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Bailey & Love’s SHORT PRACTICE of SURGERY

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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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Henry Hamilton Bailey 1894–1961

Robert J. McNeill Love 1891–1974

Skilled surgeons, inspirational teachers, dedicated authors

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Bailey & Love’s SHORT PRACTICE of SURGERY th

Edited by

27

EDITION

Professor Sir Norman Williams

MS FRCS FMedSci FRCP FRCP(Ed) FRCA FDS(Hon) FACS(Hon) FRCS(I)(Hon) FRCS(Ed)(Hon)

Senior Clinical Advisor to the Secretary of State for Health; Past President, The Royal College of Surgeons of England 2011–2014; Emeritus Professor of Surgery, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK

Professor P. Ronan O’Connell

MD FRCS(I) FRCPS(Glas) FRCS(Ed)

Head of Section of Surgery and Surgical Specialties, University College Dublin, St Vincent’s University Hospital, Dublin, Ireland

Professor Andrew W. McCaskie

MMus MD FRCS FRCS (T&O)

Professor of Orthopaedic Surgery and Head of Department of Surgery, University of Cambridge; Honorary Consultant, Addenbrooke’s Hospital, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

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B B

First published in Great Britain in 1932 This 27th edition published in 2018 by CRC Press Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487-2742 © 2018 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 Printed on acid-free paper International Standard Book Number-13: 978-1-4987-9650-7 (Pack – Paperback and eBook) International Standard Book Number-13: 978-1-138-03166-1 (Pack – Hardback and eBook) International Standard Book Number-13: 978-1-138-03164-7 (International Student Edition; restricted territorial availability) This book contains information obtained from authentic and highly regarded sources. While all reasonable efforts have been made to publish reliable data and information, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made. The publishers wish to make clear that any views or opinions expressed in this book by individual editors, authors or contributors are personal to them and do not necessarily reflect the views/opinions of the publishers. The information or guidance contained in this book is intended for use by medical, scientific or health-care professionals and is provided strictly as a supplement to the medical or other professional’s own judgement, their knowledge of the patient’s medical history, relevant manufacturer’s instructions and the appropriate best practice guidelines. Because of the rapid advances in medical science, any information or advice on dosages, procedures or diagnoses should be independently verified. The reader is strongly urged to consult the relevant national drug formulary and the drug companies’ and device or material manufacturers’ printed instructions, and their websites, before administering or utilizing any of the drugs, devices or materials mentioned in this book. This book does not indicate whether a particular treatment is appropriate or suitable for a particular individual. Ultimately it is the sole responsibility of the medical professional to make his or her own professional judgements, so as to advise and treat patients appropriately. The authors and publishers have also 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, 978-7508400. 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. Library of Congress Cataloging‑in‑Publication Data

Names: Williams, Norman S., 1947- editor. | O’Connell, P. Ronan, editor. | McCaskie, A. W., editor. Title: Bailey & Love’s short practice of surgery / [edited by] Norman Williams, P. Ronan O’Connell, Andrew McCaskie. Other titles: Bailey and Love’s short practice of surgery | Short practice of surgery. Description: 27th edition. | Boca Raton, FL : CRC Press, 2017. Identifiers: LCCN 2017015906 (print) | LCCN 2017018725 (ebook) | ISBN 9781315111087 (General eBook) | ISBN 9781351617994 (Adobe eBook) | ISBN 9781351617987 ( ePub eBook) | ISBN 9781351617970 (Mobipocket eBook) | ISBN 9781138031661 (hardback : alk. paper) | ISBN 9781498796507 (pbk. : alk. paper) | ISBN 9781138031647 (international edition pbk. : alk. paper). Subjects: | MESH: Surgical Procedures, Operative | Perioperative Care. Classification: LCC RD31 (ebook) | LCC RD31 (print) | NLM WO 500 | DDC 617--dc23 LC record available at https://lccn.loc.gov/2017015906 Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com and the CRC Press Web site at http://www.crcpress.com

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Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Contents

Karim Brohi

17

42

Peter Lamont

139

22

161

23

170

13

Human factors, patient safety and quality improvement

Introduction to trauma

310

Peter Giannoudis & Bob Handley

Early assessment and management of severe trauma

322

Chris Moran & Dan Deakin

24

Robert Wheeler

301

PART 4: TRAUMA

Jonothan J. Earnshaw & Birgit Whitman

Surgical ethics and law

Day case surgery

Douglas McWhinnie & Ian Jackson

Robert J.C. Steele & Alastair Munro

Surgical audit and research

290

21

119

Anthony Lander

Principles of oncology

Postoperative care

105

Principles of paediatric surgery

12

278

Anand Sardesai & Fay Gilder

Hutan Ashrafian, Sanjay Purkayastha & Ara Darzi

11

Nutrition and fluid therapy

Traumatic brain injury

Principles of laparoscopic and robotic surgery

20

84

Mark G. Coleman

10

269

John MacFie

Basic surgical skills and anastomoses

9

Anaesthesia and pain relief

19

57

Pradip K. Datta, Pawanindra Lal & Sanjay De Bakshi

8

254

Vivek Mehta & Serene Hsi-Lin Chang

Tropical infections and infestations

7

18

Surgical infection

Preoperative care including the high-risk surgical patient Medha Vanarase-Pandit, Pierre Foex & Anand Sardesai

Andrew W. McCaskie & John Andrew Bradley

6

234

Roger M. Feakins

33

Tissue engineering and regeneration

5

Tissue and molecular diagnosis

16

24

Michael John Earley

4

216

PART 3: PERIOPERATIVE CARE

Wounds, healing and tissue repair

3

Gastrointestinal endoscopy

12

Shock and blood transfusion

190

2

The late Kenneth Fearon

2

Diagnostic imaging

Matthew Matson, Muaaze Ahmad & Niall Power James O. Lindsay & Philip Woodland

Metabolic response to injury

14 15

PART 1: BASIC PRINCIPLES 1

PART 2: INVESTIGATION AND DIAGNOSIS

viii x xvii xx

Preface Contributors Acknowledgements Sayings of the great

328

Harry J.C.J. Bulstrode & Antonio Belli

176

Frank B.V. Keane & Ken Mealy

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vi

Contents

25

Neck and spine

338

PART 7: HEAD AND NECK

355

43

364

44

381

45

John Crawford & Douglas Hay

26

Maxillofacial trauma David A. Koppel

27

Torso trauma Extremity trauma Lee Van Rensburg

29

Disaster surgery

409

Mamoon Rashid

30

Conflict surgery

424

Jon Clasper & Phill Pearce

History taking and clinical examination in musculoskeletal disease

The eye and orbit

672

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

686

David A. Koppel

46

The ear, nose and sinuses

703

Iain J. Nixon, Iain Hathorn & Alex Bennett

47

Pharynx, larynx and neck

725

Terry M. Jones

48

PART 5: ELECTIVE ORTHOPAEDICS 31

652

Keith R. Martin

Ken Boffard & Elias Degiannis

28

Cranial neurosurgery Harry J.C.J. Bulstrode & William P. Gray

Oral cavity malignancy

760

Andrew G. Schache

49

Disorders of the salivary glands

776

Mark McGurk & Leandros-Vassilios F. Vassiliou

436

Stephen M. McDonnell & Hemant G. Pandit

32

Sports medicine and sports injuries

463

PART 8: BREAST AND ENDOCRINE

471

50

488

51

511

52

Gina Allen

33

The spine Upper limb Hip and knee Vikas Khanduja & Wasim Sardar Khan

36

Foot and ankle

524

Bob Sharp

37

Musculoskeletal tumours

38

Infection of the bones and joints

549

Martin A. McNally & Philippa C. Matthews

39

Paediatric orthopaedics

53

The adrenal glands and other abdominal endocrine disorders

838

The breast

860

Richard C. Sainsbury

PART 9: CARDIOTHORACIC 54

561

Deborah M. Eastwood

823

Tom W.J. Lennard

534

Paul Cool & Craig Gerrand

The parathyroid glands Ruth S. Prichard

David Limb & Sam Vollans

35

800

Iain J. Nixon & Richard M. Adamson

Brian J.C. Freeman & Chris Lavy

34

The thyroid gland

Cardiac surgery

884

Jonathan R. Anderson & Mustafa Zakkar

55

The thorax

914

Carol Tan & Ian Hunt

PART 6: SKIN AND SUBCUTANEOUS TISSUE 40

Skin and subcutaneous tissue

PART 10: VASCULAR 592

Adam R. Greenbaum & Christopher L.H. Chan

41 Burns Plastic and reconstructive surgery Tim Goodacre

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Arterial disorders

942

Rob Sayers & Robert S.M. Davies

617

Michael P.H. Tyler & Sudip J. Ghosh

42

56 57

Venous disorders

969

Ian C. Chetter & Dan Carradice

633

58

Lymphatic disorders

995

Gnaneswar Atturu, David A. Russell & Shervanthi Homer-Vanniasinkam

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Contents

PART 11: ABDOMINAL 59

History and examination of the abdomen

PART 12: GENITOURINARY 1016

75

P. Ronan O’Connell

60

Abdominal wall, hernia and umbilicus The peritoneum, omentum, mesentery and retroperitoneal space

1022

The oesophagus

1047

76

Stomach and duodenum Bariatric and metabolic surgery The liver

1106 80 1144

The spleen

1176

67

The gallbladder and bile ducts

1188

The pancreas The small intestine The large intestine Intestinal obstruction The vermiform appendix The rectum

1497 1513

82 Transplantation

1532

John Andrew Bradley

1560

Pradip K. Datta

1258 1280

Appendix 2: Fundamental principles in the operating theatre and the importance of global health

1299

Index

Jürgen Mulsow

73

1477

PART 13: TRANSPLANTATION

Appendix 1: Common instruments used in general surgery

Jim Hill

72

1456

Monica Mittal, Prasanna Raj Supramaniam & Christian Becker

1240

Gordon Lawrence Carlson & Jonathan Epstein

71

Testis and scrotum

APPENDICES

Gordon Lawrence Carlson & Mattias Soop

70

Urethra and penis

1212

Satyajit Bhattacharya

69

The prostate and seminal vesicles

81 Gynaecology

Kevin C.P. Conlon

68

1423

Ian Eardley

1153

O. James Garden

The urinary bladder

Ian Eardley

Robert P. Jones & Graeme J. Poston

66

1398

David E. Neal & Greg Shaw

79

Richard Welbourn & Dimitri Pournaras

65

Kidneys and ureters

Freddie C. Hamdy

1067

Tim Underwood & John N. Primrose

64

77 78

Derek Alderson

63

1374

J. Kilian Mellon

Charles H. Knowles

62

Urinary symptoms and investigations J. Kilian Mellon

Bruce Tulloh & Stephen J. Nixon

61

vii

1563

Alan Norrish & Chris Lavy

1567

1318

David Jayne & Hiba Fatayer

74

The anus and anal canal

1339

Karen Nugent

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Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Preface to 27th Edition When Hamilton Bailey and McNeil Love published the first edition of their venerated textbook in 1932 the surgical world was a very different place to that of today. There were no antibiotics, no joint replacement, no open heart surgery, no transplantation and many other procedures that we now take for granted had simply not been invented. Medicine as a whole and surgery in particular never stands still. Surgeons continually strive to innovate so that they can tackle conditions and diseases previously thought to be beyond reach. They do this against a background of new discoveries in both the physical and biological sciences. Such breakthroughs make some surgical procedures redundant but others stimulate new approaches. This is seen in all specialties and consequently it is important for textbooks not only to keep pace with new developments but also to ensure that a balanced view is taken of their place in the therapeutic armamentarium. In developing the 27th edition of this much-loved textbook, we have striven to keep this in the forefront of our minds and those of our contributors. Nevertheless, in addition to considering the place of innovation, it is important not to ‘throw the baby out with the bathwater’. We have therefore ensured that the basic tenets of surgical practice that have stood the test of time remain where appropriate. Since the last edition great strides have been made in certain areas and we have ensured that these have been embedded in the book. For instance, in colorectal surgery a tipping point has been reached whereby more elective surgery is performed laparoscopically than by open technique. Similarly, in vascular surgery there has been an explosion in the use of interventional radiology to treat conditions that were previously the sole province of the surgeon. Stenting of aortic aneurysms (EVAR), for instance, is rapidly replacing elective open operations and, in many instances, is being used for treating leaking aneurysms, with a concomitant marked reduction in mortality. Damage control surgery is an increasingly important part of trauma management, in both civilian and conflict settings. Such developments also highlight the important role of the multidisciplinary team and the realisation that modern surgical care can no longer be provided in isolation. This concept is reiterated throughout the book and is also why the importance of human factors is emphasised in the chapter on patient safety, which is a relatively new science of how humans behave physically and psychologically in relation to particular environments. There is no more intense environment than an operating theatre, so how

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a surgical team interacts is crucial to the outcome for a patient undergoing a surgical procedure. This also applies, of course, outside the operating theatre because multidisciplinary working is now paramount to the delivery of safe and effective patient care. There is no doubt that in recent years regulation of medical practice has become tighter. Whereas in certain jurisdictions some may feel that this has become stifling, there is no doubt that regulation is here to stay. Needless to say, we should all be aware of our responsibilities to patients, both morally and ethically, and, although most need no reminding, the law is continually changing as test cases are brought before the courts. Hence, we draw the attention of the reader to the revamped chapter on ethics and the law, the tenets of which we must all abide by. Throughout the text, we have also endeavoured to point out where we and our authors think the specialty is moving. Exciting developments are on the horizon. For instance, genome sequencing will have a marked effect on how we practise in certain specialties, none more so than oncology. Robotics is likely to improve many more surgical procedures and tissue engineering will become more commonplace. In order to accommodate these advances, it has been necessary to streamline some of the more established chapters, otherwise the book would become unwieldy. As a consequence, we have ensured that the ‘Further reading’ list at the end of each chapter has been brought up to date, allowing readers to delve further if they so wish. We are very conscious that the book is popular throughout the world and consequently we have ensured that those diseases that are prevalent outside Europe and North America are included. Where relevant we have involved experts who are used to dealing with such maladies. The chapter on tropical infections and infestations is such an example. We have also endeavoured in this edition to be more consistent in its layout, ensuring that we use a similar format for tables, graphs and diagrams. Nevertheless, we have been sure to keep the biographical details of individual scientists and practitioners, which have been beloved of all readers throughout the generations. Similarly, we have retained the section on surgical instruments. Although some are now very much of historical interest, they are part of our heritage and students and indeed established practitioners will, we hope, find these vignettes fascinating. We have been told that the Summary boxes are very much appreciated by both undergraduate and postgraduate students revising, sometimes in

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Preface to 27th Edition

haste, before exams and hence our authors have ensured that these are up to date. A book as comprehensive as this could never have been completed without the dedication and professionalism of our contributors. They have invariably answered our demands with alacrity and accuracy, appreciating the responsibility that goes with informing the readership of such a respected and established textbook. We are extremely grateful for all their efforts because we are conscious that a textbook such as this can never rest on its laurels. If it is to remain in the higher echelons of surgical tomes it must have the very best contributors and we believe that we have brought together such a cadre in the present edition. This in no way diminishes the contributions of the authors from the previous edition who are no longer involved. They, for a variety of reasons including retirement, have passed on the baton. We are grateful to them for magnanimously stepping down and making way for ‘new blood’ and none more so than our previous co-editor Professor Christopher Bulstrode. Chris helped revamp the 23rd, 24th, 25th and 26th Editions and these would never have been as successful without his dedicated efforts. Chris’s place in the editorial team has been taken by Andrew McCaskie who has

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streamlined the trauma and orthopaedic sections as well as overseeing other chapters. Readers of Bailey & Love have always been an integral part of the development of the book over the years and the present editorial group relish your feedback, which we know from experience will be forthcoming. Such input is vital if the book is to continue to reach the very high standards expected from each new edition. This has been a labour of love for all of us involved in this edition and we do hope it fulfils your needs, no matter whether you are an undergraduate student exploring the exciting world of surgical practice for the first time, a postgraduate trainee studying for exams or an established consultant who wishes to refresh his or her memory. We wish you all well in your careers no matter which specialty you choose to practise in and we very much hope that the 27th and indeed subsequent editions of Bailey & Love accompany you on your travels through this most rewarding of professions. Norman S. Williams P. Ronan O’Connell Andrew W. McCaskie

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Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Contributors Richard M. Adamson MBBS FRCS(ORL-HNS) Consultant Ear, Nose and Throat Surgeon University of Edinburgh ENT Department Edinburgh, UK

Muaaze Ahmad MBChB FRCR Consultant Radiologist Barts Health NHS Trust London, UK

Derek Alderson MD

President, Royal College of Surgeons of England Emeritus Professor of Surgery University of Birmingham Honorary Consultant Surgeon University Hospitals NHS Trust Queen Elizabeth Hospital Birmingham, UK

Gina Allen BM DCH MRCP MRCGP FRCR MFSEM MScSEM DipESSR

Musculoskeletal Radiologist and Sports Physician Oxford Universityand St Lukes Radiology Oxford Ltd Oxford, UK

Jonathan R. Anderson FRCS(C-Th) FFST(Ed) Consultant Cardiothoracic Surgeon Hammersmith Hospital London, UK

Hutan Ashrafian BSc(Hons) MBBS PhD MBA MRCS Department of Surgery and Cancer and Institute of Global Health Innovation Imperial College London Bariatric and Metabolic Surgical Unit Chelsea and Westminster Hospital London, UK

Gnaneswar Atturu MS ChM FRCS

Locum Consultant Vascular and Trauma Surgeon Leeds Vascular Institute Leeds General Infirmary Leeds, UK

Sanjay De Bakshi MS(Cal) FRCS(Eng) FRCS(Ed) Head of Department of Surgery Calcutta Medical Research Institute Kolkata, India

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Christian Becker MD

Associate Professor Consultant Gynaecologist and Subspecialist in Reproductive Medicine Nuffield Department of Obstetrics and Gynaecology University of Oxford John Radcliffe Hospital Oxford, UK

Antonio Belli MD FRCS FRCS(SN)

Professor of Trauma Neurosurgery Director of the NIHR Surgical Reconstruction and Microbiology Research Centre University of Birmingham Birmingham, UK

Alex Bennett MBBS DLO FRCS(ORL-HNS) MEd DIC Consultant Ear, Nose and Throat Surgeon University of Edinburgh ENT Department Edinburgh, UK

Satyajit Bhattacharya MS MPhil FRCS

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

Ken Boffard BSc(Hons) MB BCh FRCS FRCS(Ed) FRCPS(Glas) FCS(SA) FACS(Hon)

Professor Emeritus Department of Surgery University of the Witwatersrand Trauma Director and Academic Head Netcare Milpark Academic Trauma Centre Johannesburg, South Africa

John Andrew Bradley PhD, FRCS Emeritus Professor of Surgery Cambridge University 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

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Contributors

Harry J.C.J. Bulstrode PhD

Clinical Lecturer in Neurosurgery University of Cambridge Cambridge, UK

Gordon Lawrence Carlson BSc(Hons) MBChB(Hons) MD FRCS FRCS(Gen) FRCS(Ed)

Consultant Surgeon and Honorary Professor of Surgery University of Manchester Salford Royal Hospital NHS Foundation Trust Salford, UK

Dan Carradice MBChB MD(Hons) FRCS PGC Med US(Dist) PGD(Health Econ)

Kevin C.P. Conlon MA MCh MBA FRCS(I) FACS FRCS(Ed) FRCPS(Glas) FTCD

Professor of Surgery Trinity College Dublin Consultant HPB Surgeon St. Vincent’s University Hospital Dublin, Ireland

Paul Cool MD MMedSc(Res) DipStat FRCS(Ed) FRCS(Orth)

Consultant Orthopaedic and Oncological Surgeon Robert Jones and Agnes Hunt Orthopaedic Hospital NHS Foundation Trust Oswestry, UK

John Crawford BSc MBBS FRCS FRCS(Orth)

Senior Lecturer Hull York Medical School Consultant Vascular and Endovascular Surgeon Hull and East Yorkshire Hospitals NHS Trust Hull and York, UK

Consultant Orthopaedic Spinal Surgeon Department of Neurosurgery Cambridge University Hospital NHS Foundation Trust Cambridge, UK

Christopher L.H. Chan BSc(Hons) PhD FRCS(Eng)

Professor the Lord Darzi of Denham OM KBE PC FRS

FRCS(Gen Surg)

Consultant Colorectal Surgeon Barts Health NHS Trust London, UK

Serene Hsi-Lin Chang MBBS MD FRCA

Consultant Anaesthetist Ng Teng Fong General Hospital Singapore Honorary Fellow, Pain and Anaesthesia Research Centre St Bartholomew’s Hospital and Biomedical Engineering Research Group City University London, UK

Ian C. Chetter MBChB MD FRCS PGC Med US(Dist) PGD Clin Ed

Chair of Surgery Hull York Medical School Consultant Vascular Surgeon Hull and East Yorkshire Hospitals NHS Trust Hull and York, UK

Jon Clasper CBE DPhil DM FRCSEd(Orth) Col L/RAMC

Emeritus Professor and Consultant Orthopaedic Surgeon Military Clinical Director DMG (SE) Visiting Professor in Bioengineering Imperial College London Clinical Lead The Royal British Legion Centre for Blast Injury Studies London, UK

Mark G. Coleman, MBChB MD(Hons) FRCS FRCPS(Glas) FFST(RCSEd)

Consultant Surgeon Derriford Hospital, Plymouth Senior Lecturer (Associate Professor) Plymouth University Peninsula School of Medicine and Dentistry Plymouth, UK

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FMedSci

Professor of Surgery Imperial College London St Mary’s Hospital Campus London, UK

Pradip K. Datta MBE MS FRCS(Ed) FRCS(Eng) FRCS(I) FRCS(Glas)

Honorary Consultant Surgeon Caithness General Hospital Wick, UK

Robert S.M. Davies MBChB MMedSci(Med Ed) MD FRCS

Consultant Vascular Surgeon and Honorary Senior Lecturer University Hospitals of Leicester Leicester, UK

Dan Deakin FRCS(T&O)

Consultant Orthopaedic Trauma Surgeon Nottingham University Hospital Nottingham, UK

Elias Degiannis MD PhD FRCS(Glasg) FCS(SA) FACS

Professor Emeritus, Department of Surgery University of the Witwatersrand Medical School Netcare Milpark Academic Trauma Center and Leratong Hospital Johannesburg, South Africa

Ian Eardley MA MChir FRCS(Urol) FEBU

Consultant Urologist Leeds Teaching Hospital Trust Leeds, UK

Michael John Earley MB MCh FRCS(I) FRCS(Plast)

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

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Contributors

Jonothan J. Earnshaw DM FRCS Consultant Vascular Surgeon Cheltenham General Hospital Cheltenham, UK

Deborah M. Eastwood MB FRCS

Consultant Paediatric Orthopaedic Surgeon Great Ormond St Hospital for Children and the Royal National Orthopaedic Hospital London, UK

Jonathan Epstein MA MD FRCS

Consultant Surgeon Salford Royal NHS Foundation Trust Salford, UK

Hiba Fatayer MBBS MSc MRCS

Specialist Registrar in General Surgery Leeds Teaching Hospitals NHS Trust Leeds, UK

Roger M. Feakins MB BCh BAO BA MD FRCPI FRCPath Consultant Histopathologist and Professor of Gastrointestinal Pathology Department of Histopathology Barts Health NHS Trust London, UK

The late Professor 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

O. James Garden CBE BSc MBChB MD FRCS(Ed) FRCP(Ed) FRSE FRCS(Can)(Hons) FRACS(Hons) FACS(Hons) FRCS(Hons) FCSHK(Hons) FRCS(I)(Hons)

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

Craig Gerrand MD FRCS(Ed)(T&O)

Consultant Orthopaedic Surgeon North of England Bone and Soft Tissue Tumour Service Newcastle upon Tyne Hospitals NHS Foundation Trust Newcastle upon Tyne, UK

Sudip J. Ghosh MBBS MS FRCS(Plast)

Consultant Plastic Reconstructive and Burns Surgeon Stoke Mandeville Hospital Aylesbury, UK

Peter Giannoudis MD FACS FRCS

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

Fay Gilder MBBS FRCA

Consultant Anaesthetist Cambridge University Hospitals NHS Foundation Trust Cambridge, UK

Tim Goodacre MBBS BSc FRCS

Consultant Plastic Surgeon Oxford University Hospitals NHS Foundation Trust Oxford, UK

William P. Gray MB MD FRCS(I) FRCS(SN)

Emeritus Nuffield Professor of Anaesthetics Nuffield Division of Anaesthetics John Radcliffe Hospital Oxford, UK

Professor of Neurosurgery Director Wales BRAIN Unit Neuroscience and Mental HealthResearch Institute School of Medicine Cardiff University Cardiff, UK

Brian J.C. Freeman MB BCh BAO DM(Nott) FRCS(T&O)

Adam R. Greenbaum MBBS MBA PhD FRCS(Plast) FEBOPRAS

Pierre Foex DPhil FRCA FMedSci

FRACS(Ortho) FAOrthA

Professor of Spinal Surgery University of Adelaide Head of Spinal Services Royal Adelaide Hospital Adelaide Senior Visiting Specialist Women’s and Children’s Hospital Clinical Director Centre for Orthopaedic and Trauma Research Adelaide, Australia

FACS

Consultant Plastic and Reconstructive Surgeon Auckland and the Waikato New Zealand

Freddie C. Hamdy MD MA FRCS FRCS(Ed)(Urol) FMedSci Nuffield Professor of Surgery and Professor of Urology University of Oxford Director, Division of Surgery and Oncology Oxford University Hospitals NHS Foundation Trust Oxford, UK

Bob Handley MBChB FRCS

Consultant Trauma and Orthopaedic Surgeon John Radcliffe Hospital Oxford, UK

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Contributors

Iain Hathorn BSc MBChB DOHNS PGCME FRCSEd(ORL-HNS) Consultant Ear, Nose and Throat Surgeon University of Edinburgh ENT Department Edinburgh, UK

Douglas Hay MBBS FRCS(Orth)

Consultant Orthopaedic Spinal Surgeon Department of Neurosurgery Cambridge University Hospital NHS Foundation Trust Cambridge, UK

Jim Hill MDChB ChM FRCS

Clinical Professor of Colorectal Surgery Manchester Royal Infirmary and Manchester Academic Health Science Centre Manchester, UK

Shervanthi Homer-Vanniasinkam BSc MD FRCS(Ed) FRCS Consultant Vascular Surgeon Leeds Vascular Institute Leeds General Infirmary Leeds, UK

Ian Hunt FRCS(CTh)

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

Ian Jackson MBChB FRCA

Chief Clinical Information Officer York Teaching Hospital NHS Foundation Trust York, UK

David Jayne BSc MBChB MD FRCS

Professor of Surgery University of Leeds and Leeds Teaching Hospitals NHS Trust Leeds, UK

Terry M. Jones BSc FRCSEd FRCS(ORL-HNS) MD SFHEA FASE(RCS)

Professor of Head and Neck Surgery Institute of Translational Medicine University of Liverpool Liverpool, UK

Robert P. Jones BSc MBChB PhD MRCS Lecturer in Surgery Institute of Translational Medicine University of Liverpool Liverpool, UK

Frank B.V. Keane MD FRCS FRCS(I) FRCPS(Glas)(Hons) FRCP(Ed)(Hons) FRCPI(Hons)

Joint Lead, National Clinical Programme in Surgery Royal College of Surgeons in Ireland Former Consultant Colorectal Surgeon Adelaide and Meath Hospital Dublin, Ireland

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Wasim Sardar Khan MBChB MSc PhD MRCS FRCS(Tr&Orth)

University Lecturer and Honorary Consultant Trauma and Orthopaedic Surgeon Addenbrooke’s Hospital Cambridge University Hospitals NHS Foundation Trust Cambridge, UK

Vikas Khanduja MA(Cantab) MSc FRCS FRCS(Tr&Orth)

Consultant Orthopaedic Surgeon Research Lead – Elective Clinical Trials Addenbrooke’s Hospital Cambridge University Hospitals NHS Foundation Trust Cambridge, UK

Charles H. Knowles BChir PhD FRCS

Professor of Surgery and Honorary Consultant Colorectal Surgeon Barts Health NHS Trust The Blizard Institute Barts and the London School of Medicine and Dentistry Queen Mary, University of London London, UK

David A. Koppel MB BS BDS FDS FRCS

Consultant Craniofacial/Oral and Maxillofacial Surgeon Regional Maxillofacial Unit Queen Elizabeth University Hospital, Royal Hospital for Children Glasgow, UK

Pawanindra Lal MS DNB MNAMS FIMSA FCLS FRCS(Ed) FRCS(Glas) FRCS(Eng) FACS

Director Professor of Surgery Maulana Azad Medical College (University of Delhi) and Associated Lok Nayak Hospital New Delhi, India

Peter Lamont MD FRCS FEBVS

Consultant Vascular Surgeon Bristol, Bath and Weston Vascular Network Bristol, UK

Anthony Lander PhD FRCS(Paed) DCH

Consultant Paediatric Surgeon Birmingham Children’s Hospital Birmingham, UK

Chris Lavy OBE MD MCh FRCS(Eng)

Professor of Orthopaedic and Tropical Surgery University of Oxford Honorary Consultant Spine Surgeon Oxford University Hospitals Oxford, UK

Tom W.J. Lennard MBBS MD FRCS

Professor of Surgery and Associate Dean Newcastle University Newcastle upon Tyne, UK

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Contributors

David Limb BSc FRCSEd(Orth)

Matthew Matson MRCP FRCR

James O. Lindsay PhD FRCP

Philippa C. Matthews BMBS MRCP DTM&H DPhil(Oxon)

Andrew W. McCaskie MMus MD FRCS FRCS(T&O)

Wellcome Trust Clinical Research Fellow Nuffield Department of Medicine University of Oxford Honorary Consultant in Infectious Diseases and Microbiology Oxford University Hospitals NHS Foundation Trust Oxford, UK

Consultant Orthopaedic Surgeon Leeds Teaching Hospitals Trust Leeds, UK Consultant Gastroenterologist Barts Health NHS Trust The Royal London Hospital Reader in Inflammatory Bowel Disease Queen Mary University of London London, UK Professor of Orthopaedic Surgery and Head of Department of Surgery University of Cambridge Honorary Consultant Addenbrooke’s Hospital Cambridge University Hospitals NHS Foundation Trust Cambridge, UK

Stephen M. McDonnell MBBS BSc MD FRCS(T&O)

University Lecturer and Consultant Orthopaedic Surgeon Addenbrooke’s Hospital Cambridge University Hospitals NHS Foundation Trust Cambridge, UK

John MacFie MD FRCS(Eng) FRCS(Ed) FRCS(Glas) FRCP(Ed)

Professor of Surgery and Consultant Surgeon University of Hull, York NHS Trust at Scarborough Hospital Scarborough, UK

Mark McGurk MD BDS FRCS FDSRCS DLO

Professor of Oral and Maxillofacial Surgery University College London Hospital London, UK

Martin A. McNally MB BCH MD(Res) FRCS(Ed) FRCS(Orth)

Consultant in Limb Reconstruction Nuffield Orthopaedic Centre Oxford University Hospitals Honorary Senior Clinical Lecturer in Orthopaedic Surgery University of Oxford Oxford, UK

Douglas McWhinnie MD(Hons) FRCS

Professor of Clinical Education and Consultant General and Vascular Surgeon University of Buckingham Milton Keynes University Hospital NHS Foundation Trust Milton Keynes, UK

Keith R. Martin MA BM BCh DM MRCP FRCOphth Professor of Ophthalmology University of Cambridge Cambridge, UK

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Divisional Director of Imaging Barts Health NHS Trust London, UK FRCPath

Ken Mealy MD FRCS(I) FRCS(Ed)

Joint Lead, National Clinical Programme in Surgery Royal College of Surgeons in Ireland Consultant General Surgeon Wexford General Hospital Wexford, Ireland

Vivek Mehta MBBS MD FRCA FFPMRCA

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

J. Kilian Mellon MD FRCS(Urol) Consultant Urological Surgeon Leicester General Hospital Leicester, UK

Monica Mittal Intercalated BSc MBBS MRCOG

Subspecialist Trainee in Reproductive Medicine and Surgery Specialist Registrar in Obstetrics and Gynaecology Oxford University Hospitals NHS Foundation Trust Oxford, UK

Chris Moran MD FRCS(Ed)

National Clinical Director for Trauma NHS-England Professor of Orthopaedic Trauma Surgery Nottingham University Hospital Nottingham, UK

Jürgen Mulsow MD FRCS(I)

Consultant General and Colorectal Surgeon Department of Colorectal Surgery and National Centre for Peritoneal Malignancy Mater Misericordiae University Hospital Dublin, Ireland

Alastair Munro BSc FRCR FRCP(E) FRCS(Ed) Honorary Professor School of Medicine University of St Andrews St Andrews, UK

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Contributors

David E. Neal CBE FMedSci FRCS

Senior Visiting Fellow and Professor Emeritus of Surgical Oncology University of Cambridge Cambridge, UK

Iain J. Nixon MB ChB FRCS(ORL-HNS) PhD Consultant Ear, Nose and Throat Surgeon University of Edinburgh Edinburgh, UK

Stephen J. Nixon FRCS(Ed) FRCP(Ed) Consultant Surgeon Royal Infirmary of Edinburgh Edinburgh, UK

Alan Norrish BSc(Hons) MB BChir LLM PhD FRCS(Orth)

Associate Lecturer School of Clinical Medicine University of Cambridge Consultant Orthopaedic Surgeon Cambridge University Hospitals NHS Foundation Trust Cambridge, UK

Karen Nugent MA MS MEd FRCS Consultant Colorectal Surgeon University of Southampton Southampton, UK

P. Ronan O’Connell MD FRCS(I) FRCPS(Glas) FRCS(Edin)

Professor, Head of Section of Surgery and Surgical Specialties University College Dublin St Vincent’s University Hospital Dublin, Ireland

Hemant G. Pandit DPhil FRCS(T&O)

Professor of Orthopaedic Surgery and Honorary Consultant Director of Research and Innovation University of Leeds Leeds Professor of Orthopaedic Surgery University of Oxford Oxford, UK

Phill Pearce MA MBBS MRCS RAF

Registrar in General Surgery Royal British Legion Centre for Blast Injury Studies Imperial College London London Academic Department of Military Surgery and Trauma Royal Centre for Defence Medicine Frimley Park, UK

Graeme J. Poston MS DSc FRCS(Eng) FRCS(Ed) Professor of Surgery Northwestern Hepatobiliary Unit Aintree University Hospital Liverpool, UK

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Dimitri Pournaras PhD FRCS

Registrar in Upper Gastrointestinal and General Surgery Addenbrooke’s Hospital Cambridge University Hospitals NHS Foundation Trust Cambridge, UK

Niall Power MD MRCP(I) FRCR

Consultant Radiologist Royal Free Hospital London, UK

Ruth S. Prichard MD FRCS(I)

Consultant Endocrine and Breast Surgeon St Vincent’s University Hospital Dublin, Ireland

John N. Primrose FMedSci

Professor of Surgery University of Southampton Southampton General Hospital Southampton, UK

Sanjay Purkayastha BSc MBBS MD FRCS(Gen Surg)

Consultant Surgeon General, Laparoscopic, Bariatric and Upper GI Surgery St Mary’s Hospital Imperial College Healthcare NHS Trust Senior Lecturer in Bariatric Surgery Imperial College London, UK

Mamoon Rashid FRCS FCPS(Pak)

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

Lee Van Rensburg MBBCh FRCS(Tr&Orth)

Consultant Orthopaedic Surgeon Addenbrooke’s Hospital Cambridge University Hospitals NHS Foundation Trust Cambridge, UK

David A. Russell MB ChB MD FRCS(Gen Surg)

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

Richard C. Sainsbury MBBS MD FRCS

Honorary Reader in Surgery University College London Consultant Surgeon London Breast Clinic London, UK

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B B

Contributors

Anand Sardesai MB BS MD FRCA

Bruce Tulloh MB MS(Melb) FRACS FRCS(Ed)

Rob Sayers MD FRCS

Michael P.H. Tyler MB CHM FRCS(Plast)

Andrew G. Schache PhD FDSRCS FRCS(OMFS)

Tim Underwood PhD FRCS

Consultant Anaesthetist Addenbrooke’s Hospital Cambridge University Hospitals NHS Foundation Trust Cambridge, UK Honorary Professor of Vascular Surgery Leicester Royal Infirmary Leeds, UK Clinical Senior Lecturer in Head and Neck Surgery University of Liverpool Honorary Consultant in Oral and Maxillofacial – Head and Neck Surgery Aintree University Hospitals NHS Foundation Trust Liverpool, UK

Bob Sharp BM BCh MA FRCS FRCS(Tr&Orth) Consultant Orthopaedic Surgeon Oxford University Hospitals The Nuffield Orthopaedic Centre Oxford, UK

Greg Shaw MD FRCS(Urol)

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

Consultant Plastic Reconstructive and Burns Surgeon Stoke Mandeville Hospital Aylesbury, UK Professor of GI Surgery University of Southampton Southampton, UK

Medha Vanarase-PanditMD FRCA Cert Med Ed Consultant Anaesthetist Leeds Teaching Hospitals NHS Trust Leeds, UK

Leandros-Vassilios F. Vassiliou DDS MD MSc FRCS Department of Head and Neck Guy’s Hospital London, UK

Consultant Urologist University College London Hospitals NHS Foundation Trust Honorary Senior Lecturer University College and Queen Mary College London, UK

Sam Vollans FRCS(Ed)(Orth)

Mattias Soop MD PhD

Consultant Upper Gastrointestinal and Bariatric Surgeon Honorary Reader in Bariatric Surgery University of Bristol Musgrove Park Hospital Taunton, UK

Consultant Surgeon and Honorary Reader in Surgery The University of Manchester Manchester Academic Health Science Centre Salford Royal NHS Foundation Trust Salford, UK

Robert J.C. Steele MB ChB MD FRCS(Ed) FRSE

Head of Academic Surgery and Head of Cancer Division Medical Research Institute, Division of Cancer Ninewells Hospital and Medical School Dundee, UK

Prasanna Raj Supramaniam MBChB MSc MRCOG

Specialist Registrar in Obstetrics and Gynaecology Oxford University Hospitals NHS Foundation Trust Oxford, UK

Carol Tan FRCS(C-Th)

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

Consultant Orthopaedic Surgeon Leeds Teaching Hospitals Trust Leeds, UK

Richard Welbourn MD FRCS

Robert Wheeler MS LLB(Hons) LLM FRCS

Consultant Neonatal and Paediatric Surgeon Director, Department of Clinical Law University Hospital of Southampton Southampton, UK

Birgit Whitman PhD

Head of Research Governance University of Bristol Bristol, UK

Philip Woodland MBBS PhD MRCP

Consultant Gastroenterologist Barts Health NHS Trust The Royal London Hospital Honorary Senior Lecturer in Upper GI Medicine Queen Mary, University of London London, UK

Mustafa Zakkar PhD FRCS(C-Th)

NIHR Clinical Lecturer in Cardiothoracic Surgery University of Bristol and Bristol Heart Institute Bristol, UK

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Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Acknowledgements In this day and age, it is impossible to produce a book like Bailey and Love without the contribution of numerous talented individuals. Although it is impractical to mention all those who have played a part in producing the 27th Edition, it would be remiss not to express our gratitude to the following key players. Henry Spilberg initiated the new edition as commissioning editor under the supervision of Jo Koster and was very much involved in the early planning. His role was subsequently taken over by Miranda Bromage following his departure for pastures green. Miranda’s diligence and experience has been invaluable and we are enormously indebted to her wise counsel. Cherry Allen, as Editorial Assistant has been key in liaising with the editors and the contributors, ensuring manuscripts have been received on time and has been responsible for ensuring the smooth handover of the text to the production team. The latter has been headed by Paul Bennett who has provided an extremely professional service. His and his team’s attention to detail has been very much valued and we hope is reflected in a first class product.

preparation’ by current authors Medha Vanarase-Pandit and Pierre Foex, and Kevin Tremper, Lisa Leonard and Sarah Barton, and ‘Perioperative management of the high-risk patient’ by Mridula Rai, Kevin D. Johnston, Rupert M. Pearse and Richard M. Langford. The material has been revised and updated by the current authors. Chapter 18, Anaesthesia and pain relief, contains some material from ‘Anaesthesia and pain relief’ by current author Vivek Mehta, and Richard Langford and Jagannath Halder. The material has been revised and updated by the current authors. Chapter 20, Postoperative care, contains some material from ‘Postoperative care’ by Jay Kini, current author Anand Sardesai, and Alistair Pace and Nicholas C.M. Armitage. The material has been revised and updated by the current authors.

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 23, Early assessment and management of trauma, contains some material from ‘Early assessment and management of trauma’ by Dinesh Nathwani and Joseph Windley. The material has been revised and updated by the current authors.

Chapter 7, Basic surgical skills and anastomoses, contains some material from ‘Basic surgical skills and anastomoses’ by David J. Leaper and William E.G. Thomas. The mater­ial has been revised and updated by the current author.

Chapter 24, Traumatic brain 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 9, 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 25, Neck and spine, contains some material from ‘Neck and spine’ by Ashley Poynton. The material has been revised and updated by the current authors.

Chapter 12, 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 14, Diagnostic imaging, contains some material from ‘Diagnostic imaging’ by the current authors and Gina Allen, which has been revised and updated for this edition. Chapter 17, Preoperative care including the high-risk surgical patient, contains some material from ‘Pre operative

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Chapter 26, Maxillofacial trauma, contains some material from ‘Maxillofacial trauma’ by Charles Perkins. The material has been revised and updated by the current author. Chapter 28, Extremity trauma, contains some material from ‘Extremity trauma’ by Parminder Singh. The material has been revised and updated by the current author. Chapter 31, History taking and clinical examination in musculoskeletal disease, contains some material from ‘History taking and clinical examination in musculoskeletal disease’ by

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Acknowledgements

Parminder Singh and current author Hemant G. Pandit. The material has been revised and updated by the current authors. Chapter 32, 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 authors. Chapter 33, The spine, contains some material from ‘The spine’ by the current authors and Gavin Bowden, which has been revised and updated for this edition. Chapter 34, Upper limb, contains some material from ‘Upper limb – pathology, assessment and management’ by Vinay Takwale, Irfan Khan and Srinath Kamineni. The material has been revised and updated by the current authors. Chapter 35, Hip and knee, contains some material from ‘Hip and knee’ by Hermant G. Pandit, Andrew Bernett, current author Vikas Khanduja and Richard N. Villar. The material has been revised and updated by the current authors. Chapter 36, 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 38, Infection of the bones and joints, contains some material from ‘Infection of the bones and joints’ by the current authors and Philip Bejon, which has been revised and updated for this edition. Chapter 39, Paediatric orthopaedics, contains some material from ‘Paediatric orthopaedics’ by the current author and Joanna Hicks, which has been revised and updated for this edition. Chapter 43, Cranial 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 Colm O’Brien, Hugo Henderson and Jonathan Jagger. The material has been revised and updated by the current author. Chapter 45, Cleft lip and palate: developmental abnormalities of the face, mouth and jaws, contains some material from ‘Cleft lip and palate: developmental abnormalities of the face, mouth and jaws’ by William P. Smith. The material has been revised and updated by the current author. Chapter 46, The ear, nose and sinuses, contains some material from ‘The nose and sinuses’ by Robert W. Ruckley and current author Iain J. Nixon, and ‘The ear’ by Grant

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Bates. The material has been revised and updated by the current authors. Chapter 47, Pharynx, larynx and neck, contains some material from ‘Pharynx, larynx and neck’ by Rishi Sharma, Martin Birchall, Jonathan D. Jagger and Hugo W.A. Henderson. The material has been revised and updated by the current author. Chapter 48, Oral cavity malignancy, contains some material from ‘Oropharyngeal cancer’ by William P. Smith. The material has been revised and updated by the current author. Chapter 49, Disorders of the salivary glands, contains some material from ‘Disorders of the salivary glands’, by William P. Smith. The material has been revised and updated by the current authors. Chapter 50, The thyroid glands, contains some material from ‘The thyroid and parathyroid glands’ by Zygmunt H. Krukowski. The material has been revised and updated by the current author. Chapter 51, The parathyroid glands, contains some material from ‘The thyroid and parathyroid glands’ by Zygmunt H. Krukowski. 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 current author 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 Peter McCollum, current author Ian Chetter and Kevin Burnand. The material has been revised and updated by the current authors. Chapter 58, Lymphatic disorders, contains some material from ‘Lymphatic disorders’ by current author Shervanthi Homer-Vanniasinkam and Andrew Bradbury. The material has been revised and updated by the current authors.

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Acknowledgements

Chapter 59, History and examination of the abdomen, contains some material from ‘History and examination of the abdomen’, by Mohan de Silva, V. Sitaram and Simon Paterson-Brown. The material has been revised and updated by the current author. 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 64, Bariatric and metabolic surgery, contains some material from ‘Bariatric surgery’ by John Baxter. The material has been revised and updated by the current author.

Chapter 72, The vermiform appendix, contains some material from ‘The vermiform appendix’ by P. Ronan O’Connell. The material has been revised and updated by the current author. Chapter 73, The rectum, contains some material from ‘The rectum’ by Sue Clark. The material has been revised and updated by the current author. Chapter 74, The anus and anal canal, contains some material from ‘The anus and anal canal’ by the current author and Peter Lunniss, which has been revised and updated for this edition. Chapter 76, The kidneys and ureters, contains some material from ‘The kidneys and ureters’ by Christopher G. Fowler. The material has been revised and updated by the current author. Chapter 77, 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 65, The liver, contains some material from ‘The liver’ by Rahul S. Koti, Sanjeev Kanoria and Brian R. Davidson. The material has been revised and updated by the current authors.

Chapter 79, 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 69, The small intestine, contains some material from ‘The small and large intestines’ by current author Gordon Carlson, Jonathan Epstein, Neil J. McC. Mortensen and Shazad Ashraf. The material has been revised and updated by the current authors.

Chapter 80, 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.

Chapter 70, The large intestine, 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 71, Intestinal obstruction, contains some material from ‘Intestinal obstruction’ by Marc Christopher Winslet. The material has been revised and updated by the current author.

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Chapter 81, Gynaecology, contains some material from ‘Gynaecology’ by Stephen Kennedy and Enda McVeigh. The material has been revised and updated by the current author. We acknowledge advice, beyond their chapter contribution, from Anand Sardesai in relation to anaesthetics, and Lee Van Rensburg, in relation to trauma.

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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. John 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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Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love PART Bailey & Love Bailey & Love Bailey & Love

1

Basic principles

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Metabolic response to injury...................................................................... 2

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Shock and blood transfusion...................................................................12

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Wounds, healing and tissue repair.........................................................24

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Tissue engineering and regeneration...................................................33

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Surgical infection..........................................................................................42

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Tropical infections and infestations.......................................................57

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Basic surgical skills and anastomoses..................................................84

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Principles of laparoscopic and robotic surgery.............................. 105

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Principles of paediatric surgery............................................................ 119

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Principles of oncology.............................................................................. 139

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Surgical audit and research................................................................... 161

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Surgical ethics and law............................................................................ 170

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Human factors, patient safety and quality improvement............ 176

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Bailey & Love Bailey & Love Bailey & Love Bailey & 1Love Bailey & Love Bailey & Love Chapter

Metabolic response to injury Learning objectives • Changes in body composition that accompany • Avoidable factors that compound the metabolic

To understand:

• Classical concepts of homeostasis • Mediators of the metabolic response to injury • Physiological and biochemical changes that occur

response to injury

surgical injury

In the eighteenth and nineteenth centuries, a series of eminent scientists laid the foundations of our understand­ ing 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 con­ dition for freedom and independence of existence’ (Claude Bernard); i.e. body systems act to maintain internal con­ stancy. ‘Homeostasis: the coordinated physiological process which maintains most of the steady states of the organ­ ism’(Walter Cannon); i.e. complex homeostatic responses involving the brain, nerves, heart, lungs, kidneys and spleen work to maintain body constancy. ‘There is a circumstance 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.

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

­

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 nor­ mal 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 detec­ tor–processor–effector regulated by a negative feedback loop) and more of the ‘open loop’ system, whereby only with med­ ical/surgical resolution of the primary abnormality is a return to classical homeostasis possible. As a consequence of modern understanding of the meta­ bolic 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 pres­ ence of tissue trauma/sepsis/hypovolaemia often compounds the primary problem, there is a requirement to augment arti­ ficially 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 pro­ vide organ support (critical care) while the patient comes back to a situation in which homeostasis can achieve a return to normality. -

BASIC CONCEPTS IN HOMEOSTASIS

• Concepts behind optimal perioperative care •

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. 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.

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PART 1 | BASIC PRINCIPLES Mediators of the metabolic response to injury

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 ‘stressfree’ perioperative and critical care.

THE GRADED NATURE OF THE INJURY RESPONSE 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, respira­ tory 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 circumstances, 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

3

sequelae of major injury evolve from a proinflammatory state driven primarily by the innate immune system (macro­ phages, ­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.

MEDIATORS OF THE METABOLIC RESPONSE TO INJURY The classical neuroendocrine pathways of the stress response consist of afferent nociceptive neurones, the spinal cord, thal­ amus, hypothalamus and pituitary (Figure 1.2). Corticotro­ phin-releasing factor (CRF) released from the hypothalamus increases adrenocorticotrophic hormone (ACTH) release from the anterior pituitary. ACTH then acts on the adrenals to increase the secretion of cortisol. Hypothalamic activation of the sympathetic nervous system causes release of adrenaline and also stimulates release of glucagon. Intravenous infusion of a cocktail 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 sensi­ tivity, 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.

Resting metabolic rate (%)

140 Major trauma

130

Summary box 1.2

Minor trauma

120

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

110 Normal range

100 90

●●

Starvation

80

●●

25 Nitrogen excretion (g N/day)

ve ve

20

10

20

30

40

50

60

70

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.

01_01B-B&L27_Pt1_Ch01.indd 3

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

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. Pro­ inflammatory cytokines also play a complex role in the development of peripheral insulin resistance. Other import­ ant proinflammatory mediators include nitric oxide ([NO]

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CHAPTER 1  Metabolic response to injury

Hypothalamus

PLASMA

CRF

CHANGES IN BODY METABOLISM

Pituitary ACTH

Spinal cord

GH

ADRENALINE CORTISOL

Adrenal

Sympathetic nervous system

Pancreas

IL-1 TNFα IL-6 IL-8

Injury

Adaptive immune system

HEPATIC GLUCONEOGENESIS

SKELETAL MUSCLE PROTEIN DEGRADATION GLUCAGON

Afferent noiciceptive pathways

ADIPOCYTE LIPOLYSIS

Innate immune system

INSULIN IGF-1 TESTOSTERONE T3

HEPATIC ACUTE PHASE PROTEIN SYNTHESIS

PYREXIA

HYPERMETABOLISM

Figure 1.2 The integrated 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. Bailey and Love fig. 1.02

via inducible nitric oxide synthetase [iNOS]) and a variety of prostanoids (via cyclooxygenase-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 circula­ tion (e.g. interleukin-1 receptor antagonist [IL-1Ra] and TNF-­soluble receptors [TNF-sR-55 and 75]) and act to con­ trol the proinflammatory response. A complex further series of adaptive 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 character­ ised as the CARS and results in immunosuppression and an increased susceptibility to opportunistic (nosocomial) infec­ tion. 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 proresolving 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 enhancing 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 inflamma­ tion driven dyshomeostasis.

01_01B-B&L27_Pt1_Ch01.indd 4

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

There are many complex interactions among the neu­ roendocrine, 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 proinflam­ matory cytokines and the noradrenergic system. The resulting rise in cortisol levels may form a weak feedback loop attempt­ ing to limit the proinflammatory stress response. Finally, hyperglycaemia may aggravate the inflammatory response via substrate overflow in the mitochondria, causing the for­ mation of excess oxygen free 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

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PART 1 | BASIC PRINCIPLES The metabolic stress response to surgery and trauma: the ‘ebb and flow’ model

with over half showing decreased expression and the remain­ der 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

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. ●● ●●

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 attenu­ ated by proper resuscitation, but not completely abolished. The ebb phase is characterised by hypovolaemia, decreased Injury

Ebb phase

Flow phase

Recovery

Hours

Days

Weeks

Shock

Catabolism

Anabolism

basal ­metabolic rate, reduced cardiac output, hypothermia and ­lactic acidosis. The predominant hormones regulating the ebb phase 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 hyper­ metabolic 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

Atrophy

Hypertrophy IGF-1

TNF

Myostatin

CELL MEMBRANE

PI3K Akt

Injury

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

In the natural world, if an animal is injured, it displays a char­ acteristic response, which includes immobility, anorexia and catabolism.

5

NFB

mTOR FOXO

MyoD

p70S6K 4E-BP-1 Protein synthesis

NUCLEUS

E3 ligases

Protein degradation

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.

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

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CHAPTER 1  Metabolic response to injury

(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 insu­ lin at this time is associated with significant insulin resistance and, therefore, injured patients often exhibit poor glycaemic control. The combination of pronounced or prolonged catab­ olism in association with insulin resistance places patients within this phase at increased risk of complications. Obviously, the development of complications will further aggravate the neuroendocrine and inflammatory stress responses, thus creat­ ing a vicious catabolic cycle. Summary box 1.5 Purpose of neuroendocrine changes following injury The constellation of neuroendocrine changes following injury actsto: 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. ●● ●●

imately 15–25% 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 lev­ els following surgery or trauma, but several features of stan­ dard intensive care (including bed rest, paralysis, ventilation and external temperature regulation) counteract the hyper­ metabolic driving forces of the stress response. Furthermore, the skeletal muscle wasting experienced by patients with pro­ longed catabolism actually limits the volume of metabolically active tissue (see below). Summary box 1.6 Hypermetabolism Hypermetabolism following injury:

KEY CATABOLIC ELEMENTS OF THE FLOW PHASE OF THE METABOLIC STRESS RESPONSE There are several key elements of the flow phase that largely determine the extent of catabolism and thus govern the meta­ bolic 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).

Hypermetabolism The majority of trauma patients (except possibly those with extensive burns) demonstrate energy expenditures approx­ Peripheral tissues

●●

●●

Alterations in skeletal muscle protein metabolism Muscle protein is continually synthesised and broken down with a turnover rate in humans of 1–2% per day, and with a greater amplitude of changes in protein synthesis (± twofold) than breakdown (± 0.25-fold) during the diurnal cycle. Under normal circumstances, synthesis equals break­ down 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

Central tissues Liver

Muscle Amino acids Adipose tissue

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

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 wounds. One of the main reasons why the reutilisation of amino acids derived from muscle proteo­ lysis 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.

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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PART 1 | BASIC PRINCIPLES Key catabolic elements of the flow phase of the metabolic stress response

protein synthesis is depressed, but it increases again during rest and feeding. During the catabolic phase of the stress response, mus­ cle wasting occurs as a result of an increase in muscle pro­ tein 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 14–20g/day; this is equivalent to the loss of 500g of skeletal muscle per day. It is remarkable that muscle catabolism cannot be inhib­ ited 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 met­ abolic stress in itself, and that nutritional support should be at a modest level to attenuate rather than replace energy and protein losses. 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 mor­ bidity 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.

7

Summary box 1.7 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% of daily body protein turnover. Skeletal muscle has a large mass but a low turnover rate (1–2% per day), whereas the liver has a relatively small mass (1.5 kg) but a much higher protein turnover rate (10–20% per day). Hepatic protein s­ynthesis is divided roughly 50:50 between renewal of structural proteins and synthesis of export proteins. Albu­ min is the major export protein produced by the liver and is renewed at the rate of about 10% per day. The transcapillary escape rate (TER) of albumin is about ten times the rate of synthesis, and short-term 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 sur­ gery, trauma, sepsis, cancer or autoimmune conditions, circu­ lating peripheral blood mononuclear cells secrete a range of proinflammatory cytokines, including IL-1, IL-6 and TNFα.

Myofibrillar protein

Caspases, cathepsins and calpains Ubiquitinated protein Amino acids

E1, E2, E3 ATP 19S

Tripeptidyl peptidase Ubiquitin

26S proteasome ATP

Oligopeptides

ATP

20S 19S

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 01_01B-B&L27_Pt1_Ch01.indd 7

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PART 1 | BASIC PRINCIPLES 8

CHAPTER 1  Metabolic response to injury

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 sur­ gical 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 ing a reduced hepatic synthesis rate, the fall in plasma concentration of negative acute phase reactants is thought principally to reflect increased transcapillary escape, sec­ ondary 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.

CHANGES IN BODY COMPOSITION FOLLOWING INJURY The average 70-kg male can be considered to consist of fat (13kg) and fat-free mass (or lean body mass: 57kg). In such an individual, the lean tissue is composed primarily of protein (12kg), water (42kg) and minerals (3kg) (Figure 1.7). The protein mass can be considered as two basic com­ partments, skeletal muscle (4kg) and non-skeletal muscle (8kg), which includes the visceral protein mass. The water mass (42 litres) is divided into intracellular (28 litres) and extracellular (14 litres) spaces. Most of the mineral mass is contained in the bony skeleton. 70 60

Summary box 1.8

50

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

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

Protein

40 30

Intracellular water

20

Insulin resistance Following surgery or trauma, postoperative hyperglycaemia develops as a result of increased glucose production com­ bined 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 proin­ flammatory 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 sur­ gery, insulin resistance may persist for approximately 2 weeks. Postoperative patients with insulin resistance behave in a similar manner to individuals with type II diabetes melli­ tus. 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 manipu­ lated to normalise the blood glucose level) or a conservative approach (i.e. insulin is administered when the blood glu­ cose level exceeds a defined limit and discontinued when the level falls). While some 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, others have not. The risks of adverse events follow­ ing significant hypoglycaemia as a consequence of intensive insulin therapy have led most ICUs to adopt a more conven­ tional approach to glycaemic control. It should be noted that diabetic patients whose glycaemic control has been poor prior to their critical illness pose a particular challenge.

01_01B-B&L27_Pt1_Ch01.indd 8

10

FFM or LBM

●●

Mass (kg)

Hepatic acute phase response

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.

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 also in depletion of visceral protein ­ status. Within lean issue, each 1g of nitrogen is contained within 6.25 g of protein, which is contained in approxi­ mately 36 g of wet weight tissue. Thus, the loss of 1 g of nitrogen in urine is equivalent to the breakdown of 36g of wet weight lean tissue. Protein turnover in the whole body is of the order of 150–200g per day. A normal human ingests about 70–100g protein per day, which is metabolised and excreted in urine as ammonia and urea (i.e. approximately 14g 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 adap­ tive change fails to occur, and there is a state of ‘autocan­ nibalism’, resulting in continuing urinary nitrogen losses of 10–20g N/day (equivalent to 500g of wet weight lean tissue

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PART 1 | BASIC PRINCIPLES Avoidable factors that compound the response to injury

9

Weight gain (%)

16 14 12 10 8

Sepsis and multiorgan failure

6 4

Weight loss (%)

2 2 4 6 8

2 4

6

10 12 14 16

8

10 12 14 16 18 20 22

days

Uncomplicated major surgery

per day). As with total starvation, once loss of body protein mass has reached 30–40% 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 extra­ cellular water by 6–10 litres within 24 hours. Thereafter, even with optimal metabolic care and nutritional support, total body protein will diminish by 15% in the next 10days, 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 equilib­ rium following major elective surgery. This can be achieved by blocking the neuroendocrine stress response with epidural analgesia/other related techniques and providing early oral/ 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 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 As noted previously, the main features of the metabolic response are initiated by the immune system, cardiovascu­ lar system, sympathetic nervous system, ascending reticular formation and limbic system. However, the metabolic stress

01_01B-B&L27_Pt1_Ch01.indd 9

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

Starvation

response may be further exacerbated by anaesthesia, dehy­ dration, 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 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 left atrium, initiate afferent nerve input to the central nervous system (CNS), resulting in the release of both aldo­ sterone 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 aldo­ sterone 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 extra­ cellular 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. i n t h e stomach). Such visceral oedema has been associated with reduced ­gastric emptying, delayed resumption of food intake and prolonged hospital

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PART 1 | BASIC PRINCIPLES 10

CHAPTER 1  Metabolic response to injury

Immobilisation

Adreno-sympathetic activation Wound Hypothermia Hypotension Pain

Pyrexia Acute phase response Insulin resistance

Cytokine cascade release

Futile substrate cycling Muscle protein degradation

Starvation

C a t a b o l i s m

A n a b o l i s m

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

stay. Careful limitation of intraoperative administration of balanced crystalloids so that there is no net weight gain following elective surgery has been proven to reduce post­ operative complications and length of stay.

Hypothermia Hypothermia results in increased elaboration of adrenal steroids and catecholamines. When compared with normo­ thermic 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 heat­ ing cover reduces wound infections, cardiac complications and bleeding and transfusion requirements.

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

Systemic inflammation and tissue underperfusion The vascular endothelium controls vasomotor tone and microvascular flow, and regulates trafficking of nutrients

01_01B-B&L27_Pt1_Ch01.indd 10

and biologically active molecules. When endothelial acti­ vation 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.

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 cere­ bral energy metabolism. Provision of 2 litres of intrave­ nous 4% dextrose/0.18% sodium chloride as maintenance intravenous fluids for surgical patients who are fasted pro­ vides 80 g of glucose per day and has a significant pro­ tein-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 anaesthe­ sia allow intake of clear fluids up to 2 hours before sur­ gery. Administration of a carbohydrate drink at this time reduces perioperative anxiety and thirst and decreases postoperative insulin ­resistance.

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PART 1 | BASIC PRINCIPLES Further reading

Immobility Immobility has long been recognised as a potent stimulus for inducing muscle wasting. Inactivity impairs the normal meal-derived 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 ENHANCED RECOVERY AFTER SURGERY

Functional capacity

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 sci­ entific 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 sur­ gical practice that can reduce the magnitude of surgical injury and enhance the rate of patients’ return to homeostasis and recovery. It is also important to realise that modulating the stress/inflammatory response at the time of surgery may have long-term sequelae over periods of months or longer. For example, β-blockers and statins have been shown to improve long-term survival after major surgery. It has been suggested that these effects may be due to suppression of innate immu­ nity at the time of surgery. Equally, in ‘open’ surgery the use of epidural analgesia to reduce pain, block the cortisol stress response and attenuate postoperative insulin resistance may, via effects on the body’s protein economy, favourably affect many of the patient-centred outcomes that are important to postoperative recovery. Due to the reduction in wound size and tissue trauma, it should be noted that epidural analgesia

Surgery

Multimodal ERAS intervention

Traditional care Days

Weeks

Figure 1.10 Enhanced recovery after surgery (ERAS) programmes can be modulated by multimodal enhanced recovery programmes (optimal nutritional and metabolic care to minimise the stress response).

01_01B-B&L27_Pt1_Ch01.indd 11

11

is no longer recommended for laparoscopic surgery. Patient controlled analgesia is usually sufficient. Adjuncts such as ‘one shot’ spinal diamorphine and/or a 6–12-hour infusion of intra­ venous lidocaine have been suggested to be opiate sparing, to improve gut function and enhance overall recovery. Summary box 1.11 A proactive approach to prevent unnecessary aspects of the surgical stress response ●● ●●

●● ●●

Minimal access techniques Blockade of afferent painful stimuli (e.g. epidural analgesia, spinal analgesia, wound catheters) Minimal periods of starvation Early mobilisation

FURTHER READING Bessey PQ, Watters JM, Aoki TT, Wilmore DW. Combined hormonal infusion simulates the metabolic response to injury. Ann Surg 1984; 200: 264–81. Cuthbertson DP. The disturbance of metabolism produced by bone and non-bony injury, with notes on certain abnormal conditions of bone. Biochem J 1930; 24: 1244. Fearon KCH, Ljungqvist O, von Meyenfeldt M et al. Enhanced recovery after surgery: a consensus review of clinical care for patients under­ going colonic resection. Clin Nutr 2005; 24: 466–77. Finfer S, Chittock DR, Su SY et al., NICE-SUGAR Study Investiga­ tors. Intensive versus conventional glucose control in critically ill patients. N Engl J Med 2009; 360: 1283–97. Finfer S, Chittock DR, Su SY et al., NICE-SUGAR Study Investiga­ tors. Intensive versus conventional glucose control in critically ill patients with traumatic brain injury: long term follow-up in a sub­ group of patients from the NICE-SUGAR study. Intensive Care Med 2015; 41: 1037–47. Ljungqvist O. Insulin resistance and outcomes in surgery. J Clin Endocrinol Metab 2010; 95: 4217–19. Lobo DN, Bostock KA, Neal KR et al. Effect of salt and water balance on recovery of gastrointestinal function after elective colonic resection: a randomised controlled trial. Lancet 2002; 359: 1812–18. Moore FO. Metabolic care of the surgical patient. Philadelphia, PA: WB Saunders Company, 1959. Scott MJ, Baldini G, Fearon KC et al. Enhanced Recovery After Surgery (ERAS) for gastrointestinal surgery, part 1: pathophysiological con­ siderations. Acta Anaesthesiol Scand 2015; 59: 1212–31. Van den Berghe G, Wonters P, Weckers F et al. Intensive insulin therapy in the critically ill patient. N Engl J Med 2001; 345: 1359–67. Vanhorebeek O, Langounche L, Van den Berghe G. Endocrine aspects of acute and prolonged critical illness. Nat Clin Pract Endocrinol Metab 2006; 2: 20–31. Wilmore DW. From Cuthbertson to fast-track surgery: 70 years of prog­ ress in reducing stress in surgical patients. Ann Surg 2002; 236: 643–8.

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Bailey & Love Bailey & Love Bailey & Love Bailey &2Love Bailey & Love Bailey & Love Chapter

Shock and blood transfusion Learning objectives To understand: •• The pathophysiology of shock and ischaemia– reperfusion injury •• The different patterns of shock and the principles and priorities of resuscitation

INTRODUCTION Shock is the most common and therefore the most important cause of death of surgical patients. Death may occur rapidly due to a profound state of shock, or be delayed due to the consequences of organ ischaemia and reperfusion injury. It is important therefore that every surgeon understands the pathophysiology, diagnosis and priorities in management of shock and haemorrhage.

SHOCK Shock is a systemic state of low tissue perfusion that is inade­ quate for normal cellular respiration. With insufficient delivery of oxygen and glucose, cells switch from aerobic to anaerobic metabolism. If perfusion is not restored in a timely fashion, cell death ensues.

Pathophysiology Cellular As perfusion to the tissues is reduced, cells are deprived of oxy­ gen and must switch from aerobic to anaerobic meta­bolism. The product of anaerobic respiration is not carbon dioxide but lactic acid. When enough tissue is underperfused, the accumu­ lation of lactic acid in the blood produces a systemic metabolic acidosis. As glucose within cells is exhausted, anaerobic respira­ tion ceases and there is failure of sodium/potassium pumps in the cell membrane and intracellular organelles. Intracellular lysosomes release autodigestive enzymes and cell lysis ensues. Intracellular contents, including potassium, are released into the blood stream.

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•• Appropriate monitoring and end points of resuscitation •• Use of blood and blood products, the benefits and risks of blood transfusion

Microvascular As tissue ischaemia progresses, changes in the local milieu result in activation of the immune and coagulation systems. Hypoxia and acidosis activate complement and prime neu­ trophils, resulting in the generation of oxygen free radicals and cytokine release. These mechanisms lead to injury of the capillary endothelial cells. These, in turn, further activate the immune and coagulation systems. Damaged endothelium loses its integrity and becomes ‘leaky’. Spaces between endothelial cells allow fluid to leak out and tissue oedema ensues, exacer­ bating cellular hypoxia.

Systemic CARDIOVASCULAR As preload and afterload decrease, there is a compensatory baroreceptor response resulting in increased sympathetic activity and release of catecholamines into the circulation. This results in tachycardia and systemic vasoconstriction (except in sepsis – see below). RESPIRATORY The metabolic acidosis and increased sympathetic response result in an increased respiratory rate and minute ventilation to increase the excretion of carbon dioxide (and so produce a compensatory respiratory alkalosis). RENAL Decreased perfusion pressure in the kidney leads to reduced filtration at the glomerulus and a decreased urine output. The renin–angiotensin–aldosterone axis is stimulated, resulting in further vasoconstriction and increased sodium and water ­reabsorption by the kidney.

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PART 1 | BASIC PRINCIPLES Shock

ENDOCRINE As well as activation of the adrenal and renin–angiotensin systems, vasopressin (antidiuretic hormone) is released from the hypothalamus in response to decreased preload and results in vasoconstriction and resorption of water in the renal col­ lecting system. Cortisol is also released from the adrenal cortex, contributing to the sodium and water resorption and sensitising cells to catecholamines.

Ischaemia–reperfusion syndrome During the period of systemic hypoperfusion, cellular and organ damage progresses due to the direct effects of tissue hypoxia and local activation of inflammation. Further injury occurs once normal circulation is restored to these tissues. The acid and potassium load that has built up can lead to direct myocardial depression, vascular dilatation and further hypo­ tension. The cellular and humoral elements activated by the hypoxia (complement, neutrophils, microvascular thrombi) are flushed back into the circulation where they cause further endothelial injury to organs such as the lungs and the kidneys. This leads to acute lung injury, acute renal injury, multiple organ failure and death. Reperfusion injury can currently only be attenuated by reducing the extent and duration of tissue hypoperfusion.

Classification of shock There are numerous ways to classify shock, but the most com­ mon and most clinically applicable is one based on the initi­ ating mechanism. All states are characterised by systemic tissue hypoperfu­ sion, and different states may coexist within the same patient. Summary box 2.1 Classification of shock ●● ●● ●● ●● ●●

Hypovolaemic shock Cardiogenic shock Obstructive shock Distributive shock Endocrine shock

13

Cardiogenic shock Cardiogenic shock is due to primary failure of the heart to pump blood to the tissues. Causes of cardiogenic shock include ­myocardial infarction, cardiac dysrhythmias, valvular heart disease, blunt myocardial injury and cardiomyopathy. Cardiac insufficiency may also be due to myocardial depression caused by endogenous factors (e.g. bacterial and humoral agents released in sepsis) or exogenous factors, such as pharmaceutical agents or drug abuse. Evidence of venous hypertension with pulmonary or systemic oedema may coexist with the classical signs of shock.

Obstructive shock In obstructive shock there is a reduction in preload due to mechanical obstruction of cardiac filling. Common causes of obstructive shock include cardiac tamponade, tension ­pneumothorax, massive pulmonary embolus or air embolus. In each case, there is reduced filling of the left and/or right sides of the heart leading to reduced preload and a fall in ­cardiac output.

Distributive shock Distributive shock describes the pattern of cardiovascular responses characterising a variety of conditions, including septic shock, anaphylaxis and spinal cord injury. Inadequate organ perfusion is accompanied by vascular dilatation with hypotension, low systemic vascular resistance, inadequate afterload and a resulting abnormally high cardiac output. In anaphylaxis, vasodilatation is due to histamine release, while in high spinal cord injury there is failure of sympathetic outflow and adequate vascular tone (neurogenic shock). The cause in sepsis is less clear but is related to the release of ­bacterial products (endotoxin) and the activation of cellu­ lar and humoral components of the immune system. There is maldistribution of blood flow at a microvascular level with arteriovenous shunting and dysfunction of cellular utilization of oxygen. In the later phases of septic shock there is hypovolaemia from fluid loss into interstitial spaces and there may be con­ comitant myocardial depression, complicating the clinical picture (Table 2.1).

Endocrine shock Hypovolaemic shock Hypovolaemic shock is due to a reduced circulating volume. Hypovolaemia may be due to haemorrhagic or non-haemor­ rhagic causes. Non-haemorrhagic causes include poor fluid intake (dehydration), excessive fluid loss due to vomiting, diar­ rhoea, urinary loss (e.g. diabetes), evaporation, or ‘third-spacing’ where fluid is lost into the gastrointestinal tract and interstitial spaces, as for example in bowel obstruction or pancreatitis. Hypovolaemia is probably the most common form of shock, and to some degree is a component of all other forms of shock. Absolute or relative hypovolaemia must be excluded or treated in the management of the shocked state, regardless of cause.

Endocrine shock may present as a combination of hypovolae­ mic, cardiogenic or distributive shock. Causes of endocrine shock include hypo- and hyperthyroidism and adrenal insuf­ ficiency. Hypothyroidism causes a shock state similar to that of neurogenic shock due to disordered vascular and cardiac responsiveness to circulating catecholamines. Cardiac output falls due to low inotropy and bradycardia. There may also be an associated cardiomyopathy. Thyrotoxicosis may cause a high-output cardiac failure. Adrenal insufficiency leads to shock due to hypovolaemia and a poor response to circulating and exogenous catecho­ lamines. Adrenal insufficiency may be due to pre-existing ­Addison’s disease or be a relative insufficiency due to a patho­ logical disease state, such as systemic sepsis.

Thomas Addison, 1799–1860, physician, Guy’s Hospital, London, UK, described the effects of disease of the suprarenal capsules in 1849. 

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CHAPTER 2  Shock and blood transfusion

TABLE 2.1  Cardiovascular and metabolic characteristics of shock. Hypovolaemia

Cardiogenic

Obstructive

Distributive

Cardiac output Vascular resistance

Low High

Low High

Low High

High Low

Venous pressure

Low

High

High

Low

Mixed venous saturation Base deficit

Low High

Low High

Low High

High High

Severity of shock

Moderate shock

Compensated shock As shock progresses, the body’s cardiovascular and endocrine compensatory responses reduce flow to non-essential organs to preserve preload and flow to the lungs and brain. In com­ pensated shock, there is adequate compensation to maintain central blood volume and preserve flow to the kidneys, lungs and brain. Apart from a tachycardia and cool peripheries (vasoconstriction, circulating catecholamines), there may be no other clinical signs of hypovolaemia. However, this cardiovascular state is only maintained by reducing perfusion to the skin, muscle and gastroin­ testinal tract. There is a systemic metabolic acidosis and activation ofhumoral and cellular elements within the under­ perfused organs. Although clinically occult, this state will lead to m ­ ultiple organ failure and death if prolonged, due to the ischaemia–reperfusion effect described above under Ischaemia–reperfusion syndrome. Patients with occult hypo­ perfusion (metabolic acidosis despite normal urine output and cardiorespiratory vital signs) for more than 12hours have a significantly higher mortality, infection rate and incidence of multiple organ failure (see below, Multiple organ failure).

Decompensation Further loss of circulating volume overloads the body’s com­ pensatory mechanisms and there is progressive renal, respira­ tory and cardiovascular decompensation. In general, loss of around 15% of the circulating blood volume is within n ­ ormal compensatory mechanisms. Blood pressure is usually well maintained and only falls after 30–40% of circulating volume has been lost.

Mild shock Initially there is tachycardia, tachypnoea, a mild reduction in urine output and the patient may exhibit mild anxiety. Blood pressure is maintained although there is a decrease in pulse pressure. The peripheries are cool and sweaty with prolonged capillary refill times (except in septic distributive shock).

As shock progresses, renal compensatory mechanisms fail, renal perfusion falls and urine output dips below 0.5 mL/kg per hour. There is further tachycardia, and now the blood pressure starts to fall. Patients become drowsy and mildly confused.

Severe shock In severe shock, there is profound tachycardia and hypoten­ sion. Urine output falls to zero and patients are unconscious with laboured respiration.

Pitfalls The classic cardiovascular responses described (Table 2.2) are not seen in every patient. It is important to recognise the limit­ations of the clinical examination and to recognise patients who are in shock despite the absence of classic signs. CAPILLARY REFILL Most patients in hypovolaemic shock will have cool, pale peripheries, with prolonged capillary refill times. However, the actual capillary refill time varies so much in adults that it is not a specific marker of whether a patient is shocked, and patients with short capillary refill times may be in the early stages of shock. In distributive (septic) shock, the periph­ eries will be warm and capillary refill will be brisk, despite profound shock. TACHYCARDIA Tachycardia may not always accompany shock. Patients who are on beta-blockers or who have implanted pacemakers are unable to mount a tachycardia. A pulse rate of 80 in a fit young adult who normally has a pulse rate of 50 is very abnor­ mal. Furthermore, in some young patients with penetrating trauma, where there is haemorrhage but little tissue damage, there may be a paradoxical bradycardia rather than tachycar­ dia accompanying the shocked state.

TABLE 2.2  Clinical features of shock. Lactic acidosis Urine output Conscious level Respiratory rate Pulse rate Blood pressure

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Compensated

Mild

Moderate

Severe

+ Normal Normal Normal Mild increase Normal

++ Normal Mild anxiety Increased Increased Normal

++ Reduced Drowsy Increased Increased Mild hypotension

+++ Anuric Comatose Laboured Increased Severe hypotension

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PART 1 | BASIC PRINCIPLES Resuscitation

BLOOD PRESSURE It is important to recognise that hypotension is one of the last signs of shock. Children and fit young adults are able to main­ tain blood pressure until the final stages of shock by dramatic increases in stroke volume and peripheral vasoconstriction. These patients can be in profound shock with a normal blood pressure. Elderly patients who are normally hypertensive may ­present with a ‘normal’ blood pressure for the general popu­ lation but be hypovolaemic and hypotensive relative to their usual blood pressure. Beta-blockers or other medications may prevent a tachycardic response. The diagnosis of shock may be difficult unless one is alert to these pitfalls.

Consequences Unresuscitatable shock Patients who are in profound shock for a prolonged period of time become ‘unresuscitatable’. Cell death follows from ­cellular ischaemia and the ability of the body to compensate is lost. There is myocardial depression and loss of responsive­ ness to fluid or inotropic therapy. Peripherally there is loss of the ability to maintain systemic vascular resistance and fur­ ther hypotension ensues. The peripheries no longer respond appropriately to vasopressor agents. Death is the inevitable result. This stage of shock is the combined result of the severity of the insult and delayed, inadequate or inappropriate resuscita­ tion in the earlier stages of shock. Conversely, when patients present in this late stage, and have minimal responses to ­maximal therapy, it is important that the futility of treatment is recognised and valuable resources are not wasted.

Multiple organ failure As techniques of resuscitation have improved, more and more patients are surviving shock. Where intervention is timely and the period of shock is limited, patients may make a rapid, uncomplicated recovery. However the result of pro­ longed ­systemic ischaemia and reperfusion injury is end-organ ­damage and multiple organ failure. Multiple organ failure is defined as two or more failed organ systems. There is no specific treatment for multiple organ fail­ ure. Management is supporting of organ systems, with ventila­ tion, cardiovascular support and haemofiltration/dialysis until there is recovery of organ function. Multiple organ failure cur­ rently carries a mortality of 60%; thus, prevention is vital by early aggressive identification and reversal of shock.

Summary box 2.2 Effects of organ failure ●● ●● ●● ●●

Lung: Acute respiratory distress syndrome Kidney: Acute renal insufficiency Clotting: Coagulopathy Cardiac: Cardiovascular failure

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RESUSCITATION Immediate resuscitation manoeuvres for patients presenting in shock are to ensure a patent airway and adequate oxy­ genation and ventilation. Once ‘airway’ and ‘breathing’ are assessed and controlled, attention is directed to cardiovascular resuscitation.

Conduct of resuscitation Resuscitation should not be delayed in order to definitively diagnose the source of the shocked state. However, the tim­ ing and nature of resuscitation will depend on the type of shock and the timing and severity of the insult. Rapid clinical ­examination will provide adequate clues to make an appropri­ ate first determination, even if a source of bleeding or sepsis is not immediately identifiable. If there is initial doubt about the cause of shock, it is safer to assume the cause is hypo­ volaemia and begin with fluid resuscitation, and then assess the response. In patients who are actively bleeding (major trauma, aortic aneurysm rupture, gastrointestinal haemorrhage), it is counter­ productive to institute high-volume fluid therapy without controlling the site of haemorrhage. Increasing blood pressure merely increases bleeding from the site while fluid therapy cools the patient and dilutes available coagulation factors. Thus ­operative haemorrhage control should not be delayed and resuscitation should proceed in parallel with ­surgery. Conversely, a patient with bowel obstruction and hypo­ volaemic shock must be adequately resuscitated before under­ going surgery otherwise the additional surgical injury and hypovolaemia induced during the procedure will exacerbate the inflammatory activation and increase the incidence and severity of end-organ insult.

Fluid therapy In all cases of shock, regardless of classification, hypovolaemia and inadequate preload must be addressed before other ther­ apy is instituted. Administration of inotropic or chronotropic agents to an empty heart will rapidly and permanently deplete the myocardium of oxygen stores and dramatically reduce dia­ stolic filling and therefore coronary perfusion. Patients will enter the unresuscitatable stage of shock as the myocardium becomes progressively more ischaemic and unresponsive to resuscitative attempts. First-line therapy, therefore, is intravenous access and administration of intravenous fluids. Access should be through short, wide-bore catheters that allow rapid infusion of fluids as necessary. Long, narrow lines, such as central venous catheters, have too high a resistance to allow rapid infusion and are more appropriate for monitoring than fluid replacement therapy.

Type of fluids There is continuing debate over which resuscitation fluid is best for the management of shock. There is no ideal resusci­ tation fluid, and it is more important to understand how and when to administer it. In most studies of shock resuscitation

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CHAPTER 2  Shock and blood transfusion

there is no overt difference in response or outcome between crystalloid solutions (normal saline, Hartmann’s solution, Ringer’s lactate) or colloids (albumin or commercially avail­ able products). Furthermore, there is less volume benefit to the administration of colloids than had previously been thought, with only 1.3 times more crystalloid than colloid administered in blinded trials. On balance, there is little evidence to sup­ port the administration of colloids, which are more expensive and have worse side-effect profiles. Most importantly, the oxygen carrying capacity of crys­ talloids and colloids is zero. If blood is being lost, the ideal replacement fluid is blood, although crystalloid therapy may be required while awaiting blood products. Hypotonic solutions (dextrose etc.) are poor volume expanders and should not be used in the treatment of shock unless the deficit is free water loss (e.g. diabetes insipidus) or patients are sodium overloaded (e.g. cirrhosis).

Dynamic fluid response The shock status can be determined dynamically by the car­ diovascular response to the rapid administration of a fluid bolus. In total, 250–500 mL of fluid is rapidly given (over 5–10 minutes) and the cardiovascular responses in terms of heart rate, blood pressure and central venous pressure are observed. Patients can be divided into ‘responders’, ‘transient respond­ ers’ and ‘non-responders’. Responders have an improvement in their cardiovascular status that is sustained. These patients are not actively losing fluid but require filling to a normal volume status. Transient responders have an improvement, but this then reverts to the previous state over the next 10–20 min­ utes. These patients have moderate ongoing fluid losses (either overt ­haemorrhage or further fluid shifts reducing intravascular ­volume). Non-responders are severely volume depleted and are likely to have major ongoing loss of intravascular volume, usually through persistent uncontrolled haemorrhage.

Vasopressor and inotropic support Vasopressor or inotropic therapy is not indicated as first-line therapy in hypovolaemia. As discussed above, administration of these agents in the absence of adequate preload rapidly leads to decreased coronary perfusion and depletion of myo­ cardial oxygen reserves. Vasopressor agents (phenylephrine, noradrenaline) are indicated in distributive shock states (sepsis, neurogenic shock) where there is peripheral vasodilatation, and a low systemic vascular resistance, leading to hypotension despite a high cardiac output. Where the vasodilatation is resistant to catecholamines (e.g. absolute or relative steroid deficiency) vasopressin may be used as an alternative vasopressor. In cardiogenic shock, or where myocardial depression has complicated a shock state (e.g. severe septic shock with low cardiac output), inotropic therapy may be required to increase

cardiac output and therefore oxygen delivery. The inodilator dobutamine is the agent of choice.

Monitoring The minimum standard for monitoring of the patient in shock is continuous heart rate and oxygen saturation monitoring, ­frequent non-invasive blood pressure monitoring and hourly urine output measurements. Most patients will need more aggressive invasive monitoring, including central venous pres­ sure and invasive blood pressure monitoring. Summary box 2.3 Monitoring for patients in shock Minimum ●● ●● ●● ●●

ECG Pulse oximetry Blood pressure Urine output

Additional modalities ●● ●● ●● ●●

Central venous pressure Invasive blood pressure Cardiac output Base deficit and serum lactate

Cardiovascular Cardiovascular monitoring at minimum should include con­ tinuous heart rate (ECG), oxygen saturation and pulse wave­ form and non-invasive blood pressure. Patients whose state of shock is not rapidly corrected with a small amount of fluid should have central venous pressure monitoring and con­ tinuous blood pressure monitoring through an arterial line. CENTRAL VENOUS PRESSURE There is no ‘normal’ central venous pressure (CVP) for a shocked patient, and reliance cannot be placed on an indi­ vidual pressure measurement to assess volume status. Some patients may require a CVP of 5 cmH2O, whereas some may require a CVP of 15 cmH2O or higher. Further, ventricular compliance can change from minute to minute in the shocked state, and CVP is a poor reflection of end diastolic volume (preload). CVP measurements should be assessed dynamically as response to a fluid challenge (see above). A fluid bolus (250– 500 mL) is infused rapidly over 5–10 minutes. The normal CVP response is a rise of 2–5 cmH2O which gradually drifts back to the original level over 10–20 minutes. Patients with no change in their CVP are empty and require further fluid resuscitation. Patients with a large, sustained rise in CVP have high preload and an element of cardiac insuffi­ ciency or volume overload.

Alexis Frank Hartmann, 1898–1964, paediatrician, St Louis, MO, USA, described the solution; should not be confused with the name of Henri Albert Charles Antoine Hartmann, French surgeon, who described the operation that goes by his name. Sidney Ringer, 1835–1910, Professor of Clinical Medicine, University College Hospital, London, UK.

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PART 1 | BASIC PRINCIPLES Resuscitation

CARDIAC OUTPUT Cardiac output monitoring allows assessment of not only the cardiac output but also the systemic vascular resistance and, depending on the technique used, end diastolic volume (pre­ load) and blood volume. Use of invasive cardiac monitoring with pulmonary artery catheters is becoming less frequent as new non-invasive monitoring techniques, such as Doppler ultrasound, pulse waveform analysis and indicator dilution methods, provide similar information without many of the drawbacks of more invasive techniques. Measurement of cardiac output, systemic vascular resist­ ance and preload can help distinguish the types of shock present (hypovolaemia, distributive, cardiogenic), especially when they coexist. The information provided guides fluid and vasopressor therapy by providing real-time monitoring of the cardiovascular response. Measurement of cardiac output is desirable in patients who do not respond as expected to first-line therapy, or who have evidence of cardiogenic shock or myocardial dysfunc­ tion. Early consideration should be given to instituting car­ diac output monitoring for patients who require vasopressor or inotropic support.

Systemic and organ perfusion Ultimately, the goal of treatment is to restore cellular and organ perfusion. Ideally, therefore, monitoring of organ perfu­ sion should guide the management of shock. The best measure of organ perfusion and the best monitor of the adequacy of shock therapy remains the urine output. However, this is an hourly measure and does not give a minute-to-minute view of the shocked state. The level of consciousness is an important marker of cerebral perfusion, but brain perfusion is maintained until the very late stages of shock, and hence is a poor marker of adequacy of resuscitation (Table 2.3). Currently, the only clinical indicators of perfusion of the gastrointestinal tract and muscular beds are the global meas­ ures of lactic acidosis (lactate and base deficit) and the mixed venous oxygen saturation.

17

BASE DEFICIT AND LACTATE Lactic acid is generated by cells undergoing anaerobic respira­ tion. The degree of lactic acidosis, as measured by serum lac­ tate level and/or the base deficit, is sensitive for both diagnosis of shock and monitoring the response to therapy. Patients with a base deficit over 6 mmol/L have a much higher morbid­ ity and mortality than those with no metabolic acidosis. Fur­ thermore, the length of time in shock with an increased base deficit is important, even if all other vital signs have returned to normal (see occult hypoperfusion below under End points of resuscitation). These parameters are measured from arterial blood gas analyses, and therefore the frequency of measurements is limited and they do not provide minute-to-minute data on systemic perfusion or the response to therapy. Nevertheless, the base deficit and/or lactate should be measured routinely in these patients until they have returned to normal levels. MIXED VENOUS OXYGEN SATURATION The percentage saturation of oxygen returning to the heart from the body is a measure of the oxygen delivery and extraction by the tissues. Accurate measurement is via analy­ sis of blood drawn from a long central line placed in the right atrium. Estimations can be made from blood drawn from lines in the superior vena cava, but these values will be slightly higher than those of a mixed venous sample (as there is rela­ tively more oxygen extraction from the lower half of the body). Normal mixed venous oxygen saturation levels are 50–70%. Levels below 50% indicate inadequate oxygen delivery and increased oxygen extraction by the cells. This is consistent with hypovolaemic or cardiogenic shock. High mixed venous saturations (>70%) are seen in sepsis and some other forms of distributive shock. In sepsis, there is disordered utilisation of oxygen at the cellular level, and arteriovenous shunting of blood at the microvascular level. Therefore, less oxygen is presented to the cells, and those cells cannot utilise what little oxygen is presented. Thus, venous blood has a higher oxygen concentration than normal.

TABLE 2.3  Monitors for organ/systemic perfusion. Clinical Systemic perfusion

Investigational Base deficit Lactate Mixed venous oxygen saturation

Organ perfusion Muscle

Gut

Near-infrared spectroscopy Tissue oxygen electrode Sublingual capnometry Gut mucosal pH Laser Doppler flowmetry

Kidney

Urine output

Brain

Conscious level

Tissue oxygen electrode Near-infrared spectroscopy

Christian Johann Doppler, 1803–1853, Professor of Experimental Physics, Vienna, Austria, enunciated the Doppler principle in 1842.

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CHAPTER 2  Shock and blood transfusion

Patients who are septic should therefore have mixed venous oxygen saturations above 70%; below this level, they are not only in septic shock but also in hypovolaemic or car­ diogenic shock. Although the SvO2 level is in the ‘normal’ range, it is low for the septic state, and inadequate oxygen is being supplied to cells that cannot utilise oxygen appropri­ ately. This must be corrected rapidly. Hypovolaemia should be corrected with fluid therapy, and low cardiac output due to myocardial depression or failure should be treated with ino­ tropes (dobutamine), to achieve a mixed venous saturation greater than 70% (normal for the septic state). New methods for monitoring regional tissue perfusion and oxygenation are becoming available, the most promising of which are muscle tissue oxygen probes, near-infrared spectros­ copy and sublingual capnometry. While these techniques pro­ vide information regarding perfusion of specific tissue beds, it is as yet unclear whether there are significant advantages over existing measurements of global hypoperfusion (base deficit, lactate).

End points of resuscitation It is much easier to know when to start resuscitation than when to stop. Traditionally, patients have been resuscitated until they have a normal pulse, blood pressure and urine out­ put. However, these parameters are monitoring organ systems whose blood flow is preserved until the late stages of shock. A patient therefore may be resuscitated to restore central perfusion to the brain, lungs and kidneys and yet continue to underperfuse the gut and muscle beds. Thus, activation of inflammation and coagulation may be ongoing and lead to reperfusion injury when these organs are finally perfused, and ultimately multiple organ failure. This state of normal vital signs and continued underper­ fusion is termed ‘occult hypoperfusion’. With current moni­ toring techniques, it is manifested only by a persistent lactic acidosis and low mixed venous oxygen saturation. The time spent by patients in this hypoperfused state has a dramatic effect on outcome. Patients with occult hypoperfusion for more than 12 hours have two to three times the mortality of patients with a limited duration of shock. Resuscitation algorithms directed at correcting global perfusion end points (base deficit, lactate, mixed venous oxy­ gen saturation) rather than traditional end points have been shown to improve mortality and morbidity in high-risk surgical patients. However, it is clear that, despite aggressive regimes, some patients cannot be resuscitated to normal parameters within 12 hours by fluid resuscitation alone. More research is underway to identify the pathophysiology behind this and investigate new therapeutic options.

HAEMORRHAGE Haemorrhage must be recognised and managed aggressively to reduce the severity and duration of shock and avoid death and/ or multiple organ failure. Haemorrhage is treated by arresting the bleeding – not by fluid resuscitation or blood transfusion. Although necessary as supportive measures to maintain organ

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perfusion, attempting to resuscitate patients who have ongo­ ing haemorrhage will lead to physiological exhaustion (coag­ ulopathy, acidosis and hypothermia) and subsequently death.

Pathophysiology Haemorrhage leads to a state of hypovolaemic shock. The combination of tissue trauma and hypovolaemic shock leads to the development of an endogenous coagulopathy called acute traumatic coagulopathy (ATC). Up to 25% of trauma patients develop ATC within minutes of injury and it is asso­ ciated with a four-fold increase in mortality. It is likely that ATC exists whenever there is the combination of shock and tissue trauma (e.g. major surgery). ATC is a component of trauma-induced coagulopathy (TIC), which is ultimately multifactorial (Figure 2.1). Ongoing bleeding with fluid and red blood cell resuscita­ tion leads to a dilution of coagulation factors which worsens the coagulopathy. In addition, the acidosis induced by the hypoperfused state leads to decreased function of the coagu­ lation proteases, resulting in coagulopathy and further haem­ orrhage. The reduced tissue perfusion includes reduced blood supply to muscle beds. Underperfused muscle is unable to generate heat and hypothermia ensues. Coagulation functions poorly at low temperatures and there is further haemorrhage, further hypoperfusion and worsening acidosis and hypother­ mia. These three factors result in a downward spiral leading to physiological exhaustion and death (Figure 2.1). Medical therapy has a tendency to worsen this effect. Intra­ venous blood and fluids are cold and exacerbate hypothermia. Further heat is lost by opening body cavities during surgery. Surgery usually leads to further bleeding and many crystalloid fluids are themselves acidic (e.g. normal saline has a pH of 6.7). Every effort must therefore be made to rapidly identify and stop haemorrhage, and to avoid (preferably) or limit physiological exhaustion from coagulopathy, acidosis and hypothermia. Trauma

Shock ATC

Fibrinolysis

Inflammation

Hypothermia

Haemorrhage Acidaemia

Genetics

Loss, dilution

TRAUMA-INDUCED COAGULOPATHY (TIC) Figure 2.1  Trauma-induced coagulopathy.

Definitions Revealed and concealed haemorrhage Haemorrhage may be revealed or concealed. Revealed hae­ morrhage is obvious external haemorrhage, such as exsan­ guination from an open arterial wound or from massive haematemesis from a duodenal ulcer. Concealed haemorrhage is contained within the body cavity and must be suspected, actively investigated and controlled. In

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PART 1 | BASIC PRINCIPLES Haemorrhage

trauma, haemorrhage may be concealed within the chest, abdo­ men, pelvis, retroperitoneum or in the limbs with contained vascular injury or associated with long-bone fractures. Examples of non-traumatic concealed haemorrhage include occult gastro­ intestinal bleeding or ruptured aortic aneurysm.

Primary, reactionary and secondary haemorrhage Primary haemorrhage is haemorrhage occurring immediately due to an injury (or surgery). Reactionary haemorrhage is delayed haemorrhage (within 24 hours) and is usually due to dislodgement of a clot by resuscitation, normalisation of blood pressure and vasodilatation. Reactionary haemorrhage may also be due to technical failure, such as slippage of a ligature. Secondary haemorrhage is due to sloughing of the wall of a vessel. It usually occurs 7–14 days after injury and is precip­ itated by factors such as infection, pressure necrosis (such as from a drain) or malignancy.

19

among individuals (e.g. athletes versus the obese) and vari­ ation due to confounding factors (e.g. concomitant medica­ tions, pain). Treatment should therefore be based upon the degree of hypovolaemic shock according to vital signs, preload assessment, base deficit and, most importantly, the dynamic response to fluid therapy. Patients who are ‘non-responders’ or ‘transient responders’ are still bleeding and must have the site of haemorrhage identified and controlled.

Management Identify haemorrhage External haemorrhage may be obvious, but the diagnosis of concealed haemorrhage may be more difficult. Any shock should be assumed to be hypovolaemic until proven otherwise and, similarly, hypovolaemia should be assumed to be due to haemorrhage until this has been excluded.

Immediate resuscitative manoeuvres

Surgical and non-surgical haemorrhage Surgical haemorrhage is due to a direct injury and is amenable to surgical control (or other techniques such as angioemboli­ sation). Non-surgical haemorrhage is the general ooze from all raw surfaces due to coagulopathy and cannot be stopped by surgical means (except packing). Treatment requires cor­ rection of the coagulation abnormalities.

Direct pressure should be placed over the site of external haem­ orrhage. Airway and breathing should be assessed and controlled as necessary. Large-bore intravenous access should be instituted and blood drawn for cross-matching (see Cross-matching below). Emergency blood should be requested if the degree of shock and ongoing haemorrhage warrants this.

Identify the site of haemorrhage

Degree and classification The adult human has approximately 5litres of blood (70 mL/ kg children and adults, 80 mL/kg neonates). Estimation of the amount of blood that has been lost is difficult, inaccurate and usually underestimates the actual value. External haemorrhage is obvious, but it may be difficult to estimate the actual volume lost. In the operating room, blood collected in suction apparatus can be measured and swabs soaked in blood weighed. The haemoglobin level is a poor indicator of the degree of haemorrhage because it represents a concentration and not an absolute amount. In the early stages of rapid haemorrhage, the haemoglobin concentration is unchanged (as whole blood is lost). Later, as fluid shifts from the intracellular and interstitial spaces into the vascular compartment, the haemoglobin and haematocrit levels will fall. The amount of haemorrhage can be classified into classes 1–4 based on the estimated blood loss required to produce certain physiological compensatory changes (Table 2.4). Although conceptually useful, there is variation across ages (the young compensate well, the old very poorly), variation TABLE 2.4  Traditional classification of haemorrhagic shock. Class Blood volume lost as percentage of total

01_02-B&L27_Pt1_Ch02.indd 19

1

2

3

4

40%

Once haemorrhage has been considered, the site of haemor­ rhage must be rapidly identified. Note this is not to identify the exact location definitively, but rather to define the next step in haemorrhage control (operation, angioembolisation, endoscopic control). Clues may be in the history (previous episodes, known aneurysm, non-steroidal therapy for gastrointestinal [GI] bleeding) or examination (nature of blood – fresh, melaena; abdominal tenderness, etc.). For shocked trauma patients, the external signs of injury may suggest internal haemorrhage, but haemorrhage into a body cavity (thorax, abdomen) must be excluded with rapid investigations (chest and pelvis x-ray, abdominal ultrasound or diagnostic peritoneal aspiration). Investigations for blood loss must be appropriate to the patient’s physiological condition. Rapid bedside tests are more appropriate for profound shock and exsanguinating haemor­ rhage than investigations such as computed tomography (CT) which take time. Patients who are not actively bleeding can have a more methodical, definitive work-up.

Haemorrhage control The bleeding, shocked patient must be moved rapidly to a place of haemorrhage control. This will usually be in the oper­ ating room but may be the angiography or endoscopy suite. These patients require surgical and anaesthetic support and full monitoring and equipment must be available. Haemorrhage control must be achieved rapidly to pre­ vent the patient entering the triad of coagulopathy–acidosis– hypothermia and physiological exhaustion. There should be no unnecessary investigations or procedures prior to ­haemorrhage

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PART 1 | BASIC PRINCIPLES 20

CHAPTER 2  Shock and blood transfusion

control to minimise the duration and severity of shock. This includes prolonged attempts to volume resuscitate the patient prior to surgery, which will result in further hypothermia and clotting factor dilution until the bleeding is stopped. Attention should be paid to correction of coagulopathy with blood com­ ponent therapy to aid surgical haemorrhage control. Surgical intervention may need to be limited to the min­ imum necessary to stop bleeding and control sepsis. More definitive repairs can be delayed until the patient is haemo­ dynamically stable and physiologically capable of sustaining the procedure. This concept of tailoring the operation to match the patient’s physiology and staged procedures to prevent physio­ logical exhaustion is called ‘damage control surgery’ – a term borrowed from the military which ensures continued function­ ing of a damaged ship above conducting complete repairs which would prevent rapid return to battle. Once haemorrhage is controlled, patients should be aggres­ sively resuscitated, warmed and coagulopathy corrected. Atten­ tion should be paid to fluid responsiveness and the end points of resuscitation to ensure that patients are fully resuscitated and to reduce the incidence and severity of organ failure. Summary box 2.4 Damage control surgery ●● ●● ●● ●●

Arrest haemorrhage Control sepsis Protect from further injury Nothing else

infections is now very low, in recent years it has become appar­ ent that there is an immunological price to be paid from the transfusion of heterologous blood, leading to increased mor­ bidity and decreased survival in certain population groups (trauma, malignancy). Supplies are also limited, and therefore the use of blood and blood products must always be judicious and justifiable for clinical need (Table 2.5). TABLE 2.5  History of blood transfusion. 1492

Pope Innocent VIII suffers a stroke and receives a blood transfusion from three 10-year-old boys (paid a ducat each). All three boys died, as did the pope later that year

1665

Richard Lower in Oxford conducts the first successful canine transfusions

1667

Jean-Baptiste Denis reports successful sheep–human transfusions

1678

Animal–human transfusions are banned in France because of the poor results

1818

James Blundell performs the first successful documented human transfusion in a woman suffering post-partum haemorrhage. She received blood from her husband and survived

1901

Karl Landsteiner discovers the ABO system

1914

The Belgian physician Albert Hustin performed the first non-direct transfusion, using sodium citrate as an anticoagulant

1926

The British Red Cross instituted the first blood transfusion service in the world

1939

The Rhesus system was identified and recognised as the major cause of transfusion reactions

Damage control resuscitation These concepts have been combined into a new paradigm for the management of trauma patients with active haemorrhage called damage control resuscitation (DCR). The four central strategies of DCR are: 1 Anticipate and treat acute traumatic coagulopathy. 2 Permissive hypotension until haemorrhage control. 3 Limit crystalloid and colloid infusion to avoid dilutional coagulopathy. 4 Damage control surgery to control haemorrhage and pre­ serve physiology. Damage control resuscitation strategies have been shown to reduce mortality and morbidity in patients with exsangui­ nating trauma and may be applicable in other forms of acute haemorrhage.

TRANSFUSION The transfusion of blood and blood products has become commonplace since the first successful transfusion in 1818. Although the incidence of severe transfusion reactions and

Blood and blood products Blood is collected from donors who have been previously screened before donating, to exclude any donor whose blood may have the potential to harm the patient, or to prevent possible harm that donating a unit of blood may have on the donor. In the UK, up to 450 mL of blood is drawn, a maximum of three times each year. Each unit is tested for evidence of hepatitis B, hepatitis C, HIV-1, HIV-2 and syphilis. Donations are leukodepleted as a precaution against variant Creutzfeldt– Jakob disease (this may also reduce the immunogenicity of the transfusion). The ABO and rhesus D blood groups are deter­ mined, as well as the presence of irregular red cell antibodies. The blood is then processed into subcomponents.

Whole blood Whole blood is now rarely available in civilian practice because it has been seen as an inefficient use of the limited resource. However, whole blood transfusion has significant advantages over packed cells as it is coagulation factor rich and, if fresh, more metabolically active than stored blood.

Hans Gerhard Creutzfeldt, 1885–1946, neurologist, Kiel, Germany. Alfons Maria Jakob, 1884–1931, neurologist, Hamburg, Germany. Karl Landsteiner, 1868–1943, Professor of Pathological Anatomy, University of Vienna, Austria. In 1909 he classified the human blood groups into A, B, AB and O. For this he was awarded the Nobel Prize for Physiology or Medicine in 1930.

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PART 1 | BASIC PRINCIPLES Transfusion

Packed red cells Packed red blood cells are spun-down and concentrated packs of red blood cells. Each unit is approximately 330 mL and has a haematocrit of 50–70%. Packed cells are stored in a SAG-M solution (saline–adenine–glucose–mannitol) to increase shelf life to 5 weeks at 2–6°C. (Older storage regimes included storage in CPD: citrate–phosphate–dextrose solutions, which have a shelf life of 2–3 weeks.)

Indications for blood transfusion Blood transfusions should be avoided if possible, and many previous uses of blood and blood products are now no longer considered appropriate. The indications for blood transfusion are as follows: ●● ●●

Fresh-frozen plasma Fresh-frozen plasma (FFP) is rich in coagulation factors and is removed from fresh blood and stored at −40 to −50°C with a 2-year shelf life. It is the first-line therapy in the treatment of coagulopathic haemorrhage (see below under ­Management of coagulopathy). Rhesus D-positive FFP may be given to a rhesus D-negative woman although it is pos­ sible for ­sero­conversion to occur with large volumes owing to the presence of red cell fragments, and Rh-D immunisation should be considered.

Cryoprecipitate Cryoprecipitate is a supernatant precipitate of FFP and is rich in factor VIII and fibrinogen. It is stored at −30°C with a 2-year shelf life. It is given in low fibrinogen states or factor VIII deficiency.

Platelets Platelets are supplied as a pooled platelet concentrate and contain about 250 × 109/L. Platelets are stored on a special agitator at 20–24°C and have a shelf life of only 5days. Plate­ let transfusions are given to patients with thrombocytopenia or with platelet dysfunction who are bleeding or undergoing ­surgery. Patients are increasingly presenting on antiplatelet ther­ apy such as aspirin or clopidogrel for reduction of cardiovas­ cular risk. Aspirin therapy rarely poses a problem but control of haemorrhage on the more potent platelet inhibitors can be extremely difficult. Patients on clopidogrel who are actively bleeding and undergoing major surgery may require almost continuous infusion of platelets during the course of the procedure. Arginine vasopressin or its analogues (DDAVP) have also been used in this patient group, although with lim­ ited success.

Prothrombin complex concentrates Prothrombin complex concentrates (PCC) are highly puri­ fied concentrates prepared from pooled plasma. They contain factors II, IX and X. Factor VII may be included or produced separately. It is indicated for the emergency reversal of anti­ coagulant (warfarin) therapy in uncontrolled haemorrhage.

Autologous blood It is possible for patients undergoing elective surgery to predo­ nate their own blood up to 3weeks before surgery for retrans­ fusion during the operation. Similarly, during surgery blood can be collected in a cell-saver which washes and collects red blood cells which can then be returned to the patient.

01_02-B&L27_Pt1_Ch02.indd 21

21

●●

Acute blood loss, to replace circulating volume and main­ tain oxygen delivery; Perioperative anaemia, to ensure adequate oxygen deliv­ ery during the perioperative phase; Symptomatic chronic anaemia, without haemorrhage or impending surgery.

Transfusion trigger Historically, patients were transfused to achieve a haemoglo­ bin >10 g/dL. This has now been shown not only to be unnec­ essary but also to be associated with an increased morbidity and mortality compared with lower target values. A haemo­ globin level of 6 g/dL is acceptable in patients who are not actively bleeding, not about to undergo major surgery and are not symptomatic. There is some controversy as to the opti­ mal haemoglobin level in some patient groups, such as those with cardiovascular disease, sepsis and traumatic brain injury. Although, conceptually, a higher haemoglobin level improves oxygen delivery, there is little clinical evidence at this stage to support higher levels in these groups (Table 2.6). TABLE 2.6  Perioperative red blood cell transfusion criteria. Haemoglobin level (g/dL)

Indications

8

No indication for transfusion in the absence of other risk factors

Blood groups and cross-matching Human red cells have on their cell surface many different antigens. Two groups of antigens are of major importance in surgical practice – the ABO and rhesus systems.

ABO system These proteins are strongly antigenic and are associated with naturally occurring antibodies in the serum. The system con­ sists of three allelic genes – A, B and O – which control syn­ thesis of enzymes that add carbohydrate residues to cell surface glycoproteins. A and B genes add specific residues while the O gene is an amorph and does not transform the glycoprotein. The system allows for six possible genotypes although there are only four phenotypes. Naturally occurring antibodies are found in the serum of those lacking the corresponding antigen (Table 2.7). Blood group O is the universal donor type as it contains no antigens to provoke a reaction. Conversely, group AB individ­ uals are ‘universal recipients’ and can receive any ABO blood type because they have no circulating antibodies.

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PART 1 | BASIC PRINCIPLES 22

CHAPTER 2  Shock and blood transfusion

TABLE 2.7  ABO blood group system. Phenotype

Genotype

Antigens

Antibodies

Frequency (%)

O

OO

O

Anti-A, anti-B

46

A

AA or AO

A

Anti-B

42

B

BB or BO

B

Anti-A

9

AB

AB

AB

None

3

Rhesus system The rhesus D (Rh(D)) antigen is strongly antigenic and is present in approximately 85% of the population in the UK. Antibodies to the D antigen are not naturally present in the serum of the remaining 15% of individuals, but their forma­ tion may be stimulated by the transfusion of Rh-positive red cells, or acquired during delivery of a Rh(D)-positive baby. Acquired antibodies are capable, during pregnancy, of crossing the placenta and, if present in a Rh(D)-negative mother, may cause severe haemolytic anaemia and even death (hydrops fetalis) in a Rh(D)-positive fetus in utero. The other minor blood group antigens may be associated with naturally occurring antibodies, or may stimulate the formation of anti­ bodies on relatively rare occasions.

Transfusion reactions If antibodies present in the recipient’s serum are incompatible with the donor’s cells, a transfusion reaction will result. This usually takes the form of an acute haemolytic reaction. Severe immune-related transfusion reactions due to ABO incompat­ ibility result in potentially fatal complement-mediated intra­ vascular haemolysis and multiple organ failure. Transfusion reactions from other antigen systems are usually milder and self-limiting. Febrile transfusion reactions are non-haemolytic and are usually caused by a graft-versus-host response from leukocytes in transfused components. Such reactions are associated with fever, chills or rigors. The blood transfusion should be stopped immediately. This form of transfusion reaction is rare with leu­ kodepleted blood.

patient details against the prescription and the label of the donor blood. In addition, the donor blood serial number should also be checked against the issue slip for that patient. Provided these principles are strictly adhered to the number of severe and fatal ABO incompatibility reactions can be minimised.

Complications of blood transfusion Complications from blood transfusion can be categorised as those arising from a single transfusion and those related to massive transfusion.

Complications from a single transfusion Complications from a single transfusion include: ●● ●● ●● ●●

●● ●● ●●

Complications from massive transfusion Complications from massive transfusion include: ●● ●● ●●

Cross-matching To prevent transfusion reactions, all transfusions are preceded by ABO and rhesus typing of both donor and recipient blood to ensure compatibility. The recipient’s serum is then mixed with the donor’s cells to confirm ABO compatibility and to test for rhesus and any other blood group antigen–antibody reaction. Full cross-matching of blood may take up to 45 minutes in most laboratories. In more urgent situations, ‘type specific’ blood is provided which is only ABO/rhesus matched and can be issued within 10–15 minutes. Where blood must be given emergently, group O (universal donor) blood is given (O− to females, O+ to males). When blood transfusion is prescribed and blood is admin­ istered, it is essential that the correct patient receives the cor­ rect transfusion. Two healthcare personnel should check the

01_02-B&L27_Pt1_Ch02.indd 22

incompatibility haemolytic transfusion reaction; febrile transfusion reaction; allergic reaction; infection: ●● bacterial infection (usually due to faulty storage); ●● hepatitis; ●● HIV; ●● malaria; air embolism; thrombophlebitis; transfusion-related acute lung injury (usually from FFP).

●● ●●

coagulopathy; hypocalcaemia; hyperkalaemia; hypokalaemia; hypothermia.

In addition, patients who receive repeated transfusions over long periods of time (e.g. patients with thalassaemia) may develop iron overload. (Each transfused unit of red blood cells contains approximately 250 mg of elemental iron.)

Management of coagulopathy Correction of coagulopathy is not necessary if there is no active bleeding and haemorrhage is not anticipated (not due for sur­ gery). However, coagulopathy following or during massive transfusion should be anticipated and managed aggressively. Prevention of dilutional coagulopathy is central to the dam­ age control resuscitation of patients who are actively bleeding.

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PART 1 | BASIC PRINCIPLES Further reading

This is the prime reason for delivering balanced transfusion regimes matching red blood cell packs with plasma and plate­ lets. Based on moderate evidence, when red cells are trans­ fused for active haemorrhage, it is best to match each red cell unit with one unit of FFP and one of platelets (1:1:1). This will reduce the incidence and severity of subsequent dilutional coagulopathy. Crystalloids and colloids should be avoided for the same reason. The balanced transfusion approach cannot, however, correct coagulopathy. Therefore, coagulation should be mon­ itored routinely, either with point-of-care testing (throm­ boelastometry) or with laboratory tests (fibrinogen, clotting times). Underlying coagulopathies should be treated in addi­ tion to the administration of 1:1:1 balanced transfusions. There are pharmacological adjuncts to blood component therapy. The antifibrinolytic tranexamic acid is the most com­ monly administered. It is usually administered empirically to bleeding patients because effective point-of-care tests of fibrinolysis are not yet routinely available. There is little evi­ dence to support the use of other coagulation factor concen­ trates at this time.

Blood substitutes Blood substitutes are an attractive alternative to the costly process of donating, checking, storing and administering blood, especially given the immunogenic and potential infec­ tious complications associated with transfusion. There are several oxygen-carrying blood substitutes under investigation in experimental animal or early clinical trials.

01_02-B&L27_Pt1_Ch02.indd 23

23

Blood substitutes are either biomimetic or abiotic. Biomimetic substitutes mimic the standard oxygen-carrying capacity of the blood and are haemoglobin based. Abiotic substitutes are synthetic oxygen carriers and are currently primarily per­ fluorocarbon based. Haemoglobin is seen as the obvious candidate for devel­ oping an effective blood substitute. Various engineered mol­ ecules are under clinical trials, and are based on human, bovine or recombinant technologies. Second-generation perfluorocarbon emulsions are also showing potential in clinical trials.

FURTHER READING Duchesne JC, McSwain NE Jr, Cotton BA et al. Damage control ­resuscitation: the new face of damage control. J Trauma 2010; 69: 976–90. Glen J, Constanti M, Brohi K; Guideline Development Group. Assess­ ment and initial management of major trauma: summary of NICE guidance. BMJ 2016; 353: i3051. Harris T, Thomas GO, Brohi K. Early fluid resuscitation in severe trau­ ma. BMJ 2012; 345: e5752. Nguyen HB, Jaehne AK, Jayaprakash N et al. Early goal-directed therapy in severe sepsis and septic shock: insights and comparisons to Pro­ CESS, ProMISe, and ARISE. Crit Care 2016; 20(1): 160. Pearse RM, Ackland GL. Perioperative fluid therapy. BMJ 2012; 344: e2865. Rossaint R, Bouillon B, Cerny V et al. The European guideline on man­ agement of major bleeding and coagulopathy following trauma: fourth edition. Crit Care 2016; 20: 100. Sihler KC, Nathans AB. Management of severe sepsis in the surgical patient. Surg Clin N Am 2006; 86: 1457–81.

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Bailey & Love Bailey & Love Bailey & Love Bailey &3Love Bailey & Love Bailey & Love Chapter

Wounds, healing and tissue repair Learning objectives To understand: •• Normal healing and how it can be adversely affected •• How to manage wounds of different types, of different structures and at different sites

•• Aspects of disordered healing that lead to chronic

INTRODUCTION

NORMAL WOUND HEALING

Wound healing is a mechanism whereby the body attempts to restore the integrity of the injured part. This falls far short of tissue regeneration by pluripotent cells, seen in some amphi­ bians, and is often detrimental, as seen in the problems created by scarring, such as adhesions, keloids, contractures and cirrho­ sis of the liver. Several factors may influence healing. However, a clean incised wound in a healthy person where there is no skin loss will follow a set pattern as outlined below.

This is variously described as taking place in three or four phases, the most commonly agreed being:

Summary box 3.1 Factors influencing healing of a wound ●● ●● ●●

●● ●● ●●

●●

Site of the wound Structures involved Mechanism of wounding Incision Crush Crush avulsion Contamination (foreign bodies/bacteria)a Loss of tissue Other local factors Vascular insufficiency (arterial or venous) Previous radiation Pressure Systemic factors Malnutrition or vitamin and mineral deficiencies Disease (e.g. diabetes mellitus) Medications (e.g. steroids) Immune deficiencies (e.g. chemotherapy, acquired immunodeficiency syndrome [AIDS]) Smoking

a 

In explosions, the contamination may consist of tissue such as bone from another individual.

01_03-B&L27_Pt1_Ch03.indd 24

wounds

•• The variety of scars and their treatment •• How to differentiate between acute and chronic wounds

1 the inflammatory phase; 2 the proliferative phase; 3 the remodelling phase (maturing phase). Occasionally, a haemostatic phase is referred to as occur­ ring before the inflammatory phase, or a destructive phase fol­ lowing inflammation consisting of the cellular cleansing of the wound by macrophages (Figure 3.1). The inflammatory phase begins immediately after wound­ ing and lasts 2–3 days. Bleeding is followed by vasoconstric­ tion and thrombus formation to limit blood loss. Platelets stick to the damaged endothelial lining of vessels, releasing adenosine diphosphate (ADP), which causes thrombocytic aggregates to fill the wound. When bleeding stops, the plate­ lets then release several cytokines from their alpha granules. These are platelet-derived growth factor (PDGF), plate­ let factor IV and transforming growth factor beta (TGFβ). These attract inflammatory cells such as polymorphonuclear leukocytes (PMN) and macro­phages. Platelets and the local injured tissue release vasoactive amines, such as histamine, serotonin and prostaglandins, which increase vascular perme­ ability, thereby aiding infiltration of these inflammatory cells. Macrophages remove devitalised tissue and microorganisms while regulating fibroblast activity in the proliferative phase of healing. The initial framework for structural support of cells is provided by fibrin produced by fibrinogen. A more historical (Latin) description of this phase is described in four words: rubor (redness), tumor (swelling), calor (heat) and dolor (pain). The proliferative phase lasts from the third day to the third week, consisting mainly of fibroblast activity with the production of collagen and ground substance (glycosaminogly­

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ve ve

PART 1 | BASIC PRINCIPLES Abnormal healing

consisting of osteoid (mineralised by hydroxyapatite and laid down by osteoblasts). In the remodelling phase, cortical struc­ ture and the medullary cavity are restored. If fracture ends are accurately opposed and rigidly fixed, callus formation is mini­ mal and primary healing occurs. If a gap exists, then secondary healing may lead to delayed union, non-union or malunion.

Nerve (a)

(b)

Distal to the wound, Wallerian degeneration occurs. Proxi­ mally, the nerve suffers traumatic degeneration as far as the last node of Ranvier. The regenerating nerve fibres are attracted to their receptors by neurotrophism, which is mediated by growth factors, hormones and other extracellular matrix tro­ phins. Nerve regeneration is characterised by profuse growth of new nerve fibres which sprout from the cut proximal end. Overgrowth of these, coupled with poor approximation, may lead to neuroma formation.

Tendon (c)

(d)

Figure 3.1  The phases of healing. (a) Early inflammatory phase with platelet-enriched blood clot and dilated vessels. (b) Late inflammatory phase with increased vascularity and increase in polymorphonuclear leukocytes and lymphocytes (round cells). (c) Proliferative phase with capillary buds and fibroblasts. (d) Mature contracted scar.

cans and proteoglycans), the growth of new blood vessels as capillary loops (angioneogenesis) and the re-epithelialisation of the wound surface. Fibroblasts require vitamin C to pro­ duce collagen. The wound tissue formed in the early part of this phase is called granulation tissue. In the latter part of this phase, there is an increase in the tensile strength of the wound due to increased collagen, which is at first deposited in a ran­ dom fashion and consists of type III collagen. This proliferative phase with its increase of collagen deposition is associated with wound contraction, which can considerably reduce the surface area of a wound over the first 3weeks of healing. The remodelling phase is characterised by maturation of collagen (type I replacing type III until a ratio of 4:1 is achieved). There is a realignment of collagen fibres along the lines of tension, decreased wound vascularity, and wound contraction due to fibroblast and myofibroblast activity. This maturation of collagen leads to increased tensile strength in the wound which is maximal at the 12th week post injury and represents approximately 80% of the uninjured skin strength.

ort Practice of Surgery, 26th Ed

o.uk

25

ISBN: 9781444121278

NORMAL HEALING IN SPECIFIC TISSUES

Bone The phases are as above, but periosteal and endosteal prolifer­ ation leads to the formation of callus, which is immature bone

Although repair follows the normal pattern of wound heal­ ing, there are two main mechanisms whereby nutrients, cells and new vessels reach the severed tendon. These are intrinsic, which consists of vincular blood flow and synovial diffusion, and extrinsic, which depends on the formation of fibrous adhesions between the tendon and the tendon sheath. The random nature of the initial collagen produced means that the tendon lacks tensile strength for the first 3–6 weeks. Active mobilisation pre­ vents adhesions limiting range of motion, but the tendon must be protected by splintage in order to avoid rupture of the repair.

ABNORMAL HEALING Some of the adverse influences on wound healing are listed in Summary box 3.1. Delayed healing may result in loss of function or poor cosmetic outcome. The aim of treatment is to achieve healing by primary intention and so reduce the inflammatory and proliferative responses. Summary box 3.2 Classification of wound closure and healing Primary intention Wound edges opposed Normal healing Minimal scar ●● Secondary intention Proof Stage: 2 left openFig No: 3.1a-d Wound Heals by granulation, contraction and epithelialisation Increased inflammation and proliferation Poor scar ●● Tertiary intention (also called delayed primary intention) Wound initially left open Edges later opposed when healing conditions favourable ●●

Augustus Volney Waller, 1816–1870, general practitioner of Kensington, London, UK (1842–1851), subsequently worked as a physiologist in Bonn, Germany; Paris, France; Birmingham, UK; and Geneva, Switzerland. Louis Antoine Ranvier, 1835–1922, physician and histologist who was a professor in the College of France, Paris, France, described these nodes in 1878.

01_03-B&L27_Pt1_Ch03.indd 25

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PART 1 | BASIC PRINCIPLES 26

CHAPTER 3  Wounds, healing and tissue repair

Healing by primary intention is also known as healing by first intention. This occurs when there is apposition of the wound edges and minimal surrounding tissue trauma that causes least inflammation and leaves the best scar. Delayed primary inten­ tion healing occurs when the wound edges are not opposed immediately, which may be necessary in contaminated or untidy wounds. The inflammatory and proliferative phases of healing are well established when delayed closure of the wound is car­ ried out. This is also called healing by tertiary intention in some texts and will result in a less satisfactory scar than would result after healing by primary intention. Secondary healing or healing by secondary intention occurs in wounds that are left open and allowed to heal by granulation, contraction and epithelialisation.

TYPES OF WOUNDS − TIDY VERSUS UNTIDY The site injured, the structures involved in the injury and the mechanism of injury (e.g. incision or explosion) all influence healing and recovery of function. This has led to the management of wounds based upon their classi­ fication into tidy and untidy (Table 3.1 and Figure 3.2). (a)

The surgeon’s aim is to convert untidy to tidy by removing all contaminated and devitalised tissue. Primary repair of all structures (e.g. bone, tendon, vessel and nerve) may be possible in a tidy wound, but a contami­ nated wound with dead tissue requires debridement on one or several occasions before definitive repair can be carried out (the concept of ‘second look’ surgery). This is especially true in injuries caused by explosions, bullets or other missiles, where the external wound itself may appear much smaller than the wider extent of the injured tissues deep to the sur­ face. Multiple debridements are often required after crushing injuries in road traffic accidents or in natural disasters such as earthquakes, where fallen masonry causes widespread mus­ cle damage and compartment syndromes (see Compartment syndromes below). Any explosion where there are multiple victims at the same site or where there has been a suiciderelated explosion will carry the risk of tissue and viral con­ tamination. Appropriate tests for hepatitis viruses and human immunodeficiency virus (HIV) are required. TABLE 3.1  Tidy versus untidy wounds. Tidy

Untidy

Incised

Crushed or avulsed

Clean

Contaminated

Healthy tissues

Devitalised tissues

Seldom tissue loss

Often tissue loss

MANAGING THE ACUTE WOUND The surgeon must remember to examine the whole patient according to acute trauma life support (ATLS) principles. A stab wound in the back can be missed just as easily in the reality of the accident and emergency room as in a fictitious detective novel. The wound itself should be examined, taking into con­ sideration the site and the possible structures damaged (Figure 3.3). It is essential to assess movement and s­ensation while

(b)

Figure 3.2  (a) Tidy incised wound on the finger. (b) Untidy avulsed wound on the hand.

Figure 3.3  Facial trauma – apparent tissue loss but none found after careful matching.

The term ‘debridement’ was introduced by the great French surgeon in Napoleon’s army, Dominique Jean Larrey (1766–1842). He used it to describe the removal of bullets, bits of cloth, loose bits of bone and soft tissue.

01_03-B&L27_Pt1_Ch03.indd 26

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PART 1 | BASIC PRINCIPLES Some specific wounds

watching for pain and listening to the patient. Tetanus cover should be noted and appropriate treatment carried out. A bleeding wound should be elevated and a pressure pad applied. Clamps should not be put on vessels blindly because nerve damage is likely and vascular anastomosis is ren­ dered impossible. In order to facilitate examination, adequate analgesia and/ or anaesthesia (local, regional or general) are required. General anaesthesia is often needed in children. With limb injuries, particularly those of the hand, a tourniquet should be used in order to facilitate visualisation of all structures. Due care should be taken with tourniquet application, avoiding uneven pressure and noting the duration of tourniquet time. After assessment, a thorough debridement is essential. Abrasions, ‘road rash’ (following a fall from a motorbike) and explosions all cause dirt tattooing and require the use of a scrubbing brush or even excision under magnification. A wound should be explored and debrided to the limit of blood staining. Devitalised tissue must be excised until bleeding occurs, with the obvious exceptions of nerves, vessels and tendons. These may survive with adequate revascularisation subsequently or after being covered with viable tissue such as that brought in by skin or muscle flaps. The use of copious saline irrigation or pulsed jet lavage (where the instrumentation is available) can be less destruc­ tive than knife or scissors when debriding. However, it has been suggested that pulsed jet lavage can implant dirt into a deeper plane and care should be taken to avoid this compli­ cation. Muscle viability is judged by the colour, bleeding pat­ tern and contractility. In a tidy wound, repair of all damaged structures may be attempted. Repair of nerves under magnifi­ cation (loupes or microscope) using 8/0 or 10/0 monofilament nylon is usual. Vessels such as the radial or ulnar artery may be repaired using similar techniques. Tendon repairs, particu­ larly those in the hand, benefit from early active mobilisation because this ­minimises adhesions between the tendon and the tendon sheath (see above under Tendon for extrinsic tendon healing mechanism). Skin cover by flap or graft may be required as skin closure should always be without tension and should allow for the oedema typically associated with injury and the inflammatory phase of healing. A flap brings in a new blood supply and can be used to cover tendon, nerve, bone and other structures that would not provide a suitable vascular base for a skin graft. A skin graft has no inherent blood supply and is dependent on the recipient site for nutrition.

SOME SPECIFIC WOUNDS Bites Most bites involve either puncture wounds or avulsions. Bites from small animals are common in children (Figure 3.4) and require cleansing and treatment according to the principles out­ lined in Summary box 3.3, usually under general anaesthetic. Injuries to the ear, tip of nose and lower lip are most usu­ ally seen in victims of human bites. A boxing-type injury of the metacarpophalangeal joint may result from a perforating contact with the teeth of a victim. Anaerobic and aerobic

01_03-B&L27_Pt1_Ch03.indd 27

27

Figure 3.4  Dog bite in a child.

Summary box 3.3 Managing the acute wound ●● ●● ●● ●● ●● ●● ●● ●●

Cleansing Exploration and diagnosis Debridement Repair of structures Replacement of lost tissues where indicated Skin cover if required Skin closure without tension All of the above with careful tissue handling and meticulous technique

organism prophylaxis is required as bite wounds typically have high virulent bacterial counts.

Puncture wounds Wounds caused by sharp objects should be explored to the limit of tissue blood staining. Needle-stick injuries should be treated according to the well-published protocols because of hepatitis and HIV risks. X-ray examination should be carried out in order to rule out retained foreign bodies in the depth of the wound.

Haematoma If large, painful or causing neural deficit, a haematoma may require release by incision or aspiration. In the gluteal or thigh region, there may be an associated disruption of fat in the form of a fat fracture, which results in an unsightly groove but intact skin. An untreated haematoma may also calcify and therefore require surgical exploration if symptomatic.

Degloving Degloving occurs when the skin and subcutaneous fat are stripped by avulsion from the underlying fascia, leaving neuro­vascular structures, tendon or bone exposed. A deglov­ ing injury may be open or closed. An obvious example of an open degloving is a ring avulsion injury with loss of finger

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PART 1 | BASIC PRINCIPLES 28

CHAPTER 3  Wounds, healing and tissue repair

Figure 3.5  Degloving hand injury. Figure 3.7  Meshed split-skin graft.

Figure 3.6  Degloving buttock injury.

skin (Figure 3.5). A closed degloving may be a rollover injury, typically caused by a motor vehicle over a limb. Such an injury will extend far further than expected, and much of the limb skin may be non-viable (Figure 3.6). Examination under anaes­ thetic is required with a radical excision of all non-bleeding skin, as judged by bleeding dermis. Fluoroscein can be admin­ istered intravenously while the patient is anaesthetised. Under ultraviolet light, viable (perfused) skin will show up as a fluores­ cent yellowish green colour, and the non-viable skin for exci­ sion is clearly mapped out. However, the main objection to this method is that of possible anaphylactic shock due to fluoroscein sensitivity. Most surgeons therefore rely upon serial excision until punctate dermal bleeding is obvious. Split-skin grafts can be harvested from the degloved non-viable skin and meshed (Figure 3.7) to cover the raw areas resulting from debridement.

Compartment pressures can be measured using a pressure monitor and a catheter placed in the muscle compartment. If pressures are constantly greater than 30 mmHg or if the above clinical signs are present, then fasciotomy should be performed. Fasciotomy involves incising the deep muscle fas­ cia and is best carried out via longitudinal incisions of skin, fat and fascia (Figure 3.8). The muscle will then be seen bulg­ ing out through the fasciotomy opening. The lower limb can be decompressed via two incisions, each being lateral to the subcutaneous border of the tibia. This gives access to the two posterior compartments and to the peroneal and anterior com­ partments of the leg. In crush injuries that present several days after the event, a late fasciotomy can be dangerous because dead muscle produces myoglobin which, if suddenly released into the blood stream, causes myoglobinuria with glomerular blockage and renal failure. In the late treatment of lower limb injuries, therefore, it may be safer to amputate the limb once viable and non-viable tissues have been demarcated.

High-pressure injection injuries The use of high-pressure devices in cleaning, degreasing and painting can cause extensive closed injuries through

Compartment syndromes Compartment syndromes typically occur in closed lower limb injuries. They are characterised by severe pain, pain on passive movement of the affected compartment muscles, distal sen­ sory disturbance and, finally, by the absence of pulses distally (a late sign). They can occur with an open injury if the wound does not extend into the affected compartment.

01_03-B&L27_Pt1_Ch03.indd 28

Figure 3.8  Fasciotomy of the lower leg.

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PART 1 | BASIC PRINCIPLES Chronic wounds

small entry wounds. The liquid injected spreads along fascial planes, a common site being from finger to forearm. The tis­ sue damage is dependent upon the toxicity of the substance and the injection pressure. Treatment is surgical, with wide exposure, removal of the toxic substance and thorough debridement. Preoperative x-rays may be helpful where air or lead-based paints can be seen. It should be noted that ampu­ tation rates following high-pressure injection injuries are reported as being over 45%. Delayed or conservative treat­ ment is therefore inappropriate.

CHRONIC WOUNDS A chronic wound may be defined as one that fails to heal in the expected time for a wound of that type, which is usually less than 3weeks. Delays in healing can occur at any phase but most often occur in the inflammatory phase.

29

Pressure sores These can be defined as tissue necrosis with ulceration due to prolonged pressure. Less preferable terms are bed sores, pres­ sure ulcers and decubitus ulcers. They should be regarded as preventable but occur in approximately 5% of all hospital­ ised patients (range 3–12% in published literature). There is a higher incidence in paraplegic patients, in the elderly and in the severely ill patient. The most common sites are listed in Summary box 3.5. A staging system for description of pressure sores devised by the American National Pressure Ulcer Advisory Panel is shown in Table 3.2. Summary box 3.5 Pressure sore frequency in descending order ●● ●●

Leg ulcers

●●

In resource-rich countries, the most common chronic wounds are leg ulcers. An ulcer can be defined as a break in the epi­ thelial continuity. A prolonged inflammatory phase leads to overgrowth of granulation tissue, and attempts to heal by scarring leave a fibrotic margin. Necrotic tissue, often at the ulcer centre, is called slough. The more common aetiologies are listed in Summary box 3.4. A chronic ulcer, unresponsive to dressings and sim­ ple treatments, should be biopsied to rule out neoplastic change, a squamous cell carcinoma known as a Marjolin’s ulcer being the most common. Effective treatment of any leg ulcer depends on treating the underlying cause, and diagnosis is therefore vital. Arterial and venous circulation should be assessed, as should sensation throughout the lower limb. Surgical treatment is only indicated if non-operative treatment has failed or if the patient suffers from intractable pain. Meshed skin grafts (Figure 3.7) are more successful than sheet grafts and have the advantage of allowing mobili­ sation, as any tissue exudate can escape through the mesh. It should be stressed that the recurrence rate is high in venous ulceration, and patient compliance with a regime of hygiene, elevation and elastic compression is essential.

●●

●●

●●

Ischium Greater trochanter Sacrum Heel Malleolus (lateral then medial) Occiput

TABLE 3.2  Staging of pressure sores. Stage

Description

1

Non-blanchable erythema without a breach in the epidermis

2

Partial-thickness skin loss involving the epidermis and dermis

3

Full-thickness skin loss extending into the subcutaneous tissue but not through underlying fascia

4

Full-thickness skin loss through fascia with extensive tissue destruction, maybe involving muscle, bone, tendon or joint

If external pressure exceeds the capillary occlusive pressure (over 30mmHg), blood flow to the skin ceases, leading to tis­ sue anoxia, necrosis and ulceration (Figure 3.9). Prevention

Summary box 3.4 Aetiology of leg ulcers ●●

●●

●●

●● ●● ●●

Venous disease leading to local venous hypertension (e.g. varicose veins) Arterial disease, either large vessel (atherosclerosis) or small vessel (diabetes) Arteritis associated with autoimmune disease (rheumatoid arthritis, lupus, etc.) Trauma – could be self-inflicted Chronic infection – tuberculosis/syphilis Neoplastic – squamous or basal cell carcinoma, sarcoma

Figure 3.9  Pressure ulcer.

Jean-Nicholas Marjolin, 1780–1850, surgeon, Paris, France, described the development of carcinomatous ulcers in scars in 1828.

01_03-B&L27_Pt1_Ch03.indd 29

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CHAPTER 3  Wounds, healing and tissue repair

is obviously the best treatment, with good skin care, special pressure dispersion cushions or foams, the use of low air loss and air-fluidised beds and urinary or faecal diversion in selected cases. Pressure sore awareness is vital, and the bed-bound patient should be turned at least every 2hours, with the wheel­ chair-bound patient being taught to lift themselves off their seat for 10 seconds every 10 minutes. It should be stressed that the most important treatment is to treat the cause of the pressure sore and that surgical treatment is a last resort often doomed to failure if the cause persists. Surgical management of pressure sores follows the same principles involved in acute wound treatment (Summary box 3.4). The patient must be well motivated, clinically stable with good nutrition and adhere to the preventative measures advised postoperatively. Preoperative management of the pressure sore involves adequate debridement, and the use of vacuum-assisted closure (VAC) may help to provide a suitable wound for surgical closure (see below). The aim is to fill the dead space and to provide durable sensate skin. Large skin flaps that include muscle are best and, occasionally, an intact sensory innervated area can be included (e.g. extensor fascia lata flap with lateral cutaneous nerve of the thigh). If possible, use a flap that can be advanced further if there is recurrence and that does not interfere with the planning of neighbouring flaps that may be used in the future.

Vacuum-assisted closure This is now more correctly known as negative pressure wound closure. Applying intermittent negative pressure of approx­ imately −125 mmHg appears to hasten debridement and the formation of granulation tissue in chronic wounds and ulcers. A foam dressing is cut to size to fit the wound. A perforated wound drain is placed over the foam, and the wound is sealed with a transparent adhesive film. A vacuum is then applied to the drain (Figure 3.10). Negative pressure may act by decreasing oedema, by removing interstitial fluid and by increasing blood

flow. As a result, bacterial counts decrease and cell proliferation increases, thereby creating a suitable bed for graft or flap cover.

NECROTISING SOFT-TISSUE INFECTIONS These are rare but often fatal. They are most commonly poly­ microbial infections with Gram-positive aerobes (Staphylococcus aureus, S.pyogenes), Gram-negative anaerobes (Escherichia coli, Pseudomonas, Clostridium, Bacteroides) and beta-haemo­ lytic Streptococcus. There is usually a history of trauma or surgery with wound contamination. Sometimes, the patient’s own defence mechanisms may be deficient. These infections are characterised by sudden presentation and rapid progres­ sion. The fact that deeper tissues are involved often leads to a late or missed diagnosis (Figure 3.11). Clinical signs are shown in Summary box 3.6. There are two main types of necrotising infections: clostrid­ial (gas gangrene) and non-clostridial (streptococcal gangrene and necrotising fasciitis). The variant of necrotising fasciitis with toxic shock syndrome results from Streptococcus pyogenes and is often called the ‘flesh-eating bug’ in this situ­ ation. Treatment consists of appropriate antibiotics with wide surgical excision. Tissue biopsies are essential for histological

Summary box 3.6 Signs and symptoms of necrotising infections ●● ●● ●● ●● ●● ●● ●● ●● ●●

Figure 3.10  Vacuum-assisted closure dressing of a large wound.

Unusual pain Oedema beyond area of erythema Crepitus Skin blistering Fever (often absent) Greyish drainage (‘dishwater pus’) Pink/orange skin staining Focal skin gangrene (late sign) Shock, coagulopathy and multiorgan failure

Figure 3.11  Necrotising fasciitis of the anterior abdominal wall.

Hans Christian Joachim Gram, 1853–1938, Professor of Pharmacology (1891–1900) and of Medicine (1900–1923), Copenhagen, Denmark, described this method of staining bacteria in 1884.

01_03-B&L27_Pt1_Ch03.indd 30

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PART 1 | BASIC PRINCIPLES Avoidable scarring

diagnosis and culture to obtain appropriate antibiotic sensitiv­ ity information. The raw areas resulting from excision often require skin grafting. Treatment is surgical excision, with tis­ sue biopsies being sent for culture and diagnosis. Wide raw areas requiring skin grafting often result.

SCARS The maturation phase of wound healing has been discussed above and represents the formation of what is described as a scar. The immature scar becomes mature over a period lasting a year or more, but it is at first pink, hard, raised and often itchy. The disorganised collagen fibres become aligned along stress lines with their strength being in their weave rather than in their amount (this has been compared with steel wool being slowly woven into a cable). As the collagen matures and becomes denser, the scar becomes almost acellular as the fibro­ blasts and blood vessels reduce. The external appearance of the scar becomes paler, while the scar becomes softer, flattens and its itchiness diminishes. Most of these changes occur over the first three months but a scar will continue to mature for one to two years. Tensile strength will continue to increase but would not be expected to exceed 60–80% that of normal skin. Scars are often described as being atrophic, hypertro­ phic and keloid. An atrophic scar is pale, flat and stretched in appearance, often appearing on the back and in areas of tension. It is easily traumatised as the epidermis and dermis are thinned. Excision and resuturing may only rarely improve such a scar. A hypertrophic scar is defined as excessive scar tissue that does not extend beyond the boundary of the original incision or wound. It results from a prolonged inflammatory phase of wound healing and from unfavourable scar siting (i.e. across the lines of skin tension). In the face, these are known as the lines of facial expression. A keloid scar is defined as excessive scar tissue that extends beyond the boundaries of the original incision or wound (Figure 3.12). Its aetiology is unknown, but it is associated with elevated levels of growth factor, deeply pigmented skin, an

Figure 3.12  Multiple keloid scars.

31

inherited tendency and certain areas of the body (e.g. a trian­ gle whose points are the xiphisternum and each shoulder tip). The histology of both hypertrophic and keloid scars shows excess collagen with hypervascularity, but this is more marked in keloids where there is more type III collagen. The treatment of both hypertrophic and keloid scars is difficult and is summarised in Summary box 3.7. Hypertrophic scars improve spontaneously with time, whereas keloid scars do not. Summary box 3.7 Treatment of hypertrophic and keloid scars ●● ●● ●● ●● ●●

●● ●● ●● a

Pressure – local moulds or elasticated garments Silicone gel sheeting (mechanism unknown) Intralesional steroid injection (triamcinolone) Excision and steroid injectionsa Excision and postoperative radiation (external beam or brachytherapy)a Intralesional excision (keloids only) Laser – to reduce redness (which may resolve in any event) Vitamin E or palm oil massage (unproven)

All excisions are associated with high rates of recurrence.

AVOIDABLE SCARRING If an acute wound has been managed correctly (see Summary box 3.3), most of the problems described above should not occur. However, the surgeon should always stress to the patient that there will be a scar of some description after wounding, be it planned or accidental. A dirt-ingrained (tattooed) scar is usually preventable by proper initial scrubbing and cleans­ ing of the wound (Figure 3.13). Late treatment may require excision of the scar or pigment destruction by laser. Mismatched or misaligned scars result from a failure to rec­ ognise normal landmarks, such as the lip vermilion/white roll interface, eyelid and nostril free margins and hair lines such as

Figure 3.13  Dirt-ingrained scar.

Laseris an acronym for Light Amplification by Stimulated Emission of Radiation. A laser is an intense beam of monochromatic light.

01_03-B&L27_Pt1_Ch03.indd 31

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PART 1 | BASIC PRINCIPLES 32

CHAPTER 3  Wounds, healing and tissue repair

those relating to eyebrows and moustache. Treatment consists of excision and resuturing. Poorly contoured scars can be stepped, grooved or pincush­ ioned. Most are caused by poor alignment of deep structures such as muscle or fat, but trapdoor or pincushioned scars are often unavoidable unless the almost circumferential wound can be excised initially. Late treatment consists of scar exci­ sion and correct alignment of deeper structures or, as in the case of a trapdoor scar, an excision of the scar margins and repair using W or Z-plasty techniques. Suture marks may be minimised by using monofilament sutures that are removed early (3–5 days). Sutures inserted under tension will leave marks. Wounds can be strengthened post suture removal by the use of sticky strips. Fine sutures (6/0 or smaller) placed close to the wound margins tend to leave less scarring. Subcuticular suturing avoids suture marks either side of the wound or incision.

CONTRACTURES

Figure 3.15  Post-traumatic (chainsaw) midline neck contracture.

Where scars cross joints or flexion creases, a tight web may form restricting the range of movement at the joint. This may be referred to as a contracture and can cause hyperextension or hyperflexion deformity (Figure 3.14). In the neck, it may interfere with head extension (Figure 3.15). Treatment may be simple involving, multiple Z-plasties (Figure 3.16), or more complex, requiring the inset of grafts or flaps. Splintage and intensive physiotherapy are often required postoperatively.

Figure 3.16  Multiple Z-plasty release of finger contracture.

FURTHER READING

Figure 3.14  Burn contractures showing hyperextended fingers and hyperflexed elbow.

01_03-B&L27_Pt1_Ch03.indd 32

Brown DL, Borschel GH. Michigan manual of plastic surgery. Baltimore, MD: Lippincott, Williams & Wilkins, 2004. Georgiade GS, Riefkokl R, Levin LS. Georgiade plastic, maxillofacial and reconstructive surgery, 3rd edn. Baltimore, MD: Williams & Wilkins, 1997. McGregor AD, McGregor, IA. Fundamental techniques of plastic surgery, 10th edn. Edinburgh: Churchill Livingstone, 2000. Richards AM, MacLeod T, Dafydd H. Key notes on plastic surgery. Oxford: Wiley-Blackwell, 2012. Thomas S. An introduction to the use of vacuum assisted closure. World Wide Wounds, 2001; available from: www.worldwidewounds.com. Westaby S. Wound care. London: William Heinemann Medical Books Ltd, 1985.

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ve Bailey & Love Bailey & Love Bailey & Love ve Bailey & Love Bailey & Love Bailey & 4 Love Chapter

Tissue engineering and regeneration Learning objectives To understand: •• The potential opportunities afforded by tissue engineering and regenerative medicine •• The nature of stem cells, including somatic and adult stem cells, embryonic stem cells, fetal stem cells and induced pluripotent stem cells

•• The role and range of scaffolds for tissue engineering •• The different approaches for seeding scaffolds and

INTRODUCTION

to provide treatment for a wide range of diseases, including spinal cord injury and neurodegenerative conditions, cardiovascular disease, degenerative retinal conditions, type I diabetes and diseases of the musculoskeletal system. The field of tissue engineering is of particular relevance to surgeons because many of the potential future clinical applications are for conditions where surgeons are closely involved in assessment and treatment (Table 4.1). Selected examples include

Tissue engineering and regenerative medicine are relatively new but rapidly expanding multidisciplinary fields of clinical medicine, which have the potential to revolutionise the treatment of a wide range of human diseases. The ability of tissues to undergo spontaneous repair and regeneration is highly variable but in many cases very limited. Bone, for example, is one of the few tissues able to undergo effective regeneration, so long as the defective tissue is not too extensive. Adjacent cartilage, on the other hand, in common with most tissues, has little or no propensity for spontaneous regeneration, in terms of quality and quantity, following injury or arthritic disease. The limited ability of tissues to repair themselves has driven the desire to develop cell therapy and tissue engineering approaches to repair or replace diseased and damaged tissues. In most cases this involves the implantation of cells and tissues that have been expanded in vitro (outside the body), either as a cell therapy or with cells seeded into natural or synthetically based tissue scaffolds. However, cells (with or without expansion) and cellularised or cell-free scaffolds may also be implanted into areas of tissue injury with the aim of promoting in vivo (inside the body) regeneration and repair of tissues. This chapter provides a brief overview of tissue engineering and regenerative therapy, highlighting the opportunities, challenges and likely future directions.

OPPORTUNITIES The potential impact of tissue engineering and regenerative therapies is so far-reaching that practising surgeons should be aware of the opportunities afforded to improve radically the management of patients. Stem cell therapy has the potential

01_04-B&L27_Pt1_Ch04.indd 33

bioreactor technology

•• The main safety issues and current limitations to clinical application

TABLE 4.1  Examples of tissues created by tissue engineering and conditions they may be used to treat. Tissue

Conditions treated

Skin

Burns and skin defects after excision or trauma

Cardiac muscle

Heart failure

Heart valves

Congenital and acquired valvular heart disease

Cartilage

Degenerative and traumatic joint disorders

Trachea and bronchus

Congenital and acquired stenosis and resection for malignancy

Bladder

Congenital bladder malformation, and cystectomy

Anal/bladder sphincter

Incontinence

Pancreatic islets

Insulin-dependent diabetes

Large blood vessels

Atheromatous, aneurysmal and traumatic arterial disease

Oesophagus

Benign stenosis, and resection for malignancy

Small intestine

Intestinal failure after surgical resection for Crohn’s disease, cancer or ischaemia

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PART 1 | BASIC PRINCIPLES 34

CHAPTER 4  Tissue engineering and regeneration

repair or replacement of injured or diseased cartilage, skin, pancreatic islets, bladder, intestine, heart tissue, arteries, larynx and bronchus. A longer-term goal in tissue engineering is the replacement of diseased whole organs such as the liver and kidney, although the technical challenges here are enormous. Surgeons are integral to many of the multidisciplinary research teams currently undertaking translational research in the field and will play a vital role in the future delivery and assessment of many of the treatments based on tissue engineering and regenerative therapy. In addition to its direct therapeutic application, tissue engineering also has the potential to provide in vitro tissues that can be used to model human disease and to test therapeutic drugs for efficacy and toxicity. It is important to emphasise, however, that while the potential benefit of cell therapy and tissue engineering is undeniable, there are many technical, regulatory and safety issues to be addressed for it to have wide clinical impact. Summary box 4.1 Tissue engineering and regenerative therapies have potential to provide: ●● ●● ●●

Treatment for a wide range of diseases Clinical applications in surgical assessment and treatment Models to test therapeutic efficacy and toxicity

THE KEY AREAS OF UNDERPINNING SCIENCE Advances in both the biological and physical sciences underpin the fields of tissue engineering and regenerative therapy (Figure 4.1). In the biological sciences, new discoveries in stem cell biology have been key, particularly an understanding of the different types of stem cell, and how these can be derived and directed in vitro to differentiate into specialised cell types. In material sciences, major advances in the manu­ facture of scaffolds, on which to seed cells or to encourage specific interaction with host cells, have been key. In particular, design goals relate to scaffolds that possess both the physical and the biological characteristics that allow cells to create tissues, and potentially even organs, for therapeutic purposes. Key also have been engineering advances in the develop-

Engineered tissue

Stem cell biology

Cell signalling biology

Scaffold design

Bioreactor design

Materials science and engineering Cell biology and biochemistry Figure 4.1 Underpinning science in tissue engineering and cell ­therapy.

ment of the many different types of bioreactors that provide an appropriate physical environment for growing engineered tissues in vitro, outside the body in the laboratory. There is considerable commercial interest in tissue engineering and regenerative therapy and this is contributing to the rapid pace of development in these areas. Notwithstanding the potential offered by these therapies, it should be emphasised that the whole field is still at a relatively early stage of development. While there are examples where tissue engineering and regenerative therapies have already been introduced into clinical practice (e.g. for repair of damaged cartilage), most potential regenerative therapies have not yet entered routine surgical practice, as there are considerable barriers to be overcome before this translational step can be achieved.

SOURCE OF CELLS FOR TISSUE ENGINEERING Both fully differentiated cells (somatic cells) and stem cells are being used for tissue engineering and regenerative therapy, but most of the focus is on the use of stem cells, particularly somatic stem cells (SSCs) such as mesenchymal stem cells, and induced pluripotent stem cells (iPSCs). The major features of the different cell types are listed in Table 4.2.

Somatic cells Fully differentiated specialised cells (somatic cells) obtained from normal tissues have been used for tissue engineering and

TABLE 4.2  Cells used in tissue engineering and regenerative therapy. Cell type

Somatic cells

SSCs

hESCs

Fetal cells

iPSCs

Ease of availability

Limited

Good

Moderate

Moderate

Good

Expansion in vitro

Limited

Good

Excellent

Good

Excellent

Pluripotency

No

Limited

Excellent

Limited

Excellent

Ethical concerns

No

No

Yes

Yes

Yes*

Risk of malignancy

None

Low

Moderate

Moderate

Moderate

Autologous

Yes

Yes

No

No

Yes

Likely future use

Limited

High

Limited

Limited

High

hESCs, human embryonic stem cells; iPSCs, induced pluripotent stem cells; SSCs, somatic stem cells. *Note iPSCs avoid some of the ethical issues associated with hESCs.

01_04-B&L27_Pt1_Ch04.indd 34

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PART 1 | BASIC PRINCIPLES Source of cells for tissue engineering

regenerative therapy with some degree of success. For example, skin has been engineered using cultured epithelial cells grown in vitro and used to treat patients with burn injuries. Chondrocytes have been isolated, expanded in vitro, and implanted into areas of deficient cartilage in a procedure called auto­ logous chondrocyte implantation. Bladder wall has also been engineered using a combination of smooth muscle cells and uroepithelial cells expanded in vitro and grown on a scaffold before reimplantation. Such tissues can be grown using cells obtained from the intended recipient by tissue biopsy (auto­ logous cells) or using cells obtained from deceased unrelated donors (allogeneic cells). The major advantage of the former source is that after implantation they are not rejected by the recipient’s immune system and hence there is no requirement for immunosuppression (see Chapter 82 for a description of immunosuppressive agents and their side effects). For other indications, the use of fully differentiated specialised cells is not practical in most situations because such cells are not readily available in sufficient numbers and they have only limited proliferative ability in vitro, which means their numbers cannot be readily expanded to sufficient levels. To overcome these limitations, the major focus in the field of cell therapy has been on the use of stem cells.

Stem cells Stem cells are undifferentiated or non-specialised cells that are able, through cell division, to renew themselves indefin­ itely. Crucially, they are also able, when provided with the appropriate stimuli, to differentiate into one or more of the different types of specialised cell found in tissues and organs. Because of their unique ability to undergo self-renewal when cultured in vitro and to be directed to differentiate into specialised cell types, they have enormous potential for use as cell-based therapies. There are several different types of stem cell with different characteristics, all of which have potential uses in regenerative medicine. Stem cells can be classified according to whether they are derived from the early embryo (embryonic stem cells), tissues from the fetus (fetal stem cells), later in development (adult or somatic stem cells) or whether they are derived by reprogramming adult specialised cells to become pluripotent stem cells (iPSCs).

35

(i.e. they are multipotent). Among the best characterised types of SSCs are haematopoeitic stem cells, mesenchymal stem or stromal cells (MSCs), endothelial progenitor cells and neural stem cells. While haematopoeitic stem cells are widely used for treatment of haematological malignancies, the somatic stem cell type that has been most widely used for tissue engineering and regenerative therapy is the MSC.

Mesenchymal stem and stromal cells MSCs are multipotent stromal cells that can be sourced from a variety of tissues, including bone marrow, adipose tissue and umbilical cord. Morphologically they resemble fibroblasts. They are adherent to plastic, express certain cell surface markers (CD105, CD73 and CD90), and do not express the cell surface markers associated with haematopoietic stem cells (such as CD34 and CD45). MSCs were initially shown to have the ability to be directed to differentiate into a variety of specialised cell types of the mesodermal lineages, including osteoblasts, chondrocytes, adipocytes, tenocytes and myocytes (Figure 4.2). Recent studies suggest that they may also be directed into cells of the ectoderm and endoderm lineages. Of further clinical importance, MSCs have potent trophic and anti-inflammatory properties, attributable to their ability to produce growth factors (including vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF), hepatocyte growth factor (HGF)), and prostaglandin E2. MSCs for therapeutic use can be isolated from bone marrow (iliac crest aspiration) or from subcutaneous fat (liposuction) which is less invasive and gives a high yield of MSCs. In both cases, MSCs are isolated in vitro on the basis of their adherence to plastic. They can then be used either immediately, or after expansion of their numbers by in vitro culture. Alternatively, MSCs can be differentiated into the desired lineage in vitro by addition of suitable growth factors and chemicals. The relative ease of cell acquisition has meant that autologous MSCs have been used clinically in a variety of settings such as treatment of burns and to repair defects in cartilage. More clinical evidence is required in terms of efficacy and mechanism of action, as it is not entirely clear whether a given clinical effect resulting from MSC administration is attributable to their ability to contribute directly to tissue regeneration, or due to immunomodulatory and paracrine effects resulting from their ability to release trophic mediators that promote tissue repair by recipient cells (Figure 4.2).

Adult tissue resident or somatic stem Embryonic stem cells (ESCs) cells (SSCs) In the embryo, stem cells are able to give rise to all of the

Stem cells resident in the different tissues and organs are responsible for providing replacements for specialised cells that have reached the end of their functional lifespan either through natural attrition or because of damage and disease. In certain tissues and organs, notably the bone marrow and gut, stem cells regularly divide and differentiate into specialised cells to replace senescent or damaged cells in the blood and the gastrointestinal mucosa, respectively. Stem cells in other organs, such as the heart or central nervous system, are less able to effect repair or replacement. SSCs have the capacity to differentiate into a limited number of specialised cell types

01_04-B&L27_Pt1_Ch04.indd 35

different cell types of the body (i.e. they are totipotent). ESCs are obtained from the inner cell mass of the early human blastocyst (days 4–5 after fertilisation) using embryos that have been created through in vitro fertilisation for treatment of infertility, and are surplus to those needed for reimplantation. The technique for isolating and growing hESCs in culture was developed by James Thompson at the University of Wisconsin, Madison, USA in 1998. ESCs have much greater proliferative ability than MSCs and, as already noted, can differentiate into all types of specialised cells, unlike MSCs. However, their use has major

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CHAPTER 4  Tissue engineering and regeneration

Osteoblast Mesenchymal stem and stromal cells +ve for CD90, CD73, CD105 –ve for CD34, CD45

Chondrocyte Immunomodulation

Adipocyte

Other Working with other cell populations

Differentiation into multiple lineages Other

Figure 4.2  Proposed characteristics of mesenchymal stem and stromal cells relevant to tissue engineering and regenerative medicine.

limitations, one of which is ethical. The surplus embryos used for derivation of ESCs would otherwise be discarded, but because they need to be destroyed to obtain ESCs the approach has raised major ethical and political debate. The dominant view in many countries, including the UK, is that the potential therapeutic benefits of ESCs justify their use but there are very strict guidelines for their derivation, and to date their clinical use has been very limited. Cells from ESCs would be allogeneic and therefore be at risk of immunological rejection. It would, in principle, be possible to produce ESCs that were autologous for an intended recipient by the process of somatic cell nuclear transfer, i.e. transferring the nucleus from a somatic cell of the intended recipient into an oocyte that has had its nucleus removed. The transferred somatic cell nucleus, containing the human leukocyte antigen (HLA) genes and all of the other genetic information from the donor, is turned into a pluripotent stem cell that can be used as cell therapy for the donor of the nucleus.

Fetal stem cells Stem cells can also be obtained from the blood, bone marrow and other tissues of aborted fetuses (fetal stem cells). These proliferate in vitro as efficiently as ESCs and are pluripotent. They have been used as cell therapy in a variety of clinical settings, including Parkinson’s disease, diabetes and spinal cord injury. In some studies they showed early promise but

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the magnitude of any clinical benefits is controversial. The use of fetal stem cells also poses ethical challenges, although perhaps not to the extent seen with ESCs.

Induced pluripotent stem cells (iPSCs) The discovery in 2006 by Shinya Yamanaka, building on the earlier work of John Gurdon, that certain types of specialised adult cells could be reprogrammed using genetic manipulation to become embryonic-like iPSCs was a major breakthrough. Using retroviral or lentiviral transfection to introduce a combination of transcription factors (OCT3/4, SOX2, and either Kruppel-like factor and C-MYC (together designated the OSKM reprogramming factors) or NANOG and LIN28), it was shown that specialised somatic cells can be reprogrammed to become stem cells. Moreover, iPSCs proliferate in vitro as efficiently as ESCs and are pluripotent, thereby circumventing concerns about the use of human embryos. Importantly, the development of iPSCs also means that, at least in principle, an intended recipient of stem cell therapy can themselves provide a source of stem cells (e.g. from a skin biopsy or blood sample) that can then be directed to differentiate into the desired specialised cell type for therapy; because such cells would be auto­ logous they would not provoke an immunological rejection response (Figure 4.3). Alternatively, iPSCs could be obtained from a number of volunteer donors selected on the basis of their

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PART 1 | BASIC PRINCIPLES Source of cells for tissue engineering

37

Peripheral blood – mononuclear cells Reprogramming factors

Induced pluripotent stem cells (iPSC)

Skin biopsy – keratinocytes

Differentiation factors

Cell therapy

Disease modelling

Differentiated cells Examples include: chondrocytes neurones myocytes pancreatic islet cells

Figure 4.3  Schematic diagram showing the principles of iPSC therapy. Mononuclear cells from peripheral blood or keratinocytes from a skin biopsy are cultured in vitro and then reprogrammed to become iPSC by addition of reprogramming factors. The iPSC are then expanded, and selected differentiation factors added to promote differentiation of iPSCs into the desired specialised cell type for use as therapy.

HLA type and stored to create a national or international tissue bank of iPSCs. Lines of iPSCs could then be chosen from the bank to provide a fully or partially matched cell transplant for recipients, eliminating or reducing the need for immunosuppression to prevent immunological rejection. One of the problems of reprogramming somatic cells to become iPSCs using retroviruses is that genomic integration of the virus may lead to activation of oncogenic genes, causing tumorigenesis. To reduce this risk, non-retroviral vectors have been used (such as adenovirus and Sandai virus vectors, that do not insert their own genes into the host cell genome), or plasmids, episomal vectors and synthetic RNA. There has also been much recent progress in identifying combinations of small molecules, growth factors and chemicals that mimic the effect of viral transfection with transcription factors and obviate the need for viral vectors altogether. The production process from sourcing cells (e.g. skin fibroblasts or peripheral blood mononuclear cells) to obtaining an adequate number of validated iPSCs may take several weeks.

In vitro differentiation of stem cells to specialised tissue cells There is an enormous research effort aimed at better understanding the factors responsible for cell fate decisions, and

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establishing effective and reproducible protocols that can be used to differentiate stem cells in vitro into the desired type of specialised cell. Typically such protocols use culture in chemically defined media containing cocktails of small molecules that stimulate or inhibit key signalling pathways, along with cytokines, growth factors and chemicals. Many protocols include the addition of critical amounts of Activin, bone-morphogenetic protein-4 (BMP4) and fibroblast growth factor-2 (FGF2) at specific time points during culture, but protocols vary widely. For example, exposure of iPSCs to a combination of retinoic acid and BMP4 promotes differentiation along the ectoderm and then the keratinocyte lineage. Alternatively, culture of iPSCs on a Matrigel® scaffold in defined media supplemented with ascorbic acid and exposed sequentially to a glycogen synthase kinase (GSK) inhibitor followed by an inhibitor of Wnt signalling promotes the development of immature cardiomyocytes. It is becoming increasingly clear that exposure to certain biomaterials and the physical attributes of a scaffold, including its surface characteristics, also promote stem cell differentiation along a particular lineage. Mechanical stress also influences cell fate decisions. Protocols for differentiation often promote stem cells to differentiate in steps through intermediate stages that mirror normal in vivo development. In other words, sequential exposure to different factors is used first to differentiate ESCs or

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CHAPTER 4  Tissue engineering and regeneration

iPSCs into either endoderm, mesoderm or ectoderm lineages, followed by further differentiation into the specific lineage desired. After stem cells have been subjected to in vitro differentiation, it is essential that the purity of the differentiated cells and the absence of undifferentiated stem cells are confirmed, to reduce the risk of tumour transmission. The cells must also be fully phenotyped and their function confirmed before they are used for therapeutic purposes.

SCAFFOLDS FOR TISSUE ENGINEERING The complex anatomical arrangement of the different cell types in tissues and organs is absolutely integral to their normal function, and the importance of structural integrity is evident in many diseases where deranged tissue structure and tissue remodelling is associated with a failure in function. Stem cells and their progeny are able, when cultured under conventional tissue culture conditions, to form cell sheets or small three-dimensional collections of cells (organoids), but they are not able under such conditions spontaneously to assume the complex anatomical relationships seen in normal tissues. To do so they need to be provided with an appropriate scaffold that gives physical support and shape to the engineered tissue, mimicking extracellular matrix. This allows cells to attach, and delivers the cell signals necessary to guide the cell growth, migration and differentiation to form a functional tissue. Tissue engineering typically utilises rigid or semi-rigid scaffolds (usually three-dimensional) that are porous (Figure 4.4) and act as templates on which to (a)

(b)

Figure 4.4 An example of a porous scaffold in research development, manufactured using collagen. (a) Macroscopic view of collagen scaffold. (b) Overview of a scanning electron microscopy (SEM) image that shows the structure of collagen scaffold (courtesy of Prof S Best and Prof R Cameron, University of Cambridge).

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seed donor cells and guide them to restore a functional tissue or organ that can then be implanted in the recipient. Scaffolds may be derived from intact human tissue (natural scaffolds) or from engineered implantable biomaterials (artificial scaffolds). The general requirements that a scaffold must provide are listed in Table 4.3, and the choice of scaffolds that best fulfils the requirements for tissue engineering will depend on the nature of the tissue to be engineered.

TABLE 4.3  Requirements of a scaffold used in tissue engineering. Provide structural support for cells Allow cells to attach, migrate and proliferate Enable oxygen, nutrients and regulatory factors access to all cells Deliver signals to promote cell migration and proliferation Biocompatible, non-immunogenic and ideally biodegradable

Summary box 4.2 Regenerative scaffolds can: ●● ●● ●●

Provide physical support and shape to the engineered tissue Guide cell growth, migration and differentiation Be natural or artificial

Natural scaffolds Natural scaffolds may be obtained by treatment of human (or other animal) tissues or organs to remove the resident cell types, leaving behind the extracellular matrix that preserves the intricate architecture of the tissue or organ, onto which to seed new cells. Natural scaffolds not only act as a physical scaffold that allows the natural architecture of the tissue to be preserved, but they may also provide key cell signals that guide the growth and differentiation of the cells used to repopulate the scaffold. Typically, natural scaffolds are obtained either by immersing tissues in detergent or perfusing them with detergent via the arterial tree. This effectively destroys most or all of the cellular elements of the tissue or organ but leaves the collagen-rich extracellular matrix largely intact. Variable protocols have been used successfully to achieve decellurisation, and the optimal approach probably varies according to the type of tissue or organ being used to create the scaffold. The use of natural scaffolds may be particularly suited to certain applications where deceased donor tissue is relatively easy to source, for example to engineer lengths of trachea. The use of natural scaffolds to engineer whole organs such as the kidney or liver has the advantage that the extremely intricate three-dimensional structure of the organ is preserved and this would be extremely challenging to achieve using engineered biocompatible materials. Moreover, decellularised organ scaffolds provide an opportunity to repopulate the scaffold with autologous cells derived from the potential recipient to create an organ that is not susceptible to immunological rejection, thereby avoiding the need for immunosuppressive drugs and their attendant side effects. However, a significant

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PART 1 | BASIC PRINCIPLES Scaffolds for tissue engineering

disadvantage of using decellularised scaffolds to engineer whole organs is the need to use a whole human organ for each organ to be engineered; the availability of such organs is likely to be limited. Summary box 4.3 Natural scaffolds: ●●

●●

Can be prepared by removal of the resident cell types from tissue, for example with detergent Consist of tissue extracellular matrix, which can preserve intricate anatomical structures

Artificial scaffolds The materials used to create artificial scaffolds are highly variable, and new materials are being developed continually. Different scaffold characteristics are required for engineering different types of tissue but all scaffolds need to be biocompatible and in most settings they should be biodegradable and bioreabsorbable. Scaffolds encompass both natural and synthetic materials. Natural materials used include various polysaccharides, collagen, fibrin, gelatin and cellulose, while synthetic materials include various synthetic polymers such as polylactide (PLA) and polyglycolide (PGA), and graphene. Bioactive ceramics such as calcium phosphates (e.g. hydroxyapatite) and bioactive glasses have been widely used for skeletal repair. Synthetic biodegradable polymers are commonly used and have the advantage that they can be produced under standard conditions that ensure reproducible physical characteristics. Scaffolds can also be fabricated using a blend of natural and synthetic components to optimise their performance. Most artificial scaffolds are fabricated with a porous three-dimensional structure, and a wide variety of designs are in use. The application of computational design and three-­ dimensional printing technology has revolutionised the ­development of artificial scaffolds. Hydrogel scaffolds composed of cross-linked hydrophilic polymers are also increasingly used in tissue engineering because of their favourable physical and chemical characteristics. They are able to absorb very large amounts of aqueous fluid while maintaining their three-dimensional shape and structural integrity. They are fabricated from naturally occurring (e.g. collagen and fibrin) or artificial (egg PLA) cross-linked polymers and can be impregnated with growth factors to promote cellularisation. Electrospinning technology is being utilised increasingly to produce scaffolds composed of fibres with a diameter at the nanoscale level. The fibres can be spun using blends of different synthetic polymers or blends of synthetic and natural polymers, depending on the desired characteristics of the scaffold. Scaffolds based on microspheres have also been utilised. Recent developments in materials science have led to the creation of increasingly complex and innovative artificial scaffolds for tissue engineering, including composite materials (e.g. combining ceramics with polymers to gain the advantages of each), and the production of so called ‘smart scaffolds’ having biomimetic properties that provide biophysical cues or cellular signals to instruct and guide cell behaviour.

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39

Historically, a limitation of traditional artificial scaffolds is that they do not incorporate a vasculature that can be used in the potential recipient to restore the vascular integrity of the transplanted tissue or organ. However, recent innovations that allow a vascular network to be created by three-dimensional printing suggest that this limitation may be overcome. Such technology also allows the design and production of scaffolds that have the structural properties (e.g. pore size and diffusion characteristics) needed to provide the necessary cues for cell differentiation and migration. Artificial scaffolds can be engineered to incorporate molecules that aid retention of particular cell growth factors, including angiogenic growth factors such as vascular endothelial growth factor (VEGF), to provide a local environment conducive to the growth of a functional tissue construct.

Summary box 4.4 Artificial scaffolds include: ●●

●●

Natural materials, synthetic polymers, bioactive ceramics and glasses New or ‘smart’ materials that have biomimetic properties

Approaches to cell seeding of scaffolds and bioreactors Cellularisation of scaffolds can be achieved in vitro (outside the body) by a variety of methods and the most appropriate seeding system may to some extent depend on the type of tissue being engineered (Table 4.4). This is a rapidly developing area and it is only possible here to outline the principles of different approaches to cell seeding. The aim is to achieve a rapid seeding of viable cells with high seeding efficiency and uniform and effective penetration of cells into the scaffold. Some systems incorporate mechanisms to deliver mechanical stress or electrical stimulation to promote cellularisation. The most simple but possibly least effective method is static cell seeding, where a concentrated cell suspension is placed in direct contact with the scaffold. The seeding efficiency and penetration of cells into the scaffold are generally low, although scaffolds can be coated with various agents to increase the efficiency of cell attachment. Dynamic cell seeding techniques include a range of systems in which either the scaffold is rotated in the medium containing the cells or both the scaffold and cell suspension are rotated together. Rotation in some systems occurs at

TABLE 4.4  Approaches for seeding cells into scaffolds. Static cell seeding Dynamic cell seeding Magnetic cell seeding Pressure and vacuum seeding Photopolymerised hydrogels Bioreactor perfusion systems

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CHAPTER 4  Tissue engineering and regeneration

a sufficiently high speed to generate centrifugal forces. Dynamic seeding techniques increase seeding efficiency, shorten the duration of the culture period needed and may help penetration of cells into the scaffold. Magnetic cell seeding makes use of magnetic forces to direct cells into the scaffold. Essentially, the cells are first labelled, either by using supramagnetic microbeads coated with a ligand that specifically binds to molecules on the cell surface or by culturing them with cationic liposomes that contain supramagnetic ferrous particles. Magnets are then used to attract the cells into the scaffold. This enables rapid seeding of the scaffold but a potential concern is that the magnetic particles used may have adverse effects. Photopolymerised hydrogel scaffolds offer a completely different approach to cell seeding. Essentially, the cells are suspended in an aqueous monomer solution and ultraviolet light is used to promote polymerisation of the hydrogel scaffold. Alternatively, to increase cell adherence to the surface of polymerised hydrogel scaffolds, an arginine–glycine–aspartic acid adhesion peptide can be incorporated. Another approach to cell seeding uses differential pressure or vacuum seeding systems to force cells into the pores of the scaffold. Again this reduces the time needed to seed cells but the pressures used may potentially reduce cell viability. Finally, one of the more complex approaches to cell seeding is to use scaffold perfusion systems. These may take the form of bioreactor perfusion systems for tissue engineering, or whole organ perfusion systems in the case of decellularised organ scaffolds.

CHALLENGES TO ENGINEERING TISSUE IN VITRO There are many technical challenges to successful engineering of tissues in vitro. Delivery of adequate oxygen and nutrients uniformly to three-dimensional tissue constructs is problematic, as is ensuring that the varying nutritional and growth requirements of different cell types grown simultaneously are met. The difficulties of tissue engineering vary considerably according to the nature of the tissue or organ being engineered. Flat tissues such as skin, cornea and cartilage present fewer problems than complex tubular structures such as trachea, bronchus and blood vessels. Hollow organs, such as bladder and gut, present a much greater challenge, and complex solid organs such as the liver and kidney present the greatest challenge of all. Obtaining adequate numbers of differentiated cells, maintaining their viability and ensuring that they maintain their function and do not revert to undesirable cell types are all important challenges.

IMPLANTATION OF ENGINEERED TISSUE Irrespective of the nature of the engineered scaffold and the cell types used to populate it, after it is implanted it will only effect successful repair if it becomes fully integrated into adjacent normal tissue and can be remodelled appropriately

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in the recipient. An important consideration that is often not addressed sufficiently is that many tissues in the body, notably tissues in the musculoskeletal system and the cardio­ vascular system, are subject to considerable mechanical stress. Engineered tissues are not subjected to relevant mechanical stresses during their fabrication in vitro and their behaviour in response to mechanical loading after implantation is a major determinant of their ability to perform successfully. The development of innovative high-resolution three-dimensional imaging techniques to evaluate engineered tissue before and after implantation is key to refining the design of engineered tissues and assessing their functional integration after implantation.

SAFETY CONCERNS The major safety concerns of cell-based therapy and tissue engineering are listed in Table 4.5. One of the most serious concerns is that of tumour formation and malignant transformation. The risk of tumour formation varies according to the cell type used, the genetic modification strategy used to transform the stem cells, the site of transplantation and whether the cells are autologous or allogeneic. The direct risk of tumour formation by the transplanted cells relates specifically to ESCs and iPSCs and there appears to be little risk with SSCs. The ability of stem cells to form teratomas is one of the hallmarks of pluripotency, and the risk of this happening following stem cell therapy may be reduced by ensuring that only cells that have been fully differentiated in vitro and not those that are still pluripotent are used for therapy. The risk of malignancy may also be reduced by the choice of in vitro strategy used to differentiate stem cells prior to use: use of viral vectors that do not integrate into the genome or of non-viral approaches to differentiation reduces the risk of malignant transformation. There is also interest in developing techniques for directly reprogramming somatic cells to adopt the function of a different cell type without having to make them first revert back to the pluripotent state – so-called transdifferentiation. Another major concern is that of transmitting infection. It is essential that if allogeneic stem cells are used they are screened to exclude infection and that cells and engineered tissues are prepared according to Good Manufacturing Practice (GMP) guidelines to avoid bacterial infection during in vitro culture prior to use. As already noted, if allogeneic stem cells are used for tissue engineering and regenerative therapy they may be susceptible to graft rejection, and immunosuppressive therapy may be necessary. TABLE 4.5  Risks of cell-based therapy. Tumour formation Genetic and epigenetic abnormalities Transmission of infection Poor viability and loss of function Differentiation to undesired cell-types Rejection (allogeneic cells) Side effects of immunosuppression (allogeneic cells)

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PART 1 | BASIC PRINCIPLES Further reading

FUTURE DIRECTIONS Tissue engineering and regenerative strategies hold out great hope for effectively repairing or replacing tissues in a wide number of human diseases. The field is moving rapidly, underpinned by new developments in stem cells and scaffold design. The use of mesenchymal stem and stromal cell based therapies and iPSC based therapies is likely to dominate, in conjunction with improved bioactive scaffold designs that can be reproducibly manufactured and seeded, sometimes with multiple cell types, by sophisticated bioreactors that incorporate dynamic culture systems. It is likely that patient stratification will further refine therapy options. The ability to phenotype, to genotype and to profile patients at a molecular level will allow more detailed characterisation of patient subgroups and staging of disease. This would refine the surgical approach to many diseases, including regenerative procedures. Over the next decade it is likely that major advances will be made in the clinical translation of tissue engineering and regenerative therapies across a broad range of applications. Numerous clinical studies are currently being undertaken, many with promising early results, and the number of studies

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is set to rise considerably. However, caution is required and there are many examples where engineered tissues have failed to live up to their early promise. The pace of development is so rapid that regulatory authorities will have difficulty keeping up. It is important that the clinical use of tissue engineering is subject to rigorous evaluation, and that novel developments are only used in the context of appropriate clinical trials where the potential benefits and limitations are fully examined before they are introduced into routine clinical practice. The field is becoming increasingly commercialised and the cost and practicality of regenerative therapies, especially personalised autologous therapies, will need to be addressed.

FURTHER READING Fisher S. Handbook of regenerative medicine and tissue engineering. New York: Hayle Medical, 2015. Giannoudis P, Jones E, Yang X, McGonagle D. Mesenchymal stem cells and skeletal regeneration. Cambridge: Academic Press, 2013. Van Blitterswijk C, Jan De Boer J. Tissue engineering, 2nd edn. Amsterdam: Elsevier, 2015. Warburton D. Stem cells, tissue engineering and regenerative medicine. Singapore: World Scientific, 2014.

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Bailey & Love Bailey & Love Bailey & Love Bailey &5Love Bailey & Love Bailey & Love Chapter

Surgical infection Learning objectives To understand: •• The characteristics of the common surgical pathogens and their sensitivities •• The factors that determine whether a wound will become infected •• The classification of sources of infection and their severity •• The clinical presentation of surgical infections •• The indications for and choice of prophylactic antibiotics •• The spectrum of commonly used antibiotics in surgery and the principles of therapy To learn: •• Koch’s postulates

•• The management of abscesses

HISTORY OF SURGICAL INFECTION

even later to the Romans, was that, whenever pus was 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 of laudable pus 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. An understanding of the causes of infection came in the nineteenth century. Microbes had been seen under the

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 using their skills in mummification. 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

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 hospital acquired infections

Hippocrateswas 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. Galen, 130–200, Roman physician, 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, amongst them anatomy, medicine, pathology and philosophy. His work affected medical thinking for 15 centuries after his death. (Gladiator is Latin for ‘swordsman’.) Theodoric of Cervia. Theodoric, 1210–1298, Bishop of Cervia, published a book on surgery ca. 1267. Ambroise Paré, 1510–1590, French military surgeon, also worked at the Hotel Dieu, Paris, France. Guy de Chauliac, ?1298–1368, physician and chaplain to Pope Clement VI at Avignon, France and the author of Chirurgia Magna, which was published about 1363.

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ve ve

PART 1 | BASIC PRINCIPLES History of surgical infection

microscope, but Koch laid down the first definition of infective disease (Koch’s postulates). 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 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. 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% to under 2% by the simple act of hand washing between cases, particularly between postmortem examinations and the delivery suite. He was ignored by his contemporaries and died at the age of 47 in an insane asylum before the value of his work was accepted two decades later with the recognition that infections were caused by microbes. 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 twentieth 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 his mouth while pruning roses and developed

43

abscesses of the face and eyes leading to a severe staphylococcal bacteraemia. He responded to treatment and made a partial recovery before the limited batch of penicillin ran out, following which he 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 b-lactamases, which break up the b-lactam ring present in the molecular structure of many antibiotics. The acquisition of extended spectrum b-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 over 90% 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 in such cases. 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 heavily contaminated wounds

Surgical site infection in patients who have contaminated wounds, who are immunosuppressed or who are 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 use of prophylactic

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, French chemist, bacteriologist and immunologist, Professor of Chemistry at the Sorbonne, Paris, France. Joseph Lister (Lord Lister), 1827–1912, Professor of Surgery, Glasgow, Scotland (1860–1869), Edinburgh, Scotland (1869–1877) and King’s College Hospital, London (1877–1892). Sir Alexander Fleming, 1881–1955, Professor of Bacteriology, St Mary’s Hospital, London, England, discovered Penicillium notatum in 1928. Howard Walter Florey (Lord Florey of Adelaide), 1898–1968, Professor of Pathology, the University of Oxford, Oxford, England. Sir Ernst Boris Chain, Professor of Biochemistry, Imperial College, London, England. Fleming, Florey and Chain shared the 1945 Nobel Prize for Physiology or Medicine for their work on penicillin. Hans Christian Joachim Gram, 1853–1938, Professor of Pharmacology (1891–1900) and of Medicine (1900–1923), Copenhagen, Denmark, described this method of staining bacteria in 1884.

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CHAPTER 5  Surgical infection

antibiotics in clean, non-prosthetic surgery is of less value as infection rates are low and the indiscriminate use of antibiotics simply encourages the emergence of resistant strains of bacteria.

MICROBIOLOGY OF SURGICAL INFECTION Common bacteria causing surgical infection Streptococci Streptococci form chains and are Gram positive on staining (Figure 5.1). The most important is the b-haemolytic Streptococcus, which resides in the pharynx of 5–10% of the population. In the Lancefield A–G carbohydrate antigens classification, it is the group A Streptococcus, also called Streptococcus pyogenes, that is the most pathogenic. It has the ability to spread, causing cellulitis, and to cause tissue destruction through the release of enzymes such as streptolysin, streptokinase and streptodornase. Streptococcus faecalis is an enterococcus in Lancefield group D. It is often found in synergy with other organisms, as are the g-haemolytic Streptococcus and Peptostreptococcus, which is an anaerobe. Both Streptococcus pyogenes and Streptococcus faecalis may be involved in wound infection after large bowel surgery, but the a-haemolytic Streptococcus viridans is not associated with wound infections. All the streptococci remain sensitive to penicillin and erythromycin. The cephalosporins are a suitable alternative in patients who are allergic to penicillin.

Figure 5.2  Staphylococcal pus.

Staphylococci

hospital workers, a potential source of infection after surgery. In parts of northern Europe, the prevalence of MRSA infections has been kept at very low levels using ‘search and destroy’ methods, which use screening techniques to look for MRSA in patients before they come in to hospital for elective surgery so that any carriers can be treated before their admission for surgery. Local policies on the management of MRSA depend on the prevalence of MRSA, the type of hospital, the clinical specialty and the availability of facilities. Widespread swabbing, ward closures, isolation of patients and disinfection of wards by deep cleaning all have to be carefully considered. Staphylococcal infections are usually suppurative and localised. Most hospital Staphylococcus aureus strains are now b-lactamase producers and so are resistant to penicillin, but many strains remain sensitive to flucloxacillin, vancomycin, aminoglycosides and some cephalosporins. There are several novel and innovative antibiotics becoming available that have high activity against resistant strains. Some have the advantage of good oral activity (linezolid), some have a wide spectrum (teicoplanin), some have good activity in bacteraemia (daptomycin) but all are relatively expensive, and some have side effects involving marrow, hepatic and renal toxicity. Their use is justified but needs to be controlled by tight local policies and guidelines that involve clinical microbiologists. Staphylococcus epidermidis (previously Staphylococcus albus), also known as coagulase-negative staphylococcus, was regarded as a non-pathogenic commensal organism commonly found on the skin, but is now recognised as a major threat in vascular and orthopaedic prosthetic surgery and in indwelling vascular cannulas/catheters. The bacteria form biofilms which adhere to prosthetic surfaces and limit the effectiveness of antibiotics.

Staphylococci form clumps and are Gram positive (Figure 5.2). Staphylococcus aureus is the most important pathogen in this group and is found in the nasopharynx of up to 15% of the population. It can cause suppuration in wounds and around implanted prostheses. Some strains are resistant to many common antibiotics (especially methicillin resistant Staphylococcus aureus, MRSA) and so are difficult to treat. MRSA can be found in the nose of asymptomatic carriers amongst both patients and

Clostridial organisms are gram-positive, obligate anaerobes, which produce resistant spores (Figure 5.3). Clostridium perfringens is the cause of gas gangrene, and C.tetani causes tetanus after implantation into tissues or a wound. Clostridium difficile is the cause of pseudomembranous colitis, where destruction of the normal colonic bacterial flora by

Figure 5.1 Streptococci.

Clostridia

Rebecca Graighill Lancefield, 1895–1981, American bacteriologist, classified streptococci in 1933.

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fragilis is the principal organism that acts in synergy with aerobic gram-negative bacilli to cause SSIs, including intraabdominal abscesses after colorectal or gynaecological surgery. They are sensitive to the imidazoles (e.g. metronidazole) and some cephalosporins (e.g. cefotaxime).

Sources of infection

Figure 5.3  Clostridium tetani (drumstick spores).

antibiotic therapy allows an overgrowth of the normal gut commensal C.diff to pathological levels. Any antibiotic may cause this phenomenon, although the quinolones such as ciprofloxacin seem to be the highest risk, especially in elderly or immunocompromised patients. In its most severe form, the colitis may lead to perforation and the need for emergency colectomy with an associated high mortality. Treatment involves resuscitation and antibiotic therapy with metronidazole or vancomycin. The fibrinous exudate is typical and differentiates the colitis from other inflammatory diseases; laboratory recognition of the toxin is an early accurate diagnostic test.

Aerobic gram-negative bacilli These bacilli are normal inhabitants of the large bowel. Escherichia coli and Klebsiella spp. are lactose fermenting; Proteus is non-lactose fermenting. Most organisms in this group act in synergy with Bacteroides to cause SSIs after bowel operations (in particular, appendicitis, diverticulitis and peritonitis). Escherichia coli is a major cause of urinary tract infection, although most aerobic gram-negative bacilli can be involved, particularly in relation to urinary catheterisation. There is increasing concern about the development of extended spectrum b-lactamases (ESBLs) in many of this group of bacteria, which confer resistance to many antibiotics, particularly cephalosporins. Pseudomonas spp. tend to colonise burns and tracheostomy wounds, as well as the urinary tract. Once Pseudomonas has colonised wards and intensive care units, it may be difficult to eradicate. Surveillance of cross-infection is important in outbreaks. Hospital strains become resistant to b-lactamase as resistance can be transferred by plasmids. Wound infections need antibiotic therapy only when there is progressive or spreading infection with systemic signs. The aminoglycosides and the quinolones are effective, but some cephalosporins and penicillin may not be. Many of the carbapenems (e.g. meropenem) are useful in severe infections.

Bacteroides Bacteroides are non-spore-bearing, strict anaerobes that colonise the large bowel, vagina and oropharynx. Bacteroides

The infection of a wound can be defined as the invasion of organisms into tissues following a breakdown of local and systemic host defences, leading to either cellulitis, lymphangitis, abscess formation or 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 before, during or after 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 endogenous or exogenous, depending on the source of the bacterial contamination. Endogenous organisms are present on or in the patient at the time of surgery, whereas exogenous organisms come from outside the patient. In modern hospital practice, endogenous organisms colonising the patient are by far the most common source of infection. Summary box 5.3 Classification of sources of infection ●●

●●

Endogenous: present in or on the host e.g. SSSI following contamination of the wound from a perforated appendix Exogenous: 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). The cause of hospital acquired infection (HAI)

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.

Theodor Albrecht Edwin Klebs, 1834–1913, Professor of Bacteriology successively at Prague, Czechoslovakia, Zurich, Switzerland and The Rush Medical College, Chicago, IL, USA.

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CHAPTER 5  Surgical infection

All of these natural mechanisms may be compromised by surgical intervention and treatment. 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. The more virulent the organism or the larger the extent of bacterial contamination, the more likely is wound infection to occur. Host factors are also important, so a less virulent organism or a lower level of wound contamination may still result in a wound infection if the host response is impaired (see Summary box 5.5). 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 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 5.4 Factors that determine whether a wound will become infected ●● ●● ●●

●● ●●

immunosuppression caused by radiotherapy, chemotherapy or steroids (Figures 5.4 and 5.5). Summary box 5.5 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)

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

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’

The decisive period There is up to a 4-hour interval before bacterial growth becomes established enough to cause an infection after a breach in the tissues, whether caused by trauma or surgery. This interval is called the ‘decisive period’ and 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, before bacterial growth takes a hold. The tissue levels of antibiotics during the period when bacterial contamination is likely to occur should be above the minimum inhibitory concentration (MIC90) for the expected pathogens.

Figure 5.4  Major wound infection and delayed healing presenting as a faecal fistula in a patient with Crohn’s disease on steroid treatment.

Reduced resistance to infection Reduced resistance to infection has several causes, particularly those that impair the inflammatory response. 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 immmune deficiency syndrome (AIDS) are other contributors to infection and a poor healing response, as are iatrogenic causes including the

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Figure 5.5  Delayed healing relating to infection in a patient on highdose steroids.

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can be one cause of a harmful systemic inflammatory response through the excessive release of proinflammatory cytokines and activation of macrophages (Figure 5.6). In the circumstances 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 regimes have been used. Cytokine release

MODS SIRS Figure 5.7  Major wound infection with superficial skin dehiscence.

IL-6, TNF, etc.

Macrophage

Release of endotoxin

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

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

Figure 5.6  Gut failure, colonisation and translocation related to the development of systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). IL, interleukin; TNF, tumour necrosis factor.

Minor wound infections may discharge pus or infected serous fluid but are not associated with excessive discomfort, systemic signs or delay in return home (Figure 5.8). The differentiation between major and minor and the definition of SSI is important in audits and clinical 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 1year after implanted hip and knee surgery.

PRESENTATION OF SURGICAL INFECTION Major and minor surgical site infection (SSI) Infection acquired from the environment or the staff following surgery or admission to hospital is termed hospital acquired 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. 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 5.7). The patient may have systemic signs such as tachycardia, pyrexia and a raised white cell count. Summary box 5.6 Major wound infections ●● ●● ●●

Significant quantity of pus Delayed return home Patients are systemically ill

Figure 5.8  Minor wound infection that settled spontaneously without antibiotics.

Localised infection ABSCESS An abscess presents all the clinical features of acute inflammation originally described by Celsus: calor (heat), rubor (redness), dolor (pain) and tumor (swelling). To these can be added functio laesa (loss of function: if it hurts, the infected part is not used). Abscesses 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.

Aulus Aurelius Cornelius Celsus, 25 BC–50 AD, Roman surgeon and the author of De Re Medico Libri Octo.

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CHAPTER 5  Surgical infection

TABLE 5.1  Southampton wound grading system. Grade

Appearance

Normal healing

I

Normal healing with mild bruising or erythema

Ia

Some bruising

Ib

Considerable bruising

Ic

Mild erythema

II

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 (≤2cm)

IIIb

Along wound (>2cm)

IIIc

Large volume

IIId

Prolonged (>3days)

Major complication IV

Pus

IVa

At one point only (≤2cm)

IVb

Along wound (>2cm)

V

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

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% of SSIs present after the patient has left hospital and may thus be overlooked by the surgical team. 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. Summary box 5.7 Abscesses

TABLE 5.2  The ASEPSIS wound score.

●●

Criterion

Points

Additional treatment

Antibiotics for wound infection

10

Drainage of pus under local anaesthesia

5

Debridement of wound under general anaesthesia

10

Serous dischargea

Daily 0–5

Erythema

Daily 0–5

a

Purulent exudatea Separation of deep tissues

Daily 0–10 a

Daily 0–10

Isolation of bacteria from wound

10

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

5

a

 Scored for 5 of the first 7 days only, the remainder being scored if present in the first 2 months.

Pyogenic organisms, predominantly Staphylococcus aureus, cause tissue necrosis and suppuration. Pus is composed of dead and dying white blood cells, predominantly neutrophils, that have succumbed to bacterial toxins. An abscess is surrounded by an acute inflammatory response composed of a fibrinous exudate, oedema and the cells of acute inflammation. Granulation tissue (macrophages, fibroblasts and new blood vessel proliferation) 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.

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●●

●●

●●

Abscesses need drainage Modern imaging techniques may allow guided needle aspiration Antibiotics are indicated if the abscess cavity is not left open to drain freely An open abscess cavity heals by secondary intention

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, and 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 5.9). Plain or contrast radiographs may not be helpful, but ultrasonography, computed tomo­graphy (CT), magnetic resonance imaging (MRI) and isotope labelled white cell scans are all useful and may allow guided aspiration without the need for surgical intervention. CELLULITIS AND LYMPHANGITIS Cellulitis is a non-suppurative, invasive infection of tissues, which is usually related to the point of injury.There is poor localisation in addition to the cardinal signs of spreading inflammation. Such infections presenting in surgical practice

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Figure 5.10 Streptococcal cellulitis of the leg following a minor puncture wound.

Figure 5.9 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).

are typically caused by organisms such as b-haemolytic streptococci (Figure 5.10), staphylococci (Figure 5.11) and C. perfringens. Tissue destruction, gangrene and ulceration may follow, which are caused by release of proteases. Systemic signs (the old-fashioned term is toxaemia) are common, with chills, fever and rigors. These events follow the release of toxins into the circulation, which stimulate a cytokine-mediated systemic inflammatory response even though blood cultures may be negative. Lymphangitis is part of a similar process and presents as painful red streaks in affected lymphatics draining the source of infection. Lymphangitis is often accompanied by painful lymph node groups in the related drainage area. Summary box 5.8 Cellulitis and lymphangitis ●● ●●

●●

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

Specific local wound infections GAS GANGRENE Gas gangrene is caused by C.perfringens. These gram-posi­tive, anaerobic, spore-bearing bacilli are widely found in nature, particularly in soil and faeces. This infection is particularly relevant to military and trauma surgery. Patients who are immunocompromised, diabetic or have malignant disease are at greater risk, particularly if they have wounds containing

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Figure 5.11  Staphylococcal cellulitis of the face and orbit following severe infection of an epidermoid cyst of the scalp.

necrotic or foreign material, resulting in anaerobic conditions. Military wounds provide an ideal environment as the kinetic energy of high-velocity missiles or shrapnel causes extensive tissue damage. The cavitation which follows passage of a missile through the tissues causes a ‘sucking’ entry wound, leaving clothing and environmental soiling in the wound in addition to devascularised tissue. Gas gangrene wound infections are associated with severe local wound pain and crepitus (gas in the tissues, which may also be visible on plain radiographs). The wound produces a thin, brown, sweet-smelling exudate, in which Gram staining will reveal bacteria. Oedema and spreading gangrene follow the release of collagenase, hyaluronidase, other proteases and alpha toxin. Early systemic complications with circulatory collapse and organ failure follow if prompt action is not taken. Summary box 5.9 Gas gangrene ●● ●● ●● ●●

Caused by Clostridium perfringens Gas and smell are characteristic Immunocompromised patients are most at risk Antibiotic prophylaxis is essential when performing amputations to remove dead tissue

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CHAPTER 5  Surgical infection

Antibiotic prophylaxis should always be considered in patients at risk, especially when amputations are performed for peripheral vascular disease with open necrotic ulceration. Once gas gangrene infection is established, large doses of intravenous penicillin and aggressive debridement of affected tissues are required. CLOSTRIDIUM TETANI This is another anaerobic, terminal spore-bearing, grampositive bacterium, which can cause tetanus following implantation into tissues or a wound (which may have been trivial or unrecognised and forgotten). The spores are widespread in soil and manure, and so the infection is more common in traumatic civilian or military wounds. The signs and symptoms of tetanus are mediated by the release of the exotoxin tetanospasmin, which affects myoneural junctions and the motor neurones of the anterior horn of the spinal cord. A short prodromal period, which has a poor prognosis, leads to spasms in the distribution of the short motor nerves of the face followed by the development of severe generalised motor spasms including opsithotonus, respiratory arrest and death. A longer prodromal period of 4–5 weeks is associated with a milder form of the disease. The entry wound may show a localised small area of cellulitis. Exudate or aspirate may give a sample that can be stained to show the presence of gram-positive rods. Prophylaxis with tetanus toxoid is the best preventative treatment but, in an established infection, minor debridement of the wound may need to be performed and antibiotic treatment with benzylpenicillin provided in addition. Relaxants may also be required, and the patient will require ventilation in severe forms, which are associated with a high mortality. The administration of antitoxin using human immunoglobulin ought to be considered for both at-risk wounds and established infection. The toxoid is a formalin-attenuated vaccine and should be given in three separate doses to give protection for a 5-year period, after which a single 5-yearly booster confers immunity. It should be given to all patients with open traumatic wounds who are not immunised. At-risk wounds are those when there is late presentation, when there is devitalisation of tissue or when there is wound soiling. For these wounds, a booster of toxoid should be given or, if the patient is not immunised at all, a three-dose course is given together with prophylactic benzylpenicillin, but the use of antitoxin is controversial because of the risk of toxicity and allergy. SYNERGISTIC SPREADING GANGRENE (SYNONYM: SUBDERMAL GANGRENE, NECROTISING FASCIITIS) This condition is not caused by clostridia. A mixed pattern of organisms is responsible: coliforms, staphylococci, Bacteroides spp., anaerobic streptococci and peptostreptococci have all been implicated, acting in synergy. Often, aerobic bacteria destroy the living tissue, allowing anaerobic bacteria to thrive. Abdominal wall infections are known as Meleney’s synergistic gangrene and scrotal infections as Fournier’s gangrene (Figure 5.12). Patients are almost always immunocompro-

mised, with conditions such as diabetes mellitus. The wound initiating the infection may have been minor, but severely contaminated wounds are more likely to be the cause. Severe wound pain, signs of spreading inflammation with crepitus and smell are all signs of the infection spreading. Untreated, it will lead to widespread local gangrene and systemic multisystem organ failure. The subdermal spread of gangrene is always much more extensive than appears from initial examination. Broad-spectrum antibiotic therapy must be combined with aggressive circulatory support. Locally, there should be wide excision of necrotic tissue and laying open of affected areas. The debridement may need to be extensive, and patients who survive may need large areas of skin grafting.

Systemic infection Bacteraemia Bacteraemia is unusual following superficial SSIs, which tend to drain through the wound, but common after deep space SSIs such as follow an intestinal anastomotic breakdown. It is usually transient and can follow procedures undertaken through infected tissues (particularly instrumentation in infected bile or urine). It may also occur through bacterial infection of indwelling intravenous cannulae, which should be replaced regularly in order to avoid colonisation. Bacteraemia is important when a prosthesis has been implanted, as infection of the prosthesis can occur through haematogenous spread. Aerobic gram-negative bacilli are often responsible, but Staphylococcus aureus and fungi may be involved, particularly after the use of broad-spectrum antibiotics.

Figure 5.12 A classic presentation of Fournier’s gangrene of the scrotum with ‘shameful exposure of the testes’ following excision of the gangrenous skin.

Frank Lamont Meleney, 1889–1963, Professor of Clinical Surgery, Columbia University, New York, NY, USA. Jean Alfred Fournier, 1832–1915, syphilologist, the founder of the Venereal and Dermatological Clinic, Hôpital St. Louis, Paris, France.

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Summary box 5.10

TABLE 5.3  Definitions of systemic inflammatory response syndrome (SIRS) and sepsis.

Bacteraemia

SIRS is

●● ●●

●●

Common after anastomotic breakdown Dangerous if the patient has a prosthesis, which can become infected May be associated with systemic organ failure

51

Two of: hyperthermia (>38°C) or hypothermia (90/min, no β-blockers) or tachypnoea (>20/min) white cell count >12 × 109/litre or 95% reduction in bacterial count but caution should be taken not to leave a pool of alcohol-based fluid on the skin which could ignite with diathermy and burn the patient. Theatre technique and discipline also contribute to low infection rates. Numbers of staff in the theatre and movement in and out of theatre should be kept to a minimum. Careful and regular surveillance is needed to ensure the quality of instrument sterilisation, aseptic technique and theatre ventilation. Laminar flow systems direct clean, filtered air over the operating field, with any air potentially contaminated as it passes over the incision then directed away from the patient. Operator skill in gentle manipulation and dissection of tissues is much more difficult to audit, but dead spaces and haematomas should be avoided. There is no evidence that drains, incision drapes or wound guards help to reduce wound infection. There is a high level of evidence that both the perioperative avoidance of hypothermia and the use of supplemental oxygen during recovery significantly reduce the rate of SSIs.

Moritz Kaposi, 1837–1902, Professor of Dermatology, Vienna, Austria, described pigmented sarcoma of the skin in 1872.

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Prophylactic antibiotics Prophylactic antibiotics are used when there is a risk of wound contamination with bacteria during surgery. The theoretical degree of contamination, proposed by the National Research Council (USA) over 40 years ago, relates well to infection rates (Table 5.4). The value of antibiotic prophylaxis is low in non-prosthetic clean surgery, with most trials showing no clear benefit because infection rates without antibiotics are so low. The exception to this is where a prosthetic implant is used, as the results of infection are so catastrophic that even a small risk of infection is unacceptable.There is undisputed evidence that prophylactic antibiotics are effective in reducing the risk of infection in clean-contaminated and contaminated operations. When wounds are heavily contaminated or when an incision is made into an abscess, a 5-day course of therapeutic antibiotics may be justified on the assumption that the wound is inevitably infected and so treatment is needed rather than prophylaxis. If antibiotics are given to prevent infection after surgery or instrumentation, they should be used before bacterial growth becomes established (i.e. within the decisive period). Ideally, maximal blood and tissue levels should be present at the time at which the first incision is made and before contamination occurs. Tissue levels of the antibiotic should remain high throughout the operation and antibiotics with a short tissue half life should be avoided. Intravenous administration at induction of anaesthesia is therefore optimal, as unexpected delays in the timing of surgery may occur before then and antibiotic tissue levels may fall off before the surgery starts. In long operations or when there is excessive blood loss, or when unexpected contamination occurs, antibiotics may be repeated at 4-hourly intervals during the surgery, because tissue antibiotic levels often fall faster than serum levels. There is no evidence that further doses of antibiotics after surgery are of any value in prophylaxis against infection and the practice can only encourage the development of antibiotic resistance. The choice of an antibiotic depends on the expected spectrum of organisms likely to be encountered, which will depend on the site and type of surgery and whether or not the patient has any antibiotic allergies. Hospitals in the UK now have standardised antibiotic prophylaxis policies which take account of the above factors and are only deviated from with microbiological advice. Patients with known valvular disease of the heart (or with any implanted vascular or orthopaedic prosthesis) should TABLE 5.4  SSI rates relating to wound contamination with and without using antibiotic prophylaxis. Type of surgery

Infection rate with prophylaxis (%)

Infection rate without prophylaxis (%)

Clean (no viscus opened)

1–2

1–2

Clean-contaminated (viscus opened, minimal spillage)

3

6–9

Contaminated (open viscus with spillage or inflammatory disease)

6

13–20

Dirty (pus or perforation, or incision through an abscess)

7

40

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53

have prophylactic antibiotics during dental, urological or open viscus surgery, to prevent bacterial colonisation of the valve or prosthesis during the transient bacteraemia which can occur during such surgery.

Summary box 5.12 Antibiotic prophylaxis ●● ●●

●●

●●

●●

Not required in clean surgery unless a prosthesis is implanted Use antibiotics that are effective against expected pathogens within local hospital guidelines Plan for single-shot intravenous administration at induction of anaesthesia Repeat only during long operations or if there is excessive blood loss Patients with heart valve disease or a prosthesis should be protected from bacteraemia caused by dental work, urethral instrumentation or visceral surgery

Postoperative wound infections The majority of wound infections arise from endogenous sources within the patient, but exogenous SSI may also occur from bacteria present in the ward or staff and so can be related to poor hospital standards. Strict attention to ward cleanliness, gloving before touching patient wounds and hand washing between all patient contacts are important preventive measures. An outbreak of wound infections on the ward with bacteria having the same antibiotic sensitivity profile implies an exogenous source of infection, which needs to be investigated by swabbing all staff and work surfaces. It may need temporary ward closure and a deep clean to eradicate the infection source. Now that patients are discharged more quickly after surgery and many procedures are performed as day cases, many SSIs are missed by the surgical team unless they undertake a prolonged and carefully audited follow-up with primary care doctors. Suppurative wound infections take 7–10 days to develop, and even cellulitis around wounds caused by invasive organisms (such as b-haemolytic Streptococcus) takes 3–4 days to develop. Major surgical infections with systemic signs (Figure 5.13), evidence of spreading infection, cellulitis or bacteraemia need treatment with appropriate antibiotics. The choice may need to be empirical initially but is best based on culture and sensitivities of isolates harvested at surgery or from culture of wound fluids or wound swabs. Although the identification of organisms in surgical infections is necessary for audit and wound surveillance purposes, it is usually 2–3 days before sensitivities are known (Figures 5.14 and 5.15). It is illogical to withhold antibiotics until results are available but, if clinical response is poor by the time sensitivities are known, then antibiotics can be changed. Such changes are unusual if the empirical choice of antibiotics is sensible; change of antibiotics promotes resistance and risks complications, such as C.difficile enteritis. If an infected wound is under tension, or there is clear evidence of suppuration, sutures or clips need to be removed, with curettage if necessary, to allow pus to drain adequately. In severely contaminated wounds, such as an incision made

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CHAPTER 5  Surgical infection

HOSPITAL __________________________________ __ ___ _________ ______ __ ___________ WARD

J

8th

5th6th

0 22 25 6 1018 22 611 14 22 0917 23 061 21 0 0 0 0 0 3 0 0 0 0 06 0 0 0 017 0 0 30 0 0 0 30 0

TEMPERATURE (∞CELSIUS)

39.5 39.0 38.5

Fan therapy

MINUTES

9th

10th 11th

Fan therapy

TIME

7th

f

38.0

UNIT NO

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Figure 5.14  Mixed streptococcal infection of a skin graft with very poor ‘take’.

BLOOD PRESSURE mmHg

PULSE PER MINUTE

DAY

40.5

RESPIRATION PER MINUTE

AUGUST

MONTH

SEX

FIRST NAMES

BOWELS:

DATE OF BIRTH

SURNAME

20-30

YEAR

50 40 30 20 10

Figure 5.13 Classic swinging pyrexia related to a perianastomotic wound abscess that settled spontaneously on antibiotic therapy.

for drainage of an abscess, it is logical to leave the skin open. Delayed primary or secondary closure can be undertaken when the wound is clean and granulating (Figures 5.16 and 5.17). Some heavily infected wounds may be left to heal by secondary intention, with no attempt at closure, particularly where there is a loss of skin cover and healthy granulation tissue develops (Figure 5.18). While the end result may be excessive scarring, that can always be revised with plastic surgery under clean surgical conditions at a later stage. Leaving wounds open after a ‘dirty’ operation, such as laparotomy for faecal peritonitis, is not practised as widely in the UK as in the USA or mainland Europe.

Figure 5.15 After 5–6 days of antibiotics, the infection shown in ­Figure 5.14 is under control, and the skin grafts are clearly viable.

(a)

(b)

Summary box 5.13 Surgical incisions through infected or contaminated tissues ●●

●●

●●

When possible, tissue or pus for culture should be taken before antibiotic cover is started The choice of antibiotics is empirical until sensitivities are available Heavily contaminated wounds are best managed by delayed primary or secondary closure

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Figure 5.16 (a, b) Delayed primary closure of fasciotomy wound after 3–5 days.

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PART 1 | BASIC PRINCIPLES Antimicrobial treatment of surgical infection

Figure 5.17  Skin layers left open to granulate after laparotomy for faecal peritonitis, ready for skin grafting.

Figure 5.18  Infected animal bite/wound of the upper thigh, treated by open therapy following virulent staphylococcal infection.

When taking pus from infected wounds, specimens should be sent fresh for microbiological culture. Swabs should be placed in transport medium, but the larger the volume of pus sent, the more likely is the accurate identification of the organism involved. Providing the microbiologist with as much information as possible and discussing the results with them gives the best chance of the most appropriate antibiotic treatment. If bacteraemia is suspected, but results are negative, then repeat specimens for blood culture may need to be taken. A rapid report on infective material can be based on an immediate Gram stain. Topical antiseptics should only be used on heavily contaminated wounds for a short period to clear infection as they inhibit epithelial ingrowth and so impair wound healing.

antibiotic therapy. Antibiotics alone are rarely sufficient to treat SSIs, which may also need open drainage and debridement. There are two approaches to antibiotic treatment:

ANTIMICROBIAL TREATMENT OF SURGICAL INFECTION Principles Antimicrobials may be used to prevent or treat established surgical infection. Summary box 5.14 Principles for the use of antibiotic therapy ●● ●●

●●

Antibiotics do not replace surgical drainage of infection Only spreading infections or signs of systemic infection justify the use of antibiotics Whenever possible, the organism and sensitivity should be determined

The use of antibiotics for the treatment of established surgical infection ideally requires recognition and determination of the sensitivities of the causative organisms. Antibiotic therapy should not be held back if it is indicated, the choice being empirical and later modified depending on microbiological findings. Once antibiotics have been administered, it may not be possible to grow bacteria from the wound and so the opportunity to ascertain the most appropriate antibiotic sensitivities is lost if a patient’s condition does not improve on empirical

01_05-B&L27_Pt1_Ch05.indd 55

●●

●●

55

A narrow-spectrum antibiotic may be used to treat a known sensitive infection; for example, MRSA (which may be isolated from pus) is usually sensitive to vancomycin or teicoplanin, but not flucloxacillin. Combinations of broad-spectrum antibiotics can be used when the organism is not known or when it is suspected that several bacteria, acting in synergy, may be responsible for the infection. For example, during and following emergency surgery requiring the opening of perforated or ischaemic bowel, any of the gut organisms may be responsible for subsequent peritoneal or bacteraemic infection. In this case, a broad spectrum antibiotic such as teicoplenin or meropenem effective against a wide range of aerobic bacteria is combined with metronidazole, effective against anaerobic bacteria. Alternatively, triple therapy is used with amoxacillin, gentamicin and metronidazole. The use of such broad-spectrum antibiotic strategies should be guided by specialist microbiological advice. If clincal response is poor after 3–4 days, there should be a re-evaluation with a review of charts and further investigations requested to exclude the development or persistence of infection such as a collection of pus.

Antibiotics used in treatment and prophylaxis of surgical infection Antimicrobials may be produced by living organisms (antibiotics) or by synthetic methods. Some are bactericidal, e.g. penicillins and aminoglycosides, and others are bacteriostatic, e.g. tetracycline and erythromycin. In general, penicillins act upon the bacterial cell wall and are most effective against bacteria that are multiplying and synthesising new cell wall materials. The aminoglycosides act at the ribosomal level, preventing or distorting the production of proteins required to maintain the integrity of the enzymes in the bacterial cell. Hospital and Formulary guidelines should be consulted for doses and monitoring of antibiotic therapy.

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CHAPTER 5  Surgical infection

Penicillin

Aminoglycosides

Benzylpenicillin has proved most effective against gramposi­tive pathogens, including most streptococci, the clostridia and some of the staphylococci that do not produce b-lactamase. It is still effective against Actinomyces, which is a rare cause of chronic wound infection. It may be used specifically to treat spreading streptococcal infections. Penicillin is valuable even if other antibiotics are required as part of multiple therapy for a mixed infection. Some serious infections, e.g. gas gangrene, require high-dose intravenous benzylpenicillin.

Gentamicin and tobramycin have similar activity and are effective against gram-negative Enterobacteriaceae. Gentamicin is effective against many strains of Pseudomonas, although resistance has been recognised. All aminoglycosides are inactive against anaerobes and streptococci. Serum levels immediately before and 1hour after intramuscular injection must be taken 48 hours after the start of therapy, and dosage should be modified to satisfy peak and trough levels. Ototoxicity and nephrotoxicity may follow sustained high toxic levels and therefore single, large doses may be safer. Use needs to be discussed with the microbiologist and local policies should be observed.

Flucloxacillin Flucloxacillin is resistant to b-lactamases and is therefore of use in treating infections with penicillinase-producing staphylococci which are resistant to benzylpenicillin, but it has poor activity against other pathogens. It has good tissue penetration and therefore is useful in treating soft tissue infections and osteomyelitis.

Ampicillin, amoxicillin and co-amoxiclav Ampicillin and amoxicillin are b-lactam penicillins and can be taken orally or may be given parenterally. Both are effective against Enterobacteriaceae, Enterococcus faecalis and the majority of group D streptococci, but not species of Klebsiella or Pseudomonas. Clavulanic acid has no antibacterial activity itself, but it does inactivate β-lactamases, so can be used in conjunction with amoxicillin. The combination is known as co-amoxiclav and is useful against β-lactamase producing bacteria that are resistant to amoxicillin on its own. These include resistant strains of Staphylococcus aureus, E.coli, Haemophilus influenzae, Bacteroides and Klebsiella.

Piperacillin and ticarcillin These are ureidopenicillins with a broad spectrum of activity against a broad range of gram-positive, gram-negative and anaerobic bacteria. Both are used in combination with β-lactamase inhibitors (tazobactam with piperacillin and clavulanic acid with ticarcillin). They are not active against MRSA but are used in the treatment of septicaemia, hospitalacquired pneumonia and complex urinary tract infections, where they are active against Pseudomonas and Proteus spp. and have a synergistic effect when used with aminoglycosides such as gentamicin.

Cephalosporins There are several b-lactamase-susceptible cephalosporins that are of value in surgical practice: cefuroxime, cefotaxime and ceftazidime are widely used. The first two are most effective in intra-abdominal skin and soft-tissue infections, being active against Staphylococcus aureus and most Enterobacteriaceae. As a group, the enterococci (Streptococcus faecalis) are not sensitive to the cephalosporins. Ceftazidime, although active against the gram-negative organisms and Staphylococcus aureus, is also effective against Pseudomonas aeruginosa. These cephalosporins may be combined with an aminoglycoside, such as gentamicin, and an imidazole, such as metronidazole, if anaerobic cover is needed.

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Vancomycin and teicoplanin These glycopeptide antibiotics are most active against gram-positive aerobic and anaerobic bacteria and have proved to be effective against MRSA, so are often used as prophylactic antibiotics when there is a high risk of MRSA. They are ototoxic and nephrotoxic, so serum levels should be monitored. They are effective against C. difficile in cases of pseudomembranous colitis.

Carbapenems Meropenem, ertapenem and imipenem are members of the carbapenems. They are stable to b-lactamase, have useful broad-spectrum anaerobic as well as gram-positive activity and are effective for the treatment of resistant organisms, such as ESBL-resistant urinary tract infections or serious mixed-spectrum abdominal infections (peritonitis).

Metronidazole Metronidazole is the most widely used member of the imidazole group and is active against all anaerobic bacteria. It is particularly safe and may be administered orally, rectally or intravenously. Infections caused by anaerobic cocci and strains of Bacteroides and Clostridia can be treated, or prevented, by its use. Metronidazole is useful for the prophylaxis and treatment of anaerobic infections after abdominal, colorectal and pelvic surgery and in the treatment of C.difficile pseudomembranous colitis.

Ciprofloxacin Quinolones, such as ciprofloxacin, have a broad spectrum of activity against both gram-positive and gram-negative bacteria but are particularly useful against Pseudomonas infections. Many UK hospitals have restricted their use as a preventive measure against the development of C.difficile enterocolitis.

FURTHER READING Fraise AP, Bradley C. Ayliffe’s control of healthcare associated infection: a practical handbook. London: Hodder Arnold, 2009. Fry DE. Surgical infections. London: JP Medical Ltd, 2013. Sawyer RG, Hedrick TL. Surgical infections, an issue of surgical clinics. New York: Elsevier – Health Sciences Division, 2014. Thomas WEG, Reed MWR, Wyatt MG. Oxford textbook of fundamentals of surgery. Oxford: Oxford University Press, 2016. Torok E, Moran E, Cooke F. Oxford handbook of infectious diseases and microbiology, 2nd edn. Oxford: Oxford University Press, 2016.

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ve Bailey & Love Bailey & Love Bailey & Love ve Bailey & Love Bailey & Love Bailey & 6 Love Chapter

Tropical infections and infestations Learning objectives To be able to list: •• The common surgical infections and infestations that occur in the tropics To appreciate: •• That many patients do not seek medical help until late in the course of the disease because of socioeconomic reasons To be able to describe: •• The emergency presentations of the various conditions, as patients may not seek treatment until they are very ill To be able to: •• Diagnose and treat these conditions, particularly as emergencies. The ease of global travel has connected

areas where tropical infections are common to areas where they are not. Patients with such an infection who are recently returned from the tropics will mostly present as emergencies To realise: •• That the ideal management involves a multidisciplinary approach between the surgeon, physician, radiologist, pathologist and microbiologist. In case of doubt, in a difficult situation, there should be no hesitation in seeking help from a specialist centre.

INTRODUCTION

Central and South America, where almost half the population is infected. The majority remain asymptomatic carriers. The mode of infection is via the faeco-oral route, and the disease occurs as a result of substandard hygiene and sanitation; therefore, the population from the poorer socioeconomic strata are more vulnerable. Amoebic liver abscess, the commonest extraintestinal manifestation, occurs in less than 10% of the infected population and, in endemic areas, is much more common than pyogenic abscess. Patients who are immunocompromised and alcoholics are more susceptible to infection.

Most surgical conditions in the tropics (regions of the Earth surrounding the equator) are associated with parasitic infestations and infections related to poor hygeinic conditions. With the ease of international travel, diseases that are common in the tropics may present in areas of the world where they are not commonly seen, especially as emergencies. This chapter deals with the conditions that a surgeon might occasionally see when working in an area where such diseases are uncommon. Typically the patient would be a visitor from a tropical climate or a local resident who has visited the tropics either on holiday or to work. The life cycles of the parasites will not be described. For academic interest readers may refer to the 24th edition of this book should they wish to learn details of the parasitology. The principles of surgical treatment are dealt with in the appropriate sections although, for operative details, referral to a relevant textbook is advised.

AMOEBIASIS Introduction Amoebiasis is caused by Entamoeba histolytica. The disease is common in the Indian subcontinent, Africa and parts of

01_06-B&L27_Pt1_Ch06.indd 57

Pathogenesis The organism enters the gut through food or water contaminated with the cyst. In the small bowel, the cysts hatch, and a large number of trophozoites are released and carried to the colon where flask-shaped ulcers form in the submucosa. The trophozoites multiply, ultimately forming cysts, which enter the portal circulation or are passed in the faeces as an infective form that infects other humans as a result of insanitary conditions. Having entered the portal circulation, the trophozoites are filtered and trapped in the interlobular veins of the liver. They multiply in the portal triads, causing focal infarction of hepatocytes and liquefactive necrosis as a result of proteolytic

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CHAPTER 6  Tropical infections and infestations

enzymes produced by the trophozoites. The areas of necrosis eventually coalesce to form the abscess cavity. The term ‘amoebic hepatitis’ is used to describe the microscopic picture in the absence of macroscopic abscess, a differentiation only in theory because the medical treatment is the same. The right lobe is involved in 80% of cases, the left in 10% and the remainder are multiple. One possible explanation for the more common involvement of the right lobe of the liver is that blood from the superior mesenteric vein runs on a straighter course through the portal vein into the larger lobe. The abscesses are most common high in the diaphragmatic surface of the right lobe. This may cause pulmonary symptoms and chest complications. The abscess cavity contains chocolate-coloured, odourless, ‘anchovy sauce’-like fluid that is a mixture of necrotic liver tissue and blood. There may be secondary infection of the abscess which causes the pus to smell. While pus in the abscess is sterile unless secondarily infected, trophozoites may be found in the abscess wall in a minority of cases. Untreated abscesses are likely to rupture. Chronic infection of the large bowel may result in a granulomatous lesion along the large bowel, most commonly seen in the caecum, called an amoeboma. Summary box 6.1 Amoebiasis – pathology ●●

●● ●●

●●

●●

●● ●●

Entamoeba histolytica is the most common pathogenic amoeba in humans The vast majority of carriers are asymptomatic Insanitary conditions and poor personal hygiene encourage transmission of the infection In the small intestine, the parasite hatches into trophozoites, which invade the submucosa to produce flask-shaped ulcers In the portal circulation, the parasite causes liquefactive necrosis in the liver, producing an abscess, the commonest extraintestinal manifestation The majority of abscesses occur in the right lobe of the liver A mass in the course of the large bowel may indicate an amoeboma

Clinical features The typical patient with amoebic liver abscess is a young adult male with a history of insidious onset of non-specific symptoms, such as abdominal pain, anorexia, fever, night sweats, malaise, cough and weight loss. These symptoms gradually progress to more specific symptoms of pain in the right upper abdomen and right shoulder tip, hiccoughs and a non-productive cough. A past history of bloody diarrhoea or travel to an endemic area raises the index of suspicion. Examination reveals a patient who is toxic and anaemic. The patient will have upper abdominal rigidity, tender hepatomegaly, tender and bulging intercostal spaces, overlying skin oedema, a pleural effusion and basal pneumonitis – the last feature is usually a late manifestation. Occasionally, a tinge of jaundice or ascites may be present. Rarely, the patient may present as an emergency due to the effects of rupture of an abscess into the peritoneal, pleural or pericardial cavity.

01_06-B&L27_Pt1_Ch06.indd 58

Amoeboma This is a chronic granuloma arising in the large bowel, most commonly seen in the caecum. It is prone to occur in longstanding amoebic infection that has been treated intermittently with drugs without completion of a full course, a situation that arises from indiscriminate self-medication, particularly in resource-poor countries. Hence this is more often seen in such countries. This can easily be mistaken for a carcinoma. An amoeboma should be suspected when a patient from an endemic area with generalised ill health and pyrexia has a mass in the right iliac fossa with a history of blood-stained mucoid diarrhoea. Such a patient is highly unlikely to have a carcinoma because altered bowel habit is not a feature of right-sided colonic carcinoma. While iron deficiency anaemia is a classical elective presentation of a caecal carcinoma, the same is present in an amoeboma because of chronic malnutrition.

Investigations The haematological and biochemical investigations reflect the presence of a chronic infective process: anaemia, leukocytosis, raised inflammatory markers – erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) – hypoalbuminaemia and deranged liver function tests, particularly elevated alkaline phosphatase. Serological tests are more specific, with the majority of patients showing antibodies in serum. These can be detected by tests for complement fixation, indirect haemagglutination (IHA), indirect immunofluorescence and enzyme-linked immunosorbent assay (ELISA). These tests are extremely useful in detecting acute infection in non-endemic areas. IHA has a very high sensitivity in acute amoebic liver abscess in non-endemic regions and remains elevated for some time. The persistence of antibodies in a large majority of the population in endemic areas precludes its use as a diagnostic investigation in those locations. In these cases, tests, such as counter-immunoelectrophoresis, are more useful for detecting acute infection. While flexible sigmoidoscopy is routine in any patient with blood-stained altered bowel habit, an outpatient rigid sigmoidoscopy using a disposable instrument may be a prudent first choice if amoebic infection is suspected in the presence of bloody mucoid diarrhoea. Most amoebic ulcers occur in the rectosigmoid and are therefore within reach of the sigmoidoscope; shallow skip lesions and ‘flaskshaped’ or ‘collar-stud’ undermined ulcers may be seen, and can be biopsied or scrapings can be taken along with mucus for immediate microscopic examination. The presence of trophozoites distinguishes the condition from ulcerative colitis.

Imaging techniques On ultrasound, an abscess cavity in the liver is seen as a hypoechoic or anechoic lesion with ill-defined borders; internal echoes suggest necrotic material or debris (Figure 6.1).

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59

Figure 6.1 Ultrasound of the liver showing a large amoebic liver abscess with necrotic tissue in the right lobe.

The investigation is very accurate and is used for aspiration, both diagnostic and therapeutic. Where there is doubt about the diagnosis, a computed tomography (CT) scan may be helpful (Figure 6.2). Diagnostic aspiration is of limited value except for establishing the typical colour of the aspirate, which is sterile and odourless unless it is secondarily infected. A CT scan may show a raised right hemidiaphragm, a pleural effusion and evidence of pneumonitis (Figure 6.3). An ‘apple-core’ deformity on barium enema would arouse suspicion of a carcinoma. A colonoscopy with biopsy is mandatory because the radiological and macroscopic appearance may be indistinguishable from a carcinoma. In doubtful cases, vigorous medical treatment is given, and the patient undergoes colonoscopy again in 3–4 weeks, as these masses are known to regress completely on a full course of drug therapy. If symptoms persist even partially following full medical treatment in a patient who has recently returned from an endemic area, a colonic carcinoma must be excluded forthwith. This is because a dormant colonic carcinoma may become apparent as a result of infestation with amoebic dysentery causing ‘traveller’s diarrhoea’. However, it must be borne in mind that an amoeboma and a carcinoma can coexist.

Summary box 6.2 Diagnostic pointers for infection with Entamoeba histolytica ●●

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Bloody mucoid diarrhoea in a patient from an endemic area or following a recent visit to such a country Upper abdominal pain, fever, cough, malaise In chronic cases, a mass in the right iliac fossa may be an amoeboma but caecal cancer must be excluded by colonoscopy and biopsy Sigmoidoscopy shows typical ulcers – biopsy and scrapes may be diagnostic Serological tests are highly sensitive and specific outside endemic areas Ultrasound and CT scans are the imaging methods of choice

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Figure 6.2  Computed tomographic scan showing an amoebic liver abscess in the right lobe.

Figure 6.3  Computed tomographic scans showing multiple amoebic liver abscesses with extension into the chest.

Treatment Medical treatment is very effective and should be the first choice in the elective situation, with surgery being reserved for complications. Metronidazole and tinidazole are the effective drugs. After treatment with metronidazole and tinidazole, diloxanide furoate, which is not effective against hepatic infestation, is used for 10 days to destroy any intestinal amoebae. Aspiration is carried out when imminent rupture of an abscess is expected. Aspiration also helps the penetration of metronidazole, and so reduces the morbidity when carried out with drug treatment in a patient with a large abscess. If there is evidence of secondary infection, appropriate drug treatment is added. The threshold for aspirating an abscess in the left lobe should be lower because of its proximity to the pericardium.

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CHAPTER 6  Tropical infections and infestations

Surgical treatment should be reserved for the complications of rupture into the pleural (usually the right side), peritoneal or pericardial cavities. Resuscitation, drainage and appropriate lavage with vigorous medical treatment are the key principles. In the large bowel, severe haemorrhage and toxic megacolon are rare complications. In these patients, the general principles of a surgical emergency apply, the principles of management being the same as for any toxic megacolon. Resuscitation is followed by resection of bowel with exteriorisation. Then the patient is given vigorous supportive therapy. All such cases are managed in the intensive care unit, as would any patient with toxic megacolon whatever the cause. An amoeboma that has not regressed after full medical treatment should be managed with colonic resection, particularly if cancer cannot be excluded. Summary box 6.3 Amoebiasis – treatment ●● ●●

●●

●●

●●

Medical treatment is very effective For large abscesses, repeated aspiration is combined with drug treatment Surgical treatment is reserved for complications, such as rupture into the pleural, peritoneal or pericardial cavities Acute toxic megacolon and severe haemorrhage are intestinal complications that are treated with intensive supportive therapy followed by resection and exteriorisation: subtotal colectomy with terminal ileostomy and closure of the rectal stump When an amoeboma is suspected in a colonic mass, cancer should be excluded by appropriate imaging and biopsy

ROUNDWORM (ASCARIS LUMBRICOIDES)

up to 8 weeks. The developed larvae reach the alveoli, are coughed up, swallowed and continue their maturation in the small intestine. Sometimes, the young worms migrate from the tracheobronchial tree into the oesophagus, thus finding their way into the gastrointestinal tract, from where they can migrate to the common bile duct or pancreatic duct. The mature female, once in the small bowel, produces innumer­ able eggs that are fertilised and thereafter excreted in the stool to perpetuate the life cycle. Eggs in the biliary tract can form a nidus for a stone.

Clinical features The larval stage in the lungs causes pulmonary symptoms – dry cough, chest pain, dyspnoea and fever – referred to as Loeffler’s syndrome. The adult worm can grow up to 45 cm long. Its presence in the small intestine causes malnutrition, failure to thrive, particularly in children, and abdominal pain. Worms that migrate into the common bile duct can produce ascending cholangitis and obstructive jaundice, while features of acute pancreatitis may be caused by a worm in the pancreatic duct. Small intestinal obstruction can occur, particularly in children, due to a bolus of adult worms incarcerated in the terminal ileum. This is a surgical emergency. Rarely, perforation of the small bowel may occur from ischaemic pressure necrosis from the bolus of worms. A high index of suspicion is necessary so as not to miss the diagnosis. If a person from a tropical country, or one who has recently returned after spending some time in an endemic area, presents with pulmonary, gastrointestinal, hepatobiliary and pancreatic symptoms, ascariasis should be high on the list of possible diagnoses.

Introduction

Investigations

Ascaris lumbricoides, commonly called the roundworm, is the commonest intestinal nematode to infect humans and affects a quarter of the world’s population. The parasite causes pulmonary symptoms as a larva and intestinal symptoms as an adult worm.

As with most parasitic infestations, an increase in the eosinophil count is common. Stool examination may show ova. Sputum or bronchoscopic washings may show Charcot–­ Leyden crystals or the larvae. Chest radiograph may show fluffy exudates in Loeffler’s syndrome. A barium meal and follow-through may show a bolus of worms in the ileum or lying freely within the small bowel (Figure 6.4). Ultrasound may show a worm in the common bile duct (Figure 6.5) or pancreatic duct. On magnetic resonance cholangiopancreatography (MRCP), an adult worm may be seen in the common bile duct in a patient presenting with features of obstructive jaundice (Figure 6.6). In patients with intestinal obstruction, plain abdominal radiograph may show tubular structures within dilated small bowel, denoting the presence of worms, which would also show up on a contrast CT scan as curvilinear structures.

Pathology and life cycle The eggs can survive in a hostile environment for a long time. The hot and humid conditions in the tropics are ideally suited for the eggs to turn into embryos. The fertilised eggs are present in soil contaminated with infected faeces. Faeco-oral contamination causes human infection. As the eggs are ingested, the released larvae travel to the liver via the portal system and then through the systemic circulation to reach the lung, the maturation process taking Wilhelm Loeffler, 1887–1972, Professor of Medicine, Zurich, Switzerland. Jean Martin Charcot, 1825–1893, Physician, La Salpêtrière, Paris, France. Ernst von Leyden, 1832–1910, Professor of Medicine, Berlin, Germany.

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61

Figure 6.6  Magnetic resonance cholangiopancreatography showing a roundworm in the common bile duct (CBD). The worm could not be removed endoscopically. The patient underwent an open cholecystectomy and exploration of the CBD. BARIUM SEEN INSIDE THE ROUNDWORM

Summary box 6.4 Ascariasis – pathogenesis

Figure 6.4  Barium meal and follow-through showing roundworms in the course of the small bowel with barium seen inside the worms in an 18-year-old patient who presented with bouts of colicky abdominal pain and bilious vomiting, which settled with conservative management (courtesy of Dr P Bhattacharaya, Kolkata, India).

●● ●●

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It is the commonest intestinal nematode affecting humans Typically found in a humid atmosphere and poor sanitary conditions, hence is seen in the tropics and resource-poor countries Larvae cause pulmonary symptoms; adult worms cause gastrointestinal, biliary and pancreatic symptoms Distal ileal obstruction is due to a bolus of worms; ascending cholangitis and obstructive jaundice from infestation of the common bile duct Acute pancreatitis occurs when a worm is lodged in the pancreatic duct Perforation of the small bowel is rare

Treatment

Figure 6.5  Ultrasound scan showing a roundworm in the common bile duct (CBD). The patient presented with obstructive jaundice and had asymptomatic gallstones. On endoscopic retrograde cholangiopancreatography, part of the worm was seen outside the ampulla in the duodenum and was removed through the endoscope. Subsequent laparoscopic cholecystectomy was uneventful.

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The pulmonary phase of the disease is usually self-limiting and requires symptomatic treatment only. For intestinal disease, patients should ideally be under the care of a physician for treatment with anthelmintic drugs. Certain drugs may cause rapid death of the adult worms and, if there are many worms in the terminal ileum, the treatment may actually precipitate acute intestinal obstruction from a bolus of dead worms. Children who present with features of intermittent or subacute obstruction should be given a trial of conservative management in the form of intravenous fluids, nasogastric suction and hypertonic saline enemas. The last of these helps to disentangle the bolus of worms and also increases intestinal motility. Surgery is reserved for complications, such as intestinal obstruction that has not resolved on a conservative regime, or when perforation is suspected. At laparotomy, the bolus of worms in the terminal ileum is milked through the ileocaecal valve into the colon for natural passage in the stool.

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Postoperatively, hypertonic saline enemas may help in the extrusion of the worms. Strictures, gangrenous areas or perforations need resection and anastomosis. If the bowel wall is healthy, enterotomy and removal of the worms may be performed (Figure 6.7). Rarely, when perforation occurs due to roundworm, the parasites may be found lying free in the peritoneal cavity. It is safer to bring out the site of perforation as an ileostomy because, in the presence of a large number of worms, the ­closure of an anastomosis may be at risk of breakdown from the activity of the worms. When a patient is operated upon as an emergency for a suspected complication of roundworm infestation, the actual diagnosis at operation may turn out to be acute appendicitis, typhoid perforation or a tuberculous stricture, and the presence of roundworms is an incidental finding. Such a patient requires the appropriate surgery depending upon the primary pathology. Common bile duct or pancreatic duct obstruction from a roundworm can be treated by endoscopic removal, failing which laparoscopic or open exploration of the common bile duct is necessary. Cholecystectomy is also carried out. A full course of antiparasitic treatment must follow any surgical intervention.

Summary box 6.5 Ascariasis – diagnosis and management ●●

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Barium meal and follow-through will show worms scattered in the small bowel Ultrasound may show worms in the common bile duct and pancreatic duct Plain abdominal radiograph and contrast CT scan will show the worms as tubular or curvilinear structures Conservative management with anthelmintics is the first line of treatment even in obstruction Surgery is a last resort – various options are available

(a)

(b)

ASIATIC CHOLANGIOHEPATITIS Introduction This disease, also called oriental cholangiohepatitis, is caused by infestation of the hepatobiliary system by Clonorchis sinensis. It has a high incidence in the tropical regions of South East Asia, particularly amongst those living in the major sea ports and near river estuaries. The organism, which is a type of liver fluke, resides in snails and fish that act as intermediate hosts. Ingestion of infected fish and snails, when eaten raw or improperly cooked, causes the infection in humans and other fish-eating mammals, which are the definitive hosts.

Pathology In humans, the parasite matures into the adult worm in the intrahepatic biliary radicles where they may reside for many years. The intrahepatic bile ducts are dilated, with epithelial hyperplasia and periductal fibrosis. These changes may lead to dysplasia, causing cholangiocarcinoma – the most serious and dreaded complication of this parasitic infestation. The eggs or dead worms may form a nidus for stone formation in the gallbladder or common bile duct, which becomes thickened and much dilated in the late stages. Intrahepatic bile duct stones are also caused by the parasite producing mucin-rich bile. The dilated intrahepatic bile ducts may lead to cholangitis, liver abscess and hepatitis.

Diagnosis The disease may remain dormant for many years. Clinical features are non-specific and include fever, malaise, anorexia and upper abdominal discomfort. The complete clinical picture can consist of fever with rigors due to ascending cholangitis, obstructive jaundice, biliary colic and pruritus from stones in the common bile duct. Acute pancreatitis may occur because of obstruction of the pancreatic duct by an adult worm. Particularly when presenting in non-endemic areas, it should be noted that if a person from an endemic area complains

(c)

Figure 6.7  (a) Roundworms seen through the bowel wall (arrowed). (b) Roundworm being removed through enterototomy. (c) Removed roundworms.

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of symptoms of biliary tract disease, Clonorchis infestation should be high in the differential diagnosis. In advanced cases, liver function tests are abnormal. Confirmation of the condition is by examination of stool or duodenal aspirate, which may show the eggs or adult worms. Ultrasound scan findings may be characteristic, showing uniform dilatation of small peripheral intrahepatic bile ducts with only minimal dilatation of the common hepatic and common bile ducts, although the latter are much more dilated when the obstruction is caused by stones. The thickened duct walls show increased echogenicity and non-shadowing echogenic foci in the bile ducts representing the worms or eggs. Endoscopic retrograde cholangiopancreatography (ERCP) will confirm these findings. Summary box 6.6 Asiatic cholangiohepatitis – pathogenesis and diagnosis ●● ●● ●●

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Occurs in the Far Eastern tropical zones The causative parasite is Clonorchis sinensis Produces bile duct hyperplasia, intrahepatic duct dilatation and stones Increases the risk of cholangiocarcinoma May remain dormant for many years When active, there are biliary tract symptoms in a generally unwell patient Stool examination for eggs or worms is diagnostic Ultrasound scan of the hepatobiliary system and ERCP are also diagnostic

Treatment Praziquantel and albendazole are the drugs of choice. However, the surgeon faces a challenge when there are stones not only in the gallbladder but also in the common bile duct. Cholecystectomy with exploration of the common bile duct is performed when indicated. Repeated washouts are necessary during the exploration, as the common bile duct is dilated and contains stones, biliary debris, sludge and mud. This should be followed by choledochoduodenostomy. As this is a disease with a prolonged and relapsing course, some surgeons prefer to do a choledochojejunostomy to a Roux loop. The Roux loop is brought up to the abdominal wall, referred to as ‘an access loop’, which allows the interventional radiologist to deal with any future stones. As a public health measure, people who have emigrated from an endemic area should be offered screening for Clonorchis infestation in the form of ultrasound of the hepatobiliary system. This condition can be diagnosed and treated, and even cured, when it is in its subclinical form. Most importantly, the risk of developing the dreadful disease of cholangiocarcinoma is eliminated.

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Summary box 6.7 Asiatic cholangiohepatitis – treatment ●● ●●

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Medical treatment can be curative in the early stages Surgical treatment is cholecystectomy, exploration of the common bile duct and some form of biliary–enteric bypass Prevention – consider offering hepatobiliary ultrasound as a screening procedure to recently arrived migrants from endemic areas

FILARIASIS Introduction Filariasis is mainly caused by the parasite Wuchereria bancrofti carried by the mosquito. Variants of the parasite called Brugia malayi and Brugia timori are responsible for causing the disease in about 10% of those infected. The condition affects more than 120 million people worldwide, two-thirds of whom live in India, China and Indonesia. According to the World Health Organization (WHO), after leprosy, filariasis is the most common cause of long-term disability. Once the host has been bitten by the mosquito, the matured eggs enter the human circulation to hatch and grow into adult worms; the process of maturation takes almost a year. The adult worms mainly colonise the lymphatic system.

Diagnosis It is mainly males who are affected, because females generally cover a greater part of their bodies with clothing, thus making them less prone to mosquito bites. In the acute presentation, there are episodic attacks of fever with lymphadenitis and lymphangitis. Occasionally, adult worms may be felt subcutaneously. Chronic manifestations appear after repeated acute attacks over several years. The adult worms cause lymphatic obstruction, resulting in massive lower limb oedema. Obstruction to the cutaneous lymphatics causes skin thickening, not unlike the ‘peau d’orange’ appearance in breast cancer, thus exacerbating the limb swelling. Secondary streptococcal infection is common. Recurrent attacks of lymphangitis cause fibrosis of the lymph channels, resulting in a grossly swollen limb with thickened skin, producing the condition of elephantiasis (Figure 6.8). Bilateral lower limb filariasis is often associated with scrotal and penile elephantiasis. Early on, there may be a hydrocoele underlying scrotal filariasis (Figure 6.9). Chyluria and chylous ascites may occur. A mild form of the disease can affect the respiratory tract, causing dry cough, and is referred to as tropical pulmonary eosinophilia. The condition of filariasis is clinically very obvious, and thus investigations in the full-blown case are superfluous. Eosinophilia is common, and a nocturnal peripheral blood smear may show

Cesar Roux, 1857–1934, Professor of Surgery and Gynaecology, Lausanne, Switzerland, described this method of forming a jejunal conduit in 1908. Otto Eduard Heinrich Wucherer, 1820–1873, German physician who practised in Brazil, South America. Joseph Bancroft, 1836–1894, English physician who worked in Australia. Peau d’orangeis French for ‘orange skin’.

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Figure 6.9  Filariasis of the scrotum and penis (courtesy of Professor Ahmed Hassan Fahal, FRCS MD MS, Khartoum, Sudan).

HYDATID DISEASE Introduction and pathology Figure 6.8  Left lower limb filariasis – elephantiasis (courtesy of Professor Ahmed Hassan Fahal, FRCS MD MS, Khartoum, Sudan).

the immature forms, or microfilariae. The parasite may also be seen in chylous urine, ascites and hydrocoele fluid.

Treatment Medical treatment with diethylcarbamazine is very effective in the early stages before the gross deformities of elephantiasis have developed. In the early stages of limb swelling, intermittent pneumatic compression helps, but the treatment has to be repeated over a prolonged period. A hydrocoele is treated by the usual operation of excision and eversion of the sac with, if necessary, excision of redundant skin. Operations for reducing the size of the limb are hardly ever done these days because the procedures are so rarely successful. Summary box 6.8 Filariasis ●●

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Caused by Wuchereria bancrofti, which is carried by the mosquito Lymphatics are mainly affected, resulting in gross limb swelling Eosinophilia occurs; immature worms may be seen in a nocturnal peripheral blood smear Gross forms of the disease cause a great deal of disability and misery Early cases are very amenable to medical treatment Intermittent pneumatic compression gives some relief The value of various surgical procedures is largely unproven and hence they are rarely performed

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Hydatid disease is caused by Ecchinococcus granulosus, commonly called the dog tapeworm. The disease is globally distributed and, while it is common in the tropics, it is much less common in other countries; for example, in the UK the occasional patient may come from a rural sheep-farming community. The dog is the definitive host and is the commonest source of infection transmitted to the intermediate hosts – humans, sheep and cattle. In the dog, the adult worm reaches the small intestine, and the eggs are passed in the faeces. These eggs are highly resistant to extremes of temperature and may survive for long periods. In the dog’s intestine, the cyst wall is digested, allowing the protoscolices to develop into adult worms. Close contact with an infected dog causes contamination by the oral route, with the ovum thus gaining entry into the human gastrointestinal tract. The cyst is characterised by three layers, an outer pericyst derived from compressed host organ tissues, an intermediate hyaline ectocyst, which is non-infective, and an inner endocyst that is the germinal membrane and contains viable parasites which can separate forming daughter cysts. A variant of the disease occurs in colder climates caused by Echinococcus multilocularis, in which the cyst spreads from the outset by actual invasion rather than expansion.

Classification In 2003, the WHO Informal Working Group on Echinococcosis (WHO-IWGE) proposed a standardised ultrasound classification based on the status of activity of the cyst. This is universally accepted, particularly because it helps to decide on the appropriate management. Three groups have been recognised: ●●

Group 1: Active group – cysts larger than 2cm and often fertile.

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Group 2: Transition group – cysts starting to degenerate and entering a transitional stage because of host resistance or treatment, but may contain viable protoscolices. Group 3: Inactive group – degenerated, partially or totally calcified cysts; unlikely to contain viable protoscolices.

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(a)

Clinical features As the parasite can colonise virtually every organ in the body, the condition can be protean in its presentation. When a sheep farmer, who is otherwise healthy, complains of a gradually enlarging painful mass in the right upper quadrant with the physical findings of a liver swelling, a hydatid liver cyst should be considered. The liver is the organ most often affected. The lung is the next most common. The parasite can affect any organ (Figures 6.10 and 6.11) or several organs in the same patient (Figure 6.12). The disease may be asymptomatic and discovered coincidentally at postmortem or when an ultrasound or CT scan is done for some other condition. Symptomatic disease presents with a swelling causing pressure effects. Thus, a hepatic lesion causes dull pain from stretching of the liver capsule, and a pulmonary lesion, if large enough, causes dyspnoea. Daughter cysts may communicate with the biliary tree, causing obstructive jaundice and all the usual clinical features associated with it in addition to symptoms attributable to a parasitic infestation (Figure 6.13). Features of raised intracranial pressure

(b)

Figures 6.11 Anteroposterior (a) and lateral (b) views of computed tomographic scans showing a large hydatid cyst of the right adrenal gland. The patient presented with a mass in the right loin and underwent an adrenalectomy (courtesy of Dr P Bhattacharaya, Kolkata, India).

Figure 6.10  Computed tomographic scan showing a hydatid cyst of the pancreas. A differential diagnosis of hydatid cyst or a tumour was considered. At exploration, the patient was found to have a hydatid cyst, which was excised followed by 30 months of treatment with albendazole, and remains free of disease. Figure 6.12 Computed tomographic scan showing disseminated hydatid cysts of the abdomen. The patient was started on alben­ dazole but was lost to follow-up (courtesy of Dr P Bhattacharaya, Kolkata, India).

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Diagnosis There should be a high index of suspicion. Investigations show a raised eosinophil count; serological tests, such as ELISA and immunoelectrophoresis, point towards the diagnosis. Ultrasound and CT scan are the investigations of choice. The CT scan shows a smooth space-occupying lesion with several septa. Ultrasound of the biliary tract may show abnormality in the gallbladder and bile ducts, when hydatid infestation of the biliary system should be suspected. Ultimately, the diagnosis is made by a combination of good history and clinical examination supplemented by serology and imaging. Summary box 6.9 Hydatid disease – diagnosis ●● ●●

Figure 6.13  Magnetic resonance cholangiopancreatography showing a large hepatic hydatid cyst with daughter cysts communicating with the common bile duct, causing obstruction and dilatation of the entire biliary tree (courtesy of Dr B Agarwal, New Delhi, India).

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or unexplained headaches in a patient from a sheep-rearing community should raise the suspicion of a cerebral hydatid cyst. The patient may present as an emergency with severe abdominal pain following minor trauma, when the CT scan may be diagnostic (Figure 6.14). Rarely, a patient may present as an emergency with features of anaphylactic shock without any obvious cause. Such a patient may subsequently cough up white material that contains scolices that have travelled into the tracheobronchial tree from rupture of a hepatic hydatid on the diaphragmatic surface of the liver.

Figure 6.14  Computed tomographic (CT) scan of the upper abdomen showing a hypodense lesion of the left lobe of the liver; the periphery of the lesion shows a double edge. This is the lamellar membrane of the hydatid cyst that separated after trivial injury. The patient was a 14-year-old girl who developed a rash and pain in the upper abdomen after dancing. The rash settled down after a course of antihistamines. The CT scan was performed 2weeks later for persisting upper abdominal pain.

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In the UK, the usual sufferer is a sheep farmer While any organ may be involved, the liver is by far the most commonly affected Elective clinical presentation is usually in the form of a painful lump arising from the liver Anaphylactic shock due to rupture of the hydatid cyst is the emergency presentation CT scan is the best imaging technique – the diagnostic feature is a space-occupying lesion with a smooth outline with septa

Treatment Here, the treatment of hepatic hydatid is outlined because the liver is most commonly affected, but the same general principles apply whichever organ is involved. These patients should be treated in a tertiary unit where good teamwork between an expert hepatobiliary surgeon, an experienced physician and an interventional radiologist is available. Surgical treatment by minimal access therapy is best summarised by the mnemonic PAIR (puncture, aspiration, injection and reaspiration). This is done after adequate drug treatment with albendazole, although praziquantel has also been used, both of these drugs being available only on a ‘named patient’ basis. Whether the patient is treated only medically or in combination with surgery will depend upon the clinical group (which gives an idea as to the activity of the disease), the number of cysts and their anatomical position. Radical total or partial pericystectomy with omentoplasty or hepatic segmentectomy (especially if the lesion is in a peripheral part of the liver) are some of the surgical options. During the operation, scolicidal agents are used, such as hypertonic saline (15– 20%), ethanol (75–95%) or 1% povidone iodine (although some use a 10% solution). This may cause sclerosing cholangitis if biliary radicles are in communication with the cyst wall. A laparoscopic approach to these procedures is being tried (see below). Obviously, cysts in other organs need to be treated in accordance with the actual anatomical site, along with the general principles described. An asymptomatic cyst which is inactive (group 3) may be left alone.

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Summary box 6.10

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(a)

Hydatid cyst of the liver – treatment ●●

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Ideally managed in a tertiary unit by a multidisciplinary team of hepatobiliary surgeon, physician and interventional radiologist Leave asymptomatic and inactive cysts alone – monitor size by ultrasound Active cysts should first be treated by a full course of albendazole Several procedures are available – PAIR, pericystectomy with omentoplasty and hepatic segmentectomy; appropriate management is customised according to the particular patient and organ involved Increasingly, a laparoscopic approach is being tried

Laparoscopic management Currently, surgeons trained in minimal access surgery perform hydatid surgery using minimal access. Laparoscopic marsupialisation of the cyst (de-roofing), consisting of removal of the cyst containing the endocyst along with daughter cysts, is the most common procedure. In the initial steps, the cyst is aspirated, taking care not to spill any contents, using povidone iodine or hypertonic saline as a scolicidal agent. Any communication with the biliary tree is oversewn and pedicled omentum is sutured to the margins of the cyst. If the cyst is small, superficial and in the left lobe, cystopericystectomy is performed at centres experienced enough to do more advanced surgery, removing the entire cyst intact.

(b)

Pulmonary hydatid disease The lung is the second commonest organ affected after the liver. The size of the cyst can vary from very small to a considerable size. The right lung and lower lobes are slightly more often involved. The cyst is usually single, although multiple cysts do occur and concomitant hydatid cysts in other organs, such as the liver, are not unknown. The condition may be silent and found incidentally. Symptomatic patients present with cough, expectoration, fever, chest pain and sometimes haemoptysis. Silent cysts may present as an emergency due to rupture or an allergic reaction. Uncomplicated cysts present as rounded or oval lesions on chest radiography. Erosion of the bronchioles results in air being introduced between the pericyst and the laminated membrane and gives a fine radiololucent crescent, the ‘meniscus or crescent sign’ (Figure 6.15). This is often regarded as a sign of impending rupture. When the cyst ruptures, the crumpled collapsed endocyst floats in the residual fluid, giving rise to the ‘water-lily’ sign on CT scan (Figure 6.16). Rupture into the pleural cavity results in pleural effusion. CT scan defines the pathology in greater detail. The mainstay of treatment of pulmonary hydatid is surgery. Medical treatment is less successful and considered when surgery is not possible because of poor general condition or diffuse disease affecting both lungs, or recurrent or ruptured cysts. The principle of surgery is to preserve as much viable lung tissue as possible. The exact procedure can vary: cystotomy, capittonage, pericystectomy, segmentectomy or occasionally pneumonectomy.

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Figures 6.15 Chest radiographs: (a) showing a smooth rounded cystic lesion in the right lower lobe; (b) showing a ‘meniscus or crescent’ sign (courtesy of Professor Saibal Gupta, MS, FRCS, Professor of Cardiovascular Surgery, Kolkata, India and Dr Rupak Bhattacharya, Kolkata, India).

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stigma. History records that in the distant past sufferers were made to wear cow bells so that other people could avoid them. The use of the term ‘leper’, still used metaphorically to denote an outcast, does not help to break down the social barriers that continue to exist against the sufferer.

Pathology

Figure 6.16 Computed tomographic scan showing the ‘water-lily’ sign. A young mountaineer, while on a high altitude trip, complained of sudden shortness of breath, cough and copious expectoration consisting of clear fluid and flaky material. At first thought to be due to pulmonary oedema, it turned out to be ruptured hydatid cyst, successfully treated by surgery (courtesy of Professor Saibal Gupta, MS, FRCS, Professor of Cardiovascular Surgery, Kolkata, India and Dr Rupak Bhattacharya, Kolkata, India).

Summary box 6.11 Pulmonary hydatid disease ●● ●● ●● ●●

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The second most common organ involved Size of the cyst has a wide variation May present as an incidental finding Clinical presentation may be elective or as an emergency due to rupture Plain radiograph shows ‘meniscus or crescent’ sign; CT shows ‘water-lily’ sign Ideal treatment is surgical – various choices are available

LEPROSY

The bacillus inhabits the colder parts of the body – hence it is found in the nasal mucosa and skin in the region of the ears, thus involving the facial nerve as it exits from the stylomastoid foramen. The disease is transmitted from the nasal secretions of a patient, the infection being contracted in childhood or early adolescence. After an incubation period of several years, the disease presents with skin, upper respiratory or neurological manifestations. The bacillus is acid fast but weakly so when compared with Mycobacterium tuberculosis. The disease is broadly classified into two groups – lepromatous and tuberculoid. In lepromatous leprosy, there is widespread dissemination of abundant bacilli in the tissues, with macrophages and few lymphocytes. This is a reflection of the poor immune response, resulting in depleted host resistance from the patient. In tuberculoid leprosy, on the other hand, the patient shows a strong immune response with scant bacilli in the tissues, epithelioid granulomas, numerous lymphocytes and giant cells. The tissue damage is inversely proportional to the host’s immune response. There are various grades of the disease between the two main spectra. Summary box 6.12 Mycobacterium leprae – pathology ●●

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Introduction

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Leprosy, also called Hansen’s disease, is a chronic infectious disease caused by an acid-fast bacillus, Mycobacterium leprae, that is widely prevalent in the tropics. Globally, India, Brazil, Nepal, Mozambique, Angola and Myanmar account for 91% of all cases; India alone accounts for 78% of the world’s disease. Patients suffer not only from the primary effects of the disease but also from social discrimination, sadly compounded by use of the word ‘leper’ for one afflicted with this disease. Close contact over a long duration (several years) is required for disease transmission. Ignorance of this fact on the part of the general public results in ostracism and social

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Leprosy is a chronic curable infection caused by Mycobacterium leprae It occurs mainly in tropical regions and resource-poor countries The majority of cases are located in the Indian subcontinent Transmission is through nasal secretions, the bacillus inhabiting the colder parts of the body It is attributed to poor hygiene and insanitary conditions The incubation period is several years The initial infection occurs in childhood Lepromatous leprosy denotes a poor host immune reaction Tuberculoid leprosy occurs when host resistance is stronger than the virulence of the organism

Clinical features and diagnosis The disease is slowly progressive and affects the skin, upper respiratory tract and peripheral nerves. In tuberculoid leprosy, the damage to tissues occurs early and is localised to one part of the body, with limited deformity of that organ. Neural involvement is characterised by thickening of the nerves, which are tender. There may be asymmetrical well-defined

wing to the stigma attached to the word ‘leper’, RG Cochrane suggested that the best name for leprosy is ‘Hansen’s disease’. O Gerhard Henrik Armauer Hansen, 1841–1912, physician in charge of a leper hospital near Bergen, Norway. Robert Greenhill Cochrane, 1899–1985, medical missionary who became an international authority on leprosy; he devoted his time to leprosy patients in South East Asia, particularly India.

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Figure 6.18  Frontal view of the face showing eye changes in leprosy – paralysis of orbicularis oculi and loss of eyebrows.

Figure 6.17  Lateral view of the face showing collapse of the nasal bridge due to destruction of nasal cartilage by leprosy.

anaesthetic hypopigmented or erythematous macules with elevated edges and a dry and rough surface – lesions called leprids. In lepromatous leprosy, the disease is symmetrical and extensive. Cutaneous involvement occurs in the form of several pale macules that form plaques and nodules called lepromas. The deformities produced are divided into primary, which are caused by leprosy or its reactions, and secondary, resulting from effects such as anaesthesia of the hands and feet. Nodular lesions on the face in the acute phase of the lepromatous variety are known as ‘leonine facies’ (looking like a lion). Later, there is wrinkling of the skin, giving an aged appearance to a young individual. There is loss of the

(a)

(b)

eyebrows and destruction of the lateral cartilages and septum of the nose with collapse of the nasal bridge and lifting of the tip of the nose (Figure 6.17). There may be paralysis of the branches of the facial nerve in the bony canal or of the zygomatic branch. Blindness may be attributed to exposure keratitis or iridocyclitis. Paralysis of the orbicularis oculi causes incomplete closure of the eye, epiphora and conjunctivitis (Figure 6.18). The hands are typically clawed (Figure 6.19) because of involvement of the ulnar nerve at the elbow and the median nerve at the wrist. Anaesthesia of the hands makes these patients vulnerable to frequent burns and injuries. Similarly, clawing of the toes (Figure 6.20) occurs as a result of involvement of the posterior tibial nerve. When the lateral popliteal nerve is affected, it leads to foot drop, and the nerve can be felt to be thickened behind the upper end of the fibula. Anaesthesia of the feet predisposes to trophic ulceration (Figure 6.21), chronic infection, contraction and autoamputation. Involvement of the testes causes atrophy,

Figures 6.19  (a, b) Typical bilateral claw hand from leprosy due to involvement of the ulnar and median nerves.

Figure 6.20 Claw toes from involvement of the posterior tibial nerve by leprosy; also note autoamputation of toes of the right foot.

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Figure 6.21  Bilateral trophic ulceration of the feet due to anaesthesia of the soles resulting from leprosy; also note claw toes on the left foot.

which in turn results in gynaecomastia (Figure 6.22). Confirmation of the diagnosis is obtained by a skin smear or skin biopsy, which shows the classical histological and microbiological features. Summary box 6.13 Leprosy – diagnosis ●●

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Typical clinical features and awareness of the disease should help to make a diagnosis The face has an aged look, with collapse of the nasal bridge and ocular changes Thickened peripheral nerves, patches of anaesthetic skin, claw hands, foot drop and trophic ulcers are characteristic Microbiological examination of the acid-fast bacillus and typical histology on skin biopsy are confirmatory

Treatment A herbal derivative from the seeds of Hydrocarpus wightiana called chalmoogra oil was the mainstay of treatment, with some success, until the advent of dapsone (diamino-diphenyl sulphone). Dapsone, one of the principal drugs, was a derivative of prontosil red (Domagk). This is used according to

Figure 6.22  Typical leonine facies and gynaecomastia in leprosy.

the WHO guidelines along with rifampicin and clofazimine. During treatment, the patient may develop acute manifestations. These are controlled with steroids. Multiple drug therapy for 12 months is the key to treatment. A team approach between an infectious diseases specialist, plastic surgeon, ophthalmologist, and hand or orthopaedic surgeon is important. Surgical treatment is indicated in advanced stages of the disease for functional disability of limbs, cosmetic disfigurement of the face and visual problems. These entail major reconstructive surgery, the domain of the plastic surgeon. Surgery for deformities in the hand is aimed at returning the ability to achieve a grasp and a pinch grip. Tendon transfers are used to recreate the function of the lumbricals which have been lost due to damage to the ulnar nerve. In the foot, damage to the common peroneal nerve leads to a foot drop due to paralysis of tibialis anterior. If a foot-drop splint is not adequate then once again a tendon transfer (tibialis posterior into the dorsum of the foot) will improve function. Ulcers resulting from an insensate foot should be completely debrided followed by protection with a plaster cast.

Gerhard Domagk, 1895–1964, German physician, Lecturer in Pathologic Anatomy, University of Munster, Germany, discovered prontosil in 1935, for which he was awarded the Nobel Prize for Physiology or Medicine in 1939. Paul Wilson BrandCBE, FRCS, 1914–2003, was born to missionary parents in Southern India, and qualified in London in 1943. He himself was a dedicated missionary who was ‘An extraordinary gifted orthopaedic surgeon who straightened crooked hands and unravalled the riddle of leprosy.’ As a pioneer in tendon transfer techniques, he established and practised initially in New Life Center, Vellore, South India and Schieffelin Leprosy Research Centre, Karigiri, South India. Initially he trained as a carpenter and builder and maintained that his training as a carpenter helped him in his expertise in tendon transplantation. When he was awarded the CBE, his wife, Margaret, came to know about it when she found a letter from Her Majesty’s Government informing him of the award, while emptying the pockets of his trousers before they were put into the wash. He later moved to Louisiana State University, Baton Rouge, LA, where he continued his work, and finally to Seattle as Emeritus Professor of Orthopaedics in the University of Washington, Seattle, USA. Margaret Brand, alongside her husband, Paul Brand, also contributed immensely to the health of leprosy patients by concentrating on research to prevent blindness in leprosy. She became known as ‘the woman who first helped lepers to see’. Frank Tovey OBE, b.1927, another English surgeon at about the same time (1951–1967), also performed extensive tendon transfers, facial and other reconstructive surgery on leprosy patients in Southern India in the State of Mysore. In this he was helped by his wife, Winifred, who organised the physiotherapy and rehabilitation of the patients and established village diagnostic and treatment centres).

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The general surgeon may be called upon to treat a patient when the deformity is so advanced that amputation is required or an abscess needs drainage as an emergency. All surgical procedures obviously need to be done under antileprosy drug treatment. This is best achieved by a team approach. Educating patients about the dreadful sequelae of the disease so that they seek medical help early is important. It is also necessary to educate the general public that patients suffering from the disease should not be made social outcasts.

toma, invasion to deeper tissues occurs earlier and is more extensive. The tendons and nerves are spared until late in the disease. This may explain the rarity of neurological and trophic changes even in patients with long-standing disease. Trophic changes are rare because the blood supply is adequate. Summary box 6.15 Mycetoma – pathogenesis ●●

Summary box 6.14

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Leprosy – treatment ●● ●● ●●

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Multiple drug therapy for a year Team approach Surgical reconstruction requires the expertise of a hand surgeon, orthopaedic surgeon and plastic surgeon Education of the patient and general public should be the keystone in prevention

MYCETOMA (This section has been contributed by: Professor Ahmed Hassan Fahal MBBS, FRCS, FRCSI, FRCSG, MD, MS, FRCP (London), Professor of Surgery, University of Khartoum, Khartoum, Sudan)

Introduction Mycetoma is a chronic, specific, granulomatous, progressive, destructive inflammatory disease, which involves the skin, subcutaneous tissues and deeper structures. The causative organism may be true fungi, when the condition is called eumycetoma; when caused by bacteria it is called actinomycetoma. The pathognomonic feature is the triad of painless subcutaneous mass, multiple sinuses and seropurulent discharge. It causes tissue destruction, deformity, disability, and death in extreme cases.

Epidemiology and pathogenesis The condition predominently occurs in the ‘mycetoma belt’ that lies between the latitudes 15° south and 30° north, comprising the countries of Sudan, Somalia, Senegal, India, Yemen, Mexico, Venezuela, Columbia, Argentina and a few others. The route of infection is inoculation of the organism that is resident in the soil through a traumatised area. Although in the vast majority there is no history of trauma, the portal of entry is always an area of minor unrecognised trauma in a bare-footed individual walking in a terrain full of thorns. Hence the foot is the commonest site affected. Mycetoma is not contagious. Once the granuloma forms it increases in size, and the overlying skin becomes stretched, smooth, shiny and attached to the lesion. Areas of hypo- or hyperpigmentation sometimes develop. Eventually it invades the deeper structures. This is usually gradual and delayed in eumycetoma. In actinomyce-

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Mostly occurs in the ‘mycetoma belt’ There are two types – eumycetoma and actinomycetoma Caused by fungi or bacteria entering through a site of trauma which may not be apparent; hence the foot is most commonly affected Produces a chronic, specific, granulomatous, progressive, destructive inflammatory lesion Results in tissue destruction, deformity, disability and sometimes death

Clinical presentation As mycetoma is painless, presentation is late in the majority. It presents as a slowly progressive, painless, subcutaneous swelling commonly at the site of presumed trauma. The swelling is variable in its physical characteristics: firm and rounded, soft and lobulated, rarely cystic, and is often mobile. Multiple secondary nodules may evolve; they may suppurate and drain through multiple sinus tracts. The sinuses may close transiently after discharge during the active phase of the disease. Fresh adjacent sinuses may open while some of the old ones may heal completely. They coalesce and form abscesses, the discharge being serous, serosanguineous or purulent. During the active phase of the disease the sinuses discharge grains, the colour of which can be black, yellow, white or red depending upon the organism. Pain supervenes when there is secondary bacterial infection. The common sites affected are those that come into ­contact with soil during daily activities: the foot in 70% (­Figure 6.23) and the hand in 12% (Figure 6.24). In endemic areas the knee (Figure 6.25), arm, leg, head and neck (Figure 6.26), thigh and perineum (Figure 6.27) can

Figure 6.23  Mycetoma of the foot.

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Figure 6.24  Mycetoma of the hand.

Fibure 6.27 Extensive sattelite inguinal actinomycetoma from a primary foot lesion involving the anterior abdominal wall and perineum.

Figure 6.25  Mycetoma of the knee.

be involved. Rare sites are the chest, abdominal wall, facial bones, mandible, testes, paranasal sinuses and eye. In some patients there may be areas of local hyperhidrosis over the lesion. This may be due to sympathetic overactivity or increased local temperature due to raised arterial blood flow caused by the chronic inflammation. In the majority of patients, the regional lymph nodes are small and shotty. Lymphadenopathy is common. This may be due to secondary bacterial infection, lymphatic spread of mycetoma or a local immune response to the disease. The condition remains localised; constitutional disturbances are a sign of secondary bacterial infection. Cachexia and anaemia from malnutrition and sepsis may be seen in late cases. It can be fatal, especially in cases of cranial mycetoma.

Spread

Figure 6.26  Actinomycetoma of the head and neck.

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Local spread occurs predominantly along tissue planes. The organism multiplies to form colonies which spread along the fascial planes to skin and underlying structures. Lymphatic spread, more common in actinomycetoma, occurs to the regional lymph nodes, and increases with repeated inadequate surgical excision procedures. During the active phase of the disease, these lymphatic satellites may suppurate and discharge; lymphadenopathy may also be due to secondary bacterial infection. Spread via the blood stream can occur. The apparent clinical features of mycetoma are not always a reliable indicator of the extent and spread of the disease. Some small lesions with few sinuses may have many deep connecting tracts, through which the disease can spread quite extensively. Therefore surgery in mycetoma under local anaesthesia is contraindicated.

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Differential diagnosis Mycetoma should be distinguished from Kaposi’s sarcoma, malignant melanoma, fibroma and foreign body (thorn) granuloma. A radiograph that demonstrates the presence of bone destruction in the absence of sinuses is suggestive of tuberculosis. The radiological features of advanced mycetoma are similar to those of primary osteogenic sarcoma. Primary osseous mycetoma is to be differentiated from chronic osteomyelitis, osteoclastoma, bone cysts and syphilitic osteitis. In endemic areas the dictum should be ‘any subcutaneous swelling must be considered a mycetoma until proven otherwise’.

Diagnosis Several imaging techniques are available to confirm the diagnosis: plain radiography, ultrasound, CT and magnetic resonance imaging (MRI).

Plain radiograph In the early stages, soft tissue shadows (often multiple) with calcification and obliteration of the fascial planes may be seen. As the disease progresses, the cortex may be compressed from the outside by the granuloma, leading to bone scalloping. Periosteal reaction with new bone spicules may create a sun-ray appearance and Codman’s triangle, not unlike an osteogenic sarcoma (Figure 6.28). Late in the disease, there may be multiple punched-out cavities throughout the bone.

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Ultrasound This can differentiate between eumycetoma and actinomycetoma as well as between mycetoma and other conditions. In eumycetoma, the grains produce numerous sharp bright hyper-reflective echoes. There are multiple thick-walled cavities with absent acoustic enhancement. In actinomycetoma, the findings are similar but the grains are less distinct. The size and extent of the lesion can be accurately determined ultrasonically, a finding useful in planning surgical treatment.

MRI This helps to assess bone destruction, periosteal reaction, and particularly soft tissue involvement (Figure 6.29). MRI usually shows multiple 2–5mm lesions of high signal intensity, which indicates the granuloma, interspersed within a low-intensity matrix denoting the fibrous tissue. The ‘dot-in-circle sign’, which indicates the presence of grains, is highly characteristic.

CT scan CT findings in mycetoma are not specific but are helpful to detect early bone involvement. (a)

Granuloma

Soft tissue swelling

Dot-in-circle sign

Cavity (b)

Periosteal reaction

Figure 6.28  Plain x-ray of the knee showing multiple large cavities involving the lower femur, upper tibia and fibula, with well-defined margins and periosteal reaction typical of eumycetoma.

Figure 6.29  (a) Magnetic resonance imaging (MRI) of the foot showing multiple lesions of high signal intensity, which indicates granuloma, interspersed within a low-intensity matrix, which is the fibrous tissue and the ‘dot-in-circle sign’, which indicates the presence of grains. (b) MRI showing massive upper thigh and lower abdominal actinomycetoma.

Moritz Kaposi, 1837–1902, Hungarian born, Professor of Dermatology, University of Vienna, Austria, was born to a Jewish family; originally his surname was Kohn. When he converted to Catholicism in 1871, he changed his surname to Kaposi. He described the sarcoma in 1872. The viral cause was discovered in 1994. Ernest Codman, 1869–1940, American surgeon. Codman’s triangle can be seen in osteosarcoma, Ewing’s sarcoma and subperosteal abscess and haematoma.

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Histopathological diagnosis Deep biopsy is obtained under general or regional anaesthesia, although the chance of local spread is high. The biopsy should be adequate, contain grains and should be fixed immediately in 10% formal saline. Three types of host tissue reaction occur against the organism. ●●

●●

●●

Type I: the grains are usually surrounded by a layer of polymorphonuclear leukocytes. The innermost neutrophils are closely attached to the surface of the grain, sometimes invading the grain and causing its fragmentation. The hyphae and cement substance disappear and only remnants of brown pigmented cement are left behind. Outside the zone of neutrophils there is granulation tissue containing macrophages, lymphocytes, plasma cells and few neutrophils. The mononuclear cells increase in number towards the periphery of the lesion. The outermost zone of the lesion consists of fibrous tissue. Type II: the neutrophils largely disappear and are replaced by macrophages and multinucleated giant cells which engulf grain material. This consists largely of pigmented cement substance although hyphae are sometimes identified. Type III: this is characterised by the formation of a well organised epithelioid granuloma with Langhan’s type giant cells. The centre of the granuloma will sometimes contain remnants of fungal material.

Fine needle aspiration cytology (FNAC) Fine needle aspiration cytology (FNAC) can yield an accurate diagnosis and helps in distinguishing between eumycetoma and actinomycetoma. The technique is simple, rapid and sensitive.

Culture A variety of microorganisms are capable of producing mycetoma that can be identified by their textural description, morphology and biological activities in pure culture. Deep surgical biopsy is always needed to obtain the grains which are the source of culture. The grains extracted through the sinuses are usually contaminated and not viable and hence should be avoided. Several media may be used to isolate and grow these organisms. In the absence of the classical triad of mycetoma, the demonstration of significant antibody titres against the causative organism may be of diagnostic value and aid follow up. The common serodiagnostic tests are immunoelectrophoresis and ELISA.

Summary box 6.16 Mycetoma – diagnosis ●● ●●

●●

●● ●● ●● ●● ●●

Usually presents late as it is painless Triad of painless subcutaneous mass, multiple sinuses and seropurulent discharge Clinical picture may be deceptive as there may be deepseated extension May spread to lymph nodes Can be confused with Kaposi’s sarcoma Radiologically can be mistaken for osteosarcoma MRI shows typical ‘dot-in-circle’ sign Open biopsy and FNAC are confirmatory

Management Ideally this should be a combined effort between the physician and the surgeon. In actinomycetoma, combined drug therapy with amikacin sulphate and co-trimoxazole in the form of cycles is the treatment of choice. Amoxicillin– clavulanic acid, rifampacin, sulphonamides, gentamicin and kanamycin are used as a second line of treatment. Long-term drug treatment can have serious side effects. In eumycetoma, ketoconazole, intraconazole and voriconazole are the drugs of choice. They may need to be used for up to a year. Use of these drugs should be closely monitored for side effects. While not curative, these drugs help to localise the disease by forming thickly encapsulated lesions which are then amenable to surgical excision. Medical treatment for both types of mycetoma must continue until the patient is cured and also in the postoperative period.

Surgical treatment Surgery is indicated for small localised lesions, resistance to medical treatment or for a better response after medical treatment in patients with massive disease. Excision may need to be much more extensive than suggested at first on clinical appearance because the disease may extend to deeper planes which are not clinically apparent. The surgical options are wide local and debulking excisions and amputations. Amputation, used as a life-saving procedure, is indicated in advanced mycetoma (Figure 6.30) refractory to medical treatment with severe secondary bacterial infection.The amputation rate is 10–25%. Postoperative medical treatment should continue for an adequate period to prevent recurrence. The recurrence rate varies from 25 to 50%. This can be local or distant, to regional lymph nodes. Recurrence is usually due to inadequate surgical excision, use of local anaesthesia, lack of surgical experience, non-compliance with drugs for financial reasons and lack of health education.

Theodor Langhans, 1839–1915, Professor of Pathological Anatomy, University of Berne, Switzerland.

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twice as frequently as those of the upper limb (Figures 6.31 and 6.32). Fortunately, only 1–2% of sufferers develop paralytic symptoms but, when they do occur, the disability causes much misery (Figure 6.33). When a patient develops fever with muscle weakness, Guillain–Barré syndrome needs to be

Figure 6.31  Polio affecting predominantly the upper limb muscles with wasting of the intercostal muscles.

Figure 6.30  Hip disarticulation for a massive thigh eumycetoma.

Summary box 6.17

(a)

Mycetoma – management ●● ●● ●●

●● ●●

●●

Ideally combined management by physician and surgeon Medical treatment with appropriate long-term antibiotics In large lesions medical treatment to reduce the size followed by excision Beware of serious drug side effects Surgery in the form of wide excision and amputation as a lifesaving procedure High recurrence rate (b)

POLIOMYELITIS Introduction Poliomyelitis is an enteroviral infection that sadly still affects children in certain parts of the world – this is in spite of effective vaccination having been universally available for several decades. The virus enters the body by inhalation or ingestion. Clinically, the disease manifests itself in a wide spectrum of symptoms – from a few days of mild fever and headache to the extreme variety consisting of extensive paralysis of the bulbar form that may not be compatible with life because of involvement of the respiratory and pharyngeal muscles.

Diagnosis The disease targets the anterior horn cells, causing lower motor neurone paralysis. Muscles of the lower limb are affected

Figure 6.32  (a, b) A 12-year-old patient with polio showing marked wasting of the left upper arm muscles with flexion contractures of the left knee and hip; there is equinus deformity of the foot (courtesy of Dr SM Lakhotia, MS and Dr PK Jain, MD, DA, Kolkata, India).

Georges Guillain, 1876–1961, Professor of Neurology, The Faculty of Medicine, Paris, France. Jean Alexandre Barré, 1880–1967, Professor of Neurology, Strasbourg, France. Guillain and Barrédescribed the condition in a joint paper in 1916 whilst serving as Medical Officers in the French Army during the First World War.

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Summary box 6.18 Poliomyelitis ●● ●●

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A viral illness that is preventable Presents with protean manifestations of fever, headache and muscular paralysis without sensory loss, more frequently affecting the lower limbs Treatment is mainly medical and supportive in the early stages Surgery should only be undertaken after very careful assessment as most patients learn to live with their disabilities Surgery is considered for the various types of paralysis in the form of tendon transfers and arthrodesis, which is the domain of a specialist orthopaedic surgeon

TROPICAL CHRONIC PANCREATITIS Introduction

Figure 6.33 A young patient with polio showing paralysis of the lower limb and paraspinal muscles causing marked scoliosis and a deformed pelvis.

Tropical chronic pancreatitis is a disease affecting the younger generation from poor socioeconomic strata in resource-poor countries, seen mostly in southern India. The aetiology remains obscure, with malnutrition, dietary, familial and genetic factors being possible causes. Alcohol ingestion does not play a part in the aetiology.

Aetiology and pathology excluded. The latter has sensory symptoms and signs. Cerebrospinal fluid (CSF) analysis should help to differentiate the two conditions.

Management Surgical management is directed mainly towards the rehabilitation of the patient who has residual paralysis, the operations being tailored to the particular individual’s disability. Children especially may show improvement in their muscle function for up to 2years after the onset of the illness. Thereafter, many patients learn to manage their disability by incorporating various manoeuvres (‘trick movements’) into their daily life. The surgeon must be cautious in considering such a patient for any form of surgery. Surgical treatment in the chronic form of the disease is the domain of a highly specialised orthopaedic surgeon who needs to work closely with the physiotherapist both in assessing and in rehabilitating the patient. Operations are only considered after a very careful and detailed assessment of the patient’s needs. A multidisciplinary team, consisting of the orthopaedic surgeon, neurologist, physiotherapist, orthotist and the family, should decide upon the need for and advisability of any surgical procedure. A description of the operations for the various disabilities is beyond the scope of this book. The reader should therefore seek surgical details in a specialist textbook. In 2012, WHO declared India a polio-free country.

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Cassava (tapioca) is a root vegetable that is readily available and inexpensive and is therefore consumed as a staple diet by people from a poor background. It contains derivatives of cyanide that are detoxified in the liver by sulphur-containing amino acids. The less well-off among the population lack such amino acids in the diet. This results in cyanogen toxicity, causing the disease. Several members of the same family have been known to suffer from this condition; this strengthens the theory that cassava toxicity is an important cause because family members eat the same food. Macroscopically, the pancreas is firm and nodular with extensive periductal fibrosis, with intraductal calcium carbonate stones of different sizes and shapes that may show branches and resemble a staghorn. The ducts are dilated. Microscopically, intralobular, interlobular and periductal fibrosis is the predominant feature, with plasma cell and lymphocyte infiltration. There is a high incidence of pancreatic cancer in these patients. Summary box 6.19 Pathology of tropical chronic pancreatitis ●●

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Almost exclusively occurs in resource-poor countries and is due to malnutrition; alcohol is not a cause Cassava ingestion is regarded as an aetiological factor because of its high content of cyanide compounds Dilatation of pancreatic ducts with large intraductal stones Fibrosis of the pancreas as a whole A high incidence of pancreatic cancer in those affected by the disease

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Diagnosis The patient, usually male, is almost always below the age of 40 years and from a poor socioeconomic background. The clinical presentation is abdominal pain, thirst, polyuria and features of gross pancreatic insufficiency causing steatorrhoea and malnutrition. The patient looks ill and emaciated. Initial routine blood and urine tests confirm that the patient has type 1 diabetes mellitus. This is known as fibrocalculous pancreatic diabetes, a label that is aptly descriptive of the typical pathological changes. Serum amylase is usually normal; in an acute exacerbation, it may be elevated. A plain abdominal radiograph shows typical pancreatic calcification in the form of discrete stones in the duct (Figure 6.34). Ultrasound and CT scanning of the pancreas confirm the diagnosis. An ERCP, as an investigation, should only be done when the procedure is also being considered as a therapeutic manoeuvre for removal of ductal stones in the pancreatic head by papillotomy.

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the management of malnutrition. Treatment of pain should be along the lines of the usual analgesic ladder: non-opioids, followed by weak and then strong opioids and, finally, referral to a pain clinic. Surgical treatment is necessary for intractable pain, particularly when there are stones in a dilated duct. Removal of the stones, with a side-to-side pancreaticojejunostomy to a Roux loop, is the procedure of choice. As most patients are young, pancreatic resection is only very rarely considered, and only as a last resort, when all available methods of pain relief have been exhausted. Summary box 6.21 Treatment of tropical chronic pancreatitis ●●

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Mainly medical – pain relief, insulin for diabetes and pancreatic supplements for malnutrition Surgery is reserved for intractable pain when all other methods have been exhausted Operations are side-to-side pancreaticojejunostomy; resection in extreme cases

TUBERCULOSIS Although tuberculosis can affect all systems in the body, in the tropical world the surgeon is most often faced with tuberculosis affecting the cervical lymph nodes and the small intestine. Therefore, in this chapter tuberculous cervical lymphadenitis and tuberculosis of the small bowel will be described.

TUBERCULOUS CERVICAL LYMPHADENITIS Introduction

Figure 6.34  Plain radiograph of the abdomen showing large stones along the main pancreatic duct typical of tropical chronic pancreatitis (courtesy of Dr V Mohan, Chennai, India).

This is common in the Indian subcontinent. A young person who has recently arrived from an endemic area, presenting with cervical lymphadenopathy, should be diagnosed as having tuberculous lymphadenitis unless otherwise proven. With acquired immune deficiency syndrome (AIDS) being globally prevalent, this is not as rare in the West in the indigenous population as it used to be.

Summary box 6.20

Diagnosis

Diagnosis of tropical chronic pancreatitis

Any of the cervical group of lymph nodes (jugulodigastric, submandibular, supraclavicular, posterior triangle) can be involved. The patient has the usual general manifestations of tuberculosis: evening pyrexia, cough (maybe from pulmonary tuberculosis) and malaise; if the sufferer is a child, failure to thrive is a significant finding. Locally there will be regional lymphadenopathy where the lymph nodes may be matted; in late stages a cold abscess may form – a painless, fluctuant, mass which is not warm; significantly there are no signs of inflammation (Figure 6.35), hence it is called a ‘cold abscess’. This is a clinical manifestation of underlying caseation. Left untreated, the cold abscess, initially deep to the deep fascia, bursts through into the space just beneath the

●● ●● ●● ●●

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The usual sufferer is a type 1 diabetic under 40 years of age Serum amylase may be elevated in an acute exacerbation Plain radiograph shows stones along the pancreatic duct Ultrasound and CT scan of the pancreas confirm the diagnosis ERCP should be used as an investigation only when combined with a therapeutic procedure

Treatment The treatment is mainly medical, with exocrine support using pancreatic enzymes, treatment of diabetes with insulin and

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Figure 6.35  Cervical tuberculous: cold abscess about to burst.

superficial fascia. This produces a bilocular mass with cross fluctuation. This is called a ‘collar-stud’ abscess. Eventually this may burst through the skin, discharging pus and forming a tuberculous sinus (Figure 6.36). The latter typically has watery discharge with undermined edges.

Figure 6.36 Cervical tuberculous sinus with typical overhanging edges (courtesy of Professor Ahmed Hassan Fahal, FRCS MD MS, Khartoum, Sudan).

Summary box 6.22 Tuberculous cervical lymphadenitis ●● ●● ●● ●●

●● ●●

●● ●●

This is a common condition at any age A matted lymph nodal mass is the typical clinical feature In later stages the mass may be cystic, denoting an abscess The abscess denotes underlying caseation and does not show any features of inflammation – hence called a cold abscess Ultimately the abscess may burst, forming a sinus Diagnosis is clinched by culture of pus and biopsy of the lymph node Involvement of other systems must be excluded Treatment is mainly medical

Investigations Raised ESR and CRP, low haemoglobin and a positive ­Mantoux test are usual, although the last is not significant in a patient from an endemic area. The Mantoux test (tuberculin skin test), although in use for over a hundred years, has now been superseded by interferon-gamma (IFN-γ) release assays. This is an in vitro blood test of cellular immune response. Antigens unique to Mycobacterium tuberculosis are used to stimulate and measure T cell release of IFN-γ. This helps to earmark patients who have latent or subclinical tuberculosis and thus will benefit from treatment. Sputum for culture and sensitivity (the result may take several weeks) and staining by the Ziehl–Neelsen method for

acid-fast bacilli (the result is obtained much earlier) should be carried out. Specific investigations would include aspiration of the pus from a cold abscess for culture and sensitivity. If the mass is still in the early stages of adenitis, excision biopsy should be done. Here, part of the lymph nodes should be sent fresh and unfixed to the laboratory, who should be warned of the arrival of the specimen so that the tissue can be appropriately processed immediately.

Treatment This must be combined management between the physician and the surgeon. Tuberculous infection at other sites must be excluded and suitably managed. Medical treatment is the mainstay. The reader is asked to look up details of medical treatment in an appropriate source.

TUBERCULOSIS OF SMALL INTESTINE Introduction Infection by Mycobacterium tuberculosis is common in the tropics. In these days of international travel and increased migration, tuberculosis in general and intestinal tuberculosis in particular are no longer clinical curiosities in non-endemic countries. Any patient, particularly one who has recently

collar-stud abscess is so-called because it resembles a collar stud (which has two parts) used in shirts with detachable collars, now largely out of fashion. A Charles Mantoux, 1877–1947, physician, Le Cannet, Alpes Maritimes, France, described the intradermal tuberculin skin test in 1908. Franz Heinrich Paul Ziehl, 1859–1926, neurologist, Lubeck, Germany. Friedrich Carl Adolf Neelsen, 1854–1894, pathologist, Prosector, the Stadt-Krankenhaus, Dresden, Germany.

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arrived from an endemic area and who has features of generalised ill health and altered bowel habit, should arouse suspicion for intestinal tuberculosis. The increased prevalence of human immunodeficiency virus (HIV) infection worldwide has also made tuberculosis more common. Stricture in the terminal ileum

Pathology

Perforation in the terminal ileum

There are two types: ulcerative and hyperplastic. In both types, there may be marked mesenteric lymphadenopathy. ●●

●●

Ulcerative type: When a patient with pulmonary tuberculosis swallows infected sputum, the organism colonises the lymphatics of the terminal ileum, causing transverse ulcers with typical undermined edges. The serosa is usually studded with tubercles. Histology shows caseating granuloma with giant cells (Figure 6.37). This pathological entity, referred to as the ulcerative type, denotes a severe form of the disease in which the virulence of the organism overwhelms host resistance. Hyperplastic type: This occurs when host resistance has the upper hand over the virulence of the organism. It is caused by drinking infected unpasteurised milk. There is a marked inflammatory reaction causing hyperplasia and thickening of the terminal ileum because of its abundance of lymphoid follicles, thus resulting in narrowing of the lumen and obstruction. Macroscopically, this type may be confused with Crohn’s disease. The small intestine shows areas of stricture and fibrosis, most pronounced at the terminal ileum (Figure 6.38). As a result, there is shortening of the bowel with the caecum being pulled up into a subhepatic position.

Figure 6.38  Emergency limited ileocolic resection: specimen showing a tuberculous stricture in the terminal ileum and perforation of a transverse ulcer just proximal to the stricture.

Summary box 6.23 Tuberculosis – pathology ●●

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Increasingly being seen in non-endemic areas, mostly among immigrants from endemic areas Two types are recognised – ulcerative and hyperplastic The ulcerative type occurs when the virulence of the organism is greater than the host defence The opposite occurs in the hyperplastic type Small bowel strictures are common in the hyperplastic type, mainly affecting the ileocaecal area and presenting with obstructive symptoms In the ulcerative type, the bowel serosa is studded with tubercles Localised areas of ascites occur in the form of cocoons The lungs and other organs, particularly of the genitourinary system, may also be involved simultaneously

Clinical features

Figure 6.37  Histology of ileocaecal tuberculosis showing epithelioid cell granuloma (black arrows) with caseation (blue arrows) (courtesy of Dr AK Mandal, New Delhi, India).

Patients present electively with weight loss, chronic cough, malaise, evening rise in temperature with sweating, vague abdominal pain with distension and alternating constipation and diarrhoea. As an emergency, they present with features of distal small bowel obstruction from strictures of the small bowel, particularly the terminal ileum. Rarely, a patient may present with features of peritonitis from perforation of a tuberculous ulcer in the small bowel (Figure 6.38). Examination shows a chronically ill patient with a ‘doughy’ feel to the abdomen from areas of localised ascites. In the hyperplastic type, a mass may be felt in the right iliac fossa. In addition, some patients may present with

Burrill Bernard Crohn, 1884–1983, gastroenterologist, Mount Sinai Hospital, New York, NY, USA, described regional ileitis in 1932 along with Leon Ginzburg and Gordon Oppenhiemer.

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fistula-in-ano, which is typically multiple with undermined edges and watery discharge. As this is a disease mainly seen in certain resource-poor countries, patients may present late as an emergency from intestinal obstruction. Abdominal pain and distension, constipation and bilious and faeculent vomiting are typical of such a patient, who is usually in extremis. There may be involvement of other systems, such as the genitourinary tract, when the patient complains of frequency of micturition. Clinical examination does not show any abnormality. The genitourinary tract should then be investigated. Summary box 6.24 Tuberculosis – clinical features ●●

●●

●●

●●

Intestinal tuberculosis should be suspected in any patient from an endemic area who presents with weight loss, malaise, evening fever, cough, alternating constipation and diarrhoea and intermittent abdominal pain with distension The abdomen has a doughy feel; a mass may be found in the right iliac fossa The emergency patient presents with features of distal small bowel obstruction – abdominal pain, distension, bilious and faeculent vomiting Peritonitis from a perforated tuberculous ulcer in the small bowel can be another emergency presentation

ically with a high subhepatic caecum with the narrow ileum entering the caecum directly from below upwards in a straight line rather than at an angle (Figures 6.39 and 6.40a). Laparoscopy reveals the typical picture of tubercles on the bowel serosa, multiple strictures, a high caecum, enlarged lymph nodes, areas of caseation and ascites. Culture of the ascitic fluid may be helpful. A chest radiograph is essential (Figure 6.40b). If the patient complains of urinary symptoms, urine is sent for microscopy and culture; the finding of sterile pyuria should alert the clinician to the possibility of tuberculosis of the urinary tract, when the appropriate investigations should be done. A flexible cystoscopy would be very useful in the presence of sterile pyuria. A contracted bladder (‘thimble’ bladder) with ureteric orifices that are in-drawn (‘golf-hole’ ureter) may be seen; these changes are due to fibrosis. In the patient presenting as an abdominal emergency, urea and electrolytes show evidence of gross dehydration. A plain abdominal radiograph shows typical small bowel obstruction – valvulae conniventes of dilated jejunum and featureless ileum with evidence of fluid between the loops. Summary box 6.25 Intestinal tuberculosis – investigations ●●

●●

Investigations

●●

General investigations are the same as those for suspected tuberculosis anywhere in the body. They have been detailed in the previous section. A barium meal and follow-through (or small bowel enema) shows strictures of the small bowel, particularly the ileum, typ-

●●

(a)

●●

●●

Raised inflammatory markers, anaemia and positive sputum culture Interferon-γ release assays for subclinical infection Ultrasound of the abdomen may show localised areas of ascites Chest radiograph shows pulmonary infiltration Barium meal and follow-through shows multiple small bowel strictures particularly in the ileum, with a subhepatic caecum If symptoms warrant, the genitourinary tract is also investigated

(b)

SUBHEPATIC CAECUM

SUBHEPATIC CAECUM

Figures 6.39  (a, b) Series of a barium meal and follow-through showing strictures in the ileum, with the caecum pulled up into a subhepatic position.

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(a)

81

(b)

SUBHEPATIC CAECUM

PULMONARY INFILTRATION

Figures 6.40  Barium meal and follow-through (a) and chest radiograph (b) in a patient with extensive intestinal and pulmonary tuberculosis, showing ileal strictures with high caecum and pulmonary infiltration.

Treatment On completion of medical treatment, the patient’s small bowel is reimaged to look for significant strictures. If the patient has features of subacute intermittent obstruction, bowel resection, in the form of limited ileocolic resection with anastomosis between the terminal ileum and ascending colon, strictureplasty or right hemicolectomy, is performed as deemed appropriate. The surgical principles and options in the elective patient are very similar to those for Crohn’s disease, where resections should be kept as conservative as possible. The emergency patient presents a great challenge. Such a patient is usually from a poor socioeconomic background, hence the late presentation of acute, distal, small bowel obstruction. The patient is extremely ill from dehydration, malnutrition, anaemia and probably active pulmonary tuberculosis. Vigorous resuscitation should precede the operation. At laparotomy, the minimum life-saving procedure is carried out, such as a side-toside ileotransverse anastomosis for a terminal ileal stricture. If the general condition of the patient permits, a one-stage resection and anastomosis may be performed. Thereafter, the patient should ideally be under the combined care of the physician and surgeon for a full course of antituberculous chemotherapy and improvement in nutritional status, which may take up to 3–6 months. The patient who had a simple bypass procedure is reassessed and, when the disease is no longer active (as evidenced by return to normal inflammatory markers, weight gain, negative sputum culture), an elective right hemicolectomy is done to remove the blind loop. This may be supplemented with strictureplasty for short strictures at intervals.

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Perforation is treated by thorough resuscitation followed by resection of the affected segment. Anastomosis is performed, provided it is regarded as safe to do so, when peritoneal contamination is minimal and widespread disease is not encountered; otherwise, as a first stage, resection and exteriorisation is done followed by restoration of bowel continuity as a second stage later on after a full course of antituberculous chemotherapy and improvement in nutritional status. Summary box 6.26 Tuberculosis – treatment ●●

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Patients should ideally be under the combined care of a physician and surgeon Vigorous supportive and full drug treatment are mandatory in all cases Symptomatic strictures are treated by the appropriate resection, e.g. local ileocolic resection or strictureplasty as an elective procedure once the disease is completely under control Acute intestinal obstruction from distal ileal stricture is treated by thorough resuscitation followed by side-to-side ileotransverse bypass Once the patient has recovered with medical treatment, then the second-stage definitive procedure of right hemicolectomy is done to remove the blind loop One-stage resection and anastomosis can be considered if the patient’s general condition permits Perforation is treated by appropriate local resection and anastomosis or exteriorisation if the condition of the patient is very poor; this is later followed by restoration of bowel continuity after the patient has fully recovered with antituberculous chemotherapy

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CHAPTER 6  Tropical infections and infestations

TYPHOID Introduction Typhoid fever is caused by Salmonella typhi, also called the typhoid bacillus, a gram-negative organism. Like most infections occurring in the tropics, the organism gains entry into the human gastrointestinal tract as a result of poor hygiene and inadequate sanitation. It is a disease normally managed by physicians, but the surgeon may be called upon to treat the patient with typhoid fever because of perforation of a typhoid ulcer.

Pathology Following ingestion of contaminated food or water, the organism colonises the Peyer’s patches in the terminal ileum, causing hyperplasia of the lymphoid follicles followed by necrosis and ulceration. The microscopic picture shows erythrophagocytosis with histiocytic proliferation (Figure 6.41). If the patient is left untreated or inadequately treated, the ulcers may lead to perforation and bleeding. The bowel may perfor­ ate at several sites including the large bowel.

H antigens of Salmonella typhi and paratyphi in the patient’s serum. In endemic areas, laboratory facilities may sometimes be limited. Certain other tests have been developed that identify sensitive and specific markers for typhoid fever. Practical and cheap kits are available for their rapid detection that need no special expertise and equipment. These are MultiTest Dip-S-Ticks to detect immunoglobulin G (IgG), Tubex to detect immunoglobulin M (IgM) and TyphiDot to detect IgG and IgM. These tests are particularly valuable when blood cultures are negative (due to prehospital treatment or self-medication with antibiotics) or facilities for such an investigation are not available. In the second or third week of the illness, if there is severe generalised abdominal pain, this indicates a perforated typhoid ulcer unless otherwise proven. The patient, who is already very ill, deteriorates further with classical features of peritonitis. An erect chest radiograph or a lateral decubitus film (in the very ill, as they usually are) will show free gas in the peritoneal cavity. In fact, any patient being treated for typhoid fever who shows a sudden deterioration accompanied by abdominal signs should be considered to have a typhoid perforation until proven otherwise. Summary box 6.27 Diagnosis of bowel perforation secondary to typhoid ●●

●● ●●

●●

The patient presents in, or has recently visited, an endemic area The patient has persistent high temperature and is very toxic Positive blood or stool cultures for Salmonella typhi and the patient is already on treatment for typhoid After the second week, signs of peritonitis usually denote perforation, which is confirmed by the presence of free gas seen on radiograph

Treatment

Figure 6.41 Histology of enteric perforation of the small intestine showing erythrophagocytosis (arrows) with predominantly histiocytic proliferation (courtesy of Dr AK Mandal, New Delhi, India).

Diagnosis A typical patient is from an endemic area or has recently visited such a country and suffers from a high temperature for 2–3 weeks. The patient may be toxic with abdominal distension from paralytic ileus and may have melaena due to haemorrhage from a typhoid ulcer; this can lead to hypovolaemia. Blood and stool cultures confirm the nature of the infection and exclude malaria. Although obsolete in some parts of the world, the Widal test is still done in the Indian subcon­ tinent. The test looks for the presence of agglutinins to O and

Vigorous resuscitation with intravenous fluids and antibiotics in an intensive care unit gives the best chance of stabilising the patient’s condition. Metronidazole, cephalosporins and gentamicin are used in combination. Chloramphenicol, despite its potential side effect of aplastic anaemia, is still used occasionally in resource-poor countries. Laparotomy is then carried out. Several surgical options are available, and the most appropriate operative procedure should be chosen judiciously depending upon the general condition of the patient, the site of perforation, the number of perforations and the degree of peritoneal soiling. The alternatives are closure of the perfor­ ation (Figure 6.42) after freshening the edges, wedge resection of the ulcer area and closure, resection of bowel with or without anastomosis (exteriorisation), closure of the perforation and side-to-side ileotransverse anastomosis, ileostomy or colostomy where the perforated bowel is exteriorised after refashioning the edges.

Daniel Elmer Salmon, 1850–1914, veterinary pathologist, Chief of the Bureau of Animal Industry, Washington, DC, USA. Johann Conrad Peyer, 1653–1712, Professor of Logic, Rhetoric and Medicine, Schaffhausen, Switzerland, described the lymph follicles in the intestine in 1677. Georges Fernand Isidore Widal, 1862–1929, Professor of Internal Pathology, and later of Clinical Medicine, The Faculty of Medicine, Paris, France.

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PART 1 | BASIC PRINCIPLES Further reading

(a)

83

(b)

Figures 6.42  (a, b) Typhoid perforation of the terminal ileum.

After closing an ileal perforation, the surgeon should look for other sites of perforation or necrotic patches in the small or large bowel that might imminently perforate, and deal with them appropriately. Thorough peritoneal lavage is essential. The linea alba is closed, leaving the rest of the abdominal wound open for delayed closure, as wound infection is almost inevitable and dehiscence not uncommon. In the presence of rampant infection, laparostomy may be a good alternative. When a typhoid perforation occurs within the first week of illness, the prognosis is better than if it occurs after the second or third week because, in the early stages, the patient is less nutritionally compromised and the body’s defences are more robust. Furthermore, the shorter the interval between diagnosis and operation, the better the prognosis. Summary box 6.28 Treatment of bowel perforation from typhoid ●● ●● ●● ●● ●● ●● ●●

Manage in intensive care Resuscitate and give intravenous antibiotics Laparotomy – choice of various procedures Commonest site of perforation is the terminal ileum Having found a perforation, always look for others In the very ill patient, consider some form of exteriorisation Close the peritoneum and leave the wound open for secondary closure

FURTHER READING AMOEBIASIS Barnes SA, Lillemore KD. Liver abscess and hydatid disease In: Zinner NJ, Schwartz I, Ellis H (eds). Maingot’s abdominal operations, 10th edn, Vol. 2. New York: Appleton and Lange, McGraw-Hill, 1997, pp. 1527–45. Bruns BR, Scalea TM. Complex liver abscess. In: Complications in acute care surgery. Springer International Publishing, 2017, pp. 189–97.

ASCARIASIS Das AK. Hepatic and biliary ascariasis. J Global Infect Dis 2014; 6(2): 65. Steinberg R, Davies J, Millar AJ et al. Unusual intestinal sequelae after operations for Ascaris lumbricoides infestation. Paediatr Surg Int 2003; 19(1–2): 85–7.

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Wani RA, Parray FQ, Bhat NA et al. Non-traumatic terminal ileal perforation. World J Emerg Surg 2006; 10: 1–7.

ASIATIC CHOLANGIOHEPATITIS Choi BI, Han JK, Hong ST, Lee KH. Clonorchiasis and cholangiocarcinoma: etiologic relationship and imaging diagnosis. Clin Microbiol Rev 2004; 17(3): 540–52.

FILARIASIS Manjula Y, Kate V, Ananthakrishnan N. Evaluation of sequential intermittent pneumatic compression for filarial lymphoedema. Natl Med J India 2002; 15(4): 192–4. Lim KH, Speare R, Thomas G, Graves P. Surgical treatment of genital manifestations of lymphatic filariasis: a systematic review. World J Surg 2015; 39(12): 2885–99.

HYDATID DISEASE Barnes SA, Lillemore KD. Liver abscess and hydatid disease. In: Zinner NJ, Schwartz I, Ellis H (eds). Maingot’s abdominal operations, 10th edn, Vol. 2. New York: Appleton and Lange, McGraw Hill, 1997, pp. 1527–45. Chiodini P. Parasitic infections. In: Russell RCG, Williams NS, Bulstrode CJK (eds). Bailey & Love’s short practice of surgery, 24th edn. London: Arnold, 2004, pp. 146–74. WHO Informal Working Group. International classification of ultrasound images in cystic echinococcosis for application in clinical and field epidemiological settings. Acta Trop 2003; 85(2): 253–61.

LEPROSY Anderson GA. The surgical management of deformities of the hand in leprosy. Bone Joint J 2006; 88(3): 290–4.

MYCETOMA Fahal AH. Management of mycetoma. Expert Rev Dermat 2010; 5(1): 87–93. Hassan MA, Fahal AH. Mycetoma. In: Kamil R, Lumby J (eds). Tropical surgery. London: Westminster Publications Ltd, 2004, pp. 786–90.

TROPICAL CHRONIC PANCREATITIS Barman KK, Premlatha G, Mohan V. Tropical chronic pancreatitis. Postgrad Med J 2003; 79: 606–15.

TYPHOID Aziz M, Qadir A, Aziz M, Faizullah (2005) Prognostic factors in typhoid perforation. J Coll Phys Surg Pakistan 2005; 15(11): 704–7. Olsen SJ, Pruckler J, Bibb W et al. Evaluation of rapid diagnostic tests for typhoid fever. J Clin Microbiol 2004; 42(5): 1885–9.

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Bailey & Love Bailey & Love Bailey & Love Bailey &7Love Bailey & Love Bailey & Love Chapter

Basic surgical skills and anastomoses Learning objectives To understand: •• The principles of patient positioning and operating theatre safety •• The principles of skin and abdominal incisions •• The principles of laparoscopic trocar insertion •• The principles of wound closure

To know the principles in performing:

•• Bowel anastomoses •• Vascular anastomoses To be aware of:

•• The principles of drain usage •• The principles of diathermy and advanced energy devices

INTRODUCTION Successful outcomes in surgery depend on knowledge, skills and judgement. While this chapter concentrates on technical skill, it is important for the modern surgeon to remember that non-technical skills, such as communication, empathy and teamwork, are but a few of the skills required. We used to think of technical skill starting with ‘knife to skin’; it is also important to realise that a successful outcome for a patient is dependent on a surgeon who takes responsibility to make sure that the patient reaches that point, with all factors, such as positioning and equipment, considered first. Teamwork includes adherence to modern ‘human factors’ principles, such as team brief and debrief, and the use of safety checklists.

PATIENT POSITIONING AND SAFETY ON THE OPERATING TABLE The safety of the patient in the operating theatre is paramount at all times, and is a key responsibility of the surgeon, regardless of grade, experience or seniority. For all cases it is the surgeon’s responsibility to make sure the patient is placed on the table to maximise exposure for the procedure itself and to ensure risks of injury are avoided. These are categorised below.

Transfer to and from the operating table The transfer of the anaesthetised patient is a critical moment where there are significant risks of falls, injuries and, rarely,

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death, not to mention injury to operating theatre personnel. Staff should all receive regular training in manual handling. Patients at additional risk include the obese, elderly and emaciated. These groups require additional care and specialised equipment.

Positioning on the table Safe and effective positioning of the anaesthetised patient also requires good training, appropriate equipment and attention to detail. The surgeon should take personal responsibility to maintain safety and to make sure exposure is adequate for the procedure. This includes placement of the passive diathermy electrode (‘pad’) to minimise the risk of electrosurgical burns and to account for metallic prostheses and pacemakers. The surgeon should also make sure that ancillary equipment, such as energy generators, suction, laparoscopic stack systems and the scrub assistants, is appropriately located around the surgeon and the patient on the operating table. The operating lights should also be placed in an optimal starting position. All these actions need to be undertaken before the surgical team scrubs, including any final checks before the patient is prepped and draped.

Pressure areas Patients at risk from pressure sores include those with diabetes, immunodeficiency, obesity or malnutrition, and those undergoing prolonged procedures. The areas of the body prone to injury are the heels, sacrum and other bony prominences. These areas should receive particular attention during positioning with additional measures taken in the at-risk groups.

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Compartment syndrome Acute postoperative compartment syndrome refers, in the context of surgery, to the consequences of increased pressure in a muscle compartment, usually in the lower limb, that can result in permanent disability or amputation. This occurs as a result of underperfusion, usually during prolonged surgery, often with elevation of the leg. Postoperatively, the pressure in the affected compartment rises to the point beyond which irreversible ischaemic damage to muscles and nerves occurs. It manifests with pain, reduced power, swelling, numbness and tingling. Early recognition is essential and prompt surgical fasciotomy is required to avoid the disastrous and permanently disabling sequelae.

10

There are certain areas of the body where an anaesthetised patient can be exposed to neuropraxia (nerve injury) which in some cases can be permanent and disabling. These are the brachial plexus, ulnar nerve and common peroneal nerve. The surgeon should lead the theatre team in ensuring these areas are protected, particularly in high-risk groups and for long procedures.

to necrosis of the undercut edge. The incision is facilitated by tension being applied across the line of the incision by the fingers of the non-dominant hand, but the surgeon must ensure that at no time is the scalpel blade directed at their own fingers as any slip may result in a self-inflicted injury. Blades for skin incisions usually have a curved cutting margin, while those used for an arteriotomy or drain-site insertion have a sharp tip (Figure 7.1). Scalpels should at all times be passed in a kidney dish rather than by a direct hand-to-hand process because the latter can lead to injury. Diathermy, laser, harmonic scalpels and combination devices can be used instead of blades when opening deeper tissues, as they can reduce blood loss and save operating time, and may reduce postoperative pain.

11

Nerve injury

SKIN INCISIONS Skin incisions should be made with a scalpel, with the blade being pressed firmly down at right angles to the skin and then drawn gently across the skin in the desired direction to create a clean incision, the site and extent of which should have been clearly planned by the surgeon. It is important not to incise the skin obliquely because such a shearing mechanism can lead

23

22

Considerations for laparoscopic surgery Laparoscopic surgery requires some different considerations to open surgery to ensure patient safety and to maximise the ergonomic performance of the procedure. Often, steep angles of tilt to the side, or Trendelenberg (head down) and reverse-Trendelenberg (head up) positions are required to move the abdominal viscera, such as small bowel, away from the operative field. There is significant danger that the patient can slide, or in some cases, fall off the operating table and be injured. It is the surgeon’s responsibility to ensure the patient is safely and securely placed on the operating table with appropriate restraints if indicated. So-called ‘side boards’ or arm restraints are best avoided in laparoscopic surgery as they can interfere with the laparoscopic instruments. Any restraints must be placed in such a way as to avoid or minimise the risk of nerve injury, e.g. the brachial plexus with shoulder supports. Devices such as suction bean bags and antislip mats can be used to help secure placement of the patient. Occasionally, laparoscopic surgery is performed in a lateral position to expose the target organ, e.g. kidney or spleen, with the aid of gravity. Experience and training are required to maintain safety and security for such procedures.

85

15

ve ve

Figure 7.1 Scalpel blade sizes and shapes. The 22-blade is often used for abdominal incisions, the 11-blade for arteriotomy and the 15-blade for minor surgical procedures.

When planning a skin incision, four factors should be considered: 1 Skin tension lines (Langer’s lines). These lines represent the orientation of the dermal collagen fibres and any incision placed parallel to these lines results in a better scar (Figure 7.2). 2 Anatomical structure. Incisions should avoid bony prominences and crossing skin creases if possible, and take into consideration underlying structures, such as nerves and vessels. 3 Cosmetic factors. Any incision should be made bearing in mind the ultimate cosmetic result, especially in exposed parts of the body, as an incision is the only part of the operation the patient sees. 4 Adequate access for the procedure. The incision must be functionally effective for the procedure in hand because any compromise purely on cosmetic grounds may render the operation ineffective or even dangerous. Occasionally, it may be necessary to excise a skin lesion with a circular incision in an area where the direction of

Karl Ritter Von Langer, 1847–1888, Austrian anatomist.

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Abdominal incisions Anterior

Posterior

Figure 7.2 Langer’s lines. These depict the orientation of the dermal collagen fibres. Reproduced with permission from Thomas WEG, Senninger N (eds). Short stay surgery. Berlin: Springer-Verlag, 2008.

Langer’s lines is not apparent. However, once the circular incision has been made, it can often be observed that the circular incision is converted to an ellipse, thus indicating the lines of tension. This circular incision should then be formally converted into an elliptical incision, remembering the rule of thumb that ‘an elliptical incision must be at least three times as long as it is wide’ for the wound to heal without tension. Occasionally, ‘dog ears’ remain in the corner of elliptical incisions in spite of adequate care having been taken during formation and primary closure of an elliptical wound. In these situations, it is advisable to pick up the ‘dog ear’ with a skin hook and excise it as shown in Figure 7.3. This allows for a satisfactory cosmetic outcome.

X

Y

X

Laparoscopic surgery Similar attention to detail applies to laparoscopic surgery, where access is of equal importance to open surgery. Correct port site placement and closure are crucial to the success of the operative procedure. Laparoscopic surgery is covered in more detail in Chapter 8.

Y

ISBN: 9781444121278

Short Practice of Surgery, 26th Ed

As for skin incisions, all abdominal incisions should be planned in advance of surgery and take into consideration access to the relevant organs, surface landmarks, pain control and cosmetic outcome, e.g. transverse incisions tend to be associated with fewer respiratory complications and a better cosmetic outcome. In the past, traditional vertical midline or paramedian incisions were used for the majority of abdominal procedures, but there is a current trend to utilise transverse incisions wherever possible because these minimise post­ operative complications. The incision should be carried deeper through the subcutaneous tissues and then, depending on the site of the incision (Figure 7.4), the muscle layers should be divided or split, and the peritoneum displayed. This should be picked up between two clips and gently incised to ensure there is no damage to the underlying organs. This is particularly important in the emergency situation when there may be dilatation of the bowel. Every incision should be made with closure in mind, and the layers appropriately delineated. Mass closure of the abdominal wall is usually advocated, using large bites and short steps in the closure technique and either non-absorbable (e.g. nylon or polypropylene) or very slowly absorbable suture material (e.g. polydioxanone suture (PDS)). It has been estimated that, for abdominal wall closure, the length of the suture material should be at least four times the length of the wound to be closed to minimise the risk of abdominal dehiscence or later incisional hernia.

Proof Stage: 1

2 1 Fig No: 19.2

co.uk

4 5

7 8

X

Y

6 11

9 10

X

Y

Figure 7.3  Dealing with a ‘dog ear’ at the corner of an elliptical incision. Reproduced with permission from Thomas WEG, Senninger N (eds). Short stay surgery. Berlin: Springer-Verlag, 2008.

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3

Figure 7.4  Abdominal incisions. Reproduced with permission from Thomas WEG. Preparation and revision for the MRCS. London: ­Churchill Livingstone (Elsevier Limited), 2004. 1, Midline; 2, Kocher’s; 3, thoracoabdominal; 4, rectus split; 5, paramedian; 6, transverse; 7, McBurney’s gridiron; 8, inguinal; 9, pfannenstiel; 10, McEvedy; 11,Rutherford Morison.

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Summary box 7.1

Summary box 7.2

The benefits of laparoscopic surgery

The principles of safe laparoscopic surgery

●● ●● ●● ●● ●●

Less postoperative pain Better cosmesis Earlier return of normal physiological function Shorter hospital stay Earlier resumption of normal activities

●● ●●

●●

●●

●●

The basic principles of port (trocar) site placement in laparoscopic surgery are: 1 The umbilicus is a convenient and safe point of insertion of the first (primary) trocar because the skin here is fused to the peritoneum. Care must be taken to avoid bowel regardless of the technique employed. Great care and good technique must be employed to avoid injury to the major vessels (aorta, vena cava and iliac vessels), particularly in thin female patients, who are at greater risk. Elsewhere, the midline is safe for further (secondary) trocars, though care must be taken below the umbilicus to avoid the bladder. 2 An ‘open’ or ‘semi-open’ technique is practised by many general surgeons to minimise, if not eradicate, the possibility of injury to an underlying viscus during insertion of the primary trocar. 3 Scars should be avoided as bowel is more likely to be adherent to the undersurface; for midline scars, the primary trocar should be inserted away from the midline with an open cutdown or an optical trocar. 4 All secondary trocars should be inserted under direct vision to avoid damage to bowel, bladder and blood vessels. A ‘two-handed’ technique should be used to avoid sudden trocar movements that may inadvertently puncture a viscus. 5 Trocars should always be inserted perpendicular to the abdominal wall. Oblique insertion results in increased pressure or torque while instruments are being used, which fatigues the surgeon and causes increased trauma to the patient’s abdominal wall. This is of particular relevance in obese patients. 6 A hand’s breadth (the patient’s hand) either side of the midline is the rectus sheath which contains the epigastric vessels. By placing non-midline trocars lateral to the rectus sheath, usually in the mid-clavicular line, the epigastric vessels can be avoided. 7 Where possible, smaller diameter trocars should be used as they are associated with less postoperative pain, a lower incidence of port-site incisional hernia and better cosmesis. All port sites above 5mm in diameter should undergo suture closure of the fascial layers to reduce the possibility of port-site hernia in the acute postoperative setting and incisional hernia longer term. 8 All secondary trocars should be removed under direct vision to observe for port site bleeding. 9 Bladed trocars should be avoided near blood vessels to reduce the risk of bleeding.

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●●

87

The umbilicus is preferred for primary trocar insertion An open or semi-open technique is prefered by most surgeons Open insertion away from the umbilicus is safer if there is a midline scar Secondary trocars should be inserted and removed under direct vision All trocars should be placed perpendicular to the abdominal wall All trocar sites above 5mm in length should undergo closure of the fascial layer

Technique for laparoscopic primary trocar insertion There are a number of different techniques described for primary trocar insertion. In most cases the umbilicus is the preferred site because the skin is fused to the peritoneum, even in obese patients. The presence of a scar at the umbilicus is a relative contraindication as bowel may be adherent resulting in injury which can be overlooked and result in postoperative peritonitis. The author uses a semi-open technique for a 10–12mm trocar and this is described here: 1 The umbilical cicatrix is everted with a tissue grasping forceps such as a Littlewood’s. It is important to grasp the cicatrix directly as this is closest to the adherent peritoneum. Counter-traction is maintained throughout the subsequent steps until the primary trocar is inserted (Figure 7.5). 2 The umbilical stalk is palpated inferior to the everted cicatrix while maintaining cephalad (towards the head) traction. 3 A curved 10–12mm transverse incision is made inferior to the cicatrix (Figure 7.6). 4 The umbilical stalk is exposed with sharp and blunt dissection to reveal the decussation (crossing) of fibres just above its junction with the linea alba (Figure 7.7). 5 A 5mm vertical incision is made through the decussation with an 11-blade, taking care only to incise the fascia at this point and not to enter the peritoneum (Figure 7.8). 6 A blunt haemostat is then pushed through the preperitoneal fat and peritoneum; the surgeon will feel a ‘pop’ as the instrument enters the peritoneal cavity (Figure 7.9). 7 A blunt-tipped 10 or 12mm trocar is pushed through the same point of insertion as the haemostat and in the same direction (Figure 7.10). 8 The laparoscopic camera is used to confirm successful placement in the peritoneal cavity before insufflation with CO2 gas. 9 CO2 gas insufflation is commenced at low flow (1–4litres per minute) and increased to a maximum pressure of 15mmHg and with a maximum flow rate of 20litres per minute. 10 For patients with scars from previous abdominal surgery, the safest technique is a full open approach at Palmer’s

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Figure 7.5  The umbilical cicatrix is grasped with a tissue-grasping forceps (e.g. Littlewood’s) and everted.

Figure 7.6 A curved subumblilical incision is made.

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Figure 7.7 The skin is retracted to reveal the junction of the stalk and the linea alba.

Figure 7.8  A small vertical incision is made in the junction using an 11 bladed scalpel.

Figure 7.9  A blunt, long haemostat is used to enter the peritoneum and enlarge the incision in the umbilical stalk.

Figure 7.10 A blunt primary trocar and cannula are inserted and their position is confirmed with the laparoscopic camera before insufflation.

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PART 1 | BASIC PRINCIPLES Wound closure

point, 3cm below the left subcostal margin in the midclavicular line. Adequate lighting and good assistance with retraction are essential. 11 In obese patients with scars from previous surgery an optical blunt trocar can be used to enter the peritoneal cavity under vision.

Summary box 7.4 Types of wound healing ●●

●●

WOUND CLOSURE The suturing of any incision or wound needs to take into consideration the site and tissues involved, and the technique for closure should be chosen accordingly. There is no ideal wound closure technique that would be appropriate for all situations, and the ideal suture has yet to be produced, although many of the desired characteristics are listed in Summary box 7.3. Therefore, the correct choice of suture technique and suture material is vital, but will never compensate for inadequate operative technique, and, for any wound to heal well, there must be a good blood supply and no tension on the closure. Clean uninfected wounds with a good blood supply heal by primary intention and therefore closure simply requires accurate apposition of the wound edges. However, if a wound is left open, it heals by secondary intention through the formation of granulation tissue, which is tissue composed of capillaries, fibroblasts and inflammatory cells. Wound contraction and epithelialisation assist in ultimate healing, but the process may take several weeks or months. Delayed primary closure, or tertiary intention, is utilised when there is a high probability of the wound being infected. The wound is left open for a few days and, provided any infective process has resolved, the wound is closed to heal by primary intention. Skin grafting is another form of tertiary intention healing.

Summary box 7.3 Suture material: desired characteristsics ●● ●● ●● ●● ●● ●● ●● ●● ●● ●● ●● ●● ●●

Easy to handle Predictable behaviour in tissues Predictable tensile strength Sterile Glides through tissues easily Secure knotting ability Inexpensive Minimal tissue reaction Non-capillary Non-allergenic Non-carcinogenic Non-electrolytic Non-shrinkage

89

●●

Primary intention Clean wound Secondary intention Healthy granulation tissue Overexuberant granulation tissue Infected sloughy wound Black eschar Tertiary intention Delayed closure Skin grafting

When choosing suture materials, there are certain specific requirements depending on the tissues to be sutured; for example, vascular anastomoses require smooth, non-absorbable, non-elastic material, while biliary anastomoses require an absorbable material that will not promote tissue reaction or stone formation. When using absorbable material, the time for which wound support is required and maintained will vary according to the tissues in which it is inserted. Furthermore, certain tissues require wound support for longer than others, for example muscular aponeuroses compared with subcutaneous tissues. It is therefore crucial for the surgeon to select the suture material and suture technique that will most effectively achieve the desired objective for each wound closure or anastomosis.

Suture materials History Sutures are best made of soft thread, not too hard twisted that it may sit easier on the tissue, nor are too few nor too many of either of them to be put in. Aurelius Cornelius Celsus, 25bc–ad50

Multiple examples of early surgery abound, with East African tribes ligating blood vessels with tendon strips, and closing wounds with acacia thorns pushed through the wound with strips of vegetable matter wound round these in a figure of eight. A South American method of wound closure involved using large black ants to bite the wound together with their pincers or jaws acting like skin clips, and then the ant’s body was twisted off leaving the head in place keeping the wound apposed. By 1000bc, Indian surgeons were using horsehair, cotton and leather sutures while, in Roman times, linen and silk and metal clips, called fibulae, were commonly used to close gladiatorial wounds. By the end of the nineteenth century, developments in the textile industry led to major advances, and both silk and catgut became popular as suture materials. Lister believed that catgut soaked in chromic acid

Aurelius Cornelius Celsus, Roman physician, 25bc–ad50. Joseph Lister (Lord Lister), Professor of Surgery in Glasgow, Edinburgh and King’s College Hospital, London and Vice President of Royal College of Surgeons of England, 1827–1912. Alexis Carrel, 1873–1944, surgeon from Lyons in France, worked at the Rockefeller Institute for Medical Research in New York, NY, USA. He received the Nobel Prize for Physiology or Medicine in 1912 ‘in recognition for his works on vascular suture and the transplantation of blood vessels and organs’. Gladiatorswere so called because they fought with a Roman sword called a ‘gladius’.

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(a form of tanning) prevented early dissolution in body fluids and tissues, while Moynihan felt that chromic catgut was ideal as it could be sterilised, was non-irritant to tissues, kept its strength until its work was done and then disappeared. However, catgut is no longer in use as it causes an inflammatory cellular reaction with release of proteases and may also carry the risk of prion transmission if of bovine origin.

Suture characteristics There are five characteristics of any suture material that need to be considered: 1 Physical structure. Suture material may be monofilament or multifilament. Monofilament suture material is smooth and tends to slide through tissues easily without any sawing action, but is more difficult to knot effectively. Such material can be easily damaged by gripping it with needle holder or forceps and this can lead to fracture of the suture material. Multifilament or braided sutures are much easier to knot, but have a surface area of several thousand times that of monofilament sutures and thus have a capillary action and interstices where bacteria may lodge and be responsible for persistent infection or sinuses. In order to overcome some of these problems, certain materials are produced as a braided suture, which is coated with silicone in order to make it smooth. 2 Strength. The strength of a suture material depends upon its constituent material, its thickness and how it is hand­ led in the tissues. Suture material thickness is classified according to its diameter in tenths of a millimetre (Table 7.1), although the figure assigned is also dependent upon the nature of the material, e.g. absorbable material and non-absorbable material, such as polypropylene, may differ in their designations. The tensile strength of a suture can be expressed as the force required to break it when pulling the two ends apart, but is only a useful approximation as to its strength in the tissues, because what matters is the material’s in vivo strength. Absorbable sutures show a decay of this strength with the passage of time and although a material may last in the tissues for the stated period in the manufacturer’s product profile, its tensile strength cannot be relied on in vivo for this entire period.

TABLE 7.1  Size of suture material. Metric (EurPh)

Range of diameter (mm)

USP (‘old’)

1 1.5 2 3 3.5 4 5

0.100–0.149 0.150–0.199 0.200–0.249 0.300–0.349 0.350–0.399 0.400–0.499 0.500–0.599

5–0 4–0 3–0 2–0 0 1 2

Materials, such as catgut (no longer in use in the UK), have a tensile strength that lasts only about a week, while PDS will remain strong in the tissues for several weeks. However, even non-absorbable sutures do not necessarily maintain their strength indefinitely, and may degrade with time. Those non-absorbable materials of synthetic origin, such as polypropylene, probably retain their tensile strength indefinitely and do not change in mass in the tissues, although it is still possible for them to fracture. Non-absorbable materials of biological origin, such as silk, will definitely fragment with time and lose their strength, and such materials should never be used in vascular anastomoses for fear of late fistula formation. 3 Tensile behaviour. Suture materials behave differently depending upon their deformability and flexibility. Some may be ‘elastic’, where the material will return to its original length once any tension is released, while others may be ‘plastic’, in which case this phenomenon does not occur. Sutures may be deformable, in that a circular cross-section may be converted to an oval shape, or they may be more rigid and have the somewhat irritating capacity to kink and coil. Many synthetic materials demonstrate ‘memory’, so that they keep curling up in the shape they adopted within the packaging. A sharp but gentle pull on the suture material helps to diminish this memory, but the more memory a suture material has, the lower is the knot security. Therefore, knotting technique also plays a significant role in any suture line’s tensile strength and it is important to recognise that sutures lose 50% of their strength at the knot. 4 Absorbability. Suture materials may be non-absorbable (Table 7.2) or absorbable (Table 7.3) and this property must be taken into consideration when choosing suture mater­ ials for specific wound closures or anastomoses. Sutures for use in the biliary or urinary tract need to be absorbable in order to minimise the risk of stone production. However, a vascular anastomosis requires a non-absorbable material and it is wise to avoid braided material because platelet adherence may predispose to distal embolisation. Nonabsorbable materials tend to be preferred where persistent strength is required and, as an artificial graft or prosthesis never heals fully or integrates into a host artery, persistent monofilament suture materials, such as polypropylene, are almost universally used. 5 Biological behaviour. The biological behaviour of suture material within the tissues depends upon the constituent raw material. Biological or natural sutures, such as catgut, are proteolysed, but this involves a process that is not entirely predictable and can cause local irritation, and such materials are therefore seldom used. Synthetic polymers are hydrolysed and their disappearance in the tissues is more predictable. However, the presence of pus, urine or faeces influences the final result and renders the outcome more unpredictable. There is also some evidence that, in

Berkley George Andrew Moynihan (Lord Moynihan of Leeds), 1865–1936, Professor of Clinical Surgery, University of Leeds, Leeds, UK. Moynihan felt that English surgeons knew little about the work of their colleagues both at home and abroad. Therefore, in 1909, he established a small travelling club which in 1929 became the Moynihan Chirurgical Club. It still exists today. He took a leading part in founding the British Journal of Surgery in 1913 and became the first chairman of the editorial committee until his death.

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the gut, cancer cells may accumulate at sites where sutures persist, possibly giving rise to local recurrence. For this reason, synthetic materials that have a greater predictability and elicit minimal tissue reaction may have an important non-carcinogenic property.

Barbed sutures Recently, novel suture materials have helped surgeons to reduce or eradicate the need for knot tying in some situations, such as laparoscopic surgery. These sutures have unidirectional or bidirectional barbs that secure the suture in the tissues.

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 Figure 7.11  Interrupted suture technique. Reproduced with permisthen to pass through both aspects of the suture line and sion from Royal College of Surgeons of England. The intercollegiate exit again at right angles (Figure 7.11). It is important for basic surgical skills course participants handbook, edns 1–4. London: the needle to be rotated through the tissues rather than to RCS. be dragged through, to avoid 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 X distance apart (Figure 7.12). Each suture should reach X 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 comX plete the closure by successively inserting sutures, halving the remaining deficits in the wound length. 2X 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 continu- Figure 7.12  The siting of sutures. As a rule of thumb, the distance of insertion from the edge of the wound should correspond to the thickous manner until the far end of the wound is reached (Fig- ness of the tissue being sutured (X). Each successive suture should be ure 7.13). Each throw of the continuous suture should be placed at twice this distance apart (2X). Reproduced with permission inserted at right angles to the wound, and this will mean from Royal College of Surgeons of England. The intercollegiate basic that the externally observed suture material will usually surgical skills course participants handbook, edns 1–4. London: RCS. 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 stringTitle: Bailey & Love’s Short Practice of Surgery, 26th Ed ISBN: 9781444121278 Proof Stage: 1 ing the wound by too much tension, or leaving the suture material too slack. There is www.cactusdesign.co.uk 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 verti- Figure 7.13  Continuous suture technique. Reproduced with permiscal or horizontal and tend to be used to produce either sion from Royal College of Surgeons of England. The intercollegiate eversion or inversion of a wound edge (Figure 7.14). The basic surgical skills course participants handbook, edns 1–4. London: initial suture is inserted as for an interrupted suture, but RCS. then the needle moves either 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. Title: Bailey & Love’s Short Practice of Surgery, 26th Ed

ISBN: 9781444121278

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Proof

Types

Braided or twisted multifilament. Dyed or undyed. Coated (with wax or silicone) or uncoated

Twisted

Monofilament or multifilament

Monofilament or braided multifilament Dyed or undyed

Monofilament or braided multifilament Dyed or undyed Coated (polybutylate or silicone) or uncoated

Monofilament. Dyed or undyed

Monofilament. Dyed or undyed

Silk

Linen

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Surgical steel

Nylon

Polyester

Polybutester

Polypropylene

Polymer of propylene

Infinite (>1 year)

Non-absorbable: remains encapsulated in body tissues

Non-absorbable: remains encapsulated in body tissues

Infinite (>1 year)

Polybutylene terephthalate and polytetramethylene ether glycol

Non-absorbable: remains encapsulated in body tissues

Infinite (>1 year)

Polyester (polyethylene terephthalate)

Degrades at approximately 15–20% per year

Non-absorbable Remains encapsulated in body tissues

Non-absorbable Remains encapsulated in body tissues

Fibrous encapsulation in body at 2–3 weeks Absorbed slowly over 1–2 years

Absorption rate

Loses 15–20% per year

Infinite (>1 year)

Stronger when wet Loses 50% at 6 months; 30% remains at 2 years

Loses 20% when wet; 80–100% lost by 6 months. Because of tissue reactions and unpredictability, silk is increasingly not recommended

Tensile strength

Polyamide polymer

An alloy of iron, nickel and chromium

Long staple flax fibres

Natural protein Raw silk from silkworm

Raw material

Low

Low

Low

Low

Minimal

Moderate

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

Tissue reaction

None

None

None

None

Should not be used in conjunction with prosthesis of different metal

Cardiovascular surgery, plastic surgery, ophthalmic surgery, general surgical subcuticular skin closure

Exhibits a degree of elasticity. Particularly favoured for use in plastic surgery

Cardiovascular, ophthalmic, plastic and general surgery

General surgical use, e.g. skin closure, abdominal wall mass closure, hernia repair, plastic surgery, neurosurgery, microsurgery, ophthalmic surgery

Closure of sternotomy wounds Previously found favour for tendon and hernia repairs

Ligation and suturing in gastrointestinal surgery. No longer in common use in most centres

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

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

Frequent uses

Contraindications

10/0–1 with needles

7/0–1 with needles

Monofilament: (ophthalmic) 11/10; 10/0 with needles; multifilament: 5/0–1 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: 5/0–5 with needles; multifilament: 5/0– 3/0 with needles

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

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

How supplied

92

Suture

TABLE 7.2  Non-absorbable suture materials.

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Plain

Chromic

Braided multifilament

Monofilament Dyed or undyed

Braided multifilament Dyed or undyed Coated or uncoated

Monofilament Dyed or undyed

Catgut

Catgut

Polyglactin

Polyglyconate

Polyglycolic acid

Polydioxanone (PDS)

Polyglycaprone Monofilament

Types

Suture

Copolymer of glycolite and caprolactone

Polyester polymer

Polymer of polyglycolic acid. Available with coating of inert, absorbable surfactant poloxamer 188 to enhance surface smoothness; 87% excreted in urine within 3 days

21 days maximum

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

Mild

Moderate

High

Tissue reaction

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

Mild

Minimal

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

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

Phagocytosis and enzymatic degradation within 90 days

Lost within 21–28 days Marked patient variability Unpredictable and not recommended

Approximately 60% remains at 2 weeks Approximately 30% remains at 3 weeks

Phagocytosis and enzymatic degradation within 7–10 days

Absorption rate

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

Tensile strength retention in vivo

Copolymer of glycolic Approximately 70% acid and trimethylene remains at 2 weeks carbonate Approximately 55% remains at 3 weeks

Copolymer of lactide and glycolide in a ratio of 90:10, coated with polyglactin and calcium stearate

Collagen derived from healthy sheep or cattle Tanned with chromium salts to improve handling and to resist degradation in tissue

Collagen derived from healthy sheep or cattle

Raw material

TABLE 7.3  Absorbable suture materials.

No use for extended support

Not for use in association with heart valves or synthetic grafts, or in situations in which prolonged tissue approximation under stress is required

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

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

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

As for plain catgut Synthetic absorbables superior

Not for use in tissues that heal slowly and require prolonged support Synthetic absorbables are superior

Contraindications

Subcuticular in skin, ligation, gastrointestinal and muscle surgery

Uses as for other absorbable sutures, in particular where slightly longer wound support is required

Uses as for other absorbable sutures, in particular where slightly longer wound support is required

Popular in some centres as an alternative to Vicryl and PDS

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

As for plain catgut

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

Frequent uses

8/0–2 with needles

Polydioxanone suture (PDS) 10/0–2 with needles

9/0–2 with needles; 9/0–2 without needles

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

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(a)

(b) Figure 7.14  (a, b) 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.

Figure 7.15 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.

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 7.15). 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 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.

closer the needle holder is to the tip of the needle, the greater the accuracy of suture placement and the less the degree of rotation of the surgeon’s hand required in suturing. The needle should never be grasped nearer than one-third of the way back from the rear of the needle. 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 reverse cutting in which the cutting edge is on the outside (Figure 7.16). Round­bodied 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 bloodborne infectious diseases. 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 vagina, 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.

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

The knot must be tied firmly, but without strangulating the tissues. ●● The knot must be unable to slip or unravel. ove’s Short Practice of Surgery, 26th Ed ISBN: 9781444121278 Proof Stage: 1 Fig No: 19.8a ●● The knot must be as small as possible to minimise the Needles amount of foreign material. esign.co.uk In the past, needles had eyes in them and suture material had to ●● The knot must be tightened without exerting any ­tension be loaded into them, which was not only time consuming, but it or pressure on the tissues being ligated, i.e. the knot should meant that the needle holes in tissues were considerably larger be bedded down carefully, only exerting pressure against than the suture material being used. Currently, needles are eyecounter-pressure from the index finger or thumb. less or ‘atraumatic’, with the suture material embedded within ●● During tying, the suture material must not be ‘sawed’ as the shank of the needle. The needle has three main parts: this weakens the thread. ●● The suture material must be laid square during tying, 1 shank; otherwise tension applied during tightening may cause 2 body; & Love’s Short Practice of Surgery, 26th Ed ISBN: 9781444121278 Proof Stage: 3 19.9 Figthe No:thread. breakage or fracture of 3 point. ●● When tying an instrument knot, the thread should only design.co.uk The needle should be grasped byISBN: the needle holder approx- Proofbe grasped free19.8b end, as gripping the thread with ve’s Short Practice of Surgery, 26th Ed 9781444121278 Stage: 1 at the Fig No: imately one-third to one-half of the way back from the rear artery forceps or needle holders can damage the material of the needle, avoiding both the shank and the point. The and again result in breakage or fracture. sign.co.uk

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1/2 circle

3/8 circle

1/4 circle

5/8 circle

95

1/2 curved

Straight

J needle

Compound curve

Crosssection

Needles used for suturing the abdominal wall:

Cutting needles for stitching skin

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 7.16  Types of needle.

●●

●●

The standard surgical knot is the reef knot (Figure 7.17), with a third throw for security, although with monofilament sutures, such as used 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

01_07-B&L27_Pt1_Ch07.indd 95

●● ●●

●●

right tension in certain circumstances, but must be followed by a standard reef knot to ensure security. When added security is required, a surgeon’s knot using a two throw 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 1–2mm long to prevent unraveling. This is ­particularly important when using monofilament material.

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Half-hitch

Crossed half-hitch

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.

Laparoscopic wound closure

Reef or square knot

Granny knot

Laparoscopic wounds are generally 3–12 mm in length. As with all incisions they should be parallel to Langer’s lines where possible. Skin closure can be carried out with sutures, using curved or straight needles, or glue, and can be further secured with adhesive strips.

Staples

Extra half-hitch on reef knot

Surgeon's knot

Figure 7.17  Standard knotting formations.

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.

Tissue glue Tissue glue is also available, based upon a solution of n-butyl-2-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 breaking

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). 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 7.18). 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 the 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 oesophago-jejunostomy, and the shaft is either extended through a small opening in the bowel wall or secured by a further purse-string 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.

Hümer Hültl, surgeon, St Stephen’s Hospital, Budapest, Hungary, described his gastric stapler in 1908.

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●●

(a) ●●

97

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.

LAPAROSCOPIC STAPLING DEVICES Since the early 1990s, increasingly complex surgical procedures have been performed laparoscopically. This revolution in practice has gone hand-in-hand with rapid evolutions in technology to allow existing open instruments and devices to be used laparoscopically, including surgical staplers. Many of the intestinal stapling devices are now adapted to be inserted down trocars during laparoscopic surgery, and although they look very different, the principles of function are identical to their open surgical equivalent. Linear cutting staplers allow bowel and blood vessels to be sealed and divided. Linear and circular staplers also allow intracorporeal anastomoses to be performed. As with open staplers, the surgeon must be trained in their safe use and aware of the principles, including different staple sizes.

(b)

THE PRINCIPLES OF ANASTOMOSES Bowel anastomoses (c) Figure 7.18  (a–c) Standard stapling devices.

●●

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 that the cuff of bowel that remains adjacent to the staple line is of the correct length. Down in the pelvis it

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 anastomoses for many years (Figure 7.19). However, Halsted favoured a one-layer extramucosal closure, and this was subsequently advocated by Matheson as

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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CHAPTER 7  Basic surgical skills and anastomoses

clamps should be used across the lumen of the bowel. Clamps should not impinge on the mesentery or the vasculature of the bowel for fear of damage to the vessels resulting in ischaemic changes. Ideally, the bowel edges should be pink and bleeding prior to anastomosis. The gold standard for a good blood supply for any anastomosis is the presence of arterial bleeding from the marginal vessel immediately adjacent to the cut end of the bowel and the absence of venous congestion. Excessive bleeding from the bowel wall may need oversewing if natural haemostasis is inadequate. Figure 7.19 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.

Intestinal anastomoses ●●

●● ●● ●● ●●

●●

Figure 7.20 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.

it was felt to cause the least tissue necrosis or luminal narrowing (Figure 7.20). This technique has now become widely accepted, although it is essential that this is not confused with a seromuscular suture technique. The extramucosal suture must include the submucosa because this has a high collagen content and is the most stable suture in all sections of ISBN:layer 9781444121278 e’s Short Practice of Surgery, 26th Ed the gastrointestinal tract. There are several prospective randomised trials comparing two-layer and single-layer anastogn.co.uk moses demonstrating that there is probably little to choose between these techniques, provided basic essentials as highlighted in Summary box 7.5 are observed. However, catgut and silk have been replaced by synthetic, usually absorbable, polymers. In the past, great emphasis was placed on good bowel preparation prior to any anastomosis. The rationale was that, with good bowel preparation and an empty bowel, there was less likelihood of faecal contamination and therefore it was probably not necessary to apply bowel clamps (even of the soft occlusion type). However, this tradition is now being challenged, and there is evidence to suggest that conventional bowel preparation provides little benefit, and indeed at times may prove detrimental 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, atraumatic intestinal

ort Practice of Surgery, 26th Ed

o.uk

Summary box 7.5

ISBN: 9781444121278

Ensure good blood supply to both bowel ends before and after formation of anastomosis Ensure the anastomosis is under no tension Avoid risk to mesenteric vessels by clamps or sutures Use atraumatic bowel clamps to minimise contamination Interrupted and continuous single-layer suture techniques are adequate and safe Stapling devices are an alternative when speed is required or access is a major factor

For all intestinal anastomoses, the bowel ends must be brought together without tension. Stay sutures, which avoid the need for tissue forceps, are invaluable for displaying the bowel ends and help with the accurate alignment of the bowel and the placement of the sutures. If the anastomosis is being undertaken on mobile bowel, the anterior wall layer of sutures can be inserted, either in a continuous or interrupted manner, and then 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 Proof Stage: 1 Fig No: 19.14 apposition of bowel edges should be as accurate as possible and the suture bites should be approximately 3–5 mm deep and 3–5mm 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 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

Proof Stage: 1

Fig No: 19.15

Sir George Lenthal Cheatle, 1865–1951, surgeon, King’s College Hospital, London, UK.

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PART 1 | BASIC PRINCIPLES Drains

the edge of the mesentery. In certain situations, as indicated above, stapling devices are used to fashion the anastomosis, but as they are expensive, many 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.

Vascular anastomoses

(a)

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(b)

Figure 7.21  (a, b) Arteriotomy being closed by vein patch. The 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.

Vascular anastomoses require an extremely accurate closure as they must be immediately watertight at the end of the oper- suture line can be started at the apex of the arteriotomy with ation when the vascular clamps are removed. In many cases, a double-ended suture, and then carried down each side with some form of prosthetic material or graft may be used which the final knot being placed at the midpoint of the vein patch will never be integrated into the body tissues and so the integ- graft, and not at the far end. The suture should go from outrity of the suture line needs to be permanent. For this rea- side to inside on the graft and from inside to outside on the son, polypropylene is one of the best sutures because it is not artery, again to minimise the risk of intimal flap formation. biodegradable. It is used in its monofilament form, mounted When prosthetic materials or grafts are used, similar nonon an atraumatic, curved, round-bodied needle. Knot security absorbable monofilament sutures are used with the same is important, and as polypropylene is monofilament and the in–out technique to ensure eversion of the graft edge and a anastomosis often depends on one final knot, several throws smooth intimal surface. Again the needle should go from out(between six and eight) of a well-laid reef knot are required. side to inside on the graft and from inside to outside on the The suture line must be regular and watertight with a smooth artery. Double-ended sutures make the procedures easier. intimal surface to minimise the risk of thrombosis and embolus, as well as to avoid any leakage. Suture size depends Summary box 7.6 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. MicrovasVascular anastomosis cular anastomoses are made using a loupe and an interrupted ●● Non-absorbable monofilament suture material should be suture down to 10/0 size. All vessel walls must be treated with used, e.g. polypropylene great care, avoiding causing any damage to the intima. If ●● A smooth intimal suture line is essential any significant manipulation is necessary, atraumatic forceps ●● Knots require multiple throws in order to ensure security (such as DeBakey’s) are utilised. Vascular clamps should be ●● The suture must pass from within outwards on the downflow applied with great care, particularly for calcified vessels, and aspect of the anastomosis in some cases encircling rubber loops or intraluminal balloon catheters may be less traumatic for control. Vessels should always be sewn with the needle Bailey moving & Love’s Short Practice of Surgery, 26th Ed Title: ISBN: 9781444121278 Proof Stage from within to without on the downstream edge of the vessel Laparoscopic anastomosis to avoid creating an intimal flap and to fix www.cactusdesign.co.uk any atherosclerotic The same principles apply to laparoscopic anastomosis as to plaque. The tip of the needle should be inserted at right angles open anastomosis: good blood supply, the avoidance of tension to the surface of the intima and the curve of the needle fol- and gentle tissue handling. Both sutured and stapled anaslowed to prevent vessel trauma. The assistant should ‘follow’ tomoses can be performed using laparoscopic needle holders by keeping the suture taut and, once the closure is complete, and staplers adapted to laparoscopic surgery. If the ends of the the distal clamp is released first, before the final watertight bowel have been adequately mobilised, and there is a specknot is made. This allows backflow to clear any clot or air from imen extraction site (e.g. right hemicolectomy), an extrathe anastomosis. The proximal clamp can then be released, corporeal anastomosis can be performed using open surgical a process which minimises the risk of distal embolus. Suture techniques. If one or both ends of the bowel to be anastomo& Love’s of Surgery, 26th Ed ISBN: 9781444121278 Proof Stage: 1 Fig bites should be placed an Title: equalBailey distance apart,Short withPractice the bite sed cannot be exteriorised, an intracorporeal anastomosis can size dependent on the vessel diameter. Care needs to be taken be performed. In intra-abdominal surgery, enterotomies are www.cactusdesign.co.uk to avoid damaging the suture, which should not be gripped by performed in the proximal and distal ends to be anastomosed any surgical instrument. All haemostats that are used to hold and a linear stapler is used to join the two ends. The resulting any suture material should be shod with soft rubber to prevent common enterotomy is then closed with a running suture. 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. Drains are inserted to allow fluid or air that might collect at A vein patch can be used if there is any danger of steno- an operation site or in a wound to drain freely to the surface. sis or doubt about the size of the lumen (Figure 7.21). The The fluid to be drained may include blood, serum, pus, urine,

DRAINS

Michael Ellis DeBakey, b.1908, Professor of Surgery, Baylor University, Houston, TX, USA.

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faeces, bile or lymph. Drains may also allow wound irrigation in certain specific circumstances. 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 drain 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, drains were in common use ever since Lawson Tait suggested, in 1887, ‘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; their use 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.

Figure 7.22 Underwater sealed chest drain. Reproduced with permission from Thomas WEG. Basic principles. In: Kingsnorth A, Majid A (eds). Principles of surgical practice. London: Greenwich Medical, 2001.

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 However, the antagonists claim that the presence of a connected to an underwater sealed drain (Figure 7.22). This system allows air to leave the pleural cavity, but it cannot drain may: be drawn back in by the negative pressure that is created in ●● increase intra-abdominal and wound infections; the intrathoracic cavity. During the respiratory process, it ●● increase anastomotic insufficiency; should be checked that the meniscus of the fluid is swinging, ●● increase abdominal pain; to ensure that the tube is not blocked. Suction can be applied ●● increase hospital stay; to the venting tube at the bottle whenever there is significant ●● decrease pulmonary function. drainage of fluid or air expected. Between 10 and 20mm of ISBN: 9781444121278 Proof Stage: 1 Title: Bailey & Love’s Short Practice of Surgery, 26th Ed In reality, the use of drains currently tends to depend mercury is adequate to obtain a gentle flow of bubbles from www.cactusdesign.co.uk on a surgeon’s individual preference. There are randomised the chest cavity. controlled trials suggesting that their use in gastric, duodenal, small bowel, appendix and biliary surgery is unnecessary T-tube drains and may cause more problems than benefits, and this is now After exploration of the common bile duct, a T-tube (Figure reflected in current practice. There are also randomised con- 7.23) may be inserted into the duct which allows bile to drain trolled trials to suggest that they are also not required in col- while the sphincter of Oddi is in spasm postoperatively. Once orectal, liver and pancreatic surgery, and yet in today’s practice the sphincter relaxes, bile drains normally down the bile duct the majority of surgeons will still utilise drains in these forms and into the duodenum. To assist choleresis, it is often advisof surgery. The only area of alimentary tract surgery where able to convert the lumen of the limb of the T into a gutter, drains are still routinely advocated is for oesophageal surgery, which also facilitates removal. although even here the evidence is low, with the level of evidence being only 5 and the level of recommendation being Image guided drainage ‘D’ (i.e. based on expert opinion). 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 Specialist uses of drains end is often fashioned with a pigtail to discourage inadvertent There are certain clinical situations where specialist forms of removal. These techniques have been in increasing use as a less invasive method to manage both primary and secondary drainage are required.

Fig No: 19.17

Robert Lawson Tait, 1845–1899, surgeon, Birmingham, UK. Ruggero Oddi, 1864–1913, Italian physician.

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PART 1 | BASIC PRINCIPLES The principles of diathermy: electrosurgery

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Figure 7.23 T-tube. Reproduced with permission from Thomas WEG. Basic principles. In: Kingsnorth A, Majid A (eds). Principles of surgical practice. London: Greenwich Medical, 2001.

(after surgery) collections of fluid. In the context of sepsis they are often used with intravenous or oral antimicrobial therapy.

Removal of drains A drain should be removed as soon as it is no longer required because, if left in, it can itself predispose to fluid collection as a result of tissue reaction. Indeed there is evidence that by 7 days only 20% 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, 9781444121278 ove’s Short Practice of Surgery, Ed may assist any suchISBN: but 26th merely leakage to drain externally rather than to produce life-threatening peritonitis. esign.co.uk ●● 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. T-tubes are traditionally and intentionally made of latex ●●

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to stimulate fibrosis, which results in the formation of a tract to allow the drainage of bile if required. It is important to use an alternative to latex if the patient is allergic, bearing in mind the decreased potential for fibrosis of silicone-based T-tubes. The increase in less invasive means of intervention for bile duct pathology has resulted in fewer T-tubes being used. Any suction drain should have the suction taken off prior to removal of the drain. Even in the absence of suction, a blocked drain may be difficult to remove owing to the creation of a relative vacuum as it is pulled out. This can be released by twisting the drain on removal or flushing with a small volume of sterile saline under aseptic conditions. During removal of a chest drain, the patient should be asked to breathe in and hold their breath, thus doing a Valsalva manoeuvre. In this way, no air is sucked into the pleural cavity as the tube is removed. Once the drain is out, a previously inserted purse-string suture should be tied.

Laparoscopic surgery is often accompanied by ‘Enhanced Recovery after Surgery’ pathways. These pathways comprise a package of pre-, peri- and postoperative care whose objectives are to reduce complications and hospital stay. Such pathways often discourage the use of drains. However the laparoscopic surgeon should always be prepared to use drains where indicated.

THE PRINCIPLES OF DIATHERMY: ELECTROSURGERY Development of the first commercial electrosurgical device is credited to William T Bovie, who developed the first electrosurgical device while employed at Harvard University. The first use of an electrosurgical generator in an operating room occurred in 1926 at Peter Bent Brigham Hospital in Boston, Massachusetts. The operation – removal of a mass from a patient’s head – was performed by Harvey Cushing. 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 Proof Stage: 1 surgery Fig No: 19.18 intraluminal endoscopes, as in laparoscopic or down 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.

Antonio Maria Valsalva, 1666–1723, Italian physician and anatomist.

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Principle of diathermy 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.

There are two basic types of diathermy system in use, monopolar diathermy and bipolar diathermy (Figure 7.24). 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 passive 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 passive electrode, the concentrated powerful current produces heat at the operative site. However, Active cable

Active electrode

Diathermy unit

Patient plate Dispersive cable Monopolar diathermy

(a)

Active cable Two small active electrodes

Diathermy unit

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 tissues should be free from either the risk of being burned or having current passed through them.

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, 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 this occurs 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 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 machine 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 the intensity, to give a combination of both cutting and coagulation. This is known as blended current and provides both forms of diathermy activity.

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 (b)

Bipolar diathermy

Figure 7.24  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.

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Sparks from the diathermy equipment 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

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PART 1 | BASIC PRINCIPLES Principles of advanced energy devices

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 which the surgeon intended and are far more common in monopolar than bipolar diathermy. Burns 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.

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 applied to the testis.

●● ●● ●● ●●

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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 7.25). 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. Reusable instruments are subject to damage and ‘wear and tear’ through use, cleaning and sterilisation, which can lead to direct coupling that can activate an otherwise passive instrument. Therefore, it is important for the operator, assistants and scrub team to inspect such instruments for damage that may compromise safety.

Metal laparoscopic port

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

Pacemakers Diathermy currents can interfere with the working of a pacemaker, with obvious potential danger to the patient’s health. Modern pacemakers are designed to be inhibited by high frequency interference, so 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 is important for the anaesthetist to have a magnet to deactivate the device during surgery.

Laparoscopic surgery Diathermy burns are a particular hazard of laparoscopic surgery owing to relative lack of 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.

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Diathermy hook

Point of contact with bowel

Figure 7.25 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.

PRINCIPLES OF ADVANCED ENERGY DEVICES Advanced laparoscopic procedures have become widely adopted over the last 25 years. Such ‘image based surgery’ has driven a parallel explosion in novel technologies which facilitate the performance of such procedures. This is particularly the case for energy devices. Monopolar diathermy still plays a vital and effective role in laparoscopic surgery but has limitations in terms of sealing larger blood vessels and is accompanied by the risks outlined above. Therefore, surgeons have

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increasingly used advanced energy devices to facilitate dissection and to seal and divide blood vessels up to 7mm diameter. There are three main types of advanced energy device: bipolar electrosurgery, harmonic scalpel and combination devices. In all cases the surgeon needs to be aware of the characteristics of these devices and their capacity to cause thermal injury in order to use them safely.

Bipolar electrosurgery devices Advanced bipolar 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, such as the Ligasure system™ (Medtronic), involves advanced bipolar 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 7mm 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 desiccation. Therefore, the new Ligasure Advance™ (Medtronic) can dissect, seal and divide and was designed to be the only tool that a surgeon would need.

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

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white). It provides cutting precision, even through thickened scar tissue, and visibility is enhanced because less smoke is created by this system during use when compared with 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 desiccation. 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 in open surgery, such as thyroidectomy, and several plastic surgery operations, e.g. cosmetic breast surgery. There are several such devices on the market, which vary in form and function. Surgeons need to be aware of, and trained in the use of such devices to prevent, complications such as thermal injury of vital structures near to where the energy is activated. There are several manufacturers of harmonic scalpels and the latest versions can seal and divide arteries and veins up to 7mm in diameter.

Combination energy devices In the last 5 years, technology has evolved with respect to both harmonic and bipolar advanced energy devices. One product, the Thunderbeat S™ (Olympus), has combined both modalities in a single device. By simultaneously using ultrasonic vibration and bipolar diathermy, this device is able to seal and divide arteries and veins up to 7mm in diameter. There is also a ‘seal only’ mode activated by a separate button, which activates bipolar diathermy only.

FURTHER READING Carol EH Scott-Conner (Ed.) The Sages manual: Volume 1 basic laparoscopy and endoscopy. Berlin: Springer, 2012. Kirk RM. Basic surgical techniques, 6th edn. Edinburgh: Churchill Livingstone, 2010. Pignata G, Bracale U, Fabrizio Lazzara F (Eds.) Laparoscopic surgery: key points, operating room setup and equipment. Berlin: Springer, 2016. Royal College of Surgeons of England. Intercollegiate basic surgical skills course (participant handbook), 4th edn. London: Royal College of Surgeons of England, 2007. www.websurg.com (website) This is one of the best educational websites for laparoscopic surgery.

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ve Bailey & Love Bailey & Love Bailey & Love ve Bailey & Love Bailey & Love Bailey & 8 Love Chapter

Principles of laparoscopic and roboticsurgery Learning objectives To understand: •• The principles of laparoscopic and robotic surgery •• The advantages and disadvantages of such surgery

•• The safety issues and indications for laparoscopic and robotic surgery

•• The principles of postoperative care

DEFINITION Minimal access surgery is a product of modern technology and surgical innovation that aims to accomplish surgical therapeutic goals with minimal somatic and psychological trauma. This type of surgery has reduced wound access trauma, as well as being less disfiguring than conventional techniques. It can offer cost-effectiveness to both health services and employers by shortening operating times, shortening hospital stays, improving operative precision compared to open surgery in some (but not all) cases and allowing faster recuperation.

EXTENT OF MINIMAL ACCESS SURGERY The first introduction of an experimental laparoscopic procedure was by Georg Kelling of Dresden in 1901 (he termed it ‘celioscopy’ and used a Nitze-cystoscope). This was followed by Hans Christian Jacobaeus’ successful application in humans in Sweden. Despite the work of these pioneers, it took another 70 years before Patrick Steptoe applied this approach to patients in the United Kingdom in 1980, and Phillipe Mouret’s first video-laparoscopic cholecystectomy was performed in Lyon, France in 1987. However, since its mainstream adoption in the mid-1990s, minimal access ­surgery has crossed all traditional boundaries of specialties and disciplines. Shared, borrowed and overlapping technologies and information are encouraging a multidisciplinary approach that serves the whole patient, rather than a specific organ ­system. The core principles of minimal access surgery (independent of procedure or device) can be summarized by the acronym I-VITROS: ●●

Insufflate/create space – to allow surgery to take place in the minimal access setting

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●● ●● ●●

●● ●● ●●

Visualise – the tissues, anatomical landmarks and the environment for the surgery to take place Identify – the specific structures for surgery Triangulate – surgical tools (such as port placement) to optimise the efficiency of their action, and ergonomics by minimising overlap and clashing of instruments Retract – and manipulate local tissues to improve access and gain entry into the correct tissue planes Operate – incise, suture, anastomose, fuse Seal/haemostasis.

Broadly speaking, minimal access techniques can be categorised as follows:

Laparoscopy A rigid endoscope (laparoscope) is introduced through a port into the peritoneal cavity. This is insufflated with carbon dioxide to produce a pneumoperitoneum. Further ports are inserted to enable instrument access and their use for dissection (Figure 8.1). It is generally accepted that laparoscopic cholecystectomy has revolutionised the surgical management of cholelithiasis and has become the mainstay of management of uncomplicated gallstone disease. With improved instrumentation, advanced procedures, such as laparoscopic colectomies for malignancy, previously regarded as controversial, have also become fully accepted. There continues to be substantive evidence demonstrating the short-term benefits of laparoscopic surgery over open surgery with regard to postoperative pain, length of stay and earlier return to normal activities; however, the equivalence of the benefits in long-term outcomes, such as oncological quality and cancer-related survival, has not been established.

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(a)

and lumbar sympathetic chain. Extraperitoneal approaches to the retroperitoneal organs, as well as hernia repair, are now becoming increasingly commonplace, further decreasing morbidity associated with visceral peritoneal manipulation. Other, more recent, examples include subfascial ligation of incompetent perforating veins in varicose vein surgery.

Arthroscopy and intra-articular joint surgery Orthopaedic surgeons have applied arthroscopic access to the knee for some time and are applying this modality to other joints, including the shoulder, wrist, elbow and hip.

Combined approach

(b)

The diseased organ is visualised and treated by an assortment of endoluminal and extraluminal endoscopes and other imaging devices. Examples include the combined laparoendoscopic approach for the management of biliary lithiasis, colonic polyp excision and several urological procedures, such as pyeloplasty and donor nephrectomy. In some cases the application of this combined approach offers the ability to execute operations via a single incision, thereby better adhering to the minimally invasive approach. The evidence for improved outcomes using these combined approaches remains limited for the majority of procedures.

SURGICAL TRAUMA IN OPEN, MINIMALLY INVASIVE AND ROBOTIC SURGERY Figure 8.1  (a) Common laparoscopic trocars. (b) Common laparoscopic instruments (photo courtesy of Daniel Leff).

Thoracoscopy A rigid endoscope is introduced through an incision in the chest to gain access to the thoracic contents. Usually there is no requirement for gas insufflation, as the operating space is held open by the rigidity of the thoracic cavity. In specific cases, such as mediastinal tumour resection and diaphragmatic surgery, gas insufflation at low pressure (5–8mmHg) may be applied.

Endoluminal endoscopy Flexible or rigid endoscopes are introduced into hollow organs or systems, such as the urinary tract, upper or lower gastrointestinal tract, and respiratory and vascular systems.

Perivisceral endoscopy Body planes can be accessed even in the absence of a natural cavity. Examples are mediastinoscopy, retroperitoneoscopy and retroperitoneal approaches to the kidney, aorta

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Most of the trauma of an open procedure is inflicted because the surgeon must have a wound that is large enough to give adequate exposure for safe dissection at a target site. The wound is often the cause of morbidity, including infection, dehiscence, bleeding, herniation and nerve entrapment. Wound pain prolongs recovery time and, by reducing mobility, contributes to an increased incidence of pulmonary atelectasis, chest infection, paralytic ileus and deep venous thrombosis. Mechanical and human retractors cause additional trauma. Body wall retractors can inflict localised damage that may be as painful as the wound itself. In contrast, during laparoscopy, the retraction is provided by the low-pressure pneumoperitoneum, giving a diffuse force applied gently and evenly over the whole body wall, causing minimal trauma. Exposure of any body cavity to the atmosphere also causes morbidity through cooling and fluid loss by evaporation. There is also evidence that the incidence of postsurgical adhesions has been reduced by the use of the minimally invasive (laparoscopic, thoracoscopic) and robotic approaches, which has been suggested to result from less damage to deli­ cate serosal coverings. In the manual handling of intestinal loops, the surgeon and assistant disturb the peristaltic activity of the gut and provoke adynamic ileus.

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PART 1 | BASIC PRINCIPLES Limitations of minimal access surgery

Minimal access surgery has many advantages, such as a reduction in the trauma of access and exposure and an improvement in visualisation. While minimal access methods have been an established modality in some elective surgical procedures, they are now also being increasingly applied with success in emergency surgical procedures (including perforated viscus repair, such as omental patch repair of the stomach, and washout of localised perforation of diverticular disease). Summary box 8.1 Advantages of minimal access surgery ●● ●●

●● ●● ●● ●● ●●

Decrease in wound size Reduction in wound infection, dehiscence, bleeding, herniation and nerve entrapment Decrease in wound pain Improved mobility Decreased wound trauma Decreased heat loss Improved visualisation

LIMITATIONS OF MINIMAL ACCESS SURGERY Despite its many advantages, minimal access surgery has its limitations. To perform minimal access surgery with safety, the surgeon must operate remote from the surgical field, using an imaging system that provides a two-dimensional (2D) representation of the operative site. The endoscope offers a whole new anatomical landscape, which the surgeon must learn to navigate without the usual ‘open approach’ clues that make it easy to judge depth. The instruments are longer and sometimes more complex to use than those commonly used in open surgery. This results in the novice being faced with significant problems of hand–eye coordination. Here there is a well-described learning curve for novice surgeons and experienced ‘open’ surgeons when adopting the minimally invasive approach. Some of the procedures performed by these new approaches are more technically demanding and are slower to perform, and they often have a more difficult learning curve as tactile feedback to the surgeon is lost. Indeed, on occasion, a minimally invasive operation is so technically demanding that both patient and surgeon are better served by conversion to an open procedure. Unfortunately, there seems to be a sense of shame associated with conversion, which is quite unjustified. It is vital for surgeons and patients to appreciate that the decision to close or to convert to an open operation is not a complication but, instead, usually implies sound surgical judgement in favour of patient safety. Another problem occurs when there is intraoperative arterial bleeding. Haemostasis may be very difficult to achieve endoscopically because blood obscures the field of vision and there is a significant reduction of the image quality due to light absorption. Another disadvantage of laparoscopic surgery is the loss of tactile feedback in the context of some procedures (although

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many procedures have been successfully performed without ‘traditional sense’ of tactile feedback). This is an area of ongoing research in haptics and biofeedback systems. Early work suggested that laparoscopic ultrasonography might be a substitute for the need to ‘feel’ in intraoperative decision-making. The rapid progress in advanced laparoscopic techniques, in­ cluding biliary tract exploration and surgery for malignancies, has provided a strong impetus for the development of laparoscopic ultrasound. Now more developed, this technique already has advantages that far outweigh its disadvantages. In more advanced techniques, large pieces of resected tissue, such as the lung or colon, may have to be extracted from the body cavity. Occasionally, the extirpated tissue may be removed through a nearby natural orifice, such as the rectum or the mouth. At other times, a novel route may be employed. For instance, a benign colonic specimen may be extracted through an incision in the vault of the vagina. Several innovative tube systems have been shown to facilitate this extraction. Although tissue ‘morcellators, mincers and liquidisers’ can be used in some circumstances, they have the disadvantage of reducing the amount of information available to the pathologist. Previous reports of tumour implantation in the locations of port sites raised important questions about the future of the laparoscopic treatment of malignancy, but large-scale trials have shown this claim to be false. Although emerging evidence from large-scale international prospective trials implicates surgical skill as an important aetiological factor, it is important to consider the biological implications of minimally invasive strategies on the tumours. The use of carbon dioxide and helium as insufflants causes locoregional hypoxia and may also change pH. The resultant modulation of the behaviour of spilled tumour cells is increasingly being studied, although the risks of recurrence at port sites seem to be minimised by appropriate tissue handling, separating any tumours by bagging, and washing and protecting the site. Hand-assisted laparoscopic surgery is a well-developed technique. It involves the intra-abdominal placement of a hand or forearm through a minilaparotomy incision, while pneumoperitoneum is maintained. In this way, the surgeon’s hand can be used as in an open procedure. It can be used to palpate organs or tumours, reflect organs atraumatically, retract structures, identify vessels, dissect bluntly along a tissue plane and provide finger pressure to bleeding points, while proximal control is achieved. This approach has been suggested to offer technical and economic efficiency when compared with a totally laparoscopic approach, in some instances, reducing both the number of laparoscopic ports and the number of instruments required. Some advocates of the technique claim that it is also easier to learn and perform than totally laparoscopic approaches, and that there may be increased patient safety. There has been a continued improvement in dissection techniques in laparoscopic/thoracoscopic surgery beyond that of standard electrosurgery/diathermy and laser technology to improve dissection precision and haemostatic efficacy. Ultrasonic dissection, tissue fusion devices and tissue removal continue to be adopted across specialties and practitioners. This has taken place as a consequence of continuous and incremental technical improvements in devices, increased

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familiarity with their use and some improvements in cost of access. The adaptation of the technology to minimally invasive surgery grew out of the search for alternative, possibly safer, methods of dissection. Some current units combine the functions of three or four separate instruments, reducing the need for instrument exchanges during a procedure. This flexibility, combined with the ability to provide a clean, smokefree field, has the potential to improve safety and shorten operating times. Although dramatic cost savings are possible with laparoscopic cholecystectomy when compared with open cholecystectomy, the position was less clear-cut with other procedures initially. There is another factor that may complicate the computation of the cost–benefit ratio. A significant rise in the rate of cholecystectomy followed the introduction of the laparoscopic approach because the threshold for referring patients for surgery became lower. The increase in the number of procedures performed has led to an overall increase in the cost of treating symptomatic gallstones. Three-dimensional (3D) imaging systems have been available for some time, but remain expensive and currently are not commonplace, partially because many surgeons feel that 3D technology has not yet offered the ability to perform procedures with significant technical enhancement or to improve safety or outcomes across a range of operations. Stereoscopic imaging for laparoscopy and thoracoscopy is still progressing. Future improvements in these systems carry the potential to enhance manipulative ability in critical procedures, such as knot tying and dissection of closely overlapping tissues. There are, however, some drawbacks, such as reduced display brightness and interference with normal vision because of the need to wear specially designed glasses for some systems. It is likely that brighter projection displays will be developed, at increased cost. However, the need to wear glasses will not be easily overcome. Looking further to the future, it is evident that the continuing reductions in the costs of elaborate image-processing techniques will result in a wide range of transformed presentations becoming available. It should ultimately be possible for a surgeon to call up any view of the operative region that is accessible to a camera and present it stereoscopically in any size or orientation, superimposed on past images taken in other modalities. Such augmented reality systems have been available for several years but continue to improve. It is for the medical community to decide which of these many potential imaginative techniques will contribute most to effective surgical procedures.

Summary box 8.2 Limitations of minimal access surgery ●● ●● ●● ●● ●● ●●

Reliance on remote vision and operating Loss of tactile feedback Dependence on hand–eye coordination Difficulty with haemostasis Reliance on new techniques Extraction of large specimens

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ROBOTIC SURGERY A robot is a mechanical device that performs automated physical tasks according to direct human supervision, a predefined program or a set of general guidelines, using artificial intelligence techniques. In terms of surgery, robots have been used to assist surgeons during procedures. This has been primarily in the form of automated camera systems and telemanipulator systems, thus resulting in the creation of a human–machine interface. Even though laparoscopic surgery has progressed greatly over the last two decades, owing to its widespread use and dissemination in that time, there are, as discussed above, limi­ tations. To those already mentioned may be added reduced degrees of freedom of movement and ergonomically difficult positions for the surgeon. Such problems undoubtedly affect surgical precision. This has led to interest in robotic surgical systems, which currently exist as two main categories: ●●

●●

Teleoperated systems: a human surgeon performs an operation via a robot and its robotic instruments through a televisual computerised platform, either via onsite connections or remotely through the internet or other digital channels – hence the publicity of ‘operating on a patient from another country’ (such ‘remote’ operations are currently rarely performed but their existence is established). Image-guided systems: A surgical robot completes a preprogrammed surgical task which is guided by preoperative imaging and real-time anatomical constraints and cues through the application of inbuilt navigation systems.

In the current era the concept of the master–slave system prevails (where the surgeon is the master, i.e. the operator, and the robot is the slave). The two are linked by underlying hardware and software components within an advanced computer construction. Such devices have been available for the past 30 years and have become more available during the past two decades. They still remain a relative rarity owing to a multitude of factors including cost, applicability and benefits for a particular operation/pathology, training requirements and the support that is necessary, beyond just that of the individual surgeon but rather at whole institution level. Since their first clinical use in 1985, with the PUMA 560 being used for a brain biopsy, surgical robots have been considered to offer many benefits, which have arisen as a result of new technology in lenses, cameras and computer software. Just as laparoscopic surgery benefited from advances in light technology, allowing the targeted transmission of light down tubing, robotic surgery benefited from computer integration of mechanical (surgical) arms that paved the way for computer-integrated surgery (CIS). The advantages of robotic surgery are two-fold: first for the patient (as for laparoscopic surgery, see Summary box 8.1) and second for the surgeon. The advantages for the surgeon include better visualisation (higher magnification) with stereoscopic views; elimination of hand tremor allowing greater precision; improved manoeuvring as a result of the ‘robotic wrist’, which in some systems allows up to seven degrees of freedom; and the fact that large external movements of the surgical hands can be scaled down and transformed to limited internal movements of the

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PART 1 | BASIC PRINCIPLES Robotic surgery

‘robotic hands’, extending the surgical ability to perform complex technical tasks in a limited space. Also, the surgeon is able to work in an ergonomic environment with less stress and to achieve higher levels of concentration. The computer may also be able to compensate for the beating movement of the heart, making it unnecessary to stop the heart during cardiothoracic surgery. There may also be less need for assistance once surgery is under way. Many surgical specialties have embraced the progression of robot-assisted techniques, including general surgery, cardiothoracic surgery, urology, orthopaedics, ear, nose and throat (ENT) surgery, gynaecology and paediatric surgery. Specialties that use microsurgical techniques also benefit

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from this technology. Current robotic systems were designed to offer multifunctionality including multi-anatomy and speciality capability in both operating theatre and remote environments. In the current era, however, these devices seem most often applied in pelvic surgery (typically urology, colorectal and gynaecology) within inhouse operating areas. One major operative barrier to adoption remains the pro­ hibitive costs for many healthcare environments. As a result the current robotic surgical market is dominated by the master– slave da Vinci system (Intuitive Surgical, MenloPark, CA, USA) (Figure 8.2), although there are several other commercially available robots and a market open to a small number of new entrants, but also a history of unsuccessful (financially

(a)

(b)

(c)

(d)

Figure 8.2  (a) The DaVinci Xi system. (b) The surgical console. (c) The robotic arms draped for a robotic coronary artery bypass grafting procedure. (d) Robotic distal coronary anastomosis.

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or functionally) or withdrawn/ removed devices. This is partly because of the high cost of design and development of new robot technologies and surgical instruments compatible with them, which all require design, translation and intellectual property costs. In addition to the remote master–slave platform design, direct robot systems exist and include: ●● ●● ●● ●● ●●

tremor suppression robots; active guidance systems; articulated mechatronic devices; force control systems; haptic feedback devices.

Each of these systems offers different advantages to the operating surgeon, ranging from reducing the need for assistants and providing better ergonomic operating positions to providing experienced guidance from surgeons not physically present in the operating theatre.

Robotic surgery – the first 30 years The largest systematic overview of all robot surgical procedures from inception and covering the field’s first 30 years revealed only 99 prospective or randomised studies reporting clinical outcomes from over 28 000 peer-reviewed research articles that mentioned the term ‘robotic surgery’. The 99 studies revealed data from approximately 14 500 patients in trials undergoing robotic surgical procedures versus open and minimally invasive operations. The overall pooled results, regardless of specialty, revealed a decrease in blood loss and blood transfusion rate with robotic surgery when compared with both open surgery and minimally invasive surgery. Specifically, when compared with open surgery, robotic procedures demonstrated that there was a reduction in length of hospital stay and overall complication rate. However, robotic procedures did suffer from significantly longer operative times and their cost-effectiveness varied depending on operative site, technique, patient and healthcare setting. While this reveals an overall perspective from the first 30 years of robotics surgery, there remains an incumbent need to offer clearer clinical evidence regarding the most apposite operative method and technology for each individual patient.

PREOPERATIVE EVALUATION Preparation of the patient Although the patient may be in hospital for a shorter period, careful preoperative management is essential to minimise morbidity.

History Patients must be fit for general anaesthesia and open operation if necessary. Potential coagulation disorders (e.g. associated with cirrhosis) are particularly dangerous in laparoscopic surgery. As adhesions may cause problems, previous abdominal operations or peritonitis should be documented.

Summary box 8.3 Preparation for laparoscopic or robotic surgery ●●

●● ●● ●● ●● ●●

Overall fitness: cardiac arrhythmia, emphysema, medications, allergies Previous surgery: scars, adhesions Body habitus: obesity, skeletal deformity Normal coagulation Thromboprophylaxis Informed consent

Examination Routine preoperative physical examination is required as for any major operation. Although, in general, laparoscopic/ thoracoscopic surgery allows quicker recovery, it may involve longer operating times and the establishment of the pneumoperitoneum may provoke cardiac arrhythmias. Severe chronic obstructive airways disease and ischaemic heart disease may be contraindications to the laparoscopic approach. Particular attention should be paid to the presence or absence of jaundice, abdominal scars, palpable masses or tenderness. Moderate obesity does not increase operative difficulty significantly, but massive obesity may make pneumoperitoneum difficult and standard instrumentation may be too short. Access may prove difficult in very thin patients, especially those with severe kyphosis.

Premedication Premedication is the responsibility of the anaesthetist, with whom coexisting medical problems should be discussed.

Prophylaxis against thromboembolism Venous stasis induced by the reverse Trendelenburg position during laparoscopic surgery may be a particular risk factor for deep vein thrombosis, as is a lengthy operation and the obesity of many patients. Subcutaneous low molecular weight heparin and antithromboembolic stockings should be used routinely, in addition to pneumatic leggings during the operation. Patients already taking warfarin for other reasons should have this stopped temporarily or converted to intravenous heparin, depending on the underlying condition, as it is not safe to perform laparoscopic surgery in the presence of a significant coagulation deficit.

Urinary catheters and nasogastric tubes In the early days of laparoscopic surgery, routine bladder catheterisation and nasogastric intubation were advised. Most surgeons now omit these, but it remains essential to check that the patient is fasted and has recently emptied their bladder, particularly before the blind insertion of a Verres needle. However, currently, most general surgeons prefer the direct cut-down technique into the abdomen for the introduction of the first port for the establishment of the pneumoperitoneum (Hasson technique and modified Hasson approaches). More

Janos Verres, 1903–1979, chest physician and chief of the Department of Internal Medicine, The Regional Hospital, Kapuvar, Hungary. Harrith Hasson, Professor of Gynaecology, Chicago, IL, USA.

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recently, direct optical entry has been used, especially in the setting of bariatric surgery.

Informed consent The basis of many complaints and much litigation in surgery, especially laparoscopic surgery, relates to the issue of informed consent. It is essential that the patient understands the nature of the procedure, the risks involved and, when appropriate, the alternatives that are available. A locally prepared explanatory booklet concerning the laparoscopic procedure to be undertaken is extremely useful. In an elective case, a full discussion of the proposed operation should take place in the outpatient department with a surgeon of appropriate seniority, preferably the operating surgeon, before the decision is made to operate. On admission, it is the responsibility of the operating surgeon and anaesthetist to ensure that the patient has been fully counselled, although the actual witnessing of the consent form may have been delegated. The patient should understand what laparoscopic surgery involves and that there is a risk of conversion to open operation. If known, this risk should be quantified, for example the increased risk with acute cholecystitis or in the presence of extensive upper abdominal adhesions. The conversion rate will also vary with the experience and practice of the surgeon. Common complications should be mentioned, such as shoulder tip pain and minor surgical emphysema, as well as rare but serious complications, including injury to the bile ducts and visceral injury from trocar insertion or diathermy. Preparation is very similar to that for open surgery and aims to ensure that: ●● ●● ●● ●●

The patient is fit for the procedure. The patient is fully informed and has consented. Operative difficulty is predicted when possible. Appropriate theatre time and facilities are available (especially important for robotic cases).

THEATRE SET UP AND TOOLS Operating theatre design, construction and layout are key to its smooth running on a daily basis. Originally, the video and diathermy equipment and other key tools used in laparoscopic surgery were moved around on stacks, taking up valuable floor space and cluttering up the theatre environment, which was not always ergonomic for the operating team. New theatres are designed with moveable booms that come down from the ceiling; these are easy to place and do not have long leads or wires trailing behind them (Figure 8.3). The equipment consists of at least two high-resolution liquid crystal display (LCD) monitors (and, more recently, high definition (HD) monitors for even clearer images), the laparoscopic kit for maintaining pneumoperitoneum and the audiovisual kit. The advent of DVD and other digital recording equipment has also led to these being incorporated into the rigs so that cases can be recorded with ease. This is further facilitated by cameras being inserted into the light handles of the main overhead lights so that open surgery can also be recorded without distracting the surgeons.

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Figure 8.3  Modern laparoscopic theatre set up.

Image quality is vital to the success of laparoscopic surgery. New camera and lens technology allows the use of smaller cameras. Many centres now use 5-mm laparoscopes routinely. Automatic focusing and charge-coupled devices (CCDs) are used to detect different levels of brightness and adjust for the best image possible. Flat panel monitors with HD images are used to give the surgeon the best views possible and 3D technology is now being used for visualisation more routinely in some centres. The usability of the kit has also improved; touch screen panels and even voice-activated systems are now available on the market. As minimally invasive and robotic procedures have become routine in some institutions, the dedicated theatre team for such procedures has also evolved. Surgeons and anaesthetists, as well as scrub and circulating nurses, have become familiar with working with the equipment and each other. The efficient working of the team is crucial to high-quality surgery and quick yet safe turnover. Laparoscopic tools have also changed. Disposable equipment is more readily available, which does unfortunately increase the cost of the surgery. However, easy to use, ergonomically designed and reliable surgical tools are essential for laparoscopic and robotic surgery. Simple designs for new laparoscopic ports are now being studied, with the aim of reducing the incidence of port-site hernias; see-through (optical) ports that allow the surgeon to cut down through the abdomen while observing the layers through the cameras, and new light sources within the abdomen may be simple ideas that affect surgical technique in the near future.

GENERAL INTRAOPERATIVE PRINCIPLES Laparoscopic and thoracoscopic principles have specific principles that require careful clinical consideration. As such, they are not purely a less invasive equivalent of an open operation. For example, laparoscopic cholecystectomy is now the ‘gold standard’ for operative treatment of symptomatic gallstone disease. The main negative aspect of the technique is the increased incidence of bile duct injury compared with open cholecystectomy. Better understanding of the mechanisms of injury, coupled with proper training, will avoid most of these errors. The following sections highlight the important

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technical steps that should be taken during any form of laparoscopic surgery to avoid complications.

Creating a pneumoperitoneum There are two methods for creation of a pneumoperitoneum: open and closed. The closed method involves blind puncture using a Verres needle. Although this method is fast and relatively safe, there is a small but significant potential for intestinal or vascular injury on introduction of the needle or first trocar. The routine use of the open technique for creating a pneumoperitoneum avoids the morbidity related to a blind puncture. To achieve this, a 1 cm vertical or transverse incision is made at the level of the umbilicus. The umbilicus carries importance as it is a reliable anatomical landmark deriving from the embryological coalescence of the rectus sheath and peritoneum and is devoid of other myofascial planes that could complicate subsequent entry into the peritoneum. Two small retractors are used to dissect bluntly the subcutaneous fat and expose the midline fascia. Two sutures are inserted each side of the midline incision (into the rectus sheath confluence), followed by the creation of a 1cm opening in the fascia. Free penetration into the abdominal cavity is confirmed by the gentle introduction of a finger. Finally, a Hasson trocar (or other blunt-tip trocar) is inserted and anchored with the fascial sutures (Figure 8.4). This is considered the Hasson or ‘modified Hasson’ approach. The term ‘modified’ is used here to denote the same principle as the original Hasson with the midline exposure and access, except that the exact technique has been changed to suit an individual surgeon, such as the adoption of a particular angle of retraction of the umbilicus before an incision into the midline is made to get access to the peritoneum. Rarely, a third, or combination, approach may be employed. Here an open technique is followed with a smaller than usual midline incision. Once access to the peritoneum is visualised, a Verres needle is inserted under direct vision, and then insufflation is carried out. This small open approach then allows the introduction of a laparoscopic port with a

Figure 8.4  Open technique with Hasson port. Apply safe principles of closed technique.

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view to reducing trauma of the pneumoperitoneum. Such an approach may have benefits for complex cases, such as those for ‘re-do’ procedures, where the risk of umbilical adhesions during pneumoperitoneum may be high. The open technique may initially appear time consuming and even cumbersome; however, with practice, it is quick, efficient and safe overall. Optical entry to the abdomen under direct vision using optical ports (especially in bariatric surgery) is gaining favour with many laparoscopic surgeons. This allows quick and safe entry to the peritoneal cavity using bladeless see-through trocars that allow the different layers to be dissected through using the laparoscope within an optical port to be inserted into the abdomen.

Preoperative problems Previous abdominal surgery Previous abdominal surgery is no longer a contraindication to laparoscopic surgery, but preoperative evaluation is necessary to assess the type and location of surgical scars. As mentioned earlier, the open technique for insertion of the first trocar is safer. Before trocar insertion, the introduction of a fingertip helps to ascertain penetration into the peritoneal cavity and also allows adhesions to be gently removed from the entry site. After the tip of the cannula has been introduced, a laparoscope is used as a blunt dissector to tease adhesions gently away and form a tunnel towards the quadrant where the operation is to take place. This step is accomplished by a careful pushing and twisting motion under direct vision. With experience, the surgeon learns to differentiate visually between thick adhesions that may contain bowel and should be avoided and thin adhesions that would lead to a window into a free area of the peritoneal cavity.

Obesity Laparoscopic and robotic surgery has proved to be safe and effective in the obese population. In fact, some procedures are less difficult than their open counterparts for the morbidly obese patient, e.g. in bariatric surgery. Technical difficulties occur, however, in obtaining pneumoperitoneum, reaching the operative region adequately and achieving adequate exposure in the presence of an obese colon. Increased thickness of the subcutaneous fat makes insufflation of the abdominal cavity more difficult. With the closed technique, a larger Verres needle is often required for morbidly obese patients. Pulling the skin up for fixation of the soft tissues is better accomplished with towel clamps. Only moderate force should be used, to avoid separating the skin farther from the fascia. The needle should be passed at nearly a right angle to the skin and preferably above the umbilicus, where the peritoneum is more firmly fixed to the midline. The open technique of inserting a Hasson trocar is easier and safer for obese patients, but technically demanding in morbidly obese patients, where optical entry is now more commonplace. The main difficulty is reaching the fascia. A larger skin incision (1–3cm), starting at the umbilicus and extending superiorly, may facilitate this. To reach the operative area adequately, the location of some of the ports has to be modified and, in some instances, larger and

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longer instruments are necessary. When the length of the laparoscope appears to be insufficient to reach the operative area adequately, the initial midline port should be placed nearer to the operative field. Recently, the use of optical port entry for laparoscopic bariatric surgery has revolutionised port entry for morbid obesity cases.

Operative problems Intraoperative perforation of a viscus Perforation of any viscus, such as bowel, solid organs and blood vessels (including the aorta), is a potential hazard of using the laparoscopic approach and these complications may be minimised with surgical experience, education, preparation and patient selection. One example, in a common laparoscopic procedure such as cholecystectomy, includes perforation of the gallbladder. This is more com­ mon with the laparoscopic technique than with the open technique (see also Chapter 67). Some authors have reported an incidence of up to up to 30%, but it does not appear to be a factor in increasing the early postoperative morbidity. However, it is well known that bile is not a sterile fluid and bacteria can be present in the absence of cholecystitis. Unless the perforation is small, closure with endoloops or endoclips should be attempted to avoid contamination prior to extraction, which should be with the use of an endobag. Bilious leakage should be suctioned and washed out. If there is stone spillage, every attempt must be made to collect and extract the stones, and if there is a possibility of stones being retained in the peritoneum, then an ultrasound should be arranged 6weeks postoperatively to assess a collection around a stone and the patient should be informed of this outcome postoperatively.

Antibiotics to manage known sepsis or septicaemia in a patient undergoing surgery Operating on a patient with established septicaemia or sepsis is not typically recommended unless the operation will contribute to removing or minimising infectious origins. Where necessary pre-, peri- and postoperative antibiotics should be administered, in accordance with local microbiological advice.

Antibiotics to prevent infections and sepsis A single dose of antibiotics should be administered within 1hour of skin incision; in contaminated, semi-contaminated or complex procedures, additional doses should be administered, based on local microbiological advice.

Bleeding In some of the larger series, bleeding has been the most common cause of conversion to an open procedure. Bleeding plays a more important role in laparoscopic surgery because of factors inherent to the technique. These include a limited field that can easily be obscured by relatively small amounts of blood, magnification that makes small arterial bleeding appear to be a significant haemorrhage and light absorption that obscures the visual field.

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HOW TO AVOID BLEEDING As in any surgical procedure, the best way to handle intraoperative bleeding is to prevent it from happening. This can usually be accomplished by identifying patients at high risk of bleeding, having a clear understanding of the laparoscopic anatomy and employing careful surgical technique. Risk factors that predispose to increased bleeding include: ●● ●● ●● ●●

cirrhosis; inflammatory conditions (acute cholecystitis, diverticulitis); patients on clopidogrel and or dipyridamole; coagulation defects: these are contraindications to a laparoscopic procedure.

BLEEDING FROM A MAJOR VESSEL Damage to a large vessel requires immediate assessment of the magnitude and type of bleeding. When the bleeding vessel is identified, a fine-tip grasper can be used to grasp it and apply either electrocautery or a clip, depending on its size. When the vessel is not identified early and a pool of blood forms, compression should be applied immediately with a blunt instrument, a cotton swab (ENT or mastoid swab) or with the adjacent organ. Good suction and irrigation are of utmost importance. Once the area has been cleaned, pressure should be released gradually to identify the site of bleeding. Insertion of an extra port may be required to achieve adequate exposure and at the same time to enable the concomitant use of a suction device and an insulated grasper. Although most bleeding vessels can be controlled laparoscopically, judgement should be used in deciding when not to prolong bleeding, but to convert to an open procedure at an early stage. Surgicel® (absorbable fibrillar oxidized cellulose polymer) or other clot-promoting strips, tissue glues or other haemostatic agent may also be used laparoscopically to aid haemostasis. If at any stage bleeding is difficult to stem laparoscopically, there should be no delay in converting to an open procedure in the interests of patient safety. BLEEDING FROM ORGANS ENCOUNTERED DURING SURGERY Intraoperative bleeding from organs can usually be prevented by performing the dissection in the correct plane. As previously mentioned, the common laparoscopic example of a cholecystectomy requires understanding the management of bleeding from the gallbladder bed. When a bleeding site appears during detachment of the gallbladder, the dissection should be carried a little farther to expose the bleeding point adequately. Once this step has been performed, direct application of electrocautery usually controls the bleeding. If bleeding persists, indirect application of electrocautery is useful because it avoids detachment of the formed crust. This procedure is accomplished by applying pressure to the bleeding point with a blunt, insulated grasper and then applying electrocoagulation by touching this grasper with a second insulated grasper that is connected to the electrocautery device. One must be careful to keep all conducting surfaces of the graspers within the visual field while applying the electrocautery current.

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BLEEDING FROM A TROCAR SITE Bleeding from the trocar sites is usually controlled by applying upwards and lateral pressure with the trocar itself. Considerable bleeding may occur if the falciform ligament is impaled with the substernal trocar or if one of the epigastric vessels is injured. If significant continuous bleeding from the falciform ligament occurs, haemostasis is achieved by percutaneously inserting a large, straight needle at one side of the ligament. A monofilament suture attached to the needle is passed into the abdominal cavity and the needle is exited at the other side of the ligament using a grasper (Figure 8.5). The loop is suspended and compression is achieved. Maintaining compression throughout the procedure usually suffices. After the procedure has been completed, the loop is removed under direct laparoscopic visualisation to ensure complete haemostasis. When significant continuous bleeding from the abdominal wall occurs, haemostasis can be accomplished either by pressure or by suturing the bleeding site. Pressure can be applied using a Foley balloon catheter. The catheter is introduced into the abdominal cavity through the bleeding trocar site wound, the balloon is inflated and traction is placed on the catheter, which is bolstered in place to keep it under tension. The catheter is left in situ for 24 hours and then removed. Although this method is successful in achieving haemostasis, the authors favour direct suturing of the bleeding vessel. This manoeuvre is accomplished by extending the skin incision by 3 mm at both ends of the bleeding trocar site wound. Two figure-of-eight sutures are placed in the path of the vessel at both ends of the wound. Devices such as the EndoClose may also be used to apply transabdominal sutures under direct laparoscopic view to close port sites that bleed. EVACUATION OF BLOOD CLOTS The best way of dealing with blood clots is to avoid them. As mentioned, careful dissection and identification of the cystic artery and its branches, as well as identifying and carrying out dissection of the gallbladder in the correct plane, help to prevent bleeding from the cystic vessels and the hepatic bed. Nevertheless, clot formation takes place when unsuspected bleeding occurs or when inflammation is severe and a clear plane is not present between the gallbladder and the hepatic

Figure 8.5  Management of bleeding from a surgical trocar site.

bed. The routine use of 5000–7000 units of heparin per litre of irrigation fluid helps to avoid the formation of clots. When extra bleeding is foreseen, a small pool of irrigation fluid can be kept in the operative field to prevent clot formation. After clots have formed, a large bore suction device should be used for their retrieval. Care should be taken to avoid suctioning in proximity to placed clips.

Principles of electrosurgery during laparoscopic surgery Electrosurgical injuries during laparoscopy are potentially serious. The vast majority occur following the use of mono­ polar diathermy. The overall incidence is between one and two cases per 1000 operations. Electrical injuries are usually unrecognised at the time that they occur, with patients commonly presenting 3–7 days after injury with complaints of fever and abdominal pain. As these injuries usually present late, the reasons for their occurrence are largely speculative. The main theories are: (1) inadvertent touching or grasping of tissue during current application; (2) direct coupling between a portion of bowel and a metal instrument that is touching the activated probe (Figure 8.6); (3) insulation breaks in the electrodes; (4) direct sparking to bowel from the diathermy probe; and (5) current passage to the bowel from recently coagulated, electrically isolated tissue. Bipolar diathermy is safer and should be used in preference to mono­ polar diathermy, especially in anatomically crowded areas. If monopolar diathermy is to be used, important safety measures include attainment of a perfect visual image, avoiding excessive current application and meticulous attention to insulation. Alternative methods of performing dissection, such as the use of ultrasonic devices, may improve safety.

POSTOPERATIVE CARE The postoperative care of patients after laparoscopic surgery is generally straightforward, with a low incidence of pain or other problems. The most common routine postoperative symptoms are a dull upper abdominal pain, nausea and pain

Figure 8.6  Direct coupling between bowel and laparoscope, which is touching the activated probe.

Frederic Eugene Basil Foley, 1891–1966, urologist, Ankher Hospital, St Paul, MN, USA.

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PART 1 | BASIC PRINCIPLES Postoperative care

around the shoulders (referred from the diaphragm). There has been some suggestion that the instillation of local anaesthetic to the operating site and into the suprahepatic space, or even leaving 1litre of normal saline in the peritoneum, serves to decrease postoperative pain. It is a good general rule that if the patient develops a fever or tachycardia, or complains of severe pain at the operation site, something is wrong and close observation is necessary. In this case, routine investigation should include a full blood count, Creactive protein (CRP) measurement, liver function tests, an amylase test and, probably, an ultrasound scan of the upper abdomen to detect fluid collections. If bile duct leakage is suspected, endoscopic retrograde cholangiopancreatography (ERCP) may be needed. If in doubt, relaparoscopy or laparotomy should be performed earlier rather than later. Death following technical errors in laparoscopic cholecystectomy has often been associated with a long delay in deciding to re-explore the abdomen. In the absence of problems, patients should be fit for discharge within 24 hours. They should be given instructions to telephone the unit or their general practitioner and to return to the hospital if they are not making satisfactory progress.

Nausea About half of patients experience some degree of nausea after laparoscopic surgery and, rarely, this may be severe. It usually responds to an antiemetic, such as ondansetron, and settles within 12–24 hours. It is made worse by opiate analgesics and these should be avoided.

Shoulder tip pain The patient should be warned about this preoperatively and told that the pain is referred from the diaphragm and not due to a local problem in the shoulders. It can be at its worst 24 hours after the operation. It usually settles within 2–3 days and is relieved by simple analgesics, such as paracetamol.

Abdominal pain Pain in one or other of the port site wounds is not uncommon and is worse if there is haematoma formation. It usually settles very rapidly. Increasing pain after 2–3 days may be a sign of infection and, with concomitant signs, antibiotic therapy is occasionally required. Occasionally, herniation through a port may account for localised pain and this can sometimes be due to a Richter’s hernia, such that the patient exhibits no sign of intestinal obstruction. Successful laparoscopic surgery should not cause a patient increasing or undue pain. If there are any clinical concerns postoperatively due to worsening pain, tachycardia and or pyrexia, senior review with a view to imaging, or increasingly commonly relaparoscopy, should be considered.

Analgesia A 100-mg diclofenac suppository may be given at the time of the operation (if this medication is not contraindicated). It is important that the patient provides separate consent for this

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if the suppository is to be administered peroperatively. Suppositories may be administered a further two or three times postoperatively for relief of more severe pain. Otherwise, 500–1000 mg of paracetamol 4-hourly usually suffices (orally or, if more pain, intravenously). Opiate analgesics cause nausea and should be avoided unless the pain is very severe. In this case, suspect a postoperative complication (as above). The majority of patients require between one and four doses of 1g of paracetamol postoperatively. Severe pain after routine laparoscopic cases should warn the clinician that there may be an iatrogenic or surgical cause of this pain that may need further investigation with blood tests, imaging and even relaparoscopy

Orogastric tube An orogastric tube may be placed during the operation if the stomach is distended and obscuring the view. It is not necessary in all cases. It should be removed as soon as the operation is over and before the patient regains consciousness. This is more routinely used in bariatrics and oesophagogastric surgery, where a larger (32F or 34F) tube is used.

Oral fluids There is no significant ileus after laparoscopic surgery, except in resectional procedures, such as colectomy or small bowel resection. Patients can start taking oral fluids as soon as they are conscious; they usually do so 4–6 hours after the end of the operation.

Oral feeding Provided that the patient has an appetite, a light meal can be taken 4–6 hours after the operation. Some patients remain slightly nauseated at this stage, but almost all eat a normal breakfast on the morning after the operation. Patients will require advice about what they can eat at home. They should be told that they can eat a normal diet but should avoid excess. It seems sensible to avoid high-fat meals for the first week, although there is no clear evidence that this is necessary.

Urinary catheter This depends on the operation. If a urinary catheter has been placed in the bladder during an operation with likely short stay, it should be removed before the patient regains consciousness if the procedure has proceeded well. The patient should be warned of the possibility and symptoms of postoperative cystitis and told to ask advice in the unlikely event of this occurring.

Drains The use of postoperative drains in laparoscopy patients depends on the operation performed. Drains are used to assess postoperative blood loss if this is a clinical concern or to assess the nature of intraperitoneal fluids, depending on procedure

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and postoperative monitoring needs. Some surgeons drain the abdomen at the end of laparoscopic cholecystectomy, although this is controversial. If a drain is placed to vent the remaining gas and peritoneal fluid, it should be removed within 1hour of the operation. If it has been placed because of excessive hepatic bleeding or bile leakage it should be removed when that problem has resolved, usually after 12–24 hours. Continued blood loss from a drain is an indication for re-exploration of the abdomen. Summary box 8.4 Surgical principles ●● ●● ●● ●● ●● ●● ●●

Meticulous care in the creation of a pneumoperitoneum Controlled dissection of adhesions Adequate exposure of operative field Avoidance and control of bleeding Avoidance of organ injury Avoidance of diathermy damage Vigilance in the postoperative period

DISCHARGE FROM HOSPITAL Patient discharge is based on clinical indicators and their fitness for recuperating in a non-hospital environment. One of the core drivers for the application of minimally invasive surgery is an earlier recovery and therefore discharge from hospital. For the common laparoscopic procedure of cholecystectomy, most surgeons discharge a significant proportion of their laparoscopic cholecystectomy patients on the day of surgery, but some are kept in overnight and discharged the following morning. Patients should not be discharged until they are seen to be comfortable, have passed urine and are eating and drinking satisfactorily. They should be told that if they develop abdominal pain or other severe symptoms they should return to the hospital or to their general practitioner. Even for more major cases, including procedures such as laparoscopic anterior resection, some units have demonstrated a safe and feasible protocol for a 23-hour stay.

Skin sutures If non-absorbable sutures or skin staples have been used, they can be removed from the port sites after 7days.

Mobility and convalescence Patients can get out of bed to go to the toilet as soon as they have recovered from the anaesthetic and they should be encouraged to do so. Such movements are remarkably pain free when compared with the mobility achieved after an open operation. Similarly, patients can cough actively and clear bronchial secretions, and this helps to diminish the incidence of chest infections. Many patients are able to walk out of hospital on the evening of their operation and almost all are fully mobile by the following morning. Thereafter, the postoperative recovery is variable. Some patients prefer to take things

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quietly for the first 2–3 days, interspersing increasing exercise with rest. After the third day, patients will have undertaken increasing amounts of activity. The average return to work is about 10 days.

THE PRINCIPLES OF COMMON LAPAROSCOPIC PROCEDURES The principles of common laparoscopic procedures are described in the appropriate chapters: ●● ●● ●● ●● ●● ●● ●●

laparoscopic cholecystectomy (Chapter 67); laparoscopic inguinal hernia repair (Chapter 60); laparoscopic antireflux surgery (Chapter 63); laparoscopic appendicectomy (Chapter 72); laparoscopic bariatric surgery (Chapter 64); laparoscopic colectomy/anterior resection (Chapters 70 and 73); laparoscopic upper gastrointestinal (GI) surgery (Chapters 62, 63 and 69)

Other elective minimally invasive (laparoscopic, thoracoscopic) or robotic procedures that are now widely utilised in certain specialist centres include: ●● ●● ●● ●● ●● ●● ●● ●● ●● ●● ●●

colectomy; gastrectomy; splenectomy; nephrectomy; adrenalectomy; prostatectomy (typically robotic); thyroid and parathyroid surgery; aortic aneurysm surgery; single-vessel coronary artery bypass surgery; video-assisted thorascopic surgery (VATS); laparoscopic hernia surgery (inguinal, femoral, paraumbilical, incisional).

Laparoscopy has also been used in certain emergency situations (in stable patients) in the hands of experienced laparoscopic surgeons. These include laparoscopic appen­ dicectomy (typically the most common minimally invasive emergency procedure), repair of a perforated duodenal ulcer, laparoscopic cholecystectomy in severe cholecystitis (so-called ‘hot’ cholecystectomies), and treatment of intestinal obstruction secondary to adhesions, strangulated hernia repairs and, also, the laparoscopic evaluation of stable trauma patients. Procedures that have been carried out using robotically assisted minimally invasive surgery include all of those listed above. Currently, robotic surgery still has certain disadvantages: ●● ●● ●● ●● ●● ●● ●● ●●

increased cost; increased set up of the system and operating time; socioeconomic implications; significant risk of conversion to conventional techniques; prolonged learning curve; multiple repositioning of the arms can cause trauma; haemostasis; collision of the robotic arms in extreme positions.

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PART 1 | BASIC PRINCIPLES The future

Until these are overcome, by continued development of the technology and the drive of surgeons to progress in the field, robotically assisted surgery will not be commonplace. However, the potential for such systems is immense and continued research and clinical trials will pave the way for future generations of surgeons and patients alike.

FURTHER DEVELOPMENTS THAT HAVE MADE MINIMALLY INVASIVE SURGERY EVEN LESS INVASIVE Single incision laparoscopic surgery Laparoscopy has reduced the trauma from surgery, compared with open techniques, and is now used routinely for benign and oncological surgery in many centres. However, there is continued work on how to reduce the trauma and scarring from the incisions used in laparoscopic surgery because multiple port sites are needed for most procedures. Natural orifice transluminal endoscopic surgery (NOTES) (see below) addresses this but, at present, the safety of the transgastric route is not sufficient for the routine use of this approach to surgery. Advanced laparoscopists have therefore turned to focussing on the single incision for open entry via the umbilicus as an alternative. Single incision laparoscopic surgery (SILS) is a technique adopted by some surgeons to insert all the instrumentation via a single incision, through a multiple channel port via the umbilicus, to carry out the procedure. The benefit is that only one incision, through a natural scar (the umbilicus), is made, therefore these procedures are virtually ‘scarless’. Second, the use of fewer port sites around the abdomen gives the potential for less pain, less risk of port site bleeding and reduced incidence of port site hernia. This technique has many other synonyms, including laparoendoscopic single site surgery (LESS) and single port access (SPA) surgery among many others, although SILS has gained the most recognition. It does require specially manu­ factured multichannel ports and often roticulating instruments. There has been an explosion of activity in SILS procedures in the last few years and, in some units, laparoscopic cholecystectomies and hernias are routinely started as SILS cases. The clinical benefit and cost-effectiveness of this technique, which has a difficult and steep learning curve and specific instrument requirements, remain under review, although it has been adopted as a routine approach for some procedures in some units. Early evidence understandably demonstrated better cosmetic outcomes and less pain in the immediate postoperative period; however, this needs to be further corroborated with higher levels of evidence with longer-term follow-up results. Specifically, because the SILS approach was not designed for improving clinical outcomes when compared with standard minimally invasive approaches, any improvements in pain and cosmesis between SILS and standard minimally invasive approaches require further elucidation.

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Natural orifice translumenal endoscopic surgery (NOTES) This technique, whereby surgeons enter the peritoneal cavity via endoscopic puncture of a hollow viscus, has been much publicised in recent years. The NOTES approach has been utilised in nearly every body system and operative speciality addressing the pelvis, abdomen and thorax. Worldwide adoption rates compared to standard open and minimally invasive approaches remain very low. Transvaginal NOTES cholecystectomies have been performed in humans successfully, although hybrid procedures (joint laparoscopy and NOTES) are still employed regularly for safety reasons. The closure of the visceral puncture site is the issue that has prevented widespread uptake of this technique, as transgastric and transcolonic closure of peritoneal entry sites in a routinely safe way remains unperfected for general use. Also, the equipment needed has significant cost and training needs (including surgeons and a large variety of ancillary team members that range from scrub nurses to anaesthetists) and requires a large number of practitioners in the team at present. Nevertheless, it has much promise to be a technique for truly scarless surgery in the future and much research continues in this field, which is less widely adopted at present than SILS.

THE FUTURE Although there is no doubt that minimal access surgery has changed the practice of surgeons, it has not changed the nature of disease. The basic principles of good surgery still apply, including appropriate case selection, excellent exposure, adequate retraction and a high level of technical expertise. If a procedure makes no sense with conventional access, it will make no sense with a laparoscopic approach. Laparoscopic and robotic surgery training is key to allow the specialty to progress. The pioneers of yesterday have to teach the surgeons of tomorrow not only the technical and dextrous skills required, but also the decision-making and innovative skills necessary for the field to continue to evolve. Training is often perceived as difficult, as trainers have less control over the trainees at the time of surgery and caseloads may be smaller, especially in centres where laparoscopic and robotic procedures are not common. However, trainees now rightly expect exposure to these procedures, and training systems should be adaptable for international exposure so that these techniques can be disseminated worldwide. The predominant video and digital component of these new techniques opens the door for simulation approaches for training in these modalities, which has demonstrated benefits in reducing learning curves and in turn is aimed at improving patient outcomes. The ultimate goal for this educational approach is to develop expert surgeons through the ‘totally safe’ and ‘risk free’ environment of simulation before they actually have to operate on patients. The current status for laparoscopic trainees reflects their decreased experience in open approaches so that they feel less comfortable converting cases such as laparoscopic cholecystectomies to open cases. It is important that the ‘straight to minimally invasive’ trainees continue to have

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training in open skills so that they can apply both approaches where necessary. Improvements in instrumentation, the continued progress of robotic surgery and the development of structured training programmes are key to the future of minimal access surgery. The use of robots in surgery has increased dramatically in the last decade. Indeed, robots are now available not only for assisting in surgery, but also for aiding in the perioperative management of surgical patients. The remote presence systems (In Touch Health, Santa Barbara, CA, USA) allow clinicians to assess patients in real time and interact with them while they are not on site or even on a different continent. Applying established devices in different contexts also offers the introduction of innovation; for example, the LABEL procedure (Laser Assisted Bile duct Exploration by Laparoendoscopy for choledocholithiasis) was developed when the concept of laser stone management in urology was applied to laparoscopic biliary tree surgery. Continued advances in related technologies, such as computer science, will allow the incorporation of augmented reality systems alongside robotic systems to enhance surgical precision in image-guided surgery. Endoluminal robotic surgery remains in its infancy, but systems are being developed that will enable navigation within the colon to allow surgery on lesions in spaces that are accessible from the outside without an exterior incision being made. The advent of nanotechnology should also bring about much change in surgery. Miniaturisation may be possible, potentially allowing surgery at a cellular level to be carried out. At present, work has already started on single-port laparoscopy (see above under Single incision laparoscopic surgery), in which a single port may act as a camera and have unfolding instruments that open up once they are inside the peritoneum to perform the surgery, therefore reducing the number of port sites needed. Extensive research is also being carried out in the field of NOTES. Minimising the potential contamination of the peritoneum and the ability to carry out a safe closure of the peritoneal entry site are the main technical challenges of this type of minimally invasive and essentially ‘scarless’ or ‘incisionless’ surgery. It is certain that there is much that is new in minimal access surgery. Only time will tell how much of what is new is truly better. Specifically, the future evolution of robotic systems includes full integration with next generation technologies such as advanced augmented reality, autobionics, neuromorphic visual processing and real-time diagnostics and theranostics, exemplified by the i-Knife (real-time tissue metabolic profiling and tissue-level diagnosis, developed by Zoltan Takats at Imperial College London). Large master–slave constructions with multiple arms are likely to give way to flexible access bio-inspired (FAB) systems. These will probably offer full robotic arm articulation in much more portable devices with low energy needs. They would be totally modular with integrated imaging and would have platforms to offer multipurpose usage to increase utilisation and cost efficiency. These

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systems would also result in a smaller physical footprint, with cheaper devices offering more utility, precision and dexterity on platforms that allow both master–slave and direct functionality. One major obstacle in minimally invasive technology includes the ‘Achilles heel’ of cost efficiency and device financing in an increasingly rationed global healthcare environment; this is an issue which will require surgical liaison with hospital management and national policy providers. Surgeons need to continue to have a dialogue, discussing their experiences and ideas regarding all the minimally invasive approaches. None of these techniques needs to exist in isolation. The future can offer hybridisation of these approaches, including a vast array of possibilities such as Robotic-SILS, Robotic-NOTES or even endoscopic NOTES-augmented SILS (endoscopes passed through a SILS port). Such crossfertilisation can offer new innovation and techniques; thus, harvesting the advantages of newer procedures and discarding the individual weaknesses of others can ultimately improve patient outcomes and results. The cleaner and gentler the act of operation, the less the patient suffers, the smoother and quicker his convalescence, the more exquisite his healed wound. Berkeley George Andrew Moynihan (1920)

FURTHER READING Acharya MN, Ashrafian H, Athanasiou T, Casula R. Is totally endoscopic coronary artery bypass safe, feasible and effective? Interact Cardiovasc Thorac Surg 2012; 15(6): 1040–6. Antonakis PT, Ashrafian H, Isla AM. Laparoscopic gastric surgery for cancer: where do we stand? World J Gastroenterol 2014; 20(39): 14280–91. Ashrafian H, Darzi A, Athanasiou T. Autobionics: a new paradigm in regenerative medicine and surgery. Regen Med 2010; 5(2): 279–88. Ashrafian H, Navarro-Sanchez A, Athanasiou T, Sherman DI, Isla A. Thoracoscopic esophageal repair of a spontaneous Barrett’s ulcer perforation. Ann Thorac Surg 2015; 99(1): 331–3. Athanasiou T, Ashrafian H, Rao C, Yang GZ, Darzi A. The tipping point of robotic surgery in healthcare: from master–slave to flexible access bio-inspired platforms. Surg Technol Int 2011; 21: 28–34. Athanasiou T, Ashrafian H, Rowland SP, Casula R. Robotic cardiac surgery: advanced minimally invasive technology hindered by barriers to adoption. Future Cardiol 2011; 7(4): 511–22. Hoeckelmann M, Rudas IJ, Fiorini P, Kirchner F, Haidegger T. Current capabilities and development potential in surgical robotics. Int J Adv Robot Syst 2015; 12. Navarro-Sanchez A, Ashrafian H, Laliotis A, Qurashi K, Martinez-Isla A. Single-stage laparoscopic management of acute gallstone pancreatitis: outcomes at different timings. Hepatobiliary Pancreat Dis Int 2016; 15(3): 297–301. Navarro-Sanchez A, Ashrafian H, Segura-Sampedro JJ, Martinez-Isla A. LABEL procedure: laser-assisted bile duct exploration by laparoendoscopy for choledocholithiasis: improving surgical outcomes and reducing technical failure. Surg Endosc 2017; 31(5): 2103–8. Tan A, Ashrafian H, Scott AJ et al. Robotic surgery: disruptive innovation or unfulfilled promise? A systematic review and meta-analysis of the first 30 years. Surg Endosc 2016; 30(10): 4330–52.

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ve Bailey & Love Bailey & Love Bailey & Love ve Bailey & Love Bailey & Love Bailey & 9 Love Chapter

Principles of paediatric surgery Learning objectives At the end of this chapter, you will be able to: •• Describe clinically important differences between adults and children •• Explain the principles of trauma management in children •• Safely prescribe perioperative fluids in children

INTRODUCTION Premature and term neonates differ in their anatomy, physi­ ology, neurology, psychology, pathology and pharmacology, just as infants differ from school-age children and adolescents from adults. These differences underpin the principles of pae­ diatric surgery. As you progress through this chapter and con­ sider children of different ages (Table 9.1) you should make your own list of differences and their clinical implications; a few examples appear in Table 9.2 and in Figure 9.1 to get you started. Paediatric surgeons study developmental biology and ter­ atology but because some anomalies first present to adult ser­ vices (e.g. duplications, malrotation) this knowledge can help adult surgeons. Adult services also need to cater for the tran­ sitional needs of those graduating to adulthood, sometimes after complex paediatric surgical care. Most children escape the comorbidities of degenerative diseases but no longer are they free from lifestyle problems. Paediatric bariatric surgery TABLE 9.1  Common terms. Preterm

width)

Figure 9.1  Topographical differences in the abdomen.

Figure 9.2  Summary of upper airway anatomy in an infant.

TABLE 9.3  Basic paediatric data. (a) Weight Age

pulmonary evaporation and their surface area to weight ratio is higher. Consider these when managing sick children in the Emergency Department, anaesthetic room or theatre. These environments must be warm and the infant’s head (20% of surface area, cf. 9% in an adult) should be insulated. Infusions are warmed and respiratory gases both warmed and humidi­ fied. Core temperature is monitored and safe direct warming is needed for lengthy operations.

AIRWAY

Anatomical differences in the airway have clinical implica­ tions (see Figure 9.2). The infant’s large head and short neck predispose to flexion. The large tongue can obstruct the air­ way when the infant is unconscious and impede the airway ISBN: posteriorly 9781444121278 26th Ed Short Practice of Surgery, and laryngoscopy. The epiglottis projects and the larynx is high; a straight-bladed laryngoscope is favoured in .co.uk those under 1year of age. Uncuffed tubes are preferred as the cricoid ring is the narrowest region (cf. the larynx in an adult) and this is covered in loose epithelium that is easily irritated; damage can result in subglottic stenosis.

PERIOPERATIVE FLUIDS IN CHILDREN

Weight (kg)

Term neonate

3.5

1 year

10

5 years

20

10 years

30

(b)  Vital signs Age (years)

Heart rate (bpm)

Systolic blood pressure (mmHg)

Respiratory rate (b/min)

10%) in decreased skin turgor, drowsiness, tachycardia and poor capillary refill (>2seconds) and signs of hypovolaemia. Children develop hyponatraemic encephalopathy at higher sodium levels than adults because they have a higher brain:skull ratio. A few children have had symptomatic hypo­ natraemic encephalopathy attributable to poor prescription and monitoring of fluids; some have died and others have

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Proof Stage:

estimates the weight from the height. Systolic blood pressure = 80 + (age in years × 2) mmHg. Circulating blood volume = 80mL/kg (90mL/kg in infants).

permanent neurological disability. Problems have arisen when: (1) hypotonic maintenance fluids (e.g. 0.18% saline) have been inappropriately given to resuscitate or replace loses, or (2) maintenance fluids have been given in excess (3–5 times requirements). UK National Guidelines are that maintenance fluid admin­ istration should contain sodium levels of 131–154mmol/L.

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PART 1 | BASIC PRINCIPLES Operative surgery

Learning objectives for this section are to: ●● ●● ●● ●● ●●

Know the four reasons for giving intravenous (IV) fluids. Be able to calculate fluid rates for children of different weights (see Table 9.3). Understand the risks of low-sodium containing fluids. Understand how the body’s response to stress and illness affects fluid balance. Know how to recognise and manage hyponatraemia ( 0.85) 4 weeks' duration, current or within last 6 months

Colour venous duplex Superficial venous disease

Mixed deep and superficial disease

Consent Quality-of-life score Photoplethysmography Randomisation

Consent Quality-of-life score Photoplethysmography Randomisation

Group A

Group A

Group B

Group B

the grant submission date to ensure appropriate authorisation from institutions. A data collection form should be designed or a computer collection package developed. If data are collected on computer, appropriate safeguards for privacy, confidentiality and data quality will be necessary to comply with legislation. At this stage it is important to consider any validation requirements and needs for open access either in a recognised archive (e.g. the UK Data Archive) or an institutional repository. Any form of data collection needs to be quality assured. The quality assurance process will include training, Standard Operating Procedures as well as monitoring and checking a certain sample of the data. At the end of data collection and analysis, a final data base with all data should be locked and kept for future reference in a safe location. A data archiving policy with a nominated data custodian should be in place. Research is no longer confined by institutional or even geographical boundaries. Communication by the internet can be a valid way to co-ordinate internalional research. The Global Surgical Outcomes Collaboration (www.globalsurg.org) is a group of young surgeons performing collaborative research with internet data collection. Some publishers require registration of a study at the time of study set up on a publically available database (e.g. ISRCTN). It is becoming increasingly popular to consider publication of a protocol paper.

Regulatory framework In the UK, the implementation of the research governance framework by the Department of Health, or its planned successor UK Policy Framework for Health and Social Care, provides a framwork that enhances the integrity of the study and includes requirements for sponsorship by an institution to ensure the following: peer review, independent ethics review, compliance with data protection principles, financial probity, dissemination and management of intellectual property. Sponsorship is defined by the HRA as the individual, company, institution or organisation that takes on ultimate responsibility for the initiation, management (or arranging the initiation and management) of and/or financing (or arranging the financing) for that research. The sponsor takes primary responsibility for ensuring that the design of the study meets appropriate standards and that arrangements are in place to ensure appropriate conduct and reporting. http://www.hra. nhs.uk/resources/before-you-apply/roles-and-­responsibilties/ sponsor/

Group A: compression bandaging Group B: compression bandaging + surgery

Peer review

Outcomes Ulcer healing and recurrence rates Venous function tests Quality of life and cost–benefit

Once the protocol is finalised, formal peer review is needed. In the UK, evidence of peer review will be needed before submitting an application to a research ethics committee and for HRA approval.

Figure 11.1  ESCHAR trial: completed in Gloucestershire, UK (Gohel MS et al. British Journal of Surgery 2005; 92: 291–7. Copyright British Journal of Surgery Society Ltd. Permission is granted by John Wiley & Sons Ltd on behalf of the BJSS Ltd.) ABPI, ankle–brachial pressure index.

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●● ●●

If the research is part of a university course, the university (usually the student supervisor) should undertake this review. Surgeons working for the NHS can arrange their own peer review by experts who are not connected with the study.

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CHAPTER 11  Surgical audit and research

●●

Alternatively, most Research and Development Support Units (NHS) will give guidance through the review process. Many funders of research will undertake their own independent peer review. There is usually feedback from this process that can provide valuable advice about the study.

Ethics In the first instance, common sense is the best guide to whether or not a study is ethical. It is still important to seek advice from an independent research ethics committee whenever research is contemplated. In the UK the requirement is that a NHS Research Ethics Committee (NHS REC) provides an independent ethical review of all health and social care research if it involves patients and/or carers. The Government arrangment for Research Ethics Commitees (GafREC) provide detailed guidance about NHS REC review requirements. The application for NHS REC review should be made using the Integrated Research Administraion System (IRAS). IRAS is a single system for applying for the permissions and approvals for health and social care/community care research in the UK. It enables entry of information about the project once instead of duplicating information in separate application forms. IRAS captures the information needed for the relevant approvals from the following review bodies: ●● ●● ●● ●● ●● ●● ●● ●● ●●

Administration of Radioactive Substances Advisory Committee (ARSAC); Confidentiality Advisory Group (CAG); Gene Therapy Advisory Committee (GTAC); Health Research Authority (HRA) for projects seeking HRA approval; Medicines and Healthcare products Regulatory Agency (MHRA); NHS/HSC R&D offices; NHS/HSC Research Ethics Committees; National Offender Management Service (NOMS); Social Care Research Ethics Committee.

Once all the relevant forms and associated study documentation have been completed, guidance provided by the HRA and the Research Ethics Service should be followed for submission of the request for ethical review and HRA approval. If the study does not require review by an NHS REC, the need for an independent ethical review should still be considered. Universities have developed their own ethical review infrastructure and this will be institute specific and location specific. For collaborative research, local ethical review should be obtained where possible, and developing a local ethics infrastructure should be considered if it does not already exist. Duplicaton of ethical review should be avoided. Ethics committees prefer to see fully developed trial protocols but it is often possible to get some preliminary advice from the NHS REC Manager. Ethics committee forms may seem long and detailed, but it is important that these are filled in correctly and it helps to prepare the investigators for all practical aspects of the project. All dealings with ethics committees should be intelligent and courteous. It is important to attend the meeting at which the study will be discussed,

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if invited, as it provides a forum for direct communication in relation to the study. It can save time as possible concerns of the ethics committee can be addressed at the time, avoiding lengthy correspondence.

Regulatory approvals In the case of interventional clinical or device trials, the European Union Clinical Trial Directives apply, which are regulated by the Medicines and Health Care products Regulatory Agency (MHRA) in the UK. A clinical trial should be registered with the European Clinical Trials Database before applying to the MHRA for a Clinical Trial Authorisation via the common European submission portal. This can be a complicated and trying process, and support should be sought from the investigators’ employing institution. Editors of the major surgical journals now agree that all clinical trials should have been registered before an article relating to a trial can be published. All studies undertaken with NHS patients and/or carers will need HRA approval and confrmation of capacity and capability from NHS sites. Studies involving animals require approval from statutory licensing authorities. Reporting on animal research should employ ARRIVE guidelines (Animal Research: Reporting of In Vivo Experiments).

Research integrity The principles and responsibilities set out in the Singapore Statement on Research Integrity in 2010 was the first international effort to encourage the development of unified policies, guidelines and codes of conduct, with the long-term goal of fostering greater integrity in research worldwide. The European Code of Conduct followed and in 2012 Universities UK, in collaboration with major funders of research, developed ‘the Concordat to support research integrity’, which sets out key commitments to ensure a high standard in research. All highlight the principles and professional responsibilities of researchers and research instituions that are fundamental to the integrity of research wherever it is undertaken. These centre around: ●● ●● ●● ●●

honesty in all aspects of research; accountability and transparentcy in the conduct of research; professional courtesy and fairness in working with others; good stewardship of research.

A study should not under any circumstances commence until the correct approval has been granted and compliance with the principles of research integrity is ensured. Any challenge to the integrity of research can be time-consuming and career-limiting.

STATISTICAL ANALYSIS Both audit and research commonly require statistical analysis. Many surgeons find the statistical analysis of a project the most difficult part. It is also the most commonly criticised part

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PART 1 | BASIC PRINCIPLES Analysing a scientific article

of papers written by clinicians. There are many useful books about statistics that can be consulted (see Further reading); if in any doubt, a statistician will be pleased to give assistance. Statisticians like to be consulted before research or audit has been conducted rather than being presented with the data at the end; they often give helpful advice over study design and can be an important part of the project team. The following terms are frequently used when summarising statistical data: ●● ●●

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Mean: the result of dividing the total by the number of observations (the average); Median: the middle value with equal numbers of observations above and below – used for numerical or ranked data; Mode: the value with the highest frequency observed – used for nominal data collection; Range: the largest to the smallest value.

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it is possible that they are unlikely to have major clinical significance.

Computer software packages available Statistical computer packages offer a quick way of analysing descriptive statistics such as mean, median and range, as well as the most commonly used statistical tests such as the chisquared test. Various packages are available commercially and are useful tools in data analysis.

ANALYSING A SCIENTIFIC ARTICLE

The simplest way to analyse an article from a scientific journal is to look at the checklist of requirements for good scienThe most important decision for analysis is whether the tific research. A group of scientists and editors developed the distribution of the data is normal (i.e. parametric or non-­ CONSORT (Consolidated Standards of Reporting Trials) parametric). Normally, distributed data have a symmetrical, statement to improve the quality of reporting of RCTs. Lookbell-shaped curve, and the mean, median and mode all lie at ing in detail at the study design is often the best way of decidthe same value. The type of data collected determines which ing whether a trial is any good. The CONSORT document includes a checklist for the conduct of good randomised tristatistical test should be used. als (Table 11.4). Often clinicians overlook biases that others 1 Numerical and normally distributed (e.g. blood pressure) – use unpaired t-test to compare two groups or paired t-test to assess whether a variable has changed between two time TABLE 11.4  Checklist for authors. points. Heading Sub-heading Descriptor 2 Numerical but not normally distributed (e.g. tumour size) Title Identify as randomised trial – use Mann–Whitney U-test to compare two groups or a Abstract Structured format Wilcoxon signed rank test to assess whether a variable has increased/stayed the same/decreased between two time Introduction Prospectively defined hypotheses, clinical objective points. 3 Categorical (e.g. admitted or not admitted to an intenMethods Protocol Study population sive care unit) – can use chi-squared test to compare two Intervention, timing groups. ●●

(Note: the use of these and any other statistical tests may benefit from professional advice.) Confidence intervals are the best guide to the possible range in which the true differences are likely to lie. A confidence interval that includes zero usually implies a lack of statistical significance. Scientists usually employ probability (P-values) to describe statistical chance. A P-value 500 mL blood loss (7 mL/kg in children)? No Yes, and adequate intravenous access and fluids planned

Anaesthesia team reviews: are there any patient-specific concerns?

The name of the procedure recorded

How the specimen is labelled (including patient name) Whether there are any equipment problems to be addressed Surgeon, anaesthesia professional and nurse review the key concerns for recovery and management of this patient

Nursing team reviews: has sterility (including indicator results) been confirmed? are there equipment issues or any concerns? Has antibiotic prophylaxis been given within the last 60 minutes? Yes Not applicable Is essential imaging displayed? Yes Not applicable

Figure 13.5  World Health Organisation Surgical Safety Checklist (First Edition).

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Even in comparison to aviation, managing patients involves an enormous amount of coordinated, time-pressured decision making and potential delays. Checklists are simple reminders of what to do, and unless they are coupled with attitude change and efforts to remove barriers to actually using them, they will have limited impact. Finally, if one begins to believe that safety is simple and that all it requires is a checklist, there is a danger of abandoning other important efforts to achieve safer, higher quality care.

Technical and operative errors In surgery, the person rather than systems approach emphasises the accountability of the surgeon who, unlike colleagues in other medical disciplines, when operating, is an instrument of the treatment. During a surgical procedure, for example, there may be a specific action that, of itself, may be the error, such as the inadvertent cutting of the common bile duct during a cholecystectomy (Figure 13.6). The practical value of this kind of interpretation is that, provided latent conditions are excluded, it gives a sense of responsibility to the surgeon and it may also help to point to the most effective pathway for remediation, by counselling or retraining, as against reassessing the system and putting in place further safeguards.

not carry negative connotations for trainee surgeons who might be at the conscious processing stage but still perform a perfectly good operation, although it might take longer and be more tiring. Failures in operative technique include: ●●

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cognitive errors of judgment, such as failure or late conversion of a difficult laparoscopic procedure into an open one; procedural, when the steps of an operation are not followed or omitted; executional, when, for example, too much force is used which may result in damage that may or may not have consequences; misinterpretation, which is unique to minimal access surgery and is a function of the misreading of a two dimensional image; misuse of instrumentation, such as with energised dissection modalities (e.g. diathermy); missed iatrogenic injury either at the time of surgery or diagnosed late.

Never events Many national health services and institutions now require that all incidents are managed, reported and investigated. Incidents can be defined as events that could have or did result in unintended and/or unnecessary serious harm. One subset of serious incidents is a Never or Serious Reportable Event. These events are wholly preventable; for example, a retained abdominal swab or instrument, where guidance providing strong systemic protective barriers should have been implemented, namely checklists. Each Never Event type has the potential to cause serious patient harm or death. However, serious harm or death is not required to have occurred for that incident to be categorised as a Never or Serious Reportable Event.

Newer concepts of approaches to safety

Figure 13.6  Radiograph showing an iatrogenic bile duct injury.

Central to operative performance is proficiency, which is an acquired state, honed by sound teaching, practice and repetition, by which a surgeon consistently performs operations with good outcomes. In cognitive psychology, high surgical proficiency is a state of automatic unconscious processing, with the execution being effortless, intuitive and untiring, as opposed to non-proficient execution which is characterised by conscious control processing requiring constant attention and resulting in slow, deliberate execution and inducing fatigue. The transition from one state to the other is better known as the ‘learning curve’. This should

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Safety I is the approach to patient safety that has been described so far. It is predicated on identifying errors after the event and aims to prevent them from occurring or recurring in the future. Because healthcare is much more complex than such a linear model suggests, it is felt that that there is a need to switch our efforts to enable getting things to go right more often – a concept called Safety II. This acknowledges that healthcare work is resilient and that everyday performance succeeds much more often than it fails. This is because clinicians constantly adjust what they do to match the conditions. Working flexibly, and actively trying to increase their capacity to deliver more care more effectively, is key to this new approach. At its heart, proactive safety management focuses on how everyday performance usually succeeds rather than why it occasionally fails, and actively strives to improve the former rather than simply preventing the latter.

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PART 1 | BASIC PRINCIPLES Clinical outcomes and audit

Summary box 13.5 Patient safety and the surgeon and newer concepts on safety ●●

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Errors that can be made by surgeons in their overall management of patients Errors that occur in the operating theatre and how they can be mitigated The role of checklists in patient safety Performance proficiency and understanding technical and operative failures Getting things right more often may be a better approach than identifying errors after the event

QUALITY IMPROVEMENT Quality improvement (QI) comes into play when we need to design or redesign healthcare processes and systems in response to a quality gap in order to ensure more efficient, safe, timely, effective, patient-centred and equitable care. Although safety is just a single aspect, it is self-apparent that improving any one of these components will likely have a beneficial effect on the other. Cost is also an important adjunct to quality improvement.The concept of value – the quotient of what is delivered divided by the cost – is an increasingly important metric in healthcare. The scope for QI is enormous and can range from redesigning how teams deliver care in clinical microsystems that make up healthcare organisations to large-scale reconfigur­ ations of specialist services such as stroke care and cancer care. It may even extend to redesigning training, budgeting processes and information systems and it requires leadership and cultures that both understand and value quality improvement. Improvements come from the intentional actions of staff equipped with the skills and data needed to bring about changes in patient care either directly or indirectly, and they require substantial and sustained commitment of time and resource.

QUALITY MEASURES Quality measuresare tools that help usmeasureor quantify healthcare processes, outcomes, patient perceptions and ­organisational structures or systems that are associated with the ability to provide high-quality health care and/or that relate to one or morequalitygoals for healthcare. Measurement is important to determine whether changes that are believed to lead to improvements in quality do in fact result in improvements. Improvement efforts require different methods from those used in research, being concerned more with testing of how to introduce best practice rather than determining what that developing best practice should be. Process measures reflect the procedures and practices implemented by staff in the planning prescribing, delivery and evaluation of care – these may be specific to a clinical process, a service or administrative process. An example of a clinical process might be the starting times of operating lists. Process improvement measures should be associated with

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b­ etter outcomes of care and, ideally, should be important from a patient’s perspective – reducing delays in starting times in the example cited. The patient’s surgical journey is a composite of multiple processes. Measurement for improvement less commonly involves comparisons among sites and against thresholds but more commonly involves tracking processes and outcomes in the same site over time. Outcome indicators are specific, observable and measurable changes that represent the achievement of anoutcome of a quality improvement measure. Clinical outcome measures refer specifically to outcomes of healthcare interventions whether they are to do with diagnosis, treatment or that care received by service users. Ideally, they should be outcomes that are important to patients rather than to the health provider, and there should be evidence that they reflect the quality of the interventions and their effect. Outcome measures are what are commonly used in clinical audit when compared with evidenced-based standards of clinical care. Patient perception and the principles of patient centred-­ care should be an important part of QI particularly in those areas that directly affect their care, such as: ●● ●● ●● ●● ●● ●● ●● ●●

the speed of their access to reliable health advice; the effectiveness of their treatment delivered by trusted professionals; the continuity of their care and its smooth transitions; the involvement of, and support for, their family and ­carers; the availability of clear, comprehensible information and support for self-care; their involvement in decisions and the respect for their preferences; the emotional support, empathy and respect provided; the attention paid to their physical and environmental needs.

Organisational structure and systems refers to the avail­ ability of resources required to deliver care. These include the care environment and facilities, the available equipment and the organisation’s documented policies, procedures, protocols and guidelines. The consistent consensus view is that good-quality improvement or clinical audit has to have at least four essential stages of activity to be considered high quality: ●● ●● ●● ●●

preparation and planning, measuring performance; implementing change; sustaining improvement (including reaudit).

The collection and interpretation of reliable data is of fundamental importance to any QI exercise (Table 13.4).

CLINICAL OUTCOMES AND AUDIT Put simply, clinical auditis that part of clinical governance that finds out if healthcare is being provided in line with standards and it allows care providers and patients know how

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TABLE 13.4  Three pioneers of quality improvement and their quotes on data. William Edwards Denning (1900–1993)

American engineer, statistician, professor, author, lecturer and management consultant. Pioneered the PDSA (Plan, Do, Study, Act) cycle

“In God we trust, all others bring data.”

Peter Ferdinand Drucker (1909–2005)

Austrian-born American management consultant and educator

“What gets measured gets improved.”

Donald Berwick (Born 1946)

American paediatrician. Former President and Chief Executive Officer of the Institute of Health Care Improvement

Sequence of reactions that challenge data: “The data are wrong.” “The data are right but it’s not a problem.” “The data are right; it is a problem but not my problem.” “I accept the burden of improvement.”

their service is doing and where there could be improvements. The aim is to allow quality improvement to take place where it will be most helpful and will improve outcomes for patients. Clinical audits can look at care nationwide or locally within hospitals and their departments, in GP practices or anywhere healthcare is provided. Measuring clinical outcomes as part of the quality improvement cycle aims to: ●●

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improve the quality of clinical care with shorter hospital stays, better outcomes and fewer complications, reduced readmissions and greater patient satisfaction; inform the development of national clinical audits, including driving participation, data completeness and accuracy; support shared decision making and empowerment of patients, including their treatment options and choice of provider; improve the oversight and management of clinicians, their teams and practises and thus reassuring patients that their clinical care is being actively monitored and improved; help medical specialty associations to become increasingly transparent and patient focused; support team and individual quality improvement including providing information for appraisal and revalidation; learn from, spread and celebrate best practice.

‘Best practice’ dictates that surgeons should not just be aware of their clinical activity and outcomes but also endeavour to benchmark their activity against national and international norms. (Surgical audit is further addressed in Chapter 11.) There is limited evidence that audit as presently defined and used is meeting health policy makers’ aspirations. The alternative, systems-based QI methods, discussed below, although they have produced many successful improvements within healthcare services, have still not yet been scientifically proven to be more impactful.

THE PROCESS OF SURGICAL CARE The process of QI can perhaps be best illustrated by understanding and optimising the efficiency of the patient journey at each step across the healthcare domains from the patient’s home and primary care through the hospital system and then back out into the community. For example, while many ill-

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nesses and injuries require hospitalisation, a QI exercise might be the introduction of an admission avoidance policy for selected, appropriate patients attending Emergency Departments who could be better managed at home or in the community, thus providing an overall benefit to those patients in terms of safety, economy and choice. Patients attend surgeons in many different settings depending on whether they present electively or urgently (scheduled or unscheduled). An elective journey is usually predictable and starts out as a referral from primary care and commonly requires an outpatient visit and investigations. If a surgical procedure is required, then we recognise that it is best that the patient is fully assessed from a surgical and anaesthetic perspective prior to admission within a preadmission assessment clinic. Once assessed, the patient should be admitted as a day case, wherever possible, or on the day of surgery or as short a time as possible before surgery as an inpatient. Preoperative checking is followed by the theatre journey, which includes reception, anaesthesia, the surgery itself and recovery – each, in their own way, a series of complex interventions. Returning to the ward and recovery demands another set of skills, procedures and processes followed by a final ‘discharge from hospital’ process. The urgent or unscheduled journey is different because it is unpredictable for any single individual, although patterns of presentation do emerge when managing large numbers. The patient commonly presents at the Emergency Department of a hospital either as a self-referral, primary care referral or by ambulance. The journey begins with triage by a team who assess the severity of the illness (using, for example, the Manchester scoring system) and then directing the patient to the appropriate area, which might include, for example, a resuscitation unit, a rapid assessment and treatment unit, an acute surgical assessment unit (or medical assessment for medical patients), a minor injuries unit or an ambulatory care unit. The objective is to be seen as soon as possible by a senior decision maker, so that the patient can be treated or discharged as expeditiously as possible or, if admission and surgery is required, then this too can be expedited. Thereafter the journey follows a similar course to that of an elective admission. This simple outline of surgical patients’ journeys serves to illustrate the very many individual steps or processes in that journey. The scope for errors, delays and inefficiencies from a patient’s perspective is almost limitless. Instituting QI aims at their mitigation.

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PART 1 | BASIC PRINCIPLES The quality improvement pathway

Good surgical practice has, for many years, dictated that surgeons should be aware of their clinical outcomes including their complications, re-admission rates and standardised mortality rates. It is now also incumbent on surgeons and their teams to measure the performance of their surgical processes against best practice. These include the average length of stay of their patients, their day case and day of admission rates, bed occupancy and, as activity-based funding becomes more prevalent, their consumption of institutional costs.

THE QUALITY IMPROVEMENT PATHWAY QI can be applied to almost any step, process or activity. The Scottish Improvement Hub recommends seven stages that might be undertaken in a QI exercise: ●● ●● ●● ●● ●● ●● ●●

discovering – is about defining the aims and vision; for example, what the problem is and what data is available; exploring – is about defining the present state and visualising the future state; designing – is about defining how to move from the present state to the future state and identifying the priorities; refining – is about testing change, learning from the data and identifying the benefits; introducing – is about managing communications and building the will and culture to change; spreading – is about showing the improvements, telling the story and disseminating the message; closing – is about capturing and sustaining the learning.

Each step can then be accompanied by any number of established organisational and graphical tools and methodologies appropriate to the design and planning of each step and suitable for the QI improvement exercise being undertaken (Table 13.5). Emergency departments, wards and operating theatres are fertile grounds for process and performance improvement. Bundled educational programmes, such as the Productive Series (for wards and theatres, for example) introduced by the former NHS Institute for Innovation and Improvement, supports teams to redesign and streamline the way they manage and work within specific areas. TABLE 13.5  Examples of tools used in quality improvement. Organisational

Graphical

Root cause analysis Benefits realisation planning Demand and capacity planning Process mapping Value stream mapping Kanban and 5 ‘S’

Driver diagrams Fishbone cause and effect diagrams Spaghetti diagrams Box, frequency and scatter plots Pareto and run charts

Lean Arguably, the most successful example of system redesign in an industrial setting has been the Toyota Production System from which much of the thinking can be applied to health-

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care. ‘Kaizen’ is the Japanese for improvement. At Toyota, production line personnel are expected to stop the production line when an abnormality is noticed and, along with their supervisor, initiate kaizen. A single cycle of kaizen activity is defined as ‘plan, do, study and act’, also known as thePDSA cycle. The same application can be used in healthcare, with many sequential cycles growing to ‘continuous improvement’. Lean manufacturing is a management philosophy that is also derived mostly from the Toyota Production System.Defining Lean is difficult; it is in essence the elimination of waste through continuous improvement. Identifying waste leads inevitably to the need to define customer value and reducing waste requires elimination of error. This approach has found widespread application in industry. In medical settings, there is extensive evidence of its benefits in improving efficiency, reducing costs and improving patient satisfaction. Operating theatres provide a good example of how lean principles can be applied in healthcare. Lean states that, in manufacturing, there are broadly seven types of waste that need eliminating in order to improve productivity: the same could be applied to perioperative care. For example: ●●

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Overproduction. Such as: ordering unnecessary preop­ erative tests. Solution: optimising evidence-based preassessment. Inventory. Such as: purchasing of excessive drug stock before it is required. Solution: alphabetically ordered drug cupboards with only 1–2 boxes of commonly used drugs. Waiting. Such as: surgeons waiting for a patient to come down to theatre and sitting in the coffee room doing nothing. Solution: improve communications and, maybe, engage more porters. Waste of transportation. Such as: wasting time transferring patients from the admitting ward to the theatre or vice versa. Solutions: better design of the theatre complex to optimise patient flow, simplifying mode of transport and better communications and handover. Waste of overprocessing. Such as: giving patients a nerve block, a spinal and a general anaesthetic for a joint replacement. Solution: general anaesthetic and local infiltration may be equivalent and quicker. Defect. Such as: patients arrive in theatre with incomplete or inappropriate preoperative paperwork. Solution: more robust checking systems before patients come to theatre. Motion. Such as: constant repetitive movement around theatre and the anaesthetic room to get drugs, equip­ mentand disposal of waste. Solution: a ‘motion efficient’ theatre where everything is easily available with minimal movement, and similar layouts in multitheatre complexes.

Six sigma Six sigma is another scientific business performance methodology that has been adopted for use in healthcare. The fundamental objective of the Six Sigma methodology is the implementation of a measurement-based strategy that focuses on process improvement and variation reduction. One of its sub-methodologies is DMAIC (Define, Measure, Analyse, Improve, Control), which is an improvement system for

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existing processes falling below specification and requiring incremental improvement.

Systems thinking and leadership In a system as fraught with complexity as healthcare, ‘systems’ thinking allows the whole system to be viewed and the relationships of the parts rather than just the isolated parts. Healthcare is a shared resource with many interdependencies; for surgery these include anaesthesia and critical care and all those specialties we require to work with to manage comorbid patients. If quality problems exist primarily because of system problems, solutions are more likely in those systems where relationships and integration are considered important, where emphasis is placed on communication, team building, conflict management, behavioural and skill competencies, process management, and education; many of the features discussed under HF. Systems frameworks should never be punitive. They should have leaders who are systems thinkers and foster a culture of continuous QI. Those leaders should be visible at the front line and be champions of a supportive practice environment. Improvement in the quality of care does not occur by chance. Nor will a programme team, armed with just organisational and graphical tools succeed in producing sustainable change. The underlying, central and agreed principles must include the creation of value for the patient, a constancy of purpose and systems thinking. These should be enabled by the intentional actions of trained staff supported by humble leadership and respect for individuals. Such a culture adjustment also requires integrated and coherent strategies and a sustained commitment of time, patience and resources.

INVESTING IN QI AND ITS EDUCATION Healthcare as a sector has been late in recognising the important contribution that the theory and practice of QI are able to make in delivering better value care. The experience of a relatively small number of healthcare organisations that have successfully done so, such as the Virginia Mason Medical Centre in Seattle, is a challenge to others to invest in acquiring the necessary skills and capabilities.

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A recent report of the Academy of the Medical Royal Colleges of UK and Ireland (2016) has argued that QI should be at the heart of medical training and that there is a pressing need to develop QI learning across the continuum of medical education. Their report sets out to enable education bodies to embed QI education into their curricula while asserting that it is as important as learning anatomy, biochemistry and physiology and a skill as important as CPR. Summary box 13.6 Understanding QI and its application in healthcare ●● ●● ●● ●●

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The definition of QI and its relationship to clinical audit The different kinds of quality measures The patient surgical journey and its potential for improvement Examples of QI pathways, organisational methodologies and tools What system thinking is and its importance alongside leadership The requirement for more education and training in QI

FURTHER READING Academy of Medical Royal Colleges. Quality improvement – training for better outcomes. Key Findings, 2016. http://www.aomrc.org.uk/publications/reports-a-guidance Ham C, Berwick D, Dixon J. Improving quality in the English NHS – a strategy for action. The Kings Fund, 2016. http://www.kingsfund.org. uk/publications/quality-improvement Haugen AS, Softeland E, Almeland SK et al. Effect of the World Health Organization checklist on patient outcomes. Ann Surg, 2015; 261: 821–8. Institute of Medicine. Crossing the quality chasm: a new health system for the 21st century. Washington, DC: National Academies Press, 2001. Kohn LT, Corrigan JM, Donaldson MS (eds). To err is human – building a safer health system. Washington, DC: National Academies Press, 2000: 312. Langley GL, Moen R, Nolan KM, et al. The improvement guide: a practical approach to enhancing organizational performance, 2nd edn. San Francisco: Jossey-Bass Publishers, 2009. Makary MA, Daniel M. Medical error – the third leading cause of death in the US. BMJ 2016; 353: i2139. Neily J, Mills PD, Young-Xu Y, et al. Association between implementation of a medical team training program and surgical mortality JAMA, 2010; 304(15): 1693–1700. NHS Scotland. Quality improvement hub. http://www.qihub.scot.nhs.uk/ default.aspx Timmons S, Baxendale B, Buttery A, et al. Implementing human factors in clinical practice. Emerg Med J Online First, 2014; 32: 368–72.

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Investigation and diagnosis

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Gastrointestinal endoscopy................................................................... 216

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Tissue and molecular diagnosis........................................................... 234

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Diagnostic imaging Learning objectives To understand: •• The advantages of good working relationships and close collaboration with the imaging department in planning appropriate investigations •• The basic principles of radiation protection and know the law in relation to the use of ionising radiation

•• The principles of different imaging techniques and their

INTRODUCTION

HOW TO REQUEST IMAGING

Appropriate surgical management of the patient relies on correct diagnosis. While clinical symptoms and signs may provide a firm diagnosis in some cases, other conditions will require the use of supplementary investigations including imaging techniques. The number and scope of imaging techniques available to the surgeon have dramatically increased within a generation, from a time when radiographs alone were the mainstay of investigation. The development of ultrasound and colour Doppler, computed tomography (CT) and magnetic resonance imaging (MRI) has enabled the surgeon to make increasingly confident diagnoses and has reduced the need for diagnostic surgical techniques such as explorative laparotomy. Faced with such a plethora of imaging to choose from, it is important that the patient is not sent on a journey through multiple unnecessary examinations. As a basic principle, the simplest, cheapest test should be chosen that it is hoped will answer the clinical question. This necessitates knowledge of the potential complications and diagnostic limitations of the various methods. For example, in a patient presenting with the clinical features of biliary colic, an ultrasound examination alone may give enough information to enable appropriate surgical management. In more complex cases, it may be more efficient to opt for a single, more expensive investigation, such as CT, rather than embarking on multiple simpler and cheaper investigations that may not yield the answer. The choice of technique is often dictated by equipment availability, expertise and cost, as well as the clinical presentation. However, it must be emphasised that, not infrequently, the most valuable investigation is prior imaging; this not only reduces the cost and the amount of radiation a patient receives but very often improves patient care.

Best practice depends on close collaboration between the radiologist and the referrer and must take into account local expertise and access to facilities. When requesting imaging, consider what it is that you want to know from the investigation. Give a provisional diagnosis or state the clinical problem. If there is uncertainty over the best method to answer the clinical problem, then discussion with a radiologist is always worthwhile, informally or within the context of a clinicoradiological meeting or a multidisciplinary team (MDT) meeting. As well as the basic demographic information stored on the radiology information system (RIS), it is important to provide relevant past medical history, e.g. diabetes, epilepsy, renal failure, allergies and anticoagulation, all of which can affect which contrast agent can be given safely, and the date of the last menses in women of childbearing potential.

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advantages and disadvantages in different clinical scenarios •• The role of imaging in directing treatment in various surgical scenarios

INTERPRETING IMAGES While the role of the Imaging department is to provide radiological reports for imaging examinations performed, it is ­nevertheless good clinical practice to be able to evaluate your patients’ examinations, and a systematic approach is ­encouraged. The systematic approach to examining a radiograph varies according to the part of the body being imaged. For instance, for a radiograph of an extremity, the alignment, the cortices and the medullary cavity of the individual bones, the joints and the soft tissues all need to be assessed on each view.

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PART 2 | INVESTIGATION AND DIAGNOSIS Current legislation

Summary box 14.1 A simple system for checking radiographs Label Site Side (check Quality Compare

Name of patient Date of examination marker) What part is the film centered on? Does the film cover the whole area required? Is there more than one view? Is the penetration appropriate? How have the appearances changed from previous images? Conclude Is the diagnosis clear? Is further imaging needed?

HAZARDS OF IMAGING Contrast media There has been a dramatic increase in the use of contrast agents in recent years, mainly related to the increasing use of CT. Potential problems include allergic reaction and nephrotoxicity. Reactions are rare: serious reactions occur in about 1:2500 cases and life- threatening reactions in about 1:25 000 cases. The risk of sudden death, however, has not changed with the new agents. Local policies for dealing with patients at increased risk vary between departments and, indeed, between countries. Advice from the Royal College of Radiologists (RCR) in the UK does not recommend routine steroid prophylaxis for patients at increased risk of allergic reaction, but rather the use of low osmolality contrast media(LOCM) or iso-osmolar media, and observation of the patient for 30 minutes after injection with the intravenous cannula still in situ, since most serious reactions occur shortly after injection. Guidelines from the European Society of Uroradiology (ESUR), however, continue to advocate the use of steroids. In patients with diabetes or renal impairment, a recent creatinine level should be available. The radiologist should be informed of any history of renal impairment, as all contrast media are nephrotoxic in patients with impaired renal function. The risks and benefits of contrast administration need to be carefully assessed in these patients and, if contrast is given, the patient should be well hydrated and the lowest dose of a LOCM should be given. The British RCR does not recommend the routine use of N-acetylcysteine for renal protection. Concerns about lactic acidosis in patients on metformin receiving contrast led to various recommendations for stopping the metformin. The latest RCR recommendations are that it can be continued in patients with normal renal function. If there is a raised creatinine or reduced estimated glomerular filtration rate (eGFR) below 60 then any decision to stop metformin should be made with the radiologist and the physician managing the patient’s diabetes. Gadoliniumcontaining contrast agents are used in MRI examinations. Allergic reactions to these agents are very rare. However, they can be nephrotoxic in patients with renal failure. In addition, they are associated with a risk of nephrogenic systemic

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fibrosis (NSF), an extremely rare but serious life-threatening condition whereby connective tissue forms in the skin causing it to become coarse and hard. NSF may also affect other organs, including joints, muscle, liver and heart. High-risk gadolinium-containing contrast agents are contraindicated in severe renal failure, in neonates and in the perioperative period of liver transplantation, and are not recommended in pregnancy. However, lower-risk gadolinium preparations are available that may be used with caution. Liver-specific contrast agents for MRI, selectively taken up by hepatocytes, are increasingly used to characterise liver lesions and in cancer staging.

HAZARDS OF IONISING RADIATION The majority of ionising radiation comes from natural sources on the earth and cosmic rays, and this makes up the background radiation. However, medical exposure accounts for around 15% of the total received by humans. The effects of ionising radiation can be broadly divided into two groups. The first group comprises predictable, dose-dependent tissue effects and includes, for example, the development of cataracts in the lens of the eye. These effects are important for those chronically exposed to radiation, including those using image intensifiers regularly. The second group comprises the all-ornothing effects such as the development of cancer (termed stochastic). These effects are not dose dependent, but increase in likelihood with increased radiation dose. The risk of radiation-induced cancer for plain films of the chest or extremities is very small, of the order of 1:1 000 000. However, that risk rises considerably for highdose examinations such as CT of the abdomen or pelvis, where the estimated lifetime excess risk of cancer increases to the order of 1:1000. Use of CT has increased dramatically in the last 20 years, with a 12-fold increase in the UK, and it has been estimated that up to 30% of these examinations may be unnecessary. Obviously, the risk of such examinations has to be balanced against the benefit to the patient in terms of increased diagnostic yield, and must also be viewed in the context that the lifetime risk of cancer for people generally is about 1:3. Nevertheless, the increased risk is important since it is iatrogenic and applied to a large population. Therefore, techniques that do not use ionising radiation, such as ultrasound and MRI, should be carefully considered as alternatives, particularly in children and young people.

CURRENT LEGISLATION In the UK, the Ionising Radiation (Medical Exposure) Regulations (IRMER) introduced in 2000, and amended in 2006, impose on the radiologist the duty to the patient to make sure that all studies involving radiation (plain radiographs, CT and nuclear medicine) are performed appropriately and to the highest standards. Inappropriate use of radiation is a criminal offence, so investigations involving radiation need careful consideration in order to prevent wasteful use of radiology.

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CHAPTER 14  Diagnostic imaging

Summary box 14.3 gives a summary of the responsibilities of both the radiologist and the referrer. The RCR produces an evidence-based guidance tool, called iRefer, which is widely available on line. Table 14.1, showing the radiation doses for common procedures, is taken from this publication, now in its seventh edition.

Summary box 14.2 Wasteful use of radiology Results unlikely to affect patient management Positive finding unlikely Anticipated finding probably irrelevant for management

Do I need it?

Summary box 14.3

Investigating too often

Responsibilities

Before disease could be expected Do I need it now? to have progressed or resolved

●●

Repeating investigations done previously

●● ●●

Other hospital (?) GP (?)

●●

Has it been done already?

Failing to provide adequate information

●● ●●

Therefore wrong test performed or Have I explained the essential view omitted problem? Requesting wrong investigation Discuss with radiologist Over-investigating

Is this the best test? Are too many investigations being performed?

After: IRefer gudelines, Making the best use of radiology, 7th edition. Royal College of Radiologists, 2012.

Radiologists have a legal responsibility to keep imaging as safe as possible The referrer has a duty to balance risk against benefit The referrer must provide adequate clinical details to allow justification of the examination Avoid using portable (mobile) x-ray machines whenever practical Take all precautions when using an image intensifier The gonads, eyes and thyroid are especially vulnerable to radiation and should be protected

There are special considerations for portable and fluoroscopy units. The longer an operator keeps the fluoroscopy unit running, the higher the dose of radiation to all in the vicinity. Portable x-ray machines and fluoroscopic imaging equipment use much more radiation to achieve the same result. The staff, and patients in the next bed, are at risk

TABLE 14.1 Typical effective doses from diagnostic medical exposure in the 2000s. Diagnostic procedure Radiographic examinations Limbs and joints (except hip) Chest (single posteroanterior film) Skull Thoracic spine Lumbar spine Hip Pelvis Abdomen Intravenous urography (IVU) Barium swallow Barium meal Barium follow-through Barium enema CT head CT chest CT abdomen or pelvis Radionuclide studies Lung ventilation (133Xe) Lung perfusion (99mTc) Kidney (99mTc) Thyroid (99mTc) Bone (99mTc) Dynamic cardiac (99mTc) PET head (18F-FDG)

Typical effective dose (mSv) 90 minutes Reduced mobility for more than 3 days Pregnancy/puerperium Varicose veins with phlebitis Drugs, e.g. oestrogen contraceptive, HRT, smoking Known active cancer or on treatment, significant medical comorbidities, critical care admission Family/personal history of thrombosis, e.g. deficiencies in antithrombin III, protein S and C

Thomas Addison, 1795–1860, physician, Guy’s Hospital, London, UK, described the effects of disease of the suprarenal capsules in 1849.

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platelet agents or anticoagulants. If it is felt that the neurological and cardiovascular thrombotic risks are low, antiplatelet agents should be withdrawn (7 days for aspirin, 10 days for clopidogrel). If the thrombotic risks are perceived to be high and the patient is undergoing surgery with a high risk of bleeding, aspirin alone should be continued. Anticonvulsants and anti-Parkinson medication is continued perioperatively to help early mobilisation of the patient. Lithium should be stopped 24 hours prior to surgery; blood levels should be measured to exclude toxicity. The anaesthetist should be informed if patients are on psychiatric medications such as tricyclic antidepressants or monoamine oxidase inhibitors, as these may interact with anaesthetic drugs.

Musculoskeletal disorders Rheumatoid arthritis can lead to an unstable cervical spine with the possibility of spinal cord injury during intubation. Therefore, flexion and extension lateral cervical spine radiographs should be obtained in symptomatic patients (Figures 17.4 and 17.5). Assessment of the severity of renal, cardiac valvular and pericardial involvement as well as restrictive lung disease, should be carried out. Rheumatologists will advise on steroids and disease-modifying drugs so as to balance immunosuppression (chance of infections) against the need to stabilise the disease perioperatively (stopping disease modifying drugs can lead to flare-up of the disease). In ankylosing spondylitis patients, in addition to the problems discussed above, techniques of spinal or epidural anaesthesia are often challenging. Patients with systemic lupus erythematosus may exhibit a hypercoagulable state along with airway difficulties. With certain types of orthopaedic operations, such as joint replacement, antibiotic prophylaxis will be required, and will usually follow specific local or national guidelines.

Airway assessment The ability to intubate the trachea and oxygenate the patient are basic and crucial skills of the anaesthetist. The ease or difficulty encountered when performing airway manoeuvres can be predicted by simple examination findings of full mouth opening (modified Mallampati class), jaw protrusion, neck movement and thyromental distance. The anaesthetist should look for loose teeth, obvious tumours, scars, infections, obesity, thickness of the neck, etc., which will indicate difficulty in visualising the airway. When more than one of the above tests are positive, the chances of experiencing difficulty in obtaining and securing the airway become greater. To obtain the modified Mallampati class, the anaesthetist sits in front of the patient who is asked to open their mouth and protrude the tongue (Figure 17.6). The higher the grade, the higher the risk in obtaining and securing an airway (Table 17.4).

Figure 17.4  Extension view of cervical spine in patient with rheumatoid arthritis.

Figure 17.5  Flexion view in the same patient as in Figure 17.4. Note the large increase in the atlantodens interval, implying significant instability at this level.

Preoperative assessment in emergency surgery In urgent or emergency surgery the principles of preoperative assessment should be the same as in elective surgery, except that the opportunity to optimise the condition is limited by time constraints. Medical assessment and treatments should be started (e.g. as per Advanced Trauma Life Support guidelines) even if there is no time to complete them before the start of the surgical procedure. Some risks may be reduced but some may persist and, whenever possible, these need to be explained to the patient.

SR Mallampatipublished the original article suggesting that the size of the base of the tongue is an important factor determining the degree of difficulty of direct laryngoscopy in the Canadian Anaesthetists’ Society Journal in 1985. The original Mallampati classifications was modified from a total of three to four classes by GLT Sampsoon and JRB Young after reviewing a series of obstetric and general surgical patients who had had difficult intubations.

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anxiety result in increased demands for oxygen delivery to the tissues. This demand increases from an average of 110 mL/ min/m2 at rest to 170 mL/min/m2 in the postoperative period. Most patients meet this increase in demand by increasing their cardiac output and tissue oxygen extraction. Patients who are unable to meet these demands, as a result of a limited cardiorespiratory reserve, are at a risk of oxygen debt. Occult hypovolemia resulting from fluid shift or blood loss can further impair oxygen delivery. Splanchnic vasoconstriction to compensate for this may result in gut ischaemia. Those with coronary or cerebrovascular disease are also at a higher risk of myocardial ischaemia or stroke.

Factors contributing to risk

Figure 17.6  Normal mouth opening view.

TABLE 17.4  Airway assessment (Samsoon and Young modified Mallampati test). ●● ●● ●● ●●

Fauces, pillars, soft palate and uvula seen Fauces, soft palate with some part of uvula seen Soft palate seen Hard palate only seen

Grade 1 Grade 2 Grade 3 Grade 4

Summary box 17.6 Preoperative assessment for emergency surgery ●● ●● ●● ●●

Start. Similar principles to that for elective surgery Constraints. Time, facilities available Consent. May not be possible in life-saving emergencies Organisational efforts. For example, local/national algorithms for treatment of the patient with multiple injuries

ASSESSMENT OF THE HIGHRISK PATIENT Despite higher-risk patients presenting for surgery, the perioperative mortality has decreased significantly over the last half a century, especially in resource-rich countries. In a published systematic review in The Lancet (Bainbridge et al., 2012), perioperative mortality has declined from 10 603 per million (95% CI: 10 423–10 784) in the 1970s to 1176 per million (1148–1205) in the 1990s–2000s (p70 years with limited physiological reserve in one or more vital organs Extensive surgery for carcinoma Acute abdominal catastrophe with haemodynamic instability (e.g. peritonitis) Acute massive blood loss >8 units Septicaemia Positive blood culture or septic focus Respiratory failure: PaO2 0.4 or mechanical ventilation >48 h Acute renal failure: urea >20 mmol or creatinine >260 mmol/L (Based on clinical criteria used by Shoemaker and colleagues modified by Boyd.)

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TABLE 17.6  Surgery specific estimates of risk High risk (cardiac risk >5%)

Intermediate risk (cardiac risk 1–5%)

Low risk (cardiac risk 10% should be conducted under the direct supervision of consultant surgeon or anaesthetist, unless the consultants are satisfied with the seniority and competence of the staff managing these patients. Moreover, those with a mortality >10% should be managed in the critical care facility. Depending on particular comorbidities, it may be possible for a patient’s underlying conditions to be improved by optimising their medical therapy. Additional physiological

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Identify the high-risk patient Assess the level of risk Detailed preoperative assessment Adequate resusciatation Optimise medical management Investigation to define the underlying surgical problem Immediate and definitive treatment of underlying problems Consider admission to a critical care facility postoperatively

Identification of the high-risk patient A number of scoring systems have been developed over the years with the aim of identifying high-risk patients (Table 17.8).

American Society of Anaesthesiologists system The American Society of Anaesthesiologists (ASA) scoring system is widely used. Although not designed to be used as a risk prediction score, it has a quantitative association with the predicted percentage of postoperative mortality (Table 17.9). However, it does not account for age or nature of surgery and the term ‘systemic disease’ in ASA grading introduces an element of ‘subjectivity’.

Metabolic equivalent As discussed earlier, overall functional physical fitness can be judged by the ability to tolerate metabolic equivalent tasks (METs) (Table 17.10). One MET is equivalent to the oxygen consumption of an adult at rest (~3.5 mL/kg/min). Different tasks are assigned a number of METs. If the patient is able to perform >4 METs (e.g. climbing at least one flight of stairs) they are considered suitable candidates for major surgery. However, once again this depends on a subjective assessment of the ability of a patient and may be overestimated by them. Objective indices based on weighted scores pertaining to surgery and comorbidity, have been created to stratify cardiac risk. Examples include the Goldman cardiac risk index and

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TABLE 17.8  Surgical risk scores classified by outcome measures and need for intraoperative information. Scores predicting mortality

Scores predicting morbidity

Scores not requiring operative information

ASA APACHE-II Donati score Hardman index Glasgow aneurysm score Sickness assessment Boey score Hacetteppe score Physiological POSSUM ACS NSQIP surgical risk score

ASA APACHE-II Goldman cardiac risk index Veltkamp score VA respiratory failure score VA pneumonia prediction index ACS NSQIP surgical risk score

Scores requiring operative information

Mannheim peritonitis index Reiss index Fitness score POSSUM P-POSSUM Cleveland colorectal model Surgical risk scale

POSSUM P-POSSUM

APACHE-II, Acute Physiology and Chronic Health Evaluation II; VA, Veterans Affairs; P-POSSUM, Portsmouth-POSSUM; see text for additional abbreviations. (Modified from Rex TE, Bates T. World J Emerg Surg 2007; 2: 16.)

TABLE 17.9  Operative mortality by ASA grade. ASA Grade

Description

30 day mortality (%)

I II

Healthy Mild systemic disease, no functional limitation Severe systemic disease, definite functional limitation Severe systemic disease, constant threat to life Moribund patient unlikely to survive 24 hours with or without operation Emergency operation

0.1 0.7

III IV V E

3.5 18.3 93.3

TABLE 17.10  Metabolic equivalent of task (MET).

●● ●● ●● ●● ●●

Risk factors

Risk of major cardiac complications (%)

History of ischaemic heart disease History of compensated or prior heart failure History of cerebrovascular disease Diabetes mellitus Renal insufficiency (creatinine >177 µmol/L) High-risk surgery

Number of factors 0 = 0.4 1 = 0.9 2 = 7.0 3+ = 11.0

(From Boyd O, Jackson N. Crit Care 2005; 9: 390–6.)

●●

TABLE 17.11  The revised cardiac risk index (RCRI) of Lee.

1 MET = 3.5 mL O2/kg/min (oxygen consumption by 40-yearold,70 kg man at rest) 1 MET = eating and dressing 4 MET = climbing 2 flights of stairs 6 MET = short run >10 MET = able to participate in strenuous sport Patients who can exercise at 4 METS or above have lower risk of perioperative mortality

the revised cardiac risk index (RCRI) of Lee (Table 17.11). Although they can predict risk of cardiac complications, they are not designed to predict mortality.

POSSUM score The POSSUM score (Physiologic and Operative Severity Score for the enUmeration of Mortality and Morbidity) and its modifications (P-POSSUM, CR-POSSUM) are used to predict all-cause mortality in postoperative critical care patients as well as non-cardiac morbidity.

ACS NSQIP score The American College of Surgeons (ACS) National Surgical Quality Improvement Programme (NSQIP) surgical risk score estimates the chance of a complication or death after surgery for more than a thousand different surgical procedures. It compares the patient’s risk with an average person’s risk. It is a web based tool done preoperatively. The risk is calculated based on surgical procedure and 19 patient-specific preoperative risk factors.

Cardiopulmonary exercise testing Cardiopulmonary exercise testing (CPET) can be used as a screening tool to identify high-risk patients. The oxygen (O2) consumption and carbon dioxide (CO2) production of the patient are measured while they undergo a 10 minute period of incrementally demanding exercise (usually on a cycle ergometer) up to their maximally tolerated level (Figure 17.7). CPET is based on the principle that when a subject’s delivery of O2 to active tissues becomes inadequate, anaerobic metabolism begins; lactate is buffered by bicarbonate and the resulting CO2 increases out of proportion to the escalation in physical difficulty and O2 consumption. The ‘anaerobic threshold’ (AT) is the O2 consumption in mL/kg/min above

Lee Goldman, b.1948, Dean of Health Sciences and Medicine, Columbia University, New York, NY, USA, since 2006. He developed his Index in 1977. Thomas H Lee, Professor of Medicine, Harvard Medical School, Professor of Health Policy and Management, Harvard School of Public Health, Boston, MA, USA.

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hypotension, tachycardia and procoagulant states (of which the inflammatory response to surgery is an example). Preparation of these patients for surgery should aim to optimise myocardial oxygen supply and demand ratio and so minimise the risk of myocardial ischaemia developing. This work may involve further investigations or even the decision to postpone non-cardiac surgery for 3–6 months after an MI. Some patients may require preoperative revascularisation, using either a coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI) with a stent or angioplasty.

Minimising myocardial ischaemia

Figure 17.7  Cardiopulmonary exercise testing (CPET).

which this occurs. Peak oxygen consumption (VO2) is also measured. They are the end product of a subject’s combined respiratory, cardiac, vascular and musculoskeletal fitness, and subjects with either an AT above a somewhat arbitrary cutoff of 11 and a VO2 below 15 mL/kg/min are at higher risk of morbidity and mortality after surgery. When CPET is not available, a simple walk test, such as the 6-minute walk test (6MWT) and the incremental shuttle walk test (ISWT), can be used to assess the functional capacity of the patient. They depend on the patient’s ability to walk for a fixed 6 minute period or at increasing speed over a flat surface.

Optimisation of the high-risk patient As discussed above, all coexisting disease processes should be reviewed and optimised. Simple measures include stopping smoking (maximal benefit only seen if stopped for 8 weeks prior to surgery), reducing alcohol intake, losing weight, improving nutrition and/or haemoglobin levels. In the high-risk group there may a need for more complex investigations, review of medication or even consideration of further surgery. Patients scheduled for abdominal aortic aneurysm (AAA) repair surgery for example, frequently require carotid duplex scans. If the scans reveal a significant blockage and a high risk of perioperative stroke, a carotid endarterectomy may be indicated prior to AAA repair. All high-risk patients benefit from multidisciplinary team care and the involvement of experienced physicians in the peri­ operative period. The impact and management of the comorbidities that commonly contribute to risk are outlined below.

Ischaemic heart disease Perioperative myocardial infarction (MI) is associated with a high mortality (15–25%). Ischaemia, and ultimately MI, occur when the supply of oxygen to the myocardium is exceeded by its demand. This situation can be precipitated by

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Anaesthesia techniques that dampen the stress response to surgery (especially minimising pain) and provide a good degree of cardiac stability should be used. Anaesthesia should avoid tachycardia, systolic hypertension and diastolic hypotension, and may be facilitated by the use of invasive arterial blood pressure monitoring. Blood loss must be accurately monitored and haemoglobin maintained at a level suitable for the patient’s cardiac risk factors. Perioperative use of β-blockers may be considered but this is controversial. Troponin testing allows early diagnosis of perioperative MIs, but there are limited reperfusion options due to risk of bleeding from the surgical site. Admission to HDU should be considered for patients with IHD and supplemental oxygen therapy continued for 3–4 days.

Cardiac failure Left ventricular failure is the end result of several conditions including IHD, hypertension, cardiomyopathies and valve dysfunction. Decompensated heart failure puts the patient at risk of multiorgan failure. Those with ejection fractions of less than 35%, and in whom the failure is undiagnosed or its severity underestimated, are at the highest risk. The patient’s functional capacity needs to be assessed and surgery may have to be delayed for investigations such as an echocardiogram and/or for optimisation of medical therapy. Drugs used in chronic heart failure have significant implications for perioperative care, and β-blockers and probably ACE inhibitors (unless renal perfusion is to be significantly affected) should be continued. Anaesthesia should ensure minimal myocardial depression and change in afterload during surgery. Arrhythmias must be rapidly brought under control, particularly AF, and correcting any electrolyte imbalance is crucial in this respect. Invasive monitoring of trends in central venous and arterial pressure monitoring may help management, particularly when large fluid shifts are expected to occur.

Respiratory failure Around 1.5% of patients develop lower respiratory tract infection after surgery with a 30-day mortality over 20%. Surgery, particularly open abdominal procedures under general anaesthesia, result in changes to respiratory physiology. The functional residual capacity of the lungs is reduced. This combined with the respiratory depressant effect of residual anaesthetic agents, the patient’s limited mobility and pain from surgery causes atelectasis (failure of gas exchange due to alveolar collapse) and predisposes patients to postoperative

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respiratory infection. Other complications including bronchospasm, pneumothorax and acute respiratory distress syndrome (ARDS) contribute as much to morbidity and length of hospital stay as cardiac complications. Respiratory failure defined as a PaO2 30 (Figure 21.2). Traditional guidelines are conservative about obesity due to fears of intra- and postoperative complications. Although there is an increased incidence of non-serious respiratory complications intraoperatively and in the immediate postoperative recovery

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

21

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

25

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

32

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

37

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

41

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

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

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 21.2  Body mass index calculator. Adolphe Quetelet, 1796–1874, Belgian mathematician, astronomer and statistician, 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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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 and achievable in advanced units. Patients established on nasal positive airway pressure for obstructive sleep apnoea can be managed successfully.

Anticoagulants Patients are generally on oral anticoagulants due to atrial fibrillation, previous thromboembolism or because they have a metal heart valve. It is therefore important to review these patients carefully before deciding to discontinue their anticoagulant for their operation. When it is felt that surgery will require its discontinuation, this should be discussed with their cardiologist and the risks involved explained to the patient.

Social criteria Safe and comfortable discharge home requires the patient to be accompanied by a responsible and physically able adult. A journey time to home of 1 hour or less is advocated, but the comfort of the journey rather than the time involved is more relevant. Home circumstances require appropriate toilet facilities and the means of contacting the hospital should complications occur.

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, with entry to abdominal and thoracic cavities 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. With day surgery now applicable to more major and prolonged procedures, patients should undergo a venous thromboembolism risk assessment and have prophylaxis provided if required.

PREOPERATIVE ASSESSMENT The evaluation and optimisation of a patient’s fitness for surgery is known as preoperative assessment (see Chapter 17) and is best performed by a specialist nursing team with support from an anaesthetist with an interest in day surgery. All elective surgical patients should be initially regarded as suitable for day surgery until proved otherwise. 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.

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Summary box 21.3 Preoperative assessment ●● ●● ●●

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

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. When mixed lists of day and inpatient cases are planned, then day cases are scheduled first. The mixing of day and complex 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, there is a risk of cancellation or 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 (see Chapter 18). 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 non-steroidal anti-inflammatory drug, such as ibuprofen. Intraoperative anaesthesia can be maintained by any of the traditional inhalational agents. Total intravenous anaesthesia (TIVA) 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 (15. The majority of hospital admissions with injury have low ISS values, ranging between the values 4 and 8, and are secondary to single isolated limb fractures and isolated mild head injury. Overall, major trauma affects approximately 15% of all injured patients. The total number of casualties from RTA alone reported to the police in Great Britain during 2015 was 186 189, which was around 4% lower when compared with 2014. Of these, 21 657 people were seriously injured, among whom 1730 lost their lives, representing a 3% decrease compared with 2014. Across Europe, according to the data presented by the European Transport Safety Council’s Performance Index (PIN) report, it appears that fatalities rose in the majority of countries. Of the 32 countries covered, 21 had an increase in the number of fatalities in 2015, ten had a decrease, and one remained unchanged. Since countries do not use the same definition of serious injury, international comparisons are based on road deaths per million inhabitants (Figure 22.1). The United Kingdom as a whole had 27.7 deaths per million inhabitants in 2015. The only European countries with a better rate than this in 2015 were Sweden with 26.6, Malta with 25.6 and Norway with 22.6. The UK and Sweden have been consistently at the head of this table for a number of years. A large proportion of the severely injured survivors experience long-term or permanent disability as a result of their injuries. Almost 30% of them are no longer able to return to their previous occupation and a great deal of time is lost from work. These individuals end up having profound changes in their lifestyle, with long-term pain and suffering. It should be emphasised that an injury not only affects the injured person but also affects everyone who is involved in the injured person’s life. The impact of the modern epidemic of road traffic

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311

100 *Countries with provisional fatality figures.

Road deaths per million inhabitants

90

Countries marked with a red outline have fewer than 150 deaths per year and therefore the fatality rate can vary significantly between years.

80 70 60 50 40 30 20

BG

LV

RO

HR

LT*

PL

EL*

CZ

CY

RS*

BE*

LU

PT*

SI

IT*

AT*

FR

EE

SK

FI

DE*

IL

NL

ES*

IE*

DK

CH

UK

GB

SE

MT

NO*

10

Figure 22.1  Number of road deaths per million inhabitants.

accidents on the universal epidemic of violent injury cannot be overstated. The annual direct medical cost of injuries treated in hospitals and additional care facilities is estimated to be £3.7 billion. Moreover, additional costs, due to loss of earnings, loss of productivity and quality of life damage, increase the total sum significantly. While young patients are involved in road traffic accidents characterised by high energy transfer, older patients may sustain injuries from falls (low energy transfer). The most common group to be admitted to hospital in the UK are older patients who have sustained a ‘fragility’ fracture. Approximately 65 000 to 70 000 patients are admitted annually with proximal femoral fractures, among whom 30% over the age of 65 will die within a year of the incident. Most of the rest will end up having diminished independence and functional capacity. It is therefore no surprise that this particular cohort of patients, which will increase in the coming years owing to the anticipated increase in life expectancy, is thought to represent a huge burden on healthcare services and society in general. In general terms, the vast majority of injuries sustained are not limb threatening or life threatening. They are straightforward and most patients are expected to recover fully and return to their preinjury status. Nonetheless, the challenge remains to appreciate and diagnose the injuries at an early

Summary box 22.1 Trauma: the magnitude of the problem ●● ●●

●●

●●

The vast majority of injuries are not life or limb threatening Severe trauma continues to be a major cause of death in young patients Older patients with fragility fractures pose an additional burden to the healthcare system Look for important features of injuries that could influence the outcome

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stage, with an awareness of important features that may influence the outcome. For instance, we must be vigilant not to miss nonaccidental injury (NAI) in children (see Chapter 39) and injuries in other age groups related to an underlying disease process rather than the injury itself, for example pathological fractures. Of note, it has been shown that in 66% of cases when children die as a result of abuse, there has been some pre­ vious interaction with a health professional or social services but the seriousness of the situation was not fully appreciated.

THE MANAGEMENT OF TRAUMA From the moment that injury is sustained, every aspect of decision making and management is essential in terms of the survival of the victim. Our initial assessment and concepts of management have specific objectives and are usually based on knowledge acquired over a long period of time in practice. A better understanding of the physiological processes underpinning the host responses to an acute threat to our homeostatic mechanisms, together with protocols formulated to allow clinicians to use standardised measures and to speak a common language, have revolutionised the way we manage patients. All of the above help to reduce delays, particularly when under pressure to make a decision. However, it remains crucial to understand the reasoning as to why we are carrying them out. In trauma, as in other acute conditions, the patient is particularly reliant upon the clinician. A patient with a chronic condition is familiar with the nature of their problem and the way in which it is progressing. The surgeon may offer a remedy and the patient may consider the potential benefits and choose appropriately whether to accept it. The injured patient does not know what will happen without treatment and so relies on their surgeon to inform them of both the natural history and the potential benefits of any intervention. The implication is that as surgeons we have a duty to be aware of both.

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The significance of time in the outcome Injury can occur in the blink of an eye. In the seconds prior to the application of the external injury force or vector, the patient is at their normal baseline, which can be called time zero. All subsequent events, including the acute physiological response to injury, the body’s internal mechanisms to maintain homeostasis (to compensate for the sequelae of trauma), the healing processes and the actions instigated by health professionals, are associated with a ‘timeline’. Being familiar with the ‘timeline principle’, one should be aware that there is a critical time window in which we can intervene for a positive treatment outcome, before the loss of compensatory mechanisms. Moreover, the timeline allows evaluation of any progress made from time zero to other important events and to reflect on whether a specific course of action could have been performed better. Overall, interventions can be distinguished as emergency (life saving), acute (restoring haemodynamic stability) and delayed or semielective, focusing on the treatment of postfracture fixation complications (non-union, infection and malunion from the orthopaedic trauma point of view). It is essential to appreciate that the physiological crisis initiated in the immediate aftermath of trauma will continue to evolve and the risk of mortality is substantial unless the correct and timely interventions are performed. For instance, conditions such as airway obstruction, tension haemothorax and haemopericardium can progress very rapidly if left untreated and should be given priority in terms of our initial medical response to the injured patient. Thus, the seriousness and the immediate impact of a specific clinical condition should be prioritised and treated in a systematic approach (what kills first should be managed first). This concept of the hierarchy of medical responses can only be applied and become effective when we are in a position to diagnose early the underlying clinical conditions (Figure 22.2). The ATLS (Advanced Trauma Life Support) system delineates an order of priorities set by ABCD; that is, airway, breathing, circulation and disability (neurology). This hierarchy of priorities is instituted upon the ‘time dependence’ principle. The clinician should bear in mind that a successful management plan is dependent on, first, the time needed to evaluate and diagnose the nature of the problem and, second, the time taken to respond effectively to the condition discovered (Figure 22.3). Evaluating and diagnosing a condition can be challenging, as the initial clinical signs may be non-specific. The clinical condition will continue to evolve as the time progresses, but by the time the diagnosis has been made it may be too late to prevent mortality. Taking into consideration the mechanism of the accident and promptly requesting special investigations, for example computed tomography (CT), the underlying diagnosis can be made punctually, thus allowing intervention in a timely fashion. A patient presenting following a road traffic accident with a scalp laceration and a reduced Glasgow Coma Scale (GCS) score of 13/15 represents an example of such a scenario, where a drop in the GCS could be related to a head injury or to

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Ischaemic limb Extradural haematoma Intra-abdominal bleeding Airway obstruction 0

Time

Figure 22.2 Estimated time from incident to death or irretrievable damage for various conditions.

Overall timeline for generic injury Death Assessment time Response time 0

Time

Figure 22.3 Diagrammatic representation of the relationship bet­ ween assessment and response times. In this example, there is time to assess and respond effectively before death.

the presence of shock and hypoxia. An injury to the brain can deteriorate with the development of an expanding haematoma, which can be diagnosed with a head CT prior to the presentation of clinical signs. Surgical decompression can be organised speedily, reducing the risk of morbidity and mortality. In this situation, if the time taken to make the diagnosis was prolonged and the clinical signs had presented prior to treatment intervention, it may be too late to prevent the death of the patient (Figure 22.4). This clinical case scenario demonstrates the principle that we need to introduce a treatment response even before we have made the definitive diagnosis if we want to save the patient’s life. It is clear, therefore, that the ‘timeline concept’ is critical in the safe management of trauma patients. Reducing the diagnosis time and response time of our interventions is dependent not only on the clinical staff but also on the availability of resources. Recently, the 24/7 availability of the trauma team and the designation of regional hospitals to operate as Level I Trauma Centres, with the availability of all disciplines and appropriate equipment on site, has provided the necessary foundation for the development of a unified trauma care system in England. Indeed, the first reports published on its effectiveness in saving lives have been very positive. The ‘timeline concept’ that has been discussed in the management of patients with multiple trauma can be applied

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Summary box 22.2 The importance of time The ‘timeline concept’ is an essential component of trauma management Assessment should be completed within a set time The time to respond is limited Both assessment and response should take place in the time window prior to irreversible damage or death

●●

●● ●● ●●

Evolving assessment for extradural haematoma (a) Fracture on imaging

Haematoma on imaging

Subtle clinical signs

The assessment of trauma

(b) Transfer

Anaesthetise

Decompress

Overall timeline for extradural haematoma

Death

(c) 0

Time

Figure 22.4 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.

to patients with isolated injuries. The key issue, irrespective of the type of patient managed, with or without multiple injuries, is to reduce unnecessary delays in making the diagnosis and initiating appropriate treatment. Such a global approach would save lives, minimise morbidity and would make the healthcare system more efficient in terms of resource utilisation, as well as cost-effectiveness. Finally, it should not be forgotten that all clinical conditions are characterised by a dynamic process. This implies that our observations and analysis of the situation can change rapidly and to an extent that interventions would have to be modified accordingly. Ongoing evaluation of the patient is therefore essential in order to identify and respond to the changes noted in a timely fashion (as previously discussed). The initial primary survey, applied according to the ATLS protocol in trauma patients, should be followed by secondary and tertiary clinical assessment, even after the acute phase of treatment has been completed successfully. Ongoing monitoring of vital organ activity, ordering of the necessary biochemical and radiological investigations and recording of all the findings in a single place can allow easier evaluation

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and identification of trends over time to facilitate prompt intervention. Such a strategy may reduce the risk of having un­diag­nosed injuries and delays in their treatment. A number of studies have been published reporting on missed injuries and making some recommendations on how to avoid this. The timeline following an injury is continuous, and the accumulated documentation may become voluminous, complex and confusing. It is helpful periodically to make the effort to stand back and summarise the situation. The UK National Institute for Health and Care Excellence (NICE), in their recent Trauma Guidelines, recognise this and advise that a plain language summary of the situation directed at the patient’s family doctor, but intelligible and available to the patient or carers, should be available within 24 hours.

ASSESSMENT AND RESPONSE

Clinically obvious

Components of response time Refer

313

The initial assessment of the trauma patient, besides the clinical examination, should include analysis of the interactions between the patient, the mechanism of injury and the extent of the injury sustained. Being able to synthesise the inter-relationships among these parameters is essential to addressing the pressures of the ‘timeline concept’ previously discussed. The associations among these three factors are usually very clear, but can be hidden. For instance, a 50-year-old male restrained passenger in a car involved in a head-on collision with another vehicle may sustain rib fractures, a sternal fracture, thoracic spine fracture and possibly cardiac contusion. Abdominal injuries could also be suspected but, overall, the clinician, knowing the mechanism, can proceed quickly in making the diagnosis and initiating treatment. However, in cases where no association can be synthesised (between the mechanism of the accident, the patient’s condition and the clinical signs observed) the reasons behind this ‘picture’ should be sought, for example the reported mechanism may have been underestimated. We will now analyse how the clinician can make best use of the information available. Summary box 22.3 The assessment of trauma ●● ●● ●●

Include the information formula: mechanism + patient = injury Look for both obvious and less obvious features Identify more reasons when the above formula does not make sense

Mechanisms Mechanisms may be blunt, penetrating or even of a combined nature (Table 22.1). Blunt trauma can be categorised as direct or indirect, and continues to be the most common mechanism. In a direct mechanism, the damage is localised to the site of injury. In contrast, in an indirect mechanism the damage occurs at a distant site after transmission of the force

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TABLE 22.1  Examples of patterns of injury. Mechanism

Obvious features

Covert injuries

Left-sided impact Lateral compression of Splenic rupture the pelvis from road traffic accident Left-sided Extradural haematoma pneumothorax Chance fracture of the lumbar spine

Duodenal rupture

Dislocated knee

Popliteal artery disruption

Head injury

Cervical spine fracture

Electrocution

Burn on hand and collapse

Posterior dislocation of the shoulder

Dashboard impact

Knee wound

Posterior dislocation of the hip

Flexion distraction (lap belt)

exerted. For example, a direct kick to the medial aspect of the mid-shaft of the tibia in a footballer by an opponent will induce an isolated tibial fracture. Such an injury represents a direct mechanism with bruising and ecchymosis at the area of the force exertion. On the other hand, a fall from a height of 1metre with a twisting moment as the foot hits the ground can lead to a spiral fracture of the distal tibia. In this situation, the vector of the force was transmitted through the body’s tissues to a location some distance away from its original point of application. In this case, other injuries should also be looked for, such as a fibular fracture or even an ipsilateral tibial plateau fracture, around the knee joint area. Similarly, a motor vehicle crash associated with direct trauma of the knee joint of the driver on the dashboard of the car could induce a fracture dislocation of the acetabulum and hip joint (transmission of force from the knee joint to the hip socket – an indirect blunt mechanism) (Figure 22.5). The ‘timeline concept’ previously discussed may or may not be urgent, depending on the location and type of injury sustained. For instance, a minimally displaced tibial fracture that a footballer has sustained can be treated satisfactorily for some time after the moment of injury but, in contrast, a fracture of the acetabulum with a hip dislocation (as described above) represents an emergency owing to the potential development of neurovascular complications (damage to sciatic nerve; avascular necrosis of the femoral head). Therefore, the clinician’s decision-making process should take into account both the peculiarities of the type of injury sustained and the anatomical location involved. Moreover, it should be appreciated that the conduction of energy in an indirect mechanism, which is transferred via the soft tissues or fluid, can be difficult both to understand and to diagnose (accurately and promptly). For example, the rise in pressure secondary to a lower abdominal force could be passed to the vascular tree (aorta), leading to unexpected haemorrhage and death. All in all, one can argue that the effects of direct mechanisms are easier to comprehend than those of indirect ones.

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Figure 22.5 The injury force in a car accident can be transmitted from the dashboard, to the knee and then to the hip, which is the site of injury.

Penetrating mechanisms can be divided into those caused by sharp objects and those induced by firearms (see Chapter 30). With regard to injuries caused by sharp objects, it is necessary to take into account the length of the sharp object, its surface area and the size of the entry point. The sharp object, for example a pair of scissors, will cause damage to the underlying tissues that it contacts (skin, subcutaneous fat, fascia, etc.). Local examination will confirm the extent of the injury and the need for wound exploration. Being familiar with the relevant anatomy of the area involved allows assessment of the peripheral nerve function, and tendon and muscle integrity. Here again the ‘timeline concept’ of prompt assessment and response (treatment) can be crucial in cases where there is vascular injury, a compartment syndrome due to internal bleeding or even joint penetration that could lead to septic arthritis. Knowledge of the anatomical structures at risk is essential to making the right decision in a timely fashion. This is particularly critical for penetrating wounds over the torso (see Chapter 27), because it is not always easy to establish the track that the sharp object has followed. In this context, it should not be forgotten that the abdominal structures extend higher than anticipated, and as high as the level of the fifth rib in expiration.

Summary box 22.4 Sharp object injuries ●● ●● ●●

Think about the length of the sharp object involved Knowledge of the local anatomy is essential Remember that abdominal structures at risk of injury extend high into the chest

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Firearms induce penetrating injuries, which are more difficult to comprehend than incisional injuries caused by sharp objects. For instance, a high velocity projectile (bullet) causes extensive damage to the tissues as it travels, inducing lateral acceleration far from the point of impact, and producing either a permanent or a temporary cavity (see Chapter 30). The importance of the temporary cavity is that it lasts only for milliseconds and usually is not evident during the clinical examination. It is important to be aware that this temporary cavity usually extends far from the boundaries of the apparent injury (Figure 22.6). Awareness of this phenomenon will ensure that the surgeon carries out sufficient exploration and wound excision.

(a)

315

Summary box 22.5 Firearm injuries ●●

●● ●●

High velocity bullets induce permanent and temporary cavitation Temporary cavitation can contain foreign material Low velocity bullets induce similar damage to knives

Patient factors All patients possess a unique profile and medical history and so will react and respond differently to a given traumatic incident. Children and adults of different ages will sustain different injuries as a result of the same mechanism. For instance, a car hitting a pedestrian will induce different injuries in an adult, compared with a child (Figure 22.7). It is important to consider the other aspects of the patient’s history. Past medical history, medication and allergy risk will direct not only the clinical assessment but also the treatment.

Obvious injuries Some injuries are very obvious and can be identified before details of the mechanism or patient are known. One can take advantage of this, as the presence of an obvious injury can inform and lead to the identification of another which is less obvious. Obvious injuries are usually visible externally. It is therefore no surprise that at the end of the ABCD protocol there is also an E, referring to exposure and the need to look for other signs of injury. Bruising to the scrotum of a motorcyclist following a collision with a car suggests a pelvic fracture. Contusion over the greater trochanter of the proximal femur in an older patient experiencing difficulty with straight leg raise points to a neck of femur fracture. Finger-shaped bruises on a child’s arms or thighs suggest NAI. The presence of a seat belt mark on the lower abdomen of a patient involved in a car crash and who has substantial abdominal pain points to damage inside the abdomen. Thus, exposure of the trauma patient should be routine practice in order to avoid missing the ‘obvious’.

(b)

(c)

Figure 22.6 A projectile passing through a gelatin block: (a) low energy transfer; (b) high energy transfer; (c) the effect of high energy transfer on tissues (courtesy of Professor J Ryan).

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Hidden factors MECHANISMS When analysis of the relationship of the formula ‘mechanism + patient = injury’ does not seem to add up, then the hidden information may be contained in the mechanism. Occasionally, it is observed that there has been a deliberate attempt to misinform. While the majority of alert and orientated patients tell the truth, others, in order to protect themselves or others, may fabricate a mechanism. This may mislead the clinician and lead them to look for the wrong pattern of injuries. For instance, a young patient with a calcaneal fracture may report that this was the result of a fall into a hole in the road, when in fact it had occurred during a burglary, following a fall from a height of 10 metres. This can delay the accurate diagnosis of the specific injury and may prevent the diagnosis of other important injuries, such as a lumbar spine fracture. Although the patient should be given the chance to tell their

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22.9 cm (9 in)

Adult

22.9 cm 19.0 cm 17.8 cm (9 in) 16.5 cm 15.2 cm (7.5 in) (7 in) (6.5 in) (6 in)

15 years

Adult

15 y

10 y

5y

3y

1y

10 years

5 years

3 years 1 year

Figure 22.7  Body proportions at various ages and anatomical location of injuries when hit by a car.

story, it should not always be believed, particularly if there are inconsistencies. A hidden mechanism can also arise when the patient is unable to give their history of events, for instance patients who are unconscious. The physically and mentally vulner­ able include older patients, perhaps with dementia, and very young children. The difficulty or inability to report the injury is compounded by the fact that it might relate to criminal activity (e.g. NAI). Parameters that should alert the clinician and raise suspicion of NAI include: ●● ●● ●● ●● ●●

external signs of injuries not consistent with the mechanism reported; long bone fractures in a preambulatory child; inconsistent or changing history; aggressive or unusual behaviour of carers at interview; posterior rib injuries.

It must be emphasised that the clinician, in addition to diagnosis and treatment, must also protect the patient from further harm. This is of paramount importance when dealing with vulnerable individuals (children and the elderly). If the early signs of abuse are ignored or not taken seriously, it may not be possible to prevent later episodes, where serious harm may occur. While NAI is a serious issue to address, mecha-

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nisms are usually in place and can be followed by passing on the problem to the appropriate team and professionals (see Chapter 39). Another important issue is the fact that any obvious injuries may provide important evidence regarding the mechanism, which may be important to a criminal investigation. We must endeavour, without compromising treatment, not to affect such evidence by our medical actions and bear in mind that forensic evidence may be needed for a conviction at a later stage. Furthermore, the importance is made more apparent if we consider that the victim of an attack may subsequently be a murder victim.

Summary box 22.6 Hidden mechanisms ●● ●● ●●

●●

The vast majority of conscious patients will tell the truth Patients involved in criminal activity may not tell the truth Fear of abuse may prevent vulnerable patients from telling the truth Clinicians have the responsibility to take action when NAI is suspected

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PATIENTS In circumstances where the injury and mechanism are inconsistent, one should consider the possibility that the patient may have an unknown pre-existing condition. For example, an apparently healthy middle-aged woman who bends to lift a box and sustains a fracture at the thoracolumbar junction of her spine may have pathological weakness of the vertebral bone, such as advanced osteoporosis. Treatment should not be confined to the local injury, but should extend to appropriate investigation and treatment of the underlying fragility of the skeleton, thus reducing the risk of further fracture. Similarly, fractures may be secondary to an undiagnosed or poorly controlled medical condition. For example, a patient presenting with a scalp laceration and a wrist fracture may have fallen as a result of a transient ischaemic attack (a hidden patient factor). In this situation, it is essential to include a medical secondary survey to identify the real cause of the injuries sustained and prevent further trauma. INJURIES When analysis of the formula ‘mechanism + patient = injury’ has failed to identify hidden injury, there are two other approaches: 1 the look everywhere approach; 2 the focused exclusion approach. Look everywhere approach. This represents the secondary and tertiary elements of the ATLS system and involves a detailed secondary survey, from top to bottom and at different time points: soon after the initial treatment phase when measures relating to saving the patient’s life have been completed, the day after injury, e.g. during a ward round, or several days after injury, e.g. when the patient first wakes up in the intensive care environment. The implementation of whole body CT (WBCT) (scanning the whole body) in all major trauma centres has allowed the clinical team to pick up injuries early. Such injuries would have been missed in the past when reliance was made on the initial radiographs of the chest, pelvis and cervical spine. The threshold for using more WBCT has been lowered substantially. There is no doubt that WBCT scan algorithms have been shown to accelerate diagnostic work-up, but their effect on survival is controversial. Moreover, concerns have been voiced about the overexposure of patients to radiation with the increasing and often uncritical use of this type of scan. The effective radiation dose to all organs from a single full-body CT is 12–16 millisieverts (mSv). Survivors of the atomic bomb whose radiation dose ranged 5–100 mSv had a statistically significant increase in the risk of solid cancers. Overall, the risks associated with one scan are relatively modest, approximately 1 in 1250, or 0.08%. However, it has been reported that widespread liberal CT use is responsible for 1.5–2.0% of all cancers in the USA. Of interest, WBCT equates to 76 chest x-rays or 6 months of background radiation. It has been suggested that it should be requested wisely and that developing a triaging protocol can minimise the critisim of its overuse.

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317

Focused exclusion approach. This is based on the knowledge that some specific injuries are missed on a remarkably regular basis. Such injury patterns include metatarsal and metacarpal fractures, scaphoid fractures, perilunate dislocations and posterior shoulder dislocations. When such injuries are suspected, a detailed focused history, clinical examination and appropriate investigations should be carried out to either confirm or exclude them.

Summary box 22.7 Trauma assessment ●● ●● ●●

Knowledge of timelines for important diagnoses is essential Initial assessment should focus on what kills first Screen high-risk patients before clinical signs become apparent, as it may be too late to intervene once signs develop

THE RESPONSE TO TRAUMA Completion of the initial assessment according to the formula (patient + mechanism = injury) should provide the necessary information to formulate and execute a ‘response’ (treatment). During this stage of care, the response to injury will continue to evolve and decompensation may occur unexpectedly. Vigilance is required throughout management to identify the potential exhaustion of reserve mechanisms.

The patient’s response to injury From the time of the accident, a cascade of physiological responses will be upregulated to maintain survival. All such responses are part of homeostatic mechanisms that alter with the time elapsed following injury. The timing and nature of interventions should be altered accordingly. Important patient responses that require prompt attention, in order to avoid a subsequent negative impact on the patient’s haemodynamic condition, include the body temperature, oxygenation and organ perfusion. A decline in body temperature is a frequent finding after injury and may be due to exposure, blood loss and inactivity. Measures should be taken not only to prevent further reduction in temperature but also to restore it. Covering the patient with appropriate blankets during transportation, resuscitation and in the theatre environment will minimise the risk of hypothermia, coagulation disturbances and ongoing bleeding. Patient oxygenation can be optimised with the administration of inspired oxygen or ventilation if needed. Blood loss can give rise to an altered level of consciousness, low blood pressure, reduced perfusion of the extremities (skin discolouration) and tachycardia. By way of response, endogenous clotting factors are activated to stop the bleeding and to maintain adequate circulatory volume. A further consideration is that traumatised lung parenchyma cannot tolerate surplus fluid. Therefore, the latest resuscitation guidelines advocate a reduction in crystalloid administration and the

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early transfusion of blood products. Furthermore, there is a need to quickly identify and stop the source of bleeding. Another important part of the response to injury is the activation of the immune–inflammatory system. Acute phase mediators are released systemically, stimulating cellular elements (polymorphonuclear leukocytes) to interact with the endothelium. Under certain circumstances, extravasation of leukocytes may take place, with possible autodestruction. Clinical decisions should aim to minimise the risk of an exaggerated immune–inflammatory reaction. Surgical procedures, which can act as a second hit, where injury is considered the first hit, should be carefully timed and selected.

The medical response to injury Initial management Where resources are available, a patient found to have sustained serious injuries at the scene of the accident will lead the paramedics to activate ‘the trauma team on call’, allowing personnel to await the patient’s arrival in the resuscitation room. The team leader, according to the ATLS protocol, will assign trained nurses and doctors to specific tasks. Protective clothing, such as gloves and lead aprons, is required to protect the personnel from fluids and radiation exposure. Following the ATLS protocol should be a routine process, involving experienced team members and ideally avoiding careless delays, which may compromise the response time. Potential problems can be predicted. The involvement of different disciplines in assessing and planning treatment of injuries in different body areas may lead to issues around priority, which can lead to confusion and uncertainty: ‘Who should go first?’ ‘What investigation should be next?’ It is the role of the team leader to ensure that this is avoided and that decisions which may be critical for the patient’s wellbeing are executed smoothly. In situations where the system operates according to locally developed protocols, someone should have the responsibility of overruling the protocol if this would be to the best interest of the patient, in order to keep the process rolling. Following common pathways to manage patients can save time and reduce errors. The management of hip fractures in older age groups has improved in the UK with the regulated and monitored involvement of surgeons, geriatricians and anaesthetists. However, early labelling can also be misleading and troublesome. For instance, an older female patient with multiple medical problems might, after falling down a step, sustain an ankle fracture and be given the label ‘ankle fracture’. Once the label is given the ‘pathway’ is set and she may be placed in a plaster of Paris back slab and be admitted for fixation under the care of someone who thinks primarily about mechanical matters. The so-called ‘accidental benign falls’ may be associated with more severe pathology and injuries. Furthermore, a patient may fall as a result of a medical condition (e.g. a mini stroke) and, in addition to an ankle fracture, may sustain other injuries including fractures of the pubic ramus and ribs. The wrong label may disguise the seriousness of the injuries sustained and the fact that the patient’s condition may rapidly deteriorate, putting their life at risk.

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The first person in the diagnostic chain has disproportionate responsibility. Early labelling after inappropriate assessment can be incorrect and direct the patient to the wrong care pathway. In general terms, all patients, and particularly vulnerable patients, should undergo physiological triage to reduce the risk of being wrongly assigned.

Beyond the first hour Following the initial assessment and management according to the ATLS protocol, and when the end points of resuscitation have been accomplished, further interventions are necessary in a patient with multiple injuries. The presence of an open book pelvic fracture, a lumbar spine fracture, a femoral fracture, a liver laceration and a tarsometatarsal dislocation are examples of outstanding injuries waiting treatment. The timing of the initiation of fixation, the type of fixation to use and the priority of various injuries have been points of discussion for some years. The original work by Bone et al. in the 1980s, demonstrating the benefits of early fracture fixation of all injuries, led to the acceptance and wide application of the so called ‘early total care’ (ETC) philosophy. This practice became the gold standard of treatment for patients with multiple injuries. However, in some specific patient groups, for example those with severe chest and/or head injuries or those in an extreme physiological state (with ongoing bleeding from different sources such as abdomen, pelvis and chest), it was observed that the ETC concept led to early complications and mortality. Knowledge acquired at the molecular level related to the immune–inflammatory response to injury and the concepts of the phenomena of the first hit (the impact exerted on the homeostatic mechanisms as a result of the original trauma sustained) and the second hit (the additional physiological stress induced by surgical procedures) led to the acceptance and implementation of the so call ‘damage control orthopaedics’ (DCO) philosophy, which is called damage control surgery (DCS) in more generalised settings (see later chapters). The stages of DCO are: ●● ●● ●● ●● ●●

resuscitation; haemorrhage control; decompression; decontamination; fracture splintage.

In the DCO concept, initially any long bone fractures and the pelvis are temporarily stabilised with the use of external fixators. Definitive stabilisation of the fractures (conversion of the external fixators to intramedullary (IM) nailing for the femur and plating of the pelvis) would take place usually 4 days later, when the physiological state of the patient has been stabilised. In contrast, a patient with similar injuries who has stable physiology throughout would be managed with IM nailing of the femoral fracture and plating of the pelvis within the first 24–36 hours: the ETC approach. The two strategies of fracture fixation, the ETC and DCS, are currently practised on the basis of some specific criteria. The vast majority of poly­trauma patients are suitable for ETC (80–90%). Specific criteria are shown in Table 22.2.

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TABLE 22.2  Criteria for damage control surgery (DCS) and early total care (ETC). Criteria for DCS

Criteria for ETC

Hypothermia: 90 mmHg should be the target if a head injury is suspected. Small boluses of IV fluids (e.g. 250mL of O negative blood, or normal saline if blood is not immediately available) should be administered to achieve this target, which should result in a palpable radial pulse. Excessive intravenous crystalloid or colloid solutions should be avoided because they cause haemodilution, increase coagulopathy and increase the risk of adult respiratory distress syndrome (ARDS). However, the key to this approach of permissive hypotension is that it is time limited. The primary source of haemorrhage must be identified and controlled as soon as possible. Severely injured hypovolaemic patients should be resuscitated with blood and blood products, not crystalloid/colloid fluids. These must be warmed. All hospitals managing severe trauma should have a massive transfusion protocol which aims to provide blood and blood products in a ratio of 1 packed red cells:1 fresh frozen plasma:1 platelets. TRANEXAMIC ACID Tranexamic acid is an antifibrinolytic drug that reduces the risk of mortality from bleeding in both blunt and penetrating trauma. One gram is given intravenously over 10 minutes, followed by a further 1g dose over 8hours. Tranexamic acid should be given to all trauma patients suspected to have significant haemorrhage, including those with a systolic blood pressure of 30mL per hour. The patient should not have hypothermia (temperature 5 mmol/L – DCS (see Chapters 22 and 27)

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Traumatic brain injury Learning objectives To understand: •• The physiology of cerebral blood flow and the pathophysiology of raised intracranial pressure •• The classification and assessment of head injury

INTRODUCTION Head injury accounts for 3–4% of emergency department attendances, with around 1500 cases per 100000 population per year in the UK. Annual mortality attributable to head injury is estimated at 9 per 100000, and it remains the leading cause of death and disability from childhood to early middle age, with an estimated 2% of the US population suffering long-term disability as a result of head injury. Road traffic accidents are the leading cause of head injury, being responsible for up to 50% of cases. Other common mechanisms of injury include falls and assault. There is significant geographical variation, for example firearms are the third leading cause in the US. Significant traumatic brain injury can be considered a combination of the primary injury sustained on impact, and secondary injury developing in the following hours and days. Understanding the importance of intracranial pressure and related parameters is key to minimising secondary injury and improving outcomes.

INTRACRANIAL PRESSURE Intracranial pressure and cerebral blood flow The brain depends on continuous perfusion for oxygen and glucose delivery, and hence survival. Normal cerebral blood flow (CBF) is about 55 mL per minute for every 100 grams of brain tissue. Ischaemia results when this rate drops below 20mL per minute, and even lower levels will result in infarction unless promptly corrected. Flow depends on cerebral perfusion pressure (CPP), the difference between mean arterial pressure (MAP) and intracranial pressure (ICP).

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•• Management and sequelae of minor and mild traumatic brain injury

•• Medical and surgical management of moderate and severe traumatic brain injury

Summary box 24.1 Intracranial pressure (ICP) ●●

●●

A continuous supply of oxygenated blood is essential for brain survival Raised ICP can compromise cerebral perfusion, resulting in a cycle of secondary brain injury and swelling

CPP (75–105mmHg) = MAP (90–110mmHg) – ICP (5–15 mmHg) Typical normal values are given in parentheses. In fact, in the normal brain, variations in vascular tone maintain a constant CBF across a range of MAP between 50 and 150mmHg (or higher in the setting of chronic hypertension), and a corresponding range of CPP, the process of cerebral auto­ regulation.

The Monro Kellie doctrine and herniation syndromes Alexander Monro observed in 1783 that the cranium is a ‘rigid box’ containing a ‘nearly incompressible brain’. Any expansion in the contents, especially haematoma and brain swelling, may be initially accommodated by exclusion of fluid components, venous blood and cerebrospinal fluid (CSF). Further expansion is associated with an exponential rise in ICP (Figure 24.1) Uncontrolled increases in ICP result in cerebral herniation (Figure 24.2). Typically, herniation of the uncus of the temporal lobe over the tentorium results in pupil abnormalities (see Pupils below), usually occurring first on the side of any expanding haematoma. Cerebellar tonsillar herniation through the foramen magnum compresses medullary vasomotor and respiratory centres, classically producing Cushing’s

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Normal Venous blood

Arterial blood

Brain

CSF

Skull

1

Mass lesion – compensation phase Venous Arterial blood blood

2 Brain

Mass

CSF

Skull

4

3

Venous blood

Mass lesion – brain herniation Arterial blood

Brain

(a)

Mass

Skull

90 Intracranial pressure (mmHg)

5

CSF

80 Brain herniation

70 60

Figure 24.2  Brain herniation. Herniation of the cingulate gyrus under the falx cerebri is termed subfalcine herniation (1). (2) Midline shift is evident. (3) Uncal herniation: the temporal lobe is herniating over the tentorium cerebelli where it can compress the third nerve. (4) Central herniation and (5) tonsillar herniation result in brainstem compromise, manifesting as Cushing’s triad.

50 40

Compensation

30

Point of decompensation

20 10 0

10 20 30 40 50 60 70 80 90 100 110 120

(b)

Mass lesion size (arbitrary units)

Figure 24.1  The Monro Kellie doctrine accounts for the ability of the intracranial compartment to accommodate expanding mass lesions, primarily by excluding venous blood and cerebrospinal fluid (CSF), and the rapid rise in pressure associated with exhaustion of this compensation.

triad – hypertension, bradycardia and irregular respiration. The patient is then said to be ‘coning’, and brainstem death will result without immediate intervention.

CLASSIFICATION OF HEAD INJURY Severity of head injury is classified according to the postresuscitation Glasgow Coma Scale (GCS) (Table 24.1), as it is the GCS score, and in particular the motor score (see Table 24.4), that is the best predictor of neurological outcome. In broad terms, significantly obtunded patients have moderate injuries and comatose patients have severe injuries; alcohol and drug effects often complicate the classification.

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TABLE 24.1  Head injury classification using the Glasgow Coma Scale (GCS) score. Minor head injury

GCS 15 with no loss of consciousness (LOC)

Mild head injury

GCS 14 or 15 with LOC

Moderate head injury

GCS 9–13

Severe head injury

GCS 3–8

MINOR AND MILD HEAD INJURY After exclusion of associated cervical spine injury, the major concern for these patients is to avoid discharge during the ‘lucid interval’ that may precede delayed deterioration due to an expanding intracranial haematoma. In general, patients with isolated head injuries and without ongoing deficits can safely be discharged from the emergency department, provided they meet suitable criteria, for instance those provided by the UK National Institute for Heath and Care Excellence (Table 24.2). Summary box 24.2 Minor and mild head injury ●●

●●

●●

Decisions on imaging and discharge are best made guided by published criteria In preverbal children and other vulnerable groups, nonaccidental injury must be considered Amnesia, confusion, headaches and somnolence are typical features of concussion

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TABLE 24.2  National Institute for Health and Care Excellence discharge criteria in minor and mild head injury. ●● ●● ●● ●● ●●

GCS 15/15 with no focal deficits Normal CT brain if indicated (see below) Patient not under the influence of alcohol or drugs Patient accompanied by a responsible adult Verbal and written head injury advice: seek medical attention if: ●● Persistent/worsening headache despite analgesia ●● Persistent vomiting ●● Drowsiness ●● Visual disturbance ●● Limb weakness or numbness

CT, computed tomography; GCS, Glasgow Coma Scale.

TABLE 24.3  National Institute for Health and Care Excellence guidelines for computed tomography (CT) in head injury. Indications for CT imaging within 1 hour GCS 30 minutes

Patients who do not meet all the discharge criteria will need admission for a further period of observation, and/or brain imaging. Early computed tomography (CT) imaging is desirable in patients with a persistent reduced conscious level, focal deficits, suspected fractures or risk factors for intracranial bleed (Table 24.3). Significant clinical or radiological abnormalities should be discussed with the neurosurgical service. Many of these patients will struggle with features of concussion for a period after their injury, with headaches and somnolence typical. Follow-up by a head injury specialist nurse or equivalent is therefore desirable.

head injury without imaging abnormalities; loss of consciousness (LOC) at the time of injury is not a prerequisite. Key features include confusion and amnesia. The patient may be lethargic, 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 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. 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 TRAUMATIC BRAIN INJURY Resuscitation and evaluation Resuscitation is performed according to Advanced Trauma and Life Support (ATLS) guidelines, beginning with management of the airway and cervical spine control, and proceeding to assess and manage breathing and circulation. History obtained in parallel is key to shaping ongoing management.

History Mechanism In moderate and severe traumatic brain injury (TBI), history must be obtained from witnesses and paramedics. Highenergy mechanisms of injury, including fall from a height or high-speed road traffic accident (RTA), will require careful clinical and radiological exclusion of associated multi­system

Non-accidental injury Head injury in children and vulnerable adults may be due to abuse. Significant findings include delayed presentation, injuries of disparate age, retinal haemorrhages, bilateral chronic subdural haematomas, multiple skull fractures and neurological injury without external signs of trauma.

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

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Summary box 24.3 History Bystanders and paramedics may give vital information on the: preinjury state (fits, alcohol, chest pain) mechanism and energy involved in the injury (speed of vehicles, height fallen) ●● conscious state and haemodynamic stability of the patient after the accident ●● length of time taken for extrication Check the medication history especially anticoagulants and antiplatelet agents ●● ●●

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and spinal injury (see Chapter 25). In the case of RTAs in particular, extraction time and evidence of hypoxia or haemodynamic instability at the scene is important information to obtain from the paramedics. Falls and crashes are often caused by a primary medical problem such as myocardial infarction, hypoglycaemia or subarachnoid haemorrhage, with implications for management.

Neurological progression A specific check should be made for any loss of consciousness at the time of injury, and its duration. The GCS and pupil responses at the scene and on arrival in the emergency department should be obtained and documented. They should also be checked regularly thereafter; deterioration in GCS is an important index of developing, and potentially reversible, secondary injury. It is also useful to assess the extent of amnesia, retrograde (events prior to the injury) and anterograde (events afterwards). If the patient was intubated at the scene of the accident it is valuable to know whether the patient was moving all four limbs before this.

Past medical history Details of the patient’s medical background should be obtained, including allergies and normal medications. Of particular note here, are antiplatelet agents, potentially requiring platelet transfusion especially if surgery is required, and anticoagulants, which may need reversal.

Examination: primary survey ATLS guidelines address a fundamental priority, ensuring uninterrupted perfusion of the brain with oxygenated blood. This is especially important after a head injury given the disturbance to intracranial autoregulation and the sensitivity of the primary injured brain tissue to further insult. Bleeding from scalp lacerations may require management as part of the primary survey, as the blood loss can be substantial and ongoing. Check the responsiveness of the pupils, conscious level and for any gross focal neurological deficits. Blood glucose level should also be measured as early as possible as hypoglycaemia is very dangerous and easily reversible.

Pupils The pupil size should be recorded in millimetres, and reactivity documented as present, sluggish or absent. Uncal herniation (Figure 24.2) can compress the third nerve, compromising the parasympathetic supply to the pupil. Unopposed sympathetic activity produces a sluggish enlarged pupil, progressing to fixed and dilated under continued compression. Established pupil changes may reflect pathology anywhere in the eye or the reflex loop made up by the optic nerve, the oculomotor nerve and the brainstem. Direct ocular trauma or nerve injury in association with a skull base fracture can cause mydriasis (dilated pupil) present from the time of injury. Pre-existing discrepancy in pupil size (anisocoria), as a result of Holmes–Adie pupil or cataracts for example, may also complicate assessment.

Glasgow Coma Scale score The GCS is the sum of scores on three components as detailed in Table 24.4. The breakdown of the GCS into eye opening, verbal and motor components should always be recorded and used when communicating the status to other doctors. Remember that the score represents the best performance elicited, so a patient flexing in response to a painful stimulus on the left and localising on the right scores ‘M5’. A sternal or supraorbital rub, or trapezius squeeze represents an appropriate painful stimulus.

Neurological deficit Gross focal neurological deficits, such as paraplegia, may be evident at the primary survey, and an assessment to exclude such deficit should be carried out, especially if the patient is to

TABLE 24.4  Glasgow Coma Scale score for head injury. Eyes open

Verbal

Summary box 24.4 Primary survey ●● ●● ●●

●●

Ensure adequate oxygenation and circulation Exclude hypoglycaemia Check pupil size and response and Glasgow Coma Scale score as soon as possible Check for focal neurological deficits before intubation, if possible

331

Motor

Spontaneously

4

To verbal command

3

To painful stimulus

2

Do not open

1

Normal oriented conversation

5

Confused

4

Inappropriate/words only

3

Sounds only

2

No sounds

1

Intubated patient

T

Obeys commands

6

Localises to pain

5

Withdrawal/flexion

4

Abnormal flexion

3

Extension

2

No motor response

1

Sir Gordon Morgon Holmes, 1876–1965, physician, The National Hospital for Nervous Diseases, Queen’s Square, London, UK. William John Adie, 1886–1935, physician, The National Hospital for Nervous Diseases, Queen’s Square, London, UK.

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be intubated so that subsequent examination will be impossible. Detailed neurological examination is included in the secondary survey.

Examination: secondary survey A full secondary survey will be required. Particular attention must be paid to head, neck and spine.

Head Examination of the head should include inspection and palpation of the scalp for evidence of subgaleal haematoma and scalp lacerations, which may bleed profusely, and potentially overlie fractures. Examine the face for evidence of fractures, especially to the orbital rim, zygoma and maxilla. Clinical evidence of a skull base fracture may include Battle’s sign (Figure 24.3), and ‘racoon’ or ‘panda’ eyes (bilateral periorbital bruising). Haemotympanum, or overt bleeding from the ear if the tympanic membrane has ruptured, and CSF rhinnorrhoea or otorrhoea are also highly suggestive of a fracture of the base of the skull. A complete examination of the cranial nerves will reveal, for example, facial or vestibulo-cochlear nerve damage associated with skull base fracture. Midbrain or brainstem dysfunction may produce gaze paresis (inability of eye to look across beyond the midline), dysconjugate gaze (inability of the eyes to work together) or roving eye movements. Inspect the conjunctiva and cornea of the eyes, and the retina using an

ophthalmoscope, looking for hyphaema (blood in the anterior chamber of the eye), papilloedema or retinal detachment. Blood in the mouth may be due to tongue-biting at seizure. The GCS and pupil status, assessed as part of the primary survey, require re-evaluation at the secondary survey and regularly thereafter.

Neck and spine Studies have demonstrated an incidence of cervical fracture of up to 10% in association with moderate and severe TBI. Cervical spine injury must be presumed in the context of head injury until actively excluded. In a high-energy mechanism such as RTA or fall from a height, thoracic and lumbar spine injuries must also be excluded. Plain radiographs can be of limited value in excluding significant cervical spine injury. Even CT imaging does not exclude the possibility of significant ligamentous injury. Therefore, whenever feasible, these patients should be managed in a hard collar until the neck can be cleared clinically. A peripheral nerve examination with documentation of limb tone, power, reflexes and sensation needs to be performed early to identify spinal pathology. This is especially important in patients who may subsequently be intubated and ventilated, when this assessment will no longer be possible. Obtunded patients should move all four limbs in response to an appropriate painful stimulus. The patient will need to be log-rolled to palpate for thor­ acic or lumbar deformity, and any cervical collar should be removed at this stage to allow palpation of the cervical spine, before it is replaced. If there is associated spinal injury, a thor­ acic sensory level is much more easily established by sensory examination on the back. A per rectal examination is also performed at log-roll, assessing for anal tone, sensation in the awake patient and anal wink (sphincter seen to contract in response to a pinprick stimulus). Priapism is a strong predictor of severe cord injury even in intubated patients. Summary box 24.5 Secondary survey ●●

●●

●●

Battle’s sign, periorbital bruising and blood in ears/nose/ mouth may point to base of skull fracture Cervical spine fractures are common and must be actively excluded Log-roll to check whole spine for steps and tenderness, and for per rectum exam

Surgical management Fractures: skull vault Figure 24.3  Battle’s sign. A skull base fracture may be associated with bruising over the mastoid process.

Closed linear fractures of the skull vault are managed conservatively. Open or comminuted fractures should be considered for debridement and prophylactic antibiotic therapy.

William Henry Battle, 1855–1936, surgeon, St Thomas’s Hospital, London, UK. A racoonis a small mammal native to North and Central America that has a pale face with dark rings round its eyes.

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(a)

(b)

Figure 24.4 A right frontal comminuted depressed skull fracture, with a linear undisplaced fracture of the right parietal bone visible posteriorly.

Depressed skull fractures involve inward displacement of a bone fragment by at least the thickness of the skull (Figures 24.4 and 24.5). They occur when small objects hit the skull at high velocity. They are usually compound (open) fractures, and are associated with a high incidence of infection, neurological deficit and late-onset epilepsy. These fractures require exploration and elevation, especially where intracranial air is present pointing to a breach in the dura mater. Fractures that involve the air sinuses should generally be managed as open fractures, using broad spectrum antibiotics with or without exploration.

(c)

Fractures: skull base Clinical signs of skull base fracture include bleeding or CSF leak from the ears (otorrhoea) or nose (rhinnorrhea), and bruising behind the ear (Figure 24.3) or around the eyes. Skull base fractures may be complicated by pituitary dysfunction, arterial dissection or cranial nerve deficits, with anosmia, facial palsy or hearing loss typical. CSF leak will generally resolve spontaneously but persistent leak can result in meningitis so repair may be required. Blind nasogastric tube placement is contraindicated in these patients.

Extradural haematoma Extradural haematoma (Figure 24.6) is a neurosurgical emergency. It results from rupture of an artery, vein or venous sinus, in association with a skull fracture. The classical injury is a fracture to the thin squamous temporal bone, with associated damage to the middle meningeal artery. Transient loss of consciousness is typical, and the patient may then present in the subsequent lucid interval with headache but without any neurological deficit. As the haematoma expands, compensation is exhausted (see Monro Kellie doctrine above), with rapid deterioration. There is contralateral hemiparesis,

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Figure 24.5  A small depressed skull fracture of the parietal bone visible on axial bone windows (a), visualised on bone vault reconstructions (b) and with an underlying breach of dura (c).

Summary box 24.6 Extradural haemorrhage ●●

●● ●● ●●

Can follow relatively minor trauma with brief loss of consciousness Followed by a lucid interval and then sudden deterioration Lentiform lesion on computed tomography Require immediate transfer to a neurosurgical unit for decision on evacuation

reduced conscious level and ipsilateral pupillary dilatation, the cardinal signs of brain compression and herniation. Although this classical presentation occurs in only onethird of cases, it emphasises the potential for rapid avoidable

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(a)

and brain, constrained by the adherence of the dura to the skull. Mass effect may be evident, with compression of surrounding brain and midline shift. Areas of mixed density suggest active bleeding. A skull fracture will usually be evident. Extradural haematoma mandates urgent transfer to the most accessible neurosurgical facility, for immediate evacuation in deteriorating or comatose patients or those with large bleeds, and for close observation with serial imaging in other cases. The prognosis for promptly evacuated extradural haematoma, without associated primary brain injury, is excellent.

Acute subdural haematoma Acute subdural haematoma (Figure 24.7a) is encountered in two broadly distinct contexts. Firstly, high-energy injury mechanisms can result in the rupture of cortical surface vessels with significant associated primary brain injury. This results in expanding haematoma with rapid deterioration and (b)

(a)

(c) (b)

Figure 24.6  (a) A large left extradural haematoma (note the biconvex shape) exerts mass effect; a smaller right acute subdural haematoma is also evident. (b) Right frontal intracerebral haematoma extending into the lateral ventricle is evident. There is a small right posterior extradural haematoma and traumatic subarachnoid bleeding in the sulci of the right hemisphere. (c) A surgical temporal bone exposure showing a linear skull fracture with underlying extradural haematoma visible through a burr hole.

secondary brain injury in patients with minimal primary injury. On CT, extradural haematomas appear as a lentiform (lens-shaped or biconvex) hyperdense lesion between skull

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Figure 24.7  (a) Right-sided acute subdural haematoma (hyperdense). The substantial midline shift reflects brain swelling as well as bleeding; this is a high-energy injury. (b) Bilateral chronic subdural haematomas: the left is mixed density, the hypodense material representing old blood and the higher density indicating more recent bleeding, probably loculated so requiring a craniotomy to evacuate. The bleed on the right is isodense, indicating intermediate age.

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developing signs of raised ICP, reminiscent of extradural haematoma without the lucid interval. These collections require prompt evacuation, typically by craniotomy or craniectomy. In a second group of patients, older and often anticoagulated, a lower-energy injury leads to venous bleeding around the brain. Depending on the total volume of bleeding, the resulting haematoma may present early as acute subdural haematoma, after delay and osmotic expansion as chronic subdural haematoma or may even remain clinically silent. This latter group may present much later with a further ‘acute-onchronic’ subdural haematoma. On diagnosis, clotting function should be corrected wherever possible. Bleeds of significant size, with significant associated midline shift or with deteriorating neurology, require urgent evacuation. Smaller bleeds in neurologically stable patients may be managed conservatively, at least initially: liquefaction of the clot over 7–10 days after the bleed may allow for a much less invasive evacuation through burr holes. Summary box 24.7 Acute subdural haemorrhage ●● ●●

High-energy injury, or elderly/anticoagulated Generally requires urgent evacuation by craniotomy/ craniectomy

Since the dura is not adherent to the brain as it is to the skull, subdural blood is free to expand across the brain surface giving a diffuse concave appearance.

Chronic subdural haematoma Chronic subdural haematoma (Figure 24.7b) is a common cause of acute neurological deterioration in the elderly. Cerebral atrophy in this age group results in stretching of cortical– dural bridging veins, which are then vulnerable to rupture. The resulting haematoma can expand over days or weeks by osmosis, ultimately producing symptoms of raised ICP or focal deficits. There is usually a history of recent injury, but especially in the context of antiplatelet or anticoagulant medication even apparently trivial impacts may be responsible.

335

or hyperdense, and mixed density can indicate an acute-onchronic subdural haematoma. Anticoagulation should be reversed, either by administration of vitamin K, or urgently by transfusion of recombinant clotting factors in patients who have deteriorated acutely. Conservative management, sometimes with administration of corticosteroids, can be considered for small bleeds without symptoms or with headache alone. For the majority, drainage is performed using burr holes. Urgency is dictated by the clinical condition of the patient and imaging evidence of mass effect. If clinically stable, a delay of 7–10 days may be considered to allow platelet function to normalise after withdrawal of aspirin/clopidogrel.

Traumatic subarachnoid haemorrhage Trauma is the commonest cause of subarachnoid haemorrhage (Figures 24.6b, 24.8), and this is managed conservatively. It is not usually associated with significant vasospasm, which characterises aneurysmal subarachnoid haemorrhage (see later). The possibility of spontaneous subarachnoid haemorrhage leading to collapse and so causing a head injury needs to be borne in mind, and formal or CT angiography may be required to exclude this. Summary box 24.9 Specific head injuries ●●

●● ●●

●●

Traumatic vs. primary subarachnoid haemorrhage is an important distinction Cerebral contusions arise adjacent to rough bone surfaces Diffuse axonal injury results from extreme accelerations of the skull contents Arterial dissection is associated with fractures of the skull base

Summary box 24.8 Chronic subdural haemorrhage ●● ●●

●● ●●

Common in the elderly especially those on anticoagulants Clinical deficits result from osmotic expansion of a degrading clot over days/weeks Diffuse hypodense lesion on computed tomography Burr hole drainage is usually preferred.

On presentation, it is important to exclude coexisting electrolyte disturbance and infections, which may contribute to clinical impairment. Imaging reveals diffuse hypodensity overlying the brain surface. Recent bleeding may be isodense

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Figure 24.8 A large right extradural haematoma is evident. There are widespread cerebral contusions most prominent in the left frontal lobe. There is traumatic subarachnoid blood in the third and lateral ventricles.

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Cerebral contusions Contusions are common and are found predominantly where brain is in contact with the irregularly ridged inside of the skull, i.e. at the inferior frontal lobes and temporal poles. ‘Coup contre-coup’ contusions are brain injury at the site of impact and where the brain is struck by the inside of the skull on the far side, as the skull and brain accelerate and then decelerate out of synchrony with each other. Contusions appear heterogenous on CT, reflecting their composition of injured brain matter interspersed with acute blood (Figure 24.8). Contusions rarely require surgical intervention, but may warrant delayed evacuation to reduce mass effect.

Diffuse axonal injury This is a form of primary brain injury, seen in high-energy accidents, and which usually renders the patient comatose. It is strictly a pathological diagnosis made at postmortem, but haemorrhagic foci in the corpus callosum and dorsolateral rostral brainstem on CT may be suggestive, although the CT often appears normal.

Arterial dissection Cerebral arterial dissection occurs spontaneously or in the context of trauma. In the hours after significant trauma, dissection of the carotid extracranially, or at the skull base in association with fractures, is most common. It presents with headache, neck pain and focal ischaemic deficits, due to occlusion by mural haematoma, thrombus and thromboembolism. Intracranial dissection often affects the vertebral artery and may result in subarachnoid bleeding.

Medical management From initial resuscitation, through surgical intervention and into the subsequent phase of intensive care management, medical management strategies aim to minimise secondary brain injury, through avoidance of hypoxia and hypotension and control of ICP. Unchecked, secondary injury leads to a further cycle of deterioration (Figures 24.2 and 24.9).

Summary box 24.10 Medical management of head injury ●●

●●

●●

●●

First-line ICP control involves optimising sedation, ventilation and serum sodium levels Paralysis and external ventricular CSF drainage are important adjuncts There is little evidence for benefit with therapeutic hypothermia, barbiturate coma or decompressive craniectomy Check pituitary function, consider seizure prophylaxis, commence enteral nutrition within 72 hours

The role of neurosurgical centres Early discussion of patients and imaging with the regional neurosurgical service is advisable. UK trauma audit and research network data show higher mortality in patients with

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Raised intracranial pressure Deranged autoregulation

Necrosis Inflammation Hypotension

Reduced cerebral perfusion

Secondary brain injury Hypoxia

Increased metabolic requirements – seizure, pyrexia, inflammation

Figure 24.9  Brain swelling and mass lesions contribute to a raised intracranial pressure, which compromises perfusion, leading to secondary brain injury and further swelling.

severe TBI managed in non-neurosurgical centres, and this is reflected in NICE guidelines, which recommend early transfer irrespective of the need for surgery.

Control of intracranial pressure Intubation and ventilation is required early in the management of severe brain injury for airway control. It is often required in moderate brain injury to facilitate the safe management and transfer of unstable and frequently agitated patients and in order to control ICP. UK trauma audit and research network data indicate that severe TBI survival is better in a neurosurgical centre, irrespective of the need for surgery. Where there is evidence of raised ICP, for example pupil changes, a bolus of mannitol may be administered to control pressure temporarily while scanning and transferring the patient. Management of the intubated patient, following evacuation of any focal haematomas, is guided by ICP monitoring using a bolt ICP monitor, or else an external ventricular drain inserted into the lateral ventricle, which can also contribute to ICP control by permitting CSF drainage. A sustained rise of ICP over 20–25 mmHg above normal is associated with a poor outcome, and maintenance of a cerebral perfusion pressure of at least 60 mmHg is important in preventing secondary injury. ICP can be controlled by simple measures including raising the head of the bed and loosening the collar to improve venous drainage. Seizures and pyrexia should be actively controlled. Medical management titrated to ICP includes escalating doses of sedatives, analgesics and ultimately muscle relaxants. Target ventilatory and circulatory parameters are set out in Table 24.5. Where these measures fail, neurointensivists may seek to control brain swelling using mannitol or hypertonic saline infusions. Where autoregulation is preserved, inducing high cerebral perfusion pressure may reduce ICP through vasoconstriction. A range of further interventions are effective in controlling ICP, but evidence for long-term outcome benefit is limited or absent. These include induction of therapeutic hypothermia or thiopentone coma and surgical decompressive craniectomy.

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TABLE 24.5  Key parameters to maintain in head-injured patients in neurointensive care. pCO2 = 4.5–5.0 kPa pO2>11 kPa

severity, especially the presence of intracerebral haemorrhage, and depressed skull fractures and tears of the dura. Antiepileptics, typically phenytoin, are administered prophylactically to patients at high risk of seizures.

MAP = 80–90 mmHg

Nutrition

ICP 60 mmHg [Na+] >140 mmol/L [K+] >4 mmol/L

Pituitary dysfunction 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 a water retention 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, ADH secretion may be compromised in the context of trauma, producing diabetes insipidus resulting in hypernatraemia. 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% (mild TBI) and 60% (severe TBI with exacerbating features). Risk factors include injury

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337

Outcomes and sequelae The long-term sequelae of moderate and severe traumatic brain injury include headache, memory and cognitive impairments, contributing to the postconcussive syndrome described above. Rehabilitation represents a complex and prolonged multidisciplinary challenge. 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 24.6. Good recovery implies independence and potential to return to work rather than a full return to previous capacity. TABLE 24.6  Glasgow outcome score (GOS). Good recovery

5

Moderate disability

4

Severe disability

3

Persistent vegetative state

2

Dead

1

FURTHER READING Greenberg MS. Handbook of neurosurgery, 8th edn. Stuttgart: Thieme Medical Publishers, 2016. Samandouras G (ed). The neurosurgeon’s handbook. Oxford: Oxford University Press, 2010.

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Bailey & Love Bailey & Love Bailey & Love Bailey &25 Love Bailey & Love Bailey & Love Chapter

Neck and spine Learning objectives To be familiar with: •• The accurate assessment of spinal trauma •• The basic management of spinal trauma and the major pitfalls

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

ANATOMY OF THE SPINE AND SPINAL CORD Spinal column anatomy The vertebral column is composed of a series of motion segments (Figure 25.1). A motion segment consists of two adjacent vertebrae, their intervertebral disc and ligamentous restraints (Figure 25.2).

1 5 3

2

4

Vertebral body

Facet joints

Pedicle

Figure 25.2 Ligamentous spinal restraints. (1) Anterior longitudinal ligament, (2) intervertebral disc and posterior longitudinal ligament, (3) facet joint capsule, (4) interspinous ligament, (5) supraspinous ligament.

Atlas (inferior view) Posterior tubercle

Figure 25.1  The spinal motion segment.

Axis (posterosuperior view) Dens

Posterior arch

Superior articular facet

Posterior articular facet

Regional variations Upper cervical spine anatomy is designed to facilitate motion (Figure 25.3), and stability here is dependent on ligamentous restraints (Figure 25.4). Vertebral anatomy from C3 to C7 is similar. The cervicothoracic (Figure 25.5) and thoracolum­ bar junctions (Figure 25.6) are transitional zones where the

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Inferior articular Anterior facet arch

Anterior tubercle

Spinous process

Figure 25.3  Atlantoaxial bony anatomy.

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339

Ascending band Cruciate ligament

Transverse band

Posterior longitudinal ligament Figure 25.4  Atlantoaxial ligaments.

Figure 25.6 Coronal T2-weighted magnetic resonance image demonstrating a fracture dislocation at the thoracolumbar junction.

divided into three columns: anterior, middle and posterior (Figure 25.7) If two or more columns of the spine are injured the spine is considered unstable. The AO classifications (Magerl and AO Spine Subaxial Classification System) are based on the mechanism of injury and used to assess spinal stability. Summary box 25.1 Figure 25.5  Cervicothoracic facet subluxation (arrow) (easily missed with inadequate x-rays).

Spinal column anatomy ●●

●●

spine changes from a mobile section (cervical and lumbar) to a more fixed one (thoracic). These two areas are common sites of injury.

Upper cervical spine stability is dependent on ligamentous restraints The cervicothoracic and thoracolumbar junctions are common sites of injury

Spinal neuroanatomy

Spinal stability Spinal stability is the ability of the spine to withstand physio­ logical loads with acceptable pain, avoiding progressive deformity or neurological deficit. The spinal column can be

The spinal cord extends from the foramen magnum to the L1/ L2 level, where it ends as the conus medullaris in adults (lower in children) (Figure 25.8). Below this level lies the cauda equina. Figure 25.9 illustrates a cross-section of the spinal

Anterior

Middle

Posterior

Figure 25.7  The three-column model of spinal stability.

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graphically arranged; proximal body function is represented centrally, with distal body function arranged peripherally. Cord

PATIENT ASSESSMENT Basic points

Conus medullaris

The advanced trauma life support (ATLS) principles apply in all cases (see Chapters 22 and 23). The spine should initially be immobilised using full spinal precautions, on the assump­ tion that every trauma patient has a spinal injury until proven otherwise (Figure 25.10). The finding of a spinal injury makes it more (not less) likely 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 (Figure 25.11). They should only be used for transferring patients.

Cauda equina

Figure 25.8  The spinal cord ends at T12/L1 at the conus medullaris, which gives rise to the cauda equina.

Dorsal column Lateral column

Fasciculus gracilis

Dorsal sulcus

Fasciculus cuneatus

S L

T C C

C Ventral Ventral column fissure

T

T L

L S

Lateral corticospinal tract Lateral spinothalamic tract

Figure 25.10  Spinal immobilisation.

Anterior spinothalamic tract

Figure 25.9  A cross-section of the spinal cord.

cord. The lateral spinothalamic tracts transmit the sensations of pain and temperature, the lateral corticospinal tracts are responsible for motor function and the posterior columns transmit position, vibration and deep pressure ­sensation. 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 topo­

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Figure 25.11 Pressure sores may develop rapidly in insensate patients.

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The unconscious patient Definitive clearance of the spine may not be possible in the initial stages and spinal immobilisation should then be main­ tained, until MRI or equivalent can be used to rule out an unstable spinal injury.

Summary box 25.2 Patient assessment ●● ●● ●●

●●

Use 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% 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.

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

Spinal examination The overlying skin should be inspected (e.g. for possible penetrating wounds) and the entire spine must be palpated. A formal spinal log roll must be performed to achieve this ­(Figure 25.12). Significant swelling, tenderness, palpable steps or gaps suggest a spinal injury. A rectal examination should be undertaken to assess anal tone and perianal sen­ sation (see Neurological examination). Seatbelt marks on the abdomen and chest must be noted, as these suggest a high-energy accident.

Neurological examination The American Spinal Injury Association (ASIA) neurolog­ ical evaluation system (Figure 25.13) is an internationally accepted method of neurological evaluation. Motor function is assessed using the Medical Research Council (MRC) grading system (0–5) in key muscle groups

Figure 25.12  Spinal log roll.

(Figure 25.13). A motor score can then be calculated (max­ imum 100). Sensory function (light touch and pin prick) is assessed using the dermatomal map (Figure 25.13). A total sensory score is then calculated. Rectal examination is performed to assess anal tone, vol­ untary anal contraction and perianal sensation.

Level of neurological impairment The ASIA Neurological Impairment Scale is based on the Frankel classification of spinal cord injury: ●● ●● ●● ●● ●●

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

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Figure 25.14  Large prevertebral haematoma (arrows).

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Figure 25.17 Axial computed tomography demonstrating a thoracolumbar fracture dislocation.

a

b

c

Figure 25.15 The anterior (a), posterior (b) and spinolaminar (c) lines are useful in identifying anterior translation on lateral x-rays of the neck.

Magnetic resonance imaging Magnetic resonance imaging (MRI) is indicated in all cases with neurological deficit and where assessment of ligamen­ tous structures is important (Figure 25.18).

Dynamic imaging Lateral flexion–extension radiographs of the cervical spine should not be undertaken acutely although they can have a role in assessing spinal stability in the longer term.

Figure 25.16 Lateral cervical spine x-ray showing obvious spinal instability with marked sagittal angulation and translation. This patient walked into the outpatient department.

Computed tomography Computed tomography (CT) scanning with two-dimensional (2D) reconstruction remains the gold standard in spinal trauma and is indicated for patients with suspected or visi­ ble injuries on plain radiographs (Figure 25.17). Patients undergoing a head CT scan for closed head injury should also have a cervical screening CT. Often CT scans of the chest and abdomen are performed as part of the assessment of poly­ trauma patients and will usually include the spine.

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Figure 25.18 Sagittal T2-weighted magnetic resonance imaging scan demonstrating a cervical spine subluxation and spinal cord contusion.

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In many cases of spinal trauma, formal open reduction and stabilisation using internal fixation is also required (Figure 25.20).

Summary box 25.4 Diagnostic imaging of spinal injuries ●●

●●

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

CLASSIFICATION AND MANAGEMENT OF SPINAL AND SPINAL CORD INJURIES Basic management 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 25.19). (a)

(b)

Figure 25.19  Skeletal traction using skull tongs.

(c)

(d)

Figure 25.20  (a) Thoracolumbar fracture dislocation, (b) treated with open reduction and posterior fixation. (c) Bifacetal cervical spine dislocation. (d) Posterior stabilisation following closed reduction.

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A halo brace can be used to perform a closed realignment and immobilisation of cervical fractures (Figure 25.21).

345

(a)

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

Decompression of the neural elements Realignment of the spine and correction of the spinal defor­ mity may achieve an indirect decompression. A direct decom­ pression of the neural elements may also be indicated if there are bone fragments causing residual compression or a signif­ icant haematoma (Figure 25.22). The timing of surgery in spinal cord trauma remains controversial.

Corticosteroids Corticosteroids are no longer indicated in acute spinal cord injury because of a lack of evidence to support efficacy. Steroids do have a role in non-traumatic spinal cord compres­ sion e.g. malignant spinal cord compression (MSCC).

(b)

Figure 25.22  (a) Sagittal T2-weighted magnetic resonance imaging scan showing an L1 burst fracture and neural compression; (b) treated with combined anterior and posterior surgery.

SPECIFIC SPINAL INJURIES Figure 25.21  External immobilisation using a halo jacket.

Summary box 25.5 Management of spinal trauma ●● ●● ●●

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

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Upper cervical spine (skull–C2) Occipital condyle fracture This is a relatively stable injury often associated with head injuries and is best treated in a hard collar for 6–8 weeks.

Occipitoatlantal dislocation This injury is usually caused by high energy trauma and is often fatal. The dislocation may be anterior, posterior or

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­vertical (Figure 25.23). Power’s ratio (Figure 25.24) is used to assess skull translation. Treatment is with a halo brace or occipitocervical fixation.

Mass deviation (a)

(b)

Atlas fracture (Jefferson fracture) Fracture of the C1 ring is associated with axial loading of the cervical spine and may be stable or unstable (Figure 25.25a, b). Associated transverse ligament rupture may occur (Figure 25.25c). Most are treated non-operatively in a cervical collar or halo brace.

(c)

Figure 25.25 Stable (a) versus unstable (b) Jefferson’s fracture of C1. (c) Open mouth view of C1/2 demonstrating C1 lateral mass deviation (arrows). Rupture of the transverse ligament is present when the combined lateral mass deviation exceeds 6.9mm.

Atlantoaxial instability Figure 25.23  Vertical occipitocervical dislocation.

This is defined as non-physiological movement between C1 and C2. It can be translational or rotatory and resolves either spontaneously or with traction followed by a cervical collar. Isolated, traumatic transverse ligament rupture leading to C1/2 instability is uncommon and is treated with posterior C1/2 fusion (Figure 25.26).

Odontoid fractures B A

O C

There are three types of odontoid peg fracture (Figure 25.27). Neurological injury is rare. The majority of acute injuries are treated non-operatively in a hard collar or halo jacket for 3months. Internal fixation with an anterior com­ pression screw is indicated for displaced fractures (Figure 25.28), and a posterior C1/2 fusion is considered in cases of non-union. In the elderly, treatment in a soft collar should be considered on the basis that a relatively stable pseudarthrosis will occur.

Figure 25.24  Power’s ratio. BC/OA ≥1 indicates anterior translation, ≤0.75 indicates posterior translation.

Barry Powers, contemporary, Chief and Clinical Professor of Radiology, Duplin General Hospital, Kenansville, NC, USA, described his ratio in 1979. Sir Geoffrey Jefferson, 1886–1961, Professor of Neurosurgery, University of Manchester, UK, 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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(a)

347

(a)

(b)

(b)

Figure 25.26  (a) Atlantoaxial subluxation. (b) C1/2 posterior fusion using C1 lateral mass and C2 pedicle screws.

Figure 25.28  (a) Type II odontoid fracture (arrow); (b) treated with an anterior compression screw. Type I

Type II

Type III

Figure 25.27  Types of odontoid fracture.

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Traumatic spondylolisthesis of the axis (hangman’s fracture) This is a traumatic spondylolisthesis of C2 on C3. There a four types with varying degrees of instability (Figure 25.29). Those with significant displacement or associated facet dislocation are treated operatively, usually with posterior stabilisation.

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(a)

(a)

(b)

(b)

Figure 25.29  (a) Hangman’s fractures of C2 with minimal forward translation (arrow). (b) C2/3 subluxation with spinal cord contusion.

Subaxial cervical spine (C3–C7) The pattern of lower cervical spine injury depends on the mechanism of trauma. These include compression fractures (hyperflexion), burst fractures (axial compression) and facet subluxation/dislocation injuries (distraction–flexion), teardrop fractures (hyperextension) and fracture of posterior ele­ ments. The more severe injuries are accompanied by spinal cord injury (Figure 25.30a). Operative intervention may be required to decompress the spinal cord, and to stabilise the spine with internal fixation (Figure 25.30b). Facet subluxation/dislocation ranges in severity from minor instability to complete dislocation with spinal cord injury (Figure 25.31).

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Figure 25.30  (a) Cervical burst fracture with spinal cord contusion; (b) treated by anterior decompression and reconstruction.

Fractures in patients with ankylosing spondylitis Ankylosing spondylitis is a seronegative inflammatory disor­ der that causes autofusion of the spine. These patients have a higher risk of spinal fractures and spinal cord injury than the normal population. Senior advice should be obtained, because application of a cervical collar may be contraindi­ cated, and patients should be managed instead in a position of comfort. Surgical stabilisation is commonly indicated.

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(a)

80

(b)

Figure 25.31  C5/6 bifacetal dislocation (arrows).

Summary box 25.6 Cervical spine injuries ●●

●●

67

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

Thoracic and thoracolumbar fractures The system developed by the AO (Arbeitsgemeinschaft für Osteosynthesefragen) can be used to classify these fractures. There are three main injury types, A, B and C, with increas­ ing instability and risk of neurological injury. Type A fractures are vertebral body compression fractures. Type B injuries involve distraction of the anterior or posterior elements and type C injuries are rotational and often coexist with Type A or Type B injuries. The majority of type B and type C injuries require surgical stabilisation.

Thoracic spine (T1–T10) Osteoporotic wedge compression fractures in the elderly are the commonest injury in this group. Most of these fractures heal, but symptomatic fractures can be treated with percuta­ neous bone cement augmentation, known as vertebroplasty or kyphoplasty (Figure 25.32).

Figure 25.32  (a) Lateral x-ray showing multiple osteoporotic compression fractures. (b) Reduction in thoracic kyphotic deformity following four-level kyphoplasty.

In trauma cases, unstable fractures are associated with sig­ nificant 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 a sternal fracture (Figure 25.33) also carries a significant risk of aortic rupture. Multiple posterior rib frac­ tures and rib dislocations above and below a thoracic spinal injury signify a major rotational injury to the chest and can be associated with vascular injury and significant pulmonary contusion (Figure 25.34). Multimodality diagnostic imag­ ing is recommended. Surgery is appropriate for most thoracic injuries if unstable.

AO, Arbeitsgemeinschaft für Osteosynthesefragen, may be translated from the German as ‘Working Party on Problems of Bone Repair’.

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Thoracolumbar spinal fractures (T11–L2) The thoracolumbar junction is especially prone to injury. This can vary from a from minor wedge fracture to spinal dislocation (Figure 25.35). Burst fractures are comminuted fractures of the vertebral body. They are characterised by wid­ ening of the distance between the pedicles, and can be associ­ ated with retropulsion of bone fragments into the spinal canal (Figure 25.36). Anterior surgery for this type of fracture is now very rarely used and the current treatment principles involve posterior fixation (Figure 25.37). Chance fractures

A

Figure 25.33  Sagittal CT reconstruction showing an upper thoracic spine fracture dislocation (long arrow) and associated sternal fracture (short arrow).

Figure 25.34  Rotational (type C) injury at the thoracolumbar junction. Note rib fractures (long arrows) and dislocation (short arrow), and presence of chest tube.

(a)

Figure 25.35 Total spinal sagittal computed tomography reconstruction demonstrating a thoracolumbar fracture dislocation (long arrow) and fracture of L5 (short arrow).

(b)

Figure 25.36 Lumbar burst fracture with increase in interpedicular distance (a) (arrow) and spinal canal compromise (b).

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(a)

351

(b)

Figure 25.37  Lumbar burst fracture at L2 (a), and posterior instrumentation with indirect reduction (b).

are flexion–distraction injuries of the thoracolumbar junction and are classically associated with the use of lap-belts (Figure 25.38). Duodenal, pancreatic and/or aortic ruptures are also associated with these injuries.

Lumbar spinal fractures (L3–S1) Most fractures of the lower lumbar spine can be treated non-surgically because the incidence of neurological injury is lower. The neural canal is more capacious at this level (the spinal cord terminates at L1/L2). Owing to the lumbar lor­ dosis, patients with these injuries are less likely to develop a kyphotic deformity than those with injuries at the thoraco­ lumbar junction.

Summary box 25.7 Thoracic and thoracolumbar fractures ●●

Figure 25.38  A bony Chance fracture at the thoracolumbar junction (arrow) secondary to a lap-belt injury.

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

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

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EPIDEMIOLOGY OF SPINAL CORD INJURY The incidence and causation of spinal cord injury (SCI) vary globally and reflect the demographics and industrialisation of society. The worldwide annual incidence is 15–40 cases per million (according to the National Spinal Cord Injury Sta­ tistical Center, University of Alabama at Birmingham: spinal cord injury facts and figures, April 2009). Road traffic acci­ dents remain the leading cause of spinal cord injuries world­ wide. Males in the third decade of life are the most likely group to sustain serious spinal cord injury.

Summary box 25.9 Pathophysiology of spinal cord injury ●●

●●

●●

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

Identification of shock

EVOLUTION OF THE MANAGEMENT OF SPINAL CORD INJURY

Three categories of shock may occur in spinal trauma

The development of specialised SCI centres has dramatically improved the survival rates, health and functional outcomes of individuals with SCI. The first SCI centre was estab­ lished in the USA in 1936 by Dr Donald Munro. In 1944 The National Spinal Injuries Centre was established at Stoke Mandeville, England, by Sir Ludwig Guttmann.

●●

●●

●●

Summary box 25.8 Spinal cord injury ●● ●●

Hypovolaemic shock. Hypotension with tachycardia and cold clammy peripheries. This is most often due to haemor­ rhage. It should be treated with appropriate resuscitation. Neurogenic shock. This presents with hypotension, a normal heart rate or bradycardia and warm peripheries. This is due to unopposed vagal tone resulting from cervi­ cal spinal cord injury at or above the level of sympathetic outflow (T1/T5). It should be treated with inotropic sup­ port, and care should be taken to avoid fluid overload. Spinal shock. Spinal shock is a temporary physiological disorganisation of spinal cord function that starts within minutes following the injury. The length of effect is vari­ able, but it can last 6weeks or longer. It is characterised by paralysis, decreased tone and hyporeflexia. Once it has resolved the bulbocavernosus reflex (Figure 25.39) returns.

The incidence of spinal cord injury remains constant The outcome is improved in regional/national spinal cord injury centres

PATHOPHYSIOLOGY OF SPINAL CORD INJURY The primary injury This is the direct insult to the neural elements and occurs at the time of the initial injury.

The secondary injury Haemorrhage, oedema and ischaemia result in a biochemical cascade that causes the secondary injury. This may be accen­ tuated by hypotension, hypoxia, spinal instability and/or per­ sistent compression of the neural elements. Management of spinal cord injury must focus on minimising secondary injury.

Figure 25.39 The bulbocavernosus reflex (this can be elicited in females by traction on the Foley catheter).

Sir Ludwig Guttmannis considered by many to be the father of spinal cord medicine. He was a leading neurosurgeon in Germany, working at the Jewish Hospital in Breslau. He fled to England in 1939.

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Level of neurological injury The level of neurological injury is simply the most caudal neurological level with normal neurological function.

Complete versus incomplete spinal cord injury A spinal cord injury is incomplete when there is preservation of perianal sensation.

Types of incomplete spinal cord injury There are several types of incomplete spinal cord injuries. These include: ●● ●● ●● ●● ●●

central cord syndrome; Brown-Séquard syndrome (hemisection); anterior spinal syndrome; posterior cord syndrome; cauda equina syndrome.

353

REHABILITATION AND PATIENT OUTCOME The goal of spinal cord injury rehabilitation is based on a multidisciplinary approach. There is a focus on goal-setting, maximising remaining neurological function and reintegra­ tion into employment and society. The level of neurological impairment determines the functional outcome (Table 25.1).

Prognosis of spinal cord injury Despite continuing improvements in patient care, life expectancy remains below normal following SCI. The ­ median life expectancy is 33 years, but varies considerably (Table 25.2). The prognosis for neurological recovery is strongly influ­ enced by factors such as the level and completeness of the injury, ventilator dependence and the age at presentation.

TABLE 25.1 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

C5

Power wheelchair, dress upper body, self-feed with aids, wash face with assistance

C6

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

C7

Manual wheelchair, independent transfer, dressing (with aids), feeding, bathing, self-care. Bladder and bowel care with assistance

C8–T4

Independent with most activities of daily living, and bowel and bladder care

T5–T12

As above but with more ease. Independent with all self-care

L1–L5

Independent. Walk with short or long leg braces

S1–S5

Independent, able to walk if able to push off (S1) (may need brace). Bladder, bowel and sexual function may remain compromised

TABLE 25.2  Life expectancy (years) post injury by severity of injury and age at injury. Age at injury

No SCI

Motor functional at any level

Para

Low tetra (C5–C8)

High tetra (C1–C4)

Ventilator-dependent at any level

(a) For people who survive the first 24 hours 20

58.4

52.8

45.6

40.6

36.1

16.6

40

39.5

34.3

28.0

23.8

20.2

7.1

60

22.2

17.9

13.1

10.2

7.9

1.4

(b) For people surviving at least 1 year post injury 20

58.4

53.3

46.3

41.7

37.9

23.3

40

39.5

34.8

28.6

24.7

21.6

11.1

60

22.2

18.3

13.5

10.8

8.8

3.1

SCI, spinal cord injury.

Charles Edward Brown-Séquard, 1817–1894, physiologist and neurologist who held a number of academic posts, amongst them Physician, The National Hospital for Nervous Diseases, Queen’s Square, London, UK (1860–1864), Professor of Medicine at Harvard University, Boston, MA, USA (1864–1878) and at the College de France, Paris, France (1878–1894). He described his syndrome in 1851.

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Complications associated with spinal cord injury Pressure ulcers Many are preventable. Patients should be turned regularly on an appropriate mattress to minimise the risk of skin break­ down

Pain and spasticity Neurogenic pain is common. Once reflex activity returns following cord injury, spasticity may occur and can be prob­ lematic. Intrathecal infusion of baclofen may be required in resistant cases.

Autonomic dysreflexia This is a paroxysmal syndrome of hypertension, hyperhydrosis (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 (PTS) may occur in up to 28% of SCI patients up to 30 years following injury. Approximately 30% of cases are symptomatic. Clinically, patients present with segmental pain at or above the level of injury, sensory loss, progressive asymmetrical weakness or increased spastic­ ity. This warrants early MRI assessment. Expanding cavities require neurosurgical intervention.

Thromboembolic events Deep vein thrombosis (DVT) occurs in 30% of patients with SCI. Fatal pulmonary embolus is reported in 1–2% of cases. Thomboprophylaxis with compression stockings and low

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molecular weight heparin is indicated, provided there are no contraindications.

Osteoporosis, heterotopic ossification and contractures Disuse osteoporosis is an inevitable consequence of SCI and fragility fractures may occur. Heterotopic ossification may affect the hips, knees, shoulders and elbows. It occurs in 25% of spinal cord injured patients. Surgery is appropri­ ate 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. Ber­ lin, Heidelberg: Springer-Verlag, 1998. Bridwell KH, DeWald RL (eds). The textbook of spinal surgery, 3rd edn. Philadelphia: Lipponcott, Williams and Wilkins, 2011, pp.1377–473. 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&ItemID=31562 &MId=4607&wversion=Staging Cotler JM, Simson MJ, An HS et al. (eds). Surgery of spinal trauma. Phil­ adelphia: Lippincott, Williams and Wilkins, 2000. Denis F. The three column spine and its significance in the classification of acute thoracolumbar spinal injuries. Spine 1983; 8(8): 817–31. Dimar JR. Early versus late stabilisation of the spine in the polytrauma patient. Spine 2010; 35(21S): S187–S192. Fardon DF, Herzog RJ, Mink JH et al. (eds). Orthopaedic knowledge update – spine. Rosemont, IL: American Academy of Orthopaedic Sur­ geons, 1997. Fehlings MG. Essentials of spinal cord injury. Basic research to clinical practice. Stuttgart: Thieme, 2013. Focus issue. Spinal trauma. Spine 2006; 31(11S): S1–104. Panjabi M, White A. Functional anatomy of the spine. Oxford: Butter­ worth-Heinemann Ltd, 1990.

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Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & 26Love Chapter

Maxillofacial trauma Learning objectives To be able to: •• Identify and understand the significance of potentially life-threatening injuries to the face, head and neck To have: •• A systematic methodology for examining facial injuries To know: •• The classification of facial fractures

To understand:

•• The diagnosis and management of fractures of the middle third of the facial skeleton and the mandible

•• The principles of the diagnosis and management of facial soft tissue injuries To appreciate: •• The management of dental injuries

EMERGENCY ASSESSMENT AND TREATMENT The management of a patient with facial trauma must begin with an immediate assessment of the airway, breathing and circulation in keeping with the advanced trauma life support (ATLS) principles (see Chapter 23). If the patient has facial or midface bleeding they may sit forward or be placed on their side (Figure 26.1) to minimise the risk of blood and/or dental fragments obstructing the airway. The use of good light and high volume suction is often helpful. The midface, when fractured, is displaced downwards and backwards (Figure 26.2), and if this occurs in combination with a mandibular fracture, particularly if the anterior mandible is comminuted, the tongue is also displaced downwards and backwards, adding to the airway compromise and creating the risk of obstruction (Figure 26.3). In

Figure 26.1  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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Figure 26.2  A blow from the front of the face may separate the facial skeleton from the base of the skull and thrust it downwards and backwards.

these circumstances intubation is indicated, but emergency procedures can be employed to buy time. In the obtunded or unconscious patient the maxilla can be grasped by hand, disimpacted and pulled forwards. In addition, the tongue can be pulled forwards and held forwards, with a large suture or towel clip, to help clear the airway. If intubation is not possible a surgical airway is indicated. Massive, life-threatening bleeding is usually only seen in the context of major trauma, lacerations, blast, ballistic, penetrating or gunshot injuries. Significant bleeding, usually from the pterygoid venous plexus and/or the rich blood supply of the nose, can be seen in central midface injuries. Management of massive midface bleeding may require intubation and the placement of anterior and or posterior nasal packs. There are specific inflatable nasal balloons that

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can facilitate the immediate management, however Foley catheters may also be utilised. Once the patient has been stabilised a more formal assessment may be performed.

Where skull fractures occur in combination with facial fractures or the fractures extend into the frontal or ethmoidal sinuses, they are classified as craniofacial, and a joint neurosurgical and maxillofacial approach is necessary. If fractures occur at all levels of the face the term panfacial is utilised. This does not necessarily alter the management of the individual fracture components, however it does imply a significant degree of force and one must be suspicious of other injuries, especially head injuries. As with all trauma patients, associated injuries, including chest and abdominal trauma, must be actively excluded. In considering the bony injuries, the fractures may be displaced or undisplaced and comminuted or non-comminuted. In the past, and with particular reference to mandibular fractures, stability was also considered, however with modern treatment methods this is a less important factor.

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Figure 26.3  Loss of nasopharyngeal space and oedema of the soft palate and tongue (arrows) may close off the airway in severe maxillofacial injuries, 2–3 hours after injury.

Lacerations are crushing injuries where the soft tissues are compressed between the underlying bone and some form of blunt object. Incised wounds are caused by a cutting implement, such as a knife or glass. Often the injuries are a combination of the two. Either type of wound can occur with or without tissue loss. Where the injury results in a communication between the skin and the mucosa of the oral cavity the wound is termed ‘through and through’.

Summary box 26.1

Summary box 26.2

Emergency assessment

Classification of facial injuries

●●

●●

Airway, breathing, circulation with cervical spine control is the starting point Do not let dramatic facial injuries distract from other potentially life-threatening injuries

CLASSIFICATION OF FACIAL INJURIES Bony injuries and fractures The facial skeleton can be divided into thirds vertically: ●● ●● ●●

upper face (from level of canthi upwards); midface (from maxillary teeth to canthi); lower face (mandible and mandibular teeth).

In addition, the midface can be divided into central and lateral portions. The central midface is the naso-orbital– ethmoidal complex and the lateral portion comprises the cheekbones (Malar bones, zygomatic bones or zygomatic– maxillary complex). The eye socket can be considered as a separate entity, because orbital fractures can occur in isolation or as part of a constellation of multiple fractures. Orbital fractures can affect the orbital floor, medial and/or lateral walls and the roof of the orbit.

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●● ●● ●●

Divide the face into thirds Assess orbit independently Assess bony and soft tissue injuries

CLINICAL ASSESSMENT History As with all aspects of surgical diagnosis, the history is paramount. As much information as possible should be obtained about the mechanism of injury, the past medical history and the postinjury course. This will be directly from the patient, friends, family, witnesses and emergency services. Knowledge of the mechanism of injury will often help to identify the potential occult injuries that are not obvious on first inspection. As the craniofacial region is so richly vascularised, the often dramatic appearance seen in major facial trauma has the potential of distracting the unwary clinician from potentially more important injuries.

Examination Primary survey Initially, the primary survey is aimed at the airway: controlling bleeding, restoring and maintaining the circulation and

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Soft tissue injuries and lacerations

PART 4 | TRAUMA Clinical assessment

assessing for neurological deficits, with cervical spine control. The more detailed secondary survey is aimed at a definitive examination, with the clear expectation that this will need to be repeated on several occasions. The face, head and neck should be inspected and wounds cleaned and assessed for tissue loss, and then dressed to control any bleeding not addressed in the primary survey. Their size, location and depth should be carefully recorded in the case notes. Large and obvious foreign bodies should be removed but care should be exercised with penetrating wounds involving large fragments or blades which potentially penetrate deep structures. These should be removed in the operating theatre, in more controlled conditions, after imaging (note also glass that may injure the assessing surgeon). On occasions it is helpful to administer local anaesthetic for the examination and (temporary) repair of facial lacerations, particularly if a single vessel continues to bleed. In these circumstances it is very helpful to perform a thorough examination of the key sensory and motor nerves that may have been injured, before the local anaesthetic makes this assessment meaningless. This principle also applies to the management of those patients for whom intubation is imminent. While this may be difficult, a brief assessment of Glasgow Coma Scale (GCS) score, eye function (motility and acuity), facial and trigeminal nerves and cervical spine pain and function prior to the induction of anaesthesia can be very helpful in ongoing management.

Secondary survey The secondary survey examination should be systematic because it is easy to be distracted and miss potentially important injuries that leave only a small external sign, e.g. a small entry wound from a stabbing to the back of the neck. The surface inspection should include the back of the neck, the whole scalp and then move to the frontal view. At this time it is helpful to perform a formal cranial nerve examination; of particular importance are cranial nerves II, III, IV, VI, V and VII.

Further examination Examination of the eyes should then take place to exclude globe or retinal injury, as well as to assess acuity, test for diplopia and assess motility. This is possible even in the most swollen of eyes because one can gently prise the eyelids apart with cotton wool buds (or microbiology swabs). These are held parallel to the eyelids and gently pushed into the oedematous tissue close to the eyelashes, rotating the swabs to open the eye. A colleague can then examine the eye. The position of the globe – whether there is proptosis or enophthalmos – and visual acuity (utilising a Snellin chart) in each eye, and whether there is diplopia in all nine positions of gaze, should be recorded. The intraoral examination is facilitated by the use of good light (a headlight is helpful) and suction to allow removal of blood and saliva. The teeth should be examined and their presence or absence noted. Dental injuries should be classified. Teeth may be knocked out in an injury (termed avulsion), displaced but still attached to soft tissues and/or bone (termed subluxation) or fractured. If a tooth is mobile it may

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be subluxated or have a root fracture (detected on a radiograph). It is important to account for all missing teeth or tooth fragments as aspiration of an avulsed tooth or tooth fragment is a major risk. If there is any doubt about the location of missing teeth a chest radiograph should be obtained. If there is a fracture of the mandible, the overlying mucosa is often torn and there may be an associated haematoma in the floor of the mouth (Figure 26.4). A key assessment is that of the dental occlusion (the way in which the teeth bite together). Patients are able to discriminate tiny alterations in their occlusion. These occlusal changes may represent dental injuries or, more commonly, displaced fractures of the maxilla and/or mandible. Palpation of the bony contours of the facial bones should identify sites of tenderness, steps and asymmetry. This can start at the supraorbital margins, move around the infraorbital margins and then along the zygomatic arches, moving onto the condylar heads of the mandible and then running along the lower border of the mandible.

Investigations The investigations required fall into two major categories: first, those required to confirm the provisional and specific clinical diagnosis with regard to the facial injuries and, second, those to assess and manage the systemic condition of the patient. Systemic investigations will be governed by the general state of the patient and the past medical history. Typically, they will include routine laboratory (haematological and biochemical) investigations and radiological (for example the cervical spine) and other imaging. Specific head and neck investigations are utilised and the general trend is away from plain radiology towards computed tomography (CT) scanning. If the clinical picture suggests an isolated mandibular fracture, plain radiographs at right angles to each other (rotational tomograph, orthopantomogram (Figure 26.5) and a posteroanterior (PA) mandible) may suffice, but clinicians should have a low threshold for crosssectional imaging, particularly if a head or cervical spine CT

Figure 26.4  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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SPECIFIC INJURIES

(a)

Mandibular fractures Mandibular fractures typically occur at specific sites (Figure 26.6). As with all fractures the principles of reduction, fixation, immobilisation and then rehabilitation apply to facial fractures. In previous years the reduction and immobilisation was often achieved by wiring the teeth together, known as intermaxillary fixation (IMF). However, in recent years this technique has largely been superseded by the use of open reduction and internal fixation (ORIF) techniques (Figure 26.7) utilising titanium fixation plates secured with screws. In general, the facial bones heal well and undisplaced fractures or those treated with ORIF heal after about 4 weeks. If the patient has had IMF a liquid diet is required and those who have had an ORIF procedure must also remain on a very soft sloppy diet for the same period. In general, straightforward mandibular fractures treated with ORIF techniques have 2mm diameter screws engaging a single bone cortex (monocortical). These small plates are said to be load sharing, in that the fractures are reduced and load is shared between the native bone and the plate. With more complex or comminuted fractures, larger plates and screws (up to 2.7 mm diameter) may be utilised; these are termed fracture or reconstruction plates. They are regarded as load bearing, and bicortical fixation may also be utilised.

(b)

1

2

3

Figure 26.6  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.

Figure 26.5  (a) Rotational tomogram showing a right mandibular body fracture. (b) Posterioanterior (PA) mandible showing the same mandibular body fracture.

is indicated. The additional information from 1 mm imaging cuts through the facial skeleton is worth the additional radiation dose, especially if plain radiography has been avoided. Summary box 26.3 History, examination and investigation ●● ●●

The history, particularly the mechanism of injury, is vital For simple injuries radiographs in two planes are required, but increasingly cross-sectional imaging is the norm: CT scanning

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Figure 26.7  Intraoperative photograph showing a comminuted mandibular fracture reduced and fixed with a combination of 2mm mini plates (monocortical) and a larger fracture plate with bicortical screws.

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The timing of the definitive treatment of mandibular fractures is dependent on the general state of the patient; however, optimal timing is for treatment within 24–48 hours post injury. Condylar neck fractures are increasingly being treated with open reduction and internal fixation techniques, with better technology and the use of endoscopically assisted surgery. This can be done via intraoral approaches. Undisplaced or minimally displaced condylar neck fractures can be treated non-operatively or with elastic IMF.

Summary box 26.4 Mandibular fractures ●●

●●

●●

Mandibular fractures are diagnosed clinically, often because of deranged dental occlusion Numbness over the distribution of the mental nerve is common Treatment is primarily with open reduction and internal fixation

Fractures of the zygomatico-orbito complex (ZMC) ZMC (malar/cheekbone) fractures are the commonest facial fractures and have been classified in a variety of different ways. However, from a clinical perspective, considering the cheekbone as a four-legged stool is helpful – the four legs are comprised of the zygomatic arch running anteroposteriorly, the zygomatic process running vertically (to join the frontozygomatic process of the frontal bone at the frontozygomatic (FZ) suture), the infraorbital rim running horizontally and the maxillary buttress running vertically (Figure 26.8).

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With the exception of isolated zygomatic arch, isolated infraorbital rim and extensively comminuted fractures, if the ZMC is fractured then all four legs of the stool are fractured and displacement occurs about two axes, running vertically through the line from the FZ suture to the maxillary buttress or running anteroposteriorly along the zygomatic arch. All ZMC fractures (with the exception of isolated zygomatic arch and isolated infraorbital rim fractures) involve the bony orbit, and careful assessment of ocular position and function is necessary. On examination there is often periorbital bruising and swelling and subconjunctival haemorrhage with no posterior limit is often seen (Figure 26.9). On palpation (or inspection), bowing or depression of the zygomatic arch may be detected. Bony steps and tenderness at the frontozygomatic suture, the infraorbital rim or the zygomatic buttress may also be detected. Altered sensation over the distribution of the infraorbital nerve is common, as a result of either direct trauma or crushing of the nerve as it exits the maxilla or runs along the orbital floor. As with mandibular fractures, the role of plain radiography is diminishing and cross-sectional imaging utilising CT scanning is the standard investigation except for the simplest fractures. In terms of management, the mainstay of treatment is ORIF with fixation at one of the four ‘legs of the stool’, namely the frontozygomatic suture, the buttress region, the infra­ orbital rim or the zygomatic arch. The necessity for single, double, triple or four-point fixation will depend on the stability of the fracture post reduction and the degree of comminution. Uncomplicated ZMC fractures are generally treated within 10 days of injury. Summary box 26.5 Fractures of the ZMC ●● ●● ●●

Figure 26.8  The ‘four legs of the stool’.

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Fractures of the zygomatico-orbital complex are common Eye injuries should be actively excluded CT scanning is the investigation of choice

Figure 26.9  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.

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Maxillary fractures Maxillary fractures are traditionally classified after René Le Fort’s work, in which he recreated the maxillary fractures utilising cadavers and a sandbag. Interestingly, the numbering, in modern usage, has become reversed from the original: the Le Fort I fracture being inferior and the Le Fort III being superior (Figure 26.10). While the classification is simple, real life presentations are often not. CT scanning and the use of open surgical techniques have demonstrated that the described patterns are not often adhered to and that comminution is the norm. Midface fractures are often accompanied by significant facial swelling and this makes palpation of the skeleton difficult. The characteristic finding is of a mobile maxilla which tends to be displaced backwards and inferiorly. This can compromise the airway (see above) and results in an anterior open bite (inability to close the front teeth together). There

is often infraorbital nerve injury resulting in altered sensation and, with upper level (Le Fort II and III) fractures, the orbit is involved to a greater or lesser degree. The treatment of maxillary fractures, in all but the entirely undisplaced fractures, involves ORIF techniques utilising a variety of miniplates (1.5/1.7 mm diameter screws) and/or microplates (1.0/1.2mm diameter screws). Fixation is usually placed along the main facial buttresses (the ‘four legs of the stool’) for optimal strength and bone quality to be able to hold the screws (Figure 26.11). Summary box 26.6 Maxillary fractures ●●

●●

Maxillary fractures indicate significant force transfer – other associated injuries should be excluded Bleeding from the pterygoid venous plexus may be occult

Orbital fractures

(a)

The bones that comprise the orbit can be fractured and, in order of frequency, the floor, medial wall, lateral wall and roof may be disrupted either in combination or as isolated injuries. The mechanism of this is unclear and, particularly with isolated injuries, it may be that a rapid increase in pressure within the confined space of the orbit, typically, for example, when a squash ball hits the eye, results in fracture of the very thin floor and/or medial wall. Alternatively, forces are transmitted from the outer bony orbital rim, which is possibly

(b)

(c) Figure 26.10 Maxillary fractures as classified by Le Fort. (a) LeFortI; (b) Le Fort II; (c) Le Fort III.

Figure 26.11  The buttresses of the face.

René Le Fort, 1869–1951, French surgeon, classified facial fractures after macabre research in which he dropped rocks and other heavy objects on the faces of cadavers.

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temporarily deformed, causing the buckling and fracturing of the thin, vulnerable walls. It is likely that both of these mechanisms have a role in the genesis of orbital fractures. In any orbital injury the eye must be examined carefully, even if there is significant swelling. Pupillary response, visual acuity (utilising a pinhole to correct for missing glasses), ocular motility and the results of careful ophthalmoscopy (including the anterior chamber, lens and fundus) should be documented. Binocular diplopia indicates a motility issue; however, monocular diplopia suggests a problem within the globe such as a dislocated lens or retinal detachment. In general, orbital floor fractures lead to ocular motility problems, primarily restriction of upgaze due to trapping of the orbital fat and associated fibrous septae. However, on occasion the inferior rectus or inferior oblique muscles may also be trapped. Inferior rectus entrapment is much more common in children and this needs to be treated as an emergency because muscle necrosis can occur, leading to irreversible damage. In these cases the orbital floor appears, on imaging, undisplaced, i.e. a trap door defect has opened and then closed again, entrapping the muscle. In addition to motility problems, orbital wall fractures can lead to changes in globe position, with dropping of the globe (hypoglobus) or sinking in of the globe (enophthalmos) (Figure 26.12). In many cases such changes in globe position are masked in the immediate postinjury phase by oedema and only become obvious as this resolves. A retrobulbar haemorrhage is a surgical emergency because when left untreated it can lead to blindness. It presents with decreasing visual acuity, increasing pain, loss of pupillary response and a tense proptosis. Should this diagnosis be suspected medical management should be initiated with acetazolamide, mannitol and steroids; however, the main treatment is surgical, with lateral canthotomy and cantholysyis forming the initial intervention. Investigation of orbital injuries requires CT scanning (Figure 26.13) but if a retrobulbar haemorrhage is suspected treatment should be given prior to scanning. With the exception of retrobulbar haemorrhages and paediatric orbital fractures, the definitive treatment can be delayed for 7–10 days (Figure 26.14). This allows oedema to settle and globe motility and position to be assessed more

Figure 26.12 Previously undiagnosed left orbital blow-out fracture, presenting 3months after the initial injury. Enophthalmos and lowered pupillary level are evident.

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Figure 26.13 Coronal computed tomography scan showing a left orbital blow-out fracture, with evident soft tissue herniation into the maxillary antrum (arrrow).  

accurately. Reconstruction of the orbital rim is usually accomplished with ORIF techniques and the orbital walls repaired with autologous materials such as cranial bone or rib grafts, but proving more popular are preformed titanium implants or patient-specific custom-made implants. Summary box 26.7 Orbital fractures ●● ●●

Visual acuity and motility must be assessed In children, orbital floor injuries should be assessed and treated as emergencies because muscle injury may be permanent, resulting in reduced ocular motility

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Figure 26.14 Computed tomography scan showing retrobulbar haemorrhage and severe proptosis.  

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Naso-orbito ethmoidal fractures These central upper midface fractures can range from simple undisplaced nasal bone fractures to complex comminuted fractures, impacted into the anterior cranial fossa, in the region of the cribriform plate. Typically they are caused by a blow to the bridge of the nose. The more severe fractures present with periorbital ecchymosis, swelling and nasal bleeding with the bridge of the nose depressed and the nasal tip rotated upwards, allowing the nostrils to be seen straight on (‘piggy nose’). The nasal septum is often disrupted and should be inspected for haematomas. Cerebrospinal fluid (CSF) may be seen to be leaking. However, in the initial assessment it is often difficult to make this diagnosis with any certainty. Disruption of the attachment of the medial canthal ligaments can result in traumatic telcanthus – this is due to traumatic detachment of the ligament from its bony insertion or, more commonly, comminution of the naso-orbital ethmoidal complex with the canthal insertion intact, but with a small fragment of displaced bone. Investigation is necessary with CT scanning (Figure 26.15) for all but the simplest nasal bone fractures. Treatment is usually delayed for 7–10 days post injury and generally necessitates ORIF and repositioning of the fragments with the medial canthi attached. If a formal canthopexy is required, this can be achieved with stainless steel wires or specialised canthopexy wires. Summary box 26.8

Figure 26.15  Coronal computed tomography scan posteriosuperior impaction of the naso-orbito complex.

showing

fat or bone. Unless there are other pressing imperatives treatment is usually delayed for 7–14 days.

Naso-orbito ethmoidal fractures ●●

●●

Naso-orbito ethmoidal injuries indicate significant force transfer Other associated injuries should be excluded, particularly craniofacial/anterior cranial fossa injuries

Summary box 26.9 Craniofacial fractures ●●

●●

Usually managed by a multispecialty team involving neurosurgery, ear, nose & throat (ENT) and oral & maxillofacial surgery Significant head injuries are common

Craniofacial fractures These are fractures that involve the cranial cavity and the facial bones in continuity. In many cases they involve the frontal and ethmoidal sinuses, creating a communication between the cranial cavity and the nasal air sinuses. If this is combined with a dural tear, CSF will leak into the nose and is detected as CSF rhinorrhoea with or without a salty taste. In these circumstances antibiotics are not indicated and the threshold for surgical intervention is quite variable between surgeons. The most common site of injury is the posterior wall of the frontal sinus, however fractures of the ethmoid and sphenoid sinus can also cause CSF leaks. Most surgeons would treat persistent leaks lasting 10 days with surgical intervention, and mostly this is done with an open anterior fossa repair (necessitating a frontal craniotomy). In a limited number of cases the CSF leak can be repaired endoscopically. In most patients the treatment involves cranialisation of the frontal sinus with obliteration of the frontonasal duct. Although some surgeons advocate reconstruction of the posterior sinus wall, others will obliterate the sinus with

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Panfacial fractures In cases where there are fractures at all levels of the facial skeleton (upper, mid and lower face) the term panfacial fracture is used, and these fractures can present particular management challenges. First, multiple-level fractures indicate a significant amount of force and therefore energy transfer, hence associated injuries to the brain, cervical spine and other organs are much more common. Second, reconstruction of the multiple fractures is much more difficult because there is little normal anatomy to act as a guide. Each component of the panfacial fracture is treated in the same way as an isolated fracture would be, but sequencing the repair is challenging. The options are top down (craniofacial, zygomatico-orbital, maxillary and finally mandibular), bottom up, inside out (starting centrally and working laterally) or outside in. Most surgeons experienced in managing this type of injury would tailor the sequence to the particular fracture pattern to optimise the use of normal or near normal anatomy as a guide.

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PART 4 | TRAUMA Further reading

There are some particular pitfalls: obtaining adequate cheekbone projection anteroposteriorly while making the zygomatic arch too prominent, over-impacting the anterior maxilla, and an anterior mandibular fracture being fixed with the mandibular angles flared outwards.

Dental injuries The primary (deciduous) dentition is usually fully erupted by 2.5 years, and the first permanent teeth (lower incisors) usually erupt at about the age of 6. Between the ages of 5 and 13 the primary dentition is shed and replaced by the secondary teeth. If an adult whole tooth is avulsed it should be cleaned gently in saline and reimplanted; the sooner that this can happen the better the prognosis (avulsed deciduous teeth are not reimplanted). This is best achieved under local anaes­thesia and after irrigation and debridement of the socket. The patient should then be referred urgently to a dentist for ongoing care; in many cases the tooth may need to be splinted to immobilise it and ensure that it is protected from the dental occlusion. Fractures of the teeth may involve the enamel only, the enamel and dentine or the enamel, dentine and pulp. Once the dentine is exposed the fractured tooth can be exquisitely painful and benefits from a simple dental dressing – in the first instance local anaesthetic infiltrated in the region of the apex of the root is helpful in reducing pain pending a specialist dental assessment. If the pulp is exposed, local anaesthetic applied topically to the exposed pulp can also give some pain relief. Summary box 26.10 Dental injuries ●●

●●

●●

It is important to account for all missing teeth and/or dental fragments – a chest radiograph may be indicated Exposed dentine and pulp can be exquisitely painful and referral for emergency dental treatment can be very helpful Avulsed teeth should be reimplanted as soon as possible

Soft tissue injuries Lacerations and wounds Facial lacerations and incised wounds often bleed quite profusely as a result of the excellent blood supply. This has the benefit of excellent healing and therefore wounds should only be debrided of frankly necrotic tissue. In assessing facial soft tissue wounds it is important to check the function of the facial nerve and the patency of the parotid duct because both of these structures require repair should they be involved in the injury. Uncomplicated wounds with no tissue loss should be cleaned and closed in layers under either local or general anaesthesia. If the skin is contaminated with dirt it should be scrubbed clean with a brush to prevent dirt tattooing. Usually, absorbable sutures are utilised intraorally and for the deep layers. It is important for good closure that the muscle layers are accurately opposed. The final skin layer should be closed with a monofilament suture (in children this can be absorbable). For some small linear incised wounds cyanoacrylate glue can be utilised.

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Wounds involving the eyelid margins and crossing the vermillion of the lip need special attention to detail and very careful approximation of all the involved layers such that referral to a specialist should be considered by the inexperienced surgeon. Where there has been skin loss the management depends on the size of the defect, the elasticity of the surrounding skin and the circumstances. Small defects can be closed with direct closure, but for larger defects the mobilisation of local skin flaps may be necessary. When there is greater tissue loss, skin grafting and/or free tissue transfer may be required.

Parotid duct The parotid duct may be damaged as a result of an incised wound or a crushing injury. This is usually obvious as saliva leaking into the wound and should this be the case the buccal branch of the facial nerve is often injured at the same time. If the duct is transected or damaged this should be repaired over a cannula inserted into the parotid papilla. This is usually best achieved with magnification (loupes or microscope) under the controlled conditions of general anaesthetic.

Facial nerve Facial nerve injuries are best repaired primarily, and the biggest challenge to achieving this is not identifying the motor deficit at presentation. In general, injuries that lie behind a line from lateral canthus or the eye to the angle of the mouth are repairable and this should be attempted. Again, this is best achieved under microscope magnification and a nerve stimulator/monitor is very helpful in identifying the cut nerve ends.

Animal and human bites Unlike those elsewhere on the body, facial bites should be closed primarily and not left open. The abundant blood supply renders this normal precaution unnecessary. All bites should be debrided carefully and closed in the usual way; however, antibiotics, in accordance with local protocols, should be prescribed. If there is significant tissue loss consideration should be given to a staged reconstruction. Summary box 26.11 Soft tissue injuries ●●

●● ●●

Examination of both motor and sensory nerve function should be conducted prior to the administration of local anaesthetic Tissue loss can occur and usually warrants specialist referral Careful cleaning (debridement) with removal of all dirt minimises the chances of wound tattooing

FURTHER READING Brennan P, Schliephake H, Ghali GE, Cascarini L. Maxillofacial surgery, 3rd edn. London: Churchill Livingstone, 2017. Fonseca R, Barber HD, Powers M, Frost DE. Oral and maxillofacial trauma, 4th edn. Philadelphia: Saunders, 2012. Perry M, Holmes S. Atlas of operative maxillofacial trauma surgery: primary repair of facial injuries. Berlin: Springer, 2014.

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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

•• The use of special investigations and their limitations •• The operative approaches to the thoracic cavity •• The special features of an emergency room thoracotomy

INTRODUCTION

citation is therefore the preservation of normal physiology. Techniques such as ‘damage control resuscitation’ and ‘dam­ age control surgery’ have dramatically improved survival through an understanding of the best techniques required to restore physiological stability (see Chapters 1, 22 and 23).

Because injury does not respect anatomical boundaries, divi­ sion of the body into abdomen and thorax is artificial, and injury to the torso, with its associated physiological conse­ quences, is more appropriate. The torso is generally regarded as the main part of the human body, primarily made up of the chest, abdomen and pelvis, not including the head, neck, arms and legs. About 42% of all deaths are the result of brain injury, but some 39% of all trauma deaths are caused by major haemorrhage, usually from torso injury (Figure 27.1). Although initially, injury was treated on an anatom­ ical basis, it has become clear that physiology should be the over-riding consideration, and the driver of successful resus­

Other 4% MOF 7%

for haemorrhage control

•• The indications for and techniques of the trauma laparotomy

•• The philosophy of damage control surgery •• The management of trauma to the pelvis

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 27.1  Causes of death in trauma. CNS, central nervous system; MOF, multiple organ failure.

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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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PART 4 | TRAUMA Thoracic injury

The mediastinum

TABLE 27.1 ATLS® principles of resuscitation.

The zone overlying the mediastinum with its major vessels and the heart is also an extremely high-risk area for penetrat­ ing wounds. Any wound in this region should immediately raise the suspicion of a major vascular or an associated cardiac injury, even in the absence of initial gross physical signs.

A

Airway

B

Breathing

C

Circulation

D

Disability (neurology)

E

Environment and Exposure

Diaphragm The thorax and abdomen are separated by the diaphragm, which is mainly responsible for breathing, and moves during breathing between the fourth and 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 investi­ gated as if both cavities had been penetrated (Figure 27.2). In blunt trauma, rupture of the diaphragm can result in migra­ tion of abdominal viscera into the chest.

Summary box 27.1 Junctional zones ●● ●●

●● ●● ●●

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 arterial inflow and venous outflow. Angioembolisation can be a very useful adjunct to treatment, especially with deep pelvic injuries.

●●

individual, bleeding may only produce subtle changes in vital measures and therefore be difficult to assess (Table 27.2). Although obvious injury may be present, traditional indica­ tors (such as pulse rate), in isolation, are unreliable. Bleeding occurs from five major sites – ‘one on the floor and four more’:

●●

Pelvic structures

Between neck and the thorax Between thorax and the abdomen Between the abdomen, the pelvic structures and the groin

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●●

external – ‘floor’; chest; abdomen (including the retroperitoneum); pelvis; extremities.

THORACIC INJURY Thoracic injury accounts for 25% of all severe injuries. In a further 25%, it may be a significant contributor to the sub­ sequent death of the patient. In most of these patients, the cause of death is haemorrhage. About 80% of patients with chest injury can be managed non-operatively. The key to a good outcome is early physiological resuscitation followed by a correct diagnosis. TABLE 27.2  Clinical indicators of potential ongoing bleeding in torso trauma. Physiological

Increasing respiratory rate Increasing pulse rate

CRITICAL PHYSIOLOGY

Falling blood pressure

Resuscitation of all injuries to the chest and abdomen should follow traditional ATLS® principles (Table 27.1 and Chapters 22 and 23). Bleeding is the major problem. This may be obvious at the time of evaluation; however, in the young physically fit

Rising serum lactate Anatomical

Visible bleeding Injury in close proximity to major vessels Penetrating injury with a retained missile

Liver Spleen Kidney

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Figure 27.2 The anatomical extent of the abdomen.

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CHAPTER 27  Torso trauma

Investigation Routine investigation in the emergency department of injury to the chest is based on clinical examination, supplemented by chest radiography.

Ultrasound – extended focused assessment with sonar for trauma Ultrasound can be used to differentiate between contusion and the actual presence of blood. Extended focused assess­ ment with sonar for trauma (eFAST) is becoming the most common investigation. The technique uses sonar assessment in the chest, looking for a cardiac tamponade or free blood and air in the hemithorax on each side, and assessment for blood in the abdominal cavity, in the paracolic gutters, sub­ diaphragmatic spaces and pelvis.

Underwater chest drain In the physiologically grossly unstable patient, where physical examination is inconclusive and there is no time for radiolog­ ical investigations, insertion of an underwater chest drainage tube can be a diagnostic procedure as well as a therapeutic one, and the benefits of insertion often outweigh the risks.

with migration of abdominal contents into the chest can be detected by CT scan, in injury without migration the diagno­ sis will not be obvious. CT scanning has replaced angiography as the diagnostic modality of choice for the assessment of the thoracic aorta and mediastinal vessels. The pitfalls of investigation are: ●●

●●

●●

●●

●●

Chest radiograph In those cases where the patient is haemodynamically unsta­ ble or the spine is at risk, an anteroposterior (AP) supine chest radiograph is usually the simplest initial investigation, and will provide good information regarding tracheal devia­ tion, lung and mediastinal pathology, as well as skeletal injury. In penetrating injury, it may be more helpful for the radio­ graph to be performed with the patient positioned erect, as this will best reveal a small pneumothorax, fluid meniscus, air–fluid level or the presence of free gas under the diaphragm, indicating the presence of a hollow abdominal viscus perfora­ tion. Note that up to 300 mL of blood may pool behind the domes of the diaphragm, and may not be visible even in the erect view. The presence of thoracic skeletal injury should alert the clinician to the possibility of adjacent thoracic or abdominal visceral injury. Rupture of the thoracic aorta can be related to fractures of the first and second rib, bilateral clavicular frac­ ture and fracture of the sternum, thoracic spine or scapula. Fracture of the lower ribs can be related to injury of liver or spleen. Fracture of ribs, irrespective of site, can be related to injury to the lung parenchyma or thoracic wall vasculature, causing pneumothorax, haemothorax or lung contusion.

Computed tomography scan The computed tomography (CT) scan with contrast allows for three-dimensional reconstruction of the chest and abdo­ men, as well as of the bony skeleton. It has become the princi­ pal and most reliable examination for major injury in thoracic trauma. In blunt chest trauma, the CT scan will allow the definition of fractures, as well as showing haematomas, pneu­ mothoraces 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. However, although the presence of an isolated rupture of the diaphragm

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failure to assess tracheal shift immediately above the sternal notch clinically (deviation of the trachea occurs away from the affected side in tension pneumothorax, and towards the affected side in lung collapse); failure to percuss and auscultate both front and back in a supine patient (an inflated lung will ‘float’ on a haemotho­ rax, so auscultation from the front may sound normal); failure to pass a nasogastric tube if rupture of the dia­ phragm is suspected; a chest radiograph will show the nasogastric tube apparently within the chest cavity; a supine chest radiograph can show a haemothorax as a homogenous increase in opacity of the hemithorax; this can cause confusion between the darker side and the lighter side, as to which may be a haemothorax (less radiolucent), or a pneumothorax (more radiolucent). Look carefully for lung markings, and don’t drain the wrong side; pursuing radiological investigation (radiography or CT scan) instead of resuscitation in the unstable patient.

Summary box 27.2 Investigation of chest injuries ●● ●● ●● ●● ●●

Directly or indirectly involved in >50% of trauma deaths 80% can be managed non-operatively A chest radiograph is the investigation of first choice A chest drain can be diagnostic as well as therapeutic A spiral CT scan provides rapid diagnoses in the chest and abdomen

Management In penetrating injury, most patients who have suffered injury to the chest can be managed with appropriate resuscitation and insertion of an intercostal drain. 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 patient with an open pneumothorax is converted into an unstable patient with a 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, particularly in the presence of a flail chest, there can be an associated lung contusion. The patient in extremis with exsanguinating chest haem­ orrhage will be discussed in the section on Emergency depart­ ment thoracotomy (EDT) later in the chapter.

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Summary box 27.3 Closed management of chest injuries ●●

●● ●●

About 80% of chest injuries can be managed with the insertion of an intercostal drain only Do not close a sucking chest wound until a drain is in place If bleeding persists, the chest will need to be opened and direct haemostatic control is obtained

Life-threatening injuries can be remembered as the ‘deadly dozen’. Six are immediately life threatening and should be sought for and managed during the primary survey and six are potentially life threatening and should be detected during the secondary survey (Table 27.3). 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 con­ sultation 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 distor­ tion can be insidious and progressive and can make delayed intubation more difficult if not impossible.

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 a parenchymal lung injury and air leak that did not spontaneously close, iatrogenic lung injury (e.g. due to central venepuncture) and mechanical positive pressure ventilation.

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The clinical presentation is dramatic. The patient is increasingly restless with tachypnoea, dyspnoea and distended neck veins (similar to pericardial tamponade). Clinical exam­ ination may reveal tracheal deviation; this is a late finding and is not necessary to clinically confirm diagnosis. There will also be hyper-resonance and decreased or 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 27.3). Treatment consists of immediate decompression, initially by rapid insertion of a large-bore cannula into the second intercostal space in the mid-clavicular line of the affected side, 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 ten­ sion 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 compres­ sion of the heart and obstruction of the venous return, leading to decreased filling of the cardiac chambers during diastole. 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 central venous pressure elevation, decline in arterial pres­ sure with tachycardia and muffled heart sounds. However, in cases in which major bleeding from other sites has taken place, the neck veins may be flat. A central line should be inserted, checking for a rising central venous pressure. A high index of suspicion and further diagnostic investigations will be needed to make the diagnosis is those cases that are not clinically obvious. These include an eFAST showing fluid in the pericardial sac. This is the most expeditious and reliable diagnostic tool, or chest radiography looking for an enlarged heart shadow.

TABLE 27.3  The ‘deadly dozen’ threats to life from chest injury. Immediately life threatening

Airway obstruction Tension pneumothorax Pericardial tamponade Open pneumothorax Massive haemothorax Flail chest

Potentially life threatening

Aortic injuries Tracheobronchial injuries Myocardial contusion Rupture of diaphragm Oesophageal injuries Pulmonary contusion

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Figure 27.3  Radiological appearance of a tension pneumothorax.

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CHAPTER 27  Torso trauma

Needle pericardiocentesis has been suggested. 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 cor­ rect immediate treatment of tamponade is operative, either via a subxiphoid window, or by open surgery (sternotomy or left thoracotomy), with repair of the heart in the operating theatre if time allows or otherwise in the emergency room. Summary box 27.4 Pericardial tamponade ●●

●●

●●

●●

The presentation is similar to a tension pneumothorax – deteriorating cyanosis, tachycardia and agitation eFAST is diagnostic and may also detect free fluid in the abdomen or pericardium 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 immediate equilibration between intrathoracic and atmospheric pressure. If the opening in the chest wall exceeds about two-thirds of the diameter of the trachea, then with each inspiratory cycle, air will be preferentially drawn through the defect, rather than through the trachea. Air accumulates in the hemithorax (rather than in the lung) with each inspiration, leading to profound hypoventilation on the affected side and hypoxia. If there is a valvular effect, increas­ ing amounts of air in the pleura will result in a tension pneu­ mothorax (see above). 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.

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 secondary to fractures of the ribs. In penetrating injury, a variety of viscera, both thoracic and abdominal (with blood leaking through a hole in the diaphragm from the positive pressure abdomen into the negative pressure thorax) may be involved. Accumulation of blood in a haemothorax can significantly compromise respiratory efforts, compressing the lung and

preventing adequate ventilation. Presentation is with haem­ orrhagic shock, flat neck veins, unilateral absence of breath sounds and dullness to percussion. The initial treatment con­ sists of correcting the hypovolaemic shock, insertion of an intercostal drain and, in some cases, intubation. Initial drain­ age of more than 1500 mL of blood or ongoing haemorrhage of more than 200 mL/h over 3–4 hours is generally considered an indication for urgent thoracotomy. Blood in the pleural space should be removed as com­ pletely and rapidly as possible to prevent ongoing bleeding, an empyema or fibrothorax later. Clamping a chest drain to tamponade a massive haemothorax is not helpful. The following points are important in the management of an open pneumothorax/haemothorax: ●● ●● ●● ●● ●● ●●

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; clot occlusion of a chest drainage tube may result in ‘no’ drainage, even in the presence of ongoing bleeding; a second drain is sometimes necessary (but see Tracheo­ bronchial injuries); a chest radiograph can help identify the presence of blood; physiotherapy and active mobilisation should begin as soon as possible.

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 typically also produces an underlying pulmonary contusion. The diag­ nosis is made clinically in patients who are not ventilated, not by radiography. To confirm the diagnosis the chest wall can be observed for paradoxical motion of a chest wall seg­ ment. On inspiration, the loose segment of the chest wall is displaced inwards and therefore less air moves into the lungs. On expiration, the segment moves outwards (paradoxical respiration). Voluntary splinting of the chest wall occurs as a result of pain, so mechanically impaired chest wall move­ ment and the associated lung contusion all contribute to the hypoxia. There is a high risk of developing a pneumothorax or haemothorax. The CT scan, with contrast to display the vascular structures and a 3-D reconstruction of the chest wall, is the gold standard for diagnosis of this condition. Traditionally, mechanical ventilation was used to ‘inter­ nally splint’ the chest, but had a price in terms of intensive care unit resources and ventilation-dependent morbidity. Currently, treatment consists of oxygen administration, ade­ quate analgesia (including opiates) and physiotherapy. If a chest tube is in situ, topical intrapleural local analgesia intro­ duced via the tube, can also be used. Ventilation is reserved for cases developing respiratory failure despite adequate anal­ gesia and oxygen. Surgery to stabilise the flail segment using internal fixation of the ribs may be useful in a selected group of patients with isolated or severe chest injury and pulmonary contusion.

in situis Latin for ‘in place’.

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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 haemodynamically stable. For this subgroup of immediate (a)

369

survivors, salvage is frequently possible if aortic rupture is identified and treated early. Aortic disruption should be clinically suspected in patients with gross asymmetry in systolic blood pressure (between the two upper limbs, or between upper and lower limbs), widened pulse pres­ sure and chest wall contusion. Erect chest radiography can also suggest thoracic aortic disruption, the most common radiological finding being a widened mediastinum (Figure 27.4). The diagnosis is confirmed by a CT scan of the medi­ astinum (Figure 27.5), or possibly by transoesophageal (b)

Widened mediastinum

Depressed left main bronchus

Figure 27.4  (a) Chest radiograph showing a widened mediastinum. (b) Aortogram showing aortic disruption.

3D reconstruction showing aortic disruption

2D reconstruction showing aortic disruption

Figure 27.5 Computed tomography scans showing aortic disruption.

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CHAPTER 27  Torso trauma

echocardio­ graphy, in unstable patients who cannot be moved to the scanner. Initially, management consists of control of the systolic arterial blood pressure (to less than 120 mmHg). There­ after, an endovascular intra-aortic stent (Figure 27.6) 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 compro­ mise 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. Bronchoscopy is diagnostic. Treatment involves intubation of the unaffected bronchus followed by operative repair. Referral to a trauma centre is advised.

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. 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 with 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 abdominal contents. Blunt injury to the diaphragm is usually caused by a com­ pressive force applied to the pelvis and abdomen. The dia­ phragmatic rupture is usually large, with herniation of the abdominal contents into the chest. Diagnosis of diaphrag­ matic rupture can easily be missed in the acute phase, and may only be discovered at operation, or through the presenta­ tion of complications. 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, ultra­ sound and diagnostic peritoneal 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. The thorax is at negative pressure and the abdomen is at positive pressure. A complication of a breach of the dia­ phragm is herniation of abdominal contents into the chest. This may present much later, and strangulation of any of the contents can then occur, with a high mortality rate. 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.

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 saliva, foods or fluids), subcutaneous or mediastinal emphy­ sema, pleural effusion, air in the perioesophageal space and unexplained fever. Mediastinal and deep cervical emphysema are evidence of an aerodigestive injury until proven other­ wise. 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 of any defect and drainage.

Pulmonary contusion

Figure 27.6  Aortic tear showing the presence of a stent.

Pulmonary contusion occurs more frequently following blunt trauma, usually associated with a flail segment or fractured ribs. This is a very common, potentially lethal injury and the major cause of hypoxaemia after blunt trauma. Following gunshot wounds, there is an area of contusion from the shock wave of the bullet. The natural progression of pulmonary contusion is worsen­ ing hypoxaemia for the first 24–48 hours. Chest radiographic

Charles Thomas Stent, 1805–1885, dentist, Brighton, UK.

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findings may be 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 administra­ tion, 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.

EMERGENCY THORACIC SURGERY Emergency thoracic surgery is an essential part of the arma­ mentarium of any surgeon dealing with major trauma. A timely surgical intervention for the correct indications can be the key step in saving an injured patient’s life. It is important to make a distinction between: ●● ●● ●●

immediate thoracotomy in the ED for the control of hae­ morrhage, cardiac tamponade or internal cardiac massage; emergency sternotomy for anterior mediastinal structures and heart; planned thoracotomy for definitive correction of the problem – this usually takes place in the more controlled envir­onment of the operating theatre.

The clinical decision as to whether a patient requires ED surgery or can be transferred to the operating room can be complex. It is far better to perform a thoracotomy in the operating room, 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 pres­ sure, there is no choice but to proceed immediately with a left anterolateral thoracotomy. In certain circumstances, when care is futile, it may not need to be performed at all. A resusci­ tation room thoracotomy following blunt trauma has limited indications and is rarely successful.

Emergency department thoracotomy or sternotomy 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. In certain situations, EDT is considered futile: ●● ●● ●●

CPR in the absence of endotracheal intubation for more than 5 minutes; CPR for more than 10 minutes (despite endotracheal intubation); blunt trauma when there have been no signs of life at the scene (see above).

The survival rates for EDT in patients with penetrating trauma in whom the blood pressure is falling despite adequate resuscitation are shown in Table 27.4.

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371

TABLE 27.4  Survival rates for thoracotomy in patients with penetrating trauma. Blood pressure despite resuscitation

Survival (%)

>60 mmHg

60%

>40 mmHg

30%

100 mL of free blood; however, it is very operator dependent and, especially if the patient is very obese or the bowel is full of gas, it may be unreliable. Hollow viscus injury and solid organ injury are difficult to diagnose, even in experienced hands, as small amounts of gas or fluid are difficult to assess, and eFAST a low sensitivity (29–35%) for organ injury without haemoperitoneum. eFAST is also unreliable for excluding injury in penetrating trauma. If there is doubt, the eFAST examination can be repeated.

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Summary box 27.5 Utilisation of eFAST ●● ●● ●● ●● ●●

●●

Detects free fluid in the abdomen or pericardium Will not reliably detect less than 100 mL of free blood Does not directly identify injury to hollow viscus Cannot reliably exclude injury in penetrating trauma May need repeating or supplementing with other investigations Is unreliable for assessment of the retroperitoneum

Diagnostic peritoneal lavage Diagnostic peritoneal lavage (DPL) is a test used to assess the presence of blood or contaminants 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 cau­ dally and posteriorly. The cannula is aspirated for blood (>10mL is deemed as positive) and, following this, 1000mL of warmed Ringer’s lactate solution is allowed to run into the abdomen and is then drained out via the same route. The presence of >100 000 red cells/μL or >500 white cells/μL is deemed positive (this is equivalent to 20mL of free blood in the abdominal cavity), as is the presence of vegetable fibre or a raised amylase level. In penetrating trauma, a minimum of one-tenth of the above would be regarded as evidence of peri­ toneal penetration or intraperitoneal injury. 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 eFAST (see above), it remains the standard in many institutions where eFAST is not available or is unreliable. DPL is especially use­ ful in the hypotensive, unstable patient with multiple injuries as a means of excluding intra-abdominal bleeding.

373

Laparoscopy Laparoscopy or thoracoscopy may be a valuable screening investigation in stable patients with penetrating trauma, to detect or exclude peritoneal penetration and/or diaphrag­ matic injury. Laparoscopy may be divided into: ●● ●● ●●

Screening: used to exclude a penetrating injury with breach of the peritoneum. Diagnostic: finding evidence of injury to viscera. Therapeutic: used to repair the injury.

In most institutions, evidence of penetration requires a lap­ arotomy to evaluate organ injury, as it is difficult to exclude all intra-abdominal injuries laparoscopically. When used in this role laparoscopy reduces the non-therapeutic laparotomy rate. There is no place for laparoscopy in the unstable patient.

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 (Figure 27.8). The liver is usually compressed between the impacting object and the rib cage or vertebral column. Most injuries are relatively minor and can be man­ aged non-operatively. Penetrating trauma to the liver is relatively common. Bul­ lets 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 pene­ trating wounds require operative management and 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.

Computed tomography scan CT has become the ‘gold standard’ for the intra-abdominal diagnosis of injury in the stable patient. The scan can be per­ formed 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 intraperitoneal injury. The following points are important when performing CT: ●● ●● ●●

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.

Figure 27.8  Compression injury to the liver, bursting the liver substance.

Sydney Ringer, 1835–1910, Professor of Clinical Medicine, University College Hospital, London, UK.

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Injury in which there is a suggestion of a vascular compo­ nent should be reimaged, as there is a significant risk of the development of subsequent ischaemia, false aneurysms, arte­ riovenous fistulae or haemobiliary fistula. It is advised that all patients should be rescanned prior to discharge. Liver injury can be graded and managed using the Amer­ ican Association for the Surgery of Trauma (AAST) Organ Injury Scale (OIS) (www.aast.org/injury).

Management The operative management of liver injuries can be sum­ marised as ‘the four Ps’: ●● ●● ●● ●●

push; Pringle; plug; pack.

penetrating injuries of the liver, unless haemostasis cannot be controlled by other means. 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% 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. 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 27.6 Liver trauma

At laparotomy the liver is reconstituted and bleeding is controlled by direct bimanual compression to achieve its normal architecture as best as possible (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 27.9). This has the effect of reduc­ ing 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 using silicone tubing or a Sengstaken– Blakemore tube, and, after controlling any arterial bleeding, the liver can then be packed (see Damage control surgery, below). Bleeding points should be controlled locally when possi­ ble, and such patients if required, subsequently undergo subse­ quent angioembolisation. It is not usually necessary to suture

●● ●●

●● ●●

●●

●●

Blunt trauma occurs as the result of direct compression Penetrating trauma of the upper abdomen or lower thorax can damage the liver CT scanning is the investigation of choice 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 (which should be stented) Closed suction drainage should always be used

Biliary injuries Isolated traumatic biliary injuries are rare and occur mainly from penetrating trauma, often 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, or even ligated.

Spleen

Hepatic artery

Portal vein

Figure 27.9  The Pringle manoeuvre.

Splenic injury occurs from direct blunt trauma. Most iso­ lated splenic injuries, especially in children, can be managed non-operatively. However, in adults, especially in the pres­ ence of other injury or physiological instability, laparotomy 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. In certain situations, selective angioembolisation of the spleen can play a role. Following splenectomy there are significant, though tran­ sient, changes to blood physiology. The platelet and white count rise and may mimic sepsis. Innoculation against Pneumococcus is advisable within 2–3 weeks, by which time the patient’s immune system has recovered.

James Hogarth Pringle, 1863–1941 (Australian born), surgeon, The Royal Infirmary, Glasgow, UK. Robert William Sengstaken, 1923–1978, surgeon, Garden City, NY, USA and Arthur Hendley Blakemore, 1897–1970, Associate Professor of Surgery, The College of Physicians and Surgeons, Columbia University, New York, NY, USA, designed a tube with two in-built balloons for the treatment of oesophageal varices. The tube was passed and the distal balloon inflated. The tube was drawn backwards until the distal balloon was held at the oesophageal hiatus. The proximal balloon was inflated, allowing the tamponade of any varices in the distal oesophagus.

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Pancreas

Small bowel

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 accu­ rate diagnosis. Amylase or lipase estimation is insensitive. In penetrating trauma, injury may only be detected during lap­ arotomy. Classically the pancreas should be treated with conserva­ tive surgery and closed suction drainage. Injuries are treated according to the OIS system of the AAST. Injuries to the pancreatic body to the left of the superior mesenteric vessels and to the tail are treated by closed suction drainage alone, 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 pancre­ atectomy may be necessary. The pylorus can be temporarily closed (pyloric exclusion) in association with a gastric drain­ age procedure, to minimise pancreatic enzyme stimulation by gastric juice or distension. A Whipple’s procedure (pancre­ aticoduodenectomy) is rarely needed and should not be per­ formed 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.

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. Penetrating trauma is also a common cause of injury. Small bowel injuries need urgent repair. Haemorrhage control takes priority and these wounds can be temporarily controlled with simple sutures. In blunt trauma with mesen­ teric vessel damage, the bowel ischaemia that results will dictate the extent of a resection. Resections should be care­ fully 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 lowenergy wounds, primary repair can be performed, whereas more destructive wounds associated with military type weapons require resection and anastomosis. Damage control ‘clip and drop’ of damaged or resected bowel may be necessary.

Stomach Most stomach injuries are caused by penetrating trauma. Blood presence is diagnostic if found in the nasogastric tube, in the absence of bleeding from other sources. 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 Duodenal injury is frequently associated with injuries to the adjoining pancreas. Like the pancreas, the duodenum lies ret­ roperitoneally and so injuries are hidden, discovered late or at laparotomy performed for other reasons. CT is the diagnostic modality of choice. The only sign may be gas or a fluid collec­ tion in the periduodenal tissue, and leakage of oral contrast, administration of which may improve accuracy of diagnosis. Smaller injuries can be repaired primarily. The first, third and fourth parts of the duodenum behave like small bowel, and can be repaired in the same fashion. The second part of the duodenum is fixed to the head of the pancreas with a common blood supply, and may have a poorer blood sup­ ply compared to the remainder. Major trauma, especially if the head of the pancreas is simultaneously injured, should be treated as part of a damage control procedure and be referred for definitive care.

375

Colon Injuries to the colon from blunt injury are relatively infre­ quent, and are more frequently a penetrating injury. If rel­ atively little contamination is present and the viability is satisfactory, such wounds can be repaired primarily. If, how­ ever, there is extensive contamination, the patient is physi­ ologically unstable or the bowel is of doubtful viability, then the bowel can be closed off (‘clip and drop’). A defunctioning colostomy can be formed later or the bowel reanastomosed once the patient is stable.

Rectum Only 5% 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 intestinal or rectal injury. These inju­ ries are often associated with bladder and proximal urethral injury. With intraperitoneal injuries, the rectum is managed as for colonic injuries. Full-thickness extraperitoneal rectal inju­ ries 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 no longer used.

Renal and urological tract injury In the stable patient, CT scanning with contrast is the inves­ tigation of choice. For assessment of bladder injury a cystogram should be performed. A minimum of 300 mL of contrast is instilled into the bladder via a urethral catheter. The large volume is

Allen Oldfather Whipple, 1881–1963, Valentine Mott Professor of Surgery, The College of Physicians and Surgeons, Columbia University, New York, NY, USA. Henri Albert Charles Antoine Hartmann, 1860–1952, Professor of Clinical Surgery, Faculty of Medicine, The University of Paris, Paris, France.

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essential because a small volume may not distend the bladder enough to produce a leak from a small bladder injury once the cystic muscle is contracted. It is important to assess the films as follows: ●● ●●

1

two views – AP and lateral (and sometimes oblique); two occasions – full and postmicturition.

2

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 trauma. Most ureters can be repaired or diverted if necessary, or may even be ligated as part of Damage control procedures. Intraperitoneal rupture of the bladder, usually from direct blunt injury, will require surgical repair. Extraperitoneal rup­ ture is usually associated with a fracture of the pelvis and will heal with adequate urine drainage via the transurethral route. Suprapubic drainage is reserved for when this is not possible.

2

3

Figure 27.10 The zones of the retroperitoneum. Zone 1: central; zone 2: lateral; zone 3: pelvic.

Summary box 27.7 Injuries to structures in the abdomen ●●

●● ●●

●●

●●

●●

In children, splenic injury can be managed non-operatively in most cases, but not if haemodynamically unstable Duodenal injuries are often associated with pancreatic trauma Bowel injuries need urgent definitive repair, or isolation using resection or by stapling Rectal injuries may be best managed initially with a diverting colostomy Kidney and urinary tract injury is best diagnosed with enhanced CT scanning Intraperitoneal bladder tears need formal repair and drainage

Retroperitoneum Injury to the retroperitoneum is often difficult to diagnose, especially in the presence of other injury, when the signs may be masked. Diagnostic tests (such as ultrasound and DPL) may be negative. The best diagnostic modality is CT, but this requires a physiologically stable patient. The retroperitoneum is divided into three zones (Figure 27.10) for the purposes of intraoperative management: In blunt trauma: ●●

●●

●●

Zone 1 (central): central haematomas should always be explored, once proximal and distal vascular control has been obtained. Zone 2 (lateral): lateral haematomas should only be explored if they are expanding or pulsatile. They are usu­ ally renal in origin and can be managed non-operatively, though they may sometimes require angioembolisation. Zone 3 (pelvic): as with zone 2, these should only be explored if they are expanding or pulsatile. Pelvic haema­ tomas are exceptionally difficult to control and, whenever possible, should not be opened; they are best controlled with compression or extraperitonea packing, and if the bleeding is arterial in origin, with angioembolisation.

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In penetrating trauma, every injury should be explored for damage to structures along the wound track (e.g. ureter), unless preoperative investigation allows non-surgical man­ agement of the injury.

THE PELVIS Although mortality following severe pelvic fractures has decreased dramatically with better methods of controlling haemorrhage, these patients still represent a significant chal­ lenge to every link of the treatment chain. Mortality rates exceeding 40% have recently been reported. Further, pel­ vic bleeding as one of the ‘hidden bleeding sources’ is still underestimated or missed, as retrospective chart analyses of potentially preventable deaths have revealed. Extreme force is required to disrupt the pelvic ring, and associated injuries and extrapelvic bleeding sources are common (up to 50% of cases). The haemodynamically unstable patient with severe pelvic fracture has a 90% risk of associated injuries, and a 30% risk of intra-abdominal bleeding. To save these patients, three questions need to be addressed: ●● ●● ●●

Is the patient at high risk of massive bleeding? Where is the source of the bleeding? How to stop the bleeding?

Anatomy The surgical anatomy of the pelvis is a key to the understand­ ing of pelvic injuries. ●●

●●

The pelvic inlet is circular, a structure that is immensely strong, but routinely gives way at more than one point should sufficient force be applied to it. Therefore, iso­ lated fractures of the anterior or posterior pelvic ring are uncommon. The forces required to fracture the pelvic ring do not respect the surrounding organ systems.

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PART 4 | TRAUMA The pelvis

●●

●●

●●

●●

●●

The pelvis has a rich collateral blood supply, especially across the sacrum and posterior part of the ileum. The cancellous bone of the pelvis also has an excellent blood supply. Most pelvic haemorrhage emanates from venous injury and fracture sites. However, in the haemodynam­ ically unstable patient with severe pelvic injury, arterial bleeding is more frequent. Important for the treatment is that the surgeon has to deal both with arterial and venous bleeding. Postmortem examination has shown that the extrapelvic peritoneal space can accommodate more than 3000mL. However, in the case of a severe pelvic fracture where the retroperitoneal compartment is disrupted and the external bony barrier is not stable, haematoma may extend upwards towards the mediastinum (‘chimney effect’) or downwards into the medial thigh in case of rupture of the pelvic floor. All iliac vessels, the sciatic nerve roots (including the lum­ bosacral nerve) and the ureters cross the sacroiliac joint; disruption of this joint may cause severe haemorrhage and sometimes cause arterial obstruction of the internal iliac artery and sciatic nerve palsy. Injuries to the ureters are rare. The pelvic viscera are suspended from the bony pelvis by condensations of the endopelvic fascia. Shear forces acting on the pelvis will transmit these to pelvic viscera, leading to avulsion and shearing injuries. The pelvis also includes the acetabulum, a major structure in weight transfer to the leg. Inappropriate treatment will lead to severe disability.

Classification Pelvic ring fractures can be classified into three types, using the Tile classification (for subtypes and other classifications see Further reading), based on the severity of the fracture (and reflecting the energy required to cause it) (Figure 27.11). However, no fracture pattern can exclude significant haemorrhage.

Type A Type A are the most common fractures and are completely stable. They result from lateral compression, which causes compression fractures of the pubic rami or compression frac­ ture of the sacrum posteriorly.

Type B These fractures are partially stable, and there is disruption of the anterior pelvis and partial disruption of the posterior pel­ vis. The pelvis can open and close ‘like a book’, but because the sacroiliac ligaments remain intact, there is no vertical displacement. Internal or external stabilisation is required. Blood loss can be significant.

Type C This fracture is completely unstable. Both anterior pelvis and the entire posterior pelvic complexes are disrupted and the

377

Type A

Type B

Type C Figure 27.11  Tile classification of fractures of the pelvis.

disrupted pelvic bones are free to displace horizontally and vertically. In both type B and type C pelvic injuries, there is a high risk of associated abdominal injuries (bowel perforation or mesenteric laceration) and rupture of the diaphragm.

Clinical examination Pelvic fractures should be easily identified if ATLS guidelines are followed (i.e. clinical palpation and compression of the pelvic brim from sacroiliac joint to pubic symphysis, and a routine chest and pelvic radiograph for any blunt injury in a patient unable to walk). Clinical examination may reveal instability. Any instability felt indicates the presence of major pelvic fracture, associated with life-threatening blood loss, and requires appropriate measures. The absence of clinical instability does not, however, preclude an unstable pelvic fracture. One-third of such trauma victims with pelvic ring fractures present with circulatory instability on arrival. Inspection of the skin may reveal lacerations in the groin, perineum or sacral area, indicating an open pelvic fracture, the result of gross deformation. Evidence of perineal injury or haematuria mandates radiological evaluation of the urinary tract from below upwards (retrograde urethrogram followed by cystogram or CT cystogram and an excretory urogram, as appropriate) when the physiology allows. Inspection of the urethral meatus may reveal a drop of blood, indicating ure­ thral damage.

Marvin Tile, b.1933, orthopaedic surgeon, Sunnybrook Medical Centre, Toronto, Canada.

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Inspection of the anus may reveal lacerations to the sphinc­ ter mechanism. Rectal examination may reveal blood in the rectum and/or discontinuity of the rectal wall, indicating a rectal laceration. In male patients, the prostate is palpated; a high-riding prostate indicates a complete urethral avulsion. A full neurological examination is performed of the perineal area, sphincter mechanism and femoral and sciatic nerves.

Diagnosis Radiograph Examination of a plain radiograph of the pelvis requires an understanding of the mechanism of injury and a decision on the stability of the pelvic rim. An open book type mechanism causes one or both ilea to rotate externally (opening, like a book). A lateral compres­ sion mechanism causes the pelvis to collapse. An ‘open-book fracture’ is seen as a widening of the pubic symphysis or wid­ ening at the site of a fracture in the pubic ramus. Not only is there disruption of the bony pelvis, but also tearing of the pel­ vic floor and thus the pelvic venous plexus is at risk. The more unstable the pelvis, the more likely the structures are to be damaged. When the pelvis collapses from a lateral compres­ sion injury, the pubic bones usually fracture. Displacement of the anterior pelvis by greater than 2 cm indicates at least partial instability. A vertical shear disruption of the sacroiliac joint, with apparent shortening of the limb on the affected side implies significant energy of injury. FAST may be unreliable as it does not localise intraabdominal bleeding in these patients. CT is the diagnostic modality of choice in the haemo­ dynamically stable patient, and CT angiography is particu­ larly helpful to provide details of both the anatomy of the facture, as well as details of the origin of the bleeding (venous or arterial).

Management The treatment of bleeding is to stop the bleeding! The priorities for resuscitating patients with pelvic frac­ tures are no different from the standard. These injuries can produce a real threat to the circulation, and management is geared toward controlling this threat. Initial management requires the use of a compression binder or a sheet, applied around the true pelvis at the level of the greater trochanters (‘reduce the pelvic volume’), a potentially lifesaving proce­ dure that has to be done in the emergency room. 85% of bleeding originating from the pelvis is of venous ori­ gin and can be controlled by non-operative means, including compression either by binding or external fixator, or by extra­ peritoneal packing (i.e. packing the loose space between the bony wall of the pelvis and the peritoneum) to compress the pelvic veins. If other sources of bleeding have been ruled out, the extraperitoneal pelvic packing is done without entering the peritoneal cavity. This may be combined with external fixation. If the bleeding is of arterial origin, interventional angio­ embolisation is the next choice for bleeding control. The techniques for bleeding control (compression, packing, fix­ ation and angioembolisation) do not exclude each other but

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rather may complement each other. Persistent bleeding after packing may require angioembolisation and vice versa. Severe pelvic injuries require a multidisciplinary team approach. If adequate orthopaedic experience is unavailable, consideration should be given towards early transfer of this patient to an institution with the necessary expertise. If the source of the bleeding is in doubt or FAST/CT results are positive, showing a significant amount of blood in the peritoneal cavity, concurrent intra-abdominal injury cannot be excluded, and it is wise to perform an exploratory laparotomy to treat or rule out intra-abdominal bleeding.

Summary In summary, a haemodynamically normal patient can be safely transferred for stabilisation of unstable fractures within hours after injury and following control of the associated damage. Summary box 27.8 Pelvic injury ●●

●● ●●

●●

●●

●●

Associated injuries can only be managed once the patient is haemodynamically stable Decision on the stability is of paramount importance Procedures for damage control may be the only available option External stabilisation of the pelvic ring is the basis of all treatment If necessary, further bleeding control can be achieved either by angioembolisation or extraperitoneal packing Most associated injuries can be managed once the patient is haemodynamically stable

DAMAGE CONTROL Following major injury, protracted surgery in the physiologi­ cally unstable patient can in itself prove fatal. Patients with the ‘deadly triad’ (hypothermia, acidosis and coagulopathy) are those at highest risk. ‘Damage control’ or ‘damage lim­ itation surgery’ is a concept that originated from naval ship­ building strategy, whereby ships were designed so that the damage was kept ‘local’ and which allowed only the minimal repairs needed to prevent it from sinking, while definitive repairs waited until it had reached port. The technique has been adopted following major trauma, and includes initial care and resuscitation (damage control resuscitation) and the surgical correction of the injury (damage control surgery). The minimum amount of surgery needed to stabilise the patient’s condition may be the safest course until the physi­ ological derangement can be corrected. Damage control sur­ gery is restricted to only two goals: ●● ●●

stopping any active surgical bleeding; controlling any contamination.

Once these goals have been achieved then the opera­ tion is suspended and the abdomen temporarily closed. The patient’s resuscitation then continues in the intensive care unit, where other therapeutic interventions can take place.

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PART 4 | TRAUMA Damage control

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.

TABLE 27.7  Indications for damage control surgery. Anatomical

Inability to achieve haemostasis Complex abdominal injury, e.g. liver and pancreas

Damage control resuscitation

Combined vascular, solid and hollow organ injury, e.g. aortic or caval injury

The concept of damage control has been broadened to include the techniques used in resuscitation as well as in surgery. The time in the ED is minimised and the majority of resuscita­ tion of the patient is carried out in the operating room and not in the resuscitation bay (Table 27.6). The resuscitation is individualised through repeated point of care testing, of haemoglobin, acidosis (pH and lactate) and 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 hypo­ thermia in these serious injuries are predicted and attempts are made to avoid them rather than react to them.

Inaccessible major venous injury, e.g. retrohepatic vena cava

Damage control surgery The decision whether damage control surgery is the appropriate course should be made early (Table 27.7) 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 con­ trol and limitation of contamination, achieved using a range of abbreviated techniques including simple ligation of bleed­ ing vessels, shunting of major arteries and veins, drainage, temporary stapling 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 abdominal fluid. This technique is known as the ‘Vacpac’ or ‘Opsite® sandwich’ (Figure 27.12). 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 recon­ struction 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.

379

Demand for non-operative control of other injuries, e.g. fractured pelvis Anticipated need for a time-consuming procedure Physiological (decline of physiological reserve)

Temperature 60 s >10 units blood transfused Systolic blood pressure 60 min

Environmental Operating time >60 min (core temperature loss in usually 2°C/h) Inability to approximate the abdominal incision Desire to reassess the intra-abdominal contents (directed relook)

(a)

Outer layer (Opsite®/Ioban®)

Inner layer (Opsite®/Ioban®) Abdominal swab/ cotton drape

Abdominal content

Suction drains (b)

TABLE 27.6  The stages of damage control surgery. Stage I

Patient selection

II

Control of haemorrhage and control of contamination

III

Resuscitation continued in the intensive care unit

IV

Definitive surgery

V

Abdominal closure

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Figure 27.12  (a) Diagram showing temporary skin closure in damage control. (b) Abdominal closure following damage control surgery showing an Opsite® closure.

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CHAPTER 27  Torso trauma

The abdomen is closed as soon as possible, bearing in mind the risks of abdominal compartment syndrome (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 sur­ gical 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 pro­ cedures available, such as staplers, to minimise the operative time. Often, damage control surgery is the definitive surgery. The indications and techniques for emergency thoracic surgery 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 that are the main tasks. Subsequent definitive management can be carried out at a later stage. Summary box 27.9 Damage control ●●

●●

●●

●●

Resuscitation is carried out in the operating room using biologically active fluids (i.e. blood) – damage control resuscitation (DCR) 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

ABDOMINAL COMPARTMENT SYNDROME AND THE OPEN ABDOMEN Raised intra-abdominal pressure has far-reaching conse­ quences for the patient; the syndrome that results is known as ACS. ACS is a major cause of morbidity and mortality in the critically ill patient and its early recognition is essential (Table 27.8). In all cases of abdominal trauma in which the develop­ ment of ACS in the immediate postoperative phase is consid­ ered a risk, the abdomen should be left open and managed as for damage control surgery.

INTERVENTIONAL RADIOLOGY 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 follow­ ing demonstration of ongoing bleeding in splenic and renal injury is a valuable technique.

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TABLE 27.8  Effect of raised intra-abdominal pressure on individual organ function. Organ

Effect

Renal

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

NON-OPERATIVE MANAGEMENT Non-operative management is generally 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 oper­ ated patients.

ANTIBIOTICS IN TORSO TRAUMA There is no level 1 evidence to recommend the use of antibi­ otics for the insertion of chest drains. However, prophylactic antibiotics prior to surgery should be used in all cases of pen­ etrating abdominal trauma. Unless there is major contamina­ tion, a single dose is sufficient.

FURTHER READING American Association for the Surgery of Trauma. Organ Injury Scaling System. Available online at: http://www.aast.org (accessed February 2016). American College of Surgeons. Advanced trauma life support course manual for doctors, 9th edn. Chicago: American College of Surgeons, 2015. Boffard KD (ed). Definitive surgery of trauma care, 4th edn. London: Taylor and Francis, 2015. Eastern Association for the Surgery of Trauma. Guidelines for prac­ tice management: evidence-based guidelines. Available online at: http//:www.east.org (accessed February 2016). Mattox LK, Moore EE, Feliciano DV (eds). Trauma, 7th edn. New York: McGraw Hill, 2013. Tornetta P, Court-Brown CM, Heckman JD et al. Rockwood and Green’s fractures in adults, 8th edn. Lippincott Williams and Wilkins, 2014. World Society for Abdominal Compartment Syndrome. Abdominal compartment syndrome. Available online at: http//:www.wsacs.org (accessed February 2016).

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Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & Love Bailey & 28Love 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

INTRODUCTION

into the common anatomical injury patterns. For example, a head on collision between two cars each travelling at 40 miles per hour coming to a dead stop should be interpreted by the history taker as a rapid deceleration injury, which then allows anticipation of likely injuries, such as rupture of the aortic arch. Similarly, a fall on the outstretched hand might be associated with wrist, elbow, shoulder and clavicular injuries. Following the history of the presenting complaint, it is important to collect information beyond that of the injury and the AMPLE mnemonic is an abbreviated system taught in ATLS.

In several chapters the importance of life-threatening trauma is emphasised, but numerically for every patient that dies following a traumatic event, there are three that are left with a lifelong functional impairment. Appropriate treatment of extremity trauma is important to return the patient to optimal function as quickly and as safely as possible. The management of extremity trauma is step-wise and involves initially saving the patient’s life by the identification and treatment of life and limb threatening injuries first, according to the Advanced Trauma Life Support (ATLS) principles. Treatment depends on injury specific factors, patient factors and surgeon factors, including the resources available. It is imperative for the clinician to involve the patient in the decision making process when it comes to the choice of treatment for that individual. Moreover, treatment priorities, functional demands and risk versus benefit vary from individual to individual.

DIAGNOSIS The diagnosis of extremity trauma begins with the taking of a pertinent history followed by focussed physical examination and appropriate special tests.

History It is important to ascertain the mechanism of injury and the amount of force involved in the injury. Take time to gather sufficient detail in order to do this. Certain injury mechanisms result in classical injury patterns; for example, electrocution or seizure activity may lead to a posterior dislocation of the shoulder. In your mind translate the mechanism of injury

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fractures

•• The range of available treatments •• How to select an appropriate treatment

A: Allergies M: Medication – important to ask about anticoagulant and antiplatelet therapies, corticosteroid use and any possible immunosuppressive treatment P: Past medical and surgical history – has the patient had an anaesthetic in the past and were there any complications L: Last time – something to eat or drink E: Events – events that led to the injury In the multiply injured patient or patients with altered levels of consciousness, gain as much collateral history as possible. Listen to the account of pre-hospital personnel; for example, the amount of cabin intrusion in a vehicle or whether a collision was head on or a side on.

Examination An initial general examination, including vital signs and general assessment, should be conducted. Is this an isolated injury or do you need to start right at the beginning, considering the A, B, C approach as advocated by ATLS? Examination of the individual extremity only begins once you are sure the patient is stable and life- and limb-threatening conditions have been excluded.

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It is crucial to undertake a thorough top to toe evaluation in the secondary survey. Often the minor extremity injuries are missed (Figure 28.1) and can cause significant long-term problems (Table 28.1). A top to toe evaluation is is achieved by a systematic approach (see Chapter 31 and Apley’s system of orthopaedics and fractures [Further reading]) to the injured extremity: ●● ●● ●● ●● ●●

look; feel; move (active and passive); special tests; special investigations.

TABLE 28.1  Extremity injuries that 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

(a)

Ensure you examine the joint above and the joint below the site of injury. Consider the events and mechanism of injury and examine the areas that could possibly be affected. For example, a patient who falls from a height may fracture the calcaneus, which is an obvious diagnosis with a very swollen hindfoot and extremely tender heel. The concomitant lumbar spine fracture may not become evident until a few days later when the distracting pain in the heel starts to subside.

Look

(b)

It is important to look at the whole limb, back and front, noting any localised swelling, bruising and any obvious deformity. A shortened externally rotated leg in an older patient suggests a fracture of the proximal femur. A slightly flexed, adducted internally rotated leg might suggest a posterior dislocation of the hip. Any break in the skin or abrasion needs to be noted and the treating orthopaedic surgeon informed, even if you do not think it communicates with the fracture. A graze over the knee in a closed tibial fracture may preclude intramedullary nailing until the wound has healed over, or perhaps an alternative treatment may have to be considered. Ideally a photograph (with appropriate consent) should be taken to document the injury and obviate the need for repeated manipulation of the dressings (see Open fractures). Note the colour of the limb and the degree of general swelling. A compartment syndrome may still be present even when a limb does not appear to be very swollen (see Compartment syndrome), but if it is grossly swollen, note, document and pass on the information. Look for pre-existing scars; a scar at the back of the elbow or over the cubital tunnel might signify an anterior transposition of the ulna nerve. Scars might signify previous metalwork that remains in situ or has been removed in the past.

Feel Figure 28.1  (a) Missed dislocation of metatarsophalangeal joint of the little toe, picked up at 8 weeks. (b) Initial trauma computed tomography angiogram. In retrospect, on close inspection the dislocation is visible on the angiogram; do not be distracted by the obvious femoral shaft fracture.

Start gently examining the limb away from the zone of obvious injury, gaining the patients trust and gathering as much information as possible before and without causing the patient pain or discomfort. Feel for bony tenderness and note

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.

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the degree of swelling and tenseness of the compartments. It should be noted that it is not possible to exclude a compartment syndrome based on how tense the limb feels. The deep posterior compartment of the lower leg cannot be felt when palpating the skin. The characteristic crepitus of subcutaneous air can be felt in the setting of open fractures, air jet injuries and around the chest in the presence of a pneumothorax. The examiner should feel for pulses and assess capillary return (see Neurovascular examination) as well as feeling for temperature changes.

Move Movement as part of the examination should once again be approached carefully and without causing the patient pain and discomfort. Two types of movement can be assessed: 1 active – active movement is movement initiated and maintained by the patient; 2 passive – passive movement is when the examiner moves the limb.

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Laceration or rupture of major vessels may result in lifeand limb-threatening injury and should be dealt with as an emergency (see ATLS guidelines). Complete laceration or occlusion of a major vessel is obvious and seldom missed. In contrast, occult vessel injuries must be considered and actively excluded. In 30% of knee dislocations (tibio–femoral dislocation) a vascular injury will occur (Figure 28.2). The presence of palpable pulses does not exclude a significant vascular injury and an intimal flap may develop, progress and thrombose over time. Repeated evaluation is necessary, before and after any intervention (manipulation/cast). In injuries commonly associated with vascular injury, such as knee dislocations, occult injury should be actively excluded with an angiogram. If an angiogram is not performed, repeated thorough vascular evaluation of the limb should be undertaken for the first 24–48 hours. (a)

Special tests There are often special tests to detect injury in precise anatomical locations and many are described elsewhere in the book; for example, looking for a ruptured Achilles tendon by placing the patient prone with the foot over the edge of the bed and squeezing the calf; plantarflexion of the foot and ankle then suggests the Achilles tendon is intact. The examiner should be aware of gravity simulating active movements. For example, a leg lying flat, fully extended on the couch does not mean the extensor mechanism of the knee is intact. In all knee injuries make sure the patient can actively straight leg raise and get their leg off the couch. Similar pitfalls exist in the upper limb with gravity straightening the elbow. In order to assess triceps function and elbow extension, ensure the patient can actively extend against resistance from the examiner or against gravity. Beware of trick movements. Patients with a complete rupture of the quadriceps can still walk with the leg locked in full to slight hyperextension by using the iliotibial band. Patients with complete rupture of the Achilles tendon can still actively plantar flex the foot and ankle using the long toe flexors.

(b)

Neurovascular examination This is an important part of extremity examination and summary terms such as ‘neurovascularly intact’ are best avoided. It is preferable to clearly document the examination performed and its findings, along with a conclusion about the function of the particular neurological or vascular anatomy tested. On occasion you may not be able to examine all movements due to injury or casts. It is important to examine and document findings before and after any manipulation or cast application, to ensure no change. A radial nerve palsy in association with a humeral shaft fracture that occurs at the time of injury may be treated expectantly. If, however, radial nerve function is lost after application of a cast or brace, the nerve should be explored. Most peripheral nerves have a motor and sensory component; document both sensibility and motor function.

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Figure 28.2  (a) Initial anterior tibio–femoral dislocation. (b) Postreduction computed tomography angiogram showing complete blockage of the popliteal artery with reconstitution distally from a collateral blood supply.

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Investigations

(a)

The mainstay of extremity trauma investigation remains radiography of the affected limb to see if there is a bony injury. However, this is not the sole investigation available.

Haematological investigations Simple haematological investigations are seldom useful in the evaluation of single limb injury. In the polytrauma patient a full blood count, serum biochemistry, clotting factor and creatinine kinase may be useful. A blood gas, including PH, base excess and lactate, can be useful to show the severity of the injury and the response to resuscitation.

Ultrasound Ultrasound is very useful to define soft tissue injuries. Fractures of the bones can be visualised on ultrasound but generally it is reserved for the soft tissues. One limitation of ultrasound is the variability depending on the experience of the sonographer.

(b)

Radiography Radiographs are the mainstay in the initial evaluation of suspected extremity trauma. The rule of 2’s should be remembered: ●●

●● ●●

●●

2 views – ensure acquisition of 2 views in orthogonal planes to avoid missing a fracture out of plane on the first radiograph view. For shoulder injuries ensure at least an AP and axillary or modified axillary view (Figure 28.3); 2 joints – radiographs are required of the joint above and the joint below the fracture; 2 occasions – sometimes the fracture may not be initially visible; a second series of radiographs should be undertaken after 10–14 days if suspicion of bony injury persists. The classic injury here is a scaphoid fracture. If initial scaphoid views are normal, consider repeating them 10–14 days later, if pain and tenderness in the anatomical snuff box persists; 2 sides – in paediatric injuries it can be useful to consider a radiograph from the opposite and uninjured side if doubt exists. With improved access to atlases of normal variants this is less important.

(c)

Computed axial tomography Computed axial tomography (CT) is very good for characterising the bony anatomy of injuries, allowing for multiplanar reconstruction of injury anatomy and providing other 3D information. It is very useful for periarticular injuries, where the exact characterisation of the bony injury is essential. Surface volume rendering is a useful addition allowing for easier visualization of the injury (see Figure 28.1b). CT angiography (see Figure 28.2b) may be added, providing information on the vascular anatomy. One disadvantage of CT is the dose of radiation involved.

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Figure 28.3  Radiographic series of the same patient demonstrating the value of 2 views in 2 planes and the true value of the axillary view in shoulder trauma. (a) Anteroposterior radiograph of the shoulder, initially reported as normal. (b) Lateral scapula radiograph, initially reported as normal; humeral head slightly posteriorly directed. (c) Axillary view – true value of axillary view shown with obvious posterior dislocation of the glenohumeral joint.

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Magnetic resonance imaging Magnetic resonance imaging (MRI) provides 3D information without the radiation involved in CT. It provides useful information, particularly about the soft tissues. MRI can provide information on the blood supply to the bone; for example, avascular necrosis of the proximal pole of the scaphoid. One disadvantage of MRI is the time taken to acquire the image; patients suffering from claustrophobia find the experience traumatic. Another issue is that the magnetic field may be disrupted by non-ferrous metal and the presence of ferrous metal contraindicates an MRI. MRI angiography can also be performed providing information about the vascular anatomy.

Nuclear medicine scans Technetium 99 nuclear medicine scans register osteoblastic activity and may be used to demonstrate occult fractures; for example, an undisplaced scaphoid fracture. Summary box 28.1 History, examination and investigations ●● ●● ●● ●● ●●

●●

Follow a systematic approach History requires sufficient detail of injury History can be organised in the AMPLE format Examination follows look, feel, move, special tests approach Investigations will include radiographs with rule of 2s observed Selective use of special investigations can help diagnosis

DESCRIPTION AND CLASSIFICATION OF THE INJURY Soft tissue injury There are several classification systems for soft tissue injuries, the Tscherne classification for closed injuries, the Gustilo and Anderson for open injuries (Table 28.2) and the Ganga classification of severe open injuries. The first step of soft tissue injury characterisation is to decide if this is an open or closed fracture. An open fracture being any fracture where the fracture haematoma communicates with a breach in the epithelial lining, not just skin. For example, an open pelvic fracture may communicate with the vagina or rectum and a mandibular fracture through the mucosa of the mouth (see Open fractures). Consider all the soft tissues crossing the zone of injury, as it is possible to get a closed rupture or avulsion of tendons without a break in the skin. Consider the possibility of a neurovascular injury. (see Neurological injury). Severe soft tissue injury in the presence or absence of a fracture may still lead to compartment syndrome (see Compartment syndrome).

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TABLE 28.2  Gustilo and Anderson open fracture classification. Type I

A low energy open fracture with a wound less than 1 cm long and clean

II

An open fracture with a laceration more than 1 cm long without extensive soft tissue damage, flaps or avulsion

III

Characterised by high energy injury irrespective of the size of the wound. Extensive damage to soft tissues, including muscles, skin, and neurovascular structures, and a high degree of contamination. Multifragmentary and unstable fractures

Subgroups of type III A

Adequate soft tissue cover of a fractured bone after stabilisation

B

Inadequate soft tissue cover of a fractured bone after stabilisation (i.e. flap coverage required)

C

Open fracture associated with an arterial injury requiring repair

Source: Gustilo RB, Mendoza RM, Williams DN. Problems in the management of type III (severe) open fractures: a new classification of type III open fractures. J Trauma 1984; 24: 742–6.

Neurological injury Seddon classified nerve injuries into neurapraxia, axonotmesis and neurotmesis: ●●

●●

●●

neurapraxia – no loss of nerve sheath continuity or peripheral Wallerian degeneration. Recovery potential good may take months if the pressure is removed from the nerve; axonotmesis – nerve sheath remains intact, with internal nerve fibre damage with Wallerian degeneration. The neural tube (endoneurium) can guide the regenerating nerve fibres to their target. Good potential for recovery; nerve fibre regrowth is at 1 mm per day; neurotmesis – complete division of the nerve, nerve sheath and nerve fibre. Functionally poor outcome without surgical intervention to restore continuity of the nerve sheath.

Although the Seddon classification is useful in understanding the pathoanatomy, the critical discriminator in defining recovery, and need for possible surgical intervention, is the presence or lack of continuity of the enveloping nerve sheath.

Bony injury Description Describing the bony injury depends on several characteristics and includes the: ●● ●● ●●

name of the bone that has been injured; region of bone injured; pattern of fracture line: transverse, oblique, spiral, segmental or multifragmentary (Figure 28.4);

Ramon Balgoa Gustilo, surgeon, Hennepin County Medical Center, Minneapolis, MN, USA. John T Anderson, surgeon, Hennepin Medical Center, Minneapolis, MA, USA. Sir Herbert J Seddon, trained at St Barts, London University, and the Royal National Orthopaedic Hospital, Stanmore, UK. He became the second Nuffield Professor of Orthopaedic Surgery in Oxford.

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presence of compression; compression fractures occur when cancellous bone collapses; vertebral wedge compression fracture; presence of displacement of the fracture fragments, undisplaced or displaced; type and degree of displacement (Figure 28.4): ●● angulation; ●● translation; ●● rotation (Figure 28.5); ●● shortening; presence of pre-existing pathology; associated joint pathology, dislocation or subluxation.

●●

●● ●●

●● ●●

(a)

(b)

In children and adolescents the fracture line may be incomplete due to the plastic, less brittle nature of their bones (Figure 28.6) These incomplete fractures are called greenstick fractures, where one tension cortex fails. If the compression cortex buckles, they are called torus or buckle fractures. Paediatric bone may also simply undergo plastic deformation without a visible fracture line.

Spiral

Oblique

Transverse

Figure 28.5 Describing fractures: the importance of rotation. (a) Anteroposterior (AP) view of the knee seen at the top of the radiograph and lateral view of the ankle at the bottom, showing a spiral fracture at the junction of the middle and distal thirds of the tibia. (b) AP radiograph of the ankle on the same patient. Note the varied diameter of the fracture fragments; this implies rotational deformity. The distal fragment has translated laterally by 50%. There is no significant angulation on this view.

Segmental

(c)

(a)

Angulation

Translation

Shortening

(d)

(b)

Rotation

Figure 28.6 Types of bony injury: (a) uninjured bone; (b) adult transverse fracture failure across the whole bone; (c) greenstick fracture; the bone has failed on the tension side; (d) torus or buckle fracture; the bone has failed on the compression side.

Figure 28.4  Descriptive terms for fractures.

Summary box 28.2 Describing an injury Use plain language to describe: ●● ●● ●●

Location Soft tissue component Bony injury

Classification For each specific bony injury there may be several injury specific classification systems.

ve’s Short Practice of Surgery, 26th Ed

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AO CLASSIFICATION The AO (Arbeitsgemeinschaft fur Osteosynthesefragen) system provides a comprehensive classification of all fractures (Figure 28.7). The first number defines the bone injured and the second number the segment of bone injured: proximal metaphysis, diaphysis, distal metaphysis. The letter and number that follows further defines the nature of the injury (Figure 28.8). For example, the previously described humeral fracture would be 12-A1 (1 humerus, 2 diaphysis, A simple, 1 spiral). (For more detail see Further reading.)

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1 Proximal metaphysis Humerus 1

2 Diaphysis

3 Distal metaphysis

Radius and ulna 2

GROWTH PLATE INJURY CLASSIFICATION In children and adolescent injuries involvement of the growth plate (physis) can lead to abnormal growth or growth arrest, either complete or partial. Complete growth arrest will result in length abnormalities and partial growth arrest might result in angular deformities. The severity of injury to the physis is classified in the Salter–Harris classification which considers whether the fracture line passes through the epiphysis, physis, metaphysis or combinations of all above. Salter–Harris described five and Mercer Rang added the sixth (Figure 28.9): ●● ●●

Femur 3 ●●

3 Distal metaphysis

Tibia 4

4 Malleolar segment

Figure 28.7 The AO classification system: the first two numbers specify the site of the fracture.

Diaphyseal types

Metaphyseal types

A – After reduction complete contact between the two main fragments (>95%) (a)

●●

●●

I

II

III

IV

V

VI

A – Extra-articular

B – Partial articular; some part of the joint remains in continuity with the diaphysis

(b) C – After reduction no contact between the two main fragments (segmental)

(c)

●●

Type I – simple fracture line just involving the physis. Seldom affects growth. Type II – fracture line through the physis exiting through the metaphysis, producing a metaphyseal fragment. Seldom affects growth. Type III – fracture line through the physis exiting through the epiphysis (intra-articular). Seldom affects growth, but intra articular affecting joint surface. Type IV – fracture line across epiphysis, cross physis and across metaphysis. This injury can cause focal fusion of the physis leading to abnormal growth. Type V – a crush injury of the physis. Growth disturbance is common and may be the first radiological sign of an injury. Type VI – injury to perichondral structures by direct trauma. Rare injury, high chance of abnormal growth.

(a) B – After reduction partial contact between the two main fragments (wedge fracture)

(b)

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C – Complete articular; an intra-articular fracture with none of the joint attached to the diaphysis

(c)

Figure 28.8 The AO classification system: the letter defines the nature of the fracture.

Figure 28.9  The Salter–Harris classification of growth plate injuries.

Robert Bruce Salter, 1924–2010, Professor of Orthopaedic Surgery, The University of Toronto, Ontario, Canada. A pioneer in the field of paediatric orthopaedic surgery, he received international awards for medical science and the Distinguished Achievement for Orthopaedic Research award. W Robert Harris, 1922–2005, formerly Professor, University of Toronto, President Canadian Orthopaedic Foundation (1968) and President of the Canadian Orthopaedic Association (1975 and 1976).

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FRACTURE HEALING It is useful to review fracture healing, as it relates to treatment and outcome. Following a fracture, bone can heal in two different ways: direct (primary) bone healing or indirect (secondary) bone healing: ●●

●●

Direct bone healing, as the name implies, heals directly with bone and without callus formation. It happens in an environment of cortical apposition and absolute stability with no movement or gap between the fracture fragments. The normal osteoclastic-mediated remodelling of bone is directed across the fracture interface. Osteoclastic cutting cones cut across the fracture line, with following osteoblasts laying down lamellar bone across the fracture. Indirect bone healing involves a transition from one tissue to another with callus formation. It is the most common form of bone healing. Following the injury, haematoma fills the gap at the fracture site. In response to a varying strain and under the influence of bone stimulating factors, the tissue undergoes differentiation, from haematoma to fibrous tissue and then to soft callus, followed by mineralisation and formation of mature bone. The amount of strain determines the nature of tissue it differentiates into; under 100% leads to fibrous tissue, under 10% soft callus, less than 2% hard callus and progressive mineralisation. Hence a little movement is good, too much movement is bad.

Consolidation Follows union and demonstrates that the bone has returned to normal strength. Radiologically it is demonstrated by the return of the normal cortical pattern.

Remodelling In children, and to a lesser degree in adults, bone remodels based on the forces passing through it.

Summary box 28.3 Fracture healing ●● ●●

TREATMENT The main principle of extremity fracture management builds on the classical concept of reduction and stabilisation of the fracture. Treatment can be considered under the following headings (see Apley’s system of orthopaedics and fractures [Further reading]): ●● ●● ●● ●●

Terminology of bone healing after fracture Union The fracture has healed sufficiently from a clinical perspective to withstand physiological loads, with very little pain and minimal tenderness at the fracture site. Radiologically a fracture has united when the callus bridges the fracture site.

Delayed union This description can be applied to a fracture that is slow to heal and which has not healed in the expected time frame.

Direct - cortical apposition and absolute stability Indirect – secondary bone healing, requires some movement

reduce; hold; heal; rehabilitate.

The main objective of any treatment is to return the patient to normal function as soon and as safely as possible. Broadly speaking, treatment may be operative or non-operative, with differing risks and benefits (Table 28.3).

Reduce The first thing to consider is the degree of displacement of the fracture fragments. It is useful to ask the following question: if the bone were to heal in this position, would it be compatible with optimum function in the short and long term? In general, fractures involving the articular joint surface need to be reduced perfectly back to their original anatomical

Non-union This description can be applied to a fracture that has not healed and shows no potential to heal without further intervention. A non-union can also be defined as a fracture that fails to demonstrate clinical or radiological improvement over 3 months. In general, you do not describe a fracture as ‘nonunion’ until 6 months after the injury. There are a number of different types of non-union: atrophic, hypertrophic and infected. It is useful to consider certain factors with regard to the non-union; the biology of the fracture, the mechanical environment and the host (patient factors like diabetes and smoking). In an atrophic non-union, the problem is generally a biological one, with a lack of stimulus or blood supply. A hypertrophic non-union generally occurs when there is too much movement at the fracture site.

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TABLE 28.3  Risks and benefits of fracture treatment. Benefits

Risks

Pain relief

Anaesthesia

Prevention of infection

Introduction of infection

Restoration of anatomy

Damage to soft tissues and neurovascular structures

Early movement of the limb Early movement of the patient

Devitalising bone

Improved function

Need for implant removal

Reduced risk of secondary arthritis

Financial cost (cost of treatment)

Financial cost (time off work)

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position, to restore normal joint movement in the short term and avoid degenerative joint disease in the long term – intra-articular fracture = anatomical reduction. Fractures that do not involve the joint surface generally require restoration of mechanical alignment of the joints above and below. The fracture fragments do not need to be reduced perfectly. Focus on acceptable alignment, length and rotation – extra-articular fracture = mechanical alignment. In children an extra articular fracture has the ability to remodel, and therefore an increased degree of displacement can be accepted. If a fracture requires reduction, it can be reduced open or closed. A closed reduction is where the bones are manipulated and moved without exposing the bone. Often the best way to reduce a fracture is to reverse the sequence of injury, without tearing or further damaging the intact soft tissues and periosteum. On occasion this may mean exaggerating the deformity (Figure 28.10). Open reduction is utilised if an acceptable closed reduction is not achieved or likely to succeed. A combination of closed and open methods can be used to reduce a fracture. Care should be taken during an open reduction not to unduly devitalise the fracture fragments by stripping intact periosteum. A balance between maintaining a blood supply to the Compression surface

Ground reaction (a)

fracture fragments (biology) and achieving anatomical reduction needs to be maintained. Adequacy of reduction is complex and depends on many factors. If intra-articular, the joint surface involved needs to be considered. By way of an example, 2 mm of residual displacement of the articular surface may be accepted in the patella and tibial plateau and may be acceptable in fractures involving the distal radius, but is not acceptable in the condylar joints of the fingers. In general consider the relative thickness of the articular surface involved. On occasion consideration on how you intend to subsequently hold the fracture may affect the primary form of reduction.

Summary box 28.4 Reduction ●●

●● ●●

●●

Body weight Tension surface

Volar surface fails in tension

Hold (e) Increase deformity and restore soft-tissue hinge

If the fracture fragments are in an acceptable position, or have been reduced into an acceptable position, they then need to be held in that position until they heal. When choosing a method to hold a fracture the aim is to: ●●

●●

(f)

Maximum displacement

Close soft-tissue hinge

●●

(c)

●●

(g)

●● ●●

With the injury force removed the bones often recoil to bayonet apposition

Hold position with three point fixation

(h)

Figure 28.10  (a–d) Representation of how the mechanism of injury causes the bony and soft-tissue injury. (e–h) Representation of how the residual mechanical properties of the tissues may be used to effect and hold a reduction.

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optimise the biological and mechanical environment to create the most favourable conditions possible for fracture healing; minimise the period of disability by speeding up the healing process or providing enough stability to return to normal function while the fracture heals.

There are several methods of holding fracture fragments in place: ●●

(d)

Reduction has two components: reducing the fragments and assessing adequacy of reduction Reduction can be performed open or closed The principle is to reverse the movement which created the fracture Over-angulation allows the intact periosteum to guide the fragments into position

Position at presentation

Dorsal surface periosteum hinges

(b)

389

●●

plaster cast/ splints; traction; Kirschner (K-) wires; external fixation; plates and screws intramedullary nails.

Note: Arthroplasty may be used where fragments cannot be held together. On occasion a combination of holding methods may be used; for example, K-wires and a moulded cast in the case of a simple extra-articular distal radial fracture. It is important to consider the way of holding the reduction in terms of outcome and ensure this is part of the overarching goal to optimise the patient’s return to function as safely and fast as possible. Fig No: 29.9a 25/10/2017 08:21

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For example, a displaced clavicle fracture in a 10 year old has a 99% chance of sound union within a few months if treated non-operatively. In contrast, a displaced multifragmentary mid-third clavicle in a 35-year-old female will carry a 35% chance of going on to a non-union at 6 months. Therefore, even though this fracture may heal with non-operative treatment, with appropriate explanation and shared decision making, a patient may choose to have surgery early in order to get back to normal function as soon as possible. Stability can be absolute or relative: ●●

●●

Absolute stability. Implies no displacement or movement and is achieved by accurate anatomical reduction with compression across the fracture fragments to optimise the environment for direct bone healing. This is desirable in intra-articular fractures, where callus at the fracture site might inhibit movement. Intra-articular fractures require an anatomical reduction and absolute stability. Relative stability. Allows a little movement at the fracture site, optimising the environment for callus formation and indirect bone healing.

Selected examples of achieving absolute and relative stability are shown in Figure 28.11.

Plaster cast and splints Plaster casts and splints are generally used to hold stable fractures or supplement the fixation of unstable fractures (e.g. below elbow cast applied to a distal radial fracture after K-wire fixation [see below]).

Plaster casts come in two forms: plaster of Paris and synthetic casting materials. Plaster of Paris is the preferred method in acute fractures and, where more support is needed, it is easier to mould plaster of Paris than a synthetic cast. In acute injuries, where there is a risk of swelling and compartment syndrome, a backslab will often be applied. A backslab is not always positioned on the dorsal surface as the name suggests, but is a partial cast where a layer of plaster of Paris or synthetic cast is applied along roughly half the circumference. An alternative to a backslab includes a full cast that is split along its full length to allow for swelling. The use of an incomplete cast does not remove the risk of swelling and compartment syndrome and must always be accompanied by close clinical observation. Moulding of the cast is an art form requiring appropriate skill to achieve the desired effect. Three point moulding is used to control the position, often using the intact dorsal periosteal hinge to mould against (see Figure 28.11). Often, a correctly moulded cast will look crooked, leading to the adage ‘Bent casts make straight bones’ (Figure 28.12). Commercially available upper limb and lower limb splints provide comfort, support and social protection to stable fractures. Ease of application and the ability to remove make them very useful for patients to return to activities of daily living including bathing and showering. The advantages and disadvantages of plaster cast and splint usage are described in Table 28.4.

Absolute stability Lag screw

(a)

Relative stability Bridge plating

(d) Compression plating

(b)

Intramedullary nail

(e) Compression with a ring fixator

(c)

Bridging with a ring fixator

(f)

Figure 28.11  (a–f) How absolute and relative stability can be achieved. The same implants may be used to achieve different mechanical effects.

Plaster of Parisis a white crystalline powder, calcium sulphate hemihydrate CaSO4-0.5H­2O, which sets hard when water is added to it.

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TABLE 28.5  Advantages and disadvantages of traction. Advantages

No wound in zone of injury No interference with fracture site Materials cheap Adjustable

(a)

Disadvantages

Restricts mobility of patient Expensive in hospital time Skin pressure complications Pin site infection Thromboembolic complications

(b) Figure 28.12  (a) The position achieved at the end of the manipulation described in Figure 28.10. (b) Demonstration of how by moulding the cast the intact periosteum is kept under tension and the bone under compression; thus, the remaining mechanical properties are used to achieve stability.

TABLE 28.4  Advantages and disadvantages of casting and splinting. Advantages

No wound No interference with fracture site

one place and limit return to normal function. (See Table 28.5 for advantages and disadvantages.) Traction is often used in the treatment of femoral shaft fractures in adults as a temporary measure for comfort and to allow transfer of the patient, until definitive fixation can be undertaken. A Thomas splint is applied to the limb initially in a static fashion (Figure 28.13a) and then, once in bed, balanced traction is applied to help pull the leg out to length and pull the splint off the ischial tuberosity (Figure 28.13b). The anchor point on the limb may be either skin, by applying an adhesive or non-adhesive bandage, or skeletal traction, where a pin is placed in the proximal tibia or distal femur. A common everyday example of traction is the use of a collar and cuff in proximal humeral fractures. When the patient is upright, the lower part of the arm, under the action

Cheap Adjustable

(a)

No implants to remove Disadvantages

Limited access to the soft tissues Cumbersome (particularly in the elderly) Interferes with function

rt Practice of Surgery, 26th Ed

ISBN: 9781444121278 Poor mechanical stability

uk

‘Plaster disease’ – joint stiffness and muscle wasting

Proof Stage: 1

Fig No: 29.10a (b)

Traction

Traction is defined as a stretching force on a limb to pull a fracture straight. After appropriate pain control, simply pulling on the limb using manual traction will help realign fracture fragments, returning overall length and alignment. If the fracture is simple and off ended, it may require more than simply pulling to reduce it (see reduction in Figure 28.10). Once reduced, however, continued longitudinal traction will often ISBN: 9781444121278 Proof Stage: 1 ractice of Surgery, 26th Edit reduced. hold A traction force can be applied and maintained by a variety of systems and techniques. It is easy to apply traction to any extremity; however, it is cumbersome and requires a fixed point to pull on. This can require the patient to be fixed to

Weight Figure 28.13  (a) Static traction with a Thomas splint. The force and counterforce contained within a static system. The load is applied Fig No:are 29.10b to the patient through the tibial traction pin via a cord tightened with a Spanish windlass. The counterforce is applied through pressure by the splint on the ischial tuberosity. (b) A dynamic system in which the load is applied by weights suspended from the tibial pin and the counterforce is the patient’s own weight.

Hugh Owen Thomas, 1834–1891, general practitioner of Liverpool, UK, 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.

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of gravity, provides longitudinal traction, thus aligning the fracture fragments.

Kirschner wires Kirschner wires (also called K-wires) are smooth, nonthreaded, thin flexible wires often between 0.9 and 2.5 mm in diameter. They are used to hold small fragments in place. They may be used in a temporary fashion intraoperatively to hold fracture fragments in place until definitive fixation with plates and screws can be performed. They are inexpensive and simple to use. Moreover, they are extensively used for definitive fixation of injuries around the hand and wrist. The flexible nature of the wires can often require supplementation, as a hybrid construct of K-wires and plaster cast fixation. In distal radial fractures the wires are placed percutaneously after closed reduction, the trailing end of the wire is left proud of the skin and the end bent to limit wire migration. K-wires around the distal radius can be removed in the clinic setting 4–6 weeks after insertion. Complications of K-wires include pin site infection, wire breakage, loss of fixation and wire migration. Wire migration may be a potentially serious problem in certain locations. It is not advisable to use non-threaded K-wires around the shoulder girdle and clavicle as migration into the thoracic cavity and heart has been reported (Table 28.6).

External fixation External fixation involves percutaneous placement of metal rods or fine wires into bone to anchor a metal frame on the outside (Table 28.7). The frame construct itself may be comTABLE 28.6  Indications for K-wire insertion. Temporary fixation Definitive fixation – with small fracture fragments (e.g. wrist fractures and hand injuries) Tension band wiring (fractures of the patella and olecranon) Temporary immobilisation of a small joint

TABLE 28.7  Advantages and disadvantages of external fixation. Advantages

No interference with fracture site Adjustable after application: alignment; biomechanics Soft tissues accessible for plastic surgery Rapid stabilisation of fracture Hardware easy to remove

Disadvantages

Pin site infection Interferes with plastic surgical procedures Soft-tissue tethering Cumbersome for the patient

prised of tubular rods with connectors, or circular ring constructs ‘ilizarov’ type of frame. Hybrid variations are infinite, with combinations of anchor fixation modalities and frame constructs. The Taylor spatial frame allows for gradual correction of deformity (Figure 28.14). The major drawback of external fixation is that they can be cumbersome to the patient and pin site infection can be a problem (Table 28.7). Specific indications for external fixators include: ●●

●●

●●

●● ●●

emergency stabilisation of a long bone fracture in the polytrauma patient thought too unwell to have other interventions; ‘damage control orthopaedics’; stabilisation of a dislocated joint after reduction (e.g. a spanning fixator across the knee joint while the vascular surgeons repair an arterial injury with a knee dislocation); complex periarticular fractures to provide temporary stabilisation and allow the soft tissue damage to recover before definitive fixation (e.g. a distal tibial [pilon] fracture); fractures associated with infection; treating fractures with bone loss.

Plates and screws Plates and screws can be used in many different ways. A ‘lag screw’ can be used to generate compression across a fracture site, optimising the environment for direct bone healing. Similarly, compression can be achieved using a dynamic compression plate. A plate might also be used simply to neutralise forces, buttress a fracture or work as an internal external fixator (see Figure 28.11). In general, plates and screws are used where possible in articular and periarticular fractures where an anatomical reduction is required, often via open means, followed by the application of the plate and screws to achieve a rigid construct. In extra-articular fractures, where mechanical alignment is required together with relative stability, one option is the use of locking plate technology. This allows a closed reduction and percutaneous placement of the plate with locking screws to create an internal construct, which behaves like an external fixator. Injury-specific plating systems have revolutionised the ability to treat certain injuries, with plates pre-bent and pre-shaped for specific anatomical regions and specific injury patterns. (See Table 28.8 for the advantages and disadvantages of plate fixation.)

Intramedullary nails Diaphyseal fractures are best suited for intramedullary nailing. Where mechanical alignment is required together with relative stability, they allow for indirect bone healing. After nail insertion, mechanical alignment is checked particularly for length, alignment and rotation. Locking screws are then placed proximally and distally to maintain length and alignment. Intramedullary nailing of metaphyseal and articular fractures is a challenge. However, with improved implant

Martin Kirschner, 1879–1942, Professor of Surgery, Heidelberg, Germany, introduced the use of skeletal traction wires in 1909. 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.

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(d)

(a)

(b)

(c)

Figure 28.14  (a) Monolateral tubular frame with metal rod (half pin anchorage to bone. (b) Circular ring fixator with fine wire anchorage to bone. (c) Hybrid circular/tubular rod frame construct with combination of half pin and fine wire anchorage to bone. (d) Taylor spatial frame; allows for gradual correction of deformity.

TABLE 28.8  Advantages and disadvantages of plate and screw fixation. Advantages

Can be used when anatomical reduction is required

TABLE 28.9  A comparison of reamed versus unreamed nailing (an assumption is that nails used unreamed are usually thinner than those used reamed).

Allows early mobilisation Disadvantages

Reamed IMN

Unreamed IMN

Can provide absolute or relative stability

Insertion time

Longer

Quicker

May interfere with fracture site

Time to union

Shorter

Longer

Periosteal/soft-tissue damage

Size of implant

Larger

Smaller

Does not normally allow for immediate loadbearing

Reduction of distal fractures Easier

More difficult

Strength of construct

Less

Potential for infection Metalwork complications

More

IMN, intramedullary nail.

Possible need for plate removal

design and the ability to lock the nails very distally and in multiple directions, the indications for intramedullary nailing is expanding. Intramedullary nails may be placed in an unreamed or reamed fashion. Reaming is the process whereby the intramedullary canal is widened slightly to allow passage of a larger diameter nail, relating to the last reamer size used. Table 28.9 compares reamed to unreamed nails. Intramedullary nailing can be a technically demanding procedure. The advantages and disadvantages are summarised in Table 28.10.

Arthroplasty Arthroplasty is indicated in certain acute circumstances: articular fractures that are not reconstructible, or injuries

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TABLE 28.10  Advantages and disadvantages of intramedullary nailing. Advantages

Minimally invasive Early weight-bearing Less periosteal damage than open reduction and internal fixation Seldom need removal

Disadvantages

Increased risk of fat emboli/chest complications Infection difficult to treat Difficult to remove if broken

where the vascularity of the articular segment is compromised (e.g. displaced intracapsular femoral neck fracture in an older patient).

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The patient demographics and functional demands need to be considered in choosing arthroplasty as a treatment option. Implant longevity and level of activities following implant insertion need to be matched. Traditionally, arthroplasty for trauma was limited to hip and shoulder hemiarthroplasty. Total hip replacement, acute distal femoral replacement, radial head replacement, total and hemi-elbow arthroplasty, and reverse polarity shoulder arthroplasty are current treatment options for older patients with osteoporotic periarticular fractures. The selection of a particular technique will depend on clinical evidence and our previously stated aim to return patients to optimal function as soon as possible. It should be considered in the context that it can be expensive and require considerable other resources to make the procedure safe and long lasting.

Heal Time to fracture healing depends on several factors: patient co-morbidities, the age of the patient, bone involved (upper limb or lower limb), patient factors (diabetes), choice of treatment. Well known factors that slow down bone healing include diabetes mellitus (doubles time to union), diminished blood supply (peripheral vascular disease, vascular injury at time of injury), smoking, non-steroidal anti-inflammatory drugs and infection at the fracture site. Several chemical and mechanical methods have been attempted to enhance fracture healing, including bone marrow injections into the fracture site and other orthobiologics such as bone morphogenic proteins. Mechanical methods include controlled axial micromotion (using an external fixator), electromagnetic stimulation and low intensity pulsed ultrasound. There is good basic scientific evidence to support their theoretical benefit; however, to date there is little clinical evidence for their use in the primary treatment of closed fractures.

Rehabilitate The main aim of treatment is to return the patient to a similar level of pre-morbid function as quickly as possible. Rehabilitation begins as soon as feasible. It is often not necessary to wait until bone union before beginning rehabilitation. It is important to move the affected joints and the joints in close proximity to the fracture (e.g. elbow and shoulder exercise while in a cast for a distal radial fracture), limiting global stiffness and wasting of the muscles on that limb.

TREATMENT BY FRACTURE LOCATION In general, the principles of treatment described above are dependent on the fracture location: diaphyseal, metaphyseal and intra-articular. Table 28.11 outlines some indications for operative stabilisation.

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TABLE 28.11  Indications for surgery in limb trauma. The main indication is that operation will produce a better outcome; the principles are given below. A fracture requiring treatment that is unsuitable for non-operative measures Open fractures Failed non-operative management Multiple injuries Pathological or impending pathological fractures Displaced intra-articular fractures Fractures through the growth plate, where arrest is possible (Salter–Harris type III–V) Avulsion fractures that compromise the functional integrity of a ligament/tendon around a joint (e.g. olecranon fracture) Established non-unions or malunions

Diaphyseal fractures Extra articular fractures do not require an anatomical reduction, but rather a mechanical restoration by correction of length, alignment and rotation (Figure 28.15). Angular malunion of a diaphyseal fracture of the weight-bearing long bones will lead to abnormal joint forces on the joint above and below, leading to pain and secondary degenerative joint disease. Diaphyseal fractures are generally well suited to intramedullary fixation techniques, as previously discussed. Summary box 28.5 Diaphyseal fractures ●● ●●

●●

Restore length, alignment and rotation Consider whether primary or secondary bone healing is the objective Radius and ulna need precise reduction to function

Metaphyseal fractures In the AO classification metaphyseal fractures are classified into A type – extra-articular, B type – partial articular, and C type – complete articular. In A type fractures, joint congruity is not an issue and as such the principles of mechanical alignment, length and rotation need to be considered. Fixation of metaphyseal fractures is less predictable with intramedullary nailing, therefore plate and screw fixation, external fixation or, in the smaller joints, K-wire fixation is used. Metaphyseal fractures are close to the joint and so consideration is given to stable fixation to allow early joint movement and rehabilitation.

Intra-articular fractures AO type B and type C fractures are intra-articular and as such the principles of treating intra-articular fractures need to be respected; namely, anatomical reduction of the articular sur-

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(a)

(d)

(b)

(e)

395

(c)

(f)

Figure 28.15  (a) and (d) are C-type or segmental tibial fractures. Each was a high-energy injury; (b) and (e) show a temporary spanning external fixator applied in each case; (c) and (f) show definitive relative stability was achieved with different methods of bridging fixation. Healing was by indirect means in both cases. Despite irregularities at the fracture sites the overall position was satisfactory and function was good.

face and rigid stabilisation to allow early joint movement and avoidance of degenerative joint disease (Figure 28.16). However, these principles have to be balanced with the increased wound complications of open surgery and devitalising bone fragments with excessive exposure of the bone. Osteoporotic intra-articular fractures are a considerable challenge. Although anatomical reduction may be achieved, rigid fixation devices may cut out of soft bone. Injectable bone substitutes may be used to fill bone voids and augment

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fixation. If stable fixation is not possible, then consideration might be given to non-operative treatment and delayed joint replacement or, on occasion, primary joint replacement may be undertaken. In type C fractures where the articular surface has separated from the metaphysis, the articular surface is initially anatomically reduced with temporary K-wires or lag screws and then the articular block is reattached to the shaft (Figure 28.17).

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(a)

(a)

(b) (b) AA

BB

(c)

Figure 28.17  (a) A C-type proximal tibial articular fracture (i.e. none of the joint remains attached to the diaphysis). (b) The small plate and screws (AA) are used to compress the joint fragments, aiming for absolute stability. The heavy duty fixed angled device (BB) spans the fracture and provides relative stability Figure 28.16  A B-type or partial articular fracture. (a) Plain radiograph; (b) computed tomography clarifies the injury; (c) fixation with plate and screws achieving compression across a previously reduced fracture.

TREATMENT BY REGION (FROM TOP TO TOE) Scaphoid fracture The blood supply to the scaphoid enters distally and supplies the scaphoid in a retrograde fashion. As such, a displaced waist of scaphoid fracture interrupts the blood supply to the proximal pole, leading to avascular necrosis. An undisplaced fracture of the scaphoid may not be visible on the initial

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radiographs. If a patient is tender in the anatomical snuff box following a fall on the outstretched hand, special scaphoid view radiographs should be requested (Figure 28.18). (ai)

(aii)

397

If a fracture is not evident on the initial radiographs and the patient remains tender in the anatomical snuff box, then treat as a suspected scaphoid fracture until a fracture is actively excluded. The standard protocol of a suspected scaphoid fracture is to immobilise the wrist and examine again 10–14 days later. If tenderness remains, repeat the scaphoid views. If facilities and resources allow, an earlier diagnosis may be made with a bone scan, MRI or CT. Undisplaced fractures can be treated non-operatively in a below elbow cast. It is not necessary to include the thumb as a routine. In displaced or unstable fractures (>1 mm) consideration should be given to open reduction and rigid fixation with a headless compression screw. Complications of scaphoid fractures include: non-union, avascular necrosis, malunion and carpal instability.

Carpal instability

(b)

(c)

The most commonly involved carpal bone is the lunate. A lunate dislocation is where the lunate bone dislocates out of the radiocarpal joint. In a perilunate dislocation the lunate remains in the radiocarpal joint and the rest of the carpus dislocates around the lunate. Lunate and perilunate dislocations are easily missed unless careful attention is paid to carpal alignment on the lateral radiograph (Figure 28.19). Review of the radiographs should particularly ensure the anatomical location of the lunate in the radiocarpal fossa and that the capitate in the ‘cup’ of the lunate is maintained. (a)

(d)

(b)

Cap Rad Lun

Figure 28.18  Scaphoid fracture. (ai, aii) Anteroposterior and lateral views in which the injury is difficult to see; (b, 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 28.19  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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Acute injuries should be reduced closed initially to remove pressure from the median nerve. Anatomical carpal alignment is difficult to hold and therefore surgical reconstruction of damaged intrinsic ligaments, together with K-wire fixation of the carpal bones, is often undertaken. Ligamentous healing is slow and may be incomplete. K-wires are kept in place for 8 weeks and the wrist casted or splinted for 3 months.

(a)

Thumb metacarpophalangeal ulnar collateral ligament.

(b)

Injury to the thumb metacarpal ulnar collateral ligament is a unique injury often termed ‘game keepers’ thumb or ‘skiers’ thumb. Due to the unique anatomical arrangement of adductor policis, if the ligament undergoes complete rupture the aponeurosis may become interposed, inhibiting ligament to bone healing. A rupture of the ulnar collateral ligament should be suspected when an ulnar directed force is directed across the metacarpophalangeal (MCP) joint. A tender swelling on the ulna side of the MCP joint may signify the ‘Stener’ lesion. Increased laxity may be clinically evident, and if there is uncertainty, stress radiographs can demonstrate the degree of injury. Complete ruptures with a Stener lesion (interposed aponeurosis) require open reduction of the ligament to restore bone contact, with a suture anchor repair of the associated ulnar collateral ligament.

(c)

(d)

Distal radial fractures Extra-articular (type A) fractures of the distal radius may displace in a volar or dorsal direction. It is possible to reduce volar displaced fractures (Smith’s fracture) of the distal radius with a closed technique. However they tend to be unstable and displace if held in a cast. Hence most volar displaced extra articular distal radial fractures are reduced and held with a volar buttress plate (Figure 28.20). Most dorsally displaced fractures (Colles’ fracture) can be addressed with closed reduction and held in a cast. However, some will slip or collapse with cast treatment, and so close review for the first few weeks is advocated. Fractures with significant initial displacement and dorsal comminution are at risk of early and late collapse. After thorough counselling the patient may choose to have the fracture reduced and then held surgically with K-wires, plate and screw fixation (volar or dorsal) or external fixation. The K-wires may be placed across the fracture fragments or intrafocally, going through the fracture site. The latter can be used to help reduce the fracture and then used to lock the fracture fragments in place (Figure 28.21) Treatment is individualised based on patient and fracture pattern factors. Intra-articular fractures (types B and C) of the distal radius require anatomical reduction of the joint surface; a gap or step of less than 2 mm can be accepted in the radius. The distal radius fails fairly predictably with splitting of the

Figure 28.20 An A-type or extra-articular metaphyseal fracture. A plain lateral radiograph of this Smith-type fracture (a, b). Fracture fixed to a plate. There is no interfragmental compression. The plate is pushing against or buttressing the distal fragment (c, d).

lunate fossa fragment in the coronal plane and separation of the radial styloid. If a closed reduction can be achieved with manipulation, the fracture fragments can subsequently be held with K-wires, plate and screw fixation or external fixation. The most common form of treatment is closed reduction and percutaneous K-wire fixation, supplemented with a plaster cast for 4–6 weeks.

Forearm fractures (radius and ulna) Fractures of the diaphyseal shaft of the radius and ulna are technically, in the anatomic sense of the word, extraarticular. However, the forearm bones work together, being coupled at the proximal and distal radioulnar joints to allow

Robert William Smith, 1807–1873, Professor of Surgery, Trinity College, Dublin, Ireland, described the reverse Colles fracture in 1847. Abraham Colles, 1773–1843, President of the Royal College of Surgeons of Ireland (1802), Professor of Anatomy Physiology and Surgery (1804) and described distal radial fracture in 1814.

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399

Humeral fractures

(a)

Fractures of the diaphyseal portion of the humeral shaft are extra-articular fractures and as such require mechanical alignment. Non-operative treatment with functional bracing will achieve union in an acceptable position within 12 weeks in over 80% of cases. Gravity can provide traction on the arm and in conjunction with a humeral brace help to hold alignment and allow early range of motion of the elbow. Active shoulder abduction is avoided until fracture union, to prevent varus deformity. Shoulder movement must not be absent during treatment and so gravity assisted pendulum exercises are instituted early on to prevent shoulder stiffness. As the fracture approaches the metaphyseal region of the humerus it becomes more difficult to control with humeral bracing. Distal third extra-articular fractures of the humerus can be treated non-operatively in a humeral brace but have a tendency to go into varus. Articular fractures of the distal humerus require anatomical reduction and stable fixation to allow early joint movement. Internal fixation is indicated for displaced intra-articular fractures, non-union or delayed union, open fractures, multiple injuries and those fractures not held in an acceptable position with brace treatment. Fixation of diaphyseal fractures can be achieved with intramedullary nailing or plate and screw fixation. Plate fixation is associated with higher union rates and lower rates of reintervention. (Figure 28.22). (a)

(b)

(c)

(b) Figure 28.21  (a) K-wires placed across fracture fragments; (b) intrafocal K-wire used to help reduce the fracture.

for forearm pronation and supination. Therefore, when considering treatment the principles that apply to intra-articular fractures need to be considered: anatomic reduction and rigid fixation to allow for early joint motion. Most fractures that involve both radius and ulna in adults require open reduction, anatomic alignment and rigid plate fixation. Isolated fractures of the ulna, the so-called nightstick fracture, are a little more controversial, as non-operative management is possible but in this location risks delayed union and non-union, hence treatment depends on patient factors. Operative fixation with plate and screw fixation is technically simple and allows early predictable return to function.

Olecranon fractures Olecranon fractures may be displaced or undisplaced. Undisplaced fractures 10° is between 0.5% and 3%. The prevalence of curves >30º is between 1.5 and 3 per 1000. Risk factors for progression

include female gender, remaining skeletal growth, curve location and curve magnitude. Not all curves stabilise when skeletal maturity is reached. In long-term studies, 68% experienced curve progression; the most marked progression of 1° per year was observed in patients with thoracic curves between 50 and 75°. Idiopathic curves of less than 25° are monitored with clinical and radiographic examination. In growing children (premenarchal) with curves between 20° and 29°, a brace may be indicated. Bracing is used to prevent curve progression and generally does not lead to permanent curve correction. Curves beyond 45° are not amenable to brace treatment. Surgery in the form of corrective instrumentation and spinal fusion is indicated for curve progression beyond 40°, truncal imbalance and unacceptable cosmesis. During surgery, continuous spinal cord monitoring is used in the form of somatosensory evoked potentials (SSEP), motor-evoked potentials (MEP) and free-run and stimulated electromyographic (EMG) activity to minimise the risk of neurological damage. The risk of neurological injury is 0.4% (1 in 250).

Neuromuscular scoliosis This may be due to neuropathic disorders, such as cerebral palsy, spinocerebellar degeneration, syringomyelia, tetraplegia (Figure 33.9), spinal muscular atrophy and poliomyelitis, or myopathic disorders, such as Duchenne muscular dystrophy and myotonic dystrophy. There is good evidence that stabilisation of the spine in children with Duchenne muscular dystrophy who are able to walk (before respiratory compromise is too severe to preclude a general anaesthetic) may increase their lifespan by several years.

Congenital scoliosis This is caused by vertebral anomalies that produce a frontal plane growth asymmetry. The anomalies are present at birth, but the curvature may take years to be clinically evident. Close observation of spinal growth is required until skeletal maturity is reached. Brace treatment is ineffective for the primary structural curves, which are often short and rigid, but it may have a role in the control of compensatory curves. For progressive curves, surgical options include growing rod constructs such as magnetically controlled growing rod (MCGR) procedures, hemivertebra excision, correction and fusion or posterior instrumented correction and fusion. Summary box 33.8 Spinal deformity ●●

●● ●●

Early onset idiopathic scoliosis (5 cm retracted cuff tear attempting to abduct his shoulder, which is limited, by lack of balanced motor power, below 60°.

INVESTIGATION Tears are classified as small (less than 1 cm), intermediate (2–4 cm) and large (more than 5 cm). TREATMENT Treatment depends on the patient’s age, lifestyle and severity of symptoms. Arthroscopic or open repair with subacromial

Figure 34.12  Reverse geometry total shoulder replacement.

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Occur more commonly in older age groups 4–20% of 40–50 year olds have asymptomatic rotator cuff tears Up to 50% of 70 year olds have an asymptomatic tear Subacromial decompression is carried out to facilitate pain relief at cuff repair Acute tears may present with little pain but profound weakness Earlier repair after traumatic onset gives better results

Frozen shoulder (adhesive capsulitis, contracted shoulder) This is an idiopathic painful and stiff condition most commonly affecting females in their 50s. It is also associated with diabetes, heart or thyroid disease. HISTORY AND EXAMINATION Frozen shoulder is characterised by the onset of severe pain and may follow minor trauma. The differential diagnosis includes infection, fractures and rotator cuff tears. Initially there is severe pain but this improves with time. However, there is global loss of active and passive movement, limited by pain. The pathognomonic sign is loss of external rotation active. Radiographs are normal and distinguish it from the other ­condition that can globally and painfully affect shoulder movement: osteoarthritis. TREATMENT The clinical course can run over 1–2 years, often considerably longer in diabetic individuals, and is divided into painful, stiffening and thawing phases. If untreated, frozen shoulder will resolve, and the majority of patients are left with no functional problems. In the first phase of the condition, treatment is pain relief. Corticosteroids can also be injected locally. Despite the pain, the patient should be encouraged to perform as much active and passive movement as they can. Non-operative treatment can include distension injection of the glenohumeral joint with local anaesthetic and steroid. Operative options include manipulation under anaesthesia or arthroscopic release of the tight capsule, which usually produce pain relief and are indicated for prolonged stiffness.

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493

Summary box 34.4 Frozen shoulder (adhesive capsulitis) ●● ●● ●● ●● ●● ●●

Most commonly occurs in females in their 50s Spontaneous onset Produces severe pain followed by reduced shoulder motion Spontaneous resolution can occur over 1–2 years Differential diagnoses: calcific tendonitis and rotator cuff tear Injections, distension with saline, manipulation and surgical release may all help

Calcific tendinitis Calcium deposition within the supraspinatus tendon is believed to be part of a degenerative process, or the consequence of a partial degenerative tear of the tendon. HISTORY AND EXAMINATION There is severe, rapid onset shoulder pain with painful, restricted motion. However, in contrast to adhesive capsulitis, external rotation is possible. Subacromial calcific deposits can be seen on plain radiographs (Figure 34.13).

Figure 34.14  Rheumatoid arthritis of the shoulder.

reduction in pain and improvement in range of movement, though it is needed much less frequently since the introduction of biological therapies for rheumatoid disease. Intra-articular steroid injections may also be helpful. Shoulder replacement is complicated by poor bone stock and damage to the stabilising structures around the shoulder, especially the rotator cuff. The patient should only expect a reduction in pain. Any increase in range of movement is a bonus. Summary box 34.5 Shoulder problems in rheumatoid arthritis ●● ●● ●●

Arthroscopic synovectomy may be effective Rotator cuff tears are common Glenohumeral joint replacement improves pain but motion depends on rotator cuff involvement

Figure 34.13  Radiograph demonstrating calcific tendonitis.

TREATMENT Subacromial corticosteroid injections may help and can be accompanied by needling, aspiration or flushing of the deposits (barbotage). The condition is often self-limiting, with resorption of the calcium deposits. Surgery for resistant cases includes arthroscopic or open subacromial decompression and excision of the calcific deposits if they are prominent.

Arthritis of the shoulder Rheumatoid arthritis The glenohumeral joint is commonly involved in rheumatoid arthritis (Figure 34.14). As is typical of this condition, there is osteoporosis, destruction of the articular cartilage and synovial proliferation with pannus formation. The rotator cuff is weakened and frequently tears. Arthroscopic synovectomy may slow the progress of the joint destruction and lead to a

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Osteoarthritis of the shoulder Glenohumeral joint osteoarthritis is either primary (Figure 34.15), secondary to trauma (Figure 34.16) or end-stage rotator cuff disease i.e. cuff arthropathy (Figure 34.17). TREATMENT If medical treatment has failed, the surgical options are arthroscopic debridement or joint arthroplasty. Debridement is not predictable, but both total shoulder replacement (Figure 34.18) and hemiarthroplasty (Figure 34.19) have good results in appropriate patients. A standard total shoulder arthroplasty can be performed if the rotator cuff is intact. However, in most rheumatoid patients and all patients with cuff tear arthropathy, the cuff is deficient and either a hemiarthroplasty or a reverse polarity total shoulder arthroplasty (see Figure 34.12) should be used. Shoulder arthroplasty is an effective pain-relieving procedure, but less predictable in restoring motion, especially above shoulder level.

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Figure 34.15  Osteoarthritis of the glenohumeral joint.

Figure 34.18 Total shoulder replacement performed for osteo­ arthritis. An intact rotator cuff is essential.

Figure 34.16  Post-traumatic arthritis with malunion of the proximal humerus, collapse of the humeral head, subchondral sclerosis and osteophytes.

Figure 34.19  Shoulder hemiarthroplasty is performed for arthritis if there is a deficient rotator cuff. Figure 34.17  A massive cuff tear that has led to superior migration of the humeral head and secondary osteoarthritis of the glenohumeral joint.

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Arthrodesis of the joint is an alternative in younger patients with a history of sepsis or neurological problems (Figure 34.20). It is also used after brachial plexus injury, when nerve repairs restore hand and elbow function but the shoulder remains flail because of loss of the C5 supply. Good scapulothoracic control, tested by the ability to shrug the shoulder powerfully, is a prerequisite to successful arthrodesis. Patients retain a moderate range of movement at the shoulder girdle, as a result of scapulothoracic motion, which normally makes up one-third of apparent shoulder elevation, the remaining two-thirds being glenohumeral movement, which is lost in arthrodesis.

Figure 34.20  Arthrodesis of the shoulder.

The joint line is tender. Flexing and adducting the arm to place the hand behind the opposite shoulder reproduces pain. If symptoms are related to inferior osteophytes, impingement symptoms and signs are also present. TREATMENT An intra-articular corticosteroid injection will usually help, and even if the effect is short lived it localises the problem accurately. Surgery involves arthroscopic or open excision of the lateral 0.5–1cm of the clavicle (Figure 34.21). This gives good pain relief. In patients with symptoms that are predominantly those of impingement, arthroscopic removal of the inferior osteophytes with subacromial decompression should be performed.

Figure 34.21  Arthroscopic end-on view of the clavicle after excision of its distal end.

Summary box 34.6

Summary box 34.7

Arthritis of the shoulder

Acromioclavicular joint problems

●●

●●

●●

●●

●●

Severe cases are treated with hemiarthroplasty or total shoulder arthroplasty Total shoulder replacements should not be performed if the rotator cuff is deficient Pain relief is good following arthroplasty, though improvement in range of motion is less predictable Glenohumeral arthrodesis is an option in the young or those with a history of sepsis Post arthrodesis, motion is fair but is entirely scapulothoracic

495

●● ●●

●● ●●

●●

AC joint arthritis is common and may be asymptomatic It may become symptomatic secondary to trauma or repetitive overload Inferior clavicular osteophytes can impinge on the cuff Intra-articular steroid and local anaesthetic injection may relieve symptoms Excision of the lateral end of the clavicle gives good results

Long head of biceps tendon rupture Acromioclavicular joint arthritis Acromioclavicular joint (ACJ) arthritis is common and is often asymptomatic, noted as an incidental finding on radiographs (see Figure 34.4b). Symptoms typically arise in males aged 20–50 years. Inferior osteophytes can impinge on the underlying rotator cuff.

Rupture of the long head of biceps usually occurs in the elderly and is due to abrasion of the tendon in the bicipital groove, especially at the superior end, beneath the anterior acromion. It is associated with rotator cuff tears. Most patients present with few symptoms, although they often seek advice because of the bulge they notice in their arm.

HISTORY AND EXAMINATION There may be a history of trauma to the ACJ. Pain is activity related. There is prominence of the lateral end of the clavicle.

HISTORY AND EXAMINATION Patients feel a sense of ‘something giving way’ in front of the shoulder, sometimes with relief of pain if there was any

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present beforehand due to biceps tendinitis. The upper arm is bruised and elbow flexion produces a swelling in the front and middle of the arm (Figure 34.22). The lump will be permanent and is initially tender. Power is slightly diminished in the early stages, when there may also be cramping pains on use of the arm.

Recurrent traumatic instability HISTORY Traumatic shoulder dislocation is the commonest of all dislocations, usually first presenting in patients under 25. Usually the shoulder dislocates anteroinferiorly. Initially there is a notable traumatic event. Subsequent dislocations require less force. The shoulder may subluxate or actually dislocate (complete separation of the joint surfaces).

Figure 34.23  Apprehension test for anterior instability.

Figure 34.22  Bruising and change in the upper arm shape due to rupture of the long head of biceps.

TREATMENT Reassurance that pain and bruising will resolve is sufficient. Power improves over several months and surgery (biceps tenodesis) is not needed for function, though it may help the cosmetic appearance.

Dislocation of the shoulder and instability of the glenohumeral joint Three broad groups of shoulder instability exist.

Classification of glenohumeral instability ●● ●● ●●

Traumatic: unidirectional; involuntary; surgery is usually successful. Atraumatic: multidirectional, painful; involuntary; responds to surgery. Habitual: voluntary, with ligament laxity, painless; surgery usually contraindicated.

EXAMINATION On examination the shoulder has a full range of motion, but with forced abduction and external rotation the patient experiences apprehension (a sense of impending doom!) (Figure 34.23). INVESTIGATIONS On computed tomography (CT) or MR arthrography (Figure 34.24), detachment of the anteroinferior labrum (Bankart’s lesion) (Figures 34.25 and 34.26) and damage to the humeral head (Hill–Sach’s lesion) can often be seen. TREATMENT The relative indications for surgery are repeated dislocations, or symptoms of instability that persist after reduction of the first dislocation, that are interfering with the patient’s quality of life. Anterior instability can be treated with arthroscopic or open repair of the Bankart defect with tightening of the capsule, which prevents further dislocations in up to 90–95% of patients. Bony defects of the glenoid, and occasionally large Hill–Sachs lesions, may have to be grafted. For the less common recurrent posterior instability, repair of the ­damaged labrum and tightening of the posterior capsule is needed.

Arthur Sydney Blundell Bankart, 1879–1951, orthopaedic surgeon, The Middlesex Hospital, London, UK.

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497

(a)

Bankart lesion (b) Posterior labral injury

Figure 34.26  An end-on view of the glenoid labrum, demonstrating anteroinferior labral detachment (red) with the rotator cuff muscles (brown), long head of biceps tendon and labrum (grey).

Posterior dislocation of the shoulder

Figure 34.24  (a) Magnetic resonance (MR) arthrogram showing anterior Bankart lesion. (b) MR arthrogram showing posterior labral injury.

Summary box 34.8 Recurrent traumatic shoulder instability ●●

●● ●● ●● ●●

An appreciable force leads to the first dislocation or subluxation Subsequent dislocations/subluxations require less force The commonest direction of dislocation is anteroinferior There is a positive apprehension sign Surgical treatment repairs the labral lesion and tightens the capsule

A

B

This is a rare event but is easy to miss. The clue is often in the history, as the patient will have either had an electric shock, had an epileptic fit, or have been subject to severe restraint when their arm has been forced up their back (a half-Nelson) – all mechanisms producing forced internal rotation of the glenohumeral joint. The patient will be in severe pain and can be difficult to examine e.g. if they are psychotic and if this is why they are being restrained. For the same reason, the radiographer may only be able to get an anteroposterior (AP) view of the shoulder and, on this view, the shoulder may look normal to the unwary (Figure 34.27). It is the high ‘index of suspicion’ from the history which gives the best chance of making the diagnosis. TREATMENT This dislocation may be difficult to reduce if the posterior margin of the glenoid is embedded in the humeral head (a ‘locked’ posterior dislocation), so that open reduction is needed.

Atraumatic instability HISTORY There is usually no history of an initial injury. Instability may be multidirectional and the shoulder is usually associated with

C

D

E

Figure 34.25  Schematic representation of Bankart’s lesion, which forms a spectrum of pathology from minor labral detachment (B) to large detachments with glenoid rim fractures (bony Bankart; E).

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(a)

(b)

(c)

(d)

Figure 34.27 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 joint and further demonstrating the impacted fracture in the humeral head, or Hill–Sachs lesion.

subluxation rather than dislocation. The patient is often able to reduce the shoulder without assistance. EXAMINATION Generalised ligament laxity is common. Apprehension tests are positive, but often in more than one direction. Anterior and posterior drawing of the humeral head allows laxity to be tested (Figure 34.28). Overactivity of muscle groups such as pectoralis major should be sought, as this gives an avenue of treatment through rehabilitation. TREATMENT Specialist physiotherapy should be tried first in these patients, aiming to improve both the proprioception and firing patterns of the muscles around the shoulder (for instance biofeedback to control an overactive pectoralis major, or strengthening of underactive muscle groups). If this fails then surgery may be considered, by way of capsular tightening.

Habitual dislocation Habitual dislocators are patients who can sublux the shoulder at will, usually either anteroinferiorly or posteriorly. The manoeuvre is painless. Patients have generalised joint laxity and may subluxate the shoulder as a ‘party trick’. Patients should be advised to stop subluxating the shoulder, which may then allow the capsule to tighten naturally with age. They may benefit from assessment and advice from a specialist physiotherapist. Surgery is associated with a high failure rate and should be avoided.

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Figure 34.28  Generalised laxity can be appreciated by drawing the humeral head in anterior and posterior directions and feeling it slide up to, and possible even over, the glenoid rim. A sulcus will be produced under the acromion if the humerus is drawn inferiorly (sulcus sign).

DISORDERS OF THE ELBOW Anatomy and function The elbow joint allows flexion and extension as well as making up the proximal part of the radioulnar joint, which permits pronation and supination of the forearm. The brachial

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artery passes immediately in front of the joint, while the ulnar nerve passes lateral to the medial epicondyle, immediately behind it.

499

(a)

Tennis elbow (lateral epicondylitis) and golfer’s elbow (medial epicondylitis) These are discussed in Chapters 31 and 32.

Arthritis of the elbow Rheumatoid arthritis Surgery may be required, especially in end-stage disease ­(Figure 34.29). Arthroscopic or open radial head excision and synovectomy is effective for painful, restricted pronation and supination. Elbow arthroplasty is effective in the earliest stages for pain relief and functional restoration.

(b)

Figure 34.29  Typical end-stage unstable and destroyed rheumatoid elbow.

Figure 34.30  (a, b) Radiographs showing osteoarthritis of the elbow joint.

Osteoarthritis

and increases range of motion in earlier stages. Interposition arthroplasty (for example Achilles tendon allograft) may be considered in younger patients though it can be ­associated

Osteoarthritis of the elbow is usually primary (Figure 34.30) or secondary to trauma. HISTORY Typical patients are middle-aged males in manual occupations. Symptoms are pain, locking, crepitus and painful motion with loss of extension. Ulnar nerve entrapment symptoms may be present.

(a)

(b)

EXAMINATION There is usually loss of extension and restriction of flexion. Pronation and supination tend to be spared in comparison with rheumatoid arthritis. TREATMENT Surgery should be considered only if medical treatment fails. Arthrodesis may be offered for those performing heavy manual work (Figure 34.31), but is associated with significant residual functional loss, as a joint replacement will not survive long under heavy loading. Surgical debridement alleviates pain

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Figure 34.31  (a, b) Ankylosed elbow after tuberculosis. Arthrodesis is a surgical procedure to achieve the same end result, by excising the articular surfaces and compression plating across the joint.

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(a)

(b)

Figure 34.32  (a, b) Linked total elbow replacement.

with significant bone loss with time, possibly restricting future treatments). Prosthetic joint arthroplasty provides more predictable symptomatic relief (Figure 34.32) but high activity levels are associated with early loosening.

Summary box 34.9 Arthritis of the elbow ●●

●●

●●

Excision of the radial head improves pain and pronation– supination in rheumatoid arthritis Total elbow replacement gives good results in rheumatoid and low demand patients Arthrodesis may be the only surgical option in a high demand manual labourer

Loose bodies in the elbow

Figure 34.33  Osteochondritis dessicans of the capitellum (Panner’s disease).

The common causes are osteoarthritis, osteochondritis dissecans in the young (Figure 34.33) and synovial chondromatosis (Figure 34.34). Patients describe sudden pain and locking, and the need to manipulate the elbow for relief. Plain radiographs will usually confirm the diagnosis (Figure 34.35). Arthroscopic clearance of the joint produces good results (Figure 34.36).

Olecranon bursitis This is a relatively common disorder in which the elbow becomes red, warm, swollen and painful. Initially, septic arthritis may be suspected. However, on examination signs and symptoms are confined to the back of the elbow (Figure 34.37) and movement within an arc of 30–130° is possible. Most cases settle with anti-inflammatories. If the patient is pyrexial antibiotics should be given. Formal drainage of the bursa is indicated if purulent material is present.

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Figure 34.34  Synovial chondromatosis.

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Figure 34.35 Radiographs showing loose bodies in the elbow (arrow).

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Figure 34.38  Large chronic olecranon bursa with dense calcific deposit.

Ulnar nerve compression Compression of the ulnar nerve occurs in the cubital tunnel (behind the medial epicondyle), at the junction of the arcade of Struthers, and also at the medial intermuscular septum, as the nerve passes into the posterior compartment of the distal humerus. It can also occur as the nerve passes between the heads of the flexor carpi ulnaris (Figure 34.39). (a)

Ulnar nerve Figure 34.36 Loose bodies removed arthroscopically from the patient in Figure 34.35.

MCL FCU muscle belly

Fibrous arch of FCU (b)

Figure 34.37  Olecranon bursitis.

Chronic bursitis may be associated with calcific nodules of the bursal lining (Figure 34.38). These can be excised if they prove troublesome.

Figure 34.39  (a) Anatomy of the cubital tunnel site for ulnar nerve compression, with (b) a view of arthroscopic ulnar nerve decompression (inset). FCU, flexor carpi ulnaris; MCL, medial collateral ligament.

Sir John Struthers, 1823–1899, Professor of Anatomy, University of Aberdeen, Aberdeen, UK.

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HISTORY AND EXAMINATION Patients describe tingling/numbness in the little and ring fingers. A positive Tinel’s sign is usually present at the compression site, with wasting and weakness of the intrinsic muscles of the hand (Figure 34.40). Froment’s sign will be positive, due to weakness of the adductor pollicis (Figure 34.41). Nerve conduction studies have an unpredictable diagnostic value in the early stages. Radiographs may confirm medial osteophytes if compression is secondary to arthritis.

Summary box 34.10 Other common elbow problems ●●

●●

●●

Loose bodies cause locking and can be removed arthroscopically If the ulnar nerve is compressed, weakness and wasting will be seen in the hands Simple decompression is usually successful

TUMOURS OF THE UPPER LIMB Tumours are discussed in Chapter 37.

HAND The index finger works against the thumb for fine pinch grip; the thumb can press against the side of the flexed index finger for a key grip; the tips of the thumb, index and middle fingers provide a tripod pinch; all fingers curl for hook grip while the little and ring fingers provide the most power when making a fist. A stable wrist is required to allow good hand function.

Clinical history and physical examination Figure 34.40  Intrinsic muscle wasting on the left due to ulnar neuropathy.

History The occupation, sport and recreational activities (especially music) and hand dominance are all important items of information needed when treating a hand problem.

Examination The examination of the hand should assess perfusion, sensation, movement, power and coordination. A check should also be made for rotational malalignment of the digits (Figure 34.42). There are also a number of special tests (which are beyond the scope of this chapter) relevant to different conditions.

Figure 34.41  Froment’s sign tests the adductor pollicis. The patient is asked to hold a piece of paper in a side pinch between the thumb and the index finger. The examiner attempts to pull the paper out. Owing to weakness of the adductor pollicus, the patient will compensate by flexing the flexor pollicis longus, which is supplied by the anterior interosseous nerve.

TREATMENT Splints preventing elbow flexion at night may be useful. If symptoms persist, surgery can be performed, including ­simple nerve decompression (most cases), partial medial epicondylectomy and/or anterior transposition of the nerve. Transposition is necessary in cases of valgus deformity or if the nerve is unstable after decompression.

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Figure 34.42  Rotational deformity of the little finger.

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Investigations

503

Ulnar collateral ligament

Radiographs can be used to assess for arthritis or tumours. Electrophysiological studies may be required to assess nerve function. MRI is useful for diagnosing avascular necrosis, ligament injuries or soft tissue tumours.

Hand swelling and stiffness Swelling followed by stiffness is the arch enemy of hand reha­bilitation. The hand will swell after injury, surgery or infection. In response, the wrist flexes and then there is compensatory metacarpophalangeal joint (MCPJ) extension and interphalangeal joint (IPJ) flexion. If action is not taken this position will become permanent, as collateral ligaments shrink and tissues fibrose. Hand elevation to reduce swelling, splintage in the position of safety to prevent collateral shortening (Edinburgh position: wrist extension, MCPJ flexion, IPJ extension) and early mobilisation prevent permanent stiffness.

Figure 34.43  Magnetic resonance imaging showing rupture of the ulnar collateral ligament of the thumb (skier’s thumb).

Summary box 34.11 General principles of treatment Avoid swelling and stiffness by: ●● ●● ●●

Elevation – reduce swelling Splintage – avoid contractures Movement – pump away swelling and encourage suppleness

Thumb ulnar collateral ligament injury Chronic thumb overuse leads to stretching of the ulnar collateral ligament and instability (gamekeeper’s thumb). The ligament can also rupture acutely if the thumb is forcibly abducted (skier’s thumb). If valgus stress causes significant opening of the joint on the ulnar side then the ligament needs to be repaired surgically, as the adductor aponeurosis interposes between the torn end of the ligament and its insertion (Figure 34.43), preventing healing and causing chronic instability.

Triangular fibrocartilage complex (TFCC) The triangular fibrocartilage is a complex consisting of the ulnocarpal ligaments, extensor carpi ulnaris tendon sheath and a meniscus-like structure between the distal ulna and the carpus. It is continuous with the dorsal and volar wrist capsules and stabilises the distal radioulnar joint. It can undergo traumatic or degenerative tears, presenting with ulna-sided wrist pain and distal radioulnar instability. An MR arthrogram or wrist arthroscopy aids diagnosis (Figure 34.44). Peripheral tears of the TFCC can be repaired (open or arthroscopically), while central degenerative tears can be arthroscopically debrided.

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Figure 34.44 Magnetic resonance arthrogram showing peripheral detachment of the triangular fibrocartilage complex.

Infections Paronychia Nail bed infection is the commonest hand infection (Figure 34.45). After initial inflammation, pus accumulates beside the nail. It is best treated with incision, drainage and appropriate antibiotic therapy. This is sometimes, but not always, facilitated by partial nail removal to allow full drainage of the collection.

Felon A felon is an abscess between the specialised fibrous septae in the fingertip pulp. It causes intense pain and may lead

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an ultrasound scan or MRI can delineate the extent of the collections within the deep palmar spaces.

Arthritis Rheumatoid arthritis

Figure 34.45  Acute paronychia.

to terminal phalangeal osteomyelitis. Incision and drainage through the midline of the pulp of the finger in the location of maximal swelling, followed by intravenous antibiotics, are recommended.

Flexor tendon sheath infection Flexor tendon sheath infections present with Kanavel’s cardinal signs: the affected finger is held in flexion; there is uniform swelling over the tendon and digit; it is tender to touch; and the patient experiences pain on passive extension of the finger. Treatment is by tendon sheath irrigation using catheters inserted through small wounds at the proximal and distal ends of the affected sheath or by an open approach if the viability of the digit is threatened. This is followed by what is often an extended course of intravenous antibiotics. If infection is untreated tendon adhesions and necrosis occur. Infection can spread proximally, damaging the whole hand.

Rheumatoid arthritis presents with classic symptoms: morning stiffness, symmetrical arthritis, hand deformities and rheumatoid nodules. Diagnostic criteria include seropositive rheumatoid factor and radiographic changes (Table 34.1). The inflamed rheumatoid synovium (pannus) destroys ligaments, tendons and joints, producing pain, deformity and loss of function. Typical rheumatoid deformities in the hand include boutonnière (Figure 34.46), swan neck (Figure 34.47) and radial drift of the wrist (due to supination of the

TABLE 34.1  Radiographic differences between rheumatoid and osteoarthritis. Rheumatoid arthritis

Osteoarthritis

Periarticular osteoporosis/ subchondral erosions

Subchondral sclerosis and cysts

Periarticular soft-tissue swelling

Less pronounced swelling

Joint space narrowing

Joint space narrowing

Marginal erosions

Marginal osteophytes

Joint deformity/malalignment

Less pronounced deformities

Ankylosis

Less common ankylosis

Summary box 34.12 Treatment of hand infections ●● ●● ●●

Elevate, splint and give intravenous antibiotics Surgical drainage should include tendon sheath irrigation Early mobilisation

Mycobacterial infections

Rupture

Figure 34.46 Boutonnière deformity.

Tuberculosis may involve the tenosynovium, joints or bone. The most dramatic form is a compound palmar ganglion, with synovial swelling proximal and distal to the transverse carpal ligament, occasionally causing symptoms of carpal tunnel syndrome. The diagnosis is made by taking a biopsy. Synovectomy should be performed and the patient treated with the appropriate antibiotics.

Deep fascial space infections These infections occur in the palm but may be limited to a web space. The whole hand becomes swollen and tender as pus collects on either side of the septum. Treatment is incision and drainage with thorough washout of the wound. It is important that all deep spaces are opened: incision on both dorsal and volar sides of the hand may be needed. If in doubt

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Figure 34.47  Swan neck deformity.

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carpus), with compensatory ulnar deviation of the metacarpophalangeal joints (Figure 34.48). Pannus can cause extensor tendon ruptures, classically starting with the little finger and progressing stepwise in a radial direction (Vaughan Jackson syndrome). With progressive deformity and instability of the wrist and hand, activities such as key pinch and the opening of jars become impossible to perform. The treatment should be dictated by the patient’s levels of pain and disability, not purely on the basis of deformity.

505

young patient, a constrained ulnar head arthroplasty is preferred. 4 Arthrodesis of the wrist, thumb and some of the smaller joints: gives good pain relief and creates a stable axis against which other parts can function. 5 Metacarpophalangeal and interphalangeal joint replacements: provide pain relief and functional improvement. Total wrist arthroplasty will also provide good pain relief and some motion (Figure 34.49). 6 Tendon reconstructions: some ruptured tendons can cause significant morbidity (Figure 34.50) and are often treated either by a tendon transfer or a local joint fusion

Figure 34.48 Rheumatoid hand showing ulnar drift at the meta­ carpo­phalangeal joints.

Summary box 34.13 Manifestations of rheumatoid arthritis in the hand ●● ●● ●● ●●

●●

Swan neck, Boutonnière finger deformities Extensor tendon ruptures (Vaughan–Jackson syndrome) Flexor tendon synovitis or rupture Metacarpophalangeal joints: flexion, ulnar deviation, subluxation, dislocation Wrist: radial deviation, carpal supination, prominent ulnar head (caput ulnae), extensor tenosynovitis

Figure 34.49  Total wrist replacement.

MANAGEMENT The primary indications for surgery are: (1) pain relief; (2) functional improvement; (3) to prevent disease progression; (4) cosmesis. Patients may require many surgical procedures over time and a helpful axiom is to start proximally and work distally, alternating between motion-sacrificing and -sparing procedures. The various procedures which can be considered are: 1 Synovectomy: improves pain, increases function and prevents tendon rupture. 2 Trigger finger releases and nerve decompression surgery (carpal tunnel syndrome). 3 Distal ulna excision: reduces pain, prevents extensor tendon rupture or protects repaired extensor tendons. Distal ulna excision leads to instability and so, in the

Figure 34.50  Rupture of the extensor tendons to the little and ring fingers.

Boutonnièreis French for ‘button-hole’.

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Osteoarthritis

(a)

(b)

WRIST The radiocarpal joint can develop primary or secondary osteoarthritis (after intra-articular trauma and infection). If conservative measures have failed then operative management includes limited or total wrist arthrodesis and total wrist replacement. HAND Females are more commonly affected than males. The commonly affected joints are the distal interphalangeal (Heberden’s nodes), proximal interphalangeal (Bouchard’s nodes) and the thumb carpometacarpal joints (Figure 34.51). Symptoms rarely correlate with the appearance, either clinically or radiographically. Treatment includes splinting, physiotherapy and steroid injections. Surgical options include arthrodesis for distal (DIP) and proximal interphalangeal (PIP) joints (Figure 34.52), joint replacement (PIP and metacarpophalangeal (MCP) joints) and excision arthroplasty (excision of the trapezium for thumb carpometacarpal joint arthritis). Joint arthrodesis eliminates pain at the expense of motion, but function is often well preserved.

Other forms of arthritis in the hand Psoriasis particularly affects the interphalangeal joints, but is asymmetrical in nature and causes fusiform swelling of the digits along with nail changes. Gout causes pain, joint red-

Figure 34.52 Radiographs of the distal interphalangeal and proximal interphalangeal joints treated with arthrodesis (a) and joint replacement (b).

ness, occasionally tophi, and can be difficult to differentiate from septic arthritis. Serum urate is not always raised in acute attacks but finding negatively birefringent sodium urate crystals on microscopy of aspirated joint fluid is diagnostic.

Dupuytren’s contracture

Figure 34.51  Hand deformities secondary to osteoarthritis.

Dupuytren’s contracture is most often characterised as an autosomal dominant condition, common in northern Europe, predominantly in men in the 5th–7th decades of life. Four out of seven cases occur in those with a family history but there are also many sporadic cases. It is associated with smoking, trauma, epilepsy, AIDS, hypothyroidism and alcoholic cirrhosis. It also appears very frequently as a clinical case in postgraduate exams! The characteristic features are palmar nodules, skin puckering, cords of the palm and digits and flexion contractures of the digits (Figure 34.53). It is commonest on the ulnar side of the hand. Garrod’s knuckle pads (thickened skin on the dorsum of the PIP joint) are another feature visible on examination and seen in more severe forms of the disease (Figure 34.54). The condition can also produce cords in the penis, causing it to become curved (Peyronie’s disease) and may also produce plantar thickening (Ledderhosen disease). Intervention is indicated when the patient cannot put the affected hand flat on the table owing to fixed deformity, or when any flexion contracture develops in the PIP joint. Milder cases may be treated by needle fasciotomy or

William Heberden (Snr.), 1710–1801, physician, who practised first in Cambridge and from 1748 in London, UK, described these nodes in 1802. Charles Jacques Bouchard, 1837–1915, physician, Dean of the Faculty of Medicine, Paris, France. Baron Guillaume Dupuytren, 1777–1835, surgeon, Hôtel Dieu, Paris, France, described this condition in 1831.

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Summary box 34.14 Dupuytren’s contracture ●● ●●

●● ●●

Autosomal dominant inheritance but many sporadic cases Fibroblastic hyperplasia with resultant skin nodules, cords and deformities Intervention is indicated if hand cannot be placed flat Severe fixed flexion deformities may mean that amputation is the only surgical option

Tendon disorders Trigger digit

Figure 34.53  Dupuytren’s contracture.

Triggering occurs in the fingers or in the thumb as a result of a size mismatch between the flexor tendon and the sheath (usually at the A1 pulley) in which it glides. The patient complains of painful locking or snapping of the finger, usually when attempting to straighten a bent finger. Occasionally, it may present as a finger that is too painful to bend, associated with pain and tenderness at the A1 pulley. There is often a palpable nodule in the tendon. Management is a steroid injection into the sheath, and if this fails then surgical tendon sheath (A1 pulley) release should be performed under local anaesthesia, taking care not to cut too much of the pulley and create bowstringing of the flexor tendon. Trigger digits, especially the thumb, can occur in infants and usually resolve spontaneously.

De Quervain’s disease

Figure 34.54  Garrod’s knuckle pads.

De Quervain’s disease is caused by tenosynovitis of the abductor pollicis longus (APL) and extensor pollicis brevis (EPB) in the first dorsal wrist extensor compartment (1st EC). It is predominantly seen in middle-aged females and is associated with pregnancy (new mother’s wrist) and inflammatory arthritis. The clinical features are radial wrist pain, tenderness, swelling (Figure 34.55) and a positive Finkelstein’s test

collagenase injections, while more severe cases are managed surgically. Great care should be taken during surgery to avoid damage to the digital nerves, which may be trapped in the fibrous tissue. At the end of surgery, it may not be possible to obtain primary closure of the skin, so one should consider performing Z-plasties to lengthen the skin, full thickness skin grafting taken from the anteromedial proximal forearm (hairless) or occasionally leaving an open wound to heal by secondary intention. In late stage disease a fixed contracture of the MCP and PIP joints may develop. In these cases, excision of the fibrous bands may produce no improvement in the condition, and if the contracted finger is preventing useful function of the hand then amputation may have to be considered.

Figure 34.55  De Quervain’s disease.

Sir Archibald Edward Garrod, 1857–1936, Regius Professor of Medicine, the University of Oxford, Oxford, UK, described this condition in 1893. Francois de la Peyronie, 1678–1747, surgeon to King Louis XIV of France and founder of the Royal Academy of Surgery, Paris, France. Georg Ledderhose, 1855–1925, German surgeon, described this disease in 1894. Fritz de Quervain, 1868–1940, Professor of Surgery, Berne, Switzerland, described this form of tenosynovitis in 1895.

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(pain over the 1st EC associated with ulnar deviation of the wrist when the thumb is clasped in the palm). The management options are non-steroidal anti-inflammatories, splintage, steroid injections and surgical release of the extensor retinaculum of the first dorsal compartment. If surgery is considered, careful attention should be paid to fully releasing the APL and EPB, which frequently consist of bundles of separate tendon slips that lie in separate sheaths.

Compressive neuropathies Median nerve (carpal tunnel syndrome) The majority of cases of carpal tunnel syndrome are idiopathic. It is however, associated with diabetes, thyroid disorders, alcoholism, amyloidosis, inflammatory arthritis, pregnancy and obesity.

been shown to be highly sensitive and specific. Electrophysiological studies may confirm the diagnosis, with evidence of slowing of nerve conduction through the carpal tunnel. Non-operative treatment includes night splintage of the wrist in extension and steroid injections. If surgery is required the median nerve is surgically decompressed by incising the roof of the tunnel (transverse carpal ligament), as either an open or an endoscopic percutaneous procedure. Summary box 34.15 Carpal tunnel syndrome ●● ●● ●● ●●

HISTORY The patient presents with tingling and infrequently numbness of the volar aspects of the radial three and a half digits. Patients also complain of being woken at night by pain and tingling, and that hanging their hand out of the bed provides relief. They may also complain of clumsiness when picking up small objects or when carrying heavy ones. Symptoms and signs are often bilateral.

Night pain is common and relieved by shaking the hand Thenar wasting is an advanced sign Tinel’s, Phalen’s and Durkin’s tests are useful Treatment includes splints and surgical decompression

Ulnar nerve (Guyon’s tunnel syndrome) Ulnar nerve compression in Guyon’s canal can lead to tingling and numbness in the ring and little fingers with hypothenar wasting. There is preservation of dorsal sensation over the little and ring fingers, because although these areas are innervated by the ulnar nerve the dorsal branches do not pass through Guyon’s canal. Compression is usually due to a ganglion, ulnar artery aneurysm or a fracture of the hook of hamate.

EXAMINATION Wasting of the thenar eminence is visible (Figure 34.56) in chronic severe cases, and there is sometimes weakness of the abductor pollicis brevis. The tests for carpal tunnel compression are described in Chapter 31 but the most reliable are: (1) Tinel’s – percussion over the carpal tunnel and (2) Phalen’s test – reproduction of paraesthesia with full wrist flexion. More recently, Durkin’s compression test, in which digital pressure over the carpal tunnel reproduces the symptoms, has

Idiopathic avascular necrosis of the lunate (Kienböck’s disease, Figure 34.57) or scaphoid (Preiser’s disease) can occur. The clinical presentation is of wrist pain and the diagnosis

Figure 34.56  Thenar muscle wasting in carpal tunnel syndrome.

Figure 34.57  Avascular necrosis of the lunate (Keinbock’s).

Avascular necrosis of carpal bones

Jean Casimir Felix Guyon, 1831–1920, Professor of Genito-urinary Surgery, Paris, France. Robert Keinböck, 1871–1953, Professor of Radiology, Vienna, Austria, described this condition in 1910.

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can be confirmed with radiographs and MRI. The natural history of the condition is that it leads to collapse of the avascular carpal bones and subsequent arthritis of the carpus, which may be best treated with a partial or complete fusion of the wrist. This will at least give a strong and painless wrist. The limitation in movement caused by arthrodesis procedures is not as great as might be expected.

the flexor tendon sheath at the base of the finger (seed ganglion). Dorsal and volar wrist ganglions can cause discomfort. The swellings are smooth, fluctuant and transilluminate brightly. Mucous cysts can frequently discharge and cause nail changes (Figure 34.60). Seed ganglions can be painful when gripping. Aspiration or surgical excision can be considered. Patients should be informed regarding possible recurrence.

Ganglion cysts

Congenital malformations

Ganglion cysts are the commonest cause of a swelling in the hand and they are found most often on the dorsal (Figure 34.58) and volar (Figure 34.59) surfaces of the wrist, over the dorsum of the DIP joint (digital mucous cyst) or within

There are many congenital malformations of the upper limb and these are discussed in Chapter 39. A classification summarising the main congenital defects and based on aetiology appears as Table 34.2

(a)

509

(b)

Figure 34.58  (a) Clinical and (b) surgical appearance of a dorsal wrist ganglion.

Figure 34.59  Volar wrist ganglion.

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Figure 34.60  Myxoid cyst with changes in the nail.

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TABLE 34.2  Congenital malformations (hand and wrist) A Defects in formation due to arrested development

1 Transverse agenesis 2 Longitudinal agenesis (a) radial ray aplasia; (b) median ray aplasia; (c)ulnar ray aplasia 3 Thumb aplasia/hypoplasia

B Defects in differentiation/separation

1 Syndactyly 2 Camptodactyly 3 Clinodactyly 4 Kirner’s deformity 5 Radioulnar synostosis

C Duplications

1 Supernumerary phalanges 2 Supernumerary digits (polydactyly)

D Excess development/hyperplasia

Macrodactyly

E Insufficient development/hypoplasia

Thumb hypoplasia

F Constricting (amniotic) bands

Simple amniotic band syndrome

G Generalised skeletal anomalies

Marfan, Turner and Down syndromes

FURTHER READING Carr AJ, Cooper CD, Campbell AK et al. Clinical effectiveness and cost-effectiveness of open and arthroscopic rotator cuff repair [the UK Rotator Cuff Surgery (UKUFF) randomised trial]. Health Technol Assess 2015; 19(80): 1–218. Constant CR, Murley AH. A clinical method of functional assessment of the shoulder. Clin Orthop 1987; 214: 160–4. Dawson J, Rogers K, Fitzpatrick R, Carr A. The Oxford shoulder score revisited. Arch Orthop Trauma Surg 2009; 129(1): 119–23. Gill DR, Morrey BF. The Coonrad-Morrey total elbow arthroplasty in patients who have rheumatoid arthritis. A ten to fifteen-year follow-up study. J Bone Joint Surg Am 1998; 80: 1327–35. Mizuno N, Denard PJ, Raiss P et al. Long-term results of the Latarjet procedure for anterior instability of the shoulder. J Shoulder Elbow Surg 2014; 23(11); 1691–9.

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Neer CS. Anterior acromioplasty for the chronic impingement syndrome in the shoulder: a preliminary report. J Bone Joint Surg [Am] 1972; 54-A: 41–50. O’Driscoll SW, Bell DF, Morrey BF. Posterolateral rotatory instability of the elbow. J Bone Joint Surg Am 1991; 73: 440–6. Poppen NK, Walker PS. Normal and abnormal motion of the shoulder. J Bone Joint Surg [Am] 1976; 58-A: 195–201. Rowe CR, Patel D, Southmayd WW. The Bankart procedure: long-term end-result study. J Bone Joint Surg [Am] 1978; 60-A: 1–16. Singh JA, Sperling JW, Schleck S et al. Periprosthetic infections after total shoulder arthroplasty: A 33-year perspective. J Shoulder Elbow Surg. 2012; 21(11): 1534–41.

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ve Bailey & Love Bailey & Love Bailey & Love ve Bailey & Love Bailey & Love Bailey & 35Love Chapter

Hip and knee Learning objectives To understand: •• The anatomy and biomechanics of the hip and knee and their clinical implications •• The clinical presentation, aetiology and management of common hip and knee pathologies

•• The principles of joint replacement including important

THE HIP JOINT

ischiofemoral ligament posteriorly), the joint capsule and the labrum. The muscles running across the joint (short external rotator muscles posteriorly, the iliopsoas anteriorly and the hip abductors laterally) constitute the dynamic stabilisers. The acetabular labrum is a fibrocartilagenous structure that is triangular in cross-section and attaches to the rim of the acetabulum except at its base, where it is replaced by the transverse ligament. It helps in deepening the socket, thereby enhancing stability. It also acts as a fluid seal and thereby helps to improve joint lubrication.The femoral head derives its blood supply mainly from the retinacular branches of the medial circumflex femoral artery and there is a small contribution from the artery of the ligamentum teres.

Applied anatomy The hip is a ball and socket joint formed by the head of the femur and the cup-shaped acetabulum (Latin: little vinegar cup) (Figure 35.1). The joint allows a considerable range of movement in different planes, and is still inherently stable because of its bony anatomy and the static and dynamic stabilisers. The static stabilisers are composed of the ligaments (iliofemoral and pubofemoral ligaments anteriorly and the

Acetabulum Capsule

Iliofemoral ligament

complications

•• The advances in surgical practice in this field

Summary box 35.1 Anatomy ●●

●● ●●

●●

The hip joint is a ball and socket joint, stabilised by static and dynamic stabilisers Static stabilisers include the capsule, ligaments and labrum Dynamic stabilisers consist of the muscles acting across the joint Blood supply to the femoral head is mainly derived from the medial circumflex femoral artery

Biomechanics of the hip joint Capsule Ligamentum teres Figure 35.1  Anatomy of the hip joint.

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Interotrochanteric line

Kinetic analysis reveals that forces as high as three times body weight can be exerted across the hip joint during activities of daily living, and eight times body weight during physically demanding activities. This is primarily the result of contraction of muscles crossing the joint. The abductors, because of their

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insertion at the greater trochanter, help in supporting the pelvis when the patient stands on one leg and thereby form the basis of a Trendelenburg test (Figure 35.2).

TABLE 35.1 Aetiology of avascular necrosis of the femoral head. Sickle cell disease Haemoglobinopathies

Abductor muscles holding pelvis up

Caisson disease (‘the bends’ in divers)

Load on joint

Hyperlipidaemia Systemic lupus erythematosus Gaucher’s disease Chronic liver disease Antiphospholipid antibody syndrome Radiotherapy W weight of subject

Chemotherapy Human immunodeficiency virus Hypercoagulable states (protein C and protein S deficiency) Steroids

Biomechanical schematic representation of loads pivoted on a beam. The hip joint is the fulcrum

Anatomy of body

W

3W x

3x

4W Figure 35.2  Load on the hip joint when a subject weighing W stands on one leg. Hopping increases the load from 4 to 10W.

Summary box 35.2 Forces going through the hip joint ●● ●● ●●

Lifting leg from bed – one and a half times body weight Standing on one leg – three times body weight Running and jumping – ten times body weight

Conditions affecting the hip joint Common hip pathologies in the paediatric age group and secondary to trauma are covered in Chapters 39, 27 and 28. This chapter focuses on the acquired pathological conditions in the adult.

Avascular necrosis Avascular necrosis (AVN), or osteonecrosis of the femoral head, occurs because of an interruption in the blood supply to the femoral head that causes bone death. This leads to collapse of the femoral head, and subsequent secondary osteoarthritis. AVN can be primary (idiopathic) or secondary to other pathology (Table 35.1).

Alcohol excess Idiopathic (see Perthes’ disease, Chapter 39)

CLINICAL FEATURES AVN usually affects men aged from 35 to 45 and is bilateral in over 50% of patients. The patient is frequently asymptomatic in the early stages. As the disease progresses the patient may complain of an ache in the groin and walk with a limp; clinical examination may reveal limitation of movement. INVESTIGATIONS A weight-bearing anteroposterior (AP) radiograph of the pelvis along with a lateral radiograph will show the classical features of AVN including increased sclerosis in the early stages, and the crescent sign indicating subchondral bone resorption. In the late stages there may be flattening indicating a segmental head collapse (Figure 35.3). However, radiographs may be normal in the early stages of the disease and, therefore, the most sensitive and specific way of investigating these patients is with magnetic resonance imaging (MRI). MRI allows accurate assessment of the extent of involvement and can also identify associated bone marrow changes. This helps in early diagnosis and prediction of prognosis (Figure 35.4). In 1985, Ficat classified the disease into five stages. In 1995, Steinberg modified this classification into seven stages based upon both radiograph and MRI appearance (Table 35.2). Stages I–IV are further divided into A, B or C depending on the extent of involvement of the femoral head. TREATMENT Conservative treatment usually leads to poor results and is therefore not recommended. The choice of surgical treatment depends on whether the head has collapsed or not. In the pre-collapse group the principle is to preserve and preferably encourage revascularisation of the femoral head, whereas in

Friedrich Trendelenburg, 1844–1924, Professor of Surgery successively at Rostock (1875–1882), Bonn (1882–1895) and Leipzig (1895–1911), Germany. The Trendelenburg position was first described in 1885. A caissonis a watertight chamber used to protect construction workers during the building of underwater structures by means of pressurised air introduction. Philippe Charles Ernest Gaucher, 1854–1918, physician, Hôpital St. Louis, Paris, France, described familial splenic anaemia in 1882.

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(a)

513

TABLE 35.2 Steinberg’s classification of avascular necrosis of the femoral head based on the type of radiological change on radiography and magnetic resonance imaging (MRI).

(b)

Stage

Description

Normal or non-diagnostic radiograph, bone scan or MRI

I

Normal radiograph, abnormal MRI or bone scan

II

Sclerosis and cysts

III

Subchondral collapse, crescent sign

IV

Flattening of the head, normal acetabulum

V

Acetabular involvement

VI

Obliteration of joint space

the collapse group the aim is to bring the undamaged parts of the femoral head into the load-bearing area. The surgical treatment for the pre-collapse stage includes core decompression, which is aimed at relieving intravascular congestion in the femoral head, and thereby pain. This can be achieved with or without bone grafting; a vascularised bone graft can also be used to stimulate bone formation. Once the femoral head has collapsed, either a femoral osteotomy (which aims to transfer the weight-bearing area of the femoral head and thereby protect the collapsed segment) or a joint replacement (if degenerative changes have set in) is the preferred option (see later).

Summary box 35.3 Avascular necrosis of the femoral head ●●

●● ●●

Figure 35.3  (a, b) Radiological appearance of avascular necrosis of the femoral head.

●●

●●

●●

Patients can be asymptomatic in the early stages and therefore a high index of suspicion is necessary for initial diagnosis MRI scans are needed for early diagnosis Treatment is based on whether the patient presents before or after the femoral head has collapsed In the pre-collapse stage, treatement focuses on revascularisation In the collapsed stage, the aim is to replace the damaged joint surface Prognosis is dependent upon the extent of femoral head involvement

Osteoarthritis (OA)

Figure 35.4  Magnetic resonance imaging scan of the hip joint showing avascular necrosis and the extent of involvement of the femoral head (arrrow).

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OA is referred to as primary when no predisposing cause can be found and secondary (including traumatic) when it develops after an insult to the hip joint. A multitude of factors including genetic, biochemical and mechanical influences have been implicated in the development of primary OA. The exact mechanism for the development of primary OA remains unknown and it is therefore termed idiopathic. Femoroacetabular impingement (FAI) has been proposed as an aetiological factor responsible for the development of OA. Secondary OA develops following trauma, AVN, dysplasia, slipped capital femoral epiphysis, inflammatory arthropathy

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or other known predisposing cause. The causes of OA of the hip are given in Table 35.3.

(a)

TABLE 35.3 Aetiology of osteoarthritis. Primary Cause unknown, termed idiopathic Associations: for example, genetics, gender, obesity Secondary Trauma Avascular necrosis Inflammatory arthropathy (e.g. rheumatoid arthritis) Perthes’ disease Developmental dysplasia of the hip Slipped capital femoral epiphysis Septic arthritis Femoroacetabular impingement implicated as a possible cause

CLINICAL FEATURES Osteoarthritis of the hip affects 10–25% of those over the age of 65 years. The most consistent symptoms are groin pain and limitation of movement. The pain may also radiate down to the knee joint, and in some cases the only presenting feature may be a painful knee. In the early stages of the disease, pain is activity related but as the disease progresses the patient also complains of pain at rest. The patient frequently complains of night pain and may also find it difficult to get into a comfortable position while sleeping. Functionally, most have difficulty in putting on their shoes and socks, and getting into and out of a bath or a car. As the pain increases the joint gradually loses its movement because of muscle spasm, capsular contracture and osteophyte formation. Clinical examination may reveal gluteal muscle wasting. There may also be a limp, with a positive Trendelenburg’s test. Leg length discrepancy, usually shortening, and limitation of movement, particularly internal rotation, are consistent features. Many patients present with a fixed flexion deformity that is best elicited by a modified Thomas’ test (see Chapter 31). INVESTIGATIONS The characteristic features on radiograph are (1) a reduction of joint space, (2) sclerosis in the subchondral bone, (3) subchondral cysts and (4) osteophyte formation (Figure 35.5). Eventually, a collapsed femoral head may also be evident.

(b)

Figure 35.5 Anteroposterior (a) and enlarged anteroposterior (b) radiographs of the hip joint showing osteoarthritis.

(fusion), an osteotomy (re-alignment) or a joint replacement (Figure 3.6). More and more joint replacements are now being performed. The indications are based on limitation of lifestyle and individual needs, thereby making it a truly life-improving operation. Summary box 35.4 Osteoarthritis of the hip ●●

TREATMENT There is no specific pharmacological therapy for OA; however, conservative treatment with non-steroidal antiinflammatories, regular exercise, physiotherapy and modification of lifestyle with loss of weight does help. Patients should also be encouraged to use walking aids (usually a walking stick in the opposite hand to offload the affected jo