Bailey & Love’s Short Practice of Surgery (26th Ed.)

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Bailey & Love’s SHORT PRACTICE of SURGERY 26th EDITION

Sebaceous horn (The owner, the widow Dimanche, sold water-cress in Paris) A favourite illustration of Hamilton Bailey and McNeill Love, and well known to readers of earlier editions of Short Practice.

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Bailey & Love’s SHORT PRACTICE of SURGERY 26

EDITION

Edited by Norman S. Williams

MS FRCS FMed Sci

Professor of Surgery and Director of Surgical Innovation, Barts and the London School of Medicine and Dentistry, Queen Mary, University of London and President, The Royal College of Surgeons of England, London, UK

Christopher J.K. Bulstrode

MCh FRCS(T&O)

Emeritus Professor, University of Oxford, Oxford, UK

P. Ronan O’Connell,

MD FRCSI, FRCPS Glas.,

Head, Surgery and Surgical Specialties, UCD School of Medicine and Medical Sciences Consultant Surgeon, St Vincent’s University Hospital, Dublin, Ireland

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CRC Press Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487-2742 © 2013 by Taylor & Francis Group, LLC CRC Press is an imprint of Taylor & Francis Group, an Informa business No claim to original U.S. Government works Version Date: 20121207 International Standard Book Number-13: 978-1-4665-8514-0 (eBook - VitalBook) This book contains information obtained from authentic and highly regarded sources. Reasonable efforts have been made to publish reliable data and information, but the author and publisher cannot assume responsibility for the validity of all materials or the consequences of their use. The authors and publishers have attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright holders if permission to publish in this form has not been obtained. If any copyright material has not been acknowledged please write and let us know so we may rectify in any future reprint. Except as permitted under U.S. Copyright Law, no part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers. For permission to photocopy or use material electronically from this work, please access www.copyright.com (http://www.copyright.com/) or contact the Copyright Clearance Center, Inc. (CCC), 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400. CCC is a not-for-profit organization that provides licenses and registration for a variety of users. For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged. Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com and the CRC Press Web site at http://www.crcpress.com

Contents

Contributors

viii

Preface

xiii

Acknowledgements

xiv

Sayings of the great

xvi

PART ONE: PRINCIPLES 1. Metabolic response to injury

Kenneth Fearon

2. Shock and blood transfusion

Karim Brohi

3. Wounds, tissue repair and scars

Michael Earley

4. Basic surgical skills and anastomoses

33 50

Peter Lamont

6. Surgery in the tropics

Pradip K Datta, Pawanindra Lal and Sanjay De Bakshi

7. Principles of laparoscopic and robotic surgery 8. Principles of paediatric surgery

93 105

Anthony Lander

9. Principles of oncology

125

Robert JC Steele and Alastair J Munro

10. Surgical audit and clinical research

147

Robert Wheeler

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13. Diagnostic imaging 171 Matthew Matson, Gina Allen and Niall Power 14. Gastrointestinal endoscopy

196

James Lindsay

15. Tissue diagnosis

213

Roger Feakins

PART THREE: PERIOPERATIVE CARE 229

Medha Vanarase, Pierre Foex and Kevin Tremper

17. Anaesthesia and painrelief

238

Vivek Mehta, Richard Langford and Jagannath Haldar

18. Care in the operatingroom

247

Kath Jenkins and Hilary Edgcombe

255

Mridula Rai and Kevin D Johnston

20. Nutrition and fluid therapy

261

John MacFie

21. Postoperative care

272

Jay Kini

22. Day case surgery

281

Douglas McWhinnie and Ian Jackson

PART FOUR: TRAUMA

Jonothan Earnshaw and Birgit Whitman

11. Surgical ethics and law

PART TWO: INVESTIGATION AND DIAGNOSIS

19. Perioperative management of the high-risk surgical patient

Ara Darzi and Sanjay Purkayastha

161

Frank Keane

16. Preoperative preparation

William E. G. Thomas

5. Surgical infection

12. Patient safety

155

23. Introduction to trauma

289

Bob Handley and Peter Giannoudis

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CONTENTS

24. Early assessment and management of trauma

301

Dinesh Nathwani and Joseph Windley

25. Emergency neurosurgery

310

43. Elective neurosurgery

341

44. The eye and orbit

Charles Perkins

28. Torso trauma

351

Ken Boffard

29. Extremity trauma

364

Parminder Singh

30. Burns

470

52. The adrenal glands and other abdominal endocrine disorders

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723

741

Zygmunt H Krukowski

485

53. The breast

505

PART NINE: CARDIOTHORACIC

518 526 541

Martin McNally, Philippa Matthews and Philip Bejon Deborah Eastwood

706

778

Tom WJ Lennard

Paul Cool

41. Paediatric orthopaedics

674

PART EIGHT: BREAST AND ENDOCRINE 51. The thyroid and parathyroid glands

Bob Sharpe

40. Infection of the bones and joints

48. Pharynx, larynx and neck

463

Hemant G Pandit and Andrew Barnett

39. Musculoskeletal tumours

661

William P Smith

437

Vinay Takwale and Irfan Khan

38. Foot and ankle

47. The ear

50. Disorders of the salivary glands

Chris Lavy and Gavin Bowden

37. Hip and knee

653

William P Smith

Gina Allen

36. Upper limb – pathology, assessment and management

46. The nose and sinuses

49. Oropharyngeal cancer

Parminder J Singh and Hemant G Pandit

35. The spine

634

Rishi Sharma and Martin Birchall

PART FIVE: ELECTIVE ORTHOPAEDICS

34. Sports medicine and sports injuries

45. Cleft lip and palate: developmental abnormalities of the face, mouth and jaws

Grant Bates

417

Mamoon Rashid

33. History taking and clinical examination in musculoskeletal disease

622

Colm O’Brien, Hugo Henderson and Jonathan Jagger

Robert W Ruckley and Iain J Nixon

401

Tim Goodacre

32. Disaster surgery

605

William Gray and Harry Bulstrode

William P Smith

385

Michael Tyler and Sudip Ghosh

31. Plastic and reconstructive surgery

577

PART SEVEN: HEAD AND NECK

326

Ashley Poynton

27. Maxillofacial trauma

42. Skin and subcutaneous tissue Christopher Chan and Adam Greenbaum

Tony Belli and Harry Bulstrode

26. Neck and spine

PART SIX: SKIN AND SUBCUTANEOUS TISSUE

798

Richard Sainsbury

54. Cardiac surgery

823

Jonathan R Anderson and Mustafa Zakkar

55. The thorax

850

Ian Hunt and Carol Tan

PART TEN: VASCULAR 56. Arterial disorders

877

Robert Sayers

550

57. Venous disorders

901

Peter McCollum and Ian Chetter

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CONTENTS

58. Lymphatic disorders

923

Shervanthi Homer-Vanniasinkam and David A Russell

72. The rectum 73. The anus and anal canal 941

60. Abdominal wall, hernia and umbilicus 948 Stephen J Nixon and Bruce Tulloh

987

76. The urinary bladder

1058

78. Urethra and penis

1065

79. Testis and scrotum

1087

67. The gall bladder and bile ducts

1097

Kevin Conlon

68. The pancreas

1118

Satyajit Bhattacharya

69. The small and large intestines

1143

Gordon Carlson and Jonathan Epstein

70. Intestinal obstruction Jim Hill

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1181

1309 1340

David E Neal and Greg L Shaw

1359

Ian Eardley

1377

Ian Eardley

80. Gynaecology

O James Garden

1282

Freddie Hamdy

77. The prostate and seminal vesicles

Rahul S Koti, Sanjeev Kanoria and Brian R Davidson

66. The spleen

1271

Christopher G Fowler

1023

John Baxter

65. The liver

74. Urinary symptoms and investigations 75. The kidneys and ureters

John N Primrose and Timothy J Underwood

64. Bariatric surgery

PART TWELVE: GENITOURINARY

970

Derek Alderson

63. Stomach and duodenum

1236

Peter Lunniss and Karen Nugent

Christopher G Fowler

Charles H Knowles

62. The oesophagus

1215

Sue Clark

Mohan de Silva and V Sitaram

61. The peritoneum, omentum, mesentery and retroperitoneal space

1199

P Ronan O’Connell

PART ELEVEN: ABDOMINAL 59. History and examination of the abdomen

71. The vermiform appendix

vii

1392

Stephen Kennedy and Enda McVeigh

PART THIRTEEN: TRANSPLANTATION 81. Transplantation

1407

J Andrew Bradley

Appendix 1: Common instruments used in general surgery

1433

Pradip K Datta

Index

1437

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Contributors

Derek Alderson

MD FRCS

Barling Chair of Surgery and Head of Department, Queen Elizabeth Hospital, Edgbaston, Birmingham, UK

Gina Allen

BM DCH MRCGP MRCP FRCR

Oxford Soft Tissue Injury Clinic (Ostic), St Luke’s Hospital, Oxford, UK

Jonathan R Anderson

Department of Cardiothoracic Surgery, Imperial College Healthcare NHS Trust, Hammersmith Hospital, London, UK

Andrew Barnett

FRCS(Orth)

Consultant Orthopaedic Surgeon, Robert Jones and Agnes Hunt Orthopaedic Hospital, Gobowen, Shropshire, UK

Grant Bates

BSc BM Bch FRCS (deceased)

Philip Bejon

Ear, Nose and Throat Surgeon, John Radcliffe Hospital, Oxford and Lecturer, University of Oxford, Oxford, UK Bone Infection Unit, Nuffield Orthopaedic Centre, Oxford, UK

Tony Belli

Reader in Trauma, Neurosurgery, University of Birmingham, Birmingham, UK MS MPhil FRCS

Consultant Hepato-Pancreato-Biliary Surgeon, The Royal London Hospital, London, UK

Martin Birchall

MB ChB PhD FRCS Ac Med Sci

Professor of Surgery, University of Cambridge, and Consultant Surgeon, Addenbrooke’s Hospital, Cambridge, UK

Karim Brohi

FRCS FRCA

Professor of Trauma Sciences, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK

Harry Bulstrode

MA Cantab BMBCh MRCS(Eng)

Gordon Carlson

BSc MD FRCS

Academic Clinical Fellow in Neurosurgery, Division of Neurosciences, Southampton General Hospital, Southampton, UK Consultant Surgeon, Honorary Professor of Surgery, University of Manchester; Honorary Professor of Biomedical Science, University of Salford, Salford, UK

Christopher Chan

BSC PhD FRCS FRCS(Gen Surg)

Consultant Colorectal Surgeon, Academic Surgical Unit, Barts Health NHS Trust, London, UK

Ian Chetter

MB ChB FRCSMD FRCS(Gen Surg) PG Cert Medical

Ultrasound PG Dip Clinical Education

MD FRCS(SN)

Satyajit Bhattacharya

J Andrew Bradley

M(Cantab) FRCS FRCS(Oto) FRCS(ORL)

Professor of Surgery, Hull York Medical School, University of Hull; Honorary Consultant Vascular Surgeon, Hull and East Yorkshire NHS Trust, Academic Vascular Surgical Unit, Old Doctors Residence, Hull Royal Infirmary, Hull, UK

Sue Clark

MD FRCS(Gen Surg)

Consultant Colorectal Surgeon, St Mark’s Hospital, Harrow, UK

Kevin C Conlon

Professor of Laryngology, University College London, Consultant in Otolaryngology, Head and Neck Surgery, The Royal National Throat, Nose and Ear Hospital, UCLH NHS Trust, London, UK

Professor of Surgery, Trinity College Dublin; Consultant Surgeon, St. Vincent’s University Hospital and The Adelaide and Meath Hospital, Dublin, Ireland

Ken Boffard

Paul Cool

MD MedSc(Res) FRCS(Ed) FRCS(Orth)

Ara Darzi

PC KBE HonFrEng FmedSci

BSC(Hons) MB BCh FRCS FRCS(Ed) FRCPS(Glas) FACS

FCS(SA)

Professor and Head, Department of Surgery, Johannesburg Hospital, University of the Witwatersrand, Johannesburg, South Africa

Gavin Bowden

MB BCh FCS(SA)(Orth)

Consultant Spinal Surgeon, St Lukes Hospital, Oxford, UK

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MA MCh MBA FRCSI FACS FRCPS(Glas) FTCD

Consultant Orthopaedic and Oncological Surgeon, Robert Jones and Agnes Hunt Orthopaedic Hospital, Gobowen, Shropshire, UK Professor the Lord Darzi of Denham, Professor of Surgery, Imperial College London, St Mary’s Hospital Campus, London, UK

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CONTRIBUTORS

Pradip K Datta

MBE MS FRCS(Ed) FRCS FRCSI FRCPS(Glas)

Honorary Consultant Surgeon, Caithness General Hospital, Wick, Caithness, UK

Brian R Davidson

MD FRCS

Sanjay De Bakshi

MB BS MS FRCS FRCS(Ed)

Consultant Surgeon, Royal Free Hospital and Professor of Surgery, Hampstead Campus, University College London, London, UK Consultant Surgeon, Unit of Surgical Gastroenterology, Calcutta Medical Research Institute, Kolkata, India

Ian Eardley

Sudip Ghosh

MB BS MS FRCS(Plast)

Consultant Plastic Surgeon, Stoke Mandeville Hospital, Aylesbury, UK

Peter Giannoudis

MD FRCS

Professor of Trauma and Orthopaedic Surgery, School of Medicine, University of Leeds, Leeds, UK

Tim Goodacre

MD FRCS

Senior Clinical Lecturer and Consultant Plastic Surgeon, Oxford Radcliffe Hospitals, Oxford, UK

William Gray

MB MD FRCSI FRCS(SN)

Consultant Urologist, Department of Urology, St James University Hospital, Leeds, UK

Professor of Functional Neurosurgery, Institute of Psychological Medicine and Clinical Neurosciences, Cardiff University, Cardiff, UK

Michael Earley

Adam Greenbaum

MA MChir FRCS (Urol) FEBU

MB MCh FRCSI FRCS(Plast)

Consultant Plastic Surgeon and Associate Clinical Professor, The Children’s University Hospital, Temple Street and Mater Misericordiae University Hospital, Dublin, Ireland

Jonothan Earnshaw

MB BS MBA PhD FRCS(Plast) FEBOPRAS

Consultant Plastic Surgeon, The Aesthetic Body Centre, Hamilton, New Zealand

Jagannath Haldar

MB BS MD FRCA

Consultant Vascular Surgeon, Gloucestershire Royal Hospital, Gloucester, UK

Consultant Anaesthetist and Clinical Lead, Oxford University Hospitals NHS Trust, Honorary Clinical Lecturer, Oxford Brooke’s University, Oxford, UK

Deborah Eastwood

Freddie Hamdy

DM FRCS

FRCS

The Catterall Unit, Royal National Orthopaedic Hospital, Stanmore, Middlesex, UK

Hilary Edgcombe

BA BM BCh(Oxon) FRCA(Lon)

Jonathan Epstein

MA MD FRCS

Consultant Anaesthetist, Oxford University Hospitals, Oxford, UK Specialist Registrar in General Surgery, Hope Hospital, Salford, UK

Roger Feakins

MB BCh BAO BA MD FRCPI FRCPath

Consultant Histopathologist and NHS Professor of Gastrointestinal Pathology, Department of Histopathology, Barts Health NHS Trust, London, UK

Kenneth Fearon

MD FRCPS(Glas) FRCS(Ed) FRCS

Professor of Surgical Oncology and Honorary Consultant Colorectal Surgeon, Clinical Surgery, School of Clinical Science, University of Edinburgh, Royal Infirmary, Edinburgh, UK

Pierre Foex

DPhil FRCA FMedSci

Nuffield Division of Anaesthetics, John Radcliffe Hospital, Headley Way, Oxford, UK

Christopher G Fowler BSc MB BS MA MS FRCP FRCS(Urol) FEBU FHEA

Professor, Department of Urology, The Royal London Hospital, London, UK

O James Garden

BSc MB ChB FRCPS(Glas) FRCS(Ed) FRCP(Ed) FRCSCan

FRACS(Hon)

Regius Professor of Clinical Surgery, School of Clinical Sciences, University of Edinburgh, Royal Infirmary, Edinburgh, UK

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MD MA FRCS FRCS(Ed)(Urol) FMedSci

Director, Division of Surgery and Oncology, Oxford Radcliffe Hospitals NHS Trust, John Radcliffe Hospital, Oxford, UK

Bob Handley

MB ChB FRCS

John Radcliffe Hospital, Oxford, UK

Jim Hill

MB ChB ChM FRCS

Consultant General and Colorectal Surgeon, Manchester Royal Infirmary, Manchester, UK

Shervanthi Homer-Vanniasinkam

BSc MD FRCS(Ed) FRCS

Consultant Vascular Surgeon, The General Infirmary at Leeds; Clinical Sub-Dean, University of Leeds Medical School Chair, Translational Vascular Medicine, University of Bradford; Director, Northwick Park Institute for Medical Research, London Honorary Professor, Division of Surgical and Interventional Sciences, University College London, London, UK

Ian Hunt

MB BS BSc(Hons) FRCS(C-Th)

Consultant Thoracic Surgeon, Department of Cardiothoracic Surgery, St George’s Hospital, London, UK

Ian Jackson

MB ChB FRCA

Consultant Anaesthetist, Past President British Association of Day Surgery, York Teaching Hospital NHS Foundation Trust, York, UK

Kath Jenkins

BM BS FRCA

Consultant Anaesthetist, North Bristol NHS Trust, Bristol, UK

Kevin D. Johnston

MBChB (Hons) BDS BSc MFDSRCS FRCA

Specialist Registrar in Anaesthetics, Nuffield Department of Anaesthetics, John Radcliffe Hospital, Oxford, UK

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CONTRIBUTORS

Sanjeev Kanoria

FRCS

HPB and Liver Transplant Unit, University Department of Surgery, Royal Free Hospital, London, UK

Frank Keane

MD FRCSI FRCS FRCS(Ed) FRCPS(Glas) FRCPI

Associate Professor of Surgery, Trinity College, and Consultant Colorectal Surgeon, Adelaide and Meath Hospital, Dublin, Ireland

Stephen Kennedy

Professor of Reproductive Medicine and Head of Department, Nuffield Department of Obstetrics and Gynaecology, University of Oxford, Oxford University Hospitals NHS Trust, The Women’s Centre, Oxford, UK

Irfan Khan

MB BS MRCS

Specialty Doctor, Orthopaedics, Gloucestershire Hospitals NHS Trust, Gloucestershire, UK

Jay Kini

MB BS DA MD FFARCSI

Consultant Anaesthetist, Nuffield Department of Anaesthetics, John Radcliffe Hospital, Oxford, UK

Charles H Knowles

BChir PhD FRCS

Clinical Professor of Surgical Research and Hononary Consultant Colorectal Surgeon, Centre for Digestive Diseases, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University, London, UK

Rahul S Koti

MD FRCS

Honorary Lecturer in Surgery, Department of Surgery, University College London; Department of Surgery, Royal Free Hospital, London, UK

Zygmunt H Krukowski

PhD FRCS FRCP

Surgeon to the Queen in Scotland; Consultant Surgeon, Aberdeen Royal Infirmary; Professor of Clinical Surgery, University of Aberdeen, Aberdeen, UK

Pawanindra Lal

MS DNB FIMSA FRCS(Ed) FRCPS(Glas) FRCS FACS

Professor of Surgery, Maulona Azad Medical College & Associated Lok Nayak Hospital, New Delhi, India

Peter Lamont

MB ChB MD FRCS FEBVS

Consultant Vascular Surgeon, Department of Vascular Surgery, Bristol Royal Infirmary, Bristol, UK

Anthony Lander Phd FRCS(Paed) DCH

James Lindsay

PhD FRCP

Peter Lunniss

BSc MS FRCS

Consultant and Senior Lecturer in Gastroenterology, Digestive Diseases Clinical Academic Unit, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK Senior Lecturer, Honorary Consultant Coloproctologist, Royal London Hospital Whitechapel, London, UK

Peter McCollum

BA MB BCh BAO MCh FRCSI FRCS(Ed)

Professor of Vascular Surgery, Hull York Medical School; Honorary Consultant Vascular Surgeon, Hull & East Yorkshire Hospitals NHS Trust, Hull Royal Infirmary, Hull, UK

John MacFie

MB ChB R Nutr MD FRCS FRCP

Professor of Surgery/Consultant Surgeon, PGMI, University of Hull/Scarborough Hospital, Scarborough, UK

Martin McNally

MD FRCS(Ed) FRCS(Orth)

Consultant in Limb Reconstruction Surgery, Bone Infection Unit, Nuffield Orthopaedic Centre; Honorary Senior Lecturer in Orthopaedics

Enda McVeigh

Senior Fellow in Reproductive Medicine, Nuffield Department of Obstetrics and Gynaecology, University of Oxford, Oxford University Hospitals NHS Trust, The Women’s Centre, Oxford, UK

Douglas McWhinnie

MD(Hons) FRCS

Consultant General and Vascular Surgeon, Past President British Association of Day Surgery, Milton Keynes NHS Foundation Trust, Milton Keynes, UK

Matthew Matson

MRCP FRCR

Consultant Radiologist, Royal London Hospital, London, UK

Philippa Matthews

MSc MRCP FRCPath DPhil

Academic Clinical Lecturer in Infectious Diseases and Microbiology, Oxford University Hospitals NHS Trust, Oxford, UK

Vivek Mehta

MD FRCA FFPMRCA

Consultant Paediatric Surgeon, Birmingham Children’s Hospital, Birmingham, UK

Consultant in Pain Medicine, Deputy Director, Pain and Anaesthesia Research Centre, St Bartholomew’s and Royal London Hospitals, Barts Health NHS Trust, London, UK

Richard Langford

Alastair J Munro

MD FRCA FFPMRCA

Professor of Anaesthesia and Pain Medicine and Directory, Pain and Anaesthesia Research Centre, St Bartholomew’s and Royal London Hospitals, Barts Health NHS Trust, London UK

Chris Lavy

OBE MD MCh FRCS

Honorary Professor and Consultant Orthopaedic Surgeon, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), University of Nuffield, Nuffield Orthopaedic Centre, Oxford, UK

Dinesh Nathwani

Tom WJ Lennard

David E Neal

MD FRCS

Professor of Surgery, Newcastle University, Newcastle upon Tyne, UK

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BSc FRCP(E) FRCR

Professor of Radiation Oncology, University of Dundee, Tayside Cancer Centre, Ninewells Hospital and Medical School, Dundee, UK MB ChB MSc FRCSI(Tr & Orth)

Consultant and Honorary Senior Clinical Lecturer, Department of Trauma and Orthopaedic Surgery, Imperial College Healthcare, Academic Health Sciences Centre, London, UK FMedSci MS FRCS

University Department of Oncology, Addenbrooke’s Hospital, Cambridge, UK

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CONTRIBUTORS

Stephen J Nixon

FRCS(Ed) FRCP(Edin)

Consultant Surgeon, Department of Surgery, Royal Infirmary of Edinburgh, Edinburgh, UK

Iain J Nixon

MB ChB FRCS(Ed)(ORL-HNS)

Clinical Fellow, Head and Neck Service, Memorial Sloan Kettering Cancer Center, New York, NY, USA

Karen Nugent

MA MS FRCS

Colm O’Brien

MD FRCS FRCOphth

Professorial Surgical Unit, Southampton General Hospital, Southampton, UK Professor of Ophthalmology and Consultant Ophthalmic Surgeon, University College Dublin and Mater Misericordiae University Hospital, Dublin, Ireland

P Ronan O’Connell

MD FRCSI FRCPS(Glas)

Professor of Surgery, University College Dublin; Consultant Surgeon, St Vincent’s University Hospital, Dublin, Ireland

Hemant G Pandit

FRCS(Orth) DPhil (Oxford)

Honorary Senior Clinical Lecturer in Orthopaedics, Nuffield Orthopaedic Centre and Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), Oxford, UK

Charles Perkins

FDSRCS FFDRCSI FRCS

Consultant Oral and Maxillofacial Surgeon, Department of Oral and Maxillofacial Surgery, Gloucestershire Royal Hospital, Gloucester, UK

Niall Power

Royal London Hospital, London, UK

Ashley Poynton

MD FRCSI FRCS(TrandOrth)

Consultant Spinal Surgeon, National Spinal Injuries Unit, Mater Misericordiae University Hospital, Dublin, Ireland

John N Primrose

MB ChB(Hons) FRCS MD

Professor, University Surgical Unit, Southampton General Hospital, Southampton, UK

Sanjay Purkayastha

BSc MB BS MD FRCS(Gen Surg)

Locum Consultant, General & Bariatric Surgery, St Mary’s Hospital, Paddington, Imperial College Healthcare NHS Trust, London, UK

Mridula Rai

MB BS MD FRCA

Consultant Anaesthetist, Nuffield Department of Anaesthetics, Modular Building, John Radcliffe Hospital, Oxford, UK

Mamoon Rashid

FRCS FCPS(Pak)

David A Russell

MB ChB MD FRCS(Gen Surg)

Consultant Vascular Surgeon, Leeds Vascular Institute, Leeds General Infirmary, Leeds, UK

Richard Sainsbury

MD FRCS

Consultant Breast Surgeon, Southampton University Hospitals NHS Foundation Trust, Southampton, UK

Anand Sardesai

MB BS MD FRCA

Consultant Anaesthetist, Addenbrook’s Hospital, Cambridge, UK

Robert Sayers

Professor of Vascular Surgery, Leicester Royal Infirmary, Leicester, UK

Rishi Sharma

MRCS DOHNS

Specialist Registrar, Ear Nose and Throat Surgery, Guy’s and St Thomas’ Hospital, London, UK

Bob Sharp

BMBCh MA FRCS FRCS(Tr & Orth)

Consultant Orthopaedic Surgeon, Oxford University Hospitals, The Nuffield Orthopaedic Centre, Oxford, UK

Greg L Shaw

MD FRCS(Urol)

Clinical Lecturer in Urology, Cambridge University, Cambridge, UK

Mohan de Silva

MS FRCS(Ed) FCSSL

Professor of Surgery and Dean, Faculty of Medical Sciences, University of Sri Jayawardenepura Gangodawila, Nugegoda, Colombo, Sri Lanka

Parminder J Singh

MB BS MRCS FRCS(Tr & Orth) MS

Consultant Orthopaedic Surgeon, Maroondah Hospital and Honorary Senior Lecturer, Monash and Deakin University, Melbourne, Australia

V Sitaram

MS FRCPS(Glas)

Professor of Surgery, Department of Hepatic, Pancreatic & Biliary (HPB) Surgery, Christian Medical College, Vellore, India

William P Smith

FDSRCS FRCS(Ed) FRCS

Robert JC Steele

MB ChB MD FRCS(Ed)

Consultant Maxillofacial Surgeon, Northampton General Hospital NHS Trust, Northampton, UK Professor, Head of Academic Surgery, Ninewells Hospital and Medical School, Dundee, UK

Vinay Takwale

MB MS FRCS(Tr & Orth)

Consultant Orthopaedic Surgeon, Gloucestershire Hospital, Gloucester, UK

Professor of Plastic and Reconstructive Surgery, Shifa College of Medicine; Consultant Plastic Surgeon and Programme Director, Shifa International Hospital, Islamabad, Pakistan

Carol Tan

Robert W Ruckley

William EG Thomas

MB ChB FRCS FRCS(Ed)

Consultant Ear Nose and Throat and Head and Neck Surgeon (retired), Darlington Memorial Hospital, Darlington, UK

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MB ChB FRCS(C-Th)

Consultant Thoracic Surgeon, St George’s Hospital, London, UK MS FRCS FSACS(Hon)

Consultant Surgeon and Honorary Senior Lecturer in Surgery, Sheffield, UK

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CONTRIBUTORS

Kevin Tremper

PhD MD

Robert B Sweet Professor and Chair, Department of Anesthesiology, University of Michigan, Ann Arbor, MI, USA

Bruce Tulloh

MB MS(Melb) FRACS FRCS(Ed)

Department of Surgery, Royal Infirmary of Edinburgh, Edinburgh, UK

Michael Tyler

FRCS(Plast) MB CHM

Stoke Mandeville Hospital, Aylesbury, UK

Timothy J Underwood

BSc(Hons) MB BS PhD FRCS

MRC Clinician Scientist and Honorary Consultant Surgeon, University Surgical Unit, Southampton General Hospital, Southampton, UK

Medha Vanarase

Robert Wheeler

MS FRCS FRCPCH LLB(Hons) LLM

Birgit Whitman

PhD

Joseph Windley

MB BS BSc(Hons) MRCS

Mustafa Zakkar

PhD

Consultant Paediatric Surgeon, Child Health, University Hospitals of Southampton, Southampton, UK Head of Research Governance, University of Bristol, Bristol, UK Specialist Registrar, Department of Trauma and Orthopaedic Surgery, Imperial College Healthcare, Academic Health Sciences Centre, London, UK Department of Cardiothoracic Surgery, Imperial College Healthcare NHS Trust, Hammersmith Hospital, London, UK

MB BS MD FRCA(Cert Ed)

Consultant Anaesthetist, Oxford Radcliffe Hospitals NHS Trust, Oxford, UK

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Preface

In this age of rapid electronic access to scientific papers and erudite surgical opinion one has to ask whether there is still a place for a comprehensive surgical textbook that takes several years to compile and risks losing its immediacy. The success of the 25th edition of Bailey & Love together with the numerous positive communications we have received since its publication suggest that the answer is very much in the affirmative. However, it is essential that in producing further editions cognisance is taken of what the “customer” wants. Consequently before preparing the 26th edition of this venerable text we conducted considerable market research as to what had succeeded in the previous edition, what had been omitted and how we could improve content and presentation. Readers from a range of backgrounds from undergraduates to hard bitten and, dare we say, cynical senior consultants were asked for their opinion. Their musings and frank criticisms were all taken very seriously and many of their suggestions were adopted for this edition. A few chapters were removed or consolidated into others; new chapters have been added focusing on the important topics of patient safety, day case surgery and bariatric surgery. All existing chapters have been radically revised and have been thoroughly brought up to date. We have attempted to ensure more conformity with regard to illustrations; however, we have kept faith with Hamilton Bailey and McNeil Love’s original concept of ensuring clinical photographs are liberally used to not only enhance the text but more importantly illuminate a clinical point. Many new photographs have been introduced, some of which have been provided by our readers, which is very much a Bailey & Love tradition. Although we have been ruthless in removing old material we make no excuse for retaining the odd original pen drawing taken from the first few editions. This is not just for nostalgia’s sake but because they illustrate a pertinent point not easily captured by a modern photograph. Another tradition beloved of readers has of course been the autobiographical notes. These have all been painstakingly researched and added to by Pradip Datta. We recognise that despite very careful attention to detail by our authors there may be an occasional error in the text that we and our proof readers have failed to spot. It would not be

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surprising in a text of this length. We apologise in advance for any errors and thank our eagle-eyed readers whom we know from experience will let us know of any that they find. This is a Bailey & Love tradition and we value all contributions that can improve accuracy. Several editions ago we introduced the concept of learning objectives and summary boxes in order to help examination candidates in their revision. The feedback regarding these innovations was extremely positive and we have attempted to ensure that these are comprehensive, standardised and liberally dispersed through the text. The authors of the chapters have been carefully chosen not just for their undoubted experience and expertise in their specialty but also their ability to write both accurately and succinctly. Writing is a skill honed by practice; it is a labour of love and takes time and patience to perfect. The best authors are like gifted musicians who, after numerous rehearsals, are able to deliver a perfect recital. It is our belief that our contributors have done just this and we the editors have attempted wherever possible to ensure there is a rhythm and harmony flowing through the pages. However, at the end of the day we appreciate it will be up to the audience to decide how successful we and our authors have been in this endeavour. It has been a pleasure and privilege to edit this historic textbook beloved of so many students and trainees through the decades. However, we are conscious that previous reputation counts for very little unless the present product meets expectations and is relevant to the present era. This thought has always been in our minds when preparing the content of the 26th edition. We very much hope it fits the bill and fulfils your requirements whether you, the reader, are studying for an exam, checking on an area of practice that you may be unfamiliar with or just refreshing your memory about some forgotten fact or biographical detail. Norman S. Williams Christopher J.K. Bulstrode P. Ronan O’Connell 2012

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Acknowledgements

Sometimes a new edition of Bailey & Love feels like a swan swimming swiftly but serenely across a lake. From afar it may look effortless (and beautiful we hope), but to those who are closer to the action you can glimpse the webbed feet paddling away furiously beneath the surface driving that swan forward. The three editors are one part of a huge orchestra too large to mention all by name. However, it is a pleasure to acknowledge some of the most notable amongst the players. Gavin Jamieson initiated the new edition as commissioning editor under the supervision of Jo Koster, who then took over following Gavin’s departure. Sarah Penny and Stephen Clausard took on the awesome responsibility of pulling all things ‘manuscript-related’ together. Susie Bond, Alyson Thomas and Theresa Mackie have done a great job with the copy editing and proof reading, while the index has been compiled ably by Christopher Boot. Mr Pradip Datta FRCS completely revamped the historical footnotes, going back all the way to the first edition to check that we had left no ‘jewels’ out of the crown. Mr Hemant Pandit FRCS, Dr Medha Vanarese FRCA and Mr Parminder Singh FRCS helped enormously with the commissioning and editing of the orthopaedic, anaesthetic and trauma chapters respectively. Chapter 4, Basic surgical skills and anastomoses, contains some material from ‘Basic surgical skills and anastomoses’ by David J. Leaper. The material has been revised and updated by the current author. Chapter 5, Surgical infection, contains some material from ‘Surgical infection’ by David J. Leaper. The material has been revised and updated by the current author. Chapter 8, Principles of paediatric surgery, contains some material from ‘Principles of paediatric surgery’ by Mark Stringer. The material has been revised and updated by the current author. Chapter 11, Surgical ethics and law, contains some material from ‘Surgical ethics’ by Len Doyal. The material has been revised and updated by the current author. Chapter 16, Preoperative preparation, contains some material from ‘Preoperative preparation’ by Lisa Leonard and Sarah J. Barton. The material has been revised and updated by the current authors.

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Chapter 18, Care in the operating room, contains some material from ‘Care in the operating room’ by Sunny Deo and Vipul Mandalia. The material has been revised and updated by the current authors. Chapter 19, Perioperative management of the high-risk surgical patient, contains some material from ‘Perioperative management of the high-risk surgical patient’ by Rupert M. Pearse and Richard M. Langford. The material has been revised and updated by the current authors. Chapter 20, Nutrition and fluid therapy, the author would like to thank Marcel Gatt MD FRCS, who provided some illustrations and helped with proofreading the text. Chapter 21, Postoperative care, contains some material from ‘Postoperative care’ by Alistair Pace and Nicholas C.M. Armitage. The material has been revised and updated by the current author. Chapter 25, Head injury, contains some material from ‘Head injury’ by Richard Stacey and John Leach. The material has been revised and updated by the current authors. Chapter 34, Sports medicine and sports injuries, contains some material from ‘Sports medicine and sports injuries’ by D.L. Back and Jay Smith. The material has been revised and updated by the current author. Chapter 36, Upper limb – pathology, assessment and management, contains some material from ‘Upper limb – pathology, assessment and management’ by Srinath Kamineni. The material has been revised and updated by the current authors. Chapter 37, Hip and knee, contains some material from ‘Hip and knee’ by Vikas Khanduja and Richard N. Villar. The material has been revised and updated by the current authors. Chapter 38, Foot and ankle, contains some material from ‘Foot and ankle’ by Mark Davies, Matthew C. Solan and Vikas Khanduja. The material has been revised and updated by the current author. Chapter 41, Paediatric orthopaedics, contains some material from ‘Paediatric orthopaedics’ by the current author and Joanna Hicks, which has been revised and updated for this edition.

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ACKNOWLEDGEMENTS

Chapter 43, Elective neurosurgery, contains some material from ‘Elective Neurosurgery’ by John Leach and Richard Kerr. The material has been revised and updated by the current authors. Chapter 44, The eye and orbit, contains some material from ‘The eye and orbit’ by Jonathan D. Jagger and Hugo W.A. Henderson. The material has been revised and updated by the current author. Chapter 48, The pharynx, larynx and neck, contains some material from ‘The pharynx, larynx and neck’ by Jonathan D. Jagger and Hugo W.A. Henderson. The material has been revised and updated by the current author. Chapter 52, The adrenal glands and other abdominal endocrine disorders, contains some material from ‘Adrenal glands and other endocrine disorders’ by Matthias Rothmund. The material has been revised and updated by the current author. Chapter 54, Cardiac surgery, contains some material from ‘Cardiac surgery’ by Jonathan Anderson and Ian Hunt. The material has been revised and updated by the current authors. Chapter 55, The thorax, contains some material from ‘The thorax’ by Tom Treasure. The material has been revised and updated by the current authors. Chapter 56, Arterial disorders, contains some material from ‘Arterial disorders’ by John A. Murie. The material has been revised and updated by the current author. Chapter 57, Venous disorders, contains some material from ‘Venous disorders’ by Kevin Burnand. The material has been revised and updated by the current authors. Chapter 58, Lymphatic disorders, contains some material from ‘Lymphatic disorders’ by Shervanthi Homer-Vanniasinkam and Andrew Bradbury. The material has been revised and updated by the current authors.

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Chapter 59, History and examination of the abdomen, contains some material from ‘History and examination of the abdomen’ by Simon Paterson-Brown. The material has been revised and updated by the current authors. Chapter 60, Abdominal wall, hernia and umbilicus, contains some material from ‘Hernias, umbilicus and abdominal wall’ by Andrew N. Kingsnorth, Giorgi Giorgobiani and David H. Bennett. The material has been revised and updated by the current authors. Chapter 61, The peritoneum, omentum, mesentery and retroperitoneal space, contains some material from ‘The peritoneum, omentum, mesentery and retroperitoneal space’ by Jerry Thompson. The material has been revised and updated by the current author. Chapter 65, The liver, contains some material from ‘The liver’ by Brian R. Davidson. The material has been revised and updated by the current authors. Chapter 69, The small and large intestines, contains some material from ‘The small and large intestines’ by Neil J. McC Mortensen and Shazad Ashraf. The material has been revised and updated by the current authors. Chapter 70, Intestinal obstruction, contains some material from ‘Intestinal obstruction’ by Marc Christopher Winslet. The material has been revised and updated by the current author. Chapter 76, The urinary bladder, contains some material from ‘The urinary bladder’ by David E. Neal. The material has been revised and updated by the current author. Chapter 78, Urethra and penis, contains some material from ‘Urethra and penis’ by Christopher G. Fowler. The material has been revised and updated by the current author. Chapter 79, Testis and scrotum, contains some material from ‘Testis and scrotum’ by Christopher G. Fowler. The material has been revised and updated by the current author.

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Sayings of the great

Both Hamilton Bailey and McNeill Love, when medical students, served as clerks to Sir Robert Hutchinson, 1871–1960, who was Consulting Physician to the London Hospital and President of the Royal College of Physicians. They never tired of quoting his ‘medical litany’, which is appropriate for all clinicians and, perhaps especially, for those who are surgically minded. From inability to leave well alone; From too much zeal for what is new and contempt for what is old; From putting knowledge before wisdom, science before art, cleverness before common sense; From treating patients as cases; and From making the cure of a disease more grievous than its endurance, Good Lord, deliver us.

Investigating Nature you will do well to bear ever in mind that in every question there is the truth, whatever our notions may be. This seems perhaps a very simple consideration; yet it is strange how often it seems to be disregarded. If we had nothing but pecuniary rewards and worldly honours to look to, our profession would not be one to be desired. But in its practice you will find it to be attended with peculiar privileges; second to none in intense interest and pure pleasures. It is our proud office to tend the fleshy tabernacle of the immortal spirit, and our path, if rightly followed, will be guided by unfettered truth and love unfeigned. In the pursuit of this noble and holy calling I wish you all God-speed. Promoter’s address, Graduation in Medicine, University of Edinburgh, August, 1876, by Lord Lister, the Founder of Modern Surgery

The patient is the centre of the medical universe around which all our works revolve and towards which all our efforts trend. J.B. Murphy, 1857–1916, Professor of Surgery, Northwestern University, Chicago, IL, USA

Surgery has undergone many great transformations during the past fifty years, and many are to be thanked for their contributions – yet when we think of how many remain to be made, it should rather stimulate our inventiveness than fuel our vanity. Sir Percival Pott, 1714–88, Surgeon, St Bartholomew’s Hospital, London, UK

To study the phenomenon of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all. Sir William Osler, 1849–1919, Professor of Medicine, Oxford, UK

If you cannot make a diagnosis at least make a decision! Sir Harry Platt, 1897–1986, Professor of Orthopaedics, Manchester, and President of the Royal College of Surgeons England, London, UK

A knowledge of healthy and diseased actions is not less necessary to be understood than the principles of other sciences. By and acquaintance with principles we learn the cause of disease. Without this knowledge a man cannot be a surgeon. … The last part of surgery, namely operations, is a reflection on the healing art; it is a tacit acknowledgement of the insufficiency of surgery. It is like an armed savage who attempts to get that by force which a civilised man would by stratagem. Hunter, 1728–1793, Surgeon, St George’s Hospital, London, UK

If the surgeon cuts a vessel and knows the name of that vessel, the situation is serious; if the anaesthetist knows the name of that vessel, the situation is irretrievable. Maldwyn Morgan 1938– Anaesthetist, Hammersmith Hospital, London, UK

To which may be added:

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PART

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Principles

1 Metabolic response to injury

2 Shock and blood transfusion

3 Wounds, tissue repair and scars

4 Basic surgical skills and anastomeses

5 Surgical infection

6 Surgery in the tropics

7 Principles of laparoscopic and robotic surgery

8 Principles of paediatric surgery

105

9 Principles of oncology

125

10 Surgical audit and clinical research

147

11 Surgical ethics and law

155

12 Patient safety

161

30/07/2012 07:29

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30/07/2012 07:29

CHAPTER

Metabolic response to injury LEARNING OBJECTIVES

BASIC CONCEPTS IN HOMEOSTASIS In the eighteenth and nineteenth centuries, a series of eminent scientists laid the foundations of our understanding of homeostasis and the response to injury. The classical concepts of homeostasis and the response to injury are:

• ‘The stability of the “milieu intérieur” is the primary condition

for freedom and independence of existence’ (Claude Bernard); i.e. body systems act to maintain internal constancy. • ‘Homeostasis: the co-ordinated physiological process which maintains most of the steady states of the organism’ (Walter Cannon); i.e. complex homeostatic responses involving the brain, nerves, heart, lungs, kidneys and spleen work to maintain body constancy. • ‘There is a circ*mstance attending accidental injury which does not belong to the disease, namely that the injury done, has in all cases a tendency to produce both the deposition and means of cure’ (John Hunter); i.e. responses to injury are, in general, beneficial to the host and allow healing/ survival. In essence, the concept evolved that the constancy of the ‘milieu intérieur’ allowed for the independence of organisms, that complex homeostatic responses sought to maintain this constancy, and that within this range of responses were the elements of healing and repair. These ideas pertained to normal physiology and mild/moderate injury. In the modern era, such concepts do not account for disease evolution following major injury/sepsis or the injured patient who would have died but for artificial organ support. Such patients exemplify less of the classical homeostatic control system (signal detector–processor–effector regulated by a negative feedback loop) and more

John Hunter, 1728–1793, surgeon, St George’s Hospital, London, UK. He is regarded as ‘The Father of Scientific Surgery’. To further his knowledge of venereal disease he inoculated himself with syphilis in 1767.

• Changes in body composition that accompany surgical injury • Avoidable factors that compound the metabolic response to injury • Concepts behind optimal perioperative care

of the ‘open loop’ system, whereby only with medical/surgical resolution of the primary abnormality is a return to classical homeostasis possible. As a consequence of modern understanding of the metabolic response to injury, elective surgical practice seeks to reduce the need for a homeostatic response by minimising the primary insult (minimal access surgery and ‘stress-free’ perioperative care). In emergency surgery, where the presence of tissue trauma/sepsis/hypovolaemia often compounds the primary problem, there is a requirement to augment artificially homeostatic responses (resuscitation) and to close the ‘open’ loop by intervening to resolve the primary insult (e.g. surgical treatment of major abdominal sepsis) and provide organ support (critical care) while the patient comes back to a situation in which homeostasis can achieve a return to normality (Summary box 1.1).

Summary box 1.1 Basic concepts ■ ■ ■

Homeostasis is the foundation of normal physiology ‘Stress-free’ perioperative care helps to preserve homeostasis following elective surgery Resuscitation, surgical intervention and critical care can return the severely injured patient to a situation in which homeostasis becomes possible once again

This chapter aims to review the mediators of the stress response, the physiological and biochemical pathway changes associated with surgical injury and the changes in body composition that occur following surgical injury. Emphasis is laid on why knowledge of these events is important to understand the rationale for modern ‘stress-free’ perioperative and critical care.

PART 1 | PRINCIPLES

To understand: • Classical concepts of homeostasis • Mediators of the metabolic response to injury • Physiological and biochemical changes that occur during injury and recovery

Claude Bernard, 1813–1878, Professor of Physiology, The College de France, Paris, France. Walter Bradford Cannon, 1871–1945, Professor of Physiology, Harvard University Medical School, Boston, MA, USA.

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M E TA B O L I C R E S P O N S E T O I N J U R Y

THE GRADED NATURE OF THE INJURY RESPONSE

MEDIATORS OF THE METABOLIC RESPONSE TO INJURY

It is important to recognise that the response to injury is graded: the more severe the injury, the greater the response (Figure 1.1). This concept not only applies to physiological/metabolic changes but also to immunological changes/sequelae. Thus, following elective surgery of intermediate severity, there may be a transient and modest rise in temperature, heart rate, respiratory rate, energy expenditure and peripheral white cell count. Following major trauma/sepsis, these changes are accentuated, resulting in a systemic inflammatory response syndrome (SIRS), hypermetabolism, marked catabolism, shock and even multiple organ dysfunction (MODS). It is important to recognise that genetic variability plays a key role in determining the intensity of the inflammatory response. Moreover, in certain circ*mstances, the severity of injury does not lead to a simple dose-dependent metabolic response, but rather leads to quantitatively different responses. Not only is the metabolic response graded, but it also evolves with time. In particular, the immunological sequelae of major injury evolve from a proinflammatory state driven primarily by the innate immune system (macrophages, neutrophils, dendritic cells) into a compensatory anti-inflammatory response syndrome (CARS) characterised by suppressed immunity and diminished resistance to infection. In patients who develop infective complications, the latter will drive ongoing systemic inflammation, the acute phase response and continued catabolism.

The classical neuroendocrine pathways of the stress response consist of afferent nociceptive neurones, the spinal cord, thalamus, hypothalamus and pituitary (Figure 1.2). Corticotrophinreleasing factor (CRF) released from the hypothalamus increases adrenocorticotrophic hormone (ACTH) release from the anterior pituitary. ACTH then acts on the adrenal to increase the secretion of cortisol. Hypothalamic activation of the sympathetic nervous system causes release of adrenalin and also stimulates release of glucagon. Intravenous infusion of a co*cktail of these ‘counter-regulatory’ hormones (glucagon, glucocorticoids and catecholamines) reproduces many aspects of the metabolic response to injury. There are, however, many other players, including alterations in insulin release and sensitivity, hypersecretion of prolactin and growth hormone (GH) in the presence of low circulatory insulin-like growth factor-1 (IGF-1) and inactivation of peripheral thyroid hormones and gonadal function. Of note, GH has direct lipolytic, insulin-antagonising and proinflammatory properties (Summary box 1.2).

Resting metabolic rate (%)

The neuroendocrine response to severe injury/critical illness is biphasic:

Major trauma

130

Minor trauma

120

■

110

Acute phase characterised by an actively secreting pituitary and elevated counter-regulatory hormones (cortisol, glucagon, adrenaline). Changes are thought to be beneficial for short-term survival Chronic phase associated with hypothalamic suppression and low serum levels of the respective target organ hormones. Changes contribute to chronic wasting

Normal range

100 90

Starvation

80 0

25 Nitrogen excretion (g N/day)

Neuroendocrine response to injury/critical illness

■

140

PART 1 | PRINCIPLES

Summary box 1.2

days

Major trauma Minor trauma

15 10

Normal range

5 0

Figure 1.1 Hypermetabolism and increased nitrogen excretion are closely related to the magnitude of the initial injury and show a graded response.

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The innate immune system (principally macrophages) interacts in a complex manner with the adaptive immune system (T cells, B cells) in co-generating the metabolic response to injury (Figure 1.2). Proinflammatory cytokines including interleukin-1 (IL-1), tumour necrosis factor alpha (TNFα), IL-6 and IL-8 are produced within the first 24 hours and act directly on the hypothalamus to cause pyrexia. Such cytokines also augment the hypothalamic stress response and act directly on skeletal muscle to induce proteolysis while inducing acute phase protein production in the liver. Proinflammatory cytokines also play a complex role in the development of peripheral insulin resistance. Other important proinflammatory mediators include nitric oxide ((NO) via inducible nitric oxide synthetase (iNOS)) and a variety of prostanoids (via cyclo-oxygenase-2 (Cox-2)). Changes in organ function (e.g. renal hypoperfusion/impairment) may be induced by excessive vasoconstriction via endogenous factors such as endothelin-1. Within hours of the upregulation of proinflammatory cytokines, endogenous cytokine antagonists enter the circulation (e.g. interleukin-1 receptor antagonist (IL-1Ra) and TNFsoluble receptors (TNF-sR-55 and 75)) and act to control the proinflammatory response. A complex further series of adaptive

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The metabolic stress response to surger y and trauma: the ‘ebb and flow’ model Hypothalamus

PLASMA

CRF

CHANGES IN BODY METABOLISM

Pituitary ACTH

Spinal cord

ADRENALIN CORTISOL

Adrenal

Sympathetic nervous system

HEPATIC GLUCONEOGENESIS

SKELETAL MUSCLE PROTEIN DEGRADATION GLUCAGON Pancreas

Injury

Afferent noiciceptive pathways

ADIPOCYTE LIPOLYSIS

Adaptive immune system

Innate immune system

IL-1 TNFα IL-6 IL-8 Insulin IGF-1 TESTOSTERONE T3

HEPATIC ACUTE PHASE PROTEIN SYNTHESIS

PYREXIA

HYPERMETABOLISM

changes includes the development of a Th2-type counterinflammatory response (regulated by IL-4, -5, -9 and -13 and transforming growth factor beta (TGFβ)) which, if accentuated and prolonged in critical illness, is characterised as the CARS and results in immunosuppression and an increased susceptibility to opportunistic (nosocomial) infection (Summary box 1.3). Within inflamed tissue the duration and magnitude of acute inflammation as well as the return to homeostasis are influenced by a group of local mediators known as specialised pro-resolving mediators (SPM) that include essential fatty acid-derived lipoxins, resolvins, protectins and maresins. These endogenous resolution agonists orchestrate the uptake and clearance of apoptotic polymorphonuclear neutrophils and microbial particles, reduce proinflammatory cytokines and lipid mediators as well as enhance the removal of cellular debris in the inflammatory milieu. Thus both at the systemic level (endogenous cytokine antagonists – see above) and at the local tissue level, the body attempts to limit/resolve inflammation driven dyshomeostasis. Summary box 1.3 Systemic inflammatory response syndrome following major injury ■ ■ ■

Is driven initially by proinflammatory cytokines (e.g. IL-1, IL-6 and TNFα) Is followed rapidly by increased plasma levels of cytokine antagonists and soluble receptors (e.g. IL-1Ra, TNF-sR) If prolonged or excessive may evolve into a counterinflammatory response syndrome

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There are many complex interactions between the neuroendocrine, cytokine and metabolic axes. For example, although cortisol is immunosuppressive at high levels, it acts synergistically with IL-6 to promote the hepatic acute phase response. ACTH release is enhanced by proinflammatory cytokines and the noradrenergic system. The resulting rise in cortisol levels may form a weak feedback loop attempting to limit the proinflammatory stress response. Finally, hyperglycaemia may aggravate the inflammatory response via substrate overflow in the mitochondria, causing the formation of excess free oxygen radicals and also altering gene expression to enhance cytokine production. At the molecular level, the changes that accompany systemic inflammation are extremely complex. In a recent study using network-based analysis of changes in mRNA expression in leukocytes following exposure to endotoxin, there were changes in the expression of more than 3700 genes with over half showing decreased expression and the remainder increased expression. The cell surface receptors, signalling mechanisms and transcription factors that initiate these events are also complex, but an early and important player involves the nuclear factor kappa B (NFκB)/relA family of transcription factors. A simplified model of current understanding of events within skeletal muscle is shown in Figure 1.3.

THE METABOLIC STRESS RESPONSE TO SURGERY AND TRAUMA: THE ‘EBB AND FLOW’ MODEL

PART 1 | PRINCIPLES

Bailey and Love Figure 1.2 The integrated fig. 1.02 response to surgical injury (first 24–48 hours): there is a complex interplay between the neuroendocrine stress response and the proinflammatory cytokine response of the innate immune system.

In the natural world, if an animal is injured, it displays a characteristic response, which includes immobility, anorexia and catabolism (Summary box 1.4).

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M E TA B O L I C R E S P O N S E T O I N J U R Y Injury

Atrophy

Hypertrophy IGF-1

TNF

Myostatin

PI3K

CELL MEMBRANE

NFB

Akt

mTOR MyoD

FOXO p70S6K 4E-BP-1

NUCLEUS

Protein synthesis

Protein degradation

E3 ligases

Summary box 1.4 Physiological response to injury The natural response to injury includes: Immobility/rest Anorexia ■ Catabolism The changes are designed to aid survival of moderate injury in the absence of medical intervention. ■

PART 1 | PRINCIPLES

■

In 1930, Sir David Cuthbertson divided the metabolic response to injury in humans into ‘ebb’ and ‘flow’ phases (Figure 1.4). The ebb phase begins at the time of injury and lasts for approximately 24–48 hours. It may be attenuated by proper resuscitation, but not completely abolished. The ebb phase is characterised by hypovolaemia, decreased basal metabolic rate, reduced cardiac output, hypothermia and lactic acidosis. The predominant hormones regulating the ebb phase INJURY EBB PHASE

FLOW PHASE

RECOVERY

HOURS

DAYS

WEEKS

Shock

Catabolism

Anabolism

Figure 1.4 Phases of the physiological response to injury (after Cuthbertson 1930).

Figure 1.3 The major catabolic and anabolic signalling pathways involved in skeletal muscle homeostasis. FOXO, forkhead box sub-group O; mTOR, mammalian target of rapamycin; MyoD, myogenic differentiation factor D; NFκB, nuclear factor kappa B; PI3K, phosphatidylinositol 3-kinase; p70S6K, p70S6 kinase; TNFα, tumour necrosis factor alpha; 4E-BP-1, eukaryotic initiation translation factor 4E binding protein 1.

are catecholamines, cortisol and aldosterone (following activation of the renin–angiotensin system). The magnitude of this neuroendocrine response depends on the degree of blood loss and the stimulation of somatic afferent nerves at the site of injury. The main physiological role of the ebb phase is to conserve both circulating volume and energy stores for recovery and repair. Following resuscitation, the ebb phase evolves into a hypermetabolic flow phase, which corresponds to SIRS. This phase involves the mobilisation of body energy stores for recovery and repair, and the subsequent replacement of lost or damaged tissue. It is characterised by tissue oedema (from vasodilatation and increased capillary leakage), increased basal metabolic rate (hypermetabolism), increased cardiac output, raised body temperature, leukocytosis, increased oxygen consumption and increased gluconeogenesis. The flow phase may be subdivided into an initial catabolic phase, lasting approximately 3–10 days, followed by an anabolic phase, which may last for weeks if extensive recovery and repair are required following serious injury. During the catabolic phase, the increased production of counter-regulatory hormones (including catecholamines, cortisol, insulin and glucagon) and inflammatory cytokines (e.g. IL-1, IL-6 and TNFα) results in significant fat and protein mobilisation, leading to significant weight loss and increased urinary nitrogen excretion. The increased production of insulin at this time is associated with significant insulin resistance and, therefore, injured patients often exhibit poor glycaemic control. The combination of pronounced or prolonged catabolism in association with insulin resistance places patients within this phase at increased risk of complications, particularly infectious and cardiovascular. Obviously, the development of complications will further aggravate the neuroendocrine and inflammatory stress responses, thus creating a vicious catabolic cycle (Summary box 1.5).

Sir David Paton Cuthbertson, 1900–1989, biochemist, Director of the Rowett Research Institute, Glasgow, UK.

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Key catabolic elements of the flow phase of the metabolic stress response

regulation) counteract the hypermetabolic driving forces of the stress response. Furthermore, the skeletal muscle wasting experienced by patients with prolonged catabolism actually limits the volume of metabolically active tissue (Summary box 1.6; see below).

Summary box 1.5 Purpose of neuroendocrine changes following injury The constellation of neuroendocrine changes following injury acts to:

Summary box 1.6

Provide essential substrates for survival Postpone anabolism ■ Optimise host defence These changes may be helpful in the short term, but may be harmful in the long term, especially to the severely injured patient who would otherwise not have survived without medical intervention. ■ ■

Hypermetabolism Hypermetabolism following injury: ■ ■

KEY CATABOLIC ELEMENTS OF THE FLOW PHASE OF THE METABOLIC STRESS RESPONSE

The majority of trauma patients (except possibly those with extensive burns) demonstrate energy expenditures approximately 15–25 per cent above predicted healthy resting values. The predominant cause appears to be a complex interaction between the central control of metabolic rate and peripheral energy utilisation. In particular, central thermodysregulation (caused by the proinflammatory cytokine cascade), increased sympathetic activity, abnormalities in wound circulation (ischaemic areas produce lactate, which must be metabolised by the adenosine triphosphate (ATP)-consuming hepatic Cori cycle; hyperaemic areas cause an increase in cardiac output), increased protein turnover and nutritional support may all increase patient energy expenditure. Theoretically, patient energy expenditure could rise even higher than observed levels following surgery or trauma, but several features of standard intensive care (including bed rest, paralysis, ventilation and external temperature

Muscle protein is continually synthesised and broken down with a turnover rate in humans of 1–2 per cent per day, and with a greater amplitude of changes in protein synthesis (± two-fold) than breakdown (± 0.25-fold) during the diurnal cycle. Under normal circ*mstances, synthesis equals breakdown and muscle bulk remains constant. Physiological stimuli that promote net muscle protein accretion include feeding (especially extracellular amino acid concentration) and exercise. Paradoxically, during exercise, skeletal muscle protein synthesis is depressed, but it increases again during rest and feeding. During the catabolic phase of the stress response, muscle wasting occurs as a result of an increase in muscle protein degradation (via enzymatic pathways), coupled with a decrease in muscle protein synthesis. The major site of protein loss is peripheral skeletal muscle, although nitrogen losses also occur in the respiratory muscles (predisposing the patient to hypoventilation and chest infections) and in the gut (reducing gut motility). Cardiac muscle appears to be mostly spared. Under extreme conditions of catabolism (e.g. major sepsis), urinary nitrogen losses can reach 14–20 g/day; this is equivalent to the loss of 500 g of skeletal muscle per day. It is remarkable that muscle catabolism cannot be inhibited fully by providing artificial nutritional support as long as the stress response continues. Indeed, in critical care, it is now recognised that ‘hyperalimentation’ represents a metabolic stress in itself, and that nutritional support should be at a modest level to attenuate rather than replace energy and protein losses.

Central tissues Liver

Muscle Amino Acids Adipose tissue

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Immune system especially Gln and Ala

Wound

Figure 1.5 During the metabolic response to injury, the body reprioritises protein metabolism away from peripheral tissues and towards key central tissues such as the liver, immune system and wound. One of the main reasons why the reutilisation of amino acids derived from muscle proteolysis leads to net catabolism is that the increased glutamine and alanine efflux from muscle is derived, in part, from the irreversible degradation of branched chain amino acids. Ala, alanine; Gln, glutamine.

PART 1 | PRINCIPLES

Hypermetabolism

Skin

Is mainly caused by an acceleration of energy-dependent metabolic cycles Is limited in modern practice on account of elements of routine critical care

Alterations in skeletal muscle protein metabolism

There are several key elements of the flow phase that largely determine the extent of catabolism and thus govern the metabolic and nutritional care of the surgical patient. It must be remembered that, during the response to injury, not all tissues are catabolic. Indeed, the essence of this coordinated response is to allow the body to reprioritise limited resources away from peripheral tissues (muscle, adipose tissue, skin) and towards key viscera (liver, immune system) and the wound (Figure 1.5).

Peripheral tissues

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M E TA B O L I C R E S P O N S E T O I N J U R Y Myofibrillar protein

Caspases, cathepsins and calpains Ubiquitinated protein Amino acids

E1, E2, E3 ATP 19S

Tripeptidyl peptidase Ubiquitin

26S proteasome ATP

Oligopeptides

20S 19S

ATP

Substrate unfolding and proteolytic cleavage

Figure 1.6 The intercellular effector mechanisms involved in degrading myofibrillar protein into free amino acids. The ubiquitin–proteasome pathway is a complex multistep process, which requires adenosine triphosphate and results in the tagging of specific proteins with ubiquitin for degradation of proteasome. E1, ubiquitin-activating enzyme; E2, ubiquitin-conjugating enzyme; E3, ubiquitin ligase.

Bailey and Love fig. 1.06

The predominant mechanism involved in the wasting of skeletal muscle is the ATP-dependent ubiquitin–proteasome pathway (Figure 1.6), although the lysosomal cathepsins and the calcium–calpain pathway play facilitatory and accessory roles. Clinically, a patient with skeletal muscle wasting will experience asthenia, increased fatigue, reduced functional ability, decreased quality of life and an increased risk of morbidity and mortality. In critically ill patients, muscle weakness may be further worsened by the development of critical illness myopathy, a multifactorial condition that is associated with impaired excitation–contraction coupling at the level of the sarcolemma and the sarcoplasmic reticulum membrane (Summary box 1.7). Summary box 1.7

PART 1 | PRINCIPLES

Skeletal muscle wasting ■ ■ ■

Provides amino acids for the metabolic support of central organs/tissues Is mediated at a molecular level mainly by activation of the ubiquitin–proteasome pathway Can result in immobility and contribute to hypostatic pneumonia and death if prolonged and excessive

Alterations in hepatic protein metabolism: the acute phase protein response The liver and skeletal muscle together account for >50 per cent of daily body protein turnover. Skeletal muscle has a large mass but a low turnover rate (1–2 per cent per day), whereas the liver has a relatively small mass (1.5 kg) but a much higher protein turnover rate (10–20 per cent per day). Hepatic protein synthesis is divided roughly 50:50 between renewal of structural

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proteins and synthesis of export proteins. Albumin is the major export protein produced by the liver and is renewed at the rate of about 10 per cent per day. The transcapillary escape rate (TER) of albumin is about ten times the rate of synthesis, and shortterm changes in albumin concentration are most probably due to increased vascular permeability. Albumin TER may be increased three-fold following major injury/sepsis. In response to inflammatory conditions, including surgery, trauma, sepsis, cancer or autoimmune conditions, circulating peripheral blood mononuclear cells secrete a range of proinflammatory cytokines, including IL-1, IL-6 and TNFα. These cytokines, in particular IL-6, promote the hepatic synthesis of positive acute phase proteins, e.g. fibrinogen and C-reactive protein (CRP). The acute phase protein response (APPR) represents a ‘double-edged sword’ for surgical patients as it provides proteins important for recovery and repair, but only at the expense of valuable lean tissue and energy reserves. In contrast to the positive acute phase reactants, the plasma concentrations of other liver export proteins (the negative acute phase reactants) fall acutely following injury, e.g. albumin. However, rather than represent a reduced hepatic synthesis rate, the fall in plasma concentration of negative acute phase reactants is thought principally to reflect increased transcapillary escape, secondary to an increase in microvascular permeability (see above). Thus, increased hepatic synthesis of positive acute phase reactants is not compensated for by reduced synthesis of negative reactants (Summary box 1.8).

Carl Ferdinand Cori, 1896–1984, Professor of Pharmacology, and later of Biochemistry, Washington University Medical School, St Louis, MI, USA and his wife Gerty Theresa Cori, 1896–1957, who was also Professor of Biochemistry at the Washington University Medical School. In 1947 the Coris were awarded a share of the Nobel Prize for Physiology or Medicine ‘for their discovery of how glycogen is catalytically converted’.

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Changes in body composition following injur y 70

Summary box 1.8

Hepatic acute phase response

■

Positive reactants (e.g. CRP): plasma concentration ↑ Negative reactants (e.g. albumin): plasma concentration ↓

Following surgery or trauma, postoperative hyperglycaemia develops as a result of increased glucose production combined with decreased glucose uptake in peripheral tissues. Decreased glucose uptake is a result of insulin resistance which is transiently induced within the stressed patient. Suggested mechanisms for this phenomenon include the action of proinflammatory cytokines and the decreased responsiveness of insulin-regulated glucose transporter proteins. The degree of insulin resistance is proportional to the magnitude of the injurious process. Following routine upper abdominal surgery, insulin resistance may persist for approximately 2 weeks. Postoperative patients with insulin resistance behave in a similar manner to individuals with type II diabetes mellitus. The mainstay of management of insulin resistance is intravenous insulin infusion. Insulin infusions may be used in either an intensive approach (i.e. sliding scales are manipulated to normalise the blood glucose level) or a conservative approach (i.e. insulin is administered when the blood glucose level exceeds a defined limit and discontinued when the level falls). Studies of postoperatively ventilated patients in the intensive care unit (ICU) have suggested that maintenance of normal glucose levels using intensive insulin therapy can significantly reduce both morbidity and mortality. Furthermore, intensive insulin therapy is superior to conservative insulin approaches in reducing morbidity rates. However, the mortality benefit of intensive insulin therapy over a more conservative approach has not been proven conclusively. The observed benefits of insulin therapy are probably simply as a result of maintenance of normoglycaemia, but the glycaemia-independent actions of insulin may also exert minor, organ-specific effects (e.g. promotion of myocardial systolic function).

CHANGES IN BODY COMPOSITION FOLLOWING INJURY The average 70-kg male can be considered to consist of fat (13 kg) and fat-free mass (or lean body mass: 57 kg). In such an individual, the lean tissue is composed primarily of protein (12 kg), water (42 kg) and minerals (3 kg) (Figure 1.7). The protein mass can be considered as two basic compartments, skeletal muscle (4 kg) and non-skeletal muscle (8 kg), which includes the visceral protein mass. The water mass (42 litres) is divided into intercellular (28 litres) and extracellular (14 litres) spaces. Most of the mineral mass is contained in the bony skeleton. The main labile energy reserve in the body is fat, and the main labile protein reserve is skeletal muscle. While fat mass can be reduced without major detriment to function, loss of protein mass results not only in skeletal muscle wasting, but

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PROTEIN

40 30

INTRACELLULAR WATER

20 10

FFM or LBM

Insulin resistance

FAT

EXTRACELLULAR WATER MINERALS

0 Figure 1.7 The chemical body composition of a normal 70-kg male. FFM, fat-free mass; LBM, lean body mass.

also depletion of visceral protein status. Within lean issue, each 1 g of nitrogen is contained within 6.25 g of protein, which is contained in approximately 36 g of wet weight tissue. Thus, the loss of 1 g of nitrogen in urine is equivalent to the breakdown of 36 g of wet weight lean tissue. Protein turnover in the whole body is of the order of 150–200 g per day. A normal human ingests about 70–100 g protein per day, which is metabolised and excreted in urine as ammonia and urea (i.e. approximately 14 g N/day). During total starvation, urinary loss of nitrogen is rapidly attenuated by a series of adaptive changes. Loss of body weight follows a similar course (Figure 1.8), thus accounting for the survival of hunger strikers for a period of 50–60 days. Following major injury, and particularly in the presence of ongoing septic complications, this adaptive change fails to occur, and there is a state of ‘autocannibalism’, resulting in continuing urinary nitrogen losses of 10–20 g N/day (equivalent to 500 g of wet weight lean tissue per day). As with total starvation, once loss of body protein mass has reached 30–40 per cent of the total, survival is unlikely. Critically ill patients admitted to the ICU with severe sepsis or major blunt trauma undergo massive changes in body composition (Figure 1.8). Body weight increases immediately on resuscitation with an expansion of extracellular water by 6–10 litres within 24 hours. Thereafter, even with optimal metabolic care and nutritional support, total body protein will diminish by 15 per cent in the next 10 days, and body weight will reach negative balance as the expansion of the extracellular space resolves. In marked contrast, it is now possible to maintain body weight and nitrogen equilibrium following major elective surgery. This can be achieved by blocking the neuroendocrine stress response with epidural analgesia and providing early enteral feeding. Moreover, the early fluid retention phase can be avoided by careful intraoperative management of fluid balance, with avoidance of excessive administration of intravenous saline (Summary box 1.9).

PART 1 | PRINCIPLES

■

50 Mass (kg)

The hepatic acute phase response represents a reprioritisation of body protein metabolism towards the liver and is characterised by:

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M E TA B O L I C R E S P O N S E T O I N J U R Y

Weight gain (%)

16 14 12 10 8

Sepsis and multiorgan failure

6 4

Weight loss (%)

2 2 4 6 8

2 4 6 8

10 12 14 16 18 20 22 days

10 12 14 16

Uncomplicated major surgery

Starvation

Summary box 1.9 Changes in body composition following major surgery/critical illness ■ ■

Catabolism leads to a decrease in fat mass and skeletal muscle mass Body weight may paradoxically increase because of expansion of extracellular fluid space

AVOIDABLE FACTORS THAT COMPOUND THE RESPONSE TO INJURY

PART 1 | PRINCIPLES

As noted previously, the main features of the metabolic response are initiated by the immune system, cardiovascular system, sympathetic nervous system, ascending reticular formation and limbic system. However, the metabolic stress response may be further exacerbated by anaesthesia, dehydration, starvation (including preoperative fasting), sepsis, acute medical illness or even severe psychological stress (Figure 1.9). Attempts to limit or control these factors can be beneficial to the patient (Summary box 1.10). Summary box 1.10 Avoidable factors that compound the response to injury ■ ■ ■ ■ ■ ■

Continuing haemorrhage Hypothermia Tissue oedema Tissue underperfusion Starvation Immobility

Volume loss During simple haemorrhage, pressor receptors in the carotid artery and aortic arch, and volume receptors in the wall of the

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Figure 1.8 Changes in body weight that occur in serious sepsis, after uncomplicated surgery and in total starvation.

left atrium, initiate afferent nerve input to the central nervous system (CNS), resulting in the release of both aldosterone and antidiuretic hormone (ADH). Pain can also stimulate ADH release. ADH acts directly on the kidney to cause fluid retention. Decreased pulse pressure stimulates the juxtaglomerular apparatus in the kidney and directly activates the renin–angiotensin system, which in turn increases aldosterone release. Aldosterone causes the renal tubule to reabsorb sodium (and consequently also conserve water). ACTH release also augments the aldosterone response. The net effects of ADH and aldosterone result in the natural oliguria observed after surgery and conservation of sodium and water in the extracellular space. The tendency towards water and salt retention is exacerbated by resuscitation with saline-rich fluids. Salt and water retention can result in not only peripheral oedema, but also visceral oedema (e.g. stomach). Such visceral oedema has been associated with reduced gastric emptying, delayed resumption of food intake and prolonged hospital stay. Careful limitation of intraoperative administration of colloids and crystalloids (e.g. Hartmann’s solution) so that there is no net weight gain following elective surgery has been proven to reduce postoperative complications and length of stay.

Hypothermia Hypothermia results in increased elaboration of adrenal steroids and catecholamines. When compared with normothermic controls, even mild hypothermia results in a two- to three-fold increase in postoperative cardiac arrhythmias and increased catabolism. Randomised trials have shown that maintaining normothermia by an upper body forced-air heating cover reduces wound infections, cardiac complications and bleeding and transfusion requirements.

Tissue oedema During systemic inflammation, fluid, plasma proteins, leukocytes, macrophages and electrolytes leave the vascular space and accumulate in the tissues. This can diminish the alveolar diffusion of oxygen and may lead to reduced renal function. Increased capillary leak is mediated by a wide variety of mediators including cytokines, prostanoids, bradykinin and nitric oxide. Vasodilatation implies that intravascular volume

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Concepts behind optimal perioperative care

STARVATION

hypermetabolism

adreno-sympathetic activation

acute phase response

wound hypothermia hypotension pain

insulin resistance futile substrate cycling

cytokine cascade release

muscle protein degradation

IMMOBILISATION

C A T A B O L I S M

Figure 1.9 Factors that exacerbate the metabolic response to surgical injury include hypothermia, controlled pain, starvation, immobilisation, sepsis and medical complications

Systemic inflammation and tissue underperfusion The vascular endothelium controls vasomotor tone and microvascular flow, and regulates trafficking of nutrients and biologically active molecules. When endothelial activation is excessive, compromised microcirculation and subsequent cellular hypoxia contribute to the risk of organ failure. Maintaining normoglycaemia with insulin infusion during critical illness has been proposed to protect the endothelium, probably in part, via inhibition of excessive iNOS-induced NO release, and thereby contribute to the prevention of organ failure and death. Administration of activated protein C to critically ill patients has been shown to reduce organ failure and death and is thought to act, in part, via preservation of the microcirculation in vital organs.

Starvation During starvation, the body is faced with an obligate need to generate glucose to sustain cerebral energy metabolism (100 g of glucose per day). This is achieved in the first 24 hours by mobilising glycogen stores and thereafter by hepatic gluconeogenesis from amino acids, glycerol and lactate. The energy metabolism of other tissues is sustained by mobilising fat from adipose tissue. Such fat mobilisation is mainly dependent on a fall in circulating insulin levels. Eventually, accelerated loss of lean tissue (the main source of amino acids for hepatic gluconeogenesis) is reduced as a result of the liver converting free fatty acids into ketone bodies, which can serve as a substitute for glucose for

cerebral energy metabolism. Provision of 2 litres of intravenous 5 per cent dextrose as intravenous fluids for surgical patients who are fasted provides 100 g of glucose per day and has a significant protein-sparing effect. Avoiding unnecessary fasting in the first instance and early oral/enteral/parenteral nutrition form the platform for avoiding loss of body mass as a result of the varying degrees of starvation observed in surgical patients. Modern guidelines on fasting prior to anaesthesia allow intake of clear fluids up to 2 hours before surgery. Administration of a carbohydrate drink at this time reduces perioperative anxiety and thirst and decreases postoperative insulin resistance.

Immobility Immobility has long been recognised as a potent stimulus for inducing muscle wasting. Inactivity impairs the normal mealderived amino acid stimulation of protein synthesis in skeletal muscle. Avoidance of unnecessary bed rest and active early mobilisation are essential measures to avoid muscle wasting as a consequence of immobility.

CONCEPTS BEHIND OPTIMAL PERIOPERATIVE CARE Current understanding of the metabolic response to surgical injury and the mediators involved has led to a reappraisal of traditional perioperative care. There is now a strong scientific rationale for avoiding unmodulated exposure to stress, prolonged fasting and excessive administration of intravenous (saline) fluids (Figure 1.10). The widespread adoption of minimal access (laparoscopic) surgery is a key change in surgical practice that can reduce the magnitude of surgical injury and enhance the rate of patients’ return to homeostasis and recovery. It is also impor-

PART 1 | PRINCIPLES

decreases, which induces shock if inadequate resuscitation is not undertaken. Meanwhile, intracellular volume decreases, and this provides part of the volume necessary to replenish intravascular and extravascular extracellular volume.

Alexis Frank Hartmann, 1898–1964, paediatrician, St Louis, MO, USA.

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M E TA B O L I C R E S P O N S E T O I N J U R Y

Functional capacity

Further reading

Table 2.7 ABO blood group system.

Phenotype

Genotype

Antigens

Antibodies

Frequency (%)

Anti-A, anti-B

AA or AO

Anti-B

BB or BO

Anti-A

None

• FFP if prothrombin time (PT) or partial thromboplastin time (PTT) >1.5 times normal

• cryoprecipitate if fibrinogen 1 year)

Infinite (>1 year)

Infinite (> 1 year)

Non-absorbable: remains encapsulated in body tissues Non-absorbable: remains encapsulated in body tissues

Non-absorbable: remains encapsulated in body tissues

Polyamide polymer Loses 15–20% per Degrades at year approximately 15–20% per year

An alloy of iron, nickel and chromium

PART 1 | PRINCIPLES

Monofilament. Dyed or undyed

Monofilament or multifilament

Surgical steel

Polybutester

Twisted

Linen

Long staple flax fibres

Braided or twisted Natural protein multifilament. Raw silk from Dyed or undyed. silkworm Coated (with wax or silicone) or uncoated

Silk

Raw material

Types

Suture

Table 4.2 Non-absorbable suture materials.

Low

Minimal

Moderate

Moderate to high Not recommended Consider suitable absorbable or non-absorbable

Tissue reaction

None

Should not be used in conjunction with prosthesis of different metal

Not for use with vascular prostheses or in tissues requiring prolonged approximation under stress Risk of infection and tissue reaction makes silk unsuitable for routine skin closure Not advised for use with vascular prostheses

Contraindications

Exhibits a degree of elasticity. Particularly favoured for use in plastic surgery Cardiovascular surgery, plastic surgery, ophthalmic surgery, general surgical subcuticular skin closure

Cardiovascular, ophthalmic, plastic and general surgery

Ligation and suturing in gastrointestinal surgery. No longer in common use in most centres Closure of sternotomy wounds Previously found favour for tendon and hernia repairs General surgical use, e.g. skin closure, abdominal wall mass closure, hernia repair, plastic surgery, neurosurgery, microsurgery, ophthalmic surgery

Ligation and suturing when long-term tissue support is necessary For securing drains externally

Frequent uses

10/0–1 with needles

7/0–1 with needles

Monofilament: 5/0–5 with needles; multifilament: 5/0– 3/0 with needles Monofilament: 11/0–2 with needles (including loops in some sizes), 4/0–2 without needles; multifilament: 6/0–2 with needles, 3/0–1 without needles Monofilament: (ophthalmic) 11/10; 10/0 with needles; multifilament: 5/0–1 with needles

3/0–1 with needles, 3/0–1 without needles

10/0–2 with needles, 4/0–1 without needles

How supplied

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Braided multifilament

Monofilament Copolymer of glycolic Dyed or acid and trimethylene undyed carbonate

Braided multifilament Dyed or undyed Coated or uncoated

Polyglactin

Polyglyconate

Polyglycolic acid

Polymer of polyglycolic acid. Available with coating of inert, absorbable surfactant poloxamer 188 to enhance surface smoothness 87% excreted in urine within 3 days Monofilament Polyester polymer Dyed or undyed

Collagen derived from healthy sheep or cattle Tanned with chromium salts to improve handling and to resist degradation in tissue Copolymer of lactide and glycolide in a ratio of 90:10, coated with polyglactin and calcium stearate

Approximately 70% remains at 2 weeks Approximately 50% remains at 4 weeks Approximately 14% remains at 8 weeks

Approximately 40% remains at 1 week Approximately 20% remains at 3 weeks

Approximately 70% remains at 2 weeks Approximately 55% remains at 3 weeks

Lost within 21–28 days Marked patient variability Unpredictable and not recommended Approximately 60% remains at 2 weeks Approximately 30% remains at 3 weeks

Lost within 7–10 days Marked patient variability Unpredictable and not recommended

Tensile strength retention in vivo

Polyglycaprone Monofilament Copolymer of glycolite 21 days maximum and caprolactone

Polydioxanone (PDS)

Chromic

Catgut

Collagen derived from healthy sheep or cattle

Plain

Catgut

Raw material

Types

Suture

Table 4.3 Absorbable suture materials.

PART 1 | PRINCIPLES

Contraindications

90–120 days

Hydrolysis minimal at 90 days Complete absorption at 180 days

Hydrolysis minimal at 2 weeks, significant at 4 weeks. Complete absorption 60–90 days

Mild

Minimal

Hydrolysis minimal until Mild 8–9 weeks. Complete absorption by 180 days

Hydrolysis minimal until Mild 5–6 weeks. Complete absorption 60–90 days

Not for use in association with heart valves or synthetic grafts, or in situations in which prolonged tissue approximation under stress is required No use for extended support

Not advised for use in tissues which require prolonged approximation under stress Not advised for use in tissues which require prolonged approximation under stress

Not advised for use in tissues which require prolonged approximation under stress

Not for use in tissues which heal slowly and require prolonged support Synthetic absorbables are superior Phagocytosis and Moderate As for plain catgut enzymatic degradation Synthetic absorbables within 90 days superior

Tissue reaction

Phagocytosis and High enzymatic degradation within 7–10 days

Absorption rate

7/0–2 with needles

8/0–2 with needles; 5/0–2 without needles

6/0–3 with needles; 5/0–3 without needles

6/0–1 with needles; 4/0–3 without needles

How supplied

Subcuticular in skin, ligation, 8/0–2 with gastrointestinal and muscle surgery needles

Uses as for other absorbable Polydioxanone sutures, in particular where slightly suture (PDS) longer wound support is required 10/0–2 with needles

Uses as for other absorbable 9/0–2 with sutures, in particular where slightly needles; 9/0–2 longer wound support is required without needles

General surgical use where absorbable sutures required, e.g. gut anastomoses, vascular ligatures. Has become the ‘workhorse’ suture for many applications in most general surgical practices, including undyed for subcuticular wound closures. Ophthalmic surgery Popular in some centres as an alternative to Vicryl and PDS

As for plain catgut

Ligate superficial vessels, suture subcutaneous tissues Stomas and other tissues that heal rapidly

Frequent uses

38 BASIC SURGICAL SKILLS AND ANASTOMOSES

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Wo u n d c l o s u r e

Suture techniques There are four frequently used suture techniques. 1 Interrupted sutures. Interrupted sutures require the needle to be inserted at right angles to the incision and then to pass through both aspects of the suture line and exit again at right angles (Figure 4.5). It is important for the needle to be rotated through the tissues rather than to be dragged through for fear of unnecessarily enlarging the needle hole. As a guide, the distance from the entry point of the needle to the edge of the wound should be approximately the same as the depth of the tissue being sutured, and each successive suture should be placed at twice this distance apart (Figure 4.6). Each suture should reach into the depths of the wound and be placed at right angles to the axis of the wound. In linear wounds, it is sometimes easier to insert the middle suture first and then to complete the closure by successively inserting sutures, halving the remaining deficits in the wound length. 2 Continuous sutures. For a continuous suture, the first suture is inserted in an identical manner to an interrupted suture, but the rest of the sutures are inserted in a continuous manner until the far end of the wound is reached (Figure 4.7). Each throw of the continuous suture should be inserted at right

angles to the wound and this will mean that the externally observed suture material will usually lie diagonal to the axis of the wound. It is important to have an assistant who will follow the suture, keeping it at the same tension in order to avoid either purse stringing the wound by too much tension, or leaving the suture material too slack. There is more danger of producing too much tension by using too little suture length than there is of leaving the suture line too lax. Postoperative oedema will often take up any slack in the suture material. At the far end of the wound, this suture line should be secured either by using an Aberdeen knot or by tying the free end to the loop of the last suture to be inserted. 3 Mattress sutures. Mattress sutures may be either vertical or horizontal and tend to be used to produce either eversion or inversion of a wound edge (Figure 4.8). The initial suture is inserted as for an interrupted suture, but then the needle either moves horizontally or vertically and traverses both edges of the wound once again. Such sutures are very useful in producing accurate approximation of wound edges, especially when the edges to be anastomosed are irregular in depth or disposition. 4 Subcuticular suture. This technique is used in skin where a cosmetic appearance is important and where the skin edges may be approximated easily (Figure 4.9). The suture material used may be either absorbable or non-absorbable. For non-absorbable sutures, the ends may be secured by means of a collar and bead, or tied loosely over the wound. When absorbable sutures are used, the ends may be secured using a buried knot. Small bites of the subcuticular tissues are

Figure 4.7 Continuous suture technique. Reproduced with permission from Royal College of Surgeons of England. The intercollegiate basic surgical skills course participants handbook, edns 1–4. London: RCS.

Figure 4.9 Subcuticular suture technique. Reproduced with permission from Royal College of Surgeons of England. The intercollegiate basic surgical skills course participants handbook, edns 1–4. London: RCS.

PART 1 | PRINCIPLES

(a)

Point Swaged eye

Body (b) Figure 4.8 Mattress suture techniques. Reproduced with permission from Royal College of Surgeons of England. The intercollegiate basic surgical skills course participants handbook, edns 1–4. London: RCS.

ove’s Short Practice of Surgery, 26th Ed

sign.co.uk 01-04-B&L_26th-Pt1_Ch04-cp.indd 39

ISBN: 9781444121278

Figure 4.10 The basic parts of a needle. Reproduced with permission from Royal College of Surgeons of England. The intercollegiate basic surgical skills course participants handbook, edns 1–4. London: RCS.

Proof Stage: 2

Title: Bailey & Love’s Short Practice of Surgery, 26th Ed

Fig No: 19.7 ISBN: 9781444121278

Proof Stage:

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BASIC SURGICAL SKILLS AND ANASTOMOSES

taken on alternate sites of the wound and then gently pulled together thus approximating the wound edges without the risk of the cross-hatched markings of interrupted sutures.

Needles In the past, needles had eyes in them and suture material had

to be loaded into them, which was not only time consuming, but it meant that the needle holes in tissues were considerably larger than the suture material being used. Currently, needles are eyeless or ‘atraumatic’ with the suture material embedded within the shank of the needle. The needle has three main parts (Figure 4.10):

3/8 circle

1/4 circle

5/8 circle

1/2 circle

1/2 curved

Straight

J needle

Compound curve

PART 1 | PRINCIPLES

Crosssection

Cutting needles for stitching skin

Needles used for suturing the abdominal wall: Round-bodied needles for peritoneum, muscles and fat Cutting needles for aponeurosis

Needles used for suturing the bowel The threads are swaged into the needles Figure 4.11 Types of needle.

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1 Shank 2 Body 3 Point.

•

Knot tying is one of the most fundamental techniques in surgery and yet is often poorly performed. The principles behind a secure knot are poorly understood by many surgeons and sadly a poorly constructed knot may thus jeopardise an otherwise successful surgical procedure. The general principles behind knot tying include:

• •

• The knot must be tied firmly, but without strangulating the tissues.

of foreign material.

• The knot must be tightened without exerting any tension

• • •

•

or pressure on the tissues being ligated, i.e. the knot should be bedded down carefully, only exerting pressure against counter-pressure from the index finger or thumb. During tying, the suture material must not be ‘sawed’ as this weakens the thread. The suture material must be laid square during tying, otherwise tension during tightening may cause breakage or fracture of the thread. When tying an instrument knot, the thread should only be grasped at the free end, as gripping the thread with artery forceps or needle holders can damage the material and again result in breakage or fracture. The standard surgical knot is the reef knot (Figure 4.12),

01-04-B&L_26th-Pt1_Ch04-cp.indd 41

Crossed half-hitch

Reef or square knot

Granny knot

Extra half-hitch on reef knot

Surgeon's knot

Figure 4.12 Standard knotting formation.

Knotting techniques

• The knot must be unable to slip or unravel. • The knot must be as small as possible to minimise the amount

Half-hitch

•

with a third throw for security, although with monofilament sutures such as for vascular surgery, six to eight throws are required for security. A granny knot involves two throws of the same type of throw and is a slip knot. It may be useful in achieving the right tension in certain circ*mstances, but must be followed by a standard reef knot to ensure security. When added security is required, a surgeon’s knot using a twothrow technique is advisable to prevent slippage. When using a continuous suture technique, an Aberdeen knot may be used for the final knot. The free end of the suture is partially pulled through the final loop several times before being pulled through a final time completely prior to cutting. When the suture is cut after knotting, the ends should be left about 1–2 mm long to prevent unraveling. This is particularly important when using monofilament material.

Alternatives to sutures Many alternatives to standard suture techniques now exist and are in common usage.

Skin adhesive strips For the skin, self-adhesive tapes or steristrips may be used where there is no tension and not too much moisture, such as after a wide excision of a breast lump. They may also be used to minimise ‘spreading’ of a scar. Other adhesive polyurethane films, such as Opsite, Tegaderm or Bioclusive, may provide a similar benefit, while such transparent dressings also allow wound inspection and may protect against cross-infection.

PART 1 | PRINCIPLES

The needle should be grasped by the needle holder approximately one-third of the way back from the rear of the needle avoiding both the shank and the point. The body of the needle is either round, triangular or flattened. Round-bodied needles gradually taper to a point, while triangular needles have cutting edges along all three sides. The actual point of the needle can be round with a tapered end, conventional cutting which has the cutting edge facing the inside of the needle’s curvature, or reversed cutting in which the cutting edge is on the outside (Figure 4.11). Round-bodied needles are designed to separate tissue fibres rather than cut through them and are commonly used in intestinal and cardiovascular surgery. Cutting needles are used where tough or dense tissue needs to be sutured, such as skin and fascia. Blunt-ended needles are now being advocated in certain situations, such as closure of the abdominal wall, in order to diminish the risk of needle-stick injuries in this era of virally transmitted disorders. The choice of needle shape tends to be dictated by the accessibility of the tissue to be sutured, and the more confined the operative space, the more curved the needle. Hand-held straight needles may be used on skin, although today it is advocated that needle holders should be used in all cases to reduce the risk of needle-stick injuries. Half circle needles are commonly utilised in the gastrointestinal tract, while J-shaped needles, quarter circle needles and compound curvature needles are used in special situations such as the vagin*, eye and oral cavity, respectively. The size of the needle tends to correspond with the gauge of the suture material, although it is possible to get similar sutures with differing needle sizes.

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Tissue glue Tissue glue is also available based upon a solution of n-butyl2-cyanoacrylate monomer. When it is applied to a wound, it polymerises to form a firm adhesive bond, but the wound does need to be clean, dry, with near perfect haemostasis and under no tension. Some specific uses have been described such as closing a laceration on the forehead of a fractious child in Accident and Emergency thus dispensing with local anaesthetic and sutures. Although it is relatively expensive, it is quick to use, does not delay wound healing and is associated with an allegedly low infection rate. Other tissue glues involve fibrin and work on the principles of converting fibrinogen to fibrin by thrombin with crosslinking by Factor XIII, and the addition of aprotinin to slow the break up of the fibrin network by plasmin. This process has good adhesive properties and has been used for haemostasis in the liver and spleen, for dural tears, in ear, nose and throat (ENT) and ophthalmic surgery, to attach skin grafts and also to prevent haemoserous collections under flaps. Fibrin glues have also been used to control gastrointestinal haemorrhage endoscopically, but do not work when the bleeding is brisk.

Staples Mechanical stapling devices were first used successfully by Hümer Hültl in Hungary in 1908 to close the stomach after resection. Today, there is a wide range of mechanical devices with linear, side-to-side and end-to-end stapling devices that can be used both in the open surgery setting and laparoscopically. Most of these devices are disposable and relatively expensive, but their cost is offset by the saving of operative time and the potential increase in the range of surgery possible (see below).

Clips

Skin clips produce a very neat scar with good wound eversion and a minimal cross-hatching effect. They can be placed faster than suture insertion and have a lower predisposition to infection as they do not penetrate entirely through the wound and do not produce a complete track from one wound edge to the other. However, they can be uncomfortable for the patient and they require a special instrument to remove them. Furthermore, they tend to be a more expensive method for wound closure than simple suture techniques.

PART 1 | PRINCIPLES

Stapling devices

In the gastrointestinal tract, stapling devices tend to apply two rows of staples, offset in relation to each other to produce a sound anastomosis (Figure 4.13). Many of them also simultaneously divide the bowel or tissue that has been stapled while other devices merely insert the staples and the bowel has to be divided separately. For all stapling devices, it is crucial for the surgeon to understand the principles behind each device and to know intimately the mechanism and function of the instrument.

• End-to-end anastomoses. Circular stapling devices allow

tubes to be joined together and such instruments are in common use in the oesophagus and low rectum. The detached stapling head/anvil is introduced into one end of the bowel, usually being secured within it by means of a purse-string suture. The body of the device is then inserted into the other end of the bowel, either via the rectum for a low

rectal anastomosis, or via an enterotomy for an oesophagojejunostomy, and either the shaft is extended through a small opening in the bowel wall or is secured by a further pursestring suture. The head/anvil is reattached to the shaft and the two ends approximated. Once the device is fully closed as indicated by the green indicator in the window, the device is fired, and after unwinding, the stapler is gently withdrawn. It is important to assess the integrity of the anastomosis by examining the ‘doughnuts’ of tissue excised for completeness. It is essential that no extraneous tissue is allowed to become interposed between the two bowel walls on closing the stapler. • Transverse anastomoses. These instruments, which come in different sizes, simply provide two rows of staples for a single transverse anastomosis. They are useful for closing bowel ends, and the larger sizes have been used to create gastric tubes and gastric partitioning. One technical point of importance is that the bowel should be divided before the instrument is reopened after firing, as the instrument is designed with a ridge along which to pass a scalpel to ensure the correct length cuff of bowel remains adjacent to the staple line. Down in the pelvis it may be helpful to use such a device with a moveable head (roticulator). • Intraluminal anastomoses. These instruments have two limbs which can be detached. Each limb is introduced into a loop of bowel, the limbs reassembled and the device closed. On firing, two rows of staples are inserted either side of the divided bowel, the division occurring by means of a built-in blade that is activated at the same time as the insertion of staples. Such an instrument may be used in fashioning a gastro-jejunostomy or jejuno-jejunostomy and is used in ileal pouch formation. • Other devices. Other devices are produced that will staple/ ligate and divide blood vessels. Skin closure may also be undertaken using hand-held stapling devices rather than individually picking up staples/clips and inserting them as described above. Many of the intestinal stapling devices are now adapted to be inserted down cannulae during laparoscopic surgery, and although they look very different, the principles of function are identical to the open surgery variety.

THE PRINCIPLES OF ANASTOMOSES Bowel anastomoses The word anastomosis comes from the Greek ‘ana’, without, and ‘stoma’, a mouth, reflecting the join of a tubular viscus (bowel) or vessel (usually arteries) after a resection or bypass procedure. Prior to the nineteenth century, intestinal surgery was limited to exteriorisation by means of a stoma or closure of simple lacerations. Lembert then described his seromuscular suture technique for bowel anastomosis in 1826, while Senn advocated a two-layer technique for closure. Kocher’s method utilised a two-layer anastomosis, first a continuous all-layer suture using catgut, then an inverting continuous (or interrupted) seromuscular layer suture using silk, which became the mainstay of bowel anatomoses for many years (Figure 4.14). However, Halsted favoured a onelayer extramucosal closure, and this was subsequently advocated by Matheson as it was felt to cause the least tissue necrosis or luminal narrowing (Figure 4.15). This techniqe has now become

Hümer Hültl, surgeon, St Stephen’s Hospital, Budapest, Hungary, described his gastric stapler in 1908. Antoine Lembert, 1802–1851, surgeon, Hôtel Dieu, Paris, France. Nicolas Senn, 1844–1908, Professor of Surgery, Rush Medical College, Chicago, IL, USA. Emil Theodor Kocher, 1841–1917, Professor of Surgery, Berne, Switzerland. In 1909, he was awarded the Nobel Prize for Physiology or Medicine for his work on the thyroid. William Stewart Halsted, 1852–1922, Professor of Surgery, Johns Hopkins Hospital Medical School, Baltimore, MD, USA. Norman Alistair Matheson, 1907–1966, formerly surgeon, Aberdeen Royal Infirmary, UK.

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The principles of anastomoses

(a)

PART 1 | PRINCIPLES

(b)

widely accepted, although it is essential that this is not confused with a seromuscular suture technique. The extramucosal suture must include the submucosa as this has a high collagen content and is the most stable suture layer in all sections of the gastrointestinal tract. There are several prospective randomised trials

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between two-layer and single-layer anastomoses demonstrating that there is probably little to choose between these techniques, provided basic essentials as highlighted in Summary box 4.3 are observed. However, catgut and silk have been replaced by synthetic, usually absorbable, polymers.

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Figure 4.14 Standard two-layer bowel anastomosis. Reproduced with permission from Kocher T, Harder F, Thomas WEG (eds). Anastomosis techniques in the gastrointestinal tract, 1st edn. Wollerau: Covidien, 2007.

Figure 4.15 Extramucosal technique taking care to include the submucosa. Reproduced with permission from Kocher T, Harder F, Thomas WEG (eds). Anastomosis techniques in the gastrointestinal tract, 1st edn. Wollerau: Covidien, 2007.

the bowel rotated and the posterior wall sutured in an identical manner to the anterior wall. As the mesenteric edge of the bowel is the most difficult, especially when a fatty mesentery is present, this angle should be dealt with first, with the final sutures being inserted at the antimesenteric border which is far more accessible and visible. The apposition of bowel edges should be as accurate as possible and the suture bites should be approximately 3–5 mm deep and 3–5 mm apart depending on the thickness of the bowel wall. The suture materials should be of 2/0–3/0 size and made of an absorbable polymer, which can be braided (e.g. polyglactin), or monofilament (e.g. polydioxanone), mounted on an atraumatic round-bodied needle. Braided, coated sutures are the easiest to handle and knot. It is crucial to make sure that only bowel of similar diameter is brought together to form an end-to-end anastomosis. In cases of major size discrepancy, a side-to-side or end-to-side anastomosis may be safer. In cases where the size discrepancy is not marked, a Cheatle split (making a cut into the antimesenteric border) may help to enlarge the lumen of distal, collapsed bowel and allow an end-to-end anastomosis to be fashioned. After all anastomoses, the mesentery should always be closed to avoid the later risk of an internal hernia through a persistent mesenteric defect. Care must be taken during closure of this defect to prevent damage to any mesenteric vessels running in the edge of the mesentery (Summary box 4.3). In certain situations, stapling devices are used to fashion the anastomosis, but as they are expensive, most surgeons reserve them for specific indications, such as oesophageal, rectal and gastric pouch procedures. Several studies have shown them not to be cost effective in routine small bowel surgery, although many surgeons still use them for ease of use and to save time. Summary box 4.3 Intestinal anastomoses

n.co.uk

PART 1 | PRINCIPLES

In the past, great emphasis was placed on good bowel prepara■ Ensure good blood supply to both bowel ends before and tion prior to any anastomosis. The rationale was that with good after formation of anastomosis. bowel preparation and an empty bowel, there was less likelihood ■ Ensure the anastomosis is under no tension. of faecal contamination and therefore it was probably not necLove’s Short Practice of Surgery, 26th Ed ISBN: 9781444121278 Proof■ Stage: 1 to mesenteric Fig No: 19.14 Avoid risk vessels by clamps or sutures. essary to apply bowel clamps (even of the soft occlusion type). ■ Use atraumatic bowel clamps to minimise contamination. However, this tradition is now being challenged, and there is ■ Interrupted and continuous single-layer suture techniques are esign.co.uk evidence to suggest that conventional bowel preparation proadequate and safe. ■ Stapling devices are an alternative when speed is required vides little benefit, and indeed at times may prove detrimental or access is a major factor. to the outcome. In spite of this, many surgeons still use some form of bowel preparation, especially for colorectal surgery. Furthermore, if there is any risk of intestinal spillage during anastomosis, when bowel is unprepared or obstructed for example, Vascular anastomoses atraumatic intestinal clamps should be used across the lumen Vascular anastomoses require an extremely accurate closure as of the bowel. Clamps should not impinge on the mesentery or they must be immediately watertight at the end of the operation the vasculature of the bowel for fear of damage to the vessels when the vascular clamps are removed. In many cases, some form resulting in ischaemic changes. Ideally, the bowel edges should of prosthetic material or graft may be used which will never be be pink and bleeding prior to anastomosis. Excessive bleeding integrated into the body tissues and so the integrity of the suture from the bowel wall may need oversewing if natural haemostasis line needs to be permanent. For this reason, polypropylene is is inadequate. one of the best sutures as it is not biodegradable. It is used in its For all intestinal anastomoses, the bowel ends must be monofilament form, mounted on an atraumatic, curved, roundbrought together without tension. Stay sutures, which avoid the bodied needle. Knot security is important, and as polypropylene need for tissue forceps, are invaluable for displaying the bowel is monofilament and the anastomosis often depends on one final ends and help with the accurate alignment of the bowel and knot, several throws (between six and eight) of a well-laid reef the placement of the sutures. If the anastomosis is being under- knot are required. The suture line must be regular and watertight taken on mobile bowel, the anterior wall layer of sutures can be with a smooth intimal surface to minimise the risk of thrombosis ’s Short Practice of Surgery, 26th either Ed 9781444121278 Proof Stage: 1 Fig No:as19.15 inserted, in a continuousISBN: or interrupted manner, and then and embolus, as well to avoid any leakage. Suture size depends Sir George Lenthal Cheatle, 1865–1951, surgeon, King’s College Hospital, London, UK.

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Drains

DRAINS Drains are inserted to allow fluid or air that might collect at an operation site or in a wound to drain freely to the surface. The fluid to be drained may include blood, serum, pus, urine, faeces,

(a)

(b)

Figure 4.16 Arteriotomy being closed by vein patch. Technique involves a double armed suture ensuring that the final knot is half way along one side of the arteriotomy. Reproduced with permission from Royal College of Surgeons of England. The intercollegiate basic surgical skills course participants handbook, edns 1–4. London: RCS.

Summary box 4.4 Vascular anastomosis ■ ■ ■ ■

Non-absorbable monofilament suture material should be used, e.g. polypropylene. A smooth intimal suture line is essential. Knots require multiple throws in order to ensure security. The suture must pass from within outwards on the downflow aspect of the anastomosis.

bile or lymph. Drains may also allow wound irrigation in certain specific circ*mstances. The adequate drainage of fluid collections prevents the development of cavities or spaces that may delay wound healing. Their use can be regarded as prophylactic in elective surgery and therapeutic in emergency surgery. Three basic principles apply in the use of drains: 1 Open drains that utilise the principle of gravity 2 Semi-open drains that work on the principle of the capillary effect 3 Closed drains systems that utilise suction. They may be placed through the wound or through a separate incision, although it has been clearly shown that placing them through the wound leads to an increased risk of wound infection. With regard to the indications for drainage, in the past drains were in common use ever since Lawson Tait in 1887 suggested ‘when in doubt drain!’ However, this edict has come under strong criticism recently and the value and use of drains has been the subject of close scrutiny, and their use still remains controversial. Protagonists suggest that the use of drains may:

• remove any intraperitoneal or wound collection of ascites, serum, bile, chyle, pancreatic or intestinal secretion;

• act as a signal for any postoperative haemorrhage or anastomotic leakage;

• provide a track for later drainage. However, the antagonists claim that the presence of a drain may:

• • • • •

increase intra-abdominal and wound infections; increase anastomotic insufficiency; increase abdominal pain; increase hospital stay; decrease pulmonary function.

In reality, the use of drains currently tends to depend on a surgeon’s individual preference. There are randomised controlled trails suggesting that their use in gastric, duodenal, small bowel, appendix and biliary surgery is unnecessary, and may cause more problems than benefits, and this is now reflected in current practice. There are also randomised controlled trials to suggest that they are also not required in colorectal, liver and pancreatic surgery and yet in today’s practice the majority of surgeons will still utilise drains in these forms of surgery. The only area of alimentary tract surgery where drains are still routinely advocated is for oesophageal surgery, although even here the evidence is low with the level of evidence being only 5 and the level of recommendation being ‘D’ (i.e. based on expert opinion).

PART 1 | PRINCIPLES

on vessel calibre: 2/0 is suitable for the aorta, 4/0 for the femoral artery and 6/0 for the popliteal to distal arteries. Microvascular anastomoses are made using a loupe and an interrupted suture down to 10/0 size. All vessel walls must be treated with great care avoiding causing any damage to the intima. If any significant manipulation is necessary, atraumatic forceps (such as DeBakey’s) are utilised. Vascular clamps should be applied with great care, particularly for calcified vessels, and in some cases encircling rubber loops or intraluminal balloon catheters may be less traumatic for control. Vessels should always be sewn with the needle moving from within to without on the downstream edge of the vessel to avoid creating an intimal flap and to fix any atherosclerotic plaque. The tip of the needle should be inserted at right angles to the surface of the intima and the curve of the needle followed to prevent vessel trauma. The assistant should ‘follow’ by keeping the suture taut, and once the closure is complete, the distal clamp is released first, before the final watertight knot is made. This allows backflow to clear any clot or air from the anastomosis. The proximal clamp can then be released, a process which minimises the risk of distal embolus. Suture bites should be placed an equal distance apart, with the bite size dependent on the vessel diameter. Care needs to be taken to avoid damaging the suture, which should not be gripped by any surgical instrument. All haemostats that are used to hold any suture material should be shod with soft rubber to prevent suture material damage. A transverse arteriotomy is less likely to stenose following closure than a longitudinal arteriotomy, but may not give adequate access, and a longitudinal arteriotomy is easier to make. Therefore, a vein patch can be used if there is any danger of stenosis or doubt about the size of the lumen (Figure 4.16). The suture line can be started at the apex of the arteriotomy with a double-ended suture, and then carried down each side with the final knot being placed at the midpoint of the vein patch graft, and not at the far end. The suture should go from outside to inside on the graft and from inside to outside on the artery, again to minimise the risk of intimal flap formation. When prosthetic material or grafts are used, similar nonabsorbable monofilament sutures are used with the same in–out technique to ensure eversion of the graft edge and a smooth intimal surface. Again the needle should go from outside to inside on the graft and from inside to outside on the artery. Doubleended sutures make the procedures easier (Summary box 4.4).

Specialist use of drains There are certain clinical situations where specialist forms of drainage are required.

Michael Ellis DeBakey, b. 1908, Professor of Surgery, Baylor University, Houston, TX, USA. Robert Lawson Tait, surgeon, Birmingham, UK, 1845–1899.

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Chest drains These are indicated for a pneumothorax, pleural effusion, haemothorax or to prevent the collection of fluid or air after thoracotomy. Once the drain has been inserted, it should be connected to an underwater sealed drain (Figure 4.17). This system allows air to leave the pleural cavity, but cannot draw it back in with the negative pressure that is created in the intrathoracic cavity. During the respiratory process, it should be checked that the meniscus of the fluid is swinging to ensure that the tube is not blocked. Suction can be applied to the venting tube at the bottle whenever there is significant drainage of fluid or air expected. Between 10 and 20 mm of mercury are adequate to obtain a gentle flow of bubbles from the chest cavity.

T-tube drains After exploration of the common bile duct, a T-tube (Figure 4.18) may be inserted into the duct which allows bile to drain while the sphincter of Oddi is in spasm postoperatively. Once the sphincter relaxes, bile drains normally down the bile duct and into the duodenum. To assist choleresis, it is often advisable to convert the lumen of the limb of the T into a gutter, which also facilitates removal.

Guided drainage

Removal of drains A drain should be removed as soon as it is no longer required, as if left in, it can itself predispose to fluid collections as a result of tissue reaction. Indeed there is evidence that by 7 days only 20 per cent of drains are still functioning. It should be stressed how important it is to define the objective of each individual drain and to ensure that once that objective has been met, the drain is removed. If a drain is used at all, the following principles may apply:

• Drains put in to cover perioperative bleeding may usually be removed after 24 hours, e.g. thyroidectomy.

• Drains put in to drain serous collections usually can be removed after 5 days, e.g. mastectomy.

• Drains put in because of infection should be left until the infection is subsiding or the drainage is minimal.

• Drains put in to cover colorectal anastomoses should be

removed at about 5–7 days. However, it should be stressed that in no way does a drain prevent any intestinal leakage, but merely may assist any such leakage to drain externally rather than to produce life-threatening peritonitis. • Common bile duct T-tubes should remain in for 10 days. However, once the T-tube cholangiogram has shown that there is free flow of bile into the duodenum and that there are no retained stones, some surgeons like to clamp the T-tube prior to removal. The 10-day period is required to minimise the risk of biliary peritonitis after removal. • Any suction drain should have the suction taken off prior to removal of the drain. • During removal of a chest drain, the patient should be asked to breathe in and hold his breath, thus doing a Valsalva manoeuvre. In this way, no air is sucked into the pleural

PART 1 | PRINCIPLES

For many intra-abdominal collections or abscesses, drains may be inserted under ultrasound or computed tomography (CT)

control. In order for such drains to remain in site, the end is often fashioned with a pigtail to discourage inadvertent removal.

Figure 4.17 Underwater seal chest drain. Reproduced with permission from Thomas WEG. Basic principles. In: Kingsnorth A, Majid A (eds). Principles of surgical practice. London: Greenwich Medical, 2001.

Figure 4.18 T tube. Reproduced with permission from Thomas WEG. Basic principles. In: Kingsnorth A, Majid A (eds). Principles of surgical practice. London: Greenwich Medical, 2001.

Ruggero Oddi, Italian physician, 1864–1913. Antonio Maria Valsalva, Italian physician and anatomist, 1666–1723.

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The principles of diathermy: electrosurger y

cavity as the tube is removed. Once the drain is out, a previously inserted purse-string suture should be tied.

Active cable

Active electrode

Diathermy unit

THE PRINCIPLES OF DIATHERMY: ELECTROSURGERY For many years, short wave diathermy has proved a most valuable and versatile aid to surgical technique. Its most common use is in securing haemostasis by means of coagulation, but by varying the strength or wave form of the current produced, it can also result in a cutting effect. Both these effects have been used in open surgery, as well as in laparoscopic surgery or down intraluminal endoscopes as in transurethral resection of the prostate. However, although diathermy is a valuable surgical tool, many accidents have occurred due to surgeons being unaware of, or not fully understanding, the principles of its use. Most accidents are avoidable if the diathermy or electrocautery is used with care. It is therefore vital for a surgeon to have a sound understanding of the principles and practice of diathermy, and how to avoid complications.

Patient plate Dispersive cable (a)

Monopolar diathermy

Active cable

The principle of diathermy

Two small active electrodes

Diathermy unit

When an electrical current passes through a conductor, some of its energy appears as heat. The heat produced depends on:

• the intensity of the current; • the wave form of the current; • the electrical property of the tissues through which the current passes;

• the relative sizes of the two electrodes.

The effects of diathermy Diathermy can be used for three purposes: 1 Coagulation: the sealing of blood vessels. 2 Fulguration: the destructive coagulation of tissues with charring. 3 Cutting: used to divide tissues during bloodless surgery. In coagulation, a heating effect leads to cell death by dehydration and protein denaturation. Bleeding is therefore stopped by a combination of the distortion of the walls of the blood vessel,

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(b)

Bipolar diathermy

Figure 4.19 The principles of diathermy. (a) Monopolar diathermy. (b) Bipolar diathermy. Reproduced with permission from Royal College of Surgeons of England. The intercollegiate basic surgical skills course participants handbook, edns 1–4. London: RCS.

coagulation of the plasma proteins, dried and shrunken dead tissue and stimulation of the clotting mechanism. In an ideal situation, intracellular temperatures should not reach boiling during coagulation, because if it does an unwanted cutting effect may be experienced. Cutting occurs when sufficient heat is applied to the tissue to cause cell water to explode into steam. The cut current is a continuous wave form and the monopolar diathermy is most effective when the active electrode is held a very short distance from the tissues. This allows an electrical discharge to arc across the gap creating a series of sparks which produce the high temperatures needed for cutting. In fulguration, the diathermy matching is set to coagulation and a higher effective voltage is used to make larger sparks jump an air gap thus fulgurating the tissues. This can continue until carbonisation or charring occurs. The voltage and power output can be varied by adjusting the duration of bursts of current, as well as its intensity to give a combination of both cutting and coagulation. This is known as blended current and provides both forms of diathermy activity.

PART 1 | PRINCIPLES

There are two basic types of diathermy system in use, monopolar diathermy and bipolar diathermy (Figure 4.19). In monopolar diathermy, which is the most commonly used form, an alternating current is produced by a suitable generator and passed to the patient via an active electrode which has a very small surface area. The current then passes through the tissues and returns via a very large surface plate (the indifferent electrode) back to the earth pole of the generator. As the surface area of contact of the active electrode is small in comparison to the indifferent electrode, the concentrated powerful current produces heat at the operative site. However, the large surface area electrode of the patient plate spreads the returning current over a wide surface area, so it is less concentrated and produces little heat. In bipolar diathermy, the two active electrodes are usually represented by the limbs of a pair of diathermy forceps. Both forceps ends are therefore active and current flows between them and only the tissue held between the limbs of the forceps heats up. This form of diathermy is used when it is essential that the surrounding tissue should be free from either the risk of being burned or having current passed through them.

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Complications of diathermy Electrocution Today, diathermy machines are manufactured to very high safety standards which minimise the risk of any part of the machine becoming live with mains current. However, as with any such instrument, there must be regular and expert servicing.

Explosion Sparks from the diathermy can ignite any volatile or inflammable gas or fluid within the theatre. Alcohol-based skin preparations can catch fire if they are allowed to pool on or around the patient. Furthermore, diathermy should not be used in the presence of explosive gases, including those which may occur naturally in the colon, especially after certain forms of bowel preparation, such as mannitol, which has now been banned for this use for this very reason.

Burns These are the most common type of diathermy accidents in both open and endoscopic surgery. They occur when the current flows in some way other than that in which the surgeon intended and are far more common in monopolar than bipolar diathermy. These may occur as a result of:

• Faulty application of the indifferent electrode with inadequate

contact area. • The patient being earthed by touching any metal object, e.g. the Mayo table, the bar of an anaesthetic screen, an exposed metal arm rest or a leg touching the metal stirrups used in maintaining the lithotomy position. • Faulty insulation of the diathermy leads, either due to cracked insulation or instruments such as towel clips pinching the cable. • Inadvertent activity such as the accidental activation of the foot pedal, or accidental contact of the active electrode with other metal instruments, such as retractors, instruments or towel clips.

PART 1 | PRINCIPLES

Channelling Heat is produced wherever the current intensity is greatest. Normally, this would be at the tip of the active electrode, but if current passes up a narrow channel or pedicle to the active electrode, enough heat may be generated within this channel or pedicle to coagulate the tissues. This can prove disastrous, for example,

• coagulation of the penis in a child undergoing circumcision; • coagulation of the spermatic cord when the electrode is

available so that these can be reset if necessary. In most cases, it is therefore wise to undertake precautions and to use bipolar diathermy wherever possible. If monopolar diathermy is required, then the patient plate should be sited as far away from the pacemaker as possible so that the path of the current does not pass through the heart or the vicinity of the pacemaker. Monitoring of the heart rate should be undertaken throughout the operation and a defibrillator should always be available in case a dysrhythmia develops at any time.

Laparoscopic surgery Diathermy burns are a particular hazard of laparoscopic surgery due to the nature of the visibility of the instrumentation and the actual structure of the instruments used. Such burns may occur by:

• Diathermy of the wrong structure because of lack of clarity of vision or misidentification.

• Faulty insulation of any of the laparoscopic instruments or equipment.

• Intraperitoneal contact of the diathermy with another metal instrument while activating the pedal.

• Inadvertent activation of the pedal while the diathermy tip is out of vision of the camera.

• Retained heat in the diathermy tip touching susceptible structures, such as bowel.

• Capacitance coupling (Figure 4.20). This is a phenomenon

in which a capacitor is created by having an insulator sandwiched between two metal electrodes. This can be created in situations where there is a metal laparoscopic port and the diathermy hook is passed through it. The insulation of the diathermy hook acts as the sandwiched insulator and by means of electromagnetic induction, the diathermy current flowing through the hook can induce a current in the metal port, which can potentially damage intraperitoneal structures. In most cases, this current is dissipated from the metal port through the abdominal wall, but if a plastic cuff is used, this dissipation of current does not occur and the danger of capacitance coupling is significantly increased. Therefore, metal ports should never be used with a plastic cuff. The danger of capacitance coupling can be prevented by using entirely plastic ports.

Metal laparoscopic port

applied to the testis.

In such situations, diathermy should not be used, or if it is necessary, then bipolar diathermy should be employed.

Pacemakers Diathermy currents can interfere with the working of a pacemaker with its obvious potential danger to the patient’s health. Modern pacemakers are designed to be inhibited by high frequency interference, so that the patient may receive no pacing stimulation at all while the diathermy is in use. Certain demand pacemakers may revert to the fixed rate of pacing and therefore it would be important for the anaesthetist to have a magnet

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Diathermy hook

Point of contact with bowel

Figure 4.20 Capacitance coupling during laparoscopic surgery. Reproduced with permission from Royal College of Surgeons of England. The intercollegiate basic surgical skills course participants handbook, edns 1–4. London: RCS.

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The principles of the ‘harmonic scalpel’

THE PRINCIPLES OF LIGASURE ‘Ligasure’ tissue fusion technology is a vessel sealing system that is used in both open and laparoscopic surgery. It actually fuses the vessel walls to create a permanent seal and is in wide use in a range of surgical specialties, including gynaecology, colorectal, urology and general surgery. It uses a combination of pressure and energy to create vessel fusion which can withstand up to three times the normal systolic pressure. New technology of the ligasure system involves advanced monopolar technology that uses the body’s own collagen and elastin to both seal and divide, allowing surgeons to reduce instrument handling when dissecting, ligating and grasping – a valuable asset particularly during laparoscopic surgery. The feedback sensing technology incorporated in the instrument is designed to manage the energy delivery in a precise manner and results in an automatic discontinuation of energy once the seal is complete, thus removing any concern that the surgeon has to use guesswork as to when the seal is complete. The newer instruments actively monitor tissue impedance and provide a real-time adjustment of the energy being delivered. Using this technology, ligasure can seal vessels of up to 7 mm diameter, with an average seal time of 2–4 seconds, as well as pedicles, tissue bundles and lymphatics with a consistent controlled and predictable effect on tissue, including less dessication. Therefore, the new Ligasure Advance™ can dissect, seal and divide and was designed to be the only tool that a surgeon would need. However, it is relatively expensive to use compared to some of the competing technology.

THE PRINCIPLES OF THE ‘HARMONIC SCALPEL’

utilises a hand-held ultrasound transducer and scalpel which is controlled by a hand switch or foot pedal. During use, the scalpel vibrates in the 20 000–50 000 Hz range and cuts through tissues, effecting haemostasis by sealing vessels and tissues by means of protein denaturation caused by vibration rather than heat (in a similar manner to whisking an egg white). It provides cutting precision, even through thickened scar tissue, and visibility is enhanced due to less smoke being created by this system during use compared to routine electrosurgery. However, the harmonic scalpel does take longer to cut and coagulate tissues than diathermy, and while diathermy can be used to coagulate a bleeding vessel at any time, the harmonic scalpel can only coagulate as it cuts. It is claimed that patients experience less swelling, bleeding and bruising after the use of the harmonic scalpel than when a conventional scalpel is used, and blood vessels are sealed with a much lower temperature than conventional diathermy and so there is less thermal damage to adjacent tissue, with less charring and dessication. Furthermore, it is suggested that the use of the harmonic scalpel reduces operative time and recovery is thus enhanced. Currently, the harmonic scalpel is in common use during laparoscopic procedures, as well as open surgery, such as thyroidectomy and several plastic surgery operations, e.g. cosmetic breast surgery.

FURTHER READING Royal College of Surgeons of England. Intercollegiate basic surgical skills course (participant handbook), 4th edn. London: Royal College of Surgeons of England, 2007. Jenkins TPN. The burst abdominal wound: a mechanical approach. Br Med J 1976; 131: 130–40. Kirk RM. Basic surgical techniques, 6th edn. Edinburgh: Churchill Livingstone, 2010.

PART 1 | PRINCIPLES

The harmonic scalpel is an instrument that uses ultrasound technology to cut tissues while simultaneously sealing them. It

Eugen (Janö) Alexander Pölya, 1876–1944, Surgeon, St Stephen’s Hospital, Budapest, Hungary. Henri Albert Charles Antoine Hartmann, 1860–1952, Professor of Clinical Surgery, The Faculty of Medicine, The University of Paris, France. Gaston Michel, 1874–1937, French surgeon. Frank Gregory Connell, 1875–1968, Professor of Surgery, Rush Medical College, Chicago, IL, USA.

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CHAPTER

Surgical infection LEARNING OBJECTIVES

To understand: • The factors that determine whether a wound will become infected • The classification of sources of infection and their severity • The indications for and choice of prophylactic antibiotics • The characteristics of the common surgical pathogens and their sensitivities • The spectrum of commonly used antibiotics in surgery and the principles of therapy • The misuse of antibiotic therapy with the risk of resistance (such as methicillin-resistant Staphylococcus aureus (MRSA)) and emergence (such as Clostridium difficile enteritis)

PHYSIOLOGY AND PRESENTATION

Surgical infection, particularly surgical site infection (SSI), has always been a major complication of surgery and trauma and has been documented for 4000–5000 years. The Egyptians had some concepts about infection as they were able to prevent putrefaction, testified by mummification skills. Their medical papyruses also describe the use of salves and antiseptics to prevent SSIs. This ‘prophylaxis’ had also been known earlier by the Assyrians, although less well documented. It was described again independently by the Greeks. The Hippocratic teachings described the use of antimicrobials, such as wine and vinegar, which were widely used to irrigate open, infected wounds before delayed primary or secondary wound closure. A belief common to all these civilisations, and indeed even later to the Romans, was that, whenever pus localised in an infected wound, it needed to be drained.

Galen recognised that this localisation of infection (suppuration) in wounds, inflicted in the gladiatorial arena, often heralded recovery, particularly after drainage (pus bonum et laudabile). Sadly, this dictum was misunderstood by many later healers, who thought that it was the production of pus that was desirable. Until well into the Middle Ages, some practitioners promoted suppuration in wounds by the application of noxious substances, including faeces, in the misguided belief that healing could not occur without pus formation. Theodoric of Cervia, Ambroise Paré and Guy de Chauliac observed that clean wounds, closed primarily, could heal without infection or suppuration. The understanding of the causes of infection came in the nineteenth century. Microbes had been seen under the microscope, but Koch laid down the first definition of infective disease (Koch’s postulates; Summary box 5.1). Koch’s postulates do not cover every eventuality though. Organisms of low virulence may not cause disease in normal hosts but may be responsible for disease in immunocompromised hosts. Some hosts may develop

Hippocrates was a Greek physician, and by common consent ‘The Father of Medicine’. He was born on the Greek island of Cos off Turkey about 460 bc and probably died in 375 bc. He lived to be about 109 years of age in an era when the life expectancy was about 32 years.

Galen, 130–200, a Roman physician, who commenced practice as surgeon to the gladiators at Pergamum (now Bregama in Turkey) and later became personal physician to the Emperor Marcus Aurelius and to two of his successors. He was a prolific writer on many subjects, among them anatomy, medicine, pathology and philosophy. His work affected medical thinking for 15 centuries after his death. (Gladiator is Latin for ‘swordsman’.)

Background

PART 1 | PRINCIPLES

To learn: • Koch’s postulates • The management of abscesses To appreciate: • The importance of aseptic and antiseptic techniques and delayed primary or secondary closure in contaminated wounds To be aware of: • The causes of reduced resistance to infection (host response) To know: • The definitions of infection, particularly at surgical sites • What basic precautions to take to avoid surgically relevant health care-associated infections

Theodoric of Cervia. Theodoric, 1210–1298, who was Bishop of Cervia, published a book on surgery about 1267. Ambroise Paré, 1510–1590, a French military surgeon, who also worked at the Hotel Dieu, Paris, France. Guy de Chauliac, ?1298–1368, was physician and chaplain to Pope Clement VI at Avignon, France. He was the author of Chirurgia Magna which was published about 1363.

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Physiology

Summary box 5.1 Koch’s postulates proving whether a given organism is the cause of a given disease ■ ■ ■ ■

It must be found in every case It should be possible to isolate it from the host and grow it in culture It should reproduce the disease when injected into another healthy host It should be recovered from an experimentally infected host

The Austrian obstetrician Ignac Semmelweis showed that puerperal sepsis could be reduced from over 10 per cent to under 2 per cent by the simple act of hand washing between cases, particularly between post-mortem examinations and the delivery suite. He was ignored by his contemporaries. Louis Pasteur recognised through his germ theory that microorganisms were responsible for infecting humans and causing disease. Joseph Lister applied this knowledge to the reduction of colonising organisms in compound fractures by using antiseptics. The principles of antiseptic surgery were soon enhanced with aseptic surgery at the turn of the century. As well as killing the bacteria on the skin before surgical incision (antiseptic technique), the conditions under which the operation was performed were kept free of bacteria (aseptic technique). This technique is still employed in modern operating theatres. The concept of a ‘magic bullet’ (Zauberkugel) that could kill microbes but not their host became a reality with the discovery of sulphonamide chemotherapy in the mid-twentieth century. The discovery of the antibiotic penicillin is attributed to Alexander Fleming in 1928, but it was not isolated for clinical use until 1941 by Florey and Chain. The first patient to receive penicillin was Police Constable Alexander in Oxford. He scratched the side of his mouth while pruning roses and developed abscesses of the face and eyes leading to a severe staphylococcal bacteraemia. He responded to treatment, made a partial recovery before the penicillin ran out, then relapsed and died. Since then, there has been a proliferation of antibiotics with broad-spectrum activity and antibiotics today remain the mainstay of antimicrobial therapy. Many staphylococci today have become resistant to penicillin. Often bacteria develop resistance through the acquisition of β-lactamases, which break up the β-lactam ring present in Joseph Lister (Lord Lister), 1827–1912, Professor of Surgery, Glasgow (1860–1869), Edinburgh (1869–1877) and King’s College Hospital, London, UK (1877–1892). He was the first to show the relation between microbial infection and surgical sepsis. He associated Pasteur’s observations on fermentation with sepsis and, using a carbolic dressing and spray, introduced the ‘antiseptic principle’ which revolutionised surgery. Asepsis in surgery has now replaced antisepsis but the dangers of sepsis are still very much with us. Sir Ernst Boris Chain, Professor of Biochemistry, Imperial College, London, UK. Fleming, Florey and Chain shared the 1945 Nobel Prize for Physiology or Medicine for their work on penicillin.

the molecular structure of many antibiotics. The acquisition of extended spectrum β-lactamases (ESBLs) is an increasing concern in some Gram-negative organisms that cause urinary tract infections because it is difficult to find an antibiotic effective against them. In addition, there is increasing concern about the rising resistance of many other bacteria to antibiotics, in particular the emergence of methicillin-resistant Staphylococcus aureus (MRSA) and glycopeptide-resistant enterococci (GRE), which are also relevant in general surgical practice. The introduction of antibiotics for prophylaxis and for treatment, together with advances in anaesthesia and critical care medicine, has made possible surgery that would not previously have been considered. Faecal peritonitis is no longer inevitably fatal, and incisions made in the presence of such contamination can heal primarily without infection in 80–90 per cent of patients with appropriate antibiotic therapy. Despite this, it is common practice in many countries to delay wound closure in patients in whom the wound is known to be contaminated or dirty. Waiting for the wound to granulate and then performing a delayed primary or secondary closure may be considered a better option (Summary box 5.2). Summary box 5.2 Advances in the control of infection in surgery ■ ■ ■

Aseptic operating theatre techniques have enhanced the use of antiseptics Antibiotics have reduced postoperative infection rates after elective and emergency surgery Delayed primary, or secondary, closure remains useful in contaminated wounds

Surgical site infection in patients who have contaminated wounds, who are immunosuppressed or undergoing prosthetic surgery, is now the exception rather than the rule since the introduction of prophylactic antibiotics. The evidence for this is of the highest level. The value of prophylactic antibiotics in clean, non-prosthetic surgery remains controversial, although SSI rates after such surgery is high when judged by close, unbiased, post-discharge surveillance, using strict definitions.

PHYSIOLOGY Microorganisms are normally prevented from causing infection in tissues by intact epithelial surfaces, most notably the skin. These surfaces are broken down by trauma or surgery. In addition to these mechanical barriers, there are other protective mechanisms, which can be divided into:

• chemical: low gastric pH • humoral: antibodies, complement and opsonins • cellular: phagocytic cells, macrophages, polymorphonuclear cells and killer lymphocytes.

All these natural mechanisms may be compromised by surgical intervention and treatment. Reduced resistance to infection has several causes (Summary box 5.3).

PART 1 | PRINCIPLES

subclinical disease and yet still be a carrier of the organism capable of infecting others. Also, not every organism that causes disease can be grown in culture, the commonly quoted one being Mycobacterium leprae which causes leprosy.

Antony von Leeuwenhoek of Delft, The Netherlands, invented the microscope, and was the first to see bacteria in 1875. He himself made more than 400 microscopes. Robert Koch, 1843–1910, Professor of Hygiene and Bacteriology, Berlin, Germany, stated his ‘Postulates’ in 1882. Ignac Semmelweis, 1818–1865, Professor of Obstetrics, Budapest, Hungary. Louis Pasteur, 1822–1895, was a French chemist, bacteriologist and immunologist who was Professor of Chemistry at the Sorbonne, Paris, France. Sir Alexander Fleming, 1881–1955, Professor of Bacteriology, St Mary’s Hospital, London, UK, discovered Penicillium notatum in 1928. Howard Walter Florey (Lord Florey of Adelaide), 1898–1968, Professor of Pathology, The University of Oxford, Oxford, UK.

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SURGICAL INFECTION Summary box 5.3 Causes of reduced host resistance to infection ■ ■ ■

Metabolic: malnutrition (including obesity), diabetes, uraemia, jaundice Disseminated disease: cancer and acquired immunodeficiency syndrome (AIDS) Iatrogenic: radiotherapy, chemotherapy, steroids

Host response is weakened by malnutrition, which can be recognised clinically, and most easily, as recent rapid weight loss that can be present even in the presence of obesity. Metabolic diseases such as diabetes mellitus, uraemia and jaundice, disseminated malignancy and acquired immune deficiency syndrome (AIDS) are other contributors to infection and a poor healing response, as are iatrogenic causes including the immunosuppression caused by radiotherapy, chemotherapy or steroids (Summary box 5.4, and Figures 5.1 and 5.2). When enteral feeding is suspended during the perioperative period, and particularly with underlying disease such as cancer, immunosuppression, shock or sepsis, bacteria (particularly aerobic Gram-negative bacilli) tend to colonise the normally sterile upper gastrointestinal tract. They may then translocate to the mesenteric nodes and cause the release of endotoxins (lipopolysaccharide in bacterial cell walls), which can be one cause of a harmful systemic inflammatory response through the excessive release of proinflammatory cytokines and activation of macrophages (Figure 5.3). In the circ*mstances of reduced host resistance to infection, microorganisms that are not normally pathogenic may start to behave as pathogens. This is known as opportunistic infection. Opportunistic infection with fungi is an example, particularly when prolonged and changing antibiotic regimens have been used. The chance of developing an SSI after surgery is also determined by the pathogenicity of the organisms present and by the size of the bacterial inoculum. Devitalised tissue, excessive dead space or haematoma, all the results of poor surgical technique, increase the chances of infection. The same applies to foreign materials of any kind, including sutures and drains. If there is a silk suture in tissue, the critical number of organisms needed to start an infection is reduced logarithmically. Silk should not

Figure 5.2 Delayed healing relating to infection in a patient on highdose steroids.

Summary box 5.4 Risk factors for increased risk of wound infection ■ ■ ■ ■ ■ ■ ■

Malnutrition (obesity, weight loss) Metabolic disease (diabetes, uraemia, jaundice) Immunosuppression (cancer, AIDS, steroids, chemotherapy and radiotherapy) Colonisation and translocation in the gastrointestinal tract Poor perfusion (systemic shock or local ischaemia) Foreign body material Poor surgical technique (dead space, haematoma)

be used to close skin as it causes suture abscesses for this reason. These principles are important to an understanding of how best to prevent infection in surgical practice (Summary box 5.5).

Cytokine release

MODS SIRS

PART 1 | PRINCIPLES

IL-6, TNF, etc. Burrill Bernard Crohn, 1884–1983, gastroenterologist, Mount Sinai Hospital, New York, NY, USA, described regional ileitis in 1932 along with Leon Ginzburg and Gordon Oppenheimer.

Macrophage

Release of endotoxin

Mesenteric nodes Translocation (failure of gut-associated lymphoid tissue , villous atrophy)

Figure 5.1 Major wound infection and delayed healing presenting as a faecal fistula in a patient with Crohn’s disease.

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Colonisation by aerobic Gramnegative bacilli (in gut failure and starvation)

Figure 5.3 Gut failure, colonisation and translocation related to the development of multiple organ dysfunction syndrome (MODS) and systemic inflammatory response syndrome (SIRS). IL, interleukin; TNF, tumour necrosis factor.

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Major and minor surgical site infections

Factors that determine whether a wound will become infected ■ ■ ■ ■ ■

Host response Virulence and inoculum of infective agent Vascularity and health of tissue being invaded (including local ischaemia as well as systemic shock) Presence of dead or foreign tissue Presence of antibiotics during the ‘decisive period’

There is a delay before host defences can become mobilised after a breach in an epithelial surface, whether caused by trauma or surgery. The acute inflammatory, humoral and cellular defences take up to 4 hours to be mobilised. This is called the ‘decisive period’, and it is the time when the invading bacteria may become established in the tissues. Strategies aimed at preventing infection from taking a hold become ineffective after this time period. It is therefore logical that prophylactic antibiotics should be given to cover this period and that they could be decisive in preventing an infection from developing. The tissue levels of antibiotics should be above the minimum inhibitory concentration (MIC90) for the pathogens likely to be encountered.

Local and systemic presentation The infection of a wound can be defined as the invasion of organisms through tissues following a breakdown of local and systemic host defences, leading to cellulitis, lymphangitis, abscess and bacteraemia. The infection of most surgical wounds is referred to as superficial surgical site infection (SSSI). The other categories include deep SSI (infection in the deeper musculofascial layers) and organ space infection (such as an abdominal abscess after an anastomotic leak). Pathogens resist host defences by releasing toxins, which favour their spread, and this is enhanced in anaerobic or frankly necrotic wound tissue. Clostridium perfringens, which is responsible for gas gangrene, releases proteases such as hyaluronidase, lecithinase and haemolysin, which allow it to spread through the tissues. Resistance to antibiotics can be acquired by previously sensitive bacteria by transfer through plasmids. The human body harbours approximately 1014 organisms. They can be released into tissues by surgery, contamination being most severe when a hollow viscus perforates (e.g. faecal peritonitis following a diverticular perforation). Any infection that follows surgery may be termed primary or secondary (Summary box 5.6).

Infection that follows surgery or admission to hospital is termed health care-associated infection (HAI). There are four main groups: respiratory infections (including ventilator-associated pneumonia), urinary tract infections (mostly related to urinary catheters), bacteraemia (mostly related to indwelling vascular catheters) and SSIs.

MAJOR AND MINOR SURGICAL SITE INFECTIONS A major SSI is defined as a wound that either discharges significant quantities of pus spontaneously or needs a secondary procedure to drain it (Figure 5.4). The patient may have systemic signs, such as tachycardia, pyrexia and a raised white count (Summary box 5.7). Summary box 5.7 Major wound infections ■ ■ ■

Significant quantity of pus Delayed return home Patients are systemically ill

Minor wound infections may discharge pus or infected serous fluid but should not be associated with excessive discomfort, systemic signs or delay in return home (Figure 5.5). The differentiation between major and minor and the definition of SSI is important in audit or trials of antibiotic prophylaxis. There are scoring systems for the severity of wound infection, which are particularly useful in surveillance and research. Examples are the Southampton (Table 5.1) and ASEPSIS systems (Table 5.2). Accurate surveillance can only be achieved using trained, unbiased and blinded assessors. Most include surveillance for a 30-day postoperative period. The US Centers for Disease Control (CDC) definition insists on a 30-day follow-up period for non-prosthetic surgery and one year after implanted hip and knee surgery.

Types of localised infection Abscess An abscess presents all the clinical features of acute inflamma-

PART 1 | PRINCIPLES

Summary box 5.5

Summary box 5.6 Classification of sources of infection ■

■

Primary: present in or on the host and so acquired from an endogenous source (such as an SSSI following contamination of the wound from a perforated appendix) Secondary or exogenous (HAI): acquired from a source outside the body such as the operating theatre (inadequate air filtration, poor antisepsis) or the ward (e.g. poor hand washing compliance)

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Figure 5.4 Major wound infection with superficial skin dehiscence.

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SURGICAL INFECTION

after the patient has left hospital and may thus be overlooked by the surgical team. Their cost and management, which may be inadequate, is transferred to primary care (Summary box 5.8). Table 5.1 Southampton wound grading system.

Grade

Appearance

Normal healing

Normal healing with mild bruising or erythema

Some bruising

Considerable bruising

Mild erythema

Erythema plus other signs of inflammation

IIa

At one point

IIb

Around sutures

IIc

Along wound

IId

Around wound

III

Clear or haemoserous discharge

IIIa

At one point only (£2 cm)

IIIb

Along wound (>2 cm)

IIIc

Large volume

IIId

Prolonged (>3 days)

Major complication

PART 1 | PRINCIPLES

Figure 5.5 Minor wound infection that settled spontaneously without antibiotics.

tion originally described by Celsus: calor (heat), rubor (redness), dolour (pain) and tumour (swelling). To these can be added functio laesa (loss of function: if it hurts, the infected part is not used). They usually follow a puncture wound of some kind, which may have been forgotten, as well as surgery, but can be metastatic in all tissues following bacteraemia. Pyogenic organisms, predominantly Staphylococcus aureus, cause tissue necrosis and suppuration. Pus is composed of dead and dying white blood cells that release damaging cytokines, oxygen free radicals and other molecules. An abscess is surrounded by an acute inflammatory response composed of a fibrinous exudate, oedema and the cells of acute inflammation. Granulation tissue (macrophages, angiogenesis and fibroblasts) forms later around the suppurative process and leads to collagen deposition. If it is not drained or resorbed completely, a chronic abscess may result. If it is partly sterilised with antibiotics, an antibioma may form. Abscesses contain hyperosmolar material that draws in fluid. This increases the pressure and causes pain. If they spread, they usually track along planes of least resistance and point towards the skin. Wound abscesses may discharge spontaneously by tracking to a surface, but may need drainage through a surgical incision. Most abscesses relating to surgical wounds take 7–10 days to form after surgery. As many as 75 per cent of SSIs present Aulus Aurelius Cornelius Celsus, 25

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Pus

IVa

At one point only (£2 cm)

IVb

Along wound (>2 cm)

Deep or severe wound infection with or without tissue breakdown; haematoma requiring aspiration

Table 5.2 The ASEPSIS wound score.

Criterion

Points

Additional treatment

Antibiotics for wound infection

Drainage of pus under local anaesthesia

Debridement of wound under general anaesthesia 10 Serous dischargea

Daily 0–5

Erythema

Daily 0–5

Purulent exudate

Daily 0–10

Separation of deep tissuesa

Daily 0–10

Isolation of bacteria from wound

Stay as inpatient prolonged over 14 days as result of wound infection

a Scored for 5 of the first 7 days only, the remainder being scored if present in the first two months.

50, a Roman surgeon. He was the author of De Re Medico Libri Octo.

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Systemic inflammator y response syndrome and multiple organ dysfunction syndrome Summary box 5.8

Summary box 5.9

Abscesses

Cellulitis and lymphangitis

■ ■ ■

■

Abscesses need drainage Modern imaging techniques may allow guided aspiration Antibiotics are indicated if the abscess is not localised (e.g. evidence of cellulitis) or the cavity is not left open to drain freely Healing by secondary intention is encouraged

Abscess cavities need cleaning out after incision and drainage and are traditionally encouraged to heal by secondary intention. When the cavity is left open to drain freely, there is no need for antibiotic therapy as well. Antibiotics should be used if the abscess cavity is closed after drainage, but the cavity should not be closed if there is any risk of retained loculi or foreign material. Thus a perianal abscess can be incised and drained, the walls curretted and the skin closed with good results using appropriate antibiotic therapy, but a pilonidal abscess has a higher recurrence risk after such treatment because a nidus of hair may remain in the subcutaneous tissue adjacent to the abscess. Some small breast abscesses can be managed by simple needle aspiration of the pus and antibiotic therapy. Persistent chronic abscesses may lead to sinus or fistula formation. In a chronic abscess, lymphocytes and plasma cells are seen. There is tissue sequestration and later calcification may occur. Certain organisms are associated with chronicity, sinus and fistula formation. Common ones are Mycobacterium and Actinomyces. They should not be forgotten when these complications occur and persist. Perianastomotic contamination may be the cause of an abscess but, in the abdomen, abscesses are more usually the result of anastomotic leakage. An abscess in a deep cavity, such as the pleura or peritoneum, may be difficult to diagnose or locate even when there is strong clinical suspicion that it is present (Figure 5.6). Plain or contrast radiographs may not be helpful, but ultrasonography, computed tomography (CT), magnetic resonance imaging (MRI) and isotope scans are all useful and may allow guided aspiration without the need for surgical intervention.

■ ■ ■

Non-suppurative, poorly localised Commonly caused by streptococci, staphylococci or clostridia Blood cultures are often negative

SYSTEMIC INFLAMMATORY RESPONSE SYNDROME AND MULTIPLE ORGAN DYSFUNCTION SYNDROME Systemic inflammatory response syndrome (SIRS) is a systemic manifestation of sepsis, although the syndrome may also be caused by multiple trauma, burns or pancreatitis without infection. Serious infection, such as secondary peritonitis, may lead to SIRS through the release of lipopolysaccharide endotoxin from the walls of dying Gram-negative bacilli (mainly Escherichia coli) or other bacteria or fungi. This and other toxins stimulate the release of cytokines from macrophages (Figure 5.3). SIRS should not be confused with bacteraemia although the two may coexist (see Table 5.3). Septic manifestations and multiple organ dysfunction syndrome (MODS) in SIRS are mediated by the release of proinflammatory cytokines such as interleukin-1 (IL-1) and tumour necrosis factor alpha (TNFα). These cytokines stimulate neu-

Cellulitis is the non-suppurative invasive infection of tissues. There is poor localisation in addition to the cardinal signs of inflammation. Spreading infection presenting in surgical practice is typically caused by organisms such as β-haemolytic streptococci (Figure 5.7), staphylococci (Figure 5.8) and C. perfringens. Tissue destruction, gangrene and ulceration may follow, which are caused by release of proteases. Systemic signs (the old-fashioned term toxaemia) are common, with chills, fever and rigors. These follow the release of toxins into the circulation, which stimulate a cytokine-mediated systemic inflammatory response even though blood cultures are negative. Lymphangitis is part of a similar process and presents as painful red streaks in affected lymphatics. Cellulitis is usually located at the point of injury and subsequent tissue infection. Lymphangitis is often accompanied by painful lymph node groups in the related drainage area (Summary box 5.9).

PART 1 | PRINCIPLES

Cellulitis and lymphangitis

Figure 5.6 Plain radiograph showing a subphrenic abscess with a gas/fluid level (white arrow). Gastrografin is seen leaking from the oesophagojejunal anastomosis (after gastrectomy) towards the abscess (black arrow).

Theodor Escherich, 1857–1911, Professor of Paediatrics, Vienna, Austria, discovered the Bacterium coli commune in 1886.

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Figure 5.7 Streptococcal cellulitis of the leg following a minor puncture wound.

PART 1 | PRINCIPLES

trophil adhesion to endothelial surfaces adjacent to the source of infection and cause them to migrate through the blood vessel wall by chemotaxis. A respiratory burst occurs within such activated neutrophils, releasing lysosomal enzymes, oxidants and free radicals, which are involved in killing the invading bacteria but which may also damage adjacent cells. Coagulation, complement and fibrinolytic pathways are also stimulated as part of the normal inflammatory response. This response is usually beneficial to the host and is an important aspect of normal tissue repair and wound healing. In the presence of severe sepsis or bacteraemia, this response may become harmful to the host if it occurs in excess, when it is known as SIRS. There are high circulating levels of cytokines and activated neutrophils which stimulate fever, tachycardia and tachypnoea. The activated neutrophils adhere to vascular endothelium in key organs remote from the source of infection and damage it, leading to increased vascular permeability, which in turn leads to cellular damage within the organs, which become dysfunctional and give rise to the clinical picture of MODS. In its most severe form, MODS may progress into multiple system organ failure (MSOF). Respiratory, cardiac, intestinal, renal and liver failure ensue in combination with Table 5.3 Definitions of systemic inflammatory response syndrome (SIRS) and sepsis.

SIRS Two of: hyperthermia (>38°C) or hypothermia (90/min, no β-blockers) or tachypnoea (>20/min)

Figure 5.8 Staphylococcal cellulitis of the face and orbit following severe infection of an epidermoid cyst of the scalp.

circulatory failure and shock. In this state, the body’s resistance to infection is reduced and a vicious cycle develops where the more organs that fail, the more likely it becomes that death will follow despite all that a modern intensive care unit can do for organ support (Summary box 5.10). Summary box 5.10 Definitions of infected states ■ ■ ■ ■

SSI is an infected wound or deep organ space SIRS is the body’s systemic response to severe infection MODS is the effect that SIRS produces systemically MSOF is the end stage of uncontrolled MODS

white cell count >12 × 109/l or 8 g/dL should be weighed against the risks Minor bleeding in an airway can have a catastrophic effect.

Deep vein thrombosis Patients suffering postoperative deep vein thrombosis (DVT) may present with calf pain, swelling, warmth, redness and engorged veins. However, most will show no physical signs. On palpation, the muscle may be tender and there is a positive Homans’ sign (calf pain on dorsiflexion of the foot), but this test is neither sensitive nor specific. Venography or duplex Doppler ultrasound is used to assess flow and the presence of thromboses. If a significant DVT is found (one that extends above the knee), treatment with intravenous heparin initially, followed by longer-term warfarin, should be started. In some patients with a large DVT, a caval filter may be required to decrease the possibility of pulmonary embolism. Most hospitals have a DVT prophylaxis protocol. This may include the use of stockings, calf pumps and pharmacological agents, such as low molecular weight heparin. No method of prophylaxis is foolproof and they all have their own complications, and so an optimal strategy needs to be developed, which is individualised to the patient and the operation that they are receiving (Table 21.2).

PART 3 | PERIOPERATIVE CARE

Table 21.2 Stratification of risk of deep vein thrombosis.

Low

Medium

Maxillofacial surgery

Inguinal hernia repair Pelvic elective and trauma surgery Abdominal surgery

Neurosurgery Cardiothoracic surgery

Gynaecological surgery

High

Total knee and hip replacement

Urological surgery

Hypothermia and shivering Anaesthesia induces loss of thermoregulatory control. Exposure of skin and organs to a cold operating environment, volatile skin preparation (which cool by evaporation), and the infusion of cold i.v. fluids all lead to hypothermia. This, in turn, leads to increased cardiac morbidity, a hypocoagulable state, shivering with imbalance of oxygen supply and demand, and immune function impairment with the possibility of wound infection. Active warming devices should be used to treat hypothermia as appropriate.

Fever About 40 per cent of patients develop pyrexia after major surgery; however, in most cases no cause is found. The inflam-

matory response to surgical trauma may manifest itself as fever, and so pyrexia does not necessarily imply sepsis. However, in all patients with a pyrexia, a focus of infection should be sought. The causes of a raised temperature postoperatively include:

• days 2–5: atelectasis of the lung; • days 3–5: superficial and deep wound infection; • day 5: chest infection, urinary tract infection and thrombophlebitis;

• >5 days: wound infection, anastomotic leakage, intracavitary collections and abscesses;

• DVTs, transfusion reactions, wound haematomas, atelectasis and drug reactions, may also cause pyrexia of non-infective origin.

Patients with a persistent pyrexia need a thorough review. Relevant investigations include full blood count, urine culture, sputum microscopy and blood cultures (Summary box 21.8). Summary box 21.8 Fever ■ ■

A very common problem postoperatively Consider problems in the lung, urine and wound

Prophylaxis against infection In patients who have had foreign material inserted during the operation, including a hip or knee prosthesis in orthopaedic surgery or aortic valves in cardiovascular surgery, up to three doses of a prophylactic antibiotic should be administered, usually one dose 30 minutes before ‘knife to skin’ and two postoperatively. Bacteria can be incorporated into the biofilm that forms on the surface of the implant, where they are protected from antibiotics and from the natural defences of the body; prophylactic antibiotics appear to reduce the risk of any contamination developing into infection by destroying bacteria before they are incorporated into the biofilm.

Pressure sores These occur as a result of friction or persisting pressure on soft tissues. They particularly affect the pressure points of a recumbent patient, including the sacrum, greater trochanter and heels. Risk factors are poor nutritional status, dehydration and lack of mobility and also include the use of a nerve block anaesthesia technique. Early mobilisation prevents pressure sores, while those who are unable to turn in bed should be turned every 30 minutes to prevent pressure sores from developing. High-risk patients may be nursed on an air filter mattress, which automatically relieves the pressure areas (Summary box 21.9). Summary box 21.9 Preventing pressure sores ■ ■ ■

Recognise patients at risk Address nutritional status Keep patients mobile or regularly turned if bed-bound

John Homans, 1877–1954, Professor of Clinical Surgery, Harvard Medical School, Boston, MA, USA.

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General postoperative problems and management

Acute confusional states can occur on recovery from anaesthesia (postoperative delirium (POD)) or a few days after surgery. The overall incidence of POD is 5–15 per cent, but is higher in the elderly with hip fractures and is associated with increased morbidity and mortality (Table 21.3). Table 21.3 Causes of confusion.

Cause Renal

Respiratory Cardiovascular

Drugs

Neurological

Idiopathic (rare)

Renal failure/uraemia Hyponatraemia and electrolyte disorders Urinary tract infection Urinary retention Hypoxia, e.g. chest infection Atelectasis Pulmonary embolism Dehydration Septic shock Myocardial infarction Chronic heart failure Arrhythmia Opiates, including heroin Hypnotics Cocaine Alcohol withdrawal Hypoglycaemia Epilepsy Encephalopathy Head injury Cerebrovascular accident Hypothyroidism Hyperthyroidism Addison’s disease

Confusion may present as anxiety, incoherent speech, clouding of consciousness or destructive behaviour, e.g. pulling out of cannulae. Risk factors for POD include pre-existing cognitive impairment (dementia), use of narcotics, benzodiazepines, alcohol (and withdrawal from it), severe illness, renal impairment and depression. Precipitating factors include use of physical restraints, addition of new medications, electrolyte and fluid abnormalities, intraoperative blood loss and admission to an intensive care unit. Treating the underlying medical problems, involving relatives or friends who are known to the patient, and pain control will all be valuable. As a last option, haloperidol may be given in titrating doses.

Drains Drains are used to prevent accumulation of blood, serosanguinous or purulent fluid or to allow the early diagnosis of a leaking surgical anastomosis. In clean surgery, such as joint replacement, blood collected in drains can be transfused back into the patient

provided that an adequate volume (>150 mL) is collected rapidly (30 (Figure 22.2). Traditional guidelines are conservative about obesity due to fears of intra- and postoperative complications. Although there is an increased incidence of

Table 22.1 The American Society of Anaesthesiologists Physical Status Classification.

Classification 1 2 3 4 5

A normal healthy patient A patient with mild systemic disease A patient with severe systemic disease A patient with severe systemic disease that is a constant threat to life A moribund patient who is not expected to survive without the operation

Reproduced with permission from: American Society of Anaesthesiologists (1963).

non-serious respiratory complications intraoperatively and in the immediate postoperative recovery period, the course of these patients is otherwise uneventful. They should, however, be managed by experienced medical and nursing staff. Hypertension, congestive cardiac failure and sleep apnoea are all more common in patients with morbid obesity, but in selected and optimised patients, a BMI up to 40 for surface procedures and 38 for laparoscopic procedures are acceptable in advanced units.

Weight in kilograms 40 45 50 55 60 65 70 75 80 85 90 95 100 105 110 115 120 125 130 135 140 1.92 11 12 14 15 16 18 19 20 22 23 24 26 27 28 30 31 33 34 35 37 38 1.92

BMI 20–25

1.90 11 12 14 15 17 18 19 21 22 24 25 26 28 29 30 32 33 35 36 37 39 1.90

BMI 25–30

1.88 11 13 14 16 17 18 20 21 23 24 25 27 28 30 31 33 34 35 37 38 40 1.88

BMI 30–35

1.86 12 13 14 16 17 19 20 22 23 25 26 27 29 30 32 33 35 36 38 39 40 1.86

BMI 35–40

1.84 12 13 15 16 18 19 21 22 24 25 27 28 30 31 32 34 35 37 38 40 41 1.84

BMI >40

1.82 12 14 15 17 18 20 21 23 24 26 27 29 30 32 33 35 36 38 39 41 42 1.82 1.80 12 14 15 17 19 20 22 23 25 26 28 29 31 32 34 35 37 39 40 42 43 1.80 1.78 13 14 16 17 19 21 22 24 25 27 28 30 32 33 35 36 38 39 41 43 44 1.78

1.74 13 15 17 18 20 21 23 25 26 28 30 31 33 35 36 38 40 41 43 45 46 1.74 1.72 14 15 17 19 20 22 24 25 27 29 30 32 34 35 37 39 41 42 44 46 47 1.72 1.70 14 16 17 19 21 22 24 26 28 29 31 33 35 36 38 40 42 43 45 47 48 1.70 1.68 14 16 18 19 21 23 25 27 28 30 32 34 35 37 39 41 43 44 46 48 50 1.68 1.66 15 16 18 20 22 24 25 27 29 31 33 34 36 38 40 42 44 45 47 49 51 1.66 1.64 15 17 19 20 22 24 26 28 30 32 33 35 37 39 41 43 45 46 48 50 52 1.64 1.62 15 17 19 21 23 25 27 29 30 32 34 36 38 40 42 44 46 48 50 51 53 1.62 1.60 16 18 20 21 23 25 27 29 31 33 35 37 39 41 43 45 47 49 51 53 55 1.60

1.56 16 18 21 23 25 27 29 31 33 35 37 39 41 43 45 47 49 51 53 55 58 1.56 1.54 17 19 21 23 25 27 30 32 34 36 38 40 42 44 46 48 51 53 55 57 59 1.54 1.52 17 19 22 24 26 28 30 32 35 37 39 41 43 45 48 50 52 54 56 58 61 1.52 1.50 18 20 22 24 27 29 31 33 36 38 40 42 44 47 49 51 53 56 58 60 62 1.50 1.48 18 21 23 25 27 30 32 34 37 39 41 43 46 48 50 53 55 57 59 62 64 1.48

Height in metres

1.58 16 18 20 22 24 26 28 30 32 34 36 38 40 42 44 46 48 50 52 54 56 1.58

Height in metres

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1.76 13 15 16 18 19 21 23 24 26 27 29 31 32 34 36 37 39 40 42 44 45 1.76

40 45 50 55 60 65 70 75 80 85 90 95 100 105 110 115 120 125 130 135 140

Weight in kilograms

Figure 22.2 Body mass index calculator. Adolphe Quetelet, 1796–1874, Belgian mathematician, astronomer and statistician who was the pioneer in establishing the criteria of obesity that became known as the Quetelet Index. In 1972 Ancel Keys (1904–2004), an American Scientist from the University of Minnesota and an expert on human nutrition, public health and epidemiology, named it the Body Mass Index.

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Perioperative management

Safe and comfortable discharge home requires the patient to be accompanied by a responsible and physically able adult to remain with them overnight. Home circ*mstances require appropriate toilet facilities and the means of contacting the hospital should complications occur. A journey time to home of an hour or less is advocated, but the comfort of the journey rather than the time involved is more relevant.

Surgical criteria Patients undergoing procedures up to 2 hours in duration can safely undergo day surgery with modern anaesthetic techniques. The degree of surgical trauma is an important determinant of success therefore entry to abdominal and thoracic cavities should be confined to minimal access techniques. Whatever the procedure, the main requirement is that there is suitable control of pain and the ability to drink and eat in a reasonable timescale (Summary box 22.2). Summary box 22.2 Selection criteria for day surgery ■

■

Medical: use physiological rather than chronological age ASA status over II requires careful review Provided that the BMI is under 40, this alone is not a contraindication Social: a responsible adult carer must be available for first 24 hours home conditions need to be suitable ability to contact hospital in an emergency Surgical: operations up to 2 hours recognised day-surgery procedures ability to eat and drink within reasonable timescale.

PREOPERATIVE ASSESSMENT The evaluation and optimisation of a patient’s fitness for surgery is known as preoperative assessment and is best performed by a specialist nursing team with support from an anaesthetist with an interest in day surgery. The assessment should be performed early in the pathway to allow time to optimise health problems before surgery. The consultation consists of a basic health screen to include the measurement of BMI, blood pressure and an assessment of past medical history with current medication recorded. Appropriate investigations are performed to ensure the patient is fit for surgery. The patient and/or their carer should be given verbal and written information regarding admission, operation and discharge (Summary box 22.3).

PERIOPERATIVE MANAGEMENT Scheduling With dedicated day surgery lists, major procedures should be scheduled early on morning lists to allow maximum recovery time. When the list is in the afternoon, the allocation of local or regional anaesthetic cases later in the day helps reduce unplanned overnight admissions following general anaesthesia. When mixed lists of day and inpatient cases are planned, then day cases should go first. Where complex inpatient surgery is undertaken, the mixing of day and inpatient cases is not advisable. The complex case may be inappropriately delayed if the day case is scheduled first and conversely if the day-case patient is scheduled later, it may result in cancellation or an unplanned overnight admission for the day case.

Anaesthesia and analgesia Successful day-surgery anaesthesia requires a multimodal approach to analgesia, while ensuring patients are given optimal dosages of anaesthetic agent. The agents used matter less than the skill of the person providing anaesthesia. Multimodal analgesia starts in the preoperative period and unless contraindicated, patients should receive full oral doses of paracetamol and a nonsteroidal anti-inflammatory drug (NSAID), such as ibuprofen. Intraoperative anaesthesia can be maintained by any of the traditional inhalational agents. TIVA (total intravenous anaesthesia) techniques using propofol are also popular and offer the advantage of reduced postoperative nausea and vomiting (PONV). The use of intraoperative analgesia will depend on the procedure being performed. When available, the anaesthetist should use short-acting opioids (fentanyl, alfentanil). Careful use of these agents can minimise the incidence of PONV. Where the choice is limited to morphine, this should be used in small doses (under 0.1 mg/kg) to minimise sedation and PONV. Wherever possible, a long-acting local anaesthetic agent, such as bupivacaine, should be injected into wounds by the surgeon. Pain levels should be routinely assessed in the postoperative recovery area. Further doses of paracetamol, fentanyl or low doses of morphine can be used to ensure that patients are comfortable prior to return to the ward (Summary box 22.4). Summary box 22.4 Optimal analgesia and anaesthesia ■

■ ■ ■

Summary box 22.3

Multimodal analgesia with paracetamol and nonsteroidal anti-inflammatory drug (NSAID) (if not contraindicated) should be given preoperatively Use long-acting local anaesthetic infiltration of the surgical wound Careful dosing of inhalational or intravenous agents should be used to maintain anaesthesia Avoid long-acting opioids, such as morphine, to reduce the incidence of sedation and postoperative nausea and vomiting (PONV)

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Social criteria

283

Preoperative assessment ■ ■ ■

On all day-surgery patients Early in the patient pathway By a specialist nursing team with anaesthetic support

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Postoperative complications The range of postoperative complications is no different from normal surgery. However, the fact that the patient will be

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discharged home within a few hours of surgery requires proactive monitoring after surgery. Haemorrhage is dealt with later in the chapter. Nausea and vomiting is not uncommon and should be managed actively to maximise successful discharge (Figure 22.3). Inadequate recovery from anaesthesia, uncontrolled nausea and vomiting and inadequate pain control are the most common anaesthetic related causes of postoperative admission.

procedures in general surgery where the British Association of Day Surgery considers at least 40 per cent of procedures can be performed on a day-case basis are shown in Table 22.2. Summary box 22.5 Surgical haemorrhage ■

Patient with severe nausea or vomiting. ■

Give IV fluids to hydrate the patient (10–15 mL/kg over 1 hour) and intravenous antiemetic e.g. cyclizine, prochlorperazine.

Review after 1 hour.

Reactionary: occurs 4–6 hours after surgery and is caused by ligature slippage, clot displacement or cessation of vasospasm, after mobilisation or coughing Secondary: occurs more than 24 hours after surgery and is due to infection eroding a vessel

Summary box 22.6 Requirements for successful day surgery

If still a problem then give a second antiemetic of different type, e.g. ondansetron, dexamethasone.

■ ■ ■

Minimal access techniques Good haemostasis Avoidance of unnecessary tissue handling or tension

Patient is hydrated and can be reassured that no further active management is possible. Offer choice if admission or to be discharged home.

Figure 22.3 Active management of postoperative nausea and vomiting (PONV).

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SURGERY For some surgical specialties, over 90 per cent of their elective workload can be achieved in day surgery. As a result, teaching and training now routinely occurs on day-surgery lists, but requires structure and close supervision. As the spectrum of procedures has increased and become more challenging, there has been a culture change among surgeons to increase their involvement in day surgery. This is important because safe and efficient day surgery demands the competence and skill of an experienced surgeon. Some surgeons have concerns regarding patient safety after discharge. The risk of postoperative haemorrhage occurring once the patient has returned home following tonsillectomy or laparoscopic surgery is often stated as a major reason to keep the patient in hospital overnight. Reactionary haemorrhage commonly occurs in the first 4–6 hours after surgery, but the patient is unlikely to have been discharged home within this time period. It may be caused by slippage of a ligature, displacement of blood clot, cessation of vasospasm, after coughing or increased mobility. Secondary haemorrhage is defined as occurring at least 24 hours after surgery, but usually presents several days later, as it is due to postoperative infection. Thus, even if the patient had stayed overnight, these postoperative bleeds are still likely to occur once the patient has returned home (Summary box 22.5). Good surgical technique requires minimal tissue traction or tension and good haemostasis. In day surgery, these attributes are even more important (Summary box 22.6). The number and variety of surgical procedures performed on a day-case basis is increasing year on year. Many developments have been pioneered by individual surgeons in isolated centres and their expertise has yet to spread to mainstream surgery. Volume

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Table 22.2 Volume procedures where 40 per cent or more should be performed on a day-case basis.

Surgery Abdominal

Excisional/treatment of anal lesions, haemorrhoidectomy, primary and recurrent inguinal/femoral herniae, laparoscopic cholecystectomy, laparoscopic fundoplication, pilonidal sinus surgery

Breast

Excision/biopsy breast lesion, sentinel node excision

Genitourinary

Laser prostatectomy, orchidectomy, circumcision, excision of hydrocoele/varicocoele/epididymis

Orthopaedic

Dupuytren’s fasciectomy, carpal tunnel release, therapeutic arthroscopy of knee or shoulder, bunion operations, removal of metalwork

Vascular

Varicose vein procedures, thoracoscopic sympathectomy

Reproduced with permission from British Association of Day Surgery (2009).

DISCHARGE The assessment of when a patient is fit for discharge is best performed by trained day-surgery nurses using strict discharge criteria (Table 22.3). While postoperative review by the surgical team is encouraged, the discharge should not be delayed by failure of their timely attendance. A suitable supply of analgesics for the management of pain should be provided. Paracetamol, NSAIDs and codeine form the basis of the drugs available in many countries.

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Further reading Table 22.3 Discharge criteria.

Vital signs stable for at least 1 hour Correct orientation as to time, place and person Adequate pain control with supply of oral analgesia Understands how to use oral analgesia supplied

285

FURTHER READING Jakobsson J. Anaesthesia for day case surgery. Oxford: Oxford University Press, 2009. Lemos P, Jarrett P, Philip B (eds). Day surgery: development and practice. Porto: Clássica Artes Gráficas, 2006. Thomas WEG, Senninger N (eds). Short stay surgery. New York: Springer, 2008.

Ability to dress and walk, where appropriate Minimal nausea, vomiting or dizziness Has taken oral fluids Minimal bleeding or wound drainage Has passed urine (if appropriate) Has a responsible adult to take them home Has a carer at home for the next 24 hours Written and verbal instructions given about postoperative care Knows when to come back for follow up (if appropriate)

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Emergency contact number supplied

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Trauma

23 Introduction to trauma

289

24 Early assessment and management of trauma

301

25 Emergency neurosurgery

310

26 Neck and spine

326

27 Maxillofacial trauma

341

28 Torso trauma

351

29 Extremity trauma

364

30 Burns

385

31 Plastic and reconstructive surgery

401

32 Disaster surgery

417

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CHAPTER

Introduction to trauma LEARNING OBJECTIVES

WHAT IS TRAUMA? Trauma is the study of medical problems associated with physical injury. The injury is the adverse effect of a physical force upon a person. There are a variety of forces that can lead to injury, including thermal, ionising radiation and chemical. However, the force involved in most injuries is mechanical. The subject of trauma therefore centres upon the deleterious effects of kinetic energy on the human frame. In the next group of chapters we will explore trauma from a variety of perspectives related to different specialties. In this introduction, we will look at the aspects that bind the whole topic together.

THE SCALE OF THE PROBLEM Trauma is recognised as a serious public health problem. In fact, it is the leading cause of death and disability in the first four decades of life and is the third most common cause of death overall. Millions of people are killed or disabled by injury each year. Of the 5 million people killed as a result of injuries in 2000, approximately 1.2 million people died of road traffic injuries, 815 000 from suicide and 520 000 from homicides. In the UK, the accidental and deliberate injury standardised death rate (SDR) is 27.28 deaths over all ages per 100 000 inhabitants per year. Hundreds of thousands who survive their injuries experience long-term or permanent disabilities, time lost from work or family responsibilities, costly medical expenses, profound change in lifestyle, pain and suffering, regardless of gender, race or economic status. An injury affects more than just the injured person; it affects everyone who is involved in the injured person’s life. The importance of the modern epidemic of motor vehicle accidents (MVA) to the global epidemic of violent injury cannot be overstated. Trauma is not just related to high-energy transfer in road accidents or to violence. The elderly fall victim makes up the most common group to be admitted to hospital following injury in the UK. Fragility fractures represent an increasing load on health services. About 70 000 patients suffer a proximal femoral fracture each year in the UK. About 30 per cent of those over the age of 65 years who suffer a proximal femoral fracture will die

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• How to respond to a trauma problem • The value of planning

within a year of the incident, and most of the others will have diminished independence and mobility. It can be appreciated that this represents a huge burden on the health services and society in general. The great majority of injuries are not life- or limb-threatening. Here the challenge is not only to treat the minor injuries, but also to differentiate between those injuries that have some important aspects and those that are genuinely straightforward. For instance, in children, one must always be alert to the potential for non-accidental injury (NAI). There is a chilling statistic that in 66 per cent of cases when children die as the result of abuse there has been some previous relevant contact with a health professional or social services. In all age groups, we need to be wary of pathological fractures; here the more important problem may not be the injury itself, but the underlying disease process (Summary box 23.1). Summary box 23.1 Trauma: the scale of the problem ■ ■ ■

Trauma is the major cause of death in the young Fragility fractures are an increasing burden Look beyond the obvious in trauma management

THE MANAGEMENT OF TRAUMA We learn how to manage trauma based on evidence, extrapolation from principle and by copying. All of our actions should have a purpose, for those based on evidence or principle this is frequently apparent. However, our actions based on mimicry and protocol may have less obvious foundations. While this may help to reduce delay when under pressure, we should also attempt to understand why we are carrying them out.

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To gain an understanding of: • The importance of time in trauma management • How to assess a trauma problem

The importance of time An identifying feature in the study of trauma is time. At time zero, the person/patient is at their normal baseline. There is then some interaction with an external force leading to injury. The

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subsequent development of pathology, the response of the body by way of compensation and healing, and the external responses by health professionals all have a timeline. The timeline may be used to compare and consider the progress from time zero to other significant events or deadlines that follow. Figure 23.1 depicts an estimate of the periods of time that may elapse from time zero to death or irretrievable damage for various injuries. It reflects the fact that some problems tend to lead to earlier death than others. An obstructed airway, a tension pneumothorax, an extradural haematoma or an ischaemic limb will all tend to progress along a characteristic timeline after the moment of initial injury if left untreated. This creates an ‘imperative of time’ that shapes and provides a basis for the hierarchy of our initial medical response to the injured patient. Thus, an obstructed airway will need emergency initial management at the scene of the accident. An ischaemic limb may be dealt with urgently once the patient has reached a definitive treatment centre. The ATLS (Advanced Trauma Life Support) system defines an order of priorities given by ABCD; that is airway, breathing, circulation and disability (neurology). This is founded upon this time dependence. To this raw diagram of the time from injury to death or irretrievable damage may be added other components. These are the time to understand or assess the nature of the problem and the time to respond effectively to that which has been discovered. Each of these will take a finite length of time and this is shown schematically for a generic condition in Figure 23.2. It can be seen that in this example there is adequate time for an orderly

Ischaemic limb Extradural haematoma Intra-abdominal bleeding

process of all the stages of assessment followed by a response before irretrievable damage or death. The block of time allocated to assessment may be broken down further. Understanding and assessing the nature of the problem usually hinges on diagnosing the injury. An injury may be found by careful physical examination or need special investigation before it is discovered. It therefore becomes obvious at different points on its timeline. An example is an evolving extradural haematoma: the initial skull fracture may be visible on radiography or computed tomography (CT); as the haematoma develops it will first be visible on CT; later, it will be suspected on careful clinical examination; and, finally, it will become clinically very obvious. This is represented in Figure 23.3a. The next feature to add to the timeline is the response time. Once an obstructed airway is identified, the response time to carry out a life-saving simple airway manoeuvre may be a matter of seconds. Thus, even at the stage when the diagnosis is clinically obvious, there may still be time to resolve the problem before irretrievable damage occurs. However, when dealing with an extradural haemorrhage, the average response time from identification of the problem to surgical resolution may be measured in hours. This may seem an unduly long time, but bringing the patient to an operating theatre with a neurosurgeon takes time to arrange, as seen in Figure 23.3b. If we now combine the various features of a timeline for the single condition of extradural haematoma, difficulties become apparent. In Figure 23.3c, it is seen that if the response is only initiated once the diagnosis has become obvious, then there may be insufficient time left to resolve the problem before death intervenes. This seems to suggest that we need to initiate a response to a problem before we are sure of its existence if we are to save the patient’s life. This apparent paradox will be explored further. However, for the moment it can be likened to the need to identify a cancer at an early stage to give the best chance of successful treatment. A common approach to such a problem is to screen the at-risk population, and the same principle applies in the management of trauma.

Airway obstruction 0

Evolving assessment for extradural haematoma (a)

Time

Fracture on imaging

Figure 23.1 Estimated time from incident to death or irretrievable damage for various conditions.

Haematoma on imaging

Subtle clinical signs

Clinically obvious

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Components of response time (b)

Overall timeline for generic injury

Refer

Transfer

Anaesthetise

Decompress

Death Overall timeline for extradural haematoma

Assessment time Response time 0

Time

Figure 23.2 Diagrammatic representation of the relationship between assessment and response times. In this example, there is time to assess and respond effectively before death.

Death

Time

Figure 23.3 Diagrammatic representation of the relationship between assessment and response times for extradural haematoma. (a) The stages of assessment; (b) the components of the response and (c) the overall time from incident to death. It can be seen that relying on obvious clinical signs gives insufficient time to respond effectively.

George Quentin Chance, formerly Director of Diagnostic Radiology, Derby Group of Hospitals, Derbyshire, England.

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Initial rehabilitation

Surgery

Assessment

MEDICAL TIMELINE Preparation for surgery

Postoperative recovery

Discussions with family

Occupational therapy assessment

Medically fit for discharge

Home alterations

SOCIAL TIMELINE Securing discharge destination

Social services assessment 0

Socially fit for discharge

Time

Figure 23.4 Social and medical timelines for an elderly patient with a proximal femoral fracture. Discharge can only occur when both are complete.

staff is that all x-rays of patients discharged are independently reviewed by a radiologist. Should their findings differ from those in the clinical record, the patient can be recalled and reassessed. Timelines reveal that things change. As a consequence, reassessment can be of vital importance. An observation, an x-ray or a blood test are only snapshots in time. Repeated observation will reveal trends that may make a diagnosis more straightforward. Modern monitoring allows this continuing vigilance to be carried out more straightforwardly. Graphical recording of results in a single place makes trends easier to follow. Although the pressure and relevance of time shapes our response to the injured, it should not be allowed to degrade it (Summary box 23.2). Summary box 23.2 The importance of time ■ ■ ■ ■

Time pressure shapes our management of trauma There is a finite time to assess There is a finite time to respond For success, these must fit into the available time before irretrievable damage or death

ASSESSMENT AND RESPONSE The breakdown of our approach to the injured into two components of assessment and response has been introduced. Although the two concepts overlap and intertwine, it is helpful to explore them separately.

The assessment of trauma

PART 4 | TRAUMA

As we will see, much of the medical preparation and planning related to trauma is aimed at reducing the diagnosis time and the response time so that they will fit into the time available before death or irretrievable damage. To revise the meanings of these terms, the diagnosis time is the time between injury and recognition of the problem and the response time is the time that elapses between identifying the problem and effective intervention being completed. We can reduce these times by using a practised, protocol-driven approach to the initial stages of the management of an injured patient. We must still think, but it does mean that we can have a pre-existing structure upon which to build those thought processes. This allows us to move forward more rapidly. This structured initial approach allows for more straightforward teamwork, standardisation of the equipment required and confidence in a difficult situation. The pressure of time determines the manner in which we deal with the multiply-injured patient. The normal sequence of history, examination, provisional diagnosis, special investigations, diagnosis and management plan is not appropriate under this pressure. When dealing with the multiply-injured, a quite different approach is needed. As will be seen, the primary survey used in ATLS combines the identification of life-threatening problems with their management. It has evolved to improve the chances of the necessary actions being taken within the time available. The system has to allow for diagnosis to be made and response completed within the timeline for the injuries sustained. Increasingly, special investigations are being lavished on the multiply-injured patient with the aim of trying to reduce further the delay to accurate diagnosis. The model of a timeline need not be restricted to the multiply-injured patient. The role of time when dealing with an elderly person who has been injured is still present, but is frequently ignored. In these cases, there may be hidden urgent issues. Thus, when dealing with the elderly, we too readily label a patient with the most obvious problem (such as a hip fracture) without performing the vital initial physiological triage. The patient may often have a primary cardiac, respiratory or neurological problem that has resulted in a fall and the response to this may be the most urgent issue. Therefore, the timeline is not only relevant to the acute and obviously urgent clinical issues. As noted at the beginning of this chapter, a timeline may be used to compare and consider the progress from time zero to other significant events or deadlines that follow. In this case, the response time to arrange a discharge from hospital for the elderly patient may be critically protracted. Figure 23.4 demonstrates that, with such a long response time, to allow for discharge at the appropriate clinical time the social planning needs to commence almost at the time of admission. This is well before it would seem clinically reasonable, but to achieve an efficient system, it can be seen to be necessary. This approach allows an emergency unit to get as close as is possible to the practice of an effective elective unit where discharge plans are made before the patient is admitted. Time also plays a part in how we deal with more minor injuries. There is a need and expectation that these patients will be dealt with rapidly; however, there is then a danger, especially with inexperienced doctors, that corners will be cut and problems missed. Focusing on the important issues without risking missing problems is a difficult skill. Although not all patients will be seen by more than one doctor, another health professional, usually a nurse, will see them and their observations should not be ignored. A common safety net for the front-line medical

291

At time zero, a person in their baseline condition comes together with an external force to produce injury. Understanding this relationship between the patient, the mechanism of injury and the injury produced is the key to understanding the problem that has to be solved. This is helpful both when making a diagnosis

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and treatment plan for an individual, and also for structuring the thinking of the management of trauma in general. The relationship can be expressed simply as: mechanism + patient = injury. The nature of these components may be quite obvious (overt) or in some way hidden (covert). We need to convert everything to the overt. We can only treat what we have found; we can only resolve the problems that we have identified. A tidy relationship between the mechanism, the patient and the resulting injury is often obvious. A previously healthy 40-yearold man falling vertically 2 metres and landing on his feet may sustain an os calcis fracture. From this position of understanding, we can move swiftly forward to confirm and treat. In many cases, there is something more to find out or to understand. It may be that the three variables just do not add up to form a complete picture. This failure of the relationship is not real but apparent. If the three variables do not fit together something has probably been misjudged, and the factor that is causing the failure of the clinical picture to ‘add up’ must be sought. It may be that some aspect of the injury has not yet been discovered, the mechanism suggested may not be genuine or there may be some aspect of the patient before the injury of which one is unaware (Summary box 23.3). To expand on this theme, we will explore how to use the available information to best effect. Summary box 23.3 The assessment of trauma ■ ■ ■

Use all of the information: mechanism, patient and injury Allow the obvious features to be a guide to the less obvious If the equation does not add up, look for more reasons

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Mechanisms Mechanisms may be blunt or penetrating. One of the easiest of these to understand is the incision caused by a knife. We are used to knives both at home when we eat and as surgeons when we operate. A knife has a sharp edge that may cut tissues with which it makes contact; these effects are easily appreciated because they happen in a timescale that we understand. A knife damages only what it can reach. A good history of the length of blade coupled with an entry point allows for a potential pattern of injury to be imagined and then individual components to be confirmed or excluded by examination, special investigation or wound exploration (Table 23.1). Thus, an incisional injury over an extremity is readily evaluated as long as the relevant anatomy is known. The distal perfusion, peripheral nerve function and tendon and muscle function can all be assessed by clinical examination. However, should joint penetration be a possibility then the problem is different. Understanding the timeline is of value. The consequences of a septic arthritis are severe and if treatment is delayed until the condition is clinically obvious, then it may be too late to prevent permanent damage. Therefore, the diagnosis of joint penetration needs to be excluded by screening the at-risk group. If a large joint is involved, for example the knee, an algorithm such as that in Figure 23.5 can help identify those joints that need formal exploration. One component of this algorithm is to fill the joint until tense with sterile saline and watch whether fluid leaks through the traumatic wound. This will show whether the joint has been penetrated. If the joint has been breached, a

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Table 23.1 Examples of patterns of injury.

Mechanism

Obvious features

Covert injuries

Left-sided impact from road traffic accident

Lateral compression of the pelvis Left-sided pneumothorax

Splenic rupture

Flexion distraction Chance fracture of the (lap belt) lumbar spine Dislocated knee

Extradural haematoma Duodenal rupture

Head injury

Popliteal artery disruption Cervical spine fracture

Electrocution

Burn on hand and collapse

Posterior dislocation of the shoulder

Dashboard impact

Knee wound

Posterior dislocation of the hip

formal procedure in an operating theatre is required. This action is now therapeutic and not exploratory. In assessing the effects of an incisional mechanism over the torso, the first step is again to decide which structures are at risk. This may seem simple, but it is not always easy to determine the direction that a blade has entered. The anatomy can also be confusing; it is worth recalling that the abdominal contents extend higher than normally expected, up to the level of the fifth rib in expiration. A notable feature of stab injuries is that they are often eminently treatable; even cardiac injuries can be treated with a realistic chance of success if identified early (Summary box 23.4). Penetrating injuries caused by firearms are not so easily understood as incisional injuries. A low-velocity projectile behaves

Wound close to knee ? joint penetration On inspection joint open No On x-ray intra-articular gas or foreign body

Yes

No Yes

Conclude joint open Requires formal washout

Yes

Insulate knee with sterile saline until tense Leakage from traumatic wound No Conclude joint is intact

Figure 23.5 Algorithm for assessing a wound that has potentially entered a joint.

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Assessment and response Summary box 23.4

293

(a)

Incisional injuries ■ ■ ■

Require knowledge of anatomy The abdominal contents extend high into the chest Even cardiac injuries are treatable if recognised early and treated quickly

more or less like a stabbing injury. However, as the velocity increases, the energy increases in line with E = ½mv2; as the amount of energy increases, the ability of the system to dissipate that introduced energy in a simple way is overcome. In the case of high-velocity projectiles, the result is not like anything we are familiar with in day-to-day life. Furthermore, these projectiles are deliberately designed to produce particular results: some are designed to kill, whereas others are designed to maim but not kill. In a military conflict, it is more disabling and demoralising to your opponent’s forces if individuals do not die but consume resources in their treatment and protection. The high-velocity bullet crushes particles of the human body in its pathway and produces lateral acceleration away from the point of impact. This motion of the tissue particles away from their original position produces a cavity. Two types of cavity are produced: (1) a permanent cavity – one that remains after the initial impact; (2) a temporary cavity – one that lasts for milliseconds, and may no longer be apparent during the physical examination of the wounded. This temporary cavitation can extend well beyond the boundaries of the apparent injury. Highspeed photography shows the dramatic nature of the temporary deformation, which happens on a very rapid timescale (Figure 23.6). Awareness of this phenomenon will encourage the treating surgeon to perform an adequate exploration and, if appropriate, a more radical wound excision than would otherwise be used (Summary box 23.5).

(b)

(c)

Summary box 23.5 Firearm injuries ■ ■ ■

Low-velocity bullets behave like knife injuries High-velocity bullets cause cavitation The temporary cavity is large and draws in foreign materials The permanent cavity is smaller and gives no clue to the extent of damage

A blunt mechanism of injury can be considered as direct or indirect. A direct mechanism is when the damage occurs at or close to the site of impact. An indirect mechanism is when the damage occurs at a distant site after transmission of that force. The following examples, in which two different mechanisms leading to fracture of the ulna are considered, may help to understand this. Should an attacker strike with a strong stick, the victim may protect their head by raising their arm. The blow will then fall on the ulna. This may cause an isolated fracture of that bone generally called a ‘nightstick fracture’ (a nightstick being a weapon of enforcement carried by the police). This is clearly a direct injury. All of the injury is concentrated at the site of application of the force; the soft tissues may be bruised, contused or lacerated at the site. A different situation occurs if a

Figure 23.6 A projectile passing through a gelatin block. (a) Low energy transfer; (b) High energy transfer. (c) The effect of high energy transfer on tissues. Photographs courtesy of Professor J Ryan.

person falls on an outstretched hand. This may lead to a fracture of the ulna, but here the mechanism is indirect. The force has been transmitted through the body’s tissues to a site at some distance from its application. It is unlikely that an ulnar fracture would occur in isolation in such circ*mstances and the ‘associated injuries’ should be sought. In this instance, the associated injury is often a dislocation of the radial head, the whole injury complex being called a Monteggia fracture dislocation. These injuries are demonstrated diagrammatically in Figure 23.7. The injury is often missed and the consequences are severe in the growing child. Thus, we should always evaluate the elbow fully (radiologically and clinically) in an apparently ‘isolated’ ulnar fracture, especially if the mechanism was indirect, usually a fall

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■

Giovanni Batista Monteggia, 1762–1815, Professor of Anatomy and Surgery, Ospedale Maggoire, Milan, Italy.

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Zone of injury

(a)

Direct force

(b) Indirect force

Figure 23.7 Two examples of a fracture of the ulna. (a) A nightstick fracture from a direct blow. (b) A Monteggia fracture from an indirect force.

onto the hand. The timeline in these circ*mstances is not pressing. The injury can be adequately treated for some weeks after it occurs, but once the diagnosis has been missed and the wrong label applied it becomes progressively more difficult to rectify. The energy transmission in an indirect mechanism may be via a solid structure, such as a bone, as in the examples above, or it may be via the soft tissues or fluid. Some of the resulting injuries can be quite unexpected. A compressive force to the abdomen will cause a rise in pressure that may be transmitted by the vascular system. A sudden back pressure at the heart can lead to damage to the valves. The results of direct mechanisms are easier to understand as the damaging effects are often more localised. Even when the patient was alert before and after the event, it can be surprisingly difficult to be sure of the mechanism as it affected the injured part. The rapidity and unexpectedness of accidents means that precision in history is often hard to obtain.

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Patient factors Individuals with different physical characteristics and medical histories will respond differently to mechanical insult. In the standard history taken, a quick categorisation of a patient is normally carried out. As we take a history, we intuitively group patients to assess the nature of their likely injuries. Children, adults and the elderly are three obvious separate groups. We anticipate different injuries in these different groups even if the mechanism is the same. A torus fracture, a Colles fracture, or fractured hip may each result from a simple fall. Similarly knowing a patient is on anticoagulants, has osteogenesis imperfecta, has a previous total knee replacement or has known metastatic disease guides assessment.

Obvious injuries Some injuries are so obvious that they may present before any mechanism or patient details are known. It may therefore be the presence of one overt injury that leads to the search for another; the obvious injury is being used just as a history would in other circ*mstances. The most obvious injuries will be those that are

visible externally. It is for this reason that there is an E at the end of ABCDE in the ATLS system: E is for exposure – look for the clues. If a wound suggests a penetrating injury then thought should be given to the underlying structures at risk. A contusion over the knee of a driver suggests a dashboard injury. Finger-shaped bruises on a child’s arms suggest non-accidental injury (NAI). A good example of a minor but obvious injury helping in a timeline is singed facial hair. This sign is often associated with carbonaceous sputum and suggests inhalational burns. Calling an anaesthetic colleague when singed nasal hair is first noted is far better than a crash call 15 minutes later when laryngeal oedema obstructs the airway of a patient with an inhalational burn. Exposing the patient comes readily to those dealing with trauma. The perils of not exposing the patient were demonstrated in an infamous case in the UK. A patient already in hospital for another problem had ‘collapsed’ by the phone within the hospital and was dealt with by the cardiac arrest team. The patient responded poorly to treatment and it was only some time later that the bullet was noticed on the chest x-ray. Following this, the bullet wound in the victim’s back was found. A helpful adage borrowed from radiology is that ‘unless you are very lucky you only find what you look for’.

Hidden factors Mechanisms

Sometimes, when the normal relationship of ‘mechanism + patient = injury’ does not seem to hold, the hidden information may be in the mechanism. The most obvious examples are in situations in which there has been a deliberate attempt to mislead. Conscious sensible patients reporting their own injuries will generally tell the truth; however, sometimes to protect themselves or others they may fabricate a mechanism. The risk here is that if the mechanism is incorrect, the wrong pattern of injuries may be anticipated. Thus, the man who fell from 6 metres when in some illegal activity does not help achieve an accurate diagnosis if he reports the mechanism as a twist to his ankle from a stumble. Similarly, if it is not admitted that an injury results from an assault, then no action can reasonably be taken to help protect that person from further aggression. This situation is most commonly encountered when the patient is the victim of abuse within a relationship. The patient should be given the opportunity to tell their story, but it should not always be believed. More commonly, the problem of a hidden mechanism arises when the patient is unable to give their own history. A very young child or an elderly person is both physically and mentally vulnerable. They may have been physically abused, but be unable to report it. In these circ*mstances, the mechanism of injury may have been criminal. A list of some of the factors that should make one suspicious of the history and suspect that NAI has occurred is given below:

• • • • • •

history clearly inconsistent with the injuries sustained; changing history; aggressive behaviour of carers at interview; injuries of different ages; posterior rib injuries; long bone fractures in a pre-ambulatory child.

The interests of the patient are paramount and so we need to

Abraham Colles, 1773–1843, Professor of Surgery, The Royal College of Surgeons in Ireland, and surgeon, Dr Steven’s Hospital, Dublin, Ireland. At the age of 28 years, he was elected as President of the College and described his fracture in 1814. In view of his major contributions, he was awarded a baronetcy in 1839, which he declined.

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Assessment and response

Summary box 23.6 Covert mechanisms ■ ■ ■ ■

Patients usually tell the truth, but may not if criminal activity is involved Fear of abuse may prevent vulnerable patients telling the truth If a non-accidental injury (NAI) is suspected, you have a responsibility to take action Patients likely to have covert medical problems need careful checking even if their injury appears to have a simple mechanical cause

Patients

When the mechanism and the injury are obvious but inconsistent, it may be that there is something previously unknown about the patient to discover. Most commonly, this is a pre-existing pathology. Thus, a healthy adult who breaks their femur following a trivial insult may well have had a pathological weakness of the bone, such as a neoplasm. Thoughtless treatment of this as a simple fracture, without tissue diagnosis, staging, etc., may result in entirely inappropriate treatment with unnecessary loss of limb or life. Injury in the older patient may be the manifestation of general health problems. The obvious injury may be the fractured proximal femur, the hidden patient factor may be the transient ischaemic attack or abnormal cardiac rhythm that caused the fall. Rather like the practice of the secondary survey looking for covert injury in the polytraumatised patient, a medical secondary survey is required as a screen in the elderly.

Injuries

Looking for the hidden injury when deduction has failed can follow two methods: 1 the look everywhere approach; 2 the focused exclusion approach.

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1 The look everywhere approach. One of the mainstays of trauma evaluation has been the secondary survey. The essence is that once the initial life-saving manoeuvres have been completed you look everywhere for further injury. This detailed examination may take place shortly after admission, the following morning on the ward round or sometimes a week later when the patient first regains consciousness. As its name suggests, the look everywhere secondary survey comes later in the sequence of the ATLS approach. However, the emphasis placed on the timeline at the beginning of this chapter and the need for early diagnosis is leading to a different approach to the traditional ‘look everywhere’ one. The ATLS system has included a plain pelvic and a chest x-ray as part of the primary survey. This may confirm a clinical diagnosis, but is also a screening tool to identify injuries that may progress to a clinical problem; the response to that injury can then be initiated earlier. The threshold for using more generalised investigations such as CT scanning, ultrasound, cardiac echo and magnetic resonance imaging (MRI) to check for these covert injuries is progressively being lowered. Some emergency departments now have CT scanners in their resuscitation rooms. A head-to-pelvis CT scan is being used to replace the early plain radiographs of the chest and the pelvis. A CT scan is more sensitive and specific and its use to identify injury before the clinical signs become obvious is certain to improve patient care. 2 The focused exclusion approach. Some important injuries or conditions are for some reason missed on a surprisingly regular basis. This suggests that a normal deductive approach is not always adequate. Classic examples are scaphoid fractures, perilunate dislocations, posterior dislocations of the shoulder and tarso-metatarsal dislocations. Therefore, if such injuries are suspected or possibly present they should be positively excluded by focused history, examination and investigation (Summary box 23.7). Summary box 23.7 Trauma assessment ■ ■ ■ ■

Know the timelines for important diagnoses Prioritise the assessment accordingly Positively exclude critical diagnoses If required, screen at-risk patients before clinical signs are apparent

The response to trauma Once an assessment has been made based on the factors of mechanism, patient and injury discussed above, the response must be planned and executed. At the same time, the patient will have an evolving response to injury. On the positive side, physiological compensatory and reserve mechanisms will be recruited and healing processes will be initiated. Countering this, there may be progressive pathophysiological responses, the consumption of limited resources and decompensation.

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not only identify injuries that need treatment, but also protect patients from further harm. The timeline of importance here is that which has shown that 66 per cent of children who die as the result of abuse have been in contact with a health or social work professional before the fatal episode. We have already accepted that to adequately treat an extradural haematoma, we must respond to subtle indicators in the history and physical examination to allow our response to begin early enough to be effective. An analogous situation applies with child abuse – if we ignore the early signs, we may be too late to prevent the later episode in which real harm is done. NAI is a very difficult problem to deal with. As clinicians we are more comfortable trying to help everyone; acting to police a situation does not come naturally. In some criminal situations, the nature of any overt injuries may provide important evidence of the mechanism. Such evidence may be affected by our medical assessment and treatment. Although we should not compromise the medical management of an injured person, it is folly not to bear in mind at every stage that the victim of an assault may need good forensic evidence at some later date to convict their assailant. Indeed, the injured victim of an assault may later become a murder victim (Summary box 23.6).

295

The patient’s response to injury The patient’s own homeostatic mechanisms will respond to the injury and there will be physiological and pathophysiological

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changes. In the light of this evolution of responses, we may alter the nature or the timing of our interventions. A simple example is body temperature. A drop in body temperature is common after injury; this may be due to exposure, inactivity, damp, blood loss or loss of vasomotor control. The body’s own thermoregulatory mechanisms may not be able to resolve the problem and so we must be prepared to support that role – body temperature should be monitored and heat loss prevented as required. It may not be possible to do this adequately in an operating theatre during a surgical procedure. Similarly, oxygenation can be monitored and support may be given by way of increased inspired oxygen or different modes of ventilation. The response to blood loss is not only an evolving situation for an individual patient, but our response to it also changes. The patient calls on compensatory mechanisms when blood is lost. As long as organ perfusion is adequate, low blood pressure is not a problem in its own right. The body has a finite resource of clotting factors and the injured lung does not tolerate excess fluid. The combination of these factors has led to a tendency to draw back from large-scale early fluid replacement with a crystalloid. Instead, the emphasis is placed on identifying and stopping the source of bleeding. The patient also mounts a generalised immunological response to trauma. This has an impact on their ability to tolerate surgical interventions. There is growing evidence that procedures should be timed and staged to better fit the conditions created by the patient’s systemic immune response.

The medical response to injury

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Initial management The structure of ATLS is discussed in Chapter 22. Reducing the elapsed time from injury to useful intervention is critical for some patients. Preparation can aid this process. When a department is made aware of the impending arrival of a seriously injured patient, a decision needs to be made as to whether to call the ‘trauma team’; this will allow a trained team of nurses and doctors to be waiting to meet the patient. While waiting, equipment is made ready, a leader is identified and each team member is given a role. Protective clothing will be needed: gloves to protect from fluids and lead aprons to protect from x-rays. For the medical and nursing staff, the beginning of the patient’s pathway can become familiar just like any routine journey and, thus, planning becomes less complex. However, if wasteful delays are to be avoided, alternatives need to be available if for some reason the routine cannot be followed. Anticipating and dealing with potential rate-limiting steps in the patient’s journey will allow delays to be avoided and further reduce the response time. The component of the response that will be the rate-limiting step will depend on local, as well as general circ*mstances. Examples of causes of delay are obtaining a CT scan, getting the patient into an operating theatre or obtaining a necessary specialist opinion. Such steps that can potentially bring the progress of the patient to a halt need to be addressed early and sometimes in a way that may seem out of the normal sequence. This is one of the major roles of the team leader who should have an overview and be able to foresee and pre-empt problems. Whenever a system is protocol driven, someone should be in a position to take the responsibility to break protocol if required to keep the overall process flowing.

Having a practised common pathway can be disadvantageous; a patient with the wrong ‘label’ may go along the wrong pathway. We all have to be wary of labelling. Should two patients with identical histories and injuries arrive in an emergency department with one on a spine board and the other in a chair, the former will be treated as if more severely injured when in fact that may not be the case. We must make our own judgements on reasonable evidence and not just rely on the labels (in this case, the cervical collars) applied by others. Labelling is most frequently a dangerous problem in the elderly. A patient with an obviously short externally rotated leg may be quickly given the label ‘NOF’ (fracture neck of femur). There are a number of problems with this practice. The focus is now on the orthopaedic label rather than the whole patient. The incorrect label may mask the fact that the patient could be dying. The patient may have fallen as a consequence of a cardiac arrhythmia or other comorbidity; the early labelling may therefore send the patient off on entirely the wrong pathway. All vulnerable patients should have a physiological triage to avoid such problems. This means assessing the airway, respiratory rate, blood pressure, pulse rate and consciousness. All of these assessments are more important, even in the elderly, than the presence of a fractured hip.

Beyond the first hour The primary survey of ATLS encourages the identification and treatment of life-threatening problems. Once these have been addressed, there may be other problems that require intervention. The timing and order of these interventions is a matter of judgement. There has been an evolution in the approach to the management of polytrauma. It has been variously said that a patient may be ‘too sick to operate on’ or that they may be ‘too sick not to operate on’. The work of Bone in particular has promoted the concept of early definitive stabilisation of long bone fractures to allow better control of the pathophysiology of trauma. Others have highlighted the need in some circ*mstances for limited early intervention, sometimes called ‘damage control surgery’. This is followed by definitive treatment when the patient is better able to tolerate it. In orthopaedic trauma, the debate has focused on whether long bone fractures should be fixed temporarily or definitively. In general surgery, the question is whether the abdomen should be definitively treated or packed. Any patient needing a sequence of interventions, e.g. laparotomy, femoral nailing, tibial nailing, should have the most important done first. Thus, if there needs to be a break in the procedures for any reason, the most important interventions will have been completed. As each component of a sequence of procedures nears its end, a decision needs to be made whether it is safe or appropriate to proceed to the next stage. Monitoring of core temperature, coagulation, base excess, etc., will allow this decision to be made on rational grounds. When necessary the patient can then be transferred to the more controlled environment of an intensive care unit and return for definitive surgery when physiologically and immunologically better able to tolerate it; this may be hours or days later. A useful adjunct is to record the treatment plan on a whiteboard in the operating theatre. This informs others of the intended pathway of treatment so that preparations can be made. An example of such a tactic is shown in Figure 23.8. Note the alternative pathway that exists should the patient’s general condition require a shorter procedure, when the femur

Nicholas Andry, 1658–1742, was born in Lyon, France. He was a priest originally and taught theology before becoming a doctor. His expertise was in parasitology and orthopaedics. His illustration of a bent tree being supported by a stake to encourage it to grow straight symbolises the art and practice of orthopaedics worldwide.

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can be temporarily stabilised with an external fixator rather than definitively fixed with a nail.

LOCAL PROTOCOLS AND GUIDELINES A general guideline, such as ATLS, deals with some aspects of patient management and is used in many institutions. However, hospitals generally have individual policies to guide or direct decision making in smaller areas of practice. Examples are prophylaxis against infection and thromboembolism, the use of steroids in spinal injury and clearance of the cervical spine. These represent the efforts of individuals within an institution to plan for common and foreseeable circ*mstances. These protocols allow for easier and quicker decision making. Their application should protect the patient and, in an increasingly litigious world, the doctor as well. ‘Clearing’ of the spine is a practice that has particular relevance to trauma. The early policy for managing the spine in polytrauma patients is straightforward; it can be summarised as ‘suspect and protect’. This approach is widely employed, and so very many patients have their spine protected. However, this is a precautionary approach and at some stage one has to have a strategy for discontinuing protection, or ‘clearing’ the spine in those patients in whom protection is not required. In the event that it is not possible to exclude spinal injury on clinical grounds, the managing clinicians may request clearance on radiological grounds. An example of such a policy for clearing the spine is given in Table 23.2. Record-keeping for the injured patient is both important and difficult. It is often said that trends in a patient’s condition are more important than isolated observations. Because an injured patient may be cared for by a large number of individuals, trends can only become apparent by reference to the sequential recorded notes. If each individual clinician records their

Plan 1. Gen Surg. Laparotomy/Splenectomy 2. Orth (plastics aware bleep 1745) 2. Left leg Wound excision plan 2. soft tissue cover 2. Spanning EX Fix femur to tibia 2. bead pouch to cover 2. 2. 2. 2.

Right femur – if well then intramedullary nail – if not then temporary external – fixator

observations in an ‘individual’ manner, it becomes very difficult to identify trends. Adoption of the Glasgow Coma Scale to monitor the level of consciousness demonstrates the advantage of using a consistent system of recording observations. Such sequential observations, especially when displayed on a single chart, demonstrate trends. The clinical evolution of a problem, such as raised intracranial pressure secondary to an extradural haematoma is then easier to identify (Summary box 23.8). Summary box 23.8 The response to trauma ■ ■ ■ ■

Guidelines and protocols speed and streamline management Pre-empt time-limiting steps to avoid delay Respond to the evolving condition of the patient Use charts to plot trends

Table 23.2 An example of a policy for clearing the spine in the obtunded patient.

Cervical spine

Fine-quality computed tomography (CT) scans of C0–T4, reformatted and assessed in the axial, sagittal and coronal planes Powers ratio to assess the atlanto-occipital junction

Thoracolumbar spine (T4 distally)

Either good-quality anteroposterior and lateral plain films or CT scans reformatted and assessed in the anteroposterior, lateral and axial planes

Equipment

Potential problems

Washout tray

1. Pneumothorax increases:– 1. then place chest drain.

Large Ex. Fix Reamers Femoral nail Image intensifier

2. 2. 2. 2.

Chest deteriorates before femur nailed:– then temporary ex. fix to femur

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Diagnosis: Ruptured spleen Open left tibial plateau, fracture closed right femoral shaft, right pneumo (minor seen CT only)

Gent beads/loban Chest drain set

Position Supine radiolucent table Antibiotics Further dose Ceph/Gent at induction Anaesth General no blocks

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297

Figure 23.8 An example of a surgical tactic on a whiteboard in the operating theatre.

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Planning an individual operation The central part of a surgeon’s work is operating. Dealing with injuries is not repetitive and so thought and planning are required. Even when an individual surgeon is involved in performing the surgery, care is delivered as part of a team. It is good practice to think through the plan for the operating theatre. Mental rehearsal of a procedure may allow potential hazards to be predicted and avoided. For example,

• As the procedure is planned, it may become apparent that

the proposed surgical approach will not allow the access required. In a whiteboard exercise, this can readily be altered. This cannot be done so easily if the first time this problem is appreciated is after the skin has been cut. • It may be decided in planning that another surgeon is better suited to perform a particular procedure.

but also informs others. The position of the patient, the surgical approach, position of the image intensifier, method of fracture reduction and instruments required, and method of fixation and implants required are all noted. Theatre staff, anaesthetic staff and radiographers can all see what is intended and it can also act as a teaching aid. A trainee may be asked to complete the whiteboard plan; they then have to commit to a plan of action and not just drift along. An important addition to the planned progress of the procedure is a list of potential problems or hazards. The strategies that will be used to deal with these problems should they arise can then be considered and prepared for (Summary box 23.9).

The use of the whiteboard in theatre, discussed earlier in the context of multiple injuries, is equally applicable for the isolated injury. An example of a surgical tactic for a segmental tibial fracture is given in Figure 23.9. This not only helps the surgeon,

Summary box 23.9 Planning an individual operation ■ ■ ■

Plan procedures before performing them Commit a plan to paper Share the surgical plan by use of a whiteboard

(a) Diagnosis Open segmental fracture left tibia Procedure – Excise wound with plastics – Plan soft tissue cover – Secure nail entry point – Ream segment through traumatic wound – Statically lock nail – Dress wound with a bead pouch – Continue antibiotics until definitive softtissue cover

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(b)

(c)

Equipment

Problems/solutions

– – – –

– Segment viable but too narrow to nail/proceed to bridge plate or ex. fix depending on soft tissue – Segment non-viable/remove segment place temp ex. fix with view to subsequent IlIizarov transport – On passing nail malalignment of proximal fragment/remove nail and place blocking screw

Radiolucent table Tourniquet (during wound excision) Soft tissue tray Washout tray 9 litres washout – Reamers – Cannulated tibial IM nail In reserve external fixator/long plates

(e)

(d) Blocking screw

Figure 23.9 (a) Theatre whiteboard with surgical tactic and (b) radiograph for a complex grade IIIb open segmental tibial fracture. One of the foreseen problems has occurred as the proximal fragment is malreduced (c). The nail was removed and an anteroposterior blocking screw was placed (highlighted) (d and e). The fracture is then well reduced.

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Conclusion

When assessing the ‘mechanism + patient = injury’ relationship, it is easy for the doctor to focus on managing the injury; however, the mechanism of injury can also be addressed, that is we should aim to prevent rather than just treat injury. When a mechanism of injury becomes particularly prevalent or has serious consequences, it is prudent to take steps to either remove the mechanism or reduce the consequences. Accidents occur in a variety of places: the home, the workplace and the roads are the most common. The strategy and motivation for prevention varies from place to place. Within the workplace there is legislation to protect employees and a tendency for an injured employee to sue the employer. Thus, although some work environments are naturally dangerous, many advances in safety have been made. Within the home, legislation has little effect on behaviour. The safety of the structure of a home may be influenced by building regulations, but the thrust is on education of the individual. It is difficult to educate adults to behave more safely and so accidents in the home remain very common. Road safety is a contentious issue. The safe management of the kinetic energy of travel would seem to be a straightforward physical problem. Great advances have been made in the technology of motor vehicles to protect drivers. Restricting speed, separating vehicles travelling in different directions and segregating motor vehicles from vulnerable road users, such as pedestrians, are not popular measures (Summary box 23.10). Summary box 23.10 Response to the mechanism of injury ■ ■ ■

The saying that ‘prevention is better than cure’ is true Legislation and education are required Prevent further abuse by responding to the initial clues

The response to patient factors Another approach to injury prevention is to alter the patient. This particularly applies to the epidemic of injuries in the elderly. Falls are the most common mechanism of injury, so one can try to address the cause or the effects of falls. Fall prevention clinics are now common. The at-risk patients are assessed and remediable causes of falls are addressed. Postural hypotension, transient ischaemic attacks and arrhythmias can be identified and treated. Elderly people will continue to fall, so we can try to minimise the effect of the fall. Schemes, such as using hip protector pads to cushion a fall, have been tried with limited success. The area most likely to expand and give results is that of strengthening the skeleton. Identifying those at risk of osteoporosis, screening them and then treating appropriately offers a hope of reducing the incidence of low energy fractures. There was initial scepticism about the expense of such treatments and the potentially huge number of people who would require them. It is now accepted that treatment targeted appropriately will be costeffective by reducing later fractures with the consequent costs of hospitalisation, morbidity and mortality. Another of the patient factors discussed earlier is when

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injury occurs in pathological tissues, the common example being a fracture of a bone with a neoplastic deposit. This should influence management in one of two ways. When there is a doubt as to whether the tumour is a primary or secondary, it is important to think before treatment. Injudicious operative management of a fracture associated with a primary deposit may prejudice proper tumour management; when the situation allows, a proper opinion should be obtained. When dealing with obvious secondary deposits, the situation is quite different. Aggressive surgical management is often justified to allow an early return to function. A patient with a limited life expectancy should not spend long periods of time rehabilitating (Summary box 23.11). Summary box 23.11 Response to patient factors ■ ■ ■

Pre-empt injury with the use of fall prevention clinics Carry out targeted osteoporosis treatment Do not treat thoughtlessly an injury that is possibly secondary to a primary neoplasm

CONCLUSION Trauma is usually the adverse consequence of a mechanical force on a patient. The prime importance of time in trauma care needs to be appreciated. At time zero, there is a relationship between the mechanism, the patient and the injury. The components of this relationship should fit together in a rational manner. When this rational fit is not apparent, great care should be taken to look for hidden injuries, pre-existing pathology or some deliberate deception in the given history. There is a timeline that progresses from the moment of injury. Prompt understanding of the problems is key in allowing an early reaction. It may not be possible to wait for overt clinical signs and so diagnoses should be positively sought and in some circ*mstances patients screened. There is a minimum response time to initiate and complete the interventions to deal with the problems. Preparation can reduce this response time. Knowledge of realistic response times is important, because only then does the clinician know the real urgency of initiating action. When presented with an injured patient, the early management is largely protocol driven. As more details become known and the patient moves towards definitive care, a more individual plan is made. This plan coordinates the different specialties and should be flexible to allow for evolving pathology. Someone should be responsible for the patient. Trauma does not just consist of care of the young injured. Increasingly, the injured patient will be elderly. The team involved needs to reflect the needs of these elderly patients. Trauma need not only be addressed by tackling the injury itself. Preventative measures should be employed when particular mechanisms can be identified as being common or important causes of injury. For example, prophylactic measures may reduce the propensity for individuals to fall or reduce the consequences of those falls when they occur. The following chapters in this section will look further at these principles as applied to specific regions or surgical disciplines (Summary box 23.12).

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The response to the mechanism of injury (injury prevention)

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INTRODUCTION TO TRAUMA Summary box 23.12 Conclusion ■ ■

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■

The management of trauma is dependent upon time Multiple specialties may be involved, but do not lose sight of the overall problem Planning increases the chances of success

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CHAPTER

Early assessment and management of trauma LEARNING OBJECTIVES

EPIDEMIOLOGY Trauma is the most common cause of death between the ages of one and 44 years worldwide. By 2020, it is estimated that more than 10 per cent of people will die from trauma. In addition to mortality, injuries have the potential to cause many other longterm health problems, with serious consequences for individuals, families, communities and health-care systems. Subsequently, this represents a significant drain on resources. The economic impact of trauma and injury is huge globally, with some figures quoted in the region of $500 billion annually.

INTRODUCTION Much effort has gone into trying to improve trauma care, with the most recent in the UK being the introduction of specialist regional ‘level one’ trauma centres, where all the required facilities and subspecialties are available on site to deal with multiplyinjured patients. It is the initial assessment that is probably the most important factor in the subsequent outcome of the trauma patient, as it is at this stage that a subsequent care pathway and protocol is formed for definitive treatment. The Advanced Trauma Life Support (ATLS) principles were introduced into practice in the late 1970s, and have since revolutionised the management of trauma (Summary box 24.1). Once the attending clinician is versed in the structure and protocol of the ATLS philosophy, it becomes very easy to apply this to any trauma event, regardless of the nature and severity of the injuries.

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• Techniques for the initial resuscitative and definitive care aspects of trauma To be able to perform: • The necessary protocols to allow early stabilization of the patient leading on to definitive care To recognize: • Patients whose management should differ from the normal

Summary box 24.1 The steps in the Advanced Trauma Life Support (ATLS) philosophy ■ ■ ■

Primary survey with simultaneous resuscitation: identify and treat what is killing the patient Secondary survey: proceed to identify all other injuries Definitive care: develop a definitive management plan

MECHANISMS OF TRAUMA Trauma can be classified in type by causation and by effect (see Table 24.1). Table 24.1 Types of injury.

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To identify: • The sequence of priorities in the early assessment of the injured patient To learn: • The principle of triage in immediate management of the injured patient • The concepts of injury recognition prediction based on the mechanism and energy of injury To apply: • The principles of primary and secondary surveys in the assessment and management of trauma

Blunt, e.g. car bonnet Penetrating, e.g. knife Blast, e.g. bomb Crush, e.g. building collapse Thermal

Blunt trauma The most common cause of blunt trauma is the motor vehicle accident (MVA). Speed is a critical factor: a 10 per cent increase in impact speed translates to a 40 per cent rise in the case fatality. Ejection from a vehicle is associated with a significantly greater incidence of severe injury. The use of seatbelts reduces the risk of

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death or serious injury for front-seat occupants by approximately 45 per cent (Figure 24.1). Although seatbelts reduce mortality overall, they can cause a specific pattern of internal injuries. Patients with seatbelt marks have been found to have a four-fold increase in thoracic trauma and an eight-fold increase in intraabdominal trauma compared with those without seatbelt marks (Figure 24.2 and Summary box 24.2). Summary box 24.2 Energy and injury prevention ■ ■

A 10 per cent increase in speed of impact increases pedestrian fatality risk by 40 per cent Seatbelts reduce the risk of injury in a vehicle by 45 per cent

In direct frontal MVAs, airbags provide a reduced risk of fatality of approximately 30 per cent. However, airbags themselves may also cause specific patterns of injury. In order to reduce the risk of airbag-induced injury, children younger than 12 years should be properly restrained in the back seat. Infants (aged 1.5 L of blood), this may lead to severe respiratory compromise, cardiac tamponade and compression of the affected lung. Inserting a chest drain to drain the blood without any accompanying effort to control the haemorrhage may lead to a rapid and terminal deterioration in the patient’s condition (Summary box 24.5). Summary box 24.5 Breathing ■ ■ ■ ■ ■

Give 100 per cent oxygen at high flow Inspect/percuss and auscultate chest Check for tension pneumothorax and immediately decompress if suspected Insert chest drain for haemothorax/pneumothorax Major vessel bleeding within the chest needs to be controlled

Circulation and control of bleeding

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Assessment here centres on three critical clinical observations: 1 Conscious level. If this is impaired or altered, in the absence of obvious head injury, one must assume that the patient has lost a significant amount of blood and that cerebral perfusion has become compromised. 2 Skin colour. A patient with pink skin and warm peripheries is rarely critically hypovolaemic, and the converse is true for a pale, ashen, grey-looking patient with ominous signs of hypovolaemia. 3 Pulse. A full, slow, regular peripheral pulse is usually the sign of relative normovolaemia, whereas a rapid, thready pulse or, worse still, one that is not peripherally palpable is a grave sign of hypovolaemic shock, and blood volume must be rapidly restored. While the primary survey is being carried out, other team members should be securing two large-bore cannulae for intravenous access. Fluid resuscitation should be titrated against the patient’s response to the initial fluid challenge and their vital signs. Potential sites for major blood loss include the chest cavity, the abdomen, the pelvis and long bone fractures. Each of these must

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be examined in turn. Surgical intervention may ultimately be required to control haemorrhage (Summary box 24.6). Summary box 24.6 Circulation ■ ■ ■

Check pulse and blood pressure Secure two large-bore cannulae, take bloods and commence fluid resuscitation Examine for evidence of blood loss and treat accordingly

Disability The neurological status of the patient should be rapidly assessed. The pupils are monitored for size and reactivity, and a GCS measured. This should be repeated regularly as the test is quick to perform and once again it is change in the score which is more important in determining how treatment is going than one isolated measurement. Other than severe head injury, other reversible causes of an altered level of consciousness include hypovolaemia, hypoglycaemia, alcohol and drug abuse. These must all be excluded or treated during the initial assessment.

Exposure The patient must be fully exposed and examined front and back using a carefully controlled log roll. Spinal alignment must be maintained during this procedure with in-line traction. Hypothermia can be rapid following trauma, and warming air blankets are vitally important in the resuscitative phase.

Adjuncts to the primary survey At the same time as intravenous access is secured, blood should taken for haematological and biochemical analysis. A ‘group and save’ and cross-match should also be requested. Additional monitoring should be attached to the patient, including a blood pressure cuff, 12-lead electrocardiography (ECG) monitoring and pulse oximetry. Arterial blood gas sampling gives a very quick idea of oxygenation, ventilation, and electrolyte imbalance. Additional adjuncts include a nasogastric tube, urinary catheter and a ‘trauma series’ of radiographs. Other, more specialised forms of imaging, such as ultrasound, computed tomography (CT) and angiography, should be considered once the patient’s condition is seen to be stable after the initial assessment and resuscitation (Summary box 24.7). Summary box 24.7 Adjuncts to the primary survey ■ ■ ■ ■ ■

Blood tests – full blood count, urea and electrolytes, clotting screen, glucose, toxicology, cross-match ECG, pulse oximetry, arterial blood gas (ABG) Two wide-bore cannulae for intravenous fluids Urinary and gastric catheters Radiographs of the cervical spine, chest and pelvis

SECONDARY SURVEY The secondary survey does not begin until after the primary survey has been completed, and all potentially life-threatening

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Special subgroup considerations

Summary box 24.8 Review of patient’s history (AMPLE) ■ ■ ■ ■ ■

Allergy Medication, including tetanus status Past medical history Last meal Events of the incident

Secondary survey physical examination Examine each region of the body for signs of injury, bony instability and tenderness to palpation.

• Head and face. Evaluate the head for penetrating injuries and

•

• •

•

depressed fractures, and any evidence of bleeding or discharge from the ears suggestive of a basal skull fracture (Chapter 25). Check the face for maxillofacial fractures and ocular injury. Inspect the mouth, mandible, zygoma, nose and ears. Exclude midfacial injury and potential airway compromise (Chapter 27). Neck. Inspect and palpate the cervical spine anteriorly and posteriorly for haematomas, crepitus, tenderness and evidence of steps on palpation. The spine is held immobilised until formally cleared clinically and radiographically (Chapter 26). Chest. Review the primary survey and perform full palpation and auscultation of the chest wall. Palpate the entire chest wall including the clavicle, sternum and ribs. Neurological. Examine the GCS regularly. Perform a full neurological examination if the patient’s condition allows. Any evidence of sensory and motor disturbance requires full spinal immobilisation and urgent review by the neurosurgeons or spinal orthopaedic surgeons with imaging as appropriate. Abdomen and pelvis. Inspect for distension, bruising or penetrating wounds. Inspect and palpate for tenderness and signs of peritonism. Palpate the iliac crests for pain which might indicate pelvic instability, resulting from ring fractures. Inspect the perineum for evidence of ecchymosis or bleeding. A rectal examination is needed to assess tone, prostate level and to look for bleeding (Chapter 28). Extremities. It is often here that attention is diverted immediately when a dramatic injury to the limbs presents itself (Figure 24.3). It is important to note that, unless there is severe haemorrhage, the injury to the limb is not immediately life threatening and focus must be maintained on the primary survey and ‘ABCDE’ sequence. Obviously, deformed limbs should be manipulated into as near anatomical alignment as possible, remembering to document the distal neurovascular status before and after the intervention.

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• Log roll. Once the patient has been evaluated anteriorly,

a log roll should be performed to inspect the back. One member of the team is responsible for maintaining in-line spinal stabilisation (usually the anaesthetist when the patient is intubated.) Three other trained staff hold the patient steady through the turn. Inspect and palpate the entire spine from occiput to sacrum, looking and feeling for tenderness and bony abnormalities. Identify any penetrating injuries or exit wounds from gunshot injuries and cover these once they have been photographed. Percuss, palpate and auscultate the posterior chest wall.

Re-evaluation This cannot be stressed enough. It is an integral process in the initial assessment of major trauma and should not stop once the patient leaves the emergency room. Continuous monitoring is invaluable here, especially of the vital signs and urinary output. It is also very important to stress that, should the patient’s condition change at any time during the initial assessment, then the primary survey must be repeated from the beginning, since additional life-threatening injuries may be declaring themselves.

Definitive care and transfer Definitive care will be discussed in subsequent chapters, but it is important to recognise that there should be as little delay as possible in reaching this stage where initial resuscitation and assessment has been completed. It has increasingly been recognised that early transfer to an appropriate care facility is the most important contributor to successful outcome. When it becomes mandatory to transfer the patient from the initial receiving hospital, the patient must be haemodynamically and cardiovascularly stable. An experienced anaesthetist should accompany the patient, the airway should be secured as necessary. Life-saving surgery may need to be performed prior to transfer for other injuries. This is called ‘damage control surgery’ (Chapter 32).

SPECIAL SUBGROUP CONSIDERATIONS The initial management of any traumatised individual initially follows the same methodical ‘ABCDE’ pathway. However, there are three very important subgroups which require special consideration: the paediatric, the elderly and the pregnant. Each will be considered separately, highlighting the differences in initial assessment and management.

Paediatric trauma Injury is the leading cause of mortality among children and adolescents. Children have a smaller body mass and, therefore, there may be a greater force applied per unit surface area for a given injury. The energy is transmitted to a body with less fat, less connective tissue and an immature skeleton; therefore, injuries to more than one organ are more frequent. As the surface area to body volume ratio of children is high, thermal energy loss is higher and hypothermia is a higher risk.

Airway and cervical spine control

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injuries have been dealt with. In the case of a severely injured patient, for example, the secondary survey may not commence until the patient has returned from the operating theatre, having had life-saving surgery for primary survey ‘ABCDE’ problems. The purpose of the secondary survey is to identify all other injuries and perform a more thorough ‘head to toe’ examination. If possible, it is here that the patient’s history is reviewed. The ‘AMPLE’ mnemonic from the ATLS group is helpful here (Summary box 24.8).

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As with any traumatised patient, control of the airway is the first priority. Anatomically, children differ from adults in that they have a smaller and more anteriorly positioned and funnelshaped larynx, floppy epiglottis, short trachea and large tongue. Nasotracheal intubation in children younger than nine years

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(c)

(d)

(b)

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Figure 24.3 (a–d) Severe degloving injuries to the upper and lower limbs following a high-speed road traffic accident. The initial appearance and severity of the injury should not detract from following the important Advanced Trauma Life Support (ATLS) sequence in evaluating and treating immediate life-threatening injuries.

should not be performed because of the possibility of damage to the cranial vault and to the fragile soft tissues causing bleeding. With respect to a definitive airway, cuffed tubes are rarely indicated for children less than nine years of age because of the delicate structures within the airway and the fact that the cricoid ring provides an adequate seal. It should also be remembered that in children, the trachea is relatively short, and care should be taken not to intubate the right main bronchus.

common cause of cardiorespiratory arrest; however, before this, hypoventilation causes a respiratory acidosis, which is the most common acid–base disturbance in the injured child. Correction must be through adequate and controlled ventilation. Flail chest and aortic rupture are uncommon in children due to the elastic nature and resilience of the underlying structures. Pulmonary contusions are not evident in the early chest x-ray, but as before, re-evaluation is necessary for the following 24–48 hours.

Breathing and ventilatory control

Circulation with haemorrhage control

The respiratory rate in the child decreases with age. Infants require 40–60 breaths per minute, whereas the older child has a rate of 20 breaths per minute (Table 24.2). Hypoxia is a

Vital signs vary with age (Table 24.2). Due to the greater physiological capacity and ability of children to compensate for fluid loss, hypotension is a very late and ominous sign of hypovolae-

Table 24.2 Paediatric vital signs.

Normal vital signs by age

Pulse (beats per min)

Systolic blood pressure (mmHg)

Respiratory rate (breaths per min)

Infant (11 kPa MAP = 80–90 mmHg ICP 60 mmHg [Na+] >140 mmol/L [K+] >4 mmol/L

Intermediate measures

On-going management of significant head injury

■ ■

■

The patient should be intubated and ventilated with adequate sedation and pressure monitoring The goal of ongoing management is to minimise secondary brain injury Key parameters include oxygenation and ventilation, blood pressure and ICP, and electrolyte balance. Pyrexia should be actively controlled A hierarchy of management strategies exists to achieve control of intracranial pressure (Figure 25.10)

An alternative strategy for managing uncontrolled intracranial hypertension is induction of thiopentone coma. This carries a high risk of complications and results in the loss of normal EEG activity and pupil responses, compromising ongoing evaluation of the patient. A multicentre randomised control trial with the aim of establishing the relative effectiveness of these interventions, the Randomised Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of Intra-Cranial Pressure (RESCUEICP), is underway (Summary box 25.12).

Pituitary dysfunction: endocrine and metabolic management Electrolyte imbalance is common in TBI, and contributes to brain swelling and to causing seizures. Diverse mechanisms are involved. Cerebral salt wasting, a poorly understood form of excretory dysregulation in association with brain insult, leads to volume depletion and hyponatraemia.The syndrome of inappropriate antidiuretic hormone (SIADH) leads to water retention

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Where initial measures fail adequately to control ICP, sedation may be escalated and supplemented with paralysis. External ventricular CSF drainage represents a useful adjunct to physiological compensation. Mannitol can be administered to control ICP temporarily. This is helpful where there is evidence of herniation, such as development of a dilated unresponsive pupil during transfer. 100 mL of 20 per cent mannitol is a typical bolus. Repeated or excessive use is counterproductive because it is an osmotic diuretic and produces hypovolaemia and hypotension. This will compromise cerebral perfusion. Administration of mannitol necessitates catheterising the patient to monitor fluid balance. Pyrexia increases brain oxygen requirements and cell damage, and so should be avoided. Active induction of therapeutic hypothermia is effective in controlling intracranial pressure, but predisposes to complications including sepsis and coagulopathy so that its overall benefit is not firmly established.

Final measures Decompressive craniectomy (Figure 25.11) involves removal of a portion of the skull vault and opening of the underlying dura, so that brain swelling can occur without the pressure increases predicted by the Monro Kellie doctrine. Generally, a unilateral or bifrontal decompressive craniectomy is performed, with the bone flap placed subcutaneously in the abdomen, then replaced (cranioplasty) weeks or months later.

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Figure 25.11 Decompressive craniectomy. A right-sided decompressive craniectomy has been performed allowing the swollen right hemisphere to herniate through the skull defect. This procedure can help to control raised intracranial pressure. The bone flap can be stored and replaced at a later date.

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and hyponatraemia in the context of pituitary damage. This is of particular concern in head injury since low serum osmotic pressure can contribute to brain swelling, so hypotonic fluids are avoided in this setting. Conversely, antidiuretic hormone (ADH) secretion may be compromised in the context of trauma, producing diabetes insipidus resulting in hypernatraemia. This may be managed with boluses of desmopressin in consultation with endocrine specialists. All aspects of pituitary function may be compromised in the setting of TBI. Routine screening of pituitary hormone levels and liaison with endocrinology is an important aspect of optimal medical management. Note that routine, rather than directed, administration of corticosteroids in severe head injury is associated with increased mortality and is not recommended.

Seizures Seizures may occur early (within 7 days) or late. The cumulative probability is between 2 per cent (mild TBI) and 60 per cent (severe TBI with exacerbating features). Risk factors include injury severity, especially the presence of ICH, and depressed skull fractures and tears of the dura. Antiepileptics, typically phenytoin, are administered prophylactically to patients at high risk of seizures.

Nutrition Enteral nutrition is preferred to intravenous parenteral nutrition on grounds of cost and associated complications, and should be commenced within 72 hours of injury. Prokinetics (e.g. metaclopramide, erythromycin) can be administered to promote absorption (Summary box 25.13).

syndrome is disputed, and it is certainly rare, it should be considered in advice to individuals engaged in sports or activities carrying a risk of further injury: symptomatic players should not return to play. After a very mild concussion, they should not play again that day; after a severe concussion, they should refrain for the rest of that season (see www.headinjury.com/ sports.htm#guidelines). Postconcussive syndrome is a loosely defined constellation of symptoms, persisting for a prolonged period after injury, and exacerbated in some patients by the potential for secondary gain (compensation). Patients may report somatic features, such as headache, dizziness and disorders of hearing and vision. They may also suffer a variety of neurocognitive and neuropsychological disturbances, including difficulty with concentration and recall, insomnia, emotional lability, fatigue, depression and personality change.

Moderate and severe injury The long-term sequelae of significant brain injury are likely to include many of the somatic and neurocognitive problems described above, combined with the effect of deficits attributable directly to the primary and secondary injury sustained. Rehabilitation represents a complex and prolonged challenge, requiring multidisciplinary coordination. The Glasgow Outcome Score is used to quantify the degree of recovery achieved after head injury, especially for research purposes, and is detailed in Table 25.5. Good recovery implies independence and potential to return to work rather than a full return to previous capacity (Summary box 25.14).

Table 25.5 Glasgow Outcome Score (GOS).

Summary box 25.13 Investigations and prophylactic measures in significant head injury ■ ■ ■ ■ ■ ■

Check pituitary function Do not give hypotonic fluids Monitor daily for electrolyte imbalance Antiepileptics can be used prophylactically Steroids should not be given routinely Enteral nutrition should be started within 72 hours

Good recovery Moderate disability Severe disability Persistent vegetative state Dead

5 4 3 2 1

Summary box 25.14 Outcomes of a head injury

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Outcomes and sequelae Mild injury: concussion, second impact syndrome and postconcussive syndrome Concussion is defined as alteration of consciousness as a result of closed head injury, but is generally used in describing mild head injury without imaging abnormalities: loss of consciousness at the time of injury is not a prerequisite. Key features include confusion and amnesia. The patient may be easily distractable, forgetful, slow to interact or emotionally labile. Gait disturbance and incoordination may be seen. It is claimed that while symptomatic following a head injury, patients may be especially vulnerable to repeat impacts. It is proposed that in the context of disordered cerebral autoregulation, a second minor injury may trigger a form of malignant cerebral oedema refractory to treatment. Although the existence of the

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■ ■ ■

Post-concussion syndrome gives persisting headaches and problems in concentrating Players concussed when playing sport should not return immediately to the field Good recovery is not necessarily a return to normal; it may be independent living

ANEURYSMAL SUBARACHNOID HAEMORRHAGE ‘Spontaneous’ aneurysmal subarachnoid haemorrhage (SAH) is due to the rupture of an aneurysm in about 80 per cent of cases. In addition to saccular aneurysms discussed below, aneurysms may develop due to infective infiltration of arterial walls in the context of bacteraemia (mycotic aneurysm). This may

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Aneur ysmal subarachnoid haemorrhage

occur following intravenous drug use or infective endocarditis. Pseudoaneurysms may also develop after trauma or after surgery.

Epidemiology Berry aneurysms of the circle of Willis develop at branch points in the arterial tree associated with turbulent blood flow (Figure 25.12). Aneurysmal bleeding has an incidence of 10–15 per 100 000 population per year. Risk factors include age, female sex, hypertension, smoking, cocaine abuse and a family history with two first-degree relatives affected. A range of genetic disorders, in particular adult polycystic kidney disease, fibromuscular dysplasia, neurofibromatosis type 1, Ehlers-Danlos and Marfan syndromes, are known to predispose patients to this condition. Anterior cerebral artery 36%

Anterior communicating artery 38%

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and photophobia often develop over hours. Intraocular haemorrhages, classically subhyaloid, may be visible on fundoscopy. The combination of subarachnoid haemorrhage and vitreous haemorrhage is known as Terson syndrome and occurs in 15–20 per cent of patients. Papilloedema should be sought, but may not be evident early in the course of a developing hydrocephalus (Summary box 25.15).

Table 25.6 World Federation of Neurological Surgeons Grading of subarachnoid haemorrhage.

Grade

Glasgow Coma Scale

Focal deficitsa

I II III IV V

15 13–14 13–14 7–12 3–9

– – + ± ±

Focal deficit = dysphasia or limb weakness.

21% Middle cerebral artery

Posterior communicating artery

■ ■ ■ ■

Clinical features Approximately one third of subarachnoid haemorrhages are incorrectly diagnosed at initial presentation. They are then at high risk of succumbing to early complications, especially a rebleed. The typical presentation of a subarachnoid haemorrhage includes a ‘thunderclap’ headache, which is both sudden and severe and is outside the patient’s normal experience. Some patients describe prodromal headaches preceding the event, potentially representing aneurysm growth or subclinical bleeds. The sudden onset occurs commonly but not exclusively during exertion, and may be associated with seizure (10 per cent), unresponsiveness (50 per cent) and vomiting (70 per cent). Sometimes it is difficult to establish whether SAH has caused a fall, or whether a fall with head injury is responsible for the SAH. Neurological examination may be normal (‘good clinical grade’, see Table 25.6), or the patient may have focal deficits and an impaired conscious level (‘poor grade’). The World Federation of Neurosurgical Societies (WFNS) grading of subarachnoid haemorrhage is measured against the condition of the patient after resuscitation rather than at the time of the onset of symptoms (ictus). Often patients are referred to as ‘good grade’ (WFNS 1-3) or ‘poor grade’ (WFNS 4 and 5) patients. A painful third nerve palsy points to compression from a posterior communicating artery aneurysm. Meningitic features of neck stiffness

Most develop from a saccular aneurysm They are most common at junctions of the circle of Willis Presentation is a thunderclap headache often during exertion If neurological examination is normal, the prognosis is good Computed tomography (CT) is the investigation of choice

Investigation CT scan is the imaging of first choice, and, when performed within 12 hours of ictus, will confirm bleeding in more than 98 per cent of cases. This makes a diagnostic lumbar puncture unnecessary (Figure 25.13). The sensitivity of CT scan, however, deteriorates to less than 50 per cent at 1 week after a bleed. In light of this, patients with a suggestive history and negative CT scan will require lumbar

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Vertebral artery

Figure 25.12 Main sites of intracranial supraclinoid aneurysms.

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Subarachnoid haemorrhage ■

Basilar artery Posterior cerebral artery

Summary box 25.15

Figure 25.13 Diffuse subarachnoid bleeding from a ruptured anterior communicating artery aneurysm extends to the prepontine and ambient cisterns around the brainstem, and into both Sylvian fissures.

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puncture, especially where presentation is delayed. The CSF supernatant should be analysed by spectrophotometry (visual inspection is not reliable) for the spectra of haemoglobin breakdown products oxyhaemoglobin and bilirubin. These are clearly detectable in samples taken at least 6 and preferably 12 hours after subarachnoid haemorrhage, but not in CSF mixed with fresh blood due to traumatic puncture and analysed immediately. Failure to exclude subarachnoid haemorrhage with an appropriate delayed lumbar puncture may necessitate formal cerebral angiography, and the risks this entails. Catheter angiography generally involves access to both vertebral and carotid arteries through the femoral artery under local anaesthetic. This allows visualisation of the vascular anatomy by injection of contrast medium with simultaneous x-ray screening (Figures 25.14 and 25.15). The serious potential risks include ischaemic stroke or arterial dissection (1–2 per cent), and renal failure or allergic reactions attributable to contrast.

(a)

(b)

Figure 25.14 There is a small saccular aneurysm of the pericallosal branch of the anterior cerebral artery.

Figure 25.15 (a) A giant aneurysm of the internal carotid; (b) angiographic embolisation (coiling) of the giant aneurysm. Note the single displaced coil passing into the distal ICA (internal carotid artery) and then the MCA (middle cerebral artery).

Management

Prevention of rebleed

Patients should be placed on bed rest with hourly neurological observations. They require strict input–output monitoring and intravenous fluid replacement with normal saline initially. Oral nimodipine at a dose of 60 mg every 4 hours has been shown to reduce the rate of poor outcome associated with delayed neurological ischaemic deficit due to cerebral vasospasm. Analgesics, laxatives, antiemetics, gastric protection and compression stockings are also likely to be necessary. After resuscitation, the priorities in subarachnoid haemorrhage are:

• to prevent rebleeding by identifying and controlling any underlying lesion;

• to recognise and manage: • neurological complications, especially vasospasm (or delayed ischaemic neurologic deficit) and hydrocephalus;

• systemic complications, including electrolyte imbalance, severe hypertension, cardiac infarct and arrhythmia, and neurogenic pulmonary oedema.

These goals are best served by early transfer of the patient to a neurosurgical centre. In elderly patients with a poor WFNS grade, a decision to offer only supportive management may be appropriate.

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CT angiography (CTA) has a high sensitivity for aneurysms and arteriovenous malformations (AVMs), but digital subtraction angiography (DSA) remains the gold standard. Aneurysms demonstrated may be removed from the circulation surgically by craniotomy and ‘clipping’, or by endovascular embolization, also known as ‘coiling’. Sometimes, mesh stents may also be used to help secure the metal coils within the aneurysm sac as part of this procedure. Class 1 evidence suggesting a lower risk of poor outcomes, at least for small anterior circulation aneurysms, has driven the uptake of coiling. However, a surgical approach remains necessary or preferable in many cases. A rebleed risk of 4 per cent in the first 24 hours, then 1.5 per cent per day thereafter is quoted for aneurysms, and 80 per cent of patients who rebleed have an eventual poor outcome. For this reason, and to permit optimal management of complications discussed later, the current consensus favours early intervention, despite the surgical challenges presented by brain swelling and blood load (Summary box 25.16).

Identification and management of complications After subarachnoid haemorrhage, even initially good grade patients may deteriorate rapidly due to reversible neurological

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Other spontaneous intracranial haemorrhage Summary box 25.16

Summary box 25.17

Treatment of subarachnoid haemorrhage

Complications of subarachnoid haemorrhage

■

Early securing of the responsible aneurysm reduces the risk of rebleed and is necessary for management of later vasospasm Endovascular treatment (‘coiling’) is generally preferred over craniotomy and clipping for aneurysms amenable to this approach ‘Good grade’ patients commonly suffer poor outcomes, primarily as a result of cerebral vasospasm

■ ■ ■

■

or systemic complications. They should be managed in a neurosurgical unit, and will require careful neurological observation, on a high dependency unit where possible. The approach to a patient who has deteriorated should follow standard principles of resuscitation, with consideration paid to the high incidence of electrolyte imbalance, cardiac infarcts and arrhythmias, and neurogenic pulmonary oedema in this group. Neurological deterioration should prompt a repeat scan to exclude evidence of rebleeding and of hydrocephalus. This is typically the communicating type, which is a common sequel of haemorrhage. Where these complications are not demonstrated, deterioration is often attributable to delayed ischaemic neurological deficit (DNID), which commonly develops 3–10 days after aneurysmal haemorrhage and can progress rapidly to infarction. The process is attributed to cerebral vasospasm in response to, and correlating with, the blood load. This process can be visualised angiographically, and the velocity of blood flow in the cerebral vasculature, measured using transcranial Doppler ultrasound (TCDs), provides an indirect assessment of the degree of stenosis. Outcomes are optimised by the prophylactic administration of nimodipine and maintenance of fluid volume, typically with 2.5–3 L/day of normal saline. In established vasospasm, the goal is to maintain cerebral perfusion. Practically this involves maintaining mean arterial pressure with aggressive fluid replacement and inotropes. This is done by the administration of fluid and inotropes. This strategy would risk rerupturing an unsecured underlying aneurysm, a factor weighing in favour of early clipping or coiling. Hyponatraemia is a frequent complication of subarachnoid haemorrhage, attributed to cerebral salt wasting in the context of fluid depletion, and otherwise to the syndrome of inappropriate antidiuretic hormone secretion. This is associated with a higher incidence of DNID, and practical management, irrespective of the underlying pathology, is based on sodium replacement, with hypertonic infusions if necessary. Fluid restriction is not appropriate in these patients since this risks further compromising perfusion (Summary box 25.17).

Prognosis Overall survival of subarachnoid haemorrhage is about 50 per cent and one third of survivors remain dependent. Only 50 per cent of WFNS grade 1 patients return to work. Treated aneurysms can regrow and rebleed, especially after coiling, so that a program of surveillance is necessary. A distinct subgroup of SAH patients suffer bleeds confined to the basal cisterns anterior to the midbrain and pons, without an underlying lesion evident on angiogram. This is termed

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Electrolyte imbalance, cardiac arrhythmias and neurogenic pulmonary oedema are common Neurological deterioration may indicate a communicating hydrocephalus Delayed ischaemic neurological deficit (DNID) is attributed to vasospasm of the cerebral vasculature typically developing 3–10 days post ictus. It is the main cause of poor outcome in good grade subarachnoid patients After securing the aneurysm, perfusion can be maintained in the context of vasospasm by artificial elevation of the arterial blood pressure

‘perimesencephalic SAH’, and is believed to represent venous bleeding. It has an excellent prognosis. Unruptured aneurysms represent a thorny management problem: incidentally detected small anterior circulation aneurysms represent a minimal bleeding risk. Screening, even in high risk groups, is therefore of questionable benefit.

OTHER SPONTANEOUS INTRACRANIAL HAEMORRHAGE Intracerebral haemorrhage Intracerebral haemorrhage may be spontaneous or traumatic. The former accounts for a 10–15 per cent of strokes and has a mortality of 40 per cent at one year. The majority occur in the context of hypertension or amyloid angiopathy, or as a complication of ischaemic stroke. Coagulation disorders, especially patients being treated with warfarin, are a major risk factor (Summary box 25.18). Summary box 25.18 Intracerebral haemorrhage ■ ■

■ ■ ■ ■

These account for 10–15 per cent of strokes The presentation, as for ischaemic stroke, may include focal neurological deficit with or without decreased conscious level High blood pressure may be chronic so should only be reduced with care Diagnosis is by computed tomography Anticoagulants should be reversed at once Craniotomy and evacuation is especially useful in young patients

Patients typically present with sudden focal deficit and reduced conscious level. Following initial resuscitation, these patients will require CT scan to establish the diagnosis, and the size and position of the bleed (Figure 25.16). They require reversal of anticoagulation, on-going hourly neurological observations and blood pressure monitoring. High blood pressure may be longstanding and associated with adaptations to autoregulation, so attempts at lowering it acutely with intravenous antihypertensives should be made only if the values are very high (e.g. MAP >130 mmHg).

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EMERGENCY NEUROSURGERY

Craniotomy and evacuation is used to alleviate raised intracranial pressure, just as it can be in a subgroup of patients with ischaemic strokes in the posterior fossa or in the middle cerebral artery territory. Surgery has no role in addressing focal deficits corresponding to direct damage from the bleed itself. Young patients with haematomas close to the cortical surface, demonstrating progressive neurological deterioration, represent good surgical candidates. Posterior fossa clot is also a strong indication for surgery because of the potential for rapid deterioration due to brainstem compression and hydrocephalus. A substantial minority of intracerebral bleeds are attributable to focal vascular lesions, and this must be considered when planning any surgery.

Vascular malformations Vascular malformations are usually congenital in origin, with certain key exceptions discussed below. They may present with headaches, pulsatile tinnitus, seizures or focal deficit, or else acutely with rupture and haemorrhage.

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Figure 25.16 Large acute intracerebral haemorrhages in the right frontal and parietal lobes are evident, with surrounding oedema and midline shift.

Arteriovenous malformations are responsible for about 10 per cent of subarachnoid haemorrhages. Vessels and calcification may be apparent on CT or magnetic resonance imaging (MRI), and the lesion is confirmed on angiography (Figure 25.17). When AVMs present with bleeding, there is an approximate 4 per cent risk of rebleed per annum. The risk is particularly high in the first 6 weeks, and where the bleed is from an aneurysm related to the AVM. This fact often weighs against treatment by radiosurgery, which typically takes more than one year to achieve complete occlusion, but may nevertheless be applied to some small, deep AVMs. Endovascular embolisation, with tissue glue, is often a useful first-line therapy, but carries significant risks and rarely achieves complete and permanent obliteration. Most patients will therefore ultimately require craniotomy, taking into account the risks of deficit associated with operation. These may be predicted using the Spetzler–Martin grading system, which is based on the size of the lesion, the eloquence of adjacent brain, and the pattern of venous drainage. Vein of Galen malformations are AVMs feeding into an embryological venous remnant dorsal to the brainstem presenting in childhood. High-flow malformations may cause cardiac failure. They may be treated by embolisation. Dural arteriovenous fistulae (DAVFs) are shunts between dural arteries and veins or sinuses. They are proposed to arise as a result of vessel remodelling in response to dural sinus thrombosis and subsequent recanalisation. They may present with subarachnoid, intracerebral or subdural bleeding, or with headache and pulsatile tinnitus. A carotid cavernous fistula is a spontaneous or traumatic DAVF between the internal carotid artery and surrounding cavernous sinus, typically producing eye pain, ocular muscle palsies and exophthalmos. Angiography is diagnostic. Cavernomas (Figure 25.18) are venous anomalies, demonstrated on MRI, but not with angiography, which may require operation if they cause progressive deficits, intractable epilepsy or recurrent bleeding.

Figure 25.17 An arteriovenous malformation supplied by the anterior cerebral, middle cerebral and middle meningeal arteries is demonstrated at the 4 o’clock position in this angiogram.

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Figure 25.18 A brainstem cavernoma.

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Acknowledgements

Related lesions, usually clinically silent, include developmental venous anomalies (DVAs) and capillary telangectasia.

SUMMARY

ACKNOWLEDGEMENTS The authors are indebted to John Leach, Consultant Neurosurgeon, Salford Hospital, Manchester, for his contributions to the structure and content of this chapter. No head injury is too slight to neglect, or too severe to be despaired of Hippocrates

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The guiding principle of management for neurosurgical emergencies is the prevention of secondary injury by ensuring satisfactory brain perfusion. This demands immediate attention to blood pressure and oxygenation, as reflected in the ATLS resuscitation algorithms, as well as intracranial pressure management. Early imaging to identify treatable pathology and timely discussion with the local Neurosurgery Centre are key to outcome.

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CHAPTER

Neck and spine LEARNING OBJECTIVES

To be familiar with: • The accurate assessment of spinal trauma • The pathophysiology and types of spinal cord injury • The basic management of spinal trauma and the major pitfalls

• The prognosis of spinal cord injury, factors affecting functional outcome, and common associated complications

EPIDEMIOLOGY OF SPINAL CORD INJURY

Vertebral body

The incidence of spinal cord injury ranges between 27 and 47 cases per million per year. Road traffic accidents remain the leading cause of spinal cord injuries worldwide. Males in the third decade of life are the most likely group to sustain serious spinal cord injury.

Facet joints

Pedicle

EVOLUTION OF THE MANAGEMENT OF SPINAL CORD INJURY There is clear evidence to show that fewer complications, decreased length of stay, and improved patient outcome occur in patients treated in specialised spinal centres (Summary box 26.1).

Figure 26.1 The spinal motion segment.

Summary box 26.1

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Spinal cord injury ■ ■

Incidence of spinal cord injury remains constant Outcome is improved in regional/national spinal cord injury centres

1 5 3

ANATOMY OF THE SPINE AND SPINAL CORD

Spinal column anatomy The vertebral column is composed of a series of motion segments (Figure 26.1). A motion segment consists of two adjacent vertebrae, their intervertebral disc and ligamentous restraints (Figure 26.2).

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Figure 26.2 Ligamentous spinal restraints. (1) Anterior longitudinal ligament, (2) intervertebral disc and posterior longitudinal ligament, (3) facet joint capsule, (4) interspinous ligament, (5) supraspinous ligament.

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Anatomy of the spine and spinal cord

327

Regional variations Upper cervical spine anatomy is designed to facilitate motion (Figure 26.3), and stability here is dependent on ligamentous restraints (Figure 26.4). Vertebral anatomy from C3 to C7 is similar. The cervicothoracic junction is a transitional zone from mobile to fixed and is thus prone to injury. It may be difficult to visualise this area on x-ray (Figure 26.5). The thoracolumbar junction is also prone to injury and is the most common area of injury outside the cervical spine (Figure 26.6). Atlas (inferior view) Posterior tubercle

Axis (posterosuperior view) Dens

Posterior arch

Superior articular facet

Posterior articular facet

Figure 26.5 Cervicothoracic facet subluxation (easily missed with inadequate x-rays).

Inferior articular Anterior facet arch

Anterior tubercle

Spinous process

Figure 26.3 Atlantoaxial bony anatomy.

Ascending band Cruciate ligament

Transverse band

Posterior longitudinal ligament

The three column concept of spinal stability The spinal column can be divided into three columns: anterior, middle and posterior (Figure 26.7). When all three columns are injured the spine is unstable. Instability may also exist in some two-column injuries (Summary box 26.2).

Figure 26.6 Coronal T2-weighted magnetic resonance image demonstrating a fracture dislocation at the thoracolumbar junction.

Spinal neuroanatomy Summary box 26.2 Spinal column anatomy ■ ■

Upper cervical spine stability is dependent on ligamentous restraints The cervicothoracic and thoracolumbar junctions are prone to injury

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The spinal cord extends from the foramen magnum to the T12/ L1 junction where it ends as the conus medullaris (Figure 26.8). Below this level lies the cauda equina. Figure 26.9 illustrates a cross-section of the spinal cord. The lateral spinothalamic tracts transmit the sensation of pain and temperature, the lateral corticospinal tracts are responsible for motor function, and the posterior columns transmit, position, vibration and deep pressure sensation.

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Figure 26.4 Atlantoaxial ligaments.

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NECK AND SPINE Anterior

Middle

Posterior

Figure 26.7 The three-column model of spinal stability.

cally arranged; proximal body function is represented centrally with distal body function arranged peripherally.

Cord

Pathophysiology of spinal cord injury Conus medullaris

The primary injury This is the direct insult to the neural elements and occurs at the time of the initial injury.

Cauda equina

The secondary injury Haemorrhage, oedema and ischaemia results in a biochemical cascade that causes the secondary injury. This may be accentuated by hypotension, hypoxia, spinal instability and/or persistent compression of the neural elements. Management of a spinal cord injury must focus on minimising secondary injury (Summary box 26.3). Summary box 26.3 Pathophysiology of spinal cord injury

Figure 26.8 The spinal cord ends at T12/L1 at the conus medullaris which gives rise to the cauda equina.

Dorsal column Lateral column

T C

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C Ventral column

Ventral fissure

T L

Lateral corticospinal tract Lateral spinothalamic tract

Anterior spinothalamic tract

Figure 26.9 A cross-section of the spinal cord.

The spinothalamic tracts cross to the opposite side of the spinal cord within three levels of entering the cord. In contrast, the corticospinal tracts and the posterior columns decussate proximally at the craniocervical level. The tracts are topographi-

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■ ■

Fasciculus Dorsal gracilis Fasciculus sulcus cuneatus S

■

The spinal cord contains various tracts that are topographically arranged Spinal cord injury involves both primary and secondary phases Therapeutic strategies are directed at reducing the secondary injury

PATIENT ASSESSMENT Basic points Advanced Trauma Life Support (ATLS) principles apply in all cases (Chapter 23). The spine should initially be immobilised on the assumption that every trauma patient has a spinal injury until proven otherwise (Figure 26.10). The finding of a spinal injury makes it more likely (not less) that there will be a second injury at another level. Spinal boards lead to skin breakdown in insensate patients, and are very uncomfortable for those with normal sensation. Therefore, they are for very short-term use only (Figure 26.11).

The unconscious patient Definitive clearance of the spine may not be possible in the initial stages and spinal immobilisation should then be maintained, until magnetic resonance imaging (MRI) or equivalent can be used to rule out an unstable spinal injury (Summary box 26.4).

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Physical examination

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PHYSICAL EXAMINATION Initial assessment The primary survey always takes precedence, followed by careful systems examination, paying particular attention to the abdomen and chest. Spinal cord injury may mask signs of intraabdominal injury.

Identification of shock Three categories of shock may occur in spinal trauma:

Figure 26.10 Spinal immobilisation.

1 Hypovolaemic shock. Hypotension with tachycardia and cold clammy peripheries. This is most often due to haemorrhage. It should be treated with appropriate resuscitation. 2 Neurogenic shock. This presents with hypotension, a normal heart rate or bradycardia and warm peripheries. This is due to unopposed vagal tone resulting from cervical spinal cord injury above the level of sympathetic outflow (C7/T1). It should be treated with inotropic support, and care should be taken to avoid fluid overload. 3 Spinal shock. There is initial loss of all neurological function below the level of the injury. It is characterised by paralysis, hypotonia and areflexia. It usually lasts 24 hours following spinal cord injury. Once it has resolved the bulbocavernosus reflex (Figure 26.12) returns.

Spinal examination The entire spine must be palpated and the overlying skin inspected. A formal spinal log roll must be performed to achieve this (Figure 26.13). Significant swelling, tenderness, palpable steps or gaps suggest a spinal injury. Wounds may be part of penetrating trauma. Seat belt marks on the abdomen and chest must be noted, as these suggest a high energy accident.

Figure 26.11 Pressure sores and ulcers may develop rapidly in insensate patients.

Summary box 26.4

■ ■ ■ ■

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Patient assessment Use Advanced Trauma Life Support (ATLS) principles in all cases of spinal injury In polytrauma cases, suspect a spinal injury A second spinal injury at a remote level may be present in 10 per cent of cases Spinal boards cause pressure sores

PERTINENT HISTORY The mechanism and velocity of injury should be determined at an early stage. A check for the presence of spinal pain should be made. The onset and duration of neurological symptoms should also be recorded.

Figure 26.12 The bulbocavernosus reflex (this can be elicited in females by traction on the Foley catheter).

Eugene Basil Foley, 1891–1966, urologist, Anker Hospital, St Louis, MN, USA.

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Level of neurological impairment The ASIA neurological impairment scale is based on the Frankel classification of spinal cord injury:

• A, complete; • B, sensation present motor absent; • C, sensation present, motor present but not useful (MRC grade 11° (compared to adjacent level).

Computed tomography CT scanning with two-dimensional reconstruction remains the most sensitive imaging modality in spinal trauma (Figure 26.18).

Magnetic resonance imaging MRI is indicated in cases with neurological deficit and where assessment of ligamentous structures is important (Figure 26.19) (Summary box 26.6).

Summary box 26.6 Diagnostic imaging of spinal injuries

Charles Edward Brown-Séquard, 1817–1894, was a physiologist and neurologist who held a number of academic posts. He came from Mauritius and in his dotage reported enhanced sexual prowess after treating himself with extract of monkey testis. Some therefore think of him as the father of endocrinology.

■ ■

Clear visualisation of the cervicothoracic junction is mandatory Plain cervical spine radiographs fail to identity 15 per cent of injuries

Hans Ludwing Frankel, formerly clinical director, The National Spinal Injuries Centre, Stoke Mandeville, UK.

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Diagnostic imaging

331

Patient Name Date/Time of Exam

Examiner Name

MOTOR

(25)

(50)

Comments:

L2 L3 L4 L5 S1

Hip flexors Knee extensors Ankle dorsiflexors Long toe extensors Ankle plantar flexors Voluntary anal contraction (Yes/No)

LOWER LIMB TOTAL (MAXIMUM)

(25)

TOTALS {

(25)

0 1 2 NT

absent impaired normal not testable

T4 T5 T6 T7 T8

T11 T12

S4–5

Palm

L 3

L 4 S1 L5

T10

L 2

L 3

Dorsum

L 4

COMPLETE OR INCOMPLETE? Incomplete Any sensory or motor function in S4–S5

ASIA IMPAIRMENT SCALE

Dorsum

S1 L5

Palm

L 2

Key Sensory Points

(MAXIMUM) (56) (56)

(50)

NEUROLOGICAL LEVEL SENSORY MOTOR

The most caudal segment with normal function

PIN PRICK

C3 C 2

C2 C3 C4 C5 C6 C7 C8 T1 T2 T3 T4 T5 T6 T7 T8 T9 T10 T11 T12 L1 L2 L3 L4 L5 S1 S2 S3 S4–5

LIGHT TOUCH

KEY SENSORY POINTS

(MAXIMUM)

Elbow flexors Wrist extensors Elbow extensors Finger flexors (distal phalanx of middle finger) Finger abductors (little finger)

UPPER LIMB TOTAL

SENSORY

KEY MUSCLES (scoring on reverse side)

ISC

STANDARD NEUROLOGICAL CLASSIFICATION OF SPINAL CORD INJURY

AMERICAN SPINAL INJURY ASSOCIATION

C5 C6 C7 C8 T1

Any anal sensation (Yes/No) PIN PRICK SCORE (max: 112) LIGHT TOUCH SCORE (max: 112)

(56) (56)

ZONE OF PARTIAL PRESERVATION SENSORY Caudal extent of partially MOTOR innervated segments

S1 S1

This form may be copied freely but should not be altered without permission from the American Spinal Injury Association.

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Figure 26.14 American Spinal Injury Association neurological evaluation.

Figure 26.15 Large prevertebral haematoma.

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spinolaminar posterior

Figure 26.16 The anterior, posterior and spinolaminar lines are useful in identifying anterior translation on lateral x-rays of the neck.

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Figure 26.17 Lateral cervical spine x-ray showing obvious spinal instability with marked sagittal angulation and translation. This patient walked into the outpatient department. Figure 26.19 Sagittal T2-weighted magnetic resonance image demonstrating a cervical spine subluxation and spinal cord contusion.

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Figure 26.18 Axial computed tomography scan demonstrating a thoracolumbar fracture dislocation.

CLASSIFICATION AND MANAGEMENT OF SPINAL AND SPINAL CORD INJURIES Basic managenent principles Spinal realignment In cases of cervical spine subluxation or dislocation, skeletal traction is necessary to achieve anatomical realignment. This is done using skull tongs (Figure 26.20). In many cases of spinal trauma, formal open reduction and stabilisation using internal fixation is also required (Figure 26.21).

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Figure 26.20 Skeletal traction using skull tongs.

A halo brace can be used to hold a closed realignment of cervical fractures (Figure 26.22).

Stabilisation The indication for operative intervention is influenced by the injury pattern, degree of instability and the presence of a neurological deficit. The only absolute indication for surgery in spinal trauma is deteriorating neurological function.

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Classification and management of spinal and spinal cord injuries (c)

(a)

(b)

Decompression involves spinal realignment and/or direct decompression of the neural elements (Figure 26.23). The timing of surgery in spinal cord trauma remains controversial.

Corticosteroids Many spinal trauma centres no longer use steroids in cases of spinal cord injury due to lack of evidence to support efficacy (Summary box 26.7).

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Summary box 26.7 Management of spinal trauma ■ ■ ■

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(d)

Figure 26.21 (a) Thoracolumbar fracture dislocation; (b) treated with open reduction and posterior fixation; (c) bifacetal cervical spine dislocation; (d) posterior stabilisation following closed reduction.

Decompression of the neural elements

333

Neurological deficit determines management Deteriorating neurological status requires surgical intervention Corticosteroids are ineffective

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NECK AND SPINE (a)

(b)

Figure 26.22 External immobilisation using a halo jacket.

SPECIFIC SPINAL INJURIES

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Upper cervical spine (skull–C2) Craniocervical dislocation This injury is usually caused by high energy trauma and is often fatal. The dislocation may be anterior, posterior or vertical (Figure 26.24). Power’s ratio (Figure 26.25) is used to assess skull translation.

Figure 26.23 (a) Sagittal T2-weighted magnetic resonance image showing an L1 burst fracture and neural compression; (b) treated with combined anterior and posterior surgery.

Atlantoaxial instability

Jefferson fractures (C1 ring)

This is uncommon and either resolves spontaneously or with traction. Isolated, traumatic transverse ligament rupture leading to C1/2 instability is uncommon and is treated with posterior C1/2 fusion (Figure 26.26).

These injuries are associated with axial loading of the cervical spine and may be stable or unstable (Figure 26.27a). Associated

Occipital condyle fracture This is a stable injury often associated with head injuries, and is best treated in a hard collar for 8 weeks.

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Sir Geoffrey Jefferson, 1886–1961, Professor of Neurosurgery, University of Manchester, UK. He became the UK’s first Professor of Neurosurgery in 1939. In 1947, he was elected a Fellow of The Royal Society, a rare distinction for a practising surgeon. Although he became a neurosurgeon, he performed the first successful embolectomy in England in 1925 at Salford Royal Hospital.

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Specific spinal injuries

335

(a)

(b) Figure 26.24 Vertical occipitocervical dislocation.

Figure 26.25 Power’s ratio. BC/OA ≥1 indicates anterior translation, ≤0.75 indicates posterior translation.

Figure 26.26 (a) Atlantoaxial subluxation. (b) C1/2 posterior fusion using C1 lateral mass and C2 pedicle screws.

transverse ligament rupture may occur (Figure 26.27b). Most are treated non-operatively in a collar or halo brace.

ated facet dislocation are treated operatively, usually with posterior stabilisation.

Odontoid fractures

Subaxial cervical spine (C3–C7)

There are three types of Odontoid peg fracture (Figure 26.28). Neurological injury is rare. The majority of acute injuries are treated non-operatively in a halo jacket or hard collar for three months. Internal fixation with an anterior compression screw is indicated in displaced fractures (Figure 26.29). Posterior C1/2 fusion is required in cases of non-union.

The pattern of lower cervical spine injury depends on the mechanism of trauma. These include wedge (hyperflexion), burst (axial compression), tear-drop fractures (hyperextension) and facet subluxation/dislocation (rotation and hyperflexion). The more severe injuries are accompanied by spinal cord injury (Figure 26.31a). Operative intervention may be required to decompress the spinal cord and stabilize the spine with internal fixation (Figure 26.31b). Facet subluxation/dislocation ranges in severity from minor instability to complete dislocation with spinal cord injury (Figure 26.32) (Summary box 26.8).

Hangman’s fracture The Hangman’s fracture is a traumatic spondylolisthesis of C2 on C3. There are four types with varying degrees of instability (Figure 26.30). Those with significant displacement or associ-

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Barry Powers, contemporary, Chief and Clinical Professor of Radiology, Duplin General Hospital, Kenansville, NC, USA, described his ratio in 1979.

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336

NECK AND SPINE mass deviation (a)

(a)

(b)

(c)

(b)

Figure 26.27 Stable (a) versus unstable (b) Jefferson’s fracture of C1. Open mouth view of C1/2 demonstrating C1 lateral mass deviation. Rupture of the transverse ligament is present when the combined lateral mass deviation exceeds 6.9 mm.

Type I Figure 26.29 Type II odontoid fracture. Treated with an anterior compression screw.

Summary box 26.8 Type II

Cervical spine injuries ■

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■

Type III Figure 26.28 Types of odontoid fracture.

Thoracic and thoracolumbar fractures The system developed by the AO (Arbeitsgemeinschaft fu˝r Osteosynthesefragen) can be used to classify these fractures. There are three main injury types (A, B and C) with increasing instability and risk of neurological injury. Type A fractures involve the vertebral body. Type B injuries have additional distraction/ disruption of the posterior elements and type C injuries are

The majority of upper cervical spinal injuries are treated non-operatively Spinal cord injury is more commonly associated with subaxial cervical spinal injuries

rotational. The majority of type B and type C injuries require surgical stabilization.

Thoracic spine (T1–T10) Osteoporotic wedge compression fractures in the elderly are the most common injury in this group. Symptomatic fractures can be treated with percutaneous bone cement augmentation, known as vertebroplasty or kyphoplasty (Figure 26.33). In trauma cases, unstable fractures are associated with significant energy transfer to the patient and may be associated with major internal injuries, such as pulmonary contusion and spinal cord injury. The combination of thoracic spine disruption and

AO (Arbeitsgemeinschaft fu˝r Osteosynthesefragen) which may be translated from the German as ‘Working Party on Problems of Bone Repair’.

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337

(a)

(b) (b)

Figure 26.30 (a) Hangman’s fractures of C2 with minimal forward translation. (b) C2/3 subluxation with spinal cord contusion.

a sternal fracture (Figure 26.34) also carries a significant risk of aortic rupture. Multiple posterior rib fractures and rib dislocations above and below a thoracic spinal injury signify a major rotational injury to the chest and are associated with vascular injury and significant pulmonary contusion (Figure 26.35). Multimodality diagnostic imaging is recommended. Surgery is appropriate in almost all unstable thoracic injuries.

Thoracolumbar spinal fractures (T11–S1)

Figure 26.32 C5/6 bifacetal dislocation.

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The thoracolumbar junction is especially prone to injury. This can vary from a minor wedge fracture to spinal dislocation (Figure 26.36). Burst fractures are comminuted fractures of the vertebral body. Usually the distance between the pedicles is widened and bone fragments are retropulsed into the spinal canal (Figure 26.37). The surgical approach can be anterior, posterior or combined. For burst fractures with neurological compromise, an anterior approach with vertebral corpectomy, canal clearance and anterior reconstruction (Figure 26.38) is often used.

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Figure 26.31 (a) Cervical burst fracture with spinal cord contusion. (b) Treated by anterior decompression and reconstruction.

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NECK AND SPINE (a)

Figure 26.35 Rotational (type C) injury at the thoracolumbar junction. Note rib fractures and dislocation, and presence of chest tube.

(b)

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Figure 26.33 (a) Lateral x-ray showing multiple osteoporotic compression fractures. (b) Reduction in thoracic kyphotic deformity following four level kyphoplasty.

Figure 26.36 Total spinal sagittal computed tomographic reconstruction demonstrating a thoracolumbar fracture dislocation and fracture of L5.

Chance fractures are flexion–distraction injuries of the thoracolumbar junction and are classically associated with the use of lap belts (Figure 26.39). Duodenal, pancreatic and/or aortic rupture, are also associated with these injuries (Summary box 26.9).

Summary box 26.9 Thoracic and thoracolumbar fractures Figure 26.34 Sagittal computed tomographic reconstruction showing an upper thoracic spine fracture dislocation and associated sternal fracture.

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■

Unstable thoracic spine fractures and thoracolumbar flexion–distraction injuries are commonly associated with vascular and/or visceral injuries

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Rehabilitation and patient outcome (a)

339

(a)

(b) (b)

Figure 26.37 Lumbar burst fracture with increase in interpedicular distance (a) and spinal canal compromise (b). Figure 26.38 Anterior spinal reconstruction for a lumbar burst fracture.

REHABILITATION AND PATIENT OUTCOME

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The goal of spinal cord injury rehabilitation focuses on maximising the remaining neurological function. The level of neurological impairment determines functional outcome (Table 26.1).

Prognosis of spinal cord injury Despite continuing improvements in patient care, life expectancy remains reduced (Table 26.2). The prognosis for neurological recovery is strongly influenced by the pattern of initial injury, the completeness of the cord injury and the age at the time of injury.

Complications associated with spinal cord injury Pain and spasticity Neurogenic pain is common. Once reflex activity returns following cord injury, spasticity may occur and can be problematic.

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Figure 26.39 A bony Chance fracture at the thoracolumbar junction secondary to a lap belt injury.

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NECK AND SPINE Table 26.1 Expected functional outcome versus level of cervical spinal cord injury.

Level of Injury

Functional goal

C3–C4

Power wheelchair with mouth or chin control. Verbalise care, communicate through adaptive equipment. May be ventilator dependent Power wheelchair, dress upper body, self-feed with aids, wash face with assistance Propel power wheelchair, possibly push manual wheelchair, transfer with assistance, dress upper body (lower body with assistance), self-groom with aids, bladder/bowel care with assistance, self-feed with splints, able to drive Manual wheelchair, independent transfer, dressing (with aids), feeding, bathing, self-care. Bladder and bowel care with assistance Independent with most activities of daily living, and bowel and bladder care As above, but with more ease. Independent with all self-care Independent. Walk with short or long leg braces Independent, able to walk if able to push off (S1) (may need brace). Bladder, bowel and sexual function may remain compromised

C5 C6 C7 C8–T4 T5–T12 L1–L5 S1–S5

Table 26.2 Life expectancy (years) for post-injury by severity of injury and age at injury.

Age at injury

No SCI

Motor functional at any level

(a) For people who survive the first 24 hours 20 58.4 52.8 40 39.5 34.3 60 22.2 17.9 (b) For people surviving at least one year post-injury 20 58.4 53.3 40 39.5 34.8 60 22.2 18.3

Para

Low tetra (C5–C8)

High tetra (C1-C4)

Ventilator-dependent at any level

45.6 28.0 13.1

40.6 23.8 10.2

36.1 20.2 7.9

16.6 7.1 1.4

46.3 28.6 13.5

41.7 24.7 10.8

37.9 21.6 8.8

23.3 11.1 3.1

SCI, spinal cord injury.

Intrathecal infusion of baclofen may be required in resistant cases.

Autonomic dysreflexia

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This is a paroxysmal syndrome of hypertension, hypohydrosis (above level of injury), bradycardia, flushing and headache in response to noxious visceral and other stimuli. It is most commonly triggered by bladder distension or rectal loading from faecal impaction.

Neurological deterioration Post-traumatic syringomyelia may cause late (>3 months postinjury) neurological deterioration and occurs in 3–5 per cent of spinal cord injury cases. Increase in pain and/or spasticity, ascending loss of sensation and deep tendon reflexes are suspicious and warrant early MRI assessment. Expanding cavities require neurosurgical intervention.

Thromboembolic events Deep vein thrombosis (DVT) occurs in 30 per cent of spinal cord-injured patients. Fatal pulmonary embolus is reported in 1–2 per cent of cases. Therefore, prophylaxis with low molecular heparin is recommended.

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Osteoporosis, heterotopic ossification and contaractures Disuse osteoporosis is an inevitable consequence of spinal cord injury, and fragility fractures may occur. Heterotopic ossification may affect hips, knees, shoulders and elbows. It occurs in 25 per cent of spinal cord-injured patients. Surgery is appropriate in selected cases. Soft tissue contractures around joints may occur due to spasticity, but can be avoided by appropriate physical therapy, positioning and splinting.

FURTHER READING Aebi M, Thalgott JS, Webb JK. AO ASIF principles in spine surgery. Berlin: Springer-Verlag, 1998. Bridwell KH, DeWald RL (eds). The textbook of spinal surgery. Philadelphia: Lippincott-Raven, 1997. British Orthopaedic Association. The initial care and transfer of patients with spinal cord injuries, 2006. Available from: www.sbns. org/rcsed/RCSEdDocuments/DocumentsView.aspx?tabID=0&ItemI D=31562&MId=4607&wversion=Staging. Cotler JM, Simson MJ, An HS et al. (eds). Surgery of spinal trauma. Philadelphia: Lippincott, Williams and Wilkins, 2000. Fardon DF, Herzog RJ, Mink JH et al. (eds). Orthopaedic knowledge update – spine. Rosemont, IL: American Academy of Orthopaedic Surgeons, 1997. Focus issue. Spinal trauma. Spine 2006; 31(11S): S1–104.

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CHAPTER

Maxillofacial trauma LEARNING OBJECTIVES

INTRODUCTION An unscarred face is important to the well-being of the individual, and thus all injuries, however trivial, should be treated thoughtfully and sympathetically, with every effort made to produce an optimal outcome. In addition, even trivial blows to the face may:

• cause injuries which compromise the airway; • directly or indirectly cause a head injury; • cause injuries to the cervical spine.

EPIDEMIOLOGY Injuries to the orofacial soft tissues and facial skeleton commonly result from sporting activities, accidents and intentional violence. There is significant variation in the aetiological causes of orofacial injuries in different parts of the world and this affects their incidence:

• Social factors. Interpersonal violence has steadily increased

and in many countries is now the most common cause of orofacial injuries. This increase is noticed to a greater extent in conurbations and urban areas. It is often fuelled by alcohol excess. • Climatic factors. The arrival of snow and freezing weather during the winter, and increased traffic volume and interpersonal violence during the warmer months of the year often produce seasonal variations in the incidence of injuries. • Road traffic accidents. Legislation and improved vehicular design have lessened the number of injuries presenting as a result of road traffic accidents. Air bag provision, seat belts, laminated windscreens and drink/drive laws have all helped in reducing orofacial injuries in the developed world.

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To understand: • The diagnosis and management of fractures of the middle third of the facial skeleton and the mandible To appreciate: • The importance of careful cleaning and accurate suturing of facial lacerations

However, the enforcing of lower speed limits has not, as yet, been shown to reduce injuries.

CLINICAL EFFECTS The mouth and nasal passages form part of the upper aerodigestive tract. Lacerations and fractures of the facial skeleton may give rise to immediate or delayed respiratory obstruction. Immediate obstruction may arise from inhalation of tooth fragments, accumulation of blood and secretions, and loss of control of the tongue in the unconscious or semiconscious patient. Patients with facial injuries should not be allowed to lie supine. They should be nursed in the semiprone position (Figure 27.1) with the head supported on the bent arm. Damaged teeth, blood and secretions can then fall out of the mouth and gravity pulls the tongue forward. As the patient is manoeuvred into the correct nursing position, the neck should be supported and held in a neutral position – a protective collar is advisable until a fracture of the cervical spine has been excluded. An intracranial injury should always be considered as a possibility, however minor the injury to the face.

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To be able to: • Recognise the life-threatening nature of facial injuries through compromise of the airway and associated head and spinal injuries To have: • A methodology for examining facial injuries To know: • The classification of facial fractures

Figure 27.1 The patient should be nursed in the semiprone position to allow secretions, blood and foreign bodies to fall from the mouth.

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Initial haemorrhage after a facial injury can be dramatic, but sustained bleeding is unusual. The most likely cause of circulatory failure in a facial injury is the accompanying skeletal fractures or a ruptured viscus. These should always be actively sought in the shocked patient. Oedema is a particular feature of all fractures of the facial skeleton and tends to develop within 60–90 minutes. Thus, a patient with a shattered face may appear to have a good airway immediately after the injury, but then swelling of the tongue, facial and pharyngeal tissues may then cause respiratory compromise. This is especially important when the middle third of the face is involved. In Le Fort III fractures (see below under The middle third), the maxilla may be thrust downwards and backwards along the base of the skull. As it does so, the posterior teeth of the upper and lower jaws contact prematurely and the mouth is held open (Figure 27.2) giving the impression of a good airway. However, as oedema develops, the soft palate and tongue may swell to meet, and close the pharyngeal airway. This leads to respiratory distress and even obstruction (Figure 27.3) (Summary box 27.1). Summary box 27.1 Facial injuries ■ ■ ■

Are potentially life-threatening May be associated with injuries to the brain and cervical spine Are cosmetically very important

EXAMINATION OF THE PATIENT

Figure 27.3 Loss of nasopharyngeal space and odema of the soft palate and tongue may close off the airway in severe maxillofacial injuries, 2–3 hours after injury.

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It is easy to be distracted from examining the whole patient by the dramatic appearance of a facial injury. The rapid onset of oedema may make examination of the face and routine head injury observations difficult – for instance, it may prove impossible to prise the eyelids apart to examine the pupils. Once the pattern and extent of soft tissue injury have been established and recorded, attention should be directed towards

the hard tissues. Regardless of the apparent site of the injury, the whole head should be examined visually and by palpation starting with the vault of the skull. The face should be examined from in front. Any asymmetry should be noted, although oedema may make this difficult. Gentle palpation gives the most information in searching for step deformities. Tenderness over sites of known weakness and potential for fracture (see below under Fractures of the facial skeleton) is a very good guide to the possibility of there being an underlying fracture. A good system is to examine from above downwards – checking first the supraorbital and infraorbital ridges, the nasal bridge and then the zygomas, including the arches. The mandible should then be examined starting at the condyles bilaterally and then following the posterior and lower border of the mandible as far as the midline. The majority of middle third injuries are accompanied by some degree of epistaxis (except isolated zygomatic arch fractures) and Le Fort II and III injuries frequently have a cerebrospinal fluid (CSF) leak particularly useful sign in 26th Ed with CSF rhinorrhoea. AISBN: 9781444121278 Title: Bailey & Love’s Short Practice of Surgery, the fractured zygoma is the frequent subconjunctival haemorrhage, which will often be found to have no posterior limit when www.cactusdesign.co.uk the patient is asked to look to the other side (Figure 27.4). Figure 27.2 A blow from the front of the face may separate the facial The patient should then be examined intraorally with good skeleton from the base of the skull and thrust it downwards and backillumination, taking note of the occlusion. The maxillary and wards. mandibular dentition normally ‘fit’ together even if the occlu-

Proof Stage:

René Le Fort, 1869–1951, was a French surgeon who classified facial fractures after macabre research in which he dropped rocks and other heavy objects on the faces of cadavers. Thomas Brian Gunning, 1813–1889, American dentist.

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placed on the forehead. If the maxilla is fractured, gentle pressure forward and backward, or side to side, will reveal movement between the examining hands. With the mandible, gentle manipulation across the suspected site of a fracture will produce ‘springing’ if a fracture is present. Lacerations of the oral mucosa may occur independently of hard tissue injuries, and can often involve the buccal mucous membrane and tongue. Degloving lacerations most commonly involve the labial sulcus and the body of the mandible. Tongue injuries require careful assessment, as the depth of lacerations is often underestimated and may be a source for significant haemorrhage, which may be delayed. Palatal lacerations tend to occur in young children who fall on to objects held in the oral cavity, especially pens and pencils. With such a history, the possibility of a retained foreign body must be considered. Figure 27.4 Fractures of the zygoma may often be associated with subconjunctival haemorrhage. This example shows no posterior border to the haemorrhage as the patient looks away from the side of the fracture.

sion is naturally irregular – if they do not, a fracture of the jaws may be suspected. All fractures involving the alveolus (the tooth-bearing portion of the jaw in the dentate patient) tear the gingivae and are compound into the mouth (Figure 27.5). A haematoma in the floor of the mouth is an indication of a fracture of the mandible, particularly in patients with no teeth of their own. The alignment of the teeth should be noted and any missing or broken teeth and dental restorations/prostheses should be carefully recorded. The occlusal plane must be examined for the presence of step defects. These indicate a likely fracture of the underlying bone. The patient should be asked to bring the teeth together, so that any occlusal anomalies may be observed. In some cases, independent movement of the fragments may also be detected. Jaw movement should be tested: deviation from the midline at rest or on opening suggests a fracture of the side to which the jaw is deviating. If a fracture of the maxilla is suspected, then the maxillary dental arch should be grasped between the index finger and thumb of one hand in the incisor region, while the other is

Checking for intact nerves Paraesthesia suggests a fracture proximally along the course of the nerve. Thus, paraesthesia of the cheek and upper lip suggests a fracture involving the infraorbital foramen or floor of the orbit, while paraesthesia of the lower lip suggests a fracture of the mandibular body. Facial palsy may indicate damage to the branches of the facial nerve involved in facial lacerations. This is common in penetrating wounds of the parotid gland. In the absence of lacerations, facial palsy may indicate a fractured temporal bone. Check visual acuity in both eyes. This may be difficult in the oedematous patient with marked periorbital oedema, but a pen torch shone directly through the lids will confirm gross optic nerve function. Where possible, pupil size and reflexes to light should be observed and recorded, as should eye movements. Check for diplopia by asking the patient to follow the light of a pen torch through a full range. Diplopia can occur with damage to the thin orbital plates of bone, particularly the floor of the orbit or from damage to the III, IV or VI cranial nerves. All findings should be recorded accurately, preferably with diagrams to include measurements of lacerations, abrasions and areas of tissue loss. Photographs of the initial injury can be very helpful if litigation is likely to follow (Summary box 27.2). Summary box 27.2

■ ■ ■

Commence with lacerations and soft tissue injuries Systematically examine bones, including the occiput and cranial vault Check dental occlusion and palpate the mouth Examine cranial nerves

ADDITIONAL INVESTIGATIONS Radiological investigations

Figure 27.5 A fracture of the right parasymphysis of the mandible, demonstrating a tear of the gingivae in the lower right lateral incisor/ canine region.

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Table 27.1 demonstrates the regularly used radiographic views utilised in the diagnosis of maxillofacial injuries. Coronal computed tomography (CT) scanning has superseded tomographic views in the diagnosis of orbital floor fractures, and coronal and axial CT scanning is often the choice of radiographic investigation in the more complex middle third fractures (Figure 27.6). A chest radiograph is indicated if there is any suggestion of inhalation of dental fragments or dental prostheses. It should be

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Examination of facial injuries ■

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M A X I L L O FA C I A L T R A U M A Table 27.1 Radiological views for specific fractures.

Site of fracture

Radiographs

Mandible: body and ramus Mandible: condyles

OPT, lateral obliques, lower occlusal, PA mandible OPT, PA mandible with mouth open, Toller transpharyngeal views OM 15° and 30°, lateral facial bones OM 15° and 30°, submentovertex OM 15° and 30° and tomograms Lateral nasal bones, occipitofrontal Lateral skull, occipitofrontal

Maxilla Zygomatic complex Orbital blow-outs Nasal bones Frontal bones

OM, posteroanterioroccipitomental; OPT, orthopantomogram; PA posteroanterior.

pantomogram (Figure 27.7), is the radiograph of choice for the mandible as it shows the whole bone from condyle to condyle.

FRACTURES OF THE FACIAL SKELETON Fractures of the facial skeleton may be divided into those of the upper third (above the eyebrows), the middle third (above the mouth) and the lower third (the mandible). Fractures tend to occur through points of weakness – the sutures and foramina – and in thin unsupported bone.

The upper third The patterns of fracture of the skull tend to be related to the site and type of trauma (sharp or blunt), but there are points of weakness in the skull, mainly involving the frontal sinuses and the supraorbital ridges.

The middle third

Figure 27.6 Computed tomographic (CT) scan showing a comminuted fracture of the right maxilla and zygomatic complex (nasal pack in place).

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remembered, however, that polymethylmethacrylate (PMMA) used in the construction of dentures is not radiopaque and so may not be visible on plain radiographs. Posteroanterior occipitomental radiographs are the optimum initial radiographs to illustrate the site and displacement of a middle third fracture. A panoramic oral radiograph, or ortho-

In 1911, Rene Le Fort classified fractures according to patterns which he created on cadavers using various degrees of force. The Le Fort classification is still used extensively today (Figure 27.8). The Le Fort I fracture effectively separates the alveolus and palate from the facial skeleton above. The fracture line runs through points of weakness from the nasal piriform aperture, through the lateral and medial walls of the maxillary sinus, running posteriorly to include the lower part of the pterygoid plates. The Le Fort II fracture is pyramidal in shape. The fracture involves the orbit, running through the bridge of the nose and the ethmoids whose cribriform plate may be fractured. It continues to the medial part of the infraorbital rim and often through the infraorbital foramen. It continues posteriorly to the pterygoid plates at the back through the lateral wall of the maxillary antrum at a higher level than the Le Fort I. The Le Fort III fracture effectively separates the facial skeleton from the base of the skull – the fracture lines run high through the nasal bridge, septum and ethmoids. This creates the potential for dural tear and CSF leak. It then passes irregularly through the bones of the orbit to the frontozygomatic suture. The zygomatic arch fractures and the facial skeleton are separated from the bones above at a high level through the lateral wall of the maxillary sinus and the pterygoid plates. The Le Fort fractures are seldom confined exactly to the original classification and combinations of any of the above fractures may occur.

Figure 27.7 An orthopantomogram demonstrating a fracture of the left angle of the mandible.

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Blow-out fractures of the orbit Direct blunt trauma to the globe of the eye may push it back within the orbit. The globe is a fairly robust structure and as it is thrust backwards, the weakest plate of bone, most commonly the orbital floor, fractures and the orbital contents herniate down into the maxillary antrum. This soft tissue herniation may trap the inferior oblique and inferior rectus muscles, leading to failure of the eye to rotate upwards. Enophthalmos and diplopia can follow, although initially both may be concealed by oedema. Paraesthesia in the distribution of the infraorbital nerve may be an important clue to the blow-out fracture. There should be a high index of suspicion of any possible orbital blow-out fracture. A coronal CT is the investigation of choice, as significant delay in treatment may be associated with less success than early diagnosis and treatment (Figure 27.9) (Summary box 27.4).

(a)

Summary box 27.4 Blow-out fractures of the orbit ■ ■

(b)

Damage to the infraorbital nerve is common, causing numbness of the cheek Any fracture that involves the orbital floor (Le Fort II and zygomatic complex) has the potential for orbital content entrapment

Figure 27.9 Previously undiagnosed left orbital blow-out fracture, pre-

This is the most common fracture of the middle third of the senting three months after the initial injury. Enophthalmos and lowered face, apart from the nose. The fractures occur through points of pupillary level are evident. weakness: the infraorbital margin, the frontozygomatic suture, the zygomatic arch and the anterior and lateral wall of the maxhort Practice of Surgery, 26th Ed ISBN: 9781444121278 Proof Stage: 1 Fig No: 27.8a illary sinus. Tears of the antral mucosa may lead to epistaxis on hort Practice of Surgery, 26th Ed ISBN: 9781444121278 Proof Stage: 2 Fig No: 27.8b Nasoethmoidal complex fractures the affected side and damage to the infraorbital nerve may cause o.uk Fractures of the nasoethmoidal complex, as opposed to isolated paraesthesia in its sensory distribution (Summary box 27.3). o.uk nasal bone fractures, are usually comminuted fractures involving the nasal bones, maxilla, infraorbital rims and the frontal bones. Summary box 27.3 Such injuries can cause significant deformity (Figure 27.10), and due to disruption of the medial canthal ligaments may cause Fractures of the zygomatic complex traumatic telecanthus (widened intercanthal distance). ■

Damage to the infraorbital nerve is common, causing numbness of the cheek

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Fracture of the zygomatic complex

Fractures of the mandible The condylar neck is the weakest part of the mandible and is the

William Johnson Walsham, 1847–1903, surgeon, St Bartholomew’s Hospital, London, UK. Morris Joseph Asch, 1833–1902, surgeon, New York Eye and Ear Hospital, New York, NY, USA.

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TREATMENT Soft tissue injuries

Figure 27.10 Nasoethmoidal complex fracture, demonstrating gross nasal deformity and traumatic telecanthus.

most frequent site of fracture (Figure 27.11), while other fractures tend to occur through unerupted teeth (the impacted wisdom tooth) or where the roots are long (the canine tooth). The mandible may fracture directly at the point of the blow, or indirectly at a point of weakness distant from the original blow. The latter is characteristically seen in the so-called ‘guardsman’ fracture, where a blow to the chin point may cause a direct fracture of the symphysis or parasymphysis of the lower jaw. Indirect transmission of the kinetic energy causes a unilateral or bilateral fracture of the mandibular condyles. Blows from below may cause the mandible to be thrust upwards fracturing the alveolus and teeth as they strike the maxillary dentition (Summary box 27.5).

Facial soft tissues have an excellent blood supply and heal well. They should be sutured as soon as possible following the injury after careful exploration, debridement and cleaning, particularly if foreign bodies are embedded in the wounds. Most lacerations can be closed using local anaesthesia. If the patient is due to have a general anaesthetic and there is a delay, then the wounds should be temporarily closed in advance, using local anaesthesia. Great care should be taken to replace tissues accurately, particularly in cosmetically important landmarks, such as the vermilion border of the lips, the eyelids and nasal contours. Muscle and underlying tissues should be brought together with absorbable sutures so that the edges of the wound lie passively within 2 mm of their final position. Then, fine monofilament sutures (5-0 or 6-0) are used to bring the wound edges together (Figure 27.12). Sutures should be placed so as to avoid compromising the blood supply of the apices of small flaps. Broad spectrum antibiotics should be prescribed. Ideally, alternate sutures should be removed from the third day with the remaining sutures removed on the fifth day. Intraoral lacerations should be closed with resorbable sutures. The depth of lacerations to mobile structures, such as the tongue and soft palate, can easily be underestimated. Failure to close the deeper layers of intraoral lacerations may lead to wound dehiscence. The subsequent scars will be thickened and uncomfortable to the patient (Summary box 27.6). Summary box 27.6 Facial lacerations ■

Summary box 27.5

■

Fractures of the mandible ■ ■

Wounds must be thoroughly cleaned of dirt and debris to avoid tattooing Replace tissues accurately, especially the vermilion border

The condylar neck is the weakest point and the most common site of mandibular fracture Indirect transmission of energy may fracture the mandibular condyle(s)

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Figure 27.11 The patterns of fracture of the mandible. (1) The neck of the condyle is the most common site, followed by (2) the angle of the mandible through the last tooth. (3) The third point of weakness is in the region of the canine tooth. A ‘guardsman’ fracture is so called because it refers to the Queen’s Guards who, when they fainted on parade, still held themselves in a position of attention. As a consequence, if they fell forward, the first point of contact with the ground would be the point of the chin. This resulted in a direct fracture of the symphysis/parasymphysis of the mandible, and indirect fractures of both mandibular condyles.

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Figure 27.12 Facial wound. The method of skin closure avoiding inversion of the wound edges. The skin suture has a greater bite of deep tissue than at the surface.

Skin loss Substantial skin and deeper tissue loss can occur as a result of human bite injuries (Figure 27.13), most commonly the nose and ear. Small areas of tissue loss can be closed by careful undermining of the surrounding soft tissues, providing that there is no significant tension on the wound edges and no distortion of the

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mating the severed portions of the duct. The two portions of the duct are then anastomosed, and the cannula left in position for several days in an attempt to prevent post-anastomotic stricture (Summary box 27.8). Summary box 27.8 Parotid duct transection ■

(b)

Cannulate from the mouth and anastomose over the stent

The lacrimal apparatus The nasolacrimal apparatus may be involved in damage to the eyelids and skeletal facial injuries involving the naso-orbital region. The tissues are generally grossly oedematous and the manipulation required to reduce the fractures adds to the difficulty of identifying the cannaliculae. Most surgeons do not attempt repair primarily, but refer to an ophthalmic surgeon if epiphora becomes a problem later, as many heal spontaneously.

Frontal bone fractures

surrounding tissues or structures. Larger areas of skin loss require careful assessment and planned reconstruction with grafts and local tissue flaps.

Facial nerve injury The branches of the facial nerve may be severed in the depths of a lateral facial wound. If this is suspected, primary repair should be attempted, particularly where clinical signs suggest that a major division is involved. Locating the divided branches in oedematous and damaged tissue can prove extremely difficult. Proximal and distal flaps in relatively normal adjacent tissue may have to be raised to identify the nerve on each side of the laceration. The severed nerve ends may then be approximated using an operating microscope. Attempt at primary repair should always be undertaken, as secondary repair is generally unsatisfactory (Summary box 27.7). Summary box 27.7 Facial nerve injury ■

Primary repair is the most appropriate treatment

Parotid duct Lacerations in the same vicinity as those which transect the facial nerve may also transect the parotid duct. The suggested management is to insert a fine cannula into the parotid duct from within the mouth and pass it posteriorly until it appears in the wound. The position of the proximal duct should then be identified and this portion passed over the cannula, so approxi-

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Fractures of the maxilla The principle of reducing and stabilising fractures of the frontal and facial bones is that the surgeon starts at the top and works down. Where no convenient lacerations exist, fractures of the frontal bone, supraorbital ridge and nasal root may be approached through a bicoronal incision, at the vault of the skull, high in the hair line. The incision is taken from just in front of each ear across the vault of the skull. The skin and galea are reflected forwards until the supraorbital ridges are exposed. The supraorbital nerves are identified and freed and the flap extended as required. The nasal bones, lateral orbital rim, frontal bones and zygomatic arches may all be exposed through this approach. The fractured bones may be reduced and fixed by stainless steel wire or titanium mini/microplates, under direct vision. Bone deficiencies in this area may be made up with free, outer cortical cranial bone grafts, with the donor sites available through the bicoronal incision. Where there has been disruption of the medial canthal ligaments, these should be identified and sutured/wired to the opposite side to restore canthal width. When the stabilisation of the upper part of the face is complete, attention may be turned to the midface. Incisions in the lower eyelid (blepharoplasty incision), lower conjunctival sac or infraorbital region are used to explore fractures of the infraorbital rim. These also give access to the orbital floor and are used to treat orbital blow-out fractures. The fractured rim may be fixed using mini/microplates or wires as above, and the floor of the orbit reconstructed with bone, titanium mesh or alloplastic material.

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Figure 27.13 Skin and cartilage loss sustained as a result of human bite injuries. (a) Nose; (b) ear.

The presence of depressed frontal bone fractures and fractures of the posterior wall of the frontal sinus require neurosurgical collaboration. However, fractures of the anterior wall of the sinus are amenable to maxillofacial techniques for reduction and fixation. Access may be through pre-existing lacerations overlying the area, but excellent access with minimal morbidity is achieved using the bicoronal scalp flap (see below). Bone fragments may then be reduced and fixed using titanium bone plates and screws. Any missing bone should be replaced with bone grafts, thereby avoiding any cosmetic forehead depression postoperatively.

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The lower part of the maxilla is approached through a gingival sulcus incision above the maxillary teeth as far back as the second molar. Fractures are fixed with plates or wires. The dental arch is restored to its original shape as far as possible so that it matches the premorbid occlusion with the mandibular arch. To achieve accurate location, dental arch bars, intermaxillary fixation screws or eyelet wires (see below) may need to be applied. Where this is anticipated, the necessary wiring is undertaken before the main part of the operation is commenced. The principle of treatment is to restore the maxillary fragments to their original position. To achieve this, usually it is necessary to reduce the maxilla first with Rowe’s disimpaction forceps, which grasp the palate between the nasal and palatal mucosa. Considerable force is sometimes required in a series of downward, forwards and sideways movements to mobilise it. After 2–3 weeks, full disimpaction is often impossible (Summary box 27.9). Summary box 27.9

(a)

(b)

Fixation of maxillary fractures ■ ■

Orbital floor deficiencies may be made up with grafts, titanium mesh or alloplasts Intermaxillary fixation may be needed to achieve the correct occlusion

Fractures of the mandible

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Fractures of the mandible were traditionally reduced indirectly and then fixed with intermaxillary fixation (IMF). IMF is simply a means of splinting the upper and lower arches of teeth together (Figure 27.14). However, the introduction of maxillofacial fixation systems utilising titanium fixtures has significantly altered the management of patients sustaining maxillofacial fractures. Prior to the introduction of these plating systems, patients would often have their jaws ‘wired together’ for a period of up to 6 weeks. Now, although patients may be placed in temporary IMF during their operative procedure, it is more often than not released at the end of the procedure when the rigid plate fixation has been applied (Figure 27.15). Mandibular fractures may be explored through intraoral or extraoral incisions according to the access required. Pre-existing

Figure 27.15 A fractured mandible treated by open reduction and fixation using a titanium miniplate. No postoperative intermaxillary fixation (IMF) has been used. (a) Posteroanterior view; (b) orthopantomogram.

lacerations overlying the mandible may be used to gain access to the fracture (Figure 27.16). To be sure of achieving a correct dental occlusion, it is wise to use temporary intraoperative IMF. There are occasions where, in spite of rigid fixation with titanium miniplates, IMF or elastic traction is still required in the postoperative period. In this event, the IMF is removed during the recovery from anaesthesia, so as not to risk complications involving the airway. The IMF may then be reapplied when the patient has fully recovered from the general anaesthetic. Fractures of the edentulous (non-tooth-bearing) mandible are generally reduced and fixed using titanium plates. In the very atrophic mandible, the raising of the periosteum should be kept to a minimum as the blood supply to the jaw may be compromised (Summary box 27.10). Summary box 27.10 Fixation of the mandible ■

Figure 27.14 Intermaxillary fixation using eyelet wires.

Plating has made long term jaw wiring almost redundant

Fractures of the mandibular condyle may cause disturbance of the occlusion with deviation of the mandible to the side of the fracture. In unilateral fractures, which are minimally displaced,

Norman Lester Rowe, 1915–1991, maxillofacial surgeon, Queen Mary’s University Hospital, Roehampton, London, UK.

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this disturbance may not be evident. However, displaced unilateral fractures and bilateral condylar fractures often present with such a disturbance and, as such, constitute an indication for open reduction and fixation of the condylar fractures to prevent the formation of an abnormal occlusion. This malocclusion develops due to the vertical pull of the muscles of mastication shortening the ramus height. The posterior teeth contact first and the anterior teeth remain apart. Functionally and cosmetically, this is undesirable and is difficult to counteract by secondary procedures. It is not adequate to simply fix the mandible in IMF, except in the most minimally displaced malocclusions. Open reduction and fixation of the fractured mandibular condyle within 7–14 days of the original injury is indicated if a significant malocclusion is evident in a unilateral condylar fracture with displacement, or a in a bilateral condylar fracture (Summary box 27.11). Summary box 27.11 Fixation of mandibular condyles ■ ■

If displaced or bilateral, with significant occlusal disturbance, surgical intervention will be required Reduction and plating helps prevent anterior open bite

the body of the zygoma or arch, according to the site of the fracture. Force is then applied in the opposite direction to the displacement of the fracture. After reduction, the position of the zygoma can be checked by palpating the bony prominences of the zygomatic arch, and the lateral and inferior orbital rims. As all fractures of the zygoma, other than those solely of the arch, involve the orbital floor, it is essential to apply a forced duction test to ensure no limitation of movement of the inferior oblique and inferior rectus muscles. For this to be done, the lower eyelid is retracted and the inferior rectus grabbed in the lower fornix. The globe can then be rotated upwards and should move freely. Any restriction in movement suggests entrapment of the infraorbital soft tissues, and the floor of the orbit should be explored as for a blow-out fracture (see below). Should the fracture be unstable, open reduction and fixation of the fracture may be necessary. The frontozygomatic suture may be exposed by a small incision just behind the lateral part of the eyebrow and visualised. Displacements may be reduced and fixed with intraosseous wires or bone plates. Occasionally, it is necessary to explore and fix fractures at the infraorbital rim (see above under Fractures of the maxilla), or at the zygomatic buttress intraorally (Summary box 27.12). Summary box 27.12 Fixation of fractures of the zygomatic complex ■ ■ ■

The arch is elevated Ocular tethering should be checked if the fracture involves the orbital floor Regular postoperative observations must be made for retrobulbar haemorrhage

All patients who have had operations involving the orbit should have formal eye observations in the postoperative period. The condition of the eye, pupil size and light reaction should be recorded. Occasional complications occur, the most serious of which is a developing retrobulbar haematoma. Increasing proptosis and loss of vision constitute a postoperative emergency requiring immediate action to reduce the pressure of the haematoma.

Fractures of the zygomatic complex

Orbital blow-out fractures

Displacement of zygomatic complex fractures is usually in a posterior direction, although it is important to assess the actual displacement by studying the occipitomental radiographs. Most fractures may be reduced by the Gillies temporal approach. This entails an incision in the hairline, superficial to the temporal fossa, about 15 mm long, at 45° to the vertical. It is deepened down to and through the temporalis fascia. A channel is prepared below the fascia and down under the body of the zygoma and arch. A Bristow or Rowe elevator is then inserted beneath

These fractures are ideally treated within 10–14 days of the original injury. The aim of treatment is to reduce any soft tissue herniation of the periorbita (Figure 27.17), restore the continuity of the orbital floor, and restore any functional deficit of ocular function caused by extraocular muscle dysfunction. The floor of the orbit is approached either through a blepharoplasty incision in the lower eyelid or through the inferior fornix. The infraorbital margin is identified and the periosteum raised, attempting to avoid displacement of the delicate fragments of bone constituting the fracture. The periorbital soft tissues are gently separated from the bone of the fracture and freed so that no trapping or soft tissue herniation into the antrum remains. Defects of the orbital floor may be made up with bone grafts or from a variety of sources, such as titanium mesh or other suitably rigid materials. These materials may be fixed in place with wires, screws or plates (Summary box 27.13).

Sir Harold Delf Gillies, 1882–1960, plastic surgeon, St Bartholomew’s Hospital, London, UK. Born in New Zealand, widely considered the ‘father of plastic surgery’, started his craft to better the lives of the victims of the First World War. Later, he became a pioneer in gender reassignment (sex change) surgery. When he was finally knighted in 1930 for his wartime work, William Arbuttinot-Lane commented ‘Better late than never!’. He excelled in most sports (cricket, rowing, golf) and despite a stiff elbow from a childhood injury was an accomplished painter.

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Figure 27.16 Comminuted fracture of the mandible approached through a pre-existing laceration.

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Walter Rowley Bristow, 1882–1947, orthopaedic surgeon, St Thomas’s Hospital, London, UK. Henri Luc, 1855–1925, otolaryngologist, in Paris, France, described his operation in 1889. Walter Whitehead, 1840–1913, surgeon, The Royal Infirmary, Manchester, UK. Whitehead’s varnish consists of iodoform, benzoin, storax and Tolu balsam in ether.

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GENERAL Fractures of the facial skeleton are almost always compound and prophylactic antibiotics are important. Penicillin/amoxycillin and metronidazole singly or in combination are ideal for those patients who are not allergic to them. All patients with fractures of the facial skeleton benefit from intraoperative and postoperative dexamethasone, to reduce facial oedema (Summary box 27.14). Summary box 27.14 General principles in facial fractures ■ ■

Figure 27.17 Coronal computed tomographic (CT) scan showing a left orbital blow-out fracture, with evident soft-tissue herniation into the maxillary antrum.

Summary box 27.13

Prophylactic antibiotics should be given Dexamethasone may help to reduce facial oedema

FURTHER READING Langdon J, Patel M, Ord R, Brennan P (eds). Operative oral and maxillofacial surgery, 2nd end. London: Hodder Arnold, 2010. Ward Booth P, Eppley B, Schmelzeisen R. Maxillofacial trauma and esthetic reconstruction. Edinburgh: Churchill Livingstone, 2003. Ward Booth P, Schendel SA, Hausamen JE. Maxillofacial surgery, 2nd edn. Edinburgh: Churchill Livingstone, 2006.

Orbital blow-out fractures Defects of the orbital floor can be made up with bone graft or with synthetic materials

George Walter Caldwell, 1866–1946, otolaryngologist who practised successively in New York, San Francisco and Los Angeles. He described his operation for suppuration in the maxillary antrum in 1893.

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CHAPTER

Torso trauma LEARNING OBJECTIVES

To understand: • That the management of trauma is based on physiology, as well as anatomy (as in general surgery) • The gross and surgical anatomy of the chest and abdomen • The pathophysiology of torso injury • The strength and weaknesses of clinical assessment in the injured patient

INTRODUCTION The torso is generally regarded as the area between the neck and the groin, made up of the thorax and abdomen. This is the largest area of the body and is commonly injured. Because injury does not respect anatomical boundaries, division of the body into abdomen and thorax is artificial, and injury to the torso, with its associated physiological consequences, is more appropriate. About 42 per cent of all deaths are the result of brain injury, but some 39 per cent of all trauma deaths are caused by major haemorrhage, usually from torso injury (Figure 28.1). Although initially injury was treated on an anatomical basis, it has become clear that physiology should be the over-riding

MOF 7%

consideration, and the driver of successful resuscitation is therefore the preservation of normal physiology. Techniques such as ‘damage control resuscitation’ and ‘damage control surgery’ have dramatically improved survival through an understanding of the best techniques required to restore physiological stability (see Chapters 24 and 32).

INJURY MECHANISMS ASSOCIATED WITH TORSO TRAUMA Injury often traverses different anatomical zones of the body, affecting structures on both sides of traditional anatomical zones. These zones are known as ‘junctional zones’.

Junctional zones Unknown 2%

The key junctional zones are: CNS 42%

• between the neck and the thorax; • between the thorax and the abdomen; • between the abdomen, the pelvic structures and the groin. These zones represent surgical challenges in terms of both the diagnosis of the area of injury and the surgical approach, which have to be balanced against the physiological stability of the patient.

Bleeding 39%

Root of the neck Bleeding + CNS 6%

Figure 28.1 Causes of death in trauma. CNS, central nervous system; MOF, multiple organ failure.

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Other 4%

• The use of special investigations and their limitations • The operative approaches to the thoracic cavity • The special features of an emergency department thoracotomy for haemorrhage control • The indications for and techniques of the trauma laparotomy • The philosophy of damage control surgery

Most injuries affecting the base of the neck also affect the upper mediastinum and thoracic inlet. Choice of access is determined by the need for surgical control of the vascular structures contained within.

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The mediastinum

The zone overlying the mediastinum with its major vessels and the heart is also an extremely high-risk area for penetrating wounds. Any wound in this region should immediately raise the suspicion of an associated cardiac or major vascular injury even in the absence of initial gross physical signs. 2

Diaphragm The thorax and abdomen are separated by the diaphragm, which is mainly responsible for breathing, and moves during breathing, between the fourth to the eighth interspace. Any penetrating injury of the lower half of the chest may therefore have penetrated the diaphragm and entered the abdomen. Injuries in this junctional zone, therefore, should be managed as if both cavities had been penetrated (Figure 28.2).

Pelvic structures and groin The pelvis contains a large plexus of vessels, both venous and arterial. Should injury occur, control of haemorrhage can prove to be exceptionally difficult and may require control of both inflow and outflow. This may involve surgical control at the groin of the external iliac and femoral vessels, as well as at the aortic and cava level. Angioembolisation can be a very useful adjunct to treatment.

Figure 28.3 The zones of the retroperitoneum. Zone 1, central; zone 2, lateral; zone 3, pelvic.

Summary box 28.1

Retroperitoneum

Junctional zones

Injury to the retroperitoneum is often difficult to diagnose, especially in the presence of other injury, when the signs may be masked. Intraperitoneal diagnostic tests (ultrasound and diagnostic peritoneal lavage) may be negative. The best diagnostic modality is the computed tomography (CT) scan, but this requires a physiologically stable patient. The retroperitoneum is divided into three zones (Figure 28.3):

■ ■ ■ ■

Neck Mediastinum Diaphragm Groin Retroperitoneum

CRITICAL PHYSIOLOGY Resuscitation of all injuries to the chest and abdomen should follow traditional Advanced Trauma Life Support (ATLS) principles (Table 28.1 and see Chapter 24). Bleeding is the major problem for diagnosis. This may be obvious at the time of evaluation; however, in the young fit individual, bleeding into the chest and abdomen may only produce subtle changes in vital measures and therefore be difficult to assess (Table 28.2). Bleeding occurs from five major sites: ‘one on the floor and four more’:

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1 Zone 1 (central): central haematomas should always be explored, once proximal and distal vascular control has been obtained. 2 Zone 2 (lateral): lateral haematomas are usually renal in origin and can be managed non-operatively, they may sometimes require angioembolisation. 3 Zone 3 (pelvic): pelvic haematomas are exceptionally difficult to control and, whenever possible, should not be opened; they should be controlled with packing (intra- or extraperitonial) and angioembolisation (Summary box 28.1).

■

Liver Spleen Kidney Figure 28.2 The extent of the abdomen.

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external (i.e. skin); chest; abdomen; pelvis; extremities (e.g. fractures).

Although obvious injury may be present, traditional indicators (such as pulse rate) are unreliable in young patients. A normal pulse for a middle-aged patient may be a significantly raised pulse for a young fit person. Table 28.1 Advanced Trauma Life Support (ATLS) principles of resuscitation.

A B C D E

Airway Breathing Circulation Disability (neurology) Environment and exposure

Table 28.2 Clinical indicators of potential ongoing bleeding in torso trauma.

Physiological

Anatomical

Increasing respiratory rate Increasing pulse rate Falling blood pressure Rising serum lactate Visible bleeding Injury in close proximity to major vessels Penetrating injury with a retained missile

THORACIC INJURY Thoracic injury accounts for 25 per cent of all severe injuries. In a further 25 per cent, it may be a significant contributor to the subsequent death of the patient. In most of these patients, the cause of death is haemorrhage. Chest injuries are often life-threatening, either in their own right or in conjunction with other system injuries. About 80 per cent of patients with chest injury can be managed nonoperatively. The key to a good outcome is early physiological resuscitation followed by a correct diagnosis.

Investigation Routine investigation in the emergency department of injury to the chest is based on clinical examination, supplemented by chest radiography. Ultrasound can be used to differentiate between contusion and the actual presence of blood. A chest tube can be a diagnostic procedure, as well as a therapeutic one, and the benefits of insertion often outweigh the risks. The pitfalls of investigation are:

• failure to auscultate both front and back (an inflated lung will

‘float’ on a haemothorax, so auscultation from the front may sound normal); • failure to pass a nasogastric tube if rupture of the diaphragm is suspected; • pursuing radiological investigation (radiography or CT scan) instead of resuscitation in the unstable patient.

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Computed tomography scan The CT scan has become the principal and most reliable examination for major injury in thoracic trauma. Scanning with contrast allows for three-dimensional reconstruction of the chest and abdomen, as well as of the bony skeleton. In blunt chest trauma, the CT scan will allow the definition of fractures, as well as showing haematomas, pneumothoraces and pulmonary contusion. In penetrating trauma, the scan may show the track or presence of the missile and allow the proper planning of definitive surgery. CT scanning has replaced angiography as the diagnostic modality of choice for the assessment of the thoracic aorta (Summary box 28.2). Summary box 28.2 Investigation of chest injuries ■ ■ ■ ■ ■

Directly or indirectly involved in 50 per cent of trauma deaths in the United States. Eighty per cent can be managed non-operatively A chest radiograph is the investigation of first choice A spiral computed tomography scan provides rapid diagnoses in the chest and abdomen A chest drain can be diagnostic as well as therapeutic

Management Most patients who have suffered penetrating injury to the chest can be managed with appropriate resuscitation and drainage of haematoma. If a sucking chest wound is present, this should not be fully closed but should be covered with a piece of plastic, closed on three sides, to form a one-way valve, and thereafter an underwater chest drain should be inserted remote from the wound. No attempt should be made to close a sucking chest wound until controlled drainage has been achieved, in case a stable open pneumothorax is converted into an unstable tension pneumothorax. In blunt injury, most bleeding occurs from the intercostal or internal mammary vessels and it is relatively rare for these to require surgery. If bleeding does not stop spontaneously, the vessels can be tied off or encircled. In blunt chest compressive injury, there is injury to the ribs and frequently to the underlying structures as well, with an associated lung contusion (Summary box 28.3).

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Summary box 28.3 Closed management of chest injuries ■ ■ ■ ■

About 80 per cent of chest injuries can be managed closed If there is an open wound, insert a chest drain Do not close a sucking chest wound until a drain is in place If bleeding persists, the chest will need to be opened

The patient in extremis with exsanguinating chest haemorrhage will be discussed in the section below under Emergency thoracotomy. Life-threatening injuries can be remembered as the ‘deadly dozen’. Six are immediately life-threatening and should be

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sought during the primary survey and six are potentially lifethreatening and should be detected during the secondary survey (Table 28.3). Table 28.3 The ‘deadly dozen’ threats to life from chest injury.

Immediately life threatening

Potentially life threatening

Airway obstruction Tension pneumothorax Pericardial tamponade Open pneumothorax Massive haemothorax Flail chest Aortic injuries Tracheobronchial injuries Myocardial contusion Rupture of diaphragm Oesophageal injuries Pulmonary contusion Figure 28.4 Radiological appearance of a tension pneumothorax.

Efficient initial assessment should focus on identifying and correcting the immediate threats to life. A high index of suspicion must be maintained thereafter to diagnose the potential threats to life as their symptoms and signs can be very subtle. Early consultation and referral to a trauma centre is advised in cases of doubt.

Immediate life-threatening injuries Airway obstruction Early intubation is very important, particularly in cases of neck haematoma or possible airway oedema. Airway distortion can be insidious and progressive and can make delayed intubation more difficult if not impossible.

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Tension pneumothorax A tension pneumothorax develops when a ‘one-way valve’ air leak occurs either from the lung or through the chest wall. Air is sucked into the thoracic cavity without any means of escape, completely collapsing then compressing the affected lung. The mediastinum is displaced to the opposite side, decreasing venous return and compressing the opposite lung. The most common causes are penetrating chest trauma, blunt chest trauma with parenchymal lung injury and air leak that did not spontaneously close, iatrogenic lung punctures (e.g. due to subclavian central venepuncture) and mechanical positive pressure ventilation. The clinical presentation is dramatic. The patient is increasingly panicky with tachypnoea, dyspnoea and distended neck veins (similar to pericardial tamponade). Clinical examination may reveal tracheal deviation. This is a late finding and is not necessary to clinically confirm diagnosis. There will also be hyper-resonance and absent breath sounds over the affected hemithorax. Tension pneumothorax is a clinical diagnosis and treatment should never be delayed by waiting for radiological confirmation (Figure 28.4). Treatment consists of immediate decompression, initially by rapid insertion of a large-bore needle into the second intercostal space in the midclavicular line of the affected hemithorax, and

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then followed by insertion of a chest tube through the fifth intercostal space in the anterior axillary line.

Pericardial tamponade Pericardial tamponade needs to be differentiated from a tension pneumothorax in the shocked patient with distended neck veins. It is most commonly the result of penetrating trauma. Accumulation of a relatively small amount of blood into the non-distensible pericardial sac can produce physiological obstruction of the heart. All patients with penetrating injury anywhere near the heart plus shock must be considered to have a cardiac injury until proven otherwise. Classically, the presentation consists of venous pressure elevation, decline in arterial pressure with tachycardia, and muffled heart sounds. A high index of suspicion and further diagnostic investigations will be needed to make the diagnosis is those cases which are not clinically obvious. This includes chest radiography looking for an enlarged heart shadow or a cardiac ultrasound showing fluid in the pericardial sac. A central line should be inserted checking for a rising central venous pressure. However, in cases in which major bleeding from other sites has taken place, the neck veins may be flat. Needle pericardiocentesis may allow the aspiration of a few millilitres of blood and this, along with rapid volume resuscitation to increase preload, can buy enough time to move the patient to the operating room. However, in penetrating injury to the heart, there is usually a substantial clot in the pericardium, which may prevent aspiration. A dry pericardiocentesis proves only that there is a ‘clot’ on both ends of the needle! Pericardiocentesis has a high potential for iatrogenic injury to the heart and it should at the most be regarded as a desperate temporising measure in a transport situation (under electrocardiogram (ECG) control). The correct immediate treatment of tamponade is operative (sternotomy or left thoracotomy), with repair of the heart in the operating theatre if time allows or otherwise in the emergency room (Summary box 28.4).

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Thoracic injur y

Pericardial tamponade ■ ■ ■ ■

The presentation is similar to a tension pneumothorax: deteriorating cyanosis tachycardia and agitation Ultrasound is diagnostic The central venous pressure may not be elevated if the circulating volume is depleted, e.g. because of other injuries Pericardiocentesis is a temporising measure only with a high complication rate and is not a substitute for immediate operative intervention

Open pneumothorax (‘sucking chest wound’) This is due to a large open defect in the chest (>3 cm), leading to equilibration between intrathoracic and atmospheric pressure. Air accumulates in the hemithorax (rather than in the lung) with each inspiration, leading to profound hypoventilation on the affected side and hypoxia. Signs and symptoms are usually proportionate to the size of the defect. If there is a valvular effect, increasing amounts of air in the pleura will result in a tension pneumothorax (see above under Tension pneumothorax). Initial management consists of promptly closing the defect with a sterile occlusive plastic dressing (e.g. Opsite®), taped on three sides to act as a flutter-type valve. A chest tube is inserted as soon as possible in a site remote from the injury site. Definitive treatment may warrant formal debridement and closure, and early referral. The following points are important in the management of an open pneumothorax:

• a common problem is using too small a tube: a 28FG or larger tube should be used in an adult;

• If the lung does not reinflate, the drain should be placed on low-pressure (5 cm water) suction;

• a second drain is sometimes necessary (but see below under Tracheobronchial injuries);

• physiotherapy and active mobilisation should begin as soon as possible.

Massive haemothorax The most common cause of massive haemothorax in blunt injury is continuing bleeding from torn intercostal vessels or occasionally from the internal mammary artery. Accumulation of blood in a hemithorax can significantly compromise respiratory efforts, compressing the lung and preventing adequate ventilation. Presentation is with haemorrhagic shock, flat neck veins, unilateral absence of breath sounds and dullness to percussion. The treatment consists of correcting the hypovolaemic shock, insertion of an intercostal drain and, in some cases, intubation. Blood in the pleural space should be removed as completely and rapidly as possible to prevent ongoing bleeding, empyema or a late fibrothorax. Clamping a chest drain to tamponade a massive haemothorax is usually not helpful. Initial drainage of more than 1500 mL of blood or ongoing haemorrhage of more than 200 mL/hour over 3–4 hours is generally considered an indication for urgent thoracotomy.

Flail chest This condition usually results from blunt trauma associated

with multiple rib fractures, and is defined as three or more ribs fractured in two or more places. The blunt force required to disrupt the integrity of the thoracic cage typically produces an underlying pulmonary contusion as well. The diagnosis is made clinically, not by radiography. On inspiration, the loose segment of the chest wall is displaced inwards and therefore less air moves into the lungs. To confirm the diagnosis, the chest wall can be observed for paradoxical motion of a chest wall segment during respiration and during coughing. Voluntary splinting of the chest wall occurs as a result of pain, so mechanically impaired chest wall movement and the associated lung contusion all contribute to the hypoxia. There is a high risk of developing a pneumothorax or haemothorax. Traditionally, mechanical ventilation was used to ‘internally splint’ the chest, but had a price in terms of intensive care unit resources and ventilation-dependent morbidity. Currently, treatment consists of oxygen administration, adequate analgesia (including opiates) and physiotherapy. If a chest tube is in situ, intrapleural local analgesia can be used as well. Ventilation is reserved for cases developing respiratory failure despite adequate analgesia and oxygen. Surgery to stabilise the flail chest may be useful in a selected group of patients with isolated or severe chest injury and pulmonary contusion.

Potentially life-threatening injuries Thoracic aortic disruption Traumatic aortic rupture is a common cause of sudden death after an automobile collision or fall from a great height. The vessel is relatively fixed distal to the ligamentum arteriosum, just distal to the origin of the left subclavian artery. The shear forces from a sudden impact disrupt the intima and media. If the adventitia is intact, the patient may remain stable. For the subgroup of immediate survivors, salvage is frequently possible if aortic rupture is identified and treated early. It should be clinically suspected in patients with asymmetry of upper or upper and lower extremity blood pressure, widened pulse pressure and chest wall contusion. Erect chest radiography can also suggest thoracic aortic disruption, the most common radiological finding being a widened mediastinum (Figure 28.5). The diagnosis is confirmed by a CT scan of the mediastinum (Figure 28.6) or possibly by transoesophageal echocardiography. Initially, management consists of control of the systolic arterial blood pressure (to less than 100 mmHg). Thereafter, an endovascular intra-aortic stent (Figure 28.7) can be placed or the tear can be operatively repaired by direct repair or excision and grafting using a Dacron graft.

Tracheobronchial injuries Severe subcutaneous emphysema with respiratory compromise can suggest tracheobronchial disruption. A chest drain placed on the affected side will reveal a large air leak and the collapsed lung may fail to re-expand. If after insertion of a second drain the lung fails to re-expand, referral to a trauma centre is advised. Bronchoscopy is diagnostic. Treatment involves intubation of the unaffected bronchus followed by operative repair.

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Summary box 28.4

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Blunt myocardial injury Significant blunt cardiac injury that causes haemodynamic instability is rare. Blunt myocardial injury should be suspected in any patient sustaining blunt trauma who develops early ECG abnormalities.

in situ is Latin for ‘in place’.

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Widened mediastinum

Depressed left main bronchus

Figure 28.5 Chest radiograph showing a widened mediastinum.

3D reconstruction Showing Aortic disruption

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2D reconstruction Showing Aortic disruption

Figure 28.6 Computed tomography scan showing aortic disruption.

Two-dimensional echocardiography may show wall motion abnormalities. A transoesophageal echocardiogram may also be helpful. There is very little evidence that enzyme estimations have any place in diagnosis. All patients with myocardial contusion diagnosed by conduction abnormalities are at risk of developing sudden dysrhythmias and should be closely monitored.

Diaphragmatic injuries Any penetrating injury below the fifth intercostal space should raise suspicion of diaphragmatic penetration and, therefore, injury to the abdominal contents.

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Blunt injury to the diaphragm is usually caused by a compressive force applied to the pelvis and abdomen. The diaphragmatic rupture is usually large, with herniation of the abdominal contents into the chest. Diagnosis of blunt diaphragmatic rupture is missed even more often than penetrating injuries in the acute phase. Most diaphragmatic injuries are silent and the presenting features are those of injury to the surrounding organs. There is no single standard investigation. Chest radiography after placement of a nasogastric tube may be helpful (as this may show the stomach herniated into the chest). Contrast studies of the upper or lower gastrointestinal tract, CT scan and diagnostic peritoneal

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underneath a flail segment or fractured ribs. This is a very common, potentially lethal injury and the major cause of hypoxaemia after blunt trauma. The natural progression of pulmonary contusion is worsening hypoxemia for the first 24–48 hours. The chest radiography findings are typically delayed. Contrast CT scanning can be confirmatory. Haemoptysis or blood in the endotracheal tube is a sign of pulmonary contusion. In mild contusion, the treatment is oxygen administration, aggressive pulmonary toilet and adequate analgesia. In more severe cases, mechanical ventilation is necessary. Normovolaemia is critical for adequate tissue perfusion and fluid restriction is not advised.

Continuing blood loss

lavage all lack positive or negative predictive value. The most accurate evaluation is by video-assisted thoracoscopy (VATS) or laparoscopy, the latter offering the advantage of allowing the surgeon to proceed to a repair and additional evaluation of the abdominal organs (Summary box 28.5). Summary box 28.5 Blunt injuries ■ ■ ■ ■

Rupture of the diaphragm is easily missed Myocardial injury must be suspected if there are abnormal ECG changes Mortality rises rapidly with delay in diagnosis of oesophageal rupture In severe pulmonary contusion ventilation may be needed

Operative repair is recommended in all cases. All penetrating diaphragmatic injury must be repaired via the abdomen and not the chest, to rule out penetrating hollow viscus injury. The thorax is at negative pressure and the abdomen is at positive pressure. A late complication of rupture of the diaphragm is herniation of the abdominal contents into the chest. Strangulation of any of the contents can then occur, and the patients have a high mortality rate.

Oesophageal injury Most oesophageal injuries result from penetrating trauma; blunt injury is rare. A high index of suspicion is required. The patient can present with odynophagia (pain on swallowing foods or fluids), subcutaneous or mediastinal emphysema, pleural effusion, air in the retro-oesophageal space and unexplained fever. Mediastinal and deep cervical emphysema are evidence of an aerodigestive injury until proven otherwise. The mortality rate rises exponentially if treatment is delayed. A combination of oesophagogram in the decubitus position and oesophagoscopy confirm the diagnosis in the great majority of cases. The treatment is operative repair and drainage.

Pulmonary contusion Pulmonary contusion occurs following blunt trauma, usually

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EMERGENCY THORACOTOMY Emergency thoracic surgery is an essential part of the armamentarium of any surgeon dealing with major trauma. A timely thoracotomy for the correct indications can be the key step in saving an injured patient’s life. Indications for thoracotomy include the need to perform:

• • • •

internal cardiac massage; control of haemorrhage from injury to the heart or lung; control of intrathoracic haemorrhage from other causes; control of massive air leak.

The clinical decision as to whether a casualty requires an emergency department thoracotomy (EDT) or can be transferred to the operating theatre can be complex. It is far better to perform a thoracotomy in the operating theatre, either through an anterolateral approach or a median sternotomy, with good light and assistance, and the potential for autotransfusion or bypass, than it is to attempt heroic emergency surgery in the resuscitation area. However, if the patient is in extremis with a falling systolic blood pressure, there is no choice but to proceed immediately with a left anterolateral thoracotomy. In certain circ*mstances, when care is futile, it may not need to be performed at all. A resuscitation room thoracotomy following blunt trauma has limited indications and is rarely successful.

Emergency department thoracotomy EDT should be reserved for those patients suffering penetrating injury in whom signs of life are still present. Patients who have received cardiopulmonary resuscitation (CPR) in the prehospital phase of their care are unlikely to survive, and electrical activity must be present. The survival rates for EDT in patients with penetrating trauma in whom the blood pressure is falling despite adequate resuscitation are shown in Table 28.4. It is important to make a distinction between:

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Figure 28.7 Aortic tear showing presence of stent.

The first principle of all care is to assess and treat the patient according to the physiology. Initial blood loss of more than 1500 mL indicates the potential for class III shock, and any ongoing bleeding must be dealt with surgically, as soon as possible. Similarly, an ongoing blood loss of more than 200 mL/hour for 3 consecutive hours requires resuscitative surgery to stop the bleeding.

• immediate thoracotomy in the emergency department for the

control of haemorrhage, cardiac tamponade, or for internal cardiac massage;

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TORSO TRAUMA Table 28.4 Survival rates for thoracotomy in patients with penetrating trauma.

Blood pressure despite resuscitation

Survival (%)

>60 mmHg >40 mmHg 100 mL of free blood; however, it is very operatorand experience-dependent and, especially if the patient is very obese or the bowel is full of gas, it may be unreliable. Hollow viscus injury is difficult to diagnose, even in experienced hands, and has a low sensitivity (29–35 per cent) for organ injury without haemoperitoneum. FAST is also unreliable for excluding injury in penetrating trauma. If there is doubt, the FAST examination should be repeated (Summary box 28.6). Summary box 28.6 Focused abdominal sonar for trauma ■ ■ ■ ■ ■

It detects free fluid in the abdomen or pericardium It will not reliably detect less than 100 mL of free blood It does not identify injury to hollow viscus It cannot reliably exclude injury in penetrating trauma It may need repeating or supplementing with other investigations

Extensions of the FAST technique to include assessment of the chest for haemothorax and pneumothorax, as well as assessment of the extremities, depend on the experience of the operator and are not yet widely accepted.

Diagnostic peritoneal lavage Diagnostic peritoneal lavage (DPL) is a test used to assess the presence of blood in the abdomen. A gastric tube is placed to empty the stomach and a urinary catheter is inserted to drain the bladder. A cannula is inserted below the umbilicus, directed caudally and posteriorly. The cannula is aspirated for blood (>10 mL is deemed as positive) and, following this, 1000 mL of warmed Ringer’s lactate solution is allowed to run into the abdomen and is then drained out. The presence of >100 000 red cells/µL or >500 white cells/µL is deemed positive (this is equivalent to 20 mL of free blood in the abdominal cavity). In the absence of laboratory facilities, a urine dipstick may be useful. Drainage of lavage fluid via a chest drain indicates penetration of the diaphragm. Although DPL has largely been replaced by FAST (see above under Focused abdominal sonar for trauma), it remains the standard in many institutions where FAST is not available or is

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unreliable. DPL is especially useful in the hypotensive, unstable patient with multiple injuries as a means of excluding intraabdominal bleeding.

Computed tomography CT has become the ‘gold standard’ for the intra-abdominal diagnosis of injury in the stable patient. The scan should be performed using intravenous contrast. CT is sensitive for blood, and individual organ injury, as well as for retroperitoneal injury. An entirely normal abdominal CT is usually sufficient to exclude injury. The following points are important when performing CT: • Despite its tremendous value, it remains an inappropriate investigation for unstable patients. • If duodenal injury is suspected from the mechanism of injury, oral contrast may be helpful. • If rectal and distal colonic injury is suspected in the absence of blood on rectal examination, rectal contrast may be helpful.

Diagnostic laparoscopy Diagnostic laparoscopy (DL) or thoracoscopy may be a valuable screening investigation in stable patients with penetrating trauma, to detect or exclude peritoneal penetration and/or diaphragmatic injury. In most institutions, evidence of penetration requires a laparotomy to evaluate organ injury, as it is difficult to exclude all intra-abdominal injuries laparoscopically. When used in this role DL reduces the non-therapeutic laparotomy rate. DL is not a substitute for open laparotomy, especially in the presence of haemoperitoneum or contamination.

INDIVIDUAL ORGAN INJURY Liver Blunt liver trauma occurs as a result of direct injury. The liver is a solid organ and compressive forces can easily burst the liver substance. The liver is usually compressed between the impacting object and the rib cage or vertebral column. Most injuries are relatively minor and can be managed non-operatively. Many are not even suspected at the time. Penetrating trauma to the liver is relatively common. Bullets have a shock wave and when they pass through a solid structure, such as the liver, they cause significant damage some distance from the actual track of the bullet. Not all penetrating wounds require operative management and a number may stop bleeding spontaneously. In the stable patient, CT is the investigation of choice. It provides information on the liver injury itself, as well as on injuries to the adjoining major vascular and biliary structures. Close proximity injury and injury in which there is a suggestion of a vascular component should be reimaged, as there is a significant risk of the development of subsequent ischaemia. Liver injury can be graded and managed using the American Association for the Surgery of Trauma (AAST) Organ Injury Scale (OIS) (www.aast.org/injury).

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Blood is not an irritant and does not initially cause any abdominal pain. Distension is subjective, and a drop in the blood pressure may be a very late sign in a young fit patient. Examination in unstable patients should take place either in the emergency department or in the operating theatre if the patient is deteriorating rapidly.

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Management The operative management of liver injuries can be summarised as ‘the four Ps’: 1 push;

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2 Pringle; 3 plug; 4 pack.

Summary box 28.7

At laparotomy, the liver is reconstituted as best as possible in its normal position and bleeding is controlled by direct compression (push). The inflow from the portal triad is controlled by a Pringle’s manoeuvre, with direct compression of the portal triad, either digitally or using a soft clamp (Figure 28.9). This has the effect of reducing arterial and portal venous inflow into the liver, although it does not control the backflow from the inferior vena cava and hepatic veins. Any holes due to penetrating injury can be plugged directly and, after controlling any arterial bleeding, the liver can then be packed (see below under Damage control surgery). Bleeding points should be controlled locally when possible and such patients should subsequently undergo angioembolisation. It is not usually necessary to suture penetrating injuries of the liver. If there has been direct damage to the hepatic artery, it can be tied off. Damage to the portal vein must be repaired, as tying off the portal vein carries a greater than 50 per cent mortality rate. If it is not technically feasible to repair the vein at the time of surgery, it should be shunted and the patient referred to a specialist centre. A closed suction drainage system must be left in situ following hepatic surgery. Penetrating injuries and deep tracts can be plugged using silicone tubing or a Sengstaken–Blakemore tube. Finally, the liver can be definitively packed, restoring the anatomy as closely as possible. Placing omentum into cracks in the liver is not recommended (Summary box 28.7).

■ ■ ■ ■ ■ ■

Blunt trauma occurs as the result of direct compression Penetrating trauma of the upper abdomen or lower thorax can damage the liver Computed tomography scanning is the investigation of choice, but only in the stable patient Surgical management consists of push, Pringle, plug and pack The hepatic artery can be tied off, but not the portal vein (stent) Closed suction should always be used

Spleen Splenic injury occurs from direct blunt trauma. Most isolated splenic injuries, especially in children, can be managed nonoperatively. However, in adults, especially in the presence of other injury, age >55 years, or physiological instability, splenectomy should be considered. The spleen can be packed, repaired or placed in a mesh bag. Splenectomy may be a safer option, especially in the unstable patient with multiple potential sites of bleeding and who is >55 years of age, due to risk of rebleed. In certain situations, selective angioembolisation of the spleen can play a role. Following splenectomy, there are significant though transient changes to blood physiology. The platelet and white count rises and may mimic sepsis.

Pancreas

Biliary injuries Isolated traumatic biliary injuries are rare, occur mainly from penetrating trauma, and often occur in association with injuries to other structures that lie in close proximity. The common bile duct can be repaired over a T-tube or drained and referred to appropriate care as part of damage control.

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Liver trauma

Hepatic artery

Portal vein

Most pancreatic injury occurs as a result of blunt trauma. The major problem is that of diagnosis, because the pancreas is a retroperitoneal organ. CT remains the mainstay of accurate diagnosis. Amylase estimation is only relatively sensitive. Classically, the pancreas should be treated with conservative surgery and closed suction drainage. Injuries are treated according to the OIS system of the AAST. Injuries to the tail are treated by closed suction drainage, with distal pancreatectomy if the duct is involved. Proximal injuries (to the right of the superior mesenteric artery) are treated as conservatively as possible, although partial pancreatectomy may be necessary. The pylorus can be temporarily closed (pyloric exclusion) in association with a gastric drainage procedure. A Whipple’s procedure (pancreaticoduodenectomy) is rarely needed and should not be performed in the emergency situation because of the very high associated mortality rate. A damage control procedure with packing and drainage should be performed and the patient referred for definitive surgery once stabilised.

Stomach Most stomach injuries are caused by penetrating trauma. Blood may be present and is diagnostic if found in the nasogastric tube. Surgical repair is required but great care must be taken to examine the stomach fully, as an injury to the front of the stomach can be expected to have an ‘exit’ wound elsewhere on the organ.

Duodenum Figure 28.9 The Pringle manoeuvre.

Duodenal injury is frequently associated with injuries to the

James Hogarth Pringle, 1863–1941, Australian-born surgeon, Royal Infirmary, Glasgow, UK. Robert William Sengstaken, born 1923, surgeon, Garden City, NY, USA. Arthur Hendley Blakemore, 1897–1970, Associate Professor of Surgery, The College of Physicians and Surgeons, Columbia University, New York, NY, USA. Allen Oldfather Whipple, 1881–1963, Valentine Mott Professor of Surgery, The College of Physicians and Surgeons, Columbia University, New York, NY, USA.

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Damage control

adjoining pancreas. Like the pancreas, the duodenum lies retroperitoneally and so injuries are hidden and only discovered late or at laparotomy performed for other reasons. The only sign may be gas in the periduodenal tissue seen at CT. Smaller injuries can be repaired primarily. Major injuries and those also involving the head of the pancreas should undergo initial damage control surgery and be referred for definitive care.

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Generally, renal injury is managed non-operatively unless the patient is unstable. The kidney can be angioembolised if required. Ureteric injury is rare and is generally due to penetrating injury. Most ureters can be repaired or diverted if necessary. Intraperitoneal ruptures of the bladder, usually from direct blunt injury, will require surgical repair. Extraperitoneal ruptures are usually associated with a fracture of the pelvis and will heal with adequate urine drainage (Summary box 28.8).

Small bowel

Colon Injuries to the colon from blunt injury are relatively infrequent, and are a more frequent penetrating injury. If relatively little contamination is present and the viability is satisfactory, such wounds can be repaired primarily. If, however, there is extensive contamination, the patient is physiologically unstable, or the bowel is of doubtful viability, then the colon can be closed off and a defunctioning colostomy formed.

Rectum Only 5 per cent of colon injuries involve the rectum. These are generally from a penetrating injury, although occasionally the rectum may be damaged following fracture of the pelvis. Digital rectal examination will reveal the presence of blood, which is evidence of colorectal injury. These injuries are often associated with bladder and proximal urethral injury. With intraperitoneal injuries, the rectum is managed as for colonic injuries. Full-thickness extraperitoneal rectal injuries should be managed with either a diverting end-colostomy and closure of the distal end (Hartmann’s procedure) or a loop colostomy. Presacral drainage is generally no longer used.

Renal and urological tract injury In the stable patient, CT scanning with contrast is the investigation of choice. For assessment of bladder injury, a cystogram should be performed. A minimum of 400 mL of contrast is instilled into the bladder via a urethral catheter. The large volume is essential because a small volume may not produce a leak from a small bladder injury once the cystic muscle has contracted. It is important to assess the films as follows:

• with two views: anteroposterior and lateral; • on two occasions: full and post-micturition.

Summary box 28.8 Injuries to structures in the abdomen ■ ■ ■ ■ ■ ■ ■

In children, splenic injury can be managed non-operatively Duodenal injuries are associated with pancreatic damage Small bowel injuries need urgent repair Large bowel injuries can be resected and stapled off Rectal injuries may be best managed initially with a defunctioning colostomy Kidney and urinary tract damage is best diagnosed with enhanced computed tomography scanning Intra-abdominal bladder tears need formal repair and drainage

ABDOMINAL COMPARTMENT SYNDROME AND THE OPEN ABDOMEN Raised intra-abdominal pressure has far-reaching consequences for the patient; the syndrome that results is known as abdominal compartment syndrome (ACS). ACS is a major cause of morbidity and mortality in the critically ill patient and its early recognition is essential (Table 28.6). In all cases of abdominal trauma in which the development of ACS in the immediate postoperative phase is considered a risk, the abdomen should be left open and managed as for damage control surgery.

DAMAGE CONTROL Following major injury, protracted surgery in the physiologically unstable patient can in itself prove fatal. Patients with the ‘deadly triad’ of hypothermia, acidosis and coagulopathy are those at highest risk. ‘Damage control’ or ‘damage limitation surgery’ is a concept that originated from naval strategy, whereby a ship which has been damaged may have minimal repairs needed to prevent it from sinking, while definitive repairs wait until it has reached port. The minimum surgery needed to stabilise the patient’s condition may be the safest course until the physiological derangement can be corrected. Damage control surgery is restricted to only two goals: 1 stopping any active surgical bleeding; 2 controlling any contamination. Once these goals have been achieved, then the operation is suspended and the abdomen temporarily closed. The patient’s resuscitation then continues in the intensive care unit. Once the physiology has been corrected, the patient warmed and the coagulopathy corrected, the patient is returned to the operating theatre for any definitive surgery.

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The small bowel is frequently injured as a result of blunt trauma. The individual loops may be trapped, causing high-pressure rupture of a loop or tearing of the mesentery. Small bowel injuries need urgent repair. Haemorrhage control takes priority and these wounds can be temporarily controlled with simple sutures. The small bowel can also be temporarily occluded until haemorrhage control has been achieved. In blunt trauma, the mesenteric vessels damage, and the bowel ischaemia which results, may dictate the extent of a resection. Resections should be carefully planned to limit the loss of viable small bowel but should be weighed against an excessive number of repairs or anastomoses. Haematomas in the small bowel mesenteric border need to be explored to rule out perforation. With low-energy wounds, primary repair can be performed after debridement of any dead tissue, whereas more destructive wounds associated with military-type weapons require resection and anastomosis.

Henri Albert Charles Antoine Hartmann, 1860–1952, Professor of Clinical Surgery, Faculty of Medicine, University of Paris, France.

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TORSO TRAUMA Table 28.6 Effect of raised intra-abdominal pressure on individual organ function.

Organ

Effect

Increase in renal vascular resistance leading to a reduction in glomerular filtration rate and impaired renal function Cardiovascular Decrease in venous return resulting in decreased cardiac output because of both a reduction in preload and an increase in afterload Respiratory Increased ventilation pressures because of splinting of the diaphragm, decreased lung compliance and increased airway pressures Visceral perfusion Reduction in visceral perfusion Intracranial effects Severe rises in intracranial pressures

Table 28.8 Indications for damage control surgery.

Anatomical

Renal

Physiological (decline of physiological reserve)

Damage control resuscitation The concept of damage control has been broadened to include the techniques used in resuscitation as well as in surgery. The time in the emergency department is minimised and the majority of resuscitation of the patient is carried out in the operating room and not in the resuscitation bay (Table 28.7). The resuscitation is individualised through repeated point of care (POC) testing of haemoglobin, acidosis (pH and lactate) and thrombo-elastography to assess clotting, and is therefore directed towards the early delivery of biologically active colloids, clotting products, and whole blood in order to buy time. The physiological disturbances that are associated with the downward spiral of acidosis, coagulopathy and hypothermia in these serious injuries are predicted and attempts are made to avoid them rather than react to them.

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Damage control surgery The decision that damage control surgery is the appropriate course should be made early (Table 28.8) and allows the whole surgical and anaesthetic team to work together to limit the time in surgery and the earliest possible admission of the patient to the intensive care unit. Damage control is a staged process. The initial focus is haemorrhage control, followed by control and limitation of contamination, achieved using a range of abbreviated techniques including simple ligation of bleeding vessels, shunting of major arteries and veins, drainage, temporary stapling off of bowel, and therapeutic packing. Following the above, the abdomen is closed in a temporary fashion using a sheet of plastic (e.g. Opsite) over the bowel, an intermediate pack to allow suction, and a further sheet of adherent plastic drape to the skin to form a watertight and airtight seal. Suction is applied to the intermediate pack area to collect

Environmental

Inability to achieve haemostasis Complex abdominal injury, e.g. liver and pancreas Combined vascular, solid and hollow organ injury, e.g. aortic or caval injury Inaccessible major venous injury, e.g. retrohepatic vena cava Demand for non-operative control of other injuries, e.g. fractured pelvis Anticipated need for a time-consuming procedure Temperature 60 s >10 units blood transfused Systolic blood pressure 60 min Operating time >60 min Inability to approximate the abdominal incision Desire to reassess the intra-abdominal contents (directed relook)

abdominal fluid. This technique is known as the ‘Vacpac’ or ‘Opsite sandwich’ (Figure 28.10). As soon as control has been achieved, the patient is transferred to the intensive care unit where resuscitation is continued. The next stage following damage control surgery and physiological stabilisation is definitive surgery. The team should aim to perform definitive anastomoses, vascular reconstruction and closure of the body cavity within 24–72 hours of injury. However, this must be individualised to the patient, the response to critical care resuscitation, and the progression of injury complexes.

Table 28.7 The stages of damage control surgery.

Stage I II III IV V

Patient selection Control of haemorrhage and control of contamination Resuscitation continued in the intensive care unit Definitive surgery Abdominal closure

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Figure 28.10 Abdominal closure following damage control surgery.

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Further reading

The abdomen is closed as soon as possible, bearing in mind the risks of ACS. The closure is not without its own morbidity. Successful closure may require aggressive off-loading of fluid and even haemofiltration to achieve this, if the patient will tolerate it. The best situation is closure of the abdominal fascia, or, if this cannot be achieved, then skin closure only. Occasionally, mesh closure can be used, with skin grafting over the mesh and subsequent abdominal wall reconstruction. Thoracic damage control is conceptually based on the same philosophy. This is that haemorrhage control and focused surgical procedures minimise further surgical insult, and lead to improved survival in the unstable trauma patient. The aim is to control bleeding and limit air leaks using the fastest procedures available to minimise the operative time. The indications and techniques for emergency thoracotomy have already been described. Damage control applies equally to the extremities. In this case, it is shunting of blood vessels, identifying and marking damaged structures, such as nerves, fasciotomy and removal of contaminated tissue which are the main tasks. Subsequent definitive management can be carried out at a later stage (Summary box 28.9).

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demonstration of ongoing bleeding in splenic and renal injury is a valuable technique.

NON-OPERATIVE MANAGEMENT Non-operative management is universally preferred for the management of solid organ injury in haemodynamically stable children. Non-operative management of solid abdominal organ injury has rapidly gained acceptance in the management of adults as well. A stable patient and accurate CT imaging are prerequisites for this approach. Failure of non-operative management is uncommon and typically occurs within the first 12 hours after injury. Therefore, if correctly selected, the vast majority of these patients will avoid surgery, require less blood transfusion, and sustain fewer complications than operated patients.

Antibiotics in torso trauma There is no level 1 evidence to recommend the use of antibiotics for the insertion of chest drains. However, they should be used in all cases of penetrating abdominal trauma.

FURTHER READING Summary box 28.9 Damage control surgery ■ ■ ■ ■

Resuscitation is carried out in the operating theatre using biologically active fluids The surgery performed is the minimum needed to stabilise the patient The aims of surgery are to control haemorrhage and limit contamination Secondary surgery is aimed at definitive repair

INTERVENTIONAL RADIOLOGY

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Interventional radiology can be useful in the management of torso trauma as both an investigative and a therapeutic tool for patients with vascular injury. Angioembolisation following

American Association for the Surgery of Trauma. Organ injury scaling system. Last accessed February 2011. Available from www.aast.org. American College of Surgeons. Advanced trauma life support course manual for doctors. Chicago, IL: American College of Surgeons, 2008. Boffard KD (ed.). Definitive surgery of trauma care, 3rd edn. London: Hodder Arnold, 2011. Eastern Association for the Surgery of Trauma. Guidelines for practice management: evidence-based guidelines. 4a: Blunt aortic injury; 4b: Blunt myocardial injury; 4c: Evaluation of blunt abdominal trauma; 4d: Non-operative management of liver and spleen; 4e: Penetrating intraperitoneal colon injuries; 4f: Pain management in blunt thoracic trauma; 4g: Prophylactic antibiotics in penetrating abdominal trauma; 4h: Prophylactic antibiotics in tube thoracostomy. Last accessed 2011. Available from www.east.org. Moore EE, Feliciano DV, Mattox LK (eds). Trauma, 6th edn. New York: McGraw Hill, 2008. World Society for Abdominal Compartment Syndrome. Abdominal compartment syndrome. Last accessed February 2011. Available from www.wsacs.org.

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CHAPTER

Extremity trauma LEARNING OBJECTIVES

To gain an understanding of: • How to identify whether an injury exists • The important injuries not to miss • The principles of the description and classification of fractures

INTRODUCTION The objective when treating any injured person is to restore maximum function with minimum risk. So, the first duty is to identify and treat any immediate threats to life. Following the Advanced Trauma Life Support (ATLS) system (see Chapter 24), management of skeletal injuries starts after the primary survey and initial resuscitation have been completed. Very occasionally, the haemorrhage associated with a fracture may be life-threatening. For example, a pelvic injury may require urgent stabilisation, or a major open fracture needs direct pressure to control blood loss.

DIAGNOSIS, DESCRIPTION AND CLASSIFICATION OF INJURY Missing an injury can be serious, both medically and legally. Table 29.1 contains a list of injuries which are notoriously easy to miss.

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Assessment: history and examination The mechanism of injury and the patient’s description of their symptoms will give the first clues to the injuries which are likely to be found. However, if the trauma was severe enough to cause one injury, then there was enough energy to cause more injuries. Therefore, the identification of one injury is not a reason for satisfaction; it is a warning to search for others. Injuries occur in patterns, e.g. a dislocated knee is often associated with a vascular injury, and a head injury may be accompanied by and mask a fractured cervical spine. In 15 per cent of cases in which a spinal fracture has been identified, there is another spinal injury at a separate site. A repeat examination on the ‘morning after’ ward round is a time for a further secondary survey to search for occult injuries. In the multiply-injured or obtunded patient, it may not be possible to obtain a history. In this case, a top-to-toe clinical examination in the secondary survey is even more important

• The range of available treatments • How to select an appropriate treatment

Table 29.1 Extremity injuries which are notorious for being missed.

Posterior dislocation of the shoulder Lateral condylar mass fracture of the distal humerus Perilunate dislocation Scaphoid fracture Tarsometatarsal fracture dislocation Compartment syndrome Vascular injury with knee dislocation Talar neck fracture Slipped upper femoral epiphysis Achilles tendon rupture

than usual. The patient’s pre-injury condition needs to be checked as this may limit recovery.

Principles of investigation A summary of the available methods of investigation is given in Table 29.2. For almost 100 years, the mainstay of the orthopaedic surgeon’s investigation has been the plain radiograph. Radiographs should include orthogonal views (two views at 90° separation) and, for long bones, should show the joints above and below the Sir John Charnley, 1911–1982, Professor of Orthopaedic Surgery, the University of Manchester, Manchester, UK. He pioneered the hip replacement operation. In 1962, he moved his practice to Wrightington Hospital, Appley Bridge, which became a place of pilgrimage for young orthopaedic surgeons from all over the world wishing to specialise in hip replacement. In the same hospital, the John Charnley Research Institute was opened by his wife in 1992. In September 2010, the Royal Mail issued a series of stamps commemorating medical breakthroughs. The 60p stamp featured John Charnley’s hip replacement operation as an x-ray. Hugh Owen Thomas, 1834–1891, a general practitioner of Liverpool, UK. He is regarded as the ‘founder of orthopaedic surgery’, although never holding a hospital appointment preferring to treat patients in their own homes. He introduced the Thomas splint in 1875. Gavriil Abramovich Ilizarov, 1921–1993, orthopaedic surgeon, Kurgan, Western Siberia, Russia. He did not attend school until he was 11 years old as his family was too poor to buy him shoes.

Sir Isaac Newton, 1642–1727, Lucasian Professor of Mathematics, Cambridge University, Cambridge, UK.

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Table 29.2 Investigation modalities.

Modality

Good for

Problems

Plain radiographs Computed tomography

Radiation. Not good for soft tissues Radiation dose. Availability. Safety in severe injuries

Ultrasound scan Magnetic resonance imaging

Fractures and dislocations. Easily available Bony spinal injury Global view in polytrauma Planning treatment of complex fractures Soft-tissue injuries Soft-tissue problems and fractures

Bone scan Fluoroscopy

Stress fractures and tumours Checking progress of surgery

(a)

(b)

(c)

(d)

should be actively sought whenever there is any chance that they may be present (Summary box 29.1). Summary box 29.1 Finding an injury ■ ■

Look specifically for ‘easily missed injuries’ Re-examine the multiply injured patient

Achilles, the Greek hero was the son of Peleus and Thetis. When he was a child, his mother dipped him in the Styx, one of the rivers of the Underworld so that he should be invulnerable in battle. The heel by which she held him did not get wet, and was, therefore, not protected. Achilles died from a wound in the heel received at the seige of Troy.

Figure 29.1 Posterior dislocation of the shoulder. (a) Anteroposterior view; (b) origin of the light bulb sign; (c) axial projection demonstrating how much easier it is to visualise the injury on this view; (d) axial projection highlighting this point and further demonstrating the impacted fracture in the humeral head, or Hill–Sachs lesion.

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injury. Other imaging modalities are now being used more frequently. Computed tomography (CT) scans are invaluable for defining more complex patterns of a fracture, particularly adjacent to a joint. They are now also being used for the global assessment of the multiply-injured person. As scan acquisition times decrease and physiological monitoring improves, the dangers for the multiply-injured patient of being isolated in a scanner are reduced and the benefits of accurate diagnosis increased. Ultrasound is used to assess soft-tissue structures, e.g. Achilles tendon or rotator cuff injuries. Magnetic resonance imaging (MRI) is used primarily to show soft-tissue injury, particularly around the knee. Injuries with a reputation for being missed, such as a posterior dislocation of the shoulder (Figure 29.1),

Operator dependency Availability and expensive Difficult to use in the ventilated patient Radiation dose Small field of view Quality Image distortion

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DESCRIPTION AND CLASSIFICATION OF MUSCULOSKELETAL INJURY Description of injury The soft-tissue injury There are two components of soft-tissue injury that need to be identified: the degree of damage to the soft-tissue envelope around the fracture and the integrity of the important structures passing through the area, primarily the arteries and nerves. A fracture is defined as open when the haematoma associated with it is exposed by a breach in an epithelial surface; this is usually skin, but is sometimes mucous membrane of the bowel or vagin*. When there is such a wound, it should be described in plain terms, e.g. ‘a ragged 6-cm laceration over the anterior aspect of the midshaft of the left tibia with contused skin edges, but no gross contamination’. To minimise contamination, the wound, with a scale beside it, should be photographed and then covered. It should not be disturbed again until definitive treatment is given in an operating theatre. Even if there is no wound, the damage to the soft-tissue envelope will need describing. There may still be bruising, swelling, contusion, tissue shearing or crushing. Severe soft-tissue swelling may make it wise to delay surgery.

Spiral

Angulation

Oblique

Transverse

Translation

Wedge

Shortening

Segmental

Rotation

Figure 29.2 Descriptive terms for fractures.

Injuries to arteries and nerves Major arterial injuries may be limb or life threatening. Distal neurovascular status should always be checked and recorded, especially if there is penetrating trauma, a dislocation or a displaced fracture. This record should be specific, e.g. ‘dorsalis pedis present’ or ‘capillary refill 5 mm), a percutaneous repair can be performed.

Hand injuries Scaphoid fracture

The scaphoid is made up of the proximal and distal poles, a tubercle and the waist. The proximal pole is completely intraarticular and receives all of its blood supply from the distal branches of the radial artery. This enters the scaphoid in a retrograde fashion (distal to proximal). Therefore, fractures across the waist of the scaphoid are most at risk of non-union or avascular necrosis. In contrast, distal pole fractures tend to heal without problems. Figure 29.24 shows a scaphoid fracture and demonstrates how awkward it can be to make the diagnosis on standard anteroposterior and lateral views of the wrist. The scaphoid is the most commonly injured carpal bone. The mechanism of injury is typically a fall onto the out-

stretched hand with the wrist in radial deviation and dorsiflexed. Fractures of the scaphoid waist occur most frequently. Examination usually reveals tenderness in the anatomical snuffbox. The suspected diagnosis is initially based on clinical findings. Plain radiographs may not show a fracture line for up to 10 days. Therefore, a patient with an equivocal examination has the wrist and thumb immobilised in a cast to reduce the risk of non-union and subsequent avascular necrosis. A repeat clinical and radiographic assessment should be performed between 10 and 14 days post-injury. If a fracture line is now seen, then the cast is reapplied for a further 6 weeks. If the radiographs are normal but clinical suspicion remains, further imaging using a bone scan or MRI should be perfomed. Open reduction (using a compression screw) is required for unstable fractures (>1 mm displacement or angulation). Complications of scaphoid fractures include non-union, avascular necrosis, malunion and carpal instability.

Lunate dislocation

The lunate forms a part of the proximal row of the carpus with the scaphoid and triquetrum. Articulating with the radius, this row forms the radiocarpal joint.

Jacques Lisfranc de St Martin, 1790–1847, Professor of Surgery and Operative Medicine, Paris, France. Franklin Adin Simmonds, 1911–1983, orthopaedic surgeon, The Rowley Bristow Hospital, Pyrford, UK.

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Management by type and region (ai)

(aii)

383

The lunate resides in the concavity of the lunate fossa of the distal radius. Interosseus ligaments hold it to the adjacent scaphoid and triquetrum. Perilunate dislocations are often unrecognised. Clinical examination reveals significant swelling of the entire carpus. In the absence of a fracture on x-ray, this is diagnostic of carpal dissociation. The diagnosis is made with plain radiographs, but these can be difficult to interpret (Figure 29.25); the lateral view demonstrates the ‘spilled tea cup sign’ with volar tilt of the lunate. Acute injuries may be initially treated with closed reduction and casting. Irreducible or unstable injuries require open reduction and stabilisation with K-wires. Note that associated injuries, such as scaphoid and radial styloid fractures, as well as median nerve injury, should be excluded.

Thumb metacarpophalangeal ulnar collateral ligament (b)

(c)

The integrity of this ligament is important for effective lateral key pinch. Injury to the ulnar collateral ligament is commonly referred to as ‘gamekeeper’s thumb’ or ‘skier’s thumb’, and is caused by the thumb being forced laterally away from the rest of the hand. Tenderness is located on the ulnar aspect of the metacarpophalangeal joint. To assess the integrity of the ligament, perform a stress test.

(a)

(d)

(b)

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Cap Rad Lun

Figure 29.24 Scaphoid fracture. (a) Anteroposterior and lateral views in which the injury is difficult to see. (b and c) Oblique views with the fracture line highlighted. (d) In this case of a young patient, the fracture was treated with early fixation.

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Figure 29.25 Perilunate dislocation. (a) A plain lateral radiograph of the wrist. (b) The outline of the perilunate dislocation is highlighted. Cap, capitate; Lun, lunate; Rad, radius.

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Cast immobilisation can be used in the treatment of partial tears with a good endpoint. A complete tear with instability (excessive opening of the joint when compared with the other side), or a displaced fracture, requires open repair as the ends of the ruptured ligament may become separated by the aponeurosis of adductor pollicis so that natural healing cannot take place (Stener lesion).

Quality of life

(a)

Pathological failure When abnormal bone gives way under normal load, this is referred to as a pathological fracture. Examples include primary bone tumours and bony metastases, osteomyelitis, metabolic bone disease (osteomalacia, Paget’s disease, osteoporosis) and haematopoietic disease (myeloma, lymphoma, leukaemia). The typical history is of a minor trauma. This alerts the surgeon to the possibility of an underlying bony pathology. Blood tests, a chest radiograph and full-length views of the fractured bone are essential. A bone scan is the most sensitive detector of skeletal disease. In a patient with a primary bone tumour, treatment must be planned to avoid disseminating the disease (see Chapter 39). In a patient who has multiple metastases and whose life span is limited, treatment is aimed at regaining immediate mobility and relief of pain. As can be seen in Figure 29.26, there is a clear rationale for aggressive treatment to restore function despite the risks. The goals of surgical treatment are to reduce pain and to splint the bone so that the patient can use it. Femoral, tibial and humeral fractures are nailed where possible. Some juxtaarticular fractures that would require protection if treated with ORIF and bone grafting may be mobilised earlier if bone cement is substituted for the graft. Prophylactic stabilisation should be considered in patients with metastases where there has been cortical bone destruction of ≥50 per cent or a femoral lesion longer than 2.5 cm, pathological fracture of the lesser trochanter and persistent pain after irradiation (Summary box 29.9). Summary box 29.9 Pathological failure ■

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■

Do not operate on what might be a primary tumour without careful thought Fractures through secondary tumours are treated aggressively to optimise early function

CONCLUSION The management of extremity trauma is in theory quite straightforward. The first step is to realise that an injury exists as a missed injury cannot be treated. The injury then needs to be understood; this generally involves description and classification. When there is clear evidence as to the best method of treatment for a particular injury, this should be followed. When such evidence is lacking, as is generally the case, the treatment of fractures is generally principle based (Summary box 29.10).

FURTHER READING Bone LR, Johnson KD, Weight J, Scheinberg RJ. Early versus delayed stabilization of femoral fractures. J Bone Joint Surg 1989; 71A: 336–40.

Time Decreased lifespan

(b) Time of injury

Function if injury had not occured Natural history Rehabilitation phase Functional phase Degenerative phase Time

(c)

Time

Figure 29.26 Comparative outcome curves for a normal adult (a), pathological fracture (b) and paediatric fracture (c). (a) The generic outcome curve for a patient with a life expectancy of >20 years. There is a rehabilitation, functional and degenerative phase to consider. (b) It is seen that the short life expectancy of a patient with a pathological fracture secondary to metastases means that only the rehabilitation phase is relevant. The patient must be able to function before bone healing. This justifies aggressive treatment. (c) The paediatric fracture with benign natural history. Any marginal early gain has to be considered in the light of great potential for long-term detriment should there be complications.

Summary box 29.10 Summary of extremity trauma ■ ■ ■ ■ ■

Realise that an injury exists Find the characteristics of the injury, describe and classify it Consider the natural history of the injury Treatment is guided by outcome if known or by principle if not Beware of injuries that are ‘easily missed’

Charnley J. The closed treatment of common fractures. Edinburgh: E&S Livingstone, 1950. Gustilo RB, Anderson JT. Prevention of infection in the treatment of 1025 open fractures of long bones. J Bone Joint Surg 1976; 8A: 453–8. Mast J, Jakob R, Ganz R. Planning and reduction technique in fracture surgery. Berlin: Springer-Verlag, 1989. Muller ME, Nazarian S, Koch P. The AO classification of fractures. Schatzker J (trans). Berlin: Springer-Verlag, 1988.

Sir James Paget, 1814–1899, surgeon, St Bartholomew’s Hospital, London, UK.

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CHAPTER

Burns LEARNING OBJECTIVES

INTRODUCTION The incidence of burn injury varies greatly between cultures. In the United Kingdom (with its population of 65 million), each year around 175 000 people visit accident and emergency (A&E) departments suffering from burns, of whom about 13 000 need to be admitted. About 1000 have severe burns requiring fluid resuscitation, and half of the victims are under 16 years of age. The majority of burns in children are scalds caused by accidents with kettles, pans, hot drinks and bath water. Among adolescent patients, the burns are usually caused by young males experimenting with matches and flammable liquids. In adults, scalds are not uncommon, but are less frequent than flame burns. Most electrical and chemical injuries occur in adults. Cold and radiation are very rare causes of burns. Associated conditions in adults, such as mental disease (attempted suicide or assault), epilepsy and alcohol or drug abuse, are underlying factors in as many as 80 per cent of patients with burns admitted to hospital in some populations. Legislation, health promotion and appliance design have reduced the incidence of burns, with regulations regarding flameretardant clothes and furniture, the promotion of smoke alarms, the design of cookers and gas fires, the almost universal use of cordless kettles and the education of parents to keep their hot water thermostat to 60°C all playing their part (Summary box 30.1).

• Techniques for treating burns and the patient • The pathophysiology of electrical and chemical burns

will see a better understanding of the control of physiology along with improvements in reconstruction and rehabilitation. A large burn injury will have a significant effect on the patient’s family and friends and the patient’s future. The importance of multidisciplinary care needs to be stressed for the adequate and effective care of the burn patient.

THE PATHOPHYSIOLOGY OF BURN INJURY Burns cause damage in a number of different ways, but by far the most common organ affected is the skin. However, burns can also damage the airway and lungs, with life-threatening consequences. Airway injuries occur when the face and neck are burned. Respiratory system injuries usually occur if a person is trapped in a burning vehicle, house, car or aeroplane and is forced to inhale the hot and poisonous gases (Summary box 30.2). Summary box 30.2 Warning signs of burns to the respiratory system ■ ■ ■ ■

Summary box 30.1 Prevention of burns A significant proportion of burns can be prevented by: ■ Implementing good health and safety regulations ■ Educating the public ■ Introducing of effective legislation

The last 50 years have seen great strides made to reduce both morbidity and mortality from burn injuries. The coming years

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To assess: • The area and depth of burns To understand: • Methods for calculating the rate and quantity of fluids to be given

Burns around the face and neck A history of being trapped in a burning room Change in voice Stridor

INJURY TO THE AIRWAY AND LUNGS Physical burn injury to the airway above the larynx The hot gases can physically burn the nose, mouth, tongue, palate and larynx. Once burned, the linings of these structures will start to swell. After a few hours, they may start to interfere with

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the larynx and may completely block the airway if action is not taken to secure an airway (Summary box 30.3). Summary box 30.3 Dangers of smoke, hot gas or steam inhalation ■ ■ ■ ■ ■

Inhaled hot gases can cause supraglottic airway burns and laryngeal oedema Inhaled steam can cause subglottic burns and loss of respiratory epithelium Inhaled smoke particles can cause chemical alveolitis and respiratory failure Inhaled poisons, such as carbon monoxide, can cause metabolic poisoning Full-thickness burns to the chest can cause mechanical blockage to rib movement

Physical burn injury to the airway below the larynx This is a rare injury as the heat exchange mechanisms in the supraglottic airway are usually able safely to absorb the heat from hot air. However, steam has a large latent heat of evaporation and can cause thermal damage to the lower airway. In such injuries, the respiratory epithelium rapidly swells and detaches from the bronchial tree. This creates casts, which can block the main upper airway.

Metabolic poisoning

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There are many poisonous gases that can be given off in a fire, the most common being carbon monoxide, a product of incomplete combustion that is often produced by fires in enclosed spaces. This is the usual cause of a person being found with altered consciousness at the scene of a fire. Carbon monoxide binds to haemoglobin with an affinity 240 times greater than that of oxygen and therefore blocks the transport of oxygen. Levels of carboxyhaemoglobin in the bloodstream can be measured. Concentrations above 10 per cent are dangerous and need treatment with pure oxygen for more than 24 hours. Death occurs with concentrations around 60 per cent. Another metabolic toxin produced in house fires is hydrogen cyanide, which causes a metabolic acidosis by interfering with mitochondrial respiration.

Inhalational injury Inhalational injury is caused by the minute particles within thick smoke, which, because of their small size, are not filtered by the upper airway, but are carried down to the lung parenchyma. They stick to the moist lining, causing an intense reaction in the alveoli. This chemical pneumonitis causes oedema within the alveolar sacs and decreasing gaseous exchange over the ensuing 24 hours (Figure 30.1), and often gives rise to a bacterial pneumonia. Its presence or absence has a very significant effect on the mortality of any burn patient.

Mechanical block on rib movement Burned skin is very thick and stiff, and this can physically stop the ribs moving if there is a large full-thickness burn across the chest.

Figure 30.1 The swelling that occurs with inflammation due to burns.

INFLAMMATION AND CIRCULATORY CHANGES The dangers to the airway and respiration described above are readily apparent, but the cause of circulatory changes following a burn are more complex. The changes occur because burned skin activates a web of inflammatory cascades. The release of neuropeptides and the activation of complement are initiated by the stimulation of pain fibres and the alteration of proteins by heat. The activation of Hageman factor initiates a number of protease-driven cascades, altering the arachidonic acid, thrombin and kallikrein pathways. At a cellular level, complement causes the degranulation of mast cells and coats the proteins altered by the burn. This attracts neutrophils, which also degranulate, with the release of large quantities of free radicals and proteases. These can, in turn, cause further damage to the tissue. Mast cells also release primary cytokines such as tumour necrosis factor alpha (TNF-a). These act as chemotactic agents to inflammatory cells and cause the subsequent release of many secondary cytokines. These inflammatory factors alter the permeability of blood vessels such that intravascular fluid escapes. The increase in permeability is such that large protein molecules can also now escape with ease. The damaged collagen and these extravasated proteins increase the oncotic pressure within the burned tissue, further increasing the flow of water from the intravascular to the extravascular space (Figure 30.2). The overall effect of these changes is to produce a net flow of water, solutes and proteins from the intravascular to the extravascular space. This flow occurs over the first 36 hours after the injury, but does not include red blood cells. In a small burn, this reaction is small and localised but, as the burn size approaches 10–15 per cent of total body surface area (TBSA), the loss of intravascular fluid can cause a level of circulatory shock. Furthermore, once the area increases to 25 per cent of TBSA, the inflammatory reaction causes fluid loss in vessels remote from the burn injury. This is why such importance is

John Hageman was a 37-year-old railroad brakeman in whom this factor deficiency was discovered by Dr Oscar Ratnoff in 1955.

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(b)

387

damage and ischaemia to the gut mucosa. This reduces gut motility and can prevent the absorption of food. Failure of enteral feeding in a patient with a large burn is a life-threatening complication. This process also increases the translocation of gut bacteria, which can become an important source of infection in large burns. Gut mucosal swelling, gastric stasis and peritoneal oedema can also cause abdominal compartment syndrome, which splints the diaphragm and increases the airway pressures needed for respiration.

Danger to peripheral circulation In full-thickness burns, the collagen fibres are coagulated. The normal elasticity of the skin is lost. A circumferential fullthickness burn to a limb acts as a tourniquet as the limb swells. If untreated, this will progress to limb-threatening ischaemia (Summary box 30.5). Summary box 30.5 Other complications of burns ■

Figure 30.2 A scald burn (a) and its laser doppler image (b) showing burn depth. Red and pink areas are superficial burns, which should heal with conservative dressings.

Summary box 30.4 The shock reaction after burns ■ ■ ■ ■ ■

Burns produce an inflammatory reaction This leads to vastly increased vascular permeability Water, solutes and proteins move from the intra- to the extravascular space The volume of fluid lost is directly proportional to the area of the burn Above 15 per cent of surface area, the loss of fluid produces shock

■

IMMEDIATE CARE OF THE BURN PATIENT Pre-hospital care The principles of pre-hospital care are:

• Ensure rescuer safety. This is particularly important in house fires and in the case of electrical and chemical injuries.

• Stop the burning process. Stop, drop and roll is a good •

•

OTHER LIFE-THREATENING EVENTS WITH MAJOR BURNS The immune system and infection The inflammatory changes caused by the burn have an effect on the patient’s immune system. Cell-mediated immunity is significantly reduced in large burns, leaving them more susceptible to bacterial and fungal infections. There are many potential sources of infection, especially from the burn wound and from the lung if this is injured, but also from any central venous lines, tracheostomies or urinary catheters present.

Changes to the intestine The inflammatory stimulus and shock can cause microvascular

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Infection from the burn site, lungs, gut, lines and catheters Malabsorption from the gut Circumferential burns may compromise circulation to a limb

• •

method of extinguishing fire burning on a person. Check for other injuries. A standard ABC (airway, breathing, circulation) check followed by a rapid secondary survey will ensure that no other significant injuries are missed. Patients burned in explosions or even escaping from fires may have head or spine injuries and other life-threatening problems. Cool the burn wound. This provides analgesia and slows the delayed microvascular damage that can occur after a burn injury. Cooling should occur for a minimum of 10 minutes and is effective up to 1 hour after the burn injury. It is a particularly important first aid step in partial-thickness burns, especially scalds. In temperate climates, cooling should be at about 15°C, and hypothermia must be avoided. Give oxygen. Anyone involved in a fire in an enclosed space should receive oxygen, especially if there is an altered consciousness level. Elevate. Sitting a patient up with a burned airway may prove life-saving in the event of a delay in transfer to hospital care. Elevation of burned limbs will reduce swelling and discomfort.

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attached to measuring the TBSA involved in any burn. It dictates the size of inflammatory reaction and therefore the amount of fluid needed to control shock (Summary box 30.4).

■

Hospital care The principles of managing an acute burn injury are the same as in any acute trauma case:

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• • • • • •

A, Airway control B, Breathing and ventilation C, Circulation D, Disability – neurological status E, Exposure with environmental control F, Fluid resuscitation.

The possibility of injury additional to the burn must be sought both clinically and from the history, and treated appropriately. The major determinants of severity of any burn injury are the percentage of TBSA that is burned, the presence of an inhalation injury and the depth of the burn (Summary box 30.6). Not all burned patients will need to be admitted to a burns unit, but the main criteria are given in Table 30.1.

Table 30.1 The criteria for acute admission to a burns unit.

Suspected airway or inhalational injury Any burn likely to require fluid resuscitation Any burn likely to require surgery Patients with burns of any significance to the hands, face, feet or perineum Patients whose psychiatric or social background makes it inadvisable to send them home Any suspicion of non-accidental injury Any burn in a patient at the extremes of age Any burn with associated potentially serious sequelae, including high-tension electrical burns and concentrated hydrofluoric acid burns

Summary box 30.6 Major determinants of the outcome of a burn ■ ■ ■

Percentage surface area involved Depth of burns Presence of an inhalational injury

Summary box 30.8 Recognition of the potentially burned airway ■ ■

Airway The burned airway creates problems for the patient by swelling and, if not managed proactively, can completely occlude the upper airway. The treatment is to secure the airway with an endotracheal tube until the swelling has subsided, which is usually after about 48 hours. The symptoms of laryngeal oedema, such as change in voice, stridor, anxiety and respiratory difficulty, are very late symptoms. Intubation at this point is often difficult or impossible owing to swelling, so acute cricothyroidotomy equipment must be at hand when intubating patients with a delayed diagnosis of airway burn. Because of this, early intubation of suspected airway burn is the treatment of choice in such patients. The time-frame from burn to airway occlusion is usually between 4 and 24 hours, so there is time to make a sensible decision with senior staff and allow an experienced anaesthetist to intubate the patient (Summary box 30.7).

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Summary box 30.7 Initial management of the burned airway ■ ■ ■

Early elective intubation is safest Delay can make intubation very difficult because of swelling Be ready to perform an emergency cricothyroidotomy, if intubation is delayed

The key in the management of airway burn is the history and early signs, rather than the symptoms. The history is of inhalation of hot gases such as in a house or car fire. Clues on examination include blisters on the hard palate, burned nasal mucosa and loss of all the hair in the nose (the anterior hairs are often burned), but perhaps the most valuable signs are the presence of deep burns around the mouth and in the neck (Summary box 30.8).

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■

A history of being trapped in the presence of smoke or hot gases Burns on the palate or nasal mucosa, or loss of all the hairs in the nose Deep burns around the mouth and neck

Breathing Inhalational injury Time is also a factor; anyone trapped in a fire for more than a couple of minutes must be observed for signs of smoke inhalation. Other signs that raise suspicion are the presence of soot in the nose and the oropharynx and a chest radiograph showing patchy consolidation. The clinical features are a progressive increase in respiratory effort and rate, rising pulse, anxiety and confusion and decreasing oxygen saturation. These symptoms may not be apparent immediately and can take 24 hours to 5 days to develop. Treatment starts as soon as this injury is suspected and the airway is secure. Physiotherapy, nebulisers and warm humidified oxygen are all useful. The patient’s progress should be monitored using respiratory rate, together with blood gas measurements. If the situation deteriorates, continuous or intermittent positive pressure may be used with a mask or T-piece. In the severest cases, intubation and management in an intensive care unit will be needed. The key, therefore, in the management of inhalational injury is to suspect it from the history, institute early management and observe carefully for deterioration.

Thermal burn injury to the lower airway These rare injuries can occur with steam injuries. Their management is supportive and the same as that for an inhalational injury.

Metabolic poisoning Any history of a fire within an enclosed space and any history of altered consciousness are important clues to metabolic poisoning. Blood gases must be measured immediately if poisoning is a possibility. Carboxyhaemoglobin levels raised above 10 per

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Assessment of the burn wound

cent must be treated with high inspired oxygen for 24 hours to speed its displacement from haemoglobin. Metabolic acidosis is a feature of this and other forms of poisoning. Once again, the key to diagnosing these injuries is suspicion from the history. Blood gas measurement will confirm the diagnosis. The treatment is oxygen.

1 1 2 2

Mechanical block to breathing

13 1½

1½ 1

1½

1½ B

ASSESSMENT OF THE BURN WOUND Assessing size

Summary box 30.9 Assessing the area of a burn ■ ■ ■

The patient’s whole hand is 1 per cent TBSA, and is a useful guide in small burns The Lund and Browder chart is useful in larger burns The rule of nines is adequate for a first approximation only

Assessing depth from the history The first indication of burn depth comes from the history (Table 30.2). The burning of human skin is temperature- and time-dependent. It takes 6 hours for skin maintained at 44°C to suffer irreversible changes, but a surface temperature of 70°C for 1 s is all that is needed to produce epidermal destruction. Taking an example of hot water at 65°C: exposure for 45 s will produce a full-thickness burn, for 15 s a deep partial-thickness burn and for 7 s a superficial partial-thickness burn (Summary box 31.10).

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1¾

2½

1¾

1½

Burn size needs to be formally assessed in a controlled environment. This allows the area to be exposed and any soot or debris washed off. Care should be taken not to cause hypothermia during this stage. In the case of smaller burns or patches of burn, the best measurement is to cut a piece of clean paper the size of the patient’s whole hand (digits and palm), which represents 1 per cent TBSA, and match this to the area. Another accurate way of measuring the size of burns is to draw the burn on a Lund and Browder chart (Figure 30.3), which maps out the percentage TBSA of sections of our anatomy. It also takes into account different proportional body surface area in children according to age. The rule of nines, which states that each upper limb is 9 per cent TBSA, each lower limb 18 per cent, the torso 18 per cent each side and the head and neck 9 per cent, can be used as a rough guide to TBSA outside the hospital environment (Summary box 30.9).

1¾

1½

Relative percentage of area affected by growth Age in years A Head B Thigh C leg

0 9 2 2

1 8 3 2

5 6 4 3

10 5 4 3

15 4 4 3

Adult 3 4 3

Figure 30.3 The Lund and Browder chart.

Table 30.2 Causes of burns and their likely depth.

Cause of burn

Probable depth of burn

Scald

Superficial, but with deep dermal patches in the absence of good first aid. Will be deep in a young infant Deep dermal Mixed deep dermal and full thickness Often deep dermal or full thickness Weak concentrations superficial; strong concentrations deep dermal Full thickness

Fat burns Flame burns Alkali burns, including cement Acid burns Electrical contact burn

Summary box 30.10 Assessing the depth of a burn ■ ■ ■ ■

The history is important – temperature, time and burning material Superficial burns have capillary filling Deep partial-thickness burns do not blanch, but have some sensation Full-thickness burns feel leathery and have no sensation

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Any mechanical block to breathing from the eschar of a significant full-thickness burn on the chest wall is obvious from the examination. There will also be carbon dioxide retention and high inspiratory pressures if the patient is ventilated. The treatment is to make some scoring cuts through the burned skin to allow the chest to expand (escharotomy). The nerves have been destroyed in the skin, and this procedure is not painful for the patient.

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Superficial partial-thickness burns

(a)

The damage in these burns goes no deeper than the papillary dermis. The clinical features are blistering and/or loss of the epidermis. The underlying dermis is pink and moist. The capillary return is clearly visible when blanched. There is little or no fixed capillary staining. Pinprick sensation is normal. Superficial partial-thickness burns heal without residual scarring in 2 weeks. The treatment is non-surgical (Figure 30.4).

Deep partial-thickness burn These burns involve damage to the deeper parts of the reticular dermis (Figure 30.5). Clinically, the epidermis is usually lost. The exposed dermis is not as moist as that in a superficial burn. There is often abundant fixed capillary staining, especially if examined after 48 hours. The colour does not blanch with pressure under the examiner’s finger. Sensation is reduced, and the patient is unable to distinguish sharp from blunt pressure when examined with a needle. Deep dermal burns take 3 or more weeks to heal without surgery and usually lead to hypertrophic scarring (Figure 30.6).

(b)

Full-thickness burns The whole of the dermis is destroyed in these burns (Figure 30.7). Clinically, they have a hard, leathery feel. The appearance can vary from that similar to the patient’s normal skin to charred black, depending upon the intensity of the heat. There is no capillary return. Often, thrombosed vessels can be seen under the skin. These burns are completely anaesthetised: a needle can be stuck deep into the dermis without any pain or bleeding.

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FLUID RESUSCITATION The principle of fluid resuscitation is that the intravascular volume must be maintained following a burn in order to provide sufficient circulation to perfuse not only the essential visceral organs such as the brain, kidneys and gut, but also the peripheral tissues, especially the damaged skin (Summary box 30.11). Intravenous resuscitation is appropriate for any child with a burn greater than 10 per cent TBSA. The figure is 15 per cent TBSA for adults. In some parts of the world, intravenous resuscitation is commenced only with burns that approach 30 per cent TBSA. If oral resuscitation is to be commenced, it is important that the water given is not salt free. It is rarely possible to undergo significant diuresis in the first 24 hours in view of the stress hormones that are present. Hyponatraemia and water intoxication can be fatal. It is therefore appropriate to give oral rehydration with a solution such as Dioralyte®. The resuscitation volume is relatively constant in proportion to the area of the body burned and, therefore, there are formulae that calculate the approximate volume of fluid needed for the

(c)

Summary box 30.11 Fluids for resuscitation ■

■ ■ ■

In children with burns over 10 per cent TBSA and adults with burns over 15 per cent TBSA, consider the need for intravenous fluid resuscitation If oral fluids are to be used, salt must be added Fluids needed can be calculated from a standard formula The key is to monitor urine output

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Figure 30.4 (a) A superficial partial-thickness scald 24 hours after injury. The dermis is pink and blanches to pressure. (b) At 2 weeks, the wound is healed but lacks pigment. (c) At three months, the pigment is returning.

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391

(a)

(b)

Figure 30.6 Hypertrophic scarring following a deep dermal burn.

(a)

(c)

Figure 30.5 (a) A deep dermal burn undergoing tangential shaving. The dead dermis is removed layer by layer until healthy bleeding is seen. The burn is pale because it was dressed with silver sulphadiazine cream, but no blanching was visible under this layer. The patient was unable to differentiate between pressure from the sharp and blunt ends of a needle. (b) A thin, split-thickness graft harvested from the thigh. (c) The thin graft is placed in the dermal remnants. The rete pegs can be seen between the remnants of the dermis through the graft.

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(b)

Figure 30.7 (a) A full-thickness burn on admission just prior to escharotomy. The wound is wrapped in cling film while in transit. The patient’s facial burn is shown in Figure 30.10. (b) Excision of the same full-thickness burn, down to healthy fat.

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resuscitation of a patient of a given body weight with a given percentage of the body burned. These regimens follow the fluid loss, which is at its maximum in the first 8 hours and slows, such that, by 24–36 hours, the patient can be maintained on his or her normal daily requirements. There are three types of fluid used. The most common is Ringer’s lactate or Hartmann’s solution; some centres use human albumin solution or fresh-frozen plasma, and some centres use hypertonic saline. Perhaps the simplest and most widely used formula is the Parkland formula. This calculates the fluid to be replaced in the first 24 hours by the following formula: total percentage body surface area × weight (kg) × 4 = volume (mL). Half this volume is given in the first 8 hours and the second half is given in the subsequent 16 hours.

tachycardia, cool peripheries and a high haematocrit), then a bolus of 10 mL/kg body weight should be given. It is important that patients are not overresuscitated, and urine output in excess of 2 mL/kg body weight per hour should signal a decrease in the rate of infusion. Other measures of tissue perfusion such as acid–base balance are appropriate in larger, more complex burns, and a haematocrit measurement is a useful tool in confirming suspected under- or overhydration. Those with cardiac dysfunction, acute or chronic, may well need more exact measurement of filling pressure, preferably by transoesophageal ultrasound or with the more invasive central line.

Crystalloid resuscitation

Escharotomy

• 100 mL/kg for 24 hours for the first 10 kg; • 50 mL/kg for the next 10 kg; • 20 mL/kg for 24 hours for each kilogram over 20 kg body

Circumferential full-thickness burns to the limbs require emergency surgery (Figure 30.8). The tourniquet effect of this injury is easily treated by incising the whole length of full-thickness burns. This should be done in the mid-axial line, avoiding major nerves (Table 30.3). One should remember that an escharotomy can cause a large amount of blood loss; therefore, adequate blood should be available for transfusion if required. Thereafter, the management of the burn wound remains the same, irrespective of the size of the injury. The burn needs to be cleaned, and the size and depth need to be assessed. Full thickness burns and deep partial-thickness burns that will require operative treatment will need to be dressed with an antibacterial dressing to delay the onset of colonisation of the wound.

Hypertonic saline

Full-thickness burns and obvious deep dermal wounds

Ringer’s lactate is the most commonly used crystalloid. Crystalloids are said to be as effective as colloids for maintaining intravascular volume. They are also significantly less expensive. Another reason for the use of crystalloids is that even large protein molecules leak out of capillaries following burn injury; however, non-burnt capillaries continue to sieve proteins virtually normally. In children, maintenance fluid must also be given. This is normally dextrose–saline given as follows:

weight.

Human albumin solution (HAS) is a commonly used colloid. Hypertonic saline has been effective in treating burns shock for many years. It produces hyperosmolarity and hypernatraemia. This reduces the shift of intracellular water to the extracellular space. Advantages include less tissue oedema and a resultant decrease in escharotomies and intubations.

Colloid resuscitation

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TREATING THE BURN WOUND

Plasma proteins are responsible for the inward oncotic pressure that counteracts the outward capillary hydrostatic pressure. Without proteins, plasma volumes would not be maintained as there would be oedema. Proteins should be given after the first 12 hours of burn because, before this time, the massive fluid shifts cause proteins to leak out of the cells. The most common colloid-based formula is the Muir and Barclay formula:

The four most common dressings for full-thickness and contaminated wounds are listed in Table 30.4.

Dressings with nanocrystalline silver • Silver sulphadiazine cream (1 per cent). This gives broad-

spectrum prophylaxis against bacterial colonisation and is particularly effective against Pseudomonas aeruginosa and also methicillin-resistant Staphylococcus aureus.

• 0.5 × percentage body surface area burnt × weight = one portion;

• periods of 4/4/4, 6/6 and 12 hours, respectively; • one portion to be given in each period.

Monitoring of resuscitation The key to monitoring of resuscitation is urine output. Urine output should be between 0.5 and 1.0 mL/kg body weight per hour. If the urine output is below this, the infusion rate should be increased by 50 per cent. If the urine output is inadequate and the patient is showing signs of hypoperfusion (restlessness with

Figure 30.8 A full-thickness burn to the upper limb with a mid-axial escharotomy. The soot and debris have been washed off.

Alexis Frank Hartmann, 1898–1964, paediatrician, St Louis, MO, USA. Thomas Laird Barclay, d. 2007, formerly plastic surgeon, The Royal Infirmary, Bradford, UK. Ian Fraser Kerr Muir, 1921–2008, formerly plastic surgeon, Aberdeen Royal Infirmary, Aberdeen, UK. Referred to as ‘a gentle giant of plastic surgery’.

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Tr e a t i n g t h e b u r n w o u n d Table 30.3 Key features of escharotomy placement.

Upper limb Hand

Lower limb Chest

General rules

Mid-axial, anterior to the elbow medially to avoid the ulnar nerve Midline in the digits. Release muscle compartments if tight. Best done in theatre and with an experienced surgeon Mid-axial. Posterior to the ankle medially to avoid the saphenous vein Down the chest lateral to the nipples, across the chest below the clavicle and across the chest at the level of the xiphisternum Extend the wound beyond the deep burn Diathermy any significant bleeding vessels Apply haemostatic dressing and elevate the limb postoperatively

393

dressing can make the difference between scar and no scar and/ or operation and no operation. Some of the options for dressing choice are described below. If the wound is heavily contaminated as a result of the accident, then it is prudent to clean the wound formally under a general anaesthetic. With more chronic contamination, silver sulphadiazine cream dressing for 2 or 3 days is very effective and can be changed to a dressing that is more efficient at promoting healing after this period. The simplest method of treating a superficial wound is by exposure. The initial exudate needs to be managed by frequent changes of clean linen around the patient but, after a few days, a dry eschar forms, which then separates as the wound epithelialises. This is often used in hot climates and for small burns on the face. However, this method is painful and requires an intensive amount of nursing support. A variation on this theme is to cover

Table 30.4 Options for topical treatment of deep burns.

(a) 1% silver sulphadiazine cream 0.5% silver nitrate solution Mafenide acetate cream Serum nitrate, silver sulphadiazine and cerium nitrate

• Silver nitrate solution (0.5 per cent). Again, this is highly

(b)

Superficial partial-thickness wounds and mixed-depth wounds Around the world, a wide variety of substances are used to treat these wounds, from honey or boiled potato peel to synthetic biological dressings with live cultured fibroblasts within the matrix. This is testament to the fact that superficial partial-thickness burns will heal almost irrespective of the dressing. Thus, the key lies with dressings that are easy to apply, non-painful, reduce pain, simple to manage and locally available. The choice of dressings does, however, become crucial in the case of burns that border on being deep dermal (Figure 30.9). Here, the choice of

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Figure 30.9 (a) A scald to the chest from boiling water, mainly superficial but in some areas close to being deep dermal. This was treated with a hydrocolloid dressing. (b) There are two tiny areas of hypertrophy indicating how close the burn was to being deep dermal. The good first aid this patient received probably made a difference to the outcome.

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effective as a prophylaxis against Pseudomonas colonisation, but it is not as active as silver sulphadiazine cream against some of the Gram-negative aerobes. The other disadvantage of this solution is that it needs to be changed or the wounds resoaked every 2–4 hours. It also produces black staining of all the furniture surrounding the patient. • Mafenide acetate cream. This is popular, especially in the United States, but is painful to apply. It is usually used as a 5 per cent topical solution, but has been associated with metabolic acidosis. • Silver sulphadiazine and cerium nitrate. This is also a very useful burn dressing, especially for full-thickness burns. It induces a hard effect on the burned skin and has been shown in certain instances, especially in elderly patients, to reduce some of the cell-mediated immunosuppression that occurs in burns. Cerium nitrate forms a sterile eschar and is specially useful in treating burns when a conservative treatment option has been chosen. Cerium nitrate has also been shown to boost cell-mediated immunity in these patients.

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the wound with a permeable wound dressing, such as Mefix® or Fixamol®. This allows the wounds to dry but, because it is a covering, it avoids the problems of the wound adhering to the sheets and clothes. A similar method of managing these types of burn is to place a Vaseline-impregnated gauze (with or without an antiseptic, such as chlorhexidine) over the wound. An alternative is a fenestrated silicone sheet (e.g. Mepitel®). These can then be backed with swabs to absorb the exudate. The Vaseline gauze or silicone layer is used to prevent the swabs adhering to the wound and reduces the stiffness of the dry eschar, preventing it from cracking so easily. The swabs need to be changed after the first 48 hours as they are often soaked. After that, they can be left for longer. More interactive dressings include hydrocolloids and biological dressings. Hydrocolloid dressings need to be changed every 3–5 days. They are particularly useful in mixed-depth burns as the high protease levels under the occlusive dressings aid with the debridement of the deeper areas of burn. They also provide a moist environment, which is good for epithelialisation. Duoderm® is a hydrocolloid dressing. There is good evidence for its value in burns. Biological, synthetic (e.g. Biobrane®) and natural (e.g. amniotic membranes) dressings also provide good healing environments and do not need to be changed. They are ideal for one-stop management of superficial burns, being easy to apply and comfortable. However, they will become detached if applied to deep dermal wounds as the eschar needs to separate. They are therefore not as useful in mixed-depth wounds (Summary box 30.12). Early debridement and grafting is the key to effectively treating deep partial- and full-thickness burns in a majority of cases. Summary box 30.12 Principles of dressings for burns ■ ■ ■

Full-thickness and deep dermal burns need antibacterial dressings to delay colonisation prior to surgery Superficial burns will heal and need simple dressings An optimal healing environment can make a difference to outcome in borderline depth burns

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ADDITIONAL ASPECTS OF TREATING THE BURNED PATIENT Analgesia Acute Analgesia is a vital part of burns management. Small burns, especially superficial burns, respond well to simple oral analgesia, paracetamol and non-steroidal anti-inflammatory drugs. Topical cooling is especially soothing. Large burns require intravenous opiates. Intramuscular injections should not be given in acute burns over 10 per cent of TBSA, as absorption is unpredictable and dangerous.

Subacute In patients with large burns, continuous analgesia is required, beginning with infusions and continuing with oral tablets,

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such as slow-release morphine. Powerful, short-acting analgesia should be administered before dressing changes. Administration may require an anaesthetist, as in the case of general anaesthesia or midazolam and ketamine, or less intensive supervision, as in the case of morphine and nitrous oxide.

Energy balance and nutrition One of the most important aspects in treating burns patients is nutrition. Any adult with a burn greater than 15 per cent (10 per cent in children) of TBSA has an increased nutritional requirement. All patients with burns of 20 per cent of TBSA or greater should receive a nasogastric tube. (Feeding should start within 6 hours of the injury to reduce gut mucosal damage.) A number of different formulae are available to calculate the energy requirements of patients (Summary box 30.13). Summary box 30.13 Nutrition in burns patients ■ ■ ■

Burns patients need extra feeding A nasogastric tube should be used in all patients with burns over 15 per cent of TBSA Removing the burn and achieving healing stops the catabolic drive

Burn injuries are catabolic in the acute episode. Successful management of the patient’s energy balance involves a number of strategies. The catabolic drive continues while the wound remains unhealed and, therefore, rapid excision of the burn and stable coverage of the wound are the most significant factors in reversing this. Obligatory energy utilisation must be reduced to a minimum by keeping the patient warm with good environmental control. The excess energy requirements must be provided for and the nutritional balance monitored by measuring weight and nitrogen balance (see Table 30.5).

Monitoring and control of infection Patients with major burns are immunocompromised, having large portals of entry to pathogenic and opportunistic bacteria and fungi via the burn wound (Summary box 30.14). They have compromised local defences in the lungs and gut due to oedema, and usually have monitoring lines and catheters, which themselves represent portals for infection. Table 30.5 Commonly used feeding formulae.

Curreri formula Sutherland formula Protein needs

Davies formula

Age 16–59 years: (25)W + (40)TBSA Age 60+ years: (20)W + (65)TBSA Children: 60 kcal/kg + 35 kcal%TBSA Adults: 20 kcal/kg + 70 kcal%TBSA Greatest nitrogen losses between days 5 and 10 20% of kilocalories should be provided by proteins Children: 3 g/kg + 1 g%TBSA Adults: 1 g/kg + 3 g%TBSA

TBSA, total body surface area.

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Surger y for the acute burn wound Summary box 30.14

Summary box 30.15

Infection control in burns patients

Surgical treatment of deep burns

■ ■ ■ ■

Burns patients are immunocompromised They are susceptible to infection from many routes Sterile precautions must be rigorous Swabs should be taken regularly A rise in white blood cell count, thrombocytosis and increased catabolism are warnings of infection

■ ■ ■ ■ ■ ■

Control of infection begins with policies on hand-washing and other cross-contamination prevention measures. Bacteriological surveillance of the wound, catheter tips and sputum helps to build a picture of the patient’s flora. If there are signs of infection, then further cultures need to be taken and antibiotics started. This is often initially on a best guess basis, hence the usefulness of prior surveillance; close liaison with a bacteriologist is essential. In patients with large burns that remain catabolic, the core temperature is usually reset by the hypothalamus above 37°C. Significant temperatures are those above 38.5°C, but often other signs of infection are more useful to the clinician. These include significant rise or fall in the white cell count, thrombocytosis, increasing signs of catabolism and decreasing clinical status of the patient.

Nursing care Burns patients require particularly intensive nursing care. Nurses are the primary effectors of many decisions that directly affect healing. Bandaged hands and joints which are stiff and painful need careful coaxing. Personal hygiene, baths and showers all become time-consuming and painful, but are vital parts of the patient’s physiotherapy. Their success or failure has a powerful psychological impact on the patient and his or her family.

Physiotherapy All burns cause swelling, especially burns to the hands. Elevation, splintage and exercise reduce swelling and improve the final outcome. The physiotherapy needs to be started on day 1, so that the message can be reinforced on a daily basis.

Psychological A major burn is an overwhelming event, outside the normal experience, which overwhelms the patient’s coping ability, suspends the patient’s sense of safety and causes post-traumatic reactions. These are normal and usually self-limiting, receding as the patient heals. The features of this intensity of experience are of intrusive reactions, arousal reactions and avoidance reactions.

SURGERY FOR THE ACUTE BURN WOUND Any deep partial-thickness and full-thickness burns, except those that are less than about 4 cm2, need surgery. Any burn of indeterminate depth should be reassessed after 48 hours. This is because burns that initially appear superficial may well deepen over that time. Delayed microvascular injury is especially common in scalds (Summary box 30.15).

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Deep dermal burns need tangential shaving and split-skin grafting All but the smallest full-thickness burns need surgery The anaesthetist needs to be ready for significant blood loss Topical adrenaline reduces bleeding All burnt tissue needs to be excised Stable cover, permanent or temporary, should be applied at once to reduce burn load

The essence of burns surgery is control. First and foremost, the anaesthetist needs good control of the patient. A wide-bore cannula should be used and the patient’s blood pressure must be monitored adequately. If a large excision is considered, then an arterial line (to monitor blood pressure) and a central venous pressure monitor are needed. The anaesthetist also needs measurements and control of the acid–base balance, clotting time and haemoglobin levels. The core temperature of the patient must not drop below 36°C, otherwise clotting irregularities will be compounded. For most burn excisions, subcutaneous injection of a dilute solution of adrenaline 1:1 000 000 or 1:500 000 and tourniquet control are important for controlling blood loss. In deep dermal burns, the top layer of dead dermis is shaved off until punctate bleeding is observed and the dermis can be seen to be free of any small thrombosed vessels (Figure 30.5a). A topical solution of 1:500 000 adrenaline also helps to reduce bleeding, as does the application of the skin graft. The use of a tourniquet during burn excisions in the limbs helps to decrease blood loss and maintain control. Full-thickness burns require full-thickness excision of the skin (Figure 30.5b). In certain circ*mstances, it is appropriate to go down to the fascia but, in most cases, the burn excision is down to viable fat. Wherever possible, a skin graft should be applied immediately. With very large burns, the use of synthetic dermis or hom*ografts provides temporary stable coverage and will allow complete excision of the wound and thus reduce the burn load on the patient. Postoperative management of these patients obviously requires careful evaluation of fluid balance and levels of haemoglobin. The outer dressings will quickly be soaked through with serum and will need to be changed on a regular basis to reduce the bacterial load within the dressing. Physiotherapy and splints are important in maintaining range of movement and reducing joint contracture. Elevation of the appropriate limbs is important. The hand must be splinted in a position of function after grafting, although the graft needs to The Guinea Pig Club. Sir Archibald McIndoe (1900–1960), born in New Zealand, was appointed in 1938 as consultant plastic surgeon to the Royal Air Force. He trained with his cousin, Sir Harold Gillies, another internationally reputed plastic surgeon. McIndoe became world famous for his pioneering work on Battle of Britain pilots who were badly burnt. His work on these airmen, who needed several operations, and using his innovative technical and psychological methods, was the start of a life-long service. The young fighter pilots were therefore referred to as ‘guinea pigs’ – thus was formed The Guinea Pig Club. McIndoe referred to his patients as ‘the boys’ who in turn called him ‘the boss’ or ‘the maestro’. To this day, some of the members of the Guinea Pig Club from all over the world still meet on an annual basis in Sussex. McIndoe founded the British Association of Plastic Surgeons (BAPS).

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■

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be applied in the position of maximal stretch. Knees are best splinted in extension, axillae in abduction. Supervised movement by the physiotherapists, usually under direct vision of any affected joints, should begin after about 5 days.

Delayed reconstruction and scar management Delayed reconstruction of burn injuries is common for large fullthickness burns. In the early healing period, acute contractures around the eye need particular attention. Eyelids must be grafted at the first sign of difficulty in closing the eyelids, and this must be done before the patient has any symptoms of exposure keratitis (Figure 30.10). Other areas that require early intervention are any contracture causing significant loss of range of movement of a joint. This is particularly important in the hand and axilla (Summary box 30.16). Summary box 30.16 Delayed reconstruction of burns ■ ■ ■ ■

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■

Eyelids must be treated before exposure keratitis arises Transposition flaps and Z-plasties with or without tissue expansion are useful Full-thickness grafts and free flaps may be needed for large or difficult areas Hypertrophy is treated with pressure garments Pharmacological treatment of itch is important

An established contracture can be treated in a number of ways. Burn alopecia is best treated with tissue expansion of the unburned hair-bearing skin. Tissue expansion is also a useful technique for isolated burns and other areas with adjacent normal skin. Z-plasty is useful in the situation in which there is a single band and a transposition flap is useful in wider bands of scarring (Figure 30.11). In areas of circumferential or very broad areas of scarring, the only real treatment is incision and replacement with tissue. By far the best tissue for replacement is from either a full-thickness graft or vascularised tissue as in a free flap. Occasionally, the situation requires the less ideal covering of split skin, possibly with an artificial dermis, such as Integra® (Figure 30.12). These last two options require prolonged scar management after their use. Hypertrophy of many scars will respond to pressure garments. These need to be worn for a period of 6–18 months. Where it is difficult to apply pressure with pressure garments, or with smaller areas of hypertrophy, silicone patches will speed scar maturation, as will intralesional injection of steroid. Itching and dermatitis in burn scar areas are common. Pharmacological treatment of itch is an essential adjunct to therapy.

MINOR BURNS/OUTPATIENT BURNS Local burn wound care Blisters Whether to remove blisters or leave them intact has been the subject of much debate. Proponents of blister removal quote laboratory studies which show that blister fluid depresses immune function, slowing down chemotaxis and intracellular killing and also acting as a medium for bacterial growth.

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Conversely, other authors advocate leaving blisters intact as they form a sterile stratum spongiosum. Leaving a ruptured blister is not advised.

Initial cleaning of the burn wound Washing the burn wound with chlorhexidine solution is ideal for this purpose.

Topical agents For initial management of minor burns that are superficial or partial thickness, dressings with a non-adherent material, such as Vaseline-impregnated gauze or Mepitel are often sufficient. These dressings are left in place for 5 days. These burns, by definition, should be healed after 7–10 days. Various topical creams and ointments have been used for the treatment of minor burns. All published comparative data show no advantage of these agents over petroleum gauze. Silver sulphadiazine (1 per cent) or Flamazine® is the most commonly used topical agent. However, it should be avoided in pregnant women, nursing mothers and infants less than two months of age because of the increased possibility of kernicterus in these patients.

Dressing the minor burn wound The aims of dressing are to decrease wound pain and to protect and isolate the burn wound. The small superficial burn requires Vaseline gauze or another non-adherent dressing, such as Mepitel, as the first layer. Following this, gauze or Kerlix® is wrapped around with sufficient tightness to keep the dressing intact, but not to impede the circulation. This is further wrapped with bandage. It is important to realise that bulkiness of dressings in the minor burn wound depends upon the amount of wound discharge. A special case is burns of the hands where dressings should be minimised so as not to impede mobilisation and physiotherapy. Synthetic burn wound dressings are popular as they:

• • • •

decrease pain associated with dressings; improve healing times; decrease outpatient appointments; lower overall costs.

Biobrane is a bilaminar dressing made up of an inner layer of knitted nylon threads coated with porcine collagen and an outer layer of rubberised silicone impervious to gases, but not to fluids and bacteria. Wounds to be dressed with Biobrane should be carefully selected. Burn wounds should be fresh (less than 24 hours), sensate, show capillary blanching and refill. Biobrane® should be applied to the wound after removal of all blisters. It should be checked at 48 hours for adherence and any signs of infection. It should be removed if any sign of infection is found. Duoderm or hydrocolloid dressings are not bulky, help in healing and can be kept in place for 48–72 hours. They provide a moist environment, which helps in re-epithelialisation of the burn wound.

Healing of burn wounds Burns that are being managed conservatively should be healed within 3 weeks. If there are no signs of re-epithelialisation in this time, the wound requires debridement and grafting.

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(a)

(b)

(c)

(d)

(e)

(f)

Figure 30.10 (a) A mixed superficial and deep burn to the face after a petrol explosion. The patient’s airway was protected prior to transfer. He has an orogastric tube and feeding has commenced. (b) The face dressed with a hydrocolloid dressing. The endotracheal tube is wired to the teeth. (c) Day 6, the swelling is still present. (d) Six weeks after injury. With the mouth wide open, the lower eyelids are pulled down, demonstrating the intrinsic and extrinsic shortening of the eyelids. (e) Three months after injury. The eyelids have been grafted but note the contracture of the lips. (f) Six months after injury. The patient has had grafts to the upper and lower lips.

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Minor burns/outpatient burns

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Infection Infection in the minor burn should be tackled very aggressively as it is known to convert a superficial burn to a partial-thickness burn and a partial- to a deep partial-thickness burn, respectively. It should be managed using a combination of topical and systemic agents. Debridement and skin grafting should also be considered.

Itching Most burn patients have itchy wounds. Histamine and various endopeptides are said to be the causative factors of itching. Antihistamines, analgesics, moisturising creams, aloe vera and antibiotics have all been tried with varying degrees of success.

Traumatic blisters Figure 30.11 A transposition flap bringing normal skin across a scarred elbow.

(a)

The healed burn wound is prone to getting traumatic blisters because the new epithelium is very fragile. Non-adherent dressings usually suffice; regular moisturisation is also useful in this condition.

(b)

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(c)

Figure 30.12 (a) A healed full-thickness leg burn prior to resurfacing with Integra. (b) The burn scar has been excised and Integra applied prior to split-thickness skin grafting. (c) Six months after Integra resurfacing. The skin is smoother and more supple, and the scar has faded.

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Non-thermal burn injur y

NON-THERMAL BURN INJURY Electrical injuries Electrical injuries are usually divided into low- and high-voltage injuries, the threshold being 1000 V (Summary box 30.17). Summary box 30.17 Electrical burns ■ ■ ■ ■ ■ ■

Low-voltage injuries cause small, localised, deep burns They can cause cardiac arrest through pacing interruption without significant direct myocardial damage High-voltage injuries damage by flash (external burn) and conduction (internal burn) Myocardium may be directly damaged without pacing interruption Limbs may need fasciotomies or amputation Look for and treat acidosis and myoglobinuria

of direct muscle damage rather than by interference with cardiac pacing. This gives rise to significant electrocardiogram changes, with raised cardiac enzymes. If there is significant damage, there is rapid onset of heart failure. In the case of a severe injury through a limb, primary amputation is sometimes the most effective management (Figure 30.13).

Chemical injuries There are over 70 000 different chemicals in regular use within industry. Occasionally, these cause burns. Ultimately, there are two aspects to a chemical injury. The first is the physical destruction of the skin and the second is any poisoning caused by systemic absorption (Summary box 30.18). Summary box 30.18 Chemical burns ■ ■ ■

Low-tension injuries Low-tension or domestic appliance injuries do not have enough energy to cause destruction to significant amounts of subcutaneous tissues when the current passes through the body. The resistance is too great. The entry and exit points, normally in the fingers, suffer small deep burns; these may cause underlying tendon and nerve damage, but there will be little damage between. The alternating current creates a tetany within the muscles, and thus patients often describe how they were unable to release the device until the power was turned off. The main danger with these injuries is from the alternating current interfering with normal cardiac pacing. This can cause cardiac arrest. The electricity itself does not usually cause significant underlying myocardial damage, so resuscitation, if successful, should be lasting.

399

Damage is from corrosion and poisoning Copious lavage with water helps in most cases Then identify the chemical and assess the risks of absorption

(a)

High-tension injuries

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(b)

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High-tension electrical injuries can be caused by one of three sources of damage: the flash, the flame and the current itself. When a high-tension line is earthed, enormous energy is released as the current travels from the line to the earth. It can arc over the patient, causing a flash burn. The extremely rapid heating of the air causes an explosion that often propels the victim backwards. The key here is that the current travelled from the line to the earth directly and not through the patient. The flash, however, can go on to ignite the patient’s clothes and so cause a normal flame burn. In accidents with overhead lines, the patient often acts as the conduction rod to earth. In these injuries, there is enough current to cause damage to the subcutaneous tissues and muscles. The entry and exit points are damaged but, importantly, the current can cause huge amounts of subcutaneous damage between these two points. These can be extremely serious injuries. The damage to the underlying muscles in the affected limb can cause the rapid onset of compartment syndrome. The release of the myoglobins will cause myoglobinuria and subsequent renal dysfunction. Therefore, during the resuscitation of these patients, efforts must be made to maintain a high urine output of up to 2 mL/kg body weight per hour. Severe acidosis is common in large electrical burns and may require boluses of bicarbonate. These patients are also at risk of myocardial damage as a result

Figure 30.13 (a) An exit wound of a high-tension injury, with a dead big toe and significant damage to the medial portion of the second toe. (b) Amputation and cover with the lateral portion of the second toe.

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The initial management of any chemical injury is copious lavage with water. There are only a handful of chemicals for which water is not helpful, for example phosphorus, which is a component of some military devices, and elemental sodium, which is occasionally present in laboratory explosions. These substances need to be physically removed with forceps; however, it is extremely rare that any medical practitioner will encounter these in his or her lifetime. The more common injuries are caused by either acids or alkalis. Alkalis are usually the more destructive and are especially dangerous if they have come into contact with the eyes. After copious lavage, the next step in the management of any chemical injury is to identify the chemical and its concentration and to elucidate whether there is any underlying threat to the patient’s life if absorbed systemically. One acid that is a common cause of acid burns is hydrofluoric acid. Burns affecting the fingers and caused by dilute acid are relatively common. The initial management is with calcium gluconate gel topically; however, severe burns or burns to large areas of the hand can be subsequently treated with Bier’s blocks containing calcium gluconate 10 per cent gel. If the patient has been burnt with a concentration greater than 50 per cent, the threat of hypocalcaemia and subsequent arrhythmias then becomes high, and this is an indication for acute early excision. It is best not to split-skin graft these hydrofluoric acid wounds initially, but to do this at a delayed stage.

Ionising radiation injury

Summary box 30.19 Radiation burns ■ ■

Local burns causing ulceration need excision and vascularised flap cover, usually with free flaps Systemic overdose needs supportive treatment

Cold injuries Cold injuries are principally divided into two types: acute cold injuries from industrial accidents and frostbite. Exposure to liquid nitrogen and other such liquids will cause epidermal and dermal destruction. The tissue is more resistant to cold injury than to heat injury, and the inflammatory reaction is not as marked. The assessment of depth of injury is more difficult, so it is rare to make the decision for surgery early. Frostbite injuries affect the peripheries in cold climates. The initial treatment is with rapid rewarming in a bath at 42°C. The cold injury produces delayed microvascular damage similar to that of cardiac reperfusion injury. The level of damage is difficult to assess, and surgery usually does not play a role in its management, which is conservative, until there is absolute demarcation of the level of injury.

FURTHER READING British Burns Association. Emergency management of burns, 8th edn. UK Course Pre-reading. British Burns Association, 2004. Herndon D (ed.). Total burn care, 3rd edn. Philadelphia, PA: Saunders and Elsevier, 2007. Pape S, Judkins K, Settle J. Burns: the first five days, 2nd edn. Romford: Smith and Nephew, 2000.

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These injuries can be divided into groups depending on whether radiation exposure was to the whole body or localised. The management of localised radiation damage is usually conservative until the true extent of the tissue injury is apparent. Should this damage have caused an ulcer, then excision and coverage with vascularised tissue is required. Whole-body radiation causes a large number of symptoms. The dose of radiation either is or is not lethal. A patient who has suffered whole-body irradiation and is suffering from acute desquamation of the skin has received a lethal dose of radiation, which can cause a particularly slow and unpleasant death. Non-

lethal radiation has a number of systemic effects related to the gut mucosa and immune system dysfunction. Other than giving iodine tablets, the management of these injuries is supportive (Summary box 30.19).

August Karl Gustav Bier, 1861–1949, Professor of Surgery, Berlin, Germany.

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CHAPTER

Plastic and reconstructive surgery LEARNING OBJECTIVES

To understand: • The spectrum of plastic surgical techniques used to restore bodily form and function • The relevant anatomy and physiology of tissues used in reconstruction

• The various skin grafts and how to use them appropriately • The principles and use of flaps • How to use plastic surgery to manage difficult and complex tissue loss

HISTORICAL CONTEXT

Sushruta, regarded as the father of modern surgery, lived in the Indian city of Kashi (now called Banaras) in 600BC (while the exact period is unclear, most scholars maintain that he practised between 600 and 1000BC). A large part of his practice was plastic surgery in the form of rhinoplasty carried out on criminals who had their noses amputated as a punishment for their crimes. His medical pursuits were recorde d in ‘Sushsruta Samhita (compendum)’.

Figure 31.1 Sir Harold Gillies operating during the First World War – ‘the birth of plastic surgery’. Picture by Henry Tonks (by kind permission of the Royal College of Surgeons of England).

ANATOMY RELATED TO RECONSTRUCTIVE SURGERY Skin The surface of the skin is important as a biological layer for homeostasis. Restoring the skin surface is therefore critical even if the underlying structures can await later reconstruction. Epidermis regenerates from deeper follicular elements, with the most superficial layer losing vascularity and acting as a barrier to fluid loss and providing important protection against invasion by microorganisms. (Epidermal keratinocytes can be artificially cultured in vitro and are used in some wound management systems.) The depth of the dermis and the amounts of elastin and skin

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Reconstructive plastic (from the ancient Greek plassein, to mould or shape – also the stem for our modern use of the materials termed ‘plastics’) surgery involves using various techniques to restore form and function to the body when tissues have been damaged by injury, cancer or congenital loss. Its origins can be traced back to ancient Egypt, with wound care depicted in hieroglyphs on papyrus, to India in the sixth century bc, where Sushruta described using the forehead flap to reconstruct a nose, and to Al-Zahrawi, the tenth-century Islamic surgical scholar from Cordoba. Modern techniques were developed after the First World War, especially with Sir Harold Gillies’ work on reconstructing facial injuries (Figure 31.1), which was enabled by new safe anaesthetic intubation (Sir Ivan Magill). Later in the twentieth century, renewed understanding of detailed soft tissue anatomy led to an explosion in the use of new flaps, which with microsurgical methods, craniofacial surgery and tissue expansion resulted in an entirely new set of techniques becoming available to surgeons for reconstructing parts. Today, the need for reconstructive plastic surgery, especially in developing nations, has never been greater. Road, war and domestic injury inflict life-diminishing effects, which plastic surgery can reduce. The reconstructive surgeon’s ‘toolbox’ is now very diverse and will continue to grow in order to address problem wounds and tissue defects, which arise as modern medical care is more successful in treating cancer, preserving life into old age and salvaging victims of trauma.

Sir Ivan Whiteside Magill, 1888–1986, anaesthetist, Westminister Hospital, London, UK. Henry Tonks, 1862–1937, commenced a career in surgery, but abandoned it for art and became, from 1917 to 1930, Slade Professor at the Westminster School of Art, London, UK.

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adnexal elements, such as sweat glands and hair follicles, vary depending on the functional requirements of the area concerned. This means that some areas are much more vulnerable to injury than others, e.g. the fine flexible elastic skin of the eyelid rapidly suffers a full-thickness burn after a flash burn, whereas thick back skin suffers only a partial loss after the same flash burn. Skin vascularity is derived from fine perforating vessels that run through underlying muscles or through fascial septal layers, and then horizontally in a subcutaneous plane from which capillaries branch (Figure 31.2). Nerves run axially out from major trunks and are less well defined than most perforating blood vessels. When local, random-pattern skin flaps are raised, they are lifted at the subcutaneous level and are nourished by the subdermal plexus of blood vessels. However, this plexus can only survive a limited distance from the more substantial arterial branches running in the fascial, septal or muscle-perforating planes. Understanding the anatomy of different parts of the skin and tissues to be moved is a key element of successful plastic surgery. Without skin, wounds heal by secondary intention with fibrosis and contracture (Figure 31.3), and underlying structures are vulnerable to necrosis, chronic infection and dysfunction.

Graft anatomy Split-thickness skin grafts Split-thickness skin grafts are harvested by taking all of the

(a)

Fascia

Skin

Direct cutaneous artery

Subcutaneous tissue

Figure 31.3 A severely contracted hand following burn to the dorsal aspect.

epidermis together with some dermis, leaving the remaining dermis behind to heal the donor site. The thicker the dermis that is taken (seen by more brisk punctate bleeding at the donor site; Figure 31.4), the more durable will be the graft once healed (although it might take longer and require more care), but also the more difficult will be donor site healing (Summary box 31.1).

(b)

PLEXUSES Subpapillary Mid-dermal (primarily venous plexus) Subdermal

Subpapillary plexus Papillary loops

Mid-dermal (primary venous plexus) Hair

Subcutaneous Prefascial

Epidermis

Subfascial

Thin split-skin graft Deeper split-skin graft Thick split-skin graft Full thickness (Wolfe) skin graft

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Local flaps

Deep Subcutaneous Subcutaneous subdermal vessels tissue plexus Reticular dermis Papillary dermis Internal artery Musculocutaneous Fasciocutaneous artery artery

Muscle Perforator artery

Perforating vessels Figure 31.2 Diagram of skin anatomy with vascular plexus. in vitro is Latin for ‘in the glass’.

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Summary box 31.1 Split-thickness skin grafts ■ ■ ■ ■

Thicker knife-gap settings give rise to fewer but brisker bleeding points on the donor site. Thicker grafts heal with less contracture and are more durable. Thinner donor sites heal better. Grafts are hairless and do not sweat (these structures are not transferred).

Full-thickness skin grafts Full-thickness grafts are harvested to incorporate the whole dermis, with the underlying fat trimmed away – unless elements of fat (or even cartilage as well) are deliberately left attached to form a composite graft. Full-thickness and composite grafts require the most careful handling and postoperative nursing to help ensure that they ‘take’ in their transplanted site.

Figure 31.4 Fine punctate bleeding from a split-thickness skin graft donor site.

How does a skin graft survive?

CLASSIFICATION The reconstructive toolbox Plastic surgery offers a variety of techniques to address clinical problems. Sometimes, a problem is managed using a ‘ladder’ approach, with the simplest methods being used first and only moving to more complex methods when absolutely necessary. However, this is frequently not the ideal approach for best outcomes. If resources permit, it is often more cost-effective and better functionally for the patient to begin with a more complex treatment, with other easier managements held in reserve as ‘lifeboats’. Plastic surgeons now prefer to think of the range of options available as a toolbox from which they can take the most appropriate method to solve a problem, taking into account available skill, resources and the consequences of failure.

The scope of plastic surgery The tools of reconstruction are used for a wide range of conditions:

• trauma: • soft-tissue loss (skin, tendons, nerves, muscle); • hand and lower limb injury; • faciomaxillary; • burns; • cancer: • skin, head and neck, breast, soft tissue sarcoma; • congenital:

• clefts and craniofacial malformations; • skin, giant naevi, vascular malformations; • urogenital; • hand and limb malformations;

• miscellaneous: • Bell’s (facial) palsy; • pressure sores; • aesthetic surgery; • chest wall reconstruction.

A few key principles that can also be applied to other surgical specialties should be observed. In many reconstructions, success depends upon good rapid wound healing, which itself depends upon attention to detail from the surgeon. Adequate debridement, careful technique, gentle handling of tissues and consideration of blood supply are all key factors that influence outcome (Table 31.1). The placement of incisions can be critical, especially in reducing the appearance of scars on the face and in areas of tension. When possible, incisions should lie in the lines of minimal tension (described by Langer, but frequently different from those originally noted) (Figure 31.5). Table 31.1 Plastic surgery principles.

Optimise wound by adequate debridement or resection Wound or flap must have a good blood supply to heal Place scars carefully – ‘lines of election’a Replace defect with similar tissue – ‘like with like’b Observe meticulous surgical technique Remember donor site ‘cost’ Lines of election – analogous to Langer’s lines of minimal skin tension. Millard DR. Principalization of plastic surgery. Boston: Little & Brown, 1986.

a b

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Split-thickness skin grafts survive initially by imbibition of plasma from the wound bed; after 48 hours, fine anastomotic connections are made, which lead to inosculation of blood. Capillary ingrowth then completes the healing process with fibroblast maturation. Because only tissues that produce granulation will support a graft, it is usually contraindicated to use grafts to cover exposed tendons, cartilage or cortical bone. Skin grafts inevitably contract, with the extent of contracture determined by the amount of dermis taken with the graft and the level of postoperative splintage and physiotherapy applied to the grafted site.

Grafts Grafts are tissues that are transferred without their blood supply, which therefore have to revascularise once they are in a new site. They include the following:

Sir Charles Bell, 1774–1842, surgeon, Middlesex Hospital, London, UK and from 1835 until his death, Professor of Surgery, the University of Edinburgh, Edinburgh, UK. Karl Ritter von Edenberg Langer, 1819–1887, Professor of Anatomy, Vienna, Austria described these lines in 1862.

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• Nerve grafts. Usually taken from the sural nerve, but smaller cutaneous nerves may be used.

• Tendon grafts. Usually taken from the palmaris longus or plantaris tendon (runs just anteromedial to the Achilles tendon) and used for injury loss or nerve damage correction.

Flaps Flaps are tissues that are transferred with a blood supply. They therefore have the advantage of bringing vascularity to the new area. Flaps can be raised to consist of any specific tissue; for skin flaps the following will illustrate the types that exist (Figure 31.6):

• Random flaps. Three sides of a rectangle, bearing no specific

Figure 31.5 Lines of relaxed skin tension.

• • Split-thickness skin grafts (of varying thickness). These are sometimes called Thiersch grafts. They are used to cover all sizes of wound, are of limited durability and will contract. They may be used to provide valuable temporary wound closure before better cosmetic secondary correction after rehabilitation. • Full-thickness skin grafts (Wolfe grafts). Used for smaller areas of skin replacement where good elastic skin that will not contract is required (such as fingers, eyelids, facial parts). • Composite skin grafts (usually skin and fat, or skin and cartilage). Often taken from the ear margin and useful for rebuilding missing elements of nose, eyelids and fingertips.

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Random flap (and delay)

Axial flap

•

• •

relationship to where the blood supply enters; the length to breadth ratio is no more than 1.5:1. This pattern can be lengthened by ‘delaying’ the flap, a process in which the cuts are partially made and the flap is part lifted at a first operation; it is then replaced, thus ‘training’ the blood supply from a single border of the rectangle. At a second procedure, it is raised further and finally transferred. Axial flaps. Much longer flaps, based on known blood vessels supplying the skin. This technique was rediscovered in the 1960s and 1970s and enables many long thin flaps to be safely moved across large distances. Pedicled/islanded flaps. The axial blood supply of these flaps means that they can be swung round on a stalk or even fully ‘islanded’ so that the business end of the skin being transferred can have the pedicle buried (Figure 31.7). Free flaps. The blood supply has been isolated, disconnected and then reconnected using microsurgery at the new site (Figure 31.8). Composite flaps. Various tissues are transferred together, often skin with bone or muscle (osseocutaneous or myocutaneous flaps, respectively).

Islanded/pedicled flap

Free flap 6

1 1.5 1

Length can be increased by delay

Donor site Can be: • Fasciocutaneous • Myocutaneous • Composite • Perforator

Figure 31.6 Skin flaps, from simple to complex. Karl Thiersch, 1822–1895, Professor of Surgery, Leipzig, Germany. He was a pioneer of free skin grafts and described his method of skin grafting in 1874. John Reissburg Wolfe, 1824–1904, ophthalmic surgeon, Glasgow, UK, described full thickness skin grafts in 1875 and in the same year used forearm skin to construct an eyelid.

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(a)

(b) (b)

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(d) Figure 31.7 (a–c) Islanded pedicled flap used from instep to resurface heel defect.

• Perforator flaps. This description refers to a whole new

subgroup of axial flaps in which tissues are isolated on small perforating vessels that run from more major blood vessels to supply the surface.

Skin substitutes One solution to the problem presented by major skin loss with inadequate skin donor sites has been to use artificially engineered skin substitutes. These vary from thin sheets of autologous keratinocytes, to artificial collagen matrices with embedded

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Figure 31.8 (a–d) Free lateral arm fasciocutaneous flap used to resurface a tendo Achilles defect.

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fibroblasts and a keratinocyte sheet covering. They are costly, but are becoming widely used, and it is likely that tissue-engineered products will continue to be developed in an attempt to solve difficult reconstructive problems.

Tissue expansion This technique is valuable in using ‘local’ tissue for reconstruction. The natural ability of tissue to expand has been harnessed clinically since the experiments of Austad and the clinical work of Radovan in the 1970s. It is a technique borrowed from nature, and it is observed during pregnancy when skin expands over the underlying mass. It involves placing a device – usually an expandable balloon constructed from silicone – beneath the tissue to be expanded and progressively enlarging the volume with fluid while the overlying tissue accommodates to the changed vascular pressure (Figure 31.9). The fluid (usually sterile saline coloured blue in Figure 31.9) is introduced via a self-sealing port attached to a filling tube that enters the balloon. It may be introduced as frequently as can be tolerated by the patient until the tissues are stretched enough to be used for reconstruction. The tissues expanded do not hypertrophy, but there are major changes in the collagen structure. The process is time-consuming, although it can be very valuable in problematic cases. It is invaluable for sharing remaining areas of scalp hair after severe burns, removing major congenital skin naevi and restoring full-thickness skin over previously grafted limb wounds. It must never be used under irradiated tissues (such as mastectomy sites), which will not expand but necrose (Summary box 31.2).

Exudate is removed and the suction pressure affects angiogenesis and tissue regeneration. The technique can be applied as part of early wound management before definitive surgical closure has been planned, or in some cases to avoid the need for surgery altogether. The foam sponge dressing is connected by a tube to a negative pressure pump that can be controlled to give intermittent suction (Figure 31.10).

Figure 31.10 VAC™ device used to temporarily close a sternal dehiscence prior to definitive debridement and flap cover.

Implants and prosthetics Summary box 31.2 Tissue expansion Advantages ■ ■ ■

Well-vascularised tissue Tissue next to defect, so likely to be of similar consistency Good colour match

Disadvantages ■ ■ ■

Multiple expansion episodes (sometimes painful) Cost of device High incidence of infection and extrusion (especially limbs)

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Vacuum-assisted closure The use of negative pressure applied to a tissue defect has positive effects on wound closure, as well as making difficult and complex wounds more manageable during the early stages of granulation.

Figure 31.9 Tissue expander.

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Many tissue deficiencies cannot be adequately reconstructed with autologous tissue, however sophisticated the technique used. In such circ*mstances, implants are part of the reconstructive surgical ‘toolbox’; they include solid and soft silicone materials, many forms of filler including collagen and polymers, and osseointegratable anchor points for prosthesis fixation. The use of fat harvested using liposuction, centrifuged down and washed, then used to inject deficient areas around the body is now commonplace. It is a form of graft transfer since the cellular fluid regains vascularity in the host tissue. It is used for restoring contour deficits after injury and tumour treatment, as well as for cosmetic deformities.

ASSESSMENT AND DIAGNOSTIC PLANNING Formation of a definitive treatment plan, carefully considering all available options for care with the whole of the patient’s needs in mind, is a vital component of wise plastic surgical practice. This is never more so than when managing major trauma cases in the acute setting or when planning major cancer management, which might be staged over a period of treatments and procedures. If the reconstructive surgeon can be involved in early wound debridement and incisions, vital flap pedicles can be protected and the functional and cosmetic outcome made optimal. This pattern of shared team care has become the norm in many units demonstrating good outcomes from major trauma salvage. The initial assessment of wounds involves adequate removal of devitalised tissue, assessment of which vital structures will

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Tr e a t m e n t a n d c o m p l i c a t i o n s

need reconstruction immediately and which might be better reconstructed later, and assessment of the degree of contamination involved, which will require further cleaning. Further planning will include the definitive soft-tissue cover of the wound and functional rehabilitation with full psychosocial rehabilitation.

407

(a)

TREATMENT AND COMPLICATIONS Split-thickness skin grafts are taken with either hand-held (Figure 31.11) or powered skin knives (Figure 31.12). The most used donor site is the thigh, with the buttock preferable in children and cosmetically sensitive individuals. For larger grafts, almost any flat surface can be harvested, including the scalp if shaved (a very good and useful donor site). The thickness of the graft harvested, ease of graft ‘take’ and donor site healing must be weighed against the lack of durability of thin split-thickness skin grafts. Split grafts can be perforated to allow exudates to escape and improve ‘take’; they can be further meshed to allow expansion (Figure 31.13). This is carried out on a device that cuts a series of slits along the skin, allowing it to expand from a ratio of anything from 1:1.5 to about 1:6. Grafts will only take on a bed on which they can become vascularised. Preparation of the wound bed is therefore an essential part of a successful graft (Figure 31.14). Graft failure is commonly caused by pus, exudate or residual dead tissue beneath the skin, haematoma or shearing forces. A clean healthy wound bed with a meshed graft tied in place to stop movement will encourage success. The group A b-haemolytic Streptococcus can destroy split grafts completely (and also convert a donor site to a full-thickness defect) and so the presence of this micro-organism is a contraindication to grafting.

(a)

(b)

(d)

(e)

(b)

Figure 31.11 Hand-held skin knife (a) and harvesting skin with handheld knife (b).

Full-thickness skin grafts Small dermal grafts (Wolfe grafts) can be taken from behind the ear, the groin creases and the neck, with easy direct closure of the donor site. Older people can sustain larger harvests because of skin laxity. Large full-thickness skin graft use is uncommon

(c)

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Split-thickness skin grafts

Figure 31.12 Power dermatome harvest of a split-thickness skin graft, with the correct method of providing skin tension (a–d), and dressing of donor site with adhesive material (e).

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(b)

Figure 31.13 Split-thickness skin graft mesher (a) and meshed skin applied to wound (b).

Flaps Local flaps A local flap is raised next to a tissue defect in order to reconstruct it. Basic patterns include (Figure 31.15):

• Transposition flap. The most basic design, leaving a graftable donor site (Figure 31.16);

• Z-plasty. For lengthening scars or tissues; • Rhomboid flap. For cheek, temple, back and flat surface defects;

• Rotation flap. For convex surfaces; • Advancement flap. For flexor surfaces; may need triangles

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Figure 31.14 Cleaning a wound of excessive granulation tissue before grafting.

and requires great care to obtain a good take. Large donor sites require secondary split-thickness skin grafting. Major secondary burn contractures of the face and flexion creases can achieve remarkable functional and cosmetic improvement using such large grafts, particularly as the remaining facial muscle function can still produce a more natural appearance than when covered by a bulky full-thickness skin flap. Smaller full-thickness grafts are useful for contracture release around sensitive facial and extremity structures.

excised at the base to make it work (commonly called Burow’s triangles); • V-to-Y advancement. Commonly used for fingertips and extremities; • Bilobed flap. For convex surfaces, especially the nose (Figure 31.17); • Bipedicle flap. For eyelids, rarely elsewhere. All flaps must be raised in the subcutaneous plane. Gentle undercutting of margins helps to close the donor site. The art of making local flaps work is to pull available local spare lax skin into the defect, so that the scar when closed sits in a good ‘line of election’. Local flaps are usually not based on specific blood vessels, but are very useful in head and neck and smaller defect reconstructions. Good planning is essential to gain the best result from these flaps (Summary box 31.3). Summary box 31.3 Local flaps

Technique

Benefits

The shape of the graft needed is drawn and copied onto a small template (paper or cloth), which is used to transfer the same shape to the donor site. Full-thickness skin is cut; grafts take best if additional underlying fat is removed, after which the graft is applied with normal skin tension and tied down with a pressure dressing. The graft will remain vulnerable to shearing forces for several weeks after application.

■ ■ ■

Best local cosmetic tissue match Often a simple procedure Local or regional anaesthesia option

Disadvantages ■ ■ ■

Possible local tissue shortage Scarring may exacerbate the condition Surgeon may compromise local resection

Karl August von Burow, 1809–1974, surgeon, Konigsberg, Germany.

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409

BILOBED FLAP Uses a flap to close a convex defect, and a second smaller flap to close the donor site

Donor defect (grafted or sometimes closed primarily)

Defect

Secondary flap Flap

Pivot point Z-PLASTY

BIPEDICLE FLAP

Two triangular transposition flaps interposed 1

A ‘bucket-handle’ flap supplied from both ends. Useful to rebuild the lower eyelid

A B

Flap

(b) B A

(a) Figure 31.15 Local flap diagrams. (a) Transposition and Z-plasty flaps; (b) bilobed and bipedicled flaps; (c) rhomboid and rotation flaps. (continued opposite)

RHOMBOID FLAP A parallelogram shaped transposition flap

Tissue defect

a‘

a‘ a

Flap a

ROTATION FLAP

In some circ*mstances, such as burn contracture release, local flaps can usefully be combined to import surplus tissue from a wide area adjacent to a scar or defect that needs removal. Examples are the W-plasty and the multiple Y-to-V plasty, which is a very versatile means of releasing an isolated band scar contracture over a flexion crease (Figure 31.18).

Distant flaps To repair defects in which local tissue is inadequate, distant flaps can be moved on long pedicles that contain the blood supply. The pedicle may be buried beneath the skin to create an island flap or left above the skin and formed into a tube. The most common means of moving flaps long distances while still attached are with a long muscular pedicle that contains a dominant blood supply (a myocutaneous flap) (Figure 31.19) or with a long fascial layer that likewise contains a major septal blood supply (a fasciocutaneous flap) (Figure 31.20). These flaps can carry large composite skin parts for reconstruction very great distances, e.g. from the abdomen to the chest (for

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Combined local flaps

(c)

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Simple rectangular (with or without Burrow’s triangle excision at base)

Burn scar with long ellipse around it

Mark a long zig-zag along the scar

Defect

Two Burrow’s triangles can be excised at base of flap to make it slide V to Y e.g. cut fingertip a‘ Flap

Y to V Usually multiple to release band scars over joints

Add in the horizontal lines to the zig-zag; each becomes b‘ a ‘Y’

The cut lines will look something like this a

a‘ b

b‘

Advance the tips of the zig-zags into the spaces

5 Area of scar shaded

The finished wound will look something like this

This is one of the most effective means of releasing moderate isolated band burn scars over flexion creases

Pad it well, and be sure to splint open when not exercising

(d)

(e)

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Figure 31.15 (continued) Local flap diagrams. (d) advancement flaps; (e) multiple Y-to-V plasty for burn scar.

(a)

(b)

(c)

Figure 31.16 (a–c) Example of transposition flap (in this case from glabellar area to inner canthal defect) (continued overleaf)

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(e)

Figure 31.16 (continued) (d and e) appearance at one month post-transfer.

breast reconstruction), from the chest to the face (for oral cancer reconstruction) and from the calf to the knee. There are a vast number of carefully described myocutaneous and fasciocutaneous flaps throughout the body, all of which are based on known blood vessels. They are reliable when the anatomy of the blood supply is known by the surgeon and the skin is raised carefully in continuity with the underlying fascia or muscle, through which the small perforating vessels run to supply the piece of skin that is being transferred. They are the (b)

Microsurgery and perforator flaps With fine instruments and materials, it has become commonplace to be able to disconnect the blood supply of the flap from its donor site and reconnect it in a distant place using the operating microscope. (c)

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(a)

‘workhorse’ of plastic surgery worldwide because they do not require complex equipment to raise them and they can solve the majority of reconstructive problems.

(d)

Figure 31.17 (a–c) Example of a bilobed flap (in this case from nose to defect on tip following excision of a basal cell carcinoma). (d) Appearance at 6 weeks post-transfer.

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(b)

Figure 31.18 (a and b) Y-to-V flap to release axillary contracture.

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Figure 31.19 Trapezius pedicled myocutaneous flap to an area of recurrent squamous carcinoma in neck.

The free tissue transfer is now the best means of reconstructing major composite loss of tissue in the face, jaws, lower limb and many other body sites, as long as resources allow it (Figure 31.21). The operative procedure is similar whether the defect is newly produced from a recent injury or cancer resection or whether it is to be used for the secondary correction of a deformity, such as rebuilding a mastectomy deformity. At the site of the defect, the surgeon must be sure that all contaminated and dead tissue has been thoroughly cleared and cleaned, a process commonly described as debridement, although that term strictly refers to the release of constricting tissue. If this removal of poorly viable tissue is in doubt, then consideration should be given to delaying the reconstruction.

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The surgeon must then find a suitable blood supply for the tissue transfer at the site to be reconstructed. A good arterial flow in and venous return out, without external tissue pressure (such as from surrounding wound induration), is of paramount importance in achieving a successful transfer. The flap is then raised (Table 31.2) and transferred using magnification (Figure 31.22). Free muscle transfers should be reanastomosed within 1–2 hours if possible; fasciocutanous flaps are more robust and can survive slightly greater ischaemic times (Summary box 31.4).

Summary box 31.4 Free tissue transfer (or free flap) Advantages ■ ■ ■

(b)

Being able to select exactly the best tissue to move Only takes what is necessary Minimises donor site morbidity

Disadvantages ■ ■ ■

More complex surgical technique Failure involves total loss of all transferred tissue Usually takes more time unless the surgeon is experienced

Muscle only

Myocutaneous Fasciocutaneous

Fascial Miscellaneous

Figure 31.20 (a) Defect at ankle with the flap to be transferred outlined and the position of the perforating vessels (identified with hand-held Doppler device) marked with crosses; (b) flap raised with preserved septal perforators to skin paddle clearly visible; (c) flap rotated into position to cover the defect; proximal donor defect covered with a splitthickness skin graft (case courtesy of Mr David Johnson FRCS(Plast)).

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Latissimus dorsi Rectus abdominis Gracilis Latissimus dorsi Transverse rectus abdominis Radial forearm flap Scapular Lateral arm Anterolateral thigh Groin Fibula (may be cutaneous as well) Forearm (taking sliver of radius bone) Iliac crest Temporoparietal Jejunum – for oesophageal reconstruction Pectoralis minor – for facial reanimation Omentum – for chest wall and limb defects

Recent developments have led to surgeons dissecting distant flaps free from the carrier muscle or fascia, to reduce the donor morbidity further. These distant ‘perforator’ flaps increase the flexibility of the use of the flap tissue while reducing donor site problems. Future flap design is moving towards individualised flaps customised in freestyle fashion for the specific reconstructive requirement demanded.

Care of flaps and monitoring

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Table 31.2 Common free tissue transfer donor sites.

After a flap has been moved, it should be observed for tissue colour, warmth and turgor, and be pressed to assess blanching and capillary refill time. Loss of arterial inflow results in pale, cold, flaccid tissue; loss of venous outflow results in blue conges-

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(b)

(c)

Figure 31.21 (a–c) Large myocutaneous free flap (latissimus dorsi) to cover an exposed cranial defect following the excision of advanced basal cell carcinoma (case courtesy of Mr David Johnson FRCS(Plast)).

tion, increased turgor, rapid capillary refill and initially a warm flap. In a pedicled flap, such venous congestion may be relieved by releasing suture tension; applying leeches to suck out excess venous blood is a last resort when no other means of restoring venous drainage can be obtained. The most common causes of flap failure are:

• poor anatomical knowledge when raising the flap (such that

the blood supply is deficient from the start); flap inset with too much tension; local sepsis or a septicaemic patient; the dressing applied too tightly around the pedicle; microsurgical failure in free flap surgery (usually caused by problems with surgical technique) • tobacco smoking by patient.

• • • •

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‘Wet, warm and comfortable’ The best advice for postoperative flap care for major tissue transfers is to keep the patient ‘wet, warm and comfortable’. This means that the patient should be well hydrated with a hyperdynamic circulation, a very warm body temperature and well-controlled analgesia to reduce catecholamine output.

Reconstructing complex areas Certain areas, such as the eyelids, nose, lips, ears, genitalia, fingers, breast and intraoral structures, often require a combination of methods to produce the most functional and acceptable outcome for the patient. Planning such reconstruction involves considering each cosmetic subunit involved in the defect and bringing the best tissue to rebuild it. An example is the Indian forehead rhinoplasty of Sushruta, which involves transposition of a pedicled fasciocutaneous flap from forehead to nose, with the donor site usually thin skin grafted, but occasionally closed primarily in small flaps. It remains the finest means of transporting cosmetically correct tissue to the nose.

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FUTURE TRENDS Vascularised composite allografting Plastic surgeons have long sought to use transplanted tissue to solve the problems posed by the most severe tissue defects. Esser, in the early twentieth century, pioneered much innovative surgery and urged research into this area. Later, Joe Murray, a plastic surgeon in the United States, undertook the first kidney transplant and was awarded the Nobel Prize for his work. Improved understanding of immunology and means of tolerance induction are now leading to the use of transplanted composite tissues for the most intractable cases of loss of tissue following injury and cancer. Limb transplantation in cases of multiple loss (especially following war injury) is becoming accepted practice in centres where all aspects of care including ethical considerations have been addressed. It is likely that sophisticated tolerance induction for donor-specific transplantation will be possible within the next decade, and lead to a rapid increase in the use of such procedures.

Tissue and bioengineering Improved understanding of tissue behaviour is leading to numerous innovations in wound manipulation using biological Johannes Fredericus Samuel Esser, 1877–1946 born in Leyden, Netherlands. A Dutch plastic surgeon who pioneered reconstructive surgery on soldiers wounded in the First World War. He is thought to have coined the term ‘stent’ in 1917 to describe his use of a dental impression compound invented in 1856 by the English dentist Charles Stent (1807–1885) to create a form for facial reconstruction. Joseph E Murray, born 1919, Professor Emeritus of Plastic Surgery, Harvard University Medical School, Boston, MA, USA. He shared the 1990 Nobel Prize for Physiology or Medicine with E Donnall Thomas for his work on organ and cell transplantation. Murray’s interest in transplantation began during his military service in the Second World War. The early experiences with skin transplantation for burns in pilots formed the basis for Murray’s interest in solid organ transplantation. He performed the world’s first kidney transplantation in identical twins in Peter Brent Brigham Hospital, Boston in 1954.

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(b) (a)

(c)

(d)

(f)

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(e)

Figure 31.22 Large ‘chimeric flap’ of latissimus dorsi and serratus anterior muscles (a) to cover a complex open wound of the foot and ankle (b), illustrating the donor site (c and d) and fully covered defect (e and f) (case courtesy of Mr David Johnson FRCS(Plast)).

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mechanisms. Tissue-engineered biological substitutes for tendon, nerve, larynx and other vital structures are becoming established, and will greatly influence the spectrum of reconstructive procedures in the coming years. Novel polymers and biologically tolerated materials are also being developed to act as nerve conduits, facial muscle substitutes and self-inflating expansion devices. The interface of new material science with reconstructive surgery is still in its infancy.

Further reading

receipt of pituitary-derived human growth hormone, cadaveric dura mater grafts, and previous brain or spinal surgery prior to 1997. Where risk factors are present, instruments must be quarantined or destroyed postoperatively.

Risks of craniotomy The risks associated with craniotomy are important to appreciate in discussing operations with patients and family, and in evaluating patients who deteriorate postoperatively. The figures quoted in brackets will vary significantly between individual procedures and even between centres:

• • • • • •

infection (5 per cent) and wound breakdown; intracerebral haemorrhage; seizures; CSF leak; permanent neurological deficit; death (1 per cent).

Brainstem death

Diagnosis requires:

• identification of the cause of irreversible coma; • exclusion of reversible causes of coma; • clinical demonstration of the absence of brainstem function. In the UK, this entails testing twice, by two clinicians, to demonstrate the absence of:

• • • • • • •

response to pain; respiratory drive (apnoea despite a pCO2 >6.7 kPa); pupillary light reflex; corneal reflex; vestibulo-ocular reflex; oculocephalic reflex; gag reflex.

FURTHER READING Greenberg MS. Handbook of neurosurgery, 7th edn. New York: Thieme, 2010. Patten J. Neurological differential diagnosis, 2nd edn. New York: Springer, 1994. Samandouras G. The neurosurgeon’s handbook. Oxford: Oxford Publishing, 2010.

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This is defined as the irreversible loss of cerebral and brainstem function. Brainstem death is legally equivalent to death, and is a pre-condition for the harvesting of organs for transplant from heart-beating donors.

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Ambroise Paré, 1510–1590. He was official surgeon to the Kings: Henry II, Francis II, Charles IX and Henry III. He is considered as one of the fathers of surgery and a modest man who said ‘I dressed him and God healed him’.

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CHAPTER

The eye and orbit LEARNING OBJECTIVES

To understand and appreciate: • The common ocular disorders and recognise ophthalmic symptoms and specific signs

OCULAR ANATOMY Adnexae The lids comprise skin, connective tissue, the orbicularis oculi (VIIth cranial nerve) and the tarsal plate, with multiple meibomian glands opening posterior to the lashes and lined with conjunctiva, which is reflected onto the sclera. The upper lid is elevated by the levator muscle (IIIrd cranial nerve) and has a horizontal strip of sympathetically innervated Müller’s muscle, giving rise to 2 mm of ptosis in Horner’s syndrome. Both lids are attached to the orbital rim by the medial and lateral canthal tendons. Both have a rich vascular supply and are innervated by the V1 division of the trigeminal nerve (Vth cranial nerve) above and the V2 division below.

• The value of special investigations • When specialist referral is appropriate

are suspended by the suspensory ligament, over 300 tiny fibres attached to the ciliary muscle. Aqueous humour arises from the ciliary processes, hydrates the vitreous gel, passes through the pupil into the anterior chamber between the iris and the cornea and then drains out through the trabecular meshwork into Schlemm’s canal in the drainage angle. The inner retina is supplied by the central retinal artery and drained by the central retinal vein (Figure 44.1).

Orbit The orbit is four-sided and pyramidal in structure, housing the globe, optic nerve, the four rectus and two oblique muscles, the lacrimal gland, orbital fat, the IIIrd, IVth, Vth and VIth cranial

Choroid Sclera

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Lacrimal system The almond-shaped lacrimal gland lies under the upper outer orbital rim and opens into the upper conjunctival fornix through 10–15 ducts. Tears are swept across the globe by the lids and evaporate or pass into the upper and lower lid puncta, and then into the canaliculi to join the common canaliculus, which passes into the lacrimal sac under the medial canthal tendon. The sac is drained by the nasolacrimal duct into the nose, opening in the inferior meatus under the inferior turbinate.

The globe The cornea is the 12-mm diameter window of the eye, 0.5 mm thick centrally; its clarity is due to the regular arrangement of collagen bundles and relative dehydration. It merges into the sclera at the corneoscleral junction (the limbus), the insertion of the bulbar conjunctiva. The sclera, which is 1 mm thick, comprises four-fifths of the wall of the eye, and gives attachment to the extraocular muscles. It is perforated by the long and short posterior ciliary arteries and the vortex veins and is contiguous with the optic nerve sheath. The uvea comprises iris, ciliary body and vascular choroid. The optic nerve is continuous with the retina and retinal pigment epithelium. The most sensitive part of the retina, the macula, lies at the posterior pole within the vascular arcade. The biconvex lens and capsule

Superior rectus

Retina

Lens

Conjunctiva Canal of Schlemm

Central retinal artery

Cornea

Optic nerve Iris

Macula

Vascular choroid Ciliary body Inferior rectus

Vitreous humour

Uvea

Figure 44.1 Anatomy of the eye.

Johannes Peter Müller, 1801–1858, Professor of Anatomy and Physiology, Berlin, Germany. Johan Friedrich Horner, 1831–1886, Professor of Ophthalmology, Zurich, Switzerland, described this syndrome in 1869. Friedrich Schlemm, 1795–1858, Professor of Anatomy, Berlin, Germany.

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Periorbital and orbital swellings

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nerves, the ophthalmic artery with its tributaries and the ophthalmic veins, which anastomose anteriorly with the face and posteriorly with the cranial cavity. Above is the frontal lobe of the brain, temporally the temporal fossa, inferiorly the maxillary sinus and nasally the lacrimal sac and ethmoidal and sphenoidal air sinuses. The optic nerve passes through the optic canal to the chiasm, with other nerves and vessels passing through the superior ophthalmic fissure.

PERIORBITAL AND ORBITAL SWELLINGS Swellings related to the supraorbital margin Dermoid cysts Dermoid cysts are usually external angular cysts although they may occur medially (Figure 44.2). They often cause a bony depression by their pressure and they may have a dumbbell extension into the orbit. They can also erode the orbital plate of the frontal bone to become attached to dura and for this reason it is important to image the area by computed tomography (CT) before excision.

Neurofibromatosis Neurofibromatosis may also produce swellings above the eye. The diagnosis can usually be confirmed by an examination of the whole body, as there are often multiple lesions. Proptosis can also result (Figure 44.3). Other ophthalmic features may be present.

Figure 44.3 Neurofibroma in the orbit with proptosis, and also similar lesions in the forehead.

Swellings of the lids These are the most common lid swellings (Figure 44.4). A meibomian cyst is a chronic granulomatous inflammation of a meibomian gland. It may occur on either upper or lower lids and presents as a smooth, painless swelling. It can be felt by rolling the cyst on the tarsal plate. It can be distinguished from a stye (hordeolum), which is an infection of a hair follicle and is usually painful. Persistent meibomian cysts are treated by incision and curettage from the conjunctival surface. Styes are treated by antibiotics and local heat. Figure 44.4 Meibomian cyst (courtesy of Mr D Spalton, FRCS).

Basal cell carcinomas (rodent ulcers) This is the most common malignant tumour of the eyelids (Figure 44.5). It is locally malignant, is more common on the lower lids and usually starts as a small pimple that ulcerates and has raised edges (‘rodent ulcer’). It is easily excised in the early stages. Histological confirmation that the excision is complete is required. More extensive lesions may require specialist techniques, such as Mohs’ micrographic surgical excision controlled by frozen section. Local radiotherapy or cryotherapy can be carried out; however, recurrence is more common, more aggressive and more difficult to detect (Summary box 44.1).

Figure 44.2 External angular dermoid.

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Meibomian cysts (chalazion)

Frederic E Mohs, 1910–2002, physician and general surgeon, University of Wisconsin, Madison, WI, USA. Developed Mohs’ micrographic surgical technique in 1938 for cutaneous malignant lesions.

Heinrich Meibom (Meibomius), 1638–1700, Professor of Medicine, History and Poetry, Helmstadt, Germany, described these glands in 1666.

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Swellings of the lacrimal system Lacrimal sac mucocele This occurs from obstruction of the lacrimal duct beyond the sac and results in a fluctuant swelling that bulges out just below the medial canthus. It can become infected to give rise to a painful tense swelling (acute dacryocystitis). If untreated it may give rise to a fistula. Treatment is by performing a bypass operation between the lacrimal sac and the nose (a dacryocystorrhinostomy (DCR)). Watering of the eye can occur due to eversion of the lower lid (ectropion), which causes loss of contact between the lower punctum and the tear film, or from reflex hypersecretion as a result of irritation of inturning lashes in entropion, and these must be distinguished from a mucocoele. Figure 44.5 Rodent ulcers (courtesy of Mr J Beare, FRCS).

Summary box 44.1 Basal cell carcinomas ■ ■ ■

Basal cell carcinomas are the most common malignant eye tumour Treatment is by excision with care with histopathological margin control All unusual lesions (especially in the elderly) should be biopsied

Other lid swellings

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Other types of lid swelling can occur but they are less common. They include sebaceous cysts, papillomas, keratoacanthomas, cysts of Moll (sweat glands) (Figure 44.6) or Zeis (sebaceous glands) and molluscum contagiosum. When molluscum contagiosum occurs on the lid margin, it can give rise to a mild viral chronic keratoconjunctivitis and should be curetted or excised. Carcinoma of the meibomian glands and rhabdomyosarcomas are rare lesions; they need to be treated by radical excision. Atypical or meibomian cysts that recur should be biopsied.

Figure 44.6 Cyst of Moll.

Lacrimal gland tumours These are swellings of the lacrimal glands, which lie in the upper lateral aspect of the orbit. Eventually, they lead to impairment of ocular movements and displacement of the globe forwards, downwards and inwards. Pathologically the tumours resemble parotid tumours and they can be pleomorphic adenomas with or without malignant change, carcinomas or mucoepidermoid tumours.

Orbital swellings Orbital swellings result in displacement of the globe and limitation of movement. A full description of orbital swellings is outside the realm of this text but some of the most common causes include the following:

• Pseudoproptosis. This results from a large eyeball, as seen in congenital glaucoma or high myopia.

• Orbital inflammatory conditions that result in orbital cellulitis (Figure 44.7).

• Haemorrhage after trauma or retrobulbar injection. • Neoplasia affecting the lacrimal gland, the

optic nerve, the orbital walls or the nasal sinuses, e.g. glioma (neurofibromatosis) (see Figure 44.3), meningioma and osteoma (Figure 44.8). • Dysthyroid exophthalmos (Figures 44.9, 44.10 and 44.11). This may be unrelated to active thyroid disease but can start after thyroidectomy and may need urgent tarsorrhaphy, large doses of steroids or even orbital lateral wall decompression if the eyeball is threatened by exposure or optic nerve compression. CT and magnetic resonance imaging (MRI) scans are useful in diagnosis.

Figure 44.7 Orbital cellulitis.

Jacob Antonius Moll, 1832–1913, ophthalmologist of The Hague, The Netherlands. Edward Zeis, 1807–1868, Professor of Surgery, Marburg (1844–1850), who later worked at Dresden, Germany, described these glands in 1835.

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Intraocular tumours

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Figure 44.11 Exophthalmos in dysthyroid eye disease.

• Pseudotumour, or malignant lymphoma. • Haemangiomas of the orbit (Figure 44.12). • Tumour metastases. These are rare. In children they usually Figure 44.8 Radiograph showing an osteoma on the nasal side of the orbit giving rise to proptosis.

arise from neuroblastomas of the adrenal gland, whereas in adults the oesophagus, stomach, breast and prostate can be sites of primary lesions.

Diagnostic aids Diagnostic aids include radiography, CT, MRI, ultrasonography and, less commonly, tomography and orbital venography.

Treatment Treatment is directed to the cause of the lesion if at all possible, taking care to prevent exposure of the eye, diplopia or visual impairment from optic nerve compression.

INTRAOCULAR TUMOURS

Figure 44.9 Computed tomogram of the orbit in dysthyroid exophthalmos, showing swollen muscles (courtesy of Dr Glyn Lloyd).

Retinoblastoma is a multicentric malignant tumour of the retina, which can be bilateral. Some are sporadic, but many are hereditary. Children with a family history should be carefully monitored from birth. It is often not spotted until the tumour fills the globe and presents as a white reflex in the pupil or as a squint (Figure 44.13). The differential diagnosis includes retinopathy of prematurity, primary hyperplastic vitreous and intraocular infections. If the tumour is large, enucleation may be required, but radiotherapy, cryotherapy, chemotherapy or laser treatment can cure small lesions. Liaison with a paediatric oncologist is essential (Summary box 44.2).

Figure 44.10 Magnetic resonance imaging scan of a coronal view of the orbit, showing enlarged muscles in thyroid disease (courtesy of Dr Juliette Britton).

Figure 44.12 Capillary haemangioma in a child. An orbital venogram demonstrates displacement of the second part of the superior ophthalmic vein (arrow) (courtesy of Dr Glyn Lloyd).

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Children

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is by light or laser coagulation, radioactive plaque, radiotherapy, enucleation and, in selected cases, local excision using hypotensive anaesthesia. Diagnosis is made by direct observation and/or ultrasound, which shows a solid tumour (Figure 44.15).

INJURIES INVOLVING THE EYE AND ADJACENT STRUCTURES Corneal abrasions and ulceration

Figure 44.13 Retinoblastoma giving rise to a white pupillary reflex (courtesy of MA Bedford, FRCS).

The cornea is frequently damaged by direct trauma or by foreign bodies (Figure 44.16). Ulceration can occur with infection or after damage to the facial nerve. Post-herpetic ulceration is common and serious if not treated. Fluorescein instillation illuminated by blue light shows up corneal ulceration at an early stage (Summary box 44.3). Summary box 44.3

Summary box 44.2

Corneal abrasions

Intraocular tumours

■

■ ■

All children with a squint should have a fundal examination to exclude a retinoblastoma A blind painful eye may hide a melanoma

Adults

A drop of fluorescein dye illuminated by a blue light reveals even the smallest corneal abrasion

Treatment is by protection (eye pads, tarsorrhaphy or a bandage contact lens) and antibiotics topically and rarely systemically: 0.5 per cent chloramphenicol or ofloxacin eye

Malignant melanoma is the most common tumour and it originates in the pigment cells of the choroid (Figure 44.14), ciliary body or iris. It can present with a reduction in vision, a vitreous haemorrhage or by the chance finding of an elevated pigmented lesion in the eye. Tumour growth is variable but, as a general rule, the more posterior the lesion, the more rapidly progressive it is likely to be. Spread may be delayed for many years; however, the liver is frequently involved, hence the advice ‘beware of the patient with a glass eye and an enlarged liver’. Treatment

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Figure 44.15 B-scan showing choroidal melanoma (courtesy of Dr Marie Reston).

Figure 44.14 Choroidal melanoma.

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Figure 44.16 Corneal foreign body.

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Injuries involving the eye and adjacent structures

drops are commonly used. The eye is made more comfortable by the use of mydriatics, such as homatropine or cyclopentolate. Herpes simplex dendrititc ulcers are treated with aciclovir ointment. In countries in the Far and Middle East, chronic infection with trachoma can cause corneal opacification and blindness. Corneal grafting is the only cure for an opaque cornea. Until recently, full thickness penetrating keratoplasty was the only corneal graft technique. This has largely been replaced by lamellar or partial thickness graft surgery, in a technique termed DSEK or ‘Descamets stripping endothelial keratoplasty’. Rarely, osteoodonto keratoprosthesis can be attempted in very severe cases of opaque corneas that are not suitable for grafting. Acanthamoeba is a rare serious cause of corneal infection. This infection usually follows the use of contact lenses. Specialist management and treatment is recommended.

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Concussion injuries Concussion injuries of the eye can give rise to several problems, which include the following:

• Iritis. Inflammation, treated with topical steroids. • Hyphaema (blood in the anterior chamber) (Figure 44.20). Rest and sedation, particularly in children, are advised because the main danger in this condition is secondary bleeding, resulting in an acute rise in intraocular pressure and blood staining of the cornea. The use of antifibrinolytic agents (ε-aminocaproic acid) has been advocated and, if the pressure rises, surgery to wash out the blood may be necessary.

Blunt injuries to the eye and orbit

Figure 44.18 Injury from a ski stick into the right brow. Vision reduced to ‘no perception of light’ (courtesy of J Beare, FRCS).

Figure 44.19 Scan of orbit from Figure 44.18 showing a massive swelling of the medial rectus (courtesy of J Beare, FRCS).

Figure 44.17 Radiograph showing a blow-out fracture of the orbit (left) with soft tissue in the antrum (courtesy of Dr Glyn Lloyd).

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The floor of the orbit is its weakest wall and in blunt trauma, such as a blow from a fist, it is often fractured without fractures of the other walls. This is called a blow-out fracture. Clinical signs are enophthalmos, bruising around the orbit, maxillary hypoaesthesia, limitation of upward gaze due to entrapment of the inferior rectus muscle leading to vertical diplopia. This occurs when the extraocular muscles or orbital septa become trapped in the fracture and can be identified as a soft-tissue mass in the antrum on a radiograph (Figure 44.17), although CT scans or tomograms may be necessary. Surgical repair of the orbital floor with freeing of the trapped contents may be necessary if troublesome diplopia persists or enophthalmos is marked. A child with an orbital floor fracture requires urgent assessment as a ‘greenstick’ fracture can result in ischaemia of a trapped inferior rectus muscle and may require urgent surgery. If an orbital haemorrhage is too extensive to examine the eye, it may be necessary to examine the eye under anaesthesia because there may be a hidden perforation of the globe. Injuries to the lids and lid margins must be repaired, and if the lacrimal canaliculi are damaged they should be repaired if possible, especially the lower canaliculus as 75 per cent of tear drainage goes through it. Blunt injuries can also cause damage to the optic nerve, which can result in blindness and a total afferent pupillary defect (Figures 44.18 and 44.19).

Figure 44.20 Hyphaema. Blood in the vitreous chamber after concussional injury.

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Figure 44.23 Facial lacerations from a windscreen injury. Beware of a perforating eye injury.

Figure 44.21 Retinal haemorrhage from a cricket bat injury (courtesy of J Beare, FRCS).

• Subluxation of the lens. This is suspected if the iris, or part of the iris, ‘wobbles’ on movement (iridodonesis).

• Secondary glaucoma. This is often associated with recession

of the drainage angle. • Retinal and macular haemorrhages and choroidal tears (Figure 44.21). • Retinal dialysis. This may lead to a retinal detachment and permanent damage to vision (Figure 44.22).

Penetrating eye injuries These occur when the globe is penetrated, often in road traffic and other major accidents (Figure 44.23), and also in injuries from sharp instruments. The compulsory wearing of seatbelts in motor vehicles has substantially reduced the incidence of this type of eye injury, by up to 73 per cent in the UK. The presence of an irregular pupil suggests prolapse of the iris and should arouse the suspicion of a penetrating injury. Treatment is prompt primary repair to restore the integrity of the globe. If a perforation is suspected, extensive eye examination should not

be attempted before anaesthesia because this may lead to further extrusion of the intraocular contents. If the fundal view is poor, ultrasonography and orbital imaging are indicated. Secondary corneal grafting, lensectomy and vitrectomy have considerably improved the visual prognosis; these must be done by an experienced eye surgeon. Injuries to the optic nerves must also be excluded in severe accidents.

Intraocular foreign bodies Intraocular foreign bodies must always be excluded when patients attend the accident and emergency department with an eye injury and a history of working with a hammer and chisel or a history of a potentially high-velocity injury. Radiography of the orbits should always be performed, and ferrous and copper foreign bodies should always be removed, sometimes requiring the use of a magnet. B-scan ultrasonography can also assist in localising foreign bodies when a vitreous haemorrhage or cataract is present. CT can be used, but MRI is contraindicated (Summary box 44.4). Summary box 44.4 Penetrating eye injuries

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■

A distorted and irregular pupil warrants the careful exclusion of a penetrating eye injury

Burns Radiation burns These occur following exposure to ultraviolet radiation after arc welding or excessive sunlight (snow blindness) and sun lamps. Such burns cause intense gritty burning pain and photophobia as a result of keratitis (corneal inflammation), which starts some hours after exposure. Mydriatic and local steroids with antibiotic drops ease the condition, and healing usually occurs after 24 hours.

Thermal burns

Figure 44.22 Retinal dialysis after concussional injury.

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If these involve the full thickness of the lids, corneal scarring may occur from exposure, and immediate corneal protection is necessary. A splash of molten metal may cause marked local necrosis and may lead to permanent corneal scarring. Treatment

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Differential diagnosis of the acute red eye

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Figure 44.24 Chemical burn showing conjunctival necrosis.

Chemical burns Chemical burns, and especially alkali burns, can be serious because ocular penetration occurs quickly and ischaemic necrosis can result (Figure 44.24). Immediate copious irrigation until the pH is neutral will ensure that the chemical is diluted as much as possible, and all particles should be removed from the fornices. Treatment can then be continued as with thermal burns. Well-fitting goggles should prevent such injuries.

DIFFERENTIAL DIAGNOSIS OF THE ACUTE RED EYE This is important in the management of minor ocular complaints and the recognition of conditions that require expert attention. Possible causes of the acute red eye include:

• • • • • •

subconjunctival haemorrhage conjunctivitis keratitis uveitis episcleritis and scleritis acute glaucoma.

Figure 44.25 Vernal conjunctivitis (spring catarrh) showing cobblestone appearance under the upper lid.

adenovirus infections must be considered. Adenoviral infections are common and usually affect one eye much more in severity and onset, tending to be more watery than sticky, and are often associated with a palpable preauricular gland. Vernal conjunctivitis (Figure 44.25) is a form of allergic conjunctivitis, characterised by itchy eyes, usually worse in the spring and early summer and often associated with other allergic problems such as hay fever. Clinically, most signs are under the upper lid, which may have a cobblestone appearance instead of a smooth surface. Giant pupillary conjunctivitis with large papillae under the upper lid may be seen in soft contact lens wearers. This is usually caused by an allergy to the sterilising solutions and lens protein and may be helped by either using a preservative-free solution or using daily-wear disposable lenses. Kaposi’s sarcoma can rarely present like a subconjunctival haemorrhage (Figure 44.26). Considerable conjunctival and corneal irritation can be caused by the lids turning in (entropion) (Figure 44.27) or turning out (ectropion) (Figures 44.28 and 44.29), and by ingrowing lashes. The lids should be repaired surgically to their normal position.

Any condition with pain, visual impairment or a pupil abnormality suggests a more serious diagnosis.

Subconjunctival haemorrhage This presents as a bright-red eye, often noticed incidentally, with only minimal discomfort and normal vision. Causes include coughing, sneezing, minor trauma, hypertension and, rarely, a bleeding disorder. Reassurance and treatment of the underlying cause are required. Most settle within a week, but can recur.

Conjunctivitis Symptoms are grittiness, redness and discharge. Causes are infective, chemical, allergic or traumatic. In the newborn, it can be serious; gonococcal and chlamydial infection must be excluded. Bacterial conjunctivitis is purulent, usually self-limiting and treated with topical broad-spectrum antibiotics. Chlamydial and

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is to remove any debris by irrigation and to instill local atropine, antibiotics and steroids to prevent superadded infection and scarring. Lid reconstruction may be necessary.

Figure 44.26 Kaposi’s sarcoma of conjunctiva.

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Figure 44.27 Entropion (courtesy of J Beare, FRCS).

Vision is not commonly affected in conjunctivitis but, with some viral infections, a keratitis may be present and result in visual impairment and pain. All of the other conditions described below are painful and usually affect vision.

Keratitis (inflammation of the cornea) Herpes simplex infection presents as a dendritic (branching) ulcer, shown easily by staining with fluorescein or Bengal Rose. It is treated with aciclovir ointment five times per day. The use of steroid drops must be avoided as this can make the condition much worse (Figure 44.30). Corneal ulceration may occur as a result of ingrowing lashes or corneal foreign bodies, marginal ulceration and infected abrasions. Infected ulcers can occur in patients wearing soft contact

Figure 44.30 Dendritic staining caused by herpes keratitis.

lenses or elderly immunocompromised individuals. Herpes zoster (shingles) may affect the ophthalmic division of the Vth nerve and can give rise to a keratitis and uveitis. It is important to avoid the use of steroid drops until a diagnosis has been made. Local anaesthetic drops should also not be given on a regular basis.

Uveitis This can be anterior (iritis) or, more rarely, posterior. In anterior uveitis, the pupil will be small, sometimes irregular, there is circumcorneal injection and there may be keratic precipitates present on the posterior surface of the cornea. Pain, photophobia and some visual loss are usually present. Posterior uveitis can present with a white eye and blurred vision. It usually takes a chronic course. Granulomatous diseases, Behc¸et’s disease, Reiter’s syndrome, toxoplasmosis and cytomegalovirus infection should be excluded. Topical systemic steroids and, sometimes, immunosuppressive drugs are useful in treating these conditions.

Episcleritis and scleritis

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Episcleritis or inflammation of the episcleral tissue often occurs as an idiopathic condition (Figure 44.31). Scleritis is a less common, more serious, condition in which the deeper sclera is involved. There is often an associated uveitis

Figure 44.28 Ectropion, lower lid (courtesy of J Beare, FRCS).

Figure 44.29 Ectropion, upper lid – chronic staphylococcal infection (courtesy of J Beare, FRCS).

Figure 44.31 Episcleritis.

Bengal Rose (or Rose Bengal) is dichlortetraiodofluorescein. Hulusi Behçet, 1889–1948, Professor of Dermatology, Istanbul, Turkey, described this disease in 1937. Hans Conrad Julius Reiter, 1881–1968, President of the Health Service, and Honorary Professor of Hygiene at the University of Berlin, Germany, described this disease in 1916.

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and severe pain. Thinning of the sclera may result. Systemic non-steroidal anti-inflammatory drugs (NSAIDs) or steroids may be required to treat the condition adequately. Scleritis is often associated with severe rheumatoid conditions. The presence of scleritis suggests that there is active systemic disease and it requires systemic work-up including renal function tests.

Acute glaucoma This usually occurs in older, often hypermetropic, patients. The cornea becomes hazy, the pupil oval, dilated and non-reacting, the vision poor and the eye feels hard. In severe cases, pain may be accompanied by vomiting and the condition can be mistaken for an acute abdominal problem. Tonometry (intraocular pressure measurement) is diagnostic. Urgent treatment to reduce the pressure with pilocarpine, acetazolamide and, if refractory, mannitol should be started, followed by YAG laser iridotomy or surgical iridectomy. The condition is usually bilateral and the second eye usually needs a prophylactic iridotomy at the same time. Except for a simple conjunctivitis and subconjunctival haemorrhage, which are self-limiting, the management of an acute red eye requires expert treatment and a specialist opinion should be sought. A painful eye with a IIIrd nerve palsy (ptosis, dilated pupil, globe down and out) often signifies an intracranial aneurysm and should be investigated immediately.

Figure 44.32 Retinal artery occlusion.

PAINLESS LOSS OF VISION This may occur in one or both eyes, and the visual loss may be transient or permanent. Possible causes are:

• Acute:

Figure 44.33 Central retinal vein occlusion.

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– obstruction of the central retinal artery (Figure 44.32); – obstruction of the central retinal vein (Figure 44.33); – ischaemic optic neuropathy; – migraine and other vascular causes; – vitreous and retinal haemorrhages; – retinal detachment (Figure 44.34); – macular hole, cyst or haemorrhage; – cystoid macular oedema, often after surgery; – hysterical blindness. • Chronic: – cataract; – glaucoma; – macular degeneration; – diabetic retinopathy; Specialist help should be sought in any case of loss of vision. The erythrocyte sedimentation rate and C-reactive protein should be measured immediately if cranial arteritis is suspected, and the carotid system should be examined for bruits and other signs of arteriosclerosis in cases of ischaemic optic neuropathy and central retinal artery occlusion. Glaucoma, hypertension, hyperviscosity syndromes and diabetes should be looked for in cases of central vein thrombosis.

RECENT DEVELOPMENTS IN EYE SURGERY In the last three decades, eye surgery has become a microsurgical specialty. Cataract surgery has been transformed by changes in local anaesthesia, implants, phacoemulsification and small-

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Figure 44.34 B-scan of a retinal detachment.

incision surgery, which allow compressible/foldable silicone or acrylic implants to be inserted through a 2-mm incision. The implant power can be more accurately measured by new formulae and the use of A-scan ultrasonography or laser wavefront

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biometry, and multifocal and accommodative lenses are now available. There are new treatments for eye disorders that involve abnormal growth of blood vessels in the back of the eye, such as the wet form of age-related macular degeneration. Monoclonal anti-vascular endothelial growth factor (VEGF) antibodies, such as the drug ranibizumab, may be injected directly into the vitreous cavity to reduce new vessel proliferation. Intravitreal steroid injections help to treat cystoid macular oedema. Developments in vitreous surgery have enabled membranes to be peeled off the retina and macular holes to be repaired. They have also increased the success rate in retinal detachment surgery with the additional use of gases and silicone oil or heavy liquid inserted into the vitreous cavity tamponading the retina. Some paralytic squints can be helped by the use of adjustable sutures or injections of botulinum toxin into the overacting muscles. Refractive errors can be treated by the excimer laser. These can be combined with laser in situ keratomeilusis (LASIK) surgery, which involves cutting a corneal flap (by femtosecond laser or surgery) and performing the laser surgery at a deeper level. There have been some concerns about defective contrast sensitivity and problems with night vision after laser correction of myopia. Phakic implants have also been used to correct high refractive errors. Corneal topography aids the accuracy of corneal and refractive surgery and the increased use and quality of CT and MRI scans has revolutionised the diagnosis of orbital and intracranial lesions involving the optic pathways (Figures 44.35, 44.36 and 44.37). Fluorescein angiography, and ocular coherence tomography (OCT) are invaluable in the diagnosis and treatment of macular conditions. The glaucoma detection (GDx) retinal nerve fibre analyser and Heidelberg retinal tomography (HRT) are increasingly used in the diagnosis and management of glaucoma.

Figure 44.36 High-resolution computed tomography through the orbits showing dense calcification of the optic nerve sheaths typical of optic nerve meningioma (courtesy of Dr Juliette Britton).

LASERS IN OPHTHALMOLOGY

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Argon blue–green or diode laser is used to treat the retina in diabetic retinopathy (pan-retinal photocoagulation from proliferative disease or focal treatment for leaky microaneurysms),

Figure 44.35 Magnetic resonance imaging scan, sagittal view. Craniopharyngioma. The mass in the suprasellar cistern is of high signal intensity because of the proteinaceous fluid that the cyst contains (courtesy of Dr Juliette Britton).

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Figure 44.37 Axial enhanced magnetic resonance imaging scan showing a mass involving the optic chiasma and extending down the optic nerves and tracts.

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Further reading

and is also used to close retinal tears or breaks that might lead to retinal detachment. Argon laser or selective laser trabeculoplasty can be used to open the drainage angle to control elevated intraocular pressure in open angle glaucoma. Trans-scleral diode photocoagulation of the ciliary body is used to treat refactory secondary glaucoma with uncontrolled ocular pressure. Laser iridotomy with the Nd:YAG laser is used to treat both the affected and fellow eye in acute angle closure glaucoma. The Nd:YAG laser is also used to photodisrupt and clean an opaque posterior capsule which occurs in 5–10 per cent of cases following cataract surgery.

Evisceration of an eyeball

SURGICAL PROCEDURES

Incision and curettage of chalazion (meibomian cyst)

Excision of an eyeball/enucleation

The lid margin is everted to allow the application of a meibomian clamp. The ring of the clamp is placed on the palpebral conjunctiva with the granuloma in the centre. An incision is made with a small blade in the axis of the gland. The herniating granulomatous tissue is removed with a curette and the cavity is scraped clean. Recurrent cysts may have to have the cyst wall dissected away with scissors. A biopsy may be necessary in atypical or recurrent cysts to exclude malignant change.

Indications include a blind, painful eye, a blind, cosmetically poor eye/intraocular neoplasm and, in cadavers, for use in corneal grafting.

The operation

Evisceration is preferred to excision in endophthalmitis, minimising the risk of orbital and intracranial spread with meningitis. The sclera is transfixed with a pointed knife a little behind the corneosclerotic junction, and the cornea is removed entirely by completing the encircling incision in the sclera. The contents of the globe are then removed with a curette, care being exercised to remove all of the uveal tract. At the end of the operation the interior must appear perfectly white. A ball orbital implant made of acrylic or hydroxyapatite is placed within the orbit behind the sclera to improve the appearance when the artificial eye is fitted.

FURTHER READING Findlay RD, Payne PAG. The eye in general practice, 10th edn. Oxford: Butterworth-Heinemann, 1997. Kanski J, Bowling B. Clinical ophthalmology: a systematic approach, 7th edn. Philadelphia, PA: Saunders, 2011. Kline LB, Bajandas FJ. Neuro-ophthalmology review manual, 6th edn. Thorofare, NJ: Slack Incorporated, 2008. Olver J, Cassidy L. Ophthalmology at a glance. Oxford: Blackwell Publishing, 2005. Wills Eye Hospital. The Wills eye manual: office and emergency room diagnosis and treatment of eye disease, 6th edn. Philadelphia, PA: Lippincott Williams & Wilkins, 2012.

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The speculum is introduced between the lids and opened. The conjunctiva is picked up with toothed forceps and divided completely all round as near as possible to the cornea. Tenon’s capsule is entered and each of the four rectus and two oblique muscle tendons is hooked up on a strabismus hook and divided close to the sclera. The speculum is now pressed backwards and the eyeball projects forwards. Blunt scissors, curved on the flat, are insinuated on the inner side of the globe, and these are used to sever the optic nerve. The eyeball can now be drawn forwards with the forceps, and the oblique muscles, together with any other strands of tissue that are still attaching the globe to the orbit, are divided. A swab, moistened with hot water and pressed into the orbit, will control the haemorrhage. If an orbital implant is inserted to give better eye movement, the muscles are sutured to the implant at the appropriate sites. The subconjunctival tissues and conjunctiva are closed in layers.

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Jacques Rene Tenon, 1724–1816, surgeon, La Salpêtrière, Paris, France.

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CHAPTER

Cleft lip and palate: developmental abnormalities of the face, mouth and jaws LEARNING OBJECTIVES

To understand: • The aetiology and classification of cleft lip and palate • The principles of reconstruction of cleft lip and palate

INTRODUCTION

AETIOLOGY

Clefts of the lip, alveolus and hard and soft palate are the most common congenital abnormalities of the orofacial structures. They frequently occur as isolated deformities, but can be associated with other medical conditions, particularly congenital heart disease. They are also an associated feature in over 300 recognised syndromes. All children born with a cleft lip and palate need a thorough paediatric assessment to exclude other congenital abnormalities. In certain circ*mstances, genetic counselling must be sought if a syndrome is suspected.

Contemporary opinion on the aetiology of cleft lip and palate is that cleft lip and palate and isolated cleft palate have a genetic predisposition and a contributory environmental component. A family history of cleft lip and palate in which the first-degree relative is affected increases the risk to 1:25 live births. Genetic influence is more significant in cleft lip/palate than cleft palate alone, in which environmental factors exert a greater influence. Environmental factors implicated in clefting include maternal epilepsy and drugs, e.g. steroids, diazepam and phenytoin. The role of antenatal folic acid supplements in preventing cleft lip and palate remains equivocal. Although most clefts of the lip and palate occur as an isolated deformity, Pierre Robin sequence remains the most common syndrome. This syndrome comprises isolated cleft palate, retrognathia and a posteriorly displaced tongue (glossoptosis), which is associated with early respiratory and feeding difficulties. Isolated cleft palate is more commonly associated with a syndrome than cleft lip/palate and cleft lip alone. Over 150 syndromes are associated with cleft lip and palate, although Stickler’s (ophthalmic and musculoskeletal abnormalities), Shprintzen’s (cardiac anomalies), Down’s, Apert’s and Treacher Collins’ syndromes are most frequently encountered (Summary box 45.1).

INCIDENCE PART 7 | HEAD AND NECK

• The key features of the perioperative care of the child with cleft lip and palate • The associated complications of cleft lip and palate and their management

The incidence of cleft lip and palate is 1:600 live births and of isolated cleft palate is 1:1000 live births. The incidence increases in Oriental groups (1:500) and decreases in the black population (1:2000). The highest incidence reported for cleft lip and palate occurs in the Indian tribes of Montana, USA (1:276). Although cleft lip and palate is an extremely diverse and variable congenital abnormality, several distinct subgroups exist, namely cleft lip with/without cleft palate (CL/P), cleft palate (CP) alone and submucous cleft palate (SMCP). The typical distribution of cleft types is:

• cleft lip alone: 15 per cent; • cleft lip and palate: 45 per cent; • isolated cleft palate: 40 per cent. Cleft lip/palate predominates in males, whereas cleft palate alone appears to be more common in females. In unilateral cleft lip, the deformity affects the left side in 60 per cent of cases.

Summary box 45.1 Cleft lip and palate ■ ■ ■

Associated with other congenital abnormalities Incidence varies between races from 1:300 to 1:2000 live births Aetiology is both genetic and environmental

Pierre Robin, 1867–1950, professor, The French School of Dentistry, Paris, France, described this syndrome in 1929. Gunnar B Stickler, 1925–2010, born in Germany, Chair of Section of Paediatrics and later Paediatric Cardiology, The Mayo Clinic, Rochester, MN, USA. Robert J Shprintzen, born 1946, surgeon, Syracuse, NY, USA. John Langdon Haydon Down (sometimes given as Langdon-Brown), 1828–1896, physician, The London Hospital, UK, published the classification of aments in 1866. Eugene Apert, 1868–1940, physician, L’Hopital des Infants-Malades, Paris, France, described this syndrome in 1906. Edward Treacher Collins, 1862–1932, ophthalmic surgeon, the Royal London Ophthalmic Hospital, and Charing Cross Hospital, London, UK, described this syndrome in 1900.

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Anatomy of cleft lip and palate

ANATOMY OF CLEFT LIP AND PALATE Cleft lip The abnormalities in cleft lip are the direct consequence of disruption of the muscles of the upper lip and nasolabial region. The facial muscles (Figure 45.1) can be divided into three muscular rings of Delaire: the nasolabial muscle ring surrounds the nasal aperture; the bilabial muscle ring surrounds the oral aperture; and the labiomental muscle ring envelops the lower lip and chin regions.

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and upper lip. The secondary palate is defined as the remainder of the palate behind the incisive foramen, divided into the hard palate and, more posteriorly, the soft palate. Cleft palate results in failure of fusion of the two palatine shelves. This failure may be confined to the soft palate alone or involve both hard and soft palate. When the cleft of the hard palate remains attached to the nasal septum and vomer, the cleft is termed incomplete. When the nasal septum and vomer are completely separated from the palatine processes, the cleft palate is termed complete (Summary box 45.2).

Unilateral cleft lip

Summary box 45.2

In the unilateral cleft lip, the nasolabial and bilabial muscle rings are disrupted on one side resulting in an asymmetrical deformity involving the external nasal cartilages, nasal septum and anterior maxilla (premaxilla) (Figure 45.2a and b). These deformities influence the mucocutaneous tissues causing a displacement of nasal skin onto the lip and a retraction of labial skin, as well as changes to the vermilion and lip mucosa. All these changes need to be considered in planning the surgical repair of the unilateral cleft lip.

Types of cleft palate ■ ■

May involve the soft palate or the soft and hard palate It is complete when nasal septum and vomer are separated from the palatine process

Bilateral cleft lip In the bilateral cleft lip, the deformity is more profound but symmetrical. The two superior muscular rings are disrupted on both sides producing a flaring of the nose (caused by lack of nasolabial muscle continuity), a protrusive premaxilla and an area of skin in front of the premaxilla devoid of muscle, known as the prolabium (Figure 45.3a and b). As in the unilateral cleft lip, the muscular, cartilaginous and skeletal deformities influence the mucocutaneous tissues, which must be respected in planning the repair of the bilateral cleft lip.

Cleft palate

A B C (a)

(b)

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Embryologically, the primary palate consists of all anatomical structures anterior to the incisive foramen, namely the alveolus

Figure 45.1 The muscle chains of the face: frontal view. The nasal cartilages are represented in blue. A, nasolabial (muscles 1–3); B, bilabial (muscles 4–6); C, labiomental (muscles 7–9); 1, transverse nasalis; 2, levator labii superioris alaeque nasi; 3, levator labii superioris; 4, orbicularis oris (oblique head) – upper lip; 5, orbicularis oris (horizontal head) – upper lip; 6, orbicularis oris – lower lip; 7, depressor anguli oris; 8, depressor labii inferioris; 9, mentalis.

Figure 45.2 (a) Schematic representation of disruption of the nasolabial and bilabial muscle chains in unilateral (left) cleft lip. A, nasolabial; B, bilabial; C, labiomental. (b) Unilateral cleft lip before muscular reconstruction.

Title: Bailey & Love’s Short Practice of Surgery, 26th Ed

ISBN: 9781444121278

Proof Stage:

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Hard palate

(a)

B C (a)

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The normal hard palate can be divided into three anatomical and physiological zones (Figure 45.5). The central palatal fibromucosa is very thin and lies directly below the floor of nose. The maxillary fibromucosa is thick and contains the greater palatine neurovascular bundle. The gingival fibromucosa lies more lateral and adjacent to the teeth.

ISBN: 9781444121278

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Fig No: 45.3a

Figure 45.4 (a) Cleft of soft palate and incomplete cleft of hard palate. (b) Muscles of the soft palate: left, cleft palate; right, normal anatomy. A, tensor palati; B, levator palati; C, palatopharyngeus; D, palatoglossus; E, musculus uvulae. Figure 45.3 (a) Schematic representation of disruption of the nasolabial and bilabial muscle chains in bilateral cleft lip. A, nasolabial; B, bilabial; C, labiomental. (b) Bilateral cleft lip before muscular reconstruction.

1 2 3

Soft palate In the normal soft palate, closure of the velopharynx, which is essential for normal speech, is achieved by five different muscles functioning in a complete but coordinated fashion. In general, the muscle fibres of the soft palate are orientated transversely with no significant attachment to the hard palate. In a cleft of the soft palate (Figure 45.4a) the muscle fibres are orientated in an anteroposterior direction, inserting into the posterior edge of the hard palate (Figure 45.4b).

Figure 45.5 The three mucosal zones of the hard palate. 1, palatal fibromucosa; 2, maxillary fibromucosa; 3, gingival fibromucosa.

Jean Delaire, Professor of Stomatology and Maxillofacial Surgery, University of Nantes, Nantes, France from 1960 until 1991.

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Principles of cleft surger y

In performing surgical closure of cleft palate the changes associated with the cleft must be understood to obtain an anatomical and functional repair. In complete cleft palate, the median part of the palatal vault is absent and the palatal fibromucosa is reduced in size. The maxillary and gingival fibromucosa are not modified in thickness, width or position.

Nose Prolabium Premaxilla Lip Alevolus Hard palate

CLASSIFICATION Any classification for such a diverse and varied condition as cleft lip and palate needs to be simple, concise, flexible and exact but graphic. It must be suitable for computerisation but descriptive and morphological. An example of such a classification is the LAHSHAL system, which is able to describe site, size and extent, as well as type of cleft (Figure 45.6). Complete clefts of the lip, alveolus and hard and soft palate are designated as capitals L, A, H and S, respectively. Incomplete clefts are recorded in lower case letters whereas microform clefts are documented with asterisks. Hence, LAHSHAL is the anatomical paraphrase of a complete bilateral cleft lip and palate. Another example, lahSh, represents an incomplete right unilateral cleft lip and alveolus with a complete cleft of soft palate extending partly onto the hard palate.

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Soft palate

Figure 45.6 LAHSAL: an anatomical representation of cleft lip (L), alveolus (A) and hard (H) and soft palate (S).

PRIMARY MANAGEMENT An antenatal diagnosis of cleft lip, whether unilateral or bilateral, is possible by ultrasound scan after 18 weeks of gestation. Isolated cleft palate cannot be diagnosed by antenatal scan. When an antenatal diagnosis is confirmed, referral to a cleft surgeon is appropriate for counselling to allay fears. Photographs of cleft lip shown to parents ‘before and after’ surgery are invaluable. Introduction to a parent support group and meeting parents of a child with a similar cleft who has undergone surgery may also be extremely helpful (Summary box 45.3).

Airway Major respiratory obstruction is uncommon and occurs exclusively in babies with Pierre Robin sequence. Hypoxic episodes during sleep and feeding can be life-threatening. Intermittent airway obstruction is more frequent and is managed by nursing the baby prone. More severe and persistent airway compromise can be managed by ‘retained nasopharyngeal intubation’ to maintain the airway. Surgical adhesion of the tongue to the lower lip (labioglossopexy) in the first few days after birth is an alternative but less commonly practised method of management (Summary box 45.4).

Summary box 45.3

Summary box 45.4

Antenatal diagnosis and counselling

Problems immediately after birth

■ ■

All but isolated cleft palate can be diagnosed by ultrasound scan after 18 weeks’ gestation Parents will need counselling and support

Feeding

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Some babies are able to feed normally but some will need assistance Breathing problems in Pierre Robin sequence may be lifethreatening

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Antenatal diagnosis

Most babies born with cleft lip and palate feed well and PRINCIPLES OF CLEFT SURGERY thrive, provided that appropriate advice is given and support ISBN: 9781444121278 Proof Stage: 2 Title: Bailey & Love’s Short Practice of Surgery, 26th Ed is available. Some mothers are successful in breastfeeding, The ultimate goal in cleft lip and palate management is a particularly when the cleft www.cactusdesign.co.uk is incomplete and confined to the patient with a normal appearance of lip, nose and face, whose lip. Good feeding patterns can be established with soft bottles speech is normal and whose dentition and facial growth fall (e.g. Mead Johnson) and modified teats (orthodontic, Nuyk). within the range of normal development. Surgical techniques are aimed at restoring normal anatomy. Simple measures, such as enlarging the hole in the teat, often suffice. Feeding plates, constructed from a dental impression of With the exception of rare conditions such as holoprosenthe upper jaw, are rarely necessary to improve feeding. Some cephaly, there is no true hypoplasia of the tissues involved babies are provided with an active plate that aims not only to on either side of the cleft. There is, however, displacement, improve feeding but also reduce the width of the cleft lip and deformation and underdevelopment of the muscles and facial palate prior to surgery. The long-term benefit of such a regime skeleton. Emphasis is placed on muscular reconstruction of the lip, nose and face, as well as muscles of the soft palate. Normal remains unproven.

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or near-normal anatomy promotes normal function, thereby encouraging normal growth and development of lip, nose, palate and facial skeleton. An in-depth understanding of the anatomy of the cleft is invaluable if the surgeon is to achieve normal, or near-normal, anatomical reconstruction (Summary box 45.5). Summary box 45.5

(a)

Surgical anatomy ■ ■ ■

Normal lip, face and nose There is underdevelopment and displacement of the muscles Restoration of normal anatomy encourages normal facial growth and function

(b)

Figure 45.7 (a and b) Skin incisions (highlighted in red) for left unilateral complete cleft lip (after Delaire).

Surgical techniques There have been many different surgical techniques and sequences advocated in cleft lip and palate management. Cleft lip repair is commonly performed between three and six months of age, whereas cleft palate repair is frequently performed between six and 18 months. The Delaire technique and sequence (Table 45.1) is one of many regimes currently practised.

(b)

(a)

(c)

Figure 45.8 (a–c) Skin incisions for bilateral complete cleft lip, showing the shaded area from Figure 45.7a. Areas for removal of excess mucosa (a) or skin (b) (after Delaire).

Cleft lip surgery

Muscular continuity is achieved by subperiosteal undermining over the anterior maxilla. Nasolabial muscles are anchored to the premaxilla with non-resorbable sutures. Oblique muscles of orbicularis oris are sutured to the base of the anterior nasal spine and cartilaginous nasal septum. Closure of the cleft lip is completed by suturing the horizontal fibres of orbicularis oris to Table 45.1 Timing of primary cleft lip and palate procedures (after achieve a functioning oral sphincter (Figures 45.9 and 45.10). Delaire). When the cleft lip is incomplete (Figures 45.11a and 45.12a), meticulous assessment of the cleft deformity is of paramount Cleft lip alone importance, as complete muscle disruption may be present leadUnilateral (one One operation ing to nasal and skeletal deformity. Full muscular exposure and side) at 5–6 months Short Practiceisofimperative Surgery, 26th Title: Bailey & Love’s reconstruction inEdmany incomplete clefts if ISBN: facial 9781444121278 Bailey & Love’s Short Practice of Surgery, 26th Ed ISBN:(Figures 9781444121278 Proof Stage: 2 Fig No: symmetry is to be achieved 45.11b and 45.12b). Bilateral (both One Title: operation Skin incisions (Figures 45.7 and 45.8) are developed to restore displaced tissues, including skin and cartilage, to their normal position, while gaining access to the facial, nasal and lip musculature.

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Cleft palate alone

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Soft palate only

One operation at 6 months

Soft and hard palate

Two operations Soft palate at 6 months Hard palate at 15–18 months

Cleft lip and palate Unilateral

Bilateral

Two operations Cleft lip and soft palate at

Cleft palate surgery Cleft palate closure can be achieved by one- or two-stage palatoplasty. The surgical principle is mobilisation and reconstruction of the aberrant soft palate musculature (Figure 45.13a and b), together with closure of the residual hard palate cleft by minimal dissection and subsequent scar formation (Figure 45.14a and b). Excess scar formation in the palate adversely affects growth and development of the maxilla. The philosophy of two-stage closure encourages a physiological narrowing of the hard palate cleft to minimise surgical dissection at the time of the second procedure (Summary box 45.6).

Shortmonths Practice of Surgery, 26th Ed ISBN: 9781444121278 Proof Stage: 2 Title: Bailey & Love’s 5–6 Fig No: 4 ISBN: 97814441212 Hard palate and gumTitle: pad Bailey & Love’s Short Practice of Surgery, 26th Ed Summary box 45.6 www.cactusdesign.co.uk with or without revision atPractice of Surgery, 26th Ed Bailey &lipLove’s Short ISBN: 9781444121278 Proof St Title: www.cactusdesign.co.uk 15–18 months Principles of surgery www.cactusdesign.co.uk

Two operations Cleft lip and soft palate at 4–5 months

Hard palate and gum pad with or without lip revision at 15–18 months

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■ ■ ■

Cleft lip surgery attaches and reconnects the muscles around the oral sphincter Cleft palate surgery aims to bring together mucosa and muscles with minimal scarring Two-stage procedures attempt to minimise dissection

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(a)

(b)

Figure 45.9 Unilateral complete cleft lip before (a) and after (b) muscular reconstruction.

SECONDARY MANAGEMENT Following primary surgery, regular review by a multidisciplinary team is essential. Many aspects of cleft care require long-term review:

• • • •

hearing speech dental development facial growth.

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Figure 45.10 Bilateral cleft lip before (a) and after (b) muscular reconstruction.

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(b)

Hearing Eustachian tube dysfunction plays a central role in the pathogenesis of otitis media with effusion in babies and children born with a cleft palate. Children with a cleft lip alone exhibit

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Figure 45.11 Unilateral incomplete cleft lip before (a) and after (b) muscle reconstruction.

the same frequency of otitis media as their age-matched noncleft counterparts. It has been recently recognised that a child with a craniofacial anomaly including cleft lip and palate is at increased risk of a sensorineural hearing deficit. All children born with a cleft lip and palate should undergo assessment before 12 months of age for sensorineural and conductive hearing loss by auditory brainstem responses (ABR) and tympanometry, respectively. Sensorineural hearing loss is managed with a hearing aid whereas the management of secretory otitis media remains more controversial. Early (6–12 months) prophylactic myringotomy and grommet insertion temporarily eliminates middle ear effusion. Regular audiological testing may be as appropriate, reserving surgery for established secretory otitis media with infection. No firm evidence is available to support the interventional approach over the conservative regime. Nevertheless, the relationship between hearing loss and potential speech problems remains important. Regular audiological assessment during childhood is of utmost importance.

Speech Initial speech assessment should be performed early (18 months) and repeated regularly to ensure that problems are identified early and managed appropriately. Common speech problems associated with cleft lip and palate are:

• Velopharyngeal incompetence. This is associated with increased nasal airflow and resonance, producing a nasal

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or ‘hypernasal’ quality to speech. It frequently reflects poor function of the soft palate associated with inadequate muscle repair. Articulation problems. These arise either as a compensatory • mechanism to overcome velopharyngeal incompetence or, less commonly, are caused by jaw/dental and occlusal abnormalities. Videofluoroscopy, nasal airflow studies (aerophonoscopy) and nasendoscopy are helpful in defining the exact mechanism of the problem, aiding management. • Speech problems. These are managed by speech and language therapy; secondary palatal surgery, either intravelar veloplasty (muscular reconstruction of soft palate) or pharyngoplasty; and speech training devices (Summary box 45.7). Summary box 45.7 Associated hearing and speech problems ■ ■ ■

Higher incidence of sensorineural and conductive hearing loss Regular hearing tests are important if speech is to develop normally Speech problems may result from airflow problems

Dental Dental anomalies are common findings in children with cleft lip and/or palate. Various phenomena including delayed tooth development, delayed eruption of teeth and morphological

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(b)

(a)

(b)

Figure 45.13 (a and b) Method of repair of cleft palate. First-stage palatoplasty to reconstruct muscles of the soft palate. Red lines represent incisions, and orange areas raw surfaces.

abnormalities are well documented. The number of teeth may be reduced (hypodontia) or increased (hyperdontia), occurring most commonly in the region of the cleft alveolus involving the maxillary lateral incisor tooth. These abnormalities can occur in both primary and secondary dentition. All children with cleft lip and palate should undergo regular dental examination. Dental management should also include preventative measures, such as dietary advice, fluoride supplements and fissure sealants. A well-maintained and disease-free dentition in childhood is an absolute prerequisite for orthodontic treatment (Summary box 45.8).

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(a)

(b)

Figure 45.14 (a and b) Schematic representation of closure of the hard palate. Second-stage palatoplasty achieved with two-layered closure. Red lines represent incisions, and orange areas raw surfaces.

Summary box 45.8 Dental problems ■ ■

Too many/too few teeth or problems with eruption of teeth are common Good dentition is essential for successful reconstructive surgery

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Figure 45.12 Bilateral incomplete cleft lip before (a) and after (b) muscular reconstruction.

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Orthodontic management

(a)

Many children with cleft lip and palate require orthodontic treatment. Orthodontic treatment is commonly carried out in two phases: 1 Mixed dentition (8–10 years) – to expand the maxillary arches as a prelude to alveolar bone graft. 2 Permanent dentition (14–18 years) – to align the dentition and provide a normal functioning occlusion. This phase of treatment may also include surgical correction of a malpositioned/retrusive maxilla by maxillary osteotomy (Figure 45.15a and b).

Secondary surgery for cleft lip and palate Good outcome in cleft lip and palate is directly attributable to the quality of the primary surgery. Secondary cleft procedures include: cleft lip revision (unilateral and bilateral); alveolar bone graft; simultaneous lip revision and alveolar bone graft; secondary palate procedures, e.g. veloplasty and pharyngoplasty, closure of a palatal fistula; • dentoalveolar procedures, including transplantation of teeth/ insertion of osseointegrated dental implants; • orthognathic surgery; • rhinoplasty.

• • • •

(b)

Cleft lip revision Indications for revisional surgery to the previously repaired cleft lip are dependent on the site and severity of the residual deformity. Revisional surgery should be delayed for two years after primary lip closure unless the surgeon is of the opinion that the initial procedure was inadequate, particularly with respect to muscular reconstruction. Indications for revision include:

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• lip deformity:

– malaligned vermilion; – asymmetrical Cupid’s bow; – muscle discontinuity or malalignment; • nasal deformity: – lateral drift of alar base; – poor nasal tip projection; – deviation of cartilaginous nasal septum into the non-cleft nostril. Residual nasal deformity is an external manifestation of incomplete reconstruction of the nasolabial muscle ring. Examples of lip revision are shown in Figures 45.16, 45.17, 45.18 and 45.19 (Summary box 45.9). Figure 45.15 Correction of midface retrusion by maxillary advancement osteotomy, before (a) and after (b) surgery.

Summary box 45.9 Cleft lip revision surgery ■ ■

Should be delayed for at least two years after primary surgery Aims to improve incomplete primary reconstruction

Alveolar bone grafting Alveolar bone grafting in a mixed dentition is a well-established procedure for patients with a residual alveolar cleft associated with cleft lip and palate. The rationale for performing alveolar bone grafting includes:

Cupid’s Bow. Cupid, the Roman god of love, is often depicted holding a double-curved bow which he uses to shoot arrows into his victims.

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(a)

(b)

(c)

(d)

Figure 45.16 (a) Revision of unilateral complete cleft lip, seen from below. (b) Skin incisions. (c) Wide exposure of nasolabial and orbicularis oris muscle. (d) Lip closure highlighting improved nasal symmetry.

• stabilisation of maxillary segments; • to promote eruption of the canine tooth into the cleft site; • to enhance bony support of the teeth adjacent to the cleft alveolus;

• to promote closure of the oronasal fistula; • to close residual fistula of the anterior palate;

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• to provide adequate bone stock to receive an osseointegrated

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dental implant where a tooth is congenitally absent.

Normally, but not universally, patients undergo a period of orthodontic treatment prior to bone grafting. The collapsed maxillary segment is expanded orthodontically to widen the

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(c)

Figure 45.17 (a) Asymmetrical Cupid’s bow. Revision of unilateral cleft lip – skin markings. (b) Identification and realignment of orbicularis oris muscle. (c) Postoperative appearance.

cleft alveolus. The surgery is best performed before the canine tooth erupts (between 8 and 11 years of age). There is a consensus that earlier bone grafting may be beneficial not only for the unerupted canine tooth but also to promote eruption and bony support to the adjacent central and lateral incisor when present. Alveolar bone grafting can also be performed simultaneously with secondary lip revision (Figure 45.20). Cancellous bone is harvested from either the iliac crest or tibial plateau. This is achieved either through an open approach or preferably through a small incision utilising a trephine. When

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Figure 45.18 (a) Revision of bilateral cleft lip with reconstruction of nasolabial muscles. (b) Skin incisions and development of philtrum. (c) Postoperative view – improved nasal and lip symmetry.

the defect is very small, alternative bone sites, e.g. mental symphysis, are sometimes advocated. Bone grafting is a highly successful procedure when carried out in experienced hands, with over 90 per cent of patients achieving acceptable interdental alveolar bone height, but it does require the interaction of surgeon and orthodontist. When the lateral incisor is absent and the canine tooth fails to erupt, surgical exposure of the canine

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(a)

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tooth may be required to aid its eruption. It is a fundamental principle that, following alveolar bone grafting, efforts should be made to ensure that a tooth erupts into the alveolar bone graft site. Failure to provide a tooth in the alveolar bone graft site usually results in bony resorption in the long term. This can be overcome by the insertion of an osseointegrated implant into the grafted site, thereby preserving bone stock (Figure 45.21) (Summary box 45.10). Summary box 45.10 Alveolar bone grafting ■ ■

Aimed at stabilising orthodontic treatment Promotes normal eruption of canine and other teeth

Orthognathic surgery

Figure 45.19 (a) Revision of left unilateral cleft lip to correct nasal deformity. (b) Skin incision. (c) Postoperative view.

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Impaired growth of the midface (maxilla) is now attributed to poor and traumatic primary surgery. Surgical techniques must endeavour to minimise scarring, although in many cases patients have a genetic predisposition to poor midfacial growth. Elective maxillary advancement or bimaxillary surgery is often indicated to restore aesthetics and dental occlusal harmony. Orthognathic

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Figure 45.20 (a) Peroperative view of alveolar bone graft demonstrating defect in alveolus (arrow) (simultaneous lip revision). (b) Cancellous bone graft (arrow) packed into defect.

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Figure 45.21 Radiographic appearance of an implant in an alveolar bone graft site.

surgery is usually performed when facial growth is complete (16 years in female patients, 19 years in male patients). The principal dentofacial deformity associated with cleft lip and palate is underdevelopment in both the horizontal and vertical direction of the maxilla. This leads to a pseudoprognathism in late adolescence, which is not correctable by orthodontic fixed-appliance therapy alone. Patients needing orthognathic surgery can be identified as early as ten years old, although planning and treatment does not commence until 14–15 years of age. Treatment with fixed appliances to align teeth in each dental arch is carried out over a period of 18–24 months as a prelude to orthognathic surgery. Orthognathic surgery may require maxillary osteotomy advancement alone (Figure 45.15a and b) or bimaxillary osteotomy and genioplasty (Figure 45.22). Rigid fixation, with or without bone grafting of the maxilla, is essential as cleft lip and palate patients undergoing orthognathic surgery have a high risk of a skeletal relapse as a result of the scarring associated with primary cleft lip and palate surgery.

(b)

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Open septorhinoplasty Following revisional cleft lip and palate surgery, orthognathic surgery and alveolar bone grafting, many patients still require definitive surgical nasal correction. In patients with cleft lip and palate, open rhinoplasty is preferred to gain access to the external cartilaginous framework, which is frequently deformed (Figure 45.23). The principal deformity is a collapse of the lower lateral cartilage on the cleft side, together with a dislocation of the cartilaginous septum into the non-cleft nostril. The open method ensures adequate access and repositioning of the cartilaginous framework as a tertiary procedure to improve nasal tip projection, correct septal deformity and relocate alar cartilages. A postauricular onlay graft to the middle crus of the cleft nostril lower lateral cartilage may be required to enhance good nasal tip projection and symmetry (Summary box 45.11). Summary box 45.11 Deformities requiring nasal reconstruction ■ ■

Collapse of the lower lateral cartilage on the cleft side Dislocation of cartilaginous septum into the non-cleft nostril

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Figure 45.22 (a) Lateral view of an adult a with previously repaired cleft lip and palate demonstrating mandibular prognathism and maxillary retrusion. (b) Postoperative appearance following maxillary advancement and mandibular setback surgery.

Summary The management of children with cleft lip and palate is complex, requiring the skill of a multidisciplinary team. Each team should include professionals who are appropriately qualified with specialist training, treating an adequate number of patients per year in centralised units. Meticulous record keeping of

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(b)

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(d)

Figure 45.23 (a) Characteristic nasal deformity of a non-functional unilateral cleft lip repair. (b) Incisions for open rhinoplasty. (c) Exposure of the cartilaginous skeleton of the external nose. (d) Repositioning of external nasal cartilages to improve nasal tip projection.

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photography, radiology, dental casts and speech recordings are indispensable to permit regular audits and improve outcomes.

DEVELOPMENTAL ABNORMALITIES OF THE TEETH AND JAWS Teeth Developmental abnormalities of the teeth can be divided into:

• abnormality in number; • defects of structure and size; • disorders of eruption of teeth.

Number Anodontia is the term that is strictly applied to congenital absence of all teeth, which may involve both deciduous and permanent dentition. This is a rare condition that is often hereditary. Partial anodontia is a much more common disorder in which there is a failure of development of the primary or, more commonly, the secondary dentition. Teeth that are most frequently absent are the third molars (wisdom teeth), second premolars and maxillary lateral incisor teeth. Partial anodontia is associated with certain congenital disorders:

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• ectodermal dysplasia; • Down’s syndrome; • cleft lip and palate. Management of partial anodontia involves prosthetic replacement of the teeth, usually in combination with orthodontic treatment. Congenitally missing teeth can be replaced with removable prostheses, fixed prostheses or, more recently, the use of osseointegrated dental implants. Additional teeth (hyperdontia) can occur alone or in association with other syndromes. Additional teeth are termed supernumerary teeth and are often impacted in the jaw with abnormal morphology. The most common site for supernumerary teeth is the maxillary incisor region, particularly in the midline (mesiodens). When additional teeth are of a similar morphology to the normal dentition, the term supplemental is appropriate. Supplemental teeth are common in the maxillary incisor and premolar regions, and less common in the wisdom tooth region when they are termed the fourth molars. Most supernumerary teeth are removed to encourage the eruption of the permanent dentition (Summary box 45.12). Summary box 45.12 Problems with numbers of teeth ■ ■

Absent teeth can be replaced with prosthetic teeth, which may involve osseointegrated implants Supernumerary teeth are often impacted and are removed to allow eruption of secondary dentition

Genetic disorders frequently include amelogenesis imperfecta and dentinogenesis imperfecta, which affect the enamel and dentine of the teeth, respectively. Both of these conditions are characterised by defects in both dentitions, in which all teeth are affected. In amelogenesis imperfecta, the defects are variable and may involve changes in structure (hypoplasia) or in mineralisation (hypocalcification). The loss of enamel leads to rapid attrition of the teeth to gum level in early adolescence. Dentinogenesis imperfecta results in soft dentine associated with short roots. Dentinogenesis imperfecta is strongly associated with osteogenesis imperfecta. Acquired conditions producing changes in the structure of the teeth may be either local or systemic. Local causes are usually the consequence of trauma to the deciduous predecessor tooth, which interferes with enamel formation (amelogenesis). Common examples of systemic causes that produce tooth structure disruption are:

• • • • •

measles rickets hypoparathyroidism tetracycline fluoride (Summary box 45.13). Summary box 45.13 Causes of defects of the structure of teeth Congenital ■ ■

Amelogenesis imperfecta Dentinogenesis imperfecta

Acquired local ■

Trauma

Acquired systemic ■ ■

Disease – measles, rickets Drugs – fluoride, tetracycline

Disorders of eruption Both primary and secondary dentition erupt in a specific sequence, although the timing of eruption does vary from child to child. Delayed eruption of teeth may involve a single tooth or may involve the entire dentition.

Local factors

There are numerous factors that impair the eruption of a single tooth. These include: • loss of space/overcrowding • additional teeth • dentigerous cysts • retention of deciduous tooth.

Systemic factors

These can prevent the eruption of multiple teeth. Examples of such conditions include:

• metabolic diseases – cretinism and rickets • osteodystrophies – cleidocranial dysostosis and fibrous dysplasia

Defects of the structure of teeth

• hereditary gingival fibromatosis.

Structural changes of the teeth can occur as a consequence of genetic disorders or environmental factors.

Management of unerupted teeth involves the removal of the obstruction to eruption, including supernumerary teeth, as well

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Developmental abnormalities of the teeth and jaws

Summary box 45.14 Management of unerupted teeth ■ ■

Remove obstruction to eruption Surgical exposure if eruption delayed

Jaws Disproportionate growth between the maxilla and mandible can occur, which results in derangement of the dental occlusion. The occlusion can be classified into three different subtypes:

• class III: the mandibular teeth are placed anterior to the maxillary teeth.

This classification is usually, but not invariably, the consequence of aberrant skeletal development of the maxilla and mandible, such that in a class II condition there is usually an underdevelopment of the mandible (mandibular retrognathia), whereas in a class III condition there may be simultaneous overgrowth of the mandible (mandibular prognathism) and underdevelopment of the maxilla (maxillary hypoplasia). In the Caucasian population, the most common deformity of the facial skeleton is an underdevelopment of the mandible (retrognathia), producing a skeletal class II relationship often associated with excessive vertical growth of the maxilla. Bimaxillary protrusion is rare but is a characteristic of African races. Condylar hyperplasia is an idiopathic condition seen in patients between 15 and 30 years of age, more common in women than men, in which there is hyperplasia or overgrowth of the neck of the mandibular condyle. This gives an asymmetrical growth to the jaw in both a vertical and horizontal plane. Facial disproportionate growth is also a characteristic of many syndromes. Examples include:

• class I: a normal relationship of upper and lower incisors and molar dentition; • class II: the mandibular teeth are placed posterior to the maxillary teeth;

• • • •

(a)

(b)

(c)

(d)

Treacher Collins’ syndrome Crouzon’s syndrome Apert’s syndrome Pierre Robin sequence.

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as the relief of crowding. Patients with cleidocranial dysostosis should undergo long-term follow up with regular radiographic assessment. Supernumerary teeth, as and when they appear, should be removed to encourage the eruption of permanent dentition in adolescence. Many patients with cleidocranial dysostosis require multiple operations to expose teeth and encourage eruption (Summary box 45.14).

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Figure 45.24 (a) Profile of class II relationship with vertical growth of maxilla and mandibular retrognathia. (b) Preoperative occlusion with anterior open bite. (c) Postoperative view following superior repositioning of maxilla, mandibular advancement and genioplasty. (d) Postoperative occlusion. Octave Crouzon, 1874–1938, physician, La Salpêtrière, Paris, France, described this condition in 1912.

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Figure 45.25 (a) Profile of class III skeletal relationship and maxillary hypoplasia and mandibular prognathism. (b) Lateral skull radiograph. (c) Profile following bimaxillary osteotomy. (d) Postoperative radiograph following bimaxillary osteotomy demonstrating internal fixation.

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Figure 45.25 continued (e) Schematic representation of bimaxillary osteotomy with maxillary advancement and mandibular retrusion.

(a)

(b)

(c)

Right lateral

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Figure 45.26 (a) Condylar hyperplasia with mandibular asymmetry. (b) Bone scan revealing increased bone activity in the right mandibular condyle. (c) Postoperative appearance following bimaxillary osteotomy to correct facial asymmetry.

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Orthognathic surgery

Summary box 45.15 Principles of orthognathic surgery ■ ■

Orthodontist aligns the dental arches Surgery then corrects the jaw deformity

FURTHER READING Markus AF, Delaire J. Functional primary closure of cleft lip. Br J Oral Maxillofac Surg 1993; 31: 281–91. Markus AF, Delaire J, Smith WP. Facial balance in cleft lip and palate. I: Normal development and cleft palate. Br J Oral Maxillofac Surg 1992; 30: 287–95. Markus AF, Delaire J, Smith WP. Facial balance in cleft lip and palate. II: Cleft lip and palate and secondary deformities. Br J Oral Maxillofac Surg 1992; 30: 296–304. Markus AF, Smith WP, Delaire J. Primary closure of cleft palate: a functional approach. Br J Oral Maxillofac Surg 1993; 31: 71–7. Smith WP, Markus AF, Delaire J. Primary closure of the cleft alveolus: a functional approach. Br J Oral Maxillofac Surg 1995; 33: 156–65.

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Orthognathic surgery is the term given to the surgical correction of deformities of the jaw. It is usually undertaken in close cooperation between orthodontic and maxillofacial surgeons. Surgery is directed at simultaneously changing the position of both maxilla and mandible at the end of the growth period. This is termed bimaxillary osteotomy. Treatment planning usually commences at the age of 12–13 years, in which the orthodontist aligns the dental arches in correct relation for each jaw. This frequently results in an accentuation of the facial deformity at the end of the orthodontic phase of treatment. Treatment normally takes two years, in which orthognathic surgery is performed towards the end of orthodontic treatment, although orthodontic treatment in the form of fixed appliances usually continues postoperatively for up to six months after surgery. Surgical planning should be meticulous and involves clinical examination and cephalometric assessment in the form of radiograph analysis, as well as study model analysis, working in close cooperation with maxillofacial technologists. Orthognathic surgery is generally carried out through intraoral incisions, in which the upper and lower jaws are mobilised by achieving osteotomy cuts with saws and drills (Figure 45.24). Following mobilisation of the mandible and maxilla, the jaws are repositioned and held with titanium plates and screws placed through an intraoral approach. This frequently avoids the use of intermaxillary fixation and allows earlier function of the jaws, as well as improved early dietary intake. Examples of orthognathic surgery are shown in Figures 45.25 and 45.26. Patients with syndromic conditions, such as hemifacial microsomia and Crouzon’s and Treacher Collins’ syndromes, require the services of a craniofacial surgeon. As these syndromes are extremely rare, management and surgery should only be carried

out in designated centres. The principal treatment is to correct the deformity from the cranium downwards, with correction of the cranial deformity within the first three years of life and correction of the residual midfacial and lower facial deformity in childhood and adolescence. The use of distraction osteogenesis in the management of craniofacial deformity has reduced the requirements for major orthognathic surgery in patients with severe facial deformity (Summary box 45.15).

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CHAPTER

The nose and sinuses LEARNING OBJECTIVES

To be familiar with: • The basic anatomy of the nose and paranasal sinuses • The principles of managing post-traumatic nasal and septal deformity • The causes and management of epistaxis • The diagnosis and management of nasal polyposis

BASIC ANATOMY OF THE NOSE AND PARANASAL SINUSES

• The clinical features of sinus infection and its treatment and potential complications • The common sinonasal tumours, their presentation, investigation and principles of treatment

Middle turbinate

The supporting structures of the nose are shown in Figure 46.1. The septum consists of the anterior quadrilateral cartilage, the perpendicular plate of the ethmoid and the vomer (Figure 46.2). The lateral wall of the nasal cavity contains the superior, middle and inferior turbinates (Figure 46.3). Opening onto the lateral

Orbit Frontal process of maxilla Lower lateral cartilage Fibroareolar tissue

nasal wall are the ostea of all of the nasal sinuses, except the sphenoid sinus (Figures 46.4 and 46.5). The nasal fossae and sinuses receive their blood supply via the external and internal carotid arteries. The external carotid artery supplies the interior of the nose via the maxillary and sphenopalatine arteries. The greater palatine artery supplies the Sphenoid sinus

Figure 46.1 The nasal skeleton.

Frontal sinus A

Frontal sinus Sphenoid sinus

Perpendicular plate of ethmoid

Vomer Palatine bone

Figure 46.2 The left side of the nasal septum.

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Nasofrontal duct MM

Maxillary ostium

Septal cartilage Anterior nasal spine

Nasolacrimal duct opening

Sphenoid ostium Openings of posterior ethmoid cells Openings of anterior ethmoid cells

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Upper lateral cartilage

Inferior turbinate Figure 46.3 The right lateral nasal wall.

Glabella Nasal bone

Superior turbinate

Figure 46.4 The right lateral nasal wall with turbinates removed to show the sinus ostia. A, insertion of superior turbinate; B, insertion of middle turbinate; C, insertion of inferior turbinate; SM, superior meatus; MM, middle meatus; IM, inferior meatus.

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TRAUMA TO THE NOSE AND PARANASAL SINUSES

Ethmoid sinus

Fracture of the nasal bones

Orbit Superior turbinate Superior meatus Middle turbinate

Maxillary antrum

Middle meatus Inferior turbinate

Maxillary ostium

Inferior meatus

Figure 46.5 Coronal section through the left maxillary and ethmoid sinuses.

Blunt injury to the nose may fracture the nasal bones (Figure 46.7). The fracture line can extend into the lacrimal bone and tear the anterior ethmoidal artery producing catastrophic haemorrhage. This may be delayed, occurring only as the soft tissue swelling subsides, reducing the tamponade effect on the torn vessel. Violent trauma to the frontal area of the nose can result in a fracture of the frontal and ethmoid sinuses with potential extension into the anterior cranial fossa. Dural tears and brain injuries, either open or closed, are then at risk from sinonasal ascending infection which may progress to meningitis or brain abscess. Cerebrospinal fluid (CSF) rhinorrhoea is a certain sign of a dural tear.

anteroinferior septum via the incisive canal. The contribution from the internal carotid artery is via the anterior and posterior ethmoidal arteries, which are branches of the ophthalmic artery (Figure 46.6). All of these arteries anastomose to form a plexus of vessels (Kiesselbach’s plexus) on the anterior part of the nasal septum. Venous drainage is via the ophthalmic and facial veins and the pterygoid and pharyngeal plexuses. Intracranial drainage into the cavernous sinus via the ophthalmic vein is of particular clinical importance because of the potential for intracranial spread of nasal sepsis.

Management of fractured nasal bones

EXAMINATION OF THE NOSE AND PARANASAL SINUSES

Septal injury

Internal inspection of the nasal fossae can be achieved to a limited extent with the use of a Thudichum’s speculum. A more thorough examination and assessment of the nose is possible with the use of either rigid or flexible endoscopes.

Fractured nasal bones are often accompanied by extensive overlying soft tissue swelling and bruising, which may hinder the assessment of any underlying bony deformity. Reviewing after 4–5 days when the soft tissue swelling has diminished will allow a better assessment of any deformity. If there is a significant degree of nasal deformity then this can be corrected by manipulation of the nasal bones under local or general anaesthesia. This should be carried out within 10–20 days of the injury while the bony fragments are still mobile. A blunt injury of moderate force may lead to lateral displacement or deformity of the septal cartilage, restricting the nasal airway. Unlike the nasal bones, the nasal septum cannot be manipulated back into position and requires a formal septoplasty

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IMAGING OF PARANASAL SINUSES Plain radiographs are of limited value in the assessment of sinus disease. A minimum of four views, namely occipitomental, occipitofrontal, submentovertical and lateral, are required to demonstrate the paranasal sinuses adequately. Computed tomography (CT) scanning is far superior in demonstrating sinus pathology. Coronal and axial scans are necessary for detailed assessment. Anterior Posterior ethmoidal ethmoidal artery artery Kiesselbach’s plexus

Facial artery

Sphenopalatine artery Greater palatine artery

Figure 46.6 Arterial blood supply to the left side of the nasal septum.

Figure 46.7 Fracture of the nasal bones with displacement of the bony nasal complex to the right side.

Wilhelm Kiesselbach, 1839–1902, Professor of Otology, Erlangen, Germany. Johann Ludwig Wilhelm Thudichum, 1829–1901, biochemist and general practitioner, London, UK.

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The nasal septum

procedure to restore the anatomy and the patency of the nasal airways. Bleeding under the mucoperichondrium of the septum will cause a septal haematoma and nasal obstruction. Untreated, a septal haematoma will progress to abscess formation and ultimately result in necrosis of the septal cartilage and nasal collapse. A septal haematoma should be treated by incision and evacuation of the blood clot, insertion of a small silicone drain and packing of the nasal fossa. A broad-spectrum prophylactic antibiotic should be prescribed (Summary box 46.1). Summary box 46.1

Summary box 46.2 Causes of septal perforations ■

■

■ ■

Nasal trauma ■ ■ ■ ■

Do not overlook a septal haematoma Displaced nasal bone fractures should be reduced within 10–20 days of injury Severe persistent epistaxis after trauma suggests lacrimal bone fracture and injury to the anterior ethmoid artery Cerebrospinal fluid rhinorrhoea indicates a fracture involving the frontal or ethmoid sinuses with a dural tear

THE NASAL SEPTUM Septal deformity Deviation of the nasal septum may occur naturally or arise as a result of nasal trauma and is readily apparent on anterior rhinoscopy (Figure 46.8). Surgical correction can be achieved by a submucous resection (SMR) of the septum, where the deformed septal cartilage is excised while preserving a dorsal strut. The alternative is a septoplasty procedure during which the septal cartilage is preserved, but the anatomical abnormalities giving rise to its deformity, such as a twisted maxillary crest or inclination of the bony septum, are corrected. Complications of septal surgery include septal perforation. If too much cartilage is excised in the SMR procedure, loss of support to the dorsum of the nose may result in a supratip depression or drooping of the tip of the nose.

■

Trauma Iatrogenic following septal surgery Nose picking Infection Syphilis Tuberculosis Vasculitis Wegener’s granulomatosis Tumours Toxins Chrome salts Cocaine Idiopathic

option is to occlude the perforation by inserting a Silastic biflanged prosthesis (Figures 46.9 and 46.10). Wegener’s granulomatosis is a systemic idiopathic autoimmune disease affecting the nose, lungs and kidneys. Mucosal granulations on the nasal septum destroy cartilage, producing a septal perforation with saddle deformity of the nose. Laboratory findings include a high erythrocyte sedimentation rate, impaired creatinine clearance and antineutrophil cytoplasmic antibodies (ANCA) in most cases.

Septal perforation Septal prosthesis

Figure 46.9 Anterior and lateral views of septal perforation occluded with prosthesis.

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Septal perforation A hole in the nasal septum causes a turbulent airflow through the nose and a resulting sensation of nasal blockage and extensive nasal crusting. The causes of septal perforation are listed in Summary box 46.2. Septal perforations seldom heal spontaneously. A great variety of operations have been described to close septal perforations, but none has met with universal success. A more certain

Narrow airway Deviated septum

Contralateral inferior turbinate hypertrophy

Figure 46.8 Coronal section through the anterior nasal fossae with deviated nasal septum to the right side.

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Figure 46.10 Silastic prosthesis for septal perforation.

Friedrich Wegener, 1907–1990, Professor of Pathology, Lübeck, Germany, described this form of granulomatosis in 1939.

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EPISTAXIS The causes of epistaxis are listed in Table 46.1. The most common site of bleeding is from Kiesselbach’s plexus in Little’s area of the anterior portion of the septum (see Figure 46.6). Anterior bleeding is common in children and young adults as a result of nose blowing or picking. In the elderly, arteriosclerosis and hypertension are the underlying causes of arterial bleeding from the posterior part of the nose. Table 46.1 Causes of epistaxis.

Local

Nose picking Nasal trauma Nasal foreign bodies Tumours Infection Granulomatous disorders Juvenile angiofibroma

Systemic

Hypertension Warfarin therapy Aspirin therapy Haemophilia Von Willebrand’s disease Leukaemia

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Haemorrhagic telangiectasia

Hereditary haemorrhagic telangiectasia (Osler’s disease) gives rise to recurrent multifocal bleeding from thin-walled vessels deficient in muscle and elastic tissue (Figure 46.11). Juvenile angiofibroma is an uncommon condition that affects adolescent boys and may lead to massive life-threatening episodes of bleeding. Diagnosis is made with contrast CT scanning or magnetic resonance imaging (MRI). Anterior bowing or indentation of the posterior antral wall (Holman–Miller or antral sign) is the classical finding but may be seen in other expansive lesions in this area. It is a very vascular tumour, which should not be biopsied because of the risk of uncontrollable haemorrhage. Excision is best carried out by a surgeon experienced in the management of the condition. Preoperative embolisation of the feeding blood vessels may help to reduce blood loss during surgery. Sometimes the tumour is managed with radiotherapy.

Figure 46.11 Osler’s disease showing the multiple telangiectasia.

epistaxis balloon catheter (Figure 46.12). The catheter is passed into the nose and the distal balloon is inflated in the nasopharynx to secure it. The proximal balloon, which is sausage shaped, is then inflated within the nasal fossa to compress the bleeding point. Although usually effective, they can be uncomfortable. Post-nasal packing may be required in refractory cases whereby a gauze pack is positioned in the nasopharynx under general anaesthesia. Endoscopic-assisted cautery or clipping of a posterior bleeding point can be an effective alternative to nasal packing. For uncontrolled life-threatening epistaxis in which the above methods have proved ineffective, haemostasis is secured by vascular ligation. Depending on the origin of bleeding, it may be necessary to ligate the internal maxillary artery in the pterygopalatine fossa and the anterior and posterior ethmoidal

Management of epistaxis Bleeding from Kiesselbach’s plexus may be controlled by silver nitrate cautery under local anaesthesia. Posterior bleeding, as seen in the elderly, may require anterior nasal packing either with Vaseline-impregnated ribbon gauze or absorbable sponge. An alternative to anterior packing is the use of an inflatable Sir William Osler, 1849–1919, Professor of Medicine successively at McGill University, Montreal, Canada; the University of Philadelphia, Pennsylvania, PA, and the Johns Hopkins University, Baltimore, MD, USA, finally becoming Regius Professor of Medicine at Oxford University, Oxford, UK in 1904.

Figure 46.12 Epistaxis balloon catheter.

James Laurence Little, 1836–1885, Professor of Surgery, the University of Vermont, Montpelier, VT, USA. Erik Adolf von Willebrand, 1870–1949, physician, Diakonissanstaltens Hospital, Helsinki, (Helsingfors), Finland, described hereditary pseudohaemophilia in 1926.

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Nasal polyps

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arteries. An alternative measure is external carotid artery ligation above the origin of the lingual artery. In Osler’s disease, anterior nasal packing is best avoided, if at all possible, because it is most likely to lead to further mucosal trauma and bleeding. High-dose oestrogen induces squamous metaplasia of the nasal mucosa and has been used effectively in treating this condition (Summary box 46.3). Summary box 46.3 Epistaxis ■ ■ ■ ■ ■ ■ ■

The most common causes are nose picking, hypertension and anticoagulant therapy Young people bleed from the anterior septum – Kiesselbach’s plexus Elderly people bleed from the posterior part of the nose Silver nitrate cautery is used to control anterior bleeding Moderate bleeding may require anterior nasal packing Severe bleeding may require anterior and posterior nasal packing Persistent bleeding may require endoscopic cautery/clipping or arterial ligation

NASAL POLYPS Pathology Nasal polyps are benign swellings of the ethmoid sinus mucosa of unknown origin. Histologically, the polyps contain a waterlogged stroma infiltrated with inflammatory cells and eosinophils. The majority of nasal polyps arise from the ethmoid sinuses, with each individual ethmoid air cell giving rise to a single polyp as its swollen mucosal lining prolapses out of the air cell to hang down inside the nasal cavity. Polyps can arise from the other nasal sinuses and a single large polyp arising from the maxillary antrum is referred to as an antrochoanal polyp (Figure 46.13).This usually fills the nose and eventually prolapses posteriorly down into the nasopharynx.

Clinical features

Figure 46.14 Nasal polyp in right nasal vestibule.

within the nose as pale semitransparent grey masses, which are mobile and insensitive when palpated with a fine probe. This allows them to be distinguished from hypertrophied turbinates (Figure 46.14). Malignancy should be considered in adults with unilateral nasal polyps, whereas in children such polyps must be distinguished from a meningocoele or encephalocoele by high-resolution CT scanning of the anterior cranial fossa. Nasal polyps are unusual in children. However, they do occur in conjunction with cystic fibrosis in 10 per cent of cases.

Management of nasal polyps Medical treatment with systemic steroids will often reduce the size of nasal polyps and give short-term relief of nasal blockage. Unfortunately, the polyps tend to recur when the treatment stops. Surgical treatment is required in patients with severe nasal obstruction and pansinusitis that is refractory to medical treatment. Polyps may be removed either by avulsion with a nasal snare or endoscopically with a powered nasal microresector (Figure 46.15). After multiple recurrences, ethmoidectomy should be considered (Summary box 46.4).

Figure 46.13 Antrochoanal polyp.

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Patients present with nasal obstruction, watery rhinorrhoea, sinus infection and often anosmia. Polyps are easily identifiable

Figure 46.15 Powered nasal microresector.

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THE NOSE AND SINUSES Summary box 46.4 Nasal polyps ■ ■ ■ ■ ■ ■ ■ ■ ■

Polyps are insensitive to touch and are mobile Simple polyps are bilateral Unilateral nasal polyps should be removed for histology Bleeding polyps may indicate malignancy Meningocoele and encephalocoele must be excluded in children with polyps Polyps can be removed with a snare or a powered microresector Recurrent polyps may require ethmoidectomy Transitional papilloma may mimic simple nasal polyps All polyps should be submitted for histology

MAXILLARY SINUSITIS

Summary box 46.5

Clinical features

Maxillary sinusitis

Local disorders, such as nasal polyps, deviated nasal septum or upper dental sepsis, may predispose to sinus infection. Patients with persistent maxillary sinusitis have a mucopurulent postnasal discharge, headache, which is variable in severity and location, facial pain and nasal obstruction. Irritation of the superior alveolar nerve may give rise to referred upper toothache. The nasal mucosa is swollen and bathed in mucopurulent secretions. Plain sinus radiographs may show a fluid level in the antrum or complete opacity (Figure 46.16). About 10 per cent of infections of the maxillary antrum are caused by dental sepsis from anaerobic organisms. The resultant mucopurulent nasal secretion has a foul taste and smell. Complications of maxillary sinusitis include acute orbital cellulitis or osteitis.

Treatment

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Adequate penetration of antibiotics into chronically inflamed sinus mucosa is doubtful and, therefore, treatment may need to

Infraorbital rim

be prolonged. Topical nasal decongestants, such as ephedrine nasal drops, will often encourage the sinus to drain. Antral lavage under local or general anaesthesia allows confirmation of the diagnosis and provides the opportunity to obtain samples for bacteriology. The antrum is entered through the inferior meatus below the inferior turbinate where the bone separating the antrum from the nasal fossa is extremely thin and can be easily penetrated by a trocar and cannula (Figure 46.17). If infection has caused a significant degree of inflammation and fibrosis of the lining of the antrum, intranasal endoscopic techniques may be employed to create a middle meatal antrostomy or enlarge the natural ostium. Endoscopic nasal surgery allows a more functional approach to diseases of the paranasal sinuses and, as a result, the indications for radical antrostomy are decreasing (Summary box 46.5).

■ ■ ■ ■ ■ ■

The most common causative organisms are Streptococcus pneumoniae and Haemophilus influenzae Anaerobic infection may result from dental sepsis Acute infection should be treated with antibiotics and topical decongestants Antral lavage is diagnostic and therapeutic Intranasal antrostomy or endoscopic middle meatal antrostomy may be required Complications of untreated infection include cellulitis, osteitis and involvement of the orbit

FRONTOETHMOIDAL SINUSITIS Chronic frontoethmoiditis gives rise to mucopurulent catarrh, frontal headache or a feeling of pressure between the eyes, nasal obstruction and hyposmia. Nasal endoscopy will confirm pus issuing from the middle meatus. The ethmoid sinuses can only be properly assessed radiologically by CT scanning, including coronal as well as axial sections. Complications include periorbital cellulitis (Figure 46.18). This may progress to cavernous sinus thrombosis and septicaemia. Spread of infection by direct bone penetration or via the diploic vein can give rise to extradural, subdural or frontal lobe abscess formation (Summary box 46.6).

Frontal sinus

Orbit

Infraorbital foramen

Nasal fossa Air/fluid level

Figure 46.16 Plain radiograph showing the fluid level in the left maxillary antrum and total opacity of the right antrum.

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Cannula

Maxillary antrum

Figure 46.17 Diagram of left maxillary antral lavage.

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Right ethmoid sinuses

Inferior turbinate

659

Osteoma

Middle turbinate

Figure 46.18 Left periorbital cellulitis complicating acute left ethmoiditis. Figure 46.19 Coronal computed tomography scan showing a small osteoma in the right ethmoid sinus adjacent to the orbit.

Frontoethmoiditis ■ ■ ■ ■ ■

Assessment is best achieved by CT scanning It may require open surgical drainage Chronic infection may require an obliterative osteoplastic flap procedure Orbital infections may threaten sight Intracranial spread may cause meningitis, cerebral abscess or cavernous sinus thrombosis

TUMOURS OF THE NOSE AND SINUSES Tumours arising in the nasal fossa may present with unilateral nasal obstruction, persistent unilateral anterior rhinorrhoea, post-nasal catarrh, epistaxis, unilateral blood-stained rhinorrhoea, facial swelling or proptosis.

Benign tumours Simple papillomas or viral warts can grow inside the nasal vestibule. They can be confused with carcinomas and are best excised for histological diagnosis. Osteomas of the nasal skeleton are not uncommon and are usually detected on radiography as an incidental finding (Figure 46.19). In symptomatic individuals, the osteoma can be removed via the frontal sinus or an external ethmoidectomy. Transitional cell papillomas can occur both in the nasal cavity and the nasal sinuses. They are sometimes referred to as inverted papillomas because histologically the hyperplastic epithelium inverts into the underlying stroma. The papillomas are covered with transitional epithelium. Calcification within the tumour may be seen on CT scanning along with sclerosis of bone at the margins of the growth (Figure 46.20). Transitional cell papillomas can undergo malignant change.

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Malignant tumours The most common malignant tumours to occur within the nasal cavity and paranasal sinuses are squamous cell carcinoma (Figure 46.21), adenoid cystic carcinoma and adenocarcinoma. Adenocarcinoma has been linked to exposure to hardwood dust in the furniture industry. Adenoid cystic carcinomas arise from minor salivary glands, which can be found in the nose. Suspicious signs of invasion of neighbouring tissues include diplopia, proptosis, loosening of the teeth (Figure 46.22), trismus, cranial nerve palsies and regional lymphadenopathy (Figure 46.23). Patients with sinus or intranasal malignancy are best managed in a combined clinic where the expertise of ear, nose and throat (ENT) surgeons, maxillofacial surgeons and radiotherapists can be employed (Summary box 46.7). Summary box 46.7 Tumours of the nose and sinuses ■ ■ ■ ■ ■ ■

Unilateral nasal blockage, discharge and bleeding are often presenting symptoms in nasal or sinus tumours Osteomas are often asymptomatic Transitional cell papilloma is the most common benign tumour – this tumour may undergo malignant change Squamous cell carcinoma is the most common malignant tumour Almost 50 per cent of sinonasal cancers arise on the lateral nasal wall and 33 per cent in the maxillary antrum Multidisciplinary management of malignant sinonasal tumours requires input from ENT surgeons, maxillofacial surgeons and radiotherapists

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Summary box 46.6

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Figure 46.20 Coronal computed tomography scan showing extensive transitional cell papilloma involving the left maxillary antrum and ethmoid sinuses.

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Figure 46.21 Squamous cell carcinoma of the nasal septum.

Figure 46.22 Maxillary antral carcinoma presenting through an oroantral fistula.

Figure 46.23 Axial computed tomography scan of paranasal sinuses showing extensive left maxillary antral carcinoma invading adjacent structures.

FURTHER READING Hosemann WG, Weber RK, Keerl RE, Lund VJ (eds). Minimally invasive endonasal sinus surgery: principles, techniques, results, complications, revision surgery. New York: Thieme, 2000. Kennedy DW, Hwang PH (eds). Rhinology: Diseases of the nose, sinuses, and skull base. New York: Thieme, 2012. Lund VJ (ed.). Rhinology, vol. 2. In: Gleeson MJ (ed.). Scott-Brown’s otorhinolaryngology: head and neck surgery, 7 edn. London: Hodder Arnold, 2008.

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CHAPTER

The ear LEARNING OBJECTIVES

INTRODUCTION The mammalian ear is an evolutionary masterpiece. Its highly complex ‘three-dimensional anatomy’ is best learnt by dissecting cadaver temporal bones.

SURGICAL ANATOMY OF THE EAR The external ear The external and middle ear develop from the first two branchial arches. The external ear canal is 3 cm in length; the outer two-thirds is cartilage and the inner third is bony. The skin on the lateral surface of the tympanic membrane is highly specialised and migrates outwards along the ear canal. As a result of this migration most people’s ears are self-cleaning. The external canal is richly innervated and the skin is tightly bound down to the perichondrium so that swelling in this region results in severe pain. The lymphatics of the external ear drain to the retroauricular, parotid, retropharyngeal and deep upper cervical lymph nodes.

The tympanic membrane and middle ear The anatomy of the tympanic membrane and ossicles is shown in Figure 47.1. The relations of the middle ear are important (Figure 47.2). The tympanic membrane and ossicles act as a transformer system converting vibrations in the air to vibrations within the fluid-filled inner ear.

The inner ear The inner ear comprises the cochlea and vestibular labyrinth (saccule, utricle and semicircular canals). These structures are embedded in dense bone called the otic capsule.

• The facial nerve can be damaged by trauma and ear disease • Chronic ear disease can lead to intracranial sepsis • There are two types of hearing loss: conductive and senorineural

The cochlea is a minute spiral of two and three-quarter turns. Within this spiral, perilymph and endolymph are partitioned by the thin Reissner’s membrane. The endolymph has a high concentration of potassium, similar to intracellular fluid, and the perilymph has a high sodium concentration and communicates with the cerebrospinal fluid (CSF). Maintenance of the ionic gradients is an active process and is essential for neuronal activity. There are approximately 15 000 hair cells in the human cochlea. They are arranged in rows of inner and outer hair cells. The inner hair cells act as mechanicoelectric transducers, converting the acoustic signal into an electric impulse. The outer hair cells contain contractile proteins and serve to tune the basilar membrane on which they are positioned. Each inner hair cell responds to a particular frequency of vibration. When stimulated, it depolarises and passes an impulse to the cochlear nuclei in the brainstem. The vestibular labyrinth consists of the semicircular canals, utricle and saccule and their central connections. The three semicircular canals are arranged in the three planes of space at right angles to each other. Like the auditory system, hair cells are present. In the lateral canals, the hair cells are embedded in a gelatinous cupula. Shearing forces, caused by angular movements of the head, produce hair cell movements and generate action potentials. In the utricle and saccule, the hair cells are embedded in an otoconial membrane that contains particles of calcium carbonate. These respond to changes in linear acceleration and the pull of gravity. Impulses are carried centrally by the vestibular nerve and connections are made to the spinal cord, cerebellum and external ocular muscles. Its function is to record the position and movements of the head.

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To be familiar with: • The anatomy of the ear • The conditions of the outer, middle and inner ear • The examination of the ear including hearing tests To understand that: • The outer layer of the tympanic membrane migrates outwards

The sensory nerve supply The external ear is supplied by the auriculotemporal branch

Bartolomeo Eustachio (Eustachius), 1513–1574, was appointed physician to the Pope in 1547, and Professor of Anatomy at Rome, Italy, in 1549. Ernst Reissner, 1824–1878, Professor of Anatomy at Dorpat, and later at Breslau, Germany (now Wroclaw, Poland), described the vestibular membrane of the cochlea in 1851.

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Middle cranial fossa Posterior cranial fossa

Antrum

Attic

Mastoid M

Hypotympanum Stylomastoid foramen

Medial Anterior

(b) Short process

VII

Lateral

of malleus

The majority of the ossicles lie out of sight in the attic

Long process of incus

Pars flaccida

Oval window

Handle of malleus Pars tensa

Stapes

Anterior bulge of ear canal Round windo w niche

Posterior

Light reflex

Figure 47.1 (a) Right tympanic membrane and (b) diagram to illustrate anatomy (courtesy of Dr Christian Deguine).

Figure 47.2 Diagram to show the relations of the middle ear (courtesy of Dr Christian Deguine). ET, Eustachian tube; M, malleus; TM, tympanic membrane; VII, facial nerve.

Taking a thorough history is the most important part of the assessment; the symptoms that need to be enquired after are listed in Table 47.1. Table 47.1 History-taking.

Earache, pain and itch Hearing loss Discharge: type, quantity and smell Tinnitus Vertigo

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Facial movements

of the trigeminal nerve (Vth) and the greater auricular nerve Speech and development (in children) (C2/3), together with branches of the lesser occipital nerve Past history: head injury, baro- or noise trauma, ototoxics, family (C2). The VIIth, IXth and Xth cranial nerves also supply small history and previous ear surgery sensory branches to the external ear. The middle ear is supplied ISBN: 9781444121278 Title: Bailey & Love’s Short Practice of Surgery, 26th Ed by the glossopharyngeal nerve (IXth). This complicated and rich sensory innervation means that www.cactusdesign.co.uk referred otalgia is common and may originate from the normal EXAMINATION OF THE EAR area of distribution of any of the above nerves. A classic example is the referred otalgia caused by cancer of the larynx (Summary The tools of the trade are shown in Figure 47.3. Examination of the ear is part of the general ear, nose and throat (ENT) examibox 47.1). nation. The Rinne and Weber tuning fork tests are used to distinguish between a conductive and a sensorineural hearing loss. Summary box 47.1 In Weber’s test, the base of a 256 Hz vibrating tuning fork is placed on the centre of the patient’s forehead so that the sound Applied anatomy is conducted through the bones of the skull (not air). If the ■ The skin on the outer surface of the eardrum migrates patient hears the sound more clearly in one ear than the other, outwards so that the ear canal is ‘self-cleaning’ then there is either a conductive loss in that ear or neurological ■ Infection of the middle ear and mastoid can easily spread to loss in the opposite ear. Rinne’s test then distinguishes between the cranial cavity these two possibilities. A 512-Hz tuning fork is placed on the ■ The facial nerve pursues a tortuous course through the mastoid bone until the patient can no longer ‘feel’ it vibrating. It middle ear is then moved so that its tips are just outside the ear. The patient ■ The ear has a rich sensory innervation so that ‘referred should now ‘hear’ the sound again if conduction is normal. otalgia’ is common The cranial nerves and especially the function of the facial ■ Cancer of the larynx can present with otalgia nerve should be examined.

Proof Stag

Friedrich Heinrich Adolf Rinne, 1819–1868, otologist, Göttingen, Germany, described his test in 1855. Friedrich Eugen Weber-Liel, 1832–1891, otologist, University of Berlin and Jena, Germany. He described the operation of tenotomy of the tensor tympani used for certain forms of partial deafness.

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Figure 47.3 Tools of the trade: a fibreoptic otoscope, with pneumatic attachment and a selection of specula. Also a 512-Hz tuning fork.

Although conversational testing can give a useful guide to the level of hearing, pure tone audiometry in a soundproof booth is the best way of establishing the air and bone hearing levels (Figure 47.4). Other common audiological tests include speech audiometry, tympanometry, stapedial reflexes, electric response audiometry, otoacoustic emissions, caloric testing and electronystagmography (see Further reading).

Radiological investigation Computed tomography (CT) scanning of the temporal bones is routinely used preoperatively to show detailed individual anatomy, as well as alerting the surgeon to anatomical variants. Pus, bone and air are shown well on high-resolution CT (Figure 47.5). Magnetic resonance imaging (MRI) is better than CT at imaging soft tissue (e.g. facial and auditory nerve) and is the best method for imaging tumours of the acoustic nerves (Figure 47.6).

CONDITIONS OF THE EXTERNAL EAR Congenital anomalies

Figure 47.4 Audiometry: the patient sits in a soundproof room and the audiologist presents sounds at different thresholds and records the responses.

Foreign bodies in the ear canal need to be treated with the greatest respect. If an object is not easily removed at the first attempt, it is better to do it with the aid of a microscope and general anaesthesia. An active two-year-old with a bead in the ear can be a formidable opponent (Figure 47.8) (Summary box 47.2). Summary box 47.2 Trauma of the external ear ■ ■

A haematoma of the pinna requires thorough drainage, antibiotics and a compressive dressing or sutures Consider general anaesthesia when attempting to remove a foreign body in a young child

Inflammation and infection Otitis externa is common and consists of generalised inflammation of the skin of the external auditory meatus. The cause is

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See Table 47.2. Table 47.2 Congenital anomalies of the external ear.

The external and middle ear originate from the first and second branchial arches, but the cochlea is neuroectodermal in origin An individual can have a congenital abnormality of the pinna and middle ear with a normal cochlea and, therefore, the potential for normal hearing. Osseointegration allows a prosthetic ear and hearing aid to be attached to the skull

Trauma A haematoma of the pinna occurs when blood collects under the perichondrium. The cartilage receives its blood supply from the perichondrial layer and will die if the haematoma is not evacuated, resulting in a cauliflower ear. A generous incision under general anaesthetic, with a pressure dressing or compressive sutures and antibiotic cover, is recommended (Figure 47.7).

Figure 47.5 The computed tomography scan shows a normal left ear; note the air-filled middle ear and the incus and stapes and the lateral and semicircular canals and internal acoustic meatus (IAM) can be seen. In the right ear, the entire middle ear and mastoid is opaque and filled with soft tissue. This is the typical appearance of cholesteatoma.

Celsus (AD 70) recommended tying the patient on a wooden plank with the affected ear downwards and hitting the plank with a hammer.

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Figure 47.6 A high resolution T2-weighted image at the level of the internal acoustic meatus (IAM) showing an intracannalicular acoustic neuroma (AN) on the left and a normal IAM on the right (courtesy of Dr Peiter Petorius).

Figure 47.8 A foreign body seen in the ear canal, the removal of which can be a challenge (courtesy of Dr Christian Deguine).

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Figure 47.9 Fungal otitis externa; note the presence of hyphae (white) and spores (black).

Figure 47.7 Haematoma of the pinna.

often multifactorial but includes general skin disorders, such as psoriasis and eczema, and trauma. Common pathogens are Pseudomonas and Staphylococcus bacteria, Candida and Aspergillus. Once the skin of the ear canal becomes oedematous, skin migration stops and debris collects in the ear canal. This acts as a substrate for the pathogens. The hallmark of acute

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otitis externa is severe pain. Movement of the pinna elicits pain, which distinguishes it from otitis media. The initial treatment is with topical antibiotics and steroid ear drops, together with analgesia. If this fails, meticulous removal of the debris with the aid of an operating microscope is required. Fungal infection can be recognised by the presence of hyphae within the canal (Figure 47.9). Fungal infection causes irritation and itch. The treatment is meticulous removal of the fungus and any debris, as well as stopping any concurrent antibiotics. Systemic antibiotics are rarely required for otitis externa but should be used if cellulitis of the pinna occurs (Figure 47.10). Necrotising otitis externa is a rare but important condition. It presents as a severe, persistent, unilateral otitis externa in an immunocompromised individual. It is important to think of the diagnosis in an elderly diabetic patient. Usually the infecting organism is Pseudomonas aeruginosa. Osteomyelitis of the skull base occurs and several cranial nerves (VII, IX, X) may be destroyed by the progressing infection. Intensive systemic antibiotics are required and the disease process should be monitored by high-resolution imaging (Summary box 47.3).

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Figure 47.11 Osteomas grow from the bony part of the ear canal in response to cold and so are found in swimmers, surfers and divers. Treatment is only required if the osteomas occlude the ear canal.

Figure 47.10 Cellulitis of the pinna.

Summary box 47.3 Types of otitis externa

■ ■

■

Acute bacterial otitis externa is very common and extremely painful; treat with topical steroids and topical antibiotics Systemic antibiotics should be reserved for cellulitis of the pinna Chronic otitis externa needs the underlying dermatitis to be treated; application of topical steroid in spirit is recommended Fungal otitis externa itches and can be diagnosed by the presence of hyphae and spores; treat with meticulous cleaning and stop antibiotics Necrotising otitis externa is a progressive skull base infection that occurs in immunocompromised individuals and can be life-threatening; intensive long-term antibiotic treatment is required

Neoplasms Benign osteomas arise from the bone of the ear canal in individuals who swim in cold water (Figure 47.11). No treatment is required unless the osteomas obstruct the canal. Other benign tumours include papillomas and adenomas. Malignant primary tumours of the external ear are either basal cell or squamous cell carcinomas (Figure 47.12). Both may present as ulcerating or crusting lesions that grow slowly and may be ignored by elderly patients. Squamous cell carcinomas metastasise to the parotid and/or neck nodes. The ear canal may be invaded by tumours from the parotid gland and post-nasal space

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Figure 47.12 Squamous cell carcinomas of the external ear usually originate from the pinna; in this case, the tumour is growing from the canal (courtesy of Mr P Beasley).

carcinomas, which ‘creep’ up the Eustachian tube. All resectable malignant tumours of the ear are treated primarily with surgery, with or without the addition of radiation therapy.

CONDITIONS OF THE MIDDLE EAR Congenital anomalies Congenital anomalies of the middle ear may be associated with other general congenital deformities. There are a number of branchial arch syndromes, e.g. Pierre Robin’s, craniofacial dysostosis, Down’s and Treacher Collins’ syndromes.

Trauma

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■

Trauma to the middle ear can result in a perforated tympanic membrane (Figure 47.13a). Such perforations usually heal spontaneously (Figure 47.13b). Trauma can also result in ossicular discontinuity and it is usually the incus that is displaced. Tympanoplasty operations are available to reconstruct the

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damaged ossicular chain and repair the tympanic membrane (Summary box 47.4).

(a)

Summary box 47.4 Congenital anomalies and trauma of the middle ear ■ ■ ■

■ ■

Congenital anomalies may be isolated or associated with general congenital deformities CT can identify middle ear abnormalities that may be corrected by surgery Traumatic perforations of the tympanic membrane usually heal spontaneously, but explosive and welding injuries do not A myringoplasty is an operation that repairs the tympanic membrane With severe head trauma, the incus can be displaced, which leads to a conductive hearing loss

(b)

Suppurative otitis media Suppurative otitis media is extremely common in childhood and is characterised by purulent fluid in the middle ear. Mastoiditis may be associated with otitis media because the mastoid air cells connect freely with the middle ear space. The tympanic membrane bulges because of pressure from the pus in the middle ear (Figure 47.14). The child suffers extreme pain until the tympanic membrane bursts. The most common infecting organisms are Streptococcus pneumoniae and Haemophilus influenzae. Appropriate systemic antibiotics should be given for 10 days. Mastoiditis (Figure 47.15) requires hospital admission and intravenous antibiotics. If the infection does not resolve quickly, a cortical mastoidectomy is required, together with a myringotomy. Mastoiditis can lead to intracranial infection.

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Otitis media with effusion (glue ear) The majority of children experience at least one episode of glue ear. It is primarily thought to be caused by poor Eustachian tube function. Initially, the negative middle ear pressure results in transudation of fluid into the middle ear space (Figure 47.16). If hypoxia continues, a mucoid exudate is produced by the glands within the middle ear mucosa. This sticky exudate is referred to as ‘glue ear’. The following symptoms may be associated with glue ear:

Figure 47.13 (a) Traumatically perforated tympanic membrane. (b) The same tympanic membrane 2 days later (courtesy of Dr Christian Deguine). (Reproduced from O’Donoghue, G.M., Bates, G.J. and Narula, A. (1991) Clinical ENT, with permission from Oxford University Press, Oxford.)

hearing impairment, which often fluctuates; delayed speech; behavioural problems; recurrent ear infections, which occur because the exudate is an ideal culture medium for micro-organisms; • reading and learning difficulties at school.

• • • •

The otoscopic findings with glue ear The otoscopic findings of exudative glue ear are of a dull drum that is immobile on pneumatic otoscopy. The tympanic membrane is retracted and radial blood vessels may be present (Figure 47.17). In children first presenting with bilateral glue ear, 50 per cent will be better within 6 weeks. Initially, a ‘wait and watch’ policy is therefore appropriate. If a bilateral conductive hearing loss persists, the child will miss out on educational opportunities

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Figure 47.14 Acute otitis media of the left ear; note the bulging tympanic membrane.

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(a)

(b)

Figure 47.15 Child with acute mastoiditis whose tympanic membrane is shown in Figure 47.14.

Figure 47.16 The initial serous transudate of glue ear, left ear (courtesy of Dr Christian Deguine). (Reproduced from O’Donoghue, G.M., Bates, G.J. and Narula, A. (1991) Clinical ENT, with permission from Oxford University Press, Oxford.)

and may not fulfil his or her academic potential; in these circ*mstances, treatment is required. Medical treatment is of limited value. The Otovent® device may improve Eustachian tube function and is worth trying. Insertion of ventilation tubes (grommets) (Figure 47.18) and adenoidectomy are effective. The controversy is not whether surgery works, but when to intervene. A middle ear effusion in adults is relatively rare and, when

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it occurs, it does not usually last long. The condition is often associated with an upper respiratory tract infection. A persistent unilateral effusion in an adult should always be viewed with suspicion. A nasopharyngeal carcinoma may cause the effusion by blocking the opening of the Eustachian tube in the post-nasal space. This is the most common carcinoma in men in southern China (Summary box 47.5). Summary box 47.5 Acute suppurative otitis media and glue ear ■ ■ ■ ■

Acute suppurative otitis media can progress to mastoiditis Glue ear is very common in children and usually resolves without treatment Persistent hearing loss and/or recurrent acute otitis media is best treated with grommets and/or an adenoidectomy A persistent middle ear effusion in an adult is rare and may be caused by a cancer of the post-nasal space, especially in Chinese and Asian races

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Figure 47.17 (a) Left exudative glue ear. The tympanic membrane is dull and retracted. The light reflex has gone and there are radial blood vessels. The drum does not move with pneumatic otoscopy. (b) Right ear. Advanced exudative glue ear with retraction pockets (courtesy of Dr Christian Deguine). (Reproduced from O’Donoghue, G.M., Bates, G.J. and Narula, A. (1991) Clinical ENT, with permission from Oxford University Press, Oxford.)

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Figure 47.18 Ventilation tube in tympanic membrane, left ear (courtesy of Dr Christian Deguine).

Chronic suppurative otitis media Chronic suppurative otitis media (CSOM) may involve the pars tensa and the middle ear and is referred to as tubotympanic disease; it results from trauma or infection. When perforated, the tympanic membrane usually repairs itself, but if the outer layer of the tympanic membrane fuses with inner mucosa a chronic perforation results (Figure 47.19). The patient’s main symptoms are of an intermittent mucoid discharge associated with a mild

(a)

conductive hearing loss. It is rare for this type of disease to be associated with intracranial complications. A diagnosis is made on otoscopy and the tuning forks usually suggest a conductive hearing impairment. The first-line treatment is topical antibiotics and steroid drops and, on occasion, microsuction. If medical treatment fails, it may be necessary to graft the tympanic membrane. Atticoantral CSOM (often associated with cholesteatoma) is important because of the complications associated with it. A retraction pocket develops in the pars flaccida and, if the squamous epithelium cannot migrate out of this pocket, a cholesteatoma results. A low-grade osteomyelitis gives the discharge its characteristic faecal smell. Invariably, the discharge is accompanied by hearing loss and mild discomfort. The patient may simply put up with these symptoms until a severe complication occurs. The hearing loss that is caused by cholesteatoma may be conductive as a result of ossicular erosion or sensorineural as a result of cochlea damage. Vestibular symptoms may occur because of erosion of the semicircular canals or the migration of toxins into the vestibule. Erosion of the facial nerve is relatively unusual. The close proximity of the middle ear and mastoid to the middle and posterior cranial fossae means that intracranial sepsis can result from chronic ear disease. The infection spreads to the dura via emissary veins, which connect the middle ear mucosa to the dura, or by direct extension of the disease through the bone. Meningitis, extradural, subdural or intracerebral abscess, or a combination of these may occur. Diagnosis should be suspected on otoscopy (Figure 47.20). Pus, crusts, granulations or a whitish debris in the attic are hallmarks of the disease. Examination under the microscope, audiometry and, sometimes, CT scanning are indicated. The treatment is surgical and follows the principle of exposing the disease, excising the disease and then exteriorising the affected area. Three commonly applied operations for this disease are an atticotomy, modified radical mastoidectomy or combined approach tympanoplasty (Summary box 47.6). Summary box 47.6

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Chronic suppurative middle ear disease ■

■

(b)

Long process of incus Stapes crura

Malleus Facial nerve

Stapedius muscle

A rim of tympanic membrane remains

Round window niche

Eustachian tube opening

Figure 47.19 (a) Tubotympanic chronic suppurative otitis media showing central perforation, right ear. (b) Anatomy (courtesy of Dr Christian Deguine).

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Tubotympanic CSOM, in which there is a hole in the eardrum and frequently a mucoid discharge; this is seldom serious Atticoantral CSOM (cholesteatoma). In this condition, squamous epithelium has invaded a retraction pocket in the attic part of the eardrum and is known as a cholesteatoma. Presents with hearing loss and faecal smell from the ear. It is a common cause of intracranial sepsis

Tuberculous otitis media This is an important cause of suppuration in many countries. The diagnosis should always be considered in any ear that fails to respond to standard therapy.

Otosclerosis This is a condition in which new abnormal spongy bone is laid down in the temporal bone. Of particular importance is the bone that is laid down around the footplate of the stapes, which

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impedes the mobility of the stapes and results in a conductive hearing loss (Figure 47.21). A diagnosis should be suspected in any patient with a conductive hearing loss and a normal tympanic membrane. A similar type of stapes fixation occurs in osteogenesis imperfecta and is known as van der Hoeve’s syndrome. Otosclerosis is often bilateral. The treatment options are simple reassurance, a hearing aid or a stapedotomy operation (Figure 47.22).

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(a)

Neoplasms Middle ear tumours are rare with the most common being a glomus tumour (Figure 47.23). Glomus tumours arise from non-chromaffin paraganglionic tissue. The carotid body tumour arising in the neck is an example of this type of tumour. In the temporal bone, three types of glomus tumour are recognised and classification depends on the location: glomus tympanicum (arising in the middle ear), glomus jugularae (arising next to the jugular bulb) and glomus vagali (skull base). Pulsatile tinnitus is a classic symptom and the hearing loss that occurs may be either conductive or sensorineural. Palsies of the VIIth, IXth, Xth, XIth and/or XIIth nerves may occur. The classic sign is a cherry-red mass lying behind the tympanic membrane. An audible bruit may be heard with a stethoscope over the temporal bone. The treatment of choice is preoperative embolisation followed by surgical excision. Radiotherapy is also effective. Squamous cell carcinoma may also occur within the middle ear. It usually presents with deep-seated pain and a blood-stained discharge. Facial paralysis often occurs. Squamous carcinomas usually arise in a chronically discharging ear and can arise in a chronically infected mastoid cavity. Radical surgical excision, with or without radiotherapy, provides the only chance of cure (Summary box 47.7).

(b)

Figure 47.21 Section of normal stapes (a) and section of stapes affected by otosclerosis (b).

(c)

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(a)

(b)

Figure 47.20 (a) Empty attic retraction pocket, right ear. (b) Attic crust covering cholesteatoma, right ear. (c) Attic erosion with cholesteatoma, right ear. Jan van der Hoeve, 1878–1952, Dutch ophthalmologist, described this syndrome in 1918.

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Figure 47.23 Glomus tumour in the middle ear, left ear.

Figure 47.22 The stapedotomy operation showing the piston linking the incus to the vein graft, left ear.

Summary box 47.7 Neoplasms of the middle ear ■ ■

Highly vascular glomus tumours are rare and may present with pulsatile tinnitus Squamous cell cancer usually presents with pain and facial paralysis

CONDITIONS OF THE INNER EAR

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Congenital anomalies Congenital inner ear disorders may be associated with external or middle ear abnormalities or exist on their own. The most common anomaly is dysplasia of the membranous labyrinth, although dysplasia of the bony labyrinth and even total aplasia of the ear may occur. Intrauterine infections, including rubella, toxoplasmosis and cytomegalovirus infection, can cause inner ear damage. Perinatal hypoxia, jaundice and prematurity are also risk factors for a hearing loss. After birth, meningitis may cause profound sensorineural hearing loss. If a child’s parents suspect a hearing impairment, it is important to believe them, especially when glue ear has been excluded. In children in whom there is a suspicion of sensorineural hearing loss, brainstem-evoked audiometry is used to establish hearing thresholds (Figure 47.24). If some hearing is present, the early fitment of hearing aids can maximise the neural plasticity that is present in the developing brain. If a child has a profound hearing loss, early intervention with a cochlear implant is the ideal solution (Figure 47.25). Most cases of profound sensorineural hearing loss are due to loss of cochlear hair cells, so that an implant inserted through the round window can selectively stimulate the cochlear neurones, which usually remain intact. The results of cochlear implantation are miraculous but it is expensive technology.

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Figure 47.24 Evoked-response audiometry. A simple non-invasive objective test of hearing thresholds. (Reproduced from O’Donoghue, G.M., Bates, G.J. and Narula, A. (1991) Clinical ENT, with permission from Oxford University Press, Oxford.)

Figure 47.25 Multichannel cochlear implant (Cochlear Corporation).

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Conditions of the inner ear (a)

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Figure 47.26 Typical audiogram of presbycusis: (a) right ear; (b) left ear.

hearing aids for patients who also have presbycusis. An ENT surgeon who was a keen fisherman found that he could not hear his tinnitus when fishing next to a waterfall. From this observation, tinnitus maskers were developed (Figure 47.27). A masker provides a similar noise to the tinnitus and ‘blanks it out’.

Trauma Noise exposure

Presbycusis Presbycusis is characterised by a gradual loss of hearing in both ears, with or without tinnitus. The hearing loss usually affects the higher frequencies and a classical audiogram is shown in Figure 47.26. The consonants of speech lie within the high-frequency range, which makes speech discrimination difficult. Many patients with presbycusis are concerned that they may lose their hearing completely and they need reassurance. Hearing aid technology has improved dramatically and most patients can benefit.

Tinnitus Tinnitus is an abnormal noise that appears to come from the ear or within the head. It may have an extrinsic cause, for example the pulsatile tinnitus of a glomus tumour. Usually, however, the tinnitus is generated within the cochlea. Most people will experience tinnitus at some time in their lives. Tinnitus frequently accompanies presbycusis, as well as any other condition that damages the inner ear structures. Most individuals adapt to the presence of tinnitus, but in some patients it proves intrusive. Reassurance and relaxation therapy are highly effective as are

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Hair cells within the cochlea are damaged by sudden acoustic trauma (blast injury or gunfire) or prolonged exposure to excessive noise. The sensorineural hearing loss that results is greatest at high frequencies (particularly 4000 Hz) and is often accompanied by tinnitus (Figure 47.28). The law in the UK requires that workers are protected from noise, but in a disco an individual relies on common sense!

Head injury The otic capsule is the hardest bone in the body but, if trauma to the head is severe, temporal bone fractures may occur. These tend to be either longitudinal (80 per cent) or transverse (20 per cent). Transverse fractures usually involve the labyrinth and lead to a sensorineural hearing loss that is permanent. Profound vertigo occurs initially, followed by gradual compensation. In about 50 per cent of cases, there is an associated facial nerve paralysis.

Drug ototoxicity Certain drugs differentially affect the cochlea, causing hearing loss and tinnitus, whereas others affect the vestibular system, causing vertigo. Aminoglycosides are well known to be ototoxic, as is cis-platinum. Recognition of risk factors, such as poor renal function in patients being treated with aminoglycosides, is most important. Although many topical ear drops contain aminoglycosides, there is little evidence that such topical treatment causes sensorineural hearing loss if used for short periods.

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Figure 47.27 A tinnitus masker.

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Figure 47.28 A typical audiogram of noise damage: (a) right ear; (b) left ear.

Benign paroxysmal positional vertigo Benign paroxysmal positional vertigo (BPPV) may follow head or neck trauma. Vertigo is an illusion of movement and BPPV is characterised by intermittent attacks of vertigo that occur when the head is moved in a certain position. Typically, the vertigo only lasts for a few seconds and is not associated with other otological symptoms. Positional testing can evoke nystagmus and helps in the diagnosis of this condition. The condition is usually self-limiting, and special manoeuvres described by Epley help the majority of patients.

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Reduction in cochlear blood flow This is the most likely cause for most cases of sudden onset of severe sensorineural hearing loss. Five per cent of patients with an acoustic neuroma present with sudden sensorineural hearing loss and, therefore, radiological investigation is required to exclude this diagnosis.

Inflammation Viral infections are thought to account for acute vestibular failure. This condition is characterised by a sudden onset of vertigo. The vertigo is so severe that the patient goes to bed for 5 days. Central compensation then occurs, although recurring episodes of vertigo can occur for up to 18 months.

Menière’s disease The aetiology is not known but the pathology is well documented. There is an excessive accumulation of endolymphatic fluid (hydrops) and it is thought that the distension of the endolymphatic compartment may rupture Reissner’s membrane, which leads to mixing of endolymph and perilymph. The condition is characterised by a triad of symptoms: intermittent attacks of vertigo, a fluctuating sensorineural hearing loss and tinnitus. The patient often has a sensation of pressure in the affected ear

before an attack. The hearing loss typically affects the lower frequencies. The vertigo characteristically lasts between 30 minutes and 6 hours and is often accompanied by nausea and vomiting. The investigations include pure tone audiometry, electrocochleography and an MRI scan to exclude an acoustic neuroma. Medical treatment with betahistadine and diuretics is effective, with selective destruction of the vestibular labyrinth by percolating gentamicin through a grommet being reserved for resistant cases.

Facial paralysis Viral infections that involve the facial nerve are one of the most common causes of facial weakness (80 per cent). Bell’s palsy results from a viral infection of the facial nerve. The nerve swells and is compressed within the temporal bone. Early treatment with high-dose steroids is appropriate. Not all facial nerve palsies are due to viral infection and a thorough otoneurological examination is required. The facial nerve can be damaged at the cerebellopontine angle, within the internal auditory meatus, within the middle ear, at the skull base and within the parotid gland. It is essential to consider these potential sites of facial nerve damage in any patient with VIIth nerve paralysis (Summary box 47.8). Summary box 47.8 Facial paralysis ■ ■ ■ ■

The facial nerve passes through the middle ear and mastoid When considering a paralysis, think ‘complete’ or ‘partial’ Protect the eye: carry out a full otoneurological examination to find the cause If acute, consider steroids and antiviral agents

Prosper Menière, 1799–1862, physician, Institute for Deaf Mutes, Paris, France, described this condition in 1861. Sir Charles Bell, 1774–1842, surgeon, The Middlesex Hospital, London, UK (1812–1835), and later Professor of Surgery, the University of Edinburgh, Scotland, UK (1836–1842). John W Epley, contemporary, Director, Portland Otology Clinic, Portland, Oregon, USA, established his clinic in 1975; he developed the Epley manoeuvre for treating benign paroxysmal positional vertigo.

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Further reading

cervical nodes are palpable and >3 cm, they may be excised with the primary lesion. • If radiotherapy is used initially, as is always the case in carcinoma of the nasopharynx, then radiotherapy may also be given to the neck nodes, whatever their stage. In the case of the tongue, pharynx or larynx, however, if the node exceeds 3 cm in diameter, then surgery may be necessary for the neck nodes, even if the primary tumour is treated by chemoradiation. • If radiotherapy is used initially with resolution of the primary tumour, but there is subsequent residual or recurrent nodal disease, then this situation will require cervical lymph node dissection.

Type of neck dissection Classical radical neck dissection (Crile) The classic operation involves resection of the cervical lymphatics and lymph nodes and those structures closely associated: the internal jugular vein, the accessory nerve, the submandibular gland and the sternocleidomastoid muscle. These structures are all removed en bloc and in continuity with the primary disease if possible. The main disability that follows the operation is weakness and drooping of the shoulder due to paralysis of the trapezius muscle as a consequence of excision of the accessory nerve.

Modified radical neck dissection In selected cases, one or more of the three following structures are preserved: the accessory nerve, the sternocleidomastoid muscle or the internal jugular vein. Otherwise, all major lymph node groups and lymphatics are excised. Whichever structures are preserved should be clearly noted. George Washington Crile, 1864–1943, Professor of Surgery, Western Reserve University and one of the founders in 1921 of The Cleveland Clinic, Cleveland, OH, USA. He devised the small haemostatic forceps that goes by his name.

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Selective neck dissection In this type of dissection, one or more of the major lymph node groups is preserved along with the sternocleidomastoid muscle, accessory nerve and internal jugular vein. In these circ*mstances, the exact groups of nodes excised must be documented.

SUMMARY The anatomical and physiological performance of the pharyngolarynx is involved in the important mechanisms of breathing, coughing, voice production and swallowing. A variety of congenital, traumatic, infectious and neoplastic conditions disturb these functions, giving rise to the common symptoms of pain, swelling, hoarseness, dyspnoea and dysphagia. Squamous carcinomas are the most common malignancies, accounting for approximately 80 per cent of all head and neck tumours. Their incidence and anatomical site vary around the world, but they are mainly caused by the preventable aetiological agents of smoking and alcohol, although nasopharyngeal squamous carcinomas have additional genetic and environmental factors. These head and neck cancers have a high morbidity and mortality, and require expert treatment.

FURTHER READING British Association of Otorhinolaryngology Head and Neck Surgery. Head and neck cancer: Multidisciplinary management guidelines, 4th edn. London: Royal College of Surgeons of England, 2011. Bull P, Clarke R. Diseases of the ear, nose and throat. Oxford: Blackwell, 2007. Dhillon R, East C. Nose and throat, head and neck surgery. Amsterdam: Elsevier, 2006. Hibbert J (ed.). Scott Brown’s otolaryngology: Laryngology and head and neck surgery, 6th edn. Oxford: Butterworth-Heinemann, 1997. Lund VJ, Howard DJ. Ear, nose and throat emergencies, part II. In: Skinner DV, Swain A, Robertson C, Rodney Peyton JW (eds). Cambridge textbook of accident and emergency medicine. Cambridge: Cambridge University Press, 1997. Probst R, Grevers G, Iro H. Basic otorhinolaryngology. Stuttgart: Georg Thieme, 2006. Snow JB (ed.). Ballenger’s handbook of otorhinolaryngology, head and neck surgery, 17th edn. Hamilton, ON: BC Decker, 2007. Wei W, Sham J. Cancer of the larynx and hypopharynx. Oxford: Isis Medical Media, 2000.

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• If surgery is being used to treat the primary disease and the

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CHAPTER

Oropharyngeal cancer LEARNING OBJECTIVES

To understand: • The relationship between oral cancers and the use of alcohol and tobacco

INTRODUCTION AND EPIDEMIOLOGY In the Western world, oral/oropharyngeal cancer is uncommon, accounting for only 2–4 per cent of all malignant tumours, although there is increasing evidence that the incidence is on the increase, particularly among young people. In the Indian subcontinent, however, oropharyngeal cancer remains the most common malignant tumour, accounting for 40 per cent of all cancers.

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Epidemiology The principal aetiological agents are tobacco and alcohol. In Europe and North America, this is mainly through cigarette smoking combined with alcohol abuse. Synergism between alcohol abuse and tobacco use in the development of squamous cell carcinoma (SCC) of the head and neck is well established, although evidence is gathering that the human papillomavirus (HPV16) is becoming increasingly responsible for tumours that arise particularly in the oropharynx of younger/middle-aged patients. Risk factors associated with cancer of the head and neck are outlined in Summary box 49.1. Summary box 49.1 Risk factors associated with cancer of the head and neck ■ ■ ■ ■ ■ ■ ■

Tobacco Alcohol Areca nut/pan masala Human papillomavirus Epstein–Barr virus Plummer–Vinson syndrome Poor nutrition

In the Indian subcontinent, the use of ‘pan’ (a combination of betel nut, areca nut, lime and tobacco) as well as reverse smoking (smoking a cheroot with the burning end inside the mouth) are responsible for the high incidence of oropharyngeal

• The cardinal features of oropharyngeal cancer • The investigation and treatment of patients with oropharyngeal cancer

cancer. Betel quid appears to be the major carcinogen, although there is also a relationship between slaked lime and the areca nut and cancer.

INCIDENCE The incidence is greater in men than in women and it is predominantly a disease of the elderly (those over 60 years of age). The incidence in women is increasing, particularly in younger patients, with oral tongue cancer being the cancer that is usually, but not exclusively, present.

ANATOMY Lip and oral cavity The oral cavity extends from the skin–vermilion border of the lips anteriorly to the junction of the soft palate superiorly and the line of the circumvallate papillae on the junction of the posterior one-third and anterior two-thirds of the tongue posteriorly. The anatomical sites that are frequently involved in mouth cancer include the floor of the mouth, the lateral border of the anterior tongue and the retromolar trigone (Figure 49.1). The retromolar trigone is defined as the attached mucosa overlying the ascending ramus of the mandible posterior to the last molar tooth and extending superiorly to the maxillary tuberosity.

Oropharynx The oropharynx extends vertically from the oral surface of the soft palate to the superior surface of the hyoid bone (floor of vallecula). This includes the base of the tongue, the soft palate and the anterior and posterior tonsillar pillars, as well as the pharyngeal tonsils and the lateral and posterior pharyngeal walls. The In India, habitual chewing of the rolled betel leaf with betel nut inside it with concentrated lime and storing the quid over long periods inside the cheek results in a high incidence of cancer of the cheek. Another routine habit among southern Indian rural dwellers is to roll the tobacco leaf and then smoke by putting the lighted end into the oral cavity; this almost always results in cancer of the palate or some other part of the oral cavity.

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Pathology

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however, a group of oral pathological conditions in which an association with malignant transformation exists (Summary box 49.2). Summary box 49.2 Conditions associated with malignant transformation High-risk lesions ■ ■ ■

Erythroplakia Speckled erythroplakia Chronic hyperplastic candidiasis

Medium-risk lesions ■ ■ ■

Oral submucous fibrosis Syphilitic glossitis Sideropenic dysphagia (Paterson–Kelly syndrome)

Low-risk/equivocal-risk lesions ■ ■ ■

lateral boundaries include the pharyngeal constrictor muscles and the medial aspect of the mandible.

PATHOLOGY The anatomy of the oral cavity and the oropharynx is complex and the course of the nerves, blood vessels, lymphatic pathways and fascial planes influences the spread of disease. Fascial planes, including the periosteum, serve as barriers to the direct spread of tumours but contribute to the spread of tumours into the cervical lymph nodes. Perineural invasion acts as a conduit for the direct spread of tumours and profoundly impacts on prognosis and survival. Angioinvasion also carries a negative prognosis and correlates directly with distant metastases, particularly of oral tongue cancer.

Histology Squamous cell carcinoma is the predominant histology for tumours arising in the oral cavity and oropharynx. Tumours mainly arise from the mucosal epithelium, although malignant salivary gland tumours from the minor salivary glands are a rare but important group of lesions. Lymphomas, particularly around Waldeyer’s ring (tonsils, tongue base, lingual tonsil regions, posterior one-third of the tongue (see Figure 48.2, p. 674)), make up the last of the three principal pathological groups of oropharyngeal cancer. Chronic exposure of the mucosal surface to carcinogenic substances, i.e. tobacco and alcohol, can produce multiple subclinical sites of carcinoma that can at any stage develop into malignant tumour. This pathological process supports the preventative measures of smoking cessation and alcohol rehabilitation in patients with head and neck cancer, thereby minimising the occurrence of synchronous and metachronous tumours (see below under Field changes and second primary tumours).

Clinical features Premalignant lesions of the oral mucosa and oropharyngeal mucosa present as either:

• leukoplakia • speckled leukoplakia • erythroplakia/plasia.

Leukoplakia Leukoplakia is defined as any white patch or plaque that cannot be characterised clinically or pathologically. It is purely a descriptive term with no histological correlation. Leukoplakia varies from a small, well-circ*mscribed, hom*ogenous white plaque to an extensive lesion involving large surface areas of the oral mucosa. It may be smooth or wrinkled, fissured and vary in colour depending on the thickness of the lesion.

Speckled leukoplakia This is a variation of leukoplakia arising on an erythematous base (Figure 49.2). It has the highest rate of malignant transformation.

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Figure 49.1 Common anatomical sites (blue) for oral squamous cell carcinoma.

Oral lichen planus Discoid lupus erythematosus Discoid keratosis congenita

Premalignant lesions The majority of oral carcinomas are not preceded by or associated with clinically obvious premalignant lesions. There is,

Figure 49.2 Speckled leukoplakia on the lateral border of the tongue. Histology confirms carcinoma in situ.

Heinrich Wilhelm Gottfried Waldeyer-Hartz, 1836–1921, Professor of Pathological Anatomy, Berlin, Germany. Donald Rose Paterson, 1863–1939, surgeon, Ear, Nose and Throat Department, The Royal Infirmary, Cardiff, Wales. Adam Brown Kelly, 1865–1941, surgeon, Ear, Nose and Throat Department, The Royal Victoria Infirmary, Glasgow, Scotland.

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Erythroplakia Erythroplakia is defined as any lesion of the oral mucosa that presents as a bright red plaque which cannot be characterised clinically or pathologically as any other recognisable condition. The lesions are irregular in outline and separated from adjacent normal mucosa (Figure 49.3). The surfaces may be nodular. These lesions occasionally coexist with leukoplakia.

FIELD CHANGE AND SECOND PRIMARY TUMOURS The diffuse and chronic exposure of the mucosa of the upper aerodigestive tract to carcinogenic substances, e.g. tobacco and alcohol, causes widespread adverse changes in the mucosal epithelium. The consequence of the diffuse exposure is the development of separate tumours at different anatomical sites. These may present simultaneously, within six months (synchronous) or may be delayed (metachronous). Slaughter, in 1950, first proposed the concept of field change or ‘cancerisation’. Separate primary tumours may not represent distinct genetic mutational events but rather the same clonal origin of cells, which migrate to separate sites in the upper aerodigestive tract. Nevertheless, minimising exposure of the oropharyngeal tissues to potential insults is the cornerstone of long-term management for patients with head and neck cancer. Patients who develop a first tumour in the oral cavity and the oropharynx are more likely to develop a second primary tumour in the upper oesophagus. The overall rate of second primary tumour development is 15 per cent. In total, 80 per cent of these are metachronous tumours, of which 50 per cent develop within the first two years of initial presentation (Figure 49.4). The prevalence of synchronous second primary tumours is 4 per cent.

and ventral surface of the tongue, particularly in younger women, even in the absence of associated risk factors.

PREMALIGNANT CONDITIONS Chronic hyperplastic candidiasis Chronic hyperplastic candidiasis produces dense plaques of leukoplakia, particularly around the commissures of the mouth. The lesions occasionally extend on to the vermilion and even the facial skin (Figure 49.5). These lesions have a high incidence of malignant transformation, thought to be the result of invasion of the lesion by Candida albicans. A small percentage of patients have an associated immunological defect, which encourages the invasion of C. albicans, rendering the patient susceptible to malignant transformation. Specific management of chronic hyperplastic candidiasis includes prolonged (6 weeks) topical antifungal treatment or systemic antifungal treatment (2 weeks). If the lesions persist after medical therapy, surgical excision or laser vaporisation is strongly recommended.

Oral submucous fibrosis Oral submucous fibrosis is a progressive disease in which fibrous bands form beneath the oral mucosa. Scarring produces con-

Potential for malignant change

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The potential risk for malignant transformation:

• • • • • •

increases with increasing age of the patient; increases with increasing age of the lesion; is higher in smokers; increases with alcohol consumption; depends on the anatomical site of the premalignant lesion; is particularly high for leukoplakia on the floor of the mouth

Figure 49.3 Erythroplakia of the left soft palate and lateral pharyngeal wall.

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Figure 49.4 Metachronous tumour in the right mandibular alveolus after previous partial glossectomy and forearm flap reconstruction.

Figure 49.5 Chronic hyperplastic candidiasis of the left buccal mucosa.

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Clinical features

Sideropenic dysphagia (Plummer–Vincent and Paterson–Kelly syndromes) There is a well-known relationship between sideropenia (iron deficiency in the absence of anaemia) and the development of oral cancer. Sideropenia is common in Scandinavian women and leads to epithelial atrophy, which renders the oral mucosa vulnerable to irritation from topical carcinogens. Correction of the sideropenia with iron supplements reduces the epithelial atrophy and risk of malignant transformation.

CLASSIFICATION AND STAGING TNM staging Staging of head and neck cancer is defined by the American Joint Committee on Cancer (AJCC) and follows the TNM system. The system also takes into account the pretreatment computed tomography (CT) or magnetic resonance imaging (MRI) of the tumour. The T classification indicates the extent of the primary tumour and the N classification relates to the extent of regional neck metastases to the cervical lymph nodes; this is identical for all mucosal sites of the head and neck except for the nasopharynx. The M classification relates to distant metastasis. The risk of distant metastasis is dependent on nodal disease rather than the size of the primary tumour. Tumours close to the midline are at a greater risk of developing bilateral or contralateral cervical node metastasis. The TNM staging system is outlined in Table 49.1.

Table 49.1 The TNM staging system.

Primary tumour (T) TX Primary tumour cannot be assessed T0 No evidence of primary tumour Tis Carcinoma in situ T1 Tumour 2 but 4 cm but 6 cm in greatest dimension N2c Metastasis in bilateral or contralateral lymph nodes, none >6 cm in greatest dimension N3 Metastasis in any lymph node >6 cm Distant metastasis M0 No evidence of distant metastasis M1 Evidence of distant metastasis Stage 0 I II III IV

Tis T1 T2 T3 T1, T2, T3 T4 Any T Any T Any T

N0 N0 N0 N0 N1 N0 N2 N3 Any N

M0 M0 M0 M0 M0 M0 M0 M0 M1

Patterns of lymph node metastasis The cervical lymph nodes are divided into five principal levels as outlined in Figure 49.7. The spread of tumour from the primary site has been well addressed. SCC in the oral cavity and lips tends to metastasise to lymph nodes at levels I, II and III. However, with SCC of the oral tongue there is a risk of skip metastasis directly to lymph node levels III or IV, without the involvement of higher-level lymph node groups. Tumours arising in the oropharynx commonly metastasise to lymph node levels II, III and IV, as well as retropharyngeal and contralateral nodal groups. Distant metastases are relatively uncommon but sites involved include lung, brain, liver, bone and skin.

CLINICAL FEATURES

Figure 49.6 Oral submucous fibrosis of the right buccal mucosa and soft palate.

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Between 25 and 50 per cent of patients with cancer of the oral cavity or oropharynx present late. Many of these patients are elderly and frail and delay visiting the doctor or the dentist partly because they wear dentures and are accustomed to the discomfort and associated ulceration. Occasionally, dental and medical practitioners fail to recognise that a lesion may be

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tracture, resulting in limited mouth opening and restricted tongue movement. The condition is almost entirely confined to the Asian population and is characterised pathologically by epithelial fibrosis with associated atrophy and hyperplasia of the overlying epithelium (Figure 49.6). The epithelium also shows changes of epithelial dysplasia. Restricted mouth opening can be treated with either intralesional steroids or surgical excision and skin grafts. Research strongly indicates that oral submucous fibrosis is significantly associated with the use of pan masala areca nut, with or without concurrent alcohol use. Tobacco smoking alone is not associated with oral submucous fibrosis.

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OROPHARYNGEAL CANCER Summary box 49.3 Clinical features of oral cancer ■ ■ ■ ■

■ ■ ■ ■

Persistent oral swelling for >4 weeks Mouth ulceration for >4 weeks Sore tongue Difficulty swallowing Jaw or facial swelling Painless neck lump Unexplained tooth mobility Trismus

III V IV Figure 49.7 Cervical lymph nodes: (I) submandibular; (II) upper jugular; (III) middle jugular; (IV) lower jugular; (V) posterior triangle.

malignant and further delay referral. Moreover, early oral cancer is usually not painful until either the ulcer becomes infected or the tumour invades local sensory nerve fibres. Clinical presentation is markedly dependent on the anatomical site.

Lip cancer Lip cancer presents early as it is readily visible to the patient. It usually arises as an ulcer on the vermilion border (Figure 49.8). In total, 95 per cent of carcinomas of the lip arise on the lower lip and 15 per cent arise in the central one-third and commissures. Tumours tend to spread laterally over the mucosal surface. Lymph node metastases, usually to the submental or submandibular nodes, occur late.

Oropharynx Cancer of the oropharynx frequently presents much later than cancer of the lip and oral cavity. An ipsilateral or contralateral lump in the neck may be the single presenting complaint from a patient with a carcinoma arising from the tongue base, tonsil or soft palate. Palpable asymmetry, particularly in the tonsil, often represents submucosal infiltration of tumour. Deeper infiltration of the tongue base, pterygoid muscles or adherence of the tumour to the jaw results in poor mobility of the tongue or palate. Common clinical features of oropharyngeal cancer are outlined in Summary box 49.4.

(a)

Oral cavity

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Cancers of the oral cavity present in a variable way (Figure 49.9) but are often associated with persisting swelling or ulceration within the oral cavity (Summary box 49.3). The duration of symptoms is highly variable, from several weeks to many months. (b)

Figure 49.8 Squamous cell carcinoma of the lower lip.

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Figure 49.9 (a) Ulcerative squamous cell carcinoma of the anterior floor of the mouth. (b) Exophytic squamous cell carcinoma of the right lateral border of the tongue.

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Tr e a t m e n t

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Summary box 49.4 Clinical features of oropharyngeal cancer ■ ■ ■ ■ ■

Localised and persistent sore throat Difficulty and/or painful swallowing for >4 weeks Painless neck lump Unilateral tonsillar enlargement or ulceration Otalgia

INVESTIGATIONS

Radiography Plain radiography of the jaw is of limited value but does provide an opportunity for dental assessment. Before examination under anaesthesia, an orthopantomogram of the jaws is helpful to assess bony invasion, particularly from tumours arising on the alveolus and maxillary antrum.

Magnetic resonance imaging MRI is the investigation of choice for cancer of the oral cavity and oropharynx, as it is not distorted by metallic dental restorations and provides excellent visualisation of soft-tissue infiltration of the tumour (Figure 49.10). Ideally, it should be performed before diagnostic biopsy as biopsy frequently distorts the image of the primary tumour. The specificity and sensitivity of MRI in diagnosing cervical node metastasis are similar to that of CT. Patients who suffer with claustrophobia may have difficulty in tolerating the investigation.

Computed tomography CT is much more widely available than MRI but has limited value in oral cavity and oropharyngeal cancer. It is useful when bony invasion is suspected. CT of the thorax and abdomen is now indicated for all patients and not just those with proven cervical lymph node metastasis and large-volume disease.

Figure 49.10 Magnetic resonance imaging of a primary tumour of the left tongue base (blue arrow) and neck node metastasis (red arrow).

nodes. It involves the use of a fine-needle puncture into the mass and immediate aspiration for cytological examination. It has few complications and does not spread tumour. It requires no specialist equipment other than a 21G or 23G needle and a 10-mL syringe. Aspiration should be carried out only when the needle enters the swelling. If the specimen can be assessed immediately by an expert cytologist, then it can be sent without fixation. If there is delay in microscopic examination, then the specimen, smeared on a microscope slide, should be fixed before transfer to the laboratory. The positive yield from FNAC is dependent not only on the quality of the aspirate, but also on the skill of the cytologist.

Ultrasound Ultrasound has limited use in the management of oropharyngeal cancer. It is useful as an adjunct in FNAC to ensure accurate aspiration of a deeply seated neck node swelling.

TREATMENT General principles

Fine-needle aspiration cytology

The two principal treatment modalities of oropharyngeal cancer are surgery and radiotherapy. Small tumours can be managed either by primary radiotherapy or surgery. Large-volume disease, i.e. advanced tumour, usually requires a combination of surgery and radiotherapy. There is an increasing move to manage extensive disease of the oropharynx with chemoradiotherapy, provided that patients are medically fit to tolerate the toxicity. Factors that need to be taken into consideration include:

Fine-needle aspiration cytology (FNAC) is useful for the assessment and pathological diagnosis of enlarged cervical lymph

• the site of disease • the stage

Radionucleotide studies A radioisotope bone scan of the facial skeleton adds little to the diagnosis and assessment of oropharyngeal cancer. The scan is not specific and tends to show increased uptake wherever there is increased metabolic activity in bone. A false-positive diagnosis is common and ‘over-staging’ of the disease frequent.

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PART 7 | HEAD AND NECK

When a clinical diagnosis of oropharyngeal cancer is suspected, a comprehensive protocol of investigations should be instituted. An incisional biopsy should be carried out in all cases. Formal examination under anaesthetic is preferred in the vast majority of cases, not only to carry out the biopsy, but also to palpate and examine the extent of the tumour, which can be exquisitely tender in the conscious patient. Under the same anaesthetic, extraction of teeth with a dubious prognosis can be performed. Where available, and when the diagnosis is clear-cut, insertion of a percutaneous endoscopic gastrostomy (PEG) should be performed to facilitate feeding in the treatment phase. The biopsy should be generous and include the most suspicious area of the lesion, as well as normal adjacent tissue. Areas of necrosis or gross infection should be avoided.

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OROPHARYNGEAL CANCER

• histology • concomitant medical disease • social factors. The management of head and neck cancer involves a team approach, whereby patients are assessed objectively by several specialists who agree on an optimum treatment strategy. Cancer of the oral cavity is frequently managed with primary surgery whereas cancer of the oropharynx can be treated with either primary radiotherapy or primary surgery, or a combination, i.e. surgery for neck nodes and radiotherapy for the primary site. When the tumour invades bone, e.g. the mandible, primary surgery is deemed appropriate as radiotherapy is less effective in controlling disease. Surgery is also more appropriate for bulky advanced disease, usually followed by postoperative radiotherapy. Tumours of intermediate size, e.g. T2 and T3 tumours, are more problematic and treatment regimes more controversial, hence the need for planning by a multidisciplinary team.

Cervical node involvement When cervical lymph node involvement occurs, treatment should be geared towards a single modality to deal simultaneously with the lymph node disease and the primary tumour.

Histology The degree of differentiation of SCC does not normally influence the management of the tumour alone. Management of verrucous carcinoma, a variant of SCC, is identical to that of any other SCC. Malignant tumours of the minor salivary glands require primary surgery whereas lymphoma is managed by radiotherapy, or chemotherapy and radiotherapy, depending on the stage. Postoperative radiotherapy for minor salivary gland tumours is often indicated to reduce the risk of locoregional recurrence.

in alcohol consumption should be encouraged in all patients with premalignant lesions. A photographic record of the lesion is useful, particularly for long-term follow up. All erythroplakia and speckled leukoplakia should undergo urgent incisional biopsy. Biopsy from more than one site provides a better representation of histological changes within a lesion. Severe epithelial dysplasia and carcinoma in situ should be ablated by surgical excision or laser vaporisation. Small lesions, particularly on the lateral border of the tongue or buccal mucosa, may be managed with surgical excision and primary closure by undermining the adjacent mucosa. Larger defects can be managed with laser vaporisation and allowed to epithelialise spontaneously (Figure 49.11). With mild-to-moderate epithelial dysplasia, treatment is facilitated by elimination of causative agents. Patients who continue to smoke should be managed as for severe dysplasia and carcinoma in situ. Patients who cease smoking and areca nut/pan habits may be followed up closely at three-monthly intervals.

LIP CANCER Surgery and external beam radiotherapy are highly effective methods of treatment for lip cancer. The cure rate approaches 90 per cent for either modality. Premalignant changes on the lower lip mucosa are frequently extensive and are best managed by a lower lip shave, in which (a)

PART 7 | HEAD AND NECK

Age Modern anaesthesia and postoperative critical care facilities have allowed major head and neck surgery to be carried out on patients with significant medical comorbidity. Advancing age is now not considered to be a contraindication to major head and neck cancer surgery. Conversely, young patients should not be denied radiotherapy for fear of inducing a second malignancy, e.g. sarcoma, in later life.

Previous radiotherapy

(b)

A second course of radiotherapy to a previously irradiated site is contraindicated as the tumour is likely to be radioresistant and reirradiation will invariably result in extensive tissue necrosis.

Field change Surgery is preferred when multiple tumours are present or there is extensive premalignant change of the oropharyngeal mucosa. Radiotherapy is unsatisfactory as the entire oral cavity requires treatment, causing severe morbidity. In addition, subsequent postradiotherapy changes make the diagnosis of future premalignancy and malignancy more difficult.

Management of premalignant conditions Elimination of associated aetiological factors is the basis of the management of premalignant oral mucosal lesions. Cessation of smoking, elimination of the areca nut/pan habit and reduction

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Figure 49.11 (a) Leukoplakia with severe dysplasia of the lateral border of the tongue. (b) Laser vaporisation.

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To n g u e c a n c e r

the vermilion defect is closed by advancement of the lower labial mucosa.

Small tumours Small tumours ( 50 and significant smoking history Evidence of underlying lung disease on exam or CXR?

YES

Secondary Pneumothorax

YES

Aspirate 16–18G cannula Aspirate 2 cm or breathless

YES

Success (< 2 cm and breathing improved)

Consider discharge review in OPD in 2–4 weeks

*In some patients with a large pneumothorax but minimal symptoms conservative mangement may be appropriate

Aspirate 16–18G cannula Aspirate 30 g/L) effusion. If this becomes infected with the organisms from the lung (typically Streptococcus milleri and Haemophilus influenzae in children), the scene is set for empyema. At this stage, antibiotics may be all that is required. Aspiration or drainage to dryness in addition is preferred. 2 Over the next days, the fluid thickens to what is known as the fibrinopurulent phase. Drainage at this stage is prudent as antibiotics alone are unlikely to be curative. 3 The organising phase causes the lung to be trapped by a thick peel or ‘cortex’ for which surgical management may be required.

Leon David Abrams, formerly cardiothoracic surgeon, The United Birmingham Hospitals, Birmingham, UK.

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Presentation of lung disease

Surgical management of pleural effusions and infections Thoracoscopy or video-assisted thoracoscopic surgery The direct-vision thoracoscope has been used for many years, but its use was limited mainly to performing biopsies. The instrument had a limited view and was uncomfortable to use for any length of time. All this has changed since the advent of videoassisted thoracoscopy (Figure 55.8) where the surgeon’s hands are freed because the camera is attached to the thoracoscope, which can be operated by an assistant with the image displayed on a television screen. The surgeon is able to manipulate instruments with both hands to perform a variety of procedures. The number of ports required depends on the type and complexity of the surgery. The patient is usually positioned with the diseased side uppermost, having had a double lumen endotracheobronchial tube placed by the anaesthetist to allow for single-lung ventilation. Pneumonectomy, lobectomy and empyema drainage are all possible. However, lung biopsy and the treatment of recurrent pneumothorax are the most frequent indications. The principal advantage is that a large incision is avoided resulting in less postoperative pain and a more rapid recovery.

VATS drainage, pleural biopsy and talc pleurodesis VATS drainage, pleural biopsy and talc pleurodesis is an increasingly performed procedure for managing patients with an undiagnosed or malignant pleural effusion. It can be performed using a single or two ports and allows for direct visualisation of the pleural cavity for complete drainage, multiple pleural biopsies and excellent talc insufflation to achieve pleurodesis.

through the use of a double lumen tube, the patient is positioned disease side up, and the pleural cavity is entered. The fluid and debris are vigorously debrided, freeing the lung and allowing for re-expansion. At the end of the case, carefully positioned chest drains are placed to allow for dependent drainage. The drain/s must exit the skin anterior to the mid-axillary line otherwise the patient will have to lie on the drain(s), causing pain and possibly obstructing the tube. The drain should lie obliquely in its course through the skin and chest wall and into the pleura, or it will kink. Following the procedure, the patient requires good analgesic control, typically patient controlled analgesia (PCA) and physiotherapy to help fully re-expand the lung prior to final removal of chest drains.

Decortication If the lung fails to re-expand after drainage of the empyema, the more radical operation of decortication may be required (Figure 55.9). The fibrous cortex or peel from the entrapped underlying lung is removed so that the lung can expand to obliterate the pleural space. This is performed through a posterolateral thoracotomy and requires careful dissection to remove the parietal and visceral cortex, taking care not to damage the visceral pleura.

PRESENTATION OF LUNG DISEASE Haemoptysis

Pleural infection, particularly early in its evolution, requires drainage but once the fluid component becomes fibrinopurulent and loculated it requires surgical debridement which can often be achieved through a VATS approach. The lung is isolated

Diseases causing repeated haemoptysis include carcinoma, bronchiectasis, carcinoid tumours and some infections. Severe mitral stenosis is now a rare cause. Patients with repeated haemoptysis should be investigated, at the very least by chest radiography and bronchoscopy. Haemoptysis following trauma may be from a lung contusion or injury to a major airway. Treatment depends on the underlying cause. Common associated chest symptoms include cough with

Figure 55.8 Video-assisted thoracoscopic surgery (VATS) utilises modern thoracoscopic instruments and digital technology and avoids large incisions.

Figure 55.9 Chest computed tomography scan showing an empyema with a grossly thickened pleura.

PART 9 | CARDIOTHORACIC

VATS debridement of empyema

857

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THE THORAX

or without sputum, pain, breathlessness, hoarseness and more general symptoms of systemic upset, including fatigue and loss of weight. Occasionally, chest disease may cause palpitation due to atrial fibrillation. Any of these symptoms in association with haemoptysis requires urgent investigation.

Investigation Bronchoscopy

Flexible bronchoscopy may be performed with the patient awake and the oropharynx anaesthetised with topical lignocaine (Figure 55.10). The bronchoscope is passed into the nose or mouth and through the vocal folds under direct vision. As the scope is flexible, its tip can be directed into the segmental bronchi with ease. Tissue and sputum samples may be obtained for diagnostic purposes. There is a greater range of movement with this instrument, but the biopsies are relatively small and suction limited. Rigid bronchoscopy requires general anaesthesia in most instances. It is ideal for therapeutic manoeuvres, such as removal of foreign bodies, aspiration of blood and thick secretions, and intraluminal surgery (laser resection or stent placement). The surgeon and the anaesthetist share control of the airway. Continuous electrocardiography (ECG) and pulse oximetry monitoring are now essential. The technique involves the operator standing behind the patient and lifting the maxilla by the upper teeth, using the middle finger and forefinger of the left (a)

hand. The bronchoscope rests on the left thumb as it is introduced over the tongue in the midline. Care must be taken not to trap the lips or tongue between the teeth and the bronchoscope, and the fulcrum should be the left thumb and not the teeth. The bronchoscope is passed under direct vision into the oropharynx, behind the epiglottis, until the vocal folds are seen. Turning the instrument through 90° will help to negotiate the vocal folds; only then should the neck be extended. The tracheal rings and the carina should be easily seen. Advancing the bronchoscope into the right and left main bronchus reveals the orifices of the more peripheral bronchi. Operability of an endobronchial tumour may be assessed in terms of its location (e.g. the proximity of a lesion to the carina). Complications are rare, but include bleeding, pneumothorax, laryngospasm and arrhythmia (Summary box 55.4). Summary box 55.4 Biopsy hazards ■ ■ ■

Bleeding disorders Systemic anticoagulation Pulmonary hypertension

Other techniques of biopsy of intrathoracic lesions are often necessary to confirm diagnosis, stage disease and plan treatment. The options range from percutaneous needle biopsy under radiological control, endobronchial ultrasound, to open-lung biopsy. However, high-quality, contrast-enhanced, multi-slice helical CT scanning will reduce the requirement for invasive assessment (Table 55.4).

PART 9 | CARDIOTHORACIC

Table 55.4 Uses of bronchoscopy.

(b)

Diagnostic

Confirmation of disease: carcinoma of the bronchus; inflammatory process; infective process

Investigative

Tissue biopsy

Preoperative assessment

Before lung resection Before oesophageal resection Persistent haemoptysis

Therapeutic

Removal of secretions Removal of foreign bodies Stent placement, endobronchial resection, etc.

Airway obstruction Tracheal obstruction may present acutely as a life-threatening emergency or insidiously with little in the way of symptoms until critical narrowing and stridor occur. The more common causes of airway narrowing are outlined in Table 55.5. Table 55.5 Causes of airway narrowing.

Figure 55.10 (a) Rigid and flexible bronchoscopes. (b) View past the carina into the left main bronchus with a tumour seen in the bronchial lumen.

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Intraluminal

Inhaled foreign body Neoplasm

Intramural

Congenital stenosis Fibrous stricture (post-intubation or tuberculosis)

Extramural

Neoplasm (thyroid cancer, secondary deposits) Aortic arch aneurysm

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Malignant lung tumours

Treatment depends on the underlying cause. Tracheostomy may be required to overcome the obstruction, but there are few indications to do this as an emergency. Tracheal replacement with artificial substitutes has so far been unsuccessful, but resection of up to 6 cm of trachea is now possible. Sleeve resections of the major bronchi are also possible.

differ from all other types sufficiently for these to be managed differently from the outset on the basis of the histological classification. • Subdivisions of NSCLC according to histological characteristics are much less important, but pathological staging is critical to treatment and outcome.

Inhaled foreign bodies

Histological classification of lung cancer • Small cell lung cancers were known as oat cell cancers because

1 asymptomatic; 2 wheezing (from airway narrowing) with a persistent cough and signs of obstructive emphysema; 3 pyrexia with a productive cough from pulmonary suppuration. A chest x-ray is vital; even if the object is not radio-opaque, there may be other changes. An experienced anaesthetist is required. The procedure may be very difficult if there is a severe inflammatory reaction.

MALIGNANT LUNG TUMOURS

•

• • •

Primary lung cancer Lung cancer is one of the most common cancers throughout the world. In the UK, there are 40 000 cases a year, making it the most common cause of cancer death. From the time of diagnosis, 80 per cent of patients are dead within one year and only 5 per cent survive for five years. Surgical resection has a limited role in curative treatment because at the time of presentation many cases are locally advanced or widely disseminated and are beyond surgical cure. The proportion of lung cancers in which resection is attempted varies from fewer than 10 per cent in the UK to about 25 per cent in the United States. However, the thoracic surgeon working in a cancer team has a role in diagnosis, staging and palliation apart from resection in appropriate cases. The disease is so common that surgeons of all disciplines will encounter cases of lung cancer presenting with various manifestations. Cigarette smoking is undoubtedly the major risk factor for developing bronchial carcinoma and accounts for 85–95 per cent of all cases. To a lesser extent, atmospheric pollution and certain occupations (radioactive ore and chromium mining) contribute. The risk is related to the lifetime burden of cigarette smoking, which is commonly quoted as ‘pack-years’ (a ‘pack’ being 20 cigarettes): the number of packs smoked per day multiplied by the number of years of exposure. In the UK, the mortality rate from lung cancer for individuals smoking more than 40 cigarettes per day is over 210 deaths per 100 000 population per year. This compares with a mortality rate of less than four deaths per 100 000 population per year in non-smokers.

Pathological types

Accurate diagnosis and staging of the tumour are vital if surgery is to be considered.

Clinical features Clinical features of lung carcinoma depend on:

• the site of the lesion; • the invasion of neighbouring structures; • the extent of metastases. Common symptoms include a persistent cough, weight loss, dyspnoea and non-specific chest pain.

• Haemoptysis occurs in fewer than 50 per cent of patients presenting for the first time.

• Cough, or a changed cough, is a common presentation but non-specific in this population.

• Severe localised pain suggests chest wall invasion with the

• •

For practical purposes, lung cancers are divided into small cell and non-small cell lung cancer (NSCLC), which are seen in a ratio of about 1:4:

•

• The pattern of disease, the prognosis and the results of

•

treatment for small cell (also known as oat cell) carcinoma

of the packed nature of small dense cells. These represent about 20 per cent of all lung cancer. They tend to metastasise early to lymph nodes and by blood-borne spread. The median survival is measured in months. The tumours are very responsive to chemotherapy such that median survival may be doubled (but is still short), but they are rarely, if ever, cured. Surgery is rarely offered unless in very limited stage disease. Adenocarcinoma is now the most common of the NSCLC types, having overtaken squamous cancer. The increasing incidence is partly due to an increasing incidence in women and may be the result, in part, of a move towards lower-tar cigarettes that are inhaled more deeply to get the same effect. Squamous carcinoma typically appears as a cavitating tumour. Large cell undifferentiated is a discrete histological type of NSCLC and is included within neuroendocrine tumours. Bronchioalveolar carcinoma has a distinct pattern of growth following the pre-existing pulmonary architecture and is thus much less dense; it appears as a patchy diffuse shadow (‘ground glass’) on the radiograph, rather than a solid mass and has a histological appearance to match. After resection, it can appear in another lobe or the other side.

infiltration of an intercostal nerve. Invasion of the apical area may involve the brachial plexus, leading to Pancoast’s syndrome. Dyspnoea may come from loss of functioning lung tissue, lymphatic invasion or the development of a large pleural effusion. Pleural fluid is an ominous feature and the presence of blood in a pleural effusion suggests that the pleura has been directly invaded. Clubbing (Figure 55.11) and hypertrophic pulmonary osteoarthropathy accompany some lung cancers and may resolve with excision of the primary lesion. Invasion of the mediastinum may result in hoarseness (because of recurrent laryngeal nerve involvement), dysphagia

PART 9 | CARDIOTHORACIC

This is a fairly common occurrence in small children and is often marked by a choking incident that then apparently passes. Surprisingly large objects can be inhaled and become lodged in the wider calibre and more vertically placed right main bronchus. There are three possible presentations:

859

Henry Khunrath Pancoast, 1875–1939, Professor of Radiology, The University of Pennsylvania, Philadelphia, PA, USA, described the condition in 1932.

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THE THORAX

(because of the involvement of, or extrinsic pressure on, the oesophagus) and superior vena caval obstruction. • Small cell carcinoma is associated with the development of myopathies including the Eaton–Lambert syndrome, which is similar to myasthenia gravis (Summary box 55.5). Summary box 55.5 Symptoms of lung cancer ■ ■ ■ ■ ■ ■ ■

Haemoptysis 2, but ≤3 cm

Tumour >3, but ≤7 cma or tumour with any of the followingb: invades visceral pleura, involves main bronchus ≥2 cm distal to the carina, atelectasis/obstructive pneumonia extending to hilum, but not involving the entire lung T2a, Tumour >3, but ≤5 cma T2b, Tumour >5, but ≤7 cma

Tumour >7 cm or directly invading chest wall, diaphragm, phrenic nerve, mediastinal pleura, or parietal pericardium; or tumour in the main bronchus

Bailey & Love’s Short Practice of Surgery (26th Ed.) - Free Download PDF (2024)

References