SHORT PRACTICE of SURGERY

EDITION

Sebaceous horn

(The owner, the widow Dimanche, sold water-cress in Paris)

A favourite illustration of Hamilton Bailey and McNeill Love, and well known to readers of earlier editions of Short Practice.

SHORT PRACTICE of SURGERY

EDITION

Edited by

Norman S. Williams MS FRCS FMed Sci

Professor of Surgery and Director of Surgical Innovation,

Barts and the London School of Medicine and Dentistry,

Queen Mary, University of London and President,

The Royal College of Surgeons of England, London, UK

Christopher J.K. Bulstrode MCh FRCS(T&O)

Emeritus Professor, University of Oxford, Oxford, UK

P. Ronan O’Connell, MD FRCSI, FRCPS Glas.,

Head, Surgery and Surgical Specialties,

UCD School of Medicine and Medical Sciences

Consultant Surgeon, St Vincent’s University Hospital,

Dublin, Ireland

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Contributors Preface Acknowledgements Sayings of the great

PART ONE: PRINCIPLES 1. Metabolic response to injury Kenneth Fearon

2. Shock and blood transfusion Karim Brohi

Contents

viii 12. Patient safety 161

xiii

Frank Keane

xiv PART TWO: INVESTIGATION AND

xvi

DIAGNOSIS

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

14. Gastrointestinal endoscopy 196 James Lindsay

15. Tissue diagnosis 213 Roger Feakins

3. Wounds, tissue repair and scars 24

PART THREE: PERIOPERATIVE CARE

Michael Earley

4. Basic surgical skills and

anastomoses

William E. G. Thomas

5. Surgical infection

Peter Lamont

6. Surgery in the tropics

Pradip K Datta, Pawanindra Lal and

Sanjay De Bakshi

7. Principles of laparoscopic and

robotic surgery

Ara Darzi and Sanjay Purkayastha

16. Preoperative preparation 229 Medha Vanarase, Pierre Foex and

Kevin Tremper

17. Anaesthesia and painrelief 238

Vivek Mehta, Richard Langford and Jagannath Haldar

18. Care in the operatingroom 247

Kath Jenkins and Hilary Edgcombe 19. Perioperative management of th e high-risk surgical patient

255

Mridula Rai and Kevin D Johnston 20. Nutrition and uid therapy 261 8. Principles of paediat ric surgery 105

John MacFie

21. Postoperative care 272Anthony Lander

9. Principles of oncology 125

Jay Kini

22. Day case surgery 281Robert JC Steele and Alastair J Munro

10. Surgical audit and clinical research 147

Douglas McWhinnie and Ian Jackson

Jonothan Earnshaw and Birgit Whitman PART FOUR:

TRAUMA

11. Surgical ethics and law 155 23. Introduction to trauma 289 Robert Wheeler Bob Handley and Peter Giannoudis

vi CONTENTS

24. Early assessment and management of trauma 301 Dinesh Nathwani and Joseph Windl ey

25. Emergency neurosurgery 310 Tony Belli and Harry Bulstrode

26. Neck and spine 326 Ashley Poynton

27. Maxillofacial trauma 341 Charles Perkins

28. Torso trauma 351 Ken Boffard

29. Extremity trauma 364 Parminder Singh

30. Burns 385 Michael Tyler and Sudip Ghosh

31. Plastic and reconstructive surgery 401 Tim Goodacre

32. Disaster surgery 417 Mamoon Rashid

PART FIVE: ELECTIVE ORTHOPAEDICS

33. History taking and clinical

examination in musculoskeletal

disease 437 Parminder J Singh and Hemant G Pandit

34. Sports medicine and sports injuries 463 Gina Allen

35. The spine 470 Chris Lavy and Gavin Bowden

36. Upper limb – pathology, assessment and management 485 Vinay Takwale and Irfan Khan

37. Hip and knee 505 Hemant G Pandit and Andrew Barnett

38. Foot and ankle 518 Bob Sharpe

39. Musculoskeletal tumours 526 Paul Cool

40. Infection of the bones and joints 541 Martin McNally, Philippa Matthews

and Philip Bejon

41. Paediatric orthopaedics 550 Deborah Eastwood

PART SIX: SKIN AND SUBCUTANEOUS TISSUE 42. Skin and subcutaneous tissue 57 7 Christopher Chan and Adam Greenbaum

PART SEVEN: HEAD AND NECK

43. Elective neurosurgery 605 William Gray and Harry Bulstrode

44. The eye and orbit 622 Colm O’Brien, Hugo Henderson and

Jonathan Jagger

45. Cleft lip and palate: developmental

abnormalities of the face, mouth

and jaws 634 William P Smith

46. The nose and sinuses 653 Robert W Ruckley and Iain J Nixon

47. The ear 661 Grant Bates

48. Pharynx, larynx and neck 674 Rishi Sharma and Martin Birchall

49. Oropharyngeal cancer 706 William P Smith

50. Disorders of the salivary glands 723 William P Smith

PART EIGHT: BREAST AND ENDOCRINE 51. The thyroid and parathyroid glands 741 Zygmunt H Krukowski

52. The adrenal glands and other

abdominal endocrine disorders 778 Tom WJ Lennard

53. The breast 798 Richard Sainsbury

PART NINE: CARDIOTHORACIC

54. Cardiac surgery 823 Jonathan R Anderson and Mustafa Zakkar

55. The thorax 850 Ian Hunt and Carol Tan

PART TEN: VASCULAR

56. Arterial disorders 877 Robert Sayers

57. Venous disorders 901 Peter McCollum and Ian Chetter

CONTENTS vii

58. Lymphatic disorders 923 Shervanthi Homer-Vanniasinkam and

David A Russell

PART ELEVEN: ABDOMINAL

59. History and examination of the

abdomen 941 Mohan de Silva and V Sitaram

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

61. The peritoneum, omentum, mesentery and retroperitoneal space 970 Cha rles H Knowles

62. The oesophagus 987 Derek Alderson

63. Stomach and duodenum 1023 John N Primrose and Timothy J Underwoo d 64. Bariatric surgery 1058 John Baxter

65. The liver 1065 Rahul S Koti, Sanjeev Kanoria and

Brian R Davidson

66. The spleen 1087 O James Garden

67. The gall bladder and bile ducts 1097 Kevin Conlon

68. The pancreas 1118 Satyajit Bhattacharya

69. The small and large intestines 1143 Gordon Carlson and Jonathan Epstein

70. Intestinal obstruction 1181 Jim Hill

71. The vermiform appendix 1199 P Ronan O’Connell

72. The rectum 1215 Sue Clark

73. The anus and anal canal 1236 Peter Lunniss and Karen Nugent

PART TWELVE: GENITOURINARY

74. Urinary symptoms and investigations 1271 Christopher G Fowler

75. The kidneys and ureters 1282 Christopher G Fowler

76. The urinary bladder 1309 Freddie Hamdy

77. The prostate and seminal vesicles 1340 David E Neal and Greg L Shaw

78. Urethra and penis 1359 Ian Eardley

79. Testis and scrotum 1377 Ian Eardley

80. Gynaecology 1392 Stephen Kennedy and Enda McVeigh

PART THIRTEEN: TRANSPLANTATION 81. Transplantation 1407 J And rew Bradley

Appendix 1:

Common instruments used in general

surgery 1433

Pradip K Datta

Index 1437

Derek Alderson

MD FRCS

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

Gina Allen BM DCH MRCGP MRCP FRCR

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

Jonathan R Anderson

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

Andrew Barnett

FRCS(Orth)

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

Grant Bates BSc BM Bch FRCS (deceased)

Ear, Nose and Throat Surgeon, John Radcliffe Hospital, Oxford and Lecturer, Univer sity of Oxford, Oxford, UK

Philip Bejon

Bone Infection Unit, Nufeld Orthopaedic Centre, Oxford, UK

Tony Belli MD FRCS(SN)

Reader in Trauma, Neurosurgery, University of Birmingham, Birmingham, UK

Satyajit Bhattacharya

MS MPhil FRCS

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

Martin Birchall M(Cantab) FRCS FRCS(Oto) FRCS(ORL)

Professor of Laryngology, University College London, Consultant in Otolaryngology, Head a nd Neck Surgery, The Royal National

Throat, Nose and Ear Hospital, UCLH NHS Trust, London, UK

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

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

Gavin Bowden MB BCh FCS(SA)(Orth) Consultant Spinal Surgeon, St Lukes Hospital, Oxford, UK

Contributors

J Andrew Bradley MB ChB PhD FRCS Ac Med Sci

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

Karim Brohi

FRCS FRCA

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

Harry Bulstrode MA Cantab BMBCh MRCS(Eng)

Academic Clinical Fellow in Neurosurgery, Division of Neurosciences, Southa mpton General Hospital, Southampton, UK

Gordon Carlson

BSc MD FRCS

Consultant Surgeon, Honorary Professor of Surgery, University of Manchester; H onorary Professor of Biomedical Science, University of

Salford, Salford, UK

Christopher Chan BSC PhD FRCS FRCS(Gen Surg)

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

Ian Chetter MB ChB FRCSMD FRCS(Gen Surg) PG Cert Medical Ultrasound PG Dip Clinical Education

Professor of Surgery, Hull York Medical School, University of Hull; Honorary Consultant V ascular Surgeon, Hull and East Yorkshire

NHS Trust, Academic Vascular Surgical Unit, Old Doctors Residence, Hull Royal Inrm ary, Hull, UK

Sue Clark MD FRCS(Gen Surg)

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

Kevin C Conlon MA MCh MBA FRCSI FACS FRCPS(Glas) FTCD

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

Hospital, Dublin, Ireland

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

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

Ara Darzi PC KBE HonFrEng FmedSci

Professor the Lord Darzi of Denham, Professor of Surgery, Imperial College London, St Mar y’s Hospital Campus, London, UK

Pradip K Datta MBE MS FRCS(Ed) FRCS FRCSI FRCPS(Glas)

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

Sudip Ghosh MB BS MS FRCS(Plast)

Consultant Plastic Surgeon, Stoke Mandeville Hospital, Aylesbury, UK

Brian R Davidson

MD FRCS

Consultant Surgeon, Royal Free Hospital and Professor of Surgery, Hampstead Campus, U niversity College London, London, UK

Peter Giannoudis

MD FRCS

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

Sanjay De Bakshi MB BS MS FRCS FRCS(Ed)

Consultant Surgeon, Unit of Surgical Gastroenterology, Calcutta Medical Resear ch Institute, Kolkata, India

Tim Goodacre

MD FRCS

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

Ian Eardley MA MChir FRCS (Urol) FEBU

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

William Gray MB MD FRCSI FRCS(SN)

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

Michael Earley MB MCh FRCSI FRCS(Plast)

Consultant Plastic Surgeon and Associate Clinical Professor, The Children’s University Hospital, T emple Street and Mater Misericordiae

University Hospital, Dublin, Ireland

Adam Greenbaum MB BS MBA PhD FRCS(Plast) FEBOPRAS

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

Jonothan Earnshaw

DM FRCS

Consultant Vascular Surgeon, Gloucestershire Royal Hospital, Gloucester, UK

Jagannath Haldar

MB BS MD FRCA

Consultant Anaesthetist and Clinical Lead, Oxford University Hospitals NHS Tru st, Honorary Clinical Lecturer, Oxford Brooke’s

University, Oxford, UK

Deborah Eastwood

FRCS

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

Freddie Hamdy MD MA FRCS FRCS(Ed)(Urol) FMedSci

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

Hilary Edgcombe BA BM BCh(Oxon) FRCA(Lon)

Consultant Anaesthetist, Oxford University Hospitals, Oxford, UK

Bob Handley

MB ChB FRCS

John Radcliffe Hospital, Oxford, UK

Jonathan Epstein

MA MD FRCS

Specialist Registrar in General Surgery, Hope Hospital, Salford, UK

Jim Hill MB ChB ChM FRCS

Consultant General and Colorectal Surgeon, Manchester Royal Inrmary, Manc hester, UK

Roger Feakins MB BCh BAO BA MD FRCPI FRCPath

Consultant Histopathologist and NHS Professor of Gastrointestinal Pathology, Depar tment of Histopathology, Barts Health NHS Trust,

London, UK

Kenneth Fearon MD FRCPS(Glas) FRCS(Ed) FRCS

Professor of Surgical Oncology and Honorary Consultant Colorectal Surgeon, Cl inical Surgery, School of Clinical Science, University of

Edinburgh, Royal Inrmary, Edinburgh, UK

Shervanthi Homer-Vanniasinkam

BSc MD FRCS(Ed) FRCS

Consultant Vascular Surgeon, The General Inrmary at Leeds; Clinical Sub-

Dean, University of Leeds Medical School Chair, Translational Vascular Medicine, Unive rsity of Bradford; Director, Northwick Park

Institute for Medical Research, London Honorary Professor, Division of Surgical and Interv entional Sciences, University College

London, London, UK

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

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

Pierre Foex DPhil FRCA FMedSci

Nufeld Division of Anaesthetics, John Radcliffe Hospital, Headley Way, Oxford, UK

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

Professor, Department of Urology, The Royal London Hospital, London, U K

Ian Jackson

MB ChB FRCA

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

Kath Jenkins

BM BS FRCA

Consultant Anaesthetist, North Bristol NHS Trust, Bristol, UK

O James Garden BSc MB ChB FRCPS(Glas) FRCS(Ed) FRCP(Ed) FRCSCan FRACS(Hon)

Regius Professor of Clinical Surgery, School of Clinical Sciences, University of Edinbu rgh, Royal Inrmary, Edinburgh, UK

Kevin D. Johnston MBChB (Hons) BDS BSc MFDSRCS FRCA

Specialist Registrar in Anaesthetics, Nufeld Department of Anaesthetics, John Radcliff e Hospital, Oxford, UK

x CONTRI BUTORS

Sanjeev Kanoria

FRCS

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

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

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

Stephen Kennedy

Professor of Reproductive Medicine and Head of Department, Nufeld Department of Obstetrics and Gynaecology, University of

Oxford, Oxford University Hospitals NHS Trust, The Women’s Centre, Oxford, UK

Irfan Khan MB BS MRCS

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

Jay Kini MB BS DA MD FFARCSI

Consultant Anaesthetist, Nufeld Department of Anaesthetics, John Radcliffe Hospital, Ox ford, UK

Charles H Knowles

BChir PhD FRCS

Clinical Professor of Surgical Research and Hononary Consultant Colorectal Surgeon, Centr e for Digestive Diseases, Blizard Institute,

Barts and the London School of Medicine and Dentistry, Queen Mary University, London, U K

Rahul S Koti

MD FRCS

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

London, UK

Zygmunt H Krukowski

PhD FRCS FRCP

Surgeon to the Queen in Scotland; Consultant Surgeon, Aberdeen Royal Inrmary; Professor of Clinical Surgery, University of

Aberdeen, Aberdeen, UK

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

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

Peter Lamont MB ChB MD FRCS FEBVS

Consultant Vascular Surgeon, Department of Vascular Surgery, Bristol Royal In rmary, Bristol, UK

Anthony Lander

Phd FRCS(Paed) DCH

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

Richard Langford

MD FRCA FFPMRCA

Professor of Anaesthesia and Pain Medicine and Directory, Pain and Anaesthesia Research Centre, St Bartholomew’s and Royal London

Hospitals, Barts Health NHS Trust, London UK

Chris Lavy OBE MD MCh FRCS

Honorary Professor and Consultant Orthopaedic Surgeon, Nufeld Department of Orthopaedic s, Rheumatology and Musculoskeletal

Sciences (NDORMS), University of Nufeld, Nufeld Orthopaedic Centre, Oxford, UK

Tom WJ Lennard

MD FRCS

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

James Lindsay

PhD FRCP

Consultant and Senior Lecturer in Gastroenterology, Digestive Diseases Clinical Academ ic Unit, Barts and the London School of

Medicine and Dentistry, Queen Mary University of London, London, UK

Peter Lunniss

BSc MS FRCS

Senior Lecturer, Honorary Consultant Coloproctologist, Royal London Hospital Whitechap el, London, UK

Peter McCollum BA MB BCh BAO MCh FRCSI FRCS(Ed)

Professor of Vascular Surgery, Hull York Medical School; Honorary Consultan t Vascular Surgeon, Hull & East Yorkshire Hospitals

NHS Trust, Hull Royal Inrmary, Hull, UK

John MacFie MB ChB R Nutr MD FRCS FRCP

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

Martin McNally MD FRCS(Ed) FRCS(Orth)

Consultant in Limb Reconstruction Surgery, Bone Infection Unit, Nufeld Orthopaedic Centr e; Honorary Senior Lecturer in

Orthopaedics

Enda McVeigh

Senior Fellow in Reproductive Medicine, Nufeld Department of Obstetrics and Gyn aecology, University of Oxford, Oxford University

Hospitals NHS Trust, The Women’s Centre, Oxford, UK

Douglas McWhinnie

MD(Hons) FRCS

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

Milton Keynes, UK

Matthew Matson

MRCP FRCR

Consultant Radiologist, Royal London Hospital, London, UK

Philippa Matthews

MSc MRCP FRCPath DPhil

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

Vivek Mehta MD FRCA FFPMRCA

Consultant in Pain Medicine, Deputy Director, Pain and Anaesthesia Research Centre, St Bartho lomew’s and Royal London Hospitals,

Barts Health NHS Trust, London, UK

Alastair J Munro

BSc FRCP(E) FRCR

Professor of Radiation Oncology, University of Dundee, Tayside Cancer Ce ntre, Ninewells Hospital and Medical School, Dundee, UK

Dinesh Nathwani MB ChB MSc FRCSI(Tr & Orth)

Consultant and Honorary Senior Clinical Lecturer, Department of Trauma and Orthopa edic Surgery, Imperial College Healthcare,

Academic Health Sciences Centre, London, UK

David E Neal

FMedSci MS FRCS

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

Stephen J Nixon

FRCS(Ed) FRCP(Edin)

Consultant Surgeon, Department of Surgery, Royal Inrmary of Edinburgh, Edinburg h, UK

David A Russell MB ChB MD FRCS(Gen Surg)

Consultant Vascular Surgeon, Leeds Vascular Institute, Leeds General Inrmary, Leed s, UK

Iain J Nixon MB ChB FRCS(Ed)(ORL-HNS)

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

Richard Sainsbury

MD FRCS

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

Karen Nugent

MA MS FRCS

Professorial Surgical Unit, Southampton General Hospital, Southampton, UK

Anand Sardesai

MB BS MD FRCA

Consultant Anaesthetist, Addenbrook’s Hospital, Cambridge, UK

Colm O’Brien MD FRCS FRCOphth

Professor of Ophthalmology and Consultant Ophthalmic Surgeon, University College D ublin and Mater Misericordiae University

Hospital, Dublin, Ireland

P Ronan O’Connell

MD FRCSI FRCPS(Glas)

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

Hemant G Pandit FRCS(Orth) DPhil (Oxford)

Honorary Senior Clinical Lecturer in Orthopaedics, Nufeld Orthopaedic Centre a nd Nufeld Department of Orthopaedics,

Rheumatology and Musculoskeletal Sciences (NDORMS), Oxford, UK

Robert Sayers

Professor of Vascular Surgery, Leicester Royal Inrmary, Leicester, UK

Rishi Sharma

MRCS DOHNS

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

Bob Sharp BMBCh MA FRCS FRCS(Tr & Orth)

Consultant Orthopaedic Surgeon, Oxford University Hospitals, The Nufeld Orth opaedic Centre, Oxford, UK

Greg L Shaw

MD FRCS(Urol)

Clinical Lecturer in Urology, Cambridge University, Cambridge, UK

Charles Perkins FDSRCS FFDRCSI FRCS

Consultant Oral and Maxillofacial Surgeon, Department of Oral and Maxillofacial Surge ry, Gloucestershire Royal Hospital, Gloucester,

Mohan de Silva

MS FRCS(Ed) FCSSL

Professor of Surgery and Dean, Faculty of Medical Sciences, University of Sri Jay awardenepura Gangodawila, Nugegoda, Colombo, Sri

Lanka

Niall Power

Royal London Hospital, London, UK

Ashley Poynton MD FRCSI FRCS(TrandOrth)

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

John N Primrose MB ChB(Hons) FRCS MD

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

Sanjay Purkayastha BSc MB BS MD FRCS(Gen Surg)

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

Parminder J Singh MB BS MRCS FRCS(Tr & Orth) MS

Consultant Orthopaedic Surgeon, Maroondah Hospital and Honorary Senior L ecturer, Monash and Deakin University, Melbourne,

Australia

V Sitaram MS FRCPS(Glas)

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

William P Smith FDSRCS FRCS(Ed) FRCS

Consultant Maxillofacial Surgeon, Northampton General Hospital NHS Trust, N orthampton, UK

Robert JC Steele

MB ChB MD FRCS(Ed)

Professor, Head of Academic Surgery, Ninewells Hospital and Medical School, Dunde e, UK

Mridula Rai MB BS MD FRCA

Consultant Anaesthetist, Nufeld Department of Anaesthetics, Modular Building, John Ra dcliffe Hospital, Oxford, UK

Vinay Takwale MB MS FRCS(Tr & Orth)

Consultant Orthopaedic Surgeon, Gloucestershire Hospital, Gloucester, UK

Mamoon Rashid

FRCS FCPS(Pak)

Professor of Plastic and Reconstructive Surgery, Shifa College of Medicine; Consultant Plastic Sur geon and Programme Director, Shifa

International Hospital, Islamabad, Pakistan

Carol Tan MB ChB FRCS(C-Th)

Consultant Thoracic Surgeon, St George’s Hospital, London, UK

Robert W Ruckley

MB ChB FRCS FRCS(Ed)

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

William EG Thomas

MS FRCS FSACS(Hon)

Consultant Surgeon and Honorary Senior Lecturer in Surgery, Shefeld, UK

xii CONTRI BUTORS

Kevin Tremper

PhD MD

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

Robert Wheeler MS FRCS FRCPCH LLB(Hons) LLM

Consultant Paediatric Surgeon, Child Health, University Hospitals of Southampton, Southam pton, UK

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

Department of Surgery, Royal Inrmary of Edinburgh, Edinburgh, UK

Birgit Whitman

PhD

Head of Research Governance, University of Bristol, Bristol, UK

Michael Tyler FRCS(Plast) MB CHM

Stoke Mandeville Hospital, Aylesbury, UK

Timothy J Underwood

BSc(Hons) MB BS PhD FRCS

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

Joseph Windley MB BS BSc(Hons) MRCS

Specialist Registrar, Department of Trauma and Orthopaedic Surgery, Imperial College Healthc are, Academic Health Sciences Centre,

London, UK

Mustafa Zakkar

PhD

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

Medha Vanarase MB BS MD FRCA(Cert Ed)

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

Preface

In this age of rapid electronic access to scientic papers and erudite surgical opinion on e has to ask whether there is still a place for a

comprehensive surgical textbook that takes several years to compile and risks lo sing its immediacy. The success of the 25th edition of

Bailey & Love together with the numerous positive communications we have received since its pu blication suggest that the answer is

very much in the afrmative. However, it is essential that in producing further editions cogn isance is taken of what the “customer”

wants. Consequently before preparing the 26th edition of this venerable text we conducted con siderable market research as to what had

succeeded in the previous edition, what had been omitted and how we could impr ove content and presentation. Readers from a range of

backgrounds from undergraduates to hard bitten and, dare we say, cynical senior consultants were asked for their opinion. Their musings

and frank criticisms were all taken very seriously and many of their suggestions w ere adopted for this edition. A few chapters were

removed or consolidated into others; new chapters have been added focusing on the important topics of patient safety, day case surgery

and bariatric surgery.

All existing chapters have been radically revised and have been thoroughly brought up to date. We have attempted to ensure more

conformity with regard to illustrations; however, we have kept faith with Hamilton Bailey and M cNeil Love’s original concept of

ensuring clinical photographs are liberally used to not only enhance the text but more importa ntly illuminate a clinical point. Many new

photographs have been introduced, some of which have been provided by our rea ders, which is very much a Bailey & Love tradition.

Although we have been ruthless in removing old material we make no excuse for retaining the odd original pen drawing taken from the

rst few editions. This is not just for nostalgia’s sake but because they illustrate a pert inent point not easily captured by a modern

photograph. Another tradition beloved of readers has of course been the autobiogr aphical notes. These have all been painstakingly

researched and added to by Pradip Datta.

We recognise that despite very careful attention to detail by our authors there may be an occasi onal error in the text that we and our proof

readers have failed to spot. It would not be

surprising in a text of this length. We apologise in advance for any errors and than k our eagle-eyed readers whom we know from

experience will let us know of any that they nd. This is a Bailey & Love tradition and we v alue all contributions that can improve

accuracy.

Several editions ago we introduced the concept of learning objectives and summ ary boxes in order to help examination candidates in

their revision. The feedback regarding these innovations was extremely posit ive and we have attempted to ensure that these are

comprehensive, standardised and liberally dispersed through the text.

The authors of the chapters have been carefully chosen not just for their undou bted experience and expertise in their specialty but also

their ability to write both accurately and succinctly. Writing is a skill honed by practice; it is a labour of love and takes time and patience

to perfect. The best authors are like gifted musicians who, after numerous rehearsals, ar e able to deliver a perfect recital. It is our belief

that our contributors have done just this and we the editors have attempted wherev er possible to ensure there is a rhythm and harmony

owing through the pages. However, at the end of the day we appreciate it will be up to the audience to decide how successful we and

our authors have been in this endeavour.

It has been a pleasure and privilege to edit this historic textbook beloved of so many stu dents and trainees through the decades. However,

we are conscious that previous reputation counts for very little unless the present pro duct meets expectations and is relevant to the

present era. This thought has always been in our minds when preparing the content of the 26th edition. We very much hope it ts the bill

and fulls your requirements whether you, the reader, are studying for an exam, checking on an area of practice that you may be

unfamiliar with or just refreshing your memory about some forgotten fact or biographical detail.

Norman S. Williams Christopher J.K. Bulstrode

P. Ronan O’Connell 2012

Sometimes a new edition of Bailey & Love feels like a swan swimming swiftly but seren ely across a lake. From afar it may look

effortless (and beautiful we hope), but to those who are closer to the action you can glimpse the w ebbed feet paddling away furiously

beneath the surface driving that swan forward. The three editors are one part of a huge orchestra too large to mention all by name.

However, it is a pleasure to acknowledge some of the most notable amongst the players.

Gavin Jamieson initiated the new edition as commissioning editor under the supervision o f Jo Koster, who then took over following

Gavin’s departure. Sarah Penny and Stephen Clausard took on the awesome responsib ility of pulling all things ‘manuscript-related’

together. Susie Bond, Alyson Thomas and Theresa Mackie have done a grea t job with the copy editing and proof reading, while the

index has been compiled ably by Christopher Boot. Mr Pradip Datta FRCS completely re vamped the historical footnotes, going back all

the way to the rst edition to check that we had left no ‘jewels’ out of the crown. Mr Hemant Pan dit FRCS, Dr Medha Vanarese FRCA

and Mr Parminder Singh FRCS helped enormously with the commissioning and editing of the orthopaedic, anaesthetic and trauma

chapters respectively.

Chapter 4, Basic surgical skills and anastomoses, contains some material from ‘ Basic surgical skills and anastomoses’ by David J.

Leaper. The material has been revised and updated by the current author.

Chapter 5, Surgical infection, contains some material from ‘Surgical infection’ by David J. Lea per. The material has been revised and

updated by the current author.

Chapter 8, Principles of paediatric surgery, contains some material from ‘Principles of paedi atric surgery’ by Mark Stringer. The

material has been revised and updated by the current author.

Chapter 11, Surgical ethics and law, contains some material from ‘Surgical ethics’ by Len Doyal. The material ha s been revised and

updated by the current author.

Chapter 16, Preoperative preparation, contains some material from ‘Preoperative preparation’ by Lisa Leonard and Sarah J. Barton.

The material has been revised and updated by the current authors.

Acknowledgements

Chapter 18, Care in the operating room, contains some material from ‘Care in the operating room’ by Sunn y Deo and Vipul Mandalia.

The material has been revised and updated by the current authors.

Chapter 19, Perioperative management of the high-risk surgical patient, contains so me material from ‘Perioperative management of

the high-risk surgical patient’ by Rupert M. Pearse and Richard M. Langford. The m aterial has been revised and updated by the current

authors.

Chapter 20, Nutrition and uid therapy, the author would like to thank Marcel Gatt MD FRCS , who provided some illustrations and

helped with proofreading the text.

Chapter 21, Postoperative care, contains some material from ‘Postoperative care’ by Alistair Pace and Nicho las C.M. Armitage. The

material has been revised and updated by the current author.

Chapter 25, Head injury, contains some material from ‘Head injury’ by Richard Stace y and John Leach. The material has been revised

and updated by the current authors.

Chapter 34, Sports medicine and sports injuries, contains some material from ‘ Sports medicine and sports injuries’ by D.L. Back and

Jay Smith. The material has been revised and updated by the current author.

Chapter 36, Upper limb – pathology, assessment and management, contains some m aterial from ‘Upper limb – pathology, assessment

and management’ by Srinath Kamineni. The material has been revised and u pdated by the current authors.

Chapter 37, Hip and knee, contains some material from ‘Hip and knee’ by Vikas Khanduja and Richa rd N. Villar. The material has

been revised and updated by the current authors.

Chapter 38, Foot and ankle, contains some material from ‘Foot and ankle’ by Mark Davies, Matthew C. Solan and Vikas Khanduja.

The material has been revised and updated by the current author.

Chapter 41, Paediatric orthopaedics, contains some material from ‘Paediatric orthopaedics’ by th e current author and Joanna Hicks,

which has been revised and updated for this edition.

AC KNOWLEDGEMENTS xv

Chapter 43, Elective neurosurgery, contains some material from ‘Elective Neurosurgery’ by John Leach and R ichard Kerr. The material

has been revised and updated by the current authors.

Chapter 59, History and examination of the abdomen, contains some mate rial from ‘History and examination of the abdomen’ by

Simon Paterson-Brown. The material has been revised and updated by the curre nt authors.

Chapter 44 , The eye and orbit, contains some material from ‘The eye and orbit’ by Jonathan D. Jagger and Hugo W.A. Henderson. The

material has been revised and updated by the current author.

Chapter 60, Abdominal wall, hernia and umbilicus, contains some material fro m ‘Hernias, umbilicus and abdominal wall’ by Andrew

N. Kingsnorth, Giorgi Giorgobiani and David H. Bennett. The material has been revise d and updated by the current authors.

Chapter 48, The pharynx, larynx and neck, contains some material from ‘The pharynx, larynx and neck’ by Jonathan D. Jagger and

Hugo W.A. Henderson. The material has been revised and updated by the current author.

Chapter 61, The peritoneum, omentum, mesentery and retroperitoneal space, con tains some material from ‘The peritoneum, omentum,

mesentery and retroperitoneal space’ by Jerry Thompson. The material has been rev ised and updated by the current author.

Chapter 52, The adrenal glands and other abdominal endocrine disorders, con tains some material from ‘Adrenal glands and other

endocrine disorders’ by Matthias Rothmund. The material has been revised and updated by the current author. Chapter 65, The liver,

contains some material from ‘The liver’ by Brian R. Davidson. The material has been revised an d updated by the current authors.

Chapter 54, Cardiac surgery, contains some material from ‘Cardiac surgery’ by Jonathan Anderson and Ian Hunt. The material has

been revised and updated by the current authors.

Chapter 69, The small and large intestines, contains some material from ‘The sma ll and large intestines’ by Neil J. McC Mortensen

and Shazad Ashraf. The material has been revised and updated by the current a uthors.

Chapter 55, The thorax, contains some material from ‘The thorax’ by Tom Treasure. The material ha s been revised and updated by the

current authors.

Chapter 70, Intestinal obstruction, contains some material from ‘Intestinal obstruction’ by Marc Chr istopher Winslet. The material has

been revised and updated by the current author.

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 76, The urinary bladder, contains some material from ‘The urinary bladder ’ by David E. Neal. The material has been revised

and updated by the current author.

Chapter 57, Venous disorders, contains some material from ‘Venous disorders’ by Kevin Burnand. The material h as been revised and

updated by the current authors.

Chapter 78, Urethra and penis, contains some material from ‘Urethra and penis’ by Christopher G. Fowler. The material has been

revised and updated by the current author.

Chapter 58, Lymphatic disorders, contains some material from ‘Lymphatic disorders’ by Shervanthi Homer-Vanniasinkam and Andrew

Bradbury. The material has been revised and updated by the current authors.

Chapter 79, Testis and scrotum, contains some material from ‘Testis and scrotum’ by Christopher G. Fo wler. The material has been

revised and updated by the current author.

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. T hey never tired of quoting his ‘medical

litany’, which is appropriate for all clinicians and, perhaps especially, for those who a re 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 befo re common sense;

From treating patients as cases; and

From making the cure of a disease more grievous than its endurance,

Good Lord, deliver us.

To which may be added:

The patient is the centre of the medical universe around which all our works rev olve and towards which all our efforts trend.

J.B. Murphy, 1857–1916, Professor of Surgery, Northwestern University, Chicago, I L, USA

To study the phenomenon of disease without books is to sail an uncharted sea, whil e to study books without patients is not to go to sea at

all.

Sir William Osler, 1849–1919, Professor of Medicine, Oxford, UK

A knowledge of healthy and diseased actions is not less necessary to be understo od than the principles of other sciences. By and

acquaintance with principles we learn the cause of disease. Without this know ledge a man cannot be a surgeon. … The last part of

surgery, namely operations, is a reection on the healing art; it is a tacit acknowledg ement of the insufciency of surgery. It is like an

armed savage who attempts to get that by force which a civilised man would by stratage m.

Hunter, 1728–1793, Surgeon, St George’s Hospital, London, UK

Sayings of the great

Sayings of the great
Investigating Nature you will do well to bear ever in mind that in every question there is the tr uth, 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 d esired. But in its practice you will nd it to be attended
with peculiar privileges; second to none in intense interest and pure pleasures. It is  our proud ofce to tend the eshy 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
Surgery has undergone many great transformations during the past fty years, and man y are to be thanked for their contributions – yet
when we think of how many remain to be made, it should rather stimulate our inventiv eness than fuel our vanity.
Sir Percival Pott, 1714–88, Surgeon, St Bartholomew’s Hospital, London, UK If you c annot make a diagnosis at least make a decision!
Sir Harry Platt, 1897–1986,
Professor of Orthopaedics, Manchester, and President of the Royal College of Surgeo ns England, 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
PART
1 Principles
1 Metabolic response to injury 3
2 Shock and blood transfusion 13
3 Wounds, tissue repair and scars 24
4 Basic surgical skills and anastomeses 33
5 Surgical infection 50
6 Surgery in the tropics 68
7 Principles of laparoscopic and robotic surgery 93
8 Principles of paediatric surgery 105
9 Principles of oncology 125
10 Surgical audit and clinical research 147
11 Surgical ethics and law 155
12 Patient safety 161
CHAPTER
1
to injury Metabolic response
LEARNING OBJECTIVES
To understand:
• Classical concepts of homeostasis
• Mediators of the metabolic response to injury
• Physiological and biochemical changes that
occur during injury and recovery
• Changes in body composition that accompany surgical injury
• Avoidable factors that compound the metabolic response to injury
• Concepts behind optimal perioperative care
BASIC CONCEPTS IN HOMEOSTASIS
In the eighteenth and nineteenth centuries, a series of eminent scientists laid the foundations  of our understanding of homeostasis and the
response to injury. The classical concepts of homeostasis and the response to injury are :
• 
‘The stability of the “milieu intérieur” is the primary condition for freedom and indepen dence of existence’ (Claude Bernard); i.e. body

systems act to maintain internal constancy.

•

‘Homeostasis: the co-ordinated physiological process which

maintains most of the steady states of the organism’ (Walter Cannon); i.e. complex hom eostatic 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 prod uce both the deposition and means of cure’

(John Hunter); i.e. responses to injury are, in general, benecial to the host and allow he aling/ survival.

In essence, the concept evolved that the constancy of the ‘milieu intérieur’ allowed for the ind ependence of organisms, that complex

homeostatic responses sought to maintain this constancy, and that within this ran ge of responses were the elements of healing and repair.

These ideas pertained to normal physiology and mild/moderate injury. In the modern era, su ch concepts do not account for disease

evolution following major injury/sepsis or the injured patient who would have died bu t for articial organ support. Such patients

exemplify less of the classical homeostatic control system (signal detector–process or–effector regulated by a negative feedback loop) and

John Hunter , 1728–1793, surgeon, St George’s Hospital, London, UK. He is regarded as ‘The Father o f Scientific Surgery’. To further his knowledge of venereal

disease he inoculated himself with syphilis in 1767.

of the ‘open loop’ system, whereby only with medical/surgical resolution of the primary abnormality is a return to classical homeostasis

possible.

As a consequence of modern understanding of the metabolic response to injury, electiv e surgical practice seeks to reduce the need for a

homeostatic response by minimising the primary insult (minimal access surgery and ‘stress-free’ perioperative care). In emergency

surgery, where the presence of tissue trauma/sepsis/hypovolaemia often compound s the primary problem, there is a requirement to

augment articially homeostatic responses (resuscitation) and to close the ‘open’ loop by intervening to resolve the primary insult (e.g.

surgical treatment of major abdominal sepsis) and provide organ support (critical care) while the patient comes back to a situation in

which homeostasis can achieve a return to normality (Summary box 1.1).

Summary box 1.1

Basic concepts

Homeostasis is the foundation of normal physiology ‘Stress-free’ perioperative care helps to preserve hom eostasis following elective surgery

Resuscitation, surgical intervention and critical care can return the severely injured patient to a situation in which homeostasis becomes possible once again

This chapter aims to review the mediators of the stress response, the physiolog ical and biochemical pathway changes associated with

surgical injury and the changes in body composition that occur following surgical injury . Emphasis is laid on why knowledge of these

events is important to understand the rationale for modern ‘stress-free’ perioperative and crit ical care.

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. THE GRADED NATURE OF THE INJURY RESPON SE

It is important to recognise that the response to injury is graded: the more severe the inju ry, the greater the response (Figure 1.1). This

concept not only applies to physiological/metabolic changes but also to immunological ch anges/sequelae. Thus, following elective

surgery of intermediate severity, there may be a transient and modest rise in temperature , heart rate, respiratory rate, energy expenditure

and peripheral white cell count. Following major trauma/sepsis, these changes are a ccentuated, resulting in a systemic inammatory

response syndrome (SIRS), hypermetabolism, marked catabolism, shock and even mul tiple organ dysfunction (MODS). It is important to

recognise that genetic variability plays a key role in determining the intensity of the inam matory 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 sequelae of major injury evolve

from a proinammatory state driven primarily by the innate immune system (macrophages, ne utrophils, dendritic cells) into a

compensatory anti-inammatory response syndrome (CARS) characterised by suppres sed immunity and diminished resistance to

infection. In patients who develop infective complications, the latter will drive ongoing s ystemic inammation, the acute phase response

and continued catabolism.

140

130

Major trauma

120

Minor trauma

110

MEDIATORS OF THE METABOLIC RESPONSE TO INJURY

The classical neuroendocrine pathways of the stress response consist of afferent nociceptiv e neurones, the spinal cord, thalamus,

hypothalamus and pituitary (Figure 1.2). Corticotrophinreleasing factor (CRF) released from the hypothalamus increases

adrenocorticotrophic hormone (ACTH) release from the anterior pituitary. ACTH then acts on the adrenal to increase the secretion of

cortisol. Hypothalamic activation of the sympathetic nervous system causes release of ad renalin and also stimulates release of glucagon.

Intravenous infusion of a cocktail of these ‘counter-regulatory’ hormones (glucagon, gluco corticoids and catecholamines) reproduces

many aspects of the metabolic response to injury. There are, however, many o ther players, including alterations in insulin release and

sensitivity, hypersecretion of prolactin and growth hormone (GH) in the presence of low circulatory insulin-like growth factor-1 (IGF-1)

and inactivation of peripheral thyroid hormones and gonadal function. Of note, GH has direct lipolytic, insulin-antagonising and

proinammatory properties (Summary box 1.2).

Summary box 1.2

Neuroendocrine response to injury/critical illness

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

Acute phase characterised by an actively secreting

pituitary and elevated counter-regulatory hormones

(cortisol, glucagon, adrenaline). Changes are thought to be

beneficial for short-term survival

Chronic phase associated with hypothalamic suppression

and low serum levels of the respective target organ

hormones. Changes contribute to chronic wasting

100

Normal range

Starvation

010203040506070 days

Major trauma

Minor trauma

Normal range 5

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

The innate immune system (principally macrophages) interacts in a complex manner wit h the adaptive immune system (T cells, B cells)

in co-generating the metabolic response to injury (Figure 1.2). Proinammato ry cytokines including interleukin-1 (IL-1), tumour necrosis

factor alpha (TNFα), IL-6 and IL-8 are produced within the rst 24 hours and act direc tly on the hypothalamus to cause pyrexia. Such

cytokines also augment the hypothalamic stress response and act directly on ske letal muscle to induce proteolysis while inducing acute

phase protein production in the liver. Proinammatory cytokines also play a complex ro le in the development of peripheral insulin

resistance. Other important proinammatory mediators include nitric oxide ((NO) via ind ucible nitric oxide synthetase (iNOS)) and a

variety of prostanoids (via cyclo-oxygenase-2 (Cox-2)). Changes in organ fu nction (e.g. renal hypoperfusion/impairment) may be

induced by excessive vasoconstriction via endogenous factors such as endothelin-1.

Within hours of the upregulation of proinammatory cytokines, endogenous cytokine antagonist s enter the circulation (e.g. interleukin-1

receptor antagonist (IL-1Ra) and TNFsoluble receptors (TNF-sR-55 and 75)) and act to control the proinammatory response. A

complex further series of adaptive

The metabolic stress response to surgery and trauma: the ‘ebb and flow’ model 5

Hypothalamus CRF

PLASMA CHANGES IN BODY METABOLISM

Pituitary ACTH GH ADIPOCYTE LIPOLYSIS

Spinal cord Adrenal ADRENALIN CORTISOL

HEPATIC

GLUCONEOGENESIS

Injury Sympathetic nervous system SKELETAL MUSCLE

PROTEIN DEGRADATION

GLUCAGON

Pancreas IL-1

TNFα IL-6

IL-8

HEPATIC ACUTE PHASE PROTEIN SYNTHESIS

PYREXIA

Afferent noiciceptive

pathways Adaptive Innate immune immune system system Insulin

IGF-1

TESTOSTERONE T3

HYPERMETABOLISM

Figure 1.2

Bailey and Love

fig. 1.02

The integrated response to surgical injury (first 24–48 hours): there is a complex interplay between the n euroendocrine stress response and the

proinflammatory cytokine response of the innate immune system.

changes includes the development of a Th2-type counterinammatory response (regula ted by IL-4, -5, -9 and -13 and transforming

growth factor beta (TGFβ)) which, if accentuated and prolonged in critical illness, is c haracterised as the CARS and results in

immunosuppression and an increased susceptibility to opportunistic (nosocomial ) infection (Summary box 1.3). Within inamed tissue

the duration and magnitude of acute inammation as well as the return to homeostasis are inuenc ed by a group of local mediators

known as specialised pro-resolving mediators (SPM) that include essential fatty acid-der ived lipoxins, resolvins, protectins and maresins.

These endogenous resolution agonists orchestrate the uptake and clearance of apoptotic polymorphonuclear neutrophils and microbial

particles, reduce proinammatory cytokines and lipid mediators as well as enhance the remov al of cellular debris in the inammatory

milieu. Thus both at the systemic level (endogenous cytokine antagonists – see above) an d at the local tissue level, the body attempts to

limit/resolve inammation driven dyshomeostasis.

Summary box 1.3

Systemic inflammatory response syndrome following major injury

Is driven initially by proinflammatory cytokines (e.g. IL-1, IL-6 and TNFα)

Is followed rapidly by increased plasma levels of cytokine antagonists and soluble receptors (e.g. IL-1Ra, TNF-sR) If prolonged or excessive may evolve into a

counterinflammatory response syndrome

There are many complex interactions between the neuroendocrine, cytokine and metab olic 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 proinammatory cytokines and the noradrenergic system. The resulting rise in cortisol levels may form a weak feedback

loop attempting to limit the proinammatory stress response. Finally, hyperglycaemia may aggravate the inammatory response via

substrate overow in the mitochondria, causing the formation of excess free oxygen ra dicals and also altering gene expression to enhance

cytokine production.

At the molecular level, the changes that accompany systemic inammation are extremely comp lex. In a recent study using network-

based analysis of changes in mRNA expression in leukocytes following exposure to en dotoxin, there were changes in the expression of

more than 3700 genes with over half showing decreased expression and the rem ainder 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 simplied 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

In the natural world, if an animal is injured, it displays a characteristic response, which in cludes immobility, anorexia and catabolism

(Summary box 1.4).

Injury

Hypertrophy Atrophy

IGF-1

TNF

Myostatin

PI3K

CELL MEMBRANE

NF B

Akt

mTOR FOXO MyoD p70S6K

4E-BP-1

NUCLEUS

Protein

synthesis ProteinE3 ligases

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, nu clear 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.

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 ‘ow’ phases (Figure 1.4). The ebb

phase begins at the time of injury and lasts for approximately 24–48 hours. It may be attenua ted by proper resuscitation, but not

completely abolished. The ebb phase is characterised by hypovolaemia, decreased basal meta bolic rate, reduced cardiac output,

hypothermia and lactic acidosis. The predominant hormones regulating the eb b phase

INJURY

EBB PHASE FLOW PHASE RECOVERY

HOURS DAYS WEEKS

Shock Catabolism Anabolism

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

are catecholamines, cortisol and aldosterone (following activation of the renin–angioten sin system). The magnitude of this

neuroendocrine response depends on the degree of blood loss and the stimulat ion 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 store s for recovery and repair.

Following resuscitation, the ebb phase evolves into a hypermetabolic ow 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 ow 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. D uring the catabolic phase, the increased production of

counter-regulatory hormones (including catecholamines, cortisol, insulin and glucagon) and inammatory cytokines (e.g. IL-1, IL-6 and

TNFα) results in signicant fat and protein mobilisation, leading to signicant weight los s and increased urinary nitrogen excretion. The

increased production of insulin at this time is associated with signicant insulin resistance and, therefore, injured patients often exhibit

poor glycaemic control. The combination of pronounced or prolonged catabolism in association with insulin resistance places patients

within this phase at increased risk of complications, particularly infectious and cardiovas cular. Obviously, the development of

complications will further aggravate the neuroendocrine and inammatory stress respon ses, thus creating a vicious catabolic cycle

(Summary box 1.5).

Sir David Paton Cuthbertson, 1900–1989, biochemist, Director of the Rowett Research Institute, Glasgow, U K. Key catabolic elements of the flow phase of

the metabolic stress response 7

Summary box 1.5

Purpose of neuroendocrine changes following injury

The constellation of neuroendocrine changes following injury acts to:

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.

regulation) counteract the hypermetabolic driving forces of the stress response. Fur thermore, the skeletal muscle wasting experienced by

patients with prolonged catabolism actually limits the volume of metabolically active tissue (Sum mary box 1.6; see below).

Summary box 1.6

Hypermetabolism

Hypermetabolism following injury:

Is mainly caused by an acceleration of energy-dependent metabolic cycles

Is limited in modern practice on account of elements of routine critical care

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

There are several key elements of the ow phase that largely determine the extent of cata bolism and thus govern the metabolic and

nutritional care of the surgical patient. It must be remembered that, during the response to i njury, not all tissues are catabolic. Indeed, the

essence of this coordinated response is to allow the body to reprioritise limited res ources 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) demonstrat e energy expenditures approximately 15–25 per

cent above predicted healthy resting values. The predominant cause appears to be a complex interaction between the central control of

metabolic rate and peripheral energy utilisation. In particular, central thermodysregulatio n (caused by the proinammatory cytokine

cascade), increased sympathetic activity, abnormalities in wound circulation (isch aemic areas produce lactate, which must be

metabolised by the adenosine triphosphate (ATP)-consuming hepatic Cori cycle; h yperaemic areas cause an increase in cardiac output),

increased protein turnover and nutritional support may all increase patient energ y expenditure. Theoretically, patient energy expenditure

could rise even higher than observed levels following surgery or trauma, but sev eral features of standard intensive care (including bed

rest, paralysis, ventilation and external temperature

Alterations in skeletal muscle protein metabolism

Muscle protein is continually synthesised and broken down with a turnover rate in humans of 1–2 per cent per day, and with a greater

amplitude of changes in protein synthesis (± two-fold) than breakdown (± 0.25 -fold) during the diurnal cycle. Under normal

circumstances, synthesis equals breakdown and muscle bulk remains constant. Physiological stimu li that promote net muscle protein

accretion include feeding (especially extracellular amino acid concentration) and exercis e. Paradoxically, during exercise, skeletal

muscle protein synthesis is depressed, but it increases again during rest and feeding.

During the catabolic phase of the stress response, muscle wasting occurs as a result of an increase in muscle protein degradation (via

enzymatic pathways), coupled with a decrease in muscle protein synthesis. The major si te of protein loss is peripheral skeletal muscle,

although nitrogen losses also occur in the respiratory muscles (predisposing the p atient to hypoventilation and chest infections) and in the

gut (reducing gut motility). Cardiac muscle appears to be mostly spared. Under extreme c onditions of catabolism (e.g. major sepsis),

urinary nitrogen losses can reach 14–20 g/day; this is equivalent to the loss of 50 0 g of skeletal muscle per day. It is remarkable that

muscle catabolism cannot be inhibited fully by providing articial nutritional su pport as long as the stress response continues. Indeed, in

critical care, it is now recognised that ‘hyperalimentation’ represents a metabolic stress in itse lf, and that nutritional support should be at

a modest level to attenuate rather than replace energy and protein losses.

Peripheral tissues Central tissues

Muscle Liver Amino Acids

Adipose tissue

Skin Immune system especially

Gln and

Ala

Wound Myofibrillar protein

Figure 1.5 During the metabolic response to injury, the body reprioritises protein metabo lism away from peripheral tissues and towards key central tissues such as the

liver, immune system and wound. One of the main reasons why the reutilisation of amino acids derived from m uscle proteolysis leads to net catabolism is that the

increased glutamine and alanine efflux from muscle is derived, in part, from the irreversible degradation of branched ch ain amino acids. Ala, alanine; Gln, glutamine.

Caspases, cathepsins and calpains

Ubiquitinated protein

Amino acids E1, E2, E3 ATP

Tripeptidyl peptidase 19S Ubiquitin 26S proteasome ATP

Oligopeptides ATP

20S

Figure 1.6 The intercellular effector mechanisms involved in degrading myofibrillar protein into free amino ac ids.

19S The ubiquitin–proteasome

pathway is a complex multistep

process, which requires adenosine triphosphate and results in the tagging of specific proteins with ubiquitin for degra Substrate unfolding and dation of proteasome. E1,

ubiquitin-activating enzyme; E2, proteolytic cleavage ubiquitin-conjugating enzyme; E3, ubiquitin ligase .

Bailey and Love fig. 1.06

The predominant mechanism involved in the wasting of skeletal muscle is the ATP-dependent ubiquitin–proteasome pathway (Figure

1.6), although the lysosomal cathepsins and the calcium–calpain pathway play facilitat ory and accessory roles.

Clinically, a patient with skeletal muscle wasting will experience asthenia, increased fatigu e, reduced functional ability, decreased quality

of life and an increased risk of morbidity and mortality. In critically ill patients, m uscle weakness may be further worsened by the

development of critical illness myopathy, a multifactorial condition that is associated with impa ired excitation–contraction coupling at

the level of the sarcolemma and the sarcoplasmic reticulum membrane (Summary b ox 1.7).

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 exc essive

Alterations in hepatic protein metabolism: the acute phase protein respons e

The liver and skeletal muscle together account for >50 per cent of daily body protein turnover. Skeletal muscle has a large mass but a low

turnover rate (1–2 per cent per day), whereas the liver has a relatively small mass (1.5 kg) but a much higher protein turnover rate (10–20

per cent per day). Hepatic protein synthesis is divided roughly 50:50 between renew al of structural proteins and synthesis of export

proteins. Albumin is the major export protein produced by the liver and is renewed at the rate of about 10 per cent per day. The

transcapillary escape rate (TER) of albumin is about ten times the rate of synthesis, and shortterm changes in albumin concentration are

most probably due to increased vascular permeability. Albumin TER may be increased three-fold following major injury/sepsis.

In response to inammatory conditions, including surgery, trauma, sepsis, cancer or autoimmune conditions, circulating peripheral blood

mononuclear cells secrete a range of proinammatory cytokines, including IL-1, IL-6 and TNFα. These cytokines, in particular IL-6,

promote the hepatic synthesis of positive acute phase proteins, e.g. brinogen and C-r eactive protein (CRP). The acute phase protein

response (APPR) represents a ‘double-edged sword’ for surgical patients as it provides proteins important for recovery and repair, but

only at the expense of valuable lean tissue and energy reserves.

In contrast to the positive acute phase reactants, the plasma concentrations of other liver expo rt proteins (the negative acute phase

reactants) fall acutely following injury, e.g. albumin. However, rather than represent a reduced h epatic synthesis rate, the fall in plasma

concentration of negative acute phase reactants is thought principally to reect in creased transcapillary escape, secondary to an increase

in microvascular permeability (see above). Thus, increased hepatic synthesis of pos itive acute phase reactants is not compensated for by

reduced synthesis of negative reactants (Summary box 1.8).

Carl Ferdinand Cori , 1896–1984, Professor of Pharmacology, and later of Biochemistry, Washington University Medical School, St Louis, MI, USA and his wife Gerty

Theresa Cori, 1896–1957, who was also Professor of Biochemistry at the Washington University Medical School. In 1947 th e Coris were awarded a share of the Nobel

Prize for Physiology or Medicine ‘for their discovery of how glycogen is catalytically converted’.

Changes in body composition following injury 9

Summary box 1.8

Hepatic acute phase response

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

Positive reactants (e.g. CRP): plasma concentration ↑ Negative reactants (e.g. albumin): plasma concentration ↓ 60 FAT

50 PROTEIN

30 INTRACELLULAR WATER

Insulin resistance

Following surgery or trauma, postoperative hyperglycaemia develops as a result of incr eased glucose production combined with

decreased glucose uptake in peripheral tissues. Decreased glucose uptake is a result o f insulin resistance which is transiently induced

within the stressed patient. Suggested mechanisms for this phenomenon include the action of p roinammatory cytokines and the

decreased responsiveness of insulin-regulated glucose transporter proteins. Th e degree of insulin resistance is proportional to the

magnitude of the injurious process. Following routine upper abdominal surgery, insulin resistance may persist for approximately 2

weeks.

Postoperative patients with insulin resistance behave in a similar manner to indiv iduals with type II diabetes mellitus. The mainstay of

management of insulin resistance is intravenous insulin infusion. Insulin infusions ma y be used in either an intensive approach (i.e.

sliding scales are manipulated to normalise the blood glucose level) or a conservative ap proach (i.e. insulin is administered when the

blood glucose level exceeds a dened limit and discontinued when the level falls). Studie s of postoperatively ventilated patients in the

intensive care unit (ICU) have suggested that maintenance of normal glucose levels u sing intensive insulin therapy can signicantly

reduce both morbidity and mortality. Furthermore, intensive insulin therapy is superior to conservative insulin approaches in reducing

morbidity rates. However, the mortality benet of intensive insulin therapy ove r a more conservative approach has not been proven

conclusively. The observed benets of insulin therapy are probably simply as a result o f maintenance of normoglycaemia, but the

glycaemia-independent actions of insulin may also exert minor, organ-specic effects (e.g. promotion of myocardial systolic function).

CHANGES IN BODY COMPOSITION FOLLOWING INJURY

The average 70-kg male can be considered to consist of fat (13 kg) and fat- free mass (or lean body mass: 57 kg). In such an individual,

the lean tissue is composed primarily of protein (12 kg), water (42 kg) and minerals (3 kg) (Figure 1.7). The protein mass can be

considered as two basic compartments, skeletal muscle (4 kg) and non-skeletal mus cle (8 kg), which includes the visceral protein mass.

The water mass (42 litres) is divided into intercellular (28 litres) and extracellula r (14 litres) spaces. Most of the mineral mass is

contained in the bony skeleton.

The main labile energy reserve in the body is fat, and the main labile protein reserve is ske letal muscle. While fat mass can be reduced

without major detriment to function, loss of protein mass results not only in skeletal muscle wastin g, but

10 EXTRACELLULAR WATER

0 MINERALS

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

also depletion of visceral protein status. Within lean issue, each 1 g of nitrogen is contained w ithin 6.25 g of protein, which is contained

in approximately 36 g of wet weight tissue. Thus, the loss of 1 g of nitrogen in u rine is equivalent to the breakdown of 36 g of wet weight

lean tissue. Protein turnover in the whole body is of the order of 150–200 g per day. A normal human ingests about 70–100 g protein per

day, which is metabolised and excreted in urine as ammonia and urea (i.e. approximately 14 g N/day). During total starvation, urinary

loss of nitrogen is rapidly attenuated by a series of adaptive changes. Loss of body weight follows a similar course (Figure 1.8), thus

accounting for the survival of hunger strikers for a period of 50–60 days. Following major injury, and particularly in the presence of

ongoing septic complications, this adaptive change fails to occur, and there is a state of ‘autocann ibalism’, resulting in continuing urinary

nitrogen losses of 10–20 g N/day (equivalent to 500 g of wet weight lean tissu e per day). As with total starvation, once loss of body

protein mass has reached 30–40 per cent of the total, survival is unlikely.

Critically ill patients admitted to the ICU with severe sepsis or major blunt trauma undergo mass ive changes in body composition (Figure

1.8). Body weight increases immediately on resuscitation with an expansion of extracell ular water by 6–10 litres within 24 hours.

Thereafter, even with optimal metabolic care and nutritional support, total body protein w ill diminish by 15 per cent in the next 10 days,

and body weight will reach negative balance as the expansion of the extracellular space resolves. In marked contrast, it is now possible

to maintain body weight and nitrogen equilibrium following major elective surgery. T his can be achieved by blocking the

neuroendocrine stress response with epidural analgesia and providing early enteral fe eding. Moreover, the early uid retention phase can

be avoided by careful intraoperative management of uid balance, with avoidanc e of excessive administration of intravenous saline

(Summary box 1.9).

Sepsis and multiorgan

failure

24 68 10 12 14 16 18 20 22 days

Uncomplicated major

10 surgery

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

Summary box 1.9

Changes in body composition following major surgery/critical illness

Catabolism leads to a decrease in fat mass and skeletal muscle mass

Body weight may paradoxically increase because of expansion of extracellular fluid space

AVOIDABLE FACTORS THAT

COMPOUND THE RESPONSE TO INJURY

As noted previously, the main features of the metabolic response are initiated by th e immune system, cardiovascular system, sympathetic

nervous system, ascending reticular formation and limbic system. However, the metabolic stress response may be further exacerbated by

anaesthesia, dehydration, starvation (including preoperative fasting), sepsis, acute medic al illness or even severe psychological stress

(Figure 1.9). Attempts to limit or control these factors can be benecial to the patient (Summary bo x 1.10).

Summary box 1.10

Avoidable factors that compound the response to injury

Continuing haemorrhage

Hypothermia

Tissue oedema

Tissue underperfusion

Starvation

Immobility

Volume loss

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

initiate afferent nerve input to the central nervous system (CNS), resulting in th e release of both aldosterone and antidiuretic hormone

(ADH). Pain can also stimulate ADH release. ADH acts directly on the kidney to cau se uid retention. Decreased pulse pressure

stimulates the juxtaglomerular apparatus in the kidney and directly activates the renin–an giotensin system, which in turn increases

aldosterone release.

Aldosterone causes the renal tubule to reabsorb sodium (and consequently also conserve wate r). ACTH release also augments the

aldosterone response. The net effects of ADH and aldosterone result in the natur al oliguria observed after surgery and conservation of

sodium and water in the extracellular space. The tendency towards water and salt retentio n is exacerbated by resuscitation with saline-

rich uids. Salt and water retention can result in not only peripheral oedema, but also visceral oedema (e.g. stomach). Such visceral

oedema has been associated with reduced gastric emptying, delayed resumption of food intake and prolonged hospital stay. Careful

limitation of intraoperative administration of colloids and crystalloids (e.g. Hartmann’s solution ) so that there is no net weight gain

following elective surgery has been proven to reduce postoperative complications and length of stay.

Hypothermia

Hypothermia results in increased elaboration of adrenal steroids and catecholamines. W hen compared with normothermic controls, even

mild hypothermia results in a two- to three-fold increase in postoperative cardiac arrhythmia s and increased catabolism. Randomised

trials have shown that maintaining normothermia by an upper body forced-air heating cover reduces wound infections, cardiac

complications and bleeding and transfusion requirements.

Tissue oedema

During systemic inammation, uid, plasma proteins, leukocytes, macrophages and elec trolytes leave the vascular space and accumulate

in the tissues. This can diminish the alveolar diffusion of oxygen and may lead to reduced r enal function. Increased capillary leak is

mediated by a wide variety of mediators including cytokines, prostanoids, bradykinin and nitric ox ide. Vasodilatation implies that

intravascular volume

Concepts behind optimal perioperative care 11

STARVATION

wound

hypothermia hypotension pain

adreno-sympathetic

activation

cytokine cascade release

IMMOBILISATION

C A

hypermetabolism T

acute phase response

insulin resistance

futile substrate cycling L

muscle protein degradation I

S M

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

complications

decreases, which induces shock if inadequate resuscitation is not undertaken. Meanwhile, intrac ellular volume decreases, and this

provides part of the volume necessary to replenish intravascular and extravas cular extracellular volume.

Systemic inflammation and tissue

underperfusion

The vascular endothelium controls vasomotor tone and microvascular ow, and regula tes trafcking of nutrients and biologically active

molecules. When endothelial activation is excessive, compromised microcirculation and subsequent cellular hypoxia contribute to the

risk of organ failure. Maintaining normoglycaemia with insulin infusion during critical il lness has been proposed to protect the

endothelium, probably in part, via inhibition of excessive iNOS-induced NO release, an d thereby contribute to the prevention of organ

failure and death. Administration of activated protein C to critically ill patients h as been shown to reduce organ failure and death and is

thought to act, in part, via preservation of the microcirculation in vital organs.

Starvation

During starvation, the body is faced with an obligate need to generate glucose to su stain cerebral energy metabolism (100 g of glucose

per day). This is achieved in the rst 24 hours by mobilising glycogen stores and therea fter by hepatic gluconeogenesis from amino

acids, glycerol and lactate. The energy metabolism of other tissues is sustained by mobili sing fat from adipose tissue. Such fat

mobilisation is mainly dependent on a fall in circulating insulin levels. Eventually, accelera ted loss of lean tissue (the main source of

amino acids for hepatic gluconeogenesis) is reduced as a result of the liver conv erting free fatty acids into ketone bodies, which can

serve as a substitute for glucose for cerebral energy metabolism. Provision of 2 litres of intravenous 5 per cent dextrose as intravenous

uids for surgical patients who are fasted provides 100 g of glucose per day and has a s ignicant protein-sparing effect. Avoiding

unnecessary fasting in the rst instance and early oral/enteral/parenteral nutrit ion form the platform for avoiding loss of body mass as a

result of the varying degrees of starvation observed in surgical patients. Modern guidelines on fasting prior to anaesthesia allow intake of

clear fluids up to 2 hours before surgery. Administration of a carbohydrate drink at this time reduces perioperative anxiety and thirst and

decreases postoperative insulin resistance.

Immobility

Immobility has long been recognised as a potent stimulus for inducing muscle wasting. Inactivity impairs the normal mealderived amino

acid stimulation of protein synthesis in skeletal muscle. Avoidance of unnecessary bed res t and active early mobilisation are essential

measures to avoid muscle wasting as a consequence of immobility.

CONCEPTS BEHIND OPTIMAL

PERIOPERATIVE CARE

Current understanding of the metabolic response to surgical injury and the mediators involved has led to a reappraisal of traditional

perioperative care. There is now a strong scientic rationale for avoiding unmodulated expo sure to stress, prolonged fasting and

excessive administration of intravenous (saline) uids (Figure 1.10). The widespread ad option of minimal access (laparoscopic) surgery

is a key change in surgical practice that can reduce the magnitude of surgical injur y and enhance the rate of patients’ return to

homeostasis and recovery. It is also impor

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

tant to realise that modulating the stress/inammatory response at the time of su rgery may have long-term sequelae over periods of

months or longer. For example, β-blockers and statins have recently been shown to improve lon g-term survival after major surgery. It has

been suggested that these effects may be due to suppression of innate immunity at th e time of surgery. Equally, the use of epidural

analgesia to reduce pain, block the cortisol stress response and attenuate postoperative ins ulin resistance may, via effects on the body’s

protein economy, favourably affect many of the patient-centred outcomes tha t are important to postoperative recovery but have largely

been unmeasured to date, such as functional capacity, vitality and ability to return to work (Summary box 1.11).

FURTHER READING

Bessey PQ, Watters JM, Aoki TT, Wilmore DW. Combined hormonal infusion sim ulates the metabolic response to injury. Ann Surg

1984; 200: 264–81.

Calvano SE, Xioa W, Richards DR et al. A network-based analysis of systemic i nammation in humans. Nature 2005; 437: 1032–7.

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 surg ery: a consensus review of clinical care for patients

undergoing colonic resection. Clin Nutr 2005; 24: 466–77.

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 recov ery 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.

Van den Berghe G, Wonters P, Weckers F et al. Intensive insulin therapy in the critically ill patie nt. 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.

Varadhan KK, Neal KR, Dejong CH et al. The enhanced recovery after surgery (ERAS) pa thway for patients undergoing major elective

open colorectal surgery: a meta-analysis of randomised controlled trials. Clin Nutr 2010; 29: 434–4 0.

Wilmore DW. From Cuthbertson to fast-track surgery: 70 years of progress i n reducing stress in surgical patients. Ann Surg 2002; 236:

643–8.

Summary box 1.11

A proactive approach to prevent unnecessary aspects of the surgical stres s response

Minimal access techniques

Blockade of afferent painful stimuli (e.g. epidural analgesia) Minimal periods of starvation

Early mobilisation

Francis Daniels Moore, 1913–2001, Moseley Professor of Surgery at Peter Bent Brigham Hospital , Boston. ‘Franny’ to his colleagues, did pioneering work on metabolic

response to surgery and published his seminal work in 1959, Metabolic care of the surgical patient . At the age of 34 he became the youngest Chairman of Surgery in

Harvard’s history. His leadership led to the first ever kidney transplantation between identical twins in his department by Joe Murray in 1954. He was often regarded as

‘the ultimate communicator’.

CHAPTER

transfusion Shock and blood

LEARNING OBJECTIVES

To understand:

• The pathophysiology of shock and ischaemia– reperfusion injury

• The different patterns of shock and the principles and priorities of resusc itation

• Appropriate monitoring and end points of resuscitation

• Use of blood and blood products, the benefits and risks of blood transfusion

INTRODUCTION

Shock is the most common and therefore the most important cause of death of surgi cal patients. Death may occur rapidly due to a

profound state of shock, or be delayed due to the consequences of organ ischaem ia and reperfusion injury. It is important therefore that

every surgeon understands the pathophysiology, diagnosis and priorities in managemen t of shock and haemorrhage.

SHOCK

Shock is a systemic state of low tissue perfusion which is inadequate for normal cellular respiration. With insufcient delivery of oxygen

and glucose, cells switch from aerobic to anaerobic metabolism. If perfusion is n ot restored in a timely fashion, cell death ensues.

Pathophysiology

Cellular

As perfusion to the tissues is reduced, cells are deprived of oxygen 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 accumulation of lactic acid in the

blood produces a systemic metabolic acidosis.

As glucose within cells is exhausted, anaerobic respiration ceases and there is failure of sodium/potassium pumps in the cell membrane

and intracellular organelles. Intracellular lysosomes release autodigestive enzymes a nd cell lysis ensues. Intracellular contents, including

potassium are released into the blood stream.

Microvascular

As tissue ischaemia progresses, changes in the local milieu result in activation of the immune and c oagulation systems. Hypoxia and

acidosis activate complement and prime neutrophils, resulting in the generation of oxyge n free radicals and cytokine release. These

mechanisms lead to injury of the capillary endothelial cells. These, in turn, further activa te the immune and coagulation systems.

Damaged endothelium loses its integrity and becomes ‘leaky’. Spaces between endothel ial cells allow fluid to leak out and tissue oedema

ensues, exacerbating cellular hypoxia.

Systemic

Cardiovascular

As preload and afterload decrease, there is a compensatory baroreceptor response resu lting in increased sympathetic activity and release

of catecholamines into the circulation. This results in tachycardia and systemic vasoc onstriction (except in sepsis – see below).

Respiratory

The metabolic acidosis and increased sympathetic response result in an increased respirat ory rate and minute ventilation to increase the

excretion of carbon dioxide (and so produce a compensatory respiratory alk alosis).

Renal

Decreased perfusion pressure in the kidney leads to reduced filtration at the glo merulus and a decreased urine output. The renin–

angiotensin–aldosterone axis is stimulated, resulting in further vasoconstriction and in creased sodium and water reabsorption by the

kidney.

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 collecting system.

Cortisol is also released from the adrenal cortex contributing to the sodium and water re sorption and sensitizing the cells to

catecholamines.

Table 2.1 Cardiovascular and metabolic characteristics of shock.

Hypovolaemia Cardiogenic Obstructive Distributive

Cardiac output

Vascular resistance

Venous pressure

Mixed venous saturation Base decit

Low Low High High Low High Low Low High High Low High High Low High Low Low High High High

Ischaemia–reperfusion syndrome

During the period of systemic hypoperfusion, cellular and organ damage progress es due to the direct effects of tissue hypoxia and local

activation of inammation. 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 hypote nsion. The cellular and humoral elements

activated by the hypoxia (complement, neutrophils, microvascular thrombi) are ushed 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 duratio n of tissue hypoperfusion.

Classification of shock

There are numerous ways to classify shock, but the most common and most clinically ap plicable is one based on the initiating

mechanism (Summary box 2.1).

All states are characterised by systemic tissue hypoperfusion and different sta tes may coexist within the same patient.

Summary box 2.1

Classification of shock

Hypovolaemic shock Cardiogenic shock

Obstructive shock

Distributive shock

Endocrine shock

Hypovolaemic shock

Hypovolaemic shock is due to a reduced circulating volume. Hypovolaemia may be due to haemorrhagic or non-haemorrhagic causes.

Non-haemorrhagic causes include poor uid intake (dehydration), excessive uid loss due to vomiting, diarrhoea, urinary loss (eg.

diabetes), evaporation, or ‘third-spacing’ where fluid is lost into the gastrointest inal 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 c omponent of all other forms of shock. Absolute or

relative hypovolaemia must be excluded or treated in the management of the shocked state, r egardless of cause.

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 car diomyopathy. Cardiac insufciency may also be

due to myocardial depression due to endogenous factors (e.g. bacterial and humoral agents rel eased in sepsis) or exogenous factors, such

as pharmaceutical agents or drug abuse. Evidence of venous hypertension with pulmonar y 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 lling. Common causes of obstructive shock

include cardiac tamponade, tension pneumothorax, massive pulmonary embolus or air e mbolus. In each case, there is reduced lling of

the left and/or right sides of the heart leading to reduced preload and a fall in car diac output.

Distributive shock

Distributive shock describes the pattern of cardiovascular responses characterising a va riety 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 t here is failure of sympathetic outow and

adequate vascular tone (neurogenic shock). The cause in sepsis is less clear but is related to the re lease of bacterial products (endotoxin)

and the activation of cellular and humoral components of the immune system. There is maldistr ibution of blood ow at a microvascular

level with arteriovenous shunting and dysfunction of cellular utilization of oxyg en.

In the later phases of septic shock there is hypovolaemia from fluid loss into interstitial spa ces and there may be concomitant myocardial

depression, complicating the clinical picture (Table 2.1).

Endocrine shock

Endocrine shock may present as a combination of hypovolaemic, cardiogenic or distrib utive shock. Causes of endocrine shock include

hypo- and hyperthyroidism and adrenal insufciency. Hypothyroidism causes a sho ck state similar to that of neuro

Shock 15

Table 2.2 Clinical features of shock.

Compensated Mild Moderate Severe

Lactic acidosis +

Urine output Normal Conscious level Normal Respiratory rate Normal Pulse rate Mild in crease Blood pressure Normal ++

Normal

Mild anxiety Increased

Increased

Normal

Reduced

Drowsy

Increased

Mild hypotension +++

Anuric

Comatose

Laboured

Increased

Severe hypotension

genic shock due to disordered vascular and cardiac responsiveness to circulating catech olamines. Cardiac output falls due to low inotropy

and bradycardia. There may also be an associated cardiomyopathy. Thyrotoxicosis ma y cause a high-output cardiac failure.

Adrenal insufciency leads to shock due to hypovolaemia and a poor response to cir culating and exogenous catecholamines. Adrenal

insufciency may be due to pre-existing Addison’s disease or be a relative insufciency due to a pathological disease state, such as

systemic sepsis.

Severity of shock

Compensated shock

As shock progresses, the body’s cardiovascular and endocrine compensatory respons es reduce ow to non-essential organs to preserve

preload and ow to the lungs and brain. In compensated shock, there is adequate comp ensation to maintain central blood volume and

preserve ow to the kidneys, lungs and brain. Apart from a tachycardia and cool per ipheries (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 gastrointestinal tract. There is a

systemic metabolic acidosis and activation of humoral and cellular elements within the u nderperfused organs. Although clinically occult,

this state will lead to multiple organ failure and death if prolonged due to the ischaemia–r eperfusion effect described above under

Ischaemia–reperfusion syndrome. Patients with occult hypoperfusion (metabolic acidosis despite normal urine output and

cardiorespiratory vital signs) for more than 12 hours have a signicantly higher mortality, infe ction rate and incidence of multiple organ

failure (see below under Multiple organ failure).

Decompensation

Further loss of circulating volume overloads the body’s compensatory mechanisms and there is progressive renal, respiratory and

cardiovascular decompensation. In general, loss of around 15 per cent of the circulating blood volume is within normal compensatory

mechanisms. Blood pressure is usually well maintained and only falls after 30–40 per ce nt of circulating volume has been lost.

Mild shock

Initially there is tachycardia, tachypnoea, a mild reduction in urine output and the patie nt 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 rell times

(except in septic distributive shock).

Moderate shock

As shock progresses, renal compensatory mechanisms fail, renal perfusion f alls 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 m ildly confused.

Severe shock

In severe shock, there is profound tachycardia and hypotension. Urine output f alls 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 class ic signs.

Capillary refill

Most patients in hypovolaemic shock will have cool, pale peripheries, with prolonged capil lary rell times. However, the actual capillary

rell time varies so much in adults that it is not a specic marker of whether a patient is sho cked, and patients with short capillary rell

times may be in the early stages of shock. In distributive (septic) shock, the per ipheries will be warm and capillary rell will be brisk,

despite profound shock.

Tachycardia

Tachycardia may not always accompany shock. Patients who are on beta-block ers or who have implanted pacemakers are unable to

mount a tachycardia. A pulse rate of 80 in a t young adult who normally has a pulse rat e of 50 is very abnormal. Furthermore, in some

young patients with penetrating trauma, where there is haemorrhage but little tissue damage, there may be a paradoxical bradycardia

rather than tachycardia accompanying the shocked state.

Blood pressure

It is important to recognise that hypotension is one of the last signs of shock. Children and t young adults are able to maintain blood

pressure until the nal stages of shock by dramatic increases in stroke volume and peripher al vasoconstriction. These patients can be in

profound shock with a normal blood pressure.

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

Elderly patients who are normally hypertensive may present with a ‘normal’ blood pre ssure for the general population 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 difcult unless one is alert to these pitfalls.

Consequences

Unresuscitatable shock

Patients who are in profound shock for a prolonged period of time become ‘unresu scitatable’. Cell death follows from cellular ischaemia

and the ability of the body to compensate is lost. There is myocardial depression and los s of responsiveness to uid or inotropic therapy.

Peripherally there is loss of the ability to maintain systemic vascular resistance and fu rther 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 resuscitation in the earlier

stages of shock. Conversely, when patients present in this late stage, and have minimal res ponses 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 sur viving shock. Where intervention is timely and the period

of shock is limited, patients may make a rapid, uncomplicated recovery. However, the result of prolonged systemic ischaemia and

reperfusion injury is end-organ damage and multiple organ failure.

Multiple organ failure is dened as two or more failed organ systems (Summary box 2.2).

Summary box 2.2

Effects of organ failure

Lung: Acute respiratory distress syndrome Kidney: Acute liver insufficiency

Clotting: Coagulopathy

Cardiac: Cardiovascular failure

There is no specic treatment for multiple organ failure. Management is supporting of organ systems with ventilation, cardiovascular

support and haemoltration/dialysis until there is recovery of organ function. Multiple o rgan failure currently carries a mortality of 60

per cent; thus prevention is vital by early aggressive identication and reversal of shock.

and ventilation. Once ‘airway’ and ‘breathing’ are assessed and controlled, attention is direct ed to cardiovascular resuscitation.

Conduct of resuscitation

Resuscitation should not be delayed in order to denitively diagnose the sourc e of the shocked state. However, the timing 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 appropriate rst determination, even if a source of bleeding or sepsis i s not immediately identiable. If there is initial

doubt about the cause of shock, it is safer to assume the cause is hypovolaem ia and begin with uid resuscitation, and then assess the

response.

In patients who are actively bleeding (major trauma, aortic aneurysm rupture, gastrointestin al haemorrhage), it is counterproductive to

institute high-volume uid therapy without controlling the site of haemorrhage. Increasing blood pressure merely increases bleeding

from the site while uid 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 hypovolaemic shock must be adequate ly resuscitated before undergoing surgery

otherwise the additional surgical injury and hypovolaemia induced during the procedur e will exacerbate the inammatory activation and

increase the incidence and severity of end-organ insult.

Fluid therapy

In all cases of shock, regardless of classication, hypovolaemia and inadequate prelo ad must be addressed before other therapy is

instituted. Administration of inotropic or chronotropic agents to an empty heart will rapidly an d permanently deplete the myocardium of

oxygen stores and dramatically reduce diastolic filling and therefore coronary perfusion. P atients 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 uids. Acce ss should be through short, wide-bore

catheters that allow rapid infusion of uids as necessary. Long, narrow lines, such as central ven ous catheters, have too high a resistance

to allow rapid infusion and are more appropriate for monitoring than uid replacement ther apy.

Type of fluids

There is continuing debate over which resuscitation uid is best for the management of sh ock. There is no ideal resuscitation fluid, and it

is more important to understand how and when to administer it. In most studies of shock resuscitation 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 available products). Furthermore, there is less volume benet to the admin istration

RESUSCITATION

Immediate resuscitation manoeuvres for patients presenting in shock are to ensure a patent airway and adequate oxygenation

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. Resuscitation 17

of colloids than had previously been thought, with only 1.3 times more crystallo id than colloid administered in blinded trials. On

balance, there is little evidence to support the administration of colloids, which are more exp ensive and have worse side-effect proles.

Most importantly, the oxygen carrying capacity of crystalloids and colloids is zer o. 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 decit is free

water loss (eg. diabetes insipidus) or patients are sodium overloaded (eg. cirrhosis).

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

Dynamic fluid response

The shock status can be determined dynamically by the cardiovascular response to the r apid administration of a uid bolus. In total, 250–

500 mL of uid 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’, ‘trans ient responders’ and ‘nonresponders’.

Responders have an improvement in their cardiovascular status which is sus tained. These patients are not actively losing fluid but

require lling to a normal volume status.

Transient responders have an improvement which then reverts to the previous state over the next 10–20 minutes. These patients have

moderate ongoing uid losses (either overt haemorrhage or further uid shifts reducin g intravascular volume).

Non-responders are severely volume depleted and are likely to have major ongoing loss o f intravascular volume, usually through

persistent uncontrolled haemorrhage.

Vasopressor and inotropic support

Vasopressor or inotropic therapy is not indicated as rst-line therapy in hypovolaemia. As d iscussed above, administration of these

agents in the absence of adequate preload rapidly leads to decreased coronary perfusion and depletion of myocardial oxygen reserves.

Vasopressor agents (phenylephrine, noradrenaline) are indicated in distributive shock s tates (sepsis, neurogenic shock) where there is

peripheral vasodilatation, and a low systemic vascular resistance, leading to hyp otension despite a high cardiac output. Where the

vasodilatation is resistant to catecholamines (e.g. absolute or relative steroid dec iency) vasopressin may be used as an alternative

vasopressor.

In cardiogenic shock, or where myocardial depression complicated a shock state (e.g. severe septic shock with low cardiac output),

inotropic therapy may be required to increase cardiac output and therefore o xygen delivery. The inodilator dobutamine is the agent of

choice.

Monitoring

The minimum standard for monitoring of the patient in shock is continuous h eart rate and oxygen saturation monitoring, frequent non-

invasive blood pressure monitoring and hourly urine output measurements. Most p atients will need more aggressive invasive monitoring,

including central venous pressure and invasive blood pressure monitoring (Summary b ox 2.3).

Cardiovascular

Cardiovascular monitoring at a minimum should include continuous heart rate (ECG), o xygen saturation and pulse waveform and non-

invasive blood pressure. Patients whose state of shock is not rapidly corrected with a small amou nt of uid should have central venous

pressure monitoring and continuous 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 b e placed on an individual pressure

measurement to assess volume status. Some patients may require a CVP of 5 cmH

O, whereas some may require a CVP of 15 cmH

O or

higher. Further, ventricular compliance can change from minute to minute in the sho cked state, and CVP is a poor reection of end

diastolic volume (preload).

CVP measurements should be assessed dynamically as response to a uid challenge (see above). A uid bolus (250– 500 mL) is infused

rapidly over 5–10 minutes.

The normal CVP response is a rise of 2–5 cmH

O which gradually drifts back to the original level over 10–20 minutes. Patients wit h no

change in their CVP are empty and require further uid resuscitation. Patients with a lar ge, sustained rise in CVP have high preload and

an element of cardiac insufciency or volume overload.

Cardiac output

Cardiac output monitoring allows not only assessment of the cardiac output but also the systemic vascular resistance and, depending on

the technique used, end diastolic volume (preload) and blood volume. Use of invasive card iac monitoring using pulmonary artery

catheters is becoming less frequent as new non-invasive monitoring techniques, such as D oppler ultrasound, pulse waveform analysis

and indicator dilution methods, provide similar information without many of the draw backs of more invasive techniques.

Measurement of cardiac output, systemic vascular resistance and preload can h elp distinguish the types of shock present (hypovolaemia,

distributive, cardiogenic), especially when they coexist. The information provided g uides uid and vasopressor therapy by providing

real-time monitoring of the cardiovascular response.

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

Measurement of cardiac output is desirable in patients who do not respond as expected to rst-lin e therapy, or who have evidence of

cardiogenic shock or myocardial dysfunction. Early consideration should be given to institutin g cardiac output monitoring on patients

who require vasopressor or inotropic support.

Systemic and organ perfusion

Ultimately, the goal of treatment is to restore cellular and organ perfusion. Ideally, therefor e, monitoring of organ perfusion should guide

the management of shock. The best measures 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 musc ular beds are the global measures of lactic

acidosis (lactate and base decit) and the mixed venous oxygen saturation.

Base deficit and lactate

Lactic acid is generated by cells undergoing anaerobic respiration. The degree of lactic acidosis, as measured by serum lactate level

and/or the base decit, is sensitive for both diagnosis of shock and monitoring the response to therapy. Patients with a base decit over 6

mmol/L have a much higher morbidity and mortality than those with no metabolic acidosis. Furth ermore, the duration of time in shock

with an increased base decit 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 fre quency of measurements is limited and they do not

provide minute-to-minute data on systemic perfusion or the response to therapy. Never theless, the base decit and/or lactate should be

measured routinely in these patients until they have returned to normal levels.

Mixed venous oxygen saturation

The per cent 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 analysis of blood drawn from a long central line placed in the rig ht atrium. Estimations can be made from

blood drawn from lines in the superior vena cava, but these values will be slightly higher tha n those of a mixed venous sample (as there

is relatively more oxygen extraction from the lower half of the body). Normal mixed v enous oxygen saturation levels are 50–70 per cent.

Levels below 50 per cent indicate inadequate oxygen delivery and increased oxygen extraction by the cells. This is consistent with

hypovolaemic or cardiogenic shock.

High mixed venous saturations (>70 per cent) are seen in sepsis and some othe r forms of distributive shock. In sepsis, there is disordered

utilization of oxygen at the cellular level, and arteriovenous shunting of blood at the mic rovascular level. Thus less oxygen is presented

to the cells, and those cells cannot utilise what little oxygen is presented. Thus, venous bloo d has a higher oxygen concentration than

normal.

Patients who are septic should therefore have mixed venous oxygen saturations ab ove 70 per cent; below this level, they are not only in

septic shock but also in hypovolaemic or cardiogenic shock. Although the S

level is in the ‘normal’ range, it is low for the septic

state, and inadequate oxygen is being supplied to cells that cannot utilize oxygen appropria tely. This must be corrected rapidly.

Hypovolaemia should be corrected with uid therapy, and low cardiac output due to myo cardial depression or failure should be treated

with inotropes (dobutamine), to achieve a mixed venous saturation greater tha n 70 per cent (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 spectroscopy and sublingual capnometry. While th ese techniques provide information regarding

perfusion of specic tissue beds, it is as yet unclear whether there are signicant advantages o ver existing measurements of global

hypoperfusion (base decit, lactate).

Table 2.3 Monitors for organ/systemic perfusion.

Clinical Investigational Systemic perfusion Base decit

Lactate

Mixed venous oxygen saturation Organ perfusion Muscle

–

Gut

–

Kidney Brain

Urine output

Conscious level Near-infrared spectroscopy Tissue oxygen electrode Sublingual capno metry Gut mucosal pH

Laser Doppler owmetry

–

Tissue oxygen electrode Near-infrared spectroscopy

Haemorrhage 19 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 output. However, these parameters are monitoring organ systems whose blood ow 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 inammation and c oagulation may be ongoing and lead to

reperfusion injury when these organs are nally perfused, and ultimately multiple organ fa ilure.

This state of normal vital signs and continued underperfusion is termed ‘occult hypoperfusion’. With current monitoring techniques, it is

manifested only by a persistent lactic acidosis and low mixed venous oxygen saturation. Th e duration patients spend 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 decit, lactate, mixed venous oxygen 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 regimens, some patients cannot be resuscitated to normal parameters wit hin 12 hours by uid resuscitation alone.

More research is underway to identify the pathophysiology behind this and investigate n ew therapeutic options.

HAEMORRHAGE

Haemorrhage must be recognised and managed aggressively to reduce the seve rity and duration of shock and avoid death and/ or

multiple organ failure. Haemorrhage is treated by arresting the bleeding – no t by uid resuscitation or blood transfusion. Although

necessary as supportive measures to maintain organ perfusion, attempting to resuscitate patien ts who have ongoing haemorrhage will lead

to physiological exhaustion (coagulopathy, acidosis and hypothermia) and subsequently death.

Pathophysiology

Haemorrhage leads to a state of hypovolaemic shock. The combination of tissue tra uma and hypovolaemic shock leads to the

development of an endogenous coagulopathy called acute traumatic coagulopathy (ATC). Up to 25 per cent of trauma

Trauma Shock

ATC Haemorrhage

Fibrinolysis Inflammation Hypothermia Acidaemia Genetics Loss, dilution

TRAUMA-INDUCED COAGULOPATHY (TIC)

Figure 2.1 Trauma-induced coagulopathy.

patients develop ATC within minutes of injury and it is associated with a four-fold incre ase in mortality. It is likely that ATC exists

whenever there is the combination of shock and tissue trauma (e.g. major surgery). ATC is the component of traumainduced

coagulopathy (TIC) which is ultimately multifactorial (Figure 2.1).

Ongoing bleeding with fluid and red blood cell resuscitation leads to a dilution of coagulation facto rs which worsens the coagulopathy. In

addition, the acidosis induced by the hypoperfused state leads to decreased func tion of the coagulation proteases, resulting in

coagulopathy and further haemorrhage. The reduced tissue perfusion includes r educed blood supply to muscle beds. Underperfused

muscle is unable to generate heat and hypothermia ensues. Coagulation functions poorl y at low temperatures and there is further

haemorrhage, further hypoperfusion and worsening acidosis and hypothermia. These three fact ors result in a downward spiral leading to

physiological exhaustion and death (Figure 2.1).

Medical therapy has a tendency to worsen this effect. Intravenous blood and uids are cold and exacerbate hypothermia. Further heat is

lost by opening body cavities during surgery. Surgery usually leads to further bleeding an d many crystalloid fluids are themselves acidic

(e.g. normal saline has a pH of 6.7). Every effort must therefore be made to r apidly identify and stop haemorrhage, and to avoid

(preferably) or limit physiological exhaustion from coagulopathy, acidosis and hypother mia.

Definitions

Revealed and concealed haemorrhage

Haemorrhage may be revealed or concealed. Revealed haemorrhage is obvious extern al haemorrhage, such as exsanguination 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 trauma,

haemorrhage may be concealed within the chest, abdomen, pelvis, retroperitoneum or in the limbs with contained vascular injury or

associated with long-bone fractures. Examples of non-traumatic concealed haemorrha ge include occult gastrointestinal bleeding or

ruptured aortic aneurysm.

Primary, reactionary and secondary haemorrhage

Primary haemorrhage is haemorrhage occurring immediately due to an injury (or surgery). Re actionary haemorrhage is delayed

haemorrhage (within 24 hours) and is usually due to dislodgement of clot by resuscitati on, normalisation of blood pressure and

vasodilatation. Reactionary haemorrhage may also be due to technical failure, such a s 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 precipitated by factors

such as infection, pressure necrosis (such as from a drain) or malignancy.

Surgical and non-surgical haemorrhage

Surgical haemorrhage is due to a direct injury and is amenable to surgical contro l (or other techniques such as angioembolisation). Non-

surgical haemorrhage is the general ooze from all raw surfaces due to coagu lopathy and cannot be stopped by surgical means (except

packing). Treatment requires correction of the coagulation abnormalities.

Degree and classification

The adult human has approximately 5 litres of blood (70 mL/ kg children and adults, 80 mL/kg neonates). Estimation of the amount of

blood that has been lost is difcult, inaccurate and usually underestimates the actual value.

External haemorrhage is obvious, but it may be difcult to estimate the actual volume lo st. 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 as it repre sents a concentration and not an absolute amount. In

the early stages of rapid haemorrhage, the haemo globin concentration is unchang ed (as whole blood is lost). Later, as uid shifts from

the intracellular and interstitial spaces into the vascular compartment, the haemogl obin and haematocrit levels will fall.

The amount of haemorrhage can be classied into classes 1–4 based on the estim ated blood loss required to produce certain physiological

compensatory changes (Table 2.4). Although conceptually useful, there is variation acr oss ages (the young compensate well, the old very

poorly), variation between individuals (athletes versus the obese) and variation due to confo unding factors (e.g. concomitant

medications, pain).

Treatment should therefore be based upon the degree of hypovolaemic shock accordin g to vital signs, preload assessment, base decit

and, most importantly, the dynamic response to uid therapy. Patients who are ‘non-respo nders’ or ‘transient responders’ are still

bleeding and must have the site of haemorrhage identied and controlled.

Table 2.4 Traditional classification of haemorrhagic shock.

Class 1234 Blood volume lost as <15% 15–30% 30–40% >40% percentage of total

Management

Identify haemorrhage

External haemorrhage may be obvious, but the diagnosis of concealed haemorrhage m ay be more difcult. Any shock should be assumed

to be hypovolaemic until proved otherwise, and similarly, hypovolaemia should be assu med to be due to haemorrhage until this has been

excluded.

Immediate resuscitative manoeuvres

Direct pressure should be placed over the site of external haemorrhage. Airway and b reathing should be assessed and controlled as

necessary. Large-bore intravenous access should be instituted and blood drawn for cr oss-matching (see Cross-matching below).

Emergency blood should be requested if the degree of shock and ongoing h aemorrhage warrants this.

Identify the site of haemorrhage

Once haemorrhage has been considered, the site of haemorrhage must be rapidly iden tied. Note this is not to denitively identify the

exact location, but rather to dene the next step in haemorrhage control (operation, ang ioembolisation, endoscopic control).

Clues may be in the history (previous episodes, known aneurysm, non-steroidal therap y for gastrointestinal (GI) bleeding) or

examination (nature of blood – fresh, melaena; abdominal tenderness, etc.). For shocke d trauma patients, the external signs of injury may

suggest internal haemorrhage, but haemorrhage into a body cavity (thorax, abdomen) m ust 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 co ndition. Rapid bedside tests are more appropriate for

profound shock and exsanguinating haemorrhage than investigations such as computed tomog raphy (CT) which take time. Patients who

are not actively bleeding can have a more methodical, denitive work-up.

Haemorrhage control

The bleeding, shocked patient must be moved rapidly to a place of haemorrhage control. This will usually be in the operating room but

may be the angiography or endoscopy suites. These patients require surgical and anaesthetic sup port and full monitoring and equipment

must be available.

Haemorrhage control must be achieved rapidly so as to prevent the patient ente ring the triad of coagulopathy–acidosis– hypothermia and

physiological exhaustion. There should be no unnecessary investigations or procedures prior to h aemorrhage control to minimize 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 sh ould be paid to correction of coagulopathy with

blood component therapy to aid surgical haemorrhage control.

Surgical intervention may need to be limited to the minimum necessary to stop bleeding a nd control sepsis. More denitive repairs can be

delayed until the patient is haemodynamically stable and physiologically capable of sustai ning the procedure. This concept of tailoring

the operation to match the patient’s physiology and staged procedures to prevent physiological exha ustion is called ‘damage control

surgery’ – a term borrowed from the military which ensures continued functioning of a dam aged ship above conducting complete repairs

which would prevent rapid return to battle (Summary box 2.4).

Once haemorrhage is controlled, patients should be aggressively resuscitated, warmed a nd coagulopathy corrected. Attention should be

paid to uid responsiveness and the end points of resuscitation to ensure that patients ar e 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

Transfusion 21 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 preserve physiology.

Damage control resuscitation strategies have been shown to reduce mortality and morbidity in patients with exsanguinating trauma and

may be applicable in other forms of acute haemorrhage.

TRANSFUSION

The transfusion of blood and blood products has become commonplace since the rst s uccessful transfusion in 1818. Although the

incidence of severe transfusion reactions and infections is now very low, in recent yea rs it has become apparent that there is an

immunological price to be paid from the transfusion of heterologous blood, leading to in creased morbidity and decreased survival in

certain population groups (trauma, malignancy). Supplies are also limited, and therefore t he use of blood and blood products must always

be judicious and justiable for clinical need (Table 2.5).

Blood and blood products

Blood is collected from donors who have been previously screened before d onating, 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 ma y 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 hepa titis 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 group is determined, 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 as it is an inefcient use of the lim ited resource. However, whole blood

transfusion has signicant advantages over packed cells as it is coagulation factor ric h and, if fresh, more metabolically active than stored

blood.

Packed red cells

Packed red blood cells are spun-down and concentrated packs of red blood cells. Each u nit is approximately 330 mL and has a

haematocrit of 50–70 per cent. Packed cells are stored in a SAG-M solution (saline–a denine–glucose–mannitol) to increase shelf life to 5

weeks at 2–6°C. (Older storage regimens included storage in CPD – citrate–phosphate–d extrose solutions which have a shelf life of 2–3

weeks.)

1926

1939

Table 2.5 History of blood transfusion.

Pope Innocent VIII suffers a stroke and receives a blood transfusion from three ten-year -old boys (paid a ducat each). All three boys

died, as did the pope later that year

Richard Lower in Oxford conducts the rst successful canine transfusions

Jean-Baptiste Denis reports successful sheep–human transfusions

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

James Blundell performs the rst successful documented human transfusion in a woman su ffering post-partum haemorrhage. She

received blood from her husband and survived

Karl Landsteiner discovers the ABO system

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

The British Red Cross instituted the rst blood transfusion service in the world

The Rhesus system was identied and recognised as the major cause of transfusion re actions

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 two-year

shelf life. It is the rst-line therapy in the treatment of coagulopathic haemorrhage (see bel ow 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 due to the presence of red cell fragments, and rhesus D immunization should b e considered.

Cryoprecipitate

Cryoprecipitate is a supernatant precipitate of FFP and is rich in factor VIII and brino gen. It is stored at −30°C with a twoyear shelf life.

It is given in low fibrinogen states or factor VIII deciency.

Platelets

Platelets are supplied as a pooled platelet concentrate and contain about 250 × 10

/L. Platelets are stored on a special agitator at 20–24°C

and have a shelf life of only 5 days. Platelet transfusions are given to patients with throm bocytopenia or with platelet dysfunction who

are bleeding or undergoing surgery.

Patients are increasingly presenting on antiplatelet therapy such as aspirin or clopidog rel for reduction of cardiovascular risk. Aspirin

therapy rarely poses a problem but control of haemorrhage on the more potent platelet inhibitors can be extremely difcult. Patients on

clopidogrel who are actively bleeding and undergoing major surgery may requ ire 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 limited

success.

Hans Gerhard Creutzfeldt, 1885–1946, neurologist, Kiel, Germany. Alfons Maria Jakob, neurologist, Hamburg, Germany.

1492

1665

1667

1678

1818

1901 1914

Prothrombin complex concentrates

Prothrombin complex concentrates (PCC) are highly puried 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 emerge ncy reversal of anticoagulant (warfarin) therapy in

uncontrolled haemorrhage.

Autologous blood

It is possible for patients undergoing elective surgery to predonate their own blood up t o 3 weeks before surgery for retransfusion during

the operation. Similarly, during surgery blood can be collected in a cell-saver whic h washes and collects red blood cells which can then

be returned to the patient.

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 use. The indications for blood transfusion are as follows:

• acute blood loss, to replace circulating volume and maintain oxygen delivery;

• perioperative anaemia, to ensure adequate oxygen delivery during the periope rative phase;

• symptomatic chronic anaemia, without haemorrhage or impending surgery.

Transfusion trigger

Historically, patients were transfused to achieve a haemoglobin >10 g/dL. This has n ow been shown to not only be unnecessary but also

to be associated with an increased morbidity and mortality compared to lower target valu es. A haemoglobin 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 optimal haemoglobin level in some patient groups, such as those with cardiovascular dis ease, sepsis and traumatic brain injury.

Although conceptually a higher haemoglobin improves oxygen delivery, there is little clin ical 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 <6 Probably will benet from transfusion

6–8 Transfusion unlikely to be of benet in the absence of bleeding or impend ing surgery

>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 ant igens are of major importance in surgical practice –

the ABO and rhesus systems.

ABO system

These are strongly antigenic and are associated with naturally occurring antibodies in the seru m. The system consists of three allelic

genes – A, B and O which control synthesis of enzymes that add carbohydra te residues to cell surface glycoproteins. A and B genes add

specic residues while O gene is an amorph and does not transform the glycoprotein. Th e 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 individuals are

‘universal recipients’ and can receive any ABO blood type as they have no circ ulating antibodies.

Rhesus system

The rhesus D (Rh(D)) antigen is strongly antigenic and is present in approximately 85 per ce nt of the population in the UK. Antibodies to

the D antigen are not naturally present in the serum of the remaining 15 per c ent of individuals, but their formation 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 pr esent in a Rh(D)-negative mother, may cause

severe haemolytic anaemia and even death (hydrops fetalis) in a Rh(D)-positive fetu s in utero. The other minor blood group antigens

may be associated with naturally occurring antibodies, or may stimulate the formation of antibodies on relatively rare occasions.

Transfusion reactions

If antibodies present in the recipient’s serum are incompatible with the donor’s cells, a tra nsfusion reaction will result. This usually takes

the form of an acute haemolytic reaction. Severe immune-related transfusion reacti ons due to ABO incompatibility result in potentially

fatal complement-mediated intravascular haemolysis and multiple organ failure. Transf usion 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 bloo d transfusion should be stopped immediately. This form

of transfusion reaction is rare with leukodepleted blood.

Cross-matching

To prevent transfusion reactions, all transfusions are preceded by ABO and rhesus ty ping of both donor and recipient blood to ensure

compatibility. The recipient’s serum is then mixed with the donor’s cells to conrm ABO com patibility 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 specic’ blood is provided

which is only ABO/rhesus matched and can be issued within 10–15 minutes. Whe re blood must be given emergently, group O (universal

donor) blood is given (O− to females, O+ to males).

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.

FURTHER READING

Alam HB. An update on uid resuscitation. Scand J Surg 2006; 95: 136–45.

Duchesne JC, McSwain NE Jr, Cotton BA et al. Damage control resuscita tion: the new face of damage control. J Trauma 2010; 69: 976–

90.

Otero RM, Nguyen HB, Huang DT et al. Early goal-directed therapy in severe sepsis and septic shock revisited: concepts, controversies

and contemporary ndings. Chest 2006; 130: 1579–95.

Roussaint R, Cerny V, Coats TJ et al. Key issues in advanced bleeding care in trauma. Shock 2006; 26: 322–31.

Sihler KC, Nathans AB. Management of severe sepsis in the surgical patient. Surg Cli n N Am 2006; 86: 1457–81.

CHAPTER

repair and scars Wounds, tissue

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 wounds

• The variety of scars and their treatment

INTRODUCTION

Wound healing is a mechanism whereby the body attempts to restore the integrity of t he injured part. This falls far short of tissue

regeneration by pluripotent cells, seen in some amphibians, and is often detrimental, as s een in the problems created by scarring, such as

adhesions, keloids, contractures and cirrhosis of the liver. Several factors may inue nce healing (Summary box 3.1). However, a clean

incised wound in a healthy person where there is no skin loss will follow a set pattern as o utlined below.

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)

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

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

NORMAL WOUND HEALING

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

1 the inammatory phase;

2 the proliferative phase;

3 the remodelling phase (maturing phase).

Occasionally, a haemostatic phase is referred to as occurring before the inam matory phase, or a destructive phase following

inammation consisting of the cellular cleansing of the wound by macrophages ( Figure 3.1).

The inammatory phase begins immediately after wounding and lasts 2–3 days. Bleedin g is followed by vasoconstriction and thrombus

formation to limit blood loss. Platelets stick to the damaged endothelial lining of vesse ls, releasing adenosine diphosphate (ADP), which

causes thrombocytic aggregates to fill the wound. When bleeding stops, the platelet s then release several cytokines from their alpha

granules. These are plateletderived growth factor (PDGF), platelet factor IV and transf orming growth factor beta (TGFβ). These attract

inammatory cells such as polymorphonuclear lymphocytes (PMN) and macrophages. Pla telets and the local injured tissue release

vasoactive amines, such as histamine, serotonin and prostaglandins, which increase vascular perm eability, thereby aiding inltration of

these inammatory cells. Macrophages remove devitalised tissue and microorganisms wh ile regulating broblast activity in the

proliferative phase of healing. The initial framework for structural support of cells is pr ovided by brin produced by brinogen. A more

historical (Latin) description of this phase is described in four words: rubor (red ness), tumour (swelling), calor (heat) and dolour (pain).

The proliferative phase lasts from the third day to the third week, consisting mainly of broblast activity with the production of collagen

and ground substance (glycosaminoglycans and proteoglycans), the growth of new blood vesse ls as capillary loops (angioneogenesis)

and the re-epithelialisation of the

(a)

(b)

Figure 3.1 The phases of healing. (a) Early inflammatory phase with platelet-enriched blood clot and dilated vessels. (b) Late inflam matory phase with increased

vascularity and increase in polymorphonuclear lymphocytes and lymphocytes (round cells). (c) Proliferative phase w ith capillary buds and fibroblasts. (d) Mature

contracted scar.

wound surface. Fibroblasts require vitamin C to produce collagen. The wound tissue fo rmed 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 rst deposited in a random fashion and consists of type III collagen.

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 bres along the lines of tension, decreased wound vascularity a nd wound contraction due to fibroblast and

myobroblast activity.

Abnormal healing 25

hormones and other extracellular matrix trophins. Nerve regeneration is characterised b y profuse growth of new nerve bres which

sprout from the cut proximal end. Overgrowth of these, coupled with poor approximation, may lead to neuroma formation.

Tendon

While following the normal pattern of wound healing, there are two main mechanism s whereby nutrients, cells and new vessels reach the

severed tendon. These are intrinsic, which consists of vincular blood ow and synov ial diffusion, and extrinsic, which depends on the

formation of brous 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 rst 3–6 weeks. Active mobilisation prevents adhes ions 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 inuences 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 redu ce the inammatory and proliferative

responses (Summary box 3.2).

Healing by primary intention is also known as healing by rst intention. This occurs whe n there is apposition of the wound edges and

minimal surrounding tissue trauma that causes least inammation and leaves the best scar . Delayed primary intention healing occurs

when the wound edges are not opposed immediately, which may be necessary in conta minated or untidy wounds. The inammatory and

proliferative phases of healing are well established when delayed closure of the wound is carried out. This is also called healing by

tertiary intention in some texts and will result in a less satisfactory scar than would result a fter healing by primary intention. Secondary

healing or healing by secondary intention occurs in wounds that are left open and allow ed to heal by granulation, contraction and

epithelialisation.

Summary box 3.2

NORMAL HEALING IN SPECIFIC TISSUES

Bone

The phases are as above, but periosteal and endosteal prolifera

tion leads to callus formation, which is immature bone consist

ing of osteoid (mineralised by hydroxyapatite and laid down by

Classification of wound closure and healing

Primary intention

Wound edges opposed

Normal healing

Minimal scar

Secondary intention

Wound left open

Heals by granulation, contraction and epithelialisation

Proof Stage: 2

Increased inflammation and proliferation

Fig No: 3.1a-d

Poor scar

Tertiary intention (also called delayed primary intention)

Wound initially left open

Edges later opposed when healing conditions favourable

ISBN: 9781444121278

osteoblasts). In the remodelling phase, cortical structure and

the medullary cavity are restored. If fracture ends are accurately opposed and rigidly xed, c allus formation is minimal and primary

healing occurs. If a gap exists, then secondary healing may lead to delayed union, non -union or malunion.

Nerve

Distal to the wound, Wallerian degeneration occurs. Proximally, the nerve suffers trauma tic degeneration as far as the last node of

Ranvier. The regenerating nerve bres are attracted to their receptors by neurotr opism, which is mediated by growth factors,

Augustus Volney Waller , 1816–1870, a general practitioner of Kensington, London, UK (1842–1851), who subsequently worke d 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. 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 inuence healing and

recovery of function. This has led to the management of wounds based upon their clas sication into tidy and untidy (Table 3.1 and

Figure 3.2). 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 w ound, but a contaminated wound with

dead tissue requires debridement on one or several occasions before denitive re pair 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 surface. Multiple debridemen ts are often required after crushing

injuries in road trafc accidents or in natural disasters such as earthquakes, where f allen masonry causes widespread muscle damage and

compartment syndromes (see Compartment syndromes below). Any explo sion where

(a)

(b)

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

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.

there are multiple victims at the same site or where there has been a suicide-rela ted explosion will carry the risk of tissue and viral

contamination. Appropriate tests for hepatitis and HIV viruses are required.

Table 3.1 Tidy versus untidy wounds.

Tidy Untidy

Incised

Clean

Healthy tissues Seldom tissue loss Crushed or avulsed Contaminated

Devitalised tissues Often tissue loss

MANAGING THE ACUTE WOUND

The surgeon must remember to examine the whole patient according to acute trauma life s upport (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 ctitio us detective novel. The wound itself

should be examined, taking into consideration the site and the possible structures damag ed (Figure 3.3). It is essential to assess

movement and sensation while watching for pain and listening to the patient. Tetanus cover s hould 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 as nerve damage is likely

and vascular anastomosis is rendered impossible.

In order to facilitate examination, adequate analgesia and/ or anaesthesia (local, regional or general) are required. General anaesthesia is

often needed in children. In limb injuries, particularly those of the hand, a tourniquet sh ould be used in order to facilitate visualisation of

all structures. Due care should be taken with tourniquet application, avoiding uneven pres sure and noting the duration of tourniquet time.

After assessment, a thorough debridement is essential. Abrasions, ‘road rash’ (followin g a fall from a motorbike) and explosions all

cause dirt tattooing and require the use of a scrubbing brush or even excision under m agnication. A wound should be explored and

debrided to the limit of blood staining. Devitalised tissue must be excised until bleeding oc curs with the obvious

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

Some specific wounds 27

exception of nerves, vessels and tendons. These may survive with adequate revascular isation subsequently or by being covered with

viable tissue such as that brought in by skin or muscle aps.

The use of copious saline irrigation or pulsed jet lavage (where the instrumentation is available) can be less destructive than knife or

scissors when debriding. However, it has been suggested that pulsed jet lavage can imp lant dirt into a deeper plane and care should be

taken to avoid this complication. Muscle viability is judged by the colour, bleeding patter n and contractility.

In a tidy wound, repair of all damaged structures may be attempted. Repair of nerves under magnication (loupes or microscope) using

8/0 or 10/0 monolament nylon is usual. Vessels such as the radial or ulnar artery ma y be repaired using similar techniques. Tendon

repairs, particularly those in the hand, benet from early active mobilisation as this min imises adhesions between the tendon and the

tendon sheath (see above under Tendon for extrinsic tendon healing mechanism).

Skin cover by ap or graft may be required as skin closure should always be without tension a nd should allow for the oedema typically

associated with injury and the inammatory phase of healing. A flap brings in a new bloo d 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. Small animal bites are common in c hildren (Figure 3.4) and require cleansing

and treatment according to the principles outlined in Summary box 3.3, usually under general a naesthetic.

Ear, tip of nose and lower lip injuries are most usually seen in victims of human bites. A box ing-type injury of the metacarpophalangeal

joint may result from a perforating contact with the teeth of a victim. Anaerobic and aerobic 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

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

and human immunodeciency virus (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 decit, a haematoma may require release by incision or asp iration. In the gluteal or thigh region, there

may be an associated disruption of fat in the form of a fat fracture, which res ults 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 f rom its underlying fascia, leaving neurovascular

structures, tendon or bone exposed. A degloving injury may be open or closed. A n obvious example of an open degloving is a ring

avulsion injury with loss of nger 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 ma y be non-viable (Figure 3.6).

Examination under anaesthetic is required with a radical excision of all non-bleeding skin , as judged by bleeding dermis. Fluoroscein can

be administered intravenously while the patient is anaesthetised. Under ultraviolet light, viable ( perfused) skin will show up as a

uorescent yellowish green colour, and the non-viable skin for excision is clearly mapped out . However, the main objection to this

method is that of possible anaphylactic shock due to uoroscein sensitivity. Most surgeons therefore rely upon serial excision until

punctate dermal bleeding is obvious.

Figure 3.4 Dog bite in a child.

Figure 3.5 Degloving hand injury.

Figure 3.6 Degloving buttock injury.

Figure 3.7 Meshed split-skin graft.

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 syndromes

Compartment syndromes typically occur in closed lower limb injuries. They are c haracterised by severe pain, pain on passive movement

of the affected compartment muscles, distal sensory disturbance and, nally, by t he absence of pulses distally (a late sign). They can

occur in an open injury if the wound does not extend into the affected compartment.

Compartment pressures can be measured using a pressure monitor and a catheter place d in the muscle compartment. If pressures are

constantly greater than 30 mmHg or if the above clinical signs are present, then fasci otomy should be performed. Fasciotomy involves

incising the deep muscle fascia and is best carried out via longitudinal incisions of skin, fat and f ascia (Figure 3.8). The muscle will be

then seen bulging out through the fasciotomy opening. The lower limb can be decompr essed 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 compartments of

the leg. In crush injuries that present several days after the event, a lat e fasciotomy can be dangerous as dead muscle produces

Figure 3.8 Fasciotomy of the lower leg.

myoglobin which, if suddenly released into the bloodstream, causes myoglobinur ia with glomerular blockage and renal failure. In the

late treatment of lower limb injuries, therefore, it may be safer to amputate the lim b once viable and non-viable tissues have demarcated.

High-pressure injection injuries

The use of high-pressure devices in cleaning, degreasing and painting can cause extensive close d injuries through small entry wounds.

The liquid injected spreads along fascial planes, a common site being from nger to for earm. The tissue damage is dependent upon the

toxicity of the substance and the injection pressure. Treatment is surgical with wide exposure, rem oval 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 amputation

rates following high-pressure injection injuries are reported as being over 45 per cent. Delayed or conservative treatment is therefore

inappropriate.

CHRONIC WOUNDS

Leg ulcers

In developed countries, the most common chronic wounds are leg ulcers. An ulcer can be dene d as a break in the epithelial continuity.

A prolonged inammatory phase leads to overgrowth of granulation tissue, and attemp ts to heal by scarring leave a brotic margin.

Necrotic tissue, often at the ulcer centre, is called slough. The more common aetiologies are liste d in Summary box 3.4.

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

Necrotising soft-tissue infections 29

Figure 3.9 Pressure ulcer.

A chronic ulcer, unresponsive to dressings and simple 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 a ny leg ulcer depends on treating the underlying

cause, and diagnosis is therefore vital. Arterial and venous circulation should be as sessed, as should sensation throughout the lower limb.

Surgical treatment is only indicated if non-operative treatment has failed or if the p atient suffers from intractable pain. Meshed skin

grafts (Figure 3.7) are more successful than sheet grafts and have the advantage o f allowing mobilisation, 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.

Pressure sores

These can be dened as tissue necrosis with ulceration due to prolonged pres sure. Less preferable terms are bed sores, pressure ulcers and

decubitus ulcers. They should be regarded as preventable but occur in approximately 5 per cent of all hospitalised patients (range 3–12

per cent in published literature). There is a higher incidence in paraplegic patients, in th e elderly and in the severely ill patient. The most

common sites are listed in Summary box 3.5.

Summary box 3.5

Pressure sore frequency in descending order

Ischium

Greater trochanter

Sacrum

Heel

Malleolus (lateral then medial)

Occiput

A staging system for description of pressure sores devised by the American National Press ure Ulcer Advisory Panel is shown in Table

3.2.

If external pressure exceeds the capillary occlusive pressure (over 30 mmHg), blood ow to the skin ceases leading to tissue anoxia,

necrosis and ulceration (Figure 3.9). Prevention is obviously the best treatment with goo d skin care, special pressure dis

Table 3.2 Staging of pressure sores.

Stage Description 1

4 Non-blanchable erythema without a breach in the epidermis

Partial-thickness skin loss involving the epidermis and dermis

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

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

persion cushions or foams, the use of low air loss and air-uidised beds and urin ary or faecal diversion in selected cases. Pressure sore

awareness is vital, and the bed-bound patient should be turned at least every 2 hours, wi th the wheelchair-bound patient being taught to

lift themselves off their seat for 10 seconds every 10 minutes.

Surgical management of pressure sores follows the same principles involved in acu te wound treatment (Summary box 3.4). The patient

must be well motivated, clinically stable with good nutrition and adhere to the preven tative measures advised postoperatively.

Preoperative management of the pressure sore involves adequate debridement, and the use o f vacuum-assisted closure (VAC) may help

to provide a suitable wound for surgical closure (see below). The aim is to ll the dead space and to provide durable sensate skin. Large

skin aps that include muscle are best and, occasionally, an intact sensory innervated area c an be included (e.g. extensor fascia lata ap

with lateral cutaneous nerve of the thigh). If possible, use a ap that can be advanced further if there is recurrence and that does not

interfere with the planning of neighbouring aps that may be used in the future.

Vacuum-assisted closure

This is now more correctly known as negative pressure wound closure. Applying intermit tent negative pressure of approximately −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 t the wound. A perforated wound drain is placed over the foam, and the wound is sealed with a transparent adhesive lm. A

vacuum is then applied to the drain (Figure 3.10). Negative pressure may act by decreasing oedema, by removing interstitial uid and by

increasing blood ow. As a result, bacterial counts decrease and cell proliferation increases, ther eby creating a suitable bed for graft or

ap cover.

NECROTISING SOFT-TISSUE INFECTIONS

These are rare but often fatal. They are most commonly polymicrobial infections with G ram-positive aerobes (Staphylococcus aureus, S.

pyogenes), Gram-negative anaerobes (Escherichia coli,

Hans Christian Joachim Gram , 1853–1938, Professor of Pharmacology (1891–1900) and of Medici ne (1900–1923), Copenhagen, Denmark, described this method of

staining bacteria in 1884.

Jean-Nicholas Marjolin, 1780–1850, surgeon, Paris, France, described the development of carcinomatous ulcers in scars in 1828. Figure 3.10 Vacuum-assisted closure

dressing of a large wound.

Pseudomonas, Clostridium, Bacteroides ) and β-haemolytic Streptococcus. There is usually a history of trauma o r surgery with wound

contamination. Sometimes, the patient’s own defence mechanism may be decient. These infect ions are characterised by sudden

presentation and rapid progression. 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.

Summary box 3.6

Signs and symptoms of necrotising infections

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

There are two main types of necrotising infections: clostridial (gas gangrene) and non-clostrid ial (streptococcal gangrene and necrotising

fasciitis). The variant of necrotising fasciitis with toxic shock syndrome results from Streptococcus pyogenes and is often called the

‘esh-eating bug’ in this situation. Treatment is surgical excision with tissue biopsies being se nt 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 forma tion of what is described as a scar. The

immature scar becomes mature over a period lasting a year or more, but it is at rst pin k, hard, raised and often itchy. The disorganised

collagen bres become aligned along stress lines with their strength being in their w eave rather than in their amount (this has been

compared with steel wool being slowly woven into a cable). As the collagen matures a nd becomes denser, the scar becomes almost

acellular as the broblasts and blood vessels reduce. The external appearance of the scar becomes pale r, while the scar becomes softer,

attens and its itchiness diminishes. Most of these changes occur over the rst three months but a s car will continue to mature for one to

two years. Tensile strength will continue to increase but would not be expected to exc eed 60–80 per cent that of normal skin.

Scars are often described as being atrophic, hypertrophic and keloid. An atrophic scar is pale , at and stretched in appearance, often

appearing on the back and areas of tension. It is easily traumatised as the epidermis an d dermis are thinned. Excision and resuturing may

only rarely improve such a scar.

A hypertrophic scar is dened as excessive scar tissue that does not extend beyond the b oundary of the original incision or wound. It

results from a prolonged inammatory phase of wound healing and from unfavoura ble 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 dened as excessive scar tissue that extends beyond the boun daries of the original incision or wound (Figure 3.12). Its

aetiology is unknown, but it is associated with elevated levels of growth factor, deeply pi gmented skin, an inherited tendency and certain

areas of the body (e.g. a triangle whose points are the xiphisternum and each shoulder tip).

The histology of both hypertrophic and keloid scars shows excess collagen with hyp ervascularity, 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 Su mmary box 3.7.

Hypertrophic scars improve spontaneously with time, whereas keloid scars do not.

Summary box 3.7

Treatment of hypertrophic and keloid scars

Pressure – local moulds or elasticated garments Silicone gel sheeting (mechanism unknown)

Intralesional steroid injection (triamcinolone)

Excision and steroid injections

Excision and postoperative radiation (external beam or brachytherapy)

Intralesional excision (keloids only)

Laser – to reduce redness (which may resolve in any event) Vitamin E or palm oil massage (unproven)

All excisions have high rates of recurrence.

Figure 3.11 Necrotising fasciitis of the anterior abdominal wall. Contractures 31

Figure 3.12 Multiple keloid scars.

AVOIDABLE SCARRING

If an acute wound has been managed correctly (Summary box 3.4), 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 a fter wounding, be it planned or accidental. A

dirt-ingrained (tattooed) scar is usually preventable by proper initial scrubbing a nd cleansing 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 recognise normal landmarks, su ch as the lip vermilion/white roll interface, eyelid

and nostril free margins and hair lines such as those relating to eyebrows and moustache. Treatment consists of excision and resuturing.

Poorly contoured scars can be stepped, grooved or pincushioned. Most are caused by poor alignment of deep structures such as muscle or

fat, but trapdoor or pincushioned scars are often unavoidable unless the almos t circumferential wound can be excised initially. Late

treatment consists of scar excision and correct alignment of deeper structures or, as in the case o f a trapdoor scar, an excision of the scar

margins and repair using W- or Z-plasty techniques.

Suture marks may be minimised by using monolament 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 ma rks either side of the wound or incision.

CONTRACTURES

Where scars cross joints or exion creases, a tight web may form restricting the range of movem ent at the joint. This may be referred to

as a contracture and can cause hyperextension or hyperexion 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 aps.

Splintage and intensive physiotherapy are often required postoperatively.

Figure 3.13 Dirt-ingrained scar.

Figure 3.14 Burn contractures showing hyperextended fingers and hyperflexed elbow.

Figure 3.15 Post-traumatic (chainsaw) midline neck contracture. Laser is an acronym for Light Amplification by Stimulated Emission of Radiation. A laser is an

intense beam of monochromatic light. Figure 3.16 Multiple Z-plasty release of finger contracture.

FURTHER READING

Brown DL, Borschel GH. Michigan manual of plastic surgery. Baltimore, MD: Lippin cott, Williams & Wilkins, 2004.

Georgiade GS, Riefkokl R, Levin LS. Georgiade plastic, maxillofacial and reconstructiv e surgery, 3rd edn. Baltimore, MD: Williams &

Wilkins, 1997.

McGregor AD, McGregor, IA. Fundamental techniques of plastic surgery, 10th edn. Edinburgh, Chu rchill Livingstone, 2000.

Richards AM, MacLeod T, Dafydd H. Key notes on plastic surgery. O xford, Wiley-Blackwell, 2012.

Thomas S. An introduction to the use of vacuum assisted closure. World Wide Wounds 2005; availab le from: www.worldwide-

wounds.com.

Westaby S. Wound care. London: William Heinemann Medical Books Ltd, 1985.

CHAPTER

and anastomoses Basic surgical skills

LEARNING OBJECTIVES

To understand:

• The principles of skin and abdominal incisions

• 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, ligasure and

harmonic scalpel

INCISIONS

Skin incisions

Skin incisions should be made with a scalpel with the blade being pressed rmly down a t 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 wh ich should have been clearly planned by the

surgeon. It is important not to incise the skin obliquely as such a shearing mechanism ca n lead to necrosis of the undercut edge. The

incision is facilitated by tension being applied across the line of the incision by the nger s of the non-dominant hand, but the surgeon

must ensure that at no time is the scalpel blade directed at their own ngers as any slip ma y result in a selfinicted injury. Blades for skin

incisions usually have a curved cutting margin, while those used for an arteriotomy or d rain site insertion have a sharp tip (Figure 4.1).

Scalpels should at all times be passed in a kidney dish rather than by a direct hand-to-ha nd process as this can lead to a needle stick-like

injury. Diathermy, laser and harmonic scalpels can be used instead of blades when ope ning deeper tissues, as it is felt that they can

reduce blood loss and save operating time, and may reduce postoperative pain.

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 c ollagen bres and any incision placed parallel

to these lines result in a better scar (Figure 4.2).

2 Anatomical structure. Incisions should avoid bony prominences and crossing skin cr eases 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 t he procedure in hand as any com

Figure 4.1 Scalpel blade sizes and shapes. The 22-blade is often used for abdominal incisions, the 11-blade for a rteriotomy and the 15-blade for minor surgical

procedures.

promise purely on cosmetic grounds may render the operation ineffective or even dang erous.

Occasionally, it may be necessary to excise a skin lesion with a circular incision in an area when the direction of Langer’s lines are not

apparent. However, once the circular incision has been made, it can often be observed th at the circular incision is converted to an ellipse

thus indicating the lines of tension. This circular incision should then be formally con verted 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’

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

Posterior

Figure 4.2 Langer’s lines. These depict the orientation of the dermal collagen fibres. Reproduced with permission from T homas WEG, Senninger N (eds). Short stay

surgery. Berlin: Springer-Verlag, 2008.

outcome, e.g. transverse incisions tend to be associated with fewer respiratory complica tions and a better cosmetic outcome. In the past,

traditionally vertical midline or paramedian incisions were used for the majority of abdo minal procedures, but there is a current trend to

utilise transverse incisions wherever possible as this minimises postoperative complications. Th e incision should be carried deeper

through the subcutaneous tissues and then, depending on the site of the incision (Figure 4 .4), the muscle layers should be divided or

split, and the peritoneum displayed. This should be picked up between two clips and gen tly 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. Mas s closure of the abdominal wall is usually advocated

using large bites and short steps in the closure technique using either non-absorbab le (e.g. nylon or polypropylene) or very slowly

absorbable suture material (e.g. polydioxanone suture (PDS)). It has been estimated tha t 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 m inimise the risk of abdominal dehiscence or later

incisional hernia. Similar attention to detail applies to laparoscopic surgery, whe re access is of equal importance as correct port site

placement and closure is crucial to the success of the operative procedure.

for the wound to heal without tension. Occasionally, ‘dog ears’ remain in the cor ner of elliptical incisions in spite of adequate care

having been taken during formation and primary closure of an elliptical wound. In these situatio ns, it is advisable to pick up the ‘dog ear’

with a skin hook and excise it as shown in Figure 4.3. This allows for a satisfactory cosmetic ou tcome.

Abdominal incisions

As for skin incisions, all abdominal incisions should be planned in advance of s urgery and take into consideration access to the relevant

organs, surface landmarks, pain control and cosmetic

XY XY

ISBN: 9781444121278

Figure 4.3 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.

Figure 4.4 Abdominal incisions. Reproduced with permission from Thomas WEG. Preparation and revision for the M RCS. London: Churchill Livingstone (Elsevier

Limited), 2004. 1, Midline; 2, Kocher’s; 3, thoracoabdominal; 4, rectus split; 5, paramedian; 6, transvers e; 7, McBurney’s gridiron; 8, inguinal; 9, pfannenstiel; 10,

McEvedy; 11, Rutherford Morison.

Proof Stage: 1 Fig No: 19.2

WOUND CLOSURE

The suturing of any incision or wound needs to take into consideration the site and tissu es 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 Summ ary box 4.1. Therefore, the correct choice of suture

technique and suture material is vital, but will never compensate for inadequate

Summary box 4.1

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

operative technique, and for any wound to heal well, there must be a good bloo d supply and no tension on the closure.

Clean uninfected wounds with a good blood supply heal by primary intention and so closure simply requires accurate apposition of the

wound edges. However, if a wound is left open, it heals by secondary intention thro ugh the formation of granulation tissue, which is

tissue composed of capillaries, broblasts and inammatory cells. Wound contraction and epithelialisation assist in ultimate healing, but

the process may take several weeks or months. Delayed primary closure or tertiary in tention is utilised when there is a high probability of

the wound being infected. The wound is left open for a few days and then if a ny infective process is resolved then the wound is closed to

heal by primary intention. Skin grafting is another form of tertiary inten tion healing (Summary box 4.2).

Summary box 4.2

Types of wound healing

Primary intention

Clean wound

Secondary intention

Healthy granulation tissue Over-exuberant granulation tissue Infected sloughy wound

Black eschar

Tertiary intention

Delayed closure

Skin grafting

When choosing suture materials, there are certain specic requirements depending on the tissue s to be sutured, e.g. vascular anastomoses

require smooth, non-absorbable, non-elastic material, while biliary anastomoses require an absorbable mat erial that will not promote

tissue reaction or stone formation. When using absorbable material, the time in which wound support is required and maintained will

vary according to the tissues in which it is inserted. Furthermore, certain tissue s 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 o r anastomosis.

Suture materials

History

Sutures are best made of soft thread, not too hard twisted that it may sit easier o n 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 b lood vessels with tendons strips, and closing wounds with

acacia thorns pushed through the wound with strips of vegetable matter wound round these in a gure of eight. A South American

method of wound closure involved using large black ants to bite the wound tog ether 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 cl ips, called bulae, were commonly used to close

gladiatorial wounds. By the end of the nineteenth century, developments in th e textile industry led to major advances, and both silk and

catgut became popular as suture materials. Lister believed that catgut soaked in chromic ac id (a form of tanning) prevented early

dissolution in body uids and tissues, while Moynihan felt that chromic catgut was ideal as it could be sterilised, was nonirritant to

tissues, kept its strength until its work was done and then disappeared. However, catgut is no longer in use as it causes an inammatory

cellular reaction with release of proteases and may also carry the risk of prion transmissio n if of bovine origin.

Suture characteristics

There are ve characteristics of any suture material that need to be considered:

1 Physical structure. Suture material may be monolament or multilament. Monolament suture material is smooth and tends to slide

through tissues easily without any sawing action, but is more difcult 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. Multilament or braided sutures are much

easier to knot, but have a surface area of several thousand times that of mono lament sutures and thus have a capillary action and

interstices where bacteria may lodge and be responsible for persistent infect ion 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 constitue nt material, its thickness and how it is handled in the tissues.

Suture material thickness is classied according to its diameter in tenths of a millimetre (Table 4 .1), although

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 establishe d 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 Su rgery in 1913 and became the first chairman of the editorial

committee until his death.

Aurelius Cornelius Celsus, Roman physician, 25

–

50.

Joseph Lister (Lord Lister) , Professor of Surgery in Glasgow, Edinburgh and King’s College Hospital, Lo ndon and Vice President of Royal College of Surgeons of

England, 1827–1912. Alexis Carrel, 1873–1944, a surgeon from Lyons in France who worked at the Roc kefeller 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 su ture and the transplantation of blood vessels and organs’.

Gladiators were so called because they fought with a Roman sword called a ‘gladius’.

Table 4.1 Size of suture material.

Metric (EurPh) Range of diameter (mm)

1 0.100–0.149

1.5 0.150–0.199

2 0.200–0.249

3 0.300–0.349

3.5 0.350–0.399

4 0.400–0.499

5 0.500–0.599

USP (‘old’)

5–0

4–0

3–0

2–0

the gure assigned is also dependent upon the nature of the material, e.g. absorbable material an d non-absorbable material, such as

polypropylene, may differ in their designations. The tensile strength of a suture can be ex pressed 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, as 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 m aterial may last in the tissues for the

stated period in the manufacturer’s product prole, its tensile strength cannot be relied on in vivo for this entire period. Materials such as

catgut (no longer in use in the UK) has a tensile strength of only about a week whi le PDS will remain strong in the tissues for several

weeks. However, even nonabsorbable sutures do not necessarily maintain their strength indenitely, and may degrade with time. Those

non-absorbable materials of synthetic origin, such as polypropylene, probably retain their tensile strength indenitely 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

denitely fragment with time and lose their strength, and such materials should never be used in be preferred where persistent strength is

required and, as an articial graft or prosthesis never heals fully or integrates into a host artery, persistent monolament suture materials,

such as polypropylene, are almost universally used.

5 Biological behaviour. The biological behaviour of suture material within the tissue s 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. Man-made synthetic polym ers are hydrolysed and their disappearance in

the tissues is more predictable. However, the presence of pus, urine or faeces inuence s the nal result and renders the outcome more

unpredictable. There is also some evidence that in the gut, cancer cells may accumulate a t sites where sutures persist, possibly giving rise

to local recurrence. For this reason, synthetic materials that have a greater predictability a nd elicit minimal tissue reaction may have an

important non-carcinogenic property.

3 Tensile behaviour

vascular anastomoses for fear of late stula formation.

. Suture materials behave differently

depending upon their deformability and exibility. Some

may be ‘elastic’ in which the material will return to its original length once any tension is released, while others may be

Figure 4.5 Interrupted 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. ‘plastic’ in which case this phenomenon do es not occur.

Sutures may be deformable in that a circular cross-section may be converted to an oval sha pe, or they may be more rigid and have the

somewhat irritating capacity to kink and coil. Many synthetic materials demonstrate ‘me mory’ in which they keep curling up in the shape

that 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 less is the knot security. Therefore, knotting technique also plays a signicant role in any suture line’s

tensile strength and it is important to recognise that sutures lose 50 per cent of their strength at the knot.

4 Absorbability. Suture materials may be absorbable (Table 4.2) or non-absorbable (Tab le 4.3) and this property must be taken into

consideration when choosing suture materials for specic 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. Howev er, a vascular anastomosis requires a non-absorbable

material and it is wise

Figure 4.6 The siting of sutures. As a rule of thumb, the distance of insertion from the edge of the wound should correspon d to the thickness of the tissue being sutured

(×). Each successive suture should be placed at

to avoid braided material as platelet adherence may predis

twice this distance apart (2×). Reproduced with permission from Royal pose to distal embolisation. Non-absorbable materials tend to College of Surgeons

of England. The intercollegiate basic surgical skills course participants handbook, edns 1–4. London: RCS. Title: Bailey & Love’s Short Practice of Surgery, 26th Ed

ISBN: 9781444121278 Proof Stage: www.cactusdesign.co.uk

Suture techniques

There are four frequently used suture techniques.

1 Interrupted sutures. Interrupted sutures require the needle

to be inserted at right angles to the incision and then to pass through both aspects of the suture li ne and exit again at right angles (Figure

4.5). It is important for the needle to be rotated through the tissues rather than to be dragged th rough for fear of unnecessarily enlarging

the needle hole. As a guide, the distance from the entry point of the needle to the edge of the wou nd should be approximately the same

as the depth of the tissue being sutured, and each successive suture should be placed a t twice this distance apart (Figure 4.6). Each suture

should reach into the depths of the wound and be placed at right angles to the axis of the wo und. In linear wounds, it is sometimes easier

to insert the middle suture rst and then to complete the closure by successively insertin g sutures, halving the remaining decits in the

wound length.

2 Continuous sutures. For a continuous suture, the rst suture is inserted in an identic al manner to an interrupted suture, but the rest of

the sutures are inserted in a continuous manner until the far end of the wound i s reached (Figure 4.7). Each throw of the continuous

suture should be inserted at right

Figure 4.7 Continuous suture technique. Reproduced with permission from Royal College of Surgeons of England. The intercollegiate basic surgical skills course

participants handbook, edns 1–4. London: RCS.

angles to the wound and this will mean that the externally observed suture material will usually lie d iagonal to the axis of the wound. It

is important to have an assistant who will follow the suture, keeping it at the same tension in order to avoid either purse stringing the

wound by too much tension, or leaving the suture material too slack. There is more danger of producing too much tension by using too

little suture length than there is of leaving the suture line too lax. Postoperative oedema will often take up any slack in the suture

material. At the far end of the wound, this suture line should be secured either by using an A berdeen knot or by tying the free end to the

loop of the last suture to be inserted.

3 Mattress sutures. Mattress sutures may be either vertical or horizontal and tend to be used to produce either eversion or inversion of a

wound edge (Figure 4.8). The initial suture is inserted as for an interrupted suture, but then the needle either moves horizontally or

vertically and traverses both edges of the wound once again. Such sutures are ve ry useful in producing accurate approximation of wound

edges, especially when the edges to be anastomosed are irregular in depth or disposi tion.

4 Subcuticular suture. This technique is used in skin where a cosmetic appearance is importa nt and where the skin edges may be

approximated easily (Figure 4.9). The suture material used may be either absorbable or non-absorbable. For non-absorbable sutures, the

ends may be secured by means of a collar and bead, or tied loosely over the w ound. When absorbable sutures are used, the ends may be

secured using a buried knot. Small bites of the subcuticular tissues are

(a)

(b) Point

Figure 4.9 Subcuticular suture technique. Reproduced with permission from Royal College of Surgeons of Engla nd. The intercollegiate basic surgical skills course

participants handbook, edns 1–4. London: RCS.

Swaged eye

Body

Figure 4.8 Mattress suture techniques. Reproduced with permission from Royal College of Surgeons of England. The intercollegiate basic surgical skills course

participants handbook, edns 1–4. London: RCS.

Figure 4.10 The basic parts of a needle. Reproduced with permission from Royal College of Surgeons of Engla nd. The intercollegiate basic surgical skills course

participants handbook, edns 1–4. London: RCS.

ISBN: 9781444121278 Proof Stage: 2 Fig No: 19.7

Title:

ISBN: 9781444121278 Proof Stage:

taken on alternate sites of the wound and then gently pulled together thus approximating the wound edges without the risk of the cross-

hatched markings of interrupted sutures.

Needles

In the past, needles had eyes in them and suture material had to be loaded into them, whic h was not only time consuming, but it meant

that the needle holes in tissues were considerably larger than the suture material bein g used. Currently, needles are eyeless or

‘atraumatic’ with the suture material embedded within the shank of the needle. The needle ha s three main parts (Figure 4.10):

1/4 circle 3/8 circle 1/2 circle

5/8 circle 1/2 curved

Straight

J needle Compound curve

Crosssection

Cutting needles for stitching skin

Needles used for suturing the bowel The threads are swaged into the needles

Figure 4.11 Types of needle. Needles used for suturing the abdominal wall:

Round-bodied needles for peritoneum, muscles and fat

Cutting needles for aponeurosis

1 Shank

2 Body

3 Point.

The needle should be grasped by the needle holder approximately one-third of the way back from the rear of the needle avoiding both

the shank and the point.

The body of the needle is either round, triangular or attened. Round-bodied needles g radually 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 tap ered end, conventional cutting which has

the cutting edge facing the inside of the needle’s curvature, or reversed cutting in which th e cutting edge is on the outside (Figure 4.11).

Round-bodied needles are designed to separate tissue bres rather than cut through the m and are commonly used in intestinal and

cardiovascular surgery. Cutting needles are used where tough or dense tissue needs to be sutur ed, such as skin and fascia. Blunt-ended

needles are now being advocated in certain situations, such as closure of the abdominal wall, in order to diminish the risk of needle-stick

injuries in this era of virally transmitted disorders.

The choice of needle shape tends to be dictated by the accessibility of the tissue to be sut ured, and the more conned the operative space,

the more curved the needle. Hand-held straight needles may be used on skin, a lthough 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 comm only utilised in the gastrointestinal tract, while

J-shaped needles, quarter circle needles and compound curvature needles are used in special s ituations such as the vagina, eye and oral

cavity, respectively. The size of the needle tends to correspond with the gauge of th e 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 poorly perf ormed. The principles behind a secure knot

are poorly understood by many surgeons and sadly a poorly constructed knot may thus jeopard ise an otherwise successful surgical

procedure. The general principles behind knot tying include:

•

The knot must be tied rmly, but without strangulating the

tissues.

• The knot must be unable to slip or unravel.

•

The knot must be as small as possible to minimise the amount of foreign materia l.

•

The knot must be tightened without exerting any tension

or pressure on the tissues being ligated, i.e. the knot should be bedded down carefully , only exerting pressure against counter-pressure

from the index nger or thumb.

•

During tying, the suture material must not be ‘sawed’ as this weakens the thread.

•

The suture material must be laid square during tying, otherwise tension during tightening may cause breakage or fracture of the thread.

•

When tying an instrument knot, the thread should only be

grasped at the free end, as gripping the thread with artery forceps or needle holders can damag e the material and again result in breakage

or fracture.

• The standard surgical knot is the reef knot (Figure 4.12),

Half-hitch Crossed half-hitch

Reef or square knot Granny knot

Extra half-hitch on reef knot

Surgeon's knot

Figure 4.12 Standard knotting formation.

with a third throw for security, although with monolament sutures such as fo r vascular surgery, six to eight throws are required for

security.

•

A granny knot involves two throws of the same type of throw

and is a slip knot. It may be useful in achieving the right tension in certain circumstances, bu t must be followed by a standard reef knot to

ensure security.

•

When added security is required, a surgeon’s knot using a twothrow technique is advis able to prevent slippage.

•

When using a continuous suture technique, an Aberdeen

knot may be used for the nal knot. The free end of the suture is partially pulled through t he nal loop several times before being pulled

through a nal time completely prior to cutting.

•

When the suture is cut after knotting, the ends should be left about 1–2 mm long to prevent unrav eling. This is particularly important

when using monolament material.

Alternatives to sutures

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

Skin adhesive strips

For the skin, self-adhesive tapes or steristrips may be used where there is no tension and not too much moisture, such as after a wide

excision of a breast lump. They may also be used to minimise ‘spreading’ of a scar. Oth er adhesive polyurethane lms, such as Opsite,

Tegaderm or Bioclusive, may provide a similar benet, while such transparent dressings also allo w wound inspection and may protect

against cross-infection.

Tissue glue

Tissue glue is also available based upon a solution of n-butyl2-cyanoacrylate monomer. When it is applied to a wound, it polymerises to

form a rm adhesive bond, but the wound does need to be clean, dry, with ne ar perfect haemostasis and under no tension. Some specic

uses have been described such as closing a laceration on the forehead of a fractious ch ild 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 brin and work on the pr inciples of converting brinogen to brin by

thrombin with crosslinking by Factor XIII, and the addition of aprotinin to slow the break up of the brin network by plasmin. This

process has good adhesive properties and has been used for haemostasis in the liver a nd spleen, for dural tears, in ear, nose and throat

(ENT) and ophthalmic surgery, to attach skin grafts and also to prevent haemose rous collections under aps. Fibrin glues have also been

used to control gastrointestinal haemorrhage endoscopically, but do not work when the bleeding is brisk.

Staples

Mechanical stapling devices were rst used successfully by Hümer Hültl in H ungary 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 de vices that can be used both in the open

surgery setting and laparoscopically. Most of these devices are disposable and relatively expensiv e, but their cost is offset by the saving

of operative time and the potential increase in the range of surgery possible (see belo w).

Clips

Skin clips produce a very neat scar with good wound eversion and a minimal cross-hatc hing effect. They can be placed faster than suture

insertion and have a lower predisposition to infection as they do not penetrate entirely th rough the wound and do not produce a complete

track from one wound edge to the other. However, they can be uncomfortable for the patient and they require a special instrument to

remove them. Furthermore, they tend to be a more expensive method for wound clo sure than simple suture techniques.

Stapling devices

In the gastrointestinal tract, stapling devices tend to apply two rows of staples, offset in relation to each other to produce a sound

anastomosis (Figure 4.13). Many of them also simultaneously divide the bowel or tissue that has been stapled while other devices merely

insert the staples and the bowel has to be divided separately. For all stapling devices, it is c rucial for the surgeon to understand the

principles behind each device and to know intimately the mechanism and functio n 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 oeso phagus 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 pu rse-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 a n enterotomy for an

oesophagojejunostomy, and either the shaft is extended through a small opening in the bowel wa ll or is secured by a further pursestring

suture. The head/anvil is reattached to the shaft and the two ends approximated. Once th e device is fully closed as indicated by the green

indicator in the window, the device is red, and after unwinding, the stapler is gently withdrawn. It is important to assess the integrity of

the anastomosis by examining the ‘doughnuts’ of tissue excised for completeness . It is essential that no extraneous tissue is allowed to

become interposed between the two bowel walls on closing the stapler.

•

Transverse anastomoses. These instruments, which come

in different sizes, simply provide two rows of staples for a single transverse an astomosis. 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 ring, as the instrument is designed w ith a ridge along which to pass a scalpel to ensure

the correct length cuff of bowel remains adjacent to the staple line. Down in the pelvis it ma y 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 reassem bled 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-je junostomy 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 stapli ng devices rather than individually picking up

staples/clips and inserting them as described above. Many of the intestinal stapling devices are now adap ted to be inserted down

cannulae during laparoscopic surgery, and although they look very different, the principles of function are identical to the open surgery

variety.

THE PRINCIPLES OF ANASTOMOSES

Bowel anastomoses

The word anastomosis comes from the Greek ‘ ana’, without, and ‘stoma’, a mouth, reect ing the join of a tubular viscus (bowel) or

vessel (usually arteries) after a resection or bypass procedure. Prior to the nineteen th century, intestinal surgery was limited to

exteriorisation by means of a stoma or closure of simple lacerations. Lembert then descr ibed his seromuscular suture technique for bowel

anastomosis in 1826, while Senn advocated a two-layer technique for closure. Kocher’s met hod utilised a two-layer anastomosis, rst a

continuous all-layer suture using catgut, then an inverting continuous (or interrupted ) seromuscular layer suture using silk, which became

the mainstay of bowel anatomoses for many years (Figure 4.14). However, Halsted favoured a onelayer extramucosal closure, and this

was subsequently advocated by Matheson as it was felt to cause the least tissue necrosis or lumina l narrowing (Figure 4.15). This

techniqe has now become

Hümer Hültl , surgeon, St Stephen’s Hospital, Budapest, Hungary, described his gastric stapler in 1908.

Antoine Lembert, 1802–1851, surgeon, Hôtel Dieu, Paris, France.

Nicolas Senn, 1844–1908, Professor of Surgery, Rush Medical College, Chicago, IL, USA.

Emil Theodor Kocher, 1841–1917, Professor of Surgery, Berne, Switzerland. In 1909, he was awarded t he Nobel Prize for Physiology or Medicine for his work on the

thyroid. William Stewart Halsted, 1852–1922, Professor of Surgery, Johns Hopkins Hospital Medical Scho ol, Baltimore, MD, USA.

Norman Alistair Matheson, 1907–1966, formerly surgeon, Aberdeen Royal Infirmary, UK.

The principles of anastomoses 43

(a)

(b)

widely accepted, although it is essential that this is not confused with a seromuscular s uture technique. The extramucosal suture must

include the submucosa as this has a high collagen content and is the most stable suture layer in all sections of the gastrointestinal tract.

There are several prospective randomised trials between two-layer and single-layer anastomos es demonstrating that there is probably

little to choose between these techniques, provided basic essentials as highlighted in Summary box 4.3 are observed. However, catgut

and silk have been replaced by synthetic, usually absorbable, polymers.

the bowel rotated and the posterior wall sutured in an identical manner to the an terior wall. As the mesenteric edge of the bowel is the

most difcult, especially when a fatty mesentery is present, this angle should be dealt with r st, with the nal sutures being

inserted at the antimesenteric border which is far more accessible and visible. The appos ition of bowel edges should be as

accurate as possible and the suture bites should be approximately 3–5 mm deep and 3– 5 mm apart depending on the thickness of the

bowel wall. The suture materials should be of 2/0–3/0 size and made of an absorbabl e polymer, which can be braided (e.g. polyglactin),

or monolament (e.g. polydioxanone), mounted on an atraumatic round-bodied need le. Braided, coated sutures are the easiest to handle

and knot.

Figure 4.14 Standard two-layer bowel anastomosis. Reproduced with It is crucial to make sure that only bowel of similar diameter is permission from

Kocher T, Harder F, Thomas WEG (eds). Anastomosis brought together to form an end-to-end anastom osis. In cases of techniques in the gastrointestinal

tract, 1st edn. Wollerau: Covidien, major size discrepancy, a side-to-side or end-to-side anastomosis 2007. 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 runnin g in the edge of the mesentery (Summary

box 4.3).

In certain situations, stapling devices are used to fashion the anastomosis, but a s they are expensive, most surgeons reserve them for

specic 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

Figure 4.15 Extramucosal technique taking care to include the submusurgeons still use

them for ease of use and to save time.cosa. Reproduced with permission from Kocher T, Harder F, Thom as

WEG (eds). Anastomosis techniques in the gastrointestinal tract, 1st

edn. Wollerau: Covidien, 2007.

Summary box 4.3

In the past, great emphasis was placed on good bowel prepara

Intestinal anastomoses

tion prior to any anastomosis. The rationale was that

with good

Ensure good blood supply to both bowel ends before and

bowel preparation and an empty bowel, there was less likelihood

after formation of

anastomosis.

of faecal contamination and therefore it was probably not necISBN: 9781444121278

Proof Stage: 1 Fig No: 19.14Avoid risk to mesenteric vessels by clamps or

sutures. Use atraumatic bowel clamps to minimise contamination. Interrupted and continuous singl e-layer suture techniques are adequate and safe. Stapling devices are

an alternative when speed is required or access is a major factor.

Ensure the anastomosis is under no tension. essary to apply bowel clamps (even of the soft occ lusion type).

However, this tradition is now being challenged, and there is

evidence to suggest that conventional bowel preparation pro

vides little benet, 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 anas

tomosis, when bowel is unprepared or obstructed for example,

atraumatic intestinal 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. Excessive bleeding

from the bowel wall may need oversewing if natural haemostasis

is inadequate.

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 under

taken on mobile bowel, the anterior wall layer of sutures can be

Vascular anastomoses Vascular anastomoses require an extremely accurate closure as they must be immediately watertight at the end of

the operation when the vascular clamps are removed. In many cases, some form of prosthetic material or graft may be used which will

never be integrated into the body tissues and so the integrity of the suture line needs to be permanent. For this reason, polypropylene is

one of the best sutures as it is not biodegradable. It is used in its monolament form, moun ted on an atraumatic, curved, roundbodied

needle. Knot security is important, and as polypropylene is monolament and the anast omosis often depends on one nal knot, several

throws (between six and eight) of a well-laid reef knot are required. The suture line must be regular and watertight with a smooth intimal

surface to minimise the risk of thrombosis

inserted, either in a continuous or interrupted manner, and then

ISBN:

9781444121278 Proof Stage: 1 Fig No: 19.15and embolus, as well

as to avoid any leakage. Suture size depends

Sir George Lenthal Cheatle, 1865–1951, surgeon, King’s College Hospital, London, UK.

Drains 45

on vessel calibre: 2/0 is suitable for the aorta, 4/0 for the femoral artery and 6/0 for the poplit eal to distal arteries. Microvascular

anastomoses are made using a loupe and an interrupted suture down to 10/0 size .

All vessel walls must be treated with great care avoiding causing any damage to the intim a. If any signicant manipulation is necessary,

atraumatic forceps (such as DeBakey’s) are utilised. Vascular clamps should be applied with gre at care, particularly for calcied vessels,

and in some cases encircling rubber loops or intraluminal balloon catheters may be less traumatic for control. Vessels should always be

sewn with the needle moving from within to without on the downstream edge of the vessel to avoid creating an intimal ap and to x any

atherosclerotic plaque. The tip of the needle should be inserted at right angles to the surface of the intima and the curve of the needle

followed to prevent vessel trauma. The assistant should ‘follow’ by keeping the suture t aut, and once the closure is complete, the distal

clamp is released first, before the nal watertight knot is made. This allows backflow to cle ar any clot or air from the anastomosis. The

proximal clamp can then be released, a process which minimises the risk o f distal embolus. Suture bites should be placed an equal

distance apart, with the bite size dependent on the vessel diameter. Care needs to be taken to avoid damaging the suture, which should

not be gripped by any surgical instrument. All haemostats that are used to hold any suture materi al should be shod with soft rubber to

prevent suture material damage.

A transverse arteriotomy is less likely to stenose following closure than a longitudinal art eriotomy, but may not give adequate access,

and a longitudinal arteriotomy is easier to make. Therefore, a vein patch can be used if th ere is any danger of stenosis or doubt about the

size of the lumen (Figure 4.16). The suture line can be started at the apex of the arteri otomy with a double-ended suture, and then carried

down each side with the final knot being placed at the midpoint of the vein pa tch graft, and not at the far end. The suture should go from

outside to inside on the graft and from inside to outside on the artery, again to minimise the risk of intimal ap formation.

When prosthetic material or grafts are used, similar nonabsorbable monolament suture s are used with the same in–out technique to

ensure eversion of the graft edge and a smooth intimal surface. Again the needle shoul d go from outside to inside on the graft and from

inside to outside on the artery. Doubleended sutures make the procedures easier (Summ ary box 4.4).

DRAINS

Drains are inserted to allow uid or air that might collect at an operation site or in a wound to drain freely to the surface. The fluid to be

drained may include blood, serum, pus, urine, faeces,

(a)

(b)

Figure 4.16 Arteriotomy being closed by vein patch. Technique involves a double armed suture ensuring that the final knot is half way along one side of the arteriotomy.

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

RCS.

Summary box 4.4

Vascular anastomosis

Non-absorbable monofilament suture material should be used, e.g. polypropylene.

A smooth intimal suture line is essential.

Knots require multiple throws in order to ensure security. The suture must pass from within outwards on th e downflow aspect of the anastomosis.

bile or lymph. Drains may also allow wound irrigation in certain specic circum stances. The adequate drainage of uid collections

prevents the development of cavities or spaces that may delay wound healing. Their us e can be regarded as prophylactic in elective

surgery and therapeutic in emergency surgery. Three basic principles apply in the us e of drains:

1 Open drains that utilise the principle of gravity

2 Semi-open drains that work on the principle of the capillary effect

3 Closed drains systems that utilise suction.

They may be placed through the wound or through a separate incision, althou gh it has been clearly shown that placing them through the

wound leads to an increased risk of wound infection. With regard to the indications fo r drainage, in the past drains were in common use

ever since Lawson Tait in 1887 suggested ‘when in doubt drain!’ However, this edict has c ome under strong criticism recently and the

value and use of drains has been the subject of close scrutiny, and their use still remains controve rsial.

Protagonists suggest that the use of drains may:

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

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

• provide a track for later drainage.

However, the antagonists claim that the presence of a drain may:

• increase intra-abdominal and wound infections;

• increase anastomotic insufciency;

• increase abdominal pain;

• increase hospital stay;

• decrease pulmonary function.

In reality, the use of drains currently tends to depend on a surgeon’s individual prefere nce. There are randomised controlled trails

suggesting that their use in gastric, duodenal, small bowel, appendix and biliary surgery is unne cessary, and may cause more problems

than benets, and this is now reected in current practice. There are also randomised controlled trials to suggest that they are also not

required in colorectal, liver and pancreatic surgery and yet in today’s practice the m ajority of surgeons will still utilise drains in these

forms of surgery. The only area of alimentary tract surgery where drains are still routi nely advocated is for oesophageal surgery,

although even here the evidence is low with the level of evidence being only 5 a nd the level of recommendation being ‘D’ (i.e. based on

expert opinion).

Specialist use of drains

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

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

Chest drains

These are indicated for a pneumothorax, pleural effusion, haemothorax or to prevent the collection of uid or air after thoracotomy. Once

the drain has been inserted, it should be connected to an underwater sealed drain (Figure 4.17). This system allows air to leave the pleural

cavity, but cannot draw it back in with the negative pressure that is created in the intrath oracic cavity. During the respiratory process, it

should be checked that the meniscus of the uid is swinging to ensure that the tube is not blocked. Suction can be applied to the venting

tube at the bottle whenever there is signicant drainage of uid or air expected. Between 10 a nd 20 mm of mercury are adequate to

obtain a gentle ow of bubbles from the chest cavity.

T-tube drains

After exploration of the common bile duct, a T-tube (Figure 4.18) may be insert ed into the duct which allows bile to drain while the

sphincter of Oddi is in spasm postoperatively. Once the sphincter relaxes, bile drains normally down the bile duct and into the

duodenum. To assist choleresis, it is often advisable to convert the lumen of the limb of the T into a gutter, which also facilitates

removal.

Guided drainage

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

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

Removal of drains

A drain should be removed as soon as it is no longer required, as if left in, it can itself predispose to uid collections as a result of tissue

reaction. Indeed there is evidence that by 7 days only 20 per cent of drains are still functio ning. It should be stressed how important it is

to dene the objective of each individual drain and to ensure that once that objective ha s been met, the drain is removed. If a drain is

used at all, the following principles may apply:

• Drains put in to cover perioperative bleeding may usually be

removed after 24 hours, e.g. thyroidectomy.

• Drains put in to drain serous collections usually can be

removed after 5 days, e.g. mastectomy.

• Drains put in because of infection should be left until the

infection is subsiding or the drainage is minimal.

• Drains put in to cover colorectal anastomoses should be

removed at about 5–7 days. However, it should be stressed

that in no way does a drain prevent any intestinal leakage, but

merely may assist any such leakage to drain externally rather

than to produce life-threatening peritonitis.

• Common bile duct T-tubes should remain in for 10 days.

However, once the T-tube cholangiogram has shown that

there is free ow of bile into the duodenum and that there are

no retained stones, some surgeons like to clamp the T-tube

prior to removal. The 10-day period is required to minimise

the risk of biliary peritonitis after removal.

• Any suction drain should have the suction taken off prior to

removal of the drain.

• During removal of a chest drain, the patient should be asked

to breathe in and hold his breath, thus doing a Valsalva

Figure 4.17 Underwater seal chest drain. Reproduced with permission from Thomas WEG. Basic principl es. In: Kingsnorth A, Majid A (eds). Principles of surgical

practice. London: Greenwich Medical, 2001.

manoeuvre. In this way, no air is sucked into the pleural

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

Greenwich Medical, 2001.

Ruggero Oddi, Italian physician, 1864–1913.

Antonio Maria Valsalva, Italian physician and anatomist, 1666–1723. The principles of diathermy: electros urgery 47

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

Active cable Active electrode

Diathermy unit

THE PRINCIPLES OF DIATHERMY: ELECTROSURGERY

For many years, short wave diathermy has proved a most valuable and versatile aid to s urgical technique. Its most common use is in

securing haemostasis by means of coagulation, but by varying the strength or w ave 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 laparosc opic surgery or down intraluminal endoscopes as

in transurethral resection of the prostate. However, although diathermy is a valuable surgical too l, 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 so und understanding of the principles and practice of

diathermy, and how to avoid complications.

The 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 bipola r diathermy (Figure 4.19). In monopolar

diathermy, which is the most commonly used form, an alternating current is produced b y a suitable generator and passed to the patient

via an active electrode which has a very small surface area. The current then passes thro ugh the tissues and returns via a very large

surface plate (the indifferent electrode) back to the earth pole of the generator. As the surface area of contact of the active electrode is

small in comparison to the indifferent electrode, the concentrated powerful current prod uces heat at the operative site. However, the

large surface area electrode of the patient plate spreads the returning current over a wide s urface area, so it is less concentrated and

produces little heat.

In bipolar diathermy, the two active electrodes are usually represented by the lim bs of a pair of diathermy forceps. Both forceps ends are

therefore active and current ows between them and only the tissue held between the limb s of the forceps heats up. This form of

diathermy is used when it is essential that the surrounding tissue should be fre e from either the risk of being burned or having current

passed through them.

The effects of diathermy

Diathermy can be used for three purposes:

1 Coagulation: the sealing of blood vessels.

2 Fulguration: the destructive coagulation of tissues with charring.

3 Cutting: used to divide tissues during bloodless surgery.

In coagulation, a heating effect leads to cell death by dehydration and protein denaturation. Ble eding is therefore stopped by a

combination of the distortion of the walls of the blood vessel,

Dispersive cable

(a) Monopolar diathermy Patient plate

Active cable

Diathermy unit Two small

active electrodes

(b) Bipolar diathermy

Figure 4.19 The principles of diathermy. (a) Monopolar diathermy. (b) Bipolar diathermy. Reproduced with permission f rom Royal College of Surgeons of England. The

intercollegiate basic surgical skills course participants handbook, edns 1–4. London: RCS.

coagulation of the plasma proteins, dried and shrunken dead tissue and stimulation of the clotting mechanism. In an ideal situation,

intracellular temperatures should not reach boiling during coagulation, because if it does an unwanted cutting effect may be experienced.

Cutting occurs when sufcient heat is applied to the tissue to cause cell water to explode into steam. The cut current is a continuous

wave form and the monopolar diathermy is most effective when the active electrode is held a v ery short distance from the tissues. This

allows an electrical discharge to arc across the gap creating a series of sparks which produce the high temperatures needed for cutting.

In fulguration, the diathermy matching is set to coagulation and a higher effective voltage is used to make l arger sparks jump an air gap

thus fulgurating the tissues. This can continue until carbonisation or charring occurs. The voltage and power output can be varied by

adjusting the duration of bursts of current, as well as its intensity to give a combination of both cutting and coagulation. This is known as

blended current and provides both forms of diathermy activity.

Complications of diathermy

Electrocution

Today, diathermy machines are manufactured to very high safety standards which min imise the risk of any part of the machine becoming

live with mains current. However, as with any such instrument, there must be re gular and expert servicing.

Explosion

Sparks from the diathermy can ignite any volatile or inammable gas or uid within the theatre. Alcohol-based skin preparations can

catch re if they are allowed to pool on or around the patient. Furthermore, diathermy sh ould not be used in the presence of explosive

gases, including those which may occur naturally in the colon, especially after certain forms of bowel preparation, such as mannitol,

which has now been banned for this use for this very reason.

Burns

These are the most common type of diathermy accidents in both open and endoscopic surgery . They occur when the current ows in

some way other than that in which the surgeon intended and are far more com mon in monopolar than bipolar diathermy. These may

occur as a result of:

• Faulty application of the indifferent electrode with inadequate

contact area.

• The patient being earthed by touching any metal object, e.g.

the Mayo table, the bar of an anaesthetic screen, an exposed

metal arm rest or a leg touching the metal stirrups used in

maintaining the lithotomy position.

• Faulty insulation of the diathermy leads, either due to cracked

insulation or instruments such as towel clips pinching the

cable.

• Inadvertent activity such as the accidental activation of the

foot pedal, or accidental contact of the active electrode with

other metal instruments, such as retractors, instruments or

towel clips.

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 gene rated 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.

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

Pacemakers

Diathermy currents can interfere with the working of a pacemaker with its obvious pot ential danger to the patient’s health. Modern

pacemakers are designed to be inhibited by high frequency interference, so that the pa tient may receive no pacing stimulation at all while

the diathermy is in use. Certain demand pacemakers may revert to the xed rate of pacing and th erefore it would be important for the

anaesthetist to have a magnet available so that these can be reset if necessary. In most cases, it is th erefore wise to undertake precautions

and to use bipolar diathermy wherever possible. If monopolar diathermy is required, then the patient plate should be sited as far away

from the pacemaker as possible so that the path of the current does not pass through the hea rt or the vicinity of the pacemaker.

Monitoring of the heart rate should be undertaken throughout the operation a nd a debrillator should always be available in case a

dysrhythmia develops at any time.

Laparoscopic surgery

Diathermy burns are a particular hazard of laparoscopic surgery due to the nature of the visibility of the instrumentation and the actual

structure of the instruments used. Such burns may occur by:

•

Diathermy of the wrong structure because of lack of clarity of vision or misidentication.

•

Faulty insulation of any of the laparoscopic instruments or equipment.

•

Intraperitoneal contact of the diathermy with another metal instrument while activatin g the pedal.

•

Inadvertent activation of the pedal while the diathermy tip is out of vision of the ca mera.

•

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

•

Capacitance coupling (Figure 4.20). This is a phenomenon

in which a capacitor is created by having an insulator sandwiched between tw o 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 owing thr ough the hook can induce a current in

the metal port, which can potentially damage intraperitoneal structures. In most cases, this curren t 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 signicantly increased. Therefore, metal ports should never be used with a plastic cuff. The danger of capacitance coupling can be

prevented by using entirely plastic ports.

Metal laparoscopic port

Diathermy hook

Point of contact

with bowel

Figure 4.20 Capacitance coupling during laparoscopic surgery. Reproduced with permission from Royal C ollege of Surgeons of England. The intercollegiate basic

surgical skills course participants handbook, edns 1–4. London: RCS.

The principles of the ‘harmonic scalpel’ 49

THE PRINCIPLES OF LIGASURE

‘Ligasure’ tissue fusion technology is a vessel sealing system that is used in bo th 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 spec ialties, including gynaecology, colorectal, urology

and general surgery. It uses a combination of pressure and energy to create vessel fusio n which can withstand up to three times the

normal systolic pressure.

New technology of the ligasure system involves advanced monopolar technolog y 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 ins trument is designed to manage the energy delivery

in a precise manner and results in an automatic discontinuation of energy once the se al is complete, thus removing any concern that the

surgeon has to use guesswork as to when the seal is complete. The newer instruments actively m onitor tissue impedance and provide a

real-time adjustment of the energy being delivered. Using this technology, ligas ure can seal vessels of up to 7 mm diameter, with an

average seal time of 2–4 seconds, as well as pedicles, tissue bundles and lymphat ics with a consistent controlled and predictable effect on

tissue, including less dessication.

Therefore, the new Ligasure Advance™ can dissect, seal and divide and was designed to be the only tool that a surgeon would need.

However, it is relatively expensive to use compared to some of the competing tec hnology.

THE PRINCIPLES OF THE ‘HARMONIC SCALPEL’

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 pe dal. During use, the scalpel vibrates in the 20

000–50 000 Hz range and cuts through tissues, effecting haemostasis by sealing vessels and tiss ues by means of protein denaturation

caused by vibration rather than heat (in a similar manner to whisking an egg w hite). It provides cutting precision, even through thickened

scar tissue, and visibility is enhanced due to less smoke being created by this system during use compared to routine electrosurgery.

However, the harmonic scalpel does take longer to cut and coagulate tissues th an 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 c onventional scalpel is used, and blood vessels are

sealed with a much lower temperature than conventional diathermy and so there is less t hermal damage to adjacent tissue, with less

charring and dessication. Furthermore, it is suggested that the use of the harmonic scalpel reduces operative time and recovery is thus

enhanced. Currently, the harmonic scalpel is in common use during laparoscopic proce dures, as well as open surgery, such as

thyroidectomy and several plastic surgery operations, e.g. cosmetic breast surgery.

FURTHER READING

Royal College of Surgeons of England. Intercollegiate basic surgical skills course (participant han dbook), 4th edn. London: Royal

College of Surgeons of England, 2007.

Jenkins TPN. The burst abdominal wound: a mechanical approach. Br Med J 1976; 131: 130–40.

Kirk RM. Basic surgical techniques, 6th edn. Edinburgh: Churchill Livingstone, 2010.

Eugen (Janö) Alexander Pölya , 1876–1944, Surgeon, St Stephen’s Hospital, Budapest, Hungary.

Henri Albert Charles Antoine Hartmann, 1860–1952, Professor of Clinical Surgery, The Faculty of Medic ine, The University of Paris, France. Gaston Michel, 1874–

1937, French surgeon.

Frank Gregory Connell, 1875–1968, Professor of Surgery, Rush Medical College, Chicago, IL, USA.

CHAPTER

5Surgical infection

LEARNING OBJECTIVES

To understand:

• The factors that determine whether a wound will become infected

• The classification of sources of infection and their severity

• The indications for and choice of prophylactic antibiotics

• The characteristics of the common surgical pathogens and their sensitivi ties

• The spectrum of commonly used antibiotics in surgery and the princ iples of therapy

• The misuse of antibiotic therapy with the risk of resistance (such as methicil lin-resistant Staphylococcus aureus (MRSA)) and

emergence (such as Clostridium difficile enteritis)

To learn:

• Koch’s postulates

• The management of abscesses

To appreciate:

• The importance of aseptic and antiseptic

techniques and delayed primary or secondary closure in contaminated wounds

To be aware of:

• The causes of reduced resistance to infection (host response)

To know:

• The definitions of infection, particularly at surgical sites

• What basic precautions to take to avoid surgically relevant health care-associated infec tions

PHYSIOLOGY AND PRESENTATION

Background

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 the y were able to prevent putrefaction, testied

by mummication skills. Their medical papyruses also describe the use of salves and antiseptics to prevent SSIs. This ‘prophylaxis’ had

also been known earlier by the Assyrians, although less well documented. It was desc ribed again independently by the Greeks. The

Hippocratic teachings described the use of antimicrobials, such as wine and vine gar, which were widely used to irrigate open, infected

wounds before delayed primary or secondary wound closure. A belief common to all the se civilisations, and indeed even later to the

Romans, was that, whenever pus localised in an infected wound, it needed to be drained.

Galen recognised that this localisation of infection (suppuration) in wounds, inicted in t he gladiatorial arena, often heralded recovery,

particularly after drainage (pus bonum et laudabile). Sadly, this dictum was misunderstood by many later healers, who thought that it was

the production of pus that was desirable. Until well into the Middle Ages, some practitioners pro moted 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, c losed primarily, could heal without infection or

suppuration.

The understanding of the causes of infection came in the nineteenth century. Microb es had been seen under the microscope, but Koch

laid down the rst denition of infective disease (Koch’s postulates; Summary b ox 5.1). Koch’s postulates do not cover every

eventuality though. Organisms of low virulence may not cause disease in normal hosts bu t may be responsible for disease in

immunocompromised hosts. Some hosts may develop

Hippocrates was a Greek physician, and by common consent ‘The Father of Medicine’. He was born o n the Greek island of Cos off Turkey about 460 bc and probably

died in 375 bc. He lived to be about 109 years of age in an era when the life expectancy was ab out 32 years.

Galen , 130–200, a Roman physician, who commenced practice as surgeon to the gladiators at Pergamum (now Bregama in Turkey) and later became personal physician

to the Emperor Marcus Aurelius and to two of his successors. He was a prolific writer on many subjects, among th em 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, who was Bishop of Cervia, published a book on surgery a bout 1267.

Ambroise Paré, 1510–1590, a French military surgeon, who also worked at the Hotel Dieu, Paris, France.

Guy de Chauliac, ?1298–1368, was physician and chaplain to Pope Clement VI at Avignon, France. He w as the author of Chirurgia Magna which was published about

1363.

Physiology 51

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 caus es 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 cou ld be reduced from over 10 per cent to under 2 per cent by

the simple act of hand washing between cases, particularly between post-mortem examinations and the delivery suite. He was ignored by

his contemporaries.

Louis Pasteur recognised through his germ theory that microorganisms were responsib le for infecting humans and causing disease.

Joseph Lister applied this knowledge to the reduction of colonising organisms in com pound fractures by using antiseptics. The principles

of antiseptic surgery were soon enhanced with aseptic surgery at the turn of the century. As well as killing the bacteria on the skin before

surgical incision (antiseptic technique), the conditions under which the operation was pe rformed 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 an tibiotic penicillin is attributed to Alexander Fleming in

1928, but it was not isolated for clinical use until 1941 by Florey and Chain. The rst patient to receive penicillin was Police Constable

Alexander in Oxford. He scratched the side of his mouth while pruning roses and developed abscesses of the face and eyes leading to a

severe staphylococcal bacteraemia. He responded to treatment, made a partial recovery before the penicillin ran out, then relapsed and

died. Since then, there has been a proliferation of antibiotics with broad-spectrum ac tivity and antibiotics today remain the mainstay of

antimicrobial therapy.

Many staphylococci today have become resistant to penicillin. Often bacteria develop re sistance through the acquisition of β-lactamases,

which break up the β-lactam ring present in

Joseph Lister (Lord Lister) , 1827–1912, Professor of Surgery, Glasgow (1860–1869), Edinburgh (1869–1877) and King’s College Hospital, London, UK (1877–1892).

He was the first to show the relation between microbial infection and surgical sepsis. He associated Pasteur’s ob servations on fermentation with sepsis and, using a

carbolic dressing and spray, introduced the ‘antiseptic principle’ which revolutionised surgery. Asepsis in surgery ha s now replaced antisepsis but the dangers of sepsis

are still very much with us.

Sir Ernst Boris Chain, Professor of Biochemistry, Imperial College, London, UK. Fleming, Florey and Chain shared the 1945 Nobel Pr ize for Physiology or Medicine for

their work on penicillin.

the molecular structure of many antibiotics. The acquisition of extended spectrum β-lactamas es (ESBLs) is an increasing concern in

some Gram-negative organisms that cause urinary tract infections because it is difcult to nd an antibiotic effective against them. In

addition, there is increasing concern about the rising resistance of many other bacteria to antibio tics, in particular the emergence of

methicillin-resistant Staphylococcus aureus (MRSA) and glycopeptide-resistant enter ococci (GRE), which are also relevant in general

surgical practice.

The introduction of antibiotics for prophylaxis and for treatment, together with advance s in anaesthesia and critical care medicine, has

made possible surgery that would not previously have been considered. Faecal perito nitis is no longer inevitably fatal, and incisions

made in the presence of such contamination can heal primarily without infection in 80–9 0 per cent of patients with appropriate antibiotic

therapy. Despite this, it is common practice in many countries to delay wound closure in patients in who m the wound is known to be

contaminated or dirty. Waiting for the wound to granulate and then performing a delayed primar y or secondary closure may be

considered a better option (Summary box 5.2).

Summary box 5.2

Advances in the control of infection in surgery

Aseptic operating theatre techniques have enhanced the use of antiseptics

Antibiotics have reduced postoperative infection rates after elective and emergency surgery

Delayed primary, or secondary, closure remains useful in contaminated wounds

Surgical site infection in patients who have contaminated wounds, who are immunosuppressed or undergoing prosthetic surgery, is now

the exception rather than the rule since the introduction of prophylactic antibiotics. The eviden ce for this is of the highest level. The

value of prophylactic antibiotics in clean, non-prosthetic surgery remains controversia l, although SSI rates after such surgery is high

when judged by close, unbiased, post-discharge surveillance, using strict denitions.

PHYSIOLOGY

Microorganisms are normally prevented from causing infection in tissues by intact ep ithelial surfaces, most notably the skin. These

surfaces are broken down by trauma or surgery. In addition to these mechanical barriers, th ere are other protective mechanisms, which

can be divided into:

• chemical: low gastric pH

• humoral: antibodies, complement and opsonins

• cellular: phagocytic cells, macrophages, polymorphonuclear cells and killer lymphocytes.

All these natural mechanisms may be compromised by surgical intervention and treatme nt.

Reduced resistance to infection has several causes (Summary box 5.3).

Antony von Leeuwenhoek of Delft , The Netherlands, invented the microscope, and was the first to see b acteria in 1875. He himself made more than 400 microscopes.

Robert Koch, 1843–1910, Professor of Hygiene and Bacteriology, Berlin, Germany, stated his ‘Postulates’ in 1882.

Ignac Semmelweis, 1818–1865, Professor of Obstetrics, Budapest, Hungary.

Louis Pasteur, 1822–1895, was a French chemist, bacteriologist and immunologist who was Professor of Ch emistry at the Sorbonne, Paris, France. Sir Alexander

Fleming, 1881–1955, Professor of Bacteriology, St Mary’s Hospital, London, UK, discovered Penicilliu m notatum in 1928. Howard Walter Florey (Lord Florey of

Adelaide), 1898–1968, Professor of Pathology, The University of Oxford, Oxford, UK.

Summary box 5.3

Causes of reduced host resistance to infection

Metabolic: malnutrition (including obesity), diabetes, uraemia, jaundice

Disseminated disease: cancer and acquired

immunodeficiency syndrome (AIDS)

Iatrogenic: radiotherapy, chemotherapy, steroids

Host response is weakened by malnutrition, which can be recognised clinically, and most e asily, as recent rapid weight loss that can be

present even in the presence of obesity. Metabolic diseases such as diabetes me llitus, uraemia and jaundice, disseminated malignancy and

acquired immune deciency syndrome (AIDS) are other contributors to infection and a poor healing response, as are iatrogenic causes

including the immunosuppression caused by radiotherapy, chemotherapy or steroids (Summary box 5.4, and Figures 5.1 and 5.2).

When enteral feeding is suspended during the perioperative period, and parti cularly with underlying disease such as cancer,

immunosuppression, shock or sepsis, bacteria (particularly aerobic Gram-negative baci lli) tend to colonise the normally sterile upper

gastrointestinal tract. They may then translocate to the mesenteric nodes and cause the releas e of endotoxins (lipopolysaccharide in

bacterial cell walls), which can be one cause of a harmful systemic inammatory response throug h the excessive release of

proinammatory cytokines and activation of macrophages (Figure 5.3). In the circumstance s of reduced host resistance to infection,

microorganisms that are not normally pathogenic may start to behave as pathogen s. This is known as opportunistic infection.

Opportunistic infection with fungi is an example, particularly when prolonged an d changing antibiotic regimens have been used.

The chance of developing an SSI after surgery is also determined by the pathogenicity of the organisms present and by the size of the

bacterial inoculum. Devitalised tissue, excessive dead space or haematoma, all the results o f poor surgical technique, increase the

chances of infection. The same applies to foreign materials of any kind, including sutures and d rains. If there is a silk suture in tissue, the

critical number of organisms needed to start an infection is reduced logarithmic ally. Silk should not

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

Summary box 5.4

Risk factors for increased risk of wound infection

Malnutrition (obesity, weight loss)

Metabolic disease (diabetes, uraemia, jaundice)

Immunosuppression (cancer, AIDS, steroids, chemotherapy and radiotherapy)

Colonisation and translocation in the gastrointestinal tract Poor perfusion (systemic shock or local ischaemia )

Foreign body material

Poor surgical technique (dead space, haematoma)

be used to close skin as it causes suture abscesses for this reason. These principles are im portant to an understanding of how best to

prevent infection in surgical practice (Summary box 5.5).

Cytokine release MODS

SIRS

IL-6, TNF, etc.

Burrill Bernard Crohn , 1884–1983, gastroenterologist, Mount Sinai Hospital, New York, NY, USA, described regional ileitis in 193 2 along with Leon Ginzburg and

Gordon Oppenheimer.

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

Macrophage Release of endotoxin

Mesenteric nodes

Translocation (failure of gut-associated lymphoid tissue , villous atrophy) Colonisation by aerobic Gramne gative bacilli (in gut failure

and starvation)

Figure 5.3 Gut failure, colonisation and translocation related to the development of multiple organ dysfunc tion syndrome (MODS) and systemic inflammatory response

syndrome (SIRS). IL, interleukin; TNF, tumour necrosis factor.

Major and minor surgical site infections 53

Summary box 5.5

Factors that determine whether a wound will become infected

Host response

Virulence and inoculum of infective agent

Vascularity and health of tissue being invaded (including local ischaemia as well as systemic shock)

Presence of dead or foreign tissue

Presence of antibiotics during the ‘decisive period’

There is a delay before host defences can become mobilised after a breach in an epithe lial surface, whether caused by trauma or surgery.

The acute inammatory, humoral and cellular defences take up to 4 hours to be mobilised. This is called the ‘decisive period’, and it is

the time when the invading bacteria may become established in the tissues. Strategies aimed at preventing infection from taking a hold

become ineffective after this time period. It is therefore logical that prophylactic antibiotics sh ould be given to cover this period and that

they could be decisive in preventing an infection from developing. The tissu e levels of antibiotics should be above the minimum

inhibitory concentration (MIC

) for the pathogens likely to be encountered.

Local and systemic presentation

The infection of a wound can be dened as the invasion of organisms through tissues f ollowing a breakdown of local and systemic host

defences, leading to cellulitis, lymphangitis, abscess and bacteraemia. The infection of m ost surgical wounds is referred to as supercial

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 pr oteases 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 10

organisms. They can be released into tissues by surgery, contamination being most severe

when a hollow viscus perforates (e.g. faecal peritonitis following a diverticular perforation). Any infection that follows surgery may be

termed primary or secondary (Summary box 5.6).

Summary box 5.6

Classification of sources of infection

Primary: present in or on the host and so acquired from an endogenous source (such as an SSSI following contamination of the wound from a perforated appendix)

Secondary or exogenous (HAI): acquired from a source outside the body such as the operating theatre (inadequ ate air filtration, poor antisepsis) or the ward (e.g. poor

hand washing compliance)

Infection that follows surgery or admission to hospital is termed health care-associated infection (HAI). There are four main groups:

respiratory infections (including ventilator-associated pneumonia), urinary tract infectio ns (mostly related to urinary catheters),

bacteraemia (mostly related to indwelling vascular catheters) and SSIs.

MAJOR AND MINOR SURGICAL SITE INFECTIONS

A major SSI is dened as a wound that either discharges signicant quantities of pus spo ntaneously or needs a secondary procedure to

drain it (Figure 5.4). The patient may have systemic signs, such as tachycardia, pyrexia and a raised white count (Summary box 5.7).

Summary box 5.7

Major wound infections

Significant quantity of pus Delayed return home

Patients are systemically ill

Minor wound infections may discharge pus or infected serous fluid but should not be associ ated with excessive discomfort, systemic

signs or delay in return home (Figure 5.5). The differentiation between major and mino r and the denition of SSI is important in audit or

trials of antibiotic prophylaxis. There are scoring systems for the severity of wound inf ection, which are particularly useful in

surveillance and research. Examples are the Southampton (Table 5.1) and ASEPSIS system s (Table 5.2).

Accurate surveillance can only be achieved using trained, unbiased and blind ed assessors. Most include surveillance for a 30-day

postoperative period. The US Centers for Disease Control (CDC) denition insists on a 30-day follow-up period for non-prosthetic

surgery and one year after implanted hip and knee surgery.

Types of localised infection

Abscess

An abscess presents all the clinical features of acute inamma

Figure 5.4 Major wound infection with superficial skin dehiscence. Figure 5.5 Minor wound infection that settled spontaneously without antibiotics.

tion originally described by Celsus: calor (heat), rubor (redness), dolour (pain) and tumour (swelling). To these can be added functio

laesa (loss of function: if it hurts, the infected part is not used). They usually fo llow a puncture wound of some kind, which may have

been forgotten, as well as surgery, but can be metastatic in all tissues following b acteraemia.

Pyogenic organisms, predominantly Staphylococcus aureus, cause tissue necr osis and suppuration. Pus is composed of dead and dying

white blood cells that release damaging cytokines, oxygen free radicals and other mol ecules. An abscess is surrounded by an acute

inammatory response composed of a fibrinous exudate, oedema and the cells of acute inamm ation. Granulation tissue (macrophages,

angiogenesis and broblasts) forms later around the suppurative process and le ads 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 ma y form.

Abscesses contain hyperosmolar material that draws in uid. This increases the pressure and causes pain. If they spread, they usually

track along planes of least resistance and point towards the skin. Wound absce sses may discharge spontaneously by tracking to a surface,

but may need drainage through a surgical incision. Most abscesses relating to sur gical wounds take 7–10 days to form after surgery. As

many as 75 per cent of SSIs present after the patient has left hospital and may thu s be overlooked by the surgical team. Their cost and

management, which may be inadequate, is transferred to primary care (Summary box 5.8).

Table 5.1 Southampton wound grading system.

Grade Appearance

0 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 inammation IIa At one point

IIb Around sutures

IIc Along wound

IId Around wound

III Clear or haemoserous discharge

IIIa At one point only (£2 cm)

IIIb Along wound (>2 cm)

IIIc Large volume

IIId Prolonged (>3 days)

Major complication

IVa IVb V

Pus

At one point only (£2 cm)

Along wound (>2 cm)

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

Table 5.2 The ASEPSIS wound score.

Criterion Points Additional treatment 0 Antibiotics for wound infection 10 Drainage of pus under local anaesthesia 5 Debridement of

wound under general anaesthesia 10

Serous discharge

Daily 0–5

Erythema

Daily 0–5

Purulent exudate

Daily 0–10

Separation of deep tissues

Daily 0–10

Isolation of bacteria from wound 10

Stay as inpatient prolonged over 14 days as result 5 of wound infection

Scored for 5 of the rst 7 days only, the remainder being scored if present in the rst two mon ths.

Aulus Aurelius Cornelius Celsus, 25 BC to AD 50, a Roman surgeon. He was the author of De Re Medico Libri Octo. Systemic inflammatory response

syndrome and multiple organ dysfunction syndrome 55

Summary box 5.8 Summary box 5.9

Abscesses

Abscesses need drainage

Modern imaging techniques may allow guided aspiration Antibiotics are indicated if the abscess is not local ised (e.g. evidence of cellulitis) or the cavity is not left open

to drain freely

Healing by secondary intention is encouraged

Cellulitis and lymphangitis

Non-suppurative, poorly localised

Commonly caused by streptococci, staphylococci or clostridia

Blood cultures are often negative

Abscess cavities need cleaning out after incision and drainage and are traditionally encou raged 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 mat erial. Thus a perianal abscess can be

incised and drained, the walls curretted and the skin closed with good results us ing appropriate antibiotic therapy, but a pilonidal abscess

has a higher recurrence risk after such treatment because a nidus of hair may remain in the subcutane ous tissue adjacent to the abscess.

Some small breast abscesses can be managed by simple needle aspiration of the pus and antibiotic therapy.

Persistent chronic abscesses may lead to sinus or stula formation. In a chronic abscess, lymphocytes and plasma cells are seen. There is

tissue sequestration and later calcication may occur. Certain organisms are associated with chronicity, sinus and stula formation.

Common ones are Mycobacterium and Actinomyces. They should not be forgotten when these com plications occur and persist.

Perianastomotic contamination may be the cause of an abscess but, in the abdo men, abscesses are more usually the result of anastomotic

leakage. An abscess in a deep cavity, such as the pleura or peritoneum, may be difcult t o diagnose or locate even when there is strong

clinical suspicion that it is present (Figure 5.6). Plain or contrast radiographs may not b e helpful, but ultrasonography, computed

tomography (CT), magnetic resonance imaging (MRI) and isotope scans are all useful and may allow guided aspiration without the need

for surgical intervention.

Cellulitis and lymphangitis

Cellulitis is the non-suppurative invasive infection of tissues. There is poor localisatio n in addition to the cardinal signs of inammation.

Spreading infection presenting in surgical practice is typically caused by organisms such as β-h aemolytic streptococci (Figure 5.7),

staphylococci (Figure 5.8) and C. perfringens. Tissue destruction, gangrene and ul ceration may follow, which are caused by release of

proteases.

Systemic signs (the old-fashioned term toxaemia) are common, with chills, fever and rig ors. These follow the release of toxins into the

circulation, which stimulate a cytokine-mediated systemic inammatory response even thou gh blood cultures are negative.

Lymphangitis is part of a similar process and presents as painful red streaks in affecte d lymphatics. Cellulitis is usually located at the

point of injury and subsequent tissue infection. Lymphangitis is often accompanied by painful lymph node groups in the related drainage

area (Summary box 5.9).

SYSTEMIC INFLAMMATORY RESPONSE SYNDROME AND MULTI PLE ORGAN DYSFUNCTION SYNDROME

Systemic inammatory response syndrome (SIRS) is a systemic manifestation of sepsis , although the syndrome may also be caused by

multiple trauma, burns or pancreatitis without infection. Serious infection, such as secon dary peritonitis, may lead to SIRS through the

release of lipopolysaccharide endotoxin from the walls of dying Gram-negat ive bacilli (mainly Escherichia coli) or other bacteria or

fungi. This and other toxins stimulate the release of cytokines from macrophages (Figure 5.3). SIRS should not be confused with

bacteraemia although the two may coexist (see Table 5.3).

Septic manifestations and multiple organ dysfunction syndrome (MODS) in SIRS are m ediated by the release of proinflammatory

cytokines such as interleukin-1 (IL-1) and tumour necrosis factor alpha (TNFα). Th ese cytokines stimulate neu

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

gastrectomy) towards the abscess (black arrow).

Theodor Escherich, 1857–1911, Professor of Paediatrics, Vienna, Austria, discovered the Bacterium coli commune in 1886. Figure 5.7 Streptococcal cellulitis of the leg

following a minor puncture wound.

trophil adhesion to endothelial surfaces adjacent to the source of infection and cause them to m igrate through the blood vessel wall by

chemotaxis. A respiratory burst occurs within such activated neutrophils, releasing lysos omal enzymes, oxidants and free radicals, which

are involved in killing the invading bacteria but which may also damage adjacent c ells. Coagulation, complement and brinolytic

pathways are also stimulated as part of the normal inammatory response. This response is us ually benecial to the host and is an

important aspect of normal tissue repair and wound healing. In the presence of severe sepsis or bacteraemia, this response may become

harmful to the host if it occurs in excess, when it is known as SIRS. There are h igh circulating levels of cytokines and activated

neutrophils which stimulate fever, tachycardia and tachypnoea. The activated ne utrophils adhere to vascular endothelium in key organs

remote from the source of infection and damage it, leading to increased vascular permeability, which in turn leads to cellular damage

within the organs, which become dysfunctional and give rise to the clinical picture of MODS. In its most severe form, MODS may

progress into multiple system organ failure (MSOF). Respiratory, cardiac, intestinal, renal and liver failure ensue in combination with

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

SIRS

Two of:

hyperthermia (>38°C) or hypothermia (<36°C)

tachycardia (>90/min, no β-blockers) or tachypnoea (>20/min) white cell count >12 × 10

/l or <4 × 10

Sepsis is SIRS with a documented infection

Severe sepsis or sepsis syndrome is sepsis with evidence of one or more organ fail ures (respiratory (acute respiratory distress syndrome),

cardiovascular (septic shock follows compromise of cardiac function and fall in periphera l vascular resistance), renal (usually acute

tubular necrosis), hepatic, blood coagulation systems or central nervous system)

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

circulatory failure and shock. In this state, the body’s resistance to infection is reduced and a vicious cycle develops where the more

organs that fail, the more likely it becomes that death will follow despite all that a modern intensive care unit can do for organ support

(Summary box 5.10).

Summary box 5.10

Definitions of infected states

SSI is an infected wound or deep organ space

SIRS is the body’s systemic response to severe infection MODS is the effect that SIRS produces systemically

MSOF is the end stage of uncontrolled MODS

Bacteraemia and sepsis

Bacteraemia is unusual following supercial SSIs but common after anastomotic bre akdown (deep space SSI). It is usually transient and

can follow procedures undertaken through infected tissues (particularly instrumentation in infec ted bile or urine). It may also occur

through bacterial colonisation of indwelling intravenous cannulae. Bacteraemia is important when a prosthesis has been implanted, as

infection of the prosthesis can occur. Sepsis accompanied by MODS may follow anastomotic b reakdown. Aerobic Gram-negative bacilli

are mainly responsible, but S. aureus and fungi may be involved, particularly afte r the use of broad-spectrum antibiotics (Summary box

5.11).

Summary box 5.11

Bacteraemia and sepsis

Sepsis is common after anastomotic breakdown Bacteraemia is dangerous if the patient has a prosthesis Sep sis may be associated with MODS

Specific wound infections

Gas gangrene

This is caused by C. perfringens. These Gram-positive, anaerobic, spore-bearing bacilli are widely found in nature, particularly in soil

and faeces. This is relevant to military and traumatic surgery and colorectal operations. Pa tients who are immunocompromised, diabetic

or have malignant disease are at greater risk, particularly if they have wounds containing necrotic or foreign material, resulting in

anaerobic conditions. Military wounds provide an ideal environment as the kinetic energy o f 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 noted on p lain radiographs). The wound produces a thin,

brown, sweet-smelling exudate, in which Gram staining will reveal bacteria. Oedema a nd spreading gangrene follow the release of

collagenase, hyaluronidase, other proteases and alpha toxin. Early systemic complications with circulatory collapse and MSOF follow if

prompt action is not taken (Summary box 5.12).

Antibiotic prophylaxis should always be considered in patients at risk, especially when ampu tations 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.

Summary box 5.12

Gas gangrene

Caused by C. perfringens

Gas and smell are characteristic

Immunocompromised patients are most at risk Antibiotic prophylaxis is essential when performing amputations t o remove dead tissue

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 s ymptoms of tetanus are mediated by the release of

the exotoxin tetanospasmin, which affects myoneural junctions and the motor ne urones of the anterior horn of the spinal cord. A short

prodromal period, which has a poor prognosis, leads to spasms in the distribution of th e short motor nerves of the face followed by the

development of severe generalised motor spasms including opsithotonus, respirato ry 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 lo calised small area of cellulitis; exudate or

aspiration may give a sample that can be stained to show the presence of Gram-p ositive 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 patien t may require ventilation in severe

forms, which may be associated with a high mortality. The use 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 g ive protection for a ve-year period, after

which a single ve-yearly booster confers immunity. It should be given to all patients w ith open traumatic wounds who are not

immunised. At-risk wounds are those that present late, when there is devitalisa tion of tissue or when there is soiling. For these wounds, a

booster of toxoid should be given or, if not immunised at all, a three-dose cou rse, together with prophylactic benzylpenicillin; however,

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: colif orms, staphylococci, Bacteroides spp.,

anaerobic streptococci and peptostreptococci have all been implicated, acting in synergy. Abdominal wall infections are known as

Meleney’s synergistic hospital gangrene and scrotal infection as Fournier’s gang rene (Figure 5.9). Patients are almost always

immunocompromised 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 spreadin g inammation with crepitus and smell are

all signs of the infection spreading. Untreated, it will lead to widespread gangrene and MSOF. The subdermal spread of gangrene is

always much more extensive than appears from initial examination. Broad-spectrum antibio tic therapy must be combined with aggressive

circulatory support. Locally, there should be wide excision of necrotic tissue and laying open o f affected areas. The debridement may

need to be extensive, and patients who survive may need large areas of sk in grafting.

Clostridium tetani

This is another anaerobic, terminal spore-bearing, Gram-positive bacterium that ca n cause tetanus following implantation into

TREATMENT OF SURGICAL INFECTION

Now that patients are discharged more quickly after surgery and many procedu res 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 the β-haemolytic Streptoc occus) takes 3–4 days to develop. Major surgical

infections with systemic signs (Figure 5.10), evidence of spreading infection, cellulitis or bacter aemia need treatment with appropriate

antibiotics. The choice may need to be empirical initially but is best based on cultur e and sensitivities of isolates harvested at surgery.

Although the identication of organisms in surgical infections is necessary for audit and woun d surveillance purposes, it is usually 2–3

days before sensitivities are known (Figures 5.11 and 5.12). It is illogical to withhold antibiotics u ntil these are available but, if clinical

response is poor by the time sensitivities are known, then antibiotics can be changed. This is unusual if the empirical choice of

antibiotics is sensible; change of antibiotics promotes resistance and risks complications, such as C. d ifcile enteritis.

If an infected wound is under tension, or there is clear evidence of suppuration, suture s or clips need to be removed, with curettage if

necessary, to allow pus to drain adequately. There is no evidence that subcuticular continu ous skin closure contributes to or prevents

suppuration. In severely contaminated wounds, such as an incision made for drainage of an abscess, it is logical to leave the skin open.

Delayed primary or secondary suture can be undertaken when the wound is clean and granulating (Figures 5.13 and 5.14). Leaving

wounds open after a ‘dirty’ operation, such as laparotomy for faecal peritonitis, is not practised as w idely in the UK as in the US or

mainland Europe (Summary box 5.13).

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

Wounds are best managed by delayed primary or secondary closure

Figure 5.9 A classic presentation of Fournier’s gangrene of the scrotum with ‘shameful exposure of the testes’ following excision of the gangrenous skin.

HOSPITAL __________________________________

YEAR WARD SURNAME

DATE OF BIRTH UNIT NO

93 J

FIRST NAMES

SEX CONSULTANT

BOWELS: 0 0 0 0

MONTH

AUGUST

DAY 5

HOURS

06 1

22 25 6 10 18 22 6 11 14 22 09 17 23 11 23 0 711 22 11 MINUTES

21 0 0 0 0 0 0 0 0 0 3017 T

0300 0 030 0 0 0 0

17 06 0 0

17 0

40.5

40.0

39.5

39.0

38.5

250

38.0

240

37.5

230

37.0 220

36.5

210

36.0 200

35.5 190

35.0 180 170 34.5 170 160 34.0 160 150 150 140 140 130 130 120 120 110 110 100

100

Figure 5.10 Classic swinging pyrexia related to a perianastomotic wound abscess that settled spontaneously on an tibiotic therapy. Frank Lamont Meleney, 1889–1963,

Professor of Clinical Surgery, Columbia University, New York, NY, USA. Jean Alfred Fournier, 1832–191 5, syphilologist, the founder of the Venereal and

Dermatological Clinic, Hôpital St Louis, Paris, France. Figure 5.11 Mixed streptococcal infection o f a skin graft with very poor ‘take’.

Figure 5.12 After 5–6 days of antibiotics, the infection shown in Figure 5.11 is under control, an d the skin grafts are clearly viable.

When taking pus from infected wounds, specimens should be sent fresh for microbiolog ical culture. Swabs should be placed in transport

medium, but the larger the volume of pus sent, the more likely is the accurate identication of the organism involved. Providing the

microbiologist with as much information as possible and discussing the results with him o r her gives the best chance of the most

appropriate antibiotic treatment. If bacteraemia is suspected, but results are negative, then rep eat specimens for blood culture may need

to be taken.

A rapid report on infective material can be based on an immediate Gram stain. A erobic and anaerobic culture on conventional media

allows sensitivities to be assessed by disc diffusion. Measurements of minimum in hibitory antibiotic concentrations (MIC

in mg/L),

together with measurements of endotoxin and cytokine levels, are usually only needed for research studies.

Figure 5.13 Skin layers left open to granulate after laparotomy for faecal peritonitis. The w ound is clean and ready for secondary closure.

Many dressings are now available for use in wound care. These are listed in Table 5.4. Po lymeric lms are used as incision drapes and

also to cover sutured wounds, but are not indicated for use in wound infectio ns. Agents that can be used to help debride open infected

wounds and others to absorb excessive exudate or to encourage epithelialisation and the form ation of granulation tissue are also listed

(Figure 5.15). Most contribute to the ideal moist wound environment, and there are other s that provide an antibacterial to the wound.

There is now a plethora of dressings containing silver or povidone–iodine antiseptics, b ut the use of topical antibiotics should be avoided

because of the risks of allergy and resistance. Topical antiseptics inhibit epithelial ingrowth and sh ould only be used on supercial

wounds for a short period to clear infection from heavily contaminated wounds.

Prophylaxis

Prophylactic antibiotics

If antibiotics are given to prevent infection after surgery or instrumentation, they should be used when local wound defences are not

established (the decisive period). Ideally, maximal blood and tissue levels should be p resent at the time at which the rst incision is made

and before contamination occurs. Intravenous administration at induction of anaesthesia is optimal. In long operations or when there is

excessive blood loss or when unexpected contamination occurs, antibiotics may b e repeated at 4-hourly intervals during the surgery, as

tissue antibiotic levels often fall faster than serum levels. There is no evidence that further doses of a ntibiotics after surgery are of any

value in prophylaxis against infection and the practice can only encourage the developme nt of antibiotic resistance. The choice of an

antibiotic depends on the expected spectrum of organisms likely to be encountered, the c ost and local hospital policies, which are based

on experience of local resistance trends (Summary box 5.14).

Table 5.4 Surgical dressings.

Type Name (example) Indications and comments Debriding agents

Enzymatic agents Bead dressings

Benoxyl–benzoic acid

Aserbine–benzoic acid

Variclene–lactic acid

Varidase–streptokinase/streptodornase Debrisan

Polymeric lms

Foams Iodosorb

Other paste dressings

Opsite

Bioclusive

Tegaderm

Silastic (elastomer) Used only in necrotic sloughing skin ulcers. Provide acidic environm ent. Claimed to enhance healing with debriding

action

Activate brinolysis and liquefy pus on chronic skin ulcers Remove bacteria and excess moisture by capillary action in deep granulating

wounds. Antimicrobials

May be added but with questionable topical benet

Primary adhesive transparent dressing for sutured wounds or donor sites

Elastomeric dressing can be shaped to t deep cavities and granulating wounds. Absorb ent and non-adherent

Hydrogels Lyofoam Allevyn

Geliperm Intrasite

Hydrocolloids

Fibrous polymers

Biological membranes Simple miscellaneous Porcine skin, amnion

Gauzes: viscose/cotton with non-adherent coating (Melolin) Tulles: non-adherent parafn impregna tion Maintain moist environment.

Polymers can absorb exudate or antiseptics (but adding antiseptics is of doubtful b enet). Semi-permeable, allow gas exchange

Complete occlusion. Promote epithelialisation and granulation tissue. Maintain moisture w ithout gaseous exchange across them

Absorptive alginate dressings. Derived from natural (seaweed) source Like polymeric hydrocolloids and hydrogels, they can be used to

pack deep wounds

Used for supercial chronic skin ulcers. No proven advantage Simple absorptive dress ings only used as secondary dressings to absorb

exudate. Added antimicrobials probably confer no benet. Added charcoal absorbents may reduce swelling. Relatively cheap but of

questionable effectiveness

(a)

Comfeel Granuex Kaltostat Sorbsan

(b)

Figure 5.14 Delayed primary closure of fasciotomy wound.

Table 5.5 Suggested prophylactic regimens for operations at risk.

Type of surgery Organisms encountered Prophylactic regimen suggested Vascular

Orthopaedic

Oesophagogastric

Biliary

Small bowel

Appendix/colorectal

Staphylococcus epidermidis (or MRCNS) S. aureus (or MRSA)

Aerobic Gram-negative bacilli (AGNB)

S. epidermidis/aureus

Enterobacteriaceae

Enterococci (including anaerobic/

viridans streptococci)

Enterobacteriaceae (mainly Escherichia coli) Enterococci (including Streptococcus faecalis) Enter obacteriaceae

Anaerobes (mainly Bacteroides)

Enterobacteriaceae

Anaerobes (mainly Bacteroides)

One dose of augmentin with or without gentamicin, vancomycin or rifampicin if MRC NS/MRSA a risk

One dose of augmentin

One dose of a second-generation cephalosporin and metronidazole in severe contam ination

One dose of a second-generation cephalosporin

One dose of a second-generation cephalosporin with or without metronidazole

One dose of a second-generation cephalosporin (or gentamicin) with metronidazole (the use of oral, poorly absorbed antibiotics is

controversial)

MRCNS, multiply resistant coagulase-negative staphylococci; MRSA, methicillin-resistant Staphylococcus aureus.

Summary box 5.14

Choice of antibiotics for prophylaxis

Empirical cover against expected pathogens with local hospital guidelines

Single-shot intravenous administration at induction of anaesthesia

Repeat only during long operations or if there is excessive blood loss

Continue as therapy if there is unexpected contamination or if a prosthetic is implanted in a pati ent with a septic source Benzylpenicillin should be used if Clostridium

gas gangrene infection is a possibility

Patients with heart valve disease or a prosthesis should be protected from bacteraemia caused by dent al work, urethral instrumentation or visceral surgery

in immunocompromised patients or those whose gut ora is suppressed by antibiotic therapy. Although the need for clean hospitals,

emphasised by the media, is logical, the ‘clean your hands campaign’ is beginning to result in falls in the incidence of HAIs. Staff with

open, infected skin lesions should not enter the operating theatre. Ideally, neither should pati ents, especially if they are having a

prosthesis implanted. Antiseptic baths (usually chlorhexidine) are popular in Europe, but there is no hard evidence for their value in

reducing wound infections. Preoperative skin shaving should be undertaken in the operating t heatre immediately before surgery as the

SSI rate after clean wound surgery may be doubled if it is performed the night before; minor skin injury enhances supercial bacterial

colonisation. Cream depilation is messy and hair clipping is best, with the lowest rate of infection (Summary box 5.15).

The use of the newer, broad-spectrum antibiotics for prophylaxis should be avoided. T able 5.5 gives some examples of prophylaxis that

can be used in elective surgical operations.

Patients with known valvular disease of the heart (or with any implanted vascular or ort hopaedic prosthesis) should have prophylactic

antibiotics during dental, urological or open viscus surgery. Single doses of bro ad-spectrum penicillin, for example amoxicillin, orally or

intravenously administered, are sufcient for dental surgery. In urological instru mentation, a single dose of gentamycin is often used.

Preoperative preparation

Short preoperative hospital stay lowers the risk of acquiring MRSA, multiply resistant coag ulase-negative staphylococci (MRCNS) and

other organisms and the acquisition of HAIs. Medical and nursing staff should always wash th eir hands after any patient contact.

Alcoholic hand gels can act as a substitute for hand washing, but do not destroy the spo res of C. difcile, which may cause

pseudomembranous colitis, especially

Figure 5.15 Infected animal bite/wound of the upper thigh, treated by open therapy following virulent staphylococc al infection. Deep cavity wounds such as this can be

debrided and kept moist with many of the modern dressings listed in Table 5.4.

Table 5.6 Classification of antiseptics commonly used in general surgical practice.

Name Presentation Uses Comments Chlorhexidine (Hibiscrub) Alcoholic 0.5% Aqueous 4%

Povidone–iodine (Betadine)

Alcoholic 10% Aqueous 7.5%

Cetrimide (Savlon)

Alcohols

Hypochlorites

Hexachlorophane Aqueous

70% ethyl, isopropyl

Aqueous preparations (Eusol, Milton,

Chloramine T)

Aqueous bisphenol Skin preparation

Instrument and surface cleaning (debriding agent in open wounds?)

Skin preparation Hand washing

Has cumulative effect. Effective against Grampositive organisms and relatively stable in the presence of pus and body uids

Safe, fast-acting, broad spectrum. Some sporicidal activity. Anti-fungal iodine is not free but co mbined with polyvinylpyrrolidone

(povidone)

Pseudomonas spp. may grow in stored contaminated solutions. Ammonium compounds h ave good detergent action (surface-active

agent)

Should be reserved for use as disinfectants

Toxic to tissues

Has action against Gram-negative organisms

Summary box 5.15

Avoiding surgical site infections

Skin preparation

Skin preparation. Surgical scrub in dilute solutions in open wounds

Skin preparation

Skin preparation. Surgical scrub in dilute solutions in open wounds

Hand washing

Instrument and surface cleaning

Staff should always wash their hands between patients Length of patient stay should be kept to a minimum Preoperative shaving should be done immediately before

surgery

Antiseptic skin preparation should be standardised Attention to theatre technique and discipline

Avoid hypothermia perioperatively and ensure supplemental oxygenation in recovery

Scrubbing and skin preparation

For the rst operation of the day, aqueous antiseptics should be used for hand washing, and the scrub should include the nails.

Subsequent scrubbing should merely involve washing to the elbows, as repeated extensiv e scrubbing releases more organisms than it

removes.

One application of an alcoholic antiseptic is adequate for skin preparation of the o perative site. This leads to a more than 95 per cent

reduction in bacterial count. Antiseptics in common use are listed in Table 5.6.

Theatre technique and discipline also contribute to low infection rates. Numbers of staff in th e 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 theatre ventilation, instrument

sterilisation and aseptic technique. Operator skill in gentle manipulation and dissection of tissu es is much more difcult to audit, but dead

spaces and haematomas should be avoided and the use of diathermy kept to a min imum. There is no evidence that drains, incision drapes

or wound guards help to reduce wound infection.

There is the highest level of evidence-based medicine that the perioperative avoidance of h ypothermia and supplemental oxygen during

recovery can signicantly reduce the rate of SSIs.

Postoperative care of wounds

Similar attention to standards is needed in the postoperative care of wounds. Seconda ry (exogenous) SSIs, as well as other HAIs, can be

related to poor hospital standards. For example, outbreaks of MRSA infections are rare but serious. The presence of this organism in

wounds, and the number of MRSA bacteraemias, can be a marker of inadequate posto perative wound care, and it can be very difcult

and expensive to screen for, identify and eradicate.

Careful audit should lead to changes in practice, and follow up should ensure that audit loops are closed. It is critical that surgeons

manage their own audit; league tables kept by nonmedical or related personnel must be accurate. Scoring systems are useful in audit but,

in general, have only been used in wound infection research (Tables 5.2 and 5 .3). Nevertheless, accurate audit ought to involve the use of

trained, blinded observers in post-discharge surveillance of all HAIs, using validated and reproducible denitions.

CLASSIFICATION OF SURGICAL WOUNDS

Potential for infection

The best measure of wound contamination at the end of an operation is to sample tissue in the wound edge. The theoretical degree of

contamination, proposed by the National Research Council (USA) over 40 year s ago, relates well to infection rates (Table 5.7). When

wounds are heavily contaminated or when an incision is made into an abscess, therapeutic antib iotics may be justied. In these cases,

infection rates of more than 15 per cent are expected. There is undisputed evidence that prophylactic antibiotics are effective in clean-

contaminated and contaminated operations. Infection rates after non-prosthetic c lean surgery may be higher than expected when

carefully audited by post-discharge surveillance. Breast surgery, for example, is associated wit h a high risk of infection, or wound

complications, which may be interpreted

Bacteria involved in surgical infection 63

Figure 5.16 Streptococci.

Figure 5.17 Staphylococcal pus.

Table 5.7 Surgical site infection (SSI) rates relating to wound contamination.

Type of surgery Infection rate (%)

Rate before prophylaxis Clean (no viscus opened)

Clean-contaminated (viscus opened, minimal spillage) 1–2 <10

Contaminated (open viscus with spillage or inammatory disease) Dirty (pus or perfora tion, or incision through an abscess) 15–20 <40

The same

Gastric surgery up to 30% Biliary surgery up to 20% Variable but up to 60% Up to 6 0% or more

as a failure to heal and related to a high body mass index (BMI). The value of antibiotic prophylaxis is controversial in non-prosthetic

clean surgery, with most trials showing no clear benet.

BACTERIA INVOLVED IN SURGICAL INFECTION

Streptococci

Streptococci form chains and are Gram positive on staining (Figure 5.16). The most impo rtant is the β-haemolytic Streptococcus, which

resides in the pharynx of 5–10 per cent of the population. In the Lanceeld A–G carbohydrate a ntigens classication, it is the group A

Streptococcus, also called Streptococcus pyogenes, that is the m ost pathogenic. It has the ability to spread, causing cellulitis, and to

cause tissue destruction through the release of enzymes such as streptolysin, streptokina se and streptodornase.

Streptococcus faecalis is an enterococcus in Lanceeld group D. It is often found in synergy with other organisms, as is 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 suit able alternative in patients who are

allergic to penicillin.

The name Eusol is derived from Edinburgh University solution of lime. Rebecca Graighill Lancefield, 1895–1981, an American bacteriologist, classified streptococ ci in

1933.

Staphylococci

Staphylococci form clumps and are Gram positive (Figure 5.17). Staphylococcus aur eus is the most important pathogen in this group and

is found in the nasopharynx of up to 15 per cent of the population. It can cause ex ogenous suppuration in wounds (and implanted

prostheses). Strains resistant to antibiotics (e.g. MRSA) can cause epidemics and more sev ere infection. It is controversial but, if MRSA

infection is found in a hospital, all doctors, nurses and patients may need to be swabbe d so that carriers can be identied and treated. In

parts of northern Europe, the prevalence of MRSA infections has been kept at ver y low levels using ‘search and destroy’ methods, which

use these screening techniques and the isolation or treatment of carriers. Patients found to be pos itive on screening may be denied access

to hospital. Some MRSA strains are now also resistant to vancomycin. Local policies on the management of MRSA depend on the

prevalence of MRSA, the type of hospital or clinical specialty and the availability of facilities. W idespread swabbing, ward closures,

isolation of patients and disinfection of wards all have to be carefully considered and involv e all groups of practitioners. They may be

expensive but necessary options.

Infections are usually suppurative and localised (see above under Abscess). Most hospita l Staphylococcus aureus strains are now β-

lactamase producers and are resistant to penicillin, but most strains (MRSA) remain sensitive to ucloxacillin, vancomycin,

aminoglycosides, some cephalosporins and fusidic acid (used in osteomyelitis). There are sever al novel and innovative antibiotics

becoming available that have high activity against resistant strains. Some have th e advantage of good oral activity (linezolid), some have

a wide spectrum (tigecycline), have good activity in bacteraemia (daptomycin) but are relatively expensive, and some have side effects

involving marrow, hepatic and renal toxicity. Their use is justied but needs to be controlled b y tight local policies and guidelines that

involve clinical microbiologists.

Staphylococcus epidermidis (previously Staphylococcus albus), also known as coagulase-negative staphylococci (CNS), was regarded as

a commensal but is now recognised as a major threat in prosthetic (vascular a nd orthopaedic) surgery and in indwelling vascular

catheters. They can be multiply resistant (MRCNS) to many antibiotics and represent an importa nt cause of HAI.

Clostridia

Clostridial organisms are Gram-positive, obligate anaerobes, which produce r esistant spores (Figure 5.18). C. perfringens is the cause of

gas gangrene, and C. tetani causes tetanus after implantation into tissues or a wound (see above under Specic wound infections).

C. difcile is the cause of pseudomembranous colitis. This is another HAI, now m ore common than the incidence of MRSA bacteraemia,

which is caused by the overuse of antibiotics. The quinolones, such as ciprooxacin, seem to be most implicated, but the inappropriate

sequential use of several antibiotics puts patients most at risk, particularly in elderly or im munocompromised patients. The key symptom

of bloody diarrhoea can occur in small epidemics through poor hygiene. In its most se vere form, colitis may lead to perforation and the

need for emergency colectomy, with an associated high mortality. Treatment involve s resuscitation and antibiotic therapy with

metronidazole or vancomycin. The brinous exudate is typical and differentia tes the colitis from other inammatory diseases; the

laboratory recognition of the toxin is an early accurate diagnostic test.

Aerobic Gram-negative bacilli

These bacilli are normal inhabitants of the large bowel. E. 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 af ter bowel operations (in particular,

appendicitis, diverticulitis and peritonitis). E. coli is a major cause of the HAI of urinary tr act infection, although most aerobic Gram-

negative bacilli (AGNB) may be involved, particularly in relation to urinary catheterisati on. There is increasing concern about the

development of ESBLs in many of this group

Figure 5.18 Clostridium tetani (drumstick spores).

of bacteria, which confer resistance to many antibiotics, particularly cephalosporins.

Pseudomonas spp. tend to colonise burns and tracheostomy wounds, as well as the urina ry tract. Once Pseudomonas has colonised wards

and intensive care units, it may be difcult to eradicate. Surveillance of cross-infection is important in outbreaks. Hospital strains

become resistant to β-lactamase as resistance can be transferred by plasmids. Wound infectio ns need antibiotic therapy only when there is

progressive or spreading infection with systemic signs. The aminoglycosides are effectiv e, but some cephalosporins and penicillin may

not be. Many of the carbapenems (e.g. meropenem) are useful in severe infectio ns, whereas the quinolones have been made ineffective

through their overuse and the development of ESBLs.

Bacteroides

Bacteroides are non-spore-bearing, strict anaerobes that colonise the large bowel, vagina an d oropharynx. Bacteroides fragilis is the

principal organism that acts in synergy with AGNB to cause SSIs, including intra-abdominal abs cesses, after colorectal or

gynaecological surgery. They are sensitive to the imidazoles (e.g. metronidazole) and so me cephalosporins (e.g. cefotaxime).

PRINCIPLES OF ANTIMICROBIAL TREATMENT

Antimicrobials may be used to prevent (see above under Prophylaxis) or treat establishe d surgical infection (Summary box 5.16).

Summary box 5.16

Principles for the use of antibiotic therapy

Antibiotics do not replace surgical drainage of infection Only spreading infection or signs of systemic infe ction justifies 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 r ecognition and determination of the sensitivities

of the causative organisms. Antibiotic therapy should not be held back if it is indicate d, the choice being empirical and later modied

depending on microbiological ndings. However, once antibiotics have been administer ed, the clinical picture may become confused

and, if a patient’s condition does not rapidly improve, the opportunity to make a precise diagnosis may have been lost. It is unusual to

have to treat SSIs with antibiotics, unless there is evidence of spreading infection, bacterae mia or systemic complications (SIRS and

MODS). The appropriate treatment of localised SSIs is interventional radiological drainage of pu s or open drainage and debridement.

Theodor Albrecht Edwin Klebs , 1834–1913, Professor of Bacteriology successively at Prague, Cze choslovakia; Zurich, Switzerland; and The Rush Medical College,

Chicago, IL, USA.

Antibiotics used in treatment and prophylaxis of surgical infection 65

There are two approaches to antibiotic treatment:

1 A narrow-spectrum antibiotic may be used to treat a known sensitive infectio n; for example, MRSA (which may be isolated from

pus) is usually sensitive to vancomycin or teicoplanin, but not ucloxacillin.

2 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, durin g and following emergency surgery requiring the

opening of perforated or ischaemic bowel, any of the gut organisms may be respo nsible for subsequent peritoneal or bacteraemic

infection. In this case, a triple-therapy combination of broad-spectrum penicillin (suc h as ampicillin or mezlocillin) with an

aminoglycoside (such as gentamicin) and metronidazole, may be used per- and po stoperatively to support the patient’s own body

defences.

An alternative to the penicillins is a cephalosporin, e.g. cefuroxime. Other alternatives ar e piperacillin and tazobactam in combination or

monotherapy using a carbapenem. The use of such broad-spectrum antibiotic strateg ies should be guided by specialist microbiological

advice.

In surgical units in which resistant Pseudomonas or other Gram-negative species (su ch as Klebsiella) have become ‘resident

opportunists’, it may be necessary to rotate anti-pseudomonal and anti-Gram-negative a ntibiotic therapy (Summary box 5.17).

Summary box 5.17

Treatment of commensals that have become opportunist pathogens

They are likely to have multiple antibiotic resistance It may be necessary to rotate antibiotics

The use of these routines, subsequent wound infection and the alternation of combinations of ch emotherapy should be monitored by the

infection control team and local hospital protocols. In treating patients who have surgica l infection with systemic signs (SIRS and

MODS), a failure to respond to antibiotics may indicate that there has been a failure of i nfection source control. If response is poor after

3–4 days, there should be a re-evaluation with a review of charts and further investigat ions requested to exclude the development or

persistence of infection such as a collection of pus.

New antibiotics should be used with caution and, wherever possible, sensitivities shoul d rst be obtained. There are certain general rules

on which the choice of antibiotics may be based. For example, it is unusual for Pseudomonas aerug inosa to be found as a primary

infecting organism unless the patient has had surgical or hospital treatment. Local antibiotic sensitivity patterns vary from centre to

centre and from country to country, and the sensitivity patterns of common p athogens should be known to the hospital microbiologist

who should be involved.

ANTIBIOTICS USED IN TREATMENT AND PROPHYLAXIS OF SURGICAL INFECTION

Antimicrobials may be produced by living organisms (antibiotics) or by synthetic metho ds. Some are bactericidal, e.g. penicillins and

aminoglycosides, and others are bacteriostatic, e.g. tetracycline and erythromycin. In general, p enicillins act upon the bacterial cell wall

and are most effective against bacteria that are multiplying and synthesising new cell wal l materials. The aminoglycosides act at the

ribosomal level, preventing or distorting the production of proteins required to maintain the inte grity of the enzymes in the bacterial cell.

Hospital and Formulary guidelines should be consulted for doses and monitoring of antibiotic therapy.

Penicillin

Benzylpenicillin has proved most effective against Gram-positive pathogens, including m ost streptococci, the clostridia and some of the

staphylococci that do not produce β-lactamase. It is still effective against Actinomyces , which is a rare cause of chronic wound infection,

and may be used specically to treat spreading streptococcal infections. Penicillin is valua ble even if other antibiotics are required as part

of multiple therapy for a mixed infection. All serious infections, e.g. gas gangrene, require hi ghdose intravenous benzylpenicillin.

Flucloxacillin

This is a β-lactamase-resistant penicillin and is therefore of use in treating most com munity-acquired staphylococcal infections, but it has

poor activity against other pathogens.

Ampicillin and amoxicillin

These β-lactam penicillins can be taken orally or may be given parenterally. B oth are effective against Enterobacteriaceae, Enterococcus

faecalis and the majority of group D streptococci, but not species of Klebsiella or pseudom onads. Their use is now rare as there are more

effective alternatives.

Mezlocillin and azlocillin

These are ureidopenicillins with good activity against species of Enterobacter and Klebsiella. Azlocil lin is effective against

Pseudomonas. Each has some activity against Bacteroides and enterococci, but all are susceptible to β-lactamases. Combined with an

aminoglycoside, mezlocillin is a valuable treatment for severe mixed infections, particularly those caused by Gramnegative organisms in

immunocompromised patients.

Clavulanic acid is available combined with amoxicillin (Augmentin) and can be taken orally. This antiβ-lactamase protects amoxicillin

from inactivation by β-lactamaseproducing bacteria. It is of value in treating infections c aused by Klebsiella strains and β-lactamase-

producing E. coli but is not active against Pseudomonas spp. It can be used for localised cellulitis or supercial staphylococcal infections

and infected human and animal bites. It is available for oral or intravenous th erapy.

Cephalosporins

There are several β-lactamase-susceptible cephalosporins that are of value in surgic al practice: cefuroxime, cefotaxime and ceftazidime

are widely used. The rst two are most effective in intra-abdominal skin and soft-tissue i nfections, 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 S. aureus , is also effective against P. aeruginosa. These

cephalosporins may be combined with an aminoglycoside, such as gentamicin, and an imid azole, such as metronidazole, if anaerobic

cover is needed. Newer cephalosporins may be effective against organisms such as MR SA, but their spectra are usually limited.

Aminoglycosides

Gentamicin and tobramycin have similar activity and are effective against Gram-negativ e Enterobacteriaceae. Gentamicin is effective

against many strains of Pseudomonas, although resistance has been recognised. A ll aminoglycosides are inactive against anaerobes and

streptococci. Serum levels immediately before and 1 hour after intramuscular injection must be taken 48 hours after the start of therapy,

and dosage should be modied to satisfy peak and trough levels. Ototoxicity and nephrotoxicity m ay follow sustained high toxic levels.

These antibiotics have a marked post-antibiotic effect, and single, large doses are effectiv e and may be safer. Use needs to be discussed

with the microbiologist, and local policies should be observed.

Vancomycin

This glycopeptide is most active against Gram-positive bacteria and has proved to be effect ive against MRSA, although vancomycin

resistance is increasingly being reported. However, it is ototoxic and nephrotoxic, so serum levels should be monitored. It is effective

against C. difcile in cases of pseudomembranous colitis.

Imidazoles

Metronidazole is the most widely used member of the imidazole group and is active aga inst all anaerobic bacteria. It is particularly safe

and may be administered orally, rectally or intravenously. Infections caused by anae robic cocci and strains of Bacteroides and clostridia

can be treated, or prevented, by its use. Metronidazole is useful for the prophylaxis and trea tment of anaerobic infections after abdominal,

colorectal and pelvic surgery.

Carbapenems

Meropenem, ertapenem and imipenem are members of the carbapenems. They are s table to β-lactamase, have useful broadspectrum

anaerobic as well as Gram-positive activity and are effective for the treatment of resistant or ganisms, such as ESBLresistant urinary tract

infections or serious mixed-spectrum abdominal infections (peritonitis).

Quinolones

Quinolones, such as ciprooxacin, were active against a wide spectrum of organisms. Their wid espread use has been related to the

development of resistant organisms, and their role in treating surgical infection is limited.

HUMAN IMMUNODEFICIENCY VIRUS, AIDS AND THE SURGEON

The type I human immunodeciency virus (HIV) is one of the viruses of surgical imp ortance as it can be transmitted by body fluids,

particularly blood. It is a retrovirus that has become increasingly prevalent through sexual transmission, both homo- and heterosexual, in

intravenous drug addiction, through infected blood in treating haemophiliacs, in particu lar, and in subSaharan Africans. The risk in

surgery is probably mostly through ‘needle stick’ injury during operations.

After exposure, the virus binds to CD4 receptors with a subsequent loss of CD4

cells, T-helper cells and other cells involved in cell-

mediated immunity, antibody production and delayed hypersensitivity. Macrophages and g ut-associated lymphoid tissue (GALT) are

also affected. The risk of opportunistic infections (such as Pneumocystis carinii pneumonia, tuberculosis and cytomegalovirus) and

neoplasms (such as Kaposi’s sarcoma and lymphoma) is thereby increased.

In the early weeks after HIV infection, there may be a u-like illness and, during the phas e of seroconversion, patients present the

greatest risk of HIV transmission. It is during these early phases that drug treatment, highly a ctive anti-retroviral therapy (HAART), is

most effective through the ability of these drugs to inhibit reverse transcriptase and p rotease synthesis, which are the principal

mechanisms through which HIV can progress. Within two years, untreated HIV can progress to AIDS in 25–35 per cent of patients,

which is considered to be fatal.

Involvement of surgeons with HIV

patients (universal precautions)

Patients may present to surgeons for operative treatment if they have a surgical disease and they are known to be infected or ‘at risk’, or

because they need surgical intervention related to their illness for vascular access or a biopsy wh en they are known to have HIV infection

or AIDS. Universal precautions have been drawn up by the CDC in the United State s and largely adopted by the NHS in the UK (in

summary):

• when there is a risk of splashing, particularly with power tools, use of a full face mask ideally, or protective spectacles;

• use of fully waterproof, disposable gowns and drapes, particularly during sero conversion;

• boots to be worn, not clogs, to avoid injury from dropped sharps;

• double gloving needed (a larger size on the inside is more comfortable);

• allow only essential personnel in theatre;

• avoid unnecessary movement in theatre;

• respect is required for sharps, with passage in a kidney dish;

• a slow meticulous operative technique is needed with minimised bleeding.

After contamination

Needle-stick injuries are most common on the non-dominant index nger durin g operative surgery. Hollow needle injury carries the

greatest risk of HIV transmission. The injured part should be washed under running water and the incident reported. Local policies

dictate whether post-exposure HAART should be given. Occupational advice is requ ired after high-risk

Sub-Saharan Africans come from that part of the African continent which lies south of the Sahara Desert. Human immunodeficiency virus, AIDS and the

surgeon 67

exposure together with the need for HIV testing and the option for continuation in an operative s pecialty.

FURTHER READING

Cohen J, Powderly WG, Opal SM. Infectious diseases. St Louis, MO: Mosby, 2010.

Fraise AP, Bradley C. Ayliffe’s control of healthcare associated infection: a practical handbook. London: Hodder Arnold, 2009.

Fry DE. Surgical infections. Boston, MA: Little, Brown & Co, 1995.

Goering R, Dockrell H, Zuckerman M et al. Mims’ medical microbiology , 4th edn. St Louis, MO: Mosby, 2007.

Greenwood D, Slack RCB, Peutherer JF, Barer MR. Medical microbiology: a guide to microbia l infections: pathogenesis, immunity,

laboratory diagnosis and control. Edinburgh: Churchill Livingstone, 2007.

Howard RJ, Simmons RL. Surgical infectious diseases, 3rd edn. East Norwalk, CT: Allyn & Bacon, 1995 .

Kumar V, Abbas A, Aster J. Robbins and Cotran pathologic basis of disease, 8th edn. Philadelphia, PA: Saunders Elsevier, 2009.

Majno G. The healing hand. Man and wound in the ancient world. Cambridge, MA: Harvard Univ ersity Press, 1991.

Mandell GL, Bennett JE, Dolin R. Principles and practice of infectious diseases. Edinburgh: Chu rchill Livingstone, 2004.

Torok E, Moran E, Cooke F. Oxford handbook of infectious diseases and microbiology. Oxford : Oxford University Press, 2009.

Williams JD, Taylor EW. Infection in surgical practice. London: Hodder Arnold, 2003.

CHAPTER

6Surgery in the tropics

LEARNING OBJECTIVES

To be aware of:

• The common surgical conditions that occur in the tropics

To appreciate:

• That many patients do not seek medical help until late in the course of the d isease

To know:

• The emergency presentations of the various conditions as patients in developing cou ntries do not seek treatment until they are very ill

To be able to:

• Diagnose and treat these conditions, particularly as emergencies, because of th e ease of global travel, visitors from the tropics would

mostly present as an emergency in Western hospitals

To realise:

• That ideal management needs good teamwork between the surgeon, physician, radiol ogist, pathologist and microbiologist. In case of

doubt in a difficult situation, there should be no hesitation in seeking help from London Scho ol of Hygiene and Tropical Medicine or

Liverpool School of Tropical Medicine, the nation’s foremost tropical medicine institutions.

INTRODUCTION

Most surgical conditions in the tropics are associated with parasitic infestations. With the e ase of international travel, diseases that are

common in the tropics and developing countries may be seen in the UK, especially p resenting as emergencies.

This section deals with the conditions that a surgeon might occasionally encounter in a visito r to these shores. The life cycles of the

parasites will not be dealt with. For academic interest readers are, however, advised to r efer to the 24th edition of this book should they

wish 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 Central and

South America where almost half the population is infected. The majority remain asymp tomatic 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 most common ext raintestinal manifestation, occurs in less than 10

per cent 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.

Pathogenesis

The organism enters the gut through food or water contaminated with the cyst. In the sm all bowel, the cysts hatch, and a large number of

trophozoites are released and carried to the colon where ask-shaped ulcers form in the subm ucosa. 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 enzymes produced by the

trophozoites. The areas of necrosis eventually coalesce to form the abscess cavity. The te rm ‘amoebic hepatitis’ is used to describe the

microscopic picture in the absence of macroscopic abscess, a differentiation only in theo ry as the medical treatment is the same.

The right lobe is involved in 80 per cent of cases, the left in 10 per cent and th e rest are multiple. Involvement of the right lobe of the

liver is more common possibly because 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 t he right lobe. This may cause pulmonary

symptoms and chest complications. The abscess cavity contains chocolate-coloured, odo urless,

Amoebiasis 69

‘anchovy sauce’-like uid that is a mixture of necrotic liver tissue and blood. There m ay be secondary infection of the abscess. This

causes the pus to smell. While pus in the abscess is sterile unless secondarily infected, trophozoite s 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 larg e bowel, most commonly seen in the caecum,

called an amoeboma (Summary box 6.1).

Summary box 6.1

Amoebiasis – pathology

Entamoeba histolytica is the most common pathogenic amoeba in man

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 producing flask-shaped ulcers In the portal circulation, the parasite causes

liquefactive necrosis in the liver producing an abscess. This is the most common extraintestinal mani festation

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 on set of non-specic symptoms such as

abdominal pain, anorexia, fever, night sweats, malaise, cough and weight loss; these symptom s gradually progress to more specic

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 ab dominal rigidity, tender hepatomegaly, tender

and bulging intercostal spaces, overlying skin oedema, a pleural effusion and basal pneu monitis – the last feature is usually a late

manifestation. Occasionally, a tinge of jaundice or ascites may be present. Rarely, the patient ma y present as an emergency due to the

effects of rupture into the peritoneal, pleural or pericardial cavity.

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 c ourse, a situation that arises from indiscriminate

self-medication, particularly in developing countries.

This can easily be mistaken for a carcinoma. An amoeboma should be suspected w hen 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 diar rhoea. Such a patient is highly unlikely

to have a carcinoma as altered bowel habit is not a feature of right-sided colonic carcinoma .

Investigations

The haematological and biochemical investigations reect the presence of a chronic infec tive process: anaemia, leukocytosis, raised

inammatory markers – erythrocyte sedimentation rate (ESR) and C-reactive protein (C RP) – hypoalbuminaemia and deranged liver

function tests, particularly elevated alkaline phosphatase.

Serological tests are more specic, with the majority of patients showing antibodies in serum. These can be detected by tests for

complement xation, indirect haemagglutination (IHA), indirect immunouorescence an d enzyme-linked immunosorbent assay

(ELISA). They are extremely useful in detecting acute infection in non-endemic areas. IHA has a very high sensitivity rate in acute

amoebic liver abscess in non-endemic regions and remains elevated for some time. The persist ence of antibodies in a large majority of

the population in endemic areas precludes its use there as a diagnostic investigation. In these cases, tests such as counter-

immunoelectrophoresis are more useful for detecting acute infection.

An outpatient rigid sigmoidoscopy (using a disposable instrument) can be very useful, p articularly if the patient complains of bloody

mucoid diarrhoea. Most amoebic ulcers occur in the rectosigmoid and are therefore with in reach of the sigmoidoscope; shallow skip

lesions and ‘ask-shaped’ 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 distinguish es 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-dened borders; internal echoes suggest

necrotic material or debris (Figure 6.1). The investigation is very accurate and is used f or aspiration, both diagnostic and therapeutic.

Where there is doubt about the diagnosis, a computed tomography (CT) scan may be helpf ul (Figure 6.2).

Diagnostic aspiration is of limited value except for establishing the typical colour of the a spirate, which is sterile and odourless unless it

is secondarily infected.

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

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.

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 colonos copy and biopsy are mandatory as the

radiological and macroscopic appearance may be indistinguishable from a carcino ma. In doubtful cases, vigorous medical treatment is

given, and the patient’s colon is imaged again in 3–4 weeks, as these masses are known to regres s completely on a full course of drug

therapy. If symptoms persist even partially following full medical treatment in a patient who ha s recently returned from an endemic area,

a colonic carcinoma must be excluded forthwith. This is because a dormant coloni c carcinoma may become apparent as a result of

infestation with amoebic dysentery causing ‘traveller’s diarrhoea’. However, it must be borne i n mind that an amoeboma and carcinoma

can coexist (Summary box 6.2).

Summary box 6.2

Diagnostic pointers for infection with

Entamoeba histolytica

Bloody mucoid diarrhoea in a patient from an endemic area or following a recent visit to such a country Upper ab dominal pain, fever, cough, malaise

In chronic cases, a mass in the right iliac fossa = amoeboma

Sigmoidoscopy shows typical ulcers – biopsy and scraping may be diagnostic

Serological tests are highly sensitive and specific outside endemic areas

Ultrasound and CT scans are the imaging methods of choice

Treatment

Medical treatment is very effective and should be the rst choice in the elective sit uation, with surgery being reserved for complications.

Metronidazole and tinidazole are the effective drugs. After treatment with metronidaz ole and tinidazole, diloxanide furoate, which is not

effective against hepatic infestation, is used for 10 days to destroy any intestinal amo ebae.

Aspiration is carried out when imminent rupture of an abscess is expected. A spiration also helps in the penetration of metronidazole, and

so reduces the morbidity when carried out with drug treatment in a patient with a large abs cess. If there is evidence of secondary

infection, appropriate drug treatment is added. The threshold for aspirating an abscess in the left lobe is lower because of its predilection

for rupturing into the pericardium.

Surgical treatment should be reserved for the complications of rupture into the pleural (usually th e right side), peritoneal or pericardial

cavities. Resuscitation, drainage and appropriate lavage with vigorous medical treatme nt are the key principles. In the large bowel,

severe haemorrhage and toxic megacolon are rare complications. In these patients, the g eneral principles of a surgical emergency apply.

Resuscitation is followed by resection of bowel with exteriorisation. Then the patient is given vig orous supportive therapy. All such

cases are managed in the intensive care unit as would any patient with toxic meg acolon whatever the cause.

An amoeboma that has not regressed after full medical treatment should be managed wi th a colonic resection, particularly if cancer

cannot be excluded (Summary box 6.3).

Summary box 6.3

Amoebiasis – treatment

Medical treatment is very effective

In large abscesses, repeated aspiration is combined with drug treatment

Surgical treatment is reserved for complications such as rupture into the pleural, peritoneal or peri cardial cavities Acute toxic megacolon and severe haemorrhage are

intestinal complications that are treated with intensive supportive therapy followed by resection and exter iorisation When an amoeboma is suspected in a colonic mass,

cancer should be excluded by appropriate imaging and biopsy

Ascaris lumbricoides (roundworm) 71

ASCARIS LUMBRICOIDES (ROUNDWORM)

giopancreatography (MRCP), an adult worm may be seen in the common bile duct in a patient pr esenting with features of obstructive

jaundice (Figure 6.6) (Summary box 6.4).

Introduction

Ascaris lumbricoides, commonly called the roundworm, is the most common intestinal nematode to infest humans and affects a quarter

of the world’s population. The parasite causes pulmonary symptoms as a larva and inte stinal symptoms as an adult worm.

Pathology and life cycle

The eggs can survive in a hostile environment for a long time. The hot and humid cond itions in the tropics are ideally suited for the eggs

to turn into embryos. The fertilised eggs are present in soil contaminated with infecte d 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 process of maturation takes 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 worm migrates from the tra cheobronchial tree into the

oesophagus, thus nding its way into the gastrointestinal tract, from where it can migrate to the common bile duct or pancreatic duct.

The mature female, once in the small bowel, produces innumerable 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, d yspnoea and fever – referred to as Loefer’s

syndrome. The adult worm can grow up to 45 cm long. Its presence in the small intestin e causes malnutrition, failure to thrive and

abdominal pain. Worms that migrate into the common bile duct can produce ascending cholan gitis and obstructive jaundice, while

features of acute pancreatitis may be caused by a worm in the pancreatic duc t.

Small intestinal obstruction can occur, particularly in children, due to a bolus of adult wo rms incarcerated in the terminal ileum. This is a

surgical emergency. Rarely, perforation of the small bowel may occur from ischaemic pressu re 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 trop ical developing country, or one who has

recently returned after spending some time in an endemic area, presents with pulmonary, gastroin testinal, hepatobiliary and pancreatic

symptoms, ascariasis infestation should be high on the list of possible diagnoses.

Investigations

Increase in the eosinophil count is common, in keeping with most parasitic infestations. Stool exam ination may show ova. Sputum or

bronchoscopic washings may show Charcot–Leyden crystals or the larvae.

Chest x-ray may show fluffy exudates in Loefer’s syndrome. A barium meal and follow-thro ugh may show a bolus of worms in the

ileum or lying freely within the small bowel (Figure 6.4). An ultrasound may show a worm in th e common bile duct (Figure 6.5) or

pancreatic duct. On magnetic resonance cholan

Summary box 6.4

Ascariasis – pathogenesis

It is the most common intestinal nematode affecting humans Typically found in a humid atmosphere and p oor sanitary conditions; hence is seen in the tropics and

developing countries

Larvae cause pulmonary symptoms; adult worms cause gastrointestinal, biliary and pancreatic symptoms Distal i leal obstruction due to bolus of worms; ascending

cholangitis and obstructive jaundice from infestation of the common bile duct

Acute pancreatitis when a worm is lodged in the pancreatic duct

Perforation of the small bowel is rare

Treatment

The pulmonary phase of the disease is usually self-limiting and requires sympt omatic treatment only. For intestinal disease, patients

should ideally be under the care of a physician for treatment with anthelmintic drugs. C ertain 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 obstru ction should be given a trial of conservative

management in the form of intravenous uids, 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 regimen, and when

perforation is suspected. At laparotomy, the bolus of worms in the terminal ileum is milk ed through the ileocaecal valve into the colon

for natural passage in the stool. Postoperatively, hypertonic saline enemas may help in th e extrusion of the worms. Strictures, gangrenous

areas or perforations need resection and anastomosis. If the bowel wall is healthy, enter otomy and removal of the worms may be

performed (Figure 6.7).

As a result of perforation due to roundworm, the parasites may be found lying free in the peri toneal cavity. The site of perforation may

be brought out as an ileostomy because, in the presence of a large number of worms, closure or an anastomosis may be at risk of

breakdown from the activity of the worms. Exteriorisation, although the ideal operation in severe sepsis, is unfortunately sometimes not

done because of the reluctance on the part of the patient to accept such a procedure as goo d stoma care is not always available and follow

up inadequate in developing countries. In such circumstances, resection of the diseased ileum, closure of the distal bowel and end-to-side

ileotransverse anastomosis is a good alternative.

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 tubercul ous stricture, and the presence of roundworms is an

incidental nding. Such a patient requires the appropriate surgery depending upon the pathology.

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.

BARIUM SEEN INSIDE THE ROUNDWORM

Figure 6.4 Barium meal and follow-through showing roundworms in the course of the small bowel with barium seen inside the wo rms 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).

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 (ERCP), part of the worm was seen outside the ampulla in the duodenum and was removed through the endoscope.

Subsequent laparoscopic cholecystectomy was uneventful.

Figure 6.6 Magnetic resonance cholangiopancreatography (MRCP) showing a roundworm in the common bile d uct (CBD). The worm could not be removed

endoscopically. The patient underwent an open cholecystectomy and exploration of the CBD.

Figure 6.7 Roundworms removed at laparotomy in a 16-year-old patient who presented with acute intestinal obstruction (co urtesy of the Pathology Museum, Calcutta

Medical Research Institute, Kolkata, India).

Common bile duct or pancreatic duct obstruction from a roundworm can be tre ated by endoscopic removal, failing which open

exploration of the common bile duct is necessary. Cholecystectomy is also carried out. A full course of anti-parasitic treatment must

follow any surgical intervention (Summary box 6.5).

Summary box 6.5

Ascariasis – diagnosis and management

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

Conservative management with anthelmintics is the first line of treatment even in obstruction

Surgery is a last resort – various options are available

Filariasis 73

ASIATIC CHOLANGIOHEPATITIS

Summary box 6.6

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 among those living in the major sea ports and river estuaries. The

organism, which is a type of liver uke, resides in snails and fish that act as intermedia te hosts. Ingestion of infected sh and snails when

eaten raw or partly cooked causes the infection in humans and other sh-eating mammals, w hich are the denitive hosts.

Pathology

In humans, the parasite matures into the adult worm in the intra hepatic biliary r adicles where they may reside for many years. The

intrahepatic bile ducts are dilated with epithelial hyperplasia and periductal brosis. These c hanges may lead to dysplasia causing

cholangiocarcinoma – the most serious complication of this parasitic infestation.

The eggs or dead worms may form a nidus for stone formation in the gall bladder or co mmon bile duct, which becomes thickened and

much dilated in the late stages. Intrahepatic bile duct stones are also caused by the paras ite 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-specic, suc h as fever, malaise, anorexia and upper

abdominal discomfort. The complete clinical picture can consist of fever with rigors due to as cending cholangitis, obstructive jaundice

due to stones, biliary colic and pruritis. Acute pancreatitis may occur because of obstruc tion of the pancreatic duct by an adult worm. If

any person or an emigrant to the West from an endemic area complains of symptoms of biliary tract disease, Clonorchis infestation

should be considered in the differential diagnosis.

In advanced cases, liver function tests are abnormal. Conrmation of the condition is by exam ination of stool or duodenal aspirate, which

may show the eggs or adult worms. Ultrasound scan ndings can be characteristic, sho wing the uniform dilatation of small peripheral

intrahepatic bile ducts with only minimal dilatation of the common hepatic and co mmon bile ducts, although the latter are much more

dilated when the obstruction is caused by stones. The thickened duct walls show inc reased echogenicity and non-shadowing echogenic

foci in the bile ducts representing the worms or eggs. Endoscopic retrograde c holangiopancreatography (ERCP) will conrm these

ndings (Summary box 6.6).

Treatment

Praziquantel and albendazole are the drugs of choice. However, the surgeon f aces a challenge when there are stones not only in the gall

bladder but also in the common bile duct. Cholecystectomy with exploration of the comm on bile duct is performed when indicated.

Repeated washouts are necessary during the exploration, as the common bile du ct is dilated and

Asiatic cholangiohepatitis – pathogenesis and diagnosis

Occurs in the Far Eastern tropical zones

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 hepatobiliary system and ERCP are a lso diagnostic

contains stones, biliary debris, sludge and mud. This should be followed by c holedochoduodenostomy. As this is a disease with a

prolonged and relapsing course, some surgeons prefer to do a choledochojeju nostomy to a Roux loop. The Roux loop is brought up to

the abdominal wall, referred to as ‘an access loop’, which allows the interventional ra diologist to deal with any future stones.

As a public health measure, people who have emigrated to the West from an endemi c area should be offered screening for Clonorchis

infestation in the form of ultrasound of the hepatobiliary system. This condition can be d iagnosed and treated and even cured when it is in

its subclinical form. Most importantly, the risk of developing the dreadful disease of ch olangiocarcinoma is eliminated (Summary box

6.7).

Summary box 6.7

Asiatic cholangiohepatitis – treatment

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 mig rants to the West from endemic areas

FILARIASIS

Introduction

Filariasis is mainly caused by the parasite Wuchereria bancrofti carried by the mosquito. A variant of the parasite called Brugia malayi

and B. timori is responsible for causing the disease in about 10 per cent of suff erers. The condition affects more than 90 million people

worldwide, two-thirds of whom live in India, China and Indonesia. According to the World Health Organization (WHO), lariasis is the

second most common cause, after leprosy, of long-term disability.

Once bitten by the mosquito, the matured eggs enter the human circulation to hatch an d grow into adult worms; the process of

maturation takes about one year. The adult worms mainly colonise the lymphatic system.

Cesar Roux, 1857–1934, Professor of Surgery and Gynaecology, Lausanne, Switzerland, described this m ethod of forming a jejunal conduit in 1908. Figure 6.8 Left

lower limb filariasis – elephantiasis (courtesy of Professor Ahmed Hassan Fahal, Khartoum, Sudan).

Diagnosis

It is mainly males who are affected because females, in general, cover a greater part of their bod ies, thus making them less prone to

mosquito bites. In the acute presentation, there are episodic attacks of fever with lymphaden itis and lymphangitis.

Occasionally, adult worms may be felt subcutaneously. Chronic manifestations appear after repea ted acute attacks over several years.

The adult worms cause lymphatic obstruction resulting in massive lower limb oedem a. Obstruction to the cutaneous lymphatics causes

skin thickening, not unlike the ‘peau d’orange’ appearance in breast cancer, thus exacer bating the limb swelling. Secondary

streptococcal infection is common. Recurrent attacks of lymphangitis cause brosis of the lymph channels, resulting in a grossly swollen

limb with thickened skin producing the condition of elephantiasis (Figure 6.8). Bilateral lower limb lariasis is often associated with

scrotal and penile elephantiasis. Early on, there may be a hydrocoele underlying scrota l lariasis (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 superuous. Eosinophilia is common, and a nocturnal peripheral blood smear ma y show the immature forms or microlariae. The

parasite may also be seen in chylous urine, ascites and hydrocoele uid.

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, intermit

Figure 6.9Filariasis of the scrotum (courtesy of Professor Ahmed Hassan Fahal, Khartoum, Sudan).

tent pneumatic compression helps, but the treatment has to be repeated over a prolonged perio d.

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 pro cedures are rarely successful (Summary box

6.8).

Summary box 6.8

Filariasis

Caused by Wuchereria bancrofti that is carried by the mosquito

Lymphatics are mainly affected, resulting in gross limb swelling

Eosinophilia; immature worms 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

HYDATID DISEASE

Introduction and pathology

Commonly called dog tape worm, hydatid disease is caused by Ecchinococcus granulosus. Wh ile it is common in the tropics, in the UK,

the occasional patient may come from a rural sheepfarming community.

The dog is the denitive host and, as a pet, is the most common 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

Otto Eduard Heinrich Wucherer , 1820–1873, a German physician who practised in Brazil, South Americ a. Peau d’orange is French for ‘orange skin’.

Joseph Bancroft, 1836–1894, an English physician who worked in Australia.

Figure 6.10 Computed tomographic scan showing a hydatid cyst of the pancreas. A differential dia gnosis of hydatid cyst or a tumour was considered. At exploration, the

patient was found to have a hydatid cyst, which was excised followed by a 30-month treatment with albendazole. The patient remains free of disease.

wall is digested, allowing the protoscolices to develop into adult worms. Close contact with th e infected dog causes contamination by the

oral route, with the ovum thus gaining entry into the human gastrointestinal tract.

(a)

The cyst is characterised by three layers, an outer pericyst derived from compresse d host organ tissues, an intermediate hyaline ectocyst

which is non-infective and an inner endocyst that is the germinal membrane a nd contains viable parasites which can separate forming

daughter cysts. A variant of the disease occurs in colder climates caused by Echino coccus 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) propose d a standardised ultrasound classication based

on the status of activity of the cyst. This is universally accepted, particularly because it h elps to decide on the appropriate management.

Three groups have been recognised:

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

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 calcied cysts; unlikely to contain viable protoscolices.

Clinical features

As the parasite can colonise virtually every organ in the body, the condition ca n be protean in its presentation. When a sheep farmer, who

is otherwise healthy, complains of a gradually enlarging painful mass in the right upper quadran t with the physical ndings of a liver

swelling, a hydatid liver cyst should be considered. The liver is the organ most often af fected. The lung is the next most common. The

parasite can affect any organ (Figures 6.10 and 6.11) or several organs in the sam e patient (Figure 6.12).

The disease may be asymptomatic and discovered coinciden

(b)

Figure 6.11 Anteroposterior (a) and lateral (b) views of computed tomographic scans showing a large hy datid 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 6.12 Computed tomographic scan showing disseminated hydatid cysts of the abdomen. The patient was started on albendazole and lost to follow up (courtesy of

Dr P Bhattacharaya, Kolkata, India).

Figure 6.13 Magnetic resonance cholangiopancreatography (MRCP) showing a large hepatic hydat id 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).

tally at post-mortem or when an ultrasound or CT scan is done for some other condition. S ymptomatic disease presents with a swelling

causing pressure effects. Thus, a hepatic lesion causes dull pain from stretching of th e liver capsule, and a pulmonary lesion, if large

enough, causes dyspnoea. Daughter cysts may communicate with the biliary tree causing ob structive 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 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 t rauma when the CT scan may be diagnostic

(Figure 6.14). Rarely, a patient may present as an

Figure 6.14 Computed tomographic (CT) scan of the upper abdomen showing a hypodense lesion of the left lob e 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-yea r-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 done 2 we eks later for persisting upper abdominal pain.

emergency with features of anaphylactic shock without any obvious cause. S uch a patient may subsequently cough up white material

that contains scolices that have travelled into the tracheobronchial tree from rupture of a hepati c hydatid on the diaphragmatic surface of

the liver.

Diagnosis

There should be a high index of suspicion. Investigations show a raised eosinophil count; sero logical tests such as ELISA and

immunoelectrophoresis point towards the diagnosis. Ultrasound and CT scan ar e the investigations of choice. The CT scan shows a

smooth space-occupying lesion with several septa. An ultrasound of the biliary trac t may show abnormality in the gall bladder and bile

ducts. Hydatid infestation of the biliary system should then be suspected. Ultimately , the diagnosis is made by a combination of good

history and clinical examination supplemented by serology and radiological imaging tech niques (Summary box 6.9).

Summary box 6.9

Hydatid disease – diagnosis

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 modality – the diagnostic feature is a space-occupying lesion with a smooth outline with sept a

Treatment

Here, the treatment of hepatic hydatid is outlined as the liver is most commonly affected, but th e same general principles apply

whichever organ is involved.

These patients should be treated in a tertiary unit where good teamwork between a n expert hepatobiliary surgeon, an experienced

physician and an interventional radiologist is available. Surgical treatment by minimal acc ess 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 these drugs being available only on a ‘named pati ent’ 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 its activity), the number of cysts and their anatomical position. Radical total or partia l 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 per cent), ethanol (75–95 per c ent) or 1 per cent povidone iodine, although

some use a 10 per cent 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.

Obviously, cysts in other organs need to be treated in accordance with the actual anatom ical site along with the general principles

described. An asymptomatic cyst which is inactive (group 3) may just be observed (Summar y box 6.10).

Summary box 6.10

Hydatid cyst of the liver – treatment

Ideally managed in a tertiary unit by a multidisciplinary team of hepatobiliary surgeon, physician and interventiona l 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; it is impor tant to choose the most appropriate option for the

particular patient and organ involved

Increasingly, a laparoscopic approach is being tried

Pulmonary hydatid disease

The lung is the second most common organ affected after the liver. The size of the cyst can vary from being very small to a considerable

size. The right lung and lower lobes are slightly more often involved. The cyst is usually s ingle, although multiple cysts do occur and

concomitant hydatid cysts in other organs like the liver are not unknown. The conditio n may be silent and found incidentally.

Symptomatic patients present with cough, expectoration, fever, chest pain and so metimes 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 x-ray. Erosion of the bronchioles results in air being introduced between

the pericyst and the laminated membrane and gives a ne radiolucent 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 c ollapsed endocyst floats in the residual uid giving

rise to the ‘water-lily’ sign on CT scan (Figure 6.16). Rupture into the pleura l cavity results in pleural effusion. CT scan denes the

pathology in greater detail.

The mainstay of treatment of hydatidosis of the lung is surgery. Medical treatment is less successful and considered when surgery is not

possible because of poor general condition or diffuse

(a)

(b)

Figure 6.15 Chest x-ray: (a) a smooth rounded cystic lesion in the right lower lobe; (b) ‘meniscus or crescent’ sign (c ourtesy of Professor Saibal Gupta, Professor of

Cardiovascular Surgery, Kolkata, India and Dr Rupak Bhattacharya, Kolkata, India).

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, copious expectoration consisting of clear fluid and flaky material. At first thought to be due to p ulmonary oedema, it turned out to be a ruptured hydatid cyst,

which was successfully treated by surgery (courtesy of Professor Saibal Gupta, Professor of C ardiovascular Surgery, Kolkata, India and Dr Rupak Bhattacharya,

Kolkata, India).

disease affecting both lungs, or recurrent or ruptured cysts. The principle of surgery is to prese rve as much of viable lung tissue as

possible. The exact procedure can vary: cystotomy, capittonage (suturing together the walls), pericystectomy, segmentectomy or

occasionally pneumonectomy (Summary box 6.11).

Summary box 6.11

Pulmonary hydatid disease

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 emergency due to rupture

Plain x-ray shows ‘meniscus or crescent’ sign; CT shows ‘water-lily’ sign

Ideal treatment is surgical – various choices are available

effects of the disease but also from social discrimination, sadly compounded by the inappropr iate term ‘leper’ for one aficted with this

disease.

Only close contact over a long time of several years causes the disease to spread. Ignorance of this fact on the part of the general public

results in ostracism from social stigma. History records that in the distant past sufferers were mad e to wear cow bells so that other people

could avoid them. The use of the term ‘leper’, still used metaphorically to denote an outcast, do es not help to break down the social

barriers that continue to exist against the sufferer.

Pathology

The bacillus inhabits the colder parts of the body – hence found in the nasal mucosa a nd skin in the region of the ears thus involving the

facial nerve as it exits from the stylomastoid foramen. The disease is transmitted fro m the nasal secretions of a patient, the infection

being contracted in childhood or early adolescence. After an incubation period of s everal years, the disease presents with skin, upper

respiratory or neurological manifestations. The bacillus is acid fast but weakly so compared with Mycobacterium tuberculosis.

The disease is broadly classied into two groups – lepromatous and tuberculoid. In lepr omatous leprosy, there is widespread

dissemination of abundant bacilli in the tissues with macrophages and a few lymphocyte s. This is a reection of the poor immune

response, resulting in depleted host resistance from the patient. In tuberculoid lepro sy, on the other hand, the patient shows a strong

immune response with scant bacilli in the tissues, epithelioid granulomas, numerous lymphoc ytes and giant cells. The tissue damage is

inversely proportional to the host’s immune response. There are various grades of the diseas e between the two main spectra (Summary

box 6.12).

Summary box 6.12

Mycobacterium leprae – pathology

Leprosy is a chronic curable infection caused by Mycobacterium leprae

It occurs mainly in tropical regions and developing countries The majority of cases are located in the Indi an 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 resistan ce is stronger than virulence of the organism

LEPROSY

Introduction

Leprosy, also called Hansen’s disease, is a chronic infectious disease caused by th e acid-fast bacillus, Mycobacterium leprae, that is

widely prevalent in the tropics. Globally, India, Brazil, Nepal, Mozambique, Angola and Myan mar (Burma) account for 91 per cent of all

the cases; India alone accounts for 78 per cent of the world’s disease. Patients suffe r not only from the primary

Clinical features and diagnosis

The disease is slowly progressive and affects the skin, upper respiratory tract and perip heral nerves. In tuberculoid leprosy, the damage

to tissues occurs early and is localised to one part of the body with limited defo rmity of that organ. Neural involvement

Robert Greenhill Cochrane , 1899–1985, a medical missionary who became an international authority on leprosy; he devoted his t ime to leprosy patients in South East

Asia, partcularly India.

Owing to the stigma attached to the word ‘leper’, RG Cochrane suggested that the best name for leprosy is Hansen’s disease. Gerhard Henrik Armauer Hansen, 1841–

1912, a physician in charge of a leper hospital near Bergen, Norway. Leprosy 79

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

is characterised by thickening of the nerves, which are tender. There may be a symmetrical well-dened anaesthetic hypopigmented or

erythematous macules with elevated edges and a dry and rough surface – lesions c alled leprids. In lepromatous leprosy, the disease is

symmetrical and extensive. Cutaneous involvement occurs in the form of several pale m acules 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).

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

Later, there is wrinkling of the skin giving an aged appearance to a young in dividual. There is loss of the eyebrows and destruction of the

lateral cartilages and septum of the nose with collapse of the nasal bridge and liftin g 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 o f the eye, epiphora and conjunctivitis (Figure 6.18).

The hands are typically clawed (Figure 6.19) because of involvement of the ulnar ne rve 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 po pliteal 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 fee t predisposes to trophic ulceration

(a)

(b)

Figure 6.19 (a and 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 autoamp utation of toes of the right foot.

(Figure 6.21), chronic infection, contraction and autoamputation. Involvement of the te stes causes atrophy, which in turn results in

gynaecomastia (Figure 6.22). Conrmation of the diagnosis is obtained by a sk in smear or skin biopsy, which shows the classical

histological and microbiological features (Summary box 6.13).

Summary box 6.13

Leprosy – diagnosis

Typical clinical features and awareness of the disease should help to make a diagnosis

The face has an aged look about it with collapse of the nasal bridge and eye changes

Thickened peripheral nerves, patches of anaesthetic skin, claw hands, foot drop and trophic ulcers a re 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 chalm oogra oil was the mainstay of treatment with some success

until the advent of dapsone (diamino-diphenyl sulphone). Dapsone, one of the principa l drugs, was a derivative of prontosil red. This is

used according to the WHO guidelines along with rifampicin and clofazimine. During treatm ent, the patient may develop acute

manifestations. These are controlled with steroids. Multiple drug therapy for 12 mo nths is the key to treatment. A team approach

between an infectious diseases specialist, plastic surgeon, ophthalmologist, hand and orth opaedic surgeon is important.

Surgical treatment is indicated in advanced stages of the disease for functional d isability of limbs, cosmetic disgurement of the face and

visual problems. These entail major reconstructive surgery, the domain of the plastic sur geon. Deformities of the hands and feet require

various forms of tendon transfer, which need to be carried out by specialist hand or orth opaedic surgeons.

The general surgeon may be called upon to treat a patient when the deformity is so advanced that it requires amputation, or when

abscesses need to be drained as an emergency.

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.

All surgical procedures obviously need to be done under antileprosy drug treatment. T his is best achieved by a team approach. Educating

the patients about the dreadful sequelae of the disease so that they seek medical h elp early is important. It is also necessary to educate

the general public that patients suffering from the disease should not be made s ocial outcasts (Summary box 6.14).

Summary box 6.14

Leprosy – treatment

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

Figure 6.22 Typical leonine facies in leprosy and gynaecomastia in leprosy.

Gerhard Domagk , 1895–1964, German physician, Lecturer in Pathologic Anatomy, University of Munst er, Germany, discovered prontosil in 1935, for which he was

awarded the Nobel Prize for Physiology or Medicine in 1939.

Paul Wilson Brand, 1914–2003, born to missionary parents in Southern India, qualified London 1943 CBE , FRCS. He himself was a dedicated missionary who was ‘an

extraordinary gifted orthopaedic surgeon who straightened crooked hands and unravelled the riddle of l eprosy.’ As a pioneer in tendon transfer techniques, he

established and practised initially in New Life Center, Vellore, South India and Schieffelin Leprosy Researc h 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 i n tendon transplantation. 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 leprosy patients by con centrating on research to prevent blindness in leprosy. She

became known as ‘the woman who first helped lepers to see’.

Frank Tovey OBE (b.1921), another English surgeon. At about the same time (1951– 1967) in Southern India in the state of Mysore, as a general surgeon, also

performed extensive tendon transfers, facial and other reconstructive surgery on leprosy patients; in this h e was helped by his wife, Winifred, who organised the

physiotherapy and rehabilitation of the patients and established village diagnostic and treatment centres.

MYCETOMA

(This section has been contributed by Professor Ahmed Hassan Fahal MBBS, FRCS, FR CSI, MD, MS, FRCP(Lond) Professor of

Surgery, University of Khartoum, Khartoum, Sudan)

Introduction

Mycetoma is a chronic specic, granulomatous, progressive, destructive inamm atory disease, which involves subcutaneous tissues

spreading to the skin 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 i n 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, A rgentina and a few others. The route of infection

is inoculation of the organism that is resident in the soil through a traumatised ar ea. 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-fo oted individual walking in a terrain full of thorns.

Hence the foot is the most common site affected. Mycetoma is not contagious.

Once the granuloma forms it increases in size, the overlying skin becomes stretched, sm ooth, 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 actinomycetoma, invasion to deeper tissues occurs earlier and is more e xtensive. The tendons and the nerves are spared

until late in the disease. This may explain the rarity of neurological and trophic change s even in patients with long-standing disease.

Trophic changes are rare because the blood supply is adequate (Summary box 6.15).

Summary box 6.15

Mycetoma – pathogenesis

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 foot 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 characteristic s: rm and rounded, soft and lobulated,

rarely cystic and is often mobile. Multiple secondary nodules may evolve; they may sup purate and drain through multiple sinus tracts.

The sinuses may close transiently after discharge during the active phase of the disease. Fre sh adjacent sinuses may open while some of

the old ones may heal completely. They coalesce and form abscesses, the discharge bein g serous, serosanguinous 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 may supervene when there is secondary bacterial infection.

In some patients there may be areas of local hyperhidrosis over the lesion. This m ay be due to sympathetic overactivity or increased local

temperature due to raised arterial blood flow caused by the chronic inammation. In the majority of patients, the regional lymph nodes

are small and shotty. Lymphadenopathy is common. This may be due to secondary bacterial i nfection, lymphatic spread of mycetoma or

a local immune response to the disease.

The common sites affected are those that come into contact with soil during daily activities: foot in 70 per cent (Figure 6.23) and hand in

12 per cent (Figure 6.24). In endemic areas, the

Figure 6.23 Mycetoma of foot.

Figure 6.24 Mycetoma of hand.

Figure 6.25 Mycetoma of knee.

Figure 6.26 Actinomycetoma of head and neck.

Fibure 6.27 Extensive satellite inguinal actinomycetoma from primary foot lesion involving anterior abdomina l wall and perineum.

knee (Figure 6.25), arm, leg, head and neck (Figure 6.26), thigh and perineum ( Figure 6.27) can be involved. Rare sites are chest,

abdominal wall, facial bones, mandible, testes, paranasal sinuses and eye.

The condition remains localised; constitutional disturbances are a sign of secondary bacter ial infection. Cachexia and anaemia from

malnutrition and sepsis may be seen in late cases. It can be fatal, especially in c ases of cranial mycetoma.

Spread

Local spread occurs predominantly along tissue planes. The organism multiplies for ming colonies which spread along the fascial planes

to skin and underlying structures. Lymphatic spread occurs to the regional lymp h nodes. During the active phase of the disease, these

lymphatic satellites may suppurate and discharge. Lymphatic spread is more common in actinomycetoma and its incidence is augmented

by repeated inadequate surgical excision; lymphadenopathy may also be due to seconda ry bacterial infection. Spread by blood stream

can occur.

The apparent clinical features of mycetoma are not always a reliable indicator of the e xtent and spread of the disease. Some small lesions

with few sinuses may have many deep connecting tracts, through which the disease can sp read quite extensively; therefore, surgery in

mycetoma under local anaesthesia is contraindicated.

Differential diagnosis

Mycetoma should be distinguished from Kaposi’s sarcoma, malignant melanoma, brom a and foreign body (thorn) granuloma. In an x-

ray the presence of bone destruction in the absence of sinuses is suggestive of tuberculosis. The radiological features of advanced

mycetoma are similar to primary osteogenic sarcoma. Primary osseous mycetoma is to be dif ferentiated from chronic osteomyelitis,

osteoclastoma, bone cysts and syphilitic osteitis.

Moritz Kaposi , 1837–1902, Hungarian born, Professor of Dermatology, University of Vienna, Austria. Was b orn 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.

Soft tissue swelling

Cavity

Periosteal

reaction

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

typical of eumycetoma.

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 conrm the diagnosis: plain x-ray, ultrasoun d, CT scan and magnetic resonance imaging

(MRI).

Plain x-ray

In the early stages, soft tissue shadow which may be multiple may be seen with c alcication and obliteration of the fascial planes. As the

disease progresses, the cortex may be compressed from outside by the granuloma leading to b one scalloping. Periosteal reaction with

new bone spicules may create a sun-ray appearance and Codman’s triangle, not un like in osteogenic sarcoma (Figure 6.28). Late in the

disease, there may be multiple punched-out cavities throughout the bone.

Ultrasound

Ultrasound can differentiate between eumycetoma and actinomycetoma as well as betwe en mycetoma and other conditions. In

eumycetoma, the grains produce numerous sharp bright hyper-reective echoes. There are multiple thick-walled cavities with absence of

acoustic enhancement. In actinomycetoma, the findings are similar but the grains are less disti nct. The size and extent of the lesion can

be accurately determined ultrasonically, a nding useful in planning surgical treatm ent.

MRI

This helps to assess bone destruction, periosteal reaction and particularly soft ti ssue involvement (Figure 6.29). MRI usually

Granuloma

Dot-in-circle sign

Figure 6.29 Magnetic resonance imaging of foot showing multiple lesions of high signal intensity, which indicates granulo ma, interspersed within a low-intensity matrix

which is the fibrous tissue and the ‘dot-incircle sign’, which indicates the presence of grains.

shows multiple 2–5 mm lesions of high signal intensity which indicates the granu loma, interspersed within a low-intensity matrix

denoting the brous tissue. The ‘dot-in-circle sign’, which indicates the presen ce of grains, is highly characteristic.

CT scan

CT findings in mycetoma are not specic but are helpful to detect early bone involvement.

Histopathological diagnosis

Deep biopsy is obtained under general or regional anaesthesia although the chance of lo cal spread is high. The biopsy should be

adequate, contain grains and should be xed immediately in 10 per cent formal saline.

Three types of host tissue reaction occur against the organism. In 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

causing its fragmentation. The hyphae and cement substance disappear and only remn ants of brown pigmented cement are left behind.

Outside the zone of neutrophils there is granulation tissue containing macrophages, lymphocyte s, 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 brous tissue.

In Type II tissue reaction, the neutrophils largely disappear and are replaced by mac rophages and multinucleated giant cells which engulf

grain material. This consists largely of pigmented cement substance although hyphae are sometime s identied. Type III reaction is

characterised by the formation of a wellorganised epithelioid granuloma with Langhan’ s type giant cells. The centre of the granuloma

sometimes contains remnants of fungal material.

Fine needle aspiration cytology

Fine needle aspiration cytology (FNAC) can yield an accurate diagnosis and helps in di stinguishing between eumycetoma and

actinomycetoma. The technique is simple, rapid and sensitive.

Ernest Codman, 1869–1940, American surgeon. This appearance can be seen in osteosarcoma, Ewing’s s arcoma and subperosteal abscess and haematoma. Theodor

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

Culture

A variety of microorganisms are capable of producing mycetoma. These can be identied by th eir textural description, morphological

and biological activities in pure culture. Deep surgical biopsy is always needed to obtain the gr ains 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 signicant antibo dy titres against the causative organism may be

of diagnostic value and for follow up. The common serodiagnostic tests are immunoelec trophoresis and ELISA (Summary box 6.16).

Summary box 6.16

Postoperative medical treatment should continue for an adequate period to prevent recu rrence. The recurrence rate varies from 25 to 50

per cent. This can be local or distant to regional lymph nodes. Recurrence is us ually due to inadequate surgical excision, use of local

anaesthesia, lack of surgical experience, non-compliance of drugs due to nan cial reasons and lack of health education (Summary box

6.17).

Summary box 6.17

Mycetoma – management

Ideally combined management by physician and surgeon Medical treatment with appropriate long-term a ntibiotics 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 life-saving procedure

High recurrence rate

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 will be confirmatory

Management

Ideally, this should be a team effort between the physician and the surgeon. In actinomyc etoma, combined drug therapy with amikacin

sulphate and co-trimoxazole in the form of cycles is the treatment of choice. Amo xicillin–clavulanic acid, rifampacin, sulphonamides,

gentamicin and kanamycin are used as a second line of treatment. Long-term drug tre atment is beset with 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 by the physician for side effects. While not being curative, these drugs help to localise the

disease by forming thickly encapsulated lesions which are then amenable to surg ical excision. Medical treatment for both types of

mycetoma must continue until the patient is cured and also in the postoperative p eriod.

Surgical treatment

Surgery is indicated in small localized lesions, resistance to medical treatment or for better response after medical treatment in patients

with massive disease. Excision may need to be much more extensive than suggested at rst on clinical appearance because the disease

may extend to deeper planes which are not clinically apparent. The surgical options are w ide local and debulking excisions and

amputations. Amputation, used as a life-saving procedure, is indicated in advanced mycetoma refractory to medical treatment with severe

secondary bacterial infection.The amputation rate is 10–25 per cent.

POLIOMYELITIS

Introduction

Poliomyelitis is an enteroviral infection that sadly still affects children in developing countries – th is 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 a nd 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. Mu scles of the lower limb are affected twice as

frequently as those of the upper limb (Figures 6.30 and 6.31).

Figure 6.30 Polio affecting predominantly the upper limb muscles with wasting of the intercostal musc les.

Poliomyelitis 85

(a)

(b)

Figure 6.31 (a and b) A 12-year-old patient with polio showing marked wasting of the left upper arm muscles with flex ion contractures of the left knee and hip; there is

equinus deformity of the foot (courtesy of Dr SM Lakhotia and Dr PK Jain, Kolkata, India).

Fortunately, only 1–2 per cent of sufferers develop paralytic symptoms but, when they do occur, the disability causes much misery

(Figure 6.32). When a patient develops fever with muscle weakness, Guillain– Barré syndrome needs to be excluded. The latter has

sensory symptoms and signs, and cerebrospinal uid (CSF) analysis should help to diff erentiate between the two conditions.

Management

Surgical management is directed mainly towards the rehabilitation of the patient who has residual paralysis, the operations being tailored

to that particular individual’s disability. Children especially may show improve ment in their muscle function for up to two years 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 f orm of surgery.

Surgical treatment in the chronic form of the disease is the domain of a highly special ised orthopaedic surgeon who needs

Figure 6.32 A young patient with polio showing paralysis of the lower limb and paraspinal muscles causing mar ked scoliosis and a deformed pelvis.

to work closely with the physiotherapist both in assessing and rehabilitating the pat ient. Operations are only considered after a very

careful and detailed assessment of the patient’s needs. A multidisciplinary team consistin g of the orthopaedic surgeon, neurologist,

physiotherapist, orthotist and the family, should decide upon the need for and advisabilit y of any surgical procedure (Summary box

6.18).

A description of the operations for the various disabilities is beyond the scope o f this book. The reader should therefore seek surgical

details in a specialist textbook. In 2012, WHO has declared India a polio-free country.

Summary box 6.18

Poliomyelitis

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 thei r disabilities

Surgery is considered for the various types of paralysis in the form of tendon transfers and arthrodesis, which is the domain of a specialised orthopaedic surgeon

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 Barré described this condition in a joint paper in 1916 while serving as Medical Officers in th e French Army during the First World War.

TROPICAL CHRONIC PANCREATITIS

Introduction

Tropical chronic pancreatitis is a disease affecting the younger generation from poor socioecono mic strata in developing countries, seen

mostly in southern India. The aetiology remains obscure with malnutrition, dietary, fa milial and genetic factors being possible causes.

Alcohol ingestion does not play a part in the aetiology.

Aetiology and pathology

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 detoxied in the liver by su lphur-containing amino acids. The less well-off

among the population lack such amino acids in the diet. This results in cyanogen toxicity caus ing the disease. Several members of the

same family have been known to suffer from this condition; this strengthens the theory that c assava toxicity is an important cause

because family members eat the same food.

Macroscopically, the pancreas is rm and nodular with extensive periductal bro sis, with intraductal calcium carbonate stones of

different sizes and shapes that may show branches and resemble a staghorn. The duc ts are dilated. Microscopically, fibrosis is the

predominant feature – intralobular, interlobular and periductal – with plasma cell and lymphocy te inltration. There is a high incidence

of pancreatic cancer in these patients (Summary box 6.19).

Summary box 6.19

Pathology of tropical chronic pancreatitis

Almost exclusively occurs in developing 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 Dilatatio n of pancreatic ducts with large intraductal stones

Fibrosis of the pancreas

A high incidence of pancreatic cancer in those affected by the disease

Figure 6.33 Plain x-ray of the abdomen showing large stones along the main pancreatic duct typical of tropical chr onic pancreatitis (courtesy of Dr V Mohan, Chennai,

India).

being considered as a therapeutic manoeuvre for removal of ductal stones in the pancreatic head by papillotomy (Summary box 6.20).

Summary box 6.20

Diagnosis of tropical chronic pancreatitis

The usual sufferer is a type 1 diabetic under 40 years of age

Serum amylase may be elevated in an acute exacerbation Plain x-ray shows stones along the pancreatic du ct

Ultrasound and CT scan of the pancreas confirm the diagnosis

ERCP may be used as a supplementary investigation and a therapeutic procedure

Diagnosis

The patient, usually male, is almost always below the age of 40 years and from a poor backgrou nd. The clinical presentation is

abdominal pain, thirst, polyuria and features of gross pancreatic insufciency ca using steatorrhoea and malnutrition. The patient looks ill

and emaciated.

Initial routine blood and urine tests conrm that the patient has type 1 diabetes mellitus. Th is is known as brocalculous 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 x-ray shows typical pancreatic calcication in the form of discrete stones in the duct (Figure 6.33).

Ultrasound and CT scanning of the pancreas conrm the diagnosis. An ERCP as an investigation should only be done when the

procedure is also

Treatment

The treatment is mainly medical with exocrine support using pancreatic enzymes, treatm ent of diabetes with insulin and the management

of malnutrition. Treatment of pain should be along the lines of the usual analgesic ladder: no n-opioids, followed by weak and then strong

opioids and, nally, 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 choic e. As most patients are young, pancreatic resection is only

very rarely considered, and then only as a last resort, when all available methods of pain relief have been exhausted (Summary box 6.21).

Tuberculous cervical lymphadenitis 87

Summary box 6.21

Treatment of tropical chronic pancreatitis

Mainly medical – pain relief, insulin for diabetes and pancreatic supplements for malnutrition

Surgery is reserved for intractable pain

Procedures are side-to-side pancreaticojejunostomy; resection in extreme cases

TUBERCULOSIS

While tuberculosis can affect all systems in the body, in the tropical developing world the surgeo n is most often faced with tuberculosis

affecting the cervical lymph nodes and the small intestine. Therefore in this chapter, tuberculou s cervical lymphadenitis and tuberculosis

of the small bowel will be described.

TUBERCULOUS CERVICAL LYMPHADENITIS

Introduction

This is common in the Indian subcontinent. A young person who has recently arriv ed in the UK from an endemic area, presenting with

cervical lymphadenopathy, should be diagnosed as having tuberculous lymphaden itis unless otherwise proven. With acquired immune

deciency syndrome (AIDS) being globally prevalent, this is not as rare in the West in the indigenous population as it used to be.

Diagnosis

Any of the cervical group of lymph nodes (jugulodigastric, submandibular, supraclavic ular, posterior triangle) can be involved.

Figure 6.34 Cervical tuberculous cold abscess about to burst (courtesy of Professor Ahmed Hassan Fahal, Khartoum, Sudan).

Figure 6.35 Cervical tuberculous sinus with typical overhanging edges (courtesy of Professor Ahmed Hassan Fah al, Khartoum, Sudan).

The patient has the usual general manifestations of tuberculosis: evening pyrexia, cough (may be from pulmonary tuberculosis), malaise,

and if the sufferer is a child, failure to thrive is a signicant nding. Locally there will be regional lymphadenopathy where the lymph

nodes may be matted; in late stages, a cold abscess may form – a painless, uc tuant, mass, not warm; signicantly, there are no signs of

inammation (Figure 6.34), hence called a ‘cold abscess’. This is a clinical manife station of underlying caseation.

Left untreated, the cold abscess initially deep to the deep fascia now bursts through into the space just beneath the superficial fascia. This

produces a bilocular mass with cross uctuation. This is called a ‘collar-stud’ abscess. E ventually, this may burst through the skin

discharging pus and forming a tuberculous sinus (Figure 6.35). The latter typically has wa tery discharge with undermined edges

(Summary box 6.22).

Summary box 6.22

Tuberculous cervical lymphadenitis

This is a common condition at any age

Matted lymphnodal mass is the typical clinical feature In later stages the mass may be cystic denoting an ab scess The abscess denotes underlying caseation and does not

show any features of inflammation – hence called 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

Collar-stud abscess is so called because it resembles a collar stud (which has two parts) used in shirts with de tachable collars, now largely out of fashion.

Investigations

Raised ESR and CRP, low haemoglobin and a positive Mantoux test are usual, although the last is not signicant in a patient from an

endemic area. The Mantoux test (tuberculin skin test), although in use for over a hun dred years, has now been superseded by interferon

gamma (IFNγ) release assays. This is an in vitro blood test of cellular immune response. Antigens u nique to Mycobacterium tuberculosis

are used to stimulate and measure T-cell release of IFNγ. This helps to earmark patients who have latent or subclinical tuberculosis and

thus benet from treatment.

Sputum for culture and sensitivity (the result may take several weeks) and staining by th e Ziehl–Neelsen method for acidfast bacilli (the

result is obtained much earlier) should also be done.

Specic investigations include aspiration of the pus in a cold abscess for culture and sens itivity. If the mass is still in the early stages of

adenitis, excision biopsy should be done. Here, part of the lymph nodes shou ld be sent fresh and unxed to the laboratory who should be

warned of the arrival of the specimen so that the tissue can be appropriately p rocessed immediately.

Figure 6.36 Histology of ileocaecal tuberculosis. C: caseation. Black arrows show epithelioid granuloma with multi-nucleated giant cells. Yellow arrow shows acid-fast

bacilli on Ziehl–Neelsen staining. (Courtesy of Dr Rosslyn Rankin, Raigmore Hospital, Inverness, Scotland.)

Treatment

This must be a 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 refer to deta ils of medical treatment in an appropriate source.

follicles, thus causing narrowing of the lumen and obstruction. In both types th ere may be marked mesenteric lymphadenopathy.

Macroscopically, this type may be confused with Crohn’s disease. The small intestine sh ows areas of stricture and brosis most

pronounced at the terminal ileum (Figure 6.37). As a result, there is shortenin g of the bowel with the caecum being pulled up into a

subhepatic position (Summary box 6.23).

TUBERCULOSIS OF SMALL INTESTINE

Summary box 6.23 Introduction

Infection by Mycobacterium tuberculosis is common in the tropics. In these days of internat ional travel and increased migration to the

UK, tuberculosis in general and intestinal tuberculosis in particular are no longer cli nical curiosities in the West. Any patient, particularly

one who has recently arrived from an endemic area and who has features of genera lised ill health and altered bowel habit, should arouse

the suspicion of intestinal tuberculosis. The increased incidence of human immunode ciency virus (HIV) infection worldwide has also

made tuberculosis more common.

Tuberculosis – pathology

Increasingly being seen in the UK, mostly among immigrants Two types are recognised – ulcerative and h yperplastic 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

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 ge nitourinary system, may also be involved simultaneously

Pathology

When a patient with pulmonary tuberculosis swallows infected sputum, the organis m 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 6.36). This pathological entity, referred to as the ulce rative type, denotes a severe form of the disease

in which the virulence of the organism overwhelms host resistance.

The other variety, called the hyperplastic type, occurs when host resistance has the u pper hand over the virulence of the organism. It is

caused by the drinking of infected milk. There is a marked inammatory reaction causing hyp erplasia and thickening of the terminal

ileum because of its abundance of lymphoid

Clinical features

Patients present electively with weight loss, chronic cough, malaise, evening rise in t emperature with sweating, vague abdominal pain

with distension and alternating constipation and diarrhoea. As an emergency, they pr esent with features of distal small bowel obstruction

from strictures of the small bowel, particularly the terminal ileum. Rarely, a patient may presen t

Burrill Bernard Crohn , 1884–1983, gastroenterologist, Mount Sinai Hospital, New York, NY, USA, described regional ileitis in 193 2 along with Leon Ginzburg and

Gordon Oppenheimer.

Charles Mantoux , 1877–1947, physician, Le Cannet, Alpes Maritimes, France, described the intradermal t uberculin 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, Germa ny.

Tuberculosis of small intestine 89

of micturition. Clinical examination does not show any abnormality. The genitourinary tr act should then be investigated (Summary box

6.24).

Stricture in

terminal ileum

Perforation in terminal ileum

Figure 6.37 Emergency limited ileocolic resection: specimen showing tuberculous stricture in the terminal ileum and perforation of a transverse ulcer just proximal to the

stricture.

Summary box 6.24

Tuberculosis – clinical features

Intestinal tuberculosis should be suspected in any patient from an endemic area who presents with we ight loss, malaise, evening fever, cough, alternating constipation

and diarrhoea and intermittent abdominal pain with distension The abdomen has a doughy feel; a mass ma y be found in the right iliac fossa

The emergency patient presents with features of distal small bowel obstruction – abdominal pain, d istension, bilious and faeculent vomiting

Peritonitis from a perforated tuberculous ulcer in the small bowel can be another emergency present ation

with features of peritonitis from perforation of a tuberculous ulcer in the small bowel (Figure 6 .37).

Examination shows a chronically ill patient with a ‘doughy’ feel to the abdomen f rom 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 stula-in-ano, which is typically multiple with

undermined edges and watery discharge.

As this is a disease mainly seen in developing countries, patients may present late a s an emergency from intestinal obstruction.

Abdominal pain and distension, constipation and bilious and faeculent vomiting a re typical of such a patient who is in extremis.

There may be features of other system involvement, such as the genitourinary tr act, when the patient complains of frequency

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 bow el, particularly the ileum, typically with a

high subhepatic caecum with the narrow ileum entering the caecum directly from bel ow upwards in a straight line rather than at an angle

(Figures 6.38 and 6.39a). Laparoscopy reveals the typical picture of tubercles on t he bowel serosa, multiple strictures, a high caecum,

enlarged lymph nodes, areas of caseation and ascites. Culture of the ascitic uid may be he lpful. A chest x-ray is essential (Figure 6.39b).

If the patient complains of urinary symptoms, urine is sent for microscopy and culture; the nding of sterile pyuria should alert

(a)

SUBHEPATIC

CAECUM

(b)

SUBHEPATIC

CAECUM

Figure 6.38 (a and b) Series of a barium meal and follow-through showing strictures in the ileum with the caecum pulled up into a subhepatic position.

(a)

SUBHEPATIC

CAECUM

the clinician to the possibility of tuberculosis of the urinary tract, when the appropriate inves tigations should be done. A exible

cystoscopy would be very useful in the presence of sterile pyuria. A contracted bl adder (‘thimble’ bladder) with ureteric orices that are

in-drawn (‘golf-hole’ ureter) may be seen; these changes are due to brosis.

In the patient presenting as an abdominal emergency, urea and electrolytes sh ow evidence of gross dehydration. Plain abdominal x-ray

shows typical small bowel obstruction – valvulae conniventes of dilated jejunum and fea tureless ileum with evidence of uid between the

loops (Summary box 6.25).

Summary box 6.25

Intestinal tuberculosis – investigations

Raised inflammatory markers, anaemia and positive sputum culture

Interferon-gamma release assays for subclinical infection is done

Ultrasound of the abdomen may show localised areas of ascites

Chest x-ray shows pulmonary infiltration

Barium meal and follow-through shows multiple small bowel strictures particularly in the ileum with a subhepatic ca ecum If symptoms warrant, the genitourinary tract

is also investigated

Treatment

On completion of medical treatment, the patient’s small bowel is reimaged to look for sign icant strictures. If the patient has

(b)

PULMONARY INFILTRATION

Figure 6.39 Barium meal and follow-through (a) and chest x-ray (b) in a patient with extensive intestina l and pulmonary tuberculosis, showing ileal strictures with high

caecum and pulmonary infiltration.

features of subacute intermittent obstruction, bowel resection, in the form of limited ileocolic resection (Figure 6.37) with anastomosis

between the terminal ileum and ascending colon, strictureplasty or right hemicolectomy, i s performed as deemed appropriate. The

surgical principles and options in the elective patient are very similar to those f or Crohn’s disease.

The emergency patient presents a great challenge. Such a patient is usually from a poor socio economic 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 lapar otomy, 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 anti-tuberculous

chemotherapy and improvement in nutritional status; this may require three to six months of care. The patient who had a simple bypass

procedure is reassessed and, when the disease is no longer active (as evidenced by return to normal of inammatory markers, weight

gain, negative sputum culture), an elective right hemicolectomy is done. This may b e supplemented with strictureplasty for short

strictures at intervals.

Perforation is treated by thorough resuscitation followed by resection of the affected segment. An astomosis is performed provided it is

regarded as safe to do so when peritoneal contamination is minimal and widespread dise ase is not encountered; otherwise, as a rst stage,

resection and exteriorisation is done followed by restoration of bowel continuity as a second stage

Typhoid 91

later on after a full course of anti-tuberculous chemotherapy and improvement in nutritional status (Summary box 6.26).

Summary box 6.26

Tuberculosis – treatment

Patients should ideally be under the combined care of a physician and surgeon

Vigorous supportive and full drug treatment is mandatory in all cases

Symptomatic strictures are treated by the appropriate resection, e.g. local ileocolic resection or stricturep lasty 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-s ide ileotransverse bypass

Once the patient has recovered with medical treatment, then the second-stage definitive procedure of right hemico lectomy 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 co ndition of the patient is very poor; this is later followed by restoration o f

bowel continuity after the patient has fully recovered with antituberculous chemotherapy

TYPHOID

Introduction

Typhoid fever is caused by Salmonella typhi, also called the typhoid bacillus. T his is a Gram-negative organism. Like most infections

occurring in developing countries in the tropics, the organism gains entry into the human gastroi ntestinal tract as a result of poor hygiene

and inadequate sanitation. It is a disease normally managed by physicians, but the surgeon i s 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 s hows erythrophagocytosis with histiocytic

proliferation (Figure 6.40). If the patient is left untreated or inadequately treated, the ul cers may lead to perforation and bleeding. The

bowel may perforate at several sites including the large bowel.

Diagnosis

A typical patient is from an endemic area or who has recently visited such a country an d suffers from a high temperature for 2–3 weeks.

The patient may be toxic with abdominal distension from paralytic ileus. The patient may have melaena due to haemorrhage from a

typhoid ulcer; this can lead to hypovolaemia.

Blood and stool cultures conrm the nature of the infection and exclude malaria. Al though obsolete in the UK, the Widal

Figure 6.40 Histology of enteric perforation of the small intestine showing erythrophagocytosis (arrows) with p redominantly histiocytic proliferation (courtesy of Dr AK

Mandal, New Delhi, India).

test is still done in the Indian subcontinent. The test looks for the presence of agglutin ins to O and H antigens of Salmonella typhi and

paratyphi in the patient’s serum. In endemic areas, laboratory facilities may sometimes be limited. Cer tain other tests have been

developed which identify sensitive and specic markers for typhoid fever. Practical and cheap kits are available for their rapid detection

that need no special expertise and equipment. These are Multi-Test Dip-S-Ticks to detect immunogl obulin 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 pre-hospital 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 hera lds a perforated typhoid ulcer. The

patient, who is already very ill, deteriorates further with classical features of pe ritonitis. An erect chest x-ray or a lateral decubitus lm

(in the very ill, as they usually are) will show free gas in the peritoneal cavity. In fa ct, any patient being treated for typhoid fever who

shows a sudden deterioration accompanied by abdominal signs should be considered to h ave a typhoid perforation until proven otherwise

(Summary box 6.27).

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 typ hi 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 x-ray

Daniel Elmer Salmon , 1850–1914, Veterinary Pathologist, Chief of the Bureau of Animal Industry, Wash ington 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, Facul ty of Medicine, Paris, France. He developed the test in 1896 to

diagnose typhoid fever.

Treatment

Vigorous resuscitation with intravenous uids and antibiotics in an intensive car e unit gives the best chance of stabilising the patient’s

condition. Metronidazole, cephalosporins and gentamicin are used in combination. Chlo ramphenicol, despite its potential side effect of

aplastic anaemia, is still used occasionally in developing countries. Laparotomy is then c arried out.

Several surgical options are available, and the most appropriate operative procedure sh ould be chosen judiciously depending upon the

general condition of the patient, the site of perforation, the number of perforations an d the degree of peritoneal soiling. The alternatives

are closure of the perforation (Figure 6.41) after freshening the edges, wedge resectio n 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. A fter 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 ab dominal wound open for delayed

closure, as wound infection is almost inevitable and dehiscence not uncommon. In th e presence of rampant infection, laparostomy may

be a good alternative.

(a)

(b)

Figure 6.41 (a and b) Typhoid perforation of the terminal ileum.

When a typhoid perforation occurs within the rst 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 defen ces are more robust. Furthermore, the

shorter the interval between diagnosis and operation, the better is the prognosis (Summary box 6 .28).

Summary box 6.28

Treatment of bowel perforation from typhoid

Manage in intensive care

Resuscitate and give intravenous antibiotics

Laparotomy – choice of various procedures

Most common 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

Adeniran JO, Taiwo JO, Abdur-Raham LO. Salmonella intestinal perforation (27 perforatio ns in one patient, 14 perforations in another):

are the goal posts changing? J Indian Assoc Pediatr Surg 2005; 10: 248–51.

Aziz M, Qadir A, Aziz M, Faizullah. Prognostic factors in typhoid perforation. J Coll Phys Surg P akistan 2005; 15: 704–7.

Barman KK, Premlatha G, Mohan V. Tropical chronic pancreatitis. Postgrad Me d J 2003; 79: 606–15.

Barnes SA, Lillemore KD. Liver abscess and hydatid disease. In: Zinner NJ, Schwartz I, E llis H (eds). Maingot’s abdominal operations,

10th edn, Vol. 2. New York: Appleton and Lange, 1997: 1527–45.

Chiodini P. Parasitic infections. In: Russell RCG, Williams NS, Bulstrode CJK (eds). Bailey & L ove’s short practice of surgery, 24th

edn. London: Arnold, 2004: 146–74.

Choi BI, Han JK, Hong ST, Lee KH. Clonorchiasis and cholangiocarcinoma: etiologic relationship and imaging diagnosis. Clin

Microbiol Rev 2004; 17: 540–52.

Fahal AH. Management of mycetoma. Expert Rev Dermat 2010; 5: 87–93.

Fahal AH. Mycetoma: clinico-pathological monograph. Universi ty of Khartoum Press, Khartoum, 2006.

Hassan MA, Fahal AH. Mycetoma. In: Kamil R, Lumby J (eds). Tropical surgery . London: Westminster Publications Ltd. 2004: 786–

790.

Olsen SJ, Pruckler J, Bibb W et al. Evaluation of rapid diagnostic tests for typh oid fever. J Clin Microbiol 2004; 42: 1885–9.

Manjula Y, Kate V, Ananthakrishnan N. Evaluation of sequential intermittent pneu matic compression for larial lymphoedema. Natl

Med J India 2002; 15: 192–4.

Steinberg R, Davies J, Millar AJ et al. Unusual intestinal sequelae after operations for Ascaris lumbricoi des infestation. Paediatr Surg Int

2003; 19: 85–7.

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

WHO Informal Working Group. International classication of ultrasound images in cy stic echinococcosis for application in clinical and

eld epidemiological settings. Acta Trop 2003; 85: 253–61.

World Health Organization. Leprosy – global situation. Wkly Epidemiol Rec 2000; 75: 225–32.

World Health Organization. The World Health Report – bridging the gaps. World H ealth Forum 1995; 16: 377–85.

CHAPTER

laparoscopic and robotic surgery Principles of

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 marriage of modern technology and surgical innovatio n 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 disguring

than conventional techniques. With increasing experience, it offers cost-effectiveness b oth to health services and to employers by

shortening operating times, shortening hospital stays and allowing faster recupera tion.

EXTENT OF MINIMAL ACCESS SURGERY

Minimal access surgery has crossed all traditional boundaries of specialties and disciplines. Sha red, borrowed and overlapping

technologies and information are encouraging a multidisciplinary approach that serves t he whole patient, rather than a specic organ

system. Broadly speaking, minimal access techniques can be categorised as follows.

Laparoscopy

A rigid endoscope (laparoscope) is introduced through a port into the peritoneal cavit y. This is insufated with carbon dioxide to

produce a pneumoperitoneum. Further ports are inserted to enable instrument access and t heir use for dissection (Figure 7.1). There is

little doubt that laparoscopic cholecystectomy has revolutionised the surgical manageme nt of cholelithiasis and has become the mainstay

of management of uncomplicated gallstone disease. With improved instrumentation, advanced p rocedures, such as laparoscopic

colectomies for malignancy, previously regarded as controversial, have also be come fully accepted. There has been an increasing

evidence base showing the short-term benets of laparoscopic surgery over open surgery with regards t o postoperative pain, length of

stay, earlier return to normal activities, but maintaining equivalence of the benets of th e long-term outcomes, such as oncological

quality and cancer-related survival.

Figure 7.1 Basic laparoscopic instruments (photo courtesy of Daniel Leff).

Thoracoscopy

A rigid endoscope is introduced through an incision in the chest to gain access to th e thoracic contents. Usually there is no requirement

for gas insufation as the operating space is held open by the rigidity of the thorac ic cavity.

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 (see Chapter 14).

Perivisceral endoscopy

Body planes can be accessed even in the absence of a natural cavity. Examples are mediastin oscopy, retroperitoneoscopy and

retroperitoneal approaches to the kidney, aorta and lumbar sympathetic chain. Extrap eritoneal approaches to the retroperitoneal organs,

as well as hernia repair, are now becoming increasingly commonplace, furth er decreasing morbidity associated with visceral peritoneal

manipulation. Other, more recent, examples include subfascial ligation of incompe tent perforating veins in varicose vein surgery.

Arthroscopy and intra-articular joint surgery

Orthopaedic surgeons have long used arthroscopic access to the knee and have now mo ved their attention to other joints, including the

shoulder, wrist, elbow and hip.

Combined approach

The diseased organ is visualised and treated by an assortment of endoluminal and extralumina l endoscopes and other imaging devices.

SURGICAL TRAUMA IN OPEN,

LAPAROSCOPIC AND ROBOTIC

SURGERY

Most of the trauma of an open procedure is inicted because the surgeon must ha ve a wound that is large enough to give adequate

exposure for safe dissection at the target site. The wound is often the cause of mor bidity, including infection, dehiscence, bleeding,

herniation and nerve entrapment. Wound pain prolongs recovery time and, by reducin g mobility, contributes to an increased incidence of

pulmonary atelectasis, chest infection, paralytic ileus and deep venous thrombos is.

Mechanical and human retractors cause additional trauma. Body wall retractors tend to inict loc alised 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 tra uma.

Exposure of any body cavity to the atmosphere also causes morbidity through cooling a nd uid loss by evaporation. There is also

evidence to suggest that the incidence of post-surgical adhesions has been reduced by t he use of the laparoscope because there is less

damage to delicate serosal coverings. In handling intestinal loops, the surgeon and assistant disturb the peristaltic activity of the gut and

provoke adynamic ileus.

Minimal access surgery has many advantages, such as a reduction in the trauma of acce ss and exposure and an improvement in

visualisation (Summary box 7.1).

Summary box 7.1

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 vision

LIMITATIONS OF MINIMAL ACCESS SURGERY

Despite its many advantages, minimal access surgery has its limitations. To perform min imal access surgery with safety, the surgeon

must operate remote from the surgical eld, using an imaging system that provides a tw o-dimensional representation of the operative site.

The endoscope offers a whole new anatomical landscape, which the surgeon must lear n to navigate without the usual clues that make it

easy to judge depth. The instruments are longer and sometimes more complex to us e than those commonly used in open surgery. This

results in the novice being faced with signicant problems of hand–eye coordination.

Some of the procedures performed by these new approaches are more techn ically demanding and are slower to perform and often have a

more difcult 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 o pen procedure. Unfortunately, there seems to

be a sense of shame associated with conversion, which is quite unjustied. It is vital for surgeons and patients to appreciate that the

decision to close or convert to an open operation is not a complication but, ins tead, usually implies sound surgical judgement.

Another problem occurs when there is intraoperative arterial bleeding. Haemostas is may be very difcult to achieve endoscopically

because blood obscures the eld of vision and there is a signicant reduction of the image qualit y owing to light absorption.

Another disadvantage of laparoscopic surgery is the loss of tactile feedback; this is an area of o ngoing 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 , including biliary tract exploration and surgery

for malignancies, has provided a strong impetus for the development of laparoscopic ultr asound. Now more developed over the last

decade, this technique already has advantages that far outweigh its disadvantages.

In more advanced techniques, large pieces of resected tissue, such as the lung or colo n, may have to be extracted from the body cavity.

Occasionally, the extirpated tissue may be removed through a nearby natural orice, 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 thro ugh 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 amou nt of information available to the pathologist. Previous

reports of tumour implantation in the locations of port sites raised important questions a bout the future of the laparoscopic treatment of

malignancy, but large-scale trials have shown this claim to be false. Although emerging evide nce from large-scale international

prospective trials implicate surgical skill as an important aetiological factor, it is imp ortant to consider the biological implications of

minimally invasive strategies on the tumours. The use of carbon dioxide and helium a s insufants causes locoregional hypoxia and may

also change pH. The

Robotic surgery 95

resultant modulation of spilled tumour cell behaviour is only now being elucidated.

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, reect organs atraum atically, retract structures, identify vessels, dissect bluntly

along a tissue plane and provide nger pressure to bleeding points, while proximal cont rol is achieved. In addition, several reports have

suggested that this approach is more economical than a totally laparoscopic approach, reduc ing 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 is a growing need for improvement in dissection techniques in laparoscopic surg ery and, specically, for improving the safe use of

electrosurgery and lasers. Ultrasonic dissection, tissue fusion devices and tissue removal have bee n utilised by a growing number of

specialties for several years. The adaptation of the technology to laparoscopic surgery g rew out of the search for alternative, possibly

safer, methods of dissection. The current units combine the functions of three or four separate in struments, reducing the need for

instrument exchanges during a procedure. This exibility, combined with the ability to provide a clean, smoke-free eld, improves safety

while shortening operating times.

Although dramatic cost savings are possible with laparoscopic cholecystectomy, the pos ition was less clear-cut with other procedures

initially. There is another factor that may complicate the computation of the cost–benet r atio. A signicant rise in the rate of

cholecystectomy followed the introduction of the laparoscopic approach as the threshold for r eferring patients for surgery lowered. The

increase in the number of procedures performed has led to an overall increase i n the cost of treating symptomatic gallstones.

Three-dimensional imaging systems are available, but remain expensive and current ly are not commonplace. Stereoscopic imaging for

laparoscopy is still progressing. Future improvements in these systems will greatly e nhance manipulative ability in critical procedures,

such as knot tying and dissection of closely underlying tissues. There are, how ever, some drawbacks, such as reduced display brightness

and interference with normal vision because of the need to wear specially designed glasses f or 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 e laborate image-processing techniques will result

in a wide range of transformed presentations becoming available. It will ultimately be poss ible 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 ori entation, superimposed on past images

taken in other modalities. Such augmented reality systems are being developed at present, but are currently in relative infancy. It is for

the medical community to decide which of these many potential imaginative techniques will contribute most to effective surgical

procedures (Summary box 7.2).

Summary box 7.2

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

ROBOTIC SURGERY

A robot is a mechanical device that performs automated physical tasks according to dire ct human supervision, a predened program or a

set of general guidelines using articial intelligence techniques. In terms of surgery, robots hav e been used to assist surgeons during

procedures. This has been primarily in the form of automated camera systems a nd telemanipulator systems, thus resulting in the creation

of a human–machine interface.

Even though laparoscopic surgery has progressed greatly over the last two decades, there are lim itations. These include the restriction to

two-dimensional views, reduced degrees of freedom of movement, little or no tactil e feedback and ergonomically difcult positions for

the surgeon. Such problems undoubtedly affect surgical precision. This has led to interest in robotic master–slave systems (where the

surgeon is the master, i.e. the operator, and the robot is the slave). Such devic es have been under trial during the last ten years. They

offer many benets, which have arisen as a result of new technology in lenses, cameras and c omputer software. The advantages are two-

fold: rst for the patient (as for laparoscopic surgery, Summary box 7.1) and second for the surgeon. The advantages for the surgeon

include better visualisation (higher magnication) with stereoscopic views; elimination of ha nd tremor allowing greater precision;

improved manoeuvring as a result of the ‘robotic wrist’, which allows seven degrees of freedom ; and the fact that large external

movements of the surgical hands can be scaled down and transformed to limited interna l movements of the ‘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 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. Ther e may also be less need for assistance once surgery

is under way.

Many surgical specialties have embraced the progression of robot-assisted techniques, includi ng general surgery, cardiothoracic surgery,

urology, orthopaedics, ear, nose and throat (ENT) surgery and paediatric surgery. Specialities t hat use microsurgical techniques will

particularly benet in the future.

There are different robotic systems available (see Figures 7.2, 7.3, 7.4 and 7.5). Robotic c amera systems include AESOP (Computer

Motion, Goleta, CA, USA) and EndoAssist (Armstrong Healthcare, High Wycombe, UK) . Telerobotic manipulators include the da Vinci

(Intuitive Surgical, Menlo Park, CA, USA) and ZEUS (Computer Motion) m anipulators. Finally, telerobotics and telementoring has been

combined in systems such as SOCRATES (Computer Motion). All of these systems offer different advantages to the operating surgeon,

Figure 7.2 da Vinci manipulators used during robotic laparoscopic cholecystectomy. This demonstrates the robotic graspe r holding and retracting the gall bladder neck,

while the robotic hook is used to free the overlying omentum on the gall bladder and cystic duct (courtesy of the Department of Biosurgery and Surgical Technology,

Imperial College, London).

Figure 7.3 da Vinci console (photo courtesy of Daniel Leff).

ranging from reducing the need for assistants and providing better ergonomic operatin g positions to providing experienced guidance from

surgeons not physically present in the operating theatre.

Figure 7.4 da Vinci console, binocular viewer (photo courtesy of Daniel Leff).

Figure 7.5 Slave unit: da Vinci arms set up in a virtual operating theatre (photo courtesy of Daniel Leff).

PREOPERATIVE EVALUATION

Preparation of the patient

Although the patient may be in hospital for a shorter period, careful preoperative managem ent is essential to minimise morbidity.

History

Patients must be t for general anaesthesia and open operation if necessary. Potential coagul ation disorders (e.g. associated with

cirrhosis) are particularly dangerous in laparoscopic surgery. As adhesions may cause proble ms, previous abdominal operations or

peritonitis should be documented.

Examination

Routine preoperative physical examination is required as for any major operation. Although, in general, laparoscopic surgery allows

quicker recovery, it may involve longer operating times and the establishment of the pneum operitoneum may provoke cardiac

arrhythmias. Severe chronic obstructive airways disease and ischaemic heart disea se may be contraindications to the laparoscopic

approach.

Theatre set up and tools 97

Particular attention should be paid to the presence or absence of jaundice, abdominal scars, palpable masses or tenderness.

Moderate obesity does not increase operative difculty signicantly, but massive obesity may make pneumoperitoneum difcult and

standard instrumentation may be too short. Access may prove difcult in very thin p atients, especially those with severe kyphosis.

Premedication

Premedication is the responsibility of the anaesthetist, with whom coexisting medical problems sho uld be discussed.

Prophylaxis against thromboembolism

Venous stasis induced by the reverse Trendelenburg position during laparoscopic surgery may b e a particular risk factor for deep vein

thrombosis, as is a lengthy operation and the obesity of many patients. Subcutan eous 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 intrav enous heparin, depending on the underlying

condition, as it is not safe to perform laparoscopic surgery in the presence of a signicant c oagulation decit.

Urinary catheters and nasogastric tubes

In the early days of laparoscopic surgery, routine bladder catheterisation and nasogastr ic intubation were advised. Most surgeons now

omit these, but it remains essential to check that the patient is fasted and has recently e mptied the bladder, particularly before the blind

insertion of a Verres needle. However, currently, most general surgeons prefer the direct cu t-down technique into the abdomen for the

introduction of the rst port for the establishment of the pneumoperitoneum (Hasson technique) . More 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 laparos copic surgery, relates to the issue of informed consent. It

is essential that the patient understands the nature of the procedure, the risks inv olved 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 o perate. On admission, it is the responsibility of

the operating surgeon and anaesthetist to ensure that the patient has been fully counselled, althou gh 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 quantied, for example the increased risk wi th acute cholecystitis or in the presence of

extensive upper abdominal adhesions. The conversion rate will also vary with the e xperience and practice of the surgeon. Common

complications should be mentioned, such as shoulder tip pain and minor surgical emphysema, a s well as rare but serious complications,

including injury to the bile ducts and visceral injury from trocar insertion or diath ermy.

A few patients may insist on having an open procedure (probably inuenced by accou nts of mishaps) and the surgeon should be

prepared to offer this, although most will opt for laparoscopy if the surgeon has ex tensive experience and an impressive safety record.

When obtaining consent for robotic surgery, patients should be offered appropriate lite rature so that they are able to provide fully

informed consent. As these procedures are still not routine, this should be carried out by the operating surgeon and, if the procedure is in

the context of a clinical trial, the appropriate ethical approval and subsequent paperwork should be available to the patient before signing

the consent form (Summary box 7.3).

Summary box 7.3

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

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 is key to its smooth running on a daily basis. Or iginally, the video and diathermy

equipment and other key tools used in laparoscopic surgery were moved around on stacks , taking up valuable oor space and cluttering

up the theatre environment, which was not always ergonomic for the operating tea m. 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 7.6). The

equipment consists of at least two high-resolution LCD monitors (and, more recently, high denition (HD) monitors for even clearer

images), the laparoscopic kit for maintaining pneumoperitoneum and the audiovisua l 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 record ed 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.

Image quality is vital to the success of laparoscopic surgery. New camera and lens technology a llows 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 u sed to give the surgeon the best views

possible and three-dimensional technology is now starting to be used for visualisation m ore

Janos Verres, 1903–1979, chest physician and chief of the Department of Internal Medicine, The Region al Hospital, Kapuvar, Hungary. Harrith Hasson, Professor of

Gynaecology, Chicago, IL, USA.

Figure 7.6 Modern laparoscopic theatre set up (photo courtesy of Daniel Leff).

routinely in some centres. The usability of the kit has also improved; touch screen pan els and even voice-activated systems are now

available on the market.

As minimally invasive and robotic procedures have become routine in some institutions, the d edicated 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 efcient working of the team is crucial to high-quality s urgery and quick yet safe turnover times.

Laparoscopic tools have also changed. Disposable equipment is more readily available, which do es unfortunately increase the cost of the

surgery. However, easy to use, ergonomically designed and reliable surgical tools are esse ntial 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 o bserving the layers through the cameras, and

new light sources within the abdomen may be simple ideas that affect surgical techniqu e in the near future.

GENERAL INTRAOPERATIVE PRINCIPLES

Laparoscopic cholecystectomy is now the ‘gold standard’ for operative treatment of sympto matic 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 follow ing sections highlight the important

technical steps that should be taken during any form of laparoscopic surgery to avoid c omplications.

Creating a pneumoperitoneum

There are two methods for creation of a pneumoperitoneum: open and closed. The closed me thod involves blind puncture using a Verres

needle. Although this method is fast and relatively safe, there is a small but signicant po tential for intestinal or vascular injury on

introduction of the needle or rst 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 m ade at the level of the umbilicus. 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, followed by the creation of a 1-cm opening in the fascia. Free penetr ation into the abdominal cavity is conrmed by the gentle

introduction of a nger. Finally, a Hasson trocar (or other blunt-tip trocar) is inserted and a nchored with the fascial sutures (Figure 7.7).

The open technique may initially appear timeconsuming and even cumbersome; howeve r, with practice, it is quick, efcient and safe

overall. Optical entry to the abdomen under direct vision using optical ports (especiall y 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 layer to be dissected through using the laparoscope within an optical port to be inserted into the abdomen.

Figure 7.7 Open technique with Hasson port. Apply safe principles of closed technique.

Preoperative problems

Previous abdominal surgery

Previous abdominal surgery is no longer a contraindication to laparoscopic surgery, but preop erative evaluation is necessary to assess the

type and location of surgical scars. As mentioned earlier, the open technique for insertion of the rst trocar is safer. Before trocar

insertion, the introduction of a ngertip 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 lapar oscope 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 w indow into a free area of the peritoneal cavity (Figure

7.8).

Obesity

Laparoscopic and robotic surgery have proved to be safe and effective procedures in the obese population. In fact, some procedures are

less difcult than their open counterparts for the

General intraoperative principles 99

Figure 7.8 Intra-abdominal adhesion.

morbidly obese patient, e.g. in bariatic surgery. Technical difculties occur, however, in obtaining pneumoperitoneum, reaching the

operative region adequately and achieving adequate exposure in the presence o f an obese colon. Increased thickness of the subcutaneous

fat makes insufation of the abdominal cavity more difcult. With the closed technique , a larger Verres needle is often required for

morbidly obese patients. Pulling the skin up for xation of the soft tissues is be tter accomplished with towel clamps. Only moderate

force should be used to avoid separating the skin farther away from the fascia. The ne edle should be passed at nearly a right angle to the

skin and preferably above the umbilicus where the peritoneum is more rmly x ed to the midline. The open technique of inserting a

Hasson trocar is easier and safer for obese patients, but technically demanding in morbidly ob ese patients, where optical entry is now

more commonplace. The main difculty is reaching the fascia. A larger skin incision (1–3 cm) , starting at the umbilicus and extending

superiorly, may facilitate this. To reach the operative area adequately, the location of som e of the ports has to be modied and, in some

instances, larger and longer instruments are necessary. When the length of the laparoscop e appears to be insufcient to reach the

operative area adequately, the initial midline port should be placed nearer to the op erative eld. Recently, the use of optical port entry for

laparoscopic bariatric surgery has revolutionised port entry for morbid obesity cases.

Operative problems

Intraoperative perforation of the gall bladder

Perforation of the gall bladder is more common with the laparoscopic technique than with t he open technique (see also Chapter 67).

Some authors have reported an incidence of up to 30 per cent, 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 uid 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. If there is stone spillage, every attempt must be made to collect an d extract the stones and if there is a

possibility of stones retained in the peritoneum, then an ultrasound should be arranged 6 weeks postoperatively to assess a collection

around a stone and the patient should be informed of this outcome postoperatively.

Bleeding

In some of the larger series, bleeding has been the most common cause for conversion to an open procedure. Bleeding plays a more

important role in laparoscopic surgery because of factors inherent to the techniq ue. These include a limited eld that can easily be

obscured by relatively small amounts of blood, magnication that makes small arte rial bleeding appear to be a signicant haemorrhage

and light absorption that obscures the visual eld.

How to avoid bleeding

As in any surgical procedure the best way to handle intraoperative bleeding is to preven t 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;

• inammatory 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 typ e of bleeding. When the bleeding vessel is identied, a

ne-tip grasper can be used to grasp it and apply either electrocautery or a clip, depending on it s size. When the vessel is not identied

early and a pool of blood forms, compression should be applied immediately with a blu nt instrument, a cotton swab (ENT or mastoid

swab) or with the adjacent organ. Good suction and irrigation are of utmost importance. O nce 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 ach ieve adequate exposure and at the

same time to enable the concomitant use of a suction device and an insulated g rasper. Although most of the bleeding vessels can be

controlled laparoscopically, judgement should be used in deciding when not to prolong bleedi ng, but to convert to an open procedure at

an early stage. Surgicell or other clot-promoting strips, or tissue glues may also be used lap aroscopically to aid haemostasis. If at any

stage bleeding is difcult to stem laparoscopically, then there should be no delay to conver t to open in the interests of patient safety.

Bleeding from the gall bladder bed Bleeding from the gall bladder bed can usu ally be prevented by performing the dissection in the

correct plane. When a bleeding site appears during detachment of the gall bladder, the dissectio n should be carried a little farther to

adequately expose the bleeding point. Once this step has been performed, direct applica tion of electrocautery usually controls the

bleeding. If bleeding persists, indirect application of electrocautery is useful becaus e it avoids detachment of the formed crust. This

procedure is accomplished by applying pressure to the bleeding point with a blunt, insula ted 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 applyin g the electrocautery current.

Bleeding from a trocar site

Bleeding from the trocar sites is usually controlled by applying upwards and later al pressure with the trocar itself. Considerable bleeding

may occur if the falciform ligament is impaled with the substernal trocar or if one of the epigas tric vessels is injured. If signicant

continuous bleeding from the falciform ligament occurs, haemostasis is achieved by percutane ously inserting a large, straight needle at

one side of the ligament. A monolament 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 7.9). The loop is suspended and compression is achieved. Maintaining compression

throughout the procedure usually sufces. After the procedure has been completed, th e loop is removed under direct laparoscopic

visualisation to ensure complete haemostasis. When signicant continuous bleeding from the a bdominal wall occurs, haemostasis can be

accomplished either by pressure or by suturing the bleeding site. Pressure can be app lied using a Foley balloon catheter. The catheter is

introduced into the abdominal cavity through the bleeding trocar site wound, the balloon is inated 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 remo ved. Although this method is

successful in achieving haemostasis, the authors favour direct suturing of the bleeding vessel. This ma noeuvre is accomplished by

extending the skin incision by 3 mm at both ends of the bleeding trocar site wound. Tw o gure-of-eight sutures are placed in the path of

the vessel at both ends of the wound. Devices such as the EndoClose may also b e 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 dissectio n and identication of the cystic artery and its

branches, as well as identifying and carrying out dissection of the gall bladder in the correct plane, help to prevent bleeding from the

cystic vessels and the hepatic bed. Nevertheless, clot formation takes place when unsuspected bl eeding occurs or when inammation is

severe and a clear plane is not present between the gall bladder and the hepatic 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 uid can be kept

in the operative eld 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 occ ur following the use of monopolar diathermy.

The overall incidence is between one and two cases per 1000 operations. Elect rical 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 ins trument that is touching the activated probe

(Figure 7.10); (3) insulation breaks in the electrodes; (4) direct sparking to b owel 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 monopolar

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 insulatio n. 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 straightforwa rd with a low incidence of pain or other problems.

The most common routine postoperative symptoms are a dull upper abdominal pain, nau sea and pain around the shoulders (referred from

the diaphragm). There has been some suggestion that the instillation of local anaesthetic t o the operating site and into the suprahepatic

space, or even leaving 1 litre of normal

Figure 7.9 Port-side bleeding controlled with sutures. Figure 7.10 Direct coupling between bowel and laparoscope, which is touchin g the activated probe.

Frederic Eugene Basil Foley, 1891–1966, urologist, Ankher Hospital, St Paul, MN, USA. Discharge from hospital 101

saline in the peritoneum, serves to further decrease postoperative pain. It is a good gene ral rule that if the patient develops a fever or

tachycardia or complains of severe pain at the operation site, something is wrong and c lose observation is necessary. In this case, routine

investigation should include a full blood count, C reactive protein (CRP) measurement, liver f unction tests, an amylase test and,

probably, an ultrasound scan of the upper abdomen to detect uid collections. If bile du ct leakage is suspected, endoscopic retrograde

cholangiopancreatography (ERCP) may be needed. If in doubt, relaparoscopy or lapa rotomy should be performed earlier rather than

later. Death following technical errors in laparoscopic cholecystectomy has often been a ssociated with a long delay in deciding to re-

explore the abdomen.

In the absence of problems, patients should be t 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 su rgery and rarely this is severe. It usually responds to an

antiemetic, such as ondansetron, and settles within 12–24 hours. It is made worse by opiate a nalgesics and these should be avoided.

Shoulder tip pain

The patient should be warned about this preoperatively and told that the pain is referred f rom 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 w ithin 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 conc omitant signs, antibiotic therapy is occasionally required.

Occasionally, herniation through a port may account for localised pain and this can so metimes be due to a Richter’s hernia, such that the

patient exhibits no sign of intestinal obstruction. Successful laparoscopic surgery should not cause the patients 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. It is important that the patient provides separate consent for

this if the suppository is to be administered peroperatively. Suppositories may be adminis tered a further two or three times

postoperatively for relief of more severe pain. Otherwise, 500–1000 mg of paracetamol 4-hourly usually sufces (orally or if more pain,

intravenously). Opiate analgesics cause nausea and should be avoided unless the pain is ve ry severe. In this case, suspect a postoperative

complication (as above). The majority of patients require between one and four doses of 1 g of paracetam ol postoperatively. Severe pain

after routine laparoscopic cases, should warn the clinician that there may be an iatroge nic 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 obscuri ng 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 us ed.

Oral fluids

There is no signicant ileus after laparoscopic surgery, except in resectional procedures , such as colectomy or small bowel resection.

Patients can start taking oral uids 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 a fter 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 rst week, although there is no clear evidence that this is necessary.

Urinary catheter

If a urinary catheter has been placed in the bladder during the operation, it should be removed before the patient regains consciousness.

The patient should be warned of the possibility and symptoms of postoperative cys titis and told to seek advice in the unlikely event of

this occurring.

Drains

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 uid, it should be removed within 1 hour of the operation. If it has been placed because of excessive

hepatic bleeding or bile leakage it should be removed when that problem has resolve d, usually after 12–24 hours. Continued blood loss

from a drain is an indication for reexploration of the abdomen (Summary box 7.4).

Summary box 7.4

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

Most surgeons discharge a signicant 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 u ntil they are seen to be comfortable, passed urine

and eating and drinking satisfactorily. They should be told that if they develop abdomina l pain or other severe symptoms then they

should return to the hospital or to their general practitioner. Even for more major cases, incl uding 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 sit es after 7 days.

Mobility and convalescence

Patients can get out of bed to go to the toilet as soon as they have recovered from th e anaesthetic and they should be encouraged to do so.

Such movements are remarkably pain free when compared with the mobility achieved a fter 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 quietly for the rst 2–3 days, in terspersing increasing exercise with rest. After

the third day, patients will have undertaken increasing amounts of activity. The avera ge return to work is about 10 days.

THE PRINCIPLES OF COMMON

LAPAROSCOPIC PROCEDURES

The principles of common laparoscopic procedures are described in the appropriate c hapters:

• laparoscopic cholecystectomy (Chapter 63);

• laparoscopic inguinal hernia repair (Chapter 57);

• laparoscopic antireux surgery (Chapter 59);

• laparoscopic appendicectomy (Chapter 67).

• laparoscopic bariatric surgery (Chapter 64)

•

laparoscopic colectomy/anterior resection (Chapters 69 and 72)

•

laparoscopic upper gastrointestinal (GI) surgery (Chapters 62, 63 and 64)

Other elective laparoscopic or minimally invasive procedures that are becoming more widely ut ilised in certain specialist centres include:

• colectomy;

• gastrectomy

• splenectomy;

• nephrectomy;

• adrenalectomy;

• prostatectomy;

• 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 pat ients) in the hands of experienced laparoscopic surgeons.

These may include diagnostic laparoscopy, repair of a perforated duodenal ulcer, lapa roscopic appendicectomy, treatment of intestinal

obstruction secondary to adhesions, strangulated hernia repairs and, also, the laparoscopic evalu ation 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;

• signicant 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.

Until these are overcome, by continued development of the technology and the dri ve of surgeons to progress in the eld, robotically

assisted surgery will not be commonplace. However, the potential for such systems is immense a nd continued research and clinical trials

will pave the way for future generations of surgeons and patients alike.

FURTHER DEVELOPMENTS THAT HAVE MADE MINIMALLY INVASIV E SURGERY EVEN LESS INVASIVE

Single incision laparoscopic surgery Laparoscopy has reduced the trauma from surgery compared to open techniques and is now used

routinely for benign and oncological surgery in many centres. However, there is contin ued work on how to reduce the trauma and

scarring from the incisions used in laparoscopic surgery as multiple port sites are needed for most procedures. Natural orice

translumenal endoscopic surgery (NOTES) (see below) addresses this but at present, the safety of the transgastric route is not sufcient

for the routine use of this approach to surgery. Advanced laparoscopists have t herefore turned to focussing on the single incision for

open entry via the umbilicus as an alternative. Single incision laparoscopic surgery (SIL S) 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

benet is that only one incision, through a natural scar (the umbilicus), is made therefore th ese procedures are virtually ‘scarless’.

Second, less port sites around the abdomen have the potential for less pain, less risk of p ort 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. It does require specially manufactured multichannel ports an d 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. However, the clinical benet for this technique which has a di fcult and steep learning curve is still

awaited from randomised trials being carried out internationally. Non-randomised data have shown understandably better cosmetic

outcomes and even less pain in the immediate postoperative period, however, this needs to be further corroborated with randomised data.

The future 103

Natural orifice translumenal endoscopic surgery

This technique, whereby surgeons enter the peritoneal cavity via endoscopic puncture of a hollow viscus, has been much publicised in

recent years. Transvaginal NOTES cholecystectomies have been performed in human s successfully, but most still use hybrid procedures

for safety reasons with direct laparoscopic guidance. The closure of the visceral puncture site is the issue that really has prevented

widespread uptake of this technique, as transgastric and transcolonic closure of peritone al entry sites in a routinely safe way is not yet

perfected. Also, the equipment needed has signicant cost and requires a large number of practitioners in the team at present.

Nevertheless, it has much promise to be a technique for truely scarless surgery in the future an d much research is being carried out on

this eld which is less widely adpoted at present compared to 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, ex cellent 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 yesterd ay have to teach the surgeons

of tomorrow not only the technical and dextrous skills required, but also the decisionmaking a nd innovative skills necessary for the eld

to continue to evolve. Training is often perceived as difcult, as trainers have less control over the trainees at the time of surgery and

case loads may be smaller, especially in centres where laparoscopic and ro botic procedures are not common. However, trainees now

rightly expect exposure to these procedures and training systems should be adaptable f or international exposure so that these techniques

can be disseminated worldwide.

Improvements in instrumentation, the continued progress of robotic surgery and the d evelopment of structured training programmes are

the key to the future of minimal access surgery. The use of robots in surgery has incre ased dramatically in the last decade. Indeed, robots

are now available not only for assisting in surgery, but also for aiding in the per ioperative management of surgical patients. The remote

presence systems (In Touch Health, Santa Barbara, CA, USA; Figures 7.11 a nd 7.12) allow clinicians to assess patients in real time and

interact with them while they are not on site or even if in a different continent. Continued adva nces in related technologies, such as

computer science, will allow the incorporation of augmented reality systems alongsid e robotic systems to enhance surgical precision in

image-guided surgery. Endoluminal robotic surgery is in its infancy, but systems ar e being developed that will enable navigation within

the colon to allow surgery on lesions in spaces that are accessible from the outside witho ut an exterior incision being made. The advent

of nanotechnology will also bring about much change in surgery. Miniaturisation will be po ssible, potentially allowing surgery at a

cellular level to be carried out.

At present, work has already started on single-port laparoscopy (see above under Sing le incision laparoscopic surgery),

Figure 7.11 Remote presence robot (courtesy of the Department of Biosurgery and Surgical Tech nology, Imperial College, London).

Figure 7.12 Remote presence console (courtesy of the Department of Biosurgery and Surgical Technol ogy, Imperial College, London).

in which a single port may act as a camera and have unfolding instruments open u p once they are inside the peritoneum to perform the

surgery, therefore reducing the number of port sites needed. Extensive resea rch is also being carried out in the eld of NOTES.

Minimising the potential contamination of the peritoneum and the ability to carry out a sa fe 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 tel l how much of what is new is truly better.

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

Ballantyne GH, Marescaux J, Giulianotti PC (eds). Primer of robotic and tel erobotic surgery. Philadelphia, PA: Lippincott Williams &

Wilkins, 2004.

Chow AG, Purkayastha S, Zacharakis E, Paraskeva P. Single-incision laparoscopic surgery for right hemicolectomy. Arch Surg 2011;

146: 183–6.

Chow A, Purkayastha S, Aziz O et al. Single-incision laparoscopic su rgery for cholecystectomy: a retrospective comparison with 4-port

laparoscopic cholecystectomy. Arch Surg 2010; 145: 1187–91.

Chow A, Purkayastha S, Paraskeva P. Appendicectomy and cholecystectomy using sin gle-incision laparoscopic surgery (SILS): the first

UK experience. Surg Innov 2009; 16: 211–7.

Chow A, Purkayastha S, Aziz O, Paraskeva P. Single-incision laparoscopic surgery for cholecystectomy: an evolving technique. Surg

Endosc 2010; 24: 709–14.

Gill IS, Sung GT, Ballantyne GH (eds). Robotics in surgery. Surg Clin N Am 2 003; 83: 15–16.

Purkayastha S, Athanasiou T, Casula R, Darzi A. Robotic surgery: a review. Hosp Med 2004; 65: 153–9.

Berkley George Andrew Moynihan (Lord Moynihan of Leeds), 1855–1936, Professor of Clinical Surger y, The University of Leeds, Leeds, UK. CHAPTER

paediatric surgery Principles of

LEARNING OBJECTIVES

To recognize and learn:

• The important differences between adults and children which have c linical implications

• The principles of trauma management in children

• How to safely prescribe perioperative fluids in children

• How to avoid the pitfalls that lead to a missed or delayed diagnosis f or common emergency conditions

• A collection of congenital malformations managed by neonatal surgeons that may present later to general surgeons

• The common safeguarding issues in children and know how to pro ceed if abuse is suspected

INTRODUCTION

Premature and term neonates differ in their anatomy, physiology, neurology, psycholo gy, pathology and pharmacology, just as infants

differ from school-age children and adolescents from adults (Table 8.1). These differenc es underpin the principles of paediatric surgery.

A few examples appear in Table 8.2 and in Figure 8.1, but are not exhaustive.

A knowledge of teratology is fundamental to paediatric surgery, but since some anom alies rst present to adult services (e.g.

duplications, malrotation) this knowledge can occasionally pay dividends to su rgeons dealing with adults. Adult surgical services also

need to cater for the transitional needs of those graduating to adulthood, sometimes after com plex paediatric surgical attention. Generally,

children escape the comorbidities of degenerative diseases, but lifestyle problems, such as obesity , drug abuse and sexually transmitted

diseases are no longer rare.

We start with three important areas: (1) thermoregulation, (2) airway and (3) uid manageme nt, and then outline trauma, some common

problems in older children, a collection of neonatal surgical conditions, oncology and sa feguarding children.

Implications

Table 8.2 Some example differences between adults and children. Infants and small children have a wide abdomen, a broad costal margin and a

shallow pelvis

The edge of the liver comes below the costal margin and the bladder is largely intra-ab dominal

The ribs are more horizontal and are exible The umbilicus is relatively low lying

Transverse supraumbilical incisions give greater access than vertical midline ones for open surgery Trauma (including surgical access)

can easily damage the liver or bladder

The geometry of the ribs means that ventilation requires greater diaphragmatic movement. Th eir flexibility means that rib fractures are

rare and often a sign of abuse

A stoma in the lower abdomen of a neonate must be carefully sited for its bag not to in terfere with the umbilicus

Table 8.1 Common terms. Preterm Full term Neonate Infant

Child

<37 completed weeks’ gestation

Between 37 and 42 completed weeks of gestation Newborn baby up to 28 days of age

Up to 1 year of age

All ages up to 16 years, but often divided into preschool child (usually <5 years), child an d adolescent (puberty up to 16 years)

Facts

MAINTAINING TEMPERATURE

In comparison with older children, infants have less subcutaneous fat, immature vasomo tor control, greater heat loss from pulmonary

evaporation, and their surface area to weight ratio is higher. These need to be consid ered when managing sick children in the accident

and emergency department, anaesthetic room or operating theatre. These environments mu st be warm

Costal margin

Umbilicus

Pubic

symphysis Narrow nostrils Loose teeth

Large tongue

Compressible floor of mouth

High anterior larynx

Horseshoe-shaped epiglottis

Infant

(width > height) Adolescent (height > width)

Figure 8.1 Topographical differences in the abdomen. Figure 8.2 Summary of upper airway anatomy in an infant.

Table 8.3 Basic paediatric data.

and the infant’s head (20 per cent of surface area compared with 9 per cent in an adult) s hould be insulated. Infusions are warmed, and

respiratory gases both warmed and humidied. The core temperature is monitored and sa fe direct warming is needed for lengthy

operations.

AIRWAY

There are a number of differences in the airway and these have clinical implicatio ns (see Figure 8.2). The infant’s large head and short

neck predispose to flexion. The large tongue can obstruct the airway when unconsc ious and impede the airway and laryngoscopy. The

epiglottis projects posteriorly and the larynx is high, favouring a straight-bladed laryngo scope in those under one year of age. Uncuffed

tubes are preferred as the cricoid ring is the narrowest area (compared with the larynx in an adult)

ISBN: 9781444121278 and this is covered in loose epithelium that is easily irrita ted and

damage can result in subglottic stenosis.

(a) Weight Age Weight (kg)

Term neonate

1 year

5 years

10 years

(b) Vital signs

3.5

Age (years)

Heart rate (bpm) Systolic blood

Respiratorypressure rate (b/min)(mmHg)

<1 110–160

2–5 90–140

Proof Stage: 2 Fig No: 6.1 5–12 80–120

70–90 30–40

80–100 25–30

90–110 20–25

PERIOPERATIVE FLUIDS IN CHILDREN

Title:

Weight

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

Daily uid requirement

(mL/kg/hour)

(mL/kg/day) ISBN: 9781444121278 Proof Stage: Before prescribing uids (or drugs), the child’s weight must be

www.cactusdesign.co.uk known, their vital signs and their uid and electrolyte require

ments should be considered in relation to normal values and ranges (see Table 8.3). Dehy dration is difcult to assess: moderate

dehydration (5 per cent loss of total body water) may manifest in poor urine outp ut, dry mouth, and sunken eyes and fontanelle; severe

dehydration (>10 per cent) in decreased skin turgor, drowsiness, tachycardia and poor cap illary rell (>2 s) and signs of hypovolaemia.

Children develop hyponatraemic encephalopathy at higher sodium levels than adults because th ey have a higher brain–skull ratio. A few

children have had symptomatic hyponatraemic encephalopathy attributable to poor prescriptio n and monitoring of uids, some have died

and others have permanent neurological disability. Problems have arisen when (1) hyp otonic maintenance uids (e.g. 0.18 per cent

saline), have been inappropriately given to resuscitate or replace losses or (2) maintena nce uids have been given in excess (three to ve

times that required).

Neonate

Older child:

First 10 kg

Second 10 kg

Each subsequent kg 120–150 5

100 4

50 2

20 1

(d) Maintenance electrolyte requirements

Weight Sodium

Potassium

Energy (mmol/kg/

(mmol/kg/day)

(kcal/kg/ day) day)

<10 kg >10 kg 2–4 1.5–2.5 110 1–2 0.5–1.0 40–75

Approximate guide: weight (kg) = 2 × (age in years +4), or use a Broselow tape which estimates the w eight from the height.

Systolic blood pressure = 80 + (age in years × 2) mmHg.

Circulating blood volume = 80 mL/kg (90 mL/kg in infants).

Operative surgery 107 Tonicity and osmolarity

The term ‘isotonic’ is now considered in relation to the tonicity of the electrolyte compon ents of uids. Thus, isosmolar fluids such as

0.18 per cent saline with 4 per cent glucose and hyperosmolar uids such as 0.45 per cent saline with 5 per cent glucose are now

considered ‘hypotonic’ because the glucose is ignored. The National Patient S afety Agency (NPSA) in 2007 instructed that all stocks of

0.18 per cent saline with 4 per cent glucose be removed from non-specialised area s to reduce the risks of hyponatraemia from

inappropriate prescription.

Prescribing intravenous fluids

The four reasons for prescribing uids are detailed in Summary box 8.1. The body’s respons e to stress is to hold on to water and this

promotes hyponatraemia. The stresses that drive the nonosmotic retention of water inclu de trauma, head injury, chest infections and the

postoperative state. Restricting maintenance fluids to 70 per cent is thus appropriate for 24 hour s after major

Summary box 8.1

Fluids in children

Fluids are given intravenously for four reasons:

Circulatory support in resuscitating vascular collapse. (Given as a bolus of 10 or 20 mL/kg ov er periods up to 20 minutes with close monitoring of the response. Can be

repeated up to 40 mL/kg, then seek urgent help)

0.9 per cent saline

Blood

4.5 per cent albumin

Colloid

Replacement of previous fluid and electrolyte deficits. (Given over a longer period up to 48 hours with clini cal and biochemical review)

0.9 per cent saline + 0.15 per cent KCl

Hartmann’s solution

Replacement of ongoing losses (or a fluid tailored to the losses, e.g. 4.5 per cent albumin if protein loss is great. Replace losses mL for mL)

0.9 per cent saline + 0.15 per cent KCl

Hartmann’s solution

Maintenance outside neonatal period (hypotonic 0.18 per cent saline should not be used outside the neonatal per iod)

0.45 per cent saline + 0.15 per cent KCl in 2.5–5 per cent glucose

Hartmann’s ± glucose

0.9 per cent saline + 0.15 per cent KCl ± glucose Maintenance in the neonate

In term neonates in the first 48 hours of life, 10 per cent glucose at 60 mL/kg per day

Sodium 0.18 per cent and potassium 0.15 per cent are added on day 2

From day 3, around 4–5 mL/kg per hour or 100–

120 mL/kg per day

Preterm babies or those <2 kg may require 180 mL/kg/day of fluid

Consider impaired gluconeogenesis: monitor and keep glucose above 2.6 mmol/L

surgery. The liberation of the uid rate is guided by the results of daily electrolyte levels . Urine output will often be reduced after major

surgery, but a common response to this can be to inappropriately increase maintenance uid. A bolus of uid is only appropriate if

hypovolaemia is evident and needs correction.

In the surgical setting, hyponatraemia is usually a consequence of too much free water and not insufcient sodium. If mild and

asymptomatic (e.g. 130 mmol/L) then uid restriction is appropriate. If symptom atic with headache, lethargy or seizures and the Na level

is <125 mmol/L, a rapid infusion of 4 per cent hypertonic saline is needed and paediatric inten sive care unit (PICU) admission.

HISTORY AND EXAMINATION

Time, patience and a genuine interest will help to establish a good rapport with th e child and their parents or carers. An opportunistic

rather than a systematic approach to the history and examination may be needed, but appropria te areas must be covered. Do not forget to

explore perinatal problems and the family and social background. Children should be to ld what to expect from an examination,

investigation or surgical procedure in terms that they can understand. Fear, anxiety and pain can be reduced by involving the parents and

by looking after the child in an appropriate environment. General health concer ns are best discussed with a paediatrician.

OPERATIVE SURGERY

A well-prepared patient who has not been excessively starved (Summary box 8.2), with ap propriate consent, is anaesthetised in a child-

friendly anaesthetic room. Surgery demands meticulous and gentle technique, strict h aemostasis, ne suture materials and often

magnication aids. Basic principles apply: maintaining well-vascularised tissues, avoiding tens ion, minimising tissue necrosis and

contamination. The intestine can be anastomosed with single-layer interrupted extra mucosal sutures. Abdominal wounds are closed with

absorbable sutures using a layered or a mass closure. Wound dehiscence is rare and usually the result of poor technique. Clean skin

incisions are best closed with absorbable subcuticular sutures. Endoscopic minimally inv asive approaches can be used at all ages to

achieve the same advantages as in adults, but instruments and insufation pressures must be tailored to the size of the child.

Postoperatively, children recover swiftly. Analgesia must be adequate and appropriate, recognisin g the potential for respiratory

depression with opioids. Appropriately trained staff monitor the airway, vital signs, oxygen saturation, uid balance, temperature, pain

control and glucose levels during recovery (Summary box 8.3).

Summary box 8.2

Starvation instructions

Two hours for clear fluids Four hours for breast milk Six hours for solids

Summary box 8.3

Surgical technique in children

Gentle tissue handling

Abdominal incisions can be closed with absorbable sutures Bowel can be anastomosed with interrupted sing le-layer extramucosal sutures

Skin can be closed with absorbable subcuticular sutures

Stomas are necessary in some children. A gastrostomy may be required for nu tritional support, particularly in the neurologically disabled

child. Temporary intestinal stomas are used in the management of anorectal malform ations, necrotising enterocolitis and Hirschsprung’s

disease. Infants with a proximal stoma and high losses frequently require salt or bicarbon ate supplements to avoid decits, which can

cause poor weight gain and acidosis.

Surgeons who operate on children should consider the longterm outcomes of surgical d isease and its treatment during maturation and

adult life. For example, ileal resection in the neonate may later be complicated b y vitamin B12 deciency, malabsorption of fat-soluble

vitamins, gallstones, renal oxalate stones and perianastomotic ulceration. Long-term concern s include the impact on continence, fertility,

sexual activity, psychosocial adaptation, and the potential risk of late malignancy (e.g. undescen ded testis, choledochal cyst, duplication

cysts).

PAEDIATRIC TRAUMA

Trauma remains a leading cause of death in children and adolescents worldwide. Many of these deaths are avoidable if prompt treatment

is given well. Surgeons should attend the Advanced Trauma Life Support (ATLS) programm e which covers trauma in children. Some of

the important differences for children follow:

•

Avoid overextension of the neck which can obstruct the

airway.

• Use a Broselow tape if the weight is not known.

•

Blood pressure is often normal until >25 per cent of the circulating blood volume is lost.

•

Cardiorespiratory arrest is usually due to hypoxia and not vascular disease.

• Diagnostic peritoneal lavage is obsolete in children. Resuscitation

For information related to uids, see Summary box 8.1. High

1–3 cm

Figure 8.3 The intraosseous needle is inserted into the medullary cavity of the proximal tibia about 1–3 cm below the tibi al tuberosity.

however, is straightforward and particularly useful in children (Figure 8.3).

A major spinal cord injury can be present in a child without radiographic abnormalities. After major trauma, a cervical spine injury

should be assumed and the neck immobilised until cross-sectional imaging ‘clears’ the spine. Other considerations include intravenous

analgesia and, in the unconscious or ventilated child or those with major abdominal injur ies, a nasogastric tube (orogastric if suspicion of

a basal skull fracture) and a urethral catheter (if no evidence of a urethral injury).

Secondary survey and emergency management

Chest trauma

Children have elastic ribs that rarely fracture but deformation causes lung contusions. A major thoracic injury may exist despite a normal

chest radiograph. The airway is secured, oxygen is given and hypovolaemia is corrected . A tension pneumothorax should be suspected

clinically before the chest x-ray is requested and immediate needle thoracocentesis (secon d intercostal space, mid-clavicular line)

performed. A chest drain is then placed (fth intercostal space, mid-axillary li ne). Massive haemothorax needs a chest drain. Cardiac

tamponade may fol

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

low blunt or penetrating injury and requires emergency needle

ISBN: 9781444121278 Proof Stage: flow

oxygen is required if there is cardiorespiratory compromise,

and endotracheal intubation and ventilation are required if oxy

www.cactusdesign.co.uk

genation is inadequate or to control a ail chest or in children

with a serious head injury (Glasgow Coma Score ≤8). Seriously

injured children require two large peripheral intravenous can

nulae. The long saphenous at the ankle, femoral, external jugu

lar and, in babies, scalp veins can be used. Central venous access

should only be attempted by an expert. Intraosseous infusion

pericardiocentesis. Diaphragmatic rupture after blunt abdominal trauma is detected by chest r adiography or computed tomography (CT)

scan; surgical repair is undertaken once the patient is stable (Figure 8.4).

Abdomen

Blunt trauma is more common than penetrating trauma. The liver and spleen are more v ulnerable in children being less well protected by

the rib cage. The abdomen is inspected for patterned

The Glasgow Coma Score was introduced in 1977 by William Bryan Jennet, Professor

of Neurosurgery, and Graham Michael Teasdale, a neurosurgeon at the University

Department of Neurosurgery at the Institute of Neurological Sciences, The Southern

General Hospital, Glasgow, UK. Professor Teasdale was later knighted and became

President of the Royal College of Physicians and Surgeons of Glasgow.

bruising from seatbelts (Figure 8.5) or tyres. Compression will have been against the rig id skeleton. Intra-abdominal or intrathoracic

bleeding should be considered promptly in the shocked child if external bleeding has no t been profuse. Plasma amylase levels may be

normal despite pancreatic injury (Figure 8.6).

Paediatric trauma 109

Figure 8.4 Traumatic diaphragmatic rupture.

Figure 8.5 Bruises from a lap belt.

Imaging

Focused assessment with sonography for trauma (FAST) looks for uid in the perihepatic a nd hepatorenal space, the perisplenic area,

the pelvis and the pericardium. It has a role in children but it does not detect solid organ in juries nor replace CT. In the

haemodynamically stable child, a CT scan with intravenous contrast is required (Figure 8.7).

Bowel perforation or deep penetrating trauma require a laparoscopy or laparotomy. Is olated blunt splenic and/or liver injuries identied

on a CT scan can be safely and effectively managed non-operatively (Summa ry box 8.4) in the majority of children, so avoiding surgery

and the long-term risks of splenectomy.

Summary box 8.4

Requirements for successful non-operative management of isolated blunt liver o r spleen trauma

Haemodynamic stability after resuscitation with no more than 60 mL/kg of fluid

A good-quality computed tomographic scan

No evidence of hollow visceral injury

Close monitoring and the immediate availability of surgical expertise and facilities

Figure 8.6 Abdominal computed tomographic scan showing a transection through the neck of the pancreas (arrow) from a bicycle handlebar injury.

Ongoing intra-abdominal bleeding requires a laparotomy, though angiography and arterial embolisation can be useful in some. Bile leaks

are uncommon and can usually be managed by an interventional radiological techn ique. Uncomplicated unoperated cases of liver/spleen

trauma can be discharged after 5–7, days but activity is restricted for 3–6 weeks and contac t sports avoided for between two and three

months. Blunt renal trauma can be managed conservatively, but an acutely non-functio ning kidney following abdominal trauma may

need urgent exploration with a view to revascularisation.

Summary box 8.5

Paediatric trauma

Use Advanced Trauma Life Support (ATLS) principles Overextension of the neck will compromise the ai rway Cervical spine injury can be present without radiographic

signs

Intraosseous vascular access is helpful in small children Lung contusion can occur without rib fractures

Patterned skin bruising suggests underlying organ injury In a stable child, abdominal injuries are best asses sed by computed tomography

Isolated liver or splenic injury can usually be managed nonoperatively

Patterns of injury

• Lap belts: the small intestine or lumbar spine.

•

Bicycle handlebars: pancreatic, duodenal or liver trauma

(Figure 8.6).

• Straddle injuries: the urethra and pelvis.

•

Run-over injuries: severe crushing of the chest, and/or abdomen and/or pelvis.

The main principles for managing trauma in children appear in Summary box 8.5.

Figure 8.7 Abdominal computed tomographic scan after intravenous contrast in an 11-year-old boy showing a ruptured spleen (succ essfully managed non-operatively).

COMMON PAEDIATRIC SURGICAL CONDITIONS

Inguinoscrotal disorders

Most genital abnormalities in boys are the result of abnormal development. The testis develops f rom the urogenital ridge on the posterior

abdominal wall. Gonadal induction to form a testis is regulated by genes on the Y chromo some. In the abdominal descent, the testis

migrates towards the internal ring, guided by mesenchymal tissue (gubernaculum). Descent int o the scrotum is mediated by testosterone

from the fetal testis. A tongue of peritoneum precedes the migrating testis through the inguina l canal; this is the processus vaginalis. This

peritoneal pouch normally becomes obliterated after birth, but failure to do so leads to the deve lopment of an inguinal hernia or

hydrocoele (Figure 8.8).

Inguinal hernias

Inguinal hernias in children are almost always indirect and due to a patent processus vaginalis. They are more frequent in boys, especially

if premature. An inguinal hernia will develop in at least one in 50 boys and about 15 p er cent are bilateral. Rarely, bilateral inguinal

hernias in a phenotypic girl may be the pre

Bowel Thinly patent track

(a) (b)

Figure 8.8 (a) Inguinal hernia and (b) hydrocoele in children are the result of incomplete obliteration of the processu s vaginalis.

Figure 8.9 A left inguinal swelling. Clinical examination is needed to confidently distinguish a hydrocoele from an in guinal hernia.

senting feature of androgen insensitivity syndrome (testicular feminisation) and the hernia sac may then contain a testis.

An inguinal hernia typically causes an intermittent swelling in the groin or scrotum on cr ying or straining (Figure 8.9). Unless an

inguinal swelling is observed, the diagnosis relies on the history and the prese nce of palpable thickening of the spermatic cord (or round

ligament in girls). Some inguinal hernias present as a rm, tender, irreducible lump in the g roin or scrotum because of incarceration at

the external ring. The infant may be irritable and vomit. Most incarcerated her nias in children can be successfully reduced by sustained

gentle compression (‘taxis’) aided by cautious analgesia. Repair is delayed for 24 hours to let th e oedema settle. If truly irreducible,

emergency surgery is required because of the risk of vascular compromise to the bowel, ovary or testis.

Inguinal herniotomy is performed via an inguinal skin crease incision, opening Scarp a’s fascia and then the external oblique. The

cremaster is cut and, through an initially small opening, the cord grasped and gen tly delivered. The vas and vessels are separated from

the sac which is then divided and proximally ligated. Outside the neonatal period, ingui nal herniotomy is treated as day-case surgery

(Summary box 8.6).

Summary box 8.6

Inguinal hernias

More common in premature boys

15 per cent bilateral

Indirect with a patent processus vaginalis

Groin lump that appears on straining or crying

Incarcerated inguinal hernias can usually be reduced with gentle pressure

In infants, they can transilluminate like a hydrocoele making the test redundant when the distinction is diff icult

If reduction is impossible, emergency surgery is needed Infants need repair promptly to prevent the risk o f

strangulation

The hernial sac is isolated, ligated and divided

Hydrocoeles

A patent processus vaginalis may allow only peritoneal uid to track down aroun d the testis to form a hydrocoele. Hydrocoeles are

unilateral or bilateral, asymptomatic, non-tender scrotal swellings. They may be t ense or lax, but typically transilluminate. The majority

resolve spontaneously as the processus continues to obliterate, but surgical ligation is rec ommended in boys older than three years of age.

Undescended testes are palpable or impalpable At birth, about 4 per cent of full-term bo ys have unilateral or bilateral undescended

testes, but by one year of age it is <1 per cent and it changes little thereafter. Th e incidence is higher in preterm infants because the testis

descends through the inguinal canal during the third trimester. A normal testis reaches the b ase of the scrotum with a good length of cord

above it. Testes cannot be palpated in the inguinal canal, but can be milked from there into the supercial pouch (palpable undescended

testis) or in to the scrotum with a good length of cord (normal). A retractile testis can be manipulated into the base of the scrotum

without tension, but is pulled up by the cremaster muscle. With time, retractile testes reside p ermanently in the scrotum; however, follow

up is advisable as, rarely, the testis ascends into the inguinal canal. The ascending testis needs an orchidopexy. An ectopic testis lies

outside its normal line of descent, often in the perineum (Summary box 8.7).

Summary box 8.7

The undescended testis

A retractile testis reaches the base of the scrotum, but retracts

An undescended testis may be palpable or impalpable An ectopic testis lies outside the normal line of desce nt Palpable undescended testes undergo a single stage

orchidopexy

Impalpable undescended testes usually require a two stage orchidopexy

Orchidopexy around one year of age improves fertility and may reduce the risk of malignancy

A palpable undescended testis should undergo a day-case orchidopexy around one year of age. The testis is mobilised through an

inguinal incision, preserving the vas deferens and testicular vessels. The associat ed patent processus vaginalis is ligated and divided, and

the testis is placed in a subdartos scrotal pouch.

Impalpable undescended testes are either absent or located in the abdomen or inguinal canal. There is no benet from imaging and

these are best managed with a laparoscopy (Figure 8.10) and usually a staged approach .

The benets of orchidopexy include:

• Fertility. To optimise spermatogenesis, the testis needs to be in the scrotum b elow body temperature at a young age. Orchidopexy

around one year of age is currently recommended. Fertility after orchidopexy for a un ilateral

Figure 8.10 Laparoscopic view of a right-sided intra-abdominal testis visible at the internal ring. Va s (single arrow) and testicular vessels (double arrow).

undescended testis is near normal. Men with a history of bilateral intra-abdominal testes are often i nfertile.

•

Malignancy. Undescended testes are histologically abnormal

and at an increased risk of malignancy. The greatest risk is for bilateral intra-abdominal teste s. Early orchidopexy for a unilateral

undescended testis may reduce the risk, but this is not proven.

•

Cosmetic and psychological. In an older boy, a prosthetic testis can be inserted to replace an absent on e.

The acute scrotum

Testicular torsion is most common in adolescents, but may occur at any age, including in the perinatal period. The pain is not always

scrotal and may be felt in the groin or lower abdomen. Oedema and erythema of the sc rotal skin can be absent. Sometimes there is a

history of previous transient episodes. Torsion of the testis must be relieved within 6–8 hours of the onset of symptoms for there to be a

good chance of testicular salvage. At operation, viability of the testis is assessed after derotation. If salv ageable, three-point xation of

both testes with non-absorbable sutures is performed. Expert assessment of testicular blood ow by colour Doppler ultrasound may help

in the differential diagnosis, but the scrotum must be explored urgently if torsion cannot be excluded.

Torsion of a testicular or epididymal appendage characteristically affects boys just before puberty (Fig ure 8.11), possibly because of

enlargement of the hydatid in response to gonadotrophins. A hydatid of Morgagni is an embryological remnant found on the upper pole

of the testis or epididymis. The pain often increases over a day or two. Occasionally, the torted hydatid can be felt or seen (blue dot sign).

Excision of the appendage leads to rapid resolution of symptoms. Viral or bacterial epididymo-orchitis may cause an acute scrotum in

infants and toddlers, but the diagnosis is often only made after scrotal exploration. Othe r conditions that rarely cause acute scrotal

symptoms and signs include idiopathic scrotal oedema (typically painless, erythematous scrotal swelling in a young boy extending from

the scrotum into the groin and towards the anus), an

Giovanni Batista Morgagni, 1682–1771, Professor of Anatomy, Padua, Italy for 59 years. He is regarded as ‘The Founder of Morbid Anatomy’. Epididymitis Hydatid

Testicular torsion torsion

0 5 10 15 Age (years)

Figure 8.11 Acute scrotal pathology at different ages.

incarcerated inguinal hernia, vasculitis or a scrotal haematoma (Summary box 8.8).

Summary box 8.8

Diagnosis and treatment of the acute scrotum

Torsion of the testis must be assumed until proven otherwise Testicular torsion can present with acute ingui nal or abdominal pain

Urgent surgical exploration is crucial if testicular torsion cannot be excluded

Torsion of a testicular appendage usually occurs just before puberty

An incarcerated inguinal hernia must be considered in the differential diagnosis

The penis

Hypospadias

In hypospadias, seen in 1:300 boys, the urethra opens proximally and ventrally. Most com monly, the opening is just proximal to the

glans, but it can open on the penile shaft or onto the perineum. It is attributed to failure o f complete urethral tubularisation in the fetus.

The foreskin is decient ventrally and there is a variable degree of chordee (a ventr al curvature of the penis most apparent on erection)

(Figure 8.12). Glanular hypospadias needs correction for cosmetic reasons but more proximal anomalies interfere with micturition and

erection. In a newborn with severe hypospadias and bilateral undescended testes, disorders of sexual development (DSD) should be

considered. A distal hypospadias is usually repaired before two years of age in one or two sta ges. Proximal varieties require complex

staged procedures. Surgery aims to achieve a terminal urethral meatus so that th e boy can stand to micturate with a normal stream, a

straight erection and a penis that looks normal. Ritual circumcision is contraindic ated in infants with hypospadias because the foreskin is

often required for the reconstruction.

The foreskin and circumcision

At birth, the foreskin is adherent to the glans penis. These adhesions separate spontaneo usly with time, allowing the foreskin to become

retractile. At one year of age, about 50 per cent of boys have a non-retractile foreskin. By four years, this has declined

Figure 8.12 Hypospadias: note the hooded foreskin and the ventral meatus.

to 10 per cent and by 16 years to just 1 per cent. Ballooning of the normal non-retractile fore skin on micturition brings many young boys

to doctors and explanation and reassurance are required, but no operation. Gentle retraction of the foreskin at bath times helps to

maintain hygiene, but forcible retraction should never be attempted. The presence of p reputial adhesions, when the foreskin remains

partially adherent to the glans, is normal and resolves spontaneously.

Circumcision has been an important tradition in Jewish, Muslim and other cultures. Propo nents observe that circumcision reduces the

incidence of urinary tract infection in infant boys; however, circumcision is not w ithout risk of signicant morbidity. The medical

indications for circumcision are:

• Phimosis. This term is often wrongly applied to describe a normal, non-retractile foreskin. T rue phimosis is seen as a whitish scarring

of the foreskin and is rare before ve years of age (Figure 8.13). It is caused by a localised ski n disease known as balanitis xerotica

obliterans (BXO), which also affects the glans penis and can cause urethral meatal stenosis.

• Recurrent balanoposthitis. A single episode of inammation of the foreskin, some times with a purulent discharge, is not uncommon

and usually resolves spontaneously; antibiotics are sometimes needed. Recurrent attacks are unusual but may be an indication for

circumcision.

• Recurrent urinary tract infection. Circumcision is occasionally justied in boys with an abnormal upper urinary tract anomaly and

recurrent urinary infection. It may also help boys with spina bida who need to pe rform clean intermittent urethral catheterisation.

An emerging but controversial indication for circumcision is in the prevention of sexually acquired human immunodeciency virus

(HIV) infection in communities where this is common; large clinical trials have shown that c ircumcision reduces the risk of HIV

transmission.

Figure 8.13 True phimosis from balanitis xerotica obliterans.

Circumcision for medical reasons is best performed under general anaesthesia. A lo ng-acting local anaesthetic regional block can be

given to reduce postoperative pain. Circumcision is not a trivial operation; bleeding and infection are well-recognised complications and

more serious hazards, such as injury to the glans, may occur if the procedure is no t carried out well (Summary box 8.9).

Summary box 8.9

Circumcision

Medical indications are balanitis xerotica obliterans and recurrent balanoposthitis, paraphimosis, scarring fro m trauma

Circumcision is not indicated for an otherwise healthy nonretractile foreskin

Complications include bleeding, poor cosmesis (too much or too little skin removed) and trauma to the glans or ureth ra Falciform ligament

Umbilical cord

Umbilical vein

Ilieum with

Merkels diverticulum

Umbilical ring

Allantois (urachus)

Becomes medial

umbilical fold

Umbilical

artery

Becomes median

umbilical fold

Bladder

Figure 8.14 Structures at the umbilicus.

Infantile hypertrophic pyloric stenosis Infantile hypertrophic pyloric stenosis (IH PS) presents with non-bilious projectile vomiting

between 2 and 8 weeks of age and is only rarely seen after 13 weeks. It is easily di stinguished from many other serious causes of

vomiting, such as infections, because the baby is particularly hungry. IHPS is a progressive cond ition and a detailed history helps

distinguish it from the more common gastro-oesophageal reux (GOR) which is commonly seen in infancy. In the UK, it affects 1:300

infants with a male to female ratio of 4:1. However, if a girl has IHPS her off spring have a high chance of developing it, suggesting a

genetic predisposition.

The non-bilious nature is stressed here to contrast the condition with the bilious vomiting of the potentially life-threatening malrotation

and volvulus seen occasionally in neonates.

IHPS can be diagnosed clinically. During a test feed, there is visible gastric peristalsis passing fr om left to right across the upper

abdomen and in a relaxed baby the pyloric ‘tumour’ is palpable as an ‘olive’ in th e right upper quadrant. The diagnosis

Midline hernias

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Title: Bailey & Love’s Short Practice of Surgery, 26th Ed can be conrmed by an ultrasound, which sho ws the thickened Proof Stage: pyloric

muscle. IHPS is readily treated by surgery but the infant must be adequately rehy drated and the hypochloraemic-hypokalaemic alkalosis

corrected; this may take 48 hours. In most

In the embryo, the umbilical ring is a relatively large defect in

the ventral abdominal wall transmitting several structures that

connect the fetus to the placenta (Figure 8.14). An umbilical

hernia is common and caused by incomplete closure of the

umbilical ring; incarceration is very rare. Most umbilical hernias

resolve spontaneously by four years of age. Supraumbilical her

nias are through defects in the linea alba just above the umbili

cal ring and these do not close, but are still repaired at around

four years of age. Epigastric hernias are defects higher still that

allow a small amount of preperitoneal fat to prolapse. They are

repaired if symptomatic.

babies, the dehydration and alkalosis can be corrected by giving 150–180 mL/kg per day of 0.4 5 per cent saline with 0.15 per cent KCl in

5 per cent glucose. Oral feeding is discontinued and the stomach emptied with an 8–10 Fr nasogastric tube; ongoing gastric losses should

be replaced with normal saline containing potassium chloride.

Ramstedt’s pyloromyotomy is performed through an incision around the umbilicus . The pyloric tumour is delivered by gentle traction on

the stomach. A serosal incision is made and the tumour spread (Figure 8.15). The end result s hould be an intact bulging submucosa from

duodenal fornix to gastric antrum. Perforation of the duodenal fornix is uncommon and not serious provided that it is recognised and

repaired immediately.

Wilhelm Conrad Ramstedt, 1867–1963, surgeon, The Rafaelklinik, Münster, Germany, performed his firs t pyloromyotomy in 1911.

Postoperatively, intravenous uids are continued until oral feeding is re-established within 24 ho urs. Occasionally, the baby has small

vomits on the rst few feeds but this resolves after 72 hours. If it persists, then an in complete myotomy or GOR should be considered.

Surgical complications include duodenal perforation, haemorrhage, wound infe ction and wound dehiscence – all are uncommon and

avoidable. Pyloromyotomy has no signicant long-term sequelae (Summary box 8.10).

Summary box 8.10

Infantile hypertrophic pyloric stenosis

Most commonly affects boys aged 2–8 weeks

Projectile vomiting after feeds

Test feed or ultrasound to confirm the diagnosis Gastric peristalsis can be seen and an ‘olive’ felt Hypochl oraemic metabolic alkalosis must be corrected before surgery

Pyloromyotomy splits the hypertrophied muscle leaving the mucosa intact

Table 8.4 Vomiting in infancy.

Bile-stained Neonate

Older infant Intestinal malrotation with volvulus

Duodenal atresia/stenosis (Down syndrome, antenatal diagnosis) Jejunal/ileal atresia (often isolat ed anomalies)

Hirschsprung’s disease

Anorectal malformations

Meconium ileus (cystic brosis)

Necrotising enterocolitis (an acquired condition in the

premature)

Incarcerated inguinal hernia

Intestinal malrotation with volvulus

Intussusception (often non-bilious initially)

Incarcerated inguinal hernia

Non-bilious

Other common or serious causes of vomiting in infancy are shown in Table 8.4.

Gastro-oesophageal reux is common and tends to resolve spontaneously with maturity. Persiste nt symptoms respond to thickened feeds

and anti-reux medication. Complications, such as failure to thrive or respiratory problems, de mand further investigation and, in some

cases, fundoplication.

Intussusception

Most intussusceptions (Figure 8.16) in children are seen from two months to two year s of age. They are life-threatening. Intussusception

typically causes a strangulating bowel obstruction, which can progress to gangrene and perforation. Intussusception is classied

according to the site of the intussusceptum and intussuscipiens. In children, more than 8 0 per

Infantile hypertrophic pyloric stenosis

Gastro-oesophageal reux

Feeding difculties (technique/volume)

Non-specic marker of illness, e.g. infection (urinary tract infection, meningitis, gastroen teritis, respiratory, metabolic disorder, raised

intracranial pressure, congenital adrenal hyperplasia)

cent are ileocolic, beginning several centimetres proximal to the ileocaecal valve with their ape x found in the ascending or transverse

colon.

In the majority, the cause is hyperplasia of Peyer’s patches (lymphoid tissue), w hich may be secondary to a viral infection. In 10 per cent

of children, intussusception is secondary to a pathological lead point, such as a Meckel’s diver ticulum, enteric

Figure 8.15 Pyloromyotomy for infantile hypertrophic pyloric stenosis. Figure 8 .16 Ileocolic intussusception causing small bowel obstruction.

duplication cyst or even a small bowel lymphoma. Such cases are more likely in children over the age of two years and in those with

recurrent intussusception.

Classically, a previously healthy infant presents with colicky pain and vomiting (milk, the n bile). Between episodes, the child initially

appears well. Later, they may pass a ‘redcurrant jelly’ stool. Clinical signs incl ude dehydration, abdominal distension and a palpable

sausage-shaped mass in the right upper quadrant. Rectal examination may reveal blood or rarely the apex of an intussusceptum

(Summary box 8.11).

Summary box 8.11

Presentation of intussusception

Bilious vomiting in an infant is a sign of intestinal obstruction until proved otherwise

Intussusception classically presents with colicky pain and vomiting

Intussusception should be considered in any infant with bloody stools

Age range is between 2 and 24 months of age

A plain radiograph is rarely requested but if done it commonly shows signs of small bo wel obstruction and a soft-tissue opacity.

Diagnosis is conrmed on an abdominal ultrasound. After resuscitation with in travenous uids, broad-spectrum antibiotics and

nasogastric drainage, non-operative reduction is attempted using an air enema (Figu re 8.17). Successful reduction is recognised if air

ows into the small bowel, together

Figure 8.17 Air enema reduction of an intussusception (the arrows mark the soft tissue shadow of the intussusc eptum).

with later resolution of symptoms and signs. An air enema is contraindicated if t here is peritonitis, perforation or shock. More than 70

per cent of intussusceptions can be reduced nonoperatively. Strangulated bowel and pa thological lead points are unlikely to reduce.

Perforation of the colon during pneumatic reduction is a recognised hazard, but is rare. Recurrent intussusception occurs in up to 5 per

cent of patients after nonoperative reduction (Summary box 8.12).

If an operative reduction is needed, this is usually performed open. The intussusception is milked distally by gentle compression from its

apex. Both the intussusceptum and the intussuscipiens are inspected for areas of non-via bility. An irreducible intussusception or one

complicated by infarction or a pathological lead point requires resection and primary anasto mosis.

Summary box 8.12

Management of intussusception

Bowel infarction will result without treatment

Most are ileocolic

Diagnosis can be confirmed by ultrasound scan

Fluid and electrolyte resuscitation is essential

Most intussusceptions can be reduced non-operatively using an air enema

If there are signs of peritonitis or perforation, then an emergency operation is needed

Acute abdominal pain in children over three years of age

Between one-third and one-half of children admitted to hospital with acute abdo minal pain have non-specic abdominal pain (NSAP).

Another one-third have acute appendicitis. Relatively benign conditions, such as cons tipation and urinary tract infection (UTI), account

for most of the remainder. A small proportion of children have more serious pathology .

History and examination

Time and patience are required to accurately evaluate the child with acute abdomin al pain. The child may be frightened and the parents

worried. Young children nd it difcult to accurately describe or localise abdominal pain, b ut can often give a good history. The

abdomen, genitalia, chest, throat and neck are examined. The abdomen may ne ed reassessment after analgesia and a number of reviews.

A gentle abdominal examination of the sleeping toddler, before removing their clothes, may revea l tenderness, guarding or a mass.

Rectal examination is only performed if a pelvic appendicitis is suspected and should be by the surgeon whose decision will be altered

by the ndings. Active observation acknowledges that a denitive diagnosis i s not always possible when the patient is rst seen. The

surgeon reassesses the child after a few hours whilst rehydrating with intravenous uid s or allowing clear uids and simple analgesics.

This approach reduces the need for investigations and can reduce the negative appendicectomy r ate to as low as 4 per cent (Summary

box 8.13).

Peter Ferry Jones, 1920–2009, Professor of Clinical Surgery, The University of Aberdeen, Aberdeen, UK . Summary box 8.13

management with antibiotics and an interval appendicectomy can be considered 6 week s later (Summary box 8.14). Work up of

children with acute abdominal pain

A careful history and examination and active observation are paramount

Routine tests include full blood count (FBC), C-reactive protein (CRP), urine analysis, microscop y and culture Other tests may be helpful after a period of observation:

abdominal ultrasound scan (can diagnose pelvic and urinary tract pathology, intussusception an d other conditions)

Occasionally helpful tests: a plain supine abdominal radiograph (particularly in the preschool ch ild with pain and vomiting), computed tomography scan in complex

patients

Selective specific investigations: blood culture, stool culture, plasma amylase, diagnostic laparoscopy

Acute non-specific abdominal pain

The clinical features of NSAP are similar to acute appendicitis, but the pain is poorly loca lised, not aggravated by movement and rarely

accompanied by guarding. The site and severity of maximum tenderness often vary during th e course of repeated examinations.

Symptoms are typically self-limiting within 48 hours. The aetiology of non-specic abdominal pain in children is obscure, but viral

infections and transient intussusception account for some cases. Viral infections can cause reactive lymphadenopathy, fever and diffuse

abdominal pain. In some children, recurrent acute abdominal pain can be organic or sometimes an expression of underlying psychosocial

problems or abuse.

Acute appendicitis and its pitfalls

Classically, there is anorexia and a few episodes of vomiting with central abdominal pain which settles in the right iliac fossa. In early

acute appendicitis, there is a fever of 37.3–38.4°C and localised tenderness. Finding pe rsistent guarding in the right iliac fossa on

repeated examination is the key to making the diagnosis and distinguishing it from NSAP which usually resolves over 24 to 48 hours.

NSAP does not have persistent guarding. Acute appendicitis is a clinical diagnosis and in vestigations may help, but cannot replace

regular expert clinical review. The pitfalls include wrongly making the diagnosis of gast roenteritis when there are loose stools or

attributing pain on micturition and pyuria to a UTI. Both of these can occur when there is a pelvic appendicitis or a pelvic collection.

Consider also referred pain from a possible right lower lobe pneumonia and remember that if antibiotics have been given the signs may

be subdued and presentation can be delayed. The diagnosis can be difcult in those und er ve years of age. However, many patients

under the age of ve present with a perforated appendix, not because the diagnosis is m ade late but rather the omentum is less well

developed and inammation is not well contained. The treatment starts with resuscitation with intravenous uids, analgesia and broad-

spectrum antibiotics. Appendicectomy can be performed laparoscopically or through a muscle-splitting right iliac fossa incision. An

appendix mass in a child who is not obstructed may respond to conservative

Summary box 8.14

Acute appendicitis

Anorexia, vomiting, low-grade fever

Tenderness and guarding in the right iliac fossa Exclude referred pain from right lower lobe pneumonia Take special care in the preschool child

Surgery is the treatment of choice after resuscitation and antibiotics

Other causes of acute abdominal pain in children

• Intestinal obstruction. Consider intussusception, inguinal hernia, adhesio ns and secondary to a Meckel’s diverticulum.

• Constipation. Often over-diagnosed as a cause of acute

abdominal pain, particularly as the plain x-ray of a dehydrated ill child frequently shows faecal loading. Constipation is more often a

cause of acute abdominal pain in a child who has been treated for Hirschsprun g’s disease or an anorectal malformation.

• Urinary tract disorders. Urinary tract infection is an uncommon ca use of acute abdominal pain. Urinary symptoms, fever and

vomiting tend to predominate. Urinalysis, microscopy and culture are useful, but a sterile pyuria may accompany acute appendicitis.

Boys with pelviureteric junction obstruction can present with acute or recurrent abdom inal pain and no urinary symptoms.

• Gastroenteritis. May cause colicky abdominal pain. Onset of pain before the diarrhoea and the presence of lower abdominal

tenderness should raise the suspicion of appendicitis.

• Tropical diseases. Ascariasis, typhoid and amoebiasis can cause acute a bdominal pain.

There are numerous rarer causes of acute abdominal pain in children including Henoch–Sch önlein purpura, sickle cell disease, primary

peritonitis, acute pancreatitis, biliary colic, testicular torsion, gynaecological pathology (e. g. ovarian cysts and tumours, pelvic

inammatory disease, haematometrocolpos) and urinary stone disease (Summary box 8.15).

Summary box 8.15

Rare causes of acute abdominal pain in children

Obstruction from intussusception, adhesions, Meckel’s diverticulum or an inguinal hernia

Constipation

Urinary tract disorders

Gastroenteritis

Ascariasis

Typhoid

Urinary tract infection

Urinary tract infections in children may be due to a urinary tract abnormality which may carry a risk of developing renal scarring from

ascending infection. Infection and obstruction is particularly hazardous. Olde r children complain of dysuria and frequency, whereas

infants present with vomiting, fever and/or poor feeding. Urine specimens from children are easily contaminated during collection and

results must be interpreted with care. A proven infection is investigated by an ultrasound scan. Mic turating cystography and radioisotope

renography are helpful in excluding vesicoureteric reux and renal scarring. Treatment aims to reliev e symptoms, correct causes and

prevent renal scarring. Vesicoureteric reux may resolve spontaneously, some may need antibiotic prophylaxis or, in a very small

number of cases, an endoscopic treatment or a reimplantation of the ureter.

Eduard Heinrich Henoch, 1820–1910, Professor of Diseases of Children, Berlin, Germany, described this form of purpura in 1868. Johann Lucas Schönlein, 1793–1864,

Professor of Medicine, Berlin, Germany, published his description of this form of purpura in 1837.

Children with neuropathic bladders (e.g. spina bida) are at risk of seconda ry upper renal tract complications. Management of these

children must take into account their dexterity and motivation. An adequate capacity, lo w-pressure bladder can frequently be managed by

clean intermittent catheterisation, but a high pressure bladder is hazardous and other strategies, such as bladder augmentation, may be

necessary. Some of these children empty their bladder via a non-reuxing cathete risable channel fashioned from the appendix, the bowel

or a redundant ureter interposed between the abdominal wall and bladder (Mitrofanoff).

Anorectal problems

Constipation

The passage of hard or infrequent stools is common in children in the West. Severe constip ation may be secondary to an anal fissure,

Hirschsprung’s disease, an anorectal malformation or a neuropathic bowel. A detailed history and examination of the abdomen, anus and

spine will identify most causes. Rectal examination and plain abdominal radiography ma y be helpful in severe cases. In the absence of

specic underlying pathology, the child is best managed jointly with a paediatrician using a combination of diet, extra uids, reward

systems, laxatives and, in some cases, psychological intervention.

Rectal prolapse

Mucosal rectal prolapse can occur in toddlers and is exacerbated by straining or squatting on a p otty. It is typically intermittent and

frequently self-limiting. Rarely, it may be secondary to cystic fibrosis or spinal dysraphism. The differential diagnosis includes a

prolapsing rectal polyp. Underlying factors such as constipation should be treated. Recu rrent symptomatic prolapse usually responds to

injection sclerotherapy. Strapping the buttocks is ineffective.

Rectal bleeding

Unlike in adults, malignancy is an exceptionally rare cause of rectal bleeding. In newborns, th e life-threatening causes are malrotation

and necrotising enterocolitis and in older infants and children, intussusception. The quant ities of blood loss are small, but the conditions

serious. Other causes include anal ssures, juvenile polyps (Figure 8.18) and certain ga stroenteritides (e.g. Campylobacter infection).

The four-year-old patient who presents with an Hb of 4 gm/ dL will most likely have bl ed profusely from an ulcer adjacent to a Meckel’s

diverticulum containing ectopic gastric mucosa (Figure 8.19). A technetium scan ma y conrm the presence of

Figure 8.18 Colonic juvenile polyp: these are typically pedunculated.

Figure 8.19 Meckel’s diverticulum containing ectopic gastric mucosa.

ectopic gastric mucosa (Figure 8.20). A Meckel’s diverticulum may also be compl icated by an obstructing band between the

diverticulum and the umbilicus, diverticulitis, intussusception, intestinal volvulus or pe rforation.

Swallowed or inhaled foreign bodies

Coins are the most frequently swallowed foreign bodies in children. Once beyond the c ardia, they are usually passed in a few days. A

plain radiograph of the abdomen, chest and neck should establish the site of r adio-opaque objects. Oesophageal objects can be removed

endoscopically under general anaesthesia. Button batteries must be removed within hou rs. If they remain in the oesophagus they can

cause gastrointestinal perforation into the trachea. Batteries in the stomach are either removed urgently or followed very closely with

repeat x-rays over a couple of days. The need to remove sharp objects depends on the ir size, the age of the child and their position in the

gut. Ingested magnets can cause entero-enteric stulae when they x to one another in adjacent loops of bowel.

Inhaled foreign bodies cause sudden-onset coughing and stridor. If there is worsening dyspno ea or signs of hypoxia, then the infant

should be given back blows in a head-down position. A Heimlich manoeuvre can be used in older children. A foreign body is suggested

by: a unilateral wheeze, decreased transmitted breath sounds and a hyperinated lu ng from air trapping on an expiratory chest x-ray

(Figure 8.21). A rigid bronchoscopy with a ventilating bronchoscope and appropriate optical forceps are needed to assess and remove

objects (Summary box 8.16).

Paul Mitrofanoff, born 1934, Professor of Paediatric Surgery, Rouen, France. Henry J Heimlich, born 19 20, thoracic surgeon, Xavier University, Cincinnati, OH, USA.

Figure 8.20 A positive Meckel’s scan.

Summary box 8.16

Swallowed and inhaled objects

Most swallowed objects pass spontaneously

Batteries need watching – they must pass quickly if their contents are not to leak

Objects jammed in the airway or oesophagus need removing promptly

CONGENITAL MALFORMATIONS

Around 2 per cent of babies are born with one or more major structural anomalies ca used by genetic defects or teratogenic insults. Some

are diagnosed antenatally and surgeons are involved in prenatal counselling. Terminatio n of pregnancy or a planned delivery in a

specialist centre are options for severe malformations. Prenatal diagnosis may in clude checking the karyotype (e.g. Down syndrome

(trisomy 21)) or testing for genetic disorders, such as cystic brosis.

The incidence of congenital malformations is variable (Table 8.5). Some examples relevan t to the general surgeon are briey outlined in

the following sections.

Oesophageal atresia

A blind proximal pouch with a distal tracheo-oesophageal stula is the most common typ e (Figure 8.22). Affected infants present soon

after birth with drooling and cyanotic episodes on attempting to feed. There may have been poly hydramnios due to failure to swallow

amniotic uid. The diagnosis is conrmed when a nasogastric tube goes no further than the upper oesophageal pouch on the chest x-ray

and abdominal gas signies the

John Langdon Haydon Down (sometimes given as Langdon-Down), 1838–1896, physician, The London Hospital, London, UK, pub lished ‘Observations on an ethnic

classification of idiots’ in 1866.

Figure 8.21 An inspiratory (left) and expiratory (right) chest radiograph demonstrating left-sided pulmonary air trapping after inhalation of a radiolucent foreign body.

tracheo-oesophageal stula (Figure 8.22). Associated anomalies are common and in clude cardiac, renal and skeletal defects. Repair is

usually via a right-sided extrapleural thoracotomy within a day or two of birth. The stula is d ivided and the tracheal side closed. The

oesophageal ends are then anastomosed. Postoperative complications include anastomot ic leak, stricture, recurrent stula formation and

gastro-oesophageal reux. Infants with pure oesophageal atresia and no tracheo-oesopha geal stula are usually best managed by a

temporary gastrostomy and delayed primary repair or an oesophageal replaceme nt. Except for verylow-birth weight babies and those

with major congenital heart disease, most infants with repaired oesophageal atresia have a good prognosis.

Congenital diaphragmatic hernia

Typically in congenital diaphragmatic hernia (CDH), there is a left-sided posterolateral dia phragmatic defect allowing herniation of

abdominal viscera into the chest (Figure 8.23). Many are detected antenatally and the prognosis relates to the sever

ity of the associated pulmonary hypoplasia. Despite intensive respiratory suppo rt or extracorporeal membrane oxygenation (ECMO), up

to 30 per cent of babies with a CDH die from res

Table 8.5 Incidence of selected malformations.

Abnormality Incidence Thoracic

Cardiac

Gastrointestinal

Hepatobiliary

Urogenital Congenital diaphragmatic hernia 1:3000

Oesophageal atresia/tracheo1:3500

oesophageal stula

Congenital heart disease 1:150 Gastroschisis 1:7500 Hirschsprung’s disease 1:5000 An orectal malformations 1:4–5000 Biliary atresia

1:17 000 Choledochal cyst 1:50 000 Hypospadias 1:300 Pelviureteric junction dysfunc tion 1:1000

Figure 8.22 Oesophageal atresia with a distal tracheo-oesophageal fistula.

piratory failure. If the baby can be stabilised, the diaphragmatic defect is repaired. Small diap hragmatic hernias may present with

respiratory or gastrointestinal symptoms in later childhood.

Intestinal atresias

Duodenal atresia may take the form of a membrane or the proximal and distal duodenum may b e completely separated. Prenatal

ultrasound nds a ‘double bubble’ in the fetal abdomen with polyhydramnios. There is an association with Down syndrome. Postnatally,

there is bilious vomiting if the atresia is distal to the ampulla. A plain abdominal x -ray also shows the

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Figure 8.23 Left-sided congenital diaphragmatic hernia.

Figure 8.24 Neonatal abdominal x-ray showing the ‘double bubble’ of duodenal atresia.

double bubble (Figure 8.24). Repair is by duodenoduodenostomy (Figure 8.25). Occa sionally, there is a duodenal membrane with a

modest central perforation, which may delay symptoms until later childhood.

Jejunal/ileal atresia varies from an obstructing membrane through to widely separated blind-end ed bowel ends associated with a

mesenteric defect. Small bowel atresias may be single or multiple and are probably secondar y to a prenatal vascular or mechanical insult

causing sterile infarction of a segment of gut. They present with intestinal obstruction soon after birth. T he proximal bowel is often

extremely dilated and needs to be tapered or excised prior to anastomosis to th e distal bowel (Figure 8.26).

Meconium ileus is a cause of intestinal obstruction from inspissated meconium in the termin al ileum in neonates, most of whom have

cystic brosis. Meconium is a sterile mixture of epithelial cells, mucin and bile. Babies with un complicated meconium ileus (no

associated atresia, volvulus or perforation) can sometimes be managed with hyperosmolar c ontrast enemas to clear the meconium.

Meconium peritonitis is consequent upon a fetal intestinal Proof Stage:perf oration. The baby is born with a rm, distended,

discoloured abdomen and signs of obstruction. An abdominal x-ray shows dilated intestinal loops and areas of calcication.

Occasionally, the perforation has resolved spontaneously before birth, but most neonates with meco nium peritonitis will need surgery.

Intestinal malrotation . By the 12th week of gestation, the mid-gut has returne d to the fetal abdomen from the extraembryonic coelom

and has begun rotating counterclockwise around the superior mesenteric artery axis. In c lassical intestinal malrotation, this process

fails; the duodenojejunal exure lies to the right of the midline and the caecum is central, cr eating a narrow base for the small bowel

mesentery, which predisposes to mid-gut volvulus (Figure 8.27). Malrotation with volvulus is life-threatening and typically presents with

bilious vomiting. Bile-stained vomiting in the infant is a sign of intestinal obstruction un til proved otherwise.

C D

(a)

(b)

Figure 8.25(b) (a) Duodenal atresia and (b) the incisions (A–D) used to repair it.

Figure 8.27 (a) Contrast showing malrotation with a volvulus. (b) The narrow origin of the small bowel me sentery predisposes to mid-gut volvulus.

(a)

(b)

As the gut strangulates, the baby may pass blood-stained stools and becomes progre ssively more ill. An upper gastrointestinal contrast

study conrms the malrotation (Figure 8.27). Resuscitation and urgent surgery are needed to untwist the volvulus, widen the base of the

small bowel mesentery, straighten the duodenum and position the bowel in a non-rotated position with the small bowel on the right and

the colon on the left

Figure 8.26

Small bowel atresia.

ISBN:

9781444121278

(Ladd’s procedure). The appendix is usually removed to avoid

Proof Stage: 2 Fig No: 6.25a leaving it in an abnormal site within the abdomen. William Edward Ladd, 1880–1967, Professor of Child Surgery, The

University of Harvard, Boston, MA, USA. Figure 8.28 A newborn infant with gastroschisis.

Figure 8.29 Exomphalos major.

Abdominal wall defects

Gastroschisis is now the most common anomaly in babies born to mothers under 20 yea rs of age. The fetal gut prolapses through a

defect to the right of the umbilicus. At birth, the bowel is nonrotated, foreshortened and covered by a brinous peel (Figure 8.28). After

reduction of the bowel, which may need to be staged using a silo, and closur e of the defect, gastroschisis has a good prognosis, although

gut dysmotility delays recovery. Some infants have an intestinal atresia and some boys h ave undescended testes but other anomalies are

rare.

Exomphalos is quite a different anomaly in which the intestines and sometimes the liver are cover ed with a membranous sac from which

the umbilical cord arises (Figure 8.29). It may be associated with chromosom al or cardiac anomalies.

Biliary atresia

In biliary atresia, the extrahepatic bile ducts are occluded causing obstructive jaundice (c onjugated hyper-bilirubinaemia) and

progressive liver brosis in early infancy. It should be considered if jaundice persists after 2 weeks of age. Fat malabsorption can lead to

a coagulopathy correctable with vitamin K. An abdominal ultrasound scan may show a small gall bladder and no visible

Figure 8.30 A duplicated colon.

bile ducts and a biliary radionuclide scan may show no excretion. A liver biopsy may sh ow proliferation of small bile ducts. It is treated

by a Kasai porto-enterostomy in which the occluded extrahepatic bile ducts are excised and a je junal Roux loop anastomosed to the

hepatic hilum. Effective drainage is more likely with surgery before 8 weeks of age and may obviate the subsequent need for liver

transplantation.

Alimentary tract duplications

Alimentary tract duplications are rare. They are usually single, variable in size, and spherical or tu bular. Most are located on the

mesenteric border of the intestine. Typically, they are lined by alimentary tract mucosa and sh are a common smooth muscle wall and

blood supply with the adjacent bowel, with which they may communicate. Duplication s can contain heterotopic gastric mucosa and be

associated with spinal anomalies. Most duplications present in infancy or early childhood with intestinal obstruction, haemorrhage,

intussusception or perforation (Figure 8.30). Rarely, they present in adults and sometim es with a malignancy which has been reported

more often with rectal duplication cysts. Complete excision is the treatment of choice.

Hirschsprung’s disease

Hirschsprung’s disease is characterised by the congenital absence of intramural ganglio n cells (aganglionosis) and the presence of

hypertrophic nerves in the distal large bowel. The absence of ganglion cells is due to a failure of migration of vagal neural crest cells into

the developing gut. The affected gut is in spasm causing a functional bowel obstruction. The agang lionosis is restricted to the rectum and

sigmoid colon in 75 per cent of patients (short segment), involves the proxim al colon in 15 per cent (long segment) and affects the entire

colon and a portion of terminal ileum in 10 per cent (total colonic aganglionosis). A transiti on zone exists between the dilated, proximal,

normally innervated bowel and the narrow, distal aganglionic segment.

Hirschsprung’s disease may be familial or associated with Down syndrome or o ther genetic disorders. Gene mutations

Michael R Harrison , born 1943, Chief of Paediatric Surgery, San Francisco, CA, USA. A pioneer of fetal surgery.

Morio Kasai, 1922–2008, formerly Professor of Surgery, The University of Tokyo, Tokyo, Japan.

Harald Hirschsprung, 1830–1916, physician, The Queen Louise Hospital for Children, Copenhagen, Den mark, described congenital megacolon in 1887.

Figure 8.31 Barium enema in an infant showing a ‘transition zone’ in the proximal sigmoid colon between the dilated proximal normally innervated bowel and the

contracted aganglionic rectum.

have been identied on chromosome 10 (involving the RET proto-oncogene) and on chromosome 13 in some patients. Hirschsprung’s

disease typically presents in the neonatal period with delayed passage of meconium, abdominal dis tension and bilious vomiting, but it

may not be diagnosed until later in childhood or even adult life, when it manifests as seve re chronic constipation. Enterocolitis is a

potentially fatal complication of the disease.

The diagnosis requires an adequate rectal biopsy and an experienced pathologist. A con trast enema may show the narrow aganglionic

segment, a cone and the dilated proximal bowel (Figure 8.31). Surgery aims to remove the agan glionic segment and ‘pull-through’

ganglionic bowel to the anus (e.g. Swenson, Duhamel, Soave and transanal procedures) and can be done in a single stage or in several

stages after rst establishing a proximal stoma in normally innervated bowel. Most patients ac hieve good bowel control, but a signicant

minority experience residual constipation and/or faecal incontinence or further enterocolit is.

Anorectal malformations

The anus is either imperforate or replaced by a stula which does not pass through the muscle complex and opens away from the

specialised skin which represents the true anal site. The sacrum and genitourinary trac t are often abnormal. In boys, there may be a

rectoperineal stula, but the most common anomaly is an imperforate anus with a rectobulbar urethral stula (Figure 8.32). In girls, the

most common anomalies are a stula opening in the posterior vestibule behind the vagina o r on the perineum. Cloacal malformations, in

which the rectum and genitourinary tract share a common outow channel, are also seen in g irls.

Orvar Swenson, born 1909, Professor of Surgery, Northern University, Chicago, IL, USA.

(a)

(b)

Figure 8.32 (a) An imperforate anus in a neonate associated with (b) a rectourethral fistula, visible on a contrast st udy performed via a sigmoid colostomy. The bladder is

filled with contrast via the fistula and the radio-opaque dot has been placed on the infant’s pe rineum over the normal site of the anus. B, bladder; R, rectum.

Where there is a stula, meconium can be passed and the diagnosis can be delayed for months because the perineum has not been

inspected carefully. Most low malformations are treated by an anoplasty soon after birth. High er, more complex defects need a temporary

colostomy, detailed investigation and then reconstructive surgery. Functional outcome is related to the type of malformation (low defects

are associated with constipation, higher defects with faecal incontinence) and the in tegrity of the sacrum and pelvic muscles. For children

with residual intractable faecal incontinence, antegrade colonic enemas administered via a catheterisa ble appendicostomy (Figure 8.33)

(the Malone/

Bernard George Duhamel, 1917–1996, Professor of Surgery, Hopital St. Denis, Paris, France. F Soave, tw entieth century Italian paediatric surgeon.

Figure 8.33 Appendicostomy for the delivery of antegrade colonic enemas.

ACE procedure) enable the child to achieve social continence. Causes of intestinal obstr uction are summarised below (Summary box

8.17).

Summary box 8.17

Congenital causes of intestinal obstruction

Intestinal atresia: may be multiple

Cystic fibrosis: can present with intestinal obstruction from inspissated meconium

Intestinal malrotation: predisposes to potentially lethal midgut volvulus

Alimentary tract duplications: may present with obstruction, haemorrhage or intussusception

Hirschsprung’s disease: typically presents with delay in passing meconium after birth

Anorectal malformations

Urinary tract malformations

Many of these malformations are now detected by prenatal ultrasound scan. O thers present in childhood with urinary infection,

obstruction or an abdominal mass. Urinary tract disorders in children are inves tigated by urine microscopy and culture, ultrasound scan,

assessment of renal function and a combination of radioisotope renography (upta ke and excretion), contrast radiology and endoscopy.

In many infants, prenatally diagnosed mild to moderate hydronephrosis resolves spontaneously . Those with more signicant

pelviureteric junction obstruction may be asymptomatic or present in later childhood with urinary tract infection or loin pain. Pyeloplasty

is indicated for symptoms or impaired

Paediatric surgical oncology 123

Figure 8.34 Operative appearance of neonatal necrotising enterocolitis.

renal function. In boys, partial membranous obstruction in the posterior urethra (valves) c an cause a severe prenatal obstructive uropathy.

This condition demands urgent investigation and treatment soon after birth to preserve blad der and kidney function. Renal failure

develops in about one-third of affected boys despite early endoscopic ablation of the obstru cting valves. Other congenital urinary tract

malformations include ureteric abnormalities (e.g. duplex, ureterocoele, vesicoureteric re ux), multicystic dysplastic kidney and bladder

exstrophy.

Necrotising enterocolitis is an acquired inammatory condition of the neonatal gut, mostly affecting premature infants. Immaturity,

formula feeds (breast milk is protective), bacterial infection and impaired gut blood ow a re implicated in the pathogenesis. The neonate

becomes septic with abdominal distension, bloody stools and bilious aspirates. Patchy or extensive pneumatosis intestinalis progresses to

necrosis and perforation (Figure 8.34). It commonly affects the terminal ileum and colon. Small intestinal loss can be sufcient to cause

severe intestinal failure. Milder cases respond to antibiotics, gut rest and parenteral nutrition, but s evere cases need an urgent

laparotomy. The mortality remains over 30 per cent.

PAEDIATRIC SURGICAL ONCOLOGY

Although less common in children than adults, neoplasms are a leading cause of death (along with trauma) in those over one year of age.

In the western countries, leukaemia, central nervous system (CNS) tumours, lymphomas, neur oblastomas and nephroblastomas account

for most paediatric malignancies. Neuroblastoma and nephroblastoma are among the mor e common solid abdominal tumours. The

prognoses for these cancers have improved after numerous multicentre trials.

Neuroblastoma is a malignancy of neuroblasts in the adrenal medulla or sympathet ic ganglia and typically presents as an abdominal or

paravertebral mass. These cells metastasise to lymph nodes, bone and the liver, and they raise urinary catecholamine levels. Small

localised tumours are excised. More advanced tumours require surgery after chemotherapy. Survival relates to tumour biology and stage

(>90 per cent for small localised tumours, <50 per cent for advanced tumours).

Wilms’ tumour (nephroblastoma) is a malignant renal tum our derived from embryonal cells; it typically affects children aged from

one to four years. A mutation in the Wilms’ tumour suppressor gene (WT1) is responsible for som e cases. It usually presents as an

abdominal mass. The tumour extends into the renal vein and vena cava and metastasises to lymp h nodes and lungs. Treatment is with

chemotherapy and surgery. Survival depends on tumour spread, completeness of excision and the histological appearance, but exceeds

70 per cent even with advanced tumours.

SAFEGUARDING

All staff must be able to recognise abuse and neglect, and know the law and the ir local child safeguarding contacts. In the UK, three

children die each week from neglect or abuse and half of these are at the hands of their pa rents. One per cent of accident and emergency

attendances are from abuse. Consider abuse if any of the following are pres ent:

•

bruises away from bony prominences (face, back, abdomen,

arms, buttocks, ears and hands);

• bruises in clusters or in the pattern of an implement;

• multiple injuries at different stages of healing;

•

different types of injury (e.g. soft tissue, burns or scalds, cuts and bruises);

•

rib fractures; bite marks (it is difcult to distinguish adult from child bites, but adult bites are asso ciated with fatal abuse);

•

signicant delay between the injury and seeking medical

advice;

• an inconsistent or vague history;

• inappropriate parental behaviour.

ACKNOWLEDGEMENTS

This chapter owes much to the framework laid by Professor Mark Stringer who wrote the two previous editions.

FURTHER READING

Advanced Paediatric Life Support Group. Advanced paediatric life support. The pract ical approach, 8th edn. Oxford: Blackwell

Publishing, 2011.

Burge DM, Grifths DM, Steinbrecher HA, Wheeler RA (eds). Paediatric surgery, 2nd edn. London: Hodder Arnold, 2005.

Gearhart JP, Rink RC, Mouriquand PDE (eds). Pediatric urology. Philadelphia, PA: W B Saunders, 2007.

Najmaldin AS, Rothenberg S, Crabbe DCG, Beasley S (eds). Operative endoscop y and endoscopic surgery in infants and children.

London: Hodder Arnold, 2005.

National Patient Safety Agency. Reducing the risk of hyponatraemia when administering in travenous infusions to children. London:

NPSA, 2007.

Oldham KT, Colombani PM, Foglia RP, Skinner MA (eds). Principles and prac tice of pediatric surgery. Philadelphia, PA: Lippincott

Williams & Wilkins, 2005.

Parikh D, Crabbe D, Auldist A, Rothenberg S (eds). Pediatric thoracic surgery. B erlin: Springer, 2009.

Puri P, Hollwarth ME (eds). Pediatric surgery: diagnosis and management. New York: Springer, 2009.

Sinha CK, Davenport M. Handbook of pediatric surgery. London: Springer, 2009.

Spitz L, Coran AG (eds). Rob and Smith’s Operative surgery. Pediatric surgery , 6th edn. London: Hodder Arnold, 2006.

Stringer MD, Oldham KT, Mouriquand PDE (eds). Pediatric surgery and urology: long-term outcom es, 2nd edn. New York: Cambridge

University Press, 2006.

Max Wilms , 1867–1918, Professor of Surgery, Heidelberg, Germany.

John W Broviac, formerly nephrologist, University of Washington, Washington DC, USA. Robert O Hickm an, formerly nephrologist, University of Washington,

Washington DC, USA.

CHAPTER

oncology Principles of

LEARNING OBJECTIVES

To understand:

• The biological nature of cancer

• The principles of cancer prevention and early

detection

To appreciate:

• The principles of cancer aetiology and the major

known causative factors

• The likely shape of future developments in cancer management

• The multidisciplinary management of cancer

• The principles of palliative care

WHAT IS CANCER?

History

The name ‘cancer’ comes from the Greek and Latin words for a crab, and refers to the claw-like blood vessels extending over the surface

of an advanced breast cancer.

The study of cancer has always been part of clinical medicine: theories have mov ed from divine intervention, through the humours, and

are now rmly based on the cellular origin of cancer. Rudolf Virchow is cred ited with being the rst to demonstrate that cancer is a

disease of cells that progresses as a result of abnormal proliferation encapsulated by his fam ous dictum ‘omnis cellula e cellula’ (every

cell from a cell). In 1914, Theodor Boveri pointed out the importance of chromosomal ab normalities in cancer cells and, by the 1940s,

Oswald Avery had shown that DNA was the genetic material within the chromos omes. In 1953, the key discovery by Watson and Crick

of the structure of DNA paved the way for the study of what has become known as the mo lecular biology of cancer enabling us to

investigate, and, in some cases, understand, the biochemical mechanisms whereby cancer c ells are formed and which mediate their

abnormal behaviour.

The psychopath within

Cancer cells are psychopaths. They have no respect for the rights of other cells . They violate the democratic principles of normal cellular

organisation. Their proliferation is uncontrolled; their ability to spread is unbo unded. Their inexorable, relentless progress destroys rst

the tissue and then the person.

In order to behave in such an unprincipled fashion, cells have to acquire a number of characteristics before they are fully malignant. No

one characteristic is sufcient, and not all characteristics are necessary. These features, b ased on an article by Hanahan and Weinberg,

are given in Summary box 9.1.

Summary box 9.1

Malignant transformation

Establish an autonomous lineage:

resist signals that inhibit growth

acquire independence from signals stimulating growth

Obtain immortality

Evade apoptosis

Acquire angiogenic competence

Acquire the ability to invade

Acquire the ability to disseminate and implant

Evade detection/elimination

Genomic instability

Jettison excess baggage

Subvert communication to and from the environment/milieu Develop ability to change energy metabolism

Francis Harry Compton Crick , 1916–2004, a British molecular biologist who worked at the Cavendish Laboratory, Cambridge, UK and late r at the Salk Institute, San

Diego, CA, USA. Watson and Crick shared the 1962 Nobel Prize for Physiology or Medicine with Maurice Hugh Frederick Wilkins, 1916–2004, of King’s College,

London.

Rudolf Ludwig Carl Virchow , 1821–1902, Professor of Pathology, Berlin, Germany. Theodor Heinrich Boveri, 1862–1913, Professor of Zoology and Comparative

Anatomy, Wurzburg, Germany.

Oswald Theodore Avery, 1877–1955, a bacteriologist at the Rockefeller Institute, New York, NY, USA.

James Dewey Watson, born 1928, an American biologist who worked at Cambridge, UK, and late r became Director of the Cold Spring Harbor Laboratory, New York,

NY, USA. Douglas Hanahan, born 1951, American biologist and director of the Swiss Institute for Experimental Cancer Research (ISREC), Lau sanne, Switzerland.

Robert A Weinberg, born 1942, The Whitehead Institute of Biomedical Research and Department of Biology, The Massachusetts Institute of Te chnology, Cambridge,

MA, USA.

Establish an autonomous lineage

This involves developing independence from the normal signals that control supply an d demand. The healing of a wound is a

physiological process; the cellular response is exquisitely coordinated so that proliferatio n occurs when it is needed and ceases when it is

no longer required. The whole process is controlled by a series of signals tell ing cells when to divide and when not to divide. Cancer cells

escape from this normal system of checks and balances: they grow and proliferate in the absence of external stimuli regardless of signals

telling them not to do so. Oncogenes, an aberrant form of normal cellular genes, are a key factor in this process. They were originally

identied as sequences within the genome of viruses that could cause cancer and initially thought to be viral in origin but, surprisingly,

turned out to be parts of the normal genome that were hitch-hiking between cells, using the virus as a vector. Viral oncogenes (vonc) had

sequence homology with normal cellular genes (conc) and are now presumed to be m utated versions of genes concerned with normal

cellular husbandry. The implication of this is that we all carry within us genetic sequenc es that, through mutation, can turn into active

oncogenes and thereby cause malignant transformation.

Obtain immortality

According to the Hayick hypothesis, normal cells are permitted to undergo only a nite num ber of divisions. For humans, this number

is between 40 and 60. The limitation is imposed by the progressive shortening of the end of the chromosome (the telomere) that occurs

each time a cell divides. Telomeric shortening is like a molecular clock and, when its time is up, the lineage will die out. Cancer cells can

use the enzyme telomerase to rebuild the telomere at each cell division, so there is no telomeri c shortening and the lineage will never die

out. The cancer cell has achieved immortality.

Evade apoptosis

Apoptosis is a form of programmed cell death which occurs as the direct resu lt of internal cellular events instructing the cell to die, rather

than external events. Unlike necrosis, apoptosis is an orderly process. The cell dismantles its elf neatly for disposal (Figure 9.1). There is

a minimal inammatory response. Apoptosis is a physiological process rediscovered in 1972 and named from the Greek αηοητωσιξ,

meaning the act of falling. Cells that nd themselves in the wrong place normally die by apoptosis and this is an important self-

regulatory mechanism in growth and development. Genes, such as p53, that c an activate apoptosis function as tumour suppressor genes.

Loss of function in a tumour suppressor gene will contribute to malignant transform ation. Cancer cells will be able to evade apoptosis,

which means that the wrong cells can be in the wrong places at the wrong times.

Acquire angiogenic competence

A mass of tumour cells cannot, in the absence of a blood supply, grow beyond a diame ter of about 1 mm. This places a severe restriction

on the capabilities of the tumour: it cannot grow much larger or spread widely within the bo dy. If, however, the mass of tumour cells is

able to attract or construct a blood supply, then it may then quit its dormant state and beh ave in a far more aggressive fashion. The ability

of a tumour to form blood vessels is termed ‘angiogenic competence’ and is a key feature of malignant transformation.

Leonard Hayflick , born 1928, while working at the Wistar Institute in Philadelphia in 1962, he noted that normal mammalian cells growing in culture had a limited,

rather than an indefinite, capacity for self-replication.

Figure 9.1 Electron micrograph of apoptotic bodies engulfed by a macrophage.

Acquire the ability to invade

Cancer cells have no respect for the structure of normal tissues. They acquire the ability to breach the basement membrane and thus gain

direct access to blood and lymph vessels using three main mechanisms to facilitate invasion: (1) they cause a rise in the interstitial

pressure within a tissue; (2) they secrete enzymes that dissolve extracellular matrix; and (3) they acquire motility. Unrestrained

proliferation and a lack of contact inhibition enable cancer cells to exert pressure d irectly on the surrounding tissue and push themselves

beyond normal limits. They secrete collagenases and proteases that chemically dissolve any extr acellular boundaries that would

otherwise limit their spread through tissues and by modulating the expression of cell sur face molecules called integrins, are able to

detach themselves from the extracellular matrix. The abnormal integrins associated with malignancy can also transmit signals from the

environment to the cytoplasm and nucleus of the cancer cells (‘outside-in signa lling’), and these signals can induce increased motility.

Acquire the ability to disseminate and implant

Once cancer cells gain access to vascular and lymphovascular spaces, they have acquir ed the potential to use the body’s natural transport

mechanisms to distribute themselves throughout the body, although this will not, of itself, c ause tumours to develop at distant sites. They

also need to acquire the ability to implant. As Paget pointed out over a century ago, there is a crucial relationship here between the seed

(the tumour cell) and the soil (the distant tissue). Most of the cancer cells discharged into the circulation probably do not form viable

metastases: circulating cancer cells can be identied in patients who never develop c linical evidence of metastatic disease. Clumping

may be important in permitting metastases: outer cells protecting inner cells from immunological attack. These outer protective cells

may, on occasion, be normal lymphocytes.

What is cancer? 127

Cancer can spread in this embolic fashion, but also when individual cells migrate and im plant. Whether spread occurs in groups or

individually, the cells still have to cross the vascular endothelium (and basement membra ne) to gain access to the tissue itself. Cancer

cells probably implant themselves in distant tissues by exploiting, and subverting, the nor mal inammatory response. By expressing

inammatory cytokines, the cancer cells can fool the endothelium of the host tissue into b ecoming activated and allowing cancer cells

access to the extravascular space. Activated endothelium expresses receptors that bind to integrins and selectins on the surface of

leukocytes, and this allows the leukocytes to move across the endothelial barrier.

may, tomorrow, be essential. This can leave cancer cells vulnerable to external stress an d may, in part, explain why some cancer

treatments work.

Subvert communication to and from the

environment/milieu

Providing false information is a classic military strategy. Degrading the command and co ntrol systems of the enemy is an essential

component of modern warfare. Cancer cells almost certainly use similar tactics in their battle f or control over their host. Given the

complexity of communication between and within cells, this is not an easy statement to prov e or disprove. Nor does it offer any easy

targets for therapeutic manipulation.

Evade detection/elimination

Cancer cells are simultaneously both ‘self’ and ‘not self’. Although derived from norm al cells (‘self’), they are, in terms of their genetic

make up, behaviour and characteristics, foreign (‘not self’). As such, they ought to provoke an immune response and be eliminated and it

is entirely possible that malignant transformation is a more frequent event than the em ergence of clinical cancer. The possible role of the

immune system in eliminating nascent cancers was proposed by Paul Ehrlich in 1909 and revisi ted by both Sir Frank McFarlane Burnet

and Lewis Thomas in the late 1950s. Cancer cells, or at least those that give rise to clinical disease , appear to gain the ability to escape

detection by the immune system. This may be by suppressing the expression of tumour- associated antigens, or it may be through actively

coopting one part of the immune system to help the tumour to escape detection by other parts of the immune surveillance system.

Genomic instability

A cancer is a genetic ferment. Cells are dividing without proper checks and balances. Muta tions are arising all the time and some,

particularly those in tumour suppressor genes, may have the ability to encourag e the development and persistence of further mutations.

This gives rise to the phenomenon of genomic instability – as it evolves, a cancer contains an increasing variety and number of genetic

aberrations: the greater the number of such abnormalities, the greater the chance of incre asingly deviant behaviour.

Jettison excess baggage

Cancer cells are geared to excessive and remorseless proliferation. They do not need to develop or retain those specialised functions that

make them good cellular citizens. They can therefore afford to repress or permanently lose those genes that control such functions. This

may bring some short-term advantages. The longer-term disadvantage is that wh at is today superuous

Develop ability to change energy metabolism Blood ow in tumours is often sporadic a nd unreliable. As a result, cancer cells may have

to spend prolonged periods starved of oxygen – in a state of relative hypoxia. Compar ed to the corresponding normal cells, some cancer

cells may be better able to survive in hypoxic conditions. This ability may enable tumour s to grow and develop despite an impoverished

blood supply. Cancer cells can alter their metabolism even when oxygen is abundant, th ey break down glucose but do not, as normal

cells would do, send the resulting pyruvate to the mitochondria for conversion, in an ox ygen-dependent process, to carbon dioxide. This

is the phenomenon of aerobic glycolysis, or the Warburg effect and leads to the produ ction of lactate. In an act of symbiosis, lactate-

producing cancer cells may provide lactate for adjacent cancer cells which are then able to use it, via the citric acid cycle, for energy

production. This cooperation is similar to that which occurs in skeletal muscle during exe rcise.

Malignant transformation

The characteristics of the cancer cell arise as a result of mutation. Only very rarely is a s ingle mutation sufcient to cause cancer;

multiple mutations are usually required. Colorectal cancer provides the classical example of how multiple mutations are necessary for

the complete transformation from normal to malignant cell. Vogelstein and colleagues id entied the genes required and also postulated

not only that it is necessary to have mutations in all the relevant genes, but also that these mutations must be acquired in a specic

sequence.

Cancer is usually regarded as a clonal disease. Once a cell has arisen with all the muta tions necessary to make it fully malignant, it is

capable of giving rise to an innite number of identical cells, each of which is fully malig nant. These cells divide, invade, metastasise and

destroy but, ultimately, each is the direct descendant of that original, primordial, transformed cell. There is certainly evidence, mostly

from haematological malignancies,

Stephen Paget , 1855–1926, surgeon, The West London Hospital, London, UK. Paget’s ‘seed and soil’ hypothesis is conta ined in his paper ‘The distribution of

secondary growths in cancer of the breast’, in the Lancet, 1889.

Paul Ehrlich, 1854–1915, Professor of Hygiene, The University of Berlin, and later Director of The Institute for Infectious Diseas es, Berlin, Germany. In 1908, he shared

the Nobel Prize for Physiology or Medicine with Elie Metchnikoff, 1845–1916, ‘in recognition of his work on immunity’. Metchnikoff was Professor of Zoology at

Odessa in Russia, and later worked at the Pasteur Institute in Paris, France.

Sir Frank McFarlane Burnett, 1899–1985, an Australian virologist, at the Walter and Eliza Hall Institute, Melbourne, Australia. Burnett shared the 1960 Nobel Prize for

Physiology or Medicine with Sir Peter Brian Medawar, 1915–1987, Jodrell Professor of Zoology, University College, L ondon, UK, ‘for their discovery of acquired

immunological tolerance’.

Otto Warburg, 1883–1970, chemist, Director of the Kaiser Wilhelm Institute for Cell Physiology, Berlin-Dahlem. Awarded the Nobel Prize for Physiology or Medicine

in 1931 for ‘his discovery of the nature and mode of action of the respiratory enzyme’.

Lewis Thomas, 1913–1993, an American pathologist and immunologist, who became President of the Sloa n Kettering Memorial Institute, New York, NY, USA. Bert

Vogelstein, born 1949, molecular biologist, Johns Hopkins Hospital, Baltimore, MD, USA.

to support the view that tumours are monoclonal in origin, but recent evidenc e challenges the universality of this assumption. Some

cancers may arise from more than one clone of cells. Epigenetic modication refers to hereditabl e changes in DNA that are not related to

the nucleotide sequence of the molecule. Epigenetic modication may give rise to distinct can cer cell lineages with differing biological

properties. The interactions between cells from each lineage and the tissue within which such cell s nd themselves may determine the

overall clinical behaviour of a tumour.

Two mechanisms may help to sustain and accelerate the process of malignant trans formation: genomic instability and tumour-related

inammation.

Genomic instability

If a tumour is a genetic ferment, then there is abundant opportunity for mutations to occ ur in the DNA of tumour cells, some of these

mutations (for example, those occurring in tumour suppressor genes) may themselve s be capable of facilitating the persistence of further

mutations and so the pace of malignant transformation can be accelerated.

Tumour-related inflammation

If a tumour provokes an inammatory response, then the cytokines and other factors p roduced as a result of that response may act to

promote and sustain malignant transformation. Growth factors, mutagenic ROS (reac tive oxygen species), angiogenic factors, anti-

apoptotic factors, may all be produced as part of an inammatory process and all may con tribute to the progression of a tumour.

A recurring theme in the molecular biology of cancer is that systems and pathwa ys can behave unpredictably – activation may

sometimes promote, and sometimes inhibit, growth and transformation. This has important impl ications for therapy – treatments

designed to inhibit the growth and spread of cancer may, occasionally, have prec isely the opposite effect. The most consistent feature of

cancer is its lack of consistency. growth (Figure 9.2). This Gompertzian pattern has sev eral important implications for the diagnosis and

treatment of cancer (Summary box 9.2).

Summary box 9.2

Clinical implications of Gompertzian growth

The majority of the growth of a tumour occurs before it is clinically detectable

By the time they are detected, tumours have passed the period of most rapid growth, that period when they might be most sensitive to anti-proliferative drugs

There has been plenty of time, before diagnosis, for individual cells to detach, invade, implant and form distant metastases – in many patients cancer may, at

presentation, be a systemic disase.

‘Early tumours’ are genetically old: plenty of time for mutations to have occurred, mutations that might confer spontaneous drug resistance (a probability greatly

increased by the existence of cell loss)

The rate of regression of a tumour will depend upon its age (the Norton–Simon hypothesis extends t his: the rate of regression of a tumour will depend upon its growth

rate at the time of treatment)

108

Limit of clinical detection

The growth of a tumour

If it is accepted that a cancer starts from a single transformed cell, then it is possible, using stra ightforward arithmetic, to describe the

progression from a single cell to a mass of cells large enough to kill the host. The division o f a cell produces two daughter cells. The

relationship 2

will describe the number of cells produced after n generations of division. There are between 10

and 10

cells in a

typical human being. A tumour 10 mm in diameter will contain about 10

cells. As 2

= 10

, this implies that it would take 30

generations to reach the threshold of clinical detectability and, as 2

= 3 × 10

, fewer than 15 subsequent generations to produce a

tumour that, through sheer bulk alone, would be fatal. This is an oversimplication because cell loss is a feature of many tumours and,

for squamous cancers, as many as 99 per cent of the cells produced may be lost, mainly by exf oliation. It will, in the presence of cell

loss, take many cellular divisions to produce a clinically evident tumour – abundant oppor tunity for further mutations to occur during the

preclinical phase of tumour growth. The growth of a typical human tumour can be described by a n exponential relationship, the doubling

time of which increases exponentially – so-called Gompertzian

1 0 100 200 300 400 500 600 Time

Figure 9.2 The Gompertzian curve describing the growth of a typical tumour. In its early stages, growth is exponential b ut, as the tumour grows, the growth rate slows.

This decrease in growth rate probably arises because of difficulties with nutrition and oxygenation. The tumour cells are in competition: not only with the tissues of the

host, but also with each other.

Benjamin Gompertz , 1779–1865, an insurance actuary who was interested in calculating annuities. To do this, he needed to describe mathematically the relationship

between life-expectancy and age. He was able to do this using the function that bears his name . The Gompertzian function provides an excellent fit to data points

plotting tumour size against time.

THE CAUSES OF CANCER

The interplay between nature and nurture Both inheritance and environment are import ant determinants of cancer development.

Although environmental factors have been implicated in more than 80 per cent of cases, this still leaves plenty of scope for the role of

genetic inheritance: not just the 20 per cent of tumours for which there is no clear environ mental contribution but also, as environment

alone can rarely cause cancer, the genetic contribution to the 80 per cent of tumours to which env ironmental factors contribute.

Knowledge about the causes of cancer can be used to design appropriate strategies for preve ntion or earlier diagnosis. As more is

discovered about the genes associated with cancer, genetic testing and counsel ling will play an increasing role in its prevention. These

considerations are incorporated into Table 9.1 on the inherited cancer syndromes, and Table 9.2 on the environmental contribution to

cancer.

Table 9.1 Inherited syndromes associated with cancer.

Syndrome

Familial adenomatous polyposis (FAP)/ Gardner syndrome

Gene(s) Inheritance implicated

APC gene D

Hereditary non-polyposis colorectal cancer (HNPCC)

HNPCC1

HNPCC2

HNPCC3

Peutz–Jeghers syndrome

DNA mismatch D repair genes

(MLH1, MSH2, MSH6)

MSH2

MLH1

PMS1

STK11 D

Cowden’s syndrome PTEN D

Retinoblastoma RB D

Multiple endocrine neoplasia (MEN) type 1

MEN type 2A

Menin D

RET D

Associated tumours and

abnormalities

Colorectal cancer under the age of 25 years

Papillary carcinoma of the thyroid

Cancer of the ampulla of Vater

Hepatoblastomas

Primary brain tumours (Turcot’s

syndrome)

Osteomas of the jaw

CHRPE (congenital hypertrophy of the retinal pigment epithelium)

Colorectal cancer (typically in the 40s and 50s)

Strategies for prevention/early diagnosis

Prophylactic panproctocolectomy

Surveillance colonoscopies/

polypectomies

Non-steroidal anti-inammatory drugs

Endometrium, stomach, hepatobiliary (Lynch’s syndrome 1)

Bowel cancer, breast cancer, freckles round the mouth

Multiple hamartomas of skin, breast and mucus membranes

Breast cancer

Neuroendocrine tumours

Endometrial cancer, thyroid cancer

Retinoblastoma

Pinealoma

Osteosarcoma

Parathyroid tumours

Islet cell tumours

Pituitary tumours

Medullary carcinoma of the thyroid Phaeochromocytoma

Parathyroid tumours

Eldon J Gardner , born 1909, Professor of Zoology, Utah State University, Salt Lake City, UT, USA.

Abraham Vater, 1684–1751, Professor of Anatomy and Botany, and later of Pathology and Therapeutics, Wittenbur g, Germany. Jacques Turcot, born 1914, surgeon,

Hôtel Dieu de Quebec Hospital, Quebec, Canada.

Henry T Lynch, born 1928, oncologist, Chairman of the Department of Preventive Medicine, Creighton School of Medicine, Californ ia, USA.

John Law Augustine Peutz, 1886–1968, Chief Specialist for Internal Medicine, St John’s Hospital, The Hague, The Netherl ands.

Harold Joseph Jeghers, 1904–1990, Professor of Internal Medicine, The New Jersey College of Medicine and Dentistry, Jersey C ity, NJ, USA.

One of the few clinical syndromes named after the patient rather than the clinician, Rachel Cowden was, in 1963, the first p atient described with the syndrome. She died

from breast cancer at the age of 20.

Surveillance colonoscopy, mammography

Active surveillance

Surveillance of the uninvolved eye

Awareness of associations and paying attention to relevant symptoms

Regular screening of blood pressure, serum calcitonin and urinary catecholamines

Prophylactic thyroidectomy

Table 9.1 Inherited syndromes associated with cancer – continued.

Syndrome

MEN type 2b

Gene(s) Inheritance implicated

RET D

Li–Fraumeni syndrome p53 D

Familial breast cancer BRCA1, BRCA2 D

Familial cutaneous malignant melanoma Basal cell naevus

syndrome (Gorlin)

CDNK2A, CDK4 D

Associated tumours and

abnormalities

Medullary carcinoma of the thyroid Phaeochromocytoma

Mucosal neuromas

Ganglioneuromas of the gut

Sarcomas

Leukaemia

Osteosarcomas

Brain tumours

Adrenocortical carcinomas

Breast cancer

Ovarian cancer

Papillary serous carcinoma of the

peritoneum

Prostate cancer

Cutaneous malignant melanoma

PTCH D

Von Hippel–Lindau syndrome

VHL D

Neurobromatosis type 1 NF1 D

Neurobromatosis type 2 NF2 D

Xeroderma pigmentosum

Ataxia telangiectasia Decient R nucleotide

excision repair (XPA, B, C)

AT R

Bloom’s syndrome BLM helicase R

Basal cell carcinomas

Medulloblastoma

Bid ribs

Renal cancer

Phaeochromocytoma

Haemangiomas of the cerebellum and

retina

Astrocytomas

Primitive neuroectodermal tumours Optic gliomas

Multiple neurobromas

Acoustic neuromas

Spinal tumours

Meningiomas

Multiple neurobromas

Skin sensitive to sunlight; early onset of cutaneous carcinomas (SCCs, BCCs)

Strategies for prevention/early diagnosis

Regular screening of blood pressure, serum calcitonin and urinary

catecholamines

Prophylactic thyroidectomy

Very difcult, as the pattern of tumours is so heterogeneous and varies from patient to patient

Screening mammography

Pelvic ultrasound

Prostate-specic antigen in males Prophylactic mastectomy

Prophylactic oophorectomy

Avoid exposure to sunlight, careful surveillance

Careful surveillance, awareness of diagnosis (look for bid ribs on x-ray)

Urinary catecholamines

A difcult problem; maintain a high index of suspicion concerning any rapid changes in the growth or character of any nodule

Avoidance of sun exposure

Active surveillance and early treatment Retinoids for chemoprevention

Progressive cerebellar ataxia Leukaemia

Lymphoma

Breast

Melanoma

Upper gastrointestinal

Sensitivity to UV light

Leukaemia

Lymphoma

BCC, basal cell carcinoma; D, dominant; R, recessive; SCC, squamous cell carcinoma; UV, ultraviolet.

Frederick P Li , born 1940, Professor of Medicine, Harvard University Medical School, Boston, MA, USA. Joseph F Fraumeni, born 1933, Director of Cancer

Epidemiology and Genetics, The National Cancer Institute, Bethesda, MD, USA. Robert Gorlin, 1923–2006, Professor of Dentistry , The University of Minnesota,

Minneapolis, MN, USA.

Eugen von Hippel, 1867–1939, Professor of Ophthalmology, Göttingen, Germany.

Arvid Lindau, 1892–1958, Professor of Pathology, Lund, Sweden.

David Bloom, born 1892, a dermatologist at the Skin and Cancer Clinic, New York University, New York, NY, USA , described the syndrome in 1954.

Active surveillance

Table 9.2 Environmental causes of cancer (and suggested measures for reducing their impact).

Environmental/behavioural factor Associated tumours Strategy for prevention/early diagnosis

Tobacco Lung cancer

Head and neck cancer

Alcohol

UV exposure

Ionising radiation

Viral infections HPV

HIV

Hepatitis B Head and neck cancer Oesophageal cancer

Hepatoma

Melanoma

Non-melanoma skin cancer

Leukaemia

Breast

Lymphoma

Thyroid

Cervix

Penis

Kaposi’s sarcoma

Lymphomas

Germ cell tumours

Anal cancer

Hepatoma

Other infections Bilharzia Bladder cancer

Inhaled particles

Chemicals

Helicobacter pylori

Asbestos

Wood dust

Environmental

pollutants/chemicals used in industry

Medical Alkylating agents used in cytotoxic chemotherapy Immunosuppressive treatment

Stilbestrol

Tamoxifen Stomach cancer

Mesothelioma

Paranasal sinus cancers

Angiosarcoma (vinyl

chloride)

Bladder cancer (aniline dyes, vulcanisation of rubber)

Lung, nasal cavity (nickel)

Skin (arsenic)

Lung (beryllium, cadmium, chromium)

All sites (dioxins)

Leukaemia

Lymphoma

Lung cancer

Kaposi’s sarcoma

Adenocarcinoma of the vagina in daughters of treated mothers

Endometrial cancer

Fungal and plant toxins

Aatoxins Hepatoma

Ban tobacco

Ban smoking in public places Punitive taxes on tobacco

Avoid excess alcohol

Surveillance of high-risk individuals

Avoid excessive sun exposure, avoid sunbeds

Limit medical exposures to the absolute minimum; safety precautions at nuclear facilities; monitor radiation workers

Avoid unprotected sex

Vaccination

Avoid unprotected sex

Anti-retroviral therapy

Avoid contaminated injections/infusions Vaccination

Treatment of infection

Cystoscopic surveillance

Eradication therapy

Protection of exposed workers

Protection of exposed workers; avoid chemical discharge and spillages

Avoid overtreatment; only combine drugs with ionising radiation when absolutely necessary

As low a dose as possible, for as short a period as possible

Use of stilbestrol curtailed

Biopsy if patient on tamoxifen develops uterine bleeding

Appropriate food storage, screen for fungal contamination of foodstuffs

Table 9.2 Environmental causes of cancer (and suggested measures for reducing their impact) – continued.

Environmental/behavioural factor Associated tumours Strategy for prevention/early diagnosis

Obesity/lack of physical exercise

Breast

Endometrium Kidney

Colon

Oesophagus

Maintain ideal body weight, regular exercise

HIV, human immunodeciency virus; HPV, human papillomavirus; UV, ultraviolet.

THE MANAGEMENT OF CANCER

Management is more than treatment

The traditional approach to cancer concentrates on diagnosis and active treatme nt. This is a very limited view that, in terms of the public

health, may not have served society well. It implies a fatalistic attitude to the occurr ence of cancer and an assumption that, once active

treatment is complete, there is little more do be done. Prevention is forgotten and rehabilitation igno red. Cancer management can be

considered as taking place along two axes: one an axis of scale, from the individ ual to the world population; the other based on the

unnatural history of the disease, from prevention to rehabilitation or palliative care (see Figure 9.3).

Prevention

Table 9.2 summarises the approaches that can be used in the prevention of cancer. I n 1998, Sir Richard Doll estimated that 30 per cent of

cancer deaths were due to tobacco use and that up to 50 per cent of cancer deaths were rel ated to diet. Even allow

PreventionStaging Treatment Follow-up Rehabilitation (Palliation, terminal care)

Individual (primary care)

Family (primary

care)

Community (local

hospital)

Region (tertiary centre)

Country (national health-care

system) Continent

World (WHO)

Within this space we can categorise all aspects of cancer management: from an individual person’s

decision to give up smoking, to the World Health Organization’s decision to recommend morphine rather than radiotherapy to treat cancer-related pain in the developing

world

Figure 9.3 The management of cancer spans the natural history of the disease and all humankind, from the individual to the populatio n of the world. WHO, World

Health Organization.

Sir William Richard Shaboe Doll , 1912–2005, Regius Professor of Medicine, Oxford University, Oxford, UK, and Sir Austin Bradfo rd Hill, Professor of Medical

Statistics, The London School of Hygiene and Tropical Medicine, London, UK, published one of the definitive r eports linking smoking to lung cancer in 1950.

ing for overlap (smokers often have a poor diet), these are impressive gures and add some perspective to the often inated claims made

for the achievements of cancer treatment. Doll estimated that cancers related to occupatio n accounted for less than 4 per cent of cancer

deaths, and that environmental pollution accounted for less than 5 per cent of deaths.

Screening

Screening involves the detection of disease in an asymptomatic population in order to im prove outcomes by early diagnosis. It follows

that a successful screening programme must achieve early diagnosis, and that th e disease in question has a better outcome when treated at

an early stage. The criteria that must be fullled for the disease, screening test and th e screening programme itself are given in Summary

box 9.3.

Summary box 9.3

Criteria for screening

The disease

Recognisable early stage

Treatment at an early stage more effective than at a later stage

Sufficiently common to warrant screening

The test

Sensitive and specific

Acceptable to the screened population

Safe

Inexpensive

The programme

Adequate diagnostic facilities for those with a positive test

High-quality treatment for screen-detected disease to minimise morbidity and mortality

Screening repeated at intervals if the disease is of insidious onset

Benefit must outweigh physical and psychological harm

Merely to prove that screening picks up disease at an early stage, and that the outc ome is better for patients with screendetected disease

than for those who present with symptoms, is an insufcient criterion for the su ccess of a screening programme. This is because of

inherent biases in screening (lead time bias, selection bias and length bias), which make screen -detected disease appear to be associated

with better outcomes than symptomatic disease. Lead time bias describes the phen omenon whereby early detection of a disease will

always prolong survival from the time of diagnosis when compared with disease picked up at a later stage in its development whether or

not the screening process has altered the progression of the tumour (Figure 9.4). Selection bi as describes the nding that individuals who

accept an invitation for screening are, in general, healthier than those who do not. It foll ows that individuals with screendetected disease

will tend, independently of the condition for which screening is being performed, to l ive longer. Length bias is brought about by the fact

that slow-growing tumours are likely to be picked up by screening, whereas fast-growing tumours are likely to arise and produce

symptoms in between screening rounds. Thus, screen-detected tumours will tend to be l ess aggressive than symptomatic tumours.

Because of these biases, it is essential to carry out population-based randomised controlled trials and to compare mortality rate in a whole

population offered screening (including those who refuse to be screened and those who devel op cancer after a negative test) with

mortality rate in a population that has not been offered screening.

Fatal

C B Clinically detectable

Detected by screening

Tumour a Tumour b x y

01 23 45 67 89 10

Time

Figure 9.4 Lead time and length bias. Tumour ‘a’ is a steadily growing tumour; its progress is uninfluenced by any tr eatment. The arrows indicate the timing of tests in a

screening programme. The horizontal lines indicate three thresholds: detectability by screening; clinica l detectability; and death due to tumour progression. Point A

indicates the time at which the tumour would be diagnosed in a screening programme and point B indicates the time at which the tumour would be diagnosed clinically,

that is in the absence of any screening programme. If the date of diagnosis is used as the start time for meas uring survival, then it is clear that, in the absence of any effect

from treatment, the screening programme will artefactually add to the survival time. The amount of ‘incr eased’ survival is equal to y − x years, in this example, just over

two years. This artefactual inflation of survival time is referred to as lead time bias. Tumour ‘b’ is a rapidly growing t umour; again, its progress is uninfluenced by

treatment. It grows so rapidly that, in the interval between two screening tests, it can cross both the threshol d for detectability by screening and that of clinical

detectability. It will continue to progress rapidly after diagnosis, and the measured survival time will be short. This phenomenon, whereby those tumours that are

‘missed’ by the screening programme are associated with decreased survival, is called length bias.

This research design has been applied to both breast cancer and colorectal cancer: i n both cases, there was reduction in diseasespecic

mortality.

Diagnosis and classification

Accurate diagnosis is the key to the successful management of cancer. Diagnosis lies at the heart of the epidemiology of cancer; if there

is an inaccurate picture of the pattern of a disease, reliable inferences about its distributio n and causes cannot be drawn. Precise diagnosis

is crucial to the choice of correct therapy; the wrong operation, no matter how superbly performed, is useless. An unequivocal diagnosis

is the key to an accurate prognosis. Only rarely can a diagnosis of cancer condently b e made in the absence of tissue for pathological or

cytological examination. Cancer is a disease of cells and, for accurate diagnosis, the abn ormal cells need to be seen. Different tumours

are classied in different ways: most squamous epithelial tumours are simply classed as w ell (G1), moderate (G2) or poorly (G3)

differentiated (Figure 9.5). Adenocarcinomas are also often classied as G1, 2 or 3, but prostate cancer is an exception with widespread

use of the Gleason system. The Gleason system grades prostate cancer according to the degree of differentiation of the two most

prevalent architectural patterns. The nal score is the sum of the two grades and can va ry from 2 (1 + 1) to 10 (5 + 5), with the higher

scores indicating poorer prognosis. The management of malignant lymphomas is based rmly upon histopathological classication: the

rst distinction is between Hodgkin’s lymphoma (HL) and non-Hodgkin’s lymphoma ( NHL). Each of these main types of lymphoma is

then subclassied according to a different scheme. The World Health Organization/Rev ised European–American Lymphoma

(WHO/REAL) system classies Hodgkin’s lymphoma into classical HL (nodular scleros is HL; mixed cellularity HL; lymphocyte

depletion HL; lymphocyte-rich classical HL) and nodular lymphocyte-predominant HL. The WHO/REAL classication of NHL is

considerably more complex and recognises 27 distinct pathological subtypes. It is perha ps no coincidence that the non-surgical treatment

of lymphomas is, by and large, more successful than the non-surgical treatment of solid tumours. This suggests that precise and accurate

subtyping of tumours enables appropriate selection of treatment and, in turn, this is asso ciated with better outcome.

Investigation and staging

It is not sufcient simply to know what a cancer is; it is imperative to know its site and ex tent. If it is localised, then locoregional

treatments such as surgery and radiation therapy may be curative. If the disease is widespread, then, although such local interventions

may contribute to cure, they will be insufcient, and systemic treatment, for examp le with drugs or hormones, will be required. Staging

is the process whereby the extent of disease is mapped out. Formerly, staging was a fairly crude process, but nowadays it is a highly

sophisticated process, heavily reliant on the technology of modern imaging. These technological a dvances bring with them the

implication that patients staged as having localised disease in 2012 are not com parable to patients described in 1985 as having localised

disease. Many of these latter patients would have had occult metastatic disease detected had they been imaged using current technology.

This

Donald F Gleason, born 1920, pathologist, The University of Minnesota, Minneapolis, MN, USA.

Thomas Hodgkin, 1798–1866, Curator of the Museum and Demonstrator of Morbid Anatomy, Guy’s Ho spital, London, UK, described lymphadenoma in 1832.

Three carcinomas showing different degrees of differentiation. Left to right: well-differentiated, moderat ely differentiated and poorly Figure 9.5

differentiated.

leads to the paradox of stage shift, also named the Will Rogers phenomenon b y Alvan Feinstein. A change in staging system, or in the

techniques used to provide baseline information concerning staging, can produce ‘ben ets’ to patients at all stages of the disease. These

benets are, however, entirely artefactual and depend simply upon patients in ea ch stage being enriched by patients with improved

prognosis. The important cross-check to protect against being misled by stage shift is that th e prognosis for the entire group (i.e. all

stages pooled) has not been changed. Table 9.3 shows a worked example of stage shift.

The International Union against Cancer (UICC) is responsible for the TNM (tumou r, nodes, metastases) staging system for cancer. This

system is compatible with, and relates to, the American Joint Committee on Cancer (AJC C) system for stage grouping of cancer.

Examples of clinicopathological staging systems for colon cancer are shown in Tables 9 .4 and 9.5.

Therapeutic decision making and the multidisciplinary team

As the management of cancer becomes more complex, it becomes impossible for any in dividual clinician to have the intellectual and

technical competence that is necessary to manage all the patients presenting with a particular ty pe of

Table 9.3 Stage shift.

Before new staging test After new staging test

Stage Distribution (per cent) Cure rate Number cured (per cent)

Stage Distribution (per cent) Cure rate (per cent)

Number cured ‘Improvement’ in cure rate (per cent)

I 70

II 10

III 10

IV 10

All 100

90 63 80 8 80 8 50 5 84 I 50 II 10 III 10 IV 30 All 100 94 80 80 70 47 4 8 0 8 0 2 1 20 84 0

The cure rate improves in both stage I and stage IV, and there is no change in cure rates for stage II and stage III, after the introduction of a new staging investigation.

The overall cure rate is, however, unchanged.

Alvan Feinstein , 1926–2001, American Clinician and Epidemiologist.

Will Rogers (properly William Penn Adair Rogers), 1879–1935, American Actor, Humorist and Wit.

There is much confusion about the use of the terms ‘multidisciplinary’ and ‘multiprofessional’: we use ‘mu ltidisciplinary’ to imply the presence of various medically

qualified specialists (pathologists, radiologists, etc.) and ‘multiprofessional’ implies the presence of specialists from non-medical backgrounds (nurses, social workers,

radiographers).

Table 9.4 Staging of colorectal cancer.

TNM

TX, Primary tumour cannot be assessed

T0, No evidence of primary tumour

Tis, Intraepithelial or intramucosal carcinoma

T1, Tumour invades submucosa

T2, Tumour invades muscularis propria

T3, Tumour invades through the muscularis propria into the subserosa or into retroper itoneal (pericolic or perirectal) tissues

a, Minimal invasion: <1 mm beyond muscularis b, Slight invasion: 1–5 mm beyond musc ularis c, Moderate invasion: >5–15 mm beyond

muscularis d, Extensive invasion: >15 mm beyond muscularis

T4, Tumour directly invades beyond bowel a, Direct invasion into other organs or stru ctures b, Perforates visceral peritoneum

NX, Regional lymph nodes cannot be assessed

N0, No metastases in regional nodes

N1, Metastases in 1–3 regional lymph nodes

N2, Metastases in ≥4 regional lymph nodes

MX, Not possible to assess the presence of distant metastases M0, No distant metastases

M1, Distant metastases present

Table 9.5 Relationships between staging systems for colorectal cancer.

Summary box 9.4

TNM AJCC Dukes Modied Astler–Coller

TisN0M0 0– –

T1N0M0 I AA T2N0M0 I A B1 T3N0M0 IIA B B2 T4N0M0 IIB B B3 T1 or T2 N 1M0 IIIA C C1 T3 or T4 N1M0 IIIB C C2, C3 Any

T N2M0 IIIC C C1, C2, C3 Any T Any N M1 IV D –

Members of the multiprofessional team

Site-specialist surgeon

Surgical oncologist

Plastic and reconstructive surgeon

Clinical oncologist/radiotherapist

Medical oncologist

Diagnostic radiologist

Pathologist

Speech therapist

Physiotherapist

Prosthetist

Clinical nurse specialist (rehabilitation, supportive care) Palliative care nurse (symptom control, palliation) Social worker/counsellor

Medical secretary/administrator

Audit and information coordinator

tumour. The formation of multidisciplinary teams represents an attempt to make cert ain that each and every patient with a particular type

of cancer is managed appropriately. Teams should not only be multidisciplinary, they should be multiprofessional (Summary box 9.4).

The advantages and disadvantages of multidisciplinary teams are summarised in Table 9.6.

Principles of cancer surgery

For most solid tumours, surgery remains the denitive treatment and the only real istic hope of cure. However, surgery has several

Vernon B Astler , surgeon, The Medical School of the University of Michigan, Ann Arbor, MI, USA. Fred erick A Coller, pathologist, The Medical School of the

University of Michigan, Ann Arbor, MI, USA. Cuthbert Esquire Dukes, 1890–1977, pathologist, St Mark’ s Hospital, London, UK.

Table 9.6 The advantages and disadvantages of the multidisciplinary team.

Advantages Disadvantages Open debate concerning management

Patient has the advantage of many simultaneous opinions from many different specialtie s

Decision making is open, transparent and explicit

Team members educate each other

A useful educational experience for trainees and students An opportunity for rampant egotism and showing off

Less condent and less articulate members of the team may not be able to express their views, even though their views may be extremely

important

May degenerate into a rubber-stamping exercise in which the class solutions impl ied by guidelines are unthinkingly applied to disparate

individuals

Decisions are made in the absence of patients and their carers: the commodication of the pers on

Clinicians are able to avoid having to take responsibility for their decisions and their actions: the gleaf of ‘corporate responsibility’

Time-consuming and resource intensive: takes busy clinicians away from clinical p ractice for hours at a time

roles in cancer treatment including diagnosis, removal of primary disease, removal of m etastatic disease, palliation, prevention and

reconstruction.

Diagnosis and staging

In most cases, the diagnosis of cancer has been made before denitive surgery is carried out but, occasionally, a surgical procedure is

required to make the diagnosis. This is particularly true of patients with malignant ascites where laparoscopy has an important role in

obtaining tissue for diagnosis. Laparoscopy is also widely used for the staging of intr a-abdominal malignancy, particularly oesophageal

and gastric cancer. By this means, it is often possible to diagnose widespread peritoneal disease a nd small liver metastases that may have

been missed on cross-sectional imaging. Laparoscopic ultrasound is a particularly useful adjun ct for the diagnosis of intrahepatic

metastases. Other examples in which surgery is central to the diagnosis of cancer i nclude orchidectomy where a patient is suspected of

having testicular cancer and lymph node biopsy in a patient with lymphoma. R ecently, sentinel node biopsy in melanoma and breast

cancer has attracted a great deal of interest. Here, a radiolabelled colloid is injected into or around the primary tumour, and the regional

lymph nodes are scanned with a gamma camera that will pinpoint the lymph node nearest to the tumour. This lymph node can then be

removed for histological diagnosis. Until recently, staging laparotomy was an important aspect of the staging of lymphomas but, with

more accurate cross-sectional imaging and the much more widespread use of chemothera py, this practice is now largely redundant.

evidenced by the randomised trials of radical versus simple mastectomy for breast cance r. It is important, however, to appreciate that

high-quality, meticulous surgery taking care not to disrupt the primary tumour at the time of excision is of the utmost importance in

obtaining a cure in localised disease and preventing local recurrence.

Removal of metastatic disease

In certain circumstances, surgery for metastatic disease may be appropriate. T his is particularly true for liver metastases arising from

colorectal cancer where successful resection of all detectable disease can lead to long-te rm survival in about one-third of patients. With

multiple liver metastases, it may still be possible to take a surgical approach by using in situ ablation with cryotherapy or radiofrequency

energy. Another situation where surgery may be of value is pulmonary resection for iso lated lung metastases, particularly from renal cell

carcinoma.

Palliation

In many cases, surgery is not appropriate for cure but may be extremely valuab le for palliation. A good example is the patient with a

symptomatic primary tumour who also has distant metastases. In this case, removal of th e primary may improve the patient’s quality of

life, but will have little effect on the ultimate outcome. Other examples include bypass procedure s, such as an ileotransverse anastomosis

to alleviate symptoms of obstruction caused by an inoperable caecal cancer or bypassing an unresectable carcinoma at the head of the

pancreas by cholecysto- or choledochojejunostomy to alleviate jaundice.

Removal of primary disease

Radical surgery for cancer involves removal of the primary tumour and as much of the sur rounding tissue and lymph node drainage as

possible in order not only to ensure local control but also to prevent spread of the tumo ur through the lymphatics. Although the principle

of local control is still extremely important, it is now recognised that ultraradical surgery prob ably has little effect on the development of

metastatic disease, as

Principles underlying the non-surgical treatment of cancer

The relationship between dose and response and the principle of selective toxicity

Non-surgical treatments, in common with surgery, have the potential to cause h arm as well as benet. Surgery is difcult to quantify; it

is hard to describe a mastectomy in units of measure. Both drugs and radiation can be expre ssed in reproducible units: milligrams in the

case of drugs; Grays (Gy) in the case of radiation. Thus, in contrast to surgery, it is pos sible to construct dose–response relationships for

both the benets (such as tumour cure rate) and harms (such as tissue damage that is bo th severe and permanent) associated with non-

surgical interventions. These curves (see Figure 9.6) have the same general shape: they are s igmoidal. The practical consequence of this

is that, over a relatively narrow dose range, we move from failure to success, f rom tolerability to disaster. In theory, it is possible to

calculate an optimal dose for treating each tumour using dose– response curves: the dos e is that which is associated with the

Louis Harold Gray , 1905–1965, director, The British Empire Cancer Campaign Research Unit in Radiobiol ogy, Mount Vernon Hospital, Northwood, Middlesex, UK. A

Gray (Gy) is the SI unit for the absorbed dose of ionising radiation.

maximal probability of an uncomplicated cure. Lying behind the concept of the probability of an uncomplicated cure is the principle of

selective toxicity: the treatment should be selectively toxic to the tumour and, as far as possib le, should spare the normal tissues from

damage. It is this simple principle that underpins both the selection of agents used to treat cancer and the schedules employed to deliver

them. Although the graphical representations of the relationships between dose, response and th e probability of uncomplicated cure are

conceptually simple and intuitively appealing, they are, in clinical practice, impractical. The cons truction of full dose–response curves

for all possible combinations of tumours and normal tissues is neither feasible nor ethical. Reliance, when it comes to dening optimal

doses and schedules, must be on incomplete clinical data and a knowledge of the general shape of the relationship between dose and

response.

100

80 Tumour control 70

60 Serious toxicity 60

40 40 30

0 20 10

0 01020304050 60 70 80

Dose 020406080 100 Dose

100

Tumour control 50 Serious toxicity 60 40

30 40 20 20 10

0 0 0 15 30 45 60 75 90 Dose 0 15 30 45 60 75 90 Dose

Figure 9.6 A schematic illustration of the relationship between dose, response and the probability of uncomplicated cure. T he upper figures show ideal circumstances

with steep dose–response relationships for both normal tissue damage and tumour control. The lower figu res show something more like the real world. The dose–

response relationship for tumour control is flatter, because tumours are heterogeneous and, consequently, the probability of uncomplicated cure is lower – even for the

optimal dose (40 per cent in the lower figure compared with 70 per cent in the upper figure).

in situ is Latin for ‘in the place’. Tumour Surgery

Radiotherapy

Nodes Chemotherapy

Metastases

Figure 9.7 Schematic diagram to show the spatial scope of cancer treatments. Chemotherapy is systemic; surgery is mainly a local treatment. Radiotherapy is usually

local or locoregional, but can, as in radioiodine therapy for thyroid cancer, be systemic.

tion that much of what is done is unnecessary or futile, or both. The need for adjuvant the rapy, to treat the risk that residual disease might

be present after apparently curative surgery, is an acknowledgement of the current inability to detect or predict, with sufcient precision,

the presence of residual disease. It also explains why the incremental benets from adjuv ant treatments are so small and why the

existence of these benets can only be proven using randomised controlled trials, includ ing many thousands of patients. As illustrated in

Figures 9.8 and 9.9, our current approach to the selection of patients for post-surgical adjuvan t treatment is both intellectually

impoverished and inefcient. Patients may be far better off if, rather than so much time and ef fort having been invested in attempting to

discover new ‘cures’ for cancer, equivalent resources had been devoted to devising clinically useful tests to detect residual cancer cells

persisting after apparently successful initial therapy. Had this been the case, we migh t now be better able to distinguish between those

patients with systemic disease at presentation and those with truly localised disease.

General strategies in the non-surgical management of cancer

Curative surgery for cancer is guided by one simple principle: the physical rem oval of all identiable disease. The principles underlying

the non-surgical management of cancer are more complex. First, the spatial dis tribution of the effects of our therapies have to be

considered: surgery and radiotherapy are local or, at best, locoregional treatments; drugs offer a therapy that is systemic (Figure 9.7).

Second, there is the question of the intent underlying the treatment. Occasionally, radiotherapy , chemotherapy or the combination of the

two may be used with curative intent (Table 9.7). More usually, chemotherapy o r radiotherapy is used to lower the risk of recurrence

after primary treatment with surgery, so-called adjuvant therapy. Implicit within the concept of adjuvant therapy is the realisa

Radiotherapy

Within a month of their discovery in 1895, x-rays were being used to treat cancer. Despite over 100 years of use and despite some

outstanding clinical achievements, it is still not known how best to use radiation to treat cance r. In part this is because it is not known

precisely how radiation treatment affects tumours or normal tissues. Until about 20 years ago, it w as assumed that the biological effects

of radiation resulted from radiationinduced damage to the DNA of dividing cells. Nowa days, it is known that, although this undoubtedly

explains some of the biological effects of radiation, it does not provide a full explanat ion. Radiation can, both directly and indirectly,

inuence gene expression: over 100 radiation-inducible effects on gene exp ression have now been described. These changes in gene

expression are responsible for a considerable proportion of the biological effect s of radiation upon tumours and normal tissues. In this

sense, radiotherapy is a precisely targeted form of gene therapy for cancer.

Table 9.7 Examples of malignancies that may be cured without the need for surgical excision.

Malignancy Potentially curative treatment

Leukaemia

Lymphoma

Small cell lung cancer

Tumours of childhood (rhabdomyosarcoma, Wilms’ tumour) Early laryngeal cancer

Advanced head and neck cancer

Oesophageal cancer

Squamous cell cancer of the anus

Advanced cancer of the cervix

Medulloblastoma

Skin tumours (BCC, SCC)

BCC, basal cell carcinoma; SCC, squamous cell carcinoma.

Max Wilms, 1867–1918, Professor of Surgery, Heidelberg, Germany. Hubert Rodney (‘Rod’) Withers, Professor of Radiation Oncology at the University of California,

Los Angeles.

Chemotherapy (±radiotherapy)

Radiotherapy

Chemoradiation (synchronous chemotherapy and radiotherapy) Chemoradiation (sync hronous chemotherapy and radiotherapy)

Chemoradiation (synchronous chemotherapy and radiotherapy) Radiotherapy (±chem otherapy)

Radiotherapy (±chemotherapy)

Radiotherapy

100 patients operated upon for cure

70 with no residual cancer

15 resistant to adjuvant therapy

15 relapse despite adjuvant therapy

The practicalities of radiation therapy are reasonably straightforward: dene the target to treat; design the optimal technical set up to

provide uniform irradiation of that target; and choose that schedule of treatmen t that delivers radiation to that target

30 with

so as to maximise the therapeutic ratio (Figure 9.10). One of residual cancer the main problems with as sessing a therapeutic ratio for

a given schedule of radiation is that there is a dissociation between the a cute effects on normal tissues and the late damage. The acute

sensitive to

reaction is not a reliable guide to the adverse consequences

adjuvant therapy

of treatment in the longer term. As the late effects following irradiation can take over 2 0 years to develop, this poses an obvious

difculty: if the radiation schedule is changed, it will

be known within two or three years whether or not the new

5 relapse (inadequate schedule has improved tumour control; it may, however, be two therapy,

toxicity, etc.) decades before it is known, with any degree of certainty, whether

Futile therapy

Unnecessary therapy Beneficial therapy No therapy

despite adjuvant

the new technique is safe. Fractionated radiotherapy selectively

therapy spares late, as opposed to immediate, effects. For any given total

dose, the smaller the dose per treatment (the larger the number 10 patients whose of fractions), the less severe the l ate effects will be. The

problem residual disease was is that the greater the number of fractions of daily treatment, eradicated b y

adjuvant therapy

the longer the overall treatment time and the greater the opportunity for the tumour to p roliferate during treatment. All fractionation is a

compromise. Thirty years ago, Withers dened the

Net benefits four Rs of radiotherapy (see Summary box 9.5); subsequently, a

20%

70%

10%

90% treated

fifth ‘R’ (intrinsic radiosensitivity) has been added. The clinical inappropriately

practice of radiation oncology operates within the limits dened by these ve Rs.

10% treated

Chemotherapy and biological therapies

appropriately

Selective toxicity is the fundamental principle underlying the use of chemotherapy in clinical practice. The importance of the principle is

further emphasised by the fact that, by itself, chemotherapy is rarely sufcien t to cure cancer. Chemotherapy is often (in effect, if not

intent) a palliative rather than a cura

Figure 9.8 The concept of adjuvant therapy.

100 patients operated

upon for cure

Imperfect but clinically adequate test for residual disease

60 with no residual cancer, none are

treated

40 with

residual cancer, all are treated

10 with no 15 resistant to residual disease adjuvant therapy 15 sensitive to adjuvant therapy

15 relapse despite adjuvant therapy 5 relapse (inadequate therapy, toxicity, etc.)

despite adjuvant therapy

Net benefits Futile therapy Unnecessary therapy Beneficial therapy No therapy

20% 30% treated

10%

inappropriately

10% 70% treated

60%

appropriately

10 patients whose residual disease was eradicated by adjuvant therapy

Figure 9.9 The concept of adjuvant therapy and testing for minimal residual disease.

Summary box 9.5

The five Rs of radiotherapy

Repair . If given sufficient time between fractional doses of radiation, cells will repair the radiation-induced damage . Repair half-times are typically 3–6 hours.

Fractionation offers a means whereby any differentials in repair capacity between tumour and normal ce lls may be exploited. Reoxygenation. Hypoxic cells are

relatively radioresistant compared with well-oxygenated cells. Normal tissues are well oxyge nated; tumours are often hypoxic. This is an obvious therapeutic

disadvantage.

Repopulation. As radiotherapy kills cancer cells, rapid proliferation of tumour cells is stimulated. Thus, during protracte d treatment, production of cells by the tumour

may equal, or even exceed, radiation-induced cell loss. It is thus better that the overall tr eatment time is as short as possible. Redistribution. The sensitivity of cells to

radiation varies according to their position within the cell cycle. This may lead to a degree of synchronisation o f cellular division within the tumour: ideally, fractions of

radiotherapy should be timed to coincide with vulnerable phases of the cell cycle (late G2 and M).

Radiosensitivity. Low-dose rate irradiation experiments demonstrate that cells derived fr om tumours differ in their intrinsic sensitivity to radiation. Some cells are so

intrinsically resistant to treatment that no clinically viable schedule of radiation therapy would eliminate them. Conversely, some cells may be so sensitive that virtually

any schedule would be successful – the majority of cells will lie somewhere between these extre mes.

tive intervention. As such, its use should be inuenced by the cardinal principle of palliative treatment: treatment aimed at relieving

symptoms should not, itself, produce unacceptable symptoms. The cure of a diseas e should not be more grievous than its endurance.

There are now over 95 different drugs licensed by the US Food and Drug Administration (FD A) for the treatment of cancer. Of these,

over 65 per cent are cytotoxic drugs, 15 per cent are hormonal therapies and 15 per c ent are designed to interact with specic molecular

targets – so-called targeted therapies. Over 50 per cent of these agents have been lice nsed since 1990: in terms of potential progress,

achievement over the past 15 years has equalled that of the previous 40 years. There are now many more options than there were 20

years ago and, perhaps more importantly, lessons have been learnt about how better to deploy resources. The classes of cytotoxic drugs,

their mode of action and clinical indications are summarised in Table 9.8.

The newer ‘targeted’ therapies available for treating cancer present particular d ilemmas. They offer modest prolongation of survival,

often with minimal toxicity, but at considerable financial cost. When compared with conven tional therapies, these drugs typically cost

over £50 000 (US$94 000) per quality-adjusted life-year gained and, when overall re sources are limited, they may be considered

unaffordable. Table 9.9 puts into context the cost-effectiveness of various clinical interventions. The current cost of targeted therapies

should not obscure their importance: they represent the rst attempts to translate advances in molecular biology into clinical practice.

The discoveries of the mid-twentieth century are nally bearing fruit. One featu re that is emerging is the exquisite selectivity of these

treatments – they will only target specic subsets of tumours. The kinase inhibitor PLX4032 will only be effective in patients with

melanoma whose tumours have the V600E BRAF mutation; cetuximab is only ef fective in patients with colorectal cancer who have

wild-type (non-mutated) ras; imatinib is particularly effective in patients with gastroi ntestinal stromal tumours (GIST) who have

mutations in exon 11 of the Kit gene, patients with mutations in exon 9 may still respond to im atinib but will require higher doses,

patients without mutations in Kit are far less likely to respond to imatinib.

The next decade will see a major shift in the medical management of cancer – from cell destruction to cellular reprogramming. As a

result, cancer therapies are likely to become less acutely toxic, but the longer-term conse quences of such sophisticated manipulations

may be uncertain and unpredictable.

Principles of combined treatment

Cytotoxic drugs are rarely used as single agents; radiotherapy and chemotherapy are often giv en together. The rationale behind

combination, as opposed to single-agent, drug therapy is straightforward and is analogou s to that for combined antibiotic therapy: it is a

strategy designed to combat drug resistance. By the time of diagnosis, many tumours w ill contain cancer cells that, through spontaneous

mutation, have acquired resistance to cytotoxic drugs. Unlike antibiotic resistance, there is no need for previous exposure to the drug.

Spontaneous mutation rates are high enough to allow chance to permit the develop ment, and subsequent expansion, of clones of cells

resistant to drugs to which they have never been exposed. If drugs were used as single agents, th en the further expansion of these de novo

resistant subclones would limit cure. The problem can be mitigated by combining dru gs from the outset.

The choice of drugs for combination therapy is based upon three main principles: (1) us e drugs active against the disease in question; (2)

use drugs with distinct modes of action; and (3) use drugs with non-overlapping toxicit ies. By using drugs with different biological

effects, for example by combining an anti-metabolite with an agent that actively damage s DNA, it may be possible to obtain a truly

synergistic effect. It is inadvisable to combine drugs with similar adverse effects: combining tw o highly myelosuppressive drugs may

produce an unacceptably high risk of neutropenic sepsis. Where possible, combination s should be based upon a consideration of the

toxicity proles of the drugs concerned (Summary box 9.6).

Summary box 9.6

Basic principles of combined therapy

Use effective agents

Use agents with different modes of action (synergy) Use agents with non-overlapping toxicities Consider s patial cooperation

In considering the combination of radiotherapy and chemotherapy, radiation could be considered as just another drug.

A synergistic effect is one in which the damage caused by giving the agents together is greater than the da mage caused when the drugs are given separately.

Target definition

• Knowledge of

• anatomy

• patterns and probability of spread of disease

• Cross-sectional imaging

• CT, MRI

• Functional imaging

• positron emission tomography (PET)

• functional MRI

Radiotherapy dose prescription

• Optimise the therapeutic ratio

•choose that combination of total dose, number of treatments

(fractions) and overall treatment time so that the damage to normal tissues is minimised and the effects on t umour are maximised

Technical set-up

• Optimal use of radiation beams

• simulate the ‘beam’s-eye view’ of the target

• diagnostic quality screening and films

• images digitally reconstructed from CT planning images

• three-dimensional planning

• careful shaping of beams (‘conformal therapy’)

• alter energy profile across the beam to sculpt the dose distribution to complex shapes (‘intensit y modulated radiation therapy’ – IMRT)

• Optimal delivery of treatment

• ensure day-to-day reproducibility of set-up

• online verification (portal imaging)

• reference tattoos

• immobilisation of patient (moulds, shells)

• ensure that only the target is treated

• eliminate effect of physiological movement (breathing, peristalsis): ‘image-guided radiation th erapy’ – IGRT

• quality control and cross-checking procedures throughout the whole process from target def inition to follow-up

Figure 9.10 The processes involved in clinical radiotherapy. CT, computed tomography; MRI, magnetic resonance imaging.

There is, in addition to synergy and toxicity, another factor to consider in the combinatio n of drugs and radiation – the concept of spatial

cooperation. Chemotherapy is a systemic treatment; radiotherapy is not, but it is able to reach sit es, such as the central nervous system

and testis, which drugs may not reach effectively. This is why, for example, in patients treated primarily with chemotherapy for

leukaemias, lymphomas and small cell lung cancer, prophylactic cranial irradiatio n is part of the treatment protocol.

Palliative therapy

The distinction between palliative and curative treatment is not always clear cut and will bec ome increasingly blurred as professional and

public attitudes towards the management of cancer change. Ten years ago, cancer was perceived as a disease that was either cured or not;

patients either lived or died. There was little appreciation that, for many patients, cancer might be a chronic disease. Nowadays, many of

the so-called curative treatments are simply elegant exercises in growth delay. Five-year surviv al is not necessarily tantamount to cure.

With the development of targeted therapies that regulate, rather than eradicate, cancer, this sit uation is likely to continue. The aim of

treatment will be growth control rather than the extirpation of every last cancer cell. Patients w ill live with their cancers, perhaps for

years. They will die with cancer, but not necessarily of cancer. Against this backgrou nd, the distinction between curative and palliative

therapy seems somewhat arbitrary, nevertheless the control and relief of symptoms is crucial to the successful management of patients

with cancer. Much of the fear associated with cancer is due to past failures to c ontrol symptoms.

Patients fear the symptoms, distress and disruption associated with cancer almost as much as they fear the disease itself. Palliative

treatment has as its goal the relief of symptoms. Sometimes, this will involve treating the underlying problem, as with palliative

radiotherapy for bone metastases. Sometimes, it may be inappropriate to treat the cance r itself, but that does not imply that there is

nothing more to be done; there may be better ways to assuage the distress and discomfort cause d by the tumour. Palliative medicine in

the twenty-rst century is about far more than optimal control of pain: its scope is wid e, its impact immense (Table 9.10). The most

important factor in the successful palliative management of a patient with cancer is

Table 9.8 A summary of chemotherapeutic and biological agents currently used in cancer treatment.

Class Examples Putative mode of action Tumour types that may be sensitive to drug Drugs that interfere with mitosis

Vincristine, vinblastine Interfere with the formation of microtubules: ‘spindle poisons’

Taxanes: taxol, paclitaxel

Stabilise microtubules

Drugs that interfere with DNA synthesis (anti-metabolites) 5-Fluorouracil (5-FU)

Capecitabine

Methotrexate Inhibition of thymidylate synthase, false substrate for both DNA and RNA syn thesis

Orally active prodrug that is metabolised to 5-FU. Inhibition of thymidylate synthase, fa lse substrate for both DNA and RNA synthesis

Inhibition of dihydrofolate reductase

6-Mercaptopurine

6-Thioguanine

Cytosine arabinoside Inhibits de novo purine synthesis Inhibits de novo purine synthesis Fa lse substrate in DNA synthesis

Gemcitabine Inhibits ribonucleotide reductase

Drugs that directly damage DNA or interfere with its function

Mitomycin C DNA cross-linking, preferentially active at sites of low oxygen tens ion (a bioreductive drug)

Cisplatinum Forms adducts between DNA strands and interferes with replication

Carboplatin Forms adducts between DNA strands and interferes with replicat ion

Oxaliplatin

Doxorubicin Forms adducts between DNA strands and interferes with replication

Intercalates between DNA strands and interferes with replication

Cyclophosphamide

Ifosfamide

Bleomycin A prodrug converted via hepatic cytochrome p450 to phosphoram ide mustard; causes DNA crosslinks

Related to cyclophosphamide, causes DNA crosslinks

DNA strand breakage via formation of metal complex

Lymphomas

Leukaemias

Brain tumours

Sarcomas

Breast cancer

Non-small cell lung cancer Ovarian cancer

Prostate cancer

Head and neck cancer

Breast cancer

Gastrointestinal cancer Breast cancer

Gastrointestinal cancer

Breast cancer

Bladder cancer

Lymphomas

Cervix cancer

Leukaemias

Lymphomas

Non-small cell lung cancer Pancreatic cancer

Anal cancer

Bladder cancer

Gastric cancer

Head and neck cancer Rectal cancer

Germ cell tumours

Ovarian cancer

Non-small cell lung cancer Head and neck cancer Oesophageal cancer

Germ cell tumours

Ovarian cancer

Non-small cell lung cancer Head and neck cancer

Colorectal cancer

Breast cancer

Lymphomas

Sarcomas

Kaposi’s sarcoma

Breast cancer

Lymphomas

Sarcomas

Small cell lung cancer Sarcomas

Germ cell tumours Lymphomas

Table 9.8 A summary of chemotherapeutic and biological agents currently used in cancer treatment – continued.

Class Examples Putative mode of action Tumour types that may be sensitive to drug

Drugs that directly damage DNA or interfere with its function – continued

Irinotecan Inhibits topoisomerase 1 and thereby prevents the DNA from unwinding and repairing during replication

Colorectal cancer

Etoposide

Trabectedin

Dacarbazine

Temozolomide

Actinomycin D

Hormones Tamoxifen Anastrazole

Inhibitors of tyrosine kinases

Exemestane

Letrozole

Leuprolide

Goserelin

Buserelin

Cabergoline

Bromocriptine

Cyproterone acetate Flutamide

Nilutamide

Bicalutamide

Getinib

Inhibits topoisomerase 2; prevents the DNA from unwinding and repairing during replic ation

Binds to minor groove of the DNA double helix and inhibits transcription

A nitrosourea that requires activation by hepatic cytochrome p450. Methylates g uanine residues in DNA

A nitrosourea but, unlike dacarbazine, does not require activation by hepatic cytochrome p450. Methylates guanine residues in DNA

Intercalation between DNA strands, DNA strand breaks

Blocks oestrogen receptors

An aromatase inhibitor that blocks postmenopausal (non-ovarian) oestrogen production

Analogue of gonadotrophin-releasing hormone; continued use produces

downregulation of the anterior pituitary with a consequent fall in testosterone l evels

Analogue of gonadotrophin-releasing hormone; continued use produces

downregulation of the anterior pituitary with a consequent fall in testosterone l evels

Analogue of gonadotrophin-releasing hormone; continued use produces

downregulation of the anterior pituitary with a consequent fall in testosterone l evels

Blocks prolactin release, a long-acting dopamine agonist

Dopamine agonist, blocks stimulation of the anterior pituitary

Blocks the effect of androgens

Inhibits EGFR tyrosine kinase

Small cell lung cancer Germ cell tumours Lymphomas

Soft tissue sarcoma

Brain tumours

Sarcoma

Melanoma

Glioblastoma multiforme Melanoma

Rhabdomyosarcoma Wilms’ tumour

Breast cancer

Prostate cancer

Prolactin-secreting pituitary tumours

Pituitary tumours

Prostate cancer

Non-small cell lung cancer

Table 9.8 A summary of chemotherapeutic and biological agents currently used in cancer treatment – continued.

Class Examples Putative mode of action Tumour types that may be sensitive to drug Inhibitors of tyrosine kinases – continued Imatinib

Erlotinib Blocks the ability of mutant BCR-ABL fusion protein to bind ATP

Inhibition of mutant c-KIT

Inhibits EGFR tyrosine kinase

Sunitinib Promiscuous tyrosine kinase inhibitor (PDGFR, VEGFR, cKit, FLT3)

Lapatinib

Crizotinib

Pazopanib

Sorafenib

Protease inhibitors Dasatinib Bortezomib

Differentiating agents Farnesyl transferase inhibitors

All trans-retinoic acid Lonafarnib

Tipifarnib

BRAF kinase inhibitor Histone deacetylase inhibitors (HDACi)

mTOR inhibitors

PLX4032 Vorinostat

Inhibits tyrosine kinases associated with EGFR and HER

Inhibits ALK and cMET receptor tyrosine kinases

Promiscuous tyrosine kinase inhibitor – VEGFRs, PDGFR, cKit

Promiscuous tyrosine kinase inhibitor (PDGFR, VEGFR, cKit, FLT3)

BCR-ABL TKI

Interferes with proteasomal degradation of regulatory proteins; in particular, pr events NF kappa B from preventing apoptosis

Induces terminal differentiation

Inhibition of farnesyl transferase and

consequent inactivation of ras-dependent signal transduction

Inhibition of farnesyl transferase and

consequent inactivation of ras-dependent signal transduction

Blocks MAP kinase pathway

Inhibition of HDAC

Chronic myeloid leukaemia

Gastrointestinal stromal tumours (GIST) Non-small cell lung cancer

Pancreatic cancer

Renal cancer

GIST refractory to imatinib

Breast cancer

Lung cancer, Neuroblastoma, Lymphoma

Renal cancer

Renal cancer, Thyroid cancer

CML

Multiple myeloma

Acute promyelocytic leukaemia Leukaemia

Acute leukaemia

Myelodysplastic syndrome

Melanoma

Cutaneous T-cell lymphoma

Temsirolimus Everolimus Inhibits mTOR Inhibits mTOR

Antibodies directed to cell surface antigens

Trastuzumab Cetuximab Antibody directed against HER2 receptor Antibody directed a gainst EGFR receptor

Inducers of apoptosis Bevacizumab Rituximab

Alemtuzumab Arsenic trioxide

Immunological mediators

Interferon alpha-2b

Thalidomide Antibody directed against VEGFR Antibody against CD20 antigen

Antibody against CD52 antigen

Induces apoptosis by caspase inhibition, inhibition of nitric oxide

Activates macrophages, increases the cytotoxicity of T lymphocytes, inhibits cell division ( and viral replication)

Anti-inammatory, stimulates T cells, antiangiogenic

Renal cancer

Mantle-cell lymphoma,

Renal cancer

Breast cancer

Colorectal cancer

Head and neck cancer

Colorectal cancer

Lymphomas

Acute promyelocytic leukaemia

Renal carcinoma Melanoma

Hairy cell leukaemia

Myeloma

Table 9.8 A summary of chemotherapeutic and biological agents currently used in cancer treatment – continued.

Class Examples Putative mode of action Tumour types that may be sensitive to drug

Immunological Ipilimumab mediators – continued

A monoclonal antibody that blocks cytotoxic T-lymphocyte antigen-4 and acts as a potentiator of T- cell mediated anti-tumour responses

Melanoma

CML, chronic myeloid leukaemia; EGFR, epidermal growth factor receptor; FLT3, FMS-like tyrosine kina se; mTOR , mammalian target of rapamycin; NF, nuclear

factor; PDGFR, plateletderived growth factor receptor; TKI, tyrosine kinase inhibitor; VEGFR, vascular en dothelial growth factor receptor.

Table 9.9 Estimates of cost-effectiveness for a selection of interventions

Intervention Approximate cost per QALY in 2005 US$

Universal antenatal screening for HIV

Laparoscopic inguinal hernia repair versus expectant management in adults with inguina l hernia Annual mammograms from age 40 (cost

per QALY over and above screening every 2 years aged 50 to 70) Annual CT chest screening for lung cancer in a 60-year-old male ex-

smoker versus no screening Erlotinib versus usual care in the treatment of relapsed non -small cell lung cancer

Trabectedin versus best supportive care for advanced soft tissue sarcoma

Smoking cessation programme implemented at the time of surgery for lung cancer

Stroke unit care versus usual care in survivors of acute stroke

Adjuvant radiotherapy for T1 breast cancer: whole breast radiotherapy (long course) versus short course partial breast irradiation

Adding trastuzumab to adjuvant chemotherapy for HER2 receptor-positive breast canc er

Adding trastuzumab to conventional chemotherapy for advanced gastric cancer

Sunitinib compared with interferon for metastatic renal cancer

FDG-PET-CT in the follow up of non-small cell lung cancer patients after radical radio therapy with or without chemotherapy

Letrazole vs. tamoxifen in the rst-line management of post-menopausal women with ad vanced breast cancer 30 725

660

145 160

2.6 million 75 750

96 000

16 400

1750

630 000

18 900

80 000

52 500

91 500

130 000

Calculations are based on sources identied via the CEA register (https://research.tufts-nemc.org/cear4/defa ult.aspx), last accessed March 21, 2011 QALY, quality

adjusted life year

early referral. Transition between curative and palliative modes of management sho uld be seamless.

End-of-life care

End-of-life care is distinct from palliative care. Patients treated palliatively may su rvive for many years; end-of-life care concerns the

last few months of a patient’s life. Many issues, such as symptom control, are common t o both but there are also problems that are

specic to the sense of approaching death. These may include a heightened sense of spiritu al need, profound fear and the specic needs

of those who are facing bereavement. The concept of the ‘good death’ has be en embedded in many cultures over many centuries. Health-

care professionals deal with many deaths and sometimes forget that the patient who hopes for a ‘good death’ has only one chance to get

it right. This is why end-of-life care is worth considering in its own right and not as a mere appendage to palliative care. Some of the

issues unique to end-of-life care are summarised in Summary box 9.7.

Summary box 9.7

End of life issues

Appropriateness of active intervention Euthanasia

Physician-assisted suicide

Living wills

Bereavement

Spirituality

Support to allow death at home

The problem of the medicalisation of death

Table 9.10 An outline of the domains and interventions included within palliative and supportive care.

Type of support Symptom assessment

Quality of life assessment Symptom relief

Psychosocial interventions

Physical and practical support

Information and knowledge

Nutritional support

Social support

Financial support Pain, anorexia, fatigue, dyspnoea, etc. Treatment-related toxicity

Drugs

Surgery

Radiotherapy

Complementary therapies

Acupuncture

Homeopathy

Aromatherapy, etc.

Psychological support

Relaxation techniques

Cognitive behavioural therapy

Counselling

Group therapy

Music therapy

Emotional support

Physiotherapy

Occupational therapy

Speech therapy

Macmillan

Maggie’s centres

Dietary advice

Nutritional supplements

Patients

Relatives and carers

Ensure uptake of entitlements

Grants from charities, e.g. Macmillan Cancer Relief

FURTHER READING

Bailar JC, Gornik HL Cancer undefeated. N Engl J Med 1997; 336: 1569–74.

Barcellos-Hoff MH. It takes a tissue to make a tumor: epigenetics, cancer and the microenvironm ent. J Mammary Gland Biol Neoplasia

2001; 6: 213–21.

Capasso LL Antiquity of cancer. Int J Cancer 2005; 113: 2–13.

Doll R. Epidemiological evidence of the effects of behaviour and the environment on the risk of human cancer. Rec Res Cancer Res

1998; 154: 3–21.

Feinberg AP, Ohlsson R, Henikoff S. The epigenetic progenitor origin of human cancer. Nature Rev Genet 2006; 7: 21–33.

Feinstein AR, Sosin DM, Well CK. The Will Rogers phenomenon. Stage migrat ion and new diagnostic techniques as a source of

misleading statistics for survival in cancer. N Engl J Med 1985; 312: 1604–8.

Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell 2011; 144: 646–74 .

Kerr JF, Wyllie AH, Currie AR. Apoptosis: a basic biological phenomenon with wide-r anging implications in tissue kinetics. Br J

Cancer 1972; 26: 239–57.

Vogelstein B, Kinzler KW. Cancer genes and the pathways they control. Nature Med 2004; 10: 789–99.

Spiritual support CHAPTER

clinical research Surgical audit and

LEARNING OBJECTIVES

To understand:

• The planning and conduct of audit and research

• How to write up a project

• How to review a journal article and determine its

value

INTRODUCTION

It is essential for a surgeon to understand the educational and legal framework in w hich he or she works. The agenda for medical

education and clinical governance requires surgeons to expand their skills to encompass audit a nd clinical research capabilities as useful

tools for continued outcome measurement, service improvement and innovations for the b enet of patient care.

The aim of this chapter is to enable improvements in patient experience as a re sult of a successful audit cycle or by recognising the need

for clinical research to determine a new and innovative way of treatment. It will also show how to keep track of personal clinical results.

In addition, much clinical work is tedious and repetitive. Rigorous evaluation of even the m ost simple techniques and conditions can help

to keep a surgeon stimulated throughout a long career and ensure good outcomes for patients, with cost benets to the provider and a

benet to society as a whole.

Large numbers of clinical papers appear in the surgical literature every year. Many are awed, and it is important that a surgeon has the

skills to examine publications critically. The best way to develop a critical understanding of t he research and audit undertaken by others

is to perform studies of one’s own. The hardest part of audit and research is writing it up, and the hardest article to write is the rst. This

chapter also contains the information required to write a surgical paper and to e valuate the publications of others.

AUDIT OR RESEARCH?

Health professionals are expected to undertake audit and service evaluation as part of qua lity assurance. These usually involve minimal

additional risk, burden or intrusion for participants. It is important to determine at a n early stage whether a project is audit or research,

and sometimes that is not as easy as it seems. The decision will determine the framework in which the study is undertaken. In the UK,

the National Research Ethics Service has developed helpful guidance for the denition of research, audit, service evaluation and public

health surveillance. Although developed as national guidance, it is a useful guide to decision-making generally (www.nres.npsa.nhs.uk/

applications/is-your-project-research/) (Table 10.1).

AUDIT AND SERVICE EVALUATION

Clinical audit is a process used by clinicians who seek to improve patient care. The process involves comparing aspects of care

(structure, process and outcome) against explicit criteria and dened standards. Keeping trac k of personal outcome data and contributing

to a clinical database ensures that a surgeon’s own performance is monitored continuously and can be compared with a national dataset

to ensure compliance with agreed standards. It is also an essential component of reva lidation for the individual surgeon in the UK. If the

care falls short of the criteria chosen, some change in the way that care is organised should be proposed. This change may be required at

one of many levels. It might be an individual who needs training or surgical equipment that needs replacing. At times, the change may

need to take place at the team level. Sometimes, the only appropriate action is change at a n institutional level (e.g. a new antibiotic

policy), regional level (provision of a tertiary referral centre) or, indeed, national le vel (screening programmes and health education

campaigns).

Essentially, two types of audit may be encountered: national audits (e.g. in the UK, th e National Institute for Health and Clinical

Excellence (NICE)) and local/hospital audits. Both are designed to improve the quality of care. In an ideal world, national audits should

be driven by needs identied in local and hospital-based audits that are closest to the patient. For example, hospital topics are often

identied at the departmental morbidity and mortality meetings, where issues related to pa tient care are discussed. The reporting process

might identify a possible national issue, and a national audit could be designed to be completed by the local audit department and

surgical teams. The Vascular Society of Great Britain and Ireland is working continually w ith all its members in an evaluation of process

and outcomes for major vascular operations. This is driven by

Table 10.1 Research, audit or service evaluation?

Research Clinical audit Service evaluation

The attempt to derive generalisable new knowledge including studies that aim to generate hypothes es as well as studies that aim to test

them

Quantitative research – designed to test a hypothesis

Qualitative research – identies/explores themes following established methodology Addresses clea rly dened questions, aims and

objectives

Quantitative research – may involve evaluating or comparing interventions, pa rticularly new ones

Designed and conducted to produce information to inform the delivery of best care Desig ned and conducted solely to dene or judge

current care

Designed to answer the question: ‘Does this service reach a predetermined sta ndard?’ Designed to answer the question: ‘What standard

does this service achieve?’

Measures against a standard

Involves an intervention in use only. (The choice of treatment is that of the clinician and patient according to guidance, professional

standards and/or patient preference)

Measures current service without reference to a standard

Involves an intervention in use only. (The choice of treatment is that of the clinician and patient according to guidance, professional

standards and/or patient preference)

Qualitative research – usually involves studying how interventions and relationsh ips are experienced

Usually involves collecting data that are additional to those for routine care, but may include data collected routinely. May involve

treatments, samples or investigations additional to routine care

Quantitative research – study design may involve allocating patients to intervention groups

Qualitative research uses a clearly dened sampling framework underpinned by conceptua l or theoretical justications

May involve randomisation

Usually involves analysis of existing data, but may include administration of simple interviews o r questionnaires

No allocation to interventions: the health professional and patient have chosen interve ntion before clinical audit

No allocation to intervention: the health professional and patient have chosen intervention before serv ice evaluation

No randomisation No randomisation

Although any of the above may raise ethical issues, under current guidance, research requires ethics com mittee review, whereas audit and service evaluation do not.

Advice (in the UK) from National Research Ethics Service (www.nres.npsa.nhs.uk/). Based on informat ion by the National Research Ethics Service.

a Quality Improvement Programme (www.aaaqip.org.uk) that was originally designed to feedback outcomes in aortic surgery to

individual units, but which has been extended to include other high risk vascular procedure s, such as carotid endarterectomy and leg

amputation. Issues that are of local importance are addressed within the local hospita l or hospital trusts (in the UK).

Audits are formal processes that require a structure. The following steps are essential to establish an audit cycle:

1 Dene the audit question in a multidisciplinary team.

2 Identify the body of evidence and current standards.

3 Design the audit to measure performance against agreed standards based on strong evide nce. Seek appropriate advice (local audit

department in UK).

4 Measure over an agreed interval.

5 Analyse results and compare performance against agreed standards.

6 Undertake gap analysis:

a. If all standards are reached, reaudit after an agreed interval.

b. If there is a need for improvement, identify possible interventions such as tra ining, and agree with the involved parties.

7 Reaudit.

Research study

During the design of the audit project, it might become apparent that there is a limite d body of evidence available. In this case, the study

should be structured as a research proposal. Research is designed to generate ne w knowledge and might involve testing a new treatment

or regimen.

IDENTIFYING A RESEARCH TOPIC

The hardest part of research is to come up with a good idea. Once an idea has been formed, o r a question asked, it needs to be

transformed into a hypothesis. It is helpful to approach surgeons who regularly publish articles and who have a special interest in the

surgical area being considered. As ideas are suggested, keep thinking whether the ques tion posed really matters. Spend some time

rening the question because this is probably the most important part of the study . Choosing the wrong topic at this stage can lead to

many wasted hours. Once a topic has been identied, do not rush into the stud y. It is worth spending considerable time investigating the

subject in question. The worst possible outcome is to nd at the end of a long arduo us study that the research has already been done.

First port of call for information is the internet (with assistance as needed from a medica l library). Look for current articles about the

proposed research; review articles and meta-analyses can be particularly helpfu l. At this stage, most clinicians go to an electronic library

and perform a database search. It is very important to learn how to do an accurate and efcient search as early as possible. Details are

beyond the scope of this chapter, but most librarians will help out if a little interest and en thusiasm is shown. Current techniques involve

searching on Medline or other collected databases such as Google Scholar, but as ele ctronic information advances and the web becomes

more user friendly, new search strategies may emerge. Collections of reviews ar e becoming available – the Cochrane Collaboration

brings together evidence-based medical information and is available in most libraries (Ta ble 10.2).

Once a stack of articles on the subject has been obtained, it is important that these are carefully p erused. Don’t just read the abstract on

Medline! If the proposed project is still looking good after some thorough reading, it is worth further discussion with colleagues who

have written a paper on a similar subject. All scientists are attered by interest in their work. N ow it should be possible to start to plan the

research project.

PROJECT DESIGN

During the rst phase, it is important to keep in the mind some important questions (Summ ary box 10.1).

Summary box 10.1

Questions to answer before undertaking research

Why do the study?

Will it answer a useful question?

Is it practical?

Can it be accomplished in the available time and with the available resources?

What findings are expected?

What are the research governance requirements? What are the ethical issues?

What impact could it have?

Time spent carefully designing a potential project is never wasted. There are many differ ent types of scientic study. The design used

depends on the study. A randomised controlled trial (RCT) is regarded as one of the best methods of scientic research, however that

much surgical practice has been advanced through other different types of study such as th ose listed in Table 10.3. For example, testing a

new type of operation often requires a pilot study to assess feasibility that is then follow ed by a formal RCT. The introduction of

innovative surgical techniques may require novel handling, and recomendatio ns have been made by the IDEAL collaborators (see