Apley\'s System of Orthopaedics and Fractures 9th ed

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Apley’s System of Orthopaedics and Fractures

Alan Graham Apley 1914–1996 Inspired teacher, wise mentor and joyful friend

Louis Solomon MD FRCS Emeritus Professor of Orthopaedics Bristol UK David Warwick MD FRCS FRCSOrth Eur Dip Hand Surg Consultant Hand Surgeon Reader in Orthopaedic Surgery University of Southampton Southampton UK Selvadurai Nayagam BSc MChOrth FRCSOrth Consultant Orthopaedic Surgeon Royal Liverpool Children’s Hospital and The Royal Liverpool University Hospital Liverpool UK

Apley’s System of Orthopaedics and Fractures Ninth Edition

First published in Great Britain in 1959 by Butterworths Medical Publications Second edition 1963 Third edition 1968 Fourth edition 1973 Fifth edition 1977 Sixth edition 1982 Seventh edition published in 1993 by Butterworth Heineman. Eight edition published in 2001 by Arnold. This ninth edition published in 2010 by Hodder Arnold, an imprint of Hodder Education, an Hachette UK Company, 338 Euston Road, London NW1 3BH http://www.hodderarnold.com © 2010 Solomon, Warwick, Nayagam All rights reserved. Apart from any use permitted under UK copyright law, this publication may only be reproduced, stored or transmitted, in any form, or by any means, with prior permission in writing of the publishers or in the case of reprographic production, in accordance with the terms of licences issued by the Copyright Licensing Agency. In the United Kingdom such licences are issued by the Copyright Licensing Agency: 90 Tottenham Court Road, London W1T 4LP Whilst the advice and information in this book are believed to be true and accurate at the date of going to press, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made. In particular (but without limiting the generality of the preceding disclaimer) every effort has been made to check drug dosages; however it is still possible that errors have been missed. Furthermore, dosage schedules are constantly being revised and new side-effects recognized. For these reasons the reader is strongly urged to consult the drug companies’ printed instructions before administering any of the drugs recommended in this book.

British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloging-in-Publication Data A catalog record for this book is available from the Library of Congress ISBN-13 ISBN-13 [ISE]

978 0 340 942 055 978 0 340 942 086 (International Students’ Edition, restricted territorial availability)

1 2 3 4 5 6 7 8 9 10 Commissioning Editor: Gavin Jamieson Project Editor: Francesca Naish Production Controller: Joanna Walker Cover Designer: Helen Townson Indexer: Laurence Errington Additional editorial services provided by Naughton Project Management. Cover image © Linda Bucklin/stockphoto.com Typeset in 10 on 12pt Galliard by Phoenix Photosetting, Chatham, Kent Printed and bound in India by Replika Press What do you think about this book? Or any other Hodder Arnold title? Please visit our website: www.hodderarnold.com

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Dedication

To our students, trainees and patients, all of whom have helped to make our lives interesting, stimulating and worthwhile; and also to our wives and children (and grand-children) who have tolerated our absences – both material and spiritual – while preparing this new edition.

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Contents

Contributors Preface Acknowledgements List of abbreviations used PART 1:

GENERAL ORTHOPAEDICS 1 Diagnosis in orthopaedics Louis Solomon, Charles Wakeley 2 Infection Louis Solomon, H. Srinivasan, Surendar Tuli, Shunmugam Govender 3 Inflammatory rheumatic disorders Christopher Edwards, Louis Solomon 4 Crystal deposition disorders Louis Solomon 5 Osteoarthritis Louis Solomon 6 Osteonecrosis and related disorders Louis Solomon 7 Metabolic and endocrine disorders Louis Solomon 8 Genetic disorders, skeletal dysplasias and malformations Deborah Eastwood, Louis Solomon 9 Tumours Will Aston, Timothy Briggs, Louis Solomon 10 Neuromuscular disorders Deborah Eastwood, Thomas Staunton, Louis Solomon 11 Peripheral nerve injuries David Warwick, H. Srinivasan, Louis Solomon 12 Orthopaedic operations Selvadurai Nyagam, David Warwick

PART 2:

ix xi xiii xv

3 29 59 77 85 103 117 151 187 225 269 303

REGIONAL ORTHOPAEDICS 13 The shoulder and pectoral girdle Andrew Cole, Paul Pavlou 14 The elbow and forearm David Warwick 15 The wrist David Warwick, Roderick Dunn 16 The hand David Warwick, Roderick Dunn 17 The neck Stephen Eisenstein, Louis Solomon 18 The back Stephen Eisenstein, Surendar Tuli, Shunmugam Govender

337 369 383 413 439 453

19 The hip Louis Solomon, Reinhold Ganz, Michael Leunig, Fergal Monsell, Ian Learmonth 20 The knee Louis Solomon, Theo Karachalios 21 The ankle and foot Gavin Bowyer PART 3:

Epilogue: Global Orthopaedics Christopher Lavy, Felicity Briggs Index

CONTENTS

547 587

FRACTURES AND JOINT INJURIES 22 The management of major injuries David Sutton, Max Jonas 23 Principles of fractures Selvadurai Nayagam 24 Injuries of the shoulder, upper arm and elbow Andrew Cole, Paul Pavlou, David Warwick 25 Injuries of the forearm and wrist David Warwick 26 Hand injuries David Warwick 27 Injuries of the spine Stephen Eistenstein, Wagih El Masry 28 Injuries of the pelvis Louis Solomon 29 Injuries of the hip and femur Selvadurai Nayagam 30 Injuries of the knee and leg Selvadurai Nayagam 31 Injuries of the ankle and foot Gavin Bowyer

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493

627 687 733 767 787 805 829 843 875 907

935 939

Contributors

Principal Authors Louis Solomon MD FRCS Eng FRCS Ed Emeritus Professor of Orthopaedic Surgery Honorary Consultant Orthopaedic Surgeon Bristol Royal Infirmary, Bristol, UK Selvadurai Nayagam BSc, MChOrth FRCSOrth Consultant Orthopaedic Surgeon Royal Liverpool Children’s Hospital and The Royal Liverpool University Hospital Liverpool, UK David Warwick MD BM FRCS FRCS (Orth) Eur Dip Hand Surg Consultant Hand Surgeon Reader in Orthopaedic Surgery University of Southampton, Southampton, UK

Timothy William Roy Briggs MD(Res) MCh(Orth) FRCS FRCS Ed Professor and Consultant Orthopaedic Surgeon Joint Medical Director Joint Training Programme Director Royal National Orthopaedic Hospital Stanmore, UK Tumours Andrew Spencer Cole BSc MBBS FRCS(TR&Orth) Consultant Orthopaedic Surgeon Southampton University Hospitals Southampton, UK The Shoulder and Pectoral Girdle Injuries of the Shoulder and Upper Arm and elbow Roderick Dunn MBBS DMCC FRCS(Plast) Consultant Plastic, Reconstructive and Hand Surgeon, Odstock Centre for Burns, Plastic and Maxillofacial Surgery, Salisbury District Hospital Salisbury, UK The Wrist and The Hand: Congenital Variations

Contributing Authors Will Aston BSc, MBBS, FRCS Ed(TR&Orth) Consultant Orthopaedic Surgeon Royal National Orthopaedic Hospital Stanmore, UK Tumours Gavin William Bowyer MA MChir FRCS(Orth) Consultant Trauma and Orthopaedic Surgeon and Honorary Senior Lecturer Southampton University Hospitals Southampton, UK The Ankle and Foot Injuries of the ankle and foot Felicity Briggs MA(Oxon) UK Research Assistant and Graduate Medical Student Epilogue: Global Orthopaedics

Deborah Eastwood FRCS Consultant Orthopaedic Surgeon and Hon Senior Lecturer University College London; Great Ormond Street Hospital for Children London, UK Genetic Disorders, Dysplasias and Malformations Neuromuscular Disorders Christopher J Edwards BSc MBBS FRCP MD Consultant Rheumatologist & Honorary Senior Lecturer Associate Director Wellcome Trust Clinical Research Facility Southampton University Hospitals NHS Trust Southampton General Hospital, UK Inflammatory Rheumatic Disorders

Stephen Eisenstein PhD FRCS(Ed) Hon Professor, Keele University; Emeritus Director Centre for Spinal Studies; The Robert Jones and Agnes Hunt Orthopaedic Hospital, Shropshire, UK The Neck The Back Injuries of the Spine Reinhold Ganz MD Professor and Chairman Emeritus Orthopaedic Department Inselspital University of Bern, Switzerland The Hip: Femoro-acetabular Impingement Shunmugam Govender MBBS MD FRCS FC(Orth) (SA) Professor and Head of Department of Orthopaedics; Director of Spinal Services King George V Hospital; Nelson R Mandela School of Medicine Durban, South Africa Infection The Back: Infections of the Spine Max Jonas MBBS FRCA Consultant and Senior Lecturer in Critical Care Southampton University Hospitals NHS Trust Southampton, UK The Management of Major Injuries Theo Karachalios MD DSc Associate Professor in Orthopaedics, School of Health Sciences, University of Thessalia University General Hospital of Larissa Hellenic Republic The Knee

CONTRIBUTORS

Christopher Lavy OBE MD MCh FRCS Hon Professor and Consultant, Nuffield Department of Orthopaedic Surgery, University of Oxford, UK Epilogue: Global Orthopaedics

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Ian Douglas Learmonth MB ChB FRCS Ed FRCS FCS(SA)Orth Emeritus Professor, ; Honorary Consultant, University Hospitals, Bristol; Honorary Consultant, North Bristol Trust, UK Total Hip Replacement Michael Leunig MD Head of Orthopaedics, Lower Extremities Schulthess Klinik, Zurich, Switzerland The Hip: Femoro-Acetabular Impingement

Wagih S El Masry FRCS FRCP Consultant Surgeon in Spinal Injuries; Director, Midlands Centre for Spinal Injuries President International Spinal Cord Society (ISCOS) RJ & AH Orthopaedic Hospital, Oswestry, UK Injuries of the Spine Fergal P Monsell MSc FRCS FRCS(Orth) Consultant Paediatric Orthopaedic Surgeon Bristol Royal Hospital for Children Bristol, UK The Hip: Disorders in Children Paul Pavlou BSc (Hons) MB BS MRCS Orthopaedic Registrar, Wessex training scheme The Shoulder and Pectoral Girdle Injuries of the Shoulder H. Srinivasan MB BS FRCS FRCS Ed DSc (Hon) Formerly Senior Orthopaedic Surgeon Central Leprosy Teaching & Research Institute Chengalpattu (Tamil Nadu), India; Director Central JALMA Institute for Leprosy (ICMR), Agra (UP), India; and Editor Indian Journal of Leprosy Infection and Peripheral Nerve Disorders: Leprosy Thomas G Staunton MB FRCP(C) FRCP Consultant Neurologist Norfolk and Norwich University Hospital; Consultant Clinical Neurophysiologist Robert Jones and Agnes Hunt Orthopaedic Hospital, Shropshire, UK Neuromuscular Disorders: Neurophysiological Studies David Sutton BM DA FRCA Department of Anaesthetics Southampton General Hospital Southampton, UK Management of Major Injuries Surendar Mohan Tuli MBBS MS PhD Senior Consultant in Spinal Diseases and Orthopaedics, Vimhans Hospital, New Delhi, India Infection: Tuberculosis of Bones and Joints The Back Charles J Wakeley BSc MBBS FRCS FRCS Ed FRCR Consultant Radiologist, Department of Radiology University Hospital Bristol NHS Foundation Trust Bristol, UK Diagnosis in Orthopaedics: Imaging

Preface

When Alan Apley produced the first edition of his System of Orthopaedics and Fractures 50 years ago he saw it as an aid to accompany the courses that he conducted for aspiring surgeons who were preparing for the FRCS exams. With characteristic humour, he called the book ‘a prophylactic against writer’s cramp’. Pictures were unnecessary: if you had any sense (and were quick enough to get on the heavily oversubscribed Apley Course) you would be treated to an unforgettable display of clinical signs by one of the most gifted of teachers. You also learnt how to elicit those signs by using a methodical clinical approach – the Apley System. The Fellowship exam was heavily weighted towards clinical skills. Miss an important sign or stumble over how to examine a knee or a finger and you could fail outright. What Apley taught you was how to order the steps in physical examination in a way that could be applied to every part of the musculoskeletal system. ‘Look, Feel, Move’ was the mantra. He liked to say that he had a preference for four-letter words. And always in that order! Deviate from the System by grasping a patient’s leg before you look at it minutely, or by testing the movements in a joint before you feel its contours and establish the exact site of tenderness and you risked becoming an unwilling participant in a theatrical comedy. Much has changed since then. With each new edition the System has been expanded to accommodate new tests and physical manoeuvres developed in the tide of super-specialisation. Laboratory investigations have become more important and imaging techniques have advanced out of all recognition. Clinical classifications have sprung up and attempts are now made to find a numerical slot for every imaginable fracture. No medical textbook is complete without its ‘basic science’ component, and advances are so rapid that changes become necessary within the period of writing a single edition. The present volume is no exception: new bits were still being added right up to the time of proof-reading. For all that, we have retained the familiar structure of the Apley System. As in earlier editions, the book is divided into three sections: General Orthopaedics,

covering the main types of musculoskeletal disorder; Regional Orthopaedics, where we engage with these disorders in specific parts of the body; and thirdly Fractures and Joint Injuries. In a major departure from previous editions, we have enlisted the help of colleagues who have particular experience of conditions with which we as principal authors are less familiar. Their contributions are gratefully acknowledged. Even here, though, we have sought their permission to ‘edit’ their material into the Apley mould so that the book still has the sound and ‘feel’ of a single authorial voice. For the second edition of the book, in 1963, Apley added a new chapter: ‘The Management of Major Accidents’. Typically frank, he described the current arrangements for dealing with serious accidents as “woefully inadequate” and offered suggestions based on the government’s Interim Report on Accident Services in Great Britain and Ireland (1961). There has been a vast improvement since then and the number of road accident deaths today is half of what it was in the 1960’s (Department of Transport statistics). So important is this subject that the relevant section has now been re-written by two highly experienced Emergency and Intensive Care Physicians and is by far the longest chapter in the present edition. Elsewhere the text has been brought completely up to date and new pictures have been added. In most cases the illustrations appear as composites – a series of images that tell a story rather than a single ‘typical’ picture at one moment in the development of some disorder. At the beginning of each Regional chapter, in a run of pictures we show the method of examining that region: where to stand, how to confront the patient and where to place our hands. For the experienced reader this may seem like old hat; but then we have designed this book for orthopaedic surgeons of all ages and all levels of experience. We all have something to learn from each other. As before, operations are described only in outline, emphasising the principles that govern the choice of treatment, the indications for surgery, the design of the operation, its known complications and the likely outcome. Technical procedures are learnt in simulation

PREFACE

courses and, ultimately, in the operating theatre. Written instructions can only ever be a guide. Drawings are usually too idealised and ‘in theatre’ photographs are usually intelligible only to someone who has already performed that operation. Textbooks that grapple with these impediments tend to run to several volumes. The emphasis throughout is on clinical orthopaedics. We acknowledge the value of a more academic approach that starts with embryology, anatomy, biomechanics, molecular biology, physiology and pathology before introducing any patient to the reader. Instead we have chosen to present these ‘basic’ subjects in small portions where they are relevant to the clinical disorder under discussion: bone growth and metabolism in the chapter on metabolic bone disease, genetics in the chapter on osteodystrophies, and so forth. In the preface to the last edition we admitted our doubts about the value of exhaustive lists of references at the end of each chapter. We are even more divided

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about this now, what with the plethora of ‘search engines’ that have come to dominate the internet. We can merely bow our heads and say we still have those doubts and have given references only where it seems appropriate to acknowledge where an old idea started or where something new is being said that might at first sight be questioned. More than ever we are aware that there is a dwindling number of orthopaedic surgeons who grew up in the Apley era, even fewer who experienced his thrilling teaching displays, and fewer still who worked with him. Wherever they are, we trust that they will recognise the Apley flavour in this new edition. Our chief concern, however, is for the new readers who – we hope – will glean something that helps them become the next generation of teachers and mentors. LS SN DJW

Acknowledgements

Fifty years ago Apleys’ System of Orthopaedics and Fractures was written by one person – the eponymous Apley. As the years passed and new editions became ever larger, a second author appeared and then a third. Throughout those years we have always been able to get help (and sometimes useful criticism) from willing colleagues who have filled the gaps in our knowledge. Their words and hints are scattered among the pages of this book and we are forever grateful to them. For the present edition we have gone a step further and enlisted a number of those colleagues as nominated Contributing Authors. In some cases they have brought up to date existing chapters; in others they have added entirely new sections to a book that has now grown beyond the scope of two or three specialists. Their names are appropriately listed elsewhere but here we wish to thank them again for joining us. They have allowed us to mould their words into the style of the Apley System so that the text continues to carry the flavour of a unified authorial voice. We are also grateful to those colleagues who have supplied new pictures where our own collections have fallen short. In particular we want to thank Dr Santosh Rath and Dr G.N. Malaviya for pictures of peripheral deformities in leprosy, Mr Evert Smith for pictures (and helpful descriptions) of modern implants in hip replacement operations, Dr Peter Bullough who allowed us to reprint two of the excellent illustrations in his book on Orthopaedic Pathology, and Dr Asif Saifuddin for permission to use some images from his book on Musculoskeletal MRI. Others who gave us generous assistance with pictures

are Fiona Daglish, Colin Duncan, Neeraj Garg, Nikolaos Giotakis, Jagdeep Nanchahal and Badri Narayan. We have been fortunate in having friends and family around us who have given us helpful criticism on the presentation of this work. Caryn Solomon, a tireless internet traveller, found the picture for the cover and Joan Solomon gave expert advice on layout and design. James Crabtree stepped in as a model for some ‘clinical’ pictures. We are grateful to all of them. Throughout the long march to completion of this work we have enjoyed the constant help and collaboration of Francesca Naish, Gavin Jamieson, Joanna Walker and Helen Townson (our Editorial Manager, Commissioning Editor, Production Manager and Design Manager respectively) at Hodder Arnold. No problem was too complex and no obstacle too great to withstand their tireless efforts in driving this work forward. Nora Naughton and Aileen Castell (Naughton Project Management) were in the background setting up the page copies, patiently enduring the many amendments that came in over the internet. Their attention to detail has been outstanding. Finally, we want to express our deepest thanks to those nearest to us who added not a word to the text but through their support and patience made it possible for us to take so much time beyond the everyday occupations of family life to produce a single book. L. S. D.W. S. N.

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List of abbreviations used

ACA ACE ACL ACTH AFP AIDP AIDS AL ALI AM AMC ANA anti-CCP AP APC APC ARCO ARDS ARDS ARM AS ATLS AVN BASICS BCP BMD BMP BSA BVM CDH CFD CMAP CMC CMI CNS COMP CORA CPM CPPD

angulation correction axis angiotensin-converting enzyme anterior cruciate ligament adrenocorticotropic hormone alpha-fetoprotein acute inflammatory demyelinating polyneuropathy acquired immune deficiency syndrome anterolateral acute lung injury anteromedial arthrogryposis multiplex congenita antinuclear antibodies anti-cyclic citrullinated peptide antibodies anteroposterior antigen-presenting cell anteroposterior compression (injuries) Association Research Circulation Osseous adult respiratory distress syndrome acute respiratory distress syndrome awareness, recognition, management ankylosing spondylitis advanced trauma life support avascular necrosis British Association for Immediate Care basic calcium phosphate bone mineral density bone morphogenetic protein body surface area bag-valve-mask congenital dislocation of the hip congenital femoral deficiency compound muscle action potential carpo-metacarpal cell-mediated immunity central nervous system cartilage oligometric matrix protein centre of rotation of angulation continuous passive motion calcium pyrophosphate dihydrate

CRP CRPS CSF CT CVP DDH dGEMRIC DIC DIP DISH DISI DMARDs DRUJ DTH DVT DXA ECRB ECRL EDF EDG EEG EMG EMS ENL ESR ETA FAI FAST FDP FDS FFOs FPB FPE FPL GABA GAGs GCS GMFCS GPI HA

C-reactive protein complex regional pain syndrome cerebrospinal fluid computed tomography central venous pressure developmental dysplasia of the hip delayed gadolinium-enhanced MRI of cartilage disseminated intravascular coagulation distal interphalangeal (joint ) diffuse idiopathic skeletal hyperostosis dorsal intercalated segment instability disease-modifying antirheumatic drugs distal radio-ulnar joint delayed type hypersensitivity deep vein thrombosis dual-energy x-ray absorptiometry extensor carpi radialis brevis extensor carpi radialis longus elongation-derotation-flexion extensor diversion graft electroencephalography electromyography emergency medical service erythema nodosum leprosum erythrocyte sedimentation rate estimated time of arrival femoro-acetabular impingement focussed assessment sonography in trauma flexor digitorum profundus flexor digitorum superficialis functional foot orthoses flexor pollicis brevis fatal pulmonary embolism flexor pollicis longus gamma-aminobutryic acid glycosaminoglycans Glasgow Coma Scale gross motor function classification system general paralysis of the insane hydroxyapatite

HEMS HGPRT HHR HIV HLA HMSN HRT ICP ICU IL INR IP IRMER ITAP IVF JIA LCL LMA LMN LMWH MCL MCP M-CSF MED MHC MIC MIPO MIS MODS

ABBREVIATIONS

MPM MPS MRI MRSA

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MTP NCV NP NSAIDs OA OI OP OPG OPLL PA PACS PAFC PAOP PCL

helicopter emergency medical service hypoxanthine-guanine phosphoribosyltransferase humeral head replacement human immunodeficiency virus human leucocyte antigen hereditary motor and sensory neuropathy hormone replacement therapy intracerebral pressure intensive care unit interleukin international normalized ratio interphalangeal Ionising Radiation Medical Exposure Regulations intra-osseous transcutaneous amputation prosthesis in vitro fertilization juvenile idiopathic arthritis lateral collateral ligament laryngeal mask airway lower motor neuron low molecular weight heparin medial collateral ligament metacarpo-phalangeal (joint) macrophage colony-stimulating factor multiple epiphyseal dysplasia major histocompatibility complex minimal inhibitory concentration minimally invasive percutaneous osteosynthesis minimally invasive surgery multiple organ failure or dysfunction syndrome mortality prediction model mucopolysaccharidoses magnetic resonance imaging methicillin-resistant Staphylococcus aureus metatarsophalangeal (joint) nerve conduction velocity nasopharyngeal non-steroidal anti-inflammatory drugs osteoarthritis osteogenesis imperfecta oropharyngeal osteoprotegerin ossification of the posterior longitudinal ligament posteroanterior Picture Archiving and Communication System pulmonary artery flotation catherization pulmonary artery occlusion pressure posterior cruciate ligament

PCR PD PE PEA PEEP PET PFFD PIP PL PM PMMA PNS PPE PPS PTH PTS PVNS QCT QUS RA RANKL RF RR RSD RSI SACE SAMU SAPHO SCFE SCIWORA SDD SE SED SEMLS SIRS SLAP SLE SMR SMUR SNAP SNPs SONK SOPs SPECT SSEP STIR STT SCIWORA

polymerase chain reaction proton density pulmonary embolism pulseless electrical activity positive end-expiratory pressure positron emission tomography proximal focal femoral deficiency proximal interphalangeal (joint) posterolateral posteromedial polymethylmethacrylate peripheral nervous system personal protective equipment post-polio syndrome parathyroid hormone post-thrombotic syndrome pigmented villonodular synovitis quantitative computed tomography quantitative ultrasonometry radiographic absorptiometry and rheumatoid arthritis receptor activator of nuclear factorligand rheumatoid factor reversal reaction reflex sympathetic dystrophy rapid sequence induction serum angiotensin converting enzyme Services de l’Aide Medical Urgente for synovitis, acne, pustulosis, hyperostosis and osteitis slipped capital femoral epiphysis spinal cord injury without obvious radiographic abnormality digestive tract spin echo spondyloepiphyseal dysplasia single event multi-level surgery systemic inflammatory response superior labrum, anterior and posterior (tear) systemic lupus erythematosus standardized mortality ratio Services Mobile d’Urgence et de Reamination sensory nerve action potential single nucleotide polymorphisms ‘spontaneous’ osteonecrosis of the knee standard operating procedure single photon emission computed tomography somatosensory evoked responses short-tau inversion recovery scaphoid-trapezium-trapezoid arthritis spinal cord injury without radiographic abnormality

TAR

TB 99m Tc-MDP TE TFCC TIP TNF TR TSR UHMWPE UMN

prompts one to remember thrombocytopaenia with absent radius syndrome tuberculosis 99m Tc-methyl diphosphonate time to echo triangular fibrocartilage complex terminal interphalangeal (joint) tumour necrosis factor repetition time total shoulder replacement ultra-high molecular weight polyethylene upper motor neuron

US ultrasound VACTERLS refers to the systems involved and the defects identified: vertebral, anal, cardiac, tracheal, esophageal, renal, limb and single umbilical artery. VCT voluntary counselling and testing VISI volar intercalated segment instability VP ventriculo-peritoneal VS vertical shear VTE venous thromboembolism VQC ventilation-perfusion WBC white blood cell XLPE highly cross-linked polyethylene

ABBREVIATIONS xvii

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Section 1 General Orthopaedics 1 2 3 4 5 6 7 8 9 10 11 12

Orthopaedic diagnosis Infection Inflammatory rheumatic disorders Crystal deposition disorders Osteoarthritis Osteonecrosis and related disorders Metabolic and endocrine disorders Genetic disorders, skeletal dysplasias and malformations Tumours Neuromuscular disorders Peripheral nerve injuries Orthopaedic operations

3 29 59 77 85 103 117 151 187 225 269 303

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Orthopaedic diagnosis Louis Solomon, Charles Wakeley

Orthopaedics is concerned with bones, joints, muscles, tendons and nerves – the skeletal system and all that makes it move. Conditions that affect these structures fall into seven easily remembered pairs: 1. 2. 3. 4. 5. 6. 7.

Congenital and developmental abnormalities. Infection and inflammation. Arthritis and rheumatic disorders. Metabolic and endocrine disorders. Tumours and lesions that mimic them. Neurological disorders and muscle weakness. Injury and mechanical derangement.

Diagnosis in orthopaedics, as in all of medicine, is the identification of disease. It begins from the very first encounter with the patient and is gradually modified and fine-tuned until we have a picture, not only of a pathological process but also of the functional loss and the disability that goes with it. Understanding evolves from the systematic gathering of information from the history, the physical examination, tissue and organ imaging and special investigations. Systematic, but never mechanical; behind the enquiring mind there should also be what D. H. Lawrence has called ‘the intelligent heart’. It must never be forgotten that the patient has a unique personality, a job and hobbies, a family and a home; all have a bearing upon, and are in turn affected by, the disorder and its treatment.

HISTORY ‘Taking a history’ is a misnomer. The patient tells a story; it is we the listeners who construct a history. The story may be maddeningly disorganized; the history has to be systematic. Carefully and patiently compiled, it can be every bit as informative as examination or laboratory tests. As we record it, certain key words and phrases will inevitably stand out: injury, pain, stiffness, swelling, deformity, instability, weakness, altered sensibility and loss of function or inability to do certain things that were easily accomplished before.

Each symptom is pursued for more detail: we need to know when it began, whether suddenly or gradually, spontaneously or after some specific event; how it has changed or progressed; what makes it worse; what makes it better. While listening, we consider whether the story fits some pattern that we recognize, for we are already thinking of a diagnosis. Every piece of information should be thought of as part of a larger picture which gradually unfolds in our understanding. The surgeonphilosopher Wilfred Trotter (1870–1939) put it well: ‘Disease reveals itself in casual parentheses’.

SYMPTOMS Pain Pain is the most common symptom in orthopaedics. It is usually described in metaphors that range from inexpressively bland to unbelievably bizarre – descriptions that tell us more about the patient’s state of mind than about the physical disorder. Yet there are clearly differences between the throbbing pain of an abscess and the aching pain of chronic arthritis, between the ‘burning pain’ of neuralgia and the ‘stabbing pain’ of a ruptured tendon. Severity is even more subjective. High and low pain thresholds undoubtedly exist, but to the patient pain is as bad as it feels, and any system of ‘pain grading’ must take this into account. The main value of estimating severity is in assessing the progress of the disorder or the response to treatment. The commonest method is to invite the patient to mark the severity on an analogue scale of 1–10, with 1 being mild and easily ignored and 10 being totally unbearable. The problem about this type of grading is that patients who have never experienced very severe pain simply do not know what 8 or 9 or 10 would feel like. The following is suggested as a simpler system: • Grade I (mild) Pain that can easily be ignored. • Grade II (moderate) Pain that cannot be ignored, interferes with function and needs attention or treatment from time to time.

GENERAL ORTHOPAEDICS

1

• Grade III (severe) Pain that is present most of the time, demanding constant attention or treatment. • Grade IV (excruciating) Totally incapacitating pain. Identifying the site of pain may be equally vague. Yet its precise location is important, and in orthopaedics it is useful to ask the patient to point to – rather than to say – where it hurts. Even then, do not assume that the site of pain is necessarily the site of pathology; ‘referred’ pain and ‘autonomic’ pain can be very deceptive. Referred pain Pain arising in or near the skin is usually localized accurately. Pain arising in deep structures is more diffuse and is sometimes of unexpected distribution; thus, hip disease may manifest with pain in the knee (so might an obturator hernia). This is not because sensory nerves connect the two sites; it is due to inability of the cerebral cortex to differentiate clearly between sensory messages from separate but embryologically related sites. A common example is ‘sciatica’ – pain at various points in the buttock, thigh and leg, supposedly following the course of the sciatic nerve. Such pain is not necessarily due to pressure on the sciatic nerve or the lumbar nerve roots; it may be ‘referred’ from any one of a number of structures in the lumbar spine, the pelvis and the posterior capsule of the hip joint. Autonomic pain We are so accustomed to matching

pain with some discrete anatomical structure and its known sensory nerve supply that we are apt to dismiss any pain that does not fit the usual pattern as ‘atypical’ or ‘inappropriate’ (i.e. psychologically determined). But pain can also affect the autonomic nerves that accompany the peripheral blood vessels and this is much more vague, more widespread and often associated with vasomotor and trophic changes. It is poorly understood, often doubted, but nonetheless real.

(3)

(1)

(4) (2)

(a)

(4)

(b)

1.1 Referred pain Common sites of referred pain: (1) from the shoulder; (2) from the hip; (3) from the neck; (4) from the lumbar spine.

body or a torn meniscus becoming trapped between the articular surfaces of the knee. Unfortunately, patients tend to use the term for any painful limitation of movement; much more reliable is a history of ‘unlocking’, when the offending body slips out of the way.

Swelling Swelling may be in the soft tissues, the joint or the bone; to the patient they are all the same. It is important to establish whether it followed an injury, whether it appeared rapidly (think of a haematoma or a haemarthrosis) or slowly (due to inflammation, a joint effusion, infection or a tumour), whether it is painful (suggestive of acute inflammation, infection or a tumour), whether it is constant or comes and goes, and whether it is increasing in size.

Deformity Stiffness Stiffness may be generalized (typically in systemic disorders such as rheumatoid arthritis and ankylosing spondylitis) or localized to a particular joint. Patients often have difficulty in distinguishing localized stiffness from painful movement; limitation of movement should never be assumed until verified by examination. Ask when it occurs: regular early morning stiffness of many joints is one of the cardinal symptoms of rheumatoid arthritis, whereas transient stiffness of one or two joints after periods of inactivity is typical of osteoarthritis. Locking ‘Locking’ is the term applied to the sudden

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inability to complete a particular movement. It suggests a mechanical block – for example, due to a loose

The common deformities are described by patients in terms such as round shoulders, spinal curvature, knock knees, bow legs, pigeon toes and flat feet. Deformity of a single bone or joint is less easily described and the patient may simply declare that the limb is ‘crooked’. Some ‘deformities’ are merely variations of the normal (e.g. short stature or wide hips); others disappear spontaneously with growth (e.g. flat feet or bandy legs in an infant). However, if the deformity is progressive, or if it affects only one side of the body while the opposite joint or limb is normal, it may be serious.

Weakness Generalized weakness is a feature of all chronic illness, and any prolonged joint dysfunction will inevitably

PAST HISTORY 1.2 Deformity This young girl complained of a prominent right hip; the real deformity was scoliosis.

lead to weakness of the associated muscles. However, pure muscular weakness – especially if it is confined to one limb or to a single muscle group – is more specific and suggests some neurological or muscle disorder. Patients sometimes say that the limb is ‘dead’ when it is actually weak, and this can be a source of confusion. Questions should be framed to discover precisely which movements are affected, for this may give important clues, if not to the exact diagnosis at least to the site of the lesion.

Instability The patient may complain that the joint ‘gives way’ or ‘jumps out of place’. If this happens repeatedly, it suggests abnormal joint laxity, capsular or ligamentous deficiency, or some type of internal derangement such as a torn meniscus or a loose body in the joint. If there is a history of injury, its precise nature is important.

Change in sensibility Tingling or numbness signifies interference with nerve function – pressure from a neighbouring structure (e.g. a prolapsed intervertebral disc), local ischaemia (e.g. nerve entrapment in a fibro-osseous tunnel) or a peripheral neuropathy. It is important to establish its exact distribution; from this we can tell whether the fault lies in a peripheral nerve or in a nerve root. We should also ask what makes it worse or better; a change in posture might be the trigger, thus focussing attention on a particular site.

Loss of function Functional disability is more than the sum of individual symptoms and its expression depends upon the needs of that particular patient. The patient may say ‘I can’t stand for long’ rather than ‘I have backache’; or

Patients often forget to mention previous illnesses or accidents, or they may simply not appreciate their relevance to the present complaint. They should be asked specifically about childhood disorders, periods of incapacity and old injuries. A ‘twisted ankle’ many years ago may be the clue to the onset of osteoarthritis in what is otherwise an unusual site for this condition. Gastrointestinal disease, which in the patient’s mind has nothing to do with bones, may be important in the later development of ankylosing spondylitis or osteoporosis. Similarly, certain rheumatic disorders may be suggested by a history of conjunctivitis, iritis, psoriasis or urogenital disease. Metastatic bone disease may erupt many years after a mastectomy for breast cancer. Patients should also be asked about previous medication: many drugs, and especially corticosteroids, have long-term effects on bone. Alcohol and drug abuse are important, and we must not be afraid to ask about them.

1

Orthopaedic diagnosis

‘I can’t put my socks on’ rather than ‘My hip is stiff’. Moreover, what to one patient is merely inconvenient may, to another, be incapacitating. Thus a lawyer or a teacher may readily tolerate a stiff knee provided it is painless, but to a plumber or a parson the same disorder might spell economic or spiritual disaster. One question should elicit the important information: ‘What can’t you do now that you used to be able to do?’

FAMILY HISTORY Patients often wonder (and worry) about inheriting a disease or passing it on to their children. To the doctor, information about musculoskeletal disorders in the patient’s family may help with both diagnosis and counselling. When dealing with a suspected case of bone or joint infection, ask about communicable diseases, such as tuberculosis or sexually transmitted disease, in other members of the family.

SOCIAL BACKGROUND No history is complete without enquiry about the patient’s background. There are the obvious things such as the level of care and nutrition in children; dietary constraints which may cause specific deficiencies; and, in certain cases, questions about smoking habits, alcohol consumption and drug abuse, all of which call for a special degree of tact and non-judgemental enquiry.

5

GENERAL ORTHOPAEDICS

1

Find out details about the patient’s work practices, travel and recreation: could the disorder be due to a particular repetitive activity in the home, at work or on the sportsfield? Is the patient subject to any unusual occupational strain? Has he or she travelled to another country where tuberculosis is common? Finally, it is important to assess the patient’s home circumstances and the level of support by family and friends. This will help to answer the question: ‘What has the patient lost and what is he or she hoping to regain?’

EXAMINATION In A Case of Identity Sherlock Holmes has the following conversation with Dr Watson. Watson: You appeared to read a good deal upon [your client] which was quite invisible to me. Holmes: Not invisible but unnoticed, Watson.

6

Some disorders can be diagnosed at a glance: who would mistake the facial appearance of acromegaly or the hand deformities of rheumatoid arthritis for anything else? Nevertheless, even in these cases systematic examination is rewarding: it provides information about the patient’s particular disability, as distinct from the clinicopathological diagnosis; it keeps reinforcing good habits; and, never to be forgotten, it lets the patient know that he or she has been thoroughly attended to. The examination actually begins from the moment we set eyes on the patient. We observe his or her general appearance, posture and gait. Can you spot any distinctive feature: Knock-knees? Spinal curvature? A short limb? A paralysed arm? Does he or she appear to be in pain? Do their movements look natural? Do they walk with a limp, or use a stick? A tell-tale gait may suggest a painful hip, an unstable knee or a foot-drop. The clues are endless and the game is played by everyone (qualified or lay) at each new encounter throughout life. In the clinical setting the assessment needs to be more focussed. When we proceed to the structured examination, the patient must be suitably undressed; no mere rolling up of a trouser leg is sufficient. If one limb is affected, both must be exposed so that they can be compared. We examine the good limb (for comparison), then the bad. There is a great temptation to rush in with both hands – a temptation that must be resisted. Only by proceeding in a purposeful, orderly way can we avoid missing important signs. Alan Apley, who developed and taught the system used here, shied away from using long words where short ones would do as well. (He also used to say ‘I’m

neither an inspector nor a manipulator, and I am definitely not a palpator’.) Thus the traditional clinical routine, inspection, palpation, manipulation, was replaced by look, feel, move. With time his teaching has been extended and we now add test, to include the special manoeuvres we employ in assessing neurological integrity and complex functional attributes.

Look Abnormalities are not always obvious at first sight. A systematic, step by step process helps to avoid mistakes. Shape and posture The first things to catch one’s attention are the shape and posture of the limb or the body or the entire person who is being examined. Is the patient unusually thin or obese? Does the overall posture look normal? Is the spine straight or unusually curved? Are the shoulders level? Are the limbs normally positioned? It is important to look for deformity in three planes, and always compare the affected part with the normal side. In many joint disorders and in most nerve lesions the limb assumes a characteristic posture. In spinal disorders the entire torso may be deformed. Now look more closely for swelling or wasting – one often enhances the appearance of the other! Or is there a definite lump? Skin Careful attention is paid to the colour, quality

and markings of the skin. Look for bruising, wounds and ulceration. Scars are an informative record of the past – surgical archaeology, so to speak. Colour reflects vascular status or pigmentation – for example the pallor of ischaemia, the blueness of cyanosis, the redness of inflammation, or the dusky purple of an old bruise. Abnormal creases, unless due to fibrosis, suggest underlying deformity which is not always obvious; tight, shiny skin with no creases is typical of oedema or trophic change.

1.3 Look Scars often give clues to the previous history. The faded scar on this patient’s thigh is an old operation wound – internal fixation of a femoral fracture. The other scars are due to postoperative infection; one of the sinuses is still draining.

General survey Attention is initially focussed on the

symptomatic or most obviously abnormal area, but we must also look further afield. The patient complains of the joint that is hurting now, but we may see at a glance that several other joints are affected as well.

Feeling is exploring, not groping aimlessly. Know your anatomy and you will know where to feel for the landmarks; find the landmarks and you can construct a virtual anatomical picture in your mind’s eye. The skin Is it warm or cold; moist or dry; and is sen-

sation normal? The soft tissues Can you feel a lump; if so, what are its

characteristics? Are the pulses normal? The bones and joints Are the outlines normal? Is the synovium thickened? Is there excessive joint fluid? Tenderness Once you have a clear idea of the structural features in the affected area, feel gently for tenderness. Keep your eyes on the patient’s face; a grimace will tell you as much as a grunt. Try to localize any tenderness to a particular structure; if you know precisely where the trouble is, you are halfway to knowing what it is.

Move ‘Movement’ covers several different activities: active movement, passive mobility, abnormal or unstable movement, and provocative movement.

Passive movement Here it is the examiner who moves the joint in each anatomical plane. Note whether there is any difference between the range of active and passive movement. Range of movement is recorded in degrees, starting from zero which, by convention, is the neutral or anatomical position of the joint and finishing where movement stops, due either to pain or anatomical limitation. Describing the range of movement is often made to seem difficult. Words such as ‘full’, ‘good’, ‘limited’ and ‘poor’ are misleading. Always cite the range or span, from start to finish, in degrees. For example, ‘knee flexion 0–140°’ means that the range of flexion is from zero (the knee absolutely straight) through an arc of 140 degrees (the leg making an acute angle with the thigh). Similarly, ‘knee flexion 20–90°’ means that flexion begins at 20 degrees (i.e. the joint cannot extend fully) and continues only to 90 degrees. For accuracy you can measure the range of movement with a goniometer, but with practice you will learn to estimate the angles by eye. Normal ranges of movement are shown in chapters dealing with individual joints. What is important is always to compare the symptomatic with the asymptomatic or normal side. While testing movement, feel for crepitus. Joint crepitus is usually coarse and fairly diffuse; tenosynovial crepitus is fine and precisely localized to the affected tendon sheath.

1

Orthopaedic diagnosis

Feel

degree of mobility and whether it is painful or not. Active movement is also used to assess muscle power.

Active movement Ask the patient to move without

your assistance. This will give you an idea of the

Unstable movement This is movement which is inherently unphysiological. You may be able to shift or angulate a joint out of its normal plane of movement, thus demonstrating that the joint is unstable. Such abnormal movement may be obvious (e.g. a wobbly knee); often, though, you have to use special manoeuvres to pick up minor degrees of instability.

One of the most telling clues to diagnosis is reproducing the patient’s symptoms by applying a specific, provocative movement. Shoulder pain due to impingement of the subacromial structures may be ‘provoked’ by moving the joint in a way that is calculated to produce such impingement; the patient recognizes the similarity between this pain and his or her daily symptoms. Likewise, a patient who has had a previous dislocation or subluxation can be vividly reminded of that event by stressing the joint in such a way that it again threatens to dislocate; indeed, merely starting the movement may be so distressing that the patient goes rigid with anxiety at the anticipated result – this is aptly called the apprehension test.

Provocative movement

(a)

(b)

1.4 Feeling for tenderness (a) The wrong way – there is no need to look at your fingers, you should know where they are. (b) It is much more informative to look at the patient’s face!

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GENERAL ORTHOPAEDICS

1

(a)

(b)

(d)

(c)

(e)

(f)

1.5 Testing for movement (a) Flexion, (b) extension, (c) rotation, (d) abduction, (e) adduction. The range of movement can be estimated by eye or measured accurately using a goniometer (f).

(a)

(b)

(c)

(d)

1.6 Move (a) Active movement – the patient moves the joint. The right shoulder is normal; the left has restricted active movement. (b) Passive movement – the examiner moves the joint. (c) Unstable movement – the joint can be moved across the normal planes of action, in this case demonstrating valgus instability of the right knee. (d) Provocative movement – the examiner moves (or manipulates) the joint so as to provoke the symptoms of impending pain or dislocation. Here he is reproducing the position in which an unstable shoulder is likely to dislocate.

8

Test

Caveat

The apprehension test referred to in the previous paragraph is one of several clinical tests that are used to elicit suspected abnormalities: some examples are Thomas’ test for flexion deformity of the hip, Trendelenburg’s test for instability of the hip, McMurray’s test for a torn meniscus of the knee, Lachman’s test for cruciate ligament instability and various tests for intra-articular fluid. These and others are described in the relevant chapters in Section 2. Tests for muscle tone, motor power, reflexes and various modes of sensibility are part and parcel of neurological examination, which is dealt with on page 10.

We recognize that the sequence set out here may sometimes have to be modified. We may need to ‘move’ before we ‘look’: an early scoliotic deformity of the spine often becomes apparent only when the patient bends forwards. The sequence may also have to be altered because a patient is in severe pain or disabled: you would not try to move a limb at all in someone with a suspected fracture when an x-ray can provide the answer. When examining a child you may have to take your chances with look or feel or move whenever you can!

TERMINOLOGY

Sagittal plane

Coronal plane

Transverse plane

1.7 The principal planes of the body, as viewed in the anatomical position: sagittal, coronal and transverse.

1

Orthopaedic diagnosis

Colloquial terms such as front, back, upper, lower, inner aspect, outer aspect, bow legs, knock knees have the advantage of familiarity but are not applicable to every situation. Universally acceptable anatomical definitions are therefore necessary in describing physical attributes. Bodily surfaces, planes and positions are always described in relation to the anatomical position – as if the person were standing erect, facing the viewer, legs together with the knees pointing directly forwards, and arms held by the sides with the palms facing forwards. The principal planes of the body are named sagittal, coronal and transverse; they define the direction across which the body (or body part) is viewed in any description. Sagittal planes, parallel to each other, pass vertically through the body from front to back; the midsagittal or median plane divides the body into right and left halves. Coronal planes are also orientated vertically, corresponding to a frontal view, at right angles to the saggital planes; transverse planes pass horizontally across the body. Anterior signifies the frontal aspect and posterior the rear aspect of the body or a body part. The terms ventral and dorsal are also used for the front and the back respectively. Note, though, that the use of these terms is somewhat confusing when it comes to the foot: here the upper surface is called the dorsum and the sole is called the plantar surface. Medial means facing towards the median plane or

midline of the body, and lateral away from the median plane. These terms are usually applied to a limb, the clavicle or one half of the pelvis. Thus the inner aspect of the thigh lies on the medial side of the limb and the outer part of the thigh lies on the lateral side. We could also say that the little finger lies on the medial or ulnar side of the hand and the thumb on the lateral or radial side of the hand. Proximal and distal are used mainly for parts of the limbs, meaning respectively the upper end and the lower end as they appear in the anatomical position. Thus the knee joint is formed by the distal end of the femur and the proximal end of the tibia. Axial alignment describes the longitudinal arrangement of adjacent limb segments or parts of a single bone. The knees and elbows, for example, are normally angulated slightly outwards (valgus) while the opposite – ‘bow legs’ – is more correctly described as varus (see on page 13, under Deformity). Angulation in the middle of a long bone would always be regarded as abnormal. Rotational alignment refers to the tortile arrangement of segments of a long bone (or an entire limb) around a single longitudinal axis. For example, in the anatomical position the patellae face forwards while the feet are turned slightly outwards; a marked difference in rotational alignment of the two legs is abnormal. Flexion and extension are joint movements in the sagittal plane, most easily imagined in hinge joints like the knee, elbow and the joints of the fingers and toes. In elbows, knees, wrists and fingers flexion means bending the joint and extension means straightening it. In shoulders and hips flexion is movement in an anterior direction and extension is movement posteriorwards. In the ankle flexion is also called plantarflexion (pointing the foot downwards) and extension is called dorsiflexion (drawing the foot upwards). Thumb movements are the most complicated and are described in Chapter 16. Abduction and adduction are movements in the coronal plane, away from or towards the median plane. Not quite for the fingers and toes, though: here abduction and adduction mean away from and towards the longitudinal midline of the hand or foot! Lateral rotation and medial rotation are twisting movements, outwards and inwards, around a longitudinal axis. Pronation and supination are also rotatory movements, but the terms are applied only to movements of the forearm and the foot. Circumduction is a composite movement made up of a rhythmic sequence of all the other movements. It is possible only for ball-and-socket joints such as the hip and shoulder. Specialized movements such as opposition of the thumb, lateral flexion and rotation of the spine, and inversion or eversion of the foot, will be described in the relevant chapters.

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GENERAL ORTHOPAEDICS

1

NEUROLOGICAL EXAMINATION If the symptoms include weakness or incoordination or a change in sensibility, or if they point to any disorder of the neck or back, a complete neurological examination of the related part is mandatory. Once again we follow a systematic routine, first looking at the general appearance, then assessing motor function (muscle tone, power and reflexes) and finally testing for sensory function (both skin sensibility and deep sensibility).

Appearance Some neurological disorders result in postures that are so characteristic as to be diagnostic at a glance: the claw hand of an ulnar nerve lesion; drop wrist following radial nerve palsy; or the ‘waiter’s tip’ deformity of the arm in brachial plexus injury. Usually, however, it is when the patient moves that we can best appreciate the type and extent of motor disorder: the dangling arm following a brachial plexus injury; the flail lower limb of poliomyelitis; the symmetrical paralysis of spinal cord lesions; the characteristic drop-foot gait following sciatic or peroneal nerve damage; and the jerky, ‘spastic’ movements of cerebral palsy. Concentrating on the affected part, we look for trophic changes that signify loss of sensibility: the smooth, hairless skin that seems to be stretched too tight; atrophy of the fingertips and the nails; scars that tell of accidental burns; and ulcers that refuse to heal. Muscle wasting is

important; if localized and asymmetrical, it may suggest dysfunction of a specific motor nerve.

Muscle tone Tone in individual muscle groups is tested by moving the nearby joint to stretch the muscle. Increased tone (spasticity) is characteristic of upper motor neuron disorders such as cerebral palsy and stroke. It must not be confused with rigidity (the ‘lead-pipe’ or ‘cogwheel’ effect) which is seen in Parkinson’s disease. Decreased tone (flaccidity) is found in lower motor neuron lesions; for example, poliomyelitis. Muscle power is diminished in all three states; it is important to recognize that a ‘spastic’ muscle may still be weak.

Power Motor function is tested by having the patient perform movements that are normally activated by specific nerves. We may learn even more about composite movements by asking the patient to perform specific tasks, such as holding a pen, gripping a rod, doing up a button or picking up a pin. Testing for power is not as easy as it sounds; the difficulty is making ourselves understood. The simplest way is to place the limb in the ‘test’ position, then ask the patient to hold it there as firmly as possible and resist any attempt to change that position. The normal limb is examined first, then the affected limb, and the two are compared. Finer muscle actions, such as those of the thumb and fingers, may be reproduced by first demonstrating the movement yourself, then testing it in the unaffected limb, and then in the affected one. Muscle power is usually graded on the Medical Research Council scale: Grade 0 Grade 1 Grade 2 Grade 3 Grade 4 Grade 5

No movement. Only a flicker of movement. Movement with gravity eliminated. Movement against gravity. Movement against resistance. Normal power.

It is important to recognize that muscle weakness may be due to muscle disease rather than nerve disease. In muscle disorders the weakness is usually more widespread and symmetrical, and sensation is normal.

Tendon reflexes

10

1.8 Posture Posture is often diagnostic. This patient’s ‘drop wrist’ – typical of a radial nerve palsy – is due to carcinomatous infiltration of the supraclavicular lymph nodes on the right.

A deep tendon reflex is elicited by rapidly stretching the tendon near its insertion. A sharp tap with the tendon hammer does this well; but all too often this is performed with a flourish and with such force that the finer gradations of response are missed. It is better to employ a series of taps, starting with the most forceful and reducing the force with each successive tap until there is

Table 1.1 Nerve root supply and actions of main muscle groups Sternomastoids

Spinal accessory C2, 3, 4

Trapezius

Spinal accessory C3, 4

Diaphragm

C3, 4, 5

Deltoid

C5, 6

Supra- and infraspinatus

C5, 6

Serratus anterior

C5, 6, 7

Pectoralis major

C5, 6, 7, 8

Elbow flexion

C5, 6

extension

C5, 6

Pronation

C6

Wrist extension

C6, (7)

Finger extension flexion ab- and adduction Hip flexion

Forceful stroking of the sole normally produces flexion of the toes (or no response at all). An extensor response (the big toe extends while the others remain in flexion) is characteristic of upper motor neuron disorders. This is the Babinski sign – a type of withdrawal reflex which is present in young infants and normally disappears after the age of 18 months.

C7, 8, T1 C8, T1 L1, 2, 3 L5, S1 L2, 3, 4

abduction

L4, 5, S1

Knee extension

L(2), 3, 4 L5, S1 L4, 5

plantarflexion

S1, 2

inversion

L4, 5

eversion

L5, S1

Toe extension

The plantar reflex

C7

adduction

Ankle dorsiflexion

The superficial reflexes are elicited by stroking the skin at various sites to produce a specific muscle contraction; the best known are the abdominal (T7–T12), cremasteric (L1, 2) and anal (S4, 5) reflexes. These are corticospinal (upper motor neuron) reflexes. Absence of the reflex indicates an upper motor neuron lesion (usually in the spinal cord) above that level.

C7, (8)

extension

flexion

Superficial reflexes

1

C7

Supination

flexion

from the normal central inhibition and there is an exaggerated response to tendon stimulation. This may manifest as ankle clonus: a sharp upward jerk on the foot (dorsiflexion) causes a repetitive, ‘clonic’ movement of the foot; similarly, a sharp downward push on the patella may elicit patellar clonus.

Orthopaedic diagnosis

no response. Comparing the two sides in this way, we can pick up fine differences showing that a reflex is ‘diminished’ rather than ‘absent’. In the upper limb we test biceps, triceps and brachioradialis; and in the lower limb the patellar and Achilles tendons. The tendon reflexes are monosynaptic segmental reflexes; that is, the reflex pathway takes a ‘short cut’ through the spinal cord at the segmental level. Depression or absence of the reflex signifies interruption of the pathway at the posterior nerve root, the anterior horn cell, the motor nerve root or the peripheral nerve. It is a reliable pointer to the segmental level of dysfunction: thus, a depressed biceps jerk suggests pressure on the fifth or sixth cervical (C5 or 6) nerve roots while a depressed ankle jerk signifies a similar abnormality at the first sacral level (S1). An unusually brisk reflex, on the other hand, is characteristic of an upper motor neuron disorder (e.g. cerebral palsy, a stroke or injury to the spinal cord); the lower motor neuron is released

L5

flexion

S1

abduction

S1, 2

1.9 Examination Dermatomes supplied by the spinal nerve roots.

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GENERAL ORTHOPAEDICS

1

12

Sensibility Sensibility to touch and to pinprick may be increased (hyperaesthesia) or unpleasant (dysaesthesia) in certain irritative nerve lesions. More often, though, it is diminished (hypoaesthesia) or absent (anaesthesia), signifying pressure on or interruption of a peripheral nerve, a nerve root or the sensory pathways in the spinal cord. The area of sensory change can be mapped out on the skin and compared with the known segmental or dermatomal pattern of innervation. If the abnormality is well defined it is an easy matter to establish the level of the lesion, even if the precise cause remains unknown. Brisk percussion along the course of an injured nerve may elicit a tingling sensation in the distal distribution of the nerve (Tinel’s sign). The point of hypersensitivity marks the site of abnormal nerve sprouting: if it progresses distally at successive visits this signifies regeneration; if it remains unchanged this suggests a local neuroma. Tests for temperature recognition and two-point discrimination (the ability to recognize two touchpoints a few millimetres apart) are also used in the assessment of peripheral nerve injuries. Deep sensibility can be examined in several ways. In the vibration test a sounded tuning fork is placed over a peripheral bony point (e.g. the medial malleolus or the head of the ulna); the patient is asked if he or she can feel the vibrations and to say when they disappear. By comparing the two sides, differences can be noted. Position sense is tested by asking the patient to find certain points on the body with the eyes closed – for example, touching the tip of the nose with the forefinger. The sense of joint posture is tested by grasping the big toe and placing it in different positions of flexion and extension. The patient (whose eyes are closed) is asked to say whether it is ‘up’ or ‘down’. Stereognosis, the ability to recognize shape and texture by feel alone, is tested by giving the patient (again with eyes closed) a variety of familiar objects to hold and asking him or her to name each object. The pathways for deep sensibility run in the posterior columns of the spinal cord. Disturbances are, therefore, found in peripheral neuropathies and in spinal cord lesions such as posterior column injuries or tabes dorsalis. The sense of balance is also carried in the posterior columns. This can be tested by asking the patient to stand upright with his or her eyes closed; excessive body sway is abnormal (Romberg’s sign).

sign, a full examination of the central nervous system will be necessary.

EXAMINING INFANTS AND CHILDREN Paediatric practice requires special skills. You may have no first-hand account of the symptoms; a baby screaming with pain will tell you very little, and overanxious parents will probably tell you too much. When examining the child, be flexible. If he or she is moving a particular joint, take your opportunity to examine movement then and there. You will learn much more by adopting methods of play than by applying a rigid system of examination. And leave any test for tenderness until last! INFANTS AND SMALL CHILDREN The baby should be undressed, in a warm room, and placed on the examining couch. Look carefully for birthmarks, deformities and abnormal movements – or absence of movement. If there is no urgency or distress, take time to examine the head and neck, including facial features which may be characteristic of specific dysplastic syndromes. The back and limbs are then examined for abnormalities of position or shape. Examining for joint movement can be difficult. Active movements can often be stimulated by gently stroking the limb. When testing for passive mobility, be careful to avoid frightening or hurting the child. In the neonate, and throughout the first two years of life, examination of the hips is mandatory, even if the child appears to be normal. This is to avoid missing the subtle signs of developmental dysplasia of the hips (DDH) at the early stage when treatment is most effective. It is also important to assess the child’s general development by testing for the normal milestones which are expected to appear during the first two years of life.

NORMAL DEVELOPMENTAL MILESTONES Newborn

Grasp reflex present Morrow reflex present

3–6 months

Holds head up unsupported

6–9 months

Able to sit up

Cortical and cerebellar function

9–12 months

Crawling and standing up

A staggering gait may imply an unstable knee – or a disorder of the spinal cord or cerebellum. If there is no musculoskeletal abnormality to account for the

9–18 months

Walking

18–24 months

Running

PHYSICAL VARIATIONS AND DEFORMITIES

JOINT LAXITY Children’s joints are much more mobile than those of most adults, allowing them to adopt postures that would be impossible for their parents. An unusual degree of joint mobility can also be attained by adults willing to submit to rigorous exercise and practice, as witness the performances of professional dancers and athletes, but in most cases, when the exercises stop, mobility gradually reverts to the normal range. Persistent generalized joint hypermobility occurs in about 5% of the population and is inherited as a simple mendelian dominant. Those affected describe themselves as being ‘double-jointed’: they can hyperextend their metacarpophalangeal joints beyond a right angle, hyperextend their elbows and knees and bend over with knees straight to place their hands flat on the ground; some can even ‘do the splits’ or place their feet behind their neck!

1.10 Tests for joint hypermobility Hyperextension of knees and elbows; metacarpophalangeal joints extending to 90 degrees; thumb able to touch forearm.

It is doubtful whether these individuals should be considered ‘abnormal’. However, epidemiological studies have shown that they do have a greater than usual tendency to recurrent dislocation (e.g. of the shoulder or patella). Some experience recurrent episodes of aching around the larger joints; however, there is no convincing evidence that hypermobility by itself predisposes to osteoarthritis. Generalized hypermobility is not usually associated with any obvious disease, but severe laxity is a feature of certain rare connective tissue disorders such as Marfan’s syndrome, Ehlers–Danlos syndrome, Larsen’s disease and osteogenesis imperfecta.

Deformity The boundary between variations of the normal and physical deformity is blurred. Indeed, in the development of species, what at one point of time might have been seen as a deformity could over the ages have turned out to be so advantageous as to become essential for survival. So too in humans. The word ‘deformity’ is derived from the Latin for ‘misshapen’, but the range of ‘normal shape’ is so wide that variations should not automatically be designated as deformities, and some undoubted ‘deformities’ are not necessarily pathological; for example, the generally accepted cut-off points for ‘abnormal’ shortness or tallness are arbitrary and people who in one population might be considered abnormally short or abnormally tall could, in other populations, be seen as quite ordinary. However, if one leg is short and the other long, no-one would quibble with the use of the word ‘deformity’! Specific terms are used to describe the ‘position’ and ‘shape’ of the bones and joints. Whether, in any particular case, these amount to ‘deformity’ will be determined by additional factors such as the extent to which they deviate from the norm, symptoms to which they give rise, the presence or absence of instability and the degree to which they interfere with function.

1

Orthopaedic diagnosis

OLDER CHILDREN Most children can be examined in the same way as adults, though with different emphasis on particular physical features. Posture and gait are very important; subtle deviations from the norm may herald the appearance of serious abnormalities such as scoliosis or neuromuscular disorders, while more obvious ‘deformities’ such as knock knees and bow legs may be no more than transient stages in normal development; similarly with mild degrees of ‘flat feet’ and ‘pigeon toes’. More complex variations in posture and gait patterns, when the child sits and walks with the knees turned inwards (medially rotated) or outwards (laterally rotated) are usually due to anteversion or retroversion of the femoral necks, sometimes associated with compensatory rotational ‘deformities’ of the femora and tibiae. Seldom need anything be done about this; the condition usually improves as the child approaches puberty and only if the gait is very awkward would one consider performing corrective osteotomies of the femora.

Varus and valgus It seems pedantic to replace ‘bow

legs’ and ‘knock knees’ with ‘genu varum’ and ‘genu valgum’, but comparable colloquialisms are not available for deformities of the elbow, hip or big toe; and, besides, the formality is justified by the need for clarity and consistency. Varus means that the part distal to the joint in question is displaced towards the median plane, valgus away from it. Kyphosis and lordosis Seen from the side, the normal spine has a series of curves: convex posteriorly in the thoracic region (kyphosis), and convex anteriorly in the cervical and lumbar regions (lordosis). Excessive curvature constitutes kyphotic or lordotic deformity (also sometimes referred to as hyperkyphosis and

13

GENERAL ORTHOPAEDICS

1

(a)

(b)

(c)

1.11 Varus and valgus (a) Valgus knees in a patient with rheumatoid arthritis. The toe joints are also valgus. (b) Varus knees due to osteoarthritis. (c) Another varus knee? No – the deformity here is in the left tibia due to Paget’s disease.

hyperlordosis). Colloquially speaking, excessive thoracic kyphosis is referred to as ‘round-shouldered’. Scoliosis Seen from behind, the spine is straight. Any

curvature in the coronal plane is called scoliosis. The position and direction of the curve are specified by terms such as thoracic scoliosis, lumbar scoliosis, convex to the right, concave to the left, etc.

2.

3.

Postural deformity A postural deformity is one which

the patient can, if properly instructed, correct voluntarily: e.g. thoracic ‘kyphosis’ due to slumped shoulders. Postural deformity may also be caused by temporary muscle spasm.

4.

Structural deformity A deformity which results from a

permanent change in anatomical structure cannot be voluntarily corrected. It is important to distinguish postural scoliosis from structural (fixed) scoliosis. The former is non-progressive and benign; the latter is usually progressive and may require treatment. This term is ambiguous. It seems to mean that a joint is deformed and unable to move. Not so – it means that one particular movement cannot be completed. Thus the knee may be able to flex fully but not extend fully – at the limit of its extension it is still ‘fixed’ in a certain amount of flexion. This would be called a ‘fixed flexion deformity’.

5. 6.

flexor aspect of a joint, e.g. due to a burn or following surgery. Contracture of the subcutaneous fascia The classical example is Dupuytren’s contracture in the palm of the hand. Muscle contracture Fibrosis and contracture of muscles that cross a joint will cause a fixed deformity of the joint. This may be due to deep infection or fibrosis following ischaemic necrosis (Volkmann’s ischaemic contracture). Muscle imbalance Unbalanced muscle weakness or spasticity will result in joint deformity which, if not corrected, will eventually become fixed. This is seen most typically in poliomyelitis and cerebral palsy. Tendon rupture, likewise, may cause deformity. Joint instability Any unstable joint will assume a ‘deformed’ position when subjected to force. Joint destruction Trauma, infection or arthritis may destroy the joint and lead to severe deformity.

‘Fixed deformity’

CAUSES OF JOINT DEFORMITY There are six basic causes of joint deformity: 14

1. Contracture of the overlying skin This is seen typically when there is severe scarring across the

CAUSES OF BONE DEFORMITY Bone deformities in small children are usually due to genetic or developmental disorders of cartilage and bone growth; some can be diagnosed in utero by special imaging techniques (e.g. achondroplasia); some become apparent when the child starts to walk, or later still during one of the growth spurts (e.g. hereditary multiple exostosis); and some only in early adulthood (e.g. multiple epiphyseal dysplasia). There are a myriad genetic disorders affecting the skeleton, yet

BONY LUMPS A bony lump may be due to faulty development, injury, inflammation or a tumour. Although x-ray examination is essential, the clinical features can be highly informative. A large lump attached to bone, or a lump that is getting bigger, is nearly always a tumour.

Size

Site A lump near a joint is most likely to be a tumour (benign or malignant); a lump in the shaft may be fracture callus, inflammatory new bone or a tumour. Margin A benign tumour has a well-defined margin; malignant tumours, inflammatory lumps and callus have a vague edge. Consistency A benign tumour feels bony hard; malig-

nant tumours often give the impression that they can be indented. Tenderness Lumps due to active inflammation, recent callus or a rapidly growing sarcoma are tender. Multiplicity Multiple bony lumps are uncommon: they occur in hereditary multiple exostosis and in Ollier’s disease.

1

JOINT STIFFNESS The term ‘stiffness’ covers a variety of limitations. We consider three types of stiffness in particular: (1) all movements absent; (2) all movements limited; (3) one or two movements limited. All movements absent Surprisingly, although movement is completely blocked, the patient may retain such good function that the restriction goes unnoticed until the joint is examined. Surgical fusion is called ‘arthrodesis’; pathological fusion is called ‘ankylosis’. Acute suppurative arthritis typically ends in bony ankylosis; tuberculous arthritis heals by fibrosis and causes fibrous ankylosis – not strictly a ‘fusion’ because there may still be a small jog of movement.

Orthopaedic diagnosis

any one of these conditions is rare. The least unusual of them are described in Chapter 8. Acquired deformities in children may be due to fractures involving the physis (growth plate); ask about previous injuries. Other causes include rickets, endocrine disorders, malunited diaphyseal fractures and tumours. Acquired deformities of bone in adults are usually the result of previous malunited fractures. However, causes such as osteomalacia, bone tumours and Paget’s disease should always be considered.

All movements limited After severe injury, movement may be limited as a result of oedema and bruising. Later, adhesions and loss of muscle extensibility may perpetuate the stiffness. With active inflammation all movements are restricted and painful and the joint is said to be ‘irritable’. In acute arthritis spasm may prevent all but a few degrees of movement. In osteoarthritis the capsule fibroses and movements become increasingly restricted, but pain occurs only at the extremes of motion. Some movements limited When one particular move-

ment suddenly becomes blocked, the cause is usually mechanical. Thus a torn and displaced meniscus may prevent extension of the knee but not flexion. Bone deformity may alter the arc of movement, such that it is limited in one direction (loss of abduction in coxa vara is an example) but movement in the opposite direction is full or even increased. These are all examples of ‘fixed deformity’.

DIAGNOSTIC IMAGING The map is not the territory Alfred Korzybski

PLAIN FILM RADIOGRAPHY

1.12 Bony lumps The lump above the left knee is hard, well-defined and not increasing in size. The clinical diagnosis of cartilage-capped exostosis (osteochondroma) is confirmed by the x-rays.

Plain film x-ray examination is over 100 years old. Notwithstanding the extraordinary technical advances of the last few decades, it remains the most useful method of diagnostic imaging. Whereas other methods may define an inaccessible anatomical structure more accurately, or may reveal some localized tissue change, the plain film provides information simultaneously on the size, shape, tissue ‘density’ and bone architecture – characteristics which, taken together,

15

1

will usually suggest a diagnosis, or at least a range of possible diagnoses.

GENERAL ORTHOPAEDICS

The radiographic image X-rays are produced by firing electrons at high speed onto a rotating anode. The resulting beam of x-rays is attenuated by the patient’s soft tissues and bones, casting what are effectively ‘shadows’ which are displayed as images on an appropriately sensitized plate or stored as digital information which is then available to be transferred throughout the local information technology (IT) network. The more dense and impenetrable the tissue, the greater the x-ray attenuation and therefore the more blank, or white, the image that is captured. Thus, a metal implant appears intensely white, bone less so and soft tissues in varying shades of grey depending on their ‘density’. Cartilage, which causes little attenuation, appears as a dark area between adjacent bone ends; this ‘gap’ is usually called the joint space, though of course it is not a space at all, merely a radiolucent zone filled with cartilage. Other ‘radiolucent’ areas are produced by fluid-filled cysts in bone. One bone overlying another (e.g. the femoral head inside the acetabular socket) produces superimposed images; any abnormality seen in the resulting combined image could be in either bone, so it is important to obtain several images from different projections in order to separate the anatomical outlines. Similarly, the bright image of a metallic foreign body superimposed upon that of, say, the femoral condyles could mean that the foreign body is in front of, inside or behind the bone. A second projection, at right angles to the first, will give the answer. Picture Archiving and Communication System (PACS) This

is the system whereby all digitally coded images are filed, stored and retrieved to enable the images to be sent to work stations throughout the hospital, to other hospitals or to the Consultant’s personal computer.

Radiographic interpretation Although radiograph is the correct word for the plain image which we address, in the present book we have chosen to retain the old-fashioned term ‘x-ray’, which has become entrenched by long usage. The process of interpreting this image should be as methodical as clinical examination. It is seductively easy to be led astray by some flagrant anomaly; systematic study is the only safeguard. A convenient sequence for examination is: the patient – the soft tissues – the bone – the joints.

16

THE PATIENT Make sure that the name on the film is that of your patient; mistaken identity is a potent source of error.

The clinical details are important; it is surprising how much more you can see on the x-ray when you know the background. Similarly, when requesting an x-ray examination, give the radiologist enough information from the patient’s history and the clinical findings to help in guiding his or her thoughts towards the diagnostic possibilities and options. For example, when considering a malignant bone lesion, simply knowing the patient’s age may provide an important clue: under the age of 10 it is most likely to be a Ewing’s sarcoma; between 10 and 20 years it is more likely to be an osteosarcoma; and over the age of 50 years it is likely to be a metastatic deposit. THE SOFT TISSUES Muscle planes are often visible and may reveal wasting or swelling. Bulging outlines around a hip, for example, may suggest a joint effusion; and soft-tissue swelling around interphalangeal joints may be the first radiographic sign of rheumatoid arthritis. Tumours tend to displace fascial planes, whereas infection tends to obliterate them. Generalized change

Localized change Is there a mass, soft tissue calcifica-

tion, ossification, gas (from penetrating wound or gas-forming organism) or the presence of a radioopaque foreign body? THE BONES Shape The bones are well enough defined to allow

one to check their general anatomy and individual shape. For example, for the spine, look at the overall Articular cartilage Epiphysis Physis (growth plate) Metaphysis Apophysis

Diaphysis

Cortex Medulla

Physis Epiphysis

1.13 The radiographic image X-ray of an anatomical specimen to show the appearance of various parts of the bone in the x-ray image.

1

(b)

(c)

(d)

(e)

(f)

1.14 X-rays – bent bones (a) Mal-united fracture. (b) Paget’s disease. (c) Dyschondroplasia. (d) Congenital pseudarthrosis. (e) Syphilitic sabre tibia. (f) Osteogenesis imperfecta.

vertebral alignment, then at the disc spaces, and then at each vertebra separately, moving from the body to the pedicles, the facet joints and finally the spinous appendages. For the pelvis, see if the shape is symmetrical with the bones in their normal positions, then look at the sacrum, the two innominate bones, the pubic rami and the ischial tuberosities, then the femoral heads and the upper ends of the femora, always comparing the two sides. Generalized change Take note of changes in bone ‘den-

sity’ (osteopaenia or osteosclerosis). Is there abnormal trabeculation, as in Paget’s disease? Are there features suggestive of diffuse metastatic infiltration, either sclerotic or lytic? Other polyostotic lesions include fibrous dysplasia, histiocyotis, multiple exostosis and Paget’s disease. With aggressive looking polyostotic

(a)

(b)

(c)

Orthopaedic diagnosis

(a)

lesions think of metastases (including myeloma and lymphoma) and also multifocal infection. By contrast, most primary tumours are monostotic. change Focal abnormalities should be approached in the same way as one would conduct a clinical analysis of a soft tissue abnormality. Start describing the abnormality from the centre and move outwards. Determine the lesion’s size, site, shape, density and margins, as well as adjacent periosteal changes and any surrounding soft tissue changes. Remember that benign lesions are usually well defined with sclerotic margins (Fig. 1.15b) and a smooth periosteal reaction. Ill-defined areas with permeative bone destruction (Fig. 1.15c) and irregular or spiculated periosteal reactions (Fig. 1.15d) suggest an aggressive lesion such as infection or a malignant tumour.

Localized

(d)

(e)

1.15 X-rays – important features to look for (a) General shape and appearance, in this case the cortices are thickened and the bone is bent (Paget’s disease). (b,c) Interior density, a vacant area may represent a true cyst (b), or radiolucent material infiltrating the bone, like the metastatic tumour in (c). (d) Periosteal reaction, typically seen in healing fractures, bone infection and malignant bone tumours – as in this example of Ewing’s sarcoma. Compare this with the smooth periosteal new bone formation shown in (e).

17

GENERAL ORTHOPAEDICS

1

1.16 Plain x-rays of the hip Stages in the development of osteoarthritis (OA). (a) Normal hip: anatomical shape and position, with joint ‘space’ (articular cartilage) fully preserved. (b) Early OA, showing joint space slightly decreased and a subarticular cyst in the femoral head. (c) Advanced OA: joint space markedly decreased; osteophytes at the joint margin. (d) Hip replacement: the cup is radiolucent but its position is shown by a circumferential wire marker. Note the differing image ‘densities’: (1) the metal femoral implant; (2) the polyethylene cup (radiolucent); (3) acrylic cement impacted into the adjacent bone. (a)

(b) 3 2 1

(c)

(d)

THE JOINTS The radiographic ‘joint’ consists of the articulating bones and the ‘space’ between them. The joint space is, of course, illusory; it is occupied by a film of synovial fluid plus radiolucent articular cartilage which varies in thickness from 1 mm or less (the carpal joints) to 6 mm (the knee). It looks much wider in children than in adults because much of the epiphysis is still cartilaginous and therefore radiolucent. Lines of increased density within the radiographic articular ‘space’ may be due to calcification of the cartilage or menisci (chondrocalcinosis). Loose bodies, if they are radio-opaque, appear as rounded patches overlying the normal structures.

The ‘joint space’

Shape Note the general orientation of the joint and the

congruity of the bone ends (actually the subarticular bone plates), if necessary comparing the abnormal with the normal opposite side. Then look for narrowing or asymmetry of the joint ‘space’: narrowing signifies loss of hyaline cartilage and is typical of infection, inflammatory arthropathies and osteoarthritis. Further stages of joint destruction are revealed by irregularity of the radiographically visible bone ends and radiolucent cysts in the subchondral bone. Bony excrescences at the joint margins (osteophytes) are typical of osteoarthritis. Erosions Look for associated bone erosions. The posi-

18

tion of erosions and symmetry help to define various

types of arthropathy. In rheumatoid arthritis and psoriasis the erosions are peri-articular (at the bare area where the hyaline cartilage covering the joint has ended and the intracapsular bone is exposed to joint fluid). In gout the erosions are further away from the articular surfaces and are described as juxta-articular. Rheumatoid arthritis is classically symmetrical and predominantly involves the metacarpophalangeal and proximal interphalangeal joints in both hands. The erosions in psoriasis are usually more feathery with ill-defined new bone at their margins. Illdefined erosions suggest active synovitis whereas corticated erosions indicate healing and chronicity.

Diagnostic associations However carefully the individual x-ray features are observed, the diagnosis will not leap ready-made off the x-ray plate. Even a fracture is not always obvious. It is the pattern of abnormalities that counts: if you see one feature that is suggestive, look for others that are commonly associated. • Narrowing of the joint space + subchondral sclerosis and cysts + osteophytes = osteoarthritis. • Narrowing of the joint space + osteoporosis + periarticular erosions = inflammatory arthritis. Add to this the typical distribution, more or less symmetrically in the proximal joints of both hands, and you must think of rheumatoid arthritis.

Limitations of conventional radiography Conventional radiography involves exposure of the patient to ionizing radiation, which under certain circumstances can lead to radiation-induced cancer. The Ionising Radiation Medical Exposure Regulations (IRMER) 2000 are embedded in European Law, requiring all clinicians to justify any exposure of the patient to ionizing radiation. It is a criminal offence to breach these regulations. Ionizing radiation can also damage a developing foetus, especially in the first trimester. As a diagnostic tool, conventional radiography provides poor soft-tissue contrast: for example, it cannot distinguish between muscles, tendons, ligaments and hyaline cartilage. Ultrasound (US), computed tomography (CT) and magnetic resonance imaging (MRI) are now employed to complement plain x-ray examination. However, in parts of the world where these techniques are not available, some modifications of plain radiography still have a useful role.

X-RAYS USING CONTRAST MEDIA Substances that alter x-ray attenuation characteristics can be used to produce images which contrast with those of the normal tissues. The contrast media used

(a)

(b)

in orthopaedics are mostly iodine-based liquids which can be injected into sinuses, joint cavities or the spinal theca. Air or gas also can be injected into joints to produce a ‘negative image’ outlining the joint cavity. Oily iodides are not absorbed and maintain maximum concentration after injection. However, because they are non-miscible, they do not penetrate well into all the nooks and crannies. They are also tissue irritants, especially if used intrathecally. Ionic, watersoluble iodides permit much more detailed imaging and, although also somewhat irritant and neurotoxic, are rapidly absorbed and excreted.

Sinography Sinography is the simplest form of contrast radiography. The medium (usually one of the ionic watersoluble compounds) is injected into an open sinus; the film shows the track and whether or not it leads to the underlying bone or joint.

1

Orthopaedic diagnosis

• Bone destruction + periosteal new bone formation = infection or malignancy until proven otherwise. • Remember: the next best investigation is either the previous radiograph or the subsequent follow-up radiograph. Sequential films demonstrate either progression of changes in active pathology or status quo in longstanding conditions.

Arthrography Arthrography is a particularly useful form of contrast radiography. Intra-articular loose bodies will produce filling defects in the opaque contrast medium. In the knee, torn menisci, ligament tears and capsular ruptures can be shown. In children’s hips, arthrography is a useful method of outlining the cartilaginous (and therefore radiolucent) femoral head. In adults with avascular necrosis of the femoral head, arthrography may show up torn flaps of cartilage. After hip replacement, loosening of a prosthesis may be revealed by seepage of the contrast medium into the cement/bone interface. In the hip, ankle, wrist and

(c)

1.17 Contrast radiography (a) Myelography shows the outline of the spinal theca. Where facilities are available, myelography has been largely replaced by CT and MRI. (b) Discography is sometimes useful: note the difference between a normal intervertebral disc (upper level) and a degenerate disc (lower level). (c) Contrast arthrography of the knee shows a small popliteal herniation.

19

GENERAL ORTHOPAEDICS

1

shoulder, the injected contrast medium may disclose labral tears or defects in the capsular structures. In the spine, contrast radiography can be used to diagnose disc degeneration (discography) and abnormalities of the small facet joints (facetography).

Myelography Myelography was used extensively in the past for the diagnosis of disc prolapse and other spinal canal lesions. It has been largely replaced by non-invasive methods such as CT and MRI. However, it still has a place in the investigation of nerve root lesions and as an adjunct to other methods in patients with back pain. The oily media are no longer used, and even with the ionic water-soluble iodides there is a considerable incidence of complications, such as low-pressure headache (due to the lumbar puncture), muscular spasms or convulsions (due to neurotoxicity, especially if the chemical is allowed to flow above the middorsal region) and arachnoiditis (which is attributed to the hyperosmolality of these compounds in relation to cerebrospinal fluid). Precautions, such as keeping the patient sitting upright after myelography, must be strictly observed. Metrizamide has low neurotoxicity and at working concentrations it is more or less isotonic with cerebrospinal fluid. It can therefore be used throughout the length of the spinal canal; the nerve roots are also well delineated (radiculography). A bulging disc, an intrathecal tumour or narrowing of the bony canal will produce characteristic distortions of the opaque column in the myelogram.

PLAIN TOMOGRAPHY Tomography provides an image ‘focused’ on a selected plane. By moving the tube and the x-ray film in opposite directions around the patient during the exposure, images on either side of the pivotal plane are deliberately blurred out. When several ‘cuts’ are studied, lesions obscured in conventional x-rays may be revealed. The method is useful for diagnosing segmental bone necrosis and depressed fractures in cancellous bone (e.g. of the vertebral body or the tibial plateau); these defects are often obscured in the plain x-ray by the surrounding intact mass of bone. Small radiolucent lesions, such as osteoid osteomas and bone abscesses, can also be revealed. A useful procedure in former years, conventional tomography has been largely supplanted by CT and MRI.

COMPUTED TOMOGRAPHY (CT) Like plain tomography, CT produces sectional images through selected tissue planes – but with much greater resolution. A further advance over conventional tomography is that the images are trans-axial (like transverse anatomical sections), thus exposing anatomical planes that are never viewed in plain film x-rays. A general (or ‘localization’) view is obtained, the region of interest is selected and a series of crosssectional images is produced and digitally recorded. ‘Slices’ through the larger joints or tissue masses may be 5–10 mm apart; those through the small joints or intervertebral discs have to be much thinner.

(a)

(c)

20

(b)

(d)

1.18 Computed tomography (CT) The plain x-ray (a) shows a fracture of the vertebral body but one cannot tell precisely how the bone fragments are displaced. The CT (b) shows clearly that they are dangerously close to the cauda equina. (c) Congenital hip dislocation, defined more clearly by (d) three-dimensional CT reconstruction.

1

(b)

(c)

1.19 CT for complex fractures (a) A plain x-ray shows a fracture of the calcaneum but the details are obscure. CT sagittal and axial views (b,c) give a much clearer idea of the seriousness of this fracture.

New multi-slice CT scanners provide images of high quality from which multi-planar reconstructions in all three orthogonal planes can be produced. Three-dimensional surface rendered reconstructions and volume rendered reconstructions may help in demonstrating anatomical contours, but fine detail is lost in this process.

Clinical applications Because CT achieves excellent contrast resolution and spatial localization, it is able to display the size, shape and position of bone and soft-tissue masses in transverse planes. Image acquisition is extremely fast. The technique is therefore ideal for evaluating acute trauma to the head, spine, chest, abdomen and pelvis. It is better than MRI for demonstrating fine bone detail and soft-tissue calcification or ossification. Computed tomography is also an invaluable tool for assisting with pre-operative planning in secondary fracture management. It is routinely used for assessing injuries of the vertebrae, acetabulum, proximal tibial plateau, ankle and foot – indeed complex fractures and fracture-dislocations at any site. It is also useful in the assessment of bone tumour size and spread, even if it is unable to characterize the tumour type. It can be employed for guiding softtissue and bone biopsies.

Limitations An important limitation of CT is that it provides relatively poor soft-tissue contrast when compared with MRI. A major disadvantage of this technique is the relatively high radiation exposure to which the patient is subjected. It should, therefore, be used with discretion.

Orthopaedic diagnosis

(a)

MAGNETIC RESONANCE IMAGING (MRI) Magnetic resonance imaging produces cross-sectional images of any body part in any plane. It yields superb soft-tissue contrast, allowing different soft tissues to be clearly distinguished, e.g. ligaments, tendons, muscle and hyaline cartilage. Another big advantage of MRI is that it does not use ionizing radiation. It is, however, contra-indicated in patients with pacemakers and possible metallic foreign bodies in the eye or brain, as these could potentially move when the patient is introduced into the scanner’s strong magnetic field. Approximately 5% of patients cannot tolerate the scan due to claustrophobia, but newer scanners are being developed to be more ‘open’.

MRI physics The patient’s body is placed in a strong magnetic field (between 5 and 30 000 times the strength of the earth’s magnetic field). The body’s protons have a positive charge and align themselves along this strong external magnetic field. The protons are spinning and can be further excited by radiofrequency pulses, rather like whipping a spinning top. These spinning positive charges will not only induce a small magnetic field of their own, but will produce a signal as they relax (slow down) at different rates. A proton density map is recorded from these signals and plotted in x, y and z coordinates. Different speeds of tissue excitation with radiofrequency pulses (repetition times, or TR) and different intervals between recording these signals (time to echo, or TE) will yield anatomical pictures with varying ‘weighting’ and characteristics. T1 weighted (T1W) images have a high spatial resolution and provide good anatomical-looking pictures. T2 weighted (T2W) images give more information about the physiological characteristics of the tissue. Proton density (PD) images are also described as

21

GENERAL ORTHOPAEDICS

1

(a)

1.21 MRI A case of septic arthritis of the ankle, suspected from the plain x-ray (a) and confirmed by MRI (b). 1.20 Magnetic resonance imaging MRI is ideal for displaying soft-tissue injuries, particularly tears of the menisci of the knee; this common injury is clearly shown in the picture.

‘balanced’ or ‘intermediate’ as they are essentially a combination of T1 and T2 weighting and yield excellent anatomical detail for orthopaedic imaging. Fat suppression sequences allow highlighting of abnormal water, which is particularly useful in orthopaedics when assessing both soft tissue and bone marrow oedema.

Intravenous contrast Just as in CT, enhancement by intravenous contrast relies on an active blood supply and leaky cell membranes. Areas of inflammation and active tumour tissue will be highlighted. Gadolinium compounds are employed as they have seven unpaired electrons and work by creating local magnetic field disturbances at their sites of accumulation.

Indirect arthrography Gadolinium compounds administered intravenously will be secreted through joint synovium into joint effusions resulting in indirect arthrography. However, there is no additional distension of the joint, which limits its effect.

Direct arthrography

22

(b)

Direct puncture of joints under image guidance with a solution containing dilute gadolinium (1:200 concentration) is routinely performed. This provides a positive contrast within the joint and distension of the joint capsule, thereby separating many of the closely applied soft-tissue structures that can be demonstrated on the subsequent MRI scan.

Clinical applications Magnetic resonance imaging is becoming cheaper and more widely available. Its excellent anatomical detail, soft-tissue contrast and multi-planar capability make it ideal for non-invasive imaging of the musculoskeletal system. The multi-planar capability provides accurate cross-sectional information and the axial images in particular will reveal detailed limb compartmental anatomy. The excellent soft-tissue contrast allows identification of similar density soft tissues, for example in distinguishing between tendons, cartilage and ligaments. By using combinations of T1W, T2W and fat suppressed sequences, specific abnormalities can be further characterized with tissue specificity, so further extending the diagnostic possibilities. In orthopaedic surgery, MRI of the hip, knee, ankle, shoulder and wrist is now fairly commonplace. It can detect the early changes of bone marrow oedema and osteonecrosis before any other imaging modality. In the knee, MRI is as accurate as arthroscopy in diagnosing meniscal tears and cruciate ligament injuries. Bone and soft-tissue tumours should be routinely examined by MRI as the intraosseous and extra-osseous extent and spread of disease, as well as the compartmental anatomy, can be accurately assessed. Additional use of fat suppression sequences determines the extent of peri-lesional oedema and intravenous contrast will demonstrate the active part of the tumour. Intravenous contrast is used to distinguish vascularized from avascular tissue, e.g. following a scaphoid fracture, or in defining active necrotic areas of tumour, or in demonstrating areas of active inflammation. Direct MRI arthrography is used to distend the joint capsule and outline labral tears in the shoulder and the hip. In the ankle, it provides the way to demonstrate anterolateral impingement and assess the integrity of the capsular ligaments.

Limitations

DIAGNOSTIC ULTRASOUND High-frequency sound waves, generated by a transducer, can penetrate several centimetres into the soft tissues; as they pass through the tissue interfaces some of these waves are reflected back (like echoes) to the transducer, where they are registered as electrical signals and displayed as images on a screen. Unlike xrays, the image does not depend on tissue density but rather on reflective surfaces and soft-tissue interfaces. This is the same principle as applies in sonar detection for ships or submarines. Depending on their structure, different tissues are referred to as highly echogenic, mildly echogenic or echo-free. Fluid-filled cysts are echo-free; fat is highly echogenic; and semi-solid organs manifest varying degrees of ‘echogenicity’, which makes it possible to differentiate between them. Real-time display on a monitor gives a dynamic image, which is more useful than the usual static images. A big advantage of this technique is that the equipment is simple and portable and can be used almost anywhere; another is that it is entirely harmless.

Clinical applications Because of the marked echogenic contrast between cystic and solid masses, ultrasonography is particularly useful for identifying hidden ‘cystic’ lesions such as haematomas, abscesses, popliteal cysts and arterial aneurysms. It is also capable of detecting intra-articular fluid and may be used to diagnose a synovial effusion or to monitor the progress of an ‘irritable hip’. Ultrasound is commonly used for assessing tendons and diagnosing conditions such as tendinitis and partial or complete tears. The rotator cuff, patellar ligament, quadriceps tendon, Achilles tendon, flexor tendons and peroneal tendons are typical examples. The same technique is used extensively for guiding needle placement in diagnostic and therapeutic joint and soft-tissue injections. Another important application is in the screening of newborn babies for congenital dislocation (or dysplasia) of the hip; the cartilaginous femoral head and

Doppler ultrasound Blood flow can be detected by using the principle of a change in frequency of sound when material is moving towards or away from the ultrasound transducer. This is the same principle as the change in frequency of the noise from a passing fire engine when travelling towards and then away from an observer. Abnormal increased blood flow can be observed in areas of inflammation or in aggressive tumours. Different flow rates can be shown by different colour representations (‘colour Doppler’).

1

Orthopaedic diagnosis

Despite its undoubted value, MRI (like all singular methods of investigation) has its limitations and it must be seen as one of a group of imaging techniques, none of which by itself is appropriate in every situation. Conventional radiographs and CT are more sensitive to soft-tissue calcification and ossification, changes which can easily be easily overlooked on MRI. Conventional radiographs should, therefore, be used in combination with MRI to prevent such errors.

acetabulum (which are, of course, ‘invisible’ on x-ray) can be clearly identified, and their relationship to each other shows whether the hip is normal or abnormal. Ultrasound imaging is quick, cheap, simple and readily available. However, the information obtained is highly operator dependent, relying on the experience and interpretation of the technician.

RADIONUCLIDE IMAGING Photon emission by radionuclides taken up in specific tissues can be recorded by a gamma camera to produce an image which reflects physiological activity in that tissue or organ. The radiopharmaceutical used for radionuclide imaging has two components: a chemical compound that is chosen for its metabolic uptake in the target tissue or organ, and a radioisotope tracer that will emit photons for detection.

Isotope bone scans For bone imaging the ideal isotope is technetium99m (99mTc): it has the appropriate energy characteristics for gamma camera imaging, it has a relatively short half-life (6 hours) and it is rapidly excreted in the urine. A bone-seeking phosphate compound is used as the substrate as it is selectively taken up and concentrated in bone. The low background radioactivity means that any site of increased uptake is readily visible. Technetium-labelled hydroxymethylene diphosphonate (99mTc-HDP) is injected intravenously and its activity is recorded at two stages: (1) the early perfusion phase, shortly after injection, while the isotope is still in the blood stream or the perivascular space thus reflecting local blood flow difference; and (2) the delayed bone phase, 3 hours later, when the isotope has been taken up in bone tissue. Normally, in the early perfusion phase the vascular soft tissues around the joints produce the sharpest (most active) image; 3 hours later this activity has faded and the bone outlines are shown more clearly, the greatest activity appearing in the cancellous tissue at the ends of the long bones.

23

GENERAL ORTHOPAEDICS

1

(a)

(b)

1.22 Radionuclide scanning (a) The plain x-ray showed a pathological fracture, probably through a metastatic tumour. (b) The bone scan revealed generalized secondaries, here involving the spine and ribs.

the site of abnormality and it should always be viewed in conjunction with other modes of imaging. Bone scintigraphy is relatively sensitive but nonspecific. One advantage is that the whole body can be imaged to look for multiple sites of pathology (occult metastases, multi-focal infection and multiple occult fractures). It is also one of the only techniques to give information about physiological activity in the tissues being examined (essentially osteoblastic activity). However, the technique carries a significant radiation burden (equivalent to approximately 200 chest x-rays) and the images yielded make anatomical localization difficult (poor spatial resolution). For localized problems MRI has superseded bone scintigraphy as it yields much greater specificity due to its superior anatomical depiction and tissue specificity.

Other radionuclide compounds Gallium-67 ( 67Ga) Gallium-67 concentrates in inflam-

Changes in radioactivity are most significant when they are localized or asymmetrical. Four types of abnormality are seen: Increased activity in the perfusion phase This is due to

increased soft-tissue blood flow, suggesting inflammation (e.g. acute or chronic synovitis), a fracture, a highly vascular tumour or regional sympathetic dystrophy. Decreased activity in the perfusion phase This is much less common and signifies local vascular insufficiency.

Indium-111-labelled leucocytes (111I) The patient’s own

white blood cells are removed and labelled with indium-111 before being re-injected into the patient’s blood stream. Preferential uptake in areas of infection is expected, thereby hoping to distinguish sites of active infection from chronic inflammation. For example, white cell uptake is more likely to be seen with an infected total hip replacement as opposed to mechanical loosening. However, as this technique is expensive and still not completely specific, it is seldom performed.

Increased activity in the delayed bone phase This could be due either to excessive isotope uptake in the osseous extracellular fluid or to more avid incorporation into newly forming bone tissue; either would be likely in a fracture, implant loosening, infection, a local tumour or healing after necrosis, and nothing in the bone scan itself distinguishes between these conditions.

SINGLE PHOTON EMISSION COMPUTED

Diminished activity in the bone phase This is due to an

TOMOGRAPHY

absent blood supply (e.g. in the femoral head after a fracture of the femoral neck) or to replacement of bone by pathological tissue.

24

matory cells and has been used to identify sites of hidden infection: for example, in the investigation of prosthetic loosening after joint replacement. However, it is arguable whether it gives any more reliable information than the 99mTc bone scan.

CLINICAL APPLICATIONS Radionuclide imaging is useful in many situations: (1) the diagnosis of stress fractures or other undisplaced fractures that are not detectable on the plain x-ray; (2) the detection of a small bone abscess, or an osteoid osteoma; (3) the investigation of loosening or infection around prostheses; (4) the diagnosis of femoral head ischaemia in Perthes’ disease or avascular necrosis in adults; (5) the early detection of bone metastases. The scintigraphic appearances in these conditions are described in the relevant chapters. In most cases the isotope scan serves chiefly to pinpoint

Single photon emission computed tomography (SPECT) is essentially a bone scan in which images are recorded and displayed in all three orthogonal planes. Coronal, sagittal and axial images at multiple levels make spatial localization of pathology possible: for example, activity in one side of a lumbar vertebra on the planar images can be further localized to the body, pedicle or lamina of the vertebra on the SPECT images.

POSITRON EMISSION TOMOGRAPHY Positron emission tomography (PET) is an advanced nuclear medicine technique that allows functional im-

BONE MINERAL DENSITOMETRY Bone mineral density (BMD) measurement is now widely used in identifying patients with osteoporosis and an increased risk of osteoporotic fractures.

Various techniques have been developed, including radiographic absorptiometry (RA), quantitative computed tomography (QCT) and quantitative ultrasonometry (QUS). However, the most widely used technique is dual energy x-ray absorptiometry (DXA). RA uses conventional radiographic equipment and measures bone density in the phalanges. QCT measures trabecular bone density in vertebral bodies, but is not widely available and involves a higher dose of ionizing radiation than DXA. QUS assesses bone mineral density in the peripheral skeleton (e.g. the wrist and calcaneus) by measuring both the attenuation of ultrasound and the variation of speed of sound through the bone. DXA employs columnated low-dose x-ray beams of two different energy levels in order to distinguish the density of bone from that of soft tissue. Although this involves the use of ionizing radiation, it is an extremely low dose. A further advantage of DXA is the development of a huge international database that allows expression of bone mineral density values in comparison to both an age and sex matched population (Z score) and also to the peak adult bone mass (T score). The T score in particular allows calculation of relative fracture risk. Individual values for both the lumbar spine and hips are obtained as there is often a discrepancy between these two sites and the fracture risk is more directly related to the value at the target area. By World Health Organization (WHO) criteria, T scores of 40 per cent carries a worse prognosis) and the stage of the lesion (Patel et al., 1998).

Treatment Treatment is conservative in the first instance and consists of measures to reduce loading of the joint and analgesics for pain. If symptoms or signs increase, operative treatment may be considered. Surgical options include arthroscopic debridement,

drilling with or without bone grafting, core decompression of the femoral condyle at a distance from the lesion, and (for patients with persistent symptoms and well-marked articular surface damage) a valgus osteotomy or unicompartmental arthroplasty. Resurfacing with osteochondral allografts has also been employed, with variable results.

CHARCOT’S DISEASE Charcot’s disease (neuropathic arthritis) is a rare cause of joint destruction. Because of loss of pain sensibility and proprioception, the articular surface breaks down and the underlying bone crumbles. Fragments of bone and cartilage are deposited in the hypertrophic synovium and may grow into large masses. The capsule is stretched and lax, and the joint becomes progressively unstable.

Clinical features The patient chiefly complains of instability; pain (other than tabetic lightning pains) is unusual. The joint is swollen and often grossly deformed. It feels like a bag of bones and fluid but is neither warm nor tender. Movements beyond the normal limits, without pain, are a notable feature. Radiologically the joint is subluxated, bone destruction is obvious and irregular calcified masses can be seen.

Treatment Patients often seem to manage quite well despite the bizarre appearances. However, marked instability may demand treatment – usually a moulded splint or caliper will do – and occasionally pain becomes intolerable. Arthrodesis is feasible but fixation is difficult and fusion is very slow. Replacement arthroplasty is not indicated.

HAEMOPHILIC ARTHRITIS

(a)

574

(b)

20.33 Osteonecrosis (a) X-ray showing the typical features of subarticular bone fragmentation and surrounding sclerosis situated in the highest part (the dome) of the medial femoral condyle. (In osteochondritis dissecans, the necrotic segment is almost always on the lateral surface of the medial femoral condyle.) (b) In this case the medial compartment was ‘unloaded’ by performing a high tibial valgus osteotomy. The patient remained pain-free for 6 years before dying of leukaemia.

The knee is the joint most commonly involved in bleeding disorders. Repeated haemorrhage leads to chronic synovitis and articular cartilage erosion. Movement is progressively restricted and the joint may end up deformed and stiff.

Clinical features Fresh bleeds cause pain and swelling of the knee, with the typical clinical signs of a haemarthrosis (see Chapter 5). Between episodes of bleeding the knee often

20

The knee

(a)

(b)

(c)

(d)

(e)

20.34 Extensor mechanism lesions These follow resisted action of the quadriceps; they usually occur at a progressively higher level with increasing age (a). (b) Osgood-Schlatter’s disease – the only one that usually does not follow a definite accident; (c) gap fracture of patella; (d) ruptured quadriceps tendon (note the suprapatellar depression); (e) ruptured rectus femoris causing a lump with a hollow below.

continues to be painful and somewhat swollen, with restricted mobility. There is a tendency to hold the knee in flexion and this may become a fixed deformity. X-rays Radiographic examination may show little

abnormality, apart from local osteoporosis. In more advanced cases the joint space is narrowed and large ‘cysts’ or erosions may appear in the subchondral bone.

age. In the elderly the injury is usually above the patella; in middle life the patella fractures; in young adults the patellar ligament can rupture. In adolescents the upper tibial apophysis is occasionally avulsed; much more often it is merely ‘strained’. Tendon rupture sometimes occurs with minimal strain; this is seen in patients with connective tissue disorders (e.g. SLE) and advanced rheumatoid disease, especially if they are also being treated with corticosteroids.

Treatment Both the haematologist and the orthopaedic surgeon should participate in treatment. The acute bleed may need aspiration, but only if this can be ‘covered’ by giving the appropriate clotting factor; otherwise it is better treated by splintage until the acute symptoms settle down. Flexion deformity must be prevented by gentle physiotherapy and intermittent splintage. If the joint is painful and eroded, operative treatment may be considered. However, although replacement arthroplasty is feasible, this should be done only after the most searching discussion with the patient, where all the risks are considered, and only if a full haematological service is available.

RUPTURE ABOVE THE PATELLA Rupture may occur in the belly of the rectus femoris. The patient is usually elderly, or on long-term corticosteroid treatment. The torn muscle retracts and forms a characteristic lump in the thigh. Function is usually good, so no treatment is required. Avulsion of the quadriceps tendon from the upper pole of the patella is seen in the same group of people. Sometimes it is bilateral. Operative repair is essential.

RUPTURE BELOW THE PATELLA RUPTURES OF THE EXTENSOR APPARATUS Resisted extension of the knee may tear the extensor mechanism. The patient stumbles on a stair, catches his or her foot while walking or running, or may only be kicking a muddy football. In all these incidents, active knee extension is prevented by an obstacle. The precise location of the lesion varies with the patient’s

This occurs mainly in young people. The ligament may rupture or may be avulsed from the lower pole of the patella. Operative repair is necessary. Pain and tenderness in the middle portion of the patellar ligament may occur in athletes; CT or ultrasonography will reveal an abnormal area. If rest fails to provide relief the paratenon should be stripped (King et al., 1990). Partial rupture or avulsion sometimes leads to a traction tendinitis and calcification in the patellar ligament – the Sinding–Larsen Johansson syndrome (see below).

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20

PELLEGRINI–STIEDA DISEASE X-rays sometimes show a plaque of bone lying next to the femoral condyle under the medial collateral ligament. Occasionally this is a source of pain. It is generally ascribed to ossification of a haematoma following a tear of the medial ligament, though a history of injury is not always forthcoming. Treatment is rarely needed.

(a)

(b)

20.35 Osgood–Schlatter’s disease This boy complained of a painful bump below the knee. X-ray shows the traction injury of the tibial apophysis.

OSGOOD–SCHLATTER DISEASE (‘APOPHYSITIS’ OF THE TIBIAL TUBERCLE) In this common disorder of adolescence the tibial tubercle becomes painful and ‘swollen’. Although often called osteochondritis or apophysitis, it is nothing more than a traction injury of the apophysis into which part of the patellar tendon is inserted (the remainder is inserted on each side of the apophysis and prevents complete separation). There is no history of injury and sometimes the condition is bilateral. A young adolescent complains of pain after activity, and of a lump. The lump is tender and its situation over the tibial tuberosity is diagnostic. Sometimes active extension of the knee against resistance is painful and x-rays may reveal fragmentation of the apophysis. Spontaneous recovery is usual but takes time, and it is wise to restrict such activities as cycling, jumping and soccer. Occasionally, symptoms persist and, if patience or wearing a back-splint during the day are unavailing, a separate ossicle in the tendon is usually responsible; its removal is then worthwhile.

TENDINITIS AND CALCIFICATION AROUND THE KNEE

CALCIFICATION IN THE MEDIAL LIGAMENT

576

Acute pain in the medial collateral ligament may be due to a soft calcific deposit among the fibres of the ligament. There may be a small, exquisitely tender lump in the line of the ligament. Pain is dramatically relieved by operative evacuation of the deposit.

PATELLAR ‘TENDINOPATHY’ (SINDING– LARSEN JOHANSSON SYNDROME). This condition was described independently by Sinding-Larsen in 1921 and Johansson in 1922. Following a strain or partial rupture of the patellar ligament the patient (usually a young athletic individual) develops a traction ‘tendinitis’ characterised by pain and point tenderness at the lower pole of the patella. Sometimes, if the condition does not settle, calcification appears in the ligament (Medlar and Lyne, 1978). CT or ultrasonography may reveal the abnormal area in the ligament. A similar disorder has been described at the proximal pole of the patella. The condition is comparable to Osgood-Schlatter’s disease and usually recovers spontaneously. If rest fails to provide relief, the abnormal area is removed and the paratenon stripped (King et al., 1990; Khan et al., 1998).

SWELLINGS OF THE KNEE The knee is prone to a number of disorders which present essentially as ‘swelling’; and, because it is such a large joint with a number of synovial recesses, the swelling is often painless until the tissues become tense. Conditions to be considered can be divided into four groups: swelling of the entire joint; swellings in front of the joint; swellings behind the joint; and bony swellings.

ACUTE SWELLING OF THE ENTIRE JOINT POST-TRAUMATIC HAEMARTHROSIS Swelling immediately after injury means blood in the joint. The knee is very painful and it feels warm, tense and tender. Later there may be a ‘doughy’ feel. Movements are restricted. X-rays are essential to see if there is a fracture; if there is not, then suspect a tear of the anterior cruciate ligament. The joint should be aspirated under aseptic conditions. If a ligament injury is suspected, examination under anaesthesia is helpful and may indicate the need for operation; otherwise a crepe bandage is applied and the leg cradled in a back-splint. Quadriceps exercises are practised from the start. The patient may get up when comfortable, retaining the back-splint until muscle control returns.

20

(c)

The knee

(a)

(b)

(d)

(e)

(f)

20.36 Swollen knees Some causes of chronic swelling in the absence of trauma: (a) tuberculous arthritis; (b) rheumatoid arthritis; (c) Charcot’s disease; (d) villous synovitis; (e) haemophilia; (f) malignant synovioma.

BLEEDING DISORDERS In patients with clotting disorders, the knee is the most common site for acute bleeds. If the appropriate clotting factor is available, the joint should be aspirated and treated as for a traumatic haemarthrosis. If the factor is not available, aspiration is best avoided; the knee is splinted in slight flexion until the swelling subsides. ACUTE SEPTIC ARTHRITIS Acute pyogenic infection of the knee is not uncommon. The organism is usually Staphylococcus aureus, but in adults gonococcal infection is almost as common. The joint is swollen, painful and inflamed; the white cell count and ESR are elevated. Aspiration reveals pus in the joint; fluid should be sent for bacteriological investigation, including anaerobic culture. Treatment consists of systemic antibiotics and drainage of the joint – ideally by arthroscopy, with irrigation and complete synovectomy; if fluid reaccumulates, it can be aspirated through a wide-bore needle. As the inflammation subsides, movement is begun, but weightbearing is deferred for 4–6 weeks. TRAUMATIC SYNOVITIS Injury stimulates a reactive synovitis; typically the swelling appears only after some hours, and subsides spontaneously over a period of days. There is inhibition of quadriceps action and the thigh wastes. The knee may need to be splinted for several days but movement should be encouraged and quadriceps exercise is essential. If the amount of fluid is considerable, its aspiration hastens muscle recovery. In addition, any internal injury will need treatment.

ASEPTIC NON-TRAUMATIC SYNOVITIS Acute swelling, without a history of trauma or signs of infection, suggests gout or pseudogout. Aspiration will provide fluid which may look turbid, resembling pus, but it is sterile and microscopy (using polarized light) reveals the crystals. Treatment with anti-inflammatory drugs is usually effective.

CHRONIC SWELLING OF THE JOINT The diagnosis can usually be made on clinical and x-ray examination. The more elusive disorders should be fully investigated by joint aspiration, synovial fluid examination, arthroscopy and synovial biopsy. ARTHRITIS The commonest causes of chronic swelling are osteoarthritis and rheumatoid arthritis. Other signs, such as deformity, loss of movement or instability, may be present and x-ray examination will usually show characteristic features. SYNOVIAL DISORDERS Chronic swelling and synovial effusion without articular destruction should suggest conditions such as synovial chondromatosis and pigmented villonodular synovitis. The diagnosis will usually be obvious on arthroscopy and can be confirmed by synovial biopsy. The most important condition to exclude is tuberculosis. There has been a resurgence of cases during the last ten years and the condition should be seriously

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20 20.37 Lumps around the knee In front: (a) prepatellar bursa; (b) infrapatellar bursa; (c) Osgood–Schlatter disease. (a)

(b)

(c)

On either side: (d) cyst of lateral meniscus; (e) cyst of medial meniscus; (f) cartilagecapped exostosis. (d)

(e)

(f)

Behind: (g) semimembranosus bursa; (h) arthrogram of popliteal cyst; (i) leaking cyst. (g)

(h)

(i)

considered whenever there is no obvious alternative diagnosis. Investigations should include Mantoux testing and synovial biopsy. The ideal is to start antituberculous chemotherapy before joint destruction occurs.

SWELLINGS IN FRONT OF THE JOINT PREPATELLAR BURSITIS (‘HOUSEMAID’S KNEE’) The fluctuant swelling is confined to the front of the patella and the joint itself is normal. This is an uninfected bursitis due not to pressure but to constant friction between skin and bone. It is seen mainly in carpet layers, paving workers, floor cleaners and miners who do not use protective knee pads. Treatment consists of firm bandaging, and kneeling is avoided; occasionally aspiration is needed. In chronic cases the lump is best excised. Infection (possibly due to foreign body implantation) results in a warm, tender swelling. Treatment is by rest, antibiotics and, if necessary, aspiration or excision. INFRAPATELLAR BURSITIS (‘CLERGYMAN’S KNEE’) The swelling is below the patella and superficial to the patellar ligament, being more distally placed than prepatellar bursitis; it used to be said that one who prays kneels more uprightly than one who scrubs! Treatment is similar to that for prepatellar bursitis. Occasionally the bursa is affected in gout.

578

OTHER BURSAE Occasionally a bursa deep to the patellar tendon or the pes anserinus becomes inflamed and painful. Treatment is non-operative.

SWELLINGS AT THE BACK OF THE KNEE SEMIMEMBRANOSUS BURSA The bursa between the semimembranosus and the medial head of gastrocnemius may become enlarged in children or adults. It presents usually as a painless lump behind the knee, slightly to the medial side of the midline and most conspicuous with the knee straight. The lump is fluctuant but the fluid cannot be pushed into the joint, presumably because the muscles compress and obstruct the normal communication. The knee joint is normal. Occasionally the lump aches, and if so it may be excised through a transverse incision. However, recurrence is common and, as the bursa normally disappears in time, a waiting policy is perhaps wiser. POPLITEAL ‘CYST’ Bulging of the posterior capsule and synovial herniation may produce a swelling in the popliteal fossa. The lump, which is usually seen in older people, is in the midline of the limb and at or below the level of the joint. It fluctuates but is not tender. Injection of radio-opaque medium into the joint, and x-ray, will show that the ‘cyst’ communicates with the joint. The condition was originally described by Baker, whose patients were probably suffering from tuberculous synovitis. Nowadays it is more likely to be caused by rheumatoid or osteoarthritis, but it is still often called a ‘Baker’s cyst’. Occasionally the ‘cyst’ ruptures and the synovial contents spill into the muscle planes causing pain and swelling in the calf – a combination which can easily be mistaken for deep vein thrombosis.

possible. Before withdrawing the instrument, saline is squeezed out. A firm bandage is applied; the arthroscopic portals are often small enough not to require sutures. Postoperative recovery is remarkably rapid.

POPLITEAL ANEURYSM This is the commonest limb aneurysm and is sometimes bilateral. Pain and stiffness of the knee may precede the symptoms of peripheral arterial disease, so it is essential to examine any lump behind the knee for pulsation. A thrombosed popliteal aneurysm does not pulsate, but it feels almost solid.

COMPLICATIONS Intra-articular effusions and small haemarthroses are fairly common but seldom troublesome. Reflex sympathetic dystrophy (which may resemble a low-grade infection during the weeks following arthroscopy) is sometimes troublesome. It usually settles down with physiotherapy and treatment with non-steroidal anti-inflammatory drugs; occasionally it requires more radical treatment (see pages 261 and 723).

BONY SWELLINGS AROUND THE KNEE Because the knee is a relatively superficial joint, bony swellings of the distal femur and proximal tibia are often visible and almost always palpable. Common examples are cartilage-capped exostoses (osteochondromata) and the characteristic painful swelling of Osgood–Schlatter disease of the tibial tubercle (see below).

PRINCIPLES OF KNEE OPERATIONS

ARTHROSCOPY Arthroscopy is useful: (1) to establish or refine the accuracy of diagnosis; (2) to help in deciding whether to operate, and (3) to perform certain operative procedures. Arthroscopy is not a substitute for clinical examination; a detailed history and meticulous assessment of the physical signs are indispensable preliminaries and remain the sheet anchor of diagnosis. TECHNIQUE Full asepsis in an operating theatre is essential. The patient is anaesthetized (though local anaesthesia may suffice for short procedures) and a thigh tourniquet applied. Through a tiny incision, a trocar and cannula is introduced; sometimes, saline is injected to distend the joint before it is punctured. Entry into the joint is confirmed when saline flows easily into the joint or, if the joint was distended previously, by the outflow when the trocar is withdrawn. A fibreoptic viewer, light source and irrigation system are attached; a small television camera and monitor make it much easier for the operator to concentrate on manipulating the instruments with both hands (‘triangulation’). All compartments of the joint are now systematically inspected; with special instruments and, if necessary, through multiple portals, biopsy, partial meniscectomy, patellar shaving, removal of loose bodies, synovectomy, ligament replacement and many other procedures are

20

The knee

The swelling may diminish following aspiration and injection of hydrocortisone; excision is not advised, because recurrence is common unless the underlying condition is treated.

LIGAMENT RECONSTRUCTION The collateral and cruciate ligaments and the knee capsule are important constraints which allow normal knee function; laxity or rupture of these structures, either singly or in combination, is often the source of recurrent episodes of ‘giving way’. Although a significant proportion of such injuries are treated non-operatively, complete ruptures may require surgery in ‘high-demand’ individuals. Surgery for ligament reconstruction includes: 1. Repair, usually for collateral ligament midsubstance ruptures when they are found in combination with cruciate ligament injuries. This repair can be a simple end-to-end suture. 2. Substitution, usually for anterior cruciate ruptures: the semitendinosus and gracilis, either one or two bundle technique, can be carefully anchored to the femur and tibia ensuring that stability is restored without loss of knee movement. Another method is to use an autologous graft from the patellar tendon. 3. Tenodesis, using a variety of tendons which are passed either through bony or soft-tissue tunnels to ‘check’ the abnormal movement resulting from ligament rupture.

OSTEOTOMY Osteotomy above or below the joint used to be a popular method of treating arthritis of the knee, especially when articular destruction was more or less limited to one compartment and the knee had developed a varus or valgus deformity. With the development of joint replacement techniques, the operation gradually fell into disuse, or at best was seen as a temporizing measure to buy time for patients who would ultimately undergo some form of arthroplasty. However, improvements in technique and the introduction of

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20

operations for meniscal and articular cartilage repair have led to renewed interest in this procedure. The rationale for osteotomy is based on both biomechanical and physiological principles. Malalignment of the limb results in excessive loading and stress in part of the joint and consequently increased damage to the articular cartilage in that area – the medial compartment if the knee is in varus and the lateral compartment in a valgus knee. As the articular surface is destroyed, the deformity progressively increases. Osteotomy and repositioning of the bone fragments, by correcting the deformity, will improve the loadbearing mechanics of the joint. Furthermore, it will reduce the intraosseous venous congestion, and this may relieve some of the patient’s pain. INDICATIONS Severe varus or valgus deformity (e.g. due to a growth defect, epiphyseal injury or a malunited fracture) may of itself call for a corrective osteotomy, and the operation may also prevent or delay the development of osteoarthritis.

Deformity of the knee

Localized articular surface destruction Patients with unicompartmental osteoarthritis or advanced localized osteonecrosis, particularly when this is associated with deformity in the coronal plane, may benefit from an osteotomy which offloads the affected area. Provided the joint is stable and has retained a reasonable range of movement, this offers an acceptable alternative to a unicompartmental arthroplasty. Usually it is the medial compartment that is affected and the knee exhibits a varus deformity. By realigning the joint, load is transferred from the medial compartment to the centre or a little towards the lateral side. Slight over-correction may further offload the medial compartment but marked valgus should be avoided as this will rapidly lead to cartilage loss in the lateral compartment. Published results suggest that the operation provides substantial improvements in pain and function over a 7–10-year period (Dowd et al., 2006). reconstructions The introduction of meniscal and articular cartilage reconstruction techniques has led to considerable interest in applying the favourable biomechanical effects of osteotomy to the younger patient who has a full-thickness chondral lesion or an absent meniscus. Similarly, osteotomy in conjunction with either simultaneous or staged cruciate ligament reconstruction appears to be beneficial in patients who have a combination of instability and pain from limb malalignment (Giffin and Fintan, 2007).

Intra-articular

580

TECHNIQUE For sound biomechanical reasons, a varus deformity is best corrected by a valgus osteotomy at the proximal

end of the tibia, whereas a valgus deformity should be corrected by a varus osteotomy at the femoral supracondylar level. Angles must be accurately measured and the position of correction carefully mapped out on x-rays before starting the operation. A high tibial valgus osteotomy can be performed either by removing a pre-determined wedge of bone based laterally and then closing the gap (closing wedge technique) or by opening a wedge-shaped gap on the medial side (opening wedge technique). In the lateral closing wedge method the fibula must first be released either by dividing it lower down or by disrupting the proximal tibio-fibular joint. The tibia is divided just above the insertion of the patellar ligament. Two transverse cuts are made, one parallel to the joint surface and another just below that, angled to create the desired laterally based wedge. The wedge of bone is removed and the fragments are then approximated and fixed in the corrected position either with staples or with compression pins. The limb is immobilized in a cast for 4–6 weeks, by which time the osteotomy should have started to unite. An opening wedge valgus osteotomy on the medial side offers some advantages: the ability to adjust the degree of correction intra-operatively and the option to correct deformities in the sagittal plane as well as the coronal plane; it also makes it unnecessary to disrupt the tibio-fibular joint. However, there are also disadvantages: the newly-created gap must be filled with a bone graft and a long period of restricted weightbearing is needed after the procedure; there is also a higher rate of non-union or delayed union. These drawbacks can be mitigated by stabilizing the fragments with an external fixator applied to the medial side, waiting for about 5 days and then opening the gap very gradually, allowing it to fill with callus (hemicallotasis). Cast immobilization is unnecessary. The external fixator usually remains in place for 10–12 weeks. If a varus osteotomy is required – usually for active patients with isolated lateral compartment disease and valgus deformity of the knee – this is performed at the supracondylar level of the femur. The method most commonly employed is a medial closing wedge osteotomy, designed to place the mechanical axis at zero. The fragments should be firmly fixed with a blade-plate; in many cases postoperative cast immobilization will also be needed. RESULTS High tibial valgus osteotomy, when done for osteoarthritis, gives good results provided (1) the disease is confined to the medial compartment, and (2) the knee has a good range of movement and is stable. Relief of pain is good in 85 per cent of cases in the first year but drops to approximately 60 per cent after 5 years. A recent review has shown that modern medial

COMPLICATIONS Compartment syndrome in the leg This is the most important early complication of tibial osteotomy. Careful and repeated checks should be carried out during the early postoperative period to ensure that there are no symptoms or signs of impending ischaemia. Early features of compartment compression in the leg are sometimes mistaken for those of a deep vein thrombosis; this mistake should be avoided at all costs because the consequent delay in starting treatment could make the difference between complete recovery and permanent loss of function. Peroneal nerve palsy Overzealous attempts at correcting a longstanding valgus deformity can stretch and damage the peroneal nerve. Poor cast techniques may do the same, which is a good reason why postoperative cast application should not be left to an unsupervised junior assistant.

Under- or overcorrection of the deformity are really failures in technique. With medial compartment osteoarthritis, unless a slight valgus position is obtained, the result is liable to be unsatisfactory. However, marked overcorrection is not only mechanically unsound but the cosmetic defect is liable to be bitterly resented by the patient.

Failure to correct the deformity

These complications can be avoided by ensuring that fixation of the bone fragments is stable and secure.

Delayed union and non-union

INDICATIONS In the past – and even today in some parts of the world – the main indications for arthrodesis of the knee were (and are) irremediable instability due to the late effects of poliomyelitis and painful loss of mobility due to tuberculosis or chronic pyogenic infection. In countries with advanced medical facilities the commonest indication is failed total knee replacement (either septic or aseptic).

20

The knee

opening wedge osteotomy techniques can achieve satisfactory postoperative alignment in 93 per cent of patients and survivorship rates of 94 per cent at 5year, 85 per cent at 10-year, and 68 per cent at 15year follow-up, with conversion to total knee arthroplasty as the end point (Brower et al., 2007; Virolainen and Aro, 2004). The clinical results of distal femoral varus osteotomy have been good in selected patients. Substantial improvements in pain and function can be expected in approximately 90 per cent of patients (Preston et al., 2005).

CONTRAINDICATIONS Contraindications include severe general disability because of age or multiple joint disease, especially if associated with problems in the ipsilateral hip or ankle; amputation or knee fusion of the opposite limb; and persistent non-union of a peri-articular fracture or massive peri-articular bone loss. Finally, patient reluctance may be an important factor. A short period in a plaster cylinder before operation may convince the patient that a rigidly stiff leg is better than a painful and unstable knee. TECHNIQUE A vertical midline incision is used. If the operation is for tuberculosis the diseased synovium is excised; otherwise it is disregarded. The posterior vessels and nerves are protected and the ends of the tibia and femur removed by means of straight saw cuts, aiming to end with 15 degrees of flexion and 7 degrees of valgus as the position of fusion. Charnley’s method, using thick Steinman pins inserted parallel through the distal femur and proximal tibia, and connecting these with compression clamps, was for many years the standard method. Nowadays, multiplanar external fixation is used, or if the joint is not infected, a long intramedullary nail which may be unlocked or locked.

KNEE REPLACEMENT

ARTHRODESIS

INDICATIONS The main indication for knee replacement is pain, especially when this is combined with deformity and instability. Most replacements are performed for rheumatoid arthritis or osteoarthritis.

Arthrodesis of the knee has long been considered a demanding procedure that is subject to a variety of postoperative complications and often results in marginal or unacceptable outcomes. A stiff knee is a considerable disability; it makes climbing difficult and sitting in crowded areas distinctly awkward. Consequently, it is not often performed. For these reasons, arthrodesis has typically been held in reserve as a final salvage procedure for patients with irretrievably failed total knee arthroplasties and other comparable conditions.

TYPES OF OPERATION Partial replacement The role of unicompartmental replacement has yet to be firmly established. Early results for medial compartment osteoarthritis were promising but longer-term studies have highlighted the need for meticulous and exacting surgical technique to avoid high revision rates. Following a successful operation, relief of pain and restoration of function can be impressive, but for the present it is reserved for older patients; tibial and femoral osteotomies are used in the younger population.

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Patellar resurfacing, a kind of partial replacement, is rarely performed alone; usually it is combined with surface replacement of the condyles. Minimally constrained total replacement The term ‘minimally constrained’ is used for prostheses where some of the stability after replacement is provided by the prosthesis and some through preservation of the knee ligaments. Most modern minimally constrained designs allow sacrifice of the anterior cruciate ligament; some even allow both cruciates to be removed without detriment to the long-term survival of the prosthesis. ‘Totally unconstrained’ devices, where both cruciates are preserved, are rarely used because results are poor compared to the minimally constrained group. At operation all the articular surfaces are replaced – with metal on the femoral side, polyethylene on a metal tray on the tibial side and polyethylene alone on the patella. It is important to ensure correct placement of the implants so as to reproduce the normal mechanics of the knee as closely as possible. The tibial and patellar components are fixed with cement, whereas the femoral component may be press-fitted. Bone defects may be filled either with bone graft, metal augmentation wedges or cement. The development of suitable prostheses and instrumentation in recent years has led to vast improvements in technique, so the results are now similar to those of hip replacement. Constrained joints Artificial joints with fixed hinges are used when there is marked bone loss and severe instability. Their main value nowadays is to provide a mobile joint following resection of tumours at the bone ends. The lack of rotation in these implants places severe stresses on the bone/implant interfaces and they are liable to loosen, to break or to erode the tibial or femoral shafts unless physical activity is severely restricted. Moreover, a considerable amount of bone has to be removed, and this makes a subsequent arthrodesis difficult. Minimally invasive total knee replacement This is in its early stage of development and is not yet widely used. Early results suggest that it provides some benefits over conventional total joint replacement: less pain, faster recovery, better quadriceps strength and a better range of movement.

TECHNIQUE It is important: (1) to overcome deformity (the knee should finally be about 7 degrees valgus); (2) to promote stability (by tailoring the bone cuts so that the collateral ligaments are equally tense in both flexion and extension); and (3) to permit rotation (otherwise cemented prostheses are liable to loosen).

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COMPLICATIONS General As with all knee operations (except arthroscopy) in which a tourniquet is used, there is a

high incidence of deep vein thrombosis. Prophylaxis, either pharmacological (anticoagulants) or mechanical (foot pumps, compression stockings), is recommended. The methods of preventing and treating infection are similar to those used in hip replacement. For established and intractable infection, treatment by debridement and antibiotics, or by exchange replacement in one or two stages, are obvious possibilities, though probably the safest salvage operation is arthrodesis; this is especially applicable in immunosuppressed patients and in those with resistant bacteria.

Infection

Loosening Covert infection is only one cause of

implant loosening. Aseptic loosening results from faulty prosthetic design, inaccurate bone shaping, incorrect placement of the implants or a combination of these factors. Revision surgery for loose prostheses must deal with the cause, be it malposition of the prosthesis, accumulation of wear debris or infection. A loose prosthesis can be re-cemented, but unless the cause is dealt with, loosening will recur. Patellar problems Although relatively uncommon, these can be very disabling. They include: (1) recurrent patellar subluxation or dislocation, which may need realignment; and (2) complications associated with patellar resurfacing, such as loosening of the prosthetic component, fracture of the remaining bony patella, and catching of soft tissues between the patella and the femur. Patellar tracking as assessed on the operating table after implantation of the prosthesis is important. Any tendency to sublux must be corrected: common causes are unequal soft-tissue tension (for which a lateral release will be needed), a tibial component placed in internal rotation and/or a femoral component placed in internal rotation. The risk of patellar fracture postoperatively can also be lessened if care is taken not to divide the geniculate vessels when performing a lateral release.

NOTES ON APPLIED ANATOMY The knee joint combines two articulations – tibiofemoral and patello-femoral. The bones of the tibiofemoral joint have little or no inherent stability; this depends largely upon strong static and dynamic stabilizers such as ligaments and muscles. The patellofemoral joint is so shaped that the patella moves in a shallow path (or track) between the femoral condyles; if this track is too shallow the patella readily dislocates, and if its line is faulty the patellar articular cartilage is subject to excessive wear. One important function of the patella is to increase the power of extension; it lifts

does not occur medially) but remains stable concerning spinning kinematics, while the contact area transfers from an anterior pair of tibio-femoral surfaces at 10 degrees to a posterior part at about 30 degrees. Thus, because of the shapes of the bones, the medial contact area moves backwards with flexion to 30 degrees but the condyle does not. On the lateral side a variable spinning motion in mid-flexion (60 degrees) and a rolling motion up to 120 degrees of flexion are observed. Laterally, the femoral condyle and the contact area move posteriorly but to a variable extent in the mid-flexion (roll-back) causing tibial internal rotation to occur with flexion around a medial axis. Flexion beyond 120 degrees can only be achieved passively. Medially, the femur rolls back onto the posterior horn. Laterally, the femur and the posterior horn drop over the posterior tibia. New knee prostheses have been designed to reflect contemporary data regarding knee kinematics. Situated as they are between these complexly moving surfaces, the fibrocartilaginous menisci are prone to injury, particularly during unguarded movements of extension and rotation on the weightbearing leg. The medial meniscus is especially vulnerable because, in addition to its loose attachments via the coronary ligaments, it is firmly attached at three widely separated points: the anterior horn, the posterior horn and to the medial collateral ligament. The lateral meniscus more readily escapes damage because it is attached only at its anterior and posterior horns and these are close to each other. The function of the menisci is not known for certain, but they certainly increase the contact area between femur and tibia. They play a significant part in weight transmission and this applies at all angles of flexion and extension; as the knee bends they glide backwards, and as it straightens they are pushed forwards. The deep portion of the medial collateral ligament, to which the meniscus is attached, is fan-shaped and blends with the posteromedial capsule. It is, therefore, not surprising that medial ligament tears are often associated with tears of the medial meniscus and of the posteromedial capsule. The lateral collateral ligament is situated more posteriorly and does not blend with the capsule; nor is it attached to the meniscus, from which it is separated by the tendon of popliteus. The two collateral ligaments resist sideways tilting of the extended knee. In addition, the medial ligament prevents the medial tibial condyle from subluxating forwards. Forward subluxation of the lateral tibial condyle, however, is prevented, not by the lateral collateral ligament but by the anterior cruciate. Only when the medial ligament and the anterior cruciate are both torn can the whole tibia subluxate forwards (giving a marked positive anterior drawer sign). Backward subluxation of the tibia is prevented by the powerful posterior cruciate ligament in combination

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The knee

the quadriceps forwards, thereby increasing its moment arm. The patellar tendon is inserted into the upper pole of the patella. It is in line with the shaft of the femur, whereas the patellar ligament is in line with the shaft of the tibia. Because of the angle between them (the Qangle) quadriceps contraction would pull the patella laterally were it not for the fibres of vastus medialis, which are transverse. This muscle is therefore important and it is essential to try to prevent the otherwise rapid wasting that is liable to follow any effusion. The shaft of the femur is inclined medially, while the tibia is vertical; thus the normal knee is slightly valgus (average 7 degrees). This amount is physiological and the term ‘genu valgum’ is used only when the angle exceeds 7 degrees; significantly less than this amount is genu varum. During walking, weight is necessarily taken alternately on each leg. The line of body weight falls medial to the knee and must be counterbalanced by muscle action lateral to the joint (chiefly the tensor fascia femoris). To calculate the force transmitted across the knee, that due to muscle action must be added to that imposed by gravity; moreover, since with each step the knee is braced by the quadriceps, the force that this imposes also must be added. Clearly the stresses on the articular cartilage are (as they also are at the hip) much greater than consideration only of body weight would lead one to suppose. It is also obvious that a varus deformity can easily overload the medial compartment, leading to cartilage breakdown; similarly, a valgus deformity may overload the lateral compartment. For several decades, the prevailing opinion was that the movements of the knee are guided by the cruciate ligaments functioning as a crossed four-bar link. For a knee guided by a four-bar link, this implies that the axis of rotation of the tibia relative to the femur must be at the crossing point of the cruciate ligaments. An important kinematic consequence of the four-bar link is the phenomenon known as ‘roll-back’. Roll-back is a progressive movement of the femur backward on the tibia with flexion. The opposite – roll-forward – would then occur during knee extension. However, recent published work on normal knee kinematics has shown that the knee does not work as a crossed four-bar link. Modern knee kinematics are better understood by dividing the flexion arc into three parts (Freeman and Pinskerova, 2005). From full extension to 20 to 30 degrees of flexion, tibial internal rotation is coupled with flexion and on the lateral side a counter-translation nearing full extension is observed. Knee activities take place mainly between 20 degrees and 120 degrees. Over this arc, the articulating surfaces of the femoral condyles are circular in sagittal section and rotate around a centre. The medial condyle does not move anteroposteriorly (roll-back

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with the arcuate ligament on its lateral side and the posterior oblique ligament on its medial side. The cruciate ligaments are crucial, in the sense that they are essential for stability of the knee. The anterior cruciate ligament prevents forward displacement of the tibia on the femur and, in particular, it prevents forward subluxation of the lateral tibial condyle, a movement that tends to occur if a person who is running twists suddenly. The posterior cruciate ligament prevents backward displacement of the tibia on the femur and its integrity is therefore important when progressing downhill.

REFERENCES AND FURTHER READING Apley AG. The diagnosis of meniscus injuries: some new clinical methods. J Bone Joint Surg 1947; 29: 78–84. Bentley G. Articular cartilage changes in chondromalacia patellae. J Bone Joint Surg 1985; 67B: 769–774. Bowen JR, Leahy JL, Zhang Z, MacEwen GD. Partial epiphyseodesis at the knee to correct angular deformity. Clin Orthop 1985; 198: 184–90. Brower RW, van Raaij TM, Bierma-Zeinstra SM et al. Osteotomy for treating knee osteoarhtritis. Cochrane Database Syst Rev 2007; 18(3): CD004019. Coventry MB. Upper tibial osteotomy for osteoarthritis. J Bone Joint Surg 1985; 67A: 1136–40. Crotty JM, Monu JU, Pope TL Jr. Magnetic resonance imaging of the musculoskeletal system. Part 4. The knee. Clin Orthop Relat Res 1996; 330: 288–303. Dandy DJ. Chronic patellofemoral instability. J Bone Joint Surg 1995; 78B: 328–35. Dimakopoulos P, Patel D. Partial excision of discoid meniscus. Acta Orthop Scand 1990; 61: 1–40. Dowd GS, Somayaji HS, Uthukuri M. High tibial osteotomy for medial compartment osteoarthritis. Knee 2006; 13: 87–92 Ficat RP, Hungerford DS. Disorders of the Patello-femoral Joint, Williams & Wilkins, Baltimore, 1977. Freeman MA, Pinskerova V. The movement of the normal tibiofemoral joint. J Biomech 2005; 38: 197–208. Giffin R, Fintan S. The role of the high tibial osteotomy in the unstable knee. Sports Med Arthrosc 2007; 15: 23–31 Goodfellow J, Hungerford DS, Zindel M. Patello-femoral joint mechanics and pathology. 1. Functional anatomy of the patello-femoral joint. J Bone Joint Surg 1976; 58B: 287–90. Goodfellow J, Hungerford DS, Woods C. Patellofemoral joint mechanics and pathology. 2. Chondromalacia patellae. J Bone Joint Surg 1976; 58B: 291–9. Goodfellow JW, Kershaw CJ, Benson MKD’A, O’Connor JJ. The Oxford knee for unicompartmental osteoarthritis. J Bone Joint Surg 1988; 70B: 692–701. Grelsamer RP. Unicompartmental osteoarthrosis of the knee. J Bone Joint Surg 1995; 77A: 278–92

Inone M, Shino K, Hirose H et al. Subluxation of the patella. Computed tomography analysis of patellofemoral congruence. J Bone Joint Surg 1988; 70A: 1331–7. Insall JN, Salvati E. Patella position in the normal knee joint. Radiology 1971; 101: 101. Karachalios T, Hantes M, Zibis AH et al. Diagnostic accuracy of a new clinical test (the Thessaly test) for early detection of meniscal tears. J Bone Joint Surg 2005; 87A: 955–62. Kay PR, Freemont AJ, Davies DRA. The aetiology of multiple loose bodies. J Bone Joint Surg 1989; 71B: 501–4. Khan KM, Maffulli N, Coleman BD et al. Patellar tendinopathy: some aspects of basic science and clinical management. Br J Sports Med 1998; 32: 346–55. King JB, Perry DJ, Mourad K, Kumar SJ. Lesions of the patellar ligament. J Bone Joint Surg 1990; 72B: 46–48. Kocher MS, Tucker R, Ganley TJ, Flynn JM. Management of osteochondritis dissecans of the knee. Current concepts review. Am J Sports Med 2006; 34: 1181–91. Liu SH, Mirzayan R. Current review. Functional knee bracing. Clin Orthop Res 1995; 317: 273–81. Mann G, Finsterbush A, Franfkl U et al. A method of diagnosing small amounts of fluid in the knee. J Bone Joint Surg 1991; 73B: 346–7. Maquet PGJ. Biomechanics of the Knee. Springer, Berlin, 1976. Medlar RC, Lyne ED. Sinding-Larsen Johansson disease. J Bone Joint Surg 1978; 60A: 1113–6. Men HX, Bian CH, Yang CD et al. Surgical treatment of the flail knee after poliomyelitis. J Bone Joint Surg 1991; 73B: 195–8. Merchant AC, Mercer RL, Jacobsen RH, Cool CR. Roentgenographic analysis of patellofemoral congruence. J Bone Joint Surg 1974; 56A: 1391–6. Oei EHG, Nikken JJ, Verstijen ACM et al. MR Imaging of the menisci and cruciate ligaments: A systematic review. Radiology 2003; 226: 837–48. Paletta GA Jr, Laskin RS. Total knee arthroplasty after a previous patellectomy. J Bone Joint Surg 1995; 77A: 1708–12. Parisien JS. Arthroscopic treatment of cysts of the menisci. Clin Orthop Related Res 1990; 257: 154–8. Patel DV, Breazeale NM, Behr CT et al. Osteonecrosis of the knee: current clinical concepts. Knee Surg Sports Traumatol Arthrosc 1998; 6: 2–11. Preston CF, Fulkerson EW, Meislin R, Di Cesare PE. Osteotomy about the knee: applications, techniques and results. J Knee Surg 2005; 18(4): 258–72 Salenius P, Vankka E. The development of the tibiofemoral angle in children. J Bone Joint Surg 1975; 57A: 259–61. Schenck RC Jr, Goodnight JM. Osteochondritis dissecans. J Bone Joint Surg 1996; 78A: 439–56. Sherman OH, Fox JM, Snyder SJ, et al. Arthroscopy – ‘No Problem Surgery’: An analysis of complications in two thousand six hundred and forty cases. J Bone Joint Surg 1986; 68A: 256–65.

Thomee R, Augustsson J, Karlsson J. Patellofemoral pain syndrome: A review of current issues. Sport Medicine 1999; 28: 245–62. Virolainen P, Aro HT. High tibial osteotomy for the treatment of osteoarthritis of the knee of the knee: a review of

the literature and meta-analysis of follow up studies. Arch Orthop Trauma Surg 2004; 124(4): 258–61. Yamamoto T, Bullough PG. Spontaneous osteonecrosis of the knee: the result of subchondral insufficiency fracture. J Bone Joint Surg 2000; 82A: 858–66.

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The ankle and foot

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Gavin Bowyer

CLINICAL ASSESSMENT

SYMPTOMS Adults with foot and ankle problems often present complaining of pain, swelling, deformity and impaired function including difficulties with work, social and domestic activities. Questions should include those that flag up the possibility of neoplastic or generalized inflammatory disease and diabetes. Pain over a bony prominence or a joint is probably due to some local disorder; ask the patient to point to the painful spot. Symptoms tend to be well localized to the structures involved, but vague pain across the forefoot (metatarsalgia) is less specific and is often associated with uneven loading and muscle fatigue. Often the main complaint is of shoe pressure on a tender corn over a toe joint or a callosity on the sole. Osteoarthritic pain at the first metatarsophalangeal (MTP) joint is often better in firm-soled shoes; hallux valgus/bunions will be exacerbated by close-fitting shoes; a functionally or mechanically unstable ankle often feels better in boots; metatarsalgia is worse in shoes with a higher heel. Morton’s neuroma or a prominent metatarsal head feels like a marble or pebble in the shoe. Deformity is sometimes the main complaint; the patient may abhor a ‘crooked toe’ or a ‘twisted foot’, even if it is not painful, and parents often worry about their children who are ‘flat-footed’ or ‘pigeon-toed’. Elderly patients may complain chiefly of having difficulty fitting shoes. Swelling is common, even in normal people, but it gains more significance if it is unilateral or strictly localized. Instability of the ankle or subtalar joint produces repeated episodes of the joint ‘giving way’. Ask about any previous injury (a ‘twisted ankle’). Numbness and paraesthesia may be felt in all the toes or in a circumscribed field served by a single nerve or one of the nerve roots from the spine. General questions that help in reaching a diagnosis,

assessing the impact of the condition on function and deciding on treatment in foot and ankle problems are: Have you any pain or stiffness in your muscles, joints or back? Can you dress yourself completely without any difficulty? Can you walk up and down stairs without any difficulty?

SIGNS WITH PATIENT UPRIGHT It is important to see the patient stand, as deformities will often be much better shown once the patient is weightbearing. The patient, whose lower limbs should be exposed from the knees down, stands first facing the surgeon, then with his or her back to the surgeon. Ask the patient to rise up on tiptoes and then settle back on the heels. Note the posture of the feet throughout this movement. Normally the heels are in slight valgus while standing and inverted on tiptoes; the degree of inversion should be equal on the two sides, showing that the subtalar joint is mobile and the tibialis posterior functioning. Viewed from behind, if there is excessive eversion of one foot, the lateral toes are more easily visible on that side (the ‘too-many-toes’ sign). Gait Observing the gait also helps to identify dynamic

problems and pathology on other lower limb joints. The patient is asked to walk normally. Note whether the gait is smooth or halting and whether the feet are well balanced. Gait is easier to analyze if concentrating on the sequence of movements that make up the walking cycle. It begins with heel-strike, then moves into stance, then push-off and finally swing-through before making the next heel-strike. The stance phase itself can be further divided into three intervals: (1) from heel-strike to flat foot; (2) progressive ankle dorsiflexion as the body passes over the foot; (3) ankle plantarflexion leading to toe-off. Gait may be disturbed by pain, muscle weakness, deformity or stiffness. The position and mobility of each ankle is of prime importance. A fixed equinus deformity results in the heel failing to strike the

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(a)

(e)

(b)

(c)

(f)

(d)

(g)

21.1 Examination with patient standing Look at the patient as a whole, first from in front and from behind. (a,b) The heels are normally in slight valgus and should invert equally when a patient stands on his/her toes. (c) This patient has flat feet (pes planus), while the patient in (d) has the opposite deformity, varus heels and an abnormally high longitudinal arch – pes cavus (e). From the front you can again notice (f) the dropped longitudinal arch in the patient with pes planus, as well as the typical deformities of bilateral hallux valgus and overriding toes. (g) Corns on the top of the toes are common.

ground at the beginning of the walking cycle; sometimes the patient forces heel contact by hyperextending the knee. If the ankle dorsiflexors are weak, the forefoot may hit the ground prematurely, causing a ‘slap’; this is referred to as foot-drop (or drop-foot). During swingthrough the leg is lifted higher than usual so that the foot can clear the ground (a high-stepping gait).

Hindfoot and midfoot deformities may interfere with level ground-contact in the second interval of stance; the patient walks on the inner or outer border of the foot. Toe contact, especially of the great toe, is also important; pain or stiffness in the first MTP joint may prevent normal push-off.

SIGNS WITH PATIENT SITTING OR LYING A systematic approach to examination, following the ‘look, feel, move’ steps, will lead to a diagnosis in the majority of cases. Next the patient is examined lying on a couch, or it may be more convenient if he or she sits opposite the examiner and places each foot in turn on the examiner’s lap.

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21.2 Gait – the three rockers of ankle-stance phase The first rocker begins with heel-strike – if the anterior compartment muscles are weak, a ‘foot-slap’ is noticeable; or if the ankle is in fixed equinus, this rocker may be absent altogether. In mid-stance, the centre of gravity of the body (and ground reaction force) moves from a position posterior to the ankle joint to anterior (second rocker). The third rocker produces an acceleration force that shifts the fulcrum of the pivot forwards to the metatarsal heads, just prior to toe-off (Gage, 1991).

Look The heel is held square so that any foot deformity can be assessed. The toes and sole should be inspected for skin changes. The foot shows areas of overload by producing callosities, and there are often corresponding areas of wear and signs of overload on the footwear. Thickening and keratosis may be seen over the proximal toe joints or on the soles. Atrophic changes in the

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(a)

(b)

(c)

The ankle and foot

h

21.3 Foot – surface anatomy Medial aspect: a, tendon of tibialis anterior; b, medial malleolus; c, tendon of tibialis posterior; d, sulcus behind medial malleolus; e, extensor tendons of toes; f, lateral malleolus; g, peroneal tendons curving behind the lateral malleolus; h, anterior metatarsal arch.

skin and toe-nails are suggestive of a neurological or vascular disorder. Deformity may be in the ankle, the foot or toes. A foot that is set flat on the ground at a right angle to the tibia is described as plantigrade; if it is set in fixed plantarflexion (pointing downwards) it is said to be in equinus; a dorsiflexed position is called calcaneus. Common defects are a ‘flat-footed’ stance (pes valgus); an abnormally high instep (pes cavus); a downward-arched forefoot (pes plantaris); lateral deviation of the great toe (hallux valgus); fixed flexion of a single interphalangeal (IP) joint (hammer toe) or of all the toes (claw toes). Swelling may be diffuse and bilateral, or localized; unilateral swelling nearly always has a surgical cause and bilateral swelling is more often ‘medical’ in origin. Swelling over the medial side of the first metatarsal head (a bunion) is common in older women. Corns are usually obvious; callosities must be looked for on the soles of the feet.

Feel Pain and tenderness in the foot and ankle localize very well to the affected structures – the patient really does show us where the problem is. The skin temperature is assessed and the pulses are felt. Remember that one in every six normal people does not have a dorsalis pedis artery. If all the foot pulses are absent, feel for the popliteal and femoral pulses; the patient may need further evaluation by Doppler ultrasound. If there is tenderness in the foot it must be precisely localized, for its site is often diagnostic. Any swelling, oedema or lumps must be examined. Sensation may be abnormal; the precise distribution of any change is important. If a neuropathy is suspected (e.g. in a diabetic patient) test also for vibra-

tion sense, protective sensation and sense of position in the toes.

Move The foot comprises a series of joints that should be examined methodically: • Ankle joint – With the heel grasped in the left hand and the midfoot in the right, the ranges of plantarflexion (flexion) and dorsiflexion (extension) are estimated. Beware not to let the foot go into valgus during passive dorsiflexion as this will give an erroneous idea of the range of movement. • Subtalar joint – It is important to ‘lock’ the ankle joint when assessing subtalar inversion and eversion. This is done simply by ensuring that the ankle is plantigrade when the heel is moved. It is often easier to record the amount of subtalar movement if the patient is examined prone. Inversion is normally greater than eversion. • Midtarsal joint – One hand grips the heel firmly to stabilize the hindfoot while the other hand moves the forefoot up and down and from side to side. • Toes – The MTP and IP joints are tested separately. Extension (dorsiflexion) of the great toe at the MTP joint should normally exceed 70 degrees and flexion 10 degrees.

Stability Stability is assessed by moving the joints across the normal physiological planes and noting any abnormal ‘clunks’. Ankle stability should be tested in both coronal and sagittal planes, always comparing the two joints. Patients with recent ligament injury may have to be examined under anaesthesia.

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WHERE DOES IT HURT; WHERE IS IT TENDER?

REGIONAL ORTHOPAEDICS

Anterior ankle joint line – impingement from osteophytes in OA Anterolateral angle of ankle joint – lateral gutter impingement in post-traumatic ankle with soft tissue problems Bony tip/lateral malleolus – ankle fracture (Ottawa guidelines) Posterior/inferior to lateral malleolus – peroneal tenosynovitis or tear Posterior to medial malleolus/line of tibialis posterior – tibialis posterior tendinitis or tear, and in plano-valgus collapse of hindfoot Base of fifth metatarsal – fracture/insertional problem with peroneus brevis Achilles tendon – Achilles tendinitis/paratendinitis Achilles insertion – insertional tendinitis Retrocalcaneal bursa – bursitis Plantar fascia – plantar fasciitis Medial to first MTP joint – bunion Dorsal to first MTP joint – OA, hallux limitus/rigidus Beneath first MTP joint – sesamoiditis Beneath metatarsal heads – ‘metatarsalgia’ In third interspace – Morton’s neuroma

Medial and lateral stability are checked by stressing the ankle first in valgus and then in varus. Anteroposterior stability is assessed by performing an anterior ‘drawer test’: the patient lies on the examination couch with hips and knees flexed and the feet resting on the couch surface; the examiner grasps the distal tibia with both hands and pushes firmly backwards, feeling for abnormal translation of the tibia upon the talus. Another way of doing this is to stabilize the distal tibia with one hand while the other grasps the heel and tries to shift the hindfoot forwards and backwards. The same tests can be performed under x-ray and the positions of the two ankles measured and compared.

Muscle power Power is tested by resisting active movement in each direction. The patient will be more cooperative if the movement required is demonstrated precisely. While the movement is held, feel the muscle belly and tendon to establish whether they are intact and functioning.

Shoes Footwear often adds additional clues when examining the foot and ankle, providing valuable information about faulty stance or gait.

General examination If there are any symptoms or signs of vascular or neurological impairment, or if multiple joints are affected, a more general examination is essential.

IMAGING

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21.4 Normal range of movement All movements are measured from zero with the foot in the ‘neutral’ or ‘anatomical’ position: thus, dorsiflexion is 0–15 degrees and plantarfexion 0–40 degrees. Inversion is about 30 degrees and eversion 15 degrees.

There are practical problems with imaging in children, and babies in particular because: (1) babies tend not to keep still during examination; (2) their bones are not completely ossified and their shape and position may be hard to define.

Stress x-rays These complement the clinical tests for ankle stability. The patient should be completely relaxed; if the ankle is too painful, stress x-rays can be performed under regional or general anaesthesia. Both ankles should be examined, for comparison.

CT provides excellent coronal views and is important in assessing fractures and congenital bony coalitions.

CT scan

Radioscintigraphy Radioisotope scanning, though non-

specific, is excellent for localizing areas of abnormal blood flow or bone remodelling activity; it is useful in the diagnosis of covert infection. MRI and ultrasound These methods are used to demonstrate soft tissue problems, such as tendon and ligament injuries.

PEDOBAROGRAPHY A record of pressures beneath the foot can be obtained by having the patient stand or walk over a

(a)

(b)

(c)

force plate; sensors in the plate produce a dynamic map of the peak pressures and the time over which these are recorded can be obtained. Although this is sometimes helpful in clinical decision making, or for comparing pre- and postoperative function, the investigation is used mainly as a research tool.

CONGENITAL DEFORMITIES Congenital deformities of the foot are common. Many appear as part of a more widespread genetic disorder; only those in which the foot is the main (or only) problem are considered in this section. Isolated abnormalities of the toes are also dealt with elsewhere.

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The ankle and foot

X-rays In the adult, the standard views of the ankle are anteroposterior (AP), mortise (an AP view with the ankle internally rotated 15–20 degrees) and lateral. Although the subtalar joint can be seen in a lateral view of the foot, medial and lateral oblique projections allow better assessment of the joint. These views are often used to check articular congruity after treatment of calcaneal fractures. The calcaneum itself is usually x-rayed in axial and lateral views, but a weightbearing view is helpful in defining its relationship to the talus and tibia. The foot, toes and intertarsal joints are well displayed in standing anteroposterior and medial oblique views, but occasionally a true lateral view is needed.

TALIPES EQUINOVARUS (IDIOPATHIC CLUB-FOOT) The term ‘talipes’ is derived from talus (Latin = ankle bone) and pes (Latin = foot). Equinovarus is one of several different talipes deformities; others are talipes calcaneus and talipes valgus. In the full-blown equinovarus deformity the heel is in equinus, the entire hindfoot in varus and the midand forefoot adducted and supinated. The abnormality is relatively common, the incidence ranging from 1–2 per thousand births; boys are affected twice as often as girls and the condition is bilateral in one-third of cases. The exact cause is not known, although the resemblance to other disorders suggests several possible mechanisms. It could be a germ defect, or a form of

(d)

21.5 X-rays (a) AP view of the ankle in a young woman who complained that after twisting her right ankle it kept giving way in high-heeled shoes. The x-ray looks normal; the articular cartilage width (the ‘joint space’) is the same at all aspects of the joint. The inversion stress view (b) shows that the talus tilts excessively; always x-ray both ankles for comparison and in this case the left ankle (c) does the same. She has generalized joint hypermobility, not a torn lateral ligament. (d) X-rays of the feet should be taken with the feet flat on the ground.

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arrested development. Its occurrence in neurological disorders and neural tube defects (e.g. myelomeningocele and spinal dysraphism) points to a neuromuscular disorder. Severe examples of club-foot are seen in association with arthrogryposis, tibial deficiency and constriction rings. In some cases it is no more than a postural deformity caused by tight packing in an overcrowded uterus.

Pathological anatomy The neck of the talus points downwards and deviates medially, whereas the body is rotated slightly outwards in relation to both the calcaneum and the ankle mortise (Herzenberg et al., 1988). The posterior part of the calcaneum is held close to the fibula by a tight calcaneo-fibular ligament, and is tilted into equinus and varus; it is also rotated medially beneath the ankle. The navicular and entire forefoot are shifted medially and rotated into supination (the composite varus deformity). The skin and soft tissues of the calf and the medial side of the foot are short and underdeveloped. If the condition is not corrected early, secondary growth changes occur in the bones; these are permanent. Even with treatment the foot is liable to be short and the calf may remain thin.

border and through that of the calcaneum parallel to its lateral border; they normally cross at an angle of 20–40 degrees (Kite’s angle) but in club-foot the two lines may be almost parallel. Incomplete ossification makes it difficult to decide exactly where to draw these lines and this means that there is a considerable degree of interobserver variation. The lateral film is taken with the foot in forced dorsiflexion. Lines drawn through the midlongitudinal axis of the talus and the lower border of the calcaneum should meet at an angle of about 40 degrees. Anything less than 20 degrees shows that the calcaneum cannot be tilted up into true dorsiflexion; the foot may seem to be dorsiflexed but it may actually have ‘broken’ at the midtarsal level, producing the socalled rocker-bottom deformity.

(a)

(b)

(c)

(d)

Clinical features The deformity is usually obvious at birth; the foot is both turned and twisted inwards so that the sole faces posteromedially. More precisely, the ankle is in equinus, the heel is inverted and the forefoot is adducted and supinated; sometimes the foot also has a high medial arch (cavus), and the talus may protrude on the dorsolateral surface of the foot. The heel is usually small and high, and deep creases appear posteriorly and medially; some of these creases are incomplete constriction bands. In some cases the calf is abnormally thin. In a normal baby the foot can be dorsiflexed and everted until the toes touch the front of the leg. In club-foot this manoeuvre meets with varying degrees of resistance and in severe cases the deformity is fixed. The infant must always be examined for associated disorders such as congenital hip dislocation and spina bifida. The absence of creases suggests arthrogryposis; look to see if other joints are affected.

(e)

X-rays

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X-rays are used mainly to assess progress after treatment. The anteroposterior film is taken with the foot 30 degrees plantarflexed and the tube likewise angled 30 degrees perpendicular. Lines can be drawn through the long axis of the talus parallel to its medial

21.6 Talipes equinovarus (club-foot) (a) True club-foot is a fixed deformity, unlike (b) postural talipes, which is easily correctable by gentle passive movement. (c,d) With true club-foot, the poorly developed heel is higher than the forefoot, which points downwards and inwards (varus). (e) Always examine the hips for congenital dislocation and the back for spina bifida (as in the case shown here).

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(d)

(c)

(e)

The ankle and foot

(a)

(b)

21.7 Talipes equinovarus – x-rays The left foot is abnormal. In the anteroposterior view (a) the talocalcaneal angle is 5 degrees, compared to 42 degrees on the right. In the lateral views, the left talocalcaneal angle is 10 degrees in plantarflexion (b) and 15 degrees in dorsiflexion (c). In the normal foot the angle is unchanged at 44 degrees, whatever the position of the foot (d,e).

Treatment The aim of treatment is to produce and maintain a plantigrade, supple foot that will function well. There are several methods of treatment but relapse is common, especially in babies with associated neuromuscular disorders. CONSERVATIVE TREATMENT Treatment should begin early, preferably within a day or two of birth. This consists of repeated manipulation and adhesive strapping that maintains the correction; the manipulations are taught to the child’s mother, who is then able to carry out gentle stretches on a regular basis with the strapping still in place. Treatment is supervised by a physiotherapist, who alters the strapping as correction is gradually obtained. If this level of care is not available, it may be better to hold position by applying a light plaster cast (over a protective layer of strapping), which is soaked off and changed every week. The three main components of the deformity are always corrected in the following order. First the forefoot must be brought into rotational alignment with the hindfoot; paradoxically this is done by increasing the supination deformity of the forefoot so that it corresponds with the relatively more supinated hindfoot. Next, both hindfoot and forefoot are together gradually brought out of varus and supination; correction is assisted by keeping the fulcrum on the lateral side of the head of the talus. Finally, equinus is corrected by bringing the heel down and dorsiflexing the foot. It may be necessary, en route, to perform percutaneous

tendo Achillis lengthening in order to overcome the equinus (Ponsetti, 1992). The objective (ideally) is to achieve not only correction but overcorrection. The position should be checked by x-ray in order to ensure that there is no rocker-bottom defect; attempts to overcome equinus before the other deformities are corrected may ‘break’ the foot in the midtarsal region. Resistant cases will usually declare themselves after 8–12 weeks of serial manipulations and strapping. The surgeon then faces a choice of early surgery or continued conservative treatment. The results of early operation, in particular neonatal surgery, have not been shown to be better than those of late surgery. Delaying surgery until the child is near walking age has the advantages of operating on a larger foot (making surgery easier) and using the forces in normal walking to help maintain the correction obtained at surgery. This delayed operative approach is suitable for severe, rigid deformities; however, for less severe cases it may be preferable to operate at around 6 months of age, but manipulation and splintage must still be continued until the child is walking.

OPERATIVE TREATMENT The objectives of club-foot surgery are: (1) the complete release of joint ‘tethers’ (capsular and ligamentous contractures and fibrotic bands); (2) lengthening of tendons so that the foot can be positioned normally without undue tension. A detailed knowledge of the pathological anatomy is a sine qua non.

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Access to the involved structures is through either an extended posteromedial incision (Turco, 1971), a posterior curved transverse incision extended anteriorly on both medial and lateral sides (‘Cincinatti’ – Crawford et al., 1982), or a posterolateral incision combined with a separate curved medial incision (Caroll, 1994). The tendo Achillis and tibialis posterior tendons are lengthened through Z-divisions; the posterior capsules of the ankle and subtalar joints

21.8 Congenital talipes equinovarus – treatment Firstline treatment is non-operative. This may be by manipulation and strapping (a) or serial casting (b). If insufficient correction is achieved, a formal open release may be needed (c). Severe relapses need more radical forms of treatment such as the Ilizarov fixator (d). After successful correction of deformity, relapses may be prevented by using Dennis Browne boots in infants (e) or moulded ankle–foot orthoses (f) in older children.

(a)

(d)

(e)

(b)

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often have to be divided to allow adequate correction of hindfoot equinus. Sometimes flexor digitorum longus and flexor hallucis longus also require attention. The calcaneo-fibular ligament, a key structure in keeping the calcaneum malrotated, is then released. A complete subtalar release is performed to allow the hindfoot to be corrected. The superficial deltoid ligament is freed on the medial side but the deep part is preserved to prevent ankle instability.

(c)

(f)

LATE OR RELAPSED CLUB-FOOT Late presenters often have severe deformities with secondary bony changes, and the relapsed club-foot is complicated by scarring from previous surgery. If the child is young (aged 4–7), a revision of the soft tissue releases may be considered together with a shortening of the lateral side of the foot by calcaneo-cuboid fusion or cuboid enucleation (The Dilwyn–Evans operation – Evans, 1961). Calcaneal osteotomies, in the form of lateral closing wedges or lateral translations, improve heel varus. Tendon transfers, once popular, now have a more limited role; a split tibialis anterior tendon transfer to the dorsum of the base of the fourth metatarsal may help balance weak evertors, whereas a transfer of tibialis posterior through the interosseous membrane to the dorsum will act as a dorsiflexor in neurological cases. Tendon transfers work well only if the joints are mobile, and this is seldom the case in these patients. Gradual correction by means of a circular external fixator (the Ilizarov method) has gained popularity in treating difficult relapsed cases and severe deformities; the early results are encouraging. Full corrections can be achieved even in feet severely scarred from previous surgery, and there is often an increase in the size of the foot, which is thought to be due to an increase in the blood supply during distraction. The procedure can be painful and long and for the time being it is best reserved for these very difficult cases. Despite initially successful surgery, deformities do still recur. A deformed, stiff and painful foot in an adolescent is best salvaged by corrective osteotomies and fusions. The distorted anatomy makes triple arthrodesis a real challenge but it is possible to end up with a plantigrade, stable and pain-free foot.

METATARSUS ADDUCTUS Metatarsus adductus varies from a slightly curved forefoot to something resembling a mild club-foot. The majority (90 per cent) either improve spontaneously or can be managed non-operatively using serial corrective casts followed by straight-last shoes. The more severe examples need operation. Extensive capsulectomies of the tarso-metatarsal joints followed by prolonged splintage have fallen out of favour because of the risk of early degenerative arthritis in the repositioned joints. Variations of the Dilwyn Evans procedure (which aims to balance the lengths of the medial and lateral columns of the foot), often in combination with basal metatarsal osteotomies, are suitable for the small percentage of children who require surgical treatment.

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The ankle and foot

Correction of the forefoot deformity is carried out by releasing the contractures around the talonavicular and calcaneocuboid joints. The interosseous ligament in the sinus canal should be preserved, especially in children with ligamentous laxity, as division may lead to overcorrection. Finally, the origin of the intrinsic muscles and plantar fascia from the calcaneum may need to be divided to reduce any cavus or plantaris deformity. The foot, in its corrected position, is immobilized in a plaster cast. K-wires are sometimes inserted across the talonavicular and subtalar joints to augment the hold. The wires and cast are removed at 6–8 weeks, after which hobble boots or a custom-made ankle– foot orthosis is used, depending on whether the child has started walking. Stretching exercises that were performed prior to surgery are continued. The period of splintage varies: some surgeons wait until active dorsiflexion and eversion are established whereas others recommend some form of splintage until skeletal maturity.

TALIPES CALCANEOVALGUS Calcaneovalgus is a common deformity that presents in the newborn as an acutely dorsiflexed foot. There is a deep crease (or several wrinkles) on the front of the ankle, and the calcaneum juts out posteriorly. Unlike congenital vertical talus (which also presents as an acutely dorsiflexed foot) this deformity is flexible. In addition, the anterior creases in congenital vertical talus are located over the midfoot. Calcaneovalgus is usually bilateral. There is an association with hip dysplasia, especially if it presents on one side only; examination of the hips followed by ultrasound or x-ray examination is therefore recommended. This is a postural deformity, probably due to abnormal intrauterine positioning, and it often corrects spontaneously in the neonatal period. Severe deformities occasionally require serial casts for correction.

21.9 Metatarsus adductus In contrast to club-foot, the deformity here is limited to the forefoot.

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foot the dorsally subluxated navicular returns to the normal position. The only effective treatment is by operation, ideally before the age of 2 years. Correction is done in one stage through separate incisions. The tendo Achillis is lengthened, with capsulotomies of the ankle and subtalar joints; via a medial approach the talonavicular joint is reduced and the tibialis anterior tendon is transferred to the neck of the talus; if necessary, the lateral structures are lengthened or released. The reduced position is held with a K-wire transfixing the talonavicular joint and plaster immobilization for 8–12 weeks (the wire can be removed at 6 weeks). Reasonably good results have been reported with this method (Duncan and Fixsen, 1999).

REGIONAL ORTHOPAEDICS

Treatment

21.10 Talipes calcaneovalgus Bilateral calcaneovalgus. This benign ‘deformity’ can be easily corrected without hurting the baby. Over time it usually corrects spontaneously.

PES PLANUS AND PES VALGUS (‘FLAT-FOOT’)

CONGENITAL CONVEX PES VALGUS (CONGENITAL VERTICAL TALUS) This rare condition is seen in infants, usually affecting both feet. Superficially it resembles other types of valgus foot, but the deformity is more severe; the medial arch is not only flat, it is the most prominent part of the sole, producing the appearance of a rocker-bottom foot. The hindfoot is in equinus and valgus and the talus points almost vertically towards the sole; the forefoot is abducted, pronated and dorsiflexed, with subluxation of the talonavicular joint. Passive correction is impossible; by the time the child is seen, the tendons and ligaments on the dorsolateral side of the foot are usually shortened. The calcaneum is in equinus and the talus points into the sole of the foot, with the navicular dislocated dorsally onto the neck of the talus. It is important to repeat the lateral x-ray with the foot maximally plantarflexed; in congenital vertical talus the appearance will be unchanged, whereas in flexible flat-

X-ray features

“Our feet are no more alike than our faces.” This truism from a British Medical Journal editorial sums up the problem of ‘normally abnormal’ feet. The medial arch may be normally high or normally low. The term ‘flatfoot’ applies when the apex of the arch has collapsed and the medial border of the foot is in contact (or nearly in contact) with the ground; the heel becomes valgus and the foot pronates at the subtalar-midtarsal complex. The problems associated with flat-foot differ in babies, children and adults and these three categories will therefore be considered separately.

FLAT-FOOT IN CHILDREN AND ADOLESCENTS Flat-foot is a common complaint among children. Or rather their parents, grandparents, and assistants in the shoe-shop – the children themselves usually don’t seem to notice it!

21.11 Congenital vertical talus (a) The infant’s foot is in marked valgus and has a rocker-bottom shape. The deformity is rigid and cannot be corrected. (b) X-ray shows the vertical talus pointing downwards towards the sole and the other tarsal bones rotated around the head of the talus.

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(a)

(b)

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Stiff (or ‘rigid’) flat-foot A deformity that cannot be corrected passively should alert the examiner to an underlying abnormality. Congenital vertical talus is dealt with earlier. In older children, conditions to be considered are: (1) tarsal coalition; (2) an inflammatory joint disorder; (3) a neurological disorder. Compensatory flat-foot This is a spurious deformity that occurs in order to accommodate some other postural defect. For example, a tight tendo Achillis (or a mild fixed equinus) may be accommodated by everting the foot; or if the lower limbs are externally rotated the body weight falls anteromedial to the ankle and the feet go into valgus – the Charlie Chaplin look.

Clinical assessment Although there is usually nothing to worry about, the parents’ concerns should not be dismissed without a proper assessment of the child. Enquire about neonatal problems and a family history. Watch the child stand and note the position of the heels from behind. Are they in neutral or valgus, and do they invert when the child stands on tiptoe? The tiptoe test will confirm a mobile subtalar joint and functioning tibialis posterior tendon. Let the child walk: is the gait normal for the child’s age? Are the heels set flat during the stance phase, or does the child have tight Achilles tendons? Examine the foot and note its shape. In the neonate, the rare congenital vertical talus presents as a stiff, acutely dorsiflexed and very flat (almost rocker-bottom) foot. Palpate for tenderness: are there signs of arthritis or infection? Test the movements in the ankle as well as the subtalar and midtarsal joints: a tight Achilles tendon may be ‘constitutional’ or part of a neuromuscular problem. Try to correct the flat-foot by gentle passive manipulation. Perform Jack’s test (see earlier) to distinguish between a flexible and a stiff (‘rigid’) deformity. The spine, hips and knees also should be examined. The clinical assessment is completed by a swift general examination for joint hypermobility and signs of neuromuscular abnormalities.

(a)

21.12 Mobile flat feet (a) Standing with the feet flat on the floor, the medial arches appear to have dropped and the heels are in valgus. (b) When the patient goes up on his toes, the medial arches are restored, indicating that these are ‘mobile’ flat feet. If this does not occur, look carefully for a tarsal coalition.

extensor tendons are in spasm. X-rays and computed tomography (CT) may show one or several of a variety of unions or partial unions between adjacent tarsal bones; the commonest are talocalcaneal, calcaneonavicular and talonavicular coalitions. The anomaly is inherited as an autosomal dominant condition and is present at birth but it becomes symptomatic only when the abnormal fibrous syndesmosis matures into a stiffer, cartilaginous synchondrosis that later ossifies to become a rigid bar. The child, usually at puberty or during early adolescence, develops an increasingly stiff flat-foot deformity. Pain may be due to abnormal tarsal stress or even fracture of an ossified bar. The picture differs from that of the more common ‘idiopathic’ flat-foot in that the deformity is more or less rigid, with spasm of the peroneal muscles. The diagnosis is confirmed by x-ray and/or CT, but other causes of rigid flat-foot must be excluded (e.g. inflammatory arthritis and infection of the hind- or midfoot).

(a)

PERONEAL SPASTIC FLAT-FOOT (TARSAL COALITION) Older children and teenagers sometimes present with a painful, rigid flat-foot in which the peroneal and

(b)

The ankle and foot

Flexible flat-foot Flexible pes valgus appears in toddlers as a normal stage in development, and it usually disappears after a few years, when medial arch development is complete; occasionally, though, it persists into adult life. The arch can often be restored by simply dorsiflexing the great toe (Jack’s test), and during this manoeuvre the tibia rotates externally (Rose et al., 1985). Many of these children have ligamentous laxity and there may be a family history of both flat feet and joint hypermobility.

(b)

21.13 Tarsal coalition (a) X-ray appearance of a calcaneonavicular bar. (b) CT image showing incompletely ossified talocalcaneal bars bilaterally (arrows).

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Imaging X-rays are unnecessary for asymptomatic, flexible flat feet. For pathological flat feet (which are usually painful or stiff) standing anteroposterior, lateral and oblique views may help to identify underlying disorders. On the lateral view, ‘beaking’ of the head of the talus suggests the presence of a tarsal coalition. Narrowing of the talocalcaneal joint, which is sometimes seen in talocalcaneal coalition, is easily mistaken for ‘arthritis’. Calcaneonavicular bars, if ossified, can be seen in oblique views of the foot. CT scanning is the most reliable way of demonstrating tarsal coalitions. Radioscintigraphy is occasionally used if a covert infection or osteoid osteoma is suspected. It may also help to identify a ‘hot’ accessory navicular before advocating its removal.

Treatment Physiological flat-foot Young children with flexible flat

feet require no treatment. Parents need to be reassured and told that the ‘deformity’ will probably correct itself in time; even if it does not fully correct, function is unlikely to be impaired. Some parents will cite examples of other children who were helped by insoles or moulded heel-cups. These appliances serve mainly to alter the pattern of weightbearing and hence that of shoe wear; simply put, they are more effective in treating the shoes than the feet. Flat-foot associated with a tight tendo Achillis and restricted dorsiflexion at the ankle may benefit from tendon-stretching exercises.

Tight tendo Achillis

Accessory navicular Sometimes the main complaint (with a flexible flat-foot) is tenderness over an unusually prominent navicular on the medial border of the midfoot. X-rays may show an extra ossicle at this site – the accessory navicular. Symptoms are due to pressure (and possibly a ‘bursitis’) over the bony prominence, or repetitive strain at the synchondrosis between the accessory ossicle and the navicular proper. If symptoms warrant it, the accessory bone can be shelled out from within the tibialis posterior tendon. If the medial arch has ‘dropped’ significantly, the tibialis posterior tendon can be used as a ‘hitch’ by reinserting it through a hole drilled in the navicular and suturing the loop with the foot held in maximum inversion (Kidner’s operation). Rigid flat-foot (tarsal coalition) One of the problems with

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treatment of this condition is that the presence of a tarsal coalition is not necessarily the cause of the patient’s symptoms; the anomaly is sometimes discovered as an incidental finding in asymptomatic feet. For this reason the initial treatment should always

be conservative. A walking plaster is applied with the foot plantigrade and is retained for 6 weeks; splintage with an outside iron and inside T-strap may have to be continued for another 3–6 months. Obviously if an inflammatory joint disorder is discovered, this will have to be treated. If symptoms do not settle, operative treatment is needed. A calcaneonavicular bar can be resected without much difficulty through a lateral approach, and the operation may be performed before puberty; a portion of the bar is removed and the gap filled with fat or a piece of muscle (e.g. extensor digitorum brevis) to prevent recurrence. Talocalcaneal coalitions are more difficult to deal with and it may be wiser to wait until after the patient reaches puberty and then perform a triple arthrodesis.

FLAT-FOOT IN ADULTS As in children, the usual picture is of a flexible flatfoot with no obvious cause. However, underlying disorders are common enough to always warrant a careful search for abnormal ligamentous laxity, tarsal coalitions, disorders of the tibialis posterior tendon, post-traumatic deformity, degenerative arthritis, neuropathy and conditions resulting in muscular imbalance. Painful acquired flat-foot often results from tibialis posterior dysfunction. Tibialis posterior tendon dysfunction affects predominantly women in later midlife. It is usually of insidious onset, affecting one foot much more than the other, and with identifiable systemic factors such as obesity, diabetes, steroids or surgery. There may be recollection of a minor episode of trauma, such as a twisting injury to the foot. The patient experiences aching discomfort in the line of the tibialis posterior tendon, often radiating up the inner aspect of the lower leg. The foot often feels ‘tired’. As the tendon stretches out the foot drifts into plano-valgus, producing the typical acquired flat-foot deformity. As the tendon ruptures the ache or pain will often improve, temporarily, but as the foot deformity then worsens the plantar fascia becomes painful and there may be lateral hindfoot pain as the fibula starts to impinge against the calcaneum.

Pathology The tibialis posterior is a powerful muscle, with a short excursion of its tendon and a strong mechanical advantage as a foot inverter acting to help maintain the medial longitudinal arch of the foot. This tendon is probably inflamed more commonly and ruptures more frequently than the Achilles tendon. There is usually an initial tenosynovitis. Tendon elongation and rupture are probably related to an area of hypovascularity in the tendon. Once the tendon elongates

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(b)

(c)

21.14 Flat-foot in adults – clinical features (a) The medial arches have dropped and the feet appear to be pronated. (b) The medial border of the foot is flat and the tuberosity of the navicular looks prominent. (c) The heels are in valgus and the toes are visible lateral to the outer edge of the heel on the left side (the ‘too-many-toes’ sign).

the pathology is then related to the loss of powerful hindfoot inversion, probably confounded by associated stretching of the related ligaments, in particular the spring ligament and the plantar fascia.

posterior cannot stabilize and invert the heel, impairing the heel-raise action of the Achilles tendon.

Examination

Weightbearing x-rays show the altered foot axes. The tendon can be assessed with ultrasound or magnetic resonance imaging (MRI) scan.

There is usually swelling and tenderness in the line of tibialis posterior, at and distal to the medial malleolus. The hindfoot collapse is best appreciated by viewing the patient from behind, when the valgus deformity of the heel is appreciated, and the forefoot abduction leads to ‘too many toes’ being seen from this position, compared to the contralateral foot. It is difficult for the patient to do a single leg heel raise, as the tibialis

(a)

(b)

21.15 Footprints Footprints made with the aid of an ink pad show the difference between normal sole contact and flat-footed contact. (a) Normal footprint, showing the main contact areas across the anterior metatarsal arch, the lateral border of the foot and the heel, with a ‘hollow’ corresponding to the medial arch. (b) Flat-footed contact, across the sole to the medial side of the foot.

The ankle and foot

(a)

Imaging

Treatment The key point is to recognize the condition. If it is in the early stages then relative rest (sticks or crutches), support with a temporary insole, elasticated foot/ ankle support and oral non-steroidal anti-inflammatory drugs (NSAIDs) may be effective. Whether or not to inject the tendon sheath with corticosteroid is contentious; but to inject the tendon itself is just plain wrong! These temporary measures may offer the opportunity to institute more permanent solutions, such as modification of weight and activity, and assessment for definitive orthotics. ORTHOSES Functional foot orthoses (FFOs) have a role to play in the adult flexible but symptomatic flat-foot. These appliances (usually called orthotics) are used to correct abnormal foot function or biomechanics and, in so doing, they also correct for abnormal lower extremity function; they are very much more than an ‘arch support’. Orthotics are useful in the treatment of a range of painful conditions of the foot and lower extremities, in particular first MTP joint arthritis, metatarsalgia, arch and instep pain, ankle pain and heel pain. Since abnormal foot function may cause abnormal leg, knee and hip function, orthotics can be used to treat painful tendinitis and bursitis conditions in the ankle, knee and hip, as well as exercise-induced leg pain (‘shin splints’). Some types of FFOs are also

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designed to accommodate painful areas on the soles of the feet (like accommodative foot orthoses). Orthoses may be made of flexible, semi-rigid or rigid plastic or graphite materials. They are relatively thin and fit easily into several types of shoe. They are fabricated from a three-dimensional model of the foot or scanning the foot with a mechanical or optical scanner. Assessment for orthotics can be performed by a podiatrist, who can also advise on whether the usual/intended footwear will accommodate such a device and offer the support needed for it to be effective. ‘Off-the-shelf’ insoles are cheaper, but there are several advantages to prescription foot orthoses. They are custom-made to precisely fit each foot, and are made in relatively rigid, durable materials with a minimal chance of discomfort or irritation to the foot and a greater potential to relieve pain.

neuropathies and spinal cord abnormalities (tethered cord syndrome, diastematomyelia) are the commonest in Western countries but poliomyelitis is the most common cause worldwide. Occasionally the deformity follows trauma – burns or a compartment syndrome resulting in Volkmann’s contracture of the sole.

PHYSIOTHERAPY Local treatment of the associated inflammation with physiotherapy might be of benefit. Assessment of the hindfoot biomechanics by a podiatrist might help to prevent progression, and could offer protection to the contralateral side, which is often much less severely affected.

Pathology

SURGERY If the condition does not improve with a few weeks of conservative treatment, or the patient presents several months after onset of the symptoms, then surgical intervention should be considered. Options include surgical decompression and tenosynovestomy, or reconstruction of the tendon. The latter is often combined with a calcaneal osteotomy to help to protect the tendon and improve the axis. If there is already degeneration in the hindfoot joints then triple arthrodesis might be indicated (fusing the subtalar, calcaneo-cuboid and talonavicular joints – the ankle joint is not arthrodesed in this procedure, so foot plantarflexion and dorsiflexion are maintained).

PES CAVUS (HIGH-ARCHED FEET)

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In pes cavus the arch is higher than normal, and often there is also clawing of the toes. The close resemblance to deformities seen in neurological disorders where the intrinsic muscles are weak or paralyzed suggests that all forms of pes cavus are due to some type of muscle imbalance. There are rare congenital causes, such as arthrogryposis, but in the majority of cases pes cavus results from an acquired neuromuscular disorder see Box opposite. A specific abnormality can often be identified; hereditary motor and sensory

NEUROMUSCULAR CAUSES OF PES CAVUS Muscular dystrophies

Duchenne, Becker

Neuropathies

HMSN I and II

Cord lesions

Poliomyelitis, syringomyelia, diastomatomyelia, tethered cord

Cerebral disorders

Cerebral palsy, Friedreich’s ataxia

The toes are drawn up into a ‘clawed’ position, the metatarsal heads are forced down into the sole and the arch at the midfoot is accentuated. Often the heel is inverted and the soft tissues in the sole are tight. Under the prominent metatarsal heads callosities may form.

Clinical features Patients usually present at the age of 8–10 years. Deformity may be noticed by the parents or the school doctor before there are any symptoms. There may be a past history of a spinal disorder, or a family history of neuromuscular defects. As a rule both feet are affected. Pain may be felt under the metatarsal heads or over the toes where shoe pressure is most marked. Callosities appear at the same sites and walking tolerance is reduced. Enquire about symptoms of neurological disorders, such as muscle weakness and joint instability. The overall cavus deformity is usually obvious; in addition the toes are often clawed and the heel may be varus. Closer inspection will show the components of the high arch; this is important because it leads to an understanding of the responsible deforming forces. Rang (1993) presented a tripod analogy that simplifies the problem. The foot is likened to a tripod of which the calcaneus, fifth metatarsal and first metatarsal form the legs. Combinations of deformities affecting one or more of these ‘legs’ produce the common types of high arch, namely plantaris, cavovarus, calcaneus and calcaneo-cavus (Fig. 21.17). The toes are held cocked up, with hyperextension at the MTP joints and flexion at the IP joints. There may

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(b)

The ankle and foot

(a)

(c)

21.16 Pes cavus and claw-toes (a) Typical appearance of ‘idiopathic’ pes cavus. Note the high arch and claw-toes. (b) This is associated with varus heels. (c) Look for callosities under the metatarsal heads.

be callosities under the metatarsal heads and corns on the toes. Early on the toe deformities are ‘mobile’ and can be corrected passively by pressure under the metatarsal heads; as the forefoot lifts, the toes flatten out automatically. Later the deformities become fixed, with the MTP joints permanently dislocated. Mobility in the ankle and foot joints is important. In the cavo-varus foot, the heel is inverted. The block test (Coleman et al., 1984) is useful to check if the deformity is reversible (Fig. 21.18); if it is, this signifies that the subtalar joint is mobile. If the cavus deformity has been present for a long time, then movements of the ankle, subtalar and midtarsal joints are usually limited. A neurological examination is important to try to identify a reason for the deformity. Disorders such as hereditary sensory and motor neuropathy and Friedreich’s ataxia must always be excluded, and the spine should be examined for signs of dysraphism.

Imaging Weightbearing x-rays of the foot contribute further to the assessment of the deformity and the state of the normal

plantaris

individual joints. On the lateral view, measurement of the calcaneal pitch and Meary’s angle help to determine the components of the high arch (Fig. 21.19). In a normal foot the calcaneal pitch is between 10 and 30 degrees, whereas Meary’s angle, formed by the axes of the talus and first metatarsal, is zero, i.e. these axes are parallel. In a calcaneus deformity, the calcaneal pitch is increased; in a plantaris deformity, Meary’s lines meet at an angle. MRI scans of the spine will exclude a structural disorder, especially if this is more common than polio as a cause of high-arched feet in the region.

Treatment Often no treatment is required; apart from the difficulty of fitting shoes, the patient has no complaints. In general, patients need treatment only if they have symptoms. However, the problem with high-arched feet is that it is often a progressive disorder that becomes more difficult to treat when the deformities are fixed; therefore treatment should start before the feet become stiff. Non-operative treatment

Foot deformity

cavo-varus

calcaneus

calcaneo-cavus

Tibia 5th MT

1st MT OS Calcis (a)

(b)

(c)

(d)

(e)

21.17 The tripod analogy for high-arched feet This simplifies understanding of the various types of pes cavus. (a) The calcaneum, first and fifth metatarsals of the foot are likened to the spokes of a tripod. (b) When the first and fifth rays are drawn closer to the heel, a plantaris deformity is present. In a cavo-varus deformity (c), the first ray alone is drawn towards the heel, which itself is in varus. In calcaneus (d), the heel is pushed plantarwards. Finally, a calcaneo-cavus deformity is present (e) when the heel is in calcaneus and the first ray is drawn in.

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21.18 Coleman’s block test This simple test is used on a high-arched foot to see if the heel is flexible. (a) Normal stance showing the varus position of the heel. (b) With the patient standing on a low block to permit the depressed first metatarsal to hang free, the heel varus is automatically corrected if the subtalar joint is mobile. (a)

(b)

21.19 Weightbearing x-rays in foot deformities Nonweightbearing films are notorious for ‘hiding’ the true components of foot deformities. In standing lateral views, some measurements are useful in describing the type of high-arched foot: (a) the axes of the talus and first metatarsal are parallel in normal feet but cross each other in a plantaris deformity (Meary’s angle); (b) the calcaneal pitch is greater than 30 degrees in calcaneus deformities.

in the form of custom-made shoes with moulded inserts may provide some relief but does not alter the deformity or influence its progression. Surgery is often needed and the type of procedure will depend on the child’s age, underlying cause, site and flexibility of the individual deformities and type of muscle imbalance. The aim of surgery is to provide a pain-free, plantigrade, supple but stable foot. The methods available are soft tissue releases, osteotomies and tendon transfers. However, the deformity first needs to be corrected before a tendon transfer is considered; additionally, the transfer only works if the joints are mobile.

An equinus contracture is dealt with by lengthening of the tendo Achillis and posterior capsulotomies of the ankle and subtalar joints. The varus hindfoot, if shown to be reversible by Coleman’s block test, may benefit from a release of the plantar fascia (the tight fascia acts as a contracted windlass on weightbearing, accentuating the deformity). However, if the subtalar joint is stiff, then calcaneal osteotomy will be needed; two types are commonly used: (1) the lateral closing wedge (an opening wedge on the medial side is a comparable operation but is fraught with wound problems); (2) a lateral translation osteotomy. Treatment of a calcaneo-cavus deformity (which is the least common type of high arch) differs according to the age of the child. In young children (who usually have a neurological problem) tendon transfers, e.g. transferring the tibialis anterior through the interosseous membrane to the calcaneum, may be combined with tenodesis of the ankle using the tendo Achillis (Banta et al., 1981). Older children may need crescentic calcaneal osteotomies, which will correct both varus and calcaneus deformities (Samilson, 1976) or variations of a triple arthrodesis (Cholmeley, 1953). Midfoot deformities are usually cavus (plantarflexed first metatarsal) or plantaris (plantarflexed first and fifth metatarsals). The Jones tendon transfer helps elevate the depressed first metatarsal by using the extensor hallucis longus tendon as a sling through the neck of the first metatarsal. Often the peroneus longus is overactive and is partly responsible for pulling the first metatarsal down; some balance is restored by dividing this tendon on the lateral side of the foot and attaching the proximal end to the peroneus brevis, thereby

21.20 Treatment of pes cavus 1 In a normal foot (a), the point of contact of the heel is slightly lateral to the centre of the ankle, producing an eversion lever when weight is borne. In a varus heel (b) excising a wedge of bone from the lateral side, or (c) performing a lateral translation osteotomy.

602

(a)

(b)

(c)

21

(b)

(c)

(d)

21.21 Treatment of pes cavus 2 (a,b) If the great toe is clawed and the first metatarsal depressed, reducing the subluxation at the metatarsophalangeal joint by simply elevating the neck of the metatarsal often reduces the severity of the cavus deformity. The surgical equivalent of this effect is (c,d) the Robert Jones tendon transfer: the extensor hallucis longus tendon is detached distally and transferred to the neck of the first metatarsal; the interphalangeal joint is then either fused or tenodesed.

removing the deforming force and improving the power of eversion simultaneously. Occasionally the deformity affecting the first metatarsal is fixed, in which case a dorsal closing wedge osteotomy at the base of the metatarsal is needed. A plantaris deformity is treated along similar lines for the first ray, and combined with a plantar fascia release if the deformity is mobile, but basal metatarsal osteotomies or even a wedge resection and arthrodesis across the midfoot are needed for rigid deformities. In severe examples and in those who have either relapsed or who have responded poorly with soft tissue releases and osteotomies, salvage surgery in the form of a triple arthrodesis is recommended; it produces a stiff but plantigrade and pain-free foot. Clawed toes Correction of a clawed first toe is by the Jones tendon transfer, which involves either a tenodesis or fusion of the IP joint. Clawing of the lesser toes is treated with a flexor tendon transfer to the extensor hood of each toe, and MTP joint capsulotomies if the toes are still passively correctable; however, if the deformities are fixed, proximal IP fusion is needed.

HALLUX VALGUS Hallux valgus is the commonest of the foot deformities (and probably of all musculoskeletal deformities). In people who have never worn shoes the big toe is in line with the first metatarsal, retaining the slightly fanshaped appearance of the forefoot. In people who habitually wear shoes the hallux assumes a valgus position; but only if the angulation is excessive is it referred to as ‘hallux valgus’. Splaying of the forefoot, with varus angulation of the first metatarsal, predisposes to lateral angulation of the big toe in people wearing shoes – and most of

The ankle and foot

(a)

all in those who wear high-heeled shoes. Metatarsus primus varus may be congenital, or it may result from loss of muscle tone in the forefoot in elderly people. Hallux valgus is also common in rheumatoid arthritis, probably due to weakness of the joint capsule and ligaments. Heredity plays an important part; a positive family history is obtained in over 60 per cent of cases.

Pathological anatomy The elements of the deformity are lateral deviation and rotation of the hallux, together with a prominence of the medial side of the head of the first metatarsal (a bunion). Lateral deviation of the hallux may lead to overcrowding and deformity of the other toes and sometimes overriding of adjacent toes. When the valgus deformity exceeds 30 or 40 degrees, the great toe rotates into pronation so that the nail faces medially and the sessamoid bones of flexor hallucis brevis are displaced laterally; in severe deformities the tendons of flexor and extensor hallucis longus bowstring on the lateral side, thus adding to the deforming forces. The contracted adductor hallucis and lateral capsule contribute further to the fixed valgus deformity. Prominence of the first metatarsal head is due to subluxation of the MTP joint; increasing shoe pressure on the medial side leads to the development of an overlying bursa and thickened soft tissues, additional changes that combine to form the defining ‘bunion’ that eventually accompanies the great-toe deformity. When exposed at operation, the medial prominence looks like an exostosis (because of a deep sagittal sulcus on the head of the metatarsal) but there is no true exostosis. In longstanding cases the MTP joint becomes osteoarthritic and osteophytes may then add to the prominence of the metatarsal head.

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21.22 Hallux valgus (a,b) This girl’s feet are well on the way to becoming as deformed as those of her mother (c,d). Hallux valgus is not uncommonly familial. X-rays should be taken with the patient standing to show the true metatarsal and digital angulation.

(a)

(b)

(c)

(d)

Clinical features The commonest complaints are pain over the bunion, worries about cosmesis and difficulty fitting shoes. Often there is also deformity of the lesser toes and pain in the forefoot. With the patient standing, planovalgus hindfoot collapse may become apparent. The great toe is in valgus and the bunion varies in appearance from a slight prominence over the medial side of the first metatarsal head to a red and angrylooking bulge that is tender. The MTP joint often retains a good range of movement, but in longstanding cases it may be osteoarthritic. Always check the circulation and sensation.

X-rays

604

Standing views will show the degree of metatarsal and hallux angulation. Lines are drawn along the middle of the first and second metatarsals and the proximal phalanx of the great toe; normally the intermetatarsal angle is less than 9 degrees and the valgus angle at the MTP joint less than 15 degrees. Any greater degree of angulation should be regarded as ‘hallux valgus’. Not all types of valgus deformity are equally progressive and troublesome. Based on the x-ray appearances, patients with hallux valgus can be divided into three types (Piggott, 1960): (1) those in whom the MTP joint is normally centred but the articular surfaces, though congruent, are tilted towards valgus;

(2) those in whom the articular surfaces are not congruent, the phalangeal surface being tilted towards valgus; (3) those in whom the joint is both incongruent and slightly subluxated (Fig. 21.23). Type 1 is a stable joint and any deformity is likely to progress very slowly or not at all. Type 2 is somewhat unstable and likely to progress. Type 3 is even more unstable and almost certain to progress.

Treatment ADOLESCENTS Many young patients are asymptomatic, but worry over the shape of the toe and an anxious mother keen not to let the condition become as severe as her own will bring the patient to the clinic. It is wise to try conservative measures first, mainly because surgical correction in this age group carries a 20–40 per cent recurrence rate. This consists essentially of encouraging the patient to wear shoes with wide and deep toeboxes, soft uppers and low heels – ‘trainers’ are a good choice. If x-rays show a type 1 (congruous) deformity, the patient can be reassured that it will progress very slowly, if at all. If there is an incongruous deformity, surgical correction will sooner or later be required. There are a number of non-operative strategies that may be adopted to deal with the deformity and the resulting limitations, but none that will get rid of the bunion itself. Accommodating, comfortable shoes can help, but are not acceptable for some patients (or

21

The ankle and foot

(a)

(b)

(c)

(d)

(e)

21.23 X-rays (a) The intermetatarsal angle (between the first and second metatarsals) as well as the metatarsophalangeal angle of the hallux are recorded. Piggott (1960) defined three types of hallux valgus, based on the position and tilt of the first MTP articular surfaces: In normal feet (b) the articular surfaces are parallel and centred upon each other. In congruent hallux valgus (c) the lines across the articular surfaces are still parallel and the joint is centred, but the articular surfaces are set more obliquely to the long axes of their respective bones. In (d) the deviated type of hallux valgus, the lines are not parallel and the articular surfaces are not congruent. In the subluxated type (e) the surfaces are neither parallel nor centred.

professions). Lace-up or Velcro-fastening shoes are better than slip-ons, and flat shoes are probably better than those with a raised heel. Bunion pads (like a Polo/doughnut shape) can help to offload the tender bunion, but strapping and overnight splints are probably a waste of money with no quality research to support their use. Chiropody can help by taking care of the callosities and skin compromise. Podiatrists may help to correct the foot biomechanics, but there is no good evidence that antipronatory orthoses are effective in the longer term management of the bunion. Diabetic services often provide specialized foot-care. In the adolescent with mild deformities, where the hallux valgus angle is less than 25 degrees, correction can be obtained by either a softtissue rebalancing operation (see later) or by a

Operative treatment

(a)

(b)

(c)

(d)

metatarsal osteotomy. If the x-ray shows a congruent articulation, the deformity is largely bony and therefore amenable to correction by a distal osteotomy. If the MTP articulation is incongruent the deformity is in the joint and soft-tissue realignment is indicated. The tight structures on the lateral side (adductor hallucis, transverse metatarsal ligament, and lateral joint capsule) are released; the prominent bone on the medial side of the metatarsal head is pared down and the capsule on the medial side is reefed. In moderate and severe deformities the hallux valgus angle may be greater than 30 degrees and intermetatarsal angle wider than 15 degrees. If the MTP joint is congruent, a distal osteotomy combined with a corrective osteotomy of the base of the proximal phalanx (Aikin’s osteotomy) is recommended. For greater deformities, if the joint is subluxed, a softtissue adjustment is needed as well as a proximal metatarsal osteotomy. This basal osteotomy is carried

(e)

(f)

21.24 Hallux valgus – treatment (a) Basal osteotomy with bone graft inserted. (b) Mitchell’s osteotomy. (c) Wilson’s osteotomy. (d) Before and after basal osteotomy and capsulorrhaphy. (e) Keller’s operation. (f) Arthrodesis.

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21

out to reduce a wide intermetatarsal angle; care is needed not to injure an open physis or else growth of the metatarsal will be stunted. ADULTS In the adult, when self-care is insufficient and the bunion is causing pain and difficulty with footwear, surgical options are appropriate. Recurrent infection or ulceration are also indications for operative treatment. The type of surgery proposed will depend on the level and extent of the deformity. This will usually comprise: (1) an osteotomy to re-align the first metatarsal; (2) soft tissue procedures to rebalance the joint. A number of different osteotomy patterns have been described and named after their ‘inventors’ or the pattern of bone cut (chevron, scarf etc.), or the part of the metatarsal that is osteotomized (distal usually if there is less deformity, proximal or basal for greater deformity). These procedures are reviewed in a paper by Robinson and Limbers (2005). There is convincing evidence to show that a distal osteotomy is associated with reduced pain and increased ability to work in the medium to long term; the safety profile is good, with a less than 10 per cent complication rate and with many procedures being performed as day-case operations and without plaster immobilization in the postoperative period. Patient satisfaction with bunion surgery is generally good, with 75 per cent being satisfied with the outcome. ELDERLY PATIENTS Hallux valgus in the elderly is best treated by shoe modifications; where this fails, and in those whose

functional demands are low, treatment by excision arthroplasty is usually successful. In the classic Keller’s operation, the proximal third of the proximal phalanx, as well as the bunion prominence, are removed. This used to be the most common operation for hallux valgus but it has fallen into disuse because of the high rate of recurrent deformity and complications such as loss of control over great toe movement, overload of the other metatarsals, metatarsalgia and dubious cosmetic improvement.

Complications Recurrent infection and ulceration are particular problems in the diabetic foot and are an indication for surgery, rather than a contraindication. Transfer metatarsalgia may occur if the realignment or shortening of the first ray does not take account of the relative lengths of the lesser metatarsals, which then become prominent and overloaded; a metatarsal stress fracture sometimes occurs. Forefoot corrective surgery should strive to produce a balanced forefoot with appropriately distributed weightbearing. Complex regional pain syndrome is a potential complication of all foot operations.

HALLUX RIGIDUS ‘Rigidity’ (or stiffness) of the first MTP joint occurs at almost any age from adolescence onwards. In young people it may be due to local trauma or osteochrondritis dissecans of the first metatarsal head. In older people it is usually caused by longstanding joint disorders such as gout, pseudogout or osteoarthritis (OA), and is very often bilateral. In contrast to hallux valgus, men and women are affected with equal frequency. A family history is common.

Clinical features

(a)

606

(b)

21.25 Hallux valgus – treatment (a) X-ray before operation. (b) X-ray after distal osteotomy.

Pain on walking, especially on slopes or rough ground, is the predominant symptom. The patient eventually develops an altered gait, trying to offload the first MTP joint by transferring weight across to the lesser toes; there is also impaired power in toe-off during the gait cycle. The great toe is straight and often has a callosity under the medial side of the distal phalanx. The MTP joint feels knobbly; a tender dorsal ‘bunion’ (actually a large osteophyte) is diagnostic. Dorsiflexion is restricted and painful, and there may be compensatory hyperextension at the interphalangeal joint. The outer side of the sole of the shoe may be unduly worn – the result of rolling the foot outwards to avoid pressing on the big toe.

21

(b)

(c)

21.26 Hallux rigidus (a) In normal walking, the big toe dorsiflexes (extends) considerably. With rigidus (b), dorsiflexion is limited. (c) The usual cause is OA of the first MTP joint.

The ankle and foot

(a)

It is important to check the state of the other joints in the foot in order to rule out a polyarthropathy. The features are essentially those of OA: narrowing of the joint space, subchondral sclerosis and marginal osteophytes. There may be signs of recent or old osteochondritis (‘squaring’ of the metatarsal head).

X-rays

(a)

Treatment If the condition is not interfering with activity then it can be left alone and the patient reassured. Intermittent attacks of pain can be relieved by an intra-articular injection of corticosteroid and local anaesthetic. If, however, the condition is painful and restricting of activity then the risks of long-term NSAIDs must be balanced against those of surgical intervention. Some orthotic devices will offload or reduce movement at the first MTP joint, but these are usually fulllength insoles and relatively bulky – they may not fit in a smart shoe (at least not when the foot is in it as well!) A rocker-soled shoe can abolish pain by allowing the foot to ‘roll’ without the necessity for dorsiflexion at the MTP joint; many people are unwilling to wear such shoes. OPERATIVE TREATMENT Pain at the first MTP joint that is intrusive or limits activity should be an indication for referral. In limited arthritic disease, simply removing the dorsal osteophyte (cheilectomy) might be effective, and may be coupled with an extension osteotomy in the proximal phalanx, to alter the loadbearing region of the articulation. If the joint is more arthritic then a fusion or arthrodesis offers a good chance of returning the patient to function, walking comfortably without a limp. The joint should be fused in 10 degrees of valgus and 10–15 degrees of dorsiflexion in relation to the sole of the foot, or with about 5–10 mm clearance between the line of the sole of the foot and the pulp of the great toe. Too little dorsiflexion will cause pain during toe-off and too much will result in the toe

(b)

21.27 ‘Bunions’ Compare the two types of bunion: (a) Dorsal bunion in hallux rigidus and (b) medial bunion in hallux valgus.

pressing against the shoe upper. Female patients may be concerned that they will be unable to wear shoes with a higher heel if the toe is fused, but in fact the majority are able to wear footwear that can include moderate heels. Arthroplasty is more controversial. Keller’s operation (an excisional arthroplasty), carries a high risk of complications and seldom brings improvement in function; the procedure is no longer recommended. Interposition arthroplasty has from time to time been popular and can provide excellent pain relief, especially in patients with advanced OA. A simple capsular arthroplasty is probably the safest. Silicone implants were often used in the past, but silicone-related complications were common and the operation is no longer recommended for hallux rigidus. Metallic implants have fared better (in experienced hands) but these also produce variable long-term results.

DEFORMITIES OF LESSER TOES The commonest deformities of the lesser toes are ‘claw’, ‘hammer’ and ‘mallet’. These terms are often used interchangeably, leading to confusion. Claw toe is characterized by hyperextension at the MTP joint and flexion at both IP joints. Hammer toe is an acute flexion deformity of the proximal IP joint only; in severe examples there may

607

REGIONAL ORTHOPAEDICS

21

be some extension at the MTP joint. The distal IP joint is either straight or hyperextended. Mallet toe is a flexion deformity of the distal IP joint.

FIXED DEFORMITY When the deformity is fixed, it may either be accepted and accommodated by special footwear or treated by one of the following operations: 1. Interphalangeal arthrodesis – If there is no joint disease, proximal IP arthrodesis and dorsal capsulotomy of the MTP joints permits active flexion of the MTP joints by the long flexors. This is sometimes combined with transfer of the extensor hallucis longus to the first metatarsal, thus removing a deforming force while retaining the muscle as a forefoot stabilizer. 2. Joint excision – Fixed claw deformities, usually associated with destruction of the MTP joints (e.g. in rheumatoid arthritis), can be dealt with by excision arthroplasties of the MTP joints – preferably removal of only the bases of the proximal phalanges and trimming of the metatarsal heads. This can usually be achieved through two longitudinal incisions on the dorsum of the foot. If the great toe is affected, a modified Keller’s operation is performed. The base of the proximal phalanx is excised and the plantar pad (which is often displaced in these deformities) is returned to its normal position beneath the metatarsal head; the space between the metatarsal and phalanx is then filled by suturing the long extensor tendon to the flexor. 3. Amputation – Toes that are severely contracted, dislocated and ulcerated are worse than none. If the circulation is satisfactory and the patient is willing to accept the appearance, amputation of all ten toes is a useful palliative operation.

CLAW TOES The IP joints are flexed and the MTP joints hyperextended. This is an ‘intrinsic-minus’ deformity that is seen in neurological disorders (e.g. peroneal muscular atrophy, poliomyelitis and peripheral neuropathies) and in rheumatoid arthritis. Usually, however, no cause is found. The condition may also be associated with pes cavus.

Clinical features The patient complains of pain in the forefoot and under the metatarsal heads. Usually the condition is bilateral and walking may be severely restricted. At first the joints are mobile and can be passively corrected; later the deformities become fixed and the MTP joints subluxed or dislocated. Painful corns may develop on the dorsum of the toes and callosities under the metatarsal heads. In the most severe cases the skin ulcerates at the pressure sites.

Treatment FLEXIBLE DEFORMITY So long as the toes can be passively straightened the patient may obtain relief by wearing a metatarsal support or by having a transverse metatarsal bar fitted to the shoe. A daily programme of intrinsic muscle exercises is important. If these measures fail to relieve discomfort, an operation is indicated. ‘Dynamic’ correction is achieved by transferring the long toe flexors to the extensors. The operation at one stroke removes a powerful IP flexor and converts it to a MTP flexor and IP extensor.

(a)

608

(b)

HAMMER TOE The proximal IP joint is fixed in flexion, while the distal joint and the MTP joint are extended. The second toe of one or both feet is commonly affected, and

(c)

(d)

21.28 Disorders of the lesser toes (a) Hammer-toe deformity. (b,c) Claw toes. This patient suffered from peroneal muscular atrophy, a neurological disorder causing weakness of the intrinsic muscles and cavus feet. (d) Overlapping fifth toe.

Treatment Operative correction is indicated for pain or for difficulty with shoes. The toe is shortened and straightened by excising the joint. An ellipse of tissue (including the corn and the underlying extensor tendon) is removed and the proximal IP joint is entered; the articular surfaces are nibbled away and the raw ends of the proximal and middle phalanges are brought together with the toe almost straight. The position is held by a longitudinally placed K-wire, which is retained for 6 weeks. An alternative (and some would say preferable) operation is simple excision of the head of the proximal phalanx, or excision of both articular surfaces, without formal arthrodesis; the toe is splinted for 3 weeks to allow healing in the corrected position. If the MTP joint is dislocated, a dorsal capsulotomy and elongation of the extensor tendon may be necessary; the toe is held in position by driving the K-wire more proximally, or by inserting a second wire.

transfer of the long extensor tendon beneath the proximal phalanx to the abductor digiti minimi (Lapidus, 1942). COCK-UP DEFORMITY The MTP joint is dislocated and the little toe sits on the dorsum of the metatarsal head. Operative treatment is usually successful: through a longitudinal plantar incision, the proximal phalanx is winkled out and removed; the wound is closed transversely, thus pulling the toe out of the hyperextended position. TAILOR’S BUNION An irritating or painful bunionette may form over an abnormally prominent fifth metatarsal head. If the shoe cannot be adjusted to fit the bump, the bony prominence can be trimmed, taking care not to sever the tendon of the fifth toe abductor. If the metatarsal shaft is bowed laterally (as is often the case), it can be straightened by performing either a distal osteotomy or a varus correction at the base of the metatarsal.

TUBERCULOUS ARTHRITIS (see also Chapter 2) Tuberculous infection of the ankle joint begins as a synovitis or as an osteomyelitis and, because walking is painful, may present before true arthritis supervenes. The ankle is swollen and the calf markedly wasted; the skin feels warm and movements are restricted. Sinus formation occurs early.

MALLET TOE

21.29 Tuberculous arthritis of the ankle (a) The swelling of the left ankle is best seen from behind; (b) shows regional osteoporosis and joint destruction.

In mallet toe it is the distal IP joint that is flexed. The toe-nail or the tip of the toe presses into the shoe, resulting in a painful callosity. If conservative treatment (chiropody and padding) does not help, operation is indicated. The distal IP joint is exposed, the articular surfaces excised and the toe straightened; flexor tenotomy may be needed. A thin K-wire is inserted across the joint and left in position for 6 weeks.

FIFTH TOE DEFORMITIES OVERLAPPING FIFTH TOE This is a common congenital anomaly (Fig. 21.28d). If symptoms warrant, the toe may be straightened by a dorsal V/Y-plasty, reinforced by transferring the flexor to the extensor tendon. Tight dorsal and medial structures may have to be released. The toe is held in the overcorrected position with tape or K-wire for 6 weeks. Severe deformities or relapses may need a

21

The ankle and foot

hyperextension of the MTP joint may go on to dorsal dislocation. Shoe pressure may produce painful corns or callosities on the dorsum of the toe and under the prominent metatarsal head. The cause is obscure: the similarity to boutonnière deformity of a finger suggests an extensor dysfunction, a view supported by the frequent association with a dropped metatarsal head, flat anterior arch and hallux valgus. A simpler explanation is that the toe was too long or the shoe too short.

(a)

(b)

609

21

X-rays show regional osteoporosis, sometimes a bone abscess and, with late disease, narrowing and irregularity of the joint space.

REGIONAL ORTHOPAEDICS

Treatment In addition to general treatment (Chapter 2) a removable splint is used to rest the foot in neutral position. If the disease is arrested early, the patient is allowed up non-weightbearing in a calliper; gradually taking more weight and then discarding the calliper altogether. Following arthritis, weightbearing is harmless, but stiffness is inevitable and usually arthrodesis is the best treatment.

RHEUMATOID ARTHRITIS (see also Chapter 3) The ankle and foot are affected almost as often as the wrist and hand. Early on there is synovitis of the MTP, intertarsal and ankle joints, as well as of the sheathed tendons (usually the peronei and tibialis posterior). As the disease progresses, joint erosion and tendon dysfunction prepare the ground for increasingly severe deformities.

FOREFOOT Pain and swelling of the MTP joints are among the earliest features of rheumatoid arthritis. Shoes feel uncomfortable and the patient walks less and less. Tenderness is at first localized to the MTP joints; later the entire forefoot is painful on pressing or squeezing. With increasing weakness of the intrinsic muscles and joint destruction, the characteristic deformities appear: a flattened anterior arch, hallux valgus, claw toes and prominence of the metatarsal heads in the sole (patients say it feels like walking on pebbles). Subcutaneous nodules are common and may ulcerate.

(a)

610

(b)

Dorsal corns and plantar callosities also may break down and become infected. In the worst cases the toes are dislocated, inflamed, ulcerated and useless. X-rays show osteoporosis and peri-articular erosion at the MTP joints. Curiously – in contrast to the situation in the hand – the smaller digits (fourth and fifth toes) are affected first.

Treatment During the stage of synovitis, corticosteroid injections and attention to footwear may relieve symptoms; operative synovectomy is occasionally needed. Once deformity is advanced, treatment is that of the claw toes and hallux valgus. Sometimes specially made shoes will accommodate the toes in relative comfort. If this does not help, the most effective operation is excision arthroplasty in order to relieve pressure in the sole and to correct the toe deformities. For the hallux, an alternative is MTP fusion. Forefoot surgery is more likely to succeed if the hindfoot is held in the anatomical position. It is important, therefore, to treat the foot as a whole and attend also to the proximal joints.

ANKLE AND HINDFOOT The earliest symptoms are pain and swelling around the ankle. Walking becomes increasingly difficult and, later, deformities appear. On examination, swelling and tenderness are usually localized to the back of the medial malleolus (tenosynovitis of tibialis posterior) or the lateral malleolus (tenosynovitis of the peronei). Less often the ankle swells (joint synovitis) and its movements are restricted. Inversion and eversion may be painful and limited; subtalar erosion is common. In the late stages the tibialis posterior may rupture (all too often this is missed), or become ineffectual with progressive erosion of the tarsal joints, and the foot gradually drifts into severe valgus deformity. X-rays show osteoporosis and, later, erosion of the tarsal and ankle joints. Soft tissue swelling may be marked.

(c)

21.30 Rheumatoid arthritis (a,b) Forefoot deformities are similar to those in non-rheumatoid feet but more severe. They are due to a combination of joint erosion and tendon attrition. (c) Swelling and deformity of the hindfoot due to a combination of arthritis and tenosynovitis. In this case, both the ankle and the subtalar joints are affected.

loarthropathies. This appears in the foot as plantar fasciitis and Achilles tendinitis. Splintage and local injection of triamcinolone are helpful.

(a)

(b)

21.31 Rupture of tibialis posterior tendon (a) This patient with rheumatoid arthritis suddenly developed a painful valgus foot on the left. (b) The deformity was well controlled by a lightweight orthosis, and operative repair was unnecessary.

Treatment In the stage of synovitis, splintage is helpful (to allow inflammation to subside and to prevent deformity) while waiting for systemic treatment to control the disease. Initially, tendon sheaths and joints may be injected with methylprednisolone, but this should not be repeated more than two or three times because of the risk of tendon rupture. A lightweight below-knee calliper with an inside supporting strap restores stability and may be worn almost indefinitely. If the synovitis does not subside, operative synovectomy is advisable. Frayed tendons cannot be repaired and, although tendon replacement is technically feasible, progressive erosion of the hindfoot joints will countervail any improvement this might achieve. In the very late stage, arthrodesis of the ankle and tarsal joints can still restore modest function and abolish pain. The place of arthroplasty is not yet firmly established.

Swelling, redness, heat and exquisite tenderness of the MTP joint of the great toe (‘podagra’) is the epitome of gout. The ankle joint, or one of the toes, may be similarly affected – especially following a minor injury. The condition may closely resemble septic arthritis, but the systemic features of infection are absent. The serum uric acid level may be raised. Treatment with anti-inflammatory drugs will abort the acute attack of gout; until the pain subsides the foot should be rested and protected from injury.

The ankle and foot

GOUT (see also Chapter 4)

21

Chronic tophaceous gout Tophi may appear around any of the joints. The diagnosis is suggested by the characteristic x-ray features and confirmed by identifying the typical crystals in the tophus. Treatment may require local curettage of the bone lesions.

Pain under the heel due to plantar fasciitis is another manifestation of gout, though the association may be hard to prove in any particular case.

Plantar fasciitis

OSTEOCHONDRITIS DISSECANS OF THE TALUS Unexplained pain and slight limitation of movement in the ankle of a young person may be due to a small osteochondral fracture of the upper surface of the talus, though the injury may have been forgotten. X-rays taken at appropriate angles to produce tangential views of the talar surface show the small bony separation (no more than a few millimetres in diameter) at either the anteromedial or posterolateral part of the superior surface of the talus. MRI is also helpful and the lesion may be visualized directly by arthroscopy.

SERONEGATIVE ARTHROPATHIES The seronegative arthropathies are dealt with in Chapter 3. These conditions are similar to rheumatoid arthritis, but there are differences in the pattern of joint involvement, the severity of the changes and the soft tissue features. The clinical features are often asymmetrical and the ankle and hindfoot tend to be more severely affected than the forefoot. However, in psoriatic arthritis the toe joints are sometimes completely destroyed. An inflammatory reaction around the insertions of tendons and ligaments is a feature of the spondy-

(a)

(b)

21.32 Gout (a) The classical image of gout in the big toe. An inflamed 1st MTP joint. (b) X-ray showing large erosions due to tophi at the first metatarsal head.

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21

ANKLE OSTEOARTHRITIS

REGIONAL ORTHOPAEDICS

(see also Chapter 5)

(a)

(b)

21.33 Osteochondritis dissecans (a) Osteochondritis dissecans at the common site, the anteromedial part of the articular surface of the talus. (b) More extensive lesions can lead to secondary OA of the ankle.

Treatment depends on the degree of cartilage damage. As long as the articular cartilage is intact, it is sufficient to restrict activities. Once it is softened, arthroscopic drilling may be helpful. A loose fragment may need to be removed, but often the symptoms are insufficient to warrant intervention.

ATRAUMATIC OSTEONECROSIS OF THE TALUS (see also Chapter 6)

612

Osteonecrosis of the talus is a well-recognized complication of trauma (dislocation or fracture of the neck of the talus). Atraumatic osteonecrosis, though less common than its counterpart in the femoral head, is associated with the same group of systemic disorders as the latter (hypercortisonism, alcoholism, systemic lupus erythematosus, Gaucher’s disease, sickle-cell disease etc.) and is often one of multiple sites affected. Patients complain of pain, which is often aggravated by weightbearing, and gradually increasing restriction of movement. X-rays and MRI show the typical features of osteonecrosis, almost always involving the posterolateral part of the talar dome. Lesions can be staged according to Ficat’s radiographic classification (see Chapter 6). For purposes of treatment, it is important to distinguish between ‘pre-collapse’ and ‘collapse’ of the talar dome. Conservative treatment is sometimes effective; the ankle is more forgiving than the hip and patients may cope for some years on simple analgesics and restricted weightbearing. If symptoms persist and interfere significantly with function, operative treatment may be needed. During the pre-collapse phase, core decompression is worth trying as a first approach. If this fails, ankle arthrodesis is indicated (Delanois et al., 1998).

OA of the ankle is far less common than OA of the hip or knee; when it does occur it is almost always secondary to some underlying disorder: a malunited fracture, recurrent instability, osteochondritis dissecans of the talus, avascular necrosis of the talus or repeated bleeding with haemophilia. Sometimes, however, the ankle is involved in generalized OA and crystal arthropathy (See Chapter 4).

Clinical features The presentation is usually with pain and stiffness localized to the ankle, particularly noticed at ‘start up’, when first standing up from rest. Patients often indicate the site of pain as being transversely across the front of the ankle. The ankle is usually swollen, with palpable anterior osteophytes and tenderness along the anterior joint line. Dorsiflexion (extension) and plantarflexion at the ankle are often restricted. If heel inversion and eversion movements are restricted then suspect subtalar joint involvement. Gait is often anatalgic, offloading the affected leg; the foot is often turned outwards as the patient walks through on the affected ankle, to compensate for the loss of ankle movement. X-rays show the typical features of OA; the predisposing disorder is almost always easily detected.

Treatment When the condition flares up, minor, generally nonintrusive symptoms can be managed with analgesia or NSAIDs. Relative rest of the joint might be achieved with the use of a walking stick; weight loss might be appropriate. Activity such as walking, cycling and swimming can be encouraged.

(a)

(b)

21.34 OA (a) The obvious malalignment that followed an old injury has led to OA. (b) In this ankle the narrowed joint space and subarticular cysts are characteristic of OA; the cause is not clear, though it may have been trauma.

Physiotherapy can be helpful in improving the range of movement, correcting gait and ensuring correct use of walking aids. An ankle support or brace may help.

DIABETIC FOOT The complications of longstanding diabetes mellitus often appear in the foot, causing chronic disability. More than 30 per cent of patients attending diabetic clinics have evidence of peripheral neuropathy or vascular disease and about 40 per cent of non-traumarelated amputations in British hospitals are for complications of diabetes. Factors affecting the foot are: (1) a predisposition to peripheral vascular disease; (2) damage to peripheral nerves; (3) reduced resistance to infection; (4) osteoporosis. Peripheral vascular disease Atherosclerosis affects mainly the medium-sized vessels below the knee. The patient may complain of claudication or ischaemic changes and

(a)

(b)

Early on, patients are usually unaware of the abnormality but clinical tests will discover loss of vibration and joint position sense and diminished temperature discrimination in the feet. Symptoms, when they occur, are mainly due to sensory impairment: symmetrical numbness and paraesthesia, dryness and blistering of the skin, superficial burns and skin cracks or ulceration due to shoe scuffing or localized pressure. Motor loss usually manifests as claw toes with high arches and this, in turn, may predispose to plantar ulceration.

Peripheral neuropathy

21

The ankle and foot

OPERATIVE TREATMENT Ankle arthritis that is interfering with the activities of daily living and limiting work, social or domestic function warrants consideration for operative treatment. Depending on the severity of the condition, ankle surgery such as arthroscopic or open removal of anterior osteophytes (cheilectomy) might be offered, and consideration may be given to ankle arthrodesis; the ideal position for fusion is at zero in the sagittal plane (the foot therefore plantigrade) and 5 degrees of valgus. Total ankle arthroplasty is not as well established as hip and knee arthroplasty, but encouraging results are being reported.

ulceration in the foot. The skin feels smooth and cold, the nails show trophic changes and the pulses are weak or absent. Doppler studies should corroborate the clinical findings. Superficial ulceration occurs on the toes, deep ulceration typically under the heel; unlike neuropathic ulcers, these are painful and tender. Digital vessel occlusion may cause dry gangrene of one or more toes; proximal vascular occlusion is less common but more serious, sometimes resulting in extensive wet gangrene.

Neuropathic joint disease ‘Charcot joints’ occur in less than 1 per cent of diabetic patients, yet diabetes is the commonest cause of a neuropathic joint in Europe and America (leprosy and tertiary syphilis being the other common causes worldwide). The mid-tarsal joints are the most commonly affected, followed by the MTP and ankle joints. There is usually a provocative incident, such as a twisting injury or a fracture, following which the joint collapses relatively painlessly. X-rays show marked and fairly rapid destruction of the articular surfaces. These changes are easily mistaken for infection but the simultaneous involvement of several small joints and the lack of systemic signs point to a neuropathic disorder. Joint aspiration and microbiological investigation will also help to exclude infection.

(c)

21.35 The diabetic foot 1 (a) Ulceration in a patient with poorly controlled diabetes. (b,c) Despite the severe changes in these two patients with diabetic neuropathy, the feet were relatively painless.

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21

In late cases there may be severe deformity and loss of function. A rocker-bottom deformity from collapse of the midfoot is diagnostic. There is a generalized loss of bone density in diabetes. In the foot the changes may be severe enough to result in insufficiency fractures around the ankle or in the metatarsals.

REGIONAL ORTHOPAEDICS

Osteoporosis

614

Infection Diabetes, if not controlled, is known to have

a deleterious effect on white cell function. This, combined with local ischaemia, insensitivity to skin injury and localized pressure due to deformity, makes sepsis an ever-recurring hazard.

Management The orthopaedic surgeon will usually be one member of a multidisciplinary team comprising a physician (or endocrinologist), surgeon, chiropodist and orthotist. The best way of preventing complications is to insist on regular attendance at a diabetic clinic, full compliance with medication, examination for early signs of vascular or neurological abnormality, advice on foot care and footwear and a high level of skin hygiene. Examination for early signs of neuropathy should include the use of Semmes–Weinstein hairs (for testing skin sensibility) and a biothesiometer (for testing vibration sense). Peripheral vascular examination is enhanced by using a Doppler ultrasound probe. Ulcers must be swabbed for infecting organisms; frequently, multiple bacterial types are isolated (anaerobes make a regular appearance). X-ray examination may reveal periosteal reactions, osteoporosis, cortical defects near the articular margins and osteolysis – often collectively described as ‘diabetic osteopathy’. Great care is needed with nail trimming; skin cracks should be kept clean and covered and ulcers should be treated with local dressings and antibiotics if necessary. Occasionally, septicaemia calls for admission to hospital and treatment with intravenous antibiotics. Ischaemic changes need the attention of a vascular surgeon who can advise on ways of improving the local blood supply. Arteriography may show that bypass surgery is feasible. Dry gangrene of the toe can be allowed to demarcate before local amputation; severe occlusive disease with wet gangrene may call for immediate amputation. Indolent neuropathic ulcers require patient dressing and, if infected, antibiotic treatment. Total contact casts may avoid the need for prolonged inpatient stays or bed rest (Coleman et al., 1984). If a bony ‘high spot’ is identified, it should be trimmed or excised. Custom-made shoes with total contact insoles must follow the successful healing of these ulcers to avoid recurrence. Insufficiency fractures should be treated, if possible, without immobilizing the limb; or, if a cast is essen-

tial, it should be retained for the shortest possible period. Neuropathic joint disease is a major challenge. Arthrodesis is fraught with difficulty, not least a very poor union rate, and sometimes is simply not feasible. ‘Containment’ of the problem in a weight-relieving orthosis may be the best option. Bone or joint infection is an ever-present risk and should be borne in mind in the differential diagnosis of insufficiency fractures and neuropathic joint erosion. This will require urgent treatment.

DISORDERS OF THE TENDO ACHILLIS

ACHILLES TENDINITIS Athletes, joggers and hikers often develop pain and swelling around the tendo Achillis, due to local irritation of the tendon sheath or the paratenon.

Pathology The condition usually affects the ‘watershed’ area about 4 cm above the insertion of the tendon, an area where the blood supply to the tendon is poorer than elsewhere. The tendon sheath or the flimsy tissue around it may become inflamed. In a minority of cases the changes appear at the tendon insertion, or there may be inflammation of the retrocalcaneal bursa just above the calcaneum and deep to the tendon; anatomical deformity of the posterior part of the calcaneum may contribute to the pathogenesis.

Clinical features The condition may come on gradually, or rapidly following a change in sporting activity (or a change of sports footwear). Less commonly there is a history of direct trauma to the Achilles tendon. The area above the heel may look inflamed and function is inhibited because of pain in the heel-cord, especially at pushoff. The tendon feels thickened in the watershed area about 4 cm above its insertion. In chronic cases an ultrasound scan may be helpful in confirming the diagnosis. If the onset is very sudden, suspect tendon rupture (see later).

Treatment If the condition starts acutely, it will often settle within about 6 weeks if treated appropriately. Referral for early physiotherapy is important. In the interim, advice on rest, ice, compression and elevation (RICE) and the use of an NSAID (oral or topical) are helpful.

When the symptoms improve, stretching exercises, followed by a muscle strengthening programme, should be advised. The use of a removeable in-shoe heel-raise might be helpful. If there is a plano-valgus hindfoot, correction with orthotics will often bring about improvement and reduce the risk of recurrence. When the onset is insidious and treatment is started late, symptoms will be prolonged and may last for 9 months or longer. Operative treatment is seldom necessary but if symptoms fail to settle with physiotherapy then surgery may be appropriate – even more so if there is suspicion of an acute (or missed) tendon rupture. This will involve some type of ‘decompressive’ operation. Treatments such as radiofrequency coblation or extracorporeal shockwave lithotripsy are now showing some promise.

up and stretch before sport, previous injury or tendinitis and corticosteroid injection.

Potential pitfalls

Differential diagnosis

Injection with corticosteroids should be avoided. Tendon rupture is a real risk and could well give rise to litigation. Do not diagnose ‘partial rupture’ of the Achilles tendon; this should only be entertained if there is clearly some discontinuity of the tendon on ultrasound scan.

Incomplete tear A complete rupture is often mistaken

A ripping or popping sensation is felt, and often heard, at the back of the heel. This most commonly occurs in sports requiring an explosive push-off: squash, badminton, football, tennis, netball. The patient will often report having looked round to see who had hit them over the back of the heel, the pain and collapse are so sudden. The typical site for rupture is at the vascular watershed about 4 cm above the tendon insertion onto the calcaneum. The condition is often associated with poor muscle strength and flexibility, failure to warm

(a)

(b)

Examination Plantarflexion of the foot is usually inhibited and weak (although it may be possible, as the long flexors of the toes are also ankle flexors). There is often a palpable gap at the site of rupture; bruising comes out a day or two later. The calf squeeze test (Thompson’s or Simmond’s test) is diagnostic of Achilles tendon rupture: normally, with the patient prone, if the calf is squeezed the foot will plantarflex involuntarily; if the tendon is ruptured the foot remains still. Clinical assessment is often sufficient. Ultrasound scans must be used to confirm or refute the diagnosis.

The ankle and foot

ACHILLES TENDON RUPTURE

21

for a partial tear (which is rare). The mistake arises because, if a complete rupture is not seen within 24 hours, the gap is difficult to feel; moreover, the patient may by then be able to stand on tiptoe (just), by using his or her long toe flexors. A tear at the musculotendinous junction causes pain and tenderness halfway up the calf. This recovers with the aid of physiotherapy and raising the heel of the shoe.

Tear of soleus muscle

Treatment If the patient is seen early, the ends of the tendon may approximate when the foot is passively plantarflexed. If so, a plaster cast or special boot is applied with the foot in equinus; rehabilitation and physiotherapy regimes vary, but it is probably safe, and may be better for eventual tendon strength, to commence physiotherapy within 4–6 weeks. A shoe with a raised heel should be worn for a further 6–8 weeks. The ‘re-rupture rate’ is about 10 per cent.

(c)

21.36 Tendo Achillis (a) The soleus may tear at its musculotendinous junction (1), but the tendo Achillis itself ruptures about 5 cm above its insertion (2). (b) The depression seen in this picture at the site of rupture later fills with blood. (c) Simmonds’ test: both calves are being squeezed but only the left foot plantarflexes – the right tendon is ruptured.

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21

Operative repair is associated with an earlier return to function, better tendon and calf muscle strength and a lower re-rupture rate. Supported rehabilitation and physiotherapy are commenced early (within a week or two of repair) There are, however, risks associated with operative tendon repair, including wound healing problems and sural nerve neuroma. For ruptures that present late, reconstruction using local tendon substitutes (e.g. flexor hallucis longus tendon) or strips of fascia lata is still possible.

PARALYZED FOOT Weakness or paralysis of the foot may be symptomless, or may present in one of three characteristic ways: the patient may: (1) complain of difficulty in walking; (2) ‘catch his toe’ on climbing stairs (due to weak dorsiflexion); (3) stumble and fall (due to instability).

Clinical features Upper motor neuron lesions Spastic paralysis may occur in children with cerebral palsy or in adults following a stroke. Muscle imbalance usually leads to equinus or equinovarus deformity. The reflexes are brisk but sensation is normal. The entire limb (or both lower limbs) is usually abnormal. Lower motor neuron lesions Poliomyelitis was (and in some parts of the world still is) a common cause of foot paralysis. If all muscle groups are affected, the foot is flail and dangles from the ankle; if knee extension is also weak, the patient cannot walk without a calliper. With unbalanced weakness, the foot develops fixed deformity; it may also be smaller and colder than normal, but sensation is normal. Other lower motor neuron disorders such as spinal cord tumours, peroneal muscular atrophy and severe nerve root compression are rare causes of foot weakness or deformity.

616

Peripheral nerve injuries The sciatic, lateral popliteal or peroneal nerve may be affected. The commonest abnormalities are drop-foot and weakness of peroneal action. Postoperative or postimmobilization drop-foot may be due to pressure on the lateral popiteal or on the peroneal nerve as the leg rolls into external rotation. In addition to motor weakness there is an area of sensory loss. Unless the nerve is divided, recovery is possible but may take many months. ‘Peroneal nerve lesion’ is sometimes diagnosed after a hip operation. Beware! This is more often due to injury of the peroneal portion of the sciatic nerve.

Treatment The weakness may need no treatment at all, or only a drop-foot splint. Drop-foot due to nerve palsy can be treated by transferring the tibialis posterior through the interosseous membrane to the midtarsal region. Spastic paralysis is treated by tendon release and transfer, but great care is needed to prevent overaction in the new direction. Thus, a spastic equinovarus deformity may be converted to a severe valgus deformity by transferring the tibialis anterior to the lateral side; this is avoided if only half the tendon is transferred. Fixed deformities must be corrected first before doing tendon transfers. If no adequate tendon is available to permit dynamic correction, the joint may be reshaped and arthrodesed; at the same time muscle rebalancing (even of weak muscles) is necessary, otherwise the deformity will recur.

PAINFUL ANKLE Except after trauma or in rheumatoid arthritis, persistent pain around the ankle usually originates in one of the peri-articular structures or the talus rather than the joint itself. Conditions to be looked for are chronic ligamentous instability, tenosynovitis of the tibialis posterior or peroneal tendons, rupture of the tibialis posterior tendon, osteochondritis dissecans of the dome of the talus or avascular necrosis of the talus. Tenosynovitis Tenderness and swelling are localized to

the affected tendon, and pain is aggravated by active movement – inversion or eversion against resistance. Local injection of corticosteroid usually helps. Rupture of tibialis posterior tendon Pain starts quite suddenly and sometimes the patient gives a history of having felt the tendon snap. The heel is in valgus during weightbearing; the area around the medial malleolus is tender and active inversion of the ankle is both painful and weak. In physically active patients, operative repair or tendon transfer using the tendon of flexor digitorum longus is worthwhile. For poorly mobile patients, or indeed anyone who is prepared to put up with the inconvenience of an orthosis, splintage may be adequate (see Fig. 21.31). Osteochondritis dissecans of the talus Unexplained pain and slight limitation of movement in the ankle of a young person may be due to a small osteochondral fracture of the dome of the talus. Tangential x-rays will usually show the tiny fragment. MRI is also helpful and the lesion may be visualized directly by arthroscopy. If the articular surface is intact, it is sufficient to simply

21

(b)

(c)

21.37 The paralyzed foot (a) In spina bifida – the small ulcer is an indication of insensitive skin. (b) Poliomyelitis and (c) peroneal muscular atrophy, in both of which sensation is normal.

restrict activities. If the fragment has separated, it may have to be removed.

a little and strenuous activities restricted for a few weeks.

Avascular necrosis of the talus The talus is one of the preferred sites of ‘idiopathic’ necrosis. The causes are the same as for necrosis at other more common sites such as the femoral head. If pain is marked, arthrodesis of the ankle may be needed.

Calcaneal bursitis Older girls and young women often

Chronic instability of the ankle This subject is dealt with

in Chapter 3.

PAINFUL FEET “My feet are killing me!” This complaint is common but the cause is often elusive. Pain may be due to: (1) mechanical pressure (which is more likely if the foot is deformed or the patient obese); (2) joint inflammation or stiffness; (3) a localized bone lesion; (4) peripheral ischaemia; (5) muscular strain – usually secondary to some other abnormality. Remember, too, that local disorders may be part of a generalized disease (e.g. diabetes or rheumatoid arthritis), so examination of the entire patient may be indicated. Specific foot disorders that cause pain are considered later.

The ankle and foot

(a)

complain of painful bumps on the backs of their heels. The posterolateral portion of the calcaneum is prominent and shoe friction causes retrocalcaneal bursitis. Symptoms are worse in cold weather and when wearing high-heeled shoes (hence the use of colloquial labels such as ‘winter heels’ and ‘pumpbumps’). Treatment should be conservative – attention to footwear (open-back shoes are best) and padding of the heel. Operative treatment – removal of the bump

(a)

(b)

Two common causes of heel pain are traction ‘apophysitis’ and calcaneal bursitis:

(c)

(d)

Traction ‘apophysitis’ (Sever’s disease) This condition usually occurs in boys aged about 10 years. It is not a ‘disease’ but a mild traction injury. Pain and tenderness are localized to the tendo Achillis insertion. The x-ray report usually refers to increased density and fragmentation of the apophysis, but often the painless heel looks similar. The heel of the shoe should be raised

21.38 Painful heel (a) Sever’s disease – the apophysis is dense and fragmented. (b) Bilateral ‘heel bumps’. (c) The usual site of tenderness in plantar fasciitis. (d) X-ray in patients with plantar fasciitis often shows what looks like a spur on the undersurface of the calcaneum. In reality this is a two-dimensional view of a small ridge corresponding to the attachment of the plantar fascia. It is doubtful whether the ‘spur’ is responsible for the pain and local tenderness.

POSTERIOR HEEL PAIN

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REGIONAL ORTHOPAEDICS

21

or dorsal wedge osteotomy of the calcaneum – is feasible but the results are unpredictable; despite the reduction in the size of the bumps, patients often continue to experience discomfort, potentially added to by an operation scar.

INFERIOR HEEL PAIN Any bone disorder in the calcaneum can present as heel pain: a stress fracture, osteomyelitis, osteoid osteoma, cyst-like lesions and Paget’s disease are the most likely. X-rays usually provide the diagnosis.

Calcaneal bone lesions

PLANTAR FASCIITIS This is an annoying and painful condition that limits function. There is pain and tenderness in the sole of the foot, mostly under the heel, with standing or walking. The condition usually comes on gradually, without any clear incident or injury but sometimes there is a history of sudden increase in sporting activity, or a change of footwear, sports shoes or running surface. There may be an associated tightness of the Achilles tendon. The pain is often worse when first getting up in the morning, with typical hobbling downstairs, or when first getting up from a period of sitting – the typical start-up pain and stiffness. The pain can at times be very sharp, or it may change to a persistent background ache as the patient walks about. The condition can take 18–36 months or longer to resolve, but is generally self-limiting, given time.

Pathology The plantar fascia or aponeurosis is a dense fibrous structure that originates from the calcaneum, deep to the heel fat pad, and runs distally to the ball of the foot, with slips to each toe. The plantar fascia stiffens and becomes less pliable with age. The fascia is probably not actually inflamed in this condition, at least not beyond the first week or two of onset. There may be micro-tears in the fascia, and the fascia thickens. The term ‘plantar fasciitis’ is apt in some cases, as the condition is sometimes associated with inflammatory disorders such as gout, ankylosing spondylitis and Reiter’s disease, in which enthesopathy is one of the defining pathological lesions.

Clinical features

618

There is localized tenderness, usually at the medial aspect beneath the heel and sometimes in the midfoot. This is essentially a clinical diagnosis. If there are features suggesting an inflammatory disease (seroneg-

ative arthropathy) then blood tests may be indicated. An ultrasound scan shows the thickening and sometimes the Doppler test shows increased local blood flow and neovascularization, but this investigation is not indicated in every case. A plain lateral x-ray can help to exclude a stress fracture, and will often show what looks like a bony spur on the undersurface of the calcaneum. The ‘spur’ is, in fact, a bony ridge that looks sharp and localized in the two-dimensional x-ray image; it is an associated, not a causative, feature in plantar fasciitis. Patients, and sometimes doctors, can become fixated on the idea of a spur of bone causing the symptoms by digging into the plantar fascia, and cannot conceive of how the condition could possibly resolve whilst the spur remains – but it can and does get better. MRI can be helpful in excluding a calcaneal stress fracture, which is an important differential diagnosis.

Treatment Relative rest and NSAIDs can be helpful in settling the condition in the early stages, with NSAIDs either orally or topically. An analysis of causative factors (footwear, sports and exercise factors) can help the patient to overcome the condition. There is an important role for the patient in managing the condition, with stretching exercises and massage; self-help advice sheets are available. Patients might expect (or dread!) an injection into the plantar fascia, and they are right to be apprehensive. There is no convincing research to support this, and there is evidence to show that it can lead to rupture of the plantar fascia (which will often immediately ease the symptoms, but leads to a painful flatfoot and impairs sporting function). A physiotherapist can help to educate the patient about the condition and its likely progress, and can emphasize the need for a regular stretching regime for 8–12 weeks, supplemented with local massage (for instance with a foot roller, golf ball, frozen water bottle). Local manual treatments from the physiotherapist can help, as can the use of taping and a cushioned heel pad. Night splints have been tried, to keep the foot up in a plantigrade position overnight, preventing stiffening in the Achilles and plantar fascia; there is logic in this, but no clear evidence for its efficacy, and trials have been hampered by poor compliance. Podiatric assessment of the hindfoot biomechanics may identify predisposing factors such as plano-valgus hindfoot alignment, which can be corrected with orthotics. OPERATIVE TREATMENT Patients may lose heart and demand that something be done. However, there is no reliable surgical proce-

21

Potential pitfalls

(a)

(b)

It is important not to miss a manifestation of a systemic disease such as an inflammatory arthropathy (often seronegative), a peripheral neuropathy (usually diabetic) or a stress fracture. If a corticosteroid steroid injection is used it should be done cautiously with a small dose into a limited area, and after appropriate warnings to the patient. Excising a ‘spur’ is usually a vain endeavour.

Differential diagnosis Chronic pain and tenderness directly over the fat pad under the heel sometimes follows a direct blow to the area, e.g. in a fall from a height. The condition is also seen in athletes and has been attributed variously to separation of the fat pad from the bone, loss of its normal shock-absorbing effect and atrophy. Non-specific ‘inflammation’ has also been blamed. Treatment is palliative: wearing soft-soled shoes or shock-absorbing heel cups, foot baths and anti-inflammatory agents. Painful fat pad

Nerve entrapment Entrapment of the first branch of the lateral plantar nerve has been reported as a cause of heel pain. The commonest complaint is pain after sporting activities. Characteristically, tenderness is maximal on the medial aspect of the heel, where the small nerve branch is compressed between the deep fascia of abductor hallucis and the edge of the quadratus plantae muscle. Diagnosis is not easy, because the symptoms and signs may mimic those of plantar fasciitis. Treatment, in the first instance, is conservative: a long trial (6–8 months) of shock-absorbing orthoses, foot baths, anti-inflammatory preparations and one or two corticosteriod injections. Only if these measures fail to give relief should surgical decompression of the nerve be considered.

PAIN OVER THE MIDFOOT In children, pain in the midtarsal region is rare: one cause is Kohler’s disease (osteochondritis of the navicular). The bony nucleus of the navicular becomes dense and fragmented. The child, under the age of 5,

(c)

The ankle and foot

dure for this condition. Limited fasciotomy to release part of the plantar fascia can help in some cases, but there is a significant risk of complications including worsening of the condition. Promising new interventions include shockwave lithotripsy and localized radiofrequency (coblation) therapy, but these have yet to be fully tested in rigorous and large-scale studies.

(d)

21.39 Pain over the midfoot (a) Köhler’s disease compared with (b) the normal foot. (c,d) The bump on the dorsum of the foot due to OA of the first cuneiformmetatarsal joint.

has a painful limp and a tender warm thickening over the navicular. Usually no treatment is needed as the condition resolves spontaneously. If symptoms are severe, a short period in a below-knee plaster helps. A comparable condition occasionally affects middle-aged women (Brailsford’s disease); the navicular becomes dense, then altered in shape, and later the midtarsal joint may degenerate. In adults, especially if the arch is high, a ridge of bone sometimes develops on the adjacent dorsal surfaces of the medial cuneiform and the first metatarsal (the ‘overbone’). A lump can be seen, which feels bony and may become bigger and tender if the shoe presses on it. If shoe adjustment fails to provide relief the lump may be bevelled off.

GENERALIZED PAIN IN THE FOREFOOT Metatarsalgia Generalized ache in the forefoot is a common expression of foot strain, which may be due to a variety of conditions that give rise to faulty weight distribution (e.g. flattening of the metatarsal arch, or undue shortening of the first metatarsal), or merely the result of prolonged or unaccustomed walking, marching, climbing or standing. These conditions have this in common: they give rise to a mismatch between the loads applied to the foot, the structure on which those loads are acting, and the muscular effort required

619

REGIONAL ORTHOPAEDICS

21

to maintain the structure so that it can support those loads. Aching is felt across the forefoot and the anterior metatarsal arch may have flattened out. There may even be callosities under the metatarsal heads. Treatment involves: (1) dealing with the mechanical disorder (correcting a deformity if it is correctable, supplying an orthosis that will redistribute the load, fitting a shoe that will accommodate the foot); and (2) performing regular muscle strengthening exercises, especially for the intrinsic muscles that maintain the anterior (metatarsal) arch of the foot. A good ‘do-ityourself’ exercise is for the patient to stand barefoot on the floor, feet together, and then drag their body forwards by repeatedly crimping the toes to produce traction upon the floor. Ten minutes a day should suffice. Pain in metatarsophalangeal joints Inflammatory arthritis (e.g. rheumatoid disease) may start in the foot with synovitis of the MTP joints. Pain in these cases is associated with swelling and tenderness of the forefoot joints and the features are almost always bilateral and symmetrical.

LOCALIZED PAIN IN THE FOREFOOT Whereas metatarsalgia involves the entire forefoot, localized pain and tenderness is related to a specific anatomical site in the forefoot and could be due to a variety of bone or soft tissue disorders: ‘sesamoiditis’, osteochondritis of a metatarsal head (Freiberg’s disease), a metatarsal stress fracture or digital nerve entrapment (Morton’s disease).

Sesamoiditis Pain and tenderness directly under the first metatarsal head, typically aggravated by walking or passive dorsi-

(a)

620

(b)

flexion of the great toe, may be due to sesamoiditis. This term is a misnomer: symptoms usually arise from irritation or inflammation of the peritendinous tissues around the sesamoids – more often the medial (tibial) sesamoid, which is subjected to most stress during weightbearing on the ball of the foot. Acute sesamoiditis may be initiated by direct trauma (e.g. jumping from a height) or unaccustomed stress (e.g. in new athletes and dancers). Chronic sesamoid pain and tenderness should signal the possibility of sesamoid displacement, local infection (particularly in a diabetic patient) or avascular necrosis. Sesamoid chondromalacia is a term coined by Apley (1966) to explain changes such as fragmentation and cartilage fibrillation of the medial sesamoid. X-rays in these cases may show a bipartite or multipartite medial sesamoid, which is often mistaken for a fracture. Treatment, in the usual case, consists of reduced weightbearing and a pressure pad in the shoe. In resistant cases, a local injection of methylprednisolone and local anaesthetic often helps; otherwise the sesamoid should be shaved down or removed, taking great care not to completely interrupt the flexor hallucis brevis tendon.

Freiberg’s disease (osteochondritis; osteochondrosis) Osteochondritis (or osteochondrosis) of a metatarsal head is probably a type of traumatic osteonecrosis of the subarticular bone in a bulbous epiphysis (akin to osteochondritis dissecans of the knee). It usually affects the second metatarsal head (rarely the third) in young adults, mostly women. The patient complains of pain at the MTP joint. A bony lump (the enlarged head) is palpable and tender and the MTP joint is irritable. X-rays show the head

(c)

(d)

21.40 Pain in the forefoot (a) Long-standing deformities such as dropped anterior arches, hallux valgus, hammer-toe, curly toes and overlapping toes (all of which are present in this patient) can cause metatarsalgia. Localized pain and tenderness suggest a more specific cause. (b,c) Stages in the development of Freiberg’s disease. (d) Periosteal new-bone formation along the shaft of the second metatarsal, the classic sign of a healing stress fracture.

Stress fracture Stress fracture, usually of the second or third metatarsal, occurs in young adults after unaccustomed activity or in women with postmenopausal osteoporosis. The dorsum of the foot may be slightly oedematous and the affected shaft feels thick and tender. The x-ray appearance is at first normal, but later shows fusiform callus around a fine transverse fracture. Long before x-ray signs appear, a radioisotope scan will show increased activity. Treatment is either unnecessary or consists simply of rest and reassurance.

Interdigital nerve compression (Morton’s metatarsalgia) Morton’s metatarsalgia is a common problem, with neuralgia affecting a single distal metatarsal interspace, usually the third (affecting the third and fourth toes), sometimes the second (affecting the second and third toes), rarely others. The patient typically complains of pain on walking, with the sensation of walking on a pebble in the shoe, or of the sock being rucked-up under the ball of the foot. The pain is worse in tight footwear and often has to be relieved by removing the footwear and massaging the foot. Activities that load the forefoot (running, jumping, dancing) exacerbate the condition, which often consists of severe forefoot pain and then a reluctance to weightbear. In Morton’s metatarsalgia the pain is typically reproduced by laterally compressing the forefoot whilst also compressing the affected interspace – this produces the pathognomic Mulder’s click as the ‘neuroma’ displaces between the metatarsal heads. This is essentially an entrapment or compression syndrome affecting one of the digital nerves, but secondary thickening of the nerve creates the impression of a ‘neuroma’. The lesion, and an associated bursa, occupy a restricted space between the distal metatarsals, and are pinched, especially if footwear also laterally compresses the available space. Treatment A step-wise treatment programme is advis-

able. Simple offloading of the metatarsal heads by using a metatarsal dome insole and wider fitting shoes may help. If symptoms do not improve with these measures then a steroid injection into the interspace will bring about lasting relief in about 50 per cent of cases.

Surgical intervention is often successful; the nerve should be released by dividing the tight transverse intermetatarsal ligament; this can be done through either a dorsal longitudinal or a plantar incision; most surgeons will also excise the thickened portion of the nerve. This is successful in about 90 per cent of patients; the remaining 10 per cent will continue to experience varying degrees of discomfort.

TARSAL TUNNEL SYNDROME Pain and sensory disturbance in the medial part of the forefoot, unrelated to weightbearing, may be due to compression of the posterior tibial nerve behind and below the medial malleolus. Sometimes this is due to a space-occupying lesion, e.g. a ganglion, haemangioma or varicosity. The pain is often worse at night and the patient may seek relief by walking around or stamping the foot. Paraesthesia and numbness may follow the characteristic sensory distribution, but these symptoms are not as well defined as in other entrapment syndromes. The diagnosis is difficult to establish but nerve conduction studies may show slowing of motor or sensory conduction.

21

The ankle and foot

to be flattened and wide, the neck thick and the joint space apparently increased. If discomfort is marked, a walking plaster or moulded sandal will help to reduce pressure on the metatarsal head. If pain and stiffness persist, operative synovectomy, debridement and trimming of the metatarsal head should be considered. Pain relief is usually good and the range of dorsiflexion is improved.

To decompress the nerve it is exposed behind the medial malleolus and followed into the sole; sometimes it is trapped by the belly of adductor hallucis arising more proximally than usual.

Treatment

SKIN DISORDERS Painful skin lesions are important for two reasons: (1) they demand attention in their own right; (2) postural adjustments to relieve pressure may give rise to secondary problems and metatarsalgia.

Corns and calluses These are hyperkeratotic lesions that develop as a reaction to localized pressure or friction. Corns are fairly small and situated at ‘high spots’ in contact with the shoe upper: the dorsal knuckle of a claw toe or hammer toe, or the tip of the toe if it impinges against the shoe. Soft corns also appear on adjacent surfaces of toes that rub against each other. Treatment consists of paring the hyperkeratotic skin, applying felt pads that will prevent shoe or toe pressure, correcting any significant deformity (if necessary by operation) and attending to footwear. Calluses are more diffuse keratotic plaques on the soles – either under prominent metatarsal heads or under the heel. They are seen mainly in people with ‘dropped’ metatarsal arches and claw toes, or varus or

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21

21.41 Skin lesions (a) Corns. (b) Callosities in a patient with claw toes and a ‘dropped’ anterior metatarsal arch. (c) A typical pressure ulcer in a patient with longstanding diabetic neuropathy. (d) Keratoderma blenorrhagica, a complication of Reiter’s disease.

(a)

(b)

(c)

(d)

valgus heels. Treatment is much the same as for corns; it is important to redistribute foot pressure by altering the shoes, fitting pressure-relieving orthoses and ensuring that the shoes can accommodate the malshaped feet. Surgical treatment for claw toes may be needed.

Plantar warts Plantar warts resemble calluses but they tend to be more painful and tender, especially if squeezed. They can be distinguished from calluses by paring down the hyperkeratotic skin to expose the characteristic papillomatous ‘core’, which is seen to be dotted with fine blood vessels. These are viral lesions but it is usually local pressure that renders them painful. Treatment is frustrating as they are difficult to eradicate. Salicylic acid plasters are applied at regular intervals, and smaller lesions may respond to cryosurgery. Surgical excision is avoided as this usually leaves a painful scar at the pressure site.

Foreign body ‘granuloma’

622

The sole is particularly at risk of penetration by small foreign bodies (usually a thorn, a splinter or a piece of glass), which may give rise to a painful lump resembling a wart or callus. This diagnosis should always be considered if the ‘callosity’ is situated in a non-

pressure area. X-rays may help to detect the foreign body. Treatment consists of removing the object; the reactive lesion heals quickly.

TOE-NAIL DISORDERS The toe-nail of the hallux may be ingrown, overgrown or undergrown. The nail burrows into the nail groove; this ulcerates and its wall grows over the nail, so the term ‘embedded toe-nail’ would be better. The patient is taught to cut the nail square, to insert pledgets of wool under the ingrowing edges and to keep the feet clean and dry at all times. If these measures fail, the portion of germinal matrix that is responsible for the ‘ingrow’ should be ablated, either by operative excision or by chemical ablation with phenol. The phenol is applied to the exposed matrix with a cotton bud for 3 minutes and then washed off with alcohol, which neutralizes the caustic effect. Rarely is it necessary to remove the entire nail or completely ablate the nail bed.

Ingrown toe-nails

Overgrown toe-nails (onychogryposis) The nail is hard, thick and curved. A chiropodist can usually make the patient comfortable, but occasionally the nail may need excision.

21.42 Toe-nail disorders (a) Ingrown toe-nails. (b) Overgrown toe-nail (onychogryposis). (c,d) Exostosis from the distal phalanx, pushing the toe-nail up.

(c)

The ankle and foot

(a)

21

(b)

(d)

Undergrown toe-nails A subungual exostosis grows on

the dorsum of the terminal phalanx and pushes the nail upwards. The exostosis should be removed.

NOTES ON APPLIED ANATOMY The ankle and foot function as an integrated unit, and together provide stable support, proprioception, balance and mobility.

ANKLE The ankle fits together like a tenon and mortise; the tibial and fibular parts of the mortise are bound together by the inferior tibiofibular ligament, and stability is augmented by the collateral ligaments. The medial ligament fans out from the tibial malleolus to the talus, the superficial fibres forming the deltoid ligament. The lateral ligament has three thickened bands: the anterior and posterior talofibular ligaments and, between them, the calcaneofibular ligament. Tears of these ligaments may cause tilting of the talus in its mortise. Forced abduction or adduction may disrupt the mortise altogether by (1) forcing the tibia and fibula apart (diastasis of the tibiofibular joint); (2) tearing the collateral ligaments; (3) fracturing the malleoli.

FOOT The footprint gives some idea of the arched structure of the foot. This derives from the tripodial bony framework between the calcaneum posteriorly and the first and fifth metatarsal heads. The medial arch is high, with the navicular as its keystone; the lateral arch is flatter. The anterior arch formed by the metatarsal bones thrusts maximally upon the first and fifth metatarsal heads and flattens out (spreading the foot) during weightbearing; it can be pulled up by contraction of the intrinsic muscles, which flex the MTP joints.

MOVEMENTS The ankle allows movement in the sagittal plane only (plantarflexion and dorsiflexion). Adduction and abduction (turning the toes towards or away from the midline) are produced by rotation of the entire leg below the knee; if either is forced at the ankle, the mortise fractures. Pronation and supination occur at the intertarsal and tarsometatarsal joints; the foot rotates about an axis running through the second metatarsal, the sole turning laterally (pronation) or medially (supination) – movements analogous to those of the forearm. The combination of plantarflexion, adduction and supination is called inversion; the opposite movement of dorsiflexion, abduction and pronation is eversion.

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21

(a)

(b)

(c)

21.43 Footprints (a) The normal foot, (b) flat-foot (the medial arch touches the ground), and (c) cavus foot (even the lateral arch barely makes contact).

Inversion and eversion are necessary for walking on rough ground or across a slope. If the joints at which they occur are arthrodesed in childhood, a compensatory change may occur at the ankle so that it becomes a ball-and-socket joint.

FOOT POSITIONS AND DEFORMITIES A downward-pointing foot is said to be in equinus; the opposite is calcaneus. If only the forefoot points downwards the term ‘plantaris’ is used. Supination with adduction produces a varus deformity; pronation with abduction causes pes valgus. An unusually high arch is called pes cavus. Many of these terms are used as if they were definitive diagnoses when, in fact, they are nothing more than Latin translations of descriptive anatomy.

REFERENCES AND FURTHER READING Apley AG. Open sessamoid. Proc R Soc Med 1966; 59: 120. Banta J, Sutherland DH, Wyatt M. Anterior tibialis transfer to os calcis with Achilles tenodesis for calcaneal deformity in myelomeningocoele. J Paediatr Orthop 1981; 1: 125–30. Caroll NC. Technique of plantar fascia release and calcaneocuboid joint release in clubfoot surgery. In: Simons

624

GW (Ed.) The Clubfoot. Springer-Verlag, New York, 1994, pp 246–52. Cholmeley JA. Elmslie’s operation for the calcaneus foot. J Bone Joint Surg 1953; 35B: 46–9. Coleman WC, Brand PW, Birke JA. The total contact cast. A therapy for plantar ulceration on insensitive feet. J Am Podiatry Med Assoc 1984; 74: 548–52. Coughlin MJ, Shurnas PS. Hallux rigidus: demographics, etiology, and radiographic assessment. Foot Ankle Int 2003; 24: 731–43. Crawford A, Marxen J, Osterfeld D. The Cincinatti incision: A comprehensive approach for surgical procedures of the foot and ankle in childhood. J Bone Joint Surg 1982; 64A: 1355–8. Delanois RE, Mont MA, Yoon TR et al. Atraumatic osteonecrosis of the talus. J Bone Joint Surg 1998; 80A: 529–36. Duncan RD, Fixsen JA. Congenital convex pes valgus. J Bone Joint Surg 1999; 81B: 250–4. Evans D. Relapsed clubfoot. J Bone Joint Surg 1961; 43B: 722–33. Gage JR. Gait Analysis in Cerebral Palsy. MacKeith Press, New York, 1991. Herzenberg JE, Carroll NC, Christofersen MR, Lee EH, White S, Munroe R. Clubfoot analysis with threedimensional computer modeling. J Paediatr Orthop 1988; 8: 257–62. Lapidus PW. Transplantation of the extensor tendon for correction of the overlapping fifth toe. J Bone Joint Surg 1942; 24: 555–9. Piggott H. The natural history of hallux valgus in adolescence and early adult life. J Bone Joint Surg 1960; 42B: 749–60. Ponsetti IV. Treatment of congenital club foot. J Bone Joint Surg 1992; 74A: 448–54. Rang M. High arches. In: Wenger DR, Rang M (Eds) The Art and Practice of Children’s Orthopaedics. Raven Press, New York, 1993, pp 168–79. Robinson AHN, Limbers JP. Modern concepts in the treatment of hallux valgus. J Bone Joint Surg 2005; 87B: 1038–45. Rose GK, Welton EA, Marshall T. The diagnosis of flat foot in the child. J Bone Joint Surg 1985; 67B: 71–8. Samilson RL. Proscentic osteotomy of the os calcis for calcaneocavus feet. In: Bateman JE (Ed.) Foot Science. WB Saunders, Philadelphia, 1976, p. 18. Turco V. Surgical correction of the resistant clubfoot. One stage posteromedial release with internal fixation; a preliminary report. J Bone Joint Surg 1971; 53A: 477–97.

Section 3 Fractures and Joint Injuries 22 23 24 25 26 27 28 29 30 31

The management of major injuries Principles of fractures Injuries of the shoulder, upper arm and elbow Injuries of the forearm and wrist Hand injuries Injuries of the spine Injuries of the pelvis Injuries of the hip and femur Injuries of the knee and leg Injuries of the ankle and foot

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The management of major injuries

22

David Sutton, Max Jonas

100%

INTRODUCTION Aetiology of major trauma Trauma is the commonest cause of death in people from 1–44 years of age throughout the developed world. The largest proportion of deaths (1.2 million per year) result from road accidents. The World Health Organization (WHO) predicts that by 2020 road traffic injuries will rank third in the causes of premature death and loss of health from disability (Peden et al., 2004). In the UK vehicular accidents causing death or serious injury are usually car related (Figs 22.1 and 22.2).

Other

80%

Bus or coach

60%

Car occupant

Motorcyclist 40% Pedal cyclist 20%

Global Percentage of Deaths due to Injury (1999) 5.0%

5.0%

Pedestrian 0%

11.0%

4.0% 14.0%

23.0%

17.0% 0.3% 18.0%

All 22.2 Proportion of casualties by road user type (UK 2007 Department of Transport data).

For every death from trauma, three victims suffer permanent disability. As well as causing personal tragedy, this represents an enormous drain on a nation’s healthcare economy; timely and effective management of major injuries can reduce both morbidity and mortality.

Mode of death

War

Homicide and Violence

Self-Inflicted

Other Unintentional Injuries

Landmines

Road Traffic

Poisoning

Falls

Fire

Source: WHO 22.1 Global percentage of deaths due to injury (1999) (World Health Organization, Department of Violence and Injury Prevention).

Mortality subsequent to major trauma is dependent on a number of factors, of which the economic level of a nation is a major determinant. The 2004 WHO report (Mock et al., 2004) cites mortality rates for seriously injured adults, i.e. those with an injury severity score (ISS) of 9 or higher. ISS will be described in greater detail in a subsequent section. The overall mortality rate, including pre-hospital and in-hospital deaths, is 35 per cent in high-income nations, but rises to 55 per cent in middle-income economies and

63 per cent in low-income economies. More seriously injured patients (ISS 15–24) reaching hospital show a six-fold increase in mortality in low-income economies. Road traffic deaths and serious injuries show a peak incidence in young people between the ages of 17 (age of learning to drive) and 23. There is a stark contrast between major trauma mortality in a high-income country hospital (6 per cent) and in a rural area of a low-income country (36 per cent). These statistics demonstrate the impact that a high-income economy with a developed emergency medical system can have on the outcomes of major trauma. Deaths as a result of trauma classically follow a trimodal pattern, with three waves following the injury. Some 50 per cent of fatally injured casualties die from non-survivable injuries immediately, or within minutes after the accidents; 30 per cent survive the initial trauma, but die within 1–3 hours; the remaining 20 per cent die from complications at a late stage during the 6 weeks after injury. This trimodality represents civilian trauma deaths; combat deaths in a war fit a bimodal distribution, with merging of the second and third peaks due to the penetrative nature of the injuries and the extended timelines of advanced medical care (Clasper and Rew, 2003). The initial mortality peak is usually due to non-survivable central nervous system or cardiovascular disruption. The severe nature of the injuries, the immediate nature of the deaths and the usual location in the pre-hospital environment means that very few of these casualties can be saved. However, a small proportion die as a result of early airway obstruction and external haemorrhage, and these deaths can be prevented by immediate first-aid measures. A significant proportion of head-injured casualties who die on the scene succumb not to the primary brain injury but to

Death rate

FRACTURES AND JOINT INJURIES

22

0

1

2

3 0 1 2 3 4 5 6 Weeks

Hours

22.4 Death following trauma The trimodal pattern of mortality following severe trauma.

secondary brain injury caused by the hypoxia and hypercarbia associated with airway obstruction and respiratory dysfunction. The second peak of deaths during the first few hours after injury is most often due to hypoxia and hypovolaemic shock. A significant proportion of these deaths can be avoided with an effective emergency medical service (EMS); hence, this period has been called ‘the golden hour’. One-third of all deaths occurring after major injury may be preventable in hospitals with appropriate resources (Commission on the Provision of Surgical Services, 1988). The third peak in the cumulative mortality rate within the 6 weeks following injury is largely due to multisystem failure and sepsis. These complications of trauma need a high level of intensive care, but can be reduced by early and effective treatment during the preceding phases of casualty management.

1200 Car passenger Car driver Motorcycle rider/passenger Pedal cyclist Pedestrian

1000 800 600 400 200 0 0

628

5

10

15

20

25

30

35

40

45

50

55

60

65

70

75

80

22.3 Deaths and serious injuries by road user type and age (UK 2007 Department of Transport data).

85

90⫹

22

Sequence of management

PRE-HOSPITAL MANAGEMENT Essential elements include: 1. 2. 3. 4. 5. 6. 7.

Organization. Safety on scene. Immediate actions and triage. Assessment and initial management. Extrication and immobilization. Transfer to hospital. Air ambulances.

22.5 Acid burns Patient with acid burns to his ear and chest from spilt battery acid during a car accident.

The most integrated system is probably the French Services de l’Aide Medical Urgente (SAMU): all emergencies are triaged by a control room team, which includes a doctor, and an appropriate response is mounted. For major cases, intervention is provided by Services Mobile d’Urgence et de Reanimation (SMUR) teams – hospital-based medical teams with sophisticated equipment and access to a range of transport including helicopters. SMUR teams can deliver an advanced level of care on scene with rapid transfer to an appropriate hospital, and European experience (Frankema et al., 2004) is that a doctor-led pre-hospital service leads to a 2.8-fold improvement in mortality for seriously injured patents. However, the service is very expensive and demands a high number of experienced medical staff (Earlam, 1997).

The management of major injuries

In developed healthcare systems, an effective EMS is available to initiate management at the scene of the injury and transfer the casualty rapidly to hospital. Immediate first-aid manoeuvres such as opening the airway and controlling external haemorrhage with direct pressure are life-saving interventions that require minimal equipment and training. More complex treatment requires specialist equipment and expert training not always available at the scene, and rapid transfer to a medical centre is mandatory. However, medical teams can deliver advanced management to entrapped casualties. Such treatment is difficult to deliver in vehicles and aircraft, and a balance has to be drawn between delaying to give treatment on scene and transferring an unstable casualty. In sophisticated healthcare systems, casualties are taken to the nearest hospital offering comprehensive Emergency Department management. Treatment is centred on evaluation, resuscitation and stabilization. This phase merges into definitive care in the operating theatre, with control of airway, ventilation and surgical management of haemorrhage. Musculoskeletal injuries are initially stabilized, followed by definitive treatment. Level 2 or 3 critical care may be required to minimize complications and prevent third-phase deaths, and prolonged rehabilitation may be necessary to address the needs of casualties with brain injuries and complex musculoskeletal damage.

Safety on scene and personal protective equipment Hospital doctors in acute specialties may be required to form part of a medical team to manage trauma cases on scene. Although surgery on entrapped

Organization Provision of a pre-hospital EMS depends on economic resources, and varies from no provision in rural, low-income countries to sophisticated services linked to hospital care in developed economies. The EMS in most countries is based on ambulances crewed by medical technicians or paramedics. Medical support is variable, ranging from volunteer doctors in the UK by the British Association for Immediate Care (BASICS) to hospital-based teams in North America.

(a)

(b)

22.6 Medical personal protective equipment (PPE) (a) Inadequate PPE. (b) Correct PPE.

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FRACTURES AND JOINT INJURIES

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casualties is a rare event, surgeons may be sent out for serious or major incidents, and so some knowledge of pre-hospital care is important. The scene of a traumatic incident is invariably hazardous, and the immediate priority for a doctor on scene is personal safety; if this is neglected, the doctor can become a casualty rather than a rescuer. Some hazards are obvious, such as unstable wreckage, jagged metal debris and fire. However, there are concealed hazards that can injure the unwary. Undeployed airbags can be triggered, and a variety of toxic chemicals can be released, such as battery acid. All members of pre-hospital medical teams should therefore be equipped with personal protective equipment (PPE) and clothing appropriate to the incident, and this should be deployed before the scene is entered (Calland, 2000). The safety of the immediate scene will normally be the responsibility of the fire service, with police controlling the incident overall. Nations’ differing EMS will have their own specific regulations covering the specification of PPE for doctors working in the pre-hospital environment. As a rule, PPE must protect the head, eyes, hands, feet, limbs and body to an appropriate extent against physical, chemical, thermal and acoustic risks. Full chemical, biological, radiological and nuclear protection is a specialist requirement rarely applicable to doctors outside a military setting.

Immediate actions and triage

630

The initial action of a doctor arriving on scene is to establish safety – personal safety, scene safety and casualty safety. Contact should be made with the officers commanding medical, fire and police emergency services for a situation report and direction to casualties on a priority basis. Communications should be established. In the event of multiple casualties, priorities are established by triage. Triage is a system of medical sorting originating from the Napoleonic battlefields to identify casualties in an order of priority for evacuation and treatment. In trauma management, triage is used when the number of casualties is greater than can be managed simultaneously by the medical personnel available. There are two stages applicable in the pre-hospital environment: a triage sieve and a triage sort (Hodgetts and Porter, 2002). The triage sieve is a quick and uncomplicated system based on simple clinical observation of a casualty’s ability to walk, breathe and maintain a pulse. It can be performed by trained but non-clinical personnel. The triage sort requires a degree of clinical training and uses physiological measurements to score casualties and place them into priority groups. Both triage systems place casualties into four colour-coded, priority categories:

Priority 1 Priority 2 Priority 3 Priority 4

Immediate Urgent Delayed Dead

In the event of an overwhelming number of casualties, an expectant category can be used. This identifies casualties whose injuries suggest that survival is unlikely, enabling medical resources to be deployed to those more likely to survive. In the event of improved resources, expectant casualties are re-categorized as Priority 1. The category of a casualty does not necessarily dictate the order of evacuation or treatment; for example, the ‘walking wounded’ and uninjured (Priority 3) may be evacuated first (‘reverse triage’).

Assessment and initial management Once safety, command, communications and priorities have been established, patients can be given individual attention. This calls for an organized approach involving awareness, recognition and management (ARM). AWARENESS Awareness of the environment, pattern of damage to a vehicle and the nature of the incident can help the attending doctor predict the likely injuries and facilitate their early recognition. For example, ejection from a vehicle or death of an occupant increases the likelihood of serious injury. Particular impaction patterns and intrusion of wreckage into the passenger compartment can suggest specific injuries; a bulls-eye fracture of a windscreen from inside a car indicates impaction of the passenger’s head against the windscreen and likely head, maxillofacial and neck injuries. Entrapment in a fire is associated with smoke inhalation and possible inhalational burns. RECOGNITION Recognition of injuries is based on a rapid and systematic questioning and examination of the casualty. An immediate assessment is made of the airway, breathing and circulation – the ‘ABC’ of trauma assessment. An instant assessment can be made by questioning the patient and eliciting a verbal response; the ability to speak means that the brain is being perfused with oxygenated blood and hence the patient has a patent airway, is breathing and has an adequate circulation. Head injury leading to loss of consciousness is the most common cause of airway obstruction and consequent hypoxia and hypercarbia; lack of response to command or painful stimulus indicates a significant level of coma. Access to an entrapped casualty may be extremely limited, but an assessment can usually be made of the airway and

breathing, presence of peripheral pulses and peripheral perfusion, head, chest, abdomen, pelvis and limbs. This initial assessment guides immediate management and the urgency of extrication and transfer to hospital.

Airway The airway is opened initially with the ‘bare

hands’ manoeuvres of chin lift and jaw thrust; the head should not be extended and should be kept in a neutral position. If blood, saliva or vomit are present in the airway, suction should be used. If ‘bare hands’ techniques are not adequate, an oropharyngeal airway or nasopharyngeal (NP) airway should be carefully placed to prevent the posterior aspect of the tongue obstructing the pharynx. NP airways are particularly useful in casualties with obstructing airways who have retained enough of a gag reflex to resist oropharyngeal airways, however they should be used cautiously in casualties with clinically apparent basal skull fractures. If these manoeuvres are unsuccessful, there is a range of supraglottic devices such as the laryngeal mask airway (LMA), which can be inserted in difficult situations. Definitive airway securement with intubation or

Breathing Once the airway is opened and secure, an

assessment of the casualty’s breathing is made. If breathing is clearly adequate, oxygen is administered from a high flow, non-re-breathing reservoir mask. With a flow rate of 15 L/minute, approximately 85 per cent oxygen is delivered; there is no place for lower concentrations of oxygen in this situation. If there is any doubt that breathing is adequate, then ventilation must be supported with a bag–valve–mask (BVM) assembly. This should have a reservoir attached with oxygen flows of 15 L/minute. BVM ventilation is a difficult skill even in ideal situations, but chances of success can be improved with a two-person technique; one person holds the mask in place over the face with both hands and pulls the jaw up into the mask to open up the airway, whilst the second squeezes the bag. Adequacy of oxygenation should be judged by clinical assessment of lip colour to detect cyanosis, or use of a pulse oximeter. Adequacy of ventilation can be judged by clinical assessment of chest expansion and breath sounds, or use of a chemical or electronic endtidal carbon dioxide (EtCO2) monitor, if a supraglottic airway device or tracheal tube is in place. Absence of breath sounds indicates a pneumothorax or haemothorax, and when associated with deviation of the trachea and hyper-resonance, a tension pneumothorax. A tension pneumothorax is an immediately life-threatening injury, and is treated in the first instance by decompression with a large-bore (14gauge) intravenous cannula through the second intercostal space in the mid-clavicular line. This converts the tension pneumothorax into a simple pneumothorax; definitive treatment of a simple pneumothorax in a spontaneously breathing casualty is to insert a widebore chest drain in the 5th intercostal space, anterior to the mid-axillary line, with the drain being connected to a Heimlich-type valve. However, if the casualty is breathing and stable with a simple pneumothorax, rapid transfer to hospital is preferable.

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The management of major injuries

MANAGEMENT Management of injuries is prioritized on treating the most immediately life-threatening injuries first, traditionally following the ABCDE sequence. The exception to this is the casualty suffering external, peripheral haemorrhage. Military experience has shown that bleeding from limb wounds is a leading cause of combat casualty deaths, a significant proportion of which are avoidable. This has led to the development of a CABC sequence, where C stands for catastrophic haemorrhage (Hodgetts et al., 2006). Life-threatening, external bleeding is controlled, and then the usual ABC sequence is followed. As casualties with airway obstruction succumb within minutes, securing a patent airway is always a priority. Once the airway is open, the casualty must be oxygenated and ventilated if breathing is not adequate. Further circulatory compromise is addressed primarily by control of external haemorrhage; an intravenous cannula should be placed, but fluids must be administered cautiously (see later). During this immediate management phase, the assumption is always made that damage to the cervical and thoraco-lumbar spine may have occurred. The stability of the cervical spine must be protected at all times until the neck can be cleared from the risk of injury. Stabilization is achieved by two methods: manual immobilization, or securement with head blocks, head straps and a rigid cervical collar. The thoraco-lumbar spine is protected by immobilization with straps on a long spinal board or other extrication device.

cricothyroidotomy is very difficult in entrapped casualties. Without the use of anaesthetic drugs and muscle relaxants, casualties can only be intubated when jaw tone and protective reflexes have disappeared immediately prior to cardiac arrest. The survival rates of intubation in this situation are, not surprisingly, very poor, however intubation with a rapid sequence of anaesthetic induction remains the gold standard of airway securement for trauma casualties, as it offers reliable protection from airway leaks and aspiration. Prolonged attempts at intubation should not be made without effective oxygenation and ventilation; casualties do not die from not being intubated, they die from hypoxia and hypercarbia. Accumulating evidence suggests that only practitioners with an appropriate level of anaesthetic training should be attempting rapid-sequence induction and intubation.

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Open or sucking pneumothoraces should be covered with an occlusive dressing secured on three sides – the open fourth side prevents a tension pneumothorax developing. Positive-pressure ventilation is likely to accelerate the conversion of a simple pneumothorax into a tension pneumothorax. If the casualty is intubated and ventilated, and a pneumothorax suspected, a simple thoracostomy is made in the 5th intercostal space, anterior to the mid-clavicular line. This allows a tension pneumothorax to decompress; however, the lung can still be inflated as the casualty is being ventilated. A thoracostomy is made by making a 3 cm horizontal incision immediately above the 6th rib, just anterior to the mid-axillary line, dissecting the subcutaneous tissues with large, straight Spencer Wells forceps until the chest cavity is entered. A finger is used to open up the thoracostomy and ensure no vital structures are felt. External haemorrhage is controlled primarily by direct pressure with a dressing, and limb elevation if possible. Other methods used are wound packing, the windlass technique, indirect pressure and use of a tourniquet; haemostatic dressings can also be used at any stage (Lee et al., 2007). The windlass technique involves the application of a dressing directly over the wound, which is then held in place with an appropriate bandage, knotted over the wound. A pen or similar object is placed under the knot, rotated to exert direct pressure over the site of the haemorrhage, and then secured. Tourniquets have been discouraged in contemporary, civilian, pre-hospital care, due to the significant risk of serious complications. Inappropriately applied tourniquets can increase bleeding (from a venous tourniquet effect), result in distal limb ischaemia, and cause direct pressure damage to skin, muscle and nerves. However, with limb injuries resulting in catastrophic haemorrhage, judicious use of tourniquets can be life saving. Civilian indications include (Hodgetts et al., 2006):

Circulation

• life-threatening limb haemorrhage due to shooting, stabbing and industrial or farming accidents; • haemorrhagic, traumatic amputation; • limb haemorrhage not controllable with direct pressure, or where direct pressure cannot be applied due to inaccessibility of wound from entrapment; • multiple casualties with lack of manpower to apply direct pressure.

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If possible, a wide-bore cannula should be sited in a large vein, or intraosseus access achieved with a placement device such as the EZ-IO®, FAST1™ or BIG Bone Injection Gun. Administration of intravenous fluids should be judicious in the pre-hospital environment; rapid infusion of large volumes of fluids can

raise the blood pressure and bleeding can resume that has previously stopped due to low pressure. The blood pressure drops again, and more fluid administration causes increasing anaemia. Large volumes of intravenous fluid administered to casualties with haemorrhage have been shown to increase mortality, and current guidance in the UK (National Institute for Clinical Excellence, 2004) is to titrate fluids against the presence of a radial pulse in 250 mL boluses, with a crystalloid solution such as Ringer’s lactate or Hartmann’s compound sodium lactate being the preferred fluid (large, infused volumes of sodium chloride 0.9 per cent can be associated with the development of a hyperchloraemic acidosis and should be avoided). Severe, unresponsive shock is likely to be the result of uncontrollable bleeding externally or into the chest, abdomen, pelvis and multiple long bones (embodied in the aperçu ‘onto the floor and four more’). Loss of cardiac output can also be due to tension pneumothorax or cardiac tamponade. Cardiac tamponade is most commonly associated with penetrating trauma of the chest within the nipple lines anteriorly or scapulae posteriorly. Severe shock leading to pulseless electrical activity (PEA) or asystolic cardiac arrest is an indication for bilateral thoracostomies and/or clam-shell opening of the chest and incision of the pericardium. These manoeuvres will treat the reversible causes of trauma cardiac arrest – hypoxia, hypovolaemia, tension pneumothorax and cardiac tamponade, and may precede intubation, ventilation and intravenous cannulation in this dire, pre-mortem situation. Disability The casualty is quickly assessed for neurological disability using the Glasgow Coma Scale (GCS) and assessment for pupillary size and inequality.

Extrication and immobilization More complex management is often impractical in an entrapped casualty, and so extrication becomes a priority. This should be done with regard to spinal protection, usually using spinal boards or other rigid immobilization devices. Fractured limbs should be splinted in an anatomical position to preserve neurovascular function. Analgesia may be necessary to extricate an injured casualty, and this can be achieved with inhalational or intravenous agents. The initial manoeuvre in the extrication process is manual immobilization of the cervical spine. This can be done from behind the casualty (typically in seated casualties entrapped in vehicles with a rescuer in the rear of the vehicle), or from the front and side if access is limited. A stiff cervical collar is sized and fitted at the earliest opportunity, but manual immobilization is still mandatory until the casualty can be placed on a spinal board.

intravenously, and a general anaesthetic in doses of 2– 4 mg/kg. The advantage of ketamine is that it does not cause respiratory depression, and the casualty’s airway is more predictably maintained. Doses and administration times of all drugs given should be noted.

Transfer to hospital Delayed or prolonged transfer to hospital is associated with poor outcomes, and every effort should be made to minimize the on-scene times for injured casualties. There is a balance between ‘scoop and run’ and ‘stay and play’ management. The airway must be secured, and life-threatening chest injuries (e.g. tension pneumothorax) and catastrophic, external haemorrhage dealt with before transfer commences. Prolonged attempts at complex management on scene are disadvantageous, and should be limited to life-saving interventions where possible. The appropriate method of transport should be chosen, with helicopters offering some advantage for long-distance transfers or rescue from remote and rough terrain. Police escorts can be used to aid ambulance progress, and a balance sought between speed of transfer and violent movement of the casualty and attendants. The appropriate destination hospital should be chosen for the casualty’s likely injuries, and this may mean bypassing a small unit that does not have the appropriate facilities. Wherever possible, the receiving medical team should be directly advised of the estimated time of arrival (ETA) and the identified injuries, enabling an appropriate trauma team to be standing by. During the transfer, the casualty’s vital signs should be monitored clinically and with available equipment. Conscious casualties should be constantly assessed by speaking to them, and a decrease in conscious level detected early. ECG and pulse should be continuously monitored, blood pressure measured with a non-invasive blood pressure (NIBP) monitor, and oxygen saturations measured if peripheral perfusion allows. EtCO2 monitors are useful for gauging adequacy of ventilation in intubated and ventilated casualties. The casualty’s airway must be maintained at all times, and oxygenation and ventilation maintained. Oxygen saturations should be maintained above 95 per cent if possible, and ventilated casualties have their EtCO2 maintained at a low normal level (4.0–4.5 kPa). Haemorrhage is controlled with direct pressure, and Hartmann’s solution titrated intravenously to maintain a palpable radial pulse. If the patient deteriorates en route, the medical attendant must decide whether to attempt resuscitation whilst on the move, stop and resuscitate or make a run for the nearest hospital. This decision will

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Further immobilization and extrication may be impossible until wreckage has been cleared enough to enable an extrication device to be positioned under the casualty. Managing wreckage is a specialist skill that is the province of the Fire and Rescue crews; however, the pre-hospital doctor should be familiar with the techniques used to advise how extrication can be managed without causing additional injury to the casualty. Common manoeuvres in road vehicle wreckage are removal of glass and doors, a dashboard roll to lift the dashboard off trapped limbs, and removal of the roof by cutting through the A, B and C pillars. The seat can then be carefully flattened, and a long spinal board slid under the casualty from the rear of the vehicle, minimizing movement of the spinal column. If a casualty is deteriorating fast, the rescue crews should be advised and a rapid extrication carried out. Limb fractures and dislocations should be reduced and the limb returned, if possible, to its anatomical position with gentle traction and straightening. This may require analgesia. Note that some injuries such as posterior hip dislocations may prevent an anatomical alignment, and the limb must not be forced. The limb should then be splinted with traction, gutter or vacuum splints as appropriate. This reduces pain and haemorrhage, and minimizes neurovascular damage. Femoral traction splints such as the Thomas are effective for mid-shaft femur fractures, providing the pelvic ring is intact. The traction reduces the fracture, and the fusiform compression of the fracture haematoma reduces further bleeding. A unilateral, closed, femoral fracture can cause a 1.5 L blood loss – 30 per cent of the adult blood volume and enough to cause significant shock without other injury. Open-book pelvic fractures cause uncontrollable retroperitoneal bleeding. Blood loss can be minimized by stabilizing and reducing the fracture using specialist, pelvic compression devices or a rolled sheet around the pelvis and twisted above. Analgesia may be necessary to extricate an injured casualty. This can be administered by inhalation with Entonox, a 50:50 mixture of nitrous oxide and oxygen, delivered via a breath-actuated regulator valve and mask or mouthpiece. Parenteral analgesics should only be given intravenously, and titrated cautiously against effect. Other routes of administration are very unpredictable, especially in shocked casualties. Pure opioid agonists such as morphine, diamorphine and fentanyl are most effective, but it should be noted that there is a wide variation in response between individuals, and care should be taken not to cause respiratory depression by overdosage. Partial opioid agonists such as nalbuphine are used, but have a degree of narcotic antagonism that can make further administration of opioids unpredictable. Ketamine is a very useful drug that is a powerful analgesic in doses of 0.5 mg/kg

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depend on the nature of the intervention required and the ETA at the hospital. Contemporaneous records are almost impossible to maintain during a transfer, but electronic equipment can usually download a paper or electronic record. If not, notes should be made as soon as possible after arrival at the hospital. On arrival, the medical attendant should remain part of the resuscitation team until an effective handover can be made.

Helicopters and air ambulances A helicopter emergency medical service (HEMS) is ideal, but is expensive to run. HEMS (London) data show that the primary life-saving benefit is the rapid delivery of advanced resuscitation skills to the scene. The most essential life-saving skill is advanced airway management, and this requires an anaesthetically trained doctor who can perform a rapid sequence anaesthetic induction and manage tracheal intubation in difficult circumstances. International data show that, as a result of these interventions, there is a reduction of 15 per cent in death from head injuries, and a reduction of between 5 and 7 days in intensive care stays. However, the availability of appropriately trained doctors is variable; many HEMS are crewed by paramedics only, and this reduces the effectiveness of the service to less advanced life support and rapid delivery and evacuation of casualties to an appropriate facility. A common standard for response times in the UK and Europe is 12 minutes from call-out to arrival. This ability to transport casualties quickly over large distances also means that smaller, less well-equipped and well-staffed hospitals can be bypassed in favour of large, specialist centres. A wide variety of helicopters are used internationally for HEMS work, ranging from large aircraft such as the Sikorsky S61-N to smaller craft like the Bolkow 105-DBS. A feature common to all HEMSs is that the helicopter is twin-engined for safety and flexibility of flight paths. As costs rise dramatically with increased size of the helicopter, HEMS aircraft are a compromise. With the exception of military and Coastguard craft, the size is usually restricted.

Cramped cabin space and poor patient access in these helicopters greatly restrict the patient interventions possible during flight. The aircraft are noisy and vibration considerable, so monitoring the patient’s condition is difficult. These factors make it essential that the patient is stabilized and immobilized prior to transfer; the airway must be secured and protected, ventilation maintained, haemorrhage controlled and intravenous access for fluid administration preserved. Monitoring should be reliable, and the ECG, blood pressure, oxygen saturations and end-tidal carbon dioxide observed. Safety is paramount for doctors working with helicopters, and all personnel should be trained and familiar with safety guidelines. The helicopter should not be exited until directed by the crew. If asked to disembark whilst the rotor blades are revolving, personnel must keep their heads down and be aware that the rotor disc droops as it slows and may come below head height, especially uphill if landing on an incline.

HOSPITAL MANAGEMENT Upon reaching hospital, the following are important in hospital management: 1. 2. 3. 4. 5.

Organization. Trauma teams. Assessment and management. The ATLS concept. Initial management. Systemic management.

Organization The aim of any integrated EMS is to “get the right patient to the right hospital in the right amount of time” (Trunkey). Regional services were set up in the USA in 1973, with three levels of hospital designated as able to manage trauma to differing levels: Level III centres: capable of treating most trauma victims, and stabilizing critically ill patients prior to transfer. 22.7 HEMS helicopter interior (a) Interior of Bolkow 105-DBS showing medical attendant seat (facing) and restricted patient access (stretcher on right). (b) Rear clam-shell doors for patient loading.

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(a)

(b)

Level II centres: capable of managing almost all critically ill patients, but not offering all subspecialties. Level I centres: able to manage all trauma patients with all specialist needs provided on site.

Trauma teams Casualties who have survived their initial trauma and reached hospital alive need rapid assessment and appropriate resuscitation to avoid their dying during the ‘golden hour’. Crucial to the effective management of seriously injured casualties is the immediate availability of appropriately trained and experienced doctors and healthcare professionals, and this need has led to the development of the trauma team concept. The team is led by a senior doctor with advanced trauma skills, whose base specialty is less important than his or her training and experience. The trauma team is preferably activated by the pre-hospital practitioners according to a set of standard criteria, and should therefore be awaiting the casualty as they

• First-tier response: Emergency department physician Physician anaesthetist Emergency department nurses Radiographer • First- or second-tier response: Surgeon from appropriate specialty Intensive care specialists Specific specialists, e.g. paediatric, obstetric, ear, nose and throat (ENT), maxillofacial etc. The development of emergency medicine, and the increasing availability of experienced and senior emergency medicine doctors with sophisticated trauma imaging availability on a ‘round the clock’ basis, has enabled a two-tier call-out for trauma teams. Initial assessment and resuscitation rarely requires immediate specialist surgical skills; once the initial assessment and imaging has been completed, the appropriate specialist surgeon can be called in or stood by in the operating theatre for definitive surgical management of specific injuries. Trauma teams should function in an appropriate environment, and most hospitals will have a resuscitation room with all required equipment immediately available. Personal protective equipment to include gowns, gloves and eye protection must be available. A sophisticated resuscitation room will have anaesthetic delivery systems, equipment and drugs for airway management, intravenous fluid and rapid administration systems for shock management, and a variety of surgical packs for specific interventions such as chest drain insertion etc. Patient trolleys should be compatible with the taking of x-rays, and the x-ray equipment can be built onto an overhead gantry. Ultrasound imaging equipment should be available for central venous cannulation and Focussed Assessment Sonography in Trauma (FAST). Both the environment and intravenous fluids should be warmed to minimize hypothermia.

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However, the development and integration of this system was patchy, and the expense of such a system prevents full development in many countries. There are also arguments as to whether such a system, which may be effective in a society with a high level of penetrating trauma, is appropriate for all environments. In the UK, an experimental trauma centre and regional trauma system was set up in the Northwest Midlands in 1991–1992, and examined over the first 4 years. The assessment found little evidence of an integrated trauma system having developed, and there was no reliable evidence that survival rates from major trauma in the region had improved (Nicholl and Turner, 1997). However, after another 5 years, significant improvements in survival were noted (Oakley et al., 1998). This suggests that regional trauma systems take some time to develop to maximum effectiveness, but do demonstrate reductions in mortality. These findings are backed up by a meta-analysis of US and Canadian trauma centres. Regionalized trauma systems are now operational in many countries, including the USA, Canada, Australia, and across Europe. In the UK, a nationally funded enquiry in 2007 advocated regionalization of trauma care and the establishment of Level 1 trauma centres (Findlay et al., 2007). However, in many or most health care economies, the majority of available hospitals will not have all the specialist staff and facilities to adequately manage major injuries. Each hospital must therefore have standard operating procedures (SOPs) for assessing, managing and if indicated, transferring trauma casualties, depending on the facilities available.

arrive at the hospital. Team members would normally include the following personnel:

The ATLS concept Major musculoskeletal injuries can be dramatic and distracting, but it is rare for them to be immediately life-threatening in the absence of catastrophic haemorrhage. The classic mistake when treating trauma is to focus on the attention-grabbing compound fracture, and miss the obstructing airway, which is far more likely to cause a ‘golden hour’ death. Hence the most immediately life-threatening injuries should always be treated first. However, although this principle has been known for generations, in the stress of the moment a logical sequence may not be followed unless the treating doctor is trained and practised. To meet this need,

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a number of training systems have been developed over the years, of which the best known is the Advanced Trauma Life Support Program for Doctors (ATLS®) (American College of Surgeons Committee on Trauma, 2005), developed by the American College of Surgeons Committee on Trauma. The 2004 7th edition has been revised with updates from international ATLS subcommittees to reflect trauma developments across the world (Kortbeek et al., 2008). ATLS originates from 1976, when James Styner, an orthopaedic surgeon, crashed his light aircraft in rural Nebraska with his wife and four children on board. His wife was killed instantly and three of his four children sustained critical injuries. Having arrived at the nearest hospital, Styner found that the care delivered to his family was inadequate and inappropriate, and this stimulated him to initiate a trauma care training programme that became ATLS. The course has since become an internationally recognized standard and is currently taught in over 40 countries worldwide. The ATLS course is based on validated teaching techniques, and uses a system of core content lectures and practical skill stations to develop skills that are practised and finally tested in simulated trauma scenarios. The system taught is based on a three-stage approach: 1. Primary survey and simultaneous resuscitation – a rapid assessment and treatment of life-threatening injuries. 2. Secondary survey – a detailed, head-to-toe evaluation to identify all other injuries. 3. Definitive care – specialist treatment of identified injuries.

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The primary and secondary surveys constitute the initial assessment and management, which leads to the definitive care of the casualty following transfer if required. The intention of ATLS is to train doctors who do not manage major trauma on a regular basis, but it is applicable to any trauma situation as an underlying system on which to base management of an injured casualty. The sequence is taught assuming one nonspecialist doctor supported by one nurse, working on a single casualty, but the various components can be performed simultaneously if a team is available. The training is didactic, but the use of specialist skills (e.g. anaesthetic) should not be excluded. Although the course is updated on a 4-yearly basis, there is an inevitable time lag, and fast-developing areas such as imaging may introduce changes to local trauma management not found in current ATLS courses. There are also national and local variations in practice that need to be taken into account, and these are discussed later in this chapter; however ATLS has stood the test of time and remains the most widely recognized basis for trauma management internationally.

Initial assessment and management The initial assessment and management is part of a sequence leading to the transfer and definitive care of a casualty. During the primary and secondary surveys, a number of monitoring and investigative adjuncts are used alongside clinical examination as given in Figure 22.8 and the accompanying Box. THE ABCs The underlying principle of ATLS is to identify the most immediately life-threatening injuries first and start resuscitation. As a general rule, airway obstruction kills in a matter of minutes, followed by respiratory failure, circulatory failure and expanding intracranial mass lesions. This likely sequence of deterioration has led to the development of the trauma ‘ABCs’, a planned sequence of management predicated on treating the most lethal injuries first. Throughout this sequence, the assumption is made (until proved otherwise) that there may be an unrecognized and unstable cervical spine injury. Hence, the sequence is:

Injury

Definitive care

Primary survey

Transfer

Adjuncts

Resuscitation

Re-evaluation

Re-evaluation

Secondary survey Adjuncts

22.8 Algorithm of ATLS initial assessment and management

ADJUNCTS TO PRIMARY SURVEY Vital signs ECG Pulse oximetry End-tidal carbon dioxide Arterial blood gases Urinary output Urethral catheter (unless contra-indicated) Naso-gastric tube (unless contra-indicated) Chest x-ray Pelvic x-ray

A B C D E

As previously described, catastrophic haemorrhage may be controlled before the airway, designated by the ABC sequence; however, death is ultimately caused by cerebral anoxia, regardless of whether the anoxia is a result of airway obstruction, respiratory failure, shock or old age. Hence, the goal of resuscitation is to preserve the perfusion of the brain with oxygenated blood. TRIAGE Triage, as described in the pre-hospital section of this chapter, is medical sorting to prioritize multiple casualties for resuscitation, and is used when the number of casualties outstrips the available resources. The initial two phases of triage, usually pre-hospital, are the sieve and the sort, to group casualties into the four priority groups of immediate, urgent, delayed or dead. Within the ATLS® system, multiple casualties are triaged by rapidly assessing each patient’s ABCs. Those with the most immediately life-threatening injuries are treated first; these are injuries of the: Airway: Breathing: Circulation:

Actual or impending obstruction Hypoxia or ventilatory failure External haemorrhage or shock

Priority 1 Priority 2 Priority 3

PRIMARY SURVEY AND RESUSCITATION During the primary survey, life-threatening conditions are identified and resuscitation started simultaneously, again following the ABCDE sequence. The Awareness Recognition Management system enables the treating doctor to focus rapidly on the likely problems; for example:

Awareness – a head injury is the most likely cause of unconsciousness and obstructed airway in trauma casualties. Recognition – an obstructed airway is recognized by looking, listening and feeling for the diagnostic signs. Management – the airway is established with simple ‘bare hands’ manoeuvres, airway adjuncts, advanced airway interventions or surgical airway techniques. As each stage in the ABCs is completed, the casualty is re-evaluated for deterioration or improvement; on completion of the breathing assessment, the airway is re-examined and the airway and breathing reassessed before moving onto the circulation etc. A – Airway and cervical spine control The cervical spine is stabilized immediately on the basis that an unstable injury cannot initially be ruled out. There are two techniques for this:

• manual, in-line immobilization • cervical collar, head supports and strapping.

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Airway with cervical spine protection. Breathing. Circulation with haemorrhage control. Disability or neurological status. Exposure and Environment – remove clothing, keep warm.

Simultaneously, the airway is examined for obstruction by looking, listening and feeling for signs such as respiratory distress, use of auxiliary muscles of respiration, decreased conscious level and lack of detectable breath on hand or cheek. The airway is supported initially by lifting the chin or thrusting the jaw forward from under the angles of the mandible. Secretions and blood are carefully suctioned, and oropharyngeal or NP airways used to hold the tongue forward. If these simple manoeuvres are unsuccessful, the options are supraglottic airway devices (e.g. the laryngeal mask airway), tracheal intubation or surgical airway. All these techniques can be performed without extending the neck. A clear airway does not mean the casualty is breathing adequately enough to enable peripheral tissue oxygenation. As soon as the airway is

B – Breathing

22.9 Triage priorities (a) Priority 1 – Airway: severe face and neck wounds. (b) Priority 2 – Breathing: severe chest wounds; (c) Priority 3 – Circulation: severe bleeding and shock.

(a)

(b)

(c)

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secured, the chest must be exposed and examined by looking, listening and feeling. Adequate and symmetrical excursion, bruising, open wounds and tachypnoea are looked for, and the chest is auscultated for abnormal or absent breath sounds, which indicate a pneumothorax or haemothorax. The trachea is palpated in the supra-sternal notch to detect the deviation caused by a tension pneumothorax, and the chest is percussed for the hyper-resonance of a tension pneumothorax or dullness of a haemothorax. A tension pneumothorax must be treated immediately if the diagnostic signs of absent breath sounds, hyper-resonance and deviated trachea are found. Initial management is decompression with a 14-gauge cannula placed in the second intercostal space in the midclavicular line, followed by chest drain placement. If there is any doubt as to the adequacy of the casualty’s breathing and oxygenation, ventilation should be started with a reservoir BVM assembly using highflow oxygen. Any trauma casualty who has required intubation must be ventilated. C – Circulation with haemorrhage control The circulation

is assessed by looking for external bleeding and the visible signs of shock such as pallor, prolonged capillary refill and decreased conscious level. The heart is auscultated to detect the muffled sounds of cardiac tamponade, and poor perfusion assessed by feeling for clammy and cool skin. The peripheral and central pulses are palpated to detect tachycardia and diminished or absent pulse pressure. External bleeding is controlled by pressure, and two 14-gauge cannulae sited for administration of in fluids and blood. Blood samples can be drawn from the cannulae for baseline diagnostic tests and transfusion cross-matching. As blood is available quickly in a hospital setting, warmed, crystalloid intravenous fluids can be given in an initial volume of 2 L to maintain cardiac output. D – Disability The key element of assessing a patient’s

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neurological status is the Glasgow Coma Score (GCS) (Table 22.1). This score records eye opening, the best motor response and the verbal response, giving a score of between 15 for normal responses, and 3 for no responses. Repeat GCS scoring can track deterioration in the conscious level, and indicate the need for elective intubation and ventilation. It is much more precise than the AVPU score (Aware, Verbally responsive, Pain responsive and Unresponsive). The classic pitfall of intoxication should be considered, but a lowered GCS is assumed to be secondary to a cerebral injury until proved otherwise. The pupils are examined for any difference in size indicating raised intra-cerebral pressure, and unresponsive pupils, fixed at mid-point, which can indicate serious brain damage.

Table 22.1 Glasgow Coma Score Response

Score

Eye opening: Spontaneous On command On pain Nil

4 3 2 1

Best motor response: Obeys Localizes pain Normal flexor Abnormal flexor Extensor Nil

6 5 4 3 2 1

Verbal response: Orientated Confused Words Sounds Nil

5 4 3 2 1

E – Exposure and environment The patient should have

all clothing removed to enable a full examination of the entire body surface area to take place. This will require log rolling to examine the posterior aspects, and allow removal of any glass or debris. The casualty should be kept warm to maintain body temperature as close to 37ºC as possible, and all fluids and ventilated gases warmed. Although patient cooling is used in some specialist situations, this is not indicated in the initial resuscitation. A hypothermic patient becomes peripherally shut down and acidotic, and if shivering, has greatly increased oxygen demands. ADJUNCTS TO PRIMARY SURVEY A number of monitoring and diagnostic adjuncts are used to supplement the primary survey and resuscitation, in addition to vital signs monitoring and haematological assays: • Electrocardiographic (ECG) monitoring – used to monitor heart rate and detect arrhythmias and ischaemic changes. • Pulse oximetry – measures arterial oxygen saturations (SaO2) and monitors peripheral tissue perfusion (this is unreliable in low-output states, hypothermia and with motion artefact). • End-tidal carbon dioxide monitoring (EtCO2) – gives an estimation of arterial carbon dioxide partial pressure in intubated and ventilated patients, allowing optimization of lung ventilation. It also confirms tracheal intubation and alerts the practitioner to a drop in cardiac output. • Arterial blood gases (ABGs) – allows quantification of arterial oxygen and carbon dioxide partial pressures with acid–base balance. This will also give the haemoglobin, sodium and potassium levels.

(NOTE: lateral cervical spine x-rays do not exclude fractures or unstable necks and so do not alter management; although important, they can be left until the secondary survey.) SECONDARY SURVEY The secondary survey is a detailed, head-to-toe evaluation to identify all injuries not recognized in the primary survey. It takes place after the primary survey has been completed, if the patient is stable enough and not in immediate need of definitive care; it may, in fact, take place after surgery, or on the intensive care unit (ICU). The importance of the secondary survey is that relatively minor injuries can be missed during the primary survey and resuscitation, but cause longterm morbidity if overlooked, for example small joint dislocations. The components of the secondary survey are: • • • • • •

history physical examination ‘tubes and fingers in every orifice’ neurological examination further diagnostic tests re-evaluation.

The history The patient’s ongoing experience of his or

her injuries, as well as details of events immediately before, during and after the injury should be recorded. Particularly important is to establish whether the trauma was subsequent to a medical collapse: did the patient suffer a myocardial infarct causing a car crash, or was the infarct a result of hypovolaemia? With the increasing proportion of the elderly in developed societies, more patients are receiving chronic treatment for hypertension etc., which can have a profound effect on their response to hypovolaemia. An example of this is a combination of beta-blockers and angiotensinconverting enzyme (ACE) inhibitors, which cause a profound drop in blood pressure if the patient’s cardiac output is minimally compromised. A useful mnemonic is AMPLE: allergies; medications; past illnesses; last meal; events and environment. Examination follows a logical sequence from the head down to the extremities, including a

Examination

log-roll to ensure that all the body surfaces are examined. The guiding injunctions are look, listen and feel. The head is examined for contusions, lacerations and clinically detectable fractures. The eyes and ears are examined for local damage, and examined internally with an ophthalmoscope/otoscope for signs of bleeding etc. Bleeding from the ears can indicate a basal skull fracture. The GCS should be repeated. The face is examined for signs of fractures with a consequent risk of airway obstruction – contusion, laceration, deformity, malocclusion of teeth and crepitus. Cerebrospinal fluid issuing from the nose (rhineorrhoea) is indicative of a basal skull fracture. All aspects of the neck are examined for contusions, lacerations, swelling, tenderness, and a step in the cervical spine indicative of fracture/dislocation. Minorlooking contusions over the anterior neck can be indicative of underlying damage to the laryngeal and tracheal structures, which are associated with airway obstruction. A lateral cervical spine x-ray is taken at this stage. The chest is inspected for deformity, contusions such as the classic ‘seat belt’ sign and open, possibly penetrating, wounds. A stethoscope is used to auscultate the lungs, comparing left and right apices and bases to identify the loss of breath sounds, indicating a pneumothorax. Feel for tenderness and crepitus due to fractured ribs and sternum, which may also be associated with underlying lung and heart contusions. Percussion can reveal the hyper-resonance of a tension pneumothorax, and the dullness of a haemothorax. The abdomen is inspected for contusions and wounds, and auscultated for the absence of bowel sounds indicative of visceral damage. Palpation primarily detects rigidity and tenderness in the conscious patient, and percussion can identify gastric distension, but these are unreliable in many trauma casualties. The early use of specialist imaging such as ultrasound and computed tomography (CT) is indicated. Discrete areas such as the perineum, rectum and vagina should not be forgotten, and must be examined for bleeding, contusions, lacerations etc. The key indicators for pelvic fracture are unequal leg length and pain or crepitus on palpation or gentle compression of the pelvis. If these signs are positive, a pelvic fracture is indicated, with the risk of profound haemorrhage. The examination should not be repeated. All four limbs are examined for contusions, deformity and pallor. Pain and crepitus on palpation are indicative of underlying fracture or dislocation, and this examination should not be repeated if positive. Distal pallor and absence of pulses suggest a vascular injury, and sensory loss, neurological damage. X-rays that include the joint above and below the injury site are indicated.

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The management of major injuries

• Urethral catheter – allows measurement of hourly urine output (unless contraindicated, e.g. in the case of a ruptured urethra). • Nasogastric tube – decompresses the stomach and helps prevent aspiration (unless contraindicated, e.g. because of a basal skull fracture). • Chest x-ray – for diagnosis of life-threatening chest injuries such as pneumothorax, which will require early treatment. • Pelvic x-rays – enable a fractured pelvis to be diagnosed, which will alert to the likelihood of retroperitoneal bleeding.

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22

640

Table 22.2 Palpable pulses at different blood pressures Pulses palpable

Likely systolic blood pressure

Carotid, femoral, radial

> 80 mmHg

Carotid, femoral

> 70 mmHg

Carotid

> 60 mmHg

No pulse

< 60 mmHg

A rapid neurological assessment is carried out to detect lateralizing signs, loss of sensation and motor power, and abnormality of reflexes. Levels of sensory loss should be carefully documented to enable deterioration or improvement to be quantified. X-rays and CT may be indicated to detect spinal fractures. Imaging Imaging techniques are developing rapidly, and changing practice. The use of chest and pelvis x-rays is still standard in the primary survey, but false-negative results with cervical spine radiographs limits their use. The incidence of spinal cord injury without radiographic abnormality (SCIWORA) is around 10 per cent of all spinal injuries, and is more common in children. CT scans have in the past had the drawback that sending an unstable casualty for a lengthy procedure in a remote radiology department is too dangerous. However, modern spiral CT scanners are fast, and if located adjacent to the Emergency Department, a whole-body trauma CT can be completed in minutes. The risk of patient instability may therefore be outweighed by the benefit of a CT scan in enabling accurate diagnosis, and this technique is becoming a gold standard. Magnetic resonance imaging (MRI) is not usually available as an emergency procedure, and is not safe with an unstable casualty. However, its ability to identify soft-tissue injuries is of use in diagnosing SCIWORA; removal of spinal precautions may not be safe until an MRI has excluded unstable spinal injuries. Ultrasound scanning is often helpful, particularly for diagnosing intra-abdominal bleeding. In many departments focussed assessment with sonography in trauma (FAST) has largely supplanted diagnostic peritoneal lavage; however, its usefulness is limited to detecting fluid in the peritoneum, and it will not reliably enable diagnosis of specific visceral injuries. Though it remains a quick and useful Emergency Department adjunct, it does not provide the diagnostic information of CT.

PAIN MANAGEMENT Pain management has in the past been underemphasized, due to concerns about masking surgical signs

and the risks of sedation and respiratory depression. However, in expert hands, there are various techniques that can be used in the hospital setting. Intravenous analgesia – This is the most commonly preferred technique, with morphine being the usual drug. Morphine is a pure agonist opioid and should be diluted and titrated against patient response as there is a wide variation in effect between individuals. It also provides a degree of mental detachment and euphoria useful in the trauma patient, but has the side effects associated with opioids of respiratory depression, sedation, hypotension, nausea and dysphoria. Being a pure agonist, its effects can be reversed with naloxone. Respiratory depression can be reversed whilst preserving analgesia with the respiratory stimulant doxapram. Partial agonists such as buprenorphine should be avoided as they are not fully reversed by naloxone. An anti-emetic such as cyclizine or ondansetron should be given with morphine to minimize nausea. Inhalational analgesia – Nitrous oxide/oxygen 50:50 mix (Entonox) is useful for short-term analgesia when moving patients or aligning fractures. However, nitrous oxide diffuses into air-filled closed cavities such as a pneumothorax, and will expand the volume by a factor of four, potentially causing an undrained pneumothorax to tension. Nerve blocks – Nerve blocks can be used with great effect in some limb injuries, but should only be administered after discussion with an orthopaedic surgeon due to the risk of masking a compartment syndrome. Femoral nerve blocks are technically straightforward and can be used for mid-shaft femur, anterior thigh and knee injuries. INTRA-HOSPITAL AND INTER-HOSPITAL TRANSFER Few hospitals enjoy the luxury of having the Emergency Department, radiology, operating theatres and ICUs all in the same location, and so transfer of seriously injured casualties is inevitable at some point. Transfer is indicated when the patient’s needs exceed what can be delivered with the resources immediately available. The transfer may be between units within the same hospital, from a small hospital to a larger facility (e.g. a Level I trauma centre), or to a specialist unit (e.g. burns, neurosurgical or cardiothoracic). Even the shortest transfer within a hospital is fraught with hazard as monitoring and resuscitation are difficult on the move, and so must be carefully planned. A number of questions should be answered before the transfer is initiated: When? Where? Who? What way? With? When to transfer is determined by the condition of the casualty and the urgency of definitive care. Patient outcome is directly related to time from injury to definitive care, so delays should be minimized. However, transferring partially assessed and unstable patients is dangerous, and so transfer is not usually

spinal injury cannot be excluded. This may require immobilization on a spinal board with a cervical collar and head restraints; bear in mind that closely fitting cervical collars can raise intracerebral pressure, and prolonged restraint on a spinal board results in pressure injuries. The casualty should be transferred on an appropriate trolley, and a medical kit with equipment for ABC interventions must be carried. Full monitoring to include ECG, NIBP/intra-arterial BP, SaO2 and EtCO2 should be available. For transfers between hospitals, an appropriate form of transport must be available. With the casualty should go a full set of paperwork to include patient identity and documentation of the full initial assessment; it is particularly important to note whether the secondary survey has been carried out, with any injuries duly noted. If the urgency of the transfer has taken precedence over the secondary survey, then this should be highlighted so the survey can be completed after the initial, life-saving, definitive care. Results of all blood tests and investigations such as x-rays must accompany the patient.

22

The management of major injuries

contemplated until the primary survey and resuscitation have been completed. Ideally, the patient should be stable when transferred, but this may not be possible if bleeding is severe. Definitive care may be so urgent that intervention is required before the secondary survey is reached, e.g. for evacuation of an expanding intracerebral bleed. Transfer should not be delayed for investigations such as cervical spine x-ray, which will not change management. However, it is crucial that the ABCs are addressed; the airway should be secured and protected, the patient must be oxygenated and ventilated optimally, and shock should be addressed. Where to transfer the casualty to is determined by the definitive care required and the best facility available that can offer that care. Multiply-injured patients may have injuries requiring input from differing surgical specialties such as neurosurgery and general surgery; in this situation, the definitive care surgeons must decide on the priorities, having assessed the patient. The back of the head should always be examined as injuries at the back of the head may sometimes be missed (Fig. 22.10). In life-threatening circumstances (e.g. with expanding intracerebral and intraabdominal bleeds), the patient may require simultaneous management of both injuries. Who conducts the transfer is determined by the staff available. The transferring physician should have an appropriate set of critical care competencies including advanced airway skills – this is not a job for the nearest junior doctor. Transfer should be authorized by the senior doctor with responsibility for the patient, and an appropriate team of nurses, technicians and paramedics should accompany the patient. The referring doctor should have direct communication with the receiving doctor, who should be briefed on the patient’s condition, destination and ETA. In which way the transfer is achieved depends on factors such as whether the transfer is between hospitals or within units of the same facility. The casualty must be secured and full spinal stabilization in place if

DEFINITIVE CARE Definitive care describes the specialist care required to manage the injuries identified during the initial assessment and subsequent investigations. This may be specialist surgery to address a particular problem (e.g. neurosurgical evacuation of an intracerebral bleed), or critical care management on an ICU to provide systemic support (e.g. oxygenation and ventilation of patients with severe lung contusions).

SYSTEMIC MANAGEMENT Accurate and effective management of a casualty with multiple injuries depends on a logical progression of examination, moving through the systems in a sequence most likely to identify the most immediately life-threatening injuries first. Using the ARM system described earlier helps structure the approach: Awareness – use the history and accident mechanism to predict likely injuries and anticipate problems. Recognition – examine the patient logically using the look – listen – feel sequence to identify the physical signs of injury. Management – having identified injuries, implement the most effective and life-saving interventions first.

22.10 The head Failure to examine the back of the head may result in missed injuries!!

Systemic management may progress simultaneously in a hospital location with a trauma team; in the absence of a team, work through the systems following the ABCDE format. The exception to this would be control of catastrophic haemorrhage preceding airway management.

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A – Airway and cervical spine Management of the airway in all forms can be implemented whilst protecting the cervical spine. Until the airway is both secured and protected, this is best done by in-line immobilization, as use of a stiff cervical collar makes intubation difficult. Conventionally, in-line immobilization is performed with the practitioner standing at the head of the casualty, holding the head on both sides with the hands and maintaining it in a neutral position, in line with the neck and torso. This can make airway management difficult, with the inline immobilizer squatting awkwardly to one side. An alternative and more effective stance is for the immobilizer to stand to one side of the casualty’s shoulder and immobilize the head from below. An additional technique is to stand at the casualty’s head and support the head between the forearms whilst linking the hands behind the neck. This effectively immobilizes the cervical spine, but makes examination of the posterior neck difficult, and is uncomfortable for a tall practitioner. Once the airway is secured and protected, the trinity of stiff collar, head blocks and tape should be implemented. Whatever techniques are used, the cervical spine should be immobilized at all times until an unstable injury is excluded – this may require CT or MRI scanning, and be after definitive care. AIRWAY – AWARENESS Head injury This is by far the most common cause of airway compromise in the trauma patient. As the level of consciousness decreases, so does muscle tone, and the pharynx collapses around the glottis, obstructing the airway. In the supine position, the tongue drops backwards, plugging the glottis anteriorly. Airway obstruction can be sudden or insidious, and partial or complete, but will result in damaging hypoxia and hypercarbia, which are particularly dangerous in a head-injured casualty. Maxillofacial trauma Disruption of the facial bones allows the face to fall back, compressing and obstructing the pharynx. This is associated with soft tissue swelling and bleeding, which further obtund the airway. Typically, these patients need to sit up to allow the face to fall away from the pharynx and open up the airway. Neck trauma Penetrating or blunt-force trauma results

in haemorrhage and swelling, which compresses, distorts and obstructs the upper airway. This can progress rapidly and make tracheal intubation impossible and surgical airway difficult.

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Laryngeal trauma Blunt force trauma from impact to the anterior neck (on a car steering wheel, for example) can disrupt the larynx and fracture the cartilaginous

(a)

(b)

22.11 Mandibular fracture (a,b) Patient with a mandibular fracture showing the characteristic position to maintain the airway.

structures, leading to immediate or incipient airway obstruction. Signs can be subtle; contusion over the larynx with a hoarse voice, coughing of bright red blood and surgical emphysema should alert the practitioner to the likelihood of sudden airway obstruction. Inhalational burns Inhaling super-heated air burns the airway and can result in rapid development of swelling and airway obstruction. Signs such as facial burns, smoke staining and singed nasal hair suggest an inhalational burn, requiring early and expert intubation.

AIRWAY – RECOGNITION Airway obstruction and respiratory failure may be obvious (to an experienced clinician), but early signs can sometimes be subtle and need systematic examination to detect: Look

Agitation, aggression, anxiety – suggest hypoxia. Obtunded conscious level – suggests hypercarbia. Cyanosis – blue discoloration of nail beds and lips caused by hypoxaemia due to inadequate oxygenation. Sweating – increased autonomic activity. Use of accessory muscles of ventilation; casualty classically sitting forward splinting chest, and using neck and shoulder muscles to aid breathing. May also display flared nostrils. Tracheal tug and intercostal retraction – caused by exaggerated intrathoracic pressure swings. Listen

Noisy breathing – collapsing pharyngeal muscles obstruct airway leading to snoring sounds. Stridor – air flow through an obstructing upper airway changes from laminar to turbulent, resulting in the typical hoarse wheeze of stridor – a sinister sign, as even minimal further reduction in the airway lumen can result in critical airway obstruction.

22

(c)

22.12 Pharyngeal airways preventing the tongue from falling back across the glottis (a) Open airway. (b) Obstructed airway. Collapse of pharynx and tongue across glottis. (c) Airway secured with oropharyngeal airway.

(a)

Hoarse voice (dysphonia) – functional damage to larynx. Absence of noise – may indicate complete airway obstruction or apnoea. Feel

Feel for passage of air through mouth and nose with palm of hand; very sensitive for detecting air flow. Palpation of the trachea in supra-sternal notch will detect the deviation associated with a tension pneumothorax. AIRWAY – MANAGEMENT A range of manoeuvres is available to secure a patent airway, ranging from ‘bare hands’ techniques to a surgical airway. All these techniques can be performed without extending the head and compromising an unstable cervical spine. The anaesthetic ‘sniffing the early morning air’ position (head extended and neck flexed) should not be used in the trauma patient. Bare hands techniques and the use of pharyngeal airways are used together to pull the pharyngeal tissues and tongue off the posterior pharyngeal wall and away from the glottis, opening up the airway. Supra-glottic airway devices (e.g. the laryngeal mask airway) provide more reliable airway maintenance, but only intubation and the surgical airway will provide a definitive airway that is both secured and protected. All the non-surgical airway manoeuvres described are applicable to children, but require some modification in technique to accommodate their anatomical and physiological differences. Surgical cricothyroidotomy is not recommended in children under 12 years of age, as the cricoid cartilage can be damaged, leading to tracheal collapse.

Chin lift The chin is lifted forwards with the practitioner positioned at the casualty’s head or side, using one hand. This pulls the jaw and pharyngeal structures forward off the posterior pharyngeal wall and glottis, and opens up the airway.

The management of major injuries

(b)

Jaw thrust This is a more assertive manoeuvre that is

effective in patients with small jaws or thick necks, or who are edentulous. From the casualty’s head, the thenar eminences are rested on the casualty’s maxillae (assuming no obvious fracture), and the four fingers positioned under the angles of the mandible. Using the thenar eminences to provide a counterpoint on the maxillae, the mandible is lifted up and forwards to open up the airway as with chin lift. Considerable pressure can be exerted without displacing the head on the neck, and the manoeuvre can be combined with application of a BVM assembly for ventilation of the lungs.

22.13 Chin lift

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FRACTURES AND JOINT INJURIES

22

22.14 Jaw thrust

22.15 Jaw thrust with O2 mask

Release of chin lift and jaw thrust almost inevitably results in loss of the airway, and progression to airway adjuncts will be required to free up the practitioner.

A correctly sized OP airway should neither project up beyond the teeth, nor disappear into the buccal cavity. Use of the OP airway may need to be combined with chin lift or jaw thrust to maintain a patent airway, as they should only be used in obtunded patients with absent gag reflexes.

The oropharyngeal, or Guedel, airway is a curved and flattened, hard, plastic tube with a proximal flange, which is shaped and sized to hold the tongue and pharynx off the posterior pharyngeal wall. They are available in a range of sizes from neonate to large adult; selection of the correct size is important, as the pharyngeal tissues will collapse across the end of too small a device, whilst one too large will risk impinging on the glottis. The correct size is selected by lining up the OP airway alongside the patient’s jaw; the flange to tip length of the OP airway should match the distance from the corner of the patient’s mouth to the external auditory canal. The OP airway is inserted above the tongue, initially with the concave aspect upwards. As the tip passes over the tongue, the OP airway is rotated so the concave aspect slides over the tongue, and slipped into the pharynx until the flange rests on the incisors.

Nasopharyngeal (NP) airway The NP airway is a soft, plastic tube with a smooth, distal bevel and a proximal flange. Some makes have a safety pin to insert through the flange to prevent the NP airway disappearing into the nose. It is supplied in a number of internal diameter sizes, and should be selected according to the approximate size of the casualty’s little finger. The NP airway is lubricated with aqueous jelly, and inserted along the floor of the nasal cavity into the nasopharynx. The NP airway should not be inserted up the nose as this risks haemorrhage from the mucosa and turbinates, further compromising the airway, and also introduces the possibility of entering the cranial cavity through a basal skull fracture. NP airways are particularly useful as they can be tol-

22.16 OP airway (Guedel)

22.17 OP airway – correct position

Oropharyngeal (OP) airway

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22

22.19 NP airway – correct position

erated by responsive casualties with obstructing airways. They also provide access to suction the nasopharynx with a soft suction catheter.

advantages that it is more effective than other airway devices, but does not require the skill and training required for successful tracheal intubation. Mounting international evidence suggests that intubation performed by practitioners without anaesthetic training can be detrimental to patient survival, and in the UK the ambulance service regulatory body (Joint Royal Colleges Ambulance Service Liaison Committee, 2008) has removed tracheal intubation as a core paramedic skill, and recommends the use of supra-glottic airway devices. The LMA is available in a range of sizes from neonatal to large adult; for adult use, a size 3 will fit small women, size 4 larger women and smaller men, and size 5, larger men. The device consists of a cuffed distal portion shaped to fit into the oropharynx over the glottis. The cuff is inflated with air to fit snugly against the pharynx, but does not seal as does a tracheal tube cuff, and hence does not reliably protect the airway. The LMA is lubricated and inserted over the tongue with the open end of the cuffed distal portion positioned inferiorly. The device is slipped around the oropharynx until it is snugly positioned over the glottis, and the cuff inflated according to the size of the device (#3 20 mL, #4 30 mL, #5 40 mL). As the laryngeal mask, in common with other supra-glottic airway devices, does not provide a definitive and protected airway, consideration should be given to its being replaced with a tracheal tube at the earliest opportunity.

Oropharyngeal suction Secretions and blood should be cleared with a specialist pharyngeal sucker such as the Yankauer. Care should be taken not to damage the soft tissues, and as a general rule, the sucker should not be passed further than can be seen. Suction of the oronasopharynx with a Yankauer sucker, under direct vision using a laryngoscope, is effective in the obtunded patient. Supra-glottic airway devices These are devices that function between an OP airway and a tracheal tube, and include multi-lumen oesophageal airway devices (e.g. Combitube), the laryngeal tube airway, and the laryngeal mask airway. The most commonly used device is the laryngeal mask airway (LMA). The LMA was developed by Dr Archie Brain and introduced initially in the UK for anaesthetic use in the late 1980s. Since then it has found an international role for resuscitation and trauma airway management, with the

Oro-tracheal intubation is the preferred method for securing and protecting the compromised airway in the trauma patient. However, it is a difficult procedure with minimal survival rates in un-anaesthetized, trauma casualties; un-anaesthetized casualties can normally only be intubated when protective reflexes are absent, allowing a view of the vocal cords on laryngoscopy. Lack of reflexes to this degree is associated with terminally deep levels of

The management of major injuries

22.18 NP airway

Tracheal intubation

22.20 Supraglottic airways

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coma, when casualties are at the point of death. Casualties requiring a definitive airway should therefore be identified early, and expert assistance sought from an anaesthetist or critical care physician. The indications for oro-tracheal intubation are:

FRACTURES AND JOINT INJURIES

• apnoea • inability to maintain airway by other means. • need to protect airway from aspiration of blood and stomach contents • impending airway obstruction, e.g. inhalational burn, expanding neck haematoma, facial fractures • closed head injury with GCS below 8 • inability to maintain adequate oxygenation and ventilation with face mask or BVM assembly.

646

Nasotracheal intubation is indicated only in a spontaneously breathing patient, and has a poor success rate with a high incidence of complications such as nasal haemorrhage. Trauma tracheal intubation should be performed with a rapid sequence induction (RSI) anaesthetic; after pre-oxygenation, anaesthesia is rapidly induced with an intravenous agent, cricoid pressure applied to hold the oesophagus closed and prevent passive reflux of stomach contents, the patient paralyzed with suxamethonium and a tracheal tube placed under direct vision with use of a laryngoscope. The tracheal tube cuff is inflated until no leak is detected, and the cricoid pressure not released until the anaesthetist confirms the tracheal tube is secure. This procedure should not be performed by any practitioner without the necessary training and experience in anaesthetic techniques, as injudicious use of muscle relaxants can lead to immediate loss of the airway and a ‘can’t intubate, can’t ventilate’ scenario. If a non-anaesthetically trained, trauma practitioner has to attempt intubation in extremis, the following sequence should be followed: 1. Select appropriately sized tracheal tube; size 8 (internal diameter) will be appropriate for most men and most women. 2. Leave tube uncut but ensure proximal connector is securely attached. 3. Have a smaller diameter tube available as back up. 4. Lubricate the cuff and test inflate, then deflate, to detect cuff leakage. 5. Have two functioning laryngoscopes available with bright lights. 6. Have intubating bougie or catheter available. 7. Maintain head and neck immobilized in neutral, in-line position. 8. Pre-oxygenate the patient, if possible, with a BVM assembly. 9. Use a laryngoscope in the left hand to visualize the vocal cords. 10. Insert, intubating the bougie through the cords

and slide the tracheal tube over the bougie into the trachea, then remove the bougie. 11. Connect the self-inflating resuscitation bag to the tracheal tube directly or with a catheter mount, via a heat/moisture exchanger (HME) filter. 12. Inflate the cuff until no air leak is audible during ventilation. 13. Secure the tracheal tube with ties or tapes. 14. Confirm intubation with chest auscultation and EtCO2 detection, and ventilate the patient with 100 per cent oxygen to normal EtCO2 levels. All intubated, trauma patients should be ventilated, as it is unlikely that they would be able to maintain adequate oxygenation and ventilation spontaneously. Needle cricothyroidotomy Needle cricothyroidotomy is

the insertion of a needle through the cricothyroid membrane into the trachea to allow jet insufflation of the lungs with oxygen. It is used in emergency ‘can’t intubate, can’t ventilate’ situations to buy time whilst expert assistance is sought, or a definitive surgical airway prepared. Oxygenation is achievable, but ventilation limited, so carbon dioxide accumulates and the EtCO2 rises. Specialist equipment is available (e.g. ventilation with a Sanders injector driven from a highpressure oxygen source, via a curved cricothyroid needle). However, a system can be rapidly assembled from routinely available components. The following sequence should be followed: 1. Prepare a 12- or 14-gauge, preferably unported, intravenous cannula, and attach it to a 10 mL syringe. 2. Prepare a length of oxygen tubing with a distal Y connector, three-way tap or cut side-hole, and attach it to a cylinder or wall oxygen source with a flow rate set at 15 L/minute. 3. Prepare skin with 2 per cent chlorhexidine in 70 per cent isopropyl alcohol, and insert the cannula through the patient’s cricothyroid membrane in the midline, angled caudally at 45 degrees, aspirating air as the trachea is entered. 4. Slide the cannula fully into the trachea over the trochar and secure manually or with tape. 5. Attach the Y connector end of the oxygen tubing to the cannula. 6. Occlude the Y connector for 1 second to allow lung insufflation. 7. Allow a 4-second pause with the Y connector un-occluded to allow lung deflation. 8. Continue 1:4 cycles of insufflations until a definitive airway is secured. Complications of needle cricothyroidotomy and jet insufflation are commonly misplacement, surgical emphysema and barotrauma. It should only be attempted if intubation and other airway maintenance techniques have failed.

Surgical cricothyroidotomy Surgical cricothyroidotomy

1. Prepare skin over cricothyroid membrane with 2 per cent chlorhexidine in 70 per cent isopropyl alcohol, and infiltrate with local anaesthetic if the patient is aware. 2. Prepare an appropriate tracheal tube; a 6 mm internal diameter, reinforced/armoured tracheal tube is optimal, as this allows use of an intubating bougie and will not kink and obstruct. Alternatively, a tracheostomy tube with obturator can be used. 3. Prepare a scalpel, ideally with a curved No. 10 blade. 4. Prepare an intubating bougie or catheter, e.g. Cook Medical Frova intubation catheter. 5. Identify the cricothyroid membrane; place a finger on the thyroid cartilage prominence and roll it down onto a notch of cricothyroid membrane. 6. Tension skin over the cricothyroid membrane with the thumb and fore-finger on either side. 7. Make a single, 1–2 cm transverse incision through the skin and cricothyroid membrane into the trachea. 8. Without releasing skin tension, insert the intubation catheter through the incision and pass it inferiorly down the trachea. 9. Slide the tracheal tube over the intubation catheter into the trachea until the cuff is in the lumen of the trachea. 10. Inflate the cuff until the leak is sealed on ventilation. 11. Ventilate with a self-inflating bag and high-flow oxygen. 12. Secure the tracheal tube with ties or tape. 13. Confirm that both lungs are ventilated; if one-lung ventilation is detected (usually on the right), deflate the cuff, pull back the tracheal tube and re-inflate the cuff. Surgical cricothyroidotomy can be a difficult procedure in casualties with challenging anatomy, and complications can be serious; this procedure should only be used if oro-tracheal intubation has been attempted and failed. Complications include haemorrhage, damage to laryngeal structures, false passage formation, misplacement of the tracheal tube, surgical emphysema and barotrauma.

Take-home message Whatever the means of airway management used, the goal is to secure and protect the airway. The focus should be on oxygenation and ventilation, not intubation. Casualties die from hypoxia and hypercarbia, not failure of intubation.

B – Breathing and chest injuries Of severely injured patients admitted to hospital in the UK, 20 per cent have chest injuries (Joint Royal Colleges Ambulance Service Liaison Committee (JRCALC), 2008), and thoracic trauma is a significant cause of mortality (Findlay et al., 2007). However, the majority of chest injuries are not fatal and do not require specialist, surgical intervention. BREATHING/CHEST INJURY – AWARENESS The proportion of penetrating to blunt chest injuries varies between countries, and between rural and urban environments. Only 10 per cent of blunt chest injuries and 20 per cent of penetrating injuries require thoracotomy (Findlay et al., 2007; Joint Royal Colleges Ambulance Service Liaison Committee (JRCALC), 2008). Non-surgical management centres on supportive treatment of contused lungs and the insertion of chest drains. However with blunt trauma, the force of impact and energy transfer to the lung parenchyma should alert the clinician to the likelihood of severe intrathoracic damage and the potential for progressive cardiopulmonary problems. Early recognition and management of immediately life-threatening injuries in the primary survey is imperative, with early imaging repeated as necessary. Potentially life-threatening injuries are sought during the secondary survey, and sophisticated imaging modalities such as CT and MRI may be indicated. Major chest injuries will require urgent referral to a specialist thoracic or cardiothoracic surgeon, and a surgeon capable of immediate thoracotomy must be available in hospitals designated as receiving major trauma cases.

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The management of major injuries

is the insertion of a tracheal or tracheostomy tube through an incision in the cricothyroid membrane into the trachea. It is used in emergency situations when oro-tracheal intubation has been attempted, and failed, and will both secure and protect the airway. Adequate ventilation is just as achievable as with oro-tracheal intubation, and 100 per cent oxygen can be delivered. The following sequence should be followed:

BREATHING/CHEST INJURY – RECOGNITION The patient’s chest, neck and abdomen must be fully exposed to allow assessment of the chest. Examination should be systematic: Look • Respiratory rate – tachypnoea is indicative of hypoxia. • Shallow, gasping or laboured breathing – suggests

respiratory failure. • Cyanosis – indicates hypoxia. • Plethora and petechiae – suggest asphyxia and chest

crushing. • Paradoxical respiration; ‘pendulum’ breathing with

asynchronization between chest and abdomen, resulting in a seesaw motion – indicates respiratory failure or structural damage.

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22

• Unequal chest inflation – suggestive of pneumoth-

orax or flail chest. • Bruising and contusions – indicate significant energy transfer and consequent underlying lung contusion and potential hypoxia (e.g. ‘seat belt’ sign). • Penetrating chest injuries – potential for pneumothorax and open, sucking pneumothorax. • Distended neck veins – increased venous pressure secondary to a tension pneumothorax or cardiac tamponade. Listen • Absent breath sounds – indicate apnoea or tension

pneumothorax. breathing/crepitations/stridor/wheeze – suggest a partially obstructed airway, blood and secretions in airways, tracheal or bronchial damage. • Reduced air entry unilaterally – indicate a pneumothorax, haemothorax or haemo-pneumothorax, and flail chest. • Noisy

Feel • Tracheal deviation – indicative of tension pneu-

mothorax, shifting the mediastinum (Note: the trachea is felt inferiorly in the suprasternal notch; do not confuse it with the larynx, which is extra-thoracic and hence does not shift.) • Tenderness – suggests significant chest wall contusion and/or fractured ribs • Crepitus/instability – underlying fractured ribs • Surgical emphysema (classic ‘bubble wrap’ feel to subcutaneous tissues on palpation, due to presence of air forced into tissues under pressure) – tension pneumothorax, ruptured bronchi or trachea, and fractured larynx. BREATHING/CHEST INJURY – MANAGEMENT Immediate management is to stabilize the cervical spine, control catastrophic limb haemorrhage, secure the airway, administer oxygen at high flow and ventilate the lungs if breathing is absent or inadequate. It is vital to rapidly identify and manage immediately life-threatening chest injuries during the primary survey, as positive-pressure ventilation of the lungs can cause a rapid deterioration; a simple pneumothorax can be converted to a tension pneumothorax, and a tension pneumothorax will increase in pressure, leading to sudden collapse and cardiac arrest. Hence, if a patient is intubated and ventilated, signs of a pneumothorax must immediately be sought and, if present, decompressed and drained. Potentially life-threatening injuries can then be identified during the secondary survey.

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TENSION PNEUMOTHORAX A tension pneumothorax is the build-up of air under pressure in the pleural cavity, leading to compression and collapse of the underlying lung. The resultant

IMMEDIATELY LIFE-THREATENING CHEST INJURIES (PRIMARY SURVEY) 1. Tension pneumothorax 2. Open pneumothorax (sucking chest wound) 3. Massive haemothorax 4. Cardiac tamponade 5. Flail chest 6. Disruption of tracheal–bronchial tree

ventilation–perfusion mismatch leads to hypoxia. However, the life-threatening, terminal event is a shift of the mediastinum away from the affected side, kinking the great vessels and obstructing venous return to the heart. This results in a deadly combination of hypoxia and loss of cardiac output, with a pulseless electrical activity (PEA) cardiac arrest. Diagnosis should usually be clinical, not radiological, and the clinician should look specifically for the three cardinal signs: • absent breath sounds – on the side of the pneumothorax • deviated trachea – away from the side of the tension pneumothorax • hyper-resonance – on the side of the pneumothorax. The neck veins may be distended, as venous return is obstructed; however, this may not be readily visible, and is unreliable with concurrent hypovolaemia. There is an argument for radiological diagnosis if this is immediately available in the resuscitation room, and the patient is not exhibiting cardiovascular compromise; a tension pneumothorax can be mimicked by other conditions such as endo-bronchial intubation with distal lung collapse. The immediate management is decompression (needle thoracocentesis) of the tensioning pneumothorax by insertion of a 14-gauge cannula into the pleural cavity through the second intercostal space, in the mid-clavicular line. Diagnostically, a hiss is heard as air under pressure escapes. However, this is unreliable, and the relatively short 50 mm intravenous cannulae commonly used may not penetrate a thick chest wall in muscular or obese casualties. Presence of the cannula within the pleura is likely if air can be aspirated with a syringe, and use of the longer 140 mm cannulae will make correct placement more likely. Once sited, the cannula should be left open to reduce the risk of re-tensioning. Needle decompression should not be performed if the only sign elicited is reduced or absent breath

ineffective in practice, and an occlusive dressing with immediate chest drain may be more reliable. The patient may need intubating and ventilating.

sounds, as there are associated complications such as misplacement and damage to the underlying lung. Insertion of a needle into the pleural cavity will convert a tension pneumothorax into a simple pneumothorax, which will in turn need draining. In an intubated and ventilated patient, immediate thoracostomies can be performed prior to formal chest drain insertion; the positive-pressure ventilation of the lungs will enable the lungs to be satisfactorily inflated. If immediately available, a controlled chest drain insertion is preferable to a blind needle decompression. OPEN PNEUMOTHORAX (SUCKING CHEST WOUND) An open wound in the chest wall will immediately result in a simple pneumothorax as intrathoracic pressure equilibrates with atmospheric pressure. If the defect is greater than some two-thirds of the diameter of the trachea (which has a lateral diameter of 20–25 mm), air is preferentially drawn into the pleural cavity rather than into the lungs via the trachea. This causes paradoxical respiration, where the lung deflates on inspiration, with resulting hypoventilation and hypoxia. If a flap valve effect occurs, the intra-pleural pressure will rise with each breath, leading to a tension pneumothorax. Specific, immediate management is the application of an occlusive dressing, sealed on three sides, but leaving the third side open to allow any build up of positive intra-pleural pressure to vent. This can be

The management of major injuries

22.21 Left-sided tension pneumothorax

MASSIVE HAEMOTHORAX The chest cavity presents an enormous potential space in which blood can accumulate following both blunt and penetrating chest injury (one of the four of ‘bleeding onto the floor and four more’). 1500 mL or one-third of the patient’s blood volume can rapidly accumulate, leading to a combination of hypoxia and shock. Smaller haemothoraces are usually due to lung parenchymal tears, fractured ribs and minor venous injuries and are self-limiting. Massive bleeds are usually due to arterial damage, which is more likely to require surgical repair and pulmonary lobectomy. Diagnosis is based on the presence of hypoxia, reduced chest expansion, absent breath sounds and/or dullness to chest percussion, and hypovolaemic shock. Supine chest percussion may not demonstrate dullness, and supine x-rays may not reveal moderate haemothoraces. Specific management is by the insertion of a chest drain, correction of hypovolaemia and blood transfusion. If the total volume of blood initially drained is greater than 1500 mL, or the bleeding continues at 200 mL/hour, or the patient remains haemodynamically unstable, surgical referral and thoracotomy is indicated.

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CARDIAC TAMPONADE Cardiac tamponade is the accumulation of blood within the pericardium, restricting the ability of the heart to fill, and resulting in a progressive loss of cardiac output leading to PEA cardiac arrest. It is more commonly associated with penetrating rather than blunt trauma, especially stab wounds between the nipple lines or scapulae, and gunshot wounds. Clinical diagnosis can be difficult, as the signs can be subtle and difficult to elicit in the trauma room. The three classic diagnostic criteria constitute Beck’s Triad: 1. Distended neck veins due to elevated venous pressure. 2. Muffled heart sounds. 3. Fall in arterial blood pressure. If an arterial line is present, a fall in systolic blood pressure may be seen on inspiration (pulsus paradoxus). If a central venous pressure (CVP) line is in situ, a rise in CVP may be seen on inspiration, in contrast to its normal fall on inspiration (Kussmaul’s sign). Reliable diagnosis may require sophisticated imaging. No change is seen on standard chest x-rays, but CT scanning, MRI scanning, FAST ultrasound and trans-oesophageal echo-cardiogram (TOE) can all be used to confirm the diagnosis.

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Management has two components; relieving the pressure within the pericardium by draining the accumulated blood, and stopping the source of the bleeding to prevent re-accumulation. Since the bleeding is likely to come from the heart, immediate surgical repair to the myocardium may be required, and surgical assistance should be sought early. Classically, aspiration of blood from the pericardium is achieved by needle peri-cardiocentesis, which should be viewed as a diagnostic procedure rather than curative. The ECG is monitored, and a long cannula (16–14 gauge, 14 cm as above) is attached to a syringe. The skin is prepared, pierced with the cannula to the left of the xiphisternum, and the cannula directed towards the pericardium in the direction of the left scapula tip. As the pericardium is entered, blood is aspirated. The needle can then be removed from the cannula, and a three-way tap attached to the cannula to allow further aspirations. Advancement too far will cause the tip of the cannula needle to enter the myocardium, which will be seen on the ECG as ventricular ectopics, widening QRS complexes or ST-T wave changes. Pericardiocentesis can be performed under ultrasound guidance. Alternative and more definitive procedures are subxiphoid pericardial window, or emergency thoracotomy and pericardiotomy. These are optimally performed in the operating theatre if the patient’s condition allows. FLAIL CHEST Massive impact to the chest wall can result in multiple rib fractures, and this is more common in older people who have less flexible rib cages. The multiple fractures, particularly if anterior and posterior, can result in a loss of the structural integrity of the chest wall, and a segment can ‘float’; as the patient inspires, the flail segment is sucked in and the lung cannot inflate (paradoxical respiration). This results in hypoxia and ventilatory compromise. However, the force required to cause this injury inevitably causes a severe, underlying lung contusion, and this is the more significant cause of the hypoxia. The associated, severe pain further compromises the respiratory function, and respiratory failure can ensue. Diagnosis is by clinical examination, chest x-rays to reveal the fractures and lung contusion, and arterial blood gases to quantify the hypoxia. Management is initially supportive with administration of oxygen and analgesia. Advanced pain relieving methods such as epidurals may be required. Profound hypoxia may require that patients are intubated and ventilated until the contusion has adequately resolved, and pain can be controlled. Intravenous fluids may need to be restricted to avoid overload and worsening hypoxia. Very rarely, fractured ribs or costo-chondral disruption may require surgical stabilization.

DISRUPTION OF TRACHEOBRONCHIAL TREE Major disruption of the tracheobronchial tree can result in a broncho-pleural fistula; the disrupted trachea or bronchus allows an air leak into the pleura which, if large enough, will not allow inflation of the lung, even with a large-bore chest drain in situ. Diagnosis is made by the presence of a persistent pneumothorax, pneumomediastinum, pneumopericardium or air below the deep fascia of the neck, often in patients who have suffered a deceleration injury. Immediate management with tracheal intubation may not be successful, as the air leak may prevent inflation of either lung. In this situation, endobronchial intubation of the opposite lung or use of a bronchial blocker may be required before adequate lung ventilation can be achieved, and this may need the services of a thoracic anaesthetist. SIMPLE PNEUMOTHORAX A simple pneumothorax results from air entering the pleural cavity, causing collapse of the lung with a resulting ventilation–perfusion mismatch and hypoxia. As the air is at atmospheric pressure, and there is no one-way valve effect, no mediastinal shift develops, and cardiac output is maintained. The cause is usually a lung laceration, which can follow both blunt and penetrating chest trauma or thoracic spine fracture–dislocations. The diagnosis is made during the primary or secondary survey, primarily by the absence or reduction of breath sounds. Hyper-resonance may not be obvious, and a chest x-ray may be required to confirm the pneumothorax. If the pneumothorax is stable, definitive treatment with a chest drain can be deferred to the secondary survey. However, a simple pneumothorax can develop into a tension pneumothorax at any time, and so a high index of suspicion should be maintained.

POTENTIALLY LIFE-THREATENING CHEST INJURIES (SECONDARY SURVEY) 1. Simple pneumothorax 2. Haemothorax 3. Pulmonary contusion 4. Tracheobronchial tree injury 5. Blunt cardiac injury 6. Traumatic aortic disruption 7. Traumatic diaphragmatic injury 8. Mediastinal traversing wounds 9. Simple pneumothorax

1. Confirm the correct side on the chest x-ray. 2. Identify the fifth intercostal space, just anterior to the mid-axillary line on the affected side. 3. Prepare the skin with 2 per cent chlorhexidine in 70 per cent isopropyl alcohol or alcoholic iodine. 4. Infiltrate the skin and subcutaneous tissues with lignocaine if the patient is aware. 5. Make a 2–3 cm, horizontal incision through the skin, just above the sixth rib (to avoid the intercostals vessels below the fifth rib). 6. Bluntly dissect through the subcutaneous tissues with a straight forceps, and puncture the parietal pleura with the tips. 7. Insert your gloved little finger through the incision into the chest cavity and sweep the finger around to ensure the cavity is empty and your incision is above the diaphragm (no viscus is felt). 8. Grasp the tip of an appropriately sized thoracostomy tube between the tips of the forceps and introduce through the incision into the chest cavity; unclamp the forceps and slide the tube posteriorly along the inside of the chest wall. 9. Attach the tube to an underwater drain or Heimlich valve and observe for tube fogging and underwater bubbling. 10. Suture the chest drain in place and apply a dressing. 11. Check lung reinflation with a chest x-ray. The important steps are illustrated in Figure 22.22. Haemothorax Haemothoraces are primarily caused by lung lacerations or damage to intercostals and internal mammary vessels. Thoracic spine fracture dislocations can also result in haemothoraces. They are normally self-limiting, and rarely require operative intervention. Diagnosis can be difficult in the supine patient as breath sounds will remain present. Dullness to percussion will be posterior and not reliable. Supine chest x-rays will not reveal moderate amounts of blood, although erect films are more sensitive; even with an

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The management of major injuries

Intubation and ventilation in the presence of a pneumothorax predisposes to the development of a tension pneumothorax, and so chest drains should immediately be placed. Anaesthesia with a nitrous oxide-based anaesthetic will increase the air space by a factor of four, and can therefore cause rapid tensioning, as can air transport at altitude. In these situations, chest drains should be placed prophylactically, and it is good practice to insert chest drains in casualties prior to transfer in case a tension pneumothorax develops en route. Chest drain insertion is a procedure with the potentially dangerous complication of visceral damage, and the classic chest drain technique using a pointed trochar should not be used. The appropriate technique is:

(e)

(f)

22.22 Chest drain insertion sequence (a) Chest x-ray to confirm correct side. (b) Identify the fifth intercostal space, just anterior to the mid-axillary line on affected side. (c) Insert gloved little finger through the incision into the chest cavity and finger sweep to ensure cavity is empty and the incision is above the diaphragm (no viscus is felt). (d) Grasp the tip of an appropriately sized thoracostomy tube between tips of forceps and introduce through incision into chest cavity. Unclamp forceps and slide tube posteriorly along inside of chest wall. (e) Attach tube to underwater drain or Heimlich valve and observe for tube fogging and underwater bubbling. (f) Check lung reinflation with chest x-ray.

erect film, 400–500 mL of blood are required to obliterate the costo-phrenic angle. The diagnosis may require the use of FAST or CT scanning. An acute haemothorax visible on chest x-ray is treated with a large calibre chest drain, inserted using the technique described earlier. If more than 1500 mL are drained initially, or drainage continues at 200 mL/hour or faster, thoracotomy should be considered. PULMONARY CONTUSION Pulmonary contusion is the commonest potentially life-threatening chest injury, occurring in 20 per cent

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of casualties with an injury severity score (ISS) of > 15. Mortality ranges from 15–20 per cent and 40–60 per cent of patients will require ventilating. Blunt force trauma to the chest wall, or crushing injury, will contuse the underlying lung, which then becomes oedematous and haemorrhagic, with subsequent collapse and consolidation. This causes a ventilation–perfusion mismatch and hypoxia, dependant on the extent of the contusion and limitation of the patient’s ventilation by pain. About half of these patients will develop bilateral acute respiratory distress syndrome (ARDS), a systemic inflammatory response to the injury. Pulmonary contusion may not be associated with obvious rib fractures, particularly in children and teenagers with pliable rib cages. The initial chest x-ray may not reveal the extent of the contusion, which can develop over the following 48 hours. The diagnosis should be made taking into account the mechanism of injury and the degree of hypoxia revealed by oximeter saturation readings and arterial blood gas estimations. Treatment is with supportive measures and oxygen administration. Patients with severe hypoxia despite inspired oxygen (e.g. PaO2 < 8.5 kPa or SaO2 < 90 per cent) should be considered for elective ventilation. Pre-existing pulmonary disease should be taken into account. TRACHEOBRONCHIAL TREE INJURY Tracheobronchial tree injuries are rare, but can easily be overlooked as signs can be subtle. Some 3 per cent of chest-crushing injuries are associated with upper airway injuries, but most trachea-bronchial tree injuries are within 1 inch of the carina. Patients frequently present with haemoptysis, surgical emphysema and a simple or tension pneumothorax. The pneumothorax may be resistant to re-inflation with a chest drain, and a post-drain and persistent air leak suggests the presence of a bronchopleural fistula. CT and MRI imaging may confirm the diagnosis, but bronchoscopy may be required.

Treatment is initially with one or more, large chest drains that may need a high-volume/low-pressure pump to allow lung re-inflation. Persistent bronchopleural fistulae may require operative intervention. Major tracheobronchial injuries are immediately lifethreatening, and management is described earlier. BLUNT CARDIAC INJURY Blunt cardiac injury follows a direct blow to the anterior chest, and is associated with a fractured sternum. This can result in myocardial contusion, or more rarely, chamber rupture and valvular disruption. The myocardial damage can result in hypotension due to myocardial dysfunction, conduction abnormalities, and dysrhythmias. Sudden onset of dysrhythmias can result in death from ventricular fibrillation. Management is supportive, and the patient should be monitored closely for a minimum of 24 hours, following which the risk of sudden dysrhythmias diminishes substantially. TRAUMATIC AORTIC DISRUPTION Blunt aortic injury is a deceleration injury commonly following high-speed road traffic crashes (RTCs) and falls from a height. Up to 15 per cent of deaths from road vehicle collisions are a result of damage to the thoracic aorta (Williams et al., 1994). Most injuries occur in the proximal thoracic aorta, where the relatively mobile aortic arch can move against the fixed descending aorta near the ligamentum arteriosum. Complete transection or rupture is immediately fatal, but the haematoma can be contained by the adventitial layer of the aortic wall, enabling the patient to survive to reach hospital. Specific clinical signs and symptoms are often absent, and the mechanism of injury should provoke a high index of suspicion. Diagnosis is aided by chest x-ray findings, classically of a widened mediastinum (note that an anteroposterior (AP) film will magnify a normal width mediastinum), loss of the aortic knuckle

22.23 Ruptured aorta (a) Angiogram showing a rupture of the arch of the aorta. (b) CT scan showing the haematoma around the rupture.

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TRAUMATIC DIAPHRAGMATIC INJURY Traumatic rupture of the diaphragm is associated with blunt and penetrating trauma to the abdomen. Blunt trauma is usually the result of a lateral or frontal vehicular collision, with distortion of the chest wall, shearing of the diaphragm and compressive rise in intra-abdominal pressure. Rupture is more common (in survivors) on the left side, probably because the severity of injury required to cause a right-sided rupture above the protective liver is more usually fatal. The injury is rarely found in isolation, and is associated with other chest, abdominal and pelvic injuries. Diaphragmatic ruptures associated with penetrating trauma are usually due to gunshot and stab injuries, and result in a smaller tear with less visceral tissue protruding through the diaphragm. Signs and symptoms can be subtle, and the injury missed, only becoming apparent years later as the herniation develops. The standard chest x-ray only may show an elevated but indistinct hemidiaphragm; however, the appearance of bowel gas or a nasogastric tube within the chest will help confirm the diagnosis. Contrast studies via a nasogastric tube, CT and MRI scanning are all useful adjuncts. Diaphragmatic rupture and visceral herniation may be mistaken for a haemothorax on the plain chest x-ray; however, the insertion of a finger into the chest during chest drain insertion may reveal the presence of stomach or bowel loops (hence the avoidance of sharp trochars to prevent visceral injury). Initial management is supportive with careful assessment and management of the ABCs. Careful chest drain insertion is advisable prior to transfer or anaesthesia. Definitive treatment is surgical – the diaphragmatic rupture can be repaired during a trauma laparotomy, but may require a thoracotomy or thoraco-abdominal approach. MEDIASTINAL TRAVERSING WOUNDS Penetrating objects that cross the mediastinum may cause damage to the lungs and to the major mediasti-

nal structures (the heart, great vessels, tracheobronchial tree and oesophagus). The diagnosis is made by careful examination of the chest, backed up by chest x-ray and trauma CT imaging. The significant clinical finding is an entrance wound in one hemithorax and an exit wound or radiologically visible missile in the other. Bullets and shrapnel can tumble, so the trajectory is unpredictable. The presence of fragments adjacent to the mediastinum on x-ray should raise suspicion of a traversing injury. Patients with symptomatic, haemodynamically unstable mediastinal traversing wounds should be assumed to have an ongoing haemothorax, tension pneumothorax or cardiac tamponade. Initial management is ABC resuscitation with bilateral chest drains, prior to definitive surgical management. Stable patients should undergo extensive investigation with ultrasound, trauma CT, angiography, oesophagoscopy and bronchoscopy as indicated, and on early consultation with a cardiothoracic surgeon. Stable patients should be continually re-evaluated as they can suddenly deteriorate and require urgent surgical intervention; 50 per cent of patients with mediastinal traversing wounds are haemodynamically unstable on presentation, with a doubled mortality of 40 per cent over those who are stable (Findlay et al., 2007).

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The management of major injuries

and deviation of the trachea to the right. Whilst angiography has been the gold standard diagnostic tool, the advent of multidetector helical CT scanners has supplanted the more invasive technique. Modern CT scanning has an accuracy approaching 100 per cent, and is highly specific for detecting the injury. Initial management is supportive, but a contained haematoma may rupture if the patient is hypertensive. Blood pressure should therefore be controlled in patients with suspected blunt aortic injury until CT scanning has excluded the injury. Once the injury is confirmed, the blood pressure must be controlled until the patient can be taken to the operating theatre for definitive cardiothoracic repair. Endovascular repair is possible for some blunt aortic injuries.

TAKE HOME MESSAGE The primary goal in management of traumatic chest injuries is to rapidly identify and manage the six immediately life-threatening injuries within the primary survey. The eight potentially life-threatening injuries should be sought within the primary and secondary surveys, and may require sophisticated imaging to diagnose. Only 15 per cent of chest injuries require operative intervention.

C – Circulation and shock For the healthcare professional ‘shock’ is not the commonly reported emotional condition in someone witnessing a disturbing incident. It can be broadly defined as circulatory failure, or inadequate perfusion of the tissues and organs with oxygenated blood. Untreated, or inadequately treated, shock leads to organ damage and ultimately death from multi-organ failure. Recognition of shock, diagnosis of the cause and subsequent management are therefore important steps in the resuscitation and care of the seriously ill or traumatized patient. The C for circulation follows the A for airway and B for breathing, but in the presence of catastrophic, external bleeding from limb wounds, control of the bleeding takes precedence. This is the ABC sequence, and holds true in a hospital environment if the airway and catastrophic limb bleed cannot be managed simultaneously by the trauma team.

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CIRCULATION AND SHOCK – AWARENESS There are five main types of shock that can be grouped into two pathogenic groups:

The majority of patients presenting with shock following a major injury will be suffering from hypovolaemic shock; however, any patient can present with a combination of types of shock.

within the bowel secondary to bowel damage caused by ischaemia. The profound vasodilatation that results dramatically reduces afterload; even with a normal circulating blood volume and raised cardiac output, the patient’s blood pressure falls and the pulse pressure widens, e.g. 110/70 Æ 90/30. Oxygen consumption increases, and despite the high cardiac output, tissue perfusion and oxygenation are reduced, and organ damage results. The toxins can also damage the myocardium and cause capillary leakage, complicating the presentation with elements of cardiogenic and hypovolaemic shock.

Hypovolaemic shock Hypovolaemic shock results from

Neurogenic shock

1. Vasoconstrictive: hypovolaemic and cardiogenic shock. 2. Vasodilative: septic, neurogenic and anaphylactic shock.

a loss of volume within the circulation; it may be due to whole blood loss from haemorrhage, or plasma and fluid loss from burns or severe medical conditions. As the circulating blood volume decreases, compensatory mechanisms are triggered to preserve blood pressure and vital organ perfusion. These mechanisms can maintain systolic blood pressure up to around 30 per cent blood loss in a fit patient. Above this, compensation increasingly fails until unconsciousness, followed by death at around 50 per cent blood loss. Early compensatory mechanisms are tachycardia and peripheral vasoconstriction with a narrowed pulse pressure [vasoconstriction raises the diastolic blood pressure, bringing it closer to the systolic, e.g. 120/60 Æ 120/90]. Further compensations include tachypnoea, shift of fluid from tissues into circulation and reduced urine output. Some injuries mimic hypovolaemic shock, classically tension pneumothorax and cardiac tamponade; the low-output state follows obstruction to the venous return and cardiac output, respectively. Peripheral vasoconstriction is not a feature of these conditions in the absence of hypovolaemia, unlike cardiogenic shock, and the veins remain full. Cardiogenic shock Cardiogenic shock results from a decrease in myocardial contractility, and hence a reduction in stroke volume and cardiac output. This classically follows myocardial infarction or severe ischaemia, but can follow trauma damage to the myocardium from blunt or penetrating injury, e.g. fracture of the sternum. The disproportionate vasoconstriction is due not to hypovolaemia, but an outpouring of catecholamines and the profound autonomic stimulus, which can put further strain on the heart by causing vasoconstriction and increasing afterload. Trauma patients may present with cardiogenic shock if the cardiac event precedes, and indeed causes, the traumatic event.

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Septic shock This results from the entry of toxins into the circulation, which poison the vasoconstrictive mechanisms within the blood vessels. These toxins usually come from infection, or are released from

Neurogenic shock is produced by high spinal cord injury, which disrupts the sympathetic nerves controlling vasoconstriction. The peripheral vasculature relaxes and becomes profoundly dilated, reducing pre-load and afterload. Even with a raised cardiac output, the patient cannot maintain an adequate blood pressure, and shock ensues. Neurogenic shock is not caused by an isolated head injury, and is different from ‘spinal shock’, which is a temporary flaccidity following spinal damage. Since neurogenic shock is always related to traumatic spinal cord damage, it is likely to co-exist with a degree of hypovolaemia from associated trauma.

Anaphylactic shock This is a type of allergic reaction.

Exposure to an antigen to which an individual has previously been sensitized triggers off a cascade reaction. The mast cells degranulate and release large quantities of histamine into the bloodstream. Other vasoactive substances are released, and profound vasodilatation is caused. Massive capillary leakage results in sudden oedema, which with loss of fluid into the bowel causes hypovolaemia [1 mm depth of oedema across the body surface equates to a 1.5 L fluid loss]. This picture is complicated by other effects such as bronchospasm. Anaphylaxis can be triggered by many common antigens such as shellfish or peanuts. Of particular significance to the hospital practitioner are allergies to drugs and latex. CIRCULATION AND SHOCK – RECOGNITION Recognition of shock is relatively easy in the late stages when signs of underperfusion are obvious. Earlier stages of shock present with more subtle signs that require careful patient examination to elucidate; for example, the systolic blood pressure may not drop significantly until 30 per cent of the patient’s blood volume has been lost. Hypovolaemic shock passes through a number of clinical stages as blood loss increases, and these have been grouped into four classes of shock, with increasingly apparent signs [adult blood volume is approximately 7 per cent of ideal body weight, or 5 L for a non-obese man weighing 70 kg]. It should be remembered, however, that the development and progression of shock is a continuum.

CLASSES OF SHOCK Class 1 – < 15 per cent loss blood volume (< 750 mL in a male weighing 70 kg) (no change in BP, pulse pressure, respiratory rate or capillary refill) • minimal tachycardia < 100 bpm • skin pallor possible Class 2 – 15–30 per cent loss blood volume (750–1500 mL) (no change in systolic blood pressure) • Ø peripheral perfusion with cool, pale, clammy skin • ≠ capillary refill > 2 seconds • tachycardia > 100 bpm • Ø pulse pressure as diastolic BP rises • increased respiratory rate (tachypnoea) of 20–30 bpm • subtle mental status changes: anxiety, fear, aggression Class 3 – 30–40 per cent loss blood volume (1500– 2000 mL) marked tachycardia > 120 bpm • measurable fall in systolic blood pressure from patient’s normal, e.g. < 100 mmHg • thready peripheral pulses • flat/empty veins • marked tachypnoea > 30 bpm • significant mental status changes: agitated ++ • dropping urine output Class 4 – > 40 per cent loss blood volume (> 2000 mL) • severe tachycardia > 140 bpm • moribund, decreased conscious level • significant drop in systolic blood pressure, e.g. < 70 mmHg • impalpable peripheral pulses, weak central pulses • respiratory distress • central and peripheral cyanosis • minimal urine output

loss, but they deteriorate very rapidly when they decompensate. The pulse rate is a good indicator of shock level, as is the respiratory rate; tables showing normal parameters for children at different ages are available. A reasonable approximation of blood pressure can be gained from palpating pulses. However, practitioners tend to overestimate the blood pressure if pulses are palpable, although there is wide variation (Deakin and Low, 2000). Recognition of shock therefore depends on a rapid clinical assessment of the patient, with measurement of the appropriate vital signs. The look, listen, feel sequence should be applied to identify the signs of hypovolaemic shock; blood pressure and pulse alone are not adequate. Look and listen

• • • •

peripheral/central cyanosis and pallor sweating tachypnoea and respiratory distress change in mental status – anxiety, fear, aggression, agitation • depressed level of consciousness or unconsciousness

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Blood loss of greater than 50 per cent (> 2500 mL) results in loss of consciousness, pulse and blood pressure, and finally respiration, causing a hypovolaemic PEA cardiac arrest. The values shown in Table 22.1 relate to adults and children above the age of 12. Younger children compensate more effectively to a greater degree of blood

Feel

• Peripheral perfusion poor – cool, clammy, shut down • Capillary refill time > 2 seconds (this is unreliable in cold and frightened patients) • Pulse rate and character – tachycardia and thready pulse • Loss of pulses – radials, then femorals, then carotids as severity of shock increases • Blood pressure – initially a raised diastolic with narrowed pulse pressure, then drop in systolic and diastolic, and finally an unrecordable blood pressure. Observation of these factors will usually enable an assessment to be made of the presence and level of shock, and the likely degree of blood loss. This will act as a guide to whether volume replacement is indicated, and if so how much. Hypovolaemic shock that remains unresponsive to treatment is likely to be due to bleeding into the body cavities or potential spaces, and evidence of this should be sought. Diagnosis may be helped by trauma imaging such as FAST or CT. A useful reminder of where to look is the catchy slogan: bleeding onto the floor and four more (i.e. external bleeding and chest, abdomen, pelvis/retroperitoneum, long bones). Bear in mind, though, that there are other forms of shock that need to be excluded. Cardiogenic shock can mimic many of the signs of hypovolaemic shock. The history will give a good indication of the likely cause. The veins tend to be full in cardiogenic shock, and cyanosis more profound.

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There may be other diagnostic signs present such as pulmonary oedema. Septic, neurogenic and anaphylactic shock are characterized by vasodilatation as opposed to vasoconstriction. The veins tend to be full, and the peripheral pulses easily palpable and bounding. Peripheral perfusion may be good, with warm and flushed peripheries, but the skin may be mottled or cyanosed with sepsis. CIRCULATION AND SHOCK – MANAGEMENT Control of the airway (with cervical spine control), optimal oxygenation and ventilation are prerequisites to shock management. Immediate management of haemorrhagic shock depends on control of the bleeding and administration of intravenous fluids and blood to restore intravascular volume and haematocrit. Control of haemorrhage This is achieved by direct pressure on the bleeding wounds with appropriate dressings, and elevation where practicable. Continuing developments from military experience have led to the introduction of additional measures to control external and limb bleeding. Wounds can be packed with a dressing, and a circumferential bandage applied around and over the packed wound. The bandage can then be twisted in a windlass technique to press the pack down into the wound. Specialist bandages have been designed for this purpose, such as the Oales™ Modular Bandage. This incorporates a gauze bandage for wound packing, with a plastic cup to compress into the packed wound beneath a circumferential, elastic bandage. Tourniquets have been developed for controlling peripheral limb haemorrhage, with devices such as the Combat Application Tourniquet (C-A-T™). The C-AT™ is a single-handed device that uses a windlass system with a free moving internal band to provide circumferential pressure around the extremity. Once tightened and bleeding stopped, the windlass is locked in place. A Velcro® strap is then applied for further securing of the windlass during casualty evacuation. Once in place and controlling the bleeding, the tourniquet should not be loosened or removed until a surgeon is available to definitively repair the injury.

Windlass strap

Windlass rod

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Haemostatic dressings are useful for emergency control of arterial and venous haemorrhage from proximal sites where tourniquets cannot be applied (Mahoney et al., 2005). Quikclot™ (granular zeolite, derived from volcanic rock) can effectively control devastating haemorrhage from large vessels, but generates tissue temperatures up to 570ºC, potentially causing tissue necrosis. HemCon™ (chitosan, derived from crushed shellfish) is an alternative, which has the advantage of not producing an exothermic reaction. Clamping of bleeding points is difficult and can damage vessels; this should remain the province of the experienced surgeon. Fracture of the pelvis can result in devastating retroperitoneal haemorrhage; this can be reduced by compressing the pelvis to approximate the bleeding fracture sites. Compression can be achieved manually, with a towel or blanket passed under the patient and tightened from both sides above the pelvis, or with specialized devices such as the SAM Sling™. This is a ratchet system compression belt for applying circumferential pressure around the pelvis. MAST trousers are impracticable and now rarely used. Intravenous access must be secured at the earliest opportunity; this can be very difficult in later stages of shock. The size of the cannula is important because of its effect on flow, which is directly proportional to the fourth power of the radius of the cannula (Poiseuille’s Law). As an example, halving the radius of a cannula reduces the flow rate by a factor of 16. Flow is also reduced as the cannula lengthens. Clearly it is difficult, if not impossible, to keep up with major haemorrhage without a minimum of two short, large-bore cannulae. Hence, the ATLS® guideline for in-hospital trauma cannulation is insertion of two cannulae, minimum size 16-gauge, but preferably 14-gauge, into large peripheral veins, typically in the antecubital fossae.

Peripheral venous cannulation

This is an option reserved for those with appropriate expertise; it can be very difficult and carries a significant risk of life-threatening complications (pneumothorax and arterial damage most commonly). In the UK, the use of two-

Central venous cannulation

Self-adhering band

Windlass clip

22.24 The C-A-T™ tourniquet (a) Tourniquet in use. (b) Tourniquet components.

22

dimensional (2D) ultrasound imaging is strongly recommended in the routine siting of the CVP line. Access to the internal jugular can be difficult in a trauma patient, especially if he or she is immobilized with a stiff cervical collar and head blocks in place. The subclavian approach has the highest incidence of complications; femoral cannulation is a safer option than either central approach and a long cannula can often be sited in the femoral vein, medial to the femoral artery. Intraosseous cannulation has previously been reserved for young children up to the age of about 5 years, where intravenous cannulation is not possible. The bone cortex is thin and relatively soft in children, and the marrow plentiful and vascular. A specialized 16-gauge intraosseus needle can be pushed or screwed into the bone of the tibia, below and medial to the knee joint. Response time to drug administration is close to IV administration, and entire resuscitations can be performed through intraosseus cannulae, including all anaesthetic drugs and fluids. Intraosseus cannulation for adults has been validated, and specialist equipment is available for siting the cannulae through the thick and tough adult bone cortex. The Bone Injection Gun (BIG) is a springloaded device that fires a cannula through the cortex Intraosseus cannulation

22.26 Cannulas A 16-gauge cannula (grey tap) has a 20 per cent smaller diameter but 40 per cent less flow than a 14-gauge cannula (orange tap).

The management of major injuries

(a)

22.25 SAM Sling™ ratcheted compression belt in use

(b)

22.27 Intraosseous cannulation. (a) The Cook paediatric intraosseus needle. (b) Intraosseous needle in place in the medial proximal tibia.

of the tibia. The FAST1® is designed to manually push a cannula into the manubrium. The more recent EZ-IO® system consists of a hand-held electric drill to ‘drill’ a cannula through the cortex of the tibia or humeral head. Fluid administration has for long been a controversial issue. The traditional ATLS approach for trauma circulation resuscitation, based on military experience, is to site two large-bore intravenous cannulae and administer an initial bolus of 2 L of warmed Ringer’s lactate or Hartmann’s solution. This is certainly successful in improving perfusion in bleeding patients, but is now not recommended for pre-hospital use where haemorrhage cannot be surgically controlled and blood is not available for transfusion. Casualties bleeding to a level 3 or 4 shock can reach a steady state as the blood pressure drops to a point where active bleeding may cease. Restoring vascular volume with crystalloids or colloids can restore the blood pressure to a point where bleeding resumes; further administration of clear fluids repeats the cycle until the haemoglobin level drops below a point where adequate oxygen can be carried.

Fluid administration

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22

Cardiac arrest and death then result from anaemic hypoxia. In the UK, NICE guidance on Pre-hospital Initiation of Fluid Replacement Therapy in Trauma (National Institute for Clinical Excellence, 2004), relating to traumatized casualties with likely haemorrhage, is to titrate intravenous crystalloid fluids in 250 mL boluses against the radial pulse. If a radial pulse cannot be felt, the fluids are administered until the pulse returns, then withheld. NICE emphasizes the importance of not delaying transfer to hospital, and suggest fluids are administered if necessary en route. In penetrating chest wounds, fluids are titrated against a palpable central pulse. This strategy is known as permissive hypotension. Assuming O Rhesus-negative blood is immediately available in the Emergency Department, the blood pressure can be brought up with crystalloids pending rapid transfusion. In UK practice, non-albumin colloid solutions are commonly used as plasma expanders (gelatine and starch formulations). These have a theoretical advantage in that they stay within an undamaged circulation for longer than crystalloids (saline and Hartmann’s). However, there is little robust evidence that there is a practical advantage, particularly as any shocked patient will develop leaky capillaries and nullify the benefit of colloids. There is a risk of allergic reactions to these colloids, and NICE guidelines recommend the use of crystalloids only. Large volumes (> 2 L) of normal saline 0.9 per cent can cause a hyperchloraemic acidosis, and a lactated, balanced electrolyte solution such as Ringer’s lactate or Hartmann’s is preferable. The dynamic response to a fluid challenge will give information as to whether bleeding is continuous or controlled. A 2 L volume of warmed Hartmann’s is initially given (20 mL/kg in children), and the response in vital signs recorded: Rapid responders – respond rapidly and remain haemodynamically normal, having lost < 20 per cent blood volume. No further fluid is required and surgical intervention may be required. Transient responders – respond to the initial bolus, then deteriorate, having lost 20–40 per cent blood volume. These patients will need further fluid administration and blood transfusion, with probable surgical intervention. Non-responders – show minimal or no response to the initial bolus. These patients are likely to require immediate transfusion and surgery to stop exsanguinating haemorrhage. There may be other causes such as tension pneumothorax, cardiac tamponade or non-haemorrhagic shock.

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Fluids should be titrated against response, with optimum organ and peripheral tissue perfusion the goal. Blood pressure, pulse rate, peripheral perfusion

and CVP are all used to assess response. Serial measurement of metabolic acidosis parameters such as bicarbonate, base deficit and lactate levels can be used to gauge adequate response to fluid therapy. More sophisticated methods such as oesophageal Doppler and arterial waveform analysis are also used in the critical care setting. The use of hypertonic saline has been successfully demonstrated, and may have some benefits over the current use of isotonic fluids. Research with 7.5 per cent saline and dextran (as opposed to isotonic 0.9 per cent) suggests that mean arterial blood pressure and oxygen delivery are improved. Capillary damage is lessened, and organ perfusion improved, with a much larger increase in the intravascular volume. Short-term survival is improved, but the role of hypertonic solutions has yet to be determined. The ultimate goal of synthetic, oxygen-carrying fluids has been researched for decades, but as yet nothing has effectively replaced the supremely efficient red blood cell. Blood transfusion should be given early if haemorrhagic shock is demonstrated, with O Rhesusnegative, type-specific or cross-matched blood. Transfusion should be titrated against the haematocrit, and blood products such as fresh-frozen plasma, platelet concentrates and clotting factors given during massive transfusions on the advice of the haematologists. The information given earlier refers to resuscitation of hypovolaemic patients only. Most other forms of shock will respond initially to IV fluids pending accurate assessment and diagnosis. However, shock in elderly casualties without evidence of major trauma should raise a high index of suspicion for cardiogenic shock. Infusion of even small volumes of fluid can overload the circulation and cause collapse and cardiac arrest. Elderly patients may also be on medication for hypertension etc., which can severely limit their ability to maintain an adequate blood pressure and cardiac output. A drug history should be obtained as soon as possible; patients on vasodilator drugs such as ACE inhibitors and sartans may need inotropes to support the circulation, even if the patient is hypovolaemic. In patients suffering from haemorrhagic, hypovolaemic shock the source of the bleeding must be identified and surgically or radiologically controlled. The priorities for restoring and maintaining adequate circulation are:

Take home message

• • • •

control external bleeding restore intravascular volume transfuse blood turn off the tap – call a surgeon early.

D – Disability – head injury The immediate management of the seriously headinjured patient is designed to prevent secondary

HEAD INJURIES – AWARENESS In the UK, severe head injuries account for more than 50 per cent of trauma-related deaths, and these usually follow road traffic crashes, assaults and falls (Flannery and Buxton, 2001). Injury patterns differ between countries; in the UK patients experience predominantly closed injuries, with a peak incidence in males between the ages of 16 and 25 years. A second peak occurs in the elderly, with a high incidence of chronic subdural haematomas. Only 10 per cent of head-injured patients presenting at Emergency Departments have a severe injury. The injuries can be classified into three groups based on the GCS (American College of Surgeons Committee on Trauma, 2004): Mild (80 per cent) Moderate (10 per cent) Severe (10 per cent)

GCS 13–15 GCS 9–12 GCS 3–8

Investigation, management and outcomes depend on the severity of the injury; however, this is a continuum, and the classification given earlier is only a guideline. Even mild head injuries can be associated with prolonged morbidity in the form of headaches and memory problems; only 45 per cent are fully recovered 1 year later. With moderate head injuries, 63 per cent of patients remain disabled 1 year after the trauma, and this rises to 85 per cent with severe injuries (Royal College of Surgeons of England, 1999). A knowledge of anatomy and pathophysiology is needed to understand and anticipate the development of a head injury. The scalp comprises five layers of tissue, with the mnemonic SCALP: skin, connective tissue, aponeurosis, loose areolar tissue, and periosteum. It has a generous blood supply and serious scalp lacerations can result in major blood loss and shock if bleeding is not controlled. The skull is composed of the cranial vault and the base. The vault has an inner and outer table of bone, and is particularly thin in the temporal regions, although protected by the temporalis muscle. The base of the skull is irregular, which may contribute to accelerative injuries. The floor of the cranial cavity has three distinct regions: the anterior, middle and posterior fossae: The meninges cover the brain and consist of three layers:

1. Dura mater – a tough, fibrous layer, firmly adherent to the inner skull. 2. Arachnoid mater – a thin, transparent layer, not adherent to the overlying dura and so presenting a potential space. Cerebrospinal fluid (CSF) is contained and circulates within this space. 3. Pia mater – a thin, transparent layer, firmly adherent to the underlying surface of the brain. The brain itself is divided into three main structures: 1. Cerebrum – composed of right and left hemispheres, divided into: • frontal lobes – emotions, motor function, speech • parietal lobes – sensory function, special orientation • temporal lobes – some memory and speech functions • occipital lobes – vision 2. Cerebellum – coordination and balance

22

The management of major injuries

injury and to provide the neurosurgeon with a live patient who has some hope of recovery. A significant number of fatalities from head injury are caused by the secondary and not the primary injury; prevention of this secondary brain injury is facilitated by following the ABC principles set out in ATLS®.

3. Brainstem – composed of three main structures: • midbrain – reticular activating system (alertness) • pons – relays sensory information between cerebrum and cerebellum • medulla – vital cardiorespiratory centres. The midbrain passes through a large opening in the tentorium, a fibrous membrane that divides the middle and posterior fossae. The third cranial nerve, which controls pupillary constriction, also runs through this opening, and is vulnerable to pressure damage if the cerebral hemispheres swell. This results in pupillary dilatation, an early sign of a significant rise in intracerebral pressure. The skull is in effect an enclosed, bony box containing the brain, blood vessels and the CSF. The intracerebral pressure (ICP) is normally maintained at approximately 10 mmHg, and is a balance of brain, intravascular and CSF volumes. Traumatic damage to the brain can cause swelling of the brain tissue itself, and bleeds from arteries and veins into the extradural space, subdural space or brain substance (intracerebral bleed) increase the intracerebral volume and raise the ICP. If the ICP is sustained at above 20 mmHg, permanent brain damage can result, with poor outcomes; this is the secondary brain injury. There is only limited, intracranial compensation for rising ICP, and this is largely achieved by a reduction in CSF volume (Monroe-Kelly doctrine). Once pressure compensation has reached its limits, the ICP rises rapidly in a breakaway exponential. As the pressure rises, the conscious level decreases and the GCS falls. The medial part of the temporal lobe (the uncus) herniates through the tentorial

Pathophysiology

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FRACTURES AND JOINT INJURIES

22

(a) (b)

(d)

(e)

(c)

(f)

22.28 Fractured skull – imaging (a) X-ray showing a depressed fracture of the skull. (b–f) CT scans showing various injuries: (b) a fracture; (c) an extradural haematoma; (d) a subdural haematoma and compression of the left ventricle; (e) an intracerebral haematoma; (f) diffuse brain injury with loss of both ventricles.

notch, compressing the third cranial nerve and the midbrain pyramidal tracts. This usually results in pupillary dilatation on the side of the injury, and hemiplegia on the opposite side. Pressure changes in the medulla cause a sympathetic discharge, with a rise in blood pressure and reflex bradycardia. With further pressure rise, cerebral blood flow is compromised, and ceases terminally when the ICP rises above the mean arterial pressure (MAP). Ultimately, the cerebellar tonsil is forced into the foramen magnum, resulting in a loss of vital cardiorespiratory function; this is known as brain stem or brain death, and is a terminal event.

660

Mechanism of brain injury Brain injury can be blunt or penetrating. The primary brain injury occurs at the time of the trauma, and results from sudden distortion and shearing of brain tissue within the rigid skull. The damage sustained may be focal, typically resulting from a localized blow or penetrating injury, or diffuse, typically resulting from a high-momentum impact. Sudden acceleration or deceleration can cause a contracoup injury, as the brain impacts on the side of the skull away from the impact. High-velocity missile penetrating injuries will also cause a diffuse and severe

brain injury as the resultant pressure wave moves across the brain. The secondary brain injury is pressure related, and is caused by swelling within the brain, causing a rise in ICP as described earlier. This is compounded by hypoxia, hypercarbia and hypotension. Severity of brain injury The GCS is a well-tested and objective score for assessing the severity of brain injury: 13–15 is mild; 9–13 is moderate; 8 or less is severe. Morphology of brain injury Skull fractures are seen in the cranial vault or skull base; they may be linear or stellate, and open or closed. The significance of a skull fracture is in the energy transfer to the brain tissue as a result of the considerable force required to fracture the bone. Open skull fractures may tear the underlying dura, resulting in a direct communication between the scalp laceration and the cerebral surface, which may be extruded as ICP rises. Basal skull fractures are caused by a blow to the back of the head, or rapid deceleration of the torso with the head unrestrained, as in high-speed vehicular crashes. Fractures are rare, occurring in 4 per cent of

severe head injuries, but can cause severe damage, and are a cause of death in front-end collisions and motor sport crashes. There are key physical signs pathognomic of basal skull fracture: • peri-orbital ecchymosis (bruising – ‘raccoon’ or

behind ears) • oto-rhinorrhea (CSF leakage from nose and ears) • VIIth and VIIIth cranial nerve dysfunction (facial

paralysis and hearing loss) Basal skull fractures are not always visible on x-ray or CT, but blood in the sinus cavities and the clinical signs should suggest their presence. Diffuse brain injury is due to axonal disruption of the neurones and varies from minor, resulting in mild concussion, to severe, resulting in an ultimately fatal hypoxic and ischaemic insult to the brain. Extradural (epidural) haematomas are relatively uncommon, occurring in 0.5 per cent of all braininjured patients, and 9 per cent of those who are comatose (Findlay et al., 2007). The haematoma is contained outside the dura but within the skull, and is typically biconvex or lenticular in shape. They are commonly located in the temporal or temporoparietal region, and usually result from a middle meningeal artery caused by a fracture. Subdural haematomas are more common, and constitute 30 per cent of severe brain injuries (Findlay et al., 2007). They usually result from tearing of cortical surface vessels, and normally cover the entire surface of the hemisphere. Underlying brain damage is usually much more severe due to the greater energy transfer. Contusions and intracerebral haematomas are fairly common (20–30 per cent of severe brain injuries). The majority occur in the frontal and temporal lobes. Inoperative contusions can evolve into haematomas requiring surgical evacuation over a period of hours or days, and repeat CT scanning within 24 hours may be indicated. HEAD INJURIES – RECOGNITION Initial recognition of a head injury takes place in the primary survey as part of the ABCDE sequence. The airway, cervical spine, breathing and circulation must all be assessed and resuscitation commenced before the brief neurological assessment takes place, as these measures will prevent the development of a secondary brain injury. The AVPU score is an instant and useful assessment but the level of consciousness should be assessed accurately at this point, using the GCS. The pupils are assessed for equality, diameter and response to light. As there is a 5–10 per cent association of cervical spine fracture with head injury, the assumption is

• GCS < 13 on first Emergency department assessment • GCS < 15 2 hours after initial assessment • suspected open or depressed skull fracture • clinical basal skull fracture • post-traumatic seizure • focal neurological deficit • > 1 episode of vomiting • amnesia of events > 30 minutes before impact • post-injury amnesia if: age > 65 years associated with coagulopathy due to a dangerous mechanism of injury (pedestrian versus motor vehicle, ejection from motor vehicle, fall from height > 1 m).

22

The management of major injuries

‘panda’ eyes) • retro-auricular ecchymosis (Battle sign – bruising

made that the neck is unstable until proved otherwise. As the cervical spine x-ray does not rule out a fracture, full immobilization should remain in place until the neck is cleared clinically or with further imaging such as CT. A more thorough assessment of the neurological status takes place during the secondary survey. The GCS and pupils are re-evaluated, lateralizing signs are looked for, and the upper and lower limb motor and sensory function evaluated. If the patient is stable, further imaging may be indicated, and a number of guidelines exist to aid the decision. CT scanning is the primary examination of choice for patients with a clinically important brain injury (National Institute for Health and Clinical Excellence, 2007). Modern, fast, spiral CT scanners are increasingly available adjacent to Emergency Departments, enabling rapid trauma CTs in the course of minutes. All patients suffering a severe head injury require an urgent CT scan. Specific indications for a head CT are (Royal College of Surgeons of England, 1999):

HEAD INJURIES – MANAGEMENT The management of head injuries depends on the severity, as assessed by the clinical examination, GCS and CT scan. Patients with a mild head injury should be admitted and monitored, with frequent neurological observations. Should there be any deterioration, CT scanning is indicated, and referral to the local neurosurgical unit is necessary. Discharge is when a complete neurological recovery has been made and provided the patient can be supervised at home by a responsible adult. Patients sustaining moderate head injuries will need CT scanning and discussion with a neurosurgeon to decide on the need for transfer and definitive care. Other indications for neurosurgical referral, regardless of imaging findings, include: • persistent coma after initial resuscitation (GCS < 8) • unexplained confusion > 4 hours • post-admission deterioration in GCS

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FRACTURES AND JOINT INJURIES

22

• • • •

progressive, focal neurological signs seizure without full recovery definite or suspected penetrating injury CSF leak.

Patients with severe head injuries will require immediate resuscitation as described previously. The cervical spine must be immobilized whilst the airway is secured; this will require a competent, rapid sequence induction (RSI) of anaesthesia, and an anaesthetist must be involved early. Once the airway is secured and protected with a tracheal tube, the oxygenation and ventilation must be optimized. Hypoxia and hypercarbia must be avoided, but overventilation is equally damaging, as cerebral blood flow is compromised. Ventilation must be monitored with endtidal carbon dioxide analysis, and the minute volume adjusted to maintain a low-normal EtCO2 (4.5 kPa). Oxygen saturation levels should be maintained above 95 per cent, and sequential arterial blood gas estimations made to ensure the oxygen partial pressure is maintained in the normal range (> 13 kPa) as far as is possible. The circulation should be monitored to maintain intravascular filling within an appropriate range. Overfilling will worsen cerebral oedema, but hypovolaemia will result in persistent shock. Central venous pressure should be monitored, and arterial pressures kept within a normal range for that patient, with reference to the ICP. This requires expert critical care skills, and patients with a severe brain injury must be managed in an appropriate critical care unit. The rapid administration of intravenous mannitol at a dose of 0.5 mg/kg may be indicated to reduce ICP, and this should be given following discussion with the referral neurosurgeon. It can be a useful holding measure if signs of rising ICP (e.g. a dilated pupil) develop prior to or during transfer to a specialist centre. Patients with significant head injuries in units without neurosurgical capability will require transfer, on discussion with the neurosurgeons. An expanding intracerebral haematoma will need to be evacuated within 4 hours of injury to prevent serious and permanent secondary brain injury.

E – Abdominal injuries The abdomen is difficult to assess in the multiply injured trauma patient, especially when the patient is unconscious. The immediately life-threatening injury is bleeding into the abdominal cavity, and this is one of the ‘onto the floor and four more’ areas into which lethal volumes of blood may be sequestered. The abdomen is therefore examined in the primary survey as part of the circulation assessment. ABDOMINAL INJURIES – AWARENESS Abdominal injuries may be blunt or penetrating. Unrecognized abdominal injury is a cause of avoidable death after blunt trauma and may be difficult to detect. A direct blow from wreckage intrusion or crushing from restraints can compress and distort hollow viscera, causing rupture and bleeding. Deceleration causes differential movement of organs, and the spleen and liver are frequently lacerated at the site of supporting ligaments. In patients requiring laparotomy following blunt trauma, the organs most commonly injured are (Findlay et al., 2007): • • • •

spleen (40–55 per cent) liver (35–45 per cent small bowel (5–10 per cent) retroperitoneum (15 per cent).

The mechanism of injury should lead to a high index of suspicion, e.g. flexion lap-belt injuries in car crashes can rupture the duodenum, with retroperitoneal leakage and subtle signs. Early imaging and exploratory laparotomy may be required. Penetrating injuries between the nipples and the perineum may cause intra-abdominal injury, with unpredictable and widespread damage resulting from tumbling and fragmenting bullet fragments. Highvelocity rounds transfer significant kinetic energy to the abdominal viscera, causing cavitation and tissue destruction. Gunshot wounds most commonly involve the:

TAKE HOME MESSAGE Head-injured patients require early assessment and recognition of their brain injury. With severe head injuries, it should be remembered that:

662

1. A blow to the head causes a primary brain injury. 2. Hypoxia and hypercarbia cause cerebral swelling and a secondary brain injury. 3. Secondary brain injury should be minimized by optimal oxygenation, ventilation and blood pressure management.

22.29 Abdominal injury Ruptured duodenum following flexion lap belt injury.

• • • •

small bowel (50 per cent) colon (40 per cent) liver (30 per cent) abdominal vasculature (25 per cent).

• • • •

liver (40 per cent) small bowel (30 per cent) diaphragm (20 per cent) colon (15 per cent).

ABDOMINAL INJURIES – RECOGNITION The abdomen is initially examined during the primary survey to determine if shock is due to an abdominal injury. A history from the patient, bystanders and paramedics is important, as the mechanism of injury can be identified and injuries predicted. Examination of the abdomen follows the ‘look, listen, feel’ format. The patient must be fully exposed, and the anterior abdomen inspected for wounds, abrasions and contusions. The flanks and posterior abdomen and back should be examined, and this may require log rolling to both sides. Auscultation is difficult in a noisy resuscitation room, but may reveal absence of bowel sounds caused by free intraperitoneal blood or gastrointestinal fluid. Percussion and palpitation may reveal tenderness or peritonism. The genitalia and perineum should be examined, and a rectal examination performed during the log roll. Early imaging is indicated (a FAST examination will reveal the presence of intraperitoneal fluid) and can be performed in the resuscitation room; however, the technique has a high specificity but low sensitivity. Presence of fluid is an indication for laparotomy. CT scanning requires the patient to be stable, but is a much more effective diagnostic tool. Diagnostic peritoneal lavage is a technique largely supplanted by FAST and CT, but if these are unavailable it may still be used. It should be performed by the surgeon who would take the patient to the operating theatre. ABDOMINAL INJURIES – MANAGEMENT Initial management of an abdominal injury is to manage shock as described in circulation management. External bleeding is controlled with direct pressure, wound packing or haemostatic dressings. Intravenous access is established with two large-bore cannulae, and 2 L of warmed Hartmann’s or Ringer’s lactate infused at speed. If the shock remains unresponsive, further fluid is administered, and blood transfused. Confirmation of bleeding into the abdomen is an indication for immediate laparotomy, and imaging other than FAST

• • • • • •

unexplained shock rigid silent abdomen evisceration radiological evidence of intraperitoneal gas radiological evidence of ruptured diaphragm gunshot wounds.

A naso- or oro-gastric tube should be passed in all multiple trauma patients; this should be passed orally in the presence of facial and basal skull fractures. A urinary catheter should be passed unless urethral bleeding or other signs of urethral injury such as genital bruising or a high-riding prostate are present. Laparotomy is the definitive management and the province of the surgeon; general principles at initial operation are to: • control haemorrhage with ligation of vessels and packing • remove dead tissue • control contamination with clamps, suturing and stapling devices • lavage the abdominal cavity • close the abdomen without tension.

22

The management of major injuries

Stab wounds injure adjacent abdominal structures. Small wounds may result from thin-bladed knives that have penetrated deep and damaged several structures, with the most common injuries being:

may not be possible with an unstable patient. Other indications for laparotomy include:

Initial surgery may be for damage limitation rather than definitive treatment, and a second-look laparotomy at 24–48 hours may be indicated to allow: • • • • •

removal of packs removal of dead tissue definitive treatment of injuries restoration of intestinal continuity closure of musculofacial layers of the abdominal wall.

The patient will require supportive critical care, and may require ventilation on an ICU until after the second-look laparotomy. TAKE HOME MESSAGE Abdominal injuries are difficult to assess in the multiply injured patient. The immediate threat to life is bleeding into the peritoneal cavity, and early imaging with FAST and CT should be considered. Shock should be treated, and early consultation with a surgeon facilitated. Diagnostic or definitive treatment laparotomy may be required.

F – Musculoskeletal injuries In the absence of catastrophic bleeding, musculoskeletal injuries are not immediately life-threatening. They are, however, limb threatening and potentially life-threatening. Definitive management is detailed elsewhere in this book, so this section will merely put these injuries into the context of the overall management of a severely injured casualty.

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FRACTURES AND JOINT INJURIES

22

PELVIC FRACTURES Awareness The pelvis and retroperitoneum constitute one of the ‘onto the floor and four more’ spaces into which blood can be sequestered to a level resulting in non-responsive shock. A haemorrhaging fracture of the pelvis therefore becomes a life-threatening emergency, and should be considered in every patient with a serious abdominal or lower limb injury. Potential causes are road accidents, falls from a height or crush injuries. The pelvis is examined in the primary survey as part of the C – circulation assessment, once the airway and breathing have been assessed, and the cervical spine immobilized. Significant signs are swelling and bruising of the lower abdomen, thighs, perineum, scrotum or vulva, and blood at the urethral meatus. The pelvic ring should be gently palpated for tenderness side to side and front to back; however, if clinical suspicion is high, the pelvis should not be compressed for crepitus, as this can dislodge a clot from the fracture site and provoke further bleeding. If tenderness and crepitus are elicited, the examination should not be repeated. An AP x-ray should be obtained during the primary survey, and in most cases will enable a preliminary diagnosis of pelvic fracture to be made. If the patient is stable, a trauma CT scan will give more detailed information, and also provide information on intraabdominal and retroperitoneal bleeding. Recognition

Management The immediate management of a pelvic

fracture resulting in shock is to control the bleeding and restore volume as described previously. There are a number of proprietary devices available to wrap around the pelvis and apply compression to approximate the bleeding fracture sites and allow clot formation. If these are not available, manual approximation can be used; this can be facilitated with a sheet wrapped around the pelvis and twisted anteriorly. Once in place, the pelvic compression devices should not be removed until surgical interventions such as external fixation are available. Developments in interventional radiology and angiography have enabled embolization to be used to control haemorrhage from a fractured pelvis. Take home message Pelvic fractures can result in lifethreatening haemorrhage and should be recognized and managed as part of the circulation assessment during the primary survey. Pelvic compression devices should be used to minimize bleeding, and a rapid, surgical referral made for definitive management.

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SPINAL INJURIES Vertebral column injury, with or without neurological damage, must be considered in all patients with

multiple injuries. A missed spinal injury can have devastating consequences. Immediate management therefore focuses on immobilization, recognition and referral for definitive care. Awareness Spinal injuries can be stable or unstable, an unstable injury being one where there is a significant risk of fracture displacement and neurological sequelae. The mechanisms of injury are traction (avulsion), direct injury and indirect injury. Direct injuries are penetrating wounds usually associated with firearms and knives. Indirect injuries are the most common, and are typically the result of falls from a height or vehicular accidents where there is violent free movement of the neck or trunk. There is an association of cervical spinal damage with injuries above the clavicles, and some 5 per cent of head-injured patients have an associated spinal injury; 10 per cent of those with a cervical spine fracture have a second, non-contiguous spinal fracture. Regional occurrences of spinal injuries are approximately:

• • • •

cervical (55 per cent) thoracic (15 per cent) thoracolumbar junction (15 per cent) lumbosacral (15 per cent).

Spinal fractures with spinal cord transection also disrupt the sympathetic nerve supply and cause distal vasodilatation. A high spinal transection will therefore cause neurogenic shock – this is vasodilatory shock and is characterized by hypotension, a low diastolic blood pressure, widened pulse pressure, warm and well perfused peripheries and bradycardia. However, neurogenic shock can be complicated by hypovolaemic shock in multiply injured patients. The spinal column and neurological function are examined in the secondary survey, with immobilization maintained throughout. Whilst the head is immobilized manually, and the patient logrolled, the cervical spine and vertebral column from neck to sacrum are examined for:

Recognition

• • • • •

bruising, contusions and ecchymosis penetrating injury swelling or ‘bogginess’ tenderness on palpation step or misalignment between vertebrae.

A rectal examination is performed to assess anal tone. A neurological examination is carried out to identify loss of sensory and motor function. If the casualty is conscious, has no neck pain, has no distracting painful injury, is not intoxicated and has not received any analgesia, the cervical spine can be examined and a fracture clinically excluded. Head blocks, cervical collar and tape are removed, and the patient taken through a full range of active movements (i.e. patient’s voluntary movement). If there is

Initial management follows the ATLS® ABCDE sequence. The cervical spine must be immobilized at all times; deterioration of neurological function of even one myotome can cause a devastating loss of motor function, with absence of any useful function. However, only 5 per cent of multiply injured patients have cervical spine injuries, in contrast to the high percentage of patients with compromised airways; this is particularly significant with head injuries. In high spinal transections, the patient’s respiratory function may be compromised, leading to ventilatory failure. The airway must be maintained without causing neck flexion or extension, and secured and protected with careful anaesthetic induction and intubation. This can be successfully done with specialist laryngoscopes such as the McCoy (lever activated, flexing tip to lift the epiglottis), in conjunction with an intubating catheter. The procedure should be carried out by an experienced anaesthetist. Oxygenation and ventilation is optimized, monitoring SaO2 and EtCO2. The neurogenic shock will require judicious use of intravenous fluids, and may need circulatory support with vasoconstrictors and chronotropes. The spinal fracture and neurological deficits are managed by immobilization and referral to a spinal surgeon. Management

Take home message Spinal injuries should be identified

during the secondary survey and managed according

to the ABCs. Immobilization is crucial throughout, and ventilatory and circulatory failure must be recognized and managed. Injuries should be excluded clinically, or with CT and MRI, as soon as possible.

22

LONG-BONE INJURIES Long bone injuries can be spectacular, but should not distract from the injuries compromising the airway, breathing or circulation. They are limb threatening, but not immediately life-threatening, and in the absence of catastrophic bleeding can be addressed in the secondary survey.

The management of major injuries

neither pain nor neurological symptoms on movement, the cervical spine can be cleared. X-rays are of limited use in the resuscitation phase as they do not reliably exclude unstable fracture-dislocations. Hence, they do not alter initial management. Plain x-rays of the spinal column are therefore taken during the secondary survey. Since cervical fractures cannot be radiologically excluded in patients who do not meet the criteria for clinical cervical spine clearance as above, CT or MRI may be required.

Musculoskeletal injuries occur in 85 per cent of patients sustaining blunt trauma (Findlay et al., 2007). Major injuries signify significant force applied to the body, and so are associated with an increased incidence of chest, abdomen and pelvis damage. Although not immediately-life threatening, they present a potential threat to life and prejudice the integrity and survival of the limb. Crush injuries can lead to compartment syndrome, and myoglobin release with the risk of renal failure. These injuries must therefore be addressed as soon as the resuscitation priorities have been addressed.

Awareness

The casualty must be fully exposed, logrolled and examined from head to toe in all planes. The limbs are examined visually for:

Recognition

• • • • •

colour and perfusion wounds deformity (angulation and shortening) swelling discoloration and bruising.

The extremities are then palpated to detect tenderness, swelling and deformity, indicating underlying fractures and dislocations. Crepitus may be felt, but should not be specifically elicited. Peripheral circulation is assessed with palpation of pulses and capillary refill. Doppler ultrasound examination may be needed to confirm the presence of pulses – however, the presence of a pulse does not exclude compartment syndrome. X-rays should be obtained as indicated as soon as the patient is stable. Management The immediate management is to ensure

22.30 McCoy flexing tip laryngoscope

the airway and ventilation are optimized, and then control limb haemorrhage with direct pressure, tourniquets, wound packing and haemostatic dressings as described previously. Large tissue deficits may need ongoing fluid and blood replacement as immediate haemorrhage control can be difficult. Fractures and dislocations are splinted in the anatomical position where possible, to minimize neurovascular compromise, and significant analgesia may be required to facilitate this (e.g. Entonox, morphine or ketamine 0.5 mg/kg intravenously). The anatomical

665

FRACTURES AND JOINT INJURIES

22

(a)

(b)

22.31 (a) Traumatic amputation, (b) blast dressing and (c) blast dressing in situ

(c)

position should not be forced if resistance is felt, e.g. posterior hip dislocation. Tetanus toxoid should be given, and the patient referred urgently to an orthopaedic surgeon for definitive management. Significant fractures, compound fractures and dislocations may need operative intervention whilst life-saving abdominal or neurological surgery is taking place. Take home message Limb injuries are not immediately life-threatening in the absence of catastrophic haemorrhage. They should be recognized and initially managed in the secondary survey. Splinting and immobilization are instituted before prompt surgical consultation. Traumatic amputations, de-gloving injuries and blast injuries can be initially managed with specialist blast dressings.

G – Burns (thermal, chemical, electrical, cold injury)

666

A burn is a broad term that encompasses not only thermal injury to tissues from heat, but injury from electric shock, chemicals and cold. In the UK, some 250 000 burn victims attend hospital each year, of whom 16 000 are admitted; in the USA, about 1.25 million burns occur annually, with 51 000 patients hospitalized. The risk is highest in the 18–35 year age group, with a male to female ratio of 2:1 for both injury and death, and serious burns occur most frequently in children under 5 years of age. There are some 4500 burns deaths each year in the USA, and the death rate is much higher in those over the age of 65. The last two decades have seen much improvement in burns care, and the mortality rate is now 4 per cent in those treated in specialist burns centres (Schwartz and Balakrishnan, 2004).

THERMAL BURNS – AWARENESS Major burns can present a threat to life through compromise of the airway, breathing and circulation. In addition, those burned may suffer other traumatic harm due to explosions etc. and can present with any of the systemic injuries described previously. Circumferential burns around the neck can cause tissue swelling and airway obstruction, and burns around the chest may cause restrictive respiratory failure. Large burns result in significant fluid shifts, and resultant shock. In combination with coma from toxin inhalation, burns present a potent mix of assaults on a casualty’s life. Cell damage occurs at a temperature greater than 45°C (113°F) owing to denaturation of cellular protein; a burn’s size and depth are functions of the burning agent, its temperature and the duration of exposure. Thermal injury to the skin damages the skin’s ability to function as a semi-permeable barrier to evaporative water loss, resulting in free water loss in moderate to large burns. Other functions such as protection from the environment, control of body temperature, sensation and excretion can also be harmed. Systemic effects include hormonal alterations, changes in tissue acid– base balance, haemodynamic changes and haematological derangement. Massive thermal injury results in an increase in haematocrit with increased blood viscosity during the early phase, followed by anaemia from erythrocyte extravasation and destruction. Vasoactive substances are released and a systemic inflammatory reaction can result. Inhalational burns Inhalation of super-heated gases and

inhalation of toxic smoke in entrapment result in inhalational burns and smoke inhalation. Inhalational injury is now the main cause of mortality in the burns patient, and half of all fire-related deaths are due to smoke inhalation. Direct thermal injury is usually limited to the upper airway above the vocal cords, and can result in rapid development of airway obstruction due to mucosal oedema. Smoke has two noxious components: particulate matter and toxic inhalants. The particles are due to incomplete combustion, are usually less than 0.5 μm in size and can reach the terminal bronchioles, where they initiate an inflammatory reaction, leading to bronchospasm, oedema and respiratory failure. Toxic inhalants are divided into three main groups: (1) tissue asphyxiants; (2) pulmonary irritants; (3) systemic toxins. The two major tissue asphyxiants are carbon monoxide and hydrogen cyanide. Carbon monoxide poisoning is a well-known consequence of smoke inhalation injury. Severe carbon monoxide poisoning will produce brain hypoxia and coma, with loss of airway protective mechanisms, resulting in aspiration that exacerbates the pulmonary injury from smoke inhalation. The tight binding of the carbon

Depth of burns The depth of a burn is classified according to the degree and extent of tissue damage: First degree burns involve only the epidermis, and cause reddening and pain without blistering. They heal within 7 days and require only symptomatic treatment. Second degree burns extend into the dermis, and can be subdivided into superficial partial-thickness and deep partial-thickness burns. In superficial partial-thickness burns, the epidermis and the superficial dermis are injured. The deeper layers of the dermis, hair follicles, and sweat and sebaceous glands are spared. A common cause is hot water scalding. There is blistering of the skin and the exposed dermis is red and moist at the blister’s base. These burns are very painful to touch. There is good perfusion of the dermis with intact capillary refill. Superficial partialthickness burns heal in 14–21 days, scarring is usually minimal, and there is full return of function. Deep partial-thickness burns extend into the deep dermis. There is damage to hair follicles as well as sweat and sebaceous glands, but their deeper portions usually survive. Hot liquids, steam, grease, or flame usually cause deep partial-thickness burns. The skin may be blistered and the exposed dermis is pale white to yellow. The burned area does not blanch, has no capillary refill and no pain sensation. Deep partial-thickness burns may be difficult to distinguish from full-thickness burns. Healing takes 3 weeks to 2 months. Scarring is common and is related to the depth of the injury. Surgical debridement and skin grafting may be necessary to obtain maximum function. Third-degree or full-thickness burns involve the entire thickness of the skin, and all epidermal and dermal structures are destroyed. They are usually caused by flame, hot oil, steam, or contact with hot objects. The skin is charred, pale, painless, and leathery. These injuries will not heal spontaneously, as all dermal elements are destroyed. Surgical repair and skin grafting are necessary, and there will be significant scarring. Fourth-degree burns are those that extend through the skin to the subcutaneous fat, muscle, and even bone. These are devastating, life-threatening injuries. Amputation or extensive reconstruction is sometimes required.

THERMAL BURNS – RECOGNITION The initial assessment of burns takes place during the primary survey, and is designed to recognize immediately life-threatening injuries compromising the

airway, breathing and circulation and conscious level. The likelihood of coincidental traumatic injuries should be remembered. The patient is examined following the look, listen, feel format. Diagnosis of an inhalational burn is made from the history of a fire in an enclosed space and physical signs that include facial burns, singed nasal hair, soot in the mouth or nose, hoarseness, carbonaceous sputum, and expiratory wheezing. There is no single method capable of demonstrating the extent of inhalation injury. Stridor is a particularly sinister finding, as it indicates an imminent loss of the airway. Carboxyhaemoglobin levels for carbon monoxide poisoning are useful to document prolonged exposure within an enclosed space with incomplete combustion, as the cherry red skin colour is rare. Table 22.3 Diagnosis of carbon monoxide poisoning Carbon monoxide level

Physical symptoms

< 20 per cent

No physical symptoms

20–30 per cent

Headache and nausea

30–40 per cent

Confusion

40–60 per cent

Coma

> 60 per cent

Death

22

The management of major injuries

monoxide to the haemoglobin, forming carboxyhaemoglobin, is resistant to displacement by oxygen, and so hypoxia is persistent. Hydrogen cyanide is formed when nitrogen-containing polymers such as wool, silk, polyurethane, or vinyl are burned. Cyanide binds to and disrupts mitochondrial oxidative phosphorylation, leading to profound tissue hypoxia.

The chest x-ray may be normal initially; bronchoscopy and radionuclide scanning are useful in determining the full extent of injury. Arterial blood gas analysis will track hypoxia, ventilatory failure and the development of metabolic acidosis. Signs of shock are looked for, as detailed previously, and the GCS and pupillary response assessed. The patient is fully exposed to allow evaluation of the whole-body surface area. The burnt areas are assessed for depth of burn, as described earlier. This is a subjective clinical assessment. The extent of the burn is assessed and expressed as a percentage of body surface area (BSA). This can be done using the ‘rule of nines’, or with aids such as the Lund and Browder charts. The rule of nines is an approximate tool, and tends to overestimate the extent of a burn. For irregular burns, the palmar surface of the patient’s hand, including the fingers, represents approximately 1 per cent of the patient’s body surface area. Body surface areas are different in infants; they have a disproportionately larger head surface area and smaller lower limb surface area. THERMAL BURNS – MANAGEMENT The airway is secured as described previously. Inhalational burns can cause pharyngeal oedema and swelling, which can make tracheal intubation difficult if not impossible, leaving a surgical airway as the only

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22

Head and neck (9%)

FRACTURES AND JOINT INJURIES

Head and neck (21%)

9% Each arm (10%) Each arm (4.5%) 9%

Abdomen (13%) Each leg (13.5%)

Hand (1%)

Buttocks (5%) Each leg (9%)

Genital area (1%)

22.33 Burns in infants Surface areas differ markedly from those in adults.

9%

9% Each arm (4.5%)

Each leg (9%)

22.32 Burns. Rule of nines for assessment of extent of burns in adults.

668

Back (13%)

recourse. The airway may need fibre-optic assessment, and warning signs such as stridor and respiratory distress indicate the need for early intubation. This should be performed under general anaesthesia by an

experienced anaesthetist, with a range of difficult intubation equipment available. Needle cricothyroidotomy and surgical airway sets should be immediately accessible. Breathing should be supported with high-flow oxygen administered via a non-rebreathing, reservoir mask that delivers 85 per cent at a flow rate of 15 L/min. The ventilation may need support using a BVM assembly with a reservoir and high-flow oxygen. Stridor can be eased, as a holding measure pending airway securement, by administering high-flow helium and oxygen, as this gas mixture has a low density that increases flow through the obstructing airway. However, heliox is only 21 per cent oxygen and will not address hypoxia and carbon monoxide poisoning. Once the airway has been secured by tracheal intubation, the inspired oxygen concentration and ventilation should be adjusted to give optimum SaO2 levels (> 95 per cent) and low normal EtCO2 (4.5 kPa). The presence of an inhalational burn and pulmonary oedema may hinder oxygenation and ventilation, and a critical care physician should be involved early. Significant carbon monoxide levels may indicate the need for ventilation with 100 per cent oxygen and hyperbaric therapy, and an early referral should be made to a hyperbaric unit; these are often found located in diving and naval centres. Circumferential neck and chest burns may need to be incised to allow effective breathing and ventilation. The circulation should be supported in any burn patient with signs of shock or a burn less than 20 per cent BSA. Two large-bore intravenous cannulae are

palpable. If there is compromise to the circulation, surgical escharotomy will be needed. The eschar should be incised on the midlateral side of the limb, allowing the fat to bulge through. This may be extended to the hand and fingers. Escharotomy may cause substantial soft tissue bleeding. Analgesia will be required for partial-thickness burns, which are most painful. Cooling and dressing will help, but opioids may be required. These should be administered intravenously, and can be given by infusion or patient-controlled analgesia (PCA) systems. Consultation is important. A burns specialist should be involved from the outset for all patients with severe or unusual burns. Transfer will be required for these patients as outcomes are improved in specialist centres. Indications for transfer are: • partial-thickness burns > 20 per cent BSA • partial-thickness burns > 10 per cent BSA in ages 10–50 years • full-thickness burns > 5 per cent any age • partial- and full-thickness burns involving: face, eyes, ears, hands, feet, genitals, perineum, skin over major joints • significant electrical burns (and lightning) • significant chemical burns • inhalational burns • burns in patients with complicating illness, trauma, and long-term rehabilitation needs • children.

22

The management of major injuries

sited, preferably, although not necessarily, through unburned skin. If intravenous cannulation or central venous cannulation are not possible, intraosseus or intravenous cut-down techniques should be used, as shock will develop rapidly in patients with large and deep burns. Warmed Hartmann’s or Ringer’s lactate is the fluid of choice; large volumes of normal saline 0.9 per cent can cause a hyperchloraemic acidosis. Colloids and hypertonic saline have no proven beneficial role. If shock is present, 2 L should be administered as in the ATLS® guidelines for shock management. If haemorrhagic shock is excluded, the volume and rate of fluid administration is calculated according to the Parkland formula as given later. This regimen applies to partialand full-thickness burns only; superficial burns do not require intravenous fluids. The administration time is calculated from the time of the burn, not from the time of admission or time of assessment. Deeper burns are likely to cause more tissue damage and consequent fluid shifts. The Parkland formula is a guide only, and fluid administration should be titrated against response. Blood pressure, central venous pressure, pulse, peripheral perfusion and urine outputs are used, but more sophisticated techniques such as oesophageal Doppler and arterial waveform analysis may aid optimization. Fluid overload should be avoided in patients with inhalational burns and systemic inflammatory reactions. Documented anaemia may indicate the need for blood transfusion. Wound care starts in the pre-hospital environment with the removal of burnt clothing and the cooling and dressing of wounds. Rings, jewellery, watches and belts are removed as they retain heat and can cause compression as tissues swell. Wounds can initially be dressed with loose, clean, dry dressings. Alternatives are plastic sandwich wrap (known as cling film in the UK, plastic wrap in USA and cling wrap in Australia), specialized gel burns dressings or saline-moistened dressings. Cooling eases pain, but hypothermia should be avoided. Patients with circumferential deep burns of the limbs may develop eschars (thick, black, dry and necrotic tissue that constricts) with compromise of the distal circulation. Distal pulses need to be monitored closely, with a Doppler probe if not easily

CHEMICAL BURNS Most chemical burns result from exposure of the skin to strong alkalis and acids, and phosphorus, phenol and petroleum products can also damage tissue. However, 25 000 products are capable of causing chemical burns, and they account for 5–10 per cent of US burns centre admissions. Full development of chemical burns is slower than thermal injury, so the true extent of the burn can be underestimated on initial evaluation. Alkali burns tend to be more serious and deeper, as the alkalis soften and penetrate tissue, whereas acids tend to form a protective eschar.

Awareness

Definitive diagnosis depends on the history, and both the chemical involved and its

Recognition

Table 22.4 Intravenous fluid requirements in partial- and full-thickness burn patients (Parkland formula) Adults

Children

Hartmann’s or Ringer’s lactate:

Hartmann’s or Ringer’s lactate:

4 mL ¥ weight (kg) ¥ per cent BSA over initial 24 hours

3 mL ¥ weight (kg) ¥ per cent BSA over initial 24 hours plus maintenance

Half over first 8 hours from the time of burn (other half over subsequent 16 hours)

Half over first 8 hours from the time of burn (other half over subsequent 16 hours)

(Example: an adult weighing 70 kg with 40 per cent second- and third-degree burns would require 4 mL ¥ 70 kg ¥ 40 = 11 200 mL over 24 hours).

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22

domestic, low-voltage shocks are not associated with skin burns even though they may cause death from ventricular fibrillation. Alternating current (AC) shocks produce tetanic muscle spasm, which can cause the victim’s hand to clutch onto the electrical source, and the respiratory muscles can be paralyzed, resulting in respiratory arrest. Electrical muscle damage can result in rhabdomyolysis and renal failure.

Right ear

Left ear

22.34 Chemical burns Sulphuric acid burn to left ear from car battery acid in roll-over traffic accident.

concentration should be determined if possible. Alkali burns are frequently full-thickness injuries, appear pale, and feel leathery and slippery. Acid burns are often partial-thickness injuries and are accompanied by erythema and erosion. Skin is stained black by hydrochloric acid, yellow by nitric acid, and brown by sulphuric acid. Management The goal of treatment is to minimize any area of irreversible damage, and maximize salvage in the zone of reversible damage. If dry powder is present, it should be brushed off before irrigation with water, which is the mainstay of treatment. Irrigation should be commenced immediately when the injury is recognized, with copious amounts of tap water. Neutralizing agents (e.g. an acid to treat an alkali burn) should not be used, as there is a risk that heat generated by the neutralizing reaction will cause further thermal injury. After copious water irrigation, some specific treatments are possible, e.g. calcium gluconate for hydrofluoric acid burns and polyethylene glycol for phenol. An urgent referral to a burns surgeon should be made; eschar formation may make irrigation ineffective and require emergency surgical excision.

670

The assessment of an electrical shock victim should follow the ABC principles of ATLS®. The airway may be obstructed if the victim is unconscious, and prolonged apnoea may follow paralysis of the respiratory muscles. The heart may be arrested in ventricular fibrillation or asystole depending on the nature of the shock. Of high voltage electrical shock victims, 50 per cent will have a neurological injury with coma, and spinal injuries can result from violent muscle spasms. The entry and exit points should be examined for burns that may be full thickness, and the true extent of underlying muscle damage may not be apparent. There may be musculoskeletal injuries from associated trauma or muscle spasm, and all long bones should be examined and x-rayed when indicated.

Recognition

ELECTRICAL BURNS Awareness Electrical burns are caused when an individual makes contact between an electrical source and the earth, and severe, non-lethal electrical injuries constitute 3–5 per cent of admissions to US burns units. Current flows through the skin and variably through different tissues from the point of electrical contact to the ground contact, causing burns and necrosis. The physiological effects of an electric shock are related to the amount, duration, type (AC or DC), and path of current flow. Severe electrical skin burns are associated with high-voltage shocks, whereas most

The immediate priority is to avoid personal injury if the casualty is in contact with or even adjacent to a high-voltage electrical source. Initial management is to secure the airway, protect the cervical spine and oxygenate and ventilate the casualty. Intravenous access is secured, and fluids administered if the casualty is shocked. If in cardiac arrest, advanced life support should be instituted, following the appropriate Advanced Life Support algorithms for VF/VT and non-shockable arrests as indicated. The heart should be monitored for arrhythmias, which can occur in 30 per cent of high-voltage shock victims. Tissue damage may need surgical debridement, and compartment syndrome may develop, requiring fasciotomies. A urinary catheter is sited, and the urine observed for the brown discoloration indicative of development of myoglobinuria; this is treated by giving intravenous fluids to promote a diuresis, and administration of mannitol. Myoglobinuria should be considered present if a urine dipstick test registers positive for haemoglobin, but the freshly spun urine sediment shows no red blood cells. As ongoing treatment will be complex in severe electrical injuries and burns, early consultation should be made with a burns surgeon and critical care specialist. Management on a critical care unit will be required.

Management

COLD INJURY BURNS Cold injury can be systemic, leading to hypothermia, or localized, leading to localized tissue damage to varying degrees dependent on the degree of freezing.

Awareness

Hypothermia is defined as a core body temperature of below 35oC (95oF). The systemic effects depend on the severity of the drop in core temperature: 35–32oC (95–89.6oF) 32–30oC (89.6–86oF) < 30oC (< 86oF)

As core temperature drops, the conscious level deteriorates, and the airway can obstruct as coma develops. Respiratory and cardiac functions deteriorate until respiratory and cardiac arrest result. Localized cold injury is seen in three forms: 1. Frostnip – the mildest form, which is reversible on warming. 2. Frostbite – due to freezing of tissue and resultant damage from intracellular ice crystals and microvascular occlusion. There are four degrees of frostbite: • First degree – hyperaemia and oedema without skin necrosis. • Second degree – vesicle formation with partial-thickness skin necrosis. • Third degree – full-thickness and subcutaneous tissue necrosis, with haemorrhagic vesicle formation. • Fourth degree – full-thickness necrosis, including muscle and bone gangrene.

Severe hypothermia and hypothermic cardiac arrest require active internal (core) rewarming: • extracorporeal blood rewarming (cardiopulmonary, venovenous, or arteriovenous femorofemoral bypass) is the treatment of choice, especially with cardiac arrest • without equipment for extracorporeal re-warming, left-sided thoracotomy followed by pericardial cavity irrigation with warmed saline and cardiac massage is effective in systemic hypothermia < 28°C • thoracic lavage or haemodialysis is also effective • repeated peritoneal dialysis with 2 L of warm (43°C) potassium-free dialysate solution exchanged every 10–12 minutes until core temperature is raised to ~35°C • parenteral fluids warmed to 43°C • administer humidified air heated to 42°C through a face mask or tracheal tube • (NOTE: warm colonic and gastrointestinal [GI] irrigations are of less value.)

Management

Localized cold injury is initially managed in the field. The hypothermia and dehydration associated with frostbite should be addressed. Wet and constrictive clothing should be removed, the involved extremities should be elevated and wrapped carefully in dry sterile gauze, and affected fingers and toes separated. Further cold injury should be avoided. Rapid rewarming is the single most effective therapy for frostbite. As soon as possible, the injured extremity should be placed in gently circulating water at a temperature of 40–42°C (104–107.6°F) for approximately 10–30 minutes, until the distal extremity is pliable and erythematous. The current consensus is that clear blisters are aspirated or debrided and dressed. Early surgical intervention in the form of tissue debridement and amputation is not indicated; full demarcation of dead tissue can take 3–4 weeks to fully demarcate, and debridement at this point will avoid unnecessary tissue loss (Rabold, 2004).

• heated blankets, warm baths, forced hot air. It is easier to monitor and perform diagnostic and therapeutic procedures using heated blankets • warm bath re-warming is best done in a bath of

Take home message Thermal burns are assessed by depth and extent, and managed by addressing the airway, breathing and circulation. Huge volumes of intravenous fluids may be required to maintain homeostasis. Chemical burns are treated primarily by copious irrigation with water. Electrical burns may be associated with severe tissue damage and systemic disturbance, and need treatment for the local burns and systemic cardiac, respiratory and renal complications. Cold injury can be systemic hypothermia, which is treated by active external and

3. Non-freezing injury – trench foot or immersion foot, with microvascular endothelial damage, stasis and vascular occlusion. Recognition Systemic cold injury is recognized in the primary survey as the airway, breathing and circulation and neurological function are assessed. The patient is cold to the touch, and looks gray and peripherally cyanosed. Strikingly, the expired breath can feel deathly cold on the hand. A low reading rectal or oesophageal temperature probe will be needed to accurately gauge the degree of hypothermia. Local injuries are assessed during the secondary survey and the musculoskeletal survey. The affected part of the body initially appears hard, cold, white and anaesthetic, but the appearance changes frequently during treatment.

Hypothermia is treated by securing the airway, oxygenating and ventilating the patient to normal parameters, gaining intravenous access and treating shock with warmed intravenous fluids. In addition, the patient is re-warmed depending on the degree of hypothermia. Mild and moderate hypothermia is treated by active external re-warming:

22

The management of major injuries

Mild hypothermia Moderate hypothermia Severe hypothermia

40–42°C moving water (re-warming rate: ~1– 2°C/hour) The warming gradient should not be greater than this to avoid thermal injury. Re-warming should be slow to minimize peripheral dilation, which can cause hypovolaemic shock.

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22

672

internal re-warming, depending on severity, or localized tissue damage. Localized tissue damage is treated by rapid re-warming and delayed surgical debridement.

INITIAL RESPONSE TO TRAUMA The physiological effects of trauma are both widespread and predictable, invoking a range of hormonal and cellular mechanisms that have evolved to maximize the chances of survival following serious injury. These adaptations for survival can be considered as a whole body, fluid conservation and repair strategy. Following injury the first survival offensive is a plan to prevent blood loss. Direct injury to blood vessels should induce an arterial vasospasm to reduce blood loss followed by the formation of a ‘vascular patch’ consisting of a fibrin-reinforced, aggregation of platelets. If despite this strategy significant blood loss still occurs, some preservation of intravascular volume occurs by fluid redistribution between the vascular, cellular and interstitial fluid compartments. The resulting change in compartmental volumes will stimulate an endocrine response with the release of a number of renal, adrenal and pituitary hormones (renin, aldosterone, cortisol and antidiuretic hormone [ADH]). This hormonal response not only represents a secondary fluid conservation project but also heralds another survival strategy. Serious injury, which in evolutionary terms would have limited the ability to hunt and feed, produces a metabolic re-conditioning. Under endocrine guidance, cellular metabolic priorities, and the type of substrate used, change with a falling basal metabolic rate. These marked changes in metabolism represent an approach to energy conservation, allowing a channelling of reserves to damage control and repair whilst still keeping the brain fuelled. Ultimately a successful outcome following trauma (or major surgery) depends on the integration of these strategies and the maintenance of whole-body physiology. The integrity of the cardiorespiratory system is pivotal. Failure to maintain cellular (organ) perfusion, oxygenation and ATP regeneration will lead to cell apoptosis and death. Co-morbidities such as preexisting lung disease or cardiac failure will increase complications and the chance of dying. The normal physiological response to the increased metabolic demands of trauma, illness and surgery is to increase oxygen delivery in response to an increase in tissue oxygen consumption. Failure to respond to this demand will generate an oxygen debt with metabolic consequences. This limitation of oxygen availability will favour anaerobic metabolism over aerobic, reducing metabolic efficiency

ml/min/M2 200 180 160 140 120 100 80 60 40 20 0

mean increase in VO2 - 44%

colorectal

n ⫽ 200

abdominal

pre-op

abdominal aortic aneurysm

mean

post-op

22.35 Oxygen consumption before and after surgery (Older and Smith, 1988).

and generating a lactic acidosis as a consequence. This is clearly unsustainable and clinical studies show that an inability to mount a sustained cardiovascular response is directly proportional to an increase in morbidity and mortality. Survival and outcome relies on the speed of repayment of this oxygen debt. The slower the payback, the greater the ensuing complications. As a synopsis trauma and major surgery can be considered to be like running a marathon. To survive, cardiorespiratory function and cellular physiology have to remain intact. Systemic failure, for whatever reason, to maintain tissue perfusion leads to shock, which is one of the most frequently misused and misunderstood terms in medicine and the media. Correctly used it implies tissue hypoperfusion leading to cellular hypoxia and describes a medical emergency with a high mortality rate from multiple organ failure. From an intensive care perspective, the recognition and appreciation of the type of shock is essential as other reasons for hypoperfusion may coexist.

22.36 Hypoperfusion This 70-year-old man with severe sepsis developed hypoperfusion of the lower limbs. Note the typical marbling of the skin.

SHOCK

mechanisms are unable to maintain adequate tissue flow, leading to critical hypoperfusion. Obstructive shock

Reduced cardiac output

Neurogenic shock This occurs when spinal cord injury – usually at a cervical or high thoracic level – leads to loss of sympathetic tone and hence peripheral vasodilatation, venous pooling and reduced venous return. This is aggravated by the absence of direct sympathetic nervous system connection into the heart, and hence impaired compensatory responses.

Impaired performance Cardiogenic shock is an intrinsic

failure of cardiac function despite adequate circulating volume and venous return, most commonly as a result of acute myocardial infarction. Cardiogenic shock may occur following an apparently minor insult to a heart with any pre-existing functional impairment. Impaired venous return Hypovolaemic shock exists when

a fall in circulating volume of sufficient magnitude occurs such that compensatory physiological

AETIOLOGY OF CIRCULATORY SHOCK 1. Reduction in cardiac output a. HYPOVOLAEMIC SHOCK: Reduced circulating volume causing a reduction in venous return and cardiac output (e.g. haemorrhage) b. OBSTRUCTIVE SHOCK: Mechanical obstruction to normal venous return or cardiac output, e.g. tension pneumothorax, cardiac tamponade or massive pulmonary embolism c. CARDIOGENIC SHOCK: Failure of cardiac pump to maintain cardiac output, e.g. post myocardial infarction. 2. Reduction in peripheral resistance a. DISTRIBUTIVE SHOCK: A drop in peripheral resistance due to vasodilatation, which is often associated with an increase in cardiac output but not sufficient to maintain blood pressure, e.g. anaphylaxis, neurogenic shock, SIRS, septic shock b. ENDOCRINE SHOCK: In the intensive care setting hypothyroidism, hyperthyroidism and adrenal insufficiency can all lead to reduced tissue perfusion.

Reduced systemic vascular resistance

Anaphylactic shock A drug or parenteral fluid may be the trigger that provokes an immunological response with histamine release, resulting in cardiovascular instability and (potentially) respiratory distress.

The management of major injuries

‘Obstruction’ arises when venous return is compromised by raised intrathoracic or pericardial pressure (pneumothorax and cardiac tamponade), or if right ventricular ejection is blocked by a massive pulmonary embolus, resulting in right ventricular overload and impaired left heart filling. Plain x-rays may not show changes and CT angiography is the initial investigation of choice.

In health, cardiac output and the delivery of oxygen (global arterial blood flow multiplied by the blood oxygen content) and local tissue perfusion are closely matched to metabolic requirements. Shock follows a mismatch of metabolic demand to oxygen delivery at tissue level, leading to cellular hypoxia and (if uncorrected) to tissue and organ failure. The causes of circulatory shock can be classified as abnormalities of cardiac output, of systemic vascular resistance, or a combination of both.

22

Septic shock This condition is defined as severe sepsis with associated hypotension, evidence of tissue hypoperfusion that is unresponsive to fluid resuscitation. Various mechanisms are responsible for the vasodilatatory response and catecholamine resistance, which are characteristic of septic shock. It is becoming clearer that this host response does not appear to be determined by the infecting organism and there is a suggestion of genetic susceptibility being a contributory factor in dictating the severity of subsequent illness.

Diagnosis of shock Early recognition, immediate resuscitation and treatment of the underlying cause are the cornerstones of successful therapy. There may be an easily identifiable cause of shock, but often the aetiology is difficult to establish. Following massive trauma, shock may be hypovolaemic (blood loss), obstructive (tamponade or tension pneumothorax), cardiogenic (cardiac contusion), neurogenic (spinal cord injury) or anaphylactic (drug reaction). Careful examination should clarify the aetiology in most cases, and will aid in determining severity by identifying end-organ effects. Examination should be thorough and structured to avoid missing useful signs. Tests should include a full blood count and estimation of electrolytes as well as assessment of renal function, liver function, clotting and blood group/ cross-match, serum glucose, blood cultures and inflammatory markers (e.g. C-reactive protein, procal-

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22

CLINICAL EXAMINATION IN SHOCK Cardiovascular system • Pulse (rate/rhythm), blood pressure, JVP (or CVP if central line in situ), heart sounds (muffling/ murmurs), peripheral perfusion (capillary refill time/skin colour) Respiratory system • Respiratory rate, work of breathing, tracheal deviation, air entry, added sounds, oxygen saturations (relative to inspired oxygen) Abdomen • Pain, distension, peritonitis, localizing signs, urine output Central nervous system • Level of consciousness, peripheral neurological signs (e.g. power, reflexes) Other systems • Temperature, skin signs (e.g. rashes), limbs (bony integrity/perfusion)

citonin). Arterial blood gas analysis provides rapid results, and the newer analyzers often measure a serum lactate level. This is a non-specific marker, but may indicate hypoperfusion if elevated. X-ray examination, ultrasound scanning (e.g. a FAST scan) or CT may identify sources of blood loss and identify likely foci in the case of severe sepsis. An ECG and urgent echocardiography are obligatory if a cardiogenic cause of shock is suspected. Careful and regularly repeated recording of vital signs (heart rate, respiratory rate, blood pressure, oxygen saturation) and indicators of end-organ perfusion (consciousness level, urine output) are crucial. The initial severity of illness at assessment, and subsequent response to initial resuscitative and treatment measures will dictate the need for more advanced and invasive monitoring tools. Continuous invasive blood pressure and central venous pressure monitoring are generally required, and are essential if vasoactive drugs are required, both to enable safe drug delivery and to allow titration of dosing.

Advanced monitoring systems Invasive techniques that allow an estimation of cardiac output – and thereby tissue oxygen delivery – are used in the sickest patients, both as an aid to diagnosis and a guide to therapy.

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PULMONARY ARTERY FLOTATION CATHETERIZATION In pulmonary artery flotation catheterization (PAFC), a catheter is passed via a central vein through the right

heart to rest within a branch of the pulmonary artery. Inflation of the distal balloon permits measurement of the pulmonary artery occlusion pressure (PAOP), which allows an estimate of left atrial pressure and hence (it is assumed) left ventricular preload. Many errors may, however, confound this measurement. The PAFC also allows measurement of cardiac output by way of thermodilution (either by cold injectate or by proximal heating coil, allowing semi-continuous data to be recorded). This is calculated from the area under a curve of distal temperature (recorded by a thermistor at the catheter tip) plotted against time. Cardiac output is inversely proportional to this area. PAFC use has declined in popularity recently due to concern regarding the complications of what is a highly invasive modality, failure to show outcome benefit in studies of patients monitored by PAFC, and the increasing availability of alternative, less invasive monitors that generate similar data. CARDIAC OUTPUT FROM ANALYSIS OF ARTERIAL WAVEFORM Pulse contour analysis The PiCCO® cardiac output monitor employs a mathematical analysis of the shape of the arterial waveform using a dedicated femoral arterial cannula to derive cardiac output data. It is calibrated by a transpulmonary thermodilution technique, following injection of cold saline into a central line. The Lithium Dilution Cardiac Output (LiDCO®) monitor also employs the arterial

Pulse power analysis

Monitoring (non Invasive)

Early Recognition

Early Resuscitation and Treatment

History Observation Clinical Examination ECG/BP Pulse Oximetry History Clinical Examination Education Early Warning Scoring Improvement

Deterioration Monitoring (Invasive)

Arterial monitoring Bloods eg lactate CVP CO Oxygen flux

Continuing Resuscitation and Treatment 22.37 Investigation and monitoring shock

TREATMENT OF UNDERLYING CAUSE OF SHOCK Hypovolaemic • Control of haemorrhage (may require surgery) • Restoration of circulating volume (fluid and blood products) Obstructive • Needle decompression of tension pneumothorax

Management of shock

• Pericardiocentesis (tamponade)

Initial approach Initially attention should be focussed

• Thrombolysis or surgical removal of pulmonary embolus

on rapid assessment, with airway, breathing and circulation (ABC) addressed in the first instance. Highflow oxygen (FIO2 0.6 or greater) should be administered via a patent airway, and intravenous access obtained. Definitive treatment of the underlying cause of shock should be commenced alongside resuscitative measures. The aim should be to support the circulation to allow adequate tissue oxygen delivery, whilst mitigating or reversing the effects of the initial insult. This may be rapidly successful, for example in decompression of a tension pneumothorax; in other cases it may prove impossible to correct the underlying pathology (e.g. cardiogenic shock due to extensive myocardial infarction). Often large volumes are needed, guided by clinical response and monitored indicators of filling (e.g. central venous pressure). The response of these variables to a fluid challenge, and trends, are considerably more useful than ‘snapshot’ values. Indeed targeting a particular value of CVP or MAP is physiologically unsound and may be to the patient’s detriment. It is always preferable to use fluid boluses or ‘challenge techniques’ to interpret volaemic status. In ventilated patients, changes in intrathoracic pressure generate cyclical changes in systolic pressure and using the LiDCO or PiCCO monitors generates a stroke volume variation that is related to volaemic status under certain conditions. These variations in stroke volume may be more useful indicators of likely fluid responsiveness than other methods. The choice of fluid is dictated by the underlying cause of the shock and local policies. There is an optimum amount of fluid to target resuscitation and it should be recognized that overenthusiastic transfusion, as with fluid restriction, is also associated with increased complications.

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Cardiogenic • Inotropes • Anti-arrhythmics • Revascularization

The management of major injuries

waveform to derive haemodynamic data but using a power algorithm that can be used in any artery, and thus does not require insertion of a proprietary arterial line. The monitor is calibrated using either the lithium dilution technique (LiDCO plus) or using a nomogram of patient demographics with the LiDCO Rapid monitor. As with pulse contour analysis, peripheral resistance and data indicating likely fluid responsiveness are calculated beat-to-beat. It does also have, unlike many other devices, positive outcome data in high-risk patients.

• Aortic balloon counterpulsation • Surgical repair of valve lesions Distributive • Early treatment of infection (source control, e.g. drainage, early antibiotic administration)

Fluid therapy

Inotropes/vasopressors This treatment should be instituted if the patient remains hypotensive despite adequate fluid resuscitation. Again, choice is determined by aetiology: vasopressor (e.g. norepinephrine) for distributive shock and inotrope (e.g. dobutamine) for

cardiogenic shock. Combinations may be required, guided by haemodynamic data from monitoring equipment and clinical response. Significant doses of either inotropes or vasopressors should be mandatory. Cardiac output monitoring is much better than making decisions based on the arterial blood pressure. There is recent evidence that treatment with ‘physiological’ doses of corticosteroid in cases where adrenal response is inadequate may not improve outcomes as had previously been hoped. There is considered to be some benefit from the use of steroids with septic shock with an improvement in haemodynamic response but this is still the subject of considerable debate and there is a lack of cogent outcome data. The use of vasopressin has traditionally been reserved for patients with catecholamine-resistant septic shock but new evidence suggests that there may be some benefit for those requiring lower doses of noradrenaline. Tight control of blood glucose levels has also been shown to lead to improved outcomes in the sickest patients in intensive care.

Endocrine support

Shock leads to multiple organ impairment or failure. Support of other organ systems may well be required during treatment.

Systemic support

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Mortality is determined both by aetiology of circulatory shock and the response to treatment. Early recognition and prompt therapy are the most important factors.

Outcome

MULTIPLE ORGAN FAILURE Multiple organ failure or dysfunction syndrome (MODS) is the clinical appearance of a seemingly poorly controlled severe systemic inflammatory reaction, following a triggering event such as infection, inflammation or trauma. It represents the net result of altered host defence and deregulation of the inflammatory response and the immune system. The condition has emerged with medical advances as a result of increasing availability of intensive care facilities. Recognized as a syndrome in the early 1970s, progress in the management of critically ill patients has unmasked this frequently lethal cocktail of sequential pulmonary, hepatic and renal failure. This pattern of progressive organ impairment and failure complicates illnesses with diverse aetiologies and, despite progress in understanding the underlying mechanisms involved, it carries a mortality rate that remains depressingly high. MODS has now become the commonest cause of stays in surgical ITUs of more than 5 days and (among these patients) the most frequent cause of death. It is essential to differentiate MODS from postoperative or traumatic, isolated organ dysfunction, which has a different pathogenesis and markedly different survival outcomes.

Epidemiology

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Definitions of organ failure use two types of criteria based on either measures of physiological derangement (e.g. hypotension, acidosis, serum creatinine concentration) or on the treatment methods (e.g. dialysis, ventilation, etc.). The degrees of organ dysfunction, from covert physiological impairment to overt failure, coupled with the difficulties of monitoring the function of all the organs involved has led to controversies about the definition of organ failure and the clinical entities involved. This has hampered epidemiological surveys and the assessment of treatment outcomes. Confusion over the exact incidence of MODS stems from an absence of universal diagnostic criteria; many of the published studies have used differing clinical and temporal definitions of organ failure. Review of the published studies suggests that MODS develops in 5–15 per cent of patients requiring ICU admission, depending on the diagnostic

criteria used and the case-mix of the population of ICU patients studied. The outcome data is remarkably consistent between the studies, with mortality linked to the number of organs failed. The appearance of MODS broadly follows two clinical courses, differing in onset relative to the initial event, time course and sequence of organ failure. The first pattern usually follows a direct pulmonary insult, such as trauma or aspiration. In this form the overall course of the disease may be relatively short and MODS occurs as a pre-terminal event, becoming evident just prior to death. The second type is the more classical form, as found in severe sepsis, with pulmonary manifestations of acute respiratory distress syndrome (ARDS). MODS is present early in the course of the illness but does not become progressive until after a 7–10-day delay, with manifestations of hepatic and subsequently renal failure becoming apparent. The initiating events for MODS are many and diverse but by far the most common association is with severe sepsis and ARDS. The likelihood of occurrence and the progression of disease is related not only to the severity of the initiating event but also to the premorbid physiological reserve of the patient, i.e. old age and pre-existing disease such as cardiac failure, cirrhosis, drug abuse etc.

INITIATING EVENTS FOR MODS Severe sepsis • Peritonitis

Surgery • Vascular • Abdominal

Trauma • Chest injury • Burns

Medical • Pancreatitis • Aspiration

Shock • Cardiogenic • Haemorrhagic

Other • Massive transfusion

Pathogenesis MODS is now recognized as a systemic disorder resulting in widespread microvascular injury. Most of the initiating events can be characterized as infective, traumatic or ischaemic and mechanistically it is unravelling as a disorder of the host defence system, with an unregulated and exaggerated immune response, resulting in an excessive release of inflammatory mediators. It is these mediators that produce the widespread microvascular damage leading to organ failure. As a syndrome, the classical form of MODS appears to progress through four clinical phases:

1. Shock (hypoperfusion). 2. Period of active resuscitation. 3. Stable hypermetabolism (systemic inflammatory response). 4. Organ failure.

Active resuscitation If resuscitation is rapid and effective the sequence of events precipitating MODS may be aborted. However, in many cases, despite apparently adequate management the syndrome progresses, suggesting a genetic component. Systemic inflammatory response If resuscitation fails to prevent further progression of the disease, the presence of widespread cellular damage manifests after several days with a picture of panendothelial dysfunction. This endothelial damage is manifest by increased microvascular permeability with the formation of protein-rich oedema fluid. This period of hypermetabolism has characteristic features that are a consequence of the host response. This has been referred to as the systemic inflammatory response (SIRS) in the absence of proven sepsis and the sepsis syndrome when associated with an identifiable invading pathogen. Once this phase is entered the mortality rises to the 25–40 per cent range. Organ failure Failure adequately to control the inciting

event and the inexorable progression of the disease is marked in this final stage by increasing organ dysfunction, failure and death. The appearance of clinically overt organ failure is a significant prognostic event signalling another leap in the mortality rate from the 25–40 per cent range to 40–60 per cent in the early stages and 90–100 per cent as the disease progresses with increasing hepatic and renal dysfunction.

CLINICAL FEATURES OF SIR Fever Tachycardia Hyperdynamic circulation Tachypnoea Oliguria

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The management of major injuries

Shock Common to all the initiating events associated with MODS are periods of relative or total ischaemia relating to regional or global perfusion deficits, which may go clinically unrecognized, i.e. cellular hypoperfusion as discussed earlier. The severity of these deficits, the passage of time to adequate resuscitation and the reserve functional capacity of the organs concerned, appear to provide the key to the path of organ dysfunction and eventual failure.

MEDIATORS OF THE SIRS\SEPSIS RESPONSE AND MODS The metabolic and physiological alterations found in the hyperdynamic\hypermetabolic phase and the subsequent cellular damage are caused by complex interactions of endogenous and exogenous mediators. These substances are mainly released from the host endothelial and reticulo-endothelial cells, principally macrophages, in response to provocation by a variety of stimuli including ischaemia, sepsis and cytokines. Experimental administration of endogenously produced mediators such as tumour necrosis factor (TNF), interleukins IL1, IL2 and IL6 and plateletactivating factor and exogenously produced mediators such as bacterial endotoxin produce not only similar physiological effects to those found in the SIRS\sepsis syndrome, but also organ dysfunction similar to that found in patients with MODS. The wide variety of substances with vastly differing molecular structures implicated in the pathogenesis of the SIRS\sepsis syndrome, all producing the same characteristic physiological response, suggests a ‘preprogrammed’ or stereotyped host reaction. The effector systems involved in the translation of triggering injury to pathogenesis of MODS are additive and synergistic, and involve not only the endocrine and central nervous systems, but also the cellular and humoral components of the inflammatory responses. Following injury a local inflammatory response occurs resulting from the products of the damaged endothelium and platelets. Leucocytes and macrophages are presumably attracted to the area as a result of these products and secondary activation of complement, coagulation and other components of the inflammatory system occurs. If the injury is severe or persistent enough, this localized reaction may spill over into the systemic circulation, producing the systemic inflammatory response, or if identified with infection the sepsis syndrome. MODS may subsequently develop. In health, cytokine production is strongly repressed since they are produced by immune cells following activation by foreign particles, e.g. bacteria. Cytokine induction and production is then closely regulated so as to benefit the host by localizing and destroying the foreign organisms. However in certain situations, this control system appears inadequate and cytokine production becomes both inappropriate and excessive, leading to destruction of normal cells with a generalized inflammatory response. A decade of studies has underlined the importance of the immune system and these mediators in the sequence of events ultimately producing MODS. Interleukin-1 is the most extensively investigated cytokine; produced by macrophages, this polypeptide (as well as interleukin-6) can induce fever, hypermetabolism, muscle breakdown and hepatic acute phase protein synthesis. The interleukins, however, appear

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relatively late in the sequence of events as compared to TNF. TNF appears early in the systemic circulation during critical infective illness, mediating directly or indirectly many of the major features of sepsis. It is probably one of the pivotal mediators with multiple effects, producing endothelial membrane permeability changes and cell death. Many of these effects appear to be secondarily mediated by prostaglandins and TNF-induced release of other cytokines; the full extent of its actions are poorly understood.

SPECIFIC ORGAN INVOLVEMENT IN MODS Respiratory system In the majority of critically ill patients who develop MODS the lungs are the first organ to fail, the other organs following in a sequential fashion. The lung appears to be a pivotal organ in the development of MODS, appearing either to generate inflammatory mediators that aggravate peripheral endothelial dysfunction or allow the persistence of mediators in the circulation following its decreased capacity to clear and metabolize inflammatory substances. As with other organs, a spectrum of dysfunction exists ranging from minor demonstrable pathology, designated acute lung injury (ALI), to massive alterations in pulmonary pathophysiology – the so-called adult respiratory distress syndrome (ARDS). ARDS has been defined as a condition characterized by severe hypoxia despite high concentrations of supplemental oxygen, with a radiographic appearance demonstrating diffuse infiltrates in the absence of infection or any other explanation for the respiratory distress. Included in this definition are clinical values reflecting the derangement of respiratory function.

FEATURES DEFINING ARDS Hypoxia (PaO2/FiO2< 300 mmHg) Bilateral infiltrates on chest x-ray Pulmonary capillary wedge pressure < 18 mmHg or no clinical evidence of increased left atrial pressure

678

ARDS is considered to be a more severe form of ALI, in which the same criteria apply except that the hypoxia is more severe [PaO2/FiO2 < 200 mmHg regardless of positive end-expiratory pressure (PEEP)]. The pathogenesis of this lung injury has in part been suggested to be endothelial damage initiated by complement activation with subsequent

22.38 ARDS – x-ray Chest radiograph of a patient with ARDS following pulmonary contusion. Infiltrates and patchy consolidation are typical features. Note the pulmonary artery catheter in situ.

leucocyte aggregation and oxygen free radical formation. Platelet clumping and intravascular coagulation have also been implicated. Pathologically in ARDS pulmonary capillary endothelial damage causes fluid leakage and surfactant abnormalities resulting in alveolar and interstitial oedema and fibrosis. This damage to pulmonary architecture causes a reduction in functional residual capacity, increased ventilation\perfusion mismatching and a predilection for secondary infection. The net result is failure of gaseous exchange with hypoxia, hypercarbia and therefore an aggravation of the peripheral tissue hypoxia.

Cardiovascular system Under normal physiological conditions, tissue oxygen utilization is closely matched by its delivery to the tissues. Oxygen uptake by cells is normally dictated by need. Cardiac output, minute ventilation and regional blood flow in the microcirculation are regulated to prevent cellular ischaemia. If stressed in this situation, cells cope with increasing metabolic demands by increasing oxygen extraction. However, under the pathological conditions found in patients with SIRS who are developing MODS, the tissues appear unable to extract oxygen efficiently from the blood, thus resulting in cellular oxygenation having to rely on increased oxygen delivery rather than extraction – the so-called pathological oxygen, supply or flow, dependency. There may be a number of reasons for this. Microvascular inflammatory injury with endothelial and interstitial oedema hinders the diffusion of oxygen, and furthermore altered membrane characteristics of the erythrocytes render them less deformable and therefore less accessible to transit within the microcirculation.

Altered concious level

Jaundice Enzymes Albumin PT

Failure to absorb Diarrhoea GI bleeding

Tachycardia Hypotension Acidosis

Oliguria Anuria Creatinine

Platelets PT/APTT Protein C D-dimer

22.39 Physiological effects of MODS

In the hypermetabolic SIRS phase, the response to increased metabolic demands coupled with less effective utilization of oxygen must be met by an increased cardiac output. This increase, in conjunction with mediator-induced systemic vasodilation, gives rise to the hyperdynamic state characteristic of the SIRS– sepsis syndrome. Failure to meet this increased oxygen demand heralds a diminished likelihood of survival. Poor cardiac performance may also contribute to the oxygen supply–utilization disequilibrium. It is well documented in sepsis that certain circulating factors adversely affect ventricular compliance and contractility. Furthermore, if pre-existing coronary artery disease co-exists with this hyperdynamic state, myocardial ischaemia and failure may progressively ensue. The effects of this may not only cause a decrease in organ perfusion but may also aggravate existing pulmonary dysfunction with raised left atrial pressures and the generation of pulmonary oedema, further aggravating oxygen delivery.

Gastrointestinal tract The gastrointestinal tract is particularly vulnerable to the processes occurring in MODS. There is a growing body of evidence to suggest that the persistence of the SIRS–sepsis syndrome may be driven by abnormal colonization of the normally sterile upper gastrointestinal tract with pathogenic enteric bacteria. Some investigators believe that the development of MODS in the absence of a recognized focus of infection is caused by gut failure with translocation of bacteria and toxins from the gut eventually into the systemic circulation. This abnormal colonization of the gut, coupled with potentially toxic gut luminal contents, forms a deadly reservoir of pathogenic substances. The body relies on the epithelial integrity of the gut

Kidney

22

The management of major injuries

Tachypnoea Hypoxia

wall to prevent seepage of these contents into the circulation. This epithelial barrier is, however, also involved in the systemic disease process, especially as preferential redistribution of the blood from the splanchnic circulation to muscle predisposes the gut mucosa to ischaemia and membrane reperfusion injury. The epithelial barrier is then likely to fail, allowing translocation of pathogenic bacteria, or endotoxins into the portal circulation. Under normal circumstances overspill of gut luminal toxic products into the portal circulation would be cleared by hepatic reticulo-endothelial system. In the presence of MODS the hepatic clearance of these substances is greatly reduced and spillage of toxins will be washed into the pulmonary microcapillary network. The appearance of endotoxin and bacteria in the lung will activate pulmonary alveolar macrophages with local damage occurring from macrophage-derived mediator release, adding to the destruction of pulmonary architecture already occurring in ARDS.

The involvement of renal dysfunction and failure as part of classical MODS heralds a large increase in mortality. The explanation for this excess mortality is unknown; perhaps the failing kidneys act as a further source of inflammatory mediators ‘fuelling’ the systemic disease process further. The loss of intravascular volume control may exacerbate ARDS and heart failure with the potential for volume overload. In addition, institution of methods of renal support will have the potential for further activation of the reticuloendothelial cells caused by bio-incompatibility problems of the extracorporeal circuit and haemofilter/ dialyzer.

Haematological system Coagulopathy is common after major trauma. Initially this may just reflect massive fluid replacement and transfusion. Massive transfusion, the replacement of greater than one circulating blood volume (approximately 10 u of blood) in less than 24 hours, may result in diffuse microvascular bleeding from surgical wounds, intravenous catheter sites and areas of minor trauma. The source of the coagulopathy, ignoring the presumed continuing consumption, is the dilution of coagulation factors through the infusion of products deficient in these factors (e.g. packed red blood cells, crystalloids and colloids). Laboratory tests demonstrate thrombocytopaenia, hypofibrinogenemia and prolongation of the prothrobin times. An insidious complication of severe injury and blood loss is a widespread disorder of coagulation and haemostasis. This is due, at least in part, to the release of tissue thromboplastins into the circulation, en-

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dothelial damage and platelet activation. The result is a complex mixture of intravascular coagulation, depletion of clotting factors, fibrinolysis and thrombocytopaenia. Microvascular occlusion causes haemorrhagic infarctions and tissue necrosis, while deficient haemostasis leads to abnormal bleeding. This resulting coagulopathy is termed disseminated intravascular coagulation (DIC). The pathophysiology results from the generation of excessive amounts of thrombin. Thrombin generation in florid DIC is sufficiently intense that anticoagulant mechanisms such as antithrombin and activated protein C systems become ineffective. Fibrin deposition in the microvasculature undergoes fibrinolysis and promotes the consumption of clotting factors (especially fibrinogen, platelet factors V and VIII). This in turn leads to a consumptive coagulopathy characterized by thrombocytopaenia, hypofibrinogenaemia and ongoing thrombolysis. The consequences of DIC are variable but include excessive bleeding due to consumption of haemostatic factors and secondary fibrinolysis, organ dysfunction, skin infarction, haemolysis, and disseminated thrombosis. The clinical features are those of diffuse microvascular thrombosis: restlessness, confusion, neurological dysfunction, skin infarcts, oliguria and renal failure. Abnormal haemostasis causes excessive bleeding at operation, oozing drip sites and wounds, spontaneous bruising, gastrointestinal bleeding and haematuria. The diagnosis is confirmed by finding a low haemoglobin concentration, prolonged prothrombin and thrombin times, thrombocytopaenia, hypofibrinogenaemia and raised levels of fibrinogen degradation products.

Management of MODS

680

Once the clinical syndrome of MODS is established, despite major advances in ITU technology and management strategies, the chances of survival dwindle. The best treatment for MODS remains prevention. This entails early aggressive resuscitation following insult, avoidance of hypotensive episodes and removal of risk factors, e.g. by early excision of necrotic tissue, early fracture stabilization and ambulation, and appropriate antibiotic usage following drainage of sources of sepsis. Early circulatory resuscitation is of paramount importance and this should be guided by invasive monitoring. Oxygen delivery should be maximized to a point where oxygen consumption no longer rises or to the level where markers of anaerobic metabolism such as serum lactate fall. It appears that the use of less invasive clinical markers for the adequacy of the circulation, such as mean arterial pressure, temperature gradients and urine output, may not entirely reflect the success of microcirculatory resuscitation. Once the sequence of MODS is established, early appropriate institution of organ support, (e.g. endotracheal intubation and ventilation) is essential.

The treatment of ALI/ARDS remains mainly supportive and includes the management of precipitating causes. A large prospective study, supported by the National Heart Lung and Blood Institute in the USA has shown that the use of low tidal volume ventilatory strategies (6 mL/kg) and limited plateau pressure (< 30 cm H2O) was effective in reducing the mortality rate from 40 per cent to 31 per cent. Other measures to improve oxygenation – e.g. prone positioning, high-frequency ventilation, nitrous oxide inhalation and extracorporeal life support – have limited success in improving overall outcome. Renal and haematological management strategies are also largely supportive with renal replacement therapy and blood products frequently requiring expert involvement. Malnutrition is a common and major contributing factor to MODS. Nutritional starvation combined with hypermetabolism leads to structural catabolism. Unlike starvation the substrates metabolized are mixed, with a significant increase in amino-acid oxidation. With the temporal progression of MODS, direct amino-acid oxidation increasingly becomes prevalent with rapid dissolution of skeletal muscle. Metabolic support in terms of providing adequate calories and maintaining nitrogen balance is essential if lean body mass is to be preserved and ‘autocannabilism’ slowed. This has led to recommendations for early parenteral feeding (this is still controversial). Providing a calorie source for these patients requires care and a balance of substrates has to be given to prevent adding iatrogenic problems to the metabolic mayhem already occurring. Whilst it is known that glucose has a protein-sparing effect, excessive amounts confers no additive advantages and may cause complications such as fatty liver, hyperosmolarity, hyperglycaemia, and increased CO2 production, increasing the excretory load of the lungs and further exacerbating respiratory failure. The glucose load should not therefore exceed 4–5 mg/kg/minute, with a non-protein calorific load of 25–30 kcal/kg/day and 0.5–1.0 g/kg/day of lipids. Protein requirements run at 1–2 g/kg/day with modified amino acid preparations as these appear to be the most efficient protein source, producing less urea and better nitrogen retention. Rigorous attention to these details has brought improvements in prevention and outcome in MODS. Other newer treatment strategies are still largely unproven in terms of outcome. Selective decontamination of the digestive tract (SDD) by administration of non-absorbable antimicrobial agents may reduce the incidence of nosocomial pneumonia by re-sterilizing the upper gastrointestinal tract. Trials of SDD have shown some benefit but large-scale effects on antibiotic resistance from widespread use of antiobiotics are awaited. The use of aggressive early enteral

TETANUS The tetanus organism Clostridium tetani flourishes only in dead tissue. The exotoxin released passes to the central nervous system via the blood and the perineural lymphatics from the infected region. The toxin is fixed in the anterior horn cells and therefore cannot be neutralized by antitoxin. Established tetanus is characterized by tonic, and later clonic, contractions, especially of the muscles of the jaw and face (trismus, risus sardonicus), those near the wound itself, and later of the neck and trunk. Ultimately, the diaphragm and intercostal muscles may be ‘locked’ by spasm resulting in asphyxia. TREATMENT With established tetanus, intravenous antitoxin (human for choice) is advisable. Heavy sedation and muscle relaxant drugs may help; tracheal intubation and ventilation are the only options to treat respiratory muscle involvement. Prophylaxis against tetanus by active immunization with tetanus toxoid vaccine is a valuable goal. If the patient has been immunized, booster doses of toxoid are given after all but trivial skin wounds. In the nonimmunized patient prompt and thorough wound toilet together with antibiotics may be adequate, but if the wound is contaminated, and particularly with a delay before operation, antitoxin is advisable.

FAT EMBOLISM SYNDROME Fat embolism is a common phenomenon following limb fractures. Circulating fat globules larger than 10

μm in diameter occur in most adults after closed fractures of long bones and histological traces of fat can be found in the lungs and other internal organs. A small percentage of these patients develop clinical features similar to those of ARDS; this was recognized as the fat embolism syndrome long before ARDS entered the medical literature. Whether the fat embolism syndrome is an expression of the same condition or whether it is an entirely separate entity is still uncertain. The source of the fat emboli is probably the bone marrow, and the condition is more common in patients with multiple fractures.

Clinical features Early warning signs of fat embolism (usually within 72 hours of injury) are a slight rise of temperature and pulse rate. In more pronounced cases there is breathlessness and mild mental confusion or restlessness. Pathognomonic signs are petechiae on the trunk, axillae and in the conjunctival folds and retinae. In more severe cases there may be respiratory distress and coma, due both to brain emboli and hypoxia from involvement of the lungs. The features at this stage are essentially those of ARDS. There is no infallible test for fat embolism; however, urinalysis may show fat globules in the urine and the blood PO2 should always be monitored; values below 8 kPa (60 mmHg or less) within the first 72 hours of any major injury must be regarded as suspicious. A chest x-ray may show classical changes in the lungs.

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The management of major injuries

feeding in patients without an ileus may not only reduce the effects of catabolism but also prevent upper gut colonization by bacteria and hence nosocomial pneumonia by stimulation of bactericidal gastric acid secretion. Recent studies appear to suggest that this may have a positive effect on outcome. Probably the most recent advances in treatment of MODS have been in relation to modulation of the hypermetabolic inflammatory response by use of specific agents. These include monoclonal antibodies against endotoxin and TNF inhibitors of nitric oxide synthase and receptor antagonists for interleukin-1. Unfortunately interim reports of the therapeutic effectiveness are conflicting and it would appear as yet that the ‘magic bullet’ remains elusive. Again it must be emphasized that prevention is better than attempting cure for MODS, the major killer of critically ill patients in intensive care.

Management Management of severe fat embolism is supportive. Symptoms of the syndrome can be reduced with the use of supplemental high inspired oxygen concentrations immediately after injury and the incidence appears to be reduced by the prompt stabilization of long-bone fractures. Intramedullary nailing is not thought to increase the risk of developing the syndrome. Fixation of fractures also allows the patient to be nursed in the sitting position, which optimizes the ventilation–perfusion match in the lungs.

CRUSH SYNDROME This is seen when a limb is compressed for extended periods, e.g. following entrapment in a vehicle or rubble, but also after prolonged use of a pneumatic antishock garment. The crushed limb is underperfused and myonecrosis follows, leading to the release of toxic metabolites

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when the limb is freed and so generating a reperfusion injury. Reactive oxygen metabolites create further tissue injury. Membrane damage and capillary fluid reabsorption failure result in swelling that may lead to a compartment syndrome, thus creating more tissue damage from escalating ischaemia. Tissue necrosis also causes systemic problems such as renal failure from free myoglobin, which is precipitated in the renal glomeruli. Myonecrosis may cause a metabolic acidosis with hyperkalaemia and hypocalcaemia.

Clinical features and treatment The compromised limb is pulseless and becomes red, swollen and blistered; sensation and muscle power may be lost. The most important measure is prevention. From an intensive care perspective a high urine flow is encouraged with alkalization of the urine with sodium bicarbonate, which prevents myoglobin precipitating in the renal tubules. If oliguria or renal failure occurs then renal haemofiltration will be needed. If a compartment syndrome develops, and is confirmed by pressure measurements, then a fasciotomy is indicated. Excision of dead muscle must be radical to avoid sepsis. Similarly, if there is an open wound then this should be managed aggressively. If there is no open wound and the compartment pressures are not high, then the risk of infection is probably lower if early surgery is avoided.

Logical regression analysis, a multivariate statistical procedure, is used to convert a score to a predicted probability of the outcome measured, usually morbidity or mortality, using a large patient database suitable to the scoring system being developed. Finally the scoring system has to be validated on a population of patients independent from those used to develop the scoring system. Patients form a heterogeneous population and differ in many respects including age, previous health status, reason for admission and severity of illness. When comparing patients on intensive care for the purpose of research or audit, it is often difficult to standardize for all physiological variables due to the diversity of patients and their conditions. Scoring systems are therefore used to standardize for the physiological variables, age and reason for admission, allowing comparisons to be made between patients with different severity of illness. In the majority of scoring systems a high score reflects a patient who is more sick than one with a lower score (with the notable exception of the Glasgow Coma Score), but the score does not always follow a linear scale. Therefore a patient with a score of 20 is neither necessarily twice as sick nor has double the chance of dying than a patient with a score of 10. However, using logical regression it is possible to derive from the score a probability of morbidity, or mortality in hospital.

Audit

INTENSIVE CARE UNIT SCORING SYSTEMS

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The role of scoring systems in medicine has expanded since the 1950s. There are now many scoring systems catering for most organ dysfunction, disease states, trauma and critical illness. New scoring systems are regularly being developed and older systems refined. This widespread use relates to their role in communication, audit and research as well as the clinical management of patients. Scoring systems can theoretically be created from many types of variables. However, to be clinically useful, scoring systems must have predictive properties, and the information has to be unambiguous, reliable and easy to determine and collect. Ideally the variables should be frequently recorded or measured. Variables can be selected using clinical judgement and recognized physiological associations, or by using computerized searching of data collected from patient databases and relating it to outcome. The variables are then assigned a weighting in relation to their importance to the predictive power of the scoring system, again either by clinical relevance or from computerized databases.

The most common use for scoring systems is for audit. This allows ICUs to assess their performance in comparison to other units and also their own performance from year to year. If an ICU admitted patients who were not very sick, then their actual mortality on that unit would be lower than on a unit that admitted extremely sick patients and therefore it would be difficult to compare the performance between those units. This has led to the comparisons of actual mortality to a predicted mortality. The ratio of the actual to predicted mortality gives a figure for the standardized mortality ratio (SMR). Therefore an ICU with an SMR of less than 1 is theoretically performing better than expected and a unit with an SMR of more than 1 is performing worse than expected. The SMR can then be used to compare performance between units. Also if the severity of illness of patients varies, or if different types of patients are admitted from year to year, the SMR can be used to assess the performance of a unit over time. Statistical significance of different SMRs can be evaluated using confidence intervals.

Research The diversity of patients and different pathologies on the ICU makes comparisons between treatments or

Clinical management As well as quantifying the degree of physiological derangement or clinical intervention, and promoting better communication between clinicians, scoring systems can also be used to guide patient management. Some scoring systems lend themselves to sequential reassessment and thus can be used to monitor a patient’s progress over time. Also, as most research conducted in ICUs use scoring systems, the recommendations from research can sometimes be applied to subsets of patients with a severity of illness score within a certain range. This allows therapies to be directed sensibly at patients with an appropriate severity of illness. As most ITU scoring systems are an assessment of risk of mortality they have also been used to trigger admission to highdependency or intensive care.

Scoring systems on the ICU Scoring systems are often classified into three subsets: (1) anatomical (e.g. the injury severity score); (2) physiological (e.g. the GCS) and therapeutic (e.g. therapeutic intervention scoring systems). Most intensive care scoring systems are based on physiological variables; however other data are also included in the score, making simple classification very difficult. An ideal scoring system would be simple to use and be applicable to all intensive care patients irrespective of age, diagnosis and urgency of admission. It should also not be dependent upon treatment given prior to and on admission to ICU. The outcome prediction modelling should have a high sensitivity and specificity. The intensive care scoring systems are developed from large databases incorporating data from many ICUs. The data include physiological variables, co-morbidities, age, diagnoses, urgency of admission, and outcome at discharge from hospital.

Acute physiology and chronic health evaluation Knaus et al (1981) introduced the first the Acute Physiology and Chronic Health Evaluation

(APACHE) model in 1981 and revised it to APACHE II in 1985. APACHE III was presented in 1991 but as the regression analysis modelling is not in the public domain its uptake has been slow. APACHE II is made up of four basic components: (1) acute physiology score; (2) chronic health evaluation; (3) age; (4) urgency of admission to critical care. The acute physiology score is composed of 12 variables, with the most deranged measurement during the first 24 hours of admission to critical care being used to calculate the score. The original data collection for APACHE II occurred between 1979 and 1982 from ICUs in North America, and the population studied included relatively few surgical and trauma patients. Also, there have been many advances in patient care since the1980s, which have made APACHE II dated, despite its continued popularity.

Simplified acute physiology score The Simplified Acute Physiology Score (SAPS) initially used 14 variables, and did not provide any probability of survival. In 1993 it was revised to SAPS II with the data originating from European and North American ICUs. The score includes 12 physiological variables (the worst value within the first 24 hours), age, type of admission and three underlying disease variables (acquired immune deficiency syndrome (AIDS), metastatic cancer, and haematological malignancy). Using logistic regression, SAPS II can also be used to estimate the probability of survival. It is a simpler scoring system than APACHE and is also in the public domain, resulting in its widespread use, particularly in Europe. It suffers similar disadvantages to APACHE with regards to the timing of data collection, but is based on more recent and international data.

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procedures difficult. Scoring systems can be used to adjust for the differences in case-mix in patients recruited for trials, so if an intervention is used on all patients, the scoring systems can standardize for any heterogenicity between the groups prior to the intervention being initiated. Stratification of the risk of death can also be inferred from the scoring systems, allowing for investigation in different subgroups of patients in the ITU, and allowing researchers to assess response to interventions in patients at different risk of mortality.

Mortality prediction model The original mortality prediction model (MPM) was derived in the late 1980s with data from a single hospital, and differed from many of the scoring systems by not depending on physiological data but on the presence or absence of pathology. Therefore there was less of an impact by treatment on the physiology prior to and on admission to intensive care. In 1993 the MPM was revised to MPM II based on the same data set as SAPS II but with the inclusion of six extra ICUs. Initially the model was constructed of two time points: within 1 hour (MPM II0) and the first 24 hours (MPM II24) of admission. Now it can be used for 48- and 72-hour points as well, giving a prediction of mortality at those time points. Its variables include physiological parameters, age, acute diagnoses, chronic diseases, type of admission, as well as others. The MPM II0 is useful as it is minimally affected by the treatment given in an ICU.

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Therapeutic intervention scoring system The original therapeutic intervention scoring system (TISS) was devised in 1976, consisting of 76 therapeutic activities and was used initially to stratify the severity of illness. Its use for this purpose has largely been superseded by the newer scoring systems, but it is still commonly used to assess nursing workload and in resource management, for which it was not designed. A simplified TISS was developed in 1996, which included only 28 therapeutic activities.

Limitations Overall there is very little to choose between the third-generation scoring systems (APACHE III, SAPS II, MPM II) in terms of their predictive power. Despite this, APACHE II continues to dominate the literature and continues to be the most widely used score to date. The APACHE II/III and SAPS I/II scoring systems measure physiological variables during the first 24 hours of ITU admission and there has been concern that this can lead to bias. If a patient is treated prior to admission to ITU, their physiological variables will have been improved and the patients will have lower scores. Similarly if a patient is admitted to the ITU and receives inappropriate treatment over the first 24 hours, their scores will suggest that the ITU is dealing with sicker patients. Lastly, if a patient dies within 24 hours their scores before death will be very high, and therefore skew the SMR of a unit to suggest that it is admitting very sick patients. MPM II measures variables during the first hour and within the first 24 hours, thereby reducing the bias that may occur in the score when measured over 24 hours. Limitations and errors associated with the use of the scoring systems include missing data, observer error and interobserver variability. Even the method of data collection (manual data entry versus data collected automatically from monitoring systems) leads to wide variations in scores. Although the above scoring systems are useful to assess and compare outcomes in patient populations, such scores may not be appropriate to provide individual risk assessment in critically ill patients.

REFERENCES

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American College of Surgeons Committee on Trauma. Advanced Trauma Life Support® Program for Doctors. (8th edition) American College of Surgeons, Chicago, 2008. Calland V. Safety at Scene. A Manual for Paramedics and Immediate Care Doctors. Mosby, Edinburgh, 2000.

Clasper J, Rew D. Trauma life support in conflict. Br Med J 2003; 327: 1178–9. Commission on the Provision of Surgical Services. The Management of Patients with Major Injuries. The Royal College of Surgeons of England, 1988. Deakin CD, Low JL. Do Advanced Trauma Life Support guidelines accurately predict systolic blood pressure by palpation of carotid, femoral and radial pulses? An observational study. Br Med J 2000; 321: 674–5. Earlam R. Trauma Care. Helicopter Emergency Medical Service (HEMS), London, 1997. Findlay G et al. Compilers. Trauma: Who cares? A report of the National Confidential Enquiry into Patient Outcome and Death (2007). NCEPOD 2007. Flannery T, Buxton N. Modern management of head injuries. J R Coll Surg Edinb 2001; 46: 150–3. Frankema SP, Ringburg AN, Steyerberg EW et al. Beneficial effect of helicopter emergency medical services on survival of severely injured patients. Br J Surg 2004; 91: 1520–6. Hodgetts T, Mahoney P, Russell M, Byers M. ABC to ABC: redefining the military trauma paradigm. Emergency Med J 2006; 23: 745–6. Hodgetts T, Porter C. Major Incident Management System. BMJ Books, London, 2002. Joint Royal Colleges Ambulance Service Liaison Committee (JRCALC) 2008. A Joint Report from the Royal College of Surgeons of England and the British Orthopaedic Association. Better Care for the Severely Injured. The Royal College of Surgeons of England. London, 2000. Knaus WA, Zimmerman JE, Wagner DP. APACHE: Acute Physiology and Chronic Health Evaluation, a physiologically based classification system. Crit Care Med 1981; 16: 470–8. Kortbeek JB, Al Turki SA, Ali J et al. Advanced Trauma Life Support (8th edition) The Evidence for Change. J Trauma 2008; 64: 1638–50. Lee C, Porter K, Hodgetts T. Tourniquet use in the civilian prehospital setting. Emergency Med J 2007; 24: 584–7. Mock C, Lormand JD, Goosen J, Joshipura M, Peden M. Guidelines for Essential Trauma Care. World Health Organization, Geneva, 2004. Mahoney PF, Russell RJ, Russell MQ, Hodgetts TJ. Novel haemostatic techniques in military medicine. J R Army Med Corps 2005; 151: 139–41. National Institute for Clinical Excellence. Pre-hospital initiation of fluid replacement therapy in trauma. Technology Appraisal 74, January 2004. National Institute for Health and Clinical Excellence. Head injury. Triage, assessment, investigation and early management of head injury in infants, children and adults. NICE clinical guideline 56, London, September 2007. Nicholl J, Turner J. Effectiveness of a regional trauma system in reducing mortality from major trauma: before and after study. Br Med J 1997; 315: 1349–54.

Royal College of Surgeons of England. Report of the Working Party on the Management of Patients with Head Injuries. Royal College of Surgeons of England, London, 1999. Schwartz LR, Balakrishnan C. Thermal burns. In: Tintinalli JE, Kelen GD, Stapczynski JS, Ma OJ, Cline DM: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide (6th Edition) The American College of Emergency Physicians, Dallas, Texas, 2004. Williams JS, Graff JA, Uku JM, Steinig JP. Aortic injury in vehicular trauma. Ann Thorac Surg 1994; 57: 726–30.

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Oakley P, Kirby R, Redmond A, Templeton J. Effectiveness of regional trauma systems. Improvements have occurred since study. Br Med J 1998; 316: 1383. Peden M, Scurfield R, Sleet D et al. The World Report on Road Traffic Injury Prevention. World Health Organization, Geneva, 2004. Rabold MB. Frostbite and other localized cold-related injuries In: Tintinalli JE, Kelen GD, Stapczynski JS, Ma OJ, Cline DM. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide (6th Edition) The American College of Emergency Physicians, Dallas, Texas, 2004.

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Principles of fractures Selvadurai Nayagam

Fractures result from: (1) injury; (2) repetitive stress; or (3) abnormal weakening of the bone (a ‘pathological’ fracture).

INTRODUCTION A fracture is a break in the structural continuity of bone. It may be no more than a crack, a crumpling or a splintering of the cortex; more often the break is complete and the bone fragments are displaced. If the overlying skin remains intact it is a closed (or simple) fracture; if the skin or one of the body cavities is breached it is an open (or compound) fracture, liable to contamination and infection.

FRACTURES DUE TO INJURY Most fractures are caused by sudden and excessive force, which may be direct or indirect. With a direct force the bone breaks at the point of impact; the soft tissues also are damaged. A direct blow usually splits the bone transversely or may bend it over a fulcrum so as to create a break with a ‘butterfly’ fragment. Damage to the overlying skin is common; if crushing occurs, the fracture pattern will be comminuted with extensive soft-tissue damage. With an indirect force the bone breaks at a distance from where the force is applied; soft-tissue damage at

HOW FRACTURES HAPPEN Bone is relatively brittle, yet it has sufficient strength and resilience to withstand considerable stress.

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23.1 Mechanism of injury Some fracture patterns suggest the causal mechanism: (a) spiral pattern (twisting); (b) short oblique pattern (compression); (c) triangular ‘butterfly’ fragment (bending) and (d) transverse pattern (tension). Spiral and some (long) oblique patterns are usually due to low-energy indirect injuries; bending and transverse patterns are caused by high-energy direct trauma.

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the fracture site is not inevitable. Although most fractures are due to a combination of forces (twisting, bending, compressing or tension), the x-ray pattern reveals the dominant mechanism: • Twisting causes a spiral fracture; • Compression causes a short oblique fracture. • Bending results in fracture with a triangular ‘butterfly’ fragment; • Tension tends to break the bone transversely; in some situations it may simply avulse a small fragment of bone at the points of ligament or tendon insertion. NOTE: The above description applies mainly to the long bones. A cancellous bone, such as a vertebra or the calcaneum, when subjected to sufficient force, will split or be crushed into an abnormal shape.

FATIGUE OR STRESS FRACTURES These fractures occur in normal bone which is subject to repeated heavy loading, typically in athletes, dancers or military personnel who have gruelling exercise programmes. These high loads create minute deformations that initiate the normal process of remodelling – a combination of bone resorption and new bone formation in accordance with Wolff’s law. When exposure to stress and deformation is repeated and prolonged, resorption occurs faster than replacement and leaves the area liable to fracture. A similar problem occurs in individuals who are on medication that alters the normal balance of bone resorption and replacement; stress fractures are increasingly seen in patients with chronic inflammatory diseases who are on treatment with steroids or methotrexate.

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PATHOLOGICAL FRACTURES Fractures may occur even with normal stresses if the bone has been weakened by a change in its structure (e.g. in osteoporosis, osteogenesis imperfecta or Paget’s disease) or through a lytic lesion (e.g. a bone cyst or a metastasis).

TYPES OF FRACTURE Fractures are variable in appearance but for practical reasons they are divided into a few well-defined groups.

COMPLETE FRACTURES The bone is split into two or more fragments. The fracture pattern on x-ray can help predict behaviour after reduction: in a transverse fracture the fragments usually remain in place after reduction; if it is oblique or spiral, they tend to shorten and re-displace even if the bone is splinted. In an impacted fracture the fragments are jammed tightly together and the fracture line is indistinct. A comminuted fracture is one in which there are more than two fragments; because there is poor interlocking of the fracture surfaces, these are often unstable.

INCOMPLETE FRACTURES Here the bone is incompletely divided and the periosteum remains in continuity. In a greenstick fracture the bone is buckled or bent (like snapping a green

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23.2 Varieties of fracture Complete fractures: (a) transverse; (b) segmental and (c) spiral. Incomplete fractures: (d) buckle or torus and (e,f) greenstick.

CLASSIFICATION OF FRACTURES Sorting fractures into those with similar features brings advantages: it allows any information about a fracture to be applied to others in the group (whether this concerns treatment or prognosis) and it facilitates a common dialogue between surgeons and others involved in the care of such injuries. Traditional classifications, which often bear the originator’s name, are hampered by being applicable to that type of injury only; even then the term is often inaccurately applied, famously in the case of Pott’s fracture, which is often applied to any fracture around the ankle though that is not what Sir Percival Pott implied when he described the injury in 1765. A universal, anatomically based system facilitates communication and the sharing of data from a variety of countries and populations, thus contributing to advances in research and treatment. An alphanumeric classification developed by Müller and colleagues has now been adapted and revised (Muller et al., 1990;

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23.3 Müller’s classification (a) Each long bone has three segments – proximal, diaphyseal and distal; the proximal and distal segments are each defined by a square based on the widest part of the bone. (b,c,d) Diaphyseal fractures may be simple, wedge or complex. (e,f,g) Proximal and distal fractures may be extra-articular, partial articular of complete articular.

Marsh et al., 2007; Slongo and Audige 2007). Whilst it has yet to be fully validated for reliability and reproducibility, it fulfils the objective of being comprehensive. In this system, the first digit specifies the bone (1 = humerus, 2 = radius/ulna, 3 = femur, 4 = tibia/fibula) and the second the segment (1 = proximal, 2 = diaphyseal, 3 = distal, 4 = malleolar). A letter specifies the fracture pattern (for the diaphysis: A = simple, B = wedge, C = complex; for the metaphysis: A = extra-articular, B = partial articular, C = complete articular). Two further numbers specify the detailed morphology of the fracture (Fig. 23.3).

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Principles of fractures

twig); this is seen in children, whose bones are more springy than those of adults. Children can also sustain injuries where the bone is plastically deformed (misshapen) without there being any crack visible on the x-ray. In contrast, compression fractures occur when cancellous bone is crumpled. This happens in adults and typically where this type of bone structure is present, e.g. in the vertebral bodies, calcaneum and tibial plateau.

After a complete fracture the fragments usually become displaced, partly by the force of the injury, partly by gravity and partly by the pull of muscles attached to them. Displacement is usually described in terms of translation, alignment, rotation and altered length: • Translation (shift) – The fragments may be shifted sideways, backward or forward in relation to each other, such that the fracture surfaces lose contact. The fracture will usually unite as long as sufficient contact between surfaces is achieved; this may occur even if reduction is imperfect, or indeed even if the fracture ends are off-ended but the bone segments come to lie side by side. • Angulation (tilt) – The fragments may be tilted or angulated in relation to each other. Malalignment, if uncorrected, may lead to deformity of the limb. • Rotation (twist) – One of the fragments may be twisted on its longitudinal axis; the bone looks straight but the limb ends up with a rotational deformity. • Length – The fragments may be distracted and separated, or they may overlap, due to muscle spasm, causing shortening of the bone.

HOW FRACTURES HEAL It is commonly supposed that, in order to unite, a fracture must be immobilized. This cannot be so since, with few exceptions, fractures unite whether they are splinted or not; indeed, without a built-in mechanism for bone union, land animals could scarcely have evolved. It is, however, naive to suppose that union would occur if a fracture were kept moving indefinitely; the bone ends must, at some stage, be brought to rest relative to one another. But it is not mandatory for the surgeon to impose this immobility artificially – nature can do it with callus, and callus forms in response to movement, not to splintage.

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Most fractures are splinted, not to ensure union but to: (1) alleviate pain; (2) ensure that union takes place in good position and (3) permit early movement of the limb and a return of function. The process of fracture repair varies according to the type of bone involved and the amount of movement at the fracture site.

5. Remodelling – The fracture has been bridged by a cuff of solid bone. Over a period of months, or even years, this crude ‘weld’ is reshaped by a continuous process of alternating bone resorption and formation. Thicker lamellae are laid down where the stresses are high, unwanted buttresses are carved away and the medullary cavity is reformed. Eventually, and especially in children, the bone reassumes something like its normal shape.

HEALING BY CALLUS This is the ‘natural’ form of healing in tubular bones; in the absence of rigid fixation, it proceeds in five stages: 1. Tissue destruction and haematoma formation – Vessels are torn and a haematoma forms around and within the fracture. Bone at the fracture surfaces, deprived of a blood supply, dies back for a millimetre or two. 2. Inflammation and cellular proliferation – Within 8 hours of the fracture there is an acute inflammatory reaction with migration of inflammatory cells and the initiation of proliferation and differentiation of mesenchymal stem cells from the periosteum, the breached medullary canal and the surrounding muscle. The fragment ends are surrounded by cellular tissue, which creates a scaffold across the fracture site. A vast array of inflammatory mediators (cytokines and various growth factors) is involved. The clotted haematoma is slowly absorbed and fine new capillaries grow into the area. 3. Callus formation – The differentiating stem cells provide chrondrogenic and osteogenic cell populations; given the right conditions – and this is usually the local biological and biomechanical environment – they will start forming bone and, in some cases, also cartilage. The cell population now also includes osteoclasts (probably derived from the new blood vessels), which begin to mop up dead bone. The thick cellular mass, with its islands of immature bone and cartilage, forms the callus or splint on the periosteal and endosteal surfaces. As the immature fibre bone (or ‘woven’ bone) becomes more densely mineralized, movement at the fracture site decreases progressively and at about 4 weeks after injury the fracture ‘unites’. 4. Consolidation – With continuing osteoclastic and osteoblastic activity the woven bone is transformed into lamellar bone. The system is now rigid enough to allow osteoclasts to burrow through the debris at the fracture line, and close behind them. Osteoblasts fill in the remaining gaps between the fragments with new bone. This is a slow process and it may be several months before the bone is strong enough to carry normal loads.

HEALING BY DIRECT UNION Clinical and experimental studies have shown that callus is the response to movement at the fracture site (McKibbin, 1978). It serves to stabilize the fragments as rapidly as possible – a necessary precondition for bridging by bone. If the fracture site is absolutely immobile – for example, an impacted fracture in cancellous bone, or a fracture rigidly immobilized by a metal plate – there is no stimulus for callus (Sarmiento et al., 1980). Instead, osteoblastic new bone formation occurs directly between the fragments. Gaps between the fracture surfaces are invaded by new capillaries and osteoprogenitor cells growing in from the edges, and new bone is laid down on the exposed surface (gap healing). Where the crevices are very narrow (less than 200 μm), osteogenesis produces lamellar bone; wider gaps are filled first by woven bone, which is then remodelled to lamellar bone. By 3–4 weeks the fracture is solid enough to allow penetration and bridging of the area by bone remodelling units, i.e. osteoclastic ‘cutting cones’ followed by osteoblasts. Where the exposed fracture surfaces are in intimate contact and held rigidly from the outset, internal bridging may occasionally occur without any intermediate stages (contact healing). Healing by callus, though less direct (the term ‘indirect’ could be used) has distinct advantages: it ensures mechanical strength while the bone ends heal, and with increasing stress the callus grows stronger and stronger (an example of Wolff’s law). With rigid metal fixation, on the other hand, the absence of callus means that there is a long period during which the bone depends entirely upon the metal implant for its integrity. Moreover, the implant diverts stress away from the bone, which may become osteoporotic and not recover fully until the metal is removed.

UNION, CONSOLIDATION AND NON-UNION Repair of a fracture is a continuous process: any stages into which it is divided are necessarily arbitrary. In this book the terms ‘union’ and ‘consolidation’ are used, and they are defined as follows:

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Principles of fractures

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23.4 Fracture healing Five stages of healing: (a) Haematoma: there is tissue damage and bleeding at the fracture site; the bone ends die back for a few millimetres. (b) Inflammation: inflammatory cells appear in the haematoma. (c) Callus: the cell population changes to osteoblasts and osteoclasts; dead bone is mopped up and woven bone appears in the fracture callus. (d) Consolidation: woven bone is replaced by lamellar bone and the fracture is solidly united. (e) Remodelling: the newly formed bone is remodelled to resemble the normal structure.

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23.5 Fracture healing – histology Experimental fracture healing: (a) by bridging callus and (b) by direct penetration of the fracture gap by a cutting cone.

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23.6 Callus and movement Three patients with femoral shaft fractures. (a) and (b) are both 6 weeks after fixation: in (a) the Kuntscher nail fitted tightly, preventing movement, and there is no callus; in (b) the nail fitted loosely, permitting some movement, so there is callus. (c) This patient had cerebral irritation and thrashed around wildly; at 3 weeks callus is excessive.

23.7 Fracture repair (a) Fracture; (b) union; (c) consolidation; (d) bone remodelling. The fracture must be protected until consolidated. (a)

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23.8 Non-unions Aseptic non-unions are generally divided into hypertrophic and atrophic types. Hypertrophic non-unions often have florid streams of callus around the fracture gap – the result of insufficient stability. They are sometimes given colourful names, such as: (a) elephant’s foot. In contrast, atrophic non-unions usually arise from an impaired repair process; they are classified according to the x-ray appearance as (b) necrotic, (c) gap and (d) atrophic.

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• Union – Union is incomplete repair; the ensheathing callus is calcified. Clinically the fracture site is still a little tender and, though the bone moves in one piece (and in that sense is united), attempted angulation is painful. X-Rays show the fracture line still clearly visible, with fluffy callus around it. Repair is incomplete and it is not safe to subject the unprotected bone to stress. • Consolidation – Consolidation is complete repair; the calcified callus is ossified. Clinically the fracture site is not tender, no movement can be obtained and attempted angulation is painless. X-rays show the fracture line to be almost obliterated and crossed by bone trabeculae, with well-defined callus around it. Repair is complete and further protection is unnecessary. • Timetable – How long does a fracture take to unite and to consolidate? No precise answer is possible because age, constitution, blood supply, type of fracture and other factors all influence the time taken. Approximate prediction is possible and Perkins’ timetable is delightfully simple. A spiral fracture in the upper limb unites in 3 weeks; for consolidation multiply by 2; for the lower limb multiply by 2 again; for transverse fractures multiply again by 2. A more sophisticated formula is as follows. A spiral fracture in the upper limb takes 6–8 weeks to consolidate; the lower limb needs twice as long. Add 25% if the fracture is not spiral or if it involves the femur. Children’s fractures, of course, join more quickly. These figures are only a rough guide; there must be clinical and radiological evidence of consolidation before full stress is permitted without splintage. • Non-union – Sometimes the normal process of fracture repair is thwarted and the bone fails to unite. Causes of non-union are: (1) distraction and separation of the fragments, sometimes the result of interposition of soft tissues between the fragments; (2) excessive movement at the fracture line; (3) a severe injury that renders the local tissues nonviable or nearly so; (4) a poor local blood supply

and (5) infection. Of course surgical intervention, if ill-judged, is another cause! Non-unions are septic or aseptic. In the latter group, they can be either stiff or mobile as judged by clinical examination. The mobile ones can be as free and painless as to give the impression of a false joint (pseudoarthrosis). On x-ray, non-unions are typified by a lucent line still present between the bone fragments; sometimes there is exuberant callus trying – but failing – to bridge the gap (hypertrophic non-union) or at times none at all (atrophic non-union) with a sorry, withered appearance to the fracture ends.

CLINICAL FEATURES

HISTORY There is usually a history of injury, followed by inability to use the injured limb – but beware! The fracture is not always at the site of the injury: a blow to the knee may fracture the patella, femoral condyles, shaft of the femur or even acetabulum. The patient’s age and mechanism of injury are important. If a fracture occurs with trivial trauma, suspect a pathological lesion. Pain, bruising and swelling are common symptoms but they do not distinguish a fracture from a soft-tissue injury. Deformity is much more suggestive. Always enquire about symptoms of associated injuries: pain and swelling elsewhere (it is a common mistake to get distracted by the main injury, particularly if it is severe), numbness or loss of movement, skin pallor or cyanosis, blood in the urine, abdominal pain, difficulty with breathing or transient loss of consciousness. Once the acute emergency has been dealt with, ask about previous injuries, or any other musculoskeletal abnormality that might cause confusion when the x-ray is seen. Finally, a general medical history is important, in preparation for anaesthesia or operation.

GENERAL SIGNS

LOCAL SIGNS Injured tissues must be handled gently. To elicit crepitus or abnormal movement is unnecessarily painful; x-ray diagnosis is more reliable. Nevertheless the familiar headings of clinical examination should always be considered, or damage to arteries, nerves and ligaments may be overlooked. A systematic approach is always helpful: • • • •

Examine the most obviously injured part. Test for artery and nerve damage. Look for associated injuries in the region. Look for associated injuries in distant parts.

Look Swelling, bruising and deformity may be obvious, but the important point is whether the skin is intact; if the skin is broken and the wound communicates with the fracture, the injury is ‘open’ (‘compound’). Note also the posture of the distal extremity and the colour of the skin (for tell-tale signs of nerve or vessel damage).

Feel The injured part is gently palpated for localized tenderness. Some fractures would be missed if not specifically looked for, e.g. the classical sign (indeed the only clinical sign!) of a fractured scaphoid is tenderness on pressure precisely in the anatomical snuff-box. The common and characteristic associated injuries should also be felt for, even if the patient does not complain of them. For example, an isolated fracture of the proximal fibula should always alert to the likelihood of an associated fracture or ligament injury of the ankle, and in high-energy injuries always examine the spine and pelvis. Vascular and peripheral nerve abnormalities should be tested for both before and after treatment.

Move Crepitus and abnormal movement may be present, but why inflict pain when x-rays are available? It is

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X-RAY X-ray examination is mandatory. Remember the rule of twos: • Two views – A fracture or a dislocation may not be seen on a single x-ray film, and at least two views (anteroposterior and lateral) must be taken. • Two joints – In the forearm or leg, one bone may be fractured and angulated. Angulation, however, is impossible unless the other bone is also broken, or a joint dislocated. The joints above and below the fracture must both be included on the x-ray films. • Two limbs – In children, the appearance of immature epiphyses may confuse the diagnosis of a fracture; x-rays of the uninjured limb are needed for comparison. • Two injuries – Severe force often causes injuries at more than one level. Thus, with fractures of the calcaneum or femur it is important to also x-ray the pelvis and spine. • Two occasions – Some fractures are notoriously difficult to detect soon after injury, but another x-ray examination a week or two later may show the lesion. Common examples are undisplaced fractures of the distal end of the clavicle, scaphoid, femoral neck and lateral malleolus, and also stress fractures and physeal injuries wherever they occur.

Principles of fractures

Unless it is obvious from the history that the patient has sustained a localized and fairly modest injury, priority must be given to dealing with the general effects of trauma (see Chapter 22). Follow the ABCs: look for, and if necessary attend to, Airway obstruction, Breathing problems, Circulatory problems and Cervical spine injury. During the secondary survey it will also be necessary to exclude other previously unsuspected injuries and to be alert to any possible predisposing cause (such as Paget’s disease or a metastasis).

more important to ask if the patient can move the joints distal to the injury.

SPECIAL IMAGING Sometimes the fracture – or the full extent of the fracture – is not apparent on the plain x-ray. Computed tomography may be helpful in lesions of the spine or for complex joint fractures; indeed, these crosssectional images are essential for accurate visualization of fractures in ‘difficult’ sites such as the calcaneum or acetabulum. Magnetic resonance imaging may be the only way of showing whether a fractured vertebra is threatening to compress the spinal cord. Radioisotope scanning is helpful in diagnosing a suspected stress fracture or other undisplaced fractures.

DESCRIPTION Diagnosing a fracture is not enough; the surgeon should picture it (and describe it) with its properties: (1) Is it open or closed? (2) Which bone is broken, and where? (3) Has it involved a joint surface? (4) What is the shape of the break? (5) Is it stable or unstable? (6) Is it a high-energy or a low-energy

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23.9 X-ray examination must be ‘adequate’ (a,b) Two films of the same tibia: the fracture may be ‘invisible’ in one view and perfectly plain in a view at right angles to that. (c,d) More than one occasion: A fractured scaphoid may not be obvious on the day of injury, but clearly seen 2 weeks later. (e,f) Two joints: The first x-ray (e) did not include the elbow. This was, in fact, a Monteggia fracture – the head of the radius is dislocated; (f) shows the dislocated radiohumeral joint. (g,h) Two limbs: Sometimes the abnormality can be appreciated only by comparision with the normal side; in this case there is a fracture of the lateral condyle on the left side (h).

injury? And last but not least (7) who is the person with the injury? In short, the examiner must learn to recognize what has been aptly described as the ‘personality’ of the fracture.

Shape of the fracture A transverse fracture is slow to join because the area of contact is small; if the broken surfaces are accurately apposed, however, the fracture is stable on compression. A spiral fracture joins more rapidly (because the contact area is large) but is not stable on compression. Comminuted fractures are often slow to join because: (1) they are associated with more severe softtissue damage and (2) they are likely to be unstable.

Displacement 694

For every fracture, three components must be assessed:

1. Shift or translation – backwards, forwards, sideways, or longitudinally with impaction or overlap. 2. Tilt or angulation – sideways, backwards or forwards. 3. Twist or rotation – in any direction. A problem often arises in the description of angulation. ‘Anterior angulation’ could mean that the apex of the angle points anteriorly or that the distal fragment is tilted anteriorly: in this text it is always the latter meaning that is intended (‘anterior tilt of the distal fragment’ is probably clearer).

SECONDARY INJURIES Certain fractures are apt to cause secondary injuries and these should always be assumed to have occurred until proved otherwise:

TREATMENT OF CLOSED FRACTURES General treatment is the first consideration: treat the patient, not only the fracture. The principles are discussed in Chapter 22. Treatment of the fracture consists of manipulation to improve the position of the fragments, followed by splintage to hold them together until they unite; meanwhile joint movement and function must be preserved. Fracture healing is promoted by physiological loading of the bone, so muscle activity and early weightbearing are encouraged. These objectives are covered by three simple injunctions: • Reduce. • Hold. • Exercise. Two existential problems have to be overcome. The first is how to hold a fracture adequately and yet permit the patient to use the limb sufficiently; this is a conflict (Hold versus Move) that the surgeon seeks to resolve as rapidly as possible (e.g. by internal fixation). However the surgeon also wants to avoid unnecessary risks – here is a second conflict (Speed versus Safety). This dual conflict epitomizes the four factors that dominate fracture management (the term ‘fracture quartet’ seems appropriate). The fact that the fracture is closed (and not open) is no cause for complacency. The most important factor in determining the natural tendency to heal is the state of the surrounding soft tissues and the local blood supply. Low-energy (or low-velocity) fractures cause only moderate soft-tissue damage; high-energy (velocity) fractures cause severe soft-tissue damage, no matter whether the fracture is open or closed.

Tscherne (Oestern and Tscherne, 1984) has devised a helpful classification of closed injuries: • Grade 0 – a simple fracture with little or no softtissue injury. • Grade 1 – a fracture with superficial abrasion or bruising of the skin and subcutaneous tissue. • Grade 2 – a more severe fracture with deep softtissue contusion and swelling. • Grade 3 – a severe injury with marked soft-tissue damage and a threatened compartment syndrome. The more severe grades of injury are more likely to require some form of mechanical fixation; good skeletal stability aids soft-tissue recovery.

23

Principles of fractures

• Thoracic injuries – Fractured ribs or sternum may be associated with injury to the lungs or heart. It is essential to check cardiorespiratory function. • Spinal cord injury – With any fracture of the spine, neurological examination is essential to: (1) establish whether the spinal cord or nerve roots have been damaged and (2) obtain a baseline for later comparison if neurological signs should change. • Pelvic and abdominal injuries – Fractures of the pelvis may be associated with visceral injury. It is especially important to enquire about urinary function; if a urethral or bladder injury is suspected, diagnostic urethrograms or cystograms may be necessary. • Pectoral girdle injuries – Fractures and dislocations around the pectoral girdle may damage the brachial plexus or the large vessels at the base of the neck. Neurological and vascular examination is essential.

REDUCTION Although general treatment and resuscitation must always take precedence, there should not be undue delay in attending to the fracture; swelling of the soft parts during the first 12 hours makes reduction increasingly difficult. However, there are some situations in which reduction is unnecessary: (1) when there is little or no displacement; (2) when displacement does not matter initially (e.g. in fractures of the clavicle) and (3) when reduction is unlikely to succeed (e.g. with compression fractures of the vertebrae). Reduction should aim for adequate apposition and normal alignment of the bone fragments. The greater the contact surface area between fragments the more likely healing is to occur. A gap between the fragment ends is a common cause of delayed union or nonunion. On the other hand, so long as there is contact and the fragments are properly aligned, some overlap at the fracture surfaces is permissible. The exception is a fracture involving an articular surface; this should be reduced as near to perfection as possible because any irregularity will cause abnormal load distribution between the surfaces and predispose to degenerative changes in the articular cartilage. There are two methods of reduction: closed and open.

CLOSED REDUCTION Under appropriate anaesthesia and muscle relaxation, the fracture is reduced by a three-fold manoeuvre: (1) the distal part of the limb is pulled in the line of the bone; (2) as the fragments disengage, they are repositioned (by reversing the original direction of force if this can be deduced) and (3) alignment is adjusted in each plane. This is most effective when the periosteum and muscles on one side of the fracture remain intact; the soft-tissue strap prevents over-reduction

695

better alignment to be obtained; this practice is helpful for femoral and tibial shaft fractures and even supracondylar humeral fractures in children. In general, closed reduction is used for all minimally displaced fractures, for most fractures in children and for fractures that are not unstable after reduction and can be held in some form of splint or cast. Unstable fractures can also be reduced using closed methods prior to stabilization with internal or external fixation. This avoids direct manipulation of the fracture site by open reduction, which damages the local blood supply and may lead to slower healing times; increasingly, surgeons resort to reduction manoeuvres that avoid fracture-site exposure, even when the aim is some form of internal or external fixation. Traction, which reduces fracture fragments through ligamentotaxis (ligament pull), can usually be applied by using a fracture table or bone distractor.

FRACTURES AND JOINT INJURIES

23

(a)

(b)

OPEN REDUCTION Operative reduction of the fracture under direct vision is indicated: (1) when closed reduction fails, either because of difficulty in controlling the fragments or because soft tissues are interposed between them; (2) when there is a large articular fragment that needs accurate positioning or (3) for traction (avulsion) fractures in which the fragments are held apart. As a rule, however, open reduction is merely the first step to internal fixation.

(c)

23.10 Closed reduction (a) Traction in the line of the bone. (b) Disimpaction. (c) Pressing fragment into reduced position.

and stabilizes the fracture after it has been reduced (Charnley 1961). Some fractures are difficult to reduce by manipulation because of powerful muscle pull and may need prolonged traction. Skeletal or skin traction for several days allows for soft-tissue tension to decrease and a

(b)

696

(a)

HOLD REDUCTION The word ‘immobilization’ has been deliberately avoided because the objective is seldom complete immobility; usually it is the prevention of displacement. Nevertheless, some restriction of movement is needed to promote soft-tissue healing and to allow free movement of the unaffected parts.

23.11 Closed reduction These two ankle fractures look somewhat similar but are caused by different forces. The causal force must be reversed to achieve reduction: (a) requires internal rotation (b); an adduction force (c) is needed for (d).

(c)

(d)

HOLD SPEED SAFETY

MOVE

23.13 Continuous traction ‘Speed’ is the weak member of the quartet.

The available methods of holding reduction are: • • • • •

Continuous traction. Cast splintage. Functional bracing. Internal fixation. External fixation.

In the modern technological age, ‘closed’ methods are often scorned – an attitude arising from ignorance rather than experience. The muscles surrounding a fracture, if they are intact, act as a fluid compartment; traction or compression creates a hydraulic effect that is capable of splinting the fracture. Therefore closed methods are most suitable for fractures with intact soft tissues, and are liable to fail if they are used as the primary method of treatment for fractures with severe soft-tissue damage. Other contraindications to nonoperative methods are inherently unstable fractures, multiple fractures and fractures in confused or uncooperative patients. If these constraints are borne in mind, closed reduction can be sensibly considered in choosing the most suitable method of fracture splintage. Remember, too, that the objective is to splint the fracture, not the entire limb!

CONTINUOUS TRACTION Traction is applied to the limb distal to the fracture, so as to exert a continuous pull in the long axis of the bone, with a counterforce in the opposite direction (to prevent the patient being merely dragged along the bed). This is particularly useful for shaft fractures that are oblique or spiral and easily displaced by muscle contraction.

• Traction by gravity – This applies only to upper limb injuries. Thus, with a wrist sling the weight of the arm provides continuous traction to the humerus. For comfort and stability, especially with a transverse fracture, a U-slab of plaster may be bandaged on or, better, a removable plastic sleeve from the axilla to just above the elbow is held on with Velcro. • Skin traction – Skin traction will sustain a pull of no more than 4 or 5 kg. Holland strapping or oneway-stretch Elastoplast is stuck to the shaved skin and held on with a bandage. The malleoli are protected by Gamgee tissue, and cords or tapes are used for traction. • Skeletal traction – A stiff wire or pin is inserted – usually behind the tibial tubercle for hip, thigh and knee injuries, or through the calcaneum for tibial fractures – and cords tied to them for applying traction. Whether by skin or skeletal traction, the fracture is reduced and held in one of three ways: fixed traction, balanced traction or a combination of the two.

23

Principles of fractures

23.12 Hold reduction Showing how, if the soft tissues around a fracture are intact, traction will align the bony fragments.

Traction cannot hold a fracture still; it can pull a long bone straight and hold it out to length but to maintain accurate reduction is sometimes difficult. Meanwhile the patient can move the joints and exercise the muscles. Traction is safe enough, provided it is not excessive and care is taken when inserting the traction pin. The problem is speed: not because the fracture unites slowly (it does not) but because lower limb traction keeps the patient in hospital. Consequently, as soon as the fracture is ‘sticky’ (deformable but not displaceable), traction should be replaced by bracing, if this method is feasible. Traction includes:

Fixed traction The pull is exerted against a fixed point. The usual method is to tie the traction cords to the distal end of a Thomas’ splint and pull the leg down until the proximal, padded ring of the splint abuts firmly against the pelvis.

Balanced traction Here the traction cords are guided over pulleys at the foot of the bed and loaded with weights; counter-traction is provided by the weight of the body when the foot of the bed is raised.

Combined traction If a Thomas’ splint is used, the tapes are tied to the end of the splint and the entire splint is then suspended, as in balanced traction.

697

FRACTURES AND JOINT INJURIES

23

23.14 Methods of traction (a) Traction by gravity. (b,c,d) Skin traction: (b) fixed; (c) balanced; (d) Russell. (e) Skeletal traction with a splint and a knee-flexion piece.

(a)

(b)

(d)

(c)

(e)

Complications of traction In children especially, traction tapes and circular bandages may constrict the circulation; for this reason ‘gallows traction’, in which the baby’s legs are suspended from an overhead beam, should never be used for children over 12 kg in weight. Circulatory

In older people, leg traction may predispose to peroneal nerve injury and cause a dropfoot; the limb should be checked repeatedly to see that it does not roll into external rotation during traction.

Nerve injury

Pin sites must be kept clean and should be checked daily.

Pin site infection

CAST SPLINTAGE

698

HOLD

embarrassment

Plaster of Paris is still widely used as a splint, especially for distal limb fractures and for most children’s fractures. It is safe enough, so long as the practitioner is alert to the danger of a tight cast and provided pressure sores are prevented. The speed of union is neither greater nor less than with traction, but the patient can go home sooner. Holding reduction is usually no problem and patients with tibial fractures can bear weight on the cast. However, joints encased in plaster

SPEED

SAFETY MOVE

23.15 Casts ‘Move’ is the weakest member of the quartet.

cannot move and are liable to stiffen; stiffness, which has earned the sobriquet ‘fracture disease’, is the problem with conventional casts. While the swelling and haematoma resolve, adhesions may form that bind muscle fibres to each other and to the bone; with articular fractures, plaster perpetuates surface irregularities (closed reduction is seldom perfect) and lack of movement inhibits the healing of cartilage defects. Newer substitutes have some advantages over plaster (they are impervious to water, and also lighter) but as long as they are used as full casts the basic drawback is the same. Stiffness can be minimized by: (1) delayed splintage – that is, by using traction until movement has been regained, and only then applying plaster; or (2)

23

(b)

(c)

(d)

(e)

(f)

(g)

(h)

(i)

Principles of fractures

(a)

23.16 Plaster technique Applying a well-fitting and effective plaster needs experience and attention to detail. (a) A well-equipped plaster trolley is invaluable. (b) Adequate anaesthesia and careful study of the x-ray films are both indispensable. (c) For a below-knee plaster the thigh is best supported on a padded block. (d) Stockinette is threaded smoothly onto the leg. (e) For a padded plaster the wool is rolled on and it must be even. (f) Plaster is next applied smoothly, taking a tuck with each turn, and (g) smoothing each layer firmly onto the one beneath. (h) While still wet the cast is moulded away from the point points. (i) With a recent injury the plaster is then split.

starting with a conventional cast but, after a few weeks, when the limb can be handled without too much discomfort, replacing the cast by a functional brace which permits joint movement.

Technique After the fracture has been reduced, stockinette is threaded over the limb and the bony points are protected with wool. Plaster is then applied. While it is setting the surgeon moulds it away from bony prominences; with shaft fractures three-point pressure can be applied to keep the intact periosteal hinge under tension and thereby maintain reduction. If the fracture is recent, further swelling is likely; the plaster and stockinette are therefore split from top to bottom, exposing the skin. Check x-rays are essential and the plaster can be wedged if further correction of angulation is necessary. With fractures of the shafts of long bones, rotation is controlled only if the plaster includes the joints above and below the fracture. In the lower limb, the knee is usually held slightly flexed, the ankle at a right

angle and the tarsus and forefoot neutral (this ‘plantigrade’ position is essential for normal walking). In the upper limb the position of the splinted joints varies with the fracture. Splintage must not be discontinued (though a functional brace may be substituted) until the fracture is consolidated; if plaster changes are needed, check x-rays are essential.

Complications Plaster immobilization is safe, but only if care is taken to prevent certain complications. These are tight cast, pressure sores and abrasion or laceration of the skin. Tight cast The cast may be put on too tightly, or it may

become tight if the limb swells. The patient complains of diffuse pain; only later – sometimes much later – do the signs of vascular compression appear. The limb should be elevated, but if the pain persists, the only safe course is to split the cast and ease it open: (1) throughout its length and (2) through all the padding down to skin. Whenever swelling is anticipated the cast should be applied over thick padding and the plaster

699

FRACTURES AND JOINT INJURIES

23

23.17 Functional bracing (cast bracing) Despite plaster the patient has excellent joint movement. (Courtesy of Dr John A Feagin).

should be split before it sets, so as to provide a firm but not absolutely rigid splint.

Loose cast Once the swelling has subsided, the cast may no longer hold the fracture securely. If it is loose, the cast should be replaced.

Considerable skill is needed to apply an effective brace. First the fracture is ‘stabilized’: by a few days on traction or in a conventional plaster for tibial fractures; and by a few weeks on traction for femoral fractures (until the fracture is sticky, i.e. deformable but not displaceable). Then a hinged cast or splint is applied, which holds the fracture snugly but permits joint movement; functional activity, including weightbearing, is encouraged. Unlike internal fixation, functional bracing holds the fracture through compression of the soft tissues; the small amount of movement that occurs at the fracture site through using the limb encourages vascular proliferation and callus formation. Details of the rationale, technique and applications are given by Sarmiento and Latta (Sarmiento and Latta 1999, 2006).

FUNCTIONAL BRACING

INTERNAL FIXATION

Functional bracing, using either plaster of Paris or one of the lighter thermoplastic materials, is one way of preventing joint stiffness while still permitting fracture splintage and loading. Segments of a cast are applied only over the shafts of the bones, leaving the joints free; the cast segments are connected by metal or plastic hinges that allow movement in one plane. The splints are ‘functional’ in that joint movements are much less restricted than with conventional casts. Functional bracing is used most widely for fractures of the femur or tibia, but since the brace is not very rigid, it is usually applied only when the fracture is beginning to unite, i.e. after 3–6 weeks of traction or conventional plaster. Used in this way, it comes out well on all four of the basic requirements: the fracture can be held reasonably well; the joints can be moved; the fracture joins at normal speed (or perhaps slightly quicker) without keeping the patient in hospital and the method is safe.

Bone fragments may be fixed with screws, a metal plate held by screws, a long intramedullary rod or nail (with or without locking screws), circumferential bands or a combination of these methods. Properly applied, internal fixation holds a fracture securely so that movement can begin at once; with early movement the ‘fracture disease’ (stiffness and

Pressure sores Even a well-fitting cast may press upon

the skin over a bony prominence (the patella, heel, elbow or head of the ulna). The patient complains of localized pain precisely over the pressure spot. Such localized pain demands immediate inspection through a window in the cast. Skin abrasion or laceration This is really a complication of removing plasters, especially if an electric saw is used. Complaints of nipping or pinching during plaster removal should never be ignored; a ripped forearm is a good reason for litigation.

700

Technique

HOLD SAFETY SPEED

MOVE

23.18 Internal fixation ‘Safety’ is the weak member of the quartet.

23

COULD be fixed

SHOULD be fixed

K

C

A

B

MUST be fixed

L

(a)

(b)

(b)

(d)

IL

K

S

23.19 Indications staircase The indications for fixation are not immutable; thus, if the surgical skill or back-up facilities (staff, sterility and equipment) are of a low order, internal fixation is indicated only when the alternative is unacceptable (e.g. with femoral neck fractures). With average skill and facilities, fixation is indicated when alternative methods are possible but very difficult or unwise (e.g. multiple injuries). With the highest levels of skill and facilities, fixation is reasonable if it saves time, money or beds.

oedema) is abolished. As far as speed is concerned, the patient can leave hospital as soon as the wound is healed, but he must remember that, even though the bone moves in one piece, the fracture is not united – it is merely held by a metal bridge and unprotected weightbearing is, for some time, unsafe. The greatest danger, however, is sepsis; if infection supervenes, all the manifest advantages of internal fixation (precise reduction, immediate stability and early movement) may be lost. The risk of infection depends upon: (1) the patient – devitalized tissues, a dirty wound and an unfit patient are all dangerous; (2) the surgeon – thorough training, a high degree of surgical dexterity and adequate assistance are all essential and (3) the facilities – a guaranteed aseptic routine, a full range of implants and staff familiar with their use are all indispensable.

Indications

Principles of fractures

P

-U

23.20 Indications for internal fixation (a) This patella has been pulled apart and can be held together only be internal fixation. (b) Fracture dislocation of the ankle is often unstable after reduction and usually requires fixation. (c) This patient was considered to be too ill for operation; her femoral neck fracture has failed to unite without rigid fixation. (d) Pathological fracture in Paget bone; without fixation, union may not occur.

fractures). Also included are those fractures liable to be pulled apart by muscle action (e.g. transverse fracture of the patella or olecranon). 3. Fractures that unite poorly and slowly, principally fractures of the femoral neck. 4. Pathological fractures in which bone disease may prevent healing. 5. Multiple fractures where early fixation (by either internal or external fixation) reduces the risk of general complications and late multisystem organ failure (Pape et al., 2005; Roberts et al., 2005). 6. Fractures in patients who present nursing difficulties (paraplegics, those with multiple injuries and the very elderly).

Internal fixation is often the most desirable form of treatment. The chief indications are: 1. Fractures that cannot be reduced except by operation. 2. Fractures that are inherently unstable and prone to re-displace after reduction (e.g. mid-shaft fractures of the forearm and some displaced ankle

Types of internal fixation Interfragmentary screws Screws that are only partially threaded (a similar effect is achieved by overdrilling the ‘near’ cortex of bone) exert a compression or ‘lag’ effect when inserted across two fragments. The

701

23

technique is useful for reducing single fragments onto the main shaft of a tubular bone or fitting together fragments of a metaphyseal fracture.

FRACTURES AND JOINT INJURIES

Wires (transfixing, cerclage and tension-band) Transfixing

wires, often passed percutaneously, can hold major fracture fragments together. They are used in situations where fracture healing is predictably quick (e.g. in children or for distal radius fractures), and some form of external splintage (usually a cast) is applied as supplementary support. Cerclage and tension-band wires are essentially loops of wire passed around two bone fragments and then tightened to compress the fragments together. When using cerclage wires, make sure that the wires hug the bone and do not embrace any of the closelying nerves or vessels. Both techniques are used for patellar fractures: the tension-band wire is placed such that the maximum compressive force is over the tensile surface, which is usually the convex side of the bone. Plates and screws This form of fixation is useful for treating metaphyseal fractures of long bones and diaphyseal fractures of the radius and ulna. Plates have five different functions:

1. Neutralization – when used to bridge a fracture and supplement the effect of interfragmentary lag screws; the plate is to resist torque and shortening. 2. Compression – often used in metaphyseal fractures where healing across the cancellous fracture gap may occur directly, without periosteal callus. This technique is less appropriate for diaphyseal fractures and there has been a move towards the use of long plates that span the fracture, thus achieving some stability without totally sacrificing the biological (and callus producing) effect of movement. 3. Buttressing – here the plate props up the ‘overhang’ of the expanded metaphyses of long bones (e.g. in treating fractures of the proximal tibial plateau). 4. Tension-band – using a plate in this manner, again on the tensile surface of the bone, allows compression to be applied to the biomechanically more advantageous side of the fracture. 5. Anti-glide – by fixing a plate over the tip of a spiral or oblique fracture line and then using the plate as a reduction aid, the anatomy is 23.21 Internal fixation The method used must be appropriate to the situation: (a) screws – interfragmentary compression; (b) plate and screws – most suitable in the forearm or around the metaphysis; (c) flexible intramedullary nails – for long bones in children, particularly forearm bones and the femur; (d) interlocking nail and screws – ideal for the femur and tibia; (e) dynamic compression screw and plate – ideal for the proximal and distal ends of the femur; (f) simple K-wires – for fractures around the elbow and wrist and (g) tension-band wiring – for olecranon or fractures of the patella.

(a)

702

(d)

(b)

(e)

(c)

(f)

(g)

23.22 Bad fixation (how not to do it) (a) Too little. (b) Too much. (c) Too weak.

23

Principles of fractures

(a)

(b)

(c)

restored with minimal stripping of soft tissues. The position of the plate acts to prevent shortening and recurrent displacement of the fragments. Intramedullary nails These are suitable for long bones. A nail (or long rod) is inserted into the medullary canal to splint the fracture; rotational forces are resisted by introducing transverse interlocking screws that transfix the bone cortices and the nail proximal and distal to the fracture. Nails are used with or without prior reaming of the medullary canal; reamed nails achieve an interference fit in addition to the added stability from interlocking screws, but at the expense of temporary loss of the intramedullary blood supply.

Complications of internal fixation Most of the complications of internal fixation are due to poor technique, poor equipment or poor operating conditions: Infection Iatrogenic infection is now the most com-

mon cause of chronic osteomyelitis; the metal does not predispose to infection but the operation and quality of the patient’s tissues do. Non-union If the bones have been fixed rigidly with a gap between the ends, the fracture may fail to unite. This is more likely in the leg or the forearm if one bone is fractured and the other remains intact. Other causes of non-union are stripping of the soft tissues and damage to the blood supply in the course of operative fixation. Implant failure Metal is subject to fatigue and can fail

unless some union of the fracture has occurred. Stress must therefore be avoided and a patient with a broken tibia internally fixed should walk with crutches and stay

away from partial weightbearing for 6 weeks or longer, until callus or other radiological sign of fracture healing is seen on x-ray. Pain at the fracture site is a danger signal and must be investigated. Refracture It is important not to remove metal implants too soon, or the bone may refracture. A year is the minimum and 18 or 24 months safer; for several weeks after removal the bone is weak, and care or protection is needed.

EXTERNAL FIXATION A fracture may be held by transfixing screws or tensioned wires that pass through the bone above and below the fracture and are attached to an external frame. This is especially applicable to the tibia and pelvis, but the method is also used for fractures of the femur, humerus, lower radius and even bones of the hand.

Indications External fixation is particularly useful for: 1. Fractures associated with severe soft-tissue damage (including open fractures) or those that are contaminated, where internal fixation is risky and repeated access is needed for wound inspection, dressing or plastic surgery. 2. Fractures around joints that are potentially suitable for internal fixation but the soft tissues are too swollen to allow safe surgery; here, a spanning external fixator provides stability until soft-tissue conditions improve. 3. Patients with severe multiple injuries, especially if there are bilateral femoral fractures, pelvic fractures with severe bleeding, and those with limb and associated chest or head injuries.

703

FRACTURES AND JOINT INJURIES

23

(a)

(c)

23.23 External fixation of fractures External fixation is widely used for ‘damage control’ (a,b) temporary stabilization of fractures in order to allow the patient’s general condition or the state of soft tissues to improve prior to definitive surgery or (c–f) reconstruction of limbs using distraction osteogenesis. (c) A bone defect after surgical resection with gentamicin beads used to fill the space temporarily. (d) Bone transport from a more proximal osteotomy. (e) ‘Docking’ of the transported segment and (f) final union and restoration of structural integrity.

(b)

(d)

(e)

4. Ununited fractures, which can be excised and compressed; sometimes this is combined with bone lengthening to replace the excised segment. 5. Infected fractures, for which internal fixation might not be suitable.

(f)

as early as possible to ‘stimulate’ fracture healing. Some fixators incorporate a telescopic unit that allows ‘dynamization’; this will convert the forces of weightbearing into axial micromovement at the fracture site, thus promoting callus formation and accelerating bone union (Kenwright et al., 1991).

Technique

704

The principle of external fixation is simple: the bone is transfixed above and below the fracture with screws or tensioned wires and these are then connected to each other by rigid bars. There are numerous types of external fixation devices; they vary in the technique of application and each type can be constructed to provide varying degrees of rigidity and stability. Most of them permit adjustment of length and alignment after application on the limb. The fractured bone can be thought of as broken into segments – a simple fracture has two segments whereas a two-level (segmental) fracture has three and so on. Each segment should be held securely, ideally with the half-pins or tensioned wires straddling the length of that segment. The wires and half-pins must be inserted with care. Knowledge of ‘safe corridors’ is essential so as to avoid injuring nerves or vessels; in addition, the entry sites should be irrigated to prevent burning of the bone (a temperature of only 50ºC can cause bone death). The fracture is then reduced by connecting the various groups of pins and wires by rods. Depending on the stability of fixation and the underlying fracture pattern, weightbearing is started

Complications Damage to soft-tissue structures Transfixing pins or wires may injure nerves or vessels, or may tether ligaments and inhibit joint movement. The surgeon must be thoroughly familiar with the cross-sectional anatomy before operating.

If there is no contact between the fragments, union is unlikely.

Overdistraction

This is less likely with good operative technique. Nevertheless, meticulous pin-site care is essential, and antibiotics should be administered immediately if infection occurs.

Pin-track infection

EXERCISE More correctly, restore function – not only to the injured parts but also to the patient as a whole. The objectives are to reduce oedema, preserve joint movement, restore muscle power and guide the patient back to normal activity:

23

(b)

23.24 Some aspects of soft tissue treatment Swelling is minimized by improving venous drainage. This can be accomplished by: (1) elevation and (2) firm support. Stiffness is minimized by exercise. (a,c) Intermittent venous plexus pumps for use on the foot or palm to help reduce swelling. (b) A made-tomeasure pressure garment that helps reduce swelling and scarring after treatment. (d) Coban wrap around a limb to control swelling during treatment.

(c)

Principles of fractures

(a)

(d)

Prevention of oedema Swelling is almost inevitable after

a fracture and may cause skin stretching and blisters. Persistent oedema is an important cause of joint stiffness, especially in the hand; it should be prevented if possible, and treated energetically if it is already present, by a combination of elevation and exercise. Not every patient needs admission to hospital, and less severe injuries of the upper limb are successfully managed by placing the arm in a sling; but it is then essential to insist on active use, with movement of all the joints that are free. As with most closed fractures, in all open fractures and all fractures treated by internal fixation it must be assumed that swelling will occur; the limb should be elevated and active exercise begun as soon as the patient will tolerate this. The essence of soft-tissue care may be summed up thus: elevate and exercise; never dangle, never force. Elevation An injured limb usually needs to be elevated; after reduction of a leg fracture the foot of the bed is raised and exercises are begun. If the leg is in plaster the limb must, at first, be dependent for only short periods; between these periods, the leg is elevated on a chair. The patient is allowed, and encouraged, to

exercise the limb actively, but not to let it dangle. When the plaster is finally removed, a similar routine of activity punctuated by elevation is practised until circulatory control is fully restored. Injuries of the upper limb also need elevation. A sling must not be a permanent passive arm-holder; the limb must be elevated intermittently or, if need be, continuously.

23.25 Continuous passive motion The motorized frame provides continuous flexion and extension to pre-set limits.

705

FRACTURES AND JOINT INJURIES

23

Active exercise Active movement helps to pump away

oedema fluid, stimulates the circulation, prevents softtissue adhesion and promotes fracture healing. A limb encased in plaster is still capable of static muscle contraction and the patient should be taught how to do this. When splintage is removed the joints are mobilized and muscle-building exercises are steadily increased. Remember that the unaffected joints need exercising too; it is all too easy to neglect a stiffening shoulder while caring for an injured wrist or hand. Assisted movement It has long been taught that passive movement can be deleterious, especially with injuries around the elbow, where there is a high risk of developing myositis ossificans. Certainly forced movements should never be permitted, but gentle assistance during active exercises may help to retain function or regain movement after fractures involving the articular surfaces. Nowadays this is done with machines that can be set to provide a specified range and rate of movement (‘continuous passive motion’). Functional activity As the patient’s mobility improves,

an increasing amount of directed activity is included in the programme. He may need to be taught again how to perform everyday tasks such as walking, getting in and out of bed, bathing, dressing or handling eating utensils. Experience is the best teacher and the patient is encouraged to use the injured limb as much as possible. Those with very severe or extensive injuries may benefit from spending time in a special rehabilitation unit, but the best incentive to full recovery is the promise of re-entry into family life, recreational pursuits and meaningful work.

TREATMENT OF OPEN FRACTURES INITIAL MANAGEMENT

706

Patients with open fractures may have multiple injuries; a rapid general assessment is the first step and any lifethreatening conditions are addressed (see Chapter 22). The open fracture may draw attention away from other more important conditions and it is essential that the step-by-step approach in advanced trauma life support not be forgotten. When the fracture is ready to be dealt with, the wound is first carefully inspected; any gross contamination is removed, the wound is photographed with a Polaroid or digital camera to record the injury and the area then covered with a saline-soaked dressing under an impervious seal to prevent desiccation. This is left undisturbed until the patient is in the operating the-

atre. The patient is given antibiotics, usually co-amoxiclav or cefuroxime, but clindamycin if the patient is allergic to penicillin. Tetanus prophylaxis is administered: toxoid for those previously immunized, human antiserum if not. The limb is then splinted until surgery is undertaken. The limb circulation and distal neurological status will need checking repeatedly, particularly after any fracture reduction manoeuvres. Compartment syndrome is not prevented by there being an open fracture; vigilance for this complication is wise.

CLASSIFYING THE INJURY Treatment is determined by the type of fracture, the nature of the soft-tissue injury (including the wound size) and the degree of contamination. Gustilo’s classification of open fractures is widely used (Gustilo et al., 1984): Type 1 – The wound is usually a small, clean puncture through which a bone spike has protruded. There is little soft-tissue damage with no crushing and the fracture is not comminuted (i.e. a low-energy fracture). Type II – The wound is more than 1 cm long, but there is no skin flap. There is not much soft-tissue damage and no more than moderate crushing or comminution of the fracture (also a low- to moderate-energy fracture). Type III – There is a large laceration, extensive damage to skin and underlying soft tissue and, in the most severe examples, vascular compromise. The injury is caused by high-energy transfer to the bone and soft tissues. Contamination can be significant. There are three grades of severity. In type III A the fractured bone can be adequately covered by soft tissue despite the laceration. In type III B there is extensive periosteal stripping and fracture cover is not possible without use of local or distant flaps. The fracture is classified as type III C if there is an arterial injury that needs to be repaired, regardless of the amount of other soft-tissue damage. The incidence of wound infection correlates directly with the extent of soft-tissue damage, rising from less than 2 per cent in type I to more than 10 per cent in type III fractures.

PRINCIPLES OF TREATMENT All open fractures, no matter how trivial they may seem, must be assumed to be contaminated; it is important to try to prevent them from becoming infected. The four essentials are:

and Pseudomonas, both of which are near the top of the league table of responsible bacteria. The total period of antibiotic use for these fractures should not be greater than 72 hours (Table 23.1).

23

Sterility and antibiotic cover

Debridement

The wound should be kept covered until the patient reaches the operating theatre. In most cases co-amoxiclav or cefuroxime (or clindamycin if penicillin allergy is an issue) is given as soon as possible, often in the Accident and Emergency department. At the time of debridement, gentamicin is added to a second dose of the first antibiotic. Both antibiotics provide prophylaxis against the majority of Gram-positive and Gramnegative bacteria that may have entered the wound at the time of injury. Only co-amoxiclav or cefuroxime (or clindamycin) is continued thereafter; as wounds of Gustilo grade I fractures can be closed at the time of debridement, antibiotic prophylaxis need not be for more than 24 hours. With Gustilo grade II and IIIA fractures, some surgeons prefer to delay closure after a ‘second look’ procedure. Delayed cover is also usually practised in most cases of Grade IIIB and IIIC injuries. As the wounds have now been present in a hospital environment for some time, and there are data to indicate infections after such open fractures are caused mostly by hospital-acquired bacteria and not seeded at the time of injury, gentamicin and vancomycin (or teicoplanin) are given at the time of definitive wound cover. These antibiotics are effective against methicillin-resistant Staphylococcus aureus

The operation aims to render the wound free of foreign material and of dead tissue, leaving a clean surgical field and tissues with a good blood supply throughout. Under general anaesthesia the patient’s clothing is removed, while an assistant maintains traction on the injured limb and holds it still. The dressing previously applied to the wound is replaced by a sterile pad and the surrounding skin is cleaned. The pad is then taken off and the wound is irrigated thoroughly with copious amounts of physiological saline. The wound is covered again and the patient’s limb then prepped and draped for surgery. Many surgeons prefer to use a tourniquet as this provides a bloodless field. However this induces ischaemia in an already badly injured leg and can make it difficult to recognize which structures are devitalized. A compromise is to apply the tourniquet but not to inflate it during the debridement unless absolutely necessary. Because open fractures are often high-energy injuries with severe tissue damage, the operation should be performed by someone skilled in dealing with both skeletal and soft tissues; ideally this will be a joint effort by orthopaedic and plastic surgeons. The following principles must be observed:

Principles of fractures

• • • •

Antibiotic prophylaxis. Urgent wound and fracture debridement. Stabilization of the fracture. Early definitive wound cover.

Table 23.1 Antibiotics for open fractures1 Grade I

Grade II

Grade IIIA

Grade IIIB/IIIC

As soon as possible (within 3 hours of injury)

Co-amoxiclav2

Co-amoxiclav2

Co-amoxiclav2

Co-amoxiclav2

At debridement

Co-amoxiclav2 and gentamicin

Co-amoxiclav2 and gentamicin

Co-amoxiclav2 and gentamicin

Co-amoxiclav2 and gentamicin

At definitive fracture cover

Wound cover is usually possible at debridement; delayed closure unnecessary

Wound cover is usually possible at debridement. If delayed, gentamicin and vancomycin (or teicoplanin) at the time of cover

Wound cover is usually possible at debridement. If delayed, gentamicin and vancomycin (or teicoplanin) at the time of cover

Gentamicin and vancomycin (or teicoplanin)

Continued prophylaxis

Only co-amoxiclav2* continued after surgery

Only co-amoxiclav2 continued between procedures and after final surgery

Only co-amoxiclav2 continued between procedures and after final surgery

Only co-amoxiclav2 continued between procedures and after final surgery

Maximum period

24 hours

72 hours

72 hours

72 hours

1

Based on the Standards for the Management of Open Fractures of the Lower Limb, British Orthopaedic Association and British Association of Plastic, Reconstructive and Aesthetic Surgeons, 2009 2 Or cefuroxime (clindamycin for those with penicillin allergy).

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FRACTURES AND JOINT INJURIES

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(a)

(b)

23.27 Delivering the fracture Debridement is only possible if the fracture is adequately seen; for this, the fracture ends have to be delivered from within.

(c)

(d)

23.26 Wound extensions for access in open fractures of the tibia Wound incisions (extensions) for adequate access to an open tibial fracture are made along standard fasciotomy incisions: 1 cm behind the posteromedial border of the tibia and 2–3 cm lateral to the crest of the tibia as shown in this example of a two-incision fasciotomy. The dotted lines mark out the crest (C) and posteromedial corner (PM) of the tibia (a). These incisions avoid injury to the perforating branches that supply areas of skin that can be used as flaps to cover the exposed fracture (b). This clinical example shows how local skin necrosis around an open fracture is excised and the wound extended proximally along a fasciotomy incision (c,d).

The wound margins are excised, but only enough to leave healthy skin edges.

Wound excision

Thorough cleansing necessitates adequate exposure; poking around in a small wound to remove debris can be dangerous. If extensions are needed they should not jeopardize the creation of skin flaps for wound cover if this should be needed. The safest extensions are to follow the line of fasciotomy incisions; these avoid damaging important perforator vessels that can be used to raise skin flaps for eventual fracture cover.

Wound extension

Delivery of the fracture Examination of the fracture sur-

708

faces cannot be adequately performed without extracting the bone from within the wound. The simplest (and gentlest) method is to bend the limb in the manner in

which it was forced at the moment of injury; the fracture surfaces will be exposed through the wound without any additional damage to the soft tissues. Large bone levers and retractors should not be used. Removal of devitalized tissue Devitalized tissue provides a nutrient medium for bacteria. Dead muscle can be recognized by its purplish colour, its mushy consistency, its failure to contract when stimulated and its failure to bleed when cut. All doubtfully viable tissue, whether soft or bony, should be removed. The fracture ends can be nibbled away until seen to bleed.

All foreign material and tissue debris is removed by excision or through a wash with copious quantities of saline. A common mistake is to inject syringefuls of fluid through a small aperture – this only serves to push contaminants further in; 6–12 L of saline may be needed to irrigate and clean an open fracture of a long bone. Adding antibiotics or antiseptics to the solution has no added benefit.

Wound cleansing

Nerves and tendons As a general rule it is best to leave cut nerves and tendons alone, though if the wound is absolutely clean and no dissection is required – and provided the necessary expertise is available – they can be sutured.

Wound closure A small, uncontaminated wound in a Grade I or II fracture may (after debridement) be sutured, provided this can be done without tension. In the more severe grades of injury, immediate fracture stabilization and wound cover using split-skin grafts, local or distant

(b)

(d)

(c)

23

Principles of fractures

(a)

23.28 Covering the fracture The best fracture cover is skin or muscle – with the help of a plastic surgeon (a–c). If none is available, gentamicin beads can be inserted and sealed with an impervious dressing until the second operation, where a further debridement and, ideally, definitive fracture cover is obtained (d,e).

(e)

flaps is ideal, provided both orthopaedic and plastic surgeons are satisfied that a clean, viable wound has been achieved after debridement. In the absence of this combined approach at the time of debridement, the fracture is stabilized and the wound left open and dressed with an impervious dressing. Adding gentamicin beads under the dressing has been shown to help, as has the use of vacuum dressings. Return to surgery for a ‘second look’ should have definitive fracture cover as an objective. It should be done by 48– 72 hours, and not later than 5 days. Open fractures do not fare well if left exposed for long and multiple debridement can be self-defeating.

the soft tissues. The method of fixation depends on the degree of contamination, length of time from injury to operation and amount of soft-tissue damage. If there is no obvious contamination and definitive wound cover can be achieved at the time of debridement, open fractures of all grades can be treated as for a closed injury; internal or external fixation may be appropriate depending on the individual characteristics of the fracture and wound. This ideal scenario of judicious soft-tissue and bone debridement, wound cleansing, immediate stabilization and cover is only possible if orthopaedic and plastic surgeons are present at the time of initial surgery. If wound cover is delayed, then external fixation is safer; however, the surgeon must take care to insert the fixator pins away from potential flaps needed by the plastic surgeon! The external fixator may be exchanged for internal

Stabilizing the fracture Stabilizing the fracture is important in reducing the likelihood of infection and assisting recovery of

23.29 Stabilizing the limb in open fractures Spanning external fixation is a useful method of holding the fracture in the first instance (a,b). When definitive fracture cover is carried out, this can be substituted with internal fixation, provided the wound is clean and the interval between the two procedures is less than 7 days.

(a)

(b)

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FRACTURES AND JOINT INJURIES

23

(a)

(b)

(c)

(d)

23.30 Complications of fractures Fractures can become infected (a,b), fail to unite (c) or (d) unite in poor alignment.

fixation at the time of definitive wound cover as long as (1) the delay to wound cover is less than 7 days; (2) wound contamination is not visible and (3) internal fixation can control the fracture as well as the external fixator. This approach is less risky than introducing internal fixation at the time of initial surgery and leaving both metalwork and bone exposed until definitive cover several days later.

Aftercare In the ward, the limb is elevated and its circulation carefully watched. Antibiotic cover is continued but only for a maximum of 72 hours in the more severe grades of injury. Wound cultures are seldom helpful as osteomyelitis, if it were to ensue, is often caused by hospital-derived organisms; this emphasizes the need for good debridement and early fracture cover.

Bone Infection involves the bone and any implants that may have been used. Early infection may present as wound inflammation without discharge. Identifying the causal organism without tissue samples is difficult but, at best guess, it is likely to be S. aureus (including methicillin-resistant varieties) or Pseudomonas. Suppression by appropriate antibiotics, as long as the fixation remains stable, may allow the fracture to proceed to union, but further surgery is likely later, when the antibiotics are stopped. Late presentation may be with a sinus and x-ray evidence of sequestra. The implants and all avascular pieces of bone should be removed; robust soft tissue cover (ideally a flap) is needed. An external fixator can be used to bridge the fracture. If the resulting defect is too large for bone grafting at a later stage, the patient should be referred to a centre with the necessary experience and facilities for limb reconstruction.

Joints

SEQUELS TO OPEN FRACTURES Skin

710

If split-thickness skin grafts are used inappropriately, particularly where flap cover is more suited, there can be areas of contracture or friable skin that breaks down intermittently. Reparative or reconstructive surgery by a plastic surgeon is desirable.

When an infected fracture communicates with a joint, the principles of treatment are the same as with bone infection, namely debridement and drainage, drugs and splintage. On resolution of the infection, attention can be given to stabilizing the fracture so that joint movement can recommence. Permanent stiffness is a real threat; where fracture stabilization cannot be achieved to allow movement, the joint should be splinted in the optimum position for ankylosis, lest this should occur.

GUNSHOT INJURIES

Emergency treatment As always, the arrest of bleeding and general resuscitation take priority. The wounds should each be covered with a sterile dressing and the area examined for artery or nerve damage. Antibiotics should be given immediately, following the recommendations for open fractures (see Table 23.1).

Definitive treatment Traditionally, all missile injuries were treated as severe open injuries, by exploration of the missile track and formal debridement. However, it has been shown that low-velocity wounds with relatively clean entry and exit wounds can be treated as Gustilo type I injuries, by superficial debridement, splintage of the limb and antibiotic cover; the fracture is then treated as for

23

Principles of fractures

Missile wounds are looked upon as a special type of open injury. Tissue damage is produced by: (1) direct injury in the immediate path of the missile; (2) contusion of muscles around the missile track and (3) bruising and congestion of soft tissues at a greater distance from the primary track. The exit wound (if any) is usually larger than the entry wound. With high-velocity missiles (bullets, usually from rifles, travelling at speeds above 600 m/s) there is marked cavitation and tissue destruction over a wide area. The splintering of bone resulting from the transfer of large quantities of energy creates secondary missiles, causing greater damage. With low-velocity missiles (bullets from civilian hand-guns travelling at speeds of 300–600 m/s) cavitation is much less, and with smaller weapons tissue damage may be virtually confined to the bullet track. However, with all gunshot injuries debris is sucked into the wound, which is therefore contaminated from the outset.

similar open fractures. If the injury is to soft tissues only with minimal bone splinters, the wound may be safely treated without surgery but with local wound care and antibiotics. High-velocity injuries demand thorough cleansing of the wound and debridement, with excision of deep damaged tissues and, if necessary, splitting of fascial compartments to prevent ischaemia; the fracture is stabilized and the wound is treated as for a Gustilo type III fracture. If there are comminuted fractures, these are best managed by external fixation. The method of wound closure will depend on the state of tissues after several days; in some cases delayed primary suture is possible but, as with other open injuries, close collaboration between plastic and orthopaedic surgeons is needed (Dicpinigaitis et al., 2006). Close-range shotgun injuries, although the missiles may be technically low velocity, are treated as highvelocity wounds because the mass of shot transfers large quantities of energy to the tissues.

COMPLICATIONS OF FRACTURES The general complications of fractures (blood loss, shock, fat embolism, cardiorespiratory failure etc.) are dealt with in Chapter 22. Local complications can be divided into early (those that arise during the first few weeks following injury) and late.

EARLY COMPLICATIONS Early complications may present as part of the primary injury or may appear only after a few days or weeks. 23.31 Gunshot injuries (a) Closerange shotgun blasts, although technically low velocity, transfer large quantities of destructive force to the tissues due to the mass of shot. They should be treated like high-energy open fractures (b,c).

(a)

(b)

(c)

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FRACTURES AND JOINT INJURIES

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Table 23.2 Local complications of fractures Urgent

Less urgent

Late

Local visceral injury Vascular injury Nerve injury Compartment syndrome Haemarthrosis Infection Gas gangrene

Fracture blisters Plaster sores Pressure sores Nerve entrapment Myositis ossificans Ligament injury Tendon lesions Joint stiffness Algodystrophy

Delayed union Malunion Non-union Avascular necrosis Muscle contracture Joint instability Osteoarthritis

VISCERAL INJURY Fractures around the trunk are often complicated by injuries to underlying viscera, the most important being penetration of the lung with life-threatening pneumothorax following rib fractures and rupture of the bladder or urethra in pelvic fractures. These injuries require emergency treatment. Table 23.3 Common vascular injuries Injury

Vessel

First rib fracture Shoulder dislocation Humeral supracondylar fracture Elbow dislocation Pelvic fracture Femoral supracondylar fracture Knee dislocation Proximal tibial

Subclavian Axillary Brachial Brachial Presacral and internal iliac Femoral Popliteal Popliteal or its branches

either by the initial injury or subsequently by jagged bone fragments. Even if its outward appearance is normal, the intima may be detached and the vessel blocked by thrombus, or a segment of artery may be in spasm. The effects vary from transient diminution of blood flow to profound ischaemia, tissue death and peripheral gangrene.

Clinical features The patient may complain of paraesthesia or numbness in the toes or the fingers. The injured limb is cold and pale, or slightly cyanosed, and the pulse is weak or absent. X-rays will probably show one of the ‘highrisk’ fractures listed above. If a vascular injury is suspected an angiogram should be performed immediately; if it is positive, emergency treatment must be started without further delay.

Treatment All bandages and splints should be removed. The fracture is re-x-rayed and, if the position of the bones suggests that the artery is being compressed or kinked, prompt reduction is necessary. The circulation is then reassessed repeatedly over the next half hour. If there is no improvement, the vessels must be explored by operation – preferably with the benefit of preoperative or peroperative angiography. A cut vessel can be sutured, or a segment may be replaced by a vein graft; if it is thrombosed, endarterectomy may restore the blood flow. If vessel repair is undertaken, stable fixation is a must and where it is practicable, the fracture should be fixed internally.

VASCULAR INJURY The fractures most often associated with damage to a major artery are those around the knee and elbow, and those of the humeral and femoral shafts. The artery may be cut, torn, compressed or contused,

NERVE INJURY Nerve injury is particularly common with fractures of the humerus or injuries around the elbow or the knee 23.32 Vascular injury This patient was brought into hospital with a fractured femur and early signs of vascular insufficiency. The plain x-ray (a) looked as if the proximal bone fragment might have speared the popliteal artery. The angiogram (b) confirmed these fears. Despite vein grafting the patient developed peripheral gangrene (c).

712

(a)

(b)

(c)

COMPARTMENT SYNDROME

23

(see also Chapter 11). The telltale signs should be looked for (and documented) during the initial examination and again after reduction of the fracture.

Fractures of the arm or leg can give rise to severe ischaemia, even if there is no damage to a major vessel. Bleeding, oedema or inflammation (infection) may increase the pressure within one of the osseofascial compartments; there is reduced capillary flow, which results in muscle ischaemia, further oedema, still greater pressure and yet more profound ischaemia – a vicious circle that ends, after 12 hours or less, in necrosis of nerve and muscle within the compartment. Nerve is capable of regeneration but muscle, once infarcted, can never recover and is replaced by inelastic fibrous tissue (Volkmann’s ischaemic contracture). A similar cascade of events may be caused by swelling of a limb inside a tight plaster cast.

Principles of fractures

Closed nerve injuries

Clinical features

In closed injuries the nerve is seldom severed, and spontaneous recovery should be awaited – it occurs in 90 per cent within 4 months. If recovery has not occurred by the expected time, and if nerve conduction studies and EMG fail to show evidence of recovery, the nerve should be explored.

High-risk injuries are fractures of the elbow, forearm bones, proximal third of the tibia, and also multiple

Table 23.4 Common nerve injuries Injury

Nerve

Shoulder dislocation Humeral shaft fracture Humeral supracondylar fracture Elbow medial condyle Monteggia fracture–dislocation Hip dislocation Knee dislocation

Axillary Radial Radial or median Ulnar Posterior-interosseous Sciatic Peroneal

Open nerve injuries With open fractures the nerve injury is more likely to be complete. In these cases the nerve should be explored at the time of debridement and repaired at the time or at wound closure.

Acute nerve compression Nerve compression, as distinct from a direct injury, sometimes occurs with fractures or dislocations around the wrist. Complaints of numbness or paraesthesia in the distribution of the median or ulnar nerves should be taken seriously and the patient monitored closely; if there is no improvement within 48 hours of fracture reduction or splitting of bandages around the splint, the nerve should be explored and decompressed.

(a)

(b)

INDICATIONS FOR EARLY EXPLORATION Nerve injury associated with open fracture Nerve injury with fractures that need internal fixation Presence of a concomitant vascular injury Nerve damage diagnosed after manipulation of the fracture

(c)

23.33 Compartment syndrome (a) A fracture at this level is always dangerous. This man was treated in plaster. Pain became intense and when the plaster was split (which should have been done immediately after its application), the leg was swollen and blistered (b). Tibial compartment decompression (c) requires fasciotomies of all the compartments in the leg.

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FRACTURES AND JOINT INJURIES

23

fractures of the hand or foot, crush injuries and circumferential burns. Other precipitating factors are operation (usually for internal fixation) or infection. The classic features of ischaemia are the five Ps: • • • • •

Pain Paraesthesia Pallor Paralysis Pulselessness.

However in compartment syndrome the ischaemia occurs at the capillary level, so pulses may still be felt and the skin may not be pale! The earliest of the ‘classic’ features are pain (or a ‘bursting’ sensation), altered sensibility and paresis (or, more usually, weakness in active muscle contraction). Skin sensation should be carefully and repeatedly checked. Ischaemic muscle is highly sensitive to stretch. If the limb is unduly painful, swollen or tense, the muscles (which may be tender) should be tested by stretching them. When the toes or fingers are passively hyperextended, there is increased pain in the calf or forearm. Confirmation of the diagnosis can be made by measuring the intracompartmental pressures. So important is the need for early diagnosis that some surgeons advocate the use of continuous compartment pressure monitoring for high-risk injuries (e.g. fractures of the tibia and fibula) and especially for forearm or leg fractures in patients who are unconscious. A split catheter is introduced into the compartment and the pressure is measured close to the level of the fracture. A differential pressure (ΔP) – the difference between diastolic pressure and compartment pressure – of less than 30 mmHg (4.00 kilopascals) is an indication for immediate compartment decompression.

Treatment

714

The threatened compartment (or compartments) must be promptly decompressed. Casts, bandages and dressings must be completely removed – merely splitting the plaster is utterly useless – and the limb should be nursed flat (elevating the limb causes a further decrease in end capillary pressure and aggravates the muscle ischaemia). The ΔP should be carefully monitored; if it falls below 30 mmHg, immediate open fasciotomy is performed. In the case of the leg, ‘fasciotomy’ means opening all four compartments through medial and lateral incisions. The wounds should be left open and inspected 2 days later: if there is muscle necrosis, debridement can be carried out; if the tissues are healthy, the wounds can be sutured (without tension) or skin-grafted. NOTE: If facilities for measuring compartmental pressures are not available, the decision to operate will have to be made on clinical grounds. If three or more signs are present, the diagnosis is almost certain

(Ulmer, 2002). If the clinical signs are ‘soft’, the limb should be examined at 30-minute intervals and if there is no improvement within 2 hours of splitting the dressings, fasciotomy should be performed. Muscle will be dead after 4–6 hours of total ischaemia – there is no time to lose!

HAEMARTHROSIS Fractures involving a joint may cause acute haemarthrosis. The joint is swollen and tense and the patient resists any attempt at moving it. The blood should be aspirated before dealing with the fracture.

INFECTION Open fractures may become infected; closed fractures hardly ever do unless they are opened by operation. Post-traumatic wound infection is now the most common cause of chronic osteitis. The management of early and late infection is summarized under the section Sequels to open fractures (page 710).

GAS GANGRENE This terrifying condition is produced by clostridial infection (especially Clostridium welchii). These are anaerobic organisms that can survive and multiply only in tissues with low oxygen tension; the prime site for infection, therefore, is a dirty wound with dead muscle that has been closed without adequate debridement. Toxins produced by the organisms destroy the cell wall and rapidly lead to tissue necrosis, thus promoting the spread of the disease. Clinical features appear within 24 hours of the injury: the patient complains of intense pain and swelling around the wound and a brownish discharge may be seen; gas formation is usually not very marked. There is little or no pyrexia but the pulse rate is increased and a characteristic smell becomes evident (once experienced this is never forgotten). Rapidly the patient becomes toxaemic and may lapse into coma and death. It is essential to distinguish gas gangrene, which is characterized by myonecrosis, from anaerobic cellulitis, in which superficial gas formation is abundant but toxaemia usually slight. Failure to recognize the difference may lead to unnecessary amputation for the non-lethal cellulitis.

Prevention Deep, penetrating wounds in muscular tissue are dangerous; they should be explored, all dead tissue

23

(c)

23.34 Infection after fracture treatment Operative fixation is one of the commonest causes of infection in closed fractures. Fatigue failure of implants is inevitable if infection hinders union (a). Deep infection can lead to development of discharging sinuses (b,c).

Principles of fractures

(b)

(a)

should be completely excised and, if there is the slightest doubt about tissue viability, the wound should be left open. Unhappily there is no effective antitoxin against C. welchii.

Treatment The key to life-saving treatment is early diagnosis. General measures, such as fluid replacement and intravenous antibiotics, are started immediately. Hyperbaric oxygen has been used as a means of limiting the spread of gangrene. However, the mainstay of treatment is prompt decompression of the wound and removal of all dead tissue. In advanced cases, amputation may be essential.

FRACTURE BLISTERS Two distinct blister types are sometimes seen after fractures: clear fluid-filled vesicles and blood-stained ones. Both occur during limb swelling and are due to elevation of the epidermal layer of skin from the dermis (Giordano et al., 1994). There is no advantage to puncturing the blisters (it may even lead to increased local infection) and surgical incisions through blisters, whilst generally safe, should be undertaken only when limb swelling has decreased.

PLASTER AND PRESSURE SORES Plaster sores occur where skin presses directly onto bone. They should be prevented by padding the bony points and by moulding the wet plaster so that pressure is distributed to the soft tissues around the bony points. While a plaster sore is developing the patient feels localized burning pain. A window must

(a) (a)

(b)

23.35 Gas gangrene (a) Clinical picture of gas gangrene. (b) X-rays show diffuse gas in the muscles of the calf.

(b)

23.36 Pressure sores Pressure sores are a sign of carelessness. (a,b) Sores from poorly supervised treatment in a Thomas splint.

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FRACTURES AND JOINT INJURIES

23

immediately be cut in the plaster, or warning pain quickly abates and skin necrosis proceeds unnoticed. Even traction on a Thomas splint requires skill in nursing care; careless selection of ring size, excessive fixed (as opposed to balanced) traction, and neglect can lead to pressure sores around the groin and iliac crest.

LATE COMPLICATIONS

DELAYED UNION The timetable on page 692 is no more than a rough guide to the period in which a fracture may be expected to unite and consolidate. It must never be relied upon in deciding when treatment may be discontinued. If the time is unduly prolonged, the term ‘delayed union’ is used.

Causes Factors causing delayed union can be summarized as: biological, biomechanical or patient-related.

Both biology and stability are hampered by active infection: not only is there bone lysis, necrosis and pus formation, but implants which are used to hold the fracture tend to loosen.

Infection

PATIENT RELATED In a less than ideal world, there are patients who are: • • • •

Immense Immoderate Immovable Impossible.

These factors must be accommodated in an appropriate fashion.

Clinical features Fracture tenderness persists and, if the bone is subjected to stress, pain may be acute. On x-ray, the fracture line remains visible and there is very little or incomplete callus formation or periosteal reaction. However, the bone ends are not sclerosed or atrophic. The appearances suggest that, although the fracture has not united, it eventually will.

BIOLOGICAL Inadequate blood supply A badly displaced fracture of a long bone will cause tearing of both the periosteum and interruption of the intramedullary blood supply. The fracture edges will become necrotic and dependent on the formation of an ensheathing callus mass to bridge the break. If the zone of necrosis is extensive, as might occur in highly comminuted fractures, union may be hampered. Severe soft tissue damage Severe damage to the soft

tissues affects fracture healing by: (1) reducing the effectiveness of muscle splintage; (2) damaging the local blood supply and (3) diminishing or eliminating the osteogenic input from mesenchymal stem cells within muscle. Periosteal stripping Over-enthusiastic stripping of periosteum during internal fixation is an avoidable cause of delayed union.

BIOMECHANICAL Excessive traction (creating a fracture gap) or excessive movement at the fracture site will delay ossification in the callus. In the forearm and leg a single-bone fracture may be held apart by an intact fellow bone.

Imperfect splintage

716

Over-rigid fixation Contrary to popular belief, rigid fixation delays rather than promotes fracture union. It is only because the fixation device holds the fragments so securely that the fracture seems to be ‘uniting’. Union by primary bone healing is slow, but provided stability is maintained throughout, it does eventually occur.

Treatment CONSERVATIVE The two important principles are: (1) to eliminate any possible cause of delayed union and (2) to promote healing by providing the most appropriate environment. Immobilization (whether by cast or by internal fixation) should be sufficient to prevent shear at the fracture site, but fracture loading is an important stimulus to union and can be enhanced by: (1) encouraging muscular exercise and (2) by weightbearing in the cast or brace. The watchword is patience; however, there comes a point with every fracture where the illeffects of prolonged immobilization outweigh the advantages of non-operative treatment, or where the risk of implant breakage begins to loom. OPERATIVE Each case should be treated on its merits; however, if union is delayed for more than 6 months and there is no sign of callus formation, internal fixation and bone grafting are indicated. The operation should be planned in such a way as to cause the least possible damage to the soft tissues.

NON-UNION In a minority of cases delayed union gradually turns into non-union – that is it becomes apparent that the fracture will never unite without intervention. Movement can be elicited at the fracture site and pain

(a)

(b)

(c)

diminishes; the fracture gap becomes a type of pseudoarthrosis. X-ray The fracture is clearly visible but the bone on either side of it may show either exuberant callus or atrophy. This contrasting appearance has led to nonunion being divided into hypertrophic and atrophic types. In hypertrophic non-union the bone ends are enlarged, suggesting that osteogenesis is still active but not quite capable of bridging the gap. In atrophic non-union, osteogenesis seems to have ceased. The bone ends are tapered or rounded with no suggestion of new bone formation.

(d)

23

Principles of fractures

23.37 Non-union (a) This patient has an obvious pseudarthrosis of the humerus. The x-ray (b) shows a typical hypertrophic non-union. (c,d) Examples of atrophic non-union.

2. Alignment – Was the fracture adequately aligned, to reduce shear? 3. Stability – Was the fracture held with sufficient stability? 4. Stimulation – Was the fracture sufficiently ‘stimulated’? (e.g. by encouraging weightbearing). There are, of course, also biological and patientrelated reasons that may lead to non-union: (1) poor soft tissues (from either the injury or surgery); (2) local infection; (3) associated drug abuse, anti-inflammatory or cytotoxic immunosuppressant medication and (4) non-compliance on the part of the patient.

Causes Treatment

When dealing with the problem of non-union, four questions must be addressed. They have given rise to the acronym CASS:

CONSERVATIVE Non-union is occasionally symptomless, needing no treatment or, at most, a removable splint. Even if symptoms are present, operation is not the only

1. Contact – Was there sufficient contact between the fragments?

23.38 Non-union – treatment (a) This patient with fractures of the tibia and fibula was initially treated by internal fixation with a plate and screws. The fracture failed to heal, and developed the typical features of hypertrophic non-union. (b) After a further operation, using more rigid fixation (and no bone grafts), the fractures healed solidly. (c,d) This patient with atrophic nonunion needed both internal fixation and bone grafts to stimulate bone formation and union (e). (a)

(b)

(c)

(d)

(e)

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FRACTURES AND JOINT INJURIES

23

23.39 Non-union – treatment by the Ilizarov technique Hypertrophic non-unions can be treated by gradual distraction and realignment in an external fixator (a–d). Atrophic non-unions will need more surgery; the poor tissue is excised (e,f) and replaced through bone transport (g,h).

(a)

(b)

(c)

(d)

(e)

(f)

(g)

(h)

answer; with hypertrophic non-union, functional bracing may be sufficient to induce union, but splintage often needs to be prolonged. Pulsed electromagnetic fields and low-frequency, pulsed ultrasound can also be used to stimulate union. OPERATIVE With hypertrophic non-union and in the absence of deformity, very rigid fixation alone (internal or external) may lead to union. With atrophic non-union, fixation alone is not enough. Fibrous tissue in the fracture gap, as well as the hard, sclerotic bone ends is excised and bone grafts are packed around the fracture. If there is significant ‘die-back’, this will require more extensive excision and the gap is then dealt with by bone advancement using the Ilizarov technique.

MALUNION 718

When the fragments join in an unsatisfactory position (unacceptable angulation, rotation or shortening) the

fracture is said to be malunited. Causes are failure to reduce a fracture adequately, failure to hold reduction while healing proceeds, or gradual collapse of comminuted or osteoporotic bone.

Clinical features The deformity is usually obvious, but sometimes the true extent of malunion is apparent only on x-ray. Rotational deformity of the femur, tibia, humerus or forearm may be missed unless the limb is compared with its opposite fellow. Rotational deformity of a metacarpal fracture is detected by asking the patient to flatten the fingers onto the palm and seeing whether the normal regular fan-shaped appearance is reproduced (Chapter 26). X-rays are essential to check the position of the fracture while it is uniting. This is particularly important during the first 3 weeks, when the situation may change without warning. At this stage it is sometimes difficult to decide what constitutes ‘malunion’; acceptable norms differ from one site to another and these are discussed under the individual fractures.

23

(f)

(b)

(c)

(g)

(d)

(h)

(e)

Principles of fractures

(a)

(i)

23.40 Malunion – treatment by internal fixation An osteotomy, correction of deformity and internal fixation can be used to treat both intra-articular deformities (a–e) and those in the shaft of a long bone (f–i).

Treatment Incipient malunion may call for treatment even before the fracture has fully united; the decision on the need for re-manipulation or correction may be extremely difficult. A few guidelines are offered: 1. In adults, fractures should be reduced as near to the anatomical position as possible. Angulation of more than 10–15 degrees in a long bone or a noticeable rotational deformity may need correction by remanipulation, or by osteotomy and fixation.

(a)

(b)

2. In children, angular deformities near the bone ends (and especially if the deformity is in the same plane as that of movement of the nearby joint) will usually remodel with time; rotational deformities will not. 3. In the lower limb, shortening of more than 2.0 cm is seldom acceptable to the patient and a limb length equalizing procedure may be indicated. 4. The patient’s expectations (often prompted by cosmesis) may be quite different from the surgeon’s; they are not to be ignored.

(c)

23.41 Avascular necrosis (a) Displaced fractures of the femoral neck are at considerable risk of developing avascular necrosis. Despite internal fixation within a few hours of the injury (b), the head-fragment developed avascular necrosis. (c) X-ray after removal of the fixation screws.

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23

5. Early discussion with the patient, and a guided view of the x-rays, will help in deciding the need for treatment and may prevent later misunderstanding. 6. Very little is known of the long-term effects of small angular deformities on joint function. However, it seems likely that malalignment of more than 15 degrees in any plane may cause asymmetrical loading of the joint above or below and the late development of secondary osteoarthritis; this applies particularly to the large weightbearing joints.

GROWTH DISTURBANCE In children, damage to the physis may lead to abnormal or arrested growth. A transverse fracture through the growth plate is not always disastrous; the fracture runs through the hypertrophic and calcified layers and not through the germinal zone, so provided it is accurately reduced, there may not be any disturbance of growth. However fractures that split the epiphysis inevitably traverse the growing portion of the physis, and so further growth may be asymmetrical and the bone end characteristically angulated; if the entire physis is damaged, there may be slowing or complete cessation of growth. The subject is dealt with in more detail on page 727.

AVASCULAR NECROSIS Certain regions are notorious for their propensity to develop ischaemia and bone necrosis after injury (see also Chapter 6). They are: (1) the head of the femur (after fracture of the femoral neck or dislocation of the hip); (2) the proximal part of the scaphoid (after fracture through its waist); (3) the lunate (following dislocation) and (4) the body of the talus (after fracture of its neck). Accurately speaking, this is an early complication of bone injury, because ischaemia occurs during the first few hours following fracture or dislocation. However, the clinical and radiological effects are not seen until weeks or even months later.

Clinical features There are no symptoms associated with avascular necrosis, but if the fracture fails to unite or if the bone collapses the patient may complain of pain. X-ray shows the characteristic increase in x-ray density, which occurs as a consequence of two factors: disuse osteoporosis in the surrounding parts gives the impression of ‘increased density’ in the necrotic segment, and collapse of trabeculae compacts the bone and increases its density. Where normal bone meets the necrotic segment a zone of increased radiographic density may be produced by new bone formation.

BED SORES Bed sores occur in elderly or paralysed patients. The skin over the sacrum and heels is especially vulnerable. Careful nursing and early activity can usually prevent bed sores; once they have developed, treatment is difficult – it may be necessary to excise the necrotic tissue and apply skin grafts. In recent years vacuum-assisted closure (a form of negative pressure dressing) has been used for sacral bed sores.

MYOSITIS OSSIFICANS Heterotopic ossification in the muscles sometimes occurs after an injury, particularly dislocation of the elbow or a blow to the brachialis, deltoid or quadriceps. It is thought to be due to muscle damage, but it also occurs without a local injury in unconscious or paraplegic patients.

Clinical features Soon after the injury, the patient (usually a fit young man) complains of pain; there is local swelling and

Treatment

720

Treatment usually becomes necessary when joint function is threatened. In old people with necrosis of the femoral head an arthroplasty is the obvious choice; in younger people, realignment osteotomy (or, in some cases, arthrodesis) may be wiser. Avascular necrosis in the scaphoid or talus may need no more than symptomatic treatment, but arthrodesis of the wrist or ankle is sometimes needed.

23.42 Bed sores Bed sores in an elderly patient, which kept her in hospital for months.

soft-tissue tenderness. X-ray is normal but a bone scan may show increased activity. Over the next 2–3 weeks the pain gradually subsides, but joint movement is limited; x-ray may show fluffy calcification in the soft tissues. By 8 weeks the bony mass is easily palpable and is clearly defined in the x-ray.

Treatment The worst treatment is to attack an injured and slightly stiff elbow with vigorous muscle-stretching exercises; this is liable to precipitate or aggravate the condition. The joint should be rested in the position of function until pain subsides; gentle active movements are then begun. Months later, when the condition has stabilized, it may be helpful to excise the bony mass. Indomethacin or radiotherapy should be given to help prevent a recurrence.

TENDON LESIONS Tendinitis may affect the tibialis posterior tendon following medial malleolar fractures. It should be prevented by accurate reduction, if necessary at surgery. Rupture of the extensor pollicis longus tendon may occur 6–12 weeks after a fracture of the lower radius. Direct suture is seldom possible and the resulting disability is treated by transferring the extensor indicis proprius tendon to the distal stump of the ruptured thumb tendon. Late rupture of the long head of biceps after a fractured neck of humerus usually requires no treatment.

NERVE COMPRESSION Nerve compression may damage the lateral popliteal nerve if an elderly or emaciated patient lies with the

23

Principles of fractures

23.43 Myositis ossificans This followed a fractured head of the radius.

leg in full external rotation. Radial palsy may follow the faulty use of crutches. Both conditions are due to lack of supervision. Bone or joint deformity may result in local nerve entrapment with typical features such as numbness or paraesthesia, loss of power and muscle wasting in the distribution of the affected nerve. Common sites are: (1) the ulnar nerve, due to a valgus elbow following a malunited lateral condyle or supracondylar fracture; (2) the median nerve, following injuries around the wrist and (3) the posterior tibial nerve, following fractures around the ankle. Treatment is by early decompression of the nerve; in the case of the ulnar nerve this may require anterior transposition.

MUSCLE CONTRACTURE Following arterial injury or compartment syndrome, the patient may develop ischaemic contractures of the affected muscles (Volkmann’s ischaemic contracture). Nerves injured by ischaemia sometimes recover, at least partially; thus the patient presents with deformity and stiffness, but numbness is inconstant. The sites most commonly affected are the forearm and hand, leg and foot. In a severe case affecting the forearm, there will be wasting of the forearm and hand, and clawing of the fingers. If the wrist is passively flexed, the patient can extend the fingers, showing that the deformity is largely due to contracture of the forearm muscles. Detachment of the flexors at their origin and along the interosseous membrane in the forearm may improve the deformity, but function is no better if sensation and active movement are not restored. A pedicle nerve graft, using the proximal segments of the median and ulnar nerves may restore protective sensation in the hand, and tendon transfers (wrist extensors to finger and thumb flexors) will allow active grasp. In less severe cases, median nerve sensibility may be quite good and, with appropriate tendon releases and transfers, the patient regains a considerable degree of function. Ischaemia of the hand may follow forearm injuries, or swelling of the fingers associated with a tight forearm bandage or plaster. The intrinsic hand muscles fibrose and shorten, pulling the fingers into flexion at the metacarpophalangeal joints, but the interphalangeal joints remain straight. The thumb is adducted across the palm (Bunnell’s ‘intrinsic-plus’ position). Ischaemia of the calf muscles may follow injuries or operations involving the popliteal artery or its divisions. This is more common than is usually supposed. The symptoms, signs and subsequent contracture are similar to those following ischaemia of the forearm. One of the causes of late claw-toe deformity is an undiagnosed compartment syndrome.

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23

(a)

(b)

(d)

(c)

(e)

23.44 Volkmann’s ischaemia (a) Kinking of the main artery is an important cause, but intimal tears may also lead to blockage from thrombosis. A delayed diagnosis of compartment syndrome carries the same sorry fate. (b,c) Volkmann’s contracture of the forearm. The fingers can be straightened only when the wrist is flexed (the constant length phenomenon). (d) Ischaemic contracture of the small muscles of the hand. (e) Ischaemic contracture of the calf muscles with clawing of the toes.

JOINT INSTABILITY Following injury a joint may give way. Causes include the following: • Ligamentous laxity – especially at the knee, ankle and metacarpophalangeal joint of the thumb. • Muscle weakness – especially if splintage has been excessive or prolonged, and exercises have been inadequate (again the knee and ankle are most often affected). • Bone loss – especially after a gunshot fracture or severe compound injury, or from crushing of metaphyseal bone in joint depression fractures. Injury may also lead to recurrent dislocation. The commonest sites are: (1) the shoulder – if the glenoid labrum has been detached (a Bankart lesion) and (2) the patella – if, after traumatic dislocation, the restraining patellofemoral ligament heals poorly. A more subtle form of instability is seen after fractures around the wrist. Patients complaining of persistent discomfort or weakness after wrist injury should be fully investigated for chronic carpal instability (see Chapters 15 and 25).

JOINT STIFFNESS 722

Joint stiffness after a fracture commonly occurs in the knee, elbow, shoulder and (worst of all) small joints of the hand. Sometimes the joint itself has been injured;

a haemarthrosis forms and leads to synovial adhesions. More often the stiffness is due to oedema and fibrosis of the capsule, ligaments and muscles around the joint, or adhesions of the soft tissues to each other or to the underlying bone. All these conditions are made worse by prolonged immobilization; moreover, if the joint has been held in a position where the ligaments are at their shortest, no amount of exercise will afterwards succeed in stretching these tissues and restoring the lost movement completely. In a small percentage of patients with fractures of the forearm or leg, early post-traumatic swelling is accompanied by tenderness and progressive stiffness of the distal joints. These patients are at great risk of developing a complex regional pain syndrome; whether this is an entirely separate entity or merely an extension of the ‘normal’ post-traumatic soft-tissue reaction is uncertain. What is important is to recognize this type of ‘stiffness’ when it occurs and to insist on skilled physiotherapy until normal function is restored.

Treatment The best treatment is prevention – by exercises that keep the joints mobile from the outset. If a joint has to be splinted, make sure that it is held in the ‘position of safety’ (page 431). Joints that are already stiff take time to mobilize, but prolonged and patient physiotherapy can work wonders. If the situation is due to intra-articular adhesions, arthroscopic-guided releases may free the joint suffi-

ciently to permit a more pliant response to further exercise. Occasionally, adherent or contracted tissues need to be released by operation (e.g. when knee flexion is prevented by adhesions in and around the quadriceps).

Sudeck, in 1900, described a condition characterized by painful osteoporosis of the hand. The same condition sometimes occurs after fractures of the extremities and for many years it was called Sudeck’s atrophy. It is now recognized that this advanced atrophic disorder is the late stage of a post-traumatic reflex sympathetic dystrophy (also known as algodystrophy), which is much more common than originally believed (Atkins, 2003) and that it may follow relatively trivial injury. Because of continuing uncertainty about its nature, the term complex regional pain syndrome (CRPS) has been introduced (see page 261). Two types of CRPS are recognized: • Type 1 –a reflex sympathetic dystrophy that develops after an injurious or noxious event. • Type 2 – causalgia that develops after a nerve injury.

23

Principles of fractures

COMPLEX REGIONAL PAIN SYNDROME (ALGODYSTROPHY)

The patient complains of continuous pain, often described as ‘burning’ in character. At first there is local swelling, redness and warmth, as well as tenderness and moderate stiffness of the nearby joints. As the weeks go by the skin becomes pale and atrophic, movements are increasingly restricted and the patient may develop fixed deformities. X-rays characteristically show patchy rarefaction of the bone. The earlier the condition is recognized and treatment begun, the better the prognosis. Elevation and active exercises are important after all injuries, but in CRPS they are essential. In the early stage of the condition anti-inflammatory drugs and adequate analgesia are helpful. Involvement of a pain specialist who has familiarity with desensitization methods, regional anaesthesia, and use of drugs like amitriptyline, carbamazepine and gabapentin may help; this, combined with prolonged and dedicated physiotherapy, is the mainstay of treatment.

OSTEOARTHRITIS A fracture involving a joint may severely damage the articular cartilage and give rise to post-traumatic osteoarthritis within a period of months. Even if the cartilage heals, irregularity of the joint surface may

23.45 Complex regional pain syndrome (a) Regional osteoporosis is common after fractures of the extremities. The radiolucent bands seen here are typical. (b) In algodystrophy the picture is exaggerated and the soft tissues are also involved: here the right foot is somewhat swollen and the skin has become dusky, smooth and shiny. (c) In the full-blown case, x-rays show a typical patchy osteoporosis. (d) Similar changes may occur in the wrist and hand; they are always accompanied by (e) increased activity in the radionuclide scan. (a)

(d)

(b)

(e)

(c)

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cause localized stress and so predispose to secondary osteoarthritis years later. If the step-off in the articular surface involves a large fragment in a joint that is readily accessible to surgery, intra-articular osteotomies and re-positioning of the fragment may help. Often though the problem arises from areas that were previously comminuted and depressed – little can be done once the fracture has united. Malunion of a metaphyseal fracture may radically alter the mechanics of a nearby joint and this, too, can give rise to secondary osteoarthritis. It is often asserted that malunion in the shaft of a long bone (e.g. the tibia) may act in a similar manner; however, there is little evidence to show that residual angulation of less than 15 degrees can cause proximal or distal osteoarthritis.

STRESS FRACTURES A stress or fatigue fracture is one occurring in the normal bone of a healthy patient, due not to any specific traumatic incident but to small repetitive stresses of two main types: bending and compression. Bending stress causes deformation and bone responds by changing the pattern of remodelling. With repeated stress, osteoclastic resorption exceeds osteoblastic formation and a zone of relative weakness develops – ultimately leading to a breach in the cortex. This process affects young adults undertaking strenuous physical routines and is probably due to muscular forces acting on bone. Athletes in training, dancers and military recruits build up muscle power quickly but bone strength only slowly; this accounts for the high incidence of stress fractures in these groups. Compressive stresses act on soft cancellous bone; with frequent repetition an impacted fracture may result. A combination of compression and shearing stresses may account for the osteochondral fracures that characterize some of the so-called osteochondritides. ‘Spontaneous fractures’ occur with even greater ease in people with osteoporosis or osteomalacia and in patients treated with drugs that affect bone remodelling in a similar way (e.g. corticosteroids and methotrexate). These are often referred to as insufficiency fractures.

children, middle third in athletes and trainee paratroopers, distal third in the elderly); distal shaft of the fibula (the ‘runner’s fracture’); calcaneum (adults); navicular (athletes) and metatarsals (especially the second).

Clinical features There may be a history of unaccustomed and repetitive activity or one of a strenuous physical exercise programme. A common sequence of events is: pain after exercise – pain during exercise – pain without exercise. Occasionally the patient presents only after the fracture has healed and may then complain of a lump (the callus). The patient is usually healthy. The affected site may be swollen or red. It is sometimes warm and usually tender; the callus may be palpable. ‘Springing’ the bone (attempting to bend it) is often painful.

Imaging X-RAY Early on, the fracture is difficult to detect, but radioscintigraphy will show increased activity at the painful spot. Plain x-rays taken a few weeks later may show a small transverse defect in the cortex and/or localized periosteal new-bone formation. These appearances have, at times, been mistaken for those of an osteosarcoma, a horrifying trap for the unwary. Compression stress fractures (especially of the femoral neck and upper tibia) may show as a hazy transverse band of sclerosis with (in the tibia) peripheral callus. Another typical picture is that of a small osteoarticular fracture – most commonly of the dome of the medial femoral condyle at the knee or the upper surface of the talus at the ankle. Later, ischaemic necrosis of the detached fragment may render the lesion even more obvious.

Sites affected

724

Least rare are the following: shaft of humerus (adolescent cricketers); pars interarticularis of fifth lumbar vertebra (causing spondylolysis); pubic rami (inferior in children, both rami in adults); femoral neck (at any age); femoral shaft (chiefly lower third); patella (children and young adults); tibial shaft (proximal third in

(a)

(b)

23.46 Stress fracture (a) The stress fracture in this tibia is only just visible on x-ray, but it had already been suspected 2 weeks earlier when the patient first complained of pain and a radioisotope scan revealed a ‘hot’ area just above the ankle (b).

(a)

(b)

MRI The earliest changes, particularly in ‘spontaneous’ undisplaced osteoarticular fractures, are revealed by MRI. This investigation should be requested in older patients (possibly with osteoporosis) complaining of sudden onset of pain over the anteromedial part of the knee.

Diagnosis Many disorders, including osteomyelitis, scurvy and battered baby syndrome, may be confused with stress fractures. The great danger, however, is a mistaken diagnosis of osteosarcoma; scanning shows increased uptake in both conditions and even biopsy may be misleading.

23

Principles of fractures

23.47 Stress fractures Stress fractures are often missed or wrongly diagnosed. (a) This tibial fracture was at first thought to be an osteosarcoma. (b) Stress fractures of the pubic rami in elderly women can be mistaken for metastases.

Table 23.5 Causes of pathological fracture Generalized bone disease

Primary malignant tumours

1. Osteogenesis imperfecta 2. Postmenopausal osteoporosis 3. Metabolic bone disease 4. Myelomatosis 5. Polyostotic fibrous dysplasia 6. Paget’s disease

1. Chondrosarcoma 2. Osteosarcoma 3. Ewing’s tumour

Local benign conditions

Metastatic tumours

1. Chronic infection Carcinoma in breast, lung, 2. Solitary bone cyst kidney, thyroid, colon 3. Fibrous cortical defect and prostate 4. Chondromyxoid fibroma 5. Aneurysmal bone cyst 6. Chondroma 7. Monostotic fibrous dysplasia

Treatment Most stress fractures need no treatment other than an elastic bandage and avoidance of the painful activity until the lesion heals; surprisingly, this can take many months and the forced inactivity is not easily accepted by the hard-driving athlete or dancer. An important exception is stress fracture of the femoral neck. This should be suspected in all elderly people who complain of pain in the hip for which no obvious cause can be found. If the diagnosis is confirmed by bone scan, the femoral neck should be internally fixed with screws as a prophylactic measure.

PATHOLOGICAL FRACTURES When abnormal bone gives way this is referred to as a pathological fracture. The causes are numerous and varied; often the diagnosis is not made until a biopsy is examined (Table 23.5).

HISTORY Bone that fractures spontaneously, or after trivial injury, must be regarded as abnormal until proved otherwise. Older patients should always be asked about previous illnesses or operations. A malignant tumour, no matter how long ago it occurred, may be the source of a late metastatic lesion; a history of gastrectomy, intestinal malabsorption, chronic alcoholism or prolonged drug therapy should suggest a metabolic bone disorder. Symptoms such as loss of weight, pain, a lump, cough or haematuria suggest that the fracture may be through a secondary deposit. In younger patients, a history of several previous fractures may suggest a diagnosis of osteogenesis imperfecta, even if the patient does not show the classic features of the disorder.

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(a)

(b)

(c)

(d)

(e)

(f)

23.48 Pathological fractures Six examples of pathological fractures, due to: (a) primary chondrosarcoma; (b) postoperative bone infection at a screw-hole following plating of an intertrochanteric fracture; (c) Paget’s disease; (d) vertebral metastases; (e) metastasis from carcinoma of the breast and (f) myelomatosis.

EXAMINATION Local signs of bone disease (an infected sinus, an old scar, swelling or deformity) should not be missed. The site of the fracture may suggest the diagnosis: patients with involutional osteoporosis develop fractures of the vertebral bodies and corticocancellous junctions of long bones; a fracture through the shaft of the bone in an elderly patient, especially in the subtrochanteric region, should be regarded as a pathological fracture until proved otherwise. General examination may be informative. Congenital dysplasias, fibrous dysplasia, Cushing’ syndrome and Paget’ disease all produce characteristic appearances. The patient may be wasted (possibly due to malignant disease). The lymph nodes or liver may be enlarged. It should be noted whether there is a mass in the abdomen or pelvis. Old scars should not be overlooked and rectal and vaginal examinations are mandatory. Under the age of 20 the common causes of pathological fracture are benign bone tumours and cysts. Over the age of 40 the common causes are multiple myeloma, secondary carcinoma and Paget’s disease.

tebral compression in a male younger than 75 years should be regarded as ‘pathological’ until proven otherwise.

Additional investigations Local radionuclide imaging may help elucidate the diagnosis, and whole-body scanning is important in revealing or excluding other deposits. X-ray of other bones, the lungs and the urogenital tract may be necessary to exclude malignant disease. Investigations should always include a full blood count, ESR, protein electrophoresis, and tests for syphilis and metabolic bone disorders. Urine examination may reveal blood from a tumour, or Bence–Jones protein in myelomatosis.

Biopsy Some lesions are so typical that a biopsy is unnecessary (solitary cyst, fibrous cortical defect, Paget’s disease). Others are more obscure and a biopsy is essential for diagnosis. If open reduction of the fracture is indicated, the biopsy can be carried out at the same time; otherwise a definitive procedure should be arranged.

X-ray

726

Understandably, the fracture itself attracts most attention but the surrounding bone must also be examined, and features such as cyst formation, cortical erosion, abnormal trabeculation and periosteal thickening should be sought. The type of fracture, too, is important: vertebral compression fractures may be due to severe osteoporosis or osteomalacia, but they can also be caused by skeletal metastases or myeloma. Middle-aged men, unlike women, do not normally become osteoporotic: x-ray signs of bone loss and ver-

Treatment The principles of fracture treatment remain the same: reduce, hold, exercise. However the choice of method is influenced by the condition of the bone; and the underlying pathological disorder may need treatment in its own right (see Chapter 9). In most of these conditions (including Paget’s disease) the bones fracture more easily, but they heal quite well provided the fracture is

Generalized bone disease

23

(b)

(c)

(d)

Principles of fractures

(a)

23.49 Pathological fractures – treatment (a,b) Paget’s disease of the femur increases the brittleness of bone, making it more likely to fracture. Intramedullary fixation allows the entire femur to be supported. (c,d) A fracture through a solitary metastasis from a previously excised renal cell carcinoma can be resected in order to achieve cure. In this case replacement of the proximal femur with an endoprosthesis is needed.

properly immobilized. Internal fixation is therefore advisable (and for Paget’s disease almost essential). Patients with osteomalacia, hyperparathyroidism, renal osteodystrophy and Paget’s disease will need systemic treatment as well. Local benign conditions Fractures through benign cyst-

like lesions usually heal quite well and they should be allowed to do so before tackling the local lesion. Treatment is therefore the same as for simple fractures in the same area, although in some cases it will be necessary to take a biopsy before immobilizing the fracture. When the bone has healed, the tumour can be dealt with by curettage or local excision. Primary malignant tumour The fracture may need splinting but this is merely a prelude to definitive treatment of the tumour, which by now will have spread to the surrounding soft tissues. The prognosis is almost always very poor. Metastatic tumours Metastasis is a frequent cause of pathological fracture in older people. Breast cancer is the commonest source and the femur the commonest site. Nowadays cancer patients (even those with metastases) often live for several years and effective treatment of the fracture will vastly improve their quality of life. Fracture of a long-bone shaft should be treated by internal fixation; if necessary the site is also packed with acrylic cement. Bear in mind that the implant will function as a load-bearing and not a load-sharing device; intramedullary nails are more suitable than plates and screws. Fracture near a bone end can often be treated by excision and prosthetic replacement; this is especially true of femoral neck fractures.

Preoperatively, imaging studies should be performed to detect other bone lesions; these may be amenable to prophylactic fixation. Once the wound has healed, local irradiation should be applied to reduce the risk of progressive osteolysis. Pathological compression fractures of the spine cause severe pain. This is due largely to spinal instability and treatment should include operative stabilization. If there are either clinical or imaging features of actual or threatened spinal cord or cauda equina compression, the segment should also be decompressed. Postoperative irradiation is given as usual. With all types of metastatic lesion, the primary tumour should be investigated and treated as well.

INJURIES OF THE PHYSIS In children over 10 per cent of fractures involve injury to the growth plate (or physis). Because the physis is a relatively weak part of the bone, joint strains that might cause ligament injuries in adults are liable to result in separation of the physis in children. The fracture usually runs transversely through the hypertrophic or the calcified layer of the growth plate, often veering off into the metaphysis at one of the edges to include a triangular lip of bone. This has little effect on longitudinal growth, which takes place in the germinal and proliferating layers of the physis. However, if the fracture traverses the cellular ‘reproductive’ layers of the physis, it may result in premature ossification of the injured part and serious disturbances of bone growth.

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23.50 Battered baby syndrome (a–c) The fractures are not pathological but the family is. The metaphyseal lesions in each humerus are characteristic.

(a)

(b)

(c)

Classification The most widely used classification of physeal injuries is that of Salter and Harris (Salter and Harris, 1963), which distinguishes five basic types of injury: • Type 1 – A transverse fracture through the hypertrophic or calcified zone of the plate. Even if the fracture is quite alarmingly displaced, the growing zone of the physis is usually not injured and growth disturbance is uncommon. • Type 2 – This is essentially similar to type 1, but towards the edge the fracture deviates away from the physis and splits off a triangular metaphyseal fragment of bone (sometimes referred to as the Thurston– Holland fragment). • Type 3 – A fracture that splits the epiphysis and then veers off transversely to one or the other side, through the hypertrophic layer of the physis. Inevitably it damages the ‘reproductive’ layers of the physis (as these layers are closer to the epiphysis than the metaphysis) and may result in growth disturbance. • Type 4 – As with type 3, the fracture splits the epiphysis, but it extends into the metaphysis. These

1

728

2

3

fractures are liable to displacement and a consequent misfit between the separated parts of the physis, resulting in asymmetrical growth. • Type 5 – A longitudinal compression injury of the physis. There is no visible fracture but the growth plate is crushed and this may result in growth arrest. Rang (Rang, 1969) has added a Type 6, an injury to the perichondrial ring (the peripheral zone of Ranvier), which carries a significant risk of growth disturbance. The diagnosis is made usually in retrospect after development of deformity.

Mechanism of injury Physeal fractures usually result from falls or traction injuries. They occur mostly in road accidents and during sporting activities or playground tumbles.

Clinical features These fractures are more common in boys than in girls and are usually seen either in infancy or between the ages of 10 and 12. Deformity is usually minimal,

4

5

23.51 Physeal injuries Type 1 – separation of the epiphysis – which usually occurs in infants but is also seen at puberty as a slipped femoral epiphysis. Type 2 – fracture through the physis and metaphysis – is the commonest; it occurs in older children and seldom results in abnormal growth. Type 3 – an intra-articular fracture of the epiphysis – needs accurate reduction to restore the joint surface. Type 4 – splitting of the physis and epiphysis – damages the articular surface and may also cause abnormal growth; if it is displaced it needs open reduction. Type 5 – crushing of the physis – may look benign but ends in arrested growth.

23

but any injury in a child followed by pain and tenderness near the joint should arouse suspicion, and x-ray examination is essential.

X-rays

(a)

(b)

(c)

(d)

(e)

(f)

Principles of fractures

The physis itself is radiolucent and the epiphysis may be incompletely ossified; this makes it hard to tell whether the bone end is damaged or deformed. The younger the child, the smaller the ‘visible’ part of the epiphysis and thus the more difficult it is to make the diagnosis; comparison with the normal side is a great help. Telltale features are widening of the physeal ‘gap’, incongruity of the joint or tilting of the epiphyseal axis. If there is marked displacement the diagnosis is obvious, but even a type 4 fracture may at first be so little displaced that the fracture line is hard to see; if there is the faintest suspicion of a physeal fracture, a repeat x-ray after 4 or 5 days is essential. Types 5 and 6 injuries are usually diagnosed only in retrospect.

Treatment Undisplaced fractures may be treated by splinting the part in a cast or a close-fitting plaster slab for 2–4 weeks (depending on the site of injury and the age of the child). However, with undisplaced types 3 and 4 fractures, a check x-ray after 4 days and again at about 10 days is mandatory in order not to miss late displacement. Displaced fractures should be reduced as soon as possible. With types 1 and 2 this can usually be done closed; the part is then splinted securely for 3–6 weeks. Types 3 and 4 fractures demand perfect anatomical reduction. An attempt can be made to achieve this by gentle manipulation under general anaesthesia; if this is successful, the limb is held in a cast for 4–8 weeks (the longer periods for type 4 injuries). If a type 3 or 4 fracture cannot be reduced accurately by closed manipulation, immediate open reduction and internal fixation with smooth K-wires is essential. The limb is then splinted for 4–6 weeks, but it takes that long again before the child is ready to resume unrestricted activities.

Complications Types 1 and 2 injuries, if properly reduced, have an excellent prognosis and bone growth is not adversely affected. Exceptions to this rule are injuries around the knee involving the distal femoral or proximal tibial physis; both growth plates are undulating in shape, so a transverse fracture plane may actually pass through more than just the hypertrophic zone but also damage the proliferative zone. Complications such as malunion or non-union may also occur if the

23.52 Physeal injuries (a) Type 2 injury. The fracture does not traverse the width of the physis; after reduction (b) bone growth is not distorted. (c,d) This type 4 fracture of the tibial physis was treated immediately by open reduction and internal fixation and a good result was obtained. (e,f) In this case accurate reduction was not achieved and the physeal fragment remained displaced; the end result was partial fusion of the physis and severe deformity of the ankle.

diagnosis is missed and the fracture remains unreduced (e.g. fracture separation of the medial humeral epicondyle). Types 3 and 4 injuries may result in premature fusion of part of the growth plate or asymmetrical growth of the bone end. Types 5 and 6 fractures cause premature fusion and retardation of growth. The size and position of the bony bridge across the physis can be assessed by tomography or magnetic resonance imaging (MRI). If the bridge is relatively small (less than one-third the width of the physis) it can be excised and replaced by a fat graft, with some prospect of preventing or diminishing the growth disturbance (Langenskiold, 1975; 1981). However, if the bone

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FRACTURES AND JOINT INJURIES

23

(a)

(b)

(c)

(e)

23.53 Langenskiold procedure for physeal arrest Small tethers across the physis can be mapped out by MRI (a,b), then surgically removed by drilling out and curettage (c) and filling the defect with fat graft (d,e).

bridge is more extensive the operation is contraindicated as it can end up doing more harm than good. Established deformity, whether from asymmetrical growth or from malunion of a displaced fracture (e.g. a valgus elbow due to proximal displacement of a lateral humeral condylar fracture) should be treated by corrective osteotomy. If further growth is abnormal, the osteotomy may have to be repeated.

INJURIES TO JOINTS Joints are usually injured by twisting or tilting forces that stretch the ligaments and capsule. If the force is great enough the ligaments may tear, or the bone to which they are attached may be pulled apart. The articular cartilage, too, may be damaged if the joint surfaces are compressed or if there is a fracture into the joint. As a general principle, forceful angulation will tear the ligaments rather than crush the bone, but in older people with porotic bone the ligaments may hold and the bone on the opposite side of the joint is crushed instead, while in children there may be a fractureseparation of the physis.

Sprains, strains and ruptures

730

(d)

There is much confusion about the use of the terms ‘sprain’, ‘strain’ and ‘rupture’. Strictly speaking, a sprain is any painful wrenching (twisting or pulling) movement of a joint, but the term is generally reserved for joint injuries less severe than actual tearing of the capsule or ligaments. Strain is a physical effect of stress, in this case tensile stress associated with some stretching of the ligaments; in colloquial usage, ‘strained ligament’ is often meant to denote an injury somewhat more severe than a ‘sprain’, which possibly involves tearing of some fibres. If the stretching or twisting force is severe enough, the

ligament may be strained to the point of complete rupture.

STRAINED LIGAMENT Only some of the fibres in the ligament are torn and the joint remains stable. The injury is one in which the joint is momentarily twisted or bent into an abnormal position. The joint is painful and swollen and the tissues may be bruised. Tenderness is localized to the injured ligament and tensing the tissues on that side causes a sharp increase in pain.

Treatment The joint should be firmly strapped and rested until the acute pain subsides. Thereafter, active movements are encouraged, and exercises practised to strengthen the muscles.

RUPTURED LIGAMENT The ligament is completely torn and the joint is unstable. Sometimes the ligament holds and the bone to which it is attached is avulsed; this is effectively the same lesion but easier to deal with because the bone fragment can be securely reattached. As with a strain, the joint is suddenly forced into an abnormal position; sometimes the patient actually hears a snap. The joints most likely to be affected are the ones that are insecure by virtue of their shape or least well protected by surrounding muscles: the knee, ankle and finger joints. Pain is severe and there may be considerable bleeding under the skin; if the joint is swollen, this is probably due to a haemarthrosis. The patient is unlikely to permit a searching examination, but under general anaesthesia the instability can be demonstrated; it is this that distinguishes the lesion from a strain. X-ray

23

(b)

(c)

(d)

(e)

23.54 Joint injuries Severe stress may cause various types of injury. (a) A ligament may rupture, leaving the bone intact. If the soft tissues hold, the bone on the opposite side may be crushed (b), or a fragment may be pulled off by the taut ligament (c). Subluxation (d) means the articular surfaces are partially displaced; dislocation (e) refers to complete displacement of the joint.

may show a detached flake of bone where the ligament is inserted.

Treatment Torn ligaments heal by fibrous scarring. Previously this was thought inevitable and the surgeon’s task was to ensure that the torn ends were securely sutured so as to restore the ligament to its normal length. In some injuries, e.g. rupture of the ulnar collateral ligament of the metacarpophalangeal joint of the thumb, this approach is still valid. In others, however, it has changed; thus, solitary medial collateral ligament ruptures of the knee, even complete ruptures, are often treated non-operatively in the first instance. The joint is splinted and local measures are taken to reduce swelling. After 1–2 weeks, the splint is exchanged for a functional brace that allows joint movement but at the same time prevents repeat injury to the ligament, especially if some instability is also present. Physiotherapy is applied to maintain muscle strength and later proprioceptive exercises are added. This nonoperative approach has shown better results not only in the strength of the healed ligament but also in the nature of healing – there is less fibrosis (Woo et al., 2000). An exception to this non-operative approach is when the ligament is avulsed with an attached fragment of bone; reattachment of the fragment is indicated if the piece is large enough. Occasionally non-operative treatment may result in some residual instability that is clinically detectable; often this is not symptomatic, but if it is then surgical reconstruction should be considered.

DISLOCATION AND SUBLUXATION ‘Dislocation’ means that the joint surfaces are completely displaced and are no longer in contact; ‘subluxation’ implies a lesser degree of displacement, such that the articular surfaces are still partly apposed.

Clinical features

Principles of fractures

(a)

Following an injury the joint is painful and the patient tries at all costs to avoid moving it. The shape of the joint is abnormal and the bony landmarks may be displaced. The limb is often held in a characteristic position; movement is painful and restricted. X-rays will usually clinch the diagnosis; they will also show whether there is an associated bony injury affecting joint stability – i.e. a fracture-dislocation. If the dislocation is reduced by the time the patient is seen, the joint can be tested by stressing it as if almost to reproduce the suspected dislocation: the patient develops a sense of impending disaster and violently resists further manipulation.

Apprehension test

Recurrent dislocation If the ligaments and joint margins

are damaged, repeated dislocation may occur. This is seen especially in the shoulder and patellofemoral joint. Some patients acquire the knack of dislocating (or subluxating) the joint by voluntary muscle contraction. Ligamentous laxity may make this easier, but the habit often betrays a manipulative and neurotic personality. It is important to recognize this because such patients are seldom helped by operation.

Habitual (voluntary) dislocation

Treatment The dislocation must be reduced as soon as possible; usually a general anaesthetic is required, and sometimes a muscle relaxant as well. The joint is then rested or immobilized until soft-tissue swelling reduces – usually after 2 weeks. Controlled movements then begin in a functional brace; progress with physiotherapy is monitored. Occasionally surgical reconstruction for residual instability is called for.

Complications Many of the complications of fractures are seen also after dislocations: vascular injury, nerve injury, avascular

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necrosis of bone, heterotopic ossification, joint stiffness and secondary osteoarthritis. The principles of diagnosis and management of these conditions have been discussed earlier.

REFERENCES AND FURTHER READING Atkins RM. Complex regional pain syndrome. J Bone Joint Surg 2003; 85B: 1100–6. Charnley J. The Closed Treatment of Common Fractures. Churchill Livingstone, Edinburgh, 1961. Dicpinigaitis PA, Koval KJ, Tejwani NC, Egol KA. Gunshot wounds to the extremities. Bull NYU Hosp Jt Dis 2006; 64: 139–55. Giordano CP, Koval KJ, Zuckerman JD, Desai P. Fracture blisters. Clin Orthop 1994; 307: 214–21. Gustilo RB, Mendoza RM, Williams DN. Problems in the management of type III (severe) open fractures: a new classification of type III open fractures. J Trauma 1984; 24: 742–6. Kenwright J, Richardson JB, Cunningham JL et al. Axial movement and tibial fractures. A controlled randomised trial of treatment. J Bone Joint Surg 1991; 73B: 654–9. Langenskiold A. An operation for partial closure of an epiphysial plate in children, and its experimental basis. J Bone Joint Surg 1975; 57B: 325–30. Langenskiold A. Surgical treatment of partial closure of the growth plate. J Pediatr Orthop 1981; 1: 3–11. Marsh JL, Slongo TF, Agel J et al. Fracture and dislocation classification compendium – 2007: Orthopaedic Trauma Association classification, database and outcomes committee. J Orthop Trauma 2007; 21(Suppl): S1–133. McKibbin B. The biology of fracture healing in long bone. J Bone Joint Surg 1978; 60B: 150–62.

Müller M., Nazarian S, Koch P, Schatzker J. The Comprehensive Classification of Fractures of Long Bones. Springer Verlag, Berlin, Heidelberg, New York, 1990. Oestern H, Tscherne H. Pathophysiology and classification of soft tissue injuries associated with fractures. In: H. Tscherne and L. Gotzen (eds) Fractures with Soft Tissue Injuries. Springer Verlag, Berlin, 1984. Pape HC, Giannoudis PV, Kretteck C, Trentz O. Timing of fixation of major fractures in blunt polytrauma: role of conventional indicators in clinical decision making. J Orthop Trauma 2005; 19: 551–62. Rang M. The growth plate and its disorders. Churchill Livingstone, Edinburgh, 1969. Roberts CS, Pape HC, Jones AL et al. Damage control orthopaedics. Evolving concepts in the treatment of patients who have sustained orthopaedic trauma. J Bone Joint Surg 2005; 87A: 434–49. Salter RB, Harris WR. Injuries involving the epiphyseal plate. J Bone Joint Surg 1963; 45A: 587–622. Sarmiento A, Latta L. Functional fracture bracing. J Am Acad Orthop Surg 1999; 7: 66–75. Sarmiento A, Latta L. The evolution of functional bracing of fractures. J Bone Joint Surg 2006; 88B: 141–8. Sarmiento A, Mullis DL, Latta L et al. A quantitative comparative analysis of fracture healing under the influence of compression plating vs. closed weight-bearing treatment. Clin Orthop 1980; 149: 232–9. Slongo TF, Audige L. Fracture and dislocation classification compendium for children: the AO pediatric comprehensive classification of long bone fractures (PCCF). J Orthop Trauma 2007; 21(Suppl): S135–60. Ulmer T. The clinical diagnosis of compartment syndrome of the lower leg: Are clinical findings predictive of the disorder? J Orthop Trauma 2002; 16: 572–577. Woo SL, Vogrin TM, Abramowitch SD. Healing and repair of ligament injuries in the knee. J Am Acad Orthop Surg 2000; 8: 364–72.

Injuries of the shoulder, upper arm and elbow

24

Andrew Cole, Paul Pavlou, David Warwick

The great bugbear of upper limb injuries is stiffness – particularly of the shoulder but sometimes of the elbow and hand as well. Two points should be constantly borne in mind:

pulse and gently to palpate the root of the neck. Outer third fractures are easily missed or mistaken for acromioclavicular joint injuries.

• Whatever the injury, and however it is treated, all the joints that are not actually immobilized – and especially the finger joints – should be exercised from the start. • In elderly patients it is sometimes best to disregard the fracture and concentrate on regaining movement.

Imaging

FRACTURES OF THE CLAVICLE In children the clavicle fractures easily, but it almost invariably unites rapidly and without complications. In adults this can be a much more troublesome injury. In adults clavicle fractures are common, accounting for 2.6–4 per cent of fractures and approximately 35 per cent of all shoulder girdle injuries. Fractures of the midshaft account for 69–82 per cent, lateral fractures for 21–28 per cent and medial fractures for 2–3 per cent.

Mechanism of injury A fall on the shoulder or the outstretched hand may break the clavicle. In the common mid-shaft fracture, the outer fragment is pulled down by the weight of the arm and the inner half is held up by the sternomastoid muscle. In fractures of the outer end, if the ligaments are intact there is little displacement; but if the coracoclavicular ligaments are torn, or if the fracture is just medial to these ligaments, displacement may be severe and closed reduction impossible.

Radiographic analysis requires at least an anteroposterior view and another taken with a 30 degree cephalic tilt. The fracture is usually in the middle third of the bone, and the outer fragment usually lies below the inner. Fractures of the outer third may be missed, or the degree of displacement underestimated, unless additional views of the shoulder are obtained. With medial third fractures it is also wise to obtain x-rays of the sterno-clavicular joint. In assessing clinical progress, remember that ‘clinical’ union usually precedes ‘radiological’ union by several weeks. CT scanning with three-dimensional reconstructions may be needed to determine accurately the degree of shortening or for diagnosing a sternoclavicular fracture-dislocation, and also to establish whether a fracture has united.

Classification Clavicle fractures are usually classified on the basis of their location: Group I (middle third fractures), Group II (lateral third fractures) and Group III (medial third fractures). Lateral third fractures can be further sub-classified into (a) those with the coracoclavicular ligaments intact, (b) those where the coracoclavicular ligaments are torn or detached from the medial segment but the trapezoid ligament remains intact to the distal segment, and (c) factures which are intra-articular. An even more detailed classification proposed by Robinson (1998) is useful for managing data and comparing clinical outcomes.

Clinical features The arm is clasped to the chest to prevent movement. A subcutaneous lump may be obvious and occasionally a sharp fragment threatens the skin. Though vascular complications are rare, it is prudent to feel the

Treatment MIDDLE THIRD FRACTURES There is general agreement that undisplaced fractures should be treated non- operatively. Most will go on to

FRACTURES AND JOINT INJURIES

24

(a)

(b)

24.1 Fracture of the clavicle (a) Displaced fracture of the middle third of the clavicle – the most common injury. (b) The fracture usually unites in this position, leaving a barely noticable ‘bump’.

unite uneventfully with a non-union rate below 5 per cent and a return to normal function. Non-operative management consists of applying a simple sling for comfort. It is discarded once the pain subsides (between 1–3 weeks) and the patient is then encouraged to mobilize the limb as pain allows. There

is no evidence that the traditional figure-of-eight bandage confers any advantage and it carries the risk of increasing the incidence of pressures sores over the fracture site and causing harm to neurological structures; it may even increase the risk of non-union. There is less agreement about the management of displaced middle third fractures. Treating those with shortening of more than 2 cm by simple splintage is now believed to incur a considerable risk of symptomatic mal-union – mainly pain and lack of power during shoulder movements (McKee et al., 2006) – and an increased incidence of non-union. There is, therefore, a growing trend towards internal fixation of acute clavicular fractures associated with severe displacement. Methods include plating (specifically contoured locking plates are available) and intramedullary fixation. LATERAL THIRD FRACTURES Most lateral clavicle fractures are minimally displaced and extra-articular. The fact that the coracoclavicular ligaments are intact prevents further displacement and non-operative management is usually appropriate. Treatment consists of a sling for 2–3 weeks until the pain subsides, followed by mobilization within the limits of pain. Displaced lateral third fractures are associated with disruption of the coracoclavicular ligaments and are therefore unstable injuries. A number of studies have shown that these particular fractures have a higher than usual rate of non-union if treated non-operatively. Surgery to stabilize the fracture is often recom-

(a) (c)

(b)

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24.2 Severely displaced fracture (a) A comminuted fracture which united in this position (b) leaving an unsightly deformity (c). This fracture would have been better managed by (d) open reduction and internal fixation.

(d)

LATE

(a)

(b)

24.3 Fracture of the outer (lateral) third (a) The shaft of the clavicle is elevated, suggesting that the medial part of the coracoclavicular ligament is ruptured. (b) This was treated by open reduction and internal fixation, using a long screw to fix the clavicle to the coracoid process temporarily while the soft tissues healed.

mended. However the converse argument is that many of the fractures that develop non-union do not cause any symptoms and surgery can therefore be reserved for patients with symptomatic non-union. Operations for these fractures have a high complication rate and no single procedure has been shown to be better than the others. Techniques include the use of a coracoclavicular screw, plate and hook plate fixation and suture and sling techniques with Dacron graft ligaments. MEDIAL THIRD FRACTURES Most of these rare fractures are extra-articular. They are mainly managed non-operatively unless the fracture displacement threatens the mediastinal structures. Initial fixation is associated with significant complications, including migration of the implants into the mediastinum, particularly when K-wires are used. Other methods of stabilization include suture and graft techniques and the newer locking plates.

Complications EARLY Despite the close proximity of the clavicle to vital structures, a pneumothorax, damage to the subclavian vessels and brachial plexus injuries are all very rare.

Malunion All displaced fractures heal in a nonanatomical position with some shortening and angulation, however most do not produce symptoms. Some may go on to develop periscapular pain and this is more likely with shortening of more than 1.5cm. In these circumstances the difficult operation of corrective osteotomy and plating can be considered. Stiffness of the shoulder This is common but temporary; it results from fear of moving the fracture. Unless the fingers are exercised, they also may become stiff and take months to regain movement.

24

Injuries of the shoulder, upper arm and elbow

In displaced fractures of the shaft nonunion occurs in 1–15 per cent. Risk factors include increasing age, displacement, comminution and female sex. However accurate prediction of those fractures most likely to go on to non-union remains difficult. Symptomatic non-unions are generally treated with plate fixation and bone grafting if necessary. This procedure usually produces a high rate of union and satisfaction. Lateral clavicle fractures have a higher rate of nonunion (11.5–40 per cent). Treatment options for symptomatic non-unions are excision of the lateral part of the clavicle (if the fragment is small and the coracoclavicular ligaments are intact) or open reduction, internal fixation and bone grafting if the fragment is large. Locking plates and hooked plates are used.

Non-union

FRACTURES OF THE SCAPULA Mechanisms of injury The body of the scapula is fractured by a crushing force, which usually also fractures ribs and may dislocate the sternoclavicular joint. The neck of the scapula may be fractured by a blow or by a fall on the shoulder; the attached long head of triceps may drag the glenoid downwards and laterally. The coracoid process may fracture across its base or be avulsed at the tip. Fracture of the acromion is due to direct force. Fracture of the glenoid fossa usually suggests a medially directed force (impaction of the joint) but may occur with dislocation of the shoulder.

Clinical features The arm is held immobile and there may be severe bruising over the scapula or the chest wall. Because of the energy required to damage the scapula, fractures of the body of the scapula are often associated with severe injuries to the chest, brachial plexus, spine, abdomen and head. Careful neurological and vascular examinations are essential.

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FRACTURES AND JOINT INJURIES

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X-Ray Scapular fractures can be difficult to define on plain xrays because of the surrounding soft tissues. The films may reveal a comminuted fracture of the body of the scapula, or a fractured scapular neck with the outer fragment pulled downwards by the weight of the arm. Occasionally a crack is seen in the acromion or the coracoid process. CT is useful for demonstrating glenoid fractures or body fractures.

Type I

Type II

Type III

Type IV

Type V

Type VI

Classification Fractures of the scapula are divided anatomically into scapular body, glenoid neck, glenoid fossa, acromion and coracoid processes. Scapular neck fractures are the most common. Further subdivisions are shown in Table 24.1. Table 24.1 Fractures of the scapular body Fractures of the glenoid neck Intra-articular glenoid fossa fractures (Ideberg modified by Goss) Type I Fractures of the glenoid rim Type II Fractures through the glenoid fossa, inferior fragment displaced with subluxed humeral head Type III Oblique fracture through glenoid exiting superiorly (may be associated with acromioclavicular dislocation or fracture) Type IV Horizontal fracture exiting through the medial border of the scapula Type V Combination of Type IV and a fracture separating the inferior half of the glenoid

24.4 Fractures of the glenoid – classification Diagrams showing the main types of glenoid fracture.

Type VI Severe comminution of the glenoid surface Fractures of acromion process Type I Minimally displaced Type II Displaced but not reducing subacromial space Type III Inferior displacement and reduced subacromial space Fractures of coracoid process Type I Proximal to attachment of the coracoclavicular ligaments and usually associated with acromioclavicular separation Type II Distal to the coraco-acromial ligaments

Treatment Body fractures Surgery is not necessary. The patient wears a sling for comfort, and from the start practises active exercises to the shoulder, elbow and fingers.

The fracture is usually impacted and the glenoid surface is intact. A sling is worn for comfort and early exercises are begun. Isolated glenoid neck fractures

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Intra-articular fractures Type I glenoid fractures, if displaced, may result in instability of the shoulder. If the fragment involves more than a third of the glenoid surface and is displaced by more than 5 mm surgical fixation should be considered. Anterior rim fractures are approached through a delto-pectoral incision and posterior rim fractures through the posterior approach. Type II fractures are associated with inferior subluxation of the head of the humerus and require open reduction and internal fixation. Types III, IV, V and VI fractures have poorly defined indications for surgery. Generally speaking, if the head is centred on the major portion of the glenoid and the shoulder is stable a non-operative approach is adopted. Comminuted fractures of the glenoid fossa are likely to lead to osteoarthritis in the longer term.

Undisplaced fractures are treated non-operatively. Only Type III acromial fractures, in which the subacromial space is reduced, require operative intervention to restore the anatomy.

Fractures of the acromion

24.5 Glenoid fracture – imaging (a) Three-dimentional CT of a Type II glenoid fracture. (b) X-ray after open reduction and internal fixation.

(b)

Fractures of the coracoid process Fractures distal to the coracoacromial ligaments do not result in serious anatomical displacement; those proximal to the ligaments are usually associated with acromioclavicular separations and may need operative treatment. Combined fractures Whereas an isolated fracture of the glenoid neck is stable, if there is an associated fracture of the clavicle or disruption of the acromioclavicular ligament the glenoid mass may become markedly displaced giving rise to a ‘floating shoulder’ (Williams et al, 2001). Diagnosis can be difficult and may require advanced imaging and three-dimensional reconstructions. At least one of the injuries (and sometimes both) will need operative fixation before the fragments are stabilized.

Treatment The patient is resuscitated. The outcome for the upper limb is very poor. Neither vascular reconstruction nor brachial plexus exploration and repair are likely to give a functional limb.

ACROMIOCLAVICULAR JOINT INJURIES Acute injury of the acromioclavicular joint is common and usually follows direct trauma. Chronic sprains, often associated with degenerative changes, are seen in people engaged in athletic activities like weightlifting or occupations such as working with jack-hammers and other heavy vibrating tools.

Injuries of the shoulder, upper arm and elbow

(a)

24

SCAPULOTHORACIC DISSOCIATION This is a high energy injury. The scapula and arm are wrenched away from the chest, rupturing the subclavian vessels and brachial plexus. Many patients die.

Clinical features The limb is flail and ischaemic. The diagnosis is usually made on the chest x-ray. There is swelling above the clavicle from an expanding haematoma. A distraction of more than 1 cm of a fractured clavicle should give rise to suspicion of this injury.

(a)

(b)

Mechanism of injury A fall on the shoulder with the arm adducted may strain or tear the acromioclavicular ligaments and upward subluxation of the clavicle may occur; if the force is severe enough, the coracoclavicular ligaments will also be torn, resulting in complete dislocation of the joint.

Pathological anatomy and classification The injury is graded according to the type of ligament injury and the amount of displacement of the joint.

(c)

(d)

24.6 Acromioclavicular joint injuries (a) Normal joint. (b) Sprained acromioclavicular joint; no displacement. (c) Torn capsule and subluxation but coracoclavicular ligaments intact. (d) Dislocation with torn coracoclavicular ligaments.

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FRACTURES AND JOINT INJURIES

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(a)

(b)

24.7 Acromioclavicular dislocation (a) Clinically one sees a definite ‘step’ in the contour at the lateral end of the clavicle. (b) The x-ray shows complete separation of the acromioclavicular joint.

Type I is an acute sprain of the acromioclavicular ligaments; the joint is undisplaced. In Type II the acromioclavicular ligaments are torn and the joint is subluxated with slight elevation of the clavicle. In Type III the acromioclavicular and coracoclavicular ligaments are torn and the joint is dislocated; the clavicle is elevated (or the acromion depressed) creating a visible and palpable ‘step’. Other types of displacement are less common, but occasionally the clavicle is displaced posteriorly (Type IV), very markedly upwards (Type V) or inferiorly beneath the coracoid process (Type VI).

Clinical features The patient can usually point to the site of injury and the area may be bruised. If there is tenderness but no deformity, the injury is probably a sprain or a subluxation. With dislocation the patient is in severe pain and a prominent ‘step’ can be seen and felt. Shoulder movements are limited.

X-ray

ideal. There is no convincing evidence that surgery provides a better functional result than conservative treatment for a straightforward Type III injury. Operative repair should be considered only for patients with extreme prominence of the clavicle, those with posterior or inferior dislocation of the clavicle and those who aim to resume strenuous overarm or overhead activities. Whilst there is no consensus regarding the best surgical solution, there are a number of underlying principles to consider if surgery is contemplated. Accurate reduction should be the goal. The ligamentous stability can be recreated either by transferring existing ligaments (the coracoacromial or conjoined tendons), or by using a free graft (e.g., autogenous semitendinosis or a synthetic ligament). This reconstruction must have sufficient stability to prevent re-dislocation during recovery. Any rigid implants which cross the joint will need to be removed at a later date to prevent loosening or fracture. In the modified Weaver–Dunn procedure the lateral end of the clavicle is excised and the coracoacromial ligament is transferred to the outer end of the clavicle and attached by trans-osseous sutures. Tension on the repair can be reduced either by anchoring the clavicle to the coracoid with a Bosworth coracoclavicular screw (which has to be removed after 8 weeks) or by employing a Dacron sling – looped round the coracoid and the clavicle – for the same purpose. Great care is needed to avoid entrapment or damage to a nerve or vessel. Elbow and forearm exercises are begun on the day after operation and active-assisted shoulder movements 2 weeks later, increasing gradually to active movements at 4–6 weeks. Strenuous lifting movements are avoided for 4–6 months. Recent advances in instrumentation have made it

The acromioclavicular joint is not always easily visualized; anteroposterior, cephalic tilt and axillary views are advisable. In addition, a stress view is sometimes helpful in distinguishing between a Type II and Type III injury: this is an anteroposterior x-ray including both shoulders with the patient standing upright, arms by the side and holding a 5 kg weight in each hand. The distance between the coracoid process and the inferior border of the clavicle is measured on each side; a difference of more than 50 per cent is diagnostic of acromioclavicular dislocation.

Treatment

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Sprains and subluxations do not affect function and do not require any special treatment; the arm is rested in a sling until pain subsides (usually no more than a week) and shoulder exercises are then begun. Dislocations are poorly controlled by padding and bandaging, yet the role of surgery is controversial. The large number of operations suggests that none is

24.8 Modified Weaver Dunn operation The lateral end of the clavicle is excised; the acromial end of the coracoacromial ligament is detached and fastened to the lateral end of the clavicle. Tension on the ligament is lessened by placing a ‘sling’ around the clavicle and the coracoid process. (Dotted lines show former position of coracoacromial ligament).

feasible to perform this type of reconstructive surgery arthroscopically (Snow and Funk, 2006).

lows a direct blow to the front of the joint. Anterior dislocation is much more common than posterior. The joint can be sprained, subluxed or dislocated.

24

Complications

Unreduced dislocation An unreduced dislocation is ugly

and sometimes affects function. Simple excision of the distal clavicle will only make matters worse. An attempt should be made to reconstruct the coracoclavicular ligament. The Weaver–Dunn procedure may be suitable (See Figure 24.8). The more severe injuries are quite often followed by ossification of the coracoclavicular ligaments. Bony spurs may predispose to later rotator cuff dysfunction, which may require operative treatment.

Ossification of the ligaments

Secondary osteoarthritis A late complication of Type I

and II injuries is osteoarthritis of the acromioclavicular joint. This can usually be managed conservatively, but if pain is marked the outer 2 cm of the clavicle can be excised. The patient will be aware of some weakness during strenuous over-arm activities and pain is often not completely abolished.

STERNOCLAVICULAR DISLOCATIONS Mechanism of injury This uncommon injury is usually caused by lateral compression of the shoulders; for example, when someone is pinned to the ground following a road accident or an underground rock-fall. Rarely, it fol-

Clinical features Anterior dislocation is easily diagnosed; the dislocated medial end of the clavicle forms a prominent bump over the sternoclavicular joint. The condition is painful but there are usually no cardiothoracic complications. Posterior dislocation, though rare, is much more serious. Discomfort is marked; there may be pressure on the trachea or large vessels, causing venous congestion of the neck and arm and circulation to the arm may be decreased.

X-Ray Because of overlapping shadows, plain x-rays are difficult to interpret. Special oblique views are helpful and CT is the ideal method.

Treatment Sprains and subluxations do not require specific treatment. Anterior dislocation can usually be reduced by exerting pressure over the clavicle and pulling on the arm with the shoulder abducted. However, the joint usually redislocates. Not that this matters much; full function will be regained, though this may take several months. Internal fixation is unnecessary and very dangerous (because of the large vessels behind the sternum). Posterior dislocation should be reduced as soon as possible. This can usually be done closed (if necessary under general anaesthesia) by lying the patient supine with a sandbag between the scapulae and then pulling on the arm with the shoulder abducted and extended. The joint reduces with a snap and stays reduced. If this manoeuvre fails, the medial end of the clavicle is grasped with bone forceps and pulled forwards. If this too, fails (a very rare occurrence) open reduction is justified, but great care must be taken not to damage the mediastinal structures. After reduction, the shoulders are braced back with a figure-of-eight bandage, which is worn for 3 weeks.

Injuries of the shoulder, upper arm and elbow

An acute strain of the acromioclavicular joint is sometimes followed by supraspinatus tendinitis. Whether this is directly due to the primary injury or whether it results from post-traumatic oedema or inflammation of the overlying acromioclavicular joint is unclear. Treatment with anti-inflammatory preparations may help. Rotator cuff syndrome

DISLOCATION OF THE SHOULDER (a)

(b)

24.9 Sternoclavicular dislocation (a) The bump over the sternoclavicular joint may be obvious, though this is difficult to demonstrate on plain x-ray. (b) Tomography (or, better still, CT) will show the lesion.

Of the large joints, the shoulder is the one that most commonly dislocates. This is due to a number of factors: the shallowness of the glenoid socket; the extraordinary range of movement; underlying condi-

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24

tions such as ligamentous laxity or glenoid dysplasia; and the sheer vulnerability of the joint during stressful activities of the upper limb. In this chapter, acute anterior and posterior dislocations are described. Chronic instability is described in Chapter 13.

A lateral view aimed along the blade of the scapula will show the humeral head out of line with the socket. If the joint has dislocated before, special views may show flattening or an excavation of the posterolateral contour of the humeral head, where it has been indented by the anterior edge of the glenoid socket, the Hill–Sachs lesion.

ANTERIOR DISLOCATION Treatment

Mechanism of injury Dislocation is usually caused by a fall on the hand. The head of the humerus is driven forward, tearing the capsule and producing avulsion of the glenoid labrum (the Bankart lesion). Occasionally the posterolateral part of the head is crushed. Rarely, the acromion process levers the head downwards and the joint dislocates with the arm pointing upwards (luxatio erecta); nearly always the arm then drops, bringing the head to its subcoracoid position.

Clinical features Pain is severe. The patient supports the arm with the opposite hand and is loathe to permit any kind of examination. The lateral outline of the shoulder may be flattened and, if the patient is not too muscular, a bulge may be felt just below the clavicle. The arm must always be examined for nerve and vessel injury before reduction is attempted.

X-Ray The anteroposterior x-ray will show the overlapping shadows of the humeral head and glenoid fossa, with the head usually lying below and medial to the socket.

Various methods of reduction have been described, some of them now of no more than historical interest. In a patient who has had previous dislocations, simple traction on the arm may be successful. Usually, sedation and occasionally general anaesthesia is required. With Stimson’s technique, the patient is left prone with the arm hanging over the side of the bed. After 15 or 20 minutes the shoulder may reduce. In the Hippocratic method, gently increasing traction is applied to the arm with the shoulder in slight abduction, while an assistant applies firm countertraction to the body (a towel slung around the patient’s chest, under the axilla, is helpful). With Kocher’s method, the elbow is bent to 90° and held close to the body; no traction should be applied. The arm is slowly rotated 75 degrees laterally, then the point of the elbow is lifted forwards, and finally the arm is rotated medially. This technique carries the risk of nerve, vessel and bone injury and is not recommended. Another technique has the patient sitting on a reduction chair and with gentle traction of the arm over the back of the padded chair the dislocation is reduced. An x-ray is taken to confirm reduction and exclude

(c)

(a)

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(b)

(d)

24.10 Anterior dislocation of the shoulder (a) The prominent acromion process and flattening of the contour over the deltoid are typical signs. (b) X-ray confirms the diagnosis of anterior dislocation. (c,d) Two methods of reduction.

Complications EARLY Rotator cuff tear This commonly accompanies anterior dislocation, particularly in older people. The patient may have difficulty abducting the arm after reduction; palpable contraction of the deltoid muscle excludes an axillary nerve palsy. Most do not require surgical attention, but young active individuals with large tears will benefit from early repair.

The axillary nerve is most commonly injured; the patient is unable to contract the deltoid muscle and there may be a small patch of anaesthesia over the muscle. The inability to abduct must be distinguished from a rotator cuff tear. The nerve lesion is usually a neuropraxia which recovers spontaneously after a few weeks; if it does not, then surgery should be considered as the results of repair are less satisfactory if the delay is more than a few months. Occasionally the radial nerve, musculocutaneous nerve, median nerve or ulnar nerve can be injured. Rarely there is a complete infra-clavicular brachial plexus palsy. This is somewhat alarming, but fortunately it usually recovers with time. Nerve injury

24

(a)

(b)

24.11 Anterior fracture-discloation Anterior dislocation of the shoulder may be complicated by fracture of (a) the greater tuberosity or (b) the neck of the humerus – this often needs open reduction and internal fixation.

The axillary artery may be damaged, particularly in old patients with fragile vessels. This can occur either at the time of injury or during overzealous reduction. The limb should always be examined for signs of ischaemia both before and after reduction.

Vascular injury

Fracture-dislocation If there is an associated fracture of the proximal humerus, open reduction and internal fixation may be necessary. The greater tuberosity may be sheared off during dislocation. It usually falls into place during reduction, and no special treatment is then required. If it remains displaced, surgical reattachment is recommended to avoid later subacromial impingement.

Injuries of the shoulder, upper arm and elbow

a fracture. When the patient is fully awake, active abduction is gently tested to exclude an axillary nerve injury and rotator cuff tear. The median, radial, ulnar and musculocutaneous nerves are also tested and the pulse is felt. The arm is rested in a sling for about three weeks in those under 30 years of age (who are most prone to recurrence) and for only a week in those over 30 (who are most prone to stiffness). Then movements are begun, but combined abduction and lateral rotation must be avoided for at least 3 weeks. Throughout this period, elbow and finger movements are practised every day. There has been some interest in the use of external rotation splints, based on the theory that this would reduce the Bankart lesion into a better position for healing. However a recent Cochrane review has concluded that there is insufficient evidence to inform on the choices for conservative treatment and that further trials are needed to compare different types and duration of immobilization. Young athletes who dislocate their shoulder traumatically and who continue to pursue their sports (particularly contact sports) are at a much higher risk of re-dislocation in the future. With increasing advances and techniques of arthroscopy and arthroscopic anterior stabilization surgery, some are now advocating early surgery in this group of patients to repair the Bankart lesion of the anterior labrum. However a consensus on early surgery has still not been reached.

LATE Shoulder stiffness Prolonged immobilization may lead to stiffness of the shoulder, especially in patients over the age of 40. There is loss of lateral rotation, which automatically limits abduction. Active exercises will usually loosen the joint. They are practised vigorously, bearing in mind that full abduction is not possible until lateral rotation has been regained. Manipulation under anaesthesia or arthroscopic capsular release is advised only if progress has halted and at least 6 months have elapsed since injury. Unreduced dislocation Surprisingly, a dislocation of the

shoulder sometimes remains undiagnosed. This is more likely if the patient is either unconscious or very old. Closed reduction is worth attempting up to 6 weeks after injury; manipulation later may fracture the bone or tear vessels or nerves. Operative reduction is indicated after 6 weeks only in the young, because it is difficult, dangerous and followed by prolonged stiffness. An anterior approach is used, and the vessels and nerves are carefully identified before the dislocation is reduced. ‘Active neglect’ summarizes the treatment of unreduced dislocation in the elderly. The dislocation is disregarded and gentle active movements are encouraged. Moderately good function is often regained.

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24.12 Recurrent dislocation of the shoulder (a) The classic x-ray sign is a depression in the posterosuperior part of the humeral head (the HillSachs lesion). (b,c) MRI scans showing both the Hill–Sachs lesion and a Bankart lesion of the glenoid rim (arrows). (a)

(b)

(c)

If an anterior dislocation tears the shoulder capsule, repair occurs spontaneously following reduction and the dislocation may not recur; but if the glenoid labrum is detached, or the capsule is stripped off the front of the neck of the glenoid, repair is less likely and recurrence is more common. Detachment of the labrum occurs particularly in young patients, and, if at injury a bony defect has been gouged out of the posterolateral aspect of the humeral head, recurrence is even more likely. In older patients, especially if there is a rotator cuff tear or greater tuberosity fracture, recurrent dislocation is unlikely. The period of post-operative immobilization makes no difference. The history is diagnostic. The patient complains that the shoulder dislocates with relatively trivial everyday actions. Often he can reduce the dislocation himself. Any doubt as to diagnosis is quickly resolved by the apprehension test: if the patient’s arm is passively placed behind the coronal plane in a position of abduction and lateral rotation, his immediate resistance and apprehension are pathognomonic. An anteroposterior x-ray with the shoulder medially rotated may show an indentation in the back of the humeral head (the Hill–Sachs lesion). Even more common, but less readily diagnosed, is recurrent subluxation. The management of both types of instability is dealt with in Chapter 13.

Recurrent dislocation

a direct blow to the front of the shoulder or a fall on the outstretched hand.

Clinical features The diagnosis is frequently missed – partly because reliance is placed on a single anteroposterior x-ray (which may look almost normal) and partly because those attending to the patient fail to think of it. There are, in fact, several well-marked clinical features. The arm is held in internal rotation and is locked in that position. The front of the shoulder looks flat with a prominent coracoid, but swelling may obscure this deformity; seen from above, however, the posterior displacement is usually apparent.

X-Ray In the anteroposterior film the humeral head, because it is medially rotated, looks abnormal in shape (like an

POSTERIOR DISLOCATION OF THE SHOULDER Posterior dislocation is rare, accounting for less than 2 per cent of all dislocations around the shoulder.

Mechanism of injury

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Indirect force producing marked internal rotation and adduction needs be very severe to cause a dislocation. This happens most commonly during a fit or convulsion, or with an electric shock. Posterior dislocation can also follow a fall on to the flexed, adducted arm,

24.13 Posterior dislocation of the shoulder The characteristic x-ray image. Because the head of the humerus is internally rotated, the anteroposterior x-ray shows a head-on projection giving the classic ‘electric light-bulb’ appearance.

INFERIOR DISLOCATION OF THE SHOULDER (LUXATIO ERECTA) Inferior dislocation is rare but it demands early recognition because the consequences are potentially very serious. Dislocation occurs with the arm in nearly full abduction/elevation. The humeral head is levered out of its socket and pokes into the axilla; the arm remains fixed in abduction.

Mechanism of injury and pathology Treatment The acute dislocation is reduced (usually under general anaesthesia) by pulling on the arm with the shoulder in adduction; a few minutes are allowed for the head of the humerus to disengage and the arm is then gently rotated laterally while the humeral head is pushed forwards. If reduction feels stable the arm is immobilized in a sling; otherwise the shoulder is held widely abducted and laterally rotated in an airplane type splint for 3–6 weeks to allow the posterior capsule to heal in the shortest position. Shoulder movement is regained by active exercises.

Complications

The injury is caused by a severe hyper-abduction force. With the humerus as the lever and the acromion as the fulcrum, the humeral head is lifted across the inferior rim of the glenoid socket; it remains in the subglenoid position, with the humeral shaft pointing upwards. Soft-tissue injury may be severe and includes avulsion of the capsule and surrounding tendons, rupture of muscles, fractures of the glenoid or proximal humerus and damage to the brachial plexus and axillary artery.

Clinical features The startling picture of a patient with his arm locked in almost full abduction should make diagnosis quite easy. The head of the humerus may be felt in or below the axilla. Always examine for neurovascular damage.

24

Injuries of the shoulder, upper arm and elbow

electric light bulb) and it stands away somewhat from the glenoid fossa (the ‘empty glenoid’ sign). A lateral film and axillary view is essential; it shows posterior subluxation or dislocation and sometimes a deep indentation on the anterior aspect of the humeral head. Posterior dislocation is sometimes complicated by fractures of the humeral neck, posterior glenoid rim or lesser tuberosity. Sometimes the patient is too uncomfortable to permit adequate imaging and in these difficult cases CT is essential to rule out posterior dislocation of the shoulder.

Unreduced dislocation At least half the patients with

posterior dislocation have ‘unreduced’ lesions when first seen. Sometimes weeks or months elapse before the diagnosis is made and up to two thirds of posterior dislocations are not recognised initially. Typically the patient holds the arm internally rotated; he cannot abduct the arm more than 70–80 degrees, and if he lifts the extended arm forwards he cannot then turn the palm upwards. If the patient is young, or is uncomfortable and the dislocation fairly recent, open reduction is indicated. This is a difficult procedure. It is generally done through a delto-pectoral approach; the shoulder is reduced and the defect in the humeral head can then be treated by transferring the subscapularis tendon into the defect (McLaughlin procedure). Alternatively, the defect on the humeral head can be bone grafted. A useful technique for treating a defect smaller than 40 per cent of the humeral head is to transfer of the lesser tuberosity together with the subscapularis into the defect. For defects larger than this a hemiarthroplasty may be considered. Late dislocations, especially in the elderly, are best left, but movement is encouraged. Recurrent dislocation or subluxation Chronic posterior instability of the shoulder is discussed in Chapter 13.

X-ray The humeral shaft is shown in the abducted position with the head sitting below the glenoid. It is important to search for associated fractures of the glenoid or proximal humerus. NOTE: True inferior dislocation must not be confused with postural downward displacement of the humerus, which results quite commonly from weakness and laxity of the muscles around the shoulder, especially after trauma and shoulder splintage; here

24.14 Inferior dislocation of the shoulder You can see why the condition is called luxatio erecta. The shaft of the humerus points upwards and the humeral head is displaced downwards.

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the shaft of the humerus lies in the normal anatomical position at the side of the chest. The condition is harmless and resolves as muscle tone is regained.

FRACTURES AND JOINT INJURIES

Treatment Inferior dislocation can usually be reduced by pulling upwards in the line of the abducted arm, with counter-traction downwards over the top of the shoulder. If the humeral head is stuck in the soft tissues, open reduction is needed. It is important to examine again, after reduction, for evidence of neurovascular injury. The arm is rested in a sling until pain subsides and movement is then allowed, but avoiding abduction for 3 weeks to allow the soft tissues to heal.

SHOULDER DISLOCATIONS IN CHILDREN Traumatic dislocation of the shoulder is exceedingly rare in children. Children who give a history of the shoulder ‘slipping out’ almost invariably have either voluntary or involuntary (atraumatic) dislocation or subluxation. With voluntary dislocation, the child can demonstrate the instability at will. With involuntary dislocation, the shoulder slips out unexpectedly during everyday activities. Most of these children have generalized joint laxity and some have glenoid dysplasia or muscle patterning disorders (Chapter 13). Examination may show that the shoulder subluxates in almost any direction; x-rays may confirm the diagnosis.

Treatment Atraumatic dislocation should be viewed with great caution. Some of these children have behavioural or muscle patterning problems and this is where treat-

2

ment should be directed. A prolonged exercise programme may also help. Only if the child is genuinely distressed by the disorder, and provided psychological factors have been excluded, should one consider reconstructive surgery.

FRACTURES OF THE PROXIMAL HUMERUS Fractures of the proximal humerus usually occur after middle age and most of the patients are osteoporotic, postmenopausal women. Fracture displacement is usually not marked and treatment presents few problems. However, in about 20 per cent of cases there is considerable displacement of one or more fragments and a significant risk of complications due to bone fragility, damage to the rotator cuff and the prevailing co-morbidities. Deciding between operative and nonoperative treatment can be very difficult.

Mechanism of injury Fracture usually follows a fall on the out-stretched arm – the type of injury which, in younger people, might cause dislocation of the shoulder. Sometimes, indeed, there is both a fracture and a dislocation.

Classification and pathological anatomy The most widely accepted classification is that of Neer (1970) who drew attention to the four major segments involved in these injuries: the head of the humerus, the lesser tuberosity, the greater tuberosity and the shaft. Neer’s classification distinguishes between the number of displaced fragments, with displacement defined as greater than 45 degrees of angulation or 1 cm of separation. Thus, however many fracture lines there are, if the fragments are undisplaced it is regarded as a one-part fracture; if one segment is sep-

2

3

3 4

4

5 1

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(a)

1

(b)

24.15 Fractures of the proximal humerus Diagram of (a) the normal and (b) a fractured proximal humerus, showing the four main fragments, two or more of which are seen in almost all proximal humeral fractures. 1=shaft of humerus; 2=head of humerus; 3=greater tuberosity; 4=lesser tuberosity. In this figure there is a sizeable medial calcar spike; 5=suggesting a low risk of avascular necrosis.

24

(b)

(c)

(d)

24.16 X-rays of proximal humeral fractures Classification is all very well, but x-rays are more difficult to interpret than line drawings. (a) Two-part fracture. (b) Three-part fracture involving the neck and the greater tuberosity. (c) Four-part fracture. (1=shaft of humerus; 2=head of humerus; 3=greater tuberosity; 4=lesser tuberosity). (d) X-ray showing fracturedislocation of the shoulder.

arated from the others, it is a two-part fracture; if two fragments are displaced, that is a three-part fracture; if all the major parts are displaced, it is a four-part fracture. Furthermore, a fracture-dislocation exists when the head is dislocated and there are two, three or four parts. This grading is based on x-ray appearances, although observers do not always agree with each other on which class a particular fracture falls into.

Clinical features Because the fracture is often firmly impacted, pain may not be severe. However, the appearance of a large bruise on the upper part of the arm is suspicious. Signs of axillary nerve or brachial plexus injury should be sought.

X-ray In elderly patients there often appears to be a single, impacted fracture extending across the surgical neck. However, with good x-rays, several undisplaced fragments may be seen. In younger patients, the fragments are usually more clearly separated. Axillary and scapular-lateral views should always be obtained, to exclude dislocation of the shoulder. It has always been difficult to apply Neer’s classification when based on plain x-rays and not surprisingly there is a relatively high level of both inter- and intraobserver disagreement. Neer himself later noted that when this classification was developed the criteria for displacement (distance >1 cm, angulation >45 degrees) were set arbitrarily. The classification was not intended to dictate treatment, but simply to help clarify the pathoanatomy of the different fracture patterns. The advent of three-dimensional CT reconstruction has helped to reduce the degree of inter- and intra-observer error, enabling better planning of treatment than in the past. As the fracture heals, the humeral head is sometimes seen to be subluxated downwards (inferiorly); this is due to muscle atony and it usually recovers once exercises are begun.

Injuries of the shoulder, upper arm and elbow

(a)

Treatment

24.17 CT with three-dimensional reconstruction Advanced imaging provides a much clearer picture of the injury, allowing better pre-operative planning.

MINIMALLY DISPLACED FRACTURES These comprise the vast majority. They need no treatment apart from a week or two period of rest with the arm in a sling until the pain subsides, and then gentle passive movements of the shoulder. Once the fracture has united (usually after 6 weeks), active exercises are encouraged; the hand is, of course, actively exercised from the start.

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TWO-PART FRACTURES Surgical neck fractures The fragments are gently

manipulated into alignment and the arm is immobilized in a sling for about four weeks or until the fracture feels stable and the x-ray shows some signs of healing. Elbow and hand exercises are encouraged throughout this period; shoulder exercises are commenced at about four weeks. The results of conservative treatment are generally satisfactory, considering that most of these patients are over 65 and do not demand perfect function. However, if the fracture cannot be reduced closed or if the fracture is very unstable after closed reduction, then fixation is required. Options include percutaneous pins, bone sutures, intramedullary pins with tension band wiring or a locked intramedullary nail. Plate fixation requires a wider exposure and the newer locking plates offer a stable fixation without the need for extensive periosteal stripping. Fracture of the greater tuberosity is often associated with anterior dislocation and it reduces to a good position when the shoulder is relocated. If it does not reduce, the fragment can be re-attached through a small incision with interosseous sutures or, in young hard bone, cancellous screws.

Greater tuberosity fractures

Anatomical neck fractures These are very rare. In young patients the fracture should be fixed with a screw. In older patients prosthetic replacement (hemiarthroplasty) is preferable because of the high risk of avascular necrosis of the humeral head.

THREE-PART FRACTURES These usually involve displacement of the surgical neck and the greater tuberosity; they are extremely difficult to reduce closed. In active individuals this injury is best managed by open reduction and internal fixation. There is little evidence that one technique is better than another although the newer implants with

(a)

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(b)

locked plating and nailing are biomechanically superior in osteoporotic bone. FOUR-PART FRACTURES The surgical neck and both tuberosities are displaced. These are severe injuries with a high risk of complications such as vascular injury, brachial plexus damage, injuries of the chest wall and (later) avascular necrosis of the humeral head. The x-ray diagnosis is difficult (how many fragments are there, and are they displaced?). Often the most one can say is that there are ‘multiple displaced fragments’, sometimes together with glenohumeral dislocation. In young patients an attempt should be made at reconstruction. In older patients, closed treatment and attempts at open reduction and fixation can result in continuing pain and stiffness and additional surgical treatment can compromise the blood supply still further. If the fracture pattern is such that the blood-supply is likely to be compromised, or that reconstruction and internal fixation will be extremely difficult, then the treatment of choice is prosthetic replacement of the proximal humerus. The results of hemiarthroplasty are somewhat unpredictable. Anatomical reduction, fixation and healing of the tuberosities are prerequisites for a satisfactory outcome; even then, secondary displacement of the tuberosities may result in a poor functional outcome. In addition the prosthetic implant should be perfectly positioned. Be warned – these are operations for the expert; the subject is well covered by Boileau et al. (2006).

FRACTURE-DISLOCATION Two-part fracture-dislocations (greater tuberosity with anterior dislocation and lesser tuberosity with posterior) can usually be reduced by closed means.

(c)

(d)

24.18 Proximal humerus fractures – treatment (a) Three-part fracture, treated by (b) locked nail fixation. (c) Four-part fracture fixed with a locked plate; the intra-operative picture (d) shows how the plate was positioned.

Complications The patient should always be carefully assessed for signs of vascular and nerve injuries, both at the initial examination and again after any operation. The axillary nerve is at particular risk, both from the injury and from surgery.

Vascular injuries and nerve injuries

Avascular necrosis The reported incidence of avascular

necrosis (AVN) of the humeral head ranges from 10– 30 per cent in three-part fractures and 10 to over 50 per cent in four-part fractures. The ability to predict the likelihood of this outcome is important in making the choice between internal fixation and hemiarthroplasty for complex fractures. The blood-supply of the humeral head is provided mainly by the anterior circumflex artery and its ascending branch (the arcuate artery) which penetrates into the humeral head and arches across subchondrally. Additional blood-supply is provided by vessels entering the posteromedial aspect of the proximal humerus, metaphyseal vessels and vessels of the greater and lesser tuberosities that anastomose with the intraosseous arcuate artery. Thus, in threeand four-part fractures with the only supply coming from the posteromedial vessels, there may still be sufficient perfusion of the humeral head if the head fragment includes a sizeable part of the calcar on the medial side of the anatomical neck. Hertel et al. (2004) have made the point that fractures at the anatomical neck with a medial metaphyseal (calcar) spike shorter than 8 mm carry a high risk of developing humeral head avascular necrosis (see Fig. 24.15). Disruption of the medial periosteal hinge is another predictor of avascular necrosis and the presence of these two factors combined has a positive predictive value of 98 per cent for avascular necrosis of the humeral head. Contrariwise, fractures with an intact medial hinge and/or a large posteromedial metaphyseal spike carry a much better prognosis. The mere number of fracture parts, their degree of displacement and split-head fractures are rated as poor predictors of avascular necrosis, as is the presence of dislocation. of the shoulder This is a common complication, particularly in elderly patients. Unlike a frozen shoulder, the stiffness is maximal at the outset. It can be prevented, or at least minimized, by starting exercises early.

Stiffness

Malunion Malunion usually causes little disability, but loss of rotation may make it difficult for the patient to reach behind the neck or up the back.

FRACTURES OF THE PROXIMAL HUMERUS IN CHILDREN At birth, the shoulder is sometimes dislocated or the proximal humerus fractured. Diagnosis is difficult and a clavicular fracture or brachial plexus injury should also be considered. In infancy, the physis can separate (Salter–Harris I); reduction does not have to be perfect and a good outcome is usual. In older children, metaphyseal fractures or Type II physeal fractures occur. Considerable displacement and angulation can be accepted; because of the marked growth and remodelling potential of the proximal humerus, malunion is readily compensated for during the remaining growth period. Pathological fractures are not unusual, as the proximal humerus is a common site of bone cysts and tumours in children. Fracture through a simple cyst usually unites and the cyst often heals spontaneously; all that is needed is to rest the arm in a sling for 4–6 weeks. Other lesions require treatment in their own right (See Chapter 9).

(a)

24

Injuries of the shoulder, upper arm and elbow

Three-part fracture-dislocations, when the surgical neck is also broken, usually require open reduction and fixation; the brachial plexus is at particular risk during this operation. Four-part fracture-dislocations have a poor prognosis; prosthetic replacement is recommended in all but young and very active patients.

(b)

24.19 Fractures of the proximal humerus in children (a) The typical metaphyseal fracture. Reduction need not be perfect as remodelling will compensate for malunion. (b) Fracture through a benign cyst.

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Treatment

FRACTURED SHAFT OF HUMERUS

FRACTURES AND JOINT INJURIES

Mechanism of injury A fall on the hand may twist the humerus, causing a spiral fracture. A fall on the elbow with the arm abducted exerts a bending force, resulting in an oblique or transverse fracture. A direct blow to the arm causes a fracture which is either transverse or comminuted. Fracture of the shaft in an elderly patient may be due to a metastasis.

Pathological anatomy With fractures above the deltoid insertion, the proximal fragment is adducted by pectoralis major. With fractures lower down, the proximal fragment is abducted by the deltoid. Injury to the radial nerve is common, though fortunately recovery is usual.

Clinical features The arm is painful, bruised and swollen. It is important to test for radial nerve function before and after treatment. This is best done by assessing active extension of the metacarpophalangeal joints; active extension of the wrist can be misleading because extensor carpi radialis longus is sometimes supplied by a branch arising proximal to the injury.

X-ray The site of the fracture, its line (transverse, spiral or comminuted) and any displacement are readily seen. The possibility that the fracture may be pathological should be remembered.

(a)

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(b)

(c)

(d)

Fractures of the humerus heal readily. They require neither perfect reduction nor immobilization; the weight of the arm with an external cast is usually enough to pull the fragments into alignment. A ‘hanging cast’ is applied from shoulder to wrist with the elbow flexed 90 degrees, and the forearm section is suspended by a sling around the patient’s neck. This cast may be replaced after 2–3 weeks by a short (shoulder to elbow) cast or a functional polypropylene brace which is worn for a further 6 weeks. The wrist and fingers are exercised from the start. Pendulum exercises of the shoulder are begun within a week, but active abduction is postponed until the fracture has united (about 6 weeks for spiral fractures but often twice as long for other types); once united, only a sling is needed until the fracture is consolidated.

OPERATIVE TREATMENT Patients often find the hanging cast uncomfortable, tedious and frustrating; they can feel the fragments moving and that is sometimes quite distressing. The temptation is to ‘do something’, and the ‘something’ usually means an operation. It is well to remember (a) that the complication rate after internal fixation of the humerus is high and (b) that the great majority of humeral fractures unite with non-operative treatment. (c) There is no good evidence that the union rate is higher with fixation (and the rate may be lower if there is distraction with nailing or periosteal stripping with plating). There are, nevertheless, some well defined indications for surgery: • severe multiple injuries • an open fracture

(e)

24.20 Fractured shaft of humerus (a) Bruising is always extensive. (b,c) Closed transverse fracture with moderate displacement. (d) Applying a U-slab of plaster (after a few days in a shoulder-to-wrist hanging cast) is usually adequate. (e) Ready-made braces are simpler and more comfortable, though not suitable for all cases. These conservative methods demand careful supervision if excessive angulation and malunion are to be prevented.

(a)

(b)

(c)

• • • •

segmental fractures displaced intra-articular extension of the fracture a pathological fracture a ‘floating elbow’ (simultaneous unstable humeral and forearm fractures) • radial nerve palsy after manipulation • non-union • problems with nursing care in a dependent person. Fixation can be achieved with either (1) a compression plate and screws, (2) an interlocking intramedullary nail or semi-flexible pins, or (3) an external fixator. Plating permits excellent reduction and fixation, and has the added advantage that it does not interfere with shoulder or elbow function. However, it requires wide dissection and the radial nerve must be protected. Too much periosteal stripping or inadequate fixation will probably increase the risk of non-union. Antegrade nailing is performed with a rigid interlocking nail inserted through the rotator cuff under fluoroscopic control. It requires minimal dissection but has the disadvantage that it causes rotator cuff problems in a significant proportion of cases (the reported incidence ranges from 5–40 per cent). The nail can also distract the fracture which will inhibit

union; if this happens, exchange nailing and bone grafting of the fracture may be needed. Retrograde nailing with multiple flexible rods is not entirely stable. Retrograde nailing with an interlocking nail is suitable for some fractures of the middle third. External fixation may be the best option for highenergy segmental fractures and open fractures. However, great care must be taken in placing the pins as the radial nerve is vulnerable.

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Injuries of the shoulder, upper arm and elbow

24.21 Fractured shaft of humerus – treatment (a,b) Most shaft fractures can be treated in a hanging cast or functional brace, but beware the upper third fracture which tends to angulate at the proximal border of a short cast. This fracture would have been better managed by (c) intramedullary nailing (and better still with a locking nail).

Complications EARLY If there are signs of vascular insufficiency in the limb, brachial artery damage must be excluded. Angiography will show the level of the injury. This is an emergency, requiring exploration and either direct repair or grafting of the vessel. In these circumstances, internal fixation is advisable.

Vascular injury

Radial nerve palsy (wrist drop and paralysis of the metacarpophalangeal extensors) may occur with shaft fractures, particularly oblique fractures

Nerve injury

24.22 Fractured humerus – other methods of fixation (a,b) Compression plating, and (c,d,e) external fixation.

(a)

(b)

(c)

(d)

(e)

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FRACTURES AND JOINT INJURIES

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at the junction of the middle and distal thirds of the bone (Holstein–Lewis fracture). If nerve function was intact before manipulation but is defective afterwards, it must be assumed that the nerve has been snagged and surgical exploration is necessary. Otherwise, in closed injuries the nerve is very seldom divided, so there is no hurry to operate as it will usually recover. The wrist and hand must be regularly moved through a full passive range of movement to preserve joint motion until the nerve recovers. If there is no sign of recovery by 12 weeks, the nerve should be explored. It may just need a neurolysis, but if there is loss of continuity of normal-looking nerve then a graft is needed. The results are often satisfactory but, if necessary, function can be largely restored by tendon transfers (see Chapter 11). LATE Delayed union and non-union Transverse fractures sometimes take months to unite, especially if excessive traction has been used (a hanging cast must not be too heavy). Simple adjustments in technique may solve the problem; as long as there are signs of callus formation it is worth persevering with non-operative treatment, but remember to keep the shoulder moving. The rate of non-union in conservatively treated low-energy fractures is less than 3 per cent. Segmental high energy fractures and open fractures are more prone to both delayed union and non-union. Intramedullary nailing may contribute to delayed union, but if rigid fixation can be maintained (if necessary by exchange nailing) the rate of non-union can probably be kept below 10 per cent. A particularly vicious combination is incomplete union and a stiff joint. If elbow or shoulder movements are forced before consolidation of the fracture, or if an intramedullary nail is removed too soon (e.g., because of shoulder problems), the humerus may refracture and non-union is then more likely. The treatment of established non-union is operative. The bone ends are freshened, cancellous bone graft is packed around them and the reduction is held with an intramedullary nail or a compression plate.

Joint stiffness is common. It can be minimized by early activity, but transverse fractures (in which shoulder abduction is ill-advised) may limit shoulder movement for several weeks.

Joint stiffness

SPECIAL FEATURES IN CHILDREN

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Fractures of the humerus are uncommon; in children under 3 years of age the possibility of child abuse should be considered and tactful examination for other injuries performed.

Taking advantage of the robust periosteum and the power of rapid healing in children, the humeral fracture can usually be treated by applying a collar and cuff bandage for 3 or 4 weeks. If there is gross shortening, manipulation may be needed. Older children may require a short plaster splint.

FRACTURES OF THE DISTAL HUMERUS IN ADULTS Fractures around the elbow in adults – especially those of the distal humerus – are often high-energy injuries which are associated with vascular and nerve damage. Some can be reduced and stabilized only by complex surgical techniques; and the tendency to stiffness of the elbow means that with all severe injuries the striving for anatomical perfection has to be weighed up against the realities of imperfect postoperative function. The AO-ASIF Group have defined three types of distal humeral fracture: Type A – an extra-articular supracondylar fracture; Type B – an intra-articular unicondylar fracture (one condyle sheared off); Type C – bicondylar fractures with varying degrees of comminution.

TYPE A – SUPRACONDYLAR FRACTURES These extra-articular fractures are rare in adults. When they do occur, they are usually displaced and unstable – probably because there is no tough periosteum to tether the fragments. In high-energy injuries there may be comminution of the distal humerus.

Treatment Closed reduction is unlikely to be stable and K-wire fixation is not strong enough to permit early mobilization. Open reduction and internal fixation is therefore the treatment of choice. The distal humerus is approached through a posterior exposure. It is sometimes possible to fix the fracture without recourse to an olecranon osteotomy or triceps reflection. A simple transverse or oblique fracture can usually be reduced and fixed with a pair of contoured plates and screws.

TYPES B AND C – INTRA-ARTICULAR FRACTURES Except in osteoporotic individuals, intra-articular condylar fractures should be regarded as high-energy

X-Ray The fracture extends from the lower humerus into the elbow joint; it may be difficult to tell whether one or both condyles are involved, especially with an undisplaced condylar fracture. There is often also comminution of the bone between the condyles, the extent of which is usually underestimated. Sometimes the fracture extends into the metaphysis as a T- or Yshaped break, or else there may be multiple fragments (comminution). The lesson is: ‘Prepare for the worst before operating’. CT scans can be helpful in planning the surgical approach.

Treatment These are severe injuries associated with joint damage; prolonged immobilization will certainly result in a stiff elbow. Early movement is therefore a prime objective.

fractures (some would say for all Type B and C fractures – minor displacement is easily overlooked in the early post-injury x-rays). The danger with conservative treatment is the strong tendency to stiffening of the elbow and persistent pain. Good exposure of the joint is needed, if necessary by performing an intra-articular olecranon osteotomy. The ulnar nerve should be identified and protected throughout. The fragments are reduced and held temporarily with K-wires. A unicondylar fracture without comminution can then be fixed with screws; if the fragment is large, a contoured plate is added to prevent re-displacement. First the articular block is reconstructed with a transverse screw; bone graft is sometimes needed. The distal block is then fixed to the humeral shaft with medial and lateral plates. Precontoured plates with locking screws are now available. These hold the distal fragments more effectively. Postoperatively the elbow is held at 90 degrees with the arm supported in a sling. Movement is encouraged but should never be forced. Fracture healing usually occurs by 12 weeks. Despite the best efforts, the patient often does not regain full extension and in the most severe cases movement may be severely restricted. A description of this sort fails to convey the real difficulty of these operations. Unless the surgeon is more than usually skilful, the elbow may end up stiffer than if treated by activity (see below).

24

Injuries of the shoulder, upper arm and elbow

injuries with soft-tissue damage. A severe blow on the point of the elbow drives the olecranon process upwards, splitting the condyles apart. Swelling is considerable, but if the bony landmarks can be felt the elbow is found to be distorted. The patient should be carefully examined for evidence of vascular or nerve injury; if there are signs of vascular insufficiency, this must be addressed as a matter of urgency.

Undisplaced fractures These can be treated by applying

a posterior slab with the elbow flexed almost 90 degrees; movements are commenced after 2 weeks. However, great care should be taken to avoid the dual pitfalls of underdiagnosis (displacement and comminution are not always obvious on the initial xray) and late displacement (always obtain check x-rays a week after injury). If the appropriate expertise and facilities are available, open reduction and internal fixation is the treatment of choice for displaced

Displaced Type B and C fractures

ALTERNATIVE METHODS OF TREATMENT If it is anticipated that the outcome of operative treatment will be poor (either because of the degree of comminution and soft-tissue damage or because of lack of expertise and facilities) other options can be considered. Elbow replacement The elderly patient with a comminuted fracture, a low transverse fracture or osteopaenic bone, may be best served by replacement of the elbow.

24.23 Bicondylar fractures X-rays taken (a,b) before and (c,d) after open reduction and internal fixation. An excellent reduction was obtained in this case; however, the elbow sometimes ends up with considerable loss of movement even though the general anatomy has been restored. (a)

(b)

(c)

(d)

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FRACTURES AND JOINT INJURIES

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The ‘bag of bones’ technique The arm is held in a collar and cuff or, better, a hinged brace, with the elbow flexed above a right angle; active movements are encouraged as soon as the patient is willing. The fracture usually unites within 6–8 weeks, but exercises are continued far longer. A useful range of movement (45–90 degrees) is often obtained.

An alternative method of treating either moderately displaced or severely comminuted fractures is by skeletal traction through the olecranon (beware the ulnar nerve!); the patient remains in bed with the humerus held vertical, and elbow movements are encouraged. Again, meticulous internal fixation or elbow replacement are usually preferable.

Skeletal traction

Complications EARLY

(a)

(b)

24.24 Fractured capitulum Anteroposterior and lateral x-rays showing proximal displacement and tilting of the capitular fragment.

Vascular injury Always check the circulation (repeatedly!). Vigilance is required to make the diagnosis and institute treatment as early as possible. Nerve injury There may be damage to either the median or the ulnar nerve. It is important to examine the hand and record the findings before treatment is commenced. The ulnar nerve is particularly vulnerable during surgery.

longer points directly towards it. Bryan and Morrey classify these as:

LATE

CT scans can be helpful in clarifying the diagnosis.

Comminuted fractures of the elbow always result in some degree of stiffness. However, the disability may be reduced by encouraging an energetic exercise programme. Late operations to improve elbow movement are difficult but can be rewarding.

Type I Type II Type III

Complete fracture Cartilaginous shell Comminuted fracture.

Stiffness

Heterotopic ossification Severe soft-tissue damage may lead to heterotopic ossification. Forced movement should be avoided.

FRACTURED CAPITULUM This is a rare articular fracture which occurs only in adults. The patient falls on the hand, usually with the elbow straight. The anterior part of the capitulum is sheared off and displaced proximally.

Treatment Undisplaced fractures can be treated by simple splintage for 2 weeks. Displaced fractures should be reduced and held. Closed reduction is feasible, but prolonged immobilization may result in a stiff elbow. Operative treatment is therefore preferred. The fragment is always larger than expected. If it can be securely replaced, it is fixed in position with a small screw. Headless bone screws are ideally passed from front to back; alternatively, if the fragment is large enough, lag screws can be passed from back to front. If this proves too difficult, the fragment is best excised. Movements are commenced as soon as discomfort permits. The longer term outcome is not always good because of stiffness and sometimes instability.

Clinical features Fullness in front of the elbow is the most notable feature. The lateral side of the elbow is tender and flexion is grossly restricted.

X-Ray 752

In the lateral view the capitulum (or part of it) is seen in front of the lower humerus, and the radial head no

FRACTURED HEAD OF RADIUS Radial head fractures are common in adults but are hardly ever seen in children (probably because the proximal radius is mainly cartilaginous) whereas radial neck fractures occur in children more frequently.

Mechanism of injury

Clinical features This fracture is sometimes missed, but tenderness on pressure over the radial head and pain on pronation and supination should suggest the diagnosis.

X-ray Three types of fracture are identified and classified by Mason as: Type I Type II Type III

An undisplaced vertical split in the radial head A displaced single fragment of the head The head broken into several fragments (comminuted).

An additional Type IV has been proposed, for those fractures with an associated elbow dislocation. Special radial head views, rather than simple PA and lateral views are needed to fully assess the fracture. The wrist also should be x-rayed to exclude a concomitant injury of the distal radioulnar joint, which would signify damage to the interosseous membrane (acute longitudinal radioulnar dissociation).

Treatment Worthwhile pain relief can be achieved by aspirating the haematoma and injecting local anaesthetic. The arm is held in a collar and cuff for 3 weeks; active flexion, extension and rotation are encouraged. The prognosis for this injury is very good, although there is often some loss of elbow extension.

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A comminuted fracture (Type III) This is a challenging injury. Always assess for an associated soft tissue injury:

Rupture of the medial collateral ligament; Rupture of the interosseous membrane (Essex Lopresti lesion); Combined fractures of the radial head and coronoid process plus dislocation of the elbow – the ‘terrible triad’. If any of these is present, excision of the radial head is contra-indicated; this may lead to intractible instability of the elbow or forearm. The head must be meticulously reconstructed with small headless screws or replaced with a metal spacer. A medial collateral rupture, if unstable after replacing or fixing the radial head, should be repaired. Radial head excision usually gives a good long-term result if there are no contra-indications; however, wrist pain from ulnar head impaction, valgus instability of the elbow and trochleo-olecranon arthritis can develop.

Complications

Injuries of the shoulder, upper arm and elbow

A fall on the outstretched hand with the elbow extended and the forearm pronated causes impaction of the radial head against the capitulum. The radial head may be split or broken. In addition, the articular cartilage of the capitulum may be bruised or chipped; this cannot be seen on x-ray but is an important complication. The radial head is also sometimes fractured during elbow dislocation.

A single large fragment (Type II) If the fragment is displaced, it should be reduced and held with one or two small headless screws.

Joint stiffness is common and may involve both the elbow and the radioulnar joints. Even with minimally displaced fractures the elbow can take several months to recover, and stiffness may occur whether the radial head has been excised or not. Myositis ossificans is an occasional complication. Recurrent instability of the elbow can occur if the medial collateral ligament was also injured and the radial head excised.

An undisplaced split (Type I)

FRACTURE OF THE RADIAL NECK In adults, a displaced fracture of the radial neck may need open reduction; if so, a mini-plate can be 24.25 Fractured head of radius There are three main types of adult radial head fracture: (a) a chisel-like split of head, (b) a marginal fracture or (c) a comminuted fracture. Displaced marginal fractures can often be treated by (d) internal fixation.

(a)

(b)

(c)

(d)

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applied, making sure not to damage the articular surface. An alternative is to use oblique headless screws.

FRACTURES OF THE OLECRANON Two broad types of injury are seen: (1) a comminuted fracture which is due to a direct blow or a fall on the elbow; and (2) a transverse break, due to traction when the patient falls onto the hand while the triceps muscle is contracted. These two types can be further sub-classified into (a) displaced and (b) undisplaced fractures. More severe injuries may be associated also with subluxation or dislocation of the ulno-humeral joint. The fracture always enters the elbow joint and

Clinical features A graze or bruise over the elbow suggests a comminuted fracture; the triceps is intact and the elbow can be extended against gravity. With a transverse fracture there may be a palpable gap and the patient is unable to extend the elbow against resistance.

X-ray A properly orientated lateral view is essential to show details of the fracture, as well as the associated joint damage. Always check the position of the radial head – it may be dislocated.

Treatment

(a)

(b)

(c)

(d)

24.26 Fractured olecranon (a,b) Comminuted fractures, undisplaced and displaced. (c,d) Transverse fractures, undisplaced and displaced.

(a)

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therefore damages the articular cartilage. With transverse fractures, the triceps aponeurosis sometimes remains intact, in which case the fracture fragments stay together.

(b)

A comminuted fracture with the triceps intact should be treated as a severe ‘bruise’. Many of these patients are old and osteoporotic, and immobilizing the elbow will lead to stiffness. The arm is rested in a sling for a week; a further x-ray is obtained to ensure that there is no displacement and the patient is then encouraged to start active movements. An undisplaced transverse fracture that does not separate when the elbow is x-rayed in flexion can be treated closed. The elbow is immobilized by a cast in about 60 degrees of flexion for 2–3 weeks and then exercises are begun. Repeat x-rays are needed to exclude displacement. Displaced transverse fractures can be held only by splinting the arm absolutely straight – but stiffness in that position would be disastrous. Operative treatment is therefore strongly recommended. The fracture is reduced and held by tension band wiring. Oblique fractures may need a lag screw, neutralised by a tension band system or plate.

(c)

24.27 Fractured olecranon (a) Slightly displaced transverse fracture. (b) Markedly displaced transverse fracture – the extensor mechanism is no longer intact. Treatment in this case was by open reduction and tension-band wiring (c).

Complications Stiffness used to be common, but with secure internal fixation and early mobilization the residual loss of movement should be minimal. Non-union sometimes occurs after inadequate reduction and fixation. If elbow function is good, it can be ignored; if not, rigid internal fixation and bone grafting will be needed. Ulnar nerve symptoms can develop. These usually settle spontaneously. Osteoarthritis is a late complication, especially if reduction is less than perfect. This can usually be treated symptomatically.

DISLOCATION OF THE ELBOW Dislocation of the ulno-humeral joint is fairly common – more so in adults than in children. Injuries are usually classified according to the direction of displacement. However, in 90% of cases the radioulnar complex is displaced posteriorly or posterolaterally, often together with fractures of the restraining bony processes.

Mechanism of injury and pathology The cause of posterior dislocation is usually a fall on the outstretched hand with the elbow in extension. Disruption of the capsule and ligaments structures alone can result in posterior or posterolateral dislocation. However, provided there is no associated fracture, reduction will usually be stable and recurrent dislocation unlikely. The combination of ligamentous disruption and fracture of the radial head, coronoid process or olecranon process (or, worse still, several fractures) will render the joint more unstable and, unless the fractures are reduced and fixed, liable to redislocation. Once posterior dislocation has taken place, lateral shift may also occur. Soft tissue disruption is often considerable and surrounding nerves and vessels may be damaged. Although certain common patterns of fracture-dislocation are recognized (based on the particular combination of structures involved), highenergy injuries do not necessarily follow any rules. A classic example is the so-called side-swipe injury which occurs, typically, when a car-driver’s elbow, protruding through the window, is struck by another vehicle. The result is forward dislocation with fractures of any or all of the bones around the elbow; soft-tissue damage (including neurovascular injury) is usually severe.

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Injuries of the shoulder, upper arm and elbow

Displaced comminuted fractures need a plate and often bone graft. In the osteoporotic bone of lowdemand elderly patients, good results can be achieved with excision of fragments and re-attachment of triceps to the ulna. If the coronoid portion of the joint is intact it will reduce the risk of instability. Following operation, early mobilization should be encouraged.

Clinical features The patient supports his forearm with the elbow in slight flexion. Unless swelling is severe, the deformity is obvious. The bony landmarks (olecranon and epicondyles) may be palpable and abnormally placed.

(b)

24.28 Dislocation of the elbow X-rays showing (a) lateral and (b) posterior displacement.

(a)

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FRACTURES AND JOINT INJURIES

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However, in severe injuries pain and swelling are so marked that examination of the elbow is impossible. Nevertheless, the hand should be examined for signs of vascular or nerve damage.

X-ray X-ray examination is essential (a) to confirm the presence of a dislocation and (b) to identify any associated fractures. It is often only when the elbow is screened at the time of surgery that the full extent of the injury can be established.

Treatment UNCOMPLICATED DISLOCATION The patient should be fully relaxed under anaesthesia. The surgeon pulls on the forearm while the elbow is slightly flexed. With one hand, sideways displacement is corrected, then the elbow is further flexed while the olecranon process is pushed forward with the thumbs. Unless almost full flexion can be obtained, the olecranon is not in the trochlear groove. After reduction, the elbow should be put through a full range of movement to see whether it is stable. The distal nerves and circulation are checked again. In addition, an x-ray is obtained to confirm that the joint is reduced and to disclose any associated fractures. The arm is held in a collar and cuff with the elbow flexed above 90 degrees. After 1 week the patient gently exercises his elbow; at 3 weeks the collar and cuff is discarded. Elbow movements are allowed to return spontaneously and are never forced. The long-term results are usually good. DISLOCATION WITH ASSOCIATED FRACTURES Coronoid process Coronoid fractures have been classified by Regan and Morrey as: Type I

Type II

Type III

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Avulsion of the tip. A benign enough injury, but it can represent a substantial soft-tissue injury of the elbow A single or comminuted fracture of the coronoid with 50 per cent or less involved. This is usually not repaired surgically, as the elbow remains stable A single or comminuted fracture involving more than 50 per cent. If the elbow is unstable after reduction, then fixation is usually needed.

Medial epicondyle An avulsed medial epicondyle is, for practical purposes, a medial ligament disruption. If the epicondylar fragment is displaced, it must be reduced and fixed back in position. The arm and wrist are splinted with the elbow at 90 degrees; after 3 weeks movements are begun under supervision.

of radius The combination of ligament disruption and a type II or III radial head fracture is an unstable injury; stability is restored only by healing or repair of the ligaments and restoration of the radial pillar – either by fracture fixation or (in the case of a comminuted fracture) by prosthetic replacement of the radial head. The medial collateral ligament may also be repaired to protect the radial head fixation or implant from undue valgus stress.

Head

Olecranon process In the rare forward dislocation of the elbow, the olecranon process may fracture; a large piece of the olecranon is left behind as a separate fragment. Open reduction with internal fixation is the best treatment.

These severe fracture-dislocations are often associated with damage to the large vessels of the arm. The priorities are repair of any vascular injury, skeletal stabilization and soft tissue coverage. This is demanding surgery, necessitating a high level of expertise, and is best undertaken in a unit specialising in upper limb injuries.

Side-swipe injuries

In cases where the elbow remains unstable after the bone and joint anatomy has been restored, a hinged external fixator can be applied in order to maintain mobility while the tissues heal.

Persistent instability

Complications Complications are common; some are potentially so serious that the patient with a dislocation or a fracture-dislocation of the elbow must be observed with the closest attention. EARLY The brachial artery may be damaged. Absence of the radial pulse is a warning. If there are other signs of ischaemia, this should be treated as an emergency. Splints must be removed and the elbow should be straightened somewhat. If there is no improvement, an arteriogram is performed; the brachial artery may have to be explored.

Vascular injury

Nerve injury The median or ulnar nerve is sometimes

injured. Spontaneous recovery usually occurs after 6– 8 weeks. LATE Stiffness Loss of 20 to 30 degrees of extension is not

uncommon after elbow dislocation; fortunately this is usually of little functional significance. The most common cause of undue stiffness is prolonged immobilization. In the management of all elbow injuries the joint should be moved as soon as possible, with due consideration to stability of the fractures and soft tissues and without undue passive stretching of the soft tissues. For injuries requiring prolonged splintage, a

Heterotopic bone formation may occur in the damaged soft tissues in front of the joint. It is due to muscle bruising or haematoma formation; however the precise pathogenesis is not known. In former years ‘myositis ossificans’ was a fairly common complication of elbow injury, usually associated with forceful reduction and overenthusiastic passive movement of the elbow. Nowadays it is rarely seen, but it is as well to be alert for signs such as slight swelling, excessive pain and tenderness around the front of the elbow, along with tardy recovery of active movements. X-ray examination is initially unhelpful; soft-tissue ossification is usually not visible until 4–6 weeks after injury. If the condition is suspected, exercises are stopped and the elbow is splinted in comfortable flexion until pain subsides; gentle active movements and continuous passive motion are then resumed. Antiinflammatory drugs may help to reduce stiffness; they are also used prophylactically to reduce the risk of heterotopic bone formation. A bone mass which markedly restricts movement and elbow function can be excised, though not before the bone is fully ‘mature’, i.e. has well-defined cortical margins and trabeculae (as seen on x-ray).

Heterotopic ossification (myositis ossificans)

Unreduced dislocation A dislocation may not have been diagnosed; or only the backward displacement corrected, leaving the olecranon process still displaced sideways. Up to 3 weeks from injury, manipulative reduction is worth attempting but care is needed to avoid fracturing one of the bones. Other than this, there is no satisfactory treatment. Open reduction can be considered, but a wide soft tissue release is required, which predisposes to yet further stiffness. Alternatively, the condition can be left, in the hope that the elbow will regain a useful range of movement. If pain is a problem, the patient can be offered an arthrodesis or an arthroplasty. Recurrent dislocation This is rare unless there is a large coronoid fracture or radial head fracture. If recurrent elbow instability occurs, the lateral ligament and capsule can be repaired or re-attached to the lateral condyle. A cast with the elbow at 90 degrees is worn for 4 weeks.

Osteoarthritis Secondary osteoarthritis is quite common after severe fracture-dislocations. In older patients, total elbow replacement can be considered.

ISOLATED DISLOCATION OF THE RADIAL HEAD A true isolated dislocation of the radial head is very rare; if it is seen, search carefully for an associated fracture of the ulna (the Monteggia injury). In a child, the ulnar fracture may be difficult to detect if it is incomplete, either green-stick or plastic deformation of the shaft; it is very important to identify these incomplete fractures because even a minor deformity, if it is allowed to persist, may prevent full reduction of the radial head dislocation.

FRACTURES AROUND THE ELBOW IN CHILDREN The elbow is second only to the distal forearm for frequency of fractures in children. Most of these injuries are supracondylar fractures, the remainder being divided between condylar, epicondylar and proximal radial and ulnar fractures. Boys are injured more often than girls and more than half the patients are under 10 years old. The usual accident is a fall directly on the point of the elbow or – more often – onto the outstretched hand with the elbow forced into valgus or varus. Pain and swelling are often marked and examination is difficult. X-ray interpretation also has its problems: The bone ends are largely cartilaginous and therefore radiographically incompletely visualized. A good knowledge of the normal anatomy is essential if fracture displacements are to be recognized.

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Injuries of the shoulder, upper arm and elbow

hinged elbow brace, or on some occasions a hinged external fixator, can allow some movement in the flexion-extension plane whilst protecting against collateral stress. Persistent stiffness of severe degree can often be improved by anterior capsular release. However, operative treatment should not be rushed; remember that sometimes the stiffness is due to myositis ossificans, which is usually undetectable on plain x-ray examination until a month or more after injury.

Points of anatomy The elbow is a complex hinge, providing sufficient mobility to permit the upper limb to reach through wide ranges of flexion, extension and rotation, yet also enough stability to support the necessary gripping, pushing, pulling and carrying activities of daily life. Its stability is due largely to the shape and fit of the bones that make up the joint – especially the humero-ulnar component – and this is liable to be compromised by any break in the articulating structures. The surrounding soft-tissue structures also are important, especially the capsular and collateral ligaments and, to a lesser extent, the muscles. Ligament disruption is also, therefore, a destabilizing factor.

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FRACTURES AND JOINT INJURIES

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The forearm is normally in slight valgus in relation to the upper arm, the average carrying angle in children being about 15 degrees. (Published measurements range from 5 to 25 degrees). When the elbow is flexed, the forearm comes to lie directly upon the upper arm. Doubts about the normality of these features can usually be resolved by comparing the injured with the normal arm. With the elbow flexed, the tips of the medial and lateral epicondyles and the olecranon prominence form an isosceles triangle; with the elbow extended, they lie transversely in line with each other. Though all the epiphyses are in some part cartilaginous, the secondary ossific centres can be seen on xray; they should not be mistaken for fracture fragments! The average ages at which the ossific centres appear are easily remembered by the mnemonic CRITOE: Capitulum – 2 years. Radial head – 4 years. Internal (medial) epicondyle – 6 years. Trochlea – 8 years. Olecranon – 10 years. External (lateral) epicondyle – 12 years. Obviously epiphyseal displacements will not be detectable on x-ray before these ages. Fracture displacement and accuracy of reduction can be inferred from radiographic indices such as Baumann’s angle (see Fig. 24.30).

SUPRACONDYLAR FRACTURES These are among the commonest fractures in children. The distal fragment may be displaced either posteriorly or anteriorly.

Mechanism of injury Posterior angulation or displacement (95 per cent of all cases) suggests a hyperextension injury, usually due to a fall on the outstretched hand. The humerus breaks just above the condyles. The distal fragment is pushed backwards and (because the forearm is usually in pronation) twisted inwards. The jagged end of the proximal fragment pokes into the soft tissues anteri-

(a)

758

(b)

orly, sometimes injuring the brachial artery or median nerve. Anterior displacement is rare; it is thought to be due to direct violence (e.g. a fall on the point of the elbow) with the joint in flexion.

Classification Type I is an undisplaced fracture. Type II is an angulated fracture with the posterior cortex still in continuity. IIA – a less severe injury with the distal fragment merely angulated. IIB – a severe injury; the fragment is both angulated and malrotated. Type III is a completely displaced fracture (although the posterior periosteum is usually still preserved, which will assist surgical reduction).

Clinical features Following a fall, the child is in pain and the elbow is swollen; with a posteriorly displaced fracture the S-deformity of the elbow is usually obvious and the bony landmarks are abnormal. It is essential to feel the pulse and check the capillary return; passive extension of the flexor muscles should be pain-free. The wrist and the hand should be examined for evidence of nerve injury.

X-ray The fracture is seen most clearly in the lateral view. In an undisplaced fracture the ‘fat pad sign’ should raise suspicions: there is a triangular lucency in front of the distal humerus, due to the fat pad being pushed forwards by a haematoma. In the common posteriorly displaced fracture the fracture line runs obliquely downwards and forwards and the distal fragment is tilted backwards and/or shifted backwards. In the anteriorly displaced fracture the crack runs downwards and backwards and the

(c)

(d)

24.29 Supracondylar fractures X-rays showing supracondylar fractures of increasing severity. (a) Undisplaced. (b) Distal fragment posteriorly angulated but in contact. (c) Distal fragment completely separated and displaced posteriorly. (d) A rarer variety with anterior angulation.

(b)

(c)

distal fragment is tilted forwards. On a normal lateral x-ray, a line drawn along the anterior cortex of the humerus should cross the middle of the capitulum. If the line is anterior to the capitulum then a Type II fracture is suspected. An anteroposterior view is often difficult to obtain without causing pain and may need to be postponed until the child has been anaesthetized. It may show that the distal fragment is shifted or tilted sideways, and rotated (usually medially). Measurement of Baumann’s angle is useful in assessing the degree of medial angulation before and after reduction (Fig. 24.30).

Treatment If there is even a suspicion of a fracture, the elbow is gently splinted in 30 degrees of flexion to prevent movement and possible neurovascular injury during the x-ray examination. TYPE I: UNDISPLACED FRACTURE The elbow is immobilized at 90 degrees and neutral rotation in a light-weight splint or cast and the arm is supported by a sling. It is essential to obtain an x-ray 5–7 days later to check that there has been no displacement. The splint is retained for 3 weeks and supervised movement is then allowed. The capitulum normally angles forward about 30 degrees; if the capitulum is in a straight line with the humerus on the lateral x-ray, it will still remodel. Even with Type I fractures, care must be taken to recognise any medial tilt of the distal fragment on the anteroposterior x-ray, otherwise cubitus varus can result. Measure Baumann’s angle. TYPE II A: POSTERIORLY ANGULATED FRACTURE – MILD In these cases swelling is usually not severe and the risk of vascular injury is low. If the posterior cortices are in continuity, the fracture can be reduced under

general anaesthesia by the following step-wise manoeuvre: (1) traction for 2–3 minutes in the length of the arm with counter-traction above the elbow; (2) correction of any sideways tilt or shift and rotation (in comparison with the other arm); (3) gradual flexion of the elbow to 120 degrees, and pronation of the forearm, while maintaining traction and exerting finger pressure behind the distal fragment to correct posterior tilt. Then feel the pulse and check the capillary return – if the distal circulation is suspect, immediately relax the amount of elbow flexion until it improves. X-rays are taken to confirm reduction, checking carefully to see that there is no varus or valgus angulation and no rotational deformity. The anteroposterior view is confusing and unreliable with the elbow flexed, but the important features can be inferred by noting Baumann’s angle. Again, subtle medial tilt and rotation of the distal fragment must be recognised. If the acutely flexed position cannot be maintained without disturbing the circulation, or if the reduction is unstable, (and most of these fractures are unstable!) the fracture should be fixed with percutaneous crossed K-wires (take care not to skewer the ulnar nerve!). Following reduction, the arm is held in a collar and cuff; the circulation should be checked repeatedly during the first 24 hours. An x-ray is obtained after 3– 5 days to confirm that the fracture has not slipped. The splint is retained for 3 weeks, after which movements are begun. TYPES II B AND III: ANGULATED AND MALROTATED OR POSTERIORLY DISPLACED These are usually associated with severe swelling, are difficult to reduce and are often unstable; moreover, there is a considerable risk of neurovascular injury or circulatory compromise due to swelling. The fracture should be reduced under general anaesthesia as soon as possible, by the method described above, and then held with percutaneous crossed K-wires; this obviates the necessity to hold the elbow acutely flexed.

24

Injuries of the shoulder, upper arm and elbow

(a)

24.30 Baumann’s angle Anteroposterior x-rays are sometimes difficult to make out, especially if the elbow is held flexed after reduction of the supracondylar fracture. Measurement of Baumann’s angle is helpful. This is the angle subtended by the longitudinal axis of the humeral shaft and a line through the coronal axis of the capitellar physis, as shown in (a) the x-ray of a normal elbow and the accompanying diagram (b). Normally this angle is less than 80 degrees. If the distal fragment is tilted in varus, the increased angle is readily detected (c).

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FRACTURES AND JOINT INJURIES

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(a)

(e)

(b)

(f)

(g)

(d)

(h)

(i)

24.31 Supracondylar fractures – treatment (a) The uninjured arm is examined first; (b) traction of the fractured arm; (c) correcting lateral shift and tilt; (d) correcting rotation; (e) correcting backwards shift and tilt; (f) feeling the pulse; the elbow is kept well flexed while x-ray films are taken. (h) For the first 3 weeks the arm is kept under the clothes; after this (i) it is outside the clothes.

Smooth wires should be used (this lessens the risk of physeal injury) and great care should be taken not to injure the ulnar, radial and median nerves. Postoperative management is the same as for Type II A. OPEN REDUCTION This is sometimes necessary for (1) a fracture which simply cannot be reduced closed; (2) an open fracture; or (3) a fracture associated with vascular damage. The fracture is exposed (preferably through two incisions, one on each side of the elbow), the haematoma is evacuated and the fracture is reduced and held by two crossed K-wires. CONTINUOUS TRACTION Traction through a screw in the olecranon, with the arm held overhead, can be used (1) if the fracture is severely displaced and cannot be reduced by manipulation; (2) if, with the elbow flexed 100 degrees, the pulse is obliterated and image intensification is not available to allow pinning and then straightening of the elbow; or (3) for severe open injuries or multiple injuries of the limb. Once the swelling subsides, a further attempt can be made at closed reduction.

760

(c)

TREATMENT OF ANTERIORLY DISPLACED FRACTURES This is a rare injury (less than 5 per cent of supracondylar fractures). However, ‘posterior’ fractures are sometimes inadvertently converted to ‘anterior’ ones by excessive traction and manipulation. The fracture is reduced by pulling on the forearm

with the elbow semi-flexed, applying thumb pressure over the front of the distal fragment and then extending the elbow fully. Crossed percutaneous pins are used if unstable. A posterior slab is bandaged on and retained for 3 weeks. Thereafter, the child is allowed to regain flexion gradually.

Complications EARLY The great danger of supracondylar fracture is injury to the brachial artery, which, before the introduction of percutaneous pinning, was reported as occurring in over 5 per cent of cases. Nowadays the incidence is probably less than 1 per cent. Peripheral ischaemia may be immediate and severe, or the pulse may fail to return after reduction. More commonly the injury is complicated by forearm oedema and a mounting compartment syndrome which leads to necrosis of the muscle and nerves without causing peripheral gangrene. Undue pain plus one positive sign (pain on passive extension of the fingers, a tense and tender forearm, an absent pulse, blunted sensation or reduced capillary return on pressing the finger pulp) demands urgent action. The flexed elbow must be extended and all dressings removed. If the circulation does not promptly improve, then angiography (on the operating table if it saves time) is carried out, the vessel repaired or grafted and a forearm fasciotomy performed. If angiography is not available, or would cause much delay, then Doppler

Vascular injury

imaging should be used. In extreme cases, operative exploration would be justified on clinical criteria alone.

LATE Malunion is common. However, backward or sideways shifts are gradually smoothed out by modelling during growth and they seldom give rise to visible deformity of the elbow. Forward or backward tilt may limit flexion or extension, but consequent disability is slight. Uncorrected sideways tilt (angulation) and rotation are much more important and may lead to varus (or rarely valgus) deformity of the elbow; this is permanent and will not improve with growth (Fig. 24.32). The fracture is extra-physeal and so physeal damage should not be blamed for the deformity; usually it is faulty reduction which is responsible. Cubitus varus is disfiguring and cubitus valgus may cause late ulnar palsy. If deformity is marked, it will need correction by supracondylar osteotomy usually once the child approaches skeletal maturity. Malunion

(a)

(b)

FRACTURES OF THE LATERAL CONDYLE The lateral condylar (or capitellar) epiphysis begins to ossify during the first year of life and fuses with the shaft at 12–16 years. Between these ages it may be sheared off or avulsed by forceful traction.

Mechanism of injury and pathology The child falls on the hand with the elbow extended and forced into varus. A large fragment, which includes the lateral condyle, breaks off and is pulled upon by the attached wrist extensors. Sometimes there is a compression, rather than avulsion, mechanism of injury. The fracture line usually runs along the physis and into the trochlea; less often it continues through the medial epiphysis and exits through the capitulatrochlear groove. It crosses the growth plate and so is a Salter Harris Type IV injury. In severe injuries the elbow may dislocate posterolaterally; the condyle is ‘capsized’ by muscle pull and remains capsized while the elbow reduces spontaneously. The extent of this injury is often not appreciated. Because the condylar epiphysis is largely cartilaginous, the bone fragment may look deceptively small on

24

Injuries of the shoulder, upper arm and elbow

Nerve injury The radial nerve, median nerve (particularly the anterior interosseous branch) or the ulnar nerve may be injured. Tests for nerve function are described in Chapter 11. Fortunately loss of function is usually temporary and recovery can be expected in 3 to 4 months. If there is no recovery the nerve should be explored. However, if a nerve, documented as intact prior to manipulation, is then found to have failed after manipulation, then entrapment in the fracture is suspected and immediate exploration should be arranged. The ulnar nerve may be damaged by careless pinning. If the injury is recognized, and the pin removed, recovery will usually follow.

Stiffness is an ever-present risk with elbow injuries. Extension in particular may take months to return. It must not be hurried. Passive movement (which includes carrying weights) or forced movement is prohibited – this will only make matters worse and may contribute to the development of myositis ossificans. As it is, myositis ossificans is extremely rare, and should remain so if rehabilitation is properly supervised.

Elbow stiffness and myositis ossifficans

(c)

24.32 Supracondylar fracture – malunion (a) Varus deformity of the right elbow, due to incomplete correction of the varus and rotational displacements in a supracondylar fracture. (b) It is most obvious when the boy raises his arms, displaying the typical ‘gunstock deformity’. (c) X-ray showing the characteristic malunion.

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FRACTURES AND JOINT INJURIES

24

(a)

(b)

24.33 Physeal fractures of the lateral condoyle (a) The commonest is a fracture starting in the metaphysi and running along the physis of the lateral condyle into the trochlea (Salter–Harris Type II injury). (b) Less common is a fracture running right through the lateral condyle to reach the articular surface in the capitulotrochlear groove (Salter–Harris Type IV): though uncommon, this latter injury is important because of its potential for causing growth defects.

(a)

x-ray. Displacement can be quite marked due to muscle pull. The fracture is important for two reasons: (a) it may damage the growth plate and (b) it always involves the joint. Early recognition and accurate reduction are therefore essential if a poor outcome is to be avoided.

Type I:

Clinical features The elbow is swollen and deformed. There is tenderness over the lateral condyle. Passive flexion of the wrist (pulling on the extensors) may be painful.

762

(a)

(b)

(c)

(d)

(e)

(f)

(b)

24.34 Fractured lateral condyle If displacement is more than 2 mm, open reduction and internal fixation is the treatment of choice.

X-ray X-ray examination must include oblique views or else the full extent of the fracture may be missed. Two types of fracture are recognized and classified by Milch: A fracture lateral to the trochlea: the elbow joint is not involved and is stable. Type II: A fracture through the middle of the trochlea: this injury is more common; the elbow is unstable as the radius and ulna are carried along with the fragment.. The fragment is often grossly displaced and capsized, and it may carry with it a triangular piece of the metaphysis. Remember that the fragment (partly cartilaginous) is much larger than it seems on x-ray. 24.35 Fractured lateral condyle – complications (a,b) A large fragment of bone and cartilage is avulsed; even with reasonable reduction, union is not inevitable. (c) Open reduction with fixation is often wise. (d) Sometimes the condyle is capsized; if left unreduced non-union is inevitable (e) and a valgus elbow with delayed ulnar palsy (f) the likely sequel.

Treatment

Complications Non-union and malunion If the condyle is left capsized,

non-union is inevitable; with growth the elbow becomes increasingly valgus, and ulnar nerve palsy is then likely to develop. Stiffness and pain can result. Even minor displacements sometimes lead to nonunion, and even slight malunion may lead to ulnar palsy in later life; it is for these reasons that open reduction (and internal fixation) is preferred for any displaced fracture. The fracture is a Salter Harris Type IV injury and so imperfect reduction can result in growth arrest. Even if a fracture presents late (e.g. up

(a)

(d)

(b)

(e)

Occasionally condylar displacement results in posterolateral dislocation of the elbow. The only effective treatment is reconstruction of the bony and soft tissues on the lateral side.

Recurrent dislocation

SEPARATION OF THE MEDIAL EPICONDYLE

Mechanism of injury and pathology The medial epicondyle begins to ossify at the age of about 5 years and fuses to the shaft at about 16; between these ages it may be avulsed by a severe muscle or ligament strain. The child falls on the outstretched hand with the wrist and elbow extended; the elbow is wrenched into valgus. The unfused epicondylar apophysis is avulsed by tension on either the wrist flexor muscles or the medial ligament of the elbow. If the elbow subluxates (even momentarily), the small apophyseal fragment may be dragged into the joint. With more severe injuries the joint dislocates laterally.

Clinical features The diagnosis should be suspected if injury is followed by pain, swelling and bruising on the medial side of the elbow. If the joint is dislocated, deformity is of course obvious. Sensation and power in the fin-

24.36 Fractured medial epicondyle (a) Avulsion of the medial epicondyle following valgus train. (b) Avulsion associated with dislocation of the elbow; (c) after reduction. Sometimes the epicondylar fragment is trapped in the joint (d,e); the serious nature is then liable to be missed unless the surgeon specifically looks for the trapped fragment, which is emphasized in the tracings (f,g).

(c)

(f)

24

Injuries of the shoulder, upper arm and elbow

If there is no displacement the arm can be splinted in a backslab with the elbow flexed 90 degrees, the forearm neutral and the wrist extended (this position relaxes the extensor mechanism which attaches to the fragment). However, it is essential to repeat the x-ray after 5 days to make sure that the fracture has not displaced. The splint is removed after 2 weeks and exercises are encouraged. A displaced fracture requires accurate reduction and internal fixation. If the fragment is only moderately displaced (hinged), it may be possible to manipulate it into position by extending the elbow and pressing upon the condyle, and then fixing the fragment with percutaneous pins. If this fails, and for all separated fractures, open reduction and internal fixation with pins is required. The arm is immobilized in a cast; cast and pins are removed after 3 or 4 weeks.

to 3 months) open reduction and fixation should be attempted.

(g)

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24

gers should be tested to exclude concomitant ulnar nerve damage.

FRACTURES AND JOINT INJURIES

X-ray In the anteroposterior view the medial epicondylar epiphysis may be tilted or shifted downwards; if the joint is dislocated the fragment lies distal to the lower humerus. A lateral view may show the epicondyle looking like a loose body in the joint. If in any doubt, the normal side should be x-rayed for comparison (see Fig. 24.36 d–g).

Treatment Minor displacement may be disregarded. This is an extra-articular fracture, so the elbow can be mobilized as soon as the child wishes. If the epicondyle is trapped in the joint it must be freed. Manipulation with the elbow in valgus and the wrist hyperextended (to pull on the flexor muscles) may be successful; if this fails, the joint must be opened (the ulnar nerve must be visualized and protected) and the fragment retrieved and fixed back in position. Displaced fractures which are not trapped in the joint usually do not need to be operated upon: however, if there is valgus instability (because the medial collateral ligament complex is attached to the fragment) then reduction and pinning is recommended.

elbow forced into valgus; in the latter case it would be an avulsion injury. The fracture line runs through the physis, exiting in the trochlear notch or even further laterally, and the medial fragment may be displaced by the pull of the flexor muscle group.

Clinical features and x-ray This is an intra-articular fracture, resulting in considerable pain and swelling. In older children the metaphyseal component is usually easily visualized on x-ray. However, in young children much of the medial condylar epiphysis is cartilaginous and therefore not visible on x-ray, so the full extent of the fracture may not be recognized; seeing only the epicondylar ossific centre in a displaced position on the x-ray may mislead the surgeon into thinking that this is only an epicondylar fracture. In doubtful cases an arthrogram may be helpful.

Treatment Undisplaced fractures are treated by splintage; x-rays are repeated until the fracture has healed, so as to ensure that it does not become displaced. Displaced fractures are treated by either closed reduction (sometimes with percutaneous pinning) or by open reduction and fixation with pins. Postoperative management is similar to that of lateral condyle fractures.

Complications

Complications

EARLY Ulnar nerve damage is not uncommon. Mild symptoms recover spontaneously; even a complete palsy will usually recover but, if there is the possibility that the nerve is kinked in the joint, exploration should be considered.

EARLY Lateral dislocation of the elbow occasionally occurs with a severe valgus strain and avulsion of the medial condyle. Early reduction of both the dislocation and the fracture, if necessary by open operation and pinning, is important. Ulnar nerve damage is not uncommon, but recovery is usual unless the nerve is left kinked in the joint.

LATE Stiffness of the elbow is common and extension often limited for months; but, provided movement is not forced, it will eventually return.

LATE Stiffness of the elbow is common and extension often limited for months; but, provided movement is not forced, it will eventually return.

FRACTURES OF THE MEDIAL CONDYLE

764

This is much rarer than either a fracture of the lateral condyle or a separation of the medial epicondylar apophysis.

FRACTURE-SEPARATION OF THE DISTAL HUMERAL PHYSIS

Mechanism of injury

Up to the age of 7 years the distal humeral epiphysis is a solid cartilaginous segment with maturing centres of ossification. With severe injury it may separate en bloc. This is likely to occur with fairly severe violence; for example, in birth injuries or child abuse.

The injury is usually caused by a fall from a height, involving either a direct blow to the point of the elbow or a landing on the outstretched hand with the

Clinical features The child is in pain and the elbow is markedly swollen. The history may be deceptively uninformative.

In a very young child, in whom the bony outlines are still unformed, the x-ray may look normal. All that can be seen of the epiphysis is the pea-like ossification centre of the capitulum; its position should be compared with that of the normal side. Medial displacement of either the capitellar ossification centre or the proximal radius and ulna is very suspicious. In the older child the deformity is usually obvious.

Treatment If the diagnosis is uncertain, arthrography or ultrasound can help. If the fracture is undisplaced, the elbow is merely splinted for 3 weeks; if displaced then the fracture should be accurately reduced and held with smooth percutaneous wires (otherwise there is a high incidence of cubitus varus). The wires are removed at 3 weeks.

FRACTURED NECK OF RADIUS Mechanism of injury and pathology A fall on the outstretched hand forces the elbow into valgus and pushes the radial head against the capitulum. In children the bone fractures through the neck of the radius; in adults the injury is more likely to fracture the radial head.

head tilt and up to 3 mm of transverse displacement are acceptable. The arm is rested in a collar and cuff, and exercises are commenced after a week. Displacement of more than 30 degrees requires reduction. With the patient’s elbow extended, traction and varus force are applied; the surgeon then pushes the displaced radial fragment into position with his thumb. If this fails, a percutaneous implement can be used to push the fragment back into place. Open reduction is occasionally performed if significant displacement persists. The radial head tilt is corrected but internal fixation is unnecessarily meddlesome. The head of the radius must never be excised in children because this will interfere with the synchronous growth of radius and ulna. Fractures that are seen a week or longer after injury should be left untreated (except for light splintage). Following operation, the elbow is splinted in 90 degrees of flexion for a week or two and then movements are encouraged.

24

Injuries of the shoulder, upper arm and elbow

X-ray

24.37 Fractured neck of radius in a child Up to 30° of tilt is acceptable. Greater degrees of angulation should be reduced; never excise the radial head in a child.

Clinical features Following a fall, the child complains of pain in the elbow. There may be localized tenderness over the radial head and pain on rotating the forearm.

X-ray The fracture line is transverse. It is either situated immediately distal to the physis or there is true separation of the epiphysis with a triangular fragment of shaft (a Salter-Harris II injury). The proximal fragment is tilted distally, forwards and outwards. Sometimes the upper end of the ulna is also fractured or there may be a posterior dislocation of the elbow.

Treatment In children there is considerable potential for remodelling after these fractures. Up to 30 degrees of radial

SUBLUXATION OF THE RADIAL HEAD (‘PULLED ELBOW’) In young children the elbow may be injured by pulling on the arm, usually with the forearm pronated. It is sometimes called subluxation of the radial head; more accurately, it is a subluxation of the orbicular ligament which slips up over the head of the radius into the radiocapitellar joint. A child aged 2 or 3 years is brought with a painful, dangling arm: there is usually a history of the child being jerked by the arm and crying out in pain. The forearm is held in pronation and extension, and any attempt to supinate it is resisted. There are no x-ray changes. A dramatic cure is achieved by forcefully supinating and then flexing the elbow; the ligament slips back with a snap.

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FRACTURE OF THE OLECRANON IN

FRACTURES AND JOINT INJURIES

CHILDREN

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This is rare. When it does occur it is usually due to a direct blow onto the tip of the flexed elbow or a fall onto the outstretched hand. Most are undisplaced and are treated in a splint for 3 or 4 weeks. If displaced, then they should be reduced and held with wires.

REFERENCES AND FURTHER READING Boileau P, Sinnerton RJ, Chuinard C, Walch G. Arthroplasty of the shoulder. J Bone Joint Surg 2006; 88B: 562– 75. Goss TP. Fractures of the glenoid cavity. J Bone Joint Surg 1992; 74A: 299–305. Hertel R, Hempfing A, Stiehler M, Leunig M. Predictors of humeral head ischemia after intracapsular fracture of the proximal humerus. J Shoulder Elbow Surg, 2004; 13: 427–33. Jupiter JB. Complex fractures of the distal part of the humerus J Bone Joint Surg 1994; 76A: 1252–63. McKee MD, Pedersen EM, Jones C. Deficits following nonoperative treatment of displaced midshaft clavicular fractures. J Bone Joint Surg 2006; 88A: 35–40.

Modabber MR, Jupiter JB. Reconstruction for posttraumatic conditions of the elbow joint. J Bone Joint Surg 1995; 77A: 1431–46. Morrey BF. Current concepts in the treatment of fractures of the radial head, the olecranon and coronoid. J Bone Joint Surg 1995; 77A: 316–27. Neer CS II. Displaced proximal humeral fractures. Classification and evaluation. J Bone Joint Surg 1970; 52A: 1077–89. O’Hara LJ, Barlow JW, Clarke NMP. Displaced supracondylar fractures of the humerus in children. J Bone Joint Surg 2000; 82B: 204–210. Ring D, Jupiter JB. Fracture-dislocation of the elbow. J Bone Joint Surg 1998; 80A: 566–80. Robinson CM. Fractures of the clavicle in the adult. Epidemiology and classification. J Bone Joint Surg 1998; 80B: 476–84. Rockwood CA Jr, Green DP, Bucholz RW, Heckman JD (eds). Rockwood and Green’s Fractures in Adults, 4th Edition. 1996 Lippincott-Raven, Philadelphia. Snow M, Funk L. Technique of arthroscopic Weaver–Dunn in chronic acromioclavicular joint dislocation. Techniques in Shoulder and Elbow Surgery 2006; 7: 155–9. Williams GR, Naranja J, Klimkiewcz J et al. The floating shoulder: a biomechanical basis for classification and management. J Bone Joint Surg 2001; 83A: 1182–7.

Injuries of the forearm and wrist

25

David Warwick

FRACTURES OF THE RADIUS AND ULNA Mechanism of injury and pathology Fractures of the shafts of both forearm bones occur quite commonly. A twisting force (usually a fall on the hand) produces a spiral fracture with the bones broken at different levels. An angulating force causes a transverse fracture of both bones at the same level. A direct blow causes a transverse fracture of just one bone, usually the ulna. Additional rotation deformity may be produced by the pull of muscles attached to the radius: they are the biceps and supinator muscles to the upper third, the pronator teres to the middle third, and the pronator quadratus to the lower third. Bleeding and swelling of the muscle compartments of the forearm may cause circulatory impairment.

Clinical features The fracture is usually quite obvious, but the pulse must be felt and the hand examined for circulatory or neu-

ral deficit. Repeated examination is necessary in order to detect an impending compartment syndrome. X-RAY Both bones are broken, either transversely and at the same level or obliquely with the radial fracture usually at a higher level. In children, the fracture is often incomplete (greenstick) and only angulated. In adults, displacement may occur in any direction – shift, overlap, tilt or twist. In low-energy injuries, the fracture tends to be transverse or oblique; in high-energy injuries it is comminuted or segmental.

Treatment CHILDREN In children, closed treatment is usually successful because the tough periosteum tends to guide and then control the reduction. The fragments are held in a well-moulded full-length cast, from axilla to metacarpal shafts (to control rotation). The cast is applied with the elbow at 90 degrees. If the fracture is proximal to pronator teres, the forearm is supinated; if it is distal to pronator teres, then the forearm is held

25.1 Fractured radius and ulna in children Greenstick fractures (a) need only correction of angulation (b), and plaster splintage. Complete fractures (c) are harder to reduce; but provided alignment is corrected and held in plaster (d), slight lateral shift remodels with growth (e).

(a)

(b)

(c)

(d)

(e)

FRACTURES AND JOINT INJURIES

25

in neutral. The position is checked by x-ray after a week and, if it is satisfactory, splintage is retained until both fractures are united (usually 6–8 weeks). Throughout this period hand and shoulder exercises are encouraged. The child should avoid contact sports for a few weeks to prevent re-fracture. Occasionally an operation is required, either if the fracture cannot be reduced or if the fragments are unstable. Fixation with intramedullary rods is preferred, but they should be inserted with great care to avoid injury to the growth plates. Alternatively, a plate or K-wire fixation can be used. Childhood fractures usually remodel well, but not if there is any rotational deformity or an angular deformity of more than 15 degrees in children under 6 years or 10 degrees in children between 6 and 12. In those over 12 years old even slight angular deformities are unlikely to remodel satisfactorily. ADULTS Unless the fragments are in close apposition, reduction is difficult and re-displacement in the cast almost invariable. So predictable is this outcome that most surgeons opt for open reduction and internal fixation from the outset. The fragments are held by interfragmentary compression with plates and screws. Bone grafting is advisable if there is comminution. The deep fascia is left open to prevent a build-up of pressure in the muscle compartments, and only the skin is sutured. After the operation the arm is kept elevated until the swelling subsides, and during this period active exercises of the hand are encouraged. If the fracture is not comminuted and the patient is reliable, early

(a)

768

(b)

(c)

(a)

(b)

(c)

25.3 Fractured radius and ulna – cross-union If the interosseous membrane is severely damaged, even successful plating (a,b) cannot guarantee that cross-union will not occur (c).

range of movement exercises are commenced but lifting and sports are avoided. It takes 8–12 weeks for the bones to unite. With comminuted fractures or unreliable patients, immobilization in plaster is safer. OPEN FRACTURES Open fractures of the forearm must be managed meticulously. Antibiotics and tetanus prophylaxis are given as soon as possible; the wounds are copiously washed and nerve function and circulation are checked. At operation the wounds are excised and extended and the bone ends are exposed and thoroughly cleaned. The fractures are primarily fixed with compression screws and plates; if the wounds are absolutely clean, the soft tissues can be closed. If bone grafting is necessary, this is best deferred until the wounds are healed. If there is major soft-tissue loss, the bones are better stabilized by external fixation. The aim is to obtain skin cover as soon as possible; if plastic surgery services are available, these should be enlisted from the outset. If there is any question of a compartment syndrome, the wounds should be left open and closed 24–48 hours later, with a skin graft if needed.

(d)

25.2 Fractured radius and ulna in adults (a, b) These fractures are usually treated by internal fixation with sturdy plates and screws. However, removal of the implants is not without risk. (c,d) In this case, the radius fractured through one of the screw holes.

Complications EARLY Nerve injuries are rarely caused by the fracture, but they may be caused by the surgeon!

Nerve injury

osteotomy. However, it can be very difficult to calculate the deformity and subsequent correction. Removal of plates and screws is often regarded as a fairly innocuous procedure. Beware! Complications are common and they include damage to vessels and nerves, infection and fracture through a screw-hole.

25

Complications of plate removal

FRACTURE OF A SINGLE FOREARM BONE

(b)

25.4 Compartment syndrome Incisions to relieve a compartment syndrome in the forearm.

Exposure of the radius in its proximal third risks damage to the posterior interosseous nerve where it is covered by the superficial part of the supinator muscle. The proximal fragment of radius may have rotated so the nerve may not be where it is expected. Surgical technique is particularly important here; the anterior Henry approach is safest. Injury to the radial or ulnar artery seldom presents any problem, as the collateral circulation is excellent.

Vascular injury

Fractures (and operations) of the forearm bones are always associated with swelling of the soft tissues, with the attendant risk of a compartment syndrome. The threat is even greater, and the diagnosis more difficult, if the forearm is wrapped up in plaster. A distal pulse does not exclude compartment syndrome! The byword is ‘watchfulness’; if there are any signs of circulatory embarrassment, treatment must be prompt and uncompromising.

Compartment syndrome

LATE Most fractures of the radius and ulna heal within 8–12 weeks; high energy fractures and open fractures are less likely to unite. Delayed union of one or other bone (usually the ulna) is not uncommon; immobilization may have to be continued beyond the usual time. Non-union will require bone grafting and internal fixation. Delayed union and non-union

Malunion With closed reduction there is always a risk of malunion, resulting in angulation or rotational deformity of the forearm, cross-union of the fragments, or shortening of one of the bones and disruption of the distal radio-ulnar joint. If pronation or supination is severely restricted, and there is no cross-union, mobility may be improved by corrective

Fracture of the radius alone is very rare and fracture of the ulna alone is uncommon. These injuries are usually caused by a direct blow – the ‘nightstick fracture’. They are important for two reasons: • An associated dislocation may be undiagnosed; if only one forearm bone is broken along its shaft and there is displacement, then either the proximal or the distal radio-ulnar joint must be dislocated. The entire forearm, elbow and wrist should always be x-rayed. • Non-union is liable to occur unless it is realized that one bone takes just as long to consolidate as two.

Injuries of the forearm and wrist

(a)

Clinical features Ulnar fractures are easily missed – even on x-ray. If there is local tenderness, a further x-ray a week or two later is wise. X-ray The fracture may be anywhere in the radius or

ulna. The fracture line is transverse and displacement is slight. In children, the intact bone sometimes bends without actually breaking (‘plastic deformation’).

Treatment Isolated fracture of the ulna The fracture is rarely displaced; a forearm brace leaving the elbow free can be sufficient. However, it takes about 8 weeks before full activity can be resumed. Rigid internal fixation will allow earlier activity and avoids the risk of displacement or non-union. Isolated fracture of the radius Radius fractures are prone to rotary displacement; to achieve reduction in children the forearm needs to be supinated for upper third fractures, neutral for middle third fractures and pronated for lower third fractures. The position is sometimes difficult to hold in children and just about impossible in adults; if so, then internal fixation with a compression plate and screws in adults, and preferably intramedullary rods in children, is better. Middle/distal third fractures of the radius in children These

are particularly unstable, being deformed by the pull of the thumb abductors and pronator quadratus. They

769

FRACTURES AND JOINT INJURIES

25

(a)

(b)

(c)

(d)

(e)

(f)

(g)

25.5 Fracture of one forearm bone Fracture of the ulna: A fracture of the ulna alone (a) usually joins satisfactorily (b); in children the intact radius may be bowed (c). Fracture of the radius: In a child, fracture of the radius alone (d) may join in plaster (e), but in adults a fractured radius (f) is better treated by plating (g).

can be treated with an above-elbow cast in supination but, failing that, fixation with an intramedullary rod, Kirschner (K-) wires or a plate is advisable.

head usually dislocates forwards and the upper third of the ulna fractures and bows forwards. Sometimes the causal force is hyperextension.

Clinical features

MONTEGGIA FRACTUREDISLOCATION OF THE ULNA The injury described by Monteggia in the early nineteenthth century (without benefit of x-rays!) was a fracture of the shaft of the ulna associated with dislocation of the proximal radio-ulnar joint; the radiocapitellar joint is inevitably dislocated or subluxated as well. More recently the definition has been extended to embrace almost any fracture of the ulna associated with dislocation of the radio-capitellar joint, including trans-olecranon fractures in which the proximal radioulnar joint remains intact. If the ulnar shaft fracture is angulated with the apex anterior (the commonest type) then the radial head is displaced anteriorly; if the fracture apex is posterior, the radial dislocation is posterior; and if the fracture apex is lateral then the radial head will be laterally displaced. In children, the ulnar injury may be an incomplete fracture (greenstick or plastic deformation of the shaft).

Mechanism of injury

770

Usually the cause is a fall on the hand; if at the moment of impact the body is twisting, its momentum may forcibly pronate the forearm. The radial

The ulnar deformity is usually obvious but the dislocated head of radius is masked by swelling. A useful clue is pain and tenderness on the lateral side of the elbow. The wrist and hand should be examined for signs of injury to the radial nerve. X-ray With isolated fractures of the ulna, it is essential

to obtain a true anteroposterior and true lateral view of the elbow. In the usual case, the head of the radius (which normally points directly to the capitulum) is dislocated forwards, and there is a fracture of the upper third of the ulna with forward bowing. Backward or lateral bowing of the ulna (which is much less common) is likely to be associated with, respectively, posterior or lateral displacement of the radial head. Trans-olecranon fractures, also, are often associated with radial head dislocation.

Treatment The key to successful treatment is to restore the length of the fractured ulna; only then can the dislocated joint be fully reduced and remain stable. In adults, this means an operation through a posterior approach. The ulnar fracture must be accurately reduced, with the bone restored to full length, and then fixed with a plate and screws; bone grafts may be added for safety.

(b)

(c)

(d)

25.6 Monteggia fracture-dislocation (a) The ulna is fractured and the head of the radius no longer points to the capitulum. In a child, closed reduction and plaster (b) is usually satisfactory; in the adult (c) open reduction and plating (d) is preferred.

The radial head usually reduces once the ulna has been fixed. Stability must be tested through a full range of flexion and extension. If the radial head does not reduce, or is not stable, open reduction should be performed. If the elbow is completely stable, then flexion– extension and rotation can be started after very soon after surgery. If there is doubt, then the arm should be immobilized in plaster with the elbow flexed for 6 weeks.

25

Injuries of the forearm and wrist

(a)

with chronic subluxation of the radial head. Because of incomplete ossification of the radial head and capitellar epiphysis in children, these landmarks may not be easily defined on x-ray and a proximal dislocation could be missed. The x-rays should be studied very carefully and if there is any doubt, x-rays should be taken of the other side for comparison. Incomplete ulnar fractures can often be reduced closed, although considerable force is needed to straighten the ulna with plastic deformation. The position of the radial head is then checked; if it is not perfect, closed reduction can be completed by flexing and supinating the elbow and pressing on the radial head. The arm is then immobilized in a cast with the elbow in flexion and supination, for 3 weeks. Complete fractures are best treated by open reduction and fixation using an intramedullary rod or a small plate.

GALEAZZI FRACTURE-DISLOCATION OF THE RADIUS Mechanism of injury This injury was first described in 1934 by Galeazzi. The usual cause is a fall on the hand; probably with a superimposed rotation force. The radius fractures in its lower third and the inferior radio-ulnar joint subluxates or dislocates.

Clinical features Complications Nerve injuries can be caused by overenthusiastic manipulation of the radial dislocation or during the surgical exposure. Always check for nerve function after treatment. The lesion is usually a neurapraxia, which will recover by itself.

Nerve injury

Malunion Unless the ulna has been perfectly reduced, the radial head remains dislocated and limits elbow flexion. In children, no treatment is advised. In adults, osteotomy of the ulna or perhaps excision of the radial head may be needed. Non-union Non-union of the ulna should be treated by plating and bone grafting.

Special features in children The general features of Monteggia fracture-dislocations are similar to those in adults. However, it is important to remember that the ulnar fracture may be incomplete (greenstick or plastic deformation); if this is not detected, and corrected, the child may end up

The Galeazzi fracture is much more common than the Monteggia. Prominence or tenderness over the lower end of the ulna is the striking feature. It may be possible to demonstrate the instability of the radio-ulnar joint by ‘ballotting’ the distal end of the ulna (the ‘piano-key sign’) or by rotating the wrist. It is important also to test for an ulnar nerve lesion, which may occur. X-ray A transverse or short oblique fracture is seen in

the lower third of the radius, with angulation or overlap. The distal radio-ulnar joint is subluxated or dislocated.

Treatment As with the Monteggia fracture, the important step is to restore the length of the fractured bone. In children, closed reduction is often successful; in adults, reduction is best achieved by open operation and compression plating of the radius. An x-ray is taken to ensure that the distal radio-ulnar joint is reduced. There are three possibilities:

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FRACTURES AND JOINT INJURIES

25

25.7 Galeazzi fracturedislocation The diagrams show the contrast between (a) Monteggia and (b) Galeazzi fracture-dislocations. (c,d) Galeazzi type before and after reduction and plating.

COLLES’ FRACTURE

(a)

The injury that Abraham Colles described in 1814 is a transverse fracture of the radius just above the wrist, with dorsal displacement of the distal fragment. It is the most common of all fractures in older people, the high incidence being related to the onset of postmenopausal osteoporosis. Thus the patient is usually an older woman who gives a history of falling on her outstretched hand.

(b)

Mechanism of injury and pathological anatomy

(c)

(d)

The distal radio-ulnar joint is reduced and stable No further action is needed. The arm is rested for a few days, then gentle active movements are encouraged. The radio-ulnar joint should be checked, both clinically and radiologically, during the next 6 weeks. The distal radio-ulnar joint is reduced but unstable The forearm should be immobilized in the position of stability (usually supination), supplemented if required by a transverse K-wire. The forearm is splinted in an above-elbow cast for 6 weeks. If there is a large ulnar styloid fragment, it should be reduced and fixed. The distal radio-ulnar joint is irreducible This is unusual. Open reduction is needed to remove the interposed soft tissues. The triangular fibrocartilage complex (TFCC) and dorsal capsule are then carefully repaired and the forearm immobilized in the position of stability (again, usually supination, supported by a wire if needed) for 6 weeks.

FRACTURES OF THE DISTAL RADIUS IN ADULTS 772

age, transfer of energy, mechanism of injury and bone quality. With any of these fractures, the wrist also can suffer substantial ligamentous injury causing instability to the carpus or distal radio-ulnar joint. These injuries are easily missed because the x-rays may look normal.

The distal end of the radius is subject to many different types of fracture, depending on factors such as

Force is applied in the length of the forearm with the wrist in extension. The bone fractures at the corticocancellous junction and the distal fragment collapses into extension, dorsal displacement, radial tilt and shortening.

(a)

(b)

(c)

(d)

25.8 Colles’ fracture (a,b) The typical Colles‘ fracture is both displaced and angulated towards the dorsum and towards the radial side of the wrist. (c,d) Note, how, after successful reduction, the radial articular surface faces correctly both distally and slightly volarwards.

Clinical features

X-ray There is a transverse fracture of the radius at the corticocancellous junction, and often the ulnar styloid process is broken off. The radial fragment is impacted into radial and backward tilt. Sometimes there is an intra-articular fracture; sometimes it is severely comminuted.

Treatment UNDISPLACED FRACTURES If the fracture is undisplaced (or only very slightly displaced), a dorsal splint is applied for a day or two until the swelling has resolved, then the cast is completed. An x-ray is taken at 10–14 days to ensure that the fracture has not slipped; if it has, surgery may be required; if not, the cast can usually be removed after four weeks to allow mobilization. DISPLACED FRACTURES Displaced fractures must be reduced under anaesthesia (haematoma block, Bier’s block or axillary block). The hand is grasped and traction is applied in the length of the bone (sometimes with extension of the wrist to disimpact the fragments); the distal fragment is then pushed into place by pressing on the dorsum while manipulating the wrist into flexion, ulnar deviation and pronation. The position is then checked by x-ray. If it is satisfactory, a dorsal plaster slab is applied, extending from just below the elbow to the metacarpal necks and two-thirds of the way round the

25

Injuries of the forearm and wrist

We can recognize this fracture (as Colles did long before radiography was invented) by the ‘dinner-fork’ deformity, with prominence on the back of the wrist and a depression in front. In patients with less deformity there may only be local tenderness and pain on wrist movements.

circumference of the wrist. It is held in position by a crepe bandage. Extreme positions of flexion and ulnar deviation must be avoided; 20 degrees in each direction is adequate. The arm is kept elevated for the next day or two; shoulder and finger exercises are started as soon as possible. If the fingers become swollen, cyanosed or painful, there should be no hesitation in splitting the bandage. At 7–10 days fresh x-rays are taken; re-displacement is not uncommon and should be treated, if the patient’s functional demands are high, by re-manipulation and internal fixation. However, in some elderly patients with low functional demands, modest degrees of displacement should be accepted because (a) outcome in these patients is not so dependent upon anatomical perfection, and (b) fixation of the fragile bone can be very difficult. The fracture unites in about 6 weeks and, even in the absence of radiological proof of union, the slab may safely be discarded and exercises begun. IMPACTED OR COMMINUTED COLLES’ FRACTURES With substantial impaction or comminution in osteoporotic bone, manipulation and plaster immobilization alone may be insufficient. The fracture can sometimes be reduced and held with percutaneous wires, but if impaction is severe even this may not be enough to maintain length; in that case, an external fixator is used to neutralize the compressive force of the 25 tendons crossing the wrist, and bone graft or bone substitute is placed into the gap. The fixator is attached to the distal radius and the second metacarpal shaft. It should be used only as a neutralizing device; too much distraction will lead to stiffness. The fixation is removed after 5–6 weeks and exercises begun. Plate fixation is increasingly being used for some Colles’ fractures. The so-called ‘volar locking plate’ is

23° 12mm 1mm

11°

(a)

(b)

(c)

25.9 Colles‘ fracture – operative fixation (a) Comminuted Colles’ fracture reduced and held with percutaneous wires. Make sure that the articular surface angles are correctly restored (b,c).

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FRACTURES AND JOINT INJURIES

25

applied to the front of the radius through the bed of flexor carpi radialis. The screws are fixed to the plate itself and are passed into the relatively stronger subchondral bone distally. These devices, which are flourishing in the orthopaedic marketplace, allow stable fixation and thus early mobilization of the forearm. Other devices, such as a locked intramedullary nail or crossed K-wires, are also suitable for the distal radius.

Outcome As Colles himself recognized, the outcome of these fractures in an older age group with lower functional demands is usually good, regardless of the cosmetic or the radiographic appearance. Poor outcomes can often be improved by performing a corrective osteotomy. The amount of displacement that can be accepted depends on patient factors such as age, comorbidity, functional demands, handedness, and quality of bone, and treatment factors such as surgical skill and implants available. As a rule, shortening of more than 2 mm at the distal radio-ulnar joint, dorsal tilt of more than 10 degrees and dorsal translation of more than 30 per cent are likely to lead to a poor outcome and early correction should be considered. This advice applies to older osteopaenic fractures; in younger patients the tolerances are far less!

Complications EARLY Circulatory problems The circulation in the fingers must be checked; the bandage holding the slab may need to be split or loosened. Nerve injury Direct injury is rare, but compression of the median nerve in the carpal tunnel is fairly common. If it occurs soon after injury and the symptoms are mild, they may resolve with release of the dressings and elevation. If symptoms are severe or persistent, the transverse ligament should be divided. Reflex sympathetic dystrophy This condition is probably quite common, but fortunately it seldom progresses to the full-blown picture of Sudeck’s atrophy. There may

(a)

774

(b)

be swelling and tenderness of the finger joints, a warning not to neglect the daily exercises. In about 5 per cent of cases, by the time the plaster is removed the hand is stiff and painful and there are signs of vasomotor instability. X-rays show osteoporosis and there is increased activity on the bone scan. TFCC injury is more common than is generally appreciated. As the distal radius displaces dorsally, the TFCC is damaged; the ulnar styloid fracture which commonly accompanies a Colles’ fracture illustrates the forces which are transmitted to the TFCC, which attaches in part to it.

TFCC injury

LATE Malunion is common, either because reduction was not complete or because displacement within the plaster was overlooked. The appearance is ugly, and weakness and loss of rotation may persist. In most cases treatment is not necessary. Where the disability is severe and the patient relatively young, the lower 1.5 cm of the ulna may be excised to restore rotation, and the radial deformity corrected by osteotomy. Malunion

Non-union of the radius is rare, but the ulnar styloid process often joins by fibrous tissue only and remains painful and tender for several months.

Delayed union and non-union

Stiffness Stiffness of the shoulder, elbow and fingers from neglect is a common complication. Stiffness of the wrist may follow prolonged splintage. Tendon rupture Rupture of extensor pollicis longus occasionally occurs a few weeks after an apparently trivial undisplaced fracture of the lower radius. The patient should be warned of the possibility and told that operative treatment is available.

SMITH’S FRACTURE Smith (a Dubliner, like Colles) described a similar fracture about 20 years later. However, in this injury the distal fragment is displaced anteriorly (which is

(c)

(d)

25.10 Colles’ fracture-complications (a) Rupture of extensor pollicis longus; (b) malunion – CT scan showing incongruity of the distal radio-ulnar joint; (c) infected K-wire; (d) failed fixation as the wires have cut through the osteoporotic bone.

fractures should be fixed with percutaneous wires or a plate.

(a)

The distal radius and ulna are among the commonest sites of childhood fractures. The break may occur through the distal radial physis or in the metaphysis of one or both bones. Metaphyseal fractures are often incomplete or greenstick.

(b)

25.11 Smith’s fracture (a,b) Here, in contrast to Colles’ fracture, the displacement of the lower radial fragment is forwards – not backwards.

why it is sometimes called a ‘reversed Colles’). It is caused by a fall on the back of the hand.

Clinical features The patient presents with a wrist injury, but there is no dinner-fork deformity. Instead, there is a ‘garden spade’ deformity. There is a fracture through the distal radial metaphysis; a lateral view shows that the distal fragment is displaced and tilted anteriorly – the opposite of a Colles’ fracture. The entire metaphysis can be fractured, or there can be an oblique fracture exiting at the dorsal or volar rim of the radius.

X-ray

Treatment The fracture is reduced by traction, supination and extension of the wrist, and the forearm is immobilized in a cast for 6 weeks. X-rays should be taken at 7–10 days to ensure the fracture has not slipped. Unstable

(a)

(b)

(c)

Mechanism of injury The usual injury is a fall on the outstretched hand with the wrist in extension; the distal fragment is forced posteriorly (this is often called a ‘juvenile Colles’ fracture’). However, sometimes the wrist is in flexion and the fracture is angulated anteriorly. Lesser force may do no more than buckle the metaphyseal cortex (a type of compression fracture, or torus fracture).

Injuries of the forearm and wrist

DISTAL FOREARM FRACTURES IN CHILDREN

25

Clinical features There is usually a history of a fall, though this may be passed off as one of many childhood spills. The wrist is painful, and often quite swollen; sometimes there is an obvious ‘dinner-fork’ deformity. The precise diagnosis is made on the x-ray appearances.

X-ray

Physeal fractures are almost invariably Salter–Harris type I or II, with the epiphysis shifted and tilted backwards and radially. Type V injuries are unusual; sometimes they are diagnosed in retrospect when premature epiphyseal fusion occurs.

(d)

(e)

(f)

25.12 Distal forearm fractures in children (a,b) In older children the fracture is usually slightly more proximal than a true Colles’, and often merely a greenstick or buckling injury. (c,d) In young children physeal fractures are usually Salter– Harris type I or II. In this case, accurate reduction has been achieved (e,f).

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FRACTURES AND JOINT INJURIES

25

Metaphyseal injuries may appear as mere buckling of the cortex (easily missed unless appropriate views are obtained), as angulated greenstick fractures or as complete fractures with displacement and shortening. If only the radius is fractured, the ulna may be bent though not fractured.

Treatment Physeal fractures are reduced, under anaesthesia, by pressure on the distal fragment. The arm is immobilized in a full-length cast with the wrist slightly flexed and ulnar deviated, and the elbow at 90 degrees. The cast is retained for 4 weeks. These fractures very rarely interfere with growth. Even if reduction is not absolutely perfect, further growth and modelling will obliterate any deformity. Patients seen more than 2 weeks after injury are best left untreated. Buckle fractures require no more than 2 weeks in plaster, followed by another 2 weeks of restricted activity. Greenstick fractures are usually easy to reduce – but apt to re-displace in the cast! Some degree of angulation can be accepted: in children under 10, up to 30 degrees and in children over 10, up 15 degrees. If the deformity is greater, the fracture is reduced by thumb pressure and the arm is immobilized with three-point fixation in a full-length cast with the wrist and forearm in neutral and the elbow flexed 90 degrees. The cast is changed and the fracture re-x-rayed at 2 weeks; if it has re-displaced a further manipulation can be carried out. The cast is finally discarded after 6 weeks. Complete fractures can be embarrassingly difficult to reduce – especially if the ulna is intact. The fracture is manipulated in much the same way as a Colles’ fracture; the reduction is checked by x-ray and a fulllength cast is applied with the wrist neutral and the forearm supinated. After 2 weeks, a check x-ray is obtained; the cast is kept on for 6 weeks. If the fracture slips, especially if the ulna is intact, it should be stabilized with a percutaneous K-wire.

Radio-ulnar discrepancy Premature fusion of the radial

epiphysis may result in bone length disparity and subluxation of the radio-ulnar joint. If this is troublesome, the radius can be lengthened and, if the child is near to skeletal maturity, the ulnar physis fused surgically.

RADIO-CARPAL FRACTURES

FRACTURED RADIAL STYLOID This injury is caused by forced radial deviation of the wrist and may occur after a fall, or when a starting handle ‘kicks back’ – the so-called ‘chauffeur’s fracture‘. The fracture line is transverse, extending laterally from the articular surface of the radius; the fragment, much more than the radial styloid, is often undisplaced. The radial styloid can also be fractured as part of the far more serious trans-scaphoid perilunate fracture dislocation.

Treatment If there is displacement it is reduced, and the wrist is held in ulnar deviation by a plaster slab round the outer forearm extending from below the elbow to the metacarpal necks. Imperfect reduction may lead to osteoarthritis; therefore if closed reduction is imperfect the fragment should be screwed back, or held with K-wires.

FRACTURE-SUBLUXATION (BARTON’S FRACTURE) VOLAR SUBLUXATION The true Barton’s injury is a volar fracture of the distal radius associated with volar subluxation of the carpus.

Complications EARLY Forearm swelling and threatened compartment syndrome

This dire combination can be prevented by avoiding over-forceful or repeated manipulations, splitting the plaster, elevating the arm for the first 24–48 hours and encouraging exercises. LATE This late sequel is uncommon in children under 10 years of age. Deformity of as much as 30 degrees will straighten out with further growth and remodelling over the next 5 years. This should be carefully explained to the worried parents.

Malunion

776

(a)

(b)

25.13 Fractured radial styloid (a) X-ray; (b) fixation with cannulated percutaneous screw.

25

(a)

(b)

(b)

(c)

(c)

25.14 Fracture-subluxation (Barton’s fracture) (a,b) The true Barton’s fracture is a split of the volar edge of the distal radius with anterior (volar) subluxation of the wrist. This has been reduced and held (c) with a small anterior plate.

25.15 Comminuted fracture of the distal radius The ‘die punch fragment’ of the lunate fossa of the distal radius (a,b) must be perfectly reduced and fixed; here this has been achieved by closed reduction and percutaneous K-wire fixation (c). The wires can be used as ‘joy sticks’ to manipulate the fragment back before fixation.

It is sometimes mistaken for a Smith’s fracture, but it differs from the latter in that the fracture line runs obliquely across the volar lip of the radius into the wrist joint; the distal fragment is displaced anteriorly, carrying the carpus with it. Because the fragment is small and unsupported, the fracture is inherently unstable.

closed K-wiring or open reduction and plating is advisable.

Treatment The fracture can be easily reduced, but it is

just as easily re-displaced. Internal fixation, using a small anterior buttress plate, is recommended. DORSAL SUBLUXATION This is sometimes called a ‘dorsal Barton’s fracture’. Here the line of fracture runs obliquely across the dorsal lip of the radius and the carpus is carried posteriorly. The fracture is easier to control than the volar Barton’s. It is reduced closed and the forearm is immobilized in a cast for 6 weeks. If it re-displaces,

Treatment

Injuries of the forearm and wrist

(a)

COMMINUTED INTRA-ARTICULAR FRACTURES IN YOUNG ADULTS In the young adult, a comminuted intra-articular fracture is a high energy injury. A poor outcome will result unless intra-articular congruity, fracture alignment and length are restored and movements started as soon as possible. For these patients a much higher standard must be set than would be accepted for the typical osteoporotic fracture. In addition to the usual posteroanterior and lateral x-rays, oblique views and often CT scans are useful to show the fragment alignment. The simplest option is a manipulation and cast. If the anatomy is not restored, then an open reduction 25.16 High energy injuries in younger patients Perfect reduction is required.

(a)

(b)

(c)

(d)

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25

COMPLICATIONS OF RADIO-CARPAL

FRACTURES AND JOINT INJURIES

FRACTURES Associated injuries of the carpus Injuries of the carpus are easily overlooked while attention is focussed on the radius. Carpal injuries must be excluded by careful clinical and x-ray examination, occasionally supplemented by MRI or arthroscopy. Re-displacement There is a strong tendency for Barton’s fracture to re-displace if it is held in a cast; hence our preference for internal fixation.

(a)

The patient may present years later with chronic carpal instability. The wrist injury may have been overlooked at the time.

Carpal instability

Fractures into the joint and carpal instability may eventually lead to secondary osteoarthritis. It is difficult to predict when (or even whether) this is likely to occur; symptoms develop slowly and disability is often not severe. Warning symptoms are restricted wrist movement and loss of grip strength. If pain and weakness interfere significantly with function, arthrodesis of the wrist may be need, especially if it is the dominant side which is affected.

Secondary osteoarthritis

CARPAL INJURIES

(b)

25.17 Distal radius fracture Options include simple plaster (a) or external fixation (b) depending on the amount of comminution, stability of the fracture and patient demands.

may be necessary. The medial complex must be anatomically reduced, which may require open reduction through dorsal and palmar approaches and a combination of wires, plates, screws and bone grafts.

(a)

778

(b)

Fractures and dislocations of the carpal bones are common. They vary greatly in type and severity. These should never be regarded as isolated injuries; the entire carpus suffers, and sometimes, long after the fracture has healed, the patient still complains of pain and weakness in the wrist. The commonest wrist injuries are: sprains of the capsule and ligaments; fracture of a carpal bone

(c)

25.18 Don’t forget the ulna (a) Fracture of radius and ulna, both unstable. (b) Both bones fixed. (c) Ulnar styloid fracture fixed to prevent instability of distal radio-ulnar joint.

(usually the scaphoid); injury of the triangular fibrocartilage complex (TFCC) and distal radio-ulnar joint; dislocations of the lunate or the bones around it; and subluxations and ‘carpal collapse’, which may be acute or chronic.

Following a fall, the patient complains of pain in the wrist. There may be swelling or well-marked deformity of the joint. Tenderness should be carefully localized; undirected prodding will confuse both the patient and the examiner. The blunt end of a pencil is helpful in testing for point tenderness. For scaphoid

Imaging X-rays are the key to diagnosis. There are three golden rules: • Accept only high-quality films • If the initial x-rays are ‘normal’, treat the clinical diagnosis • Repeat the x-ray examination 2 weeks later.

(a)

(b)

(c)

25.19 Carpal instability – x-ray patterns (a) Normal lateral view. The radius, capitate and middle metacarpal lie in a straight line and the scaphoid axis is angled at 45º to the line of the radius. (b) Dorsal intercalated segmental instability (DISI). The lunate is tilted dorsally and the scaphoid is tilted somewhat volarwards; the axes of the capitate and metacarpals now lie behind (dorsal to) that of the radius. (c) Volar intercalated segmental instability (VISI). The lunate and scaphoid are tilted somewhat volarwards and the capitate and metacarpals lie anterior (volar) to the radius.

Initially three standard views are obtained: anteroposterior and lateral with the wrist neutral, and an oblique ‘scaphoid’ view. If these are normal and clinical features suggest a carpal injury, further views are obtained: anteroposterior x-rays with the wrist first in maximum ulnar and then in maximum radial deviation, and an anteroposterior view with the fist clenched. The examiner should be familiar with the normal x-ray anatomy of the carpus in all the standard views, so that he or she can visualize a three-dimensional picture from the two-dimensional, overlapping images of the carpal bones. In the anteroposterior x-rays note the shape of the carpus, whether the individual bones are clearly outlined and whether there are any abnormally large gaps suggesting disruption of the ligaments. The scaphoid may be fractured; or it may have lost its normal bean shape and look squat and foreshortened, sometimes with an inner circular density (the cortical ring sign) – features of an end-on view when the bone is hyperflexed because of damage to the restraining scapholunate ligament. The lunate is normally quadrilateral in shape, but if it is dislocated it looks triangular. In the lateral x-ray the axes of the radius, lunate, capitate and third metacarpal are co-linear, and the scaphoid projects at an angle of about 45 degrees to this line. With traumatic instability the linked carpal segments collapse (like the buckled carriages of a derailed train). Two patterns are recognized: dorsal intercalated segment instability (DISI), in which the lunate is torn from the scaphoid and tilted backwards; and volar intercalated segment instability (VISI), in which the lunate is torn from the triquetrum and turns towards the palm; the capitate shows a complementary dorsal tilt. There may be a flake fracture off the back of a carpal bone (usually the triquetrum). Special x-ray studies are sometimes helpful: a carpal

25

Injuries of the forearm and wrist

Clinical assessment

fractures, the ‘jump spot’ is in the anatomical snuffbox and scaphoid tubercle; for scapho-lunate injuries, just beyond Lister’s tubercle; for lunate dislocation, in the middle of the wrist; for triquetral injuries, beyond the head of the ulna; for hamate fractures, at the base of the hypothenar eminence; for triangular fibrocartilage complex injuries, over the dorsum of the ulnocarpal joint. Movements are often limited (more by pain than by stiffness) and they may be accompanied by a palpable catch or an audible clunk.

779

FRACTURES AND JOINT INJURIES

25

Principles of management

(b) (a)

‘Wrist sprain’ should not be diagnosed unless a more serious injury has been excluded with certainty. Even with apparently trivial injuries, ligaments are sometimes torn and the patient may later develop carpal instability. If the x-rays are normal but the clinical signs strongly suggest a carpal injury, a splint or plaster should be applied for 2 weeks, after which time the xrays are repeated. A fracture or dislocation may become more obvious after a few weeks, but a second negative x-ray still does not exclude a serious injury. A bone scan or MRI at this stage will confirm the diagnosis and avoid an unnecessary period of immobilization and time from work. If these tests are not readily available, then the patient should be re-examined repeatedly until the symptoms settle or a firm diagnosis is made. The more common lesions are dealt with below.

(d) (c)

FRACTURED SCAPHOID Scaphoid fractures account for almost 75 per cent of all carpal fractures although they are rare in the elderly and in children. With unstable fractures there may also be disruption of the scapho-lunate ligaments and dorsal rotation of the lunate.

(f) (e)

25.20 Carpal injuries (a,b) Normal appearances in antero-posterior and lateral x-rays. (c,d) Following a ‘sprained wrist’ this patient developed persistent pain and weakness. X-rays showed (c) scapho-lunate dissociation and (d) dorsal rotation of the lunate (the typical DISI pattern). (e,f) This patient, too, had a sprained wrist. The anteroposterior and lateral x-rays show foreshortening of the scaphoid and volar rotation of the lunate (VISI).

e

g

d f

tunnel view may show a fractured hook of hamate, and motion studies in different positions may reveal a subluxation. A radioisotope scan will confirm a wrist injury although it may not precisely localize it. MRI is sensitive and specific (especially for detecting undisclosed fractures or Kienböck’s disease), but unless very fine cuts are taken it may miss TFCC and interosseous ligament tears.

Arthroscopy 780

Wrist arthroscopy is the best way of demonstrating TFCC or interosseous ligament tears.

c

a b

25.21 X-ray appearance of the normal carpus X-ray of a normal wrist showing the shape and disposition of the eight carpal bones: (a) scaphoid; (b) lunate; (c) triquetrum overlain by pisiform; (d) trapezium; (e) trapezoid; (f) capitate; and (g) hamate.

Mechanism of injury and pathological anatomy

Clinical features The appearance may be deceptively normal, but the astute observer can usually detect fullness in the anatomical snuffbox; precisely localized tenderness in

(a)

(d)

X-ray Anteroposterior, lateral and oblique views are all essential; often a recent fracture shows only in the oblique view. Usually the fracture line is transverse, and through the narrowest part of the bone (waist), but it may be more proximally situated (proximal pole fracture). Sometimes only the tubercle of the scaphoid is fractured. It is very important to look for subtle signs of displacement or instability: e.g. obliquity of the fracture line, opening of the fracture line, angulation of the distal fragment and foreshortening of the scaphoid image. A few weeks after the injury the fracture may be more obvious; if union is delayed, cavitation appears on either side of the break. Old, un-united fractures have ‘hard’ borders, making it seem as if there is an extra carpal bone. Relative sclerosis of the proximal fragment is pathognomonic of avascular necrosis.

(b)

(e)

25

Injuries of the forearm and wrist

The scaphoid lies obliquely across the two rows of carpal bones, and is also in the line of loading between the thumb and forearm. The combination of forced carpal movement and compression, as in a fall on the dorsiflexed hand, exerts severe stress on the bone and it is liable to fracture. Most scaphoid fractures are stable; with unstable fractures the fragments may become displaced. The distal fragment, unrestrained by the scapho-lunate ligament, flexes and the proximal fragment tilts dorsally with the lunate (a DISI deformity); the hump-backed deformity of the scaphoid is permanent. The blood supply of the scaphoid diminishes proximally. This accounts for the fact that 1 per cent of distal third fractures, 20 per cent of middle third fractures and 40 per cent of proximal fractures result in non-union or avascular necrosis of the proximal fragment.

the same place is an important diagnostic sign; the scaphoid can of course also be palpated from the front and back of the wrist and it may be tender there as well. Proximal pressure along the axis of the thumb may be painful.

(c)

(f)

(g)

25.22 Fractures of the scaphoid – diagnosis (a) The initial anteroposterior view often fails to show the fracture; (b) always ask for a ‘scaphoid series’, including two oblique views. If the clinical features are suggestive of a fracture, then immobilize the wrist and repeat the x-ray 2 weeks later when the fracture is more likely to be apparent. (c) A CT scan is useful for showing the fracture configuration. The fracture may be (d) through the proximal pole, (e) the waist, or (f) the scaphoid tubercle. Occasionally these fractures are seen in children (g).

781

FRACTURES AND JOINT INJURIES

25

(a)

(f)

(b)

(c)

(g)

(d)

(e)

(h)

25.23 Fractures of the scaphoid –treatment (a) Scaphoid plaster – position and extent. (b,c) Before and after treatment: in this case radiological union was visible at 10 weeks. (d) Delayed union, treated successfully by (e) bone grafting and screw fixation. (f) Long-standing stable non-union. (g) Non-union with avascular necrosis and secondary osteoarthritis treated by (h) scaphoid excision and four-corner fusion.

Treatment

782

Fracture of the scaphoid tubercle needs no splintage and should be treated as a wrist sprain; a crepe bandage is applied and movement is encouraged. Other scaphoid fractures are treated as follows. Undisplaced fractures need no reduction and are treated in plaster; 90 per cent of waist fractures should heal. The cast is applied from the upper forearm to just short of the metacarpo-phalangeal joints of the fingers, but incorporating the proximal phalanx of the thumb. The wrist is held dorsiflexed and the thumb forwards in the ‘glass-holding’ position. The plaster must be carefully moulded into the hollow of the hand, and is not split. It is retained (and if necessary repaired or renewed) for 8 weeks. After 8 weeks the plaster is removed and the wrist examined clinically and radiologically. If there is no tenderness and the x-ray shows signs of healing, the wrist is left free; a CT scan is the most reliable means of confirming union if in doubt. If the scaphoid is tender, or the fracture still visible on x-ray, the cast is reapplied for a further 4 weeks. At

that stage, one of two pictures may emerge: (a) the wrist is painless and the fracture has healed – the cast can be discarded; (b)the x-ray shows signs of delayed healing (bone resorption and cavitation around the fracture) – union can be hastened by bone grafting and internal fixation. Displaced fractures can also be treated in plaster, but the outcome is less predictable. It is better to reduce the fracture openly and to fix it with a compression screw. This should increase the likelihood of union and reduce the time of immobilization. Some patients may not want to endure a prolonged period in plaster. Early percutaneous fixation with a compression screw, though technically demanding, can dramatically reduce the time away from work and the difficulties associated with personal care.

Complications Avascular necrosis The proximal fragment may die, especially with proximal pole fractures, and then at 2– 3 months it appears dense on x-ray. Although revascularization and union are theoretically possible,

Non-union By 3 months it may be obvious that the fracture will not unite. Bone grafting should be attempted, especially in the younger, more vigorous type of patient, because this probably reduces the chance of later, symptomatic osteoarthritis. Two types of graft are used. If the scaphoid has folded into a flexed ‘humpback’ shape, then it is approached from the front and a wedge of cortico-cancellous iliac crest graft is inserted to restore the shape of the bone. The graft is fixed with a buried screw and/or K-wires. If the scaphoid has not collapsed, the graft is inserted into

a trough carved into the front of the scaphoid and again stabilized with a screw or wires. If these techniques fail to achieve union then the options are a vascularized bone graft, scaphoidectomy with proximal-to-distal-row (four-corner) fusion, proximal row carpectomy or radio-carpal arthrodesis. In older patients, and those who are completely asymptomatic, non-union may be left untreated. Sometimes a patient is seen for the first time with a ‘sprain’, but x-rays show an old, un-united fracture with sclerosed edges; 3–4 weeks in plaster may suffice to make him or her comfortable once again, and no further treatment is required. Osteoarthritis Non-union or avascular necrosis may lead to secondary osteoarthritis of the wrist. If the arthritis is localized to the distal pole, excising the radial styloid may help. As the arthritis progresses, changes appear in the scapho-capitate joint then the capitate-lunate joint. The lunate-radius joint is never affected, thus allowing salvage procedures – either proximal row carpectomy or four-corner fusion.

(a)

(b)

(c)

(d)

(e)

(f)

(g)

(h)

25.24 Fractures of other carpal bones (a) Fracture of body of trapezium; (b) lunate fracture; (c) lunate fracture; (d) hook of hamate; (e) hook of hamate CT; (f) capitate fracture fixed (g) with a screw; (h) fracture of body of hamate.

25

Injuries of the forearm and wrist

they take years and meanwhile the wrist collapses and arthritis develops. Bone grafting, as for delayed union, may be successful, in which case the bone, though abnormal, is structurally intact. If the wrist becomes painful, the dead fragment can be excised. However, the wrist tends to collapse after this procedure; a better option would be to remove the entire proximal row of carpal bones or else to remove the scaphoid and fuse the proximal to the distal row (four-corner fusion: capitate–hamate–triquetrum–lunate).

783

25

FRACTURES OF OTHER CARPAL BONES

styloid avulsed or the articular surfaces of the ulnocarpal joint or distal radio-ulnar joint damaged.

FRACTURES AND JOINT INJURIES

Triquetrum Avulsion of the dorsal ligaments is not uncommon; analgesics and splintage for a few days are all that is required. Occasionally the body is fractured; it usually heals after 4–6 weeks in plaster.

Hamate A fracture of the hook of hamate follows a direct blow to the palm of the hand. These fractures cannot be seen on routine x-rays; a carpal tunnel view, CT or MRI is needed. The fracture does not heal readily; if symptoms are prolonged then the fragment is excised, taking care not to damage the ulnar nerve. Fractures of the body are rare. They are also difficult to define on plain x-rays. If the CT scan shows a fracture, fixation may occasionally be needed.

Trapezium The body of the trapezium can be fractured if the shaft of the first metacarpal impacts onto it; the ridge (to which the transverse carpal ligament attaches) can be fractured by a direct blow. The latter fracture can usually be seen on a carpal tunnel view rather than standard x-rays. The body fracture may need open reduction and internal fixation if displaced; the ridge fracture usually settles with splintage for a week or two.

Clinical features There is tenderness over the distal radio-ulnar joint and pain on rotation of the forearm. The distal ulna may be unstable; the piano-key sign is elicited by holding the patient’s forearm pronated and pushing sharply forwards on the head of the ulna.

Imaging and arthroscopy A lateral x-ray in pronation and supination shows incongruity of the distal radio-ulnar joint. The anteroposterior view may show an avulsed ulnar styloid. Arthrography, MRI and arthroscopy may be needed to confirm the diagnosis.

Treatment Instability usually resolves if the arm is held in supination for 6 weeks; occasionally a K-wire is needed to maintain the reduction. If the dislocation is irreducible, this may be due to trapped soft tissue, which will have to be removed. Chronic instability may require reconstructive surgery. A TFCC tear should be repaired and the ulnocarpal capsule reefed. A displaced fracture at the base of the ulnar styloid, if painful or associated with instability of the radio-ulnar joint, should be fixed with a small screw.

Capitate The capitate is relatively protected within the carpus. However, in severe trauma the wrist can be fractured; the distal fragment can rotate, in which case open reduction and internal fixation is required.

Fractures of the lunate are rare and follow a hyperextension injury to the wrist. There is a real risk of nonunion; undisplaced fractures should be immobilized in a cast for 6 weeks; displaced fractures should be reduced and fixed with a screw.

The wrist functions as a system of intercalated segments or links, stabilized by the intercarpal ligaments and the scaphoid which acts as a bridge between the proximal and distal rows of the carpus. Fractures and dislocations of the carpal bones, or even simple ligament tears and sprains, may seriously disturb this system so that the links collapse into one of several well-recognized patterns (see Chapter 16).

ULNAR-SIDE WRIST INJURIES

LUNATE AND PERILUNATE DISLOCATIONS

(see also Chapter 16)

A fall with the hand forced into dorsiflexion may tear the tough ligaments that normally bind the carpal bones. The lunate usually remains attached to the radius and the rest of the carpus is displaced backwards (perilunate dislocation). Usually the hand immediately snaps forwards again but, as it does so,

Lunate

784

CARPAL DISLOCATIONS, SUBLUXATIONS AND INSTABILITY

The distal radio-ulnar joint is often injured with a radial fracture; it can also be damaged in isolation, particularly after hyperpronation. The triangular fibrocartilage complex (TFCC) can be torn, the ulnar

the lunate may be levered out of position to be displaced anteriorly (lunate dislocation). Sometimes the scaphoid remains attached to the radius and the force of the perilunar dislocation causes it to fracture through the waist (trans-scaphoid perilunate dislocation).

wards, and the capitate and metacarpals lie behind the line of the radius (DISI pattern); if there is an associated scaphoid fracture, the distal fragment may be flexed.

25

Treatment

Clinical features

Closed reduction

Injuries of the forearm and wrist

The wrist is painful and swollen and is held immobile. If the carpal tunnel is compressed there may be paraesthesia or blunting of sensation in the territory of the median nerve, and weakness of palmar abduction of the thumb.

X-ray Most dislocations are perilunate. In the antero-posterior view the carpus is diminished in height and the bone shadows overlap abnormally. One or more of the carpal bones may be fractured (usually the scaphoid and radial styloid). If the lunate is dislocated, it has a characteristic triangular shape instead of the normal quadrilateral appearance. In the lateral view it is easy to distinguish a lunate from a perilunate dislocation. The dislocated lunate is tilted forwards and is displaced in front of the radius, while the capitate and metacarpal bones are in line with the radius. With a perilunate dislocation the lunate is tilted only slightly and is not displaced for-

The surgeon pulls strongly on the dorsiflexed hand; then, while maintaining traction, he or she slowly palmarflexes the wrist, at the same time squeezing the lunate backwards with his or her other thumb. These manoeuvres usually effect reduction; they also prevent conversion of a perilunate to a lunate dislocation. A plaster slab is applied holding the wrist neutral. Percutaneous K-wires may be needed to hold the reduction.

Open reduction Reduction is imperative, and if closed reduction fails, or if a later x-ray shows that the wrist has collapsed into the familiar DISI pattern, open reduction is performed. The carpus is exposed by an anterior approach which has the advantage of decompressing the carpal tunnel. While an assistant pulls on the hand, the lunate is levered into place and kept there by a K-wire which is inserted through the lunate into the capitate. If the scaphoid is fractured, this too can be reduced and fixed with a Herbert screw or K-wires. Where possible, the torn soft tissues should be repaired through palmar and dorsal approaches. At the end of the procedure, the wrist is splinted in a plaster slab, which is retained for 3 weeks. Finger, elbow and shoulder exercises are practised throughout this period. The K-wires are removed at 6 weeks. This injury is frequently accompanied by severe compression of the median nerve, which should be released.

SCAPHO-LUNATE DISSOCIATION

(a)

(c)

(e)

A wrist sprain may be followed by persistent pain and tenderness over the dorsum just distal to Lister’s tubercle. X-rays show an excessively large gap between the scaphoid and the lunate. The scaphoid may appear foreshortened, with a typical cortical ring sign. In the lateral view, the lunate is tilted dorsally and the scaphoid anteriorly (DISI pattern).

Treatment

(b)

(d)

(f)

25.25 Lunate and perilunate dislocations. (a,b) Lateral x-ray of normal wrist; (c,d) lunate dislocation; (e,f) perilunate dislocation.

Scapho-lunate instability causes weakness of the wrist and recurrent discomfort. If seen early (i.e. less than 4 weeks after injury) the scapho-lunate ligament should be repaired directly with interosseous sutures, protected by K-wires for 6 weeks and a cast for 8–12 weeks. If seen between 4 and 24 weeks, then the

785

FRACTURES AND JOINT INJURIES

25

(a)

(b)

(c)

25.26 Perilunate dislocation (a,b) Lunate still in its original position while the rest of the carpus is dislocated around it. (c) The dislocation has been reduced and held with K-wires. (d) The luno-triquetral ligament is re-attached with ligament anchors.

ligament is unlikely to heal. Blatt’s capsulodesis is helpful: a proximally based flap of dorsal capsule is attached to the back of the scaphoid to haul it back from flexion into a normal position. In chronic lesions without secondary osteoarthritis, a capsulodesis or ligament reconstruction is attempted. If there is severe symptomatic osteoarthritis then a limited intercarpal arthrodesis or radio-carpal arthrodesis is performed.

RADIO-CARPAL DISLOCATION

TRIQUETRO-LUNATE DISSOCIATION

MIDCARPAL DISLOCATION

A medial sprain followed by weakness of grip and tenderness distal to the head of the ulna should suggest disruption of the triquetro-lunate ligaments. X-rays show a noticeable gap between the triquetrum and the lunate, with a VISI carpal collapse pattern in the lateral view.

The extrinsic ligaments which bind the proximal to the distal row can rupture (there are, by definition, no intrinsic ligaments between these two rows). The diagnosis is difficult but is more readily suggested in those with generalized ligament laxity and a chronic wrist problem. The patient complains of a painful, recurrent snap in the wrist; the two rows can be passively ‘clunked’ apart when shifted backwards and forwards. If an acute ligament rupture is diagnosed, then repair and temporary K-wire stabilization should be carried out. In a chronic lesion, fusion of the proximal row to the distal row is the most effective treatment but this operation will restrict wrist movement and may predispose to later arthritis.

Treatment Acute tears should be repaired with interosseous sutures, supported by temporary K-wires for 6 weeks and a cast for 8–12 weeks. In chronic injuries, a ligament substitution (e.g. a slip of extensor carpi ulnaris) or a limited intercarpal fusion may be considered.

786

(d)

The most common injuries of this type involve a fracture of the anterior or posterior rim of the distal radius (Barton’s fracture – see page 776). However, occasionally the ligaments which bind the carpus to the distal radius can rupture; the carpus tends to translate medially. Repair of the ligaments and temporary K-wire stabilization is needed.

26

Hand injuries David Warwick

Hand injuries – the commonest of all injuries – are important out of all proportion to their apparent severity, because of the need for perfect function. Nowhere else do painstaking evaluation, meticulous care and dedicated rehabilitation yield greater rewards. The outcome is often dependent upon the judgement of the doctor who first sees the patient. If there is skin damage the patient should be examined in a clean environment with the hand displayed on sterile drapes. A brief but searching history is obtained; often the mechanism of injury will suggest the type and severity of the trauma. The patient’s age, occupation and ‘handedness’ should be recorded. Superficial injuries and severe fractures are obvious, but deeper injuries are often poorly disclosed. It is important in the initial examination to assess the circulation, soft-tissue cover, bones, joints, nerves and tendons. X-rays should include at least three views (posteroanterior, lateral and oblique), and with finger injuries the individual digit must be x-rayed.

GENERAL PRINCIPLES OF TREATMENT Most hand injuries can be dealt with under local or regional anaesthesia; a general anaesthetic is only rarely required.

is needed, only the injured finger should be splinted. If the entire hand needs splinting, this must always be in the ‘position of safety’ – with the metacarpo-phalangeal joints flexed at least 70 degrees and the interphalangeal joints almost straight. Sometimes an external splint, to be effective, would need to immobilize undamaged fingers or would need to hold the joints of the injured finger in an unfavourable position (e.g. flexion of the interphalangeal joints). If so, internal fixation may be required (K-wires, screws or plates). Skin damage demands wound toilet followed by suture, skin grafting, local flaps, pedicled flaps or (occasionally) free flaps. Treatment of the skin takes precedence over treatment of the fracture.

Skin cover

Generally, the best results will follow primary repair of tendons and nerves. Occasionally grafts are required.

Nerve and tendon injury

METACARPAL FRACTURES The metacarpal bones are vulnerable to blows and falls upon the hand, or the longitudinal force of the boxer’s punch. Injuries are common and the bones may fracture at their base, in the shaft or through the neck. Angular deformity is usually not very marked, and even if it persists, it does not interfere much with

If the circulation is threatened, it must be promptly restored, if necessary by direct repair or vein grafting.

Circulation

Swelling Swelling must be controlled by elevating the hand and by early and repeated active exercises. Splintage Incorrect splintage is a potent cause of stiffness; it must be appropriate and it must be kept to a minimum length of time. If a finger has to be splinted, it may be possible simply to tape it to its neighbour so that both move as one; if greater security

(a)

(b)

(c)

26.1 Splintage of the hand Three positions of the hand: (a) The position of relaxation, (b) the position of function (ready for action) and (c) the position of safe immobilization, with the ligaments taut.

FRACTURES AND JOINT INJURIES

26

(a)

(e)

(b)

(c)

(f)

function. Rotational deformity, however, is serious. Close your hand with the distal phalanges extended, and look: the fingers converge across the palm to a point above the thenar eminence; malrotation of the metacarpal (or proximal phalanx) will cause that finger to diverge and overlap one of its neighbours. Thus, with a fractured metacarpal it is important to regain normal rotational alignment. The fourth and fifth metacarpals are more mobile at their base than the second and third, and therefore are better able to compensate for residual angular deformity. Fractures of the thumb metacarpal usually occur near the base and pose special problems. They are dealt with separately below.

(d)

26.2 Metacarpal fractures (a) A spiral fracture (especially an ‘inboard’ one) can be adequately held by the surrounding muscles and ligaments but internal fixation (b) allows early mobilization. A displaced fracture (c), especially an ‘outboard’ one, can be held by a plate or transverse wires to allow early mobilization (d); multiple metacarpal fractures should be fixed with rigid plates for wires (e). A boxer’s fracture (f) should be treated by early mobilization.

practised assiduously. As the patient moves the fingers, the fracture may shorten until the intertacarpal ligaments between the metacarpal necks tighten, thus limiting further shortening and rotational deformity. Transverse fractures with considerable displacement are reduced by traction and pressure. Reduction can sometimes be held by a plaster slab extending from the forearm over the fingers (only the damaged ones). The slab is maintained for 3 weeks and the undamaged fingers are exercised. However, these fractures are usually unstable and should be fixed surgically with compression plates or percutaneous K-wires placed either across the fracture or transversely through the neighbouring undamaged metacarpals. Spiral fractures are liable to rotate; if so, they should be perfectly reduced and fixed with lag screws and a plate, or percutaneous wires.

FRACTURES OF THE METACARPAL SHAFT A direct blow may fracture one or several metacarpal shafts transversely, often with associated skin damage. A twisting or punching force may cause a spiral fracture of one or more shafts. There is local pain and swelling, and sometimes a dorsal ‘hump’.

Treatment

788

Oblique or transverse fractures with slight displacement require no reduction. Splintage also is unnecessary, but a firm crepe bandage may be comforting; this should not be allowed to discourage the patient from active movements of the fingers, which should be

FRACTURES OF THE METACARPAL NECK A blow may fracture the metacarpal neck, usually of the fifth finger (the ‘boxer’s fracture’) and occasionally one of the others. There may be local swelling, with flattening of the knuckle. X-rays show an impacted transverse fracture with volar angulation of the distal fragment.

Treatment The main function of the fifth and fourth fingers is firm flexion (‘power grip’) and, as can be readily

joint is so badly damaged that primary replacement is considered (Silastic, pyrocarbon or polythene– metal).

26

FRACTURES OF THE METACARPAL BASE

(b)

26.3 Fracture of the metacarpal head (a) Depressed head fracture which was reduced and held with buried mini-screws. (b) A ‘fight-bite’, with metacarpal head damage from an opponent’s tooth.

demonstrated on a normal hand, there is ‘spare’ extension available at the metacarpo-phalangeal (MCP) joint. Therefore in these digits, a flexion deformity of up to 40 degrees can be accepted; as long as there is no rotational deformity, a good outcome can be expected. The hand is immobilized in a gutter splint with the MCP joint flexed and the interphalangeal (IP) joints straight until discomfort settles – a week or two – and then the hand is mobilized. The patient is warned that the knuckle profile may be permanently lost. In the index and middle fingers, which function mainly in extension, no more than 20 degrees of flexion at the fracture is acceptable. If the fracture needs reduction, this can be done under a local block. The reduced finger is held with a gutter splint moulded at three points to support the fracture; the MCP joints are flexed and the IP joints are straight. Unfortunately, these fractures are usually fairly unstable because of the tone of the flexor tendons and the palmar comminution of the fracture. If there is a tendency to redisplacement, fixation should be used. Plates are not really suitable because the fracture is so distal. A bouquet of two or three bent wires passed distally through a hole in the styloid process of the fifth metacarpal base is particularly effective.

Complications Malunion, with volar angulation of the distal fragment, is poorly tolerated if this occurs in the second or third rays. The patient may be aware of a bump in the palm from the prominent metacarpal head and the digit may take on a ‘Z’ appearance as the knuckle joint hyperextends to compensate for the deformity.

Hand injuries

(a)

Excepting fractures of the thumb metacarpal, these are usually stable injuries which can be treated by ensuring that rotation is correct and then splinting the digit in a volar slab extending from the forearm to the proximal finger joint. The splint is retained for 3 weeks and exercises are then encouraged. Displaced intra-articular fractures of the base of the fourth or fifth metacarpal may cause marked incongruity of the joint. This is a mobile joint and it may, therefore, be painful. The fracture should be reduced by traction on the little finger and then held with a percutaneous K-wire or compression screw. In the long term, if painful arthritis supervenes, treatment would be with either arthrodesis or joint excision.

FRACTURE OF THE THUMB METACARPAL Three types of fracture are encountered: impacted fracture of the metacarpal base; Bennett’s fracture-dislocation of the carpo-metacarpal (CMC) joint; and Rolando’s comminuted fracture of the base.

Impacted fracture A boxer may, while punching, sustain a fracture of the base of the first metacarpal. Localized swelling and tenderness are found, and x-ray shows a transverse fracture about 6 mm distal to the CMC joint, with outward bowing and impaction. Treatment If the angulation is less than 20–30

degrees and the fragments are impacted, the thumb is rested in a plaster of Paris cast extending from the forearm to just short of the interphalangeal thumb joint with the thumb fully abducted and extended. The cast is removed after 2–3 weeks and the thumb is mobilized. If the angulation is greater than 30 degrees, then the reduced thumb web span will be noticeable and so the fracture should be reduced. The surgeon pulls on the abducted thumb and, by levering the metacarpal outwards against his own thumb, corrects the bowing. A plaster cast is applied. If the fracture is still unstable, then a percutaneous K-wire is inserted. An alternative would be a low profile plate.

FRACTURES OF THE METACARPAL HEAD

Bennett’s fracture-dislocation

These fractures occur after a direct blow. They are often quite comminuted and sometimes ‘open’. Operative reduction is usually required and fixation with small headless buried screws is ideal. Occasionally the

This fracture, too, occurs at the base of the first metacarpal bone and is commonly due to punching; however the fracture is oblique, extends into the CMC joint and is unstable.

789

FRACTURES AND JOINT INJURIES

26

(a)

(b)

(d)

(e)

26.4 Fractures of the first metacarpal base A transverse fracture (a) can be reduced and held in plaster (b). Bennett’s fracture-dislocation (c) is best held with a small screw (d) or a percutaneous K-wire (e).

The thumb looks short and the carpo-metacarpal region swollen. X-rays show that a small triangular fragment has remained in contact with the medial edge of the trapezium, while the remainder of the thumb has subluxated proximally, pulled upon by the abductor pollicis longus tendon. Treatment It is widely supposed (with little evidence)

that perfect reduction is essential. It should, however, be attempted and can usually be achieved by pulling on the thumb, abducting it and extending it. Reduction can then be held in one of two ways: plaster or internal fixation. Plaster may be applied with a felt pad over the fracture, and the first metacarpal held abducted and extended (usually best achieved by flexing the MCP joint). However, plaster only works if it is applied with great skill, and the pressure required to maintain a reduction can cause skin damage; it has, therefore, generally been abandoned in favour of surgery. Surgical fixation is achieved by passing a K-wire across the metacarpal base into the carpus. If the fragment is large and cannot be reduced and held with a wire, then open reduction and fixation with a lag screw is effective. ROLANDO’S FRACTURE This is an intra-articular comminuted fracture of the base of the first metacarpal with a T or Y configuration. Closed reduction and K-wiring or open reduction and plate fixation can be used. With more severe comminution, external fixation is needed.

METACARPAL FRACTURES IN CHILDREN

790

(c)

Metacarpal fractures are less common in children than in adults. In general they also present fewer problems: the vast majority can be treated by manipulation and plaster splintage; angular deformities will almost always be remodelled with further growth. However, rotational alignment is as important as it is in adults. Bennett’s fracture is rare; but when it does occur it

usually requires open reduction. This is, by definition, a Salter-Harris type III fracture-separation of the physis; it must be accurately reduced and fixed with a K-wire.

FRACTURES OF THE PHALANGES The fingers are usually injured by direct violence, and there may be considerable swelling or open wounds. Injudicious treatment may result in a stiff finger which, in some cases, can be worse than no finger.

FRACTURES OF THE PROXIMAL AND MIDDLE PHALANGEAL SHAFTS The phalanx may fracture in various ways: • Transverse fracture of the shaft, often with forward angulation. • Spiral fracture of the shaft, from a twisting injury. • Comminuted fracture, usually due to a crush injury and often associated with significant tendon damage and skin loss. • Avulsion of a small fragment of bone. • Metaphyseal fracture at the base of the proximal phalanx, commonly seen in osteopaenic bone. The shaft is pulled into extension and at the distal end the entire head may displace. This is most commonly seen in children. • Intra-articular fractures: At the distal end of the phalanx, the entire head may rotate or, more commonly, one condyle rotates through a longitudinal midline fracture into the joint. At the proximal end, displacement tends to lead to an angular deformity.

Treatment UNDISPLACED FRACTURES These can be treated by ‘functional splintage’. The finger is strapped to its neighbour (‘buddy strapping’)

26

(b)

26.5 Phalangeal fractures These can be treated, depending on the ‘personality’ of the fracture, experience of the surgeon and equipment available, with neighbour strapping (a), plate fixation (b), percutaneous screw fixation (c) or percutaneous wires (d).

(c)

and movements are encouraged from the outset. Splintage is retained for 2–3 weeks, but during this time it is wise to check the position by x-ray in case displacement has occurred. DISPLACED FRACTURES Displaced fractures must be reduced and immobilized. It is essential to check for rotational correction by (1) noting the convergent position of the finger when the MCP joint is flexed, and (2) seeing that the fingernails are all in the same plane. The technique depends on the fracture pattern. Most need simple manipulation and can then be held in a splint. Basal fractures with extension are manipulated and held with a dorsal blocking splint with the MCP joint at 90 degrees. Angulated basal fractures are manipulated with a pencil between the digits as a lever and then held with neighbour strapping which pulls the injured finger to the next one. Spiral fractures are held with ‘de-rotation taping’ to the next digit, using tension in the tape to unwind the fracture. Transverse fractures may be held in a gutter splint or neighbour splint. If a reduction cannot be achieved, or if it is unstable and the position slips, then surgery is needed. The technique depends upon the configuration of the fracture. K-wires are less invasive and are perfect for some fractures; other techniques include percutaneous lag screw fixation (for spiral fractures and distal condylar fractures) and plate fixation (which risks stiffness in the proximal phalanx due to the soft-tissue exposure and subsequent tendon adhesion). External fixation may be needed for comminuted fractures.

Hand injuries

(a)

(d)

CHILDHOOD FRACTURES In children the phalangeal neck can be broken, often after a crush injury. The distal fragment displaces dorsally and extends. These are serious injuries and should be reduced as soon as possible and then held with a percutaneous wire.

FRACTURES OF THE TERMINAL PHALANX The terminal phalanx, small though it is, is subject to five different types of fracture.

Fracture of the tuft The tip of the finger may be struck by a hammer or caught in a door, and the bone shattered. The fracture is disregarded and treatment is focused on controlling swelling and regaining movement. The painful haematoma beneath the finger nail should be drained by piercing the nail with a hot paper clip. If the nail bed is shattered and cosmesis is important, it should be meticulously repaired under magnification.

Mallet finger injury After a sudden flexion injury (e.g. stubbing the tip of the finger) the terminal phalanx droops and cannot be straightened actively. Three types of injury are recognized: avulsion of the most distal part of the extensor tendon; avulsion of a small flake of bone from the base of the terminal phalanx; and avulsion of a large dorsal

791

FRACTURES AND JOINT INJURIES

26

(a)

(b)

(c) (d)

(e)

bone fragment, sometimes with subluxation of the terminal interphalangeal (TIP) joint. TREATMENT The TIP joint should be immobilized in slight hyperextension, using a special mallet-finger splint which fixes the distal joint but leaves the proximal joints free. For tendinous avulsions (which usually occur painlessly) the splint should be kept in place constantly for 8 weeks and then only at night for another 4 weeks. Even if there has been a delay of 3 or 4 weeks after injury, this prolonged splintage is usually successful. Bone avulsions are also treated in a splint, but 6 weeks should suffice as bone heals quicker than tendon. Operative treatment is generally avoided, even for large bone fragments, unless there is subluxation. Surgery carries a high complication rate (wound failure, metalwork problems) without evidence that the outcome is improved. However, if there is subluxation then K-wires or small screws are used to fix the fragment in place.

792

COMPLICATIONS OF MALLET FINGER Non-union This is usually painless and treatment is not needed.

26.6 Distal phalangeal injury A fracture of the tuft (a), caused by a hammer blow, is treated by a protective dressing. The subungual haematoma should be evacuated using a red-hot paper clip tip (b) or a small drill. A mallet finger (c) is best treated with a splint for 6 weeks (d). Mallet fractures (e) are also better splinted – surgery can make the outcome worse.

Persistent droop About 85 per cent of mallet fingers recover full extension. If there is a persistent droop this can be treated by tendon repair supported by K-wire fixation of the joint, but the results are often disappointing. The alternative would be joint arthrodesis, best achieved with a buried intramedullary double-pitch screw. Swan neck deformity Imbalance of the extensor mech-

anism can cause this in lax-jointed individuals. A central slip tenotomy is straightforward and can give a very good result.

Fracture of the terminal shaft Undisplaced fractures of the shaft need no treatment apart from analgesia. If angulated, they should be reduced and held with a longitudinal K-wire through the pulp for 4 weeks. The nail is often dislocated from its fold; if so it must be carefully tucked back in and held with a suture in each corner.

Avulsion of the flexor tendon This injury is caused by sudden hyperextension of the distal joint, typically when a game player catches his

JOINT INJURIES

CARPO-METACARPAL DISLOCATION (a)

(b)

26.7 Flexor tendon avulsion (a) Large fragment and (b) smaller fragment lodged in front of the PIP joint.

finger on an opponent’s shirt. The ring finger is most commonly affected. The flexor digitorum profundus tendon is avulsed, either rupturing the tendon itself or taking a fragment of bone with it. If the bone fragment is small, or if only the tendon is ruptured, it can recoil into the palm. If the lesion is detected within a few days (and the diagnosis is easily missed if not thought about), then the tendon can be re-attached. If the diagnosis is much delayed, repair is likely to be unsuccessful. Two-stage tendon reconstruction is possible but difficult, and the finger may end up stiff. Thus, for late cases, tenodesis or fusion of the distal joint is usually preferable.

Physeal fracture

The thumb is most frequently affected and clinically the injury then resembles a Bennett’s fracturedislocation; however, x-rays reveal proximal subluxation or dislocation of the first metacarpal bone without a fracture. The displacement is easily reduced by traction and hyperpronation, but reduction is unstable and can be held only by a K-wire driven through the metacarpal into the carpus. The wire is removed after 5 weeks but a protective splint should be worn for 8 weeks because of the risk of instability. Chronic instability can occur. This is treated prior to arthritis developing, by using part of the flexor carpi radialis tendon to reconstruct the ruptured and incompetent palmar ligament of the CMC joint. The other carpo-metacarpal joints are also sometimes dislocated, typically when a motorcyclist, holding the handlebars, strikes an object and the hand is driven backwards. The hand swells up rapidly and the diagnosis is easily missed unless a true lateral x-ray is carefully examined. Closed manipulation is usually successful, although a K-wire is recommended to prevent the joint from dislocating again.

Hand injuries

Any finger joint may be injured by a direct blow (often the overlying skin is damaged), or by an angulation force, or by the straight finger being forcibly stubbed. The affected joint is swollen, tender and too painful to move. X-rays may show that a fragment of bone has been sheared off or avulsed.

26

Late presentation Late presentation or secondary

The basal physis can break, usually producing a Salter–Harris I fracture (Seymour fracture). The nail may be dislocated from its fold and the germinal matrix can be trapped in the fracture. The injury is easily overlooked if the finger is very swollen. The nail must be cleaned and carefully replaced into its bed.

arthritis is treated by joint fusion. However, if just the fifth CMC joint is involved, a neat operation is to fuse the base of the fourth to the fifth metacarpal and then excise the articular surface of the fifth. This will maintain movement at the fourth CMC, so allowing the ulnar side of the hand to ‘cup’ around during grip.

(d)

26.8 Carpo-metacarpal dislocation (a) Thumb dislocation. (b) Dislocation of the fourth and fifth CMC joints treated by closed reduction and K-wires (c). Complete carpo-metacarpal dislocation (d). (a)

(b)

(c)

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FRACTURES AND JOINT INJURIES

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METACARPO-PHALANGEAL DISLOCATION Usually the thumb is affected, sometimes the fifth finger, and rarely the other fingers. The entire finger is suddenly forced into hyperextension and the capsule and muscle insertions in front of the joint may be torn. There are two types of dislocation: Simple dislocation The finger is extended about 75 degrees. It is easily reduced by traction, firstly in hyperextension then pulling the finger around. The finger is strapped to its neighbour and early mobilization is encouraged.

the spindle-like swelling of the joint to settle and for full extension to recover. If there is a large palmar fragment with displacement, then this should be reduced and fixed. If closed reduction is successful, then an extension splint or temporary transarticular wire is used. If it cannot be reduced or remains unstable then screw fixation or a small wire loop can be used. If there is marked comminution and instability, the joint is exposed from the palmar surface, the damaged fragments are excised and the palmar plate is reattached to the base of the proximal phalanx (‘palmar-plate arthroplasty’).

Complex dislocation The avulsed palmar plate sits in

the joint, blocking reduction. Furthermore, the metacarpal head can be clasped between the flexor tendon and lumbrical tendon. The finger is extended only about 30 degrees and there is usually a tell-tale dimple in the palm. Very occasionally the fracture can be reduced closed by hyperextending the MCP joint and flexing the IP joints to release the clasp. If this fails, open reduction is required. A dorsal approach is safest. After reduction the joint is stable and should be mobilized in a neighbour-splint. This is treated by a sesamoid arthrodesis. The abductor sesamoid is fused to the underside of the metacarpal neck. This preserves some flexion yet prevents hyperextension. An alternative is formal arthrodesis. The use of a lowprofile compression plate allows early mobilization. The functional result is usually very good.

Chronic instability in the thumb MCP joint

INTERPHALANGEAL JOINT DISLOCATION Distal joint dislocation is rare; proximal joint dislocation is more common. The dislocation is easily reduced by pulling. The joint is strapped to its neighbour for a few days and movements are begun immediately. The lateral x-ray may show a small flake of bone, representing a palmar plate avulsion; this should be ignored. The patient must be warned that it can take many months (and sometimes forever) for

‘PILON’ FRACTURES OF THE MIDDLE PHALANX These are quite common injuries and can be very troublesome. The head of the proximal phalanx impacts into the base of the middle phalanx, causing the latter to splay open in several pieces. These injuries are best treated with dynamic distraction using a spring-loaded external fixator which rotates around the head of the proximal phalanx and disimpacts the distal fragment. The results can be surprisingly good.

CONDYLAR FRACTURE The basal joint surface or distal joint surface of the phalanges can be fractured, usually by an angulation force. If the fragment is not displaced, it is best to disregard the fracture, strap the finger to its neighbour and concentrate on regaining movement. An x-ray should be taken after a week to ensure there is no displacement. If the fracture is displaced, there is a risk of permanent angular deformity and loss of movement at the joint. The fracture should be anatomically reduced, either closed or by open operation and fixed with small K-wires or mini-screws. The finger is splinted for a few days and then supervised movements are commenced.

26.9 Finger dislocation (a) Metacarpo-phalangeal dislocation in the thumb occasionally buttonholes and needs open reduction; (b,c) interphalangeal dislocations are easily reduced (and easily missed if not x-rayed!).

794

(a)

(b)

(c)

VOLAR FRACTURE-DISLOCATIONS

LIGAMENT INJURIES

PROXIMAL INTERPHALANGEAL LIGAMENTS Partial or complete tears of the proximal interphalangeal ligaments are quite common, due to forced angulation of the joint. Mild sprains require no treatment but with more severe injuries the finger should be splinted in extension for 2 or 3 weeks, If the joint is frankly unstable, especially the index and middle which oppose load from the thumb, repair is considered. Occasionally, the bone to which the ligament is attached is avulsed; if the fragment is markedly displaced (and large enough), it should be re-attached. The patient must be warned that the joint is likely to remain swollen and slightly painful for at least 6–12 months. If the instability persists – which is rare – it can be treated by using spare tendon (e.g. palmaris longus) for reconstruction.

ULNAR COLLATERAL LIGAMENT OF THE THUMB METACARPO-PHALANGEAL JOINT (‘GAMEKEEPER’S THUMB’; ‘SKIER’S THUMB’)

26

Hand injuries

When the proximal interphalangeal joint dislocates, a fragment of bone may be avulsed from the base of the middle phalanx. If this fragment is large, the joint can subluxate forwards. Surgical fixation is very difficult and can lead to permanent stiffness of the joint. The fracture can be reduced by flexing the joint to 40 degrees. The joint is then held in a splint which allows flexion but not extension. The amount of extension block is reduced over the next 4 weeks and the splint is then discarded. If the fragment is large enough, then miniscrew fixation may be attempted, but failure of fixation, tendon adhesion or joint stiffness are risks.

is tested with the MP joint flexed (if extended, even a normal ligament is very lax!). In children, the injury may be accompanied by a Salter–Harris III fracture at the base of the proximal phalanx. A large bone fragment, if displaced, can be reattached from a palmar approach, using a tension band suture or small screw. Smaller fragments are treated by splintage with the MP joints flexed.

In former years, gamekeepers who twisted the necks of little animals ran the risk of tearing the ulnar collateral ligament of the thumb metacarpo-phalangeal joint, either acutely or as a chronic injury. Nowadays this injury is seen in skiers who fall onto the extended thumb, forcing it into hyperabduction. A small flake of bone may be pulled off at the same time. The resulting loss of stability may interfere markedly with prehensile (pinching) activities. The ulnar collateral ligament inserts partly into the palmar plate. In a partial rupture, only the ligament proper is torn and the thumb is unstable in flexion but still more or less stable in full extension because the palmar plate is intact. In a complete rupture, both the ligament proper and the palmar plate are torn and the thumb is unstable in all positions. If the ligament ruptures completely (usually at its distal attachment to the base of the proximal phalanx), it will not heal unless it is repaired; this is because the proximal end gets trapped in front of the adductor pollicis aponeurosis (the Stener lesion).

METACARPO-PHALANGEAL JOINTS The radial collateral ligament of the index finger is most vulnerable, although with a suitable force any ligament can be injured. The tension of the ligament

(a)

(b)

Clinical assessment On examination there is tenderness and swelling precisely over the ulnar side of the thumb metacarpo-

(c)

26.10 Skier’s thumb (a,b) The ulnar collateral ligament has ruptured. Urgent repair is indicated (c).

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FRACTURES AND JOINT INJURIES

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phalangeal joint. An x-ray is essential, to exclude a fracture before carrying out any stress tests. Laxity is often obvious but if in doubt, then the joint can be examined under local anaesthetic. If there is no undue laxity (compare with the normal side) in both extension and 30 degrees flexion, then a serious injury can be excluded. If there is more than a few degrees of laxity there is probably a complete rupture which will require operative repair.

Treatment Partial tears can be treated by a short period (2–4 weeks) of immobilization in a splint followed by increasing movement. Pinch should be avoided for 6–8 weeks. Complete tears need operative repair. Care should be taken during the exposure not to injure the superficial radial nerve branches. The Stener lesion is found at the proximal edge of the adductor aponeurosis. The aponeurosis is incised and retracted to expose the ligaments and capsule and the torn structures are then carefully repaired. Postoperatively, the joint is immobilized in a thumb splint for 6 weeks, but can be moved early in the flexion–extension plane as the ligament is isometric (i.e. the same length in flexion and extension). The thumb interphalangeal joint should be left free from the outset to avoid the adductor aponeurosis becoming adherent (which would limit flexion). A neglected tear leads to weakness of pinch. In early cases without articular damage, stability may be restored by using a free tendon graft. If this fails, or if the joint is painful, MP joint arthrodesis is reliable and leaves minimal functional deficit. In children, the injury may be accompanied by a Salter–Harris Type III fracture through the physis. This should be reduced and fixed with smooth Kwires which should not cross the growth plate.

OPEN INJURIES OF THE HAND Over 75 per cent of work injuries affect the hands; inadequate treatment costs the patient (and society) dear in terms of functional disability.

Clinical assessment Open injuries comprise tidy or ‘clean’ cuts, lacerations, crushing and injection injuries, burns and pulp defects. The precise mechanism of injury must be understood. Was the instrument sharp or blunt? Clean or dirty? The position of the fingers (flexed or extended) at the time of injury will influence the relative damage to the deep and superficial flexor tendons. A history of high pressure injection predicts major soft-tissue damage, however innocuous the wound may seem. What are the patient’s occupation, hobbies and aspirations? Is he or she right-handed or lefthanded? Examination should be gentle and painstaking. Skin damage is important, but it should be remembered that even a tiny, clean cut may conceal nerve or tendon damage. The circulation to the hand and each digit must be assessed. The Allen test can be applied to the hand as a whole or to an individual finger. The radial and ulnar arteries at the wrist are simultaneously compressed by the examiner while the patient clenches his fist for several seconds before relaxing; the hand should now be pale. The radial artery is then released; if the hand flushes it means that the radial blood supply is intact. The test is repeated for the ulnar artery. An injured finger can be assessed in the same way. The digital arteries are occluded by pinching the base of the finger. When blood is squeezed out of the finger the pulp will become noticeably pale; one digital artery is then released and the pulp should pink up; the test is repeated for the other digital artery. Sensation is tested in the territory of each nerve. Two-point discrimination may be reduced in partial injuries. In children, who are more difficult to examine, the plastic pen test is helpful: if a plastic pen is brushed along the skin it will tend to ‘stick’ due to the normal thin layer of sweat on the surface; absence of sweating (due to a nerve injury) is revealed by noting that the pen does not adhere as it should (compared to the normal side). Another observation is that the skin in the territory of a divided nerve will not wrinkle if immersed in water. 26.11 Open injuries (a) A mangled hand; (b) open finger fracture treated with external fixation.

796

(a)

(b)

26

(b)

(c)

(d)

26.12 Testing the flexor tendons Testing for (a) flexor digitorum profundus (FDP) lesser fingers, (b) flexor digitorum superficialis (FDS) lesser fingers, (c) FDP index, (d) FDS index.

Tendons must be examined with similar care. Start by testing for ‘passive tenodesis’. When the wrist is extended passively, the fingers automatically flex in a gentle and regular cascade; when the wrist is flexed, the fingers fall into extension. These actions rely upon the balanced tension of the opposing flexor and extensor tendons to the fingers; if a tendon is cut, the cascade will be disturbed. Active movements are then tested for each individual tendon. Flexor digitorum profundus is tested by holding the proximal finger joint straight and instructing the patient to bend the distal joint. Flexor digitorum superficialis is tested by the examiner holding all the fingers together out straight, then releasing one and asking the patient to bend the proximal joint. Holding the fingers out straight ‘immobilizes’ all the deep flexors (including that of the finger being tested) which have a common muscle belly. However, in the index finger this test is not 100 per cent reliable because the deep flexor is sometimes separate. It is better to ask the patient to make a ‘circle’ between thumb and index (FDP intact) and a ‘buttonhole‘ (FDS intact). If a tendon is only partly divided, it will still work although it may be painful. In full thickness skin lacerations, if there is any doubt about the integrity of the tendons, the wound should be explored. X-rays may show fractures, foreign bodies, air or paint.

Primary treatment PREOPERATIVE CARE The patient may need treatment for pain and shock. If the wound is contaminated, it should be rinsed with sterile crystalloid; antibiotics should be given as soon

Hand injuries

(a)

26.13 Hand incisions ‘Permissable’ incisions in hand surgery. Incisions must not cross a skin crease or an interdigital web or else scarring may cause contracture and deformity.

as possible. Prophylaxis against tetanus and gas gangrene may also be needed. The hand is lightly splinted and the wound is covered with an iodine-soaked dressing. WOUND EXPLORATION Under general or regional anaesthesia, the wound is cleaned and explored. A pneumatic tourniquet is essential unless there is a crush injury where muscle viability is in doubt. Skin is too precious to waste and only obviously dead skin should be excised. For adequate exposure the wound may need enlarging, but incisions must not cross a skin crease or an interdigital web. Through the enlarged wound, loose debris is picked out, dead muscle is excised and the tissues are thoroughly irrigated with isotonic crystalloid solution. A further assessment of the extent of the injury is then undertaken. TISSUE REPAIR Fractures are reduced and held appropriately (splintage, K-wires, external fixator or plate and screws) unless there is some specific contraindication. Joint capsule and ligaments are repaired. Artery and vein repair may be needed if the hand or finger is ischaemic. This done with the aid of an operating microscope. Any gap should be bridged with a vein graft. Severed nerves are sutured under an operating microscope (or at least loupe magnification) with the finest, non-reactive material. If the repair cannot be achieved without tension then a nerve graft (e.g. from the posterior interosseous nerve at the wrist) should

797

FRACTURES AND JOINT INJURIES

26

26.15 The flexor tendon sheath and pulleys Fibrous pulleys – designated A1 to A5 – hold the flexor tendons to the phalanges and prevent bowstringing during movement. A1, 3 and 5 are attached to the palmar plate near each joint; A2 and 4 have a crucial tethering effect and must always be preserved or reconstructed. 26.14 The zones of injury I – Distal to the insertion of flexor digitorum superficialis. II – Between the opening of the flexor sheath (the distal palmar crease) and the insertion of flexor superficialis. IIII – Between the end of the carpal tunnel and the beginning of the flexor sheath. IV – Within the carpal tunnel. V – Proximal to the carpal tunnel.

be performed. More recently, dissolvable nerve guides have been used to bridge the gap, allowing a biological regeneration across the gap). Extensor tendon repair is not as easy and the results not as reliable as some have suggested. Repair and postoperative management should be meticulous. Flexor tendon repair is even more challenging, particularly in the region between the distal palmar crease and the flexor crease of the proximal interphalangeal

joint where both the superficial and deep tendons run together in a tight sheath (Zone II or, more dramatically, ‘no man’s land’ because injuries in this zone are the most dangerous). Primary repair with fastidious postoperative supervision gives the best outcome but calls for a high level of expertise and specialized physiotherapy. If the necessary facilities are not available, then the wound should be washed out and loosely closed, and the patient transferred to a special centre. A delay of several days, with a clean wound, is unlikely to affect the outcome. The tendon repair must be strong and accurate enough to allow early mobilization (usually passive) so that the tendons can glide freely and independently from each other and the sheath. Four strands of locked core suture are placed 26.16 Flexor tendon repair A core suture (a) is supplemented by circumferential sutures (b). (c) The relationship of the important structures in ‘no man’s land’: 1 – the tendon sheath; 2 – flexor digitorum profundus; 3 – flexor digitorum superficialis; 4 – digital nerve; 5 – artery; 6 – extensor tendon.

(a)

798

(b)

(c)

26

(b)

(c)

26.17 Pulp and finger-tip injuries (a) Cross-finger graft for a palmar oblique finger-tip injury with exposed bone. (b) V-to-Y advancement for a transverse finger-tip injury with exposed bone. Thumb tip loss (c) must always be reconstructed – never amputate.

without handling the tendon any more than is absolutely necessary; this is supplemented by a continuous circumferential suture which strengthens the repair and smoothes it, thus making the gliding action through the sheath easier. The A2 and A4 pulleys must be repaired or reconstructed, otherwise the tendons will bowstring. Cuts above the wrist (Zone V), in the palm (Zone III) or distal to the superficialis insertion (Zone I) generally have a better outcome than injuries in the carpal tunnel (Zone IV) or flexor sheath (Zone II). Division of the superficialis tendon noticeably weakens the hand and a swan neck deformity can develop in those with lax ligaments. At least one slip should therefore always be repaired. Amputation of a finger as a primary procedure should be avoided unless the damage involves many tissues and is clearly irreparable. Even when a finger has been amputated by the injury, the possibility of reattachment should be considered (see below). Ring avulsion is a special case. When a finger is caught by a ring, the soft tissues are sheared away from the underlying skeleton. Depending on the amount of damage, skin reattachment, microvascular reconstruction or even amputation may be required. CLOSURE The tourniquet is deflated and bipolar diathermy is used to stop bleeding. Haematoma formation leads to poor healing and tendon adhesions. Unless the wound is contaminated, the skin is closed – either by direct suture without tension or, if there is skin loss, by skin grafting. Skin grafts are conveniently taken from the inner aspect of the upper arm. If tendon or bare bone is exposed, this must be covered by a rotation or pedicled flap. Sometimes a severely mutilated finger is sacrificed and its skin used as a rotation flap to cover an adjacent area of loss. In full thickness wounds without bone exposure, the wound should be thoroughly cleaned and then covered with a nonadherent dressing. This is left well alone for 7 days; the accumulation of fluid beneath the dressing is not

Pulp and finger-tip injuries

Hand injuries

(a)

usually a sign of infection and antibiotics should be avoided. The wound is inspected only infrequently, then re-covered with the non-adherent dressing, until it heals. If the open area is greater than 1 cm in diameter, healing will be quicker with a split-skin or full thickness graft but the residual pulp cover may not be as satisfactory as a wound that has been left to heal naturally by granulation and re-epithelialization. If bone is exposed and length of the digit is important for the individual patient, then an advancement flap or neurovascular island flap should be considered. The precise type of flap depends on the orientation of the cut. Otherwise, primary cover can be achieved by shortening the bone and tailoring the skin flaps (‘terminalization’). In young children, the finger-tips recover extraordinarily well from injury and they should be treated with dressings rather than grafts or terminalization. Thumb length should never be sacrificed lightly and every effort should be made to provide a long, sensate digit. Nail bed injuries Nail bed injuries are often seen in association with fractures of the terminal phalanx. If appearance is important, meticulous repair of the nail bed under magnification, replacing any loss with a split thickness nail bed graft from one of the toes, will give the best cosmetic result. In children, these injuries are associated with a physeal fracture.

DRESSING AND SPLINTAGE The wound is covered with a single layer of paraffin gauze and ample wool roll. A light plaster slab holds the wrist and hand in the position of safety (wrist extended, metacarpo-phalangeal joints flexed to 90 degrees, interphalangeal joints straight, thumb abducted). This is the position in which the metacarpo-phalangeal and interphalangeal ligaments are fully stretched and fibrosis therefore least likely to cause contractures. Failure to appreciate this point is the commonest cause of irrecoverable stiffness after injury (see Fig 16.26).

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This position is modified in two circumstances. (1) After primary flexor tendon suture, the wrist is held with a dorsal splint in about 20 degrees of flexion to take tension off the repair (too much wrist flexion invites wrist stiffness and carpal tunnel symptoms) but the interphalangeal joints must remain straight. There should be minimal restriction at the front of the fingers, otherwise the resistance can precipitate rupture of the tendon. (2) After extensor tendon repair, the metacarpo-phalangeal joints are flexed to only about 30 degrees so that there is less tension on the repair; the wrist is extended to 30 degrees and the interphalangeal joints remain straight.

used, particularly for injuries at the level of the extensor retinaculum and the metacarpo-phalangeal joint. Various protocols are followed for flexor tendon injuries, including passive, active or elastic-band assisted flexion. Early movement promotes tendon healing and excursion. In all cases the risk of rupture is balanced against the need for early mobilization. Close supervision and attention to detail are essential. Once the tissues have healed, the hand is increasingly used for more and more arduous and complex tasks, especially those that resemble the patient’s normal job, until he or she is fit to start work; if necessary, his or her work is modified temporarily. If secondary surgery is required, tendon or nerve repair is postponed until the skin is healthy, there is no oedema and the joints have regained a normal range of passive movement.

Replantation

(a)

(b)

26.18 Splintage Always splint in the safe position (wrist slightly extended, MP joint flexed, PIP extended). Only immobilize the affected ray if there is a metacarpal or phalangeal injury.

Postoperative management IMMEDIATE AFTERCARE Following an operation, the hand is kept elevated in a roller towel or high sling. If the latter is used, the sling must be removed several times a day to exercise the elbow and shoulder. Too much elbow flexion can stop venous return and make swelling worse. Antibiotics are continued as necessary. REHABILITATION Movements of the hand must be commenced within a few days at most. Splintage should allow as many joints as possible to be exercised, consistent with protecting the repair. Most extensor tendon injuries are splinted for about 4 weeks. Dynamic splintage can be

With modern microsurgical techniques and appropriate skill, amputated digits or hands can be replanted. An amputated part should be wrapped in sterile saline gauze and placed in a plastic bag, which is itself placed in watery ice. The ‘cold ischaemic time’ for a finger, which contains so little muscle, is about 30 hours, but the ‘warm time’ less than six. For a hand or forearm, the cold ischaemic time is only about 12 hours and the warm time much less. After resuscitation and attention to other potentially life-threatening injuries, the patient and the amputated part should be transferred to a centre where the appropriate surgical skills and facilities are available. INDICATIONS The decision to replant depends on the patient’s age, his or her social and professional requirements, the condition of the part (whether clean-cut, mangled, crushed or avulsed), and the warm and cold ischaemic time. Furthermore, and perhaps most importantly, it depends on whether the replanted part is likely to give better function than an amputation. The thumb should be replanted whenever possible. Even if it functions only as a perfused ‘post’ with protective sensation, it will give useful service. Multiple dig-

26.19 Avulsion This is not replantable.

800

(a)

(b)

26

its also should be replanted, and in a child even a single digit. Proximal amputations (through the palm, wrist or forearm) likewise merit an attempt at replantation.

MANAGEMENT OF BURNS Generally, hand burns should be dealt with in a specialized unit. Superficial burns are covered with moist non-adherent dressings; the hand is elevated and finger movements are encouraged. Partial thickness burns can usually be allowed to heal spontaneously; the hand is dressed with an antimicrobial cream and splinted in the position of safety. Full thickness burns will not heal. Devitalized tissue should be excised; the wound is cleaned and dressed and 2–5 days later skin-grafted. Full thickness circumferential burns may need early escharotomy to preserve the distal circulation. Skin flaps are sometimes needed in sites such as the thumb web which are prone to contracture. The hand should be splinted in the position of safety; K-wires may be needed to maintain this position. Electric burns may cause extensive damage and thrombosis which become apparent only after several days. The patient may of course need resuscitation (treating cardiac anomalies and myoglobinuria). The arm needs to be monitored and fasciotomy with debridement of dead tissue is often needed. Chemical burns should be irrigated copiously for 20 or 30 minutes, usually with water or saline but sometimes with a specific reagent (calcium gluconate for hydrogen fluoride burns, soda lime or magnesium solution for hydrochloric acid, mineral oil for sodium).

MANAGEMENT OF INJECTION INJURIES Oil, grease, solvents, hydraulic fluid or paint injected under pressure are damaging because of tension, tox-

Hand injuries

RELATIVE CONTRAINDICATIONS Single digits do badly if replanted. There is a high complication rate, including stiffness, non-union, poor sensation, and cold intolerance; a replanted single finger is likely to be excluded from use. The exception is an amputation beyond the insertion of flexor digitorum superficialis, when a cosmetic, functioning finger-tip can be retrieved. Severely crushed, mangled or avulsed parts may not be replantable; and parts with a long ischaemic time may not survive. General medical disorders or other injuries may engender unacceptable risks from the prolonged anaesthesia needed for replantation.

26.20 Frostbite

icity or both. The thumb or index finger is usually involved. Substances can gain entry even through intact skin. Air or lead paint may show on x-ray. Immediate decompression and removal of the foreign substance offers the best hope. This means an extensive dissection. The outcome is often poor, with amputation sometimes being necessary.

FROSTBITE Frostbite requires special treatment. The limb is rewarmed in a water bath at 40–42 degrees for 30 minutes. Oedema is minimized by elevation, and blisters are drained. Digits sometimes need amputation.

SECONDARY OPERATIONS The primary treatment of hand injuries should always be carried out with an eye to any future reconstructive procedures that might be necessary. These are of three kinds: • secondary repair or replacement of damaged structures • amputation of fingers • reconstruction of a mutilated hand.

Delayed repair SKIN If the skin cover is unsuitable for primary closure or has broken down it is replaced by a graft or flap. As always, the skin creases must be respected. Contractures are dealt with by Z-plasty, skin grafting, or local flaps, regional flaps or free flaps. When important volar surfaces such as the thumb or index tip are insensate, a flap of skin complete with its neurovascular supply may be transposed.

801

FRACTURES AND JOINT INJURIES

26

802

Split thickness skin contracts and so full thickness grafts are preferred. The upper inner arm can provide a fair amount of skin leaving a reasonable cosmetic defect. Larger amounts of skin can be harvested from the groin or abdomen. Bear in mind that grafts will not adhere to raw tendon or bone.

TENDONS Primary suture may have been contraindicated by wound contamination, undue delay between injury and repair, massive skin loss or inadequate operating facilities. In these circumstances secondary repair or tendon grafting may be necessary. In a late-presenting injury of the profundus tendon with an intact superficialis, advancement of a retracted tendon can cause a flexion deformity of the entire finger. Tendon grafting also is risky: the finger could end up even stiffer. Unless the patient’s work or hobby demands flexion of the distal joint and maximum power in the finger, fusion or tenodesis of the distal interphalangeal joint is a more reliable option. If both the superficialis and profundus tendons have been divided and have retracted, a tendon graft is needed. Full passive joint movement is a prerequisite. If the pulley system is in good condition and there are no adhesions, the tendons are excised from the flexor sheath and replaced with a tendon graft (palmaris longus, plantaris or a toe extensor). Rehabilitation is the same as for a primary repair. If the pulleys are damaged, the skin cover poor, the passive range of movement limited or the sheath scarred, a two-stage procedure is preferred. The tendons are excised and the pulleys reconstructed with extensor retinaculum or excised tendon. A Silastic rod is sutured to the distal stump of the profundus tendon and left free proximally either in the palm or distal forearm. Rehabilitation is planned to maintain a good passive range of movement. A smooth gliding surface forms around the rod. At least 3 months later, the rod is removed through two smaller incisions and a tendon graft (palmaris longus, plantaris or a lesser toe extensor) is sutured to the proximal and distal stumps of flexor digitorum profundus. Rehabilitation is the same as that for a primary repair. Tenolysis is sometimes indicated. After flexor tendon repair in Zone II, a poor excursion is not infrequent because of adhesions between the tendons and the sheath. There is some active movement – indicating that the tendon is intact – but not enough for good function. The passive range of movement should be good if the tenolysis is to succeed. The tendons are painstakingly freed through small windows in the flexor sheath. Postoperatively an intensive programme of movement is essential, otherwise there will be even more scar tissue than before and the tenolysis will have made matters worse.

NERVES Late-presenting nerve injuries must be carefully assessed. The results of repair deteriorate with time, particularly for motor nerves where the end plate begins to fail and the muscle begins to fibrose. If several months have passed, tendon transfer may be a more reliable alternative. If nerve repair is attempted, the scar is excised and the stumps pared back until healthy nerve is found proximally and distally; a nerve graft or tubular nerve guide is usually needed to avoid tension at the suture line. JOINTS The proximal interphalangeal joint is most prone to a flexion contracture. Active and passive exercises can be supplemented by serial static splints or dynamic splints. Surgery (capsulotomy, palmar plate and collateral ligament release) may be required but these operations themselves can invite further stiffness. Unstable or painful joints are best fused. BONES Malunion, especially if rotational, may require treatment. Non-union is very uncommon, but if present grafting may be required. Extensor tendons may stick to bone, most commonly after plate fixation of the proximal phalanx. Plate removal and tenolysis is followed by aggressive active and passive movements: a fair result is usually achieved.

AMPUTATION Indications A finger is amputated only if it remains painful or unhealed, or if it is a nuisance (i.e. the patient cannot bend it, straighten it or feel with it), and then only if repair is impossible or uneconomic. Technique In the finger-tip, the aim is a mobile digit covered by healthy skin with normal sensation. This can be achieved by local advancement flaps or neurovascular island flaps, or by bone shortening (‘terminalization’). A cross-finger flap is fairly straightforward and provides good skin cover, but sensation is limited and a flexion contracture can develop in the donor finger. The final choice depends on the patient’s requirements and the surgeon’s skill. In the thumb every millimetre is worth preserving; even a stiff or deformed thumb is worth keeping. The middle and ring fingers should not be amputated through the knuckle joint because cosmetically this is unsatisfactory and small objects will fall through the gap (‘incontinence of grip’). If the proximal phalanx can be left, the appearance is still abnormal but function is better. The extensor tendon must never be

LATE RECONSTRUCTION A severely mutilated hand should be dealt with by a hand expert. Certain options may be considered in

26

26.21 Late reconstruction The second toe has been transferred to replace the thumb, which was severed in an accident.

Hand injuries

sutured to the flexor tendon; this will act as a tether on the common belly of flexor digitorum profundus and prevent the other digits from flexing fully (the ‘Quadriga effect’). If the middle phalanx is amputated distal to the flexor digitorum superficialis insertion, the profundus tendon continues to pull, but now through the lumbrical, making the proximal interphalangeal joint paradoxically extend rather than flex. This irritating anomaly is avoided by suturing the superficialis stump to the flexor sheath or by dividing the lumbrical. For more proximal injuries, the entire finger with most of its metacarpal may be amputated; the hand is weakened but the appearance is usually satisfactory. If the middle ray is amputated through the metacarpal, the index finger may ‘scissor’ across it in flexion; this can be overcome by dividing the adjacent index metacarpal and transposing it to the stump of the middle metacarpal.

exceptional cases. If all the fingers have been lost but the thumb is present, a new finger can sometimes be constructed with cortical bone, covered by a tubular flap of skin; an alternative is a neurovascular microsurgical transfer from the second toe. If the thumb has been lost, the options include pollicization (rotating a finger to oppose the other fingers), second toe transfer and osteoplastic reconstruction (a cortical bone graft surrounded by a skin flap).

803

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Injuries of the spine

27

Stephen Eisenstein, Wagih El Masry

PATHOPHYSIOLOGY OF SPINE INJURIES Stable and unstable injuries Spinal injuries carry a double threat: damage to the vertebral column and damage to the neural tissues. While the full extent of the damage may be apparent from the moment of injury, there is always the fear that movement may cause or aggravate the neural lesion; hence the importance of establishing whether the injury is stable or unstable and treating it as unstable until proven otherwise. A stable injury is one in which the vertebral components will not be displaced by normal movements;

in a stable injury, if the neural elements are undamaged there is little risk of them becoming damaged. An unstable injury is one in which there is a significant risk of displacement and consequent damage – or further damage – to the neural tissues. In assessing spinal stability, three structural elements must be considered: the posterior osseoligamentous complex (or posterior column) consisting of the pedicles, facet joints, posterior bony arch, interspinous and supraspinous ligaments; the middle column comprising the posterior half of the vertebral body, the posterior part of the intervertebral disc and the posterior longitudinal ligament; and the anterior column composed of the anterior half of the vertebral body, the anterior part of the intervertebral disc and the anterior longitudinal ligament (Denis, 1983). All fractures involving the middle column and at least one other column should be regarded as unstable. Fortunately, only 10 per cent of spinal fractures are unstable and less than 5 per cent are associated with cord damage.

Pathophysiology Primary changes Physical injury may be limited to the

vertebral column, including its soft-tissue components, and varies from ligamentous strains to vertebral fractures and fracture-dislocations. The spinal cord and/or nerve roots may be injured, either by the initial trauma or by ongoing structural instability of a vertebral segment, causing direct compression, severe energy transfer, physical disruption or damage to its blood supply. Secondary changes During the hours and days following a spinal injury biochemical changes may lead to more gradual cellular disruption and extension of the initial neurological damage. 27.1 Structural elements of the spine The vertical lines show Denis’ classification of the structural elements of the spine. The three elements are: the posterior complex, the middle component and the anterior column. This concept is particularly useful in assessing the stability of lumbar injuries.

Mechanism of injury There are three basic mechanisms of injury: traction (avulsion), direct injury and indirect injury.

FRACTURES AND JOINT INJURIES

27

PRINCIPLES OF DIAGNOSIS AND INITIAL MANAGEMENT Diagnosis and management go hand in hand; inappropriate movement and examination can irretrievably change the outcome for the worse.

Early management

(a)

(b)

27.2 Mechanism of injury The spine is usually injured in one of two ways: (a) a fall onto the head or the back of the neck; and (b) a blow on the forehead, which forces the neck into hyperextension.

Traction injury In the lumbar spine resisted muscle effort may avulse transverse processes; in the cervical spine the seventh spinous process can be avulsed (‘clayshoveller’s fracture’).

Penetrating injuries to the spine, particularly from firearms and knives, are becoming increasingly common.

Direct injury

This is the most common cause of significant spinal damage; it occurs most typically in a fall from a height when the spinal column collapses in its vertical axis, or else during violent free movements of the neck or trunk. A variety of forces may be applied to the spine (often simultaneously): axial compression, flexion, lateral compression, flexion-rotation, shear, flexion-distraction and extension. NOTE: Insufficiency fractures may occur with minimal force in bone which is weakened by osteoporosis or a pathological lesion.

Indirect injury

Healing

806

Spinal injuries may damage both bone and soft tissue (ligaments, facet joint capsule and intervertebral disc). Non-union of fractures is very rare while malunion is common. The bone injury will usually heal; however, if the bone structures heal in an abnormal position the healed soft tissues may not always protect against progressive deformity. This may occur with flexion injuries in which there is anterior wedging of the vertebral body of more than 40 per cent. An increasing flexion-deformity (kyphosis) may occur. Injuries with a predominant soft-tissue element – for example flexion-distraction with bilateral facet dislocation and disruption of the posterior ligaments and disc – heal with fibrous tissue and can become completely stable; sometimes, however, they do not regain stability.

The adherence to the resuscitation protocol (airway with cervical spine control, breathing, circulation and haemorrhage control) supersedes the assessment of the spinal injury. Adequate oxygenation, ventilation and circulation will minimize secondary spinal cord injury. The essential principle is that if there is the slightest possibility of a spinal injury in a trauma patient, the spine must be immobilized until the patient has been resuscitated and other life-threatening injuries have been identified and treated. Immobilization is abandoned only when spinal injury has been excluded by clinical and radiological assessment.

Methods of temporary immobilization CERVICAL SPINE In-line immobilization The head and neck are supported

in the neutral position. QUADRUPLE IMMOBILIZATION A backboard, sandbags, a forehead tape and a semirigid collar are applied. Because children have a relatively prominent occiput, care must be taken to ensure that the neck is not flexed: padding may be required behind the shoulders. Thoracolumbar spine The patient should be moved without flexion or rotation of the thoracolumbar spine. A scoop stretcher and spinal board are very useful; however in the paralysed patient, there is a high risk of pressure sores – adequate padding is essential and transfer to a special bed must be undertaken as soon as possible. If the back is to be examined, or if the patient is to be placed onto a scoop stretcher or spinal board, the logrolling technique should be used.

DIAGNOSIS History A high index of suspicion is essential; symptoms and signs may be minimal; the history is crucial. Every patient with a blunt injury above the clavicle, a head injury or loss of consciousness should be considered

Examination NECK The patient may be supporting his or her head with their hands – a warning to the examiner to be equally careful! The head and face are thoroughly inspected for bruises or grazes which could indicate indirect trauma to the cervical spine. The neck is inspected for deformity, bruising or penetrating injury. The bones and soft tissues of the neck are gently palpated for tenderness and areas of ‘bogginess’, or increased space between the spinous processes, suggesting instability due to posterior column failure. The back of the neck must also be examined but throughout the entire examination the cervical spine must not be moved because of the risk of injuring the cord in an unstable injury (see below).

(a)

(b)

BACK The patient is ‘log-rolled’ (i.e. turned over ‘in one piece’) to avoid movement of the vertebral column. The back is inspected for deformity, penetrating injury, haematoma or bruising. The bone and soft-tissue structures are palpated, again with particular reference to the interspinous spaces. A haematoma, a gap or a step are signs of instability. GENERAL EXAMINATION – ‘SHOCK’ Early examination of the severely injured patent is considered in Chapter 22. The ABC sequence of advanced trauma life support (ATLS) always takes precedence. Three types of shock may be encountered in patients with spinal injury: Hypovolaemic shock is suggested by tachycardia, peripheral shutdown and, in later stages, hypotension. Neurogenic shock reflects loss of the sympathetic pathways in the spinal cord; the peripheral vessels dilate causing hypotension but the heart, deprived of its sympathetic innervation, does not respond by increasing its rate. The combination of paralysis, warm and well-perfused peripheral areas, bradycardia and hypotension with a low diastolic blood pressure suggests neurogenic shock. Over-enthusiastic use of fluids can cause pulmonary oedema; atropine and vasopressors may be required.

27

Injuries of the spine

to have a cervical spine injury until proven otherwise. Every patient who is involved in a fall from a height or a high-speed deceleration accident should similarly be considered to have a thoracolumbar injury. The safe approach is to consider the presence of a vertebral column injury in all patients with multiple injuries. Lesser injuries also should arouse suspicion if they are followed by pain in the neck or back or neurological symptoms in the limbs.

(c)

27.3 Spinal injuries – early management (a) Quadruple immobilization: the patient is on a backboard, the head is supported by sandbags and held with tape across the forehead, and a semi-rigid collar has been applied. (b,c) The log-rolling technique for exposure and examination of the back.

27.4 Spinal injuries – suspicious signs First appearances do matter. (a) With severe facial bruising always suspect a hyperextension injury of the neck. (b) Bruising over the lower back should raise the suspicion of a lumbar vertebral fracture.

(a)

(b)

807

FRACTURES AND JOINT INJURIES

27

‘Spinal shock’ occurs when the spinal cord fails temporarily following injury. Even parts of the cord without structural damage may not function. Below the level of the injury, the muscles are flaccid, the reflexes absent and sensation is lost. This rarely lasts for more than 48 hours and during this period it is difficult to tell whether the neurological lesion is complete or incomplete. If the primitive reflexes (anal ‘wink’ and the bulbocavernosus reflex) are absent, their return usually does not mark the end of ‘spinal shock’; some neurological improvement can occur as time passes. NEUROLOGICAL EXAMINATION A full neurological examination is carried out in every case; this may have to be repeated several times during the first few days. Each dermatome, myotome and reflex is tested. Cord longitudinal column functions are assessed: corticospinal tract (posterolateral cord, ipsilateral motor power), spinothalamic tract (anterolateral cord, contralateral pain and temperature) and posterior columns (ipsilateral proprioception).

Sacral sparing should be tested for. Preservation of active great toe flexion, active anal squeeze (on digital examination) and intact peri-anal sensation suggest a partial rather than complete lesion. Further recovery may occur. The unconscious patient is difficult to examine; a spinal injury must be assumed until proven otherwise. Clues to the existence of a spinal cord lesion are a history of a fall or rapid deceleration, a head injury, diaphragmatic breathing, a flaccid anal sphincter, hypotension with bradycardia and a pain response above, but not below, the clavicle. IMAGING • X-ray examination of the spine is mandatory for all accident victims complaining of pain or stiffness in the neck or back or peripheral paraesthesiae, all patients with head injuries or severe facial injuries (cervical spine), patients with rib fractures or severe seat-belt bruising (thoracic spine), and those with severe pelvic or abdominal injuries (thoracolumbar spine). This is performed during the secondary survey. • Accident victims who are unconscious should have spine x-rays as part of the routine work-up. • Elderly people and patients with known vertebral pathology (e.g. ankylosing spondylitis) may suffer fractures after comparatively minor back injury. The spine should be x-rayed even if pain is not marked. Table 27.1 Tests for nerve root motor function Nerve root

Test

C5

Elbow flexion

C6

Wrist extension

C7

Wrist flexion, finger extension

C8

Finger flexion

T1

Finger abduction

L1,2

Hip abduction

L3,4

Knee extension

L5,S1

Knee flexion

L5

Great toe extension

S1

Great toe flexion

Table 27.2 Root values for tendon reflexes

808

27.5 Spine injuries – neurological examination Dermatomes supplied by the spinal nerve roots.

Root value

Tendon reflex

C5

Biceps

C6

Brachioradialis

C7

Triceps

L3,4

Quadriceps

L5,S1

Achilles tendon

PRINCIPLES OF DEFINITIVE TREATMENT

27

The objectives of treatment are: • to preserve neurological function; • to minimize a perceived threat of neurological compression; • to stabilize the spine; • to rehabilitate the patient. The indications for urgent surgical stabilization are: (a) an unstable fracture with progressive neurological deficit and MRI signs of likely further neurological deterioration; and (b) controversially an unstable fracture in a patient with multiple injuries.

Injuries of the spine

• Pain is often poorly localized; views should include several segments above and below the painful area. • X-ray examination should be carried out with a minimum of movement and manipulation. No attempt should be made to obtain ‘flexion-andextension’ views during the initial work-up. • ‘Difficult’ areas, such as the upper cervical spine, the cervico-thoracic junction and the upper thoracic segments which are often obscured by shoulder and rib images, may require plain film tomography, CT or MRI. Odontoid fractures also are sometimes better shown on axial tomograms than on routine CT. • In addition to anteroposterior and lateral views, open-mouth views are needed for the upper two cervical vertebrae and oblique views may be needed for the cervical as well as the thoracolumbar region. • CT is ideal for showing structural damage to individual vertebrae and displacement of bone fragments into the vertebral canal. In fact, screening CT is employed routinely in many centres; the drawback is its high level of radiation exposure. • MRI is the method of choice for displaying the intervertebral discs, ligamentum flavum and neural structures, and is indicated for all patients with neurological signs and those who are considered for surgery. • CT myelography, with the intrathecal introduction of contrast agent, provides information on the dimensions of the spinal canal, impingement by fracture fragments or intervertebral disc, and root avulsion. This investigation has been largely replaced by MRI. • Three-dimensional reconstruction of CT images defines certain complex fracture patterns. Spiral CT allows high resolution sagittal reconstruction and, when available, is useful for displaying fractures of the odontoid process. • Remember that the spine may be damaged in more than one place. • Do not accept poor quality images. • Consult with the radiologist.

Patients with no neurological injury Stable injuries If the spinal injury is stable, the patient is treated by supporting the spine in a position that will cause no further strain; a firm collar or lumbar brace will usually suffice, but the patient may need to rest in bed until pain and muscle spasm subside. The exception is a burst fracture of the vertebral body: a CT should be arranged which may show displaced fragments within the spinal canal; however, even if a retropulsed fragment is identified, operative treatment is not imperative, though rehabilitation may be easier if surgery is performed. Furthermore, these patients are potentially ‘neurologically unstable’. A progressive neurological deficit may occasionally develop, which could be an indication for decompression and fusion. The correction of deformity by surgery is also controversial. It is not clear that symptoms are related to minor deformity, although a kyphosis of greater than 30 degrees may on occasions be associated with back pain in the long term. The patient should be given the choice between surgery for early mobilization and discharge, and conservative management which is likely to take longer. 27.6 X-ray diagnosis Plain xray alone may be insufficient to show the true state of affairs. (a) This x-ray showed the fracture, but it needed a CT scan (b) to reveal the large fragment encroaching on the spinal canal.

(a)

(b)

809

FRACTURES AND JOINT INJURIES

27

810

Unstable injuries If the spinal injury is unstable it

should be held secure until the tissues heal and the spine becomes stable. In the cervical spine this should be done as soon as possible by traction, using tongs or a halo device attached to the skull. If the halo is attached to a body cast the combination can be used as an external fixator for prolonged immobilization (see below). Alternatively (particularly in the thoracolumbar spine) internal fixation can be carried out. Attempts to reduce dislocations and subluxations should be made whether by adjusting the posture, by traction or by open operation if the patient so chooses.

Patients with a neurological injury Once spinal shock has recovered, the full extent of the neurological injury is assessed. Caring for patients with neurological injury requires the infrastructure of an experienced multidisciplinary team that can optimally manage their multisystem physiological impairment and malfunction, including the spinal injury. Whenever feasible, they should be transferred to a Spinal Injury Centre as soon as possible after injury. If the spinal injury is stable (which is rare), the patient can be treated conservatively and rehabilitated as soon as possible. With the usual unstable injury, conservative treatment can be still be used; this is highly demanding and is best carried out in a special unit equipped for round-the-clock nursing, 2-hourly turning routines, skin toilet, bladder care and specialized physiotherapy and occupational therapy. After a few weeks the injury stabilizes spontaneously and the patient can be got out of bed for intensive rehabilitation. This approach is applicable to almost all injuries. Early operative stabilization is preferred by many; it facilitates nursing by inexperienced carers and reduces the risk of spinal deformity. The benefit of surgery on ease and speed of rehabilitation, total period of hospitalization and neurological recovery is uncertain. A positive indication for early operative reduction or decompression and stabilization is progressive neurological deterioration with evidence (or a serious risk) of further neural compression on MRI. Patients with incomplete lesions are also sometimes considered for operation, but there is little enthusiasm for this approach in specialized centres. Significant neurological recovery occurs without surgery in the majority of those who present with sensory and/or motor sparing in the first 48–72 hours. Furthermore, such recovery can theoretically be endangered by operative manoeuvres, arterial injury, hypoxia, hypotension, hypothermia, further damage to the blood–brain barrier or sepsis associated with spinal surgery.

‘Medical treatment’ to counteract the secondary pathophysiological changes associated with cord injury has been (and still is being) pursued. Of the various methods the one that gained most attention was the use of corticosteroids. However, after several trials in the USA and elsewhere, the use of intravenous methylprednisolone is considered to be of dubious benefit and is currently viewed as an ‘option’ for patients seen within the first few hours of injury, rather than a ‘recommendation’ (Short et al., 2000; Molano et al., 2002; Hugenholtz et al., 2002).

TREATMENT METHODS Cervical spine Soft collars offer very little biomechanical support to the cervical spine and their use is restricted to minor sprains for the first few days after injury. Semirigid collars limit motion quite effectively and are widely used in the acute setting. They are not adequate for very unstable injury patterns. Four-poster braces are more stable, applying pressure to the mandible, occiput, sternum and upper thoracic spine. They can be uncomfortable.

Collars

Tongs A pin is inserted into the outer table on each side of the skull; these are mounted on a pair of tongs and traction is applied to reduce the fracture or dislocation and to maintain the reduced position.

At least four pins are inserted into the outer table of the skull and a ring is applied. The use of titanium pins and graphite ring allows an MRI scan to be performed. The halo ring can be used for initial traction and reduction of the fracture or dislocation, and then can be attached to a plaster vest. Proper positioning and torque-pressure of the pins is essential. Bear in mind that the use of a halo-vest carries a significant risk of complications such as pin loosening, pin-site infection and (in elderly patients) respiratory distress.

Halo ring

Fixation Various operative procedures are available, depending on the level and pattern of injury. Odontoid fractures can be fixed with lag screws, burst fractures can be decompressed through an anterior approach, and facet dislocations can be reduced through a posterior approach. The spine can be stabilized anteriorly with plates between the vertebral bodies or posteriorly with wires between the spinous processes, or with small plates between the lateral masses.

Thoracolumbar spine Special beds are used in the management of spinal injuries. They are designed to avoid pressure

Beds

(a)

(b)

27.7 Spine injuries – treatment (a) Standard cervical collar. (b) More rigid variety. (c) Halo-body cast.

(c)

sores (with special mattresses or the facility to turn the patient frequently). Some beds allow postural reduction of fractures. Brace A thoracolumbar brace avoids flexion by threepoint fixation. It is suitable for some burst fractures, seat-belt injuries and compression fractures. Decompression and stabilization The aim of surgery is to reduce the fracture, hold the reduction and decompress the neural elements. The surgical approach can be either anterior or posterior. The anterior approach is suitable for burst fractures with significant canal impingement or as a supplement to posterior fixation in those compression fractures with considerable loss of anterior bone stock. With an anterior approach, the spine is exposed through a transthoracic, transdiaphragmatic or transperitoneal approach depending on the level of the fracture. The vertebral body is removed so that the spinal canal is decompressed; a bone graft (rib, fibula or iliac crest) is then inserted and special plates are applied between the intact vertebral bodies above and below the injured level. The posterior approach is more suitable for flexioncompression injuries, seat-belt injuries and fracturedislocations. Some burst fractures can also be reduced indirectly from a posterior approach using implants that apply distraction to the fracture. Hook and rod

CERVICAL SPINE INJURIES

27

Injuries of the spine

systems provide fixation between intact vertebrae several segments above and below the injury. The advent of segmental spinal instrumentation, with the fixation device attached to the spinal column through pedicle screws, allows secure fixation of a much shorter implant, reaching only one or two segments away from the injury. These devices also allow correction of the deformity by distraction and extension. Bone graft is required so that a biological fusion can supplement the implants.

The patient will usually give a history of a fall from a height, a diving accident or a vehicle accident in which the neck is forcibly moved. In a patient unconscious from a head injury, a fractured cervical spine should be assumed (and acted upon) until proved otherwise. An abnormal position of the neck is suggestive, and careful palpation may elicit tenderness. Movement is best postponed until the neck has been x-rayed. Pain or paraesthesia in the limbs is significant, and the patient should be examined for evidence of spinal cord or nerve root damage.

Imaging Plain x-rays must be of high quality and should be inspected methodically. • In the anteroposterior view the lateral outlines should be intact, and the spinous processes and tracheal shadow in the midline. An open-mouth view is necessary to show C1 and C2 (for odontoid and lateral mass fractures).

27.8 Cervical spine injury Look at the position of this patient’s neck. He complained of pain and stiffness after a fall. It could have been no more than a soft-tissue strain, but x-ray examination revealed an odontoid fracture.

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(a)

(b)

27.10 Cervical spine injuries – x-ray diagnosis (a) Following a traffic accident this patient had a painful neck and consulted her doctor three times; on each occasion she was told ‘the x-rays are normal‘. But count the vertebrae! There are only six in this film. (b) When a shoulder ‘pull-down view’ was obtained to show the entire cervical spine, a dislocation of C6 on C7 could be seen at the very bottom of the film.

27.9 Cervical spine – normal x-ray In the lateral projection, four parallel lines can be traced unbroken from C1 to C7. They are formed by: (1) the anterior surfaces of the vertebral bodies; (2) the posterior surfaces of the bodies; (3) the posterior borders of the lateral masses; and (4) the bases of the spinous processes.

812

• In the lateral view the smooth lordotic curve should be followed, tracing four parallel lines formed by the front of the vertebral bodies, the back of the bodies, the posterior borders of the lateral masses and the bases of the spinous processes; any irregularity suggests a fracture or displacement. Forward shift of the vertebral body by 25 per cent suggests a unilateral facet dislocation and by 50 per cent a bilateral facet dislocation. • The lateral view must include all seven cervical vertebrae and the upper half of T1, otherwise a serious injury at the cervico-thoracic junction will be missed. If the cervico-thoracic junction cannot be seen, then the lateral view should be repeated while the patient’s shoulders are pulled down. If this fails,

then a ‘swimmer’s view’ is obtained. If this, too, fails, then tomography or a CT scan is required. • The distance between the odontoid peg and the back of the anterior arch of the atlas should be no more than 3 mm in adults and 4.5 mm in children. • Compare the shape of each vertebral body with that of the others; note particularly any loss of height, fragmentation or backward displacement of the posterior border of the vertebral body. • Examine the soft-tissue shadows. The retropharyngeal space may contain a haematoma; the prevertebral soft-tissue shadow should be less than 5 mm in thickness above the level of the trachea and less than one vertebral body’s width in thickness below. The interspinous space may be widened after ligament rupture.

Diagnostic pitfalls in children Children are often distressed and difficult to examine; more than usual reliance may be placed on the x-rays. It is well to recall some common pitfalls. An increased atlanto-dental interval (up to 4.5mm)

27

Injuries of the spine

may be quite normal; this is because the skeleton is incompletely ossified and the ligaments relatively lax during childhood. There may also be apparent subluxation of C2 on C3 (pseudosubluxation). An increased retropharyngeal space can be brought about by forced expiration during crying. Growth plates and synchondroses can be mistaken for fractures. The normal synchondrosis at the base of the dens has usually fused by the age of 6 years, but it can be mistaken for an undisplaced fracture; the spinous process growth plates also resemble fractures; and the growth plate at the tip of the odontoid can be taken for a fracture in older children. SCIWORA is an acronym for spinal cord injury without obvious radiographic abnormality. Normal radiographs in children do not exclude the possibility of spinal cord injury.

UPPER CERVICAL SPINE Occipital condyle fracture This is usually a high-energy fracture and associated skull or cervical spine injuries must be sought. The diagnosis is likely to be missed on plain x-ray examination and CT is essential. Impacted and undisplaced fractures can be treated by brace immobilization for 8–12 weeks. Displaced fractures are best managed by using a halo-vest or by operative fixation.

Occipito-cervical dislocation This high-energy injury is almost always associated with other serious bone and/or soft-tissue injuries, including arterial and pharyngeal disruption, and the outcome is often fatal. Patients are best dealt with by a multidisciplinary team of surgeons and physicians. The diagnosis can sometimes be made on the lateral cervical radiograph: the tip of the odontoid should be no more than 5mm in vertical alignment and 1mm in horizontal alignment from the basion (anterior rim of the foramen magnum). Greater distances are allowable in children. CT scans are more reliable. The injury is likely to be unstable and requires immediate reduction (without traction!) and stabilization with a halo-vest, pending surgical treatment. After appropriate attention to the more serious softtissue injuries and general resuscitation, the dislocation should be internally fixed; specially designed occipito-cervical plates and screws are available for the purpose. In severely unstable injuries, halo-vest stabilization should be retained for another 6–8 weeks.

27.11 Occipito–cervical fusion X-ray showing one of the devices used for internal fixation in occipito-cervical fusion operations.

C1 ring fracture Sudden severe load on the top of the head may cause a ‘bursting’ force which fractures the ring of the atlas (Jefferson’s fracture). There is no encroachment on the neural canal and, usually, no neurological damage. The fracture is seen on the open-mouth view (if the lateral masses are spread away from the odontoid peg) and the lateral view. A CT scan is particularly helpful in defining the fracture. If it is undisplaced, the injury

27.12 Fracture of C1 ring Jefferson’s fracture – bursting apart of the lateral masses of C1.

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27

is stable and the patient wears a semi-rigid collar or halo-vest until the fracture unites. If there is sideways spreading of the lateral masses (more than 7 mm on the open-mouth view), the transverse ligament has ruptured; this injury is unstable and should be treated by a halo-vest for several weeks. If there is persisting instability on x-ray, a posterior C1/2 fixation and fusion is needed. A hyperextension injury can fracture either the anterior or posterior arch of the atlas. These injuries are usually relatively stable and are managed with a halo-vest or semi-rigid collar until union occurs. Fractures of the atlas are associated with injury elsewhere in the cervical spine in up to 50 per cent of cases.

27.13 Fracture of C2 ‘Hangman’s fracture’ – fracture of the pars interarticularis of C2.

velocity accidents or severe falls. However, they also occur in elderly, osteoporotic people as a result of low-energy trauma in which the neck is forced into hyperextension, e.g. a fall onto the face or forehead. A displaced fracture is really a fracture-dislocation of the atlanto-axial joint in which the atlas is shifted forwards or backwards, taking the odontoid process with it. At this level about a third of the internal diameter of the atlas is free space, a third filled with the odontoid and a third with the cord; thus there is room for displacement without neurological injury. However, cord damage is not uncommon and in old people there is a considerable mortality rate.

C2 pars interarticularis fractures In the true judicial ‘hangman’s fracture’ there are bilateral fractures of the pars interarticularis of C2 and the C2/3 disc is torn; the mechanism is extension with distraction. In civilian injuries, the mechanism is more complex, with varying degrees of extension, compression and flexion. This is one cause of death in motor vehicle accidents when the forehead strikes the dashboard. Neurological damage, however, is unusual because the fracture of the posterior arch tends to decompress the spinal cord. Nevertheless the fracture is potentially unstable. Undisplaced fractures which are shown to be stable on supervised flexion–extension views (less than 3mm of C2/3 subluxation) can be treated in a semi-rigid orthosis until united (usually 6–12 weeks). Fractures with more than 3mm displacement but no kyphotic angulation may need reduction; however, because the mechanism of injury usually involves distraction, traction must be avoided. After reduction, the neck is held in a halo-vest until union occurs. C2/3 fusion is sometimes required for persistent pain and instability (‘traumatic spondylolisthesis’). Occasionally, the ‘hangman’s fracture’ is associated with a C2/3 facet dislocation. This is a severely unstable injury; open reduction and stabilization is required.

Classification Odontoid fractures have been classified by Anderson and D’Alonzo (1974) as follows: • Type I – An avulsion fracture of the tip of the odontoid process due to traction by the alar ligaments. The fracture is stable (above the transverse ligament) and unites without difficulty. • Type II – A fracture at the junction of the odontoid process and the body of the axis. This is the most common (and potentially the most dangerous) type. The fracture is unstable and prone to non-union. • Type III – A fracture through the body of the axis. The fracture is stable and almost always unites with immobilization.

Clinical features The history is usually that of a severe neck strain followed by pain and stiffness due to muscle spasm. The diagnosis is confirmed by high quality x-ray examination; it is important to rule out an associated

C2 Odontoid process fracture Odontoid fractures are uncommon. They usually occur as flexion injuries in young adults after high-

814

(a)

(b)

(c)

27.14 Odontoid fractures – classification (a) Type I – fracture through the tip of the odontoid process. (b) Type II – fracture at the junction of the odontoid process and the body. (c) Type III – fracture through the body of the axis. (Anderson and D’Alonzo, 1974.)

(b)

27.15 Fractured odontoid process (a) Anteroposterior ‘open-mouth’ x-ray showing a Type II odontoid fracture. (b) Lateral x-ray of the same patient.

occipito-cervical injury which commands immediate attention. In some cases the clinical features are mild and continue to be overlooked for weeks on end. Neurological symptoms occur in a significant number of cases.

Imaging Plain x-rays usually show the fracture, although the extent of the injury is not always obvious – e.g. there may be an associated fracture of the atlas or displacement at the occipito-atlanto level. Tomography is helpful but MRI has the advantage that it may reveal rupture of the transverse ligament; this can cause instability in the absence of a fracture.

Treatment

Type III fractures If undisplaced, these are treated in a

halo-vest for 8–12 weeks. If displaced, attempts should be made at reducing the fracture by halo traction, which will allow positioning in either flexion or extension, depending on whether the displacement is forward or backward; the neck is then immobilized in a halo-vest for 8–12 weeks. For elderly patients with poor bone a collar may suffice, though this carries a higher risk of non-union.

27

Injuries of the spine

(a)

or – in elderly patients – a rigid collar. Displaced fractures should be reduced by traction and can then be held by operative posterior C1/2 fusion; a drawback is that neck rotation will be restricted. Anterior screw fixation is suitable for Type II fractures that run from anterior-superior to posterior-inferior, provided the fracture is not comminuted, that the transverse ligament is not ruptured, that the fracture is fully reduced and the bone solid enough to hold a screw; in that case neck rotation is retained. If full operative facilities are not available, immobilization can be applied by using a halo-vest with repeated x-ray monitoring to check for stability.

LOWER CERVICAL SPINE Fractures of the cervical spine from C3 to C7 tend to produce characteristic fracture patterns, depending on the mechanism of injury: flexion, axial compression, flexion–rotation or hyperextension.

Type I fractures Isolated fractures of the odontoid tip

are uncommon. They need no more than immobilization in a rigid collar until discomfort subsides. Type II fractures These are often unstable and prone to non-union, especially if displaced more than 5 mm. Undisplaced fractures can be held by fitting a halo-vest

(a)

(b)

Posterior ligament injury Sudden flexion of the mid-cervical spine can result in damage to the posterior ligament complex (the interspinous ligament, facet capsule and supraspinous ligament). The upper vertebra tilts forward on the one below, opening up the interspinous space posteriorly.

(c)

(d)

27.16 Fractured odontoid – treatment (a) A severely displaced Type II odontoid fracture. (b) The fracture was reduced by skull traction and held by fixing the spinous process of C1 to that of C2 with wires. (c) An undisplaced Type II fracture, which was suitable for (d) anterior screw fixation.

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(a)

(b)

27.17 Cervical spine – posterior ligament injury (a) The film taken in extension shows no displacement of the vertebral bodies, but there is an unduly large gap between the spinous processes of C4 and 5. (b) With the neck slightly flexed the subluxation is obvious. NB: flexion–extension views are potentially dangerous and should be used only in specific situations under direct supervision of an experienced surgeon.

The patient complains of pain and there may be localized tenderness posteriorly. X-ray may reveal a slightly increased gap between the adjacent spines; however, if the neck is held in extension this sign can be missed, so it is always advisable to obtain a lateral view with the neck in the neutral position. A flexion view would, of course, show the widened interspinous space more clearly, but flexion should not be permitted in the early post-injury period. This is why the diagnosis is often made only some weeks after the injury, when the patient goes on complaining of pain. The assessment of stability is essential in these cases. If the angulation of the vertebral body with its neighbour exceeds 11 degrees, if there is anterior translation of one vertebral body upon the other of more than 3.5 mm or if the facets are fractured or displaced, then the injury is unstable and it should be treated as a subluxation or dislocation. If it is certain that the injury is stable, a semi-rigid collar for 6 weeks is adequate; if the injury is unstable then posterior fixation and fusion is advisable.

Wedge compression fracture

816

A pure flexion injury results in a wedge compression fracture of the vertebral body (Fig. 27.18). The middle and posterior elements remain intact and the injury is stable. All that is needed is a comfortable collar for 6–12 weeks. A note of warning: The x-ray should be carefully examined to exclude damage to the middle column and posterior displacement of the vertebral body

27.18 Cervical compression fracture A wedge compression fracture of a single cervical vertebral body. This is a stable injury because the middle and posterior elements are intact. Compare and contrast with Figure 27.19.

fragment, i.e. features of a burst fracture (see below) which is potentially dangerous. If there is the least doubt, an axial CT or MRI should be obtained.

Burst and compression-flexion (‘teardrop’) fractures These severe injuries are due to axial compression of the cervical spine, usually in diving or athletic accidents (Fig. 27.19). If the vertebral body is crushed in neutral position of the neck the result is a ‘burst fracture’. With combined axial compression and flexion, an antero-inferior fragment of the vertebral body is sheared off, producing the eponymous ‘tear-drop’ on the lateral x-ray. In both types of fracture there is a risk of posterior displacement of the vertebral body fragment and spinal cord injury. Plain x-rays show either a crushed vertebral body (burst fracture) or a flexion deformity with a triangular fragment separated from the antero-inferior edge of the fractured vertebra (the innocent-looking ‘teardrop’). The x-ray images should be carefully examined for evidence of middle column damage and posterior displacement (even very slight displacement) of the main body fragment. Traction must be applied immediately and CT or MRI should be performed to look for retropulsion of bone fragments into the spinal canal. TREATMENT If there is no neurological deficit, the patient can be treated surgically or by confinement to bed and traction for 2–4 weeks, followed by a further period of

27

(b)

(c)

immobilization in a halo-vest for 6–8 weeks. (The halo-vest is unsuitable for initial treatment because it does not provide axial traction). If there is any deterioration of neurological status while the fracture is believed to be unstable, and the MRI shows that there is a threat of cord compression, then urgent anterior decompression is considered – anterior corpectomy, bone grafting and plate fixation, and sometimes also posterior stabilization.

Fracture-dislocations Bilateral facet joint dislocations are caused by severe flexion or flexion–rotation injuries. The inferior articular facets of one vertebra ride forward over the superior facets of the vertebra below. One or both of the articular masses may be fractured or there may be a pure dislocation – ‘jumped facets’. The posterior ligaments are ruptured and the spine is unstable; often there is cord damage.

(a)

(b)

(c)

Injuries of the spine

(a)

27.19 Tear-drop fracture (a) This comminuted vertebral body fracture has produced a large anterior fragment and obvious posterior displacement of the posterior fragment. (b) In this case the anterior ‘tear-drop’ was noted but the severity of the injury was underestimated; careful examination shows that the main body fragment is displaced slightly posteriorly. The patient was treated in a collar; 3 weeks later (c) the fracture had collapsed and the large body fragment was now very obviously tilted and displaced posteriorly. By then he was complaining of tingling and weakness in his right arm. Beware the innocent tear-drop!

The lateral x-ray shows forward displacement of a vertebra on the one below of greater than half the vertebra’s antero-posterior width. The displacement must be reduced as a matter of urgency. Skull traction is used, starting with 5 kg and increasing it step-wise by similar amounts up to about 30kg; intravenous muscle relaxants and a bolster beneath the shoulders may help. The entire procedure should be done without anaesthesia (or under mild sedation only) and neurological examination should be repeated after each incremental step. If neurological symptoms or signs develop, or increase, further attempts at closed reduction should be stopped. When x-rays show that the dislocation has been reduced, traction is diminished to about 5 kg and then maintained for 6 weeks. During this time MRI can be performed to rule out the presence of an associated disc disruption. At the end of that period the patient should still wear a collar for another 6 weeks;

(d)

27.20 Cervical fracture-dislocation (a) Fracture-dislocation in the lower cervical spine. (b,c) Stages in the reduction of this fracture-dislocation by skull traction; (d) subsequent posterior wiring to ensure stability.

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27

however, it may be more convenient to immobilize the neck in a halo-vest for 12 weeks. Another alternative is to carry out a posterior fusion as soon as reduction has been achieved; the patient is then allowed up in a cervical brace which is worn for 6–8 weeks. Posterior open reduction and fusion is also indicated if closed reduction fails. The need for pre-reduction MRI is controversial. In its favour is the ability to diagnose an extruded disc fragment which may further compromise any neurological lesion but can be dealt with by anterior decompression. This is particularly applicable to elderly patients in whom immediate closed reduction may be hazardous and long periods on their backs can lead to pressure sores. An argument against pre-reduction MRI is that there is insufficient correlation between various degrees of disc extrusion and neurological deterioration to justify another surgical assault on the traumatized patient. Unilateral facet dislocation This is a flexion–rotation injury in which only one apophyseal joint is dislocated. There may be an associated fracture of the facet. On the lateral x-ray the vertebral body appears to be partially displaced (less than one-half of its width); on the anteroposterior x-ray the alignment of the spinous processes is distorted. Cord damage is unusual and the injury is stable. Management is the same as for bilateral dislocation. Sometimes complete reduction is prevented by the upper facet becoming perched upon the lower. When no further progress occurs, it is tempting to assist in the final reduction by gently manipulating the patient’s head in extension and rotation; this should be attempted only by an experienced operator. As a general rule, if closed reduction fails, open reduction and posterior fixation are advisable. After reduction, if the patient is neurologically intact the neck is immobilized in a halo-vest for 6–8

weeks. However, in about 50 per cent of the patients surgery may still have to be considered at the end of this period. If there is an associated facet fracture or recurrent dislocation in the external fixator, then posterior fusion again becomes necessary. Patients left with an unreduced unilateral facet dislocation may develop neck pain and nerve root symptoms longterm if poorly managed. Remember that halo vests can cause pressure sores over the scapula in sensory impaired patients.

Hyperextension injury Hyperextension strains of soft-tissue structures are common and may be caused by comparatively mild acceleration forces. Bone and joint disruptions, however, are rare. The more severe injuries are suggested by the history and the presence of facial bruising or lacerations. The posterior bone elements are compressed and may fracture; the anterior structures fail in tension, with tearing of the anterior longitudinal ligament or an avulsion fracture of the anterosuperior or anteroinferior edge of the vertebral body, opening up of the anterior part of the disc space, fracture of the back of the vertebral body and/or damage to the intervertebral disc. In patients with pre-existing cervical spondylosis, the cord can be pinched between the bony spurs or disc and the posterior ligamentum flavum; oedema and haematomyelia may cause an acute central cord syndrome (quadriplegia, sacral sparing and more upper limb than lower limb deficit, a flaccid upper limb paralysis and spastic lower limb paralysis). These injuries are stable in the neutral position, in which they should be held by a collar for 6–8 weeks. Healing may lead to spontaneous fusion between adjacent vertebral bodies.

5

5

5 6

6

6 7

7

(a)

818

(b)

(c)

(d)

27.21 Hyperextension injuries (a) The anterior longitudinal ligament has been torn; in the neutral position the gap will close and reduction will be stable, but a collar or brace will be needed until the soft tissues are healed. (b) X-ray in this case showed a barely visible flake of bone anteriorly at the C6/7 disc space. (c) 1 month later the traction fracture at C6/7 was more obvious, as was the disc lesion at C5/6. (d) A year later C6/7 has fused anteriorly; the patient still has neck pain due to the C5/6 disc degeneration.

Double injuries With high-energy trauma the cervical spine may be injured at more than one level. Discovery of the most obvious lesion is no reason to drop one’s guard. Two salutary examples are shown in Figures 27.22 and 27.23.

Sudden paresis will need immediate surgical decompression. With lesser symptoms and signs, one can afford to wait a few days for improvement; if this does not occur, then anterior discectomy and interbody fusion will be needed.

Neurapraxia of the cervical cord

Fracture of the C7 spinous process may occur with severe voluntary contraction of the muscles at the back of the neck; it is known as the clay-shoveller’s fracture. The injury is painful but harmless. No treatment is required; as soon as symptoms permit, neck exercises are encouraged.

Accidents causing sudden, severe axial loading with the neck in hyperflexion or hyperextension are occasionally followed by transient pain, paraesthesia and weakness in the arms or legs, all in the absence of any x-ray or MRI abnormality. Symptoms may last for as little as a few minutes or as long as two or three days. The condition has been called neurapraxia of the cervical cord and is ascribed to pinching of the cord by the bony edges of the mobile spinal canal and/or local compression by infolding of the posterior longitudinal ligament or the ligamentum flavum (Thomas et al., 1999). Congenital narrowing of the spinal canal may be a predisposing factor. Treatment consists of reassurance (after full neurological investigation) and graded exercises to improve strength in the neck muscles.

Cervical disc herniation Acute post-traumatic disc herniation may cause severe pain radiating to one or both upper limbs, and neurological symptoms and signs ranging from mild paraesthesia to weakness, loss of a reflex and blunted sensation. Rarely a patient presents with full-blown paresis. The diagnosis is confirmed by MRI or CTmyelography.

Injuries of the spine

Avulsion injury of the spinous process

27

27.22 Double cervical injuries (a) This patient with a neck injury was suspected of having an odontoid fracture. This was confirmed and a posterior stabilization was performed. Only when the brace was removed and he started flexing his neck did the x-ray show an obvious subluxation lower down (b). This was treated by anterior fusion (c).

(a)

(b)

(c)

27.23 Avulsions (a) The clay-shoveller’s fracture. Jerking the neck backwards has resulted in avulsion of one of the spinous processes – a benign injury. (b) This patient might be thought to have a similar fracture, but a subsequent flexion film (c) shows the serious nature of the injury – a severe fracture-dislocation.

(a)

(b)

(c)

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SPRAINED NECK (WHIPLASH INJURY) Soft-tissue sprains of the neck are so common after motor vehicle accidents that they now constitute a veritable epidemic. There is usually a history of a lowvelocity rear-end collision in which the occupant’s body is forced against the car seat while his or her head flips backwards and then recoils in flexion. This mechanism has generated the imaginative term whiplash injury, which has served effectively to enhance public apprehension at its occurrence. However, similar symptoms are often reported with flexion and rotation injuries. Women are affected more often than men, perhaps because their neck muscles are more gracile. There is disagreement about the exact pathology but it has been suggested that the anterior longitudinal ligament of the spine and the capsular fibres of the facet joints are strained and in some cases the intervertebral discs may be damaged in some unspecified manner. There is no correlation between the amount of damage to the vehicle and the severity of complaints.

Clinical features Often the victim is unaware of any abnormality immediately after the collision. Pain and stiffness of the neck usually appear within the next 12–48 hours, or occasionally only several days later. Pain sometimes radiates to the shoulders or interscapular area and may be accompanied by other, more ill-defined, symptoms such as headache, dizziness, blurring of vision, paraesthesia in the arms, temporomandibular discomfort and tinnitus. Neck muscles are tender and movements often restricted; the occasional patient may present with a ‘skew neck’. Other physical signs – including neurological defects – are uncommon. X-ray examination may show straightening out of the normal cervical lordosis, a sign of muscle spasm; in other respects the appearances are usually normal. In some cases, however, there are features of longstanding intervertebral disc degeneration or degenerative changes in the uncovertebral joints; it may be that these patients suffer more, and for longer spells, than others. Table 27.3 Proposed grading of whiplash-associated injuries

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Grade

Clinical pattern

0

No neck symptoms or signs

1

Neck pain, stiffness and tenderness No physical signs

2

Neck symptoms and musculoskeletal signs

3

Neck symptoms and neurological signs

4

Neck symptoms and fracture or dislocation

MRI may show early degenerative changes, but no more commonly than in the age-matched population at large; the examination is not indicated except in patients with convincing neurological signs. For purposes of comparison, the severity grading system proposed by the Quebec Task Force on Whiplash-Associated Disorders is useful.

Differential diagnosis The diagnosis of sprained neck is reached largely by a process of exclusion, i.e. the inability to demonstrate any other credible explanation for the patient’s symptoms. X-rays should be carefully scrutinized to avoid missing a vertebral fracture or a mid-cervical subluxation. The presence of neurological signs such as muscle weakness and wasting, a depressed reflex or definite loss of sensibility should suggest an acute disc lesion and is an indication for MRI. Seat-belt injuries often accompany neck sprains. They do not always cause bruising of the chest, but they can produce pressure or traction injuries of the suprascapular nerve or the brachial plexus, either of which may cause symptoms resembling those of a whiplash injury. The examining doctor should be familiar with the clinical features of these conditions.

Treatment Collars are more likely to hinder than help recovery. Simple pain-relieving measures, including analgesic medication, may be needed during the first few weeks. However, the emphasis should be on graded exercises, beginning with isometric muscle contractions and postural adjustments, then going on gradually to active movements and lastly movements against resistance. The range of movement in each direction is slowly increased without subjecting the patient to unnecessary pain. Many patients find osteopathy and chiropractic treatment to be helpful.

Progress and outcome The natural history of whiplash injury is reflected in the statistics appearing in the medical literature on this subject. Details and references are presented in a recent review by Bannister et al. (2009). Many people who are involved in road collisions do not seek medical attention at all; this is particularly the case in countries where medical and legal costs are not compensated. Some patients start improving within a few weeks and reports in the medical literature suggest that 50–60 per cent eventually make a full recovery; in most cases symptoms diminish after about 3 months and go on improving over the next year or two; however, 2–5 per cent continue to complain of symptoms and loss of functional capacity more or less

Chronic whiplash-associated disorder Those patients who, in the absence of any objective clinical or imaging signs, continue almost indefinitely to complain of pain, restriction of movement, loss of function, depression and inability to work constitute a sizeable problem in terms of medical resources, compensation claims, legal costs and – not least – personal suffering. As yet, no convincing evidence of a new pathological lesion has been adduced to account for this long-lasting disorder and it cannot be said with certainty how much of it is due to a physical abnormality and how much is an expression of a behavioural disorder. The subject is well reviewed in the Current Concepts monograph edited by Gunzburg and Szpalski (1997).

THORACOLUMBAR INJURIES Most injuries of the thoracolumbar spine occur in the transitional area – T11 to L2 – between the somewhat rigid upper and middle thoracic column and the flexible lumbar spine. The upper three-quarters of the thoracic segments are also protected to some extent by the rib-cage and fractures in this region tend to be mechanically stable. However, the spinal canal in that area is relatively narrow so cord damage is not uncommon and when it does occur it is usually complete (Bohlman, 1985). The spinal cord actually ends at L1 and below that level it is the lower nerve roots that are at risk.

Pathogenesis Pathogenetic mechanisms fall into three main groups: low-energy insufficiency fractures arising from comparatively mild compressive stress in osteoporotic bone; minor fractures of the vertebral processes due to

compressive, tensile or tortional strains; and highenergy fractures or fracture-dislocations due to major injuries sustained in motor vehicle collisions, falls or diving from heights, sporting events, horse-riding and collapsed buildings. It is mainly in the third group that one encounters neurological complications, but lesser fractures also sometimes cause nerve damage. The common mechanisms of injury are: • Flexion–compression – failure of the anterior column and wedge-compression of the vertebral body. Usually stable, but greater than 50 per cent loss of anterior height suggests some disruption of the posterior ligamentous structures. • Lateral compression – lateral wedging of the vertebral body resulting in a localized ‘scoliotic’ deformity. • Axial compression – failure of anterior and middle columns causing a ‘burst’ fracture and the danger of retropulsion of a posterior fragment into the spinal canal. Often unstable. • Flexion–rotation – failure of all three columns and a risk of displacement or dislocation. Usually unstable. • Flexion–distraction – the so-called ‘jack-knife’ injury causing failure of the posterior and middle columns and sometimes also anterior compression. • Extension – tensile failure of the anterior column and compression failure of the posterior column. Unstable.

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Injuries of the spine

indefinitely (Bannister et al., 2009). Negative prognostic indicators are increasing age, severity of symptoms at the outset, prolonged duration of symptoms and the presence of pre-existing intervertebral disc degeneration. Other factors that presage a poor outcome are a history of pre-accident psychological dysfunction, unduly frequent attendance with unrelated physical complaints, a record of unemployment and a general tendency to underachievement. It should be borne in mind that outcome studies are almost invariably based on a selected group of patients, namely those who attend for medical treatment after the accident, and little is known of the natural progress in the thousands of people who experience similar injuries and either do not develop symptoms or do not report them.

Examination Patients complaining of back pain following an injury or showing signs of bruising and tenderness over the spine, as well as those suffering head or neck injuries, chest injuries, pelvic fractures or multiple injuries elsewhere, should undergo a careful examination of the spine and a full neurological examination, including rectal examination to assess sphincter tone.

Imaging X-rays The anteroposterior x-ray may show loss of height or splaying of the vertebral body with a crush fracture. Widening of the distance between the pedicles at one level, or an increased distance between two adjacent spinous processes, is associated with posterior column damage. The lateral view is examined for alignment, bone outline, structural integrity, disc space defects and soft-tissue shadow abnormalities. Always look carefully for evidence of fragment retropulsion towards the spinal canal. Plain x-rays, while showing the lower thoracic and lumbar spine quite clearly, are less revealing of the upper thoracic vertebrae because the scapulae and shoulders get in the way

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CT and MRI Rapid screening CT scans are now routine in many accident units. Not only are they more reliable than x-rays in showing bone injuries throughout the spine, and indispensable if axial views are necessary, but they also eliminate the delay, discomfort and anxiety so often associated with multiple attempts at ‘getting the right views’ with plain x-rays. In some cases MRI also may be needed to evaluate neurological or other soft-tissue injuries.

Treatment Treatment depends on: (a) the type of anatomical disruption; (b) whether the injury is stable or unstable; (c) whether there is neurological involvement or not; and (d) the presence or absence of concomitant injuries. Details are discussed under each fracture type.

MINOR INJURIES Fractures of the transverse processes The transverse processes can be avulsed with sudden muscular activity. Isolated injuries need no more than symptomatic treatment. More ominous than usual is a fracture of the transverse process of L5; this should alert one to the possibility of a vertical shear injury of the pelvis.

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27.24 Thoracolumbar injuries – minor fractures Fracture of the transverse processes on the right at L3 and L4.

Fracture of the pars interarticularis A stress fracture of the pars interarticularis should be suspected if a gymnast or athlete or weight-lifter complains of the sudden onset of back pain during the course of strenuous activity. The injury is often ascribed to a disc prolapse, whereas in fact it may be a stress fracture of the pars interarticularis (traumatic spondylolysis). This is best seen in the oblique x-rays, but a thin fracture line is easily missed; a week or two later, an isotope bone scan may show a ‘hot’ spot. Bilateral fractures occasionally lead to spondylolisthesis. The fracture usually heals spontaneously, provided the patient is prepared to forego his (more often her) athletic passion for several months.

MAJOR INJURIES Flexion–compression injury This is by far the most common vertebral fracture and is due to severe spinal flexion, though in osteoporotic individuals fracture may occur with minimal trauma. The posterior ligaments usually remain intact, although if anterior collapse is marked they may be damaged by distraction. CT shows that the posterior part of the vertebral body (middle column) is unbroken. Pain may be quite severe but the fracture is usually stable. Neurological injury is extremely rare. Patients with minimal wedging and a stable fracture pattern are kept in bed for a week or two until pain subsides and are then mobilized; no support is needed. Those with moderate wedging (loss of 20–40 per cent of anterior vertebral height) and a stable injury can be allowed up after a week, wearing a thoracolumbar brace or a body cast applied with the back in extension. At 3 months, flexion–extension x-rays are obtained with the patient out of the orthosis; if there is no instability, the brace is gradually discarded. If the deformity increases and neurological signs appear, or if the patient cannot tolerate the orthosis, surgical stabilization is indicated. If loss of anterior vertebral height is greater than 40 per cent, it is likely that the posterior ligaments have been damaged by distraction and will be unable to resist further collapse and deformity. If the patient is neurologically intact, surgical correction and internal fixation is the preferred treatment, though if necessary even these patients can be treated conservatively with vigilant monitoring of their neurological status. In the rare cases of patients with a wedge compression fracture and neurological impairment treatment will depend on the degree of dysfunction and the risk of progression. If nerve loss is incomplete there is the potential for further recovery; any increase in kyphotic deformity or MRI signs of impending cord

(a)

d)

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(c)

(e)

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Injuries of the spine

27.25 Wedge-compression fractures (a) Central compression fracture of the vertebral body and (b) anterior wedge-compression fracture with less than 20 per cent loss of vertebral body height. In both cases the middle and posterior columns are intact; further collapse can be prevented by immobilization for 8–12 weeks in (c) a plaster ‘jacket’ or (d) a lightweight removable orthosis. (e,f) More severe and potentially unstable compression fractures may need posterior internal fixation.

(f)

neurological compression would be an indication for operative decompression and stabilization through a trans-thoracic approach. If there is complete paraplegia with no improvement after 48 hours, conservative management is adequate; the patient can be rested in bed for 5–6 weeks, then gradually mobilized in a brace. With severe bony injury, however, increasing kyphosis may occur and internal fixation should be considered.

is kept in bed until the acute symptoms settle (usually under a week) and is then mobilized in a thoracolumbar brace or body cast which is worn for about 12 weeks. Wood et al. (2003) carried out a prospective randomized trial comparing operative and non-operative treatment of stable thoracolumbar burst fractures with no neurological impairment; they found no difference in the long-term results in the two groups, but complications were more frequent in the surgical group.

Axial compression or burst injury Severe axial compression may ‘explode’ the vertebral body, causing failure of both the anterior and the middle columns. The posterior column is usually, but not always, undamaged. The posterior part of the vertebral body is shattered and fragments of bone and disc may be displaced into the spinal canal. The injury is usually unstable. Anteroposterior x-rays may show spreading of the vertebral body with an increase of the interpedicular distance. Posterior displacement of bone into the spinal canal (retropulsion) is difficult to see on the plain lateral radiograph; a CT is essential. If there is minimal anterior wedging and the fracture is stable with no neurological damage, the patient

(a)

(b)

27.26 Lumbar burst fracture Severe compression may shatter the middle column and cause retropulsion of the vertebral body (a). The extent of spinal canal encroachment is best shown by CT (b).

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(a)

(b)

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27.27 Burst fracture – treatment (a) Burst fracture in a 44-year-old man who fell from his horse; 3 months later he developed paraesthesia in both legs. (b–e) Internal fixation and grafting through a transthoracic transdiaphragmatic approach provided total stability (the Kaneda method).

Even if CT shows that there is considerable compromise of the spinal canal, provided there are no neurological symptoms or signs non-operative treatment is still appropriate; the fragments usually remodel. However, any new symptoms such as tingling, weakness or alteration of bladder or bowel function must be reported immediately and should call for further imaging by MRI; anterior decompression and stabilization may then be needed if there are signs of present or impending neurological compromise.

Jack-knife injury

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(d)

Combined flexion and posterior distraction may cause the mid-lumbar spine to jack-knife around an axis that is placed anterior to the vertebral column. This is seen most typically in lap seat-belt injuries, where the body is thrown forward against the restraining strap. There is little or no crushing of the vertebral body, but the posterior and middle columns fail in distraction; thus these fractures are unstable in flexion. The tear passes transversely through the bones or the ligament structures, or both. The most perfect example of tensile failure is the injury described by Chance in 1948, in which the split runs through the spinous process, the transverse processes, pedicles and the vertebral body. Neurological damage is uncommon, though the injury is (by definition) unstable. Xrays may show horizontal fractures in the pedicles or transverse processes, and in the anteroposterior view the apparent height of the vertebral body may be increased. In the lateral view there may be opening up of the disc space posteriorly.

The Chance fracture (being an ‘all bone’ injury) heals rapidly and requires 3 months in a body cast or well-fitting brace. Flexion–extension lateral views should then be taken to ensure that there is no unstable deformity. Severe ligamentous injuries are less predictable and posterior spinal fusion is advisable.

Fracture-dislocation Segmental displacement may occur with various combinations of flexion, compression, rotation and shear. All three columns are disrupted and the spine is

(a)

(b)

27.28 Jack-knife injuries (a) Whereas flexion usually crushes the vertebral body and leaves the posterior ligaments intact, the jack-knife injury disrupts the posterior ligaments causing only slight anterior compression. (b) The rare Chance fracture.

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Injuries of the spine

(a)

(b)

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27.29 Thoracolumbar fracture-dislocation (a) Fracture-dislocation at T11/12 in a 32-year-old woman who was a passenger in a truck that overturned. She was completely paraplegic and operation was not thought worthwhile. (b) Four weeks later the deformity has increased, leaving her with a marked gibbus. (c,d) A similar injury in a 17-year-old man, treated by open reduction and internal fixation.

grossly unstable. These are the most dangerous injuries and are often associated with neurological damage to the lowermost part of the cord or the cauda equina. The injury most commonly occurs at the thoracolumbar junction. X-rays may show fractures through the vertebral body, pedicles, articular processes and laminae; there may be varying degrees of subluxation or even bilateral facet dislocation. Often there are associated fractures of transverse processes or ribs. CT is helpful in demonstrating the degree of spinal canal occlusion. In neurologically intact patients, most fracturedislocations will benefit from early surgery. In fracture-dislocation with paraplegia, there is no convincing evidence that surgery will facilitate nursing, shorten the hospital stay, help the patient’s rehabilitation or reduce the chance of painful deformity. In fracture-dislocation with a partial neurological deficit, there is also no evidence that surgical stabilization and decompression provides a better neurological outcome than conservative treatment. If surgical decompression and stabilization are performed, this may require a combined posterior and anterior approach. In fracture-dislocation without neurological deficit, surgical stabilization will prevent future neurological complications and allow earlier rehabilitation. When specialized surgery cannot be performed, these injuries can be managed non-operatively with postural reduction, bed rest and bracing. For patients

with neurological impairment who have the benefit of being treated in a specialized spinal injuries unit, a strong case can be made for managing them also by non-operative methods.

NEURAL INJURIES In spinal injuries the displaced structures may damage the cord or the nerve roots, or both; cervical lesions may cause quadriplegia, thoracolumbar lesions paraplegia. The damage may be partial or complete. Three varieties of lesion occur: neurapraxia, cord transection and root transection.

Neurapraxia Motor paralysis (flaccid), burning paraesthesia, sensory loss and visceral paralysis below the level of the cord lesion may be complete, but within minutes or a few hours recovery begins and soon becomes full. The condition is most likely to occur in patients who, for some reason other than injury, have a small-diameter anteroposterior canal; there is, however, no radiological evidence of recent bony damage.

Cord transection Motor paralysis, sensory loss and visceral paralysis occur below the level of the cord lesion; as with cord

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concussion, the motor paralysis is at first flaccid. This is a temporary condition known as cord shock, but the injury is anatomical and irreparable. After a time the cord below the level of transection recovers from the shock and acts as an independent structure; that is, it manifests reflex activity. Within 48 hours the primitive anal wink and bulbocavernosus reflexes return. Within 4 weeks of injury tendon reflexes return and the flaccid paralysis becomes spastic, with increased tone, increased tendon reflexes and clonus; flexor spasms and contractures may develop with inadequate management.

Root transection Motor paralysis, sensory loss and visceral paralysis occur in the distribution of the damaged roots. Root transection, however, differs from cord transection in two ways: recovery may occur and residual motor paralysis remains permanently flaccid. ANATOMICAL LEVELS Cervical spine With cervical spine injuries the segmental level of cord transection nearly corresponds to the level of bony damage. Not more than one or two additional roots are likely to be transected. High cervical cord transection is fatal because all the respiratory muscles are paralysed. At the level of the C5 vertebra, cord transection isolates the lower cervical cord (with paralysis of the upper limbs), the thoracic cord (with paralysis of the trunk) and the lumbar and sacral cord (with paralysis of the lower limbs and viscera). With injury below the C5 vertebra, the upper limbs are partially spared and characteristic deformities result. The first lumbar cord segment in the adult is at the level of the T10 vertebra. Consequently, cord transection at that level spares the thoracic cord but isolates the entire lumbar and sacral cord, with paralysis of the lower limbs and viscera. The lower thoracic roots may also be transected but are of relatively little importance.

Between T1 and T10 vertebrae

Below T10 vertebra The cord forms a slight bulge (the conus medullaris) between the T10 and L1 vertebrae, and tapers to an end at the interspace between the L1 and L2 vertebrae. The L2 to S4 nerve roots arise from the conus medullaris and stream downwards in a bunch (the cauda equina) to emerge at successive levels of the lumbosacral spine. Therefore, spinal injuries above the T10 vertebra cause cord transection, those between the T10 and L1 vertebrae cause cord and nerve root lesions, and those below the L1 vertebra only root lesions. The sacral roots innervate:

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• sensation in the ‘saddle’ area (S3, S4), a strip down the back of the thigh and leg (S2) and the outer two-thirds of the sole (S1);

• motor power to the muscles controlling the ankle and foot; • the anal and penile reflexes, plantar responses and ankle jerks; • bladder and bowel continence. The lumbar roots innervate: • sensation to the groins and entire lower limb other than that portion supplied by the sacral segment; • motor power to the muscles controlling the hip and knee; • the cremasteric reflexes and knee jerks. It is essential, when the bony injury is at the thoracolumbar junction, to distinguish between cord transection with root escape and cord transection with root transection. A patient with root escape is much better off than one with cord and root transection. DIAGNOSIS Clinical examination of the back nearly always shows the signs of an unstable fracture; however, a ‘burst’ fracture with paraplegia is stable as long as the patient is in recumbency or very well braced until the fracture heals. The nature and level of the bone lesion are demonstrated by x-ray, and that of the neural lesion by CT or MRI. Neurological examination should be painstaking. Without detailed information, accurate diagnosis and prognosis are impossible; rectal examination is mandatory. Complete cord lesions Complete paralysis and anaesthesia below the level of injury suggest cord transection. During the stage of spinal shock when the anal reflex is absent (seldom longer than the first 24 hours) the diagnosis cannot be absolutely certain; if the anal reflex returns and the neural deficit (sensory and motor) persists, the cord lesion is complete. Complete lesions lasting more than 72 hours have only a small chance of neurological recovery.

Persistence of any sensation distal to the injury (peri-anal pinprick is most important) suggests an incomplete lesion. The commonest is the central cord syndrome where the initial flaccid weakness is followed by lower motor neuron paralysis of the upper limbs with upper motor neuron (spastic) paralysis of the lower limbs, and intact peri-anal sensation (sacral sparing). Bladder control may or may not be preserved from an early stage. With the less common anterior cord syndrome there is complete paralysis and anaesthesia but deep pressure and position sense are retained in the lower limbs (dorsal column sparing). The posterior cord syndrome is rare; only deep pressure and proprioception are lost.

Incomplete cord lesions

FRANKEL GRADING A well-established method of recording the functional deficit after an incomplete spinal cord injury was that described by Frankel: Grade A = Absent motor and sensory function. Grade B = Sensation present, motor power absent. Grade C = Sensation present, motor power present but not useful. Grade D = Sensation present, motor power present and useful (grade 4 or 5). Grade E =Normal motor and sensory function. Frankel observed that 60 per cent of patients with partial cord lesions (Grades B, C or D) improved (spontaneously) by one grade regardless of the treatment type and a significant number are able to walk again. Although many of the patients who present in Frankel Grade A improve to B or C, only 5 per cent of these patients improve to Frankel D or E.

MANAGEMENT OF TRAUMATIC PARAPLEGIA AND QUADRIPLEGIA With both complete and incomplete paralysis it is the overall management of the patient that is most important – from the early stages onwards. The patient must be transported with great care to prevent further damage, and preferably taken to a spinal centre. The strategy is outlined below. Skin Within a few hours anaesthetic skin may develop

large pressure sores; this can be prevented by meticulous nursing. Creases in the sheets and crumbs in bed are not permitted. Every 2 hours the patient is gently rolled onto his or her side and the back is carefully washed (without rubbing), dried and powdered. After a few weeks the skin becomes a little more tolerant and the patient can turn him- or herself. Later he or she should be taught how to relieve skin pressure intermittently during periods of sitting. If sores have been allowed to develop, they may never heal without surgical closure.

Bladder and bowel For the first 24 hours the bladder distends only slowly, but, if the distension is allowed to progress, overflow incontinence occurs and infection is probable. In special centres it is usual to manage the patient from the outset by intermittent catheterization under sterile conditions. If early transfer to a paraplegia centre is not possible, continuous drainage through a fine Silastic catheter is advised. The catheter drains in a closed manner into a disposable bag, and is changed twice weekly to prevent urethral and bladder complications, catheter blockage and infection. When infection supervenes, antibiotics are given. Bladder training is begun as early as possible. Although retention is complete to begin with, partial recovery may lead to either an automatic bladder which works reflexly or an expressible bladder which is emptied by manual suprapubic pressure. A few patients are left with a high residual urine after emptying the bladder. They need special investigations, including cystography and cystometry; transurethral resection of the bladder neck or sphincterotomy may be indicated but should not be performed until at least 3 months of bladder training have been completed. The bowel is more easily trained, with the help of enemas, aperients and abdominal exercises.

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Injuries of the spine

The Brown-Séquard syndrome (due to cord hemisection) is usually associated with penetrating thoracic injuries. There is loss of motor power on the side of the injury and loss of pain and temperature sensation on the opposite side. Most of these patients improve and regain bowel and bladder function and some walking ability. High root lesions sometimes cause confusion. Below the T10 vertebra, discrepancies between neurological and skeletal levels are due to transection of roots descending from cord segments higher than the vertebral lesion.

The paralysed muscles, if not treated, may develop severe flexion contractures. These are usually preventable by moving the joints passively through their full range twice daily. Later, splints may be necessary. With lesions below the cervical cord, the patient should be up within 6 weeks; standing and walking are valuable in preventing contractures. Callipers are usually necessary to keep the knees straight and the feet plantigrade. The callipers are removed at intervals during the day while the patient lies prone, and while he or she is having physiotherapy. The upper limbs must be trained until they develop sufficient power to enable the patient to use crutches and a wheelchair. If flexion contractures have been allowed to develop, tenotomies may be necessary. Painful flexor spasms are rare unless skin or bladder infection occurs. They can sometimes be relieved by tenotomies, neurectomies, rhizotomies or the intrathecal injection of alcohol. Heterotopic ossification is a common and disturbing complication. It is more likely to occur with high lesions and complete lesions. It may restrict or abolish movement, especially at the hip. Once the new bone is mature it should be considered for excision if it interferes with function.

Muscles and joints

Tendon transfers Some function can be regained in the upper limb by the use of tendon transfers. The aim with patients who have a low cervical cord injury is to

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use the limited number of functioning muscles in the arm to provide a primitive pinch mechanism (normally powered by C8 or T1 which, being below the level of injury, are lost). One must establish which muscles are working, which are not and which are available for transfer. • If only deltoid and biceps are working (C5, C6) then a posterior-deltoid to triceps transfer using interposition tendon grafts will replace the lost C7 function of elbow extension; this will enable the patient to orient his or her hand in space. • If brachioradialis (C6) is working, this can be transferred to become a wrist extensor (since its prime function as an elbow flexor is duplicated by biceps). A primitive thumb pinch can be achieved by the Moberg procedure in which the thumb interphalangeal joint is fused and the basal joint of the thumb is tenodesed with a loop of the redundant flexor pollicis longus. On active extension of the wrist, the basal joint of the thumb is passively flexed. • If extensor carpi radialis longus and brevis (C7) are both available, one of them can be transferred into the flexor pollicis longus to provide active thumb flexion (normally supplied by C8). Morale The morale of a paraplegic patient is liable to

reach a low ebb, and the restoration of his or her selfconfidence is an important part of treatment. Constant enthusiasm and encouragement by doctors, physiotherapists and nurses is essential. Their scrupulous attention to the patient’s comfort and toilet are of primary importance; the unpleasant smells of bowel accidents, or those associated with skin or urinary infection must be prevented. The patient should find a hobby or be trained for a new job as quickly as possible.

REFERENCES AND FURTHER READING Advanced Trauma Life Support. American College of Surgeons 1997. Anderson LD, D’Alonzo RT. Fractures of the odontoid process of the axis. J Bone Joint Surg 1974; 56A: 1663– 74. Bannister G, Amirfeyz R, Kelley S, Gargan M. Whiplash injury. J Bone Joint Injury 2009; 91B: 845–50.

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Bohlman HH. Treatment of fractures and dislocations of the thoracic and lumbar spine – current concepts review. J Bone Joint Surg 1985; 67A: 165–9. Chance CQ. Note on a type of flexion fracture of the spine. Br J Radiol 1948; 21: 452–3. Denis F. The three column spine and its significance in the classification of acute thoracolumbar spinal injuries. Spine 1983; 8: 817–31. El Masry WS. Management of Traumatic Spinal Cord Injuries: current standard of care revisited. Ad Clin Neuroscience Rehab. 2010; 10: 37–40. El Masry WS. Traumatic spinal cord injury: the relationship between pathology and clinical implications. Trauma 2006; 8: 29–46. El Masri WS. Physiological instability of the spinal cord following injury. Paraplegia 1993; 31: 273–5. Gunzburg R, Szpalski M. Whiplash injuries. Current concepts in prevention, diagnosis and treatment of the cervical whiplash syndrome. Philadelphia, Lippincott-Raven, 1997. Hugenholtz H, Cass DE, Dvorak MF. High-dose methylprednisolone for acute closed spinal cord injury: Only a treatment option. Can J Neurol Sci 2002; 29: 227–35. Katoh S, El Masry WS, Jaffray D et al. The neurologic outcome in conservatively treated patients with incomplete closed traumatic cervical spinal cord injuries. Spine; 21: 2345–2351. Molano M, Broton JG, Bean JA et al. Complications associated with prophylactic use of methylprednisolone during surgical stabilization after spinal cord injury. J Neurosurg 2002; 96: 267–72. Short DJ, El Masry WS, Jones PW. High dose methylprednisolone in the management of acute spinal cord injury: A systematic review from a clinical perspective. Spinal Cord 2000; 38: 273–86. Slucky AV, Eismont FJ. Treatment of acute injury of the cervical spine. J Bone Joint Surg 1994; 76A: 1882–95. Solomon L, Pearse MF. Osteonecrosis following low-dose short-course corticosteroids. J Orthop Rheumatol 1994; 7: 203–5. Spitzer WO, Skovron ML, Salmi LR et al. Scientific monograph of the Quebec Task Force on whiplash-associated disorders: redefining whiplash and its management. Spine 1995; 20(8): 1S–73S. Thomas BE, McCullen GM, Yuan HA. Cervical spine injuries in football players. J Am Acad Orthop Surg 1999; 7: 338–47. Wood K, Butterman G, Mehbod A et al. Operative compared with non-operative treatment of a thoracolumbar burst fracture without neurological deficit. J Bone Joint Surg 2003; 85A: 773–81.

Injuries of the pelvis

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Louis Solomon

Fractures of the pelvis account for less than 5 per cent of all skeletal injuries, but they are particularly important because of the high incidence of associated softtissue injuries and the risks of severe blood loss, shock, sepsis and adult respiratory distress syndrome (ARDS). Like other serious injuries, they demand a combined approach by experts in various fields. About two-thirds of all pelvic fractures occur in road accidents involving pedestrians; over 10 per cent of these patients will have associated visceral injuries, and in this group the mortality rate is probably in excess of 10 per cent.

Surgical anatomy The pelvic ring is made up of the two innominate bones and the sacrum, articulating in front at the symphysis pubis (the anterior or pubic bridge) and posteriorly at the sacroiliac joints (the posterior or sacroiliac bridge). This basin-like structure transmits weight from the trunk to the lower limbs and provides protection for the pelvic viscera, vessels and nerves. The stability of the pelvic ring depends upon the rigidity of the bony parts and the integrity of the strong ligaments that bind the three segments together across the symphysis pubis and the sacroil-

(a)

iac joints. The strongest and most important of the tethering ligaments are the sacroiliac and iliolumbar ligaments; these are supplemented by the sacrotuberous and sacrospinous ligaments and the ligaments of the symphysis pubis. As long as the bony ring and the ligaments are intact, load-bearing is unimpaired. The major branches of the common iliac arteries arise within the pelvis between the level of the sacroiliac joint and the greater sciatic notch. With their accompanying veins they are particularly vulnerable in fractures through the posterior part of the pelvic ring. The nerves of the lumbar and sacral plexuses, likewise, are at risk with posterior pelvic injuries. The bladder lies behind the symphysis pubis. The trigone is held in position by the lateral ligaments of the bladder and, in the male, by the prostate. The prostate lies between the bladder and the pelvic floor. It is held laterally by the medial fibres of the levator ani, whilst anteriorly it is firmly attached to the pubic bones by the puboprostatic ligament. In the female the trigone is attached also to the cervix and the anterior vaginal fornix. The urethra is held by both the pelvic floor muscles and the pubourethral ligament. Consequently in females the urethra is much more mobile and less prone to injury.

(b)

28.1 Ligaments supporting the pelvis (a) Anterior view. (b) Posterior view. Some ligaments run transversely and will resist rotational forces which separate the two halves (the posterior sacroiliac and iliolumbar ligaments can be thought of as a posterior band), whilst those that are oriented longitudinally tend to resist vertical shear.

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In severe pelvic injuries the membranous urethra is damaged when the prostate is forced backwards whilst the urethra remains static. When the puboprostatic ligament is torn, the prostate and base of the bladder can become grossly dislocated from the membranous urethra. The pelvic colon, with its mesentery, is a mobile structure and therefore not readily injured. However, the rectum and anal canal are more firmly tethered to the urogenital structures and the muscular floor of the pelvis and are therefore vulnerable in pelvic fractures.

Pelvic instability If the pelvis can withstand weightbearing loads without displacement, it is stable; this situation exists only if the bony and key ligamentous structures are intact. An anterior force applied to both halves of the pelvis forces apart the symphysis pubis. If a diastasis occurs because of capsular rupture, the extent of separation is checked by the anterior sacroiliac and sacrospinous ligaments. Should these restraints fail through the application of a still greater force, the pelvis opens like a book until the posterior iliac spines abut; because the more vertically oriented long posterior sacroiliac and sacrotuberous ligaments remain intact, the pelvis will still resist vertical shear but it is rotationally unstable. If, however, the posterior sacroiliac and sacrotuberous ligaments are damaged, then the pelvis is not only rotationally and vertically unstable, but there will also be posterior translation of the injured half of the pelvis. Vertical instability is therefore ominous as it suggests complete loss of the major ligamentous support posteriorly. It should be remembered that some fracture patterns can cause instability which mimics that of ligamentous disruption; e.g. fractures of both pubic rami may behave like symphyseal disruptions, and fractures of the iliac wing combined with ipsilateral pubic rami fractures are unstable to vertical shear.

bleeding. The pelvic ring can be gently compressed from side to side and back to front. Tenderness over the sacroiliac region is particularly important and may signify disruption of the posterior bridge. A rectal examination is then carried out in every case. The coccyx and sacrum can be felt and tested for tenderness. If the prostate can be felt, which is often difficult due to pain and swelling, its position should be gauged; an abnormally high prostate suggests a urethral injury. Enquire when the patient passed urine last and look for bleeding at the external meatus. An inability to void and blood at the external meatus are the classic features of a ruptured urethra. However, the absence of blood at the meatus does not exclude a urethral injury, because the external sphincter may be in spasm, halting the passage of blood from the site of injury. Thus every patient who has a pelvic fracture must be considered to be at risk. The patient can be encouraged to void; if he is able to do so, either the urethra is intact or there is only minimal damage which will not be made worse by the passage of urine. No attempt should be made to pass a catheter, as this could convert a partial to a complete tear of the urethra. If the urethral injury is suspected, this can be diagnosed more accurately and more safely by retrograde urethrography. A ruptured bladder should be suspected in patients who do not void or in whom a bladder is not palpable after adequate fluid replacement. This palpation is often difficult because of abdominal wall haematoma. The physical findings initially can be minimal, with normal bowel sounds, as extravasation of sterile urine produces little peritoneal irritation. Only a very small

Clinical assessment

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Fracture of the pelvis should be suspected in every patient with serious abdominal or lower limb injuries. There may be a history of a road accident or a fall from a height or crush injury. Often the patient complains of severe pain and feels as if he has fallen apart, and there may be swelling or bruising of the lower abdomen, the thighs, the perineum, the scrotum or the vulva. All these areas should be rapidly inspected, looking for evidence of extravasation of urine. However, the first priority, always, is to assess the patient’s general condition and look for signs of blood loss. It may be necessary to start resuscitation before the examination is completed. The abdomen should be carefully palpated. Signs of irritation suggest the possibility of intraperitoneal

28.2 Fractures of the pelvis This young man crashed on his motorcycle and was brought into the Accident and Emergency Department with a fractured femur. His perineum and scrotum were swollen and bruised, he was unable to pass urine and a streak of blood appeared at the external meatus. X-rays confirmed that he had a fractured pelvis.

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(e)

(b)

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(f)

Injuries of the pelvis

(a)

28.3 Pelvic fractures – x-ray diagnosis (1) (a,b) The anteroposterior view is usually taken during the initial assessment of the multiply-injured patient as part of a ‘trauma series’. It is useful in quickly diagnosing gross disruptions or fractures. The x-ray should be read systematically: Is the picture well centred? Look for asymmetry in the pubic symphysis, the pubic rami, the iliac blades, the sacroiliac joints and the sacral foramina. If the patient’s condition permits, at least two additional views should be obtained: (c,d) an inlet view with the tube titled 30° downwards and (e,f) an outlet view with the tube titled 40° upwards.

(a)

(b)

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28.4 Pelvic fractures – x-ray diagnosis (2) Oblique views are helpful for defining the ilium and acetabulum on each side. (a,b) the right oblique view; and (c,d) the left oblique view. These can be omitted if facilities for CT are available.

proportion of patients with a ruptured bladder are hypotensive, so if a patient is hypotensive another cause must be sought. Neurological examination is important; there may be damage to the lumbar or sacral plexus. If the patient is unconscious, the same routine is followed. However, early x-ray examination is essential in these cases.

Imaging of the pelvis During the initial survey of every severely injured patient, a plain anteroposterior x-ray of the pelvis should be obtained at the same time as the chest x-ray. In most cases this film will give sufficient information to make a preliminary diagnosis of pelvic fracture. The exact nature of the injury can be clarified by more

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the contrast agent to ensure that the urethra is fully distended. This technique will confirm a urethral tear and will show whether it is complete or incomplete. In a patient with possible rupture of the bladder (so long as there is no evidence of a urethral injury) a cystogram should be performed.

Types of injury

(a)

(b)

28.5 Pelvic fractures and bladder injury (a) Intravenous urogram outlining the bladder and showing the typical globular appearance due to compression by blood and extravasated urine. There is also marked gastric dilation suggesting retroperitoneal bleeding. (b) Cystogram showing extravasation of radioopaque material. This patient had a ruptured bladder.

Injuries of the pelvis fall into four groups: (1) isolated fractures with an intact pelvic ring; (2) fractures with a broken ring – these may be stable or unstable; (3) fractures of the acetabulum – although these are ring fractures, involvement of the joint raises special problems and therefore they are considered separately; and (4) sacrococcygeal fractures.

ISOLATED FRACTURES Avulsion fractures

detailed radiography once it is certain that the patient can tolerate an extended period of positioning and repositioning on the x-ray table. Five views are necessary: anteroposterior, an inlet view (tube cephalad to the pelvis and tilted 30° downwards), an outlet view (tube caudad to the pelvis and tilted 40° upwards), and right and left oblique views. If any serious injury is suspected, a CT scan at the appropriate level is extremely helpful (some would say essential). This is particularly true for posterior pelvic ring disruptions and for complex acetabular fractures, which cannot be properly evaluated on plain x-rays. Three-dimensional CT re-formation of the pelvic image gives the most accurate picture of the injury; however, with practice almost as much information can be gleaned from a good set of plain radiographs and standard CT images.

Imaging of the urinary tract

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If there is evidence of upper abdominal injury, and the patient has haematuria, an intravenous urogram is performed to exclude renal injury. This will also show whether there is any ureteric or major bladder damage. In a case of urethral rupture, the base of the bladder may be riding high (dislocated prostate) or there may be a teardrop deformity of the bladder owing to compression by blood and extravasated urine (prostate-in-situ). When a urethral injury is considered likely, an urethrogram should be undertaken using 25–30ml of water-soluble contrast agent with suitable aseptic technique. A film must be taken during injection of

A piece of bone is pulled off by violent muscle contraction; this is usually seen in sportsmen and athletes. The sartorius may pull off the anterior superior iliac spine, the rectus femoris the anterior inferior iliac spine, the adductor longus a piece of the pubis, and the hamstrings part of the ischium. All are essentially muscle injuries, needing only rest for a few days and reassurance. Pain may take months to disappear and, because there is often no history of impact injury, biopsy of the callus may lead to an erroneous diagnosis of a tumour. Rarely, avulsion of the ischial apophysis by the hamstrings may lead to persistent symptoms, in which case open reduction and internal fixation is indicated (Wootton, Cross and Holt, 1990).

Direct fractures A direct blow to the pelvis, usually after a fall from a height, may fracture the ischium or the iliac blade. Bed rest until pain subsides is usually all that is needed.

Stress fractures Fractures of the pubic rami are fairly common (and often quite painless) in severely osteoporotic or osteomalacic patients. More difficult to diagnose are stress fractures around the sacroiliac joints; this is an uncommon cause of ‘sacroiliac’ pain in elderly osteoporotic individuals and long distance runners. Obscure stress fractures are best demonstrated by radioisotope scans.

springy. Often, however, the second break is not visible – either because it reduces immediately or because the sacroiliac joints are only partially disrupted.

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Mechanisms of injury

(b)

Anteroposterior compression This injury is usually

caused by a frontal collision between a pedestrian and a car. The pubic rami are fractured or the innominate bones are sprung apart and externally rotated, with disruption of the symphysis – the so-called ‘open book’ injury. The anterior sacroiliac ligaments are strained and may be torn, or there may be a fracture of the posterior part of the ilium. (c)

(d)

28.6 Isolated injuries (a,b) Avulsion fractures. Unusually powerful muscle contraction may tear off a piece of bone at its attachment. Two examples are shown here: (a) avulsion of sartorius attachment; (b) avulsion of rectus femoris origin. (c,d) Fractured iliac blade. The bruise suggests the site of the injury. The fracture looks alarming and is certainly painful but, if the remainder of the bony pelvis is intact, it poses no threat to the patient.

Injuries of the pelvis

(a)

The basic mechanisms of pelvic ring injury are anteroposterior compression, lateral compression, vertical shear and combinations of these.

Lateral compression Side-to-side compression of the pelvis causes the ring to buckle and break. This is usually due to a side-on impact in a road accident or a fall from a height. Anteriorly the pubic rami on one or both sides are fractured, and posteriorly there is a severe sacroiliac strain or a fracture of the sacrum or ilium, either on the same side as the fractured pubic rami or on the opposite side of the pelvis. If the sacroiliac injury is much displaced, the pelvis is unstable. Vertical shear The innominate bone on one side is dis-

FRACTURES OF THE PELVIC RING It has been cogently argued that, because of the rigidity of the pelvis, a break at one point in the ring must be accompanied by disruption at a second point; exceptions are fractures due to direct blows (including fractures of the acetabular floor), or ring fractures in children, whose symphysis and sacroiliac joints are

(a)

(b)

placed vertically, fracturing the pubic rami and disrupting the sacroiliac region on the same side. This occurs typically when someone falls from a height onto one leg. These are usually severe, unstable injuries with gross tearing of the soft tissues and retroperitoneal haemorrhage. Combination injuries In severe pelvic injuries there

may be a combination of the above.

(c)

28.7 Types of pelvic ring fracture The three important types of injury are shown. (a) Anteroposterior compression with lateral rotation may cause the ‘open book’ injury, the hallmark of which is diastasis of the pubic symphysis. Widening of the anterior portion of the sacroiliac joint is best seen on an inlet view. (b) Lateral compression causing the ring to buckle and break; the pubic rami are fractured, sometimes on both sides. Posteriorly the iliac blade may break or the sacrum is crushed. (c) Vertical shear, with disruption of both the sacroiliac and symphyseal regions on one side.

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28

Stable and unstable fractures A stable pelvic ring injury is usually defined as one that will (theoretically) allow full weightbearing without the risk of pelvic deformity. Of course one cannot actually perform the test in an acutely injured patient. However, because the mechanisms which cause these injuries are fairly consistent, typical patterns and displacements are defined which make it possible to deduce the mechanism of injury, the type of ligament damage and the degree of pelvic instability. Occasionally the decision on stability cannot be made until the patient is examined under anaesthesia. Several classifications are in use. The one presented here is based on that of Young and Burgess (1986; 1987). ANTEROPOSTERIOR COMPRESSION (APC) INJURIES The ‘open book’ pattern appears as either diastasis of the pubic symphysis or fracture(s) of the pubic rami; as the pelvis is sprung open, the posterior (sacroiliac) elements also are strained. This general pattern is subclassified according to the severity of the injury: In APC-I injuries there may be only slight (less than 2 cm) diastasis of the symphysis; however, although invisible on x-ray, there will almost certainly be some strain of the anterior sacroiliac ligaments. The pelvic ring is stable. In APC-II injuries diastasis is more marked and the anterior sacroiliac ligaments (often also the sacrotuberous and sacrospinous ligaments) are torn. CT may show slight separation of the sacroiliac joint on one side. Nevertheless, the pelvic ring is still stable. In APC-III injuries the anterior and posterior sacroiliac ligaments are torn. CT shows a shift or separation of the sacroiliac joint; the one hemi-pelvis is effectively disconnected from the other anteriorly and from the sacrum posteriorly. The ring is unstable. LATERAL COMPRESSION (LC) INJURIES The hallmark of this injury is a transverse fracture of the pubic ramus (or rami), often best seen on an inlet view x-ray. There may also be a compression fracture of the sacrum. In its simplest form this would be classified as a LC-I injury. The ring is stable. The LC-II injury is more severe; in addition to the anterior fracture, there may be a fracture of the iliac wing on the side of impact. However, the ring remains stable. The LC-III injury is worse still. As the victim is run over, the lateral compression force on one iliac wing results in an opening anteroposterior force on the opposite ilium, causing injury patterns typical for that mechanism.

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VERTICAL SHEAR (VS) INJURIES The hemi-pelvis is displaced in a cranial direction, and often posteriorly as well, producing a typically asym-

metrical appearance of the pelvis. As with APC-III injuries, the hemi-pelvis is totally disconnected and the pelvic ring is unstable. COMBINATION INJURIES Combination patterns do occur but, in the main, the above classification defines the most common types of injury. The LC-II pattern is linked to abdominal, head and chest injuries; all the unstable patterns carry a high risk of severe haemorrhage and are life-threatening (Dalal et al., 1989).

Clinical features Stable ring injuries The patient is not severely shocked

but has pain on attempting to walk. There is localized tenderness but seldom any damage to pelvic viscera. Plain x-rays reveal the fractures. Unstable ring injuries The patient is severely shocked, in great pain and unable to stand. He or she may also be unable to pass urine and there may be blood at the external meatus. Tenderness is widespread, and attempting to move one or both blades of the ilium is very painful. Clinical assessment for stability is difficult; few patients will allow pulling or pushing to reveal abnormal vertical movement (Olson and Pollack, 1996). One leg may be partly anaesthetic because of sciatic nerve injury. Haemodynamic instability High-energy fractures of the

pelvis are extremely serious injuries, carrying a great risk of associated visceral damage, intra-abdominal and retroperitoneal haemorrhage, shock, sepsis and ARDS; the mortality rate is considerable. The patient should be repeatedly assessed and re-assessed for signs of blood loss and hypovolaemia. Bear in mind that, although the pelvis may be the main focus of attention, haemorrhage may occur also in areas outside the pelvis.

Imaging This may show fractures of the pubic rami, ipsilateral or contralateral fractures of the posterior elements, separation of the symphysis, disruption of the sacroiliac joint or combinations of these injuries. The films are often difficult to interpret and CT scans are much the best way of visualizing the nature of the injury.

Management EARLY MANAGEMENT Treatment should not await full and detailed diagnosis. It is vital to keep a sense of priorities and to act on any information that is already available while moving along to the next diagnostic hurdle. ‘Management’ in

this context is a combination of assessment and treatment, following the ATLS protocols. Six questions must be asked and the answers acted upon as they emerge: Is there a clear airway? Are the lungs adequately ventilated? Is the patient losing blood? Is there an intra-abdominal injury? Is there a bladder or urethral injury? Is the pelvic fracture stable or unstable?

With any severely injured patient, the first step is to make sure that the airway is clear and ventilation is unimpaired. Resuscitation must be started immediately and active bleeding controlled. The patient is rapidly examined for multiple injuries and, if necessary, painful fractures are splinted. A single anteroposterior x-ray of the pelvis is obtained. A more careful examination is then carried out, paying attention to the pelvis, the abdomen, the perineum and the rectum. The urethral meatus is inspected for signs of bleeding. The lower limbs are examined for signs of nerve injury. If the patient’s general condition is stable, further x-rays can then be obtained. If a urethral tear is suspected, an urethrogram is gently performed. The findings up to that stage may dictate the need for an intravenous urogram. By now the examining doctor will have a good idea of the patient’s general condition, the extent of the pelvic injury, the presence or absence of visceral injury and the likelihood of continued intra-abdominal or retroperitoneal bleeding. Ideally, a team of experts will be on hand to deal with the individual problems or undertake further investigations. MANAGEMENT OF SEVERE BLEEDING Severe bleeding is the main cause of death following high-energy pelvic fractures. The general treatment of shock is described in Chapter 22. If there is an unstable fracture of the pelvis, haemorrhage will be reduced by rapidly applying an external fixator. If either the expertise or the necessary equipment is lacking, unstable APC injuries can initially be managed by applying a pelvic binder to achieve side-toside compression; the rationale is to try and close the ‘open book’ and reduce the internal pelvic volume. The diagnosis of persistent bleeding is often difficult, and even when it seems clear that continuing shock is due to haemorrhage, it is not easy to determine the source of the bleeding. Patients with suspicious abdominal signs should be further investigated by peritoneal aspiration or lavage. If there is a positive diagnostic tap, the abdomen should be explored in an attempt to find and deal with the source of bleeding. However, if there is a large retroperitoneal haematoma, it should not be evacuated as this may

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Injuries of the pelvis

• • • • • •

release the tamponade effect and lead to uncontrollable haemorrhage. If there is no evidence of intra-abdominal bleeding and laparotomy is not contemplated, but the patient shows signs of continuing blood loss, then angiography should be performed with a view to carrying out embolization. If blood loss continues after embolization, angiography can again be performed to seek other sites of bleeding. However, angiography will not reveal any source of venous bleeding and repeated procedures are time-wasting. An alternative approach is the application of pelvic packing to provide a tamponade effect (Ertel et al., 2001). The management of severe haemorrhage in pelvic injuries is well-described in a recent review paper by Hak et al. (2009). MANAGEMENT OF THE URETHRA AND BLADDER Urological injury occurs in about 10 per cent of patients with pelvic ring fractures. As these patients are often seriously ill from other injuries, a urinary catheter may be required to monitor urinary output, and therefore the urologist is placed under pressure to make a rapid diagnosis of urethral damage. There is no place for passing a diagnostic catheter as this will most probably convert any partial tear to a complete tear. For an incomplete tear, the insertion of a suprapubic catheter as a formal procedure is all that is required. Around half of all incomplete tears will heal and require little long-term management. The treatment of a complete urethral tear is controversial. Primary realignment of the urethra may be achieved by performing suprapubic cystostomy, evacuating the pelvic haematoma and then threading a catheter across the injury to drain the bladder. If the bladder is floating high it is repositioned and held down by a sling suture passed through the lower anterior part of the prostatic capsule, through the perineum on either side of the bulbar urethra and anchored to the thighs by elastic bands. An alternative – and much simpler – approach is to perform the cystostomy as soon as possible, making no attempt to drain the pelvis or dissect the urethra, and to deal with the resulting stricture 4–6 months later. The latter method is contraindicated if there is severe prostatic dislocation or severe tears of the rectum or bladder neck. With both methods there is a significant incidence of late stricture formation, incontinence and impotence. TREATMENT OF THE FRACTURE For patients with very severe injuries, early external fixation is one of the most effective ways of reducing haemorrhage and counteracting shock (Poka and Libby, 1996; Hak et al., 2009). If there are no lifethreatening complications, definitive treatment is as follows.

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(a)

(b)

(c)

28.8 Internal fixation (a) Severe open-book injury with complete disruption of the symphysis pubis. (b) Reduction and stabilization by external fixator. (c) The symphysis was then firmly held by internal fixation with a plate and screws.

Isolated fractures and minimally displaced fractures These

injuries need only bed rest, possibly combined with lower limb traction. Within 4–6 weeks the patient is usually comfortable and may then be allowed up using crutches. Open-book injuries Provided the anterior gap is less

than 2 cm and it is certain that there are no displaced posterior disruptions, these injuries can usually be treated satisfactorily by bed rest; a posterior sling or a pelvic binder helps to ‘close the book’. The most efficient way of maintaining reduction is by external fixation with pins in both iliac blades connected by an anterior bar; ‘closing the book’ may also reduce the amount of bleeding. Placing the pins is made easier if two temporary pins are first inserted hugging the medial and lateral surfaces of each iliac blade and then directing the fixing pins between them. Internal fixation by attaching a plate across the symphysis should be performed: (1) during the first few days after injury only if the patient needs a laparotomy; and (2) later on if the gap cannot be closed by less radical methods.

(a)

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(b)

Fractures of the iliac blade can often be treated with bed rest. However, if displacement is marked, or if there is an associated anterior ring fracture or symphysis separation, then open reduction and internal fixation with plates and screws will need to be considered (e.g. in displaced LC-II injuries causing a leg length discrepancy greater than 1.5 cm). It is also possible to reduce and hold some of these fractures by external fixation. APC-III and VS injuries These are the most dangerous

injuries and the most difficult to treat. It may be possible to reduce some or all of the vertical displacement by skeletal traction combined with an external fixator; even so, the patient needs to remain in bed for at least 10 weeks. This prolonged recumbency is not without risk. As these injuries represent loss of both anterior and posterior support, both areas will need to be stabilized. Two techniques are used: (a) anterior external fixation and posterior stabilization using screws across the sacroiliac joint, or (b) plating anteriorly and iliosacral screw fixation posteriorly. Posterior operations are hazardous (the dangers include massive haemorrhage, neurological damage and infection)

(c)

28.9 Treatment of vertical sheer fracture (a) X-ray showing a fractured superior pubic ramus and disruption of the right sacroiliac joint. (b) This was initially treated by traction and external fixation. (c) X-ray showing the pelvic ring restored. Thereafter, the sacroiliac joint was stabilized with plates and screws.

Open pelvic fractures Open fractures are best managed by external fixation. A diversion colostomy may be necessary.

Complications Thromboembolism A careful watch should be kept for signs of deep vein thrombosis or pulmonary embolism (Montgomery et al., 1996). Prophylactic anticoagulants are advocated in some hospitals. Sciatic nerve injury It is essential to test for sciatic nerve function both before and after treating the pelvic fracture. If the nerve is injured it is usually a neuropraxia and one can afford to wait several weeks for signs of recovery. Occasionally, though, nerve exploration is necessary. Urogenital problems Urethral injuries sometimes result in stricture, incontinence or impotence and may require further treatment. Persistent sacroiliac pain Unstable pelvic fractures are

often associated with partial or complete sacroiliac joint disruption, and this can lead to persistent pain at the back of the pelvis. Occasionally arthrodesis of the sacroiliac joint is needed.

FRACTURES OF THE ACETABULUM Fractures of the acetabulum occur when the head of the femur is driven into the pelvis. This is caused either by

a blow on the side (as in a fall from a height) or by a blow on the front of the knee, usually in a dashboard injury when the femur also may be fractured. Acetabular fractures combine the complexities of pelvic fractures (notably the frequency of associated soft-tissue injury) with those of joint disruption (namely, articular cartilage damage, noncongruent loading and secondary osteoarthritis).

Patterns of fracture Several classifications of acetabular fractures are currently popular (Letournel, 1981; Müller et al., 1991; Tile, 1995). All use similar anatomical descriptions, but Tile’s universal classification has much to commend it for simplicity. The fractures are divided into four major types; though they are distinguished on anatomical grounds, it is important to recognize that they also differ in their ease of reduction, their stability after reduction and their long-term prognosis.

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Injuries of the pelvis

and should be attempted only by surgeons with considerable experience in this field. Persisting with skeletal traction and external fixation is probably safer, though the malposition is likely to leave a legacy of posterior pain. It should be emphasized that more than 60 per cent of pelvic fractures need no fixation.

Acetabular wall fractures Fractures of the anterior or posterior part of the acetabular rim affect the depth of the socket and may lead to hip instability unless they are properly reduced and fixed.

COLUMN FRACTURES The anterior column extends from the pubic symphysis, along the superior pubic ramus, across the acetabulum to the anterior part of the ilium. On the x-ray it is shown in profile by the iliopectineal line in the oblique view. Anterior column fractures are uncommon, do not involve the weightbearing area and have a good prognosis. The posterior column extends from the ischium, across the posterior aspect of the acetabular socket to the sciatic notch and the posterior part of the innominate bone. In an iliac oblique x-ray it is seen in 28.10 Acetabular fractures (a) Fractures occur through the wall (rim) or supporting columns. (b) Of particular importance is the roof (superior dome – which carries a high proportion of the load in walking).

(a)

(b)

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28

(a)

(b)

(c)

(e)

28.11 The classification of acetabular fractures There are four types of injury: (a,b) a simple fracture involving either the anterior or the posterior wall or column; (c) a transverse or (d) a T-type fracture involving two columns; (e) the bothcolumn fracture, resulting in a ‘floating’ acetabulum with no part of the socket attached to the ilium (compare this with the transverse or T-type fractures).

profile as the ilioischial line. A posterior column fracture usually runs upwards from the obturator foramen into the sciatic notch, separating the posterior ischiopubic column of bone and breaking the weightbearing part of the acetabulum. It is usually associated with a posterior dislocation of the hip and may injure the sciatic nerve. Treatment is more urgent and usually involves internal fixation to obtain a stable joint. TRANSVERSE FRACTURE This fracture runs transversely through the acetabulum, involving both the anterior and posterior columns, and separating the iliac portion above from the pubic and ischial portions below. A vertical split into the obturator foramen may coexist, resulting in a T-fracture. Note that in both transverse and T-type

(a)

838

(d)

(b)

fractures, a portion of the acetabulum remains attached to the ilium. These fractures are usually difficult to reduce and to hold reduced. COMPLEX FRACTURES Many acetabular fractures are complex injuries which damage either the anterior or the posterior columns (or both) as well as the roof or the walls of the acetabulum. Of particular note, and sometimes a cause of confusion, is the ‘both-column fracture’ – this is really a variant of the T-fracture in that the two columns are involved but the transverse part of the ‘T’ lies just above the acetabulum; effectively, no portion of the acetabulum remains connected to the rest of the pelvis. Understandably, the confusion arises when the term ‘both-column’ is used to refer to a transverse

(c)

28.12 Imaging the pelvis for acetabular fractures Although CT scans have become the standard in assessing acetabular fractures, plain x-rays have much to offer. The obturator oblique (a), standard anteroposterior (b) and iliac oblique (c) views will allow the trained eye to picture the structures involved in the injury. The iliopectineal line represents a profile of the anterior column whereas the ilioschial line defines the posterior column. The margins of the anterior and posterior walls are usually seen in all three views.

Clinical features There has usually been a severe injury; either a traffic accident or a fall from a height. Associated fractures are not uncommon and, because they may be more obvious, are liable to divert attention from the more urgent pelvic injuries. Whenever a fractured femur, a severe knee injury or a fractured calcaneum is diagnosed, the hips also should be x-rayed. The patient may be severely shocked, and the complications associated with all pelvic fractures should be excluded. Rectal examination is essential. There may be bruising around the hip and the limb may lie in internal rotation (if the hip is dislocated). No attempt should be made to move the hip. Careful neurological examination is important, testing the function of the sciatic, femoral, obturator and pudendal nerves.

Imaging At least four x-ray views should be obtained in every case: a standard anteroposterior view, the pelvic inlet view and two 45 degrees oblique views. Each view shows a different profile of the acetabulum; with practice the various landmarks (iliopectineal line, ilioischial line and the boundaries of the anterior and posterior walls) can be identified, thus providing a fairly good mental picture of the fracture type, the degree of comminution and the amount of displacement. CT

(a)

(b)

scans and three-dimensional re-formations are added refinements, and are particularly helpful if surgical reconstruction is planned.

Treatment EMERGENCY TREATMENT The first priority is to counteract shock and reduce a dislocation. Skeletal traction is then applied to the distal femur (10 kg will suffice) and during the next 3–4 days the patient’s general condition is brought under control. Occasionally, additional lateral traction through the greater trochanter is needed for central hip dislocations. Definitive treatment of the fracture is delayed until the patient is fit and operation facilities are optimal.

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Injuries of the pelvis

fracture – perhaps the term ‘high T’ would have been better! Complex fracture patterns share the following features: (1) the injury is severe; (2) the joint surface is disrupted; (3) they usually need operative reduction and internal fixation; and (4) the end result is likely to be less than perfect, unless surgical restoration has been exact.

NON-OPERATIVE TREATMENT In recent years opinion has moved in favour of operative treatment for displaced acetabular fractures. However, conservative treatment is still preferable in certain well-defined situations: (1) acetabular fractures with minimal displacement (in the weightbearing zone, less than 3 mm); (2) displaced fractures that do not involve the superomedial weightbearing segment (roof) of the acetabulum – usually distal anterior column and distal transverse fractures; (3) a both-column fracture that retains the ball and socket congruence of the hip by virtue of the fracture line lying in the coronal plane and displacement being limited by an intact labrum; (4) fractures in elderly patients, where closed reduction seems feasible; (5) patients with ‘medical’ contraindications to operative treatment (including local sepsis). Comminution in itself is not a contraindication to operative treatment, provided adequate facilities and expertise are available. Matta and Merritt (1988) have listed certain criteria which should be met if conservative treatment is expected to succeed: (1) when traction is released, the

(c)

(d)

28.13 Fractured acetabulum – conservative treatment This severely displaced acetabular fracture (a) was almost completely reduced by (b) longitudinal and lateral traction. (c) The fracture healed and the patient regained a congruent joint with a fairly good range of movement. (d) X-ray two years later.

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28

hip should remain congruent; (2) the weightbearing portion of the acetabular roof should be intact; and (3) associated fractures of the posterior wall should be excluded by CT. Non-operative treatment is more suitable for patients aged over 50 years than for adolescents and young adults. If there are medical contraindications to operative treatment, closed reduction under general anaesthesia is attempted. In all patients treated conservatively, longitudinal traction, if necessary supplemented by lateral traction, is maintained for 6–8 weeks; this will unload the articular cartilage and will help to prevent further displacement of the fracture. During this period, hip movement and exercises are encouraged. The patient is then allowed up, using crutches with minimal weightbearing for a further 6 weeks.

is useful to monitor somatosensory evoked potentials during the operation, in order to avoid damaging the sciatic nerve (separate electrodes are required for medial and lateral popliteal branches). Prophylactic antibiotics are used, and postoperatively hip movements are started as soon as possible. Some prophylaxis against heterotopic ossification is often used, usually indomethacin. The patient is allowed up, partial weightbearing with crutches, after 7 days. Exercises are continued for 3–6 months; it may take a year or longer for full function to return.

Complications Operative treatment should aim for a perfect anatomical reduction and is best undertaken in centres that specialize in this form of treatment.

OPERATIVE TREATMENT Operative treatment is indicated for all unstable hips and fractures resulting in significant distortion of the ball and socket congruence. The hip may be dislocated centrally, anteriorly or posteriorly. Patients with isolated posterior wall fractures and dislocation may require immediate open reduction and stabilization. In other cases operation is usually deferred for 4 or 5 days. Matta and Merritt (1988) have made the important point that open reduction is an operation on the pelvis and not merely the acetabular socket. Adequate exposure is essential, if possible through a single approach which is selected according to the type of fracture. The posterior Kocher–Langenbach exposure allows good access to the posterior wall and column but may have to be combined with a trochanteric osteotomy to gain adequate sight in transverse fractures. The anterior ilioinguinal approach is suited for anterior wall and column fractures. Both exposures are usually needed in T-type and both-column fractures – this is a considerable undertaking, encouraging some surgeons to adopt the singular triradiate or extended iliofemoral approaches instead. The fracture (or fractures) is fixed with lag screws or special buttressing plates which can be shaped in the operating theatre. It

Iliofemoral venous thrombosis This is potentially serious and in some clinics prophylactic anticoagulation is used. Sciatic nerve injury Nerve injury may occur either at the time of fracture or during the subsequent operation. Unless the nerve is seen to be unharmed during the operation, there can be no certainty about the prognosis. Intra-operative somatosensory monitoring is advocated as a means of preventing serious nerve damage. For an established lesion, it is worth waiting for 6 weeks to see if there is any sign of recovery. If there is none, the nerve should be explored in order to establish the diagnosis and ensure that the nerve is not being compressed. Hereterotopic bone formation Periarticular ossification is common after severe soft-tissue injury and extended surgical dissections. In cases where this is anticipated, prophylactic indomethacin is useful. Avascular necrosis Osteonecrosis of the femoral head

may occur even if the hip is not fully dislocated. The condition is probably overdiagnosed because of erroneous interpretation of the x-ray appearances following impacted marginal fractures of the acetabulum (Gruen, Mears and Tauxe, 1988).

28.14 Fractured acetabulum – internal fixation (a) X-ray and (b) three-dimensional CT before reduction, showing a large posterior fragment which needed accurate repositioning and internal fixation (c). (Courtsey of Mr RN Brueton and Dr RL Guy).

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(a)

(b)

(c)

REFERENCES AND FURTHER READING

(a)

(b)

28.15 Sacrococcygeal fractures (a) Fractured sacrum; (b) fractured coccyx.

Displaced fractures involving the weightbearing portion of the joint may result in loss of movement and early onset osteoarthritis. If a joint replacement operation is contemplated it should be deferred until the fractures have consolidated; the acetabular implant is bound to work loose if there is any movement of the innominate segments.

Loss of joint movement and secondary osteoarthritis

INJURIES TO THE SACRUM AND COCCYX A blow from behind, or a fall onto the ‘tail’ may fracture the sacrum or coccyx, or sprain the joint between them. Women seem to be affected more commonly than men. Bruising is considerable and tenderness is elicited when the sacrum or coccyx is palpated from behind or per rectum. Sensation may be lost over the distribution of sacral nerves. X-rays may show: (1) a transverse fracture of the sacrum, in rare cases with the lower fragment pushed forwards; (2) a fractured coccyx, sometimes with the lower fragment angulated forwards; or (3) a normal appearance if the injury was merely a sprained sacrococcygeal joint. Treatment If the fracture is displaced, reduction is

worth attempting. The lower fragment may be pushed backwards by a finger in the rectum. The

Dalal SA, Burgess AR, Siegel JH, et al. Pelvic fracture in multiple trauma. J Trauma 1989; 29: 981–1000. Ertel W, Keel M, Eid K, et al. Control of severe haemorrhage using C-clamp and pelvic packing in multiply injured patients with pelvic ring disruption. J Orthop Trauma 2001; 15: 468–74. Gruen GS, Mears DC, Tauxe WN. Distinguishing avascular necrosis from segmental impaction of the femoral head following an acetabular fracture. J Orthop Trauma 1988; 2: 5–9. Hak DJ, Smith WR, Suzuki T. Management of haemorrhage in life-threatening pelvic fracture. J Am Acad Orthop Surg 2009; 17: 447–57. Letournel E. Fractures of the Acetabulum 1981. Springer, Berlin, 1981. Matta JM, Merritt PO. Displaced acetabular fractures. Clin Orthop Relat Res 1988; 230: 83–97. Montgomery KD, Geerts WH, Potter HG, Helfet DL. Thromboembolic complications in patients with pelvic trauma. Clin Orthop Relat Res 1996; 329: 68–87. Müller ME, Allgower M, Schneider R, Willeneger H. Manual of Internal Fixation, 3rd edition. Springer Verlag. Berlin, Heidelberg, New York, 1991. Olson SA, Pollak AN. Assessment of pelvic ring stability after injury. Indications for surgical stabilisation. Clin Orthop Relat Res 1996; 329: 15–27. Poka A, Libby EP. Indications and techniques for external fixation of the pelvis. Clin Orthop Relat Res 1996; 329: 54–9. Tile M. Fractures of the pelvis and acetabulum. 2nd edition. Williams and Wilkins, Baltimore, 1995. Wootton JR, Cross MJ, Holt KWG. Avulsion of the ischial apophysis. J Bone Joint Surg 1990; 72B: 625–7. Young JWR, Burgess AR, Brumback RJ, Poka A. Lateral compression fractures of the pelvis: the importance of plain radiographs in the diagnosis and surgical management. Skeletal Radiol 1986; 15: 103–9. Young JWR, Burgess AR. Radiologic management of pelvic ring fractures: Systematic radiographic diagnosis. Urban and Schwarzenberg. Baltimore, 1987.

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Injuries of the pelvis

reduction is stable, which is fortunate. The patient is allowed to resume normal activity, but is advised to use a rubber ring cushion when sitting. Occasionally, sacral fractures are associated with urinary problems, necessitating sacral laminectomy. Persistent pain, especially on sitting, is common after coccygeal injuries. If the pain is not relieved by the use of a cushion or by the injection of local anaesthetic into the tender area, excision of the coccyx may be considered.

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29

Injuries of the hip and femur Selvadurai Nayagam

dashboard. The femur is thrust upwards and the femoral head is forced out of its socket; often a piece of bone at the back of the acetabulum (usually the posterior wall) is sheared off, making it a fracture-dislocation. Seat-belt restraints can reduce the number of posterior hip dislocations.

DISLOCATION OF THE HIP The magnitude of force needed to dislocate the hip, a joint particularly well-contained by virtue of its bony and soft-tissue anatomy, is so great that the dislocation is often associated with fractures – either around the joint or elsewhere in the same limb. Small fragments of bone are often chipped off, usually from the femoral head or from the wall of the acetabulum. If there is a major fragment, the injury is regarded as a fracture-dislocation. Hip dislocations are classified according to the direction of the femoral head displacement: posterior (by far the commonest variety), anterior and central (a comminuted or displaced fracture of the acetabulum).

Clinical features In a straightforward case the diagnosis is easy; the leg is short and lies adducted, internally rotated and slightly flexed. However, if one of the long bones is fractured – usually the femur – the injury can easily be missed as the limb can adopt almost any position. The golden rule is to x-ray the pelvis in every case of severe injury and, with femoral fractures, to insist on an x-ray that includes both the hip and knee. The lower limb should be examined for signs of sciatic nerve injury (Figure 29.1).

POSTERIOR DISLOCATION Mechanism of injury

X-ray

This is a posterior dislocation, usually occurring in a road accident when someone seated in a truck or car is thrown forward, striking the knee against the

(a)

(b)

In the anteroposterior film the femoral head is seen out of its socket and above the acetabulum. A

(c)

(d)

29.1 Posterior dislocation of the hip (a) This is the typical posture in a patient with posterior dislocation: the left hip is slightly flexed and internally rotated. (b) The x-ray in this case showed a simple dislocation, with the femoral head lying above and behind the acetabulum. (c) Another patient with dislocation and an associated acetabular rim fracture. However, in some cases it may need a CT scan and three-dimensional image reconstruction to appreciate the full extent of the associated acetabular injury (d).

FRACTURES AND JOINT INJURIES

29

Table 29.1 Classification of hip dislocation (Thompson and Epstein). Types

Thompson and Epstein classification of hip dislocations

I

Dislocation with no more than minor chip fractures

II

Dislocation with single large fragment of posterior acetabular wall

III

Dislocation with comminuted fragments of posterior acetabular wall

IV

Dislocation with fracture through acetabular floor

V

Dislocation with fracture through acetabular floor and femoral head

segment of acetabular rim or femoral head may have been broken off and displaced; oblique films are useful in demonstrating the size of the fragment. If any fracture is seen, other bony fragments (which may need removal) must be suspected. A CT scan is the best way of demonstrating an acetabular fracture (or any bony fragment) but detailed imaging at this stage should be undertaken only if it does not delay reduction of the dislocation unduly. Thompson and Epstein (1951) suggested a classification which is helpful in planning treatment. Types I and II are relatively simple dislocations; these are associated with either minor chip fractures (small fragments of the acetabular wall or fovea centralis) or a single large fragment from the posterior acetabular wall. In Type III the posterior wall is comminuted. type IV has an associated fracture of the acetabular floor, and Type V an associated fracture of the femoral head, which can be further subdivided according to Pipkin’s (1957) classification. (Figure 29.2)

Treatment The dislocation must be reduced as soon as possible under general anaesthesia. In the vast majority of cases this is performed closed, but if this is not achieved after two or three attempts an open reduction is required. An assistant steadies the pelvis; the surgeon starts by applying traction in the line of the femur as it lies (usually in adduction and internal rotation), and then gradually flexes the patient’s hip and knee to 90 degrees, maintaining traction throughout. At 90 degrees of hip flexion, traction is steadily increased and sometimes a little rotation (either internal or external) is required to accomplish reduction. Another assistant can help by applying direct medial and anterior pressure to the femoral head through the buttock. A satisfying ‘clunk’ terminates the manoeuvre. An important test follows, to assess the stability of the reduced hip. By flexing the hip to 90 degrees and applying a longitudinal and posteriorly-directed force, the hip is screened on an image-intensifier looking for signs of subluxation. Evidence of this should prompt a repair to the posterior wall of the acetabulum. Reduction is usually stable in type I injuries, but the hip has been severely injured and needs to be rested. The simplest way is to apply traction and maintain it for a few days. Movement and exercises are begun as soon as pain allows; continuous passive movement machines are helpful. The terminal ranges of hip movements are avoided to allow healing of the capsule and ligaments. As soon as active limb control is achieved, and this may take about 2 weeks, the patient is allowed to walk with crutches but without taking weight on the affected side. The rationale for not bearing weight is to prevent collapse of femoral head due to an unsuspected avascular change. The period of hip ‘protection’ varies according to

Pipkin classification of femoral head fractures

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Type I

Type II

Type III

Type IV

The fracture line is inferior to the fovea

The fracture fragment includes the fovea

As with types I and II but with an associated femoral neck fracture

Any pattern of femoral head fracture and an acetabular fracture (coincides with Thompson and Epstein’s type V)

29.2 Pipkin classification of femoral head fractures

Complications EARLY Sciatic nerve injury The sciatic nerve is damaged in 10–20 per cent of cases but it usually recovers. Nerve function must be tested and documented before reduction is attempted. If, after reducing the dislocation, a

sciatic nerve lesion is diagnosed, the nerve should be explored to ensure it is not trapped by the reduction manoeuvre. Recovery often takes months and in the meantime the limb must be protected from injury and the ankle splinted to overcome the foot drop.

29

Vascular injury Occasionally the superior gluteal artery is torn and bleeding may be profuse. If this is suspected, an arteriogram should be performed. The torn vessel may need to be ligated.

Injuries of the hip and femur

the risk of avascular necrosis: if the reduction was performed promptly (within 6 hours), then no more than 6 weeks should suffice, but if there was a longer delay then an extended period of 12 weeks may be wiser. Progression of weightbearing should be graduated and the hip joint monitored by x-ray (Tornetta and Mostafavi 1997). If the post-reduction x-rays or CT scans show the presence of intra-articular bone fragments or larger femoral head pieces that are incompletely reduced, an open procedure should be planned. The approach is dictated by the location of the fragment on CT scan; however, the operation is not an emergency and can be done once the patient’s condition has stabilized. The joint needs to be thoroughly washed out at the conclusion of the procedure to remove bone ‘grit’. Type II fracture-dislocations are often treated by immediate open reduction and anatomical fixation of the detached fragment, the rationale being that many large posterior wall fragments either do not reduce well or remain as a cause of instability even after reduction. However, if the patient’s general condition is suspect, or the necessary surgical skills are not available, the hip is reduced closed, as described above. Traction can be applied until conditions are appropriate for surgery – open reduction and internal fixation will remedy the source of instability, return congruity to the joint and remove any trapped bone fragments. Type III injuries are treated closed, but there may be retained fragments and these should be removed by open operation. Fixation of a comminuted posterior wall is sometimes impossible – if persistent instability is present, referral to a specialist centre, where reconstruction using a segment of iliac crest could be undertaken, is advisable. Types IV and V are treated initially by closed reduction. The indications for surgery follow the principles already outlined: instability, retained fragments or joint incongruity. In type V injuries, a femoral head fragment may automatically fall into place, and this can be confirmed by post-reduction CT. If the fragment remains unreduced, operative treatment is indicated: a small fragment can simply be removed, but a large fragment should be replaced; the joint is opened, the femoral head dislocated and the fragment fixed in position with a countersunk screw. Postoperatively, traction is maintained for 2–4 weeks and full weightbearing is deferred for 12 weeks.

Associated fractured femoral shaft When this occurs at the same time as the hip dislocation, the dislocation is often missed. It should be a rule that with every femoral shaft fracture, the buttock and trochanter are palpated, and the hip clearly seen on x-ray. Even if this precaution has been omitted, a dislocation should be suspected if the proximal fragment of a transverse shaft fracture is seen to be adducted. Closed reduction of the dislocation will be much more difficult. A prompt open reduction of the hip followed by internal fixation of the shaft fracture should be undertaken.

LATE Avascular necrosis Avascular necrosis of the femoral head has been reported in about 10 per cent of traumatic hip dislocations; if reduction is delayed by more than 12 hours, the figure rises to over 40 per cent. Changes are seen first on MRI or isotope bone scans. X-ray features such as increased density of the femoral head may not be seen for at least 6 weeks, and sometimes very much later (up to 2 years), depending on the rate of bone repair. Ischaemia is due to interruption of femoral head blood supply when the hip is dislocated. There is evidence to suggest that this results from compression, traction and arterial spasm rather than actual disruption of blood vessels (Shim 1979), which means that the consequences of ischaemia are proportional to the delay in starting treatment; blood flow is restored on reduction of the hip, especially if this is performed early – which highlights the need for emergency treatment with a target of less than 12 hours (preferably less than 6) from the time of injury. If the femoral head develops signs of fragmentation, an operation may be needed. If the necrotic segment is small, realignment osteotomy is the method of choice; for extensive femoral head collapse, usually with accompanying degenerative arthritis, the choice is between joint replacement and hip arthrodesis (never an easy procedure). Myositis ossificans This is an uncommon complication, probably related to the severity of the injury. During recovery, movements should never be forced and in severe injuries the period of rest and non-weightbearing may need to be prolonged. Small areas of ossification seen on x-ray usually bear no clinical significance.

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FRACTURES AND JOINT INJURIES

29

29.3 Anterior hip dislocation (a,b) The usual appearance of an anterior dislocation: the hip is only slightly abducted and the head shows clinically as a prominent lump.

(b)

(a)

Unreduced dislocation After a few weeks an untreated dislocation can seldom be reduced by closed manipulation and open reduction is needed. The incidence of stiffness or avascular necrosis is considerably increased and the patient may later need reconstructive surgery.

upwards. Occasionally the leg is abducted almost to a right angle. Seen from the side, the anterior bulge of the dislocated head is unmistakable, especially when the head has moved anteriorly and superiorly. The prominent head is easy to feel, either anteriorly (superior type) or in the groin (inferior type). Hip movements are impossible (Figure 29.3).

Osteoarthritis Secondary osteoarthritis is not uncommon and is due to (1) cartilage damage at the time of the dislocation, (2) the presence of retained fragments in the joint or (3) ischaemic necrosis of the femoral head. In young patients treatment presents a difficult problem.

X-ray In the anteroposterior view the dislocation is usually obvious, but occasionally the head is almost directly in front of its normal position; any doubt is resolved by a lateral film.

ANTERIOR DISLOCATION

Treatment and complications

Anterior dislocation is rare compared with posterior. Dislocation of one or even both hips may occur when a weight falls onto the back of a miner or building labourer who is working with his legs wide apart, knees straight and back bent forwards. However, nowadays the usual cause is a road accident or air crash – even a posteriorly directed force on an abducted and externally rotated hip may cause the neck to impinge on the acetabular rim and lever the femoral head out in front of its socket. The femoral head will then lie superiorly (type I - pubic) or inferiorly (type II - obturator).

The manoeuvres employed are similar to those used to reduce a posterior dislocation, except that while the flexed knee is being pulled and the hip gently flexed upwards, it should be kept adducted; an assistant then helps by applying lateral pressure to the inside of the thigh. The point of reduction is usually heard and felt. The subsequent treatment is similar to that employed for posterior dislocation. Avascular necrosis occurs in less than 10 per cent of cases.

Clinical features

CENTRAL DISLOCATION

The leg lies externally rotated, abducted and slightly flexed. It is not short, because the attachment of rectus femoris prevents the head from displacing

A fall on the side, or a blow over the greater trochanter, may force the femoral head medially 29.4 Central dislocation (a) The plain x-ray gives a good picture of the displacement, but (b) a CT scan shows the pelvic injury more clearly. (c) Skeletal traction, which often needs both longitudinal and lateral vectors, is an effective method of reduction.

846

(a)

(b)

(c)

a height or a blow sustained in a road accident. These patients often have multiple injuries and in 20 per cent there is an associated fracture of the femoral shaft. Occasionally, stress fractures of the femoral neck occur in runners or military personnel.

FRACTURES OF THE FEMORAL NECK

Pathological anatomy and classification

The femoral neck is the commonest site of fractures in the elderly. The vast majority of patients are Caucasian women in the seventh and eighth decades, and the association with osteoporosis is so manifest that the incidence of femoral neck fractures has been used as a measure of age-related osteoporosis in population studies. Other risk factors include bone-losing or bone-weakening disorders such as osteomalacia, diabetes, stroke (disuse), alcoholism and chronic debilitating disease. In addition, old people often have weak muscles and poor balance resulting in an increased tendency to fall. The association of femoral neck fracture with postmenopausal bone loss has stimulated renewed interest in screening for osteoporosis and prophylactic measures in the ‘at risk’ population (see Chapter 7). By contrast, this injury is much less common among people whose bone mass is above that of the population average, e.g. those with osteoarthritis of the hip. Femoral neck fractures are also much less common in black (Negroid) peoples than in whites and Asians. The reasons for this phenomenon are poorly understood. Slightly higher bone mass and a slower rate of bone loss after the menopause may be significant, but a qualitative difference in bone structure has also been suggested: even among people with the same bone mass, those with greater loss of trabecular interconnectivity (typical in elderly whites) will suffer fractures more easily than those with firmer structure. The incidence of femoral neck fractures is set to double over the next 30 years; this is a reflection of a higher number of individuals living beyond 65 years and a parallel rise in those affected with osteoporosis. The economic impact of treating, rehabilitating and caring for this group of patients is increasingly being recognized, with many governments and healthcare administration bodies focusing on preventive strategies.

Mechanism of injury The fracture usually results from a simple fall; however, in very osteoporotic people, less force is required –– perhaps no more than catching a toe in the carpet and twisting the hip into external rotation. Some patients may have experienced minor symptoms of a preceding stress fracture of the femoral neck. In younger individuals, the usual cause is a fall from

The most useful classification is that of Garden, which is based on the amount of displacement apparent in the pre-reduction x-rays (Garden 1961). Once fractured, the head and neck become displaced in progressively severe stages. Stage I is an incomplete impacted fracture, including the so-called abduction fracture in which the femoral head is tilted into valgus in relation to the neck. Stage II is a complete but undisplaced fracture. Stage III is a complete fracture with moderate displacement. And Stage IV is a severely displaced fracture. This is essentially a radiographic classification; the distinctive x-ray features are described below. Garden I and II fractures, which are only slightly displaced, have a much better prognosis for union and for viability of the femoral head than the more severely displaced Garden III and IV fractures (Barnes, Brown et al. 1976). This has an important influence on the choice of treatment for the various stages. However, there is little room for complacency with any of these fractures; left untreated, a comparatively benign-looking Stage I fracture may rapidly disintegrate to Stage IV. Healing of femoral neck fractures is bedevilled by two problems: the threat of bone ischaemia and tardy union. The femoral head gets its blood supply from three sources: (1) intramedullary vessels in the femoral neck; (2) ascending cervical branches of the medial and lateral circumflex anastomoses, which run within the capsular retinaculum before entering the bone at the articular margin of the femoral head; and (3) the vessels of the ligamentum teres. The intramedullary supply is always interrupted by the fracture; the retinacular vessels, also, may be kinked or torn if the fracture is displaced. In elderly people, the remaining supply in the ligamentum teres is at best fairly meagre and, in 20 per cent of cases, nonexistent. Hence the high incidence of avascular necrosis in displaced femoral neck fractures. Transcervical fractures are, by definition, intracapsular. They have a poor capacity for healing because: (1) by tearing the retinacular vessels the injury deprives the head of its main blood supply; (2) intra-articular bone has only a flimsy periosteum and no contact with soft tissues which could promote callus formation; and (3) synovial fluid prevents clotting of the fracture haematoma. Accurate apposition and impaction of bone fragments are therefore of more importance than usual. There is evidence that aspirating a haemarthro-

29

Injuries of the hip and femur

through the floor of the acetabulum. Although this is called ‘central dislocation’, it is really a fracture of the acetabulum (Figure 29.4). The condition is dealt with in the chapter on ‘Injuries of the pelvis’.

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FRACTURES AND JOINT INJURIES

29

sis increases the blood flow in the femoral head by relieving tension in the capsule, and the practice is encouraged at the time of surgery (Harper, Barnes et al. 1991; Bonnaire and Weber 2002).

Clinical features There is usually a history of a fall, followed by pain in the hip. If the fracture is displaced, the patient lies with the limb in lateral rotation and the leg looks short. Beware, not all hip fractures are so obvious. With an impacted fracture the patient may still be able to walk, and debilitated or mentally handicapped patients may not complain at all – even with bilateral fractures. In contrast, femoral neck fractures in young adults result from road traffic accidents or falls from heights and are often associated with multiple injuries. A good rule is that young adults with severe injuries – whether they complain of hip pain or not – should always be examined for an associated femoral neck fracture.

X-ray Two questions must be answered: is there a fracture, and is it displaced? Usually the break is obvious, but an impacted fracture can be missed by the unwary. Displacement is judged by the abnormal shape of the bone outlines and the degree of mismatch of the trabecular lines in the femoral head and neck and the supra-acetabular (innominate) part of the pelvis (Figure 29.5). This assessment is important because impacted or undisplaced fractures do well after inter-

nal fixation, whereas displaced fractures have a high rate of non-union and avascular necrosis. In Garden I fractures the femoral head is in its normal position or tilted into valgus and impacted on the femoral neck stump. The medial cortex may be intact. The femoral head stress trabeculae are normally aligned with the innominate trabeculae. In Garden II fractures the femoral head is normally placed and the fracture line may be difficult to discern. In Garden III fractures the anteroposterior x-ray shows that the femoral head is tilted out of position and the trabecular markings are not in line with those of the innominate bone; this is because the proximal fragment retains some contact with the neck stump and is pushed out of alignment. In Garden IV fractures the femoral head trabeculae are normally aligned with those of the innominate bone; the reason is that the proximal fragment has lost contact with the femoral neck and lies in its normal position in the acetabular socket.

Diagnosis There are four situations in which a femoral neck fracture may be missed, sometimes with dire consequences. • Stress fractures The elderly patient with unexplained pain in the hip should be considered to have a stress fracture until proved otherwise. A similar cautionary note is raised for young athletes who do regular impact-loading sports and military personnel on marching routines. The x-ray is usually normal but a bone scan, or better still an MRI, will show the lesion (Figure 29.6). 29.5 Garden’s classification of femoral neck fractures (a) Stage I: incomplete (socalled abducted or impacted) – the femoral head in this case is in slight valgus. (b) Stage II: complete without displacement. (c) Stage III: complete with partial displacement – the fragments are still connected by the posterior retinacular attachment; the femoral head trabeculae are no longer in line with those of the innominate bone. (d) Stage IV: complete with full displacement – the proximal fragment is free and lies correctly in the acetabulum so that the trabeculae appear normally aligned with those of the innominate.

848

(a)

(b)

(c)

(d)

29

(b)

(c)

29.6 Fractures of the femoral neck – diagnosis (a) An elderly woman tripped on the pavement and complained of pain in the left hip. The plain x-ray showed no abnormality. Two weeks later she was still in pain; (b) a bone scan showed a ‘hot’ area medially at the base of the femoral neck. MRI, if available, is an alternative investigation to confirm suspicions of a femoral neck fracture (c).

• Undisplaced fractures Impacted fractures may be extremely difficult to discern on plain x-ray. If there is a fracture it will show up on MRI or a bone scan after a few days. • Painless fractures A bed-ridden patient may develop a ‘silent’ fracture. Even a fit patient occasionally walks about without pain if the fracture is impacted. If the context suggests an injury, investigate – whether the patient complains or not. • Multiple fractures The patient with a femoral shaft fracture may also have a hip fracture, which is easily missed unless the pelvis is x-rayed.

Treatment Initial treatment consists of pain-relieving measures and simple splintage of the limb. If operation is delayed, a femoral nerve block may be helpful. A case for non-operative treatment of undisplaced (Garden Stages I and II) fractures can be made in treating patients with advanced dementia and little discomfort. For all others, operative treatment is almost mandatory. Displaced fractures will not unite without internal fixation, and in any case elderly people should be got up and kept active without delay if pulmonary complications and bed sores are to be prevented. Impacted fractures can be left to unite, but there is always a risk that they may become displaced, even while lying in bed, so fixation is safer. Another indication for non-operative management is an impacted Garden I fracture that is an ‘old’ injury, where the diagnosis is made only after the patient has been walking about for several weeks without deleterious effect on the fracture position. When should the operation be performed? In young patients operation is urgent; interruption of the blood supply will produce irreversible cellular changes after 12 hours and, to prevent this, an

accurate reduction and stable internal fixation is needed as soon as possible. In older patients, also, the longer the delay, the greater is the likelihood of complications. However, here speed is tempered by the need for adequate preparation, especially in the very elderly, who are often ill and debilitated. What if operation is considered too dangerous? Lying in bed on traction may be even more dangerous, and leaving the fracture untreated too painful; the patient least fit for operation may need it most. Internal fixation Notwithstanding the advances in joint replacement, for most patients the principles of treatment are as of old: accurate reduction, secure internal fixation and early activity. Displaced fractures must first be reduced: with the patient under anaesthesia, the fracture is disimpacted by applying traction with the hip held in 45 degrees of flexion and slight abduction; the limb is then slowly brought into extension and finally internally rotated; as traction is released, the fracture re-impacts in the reduced position. The reduction is assessed by x-ray. The femoral head should be positioned correctly with the stress trabeculae in the femoral head and those in the femoral neck aligned close to their normal position in both anteroposterior and lateral views, as shown in Figure 29.7. In the AP x-ray the trabeculae in the femoral head and a line along the medial border of the femoral shaft should subtend an angle of 155–180 degrees. To fix an imperfectly reduced fracture is to risk failure. If a stage III or IV fracture cannot be reduced closed, and the patient is under 60 years of age, open reduction through an anterolateral approach is advisable. However, in older patients (and certainly in those over 70) this may not be justified; if two careful attempts at closed reduction fail, prosthetic

Injuries of the hip and femur

(a)

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FRACTURES AND JOINT INJURIES

29

(a)

(c)

(b)

(d)

29.7 Garden’s index for assessing reduction in subcapital fractures On the anteroposterior x-ray (a,b), the medial femoral shaft and the axis of trabecular markings over the medial aspect of the femoral neck lie at an angle of 160°; an acceptable reduction is deemed to lie between 155° and 180°. On the lateral view (c,d), the trabecular markings would be in line (i.e. 180°) if the fracture was perfectly reduced; an acceptable reduction is within 20° of this ideal. Garden (1974) noted that there was a higher association with complications such as avascular necrosis, non-union and osteoarthritis if the quality of reduction was outside these acceptable limits.

(a)

850

(b)

replacement is preferable. Some may even argue that prosthetic replacement is always a preferable option for this older group as it carries a much lower risk of needing revision surgery. Once the fracture is reduced, it is held with cannulated screws or a sliding screw and side-plate which attaches to the femoral shaft. A lateral incision is used to expose the upper femur. When using cannulated screws, guide wires –– inserted under fluoroscopic control – are used to ensure correct placement of the fixing device. Usually three cannulated screws will suffice; they should lie parallel and extend to within 5 mm of the subchondral bone plate. It is usual to start with an inferior screw that skirts the inferior cortex of the neck but remains centred in the lateral x-ray view. This screw should be inserted through the lateral cortex of the femur at a level proximal to the lesser trochanter lest a stress riser is created and produces a subtrochanteric fracture. Two further screws are inserted more proximally, this time centred in the femoral neck on the anteroposterior x-ray but straddling the anterior and posterior margins of the femoral neck on the lateral x-ray (Figure 29.8). If a sliding screw is used, the femoral neck will first have to be reamed; a temporary guidewire should always be introduced before reaming so as to prevent the femoral head from rotating with the reamer and tearing the remaining soft-tissue attachments. Once the sliding screw is fixed, the guidewire is replaced by a single screw to reduce the risk of femoral head rotation during fracture healing – this screw must be parallel to the sliding screw or else impaction of the fracture will not occur! From the first day patients should sit up in bed or in a chair. They are taught breathing exercises, and

(c)

(d)

29.8 Femoral neck injuries – treatment (a,b) This Garden stage II fracture has been stabilized with 3 cannulated screws. (c,d) An optimum position for the screws is: one to support the inferior portion of the neck (centrally); and another two, central in level, skirting the anterior and posterior cortices of the femoral neck on the lateral x-ray. It is important the most inferior screw enters the lateral cortex of the femur proximal to the level of the inferior margin of the lesser trochanter.

29

(b)

(c)

29.9 Fracture of the femoral neck – treatment (a) A fracture as severely displaced as this (Stage IV), if treated by reduction and internal fixation, will probably end up needing revision surgery; instead it could be treated by performing a hemiarthroplasty using a cemented femoral prostheses (b). A total hip replacement (c) provides a better outcome for younger patients (50–60 year olds) with this type of fracture.

encouraged to help themselves and to begin walking (with crutches or a walker) as soon as possible. To delay weightbearing may be theoretically appropriate but is rarely practicable. This procedure carries a longer operating time, greater blood loss and a higher infection rate than internal fixation. However, in its favour is a much lower need for revision surgery (nearly four times less) when compared to internal fixation for stage III and IV fractures. The mortality rates are equivalent for the two groups but there is insufficient data to be certain there is a difference in morbidity (Masson, Parker et al. 2003). Some argue that prosthetic replacement is always preferable for stage III and IV fractures so that patients, particularly the elderly, are subject to one single surgical intervention (Figure 29.9). This is also true for patients with pathological fractures and those in whom closed reduction cannot be achieved. Hip prostheses used for femoral neck fractures are usually of the femoral part only (hemiarthroplasty) and may be inserted with or without cement. Cemented prostheses have better mobility and less thigh pain; uncemented prostheses should be reserved for the very frail where the pre-injury status suggests that mobility is unlikely to be attained after operation and those who will benefit significantly from the reduced operating time. There is little evidence to support use of bipolar prostheses over unipolar types for the elderly group; the mortality, morbidity and functional recovery following use of either are similar.

Prosthetic replacement

Injuries of the hip and femur

(a)

However, some studies suggest a longer survivorship of bipolar implants and an argument can be made for their use in younger patients. Total hip replacement for femoral neck fractures may be indicated: (1) if treatment has been delayed for some weeks and acetabular damage is suspected, or (2) in patients with metastatic disease or Paget’s disease. Hip function and quality of life are reported to be better with total hip replacement, even when compared with hemiarthroplasty, and there is some justification for using this as a preferred option in the healthy, active person who needs treatment for a stage III or IV fracture (Keating, Grant et al. 2006). Postoperatively, breathing exercises and early mobilization are important. Speed of recovery depends largely on how active the patient was before the fracture; after 2–4 months, further improvement is unlikely.

Complications General complications These patients, most of whom

are elderly, are prone to general complications such as deep vein thrombosis, pulmonary embolism, pneumonia and bed sores; not to mention disorders that might have been present before the fracture and which lead to death in a substantial proportion of cases. Notwithstanding the advances in perioperative care, the mortality rate in elderly patients may be as high as 20 per cent at 4 months after injury. Among the survivors over 80 years, about half fail to resume independent walking.

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FRACTURES AND JOINT INJURIES

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Avascular necrosis Ischaemic necrosis of the femoral

head occurs in about 30 per cent of patients with displaced fractures and 10 per cent of those with undisplaced fractures. There is no way of diagnosing this at the time of fracture. A few weeks later, an isotope bone scan may show diminished vascularity. X-ray changes may not become apparent for months or even years. Whether the fracture unites or not, collapse of the femoral head will cause pain and progressive loss of function (Figure 29.10). In patients over 45 years, treatment is by total joint replacement.

(a)

(b)

(c)

(d)

(e)

852

(f)

29.10 Fracture of the femoral neck – avascular necrosis (a) The post-reduction x-ray may look splendid but the blood supply is compromised and 6 months later (b) there is obvious necrosis of the femoral head. (c) Section across the excised femoral head, showing the large necrotic segment and splitting of the articular cartilage. (d) Fine detail x-ray of the same. (e,f) Even an impacted fracture, if it is displaced in valgus, can lead to avascular necrosis.

In younger patients, the choice of treatment is controversial. Core decompression has no place in the management of traumatic osteonecrosis. Realignment or rotational osteotomy is suitable for those with a relatively small necrotic segment. Arthrodesis is often mentioned in armchair discussions, but in practice it is seldom carried out. Provided the risks are carefully explained, including the likelihood of at least one revision procedure, joint replacement may be justifiable even in this group. Non-union More than 30 per cent of all femoral neck fractures fail to unite, and the risk is particularly high in those that are severely displaced. There are many causes: poor blood supply, imperfect reduction, inadequate fixation, and the tardy healing that is characteristic of intra-articular fractures. The bone at the fracture site is ground away, the fragments fall apart and the screw cuts out of the bone or is extruded laterally. The patient complains of pain, shortening of the limb and difficulty with walking. The x-ray shows the sorry outcome. The method of treatment depends on the cause of the non-union and the age of the patient. In the relatively young, three procedures are available: (1) if the fracture is nearly vertical but the head is alive, subtrochanteric osteotomy with internal fixation changes the fracture line to a more horizontal angle; (2) if the reduction or fixation was faulty and there are no signs of necrosis, it is reasonable to remove the screws, reduce the fracture, insert fresh screws correctly and also to apply a bone graft across the fracture, either a segment of fibula or a muscle pedicle graft; and (3), if the head is avascular but the joint unaffected, prosthetic replacement may be suitable; if the joint is damaged or arthritic, total replacement is indicated. In elderly patients, only two procedures should be considered: (1) if pain is considerable then the femoral head, no matter whether it is avascular or not, is best removed and (provided the patient is reasonably fit) total joint replacement is performed; (2) if the patient is old and infirm and pain not unbearable, a raised heel and a stout stick or elbow crutch are often sufficient. Osteoarthritis Avascular necrosis or femoral head collapse may lead, after several years, to secondary osteoarthritis of the hip. If there is marked loss of joint movement and widespread damage to the articular surface, total joint replacement will be needed.

Combined fractures of the neck and shaft Young patients with high-energy fractures of both the femoral neck and the ipsilateral femoral shaft present a special problem. Both fractures must be fixed, and

INTERTROCHANTERIC FRACTURES Intertrochanteric fractures are, by definition, extracapsular. As with femoral neck fractures, they are common in elderly, osteoporotic people; most of the patients are women in the 8th decade. However, in contrast to intracapsular fractures, extracapsular trochanteric fractures unite quite easily and seldom cause avascular necrosis.

1. there is poor contact between the fracture fragments, as in four-part intertrochanteric types (greater and lesser trochanter, proximal and distal femoral fragments), or if the posteromedial cortex is comminuted. 2. the fracture pattern is such that forces of weightbearing continually displace the fragments further, as in those with a reverse oblique pattern or with a subtrochanteric extension. 3. osteoporosis leading to poor quality grip by the fixation implants. The importance of fracture pattern is detailed in the classification by Kyle (1994) which distinguishes four basic patterns that reflect increasing instability and increasing difficulty at reduction and fixation (Figure 29.11).

Clinical features The patient is usually old and is unable to stand. The leg is shorter and more externally rotated than with a transcervical fracture (because the fracture is extracapsular) and the patient cannot lift his or her leg.

Mechanism of injury

X-ray

The fracture is caused either by a fall directly onto the greater trochanter or by an indirect twisting injury. The crack runs up between the lesser and greater trochanter and the proximal fragment tends to displace in varus.

Undisplaced, stable fractures may show no more than a thin crack along the intertrochanteric line; indeed, there is often doubt as to whether the bone is fractured and the diagnosis may have to be confirmed by scintigraphy or MRI. More often the fracture is displaced and there may be considerable comminution. The lesser and greater trochanters may be identifiable as separate fragments and this calls for caution; surgery is technically more difficult and, even with modern implants, stable fixation may be hindered because of poor bone quality.

Pathological anatomy Intertrochanteric fractures are divided into stable and unstable varieties. In essence, unstable fractures are those where:

TYPE 1 Undisplaced Uncomminuted

TYPE 2 Displaced Minimal comminuted Lesser trochanter fracture Varus

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Injuries of the hip and femur

there are several ways of doing this. The femoral neck fracture takes priority as complications following this fracture are generally more difficult to address than those of the shaft fracture. Anatomic reduction and stable fixation of the femoral neck fracture must not be compromised in order to accommodate fixation of the shaft fracture. The femoral neck fracture is reduced using closed or, if necessary, open methods. The fracture is fixed using multiple screws. The femoral shaft fracture can then be managed with a retrograde locked intramedullary nail (inserted through the knee) or by a lateral plate inserted in a submuscular fashion.

TYPE 3 Displaced Greater trochanter fracture Comminuted Varus

TYPE 4 Severely comminuted Subtrochanter extension (Also reverse oblique)

29.11 Intertrochanteric fractures – classification Types 1 to 4 are arranged in increasing degrees of instability and complexity. Types 1 and 2 account for the majority (nearly 60 per cent). The reverse oblique type of intertrochanteric fracture represents a subgroup of Type 4; it causes similar difficulties with fixation.

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Treatment Intertrochanteric fractures are almost always treated by early internal fixation – not because they fail to unite with conservative treatment (they unite quite readily), but (a) to obtain the best possible position and (b) to get the patient up and walking as soon as possible and thereby reduce the complications associated with prolonged recumbency. Non-operative treatment may be appropriate for a small group who are too ill to undergo anaesthesia; traction in bed until there is sufficient reduction of pain to allow mobilization can yield reasonable results but much depends on the quality of nursing care and physical therapy (Kaplan, Miyamoto et al. 2008).

(a)

(b)

29.12 Intertrochanteric features Two contrasting types of intertrochanteric fracture. (a) Type 2 fracture: the fracture runs obliquely downwards from the lateral to medial cortex, in this case associated with a lesser trochanter fracture and resulting in a typical varus deformity. This is an unstable fracture. (b) Type 4 ‘reverse oblique’ fracture: here the fracture line runs downwards from medial to lateral cortex, to give an even more unstable geometry.

854

Fracture reduction at surgery is performed on a fracture table that provides slight traction and internal rotation; the position is checked by x-ray and the fracture is fixed with an angled device – preferably a sliding screw in conjunction with a plate or intramedullary nail. Positioning the screw is important if it is to be prevented from cutting out of the osteoporotic bone. It should pass up the femoral neck to end within the centre of the femoral head, with the tip resting about 5 mm from the subchondral bone plate. A ‘tip-apex’ distance is described to identify a ‘sweet-spot’ for positioning this sliding screw: if within 25 mm, there is a lower risk of the screw cutting out of the femoral head (Figure 29.13). The side plate should be long enough to accommodate at least 4 screws below the fracture line. A small lesser trochanteric fragment may be ‘caught’ with additional screws.

(a)

(b)

29.13 Risk of screw cut-out The tip-apex distance is a measure that estimates the risk of screw cut-out from the femoral head. (a,b) It is the sum of the measured distances (after adjustment for magnification on the x-ray) from the tip of the screw to the apex of the femoral head – on both the AP (x) and lateral views (y). The risk of cut-out is low if the sum is less than 25 mm.

With the less common ‘reversed oblique’ fracture (where the fracture line runs downwards obliquely from medial to lateral cortex) there is a tendency for the distal fragment to shift medially under the proximal fragment as the hip screw slides in the barrel; often the screws from the slide plate lose their purchase from the femoral shaft. In these cases a 95 degree screw-plate device or an intramedullary device with a hip screw gives more stable fixation. If closed reduction fails to achieve a satisfactory position, open reduction and manipulation of the fragments will be necessary. A large posteromedial fragment (often including the lesser trochanter) may need additional fixation. The addition of bone grafts may hasten union of the medial cortex. On the occasion that anatomical reduction proves impossible, a valgus osteotomy may be needed to allow the proximal fragment to abut securely against the femoral shaft (Dimon and Hughston 1967) (Figure 29.14 c,d). Postoperatively, exercises are started on the day after operation and the patient allowed up and partial weightbearing as soon as possible.

Complications EARLY Early complications are the same as with femoral neck fractures, reflecting the fact that most of these patients are in poor health. LATE Failed fixation Screws may cut out of the osteoporotic bone if reduction is poor or if the fixation device is incorrectly positioned. If union is delayed, the implant

29

(b)

(c)

(d)

(e)

(f)

29.14 Intertrochanteric fractures – treatment Anatomic reduction is the ideal; but stable fixation is equally important. Types 1 and 2 fractures (a,b) can usually be held in good position with a compression screw and plate. If this is not possible, an osteotomy of the lateral cortex (c,d) will allow a screw to be inserted up to the femoral neck and into the head of the femur; this can be used as a lever to reduce the fracture so that the medial spike of the proximal fragment engages securely into the femoral canal; fixation is completed with a side plate. Reverse oblique fractures (e,f) are inherently unstable even after perfect reduction; here one can use an intramedullary device with an oblique screw that engages the femoral head. (Courtesy of Mr M Manning and Mr JS Albert).

itself may break. In either event, reduction and fixation may have to be re-done. Varus and external rotation deformities are common. Fortunately they are seldom severe and rarely interfere with function. Malunion

Non-union Intertrochanteric fractures seldom fail to unite. If healing is delayed (say beyond 6 months) the fracture probably will not join and further operation is advisable; the fragments are repositioned as anatomically as is feasible, the fixation device is applied more securely and bone grafts are packed around the fracture (Figure 29.15).

(a)

(b)

Injuries of the hip and femur

(a)

Pathological fractures Intertrochanteric fractures may be due to metastatic disease or myeloma. Unless patients are terminally ill, fracture fixation is essential in order to ensure an acceptable quality of life for their remaining years. In addition to internal fixation, methylmethacrylate cement may be packed in the defect to improve stability. If there is involvement of the femoral neck, replacement with a cemented prosthesis may be preferable.

(c)

(d)

29.15 Complications of treatment of intertrochanteric fractures (a,b) Failure to maintain reduction, which can be early – usually in osteoporotic bone or from poor implant seating (c,d). The implant may fracture if union is not timely. Revision surgery is complex and may involve bone grafts and a new implant.

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PROXIMAL FEMORAL FRACTURES IN CHILDREN Hip fractures rarely occur in children but when they do they are potentially very serious. The fracture is usually due to high velocity trauma; for example, falling from a height or a car accident. Pathological fractures sometimes occur through a bone cyst or benign tumour. In children under two years, the possibility of child abuse should be considered. There is a high risk of complications, such as avascular necrosis, premature physeal closure and coxa vara. At birth the proximal end of the femur is entirely cartilaginous and for several years, as ossification proceeds, the area between the capital epiphysis and greater trochanter is unusually vulnerable to trauma. Moreover, between the ages of 4 and 8 the ligamentum teres contributes very little to the blood supply of the epiphysis; hence its susceptibility to post-traumatic ischaemia.

Classification The most useful classification is that of Delbet, which is based on the level of the fracture (Hughes and Beaty 1994). Type I is a fracture-separation of the epiphysis; sometimes the epiphyseal fragment is dislocated from the acetabulum. Type II is a transcervical fracture of the femoral neck; this is the commonest variety, accounting for almost half of the injuries. Type III is a basal (cervico-trochanteric) fracture, the second most common injury. Type IV is an intertrochanteric fracture (Figure 29.16).

Diagnosis can be difficult, especially in infants where the epiphysis is not easily defined on x-ray. Type I

856

Treatment These fractures should be treated as a matter of urgency, and certainly within 24 hours of injury. Initially the hip is supported or splinted while investigations are carried out. Early aspiration of the intracapsular haematoma is advocated by some authors as a means of reducing the risk of epiphyseal ischaemia; however, the benefits are uncertain and the matter is controversial. Undisplaced fractures may be treated by immobilization in a plaster spica for 6–8 weeks. However, fracture position is not always maintained and there is a considerable risk of late displacement and malunion or non-union. Displaced type IV fractures also can be treated nonoperatively: closed reduction, traction and spica immobilization. Careful follow-up is essential; if position is lost, operative fixation will be needed. Type I, II and III fractures are treated by closed reduction and then internal fixation with smooth pins or cannulated screws. ‘Closed reduction’ means one gentle manipulation; if this fails, open reduction is performed. In small children, operative fixation is supplemented by a spica cast for 6–12 weeks.

Complications

Clinical features

(a)

fractures are easily mistaken for hip dislocation. Ultrasonography, MRI and arthrography may help. In older children the diagnosis is usually obvious on plain x-ray examination. It is important to establish whether the fracture is displaced or undisplaced; the former carries a much higher risk of complications. Type IV fractures are the least likely to give rise to complications.

(b)

Avascular necrosis of the femoral head This is the most

common (and most feared) complication; it occurs in

(c)

(d)

29.16 Proximal femoral fractures in children These are the result of strong forces or weak bone, e.g. through cysts. There are 4 types (the Delbet classification), depending on the level of the fracture: (a) Type 1 at the physeal level; (b) Type 2 through the middle of the neck; (c) Type 3 at the base of the neck and (d) Type 4 at the intertrochanteric level.

29

(b)

(c)

(d)

29.17 Femoral neck fractures in children: (a) Fracture of the femoral neck in a child is particularly worrying because, even with perfect fixation (b), there is often ischaemia of the femoral head. This fracture united and the screws were removed (c), but the radioisotope scan shows no activity in the left femoral head (d) i.e. ischaemic necrosis.

about 30 per cent of all cases. Important risk factors are (1) an age of more than 10; (2) a high velocity injury; (3) a type I or II fracture; and (4) displacement. The child complains of pain and loss of movement; x-ray changes usually appear within 3 months of injury. Treatment is problematic. Non-weightbearing, or ‘containment splintage’ in abduction and internal rotation, is sometimes advocated but there is little evidence that this makes any difference. The outcome depends largely on the size of the necrotic area; unfortunately most end up with intrusive pain and marked restriction of movement. Arthrodesis may be advisable, as a late salvage procedure. Coxa vara Femoral neck deformity may result from malunion, avascular necrosis or premature physeal closure. If the deformity is mild, remodelling may take care of it. If the neck-shaft angle is less than 110 degrees, subtrochanteric valgus osteotomy will probably be needed.

Occasionally, the greater trochanter is fractured and the fragment widely separated in a young individual. It can be fixed back in position with cancellous screws or tension band wiring. Full weightbearing is prohibited for 6–8 weeks.

Injuries of the hip and femur

(a)

SUBTROCHANTERIC FRACTURES The part of the femoral shaft around the lesser trochanter is substantially strengthened by a widening cortex and that stout pillar of bone posteromedially, the calcar femorale. Therefore, large forces are needed to cause fractures in this area – and that is usually the case when this injury is diagnosed in young adults. By contrast, in the elderly, who are the second group who sustain this fracture quite frequently, the injury is relatively trivial; here the reason is a weakening of bone in this area by osteoporosis, osteomalacia, Paget’s disease or a secondary deposit.

Diminished growth Physeal damage may result in retarded femoral growth. Limb length equalization may be needed.

ISOLATED FRACTURES OF THE TROCHANTERS In adolescents, the lesser trochanter apophysis may be avulsed by the pull of the psoas muscle; the injury nearly always occurs during hurdling. Treatment is rest, followed by return to activity when comfortable. In the elderly, separation of the lesser trochanter should arouse suspicions of metastatic malignant disease. In the elderly, part of the greater trochanter can be fractured by a direct blow after a fall. The x-ray should be scrutinised for a subtle associated intertrochanteric fracture. In the event this is absent, treatment is nonoperative and functional recovery is usually good.

(a)

(b)

(c)

29.18 Subtrochanteric fractures of the femur – warning signs on the x-ray X-ray findings that should caution the surgeon: (a) comminution, with extension into the piriform fossa; (b) displacement of a medial fragment including the lesser trochanter and, (c) lytic lesions in the femur.

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29.19 Subtrochanteric fractures – internal fixation Several methods of fixation are in use: (a) a 95° screw and plate device; (b) an intramedullary nail with proximal interlocking screw into the femoral head; and (c) a proximal femoral plate with locking screws.

(a)

(b)

Subtrochanteric fractures have several features which make them interesting (and challenging to treat): 1. Blood loss is greater than with femoral neck or trochanteric fractures – the region is covered with anastomosing branches of the medial and lateral circumflex femoral arteries which come off the profunda femoris trunk. 2. There may be subtle extensions of the fracture into the intertrochanteric region, which may influence the manner in which internal fixation can be performed. 3. The proximal part is abducted and externally rotated by the gluteal muscles, and flexed by the psoas. The shaft of the femur has to be brought into a position to match the proximal part or else a malunion is created by internal fixation.

Clinical features The leg lies in neutral or external rotation and looks short; the thigh is markedly swollen. Movement is excruciatingly painful.

X-ray

858

The fracture is through or below the lesser trochanter. It may be transverse, oblique or spiral, and is frequently comminuted. The upper fragment is flexed and appears deceptively short; the shaft is adducted and is displaced proximally. Three important features should be looked for, as the presence of any one will influence treatment: (1) an unusually long fracture line extending proximally towards the greater trochanter and piriform fossa; (2) a large, displaced fragment which includes the lesser trochanter; and (3) lytic lesions in the femur.

(c)

Treatment Traction may help to reduce blood loss and pain. It is an interim measure until the patient, especially if elderly and with multiple medical problems, is stabilized and prepared for surgery. Open reduction and internal fixation is the treatment of choice. Two main types of implant are used for fracture fixation: (a) an intramedullary nail with a proximal interlocking screw that can be directed into the femoral head or placed in the standard manner, and (b) a 95 degree hip screw-and-plate device. Both implants are suitable but there are circumstances where one may be preferable: 1. Intramedullary nails are generally stronger and can tolerate stresses for longer if healing is slow; this may be the case if the fracture is very comminuted or unstable, or if one suspects that operative dissection may have compromised bone viability. 2. An intramedullary nail is also preferable for a pathological fracture; a full-length nail should be used as there may be tumour deposits in the distal part of the femur. Key points to bear in mind when operating on these fractures are: (a) an anatomic reduction will provide the greatest surface area of contact between the fragments and reduce stresses on the implant; with intramedullary nails this has to be achieved before reaming is commenced; (b) as little soft-tissue dissection as possible to accomplish reduction should be performed; and (c) it is important that the integrity of the medial cortex (around the lesser trochanter) be established, particularly if a hip screw-and-plate device is used. Proximal interlocking screws with intramedullary nails should be directed into the femoral head if the fracture pattern extends above the lesser trochanter. If

Complications Malunion Varus and rotational malunions are fairly common. This can be prevented by careful attention to accurate reduction before internal fixation is applied. If the degree of malunion produces symptoms, it may need operative correction. Non-union This occurs in about 5 per cent of cases; it will require operative correction of any deformity, renewed fixation and bone grafting.

FEMORAL SHAFT FRACTURES The femoral shaft is circumferentially padded with large muscles. This provides advantages and disadvantages: reduction can be difficult as muscle contraction displaces the fracture; however, healing potential is improved by having this well-vascularized sleeve containing a source of mesenchymal stem cells, and open fractures often need no more than split thickness skin grafts to obtain satisfactory cover.

Mechanism of injury This is usually a fracture of young adults and results from a high energy injury. Diaphyseal fractures in

elderly patients should be considered ‘pathological’ until proved otherwise. In children under 4 years the possibility of physical abuse must be kept in mind. Fracture patterns are clues to the type of force that produced the break. A spiral fracture is usually caused by a fall in which the foot is anchored while a twisting force is transmitted to the femur. Transverse and oblique fractures are more often due to angulation or direct violence and are therefore particularly common in road accidents. With severe violence (often a combination of direct and indirect forces) the fracture may be comminuted, or the bone may be broken in more than one place (a segmental fracture).

Pathological anatomy Most fractures of the femoral shaft have some degree of comminution, although it is not always apparent on x-ray. Small bone fragments, or a single large ‘butterfly’ fragment, may separate at the fracture line but usually remain attached to the adjacent soft tissue and retain their blood supply. With more extensive comminution there is no point of firm contact between proximal and distal fragments and the fracture is completely unstable (Figure 29.20). This is the basis of a helpful classification (Winquist, Hansen et al. 1984). Fracture displacement often follows a predictable pattern dictated by the pull of muscles attached to each fragment.

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Injuries of the hip and femur

the fracture enters the piriformis fossa, then an intramedullary nail designed to be inserted at the tip of the greater trochanter is better; alternatively a 95 degree hip screw-and-plate device can be used. Postoperatively the patient is allowed partial weightbearing (with crutches) until union is secure. It is rarely feasible to impose significant weightbearing restrictions on the elderly and it would be better to choose a stronger implant (and ensure a nearanatomic reduction of the fracture) so that early loading can be tolerated.

• In proximal shaft fractures the proximal fragment is flexed, abducted and externally rotated because of gluteus medius and iliopsoas pull; the distal fragment is frequently adducted. • In mid-shaft fractures the proximal fragment is again flexed and externally rotated but abduction is less marked. • In lower third fractures the proximal fragment is adducted and the distal fragment is tilted by gastrocnemius pull.

29.20 Femoral shaft fractures – classification Winquist’s classification reflects the observation that the degrees of soft-tissue damage and fracture instability increase with increasing grades of comminution. In Type 1 there is only a tiny cortical fragment. In Type 2 the ‘butterfly fragment’ is larger but there is still at least 50 per cent cortical contact between the main fragments. In Type 3 the butterfly fragment involves more than 50 per cent of the bone width. Type 4 is essentially a segmental fracture.

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The soft tissues are always injured and bleeding from the perforators of the profunda femoris may be severe. Over one litre may be lost into the tissues and, in the case of bilateral femoral shaft fractures, the patient can become hypotensive quickly if not adequately resuscitated. Beware of the fracture at the junction of the middle and distal thirds of the femoral shaft – it can be responsible for damaging the femoral artery in the adductor canal.

Clinical features There is swelling and deformity of the limb, and any attempt to move the limb is painful. With the exception of a fracture through pathological bone, the large forces needed to break the femur usually produce accompanying injuries nearby and sometimes further afield. Careful clinical scrutiny is necessary to exclude neurovascular problems and other lower limb or pelvic fractures. An ipsilateral femoral neck fracture occurs in about 10 per cent of cases and, if present, there is a one in three chance of a significant knee injury as well. The combination of femoral shaft and tibial shaft fractures on the same side, producing a ‘floating knee’, signals a high risk of multi-system injury in the patient. The effects of blood loss and other injuries, some of which can be life-threatening, may dominate the clinical picture.

X-ray It may be difficult to obtain adequate views in the Accident and Emergency Room setting, especially views that provide reliable information on proximal or distal fracture extensions or joint involvement; these can be postponed until better facilities and easier patient positioning are possible. But never forget to xray the hip and knee as well (Figure 29.21). A baseline chest x-ray is useful as there is a risk of adult respiratory distress syndrome (ARDS) in those with multiple injuries. The fracture pattern should be noted; it will form a guide to treatment.

Emergency treatment

860

Traction with a splint is first aid for a patient with a femoral shaft fracture. It is applied at the site of the accident, and before the patient is moved. A Thomas’ splint, or one of the modern derivations of this practical device, is ideal: the leg is pulled straight and threaded through the ring of the splint; the shod foot is tied to the cross-piece so as to maintain traction and the limb and splint are firmly bandaged together. This temporary stabilization helps to control pain, reduces bleeding and makes transfer easier. Shock should be treated; blood volume is restored and maintained, and

(a)

(b)

29.21 Femoral shaft fractures – diagnosis (a) The upper fragment of this femur is adducted, which should alert the surgeon to the possibility of (b) an associated hip dislocation. With this combination of injuries the dislocation is frequently missed; the safest plan is to x-ray the pelvis with every fracture of the femoral shaft.

a definitive plan of action instituted as soon as the patient’s condition has been fully assessed.

Definitive treatment The patient with multiple injuries The association of

femoral shaft fractures with other injuries, including head, chest, abdominal and pelvic trauma, increases the potential for developing fat embolism, ARDS and multi-organ failure. The risk of systemic complications can be significantly reduced by early stabilization of the fracture, usually by a locked intramedullary nail. However, surgery to introduce a reamed intramedullary nail may produce untoward effects in those with severe chest injuries, especially when carried out within 24 hours of the fracture. It is thought the trauma of surgery and blood loss induces inflammatory changes that may increase both morbidity and mortality – this phenomenon is called ‘the second hit’, referring to a second episode of trauma, albeit surgical, on the patient. Consequently, in the multiplyinjured patient, particularly one with severe chest trauma, prompt stabilization with an external fixator may be wise; the fixator can be exchanged for an intramedullary nail when the patient’s condition stabilizes. The timing of this second procedure is problematic. Some guidance can be sought from measurement of circulating levels of interleukin-6, a pro-inflammatory cytokine (Pape, van Griensven et al.

THE ISOLATED FEMORAL SHAFT FRACTURE Traction, bracing and spica casts Traction can reduce and hold most fractures in reasonable alignment, except those in the upper third of the femur. Joint mobility can be ensured by active exercises. The chief drawback is the length of time spent in bed (10–14 weeks for adults) with the attendant problems of keeping the femur aligned until sufficient callus has formed plus reducing patient morbidity and frustration. Some of these difficulties are overcome by changing to a plaster spica or – in the case of lower third fractures – functional bracing when the fracture is ‘sticky’, usually around 6–8 weeks.

(a)

(b)

(c)

(d)

The main indications for traction are (1) fractures in children; (2) contraindications to anaesthesia; and (3) lack of suitable skill or facilities for internal fixation. It is a poor choice for elderly patients, for pathological fractures and for those with multiple injuries. The various methods of traction are described in Chapter 23. For young children, skin traction without a splint is usually all that is needed. Infants less than 12 kg in weight are most easily managed by suspending the lower limbs from overhead pulleys (‘gallows traction’), but no more than 2 kg weight should be used and the feet must be checked frequently for circulatory problems. Older children are better suited to Russell’s traction (Chapter 23) or use of a Thomas’ splint. Fracture union will have progressed sufficiently by 2–4 weeks (depending on the age of the child) to permit a hip spica to be applied and the child is then allowed up. Consolidation is usually complete by 6–12 weeks. Adults (and older adolescents) require skeletal traction through a pin or a tightly strung Kirschner wire behind the tibial tubercle. Traction (8–10 kg for an adult) is applied over pulleys at the foot of the bed. The limb is usually supported on a Thomas’ splint and a flexion piece allows movement at the knee (Figure 29.22). However, a splint is not essential; indeed, skeletal traction without a splint (Perkins’ traction) has the advantages of producing less distortion of the fracture and allowing freer movement in bed (Figure 29.23). Exercises are begun as soon as possible.

29.22 Femoral fractures – treatment by traction (a) Fixed traction on a Thomas’ splint: the splint is tied to the foot of the bed which is elevated. This method should be used only rarely because the knee may stiffen; (b) this was the range in such a case when the fracture had united. (c,d) Balanced traction: one way to minimize stiffness is to use skeletal balanced traction; the lower slings can be removed to permit knee flexion while traction is still maintained.

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Injuries of the hip and femur

2001); when the levels start to decrease, it should be safe to perform ‘second hit’ interventions. Clinically this occurs around 5–7 days after admission, but this window is by no means applicable to all patients nor is it conclusive at this time. Performing the exchange to an intramedullary nail also carries the risk of transferring contaminants from pin sites to the intramedullary nail; the earlier the operation is performed, the lower the risk. In the patient who spends a protracted period in the intensive care unit, it may be safer to use external fixation as definitive treatment, perhaps with a return to theatre later to allow insertion of new pins to increase the stability of the construct.

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(b)

(f) (c)

(a)

(d)

(e)

(g)

29.23 Femoral fractures – treatment by traction Even in the adult, traction without a splint can be satisfactory, but skeletal traction is essential. The patient with this rather unstable fracture (a) can lift his leg and exercise his knee (b,c,d). At no time was the leg splinted, but clearly the fracture has consolidated (e), and the knee range (f) is only slightly less than that of the uninjured left leg (g).

Once the fracture is sticky (at about 8 weeks in adults) traction can be discontinued and the patient allowed up and partial weightbearing in a cast or brace. For fractures in the upper half of the femur, a plaster spica is the safest but it will almost certainly prolong the period of knee stiffness. For fractures in the lower half of the femur, cast-bracing is suitable. This type of protection is needed until the fracture has consolidated (16–24 weeks).

862

Plate and screw fixation Plating is a comparatively easy way of obtaining accurate reduction and firm fixation. The method was popular at one time but went out of favour because of a high complication rate. This occurred when plates were applied through a wide open exposure of the fracture site and perfect anatomical reduction of all bone pieces. Such extensive surgery damaged the healing potential and led to tardy union and implant failure. However, plates have encountered resurgence: today, they are inserted through short incisions and placed in a submuscular plane, rather than deep to periosteum; an indirect (closed) reduction of the fracture is done; fewer screws are used, and usually placed at the ends of the plate, leading to a less rigid hold on the fracture. This technique of minimally invasive plate osteosynthesis (MIPO) has led to better union rates. However, postoperative weightbearing will need to be modified as the implant is not as strong as an intramedullary nail. The main indications for plates are (1) fractures at

either end of the femoral shaft, especially those with extensions into the supracondylar or pertrochanteric areas, (2) a shaft fracture in a growing child, and (3) a fracture with a vascular injury which requires repair (Figure 29.24). Intramedullary nailing Intramedullary nailing is the

method of choice for most femoral shaft fractures. However, it should not be attempted unless the appropriate facilities and expertise are available. The basic implant system consists of an intramedullary nail (in a range of sizes) which is perforated near each end so that locking screws can be inserted transversely at the proximal and distal ends; this controls rotation and length, and ensures stability even for subtrochanteric and distal third fractures (Figure 29.25). These important details should be remembered when using locked intramedullary nails: 1. Reamed nails have a lower need for revision surgery when compared to unreamed nails. 2. Select a nail that is approximately the size of the medullary isthmus so that it fills the canal reasonably well (after reaming) and adds to stability – small diameter nails are quicker to insert but more frequently lead to the need for revision surgery. 3. Consider alternative means of fracture fixation if the isthmus is so narrow that a large amount of canal reaming will have to be done in order to fit the smallest diameter nail available.

29

(b)

(c)

(d)

(e)

29.24 Plate fixation – past and present (a,b) Plate fixation was popular in the past, but it fell out of favour because of the high complication rate (c). Modern techniques of minimally invasive plate osteosynthesis (d,e) have shown that it still has place in the treatment of certain types of femoral shaft fracture.

4. Use a nail of sufficient length to fully span the canal. 5. Antegrade insertion (through either the piriformis fossa or the tip of the greater trochanter, depending on the design of nail) or retrograde insertion (through the intercondylar notch distally) are equally suitable techniques to use; there is a small incidence of hip and thigh pain with antegrade nails, whereas there is a small problem with knee pain with retrograde nails. Retrograde insertion of intramedullary nails is particularly useful for: obese patients; when there are bilateral femoral shaft fractures (as the procedure can be performed without the need for a fracture table and the added time for setting up

(a)

(b)

(c)

(d)

Injuries of the hip and femur

(a)

for each side); when there is a tibial shaft fracture on the same side; and if there is a femoral neck fracture more proximally, as screws can be inserted to hold this fracture without being impeded by the nail. Stability is improved by using interlocking screws; all locking holes in the nail should be used. Often there is enough shared stability between the nail and fracture ends to allow some weightbearing early on. The fracture usually heals within 20 weeks and the complication rate is low; sometimes malunion (more likely malrotation) or delayed union (from leaving the fracture site over-distracted) occurs.

(e)

29.25 Intramedullary nailing Nowadays this is the commonest way of treating femoral shaft fractures. Ideally a range of designs to suit different types of fracture should be available. (a,b) Antegrade nailing with insertion of the nail through the pyriform fossa and transverse locking screws proximally and distally. (c) Retrograde nailing with insertion of the nail through the intercondylar notch at the knee – useful for obese patients and those with bilateral femoral fractures. (d,e) Proximal locking can be achieved in other ways e.g. by using parallel screws or a sliding hip screw.

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Open medullary nailing is a feasible alternative where facilities for closed nailing are lacking. A limited lateral exposure of the femur is made; the fracture is reduced and a guidewire is passed between the main proximal and distal fragments. A small exposure to achieve reduction does not significantly affect the risk of complications or fracture healing as compared to ‘closed’ nailing. External fixation The main indications for external fixation are (1) treatment of severe open injuries; (2) management of patients with multiple injuries where there is a need to reduce operating time and prevent the ‘second hit’; and (3) the need to deal with severe bone loss by the technique of bone transport. External fixation is also useful for (4) treating femoral fractures in adolescents (Figure 29.26). Like closed intramedullary nailing, it has the advantage of not exposing the fracture site and small amounts of axial movement can be applied to the bone by allowing a telescoping action in the fixator body (with some designs of external fixator). As the callus increases in volume and quality, the fixator can be adjusted to increase stress transfer to the fracture site, thus promoting quicker consolidation. However, there are still problems with pin-site infection, pin loosening and (if the half-pins are applied close to joints) limitation of movement due to interference with sliding structures. The patient is allowed up as soon as he or she is comfortable and knee movement exercises are encouraged to prevent tethering by the half pins. Partial weightbearing is usually possible immediately but this will depend on the x-ray appearance of callus – this may take some time (more than 6 weeks) if the fixator is a rigid device. Most femoral shaft fractures will unite in under 5 months but some take longer if the fracture is badly comminuted or contact between fracture ends is poor.

Treatment of open fractures Open femoral fractures should be carefully assessed for (1) skin loss; (2) wound contamination; (3) muscle ischaemia; and (4) injury to vessels and nerves. The immediate treatment is similar to that of closed fractures; in addition, the patient is started on intravenous antibiotics. The wound will need cleansing: it should be extended to give unhindered access, contaminated areas and dead tissue must be excised and the entire area should be washed thoroughly. Stabilization of open femoral shaft fractures is best achieved with locked intramedullary nails unless there is heavy contamination or bone loss – in which case external fixation (if necessary with the capacity to deal with bone loss through distraction osteogenesis) is preferable.

Complex injuries FRACTURES ASSOCIATED WITH VASCULAR INJURY Warning signs of an associated vascular injury are (1) excessive bleeding or haematoma formation; and (2) paraesthesia, pallor or pulselessness in the leg and foot. Do not accept ‘arterial spasm’ as a cause of absent pulses; the fracture level on x-ray will indicate the region of arterial damage and arteriography may only delay surgery to re-establish perfusion. Most femoral fractures with vascular injuries will have had warm ischaemia times greater than 2–3 hours by the time the patient arrives in the operating theatre; when this exceeds 4– 6 hours, salvage may not be possible and the risk of amputation rises. This means that diagnosis must be prompt and re-establishing perfusion a priority; fracture stabilization is secondary. A recommended sequence for treatment, particularly if the warm ischaemia time is approaching the salvage threshold, is (a) to create a shunt from the femoral vessels in the groin to beyond the point of 29.26 External fixation for femoral shaft fractures in older children (a–c) External fixation is an option for treating femoral shaft fractures in adolescents. Elastic stable intramedullary nails shown in Fig 29.31 may not be strong enough for this heavier group of teenagers.

864

(a)

(b)

(c)

FRACTURE ASSOCIATED WITH KNEE INJURY Femoral fractures are frequently accompanied by injury to the ligaments of the knee. Direct blows to the knee from the dashboard of a car in an accident will damage knee ligaments as well as break the femoral shaft and femoral neck – this triad of problems should be recognized. With attention focused on the femur, the knee injury is easily overlooked, only to re-emerge as a persistent complaint weeks or months later. As soon as the fracture has been stabilized, the knee should be carefully examined and any associated abnormality treated. ‘FLOATING KNEE’ Ipsilateral fractures of the femur and tibia may leave the knee joint ‘floating’. This is a very serious situation, and other injuries are often present. Both fractures will need immediate stabilization – an anterior approach to the knee joint will allow both fractures to be stabilized by intramedullary nails – retrograde for the femur and antegrade for the tibia. It is usual to fix the femur first. COMBINED NECK AND SHAFT FRACTURES This is dealt with on page 850. The most important thing is diagnosis: always examine the hip and obtain

(a)

(b)

(c)

an x-ray of the pelvis. Both sites must be stabilized, first the femoral neck and then the femur. Parallel screw fixation of the femoral neck followed by retrograde femoral nailing is a useful way to treat this problem. PATHOLOGICAL FRACTURES Fractures through metastatic lesions should be fixed by intramedullary nailing. Provided the patient is fit enough to tolerate the operation, a short life expectancy is not a contraindication. ‘Prophylactic fixation’ is also indicated if a lytic lesion is (a) greater than half the diameter of the bone; (b) longer than 3 cm on any view, or (c) painful, irrespective of its size. Paget’s disease, fibrous dysplasia or rickets may present a problem. The femur is likely to be bowed and, in the case of Paget’s disease, abnormally hard. An osteotomy to straighten the femur may be necessary to allow a nail to be inserted fully (Figure 29.27).

29

Injuries of the hip and femur

injury using plastic catheters; (b) to stabilize the fracture (usually by plating or external fixation) and then (c) to carry out definitive vascular repair. This sequence establishes blood flow quickly and permits fracture fixation and vascular repair to be carried out without pressure of time.

PERIPROSTHETIC FRACTURES Femoral shaft fractures around a hip implant are uncommon; they may happen during primary hip surgery when reaming or preparing the medullary canal, or when forcing in an over-sized uncemented prosthesis, or during revision surgery while extracting cement or attempting to dislocate the hip if the soft tissue release has been insufficient. Sometimes the fracture occurs much later, and there are usually x-ray signs of osteolysis or implant loosening suggesting a reason for bone weakness.

(d)

(e)

29.27 Pathological fractures – internal fixation (a) Metastatic tumour, nailed before it actually causes a fracture. (b) Fibrous dysplasia with a stress fracture; (c) nailing provided the opportunity to correct the deformity. (d,e) Paget’s disease, with a fracture; in this case (because of its site) treated by fixation with a plate and screws.

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If the prosthesis is worn or loose, it should be removed and replaced by one with a long stem, thereby treating both problems. If the primary implant is neither loose nor worn it can be left in place and the fracture treated by plate fixation with structural allografts bridging the fracture (Figure 29.28).

Complications of femoral shaft fractures All the complications described in Chapter 23, with the exception of visceral injury and avascular necrosis, are encountered in femoral shaft fractures. The more common ones are as follows. EARLY Shock One or two litres of blood can be lost even with a closed fracture, and if the injury is bilateral shock may be severe. Prevention is better than cure; most patients will require a transfusion.

Fracture through a large marrow-filled cavity almost inevitably results in small showers of fat emboli being swept to the lungs. This can usually be accommodated without serious consequences, but in some cases (and especially in those with multiple injuries and severe shock, or in patients with associated chest injuries) it results in progressive respiratory distress and multi-organ failure (adult res-

Fat embolism and ARDS

(a)

866

(b)

piratory distress syndrome). Blood gases should be measured if this is suspected and signs such as shortness of breath, restlessness or a rise in temperature or pulse rate should prompt a search for petechial haemorrhages over the upper body, axillae and conjunctivae. Treatment is supportive, with the emphasis on preventing hypoxia and maintaining blood volume. Thromboembolism Prolonged traction in bed predisposes to thrombosis. Movement and exercise are important in preventing this, but high-risk patients should be given prophylactic anticoagulants as well. Vigilance is needed and full anticoagulant treatment is started immediately if thigh or pelvic vein thrombosis is diagnosed. Infection In open injuries, and following internal fixa-

tion, there is always a risk of infection. Prophylactic antibiotics and careful attention to the principles of fracture surgery should keep the incidence below 2 per cent. If the bone does become infected, the patient should be treated as for an acute osteomyelitis. Antibiotic treatment may suppress the infection until the fracture unites, at which time the femoral nail can be removed and the canal reamed and washed out. However, if there is pus or a sequestrum, a more radical approach is called for: the wound is explored, all dead and infected tissue is removed and the nail as well; the

(c)

(d)

29.28 Periprosthetic fracture This patient had two successive fractures around his hip prosthesis. The first was held with cerclage wires (a,b). As the prosthesis was secure in the femur the second fracture was fixed with a plate and screws (c,d).

LATE Delayed union and non-union The time-scale for declaring a delayed or non-union can vary with the type of injury and the method of treatment. If there is failure to progress by 6 months, as judged by serial x-rays, then intervention may be needed. A common practice is to remove locking screws from the intramedullary nail to enable the fracture to ‘collapse’ (‘dynamise’ in modern orthopaedic parlance). This can be successful in a small proportion of cases; more often it fails and results in pain as rotational control of the fracture is lost (the femur is often subject to torsional forces in walking). A better course is to remove the nail, ream the medullary canal and introduce a larger diameter nail – exchange nailing. Bone grafts should be added to the fracture site if there are gaps not closed at the revision procedure.

(a)

(b)

Malunion Fractures treated by traction and bracing often develop some deformity; no more than 15 degrees of angulation should be accepted (Figure 29.29). Even if the initial reduction was satisfactory, until the x-ray shows solid union the fracture is too insecure to permit weightbearing; the bone will bend and what previously seemed a satisfactory reduction may end up with lateral or anterior bowing. Malunion is much less likely in those treated with static interlocked nails; yet it does still occur – especially malrotation – and this can be prevented only by meticulous intra-operative and post-operative assessment followed, where necessary, by immediate correction. Shortening is seldom a major problem unless there was bone loss; if it does occur, treatment will depend on the amount and its clinical impact – sometimes all that is needed is a built-up shoe.

The knee is often affected after a femoral shaft fracture. The joint may be injured at the same time, or it stiffens due to soft-tissue adhesions during treatment; hence the importance of repeated evaluation and early physiotherapy.

Joint stiffness

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Injuries of the hip and femur

canal is reamed and washed out and the fracture is then stabilized by an external fixator. Replacement of the external fixator by another intramedullary nail can be risky, and much depends of the nature of the infecting organism (its sensitivity or resistance to antibiotics), the length of time during which the infection has been present and the quality of the surgical debridement. The long-term management of chronic osteomyelitis is discussed in Chapter 2.

Fractures which heal with abundant callus are unlikely to recur. By contrast, in those treated by internal fixation, callus formation is often slow and meagre. With delayed union or non-

Refracture and implant failure

(c)

(d)

29.29 Malalignment after treatment Treatment of femoral shaft fractures by traction can produce good results but, in some, a malunion can lead to symptoms. In this patient (a,b) the varus deformity produced knee symptoms from overloading of the medial compartment; this was relieved by corrective osteotomy and intramedullary nailing (c,d).

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union, the integrity of the femur may be almost wholly dependent on the implant and sooner or later it will fail. If a comminuted fracture is plated, bone grafts should be added and weightbearing delayed so as to protect the plate from reaching its fatigue limit too soon. Intramedullary nails are less prone to break. However, sometimes they do, especially with a slowhealing fracture of the lower third and a static locked nail; the break usually occurs through the screw-hole closest to the fracture. Treatment consists of replacing the nail and adding bone grafts. In resistant cases, the fracture site may need excising (as viability of the bone ends is poor) followed by distraction osteogenesis which simultaneously stabilizes the limb and deals with the length discrepancy (Figure 29.30).

FEMORAL SHAFT FRACTURES IN CHILDREN Mechanism Fractures of the femur are quite common in older children and are usually due to direct violence (e.g. a road accident) or a fall from a height. However, in

(a)

868

(b)

children under 2 years of age the commonest cause is child abuse; if there are several fractures in different stages of healing, this is very suspicious. Pathological fractures are common in generalized disorders such as spina bifida and osteogenesis imperfecta, and with local bone lesions (e.g. a benign cyst or tumour).

Treatment The principles of treatment in children are the same as in adults but it should be emphasized that in young children open treatment is rarely necessary. The choice of closed method depends largely on the age and weight of the child. As children get older (and larger), fractures take longer to heal and conservative treatment is more likely to result in problems associated with long hospitalization and a greater risk of malunion (Poolman, Kocher et al. 2006). Coupled to this is the cost of protracted bed occupancy. Consequently there has been a trend towards treating femoral shaft fractures in older children by operation, but the argument is flawed if this is based on cost alone – many of these children will have to return for implant removal. Perhaps it is the risk of malunion, particularly in unstable fracture patterns, that renders

(c)

(d)

29.30 Implant failure and non-union (a) This was an open injury with poor vascularity of the fracture ends. It was fixed with an intramedullary nail in the hope that it might unite. It didn’t, and one of the proximal screws broke. The fracture ends were excised; an external fixator was applied (b); and an osteotomy was performed lower down (c); then the fracture ends were brought together with distraction osteogenesis at the osteotomy site. The fracture united (d).

surgery a better option for older children and adolescents.

(a)

(b)

Operative treatment This is growing in popularity as there is: (1) a shorter in-patient stay (and for the child, a quick return home); (2) a lower incidence of malunion. Against this is the added risk of surgery, taking into account that many such fractures have good results when treated non-operatively. The tendency to adopt this approach in older children and adolescents may be justified. Surgical options include fixation with flexible intramedullary nails or trochanteric entry-point rigid nails with interlocking screws (neither of which damages the physes), plates inserted by the MIPO technique and external fixation (Figure 29.31).

Complications

29

Injuries of the hip and femur

Traction and casts Infants need no more than a few days in balanced traction, followed by a spica cast for another 3–4 weeks. Angulation of up to 30 degrees can be accepted, as the bone remodels quite remarkably with growth. Immediate spica casting has also found favour and this approach does not appear to increase the risk of complications. Children between 2 and 10 years of age can be treated either with balanced traction for 2–3 weeks followed by a spica cast for another 4 weeks, or by early reduction and a spica cast from the outset. Shortening of 1–2 cm and angulation of up to 20 degrees are acceptable. Teenagers require somewhat longer (4–6 weeks) in balanced traction, and those aged over 15 (or even younger adolescents if they are large and muscular) may need skeletal traction. Once the fracture feels firm, traction is exchanged for either a spica cast (in the case of upper third and mid-shaft fractures) or a cast-brace (for lower third fractures), which is retained for a further 6 weeks. The position should be checked every few weeks; the limit of acceptable angulation in this age group is 15 degrees in the anteroposterior x-ray and 25 degrees in the lateral.

If a satisfactory reduction cannot be achieved by traction, internal (plates or flexible intramedullary nails) or external fixation is justified. This applies to older children and those with multiple injuries.

Shortening Overlapping and comminution of the bone fragments may shorten the femur. However, anything up to 2 cm is quite acceptable in young children; indeed, some surgeons regard this as an advantage because there is a tendency for the fractured bone to grow faster for up to 2 years after the injury. This may be related to stimulation of the physes

(c)

(d)

29.31 Fixation techniques for femoral shaft fractures in children Non-operative treatment is safest for children. If surgery is indicated, options include: (a) flexible nailing; (b) trochanteric entry-point rigid nails; (c) plates and screws inserted by the minimally invasive percutaneous osteosynthesis (MIPO) technique and, (d) external fixation.

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derived from the increased blood flow that accompanies fracture healing. Unfortunately, the effect on growth is unpredictable.

should always be checked to ensure the popliteal artery was not injured in the fracture.

Angulation can usually be tolerated within the limits mentioned above. However, the fact that bone modelling is excellent in children is no excuse for casual management; bone may be forgiving but parents are not! Certainly rotational malunion is not corrected by growth or remodelling. It is probably wise to observe a malunited fracture for 2 years before offering corrective osteotomy.

to miss a proximal fracture or dislocated hip. The supracondylar fracture pattern will vary. Of importance are: (a) whether there is a fracture into the joint and if it is comminuted; (b) the size of the distal segment; and (c) whether the bone is osteoporotic. These factors influence the type of internal fixation required, if that is the chosen mode of treatment.

FRACTURES AND JOINT INJURIES

Malunion

Treatment

SUPRACONDYLAR FRACTURES OF THE FEMUR Supracondylar fractures of the femur are encountered (a) in young adults, usually as a result of high energy trauma, and (b) in elderly, osteoporotic individuals.

Mechanism and pathological anatomy Direct violence is the usual cause. The fracture line is just above the condyles, but may extend between them. In the worst cases the fracture is severely comminuted. A useful classification is from the AO group: type A fractures have no articular splits and are truly ‘supracondylar’; type B fractures are simply shear fractures of one of the condyles; and type C fractures have supracondylar and intercondylar fissures (Figure 29.32). Gastrocnemius, arising from the posterior surface of the distal femur, will tend to pull the distal segment into extension, thus risking injury to the popliteal artery.

Clinical features The knee is swollen because of a haemarthrosis – this can be severe enough to cause blistering later. Movement is too painful to be attempted. The tibial pulses

(a)

870

X-RAY The entire femur should be x-rayed so as not

(b)

(c)

29.32 The AO classification of supracondylar fractures (a) Type A fractures do not involve the joint surface; (b) type B fractures involve the joint surface (one condyle) but leave the supracondylar region intact; (c) type C fractures have supracondylar and condylar components.

Non-operative If the fracture is only slightly displaced

and extra-articular, or if it reduces easily with the knee in flexion, it can be treated quite satisfactorily by traction through the proximal tibia; the limb is cradled on a Thomas’ splint with a knee flexion piece and movements are encouraged. If the distal fragment is displaced by gastrocnemius pull, a second pin above the knee, and vertical traction, will correct this. At 4–6 weeks, when the fracture is beginning to unite, traction can be replaced by a cast-brace and the patient allowed up and partially weightbearing with crutches. Nonoperative treatment should be considered as an option if the patient is young or the facilities and skill to treat by internal fixation are absent. Elderly patients tend not do as well with the 6 weeks of enforced recumbency. Surgery Operative treatment with internal fixation

can enable accurate fracture reduction, especially of the joint surface, and early movement. If the necessary facilities and skill are available, this is the treatment of choice. For the elderly, early mobilization is so important that internal fixation is almost obligatory. Sometimes the hold on osteoporotic bone is poor (despite modern implant designs) or the patient may be old and frail, making early mobilization difficult or risky, but nursing in bed is made easier and knee movements can be started sooner. Several different devices are available: 1. Locked intramedullary nails which are introduced retrograde through the intercondylar notch – these are suitable for the type A and simpler type C fractures 2. Plates that are applied to the lateral surface of the femur: traditional angled blade-plates or 95 degree condylar screw-plates. They are suitable for type A and the simpler type C fractures. For severely comminuted type C fractures, the newer plate designs with locking screws appear to offer an advantage over other implants; they provide adequate stability, even in the presence of osteoporotic bone, but (as with compression plates) unprotected weightbearing is best avoided until union is assured.

Knee movements are started soon after operation, if wound healing allows. This limits adhesions forming within the knee joint.

Complications EARLY Arterial damage There is a small but definite risk of arterial damage and distal ischaemia. Careful assessment of the leg and peripheral pulses is essential, even if the x-ray shows only minimal displacement.

LATE Joint stiffness Knee stiffness – probably due to scarring

(a)

from the injury and the operation – is almost inevitable. A long period of exercise is needed in all cases, and even then full movement is rarely regained. For marked stiffness, arthroscopic division of adhesions in the joint or even a quadricepsplasty may be needed.

(b)

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Injuries of the hip and femur

3. Simple lag screws – these suffice for type B fractures and are inserted in parallel, with the screw heads buried within the articular cartilage to avoid abrading the opposing joint surface. They are also used to hold the femoral condyles together in type C fractures before intramedullary nails or lateral plates are used to hold the main supracondylar break (Figure 29.33).

Malunion Internal fixation of these fractures is difficult and malunion – usually varus and recurvatum – is not uncommon. Corrective osteotomy may be needed for patients who are still physically active.

(c)

(d)

29.33 Femoral condyle fractures – treatment (a) A single condylar fracture can be reduced open and held with Kirschner wires preparatory to (b) inserting compression screws. (c) T- or Y-shaped fractures are best fixed with a dynamic condylar screw and plate (d).

Non-union Modern surgical techniques of internal fixation recognize the importance of minimizing damage to the soft tissues around the fracture; where possible, only those parts that are essential for fracture reduction are exposed. The knee joint may need to be opened for reduction of articular fragments but the metaphyseal area is left untouched in order to preserve its vitality. If these precautions are taken, nonunion is unlikely. If non-union does occur, autogenous bone grafts and a revision of internal fix-

(a)

(b)

(e) (c)

(f)

(g)

(d)

29.34 Supracondylar fractures (a–c) These fractures can sometimes be treated successfully by traction through the upper tibia. (d–g) If the bone is not too osteoporotic, internal fixation is often preferable and the patient can get out of bed sooner: a dynamic condylar screw and plate for a Type A fracture (d) and a combination of lag screws and a lateral side plate for more complex fracture patterns (e,f,g).

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ation will be needed – particularly if there are signs that the fixation is working loose or has failed. Knee stiffness is another threat. Unless great care is exercised during mobilization, the ultimate range of movement at the knee may be less than that at the fracture!

FRACTURE-SEPARATION OF DISTAL FEMORAL EPIPHYSIS In the childhood or adolescent equivalent of a supracondylar fracture, the lower femoral epiphysis may be displaced – either to one side (usually laterally) by forced angulation of the straight knee or forwards by a hyperextension injury. Although not nearly as common as physeal fractures at the elbow or ankle, this injury is important because of its potential for causing abnormal growth and deformity of the knee. The fracture is usually a Salter–Harris type 2 lesion – i.e. physeal separation with a large triangular metaphyseal bone fragment (Figure 29.35). Although this type of fracture usually has a good prognosis, asymmetrical growth arrest is not uncommon and the child may end up with a valgus or varus deformity. All grades of injury, but especially Salter–Harris types 3 and 4, may result in femoral shortening. Nearly 70 per cent of the femur’s length is derived from the distal physis, so an early arrest can present a major problem.

Clinical features The knee is swollen and perhaps deformed. The pulses in the foot should be palpated because, with

forward displacement of the epiphysis, the popliteal artery may be obstructed by the lower femur.

Treatment The fracture can usually be perfectly reduced manually, but further x-ray checks will be needed over the next few weeks to ensure that reduction is maintained. Occasionally open reduction is needed; a flap of periosteum may be trapped in the fracture line. Salter– Harris types 3 and 4 should be accurately reduced and fixed. If there is a tendency to redisplacement, the fragments may be stabilized with percutaneous Kirschner wires or lag screws driven across the metaphyseal spike. The limb is immobilized in plaster and the patient is allowed partial weightbearing on crutches. The cast can be removed after 6–8 weeks and physiotherapy started.

Complications EARLY Vascular injury There is danger of gangrene unless the hyperextension injury is reduced without delay. LATE Physeal arrest Damage to the physis is not uncommon and residual deformity may require corrective osteotomy at the end of the growth period. Small areas of tethering across the growth plate can sometimes be successfully removed and normal growth restored. Shortening, if it is marked, can be treated by femoral lengthening.

REFERENCES AND FURTHER READING

(a)

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29.35 Fracture-separation of the epiphysis These fractures are not difficult to reduce and can usually be held adequately in plaster, but they must be watched carefully for several weeks.

Barnes R, Brown JT, Garden RS, et al. Subcapital fractures of the femur. A prospective review. J Bone Joint Surg 1976; 58B: 2–24. Bonnaire FA, Weber AT. The influence of haemarthrosis on the development of femoral head necrosis following intracapsular femoral neck fractures. Injury 2002; 33 Suppl 3: C33–40. Dimon JH III, Hughston JC. Unstable Intertrochanteric Fractures of the Hip. J Bone Joint Surg 1967; 49A: 440– 50. Garden RS. Low angle fixation in fractures of the femoral neck. J Bone Joint Surg 1961; 43B: 647–63. Harper WM, Barnes MR, Gregg PJ. Femoral head blood flow in femoral neck fractures. An analysis using intraosseous pressure measurement. J Bone Joint Surg 1991; 73B: 73–5. Hughes LO, Beaty JH. Fractures of the head and neck of the femur in children. J Bone Joint Surg 1994; 76A: 283– 92.

vance of biochemical markers. J Trauma 2001; 50(6): 989–1000. Pipkin G. Treatment of grade IV fracture dislocation of the hip. J Bone Joint Surg 1957; 39: 1027–42. Poolman RW, Kocher MS, Bhandari M. Pediatric femoral fractures: a systematic review of 2422 cases. J Orthop Trauma 2006; 20(9): 648–54. Shim SS. Circulatory and vascular changes in the hip following traumatic hip dislocation. Clin Orthop Relat Res 1979; 140: 255–61. Thompson VP, Epstein VP. Traumatic dislocation of the hip. J Bone Joint Surg 1951; 33A: 746–78. Tornetta P III, Mostafavi HR. Hip Dislocation: Current Treatment Regimens. J Am Acad Orthop Surg 1997; 5(1): 27–36. Winquist RA, Hansen ST Jnr, Clawson DK. Closed intramedullary nailing of femoral fractures. A report of five hundred and twenty cases. J Bone Joint Surg 1984; 66A: 529–39.

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Kaplan K, Miyamoto R, Levine BR, et al. Surgical Management of Hip Fractures: An Evidence-based Review of the Literature. II: Intertrochanteric Fractures. J Am Acad Orthop Surg 2008; 16(11): 665–73. Keating JF, Grant A, Masson M, et al. Randomized comparison of reduction and fixation, bipolar hemiarthroplasty, and total hip arthroplasty. Treatment of displaced intracapsular hip fractures in healthy older patients. J Bone Joint Surg 2006; 88A: 249–60. Kyle RF. Fractures of the Proximal Part of the Femur. J Bone Joint Surg 1994; 76A: 924–50. Masson M, Parker MJ, Fleischer S. Internal fixation versus arthroplasty for intracapsular proximal femoral fractures in adults. Cochrane Database of Systematic Reviews 2003; (2): CD001708. Pape HC, van Griensven M, Rice J, et al. Major secondary surgery in blunt trauma patients and perioperative cytokine liberation: determination of the clinical rele-

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Selvadurai Nayagam

ACUTE KNEE LIGAMENT INJURIES The bony structure of the knee joint is inherently unstable; were it not for the strong capsule, intra- and extra-articular ligaments and controlling muscles, the knee would not be able to function effectively as a mechanism for support, balance and thrust. Valgus stresses are resisted by the superficial and deep layers of the medial collateral ligament (MCL), semimembranosus tendon and its expansions, the tough posteromedial part of the capsule (referred to as the posterior oblique ligament) as well as the cruciate ligaments (Fig. 30.1a). Depending on the position of the knee, some will act as primary and others as secondary stabilizers. At 30 degrees of flexion, the MCL is the primary stabilizer. The main checks to varus angulation are the iliotibial tract and the lateral collateral ligament (LCL). Structures forming the posterolateral corner of the knee also make an important contribution to stability; they comprise the popliteus tendon, the capsule and the arcuate ligament – a condensation of fibres lying posterior to the LCL and running from the fibula over popliteus tendon to the posterior capsule (Fig. 30.1b). The iliotibial band and LCL are the primary stabilizers to a varus stress between full extension and 30 degrees of flexion; however, as flexion increases, the LCL relaxes and the posterolateral structures come into play to provide additional stability. The cruciate ligaments provide both anteroposterior and rotary stability; they also help to resist excessive valgus and varus angulation. Both cruciate ligaments have a double bundle structure and some fibres of each bundle are taut in all positions of the knee (Petersen and Zantop, 2007). The anterior cruciate has anteromedial and posterolateral bundles, whereas the posterior cruciate has anterolateral and posteromedial bundles. Anterior displacement of the tibia (as in the anterior drawer test) is resisted by the anteromedial bundle of the anterior cruciate ligament

Posterior oblique ligament including the superficial arm

Superficial medial collateral ligament

(a) (a)

Lateral gastrocnemius tendon

Semimembranosus including capsular, anterior and inferior arms Gastrocnemius

Iliotibial tract

Popliteus tendon

Popliteofibular ligament Fibular collateral ligament (b) (b)

30.1 Extracapsular restraints to valgus and varus stresses on the knee (a) Restraints on valgus stresses: the deep and superficial parts of the medial collateral ligament, semimembranosus and the posterior oblique ligament. (b) Extracapsular restraints on varus stresses: lateral collateral ligament, popliteus tendon, popliteofibular ligament and the capsule.

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(ACL) whilst the posterolateral part tightens as the knee extends. Posterior displacement is prevented by the posterior cruciate ligament (PCL), specifically by the anterolateral bundle when the knee is in near 90 degree flexion and by the posteromedial bundle when the knee is straight (Fig. 30.2). Injuries of the knee ligaments are common, particularly in sporting pursuits but also in road accidents, where they may be associated with fractures or dislocations. They vary in severity from a simple sprain to complete rupture. It is important to recognize that these injuries are seldom ‘unidirectional’; they often involve more than one structure and it is therefore useful to refer to them in functional terms (e.g. ‘anteromedial instability’) as well as anatomical terms (e.g. ‘torn MCL and ACL’).

Mechanism of injury and pathological anatomy Most ligament injuries occur while the knee is bent, i.e. when the capsule and ligaments are relaxed and the femur is allowed to rotate on the tibia. The damaging force may be a straight thrust (e.g. a dashboard injury forcing the tibia backwards) or, more commonly, a combined rotation and thrust as in a football tackle. The medial structures are most often affected but if the injury involves a twist in addition to a valgus force, the ACL also may be damaged. This twisting force in a weightbearing knee often tears the medial meniscus, causing the well-recognized triad of MCL, ACL and medial meniscal injury described by O’Donoghue. A solitary MCL injury, if sufficiently severe, can be shown to cause the knee joint to ‘open’ on the medial side when the joint is flexed to 30 degrees a valgus stress is applied, but if this is still

PL AM

(a)

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detectable when the knee is extended, then it is likely the expansions of the semimembranosus tendon, capsule and ACL are also damaged. Forces that push the tibia into varus will damage the lateral structures, but these forces are relatively uncommon; as with medial injuries, the cruciate ligaments are at risk if there is a twisting component, and a clinically detectable opening on varus stressing in an extended knee suggests that there is, in addition to a rupture of the LCL, capsular and cruciate damage. Cruciate ligament injuries occur in isolation or in combination with damage to other structures. The ACL is the more commonly affected. Solitary cruciate ligament injuries result in instability in the sagittal plane, i.e. the tibia can be pushed backwards or pulled forwards in relation to the femoral condyles. If there is accompanying damage to a collateral ligament or the capsule, then the direction of instability is often oblique and there may be a problem in controlling rotation. These oblique plane and rotatory instabilities are complex; in essence, one of the cruciate ligaments is ruptured and there is also laxity in one part of the capsule – this causes movement of the tibia on the femur, usually around an axis of the remaining intact capsule or other supporting ligament. Thus, in the more common anterolateral instability, where the ACL, lateral capsule and LCL are injured, the lateral plateau of the tibia can be made to sublux anteriorly when the tibia is rotated internally. If this is done with the knee fully extended whilst maintaining a valgus force, and the knee is then gradually flexed, a palpable reduction of this subluxation is felt at 20–30 degrees. This is the basis of the pivot shift test; it is thought the tibia rotates around the axis of an intact MCL. The common rotational instability patterns are summarized in Table 30.1, showing the likely ligaments involved and the clinical tests for assessment.

AL PM

(b)

30.2 Dual-bundle structure of the anterior and posterior cruciate ligaments (a) The anteromedial (AM) bundle of an anterior cruciate ligament is taut in 90° of knee flexion whereas the posterolateral (PL) bundle tightens in extension. (b) In contrast, it is the anterolateral (AL) bundle of the posterior cruciate ligament that is tight in 90° flexion and the posteromedial (PM) bundle tightens in extension (and therefore resists hyperextension).

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Table 30.1 Rotational instabilities of the knee Test

Positive result

Probable structures damaged

Anterolateral rotatory instability

Perform an anterior drawer test but with the foot internally rotated 30 degrees

The tibia subluxes forward to an equal or greater extent as when the foot is in a neutral position

ACL LCL Lateral aspect of knee capsule

Perform the pivot shift manoeuvre

The tibia is subluxed when the knee is extended and felt to reduce as it is gradually flexed

Anteromedial rotatory instability

Perform an anterior drawer test but with the foot externally rotated 15 degrees

The tibia subluxes forward

ACL MCL Posteromedial aspect of knee capsule (including the posterior oblique ligament and expansions of semimembranosus

Posterolateral rotatory instability

Perform a reverse (external rotation) pivot shift manoeuvre

The tibia subluxes posteriorly in the extended knee but is felt to reduce as flexion is gradually increased

PCL Popliteus tendon Arcuate ligament

Pick up the foot by grasping the medial forefoot

The knee hyperextends and tibia externally rotates. The tibia appears to be in varus

Injuries of the knee and leg

Type of instability

ACL, anterior cruciate ligament; LCL, lateral collateral ligament, MCL, medial collateral ligament; PCL, posterior cruciate ligament.

Clinical features The patient gives a history of a twisting or wrenching injury and may even claim to have heard a ‘pop’ as the tissues snapped. The knee is painful and (usually) swollen – and, in contrast to meniscal injury, the swelling appears almost immediately. Tenderness is most acute over the torn ligament, and stressing one or other side of the joint may produce excruciating pain. The knee may be too painful to permit deep palpation or much movement. For all the apparent consistency, the findings can be somewhat perverse: thus, with a complete tear the patient may have little or no pain, whereas with a partial tear the knee is painful. Swelling also is worse with partial tears, because haemorrhage remains confined within the joint; with complete tears the ruptured capsule permits leakage and diffusion. With a partial tear attempted movement is always painful; the abnormal movement of a complete tear is often painless or prevented by spasm. Abrasions suggest the site of impact, but bruising is more important and indicates the site of damage. The doughy feel of a haemarthrosis distinguishes ligament injuries from the fluctuant feel of the synovial effusion of a meniscus injury. Tenderness localizes the lesion,

but the sharply defined tender spot of a partial tear (usually medial and 2.5 cm above the joint line) contrasts with the diffuse tenderness of a complete one. The entire limb should be examined for other injuries and for vascular or nerve damage. The most important aspect of the examination is to test for joint stability. Partial tears permit no abnormal movement, but the attempt causes pain. Complete tears permit abnormal movement, which sometimes is almost painless. To distinguish between the two is critical because their treatment is different; if there is doubt, examination under anaesthesia is mandatory. Sideways tilting (varus/valgus) is examined, first with the knee at 30 degree of flexion and then with the knee straight. Movement is compared with the normal side. If the knee angulates only in slight flexion, there is probably an isolated tear of the collateral ligaments; if it angulates in full extension, there is almost certainly rupture of the capsule and cruciate ligaments as well. Anteroposterior stability is assessed first by placing the knees at 90 degrees with the feet resting on the couch and looking from the side for posterior sag of the proximal tibia; when present, this is a reliable sign of posterior cruciate damage. Next, the drawer test is carried out in the usual way; a positive drawer sign is

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diagnostic of a tear, but a negative test does not exclude one. The Lachman test is more reliable; anteroposterior glide is tested with the knee flexed 15–20 degrees. Rotational stability arising from acute injuries can usually be tested only under anaesthesia.

Treatment Imaging Plain x-rays may show that the ligament has avulsed a small piece of bone: • from the medial edge of the femur by the medial ligament • from the fibula by the lateral ligament • from the tip of the fibula, probably by a posterolateral corner injury • from the tibial spine by the anterior cruciate ligament • from the back of the upper tibia by the posterior cruciate • from the near edge of the lateral tibial condyle by the iliotibial tract or capsule (a Segond fracture, which is often associated with anterior cruciate ligament and meniscal injuries). Stress films (if necessary under anaesthesia) show whether the joint hinges open on one side (Fig. 30.3). Magnetic resonance imaging (MRI) is helpful in distinguishing partial from complete ligament tears. This may also reveal ‘bone bruising’, a hitherto poorly recognized source of pain.

Arthroscopy With severe tears of the collateral ligaments and capsule, arthroscopy should not be attempted; fluid extravasation will hamper diagnosis and may complicate further procedures. The main indication for arthroscopy, which is usually conducted after capsular

(a)

(b)

878

healing has occurred and knee motion recovered, is for reconstruction of cruciate ligament tears in those individuals who would benefit, and to deal with other internal injuries such as meniscal tears.

30.3 Stress x-rays Stress films show: (a) complete tear of medial ligament, left knee; (b) complete tear of lateral ligament. In both, the anterior cruciate also was torn.

SPRAINS AND PARTIAL TEARS The intact fibres splint the torn ones and spontaneous healing will occur. The hazard is adhesions, so active exercise is prescribed from the start, facilitated by aspirating a tense effusion, applying ice-packs to the knee and, sometimes, by injecting local anaesthetic into the tender area. Weightbearing is permitted but the knee is protected from rotational or angulatory strain by a heavily padded bandage or a functional brace. A complete plaster cast is unnecessary and disadvantageous; it inhibits movement and prevents weekly reassessment – an important precaution if the occasional error is to be avoided. With a dedicated exercise programme, the patient can usually return to sports training by 6–8 weeks. COMPLETE TEARS Isolated tears of the MCL, i.e. where the knee is stable in full extension, usually heal well enough to permit near-normal function. Operative repair is unnecessary. A long cast-brace is worn for 6 weeks and thereafter graded exercises are encouraged. Isolated tears of the LCL are rare. If the diagnosis is certain, these can be treated conservatively as for MCL tears. If the fibular styloid is avulsed, the injury is probably more severe and involves part of the posterolateral capsule and arcuate complex. Examination for posterolateral instability should be done and, if confirmed, these injuries may benefit from repair. In contrast, a fibular head fracture indicates an avulsion of the LCL as a solitary injury. Isolated tears of the ACL should, in theory, be treated by early operative reconstruction. Indeed, such are the pressures on professional sportspersons that this is often demanded. Operation may also be indicated for non-professionals if the tibial spine is avulsed; the bone fragment, with the attached ACL, is replaced and fixed under arthroscopic control and the knee is braced for 6 weeks. In all other cases it is more prudent to follow the conservative regime described earlier; the cast-brace is worn only until symptoms subside and thereafter movement and musclestrengthening exercises are encouraged. About half of these patients regain sufficiently good function not to need further treatment. The remainder complain of varying degrees of instability; late assessment will identify those who are likely to benefit from ligament reconstruction. Isolated tears of the PCL are treated conservatively. Most patients end up with little or no loss of function.

CHRONIC LIGAMENTOUS INSTABILITY

30.4 Apley’s test The knee is flexed to 90° and rotated while applying first a compression force and then a distraction force. Pain and/or clicking on compression is suggestive of a meniscal lesion.

However, some experience instability whilst walking up stairs and are sufficiently disabled to warrant late reconstruction. Combined injuries may result in significant loss of function. With concurrent ACL and collateral ligament injury, reconstruction of the ACL often obviates the need for collateral ligament treatment; however, early operation carries the risk of postoperative joint fibrosis, so it is wiser to start treatment with joint support and physiotherapy in order to restore a good range of movement before following on with ACL reconstruction. A similar approach is adopted for combined injuries involving the PCL, but here all damaged structures will need to be repaired.

Complications If the knee with a partial ligament tear is not actively exercised, torn fibres stick to intact fibres and to bone. The knee ‘gives way’ with catches of pain; localized tenderness is present and there is pain on medial or lateral rotation. The obvious confusion with a torn meniscus can be resolved by the grinding test (Fig. 30.4) or, better still, by MRI. Physiotherapy will resolve the problem caused by adhesions and rarely is manipulation under anaesthesia needed.

Adhesions

Ossification in the ligament (Pellegrini–Stieda’s disease)

Occasionally, an abduction injury is followed by ossification near the upper attachment of the medial ligament. This is usually discovered as a chance finding in x-rays of the knee and carries no prognostic significance. The knee may continue to give way. The instability tends to get worse and the repeated injury predisposes to osteoarthritis. This important subject is discussed under a separate heading later.

Instability

Functional pathology Unstable tibiofemoral relationships may result in abnormal sideways tilt (varus or valgus), excessive glide (forwards, backwards or even in an oblique direction), unnatural rotation (internal or external), or combinations of these. Seldom is only one ligament at fault. As described at the beginning of this chapter, stability is normally maintained by both primary and secondary stabilizers (not to mention the dynamic forces of surrounding muscles). In different positions, different structures come into play as primary stabilizers. Therefore, when testing for medial and lateral stability, valgus and varus stresses should be applied with the knee first in 30 degrees of flexion and then in full extension. Abnormal translation or rotation of the tibia on the femur is even more complex. A positive anterior drawer sign is the result of a torn ACL, but a solitary cruciate injury is unusual. More commonly there is anterolateral rotatory instability where, in addition to a torn ACL, the lateral capsule and LCL are torn or ‘stretched’. In this instance, not only will the anterior drawer test be positive, but the lateral tibial condyle can be made to sublux forwards as the tibia rotates abnormally around an axis through the medial condyles; this is the basis of the pivot shift phenomenon (Galway and MacIntosh, 1980). A positive posterior tibial sag and drawer sign means that the posterior cruciate ligament is torn (Fig. 30.5). Soon after injury, however, this sign is difficult to elicit unless the ligaments of the arcuate complex and popliteus also are torn. Chronic deficiency of the arcuate ligament complex causes a type of posterolateral rotatory instability that is a counterpart of the pivot shift phenomenon (Bahk and Cosgarea, 2006; Ranawat et al., 2008). Complete tears of all the posterior structures also allow the knee to hyperextend.

Injuries of the knee and leg

Instability (‘giving way’) of the knee may be obvious soon after the acute injury has healed, or it may only become apparent much later. It is usually progressive (a partial meniscectomy for a meniscal tear is likely to make it worse and create new tears) but, except in people engaged in strenuous sport, dancing or certain work activities, the disability is often tolerated without complaint. In more severe and longstanding cases, osteoarthritis may eventually supervene.

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Clinical features The patient complains of a feeling of insecurity and of giving way. With collateral ligament instability the

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30.5 Cruciate ligaments (a) Viewed from the side, any backwards displacement of the upper tibia is plainly visible and can be confirmed by (b) pushing the tibia backwards.

(a)

(b)

cause is obvious even to the patient, but with anterolateral rotatory instability the symptoms are more subtle – the knee suddenly gives way as the patient pivots on the affected side (effectively causing a pivot shift to occur). Some patients describe this jerking sensation by grinding the knuckles of clenched fists upon each other. The explanation is that, with the knee just short of full extension, the lateral tibial condyle slips forward (subluxes); then, as the knee is flexed, the iliotibial band pulls the condyle back into the reduced position with a ‘clunk’. For a sportsman, ‘cutting’ is particularly troublesome. Locking is not a feature of instability and always suggests an associated meniscal tear. In the less common posterior cruciate insufficiency, symptoms are mild unless the arcuate ligament complex also is torn or stretched; instability is sometimes felt only on climbing stairs. The joint looks normal apart from slight wasting; there is rarely tenderness but excessive movement in one or more directions can usually be demonstrated. Comparison with the normal knee is essential. A useful routine is to observe gait and knee posture in standing, then to examine for hyperextension, then

for increased tilting into varus or valgus (at 0 and 30 degrees knee flexion), followed by the drawer tests and the more specific Lachman test (see later), and finally to perform special tests for rotational instability. Start by watching the patient walk and noting knee posture and movement in the stance phase. Then ask the patient to stand on one leg – those with severe instabilities may not be able to achieve this task, whereas others who do may demonstrate the problem. Hyperextension is tested with the patient supine and the knee straight; with the patient relaxed, lift each heel in turn. Repeat the test, but this time grasp the medial forefoot – if the tibia sags posteriorly and externally rotates, this suggests that both posterior cruciate and posterolateral capsule are torn (posterolateral rotatory instability). To test stability in the coronal plane, the patient’s ankle is tucked under the examiner’s armpit whilst both hands support the knee by straddling it on either side (Fig. 30.6a). The examiner is then able to control both knee flexion and the amount of varus or valgus thrust applied;

Quadriceps contraction

(a)

880

30.6 Testing collateral ligaments (a) Side-to-side stability of the knee can be checked by holding the foot between the upper arm and body and moving the joint between supporting hands. This method is useful if the leg is large. (b) The quadriceps active test. Note the position of the examiner’s hands in supporting the thigh and resisting knee extension by the ankle. At 90° of knee flexion, a posterior sag caused by a damaged posterior cruciate ligament is corrected when the quadriceps contracts.

(b)

Modified drawer test The anterior drawer test is performed with the tibia in 30 degrees of internal rotation; if positive, it suggests anterolateral rotatory

The leg is dangled over the edge of the couch. The examiner steadies the distal femur with one hand and holds the heel firmly in the other. The knee is flexed at 30 degrees. External rotation is applied through the heel and the position of the tibial tuberosity is noted. If external rotation is greater by 15 degrees as compared to the other side, a posterolateral corner injury is suspected. If the test is repeated with the knee flexed further to 90 degrees and the external rotation is noted to increase, a posterior cruciate injury is likely too (LaPrade and Wentorf, 2002).

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Dial test

Pivot shift test The examiner supports the knee in extension with the tibia internally rotated (the subluxed position – the lateral tibial condyle is drawn in front of the femoral condyle); the knee is then gradually flexed while a valgus stress is applied. In a positive test, as the knee reaches 20 or 30 degrees, there is a sudden jerk as the tibial condyle slips backwards and reduces. The valgus stress compresses the lateral femoral condyle against the tibia and, through a jamming effect, amplifies the sudden ‘jerk’ when the condyle drops back. Another way to show this is MacIntosh’s test (Fig. 30.8). A positive pivot shift test indicates anterolateral rotatory instability. A modification of this test can be used to diagnose posterolateral rotatory instability; the tibia is held in external rotation while the knee is extended and, similarly, a valgus stress is applied as the knee is gradually flexed – a characteristic ‘clunk’ signals the change from a subluxed to a reduced position (the reverse pivot shift).

30.7 Tests for cruciate ligament instability (a) Drawer test: Wth the knee at 90° and the hamstrings relaxed, grasp the top of the patients leg and try to shift it forwards and backwards. (b) Note that there is some anterior shift when the tibia is pulled forwards (slight anterior cruciate laxity. (c) Lachman test: This is more sensitive than the drawer test. Note the position of the knee and the examiner’s hands.

(a)

(b)

instability. Likewise, a positive drawer sign with the knee in external rotation (about 15 degrees) suggests anteromedial rotatory instability (Slocum and Larson, 1968).

Injuries of the knee and leg

perform the test first with the knee straight and then flexed at 30 degrees. This manner of performing varus and valgus stressing enables even large limbs to be held and examined. Next, place the knees at 90 degrees with the soles of the feet flat on the couch and the heels lined up; the quadriceps should be relaxed. Looking from the side, note if there is any posterior sag of the upper tibia by checking the levels of the tibial tuberosities on each leg – a posterior sag is a sure sign of posterior cruciate laxity. Then support the patient’s thigh in this position to ensure the hamstring muscles are relaxed, and use the other hand to grasp the patient’s ankle (Fig. 30.6b). Ask the patient to slide the foot slowly down the couch while resisting this movement by holding on to the ankle as the quadriceps contracts, the posterior sag is pulled up and the proximal tibia shifts forward. This is the quadriceps active test (Daniel et al., 1988). Again with the knees flexed at 90 degrees and both feet resting on the couch (it is useful to sit across the couch to prevent the feet sliding forward), grasp the upper tibia with both hands, and making sure the hamstrings are relaxed, test for anterior and posterior laxity (the drawer sign). A more reliable test for anterior cruciate laxity is to examine for anterior–posterior displacement with the knee flexed to 20 degrees (the Lachman test). Hold the calf with one hand and the thigh with the other, and try to displace the joint backwards and forwards. Rotational stability can be tested in several ways:

(c)

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(a) (a)

(b)

30.9 Torn knee ligaments – MRI (a) Coronal T2weighted image showing a medial collateral ligament tear with surrounding oedema and joint effusion. (b) Sagittal T2-weighted image showing an intrasubstance tear of the anterior cruciate ligament with a large joint effusion.

other lesions, such as meniscal tears or cartilage damage, are suspected; (3) surgical treatment is anticipated. Partial meniscectomy and removal of loose cartilage tags can be performed at the same time. (b)

Treatment Most patients with chronic instability have reasonably good function and will not require an operation. The first approach should always be a supervised, disciplined and progressively vigorous exercise programme to strengthen the quadriceps and the hamstrings. At the end of 6 months the patient should be reexamined. The indications for operation are:

(c)

30.8 Cruciate ligament tears – MacIntosh’s test (a) The leg is lifted with the knee straight. (b) The fibula is pushed forwards – if the anterior cruciate is torn the lateral tibial condyle is now subluxed forwards. (c) It is held forwards while the knee is flexed; at 30–40° the condyle reduces with a jerk. This may be painful and an alternative method is to lift the straight leg by holding it with both hands just above the ankle, rotating the leg inwards, then flexing the knee. The jerk is often visible and usually painless.

Imaging MRI is a reliable method of diagnosing cruciate ligament and meniscal injuries, providing almost 100 per cent sensitivity and over 90 per cent accuracy (Fig. 30.9).

Arthroscopy 882

Arthroscopy is indicated if: (1) the diagnosis, or the extent of the ligament injury, remains in doubt; (2)

1. Recurrent locking, with MRI or arthroscopic confirmation of a meniscal tear (arthroscopic meniscectomy alone may alleviate the patient’s symptoms, though this may later lead to increased instability); 2. intolerable symptoms of giving way; 3. suboptimal function in a sportsperson or others with similarly demanding occupations (even in this group, some patients will accept the use of a knee brace for specific activities that are known to cause trouble); 4. ligament injuries in adolescents (the long-term effects of chronic instability in this group are more marked). Partial tears of the anterior cruciate ligament are more problematic and there is still much controversy about the need for surgery in these cases. The decision should be based on an assessment of the patient’s symptoms and functional capacity rather than the appearance of the ligament. Young adults with chronic anterior cruciate insufficiency and proven partial tears show diminished activity and run the risk of developing secondary problems such as meniscal

lesions, cartilage damage, increasing instability and (eventually) secondary osteoarthritis. With careful follow-up and reassessment, those most at risk can usually be identified and advised to undergo reconstructive surgery.

Medial collateral ligament insufficiency seldom causes much disability unless there is an associated anterior cruciate tear. However, if valgus instability is marked, and particularly if it is progressive, ligament reconstruction, by advancing the proximal or distal end of the ligament, restoring the tension of the posteromedial capsule and reinforcing the medial structures with the semimembranosus tendon, is justified. Isolated lateral instability is uncommon and symptoms are rarely troublesome enough to warrant surgery. If operative reconstruction is attempted, it should follow the lines described earlier. Isolated PCL insufficiency rarely causes loss of function. Conservative treatment (mainly quadriceps strengthening exercises) will usually suffice. Isolated ACL insufficiency is uncommon and can usually be managed by physiotherapy. Splints or braces may be used to speed the return to weightbearing. Patients seeking to resume competitive sport may need something more; reconstructive surgery involves replacing the torn ACL with an autologous graft, usually a strip of patellar tendon with bone attachments at either end or with hamstring tendons. Combined injuries such as anterolateral or anteromedial rotatory instability are the commonest reasons for reconstructive surgery. When the ACL is damaged together with either the medial or lateral collateral ligament, reconstruction of the ACL alone often suffices. The torn ACL is replaced by an autograft

(a)

(b)

The treatment of combined injuries in which the PCL is involved is changing; until recently, it was thought that most of these patients had good function and therefore did not need reconstructive surgery. Newer studies have shown that there is an increased risk of osteoarthritis (especially of the medial compartment) and this is seen as an indication for PCL reconstruction in patients who have more than 10–15 mm of posterior tibial translation in the drawer test. Unlike injuries involving the ACL, combination injuries involving the PCL require all damaged structures to be repaired.

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Injuries of the knee and leg

Operative treatment

(usually from the patellar tendon or from hamstring tendons) or by an allograft. Some surgeons advocate replicating the dual bundle arrangement of the original ligament. The ideal synthetic graft has yet to be developed. Postoperative care will depend on the fixation of the new ligament; in many cases a short period of splintage can be followed by regular physiotherapy to avoid joint stiffness and improve muscle control. Many patients return to sports within 6 months.

FRACTURED TIBIAL SPINE Severe valgus or varus stress, or twisting injuries, may damage the knee ligaments and fracture the tibial spine. This is, in fact, a type of traction injury – the adolescent variant of a cruciate ligament tear.

Pathological anatomy The detached bone fragment may remain almost undisplaced, held in position by the soft tissues; it may be partially displaced, the anterior end lifted away on

(c)

(d)

30.10 Tibial spine fracture (a,b) This young man injured his knee while playing football; x-rays showed a large, displaced avulsion fracture of the tibial spine. (c) An undisplaced tibial spine fracture. (d) Posterior fractures, with avulsion of the posterior cruciate ligament, are often missed.

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a posterior hinge, or it may be completely detached and displaced. Because its articular surface is covered with cartilage – invisible on x-ray – the image seen on x-ray is smaller than the actual fragment.

DISLOCATION OF KNEE The knee can be dislocated only by considerable violence, as in a road accident. The cruciate ligaments and one or both lateral ligaments are torn.

Clinical features The patient – usually an older child or adolescent – presents with a swollen, immobile knee. The joint feels tense, tender and ‘doughy’ and aspiration will reveal a haemarthrosis. Examination under anaesthesia may show that extension is blocked. There may also be associated ligament injuries; always test for varus and valgus stability and cruciate laxity.

Clinical features Rupture of the joint capsule produces a leak of the haemarthrosis, leading to severe bruising and swelling. This may be the only clue on inspection, especially if the dislocated joint has reduced spontaneously. Otherwise, the diagnosis is straightforward as there is gross deformity (Fig. 30.11). The circulation in the foot must be examined because the popliteal artery may be torn or obstructed. Repeated examination is necessary as compartment syndrome is also a risk. Common peroneal nerve injury occurs in nearly 20 per cent of cases; distal sensation and movement should be tested.

X-ray The fracture is not always obvious and a small

posterior fracture may be missed unless the x-rays are carefully examined. The fragment – often including part of the intercondylar eminence – may be undisplaced, tilted upwards or completely detached (Fig. 30.10).

In addition to the dislocation, the films occasionally reveal a fracture of the tibial spine or posterior part of the plateau (cruciate ligament avulsion), avulsion of the fibular styloid or avulsion of a fragment from the near the edge of the lateral tibial condyle (the Segond fracture). Arteriograpy is not essential if the clinical assessment of the circulation is normal. The ankle/brachial arterial pressure index (ratio of systolic pressure at the ankle relative to systolic pressure at the elbow) is a useful measure and should not be less than 0.9, but if there is any doubt an arteriogram should be obtained (Robertson et al., 2006).

X-ray

Treatment Under anaesthesia the joint is aspirated and gently manipulated into full extension. Often the fragment falls back into position and the x-ray shows that the fracture is reduced. As long as the knee extends fully, small amounts of fragment elevation can be accepted. If there is a block to full extension or if the bone fragment remains displaced, operative reduction is essential. The fragment – often larger than suspected – is restored to its bed and anchored by small screws, taking care to avoid the physis. After either closed or open reduction, a long plaster cylinder is applied with the knee almost straight; it is worn for 6 weeks and then movements are encouraged. The outcome is usually good and full movement regained; there may be some residual laxity on examination, but this rarely causes symptoms.

(a)

884

(b)

Treatment Reduction under anaesthesia is urgent; this is usually achieved by pulling directly in the line of the leg, but hyperextension must be avoided because of the danger to the popliteal vessels. If reduction is achieved,

(c)

(d)

30.11 Dislocations of the knee (a,b) Posterolateral dislocation; (c,d) anteromedial dislocation.

(a)

(b)

(c)

the limb is rested on a back-splint and the circulation is checked repeatedly during the 48 hours. Because of swelling, a plaster cylinder is dangerous. A vascular injury will need immediate repair and the limb is then more conveniently splinted with an anterior external fixator (Fig. 30.12). If possible, repair or reconstruction of the capsule and collateral ligaments should be undertaken at the same time – this may involve simple suture or reattachment of the avulsed portions to bone – in order to enable early movement of the knee with the support of a hinged knee brace. If the direct repair is tenuous, augmentation using tendon grafts may be needed. In general, early reconstruction of the torn ligaments followed by protected movement of the joint reduces the severity of joint stiffness. The cruciate ligaments can be reconstructed after knee movement has recovered, usually some 6–12 months later. Prolonged cast immobilization (usually 12 weeks) is no longer recommended as it has been shown to be less good at preserving knee function.

Complications EARLY Popliteal artery damage occurs in nearly 20 per cent of patients and needs immediate repair. Delay and an extended warm ischaemic period can result in amputation.

Arterial damage

Nerve injury The lateral popliteal nerve may be injured. Spontaneous recovery is possible if the nerve is not completely disrupted – about 20 per cent of patients can be expected to improve. If nerve conduction studies or clinical examination shows no sign of recovery, a transfer of tibialis posterior tendon through the interosseous membrane to the lateral cuneiform may help restore ankle dorsiflexion.

LATE Joint instability Anteroposterior glide or a lateral

wobble often remains but, provided the quadriceps muscle is sufficiently powerful, the disability is not severe.

(d)

Stiffness Loss of movement, due to prolonged immobilization, is a common problem and may be even more troublesome than instability. Even with early surgical reconstruction, normal knee function is elusive.

30

Injuries of the knee and leg

30.12 Knee dislocation and vascular trauma (a,b) This patient was admitted with a dislocated knee. After reduction (c) the x-ray looked satisfactory, but the circulation did not. (d) An arteriogram showed vascular cut-off just above the knee; had this not been recognized and treated, amputation might have been necessary.

ACUTE INJURIES OF EXTENSOR APPARATUS Disruption of the extensor apparatus may occur: in the quadriceps tendon, at the attachment of the quadriceps tendon to the proximal surface of the patella, through the patella and retinacular expansions, at the junction of the patella and the patellar ligament, in the patellar ligament or at the insertion of the patellar ligament to the tibial tubercle. (Note: The patellar ligament is often called the patellar tendon). In all but direct fractures of the patella, the mechanism of injury is the same: sudden resisted extension of the knee or (essentially the same thing) sudden passive flexion of the knee while the quadriceps is contracting. The patient gives a history of stumbling on a stair, catching the foot while running, or kicking hard at a muddy football. The lesion tends to occur at progressively higher levels with increasing age: adolescents suffer avulsion fractures of the tibial tubercle; young adult sportspeople tear the patellar ligament, middle-aged adults fracture their patellae; and older people (as well as those whose tissues are weakened by chronic illness or steroid medication) suffer acute tears of the quadriceps tendon.

RUPTURE OF QUADRICEPS TENDON The patient is usually elderly, may have a history of diabetes or rheumatoid disease, or may have been treated with corticosteroids. Occasionally acute rupture is seen in a young athlete. The typical injury is followed by tearing pain and giving way of the knee.

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There is bruising and local tenderness; sometimes a gap can be felt proximal to the patella. Active knee extension is either impossible (suggesting a complete rupture) or weak (partial rupture). The diagnosis can be confirmed by MRI.

Treatment Partial tears Non-operative treatment will suffice: a plaster cylinder is applied for 6 weeks, followed by physiotherapy that concentrates on restoring knee flexion and quadriceps strength.

‘Chronic’ ruptures (usually the result of delayed presentations or missed diagnoses) are difficult to repair because the ends have retracted. The gap can often be made smaller by closing the medial and lateral ends, and the remaining central gap is then covered by a full-thickness V-flap turned down from the proximal quadriceps tendon (Codivilla). A pullout or cerclage wire protects the repair. The results of acute repairs are good, with most patients regaining full power, a good range of movement and little or no extensor lag. Late repairs are less predictable.

Complete tears Early operation is needed, or else the

ruptured fibres will retract and repair will be more difficult. End-to-end suturing can be reinforced by turning down a partial-thickness triangular flap of quadriceps tendon proximal to the repair (Scuderi). If the tendon has been avulsed from the proximal pole of the patella, it should be re-attached to a trough created at that site using pull-through sutures. Postoperatively the knee is held in extension in hinged brace. Early supervised movement through the brace is important to prevent adhesions; limits to the amount of flexion can be controlled through the brace and increased as the repair heals over the next 12 weeks (Fig. 30.13).

RUPTURE OF PATELLAR LIGAMENT This is an uncommon injury; it is usually seen in young athletes and the tear is almost always at the proximal or distal attachment of the ligament. There may be a previous history of ‘tendinitis’ and local injection of corticosteroid. The patient gives a history of sudden pain on forced extension of the knee, followed by bruising, swelling and tenderness at the lower edge of the patella or more distally. X-rays may show a high-riding patella and a tell-tale flake of bone torn from the proximal or distal attachment of the ligament. MRI will help to distinguish a partial from a complete tear.

Treatment

(a)

(b)

886

30.13 Repairing ruptures of the quadriceps tendon (a) Acute ruptures can usually be sutured and reinforced with a partial-thickness flap of the quadriceps tendon (Scuderi). When the patient presents late (b), the retracted ends may have to be bridged by a full-thickness V-shaped flap (Codivilla).

ACUTE TEARS Partial tears can be treated by applying a plaster cylinder. Complete tears need operative repair or reattachment to bone. Tension on the suture line can be lessened by inserting a temporary pull-out wire to keep the distance between the inferior pole and attachment to the tibial tuberosity constant. Immobilization in full extension may precipitate stiffness – it is, after all, a joint injury – and it may be better to support the knee in a hinged brace with limits to the amount of flexion permitted. This range can be gradually increased after 6 weeks. Early repair of acute ruptures gives excellent results. Late repairs are less successful and the patient may be left with a permanent extension lag. LATE CASES Late cases are difficult to manage because of proximal retraction of the patella. A two-stage operation may be needed: first to release the contracted tissues and apply traction directly to the patella, then at a later stage to repair the patellar ligament and reinforce it with grafts of tendon from gracilis or semitendinosus. Here, again, a tension-relieving pull-out wire is helpful. Postoperatively

a hinged brace is used to hold the knee in extension with supervised knee movement and limits to the amount of flexion until the repair is healed, usually at 12 weeks.

Fracture or avulsion of the tibial tubercle usually occurs as a sports injury in young people. If the knee is suddenly forced into flexion while the quadriceps is contracting, a fragment of the tubercle – or sometimes the entire apophysis – may be wrenched from the bone. The diagnosis is suggested by the history. The area over the tubercle is swollen and tender; active extension causes pain. The lateral x-ray shows the fracture. Sometimes the patella is abnormally high, having lost part of its distal attachment. An incomplete fracture can be treated by applying a long-leg cast with the knee in extension for 6 weeks. Complete separation requires open reduction and fixation with lag screws; a cast or hinged brace is applied for 6 weeks. Osgood–Schlatter disease Repetitive strain on the patellar ligament may give rise to a painful, tender swelling over the tibial tubercle. The condition is fairly common in adolescents who are keen on sport. Treatment consists of restricting sports activities until the symptoms subside (see page 576).

FRACTURED PATELLA The patella is a sesamoid bone in continuity with the quadriceps tendon and the patellar ligament (also called the patellar tendon). There are additional insertions from the vastus medialis and lateralis into the medial and lateral edges of the patella. The extensor ‘strap’ is completed by the medial and lateral extensor retinacula (or quadriceps expansions), which bypass the patella and insert into the proximal tibia. The mechanical function of the patella is to hold the entire extensor ‘strap’ away from the centre of rotation of the knee, thereby lengthening the anterior lever arm and increasing the efficiency of the quadriceps. The key to the management of patellar fractures is the state of the entire extensor mechanism. If the extensor retinacula are intact, active knee extension is still possible, even if the patella itself is fractured.

Clinical features Following one of the typical injuries, the knee becomes swollen and painful. There may be an abrasion or bruising over the front of the joint. The patella is tender and sometimes a gap can be felt. Active knee extension should be tested. If the patient can lift the straight leg, the quadriceps mechanism is still intact. If this manoeuvre is too painful, active extension can be tested with the patient lying on his side. If there is an effusion, aspiration may reveal the presence of blood and fat droplets.

30

Injuries of the knee and leg

FRACTURES OF TIBIAL TUBERCLE

hammer or by an indirect traction force that pulls the bone apart (and often tears the extensor expansions as well). Direct injury – usually a fall onto the knee or a blow against the dashboard of a car – causes either an undisplaced crack or else a comminuted (‘stellate’) fracture without severe damage to the extensor expansions. Indirect injury occurs, typically, when someone catches the foot against a solid obstacle and, to avoid falling, contracts the quadriceps muscle forcefully. This is a transverse fracture with a gap between the fragments.

X-ray The x-ray may show one or more fine fracture

lines without displacement, multiple fracture lines with irregular displacement or a transverse fracture with a gap between the fragments (Fig. 30.14). Comparative x-rays of the opposite knee may help to distinguish normal from abnormal appearances in undisplaced fractures. Patellar fractures are classified as transverse, longitudinal, polar or comminuted (stellate). Any of these may be either undisplaced or displaced. Separation of the fragments is significant if it is sufficient to create a step on the articular surface of the patella or, in the case of a transverse fracture, if the gap is more than 3 mm wide. A fracture line running obliquely across the superolateral corner of the patella should not be confused with the smooth, regular line of a (normal) bipartite patella. Check the opposite knee; bipartite patella is often bilateral.

Treatment Undisplaced or minimally displaced fractures If there is a

Mechanism of injury and pathological anatomy

haemarthrosis it should be aspirated. The extensor mechanism is intact and treatment is mainly protective. A plaster cylinder holding the knee straight should be worn for 3–4 weeks, and during this time quadriceps exercises are to be practised every day.

The patella may be fractured, either by a direct force that cracks the bone like a tile under the blow of a

Comminuted (stellate) fracture The extensor expansions are intact and the patient may be able to lift the leg.

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(a)

(b)

(d)

30.14 Fractured patella – stellate (a,b) A fracture with little or no displacement can be treated conservatively by a posterior slab of plaster that is removed several times a day for gentle active exercises. (c,d) With severe comminutions, patellectomy is arguably the best treatment, although some surgeons would consider preserving as many useful fragments as possible.

However, the undersurface of the patella is irregular and there is a serious risk of damage to the patellofemoral joint. For this reason some people advocate patellectomy, whatever the degree of displacement. To others it seems reasonable to preserve the patella if the fragments are not severely displaced (or to remove only those fragments that obviously distort the articular surface); a hinged brace is used in extension but unlocked several times daily for exercises to mould the fragments into position and to maintain mobility. Displaced transverse fracture The lateral expansions are

torn and the entire extensor mechanism is disrupted. Operation is essential. Through a longitudinal incision the fracture is exposed and the patella repaired by the tension-band principle. The fragments are reduced and transfixed with two stiff K-wires; flexible wire is then looped tightly around the protruding K-wires and over the front of the patella (Fig. 30.15). The tears in the extensor expansions are then repaired. A plaster backslab or hinged brace is worn until active extension of

(a)

888

(c)

the knee is regained; either may be removed every day to permit active knee-flexion exercises.

Outcome Patients usually regain good function but, depending on the severity of the injury, there is a significant incidence of late patellofemoral osteoarthritis.

DISLOCATION OF PATELLA Because the knee is normally angled in slight valgus, there is a natural tendency for the patella to pull towards the lateral side when the quadriceps muscle contracts. Lateral deviation of the patella during knee extension is prevented by a number of factors: the patella is seated in the intercondylar groove, which has a high lateral ‘embankment’; the force of extensor muscle contraction pulls it firmly into the groove; and the extensor retinacula and patellofemoral ligaments guide it centrally as it tracks along the intercondylar runway. The most important static check-rein on the medial side is the medial patellofemoral ligament, a more or less distinct structure extending from the superomedial border of the patella towards the medial femoral condyle deep to vastus medialis (Conlan et al., 1993). Additional restraint is provided by the medial patellomeniscal and patellotibial ligaments and the associated medial retinacular fibres. In the normal knee, considerable force is required to wrench the patella out of its track. However, if the intercondylar groove is unusually shallow, or the patella seated higher than usual, or the ligaments are abnormally lax, dislocation is not that difficult.

(b)

30.15 Fractured patella – transverse The separated fragments (a) are transfixed by K-wires; (b) malleable wire is then looped around the protruding ends of the K-wires and tightened over the front of the patella.

Mechanism of injury While the knee is flexed and the quadriceps muscle relaxed, the patella may be forced laterally by direct

Clinical features In a ‘first-time’ dislocation the patient may experience a tearing sensation and a feeling that the knee has gone ‘out of joint’; when running, he or she may collapse and fall to the ground. Often the patella springs back into position spontaneously; however, if it remains unreduced there is an obvious (if somewhat misleading) deformity: the displaced patella, seated on the lateral side of the knee, is not easily noticed but the uncovered medial femoral condyle is unduly prominent and may be mistaken for the patella. Neither active nor passive movement is possible (Fig. 30.16). In the rare intraarticular (downward) dislocation the patella is stuck between the condyles and there is a marked prominence on the front of the knee. If the dislocation has reduced spontaneously, the knee may be swollen and there may be bruising and tenderness on the medial side. If there is fluid in the joint, aspiration may show that it is bloodstained; the presence of fat droplets suggests a concurrent osteochondral fracture. With recurrent dislocation the symptoms and signs are much less marked, though still unpleasant. After spontaneous reduction the knee looks normal, but the apprehension test is positive.

Imaging Anteroposterior, lateral and tangential (‘skyline’) x-ray views are needed. In an unreduced dislocation, the patella is seen to be laterally displaced and tilted or rotated. In 5 per cent of cases there is an associated osteochondral fracture.

MRI may reveal a soft-tissue lesion (e.g. disruption of the medial patellofemoral ligament) as well as articular cartilage and/or bone damage.

30

Treatment In most cases the patella can be pushed back into place without much difficulty and anaesthesia is not always necessary; the exception is an intra-articular (intercondylar) dislocation, which may need open reduction. If there are no signs of soft tissue rupture – i.e. there is minimal swelling, no bruising and little tenderness – cast splintage alone will usually suffice. The knee is aspirated and then immobilized in almost full extension; a small pad along the lateral edge of the patella may help to keep the medial soft tissues relaxed. The cast is retained for 2 or 3 weeks and the patient then undergoes a long period (2–3 months) of quadriceps strengthening exercises. The same approach has been advocated for more severe forms of dislocation. However, if there is much bruising, swelling and tenderness medially, the patellofemoral ligaments and retinacular tissues are probably torn and immediate operative repair will reduce the likelihood of later recurrent dislocation.

Injuries of the knee and leg

violence; this is rare. More often traumatic dislocation is due to indirect force: sudden, severe contraction of the quadriceps muscle while the knee is stretched in valgus and external rotation. Typically this occurs in field sports when a runner dodges to one side. The patella dislocates laterally and the medial patellofemoral ligament and retinacular fibres may be torn. Predisposing factors are anatomical variations such as genu valgum, tibial torsion, high-riding patella (patella alta) and a shallow intercondylar groove, as well as patellar hypermobility due to generalized ligamentous laxity or localized muscle weakness.

OPERATIVE TREATMENT The area is approached through a medial incision. If the patellofemoral ligament is avulsed from the femur, it is reattached with suitable anchors. Mid-substance tears of the ligaments are sutured directly. At the same time, if the lateral retinaculum is tight it is released. Osteochondral fragments are removed – unless they are single, large and amenable to reattachment. Postoperatively a padded cylinder cast is applied with the knee in extension; this can be renewed when the swelling has subsided. A hinged brace is substituted, which provides control for weightbearing and allows knee movement. Quadriceps exercises are encouraged.

Complications Recurrent dislocation Patients treated non-operatively for a first-time dislocation have a 15–20 per cent chance of suffering further dislocations. This depends 30.16 Dislocation of the patella (a) The right patella has dislocated laterally; the flattened appearance is typical. (b,c) Anteroposterior and lateral films of traumatic dislocation of the patella.

(a)

(b)

(c)

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30

also on whether there are other predisposing abnormalities, and prevention consists of dealing with all these conditions (the subjects of recurrent dislocation, subluxation, chronic patellar instability and patellar mal-tracking are dealt with in Chapter 20).

OSTEOCHONDRAL INJURIES Osteochondral fractures and osteochondritis dissecans are similar injuries of the articular cartilage and subchondral bone. The knee joint is a common site for both conditions. The lesion is usually located on one of the femoral condyles, the intercondylar groove or the medial facet of the patella, and is thought to be due to the patella striking the opposed articular surface.

OSTEOCHONDRAL FRACTURES The patient gives a history of patellar dislocation or a blow to the front of the knee. The joint is swollen and aspiration yields blood-stained fluid mixed with fat globules. Standard anteroposterior and lateral x-rays seldom show the abnormality; if the diagnosis is suspected, tunnel and patellar skyline views are needed, and even then the fracture may be hard to see because the damaged area consists largely of articular cartilage. MRI or arthroscopy will be more helpful.

Treatment Small fragments should be removed as they may cause symptoms. Larger fragments, and especially those from loadbearing areas, can be reattached with screws (counter-sunk or ‘headless’ small fragment screws). Postoperatively a long-leg cast is applied for 2 weeks before movement is allowed. Sometimes a large area of cartilage damage, or even a crater, is discovered on the anterior intercondylar surface. In the past this was treated by trimming any ragged parts and drilling through the crater to stimulate an inflammatory response (‘micro-fracturing’). More recently, cartilage transplantation into these defects has shown promising results.

OSTEOCHONDRITIS DISSECANS

890

Teenagers and young adults who complain of intermittent pain in the knee are sometimes found to have developed a small segment of osteochondral necrosis, usually on the lateral aspect of the medial femoral condyle. This is probably a traumatic lesion, caused by repetitive contact with the overlying patella or an

adjacent ridge on the tibial plateau. The condition is described in Chapter 6.

TIBIAL PLATEAU FRACTURES Mechanism of injury Fractures of the tibial plateau are caused by a varus or valgus force combined with axial loading (a pure valgus force is more likely to rupture the ligaments). This is sometimes the result of a car striking a pedestrian (hence the term ‘bumper fracture’); more often it is due to a fall from a height in which the knee is forced into valgus or varus. The tibial condyle is crushed or split by the opposing femoral condyle, which remains intact.

Pathological anatomy The fracture pattern and degree of displacement depend on the type and direction of force as well as the quality of the bone at the upper end of the tibia. A useful classification is that of Schatzker (Fig. 30.17): Type 1 – a vertical split of the lateral condyle This is a fracture through dense bone, usually in younger people. It may be virtually undisplaced, or the condylar fragment may be pushed inferiorly and tilted; the damaged lateral meniscus may be trapped in the crevice. Type 2 – a vertical split of the lateral condyle combined with depression of an adjacent loadbearing part of the condyle

The wedge fragment, which varies in size from a portion of the rim to a sizeable part of the lateral condyle, is displaced laterally; the joint is widened and, if the fracture is not reduced, may later develop a valgus deformity. Type 3 – depression of the articular surface with an intact condylar rim Unlike type 2, the split to the edge of the

plateau is absent. The depressed fragments may be wedged firmly into the subchondral bone. The joint is usually stable and may tolerate early movement. Type 4 – fracture of the medial tibial condyle Two types of

fracture are seen: (1) a depressed, crush fracture of osteoporotic bone in an elderly person (a low-energy lesion), and (2) a high-energy fracture resulting in a condylar split that runs obliquely from the intercondylar eminence to the medial cortex. The momentary varus angulation may be severe enough to cause a rupture of the lateral collateral ligament and a traction injury of the peroneal nerve. The severity of these injuries should not be underestimated. Type 5 – fracture of both condyles Both condyles are split but there is a column of the metaphysis wedged in between that remains in continuity with the tibial shaft.

Type 6 – combined condylar and subcondylar fractures

This is a high-energy injury that may result in severe comminution. Unlike type 5 fractures, the tibial shaft is effectively disconnected from the tibial condyles.

(a)

(b)

(c)

The knee is swollen and may be deformed. Bruising is usually extensive and the tissues feel ‘doughy’ because of haemarthrosis. Examining the knee may suggest medial or lateral instability but this is usually painful and adds little to the x-ray diagnosis. More importantly, the leg and foot should be carefully examined for signs of vascular or neurological injury. Traction injury of the peroneal or tibial nerves is not uncommon and it is important to establish whether this is present at the time of admission and before operation.

Imaging

(d)

(e)

(f)

30.17 Tibial plateau fractures (a) Type 1 – simple split of the lateral condyle. (b) Type 2 – a split of the lateral condyle with a more central area of depression. (c) Type 3 – depression of the lateral condyle with an intact rim. (d) Type 4 – a fracture of the medial condyle. (e) Type 5 – fractures of both condyles, but with the central portion of the metaphysis still connected to the tibial shaft. (f) Type 6 – combined condylar and subcondylar fractures; effectively a disconnection of the shaft from the metaphysis.

Injuries of the knee and leg

Clinical features

30

Anteroposterior, lateral and oblique x-rays will usually show the fracture, but the amount of comminution or plateau depression may not be appreciated without computer tomography (CT). This provides information on the location of the main fracture lines, the site and size of the portion of condyle that is depressed and the position of major parts of articular surface that have been displaced. Software-generated re-assembly of the axial images can provide sagittal and coronal views that aid in surgical planning (Fig. 30.18). It is important not to miss a posterior condylar component in high-energy fractures because this may require a separate posteromedial or posterolateral exposure for internal fixation. With a crushed lateral condyle the medial ligament is often intact, but with a crushed medial condyle the lateral ligament is often torn.

Treatment Treatment by traction is simple and often produces a well-functioning knee, but residual angulation is not

(a)

(b)

(c)

(d)

30.18 Tibial plateau fractures – imaging (a) X-rays provide information about the position of the main fracture lines and areas of articular surface depression. (b,c) CT reconstructions reveal the extent and direction of displacements, vital information for planning the operation. (d) The postoperative x-ray shows that perfect reduction has been achieved.

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uncommon (Apley, 1979). On the other hand, obsessional surgery to restore the shattered surface may produce a good x-ray appearance – and a stiff knee, especially if the operation is followed by prolonged immobilization (Fig. 30.19). Undisplaced type 1 fractures can be treated conservatively. The haemarthrosis is aspirated and a compression bandage is applied. The limb is rested on a continuous passive motion (CPM) machine and knee movements are begun. As soon as the acute pain and swelling have subsided (usually within 1 week), a hinged cast-brace is fitted and the patient is allowed up; however, weightbearing is not allowed for another 3 weeks. Thereafter, partial weightbearing is permitted but full weightbearing is delayed until the fracture has healed (usually around 8 weeks). Displaced fractures should be treated by open reduction and internal fixation. The condylar surface is examined and trapped fragments are released or removed. The aim is for an accurate reduction; two lag screws or a buttress plate are usually sufficient for fixation.

Type 1 fractures

Type 2 fractures If depression is slight (less than 5 mm) and the knee is not unstable, or if the patient is old and frail or osteoporotic, the fracture is treated closed with the aim of regaining mobility and function rather than anatomical restitution. After aspiration and compression bandaging, skeletal traction is applied via a threaded pin passed through the tibia 7 cm below the fracture. An attempt is made to squeeze the condyle into shape; the knee is then flexed and extended several times to ‘mould’ the upper tibia on the opposing femoral condyle. The leg is cradled on pillows and, with 5 kg traction in place, active exercises are carried

out every day. As soon as the fracture is ‘sticky’ (usually at 3–4 weeks), the traction pin is removed, a hinged cast-brace is applied and the patient is allowed up on crutches. Full weightbearing is deferred for another 6 weeks. In younger patients, and more so in those with a central depression of more than 5 mm, open reduction with elevation of the plateau and internal fixation is often preferred. A midline incision offers good exposure – together with a limited transverse arthrotomy beneath the lateral meniscus; the joint is seen to allow a check on the quality of reduction. Bone graft or a similar substitute is needed to support the elevated fragments. Small 3.5 mm screws placed in parallel just beneath the subchondral bone hold up the elevated fragments well (these are sometimes referred to as ‘raft’ screws, describing the arrangement of parallel screws, Fig. 30.20). Alternatively cannulated screws can be used. The wedge of lateral condyle is then fixed with a buttress plate – newer designs of contoured and angle-stable plates (using screws that lock into the plate) are available but are not always necessary – and early knee movement is encouraged after surgery (Fig. 30.21). A CPM machine can help with the regime of passive exercise to complement the active work; at 2 weeks the patient is allowed up in a cast-brace, which is retained until the fracture has united. Type 3 fractures The principles of treatment are similar

to those applying to type 2 fractures. However, the fact that the lateral rim of the condyle is intact means that the knee is usually stable and a satisfactory outcome is more predictable. The depressed fragments may need to be elevated through a window in the metaphysis; reduction should be checked by x-ray or arthroscopy. The elevated fragments are supported with bone grafts and the whole segment is fixed in position with ‘raft’ screws. Postoperatively, exercises are begun as soon as possible and the patient is allowed up in a cast-brace, which is retained until the fracture has united. Type 4 fracture of the medial condyle Osteoporotic crush

(a)

892

(b)

3.19 Tibial plateau fractures – fixation (a) Tomography showed significant depression and some lateral displacement of the lateral condyle. (b) Open reduction and internal fixation with a buttress plate.

fractures of the medial plateau are difficult to reduce; in the long term the patient is likely to be left with some degree of varus deformity. The principles of treatment are the same as for type 2 fractures of the lateral plateau. Medial condylar split fractures usually occur in younger people and are caused by high-energy trauma. The fracture itself is often more complex than is appreciated at first sight; there may be a second, posterior split in the coronal plane that cannot be fixed through the standard anterior approach. Good lateral x-rays or CT are needed to define the fracture pattern. There is often an underlying ligament injury on the lateral side. Stable fixation of the medial side, along the lines described for the type 2 fracture will

30

30.20 Raft screws (a–c) These small 3.5 mm cortical screws are inserted just beneath the subchondral surface and form a ‘raft’ above which the elevated fragments of the plateau are supported. In types 2, 5 or 6 injuries, they need to be supplemented by a buttress plate.

(a)

(a)

(c)

(b)

(c)

(d)

Injuries of the knee and leg

(b)

(e)

30.21 Tibial plateau fractures – fixation (a) Two or three lag screws may be sufficient for simple split fractures (type 1), though (b) a buttress plate and screws may be more secure. (c) Depression of more than 5 mm in a type 3 fracture can be treated by elevation from below and (d) supported by bone grafts and fixation. (e) Type 2 fractures require a combination of both techniques – direct reduction, elevation of depressed areas, bone grafting and buttress plate fixation.

then allow an assessment of the ligament injury. If the joint is unstable after fracture fixation, the torn structures on the lateral side may need repair. These are severe injuries that carry the added risk of a compartment syndrome. A simple bicondylar fracture, in an elderly patient, can often be reduced by traction and the patient then treated as for a type 2 injury – some residual angulation may follow (Fig. 30.22). However, it is more usual to consider stable internal fixation and early joint movement for these injuries, but surgery is not without significant risk. The danger is that the wide exposure necessary to gain access to both condyles may strip the

Types 5 and 6 fractures

supporting soft tissues, thus increasing the risk of wound breakdown and delayed union or non-union. New strategies involve spanning the knee joint with an external fixator, thereby providing provisional stability, and waiting for the soft-tissue conditions to improve – sometimes as long as 2–3 weeks. Then a double incision approach (anterior and posteromedial usually) is made, which provides access to the main fracture fragments and limits the amount of subperiosteal elevation carried out if both condyles are approached through a single anterior incision only. Buttress plates placed in a submuscular fashion are used (Fig. 30.23). An alternative method is to perform the articular reduction through a limited surgi-

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(b)

(a)

(c)

30.22 Complex plateau fractures – non-operative treatment (a) Even in this complex bicondylar fracture, non-operative treatment (b,c) with a low-traction pin makes early movement possible. (d) 10 days later the x-ray shows reasonably good reduction and the functional result was excellent.

cal exposure (this can often be done percutaneously) and to stabilize the metaphysis to the diaphysis using a circular external fixator (Fig. 30.24). This approach is less risky and can produce better results (Canadian Orthopaedic Trauma Society, 2006). Traction is used to achieve reduction; many of the fragments that have soft-tissue attachments will reduce spontaneously (ligamentotaxis). This is done by applying bone distractors across the knee joint or by traction on a traction table. If open reduction is needed or intended, the operation should be carefully planned. High-quality imaging is needed to define the fracture pattern accurately. The difficulty of fixing plateau fractures should not be

Principles in reduction and fixation

(a)

894

(d)

underestimated; operative treatment should be undertaken only if the full range of implants and the necessary expertise are available. The standard approach to the lateral part of the joint is through a longitudinal parapatellar incision. The aim is to preserve the meniscus while fully exposing the fractured plateau; this is best done by entering the joint through a transverse capsular incision beneath the meniscus. If exposure of the medial compartment is needed, a separate posteromedial incision and approach is made. Dividing the patellar ligament in a Z-fashion – whilst giving good access across the entire joint – limits the extent of knee flexion exercises after surgery, even if the ligament is repaired. A single large fragment may be re-positioned and held with lag screws and washers; a buttress plate is

(b)

(c)

30.23 Complex tibial plateau fractures – internal fixation Soft tissue trauma in high-energy complex fractures of the tibial plateau usually makes it unsafe to undertake extensive open surgery early on. Provisional stabilization by a spanning external fixator allows the swelling to reduce and the patient to rest comfortably (a). When conditions improve, and this may take as long as 2 weeks, open surgery can be undertaken. In this example two buttress plates were used to shore up the lateral and posteromedial aspects of the tibial plateau (b,c).

(a)

(b)

(c)

added for security. Comminuted, depressed fractures must be elevated by pushing the fragmented mass upwards from below; the osteoarticular surface is then supported by packing the subchondral area with cortico-cancellous grafts (obtained from the iliac crest) and held in place by inserting ‘raft’ screws and a suitably contoured buttress plate. Unless it is torn, the meniscus should be preserved and sutured back in place when the capsule is repaired. Displaced fractures with splits in both the sagittal and the coronal plane may be impossible to reduce and fix through the anterior approach; a second, posteromedial or posterolateral approach is the answer. Extensive exposure and manipulation of highly comminuted fractures can sometimes be selfdefeating. These injuries may be better treated by percutaneous manipulation of the fragments (under traction) and circular-frame external fixation. Stability is all-important; no matter which method is used, fixation must be secure enough to permit early joint movement. There is little point in ending up with a pleasing x-ray and a stiff knee. Postoperatively the limb is elevated and splinted until swelling subsides; movements are begun as soon as possible and active exercises are encouraged. The patient is allowed up as swelling subsides, and at the end of 6 weeks the patient can partial weightbear with crutches; full weightbearing is resumed when healing is complete, usually after 12–16 weeks.

developing a stiff knee. This is prevented by avoiding prolonged immobilization and encouraging movement as early as possible. Deformity Some residual valgus or varus deformity is

30

Injuries of the knee and leg

30.24 Complex tibial plateau fractures – external fixation Rather than expose the joint formally in order to reduce the fracture, this can be done percutaneously, albeit with x-ray control, and the articular fragments held with multiple screws (a,b). The tibial metaphysis is then held to the shaft using a circular external fixator (c).

quite common – either because the fracture was incompletely reduced or because, although adequately reduced, the fracture became re-displaced during treatment. Fortunately, moderate deformity is compatible with good function, although constant overloading of one compartment may predispose to osteoarthritis in later life. Osteoarthritis If, at the end of treatment, there is marked depression of the plateau, or deformity of the knee or ligamentous instability, secondary osteoarthritis is likely to develop after 5 or 10 years. This may eventually require reconstructive surgery.

FRACTURE-SEPARATION OF PROXIMAL TIBIAL EPIPHYSIS This uncommon injury is usually caused by a severe hyperextension and valgus strain. The epiphysis displaces forwards and laterally, often taking a small fragment of the metaphysis with it (a Salter–Harris type 2 injury). There is a risk of popliteal artery damage where the vessel is stretched across the step at the back of the tibia.

Complications EARLY Compartment syndrome – With closed types 4 and 5 fractures there is considerable bleeding and swelling of the leg – and a risk of developing a compartment syndrome. The leg and foot should be examined repeatedly for signs. LATE Joint stiffness With severely comminuted fractures, and

after complex operations, there is a considerable risk of

Clinical features The knee is tensely swollen and extremely tender. If the epiphysis is displaced, there may be a valgus or hyperextension deformity. All movements are resisted. The swelling may extend into the calf and a careful watch for compartment syndrome, particularly if the fracture was caused by hyperextension, is important. Salter–Harris type 1 and 2 injuries may be undisplaced and difficult to define on x-ray; a few small

X-ray

895

FRACTURES AND JOINT INJURIES

30

bone fragments near the epiphysis may be the only clue. In the more serious injuries the entire upper tibial epiphysis may be tilted forwards or sideways. The fracture is categorized by the direction of displacement, so there are hyperextension, flexion, varus or valgus types.

Treatment Under anaesthesia, closed manipulative reduction can usually be achieved. The direction of tilt may suggest the mechanism of injury; the fragment can be reduced by gentle traction and manipulation in a direction opposite to that of the fracturing force. Fixation using smooth K-wires or screws may be needed if the fracture is unstable. Occasionally, when the entire tibial epiphysis cannot be accurately reduced by closed manipulation, it is repositioned at operation and held by a screw (Figure 30.25). The rare Salter–Harris type 3 or 4 fractures also may need open reduction and fixation. Following reduction, whether closed or open, a long-leg cast is applied. For the usual hyperextension injury the knee is held flexed at 30 degrees; for the less common flexion and varus injuries the knee is kept straight. The cast is worn for 6–8 weeks, with partial weightbearing from the outset. Knee movement quickly returns when the cast is removed.

FRACTURE OF PROXIMAL END OF FIBULA Fracture of the proximal end of the fibula may be caused by either direct injury or an indirect twisting injury of the lower limb. Beware: an isolated fracture of the proximal fibula is rare; it may be merely the most visible part of a more extensive rotational injury of the leg involving a serious fracture or ligament injury of the ankle (the Maisonneuve fracture) or a major disruption of the posterolateral corner of the knee. Always x-ray the ankle and check for knee stability! The fracture itself is of little consequence and it requires no treatment. However, associated injuries are frequent and they may result in prolonged disability.

Complications Associated injuries Associated lesions, which should be

looked for in every case, are: (1) the ankle injury mentioned earlier; (2) peroneal nerve injury; (3) lateral collateral ligament injury – more usually a disruption of this ligament and the posterolateral corner – especially if the fibula styloid is avulsed; (4) peroneal nerve entrapment – an occasional late complication. Each of these conditions requires specific treatment.

Complications Epiphyseal fractures in young children sometimes result in angular deformity of the proximal tibia. This may later require operative correction. With the higher grades of injury there is a risk of complete growth arrest at the proximal tibia. If the predicted leg length discrepancy is greater than 2.5 cm, tibial lengthening (or epiphyseodesis of the opposite limb) may be needed.

DISLOCATION OF PROXIMAL TIBIOFIBULAR JOINT A blow or twisting injury may cause subluxation or dislocation of the proximal tibio-fibular joint. Isolated injuries are rare; they usually occur in parachuting or

30.25 Fracture-separation of proximal tibial epiphysis (a) This hyperextension type of fracture needs urgent reduction because the popliteal vessels are endangered. (b) A flexion type of fracture-separation, but essentially a Salter–Harris type 4 pattern; in this case reduction was held with internal fixation (c).

896

(a)

(b)

(c)

X-ray In the normal anteroposterior x-ray of the knee

the fibular head overlaps the lateral tibial condyle; in a dislocation the fibular head stands clear of the tibia, and in the lateral view the fibular head is displaced either forwards or backwards. Manual reduction is carried out by flexing the knee to 90 degrees (to relax the lateral collateral ligament) and pressing upon the fibular head; reductions are usually stable and a plaster cylinder is applied for 4 weeks. Recurrent subluxation may call for excision of the fibular head.

FRACTURES OF TIBIA AND FIBULA Because of its subcutaneous position, the tibia is more commonly fractured, and more often sustains an open fracture, than any other long bone.

1. The state of the soft tissues – The risk of complications and the progress to fracture healing are directly related to the amount and type of soft-tissue damage. Closed fractures are best described using Tscherne’s (Oestern and Tscherne, 1984) method; for open injuries, Gustilo’s grading (Table 30.2) is more useful (Gustilo et al., 1984). The incidence of tissue breakdown and/or infection ranges from 1 per cent for Gustilo type I to 30 per cent for type IIIC. 2. The severity of the bone injury – High-energy fractures are more damaging and take longer to heal than low-energy fractures; this is regardless of whether the fracture is open or closed. Lowenergy breaks are typically closed or Gustilo I or II, and spiral. High-energy fractures are usually caused by direct trauma and tend to be open (Gustilo III A–C), transverse or comminuted. 3. Stability of the fracture – Consider whether it will displace if weightbearing is allowed. Long oblique fractures tend to shorten; those with a butterfly fragment tend to angulate towards the butterfly. Severely comminuted fractures are the least stable of all, and the most likely to need mechanical fixation. 4. Degree of contamination – In open fractures this is an important additional variable.

30

Injuries of the knee and leg

similar activities. Occasionally the condition is habitual and associated with generalized ligamentous laxity. The fibular head displaces upwards, and either anterolaterally or posteromedially. There is usually pain and local tenderness; the abnormal contour over the lateral aspect of the knee is best seen when the two knees are flexed to 90 degrees on the examination couch. Always check for peroneal nerve injury.

TSCHERNE’S CLASSIFICATION OF SKIN LESIONS IN CLOSED FRACTURES

Mechanism of injury A twisting force causes a spiral fracture of both leg bones at different levels; an angulatory force produces transverse or short oblique fractures, usually at the same level. Indirect injury is usually low energy; with a spiral or long oblique fracture one of the bone fragments may pierce the skin from within. Direct injury crushes or splits the skin over the fracture; this is usually a high-energy injury and the most common cause is a motorcycle accident.

IC1

No skin lesion

IC2

No skin laceration but contusion

IC3

Circumscribed degloving

IC4

Extensive, closed degloving

IC5

Necrosis from contusion

Clinical features Pathological anatomy The behaviour of these injuries – and therefore the choice of treatment – depends on the following factors:

The limb should be carefully examined for signs of soft-tissue damage: bruising, severe swelling, crushing or tenting of the skin, an open wound, circulatory

Table 30.2 Gustilo’s classification of open fractures Grade

Wound

Soft-tissue injury

Bone injury

I

1 cm long

Moderate, some muscle damage

Moderate comminution

IIIA

Usually >1 cm long

Severe deep contusion; + compartment syndrome

High-energy fracture patterns; comminuted but soft-tissue cover possible

IIIB

Usually >10 cm long

Severe loss of soft-tissue cover

Requires soft-tissue reconstruction for cover

IIIC

Usually >10 cm long

As IIIB, with need for vascular repair

Requires soft-tissue reconstruction for cover

897

30

changes, weak or absent pulses, diminution or loss of sensation and inability to move the toes. Any deformity should be noted before splinting the limb. Always be on the alert for signs of an impending compartment syndrome.

FRACTURES AND JOINT INJURIES

X-ray The entire length of the tibia and fibula, as well

as the knee and ankle joints, must be seen. The type of fracture, its level and the degree of angulation and displacement are recorded. Rotational deformity can be gauged by comparing the width of the tibio-fibular interspace above and below the fracture. Spiral fractures without comminution are lowenergy injuries. Transverse, short oblique and comminuted fractures, especially if displaced or associated with a fibular fracture at a similar level, are highenergy injuries.

Management The main objectives are: (1) to limit soft-tissue damage and preserve (or restore, in the case of open fractures) skin cover; (2) to prevent – or at least recognize – a compartment syndrome; (3) to obtain and hold fracture alignment; (4) to start early weightbearing (loading promotes healing); (5) to start joint movements as soon as possible. The first step is to gain a clear idea of the character of the injury – what some have called the ‘fracture personality’ – which is a combination of the soft tissue condition and fracture pattern. Uncomminuted, spiral

(a)

(c)

898

fractures with minimal soft-tissue damage (including open injuries like Gustilo I) are likely to heal with a minimum of trouble; they can be treated conservatively unless there is a definite indication for surgery (see later). Fractures associated with severe soft-tissue damage (whether open or closed) and unstable fracture patterns need much more careful attention if complications are to be avoided. LOW-ENERGY FRACTURES Most low-energy fractures, including Gustilo I injuries after attention to the wounds, can be treated by non-operative methods. If the fracture is undisplaced or minimally displaced, a full-length cast from upper thigh to metatarsal necks is applied with the knee slightly flexed and the ankle at a right angle (Fig. 30.26). Displacement of the fibular fracture, unless it involves the ankle joint, is unimportant and can be ignored. If the fracture is displaced, it is reduced under general anaesthesia with x-ray control. Apposition need not be complete but alignment must be near-perfect (no more than 7 degrees of angulation) and rotation absolutely perfect. A full-length cast is applied as for undisplaced fractures (note, however, that if placing the ankle at 0 degrees causes the fracture to displace, a few degrees of equinus are acceptable). The position is checked by x-ray; minor degrees of angulation can still be corrected by making a transverse cut in the plaster and wedging it into a better position. The limb is elevated and the patient is kept under

(b)

(d)

30.26 Fractured tibia and fibula – closed treatment (1) Reduction is facilitated by bending the knee over the end of the table, with the normal leg alongside for comparison (a). The surgeon holds the position while an assistant applies plaster from the knee downwards (b). When the plaster has set, the leg is lifted and the above-knee plaster completed (c); note that the foot is plantigrade, the knee slightly bent, and the plaster moulded round the patella. A rockered boot is fitted for walking (d).

Exercise From the start, the patient is taught to exercise the muscles of the foot, ankle and knee. When he gets up, an overboot with a rocker sole is fitted and he is taught to walk correctly. When the plaster is removed, a crepe bandage or elasticated support is applied and the patient is told that he may either elevate and exercise the limb or walk correctly on it, but he must not let it dangle idly. Functional bracing With stable fractures the full-length

cast may be changed after 4–6 weeks to a functional below-knee brace that is carefully moulded to bear upon the upper tibia and patellar tendon. This liberates the knee and allows full weightbearing (Sarmiento and Latta, 2006). A snug fit is important and the fastening straps will need to be tightened as the swelling subsides. Indications for skeletal fixation If follow-up x-rays show unsatisfactory fracture alignment, and wedging fails to correct this, the plaster is abandoned and the fracture

is reduced and fixed at surgery. Indeed, many surgeons would hold that unstable fractures are better treated by skeletal fixation from the outset. This is the method of choice for internal fixation. The fracture is reduced under x-ray control and image intensification. The proximal end of the tibia is exposed; a guide-wire is passed down the medullary canal and the canal is reamed. A nail of appropriate size and shape is then introduced from the proximal end across the fracture site. Transverse locking screws are inserted at the proximal and distal ends (Fig. 30.28). Postoperatively, partial weightbearing is started as soon as possible, progressing to full weightbearing when this is comfortable. For diaphyseal fractures, union can be expected in over 95 per cent of cases. However, the method is less suitable for fractures near the bone ends.

30

Closed intramedullary nailing

Injuries of the knee and leg

observation for 48–72 hours. If there is excessive swelling, the cast is split. Patients are usually allowed up (and home) on the second or third day, bearing minimal weight with the aid of crutches. The immediate application of plaster may be unwise if skin viability is doubtful, in which case a few days on skeletal traction is useful as a preliminary measure (Fig. 30.27). After 2 weeks the position is checked by x-ray. A change from an above- to a below-the-knee cast is possible around 4–6 weeks, when the fracture becomes ‘sticky’. The cast is retained (or renewed if it becomes loose) until the fracture unites, which is around 8 weeks in children but seldom under 12 weeks in adults.

Plate fixation Plating is best for metaphyseal fractures

that are unsuitable for nailing. It is also sometimes used for unstable tibial shaft fractures in children. Previously, the disadvantages of plate fixation included the need to expose the fracture site and, in so doing, stripping the soft tissues around the fracture. This may increase the risk of introducing infection and delaying union. Newer techniques of plating overcome these disadvantages. The plate is slid across the fracture through proximal and distal ‘access incisions’ on the anterolateral aspect of the tibia and then fixed to the bone only at these levels. This method of ‘submuscular’ plating preserves the soft tissues around the fracture site better than conventional open plating, and provides a relative stability that appears to hasten

(a)

(b)

(c)

(d)

30.27 Fractured tibia and fibula – closed treatment (2) (a) Skeletal traction is used to reduce overlap, and also as provisional treatment when skin viability is doubtful. Plaster is applied 10–14 days later (b), using the technique shown in Figure 30.26, except that the skeletal pin is retained until the plaster has set. Examples of spiral and transverse fractures treated in this way are shown in (c) and (d).

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FRACTURES AND JOINT INJURIES

30

Partial weightbearing is permitted from the start and the external fixator can be replaced by a functional brace once there are signs of union (although, with modern fixators, this is usually unnecessary because fracture loading can be controlled and adjusted in the fixator).

(a)

(b)

(c)

30.28 Fractured tibia and fibula – intramedullary nailing Closed intramedullary nailing is now the preferred treatment for unstable tibial fractures. This series of x-rays shows the fracture before (a) and after (b,c) nailing. Active movements and partial weightbearing were started soon after operation.

union. Even so, full weightbearing will need to be deferred until some callus formation is evident on xray, usually at 6–8 weeks. External fixation This is an alternative to closed nailing;

it avoids exposure of the fracture site and allows further adjustments to be made if this should be needed.

HIGH-ENERGY FRACTURES Initially, the most important consideration is the viability of the damaged soft tissues and underlying bone. Tissues around the fracture should be disturbed as little as possible and open operations should be avoided unless there is already an open wound. Transverse fractures are usually stable after reduction; they can be treated ‘closed’, provided a careful watch is kept for symptoms and signs of complications (excessive pain, swelling, tightness or sensory change). Comminuted and segmental fractures, those associated with bone loss, and indeed any high-energy fracture that is inherently unstable, require early surgical stabilization. For closed fractures, external fixation and closed nailing are equally suitable; in both cases the tissues around the fracture are left undisturbed (Fig. 30.29). For open fractures, the use of internal fixation has to be accompanied by judicious and expert debridement and prompt cover of the exposed bone and implant; alternatively, external fixation can be safer if these pre-requisites cannot be met. In cases of bone loss, small defects can be treated by delayed bone grafting; larger defects will need either bone transport or compression-distraction (acute shortening to close the defect, with subsequent lengthening at a different level) with an external fixator (Chapter 12). 30.29 Fixation (a–d) This method of fixation offers the benefit of multilevel stability and can be carried out with little additional damage to the soft tissues around the injury.

900

(a)

(b)

(c)

(d)

OPEN FRACTURES A suitable mantra for the treatment of open tibial fractures is: antibiotics debridement stabilization prompt soft-tissue cover rehabilitation.

Antibiotics are started immediately. A first- or second-generation cephalosporin is suitable for Gustilo grades I–IIIA wounds but more severe grades may benefit from Gram-negative cover as well (an aminoglycoside such as gentamicin is often used). With an adequate debridement, the antibiotics are continued for 24 hours in a grade 1 fracture and 72 hours in more severe grades. However, the evidence for prolonged antibiotic use is lacking and, not surprisingly, most infections from delayed closure of open tibial wounds tend to be by nosocomial hospital-acquired bacteria. These can be multiresistant organisms that are not covered by standard antibiotics, thus good debridement of the fracture and prompt cover remain the strongest defence against infection. The wound should be photographed on first inspection in the emergency department using a Polaroid or digital camera, and then covered with a sterile dressing. The photograph can then be printed for inclusion in the patient’s case notes to serve as a record and prevent further disturbance to the wound. Adequate debridement is possible only if the original wound is extended. However, excise as little skin as possible and discuss wound extensions with a plastic surgeon, especially if there appears to be a need for local or free skin or muscle flaps. Ideally the debridement should be performed jointly with the plastic surgeon. All dead and foreign material is removed; this includes bone without significant soft-tissue attachments. Tissue of doubtful viability may be left for a second look in 48 hours. The wound and fracture site are then washed out with large quantities of normal saline. Gustilo grade I injuries can be closed primarily – being a low-energy injury with a small wound, closure should be possible without skin tension – and the fracture then treated as for closed injuries. More severe wounds should, ideally, be closed at primary surgery as long as the debridement has been thorough and the skills of a plastic surgeon are at hand. If there is tissue of doubtful viability that requires another look, or a local flap cover deemed to be inappropriate, a second planned operation is needed. This allows further debridement and, hopefully, sufficient time to plan cover by free tissue transfer. Temporary cover of the exposed bone by using antibiotic beads sealed with an impervious plastic film can help reduce bacterial colo-

30

Injuries of the knee and leg

• • • • •

nization. In general the aim should be to close the wound in the first 3–5 days. It is important to stabilize the fracture. For Gustilo I, II and IIIA injuries, locked intramedullary nailing is permissible as definitive wound cover is usually possible at the time of debridement. For more severe grades of open tibial fracture, internal fixation should be performed only at the time of definitive soft tissue cover. If this is not feasible at the time of primary debridement, the fracture should be stabilized temporarily with a spanning external fixator. Exchange of the fixator for an intramedullary nail can be done at the point when definitive soft tissue cover is carried out – ideally within 5 days of the injury. Alternatively, definitive fracture management can be carried out using external fixation. Severe grades of open fractures should, whenever possible, be managed from the outset under the combined care of an orthopaedic surgeon and a plastic surgeon.

Postoperative management Swelling is common after tibial fractures; even after skeletal fixation the soft tissues continue to swell for several days. The limb should be elevated and frequent checks made for signs of compartment syndrome (see later). After intramedullary nailing of a transverse or short oblique fracture, weightbearing can be started within a few days and increased to full weight when this is comfortable. If the fracture is comminuted or segmental, meaning that almost the entire load will be taken by the nail initially, only partial weightbearing is permitted until some callus is seen on x-ray. With plate fixation, additional support with a cast may be needed if partial weightbearing is to start soon after surgery; otherwise weightbearing is delayed for 6 weeks. Unlike fractures treated with intramedullary nails, callus formation is not seen as rapidly and this may give a poor signal for increasing the amount of weightbearing. Patients with fractures stabilized with external fixators can usually weightbear early unless there is major bone loss. Weightbearing through the fractured tibia is increased when callus is visible on x-ray; the fixator is later ‘dynamized’ to allow greater load transfer through the bone and help the callus bridge to mature. This does away with the need for exchanging the external fixator for a functional brace. However, if the pin sites are in poor condition or there is loosening of the hold on the tibia, a change to functional bracing is helpful.

Early complications VASCULAR INJURY Fractures of the proximal half of the tibia may damage the popliteal artery. This is an emergency of the first

901

FRACTURES AND JOINT INJURIES

30

902

order, requiring exploration and repair. Damage to one of the two major tibial vessels may also occur and go unnoticed if there is no critical ischaemia. COMPARTMENT SYNDROME Tibial fractures – both open and closed – are among the commonest causes of compartment syndrome in the leg. The combination of tissue oedema and bleeding (oozing) causes swelling in the muscle compartments and this may precipitate ischaemia. Additional risk factors are proximal tibial fractures, severe crush injury, a long ischaemic period before revascularization (in type IIIC open fractures), a long delay to treatment, haemorrhagic shock, difficult and prolonged operation and a fracture fixed in distraction. The diagnosis is usually suspected on clinical grounds. Warning symptoms are increasing pain, a feeling of tightness or ‘bursting’ in the leg and numbness in the leg or foot. These complaints should always be taken seriously and followed by careful and repeated examination for pain provoked by muscle stretching and loss of sensibility and/or muscle strength. Heightened awareness is all! The diagnosis can be confirmed by measuring the compartment pressures in the leg. Indeed, so important is the need for early diagnosis that some surgeons advocate the use of continuous compartment pressure monitoring for all tibial fractures (McQueen et al., 1996). This deals admirably with patients who are unconscious or uncooperative, and those with multiple injuries. It also serves as an ‘early warning system’ in less problematic cases. A split-tip 20-gauge catheter is introduced into the anterior compartment of the leg and the pressure is measured close to the level of the fracture (Heckman et al., 1994). A differential pressure (ΔP) – the difference between diastolic pressure and compartment pressure – of less than 30 mmHg (4.00 kPA) is regarded as critical and an indication for compartment decompression. Ideally the pressure should be measured in all four compartments but this is often impractical; however, if the clinical features suggest a compartment syndrome and the anterior compartment pressure is normal or borderline, pressures should be measured in the other compartments. Fasciotomy and decompression Once the diagnosis is made, decompression should be carried out with the minimum delay – and that means decompression of all four compartments at the first operation. This is best and most safely accomplished through two incisions, one anterolateral and one posteromedial. The anterolateral incision is made about 2–3 cm lateral to the crest of the tibia and extends from the level of the tibial tuberosity to just above the ankle (Fig. 30.30). The fascia is split along the length of the anterior and lateral compartments taking care not to damage the superfi-

(a)

(b)

(c)

30.30 Compartment syndrome (a) With a fracture at this level the surgeon should be constantly on the alert for symptoms and signs of a compartment syndrome. This patient was treated in plaster. Pain became intense and when the plaster was split (which should have been done immediately after its application), the leg was swollen and blistered (b). Tibial compartment decompression (c) requires fasciotomies of all the compartments in the leg.

cial peroneal nerve. A second, similar incision is made just posterior to the posteromedial border of the tibia; the fascial covering of the superficial posterior compartment is split. The deep posterior compartment is identified just above the ankle (where its fascial covering is absent) and traced proximally; the muscle bulk of the superficial compartment needs to be retracted posteriorly, exposing the fascial envelope of the deep posterior compartment, which is likewise split down its entire length. Segmental arteries that perforate the fascia from the posterior tibial artery should be preserved for possible use in local skin flaps (Fig. 30.31). The incisions are left open, a well-padded dressing is applied and the leg is splinted with the ankle in the neutral position. The fracture is treated as a grade III open injury requiring a spanning external fixator and prompt return for wound closure or skin grafting.

30

Injuries of the knee and leg

(a)

(b)

(c)

30.31 Fasciotomies for compartment decompression (a) The first incision is usually anterolateral, giving access to the anterior and lateral compartments. But this is not enough. The superficial and deep posterior compartments also must be opened; their position is shown in (b), a cross-section of the leg. This requires a second incision (b,c), which is made a finger’s breadth behind the posteromedial border of the tibia; care must be taken not to damage the deep perforators of the posterior tibial artery. Note that the two incisions should be placed at least 7 cm apart so as to ensure a sufficient skin bridge without risk of sloughing.

Outcome Compartment decompression within 6 hours

of the onset of symptoms (or critical pressure measurement) should result in full recovery. Delayed decompression carries the risk of permanent dysfunction, the extent of which varies from mild sensory and motor loss to severe muscle and nerve damage, joint contractures and trophic changes in the foot. INFECTION Open fractures are always at risk; even a small perforation should be treated with respect and debridement carried out before the wound is closed. If the diagnosis is suspected, wound swabs and blood samples should be taken and antibiotic treatment started forthwith, using a ‘best guess’ intravenous preparation; once the laboratory results are obtained, a more suitable antibiotic may be substituted. With established infection, skeletal fixation should not be abandoned if the system is stable; infection control and fracture union are more likely if fixation is secure. However, if there is a loose implant it should be removed and replaced by external fixation.

Late complications Slight shortening (up to 1.5 cm) is usually of little consequence, but rotation and angulation Malunion

deformity, apart from being unsightly, can be disabling because the knee and ankle no longer move in the same plane. Angulation should be prevented at all stages; anything more than 7 degrees in either plane is unacceptable. Angulation in the sagittal plane, especially if accompanied by a stiff equinus ankle, produces a marked increase in sheer forces at the fracture site during walking; this may result in either refracture or non-union. Varus or valgus angulation will alter the axis of loading through the knee or ankle, causing increased stress in some part of the joint. This is often cited as a cause of secondary osteoarthritis; however while this may be true for angular deformities close to the joint, long-term studies have failed to show that it applies to moderate deformities in the middle third of the bone. Rotational alignment should be near-perfect (as compared with the opposite leg). This may be difficult to achieve with closed methods, but it should be possible with locked intramedullary nailing. Late deformity, if marked, should be corrected by tibial osteotomy. Delayed union High-energy fractures are slow to unite

and liable to non-union or fatigue failure if a nail has been used. If there is insufficient contact at the fracture

903

FRACTURES AND JOINT INJURIES

30

site, either through bone loss or comminution, ‘prophylactic’ bone grafting as soon as the soft tissues have healed is recommended (Watson, 1994). If there is a failure of union to progress on x-ray by 6 months, secondary intervention should be considered. The first nail is removed, the canal reamed and a larger nail reinserted. If the fibula has united before the tibia, it should be osteotomized so as to allow better apposition and compression of the tibial fragments. Non-union This may follow bone loss or deep infection, but a common cause is faulty treatment. Either the risks and consequences of delayed union have not been recognized, or splintage has been discontinued too soon, or the patient with a recently united fracture has walked with a stiff equinus ankle. Hypertrophic non-union can be treated by intramedullary nailing (or exchange nailing) or compression plating. Atrophic non-union needs bone grafting in addition. If the fibula has united, a small segment should be excised so as to permit compression of the tibial fragments. Intractable cases will respond to nothing except radical Ilizarov techniques (Fig. 30.32). Joint stiffness Prolonged cast immobilization is liable to

cause stiffness of the ankle and foot, which may persist for 12 months or longer in spite of active exercises. This can be avoided by changing to a functional brace as soon as it is safe to do so, usually by 4–6 weeks. Osteoporosis Osteoporosis of the distal fragment is so

common with all forms of treatment as to be regarded as a ‘normal’ consequence of tibial fractures. Axial loading of the tibia is important and weightbearing should be re-established as soon as possible. After prolonged external fixation, special care should be taken to prevent a distal stress fracture. With distal third fractures, this is not uncommon. Exercises should be encouraged throughout the period of treatment. The management of the established condition is discussed in Chapter 10. Regional complex pain syndrome

FRACTURE OF TIBIA ALONE A direct injury, such as a kick or blow with a club, may cause a transverse or slightly oblique fracture of the tibia alone at the site of impact. In children, the fracture is usually caused by an indirect injury; the fibula is intact or may show plastic deformation. Local bruising and swelling are usually evident, but knee and ankle movements are possible. Transverse or slightly oblique fractures are easy to spot on x-ray even if displacement is slight. The child with a spiral fracture may be able to stand on the leg, and as the fracture may be almost invisible in an anteroposterior film, the injury can be missed unless two views are obtained; a few days later an angry mother brings the child back with a lump that proves to be callus!

Treatment If the fracture is displaced, reduction should be attempted. An above-knee plaster is applied as with a fracture of both bones; first a split plaster and then, when swelling has subsided, a complete one. A fracture of the tibia alone takes just as long to unite as if both bones were broken, so at least 12 weeks is needed for consolidation and sometimes much longer. The child with a spiral fracture, however, can be safely released after 6 weeks; and with a mid-shaft transverse fracture the surgeon may (if he or she is a skilled plasterer and reduction is perfect) replace the above-knee plaster by a short plaster gaiter.

Complications Delayed union Isolated tibial fractures, especially in the lower third, may be slow to join and the temptation is to discard splintage too soon. Even slight displacement and loss of contact at the fracture level may delay union, so internal fixation is often preferred as primary treatment. This fracture also has a tendency to drift 30.32 Fractured tibia and tibula – late complications (a) Hypertrophic non-union: the exuberant callus formation and frustrated healing process are typical. (b) Atrophic non-union: there is very little sign of biological activity at the fracture site. (c) Malunion: treated, in this case, by gradual correction in an Ilizarov fixator (d,e).

904

(a)

(b)

(c)

(d)

(e)

into varus in the later stages of healing; sometimes a fibular osteotomy is needed to allow correction of the deformity at surgery.

Isolated spiral fractures should be regarded with suspicion: they are often associated with other injuries and it is wise to obtain x-rays of the ankle and knee. A transverse or short oblique fracture may be due to a direct blow. There is local tenderness, but the patient is able to stand and to move the knee and ankle. Pain can usually be controlled by analgesic medication and the patient will need no more than an elastic bandage, from knee to toes, for 2 or 3 weeks. In the occasional case where pain is more severe, a below-knee walking cast may be necessary. Pathological fractures sometimes occur in patients with osteomyelitis or bone tumours. Treatment is that of the underlying condition.

FATIGUE FRACTURES Repetitive stress may cause a fatigue fracture of the tibia (usually in the upper half of the bone) or the fibula (most often in the lower third). This injury is seen in army recruits, mountaineers, runners and ballet dancers, who complain of pain in the leg. There is local tenderness and slight swelling. The condition may be mistaken for a chronic compartment syndrome. X-ray For the first 4 weeks there may be nothing

abnormal about the x-ray, but a bone scan shows increased activity. After some weeks periosteal new bone may be seen, with a small transverse defect in the cortex. There is a danger that these appearances may be mistaken for those of an osteosarcoma, with tragic consequences. If the diagnosis of stress fracture is kept in mind, such mistakes are unlikely.

Treatment The patient is told to avoid the stressful activity. Usually after 8–10 weeks the symptoms settle down. A short leg gaiter can be applied for comfort during weightbearing.

REFERENCES AND FURTHER READING Apley AG. Fractures of the tibial plateau. Orthop Clin North Am 1979; 10: 61–74.

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Injuries of the knee and leg

FRACTURE OF FIBULA ALONE

Bahk MS, Cosgarea AJ. Physical examination and imaging of the lateral collateral ligament and posterolateral corner of the knee. Sports Med Arthrosc 2006; 14: 12–19. Canadian Orthopaedic Trauma Society. Open reduction and internal fixation compared with circular fixator application for bicondylar tibial plateau fractures. Results of a multicenter, prospective, randomized clinical trial. J Bone Joint Surg 2006; 88A: 2613–23. Conlan T, Garth WP, Lemons JE. Evaluation of the medial soft-tissue restraints of the extensor mechanism of the knee. J Bone Joint Surg 1993; 75A: 682–93. Daniel DM, Stone ML, Barnett P, Sachs R. Use of the quadriceps active test to diagnose posterior cruciate-ligament disruption and measure posterior laxity of the knee. J Bone Joint Surg 1988; 70A: 386–91. Galway HR, MacIntosh DL. The lateral pivot shift: a symptom and sign of anterior cruciate ligament insufficiency. Clin Orthop Relat Res 1980; 147: 45–50. Gustilo RB, Mendoza RM, Williams DN. Problems in the management of type III (severe) open fractures: a new classification of type III open fractures. J Trauma 1984; 24: 742–6. Heckman MM, Whitesides TE Jr, Grewe SR, Rooks MD. Compartment pressure in association with closed tibial fractures. The relationship between tissue pressure, compartment, and the distance from the site of the fracture. J Bone Joint Surg 1994; 76A: 1285–92. LaPrade RF, Wentorf F. Diagnosis and treatment of posterolateral knee injuries. Clin Orthop Relat Res 2002; 402: 110–21. McQueen MM, Christie J, Court-Brown CM. Acute compartment syndrome in tibial diaphyseal fractures. J Bone Joint Surg 1996; 78B: 95–8. O’Donoghue D. Surgical treatment of fresh injuries to the major ligaments of the knee. J Bone Joint Surg 1950; 32A: 721–38. Oestern H, Tscherne H. Pathophysiology and classification of soft tissue injuries associated with fractures. In: Tscherne H, Gotzen L (Eds) Fractures with Soft Tissue Injuries. Springer Verlag, Berlin, 1984. Petersen WMD, Zantop TMD. Anatomy of the anterior cruciate ligament with regard to its two bundles. Clin Orthop Relat Res 2007; 454: 35–47. Ranawat A, Baker CL 3rd, Henry S, Harner CD. Posterolateral corner injury of the knee: evaluation and management. J Am Acad Orthop Surg 2008; 16: 506–18. Robertson A, Nutton RW, Keating JF. Dislocation of the knee. J Bone Joint Surg 2006; 88B: 706–11. Sarmiento A, Latta L. The evolution of functional bracing of fractures. J Bone Joint Surg 2006; 88B: 141–8. Slocum DB, Larson RL. Rotatory instability of the knee: Its pathogenesis and a clinical test to demonstrate its presence. J Bone Joint Surg 1968; 50A: 211–25. Watson JT. Treatment of unstable fractures of the shaft of the tibia. J Bone Joint Surg 1994; 76A: 1575–84.

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Injuries of the ankle and foot

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Gavin Bowyer

INTRODUCTION The foot and ankle act to both support and propel the body and are well adapted for these roles. During running and jumping, loads well in excess of 10 times body weight are transmitted through the ankle and foot. If this loading is excessive, or excessively repeated, it can lead to foot and ankle injuries. The ankle is a close-fitting hinge-like joint of which the two parts interlock like a mortise (the box formed by the distal ends of the tibia and fibula) and tenon (the upward projecting talus). The mortise bones are held together as a syndesmosis by the distal (inferior) tibiofibular and interosseous ligaments, and the talus is prevented from slipping out of the mortise by the medial and lateral collateral ligaments and joint capsule. The peroneal tendons provide additional stability. The ankle moves only in one plane (flexion/ extension), but with a complex axis of rotation, actually rolling forward as the talus goes into plantar flexion; sideways movement is prevented by the malleolar buttresses and the collateral ligaments, but the bony constraint lessens as the ankle flexes. If the talus is forced to tilt or rotate, something must give: the ligaments, the malleoli or both. Movements of the talus into internal or external rotation come about from a rotatory force upon the foot, or more commonly inversion/supination of the foot, which, through the orientation of the subtalar joint, causes external rotation of the talus. Whenever a fracture of the malleolus is seen, it is important to ask about the associated ligament injury.

ANKLE LIGAMENT INJURIES Ankle sprains are the most common of all sportsrelated injuries, accounting for over 25 per cent of cases. They are probably even more common in pedestrians and country walkers who stumble on stairways, pavements and potholes.

In more than 75 per cent of cases it is the lateral ligament complex that is injured, in particular the anterior talofibular and calcaneofibular ligaments. Medial ligament injuries are usually associated with a fracture or joint injury. A sudden twist of the ankle momentarily tenses the structures around the joint. This may amount to no more than a painful wrenching of the soft tissues – what is commonly called a sprained ankle. If more severe force is applied, the ligaments may be strained to the point of rupture. With a partial tear, most of the ligament remains intact and, once it has healed, it is able to support the weight of the body. With a complete tear, the ligament may still heal but it never regains its original form and the joint will probably be unstable.

Functional anatomy The lateral collateral ligaments consist of the anterior talofibular, the posterior talofibular and (between them) the calcaneofibular ligaments. The anterior talofibular ligament (ATFL) runs almost horizontally from the anterior edge of the lateral malleolus to the neck of the talus; it is relaxed in dorsiflexion and tense in plantarflexion. In plantarflexion the ligament essentially changes its orientation from horizontal with respect to the floor, to almost vertical. Thus the ligament at greatest stretch, and most vulnerable, with the foot plantar-flexed is the ATFL – hence the propensity for ATFL injury with the plantar-flexed, inverting, foot (down a pot-hole, off a kerb, etc). The calcaneofibular ligament stretches from the tip of the lateral malleolus to the posterolateral part of the calcaneum, thus it helps also to stabilize the subtalar joint. Maximum tension is produced by inversion and dorsiflexion of the ankle. The posterior talofibular ligament runs from the posterior border of the lateral malleolus to the posterior part of the talus. The medial collateral (deltoid) ligament consists of superficial and deep portions. The superficial fibres spread like a fan from the medial malleolus as far

31 Anterior talofibular

FRACTURES AND JOINT INJURIES

Posterior talofibular

Calcaneofibular

(a)

(b)

(c)

(d)

(e)

(f)

anteriorly as the navicular and inferiorly to the calcaneum and talus. Its chief function is to resist eversion of the hindfoot. The deep portion is intra-articular, running directly from the medial malleolus to the medial surface of the talus. Its principal effect is to prevent external rotation of the talus. The combined action of restraining eversion and external rotation makes the deltoid ligament the major stabilizer of the ankle. The distal tibiofibular joint is held by four ligaments: anterior, posterior, inferior transverse and the interosseous ‘ligament’, which is really a thickened part of the interosseous membrane. This strong ligament complex still permits some movement at the tibiofibular joint during flexion and extension of the ankle.

Pathology The common ‘twisted ankle’ is due to unbalanced loading with the ankle inverted and plantarflexed. First the anterior talofibular and then the calcaneofibular ligament is strained; sometimes the talocalcaneal ligaments also are injured. If fibres are torn there is bleeding into the soft tissues. The tip of the malleolus may be avulsed and in some cases the peroneal tendons are injured. There may be a small fracture of an adjacent tarsal bone or (on the lateral side) the base of the fifth metatarsal.

ACUTE INJURY OF LATERAL LIGAMENTS Clinical features 908

A history of a twisting injury followed by pain and swelling could suggest anything from a minor sprain

31.1 Ankle ligament injuries (a) Schematic diagram showing the mortise-and-tenon articulation and main ligaments of the ankle. (b) The three components of the lateral collateral ligament. (c) The commonest injury is a partial tear of one or other component of the lateral ligament. Following a complete tear, the talus may be displaced in the ankle mortise; the tibiofibular ligament may have ruptured as well, shown here in somewhat exaggerated form. (d) Stress x-ray showing talar tilt. (e,f) X-rays demonstrating anteroposterior instability. Pulling the foot forward under the tibia causes the talus to shift appreciably at the ankle joint; this is usually seen after recurrent sprains.

to a fracture. If the patient is able to walk, and bruising is only faint and slow to appear, it is probably a sprain; if bruising is marked and the patient unable to put any weight on the foot, this suggests a more severe injury. Tenderness is maximal just distal and slightly anterior to the lateral malleolus. The slightest attempt at passive inversion of the ankle is extremely painful. It is impossible to test for abnormal mobility without using local or general anaesthesia. With all ankle injuries it is essential to examine the entire leg and foot; undisplaced fractures of the fibula or the tarsal bones, or even the fifth metatarsal bone are easily missed and injuries of the distal tibiofibular joint and the peroneal tendon sheath cause features that mimic those of a lateral ligament strain.

Imaging About 15 per cent of ankle sprains reaching the Emergency Department are associated with an ankle fracture. This complication can be excluded by obtaining an x-ray, but there are doubts as to whether all patients with ankle injuries should be subjected to x-ray examination. Almost 2 decades ago The Ottawa Ankle Rules were developed to assist in making this decision. X-ray examination is called for if there is: (1) pain around the malleolus; (2) inability to take weight on the ankle immediately after the injury; (3) inability to take four steps in the Emergency Department; (4) bone tenderness at the posterior edge or tip of the medial or lateral malleolus or the base of the fifth metatarsal bone. If x-ray examination is considered necessary, anteroposterior, lateral and ‘mortise’ (30-degree oblique) views of the ankle should be obtained. Localized soft

Treatment Initial treatment consists of rest, ice, compression and elevation (RICE), which is continued for 1–3 weeks depending on the severity of the injury and the response to treatment. Cold compresses should be applied for about 20 minutes every 2 hours, and after any activity that exacerbates the symptoms. More recently the acronym has been extended to ‘PRICE’ by adding protection (crutches, splint or brace) and still further to ‘PRICER’, adding rehabilitation (supported return to function). The principles remain the same – a phased approach, to support the injured part during the first few weeks and then allow early mobilization and a supported return to function. An advice leaflet for patients is probably helpful. The use of non-steroidal anti-inflammatory drugs (NSAIDs) in the acute phase can be helpful, with the usual contraindications and caveats. There is evidence that in acute injuries topical non-steroidal anti-inflammatory (NSAI) gels or creams might be as beneficial as oral preparations, probably with a better risk profile. Functional treatment, i.e. ‘protected mobilization’, leads to earlier recovery of all grades of injury – without jeopardizing stability – than either rigid immobilization or early operative treatment. OPERATIVE TREATMENT If the ankle does not start to settle within 1 or 2 weeks of starting RICE, further review and investigation are called for. Persistent problems at 12 weeks after injury, despite physiotherapy, may signal the need for operative treatment. Residual complaints of ankle pain and stiffness, a sensation of instability or giving way and intermittent swelling are suggestive of cartilage damage or impinging scar tissue within the ankle. Arthroscopic repair or ligament substitution is now

effective in many cases, allowing a return to full function and sports.

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RECURRENT LATERAL INSTABILITY Recurrent sprains are potentially associated with added cartilage damage, and warrant careful investigation by MRI, arthroscopy and examination under anaesthesia.

Clinical features The patient gives a history of a ‘sprained ankle’ that never quite seems to recover and is followed by recurrent ‘giving way’ or a feeling of instability when walking on uneven surfaces. This is said to occur in about 20 per cent of cases after acute lateral collateral ligament tears (Colville, 1994). The ankle looks normal and passive movements are full, however stress tests for abnormal lateral ligament laxity may show either excessive talar tilting in the sagittal plane or anterior displacement (an anterior drawer sign) in the coronal plane. In the chronic phase these tests are painless and can be performed either manually or with the use of special mechanical stress devices. Both ankles are tested, so as to allow comparison of the abnormal with the normal side.

Injuries of the ankle and foot

tissue swelling and, in some cases, a small avulsion fracture of the tip of the lateral malleolus or the anterolateral surface of the talus may be the only corroborative signs of a lateral ligament injury. However, it is important to exclude other injuries, such as an undisplaced fibular fracture or diastasis of the tibiofibular syndesmosis. If tenderness extends onto the foot, or if swelling is so severe that the area cannot be properly examined, additional x-rays of the foot are essential. Persistent inability to weightbear over 1 week or longer should call for re-examination and review of all the initial ‘negative’ x-rays. For patients who have had persistent pain, swelling, instability and impaired function over 6 weeks or longer, despite appropriate early treatment, magnetic resonance imaging (MRI) or computed tomography (CT) will be required to assess the extent of soft tissue injury or subtle bony changes.

Talar tilt test With the ankle held in the neutral position,

the examiner stabilizes the tibia by grasping the leg with one hand above the ankle; the other hand is then used to force the heel into maximum inversion. The range of movement can be estimated clinically and compared with that of the normal ankle. The exact degree of talar tilt can also be measured by x-rays, which should be taken with the ankles in 30 degrees of internal rotation (mortise views); 15 degrees of talar tilt (or 5 degrees more than in the normal ankle) is regarded as abnormal. Inversion laxity suggests injury to both the calcaneofibular and anterior talofibular ligaments. Anterior drawer test The patient should be sitting with the knee flexed to 90 degrees and the ankle in 10 degrees of plantarflexion. The lower leg is stabilized with one hand while the other hand forces the patient’s heel forward under the tibia. In a positive test the talus can be felt sliding forwards and backwards. The position of the talus is verified by lateral x-rays; anterior displacement of 10 mm (or 5 mm more than on the normal side) indicates abnormal laxity of the anterior talofibular ligament. With an isolated tear of the anterior talofibular ligament, the anterior drawer test may be positive in the absence of abnormal talar tilt. (Note: A positive anterior drawer test can sometimes be obtained in normal, asymptomatic individuals; the finding should always be considered in conjunction with other symptoms and signs).

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31.2 Recurrent lateral instability – special tests (a) Anterior drawer test: When the heel is drawn forwards under the tibia, the abnormally lax ligaments allow the talus to displace anteriorly. (b) Talar tilt test: Forcibly inverting the ankle causes the talus to tilt abnormally in the mortise. For both tests comparison with the normal side is important.

(a)

(b)

Treatment Recurrent ‘giving way’ can sometimes be prevented by modifying shoe-wear, raising the outer side of the heel and extending it laterally. More effectively, the secondary dynamic ankle stabilizers, the peronei, can be strengthened and brought into play by specific physiotherapy regimes. Ankle exercises to strengthen the peroneal muscles are helpful, and a light brace can be worn during stressful activities. If, in spite of these measures, the patient continues to experience mechanical instability (true giving way) during everyday activities, reconstruction of the lateral ligament should be considered. More commonly the persisting problem will be functional instability, in which the patient does not trust the ankle, and there are recurrent episodes in which the patient has rapidly or suddenly to unload the ankle, probably because of inhibitory feedback from the injured ankle. Most patients with functional instability can be improved and returned to sport by arthroscopic

(a)

(b) (a)

910

debridement of the impinging tissue within the ankle joint, followed by physiotherapy. Various operations for mechanical stabilization are described; they fall mainly into two groups: (1) those that aim to repair or tighten the ligaments, (2) those that are designed to construct a ‘check-rein’ against the unstable movement. The Broström–Karlsson or Gould operation is an example of the first type: the anterior talofibular and calcaneofibular ligaments are exposed and repaired, usually by an overlapping – or ‘double-breasting’ – technique (Karlsson et al., 1988). In the second type of operation a substitute ligament is constructed by using peroneus brevis to act as a tenodesis and prevent sudden movements into varus (Chrisman and Snook, 1969). The disadvantages of the non-anatomic reconstructions are that they sacrifice or partially sacrifice the secondary stabilizers, the peroneal tendons. Postoperatively the ankle is immobilized in eversion for 2 weeks; a below-knee cast is then applied for another 4 weeks, during which time the patient can

(b)

31.3 Recurrent lateral instability – operative treatment (a) The lax anterior talofibular and calcaneofibular ligaments can be reinforced by a double-breasting technique (the Boström–Karlsson operation). (b) Another way of augmenting the lateral ligament is to re-route part of the peroneus brevis tendon so that is acts as a check-rein (tenodesis) (The Chrisman operation).

31

bear weight. Thereafter, a removable brace is worn and exercises are encouraged. The brace can usually be discarded after 3 months but it may need to be used from time to time for sports activities.

Rupture of the deltoid ligament is usually associated with either a fracture of the distal end of the fibula or tearing of the distal tibiofibular ligaments (or both). The effect is to destabilize the talus and allow it to move into eversion and external rotation. The diagnosis is made by x-ray: there is widening of the medial joint space in the mortise view; sometimes the talus is tilted, and diastasis of the tibiofibular joint may be obvious. When there is a deltoid ligament or medial malleolar injury but no apparent lateral disruption at the ankle, it is important to look for a fracture or dislocation of the proximal fibula – the highly unstable Maissoneuve injury.

Treatment Provided the medial joint space is completely reduced, the ligament will heal. The fibular fracture or diastasis must be accurately reduced, if necessary by open operation and internal fixation. Occasionally the medial joint space cannot be reduced; it should then be explored in order to free any soft tissue trapped in the joint. A below-knee cast is applied with the foot plantigrade and is retained for 8 weeks.

DISLOCATION OF PERONEAL TENDONS Acute dislocation of the peroneal tendons may accompany – or may be mistaken for – a lateral ligament strain. Tell-tale signs on x-ray are an oblique fracture of the lateral malleolus (the so-called ‘rim fracture’) or a small flake of bone lying lateral to the lateral malleolus (avulsion of the retinaculum). Treatment in a belowknee cast for 6 weeks will help in a proportion of cases; the remainder will complain of residual symptoms. Recurrent subluxation or dislocation is unmistakable; the patient can demonstrate that the peroneal tendons dislocate forwards over the fibula during dorsiflexion and eversion. Treatment is operative and is based on the observation that the attachment of the retinaculum to the periosteum on the front of the fibula has come adrift, creating a pouch into which the tendons displace. Using non-absorbable sutures through drill holes in the bone, the normal anatomy is recreated (Das De and Balasubramaniam, 1985). An alternative approach is to modify the morphology of the distal fibula, posteriorly translating a shelf of bone to constrain the tendons mechanically in a deep-

(b) (a)

31.4 Dislocation of peroneal tendons (a) On movement of the ankle, the peroneal tendons slip forwards over the lateral malleolus. (b) The anterior part of the retinaculum is being reconstructed.

Injuries of the ankle and foot

DELTOID LIGAMENT TEARS

ened posterior channel. Whichever method of stabilization is used, it is important to also assess the state of the tendons themselves, as an associated longitudinal split tear is commonly found, and this will lead to continuing pain and dysfunction around the lateral border of the ankle if it is not repaired.

TEARS OF INFERIOR TIBIOFIBULAR LIGAMENTS The inferior tibiofibular ligaments may be torn, allowing partial or complete separation of the tibiofibular joint (diastasis). Complete diastasis, with tearing of both the anterior and posterior fibres, follows a severe abduction strain. Partial diastasis, with tearing of only the anterior fibres, is due to an external rotation force. These injuries may occur in isolation, but they are usually associated with fractures of the malleoli or rupture of the collateral ligaments.

Clinical features Following a twisting injury, the patient complains of pain in the front of the ankle. There is swelling and marked tenderness directly over the inferior tibiofibular joint. A ‘squeeze test’ has been described by Hopkinson et al. (1990); when the leg is firmly compressed some way above the ankle, the patient experiences pain over the syndesmosis. Be sure, though, to exclude a fracture before carrying out the test.

X-ray With a partial tear the fibula usually lies in its normal position and the x-ray looks normal. With a complete

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tear the tibiofibular joint is separated and the ankle mortise is widened; sometimes this becomes apparent only when the ankle is stressed in abduction. There may be associated fractures of the distal tibia or fibula, or an isolated fracture more proximally in the fibula.

Treatment Partial tears can be treated by strapping the ankle firmly for 2–3 weeks. Thereafter exercises are encouraged. Complete tears are best managed by internal fixation with a transverse screw just above the joint. This must be done as soon as possible so that the tibiofibular space does not become clogged with organizing haematoma and fibrous tissue. If the patient is seen late and the ankle is painful and unstable, open clearance of the syndesmosis and transverse screw fixation may be warranted. The ankle is immobilized in plaster for 8 weeks, after which the screw is removed. However, some degree of instability usually persists.

MALLEOLAR FRACTURES OF THE ANKLE Fractures and fracture dislocations of the ankle are common. Most are low-energy fractures of one or both malleoli, usually caused by a twisting mechanism. Less common are the more severe fractures involving the tibial plafond, the pilon fractures, which are high-energy injuries often caused by a fall from a height. The patient usually presents with a history of a twisting injury, usually with the ankle going into inversion, followed by immediate pain, swelling and difficulty weightbearing. Bruising often comes out soon after injury. One such injury was described by Percival Pott in 1768, and the group as a whole was for a long time referred to as Pott’s fracture – although as with many eponyms, he was not the first to notice or describe it, and what became known by this eponym was not what he described anyway! The most obvious injury is a fracture of one or both malleoli; often, though, the ‘invisible’ part of the injury – rupture of one or more ligaments – is just as serious.

Mechanism of injury

912

The patient stumbles and falls. Usually the foot is anchored to the ground while the body lunges forward. The ankle is twisted and the talus tilts and/or rotates forcibly in the mortise, causing a low-energy fracture of one or both malleoli, with or without

associated injuries of the ligaments. If a malleolus is pushed off, it usually fractures obliquely; if it is pulled off, it fractures transversely. The precise fracture pattern is determined by: (1) the position of the foot; (2) the direction of force at the moment of injury. The foot may be either pronated or supinated and the force upon the talus is towards adduction, abduction or external rotation, or a combination of these.

Pathological anatomy There is no completely satisfactory classification of ankle fractures. Lauge-Hansen (1950) grouped these injuries according to the likely position of the foot and the direction of force at the moment of fracture. This is useful as a guide to the method of reduction (reverse the pathological force); it also gives a pointer to the associated ligament injuries. However, some people find this classification overly complicated. For a detailed description the reader is referred to the original paper by Lauge-Hansen (1950). A simpler (perhaps too simple) classification is that of Danis and Weber (Müller et al., 1991), which focuses on the fibular fracture. Type A is a transverse fracture of the fibula below the tibiofibular syndesmosis, perhaps associated with an oblique or vertical fracture of the medial malleolus; this is almost certainly an adduction (or adduction and internal rotation) injury. Type B is an oblique fracture of the fibula in the sagittal plane (and therefore better seen in the lateral xray) at the level of the syndesmosis; often there is also an avulsion injury on the medial side (a torn deltoid ligament or fracture of the medial malleolus). This is probably an external rotation injury and it may be associated with a tear of the anterior tibiofibular ligament. Type C is a more severe injury, above the level of the syndesmosis, which means that the tibiofibular ligament and part of the interosseous membrane must have been torn. This is due to severe abduction or a combination of abduction and external rotation. Associated injuries are an avulsion fracture of the medial malleolus (or rupture of the medial collateral ligament), a posterior malleolar fracture and diastasis of the tibiofibular joint.

Clinical features Ankle fractures are seen in skiers, footballers and climbers; an older group includes women with postmenopausal osteoporosis. A history of a severe twisting injury, followed by intense pain and inability to stand on the leg suggests something more serious than a simple sprain. The ankle is swollen and deformity may be obvious. The site of tenderness is important; if both the medial and lateral sides are tender, a double injury (bony or ligamentous) must be suspected.

X-ray At least three views are needed: anteroposterior, lateral and a 30-degree oblique ‘mortise’ view. The level of the fibular fracture is often best seen in the lateral view; diastasis may not be appreciated without the mortise view. Further x-rays may be needed to exclude a proximal fibular fracture. From a careful study of the x-rays it should be possible to reconstruct the mechanism of injury. The four most common patterns are shown in Figure 31.5.

Treatment Swelling is usually rapid and severe, particularly in the higher energy injuries. If the injury is not dealt with within a few hours, definitive treatment may have to be deferred for several days while the leg is elevated so that the swelling can subside; this can be hastened by using a foot pump (which also reduces the risk of deep-vein thrombosis). Fractures are visible on x-ray; ligaments are not. Always look for clues to the invisible ligament injury – widening of the tibiofibular space, asymmetry of the

(a)

(b)

31

Injuries of the ankle and foot

talotibial space, widening of the medial joint space, or tilting of the talus – before deciding on a course of action. Like other intra-articular injuries, ankle fractures must be accurately reduced and held if later mechanical dysfunction is to be prevented. Persistent displacement of the talus, or a step in the articular surface, leads to increased stress and predisposes to secondary osteoarthritis. In assessing the accuracy of reduction, four objectives must be met: (1) the fibula must be restored to its full length; (2) the talus must sit squarely in the mortise, with the talar and tibial articular surfaces parallel; (3) the medial joint space must be restored to its normal width, i.e. the same width as the tibio-talar space (about 4 mm); (4) oblique x-rays must show that there is no tibiofibular diastasis. Ankle fractures are often unstable. Whatever the method of reduction and fixation, the position must be checked by x-ray during the period of healing. UNDISPLACED FRACTURES The first step is to decide whether the injury is stable or unstable. An isolated, undisplaced Danis–Weber

(c)

(d)

31.5 Ankle fractures – classification The Danis–Weber classification is based on the level of the fibular fracture. (a) Type A – a fibular fracture below the syndesmosis and an oblique fracture of the medial malleolus (caused by forced supination and adduction of the foot). (b) Type B – fracture at the syndesmosis, often associated with disruption of the anterior fibres of the tibiofibular ligament and fracture of the posterior and/or medial malleolus, or disruption of the medial ligament (caused by forced supination and external rotation). (c) Type C – a fibular fracture above the syndesmosis; the tibiofibular ligament must be torn, or else (d) the ligament avulses a small piece of the tibia. Here, again, there must also be disruption on the medial side of the joint – either a medial malleolar fracture or rupture of the deltoid ligament.

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type A fracture is stable and will need minimal splintage: a firm bandage or stirrup brace is applied mainly for comfort until the fracture heals. Undisplaced type B fractures are potentially unstable only if the tibiofibular ligament is torn or avulsed, or if there is a significant medial-sided injury. X-rays will show if the syndesmosis or mortise is intact; if it is, a below-knee cast is applied with the ankle in the neutral (anatomical) position. The plaster may need to be split and, if so, it must be completed or replaced when swelling has subsided. A check x-ray is taken at 2 weeks to confirm that the fracture remains undisplaced. An overboot is fitted and the patient is taught to walk correctly as soon as possible. The cast can usually be discarded after 6–8 weeks. Ankle and foot movements are regained by active exercises when the plaster is removed. As with any lower limb fracture, the leg must not be allowed to dangle idly – it must be exercised and elevated. Undisplaced type C fractures are deceivingly innocent-looking but are often accompanied by disruption of the medial joint structures as well as the tibiofibular syndesmosis and interosseous membrane. These defects may become apparent only when the fracture displaces in a cast; arguably, therefore, type C fractures are better fixed from the outset.

DISPLACED FRACTURES Reduction of these joint disruptions is a prerequisite to all further treatment; knowledge of the causal mechanism (and this is where the Lauge-Hansen classification is useful) helps to guide the method of closed reduction. Although internal fixation is usually performed to stabilize the reduction, not all such fractures require surgery.

(a)

914

(b)

Displaced Weber type A fractures The medial malleolar fracture is nearly vertical and after closed reduction it often remains unstable; internal fixation of the malleolar fragment with one or two screws directed almost parallel to the ankle joint is advisable. A perfect reduction should be aimed for, with accurate restoration of the tibial articular surface. Loose bone fragments are removed. The lateral malleolar fracture, unless it is already perfectly reduced and stable, should be fixed with a plate and screws or tension-band wiring. Postoperatively a ‘walking cast’ or removable splintage boot is applied for 6 weeks; the advantage of removable splintage is that early physiotherapy can be commenced.

The most common fracture pattern is a spiral fracture of the fibula and an oblique fracture of the medial malleolus. The causal mechanism is external rotation of the ankle when the foot is caught in a supinated position. Closed reduction therefore needs traction (to disimpact the fracture) and then internal rotation of the foot. If closed reduction succeeds, a cast is applied, following the same routine as for undisplaced fractures. Failure of closed reduction (sometimes a torn medial ligament is caught in between the talus and medial malleolus) or late redisplacement calls for operative treatment. Type B fractures may also be caused by abduction; often the lateral aspect of the fibula is comminuted and the fracture line more horizontal. Despite accurate reduction (the ankle is adducted and the foot supinated), these injuries are unstable and often poorly controlled in a cast; internal fixation is therefore preferred.

Displaced Weber type B fractures

Displaced Weber type C fractures The fibular fracture is well above the syndesmosis and frequently there are

(c)

(d)

31.6 Ankle fractures – stable or unstable? (a) Stable fracture: in this Danis–Weber type B fracture the tibiofibular syndesmosis has held; the surfaces of the tibia and talus are precisely parallel and the width of the joint space is regular both superiorly and medially. (b) Slight subluxation: the syndesmosis is intact but the talus has moved laterally with the distal fibular fragment; the medial joint space is too wide, signifying a deltoid ligament rupture. It is vital, after reduction of the fibular fracture, to check that the medial joint space is normal; if it is not, the ligament has probably been trapped in the joint and it must be freed so as to allow perfect re-positioning of the talus. (c) Fracture–dislocation: in this high fibular fracture the syndesmosis has given way, the medial collatoral ligament has been torn and the talus is displaced and tilted. The fibula must be fixed to full length and the tibiofibular joint secured before the ankle can be stabilized. (d) Posterior fracture–dislocation: if the posterior margin of the tibia is fractured, the talus may be displaced upwards. The fragment must be replaced and fixed securely.

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(a)

(b)

(c)

(d)

(f)

31.7 Ankle fractures – open treatment (1) (a,b) Danis–Weber type A fractures can often be treated conservatively, but if the medial malleolar fragment involves a large segment of the articular surface, it is best treated by accurate open reduction and internal fixation with one or two screws. (c,d) An unstable fracture–dislocation such as this almost always needs open reduction and internal fixation. The fibula should be restored to full length and fixed securely; in this case the medial malleolus also needed internal fixation; (e) and (f) show the range of ankle movement a few days after operation and before a ‘walking plaster’ was applied.

associated medial and posterior malleolar fragments. An isolated type C fibular fracture should raise strong suspicions of major ligament damage to the syndesmosis and medial side of the joint. Almost all type C fractures are unstable and will need open reduction and internal fixation. The first step is to reduce the fibula, restoring its length and alignment; the fracture is then stabilized using a plate and screws. If there is a medial fracture, this also is fixed. The syndesmosis is then checked, using a hook to pull the fibula laterally. If the joint opens out, it means that the ligaments are torn; the syndesmosis is stabilized by inserting a transverse screw across from the fibula into the tibia (the ankle should be held in 10 degrees of dorsiflexion when the screw is inserted). Fracture subluxations more than 1 or 2 weeks old may prove difficult to reduce because of clot organi-

(a)

(b)

(c)

Injuries of the ankle and foot

(e)

zation in the syndesmosis. Granulation tissue should be removed from the syndesmosis and transverse tibiofibular fixation secured. After open reduction and fixation of ankle fractures, movements should be regained before applying a below-knee plaster cast, or removable support boot. The patient is then allowed partial weightbearing with crutches; the support is retained until the fractures have consolidated (anything from 6–12 weeks). Management of the syndesmosis- or diastasis-screw remains controversial. Some advocate removal of the screw when the syndesmosis has healed, and before weightbearing has commenced (6 weeks is too early, 10 weeks is probably more appropriate). Others are happy to allow early weightbearing with the screw still

Postoperative management

(d)

(e)

(f)

31.8 Ankle fractures with diastasis – open treatment (2) (a) In this type B fracture there is partial disruption of the distal tibiofibular syndesmosis. Treatment (b) required medial and lateral fixation as well a tibiofibular screw. (c) A type C fracture must, inevitably, disrupt the tibiofibular ligament; in this case the medial malleolus was intact but the deltoid ligament was torn (look at the wider than normal medial joint space). (d) By fixing the fibular fracture and using a tibiofibular screw, the ankle was completely reduced and it was therefore unnecessary to explore the deltoid ligament. (e) This patient presented 5 days after his injury; he, too, had a diastasis with disruption of the deltoid ligament (f). In this case the tibiofibular joint as well as the deltoid ligament had to be explored before the ankle could be reduced.

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in place, accepting that the screw may break (especially if four cortices are engaged). OPEN FRACTURES Open fractures of the ankle pose special problems. If the fracture is not reduced and stabilized at an early stage, it may prove impossible to restore the anatomy. For this reason unstable injuries should be treated by internal fixation even in the presence of an open wound, provided the soft tissues are not too severely damaged and the wound is not contaminated. If internal fixation seems too risky, an external fixator can be used, often as a temporary spanning option. Treatment in other respects follows the principles outlined in chapter 23.

Complications

later years. Unless the ankle is unstable, symptoms can often be managed by judicious analgesic treatment and the use of firm, comfortable footwear. However, in the longer term if symptoms become severe arthrodesis may be necessary.

PILON FRACTURES Unlike the twisting injuries that cause the common ankle fractures, this injury to the ankle joint occurs when a large force drives the talus upwards against the tibial plafond, like a pestle (pilon) being struck into a mortar. There is considerable damage to the articular cartilage and the subchondral bone may be broken into several pieces; in severe cases, the comminution extends some way up the shaft of the tibia.

EARLY Vascular injury With a severe fracture-subluxation the

pulses may be obliterated. The ankle should be immediately reduced and held in a splint until definitive treatment has been initiated. Wound breakdown and infection Diabetic patients are at greater than usual risk of developing wound-edge necrosis and deep infection. In dealing with displaced fractures, these risks should be carefully weighed against the disadvantages of conservative treatment; casts may also cause skin problems if not well padded and are less effective in preventing malunion.

Clinical features There may be little swelling initially but this rapidly changes and fracture blisters are common. The ankle may be deformed or even dislocated; prompt approximate reduction is mandatory.

X-rays This is a comminuted fracture of the distal end of the tibia, extending into the ankle joint. The fracture may

LATE Incomplete reduction Incomplete reduction is common

and, unless the talus fits the mortise accurately, degenerative changes may occur. This can sometimes be prevented by a corrective osteotomy. Non-union The medial malleolus occasionally fails to

unite because a flap of periosteum is interposed between it and the tibia. It should be prevented by operative reduction and screw fixation. Swelling and stiffness of the ankle are usually the result of neglect in treatment of the soft tissues. The patient must walk correctly in plaster and, when the plaster is removed, he or she must, until circulatory control is regained, wear a crepe bandage and elevate the leg whenever it is not being used actively. Physiotherapy is always helpful.

(a)

(b)

(c)

Joint stiffness

Algodystrophy This often follows fractures of the ankle.

The patient complains of pain in the foot; there may be swelling and diffuse tenderness, with gradual development of trophic changes and severe osteoporosis. Management is discussed in Chapter 10. Osteoarthritis Malunion and/or incomplete reduction

916

may lead to secondary osteoarthritis of the ankle in

(d)

(e)

(f)

31.9 Pilon fractures – imaging These are either (a) undisplaced (type 1), (b) minimally displaced (type 2); (c) markedly displaced (type 3). CT (d) shows that there are usually five major tibial fragments: anterolateral (al), anterocentral (ac), anteromedial (am), the medial malleolus (mm) and the posterior fragment (p). These elements are better defined by three-dimensional CT reconstruction (e,f).

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Injuries of the ankle and foot

(d)

(a)

(b)

(c)

31.10 Pilon fracture A 43-year old man suffered a high-energy comminuted fracture of the distal end of the tibia. (a) Swelling and fracture blisters around the ankle. (b,c) X-rays showing disruption of the metaphyseal–diaphyseal junction in this pilon fracture. (d) Fracture held in an external fixator. (e) Fracture blisters were de-roofed and treated with Flamazine (silver sulfadiazine); the skin has re-epithelialized and is free of (e) infection 5 days after injury.

be classified according to the amount of displacement and comminution (Rüedi and Allgöwer, 1979), though this will usually require accurate definition by CT. Rüedi type 1 is an intra-articular fracture with little or no displacement of the fragments; in type 2 there is more severe disruption of the articular surface but without very marked comminution. Type 3 is a severely comminuted fracture with displacement of the fragments and gross articular irregularity. In all cases, assessment is far better with CT scanning (preferably including three-dimensional reconstruction) than with plain x-ray examination.

obtain as much reduction as possible through ligamentotaxis) and plating through limited exposures. Recently, these injuries have been successfully treated by using a combination of indirect reduction methods and small screws to hold the articular fragments, coupled with axially stable locking plates. Circular frame fixation has also been successful. The soft-tissue swelling following these injuries is substantial. After fixation, elevation and early movement help to reduce the oedema; arterio-venous impulse devices applied to the sole of the foot are also helpful.

Treatment The three points of early management of these injuries are: span, scan, plan. Staged treatment has reduced the complication rate in these injuries. Control of soft tissue swelling is a priority; this is best achieved either by elevation and applying an external fixator across the ankle joint (the spanning external fixator, or travelling traction). It may take 2– 3 weeks before the soft tissues improve, and fracture blisters can be actively managed rather than hidden under plaster. Surgery can be planned, based on the CT scan. Once the skin has recovered, an open reduction and fixation with plates and screws (usually with bone grafting) may be possible. However, the more severe injuries (types 2 and 3) do not readily tolerate large surgical exposures for plating and significant wound breakdown and infection rates have been reported. Better results have followed wider use of indirect reduction techniques (e.g. applying a bone distractor or utilizing the spanning fixator across the joint to

(a)

(b)

31.11 Same case as 31.10 – Outcome At 3 months after minimal approach reduction and fixation with distal locking plates the fractures have healed and the joint is congruent and normally aligned.

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(a)

(b)

(c)

(d)

31.12 Physeal injuries of the distal tibia The classification suggested by Dias and Tachdjian (1978) has the merit of pointing to the required reduction manoeuvre – the reverse of the causal mechanism. (a) Supination–inversion: the fibular fracture is usually an avulsion (Salter–Harris type 1) whereas the medial malleolar fracture can be variable. (b) Pronation– eversion–external rotation: the fibular fracture is often high and transverse. (c) Supination–plantarflexion: a fracture of the distal tibia only (Salter–Harris type 1 or 2) with posterior displacement. (d) Supination–external rotation: an oblique fibular fracture coupled with a fracture of the distal tibia.

Outcome

31.13 Tillaux fracture Diagram illustrating the elements of this unusual injury.

Pilon fractures usually take several months to heal. Postoperatively, physiotherapy is focused on joint movement and reduction of swelling. There remains, however, a challenging problem with poor functional results in these complex fractures, which represent a significant soft tissue injury as well as bony jigsaw. Although bony union may be achieved, the fate of the joint is decided by the degree of cartilage injury – the ‘invisible’ factor on x-rays. Secondary osteoarthritis, stiffness and pain are still frequent late complications.

ANKLE FRACTURES IN CHILDREN Physeal injuries are quite common in children and almost a third of these occur around the ankle.

Mechanism of injury

918

The foot is fixed to the ground or trapped in a crevice and the leg twists to one or the other side. The tibial (or fibular) physis is wrenched apart, usually resulting in a Salter–Harris type 1 or 2 fracture. With severe external rotation or abduction the fibula may also fracture more proximally. The tibial metaphyseal spike may come off posteriorly, laterally or posteromedially; its position is determined by the mechanism of injury and suggests the method of reduction. With adduction injuries the tip of the fibula may be avulsed. Type 3 and 4 fractures are uncommon. They are due to a supination–adduction force. The epiphysis is split vertically and one piece of the epiphysis (usually the medial part) may be displaced. Two unusual injuries of the growing ankle are the Tillaux fracture and the notorious triplane fracture. The Tillaux fracture is an avulsion of a fragment of tibia by the anterior tibiofibular ligament; in the child

(a)

(b)

(c)

(d)

31.14 Ankle fractures in children (a) Salter–Harris type 2 injury; after reduction (b) growth has proceeded normally. (c) Salter–Harris type 3 injury; (d) the medial side of the physis has fused prematurely, resulting in distorted growth.

or adolescent this fragment is the lateral part of the epiphysis and the injury is therefore a Salter–Harris type 3 fracture. The triplane fracture occurs on the medial side of the tibia and is a combination of Salter–Harris types 2

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(b)

(c)

(d)

31.16 Triplane fracture The three fracture planes may not be seen in a single x-ray, but can be visualized from a combination of images. In this case the epiphyseal fracture is clearly seen only in the coronal plane CT scan (c).

(a)

(b)

Injuries of the ankle and foot

(a)

31.15 Tillaux fracture (a,b) This avulsion fracture of the lateral part of the physis was reduced and fixed percutaneously (c,d).

(c)

and 3 injuries. Fracture lines appear in the coronal, sagittal and transverse planes. Injury to the physis may result in either asymmetrical growth or arrested growth.

making it difficult to see both fractures in the same xray. CT scans are particularly helpful in these and other type 3 injuries.

Treatment Clinical features Following a sprain the ankle is painful, swollen, bruised and acutely tender. There may be an obvious deformity, but sometimes the injury looks deceptively mild.

Imaging Undisplaced physeal fractures – especially those in the distal fibula – are easily missed. Even a hint of physeal widening should be regarded with great suspicion and the child x-rayed again after 1 week. In an infant the state of the physis can sometimes only be guessed at, but a few weeks after injury there may be extensive periosteal new bone formation. In triplane fractures the tibial epiphysis may be split in one plane and the metaphysis in another, thus

Salter–Harris types 1 and 2 injuries are treated closed. If it is displaced, the fracture is gently reduced under general anaesthesia; the limb is immobilized in a fulllength cast for 3 weeks and then in a below-knee walking cast for a further 3 weeks. Occasionally, surgery is needed to extract a periosteal flap, which prevents an adequate reduction. Type 3 or 4 fractures, if undisplaced, can be treated in the same manner, but the ankle must be re-x-rayed after 5 days to ensure that the fragments have not slipped. Displaced fractures can sometimes be reduced closed by reversing the forces that produced the injury. However, unless reduction is near-perfect, the fracture should be reduced open and fixed with interfragmentary screws, which are inserted parallel to the physis. Postoperatively the leg is immobilized in a below-knee cast for 6 weeks.

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31

Tillaux fractures are treated in the same way as type 3 fractures. Triplane fractures, if undisplaced, can be managed closed but require vigilant monitoring for late displacement. Displaced fractures must be reduced and fixed.

Complications Malunion Imperfect reduction may result in angular deformity of the ankle – usually valgus. In children under 10 years old, mild deformities may be accommodated by further growth and modelling. In older children the deformity should be corrected by a supramalleolar closing-wedge osteotomy.

Fractures through the epiphysis (Salter–Harris type 3 or 4) may result in localized fusion of the physis. The bony bridge is usually in the medial half of the growth plate; the lateral half goes on growing and the distal tibia gradually veers into varus. MRI and CT are helpful in showing precisely where physeal arrest has occurred. If the bony bridge is small (less than 30 per cent of the physeal width) it can be excised and replaced by a pad of fat in the hope that physeal growth may be restored. If more than half of the physis is involved, or the child is near the end of the growth period, a supramalleolar closing-wedge osteotomy is indicated.

Asymmetrical growth

Shortening Early physeal closure occurs in about 2 per cent of children with distal tibial injuries. Fortunately the resulting limb length discrepancy is usually mild. If it promises to be more than 2 cm and the child is young enough, proximal tibial epiphysiodesis in the opposite limb may restore equality. If the discrepancy is marked, or the child near the end of the growth period, leg lengthening is indicated.

PRINCIPLES IN MANAGING INJURIES OF THE FOOT

920

Injuries of the foot are apt to be followed by residual symptoms and loss of function, which seem out of proportion to the initial trauma. Severe injuries affect the foot as a whole, whatever the particular bone that might be fractured. A global approach is therefore essential in dealing with these injuries, the objective being a return to full weightbearing without pain, with an appropriate propulsive gait. Identification of these injuries is particularly challenging in the patient with multiple trauma, where the more subtle foot injuries might be missed as the lifethreatening truncal injuries and limb-threatening long bone injuries distract attention from the more subtle injuries to the foot, which may nonetheless impair eventual function.

Clinical assessment The entire foot should be examined systematically, no matter that the injury may appear to be localized to one spot. Multiple fractures, or combinations of fractures and dislocations, are easily missed. The circulation and nerve supply must be carefully assessed; a well-reduced fracture is a useless achievement if the foot becomes ischaemic or insensitive. Similarly, attention must be paid to the soft tissues and functional movement of the foot; the stiff, painful foot is impaired for propulsion, and maybe even for stance. Fractures and dislocations may cause tenting of the skin; this is always a bad sign because there is a risk of skin necrosis if reduction is delayed.

Imaging Imaging routinely begins with anteroposterior, lateral and oblique x-rays of the foot. If a fracture of the talus or calcaneum, or fracture–dislocation of the midtarsal joints is suspected then special views may be helpful, but a more rewarding approach is to carry out a CT scan of the foot. CT is especially useful for evaluating fractures of the calcaneum, and MRI is helpful in diagnosing osteochondral fractures of the talus. Familiarity with the talocalcaneal anatomy is essential if fractures of the hindfoot are to be diagnosed properly.

Treatment Swelling is always a problem. Not only does it make clinical examination difficult, but more importantly it may lead to definitive treatment being delayed; fractures and dislocations are more difficult to reduce in a swollen foot. The principles are: • realign and splint the foot, keep it elevated and apply Cryo-Cuff or ice-packs and intermittent pneumatic compression foot pumps;

31.17 Talus and calcaneum The main features of these two bones, and their relationship to each other, are shown here.

• make the diagnosis, defining the extent of injury; • start definitive treatment as soon as the fracture pattern is properly defined and swelling permits.

Mechanism of injury

INJURIES OF THE TALUS Talar fractures and dislocations are relatively uncommon. They usually involve considerable violence – car accidents in which the occupants are thrown against the resistant frame of the vehicle, falls from a height, or severe wrenching of the ankle. The injuries include fractures of the neck, body, head or bony processes of the talus, dislocations of the talus or the joints around the talus, osteochondral fractures of the superior articular surface, and a variety of chip or avulsion fractures. The significance of the more serious injuries is enhanced by two important facts: (1) the talus is a major weightbearing structure (the superior articular surface carries a greater load per unit area than any other bone in the body); (2) it has a vulnerable blood supply and is a relatively common site for post-traumatic ischaemic necrosis.

Fracture of the talar neck is produced by violent hyperextension of the ankle. The neck of the talus is forced against the anterior edge of the tibia, which acts like a cleaver. If the force continues, the fracture is displaced and the surrounding joints may sublux or dislocate. Fracture of the body is usually a compression injury due to a fall from a height, or an everting force across the body, fracturing the lateral process (the snowboarders’ fracture). Avulsion fractures are associated with ligament strains around the ankle and hindfoot.

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Injuries of the ankle and foot

In the rehabilitation phase, if the foot has to be immobilized, exercise those joints that can be left free. Start weightbearing as soon as the patient will tolerate it, provided this will not jeopardize the reduction. If a removable splint will fit the purpose, use it so that non-weightbearing exercises can be started as soon as possible. Prolonged immobilization predisposes to stiffness, impaired function, localized osteoporosis and complex regional pain syndrome.

Blood vessels enter the bone from the anterior tibial, posterior tibial and peroneal arteries, as well as anastomotic vessels from the surrounding capsule and ligaments. The head of the talus is richly supplied by intraosseous vessels. However, the body of the talus is supplied mainly by vessels that enter the talar neck from the tarsal canal and then run retrograde from distal to proximal. In fractures of the talar neck these vessels are divided; if the fracture is displaced, the extraosseous plexus too may be damaged and the body of the talus is at risk of ischaemia.

Clinical features The patient has most commonly been involved in a motor vehicle accident or has fallen from a height. The foot and ankle are painful and swollen; if the fracture is displaced, there may be an obvious deformity, or the skin may be tented or split. Tenting is a dangerous sign; if the fracture or dislocation is not promptly reduced, the skin may slough and become

31.18 Injuries of the talus–x-rays (a) Talocalcaneal fracture–dislocation. (b) Undisplaced fracture of the talar neck. (c) Type III fracture of the neck. (d) Displaced fracture of the body of the talus. (e) This fracture of the body was thought to be well reduced; however, in the AP view (f) it is possible to see two overlapping outlines, indicating that the fragments are malrotated. (a)

(d)

(b)

(e)

(c)

(f)

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infected. The pulses should be checked and compared with those in the opposite foot.

FRACTURES AND JOINT INJURIES

X-ray Anteroposterior, lateral and oblique views are essential; CT scanning helps to identify associated injuries of the ankle and foot. Both malleoli, the ankle mortise, the talus and all the adjacent tarsal bones should be carefully assessed. Undisplaced fractures are not always easy to see, and sometimes even severely displaced fractures are missed in the initial assessment because of unfamiliarity with the normal appearance – sad but true.

Classification Fractures of the neck of the talus These fractures are classified according to the system devised by Hawkins (1970) and modified by Canale (1978):

• Group I – undisplaced • Group II – displaced (however little) and associated with subluxation or dislocation of the subtalar joint • Group III – displaced, with dislocation of the body of the talus from the ankle joint • Type IV – displaced vertical talar neck fracture with associated talonavicular joint disruption. Fractures of the head of the talus This is a rare injury; the fracture usually involves the talonavicular joint.

with the foot plantarflexed. Weightbearing is not permitted for the first 4 weeks; thereafter, the plaster is removed, the fracture position is checked by x-ray, a new cast is applied and weightbearing is gradually introduced. Further plaster changes or use of an adjustable splintage boot will allow the foot to be brought up, slowly, to plantigrade; physiotherapy is commenced. At 8–12 weeks the splintage is discarded and function is regained by normal use.

DISPLACED FRACTURES OF THE NECK Even the slightest displacement makes it a type II fracture, which needs to be reduced. If the skin is tight, reduction becomes urgent because of the risk of skin necrosis. Reduction must be perfect: (1) in order to ensure that the subtalar joint is mechanically sound; (2) to lessen the chance – or at any rate lessen the effects – of avascular necrosis. With type II fractures, closed manipulation under general anaesthesia can be tried first. Traction is applied with the ankle in plantarflexion; the foot is then steered into inversion or eversion to correct the displacement shown on the x-ray. The reduction is checked by x-ray; nothing short of ‘anatomic’ is acceptable. A below-knee cast is applied (with the foot still in equinus) and this is retained, non-weightbearing, for 4 weeks. Cast changes after that will allow the foot to be gradually brought up to plantigrade; however, weightbearing is not permitted until there is evidence of union (8–12 weeks).

Fractures of the body of the talus These are also uncommon. The fracture is often displaced and may cause distortion of the talocalcaneal joint. Rotational malalignment of the fragments is difficult to diagnose on plain x-ray examination; the deformity is best visualized by three-dimensional CT reconstruction. Fractures of the lateral and posterior processes These are

usually associated with ankle ligament strains. It is sometimes difficult to distinguish between a fracture of the posterior process and a normal os trigonum. A simple rule is ‘if it’s not causing symptoms it doesn’t really matter’.

(a)

(b)

Osteochondral fractures following acute trauma usually occur on the lateral part of the dome of the talus. The diagnosis is often missed when the patient is first seen and may come to light only after CT or MRI scan. Osteochondral

fractures

Treatment The general principles set out on page 920 should be observed.

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UNDISPLACED FRACTURES A split below-knee plaster is applied and, when the swelling has subsided, is replaced by a complete cast

(c)

(d)

31.19 Fractures of the talus – treatment (a) This displaced fracture of the body was reduced and fixed with a countersunk screw (b), giving a perfect result. Fractures of the neck, even if well reduced (c) are still at risk of developing ischaemic necrosis (d).

DISPLACED FRACTURES OF THE BODY Fractures through the body of the talus are usually displaced or comminuted and involve the ankle and/or the talocalcaneal joint; occasionally the fragments are completely dislocated. Minimal displacement can be accepted; a belowknee non-weightbearing cast is applied for 6–8 weeks; this is then replaced by a weightbearing cast for another 4 weeks. Horizontal fractures that do not involve the ankle or subtalar joint are treated by closed reduction and cast immobilization (as earlier). Displaced fractures with dislocation of the adjacent joints should be accurately reduced. In almost all cases open reduction and internal fixation will be needed. An osteotomy of the medial malleolus is useful for adequate exposure of the talus; the malleolus is predrilled before the osteotomy and fixed back into position after the talar fracture has been dealt with. The prognosis for these fractures is poor: there is a considerable incidence of malunion, joint incongruity, avascular necrosis and secondary osteoarthritis of the ankle or talocalcaneal joint.

DISPLACED FRACTURES OF THE HEAD The main problem is injury to the talonavicular joint. If the fragments are large enough, open reduction and internal fixation with screws is the recommended treatment. If there is much comminution, it may be better simply to excise the smaller fragments. Postoperative immobilization is the same as for other talar fractures. FRACTURES OF THE TALAR PROCESSES If the fragment is large enough, open reduction and fixation with K-wires or small screws is advisable. Tiny fragments are left but can be removed later if they become symptomatic. OSTEOCHONDRAL FRACTURES These small surface fractures of the dome of the talus usually occur with severe ankle sprains or subtalar dislocations. Most acute lesions can be treated by cast immobilization for 4–6 weeks. Occasionally a displaced fragment is large enough to warrant operative replacement and internal fixation – easier said than done! More often it is separated from its bed and is excised: the exposed bone is then drilled to encourage repair by fibrocartilage.

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Injuries of the ankle and foot

If closed reduction fails (which it often does), open reduction is essential; indeed, some would say that all type II fractures should be managed by open reduction and internal fixation without attempting closed treatment. Through an anteromedial incision the fracture is exposed and manipulated into position. Wider access can be obtained by pre-drilling and then osteotomizing the medial malleolus; after the talar fracture has been reduced, the malleolar fragment is fixed back in position with a screw. The position is checked by x-ray and the fracture is then fixed with two K-wires or a lag screw. Postoperatively a belowknee cast is applied; weightbearing is not permitted until there are signs of union (8–12 weeks). Type III fracture–dislocations need urgent open reduction and internal fixation. The approach will depend on the fracture pattern and position of displaced fragments. Osteotomy of the medial malleolus might help; the malleolus is pre-drilled for screw fixation and osteotomized and retracted distally without injuring the deltoid ligament. This wide exposure is essential to permit removal of small fragments from the ankle joint and perfect reduction of the displaced talar body under direct vision; even then, it is difficult! The position is checked by x-ray and the fracture is then fixed securely with screws. If there is the slightest doubt about the condition of the skin, the wound is left open and delayed primary closure carried out 5 days later. Postoperatively the foot is splinted and elevated until the swelling subsides; a below-knee cast or splintage boot is then applied, following the same routine as for type II injuries.

OPEN FRACTURES Fractures of the talus are often associated with burst skin wounds. In some cases the fracture becomes ‘open’ when stretched or tented skin starts sloughing. There is a high risk of infection in these wounds and prophylactic antibiotics are advisable. The injury is treated as an emergency. Under general anaesthesia, the wound is cleaned and debrided and all necrotic tissue is removed. The fracture is then dealt with as for closed injuries, except that the wound is left open and closed by delayed primary suture or skin grafting 5–7 days later, when swelling has subsided and it is certain that there is no infection. Sometimes, in open injuries, the talus is completely detached and lying in the wound. After adequate debridement and cleansing, the talus should be replaced in the mortise and stabilized, if necessary with crossed K-wires. Later definitive fixation is then performed.

Complications Malunion The importance of accurate reduction has been stressed. Malunion may lead to distortion of the joint surface, limitation of movement and pain on weightbearing. If early follow-up x-rays show redisplacement of the fragments, a further attempt at reduction is justified. Persistent malunion predisposes to osteoarthritis. Avascular necrosis Avascular necrosis of the body of the

talus occurs in displaced fractures of the talar neck. The

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incidence varies with the severity of displacement: in type 1 fractures it is less than 10 per cent; in type 2 about 30–40 per cent; and in type 3 more than 90 per cent. The earliest x-ray sign (often present by the sixth week) is apparent increased density of the avascular segment; in reality it is the rest of the tarsus that has become slightly porotic with disuse, but the avascular portion remains unaffected and therefore looks more ‘dense’. The opposite is also true: if the dome of the talus becomes osteoporotic, this means that it has a blood supply and it will not develop osteonecrosis. This is the basis of Hawkins’ sign, which should be looked for 6–8 weeks after injury. If osteonecrosis does occur, the body of the talus will eventually appear on x-ray to be more dense than the surrounding bones. Despite necrosis, the fracture may heal, so treatment should not be interrupted by this event; if anything, weightbearing should be delayed in the hope that the bone is not unduly flattened. Function may yet be reasonable. However, if the talus becomes flattened or fragmented, or pain and disability are marked, the ankle may need to be arthrodesed. Secondary osteoarthritis Osteoarthritis of the ankle and/or subtalar joints occurs some years after injury in over 50 per cent of patients with talar neck fractures. There are a number of causes: (1) articular damage due to the initial trauma; (2) malunion and distortion of the articular surface; (3) avascular necrosis of the talus. Pain and stiffness may be managed by judicious analgesic medication and orthotic adjustments, but in some cases the painful hindfoot will simply not allow a return to function; arthrodesis of the affected joints can help to relieve symptoms. Operative fusion of one joint may predispose to overload of the associated foot joints, and hence to later arthritis, but this should be accepted.

FRACTURES OF THE CALCANEUM The calcaneum is the most commonly fractured tarsal bone, and in 5–10 per cent of cases both heels are injured simultaneously. Crush injuries, although they always heal in the biological sense, are likely to be followed by long-term disability. The general attitude to these injuries at the beginning of the twentieth century (at least from an industrial point of view) was that “the man who breaks his heel-bone is finished”. This was followed by attempts, throughout the latter part of that century, to modify the outcome through open reduction and internal fixation of these fractures.

Mechanism of injury 924

In most cases the patient falls from a height, often from a ladder, onto one or both heels. The calcaneum

is driven up against the talus and is split or crushed. Over 20 per cent of these patients suffer associated injuries of the spine, pelvis or hip. Avulsion fractures sometimes follow traction injuries of the tendo Achillis or the ankle ligaments. Occasionally the bone is shattered by a direct blow.

Pathological anatomy Based largely on the work of Palmer (1948) and Essex-Lopresti (1952), it has been customary to divide calcaneal fractures into extra-articular fractures (those involving the various calcaneal processes or the body posterior to the talocalcaneal joint) and intraarticular fractures (those that split the talocalcaneal articular facet). EXTRA-ARTICULAR FRACTURES These account for 25 per cent of calcaneal injuries. They usually follow fairly simple patterns, with shearing or avulsion of the anterior process, the sustentaculum tali, the tuberosity or the inferomedial process. Fractures of the posterior (extra-articular) part of the body are caused by compression. Extra-articular fractures are usually easy to manage and have a good prognosis. INTRA-ARTICULAR FRACTURES These injuries are much more complex and unpredictable in their outcome. They are best understood by imagining the impact of the talus cleaving the bone from above to produce a primary fracture line that runs obliquely across the posterior articular facet and the body from posteromedial to anterolateral. Where it splits, the posterior articular facet depends upon the position of the foot at impact: if the heel is in valgus (abducted), the fracture is in the lateral part of the facet; if the heel is in varus (adducted), the fracture is more medial. The upward displacement of the body of the calca-

(a)

(b)

31.20 Extra-articular fractures of the calcaneum Fractures may occur through (A) the anterior process, (B) the body, (C) the tuberosity, (D) the sustentaculum tali or (E) the medial tubercle. Treatment is closed unless the fragment is large and badly displaced, in which case it will need to be fixed back in position.

(a)

(b)

of the calcaneum and can only be reduced if the lateral wall of the body is osteotomized so as to gain access to it (Eastwood et al., 1993).

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Clinical features There is usually a history of a fall from a height, or a road traffic accident; in elderly osteoporotic people even a comparatively minor injury may fracture the calcaneum. The foot is painful and swollen and a large bruise appears on the lateral aspect of the heel. The heel may look broad and squat. The surrounding tissues are thick and tender, and the normal concavity below the lateral malleolus is lacking. The subtalar joint cannot be moved but ankle movement is possible. Always check for signs of a compartment syndrome of the foot (intense pain, very extensive bruising and diminished sensation, with pain on passive toe movement).

(c)

Injuries of the ankle and foot

neum produces one of the classic x-ray signs of a ‘depressed’ fracture: flattening of the angle subtended by the posterior articular surface and the upper surface of the body posterior to the joint (Böhler’s angle). The advent of CT, and the trend towards operative reduction and fixation of displaced calcaneal fractures, have sharpened our understanding of these complex injuries. There are two important ways of assessing or classifying these injuries that are of relevance to the treating surgeon (and the patient). The work of Sanders and Gregory (1995) has helped to define the intra-articular fracture pattern and the associated outcome and prognosis. Knowledge of the variations in fracture pattern, particularly in relation to the lateral wall of the calcaneum (Eastwood et al., 1993) has improved our understanding of the anatomy that is likely to be encountered at operation, approaching from an extended L-shaped incision; the lateral joint fragment may sometimes be trapped within the body

(d)

31.21 Intra-articular fractures of the calcaneum The primary fracture line (a,b) is created by the impact of the talus on the calcaneum – it runs from posteromedial to anterolateral. Secondary fracture lines may create ‘tongue’ (c) or ‘joint depression’ (d) variants to the fracture pattern.

(a)

(b)

(c)

31.22 Intra-articular fractures of the calcaneum CT scans have allowed a better understanding of the fracture anatomy. A coronal CT scan enables the identification of three major fragments in most intra-articular fractures: the lateral joint fragment (L), the sustentaculum tali (S) and the body fragment (B). In type 1 fractures (a) the lateral joint fragment is in valgus whereas the body is in varus. In type 2 fractures (b), the sustentaculum tali is in varus and the lateral joint is elevated in relation to it. In type 3 fractures (c) the lateral joint fragment is impacted and buried within the body fragment (Eastwood et al., 1993).

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(a)

(b)

(c)

(d)

31.23 Fracture of the calcaneum – imaging (a,b) Measurement of Böhler’s angle and the x-ray appearance in a normal foot. (c) Flattening of Böhler’s angle in a fractured calcaneum. (d) The CT scan in this case shows how the articular fragments have been split apart.

X-ray Plain x-rays should include lateral, oblique and axial views. Extra-articular fractures are usually fairly obvious. Intra-articular fractures, also, can often be identified in the plain films and if there is displacement of the fragments the lateral view may show flattening of the tuber-joint angle (Böhler’s angle). For accurate definition of intra-articular fractures, CT is essential and three-dimensional reconstruction views even better. Coronal sections will show the fracture ‘geometry’ clearly enough to permit accurate diagnosis of most intra-articular fractures (Lowrie et al., 1988). With severe injuries – and especially with bilateral fractures or in the unconscious patient – it is essential to assess the knees, spine and pelvis as well.

EXTRA-ARTICULAR FRACTURES The byword for the management of extra-articular fractures is ‘mobility and function are more important than anatomical repositioning’. The vast majority are treated closed: (1) compression bandaging, ice packs and elevation until the swelling subsides; (2) exercises as soon as pain permits; (3) no weightbearing for 4 weeks and partial weightbearing for another 4 weeks. Variations from this routine relate to specific injuries. Fractures of the anterior process Most of these are avulsion fractures and many are mistaken for an ankle sprain. Oblique x-rays will show the fracture, which almost always involves the calcaneocuboid joint. If there is a large displaced fragment, internal fixation may be needed; this is followed by the usual ‘closed’ routine.

These are usually due to avulsion by the tendo Achillis; clinical signs are similar to those of a torn Achilles tendon. If the fragment is displaced, it should be reduced and fixed with cancellous screws; the foot is then immobilized in slight equinus to relieve tension on the tendo Achillis. Weightbearing can be permitted after 4 weeks.

Fractures of the tuberosity

Treatment For all except the most minor injuries, the patient is admitted to hospital so that the leg and foot can be elevated and treated with cold (ice or Cryo-Cuff) and compression until swelling subsides. This also gives time to obtain the necessary CT scans.

31.24 Calcaneal fractures – imaging Bilateral calcaneal fractures (a,b) are caused by a fall on the heels from a height or by an explosion from below. In either case the spine also may be fractured, as it was in this patient (c). With bilateral heel fractures, always x-ray the spine.

926

(a)

(b)

(c)

31.25 Extra-articular calcaneal fractures – treatment (a) Avulsion fracture of posterosuperior corner (b) fixed by a screw.

(b)

If it is certain that the subtalar joint is not involved, the prognosis is good and the fracture can be treated by the usual ‘closed’ routine. However, if there is much sideways displacement and widening of the heel, closed reduction by manual compression should be attempted. Weightbearing is avoided for 6–8 weeks; however, cast immobilization is unnecessary except if both heels are fractured or if the patient simply cannot manage a one-legged gait with crutches (e.g. those who are elderly or frail).

Fractures of the body

INTRA-ARTICULAR FRACTURES Undisplaced fractures are treated in much the same way as extra-articular fractures: compression bandaging, ice-packs and elevation followed by exercises and

(a)

(b)

non-weightbearing for 6–8 weeks. As long as vertical stress is avoided, the fracture will not become displaced; cast immobilization is therefore unnecessary and it may even be harmful in that it increases the risk of stiffness and algodystrophy. Good or excellent results can be expected in most patients with undisplaced intra-articular fractures. Displaced intra-articular fractures are best treated by open reduction and internal fixation as soon as the swelling subsides. CT has greatly facilitated this approach; the medial and lateral fragments can be clearly defined and, with suitable drawings or models, the surgical procedure can be carefully planned and rehearsed. The operation is usually performed through a single, wide lateral approach; access to the posterior facet and medial fragment is achieved by taking down the lateral aspect of the calcaneum, performing the reduction, and then rebuilding this wall. The various fragments are held with interfragmentary screws – bone grafts are sometimes added to fill in defects. The anterior part of the calcaneum and the calcaneocuboid joint also need attention; the fragments are similarly reduced and fixed. Finally a contoured plate is placed on the lateral aspect of the calcaneum to buttress the entire assembly. The wound is then closed and drained. Postoperatively the foot is lightly splinted and elevated. Exercises are begun as soon as pain subsides and after about 2 weeks the patient can be allowed up non-weightbearing on crutches. Partial weightbearing is permitted only when the fracture has healed (seldom before 8 weeks) and full weightbearing about 4 weeks after that. Restoration of function may take 6– 12 months.

Injuries of the ankle and foot

(a)

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Outcome (c)

(d)

31.26 Intra-articular calcaneal fracture – treatment (a) X-ray gives limited information, but the CT (b) shows the severe depression of the posterior calcaneal facet. This was treated operatively with a calcaneal locking plate, to reconstitute the posterior facet (arrow) and restore the height of the calcaneum (c,d).

Extra-articular fractures and undisplaced intra-articular fractures, if properly treated, usually have a good result. However, the patient should be warned that it may take 6–12 months before full function is regained, and in about 10 per cent of cases there will be residual symptoms that might preclude a return to their previous job if this involved walking on uneven surfaces or balancing on ladders.

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The outcome for displaced intra-articular fractures is much less predictable. The results of operative treatment are heavily dependent on the severity of the fracture and the experience of the surgeon (Buckley et al., 1992; Sanders et al., 1995). The Canadian multicentre study showed a shorter time off work and lower requirement for subtalar arthrodesis in those managed operatively. Results were particularly favourable with internal fixation in younger men and those not working with heavy loads or receiving workmen’s compensation. In experienced hands, for selected fractures, this is a rational treatment. However, it is not an enterprise for the tyro and unless the appropriate skills and facilities are available the patient should be referred to a specializing centre. Closed treatment, though it may be the only alternative, has a bad reputation. Crosby and Fitzgibbons (1990), in a follow up of 30 patients who had undergone closed treatment, found that 50 per cent of those with uncomplicated displaced intra-articular fractures were contemplating having an arthrodesis within 4 years of injury; only two out of 10 patients had a ‘good’ result. Those with comminuted fractures fared even worse: all of them were assessed as having a poor result. The fact remains that the heel fracture is a serious and disabling injury in many patients with heavy or physically demanding jobs; mechanical reconstruction of the bony anatomy does not necessarily improve the functional outcome.

Complications

Insufficiency of the tendo Achillis The loss of heel height

may result in diminished tendo Achillis action. If this interferes markedly with walking, subtalar arthrodesis with insertion of a bone block may alleviate the problem. Talocalcaneal stiffness and osteoarthritis Displaced intra-

articular fractures may lead to joint stiffness and, eventually, osteoarthritis. This can usually be managed conservatively but persistent or severe pain may necessitate subtalar arthrodesis. If the calcaneocuboid joint is also involved, a triple arthrodesis is better.

MIDTARSAL INJURIES Injuries in this area vary from minor sprains, often incorrectly labelled as ‘ankle’ sprains, to severe fracture–dislocations that can threaten the survival of the foot. The mechanism differs accordingly, from benign twisting injuries to crushing forces that produce severe soft tissue damage; bleeding into the fascial compartments of the foot may cause a typical compartment syndrome. Isolated injuries of the navicular, cuneiform or cuboid bones are rare. Fractures in this region should be assumed to be ‘combination’ fractures or fracture– subluxations, until proved otherwise. Remember that small flakes of bone on x-ray often have large ligaments attached to them, and that ‘midfoot sprain’ (like ‘partial Achilles tendon rupture’) is a dangerous diagnosis to make.

EARLY Intense swelling and blistering may jeopardize operative treatment. The limb should be elevated with the minimum of delay.

Swelling and blistering

About 10 per cent of patients develop intense pressure symptoms. The risk of a fullblown compartment syndrome can be minimized by starting treatment early. If operative decompression is carried out, this will delay any definitive procedure for the fracture.

Compartment syndrome

LATE Closed treatment of displaced fractures, or injudicious weightbearing after open reduction, may result in malunion. The heel is broad and squat, and the patient has a problem fitting shoes. Usually the foot is in valgus and walking may be impaired. Malunion

Lateral displacement of the body of the calcaneum may cause painful compression of the peroneal tendons against the lateral malleolus. Treatment consists of operative paring down of protuberant bone on the lateral wall of the calcaneum.

Peroneal tendon impingement

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Pathological anatomy The most useful classification is that of Main and Jowett (1975), which is based on the mechanism of injury. Medial stress injuries are caused by violent inversion of the foot and vary in severity from sprains of the midtarsal joint to subluxation or fracture–subluxation of the talonavicular or midtarsal joints. Longitudinal stress injuries are the most common. They are caused by a severe longitudinal force with the foot in plantarflexion. The navicular is compressed between the cuneiforms and the talus, resulting in fracture of the navicular and subluxation of the midtarsal joint. Lateral stress injuries are usually due to falls in which the foot is forced into valgus. Injuries include fractures and fracture–subluxations of the cuboid and the anterior end of the calcaneum as well as avulsion injuries on the medial side of the foot. Plantar stress injuries result from falls in which the foot is twisted and trapped under the body; they usually present as dorsal avulsion injuries or fracture– subluxation of the calcaneocuboid joint.

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Crush injuries usually cause open comminuted fractures of the midtarsal region.

Clinical features

X-ray Multiple views are necessary to determine the extent of the injury; be sure that all the tarsal bones are clearly shown. Tarso-metatarsal dislocation may be missed if the forefoot falls back into place; fractures of the tarsal bones or bases of the metatarsals should alert the surgeon to this possibility. Abnormality of alignment, or fracture, on any view should lead to CT scanning to better assess the extent of injury.

Treatment The foot may be bandaged until acute pain subsides. Thereafter, movement is encouraged. Be prepared to re-examine and re-x-ray the foot that does not settle within a few weeks.

Ligamentous strains

Undisplaced fractures The foot is elevated to counteract swelling. After 3 or 4 days a below-knee cast or removeable splintage boot is applied and the patient is allowed up on crutches with limited weightbearing. The plaster is retained for 4–6 weeks. Displaced fractures An isolated navicular or cuboid fracture is sometimes displaced and, if so, may need open reduction and screw fixation.

31.28 Midtarsal injuries Reconstructed CT after reduction of a severe tarso-metatarsal injury reveals associated injuries of the cuboid and the lateral cuneiform.

Injuries of the ankle and foot

The foot is bruised and swollen. Tenderness is usually diffuse across the midfoot. A medial midtarsal dislocation looks like an ‘acute club-foot’ and a lateral dislocation produces a valgus deformity; with longitudinal stress injuries there is often no obvious deformity. Any attempt at movement is painful. It is important to exclude distal ischaemia or a compartment syndrome.

These are severe injuries. Under general anaesthesia, the dislocation can usually be reduced by closed manipulation but holding it is a problem. If there is the least tendency to redisplacement, percutaneous K-wires are run across the joints to fix them in position. The foot is immobilized in a below-knee cast for 6– 8 weeks. Exercises are then begun and should be practised assiduously; it may be 6–8 months before function is regained. If accurate reduction cannot be achieved by closed manipulation, then open reduction and screw fixation is necessary; the importance of anatomical reduction cannot be overemphasized. However, missed fractures are a lost cause and open reduction will seldom improve the situation in those who present late (more than 3 weeks after injury).

Fracture–dislocation

Severely comminuted fractures defy accurate reduction. Attention should be paid to the soft tissues; there is a risk of ischaemia. The foot is splinted in the best possible position and elevated until swelling subsides. Early arthrodesis, with restoration of the longitudinal arch, is advisable, with stable fixation and interpositional bone graft block.

Comminuted fractures

(a)

(b)

31.27 Midtarsal injuries (a) X-ray showing dislocation of the talonaviclar joint. (b) X-ray on another patient showing longitudinal compression fracture of the navicular bone and subluxation of the head of the talus. This injury is often difficult to demonstrate accurately on plain x-ray.

OUTCOME A major problem with midtarsal injuries is the frequency with which fractures and dislocations are missed at the first examination, resulting in undertreatment and a poor outcome. Even with accurate reduction of midtarsal fracture–dislocations, post-traumatic osteoarthritis may develop and about 50 per cent of patients fail to regain normal function. If symptoms are persistent and intrusive, arthrodesis may be indicated.

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X-rays may be difficult to interpret; something looks wrong but it is often difficult to tell what. A systematic method for examining the foot x-rays can help to improve the pick-up rate for these injuries. Concentrate on the second and fourth metatarsals in the oblique views: the medial edge of the second should be in line with the medial edge of the second cuneiform, and the medial edge of the fourth should line up with the medial side of the cuboid. A true lateral may show the dorsal displacement of the second metatarsal base. If a fracture–dislocation is suspected (the displacement may reduce spontaneously and not be immediately detectable), stress views may reveal the abnormality, but a CT scan is a more efficient way of showing the extent of injury.

TARSO-METATARSAL INJURIES The five tarso-metatarsal (TMT) joints form a structural complex that is held intact partly by the interdigitating joints and partly by the strong ligaments that bind the metatarsal bones to each other and to the tarsal bones of the midfoot. An appreciation of the anatomy across the TMT joints is important in understanding these injuries. The second metatarsal base is set into a recess formed by the medial, intermediate and lateral cuneiforms. There is no ligament between the first and second metatarsal bases, but the plantar ligament between second metatarsal base and medial cuneiform is short and thick. In the coronal plane, the second metatarsal base forms the apex or keystone in the arch. Dislocation is rare, but important not to miss; twisting and crushing injuries are the usual causes, with the foot buckling or twisting at the midfoot– forefoot junction. The term Lisfranc injury is often used for the disruptions that occur at the midfoot– forefoot junction. Classifying these by direction of forefoot dislocation is, however, pointless – it is neither a guide to treatment nor an indication of outcome. These are often high-energy injuries with extensive damage to the whole region of the foot, and simply to assess the direction of metatarsal displacement is to miss the complexity of the injury pattern.

Treatment The method of treatment depends on the severity of the injury. Undisplaced sprains require cast immobilization for 4–6 weeks. Subluxation or dislocation calls for accurate reduction. This can often be achieved by traction and manipulation under anaesthesia; the position is then held with percutaneous K-wires or screws and cast immobilization. The cast is changed after a few days when swelling has subsided; the new cast is retained, non-weightbearing, for 6–8 weeks. The Kwires are then removed and rehabilitation exercises begun. If closed reduction fails, open reduction is essential. The key to success is the second TMT joint. Through a longitudinal incision, the base of the second metatarsal is exposed and the joint manipulated into position. Reduction of the remaining parts of the tarso-metatarsal articulation will not be too difficult. The bones are fixed with percutaneous K-wires or screws and the foot is immobilized as described earlier.

Clinical features TMT dislocation or fracture–dislocation should always be suspected in patients with pain and swelling of the foot after high-velocity car accidents and falls. Unfortunately about 20–30 per cent of these injuries are initially missed. Only with severe injury is there an obvious deformity.

(a)

930

(b)

(c)

(d)

31.29 TMT injuries (a) Dislocation of the TMT joints. (b) X-ray after reduction and stabilization with K-wires. (c) X-ray showing a high-energy fracture–dislocation involving the TMT joints. These are serious injuries that may be complicated by (d) compartment syndrome of the foot.

Complications

INJURIES OF METATARSAL BONES Metatarsal fractures are relatively common and are of four types: (1) crush fractures due to a direct blow; (2) a spiral fracture of the shaft due to a twisting injury; (3) avulsion fractures due to ligament strains; (4) insufficiency fractures due to repetitive stress.

Clinical features In acute injuries pain, swelling and bruising of the foot are usually quite marked; with stress fractures, the symptoms and signs are more insidious. X-rays should include routine anteroposterior, lateral and oblique views of the entire foot; multiple injuries are not uncommon. Undisplaced fractures may be difficult to detect and stress fractures usually show nothing at all until several weeks later.

DISPLACED FRACTURES Displaced fractures can usually be treated closed. The foot is elevated until swelling subsides. The fracture may be reduced by traction under anaesthesia and the leg immobilized in a cast – non-weightbearing – for 4 weeks. Alternatively the fracture position might be accepted, depending on the degree of displacement. For the second to fifth metatarsals, displacement in the coronal plane can be accepted and closed treatment, as above, is satisfactory. However, for the first metatarsal and for all fractures with significant displacement in the sagittal plane (i.e. depression or elevation of the displaced fragment) open reduction and internal fixation with K-wires, or better with stable fixation using a plate and small screws, is advisable. A below-knee cast is applied and weightbearing is avoided for 3 weeks; this is then replaced by a weightbearing cast for another 4 weeks. Fractures of the metatarsal neck have a tendency to displace, or re-displace, with closed immobilization. It is therefore important to check the position repeatedly if closed treatment is used. If the fracture is unstable, it may be possible to maintain the position by percutaneous K-wire or screw fixation. The wire is removed after 4 weeks; cast immobilization is retained for 4–6 weeks.

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Injuries of the ankle and foot

Compartment syndrome A tensely swollen foot may hide a serious compartment syndrome that could result in ischaemic contractures. If this is suspected, intracompartmental pressures should be measured (see Chapter 23). Treatment should be prompt and effective: through a medial longitudinal incision, or two well-spaced dorsal incisions, all the compartments can be decompressed; the wound is left open until swelling subsides and the skin can be closed without tension.

active movements are started immediately, partial weightbearing for about 4–6 weeks. At the end of that period, exercise is very important and the patient is encouraged to resume normal activity. Slight malunion rarely results in disability once mobility has been regained.

Treatment Treatment will depend on the type of fracture, the site of injury and the degree of displacement. UNDISPLACED AND MINIMALLY DISPLACED FRACTURES These can be treated by support in a below-knee cast or removable boot splint; the foot is elevated and

FRACTURES OF THE FIFTH METATARSAL BASE Forced inversion of the foot (the ‘pot-hole injury’) may cause avulsion of the base of the fifth metatarsal, with pull-off by the peroneus brevis tendon or the 31.30 Metatarsal injuries (a) Transverse fractures of three metatarsal shafts. (b) Avulsion fracture of the base of the fifth metatarsal – the pot-hole injury, or Robert Jones fracture. (c) Florid callus in a stress fracture of the second metatarsal. (d) Jones’ fracture of the fifth metatarsal.

(a)

(b)

(c)

(d)

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lateral band of the plantar fascia. Pain due to a sprained ankle may overshadow pain in the foot. Examination will disclose a point of tenderness directly over the prominence at the base of the fifth metatarsal bone. A careful assessment of the fracture pattern will provide a guide to prognosis and treatment. Again, an appreciation of the patho-anatomy explains these factors. The fifth metatarsal base extends much more proximal into the midfoot region, compared to the other metatarsal bases. It articulates with the cuboid and with the fourth metatarsal. The peroneus brevis tendon and lateral band of the plantar fascia insert onto the base of the fifth metatarsal. There is a relative watershed in the blood supply to the fifth metatarsal at the junction between the diaphysis and metaphysis. Robert Jones, a founding father and doyen of orthopaedics, described his own fracture (sustained whilst dancing), as a fracture of the fifth metatarsal about three-fourths of an inch from its base. Unfortunately, as observed above with Pott’s fractures, what has passed into history as this eponymous fracture is often not what was actually described, and the term ‘Jones fracture’ is now sometimes used for any fracture of the proximal fifth metatarsal. A more useful classification system takes account of the fracture line, and whether it is proximal, affecting the tuberosity, in the region of articulation with the fourth metatarsal, or at the metaphyseal/diaphyseal junction – the latter has a higher rate of non-union, probably as a consequence of the relatively poor blood supply in that region. Occasionally a normal peroneal ossicle in this area may be mistaken for a fracture; there is also an apophyseal ossification centre in the tuberosity.

midshaft of a metatarsal bone. Usually the second metatarsal is affected, especially if it is much longer than an ‘atavistic’ first metatarsal. The x-ray appearance may at first be normal but a radioisotope scan will show an area of intense activity in the bone. Later a hairline crack may be visible and later still (4–6 weeks) a mass of callus is seen. Unaccountable pain in elderly osteoporotic people may be due to the same lesion; x-ray diagnosis is more difficult because callus is minimal and there may be no more than a fine linear periosteal reaction along the metatarsal. If osteoporosis has not already been diagnosed, then this should be considered and assessed with bone densitometry. Metatarsal pain after forefoot surgery may also be due to stress fractures of the adjacent metatarsals, a consequence of redistributed stresses in the foot. No displacement occurs and neither reduction nor splintage is necessary. The forefoot may be supported with an elastic bandage and normal walking is encouraged.

INJURIES OF METATARSOPHALANGEAL JOINTS Sprains and dislocations of the metatarsophalangeal (MTP) joints are common in dancers and athletes. A simple sprain requires no more than light splinting; strapping a lesser toe (second to fifth) to its neighbour for a week or two is the easiest way. If the toe is dislocated, it should be reduced by traction and manipulation; the foot is then protected in a short walking cast for a few weeks.

Treatment The proximal avulsion fractures can usually be treated symptomatically, with initial rest and support, but with early mobilization and return to function. The intra-articular injuries and those at the metaphyseal–diaphyseal junction may also be treated nonoperatively, but there is a greater risk of non-union and slower return to function. The role of fixation with an interfragmentary screw or screws and plate is therefore an issue for discussion between the surgeon and the patient, depending to a large extent on the patient’s functional demands and expectations with respect to sport, activity, and time away from these.

STRESS INJURY (MARCH FRACTURE) 932

In a young adult (often a military recruit or a nurse) the foot may become painful and slightly swollen after overuse. A tender lump is palpable just distal to the

FRACTURED TOES A heavy object falling on the toes may fracture phalanges. If the skin is broken it must be covered with a sterile dressing, and antibiotics are given; a contaminated wound will require formal surgical washout and exploration. The fracture is disregarded and the patient encouraged to walk in a supportive boot or shoe. If pain is marked, the toe may be splinted by strapping it to its neighbour for 2–3 weeks.

FRACTURED SESAMOIDS One of the sesamoids (usually the medial) may fracture from either a direct injury (landing from a height on the ball of the foot) or sudden traction; chronic,

REFERENCES AND FURTHER READING Ajis A, Younger AS, Maffulli N. Anatomic repair for chronic lateral ankle instability. Foot Ankle Clin 2006; 11: 539–45. Bajammal S, Tornetta P 3rd, Sanders D, Bhandari M. Displaced intra-articular calcaneal fractures. J Orthop Trauma 2005; 19: 360–4. Blauth M, Bastian L, Krettek C, Knop C, Evans S. Surgical options for the treatment of severe tibial pilon fractures: a study of three techniques. J Orthop Trauma 2001; 15: 153–60. Bosse MJ, McCarthy ML, Jones AL et al. Lower Extremity Assessment Project (LEAP) Study Group. The insensate foot following severe lower extremity trauma: an indication for amputation? J Bone Joint Surg 2005; 87A: 2601–8. Broström L. Sprained ankles. Surgical treatment of ‘chronic’ ligament ruptures. Acta Chir Scand 1966; 132: 551–65. Buckley R, Tough S, McCormack R et al. Operative compared with nonoperative treatment of displaced intraarticular calcaneal fractures: a prospective, randomized, controlled multicenter trial. J Bone Joint Surg 2002; 84A: 1733–44. Canale ST, Kelly FB Jr. Fractures of the neck of the talus. Long-term evaluation of seventy-one cases. J Bone Joint Surg 1978; 60A: 143–56. Chrisman OD, Snook GA. Reconstruction of lateral ligament tears of the ankle: an experimental study and clinical evaluation of seven patients treated by a new modification of the Elmslie procedure. J Bone Joint Surg 1969; 51A: 904–12. Clare MP, Sanders RW. Preoperative considerations in ankle replacement surgery. Foot Ankle Clin 2002; 7: 709–20. Coetzee JC, Ly TV. Treatment of primarily ligamentous Lisfranc joint injuries: primary arthrodesis compared with

open reduction and internal fixation. Surgical technique. J Bone Joint Surg 2007; 89A(Suppl 2 Pt 1): 122–7. Coetzee JC. Making sense of Lisfranc injuries. Foot Ankle Clin 2008; 13: 695–704. Colville MR. Reconstruction of the lateral ankle ligaments. J Bone Joint Surg 1994; 76A: 1092–102. Crosby LA, Fitzgibbons T. Intra-articular calcaneal fractures: Results of closed treatment. Clin Orthop 1993; 290: 46–54. Das De S, Balasubramaniam P. A repair operation for recurrent dislocation of the peroneal tendons. J Bone Joint Surg 1985; 67B: 585–7. Dattani R, Patnaik S, Kantak A, Srikanth B, Selvan TP. Injuries to the tibiofibular syndesmosis. J Bone Joint Surg 2008; 90B: 405–10. Dias LS, Tachdjian MO. Physeal injuries of the ankle in children. Clinical Orthopaedics and Related Research 1978; 136: 230. Eastwood DM, Gregg PJ, Atkins RM. Intra-articular fractures of the calcaneum. Part 1: Pathological anatomy and classification. J Bone Joint Surg 1993; 75B: 183–8. Eastwood DM, Langkamer VG, Atkins RM. Intraarticular fractures of the calcaneum. Part 2: Open reduction and internal fixation by the extended lateral transcalcaneal approach. J Bone Joint Surg 1993; 75B: 189–95. Egol KA, Wolinsky P, Koval KJ. Open reduction and internal fixation of tibial pilon fractures. Foot Ankle Clin 2000; 5: 873–85. Eiff M, Smith A, Smith G. Early mobilization versus immobilization in the treatment of lateral ankle sprains. Am J Sports Med 1994; 22: 83–8. Espinosa N, Smerek JP, Myerson MS. Acute and chronic syndesmosis injuries: pathomechanisms, diagnosis and management. Foot Ankle Clin 2006; 11: 639–57. Essex-Lopresti P. The mechanism, reduction technique and results in fractures of the os calcis. Br J Surg 1952; 39: 395–419. Goel DP, Buckley R, deVries G, Abelseth G, Ni A, Gray R. Prophylaxis of deep-vein thrombosis in fractures below the knee: a prospective randomised controlled trial. J Bone Joint Surg 2009; 91B: 388–94. Harris AM, Patterson BM, Sontich JK, Vallier HA. Results and outcomes after operative treatment of highenergy tibial plafond fractures. Foot Ankle Int 2006; 27: 256–65. Hawkins LG. Fractures of the neck of the talus. J Bone Joint Surg 1970; 52A: 991–1002. Helfet DL, Koval K, Pappas J, Sanders RW, DiPasquale T. Intraarticular ‘pilon’ fracture of the tibia. Clin Orthop Relat Res 1994; 298: 221–8. Hopkinson WJ, St Pierre P, Ryan JB et al. Syndesmosis sprains of the ankle. Foot Ankle 1990; 10: 325. Karlsson J, Bergsten T, Lansinger O, Peterson L. Reconstruction of the lateral ligaments of the ankle for chronic-lateral instability. J Bone Joint Surg 1988; 70A: 581–588.

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Injuries of the ankle and foot

repetitive stress is more often seen in dancers and runners. The patient complains of pain directly over the sesamoid. There is a tender spot in the same area and sometimes pain can be exacerbated by passively hyperextending the big toe. X-rays will usually show the fracture (which must be distinguished from a smoothedged bipartite sesamoid). Treatment is often unnecessary, though a local injection of lignocaine helps for pain. If discomfort is marked, the foot can be supported in a removable boot/splint for 2–3 weeks. An insole with differential padding or cut-out under the sesamoid might also speed a return to sporting activities. Occasionally, intractable symptoms call for excision of the offending ossicle; care should be taken not to disrupt the flexor attachment to the proximal phalanx as this may result in great toe deformity.

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FRACTURES AND JOINT INJURIES

31

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Konradsen L, Homer P, Sondergaard L. Early mobilization treatment for grade III ankle ligament injuries. Foot Ankle 1992; 12: 69–73. Kuo RS, Tejwani NC, Digiovanni CW et al. Outcome after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg Am 2000; 82A: 1609–18. Langdon IJ, Kerr PS, Atkins RM. Fractures of the calcaneum: the anterolateral fragment. J Bone Joint Surg 1994; 76B: 303–5. Lauge-Hansen N. Fractures of the ankle. II. Combined experimental-surgical and experimental-roentgenologic investigations. Arch Surg 1950; 60: 957–85. Li X, Killie H, Guerrero P, Busconi BD. Anatomical reconstruction for chronic lateral ankle instability in the highdemand athlete: functional outcomes after the modified Broström repair using suture anchors. Am J Sports Med 2009; 37: 488–94. Lowrie IG, Finlay DB, Brenkel IJ, Gregg PJ. Computerised tomographic assessment of the subtalar joint in calcaneal fractures. J Bone Joint Surg Am 1988; 70B: 247–50. Main BJ, Jowett RL. Injuries of the midtarsal joint. J Bone Joint Surg 1975; 57B: 89–97. Michelson JD. Ankle fractures resulting from rotational injuries. J Am Acad Orthop Surg 2003; 11: 403–12. Muller ME, Allgöwer M, Schneider R, Willeneger H. Manual of Internal Fixation. (3rd edition) Springer, Berlin, 1991, pp 598–600. Nunn T, Baird C, Robertson D, Gray I, Gregori A. Fitness to drive in a below knee plaster? An evidence based response. Injury 2007; 38: 1305–07. Palmer I. The mechanism and treatment of fractures of the calcaneus. J Bone Joint Surg 1948; 30A: 2–8. Papadokostakis G, Kontakis G, Giannoudis P, Hadjipavlou A. External fixation devices in the treatment of fractures of the tibial plafond: a systematic review of the literature. J Bone Joint Surg Br 2008; 90: 1–6. Pearse EO, Klass B, Bendall SP. The ‘ABC’ of examining foot radiographs. Ann R Coll Surg Engl 2005; 87: 449–51. Philbin T, Rosenberg G, Sferra JJ. Complications of missed or untreated Lisfranc injuries. Foot Ankle Clin 2003; 8: 61–71. Porter DA. Evaluation and treatment of ankle syndesmosis injuries. Instr Course Lect 2009; 58: 575–81.

Quill GE Jr. Fractures of the proximal fifth metatarsal. Orthop Clin North Am 1995; 26: 353–61. Rammelt S, Heineck J, Zwipp H. Metatarsal fractures. Injury 2004; 35(Suppl 2): SB77–86. Ruedi TP, Allgöwer M. The operative treatment of intraarticular fractures of the lower end of the tibia. Clin Orthop 1979; 138: 105–10. Sanders R, Gregory P. Operative treatment of intra-articular fractures of the calcaneus. Orthop Clin N Am 1995; 26: 203–14. Schnetzler KA, Hoernschemeyer D. The pediatric triplane ankle fracture. J Am Acad Orthop Surg 2007; 15: 738– 47. Sirkin M, Sanders R, DiPasquale T, Herscovici D Jr. A staged protocol for soft tissue management in the treatment of complex pilon fractures. J Orthop Trauma 1999; 13: 78–84. Sirkin MS. Plating of tibial pilon fractures. Am J Orthop 2007; 36(Suppl 2): 13–17. SooHoo NF, Krenek L, Eagan MJ, Gurbani B, Ko CY, Zingmond DS. Complication rates following open reduction and internal fixation of ankle fractures. J Bone Joint Surg 2009; 91A: 1042–9. Tarkin IS, Clare MP, Marcantonio A, Pape HC. An update on the management of high-energy pilon fractures. Injury 2008; 39: 142–54. Teeny SM, Wiss DA. Open reduction and internal fixation of tibial plafond fractures. Clin Orthop 1993; 292: 108– 17. Tezval M, Dumont C, Stürmer KM. Prognostic reliability of the Hawkins sign in fractures of the talus. J Orthop Trauma 2007; 21: 538–43. Thordarson DB. Complications after treatment of tibial pilon fractures: prevention and management strategies. J Am Acad Orthop Surg 2000; 8: 253–65. Vallier HA, Nork SE, Barei DP, Benirschke SK, Sangeorzan BJ. Talar neck fractures: results and outcomes. J Bone Joint Surg 2004; 86A: 1616–24. Vander Griend R, Michelson JD, Bone LB. Fractures of the ankle and distal part of the tibia. J Bone Joint Surg 1996; 78A: 1772–83. Weinfeld SB, Haddad SL, Myerson MS. Metatarsal stress fractures. Clin Sports Med 1997; 16: 319–38.

Epilogue – Global Orthopaedics Christopher Lavy, Felicity Briggs Textbooks tend to project an idealised version of the medical world: they assume, for a start, that there is a doctor, or at least a qualified medical attendant, and a hospital or clinic where patients can be examined and treated as prescribed on the printed page; that basic equipment such as x-ray machines and CT scanners are accessible; that there are facilities for essential laboratory investigations; that the recommended drugs and surgical implants are available; that the environment is clean if not actually sterile; that a variety of operations can be performed and that an appropriate level of postoperative care will be applied. It is right that a book such as this should teach what is considered to be ‘best practice’ at the time of writing. However, we should also recognise that for the majority of people in the world these high standards are out of reach and compromises have to be made at every level of healthcare provision. It is beyond the scope of this book to discuss ways of improving conditions in disadvantaged countries. Here we simply offer a brief reminder of what exists in the wider world. GLOBAL DISTRIBUTION OF RESOURCES Modern orthopaedic surgery is expensive by virtue of the equipment and hospital facilities required and the training of surgeons and allied medical staff. Table 1 shows the disparities among a number of representative countries in terms of per capita expenditure on health per year, the number of doctors per hundred thousand population and Gross Domestic Product (GDP). The situation in poorer countries threatens to be made even worse by the migration of doctors to relatively richer countries that offer better working facilities, economic benefits and living conditions. GENERAL EFFECTS OF POVERTY AND MALNUTRITION Poverty is linked to malnutrition, which contributes to reduced immune function and increased susceptibility to infection – including osteomyelitis, septic arthritis and tuberculosis of bones and joints. The strain on resources is considerable and the incidence of chronic infection requiring long-term care is high.

Table 1 Variation in health expenditure and number of doctors compared to GDP GDP per capita in US$

Per capita total expenditure on health in US$

Doctors/ 1000 population

10,600

2, 58

0.02

Egypt

4,200

2,258

0.54

China

7,800

2,277

1.06

Thailand

9,200

2,293

0.37

Mexico

10,700

2,655

1.98

Mauritius

13,700

2,516

1.06

Latvia

16,000

2,852

3.01

Kuwait

23,100

2,538

1.53

New Zealand

26,200

2,081

2.37

Malawi

UK

31,800

2,560

2.30

USA

43,800

6,096

2.56

Cases such as the one shown in Figure 1 are rarely seen in affluent countries. Specific nutritional deficiencies also take their toll and conditions such as calcium deficiency rickets and scurvy, seldom seen in affluent countries, are not uncommon in Africa. EFFECTS OF THE HIV PANDEMIC HIV infection rates are unusually high in some parts of the world, particularly in Africa. The virus causes a de-

1 Chronic osteomyelitis with massive sequestrum

crease in helper CD4 cells, thus predisposing the patient to opportunistic local and systemic infections. On a global level one of the most important outcomes is the rise in the number of patients with tuberculosis. Though the skeleton is involved in only 1 per cent of cases, treatment (especially for spinal tuberculosis) is demanding, prolonged and expensive. If paraplegia develops, the outlook – more often than not – is hopeless.

EPIILOGUE – GLOBAL ORTHOPAEDICS

EFFECTS OF WAR INJURIES Conventional warfare is usually attended by more or less skilled medical services, advanced surgical facilities and efficient transfer of the wounded to hospitals. Small-scale conflicts that flare up in under-resourced civilian populations may cause fewer casualties but lack of experienced personnel and field services results in a proportionately greater number of serious complications and poor outcomes among the wounded. Were it not for voluntary medical organizations the death toll would be much greater than it is. Even after these conflicts have ended, people continue to suffer injuries inflicted by abandoned anti-personnel weapons, and health services in poor countries continue to be substandard. In Cambodia and Angola, for example, the presence of unexploded mines in populated areas has resulted in a high percentage of amputees among civilians. Facilities for treating these patients are poor and provision of prostheses inadequate. Knock-on effects can also be serious. In Northern Uganda, where there has been low-level conflict for many years, polio vaccination services have broken down, resulting in an increased number of children with poliomyelitis and the resulting deformities.

936

for granted. In poor countries conservative treatment and operations that do not involve the use of expensive implants and instrumentation are all that can be afforded. Similarly, the unavailability of arthroscopic equipment forces surgeons to set a higher threshold for operating on knees and shoulders. Surgical treatment of bone tumours is particularly problematic. Ideal investigative procedures are often unavailable for lack of imaging equipment and experienced pathology services. Limb salvage procedures by endoprosthetic replacement are usually out of the question because of the need for high quality prostheses, a tissue bank and specialized postoperative care. In these circumstances malignant tumours are more often treated by amputation. In organizing elective orthopaedic treatment knock-on effects must also be considered. A good example is in the management of a common condition such as congenital club-foot. In countries with well-supported child health services treatment is started soon after birth and usually follows Ponseti’s method of repeated manipulation and splintage, perhaps followed by limited surgery. This requires a level of parental participation and medical supervision that is simply not available in resource poor countries where treatment is usually started much later, return visits are sporadic and many do not get treated at all. The outcome is often severe deformity which requires prolonged and highly skilled surgical management (Fig. 2).

FRACTURE MANAGEMENT For a given fracture there is no universal ‘best practice’ method of management as so much depends on facilities, resources and personnel. A closed mid-shaft femoral fracture in a rich country where there is an available clean operating theatre, a full set of intramedullary nail sizes, an image intensifier and a fully trained operating theatre staff, may be appropriately treated by internal fixation. The patient has a low risk of complications and will return to full mobility in a short time. In a poor country with no dedicated orthopaedic theatre or team, a small number of implants and limited imaging facilities, it might be wiser to treat the same fracture conservatively because the risk of complications associated with surgery is unacceptably high. Moreover, treating a femoral fracture by traction for many weeks might well be cheaper than internal fixation, because of the lower cost of running a hospital and the lower daily cost of occupying a hospital bed. ELECTIVE ORTHOPAEDICS Elective orthopaedic treatment is also affected. In rich countries joint replacement for osteoarthritis is taken

2 Untreated club-foot

PERSONNEL ISSUES Surgeons working in countries with a high workload are often required to treat a much wider spectrum of pathology than those operating in more specialised hospitals. Indeed, in many cases a single surgeon covers the entire range of surgical specialties. This obviously reduces the level of expertise that he or she can develop in a particular field. In many countries throughout the developing world non-medically qualified assistants (‘clinical officers’) are being trained to deal with common simple conditions such as closed fractures. On the one hand this practice carries an increased risk of late complications but on the other hand the regular management of these conditions can lead to a higher degree of skill in methods of manual fracture reduction than that possessed by the qualified surgeon who does not have time to master everything! Training is a crucial part of surgery and it is important that surgeons are taught to deal with the pathology that they are eventually going to encounter, using the methods that will be available where they work. The scenario of a poor country sending its surgical trainees to better resourced centres where they learn only high cost methods of treatment is common. It often results in a trainee who returns to his or her own country with a certificate of completion of training, but no knowledge or experience of how to function in a resource limited environment. This is a problem that deserves the attention of both those who send aspiring surgeons to other countries for training, and those in recipient countries organizing training for them.

CONSENT TO TREATMENT It is always essential that the patient receives an easily understandable description of any operative procedure you have advised, as well as an honest opinion about the likely outcome and the foreseeable complications that might arise from the operation. When working in a disadvantaged community, where the patient may be poorly educated, it is much more difficult than usual to convey this information, and be sure that it has been understood, when seeking consent. The difficulty is increased if the surgeon and patient do not speak the same language and information is conveyed via an interpreter. The solution is to ask the patient to repeat the message to you in small portions, and to ensure that it is still intelligible. THE FUTURE It is not possible in a chapter to cover all the differences between orthopaedic practice in different parts of the world. What is clear is that although there are some real differences in pathology in the different geographical regions, the key differences are those of economic inequality. They are differences that have always existed, and differences that are not likely to disappear in the near future. Indeed they might well grow as international donor funds tend to be spent on public health and infectious diseases rather than on orthopaedics and fractures. The World Health Organization estimates that by 2020 road trauma will be the third biggest global cause of morbidity for males. It may be that this will cause an improvement in global funding of orthopaedic care. Whether or not this occurs it is important for those who practise orthopaedics in all countries to maintain and increase their understanding of the global issues, for training programme organizers to keep their eyes on a horizon that is not limited to their own part of the world, and for those responsible for planning and funding research to be aware of the world’s real orthopaedic problems. Best of all is for aspiring orthopaedic surgeons to spend some time working in one of the poor countries of the world.

Epilogue – Global Orthopaedics

ETHICAL AND LEGAL ISSUES The practice of orthopaedic surgery is expensive, and in Western countries continues to get more expensive as better and more complex treatments and implants are devised. Poorer countries do not have the economic capability to afford such treatments and are forced into a dilemma over treatment rationing that has both moral and legal implications. If a limited number of modern products, for example hip replacements, are available, then the decision as to which of many clinically deserving patients receives them is difficult. There is no correct solution to this problem, but often the decision is made on economic grounds: the patient who can pay has first call on the resources. This is clearly wrong, but one must also beware of having the decision taken out of the hands of the clinician and made by politicians. A related legal and ethical issue arises when less than best but cheaper than best treatment options are on offer. For example a country may not be able to

afford fracture implants made of the highest quality titanium, but may have low quality fracture plates available. The decision about whether to use equipment that is not perfect is a hard one; similarly the decision about whether to use donated or previously used, but still effective, implants, or implants, sutures and sterile supplies that are past their ‘use by’ dates. It is easy to take the moral high ground and decry such practices, but where the options are limited the practical choice – and the choice of many surgeons in the world – is between second best or nothing.

937

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Index

Note ‘vs’ indicates the differential diagnosis of two conditions.

ABC(DE) sequence hospital 641–62 primary survey 636–8, 661 pre-hospital 631–2 see also individual components abdomen in shock, examination 674 visceral injuries 662–3 examination (in major trauma) for 639 fractures causing 694 abduction definition 9 digits of hand 415, 416, 436 foot 623 hip 495 shoulder 338–9, 367 in rotator cuff tears 345 abscess Brodie’s 37 cold see cold abscess epidural 247 nerve, leprosy 55 psoas see psoas muscle thenar space 433 accessory nerve see spinal accessory nerve acetabulum anatomy 542 dysplasia 504–6 in proximal femoral focal deficiency 509, 510 fractures 837–40, 847 protrusion into pelvic cavity 507–8 in total hip arthroplasty cemented component 539 uncemented component 540 see also femoro-acetabular impingement Achilles tendon 614–16 flat-foot with tightness of 598 insufficiency with calcaneal fractures 928 rupture 615–16 tendinitis 614–15 achondroplasia 163–4 differential diagnosis 164 multiple epiphyseal dysplasia 159 achrosyndactyly, fingers 389 acid burns 669, 670 acrocephalosyndactyly 170 acromegaly 148 acromelia 155

acromio-clavicular joint injuries 737–9 osteoarthritis 364 rheumatoid arthritis 359 acromio-clavicular ligament injuries 738 acromion process fractures 736 acromioplasty 347 acrylic cement implants 331 ACTH excess 148 actinomycosis 56 action potentials 225, 270 compound muscle (CMAP) 231, 232 loss 234 sensory nerve (SNAP) 232 active movements assessing (general aspects) 7 elbow 381 assessing 370 fracture rehabilitation 705 hand, assessing 414, 415–16 knee 583 assessing 549 shoulder 367 assessing 338–9 wrist 409 assessing 385 activities daily see daily functional, fracture rehabilitation 705–6 Acute Physiology and Chronic Health Evaluation (APACHE) 683, 684 acute respiratory distress syndrome see adult respiratory distress syndrome adamantinoma 215 adaptive midcarpal instability 395 adduction definition 9 digits of hand 415, 416, 436 foot 623 hip 495 deformity in cerebral palsy 242 adductor longus tendinitis 533 adenoma parathyroid, causing hyperparathyroidism 140 pituitary, causing hyperpituitarism 147 adhesions, knee ligament tears 879 adhesive capsulitis 351–2 adiposogenital syndrome, Fröhlich’s 147

adolescents/teenagers acute suppurative arthritis, antibiotics 45 femur fracture–separation of distal epiphysis 872 shaft fractures 869 trochanteric fractures 857 flat-foot 596–7 hallux valgus 604–6 hip coxa vara (acquired) 509 subluxation 505, 506 knee region problems 554 tibial tubercle see Osgood–Schlatter disease osteochondritis dissecans of knee 890 spine idiopathic scoliosis 460, 461, 462–5 kyphosis 467, 468–9 spondylolisthesis 485 see also puberty adrenal gland cortical dysfunction 148 neuroblastoma, bone metastases 217 adrenocorticotropic hormone (ACTH) excess 148 Adson’s test 293 adult respiratory distress syndrome (ARDS) 678 femoral shaft fractures 866 treatment 680 Advanced Trauma Life Support (ATLS) 635–6 age bone, Perthes’ disease treatment and 515 bone changes with 127–9 hip disorders and 498 intervertebral disc changes with 476 knee disorders and 553–4 neuromuscular disorders and 228 tumour presentation and 188 see also adolescents; children; elderly; infants; neonates agenesis (congenital absence) radial 182 sacral 181–2 ulnar 183 vertebral 181 aggrecans 85

INDEX 940

aggressiveness, tumour, grading 191 air ambulance 633–4 airway management (major trauma) hospital 642–7 primary survey 637 pre-hospital 631 transfers in and between hospitals 641 Aitken classification of proximal femoral deficiency 183, 184, 509–10 AJC (American Joint Committee) for Cancer Staging System, soft-tissue tumours 192 Albers–Schönberg disease 166–7 Albright’s syndrome and fibrous dysplasia 195 alcohol abuse neuropathy 259 osteonecrosis 108, 110 osteoporosis 135 alendronate, osteoporosis (postmenopausal) 133 algodystrophy see complex regional pain syndrome alignment axial, definition 9 fracture 695 non-union relating to 717 knee extensors, assessment 548 patella, assessment 548 tibio-femoral 553 rotational, definition 9 alimentary (gastrointestinal) tract in multiple organ failure 679 alkali burns 669, 670 alkaline phosphatase, bone-specific 118 serum levels, measurement 130–1 alkaptonuria 179 pseudogout vs 82 alleles 151 allergic reactions, spina bifida 250 allografts, bone 318–19 allopurinol, gout 80 American Joint Committee for Cancer Staging System, soft-tissue tumours 192 amniocentesis 154 amputation (accidental), replantation see replantation amputation (surgical) 325–7 claw toes 608 complications 328 fibular deficiency, prosthetics 185 fingers 799, 802–3 leprosy 300–1 with tumours 193 amyloidosis juvenile idiopathic arthritis 75 rheumatoid arthritis 66 amyoplasia see arthrogryposis amyotrophic lateral sclerosis 255 amyotrophy, neuralgic 259–60 anaemia, hypochromic see hypochromic anaemia anaesthesia (loss of sensation) 12 anaesthesia (surgical) local, shoulder examination under 340, 355 neuraxial 309

analgesics and analgesia cerebral palsy 239 facet joint dysfunction 483 major trauma 640 burns 669 pre-hospital 633 metastatic bone disease 217 osteoarthritis 95 anaphylactic shock 654, 655, 673 Anderson and D’Alonzo classification of odontoid process fractures 814 androgens 127 aneurysm, popliteal 579 aneurysmal bone cyst 201–2 angles (reference) for osteotomies 311–12 angulation (tilt) centre of rotation of (CORA) 313–14 of fracture (deformities) 689, 694 humeral supracondylar fractures in children 759–60 non-union 719 phalanges of hand 791 animal bites, infected 434 ankle 587–625, 907–20 anatomy 623, 907–8 axes and reference angles for osteotomies 312 cerebral palsy-associated deformities 241 clinical assessment 587–91 injuries 907–20 movements 589, 623–4, 907 ankylosing spondylitis 66–70, 451 cervical spine 451 diagnosis (incl. differential diagnosis) 63, 68, 69 irritable hip 511 HLA-B27 66, 154 ankylosis in juvenile idiopathic arthritis 75 annulus fibrosus 489 degeneration 476 antalgic gait 229 antenatal diagnosis of genetic disorders 154–5 anterior (definition of term) 9 anterior cord syndrome 826 anterior drawer test ankle 590, 909 knee 875, 879 anteversion, femoral 507 antibiotics (antimicrobials/antibacterials) brucellosis 53 fractures, prophylactic 706–7 tibial fractures 901 gonorrhoeae 46 hand infections 431 bite wounds 434 septic arthritis 434 leprosy 55 osteomyelitis acute 34–5 chronic 30, 39 post-traumatic 38 pyogenic, spine 471 subacute 37 resistance to 29 in selective decontamination of gut in multiple organ failure 680 suppurative/pyogenic arthritis 45 hip 520

syphilis 48 tropical ulcer 49 tuberculosis 52, 358–9, 473 yaws 48 anticoagulants, perioperative 310 antifungal drugs deep mycoses 57 superficial mycoses 56 antiglide plates 702 antihelmintics, echinococcosis 57–8, 475 antimicrobial agents see antibiotics antithrombotics 310 AO–ASIF Group classification of distal humeral fracture 750 AO classification of femoral supracondylar fractures 870 aortic disruption, traumatic 652–3 APACHE (Acute Physiology and Chronic Health Evaluation) 683, 684 Apert’s syndrome 170 Apley’s test 553 ‘apophysitis’ calcaneal/traction 617 tibial tubercle see Osgood–Schlatter disease appearance assessing 10 wrist/hand deformity, as surgical indication 387 apposition (bone formation by) 117, 122 fracture 695 apprehension test 7, 8, 731 knee 551 in recurrent patellar dislocation 563 shoulder 354, 354–5 arachnoid mater (and head injury) 659 arachnoiditis 481 ARCO staging of osteonecrosis 108, 531, 532 ARM see awareness–recognition– management arms see upper limbs arterial blood gases, major trauma 638 arterial repair in open hand injuries 797 arterial supply see blood supply arterial waveform analysis, cardiac output from 674 arteriography, knee dislocation 884 arthritis Charcot see Charcot disease degenerative see osteoarthritis destructive/erosive see erosive arthritis; Milwaukee shoulder enteropathic see Crohn’s disease; ulcerative colitis haemophilic see haemophilic arthropathy haemorrhagic, tuberculosis vs 52 infectious causes see septic arthritis juvenile idiopathic see juvenile idiopathic arthritis knee deformities secondary to 667 neuropathic see Charcot disease polyarticular see polyarthritis reactive see Reiter’s disease rheumatoid see rheumatoid arthritis subacute, tuberculosis vs 52 tuberculous see tuberculosis viral 64 see also peri-arthritis

shoulder 365–6 in osteoarthritis 360 in rheumatoid arthritis 359–60 surface replacement see hemiarthroplasty toes claw 608 hallux rigidus 607 wrist in osteoarthritis 403, 404 in rheumatoid arthritis 401 arthroscopy, diagnostic 28 elbow 380–1 hip 28, 497–8 knee 28, 553, 555 chondromalacia patellae 566 ligament problems 878, 881 meniscectomy 560 osteoarthritis 92 shoulder 28, 341, 365 wrist 386, 780 carpal instability 396 arthroscopy, surgical femoro-acetabular impingement 527 knee 579 osteoarthritis 573 menisci 560 shoulder 365 acromioplasty 347 arthrotomy 323 articulations see joints ascorbic acid deficiency 142–3 aseptic loosening of joint implant hip 538 knee 582 aseptic non-traumatic synovitis in knee 577 aseptic non-union 692 aspirin, surgical patients 310 assessment (evaluation) in major trauma 629 hospital 636–40 pre-hospital 630–2 Association Research Circulation Osseous (ARCO) staging of osteonecrosis 108, 531, 532 ataxia in cerebral palsy 235 Friedrich’s 245, 258 gait in 230 athetosis, cerebral palsy 235 atlanto-axial joint 452 erosion 450 rotatory displacement 442–3 atlanto-dental interval in children, increased 813 atlas (C1), ring fracture 813–14 atrophy bone, non-union with 717 Sudek’s see complex regional pain syndrome audit, intensive care unit scoring systems 682 autoantibodies, rheumatoid arthritis 60 autografts, bone 317–18 autonomic nervous system 226, 226–7 assessment 230 autonomic pain 4 autosomes 151 dominant disorders 152–3 recessive disorders 153

avascular necrosis see osteonecrosis avulsion injuries cervical spine odontoid process (=type I) 814–15 spinous process 819 fingers/phalanges (hand) 790, 792 ring 799 pelvis 832 tendon see tendons trochanteric 857 awareness–recognition–management (ARM) in major trauma prehospital 630–2 primary survey in hospital 637 in systemic management 641 abdominal injuries 662–3 airway 642–7 breathing 647–53 chemical burns 669–70 circulation 654–8 cold injury burns 670–1 disability (head injury) 659–62 electrical burns 670 long-bone injuries 665 pelvic fractures 664 spinal injuries 664–5 thermal burns 666–9 axial alignment, definition 9 axial compression injuries of thoracolumbar spine 821, 823 axillary artery injury in shoulder dislocation 741 axillary nerve lesion 281–2 in shoulder dislocation 741 axis (C2), fractures, C2 814–15 axon 225, 269 degeneration acute 257, 271 chronic 257 interruption, acute 256 regeneration 271 axonotmesis 270–1 Babinski sign 11 back 453–91 clinical assessment incl. examination 453–7 in spinal trauma 807 pain see pain baclofen, cerebral palsy 239 bacteria colonization, factors enhancing 29 infection by 29–55 antibiotics see antibiotics see also microbiology ‘bag of bones’ technique, distal humeral fracture 752 Baker’s cyst 578–9 balanced traction with fractures 697 ballottement, luno-triquetral 395 bandage, haemorrhage control 656 Bankart operation 356 barbotage, rotator cuff calcifications 349 Barlow’s test 499 Barton’s fracture 776–7 baseball pitcher’s elbow 379 basic calcium phosphate crystal deposition disease 83–4 basilar impression 443 battered baby syndrome 155, 728

INDEX

arthrodesis (joint fusion) 323–4 elbow 381 hip 534–5 osteoarthritis 524 knee 581 osteoarthritis 95 ankle 613 hip 524 knee 573 wrist 403, 404 radio-carpal 399 shoulder 366 in brachial plexopathy 279 in rheumatoid arthritis 359–60 spine in cervical facet joint dislocation 818 in cervical spondylosis 447 in facet joint dysfunction 484 in idiopathic scoliosis 464, 465 toes in claw toes 608 in hallux rigidus 607 wrist in osteoarthritis 403, 404 in rheumatoid arthritis 401 arthrography (MR) see magnetic resonance arthrography arthrography (plain) 19–20 facet joints 457 hip 497 developmental dysplasia, infants 502 shoulder 340 wrist 385 carpal instability 396 arthrogryposis (incl. arthrogryposis multiplex congenita; amyoplasia) 263–4 hand 263, 391 arthropathies (joint disorders) crystal deposition see crystal deposition disorders haemophilic see haemophilic arthropathy hand/fingers 420 inflammatory see inflammatory rheumatic disorders neuropathic see neuropathic arthropathy in rotator cuff impingement, secondary 342–3 seronegative see seronegative arthropathies arthroplasty (joint replacement) 324 elbow in distal humeral fracture 751 osteoarthritis 376 hip 536–42 in femoral neck fracture 851 femoral shaft fracture risk 865–6 in osteoarthritis 524 sciatic palsy following 286, 536 implants see prosthetics knee 581–2 osteoarthritis 573 metacarpophalangeal joints in rheumatoid arthritis 427 osteoarthritis 95 elbow 376 hip 524 knee 573 shoulder 360 wrist 403, 404

941

INDEX 942

bearing surface in total hip replacement 541–2 Beck, triad of 649 Becker muscular dystrophy 264 bed(s), spinal injuries 810 bed rest, spinal tuberculosis 474 bed sores 720 Behçet’s syndrome vs ankylosing spondylitis 69 Bell’s respiratory (long thoracic) nerve lesions 280 bending stress, fracture due to 724 benign tumours (and local benign lesions) 194–205 bone 194–205 fractures with 725, 726–7 management principles 192 staging and grading 191 classification 187–8 soft-tissue 218, 219, 219–20, 220–1, 221–3, 223 Bennett’s fracture–dislocation 789 bent finger 389 biceps brachii 349–50, 379–80 avulsion of distal tendon 379–80 rheumatoid arthritis affecting synovial sheaths 359 bifocal compression–distraction 320–1 biochemical tests and features 26 metabolic bone disorders 130–1 hyperparathyroidism (primary) 141 Paget’s disease 145 rickets/osteomalacia 138 biopsy bone see bone biopsy muscle 231 synovial/synovial fluid (incl. aspirates) 26–7 rheumatoid arthritis 62 sarcoma 220–1 technique 26–7 tuberculosis 51 tumour 27, 189 giant-cell tumour 203 see also histology bisphosphonates 127 osteonecrosis 109 osteoporosis (postmenopausal) 133 Paget’s disease 146 bite wound infections 434 bladder anatomy 829 examination 830–1 imaging 832 injuries, management 835 in traumatic paraplegia/quadriplegia, management 827 blastomycosis 56 bleeding see clotting disorders; haemorrhage blisters, fractures causing 715 calcaneal 928 block test, pes cavus 601 blood gases, major trauma 638 blood loss see haemorrhage blood supply (arterial supply) in amputations, complications 328 bone 120, 121 bone grafts with 317 delayed union relating to 716

femoral head 542 foot 921 hand, repair in open injuries 797 nerves 270 pelvic 829 spine 490 wrist 411 see also circulation; haemodynamic function blood tests 26–7 rheumatoid arthritis 26, 62 blood vessels (vasculature) fractures and injuries causing damage 711–12 ankle fractures 916 elbow fracture–dislocations 756 femoral distal epiphyseal fracture– separation 872 femoral shaft fractures 864–5 femoral supracondylar fractures 870 forearm fractures 769 humeral distal fracture 752 humeral proximal fracture 741 in humeral proximal fracture– dislocation 747 humeral supracondylar fractures, children 760–1 knee dislocation 885 tibia and fibula combined fractures 901–2 hand, disorders 435 hip dislocation causing 845 poliomyelitis, dysfunction 254 sympathetic nerve supply to 270 systemic, reduced resistance in shock 673 tissues supplied by see blood supply tumours 221–2 see also peripheral vascular disease blood volume, shock due to loss of see hypovolaemic shock bloodless field 305–6 Blount’s disease 556–7 blunt injury abdomen 662 aorta 652 chest 647, 649 diaphragm 652 heart 652 body surface area in burns 667, 668 bone(s) 117–29 age, Perthes’ disease treatment and 515 age-related changes 127–9 amputation-related complications 328 avascular necrosis see osteonecrosis cysts see cysts deformities, causes 14–15 cerebral palsy 238–9 deformities, correction 311–14, 321 development 117, 118, 121–4 disorders of cartilage and see dysplasias see also ossification disease (generalized/in general) fractures in 624, 725 metabolic see metabolic disorders feeling 7 fixation see fixation fractures see fractures function/physiology 117–18 grafts 317–19

growth see growth hand avulsions 792 lesions 421 secondary operations following injuries 802 infections 30–1 biopsy 27 non-pyogenic, chronic 30 open fractures 710 predisposing factors 30 pyogenic, acute and chronic 29 treatment principles 30 see also osteitis; osteomyelitis ischaemia in Perthes’ disease 513 isotope scans see radionuclide scans lengthening see lengthening lumps associated with, examination 15 matrix 118–19 demineralized, for allografts 318 modelling 122–4 operations on 311–23 post-traumatic loss 722 radiography 16–17 erosions 18 remodelling/turnover 122–7 fracture healing 690 in Perthes’ disease 513 resorption 120, 122 hormones affecting 127 strength 128–9 structure and composition 118–20 substitutes 319, 331 in tibia and fibula combined fractures, severity of injury 897 transport (technique) 320–1 types 120 union (fracture) see delayed union; malunion; non-union; union see also entries under ostebone biopsy 27–8, 131 fibular deficiency 186 fractures (pathological) 726 metabolic disease 27, 131 rickets/osteomalacia 138 subacute recurrent multifocal osteomyelitis 42 bone cells 119–20 bone density/mass (mineral density) 128–9 factors adversely affecting 129 measurement/densitometry 25, 129–30, 131–2 indications 131 postmenopausal women 133 osteoarthritis risk relating to 90 bone-forming tumours benign 194–7 classification 187 malignant 207–11 bone marrow aspirates for repair 318 fat cell swelling, osteonecrosis due to 104 oedema syndrome 114, 530, 532 transplantation in Morquio’s syndrome 177 bone mineral 119 density see bone density exchange 124–7

bulge test 550 bullet injuries 710 bunion 589 tailor’s 609 burns non-thermal see chemical burns; electrical burns thermal (and in general) 666–72 depth 667 hand 801 inhalational 642, 666–7 bursa, subacromial, rheumatoid arthritis 359 bursitis calcaneal 617 elbow 380 hip 533 knee 578 burst injuries/fractures cervical 810, 816–17 thoracolumbar 811, 823 buttressing plates 702 C-reactive protein 26 C1 ring fracture 813–14 C2 fractures 814–15 café au lait spots fibrous dysplasia 195 NF-1 175, 223 Caffey’s disease 42–3 caisson disease 111 calcaneal bursitis 617 calcaneal fractures 924–8 calcaneocavus 601, 602 calcaneofibular ligament 907 strain 908 calcaneovalgus 595 calcaneus ‘apophysitis’ (traction ‘apophysitis’) 617 deformity 601, 602 fractures, CT 21 pain relating to 618 pitch angle 601 calcifications knee area 576 collateral ligaments 562, 576 in pseudogout 81, 82 rotator cuff 348–9 calcimimetic drug, renal osteodystrophy 142 calcitonin 126 Paget’s disease treatment 146 calcitriol see 1,25-dihydroxycholecalciferol calcium blood/serum, measurement 130 see also hypercalcaemia; hypocalcaemia in bone 119, 124 urinary, measurement 131 calcium phosphate, as synthetic bone substitute 319 calcium phosphate crystal deposition disease, basic 83–4 calcium pyrophosphate deposition disease see pseudogout calcium sulphate as synthetic bone substitute 319 calf (muscles) post-traumatic ischaemia 722 squeeze test 615

callus (bone fracture) 690 formation 690, 691 surgically-produced, distraction (callotasis) 319–20 callus (callosity on sole) 589, 621–2 cam mechanism, femoro-acetabular impingement 525, 526, 528 camptodactyly 389, 417 Camurati’s disease 167 Canale classification of talar neck fractures 922 cancellous (trabecular) bone 120 grafts 317 resorption 122 cancer see malignant tumours candidiasis 56 candle bones 167 cannulation (commonly called catheterization) in shock intraosseous 657 pulmonary artery flotation catheter 674 venous 656–7 Capener’s sign 516 capillary haemangioma 221 capitate fracture 784 capitulum fracture 752 osteochondritis dissecans 372–3 capsule, articular 86 herniation in osteoarthritis 93 capsulitis, adhesive 351–2 car accidents see road accidents carbon dioxide monitoring, end-tidal, major trauma 638 carbon implants 331 carbon monoxide poisoning 666–7, 667 carcinomatosis, multiple, osteoporosis 135 cardiac problems see heart cardiovascular system in multiple organ failure 678–9 in shock, assessment 674 carpal ligaments 411 carpal tunnel syndrome 287, 288, 288–9, 409 pregnancy 149 rheumatoid arthritis 401 carpo-metacarpal joints 437 boss 408 dislocation 793 osteoarthritis 403–4, 429 carpus (carpal bones) 393 chronic instability see instability height 409 injuries 778–84 fracture–subluxations 776–7 in osteoarthritis, operations 402–3 cartilage articular 85–6 in osteoarthritis 88, 88–9 transplantation in osteochondritis dissecans 568 bone development and role of 117, 121, 122 breakdown see chondrolysis developmental disorders of bone and see dysplasias necrosis, in slipped capital femoral epiphysis 519 see also entries under chondro-

INDEX

bone morphogenetic protein (BMP) 119 use as osteoinductive agent 319 bone tumours 187–218 benign see benign tumours classification 187–8 malignant 187, 192, 205–18, 727 in enchondromatosis 165 fractures with see tumours in Paget’s disease 146, 210–11 primary 205–16 secondary see metastatic bone tumours stress fracture vs 190, 724 management principles 192–4 staging 140–2 bony swellings, knee 579 borreliosis (Lyme disease) 64 Boston brace 463 botulinum toxin, cerebral palsy 239 boundary layer joint lubrication 87 boutonnière deformity 419 rheumatoid arthritis 425, 426, 427–8 bow legs see genu varum bowel see intestine bowing, congenital tibial 186 bowstring sign 455–6 brachial artery injury, humeral supracondylar fractures in children 760 brachial neuritis, acute 259–60 brachial plexopathy 276–80 brachioradialis tendon transfer (for wrist extension) in traumatic paraplegia/quadriplegia 828 brachydactyly, hand 390 bracing adolescent idiopathic scoliosis 463 fractures 700 femoral shaft fractures 861, 862 tibia and fibula combined fractures 899 spinal injuries cervical 810 thoracolumbar 811 Brailsford’s disease 619 brain 660 imaging in neuromuscular disorders 231 injury anatomy relevant to 659 management 661–2 mechanisms/severity/morphology 660 brainstem (and head injury) 659 breast, bone metastases from, palliation 217 breathing management (in major trauma) hospital 642, 647–53 primary survey 637–8 pre-hospital 631–2 Bristow–Laterjet operation 356 brittle bones 172–4 Brodie’s abscess 37 bronchial injury 650, 652 Broström–Karlsson operation 910 ‘brown tumours’ 137, 203 Brown-Séquard’s syndrome 246, 827 brucellosis 52–3 bucket-handle tear 559 buckle fracture (distal radius) 776

943

INDEX 944

cartilage-capped exostosis 199–200 cartilage-forming tumours benign 197–200 classification 187 malignant 205–7 cartilage oligometric matrix protein, mutation affecting 159 cast (plaster etc.) fractures 698–9 femoral shaft, adults 861, 862 femoral shaft, children 869 humeral shaft 748 metacarpal 790 tibial proximal epiphyseal fracture– separation 896 pressure sores with 699, 715 serial, cerebral palsy 240 C-A-T™ (Combat Application Tourniquet) 656 catheterization urethral, major trauma 639 vascular see cannulation Catterall classification, Perthes’ disease 513, 514 cauda equina syndrome 246, 480 cavernous haemangioma 221 cellulitis vs acute osteomyelitis 34 cemented hip implants 539 cementless hip implants 539–40 central chondrosarcoma 205, 206 central cord compression 245 central cord syndrome 826 central nervous system 225 congenital anomalies see neural tube defects in shock, examination 674 central venous cannulation in shock 656–7 centre of rotation of angulation (CORA) 313–14 ceramic-on-ceramic hip implants 541 cerclage wires 701 cerebellum functional assessment 12 head injury and 659 cerebral palsy 235–45 classification 235 diagnosis 236–9 management 239–40 regional survey 241–4 topographic distribution 236 cerebrum (in head injury) 659 haematoma 661 cervical disc prolapse (acute) 445 cervical rib 293 cervical spine 439–52 anatomy 451–2 clinical assessment 439–52 control/stabilization (incl. immobilization) 806 control/stabilization (incl. immobilization), in major trauma 637, 642–7, 661 pre-hospital 631, 632 cord compression 245 neurapraxia 819 root transection 826 injury 810–11, 811–21 children, diagnostic pitfalls 812–13

lower 815–19 upper 813–15 spondylosis see spondylosis vertebrae see vertebrae cestode worms 57–8, 475–6 Chance fracture 824 chancre 46 Charcot disease (neuropathic arthritis) 98–9 elbow 376 foot 613–14, 614 knee 574 Charcot–Marie–Tooth disease 258 Charnley, Sir J, and hip replacement systems 537, 539 chauffeur’s fracture 776–7 cheilectomy, hallux rigidus 607 chemical burns 669–70, 671 hand 801 chemotherapy 193–4 Ewing’s sarcoma 213 osteosarcoma neoadjuvant 208, 210 in Paget’s disease 211 soft-tissue tumours 219 chest drain insertion 650–1 chest injuries (thoracic injuries) fractures causing 694 in major trauma cases 647–53 examination for 639 imaging 639, 640 childbirth, brachial plexus injury 279–80 children arthritis (acute suppurative) clinical features 43–4 treatment 45 bone changes in 118, 127 burns, fluid requirements 669 cerebral palsy diagnosis 236–7 cervical spine injury, diagnostic pitfalls 812–13 coxa vara (acquired) 509 discitis 472 examination 12–13 femoral head osteonecrosis in sickle cell disease 110, 111 flat-foot 596–7 fracture(s) ankle 918–20 elbow 757–65 femur, proximal 856–7 femur, shaft 868–70 greenstick 688–9 humerus, proximal 747 humerus, shaft 750 metacarpal 790 non-union 719 phalanges (hand) 791 radius 765, 767–8, 769–70, 775–6 ulna (Monteggia’s) 771, 775–6 X-rays of both limbs 693 fracture–separation of distal femoral epiphysis 872 growth plate see physis hand injuries 790, 791 wound closure 799 Handigodu joint disease 98 hip Perthes’ disease see Perthes’ disease pyogenic arthritis 520

subluxation 504–5, 506 hip, developmental dysplasia clinical features 499 management 502–3 pathology 499 hyperpituitarism 147–8 hypopituitarism 147 knee deformities 554–7 kyphosis 467 limping, approaches 514 metastatic bone disease 217 Mseleni joint disease 97–8 neck/cervical spine deformities/anomalies 442–3, 443 X-rays 441 osteomyelitis, acute aetiopathogenesis 31–2, 32 antibiotics 35 clinical features 32 pathology 31–2 osteomyelitis, multifocal nonsuppurative 41 renal osteodystrophy 142 rickets see rickets scoliosis (idiopathic) 465 shoulder dislocation 744 skeletal dysplasias/developmental disorders, diagnosis 155–6 spina bifida diagnosis 249 spondylolisthesis 485, 486 ulnar collateral ligament injury 796 see also adolescents; infants; neonates and entries under congenital chin lift 643, 644 cholecalciferol see 1,25dihydroxycholecalciferol; 25-hydroxycholecalciferol; vitamin D chondroblastoma 198 chondrocalcinosis in pseudogout 80, 80–1, 82 chondrocytes of hyaline cartilage 85 chondrodiatasis 320 chondrodysplasia, metaphyseal 164–5 chondrodysplasia punctata (Conradi’s disease) 161, 162 chondrogenic tumours see cartilageforming tumours chondrolysis (cartilage breakdown) osteoarthritis in knee 572 slipped capital femoral epiphysis 519 chondroma see enchondroma chondromalacia in osteoarthritis 88 patellar 564–6 sesamoid 620 chondromatosis, synovial 569 chondromyxoid fibroma 197–8 chondro-osteodystrophies see dysplasias chondroplasty, patellar articular surface 566 see also osteochondroplasty chondrosarcoma 205–7 staging/grading 191, 207 chordoma 215 chorionic villus sampling 154 chromosomes 151 disorders 152, 158, 179–80 chronic pain syndrome 262 in back 488–9 see also complex regional pain syndrome

coagulation see clotting cobalt–chromium-based alloy implants 329 coccidioidomycosis 56 coccygeal injuries 841 cock-up deformity 609 cold abscess leprosy 55 tuberculosis 51, 472 cold injury 670–1, 671–2 hand 801 Coleman block test, pes cavus 601 colitis, ulcerative see ulcerative colitis collagen 170 articular cartilage 85 bone 118 hereditable defects of synthesis 170, 172 telopeptide excretion, measurement 131 types 170 collars, cervical 810 collateral ligaments (CL) ankle anatomy 907–8 lateral, acute injury 908–10 knee anatomy 583–4, 875 assessment 551, 880 calcification 562, 576 injuries 560, 875, 883 insufficiency 883 ossification of medial CL (Pellegrini– Stieda disease) 576, 879 reconstruction 579, 883 ulnar see ulnar collateral ligament Colles’ fracture 772–5 juvenile 775 reversed 774–5 colloid solutions in shock 658 Combat Application Tourniquet (C-A-T™ ) 656 combined traction with fractures 697 comminuted fractures 688, 694 femoral shaft 859 midtarsal 929 olecranon 754, 755 patella 887–8 phalangeal (hand) 790 radial distal 773 see also complex fractures common extensor compartment, tenosynovitis 407 communication (patient) with genetic and developmental disorders 156 compact bone 120 compact bone see cortical bone compact osteoma 197 compartment syndromes 295 with crush injuries 682 with fractures 713 of calcaneus 928 of forearm 769, 776 of tibia and fibula combined 898, 902 of tibial plateau 895 in haemophilia 100 with osteotomies 314 leg 581 with tarso-metatarsal injuries 931

compensatory deformities flat-foot as 597 knee region 556 complex fractures Colles’ fracture 774 CT 21 femoral shaft 864–6 pelvic 838–9 see also comminuted fractures complex regional pain syndrome (reflex sympathetic dystrophy; Sudek’s atrophy; algodystrophy) 261–2 foot operations complicated by 606 knee arthroscopy complicated by 579 malleolar fractures 916 tibia and fibula combined fractures 904 compound muscle action potentials (CMAP) 231, 232 compound palmar ganglion 408–9 compression lower limb, perioperative prophylactic 309–10 radial artery, testing 439 spinal cord 244, 245–6 see also PRICE; RICE compression–distraction, bifocal 320–1 compression–flexion injuries/fractures see flexion–compression injuries/ fractures compression injuries incl. fractures 689, 724 pelvic ring anteroposterior (ACP) 833, 834, 836 lateral (LS) 833, 834 spine cervical 816–17 pathological 727 thoracolumbar 821, 822–3 see also crush injuries compression neuropathies/palsies (nerve pressure/entrapment) 234, 287–94 cervical spondylosis vs 446 familial liability 258 foot 619, 621 fracture-related 713, 721 iatropathic 295 nerve root disease vs 234 in Paget’s disease 146 transient ischaemia of 270 ulnar nerve see ulnar nerve injury compression plate 702 computerized gait analysis 229 cerebral palsy 238 computerized tomographic myelography brachial plexopathy 277 spinal trauma 809 computerized tomography (CT) 20–1 ankle/foot 591 calcaneal fractures 926 tarsal coalition 598 back/thoracolumbar spine 457 disc prolapse 480 facet joint dysfunction 483 injuries 822 spinal tuberculosis 474 elbow 371 fractures 693 pelvic 831, 839

INDEX

cinacalcet, renal osteodystrophy 142 circulation Colles’ fracture affecting 774 failure see shock hand injury 787 open 796 major trauma, management 653–8 burns 668–9 prehospital 632 primary survey 638 traction restricting 697 see also blood supply; haemodynamic function circumduction 9 clasped thumb, congenital 391, 423 clavicle condensing osteitis 363–4 fractures 733–5 osteomyelitis 364 pseudarthrosis 183, 362–3 claw hand/finger, leprosy 54, 55, 296–7 claw toes 255, 589, 601, 603, 608 clay-shoveller’s fracture 819 cleansing, open fracture wound 708 clear-cell chondrosarcoma 205 cleft hand 183, 388–9 cleidocranial dysplasia (dysostosis) 169, 362 clergyman’s knee 578 clicking hip 493, 534 climacteric (menopause) men see men women, bone changes (incl. loss) 128 see also postmenopausal women clinodactyly 389, 417 closed fractures management 695–706 of nerve injuries 712–13 of tibia and fibula combined 897, 900 closed reduction developmental dysplasia of hip 501 fractures 695–6 calcaneal displaced intra-articular fractures 928 femoral intertrochanteric 854 femoral subtrochanteric 858–9 talar neck 922 lunate/perilunate dislocations 785 Clostridium botulinum toxin, cerebral palsy 239 Clostridium tetani and tetanus 681 Clostridium welchi and gas gangrene 714–15 closure of open wounds incl. fractures 695–706 hand 799 clothing, surgical 306–7 clotting (coagulation/bleeding) disorders knee in 574–5, 577 in multiple organ failure 679–80 osteonecrosis 103 clotting factor replacement therapy in haemophilia 100, 101 club-foot (talipes equinovarus), congenital/idiopathic 591–5 cerebral palsy 241 club-hand, radial 387

945

INDEX 946

computerized tomography (CT) – contd head injury 661 hip 497 acetabular dysplasia and hip subluxation 505 slipped capital femoral epiphysis 517 knee 553 neck/cervical spine 441 neuromuscular disorders 230–1 osteoarthritis 92 osteomyelitis (chronic) 39 osteonecrosis 107 positron emission tomography combined with (PET/CT) 25 quantitative 25, 130 shoulder 340 spinal trauma 809, 809 three-dimensional see three-dimensional CT tibial plateau fractures 891 tumours 189 Ewing’s sarcoma 212 osteosarcoma 208, 210, 211 wrist 385 condensing osteitis, clavicle 363–4 conduction studies, nerve 231–2 brachial plexopathy 277–8 condylar fractures humeral see humerus occipital 813 phalangeal (hand) 794 tibial 890–1, 891–4 congenital hyperthyroidism 149 congenital malformations (structural anomalies; developmental disorders) in general 157–86 ankle/foot 591–6 classification 157, 158, 386 diagnosis 154–6 elbow 371 forearm 371, 387 hand see hand hip 498–506, 508–10 knee 554, 554–7, 564 localized 180–6 management principles 156–7 neural tube see neural tube defects non-genetic 152 shoulder 181, 183, 361–2 spine cervical vertebrae 443–4 kyphosis 467 scoliosis 465–6 spinal canal narrowing 247 wrist/hand 183, 386–91 congenital syphilis 47–8 congenital torticollis 442 conjunctivitis, Reiter’s syndrome 70 connective tissue diseases 75–6, 158, 170–8 Conradi’s disease 161, 162 consolidation phase of fracture healing 690, 692 constriction ring syndrome 390, 417 consultation, burns specialist 669 contact healing (fracture) 690 non-union due to insufficient contact 717 contractions, muscle 228

contractures (soft-tissue) fascia see fascia hand 418 joint, correction 321 muscle see muscle skin see skin contrast MRI 22 contrast radiographs 19–20 contusions cerebral 661 pulmonary 651–2 coraco-acromial arch 367 coraco-clavicular ligament injuries 738 heterotopic ossification 739 coracoid process fractures 736, 737 corns 589, 621–2 coronal plane 9 coronoid process fractures 756 corrosion, prosthetic 329 cortical bone (compact bone) 120 in distraction osteogenesis, division 320 fibrous defect (non-ossifying fibroma) 194 grafts 317 hyperostosis, infantile 42–3 ivory exostosis on surface of (=compact osteoma) 197 resorption 122 cortical (cerebral) function, assessment 12 corticosteroids (glucocorticoids) 127 adverse effects 127 osteonecrosis 108, 110 osteoporosis 134 endogenous, excess levels 134, 148 gout 80 rheumatoid arthritis 65 shock 675 spinal cord injury 810 Cotrel–Duboussuet system 464 counselling, genetic and developmental disorders 156 coxa vara 183, 184, 508–9, 542 acquired 509 in proximal femoral neck fractures in children 857 in slipped capital femoral epiphysis 519 congenital 508–9 craniodiaphyseal dysplasia 167 craniofacial dysplasia 179 craniometaphyseal dysplasia 166 cranium see skull crepitus knee 549 in osteoarthritis 91 cretinism 149 cricothyroidotomy needle 646 surgical 647 critical illness, scoring systems 682–4 Crohn’s disease 73 ankylosing spondylitis vs 69 Reiter’s syndrome vs 71 cross fluctuation test 549 cross-linked polyethylene (XLPE), hip implants 541 crossover syndrome 406–7 cruciate ligaments anatomy 584, 876 assessment 551, 881

injuries/tears/rupture 560, 876 treatment 579, 878–9, 882–3 crush injuries (incl. fractures) calcaneum 924 limbs 665, 681–2 tibial plateau osteoporotic crush fractures 890, 892 midtarsal 929 see also compression injuries crystal deposition disorders 77–84 elbow 375 foot 611 hand 420 crystalloids in shock 658 cubital tunnel syndrome 287, 290 cubitus varus and valgus 369, 371 cuff, tourniquet 305 cumulative trauma disorders, wrist pain 407 Cushing’s syndrome and disease 148 cutaneous nerve of thigh, lateral, compression 294 cysts bone 203 aneurysmal 201–2 and cyst-like lesions 203 hydatid 58 osteoarthritic 89 simple/solitary/unicameral 200–1 ganglion, wrist 407–8 meniscal 561–2 mucous, osteoarthritis 428 popliteal 578–9 cytokines and SIRS/sepsis response 677–8 daily activities in facet joint dysfunction, modification 383 in osteoarthritis, function in 91 Danis–Weber classification of malleolar fractures 912 displaced fractures 914–15 undisplaced fractures 913–14 dantrolene, cerebral palsy 239 de Quervain’s disease 384, 406 dead space in chronic osteomyelitis, dealing with 40 dead tissue see necrosis death (mortality) in major trauma, mode 627–8 prediction model in intensive care 683 debridement chronic osteomyelitis 40 in osteoarthritis, joint 95, 376 wound from fracture 707 tibia and fibula combined fractures 901 decompression (surgical) compartments (with fractures) 714 tibia and fibula combined fractures, tibia and fibula combined fractures 902 nerve leprosy 55 median nerve 289 supracapsular nerve 293 thoracic outlet syndrome 294 tibial nerve (posterior) 621 ulnar nerve 290

Delbet classification of paediatric proximal femoral fractures 856 deletion mutations 152 deltoid posterior, tendon transfer to triceps in traumatic paraplegia/quadriplegia 828 power assessment 339 deltoid ligament 907–8 tears 911 demineralized bone matrix, allografts 318 demyelinating polyneuropathies 257 acute inflammatory 260 dendrites 225 denervation, EMG 232, 233 denosumab, postmenopausal osteoporosis 133 dens (odontoid process) fractures 814–15 dermatomes supplied by nerve roots 229, 272 desmoid tumours 220 destructive arthritis see arthritis; osteoarthritis development bone see bone disorders see congenital malformations embryonic see embryonic development devitalized tissue see necrosis diabetes 258–9, 613–14 foot disease 613–14 neuropathy 98, 258–9, 613, 614 diagnosis 3–28 dial test 881 diaphragmatic trauma 653 diaphysis aclasis 161–3 dysplasias predominantly affecting 158, 166–7 formation/development 117, 121 diarthrodial see synovial joints diastasis, distal tibio-fibular joint 911 ankle fractures with 915 diastrophic dysplasia 168–9 diet, bone affected by 127 vitamin D deficiency causing rickets/ osteomalacia 138 see also malnutrition differentiation disorders, wrist/hand 389 diffuse brain injury 661 diffuse idiopathic skeletal hyperostosis see Forestier’s disease digestive (gastrointestinal) tract in multiple organ failure 679 digit(s), congenital anomalies 183, 184, 417 see also fingers; hallux; thumb; toes digital nerve compression in foot 621 1,25-dihydroxycholecalciferol (1,25(OH)2D3; calcitriol) 124, 125, 125–6, 126 hypophosphataemic rickets/osteomalacia, administration 139 metabolic abnormalities 138 Dilwyn Evans procedure 595 diplegia 230 cerebral palsy 236, 241–2 disability (D; neurological status) in major trauma hospital 658–62

primary survey 638 secondary survey 640 pre-hospital 632 disappearing bone disease 204–5 disarticulations 327 disc, intervertebral see intervertebral discs discoid lateral meniscus 561 disease-modifying antirheumatic drugs (DMARDs), rheumatoid arthritis 65 dislocation 731 cervical spine facet joint 810, 817–18 occipito-cervical 813 clinical features 731 complications 731 elbow 755–6 recurrent 757, 763 foot 921 tarso-metatarsal joint 930 hand 793–4 hip see hip knee region 884–5, 896–7 patella see patella peroneal tendon 911 post-traumatic, recurrent 722 radial head see radius recurrent (general aspects) 731 shoulder/pectoral girdle 353, 739–44 children 756 recurrent 354, 354–5, 742, 743 traumatic causes 354, 354–5, 738, 739–44 surgical (intentional), in femoroacetabular impingement 527–8 treatment 731 wrist/carpus 784–5 see also fracture–dislocation displacement atlanto-axial joint rotatory 442–3 fracture 694 acromio-clavicular joint 737–8, 738 calcaneal fractures 927, 928 capitulum 752 clavicular 733, 734, 734–5, 735 elbow area in children 758, 759, 760–1, 762, 763, 764, 765 femoral neck 849 femoral proximal, children 856 humeral distal 751 humeral proximal 744, 745, 746 humeral supracondylar 758, 759 mechanism 688 metacarpal 788 metatarsal 931 midtarsal region 929 odontoid process fracture 815 olecranon 754–5 patella 887–8, 888 pelvis 836 phalangeal (hand) 791 physeal injuries 729 radial distal 773 radial head 753 radial neck 753 scaphoid 782 scapula 736 talus 922–3 tibia and fibula combined fractures 898 tibial plateau 895

INDEX

tension pneumothorax 648–9 thoracolumbar spinal injuries 811 decompression sickness 111 decubitus ulcers (bed sores) 720 deep fascial space infection 433 deep fibromatosis 220 deep mycoses 56, 56–7 hand 435 deep-sea divers, caisson disease 111 deep tendon reflexes see tendon reflexes deep venous thrombosis, perioperative risk 307–10 definitive care major trauma 636, 641 spinal trauma 809–10 deformities 13–16 back 456, 456–70 bone see bone causes (in general) 14 correction 311–14 elbow 369, 371–2 examination (principles) 13–16 foot see foot hand/fingers 413, 417–21 in rheumatoid arthritis 424, 425–8 hip 493, 498–519 history-taking 4 in neuromuscular disorders 228 in juvenile idiopathic arthritis, fixed/permanent 74, 75 knee 547, 547–8, 554–8 local (in genetic/developmental disorders) 155 neck 439 children 442–3 in neuromuscular disorders in adult-acquired spastic paresis 244 in cerebral palsy 238–9, 238, 241–3 history-taking 228 in paralysis see paralysis in poliomyelitis 252–3 in spina bifida 250–2 in osteoarthritis 91 in Paget’s disease 144, 145 in rheumatoid arthritis 60, 61 fixed 65, 66 hand 424, 425–8 shoulder 337 spinal see spinal column in tibial plateau fractures 895 wrist see wrist degeneration (and degenerative change) axons see axon joints in haemophilic arthropathy 100 in pseudogout 81 see also osteoarthritis meniscal 561 spine 476–8 spondylolisthesis 484, 486 triangular fibrocartilage complex 394 delayed union with fractures 716 femoral shaft 867 forearm fractures 769, 774 humeral shaft 750 surgical fractures (osteotomy) in knee area 581 tibial fractures 30, 904–5 combined with fibular fractures 903–4

947

INDEX 948

disseminated intravascular coagulation 680 distraction osteogenesis 319–21 distraction test (knee) 553 torn medial meniscus 559 distributive shock 673 treatment 675 disuse (immobilization) osteoporosis 135 divers (deep-sea), caisson disease 111 DNA 151 dominant disorders autosomal 152–3 X-linked 153 Doppler ultrasound 23 dorsal (definition of term) 9 dorsal rhizotomy in cerebral palsy, selective 240 dorsiflexion (ankle extension) 589, 623 definition 9 dorsiflexor paralysis in leprosy 298 dorsum (wrist/hand) carpal ligaments 411 distal radius malunions 397 intercalated segment instability 395, 779 malunion of distal radius 397 radio-carpal joint subluxation 777 skin 436 synovial impingement 408 ‘double crush’ phenomenon 271, 287 Down’s syndrome 179–80 drainage acute osteomyelitis 35–6 acute suppurative arthritis 45 chest, insertion technique 650–1 hand infections 431–2 drapes 306 drawer test ankle, anterior 590, 909 knee 551, 877–8, 879, 881 modified 881 shoulder 355 dressings haemostatic 656 open hand injuries 799–801 drop arm sign 2, 345 drop-finger 419, 792 drop-foot (gait) 229, 588, 616 leprosy 55, 298 poliomyelitis 255 drop-wrist 282, 296, 392 drug-induced conditions osteonecrosis 108 osteoporosis 135 drug therapy ankylosing spondylitis 69 cerebral palsy tone management 239–40 enteropathic arthritis 73 facet joint dysfunction 483 gout 80 juvenile idiopathic arthritis 75 osteoarthritis 95 osteonecrosis 109, 110 osteoporosis (postmenopausal) 133 Paget’s disease 146 psoriatic arthritis 72 Reiter’s syndrome 71 renal osteodystrophy 142

rheumatoid arthritis 65 rotator cuff calcifications 348 shock 675 spinal cord injury 810 thrombosis prophylaxis 310 dual energy x-ray absorptiometry (DXA) 25, 130 Duchenne muscular dystrophy 264 Dunn’s operation, slipped capital femoral epiphysis 518–19 duplications, digits of hand 389–90 Dupuytren’s contracture 418, 421–3 dura mater (and head injury) 659 Dwyer instrumentation 464 dysbaric osteonecrosis 111 dyschondroplasia 165 dyschondrosteosis (Lehri–Weill syndrome) 164 vs multiple epiphyseal dysplasia 159 dysgenesis, vertebral 181 dysmorphism 155 dysostosis cleidocranial (cleidocranial dysplasia) 169, 362 metaphyseal 164–5 see also pyknodysostosis dysplasias, skeletal (chondroosteodystrophies) 157–76 acetabulum see acetabulum combined/mixed 168–70 diagnosis in childhood 155–6 localized femur 183, 184 femur see femur fibula 185 hip joint see hip radius 182, 387–8 tibia 176, 185 ulna 388 osteoarthritis risk 90 spondylolisthesis in 484, 485 see also specific dysplasias dysraphism, spinal see neural tube defects dystonia 229 cerebral palsy 235, 239 dystrophia myotonica 266 dystrophic spinal deformities in neurofibromatosis type-1 176 ECG (major trauma) 638 echinococcosis (hydatid disease) 57–8 spine 475–6 effusions, knee, tests for 549–50 Ehlers–Danlos syndrome 171 elbow 369–82, 750–66 anatomy 381 clinical assessment 369–71 disorders (non-traumatic) 369–80 injuries 750–66 operations 380–1 arthroplasty see arthroplasty pulled see radius, head subluxation stiffness see stiffness elbow flexion assessment 370 deformity cerebral palsy 241 poliomyelitis 254 tendon transfer achieving 279

elderly (old age/above middle age) bone changes 128, 129 femoral fracture neck, non-union 852 trochanteric 857 hallux valgus 606 knee problems 554 kyphosis 467, 469–70 osteomyelitis (acute), antibiotics 35 osteoporosis (involutional/senile) 134, 469–70 electrical burns 670, 671 hand 801 electrical stimulation affecting bone 127 electrocardiogram (major trauma) 638 electromyography 232–4 intraoperative 235 needle 231 peripheral nerve lesions 273 electrophysiological studies see neurophysiological studies elevation (limbs) fractures 704–5 hand infections 431 see also PRICE; RICE Elmslie–Trillat procedure 563 embolism fat see fat embolism hand 435 pulmonary see pulmonary embolism see also thromboembolism embryonic development 117 wrist/hand 386 emergency medical services (EMS) 628, 629, 634 air/helicopter 634 emergency treatment femoral shaft fractures 860 gunshot injuries 710–11 pelvic fracture 834–5, 839–40 empty can test 345 enchondroma (chondroma) 197 multiple (endochondromatatosis) 165 periosteal 197–8 end-tidal carbon dioxide monitoring, major trauma 638 endochondral bone and ossification 117, 121 femoral neck, defects 508 endocrine disorders 147–9 osteoporosis 134–5, 135 shock associated with 674 see also hormone endocrine support, shock 675 endomysium 227 endoneurium 270 endosteum (endosteal membrane) 120, 122 endotracheal intubation 645–6 Engelmann’s disease 167 Enneking staging of bone tumours 191 entrapment biceps, intra-articular 350 nerve see compression neuropathies environment and exposure (primary survey in major trauma) 638 environmental factors genetic factors interacting with, disorders due to 152 local, affecting bone 127

paediatric 12–13 pelvic injuries 830–1 in shock 674 shoulder 337–9 under local anaesthetic 340, 344 spinal trauma 806–9 terminology 9 tumour 188 wrist 383–5 see also feel; listening; look; movement excision bone tumours 192–3 wound (open fracture) 707 see also specific tumours excision arthroplasty 324 toes claw 608 hallux rigidus 607 wrist in osteoarthritis 404 exercise adolescent idiopathic scoliosis 463 in fracture rehabilitation 704–6 tibia and fibula combined fractures 899 exertion, back pain following 487–8 exostosis cartilage-capped 199–200 hereditary multiple 161–3 ivory 197 exposure and environment (primary survey in major trauma) 638 exsanguination 305 EXT1/2/3 genes and hereditary multiple exostosis 162 extension (movement) ankle see dorsiflexion back (lower) 455 definition 9 digits of hand 415, 416 deformities 419 elbow 370 injury due to excessive see hyperextension injury knee 549, 583 excessive see genu recurvatum spastic (in cerebral palsy) 243 shoulder 339 wrist 385, 410 brachioradialis tendon transfer to enable, in traumatic paraplegia/quadriplegia 828 extension (wound), with open fracture 707 extensor(s), knee alignment, assessment 548 rupture 575–6, 885–6 extensor carpi radialis brevis overuse tenosynovitis 407 tendon transfer in traumatic paraplegia/quadriplegia 828 extensor carpi radialis longus tendon transfer in traumatic paraplegia/quadriplegia 828 extensor carpi ulnaris, overuse tenosynovitis 407 extensor pollicis longus rupture 419 extensor tendons fingers 437 repair of injuries 798–9 testing 416

hand, in rheumatoid arthritis 428 surgery 401 hand, tenosynovitis 400, 406–7, 408 in rheumatoid arthritis 428 external fixation 316–17, 703–4 distraction osteogenesis 320 femoral shaft fractures 864 humeral shaft fracture 749 indications/technique/complications (in general) 703–4 open fractures 708–9 pelvic fractures 836 radial distal fractures 773 tibia and fibula combined fractures 900, 901 external rotation, testing knee 549 shoulder 345 extracorporeal shockwave therapy, rotator cuff calcifications 348 extradural haematoma, traumatic 661 extrication of major trauma case 632–3 extrinsic muscles of hand 437 eye features ankylosing spondylitis 68 juvenile idiopathic arthritis 75 Reiter’s syndrome 70 face, in major trauma airway and injuries to 642 examination 639 face mask (surgeon) 307 facet (zygapophyseal) joints 482–4 ankylosing spondylitis 67 arthrography 457 cervical, dislocations 810, 817–18 dysfunction 482–4 facioscapulohumeral dystrophy 264, 265 factor VIII or IX therapy 100, 101 factor Xa inhibitor 310 familial joint laxity, generalized 170 familial pressure-sensitive neuropathies 258 family history osteoarthritis 90 recording 5 in genetic and developmental disorders 156 in neuromuscular disorders 228 fascia deep, infection 433 subcutaneous/superficial, contractures 14 palmar (Dupuytren’s) 418, 421–3 fasciculations, muscle 228 fasciitis, plantar 611, 618–19 fasciotomy (in compartment syndrome) 714 tibia and fibula combined fractures 902 fat embolism (with fractures) 681 femoral shaft fractures 866 fat pad (heel), painful 619 fat suppression MRI sequences 22 fatigue fracture see stress fracture fatty tumours 219 feel (palpation) 7 ankle/foot 589 back 454 elbow 369–70 fractures 693

INDEX

eosinophilic granuloma 204 epicondylar injuries lateral 756 medial 756 children 763–4 epicondylitis/epicondalgia 378–9 lateral see tennis elbow medial 379 epidural abscess 247 epidural anaesthesia 309 epidural haematoma, traumatic 661 epimysium 227 epineurium 270 epiphysiodesis 322 epiphysis dysplasias predominantly affecting 157–61 femoral distal, fracture–separation 872 femoral head Hilgenreiner’s epiphyseal angle 508 slipped 511, 515–19 formation/development 117, 121 in paediatric acute osteomyelitis, damage 36 physeal injuries involving 728 tibial proximal, fracture–separation 895–6 equinovarus see club-foot; pes deformities equipment operative 303 personal protective 629–30 Erb’s palsy, obstetric 279 erosions, bone, radiography 18 erosive arthritis in basic calcium phosphate crystal deposition disease 84 cervical spine 450 ethnicity (race) femoral neck fracture and 847 osteoarthritis 90 evaluation see assessment Evans (Dilwyn Evans) procedure 595 eversion, foot 623–4 evertor paralysis 298 evoked potentials, somatosensory, intraoperative 234–5 Ewing’s sarcoma 212–13 examination 6–13 ankle/foot 587–90 back see back elbow/forearm 369–71 fractures 693 pathological 725–6 hand 413–17 hip 493–6 knee 547–53 ligaments and ligamentous instability 876–7, 880–1 major trauma abdomen 663 airway 637, 647–8 breathing 638, 647–8 burns 667 circulatory failure (shock) 655 in primary survey 637, 638 in secondary survey 639–40 metabolic bone disorders 129 mononeuropathies 272–3 neck see neck neuromuscular disorders 228–30

949

INDEX 950

feel (palpation) – contd hand 414–15 hip 494–5 knee 548 in major trauma airway 637, 643 breathing 648 hypovolaemic shock 655 neck 439 shoulder 338 wrist 373–5 feet see foot felon 432 Felty’s syndrome 61 females see climacteric; postmenopausal women; pregnancy femoral nerve injury 285 stretch test 455 femoro-acetabular impingement 524–8 femur 845–72 amputation through 327 anatomy distal 583 proximal 542 anteversion 507 deficiency/dysplasia (congenital shortness) 183–5, 509–10 proximal 183, 184, 509–10 endochondral ossification of neck, defect 508 epiphyses see epiphysis fractures of head hip dislocation combined with 844 Pipkin classification 844 fractures of intertrochanteric region 853–5 fractures in major trauma, pre-hospital management 633 fractures of neck 847–53 clinical features 848 complications 851–2 diagnosis 848–9 mechanisms of injury 847–8 with metastases 218 pathological anatomy and classification 847–8 and shaft 852–3, 865 treatment 849–51 X-ray 848 fractures of proximal region in children 856–7 fractures of shaft, adults 859–68 clinical features 860 complications 866–8 hip dislocation combined with 845 mechanism of injury 859 neck fracture combined with 852–3, 865 pathological anatomy 859–60 refracture 867–8 treatment 861–6 X-ray 860 fractures of shaft, children 868–70 fractures of subtrochanteric region 857–9 fractures of supracondylar regions 870–1 fractures of trochanter 857 osteonecrosis see osteonecrosis

osteotomy acetabular dysplasia and hip subluxation 506 coxa vara 509 knee deformities 556, 580 osteonecrosis 532 slipped capital femoral epiphysis 518, 519 pistol-grip deformity of head of 525 retroversion 507 stress 725 in total hip arthroplasty cemented component 539–40 uncemented component 540 vascular necrosis of head of see Perthes’ disease fetus genetic and development disorders, diagnosis 154–5 malposition, and developmental dysplasia of hip 498 surgery see intrauterine surgery FGF receptor 3 gene and achondroplasia 164 fibroblast growth factor receptor 3 gene and achondroplasia 164 fibrodysplasia ossificans progressiva (myositis ossificans progressiva) 174– 5 fibroma chondromyxoid 197–8 non-ossifying 194 soft-tissue tumours 219 fibromatosis 219–20 fibromyalgia 262–3 fibro-osseous junction (tendons/joints) in ankylosing spondylitis 67 fibrosarcoma 220 bone 211 fibrous cortical defect 194 fibrous dysplasia 194–6 fibrous histiocytoma, malignant 211–13 fibula 30–1 deficiency 185 fractures 905 fatigue 905 malleolar fracture combined with 912, 913, 914 proximal 896 tibia fracture combined with 897 physeal injuries in children 918 Ficat–Arlet staging of femoral head necrosis 530–1 fingers acquired deformities 418–20, 423–4 rheumatoid arthritis 427–8 amputation (surgical) 799, 802–3 congenital anomalies 387, 389, 389–90 flexion deformity in cerebral palsy 241 injuries 418–19, 421, 790–3 replantation following amputation 800–1 tip 791, 799 metacarpal fractures and the functions of 788–9 osteoarthritis 428–9 polyarthritis vs 95 polyarthritis 95 tourniquets 306 Finkelstein’s test 384, 406

firearm injuries (incl. guns) 662–3, 710–11 fishmonger’s infection 434–5 fixation (stabilization) of fractures 314–17, 700–4 ankle, pilon fractures 917 cervical spine injury 811 femoral intertrochanteric fractures 854 failure 854–5 femoral neck fractures 849–51 femoral shaft fractures 860–1, 862–4 failure 867–8 femoral supracondylar fractures 870–1 humeral medial condylar fractures in children 763 humeral shaft fracture 749 indications other than metastatic bone disease 701 insufficient, causing non-union 717 malunion treated by 719 metacarpal fractures 790 in metastatic bone disease 218 prophylactic 218 open fractures 708–9 over-rigid, causing delayed union 716 pelvic fractures 836, 840 radial distal fractures 773–4 talar neck fractures 922–3 tibial fractures combined with fibula fractures 899–900, 900, 901 plateau fractures 892, 894–5 fixed deformities claw toe 608 examination for 14 hip 495 hand/fingers 419–20 in juvenile idiopathic arthritis 65, 66 in leprosy, drop-foot 298 in poliomyelitis 253 in rheumatoid arthritis 65, 66 fixed traction with fractures 697 flail chest 650 flail joint elbow 376, 378 poliomyelitis 253 flat-foot 596–600 flexible flat-foot 597 flexion ankle/foot see plantarflexion back 454–5 lateral 455 definition 9 elbow see elbow fingers 415, 436 fingers, deformity 419 in cerebral palsy 241 hip 495 hip, deformity 495 cerebral palsy 242 poliomyelitis 254 hip, femoro-acetabular impingement and 524–5 knee 549, 583 knee, deformity cerebral palsy 242–3 poliomyelitis 255 shoulder 339, 367 thumb 416 wrist 385, 410 deformity in cerebral palsy 241

forearm 369–82, 767–76 anatomy 381 congenital anomalies 371, 387 injuries 767–76 fractures 391–2, 767–70, 772–6 muscle contractures following injury 722 pronation 381 pronation deformity cerebral palsy 241 poliomyelitis 254 supination 381 forefoot generalized pain 619–20 localized pain 620–1 rheumatoid arthritis 610 foreign body ‘granuloma’, foot 622 forequarter amputation 327 Forestier’s disease (diffuse idiopathic skeletal hyperostosis) ankylosing spondylitis vs 69 osteoarthritis vs 95 four-poster braces, cervical injuries 810 fracture(s) 687–732 ankle 912–20 children 918–20 clinical features 692–4 closed see closed fractures complete vs incomplete 688–9 complex, CT 21 complications 711–23 early 711–16 infection see infection late 716–23 displacement see displacement exercise 704–6 fat embolism see fat embolism femoral see femur fibular see fibula fixation see fixation foot 621, 921–8, 929, 931–2, 932 forearm 391–2, 767–70, 772–6 hand 787–93 care in open injuries 797 metacarpal 787–90 phalangeal 790–3 healing see delayed union; healing; malunion; non-union; union injuries caused by 694–5 in juvenile idiopathic arthritis 75 limbs (in general) see limbs major trauma cases, pre-hospital management 633 mechanisms (causes) 687–8 multiple see multiple injuries open see open fractures osteoporotic (postmenopausal) 133 management 133–4 pagetoid 145 patellar 887–8 pathological 688, 725–7 femoral shaft in adults 865 femoral shaft in children 868 intertrochanteric fractures 855 see also specific types (subheading above/below) pelvic see pelvis physeal see physis recurring after internal fixation 703 shoulder 733–7

skull base 660 spinal/vertebral 664, 727, 806 cervical 810, 813–15, 816–18, 819 cord injury with 682 CT 20 in major trauma 664 thoracolumbar 821, 822, 824–5 spinal/vertebral, pathological ankylosing spondylitis 69–70 multiple myeloma 215, 855 osteoporotic (postmenopausal), management 133–4 stress/fatigue see stress fracture tibial see tibia tumour-associated see tumours types and classification 688–9 upper arm and elbow 744–55, 756, 757–65 wrist/carpus 778–84 fracture–dislocation or subluxation elbow 756–7 hand Bennett’s 789 volar 795 hip 844, 845 humerus (proximal) 746–7 midtarsal 929 radio-carpal joint (Barton’s) 776–7 radius (Galeazzi’s) 771–2 shoulder 741 spine cervical facet joints 817–18 thoracolumbar 821, 824–5 talocalcaneal joint 922 talus 923 ulna (Monteggia’s) 770–1 fracture–separation distal femoral epiphysis 872 distal humeral physis 764–5 proximal tibial epiphysis 895–6 Frankel grading of spinal cord injury 827 Freiberg’s disease 620–1 friction, prosthetics 329–30 friction test (knee) 551 Friedrich’s ataxia 245, 258 Fröhlich’s adiposogenital syndrome 147 frostbite 671 hand 801 frostnip 671 frozen shoulder 351–2 fulcrum test 355 full-thickness burns 667 function(s) hand 413, 435–6 tests 417 loss/disability elbow 369 history-taking 5 knee 547 osteoarthritis 91 shoulder 337 wrist 373, 413 functional activities, fracture rehabilitation 705–6 functional bracing see bracing fungal (mycotic) infections 55–7 hand 435 spine 475

INDEX

flexion–compression injuries/fractures cervical 816–17 thoracolumbar 821, 822–3 flexion–distraction injuries, thoracolumbar 821, 824 flexion–rotation injuries, thoracolumbar 821 flexor carpi radialis tendinitis 401 flexor carpi ulnaris tendinitis 401 flexor digitorum profundus (FDP) repair 802 testing 416 open injuries 797 flexor digitorum superficialis (FDS) repair 802 testing 416 open injuries 797 flexor pollicis brevis paresis in leprosy 296–7 flexor pollicis longus (FPL) tendon rupture in rheumatoid arthritis 401 tendon transfer to, in traumatic paraplegia/quadriplegia 828 testing 416 flexor tendons fingers 437 avulsion 792–3 repair of injuries 798–9, 802 testing 416 hand, tenosynovitis 407 rheumatoid arthritis 401, 423–4, 428 floating knee 865 fluid, knee, tests for 549–50 fluid administration (intravenous) burns 669 shock 675 in multiple trauma 658 fluid film lubrication, joints 87 fluoride 127 intoxication (fluorosis) 127, 143 fluoroscopy, wrist 386 focussed assessment with sonography (FAST), major trauma 640 fondaparinux 310 foot 587–624, 920–33 amputations 327 anatomy 623 surface 589 clinical assessment 587–91 deformities 591–609, 624 arthrogryposis 263 cerebral palsy 241, 243 examination for 587, 589 poliomyelitis 255 see also pes (and talipes) deformities drop see drop-foot injuries 621, 920–33 interdigital nerve compression 621 leprosy, nerve lesions 54, 55, 298–301 movements of ankle and 589, 623–4, 907 positions 624 spina bifida 251–2 footwear, looking at 590 foramen, intervertebral see intervertebral foramen forces fracturing, direct and indirect 687–8 hip region 542

951

INDEX 952

gadolinium-enhanced MRI 22 gait (and abnormalities and their assessment) 229–30, 587–8 in ankle/foot problems 587–8 cerebral palsy 237–8 in knee problems 548 Galeazzi’s fracture–dislocation of radius 771–2 gallium-67 scans 24 gallows traction, femoral shaft fractures 861 gamekeeper’s thumb 795–6 gamma-globulins, plasma 26 ganglion compound palmar 408–9 knee region 562 ganglion cyst, wrist 407–8 gangrene, gas 714–15 gap healing (fracture) 690 Garden classification of femoral neck fractures 847, 848 reduction and 850 Garré’s sclerosing osteomyelitis 41 gas gangrene 714–15 gastrointestinal tract in multiple organ failure 679 Gaucher’s disease (glucocerebroside storage disorder) 111–12, 177–8 clinical features 178 imaging 178 osteomyelitis vs acute haematogenous 34 acute suppurative 45 osteonecrosis 111–12 treatment 178–9 gene(s) 151 alleles of 151 mutations see mutations gene therapy 157 genetic disorders 151–80 background genetics/biology 181–2 diagnosis 154–6 inheritance patterns 152–4 management principles 156–7 neuropathies 258–60, 258 genetic factors/predisposition (in acquired disorders) 151 ankylosing spondylitis 66 developmental dysplasia of hip 498 osteoarthritis 87–8 Perthes’ disease 511 rheumatoid arthritis 59 genetic heterogenicity 154 genetic mapping 154 genetic markers 154 genome 151–2 genotype 151 genu recurvatum (knee hyperextension), poliomyelitis 255 genu valgum (valgus/knock knee) 548, 554–7 adults 557 children 554–7 spina bifida 251 varus osteotomy 580 genu varum (varus knee; bow legs) 548, 554–7 adults 557 children 554–7 valgus osteotomy 580

geographic distribution, osteoarthritis 90 giant-cell sarcoma 204 giant-cell tumour bone 202–3 tendon sheath 220 giant osteoid osteoma 196–7 gigantism 147–8 Gilula’s arcs 409 Gla protein (osteocalcin) 118, 119 Glasgow Coma Scale 638 glenohumeral joint arthrodesis 360, 366 movements 367 osteoarthritis 360 rheumatoid arthritis 359 tuberculosis 358–9 glenoid fractures 736 labrum lesions (SLAP lesions) 350–1 glide, plates preventing 702 glomerular pathology osteodystrophy 141 rickets 139 glomus tumour 221–2 gloves (surgical) 306–7 glucocerebroside storage disorder see Gaucher’s disease glucocorticoids see corticosteroids gluteal artery tear with hip dislocation, superior 845 gluteus medius tendinitis 533 goal-setting, cerebral palsy 239 Goldthwaite procedure 563 golfer’s elbow 379 gonadal hormones 126–7 insufficiency 135 gonococcal arthritis 43 Reiter’s syndrome vs 71 Gorham’s disease 204–5 Gould operation 910 gout 77–80 differential diagnosis 79 acute suppurative osteomyelitis vs 45 osteoarthritis 95 pseudogout 79, 81, 82 Reiter’s syndrome 71, 79 rheumatoid arthritis 63, 79 tumour 190 elbow 375 hand/fingers 420 tophaceous see tophaceous gout gowns 306 grading of tumours 191 grafting see transplantation granuloma eosinophilic 204 foreign body, foot 622 grasp see grip gravity, traction by 697 greenstick fractures 688–9 distal radius 776 grinding test (knee) 553 torn medial meniscus 559 grip (grasp) 417 power/strength 417, 435, 436, 437 assessment 416 growth (primarily bone) 117, 121–4 fractures affecting 720 ankle 919–20 femoral neck 857

in juvenile idiopathic arthritis 75 in leg length inequalities, interventions arrest (longer leg) 322 stimulation (shorter leg) 323 in paediatric acute osteomyelitis 36 pubertal spurt in, slipped capital femoral epiphysis during 515 wrist malformation due to arrest of 387–9 growth factors (in bone) 119 growth hormone (somatotropin) deficiency 147 oversecretion 147 growth plate see physis Guedel (oropharyngeal) airway 644 Guillain–Barré syndrome 260 gunshot injuries 662–3, 710–11 gun-stock deformity 369, 371 Gustillo classification of open fractures 706 antibiotics and 707 tibia and fibula combined 897, 901 gut see intestine Guyon’s canal, ulnar nerve compression 283, 291 habitual (voluntary) dislocation 731 knee 564 haemangioma 221 multiple (Maffuci’s disease) 165, 166 osseous 204 haemarthrosis (bleeding into joint) acute suppurative arthritis vs 44, 45 haemophilic see haemophilic arthropathy post-traumatic (incl. fractures) 714 knee 576 pseudogout vs 82 tuberculosis vs 52 haematological system in multiple organ failure 679–80 haematoma fracture site 690, 691 intracranial, traumatic 661 soft-tissue, tumour vs 190 haemochromatosis vs pseudogout 82 haemodynamic function instability with pelvic fractures 834 tests in osteonecrosis 107 see also circulation haemophilic arthropathy 99–101, 574–5 acute suppurative arthritis vs 45 knee 574–5 Haemophilus influenzae and paediatric osteomyelitis 30–1 haemorrhage (bleeding/blood loss) femoral fractures shaft 866 subtrochanteric 858 intraoperative, prevention 305–6 into joints see haemarthrosis major trauma, control 638, 656 prehospital 632 into muscle or nerve in haemophilia 100 pelvic fractures 656, 835 see also clotting disorders haemostatic dressings 656 haemothorax 638, 651 massive 649 hair removal for surgery 306

humeral fractures (proximal) 746 knee 581–2 shoulder 365 rheumatoid arthritis 360 hemi-epiphysiodesis, knee deformities 556 hemimelic epiphyseal dysplasia (dysplasia epiphysealis hemimelica) 160–1 hemiparesis 230 hemiplegia 230 cerebral palsy 236, 241 heparin, perioperative 310 hepatic 25-OHD see 25hydroxycholecalciferol hepatitis B and C infection control 307 heredity see entries under genetic herniation articular capsule in osteoarthritis 93 disc see intervertebral disc heroin addicts, osteomyelitis (acute), antibiotics 35 herpes zoster 259 herpetic whitlow 432 Herring classification, Perthes’ disease 512, 513, 514 heterotopic bone formation see ossification (heterotopic) heterozygosity 151 autosomal dominant disorders 152 autosomal recessive disorders 153 high-arched feet (pes cavus) 589, 600–3 high-energy injuries missile injuries 710, 711 tibia and fibula combined fractures 900–1 high-stepping gait 229, 587 Hilgenreiner’s epiphyseal angle 508 Hill–Sachs lesion 354, 355, 740, 742 hindfoot, rheumatoid arthritis 610–11 see also heel hip 493–545 anatomy 542–3 arthroscopy (diagnostic) 28, 497–8 axes and reference angles for osteotomies 312 cerebral palsy 241, 242, 243–4 clinical assessment 493–6 neonatal 12 developmental dysplasia (congenital dislocation) 12, 498–504 ultrasonography 23, 499, 500 diagnostic calendar 498 disarticulation through 327 dislocation acquired (non-traumatic) 506 congenital see subheading above postoperative 537–8 traumatic 843–7 imaging 496–7 plain films 18, 496–7 operations 534–42 osteoarthritis see osteoarthritis osteoporosis, transient 114, 530, 532 poliomyelitis 254 replacement, sciatic palsy following 286, 537 septic arthritis 520–1 dislocation following 506 in inflammatory bowel disease 73 spina bifida 251

nerve root levels concerned with movements of 250 Hippocratic method of shoulder reduction 740 histamine test 277 histiocytoma, malignant fibrous 211–13 histiocytosis X 204 histocompatibility complex, major (MHC) see HLA histology, osteoarthritic 89 histoplasmosis 56 history-taking 3–6 fractures 692 pathological 725 genetic and developmental disorders 156 knee ligament injuries 877 major trauma 639 metabolic bone disorders 129 neuromuscular disorders 228 peripheral nerve lesions 273 spinal trauma 806 tumours 188 HIV (human immunodeficiency virus) septic arthritis and 46 spinal tuberculosis and 474, 475 surgery and risk of transmission 307 HLA (human leucocyte/ histocompatibility/human MHC antigens) 26, 151–2 ankylosing spondylitis, HLA-B27 66, 154 psoriatic arthritis, HLA-B27 71, 72 Reiter’s syndrome, HLA-B27 70 rheumatoid arthritis 59 hold reduction, fractures 696–704 homocystinuria 179 Marfan’s syndrome vs 171, 179 homografts, bone 318–19 homozygosity 151 autosomal recessive disorders 153 hormone replacement therapy, postmenopausal 133 hormone therapy, palliative, bone metastases from breast or prostate 217 hormones as aetiological factors in developmental dysplasia of hip 498 in slipped capital femoral epiphysis 515 in bone metabolism 125 hospital (in major trauma) management in 634–72 transfer from scene to 633–4 transfer within/between 640–1 hourglass biceps 350 housemaid’s knee 578 human bites, infected 434 human immunodeficiency virus see HIV human leucocyte antigens see HLA humerus capitulum see capitulum condylar fractures lateral 761–3 medial 764 distal fracture 750–2 physeal fracture–separation 764–5

INDEX

hallux rigidus 606–7 hallux valgus 603–6 halo ring/vest, cervical injuries 810 hamate fracture 784 hammer toe 607–8, 608–9 hand 413–37, 787–803 acquired deformities 417–21 anatomy 436–7 clinical assessment 413–17 congenital anomalies 183, 184, 386–91, 417, 423 arthrogryposis 263, 391 injuries 418–19, 421, 787–803 open 796–801 treatment principles 787 nerve lesions in leprosy 54, 55, 296–8 operations late reconstructions 803 secondary 801–2 Volkmann’s ischaemic contracture 418, 722 hand–arm vibration syndrome 435 Hand–Schüller–Christian disease 204 Handigodu joint disease 98 hanging cast, humeral shaft fracture 748 hangman’s fracture, C2 814 Hansen’s disease see leprosy Harrington system 463–4 Haversian system 120 Hawkins classification of talar neck fractures 922 Hawkins–Kennedy test 343 head injury in major trauma 658–62 airway management 642 assessment incl. examination 639, 661 spastic paresis 244 headache, neck-related 439 healing acute suppurative arthritis 43 fractures 689–92 femoral neck 847 see also delayed union; malunion; nonunion; union spinal injuries 806 heart arrest in hypothermia 671 blunt injury 652 failure, Paget’s disease 146 in multiple organ failure, poor performance 678–9 output in shock monitoring 674 reduced 673, 673 shock relating to (cardiogenic shock) 654, 673 treatment 675 tamponade 632, 649 heel injuries 924–8 pain 617–18, 619 scars, leprosy 300 see also hindfoot helicopter ambulance 634 helminths (worms) 57–8, 475–6 HemCon™ 656 hemiarthroplasty (partial arthroplasty incl. surface replacement) hip 540–1 in femoral neck fracture 851

953

INDEX 954

humerus – contd epicondyle see epicondylar injuries; epicondylitis proximal, fracture 744–6 children 747 shoulder dislocation and 741 proximal, fracture–dislocation 746–7 shaft, fracture 748–50 children 750 subglenoid dislocation of the head of (luxatio erecta) 743–4 supracondylar fractures 750 children 758–60 Hunter’s syndrome 176 Hurler’s syndrome 176 hyaline cartilage 85, 117 hyalurinate 85, 87 hydatid disease see echinococcosis hydrocephalus, spina bifida cystica 248, 249 hydrogen cyanide poisoning 667 hydroxyapatite (crystalline) in bone 118, 119 synthetic, as bone substitute 319, 331 hydroxyapatite deposition disease (basic calcium phosphate crystal deposition disease) 83–4 25-hydroxycholecalciferol (25-OHD) 125 hepatic 138 inadequacy 138 hydroxyproline, urinary, measurement 131 hypercalcaemia 124–5 in metastatic bone disease 217, 218 in primary hyperparathyroidism 140 hypercortisonism (excess corticosteroid) 134, 148 hyperextension, knee non-traumatic see genu recurvatum traumatic, testing 880 hyperextension injury cervical spine 818 thoracolumbar spine 821 hyperkyphosis see kyphosis hypermobility (joint), generalized 13 benign familial 170 hyperostosis diffuse idiopathic see Forestier’s disease infantile cortical 42–3 sternoclavicular 363–4 sterno-costo-clavicular 42, 364 hyperparathyroidism 129, 140–1 ‘brown tumours’ 138, 203 primary 140, 140–1 pseudogout vs 82 secondary 136, 137, 140, 141 tertiary 140 hyperpituitarism 146, 147–8 hyperthyroidism, osteoporosis 135 hypertonic saline in shock 658 hypertrophic non-union 716–17, 718 tibia and fibula combined fractures 904 hypertrophy, biceps 350 hyperuricaemia 77, 78 congenital 179 drugs treating 80 predisposing factors 78 hypervitaminosis A and D 134 hypoaesthesia 12

hypocalcaemia 124–5 hypochondroplasia 164 multiple epiphyseal dysplasia vs 159 hypochromic anaemia 26 rheumatoid arthritis 62 hypophosphataemic rickets/osteomalacia 139–40 hypopituitarism 146, 147 hypoplasia radial 182 thumb 390 ulnar 183 hypotension in shock, permissive 658 hypothermia 671 hypothyroidism 149 multiple epiphyseal dysplasia vs 159 hypotonia, cerebral palsy 235 hypovolaemic (loss of blood volume) shock 654, 655 spinal trauma 807 treatment 675 venous return in 673 hypoxanthine-guanine phosphoribosyltransferase deficiency 179 iatropathic injuries nerves 295–6, 697 traction causing 697 ice see PRICE; RICE iliac bones adjacent to sacroiliac joints, osteitis condensans 149 iliac vessels 829 iliofemoral venous thrombosis, acetabular fractures 840 iliopsoas bursitis 533 Ilizarov method 319–21 imaging, diagnostic 15–25 ankle/foot 590–1 elbow 371 fetus 155 fractures 693 hip see hip knee 553 major trauma 640 neck 440–1 pelvis 831–2 shoulder 340–1 wrist 385–6 see also specific modalities and conditions immobilization hand infections 431 major trauma case 632–3 cervical spine see cervical spine osteoporosis associated with 135 spinal injury cases 806 immunization (surgeon) 307 immunocompromised patients, osteomyelitis (acute), antibiotics 35 impacted fractures 688 distal radius 773 impingement dorsal synovial 408 femoro-acetabular 524–8 peroneal tendon 928 impingement syndrome, shoulder 341–3 surgery 347 implants see prosthetics and implants inbreeding 154

independent lifestyle, maintenance with genetic and developmental disorders 156–7 indium-111-labelled leucocytes 24 infants acute osteomyelitis clinical features 33 complications 36 pathology 32 acute suppurative arthritis antibiotics 45 complications 45 burns and body surface area 667, 668 cerebral palsy diagnosis 236 cortical hyperostosis 42–3 coxa vara 508 examination 12 femoral shaft fractures 869 hip, developmental dysplasia clinical features 499 management 500–2 pathology 498–9 hip, subluxation 504, 505 newborn see neonates non-accidental fractures (battered baby syndrome) 155, 728 scoliosis, idiopathic 461, 465 torticollis 442 trigger thumb (congenital) 391, 423, 424 infection 29–58, 429–35, 470–6 antibiotics see antibiotics arthroplasty (incl. implant)-related 330 hip 538–9 knee 582 bone see bone; osteitis; osteomyelitis foot, diabetic 614 fractures 38, 714–15 external fixation-related 704 femoral 866–7 internal fixation-related 703 open fractures see subheading below pin-site 697 general aspects 29–30 gout vs 79 hallux valgus, recurrent 606 hand, acute 429–35 hip 520–1 joint see septic arthritis knee 570–1 open fractures 710 ankle 916 tibia and fibula combined fractures 903 polyneuropathies 256, 259–60 in rheumatoid arthritis 66 shoulder 352 spine 470–6 cervical 445, 448–50 surgical, risk reduction 306–7 of trophic/plantar ulcers in leprosy 299, 300 see also microbiology inflammatory bowel disease see Crohn’s disease; ulcerative colitis inflammatory demyelinating neuropathy, acute 260 inflammatory phase of fracture healing 690, 691

inotropes, shock 675 insertion mutations 152 in-soles (off-the-shelf), flat-foot 600 inspecting see look instability (unstable joint) ankle 587 recurrent lateral 909–10 assessment (in general) for 7 elbow 369 persistent (with fractures) 756 recurrent 377 history-taking 5 intertrochanteric fractures 853 knee 547, 879–83 assessment for 551–2, 877 in dislocation 885 ligaments, chronic 562, 879–83 in poliomyelitis 254–5 metacarpo-phalangeal joint of thumb, chronic 793 osteoarthritis 91 pelvic 829 with fractures 834 post-traumatic 722 radio-ulnar joint (distal/inferior) in Galeazzi’s fracture 772 shoulder 337, 353–8, 362–3 in biceps pathology 350 spinal 805 segmental 482 in trauma 810 wrist/carpus, chronic 392–7, 779 in radio-carpal fracture 778 instrumentation (spinal) idiopathic scoliosis 463–4 thoracolumbar trauma 811 insufficiency fractures 724 thoracolumbar 821 intensive care unit scoring systems 682–4 intercalated segment, wrist 392 dysplasia 389, 779 instability 395 intercarpal joints, chronic instability 394–7 intercarpal ligament, dorsal 411 interdigital nerve compression 621 interfragmentary screws 701 interlocked (locked) intramedullary nails/screws 316, 702 femoral supracondylar fractures 870 humeral shaft fracture 749 internal fixation 314–16, 700–4 ankle, pilon fractures 917 cervical spine injury 810 complications 702–3 femoral intertrochanteric fractures 854 failure 854–5 femoral neck fractures 849–51 femoral shaft fractures, adults 860–1, 862–4 failure 867–8 femoral shaft fractures, children 869 femoral subtrochanteric fractures 858–9 femoral supracondylar fractures 870–1 humeral lateral condylar fractures in children 763 humeral shaft fracture 749 indications (generally) 701 malunion treated by 719

in metastatic bone disease 218 prophylactic 218 open fractures 708–9 pelvic fractures 836, 840 radial distal fractures 773–4 talar fractures 922–3 tibia and fibula combined fractures 899–900, 900, 901 tibial plateau fractures 892 types 701–2 internal rotation hip 495–6 deformity in cerebral palsy 242 femoro-acetabular impingement and 524–5 knee 549 interosseous ligaments, wrist 411 interosseous muscles of hand, testing 416 interosseous nerve lesions anterior 284 compression injury 289 posterior, compression injury 291–2 interphalangeal arthrodesis, in claw toes 608 interphalangeal joints of hand (IP) 437 dislocation 794 osteoarthritis 428–9 rheumatoid arthritis 426, 427 secondary operations 802 tendon lesions affecting 419–20 interphalangeal ligament injuries, proximal 795 interposition arthroplasty elbow in osteoarthritis 376 toe in hallux rigidus 607 interscapulothoracic amputation 327 intersection syndrome 406–7 intertrochanteric fractures 853–5 intertrochanteric osteotomy 534–5 osteoarthritis 524 slipped capital femoral epiphysis 519 intervertebral discs 489 in ankylosing spondylitis 67 cervical acute prolapse/herniation 444–5, 819 anatomy 451 in spondylosis, surgery 446 chronic disease 247 degeneration 476–8 imaging (discography) 457 in facet joint dysfunction 483 infection (discitis) 472 adolescent kyphosis vs 469 prolapse/herniation/rupture, acute 247, 478–81 cervical 444–5, 819 intervertebral foramen 490 surgical enlargement in cervical spondylosis 447 intestine (bowel; gut) inflammatory disease see Crohn’s disease; ulcerative colitis malabsorption causing vitamin D deficiency 138 in multiple organ failure 679 selective decontamination 680 PTH actions 125, 126 in traumatic paraplegia/quadriplegia, management 827

INDEX

inflammatory response, systemic (SIRS) 677, 678, 679 inflammatory rheumatic disorders/arthropathies 59–76 osteoarthritis vs 94 polyarticular see polyarthritis seronegative/spinal column see seronegative arthropathies infrapatellar bursitis 578 infrapatellar procedures in recurrent patellar dislocation 563 infraspinatus weakness, testing 345 ingrown toe-nails 622 inhalational analgesia, major trauma 640 inhalational burns 642, 666–7 inheritance see entries under genetic injection(s) in facet joint dysfunction 483 nerve injury caused by 295 injection injuries to hand 801 injury (traumatic incl. tears and rupture) Achilles tendon 615–16 acute suppurative arthritis vs 44 ankle 907–20 biceps 349–50 elbow stiffness following see stiffness foot 621, 920–33 forearm see wrist/distal forearm (subheading below) and forearm fractures caused by 688–723 history-taking 692 mechanisms 687–8 X-rays for injuries at other sites 693 fractures causing 694–5 haemarthrosis following see haemarthrosis hand/fingers see fingers; hand head, spastic paresis 244 hip osteonecrosis following 528 persistent dislocation following 506 slipped capital femoral epiphysis, following 615 iatropathic see iatropathic injuries joints in see joints knee 875–90 extensors 575–6, 885–6 haemarthrosis following 576 ligaments see ligaments menisci see menisci synovitis following 577 major/multiple/complex see multiple injuries nerve see mononeuropathies osteoarthritis following see osteoarthritis osteomyelitis following 37–8 osteonecrosis following see osteonecrosis pelvic see pelvis rotator cuff 344–5 repair 347–8 shoulder see shoulder spine see spinal column; spinal cord spondylolisthesis following 486 tumours and history of 188 tumours vs 190 wrist/distal forearm 391–2, 394, 776– 86 repetitive stress-related 407 Injury Severity Score, mortality rates and 627

955

INDEX

in-toeing 507 intra-articular bleeding see haemorrhage intra-articular entrapment of biceps 350 intra-articular injuries/fractures see haemarthrosis intracranial haematoma, traumatic 661 intracranial pressure elevation, traumatic 659 management 662 intramedullary nailing 316, 702 femur shaft fractures 860–1, 862–3 subtrochanteric fractures 858–9 supracondylar fractures 870 metastatic bone disease 218 tibia and fibula combined fractures 899, 901 intramembranous (appositional bone) ossification 117, 121–2 intraoperative neurophysiological studies 234–5 intraoperative radiography 303–4 intraosseous cannulation in shock 657 intrauterine malposition and developmental dysplasia of hip 498 intrauterine surgery in developmental and genetic disorders 157 spina bifida 249–50 intravenous analgesia, major trauma 640 intravenous fluids see fluid administration intrinsic muscles of hand 437 pathology 418, 421, 437 testing 416 inversion, foot 623–4 involutional osteoporosis 134 ionizing radiation see radiation iridocyclitis in juvenile idiopathic arthritis 75 irradiation see radiation irritable joint (transient synovitis) 510–11 acute suppurative arthritis vs 44 hip 510–11 in Perthes’ disease 514 tuberculosis vs 51, 511 ischaemia bone, in Perthes’ disease 513 nerves, transient 270 ischaemic contracture, Volkmann’s see Volkmann’s ischaemic contracture ischaemic necrosis see osteonecrosis isometric contraction 228 isotonic contraction 228 isotopic scans see radionuclide scans ivory exostosis 197

956

jack-knife injury 821, 824 Jansen-type metaphyseal chondrodysplasia 164 javelin thrower’s elbow 379 jaw thrust 643–4, 644 Jefferson’s fracture 813 joint(s) (articulations) amputation affecting joint above 328 in ankylosing spondylitis 67 bleeding into see haemarthrosis calcifications in pseudogout 81, 82 contractures, correction 321 deformities see deformities degeneration see degeneration dysplasia see dysplasia

elbow, anatomy 381 feeling 7 flail see flail joint fusion (arthrodesis), osteoarthritis 95 hand anatomy 437 injuries 790, 793–5, 802 injuries involving surfaces (intraarticular fractures) 730–1 calcaneal 924–5, 927–8 hand/finger 790, 793–5, 802, 1521 humerus (distal) 750–1 instability and stiffness 722 treatment with infected fractures 710 wrist 777–8 X-ray above/below fracture 693 instability see instability irritable see irritable joint knee fluid/effusion, tests for 549–50 surface destruction (localized), osteotomy 580 laxity see laxity lubrication 87 mobility see hypermobility; laxity; movement operations 323–4 osteoarthritic, debridement 95, 376 replacement see arthroplasty in rheumatoid arthritis, pathology 60 rupture 66 shoulder, anatomy 366 stiffness see stiffness swelling see swelling synovial (diarthrodial) see synovial joints in traumatic paraplegia/quadriplegia, management 827 wrist 392–3 instability 392–7 X-rays 18–19 see also entries under arthrjoint space (radiographic) 18 narrowing 10 osteoarthritis 91 Jones’ fracture 932 juvenile Colles’ fracture 775 juvenile idiopathic arthritis (juvenile rheumatoid/chronic arthritis) 73–5 diagnosis/differential diagnosis 75 acute suppurative arthritis 45 irritable hip 511 hand/fingers 420 juvenile idiopathic scoliosis 465 juvenile osteochondrosis (Scheuermann’s disease) 467, 468–9 juxtacortical chondrosarcoma 205 juxta-patellar hollow test 550 Kaneda instrumentation 464 Kashin–Beck disease 96–7 Keller’s operation 608 ketamine in major trauma, pre-hospital 633 kidney failure osteodystrophy in 141–2 osteomalacia in 138 glomerular disease see glomerular pathology

in multiple organ failure 679 parathyroid hormone actions 126 tubules see tubules Kienböck’s disease 397–9 kinematics see movement Kirner’s syndrome 389 Klinefelter’s syndrome 180 Klippel–Feil syndrome 180–1, 362, 443 Klumpke’s palsy, obstetric 279, 280 knee 547–86, 875–90 amputation above/at/below 337 anatomy 582–4 arthroscopy see arthroscopy axes and reference angles for osteotomies 312 cerebral palsy 241, 242–3 clinical assessment 547–53 diagnostic calendar 553–4 floating 865 imaging 553 injury see injury instability see instability operations 579–82 osteonecrosis 114, 573–4 in poliomyelitis 254–5 spina bifida 251 nerve root levels concerned with movements of 250 stiffness see stiffness knife wounds, abdomen 663 knock knee see genu valgum Kocher’s method of shoulder reduction 740 Kohler’s disease 619 Kyle classification, intertrochanteric fractures 853 kyphosis (and excessive kyphosis/hyperkyphosis) 13–14, 453–4, 467–70 adolescent 468–9 ankylosing spondylitis 70 congenital 467 elderly 467, 469–70 spina bifida 250, 251 laboratory tests synovial fluid 27 tumours 189 see also specific conditions and (types of) tests Lachman test 551, 553, 878, 881 lag screw fixation 314–15 femoral supracondylar fractures 871 lag sign 345 lamellar bone 120 laminotomy 481 Langenskiold procedure for physeal arrest 729, 730 lap seat-belt injuries 824 laparotomy, abdominal injury 663 Larsen’s syndrome 171–2 laryngeal mask airway 645 laryngeal trauma 642 laryngoscope in major trauma 665 lateral (definition of term) 9 lateral flexion, back 455 lateral rotation 9 latex allergy, spina bifida 250 Lauge-Hansen classification of ankle fracture 912

limb(s) amputation see amputation axes and reference angles for osteotomies 311–12 congenital anomalies localized 182–6 small stature with disproportionate shortness of limbs 155 crush injuries see crush injuries deformities adult-acquired spastic paresis 244 cerebral palsy 241–4 treatment principles 245 fractures children see children in major trauma 633, 666 in metastatic bone disease 218 in major trauma examination 639 injuries incl. fractures 633, 666 microsurgery 324–5 osteotomy see osteotomy power loss see diplegia; hemiplegia; monoplegia; paraplegia; quadriplegia reconstruction via Ilizarov method 319–21 replantation 325 salvage (with tumours) 193 tourniquets see tourniquets see also long bones; lower limbs; upper limbs and specific portions of limbs limb girdle muscular dystrophy 264, 265–6 limp 493 child, approaches 514 lipoma 219 liposarcoma 219 Lisfranc injury 930 listening in major trauma airway 642 primary survey 637 breathing 648 hypovolaemic shock 655 Lithium Dilution Cardiac Output Monitor 674–5 liver, 25-OHD in see 25hydroxycholecalciferol load reduction in osteoarthritis 95 local anaesthesia, examination under, shoulder 340, 355 locked intramedullary nails/screws see interlocked intramedullary nails/screws locked knee 547, 560, 880 bucket-handle tear 559 recurrent 882 locoregional aspects bone mineral exchange and turnover 127 cerebral palsy 241–4 mononeuropathies 276–87 poliomyelitis 254–5 spina bifida 250–2 tumour spread 191 long bones injuries in major trauma 665 metastases causing shaft fractures 727 staging of chronic osteomyelitis 40 see also limbs

longitudinal arrest of wrist development 387 longitudinal instability of radius and ulna 394 longitudinal ligament, posterior see posterior ligament complex look (inspecting/observing) 6–7 ankle/foot 588–9 appearance overall 10 back 453–4 elbow 369 fractures 693 hand 414 hip (and lower limb) 494 knee 548–9 in major trauma airway 637, 642 breathing 647–8 hypovolaemic shock 655 neck 439 shoulder 337 wrist 373 loose bodies elbow 373 knee 560, 568–9 osteoarthritis 93 loosening casts 699 implants, aseptic see aseptic loosening of joint implant Looser zone in osteomalacia 137 Lorain syndrome 147 lordosis 13–14 loupes, operating 305 low-energy injuries missile injuries 710, 711 tibia and fibula combined fractures 898–900 lower limbs (legs) 493–624, 843–934 adult-acquired spastic paresis 244 cerebral palsy 241–3 length discrepancy 241 compression prophylaxis, perioperative 309–10, 310 congenital anomalies 183–6 deformities (in general), treatment principles 245 elevation, fractures 704–5 injuries 843–934 nerve see subheading below length see length nerve injuries 285–7 compression causing 294 pain referred from back to 453 disc prolapse 480 power with back problems, assessment 455 see also straight-leg raising test and specific portions of limbs lower motor neuron lesions, foot paralysis 616 lubrication, joint 87 lumbar spine cord compression 245–6 nerve root compression in ankylosing spondylitis 70 root transection 826 see also back; thoracolumbar spine lumbosacral plexopathy 285

INDEX

laxity (joint/ligament) examination 13 fingers/thumb 415 generalized familial 170 knee 558 non-pathological 86 shoulder, vs instability 353 leg (lower limb or lower part of lower limb) see lower limb and parts of leg Legg–Calvé–Perthes disease see Perthes’ disease Lehri–Weill syndrome see dyschondrosteosis length displaced fractures and changes in 689 leg, discrepancies/inequalities 321–3, 494 ankle fractures 920 cerebral palsy 241 correction techniques 321–3 poliomyelitis 253–4 leg, measurement 494 scoliosis 460 lengthening (bone) 319–20 shorter leg 323 leontiasis 167 lepromatous leprosy 53, 54, 260 leprosy (Hansen’s disease) 53–5, 260 peripheral nerve lesions 53, 54, 55, 296–300 Leri’s disease 167 Lesch–Nyhan syndrome 179 Letterer–Siwe disease 204 leucocytes, indium-111-labelled 24 LiDCO® cardiac output monitor 674–5 lifestyle, independent, maintenance with genetic and developmental disorders 156–7 lift-off test 345–6 ligament(s) 86 hip 542 injuries (sprains/strains/ruptures) 730–1 ankle 907–12 cervical spine 815–16 foot 929 hand/fingers 795 knee see subheading below shoulder see subheading below knee assessment 551–2, 876–7 chronic instability 562, 879–83 lax 558 in tibial plateau fractures, spontaneous reduction 894 knee, injuries 560, 875–83 femoral shaft fractures associated with 865–6 mechanism of injury and pathological anatomy 876 testing 552, 877 treatment 579, 878–9, 882–3 laxity see laxity pelvic, anatomy 829 pull (ligamentotaxis), with fractures 696 shoulder, injuries 737–8 heterotopic ossification 739 wrist 410–11

957

INDEX

lumbosacral trigger point injections in facet joint dysfunction 483 lumbricals, testing 416 lunate dislocations 784–6 fracture 784 traumatic softening (Kienböck’s disease) 397–9 lung (pulmonary non-vascular tissue) contusions 651–2 function tests in scoliosis 462 in multiple organ failure 678 direct insult in pathogenesis 676 treatment of problems 680 luno-triquetral joint dissociation 396 instability 397 testing 385, 395 lupus erythematosus, systemic see systemic lupus erythematosus Luque instrumentation 464 luxatio erecta 743–4 lying ankle/foot examination 588–90 back examination 455–6 hip examination 494 knee examination 548–53 Lyme disease 64 lymphadenopathy, rheumatoid arthritis 61 lymphoma, non-Hodgkin’s 213 lytic spondylolisthesis 484, 486

958

McCoy laryngoscope in major trauma 665 McCune–Albright (ALbright’s) syndrome and fibrous dysplasia 195 MacIntosh’s test 881 Mckusick-type metaphyseal chondrodysplasia 164 McMurray’s test 552 torn medial meniscus 559 macrodactyly, hand 390 Madelung’s deformity 390 maduramycosis 56 Maffuci’s disease 165, 166 magnesium 125 magnetic resonance arthrography 22 elbow 371 femoro-acetabular impingement 527 shoulder 340–1 rotator cuff disorders 346 SLAP lesions 351 magnetic resonance imaging (MRI) 21–3 ankle/foot 591 pes cavus 601 ankylosing spondylitis 68 arthritis acute suppurative 44 psoriatic 72 rheumatoid 62 back/thoracolumbar spine 457 degenerative disease 478 disc prolapse 480 facet joint dysfunction 483 injuries 822 pyogenic osteomyelitis 471 spinal canal stenosis 487 tuberculosis 474 clinical applications (in general) 22

contrast 22 fractures 693 carpal 780 stress 724 Gaucher’s disease 178 hip 497 acetabular dysplasia and hip subluxation 505 osteonecrosis 529–30, 531 slipped capital femoral epiphysis 517 transient osteoporosis 532 knee 553, 554 chronic ligamentous instability 882 osteonecrosis 573 patellar dislocation 889 limitations 23 major trauma 640 neck/cervical spine 441 neuromuscular disorders 231 osteoarthritis 92 osteomyelitis acute 33 chronic 39 pyogenic (spine) 471 osteonecrosis 107, 108 knee 573 physics 21–2 shoulder 340 spinal trauma 809, 809 cervical facet joint dislocation 818 whiplash injury 820 tumours 189 Ewing’s sarcoma 212 osteosarcoma 208, 209, 210, 211 wrist 386 carpal instability 396 Kienböck’s disease 398 magnification in surgery 303–4 Main–Jowett classification of midtarsal injuries 928–9 major histocompatibility complex see HLA major injuries see multiple injuries malabsorption (intestinal) causing vitamin D deficiency 138 males see men malformations see congenital malformations malignant tumours (cancer) bone see bone tumours fractures see fractures grading 191 at implant site 330 management principles 192 osteomalacia with 140 osteoporosis with 135 PET scans 25 predisposition risk (incl. malignant transformation) giant-cell tumour 203 neurofibromatosis type-1 176 osteochondroma 199 soft-tissue 218–19, 219, 220, 221–2, 223 malleolar fractures 912–16 mallet finger 418, 791–2 mallet toe 607, 608 malnutrition in multiple organ failure 680 malrotation of fractures see rotation

malunion 718–19 ankle fractures in children 920 calcaneal fractures 928 clavicular fracture 735 femoral fractures intertrochanteric 855 shaft, adults 867 shaft, children 870 subtrochanteric 859 supracondylar 871 forearm fractures 769, 774 humeral fracture–dislocations (proximal) 747 humeral lateral condylar fractures in children 763 humeral supracondylar fractures, children 761 metacarpal 789 radial distal 776 dorsal 397 talar fractures 923 tibia and fibula combined fractures 903 manipulation cerebral palsy 240 nerve injury caused by pressure of 295 mannitol 662 Maquet’s operation 566 marble bone disease 166–7 march fracture (stress fracture of metatarsal) 621, 932 Marfan’s syndrome 170–1 homocystinuria vs 171, 179 maternal screening for fetal disorders 154 neural tube defects 154, 248 maxillofacial trauma, airway in 642 mechanical disorders vs ankylosing spondylitis 69 mechanical stress see stress medial (definition of term) 9 medial rotation 9 median nerve lesions/injuries 284–5 compressive 288–94, 288, 446 leprosy 54, 55, 296, 297 regional anatomy elbow 381 hand 437 wrist 410 mediastinal injury 653 megadactyly (macrodactyly), hand 390 melorheostosis 167 men, bone changes at/following climacteric 128 osteoporosis 134 in testicular dysfunction in old age 135 meninges (and head injury) 659 meningocele 148 menisci 558–62, 561 anatomy 583 cysts 561–2 degeneration 561 discoid lateral 561 excision (meniscectomy) arthroscopic 560 complications 560, 562, 573 injuries/tears 558–61, 562 testing 552 see also cartilage menopause see climacteric

Milwaukee shoulder (rapidly destructive arthritis) 360–1 in basic calcium phosphate crystal deposition disease 84 in rotator cuff impingement syndrome 343 minimally-constrained total knee replacement 582 minimally invasive arthroplasty hip 541 knee 582 minimally invasive plate osteosynthesis, femoral shaft fractures 862 Mirel’s scoring system, metastatic bone disease 218 missile injuries (incl. guns) 662–3, 710–11 Moberg pick-up test 274, 417 mobility see movement mobilization, postoperative, early 309 monarticular osteoarthritis 93 monarticular rheumatoid arthritis vs infection 93 monofilament test 273, 274 monogenetic disorders see single gene disorders mononeuropathies (predominantly injuries) and resulting palsies 234, 256, 272–301 classification of injuries 271–2 clinical features 272–4 compression see compression neuropathies pathology 271 treatment principles 274 monoplegia 230 cerebral palsy 236 Monteggia fracture–dislocation of ulna 770–1 Morquio’s (Morquio–Brailsford) syndrome 176–7 spondyloepiphyseal dysplasia congenita vs 160 mortality see death mortise bones (ankle) 907 Morton’s metatarsalgia 621 motion see movement motor and sensory neuropathy, hereditary 258 motor function, nerve root, testing 808 motor nerves 225, 226, 269 motor neuron 227 a-lesions, foot paralysis 616 motor neuron disease 255 motor power see power motor unit recruitment 233–4 motor vehicle collisions see road accidents movement (mobility/motion) ankle/foot 589, 623–4, 907 assessing (in general) 7 back/lower spine 489–90 assessing 454–5 elbow 381 assessing 370 fractures, assessing 693 hand 436 assessing 414, 415–16 hip 495–6 femoro-acetabular impingement and 524–5

joint stiffness with all movements absent or limited 15 joint stiffness with some movements limited 15 knee 549, 583 neck, assessing 439 in osteoarthritis, limited 91 pelvic fractures complicated by loss of 840 in planes, terminology 9 range see range of movement shoulder 367 assessing 338–9 wrist 410 assessing 384, 385 see also hypermobility; immobilization and specific movements e.g. extension; flexion Mseleni joint disease 97–8 mucopolysaccharidoses 176–7 mucous cysts, osteoarthritis 428 Müller’s classification of fractures 689 multibacillary leprosy 54 multidisciplinary trauma teams 635 multifactorial disorders 152 multiple casualties, triage see triage multiple enchondromata 165 multiple epiphyseal dysplasia 157–9 multiple haemangiomata (Maffuci’s disease) 165, 166 multiple injuries (complex/major injuries incl. fractures) 627–85 aetiology 627–8 death, mode 627–8 femoral neck fractures and 849 femoral shaft fractures and 860–1, 864–6 fixation 701, 703 foot injuries and 920 hospital management 634–72 pre-hospital management 629–34 sequence of management 629 multiple mononeuropathy 256 multiple myeloma 213–15 fractures with 215, 855 osteoporosis 135, 213, 214 multiple organ failure 676–81 multi-slice CT 21 muscle(s) (skeletal) 227–8 amputation-related complications 328 back pain following activity of, transient 487 biopsy 231 compartment syndromes see compartment syndromes contractions 228 contractures 14, 228 cerebral palsy 238 fractures causing 713, 721–2 hand 418 quadriceps 564 Volkmann’s ischaemic see Volkmann’s ischaemic contracture electrical activity recording see electromyography fasciculations 228 finger 437 testing 416 haemophilic bleeding into 100

INDEX

meralgia paraesthetica 294 mesenchymal chondrosarcoma 207 mesomelia 155 metabolic disorders 131–46 bone 117, 131–46 assessment 27, 129–31 inherited 158, 176–9 polyneuropathies 256, 258–9 pseudogout vs 82 metacarpal fractures 787–90 metacarpophalangeal joints (MCPs) 437 dislocation 794 osteoarthritis 429 rheumatoid arthritis 425, 426, 427 metal implants 328–30 hip implants 541 metaphysis dysplasias predominantly affecting 158, 161–6 injuries distal forearm 776 phalanges (hand) 790 physial injuries and 728 metastatic bone tumours 216–18 fractures 218, 725 femoral shaft 865 intertrochanteric 855 metastatic infection in acute osteomyelitis 36 metatarsal bone injuries 931–2 osteochondritis of head of 620–1 osteotomy, hallux valgus 605, 605–6 metatarsalgia 587, 619–20 Morton’s 621 transfer 606 metatarsophalangeal joint (MTP) in hallux rigidus 607 in hallux valgus 603, 604 injuries 932 in lesser toe deformities 608, 609 pain 620 metatarsus adductus 595 metatarsus primus varus 603 methicillin-resistant S. aureus, treatment of acute osteomyelitis in patients at risk of 35 methylprednisolone, spinal cord injury 810 metrizamide 20 MHC see HLA microbiology osteomyelitis acute 30–1 chronic 38 post-traumatic 37 suppurative arthritis (acute) 43 microdiscectomy 481 microscope, operative 304 microsurgery 324–5 midcarpal dislocation 786 midcarpal joints 393 instability 395 symptomatic 397 midfoot pain 619 midpalmar space infection 433 midtarsal joint 928–9 injuries 928–9 movements 589 Milwaukee brace 462

959

INDEX

muscle(s) (skeletal) – contd imbalance hip dislocation due to 506 patello-femoral joint overload due to 564–5 necrosis with gas gangrene 715 nerve roots supplying 11, 229 patterning instability of shoulder 357 power see power tone see tone in traumatic paraplegia/quadriplegia, management 827 tumours derived from 223 wasting see wasting weakness see weakness see also fibromyalgia; neuromuscular system muscle fibres 228 muscular atrophy peroneal 258 spinal 255 muscular dystrophies 264–6 mutations 152 direct testing for 156 Mycobacterium hand infection 434–5 M. leprae see leprosy M. marinum 434–5 M. tuberculosis see tuberculosis mycotic infections see fungal infections myelin 225, 270 see also demyelinating polyneuropathies myelography 20 cervical 441 CT see computerized tomographic myelography disc prolapse 479–80 myeloma multiple see multiple myeloma solitary (plasmacytoma) 213 myelomeningocele 148 myofibrils 227 myogenic tumours 223 myonecrosis with gas gangrene 715 myopathic scoliosis 466–7 myositis, streptococcal necrotizing, vs acute osteomyelitis 34 myositis ossificans, post-traumatic 720–1 elbow fracture–dislocations 757 hip dislocation 845 humeral supracondylar fractures, children 761 tumour vs 190 myositis ossificans progressiva 174–5 myotonia 266

960

nail hand injuries 799 nail-fold infections 432 toe, disorders 622–3 nail–patella syndrome 169 nailing 316, 702 femur shaft fractures 860–1, 862–3 subtrochanteric fractures 858–9 supracondylar fractures 870 humeral shaft fracture 749 metastatic bone disease 218

tibia and fibula combined fractures 899, 901 nasogastric tube, major trauma 639 nasopharyngeal airway 644, 645 nasotracheal intubation 646 navicular bone (foot) accessory 598 osteochondritis 619 neck 439–52 airway affected by trauma to 642 anatomy 451–2 clinical assessment (incl. examination) 439–41 major trauma 639 spinal trauma 807 congenitally short 180–1, 362, 443 sprained 820–1 necrosis (necrotic/dead/devitalized tissue) avascular/ischaemic see osteonecrosis muscle, with gas gangrene 715 removal of dead tissue with open fractures 707–8 necrotizing myositis, streptococcal, acute osteomyelitis vs 34 needle aspiration and irrigation, rotator cuff calcifications 349 needle cricothyroidotomy 646 needle decompression (thoracocentesis), tension pneumothorax 648–9 needle electromyography 231 Neer’s classification of proximal humeral fractures 744–5 Neer’s test and sign 343 Neisseria gonorrhoeae see gonococcal arthritis neoadjuvant chemotherapy Ewing’s sarcoma 213 osteosarcoma 208, 210 neonates arthritis (acute suppurative) antibiotics 45 clinical features 43–4 aspiration (for biochemical tests) 26 cerebral palsy diagnosis 236 developmental dysplasia of hip clinical features 499 screening 500 hip examination 12 osteomyelitis (acute) antibiotics 35 complications 36 spina bifida diagnosis 248–9 management 250 neoplasms see tumours nerve(s) (predominantly peripheral) 225, 225–7, 269–70 amputation-related complications 328 blocks, major trauma 640 conduction studies see conduction studies disorders (incl. neuropathies) 255–60, 269–301 classification 256 compression neuropathy see compression neuropathies diabetes 98, 258–9, 613, 614 diagnostic/electrophysiological signs 234

hand deformities 421 leprosy 53, 54, 55, 296–300 regional survey 276–87 see also neurological disorders exploration 274 foot paralysis 616 function 225–7, 269–70 assessment 273–4 guides 275 haemophilic bleeding into 100 regional anatomy elbow 381 hand 437 wrist 410 repair 274–5 structure 225–7, 269–70 supply to hip 542 to spine 490 tension, deformity correction causing 314 transfers and grafts see transfer (tissue); transplantation and grafting tumours 222–3 disc prolapse vs 480 see also mononeuropathies; polyneuropathies nerve injuries (incl. cuts) fractures and musculoskeletal injuries causing 712–13 elbow fracture–dislocations 756 forearm fractures 769, 771, 774 hip injuries 845 humeral distal fractures 752 humeral proximal fracture– dislocations 747 humeral shaft fractures 748–9 humeral supracondylar fractures, children 761 iatropathic fractures 295–6, 697 knee dislocation 885 open fractures 708 pelvic fractures 837, 840 shoulder dislocation (anterior) 741 hand 787, 797–8, 802 humeral medial epicondylar separation in children 764 nerve roots (spinal) anatomy 490 cervical 451, 451–2 dermatomes supplied by 229, 272 disease see radiculopathy dorsal, selective division in cerebral palsy 240 imaging (radiculography) in disc prolapse 479–80 injuries 805, 825–8 lumbosacral, compression in ankylosing spondylitis 70 muscles supplied by 11, 229 spina bifida hip and knee movements and levels of 250 testing 808 nervous system, divisions 225–6 see also specific divisions neural tube defects (spinal dysraphism) 181, 248 maternal screening 154, 248 neuralgic amyotrophy 259–60

non-steroidal anti-inflammatory drugs (NSAIDs) ankle ligament injury 909 ankylosing spondylitis 69 gout 80 rheumatoid arthritis 65 rotator cuff calcifications 348 non-union 692, 716–17 ankle fractures 916 femoral fractures intertrochanteric 855 neck 852 subtrochanteric 859 supracondylar 871 forearm fractures 769, 774 humeral lateral condylar fractures in children 763 humeral shaft fractures 750 internal fixation-related 703 of osteotomy 314 knee area 581 scaphoid fracture 783 tibia and fibula combined fractures 904 nucleus pulposus 489 degeneration 476 numbness 5 ankle/foot 587 back pathology causing 453 history of 5, 228 neck pathology causing 439 see also anaesthesia; paraesthesia nutrition see diet; malnutrition Oales™ Modular Bandage 656 obesity, osteoarthritis risk 90 oblique fractures 687, 688 metacarpal 788 O’Briens test 351 observing see look obstetrics see childbirth; pregnancy obstructive shock 673, 673 treatment 675 occipital condylar fractures 813 occipito-cervical dislocation 813 occupational disorder(s) osteoarthritis as 90 wrist pain 407 occupational therapy, rheumatoid arthritis 65 ocular features see eye odontoid anomalies 443–4 fractures 810, 814–15 oedema bone marrow, transient 114, 530, 532 fracture-related 704 oestrogen 126–7 deficiency 135 see also hormone replacement therapy olecranon bursitis 380 fractures 754–5 children 766 dislocation associated with 756 Ollier’s disease 165 open-book pelvic injuries 633, 836 open fractures 706–10 ankle 916 femoral shaft 864 forearm 768

hand 797 infection see infection nerve injuries 713 pelvis 836 talus 923 tibia 900–1 and fibula combined 897, 900, 901, 903 open injuries chest wall 649 hand 796–801 open medullary nailing of femoral shaft fractures 864 open reduction fractures 696 femoral intertrochanteric 854 humeral supracondylar, children 760 talar neck 922–3 tibial plateau 894 lunate/perilunate dislocations 785 slipped capital femoral epiphysis 518– 19 operation see surgery ophthalmological features see eye opposition, thumb 416 restoration 421 organ(s) see viscera and organs organization in major trauma hospital 634–5 pre-hospital 629 oropharyngeal airway 644 oropharyngeal suction 645 orotracheal intubation 645–6 orthoses, flat-foot 599–600 Ortolani’s test 499 Osgood–Schlatter disease (apophysitis of tibial tubercle) 575, 576, 887 tumour vs 190 ossification (heterotopic bone formation) coraco-clavicular ligaments 739 elbow fracture–dislocations 757 hip, after joint replacement 537 humeral distal fractures 752 medial collateral ligament of knee (Pellegrini–Stieda disease) 576, 879 muscle see myositis ossificans pelvic fractures 840 posterior longitudinal ligament 447–8 ossification (physiological) 121–2 endochondral see endochondral bone primary and secondary centres of 117 wrist bones 410 osteitis condensing, clavicle 363–4 syphilitic 47 osteitis condensans ilii 149 osteitis deformans 143–6 osteoarthritis (OA; so-called degenerative arthritis) 64, 87–100, 360, 375–6, 402–6, 428–9, 522–4, 572–3 aetiology 87–8 Paget’s disease 145–6 ankle 612–13 malleolar fractures 916 arthroscopy 92 clinical features 90–1, 375, 402, 403–4, 522–3, 572–3 clinical variants 93–4 complications 93

INDEX

neurapraxia 270 spinal cord 825 cervical 819 neuraxial anaesthesia 309 neurilemma 222 neurilemmoma (schwannoma) benign 222 malignant 223 neuritis brachial, acute 259–60 ulnar 283–4 neuroblastoma, adrenal, bone metastases 217 neurofibroma 222–3 neurofibromatosis 175–6 scoliosis 175–6, 467 type 1 (von Recklinghausen’s disease) 175, 175–6, 223 type 2 175 neurogenic shock 654, 655, 673 spinal trauma 807 neuroimaging (brain imaging) in neuromuscular disorders 231 neurological disorders scoliosis surgery-related 464 syphilis 47 tumour-related 188 see also nerves, disorders; neuromuscular system neurological examination 10–12 back (lower spine) problems 456 disc prolapse 479 scoliosis 460 hand problems 416 major trauma see disability mononeuropathies 272–3 neck problems 439–40 neuromuscular disorders 228 spinal trauma 808 neurological injury in spinal trauma see spinal cord, injury neuroma 222 Morton’s (Morton’s metatarsalgia) 621 neuromuscular system 225–67 anatomy/components 225–8 disorders 225–67 clinical assessment 228–31 electrophysiological studies 231–5 hand in 421 pes cavus in 600 scoliosis 466–7 neurons 225, 269–70 neuropathic arthropathy/arthritis see Charcot disease (neuropathic arthritis) neuropathic scoliosis 466–7 neuropathies see nerves neurophysiological (incl. electrophysiological) studies 231–5 thoracic outlet syndrome 293–4 neurosarcoma 223 neurotmesis 271 neutralization, acid/alkali burns 670 neutralization plate 702 newborns see neonates nodes of Ranvier 225, 270 non-Hodgkin’s lymphoma 213 non-ossifying fibroma 194

961

INDEX 962

osteoarthritis (OA; so-called degenerative arthritis) – contd differential diagnosis 94–5 osteonecrosis 94, 530 rheumatoid arthritis 64, 95 elbow 375–6 endemic 96–8 hand/fingers 420, 428–9 hip 522 femoro-acetabular impingement causing 524–6 osteonecrosis vs 530 osteotomy 524, 535 plain films 18, 523 post-dislocation 846 imaging 91, 376, 402, 404, 572 knee region 572–3, 577 tibial plateau fractures 895 management 95–6, 360, 376, 523–4, 572–3 natural history 92 pathogenesis 86 pathology 88–90, 522 post-traumatic 90, 723 calcaneal fractures 928 elbow dislocation 757 femoral neck fracture 852 hip dislocation 846 pelvic fracture 840 talar fractures 924 tibial plateau fractures 895 wrist fracture 783 prevalence 90 primary/idiopathic and secondary (socalled) 88 in pseudogout 80, 81, 82 rapidly destructive 94 risk factors 90 trauma see subheading above shoulder 93, 360, 364 complicating acromioclavicular joint injury 739 spinal column 93, 477 wrist 402–6 post-traumatic 783 osteoblastoma 196–7 osteoblasts 119 bone resorption and 122 osteocalcin 118, 119 osteochondral fractures knee 890 talus 922, 923 osteochondritis (osteochondrosis) 113–14 juvenile (Scheuermann’s disease) 467, 468–9 metatarsal head 620–1 navicular 619 syphilitic 47 osteochondritis dissecans 113, 566–8, 890 capitulum 372–3 knee 566–8, 574, 890 talus 611–12, 616–17 osteochondroma 199–200 osteochondroplasty (hip) 534 femoro-acetabular impingement 528 osteoarthritis 524 osteoclasts 119–20 bone resorption and 122

osteocytes 119 osteodystrophy, renal 141–2 osteogenesis, distraction 319–21 osteogenesis imperfecta 172–4 osteogenic tumours see bone-forming tumours osteoid 119 osteoid osteoma 196 giant 196–7 osteolysis aggressive, in hip arthroplasty 538, 541 massive (Gorham’s disease) 204–5 osteoma compact 197 osteoid see osteoid osteoma osteomalacia 129, 135–40 hypophosphataemic 139–40 oncogenic 140 vitamin D-dependent 138–9 vitamin D-resistant 138 X-rays 129, 137 osteomyelitis acute haematogenous 30–42 acute suppurative arthritis vs 34, 44 in sickle cell disease see sickle cell disease chronic 36, 38–41, 364 clavicle 364 Garré’s sclerosing 41 multifocal non-suppurative 41 post-traumatic 37–8 subacute 36–7, 364 subacute recurrent multifocal 41–2 tumour vs 190 vertebral/spinal adolescent kyphosis vs 469 pyogenic see pyogenic osteon 123 osteonecrosis (avascular/ischaemic necrosis/bone death in mass) 103– 15 aetiopathogenesis 103–4 bone marrow oedema vs 114, 115 clinical features 105–6 diagnosing underlying condition 108 femoral condyle in osteochondritis dissecans 567 femoral head 528–32 in developmental dysplasia of hip 504 in sickle cell disease 110, 111 in slipped capital femoral epiphysis 519 in traumatic hip dislocations 845 femoral head and neck fractures combined 852 children 856 haemodynamic tests 107 imaging 106–7 knee 114, 573–4 osteoarthritis vs 94, 530 pathology and natural history 105 post-traumatic 104, 720 femoral head and neck see subheading above humeral head (in fracture– dislocation) 747 pelvic fracture 840 talar fractures 923–4

prevention 108–9 scaphoid post-traumatic 782–3 spontaneous 399 shoulder 361 staging the lesion 107–8 systemic disorders associated with 110–14 talar 612, 617 fractures 923–4 treatment 109 osteopathia striate 167 osteopathic scoliosis 465–6 osteopenia 132 inflammatory bowel disease 73 X-rays 130 osteopetrosis 167–8 osteopoikikosis 167 osteoporosis 113–15, 129 in ankylosing spondylitis 68 foot, in diabetes 614 hip fracture associated with 847 transient 114, 530, 532 imaging 129, 131–2 involutional/senile/elderly 134, 470 kyphosis in 469–70 osteoarthritis risk 90 osteomalacia vs 138 postmenopausal 132–4 regional 132 secondary 134–5 multiple myeloma 135, 213, 214 tibial fractures combined with fibula fractures 904 plateau crush fractures 890, 892 see also osteopenia osteoprotegerin (OPG) 124 osteosarcoma 207–11 staging/grading 191, 208 stress fracture vs 190, 724 variants 210–11 Paget’s disease 146, 210–11 osteotomy 311–14 acetabular dysplasia and hip subluxation 505, 506 coxa vara 509 hallux valgus 605, 605–6 intertrochanteric see intertrochanteric osteotomy knee region 579–81 childhood deformities 556 osteoarthritis 573 rheumatoid arthritis 572 osteoarthritis 96 hip 524, 535 knee 573 osteonecrosis of hip 532 slipped capital femoral epiphysis 519 Otto pelvis 507–8 out-toeing 507 overcorrection (intentional), club-foot 593 overgrowth fingers 390 toenails 622 overload, patello-femoral joint 564–6 overuse tenosynovitis, wrist 406, 407 oxygen tension, effects on bone 127

patterns 230 in cerebral palsy 236 peripheral nerve see mononeuropathies and specific nerves poliomyelitis 252–3 spina bifida 251 spinal cord injury 823, 825, 827–8 see also diplegia; hemiplegia; monoplegia; paraplegia; quadriplegia paraplegia Pott’s 473 spinal trauma 823, 825 management 827–8 parasitic infestations 57–8 spine 475–6 parasympathetic nervous system 226, 227 parathyroid hormone (PTH) 119, 122, 124, 125, 126 excess see hyperparathyroidism postmenopausal osteoporosis, therapeutic use 133 paresis 230 spastic, adult-acquired 244 see also weakness Parkland formula with burns 669 paronychia 169 parosteal osteosarcoma 210 pars interarticularis fractures C2 814 thoracolumbar 822 partial-thickness burns 667 passive movements assessing 7 elbow 370 knee 549 shoulder 339 wrist 385 fracture rehabilitation 705 past (previous) medical history, recording 5 genetic and developmental disorders 156 neuromuscular disorders 228 patella absent/hypoplastic, of nail–patella syndrome 169 alignment, assessment 548 chondromalacia 564–6 dislocation 888–90 recurrent 560, 562–4, 889–90 extensor rupture above 575 extensor rupture below 576 fracture 887–8 tap test 550 patella alta 548, 566 patella baja 548 patellar ligament (patellar tendon) injury 886–7 syndrome following 576 patellectomy osteoarthritis 573 patellar chondromalacia 566 recurrent patellar dislocation 563 patello-femoral joint assessment 550–1 overload (pain) syndrome 564–6 patello-femoral ligament, medial, repair 563

pauciarticular juvenile idiopathic arthritis 73–4, 74 pauciarticular osteoarthritis 93 paucibacillary leprosy 53–4, 54 Pauwels’ valgus osteotomy 509 pedobarography 591 Pellegrini–Stieda disease 576, 879 pelvis 829–41 anatomy 829–30 in cerebral palsy, deformities 244 imaging 831–2 injuries/fractures 829–41, 847 clinical assessment 830–1 haemorrhage 656, 835 major trauma 633, 639, 640, 664 open-book 633, 836 types 832–41 visceral injuries associated with 694, 829–30, 830–1, 832 instability 830 Otto 507–8 penetrating injury abdomen 662–3 chest 647 diaphragm 653 pentasaccharide, heparin 310 peri-arthritis in basic calcium phosphate crystal deposition disease 83, 84 perilunate dislocations 784–6 perimysium 227 perineurium 270 periosteum (periosteal membrane) 120, 122 chondroma 197–8 chondrosarcoma 205 osteosarcoma 210 stripping causing delayed union, overenthusiastic 716 periostitis, syphilitic 47 peripheral chondrosarcoma 205 peripheral nerves see nerves peripheral vascular disease in diabetes, foot 613, 614 peripheral venous cannulation in shock 656 peri-tendinitis crepitans 406–7 Perkins’ traction, femoral shaft fractures 861 peroneal muscular atrophy 258 peroneal nerve lesions/palsy 286–7 foot paralysis 616 post-osteotomy 581 proximal fibular fractures 896 peroneal spastic flat-foot 597–8 peroneal tendon dislocation 911 impingement 928 personal protective equipment 629–30 Perthes’ (Legg–Calvé–Perthes) disease/ avascular necrosis of femoral head irritable hip vs 511 multiple epiphyseal dysplasia vs 159 pes (and talipes) deformities calcaneocavus 601, 602 calcaneovalgus 595 cavus 589, 600–3 equinovalgus cerebral palsy 243 spina bifida 251–2 equinovarus see club-foot

INDEX

paediatrics see children; infants; neonates Paget’s disease 143–6 osteosarcoma 146, 210–11 pain 260–2 acute 261 ankle/foot 587, 616–21 site related to cause 590 autonomic 4 back 487–8 assessment 453 diagnostic approaches 487–8 in disc prolapse (acute) 479 in facet joint dysfunction 482 persistent postoperative 481 in pregnancy 149 scoliotic 459 chronic 261 syndromes of see chronic pain syndrome; complex regional pain syndrome coccygeal injury-related 841 elbow 369 femoral neck fractures without 849 grade/severity 3–4 hand 413 hip 493 causes 534 history-taking 3–4 knee 547 anterior, causes 565 in chondromalacia patellae 564–6 metastatic bone disease 217 neck 439 osteoarthritis 91 perception 261 referred 4 to lower limbs from back see lower limbs to shoulder 337 sacroiliac (with pelvic fracture), persistent 837 shoulder 337, 341 tumour-related 188 wrist 373, 387 see also analgesics; headache; tenderness palliative treatment metastatic bone disease 217–18 Paget’s sarcoma 211 palmar carpal ligaments 411 palmar fascial contractures 418, 421–3 palmar ganglion, compound 408–9 palmar skin 436 palpation see feel palsy see paralysis Pancoast’s syndrome vs thoracic outlet syndrome 294 panhypopituitarism 147 paraesthesia ankle/foot 587 back pathology causing 453 history of 228 see also anaesthesia; numbness paralysis (palsy) 230 compression see compression neuropathies deformities in 230 knee 558 foot 616 hand intrinsic muscles 421, 437 leprosy, residual 55

963

INDEX 964

pes (and talipes) deformities – contd equinus 589, 602 cerebral palsy 243 plantaris 589, 601, 602, 603 planus 596–600 valgus 596–600 cerebral palsy 241 congenital convex 596 poliomyelitis 255 varus cerebral palsy 241 poliomyelitis 255 phalangeal fractures (hand) 790–3 Phalen’s test 289 phantom limb 328 pharyngeal airways 644 phenotype 151 phosphate in bone 119, 125 dietary, affecting bone 127 serum, measurement 130 see also hypophosphataemic rickets/osteomalacia urinary, measurement 131 phosphatonins 125, 140 phosphorus 125 physical examination see examination physical therapy (incl. physiotherapy) cerebral palsy 240 facet joint dysfunction 483 flat-foot 600 osteoarthritis 95 rheumatoid arthritis 65 physical variations, assessment 13–16 physiotherapy see physical therapy physis (growth plate) dysplasias predominantly affecting 161–6 injuries/damage incl. fractures 720, 727–30 ankle 918, 920 femoral distal epiphyseal fracture– separation 872 femoral neck in children 857 humeral distal physeal fracture– separation 764–5 phalanges of hand 793 wrist 391, 774 knee (either side), stapling 555 in leg length inequalities growth arrest (longer leg) 322 stimulation (shorter leg) 323 mistaken for fracture 813 zones 121–2 pia mater (and head injury) 659 piano-key sign 784 PiCCO® cardiac output monitor 674 picture archiving and communication system (PACS) 16 pigmented villonodular synovitis 220 pilon fractures ankle 916–18 middle phalanx 794 pin(s) for fracture fixation 703–4 infection relating to 697, 704 pincer, mechanism, femoro-acetabular impingement 525, 526, 527, 528 Pipkin classification of femoral head fractures 844 Pirigoff’s operation 327

pisohamate tunnel (Guyon’s canal), ulnar nerve compression 283, 291 pisotriquetral joint testing 385 pistol-grip deformity of femoral head 525 pituitary disorders 146, 147–8 pivot shift test carpal instability 395 knee ligament injuries 552, 876, 881 plain films see X-rays plain tomography 20 planes of body 9 movements in various, terminology 9 plant thorn prick, infection 430 plantar fasciitis 611, 618–19 plantar nerve lesions lateral 287 entrapment 619 medial 287 plantar reflex 11 plantar stress injuries 928 plantar ulceration (trophic), leprosy 54, 55, 299–300 plantar venous compression, intermittent 310 plantar warts 622 plantarflexion 589, 623 definition 9 plantaris deformity 589, 601, 602, 603 plasmacytoma 214 plaster of Paris see cast plastic pen test 796 plate fixation femur shaft fractures 862 supracondylar fractures 870–1 forearm fractures, complication of plate removal 769 humeral shaft fracture 749 pelvic fractures 836 radial distal fractures 773–4 screw and (principle of) 315–16, 701–2 tibia and fibula combined fractures 899–900 platelet-derived activators for bone repair 318 plexopathy 234 brachial 276–80 lumbosacral 285 plica syndrome 569–70 pneumatic compression of leg, intermittent 310 pneumothorax 648–9 open 649 simple 650–1 tension 638, 648–9 point mutations 152 Poirier’s space 411 poliomyelitis 252–4 polyarthritis (polyarticular arthritis) differential diagnosis 63–4 fingers, vs osteoarthritis 95 inflammatory pseudogout vs 82 seronegative see seronegative arthropathies in juvenile idiopathic arthritis 73–4, 74 polyarticular arthritis see polyarthritis polyarticular osteoarthritis 93–4

polyethylene, cross-linked (XLPE), hip implants 541 polygenic disorders 152 polymethylmethacrylate implants 331 polymyalgia rheumatica 64 polyneuropathies 256, 258–60 popliteal aneurysm 579 popliteal artery damage 884, 885, 895, 901–2 popliteal cyst 578–9 popliteal fossa, examining 552 position(s) of cerebral palsy patients, good 240 foot 624 hand, posture in different resting positions 414 see also posture positron emission tomography (PET) 24–5 posterior (of body - definition of term) 9 posterior cord syndrome 826 posterior ligament complex (incl. posterior longitudinal ligament) injury 815–16 ossification 447–8 postganglionic brachial plexopathy 276–7 postmenopausal women, bone changes 128 osteoporosis 132–4 kyphosis 469–70 post-thrombotic syndrome 308–9 post-traumatic disorders see injury posture in ankylosing spondylitis 67 deformities due examining for 14 kyphosis 467, 468 scoliosis 458 examining/observing (principles) 6, 14 for deformities 14 hand in resting positions 414 neuromuscular disorders 229–30 cerebral palsy 237 see also position pot-hole injury 931–2 Pott’s disease see tuberculosis Pott’s fracture 912 power (motor) 230 assessment 10, 230, 274 ankle/foot 590 legs in back pathology 455 shoulder 339 grip see grip loss see paralysis; paresis; weakness prednisolone, rheumatoid arthritis 65 preganglionic brachial plexopathy 276–7 pregnancy 149 prenatal diagnosis of genetic disorders 154–5 see also childbirth; maternal screening pre-hospital management of major trauma 629–34 pre-implantation genetic diagnosis 154–5 Preiser’s disease 399 prenatal diagnosis of genetic disorders 154–5 preoperative period chemotherapy see neoadjuvant chemotherapy preparation 303

psychological support facet joint dysfunction 383 traumatic paraplegia/quadriplegia 828 pterygia syndrome 264 puberty bone changes following 127–8 slipped capital femoral epiphysis during growth spurt 515 see also adolescents pulled elbow 372 pulmonary artery flotation catheter in shock 674 pulmonary embolism pelvic fractures 837 perioperative risk 307–10 pulmonary non-vascular tissue see lung pulp (finger) infection 432 injuries, closure 799 pulse(s) contour analysis 674 palpable 640 power analysis 674–5 pulse oximetry 638 Putti–Platt operation 355–6 pyknodysostosis 167 Pyle’s disease 166 pyogenic (suppurative) infection bone, acute and chronic 29 joint, acute (=acute suppurative arthritis) 43–6 acute osteomyelitis complicated by 36 acute osteomyelitis vs 34, 44 hip 520 knee 577 spine/vertebrae (incl. osteomyelitis) 470–1 cervical 448–9 tendon sheaths in hand 433 wounds 38 pyridinium compounds, excretion, measurement 131 pyrophosphate, dietary, affecting bone 127 pyrophosphate arthropathy (crystal deposition), chronic 79, 80, 81 elbow 375 see also pseudogout Q angle see quadriceps angle quadriceps contractures 564 tendon rupture 885–6 wasting 548 quadriceps (Q) angle 548 in patellar chondromalacia 565–6 quadriceps active test 881 quadriplegia 230 traumatic, management 827–8 quadruple immobilization (spinal injury) 806 quantitative CT 25, 130 quantitative ultrasonometry 25 Quikclot™ 656 race see ethnicity radial artery compression, testing 439 radial nerve lesions 282, 392

compressive 291–2 in humeral shaft fractures 748–9 leprosy 45, 55, 296, 298 regional anatomy elbow 381 hand 437 wrist 410 radial tunnel syndrome 292 radiation, ionizing (irradiation) complications necrosis 112–13 nerve damage 295 intraoperative exposure to 304 radical resections of tumour 192–3 radiculography, disc prolapse 479–80 radiculopathy (nerve root disease/lesions) 256 in cervical spondylosis 446 in disc prolapse 478–9, 479 peripheral entrapment vs 234 radio-capitellar joint dislocation 770 radio-carpal joint 393 arthrodesis 399 chronic instability 394–7 dislocation 786 fractures 776–8 osteoarthritis 402–3 radio-carpal ligaments, dorsal 411 radiographs, plain see X-rays radiology see imaging and specific modalities radio-lunate ligaments 411 radionuclide scans (radioscintigraphy incl. bone scans) 23–4 ankle/foot 591 tarsal coalition 598 arthritis (acute suppurative) 44 back 457 pyogenic spinal osteomyelitis 471 fractures 693 Gaucher’s disease 178 hip 497 knee 553 osteochondritis dissecans 567 osteoarthritis 92 osteomyelitis acute 33 chronic 39 pyogenic, spine 471 osteonecrosis 106–7 tumours 189 Ewing’s sarcoma 212 metastases 217 osteoblastoma 196 osteosarcoma 208 wrist 386 radio-scapho-capitate ligament 411 radio-scapho-lunate ligament 411 radiotherapy 194 Ewing’s sarcoma 213 metastatic bone disease, palliative 217, 218 soft-tissue tumours 219 radio-ulnar joint distal/inferior 392–3 in Galeazzi’s fracture, dislocation 771–2 injuries (generally) 784 instability 393 osteoarthritis 403

INDEX

prepatellar bursitis 578 pressure(s), foot, assessment 591 see also compression pressure sores 715–16 in bed 720 plaster casts 699, 715 previous history see past medical history PRICE (protection, rest, ice, compression, elevation), ankle ligament injury 909 primary survey (major trauma) 636, 637–8 adjuncts 638–40 head injury in 661 proliferative phase of fracture healing 690 pronation 9 foot 623 forearm see forearm wrist 385 prone (lying) back examination 455 hip examination 496 knee examination 552–3 prostate, bone metastases from, palliation 217 prosthetics and implants 327–8, 328–31 amputation 327–8 fibular deficiency 185 arthroplasty 330, 331 hip see subheading below complications 329–30 hip arthroplasty 539–40 femoral shaft fracture risk 865 in limb salvage with tumours 193 materials 328–9 scoliosis (idiopathic) 463–4 failure 465 protective equipment, personal 629–30 proteoglycans 85, 87 protrusio acetabuli 507–8 provocative tests/movements 7 wrist 385 carpal instability 395 proximal (definition of term) 9 pseudarthrosis congenital clavicular 183, 362–3 tibial 176, 183–4 instrumented spine in idiopathic scoliosis 465 in non-united fracture 692 pseudoachondroplasia 168 multiple epiphyseal dysplasia vs 159 pseudoclaudication plus back pain 488 pseudogout (calcium pyrophosphate deposition disease) 80–2 differential diagnosis 63 acute suppurative osteomyelitis vs 45 gout 79, 81, 82 elbow 375 pseudo-vitamin D deficient rickets 138 psoas muscle abscess acute suppurative arthritis vs 44 in Crohn’s disease 73 lesser trochanteric avulsed by pull of 857 psoriatic arthritis 71–2 differential diagnosis 72 ankylosing spondylitis 69 osteoarthritis 95 hand/fingers 420

965

INDEX 966

radio-ulnar joint – contd distal/inferior – contd reduction 772 subluxation 392, 772, 776 testing 385 proximal, dislocation (in Monteggia’s fracture) 736–7 synostosis 183, 371 post-traumatic 377 radius deviation 385, 410 distal, dorsal malunions 397 dysplasia and deficiency 182–3, 387–8 head dislocation acquired/unreduced 372, 757, 808–9 congenital 371 head subluxation (pulled elbow) 373–4 child 765 longitudinal instability 394 styloid process excision in osteoarthritis 402 radius fracture 767–70 children 765, 767–8, 769–70 distal 772–6 children 775–6 Galeazzi’s (with dislocation of inferior radio-ulnar joint) 771–2 head 752–3 isolated 769, 769 neck 753–4, 765 children 765 styloid 776–7 range of movement/motion assessing (general aspects) 7 hip 495, 496, 497 femoro-acetabular impingement and 524–5 wrist 410 RANK (receptor activator of nuclear factor-kB) and RANKL 120, 122, 124 monoclonal antibody to RANKL in postmenopausal osteoporosis 133 Ranvier’s nodes 225, 270 Raynaud’s disease 435 reactive arthritis see Reiter’s disease realignment osteotomy knee osteoarthritis 573 rheumatoid arthritis 572 osteoarthritis 96 hip 524 osteonecrosis, hip 532 realignment procedures (in general) patellar chondromalacia 566 in recurrent patellar dislocation 563 rearfoot see heel; hindfoot recessive disorders autosomal 153 X-linked 153 recognition in major trauma see awareness– recognition–management recruitment (motor unit) 233–4 rectal examination in pelvic injury 830 reduction acromioclavicular joint injuries 738 failed 739 developmental dysplasia of hip 501 failed 503

disc prolapse (acute) 445, 481 elbow dislocations, failed 757 facet joint dislocation 818 fracture 695–6 calcaneal displaced intra-articular fractures 928 femoral distal epiphyseal fracture– separation 872 femoral intertrochanteric fractures 854 femoral neck fractures 849 femoral shaft fractures in adults 861–2 femoral shaft fractures in children 869 femoral subtrochanteric 858–9 malleolar, incomplete 916 pelvic 836, 840 radial distal 773 radial shaft (in Galeazzi’s fracture– dislocation) 771–2 talar neck 922–3 tibial plateau 894 tibial proximal epiphyseal fracture– separation 896 hip dislocation anterior 844 failure 846 posterior 846 humeral lateral condylar fractures in children 763 humeral medial condylar fractures in children 764 humeral supracondylar fractures in children 759, 760 lunate/perilunate dislocations 785 shoulder dislocation (anterior) 740 failed 740 shoulder dislocation (inferior) 744 shoulder dislocation (posterior) 743 failed 743 slipped capital femoral epiphysis 518–19 see also hold reduction referral (consultation), burns specialist 669 reflex(es) 226 tendon see tendon reflexes testing 10–11 cerebral palsy 237 in spinal trauma 808 reflex sympathetic dystrophy see complex regional pain syndrome regeneration, axonal 271 regional aspects (orthopaedics) see locoregional aspects regional trauma services 634–5 Reiter’s disease and reactive arthritis 70–1 differential diagnosis 71, 72 ankylosing spondylitis 69 brucellosis 53 gout 71, 79 rheumatoid arthritis 63 renal organ see kidney repetitive stress injury, wrist pain 407 replantation (in accidental amputation) finger/thumb 800–1 limb 325 research, intensive care unit scoring systems 682–3

resection (excision) of bone tumours 192–3 see also specific tumours respiratory distress syndrome, adult see adult respiratory distress syndrome respiratory tract/system injury 647–51 in multiple organ failure 678 in shock, assessment 674 rest disc prolapse (acute) 445, 481 hand infections 431 tuberculosis 52 spinal 474 see also PRICE; RICE resurfacing arthroplasty see hemiarthroplasty resuscitation ABCDE of see ABC(DE) sequence major trauma 637–8 head injury 662 pre-hospital 629 shock 677 reticulum cell sarcoma 213 retropharyngeal space in children, increased 813 retroversion, femoral 507 revascularization in Perthes’ disease 513 reverse (polarity) shoulder arthroplasty 365 cuff tear 365 reverse pivot shift 881 re-warming in hypothermia 671 rhabdomyoma 223 rhabdomyosarcoma 223 rheumatic disorders inflammatory 59–76 in pregnancy 149 rheumatic fever (rheumatism), acute, differential diagnosis acute osteomyelitis 34 acute suppurative arthritis vs 45 tuberculosis 51 rheumatoid arthritis 59–66, 359–60, 374, 399–401, 450–1, 521–2, 571–2, 610–11 ankle/foot 610–11 cause 59–60 cervical spine 450–1 clinical features 61–2, 360, 374, 400, 424, 450, 521–2, 571 complications 66 elbow 374, 380 gout vs 63, 79 hand/fingers 420, 424–9 hip 521–2 investigations and diagnosis 62–4, 360, 400 blood tests 26, 62 juvenile see juvenile idiopathic arthritis knee 570, 571–2, 577 osteoarthritis vs 64, 95 pathology 60–1, 399–400 prognosis 66 shoulder 359–60 treatment 64–6, 360, 400–1, 450, 522, 571–2, 610–11 wrist 392, 399–401 rheumatoid factor 26, 60, 62 diagnostic value 63

rheumatoid nodules 60–1, 62, 424–5 rhizomelia 155 rhizotomy, selective dorsal, cerebral palsy 240 rib cervical 293 hump (in scoliosis) 464 RICE (rest, ice, compression, elevation), ankle ligament injury 909 rickets 129, 135–40 hypophosphataemic 139–40 vitamin D-dependent 138–9 vitamin D-resistant 138 rigidity see stiffness ring avulsion 799 Risser’s sign 461 road accidents (cars; motor vehicles) seat belt injuries see seat-belt injuries whiplash injury 820–1 rocker-bottom deformity 593, 614 rod instrumentation, idiopathic scoliosis 463–4 Rolando’s fracture 790 Romberg’s sign 12 Roos’s test 293 rotation centre of rotation of angulation (CORA) 313–14 displacement and deformity by atlanto-axial 442–3 fractures see subheading below hand 788 fractures (malrotation) 689, 694, 718 elbow, children 759–60 hip 495–6 internal see internal rotation knee 549 instability 876, 877 lateral and medial 9 shoulder (assessment) 339, 345 see also flexion–rotation injuries rotational alignment, definition 9 rotationplasty, proximal femoral deficiency 510 rotator cuff 366–7 lesions/dysfunction 341–9 acute disc prolapse vs 445 cervical spondylosis vs 446 in osteoarthritis 93 in shoulder dislocation 741 thoracic outlet syndrome vs 294 rotator cuff syndrome 341 in acromioclavicular injury 739 rule of nines (burns) 667, 668 rupture see injury Russell’s traction, femoral shaft fractures 861

adolescent 460, 461, 462–5 patterns 461 neurofibromatosis 175, 467 spina bifida 250, 251 screening maternal see maternal screening neonatal, developmental dysplasia of hip 500 screw fixation 314–15, 701, 701–2 femur intertrochanteric fractures 854 neck fractures 850 shaft fractures 862 pelvic fractures 836 plate and (principles) 315–16, 701–2 tibial plateau fractures 892 scurvy 142–3 seat-belt injuries 820 lap belt 824 ‘second hit phenomenon’ femoral shaft fractures 860, 861 secondary survey (major trauma) 636, 639–40 segmental fracture femoral shaft 859 tibia and fibula combined fractures 900 segmental spinal instability 482 segmental spinal instrumentation in thoracolumbar trauma 811 Segond fracture 878, 884 selective decontamination of gut in multiple organ failure 680 selective dorsal rhizotomy, cerebral palsy 240 semimembranosus bursitis 578 semi-rigid cervical collars 810 sensibility/sensation 230 assessment (principles) 12, 230 cerebral palsy, assessment 238 hand, assessment 413 open injuries 796 history-taking of changes in 5 see also anaesthesia; numbness; paraesthesia sensory nerves 225, 226, 269 action potential see action potential conduction studies 232 sensory neuropathy hereditary 258 hereditary motor and 258 sepsis, multiple organ failure 676, 677–8 septic (infective) arthritis 43–6 acute suppurative see pyogenic infection brucellosis 52, 53 differential diagnosis 44–5 pseudogout 82 Reiter’s syndrome 71 hand 434 hip see hip HIV-1 and 46 inflammatory bowel disease 73 knee 577 MRI 22 Reiter’s syndrome vs 71 in sickle cell disease 111 sternoclavicular joint 363 synovial fluid analysis 26 syphilitic 47 tuberculous 49, 52 septic non-union 692

INDEX

sacral nerve roots compression in ankylosing spondylitis 70 innervation and consequence of injuries 826 sacroiliac joints in ankylosing spondylitis 67, 68 iliac bones adjacent to, osteitis condensans 149 sacroiliac pain (with pelvic fracture), persistent 837 sacroiliitis in inflammatory bowel disease 73

sacrum agenesis 181–2 injuries 841 safety in major trauma helicopter 634 at scene 629–30 sagittal plane 9 saline, hypertonic, in shock 658 Salter–Harris classification of physeal injuries 727–8 ankle 918 femur (distal) 872 tibia (proximal) 895 Salter–Thompson classification, Perthes’ disease 514 sarcoidosis 64 sarcoma bone 205–11 giant-cell 204 Paget’s disease 146, 210–11 reticulum cell 213 staging/grading 191 stress fracture vs 190, 724 soft-tissue 219, 220, 220–1, 223 chemotherapy 218 scalp injury 659 scaphoid 393 avascular necrosis 399 excision in osteoarthritis 402 fracture 780–3 see also trans-scaphoid perilunate dislocations scaphoid–trapezium–trapezoid arthritis 404–6 scapho-lunate dissociation 396 scapho-lunate joint dislocation 785–6 incompetence 395 testing 385, 395 scapho-lunate ligament failure (SLAC wrist) 402 scapula congenital elevation 181, 361–2 fractures 735–7 grating 363 instability 362–3 scapulothoracic dissociation 737 scene (of major trauma), safety on 629–30 Scheuermann’s disease 467, 468–9 Schmid-type metaphyseal chondrodysplasia 164 Schwann cells 225, 270 schwannoma see neurilemmoma sciatic nerve injury/palsy 285–6 in hip arthroplasty 286, 536 in hip dislocation 845 in pelvic fracture 837, 840 sciatic pain (sciatica) 453, 487 persistent postoperative 481 stretch tests eliciting 455, 456 scintigraphy (radionuclide scans) 23–4 SCIWORA (spinal cord injury without radiographic abnormality) 640 children 813 scleroderma, fingers 420 sclerosing osteomyelitis, Garré’s 41 scoliosis 14, 453, 458–67 cerebral palsy 239, 244 idiopathic 462–5

967

INDEX 968

septic shock 654, 655, 673 septic tarsal disorganization in leprosy 300 seronegative arthropathies/inflammatory spondyloarthropathies 66–73 ankle/foot 611 differential diagnosis 63 disc prolapse 480 in juvenile idiopathic arthritis 74 sesamoids (forefoot) fractures 932–3 sesamoiditis 620 Sever’s disease 617 sex chromosomes 151 numerical anomalies 180 single gene disorders 153 see also X chromosome; Y chromosome shape bone, radiography 16–17 joint, radiography 18 observing (body/limb etc.) 6 fracture 694 knee/patella 548, 549 shoulder 337 shearing stress, fracture caused by 724 pelvic ring (vertical shear; VS) 833, 834, 836 shifting (translation) of fracture 689, 694 Shimuzu grading of non-traumatic osteonecrosis 531–2 shingles 259 shock, circulatory 654–8, 673–6 classes 655 diagnosis 673–4 femoral shaft fractures 866 major trauma cases 654–8 prehospital management 632 management 675–6 monitoring systems 674 multiple organ failure in 677 pelvic fractures 835 spinal trauma 807 shock, spinal 246, 808 shoes, looking at 590 short-stemmed hip implants 541 shortening (pathological) in femoral shaft fractures 869–70 of intrinsic hand muscles 418 shortening (procedure) of longer bone 322–3 shortness (undergrowth) fingers 390 legs see length, leg, discrepancies neck, congenital 180–1, 362, 443 stature see stature toenails 623 shotgun injuries 711 shoulder (and pectoral girdle) 337–68 anatomy 366–7 arthroscopy (diagnostic) 28, 341, 365 clinical assessment 337–68 disarticulation at 327 disorders 341–64 injuries 733–44 fractures causing secondary 694–5 instability following 354–6 operations 364–5 arthrodesis see arthrodesis poliomyelitis 254 rapidly destructive arthritis see Milwaukee shoulder

sickle cell disease acute osteomyelitis in 111 management 35 acute osteomyelitis vs sickle cell crisis 34 acute suppurative osteomyelitis vs 45 osteonecrosis in 110–11 side-swipe elbow injuries 756 signs ankle/foot 587–90 back 453 elbow/forearm 369–71 fractures 693 hand 414 hip 493–6 knee 547–63 neck 439–40 shoulder 337–9 wrist 373–5 see also specific disorders Silfverskiöld test 238 silicon implants 330–1 Simmond calf squeeze test 615 Simplified Acute Physiology Score (SAPS) 683 Sinding-Larsen and Johansson syndrome 576 single energy x-ray absorptiometry 130 single-event multilevel surgery in cerebral palsy 243 single gene disorders 152 inheritance patterns 152–4 single photon emission computed tomography (SPECT) 24 sinography 19 sitting ankle/foot examination 588–90 cerebral palsy, posture 237 hip examination/signs 494 knee examination 548 skeletal dysplasia see dysplasia skeletal fixation see fixation skeletal maturity assessment in scoliosis 461 skeletal muscle see muscle skeletal traction with fractures 697 femoral shaft 861 humeral shaft 752 tibial plateau 892 skier’s thumb 795–6 skin amputation-related complications 328 ankle/foot disorders 621–2 examination 588–9 contractures 14 hand 418 feeling 7 with fractures in casts, abrasion/laceration 699 closed fractures of tibia and fibular 897 open fractures, management 709–10 traction see subheading below hand anatomy 436–7 contractures 418 hand, cover with injuries 787 delayed 801–2 observing 6

surgeon’s, cleaning 306 temperature, knee area 548 traction (with fractures) 697 femoral shaft fractures 861 in traumatic paraplegia/quadriplegia, care 827 skin flaps (amputation), breakdown 328 skull (in head injury) anatomy 659 basal fractures 660 traction, in cervical facet joint dislocation 817 SLAP lesions 350–1 slipped capital femoral epiphysis 511, 515–19 Smith’s fracture 774–5 snapping hip 493, 533–4 social history, recording 5–6 soft cervical collars 810 soft tissues in chronic osteomyelitis, cover 41 contractures see contractures feeling 7 in fractures care 704, 705 classification of injuries caused by fractures see Tscherne classification delayed union due to damage 716 external fixation causing damage 704 of femoral shaft, injuries 860, 864–5 tibia–fibular combined fractures and state of 897 treatment classification of injuries caused by fractures 711–14 haematoma, tumour vs 190 infrapatellar, realignment 563 neck, strain 445 radiographs of generalized vs localized change 16 shoulder, feel 338 swelling see swelling tumours 218–23 staging 191 see also viscera soleus muscle tear 615 somatic nervous system 225, 226 somatosensory evoked potentials, intraoperative 234–5 somatotropin see growth hormone sonography see ultrasonography spasmodic torticollis 451 spasticity (and spastic paresis/palsy) adult-acquired spastic paresis 244 in cerebral palsy 235, 241–2 foot 616 gait with 229 hand 421 see also peroneal spastic flat-foot specialist, burns, consultation 669 spica cast, femoral shaft fractures 861, 862 spina bifida 247–52 spinal accessory nerve lesion 280–1 scapular instability 363 spinal canal (vertebral canal) anatomy 490 stenosis 247, 448, 486–7 cervical 448 lumbar 486–7

developmental dysplasia of hip 500, 501, 501–2, 502 fractures 698–9, 705 delayed union relating to 716 femoral shaft 861 hand infections 431 open 799–800 hand injuries 787 see also cast spondylitis ankylosing see ankylosing spondylitis in inflammatory bowel disease 73 tuberculous see tuberculosis spondyloarthropathies, seronegative see seronegative arthropathies spondyloepiphyseal dysplasia 159–60, 469 spondylolisthesis 484–6 in osteoarthritis 93 spondylolysis 484 traumatic 822 spondylometaphyseal dysplasia 168 spondylosis 477 cervical 445–6 differential diagnosis 294, 446–7 Sporothrix schenckii 435 spotted bones 167 sprains 730 ankle 907 recurrent 909–10 knee 878 neck 820–1 spread of tumour distant see metastatic bone tumours local 191 Sprengel deformity 181, 361–2 Spurling’s test 439 stab wounds, abdomen 663 stability ankle/foot, assessment 589–90 elbow, assessment 370 knee, assessment 551–2, 877 shoulder, anatomy relating to 366 in tibia and fibula combined fractures 897 see also instability stabilization (physical/surgical) ankle ligament injury 909 spinal trauma thoracolumbar injuries 811 urgent 809 see also fixation; hold reduction; immobilization stabilization (physiological) of major trauma cases 628 staging of bone tumours 140–2 chondrosarcoma 191, 207 giant-cell tumour 203 osteosarcoma 191, 208 stainless steel implants 328–9 stance phase of gait ankle/foot in 587 knee in 548 standing/upright stance ankle/foot examination 587–8 back examination 453–4 in cerebral palsy, posture 237 hip examination 494–5 knee examination 548 Stanmore Instability Classification system 353

Staphylococcus aureus, methicillin-resistant, treatment of acute osteomyelitis in patients at risk of 35 stapling of physes (either side of knee) 555 stature, shortness/small with disproportionate shortness of limbs 155 normal proportions 155 surgical treatment 323 steal syndromes, Paget’s disease 144 stellate fracture, patella 887–8 sterility with open fractures 706–7 sternoclavicular hyperostosis 363–4 sternoclavicular joint dislocations 739 movements 367 septic arthritis 363 sterno-costo-clavicular hyperostosis 42, 364 sternomastoid, bilateral shortness 362 steroids see corticosteroids stiffness/rigidity ankle or foot flat-foot 597, 597–8 hallux (=hallux rigidus) 606–7 malleolar fractures 916 tibia and fibula combined fractures 904 assessment (in general) 15 back 456 elbow 369, 376–7 elbow, post-traumatic 376–7 Colles’ fracture 774 with fracture–dislocations of elbow 756–7 humeral distal fractures 752 humeral supracondylar fractures, children 761 with fractures in casts 698 hip 493 history-taking 4 knee 547 femoral shaft fractures 867 femoral supracondylar fractures 871 knee dislocation 885 tibial plateau fractures 895 neck 439 osteoarthritis 91 post-traumatic 722 rheumatoid arthritis 61 shoulder 337 in clavicular fracture 735 in Colles’ fracture 774 differential diagnosis 352 in humeral proximal fracture– dislocation 747 in humeral shaft fractures 750 in shoulder dislocation 741 wrist 373 in Colles’ fracture 774 Still’s disease (systemic juvenile idiopathic arthritis) 73, 74 Stimson’s technique (shoulder reduction) 740 stippled epiphyses (Conradi’s disease) 161, 162 stocking, compression, perioperative 309– 10 Stokes–Gritti operation 327

INDEX

osteoarthritis 93 Paget’s disease 146 spinal column (spine; vertebral column) anatomy 489 cervical see cervical spine deformities 13–14 in cerebral palsy 239, 244 developmental see subheading below in neurofibromatosis type-1 175–6 in spina bifida 250–1 in trauma, surgical correction 809 degenerative disease see degeneration developmental/congenital anomalies 180–2 management 157 fusion see arthrodesis lumbar see lumbar spine metastases 218 nerve roots see nerve roots thoracic and lumbar see lumbar spine; thoracic spine; thoracolumbar spine trauma 664–5, 805–28 definitive treatment 831–2 diagnosis 806–9 early management 806 examination 807–9 fractures see fractures healing 806 mechanisms 805–6 methods of treatment 810–11 pathophysiology 805 tuberculosis see tuberculosis see also back; vertebrae spinal cord 490 compression in ankylosing spondylitis 70 in rheumatoid arthritis 66 contrast radiography 20 functional assessment 808 injury/trauma (neurological injury/ deficits in spinal trauma) 246–7, 805, 810, 819, 825–8 cervical 819 complete vs incomplete lesions 826 failure following (=spinal shock) 246, 807–8 fractures causing 694 thoracolumbar 822–3, 825 without radiographic abnormality see SCIWORA lesions 245–7 neoplastic 247 traumatic see subheading above monitoring during surgery 234–5 tethering 249, 250–1 spinal dysraphism see neural tube defects spinal muscular atrophy 255 spinous process (cervical vertebrae), avulsion injury 819, 819 spiral fractures 687, 688, 694 femoral shaft 859 hand metacarpal 788 phalanges 790, 791 spirochaetal infections 46–8, 64 splenomegaly, rheumatoid arthritis 61 splintage acute osteomyelitis 34 acute suppurative arthritis 45 cerebral palsy 240

969

INDEX 970

storage disorders 158, 176–9 straight-leg raising test 255, 256 strains see ligaments strength bone 128–9 grip see grip streptococcal necrotizing myositis vs acute osteomyelitis 34 stress (mechanical) 127 pelvis 832 tibia or fibula 31 Wolff’s law and 123, 127, 688 see also repetitive stress injury; tension– stress principle stress fracture (fatigue fracture) 688, 724–5 differential diagnosis 724 tumour vs 190, 724 metatarsal 621, 932 tibia or fibula 905 stress X-rays ankle/foot 591 knee 878 stretch reflex 226 striped bones 167 stroke, spastic paresis 244 structural deformities examination for 14 spine kyphosis 467 scoliosis 458–60, 462 styloid process, radial excision in osteoarthritis 402 fracture 776–7 subacromial bursa, rheumatoid arthritis 359 subcondylar fractures of tibia 891 subcutaneous fascia see fascia subcutaneous infections 432–3 subdural haematoma, traumatic 661 sublaminar wiring, idiopathic scoliosis 464 subluxation hip 504–6 cerebral palsy 242, 243–4 patellar, recurrent 564 radial head 371–2 radio-ulnar joint (distal) 392, 772, 776 shoulder 353 inferior 357 posterior 357–8, 743 recurrent 354, 355, 358, 743 traumatic causes 354 wrist/carpus 784–5 see also fracture–dislocation or subluxation subscapularis assessment 345–6 subtalar joint movements 589 subtrochanteric fractures 857–9 Sudek’s atrophy see complex regional pain syndrome superficial fibromatosis 219–20 superficial mycoses 56 hand 435 superficial reflexes 11 supination 9 foot 623 forearm 381 wrist 385 supine (lying)

back examination 455–6 knee examination 548–52 support, lumbar, in facet joint dysfunction 483 supportive treatment acute osteomyelitis 34 acute suppurative arthritis 45 suppurative infection see pyogenic infection supracondylar fractures femur 870–1 humerus see humerus supracondylar osteotomy knee deformities 580 children 556 rheumatoid arthritis 572 supra-glottic airway 643, 645 suprapatellar realignment 563 suprascapsular nerve lesion 281 compressive 292–3 supraspinatus muscle 367 tendinitis see tendinitis weakness, testing 345 X-ray 346 surface area, body, burns 667, 668 surgery (operation) 303–33 adrenocortical dysfunction 148 ankylosing spondylitis 69 arthrogryposis 264 back failed 484 persistent back pain following 481 brucellosis 53 cerebral palsy 240, 241–3, 244 fetal see intrauterine surgery in genetic and developmental disorders 157 achondroplasia 164 clavicular pseudarthrosis 183 Down’s syndrome 180 enchondromatosis 165 femoral deficiency 184 fibular deficiency 185 hereditary multiple exostoses 163 intrauterine 157 Klippel–Feil syndrome 181 osteogenesis imperfecta 174 Sprengel deformity 181 tibial bowing 186 of wrist/hand, indications 387 gout 80 haemophilic arthropathy 101 hydatid cysts 58 juvenile idiopathic arthritis 75 neurophysiological studies during 234–5 osteoarthritis 96 osteomyelitis (chronic) 40–1 osteonecrosis 109 Paget’s disease 146 peripheral nerve injuries 274–6 brachial plexopathy 278–9 brachial plexopathy from birth trauma 280 leprosy 55, 296–301 median nerve 285, 289 supracapsular nerve 293 thoracic outlet syndrome 294 ulnar nerve 284, 291 peripheral nerve injuries caused by 295

preparation for 303 psoriatic arthritis 72 regional operations back see subheading above elbow 380–1 hand, secondary 801–2 hip 534–42 knee 579–82 shoulder see shoulder rheumatoid arthritis 65–6 tuberculosis 52 tumour 192–3 adamantinoma 215 aneurysmal bone cyst 202 chondroblastoma 198 chondroma 197 chondromyxoid fibroma 199 chondrosarcoma 207 chordoma 215 compact osteoma 197 eosinophilic granuloma 204 Ewing’s sarcoma 213 fibromatosis 220 fibrosarcoma of bone 211 fibrosarcoma of connective tissue 220 fibrous dysplasia 195–6 giant-cell tumour 203 metastatic bone disease, palliative 218 multiple myeloma 215 neurosarcoma 223 osteoblastoma 197 osteoid osteoma 196 osteosarcoma 208–10, 210 rhabdomyosarcoma 223 solitary bone cyst 201 synovial tumours 221 swan-neck deformity 419–20, 792 rheumatoid arthritis 425, 426, 427, 428 swelling ankle/foot 587, 920–1 calcaneal fractures 928 pilon fractures 917 bone marrow (fat cell), osteonecrosis due to 104 elbow 369 hand 413 injured 787 history-taking 4 joint acute (after injury), synovial fluid analysis 26 in osteoarthritis 91 knee 547, 576–9 shoulder 337 tumour 188 wrist 373, 407–8 swing phase of gait, knee in 548 symbrachydactyly 387, 389 Syme’s amputation 327 sympathetic nervous system 226 blood vessel innervation 270 symphalangism 391 symptoms ankle/foot 587 back 453 elbow/forearm 369 fractures 692

hand 413 hip 493 in Perthes’ disease, treatment 514 history-taking 3–4 knee 547 neck 439 shoulder 337 wrist 373 see also specific disorders synapse 225 synchondrosis mistaken for fracture 813 syndactyly, fingers 389 synostosis cervical vertebral (Klippel–Feil syndrome) 180–1, 362, 443 radio-ulnar see radio-ulnar joint wrist 389 synovial fluid 86 aspirates see biopsy synovial joints (diarthrodial joints) 117 physiology 85–7 synovial membrane (synovium) 86 knee chondromatosis 569 swelling due to disorders of 577–8 thickening 549 wrist, ganglion 408 synovial sheath see tendon sheath synovial tumours 220–1 synovitis acute atraumatic and chronic synovitis, synovial fluid analysis 26 hip, tuberculous 511, 520–1 knee aseptic non-traumatic 577 post-traumatic 577 tuberculous 577–8 pigmented villonodular 220 in pseudogout, acute 80, 81 in rheumatoid arthritis 60 ankle 610, 611 chronic 60 hand 426 shoulder 359 transient see irritable joint see also tenosynovitis syphilis 46–8, 247 syringomyelia 247 systemic disorders/illness in juvenile idiopathic arthritis 73, 74 osteonecrosis associated with 110–14 systemic inflammatory response syndrome (SIRS) 677–8, 678, 679 systemic lupus erythematosus 75–6 hand/fingers 420 systemic management in major trauma 641–72 systemic vascular resistance in shock, reduced 673

giant-cell tumour 220 inflammation see tenosynovitis tennis elbow (lateral epicondalgia) 378 radial tunnel syndrome resembling 292 tenodesis, knee area 579 tenolysis, hand injuries 802 tenosynovectomy in rheumatoid arthritis, extensor 401 tenosynovitis/tenovaginitis ankle 616 hand 428 flexor tendons 401, 423–4, 428 in rheumatoid arthritis 401, 428 suppurative 433 in tuberculosis 434 rheumatoid arthritis 61 hand 401, 428 shoulder 359 wrist 406–7, 408 tension fractures caused by 688 neck 439 nerve, deformity correction causing 314 tension-band plates 702 tension-band wires 701 tension pneumothorax 638, 648–9 tension–stress principle, soft-tissue contractures 321 tensor fasciae femoris 542–3 Terry Thomas sign 396 testicular dysfunction in old age, bone loss due to 135 Testut’s ligament 411 tetanus 681 tethering of spinal cord 249, 250–1 tetraplegia (quadriplegia) 230 thenar eminence wasting 284 thenar space abscess 433 Therapeutic Intervention Scoring System (TISS) 684 thermal injuries see burns; cold injury Thessaly test 552 thigh, compression of lateral cutaneous nerve of 294 Thomas splint, femoral shaft fractures 861 Thomas test 495 Thompson calf squeeze test 615 Thompson–Epstein classification of hip dislocation 844 thoracic nerve lesions, long 280 thoracic outlet syndrome 288 cervical spondylosis vs 294, 446–7 compression causing 292–3 thoracic spine congenital anomalies 181 cord compression 245 root transection 826 see also back; thoracolumbar spine thoracocentesis (needle decompression), tension pneumothorax 648–9 thoracolumbar spine injury 821–5 immobilization 806 root transection 826 Scheuermann’s disease 469 thorax see chest drain; chest injuries thorn prick, infection 430

INDEX

tabes dorsalis 247 tailor’s bunion 609 talipes deformities see pes (and talipes) deformities talocalcaneal joint calcaneal fracture-related complications 928 fracture–dislocation 921 injuries involving articular surfaces 924–5, 927–8

talofibular ligament, anterior 907 strain 908 talus avascular necrosis/osteonecrosis 612, 617 congenital vertical 596 injuries 921–4 osteochondritis dissecans 611–12, 616–17 tilt test 909 tamponade, cardiac 632, 649 taper slip of cemented hip implants 539 tapeworms 57–8, 475–6 TAR (thrombocytopenia with absent radius) syndrome 182 tarsal tunnel syndrome 294, 621 tarso-metatarsal injuries 930–1 tarsus coalition 597–8 neuropathic disorganization in leprosy 300 teams, trauma 635 tear see injury tear-drop fracture 816–17, 817 technetium-99m scans of bone 23–4 tumours 189 teenagers see adolescents temperature bone formation and effects of 127 skin, knee area 548 tenderness ankle/foot, site related to cause 590 bony lumps 15 feeling for 7 osteoarthritis, local 91 tendinitis Achilles 614–15 adductor longus 533 biceps 349 gluteus medius 533 knee area 576 post-traumatic 721 supraspinatus 343–4 acute calcific 348 see also tenosynovitis tendon(s) in ankylosing spondylitis 67 avulsion injuries distal biceps 379–80 fingers 792, 792–3 tumours vs 190 in Colles’ fracture, rupture 775 cut (in open fractures), management 708 finger 437 testing 416 hand assessment in open injury 797 injuries 787, 792, 792–3 lesions 418–20 repair of injuries 798–9, 802 knee region, injuries 885–6 in rheumatoid arthritis 60, 61 transfers see transfer (tissue) tendon reflexes 226 testing 10–11 spinal trauma 808 tendon sheath, synovial biceps (long head), rheumatoid arthritis 359

971

INDEX 972

three-dimensional CT clavicular fractures 733 humeral fractures (proximal) 745 pelvis 831 fractures 839 spinal trauma 809 thrombin inhibitors 310 thrombocytopenia with absent radius syndrome 182 thromboembolism pelvic fractures 837 prophylaxis 307–10 see also embolism; thrombosis thrombophilia, inherited, and Perthes’ disease 511 thrombosis deep venous see venous thrombosis osteonecrosis associated with 104 ulnar artery 435 thumb carpo-metacarpal dislocation 793 metacarpal fracture 789 metacarpo-phalangeal instability, chronic 793 movements 415 replantation 800–1 ulnar collateral ligament see ulnar collateral ligament thumb deformity congenital 391, 417 duplications 390 hypoplasia 390 in radial dysplasia 388 poliomyelitis 254 in rheumatoid arthritis 427 in spastic paresis (incl. cerebral palsy) 241, 421 traumatic 795–6 in ulnar and median nerve palsy (in leprosy) 297 in ulnar palsy (in leprosy) 296–7 thyroid disorders see hyperthyroidism; hypothyroidism thyroxine 127 tibia amputation through 327 apophyseal stress lesion (Osgood– Schlatter disease), tumour vs 190 bowing 186 dysplasia 176, 185 fractures 30, 890–6 fatigue 905 and fibula combined 897 plateau 890–5 spine 560, 883–4 tubercle 887 physeal injuries in children 918 pseudarthrosis (congenital) 176, 185–6 torsion in cerebral palsy, external 243 tubercle adolescent disorder see Osgood– Schlatter disease advancement operation (Maquet’s) 566 fractures 887 valgus osteotomy 580, 580–1 varus deformity (Blount’s disease) 556–7 tibial nerve lesions, posterior 287 compression in tarsal tunnel 294, 621

tibialis posterior pathology 598–9 pain 616 rheumatoid arthritis 610 tibio-femoral alignment 553 tibio-fibular joint distal 908 separation see diastasis proximal, dislocation 896–7 tibio-fibular ligament, inferior, tears 911–12 Tile’s classification of acetabular fractures 837 Tillaux fracture 918, 921 tilt see angulation tinea, hand 435 Tinel’s sign 12, 273 carpal tunnel syndrome 288–9 tissue typing 26 titanium alloy implants 329 TNF see tumour necrosis factor toes deformities 589, 603–11 big toes see hallux claw toes 255, 589, 601, 603, 608 lesser toes 607 in pes cavus 600–1 poliomyelitis 255 spina bifida 252 examining movements 589 fractures 932 nail disorders 622–3 tomography (plain) 20 tone (muscle) 226, 230 assessment 10, 230 cerebral palsy, management 239–40 see also dystonia; hypotonia; myotonia tongs, cervical injuries 810 tophaceous gout (and gouty tophi) 78, 79 foot 611 hand 420 osteoarthritis vs 95 torsion, tibial, in cerebral palsy, external 243 torticollis (wry neck) children 442–3 spasmodic 451 tourniquets 305–6 complications 306, 309 nerve injury 295 major trauma, management 656 prehospital 632 pressure 295, 305, 305–6 trabecular bone see cancellous bone tracheal intubation 645–6 tracheobronchial injury 650, 652 traction acetabular fracture 840 cervical facet joint dislocation 817 developmental dysplasia of hip 502 fractures 697 femoral shaft, adults 861 femoral shaft, children 869 humeral shaft 752 humeral supracondylar, children 760 tibial plateau 892, 894 nerve injury due to 295 traction (calcaneal) ‘apophysitis’ 617 traction injury to spine 806 transcervical fracture 847–8

transfemoral amputation 327 transfer (patient) in major trauma to burns unit 669 to hospital from scene 633–4 in hospital/between hospitals 640–1 transfer (tissue) nerve 275–6 brachial plexopathy 278–9 tendon 276 brachial plexopathy 279 club-foot 595 in traumatic paraplegia/quadriplegia 827–8 transfer metatarsalgia 606 transfixing wires 701 translation (shifting) of fracture 689, 694 transplantation and grafting bone 317–19 bone marrow, in Morquio’s syndrome 177 cartilage, in osteochondritis dissecans 568 nerve 275 brachial plexopathy 278 skin, hand injuries 802 trans-scaphoid perilunate dislocations 785 transtibial amputation 327 transverse arrest/deficiency in upper limb 183, 387 transverse fractures 687, 688, 694 femoral shaft 859 growth plate involvement 728 hand metacarpal 788 phalanges 790 olecranon 754 patellar 888 pelvis 838 tibia and fibula combined fractures 900 transverse plane 9 transverse process (thoracolumbar vertebrae), fractures 822 trapezial fracture 784, 784 trapezio-metacarpal joint osteoarthritis 403–4 trauma see injury Trendelenburg gait 229–30 Trendelenburg sign (standing) 493 Treponema pallidum infection 46–8 Treponema pertinue infection 48 Trethowan’s sign/line 516, 517 Trevor’s disease 160–1 triage hospital 637 pre-hospital 630 triangular fibrocartilage complex (TFCC) 392–3 disorders 394 injury 784 in Colles’ fracture 774 testing 385 triceps, deltoid tendon transfer to, in traumatic paraplegia/quadriplegia 828 trigger finger 423–4 trigger point injections in facet joint dysfunction 483 trigger thumb, congenital/infantile 391, 423, 424

tumour necrosis factor (TNF) inhibitors ankylosing spondylitis 69 psoriatic arthritis 72 SIRS/sepsis response and 678 Turner’s syndrome 180 twist (rotation) of fractures 689, 694, 718 two-point discrimination test 273 hand 273, 796 ulcer (and ulceration) decubitus (bed sores) 720 diabetic neuropathic 614 hallux valgus, recurrent 606 trophic, leprosy 54, 55, 299–300 tropical 48–9 ulcerative colitis 73 ankylosing spondylitis vs 69 Reiter’s syndrome vs 71 ulna congenital anomalies 183, 388 deviation 385, 410 fracture 767–70 children 771, 775–6 isolated 769, 770 fracture–dislocation (Monteggia’s) 770–1 longitudinal instability 394 ulnar artery, thrombosis 435 ulnar collateral ligament of thumb injuries 795–6 in rheumatoid arthritis 426 ulnar motor nerve conduction 231 ulnar nerve anatomy elbow 381 hand 437 wrist 410 ulnar nerve injury 283–4 clinical features/assessment 283, 290–1, 369 compressive 283, 287, 288, 290–1 cervical spondylosis vs 446 thoracic outlet syndrome vs 294 humeral medial epicondylar separation in children 764 leprosy 54, 55, 296, 296–7 ulnar-side wrist injuries 784 ulno-carpal impaction syndrome 394 ulno-carpal ligament 411 ulno-humeral joint dislocation 755–6 ultra-high molecular weight polyethylene implants 330 ultrasonography 23 ankle/foot 591 arthritis acute suppurative 44 psoriatic 72 rheumatoid 62 fetal 155 hip 497 developmental dysplasia 23, 499, 500 slipped capital femoral epiphysis 517 major trauma 640 osteomyelitis (acute) 33 rotator cuff disorders 346 ultrasonometry, quantitative 25 uncemented hip implants 539–40 unconscious patient in spinal trauma, examination 808

undergrowth see shortness unicameral bone cyst 200–1 union (bone fracture) 692 problems see delayed union; malunion; non-union unlocked intramedullary nails 316 unstable joint see instability upper arm injuries 744–50 upper limbs (arm) 337–427, 733–803 adult-acquired spastic paresis 244 amputations 327 cerebral palsy 241 congenital anomalies 182–3 deformities (in general), treatment principles 245 elevation fractures 705 hand infections 431 injuries 733–803 nerve see subheading below nerve injuries 276–84 compression causing 288–94 weakness due to neck pathology 439 see also specific portions of limbs upper motor neuron lesions, foot paralysis 616 upright stance see standing urate crystal deposition (in gout) 77–8, 79 see also hyperuricaemia urethra anatomy 829–30 catheterization in major trauma 639 examination 830 imaging 832 injuries, management 835 urethritis, Reiter’s syndrome 70 uricosuric agents in gout 80 urinary tract anatomy 829 examination 830–1 imaging 832 injuries (in pelvic fracture), management 835, 837 vaccination (surgeon) 307 VACTERLS 182 valgus 13 see also specific valgus deformities e.g. calcaneovalgus; genu valgum valgus osteotomy hip, in coxa vara 509 knee region 580 valgus stresses on knee, extracapsular restraints to 875 varus 13 see also specific varus deformities e.g. genu varum varus osteotomy hip in osteoarthritis 535 knee region 580 vasculitis, rheumatoid arthritis 61, 66 see also blood supply; blood vessels vasoconstrictive shock 654 vasodilative shock 654, 673 vasopressors, shock 675 vena cava filter, inferior 310 venous cannulation, in shock 656–7 venous repair in open hand injuries 797 venous return in hypovolaemic shock 673

INDEX

triplane fracture (ankle) in children 918–19 triquetral fracture 784 triquetro-lunate dissociation 786 triscaphe arthritis 404–6 trisomy 21 (Down’s syndrome) 179–80 trochanter(s) fractures between 853–5 fractures of, isolated 857 trochanteric bursitis 533 trophic ulcers, leprosy 54, 55, 299–300 tropical ulcer 48–9 trunk deformities, poliomyelitis 254 Tscherne classification of closed injuries with fractures 695 of tibia and fibula combined 897 tubercle/tuberosity calcaneal, fracture 926 humeral (greater), fractures 746 scaphoid, fracture 782 tibial see tibia tuberculoid leprosy 53, 54, 260 tuberculosis 49–52, 472–5, 520–1 ankle 609–10 brucellosis vs 53 elbow 373–4 hand, tenosynovitis 434 hip 520–1 synovitis 511, 520–1 irritable joint (transient synovitis) vs 51, 511 knee 570–1 synovial 577–8 shoulder 358–9 vertebral/spinal (Pott’s disease; tuberculous spondylitis) 449, 72–5 adolescent kyphosis vs 469 wrist 399 tubules, renal defects, rickets/osteomalacia in 139, 140 PTH actions 126 tuft fracture 791 tumour(s)/neoplasms 187–224 benign see benign tumours biopsy see biopsy bone see bone tumours clinical presentation 188 osteomalacia 140 differential diagnosis 190 stress fracture 190, 724 fractures with 188, 725 intertrochanteric 855 metastatic bone disease see metastatic bone tumours multiple myeloma 215 investigations 188–9 knee area 562 malignant see malignant tumours management principles 192–4 parathyroid, causing hyperparathyroidism 140 PET scans 25 pituitary causing hyperpituitarism 147, 148 causing hypopituitarism 147 soft-tissue see soft tissue spinal/vertebral cervical spondylosis vs 446 disc prolapse vs 445, 480

973

INDEX

venous thrombosis, deep femoral shaft fractures 866 pelvic fractures 837, 840 perioperative risk 307–10 ventilation in major trauma, pre-hospital 632 ventral (definition of term) 9 vertebrae cervical 443–51 imaging 440–1 spinous process avulsion injury 819, 819 synostosis (Klippel–Feil syndrome) 180–1, 362, 443 components/anatomy 489 congenital anomalies 180–2 cervical 443–4 kyphosis due to 467 neurofibromatosis type-1 176 disease 247 in ankylosing spondylitis 67, 68 fractures see fractures thoracolumbar, fractures involving processes 821–2 see also entries under spondylvertebral canal see spinal canal vertebral column see spinal column vibration syndrome, hand–arm 435 vibration test 12 viral arthritis 64 viscera and organs fractures causing injury to 694–5, 711–12 pelvic 694, 829–30, 830–1, 832 multiple failure 676–81 rheumatoid arthritis-related disease 61 see also soft tissues vitamin A excess 134 vitamin C deficiency 142–3 vitamin D (cholecalciferol) 125–6 dietary deficiency 138 excess/intoxication 143 metabolic pathway abnormalities 135–9 therapeutic administration in rickets dietary supplements 138 hypophosphataemic rickets 139 see also 1,25-dihydroxycholecalciferol; 25-hydroxycholecalciferol volar fracture–dislocations (hand) 795 volar intercalated segment instability (wrist) 395, 779 volar subluxation 776–7 Volkmann canals 120 Volkmann’s ischaemic contracture 418 with fractures 713, 721–2 voluntary dislocation see habitual dislocation von Recklinghausen’s disease (NF-1) 175, 175–6, 223

974

waddling gait 229–30 walking cycle, see also gait wall test 455 Wallerian degeneration 271 warfarin 310 warming in hypothermia 671 warts, plantar 622 wasting (muscle) 228 quadriceps 548 Watson’s test 395 Watson–Jones approach to hip 534 weakness complete and partial see paralysis; paresis foot 616 hand 424 test for 413 history-taking 4–5 neck pathology causing (in upper limbs) 439 neuromuscular disorders 228 poliomyelitis 253 post-traumatic joint instability causing 722 rheumatoid arthritis 61, 66, 424 shoulder, test for 345 thumb adduction 416 see also paresis wear, prosthetic 329–30 Weaver–Dunn procedure 738 wedge compression fracture cervical 816 thoracolumbar 823 wedge osteotomy, knee region 580 weightbearing in developmental dysplasia of hip, commencement 499 X-rays, in pes cavus 601 whiplash injury 820–1 Whipple’s disease vs ankylosing spondylitis 69 white blood cells, indium-111-labelled 24 whitlow, herpetic 432 WHO classification of musculoskeletal tumours 187 windlass technique 632 Winquist’s classification of femoral shaft fractures 859 wires fracture fixation external 703–4 internal 701 sublaminar, idiopathic scoliosis 464 Wolff’s law 123, 127, 688 women see climacteric; postmenopausal women; pregnancy World Health Organization classification of musculoskeletal tumours 187 wound burn, care 669 debridement see debridement open fractures

ankle, breakdown and infection 916 care (principles) 707–8 closure 708 tibia and fibula combined fractures, grade (size) in Gustillo classification 897 open injuries of hand, care 797–9 woven bone 120 fracture site 690 Wright’s test 293 wrist 373–411, 776–86 anatomy 409–11 arthroscopy (diagnostic) 28 clinical assessment 383–6 deformity 386–92 cerebral palsy 241 poliomyelitis 254 drop 282, 296, 392 extension see extension injuries see injury instability see instability wry neck see torticollis X chromosome 151 defective/absent (Turner’s syndrome) 180 single gene (X-linked) disorders 153 multiple epiphyseal dysplasia 160 X-rays (plain films/radiographs) contrast 19–20 plain film/conventional 15–19 ankle/foot 591 bone density measurements (radiographic absorptiometry) 25, 130 chest in major trauma 639, 640 diagnostic associations 18–19 elbow 371 fractures 693 hip 18, 496–7 image on 16 interpretation 16–18 intraoperative 303–4 knee 553 limitations 19 neck/cervical spine 440–1 pelvic, in major trauma 639, 640 shoulder 340 wrist 385 see also specific conditions xanthine oxidase inhibitors, gout 80 xanthoma, tendon sheath 220 XLPE hip implants 541 XXY (Klinefelter’s) syndrome 180 Y chromosome 151 yaws 48 Z-collapse (hand) 425 Zielke instrumentation 464 zygapophyseal joints see facet joints