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CLINICAL

SURGERY

ERRNVPHGLFRVRUJ

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For Elsevier Commissioning Editor: Pauline Graham Development Editor: Sally Davies Project Manager: Alan Nicholson/Louisa Talbott Designer: Stewart Larking Illustration Manager: Merlyn Harvey

CLINICAL

SURGERY THIRD EDITION Edited by

Michael M Henry

MB FRCS

Formerly Consultant Surgeon, Chelsea and Westminster and Royal Marsden Hospitals; Formerly Honorary Consultant Surgeon, National Hospital for Neurology and Elizabeth Garrett Anderson Hospital, London, UK

Jeremy N Thompson

MA MB MChir FRCS

Consultant Surgeon, Chelsea and Westminster and Royal Marsden Hospitals, London, UK Foreword by

Parveen Kumar & Michael Clark Illustrations by Gillian Lee FMAA HonFIMI AMI RMIP and Louise Perks MIMI RMIP

Edinburgh  London  New York  Oxford  Philadelphia  St Louis  Sydney  Toronto 2012

© 2012 Elsevier Ltd. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein). Third edition 2012 Second edition 2005 First edition 2001 ISBN 978-0-7020-3070-3 International ISBN 978-0-7020-3074-1 British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloging in Publication Data A catalog record for this book is available from the Library of Congress Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein.

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Contents  v

Contents

Contributors International Advisory Panel Foreword Acknowledgements Preface Abbreviations



SECTION 1 GENERAL ISSUES

  1

Surgery – what it is and what a surgeon does



J N Thompson

  2

Organisation of surgical services



D Corless

  3

Emergency medicine



J Booth

  4

Investigation of the surgical patient



A Hine and P J Shorvon

  5

The operation



P A Paraskevas, A Darzi and S Purkayastha

  6

Anaesthesia and pain control



D Dob and K Haire

  7

Perioperative management and postoperative complications



A Darzi and P A Paraskevas

  8

Wound healing and management



J N Thompson

  9

Surgical infection



S Mudan

10

The seriously ill and injured patient



N Soni and R C Bloomer

11

Practical procedures



J N Thompson

12

Principles of surgical oncology



J N Thompson

13

Organ transplantation



S H Kashi

viii xi xii xii xii xiii

3 7 15 25 53 65 81 97 109 127 149 175 187

vi  Contents



SECTION 2 REGIONAL SURGERY

14

The neck and upper aerodigestive tract



N D Stafford

15

Ear and nose



S Abramovich

16

Chest and lungs



M Dusmet

17

Cardiac surgery



J Pepper and P Kumar

18

Oesophagus, stomach and duodenum



J N Thompson

19

Bariatric surgery



G Bonanomi

20

Liver and biliary tree



S Mudan

21

The spleen



R C N Williamson and D R C Spalding

22

The pancreas



J N Thompson

23

Acute abdominal conditions



A D Spigelman

24

Small-bowel disease and intestinal obstruction



J N Thompson

25

Large bowel, including appendix



M M Henry

26

Anal and related disorders



A C J Windsor, C R G Cohen and T Campbell-Smith

27

Hernia



T McCullough and M J Hershman

28

Breast disease



P J Drew and J Winstanley

29

Arterial disease



M Jenkins and M Dialynas

30

Venous and lymphatic disorders



M Jenkins and D A Black

201 213 229 247 279 293 297 319 327 341 353 365 385 401 415 443 481

Contents  vii



SECTION 3 SURGICAL SPECIALTIES

31

Neurosurgery



P Richards and T P Lawrence

32

Surgery of the endocrine glands



D Scott-Coombes

33

Urology



C W Ogden

34

Principles of orthopaedics



M Barry and W Radford

35 Principles of management of fractures, spinal injuries   and peripheral nerve

S A Clint and D Singh

36

Principles of paediatric surgery



S Clarke

37

Ophthalmology in clinical surgery



W E Schulenburg

38

Principles of plastic surgery



N H Cawrse and P J Saxby

39

Skin disorders



J Leonard and N O’Donoghue

40

Surgery in the developing world



T E E Goodacre



Index

513 527 557 607

639 653 669 691 703 721 739

Contributors Solomon Abramovich MSc FRCS

Consultant Ear, Nose and Throat Surgeon, Department of Otolaryngology, Head and Neck Surgery, Imperial College Healthcare NHS Trust, St Mary’s Hospital, London, UK Ear and nose

Matthew Barry MBBS MS FRCS(Orth)

Consultant Orthopaedic Surgeon, Department of Orthopaedics, The Royal London Hospital, London, UK Principles of orthopaedics

Duncan Arthur Black BSc(Med Hons) MBChB FRCS(Ed) PhD

Honorary Consultant Vascular Surgeon, Department of Vascular Surgery, St Mary’s Hospital, Imperial College Healthcare NHS Trust, London,UK Venous and lymphatic disorders

Roger C Bloomer MBChB FRCA

Specialist Registrar in Anaesthetics, Imperial School of Anaesthesia, London, UK The seriously ill and injured patient

Gianluca Bonanomi MD FRCS

Consultant Surgeon, Chelsea and Westminster NHS Foundation Hospital, London; Honorary Senior Lecturer, Imperial College, London, UK Bariatric surgery

S Jeremy Booth MBBS FCEM

Consultant in Emergency Medicine, Chelsea and Westminster Hospital, London, UK Formerly: Clinical Director of Accident and Emergency Medicine, Chelsea and Westminster Healthcare NHS Trust, London Honorary Consultant in Accident and Emergency, Royal Brompton and Harefield Hospitals NHS Trust, London Immediate Past President (Accident and Emergency Section), Royal Society of Medicine Senior Examiner in Surgery to the University of London Emergency medicine

Tim Campbell-Smith BSc(Hons) MBBS FRCS (Gen Surg)

Colorectal Fellow, University College London Hospital, London, UK Anal and related disorders

Nicholas H Cawrse FRCS(Plast)

Specialist Registrar in Plastic Surgery, Abbey Ward, Royal Devon and Exeter Hospital (Wonford), Exeter, UK Principles of plastic surgery

Simon Clarke BSc(Hons) FRCS(Paed Surg) Consultant Paediatric Surgeon, Chelsea and Westminister Foundation NHS Trust; Honorary Senior Lecturer, Imperial College London, London, UK Principles of paediatric surgery

Simon Anthony Clint BSc MBBS FRCS(Tr & Orth) Specialist Registrar, Royal National Orthopaedic Hospital, Middlesex, UK Principles of management of fractures, joint injuries and peripheral nerve injuries

C Richard G Cohen MD FRCS

Consultant Colorectal Surgeon and Honorary Senior Lecturer, University College London Hospital, London, UK Anal and related disorders

David Corless BSc MD FRCS(Gen)

Consultant General and Upper Gastrointestinal Surgeon, Mid-Cheshire Hospital Foundation Trust, Cheshire and University Hospital, North Staffordshire, Staffordshire, UK Organisation of surgical services

Lord Ara Darzi PC KBE HonFrEng FMedSci

Professor of Surgery, Division of Surgery, Imperial College London, St Mary’s Hospital, London, UK The operation Perioperative management and postoperative complications

Michael Dialynas MS FRCS(Ed) FRCS(Gen Surg) Consultant Vascular Surgeon, King’s College Hospital, London, UK Arterial disease

Contributors  ix Daryl Dob BSc(Hons) MBBS FRCA

Consultant Anaesthetist, Maghill Department of Anaesthetics, Chelsea and Westminster Hospital, London, UK

Michael Philip Jenkins BSc MS FRCS FRCS (Gen Surg) FEBVS

Anaesthesia and pain control

Consultant Vascular Surgeon, Regional Vascular Unit, St Mary’s Hospital, Imperial College Healthcare NHS Trust, London, UK

Philip J Drew BSc MD(Hons) MS FRCS

Arterial disease Venous and lymphatic disorders

(Ed, Eng & Glasg) FRCS(Gen)

Professor and Consultant Breast Surgeon, Royal Cornwall HospitalTrust, Treliske Hospital, Truro, Cornwall, UK

Pankaj Kumar MA FRCS(C/Th)

Breast disease

Cardiac surgery

Michael Dusmet MD FMH

Tim P Lawrence BM MRCS

Consultant Thoracic Surgeon, Royal Brompton Hospital, London, UK Chest and lungs

Timothy E E Goodacre MBBS BSc FRCS

Florey Lecturer in Clinical Medicine and Consultant Plastic and Reconstructive Surgeon, Oxford Children’s Hospital, Oxford Radcliffe Hospitals, Headington, Oxford, UK Surgery in the developing world

Seyed Habib Kashi MB ChM FRCS

Consultant Surgeon, University Hospital of Coventry and Warwickshire NHS Trust, Coventry, UK Organ transplantation

Kevin Haire MBBS FRCA

Consultant Anaesthetist, Maghill Department of Anaesthesia, Chelsea and Westminster Hospital, London, UK Anaesthesia and pain control

Michael M Henry MB FRCS

Formerly Consultant Surgeon, Chelsea and Westminster and Royal Marsden Hospitals; Formerly Honorary Consultant Surgeon, National Hospital for Neurology and Elizabeth Garrett Anderson Hospital London, UK Large bowel, including appendix

Michael J Hershman DHMSA MSc(Hons) MS(Hons) FRCS(Eng, Ed, Glas & I) FICS

Consultant Surgeon, Stafford Hospital, Stafford, UK Hernia

Andrew L Hine MBBS MRCP FRCR

Consultant Radiologist, Department of Radiology, Central Middlesex Hospital, North-West London Hospitals NHS Trust, London, UK Investigation of the surgical patient

Consultant Cardiac Surgeon, Morriston Hospital, Swansea, UK

Neurosurgery Registrar, Department of Neurosurgery, The John Radcliffe Hospital, Oxford, UK Neurosurgery

Jonathan Leonard BSc MD FRCP

Consultant Dermatologist, St Mary’s Hospital, Imperial College Healthcare NHS Trust, London, UK Skin Disorders

Christopher P Macklin BMed BM BS FRCS DM

Consultant General and Colorectal Surgeon Mid Yorkshire Hospitals NHS Trust, Yorkshire, UK Reader

Timothy K McCullough MS FRCS

Consultant General and Colorectal Surgeon Lister Hospital, East and North Hertfordshire NHS Trust, Stevenage, Hertfordshire, UK Hernia

Satvinder Mudan BSc MBBS MD FRCS

Consultant Surgeon, Royal Marsden Hospital, London, UK Surgical infection Liver and biliary tree

Nuala O’Donoghue MBChB MRCPI

Consultant Dermatologist, Salford Royal NHS FoundationTrust, Salford, UK Skin disorders

Christopher William Ogden MS FRCS Eng(Urol) FEBU

Consultant Urologist, The Royal Marsden Hospital, Urology Unit, London, UK Urology

x  Contributors Paraskeva Paraskevas PhD FRCS

Consultant Surgeon and Senior Lecturer, Department of Biosurgery and Surgical Technology, St Mary’s Hospital, Imperial College Healthcare NHS Trust, London, UK The operation Perioperative management and postoperative complications

John Pepper MChir FRCS

Professor of Cardiothoracic Surgery, Department of Surgery, Royal Brompton Hospital, London, UK Cardiac surgery

Sanjay Purkayastha BSc(Hons) MD MRCS(Eng) MBBS(Hons)

Clinical Lecturer in Surgery, Division of Surgery, Department of Surgery and Cancer, Faculty of Medicine, St Mary’s Hospital, Imperial College Healthcare NHS Trust, London, UK The operation

Warwick Radford ChM FRCSEd(Orth)

Consultant Orthopaedic Surgeon, Chelsea and Westminster Hospital, London, UK Principles of orthopaedics

Peter Richards FRCS FRCPCH

Consultant Paediatric Neurosurgeon, Department of Neurosurgery, John Radcliffe Hospital, Oxford, UK Neurosurgery

Peter J Saxby MBChB FRCS(Plast) ChM Consultant Plastic Surgeon, Department of Plastic Surgery, Royal Devon and Exeter Hospital, Exeter, UK Principles of plastic surgery

Wilhelm Edmund Schulenburg FRCS FRCOphth

Consultant Ophthalmic Surgeon, The Western Eye Hospital Imperial College Healthcare NHS Trust, London, UK Ophthalmology in clinical surgery

David Michael Scott-Coombes MS FRCS Consultant Endocrine Surgeon, University Hospital of Wales, Cardiff, UK Surgery of the endocrine glands

Philip J Shorvon FRCP FRCR FBIR

Consultant Radiologist, Department of Radiology, Central Middlesex Hospital, North West London Hospitals NHS Trust, London, UK Investigation of the surgical patient

Dishan Singh MBChB FRCS(Orth)

Consultant Orthopaedic Surgeon, Royal National Orthopaedic Hospital, Middlesex, UK Principles of management of fractures, joint injuries and peripheral nerve injuries

Neil Soni MBChB FRCA FANZCA FJFICM MD Consultant in Anaesthesia and Intensive Care, Chelsea and Westminster Hospital NHS Trust, London, UK The seriously ill and injured patient

Duncan Richard Castell Spalding BSc(Hons) MD FRCS(Eng) FRCS(Gen Surg)

Clinical Senior Lecturer and Honorary HPB Surgeon, Hammersmith Hospital, Imperial College Healthcare NHS Trust, London, UK The spleen

Allan D Spigelman MBBS MD FRACS FRCS

Clinical Associate Dean and Professor of Surgery, Surgical Professorial Unit, UNSW St Vincent’s Hospital Clinical School, Sydney; Director of Cancer Services, St Vincent’s and Mater Health, Sydney; Director Cancer and Imunology Program, St Vincent’s Hospital, Sydney, Australia Acute abdominal conditions

Nicholas D Stafford MBChB FRCS

Professor of Head and Neck Surgery, Postgraduate Medical Institute, University of Hull, Hull, UK The neck and upper aerodigestive tract

Jeremy N Thompson MA MB MChir FRCS

Consultant Surgeon, Chelsea and Westminster and Royal Marsden Hospitals, London, UK Surgery – what it is and what a surgeon does Wound healing and management The pancreas Small bowel disease and intestinal obstruction

Robin C N Williamson MA MD MChir FRCS(Ed) FRCS(Eng)

Consultant Surgeon, Hammersmith Hospital, Imperial College Healthcare NHS Trust, London; Professor of Surgery, Imperial College London, London, UK The spleen

Alastair C J Windsor MD FRCS

Consultant Colorectal Surgeon, University College Hospital, London, UK Anal and related disorders

John Winstanley BDS MD FRCS (Eng, Glas) FDSRCPSG

Consultant Surgeon, Royal Bolton Hospital, Bolton, UK Breast disease

International Advisory Panel Hong Kong Dr Kwok Fu Jacobus Ng

Professor Abdulla I Behbehani

Professor Michael Chi Fai Tong

Lebanon Dr Youssef Comair

Departments of Anaesthesiology, Pharmacology and Pharmacy The University of Hong Kong

Department of Otorhinolaryngology, Head and Neck Surgery The Chinese University of Hong Kong

Professor David Tai Wai Yew

Professor of Anatomy and Theme Head of ‘Neuro-degeneration, Development and Repair’ School of Biomedical Sciences Faculty of Medicine The Chinese University of Hong Kong

The Vice-President of Kuwait University for Health Sciences Faculty of Medicine Kuwait University

Professor of Surgery and Chief of Division of Neurosurgery American University of Beirut Medical Center Beirut

Dr Ahmad Tayim

Orthopaedic Surgeon American University of Beirut Medical Center Beirut

India Professor N Dorairajan

Malaysia Professor Mohd Amin Jalaludin

Jordan Professor Kamal E Bani-Hani

Professor Dr Yip Cheng Har

Dean, Faculty of Medicine Jordan University of Science and Technology King Abdullah University Hospital

Department of Surgery Faculty of Medicine, University of Malaya Kuala Lumpur

Kuwait Professor Sami Asfar

Singapore Professor Khee Chee Soo

Department of Surgery Madras Medical College Chennai

Professor, Department of Surgery Faculty of Medicine, Kuwait University; Senior Consultant, Liver and Vascular Surgery Mubarak Al-Kabeer Hospital.

Consultant Otorhinolaryngologist Head and Neck Surgery Faculty of Medicine University of Malaya Kuala Lumpur

Professor of Surgery Director, National Cancer Centre Singapore Vice Dean, Clinical and Faculty Affairs, Duke-NUS Graduate Medical School

Foreword Undergraduate curricula are continually changing to suit the needs of the patient and over the last few years there has been an emphasis on communication skills, clinical skills and patient involvement. However, the basic practise of medicine and surgery remains unchanged and requires a good grounding of knowledge. Despite the onslaught of the technological age, textbooks still remain an integral part of learning. This textbook has now become well established in the undergraduate curriculum and we are delighted to see this 3rd edition. It builds on the previous editions bringing all aspects of surgery right up-todate. The book is extremely practical as well as informative. It gives an excellent insight into the life of a surgeon, starting

with the training of a surgeon, the organisational aspects of being a surgeon, and the pre- and post-operative care management of the patient. It also touches on the legal and ethical issues which are a necessary part of being a doctor. The remaining chapters take you through the various specialities in a logical fashion providing the knowledge to be able to understand surgical decisions and techniques. This new edition, once again, has been written to harmonise with our own textbook, Kumar and Clark’s Clinical Medicine. We hope that these books will be helpful companions through your career in clinical practice. Parveen J. Kumar Michael L. Clark

Preface Clinical Surgery aims to provide a comprehensive textbook of surgical disorders for both an undergraduate and postgraduate readership. The book encompasses a wide range of surgical specialties within a single volume. The Third Edition has been comprehensively revised and updated in response to comments and suggestions from our

readers, authors, Chris Macklin, Parveen Kumar and Michael Clark. An extra chapter on Bariatric Surgery has been added. We believe that these changes have further strengthened Clinical Surgery. Michael M. Henry Jeremy N. Thompson

Acknowledgements The Third Edition of Clinical Surgery follows on from the success of the first two editions. We remain grateful to those authors that contributed to the first two editions. In particular we are indebted to several authors who contributed to both the previous editions including: Shaun Appleton, Saswata Banerjee, Rolfe Birch, Reuben Canello, Richard Coombs, David Drake, Omar Faiz, Pierre Guillou, Nagy Habib, Dimitri Hadjiminas, Andrew Leather, Hamish McClure, Jonathan Northway, Michelle Slater, the late Nick Taffinder, Alison Waghorn and Gordon Williams.

We are extremely grateful to all those existing and new authors who contributed to the current edition. We would also like to thank Chris Macklin for his input as reader. We are particularly thankful to Michael Clark and Parveen Kumar who have made helpful contributions to the editorial review of this edition. Finally we are very grateful for the support and patience of Alan Nicholson, Sally Davies and Pauline Graham at Elsevier during the preparation of the Third Edition. Michael M. Henry Jeremy N. Thompson

Contents  xiii

Abbreviations A&E AAA ABGs ABPI ACE ACL ACTH ADH AEE AFP AION APC APPT APUD ARDS ARMD ATLS ATP AV AVM BMR BMT BP BPH BST CA 19-9 CABG CAD CCD CCK CCST CDC CEA CLI CNS COPD CPAP CPB CPP CQC CSF CSSD CT CVA CVP DCIS DGH DIC DIT DMSA DSA DTPA DTSI DVT ECF

accident and emergency abdominal aortic aneurysm arterial blood gases ankle:brachial pressure index angiotensin-converting enzyme anterior cruciate ligament adrenocorticotrophic hormone antidiuretic hormone activity energy expenditure alpha-fetoprotein anterior ischaemic optic neuropathy antigen-presenting cell accelerated partial thromboplastin time amine precursor uptake and decarboxylation adult respiratory distress syndrome age-related macular degeneration advanced trauma life support adenosine triphosphate (1) atrioventricular; (2) arteriovenous arteriovenous malformation basal metabolic rate best medical therapy blood pressure benign prostatic hyperplasia basic surgical training carbohydrate antigen 19-9 coronary artery bypass grafting coronary artery disease charge couple device cholecystokinin Certificate of Completion of Specialist Training Centers for Disease Control (1) carcinoembryonic antigen; (2) carotid endarterectomy critical limb ischaemia central nervous system chronic obstructive pulmonary disease continuous positive airways pressure cardiopulmonary bypass cerebral perfusion pressure Care Quality Commission cerebrospinal fluid central sterile supply department computed tomography cerebrovascular accident central venous pressure ductal carcinoma in situ district general hospital disseminated intravascular coagulation dietary-induced thermogenesis dimercaptosuccinic acid digital subtraction angiography diethylene-triamine-penta-acetic acid deep-to-superficial incompetence deep-vein thrombosis extracellular fluid

ECG ECMO EEG EGF ELISA EMG ENT ER ERCP ESR FDPs FEV1 FFA FNA FNAC FNH FSH FVC GA GCS G-CSF GFR GI GMC GnRH GORD GTN HAART hATI hCG HDU HRT HST i.m. i.v. IABP ICF ICP ICU IFN IL INR IVN IVU JVP L LA LAD LATS LCA LCIS LDH LH LHRH LMA

electrocardiogram extracorporeal membrane oxygenation electroencephalogram epidermal growth factor enzyme-linked immunosorbent assay electromyography ear, nose and throat oestrogen receptor endoscopic retrograde cholangiopancreatography erythrocyte sedimentation rate fibrin degradation products forced expiratory volume in the first second free fatty acids fine-needle aspiration fine-needle aspiration cytology focal nodular hyperplasia follicle-stimulating hormone forced vital capacity general anaesthetic Glasgow Coma Score granulocyte colony-stimulating factor glomerular filtration rate gastrointestinal General Medical Council gonadotrophin-releasing hormone gastro-oesophageal reflux disease glyceryl trinitrate highly active antiretroviral therapy human anti-tetanus immunoglobulin human chorionic gonadotrophin high-dependency unit hormone replacement therapy higher surgical training intramuscular intravenous intra-aortic balloon pump intracellular fluid intracranial pressure intensive care unit interferon interleukin international normalised ratio intravenous nutrition intravenous urogram jugular venous pressure litre local anaesthetic left anterior descending coronary artery long-acting thyroid stimulators left coronary artery lobular carcinoma in situ lactate dehydrogenase luteinising hormone luteinising hormone-releasing hormone laryngeal mask airway

xiv  Abbreviations LMWH LVEDP MAG3 MAP MCV MG MHC MODS MOSF MRCP MRI MRSA MS MSU NHS NICE NSAID NSCLC NTN NVE NYHA OA OPSI PABA PACS PAD PCA PCL PCR PCT PE PEEP PEG PET PGA PiCCO PNO PONV PPV PR PSP PTA PTC PTCA

low-molecular-weight heparin left ventricular end-diastolic pressure technetium-99m mercaptoacetyltriglycine mean arterial pressure mean corpuscular volume myasthenia gravis major histocompatibility complex multiple organ dysfunction syndrome multiple organ system failure magnetic resonance cholangiopancreatography magnetic resonance imaging methicillin-resistant Staphylococcus aureus multiple sclerosis midstream urine National Health Service National Institute for Clinical Excellence non-steroidal anti-inflammatory drug non-small-cell lung cancer National Training Number native valve endocarditis New York Heart Association osteoarthritis overwhelming postsplenectomy infection p-aminobenzoic acid picture archive and communication system peripheral arterial disease patient-controlled analgesia posterior cruciate ligament polymerase chain reaction Primary Care Trust pulmonary embolism positive end-expiratory pressure percutaneous endoscopic gastrostomy positron emission tomography persistent generalised lymphadenopathy pulse-induced contour cardiac output pneumothorax postoperative nausea and vomiting positive-pressure ventilation progesterone receptor peak systolic pressure percutaneous transluminal angioplasty percutaneous transhepatic cholangiography percutaneous transluminal coronary angioplasty

PTH PUJ PUO PVD PVE RA RAPD RAS RCA REE RP RSI RTI RVF SA SAC SCC SCFAs SCID SIRS SPECT SpR TBW TEE THI TIA TIBC TNF TNM TPN TRH TRUS TSH TSSU TUR U&E UGI UICC UTI VATS VIP VMA VVF WBC

parathyroid hormone pelviureteric junction pyrexia of unknown origin posterior vitreous detachment prosthetic valve endocarditis rheumatoid arthritis relative afferent pupillary defect renal artery stenosis right coronary artery resting energy expenditure Raynaud’s phenomenon repetitive strain injury respiratory tract infection rectovaginal fistula sinoatrial Specialist Advisory Committee small-cell carcinoma short-chain fatty acids severe combined immune deficiency systemic inflammatory response syndrome single-photon emission computed tomography Specialist Registrar total body water total energy expenditure tissue harmonic imaging transient ischaemic attack total iron-binding capacity tumour necrosis factor tumour–node–metastasis total parenteral nutrition thyrotrophin-releasing hormone transrectal ultrasound thyroid-stimulating hormone theatre sterile supply unit transurethral resection urea and electrolytes upper-gastrointestinal International Union against Cancer urinary tract infection video-assisted thoracic surgery vasointestinal peptide vanillylmandelic acid vesicovaginal fistula white blood cell

SECTION 1 GENERAL ISSUES

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1 

Surgery – what it is and what a surgeon does

The profession Surgery as an assault – psychological effects Training

3 4 4

THE PROFESSION Surgery is defined in the Oxford English Dictionary as: The art or practice of treating injuries, deformities and other disorders by manual operation or instrumental appliances.

The surgeon, therefore, attempts to make people better chiefly by the exercise of manual skills in performing ‘invasive’ procedures. In the development of medicine, surgeons have in consequence tended to be regarded as technicians, in contrast to physicians who have been seen as contemplative, analytical and devoted to the philosophical. However, these distinctions, if they ever existed, between the roles of physicians and surgeons have become increasingly blurred. Invasive procedures are frequently done within medical specialties. For example, a gastroenterologist will remove bile duct stones by endoscopic methods (ERCP) avoiding the need for surgical exploration; an interventional radiologist will deal with a narrowed artery, which would once have been bypassed using a surgical procedure. In addition, surgeons have skills in patient management other than manipulative ones; they look after many patients who might possibly need an operation but in the event do not, e.g. patients with head injuries or acute abdominal pain. A further stereotype of the surgical personality has been that of a dominant leader. The biographical accounts of pioneer surgeons contain many examples of such men, who, even if they made notable contributions to the advancement of surgery, were often dogmatic in their views and wrong as often as they were right. One early-20th century surgical master (Berkeley Moynihan) remarked that it was necessary for the surgeon to have ‘the eye of an eagle, the hand of a lady’ and, he added (in that he saw himself as a leader whom all should follow), ‘the courage of a lion’. In the development of surgery of ‘new territories’ of Moynihan’s time – the abdomen, the thorax and the head – this was probably true. But inbred dexterity and charismatic leadership have now largely given way to careful training and recognition by surgeons themselves of the limits to both their cognitive and physical skills. Current medical practice is ‘patient centred’ and based on multidisciplinary teamwork. The complexity of both modern surgical procedures and perioperative patient care

makes a well-functioning team essential. Such teams need a leader (or leaders), but leadership is in general based on discussion and consensus, and should be focused on the individual patient’s needs and wishes. Whenever possible, recommendations about patient management are ‘evidencebased’. The development of multidisciplinary and multiprofessional teams has changed the surgeon’s relationship with other doctors, nurses and healthcare workers. The members of a team share a common interest in a group of disorders. Gastroenterology is a good example: surgeons, physicians (internists in North America), radiologists and pathologists investigate and look after patients with alimentary disease and all gain from joint activities. The same is true in the care of cardiological and neurological patients. For such professional groupings to be effective, joint meetings must take place regularly at which the problems of patients and the results of investigations, such as imaging and pathological findings, are discussed and decisions reached on recommended management. Over the last few years in the United Kingdom, these multidisciplinary team meetings (MDMs or MDTs) have been formally incorporated into the management of patients with cancer and other conditions. There is also often a place for seeing and managing patients together – for example, the surgeon may meet with a gastroenterologist to discuss patients with inflammatory bowel disease, or with a radiologist to discuss a possible interventional vascular procedure. Patients requiring intensive care need close cooperation between surgeons and intensivists. The same team approach is valid for the broader matters of patient care where the close incorporation of social workers, occupational and other therapists into the decision processes about a patient may simplify return to the community and work after a major operation. Teamwork has not, however, led to a reduction in accountability – surgeons in particular are subjected to increasing scrutiny, both from within and outside the specialty (see Ch. 2). All treatments, but especially operations, carry the risk of unintended injury to the patient. Such complications of surgery often cause distress to patient and surgeon and may lead to complaint and litigation. Surgical practice is now more formally regulated by audit, which maintains a running peer-controlled check on the performance of individuals or teams. The introduction of

1 

4  Surgery – what it is and what a surgeon does

periodic re-certification or revalidation for both individual surgeons and also multidisciplinary teams is increasingly common in Western countries. External inspection and quality control, and the development of national protocols and guidelines, are common features of modern medicine. In England and Wales the Care Quality Commission (CQC) and the National Institute for Health and Clinical Excellence (NICE) undertake such roles.

SURGERY AS AN ASSAULT – PSYCHOLOGICAL EFFECTS The implied and legal view of surgery as an assault inevitably impinges on the relationship between the practitioner and the patient. The biological effects of a surgical procedure are increasingly well known and discussed in detail throughout this book (Chs 5–8), but there are important psychological matters that have been less studied and sometimes ignored by surgeons. Most patients are relatively ignorant about their body deep to their skin. One study showed, for example, that less than 10% of UK patients could accurately locate the gallbladder or define its function. A proposed attack on a structure or organ may therefore inspire alarm or dismay a patient out of proportion to what the surgeon believes to be appropriate. Irrespective of the organ or area which requires surgical attention, any physical invasion of the body creates fear, and there is a lingering belief that surgery means a close brush with death. The surgeon must understand such fears and attempt to relieve them by careful explanation of the procedure and a frank account of possible complications, including, when appropriate, the risk of death. Surgeons must recognise that certain operations have a particular psychological impact. Mastectomy for breast cancer is a good and obvious example of a severe injury to a woman’s body image (Ch. 28). There are also less visible threats such as removal of the womb (hysterectomy) with resultant loss of fertility. The circumstances in which the operation is done are also important. An urgent total colectomy with creation of an ileostomy for toxic megacolon in a young woman (Ch. 25) may be life-saving but she is unlikely to be prepared for the psychosexual consequences. A surgical procedure should always be expected to result in such benefit for the patient that the upside outweighs any downside. For example, in inflammatory bowel disease (Ch. 25), to have to put up with an ileostomy may be preferable to enduring years of frequent loose bowel motions, periodic hospitalisation, the side effects of prolonged medical therapy and the risk of cancer development. Surgeons must at all times consider the psychological impact of their advice and actions. A caring approach, considerate discussion with patient and their families, and a detailed, honest consent process will help patients overcome these problems.

simulation techniques whenever possible. For those doctors who wish to pursue a surgical career the training has become more standardised (Fig. 1.1). Currently in Great Britain and Ireland there is a 2–3-year period of core surgical training after the foundation training programmes (Years 1 and 2). This core surgical training should lead to obtaining the MRCS Diploma of the Royal Surgical Colleges of Great Britain and Ireland. Trainees are strongly advised to attend both an Advanced Trauma Life Support (ATLS) course and a Care of the Critically Ill Surgical Patient (CCrISP) course. The MRCS examination consists of two parts: an MCQ test on applied basic sciences and the principles of surgery in general and an OSCE (objective and structured clinical examination) on anatomy, surgical pathology, surgical skills, patient safety, communication skills, applied surgical science and critical care, and clinical skills in history taking and physical examination. Further training in the UK is the responsibility of the Postgraduate Medical Education and Training Board (PMETB), supported by the individual Surgical Specialist Advisory Committees (SACs). Trainees are appointed as Specialist Registrars (SpRs) to a 4–5-year specialist surgical training programme by competitive interview. On appointment they obtain a specialty National Training Number (NTN) which they keep until completion of training (or expiry of their contract). Trainees are assessed at 6 months and annually thereafter. They must pass these assessments and the Intercollegiate Specialty Examination (FRCS, or ‘exit exam’) to obtain a Certificate of Completion of Training (CCT). This confers eligibility for the Specialist Register of the General Medical Council (GMC) and to apply for Consultant (Specialist) posts.

Run through specialist training programmes Academic training

NTN (speciality) ST3 ST2

Confirm/identify speciality preference Selection into themed/generic programmes (3x4) or (2x6)

Core surgical training NTN(S) ST1

F2

TRAINING Surprisingly, training in surgery has differed markedly between regions of the world. However, these cultural differences are beginning to disappear. Increasingly medical students learn basic surgical skills such as venous cannulation and skin suturing in a clinical skills laboratory using

Career posts

Foundation programmes F1

Fig. 1.1  Structure of surgical training (2007).

Timelimited training contracts (FTSTA)

Training  5 A further optional component of surgical (and also of most other specialist) training is to spend a period in research. This is commonly undertaken after core surgical training (post-MRCS) or as an additional period of 1–2 years during specialty training. All medicine has become increasingly based on applied science. Hands-on experience of scientific method and the production of new ideas at the scientific frontier may result in a better and more perceptive clinician. How true this is in surgery is uncertain, but the prosecution of research by surgeons is regarded by most as essential to the progress of the discipline, however skill-based it may continue to be. For this to continue requires that some, if not all, surgeons gain formal training in science as applied to their discipline; most also find it exciting. FURTHER READING Surgery in general Douglas C 1975 The houseman’s tale. Canongate, Edinburgh. (A cynical but realistic novel on relatively recent hospital practice, based on the Royal Infirmary of Edinburgh)

Hger, K, Calne R, Calne R 2000 The illustrated history of surgery, 2nd edn. Routledge, Oxford Moore F 1995 A miracle and a privilege. National Academy Press, Washington. (Personal recollections of the growth of surgical biology) Mosley M, Hollingham R 2008 Blood and guts: a history of surgery. BBC Books, London Moynihan, Lord 1967 Selected writings. Pitman Medical, London Starzl T 1992 The puzzle people – memoirs of a transplant surgeon. University of Pittsburgh Press, Pittsburgh

Professional relationships and training Department of Health 2009 Reference guide to consent for examination or treatment, 2nd edn. DoH, London General Medical Council 2006 Good medical practice. General Medical Council, London General Medical Council 2008 Consent: patients and doctors making decisions together. General Medical Council, London Intercollegiate Surgical Curriculum Programme: www.iscp.ac.uk Royal College of Surgeons of England 2008 Good surgical practice

The profession Surgery as an assault – psychological effects Training

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Organisation of surgical services

The surgical team Elective surgery in the new NHS Training

8 8 8

The patient’s path to surgery

8

Minor procedures

9

Surgery, like many aspects of medicine, needs to be organised in such a way as to provide a timely and quality service. Similarly, the complexity of all branches of surgery continuously increases and requires the support of a complex infrastructure of an extended surgical team, including the surgical consultant, surgeons in training, other medical professionals such as anaesthetists, nurses and professions allied to medicine such as physiotherapists. An IT and administrative team is also needed to bring the correct patient to the correct clinic and then to the appropriate operating list. As in all systems, errors will occur and safety measures need to be inbuilt. An operation for an individual is a major life event. Anxiety and fear need to be addressed. All organisational issues need to function well to provide confidence as well as to lead to efficiency. For accountability and simplicity it remains a cornerstone of the UK health system that all patients admitted to hospital are the responsibility of a named consultant. An operation may be a single visit such as a day-case procedure with no or very little follow-up or it may be part of a complex programme of treatment, such as in cancer treatment. The early part of the 21st century has seen many changes to the provision of surgical services. New ‘providers’ of surgical care have arrived, albeit still funded in the main by the NHS. Essentially, new providers are private and by definition profit-driven organisations but they still must address all the parameters of quality as the main NHS Trusts. The complexity of the administration of each of these systems interacting has increased. It is controversial to utilise private companies within the NHS and not all professionals approve. This extra provision has probably helped reduce the time people wait for their procedures. As ‘waiting times’ reduce, quality needs to be ensured. The fact that additional providers of surgery have arrived is due mainly to the hitherto unprecedented increase in spending the UK Government has allocated to health in the last decade. This has brought the UK in line with the rest of Europe in the proportion of GDP allocated to health. The current economic situation is unlikely to lead to further

Legal and ethical issues for the surgeon Duty Negligence Consent Death and bereavement

10 11 11 11 13

additional spending. It would therefore be very difficult to predict whether the pace of change in the provision of health care and particularly surgery will continue or falter. Currently, however, the NHS is no longer the sole provider of surgical care but remains the guarantor of care still free at the point of delivery. Surgery needs to attempt to keep pace with a rapidly changing society and its expectations. Generally, increased broadband availability and instant communications make many NHS carbon-copied handwritten illegible letters obsolete. Investment and advances in IT should improve this and help with accurate data recording and analysis, which should improve patient safety, the effectiveness of care and the experience of the patient. Likewise, socio-economic changes will work through to affect surgical practice. One of the most obvious is the rise in obesity. Not only does this make most types of surgery considerably more difficult but also it adds significantly to the risks involved and the likelihood of complications. It has also spurred on surgical innovation to help such people with what is called bariatric surgery specifically designed to promote weight loss by reducing the size of the stomach and/or shortening the functional part of the small bowel. Such lifestyle-type surgery remains controversial, particularly in terms of NHS funding. There are nine surgical specialties, each with its own particular issues but sharing many common organisational issues. They are: n

n n n n n n n n

General surgery, now sub-specialising into breast, vascular, colorectal, upper gastrointestinal, endocrine and transplantation surgery Trauma and orthopaedics Urology ENT Oral and maxillofacial Paediatric Plastic surgery Cardiothoracic surgery Neurosurgery.

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8  Organisation of surgical services THE SURGICAL TEAM

The surgical consultant needs to lead a clinical team and coordinate the complex pathway to surgery alluded to above. As the complexity of surgery increases, many surgeons may become particularly specialised in a certain area. The majority of routine surgery, however, needs to be delivered with high quality in operating lists optimising the time available. Surgeons of all disciplines in the UK are required to provide emergency care and provide an elective service in their particular specialty. The generality of emergency work and the increasingly specialised elective work is an area which is influencing the organisation of surgical services, particularly in general surgery.

ELECTIVE SURGERY IN THE NEW NHS In the UK, unlike many areas of Europe and North America, patients are referred for a surgical opinion via their family doctor or general practitioner (GP). In other parts of Europe a problem with the ear, for example, may take a person directly to the relevant ENT specialist. There are advantages in both systems. In the UK it seems likely that the traditional system will continue. Now, however, the GP and patient have a choice of where this opinion may be. The majority of patients have confidence in their local hospital and currently continue to choose to have their surgery there. Patients, however, may choose to have surgery in another NHS hospital, in one of the newer Independent Treatment Centres or via a local Private Hospital Provider. Using a centralised appointment system called ‘Choose and Book’ a patient can confirm their appointment with a specialist shortly after their GP consultation, utilising appointment times dedicated to this system. The potential choice can be bewildering and difficult for patients to be truly informed about their choices. Needless to say that the concept of more providers of routine surgery is controversial and may destabilise a local Trust, which also has to train future surgeons and provide emergency surgery whilst losing the revenue of its routine work and the routine training cases. Currently, hospitals receive payment for the work done by a ‘payment by results’ system, whereby the more operations performed the more revenue received. An alternative method of payment is called a ‘block payment’ system (e.g. Wales) where a service is bought regardless of the number of cases performed. Strategic planning by the Department of Health obviously tries to calculate the need for surgery and provide the funding for it. As the requirements may differ around the country there are about 28 Strategic Health Authorities which manage the local NHS budget and commission (plan and fund) local services. Highly specialised services, for example paediatric cardiac surgery, can only be commissioned nationally. Recently, many Trusts have achieved ‘Foundation Trust’ status, which gives them some degree of financial autonomy. This may affect the range of services offered. The next few years will hopefully see the stabilisation of the routine provisions of surgical care. Many factors will influence the direction this will take, including the economic climate and the training needs of future surgeons with more stringent control of their working time by means of the European Working Time Directive (EWTD). These features may lead to the separation of emergency

surgical care and elective care to improve the efficiency and quality of both. Many Trusts have adopted a ‘consultant of the week’ system in which one surgeon looks after all the emergency cases and is freed from elective responsibility. This leads to improved continuity of care and is now widely adopted in the UK.

TRAINING The majority of hospitals in the UK have an important role in training the surgeons of the future. Traditionally there has been an apprenticeship-type component to this training with much of the service being delivered by surgeons in training. Trainees spent long hours in hospital dealing with both the daytime elective work and out of hour’s emergencies. This allowed a great deal of experience to be gained but at the expense of many unproductive hours waiting for that same experience. Recent years have seen a progressive and continuous move away from this system. The principal driving force is the EWTD, which the UK government remains committed to and which limits the time a trainee can work each day and each week and will be no more than 48 hours per week. Compulsory periods of rest are built into the system and its goal is safety by avoiding over-tired people making difficult decisions or being required to work long continuous hours. Adhering to the EWTD appears to be reducing the training opportunities for trainees and there are strongly held views that the particular requirements of surgical training cannot be met within the shortened period of training that results. However, it seems unlikely that any move back from the EWTD is planned. There are serious potential consequences for both training and emergency surgery which are probably not yet fully realised and which may influence the organisation and provision of surgical services in the years to come

THE PATIENT’S PATH TO SURGERY Definitions An elective patient is an individual with a condition that may require surgical management but in whom the matter is not sufficiently progressive to need immediate treatment. n An emergency patient, by contrast, requires assessment at once, either because of the nature of the problem (e.g. acute injury, fracture, infection or bleeding) or because of the possible rapid progression of a disease (e.g. an acute abdomen such as appendicitis). n

An emergency patient may be assessed, treated and stabilised to become an elective patient.

Elective patients In the UK the majority of patients initially see their GP with their problems. Subsequent assessment by their GP may identify a surgical problem and referral to a consultant for

Minor procedures  9 further assessment. Surgeons may also see patients referred from other medical specialists or accident and emergency (A&E) departments. The referring doctor will usually have made an assessment about the urgency of the referral, which guides the surgeon in allocating a clinic appointment. All patients who are referred need to be seen promptly and increased capacity and efficiency may lead to the majority of patients being seen in a sufficiently timely fashion such as to remove the need to classify the referrals by urgency. Currently, however, referrals are divided into those who need to be seen urgently (i.e. within 2 weeks) or routinely. Patients with suspected cancer are referred via a fasttracked system in which the patient is seen and assessed within 2 weeks. Any subsequent tests are also expedited to provide a rapid diagnosis and subsequent treatment. Additional targets to begin treatment within a timeframe have further influenced streamlining patient assessment with open access and one-stop clinics.

patient to stay in hospital overnight. Such day-case surgery requires careful planning and patient selection. It is best performed in dedicated units where the day-case processes are well established. This type of surgery lends itself to protocols, which can be followed safely and efficiently. Preoperative assessment is a key component of this process. The patient is seen, usually by a trained nurse, on a date prior to surgery to assess the patient’s fitness for the operation and general anaesthetic if that is required. The protocol will guide the necessity of additional tests such as blood tests and ECG. The procedure is further explained. Explan­ atory leaflets may be given and consent for procedures can be taken. Clinical and anaesthetic staff, depending on the patient, mix may also support this preoperative assessment. The range of cases that are suitable for day surgery continues to develop and many laparoscopic cases such as cholecystectomy can be safely performed. Currently over 50% of general surgery may be performed as a day case.

Open access  is a system in which primary care physicians can refer their patients directly to a clinical service, e.g. an endoscopy or flexible sigmoidoscopy or some minor surgery. These patients are receiving a test or treatment and are not having a comprehensive assessment.

In-patient management

One-stop clinics  provide assessment and sometimes treatment in one visit. Examples where this works well include the assessment of breast lumps where a definitive diagnosis can be achieved in one visit with clinical examination, imaging and pathology, all organised at the same visit so greatly reducing the anxiety of waiting for results. Similarly, rectal bleeding and haemorrhoids can be evaluated and treated in one visit. If more serious problems are encountered, time has also been saved as initial tests have already been done. Potentially more complex surgical problems require conventional assessment, usually in an out-patient setting. In such a consultation, a full relevant history is taken and, coupled with clinical examination, will lead to a diagnosis or further investigations. This process may result in the patient being listed for a surgical procedure. The best system also allows for a date to be agreed with the patient at that same appointment. If this is not possible, the patient is added to a waiting list but should be given an idea of the length of time to wait before surgery.

MINOR PROCEDURES No operation is minor for the patient and the clinician needs to be sensitive to a patient’s anxiety even if it is routine. A considerable proportion of minor surgery is performed in general practice. The range of cases undertaken is increasing as larger ‘poly clinics’ are built with more facilities (e.g. vasectomy, endoscopy and in some cases hernia repair).

Day-case surgery A lot of routine general, orthopaedic, ophthalmological and ENT surgery can safely be performed without requiring the

Cases that are not suitable for day surgery require in-patient care. This may involve surgery that would usually be a day case but the patient has other medical problems that require treatment or has no social support to care for him or her. Generally, however, in-patient surgery usually means more major surgery. These are cases during which a major physiological challenge is created such as blood loss, which requires prolonged observation and management afterwards. Examples would be major cancer surgery or joint replacement. The other main group of in-patient cases is emergency patients. These patients can range from being constitutionally well with a relatively minor problem such as an abscess which requires drainage to patients needing immediate lifesaving surgery due to blood loss in, for example, a patient with multiple injuries or a ruptured aortic aneurysm. Other patients may be critically ill with a surgical emergency such as a perforated intra-abdominal viscus. These patients need the physiological consequences of their illness correcting by resuscitation and then urgent surgery to deal with the cause. Surgical services in hospitals which receive such diverse emergency cases need an infrastructure which can adapt to cope with these differing cases and the availability of appropriately trained and experienced staff. The sophisticated equipment, medical infrastructure and access to critical care emergency patients need are the same as needed for complex elective cases. Often, however, elective cases and emergency cases may clash in terms of their respective needs. Hospitals may therefore separate the running of elective and emergency services so that the surgical team dealing with the emergency patients have no elective work for that day. They also have a dedicated operating theatre for any surgery required. Consequently, both elective and emergency work may proceed more efficiently. At many hospitals this system is called the ‘consultant of the week’ system, whereby one team deals with the emergency cases for a week at a time. Patients requiring certain specialist skills will still need to be ‘transferred’ to the appropriate clinician and so there still needs to be adaptability in the concurrent elective surgical services.

The surgical team Elective surgery in the new NHS Training

The patient’s path to surgery Minor procedures

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10  Organisation of surgical services

Emergency patients may be referred from their general practitioner, from A&E or from other specialists such as physicians. Emergency, life-saving surgery is very seldom indicated within the A&E. Most conditions can be stabilised to transfer to a fully equipped operating theatre. Many A&E departments may have an observation ward. Here cases usually admitted to an in-patient bed may be safely dealt with. Head injuries can be observed. Some minor surgery can be performed: for example, fracture manipulation or abscess drainage. An increasing number of hospitals now have an Admissions Unit where the majority of general surgical patients can be assessed, further tests or investigations arranged and if required the patient can be stabilised and resuscitated before transfer to theatre. Such units work well because the medical team responsible for emergencies have all the cases in one place and the nursing team become skilled in their management. Acute hospitals which receive and deal with emergency cases in both medical and surgical disciplines require a minimum range of interdependent services such as acute medicine, critical care, anaesthesia, radiology, coronary care and laboratories. They also need to be supported by networked liaison with services which may be on site or in nearby hospitals such as paediatric surgery, cardiothoracic surgery, neurosurgery, ophthalmology, ENT, maxillofacial surgery, urology and obstetrics and gynaecology. Elective operating lists need to be carefully planned. Operating lists in the UK (but not in all countries) tend to be of a set length of time such that there are two lists per day, one in the morning and one in the afternoon. These are often combined to give a team an ‘all day’ list, particularly if long or complex operations are planned. The lists therefore need to be planned to be completed in these timeframes. This operating list scheduling may have been compiled by the surgeon or structured by secretarial or administrative staff. Other factors need to be addressed to optimise the safety and efficiency of operating lists: The patients should be medically and psychologically prepared; this is best facilitated by preoperative assessment clinics where it is checked that the correct procedure is planned, and the patient’s fitness for surgery is assessed. This may involve further clinical examination and, if needed, further tests such as blood tests (including grouping and saving blood in case a transfusion is required) and an electrocardiogram (ECG) are performed. Patients are instructed where to report on the day of surgery, or the day before if more detailed planning is required, and what to bring with them as well as how long to have fasted prior to surgery. These clinics are held prior to surgery and aim to produce well-prepared patients and avoid the cancellation of operations due to unforeseen problems. Appropriately trained nurses or medical staff may run clinics. Consent may also be taken at these clinics. Complex cases should be at the start of operating lists to allow time to deal with any unexpected problems. Patients with medical problems such as diabetes should be prioritised on an operating list because of the difficulties managing their insulin. Children should ideally be operated on dedicated

paediatric lists with specialist surgeons, anaesthetists, theatre staff and equipment.

The operating suite Most students remember their first visit to an operating theatre. There is often trepidation and a feeling of ‘being in the way’. There are many professionals within an operating theatre and there is an apparent unwritten code of practice and behaviour that at first seems daunting. It is important that when a medical student first attends an operating theatre that he or she is made to feel welcome and is offered explanations of why, for example, certain areas are not touched because they are sterile. By attending theatre regularly these rituals of behaviour soon make sense and students enjoy being part of the team. More importantly, the student sees operations at first hand and gains an added understanding of the medical problem that was treated by surgery. Even if the student does not follow a surgical career, this knowledge will be invaluable in explaining issues to patients. An operating suite usually comprises several individual operating theatres. They should be easily accessible from the A&E and close to the ITU for obvious reasons. Increasingly, individual theatres are dedicated to one or two specialties. This is because each specialty often requires its own equipment and theatre layout: for example, a laminar flow theatre for orthopaedics where joint replacements are performed and theatres dedicated to minimal access surgery.

Postoperative pathway After each operation, apart from some minor cases, patients are taken to a recovery area. Patients remain vulnerable just after surgery and require special monitoring and care in this time. Recovery staff have expertise to recognise and manage problems of breathing and ventilation after general anaesthetic and to recognise surgical problems such as bleeding which occasionally necessitates further surgery. Such a recovery facility is part of a theatre complex and patients remain there until they are stable and can be safely returned to the ward for ongoing but usually less intense observation. More complex or high-risk cases may be transferred directly to a critical care facility (ITU or HDU) to continue medical treatment and observation after surgery such as ventilation. Patients who are in an ITU after surgery may require not only ventilation but also accurate monitoring and support of the other body systems. Patients typically require lines to monitor the central venous pressure (CVP) and arterial pressure (arterial line). Only with the accurate knowledge and monitoring of parameters such as these can the patient’s condition be managed well (see Ch. 10).

LEGAL AND ETHICAL ISSUES FOR THE SURGEON All doctors occupy a privileged position in society in which others may put the ultimate trust of their life in the doctor’s hands. The vast majority of doctors only ever act with the best interest of their patients at heart. The nature of medical

Legal and ethical issues for the surgeon   11 work and especially surgery requires a supporting legal framework for both patients and doctors All medical practitioners need to be aware of the legal issues related to their practice. Surgeons may be taken to court by a patient seeking compensation where negligence is deemed to have occurred. Surgeons may also face allegations of negligence through complaints made to the General Medical Council (GMC). This body regulates and advises doctors and protects patients. Most complaints about doctors can be addressed without a prolonged investigation. In potentially more serious cases a court system operates where issues of negligence are investigated and tried. The GMC, thereafter, has the powers to suspend or ‘strike a doctor off’ the medical register either temporarily or permanently. The complexity of surgery ceaselessly increases. There are many areas where patients may suffer adverse outcomes or misadventures. Society in general has higher expectations and less tolerance of these perceived failures. Patients are therefore now more likely to complain or take legal action against their doctor, hospital or both.

DUTY Before describing matters relating to negligence in more detail it would be helpful to outline a doctor’s legal duty to his or her patient and how this is interpreted in common law. Duty is the primary legal test. This is a duty of care and a duty to act in the best interest of the patient. By exercising this duty a doctor is striving to prevent disease and promote health, relieve pain and suffering and care for those who may not be cured. Surgeons often have to take very difficult decisions with and on behalf of their patients. For example, whether to proceed with highrisk surgery when potential complications could ensue. Surgeons need to always have in mind that they have a duty of care and not a duty to try to cure and operate on all their patients.

NEGLIGENCE To prove negligence it must be proved that the doctor had a duty of care, that this duty was breached with the claimant suffering as a consequence and that any resulting damage was due to this breach in care. Any claim for negligence must be brought within 3 years and the burden of proof lies with the claimant. It would be fair to say that many ‘medico-legal’ cases can be protracted and very costly. It is hard to see who, apart from solicitors, gains from this. No fault compensation or fixed tariff settlements may be a way forward. When a professional skill is involved and negligence is alleged, the question that arises is: ‘What level of skill and care does the law require?’ The evolution of common law has, over the years, provided a number of guidelines of the standards of care expected so as to avoid or counter a charge of negligence. The first and most general is: A fair, reasonable and competent degree of skill is brought to the procedure.

This should be dealt with in surgical training and clinical governance. It is any doctors’ responsibility to keep up to date and work within their limitations and seek help when needed. The second guideline relates to circumstances in which there are alternative treatments for a given condition: Failure to act in a way that a surgeon of ordinary skill would have done.

This is sometimes expressed as the practice accepted as proper by a reasonable body of medical people skilled in that particular area. Interpretation of this point can be difficult, as not infrequently seemingly contradictory views can exist. However, a doctor cannot be judged to be negligent because a contrary view exits. The third guideline is the causal chain: A direct causal link justified in terms of logic and medical knowledge must exist between the alleged negligent act and the damage or loss that has been sustained.

Proving such a link can be contentious, especially if the case is complex, and may involve difficult decisions and sometimes multiple procedures. The importance of accurate, legible, contemporaneous notes can never be overestimated in these circumstances.

CONSENT Patients may give implied consent for such matters as clinical examination, X-ray or blood tests. Explicit or written consent is needed for all invasive and surgical procedures and treatments incurring risk such as chemotherapy. Consent is not just obtaining a signature on a form prior to an operation. Informed consent is a legal entity. It must be obtained with a clear understanding of all the relevant facts and all consequences. In terms of surgery this means the diagnosis and how certain that is, the prognosis, the proposed operation and any alternative surgical or nonsurgical treatments. It should also include details of the likely outcome and risks and side effects. Generally speaking, an adult is presumed to be competent to understand the consent process and give consent for a surgical procedure. Some common problems impair reasoning and could invalidate an informed consent process. Examples may be Alzheimer’s, senile dementia and alcohol intoxication. Surgical procedures may be justly indicated where informed consent cannot be taken. Each hospital will have guidelines about consent based on national consent guidelines. In such circumstances the most senior doctor responsible should be integral to this type of decision. In life-saving scenarios with an unconscious patient surgery can take place without consent, provided what is done can be judged to be reasonable (as judged by other doctors). Consent is ideally taken by the operating surgeon. Doctors in training can very ably take consent provided they have a full understanding of the procedure and its benefits and risks, and are able easily to discuss with the operating surgeon any problem that arises. Likewise, other professionals such as nurses can be trained to take consent. Patients have rights both in civil and criminal law and these have been reaffirmed and strengthened by the Human

Legal and ethical issues for the surgeon Duty Negligence Consent

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12  Organisation of surgical services

Rights Act of 1998 which became law in 2000 and brought the provisions of the European Convention of Human Rights. If a patient suffers harm in a procedure and consent was not taken or was not adequate, this may be a factor in a claim of negligence. Thus, anything that can be construed as invading the body or mind in any way without consent is unlawful and may attract proceedings for the crime of assault and battery. For such a charge there must also be intent. Such events are extremely rare and fortunately allegations like this are also very rare. It is possible for mischievous and deluded patients to make false allegations possibly in the hope of gain. Having a witness or chaperone is vital when conducting intimate or invasive examinations or procedures. The following principles must be satisfied for the consent to be valid: n

Consent must be voluntary. n The patient must have the capacity to give consent. n The patient must have adequate knowledge to understand what they are consenting to. The complexity and possible ramifications of many surgical procedures makes taking fully informed consent nearly impossible. In North America the patient is informed of every possible complication, however rare it may be. In English law it is necessary to give sufficient information for patients to make a balanced judgement. To explain every rare potential risk may impart unnecessary anxiety in many cases for which the procedure may be usually straightforward and necessary. A grave risk of adverse complications is judged by the standards of a reputable body of medical practice – a court of law uses peer review by experienced clinicians who form expert opinions after having appraised all the facts of the cases. There is little to guide the clinician about disclosing the risks involved in a particular procedure. Case law gives some guidance and suggests that a risk of 10% should always be disclosed. Surgeons should also take into account the likelihood and seriousness of any risk for the individual patient. It is probably sensible to explain risks which occur at a level of 1% or even more rarely if the consequences are significant. Additional matters have emerged from the detailed judgements handed down in some leading cases and may be summarised as follows: n

The surgeon must weigh the balance of good and harm before treatment is recommended and is ethically required to provide information which is adequate to enable the patient to reach a balanced judgement. n The patient is entitled to reject treatment and for that purpose must understand the possibility that harm may result. n Information about the procedure may both (unduly) confuse and alarm. Implicit in the above are that: n

The surgeon should take into account the nature and severity of the patient’s condition in determining how much to disclose. n The urgency of the situation (see consent in emergency care below) and the effect of the condition to be treated

on the patient’s emotional state, must be taken into account. n A judgement must be made on the patient’s intellect and capacity to understand and deal with any information offered. Surgeons must cultivate and be trained in sensitive interpersonal and communication skills to provide balanced and impartial advice to their patients and not to unduly favour a favourite operation. False hopes should not be raised and undue fears should not be caused. If the patient requires treatment in the ITU, this should be explained and fears helped by an introduction to the unit and the staff preoperatively.

Age of consent Above the age of 16, statute law (Family Law Reform Act 1969) empowers patients to provide valid consent for their own medical, surgical or dental treatment. For those younger than 16, tradition rather than law has vested consent in parents or guardians. However, in the 1980s a Lord Justice said in a particular case: Provided the patient … is capable of understanding what is proposed and expressing his or her own wishes, I see no good reason for holding that he or she lacks the mental capacity to express them effectively and to authorise the medical man …

In light of this, the surgeon must make a clinical judgement in those under 16 as to whether: n

There is sufficient capacity in the patient to comprehend the implications of treatment n It is sensible and proper for an agreement regarding treatment to be entered into directly with the patient, independent of the views of the parents.

Mental illness and capacity The Mental Capacity Act for England and Wales (2005) has clarified the procedures to be followed when assessing an adult patient’s ability to make his or her own decision about treatment and who can make decisions for those who lack such capacity. In general, a patient is assumed to have capacity unless proven otherwise. Just because a decision seems wrong or irrational to the attending doctor does not mean that the patient lacks mental capacity. Support must be given to help a patient make her or his own decision when possible. Anything done for a patient who lacks capacity must be done in their best interests and be least restrictive of their basic rights and freedoms. In certain circumstances an independent mental capacity advocate (IMCA) must be consulted. The act also provides a framework for patients to appoint someone else to make decisions for them if they lose capacity (a Lasting Power of Attorney) and to make advance decisions about treatment.

Unconsciousness Life-saving treatment to resuscitate and stabilise can be performed without consent.

Jehovah’s Witnesses Surgeons in particular may face the occasion when a patient facing imminent death from haemorrhage refuses a blood

Legal and ethical issues for the surgeon   13 transfusion because of religious beliefs. This is a legal right but it is unlikely that any criminal proceedings would be brought against those who administer a blood transfusion to save life. However, that this is an area of difficulty is shown by a successful action by a Jehovah’s Witness because of the mental trauma which followed a blood transfusion. Jehovah’s Witnesses may also refuse blood transfusion for elective operations. All operations are performed to minimise the need to transfuse blood but many, particularly long and complex procedures, often require blood to be available. Modern equipment to aid vessel sealing help to minimise blood loss and cell-saving suction devices can re-transfuse the patient’s own blood. Likewise, in some circumstances, a patient may store their own blood preoperatively.

Undue influence Children of Jehovah’s Witnesses If there is a threat to life, the surgeon is not entitled to assume that the parent’s beliefs are shared by their children. There is a greater duty to act in the best interest of the child protected by the view that the courts do not regard children as capable of forming profound religious beliefs. In similar circumstances not related to Jehovah’s Witnesses, when it can be shown that parental or other influence has caused the patient to withhold consent for life-saving treatment, the courts have taken the view that legal liability shall not attach to those who have acted in good faith. For those just starting a medical career it may seem daunting to cope with the potential legal manifestations of everyday practise. The risk of inadvertently being entwined in legal matters can be reduced by always acting in good faith and seeking advice and counsel for any doubt. Record keeping and paperwork should be legible and in sufficient detail to reflect all decisions, particularly with such things as consent forms. All doctors in the NHS are protected by indemnity for work carried out within the NHS, provided of course the doctor followed good practise. All doctors should, however, have medical insurance (a necessary condition of employment in most countries). In the UK there are two agencies: the Medical Defence Union and the Medical Protection Society.

DEATH AND BEREAVEMENT Death comes to us all but in a surgical context may be unexpected and sudden and may be the direct consequence of efforts to try to help the patient. Sensitive and speedy handling of the physical and emotional turmoil and awareness of cultural and social differences in those bereaved are essential.

Terminal care All clinicians, including surgeons, are responsible in some way for the management of the last stages of life. The common aims are to allay suffering and maintain dignity, both of which require close and sympathetic contact with relatives. Although surgeons may feel the human and honourable need to strive against potential therapeutic defeat, it is not their task to wring the last drop of life out of their patients. For instance in extreme old age the correct management of an abdominal catastrophe may be pain relief

rather than major surgery with very little prospect of survival. These are very difficult decisions only experience can make. They are subjective and the reasons why one particular decision was taken should of course be recorded because in different circumstances elderly patients can do very well from surgery. At all times the surgeon should try to follow the wishes of the patient (including living wills), involve the relatives in difficult decisions and seek advice from colleagues if needed. It is better to anticipate the special needs of the dying in consort with the general practitioner and sometimes religious representative, especially if special care is going to be necessary. Many hospitals have protocols and pathways for patients who are dying and in need of terminal care. Groups such as Macmillan nurses can be invaluable at these difficult times.

Informing relatives This task, especially at night, may fall upon the most junior member of the medical team. At other times a senior doctor may be able to answer more questions to alleviate anxiety. Nurses can also play a key role. All questions should be answered honestly and directly. Handling these issues sensitively and with understanding is greatly appreciated by most relatives.

Death certification Trainee doctors are nearly always those responsible for the recording of death. The death certificate is a legal document and also the basis of national population statistics. It should be completed accurately to avoid subsequent wrangles, anxieties and confusion for relatives. Referral to a coroner (in England, Wales and Northern Ireland) or a procurator fiscal (in Scotland) may be necessary (Box 2.1). Many other countries have similar procedures to observe. A cause of death should be recorded rather than the mode of death (e.g. ruptured aortic aneurysm rather than shock). Box 2.1 

Reasons for referral to the coroner or procurator fiscal

Doctor: Did not treat the deceased in the final illness Did not see the deceased in the last 14 days of life Death in relation to surgical operation: During the procedure Before recovery from anaesthesia Within 24 hours Circumstances: Suspected industrial cause of death Patient in receipt of a war or industrial pension Accidental death Suspected or known – violence – neglect – poisoning or administration of drugs Medical mishap Death in police custody After abortion in mother or stillbirth of child Within 24 hours of admission to hospital Doubt and complaint: Doubt as to cause, including sudden or unexplained death Complaint by relatives

Death and bereavement

2 

14  Organisation of surgical services

Postmortem examination Opinions can be divided on the need and benefit of such examinations. Pathologists, in particular, point out that unexpected and instructive information is often discovered. Others, in contrast, often feel that functional causes such as adult respiratory distress syndrome and multi-organ system failure

are apparent during life and are not well reflected in postmortem examinations. If a death certificate cannot be issued, the death must be reported to the coroner. In other circumstances where a death certificate can be issued and a postmortem would be of value to discover more about the cause of death, the consent of the relatives must be requested.

3 

Emergency medicine

Life-saving procedures in the   Emergency Department Airway Breathing Circulation

15 15 17 18

Imaging in the trauma patient

18

The primary purpose of an Emergency Department (ED) is to diagnose and treat acute life-threatening injury and illness. Of necessity, such departments need always to be open – 24 hours a day – and adequately staffed. Inevitably, therefore, they also deal with large numbers of patients who do not strictly fall into the category of having a life-threatening illness. Emergency medicine is a rapidly expanding specialty in the UK, and all EDs now have much improved consultant supervision when compared with a decade ago. It is regrettable that some Foundation Year 2 doctors only spend 4 months in the ED; this is a vital part of their training and it is important that they get as much out of their period in the ED as possible. Because of the ready availability of the ED, all manner of patients pass through its doors. These include the lonely, people who abuse drugs, society’s misfits, and those who find conventional access to healthcare difficult. It is important that every medical student and trainee doctor sees these patients, because they have much to instruct us about the nature of humanity.

Surgical workload Only about 1% of patients who attend an ED have suffered multiple trauma. There is currently a trend to concentrate these patients into specifically designed trauma centres; however, it will still be the case that most EDs will receive multiple injured patients. A few more, although not many, come with surgical conditions which require urgent intervention: a leaking aneurysm of the abdominal aorta, a perforated abdominal viscus or a femoral artery blocked by an embolus. There is a much commoner third group of surgical patients: those who suffer from minor surgical conditions such as abscesses, paronychias and perianal haematomas. Given this wide range of presentation, it is important for patients to be prioritized – a process known as ‘triage’ (from the French word meaning ‘to sort’).

Urgent surgical conditions which cause hypovolaemic shock

19

Surgical conditions commonly seen in   the ED

20

Some aphorisms in ED medicine

22

LIFE-SAVING PROCEDURES IN THE EMERGENCY DEPARTMENT A number of surgical conditions demand immediate intervention if the patient’s life is to be saved. These are usually related to trauma – advanced trauma life support (ATLS) guidelines should be followed in the management of all trauma patients.

AIRWAY Never forget to call for help if it is apparent that the patient has a problem with their airway. A duty anaesthetist should be asked to attend urgently if there is an airway problem. It is a good principle for the inexperienced trainee doctor to call for help at an early stage before he or she gets out of depth, rather than afterwards. It is no shame, and is indeed commendable, to ask for senior and more experienced help when the situation demands. Never let one’s own pride get in the way of asking for assistance, it is a sign of maturity, not weakness, to ask for senior help when the situation demands it. In all accident victims and in anyone who is unconscious, say after a head injury, care of the airway is paramount; for example, it is quite wrong to waste time dealing with a dislocated ankle if the patient is unable to breathe because of an obstructed glottis. Always deal with the airway first (Emergency Box 3.1). The common objects which obstruct the airway are the tongue, food and dentures. The most useful instrument to have to hand is a wide-bore (Yankers) sucker. The first action to be undertaken in dealing with an unconscious patient or an accident victim is to check that the upper airway – mouth to larynx – is patent, to suck out any food and to remove dentures if these are present. It is important to bear in mind that, in trauma cases, the cervical spine must be protected by means of a stiff-neck

3 

16  Emergency medicine

!Management of airway obstruction Emergency Box 3.1 

 

n

Protect cervical spine in trauma patients Remove any foreign bodies, e.g. food, dentures n Displace tongue forwards by chin lift or jaw thrust n Insert oropharyngeal or nasopharyngeal airway if possible n Perform cricothyroidotomy if obstruction not relieved. n

Fig. 3.3  The semi-prone position for the unconscious patient.

Fig. 3.1  Oropharyngeal airway (Guedel).

Fig. 3.2  Nasopharyngeal tube for airway maintenance. cervical collar, and the spine must be kept ‘in line’ until spinal trauma has been excluded. Because the tongue has its main muscular attachment to the posterior aspect of the body of the mandible, drawing the jaw forward automatically brings the tongue with it. Therefore, obstruction caused by the tongue falling back can be dealt with by either of two simple measures: chin lift or jaw thrust. An oropharyngeal airway (Fig. 3.1) helps to keep the tongue forward. Alternatively, a nasopharyngeal tube can be inserted along the floor of the nose (Fig. 3.2). It is important to insert a safety pin at the nasal end to prevent the tube disappearing down the back of the patient’s throat. Whenever it is feasible, the unconscious patient should be kept semi-prone (Fig. 3.3). When there is an immediate need for a definitive airway, endotracheal intubation should be performed by an appropriately experienced doctor with in-line stabilisation of the cervical spine. If the trachea cannot be intubated, then this is an indication for creating a surgical airway; an example of

Fig. 3.4  Technique of jet insufflation. Carefully palpate for the cricothyroid membrane before insertion of the cannula.

where this might be the case is severe maxillofacial trauma. A cricothyroidotomy is the method used to establish a surgical airway. An incision is made directly over the cricothyroid membrane (Ch. 11) and an endotracheal tube is inserted into the upper trachea. Alternatively, the less experienced operator should pass a wide-bore intravenous trocar and cannula through the cricothyroid membrane and then remove the trocar. The stem of a Y-shaped connector is then attached to the cannula and one of the limbs of the Y is connected to an oxygen supply; insufflation of the lungs is achieved by intermittent obstruction of the remaining vent (Fig. 3.4). This procedure, although crude, can buy very valuable time for more definitive management, usually by orotracheal intubation or tracheostomy (Ch. 14).

Life-saving procedures in the Emergency Department  17 BREATHING (VENTILATION) Oxygenation of the tissues cannot be achieved, even if the airway is patent, if there is either absence of respiratory activity or impairment of cardiac output. There are four such conditions commonly encountered in the ED: n

tension pneumothorax haemothorax n flail chest n acute cardiac tamponade. n

Tension pneumothorax Aetiology There are two causes: n

closed trauma in which a fractured rib penetrates the lung n rupture of an emphysematous bulla.

Pathophysiology More air passes out through a hole in the lung during inspiration than is returned on expiration, and in the most acute examples there is one-way traffic only. With each inspiration the volume of intrapleural air increases, the intrapleural pressure rises and, in consequence, the lung collapses and the mediastinum is displaced towards the opposite side. The compressed lung causes a right-to-left shunt with cyanosis; the displaced mediastinum kinks the superior and, more importantly, the inferior vena cava, so reducing venous return and resulting in death from abolition of cardiac output.

Clinical features

Haemothorax Aetiology The cause is usually trauma to the chest as the result of either penetration (knife or projectile) or blunt injury which is usually severe, such as a fall from a height or a crush by a vehicle.

Pathophysiology The usual cause of a haemothorax is rupture of one or more intercostal arteries. The intercostal vessels are segmental in nature and come directly off the thoracic aorta; hence, haemorrhage is often brisk. Bleeding can also come from torn bronchial arteries or veins when the substance of the lung is itself lacerated. Loss of blood can be severe and is combined with compression of the lung on the affected side to produce a rightto-left shunt. Haemothorax may also be caused by an acute transection of the aorta as a result of a sudden deceleration injury.

Clinical features Symptoms In addition to a history of a physical injury, there may be chest pain and dyspnoea.

Physical findings There will usually be general features of hypovolaemia and occasionally cyanosis. Local signs are: n n n

History There may be a story of closed injury or of previous emphysema, and a conscious patient may complain of progressive dyspnoea.

Physical findings There will be gasping attempts to breathe and, in the very final stages, cyanosis. There may be distended neck veins. Local physical signs on the affected side are: n

decreased chest wall movement n a hyperresonant percussion note n absent breath sounds. In addition, although these are of late occurrence and difficult to detect, there will be: n

displacement of the trachea in the suprasternal notch away from the affected side n movement of the apex beat – laterally in a right and medially in a left pneumothorax.

Management A chest X-ray should not be done until urgent relief has been achieved by the insertion of a wide-bore needle through the second intercostal space in the midclavicular line (see Ch. 11). Formal chest drainage with an underwater seal can then be undertaken (Ch. 11) once deterioration of the patient has been averted.

n n n

bruising of the chest wall evidence of fractured ribs, including subcutaneous emphysema imprinting – a mark left on the skin by the object responsible for the injury, such as a tyre mark or other evidence of cause an entry wound, perhaps with, in a projectile injury, a complementary exit wound dull percussion note on the affected side absent or reduced breath sounds also on the affected side.

Investigation Provided there is not urgency to restore ventilation, a chest X-ray often shows shadowing on the affected side with a fluid interface with the lung. If there is also a pneumothorax, an erect film reveals a horizontal fluid level.

Management Treatment is different from that of a tension pneumothorax; a needle is inadequate for drainage. A wide-bore chest drain must be inserted and positioned so that it lies in the dependent part of the chest cavity. However, large-calibre intravenous lines and intravenous fluid resuscitation must be instituted so that blood volume is restored as the chest cavity is being decompressed. Drainage and re-expansion of the lung are frequently followed by cessation of the bleeding. However, if the rate of blood loss is greater than 200 mL/h, or if 1500 mL is drained immediately, then it is likely that an urgent thoracotomy is indicated, and a thoracic surgical team needs to be urgently contacted.

Life-saving procedures in the Emergency Department Airway Breathing (ventilation)

3 

18  Emergency medicine

Flail chest Aetiology Trauma is the only cause and, once again, may be open or closed – usually the latter.

Pathophysiology The injury is always serious and very frequently associated with an underlying contusion of the lung. The chest wall injury is a fracture of one rib (but usually more) at both the anterior and posterior ends. Thus a segment of chest wall moves independently in a paradoxical manner – inwards on inspiration and outwards on expiration. The size of the involved segment determines the degree of reduction in respiratory efficiency, which is made worse by any lung contusion which causes a right-to-left shunt.

Clinical features Symptoms The symptoms are those of hypoxia and respiratory distress.

Physical findings Apart from an external injury in penetrating trauma, physical findings may be few. Dilated neck veins are universal, and loss of a palpable apex beat may be suggestive but this may be difficult to evaluate. Heart sounds are quiet and arterial blood pressure low. Pulsus paradoxus is characteristic (decrease in systolic pressure by >10 mmHg on inspiration) but not always present.

Management Unless there is prompt relief, continuing hypoxia and death result. Tamponade caused by a stab wound requires immediate thoracotomy, if necessary at the place where injury occurred or in the ED. The thorax is entered via the left fifth rib space, the bulging pericardial sac is incised longitudinally avoiding the phrenic nerve, the blood is evacuated, and a finger is placed over the myocardial wound to arrest further bleeding while preparations are made to close the wound with simple sutures. This dramatic management results in survival of at least a quarter of victims. For those untrained in thoracotomy, time may be bought by performing needle pericardiocentesis.

Physical findings The physical findings are: n

dyspnoea n paradoxical respiration in the involved segment of chest wall.

Diagnosis Early recognition can be surprisingly difficult, particularly when breathing is shallow, but is important in that the whole thrust of management is to avoid tissue hypoxia. The majority of those with a flail chest that is causing respiratory insufficiency require positive-pressure ventilation, which can be established in the ED by intubation of the trachea and either hand or mechanical ventilation. The procedure must be continued until the flail segment has stabilised, which may take several weeks. Surgical fixation of the chest wall is only occasionally indicated.

CIRCULATION

Acute cardiac tamponade Aetiology and pathophysiology Blood accumulates within the pericardial sac and compresses the heart so that cardiac output is decreased. The source is a leak from the heart either because of a penetrating injury, such as a knife wound, or from blunt trauma. The outcome is a low cardiac output which will eventually cause death; venous return is reduced, so that there are features of right heart failure.

Clinical features History Penetrating or blunt trauma is usually obvious. The victim becomes progressively ill from low cardiac output, with confusion and eventually unconsciousness.

IMAGING IN THE TRAUMA PATIENT Any imaging must be related to the clinical state of the patient and, in particular, a competent clinical individual should accompany the patient during the procedure. There are three standard radiological views which, in trauma, should be taken: n

chest X-ray anteroposterior pelvis n cervical spine X-rays, which now form part of the secondary patient survey. n

Chest X-ray An upright (Ch. 4) chest X-ray should be obtained in any patient who has sustained trauma to the trunk – chest or abdomen. There are numerous possible abnormalities, but commonly missed diagnoses include: n

pneumothorax (see above); it is important to check that lung markings go right out to the periphery of the lung field n ruptured diaphragm n traumatic aortic dissection (Ch 29), which often reveals itself as a widened mediastinum.

Pelvis A diastasis (abnormal widening) at the symphysis pubis (Fig. 3.5) may indicate damage to the urethra (Ch. 33), which can be confirmed by urethrography. This is easily performed in the resuscitation room by inserting a urinary balloon catheter (Ch. 11) and securing it in the meatal fossa by gently inflating the balloon and instilling contrast medium under gentle pressure.

Urgent surgical conditions which cause hypovolaemic shock   19 Circulation

Imaging in the trauma patient Urgent surgical conditions   which cause hypovolaemic shock

Fig. 3.6  Method of obtaining a cross-table X-ray of the cervical spine. between the posterior aspect of the body of the first cervical vertebra and the anterior aspect of the odontoid peg is no greater than 3 mm.

Fig. 3.5  Abnormal widening of the pubic symphysis with an associated rupture of the urethra and high-riding bladder.

Concurrent with or subsequent to the information derived from these basic imaging techniques, other methods may be indicated.

Ultrasound Ultrasound images can be obtained on small, portable machines that can easily be used in the resuscitation room. This can be very useful in cases of abdominal trauma. The Focused Assessment with Sonography for Trauma (FAST scan) is a rapid, bedside, ultrasound examination performed to identify intra-peritoneal haemorrhage or pericardial tamponade. FAST examines four areas for free fluid: n

Cervical spine A cross-table cervical spine X-ray which shows all seven cervical vertebrae and the cervicothoracic junction is mandatory to avoid the possibility of a missed diagnosis of a cervical spine injury. Unrecognised, this may lead on to damage to the spinal cord. Such views are facilitated if the patient’s shoulders are pulled down (Fig. 3.6). If the cervical spine cannot be completely imaged, then a swimmer’s view can be obtained, where one arm is extended over the patient’s head, the X-ray tube is brought into the axilla, and a plate is placed on the opposite side and then exposed. There are four lines on a lateral cervical spine X-ray: prevertebral the anterior aspect of the vertebral bodies n the posterior aspect of the vertebral bodies n the spinous processes.

Perihepatic and hepato-renal space Perisplenic n Pelvis n Pericardium. n

Computed tomography (CT) This technique has transformed radiological practice, particularly in neurotrauma (Ch. 31). Spiral CT makes imaging more rapid than was previously the case and an increasing number of EDs have a CT scanner for the rapid assessment of trauma cases and selected patients with acute abdominal or chest disease. CT scanning has helped greatly in the acute management of these patients.

n n

All of these must be smooth curves. A feature which is commonly missed in interpreting these X-rays is a haematoma deep to the prevertebral fascia which clearly shows as a soft tissue swelling. Odontoid peg fractures are also commonly missed, and it is important to check that the distance

URGENT SURGICAL CONDITIONS WHICH CAUSE HYPOVOLAEMIC SHOCK Management of hypovolaemic shock is summarised in Emergency Box 3.2.

3 

20  Emergency medicine   !Management of hypovolaemic shock Emergency Box 3.2

 

n

Arrest external blood loss by pressure/elevation Insert two 14 G cannulae and take blood samples for full blood count, biochemistry, clotting studies and urgent cross match n Administer 0.9% saline 1–2 L as fast as possible, followed by plasma substitutes and blood (O-negative universal donor, type specific or fully cross matched as time permits) n Monitor pulse, blood pressure, tissue oxygenation (by pulse oximetry) and urine output (catheterisation required) n Assess/investigate and treat cause of blood loss. n

The commonest causes of non-traumatic massive blood loss are: n

ruptured abdominal aortic aneurysm (Ch. 29) ectopic pregnancy n gastrointestinal haemorrhage (usually from the upper GI tract) (Ch. 23). n

In civilian ED practice in the UK, the common traumatic causes are: n

ruptured spleen rupture of other intra-abdominal viscera such as the liver and tearing of the mesenteric vessels n long bone fractures – a single femoral shaft fracture leads to the loss of 1.5 L of blood, which is 30% of the total blood volume n pelvic fractures – several litres of blood may be lost and the patient may rapidly die from hypovolaemia. Hence, if a pelvic fracture is suspected clinically, very urgent resuscitation is required and the haemorrhage can often be abated by applying an external fixator to the pelvis in the resuscitation room. n

Ectopic pregnancy This condition should be considered in any woman who presents to the ED with acute abdominal pain and who may, even as a remote possibility, be pregnant. A denial of recent sexual intercourse is not a guarantee that the patient is not pregnant.

Clinical features History There is frequently (90%) a short history of lower abdominal pain followed by more generalised and constant pain which may also be felt in the shoulder if blood tracks up the paracolic gutters to the undersurface of the diaphragm. Dysuria is also common. Vaginal bleeding is absent in 25%.

Physical findings General features of bleeding are often apparent – pallor, circulatory collapse and air hunger may be present together with abdominal tenderness and rigidity, initially most marked in the lower abdomen. Cervical excitation also causes pain.

Management In any patient in which an ectopic pregnancy is likely, two large intravenous cannulae should be inserted even if the circulation is apparently stable; in such circumstances it may be possible to confirm the diagnosis by obtaining a positive pregnancy test. A patient with signs of hypovolaemia should go immediately to the operating room for surgery, preferably by a gynaecologist who may be able to save the affected fallopian tube.

SURGICAL CONDITIONS COMMONLY SEEN IN THE ED Soft-tissue abscesses These represent a very considerable component of the surgical work of an ED. An abscess is defined simply as a collection of pus, and the pain of an abscess is caused by the build-up of pressure in the inflamed soft tissues. It is true to say that the smaller the abscess, the greater the pain and, because an abscess may appear small, this is not a reason to underestimate the distress caused. An abscess in the finger (e.g. a pulp space abscess) is much more painful than, say, an abscess on the scrotum, because in the former there are strong fibres which connect the pulp of the fingertip to the periosteum of the distal phalanx, and also pressure rises in a confined space. Thus there is little opportunity for the abscess to expand and the tension in the affected area is high.

Diagnosis This is usually straightforward. The symptoms are of inflammation, the signs of which are heat, redness, tenderness, swelling and loss of function of the affected part. In addition there is often fluctuation.

Management Once an abscess has been diagnosed, the correct treatment is incision and drainage rather than recourse to antibiotics, although these may be administered to deal with the pos­ sibility of spread when a surgical procedure is undertaken, or any associated cellulitis. Before incision is performed, an appropriate method of anaesthesia needs to be established. For pulp space abscesses and those beside the fingernail (paronychia), ring block regional anaesthesia is suitable. A solution of 1% lidocaine (lignocaine) is introduced on either side of the base of the digit to anaesthetise the digital nerve. It takes 5 or 10 minutes for the anaesthetic to take effect; then an incision is made over the chosen point where the abscess is at its most prominent. In all abscesses, it is a cardinal error to make the incision too small. There are some abscesses which are better dealt with under general anaesthesia, e.g. in the breast, the axilla or the ischiorectal fossa. There is now a school of thought that maintains that after drainage and the use of appropriate antibiotics, the drainage site can be closed primarily. There is certainly a case for this,

Surgical conditions commonly seen in the ED  21 but caution should be observed unless drainage and excision of dead tissue are indubitably complete.

Traumatic haematoma There are two small haematomas (which cause severe pain) that can easily be dealt with in an ED: subungual and perianal.

Subungual haematoma This usually occurs when the extremities of either a finger or a toe have been damaged. Blood oozes out beneath the affected nail and, because there is initially little room for expansion, the pain soon becomes severe and requires urgent release. The old-fashioned method of trephine, in which the red hot end of a paper clip is pushed down on the nail in order to bore a hole and allow the escape of blood, is very effective, but ring block anaesthesia should be used.

Perianal haematoma See Chapter 26.

‘Minor’ wounds Relatively simple lacerations to the skin and underlying tissues are common in the ED, but a wound should never be regarded as minor. It is imperative that the basic principles of wound management are observed (Ch. 8). Chemoprophylaxis is required for all animal (including human) bites.

Tetanus prophylaxis In dealing with a laceration in the ED, consideration should always be given to whether or not the patient is immune to the effects of Clostridium tetani (Ch. 9). Tetanus is rare in developed countries but is a major cause of mortality in developing communities. The very low rates of tetanus in the UK are attributable to an effective immunisation programme and good standards of hygiene. However, previous and often repeated immunisations, as took place during the 1940s, have produced a population which is now ageing and in whom resistance to C. tetani may be on the decline. Tetanus-prone wounds are wounds including burns: n

sustained more than 6 hours before surgical treatment with a significant degree of devitalised tissue n resulting from a puncture injury n which have come into contact with soil or manure, and n where there is associated clinical evidence of sepsis, foreign body or a compound fracture. n

In a patient who has sustained such a wound, and who has received a full five dose course of tetanus vaccine at the recommended intervals, or who is up to date with their tetanus immunisation schedule, then no further doses of vaccine are recommended since within the incubation period of tetanus vaccine given at the time of the tetanus-prone injury may not boost immunity early enough to give additional protection. However, if the risk of tetanus is especially high, e.g. the wound is contaminated with stable manure, then human tetanus immunoglobulin should be given to provide immediate additional protection. If the patient’s immunisation schedule is not up to date, or if their status is unknown, a

reinforcing dose of Td/IPV (this is tetanus, diphtheria, and inactivated polio vaccine) should be given provided there are no contraindications. Further doses should be given as required to complete the recommended five dose schedule. In this situation immunoglobulin should be given for any injury which is defined as a tetanus-prone wound. The preventative dose of human tetanus immunoglobulin is 250 IU, intramuscular in most case, except if more than 24 hours have elapsed since the injury, or if there is a risk of heavy contamination or following burns, when the dose is 500 IU. For all other wounds if the patient is not up to date with his/her tetanus immunisation a reinforcing dose of Td/IPV should be given (or a course of immunisation started).

Antibiotic prophylaxis There are some wounds which, by definition, will be heavily contaminated by bacteria, e.g. agricultural injuries and human and animal bites. These should not be primarily sutured (see below) but should be thoroughly washed out with normal saline, left open and prophylactic antibiotics (Ch. 9) prescribed.

Initial examination Examination must include that part of the body distal to the wound to ensure that nerves, blood vessels and tendons have not been damaged. For example, in a laceration to the hand caused by a broken glass, all the fingers must be carefully examined to ensure that nerve and tendon function is intact. It is inadequate merely to ask the patient to make a fist – each finger must be examined, and flexor digitorum profundus and flexor digitorum superficialis tendons must have their integrity established. The possibility that there might be a foreign body should always be considered.

Management The principles of excision and suture are outlined in Chapter 8. Lacerations over the pretibial (shin) area should not be sutured because the skin is already quite tight and additional tension easily results in ischaemia of the wound edges. The correct management is for the wound edges to be approximated only, often by means of sterile adhesive plastic strips (Steristrips; see also Ch. 6) and a light dressing applied. These wounds usually heal well, although they can take many months to do so.

Head injury Definitive management is considered in Chapter 31. Initial decision-making and management in the ED are vital to subsequent success. Every year, 3 per 1000 000 of the population are admitted to hospital with head injuries; they make up approximately 20% of acute surgical admissions. The majority are admitted under the care of general surgeons and therefore it behoves those in training to have a thorough working knowledge of their initial management and to be able to detect warning signs of deterioration. They must be fully conversant with the in-house arrangements for the procedures to be undertaken

Surgical conditions commonly seen in the ED

3 

22  Emergency medicine

with such patients and must also know the lines of referral to their local neurosurgical unit.

History and progress For every victim of a head injury, the following clinical matters must be recorded, if necessary with the help of witnesses and family: n n n n n

n n n n n

time of injury time seen by the examining doctor mechanism of injury evidence of loss of consciousness period of amnesia both before (retrograde) and after sustaining the injury and whether the patient now has a continuous memory of events any visual disturbance vomiting headache fits an alcohol and drug history (if possible).

Clinical features

overriding importance – however severe the injury to the head, the airway always comes first in an attempt to ensure survival. As is also emphasised above, arterial hypotension in the presence of a head injury should not be presumed to be caused by damage to the head. Although scalp lacerations can bleed profusely, intracranial bleeding of itself does not produce hypotensive shock; the systemic response to raised intracranial pressure caused by an expanding intracranial haematoma is usually bradycardia with later hypertension. Therefore, other causes for hypotension should be sought. An algorithm for the investigation of head injuries has been produced by NICE (Fig 3.7). For further discussion on management of head injuries, see Chapter 31.

SOME APHORISMS IN ED MEDICINE

Physical findings

Always introduce yourself to the patient

Urgent findings are:

In the ED, patients are nearly always frightened and in pain. When there is time and a pressing state of emergency does not exist, an early rapport is established by introducing yourself to the patient. The patient will forgive most things related, for example, to delay if you are perceived as being a kind and caring doctor. By contrast, forgiveness is uncommon for one who is seen to be offhand. Being kind does not require any special training and is therapy needed by every patient you meet.

n

presence of blood behind the eardrum (haemotympanum) n cerebrospinal fluid coming from the nose or ears, often blood-stained (rhinorrhoea and otorrhoea) n pupillary signs, including inequality between the two sides and dilatation, particularly if unresponsive to light. The first two findings are an indication of a fracture of the base of the skull. The pupillary signs are possible indications of compression of the ocular motor (third cranial) nerve against the edge of the tentorial hiatus from critically raised intracranial pressure, perhaps because of an expanding supratentorial extradural haematoma.

Level of consciousness This is recorded against the Glasgow Coma Scale (GCS) scoring system (see Ch. 31). The initial and subsequent estimates must be, together with the time, recorded in the notes both as individual scores and as a total.

Urgent management Any patient known or suspected to have a head injury is dealt with according to the protocols laid down by the advanced trauma life support (ATLS) system (Emergency Box 3.3). As in every other circumstance of injury, the airway is of

!Advanced trauma  life support (ATLS) Emergency Box 3.3

 

A – airway maintenance with cervical spine control B – breathing and ventilation with supplemental oxygen as required C – circulation with haemorrhage control D – disability – neurological status E – exposure – completely undress patient.

Do not be distracted by the spectacular Spectacular injuries are not uncommonly seen in a busy ED. It is easy to become distracted by a patient with bilateral fractured femurs with the bone ends clearly visible, but concentration on the local injury may divert attention from a need to attend to the airway or to make sure that there is a channel for fluid replacement. The injury that is spectacular is not necessarily the one that should be attended to first.

Clinical notes are a medicolegal document, and legible, timed and signed records should be taken in every instance This good professional practice is easy to forget in the hurlyburly of an ED. However, these records are a legal document (see Ch. 2) and may later have to be made available to the patient or legal advisors, not necessarily because legal action is being taken but perhaps because an insurance claim is pending (sometimes years after the accident) which can only be dealt with properly if clear notes were taken initially. Further, if, at a later date, malpractice (Ch. 2) is alleged, comprehensive and legible clinical notes are a necessary part of the defence; by contrast, absence of a record or its incomplete nature makes defence difficult.

The diagnosis of a fracture is clinical,   not radiological A normal X-ray should not lead to a false sense of security that a fracture is absent. A classical example of this is after

Some aphorisms in ED medicine   23 Some aphorisms in ED medicine Are any of the following present?

GCS < 13 when first assessed in Emergency Department GCS < 15 when assessed in Emergency Department 2 hours after the injury Suspected open or depressed skull fracture Sign of fracture at skull base (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from ears or nose, Battle’s sign) Post-traumatic seizure Focal neurological deficit > 1 episode of vomiting Amnesia of events > 30 minutes before impact

Yes

No

Any amnesia or loss of consciousness since the injury?

Yes

No

Are any of the following present?

Age = 65 years Coagulopathy (history of bleeding, clotting disorder, current treatment with warfarin) Dangerous mechanism of injury – pedestrian or cyclist struck by a motor vehicle – occupant ejected from a motor vehicle – fall from > 1 m or 5 stairs

Yes

Request CT scan immediately

No

No imaging required now

Fig. 3.7  Investigation for clinically important brain injury. (Adapted from CG 56 Head injury: triage, assessment, investigation and early management of head injury in infants, children and adults, London: NICE, 2007. Available from www.nice.org.uk/CG56 Reproduced with permission. Note: this guidance is current at the time of going to press. All NICE guidance is subject to review.)

a fall onto the outstretched hand (Ch. 35) when there is a fracture of the head of the radius or of the scaphoid. Similarly, an elderly lady who has fallen on her hip and is complaining of local pain could have a fracture that is impacted and permits walking (Ch. 35), even if the initial X-ray looks normal – never make a diagnosis of a bruised hip; admission to hospital is the best course.

Consider carefully the diagnosis   of drunkenness It is often unsatisfactory and sometimes very dangerous for both the patient and the medical attendant to make a diagnosis of alcohol intoxication in the ED. Other conditions such as head injury and hypoglycaemia must be excluded. If the patient has sustained a head injury, then it is prudent to

3 

24  Emergency medicine

assume that confusion is caused by the head injury and is not the result of alcohol. The correct course of action is to admit the patient to hospital, and make regular neurological observations until the situation has declared itself. If the patient’s neurological condition deteriorates, then urgent CT scanning is indicated with appropriate airway management.

Never diagnose hysteria It has been known for a patient to be labelled ‘hysterical’ after a minor chest injury; the patient is then given a paper bag to breathe into and put into a cubicle, only to be found dead some time later from a tension pneumothorax. A diagnosis of psychological problems in ED should only be made after physical causes have been properly excluded.

Small wounds may result in serious injury The smaller the wound, the more likely it is that complications will be discounted or overlooked. A compound fracture of

the tibia and the fibula after a motorcycle crash is not easily missed, but a tiny cut on the finger sustained while washing the dishes may be followed by failure to detect a divided digital nerve. Serious and permanent morbidity may then result. The term ‘minor injury’ should never be used. All injuries have a potential for morbidity and should be dealt with in this light.

If there is abdominal pain, examine   the chest (and vice versa) Chest problems often cause abdominal pain, and similarly abdominal conditions may cause referred chest pain. For example myocardial infarction not infrequently presents with epigastric pain, and pleural involvement in lower lobe pneumonia can cause referred pain to the abdomen. Biliary colic may cause retrosternal pain mistaken for myocardial ischaemia and gas or fluid under the diaphragm may cause referred shoulder pain.

4 

Investigation of the   surgical patient

Haematological investigations

26

Endoscopy

48

Biochemical tests

27

Tissue sampling

50

Imaging

28 28 39 43 47

Function tests

51

Screening for surgical disease

52

Radiological imaging Ultrasound Magnetic resonance imaging Radioisotope imaging

Decision-making in the surgical patient is not often based on clinical findings alone. More frequently, investigations are undertaken to support or refute a clinical suspicion. Any investigation increases the cost of healthcare and often carries a risk both to the patient and to healthcare workers (e.g. exposure to X-rays). In consequence, investigations should only be undertaken if they are thought to contribute significantly to patient management (see also Ch. 7). It has now become customary to grade investigations by their degree of invasiveness (Ch. 1). There is not an agreed scale to define this, but the amount of compromise of the body surface and the likelihood of complications (both morbidity and mortality) are a rough guide; for example, a venepuncture is regarded as less invasive than an arterial puncture.

Objectives There are three objectives to carrying out investigations: n

to establish a diagnosis, which includes the determination of the extent of the pathological process and the planning for its surgical correction n to assess system physiological impairment (e.g. pulmonary or cardiac) and therefore the possible risk which is present if surgical treatment is needed n to screen for disorders that are common but without symptoms; however, this is only worthwhile if their presence results in a change in management (e.g. previously undiagnosed hypertension, diabetes mellitus or coronary artery disease in those who require operations for vascular disorders). There is an additional meaning of the word ‘screen’. It can be, and often is, a synonym for a group of tests designed to detect a specific abnormality, such as in clotting (see below). The surgical student should understand the difference between the two senses.

Efficacy A given investigation (just as with any clinical or laboratory observation) has a given degree of association with an underlying disease or disorder. This degree is a measure of the probability that, in a run of patients with disease X, the investigation will be positive in a given fraction of those who actually have X. For example, in patients with perforated peptic ulcer (Ch. 18), an upright chest X-ray reveals gas under the diaphragm in 60 out of 100 consecutive patients – a probability of 0.6. Observations of this kind can be incorporated into mathematical formulae using Bayes’ theorem (see ‘Further reading’) to calculate the likelihood that a given set of observations (which include clinical findings and investigations) implies the presence of a particular disease/ disorder.

Sensitivity, specificity, positive and negative predictive values Sensitivity  describes the ability of the clinical test to identify patients with a particular abnormality, even though it may also select patients who do not actually have the condition. It is calculated as: true positives true positives + false negatives

Specificity  describes the ability of the test to identify the healthy individuals who do not have that particular abnormality, even though it may miss some patients who have the condition. It is calculated as: true negatives true negatives + false positives

4 

26  Investigation of the surgical patient

Positive predictive value  describes the probability that an individual who tested positive actually has the abnormality. It is calculated as: true positives true positives + false positives

Negative predictive value  describes the probability that an individual who tested negative actually does not have the abnormality. It is calculated as: true negatives true negatives + false negatives

White cell count

False negatives are those patients who truly have the condition but were not detected by the clinical test, and false positives are those who, on subsequent analysis, turn out not to have the condition under study but had a positive test. The ideal investigation is one whose sensitivity and specificity approach unity. In practice, however, there is a tradeoff between the two ratios – the greater the sensitivity, the less the specificity, and vice versa. This matter is particularly important in screening for early disease.

Full blood count The diagnostic use of full blood count in surgical patients is less common than in assessment and screening, e.g. to ensure that the patient has a haemoglobin level sufficient for oxygen carriage during anaesthesia (see Ch. 6) and a platelet count which ensures adequate haemostasis. Nevertheless, the full blood count is the commonest haematological investigation ordered in surgical patients (Table 4.1). In diagnosis, the mean corpuscular volume (MCV) helps to identify the cause of anaemia, because chronic occult bleeding produces a low MCV (microcytic anaemia), whereas acute haemorrhage is associated with a normal value but a low haemoglobin level. A high MCV may be encountered in chronic alcoholism and vitamin B12 or folate deficiency (e.g.

Full blood count

Component Haemoglobin –Male –Female Haematocrit –Male –Female Red blood cell count –Male –Female White blood cell count Platelet count Mean corpuscular volume (MCV) Mean corpuscular haemoglobin (MCH)

A raised white cell count with neutrophilia may be indicative of the presence of bacterial infection or necrotic tissue (Ch. 9). A severe septic response, however, may be associated with an abnormally low count. Eosinophilia may be a manifestation of parasitic infestation or allergic reaction, and a high lymphocyte count can indicate the possibility of viral infection. Low white cell counts follow cytotoxic chemotherapy. Patients with HIV infection may have low numbers of lymphocytes.

Platelets

HAEMATOLOGICAL INVESTIGATIONS

Table 4.1

in patients with a previous total gastrectomy without vitamin B12 replacement, Crohn’s disease [Ch. 24] of the terminal ileum or previous resection of this part of the gut). High haemoglobin and red blood cell counts are commonly the result of severe dehydration and compensation for chronic respiratory failure. Occasionally they direct attention to the possibility of polycythaemia vera, a myeloproliferative disorder in which there is not only excessive production of normal erythrocytes but also increased production of leucocytes and platelets.

Normal value 12.5–16.5 g/dL 11.5–15.5 g/dL

Thrombocytopenia may be the result of a drug reaction (e.g. heparin), hypersplenism, an autoimmune process (idiopathic thrombocytopenic purpura), leukaemias or excessive consumption (disseminated intravascular coagulation). Thrombocytosis is seen in chronic sepsis and after splenectomy (Ch. 21) or haemorrhage.

Coagulation In certain surgical patients, disorders of the clotting mechanism are more common. A coagulation screen should be obtained in: n

obstructive jaundice in which absence of vitamin K absorption leads to lack of prothrombin synthesis (Ch. 20) n patients on anticoagulants n patients who have undergone significant haemorrhage, e.g. during operation or after trauma n patients who appear, during operation, to have coagulation defects, i.e. those with unexpectedly heavy bleeding. Coagulopathies are not common but can occur in the course of other serious illness that may require surgical management.

0.42–0.53 0.39–0.45

Disseminated intravascular coagulation (DIC)

4.4–6.5 × 1012/L 3.9–5.6 × 1012/L 4–11 × 109/L 150–400 × 109/L 80–98 fL 27–32 pg

This condition is usually part of another severe illness or widespread malignancy and is characterised by activation, within the intravascular compartment, of both the coagu­ lation and the fibrinolytic cascades. Clotting factors are consumed at a higher rate than they are replaced. The results are:

Biochemical tests  27 n

depletion of clotting factors, and coagulopathy characterised by high prothrombin time and a low platelet count and fibrinogen levels n increased circulating products of fibrin degradation (FDPs). The cause of the syndrome is probably the activation of the vascular endothelium in capillary beds, which assumes a pro-coagulant state and initiates the coagulation cascade. Many bacterial products such as endotoxin and cytokines (e.g. tumour necrosis factor, interleukin-1) are capable of inducing a pro-coagulant state in endothelial cells.

BIOCHEMICAL TESTS Table 4.2 lists the most commonly used biochemical tests.

Blood levels Previously well patients who are not taking medication can undergo minor surgery without any biochemical studies other than routine urinalysis for the presence of glucose (see below). Levels in the blood are, however, important screening tests for many surgical patients: those with a cardiovascular disorder, on diuretic treatment or with known diabetes mellitus should always have their blood levels of sodium and potassium determined before an anaesthetic. Potassium changes (usually hypokalaemia) make patients vulnerable to cardiac arrhythmias; correction is necessary and usually easy. Elevated serum urea concentration is common with dehydration or renal insufficiency, whereas serum creatinine concentration is a more reliable marker of renal disease and is usually not affected by moderate dehydration. Elevation usually signifies the loss of 50% of renal function. Creatinine clearance (calculated from 24-hour urinary and serum creatinine values) is an accurate measure of glomerular filtration rate (GFR) and should be done in those who are to undergo major vascular reconstructions (e.g. aortic aneurysm repair), when it may reveal impaired renal function.

Postoperative abnormalities in serum electrolyte concentrations are very common, chiefly because, in many surgical circumstances, the gastrointestinal tract cannot be used for the administration of maintenance fluids and electrolytes. In addition, postoperative requirements may be difficult to calculate when losses are complicated – fistulae, nasogastric suction and fluid sequestration into either the intestine or large inflamed areas. Although sepsis and inappropriate antidiuretic hormone (ADH) secretion can cause a low serum sodium concentration (hyponatraemia), the commonest cause of this is water overload. If the patient is dependent on parenteral fluid therapy, the levels of electrolyte and urea in the blood should be measured daily. Changes in serum potassium concentration are particularly likely in patients with an unusually high urine output (low potassium – hypokalaemia) or pathologically low output (raised potassium – hyperkalaemia). Prompt correction of the underlying cause is mandatory. Renal blood flow may be reduced during and after prolonged hypotension caused by uncorrected loss of blood volume or in patients with systemic sepsis. Postoperative elevations of urea and/or creatinine concentration are often the consequence of this. Serial measurements of urea concentration may provide an early warning of the development of renal failure. Other blood levels, such as calcium and enzyme concentrations, are dealt with under the heading of the disorders or disturbances which cause their change.

Urinalysis Testing of the urine has been greatly simplified by the use of dipstick and other prepackaged tests. Relevant findings in surgical patients are: n n

n

Table 4.2

Commonly used biochemical tests Normal value

Sodium Potassium Urea Creatinine Calcium Glucose Urate Total protein Albumin Bilirubin Alkaline phosphatase Aspartate aminotransferase Alanine aminotransferase Lactate dehydrogenase Creatine phosphokinase C-reactive protein

135–146 mmol/L 3.5–5.5 mmol/L 2.6–6.7 mmol/L 60–120 mmol/L 2.2–2.6 mmol/L 3.9–5.6 mmol/L 0.18–0.42 mmol/L 62–80 g/L 35–50 g/L 10 000 red blood cells/mm3; >500 white blood cells/ mm3, bacteria and vegetable matter (usually associated with a raised WBC count).

AIRWAY MANAGEMENT Any patient who is semi-conscious or unconscious must have an adequate assessment of the airway: n

Look for agitation, cyanosis, difficulty in respiratory effort and choking motions. n Listen for snoring, gurgling, stridor and gargling sounds. n Feel with the back of the hand for the exit of air with respiratory effort or see fogging of the oxygen mask on expiration.

Simple management Blood secretions should be removed from the nose and mouth with a rigid suction device. A cribriform plate fracture must be considered, and gentleness is essential.

n n

False-negative results are obtained in 2% of peritoneal lavages, usually the consequence of isolated injury to retroperitoneal organs such as the pancreas, duodenum, diaphragm, small bowel and bladder.

Chin lift First complete clearance of the mouth, if indicated, by sweeping a finger between the tongue and the upper palate; be wary of the tendency of a semi-conscious patient to bite. Chin lift (Fig. 11.20) is a simple procedure which can be done on any patient without interfering with the cervical spine: the fingers of one hand are placed under the mandible in the midline, and are then lifted gently upwards to bring the chin forwards.

Airway management  171 Airway management Surgical airway

Lift the chin Open the angle between the neck and chin After

Before

Fig. 11.20  Chin lift. Jaw thrust The angles of the lower jaw are grasped and the mandible displaced forwards. This is the method used with a mouthto-face mask with a good seal.

Oropharyngeal airway

(see Ch. 6)

A semi-conscious or agitated patient may cause difficulty, but an unconscious one usually accepts an oral airway. This should be inserted upside down with the concavity directed upwards until the soft palate is encountered. Rotation through 180° is then done, which places the concavity downwards and around the back of the tongue.

Nasopharyngeal airway

SURGICAL AIRWAY

Indications An inability to intubate the trachea is the only indication for creating a surgical airway, and this can occur for various reasons: oedema of the epiglottis fracture of the larynx n severe oropharyngeal haemorrhage n when an endotracheal tube cannot be placed through the cords. n

Anatomy

(Fig. 11.21)

The cricoid cartilage is the only circumferential support to the upper trachea in children and therefore surgical cricothyroidotomy is not recommended in children under 12 years. A 14 gauge needle/cannula can be used instead and is inserted through the cricothyroid membrane with intermittent oxygen jet insufflation. This method can lead to carbon dioxide re­tention and therefore should not be used for more than 40 minutes.

Equipment Equipment required is:

(see Ch. 6)

This is useful when a patient has an upper airway obstruction but is unable to tolerate an oropharyngeal airway. The nasal airway is inserted into one nostril. It needs first to be lubricated and then inserted into the less obstructed nostril (often it is easier to insert through one or other nostril). If difficulty is encountered with one nostril, the other is used. The turbinates are often felt to fracture as the catheter is inserted, but little force is needed for this to occur and fracture is usual. If there is a suspicion of a base of skull fracture, a nasopharyngeal tube should not be used.

n

Cricothyroidotomy

n

cricothyroidotomy set – often easily available in most resuscitation areas n surgical blade n curved arterial forceps and tracheal dilators n small endotracheal tube of internal diameter 5–7 mm; if not available, then use any type of tube – metal, rubber or plastic.

Procedure n

Feel for the laryngeal prominence of the thyroid cartilage (Adam’s apple) – more prominent in men than women. If it is difficult to be certain, then identify the hyoid bone and work the finger downwards; if it is still impossible to identify anything above what is thought to be the thyroid cartilage, it is possible that what was thought to be the thyroid cartilage is in fact the hyoid. As the finger descends in the midline, there is a palpable gap between the thyroid cartilage and the cricoid. It is through this window that emergency cricothyroidotomy is carried out. (Beneath the cricoid ring it is sometimes possible to feel the rings of the trachea but this depends on how much subcutaneous tissue is present.) (See Fig. 11.21.)

11 

172  Practical procedures Emergency tracheostomy

Chin Hyoid bone

Laryngeal prominence (Adam's apple) Thyroid cartilage Point of insertion for cricothyroidotomy Cricothyroid membrane Cricoid Rings of trachea Point of insertion for tracheostomy Sternal notch

Fig. 11.21  Cricothyroidotomy and tracheostomy incision points.

If time permits and the patient is conscious, insert local anaesthetic into the skin and subcutaneous tissues. n Make a small transverse incision through the skin and extend this through the cricothyroid membrane; a hissing sound is audible once the trachea is penetrated. Alternatively, a Seldinger technique can be used. n Use tracheal dilators and/or arterial forceps to expand the hole by separating the cricothyroid fibres (cricothyroidotomy set has appropriate instruments). n Insert a small endotracheal tube (5–7 mm internal diameter) or any other appropriate tube that is available (normal tube sizes for adults are 8–8.5 mm for women and 9–10 mm for men).

This is rare because cricothyroidotomy is the preferred emergency procedure. If the larynx has been completely disrupted by injury and the cricothyroid membrane is not intact, then an emergency tracheostomy is indicated. The tracheostomy procedure is the same as for an elective procedure except where indicated.

Elective tracheostomy It is preferable to relieve acute airways obstruction by endotracheal intubation or cricothyroidotomy and then to do an elective tracheostomy.

Open tracheostomy (emergency or elective) Equipment

Equipment required is: n

tracheostomy set – usually obtained or used in the operating room (an operating room scrub nurse usually comes with the set) n tracheal tubes of internal diameter 8–8.5 mm for women and 9–10 mm for men. If the neck is very large in diameter and the tracheal rings almost retrosternal, then a long tracheal tube should be considered.

Procedure (Fig. 11.22) The procedure can be done under general or local anaesthetic (preferably the latter) and should be performed by an experienced surgeon: n

n

n

n

n n

Tracheostomy This may be: n

emergency or elective n percutaneous or open.

n n

Indications Indications include: n n n n n n

airway obstruction head and neck surgery laryngeal trauma failed endotracheal intubation prolonged tracheal intubation prevention of pulmonary aspiration.

Ensure the patient’s neck is extended as far as possible (in trauma the possibility of injury to the cervical spine must be remembered and ideally an assistant should keep the head and neck central). Oxygen should always be given to the patient even if you think the airway is completely obstructed, because sometimes this gives the patient a few extra minutes without severe hypoxia. Make a transverse incision halfway between the cricoid and the suprasternal notch and between the medial borders of sternomastoid muscles. In an emergency, if the anatomy is unclear, a vertical incision can be made from the laryngeal prominence of the thyroid cartilage to the suprasternal notch. Separate the strap muscles vertically in the midline through the investing fascia. Identify the thyroid isthmus, although it rarely needs to be divided in the adult and can usually be retracted upwards; in the child it is more likely to require division. Find the second, third and fourth tracheal rings. Incise the trachea vertically through the second, third and fourth rings; dilate the opening with either tracheal dilators or arterial forceps and insert an endotracheal tube (ideally 7–8 mm internal diameter) and attach the oxygen supply immediately.

In an emergency n

After the insertion of the tracheostomy tube, bleeding is controlled with artery forceps and ties; often the anterior jugular vein bleeds as well as the divided thyroid isthmus. n Use a fine-bore suction tube to suck out the trachea.

Airway management  173 dilatation with the tracheal dilators and allows the tube to be inserted. The ends of the sutures should be left long so that they protrude through the incision to facilitate re-intubation should the tracheostomy be accidentally removed.

Chin

Hyoid bone

Laryngeal prominence (Adam's apple)

The same method can be used with advantage in adults. Some surgeons excise a circular piece of trachea anteriorly and others use a distally based flap. Subsequent stenosis is less likely in the adult, whichever method is adopted.

Percutaneous tracheostomy Techniques

Techniques include:

Thyroid cartilage

n

Cricothyroid membrane

serial dilatation single tapered dilator n guidewire dilatation n forceps or screw. n

Indication

Thyroid gland Incision for cricothyroidotomy Incision for tracheostomy (2/3/4 rings)

Percutaneous tracheostomy is indicated for prolonged endotracheal intubation to facilitate weaning and nursing care.

Equipment Equipment required is: n

bronchoscope 100% O2 n sedation n analgesia n neuromuscular blockade. n

Manubrium

Fig. 11.22  Tracheostomy technique.

Procedure n n

Elective and semi-elective open tracheostomy n

Before the incision into the trachea is made, check the tracheostomy tube: inflate the cuff and make sure there are no leaks; deflate the cuff and then gently lubricate the cuff and tube with lubricating jelly. Check that the connector is compatible with the anaesthetic tube and oxygen supply. n Insert the tube at the same time as the endotracheal tube is withdrawn; make an immediate connection to the oxygen supply. n Do not allow anyone to remove the endotracheal tube completely until you are certain your tracheostomy tube is in the correct position. n In a child no part of the trachea should be excised, as there is a high risk of subsequent stenosis. Therefore a vertical incision is made over the second, third and fourth tracheal rings and a heavy suture is inserted through each side of the tracheal incision; this aids

n n n n

Same position as for open tracheostomy. Infiltrate with lidocaine with adrenaline (epinephrine) over the incision site (1st and 2nd tracheal rings). Dissect down to trachea. Puncture trachea and insert guide wire or introducer. Check position of introducer/guide wire bronchoscopically. Dilate tract and introduce tracheostomy tube.

Complications of tracheostomy Potential complications include: n n n n n n n n n

loss of airway malposition or displacement of tube haemorrhage bacteraemia surgical emphysema pneumothorax occlusion of tube oesophageal injury tracheal injury.

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12 

Principles of surgical oncology

General features of malignant disease

175

Biology of malignancy

176

Clinical features of malignant disease

179

Management of malignant disease

179 179

Patient evaluation

The management of patients with cancer usually involves more than one specialist. Management decisions are made within a multidisciplinary team meeting (MDM or MDT) including surgeons, medical and clinical oncologists, radiologists, pathologists and specialists in palliative care. Increasingly, nurse specialists are also intimately involved in coordinating this multidisciplinary activity. Oncology therefore cuts across the traditional specialties, and the development of multidisciplinary teams provides a more efficient and complete service for patients. The surgeon may be called upon to assist with diagnosis, assessment of tumour staging and removal of tumour bulk and to perform surgical procedures to deal with mechanical complications. The diverse nature of surgical intervention demands considerable familiarity with the pathological basis of malignancy and the therapeutic options available. A further aspect of oncological practice is the detection of malignancy before it has caused symptoms, or the identification of which patients or groups of patients are at high risk of developing malignant diseases. Both these roles are examples of screening, which is considered at the end of this chapter. As in many other areas of medicine, the definition of terms can cause confusion. Malignancy means that a cell type has escaped normal control and is proliferating unchecked; the tissue of origin is not specified. Cancer used to mean a malignant tumour which had its origin in epithelial tissues, e.g. a squamous carcinoma of the skin or a transitional cell carcinoma of the bladder. However, this distinction has largely been lost and the terms ‘cancer’ and ‘malignancy’ are now used interchangeably.

GENERAL FEATURES OF MALIGNANT DISEASE Incidence Figures from the NHS in the UK show that malignant disease accounts for just over a quarter of all deaths

Operative surgery for malignant disease Adjuvant therapy Non-operative therapy Assessment of response to treatment Terminal care

181 181 182 183 184

Screening for malignant disease

184

(27%) in 2007, being second only to cardiovascular disease (approximately one-half). Table 12.1 shows the incidence of different types of malignancy in the UK in 2005. Lung cancer still causes the greatest number of deaths for both men and women. Breast cancer is the second commonest cause of cancer death in women. Cancer of the gastrointestinal tract is the next most common cause. Total cancer deaths continue to increase, but the incidence of deaths from certain tumours, such as stomach cancer, is declining.

Aetiology Malignancy is of diverse and multifactorial cause. No single chemical or biological factor has been definitively shown to cause human cancer. However, combinations of individual factors, such as genetic susceptibility, chemicals, occupation, lifestyle and viruses, may together induce malignant change in exposed or susceptible tissues. The assessment of a patient with suspected malignancy should include a family history and an enquiry of possible exposure to aetiological factors (Table 12.2). Their continued identification will inevitably lead to further preventative measures, comparable to the efforts being made to reduce the use of tobacco.

Epidemiology Study of the population dynamics and distribution of malignancy helps in the appropriate planning of healthcare services and resources. In addition, detailed statistics can highlight trends in incidence that point to aetiological factors and geographical variations in the occurrence of tumours. The identification of causal occupational factors (e.g. exposure to industrial carcinogenic chemicals) has been largely the result of epidemiological study. In addition, epidemiological studies can identify groups with a high risk or a poor prognosis. These can then be subject to screening or rigorous follow-up after treatment.

12 

176  Principles of surgical oncology Table 12.1

Incidence, per 100 000 population, of cancer in UK in 2005

All cancers Oesophagus Stomach Pancreas Colon/rectum Lung/bronchus Breast Kidney Prostate Non-Hodgkin’s lymphoma

Table 12.2

Men

Women

523 14 14 10 56 61 1 13 95 16

430 6 6 8 36 37 123 7 – 12

Aetiological factors associated with malignant disease

Factor Genetic: Retinoblastoma (Rb) gene Wilms’ tumour gene p53 oncogene FAP gene Polyp–cancer sequence (multiple sequential genetic mutations) Environmental: Ultraviolet light Chemicals: Benzene β-Naphthylamine Vinyl chloride Asbestos Tar, crude oil Tobacco smoke Ionising radiation Diet: Aflatoxins Smoked foods Alcohol Drugs: Alkylating agents (in patients treated for other malignant disease) Viral: Hepatitis B and C virus Epstein–Barr virus Human papilloma virus Human immunodeficiency virus

Tumour Childhood retinoblastoma Nephroblastoma Prevents malignant transformation unless mutated Colonic carcinoma in patients with familial adenomatous polyposis (FAP) Colorectal cancer

Basal cell carcinoma, malignant melanoma Leukaemia Bladder carcinoma Hepatic angiosarcoma Mesothelioma Squamous carcinoma Lung carcinoma Skin tumours, leukaemias Oesophageal carcinoma Gastric carcinoma Oropharyngeal and oesophageal cancer Leukaemias

Hepatocellular carcinoma Burkitt’s lymphoma, nasopharyngeal carcinoma Cervical carcinoma, anal cancer Kaposi’s sarcoma, B-cell lymphoma

BIOLOGY OF MALIGNANCY Carcinogenesis and growth Controlled cellular proliferation occurs during embryogenesis, hypertrophy, healing, regeneration, repair and during the metabolic response to trauma and sepsis. In many instances, cellular replication occurs because growth factors bind to specific receptors on the cell surface and induce intracellular signals which activate the nucleus and cause cell division. Within the nucleus, nucleoproteins ensure accurate DNA replication, DNA repair and DNA transcription to messenger RNA. However, these biochemical processes are susceptible to damage and malfunction by mutations, deletions or amplifications of the genes which code for many of the normal regulatory factors or their receptors. Mutations can occur either spontaneously or as a result of the interaction of aetiological factors with the DNA of the host. Malignancy is the consequence of escape from the normal controlling factors for cellular replication. At some point in the multi-step process of carcinogenesis, the transforming cell undergoes a number of genetic changes which result either in the unchecked expression of proto-oncogenes or in abrogation of the function of tumour suppressor genes. These are constituents of the human genome which are associated with normal cellular proliferation and differentiation. They become implicated in carcinogenesis when their encoded proteins are overproduced, mutated or otherwise modified so that their function is abnormally expressed, rather than regulated. This unregulated expression of normal genes may be responsible for the capacity of certain tumours to secrete proteins known as tumour markers into the circulation, e.g. carcinoembryonic antigen (CEA) for colorectal cancer and alpha-fetoprotein (AFP) for hepatocellular carcinoma. Unlike normal tissues where, in general, a cell divides only in order to replace one which has been lost, tumour cells fail to respond to the signals which regulate normal replication. The belief that all tumours contain cells proliferating more rapidly than those in normal tissues is false. Most tumours enlarge because either the proportion of cells in the proliferative phase of the cell cycle (growth fraction) is greater than normal, or there is decreased cell loss from apoptosis (physiological cell death). It has been estimated that up to 50% of tumour cells are lost as a consequence of hypoxia, exfoliation, metastasis and destruction by host defences. Despite these losses, tumour cells adapt to the physiological selection pressures of their surroundings to achieve continuous advantage over the host. A further development of this adaptive nature is progression by which tumours become more aggressive with time and contain fewer cells which resemble their parent tissue, so producing cells with metastatic potential. A fundamental concept is that change to malignant behaviour on the part of cells does not result in a single disease process. Tumours from the same tissue of origin may behave quite differently with respect to growth, invasion and metastases. This is frequently demonstrated by colonic tumours appearing as either bulky, locally invasive primary

Biology of malignancy  177 tumours without metastases or as small asymptomatic primary tumours with dissemination to other parts of the body. Carcinogenesis proceeds through multiple stages involving the interaction of different aetiological and host factors, each of which influences the tumour’s final biological behaviour and clinical manifestations.

Influence of biology on clinical course In general, a tumour is of sufficient size to be clinically palpable when it contains 109 or more cells; however, at clinical presentation most tumours have many more cells than this. Even the smallest radiologically detectable breast carcinoma contains 107–108 cells. Patients usually die when the total has reached 1012. This natural history is shown diagrammatically in Figure 12.1.

Invasion and metastasis Carcinoma in situ is a collection of malignant cells confined by their normal basement membrane. This is the earliest stage at which a tumour may be histologically identified and implies that the tissue has changed under carcinogenic influences. The cells are both functionally and structurally altered – a state of dysplasia. This process may be multifocal, which

implies that the remaining apparently normal cells are at increased risk of malignant transformation (e.g. the normal mucosa surrounding a colonic carcinoma). The advance of malignant disease is by: n

local tissue invasion through and beyond the basement membrane n distant spread of cells (metastasis) to form autonomous tumour deposits. Invasion occurs when tumour cells start to secrete enzymes capable of digesting intercellular matrix. Many of these enzymes are now being characterised and their physiological or pharmacological inhibitors identified. Prominent among these enzymes are the matrix metalloproteinases. Through continued growth, suitably equipped cells can encroach upon and destroy adjacent organs (e.g. duodenal and bile duct obstruction from a pancreatic carcinoma). Tissue resistance to invasion is variable: arteries and tendons are rarely destroyed, but lymphatics and veins are commonly breached. Tumour cells have metastatic capacity when they are able to: n

invade adjacent tissues (especially veins and lymphatics) survive in unfamiliar tissue environments – bloodstream, peritoneal cavity n sustain their own proliferation to form a focus of tumour cells. n

Normal tissue Carcinoma in situ

Early invasive carcinoma

Metastatic cancer

Advanced invasive carcinoma

Fig. 12.1  The natural history of the development of malignant disease.

General features of malignant disease Biology of malignancy

12 

178  Principles of surgical oncology

Although only about 1 in 106 tumour cells may have metastatic potential, many thousands of cells are shed from a tumour each day. Palpation or surgical manipulation of a tumour is known to increase shedding. Tumour metastases may themselves undergo further malignant progression and bear little pathological resemblance to the primary tumour.

Routes of metastasis Metastasis occurs by three routes (Fig. 12.2). Invasion of the lymphatics or veins allows the transport of viable invasive tumour cells to distant sites. The pattern of spread can be predicted for most tumours (e.g. breast and large bowel) and may be used to plan surgical removal of the primary tumour and possible sites of distant spread. Lymphatics usually accompany the arterial supply to an organ and so, in many instances, surgical removal of an organ which contains a tumour involves dissection of the arterial supply and removal of these vessels and their associated lymphatic tissue (e.g. radical gastrectomy, colectomy). Similarly, the venous drainage of an organ is an important determinant of venous metastatic spread. Because surgical manipulation of any malignant tumour causes shedding of tumour cells into lymphatics and veins, some surgical procedures have been designed to reduce this by initially dividing the blood supply, especially the veins (e.g. ligation of the inferior mesenteric vessels before mobilising a left-sided colonic tumour using a ‘no-touch’ technique – Fig. 12.3).

Distribution of metastases The organ distribution of metastases varies with the type of tumour and is related to complex interactions between the migrating tumour cell and the capillary endothelium of the organ. Metastatic deposits may become sites from which tumour cells gain access to further vessels – metastases from metastases. In this way, tumours spread from the primary to predictable local metastatic sites, and then on to other less predictable places. Some tumours have a predilection for particular metastatic sites. Gastrointestinal malignancy tends initially to metastasise to the liver via the portal venous circulation; renal and breast carcinoma to the lungs. Bony metastases are relatively common in all terminal disease but there are five tumours that commonly metastasise to bone: n

breast prostate n lung n kidney n thyroid. n

Occult micrometastases Microscopic tumour deposits, present at the time of original diagnosis and treatment but which escape detection, may emerge as metastases or recurrent disease some time later. They are of considerable importance in surgical oncology. Although they are often called recurrence, they are in fact the continued growth of residual tumour. Modern oncological management aims to include adequate treatment to deal with

Local lymph nodes

Lymphatic Distant lymph nodes

Venous to next capillary bed

Liver

Lungs Transcoelomic

Direct invasion of adjacent structures

Fig. 12.2  Routes of tumour spread.

Across peritoneum or pleura

Management of malignant disease  179 Clinical features of malignant disease Management of malignant disease

Fig. 12.3  Isolation of the tumour before surgical resection – the ‘no-touch’ technique.

such micrometastases. This involves systemic therapy additional to local surgical measures – adjuvant therapy, if given after the operation, or neoadjuvant therapy if given prior to surgical extirpation.

n n

Exposure to risk factors Family history of cancer.

Examination n

CLINICAL FEATURES OF MALIGNANT DISEASE Most of these will be found in the individual chapters of this book devoted to regions or systems. The important clinical features of ‘malignancy in general’ are given in Box 12.1.

MANAGEMENT OF MALIGNANT DISEASE Decisions about management must be made only after a full explanation of the condition and treatment options have been given to the patient and often also to his/her relatives. The advantages and risks of each treatment option, including where appropriate symptomatic treatment only, should be discussed before a treatment plan can be agreed.

PATIENT EVALUATION The following components are involved:

History n

Duration and progression of symptoms – often symptoms last for months (rarely years) and are progressive n Presence of non-specific symptoms such as fatigue, loss of appetite and weight

Identification of primary site (as suggested by the history) n Evidence of local invasion (mobility or fixation, damage to local structures) n Use of special techniques for individual circumstances – e.g. rectal examination, sigmoidoscopy n Evidence of distant spread – palpable lymph nodes, enlargement or malfunction of organs (e.g. liver enlargement and jaundice), accumulation of effusions.

Investigation Simple n n n n n n

Full blood count – may reveal blood loss, marrow failure or infiltration Serum concentrations of urea and electrolytes – evidence of renal tract obstruction or dehydration Liver function tests – the presence of hepatic metastases or biliary tract obstruction Examination of urine for cytology and/or for the presence of tumour markers Plain X-ray, especially of the chest, for primary tumour or metastases Measurement of serum tumour markers, e.g. CEA, CA 125.

More complex These investigations are determined by the suspected clinical diagnosis and include: n n

contrast examination of the GI tract ultrasound scan, usually of solid organs

12 

180  Principles of surgical oncology Box 12.1 

Clinical features suggestive of malignant disease

Palpable swelling This is most often painless. It is usually irregular and firm (unless bony in origin). It may be invading local structures and therefore fixed. Anaemia Loss of blood occurs readily from disorganised capillaries and other vessels in the tumour. Continued bleeding from a surface lesion should be viewed with suspicion. Internal bleeding (e.g. into the gut) is most often chronic and concealed; the result is iron deficiency anaemia of unknown origin. Consequences of local invasion Hollow tube obstruction is a sinister development in the natural history of a tumour. Examples of manifestations are dysphagia (oesophageal), abdominal colic (small and large bowel), jaundice (bile duct), hydronephrosis (renal tract) and bilateral leg oedema (inferior vena cava). Perforation of a hollow tube can follow invasion, with development of an acute emergency (e.g. perforation of a gastric carcinoma). Local invasion may also lead to destruction of tissue (e.g. nerves and bone) with pain. Metastatic spread This is common. Presentation is with a history of progressive general tiredness, weight loss and anorexia. Examination may reveal the signs of metastatic deposits: irregular hepatomegaly, lymphadenopathy, ascites, pleural effusion, pathological fracture, focal headache and epileptic fits (cerebral deposits). Biochemical effects This relates to the production of substances associated with clinical effects: n

n n n n

parathyroid hormone analogue (PTH-rp) causes malignancy-related hypercalcaemia; it is not uncommon in breast and neoplasms but may be seen in any tumour causing significant bone destruction antidiuretic hormone in bronchogenic carcinoma adrenocorticotrophic hormone in pituitary tumours, leading to increased corticosteroid output 5-hydroxytryptamine in carcinoid tumours adrenaline in phaeochromocytoma.

Asymptomatic detection During routine assessment of other conditions (e.g. preoperative check before herniorrhaphy), never overlook the possibility of malignant disease. Do not forget: if you do not look you cannot find.

n

computed tomography magnetic resonance imaging n positron emission tomography – PET scanning, usually with fluorodeoxy-glucose (FDG). n

Invasive These are usually directed both towards reaching a definitive diagnosis and assessing the extent of the problem: n

endoscopy, including the upper and lower GI tracts, the biliary tree and the air passages, all of which can include biopsy n laparoscopy and thoracoscopy, also with biopsy.

cytology gives an assessment only of the shape and other features of individual cells. Histological examination of a tissue sample shows the pathological architecture (the relationship between cells and their surroundings). Aspiration is done by passing a fine needle into the lesion and applying suction with a syringe. Small fragments are drawn back into the barrel and can be extracted and stained for examination under the microscope. Needle biopsy uses a needle of larger calibre often equipped with a cutting device. A tissue core is extracted, processed and sectioned, so providing an histological section. Open biopsy exposes the lesion and either removes part (incisional) or all (excisional) of it for histopathological examination. Biopsies of this nature can be processed immediately (frozen section) or by standard paraffin-embedded sections.

Guidance All the above methods may be undertaken under some form of guidance. X-ray, ultrasonography or CT scanning may have been done previously and the site marked; more commonly the needle biopsy or incision may be performed under real-time image control, most commonly by ultrasound.

Tumour staging and prognosis Staging Staging is the attempt to classify tumours into categories (stages) of their natural history by using agreed criteria which are known to be relevant to prognosis. To categorise a patient into the appropriate stage is an essential part of the decision-making process for correct treatment. Many systems have been devised for tumours of different organs or anatomical regions. Most were originally based solely upon clinical findings or sometimes upon additional findings, such as the histopathological features for an individual tumour group, e.g. the clinical staging for breast carcinoma (Ch. 27) and the Dukes classification for colorectal cancer (Ch. 24). However, the more recent and widely adopted TNM (tumour, nodes, metastases) system (Box 12.2) allows a single generic method to be applied to almost all tumours, which has the advantage of allowing for different biological behaviour because each value of T, N and M is scored independently.

Histological grade (Table 12.3) The histological grade, obtained either from a tumour biopsy or from the excised specimen, can be used in conjunction with the TNM stage to give a more accurate assessment of prognosis for an individual patient. This information allows more precise evaluation of the efficacy of different treatments on tumours of comparable stage. For example, a radical mastectomy (Ch. 28) for a histological grade 1 breast carcinoma of stage T1–N0–M0 may lead to cure, but the prognosis for long-term survival is more guarded in a tumour of similar stage but which is grade 3.

Aspiration cytology and tissue   biopsy (see also Ch. 4)

Prognostic markers

These are techniques that allow a pathological diagnosis to be reached – an essential preliminary to treatment. Aspiration

Both molecular and genetic markers which give prognostic information have been identified for some tumours. In breast

Management of malignant disease  181 Box 12.2 

The TNM staging system

Tumour n T0: primary unknown (Tis: tumour in situ) n T1: tumour < 2 cm metastases present n T2: tumour > 2 cm n T3: tumour > 5 cm (or reaching serosa in GI tract) n T4: tumour infiltrating local tissues, e.g. skin, vessels, nerves Nodes n N0: not involved n N1: local nodes involved n N2: distant nodes involved Metastases n M0: no metastases n M1: metastases present n Mx: status unknown Postoperative R0: no residual tumour R1: microscopic residual disease R2: macroscopic residual disease

Table 12.3

Histological classification

Differentiation

Features

Grade 1 – well differentiated Grade 2 – moderately differentiated Grade 3 – poorly differentiated

Forms recognisable structures of parent tissue Some degree of organisation Architecture totally disorganised; cells not recognisable from parent tissue

cancers, the presence of nuclear receptor for oestrogen indicates a good prognosis, whilst those tumours which express an excess of receptors for epidermal growth factor or the oncogene c-erbB2 have a worse prognosis. Many new ‘markers’ of prognosis are described each year.

OPERATIVE SURGERY   FOR MALIGNANT DISEASE Histological confirmation Before definitive elective treatment of a tumour there must (usually) be unequivocal histological confirmation of malignancy and an accurate assessment of the stage. However, some patients present with a surgical emergency (e.g. an obstructing carcinoma of the colon) which requires surgical intervention without either of the above items of information. In these cases a decision about the extent of surgical treatment is made on the operative findings, supplemented if possible by urgent pathological examination of tissue during the course of the procedure (frozen section).

Aim The aim of surgical management is either curative or palliative. Those with obvious widespread tumours should not be treated by a surgical effort to achieve cure; a lesser procedure may be performed (e.g. bypass of a gastrointestinal tumour) to relieve distressing symptoms such as pain or

gastrointestinal obstruction. Referral for non-surgical treatment or for palliative care is then appropriate. Surgical attempt at cure involves the total excision of all tumour-bearing tissues together with the associated lymphatic and venous drainage (e.g. radical gastrectomy). Invasion of adjacent vital structures (e.g. invasion of the trachea by an oesophageal cancer) may determine the feasibility of removing a tumour (its operability, which is not the same as curability). By contrast, involvement of non-essential structures does not prevent resection of a tumour with the invaded structures (e.g. a colonic tumour that has invaded the small bowel). How far to place the resection away from the visible growth (resection margin) is decided by knowledge of the behaviour of the tumour and its propensity to local invasion. Both are described in the appropriate sections of this book. For most neoplasms treated by surgery the technical aim is to remove the tumour, the organ in which it is contained and the regional lymph node drainage (lymphatics and nodes) all in one piece: en-bloc. Reconstruction after curative surgery is an important aspect of surgical technique. Most patients naturally wish to regain as near normal a lifestyle and self-perception as possible. An ileostomy (Ch. 24) requires more departures from usual habits than does a successful ileo-anal pouch (Ch. 26). Reconstruction after mastectomy (Ch. 28) restores body image and self-confidence. A careful, informed and sympathetic discussion with the patient is needed to reach a joint conclusion about the course of action.

ADJUVANT THERAPY One of the most challenging areas in surgical oncology is the treatment of patients with apparently early disease. Clinical experience over the last 50 years has clearly shown that curative surgery alone for tumours that seem to be localised leads to cure in only a proportion of patients. This indicates either that some patients may have undetected micrometastases at the time of presentation or that surgical intervention triggers the release and seeding of tumour cells to distant sites where their growth becomes clinically evident some time after the initial surgery. Adjuvant therapy is additional anti-neoplastic treatment which is used for some patients with tumours that are thought to have been completely removed by surgical excision. Adjuvant chemotherapy, local radiotherapy or hormone therapy, or sometimes various combinations of these, aim to destroy occult micrometastases. Success in this effort must always be balanced against the fact that adjuvant treatment will be given to a varying proportion of patients who do not have micrometastases and who therefore do not need it. Accordingly, adjuvant treatments must: n

be relatively non-toxic have been demonstrated to have efficacy against the same tumour, usually in patients with advanced disease n have been proven to improve survival in randomised trials unless being given within such a trial. n

Timing of adjuvant therapy Adjuvant therapy was traditionally used only after curative surgery. More recently, treatment has been used before

Operative surgery for malignant disease Adjuvant therapy

12 

182  Principles of surgical oncology Table 12.4  Adjuvant and neo-adjuvant therapy Tumour

Adjuvant protocol

Timing

Breast

Epirubicin, cyclophosphamide and 5-fluorouracil Cisplatin and 5-fluorouracil, or epirubicin, cisplatin and 5-fluorouracil 5-fluorouracil and oxaliplatin with folinic acid FOLFOX Chemoradiotherapy

Postoperative

Oesophagus Colorectal Rectum

Pre-operative Postoperative Pre-operative

The spectrum of electromagnetic radiation can be adjusted to increase penetration into deep tissues. Newer ‘supervoltage’ apparatus is based on this principle. This can be used to focus treatment at a tumour site from different directions, thus enhancing the destruction of tumour cells without damaging surrounding structures. The level of expertise with this fractionated radiotherapy is now such that not only is it used as palliative therapy for certain unresectable or metastatic lesions but also it is employed as an adjuvant to surgery (e.g. following wide local excision of T1–T2 breast carcinomas or before excision of a rectal carcinoma).

Other methods of application In addition to external beam irradiation mentioned above, radiotherapy can be applied in other ways. operation – neo-adjuvant therapy. Some examples of the protocols currently in use are shown in Table 12.4. A useful shrinkage of some tumours – oesophageal, rectal and breast – can be achieved by preoperative radiotherapy, and some of the many protocols for the treatment of breast cancer include postoperative radiotherapy.

NON-OPERATIVE THERAPY

Radiotherapy Knowledge of the radiotherapeutic options for a particular tumour is essential for the practising surgeon. Unfortunately, a large number of tumours are relatively radio-resistant. Examples are clear cell carcinoma of the adult kidney, adenocarcinoma of the stomach and malignant melanoma.

Principles The unit of absorbed radiation energy is the gray (Gy), 1 Gy being equivalent to 1 joule per kilogram (J/kg). Radiation acts by inducing chemical changes within the nucleus of the cell that cause damage to DNA. Irradiation depopulates a tumour of its malignant cells mainly via direct effects during mitosis, and thus its efficacy is determined by: n

the number of viable cells present intrinsic radiosensitivity of the cells n mitotic rate. n

Because irradiation damage takes place during mitosis, it follows that normal tissues, which have a high cellular turnover (such as the bone marrow and enterocytes), will also show evidence of damage within hours of irradiation. For the same reason, it may be weeks or months before the maximum effect of radiotherapy is apparent in a more slowly proliferating tumour such as basal cell carcinoma of the skin.

Dose and fractionation The total dose of radiotherapy for a tumour is calculated for each individual site and size. Modern therapy is now given in fractions of the total dose, because this minimises the unpleasant side effects of treatment, i.e.: n

local soreness skin changes n lethargy n nausea and vomiting. n

Radioactive implants These may be inserted into tumours to achieve maximum dose (brachytherapy): n

endoluminal radiation for oesophageal and rectal tumours n iridium wires for cervical carcinoma n yttrium implants for pituitary tumours.

Systemic administration of radioactive substances This can be used if the tumour is known selectively to take up known chemicals. Radioactive iodine can be taken up by cells of thyroid tumours, which incorporate it as they synthesise thyroxine.

Chemotherapy Cytotoxic drugs interfere with cell division in normal and malignant cells. Therefore the success of their use depends on: n n

intrinsic resistance of the tumour cell to the agent the toxic effect on normal tissues, which limits the dose.

The gap between the two may be very narrow.

Types of chemotherapeutic agents There are four main groups as well as additional miscellaneous agents. Many of these agents are used in varying combinations which have been developed empirically to maximise therapeutic efficacy without excessively increasing toxicity. However, their effects on normal proliferating cells result in bone marrow and intestinal toxicity.

Alkylating agents Examples of these are the nitrosoureas and epoxide compounds – cyclophosphamide, melphalan, chlorambucil – which combine with intracellular molecules such as nucleic acids, proteins (especially enzymes) and cell membranes. Damage to the enzymes which link DNA strands, critically disrupts mitosis.

Antimetabolites Antimetabolites – methotrexate, 5-fluorouracil, cytosine arabinoside and 6-mercaptopurine – disrupt the sequence of

Management of malignant disease  183 DNA by being incorporated instead of the normal nucleotide or by irreversibly binding to the constituting enzyme in order to render it ineffective.

Vinca alkaloids These bind to intracellular tubulin and inhibit microtubule formation. The latter is the spindle during mitosis, and in consequence this is arrested at metaphase.

Antimitotic antibiotics These include doxorubicin, epirubicin, actinomycin D, mitomycin C and bleomycin. The first two intercalate between opposing DNA strands and disturb DNA function. Actinomycin D and mitomycin C are inhibitors of DNA and RNA synthesis, respectively, and also generate free oxygen radicals which are toxic.

Miscellaneous agents There is a further group of agents whose mechanisms of action are varied or unknown. Cis-platinum and its less toxic derivative carboplatin react with the guanine in DNA and form cross-linkages along the DNA chain as well as between DNA strands. Other agents, such as etoposide, are tubular poisons derived from podophyllotoxin.

Biological response modification Endocrine manipulation has been used for many years to control tumours which arise from cells that are dependent on hormones for their normal growth and division. The effect is obtained in a number of ways: n

removing the endocrine organ or organs that produce the hormone – orchidectomy for prostate cancer n inhibiting hormone production with antagonists to releasing hormones – genetically engineered luteinising hormone release hormone (LHRH) for prostate cancer n blocking the stimulatory action of the hormone by using the endocrine antagonist – oestrogens in large doses for prostatic cancer to exhaust testosterone production from the testis n blocking the receptor site for the hormone on the malignant cell – tamoxifen prevents oestrogen binding in breast cancer. The discovery of receptor sites for autocrine hormones on many different tumour cells will undoubtedly lead to the construction of synthetic analogues which block receptor binding and activation. Biological therapies may also use the body’s immune system to fight the cancer. Agents used include interferon, interleukins and colony-stimulating factors. Monoclonal antibodies directed against cell growth factors have been introduced: e.g. trastuzumab for patients with HER-2 positive breast cancers, and cetuximab and bevacizumab for advanced colorectal cancer. Other monoclonal antibodies attach to the surface of tumour cells and stimulate the patient’s immune system to destroy these cells: e.g. rituximab for non-Hodgkin’s lymphoma. Monoclonal antibodies can also be used to deliver drugs or radiation directly to cancer cells and a number of clinical trials are underway.

ASSESSMENT OF RESPONSE   TO TREATMENT Clinicians must assess their therapeutic performance in two ways: n

review treatment outcome in their own patients – clinical audit n study the publications that compare current treatment with new experimental protocols. Such periodic appraisal allows advances to be incorporated into practice and outmoded treatments to be discarded.

Methods of assessment Five-year survival This has been the traditional method of outcome assessment. The figure is helpful in studying groups of patients who may receive different forms of treatment, but it gives little information that is relevant to the individual patient.

Median survival time (or median time   to recurrence) This information is more useful to clinician and patient than 5-year survival and is the preferred method. For example, the 5-year survival rate for pancreatic carcinoma treated by resectional surgery is approximately 25%, but the median survival is approximately 18 months.

Serial imaging of progression The response of inoperable or metastatic tumour to nonsurgical treatment can be gauged by serial imaging (ultrasound, CT or MRI) of the tumour. In such circumstances, duration of response is of equal importance to magnitude and is measured as the median duration of response in the patients treated. Accepted grades of response are given in Table 12.5.

Patient well-being How a patient ‘feels’ is a subjective marker of response to reduction in the bulk of a tumour and of the side effects of the treatment that is being used. A number of scales have been formulated to assess this aspect of treatment (see Box 12.3).

Table 12.5

Grading of tumour response to non-surgical therapy for solid tumours (RECIST) criteria

Grade Complete response (CR)

Assessment

Disappearance of all known lesions, confirmed at 4 weeks Partial response (PR) Decrease in tumour size by more than 30%, confirmed at 4 weeks Stable disease (SD) Less than 30% decrease or 20% increase in tumour size Progressive disease (PD) Greater than 20% increase in tumour size or of a deposit, or new lesions

Non-operative therapy Assessment of response to treatment

12 

184  Principles of surgical oncology Box 12.3 

Scales for measurement of patient well-being

Karnovsky Performance Status scale This scale provides a score, e.g.: 100 – Well, no complaints 50 – Requires considerable assistance and medical care 10 – Moribund European ECOG 0 – ECOG 1 – ECOG 2 – ECOG 3 – ECOG 4 –

Cooperative Oncology Group scale asymptomatic minor limitation moderate limitation severe limitation moribund

Table 12.6

Screening programmes

Method

Tumour

Mammography (high risk, 50–65 years) Faecal occult blood (FOB) testing Colonoscopy (genetic high-risk groups) Oesophagogastroscopy (dysplasia – high-risk groups) Serum prostate-specific antigen

Breast Colorectal Colorectal Oesophagus, stomach Prostate

Quality of life score This is obtained from a multiple-field questionnaire

TERMINAL CARE Terminal care should be seen as an integral part of oncological management and of equal importance to any of the other therapeutic disciplines. Accurate assessment of the disease will enable a prediction of the likely sequence of terminal events. Some of these (e.g. nausea) can be anticipated and prophylaxis undertaken.

Informing the patient When treatment for cure fails or when treatment for palliation begins, a full and frank discussion about the prognosis and the plan of management is essential. The patient has an absolute right to this information, which can never be justifiably withheld, even if disclosure is against the wishes of relatives. Once the patient is fully aware of the situation, referral to a team which can provide palliative care should be sought. Although not necessarily about to die at this stage, many patients are apprehensive for their future and appreciate an introduction to those who may treat them in a later phase.

Fear of death and dying For most patients with malignant disease, their abiding fear is of a painful, lingering death. Terminal care exists to alleviate both the psychological torment of impending death by counselling of patient and family and the physical problems posed by progressive malignant disease. Foremost in the aims of terminal care is keeping the patient in the familiar surroundings of home. Adequate facilities and the provision of satisfactory analgesia and nursing management must be available. There are a number of charity-based cancer nursing agencies in the UK for this purpose; they are staffed by nurses specially trained in the management of malignant disease and in dealing with its psychological impact on the patient and relatives.

SCREENING FOR MALIGNANT DISEASE Tumours might either be foreseen in those who are known to be at high risk or detected early by examining in some way or other those in the population who might be susceptible. Such activities are called screening.

Population screening. The knowledge that a large proportion of patients present with advanced disease has prompted the idea of screening the entire population. However, population screening often yields relatively few unsuspected tumours at a pathological stage which would make cure more likely. The cost of these huge projects is high. Targeted screening of high-risk groups significantly increases the number of patients detected in relation to the cost of the procedure. The cost/benefit ratio is consequently improved.

Desirable criteria for a screening programme For a screening programme to be effective, the following points are essential: n n

n n n n

The disease should be common or have defined high-risk groups. The natural history of the disease should be known, in order to define lesions which are truly localised and identify opportunities for curative treatment. Sensitive and specific methods of early detection must be available. Detection methods should be cheap, easy to use, and have a high patient compliance. Effective treatment for early disease should be available. The screening procedure must not involve significant hazard to the population tested.

Table 12.6 lists a number of tumours for which screening programmes are undergoing evaluation. However, few meet all of the above criteria.

Screening for recurrence of tumour What is often called ‘recurrence’ of a tumour is in fact the progression of ‘residual disease’. In some cases, the latter may be amenable to further surgical treatment (e.g. excision of a metastasis in the liver after primary resection of a colo­ rectal carcinoma).

Simple methods In those treated with the intention of cure, clinical assessment to detect residual tumour is often undertaken on a regular basis by follow-up and periodic examination. Features indicating the presence of disease, such as return of symptoms, enlargement of the liver or the development of

Screening for malignant disease  185 Table 12.7

Tumour markers in serum

Marker

Tumour

Prostate-specific antigen (PSA) Carcinoembryonic antigen (CEA) Alpha-fetoprotein (AFP) Beta-human chorionic gonadotrophin (β-hCG) CA 19-9 CA 125

Prostate Colorectal Hepatocellular Testicular, gestational Colorectal, pancreatic Ovarian

palpable lymph nodes are sought. When such features are found, further investigation for evidence of tumour should follow. However, by this time the disease is often re-established and incurable. Earlier diagnosis of residual or recurrent disease may allow for more effective treatment. The techniques used in population screening are appropriate, because patients who have been treated for malignant disease are, by definition, a subpopulation with a high risk of recurrence, e.g. metachronous cancer of the colon or breast.

Tumour markers These molecules (Table 12.7) are products of tumours which may be detected in body fluids or sometimes in urine in

abnormally high levels. Their use in diagnostic screening is limited by the incidence of false positives in patients with benign disease.

Other methods of detection   of residual disease Monoclonal antibodies against tumour antigens can be radiolabelled. The antibodies seek out the tumour cells and can then be detected by gamma camera scanning for sites of increased uptake (e.g. colorectal tumour deposits in the liver).

FURTHER READING Chaudry MA, Winslet MC 2009 Surgical oncology (Oxford Specialist Handbooks in Surgery). OUP, Oxford Silberman H, Silberman AW 2009 Principles and practice of surgical oncology. Lippincott, Williams & Wilkins, Philadelphia Poston GJ, Beauchamp RD, Ruers TJM 2007 Textbook of surgical oncology. Informa Healthcare, London

Terminal care

Screening for malignant disease

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13 

Organ transplantation

Basic immunology of organ   transplantation

188

Organ matching and retrieval

189

Immunosuppression in transplantation

191

Over the past 30 years, organ transplantation has become a rapidly expanding and important surgical specialty. More than any other branch of surgery, organ transplantation requires the close cooperation of several disciplines – surgeons, anaesthetists, immunologists and physicians – to achieve a successful outcome. A synopsis of its historical landmarks is provided in Box 13.1.

Essential definitions Autograft.  Free (i.e. after disconnection of the blood supply) transplantation of tissue from one part of the body to another in the same individual. Isograft.  The transfer of tissue between genetically identical individuals – in humans this is between identical twins (rejection is not a feature of auto- or isografts). Allograft.  An organ or structure transplanted from an individual of the same species. Allografts are at the moment the main class of transplant in humans. Xenograft.  The transfer of organs between dissimilar species. Presently limited to tissues that have been chemically processed to make them non-antigenic, e.g. porcine heart valves. However, this is potentially the most exciting technique because, should it prove successful, the present acute shortage of organs for transplantation would be overcome. Great progress is being made in understanding the nature of the difficulties that form a barrier to xenografting. Orthotopic graft.  The donor organ is transplanted to the same site as the recipient’s diseased one. The removal of the latter is first required, e.g. liver transplantation. Heterotopic graft.  The donor organ is inserted at a site different from its normal anatomical position, e.g. kidney transplantation to the iliac fossa.

General complications of transplantation

193

Transplantation of individual organs

194

Transplantation in children

198

The future

198

Artificial (hybrid) organ implantation.  The transplantation of bio-artificial organs, which are a combination of biomaterials and living cells, e.g. a hybrid artificial pancreas. At present this technique is experimental. Success would, as with xenografting, open a new chapter in transplantation.

Organ donation Cadaver graft.  An organ or tissue retrieved from an individual who has been pronounced dead according to criteria which differ from one culture to another (see below). There are currently three systems of cadaveric organ donation in use: ‘required request’, ‘opting out’ and ‘opting in’. These are summarised in Box 13.2; however, no matter which system is adopted, the wishes of the family of the donor are the most important factor. Living donors.  There are two classes: related donors – parents or siblings who may have some genetic advantages and a sense of family or social obligation n unrelated donors – In UK most of these are spousal or transplants from partners or friends. A small number are kidneys from individuals with a high philanthropic sense. In contrast to UK practice, internationally many kidneys come from donors who wish to make money. Although selling a kidney is outlawed in the West there is a thriving trade in other parts of the world and the moral issues are complex. n

With the continued rise in the number of patients on waiting lists in the presence of a static or falling number of available organs, a number of patients from the UK are travelling abroad, mainly to countries in Asia, for their transplants. Most UK transplant centres will now support travel by potential related donors to the UK, where the pre-donation investigations are carried out prior to transplantation if the donor is suitable.

13 

188  Organ transplantation Box 13.1 

Some landmarks in transplantation

A

Date c.

ad

300

1778 1863 1905 1933 1945 1950 1963 1966 1967 1967 1967 1981 1988

Box 13.2 

Event

C

Cosmos and Damian: believed to have attempted a leg transplant John Hunter: coined the term transplant Bert: observed ingrowth of vessels into skin grafts and defined autograft, allograft and xenograft Guthrie and Carrel: developed vascular anastomotic techniques Voronoy: first human renal transplant – failed because of ABO incompatibility Hume: first short-lived functioning renal allograft Lawler: first long-term survivor from renal grafting Starzl: first human liver allograft Lillehei: first human pancreas transplant – technical success Lillehei: first human bowel transplant – failed Starzl: first long-term survivor from liver transplantation Barnard: first successful heart transplant Shumway: first successful heart-lung transplant Grant: first long-term survivor of smallbowel transplantation

B Bf

Systems currently in use for organ donation

Required request: doctors looking after the potential donor have to ask, or refer the patient to, a retrieval coordinator who will enquire about donation. n Opting out or presumed consent: all donors are presumed to have consented unless the family on approach refuse consent or the patient has previously registered his or her wish not to consent. This system produces the highest number of donors. n Opting in or required consent: this is the system in use in the UK. Medical or nursing staff approach the family to ask about organ donation. Approximately one-third of the families refuse donation. To reduce this proportion, currently people are encouraged to register their desire for donation in the event of death on the NHS organ register. The register can be accessed prior to talking to the family. n

BASIC IMMUNOLOGY OF ORGAN TRANSPLANTATION Successful organ transplantation (with the exception of the cornea) requires the manipulation of the immunological defences of the recipient so as to overcome rejection. Because auto- and isografts do not elicit an immune response, it must be the genetic differences between the donor and the recipient that are of major importance in this process. These differences are expressed as tissue or histocompatibility antigens. The latter stimulate and lead the activation and proliferation of the immune cells and also identify cells which are the targets of the effector mechanisms induced by the immune reaction. The key cells involved in the rejection process are lymphocytes and antigen-presenting cells.

Short arm

D

Class I antigens

Class II antigens

DR

Centromere

Long arm

Fig. 13.1  Position of the major histocompatibility locus on the short arm of chromosome 6.

Major histocompatibility complex (MHC) A large group of genes is present on the short arm of human chromosome 6 (Fig. 13.1), including those that encode the class I and class II MHC molecules which are involved in the presentation of antigens to T-cells. Class I molecules are integral membrane proteins found in all nucleated cells and platelets – the classical transplantation antigens. Class II molecules are expressed on B-cells, macrophages, monocytes, antigen-presenting cells (APCs) and some T-cells.

Human leucocyte antigen (HLA) loci There are four of these on the short arm of chromosome 6: n

HLA-A – over 20 alleles have been identified HLA-B – over 30 alleles have so far been characterised n HLA-C (between A and B) – seems not to have a role in mounting the immune response n HLA-DR – appears to be clinically most important in that, if donor and recipient match for it, graft survival is improved. n

Cells involved in the immune response to a transplant Lymphocytes These are the key cells controlling the immune response. They specifically recognise foreign (non-self) material as different from the tissues of the body. Lymphocytes are of two main types: B-cells and T-cells. B-cells develop in the fetal liver and subsequently in bone marrow. Mature B-cells carry surface immunoglobulins which constitute their antigen receptor. The response to an antigenic stimulus is cell division and differentiation into plasma cells under the control of cytokines released by T-cells. T-cells develop in the thymus, which is seeded during embryonic development with lymphocytic stem cells from

Organ matching and retrieval   189 the bone marrow. T-cells then develop their antigen receptors and differentiate into two major peripheral subsets: one expresses the CD4 marker, and the other the CD8. T-cells have a number of functions, including: helping B-cells to make antibody (CD4+) n recognising and destroying cells infected with viruses (CD8+) n activating phagocytes to destroy ingested pathogens (CD4+) n controlling the level and quality of the immune response (CD8+). n

Antigen-presenting cells These are a group defined functionally by their ability to take up antigens and present them to lymphocytes in a form the latter can recognise. Some antigens are taken up by APCs in the periphery and transported to secondary lymphoid tissues. Others are intercepted as they arrive by APCs normally resident in lymph nodes and other lymphoid aggregates. B-cells recognise antigen in its native form, but T-cells recognise antigenic peptides that have been associated with self MHC molecules. In consequence, to present an antigen to a T-cell, an APC must internalise it, process it into fragments and re-express these at the cell surface in association with class II MHC molecules. In addition, many APCs provide additional stimulatory signals to lymphocytes either by direct cellular interactions or via cytokines (Fig. 13.2).

Rejection Rejection is a destructive reaction initiated by the host to foreign HLA and other non-shared antigens. The process involves: Native antigen

Cell wall Immunoglobulin

Antigen-presenting cell

n n

antigen recognition (afferent arc) activation of selected clones of T-cells and the effector mechanisms (efferent arc).

Afferent arc Two routes lead to activation: n

foreign antigen or donor antigen-presenting cells (e.g. dendritic cells) which are directly recognised by the recipient’s T-cells n intracellular processing of foreign antigens by host antigen-presenting cells and subsequent presentation of peptides to T-cells. Class II HLA antigens activate T helper (CD4+) cells, and class I HLA antigens activate cytotoxic (CD8+) T-cells.

Efferent arc There is proliferation and differentiation of the selected Tcell population. CD4+ cells (T helper – Th cells) produce interleukin-X (IL-10) which induces macrophages to produce IL-1, which in turn stimulates Th cells to produce IL-2 and other cytokines (e.g. IL-4, IL-5, IL-6). The latter cause B-cells to differentiate into plasma cells and to secrete antibody. Cytokines also stimulate CD8+ cells to become cytotoxic. The coating of target cells by antibody allows K cells (large granular lymphocytes), macrophages or granulocytes to recognise and destroy them through a variety of mechanisms (release of enzymes, reactive oxygen mediators and perforins).

Clinical patterns of rejection There are three patterns of rejection: hyperacute and acute accelerated rejection – this is the result of preformed IgG antibody and occurs within hours of exposure n acute cellular rejection – this is infiltration by activated T-cells with recruitment of acute inflammatory cells; generally seen at 7–14 days post-transplant. n chronic rejection – this is a major cause of graft attrition and is probably antibody-mediated. There is intimal hyperplasia and endarteritis obliterans. In liver transplants it is associated with loss of bile duct radicles. n

Chronic rejection is difficult to treat, but strategies that involve the newer anti-B-cell drugs (e.g. mycophenolate mofetil) or rapamycin, which is not nephrotoxic, may have a role in the future.

Cell wall MHC molecule Antigen fragment

Antigen-binding part of the TCR

Fig. 13.2  Antigen handling by B- and T-cells. TCR, T-cell receptor.

ORGAN MATCHING AND RETRIEVAL Organ matching ABO compatibility The biological rules are the same as those which govern blood transfusion. Because ABO red cell antigens are expressed on most tissue cells, ABO-incompatible allografts

Basic immunology   of organ transplantation Organ matching and retrieval

13 

190  Organ transplantation

undergo hyperacute rejection. However, the rhesus factor is expressed only on red blood cells and therefore a match for it is not required for successful transplantation.

HLA-A, HLA-B and HLA-DR matching Tissue typing (identification of the A, B and DR antigens) is carried out on the donor and the recipient by the separation of lymphocytes out of heparinised whole blood and their exposure to antibodies of known HLA-A, HLA-B and HLA-DR specificity. The technique is particularly relevant in the investigation of a family where a living donor may be available, and it also enables HLA-identical siblings to be identified. The influence of matching by tissue type on the successful outcome of organ transplantation is best established in renal transplantation, and its role in cardiac, liver and pancreatic transplantation is not yet clear.

Direct cross-matching After a suitably matched recipient has been selected, a direct cross-match is set up because any recipient may have preformed circulating antibodies capable of reacting against donor cells. These antibodies may be the result of previous blood transfusion, pregnancy, viral infections or transplants. A direct cross-match incubates donor lymphocytes with the serum of the recipient in the presence of complement, to exclude cytotoxicity from circulating antibodies.

Exchange transplantation and desensitization programmes In the United Kingdom at least 500 living kidney transplants are cancelled each year because of preformed cytotoxic antibodies. In approximately half, the cause is blood group incompatibility with the remainder presenting unacceptable anti HLA antibodies. At present there are two methods that allow these individuals to receive a transplant. One is exchange transplantation where donor A gives a kidney to recipient B and donor B donates a kidney to recipient A, thus overcoming the positive cytotoxic test. Individuals willing to exchange transplants are put onto a national register to increase the chances of finding a compatible combination. The 2nd option is a desensitization programme where over a number of session using filters or antigen columns, anti HLA antibodies are removed until their level is low enough to allow an initially incompatible transplant to proceed. There is, however, a significant risk of early rejection in these patients.

Organ retrieval Most organs for cadaveric transplantation come from those who have suffered irreversible structural brain damage after road traffic accidents or cerebrovascular catastrophes and have been diagnosed brain dead by agreed criteria (see Ch. 10). In most countries that accept this practice, organs are then retrieved while the heart continues to beat and the donor receives ventilatory and other support. Such conditions are absolute requirements for transplantations of heart, heart-lung, and small bowel. Although organs can be retrieved from brainstem-dead individuals in whom coroners

Box 13.3 

Sources of organs for transplantation

n

Cadaveric heart beating and brainstem dead Cadaveric controlled non-heart-beating (non-brainstem dead) n Cadaveric non-controlled non-heart-beating n Living related and unrelated donors n

have determined the need for a postmortem, in practice many coroners refuse permission. The majority of transplant centres are developing links with pathology departments so that organ retrieval can take place in the presence of a pathologist in a way acceptable to the coroner. As the number of brainstem-dead donors continues to fall, many centres will now accept kidneys, livers, lungs and pancreas organs retrieved from controlled non-heart-beating donors. At present the only organs transplanted from non-controlled non-heart-beating donors (for example, individuals brought to the emergency department in asystole) are renal allografts (see Box 13.3). Contraindications to organ donation are: n n

n

n n

history of disease or trauma involving the organs being considered long-standing history of diabetes mellitus, hypertension, cardiovascular or peripheral vascular disease (donors with the last three conditions are now accepted for donation but the organs are carefully assessed after retrieval to ensure they are of a satisfactory quality) prolonged periods of ischaemia because of profound hypotension or asystole (increasingly only a relative contraindication) malignancy – other than a primary brain tumour untreated systemic bacterial, fungal or viral infections – however, donors who have had bacterial infections adequately treated may still be suitable.

Chronological age in donors is usually less important than biological age. The age limit for each organ is given in Table 13.1.

Organ function in donors Function of the organ which is to be transplanted must be established. A satisfactory past medical history and physical examination are essential. A well-perfused organ – as indicated by adequate blood pressure and normal arterial blood gas tensions – is also highly desirable.

Heart Requirements are: normal blood pressure, ECG, chest X-ray and arterial blood gas tensions.

Lung and heart–lung Requirements are: n n

negative Gram stain on sputum absence of pathogens on sputum culture.

Liver Requirements are: n

adequate liver perfusion – arterial blood pressure, blood and arterial gas tensions

Immunosuppression in transplantation   191 Table 13.1

Age range for donors

Organ

Range (years)

Kidney Liver Heart and/or lung Pancreas

3–75 Neonate to 70 Neonate to 50 Neonate to 50

n

normal values for serum bilirubin, transaminase and alkaline phosphatase concentrations and a normal prothrombin time.

Kidney Requirements are: n

normal urine output and urinalysis – however, oliguria may be pre-renal because of dehydration n normal serum creatinine and urea concentrations.

Retrieval procedure Currently, the local kidney/liver team starts the procedure and is followed by the heart/lung team. The procedure for the abdominal organs is illustrated in outline in Figure 13.3. Organs are cold-perfused before removal, examined after removal to ensure they are anatomically satisfactory and then cold-preserved within double plastic bags and stored on a bed of crushed ice for transfer to the chosen transplant centre.

IMMUNOSUPPRESSION IN TRANSPLANTATION There is a difficult balance to achieve between the prevention or reversal of rejection and the morbidity that can result from loss of host defences against infection – and also, in the long term, the development of malignant disease.

Pancreas Requirements are: normal serum concentrations of amylase and glucose – hyperglycaemia often develops in acute brainstem injury because of steroid administration and intravenous infusion of crystalloid containing glucose; elevated serum glucose alone is not necessarily a contraindication.

Retrieval after cardiac arrest The continued shortage of organ donors has provided an impetus to re-examine retrieval from donors who do not have a beating heart. This may be in the controlled situation of an operating theatre where patients are moved from intensive care prior to cessation of ventilatory support or in a noncontrolled situation where patients are seen in the emergency department after a cardiac arrest. Provided rapid organ perfusion with cold preservation solution can be achieved immediately after cardiac arrest, the lungs, liver, pancreas and kidneys may be usable.

Live related donation Live related donor organs can be used for kidney, liver, pancreas, lung and small-bowel transplantation. Clearly the requirement for any organ other than the kidney must justify the operative risk of the partial resection of the relevant organ that is required. The increasing number of non-cadaveric transplants in the UK is illustrated in Figure 13.4. In Scandinavia and the USA up to half of transplants are from living donors.

Donor operation Retrieval is becoming increasingly complex because many donors are now considered, and consent is obtained for multi-organ donation. Frequently there is a harvest from one individual of: corneas, heart, lungs, liver, pancreas, kidneys, bone and skin. With the recent success of smallbowel transplantation, the retrieval of the small bowel and the right colon may also be included. A number of transplant teams are involved, and it is essential that they fully agree the order of retrieval to be used before the start of the operation.

Immunosuppressive agents Azathioprine.  Metabolised in the liver to 6-mercaptopurine, this substance is a purine antagonist and reduces the synthesis of DNA and RNA in dividing cells. Ciclosporin and tacrolimus.  These act within the cell to prevent transcription of the gene for interleukin 2 (IL-2), a cytokine involved in the efferent arc of rejection. Corticosteroids.  These agents produce potent but nonspecific immunosuppression and also have an antiinflammatory action. They work by decreasing macrophage motility and phagocytic activity and also block both IL-2 release from macrophages and its generation by Th cells. ATG.  Thymoglobulin is a rabbit anti-human thymocyte immunoglobulin. It is polyclonal in nature and depletes lymphocytes in the circulation and lymphoid organs and also masks T-cell antigens non-specifically. Monoclonal anti-CD25 antibody.  Basiliximab and daclizumab are humanized monoclonal antibodies that target the IL-2 receptor. They have largely replaced ATG. Monoclonal anti-T-cell antibody (OKT3).  This is a murine antibody to the T3 antigen of human T-cells. It produces destruction of CD3-positive T-cells which are associated with graft rejection. There are other similar monoclonal antibodies, but OKT3 is the one most widely used. Mycophenolate mofetil (MMF)  inhibits proliferation of T- and B-lymphocytes and may prove more potent than azathioprine. It may also have a role in the prevention of chronic rejection because B-lymphocytes are thought to be important in this process which now accounts for the majority of renal transplants lost in the long term. Anti-IL-2 receptor antibody.  This is a monoclonal antibody to the IL-2 receptor on human lymphocytes. By binding the

Immunosuppres-  sion in transplantation

13 

192  Organ transplantation

Liver

Pancreas

Left kidney

Right kidney

Perfusion cannula in portal vein Drainage cannula in inferior vena cava

Perfusion cannula in aorta

Fig. 13.3  Retrieval procedure for the abdominal organs.

IL-2 receptor it blocks the pathway of activation mediated through the release of IL-2.

Table 13.2

Immunosuppressive agents

Agent

Principal mode of action

Monoclonal anti-CD20 antibody.  Rituximab is a monoclonal antibody directed against the CD20 antigen on B-cells. It may have a role in treatment of some forms of antibodymediated rejection.

Corticosteroids Ciclosporin/tacrolimus Rapamycin

Sirolimus.  This macrolide antibiotic binds the FK-binding protein, but its mechanism of action is via the ‘target of Rapamune’, or TOR. It inhibits G1- to S-phase cell division and, therefore, cell proliferation, and is used for maintenance immunosuppression and the treatment of chronic rejection.

Mycophenolate mofetil

Block IL-2 release Block IL-2 gene transcription Blocks T-cell proliferation in response to IL-2 Reduces synthesis of RNA and DNA Inhibits proliferation of T- and B-lymphocytes Blocks IL-2 receptors on T-cells The monoclonal OKT3 blocks the CD3 component of the T-cell receptor The polyclonal ATG depletes lymphocytes in circulation

Azathioprine

IL-2 receptor antagonist Antilymphocytes

Rapamycin.  This drug reduces T-cell activation at a later stage in the cell cycle than ciclosporin or tacrolimus although still affecting the IL-2 signal transduction pathway. One of its main advantages is that it is not nephrotoxic (see Table 13.2).

Triple therapy Alemtuzumab  is a recombinant DNA derived humanized monoclonal antibody that is directed against CD52, a protein which is present on the surface of mature lymphocytes. This drug is gaining popularity for use in desensitisation programmes or in regimens intending to induce immune tolerance to the transplanted organ.

This is the most common standard induction and maintenance therapy, particularly in renal transplantation, and consists of: n

Clinical regimens

azathioprine – 2 mg/kg body weight, reduced to 1 mg/ kg at the end of the first week n ciclosporin − 8 mg/kg body weight adjusted according to the trough (pre-dose level) of free drug in serum n prednisolone – 0.3 mg/kg body weight.

These vary greatly from centre to centre but can be approximately categorised as follows.

The mainstay is ciclosporin. Measuring its trough level is important because an excess can be nephrotoxic, although

General complications of transplantation   193 there is recent evidence that measurement of the peak level of ciclosporin (the C2 level) may provide a more accurate measure of the exposure to the drug. Further reductions in dose follow satisfactory progress over 3 months. Another triple therapy regimen, based on tacrolimus (0.2 mg/kg) instead of ciclosporin and adjusted according to the trough level, is now being used in a number of centres and may be more effective in reducing acute rejection rates than ciclosporin. Many American centres now also use MMF in place of azathioprine in triple therapy at a dose of 2 g/day.

also increases the risk of developing malignant disease, particularly squamous cell carcinoma of the skin and some forms of lymphoma. Other complications are the outcome of the specific side effects of individual components of the suppressive regimen (see Box 13.5).

Polyclonal and monoclonal agents against T cells

Apart from graft rejection and problems with drug toxicity, organ transplants of most kinds share a variety of complications which are summarised in Table 13.3. Technical problems are directly related to the quality of surgery and show a steady decline with increasing experience.

Basiliximab, alemtuzumab, OKT3 and ATG are agents used in some protocols for induction immunosuppression; however, OKT3 and ATG are very useful agents in treatment of steroid-resistant rejection.

Experimental regimens There are a number of strategies for inducing tolerance to the transplanted organ – the aim being stopping most of the immunosuppression long term. An example is combined bone marrow and solid organ transplants together with the use of alemtuzumab, OKT3 or ATG as induction therapy.

GENERAL COMPLICATIONS OF TRANSPLANTATION

Monitoring the progress of a transplanted organ The monitoring methods available are as follows.

Transplant function n

Kidney – serum urea, electrolyte and creatinine concentrations

Complications of immunosuppression The most serious complication is an increased susceptibility to infections (see Box 13.4). Long-term immunosuppression Box 13.4 

Infective complications of immunosuppression

Bacterial n Mycobacterium tuberculosis n Listeria monocytogenes Fungal n Candida albicans n Aspergillus – various species Protozoal n Pneumocystis jiroveci n Cryptosporidium Viral n Cytomegalovirus n Epstein–Barr n Measles n Herpes simplex and zoster

Table 13.3

Box 13.5 

Complications of agents used in immunosuppression

Corticosteroids n Reduced growth in children n Impaired wound healing n Bone – osteoporosis and avascular necrosis n Diabetes mellitus n Peptic ulceration n Acute pancreatitis n Hypertension n Psychosis Azathioprine n Myelosuppression n Liver – toxicity and cholestatic jaundice n Acute pancreatitis Ciclosporin n Nephrotoxicity n Hepatotoxicity n Neurotoxicity n Gingival hypertrophy n Hypertrichosis

Complications of transplantation

Category

Nature

Possible effects

General surgical

Wound – infection, dehiscence, incisional hernia

Occasionally life-threatening Further surgery required

Systemic infection

From i.v. lines, especially in liver transplantation Consequent on immunosuppression Thrombosis Stenosis Leakage Stenosis

Vascular suture lines Visceral suture lines

Septicaemia Loss of graft In kidney – hypertension Fistula Interference with graft function (hydronephrosis, obstructive jaundice)

General complications of transplantation

13 

194  Organ transplantation

n

Liver – urea and electrolyte concentrations, liver function tests and measures of clotting activity n Pancreas – measurement of amylase and pH in urine (if the transplanted pancreas is implanted into the bladder).

added to an ever-increasing list of patients waiting for a suitable allograft (Fig. 13.4).

Indications Indication for kidney transplantation is renal failure from the following causes:

Evidence of dysfunction (from the above)

n

n

Kidney – Doppler ultrasound examination to exclude collections around it, obstruction of the ureter and arterial or venous thrombosis. In the absence of such findings, carry out percutaneous biopsy under ultrasound guidance. n Liver – ultrasound to eliminate technical problems such as bile duct obstruction or vascular thrombosis; biliary contrast studies; biopsy if an immunological problem is suspected. n Pancreas – the blood glucose level is not of value. Most transplants in the UK are combined kidney and pancreas, and the progress of the kidney can be used to monitor the pancreas. n Small bowel – see below.

n n n n n

chronic glomerulonephritis (55%) reflux nephropathy (25%) polycystic disease (8%) diabetic nephropathy (2%) malignant hypertension (1%) other causes, e.g. analgesic nephropathy (9%).

Operation The transplant is heterotopic, with the kidney placed usually in the right iliac fossa and attached to the iliac artery and vein. The ureter is joined to the bladder to make a new ureterovesical junction (Fig. 13.5). The recipient’s own kidneys are left in situ unless they are a source of recurrent urinary infection which may place the transplanted kidney at risk.

Results There is intercentre variability in graft survival, but current cadaveric graft survival rates are 80–95% at 1 year, 60–70% at 5 years and 49–56% at 10 years (Fig. 13.6).

TRANSPLANTATION OF INDIVIDUAL ORGANS End-stage failure means that the organ is no longer able to sustain life.

Kidney With increasing success, the number of allografts transplanted increased every year, but the numbers have now reached a plateau because of the limited availability of donors. However, more and more patients are being admitted to dialysis programmes and are subsequently

Liver The procedure for liver transplantation is more recent than for kidney transplantation: However, it is now an established treatment of end-stage parenchymal liver disease, including congenital metabolic disorders. Survival figures have improved because of better patient selection and clinical support, organ preservation and immunosuppressive agents. In major transplant centres, a 70–90% 1-year survival is obtained and, in those transplanted for benign disease, survivors of the first year are likely to be alive at 5 years. The

Number of transplants/Number on waiting list

5000

4000

Cadaveric transplants

3000

Living donor transplants Waiting list

2000

1000

0 1992

1993

1994

1995

1996

1997 Year

1998

1999

2000

2001

2002

Fig. 13.4  Numbers of kidney-only transplants and active waiting list in the UK at year end, 1992–2002.

2003

Transplantation of individual organs  195 Inferior vena cava

Transplantation of individual organs

a 100

Common iliac artery

% Graft survival

80

Donor renal artery Donor renal vein

60 Year of transplant (No. at risk on day 0) 1995–1997 (3504) 1998–2000 (2893) 2001–2003 (2774) 2004–2007 (3155)

40

Internal iliac vein Internal iliac artery External iliac vein

20 0

Bladder

2

6 4 8 Years since transplant

10

External iliac artery b Ureter

100

Fig. 13.5  Completed renal transplant in right iliac fossa.

results of liver transplantation in the management of primary liver tumours are universally poor, and its role in this situation remains controversial. Unlike kidney transplants, the number of organs available has been better matched to the number of recipients. However, widening indications for the transplantation of the liver and the increasing awareness by clinicians of liver transplantation as a therapeutic option will undoubtedly result in a waiting list in the near future.

% Patient survival

80

60

40

20 0

Indications Transplantation is indicated in the presence of liver failure from any of the conditions shown in Table 13.4. Although these are all disorders which make the patient a candidate, many of them are rare and thus form only a small part of the liver transplant population.

Operation The operation is a major procedure because the diseased liver may be difficult to remove and there are a number of vascular anastomoses to be made during which venous return to the heart must be maintained by bypass (Fig. 13.7). Primary failure of function may occur in up to 10% of allografts. The morbidity and mortality of this complication is high. Survival following re-transplantation for primary nonfunction is only half that seen when the first graft functions successfully.

Results The results of liver transplantation are rapidly improving. Currently the majority of centres report 1-year graft survival in excess of 70%. It is of note that over 85% of patients surviving more than 6 months after liver transplantation return to active life either at school or at work.

Year of transplant (No. at risk on day 0) 1995–1997 (3504) 1998–2000 (2893) 2001–2003 (2774) 2004–2007 (3155) 2

6 4 8 Years since transplant

10

Fig. 13.6  Survival for patients and transplants after kidney transplantation. Table 13.4

Indications for liver transplantation

Disease process

Suitable subgroups

Cirrhosis

Primary biliary Alcoholic liver disease Cryptogenic Secondary biliary Chronic

Hepatitis B and C virus infection Cholangitis Congenital anatomical disorders Inborn errors of metabolism Primary liver tumours Rare secondary tumours, e.g. neuroendocrine

Sclerosing Biliary atresia Budd–Chiari syndrome Alpha-1-antitrypsin deficiency Galactosaemia Wilson’s disease Hepatocellular carcinoma A relative indication depending on the size of the tumour and absence of extrahepatic involvement

13 

196  Organ transplantation

Gallbladder fossa

Hepatic artery Coeliac axis Portal vein Bile duct Inferior vena cava

Fig. 13.7  Completed liver transplant. Note the numerous suture lines. The gallbladder is removed.

Pancreas The large number of patients with diabetes has made transplantation of the pancreas a worthwhile goal. However, severe diabetes is often accompanied by renal disease which makes concurrent renal transplantation necessary if the patient is to be restored to health.

Indications n

Insulin-dependent diabetes with renal failure – combined pancreas and kidney transplant n Pre-uraemic diabetic with severe complications, e.g. neuropathy, retinopathy and poor control of the disease – a pancreas-only transplant is needed.

Operation The technique depends on whether a whole organ or a segmental graft is to be used. The latter is removed on a pedicle of splenic artery and vein and is revascularised using the external iliac artery and vein, with the pancreatic duct either occluded or drained into the urinary bladder. The whole organ is removed with the segment of duodenum which drains the pancreatic duct. Revascularisation is by a similar method to the segmental graft, with the duodenal loop drained into the bladder (Fig. 13.8). The latter technique has the least complications and the highest success rate. However, as experience with pancreas transplantation has increased, many centres are changing to an enteric drainage (anastomosis of donor pancreas or duodenum to the GI tract) but complication rates are high.

Results With increasing experience, 1- and 5-year graft survivals of 70% and 40%, respectively, are being reported.

However, transplantation of the whole pancreas is likely in the future to be replaced by transplantation of islet cells only.

Small bowel Small-bowel transplantation presents particular difficulties because: n

the transplant contains a large volume of lymphoid tissue (see graft–versus–host reaction below) n MHC class II antigens are constitutively expressed by the bowel epithelium n the transplanted organ is colonised with microorganisms. As a consequence of the last of these, there is breakdown of the intestinal barrier and the release of bacteria into the circulation (translocation), with consequent infection as well as an increased presentation of immune signals to the recipient.

Indications The indications in adults and children are given in Box 13.6. A combined liver and bowel replacement may be necessary if there is coexistent irreversible structural damage to the liver, such as may occur with prolonged parenteral nutrition.

Operation Proximal anastomosis of the graft is to the recipient’s jejunum; distally the new gut is brought out as an endileostomy (Fig. 13.9).

Transplantation of individual organs  197 Transplantation in children The future

Aorta Inferior vena cava Bowel Transplanted kidney

Transplanted duodenum

Transplanted prancreas Transplanted ureter Bladder

Fig. 13.8  Whole-organ pancreas transplant.

Box 13.6 

Indications for small-bowel transplant

Adults n Vascular – Superior mesenteric artery or vein thrombosis – Volvulus with irreversible damage to the gut – Desmoid tumour in the mesentery n Crohn’s disease with loss of function but without active sepsis

Duodenum Recipient jejunum

Children n Intestinal atresia with loss of most of the small bowel n Pseudo-obstruction – neurogenic failure of intestinal function n Microvillus inclusion disease n Gastroschisis with loss of small bowel n Necrotising enterocolitis – extensive resection

Results The most encouraging results have been reported in Canada where the last five small-bowel transplants have all been successful with the use of the immunosuppressive drug tacrolimus. In the USA, survivals are now at 65% at 1 year and 43% at 2 years.

Donor jejunum Stoma

Fig. 13.9  Small-bowel transplant.

Indications n

Heart, lung and heart–lung This is discussed in Chapters 16 and 17.

Cornea The cornea was the first solid tissue successfully allografted in humans. In recent years, a high success rate has made corneal transplantation the most commonly performed transplant.

Opaque cornea from any cause Thin or distorted cornea n Corneal loss – necrotising ulceration or trauma. n

Operation A button of the recipient’s cornea is removed and replaced with a corresponding graft from the donor using very fine nylon sutures. Because the cornea is avascular, rejection is not a common problem unless the recipient’s cornea has undergone neovascularisation before the transplant takes place.

13 

198  Organ transplantation

Results Worldwide, the survival of the graft is 95%, and it may be expected to last for life. Close HLA matching correlates with an improved long-term result.

TRANSPLANTATION IN CHILDREN In older children with a weight in excess of 20 kg, most transplant procedures are the same as for adults, although specially skilled personnel such as paediatric anaesthetists are required to deal with the haemodynamic problems that may arise during clamping of major vessels. Such problems are greater the younger and the smaller the child.

THE FUTURE Despite the great success of current multi-organ transplant programmes, further developments are required to improve the long-term outlook of recipients. It is difficult to imagine that there will be many more technical improvements in transplant surgery. Advances in immunology, formulation of new less-toxic immunosuppressive drugs, xenografting and the development of cellular or biomechanical approaches to organ replacement therapy are clearly the most important areas for the future.

Kidney The results of transplanting paediatric kidneys into paediatric recipients are worse than if an adult kidney is used. Accordingly, most centres now transplant the best-matched organ, provided its size is not too discrepant; access may be modified to make the procedure feasible.

Other organs For liver, heart and lung, the constraints of size are more relevant, and age matching is done. However, the increasing success of using a reduced-size liver graft has overcome the problem of supply in that area.

FURTHER READING Abbas AK, Lichtman AH, Pillai S 2009 Cellular and molecular immunology, 6th edn. Saunders, Philadelphia Forsythe JLR 2009 Transplantation: a companion to specialist surgical practice. Saunders, Philadelphia Hakim N, Danovitch G, Dausset J 2010 Transplantation Surgery – Springer Specialist Surgery Series, Springer, New York Hornick P (ed) 2006 Transplantation immunology: methods and protocols (Methods in Molecular Biology). Humana Press, Totowa Morris PJ, Knechtle SJ 2008 Kidney transplantation: principles and practice, 6th edn. Saunders, Philadelphia

SECTION 2 REGIONAL SURGERY

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Swellings in the neck  201

The neck and upper aerodigestive tract

Swellings in the neck

201 204 204

Non-neoplastic salivary gland disease Salivary gland neoplasms

207 208

Neck space infections

208

Squamous carcinoma Lymphoma

204 204 206

Vocal cord paralysis and upper airways obstruction

210

Diseases of the salivary glands

207

Common surgical procedures on the   neck

210

Benign cystic swellings Vascular tumours

Tumours of the upper aerodigestive   tract

SWELLINGS IN THE NECK The most common cause of a neck swelling is lymph node enlargement. The majority of such swellings are secondary to infection, the minority are the consequence of malignant disease. Making the correct diagnosis depends initially on a careful, thorough clinical assessment.

Clinical features History

mirror, but the advent of the fibreoptic nasoendoscope has made these sites much easier to view directly. However, even with this instrument a very small submucosal primary tumour may be overlooked. If a lymphoma is suspected then the axillae, groins and abdomen should also be examined.

Clinical diagnosis After the completion of the local examination, a first attempt can often be made at a clinical diagnosis.

Important features are: n n n n n n

the duration of the swelling progression in size associated pain other symptoms in the upper aerodigestive tract – hoarseness, dysphagia, localised sore throat, deafness systemic symptoms – weight loss, night sweats exposure to alcohol and/or tobacco – squamous carcinoma with a cervical lymph node metastasis is rare below the age of 40 in those who have not been exposed to either of these agents.

Site The site often indicates a possible origin (Fig. 14.1): n

n

Physical findings Examination of an individual lump should produce the following information: site and size relationship to other anatomical structures such as the great vessels n fixation to other structures n special features such as pulsatility, the presence of a bruit or thrill, tenderness or fluctuation.

n

n n

A thorough orodental examination must be carried out. The oral cavity and oropharynx can easily be examined using a tongue depressor and bright light. The nasopharynx and laryngopharynx used to require indirect examination with a

n

n

Parotid swellings occur immediately in front of the tragus, over the angle of the mandible or just below the lobe of the ear. An associated facial palsy suggests a malignant tumour of the gland. Submandibular gland swellings are sometimes indistinguishable from regional lymphadenopathy. In either case, fixation to the mandible may make it impossible to get above the mass. A submandibular swelling is more likely to be palpable bimanually (via the mouth). Midline submental swellings are nearly always benign and, if cystic, are commonly a thyroglossal cyst, a midline dermoid cyst or a pyramidal lobe of the thyroid, if lower in the neck. High anterior triangle swellings can be metastatic in origin, with the likely primary site in the oral cavity or oropharynx. Alternatives are a branchial cyst or carotid body tumour. Low anterior triangle swellings are either related to the thyroid gland or are metastatic nodal deposits from a primary tumour in the larynx or hypopharynx. Such lymph node masses do not move on swallowing unless they are fixed to the thyroid gland or the larynx.

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202  The neck and upper aerodigestive tract

Parotid region

Submandibular triangle Submental triangle

Upper anterior triangle Lower anterior triangle Posterior triangle Subclavicular triangle

Fig. 14.1  Sites of swelling in the neck. n

Supraclavicular swellings are more common on the left side of the neck and are often caused by disease below the level of the clavicle, e.g. carcinoma of the lung or stomach. n Posterior triangle swellings are rarely the result of metastatic carcinoma unless there are also palpable lymph nodes in the anterior triangle on the same side. More common causes are tuberculosis, toxoplasmosis and lymphoma. The last may occur in an otherwise fit and asymptomatic young adult.

Multiple cervical masses These are almost always nodal and, if accompanied by an acute systemic illness, may be caused by viral infections such as infectious mononucleosis. A more chronic presentation can be produced by tuberculosis.

Time course The time course of the swelling may be helpful in suggesting the diagnosis. Enlargement of a cervical lymph node(s) which has taken place over a few days, and which is tender, is almost always inflammatory. Lymphomas occasionally present in this way, but more commonly develop over a period of several weeks and are usually painless. Metastatic nodes have a similar pattern; although they may be tender on palpation, they rarely cause spontaneous pain unless there is invasion of the cervical or brachial plexus.

Investigation Fine-needle aspiration Fine-needle aspiration (FNA; Ch. 4 and Fig. 14.2) to obtain cell or tissue samples is the first invasive investigation to confirm a diagnosis and is best done immediately after clinical examination has been completed unless there are clinical reasons to think that it is potentially dangerous, e.g. evidence of considerable vascularity such as a bruit or thrill. A fluctuant

Fig. 14.2  Fine-needle aspiration of a parotid lump. swelling may yield pus, which is sent for culture, or either clear or opalescent liquid which suggests a branchial or other cyst. In both instances, a sample should be sent for cytological examination. A solid lump produces an aspirate which is examined cytologically and is likely to give an indication of the pathological cause. However, confirmation must nearly always be sought by other means such as endoscopy with biopsy for histology and imaging (see below) before treatment is undertaken. Cytology is not infallible.

MRI scanning This is valuable when the likely diagnosis is of metastatic nodal disease. The scan should extend from the base of the skull to the clavicles. Information is obtained about the relationship of the mass to other structures, and other impalpable swellings may be found. Indeed the scan may demonstrate the site of a primary tumour. CT and ultrasound scanning are also useful in certain clinical situations. Ultrasound-guided FNA is useful for small or deeper lesions in the neck.

Swellings in the neck  203 Other investigations These are based on the probable clinical diagnosis, particularly if the swelling(s) is thought to be of lymph node origin. The usual procedures are indicated in Table 14.1.

Further diagnostic strategy The above investigations usually provide enough information to decide whether the patient requires formal endoscopy of the upper aerodigestive tract. The diagnostic pathways are decided from the outcome of the result of FNA and endoscopy, as follows.

Cytology suggests squamous carcinoma Regardless of whether or not the primary is apparent, a formal upper aerodigestive tract endoscopy is undertaken, and must include examination of (Fig. 14.3): n n n n n n

nasopharynx oral cavity/oropharynx (with inspection of ipsilateral tonsil) hypopharynx larynx and trachea bronchi cervical oesophagus.

Table 14.1

Supplementary investigations to be considered for a lump in the neck

Possible cause

Investigation

Acute infection Tuberculosis Infectious mononucleosis Lymphoma Malignancy in lung

Full blood count (FBC) Chest X-ray, Mantoux test Monospot, FBC FBC, bone marrow Chest X-ray, CT scanning

A biopsy is taken from any suspicious lesion. Such an endoscopy will uncover a primary tumour in approximately one third of cases. In approximately 2%, a second primary is found elsewhere. If the nodal mass contains squamous carcinoma but endoscopy and scanning fail to identify a primary tumour, then treatment of the neck should be by radiotherapy (for nodal disease < 2 cm in diameter) or neck dissection (where nodes > 2 cm in diameter). PET-CT scanning should be undertaken as part of the diagnostic assessment of metastatic cervical lymphadenopathy, when no primary is clinically apparent. Ideally, the scan should be undertaken before mucosal biopsies are undertaken.

Cytology suggests lymphoma Incision or excision biopsy of an enlarged node is almost always necessary to obtain sufficient tissue to identify with confidence the histological type of lymphoma (see also below). Excisional surgery is diagnostic, not therapeutic.

Cytology is unhelpful A normal endoscopy and lack of information from FNA together indicate the need for surgical excision/incision biopsy as a last resort. The reason for trying to avoid this is that local surgery for diagnosis of a lump which is malignant may lead to seeding of tumour cells at the biopsy site. Whenever feasible, excision biopsy should be performed to reduce this hazard. Furthermore, it is best to obtain a frozen section at once and, if metastatic squamous carcinoma is confirmed, to go straight on to a radical neck dissection. If fixity of the node(s) makes this unfeasible, the wound is closed and alternative treatment, usually by radiotherapy, is undertaken. Incision, as opposed to excision, biopsy of a benign lesion should be avoided whenever possible, as it makes subsequent surgery that considerably more difficult.

Nasal cavity

Nasopharynx Oral cavity

Oropharynx

Hypopharynx

Larynx Cervical oesophagus Trachea

Fig. 14.3  Regions of the upper aerodigestive tract.

Swellings in the neck

14 

204  The neck and upper aerodigestive tract

A primary tumour is found at endoscopy If a primary tumour is found at endoscopy, the type of treatment recommended will depend on the site and size of both the primary and the cervical node metastases. A radical neck dissection should not be undertaken if the primary is known to be below the clavicle.

BENIGN CYSTIC SWELLINGS

Thyroglossal cyst Aetiology The embryonic mesoderm which ultimately develops into the thyroid gland descends from the foramen caecum of the tongue to the normal pretracheal site of the gland. The tract usually disappears, but islands of thyroid tissue may be deposited at any point along its course and develop into a cyst.

Clinical features Presentation is commonly during the second or third decades of life. The mass is usually midline, between the thyroid notch and hyoid bone, and moves upwards on protrusion of the tongue (Fig. 14.4).

Management The cyst is removed surgically. To avoid recurrence, which may be associated with sinus formation, the central portion of the hyoid bone is included in the excision because the tract can run either deep or superficial to the bone (Sistrunk’s operation).

Branchial cyst Aetiology The cause is uncertain. It is considered by some to be a remnant of the branchial complex which contributes so much to the development of the neck structures.

Clinical features Presentation is typically between the ages of 15 and 35 years with a cyst in the upper part of the anterior triangle with its posterior portion deep to the sternomastoid muscle. It is smooth, mobile and, unless infected, not tender. Occasionally the cyst communicates with the skin via a sinus. The diagnosis can be confirmed by FNA, which characteristically produces pale creamy fluid, and ultrasound scanning. Further imaging is rarely necessary. Treatment is by excision together with any sinus tract that may run from it.

VASCULAR TUMOURS

Chemodectoma – carotid body tumour Aetiology There is sometimes a family history and these tumours are more common in those who live at high altitudes. Not much else about the cause of this rare tumour is known, except that it is derived from paraganglionic cells.

Clinical features The patient usually presents in adult life with a history of a lump which is ovoid, non-tender, pulsatile and which is in the upper anterior triangle of the neck. Characteristically, it is mobile in the horizontal but not the vertical plane. However, it may be difficult to distinguish a carotid body tumour from a branchial cyst without appropriate investigation. Auscultation may reveal a bruit. A CT scan demonstrates the lesion but confirmation is best made by carotid angiography, which shows a highly vascular mass. Treatment is by surgical excision, which is usually preceded by embolisation of the tumour.

TUMOURS OF THE UPPER AERODIGESTIVE TRACT Malignant tumours are more common than benign ones and almost all are primary as opposed to secondary. Squamous carcinomas are the most common (more than 90%), followed by lymphomas, salivary gland tumours, melanomas and sarcomas.

SQUAMOUS CARCINOMA

Aetiology The most important predisposing factors are: n

Fig. 14.4  Infected thyroglossal cyst.

smoking high alcohol intake, especially of wines and spirits n presence of pre-malignant conditions. n

Tumours of the upper aerodigestive tract  205 Other factors include: n

chronic irritation from a jagged tooth chewing betel nut (common in the Indian subcontinent) n oral syphilis (very rare). n

Pre-malignant conditions Leucoplakia This is a descriptive term for a white patch or patches on the mucosa, usually of the oral cavity and larynx. It usually results from chronic irritation, although in 10% it is of unknown cause. The histological picture is often one of dysplasia, but the condition may be associated with frank malignancy. Management should be conservative, once malignancy has been excluded by biopsy. Close follow-up of the patient is essential, and further biopsies may be necessary. Causative factors should be removed if possible.

Erythroplakia These are fiery red patches of mucosa that bleed easily. They imply severe dysplasia and are often associated with the presence of an in-situ carcinoma.

Sideropenic dysphagia Erythroplakia may be associated with this syndrome in postmenopausal women; it involves dysphagia, iron deficiency anaemia and a web in the postcricoid hypopharynx. A barium swallow demonstrates the web, which may be associated with a locally dysplastic mucosa. Endoscopy and biopsy are therefore necessary, the passage of the endoscope often temporarily relieving symptoms. The condition is not, however, reversible with correction of the anaemia. Subsequent development of a postcricoid carcinoma is a distinct possibility, and the patient should be kept under observation.

Clinical examination The sequence of examination is outlined above. The primary may be readily apparent on inspection, usually as an ulcer with a raised edge. Examination is not complete without careful palpation of the neck.

Investigation The choice of investigations depends on the known or likely site of the tumour. The principles have already been outlined. The presence of an unexplained hoarse voice for longer than 6 weeks and inability to assess the larynx fully as an out­patient is an indication for direct laryngoscopy under general anaesthesia. A similar principle is observed for persistent dysphagia and the need for oesophagoscopy; a diagnosis of functional dysphagia (globus pharyngis or globus hystericus) should never be made until both a barium swallow and an oesophagoscopy have been shown to be normal, thus excluding both strictures, mucosal disease and motility disorders.

Management A multidisciplinary approach (MDM or MDT) is required. Surgery and radiotherapy are the two principal treatments, used either alone or in planned combination. The role of chemotherapy remains unclear. Eradication of the tumour is the first priority, but preservation of function (particularly of speech and swallowing) and of appearance are also important factors. Approximately 20% of patients with head and neck cancer present with such advanced disease that it is wisest and kindest to do nothing more than provide supportive care and analgesia. Whilst this may initially be at home, hospice care usually becomes necessary later because of swallowing and respiratory problems, and intractable pain. A gastrostomy or tracheostomy may be useful in referring severe digestive or respiratory tract obstruction.

Clinical features

Small tumours

These are site-specific (see Fig. 14.3).

For small or early cancers radiotherapy and surgery are equally effective and, in view of the wish to preserve function, radiotherapy is often the treatment of choice. Once a full course (60–65 Gy) of radiotherapy has been given, the irradiated volume cannot be retreated, and recurrent or new tumours, however small, which occur within the irradiated field have to be treated by surgery. Using a microscopy and CO2 laser, certain small volume carcinomas of the larynx can be excised endoscopically, with preservation of the voice.

Symptoms Nasal or sinus tumours can cause local problems, such as unilateral nasal obstruction and epistaxis, or can invade adjacent structures and give rise to clinical features that are misleading, such as diplopia, middle ear effusion or loosening of teeth. Oral cavity and oropharyngeal tumours commonly present with symptoms of local pain, referred otalgia or difficulty eating but, as with tumours of the hypopharynx, the primary may be asymptomatic and it is the presence of metastases which draws attention to the lesion. Tumours of the larynx characteristically result in hoarseness, and compromise of the airway only occurs in very advanced cases. Referred otalgia, mediated by the vagus nerve, may also be a presenting symptom. Laryngeal, hypopharyngeal and cervical oesophageal neoplasms may also cause dysphagia, initially to solid food. This is in contrast to dysphagia of neurological origin e.g. (motor neurone disease or after a cardiovascular accident), when swallowing is initially more difficult with liquids.

Large tumours The bigger the tumour, the less likely it is to be cured by radiotherapy, and this is particularly so if there is invasion of bone or cartilage. Primary surgery is better in such cases. The decision as to whether or not to add planned postoperative radiotherapy may be made before surgery or may depend on histological factors revealed by study of the operative specimen. Very close or positive margins of excision of the primary, extracapsular rupture of a lymph node or involvement of multiple levels of the neck would merit planned postoperative radiotherapy.

Benign cystic swellings Vascular tumours

Tumours of   the upper aerodigestive tract Squamous carcinoma

14 

206  The neck and upper aerodigestive tract

Given the propensity for these tumours to metastasise to the cervical nodes, these may need to be treated at the same time as the primary tumour. Small nodes can be treated by radiotherapy or surgery, and the appropriate choice may well depend on the treatment modality chosen for the primary site. Large nodes should be treated by a neck dissection. Some primary sites (e.g. tongue, bone and tonsil) carry such a high risk (50%) of microscopic nodal disease that prophylactic treatment of the ipsilateral neck should be undertaken even when there is no clinical evidence of metastasis. The modality used will usually be the same as that employed for the primary site.

Prognosis Survival rates depend on the site and size of the primary tumour, and the presence or absence of metastatic nodal disease. A patient with a tumour of the larynx is likely to fare much better than one with a tumour of the same size in the hypopharynx. This is partly the result of more ready spread of the latter to the regional lymph nodes. Once lymph node metastases have developed, the prognosis for any tumour, no matter how small the primary, worsens considerably. Failure to control the disease is almost always because recurrence takes place loco-regionally; distant metastases are unusual unless there is already advanced disease above the clavicles. Such loco-regional recurrence is most likely to occur within 2 years of the initial treatment. Overall, the 5-year survival rate for all head and neck malignancies is approximately 40%.

Surgical management Reconstruction

mediastinum for anastomosis to the pharynx in the neck (stomach pull-up procedure). Another less reliable option is to bring up a vascularised segment of transverse colon.

Restoration of speech One of the greatest handicaps which can result from the surgical treatment of head and neck tumours is the loss of voice which follows total laryngectomy. Until relatively recently, adequate speech after laryngectomy was often not achievable, the patient being doomed to a life of silence and a pen and paper. However, the last decade has seen the advent of surgical speech restoration. A tracheo-oesophageal fistula is created surgically through the posterior wall of the trachea, approximately 5 mm below the mucocutaneous junction (Fig. 14.5). A one-way valve can then be introduced into the tract, where it can be left for several months before replacement. By occluding the tracheostomy with a finger during expiration, the patient can divert air up through the valve into the pharynx. The air is set in vibration by the valve and speech can be produced.

LYMPHOMA

Pathological features The majority of lymphomas in the head and neck region are non-Hodgkin’s in type. They can be nodal or extranodal, and those found in Waldeyer’s ring (the lymphoid tissue ring located in the pharynx and to the back of the oral cavity which includes the tonsils) characteristically form a protruding mass, unlike squamous carcinomas.

The defect after surgery for a large aerodigestive tract tumour is often of considerable size, and it may be difficult to achieve a satisfactory cosmetic and functional result by direct closure. Recent advances in plastic surgical techniques have provided a variety of options, which include: Simple free grafts of split or full-thickness skin. These are only appropriate for small defects, as they rely on the tissue bed for their revascularisation. n Pedicled skin flaps. These may be random, where there is no specific nutrient artery, or axial, where the flap has a named blood supply (e.g. the pectoralis major myocutaneous flap supplied by the thoraco-acromial artery). Axial flaps are much more reliable and are not limited by the width/length ratio of the flap. n Free skin flaps and jejunal segmental transplant. A piece of forearm or lateral thigh skin or a segment of jejunum can be dissected with its own arterial supply and venous drainage which can then be anastomosed to appropriate vessels in the neck, so restoring the graft tissue’s circulation. The radial forearm flap has the great advantage that it can be raised in continuity with a piece of radial bone, which will restore continuity following resection of a segment of mandible for an oral cavity carcinoma. A transplanted length of jejunum can be used as an oesophageal replacement. n Transposed viscus. Following a laryngopharyngooesophagectomy for a postcricoid carcinoma, the stomach can be mobilised and brought up through the n

Fig. 14.5  Restoration of speech after tracheostomy.

Diseases of the salivary glands   207 Clinical features

Lymphoma

The patient presents with a local lesion or enlarged lymph node(s).

Diseases of the salivary glands

Diagnosis

Non-neoplastic salivary gland disease

Biopsy is the only method of making an exact diagnosis.

Investigation The studies to be done are the same as for lymphomas at other sites (Ch. 30). Surgery plays only a diagnostic role in management.

DISEASES OF THE SALIVARY GLANDS There are three paired salivary glands: the parotid, the submandibular and the sublingual glands. Scattered throughout the mucosa of the oral cavity and pharynx are millions of other tiny minor salivary glands. Although tumours may arise in the latter, they are rarely a site of inflammatory disease.

NON-NEOPLASTIC SALIVARY   GLAND DISEASE

Bacterial infection

Fig. 14.6  Oblique X-ray of the floor of the mouth showing two stones in the submandibular salivary duct.

Infections in the parotid or submandibular salivary gland are relatively uncommon. Bacterial parotitis tends to occur in elderly debilitated patients, probably as the result of poor oral hygiene and dehydration. Bacterial infection of the submandibular gland is more common and can occur in an otherwise well patient. Infection is frequently due to a stone lodged in the gland’s duct.

and difficult to remove, particularly if it is lodged far back in the duct, where damage to the adjacent lingual nerve may occur. In such circumstances, it is better to allow the infection to resolve with antibiotic treatment and then remove the entire gland.

Clinical features

This is a common disorder usually caused by the mumps virus. Other agents include the cytomegalovirus and Coxsackie virus. Although the gland may swell considerably, there is not as much pain or systemic upset as in bacterial infection.

Parotitis The gland swells, becomes acutely tender and the overlying skin may be erythematous. A plain X-ray may demonstrate a stone in the duct, but a contrast examination should not be done while there is acute inflammation.

Submandibular sialadenitis The appearances are the same as for parotitis. A stone may be palpable on bimanual examination. Alternatively, a stone may be identified on an intraoral dental X-ray (Fig. 14.6).

Management Parotitis Parotitis requires energetic care of the mouth, rehydration and antibiotics. If fluctuation develops, incision and drainage of the abscess is necessary, ensuring that the facial nerve is not damaged.

Submandibular sialadenitis This is treated in the same way as parotitis, but if a stone is obvious, then intraoral incision of the duct and removal of the stone under local anaesthesia may be all that is required. However, a submandibular duct stone can be very mobile

Viral parotitis

Sialectasis This is primarily a disease of the parotid gland and may be a forerunner to stone formation. Epithelial debris mixes with the saliva to produce sediment in the ducts, which in turn leads to stasis and poor emptying of the ducts when secretion is stimulated.

Clinical features and investigation Painful swelling of the gland occurs at mealtimes and can last several hours. Sialography characteristically demonstrates a snowstorm appearance of the duct system, caused by patchy cystic dilatations of the ducts interspersed with areas of stricture formation.

Management Salivary flow is increased by the use of sialogogues, such as lemon juice. Parotidectomy should be avoided if

14 

208  The neck and upper aerodigestive tract

at all possible because of the risk of damage to the facial nerve.

Connective tissue disease Keratoconjunctivitis sicca and rheumatoid arthritis (Sjögren’s disease) Salivary gland swelling occurs in about one-third of affected patients. Because the disease is associated with an abnormality in lymphocyte function, the patient is at risk of developing a lymphoma.

Benign lymphoepithelial infiltration This causes general enlargement of the submandibular and parotid glands without any of the other features of Sjögren’s disease. A sublabial mucosal biopsy demonstrates a dense lymphocytic infiltrate of the minor salivary glands. Again, there is an increased risk of lymphoma, and any further increase in size of any of the salivary glands should be viewed with suspicion and FNA carried out.

Drug-induced salivary gland swelling Certain antihypertensives, monoamine oxidase inhibitors and iodide-containing drugs can cause enlargement of the parotid, as may the contraceptive pill.

SALIVARY GLAND NEOPLASMS Most salivary gland tumours are benign. However, the smaller the gland, the higher is the chance of a tumour being malignant. Although 70% of parotid tumours are benign, 70% of minor salivary gland tumours are malignant.

Cystadenoma lymphomatosum (Warthin’s tumour or adenolymphoma) This is another common benign tumour found only in the parotid gland. It is bilateral in 10%, does not undergo malignant change and bears no connection with lymphomas.

Malignant neoplasms Malignant salivary gland tumours are rare and histologically diverse. Muco-epidermoid carcinomas can be high grade (and mimic squamous carcinoma in clinical behaviour) or low grade (when they behave in a relatively benign way). Squamous carcinoma is an aggressive tumour, which, in the parotid gland, often produces a facial nerve palsy. It is important to differentiate this disease from metastatic squamous carcinoma in an intraparotid lymph node. Adenocarcinomas and adenoid cystic carcinomas can also develop in the salivary glands. The latter has a tendency to infiltrate along nerves for considerable distances.

Management Surgical removal is the main treatment. If a malignant parotid tumour is found to directly involve the facial nerve, then that structure must be sacrificed and continuity of the nerve re-established using a segment of greater auricular or sural nerve as a graft. Unfortunately, both fine needle aspiration biopsy and frozen section biopsy are notoriously unreliable at providing an accurate morphological diagnosis of a salivary gland malignancy.

Lymphomas These tumours may develop in any of the larger salivary glands. Once the diagnosis has been made by either FNA or biopsy, treatment is by conventional methods (see Ch. 30).

Pleomorphic adenoma This is the most common benign tumour, so-called because histologically it can mimic a variety of tissues. If left untreated for many years, it can undergo malignant change, which is usually signalled by a sudden increase in the rate of enlargement.

Clinical features The history is of a painless mass, usually in the parotid, which may enlarge very slowly over a period of several years. The lump is discrete and mobile. If it occurs in the parotid it rarely results in a facial palsy (unlike a malignant tumour).

Management Surgical excision is the standard treatment. The tumour has a capsule, and rupture of this can lead to tumour seeding and recurrence. As most parotid adenomas are in the bulkier superficial lobe of the gland, a superficial parotidectomy with preservation of the facial nerve can be undertaken. A submandibular adenoma is best managed by removal of the whole gland.

NECK SPACE INFECTIONS Peritonsillar abscess (quinsy) Anatomy and pathological features The faucial tonsil lies medial to the pharyngeal constrictor muscle and has a pseudocapsule of fibrous tissue around its deep surface. A peritonsillar abscess develops when this potential space becomes infected by direct spread from acute tonsillitis. The problem is usually unilateral, and in the early stages there is a local cellulitis rather than overt abscess formation.

Clinical features History There is a background of acute tonsillitis that suddenly progresses with increasing unilateral pain and dysphagia. The patient may be unable to swallow saliva and usually has marked trismus because of reflex spasm in the adjacent pterygoid muscles.

Neck space infections  209 Physical findings

Management

A fluctuating pyrexia is invariable. The tonsil is displaced downwards and medially. There may be obvious cervical lymphadenopathy or just a vague fullness on that side of the neck.

Prompt treatment is essential because of the risk of complications. Intravenous antibiotics should be administered and a CT scan obtained to ascertain whether or not there is a collection of pus. When present, pus is drained through an incision running down the anterior border of the sternomastoid muscle.

Management In the early stages, intravenous antibiotics (penicillin and metronidazole) are given. However, if there is any suspicion of a local collection of pus, then the inflammatory mass should be drained. This is best performed with a 14 G needle and 10 mL syringe or a fine blade on a long-handled scalpel, having first sprayed the palate with lidocaine. The site of the puncture is shown in Figure 14.7.

Parapharyngeal abscess Anatomy and pathological considerations The parapharyngeal space is a potential one that is triangular in cross-section (Fig. 14.8). It lies lateral to the pharyngeal constrictors, anterior to the prevertebral fascia and deep to the deep cervical fascia. Its chief contents are the carotid tree, the internal jugular vein and the last four cranial nerves. Infection of this space is usually the consequence of dental sepsis or uncontrolled tonsillitis. Two dangerous complications may result: n n

spread of the infection inferiorly into the mediastinum mucosal oedema in the adjacent larynx and pharynx with airways obstruction.

Clinical features There is fever with diffuse swelling of the affected side of the neck and loss of the normal gutter anterior to the sternomastoid muscle.

Fig. 14.7  The site of a right-sided peritonsillar abscess, with the point of incision.

Pretracheal fascia Carotid artery

Parapharyngeal space

Internal jugular vein

Deep cervical fascia

Pharyngeal constrictors Prevertebral fascia

Fig. 14.8  The parapharyngeal space.

Salivary gland neoplasms

Neck space infections

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210  The neck and upper aerodigestive tract

!Acute airways obstruction Emergency Box 14.1 

 

Any neck space infection is a potential cause of acute airways obstruction. Failure to improve after 24 hours of intravenous antibiotics may necessitate surgical drainage and/or a tracheostomy.

almost inevitable. Damage to or division of the main vagus nerve at the base of the skull is more likely to cause the ipsilateral cord to assume a more lateralised position. Although this does not threaten the airway, it results in a very poor breathy voice and serious problems with aspiration of saliva and food.

Aetiology Common causes of distal disruption of the recurrent laryngeal nerve are:

Ludwig’s angina

(Emergency Box 14.1)

Anatomy and pathological considerations Soft-tissue infection of the floor of the mouth on both sides of the mylohyoid muscle usually results from gross dental sepsis. A combination of bacteria, which may be anaerobic, is often involved.

Clinical features A brawny swelling of the submandibular and submental triangles is present. On intraoral inspection, there is gross oedema of the mucosa of the floor of the mouth, with upward and posterior displacement of the tongue. The latter is potentially fatal, in that the tongue may obstruct the airway.

Management Treatment is initially with antibiotics, which should be chosen to include cover for anaerobic infection. Any collection of pus should be drained, if necessary using through-and-through incisions running from the floor of the mouth medial to the mandible and out into the neck. It may be necessary to maintain the airway by nasopharyngeal or nasotracheal intubation. If this is unsatisfactory, a tracheostomy is required.

n

thyroid surgery (Ch. 32) cardiac (aortic arch) surgery n carcinoma of the bronchus n carcinoma of the thyroid n carcinoma of the oesophagus. n

There is, in addition, a large idiopathic group in which the cause is never found and where spontaneous recovery is relatively common.

Diagnosis The development of a recurrent laryngeal nerve palsy should lead to a detailed search for the cause, which may require a variety of special investigations to find or exclude an intrathoracic cause.

Management The frequency with which an idiopathic palsy occurs and its likely spontaneous recovery mean that elective surgery for hoarseness, airways obstruction or aspiration should only be undertaken in those patients who have an identifiable, nonreversible cause or who have had symptoms for at least 9 months and are therefore very unlikely to recover. Patients with a unilateral palsy very rarely require a tracheostomy.

Tonsillar swelling from infectious mononucleosis

Surgical treatment

Alarming swelling of both tonsils may occur and, in extreme cases, compromise the pharyngeal airway. However, peritonsillar abscess does not occur unless a bacterial tonsillitis supervenes. Impending airways obstruction can often be prevented by using steroids.

n

VOCAL CORD PARALYSIS AND UPPER AIRWAYS OBSTRUCTION Paralysis of a vocal cord is usually the consequence of damage to the ipsilateral recurrent laryngeal nerve, which is a branch of the vagus nerve.

Anatomy and physiological features The left nerve runs a significantly longer course than the right, down into the superior mediastinum and around the arch of the aorta. Therefore it is three times more likely to be affected. When the recurrent laryngeal nerve is damaged or divided, the cord assumes a paramedian position. This may be asymptomatic or result in hoarseness; however, if both recurrent nerves are affected then acute airways obstruction is

There are two categories: n

medialisation of the vocal cord lateralisation of the vocal cord.

Medialisation is used when one cord is paralysed and the other unable to provide complete closure of the glottis. The affected cord is moved medially to improve the voice and reduce aspiration. Either a paste is injected endoscopically at two or three sites immediately lateral to the cord, or a piece of thyroid cartilage is wedged between it and the thyroid ala (thyroplasty). Lateralisation is used in an attempt to improve the airway in bilateral palsy when the cords lie in the paramedian position. A type of laser cordectomy can be undertaken, although this treatment is inevitably a compromise; as the gap between the cords is increased, the airway improves, but the voice deteriorates and aspiration becomes an increasing problem. In bilateral paralysis, a permanent tracheostomy is usually the best management. A cuffed tube will be necessary if aspiration is a serious problem.

Obstructive sleep apnoea Obstructive sleep apnoea (OSA) is an increasingly recognised condition where blockage occurs in the upper airways

Common surgical procedures on the neck  211 during sleep. This results in repeated episodes of apnoea and is particularly common in the morbidly obese. Other risk factors include male sex and age over 40 years. Diagnosis is suspected on history and confirmed by sleep studies. OSA may lead to daytime sleepiness, hypertension, cardiovascular disease, memory problems, weight gain and headaches. Treatment is usually non-surgical with the use of a dentally fitted mandibular advancement devices (MDA) or continuous positive airways pressure (CPAP) masks which help to prevent airways obstruction at night. Weight loss should be achieved in the obese patient if possible. Morbidly obese patients may benefit from bariatric surgery (see Ch. 19). In children tonsillectomy and adenoidectomy may cure the condition. In some adults surgery to reconstruct the soft tissues of the upper airway, and occasionally the bony structures may be recommended. Options include uvulopalatopharyngoplasty (UPPP – which involves removal of the tonsils, adenoids, and part of the soft palate and uvula), laser assisted uvulopalatoplasty, and radiofrequency ablation (RFA) treatment to the soft palate and tongue.

complications. Haemorrhage is the most important and may be primary (within 24 hours of surgery) or secondary (days 5–10), when it is usually the result of infection at the site of excision. A bleeding diathesis, such as von Willebrand’s disease, may present with bleeding during or after tonsillectomy.

Tracheostomy There are two types of tracheostomy (Fig. 14.9): n

After a laryngectomy, the divided trachea is brought out and sutured to the skin. n More frequently an opening is made, into the front wall of the trachea, the larynx remaining in situ. It may be a temporary or permanent, elective or emergency procedure. Whenever possible, a tracheostomy should be performed with an endotracheal tube in situ. This way, the airway

Box 14.1 

COMMON SURGICAL PROCEDURES ON THE NECK Tonsillectomy The indications for tonsillectomy are given in Box 14.1. Although the frequency of this operation has reduced, it is still a commonly performed operation, which is not without

Fig. 14.9  The two types of tracheostomy.

n

Indications for tonsillectomy

Recurrent tonsillitis with more than four attacks per year Obstructive sleep apnoea with tonsillar hypertrophy in children n Peritonsillar abscess with a past history of recurrent tonsillitis n Unilaterally enlarged tonsil with lymphoma a possibility n Malignant ipsilateral lymphadenopathy due to squamous carcinoma, with no known primary n

Vocal cord paralysis and upper airways obstruction Common surgical procedures on the neck

14 

212  The neck and upper aerodigestive tract Box 14.2 

Indications for tracheostomy

Supralaryngeal obstruction n Ludwig’s angina n Severe facial fractures n Glandular fever n Laryngeal obstruction n Epiglottitis n Laryngeal tumour n Bilateral vocal cord palsy

The indications for tracheostomy are given in Box 14.2. One of the fallacies about a tracheostomy is that the patient is unable to speak afterwards. This is not usually true. Once the operation site has healed, the initial tube is replaced by a silver or plastic one without a cuff. A speaking valve can then be attached: during quiet respiration, air travels back and forth through the tube, but on forced expiration the valve will shut, diverting the air up through the glottis where it can be set into vibration and used for phonation.

Recurrent aspiration n Coma n Myasthenia gravis n Bulbar or pseudobulbar palsy Respiratory support n Injury to the chest wall n Seriously ill or injured patients (ARDS) n Prolonged endotracheal intubation

FURTHER READING Corbridge R, Steventon N 2009 Oxford handbook of ENT and head and neck surgery, 2nd edn. Oxford University Press, Oxford

remains secure throughout the procedure. In adults, a window should be excised from the anterior tracheal wall: a trap door flap is dangerous as it can become inverted and obstruct the tracheal lumen. In children, a vertical slit controlled by stay sutures should be employed.

Clarke R, Bull PD 2007 Diseases of the ear, nose and throat (Lecture Notes Series), 10th edn. Wiley-Blackwell, Chichester Lee K J (ed) 2008 Essential otolaryngology: Head and neck surgery, 9th edn. McGraw-Hill Medical, New York

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Ear and nose

THE EAR

213

THE NOSE AND PARANASAL SINUSES

223

Diseases of the external ear

216

Diseases of the middle ear

217

Common conditions of the nose and   paranasal sinuses

224

Diseases of the inner ear

220

Tumours of the nasal cavity and sinuses

227

THE EAR Anatomy External ear This is merely the pinna and the auditory meatus (Fig. 15.1).

Middle ear (tympanic cavity) The tympanic membrane separates the external from the middle ear. The middle ear cleft comprises the Eustachian (auditory) tube and middle ear cavity which communicates with the mastoid air cells. The bony roof of the attic of the middle ear separates it from the middle cranial fossa. The middle ear cavity is in contact with the external atmosphere through the Eustachian tube, which opens into the postnasal space and contains three articulating ossicles (Fig. 15.1) – the malleus, incus and stapes – which are supported by ligaments. The annular ligament surrounds the footplate of the stapes (3.5mm2 in area) and restrains this to movement in the oval window. The second, round window, below the oval window, is covered only with a membrane, which allows the transmission of pressure and movement of fluids in the inner ear. There are two muscles in the middle ear: tensor tympani and stapedius; these pull in opposite directions and modify the motion of the ossicles, increasing their stiffness and protecting the delicate inner ear from excessive oscillation of the chain of small bones.

Inner ear There are three parts to the inner ear: n

anteriorly, the cochlea with the organ of Corti, for hearing n in the middle, the vestibule with the utricle and saccule, which are concerned with static balance and linear acceleration n posteriorly, three semicircular canals in different planes – the organ of balance, which is concerned with angular acceleration.

The otic capsule of the inner ear contains perilymph and has connection with the subarachnoid space. Inside the capsule is the membranous labyrinth with sensory cells and containing the endolymph, which is produced by stria vascularis. Endolymph is absorbed mainly by the endolymphatic sac which lies in the posterior cranial fossa between the petrous bone and the dura. The cochlear and vestibular divisions of the VIIIth nerve join and travel through the internal auditory meatus to the brainstem. The VIIth (facial) nerve also travels through the internal auditory canal and traverses the medial and posterior walls of the middle ear cavity to emerge through the stylomastoid foramen.

Physiology Hearing The eardrum and the ossicles amplify sound waves through the lever effect of the ossicles and because the area of the eardrum is more than 20 times that of the footplate of the stapes. This allows reduction of acoustic impedance when sound energy is passed from air into liquid in the labyrinth. Micromechanical oscillations of the stapes result in movement of liquid in the cochlea and motion of the basilar membrane with the sensory hair cells. The point of maximum movement of the basilar membrane is determined by the frequency of the introduced tone: high-frequency tones correspond to a place in the basal turn of the cochlea; and low-frequency tones to one in the apical turn. The movement of the cilia of the receptor hair cells generates electric impulses in the cells, and bioelectric events then follow in the auditory nerve. Sound frequency is measured in hertz (Hz) where 1 Hz is equal to 1 cycle per second. The range of frequencies which can be appreciated as sound by humans is approximately 20 to 18 000 Hz. The ear can discriminate an enormous intensity range of 100 000 : 1, and for practical measurement it can be compressed into a logarithmic decibel scale of 0–120 dB.

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214  Ear and nose

Semicircular canals

Mastoid air cells Malleus Incus

Vestibule

Auditory nerve

Cochlea

Stapes Round window Tympanic membrane

Eustachian tube

External auditory meatus

Fig. 15.1  Anatomy of the ear. Balance Movement and acceleration in any of the three planes of the semicircular canals cause movement of the endolymph with deviation of the gelatinous cupola with the embedded sensory hair cells in the semicircular canals. In the saccule and utricle, there is displacement of the sensory hair cells, which are embedded in the gelatinous otolith membrane containing particles of calcium carbonate, and respond to changes in linear acceleration or gravity force. The stimulus triggers the action potential of the vestibular nerve. All of the inputs from the labyrinth, the eyes and somatosensors relay to the brain. Central processing takes place, and responses return to the muscles to maintain posture and eye position, with the cerebellum ensuring a smooth, coordinated response. An alteration in vestibular response on one side as opposed to the other, results in imbalance in the central response which affects control of the eyes, causing them to oscillate – vestibular nystagmus.

Common symptoms Common symptoms are: n n n n n

hearing loss – congenital or acquired (sudden or progressive) aural discharge otalgia – pain in the ear tinnitus – variable noises in the ear vertigo.

Otalgia Pain in the ear may arise from pain receptors supplied by the afferent fibres of: n

the Vth and Xth cranial nerves C2 and C3, which supply the external ear n the IXth, supplying the middle ear. n

When otalgia is a presenting symptom and no local dis­ ease is found in the ear, a referred otalgia is possible from a distant area innervated by any of the above nerves. Usual causes are: n

dental disease temporomandibular joint disorders n maxillary sinusitis n inflammatory and malignant lesions of the pharynx, posterior tongue and larynx n conditions in the back of the neck and cervical spine. n

Tinnitus The subjective perception of tinnitus, which is characterised by rushing, hissing or ringing sounds of varying intensity in the ear or head, may be associated with dysfunction in the cochlea and the auditory pathway. A rhythmic pulsatile tinnitus is suggestive of vascular lesions such as: n

arteriovenous malformations arterial aneurysms n glomus tumour in the middle ear n sound transmission from major vessels in the neck. n

Tinnitus can sometimes be detected objectively on auscultation of the ear and the mastoid. Crackling sounds can be associated with dysfunction of the Eustachian tube and rhythmic myoclonus of the muscles attached to it.

Vertigo Vertigo associated with a peripheral vestibular lesion is most commonly rotatory but can be experienced as a swaying or tilting of either the patient or the surroundings. Movement and positional changes tend to make the vertigo worse. Central vestibular lesions tend to produce less intense vertigo, positional changes have less effect and the patient

The ear  215 may experience disturbance of gait and other neurological symptoms and signs.

Clinical examination Examination of the auricle and the mastoid precedes otoscopic examination. Wax should be removed if it obstructs the view, but this should not be done by syringing if a perforation of the tympanic membrane is suspected, because of a risk of introducing infection. The normal tympanic membrane reflects the directed light in the shape of a cone which is seen in the antero-inferior part of the membrane. The prominent landmark is the handle of the malleus (Fig. 15.2). The tympanic membrane is divided into the pars tensa and the pars flaccida (the upper area). It is very useful to use examination with a microscope to evaluate scars, retractions and types of perforation. The presence of perforation may allow damage to the ossicles, granulations and choleste­ atoma to be seen. The nasal cavities and posterior nasal space must be examined in order to exclude infection or tumour which may cause Eustachian tube insufficiency or blockage and consequent failure of air circulation to the middle ear. A full assessment of the head and neck is performed to exclude referred otalgia.

AC) and then firmly on the mastoid process (bone conduction [BC], a measure of sensorineural function of the cochlea). Normally sound is detected better by AC than by BC. Conductive loss means that sound conduction through the middle ear apparatus is reduced. The convention is as follows: normal – AC better than BC → Rinne test positive conductive loss – BC better than AC → Rinne test negative n sensorineural loss – AC better than BC but both reduced compared with normal → Rinne test positive and reduced. n n

Weber test. A vibrating tuning fork is placed either on the vertex of the skull or on the forehead midway between the ears. The patient indicates on which side the sound is better lateralised by bone conduction. The interpretation is as follows: n

conductive loss – sound lateralised to the affected side n sensorineural loss – sound lateralised to the side with better cochlear function.

Pure tone audiometry

Investigations Auditory function There are different types of hearing loss, as follows: conductive – from lesions in the external auditory meatus and the middle ear n sensorineural – from cochlear and retrocochlear lesions n mixed – when both types of hearing loss are present.

The hearing threshold can be measured in decibels of hearing level (dBHL) for air and bone conduction at each frequency between 250 and 8000 Hz (Fig. 15.3).

n

Tuning fork tests Rinne test. A vibrating tuning fork which generates sound at 512 Hz is placed near the external meatus (air conduction,

Incus

Attic

Stapes (footplate in the oval window)

Impedance audiometry The middle ear compliance (i.e. how much of the applied sound energy is reflected from the tympanic membrane) and middle ear pressure (the difference, if any, between pressure externally and in the cavity) can be measured with an instrument applied to the ear canal. A very low compliance could be the result of a middle ear effusion. A lower or negative

Malleus

Pars flaccida of the tympanic membrane

Pars tensa of the tympanic membrane

Light reflex Round window

Fig. 15.2  The external aspect of the tympanic membrane.

THE EAR

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216  Ear and nose a

Head positional testing

Hearing threshold (dB)

-20

This can induce benign positional vertigo (BPV) and nystagmus when the defect is thought to be in the labyrinth and the detached otolith floats in the semicircular canal of balance. BPV occurs with a short latency, lasts a few seconds and fatigues on repetition; usually it is a self-limiting condition which resolves within a few months.

0 20 40 60

Electronystagmography

80

The velocity of nystagmus can be assessed by graphic recording. Labyrinthine nystagmus is enhanced when visual input is abolished by closing the eyes or by darkness.

100

b Hearing threshold (dB)

-20 0

Caloric test

20

This test is based on the principle of cooling or heating the labyrinth by a flow of water in the external ear canal. A convection current is set up in the semicircular canal which in turn induces vertigo and nystagmus. In vestibular hypofunction these may be reduced or absent.

40 60 80 100 125 250 500 1000 2000 4000 8000 Hz

Conduction:

Bone

Air (right ear)

Fig. 15.3  An audiogram. (a) Sensorineural loss with reduced hearing levels by both air and bone conduction. (b) Conductive hearing loss with reduced hearing level by air conduction and normal bone conduction.

pressure within the middle ear than without indicates insufficiency of the Eustachian tube.

DISEASES OF THE EXTERNAL EAR Foreign bodies In these cases, there is always a danger of forcing the foreign body further into the ear canal where it may damage the drum and the middle ear. Extraction of foreign bodies should therefore be done by skilled ear, nose and throat (ENT) personnel.

Electric response audiometry Electrical responses to sound stimuli can be recorded from the cochlea, brainstem and cortex. Auditory-evoked potentials of a few microvolts can be recorded from the scalp as the ‘auditory brainstem response’ which occurs within 10 ms. This has become a useful objective test in children and in patients in whom reliability of subjective audiometric tests is doubtful. It also has wide-ranging application in neurootological diagnosis and detection of acoustic tumours.

Vestibular function Clinical

Spontaneous and positional nystagmus, eye movements, stance, gait and limbs are all tested. Nystagmus. This condition is defined as involuntary (usually rapid) rhythmic, transverse (although occasionally vertical – see below) eye movements: n

Vestibular nystagmus is a rhythmic oscillating movement of the eyes resulting from either induced stimulation of the labyrinth or vestibular disease; it has a slow vestibular and a fast cerebral correcting component trying to restore the eye position in the direction of gaze. n Labyrinthine nystagmus is always horizontal-rotatory or horizontal. n Vertical nystagmus and multiple other forms occur only in central vestibular lesions.

Trauma to the auricle Aetiology and pathological features Haematoma of the auricle occurs in boxers and those who take part in other contact sports such as rugby football. The blood extravasates between the cartilage and perichondrium. If untreated, the blood becomes organised, causing a cauliflower deformity composed of fibrous tissues. Perichondritis and abscess may develop as a consequence of secondary infection. The cartilage deprived of vascular supply may undergo necrosis, leading to marked deformity of the auricle.

Management Prevention Suitable headgear should be worn by those engaged in contact sports.

Treatment The haematoma is evacuated through a wide-bore needle or by incision of the skin. A firm dressing must be applied in order to prevent further bleeding. If a subperichon­ drial abscess forms, it should be incised and drained. Pseudomonas aeruginosa is not uncommonly cultured in these patients, and broad-spectrum antibiotics are indicated.

Diseases of the middle ear  217

Furuncle Aetiology and pathological features This is an infection of hair follicles and is usually caused by Staphylococcus aureus. Recurrent infection may have diabetes as the underlying cause.

Clinical features There may be severe earache, and any movement of the auricle (and thus of the auditory canal) or pressure on the tragus causes considerable pain. Mild hearing deficit may occur in cases of complete obturation of the ear canal. The external canal will be oedematous, with swelling in front of or behind the auricle.

Management Furuncle is treated by a combination of the insertion of an antiseptic wick and systemic antibiotics.

Otitis externa Aetiology and pathological features Environmental factors which predispose to otitis externa are: n

heat humidity n swimming n any irritation which predisposes to scratching. n

Specific causes are: n n

infection – bacterial, fungal, viral reactive inflammation – eczema, seborrhoeic dermatitis, neurodermatitis.

A spreading necrotising type with osteomyelitis of the base of the skull may develop in immunocompromised or elderly diabetic patients. Pseudomonas aeruginosa and anaerobic organisms are often found.

Clinical features In the common irritative type, discharge from the ear and, sometimes, mild pain are present. In the spreading, necrotising variant, there is systemic disturbance, more severe local symptoms and signs of spread which may include the development of a VIIth nerve palsy.

Management In the mild type, treatment is by a combination of topical antiseptics or antibiotics incorporated into steroid-containing ear drops; if the condition is particularly troublesome, this is supplemented by systemic antibiotics after culture has been obtained. Aural toilet is essential, and infected debris is removed by mopping with a cotton wool carrier or by microsuction. Fungal infection may follow after prolonged treatment with antibacterial drops. In the severe necrotising form, therapy should consist of intensive local treatment with excision of dead tissue, the administration of systemic antibiotics and control of diabetes if this is present.

DISEASES OF THE MIDDLE EAR Acute otitis media Aetiology and pathological features The incidence is highest in the first 5 years of life and thereafter it becomes infrequent. Most children have a history of preceding viral upper respiratory tract infection. Inflammation of the postnasal space and adenoids may spread via the Eustachian tube to the middle ear. Oedematous mucosa in the tube causes blockage and, if secondary bacterial infection spreads along the tube, a middle ear abscess will result. Under the age of 5 years, Haemophilus influenzae is isolated in about 30% of cases. As tension rises, rupture of the tympanic membrane occurs usually in the pars tensa. In the majority, the inflammation resolves and the tympanic membrane heals without any sequelae. However, in a small proportion, complications develop and there is loss of hearing. Other problems are: n

a chronic middle ear effusion in about 5% scarring of the tympanic membrane and the middle ear (tympanosclerosis) n chronic suppurative otitis media consequent to a non-healing perforation n progression to acute mastoiditis. n

Clinical features Symptoms Pain and hearing loss are early symptoms; if the drum perforates, a purulent discharge develops and the pain usually subsides.

Signs There is malaise and pyrexia. The drum is reddened and tense. A perforation may be visible with discharge emerging through it.

Management Amoxicillin is the preferred drug in children and should be administered for 10 days.

Acute mastoiditis Aetiology and pathological features Mastoiditis is the consequence of a preceding otitis media, and with the advent of powerful antibiotics the incidence has diminished considerably. Nevertheless, silent or masked mastoiditis can develop. There is cellulitis and osteitis in the air spaces which may go on to abscess formation. Spread can take place through the temporal bone to cause subperiosteal abscess or intracranial complications – an extradural abscess.

Clinical features Symptoms Symptoms are: n

pain fever n aural discharge n hearing loss. n

Diseases of the external ear Diseases of the middle ear

15 

218  Ear and nose

Signs Signs are: n n

erythematous swollen mastoid and external canal the ear is pushed outward and forward if subperiosteal abscess develops.

Investigation Sometimes, because of swelling in the canal, it is difficult to visualise the inflamed drum. Mastoid X-ray shows clouding of the air cells and sometimes formation of an abscess with erosion of bone.

Management Very early stages are treated with intensive parenteral antibiotics. If resolution fails to occur, the inflammatory process is decompressed by a simple cortical mastoidectomy, preserving the posterior meatal wall and the middle ear ossicles.

Otitis media with effusion The alternative names for this condition are chronic serous otitis media and glue ear.

Fig. 15.4  A grommet inserted into the anterior inferior quadrant of the left tympanic membrane.

Aetiology and pathogenesis Accumulation of non-purulent fluid in the middle ear is common in children aged between 2 and 6 years. Many causative factors have been suggested, but the most probable is low-grade inflammation with partial block and dysfunction of the Eustachian tube and interference with the free flow of air in and out of the middle ear so that negative pressure develops in the middle ear.

Clinical features Symptoms Symptoms are:

Middle ear effusion in adults Aetiology and pathogenesis Serous middle ear effusion may develop after: n

an upper respiratory tract infection allergic or vasomotor rhinitis n exposure to changes in ambient pressure such as flying or diving (barotrauma) when the Eustachian tube does not equalise pressure. n

impaired hearing delay in learning to speak and acquiring a vocabulary n other learning difficulties n inattentiveness n recurrent earaches.

In adults, carcinoma of the postnasal space invading the Eustachian tube is a rare precipitating cause.

Signs

This condition usually follows acute otitis media and has the same underlying causes. However, it may be chronic from the outset. There are two types:

n n

Many children with this condition are discovered during routine audiometric screening. Otoscopic examination reveals a lustreless immobile tympanic membrane. Sometimes fluid levels can be seen in the middle ear. In long-standing disease the drum may become thin, atrophic and retracted.

Management In many instances, reassessment after 3 months is advisable because in more than 90% the effusion will resolve spontaneously. Unresolved middle ear effusion with hearing loss requires anterior–inferior myringotomy, aspiration of the liquid and a ventilation tube (grommet) inserted into the tympanic membrane (Fig. 15.4). If there are associated features of nasal obstruction, the adenoids are curetted. The ventilation tube remains in the tympanic membrane for about 12 months, helping to restore to normal the mucus-producing mucosa of the middle ear, and is then spontaneously extruded from the tympanic membrane.

Chronic suppurative otitis media Aetiology and pathological features

n

tubotympanic suppuration, which is limited to inflammation of the mucosa n attico-antral disease with destruction involving the mastoid bone. In the former, complications are unlikely, while the latter is unsafe.

Clinical features Tubotympanic disease The discharge is mucopurulent but it may cease and reappear after an upper respiratory tract infection or if water passes through the perforation in the tympanic membrane. This opening is central in the pars tensa and does not involve the bony margins (Fig. 15.5a). An audiogram shows conductive hearing loss.

Diseases of the middle ear  219 Attico-antral disease This presents as suppuration with or without cholesteatoma. The latter is a mass of keratinised squamous epithelium which increases in size as skin desquamates. Initially it forms in the developed retraction pocket of a perforated tympanic membrane in the attic. Spread then occurs, so destroying the middle ear ossicles and the temporal bone and eroding the bony canal of the facial nerve. Hearing loss can be marked. Vertigo may be present if the cholesteatoma has eroded the bony wall of the most prominent lateral semicircular canal, causing a fistula. Otoscopy reveals a superior perforation leading into the attic or a posterior marginaltype perforation involving the bony margin Fig. 15.5b. With bony involvement, granulations are common. Flakes of cholesteatoma can be seen in the area of the attic. CT may sometimes be helpful to reveal the extent of the bony erosion and the fistula of the lateral semicircular canal of balance.

Management Tubotympanic disease Active suppurative tubotympanic disease is treated with combined antibiotic and corticosteroid ear drops. For those who do not wish to wear a hearing aid or who want to swim, repair of the tympanic membrane (myringoplasty) can be done when the perforation is dry. The tympanic membrane can be supplemented by a graft of fascia from the temporalis muscle.

Attico-antral disease Conservative treatment is ineffective in the presence of cholesteatoma. Classical radical mastoidectomy lays open the mastoid and excises the posterior meatal wall and the contents of the tympanic cavity (apart from the stapes) to create one safe cavity. Reconstruction of the tympanic membrane with a fascial graft and artificial ossicles (tympanoplasty), with the aim of improving hearing, may then be considered.

Complications of otitis media a

Pathological features The infective process in both acute and chronic otitis media may cause bone destruction and may also spread along veins, so leading to intracranial sepsis and the complications listed in Box 15.1. Figure 15.6 illustrates the complications that can arise.

Clinical features In chronic otitis media, the development of pain in the ear and headache are a warning of a possible intracranial complication. Vertigo occurs in labyrinthitis, and suppuration will lead to complete destruction of the hearing and balance organs. In developed intracranial complications the symptoms and signs are those of: n

systemic infection meningitis n raised intracranial pressure (Ch. 30) n focal neurological abnormalities. n

b

CT and MRI of the head are essential for accurate diagnosis.

Management Joint management with the neurosurgeon is essential. The underlying disease in the mastoid is explored as described above. Box 15.1 

Complications of otitis media

Intratemporal n Mastoiditis n Labyrinthitis n Facial nerve palsy

Fig. 15.5  (a) Large perforation of the tympanic membrane in the pars tensa. (b) Chronic otitis media with cholesteatoma and granulations in the attic.

Intracranial n Extradural abscess n Meningitis n Lateral sinus thrombosis n Temporal lobe abscess n Cerebellar abscess

15 

220  Ear and nose

7

6

5 4

3

1

Fig. 15.6  Complications of otitis media. 1. Mastoiditis with subperiosteal abscess. 2. Mastoiditis with pus from the air cells of the tip of the mastoid spreading into the neck. 3. Sigmoid sinus thrombosis. 4, 5 Cerebellar abscess. 6. Epidural abscess. 7. Brain abscess in the temporal lobe.

2

Otosclerosis

n

Aetiology and pathological features

n

Otosclerosis is a localised disease of bone which affects the otic capsule. It is inherited as an autosomal dominant trait with incomplete penetrance. New spongy bone forms and, if this is in the area of the stapes, there may be ankylosis and conductive deafness.

Clinical features History There is a strong family history and both ears are affected in 90% of patients. The first manifestations are in the second decade and are progressive. Pregnancy and lactation aggravate the condition.

Physical findings The tympanic membrane is normal and mobile in the presence of conductive hearing loss on an audiogram.

Management If the patient does not wish to have a hearing aid, then stapedectomy is advised. The operation restores the mobility of the ossicular chain by perforating the stapes footplate, removing the arch of the stapes and replacing this with a piston prosthesis.

DISEASES OF THE INNER EAR Sensorineural hearing loss The causes of this kind of loss are: n n

genetic abnormalities of the cochlea maternal infections during pregnancy – rubella, cytomegalovirus, syphilis

n n n n n n

perinatal hypoxia viral and bacterial labyrinthitis meningitis ototoxic drugs – gentamicin, neomycin, furosemide (frusemide), salicylates sudden idiopathic hearing loss (possibly viral or vascular) noise-induced hearing loss fracture of the temporal bone and trauma to the ear barotrauma, rupture of the round window membrane, perilymph leak.

In acquired hearing loss, the high audiometric frequencies are usually affected first, and this type of loss is associated with hair cell loss in the basal turn of the cochlea. Tinnitus is often associated with sensorineural loss. Presbycusis is sensorineural hearing loss with ageing; an audiogram reveals bilateral symmetrical high-frequency loss. Exposure to high-intensity noise causes characteristic bilateral hearing loss on the audiogram with a dip at 4000 Hz as the earliest change with depletion of hair cells at the basal turn of the cochlea.

Management Hearing aids Normal speech is at an intensity of 40–70 dB, and some form of amplification is required if the audiogram shows a hearing loss of more than 40 dB. An aid may also have a masking effect on tinnitus, which is often associated with sensorineural hearing loss. Air conduction aids consist of a miniature microphone, an amplifier and a receiver which feed the sound into the ear, and a mould in the auditory canal. The apparatus is usually

Diseases of the inner ear  221 mounted behind the ear, but the advent of microelectronics means that a more cosmetically acceptable aid can, in mild to moderate loss, be placed entirely within the auditory canal. Improved signal processing and programmable digital multichannel aids work more selectively to amplify various speech frequencies and reduce interference from ambient noise. Bone conduction aids are used when there is a congenital absence of the pinna and atresia of the canal. The aid is anchored to a titanium screw in the mastoid that has become

osseo-integrated by ingrowth of bone. Sound waves are transferred into the cochlea by bone conduction.

Cochlear implant Those who do not benefit from even the most powerful hearing aid and have profound bilateral deafness usually have a destroyed receptor organ and may be considered for a cochlear implant. In this procedure, electrodes are inserted into the spiral of the cochlea to stimulate the surviving neurons electrically (Fig. 15.7). Speech is coded in a small

a Cord to speech processor

Transmitter coil Receiver coil

Electrode array

b

Fig. 15.7  The electrodes of the cochlear implant are inserted and stimulate the surviving nerve endings. (Adapted from H.G. Hirsch. Intelligibility improvement of noisy speech for people with cochlear implants. Speech Communication 12 (1993) 261−266. Reproduced by permission of Cochlear™.)

Diseases of the inner ear

15 

222  Ear and nose

speech processor worn externally and transmitted across the skin behind the ear into the implant. The patient hears the sound (about 50% can discriminate speech without having to lip read), and their speech production improves.

Clinical features Symptoms There is a characteristic triad of symptoms which recur: n

Acoustic neuroma Clinical features The early symptoms are unilateral or markedly asymmetric sensorineural hearing loss and tinnitus. Such patients should be suspected of having an acoustic tumour unless there is a clear association with trauma or acute infection. Vertigo is rare, but patients with large tumours may have ataxia. Numbness of the side of the face (Vth nerve) follows.

Investigation The audiogram reveals unilateral sensorineural hearing loss. MRI scan of the internal auditory meatus and the posterior cranial fossa reveals even the smallest tumour (Fig. 15.8).

Management The tumour is removed by neurosurgery. The smaller the tumour, the easier is the operation and the less the likelihood of damage to the facial nerve. A proportion of tumours may not grow further and the patient may be followed up by monitoring the tumour size at 6-monthly intervals on MRI. Another option is gamma knife radiosurgery to arrest the growth of the tumour; this may be considered in particular for elderly patients.

Ménière’s disease Pathological features Endolymphatic hydrops, which causes distension of the membranous labyrinthine spaces, is thought to be a pathological feature of Ménière’s disease, but the reason for this is unknown.

attacks of vertigo fluctuating sensory hearing loss at low audiometric frequencies n tinnitus. n

Some patients also experience a sensation of fullness and pressure in the ear during the attack. Over years the hearing gradually deteriorates in the affected ear, and occasionally the disease is bilateral.

Signs There are no specific physical findings.

Management Attacks of vertigo are treated with vestibular sedatives (diazepam, cinnarizine, prochlorperazine). A salt-restricted diet is advised in an endeavour to reduce the frequency of attacks. It is thought that betahistine may have a positive prophylactic effect on the microcirculation in the cochlea, and it also has a positive effect on balance by reducing vestibular receptor resting firing rate. Surgery is indicated if medical treatment fails. Decompression of the endolymphatic sac and vestibular neurectomy does not destroy hearing and therefore is preferred to labyrinthectomy, which destroys the inner ear completely. Injections of gentamicin into the middle ear and delivery to the membranous round window through which it diffuses into the inner ear are effective in alleviating vertigo by reducing vestibular function.

Ear trauma and fracture of the skull base Pathological and clinical features Fractures of the temporal bone are associated with a severe head injury. Haematoma over the mastoid and blood in the external canal are important signs easily detected on simple clinical examination. A leak of cerebrospinal fluid (CSF) into the middle ear and through the auditory canal is a complication of fracture of the middle cranial fossa. CSF may also escape from the middle ear through the Eustachian tube – CSF rhinorrhoea. Conductive hearing loss is the result of blood in the middle ear (haemotympanum) or disruption of the ossicular chain. Vertigo or imbalance may suggest rupture of the round or oval windows. Profound deafness occurs if the fracture extends into the inner ear and may be associated with the above symptoms and also tinnitus. Fractures which involve the facial canal may produce a VIIth nerve palsy.

Management

Fig. 15.8  MRI scan showing small left acoustic tumour.

The ear canal should not be syringed, nor should drops be instilled, because of the risk of introducing infection. Antibiotics are given and any CSF leak usually settles spontaneously. At a later stage, reconstruction of the ossicle chain (ossiculoplasty) may be needed to improve hearing. Very occasionally, exploration of the facial nerve is indicated with neural repair. Compensation for vestibular dysfunction can take several months.

The nose and paranasal sinuses  223 THE NOSE AND PARANASAL SINUSES

THE NOSE AND PARANASAL SINUSES Anatomy A central septum divides the nasal cavity into two halves and supports the cartilaginous part of the nose. The anterior part is cartilage and the posterior bone. The lateral wall has three turbinates – inferior, middle and superior – with a corresponding meatus under each turbinate (Fig. 15.9). The anterior ethmoidal cells and the maxillary and frontal sinuses open into the middle meatus, and their ostia, which are close together, form the ostiomeatal complex. The posterior ethmoidal cells and the sphenoid sinus open into the superior meatus. The nasolacrimal duct opens into the inferior meatus. The relationships between the sinuses and other structures have clinical importance in the spread of infection and tumours and in trauma. The maxillary, ethmoidal and frontal sinuses are related to the orbit, and the ethmoidal and frontal sinuses to the anterior cranial fossa. The sphenoid sinus is concealed by its position. On the lateral sides of the sinus lie the cavernous venous sinus, the internal carotid artery and the IIIrd, IVth and Vth cranial nerves. The pituitary fossa intrudes into the roof. The arterial supply of the nose is provided from branches of both external and internal carotid arteries. The venous drainage is extracranial, but there are intracranial communications. The nerve supply to the nose and its sinuses is from the trigeminal nerve. The olfactory epithelium is in the branches of the superior part of the nose, and the filaments of the olfactory nerve pass through the cribriform plate. Autonomic sympathetic and parasympathetic fibres provide vasomotor innervation to the cavernous tissue in the nasal mucosa and also secretomotor control. The parasympathetic

Frontal sinus

Orbit

fibres relay in the pterygopalatine ganglion, and their stimulation causes swelling and increased secretion from the mucosa.

Physiology The functions of the nose and sinuses are: n n n n n n

air passage to and from the lungs warming, humidification and cleaning of incoming air (air conditioning) protection by mucociliary transport and immunological factors sense of smell resonators for speech production initiation of nasal reflexes – sneezing.

General features of nasal and sinus disease Clinical features Symptoms These include: n

nasal obstruction – which can be unilateral or bilateral, intermittent or permanent n mouth breathing – because of nasal obstruction, which in turn leads to dryness in the throat n discharge and postnasal drip – clear serous discharge is common in allergic conditions and mucous or purulent discharge is associated with rhinosinusitis.

Frontal sinus

Orbit

Ethmoid sinus Superior turbinate Nasal septum Middle turbinate

Maxillary sinus Inferior turbinate

Fig. 15.9  Coronal section to show the sinuses and particularly the ethmoid air cells.

15  n

n n n n

224  Ear and nose A unilateral discharge in a child probably originates from a foreign body. A bloodstained discharge with unilateral symptoms may be associated with tumour. Unilateral copious watery discharge suggests CSF rhinorrhoea facial pain – dull and well-localised, although it sometimes may radiate into the teeth and around the eyes or ear headaches, especially in sphenoiditis loss of smell bleeding cosmetic nasal deformity.

It is important to distinguish sinus pain from neuralgia, and referred pain from the teeth, temporomandibular joint or cervical spine.

Signs The anterior part of the nose can be examined using a nasal speculum and a head light. Deformities of the septum, mucosal changes, prominent vessels and inferior and middle turbinates can be seen. Nasal polyps, tumours, ulcerations and foreign bodies can be identified. The posterior nasal space with the choanae and openings of the Eustachian tubes can be examined through the mouth by introducing a small mirror behind the soft palate. Application of decongestant drops or 10% cocaine spray causes vasoconstriction and, by reducing the swelling of the mucosa, improves visibility. Cocaine also has a topical anaesthetic effect, and rigid or flexible nasal endoscopes can be used to examine the ostiomeatal complex and the posterior part of the nose and the postnasal space.

Smell A short exposure to various bottles containing pungent substances establishes whether smell is reduced or distorted.

COMMON CONDITIONS OF THE NOSE AND PARANASAL SINUSES Nasal foreign bodies It is not unusual for children to insert foreign bodies into a nostril. The object may go undetected for some time, and presentation is with symptoms of unilateral purulent and sometimes offensive discharge. A radio-opaque concealed foreign body may be seen on X-ray. It should be removed with forceps or a hook, a procedure which may require a general anaesthetic.

Fractures of the nose A nasal injury may be associated with other fractures of the face, including those of the zygoma, bony orbit and middle third of the face.

Clinical features The symptoms are: n

nasal deformity obstruction n bleeding. n

Examination of the nasal cavity may reveal: n

deviated septum septal haematoma.

Investigation

n

Imaging

Management

Plain X-ray will show if there is gross disease. CT scanning of the sinuses gives precise images and shows mucosal swelling, fluid levels or opacity as well as bony erosion by tumours. MRI is especially useful for delineating tumour spread.

Rhinomanometry Nasal resistance to airflow can be calculated from measurements of flow and transnasal pressure. However, the results do not always correspond to the subjective feeling of nasal obstruction.

Immunological Skin prick tests may identify a possible allergen. A weal of at least 2 mm diameter and greater than the reaction to the control solution is considered positive. The serum-specific IgE and the radio allergosorbent test (RAST) quantify an allergic response.

Mucociliary clearance Saccharin is placed in the front of the nose and the time (normally 20 minutes) is measured for a sensation of sweetness to be recognised as the substance reaches the pharynx on the mucous blanket.

Displaced nasal fractures may be reduced immediately or in 7–10 days after swelling has subsided. For old nasal injuries, the nasal deformity may be corrected by mobilising the external nasal pyramid by performing osteotomies of the nasal bones and rhinoplasty. A plaster of Paris splint is applied for 2 weeks to stabilise the nasal bones.

Septal haematoma and abscess Pathological features After nasal trauma a haematoma may develop between the mucoperichondrial flaps of the septum. The outcome may be that the septal cartilage is deprived of its blood supply. Secondary infection can develop, and an abscess may form. If untreated, the cartilage may undergo necrosis and the nasal bridge loses its support, leading to a saddle-type nasal deformity. Upon examination, the septum will be very swollen and fluctuant to palpation with a probe.

Management The haematoma must be incised and drained. Nasal packing should be applied so as to allow the perichondrium to adhere to the cartilage. Antibiotics should be given.

Common conditions of the nose and paranasal sinuses  225

Deviated nasal septum A septal deviation can be either traumatic or developmental. In either event, nasal obstruction results. The patient will complain of such obstruction, and the deviation will be apparent on clinical examination.

or, alternatively, the sphenopalantine artery, which is the branch of the maxillary artery in the back of the nose, can be clipped by an endoscopic intranasal approach. If the bleeding arises from the upper part, the ethmoidal arteries are ligated by gaining access through the medial wall of the orbit.

Management

Rhinosinusitis

Submucous resection (SMR) of the septum is done by elevating the mucoperichondrial flaps and resecting the deviated part of the septal cartilage and bone. In septoplasty, the cartilage is mobilised and the excision is more conservative. Excessive resection of the cartilage may lead to collapse of the nasal dorsum and tip. A septal perforation may occur if the mucoperichondrial flaps are perforated on both sides.

Aetiology and pathological features

Epistaxis Pathological features Bleeding from the anterior part of the nose is more common and less severe than that from the posterior part, where the arteries are larger and have undergone degenerative change in older patients. Several vessels anastomose in the anterior septum, known as Little’s area, which is a frequent site of origin of bleeding. Bleeding can be the consequence of local or systemic causes, which include: n n

n n n n

trauma – nose-picking, fracture, surgery tumours – angioma, angiofibroma of postnasal space, carcinoma of the nose, postnasal space or sinuses local infection with ulceration prominent vessels in Little’s area atherosclerotic degeneration of greater nasal arteries haematological – blood disease, bleeding diatheses, hereditary telangiectasia, coagulation defects, treatment with anticoagulants.

Management The nose is anaesthetised and decongested with lidocaine and phenylephrine. The bleeding vessel can be cauterised chemically with silver nitrate or by electrocautery. More accurate cauterisation of the bleeding vessels may be achieved by using a fibreoptic naso-endoscope, particularly in the posterior aspect of the nasal cavity. If the bleeding point cannot be identified or is not controlled with cautery, a Merocel expandable nasal tampon or ribbon gauze impregnated in bismuth iodoform paraffin paste (BIPP) is packed into the anterior nasal cavity. When the bleeding is from the back of the nose and anterior packing is ineffective, an epistaxis balloon is introduced through the nose into the postnasal space to occlude the posterior nares and choanae; it is then drawn forward through the nose and secured. When even a balloon is ineffective, re-insertion of a postnasal pack through the mouth and securing this in front of the nose is required and is combined with anterior packing usually under general anaesthesia. The packs remain for 48 hours, during which time antibiotics are necessary. Frequently, repeated haemorrhage may require ligation of the appropriate vessel. The external carotid artery can be ligated in the neck

Pathological changes in the nasal cavities are usually accompanied by similar mucosal changes in the sinuses. The causes are: n

allergy infective n non-allergic n autonomic n

In allergic rhinitis, inhaled substances are the most common allergens. Pollens from grass, trees and flowers are responsible for seasonal symptoms. House dust, the house dust mite, and dog and cat fur cause more-perennial symptoms. Autonomic rhinitis is a disorder of the autonomic nervous system in which a predominance of parasympathetic stimulation causes swelling of the nasal mucosa and hypersecretion. Acute infective rhinitis is that which occurs in the common cold as a result of viral infection. Secondary bacterial infection may supervene, and the common microorganisms are Haemophilus influenzae and Streptococcus pneumoniae. Sinusitis is usually an extension from the nasal infection. Any condition which interferes with mucociliary transport, drainage and ventilation, including mechanical factors such as a deviated septum, polyps, hypertrophy of the turbinates and swollen mucosa, especially around the ostiomeatal complex, predisposes to the development of infective sinusitis. Swollen mucosa blocks the natural ostia of the sinuses. Pus reduces the activity of cilia, thus leading to stasis in the sinuses. In chronic infection, the mucosa may be damaged and granulations may develop. Infections of the maxillary sinus can also develop from a dental abscess. Mycotic infections occasionally occur in immunosuppressed and diabetic patients.

Clinical features Allergic rhinitis Symptoms

Symptoms include: n

nasal itching bouts of sneezing n profuse watery discharge n postnasal drip. n

In chronic allergic rhinitis, nasal stuffiness is a prominent symptom.

Signs The mucosa will look oedematous and wet and the turbinates can become hypertrophic.

Infective rhinosinusitis Symptoms

Symptoms are usually unilateral and include:

Common conditions of   the nose and paranasal sinuses

15 

226  Ear and nose

n

pain over the affected sinus and around the eye headache n mucopurulent discharge n nasal obstruction n loss of smell. n

In chronic infection, pain may not be present.

Signs The mucosa will be congested and the turbinates swollen with muco-pus in the nasal cavity. The sinus can be tender to palpation. Sinus X-ray and CT may reveal opaque sinuses or a fluid level (Fig. 15.10). Bacteriological studies should be carried out on the muco-pus.

Management Allergic rhinitis Once the allergen is known, appropriate advice should be offered on how best to avoid it, although there is no evidence of benefit from attempts at eradication of the house dust mite. Desensitisation is possible, but carries a small risk of anaphylaxis. Antimuscarinic ipratropium bromide is sometimes helpful in autonomic rhinitis. The prophylactic use of a mast cell stabiliser (sodium cromoglicate) and steroid sprays is effective in allergic rhinitis, and they do not seem to have any adverse systemic effects. If the symptoms are not controlled by sprays, non-sedating oral antihistamines can be added. If medical treatment fails to relieve the nasal obstruction, the enlarged hypertrophic turbinates can be reduced by diathermy to the inferior turbinates.

infection do not resolve. A trocar and cannula are passed through the thin medial wall of the sinus under the inferior turbinate. The washout is examined bacteriologically. Intranasal antrostomy is a permanent large opening made under the inferior turbinate or usually by expanding the natural ostium in the middle meatus. Radical antrostomy (Caldwell–Luc operation) removes the anterior wall of the maxillary sinus above the gum. The irreversibly changed granulating mucosa is then removed. Operations on the ostiomeatal complex open the maxillary ostia, the ethmoidal air cells and fronto-ethmoidal duct, and the maxillary and sphenoid ostia, so enabling their ostia to be expanded intranasally under direct vision using a fibreoptic endoscope – endoscopic sinus surgery. External ethmoidectomy decompresses the orbit where there are orbital complications due to unresolving ethmoiditis and abscess formation. The incision is made between the medial canthus of the eye and the bridge of the nose, and after it has healed the scar is invisible. Frontal sinus trephine is indicated when the frontonasal duct remains blocked and serious complications are imminent. The incision is made below the lower margin of the eyebrow and a hole drilled through the orbital wall of the sinus. A plastic tube is left in situ to permit irrigation of the sinus. Fronto-ethmoidectomy is carried out for complications of sinus infection and when there is permanent change to the mucosa which requires its removal. It is also undertaken for mucoceles of the sinus. A large frontonasal opening is created for drainage and a plastic tube left in for several months.

Infective rhinosinusitis Initially, acute sinusitis is treated with antibiotics (amoxicillin) and decongestant drops (0.5% ephedrine, xylometazoline) which reduce the swelling of the mucosa and may improve ventilation and drainage through the natural ostia. Surgery of varying extent is required to re-establish air flow, drainage and mucociliary clearance when medical treatment has proved ineffective. Sinus washout is done under local anaesthesia with lidocaine and phenylephrine in acute sinusitis if the pain and

Complications of infective sinusitis The following may occur in acute or chronic sinusitis: n

orbital complications – periorbital cellulitis, subperiosteal abscess, blindness, suppuration of orbital contents n osteomyelitis complications – in the frontal bone and maxilla; a discharging sinus may follow n intracranial complications – meningitis, extradural, subdural and brain abscesses, cavernous sinus thrombosis. Orbital and intracranial complications more often follow infection in the adjacent ethmoidal, frontal and sphenoid sinuses. Infection spreads: n

along veins by rupture of an abscess through eroded thin bone and then periosteum n through a bony defect after injury. n

Clinical features Orbital complications Symptoms

Symptoms are:

Fig. 15.10  CT scan of the sinuses showing opaque left maxillary sinus due to sinusitis.

n n

diplopia and restricted eye movement reduction of visual acuity.

Tumours of the nasal cavity and sinuses  227 Signs Signs are: n n

swollen eyelids proptosis with displacement of the orbit outwards and downwards.

Intracranial complications Symptoms

Symptoms are: n

headache drowsiness n photophobia. n

Signs

Unilateral nasal polypoidal swellings should always be subject to biopsy and histological examination to exclude a tumour.

Management Medical treatment with topical steroid sprays can be employed if the symptoms are not severe, the polyps are small and there is no associated infection. However, in the majority, surgical removal is required. A snare or forceps is used close to the stalk, and sometimes the ethmoidal air cells are also cleared. The postoperative use of a steroid spray can reduce recurrence. A short course of systemic steroids could be considered in severe recurrent polyposis.

Signs are: n

pyrexia and rigors personality changes (frontal abscess) n fits and neurological localising signs. n

Cavernous sinus thrombosis occurs rarely and is characterised by: n

proptosis swelling of the eyelids and conjunctiva n ophthalmoplegia. n

Investigation of complications CT scan demonstrates opaque sinuses, bony defect, abscess formation in the ethmoidal and orbital areas with displacement of the eye, and brain abscess.

Nasal polyps Aetiology and pathological features Nasal polyps are pale greyish pedunculated oedematous mucosal tissue masses which project into the nasal cavity. Usually they originate in the region of the ethmoids but can arise from any part of the nose or sinuses, and usually they are multiple and bilateral. Their cause is not fully understood. They are rare in children and, if found, the possibility of mucoviscoidosis should be considered. Confusion may also occur with a congenital meningocele. In about 25% of cases, they are associated with asthma and in 8% there is a linkage with both asthma and aspirin sensitivity. Polyps have a tendency to recur following treatment.

Clinical features Symptoms Nasal obstruction is the main complaint. Loss of smell and sneezing are common. Nasal polyps may block the ostia of a sinus and predispose to development of secondary sinus infection and a mucopurulent discharge.

Signs The lesions are visible on endonasal examination, although a polyp may develop in the maxillary sinus and protrude through the ostium into the back of the nasal cavity and the postnasal space (antrochoanal polyp).

Investigation A sinus X-ray may show swollen mucosa but is not of particular help.

TUMOURS OF THE NASAL CAVITY AND SINUSES Both benign and malignant tumours in the nasal cavity and sinuses are rare.

Benign tumours Inverting papilloma The presentation is with unilateral nasal symptoms, usually of obstruction. The examination will reveal a unilateral polypoidal swelling, biopsy or removal of which will reveal the benign nature of the tumour. It has a tendency to recur and there is a small risk of malignant change. A CT scan indicates the extent of the tumour. The tumour is removed using the lateral rhinotomy approach, with the incision on the side of the nose.

Osteomas An osteoma may be an accidental finding on sinus X-ray and is more common in the frontal sinus. The frontonasal duct may be obstructed and be responsible for sinusitis or mucocele. Sometimes osteomas expand in all directions, causing pressure erosion of the bony walls of a sinus. In the presence of symptoms, they are removed using a frontoethmoidectomy or sometimes an osteoplastic frontal flap operation which lifts the anterior wall of the sinus.

Angiofibroma Found only in adolescent males, this tumour occurs in the posterior part of the nose and the postnasal space and expands towards the base of the skull. Patients present with frequent severe nose bleeds. Embolisation to reduce vascularity is carried out before removal by surgery. Radiotherapy is used in some centres.

Malignant tumours The majority of malignant tumours are of squamous cell origin. An increased occurrence of adenocarcinoma has been described in workers with wood.

Tumours of the nasal cavity and sinuses

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228  Ear and nose

Tumours arising in the nasal cavity and the ethmoids present with nasal and eye symptoms when they expand towards the orbit. Maxillary tumours present late with dental, orbital and nasal symptoms and facial swelling. Sometimes the first feature is a lymph node in the neck. Treatment in most cases is by a combination of radiotherapy and surgery. Maxillectomy may need to be combined with exenteration of the orbital contents. Craniofacial resection may be required when there is an extension of tumour into the anterior cranial fossa.

FURTHER READING Behrbohm H, Kaschke O, Nawka T, Swift A 2009 Ear, nose, and throat diseases: with head and neck surgery, 3rd edn. Thieme, Stuttgart Clarke R, Bull PD 2007 Diseases of the ear, nose and throat (Lecture Notes Series), 10th edn. Blackwell Publishing, Oxford Lalwani A 2007 Current diagnosis and treatment in otolaryngology – head and neck surgery, 2nd edn. McGraw-Hill Medical, New York

16 

Chest and lungs

Lung cancer

229

Other lung tumours

234

Principles of chest drainage

234

Pneumothorax

235

Chest trauma and haemoptysis

238

The pleura

239

LUNG CANCER Epidemiology Lung cancer was rare in the 19th century. Carcinoma of the lung is now the most common cause of cancer death in the world (almost one million deaths per year) and the third most common cause of death overall. The incidence is rising in women, and lung cancer is now the leading malignant cause of death for this group too, ahead of breast cancer. Approximately 1% of the USA’s gross national product is spent on the management of lung cancer patients. Lung cancer is strongly associated with smoking. Smoking is also often responsible for most cases of chronic obstructive pulmonary disease (COPD), but there is no direct correlation between COPD and lung cancer. As discussed below, this has important therapeutic consequences.

Aetiology Tobacco There is a very clear association between lung cancer and tobacco, often with a latent period of 10–30 years. The risk factors are the number of cigarettes consumed per day, the age of onset of smoking (those who start smoking before 16 have the greatest damage to DNA), the length of time of smoking, the type of tobacco – unfiltered, high-tar and nicotine cigarettes give the highest risk. Cigar and pipe smoking are also associated with an increased risk of lung cancer, but this is of a lesser magnitude than with cigarette smoking. Passive exposure to tobacco smoke is also a risk. Following smoking cessation the risk of developing lung cancer slowly decreases, but never reaches the level of lifelong non-smokers.

Other factors Exposure to asbestos and certain chemicals, toxic metals and radioactive compounds and byproducts (radon) also increase the risk of developing lung cancer.

Infectious lung conditions requiring   surgery

242

The mediastinum

243

Surgery for emphysema

244

Transplantation

244

Standard thoracic incisions

244

Postoperative care

245

Pathological features Lung cancers are commonly divided into small-cell carcinoma (SCC), derived from neuroendocrine cells, and nonsmall-cell lung cancer (NSCLC), of epithelial origin (Box 16.1). The figures quoted below are US data, but similar figures are seen in western Europe.

Non-small-cell carcinoma Squamous-cell carcinoma

This used to be the commonest type, accounting for 60% of lung tumours. It now represents around 30% of lung cancers in the USA. They tend to be fairly central lesions, and can be slow growing with later development of metastases. The growth starts as squamous metaplasia and progresses first to carcinoma in situ and then invasive carcinoma. Although usually solitary, there may be more than one area of primary squamous carcinoma occurring both in the lung and elsewhere in the upper aerodigestive tract at one time. Continuing to smoke after treatment encourages further de novo development of squamous carcinoma in any of these locations.

Adenocarcinoma This is now the most frequent type of lung cancer, accounting for around 40% of lung cancers in the USA. It has a tendency to be more peripheral, arising in the small bronchial glands, because of deeper inhalation of the smoke from filtered low-tar and low-nicotine cigarettes (which is the way the smoker extracts the same amount of nicotine from them). These do have a tendency to metastasise earlier. Bronchoalveolar carcinoma is a subtype of adenocarcinoma which respects the normal lung architecture. It can be multifocal and bilateral.

Large-cell carcinoma These are poorly differentiated epithelial tumours which do not meet the criteria to be classified as either squamous-cell

16 

230  Chest and lungs Box 16.1 

Pathological classification of lung tumours

Lung cancer n Small-cell carcinoma n Non-small-cell carcinoma – Squamous-cell carcinoma – Adenocarcinoma – Large-cell (undifferentiated) carcinoma Neuroendocrine tumours n Benign – typical carcinoid n Intermediate – atypical carcinoid (= well-differentiated neuroendocrine carcinoma) n Malignant – Large-cell neuroendocrine carcinoma – Small-cell carcinoma

carcinoma or adenocarcinoma. They represent 10–20% of lung tumours. They have no distinguishing distribution or macroscopic appearance.

Small-cell carcinoma and   neuroendocrine tumours Small-cell carcinoma represents around 20% of lung tumours. Histologically the cells are very small and round. This is an anaplastic tumour which may occur in multiple lung sites and is highly malignant. Hormone production is common because its cells produce amine precursors. This causes paraneoplastic symptoms in about 15% of patients: hyponatraemia, Cushing’s syndrome, neurological syndromes such as the Eaton–Lambert syndrome (a myasthenic syndrome). The typical presentation of SCC is ‘small tumour, huge nodes’. Metastases are frequently present at the time of initial diagnosis. There is a spectrum of neuroendocrine tumours which runs from the benign typical carcinoid tumours to welldifferentiated neuroendocrine carcinoma (also known as atypical carcinoids), to large-cell type neuroendocrine carcinoma and ultimately to small-cell carcinoma. These tumours are of increasing aggressiveness–typical carcinoids, are benign lesions and small-cell carcinoma is a highly aggressive and lethal lesion.

occur due to involvement of a recurrent laryngeal nerve by the tumour or metastatic lymph nodes. Dysphagia is the consequence of compression or invasion of the oesophagus in the same way.

Signs General. Clubbing of the fingers may occur in 30% and hypertrophic pulmonary osteoarthropathy in 3% with painful swelling of the wrists and ankles. These regress rapidly with complete tumour resection. A marked increase in jugular venous pressure occurs with superior vena cava obstruction, and distended veins may be visible over the upper arms and chest along with swelling of the upper body from the level of the heart up. Respiratory. Localised wheezing can indicate a partially obstructed bronchus. Inspiratory stridor indicates significant narrowing of the airway and mandates urgent referral to a specialist centre. An area of decreased air entry and/or bronchial breathing may occur due to an obstructed bronchus or pleural effusion. Percussion with dullness and associated decreased fremitus indicate an effusion. Signs of metastases. Any new neurological complaint or sign such as headache, blurred vision, hallucinations, syncope, convulsions, imbalance can indicate CNS involvement. New bone or joint pain may be the sign of metastases. Enlarged scalene or supraclavicular nodes may be loco­ regional palpable metastases; subcutaneous nodules may be skin metastases. An enlarged liver may indicate diffuse involvement. Laboratory investigations may reveal anaemia, hypercalcaemia and elevated alkaline phosphatase levels.

Staging of lung cancer The TNM staging of lung cancer was modified in 2009 (Boxes 16.2 and 16.3). This staging system can also be used for SCC, but more commonly SCC is staged as limited- or extensive-stage disease. Limited disease is when the disease is limited to one hemithorax with hilar or mediastinal disease which can be encompassed in a tolerable radiotherapy portal. The precise definition of limited/extensive disease therefore varies somewhat from centre to centre.

Clinical features of lung cancer

Evaluation of the lung cancer patient

Symptoms

The evaluation of the lung cancer patient is a three-step process:

General. Weight loss, malaise and fatigue are common, especially with more advanced disease. Respiratory. Cough is the most common symptom, occurring in nearly half of patients. Sputum production is variable. Haemoptysis on at least one occasion is frequent but is usually not massive. This symptom must never be trivialised. Dyspnoea can be caused by intrinsic or extrinsic airway obstruction and by pleural effusion with loss of function of part of the lung. Occasionally, pulmonary embolism (an expression of paraneoplastic thrombophlebitis, or Trousseau’s syndrome) can be responsible. Other chest or local symptoms. Non-specific chest pain, usually heaviness, is often described; specific local pain may be associated with invasion of the chest wall by tumour or involvement of the skeleton by metastases. Pain or numbness in the arm occurs from brachial plexus invasion by a superior sulcus tumour (Pancoast tumour). Hoarseness can

n

What is the stage of the disease? What extent of resection is necessary to completely resect the lesion (i.e. segmentectomy, lobectomy, pneumonectomy)? n Can the patient tolerate this resection? n

The process is outlined in Box 16.4 and described below.

Determination of the stage of the disease Rule out the presence of distant metastases

The four most common sites are brain (if any new neurological symptoms are present a brain MRI is mandatory), adrenals and liver (CT chest and upper abdomen and/or PET scan and/or liver ultrasound) and bone (bone scan or PET scan with additional conventional X-rays and/or CT or MRI as indicated). The CT chest scan will also evaluate the chest for

Lung cancer  231 Box 16.2 

TNM staging of lung cancer (2009)

Tumour (T) n T1a – the tumour is contained within the lung and is smaller than 2 cm across. n T1b – the tumour is contained within the lung and is between 2 and 3 cm across. n T2 – the tumour is between 3 and 7 cm across or has grown into the the main bronchus more than 2 cm below the part where it divides to go into each lung or the tumour has grown into the visceral pleura or the tumour has made part of the lung collapse. T2 tumours that are 5 cm or smaller are classed as T2a and those larger than 5 cm are T2b. n T3 – the tumour is larger than 7 cm or has grown into one of the following structures – the chest wall, the mediastinal pleura, the diaphragm, the phrenic nerve, or the pericardium or the tumour has made the whole lung collapse or there is more than one tumour nodule in the same lobe of the lung. n T4 – the tumour has grown into one of the following structures – the mediastinum, the heart, a major blood vessel, the trachea, the carina, the oesophagus, the vertebral column, the recurrent laryngeal nerve or there are tumour nodules in more than one lobe of the same lung. Nodes (N) n N0 – there is no cancer in any lymph nodes. n N1 – there is cancer in the lymph nodes nearest the affected lung (ipsilateral peribronchial and hilar). n N2 – there is cancer in lymph nodes in the mediastinum but on the same side as the affected lung or there is cancer in subcarinal lymph nodes. n N3 – there is cancer in lymph nodes on the opposite side of the chest from the affected lung or in the supraclavicular or scalene lymph nodes. Metastases (M) n M0 – there are no signs that the cancer has spread to another lobe of the lung or any other part of the body. n M1a – there are tumours in both lungs or a malignant pleural effusion or pericardial effusion. n M1b – there are lung cancer cells in distant parts of the body, such as the liver or bones. Box 16.3 

Staging of lung cancer by TNM subsets

Stage 1 lung cancer 1A 1B Stage 2 lung cancer 2A

2B Stage 3 lung cancer 3A

3B

Stage 4 lung cancer 4

T1a or T1b, N0, M0 T2a, N0, M0 T1a, N1, M0 T1b, N1, M0 T2a, N1, M0 T2b, N0, M0 T2b, N1, M0 T3, N0, M0 T1a, N2, M0 T1b, N2, M0 T2a, N2, M0 T2b, N2, M0 T3, N1, M0 T3, N2, M0 T4, N0, M0 T4, N1, M0 Any T, N3, M0 T4, N2, M0 T4, N3, M0 Any T, any N, with M1a or M1b

Box 16.4 

Management of non-small-cell lung cancer (NSCLC)

Surgery provides the best chance of cure for stages I and II NCSLC. Some very highly selected stage III patients are surgical candidates (see text) Staging of disease n Clinical signs/symptoms n CT chest and upper abdomen n Bronchoscopy n Other as dictated by clinical/biochemical findings Determination of the extent of resection required n CT chest n Bronchoscopy n FDG-PET scan Fitness of the patient n Pulmonary function n Determination of residual postoperative function n General well-being/fitness n Other comorbidities Operable patients – i.e. those with a meaningful chance of being cured and who are fit for the necessary resection – are offered surgery. All others (the majority of lung cancer patients) are referred either to the oncologist for chemotherapy and/or radiotherapy or to the palliative care specialist

the presence of an effusion or other lung lesions which could be secondary lesions.

Determine the intrathoracic stage   of the disease n

The CT often cannot distinguish between approximation and invasion of adjacent structures. This may require surgical evaluation. However, it is often possible to determine the T stage of the tumour by CT. Standard X-rays can be helpful to localise the tumour by lobe, to investigate the skeleton and to ascertain a raised hemidiaphragm (this can indicate phrenic nerve involvement). n CT is notoriously unreliable to determine N stage. PET scan has around 80–85% sensitivity but its specificity is around 95%. Every effort therefore should be made to obtain tissue confirmation of mediastinal lymph node involvement before ruling out surgery. This can be done by fine-needle transtracheal aspiration biopsy at bronchoscopy, by mediastinoscopy (or on occasion anterior mediastinotomy or VATS, video-assisted thoracic surgery) or at thoracotomy. Mediastinoscopy is performed through a small cervical incision and allows all the lymph nodes around the central airway to be identified and biopsied. However stations 5 and 6 are the subaortic and aortopulmonary nodes. They are on lateral side of the aorta and are therefore not accessible with mediastinoscopy. They can be biopsied by an anterior mediastinotomy or using VATS. n MRI is superior to CT to determine vascular, vertebral and nerve (brachial plexus) involvement by the tumour. Otherwise it offers no advantage over CT. n Bronchoscopy will determine the intrabronchial extension of the tumour if it is visible, allow detection of other intrabronchial lesions and may permit biopsies to be taken from the lesion for histological diagnosis.

Lung cancer

16 

232  Chest and lungs

Secretions can also be taken for sensitivity studies. The yield from bronchoscopy is much higher in central lesions than with peripheral ones. Tissue diagnosis from peripheral lesions is often more readily obtained by CT or fluoroscopy-guided transthoracic needle biopsy. At some point in their work-up all lung cancer patients should undergo bronchoscopy. n If there is an effusion it is mandatory to absolutely rule out pleural involvement. If cytological analysis of the fluid is negative, pleuroscopy should be performed to examine and biopsy the pleura. Cytology has a 15–20% false-negative rate even after 2–3 aspirations of pleural fluid.

Determination of the required resection The objective of a resection for lung cancer is to completely resect the lesion, with clear margins throughout, as well as the regional lymph nodes. This is why the ‘standard’ resection for lung cancer is an anatomic lobectomy with resection of the intrafissural lymph nodes and a complete mediastinal lymph node dissection. Lesser resections are reserved for exceptional patients with a small, peripheral, node-negative cancer which can be completely resected with negative margins via segmentectomy or wedge resection but who do not have sufficient functional reserve to undergo a lobectomy. The local recurrence rate is certainly higher with lesser resections, and this probably has a negative impact on survival. More-extensive resections are necessary when the tumour involves more than one lobe or the central airway in the lung. On the right side these are bilobectomies (either upper and middle lobes or middle and lower lobes) and pneumonectomy. On the left side this entails a pneumonectomy. A ‘sleeve resection’ entails a pulmonary resection with a segment of bronchus and re-anastomosis of the airway (Fig. 16.1). The extent of resection can usually be determined from the bronchoscopy and CT findings. However, in some cases it is only at the time of surgical exploration that this can be ascertained. It is therefore mandatory that the extent of resection that is physiologically tolerable by the patient be determined prior to surgery so as to allow this decision to be made safely intraoperatively.

a

Upper lobe bronchus

Bronchus intermedius

b

Fig. 16.1  A prototypical ‘sleeve resection’ – that is, a

Determination of the extent of resection   that is tolerable by the patient

right upper lobectomy. (a) The right main bronchus is divided above the takeoff of the upper lobe bronchus, and the bronchus intermedius is cut below it. This allows the airway to be resected in such a way as to ensure adequate resection margins. (b) The bronchus intermedius is then anastomosed to the right main bronchus with a running non-resorbable suture. Some surgeons use slowly resorbable sutures, others interrupted sutures.

Whenever considering surgery it is absolutely essential to obtain a careful and very complete history. The precise functional capacity of the patient must be determined (unlimited, strenuous activity; can climb 3, 2, 1 or only so many stairs; limited in activities of daily living by breathlessness). Other important points are cough and sputum production as well as other comorbid conditions. Most lung cancer patients are smokers and therefore at high risk of having coexistent coronary artery disease. This must be ruled out by history and, if necessary, other non-invasive and invasive tests to allow surgery to be performed safely. Likewise it is imperative to examine the carotids for pulse, murmurs and bruits. Finally, right heart failure after pulmonary resection can be a devastating complication with fatal outcome. There is no reliable test to predict its onset but preoperative pulmonary

hypertension is a predisposing factor and this should be ruled out if there is any suspicion. Careful physical examination is also important. The supraclavicular fossae and the base of the neck must be carefully and attentively examined for lymphadenopathy. If present the enlarged lymph nodes should be aspirated for cytology to rule out N3 disease. Pulmonary function results are always expressed as absolute and relative values. The relative values are expressed as the percent of predicted values based on the patient’s sex, age, height and weight. It is important to refer to these relative values rather than to absolute figures. It is obvious that a FEV1 (forced expiratory volume in one second) of one

Lung cancer  233 litre is quite adequate for a very small, light woman but equally inadequate for a very large, heavy man. Furthermore it is the predicted postoperative value that is the true determinant of residual function (and therefore operability) rather than the crude preoperative value. Let us take the case of a patient with adequate clinical function who has ‘very poor numbers which rule out pneumonectomy’. If the involved lung is still doing 50% of the patient’s breathing, then these values indeed rule out performing a pneumonectomy. If on the other hand the tumour has obstructed the main bronchus and the pulmonary artery and the preoperative function is equal to what the postoperative function will be, then the patient is operable. If only the airway is obstructed and the artery is permeable and there is a physiological shunt through this lung then resection could actually improve oxygenation. The decision that a patient is physiologically inoperable should only be made by a specialist unit after careful evaluation of the patient, as this is quite a complex decision process. The two strongest predictors of cardiopulmonary morbidity and mortality after pulmonary resection are the FEV1 and the DLCO (transfer factor for CO). When the predicted postoperative FEV1 and DLCO are both less than 40% of the predicted value the risk of significant morbidity and mortality become unacceptably high. There is also a risk of turning the patient who survives into a respiratory cripple. This is also an unacceptable outcome. In borderline patients the aerobic capacity is also a strong predictor of unfavourable outcomes. This is assessed by ergospirometry with measurement of the VO2 max. When pulmonary function is well preserved, no further tests are required and major resections including pneumonectomy can be performed. When there is doubt, the V/Q scan will allow the regional perfusion and ventilation to be assessed. This is then used to calculate the predicted postoperative function. Smoking cessation prior to surgery seems intuitively to be desirable. In fact it takes 2 months for there to be a true benefit in terms of sputum reduction and full restitution of mucociliary function. Nonetheless, active smoking immediately prior to surgery does increase the operative risk. In a borderline patient it can be beneficial to defer surgery for 6–8 weeks for pulmonary rehabilitation combined with smoking cessation. In current smokers undergoing ‘curative’ treatment every effort should be made to help the patient quit smoking. Smoking cessation slows the accelerated loss of lung function in COPD patients. This is important, as surgery has just deprived the patient of functional lung tissue, and respiratory failure is one of the mid- to long-term causes of death in patients who have indeed undergone a curative resection of lung cancer. Furthermore it significantly reduces the risk of developing a second primary lung cancer.

Treatment of lung cancer Non-small-cell lung cancer Unfortunately, most patients present initially with advanced disease that will not be curable with any modality. In these cases they must be referred to an oncologist so that palliative chemotherapy can be discussed. When there is pain or

obstruction, palliative radiotherapy is also often a valid option. Palliative treatment is an active treatment option that seeks optimal symptom relief. The value of this treatment must not be underestimated to maintain quality of life, and every effort must be made to obtain it for all inoperable patients, especially when they become symptomatic. Surgery should not be offered to patients with minimal chance of cure. It submits them needlessly to the risks (morbidity/ mortality) of the procedure without the benefit (chance of cure). Shields has defined a futile thoracotomy as one where the chance of cure is less than the chance of suffering major morbidity or death. Appropriate staging will ensure an exploratory thoracotomy (‘open and shut’) rate of less than 5%. There are patients in whom only exploratory thoracotomy can assess resectability, so the rate of this procedure should not be 0%. Surgery offers the best chance of cure in stage I and II lung cancer, so radiation and chemotherapy are usually reserved for patients who are unfit for surgery (or who refuse surgery). If it is the general condition of the patient that precludes surgery, radical radiotherapy may still be an option but these patients are often poor candidates for chemotherapy. If this is contraindicated, then palliative care is often the only reasonable option. If it is the patient’s poor respiratory reserve that rules out surgery, then radical radiotherapy may not be tolerable (because of radiation injury to the adjacent lung), but highly focused radiotherapy may be applicable. In this case palliative chemotherapy should be discussed. Some very highly selected stage IIIa patients can be surgical candidates. Other stage IIIa patients may be considered for inclusion in neo-adjuvant (or induction) therapy protocols. It now seems that if the mediastinal lymph nodes can be cleared of tumour by neo-adjuvant therapy, surgery remains a valid treatment option for these patients. Otherwise most surgeons would refer patients with stage IIIa disease for radical radiotherapy and/or chemotherapy. Occasional very highly selected stage IIIb patients might be appropriate candidates for inclusion in prospective trials of surgery or induction therapy (with the same caveats as for stage IIIa disease as above). This is however only exceptionally the case. These patients are usually treated with chemoand/or radiotherapy. Patients with stage IV disease because of a single, completely resectable brain metastasis and who do not have locally advanced disease can be considered for resection of the brain lesion followed by resection of the primary lesion with a 20–25% chance of 5-year survival. All other stage IV patients are usually treated with palliative chemotherapy or palliative radiotherapy. Palliative chemotherapy has a modest effect on overall survival, but its proponents believe that it can improve quality of life significantly. This is not universally accepted. Palliative radiotherapy can obtain good relief of symptoms when there is pain from invasion into the chest wall or at the site of bone metastases. It can offer relief of superior vena cava syndrome (endovascular stenting is also a useful palliative procedure in this condition). It can also be very helpful when there is symptomatic bronchial obstruction or haemoptysis.

16 

234  Chest and lungs

Small-cell lung cancer The treatment of SCC is typically combination chemotherapy. Etoposide/cisplatin in combination with radiotherapy can induce complete response in around 80% of patients with limited disease. Patients with a complete response should receive prophylactic cranial irradiation. Radiotherapy for extensive disease is palliative. The treatment of stages I and II SCC is controversial, but it does seem that surgery followed by chemotherapy can offer up to 35–40% 5-year survival. Occasionally isolated secondary deposits are resected.

Prognosis Overall, the prognosis of NSCLC is relatively poor. The 5-year survival for stage I NSCLC is around 70%. With stage II disease this falls to 40–50%. In the very highly selected stage III patients who are considered surgical candidates the 5-year survival is only around 25–30%. Otherwise it is at best 10–15%, more often much less. The median survival for stage IV disease is around 12 months, with minimal 5-year survival. Less than 20–25% of patients present with operable disease, so the overall 5-year survival for men with lung cancer in the UK is only 5–7%. Equally depressing is the very small progress in overall survival that has been made over the last 25 years and the fact that survivors develop a second primary lung cancer at a rate of 1–2% per year. The prognosis of SCC is worse, with only 3–17% of patients with limited disease surviving 5 years (and only 30–40% of patients present with limited disease). The 5-year survival for extensive disease is 2–8%. New chemotherapy treatments may improve the prognosis. Furthermore the survivors present with new second aerodigestive cancers at a rate of 2–10% per patient per year. Thus the mortality of survivors is 10 times greater than ageand sex-matched cohorts.

OTHER LUNG TUMOURS Neuroendocrine tumours The spectrum of neuroendocrine tumours spans a range starting with the benign typical carcinoids, which have an essentially normal 5- and 10-year survival following their complete resection. They are slow-growing lesions. The majority (70%) are central lesions. Up to 31% are asymptomatic. They can cause multiple symptoms over many years; some are due to obstruction such as wheezing, shortness of breath, cough and infection. Others are haemoptysis (frequent) or chest pain. An associated carcinoid syndrome is very rare (around 2%), as is Cushing’s syndrome. Complete resection is curative. Resection should always spare as much lung parenchyma as possible. Because of their central location these tumours often lend themselves to sleeve resections (see Fig. 16.1). Endoscopic resection (whatever the technique) should be reserved for frail, high-risk patients who are poor operative candidates because of the high risk of incomplete resection and recurrence. The other indication for endoscopic resection is to allow a distal pneumonitis to clear so as to permit a safe parenchyma-sparing limited resection.

Atypical carcinoids tend to be more aggressive with much more frequent lymph node metastases (30–50%). The 5-year survival is poorer at 40–76%. Large-cell neuroendocrine carcinomas are uncommon lesions with a poor prognosis. Small-cell carcinoma is discussed above.

Other rare primary pulmonary tumours There is a long list of these very rare lesions which are beyond the scope of this chapter, and the reader is referred to the excellent review chapters in the textbooks on thoracic surgery edited by Shields et al (2009) and by Patterson et al (2008). Immunosuppressed patients have an increased risk of presenting with solid organ lymphomas, and this includes the lungs. HIV-infected patients may also present with pulmonary Kaposi sarcoma. Hamartomas account for around three-quarters of all benign lung tumours. The definition of a hamartoma is an excessive focal overgrowth of mature normal cells and tissues in an organ, composed of identical cellular components. The majority are asymptomatic peripheral lung lesions which are discovered incidentally, and the obvious problem is distinguishing them from a small, early stage lung cancer. They often contain fat and cartilage. Chondrohamartomas are purely cartilaginous, as their name indicates. Central lesions can cause symptoms of obstruction. The diagnosis of hamartoma can be made on the basis of the radiological findings and the presence of fat and/or cartilage in a biopsy specimen. The usual indication for surgery is the uncertainty as to diagnosis. Simple excision is curative. Symptomatic lesions should be resected with as much of a parenchymasparing technique as feasible. Asymptomatic peripheral lesions only need to be resected if large, or growing in a young, fit patient.

PRINCIPLES OF CHEST DRAINAGE The object of chest drainage is to obtain complete evacuation of all fluid and air from the pleural space so as to allow complete re-expansion of the underlying lung. Indications for insertion of a chest drain are given in Box 16.5 and the technique described in Chapter 11. If the lung cannot re-expand despite adequate drainage then it is a trapped lung, and this condition can only be resolved surgically if clinically indicated. If drainage cannot result in evacuation of all abnormal pleural contents, either because of their loculation or coagulation, then again only surgery will resolve the condition. In many cases thoracoscopy (also called VATS, video-assisted thoracic surgery) will be all that is needed. It is often said that whenever there is a hole in the chest wall the lung will collapse. On this basis suction had routinely been applied to chest drains. In actual fact the lung will re-expand and occupy the entire pleural space unless there is a condition which prevents this – air or fluid trapped in the pleural space, for example. There is now some evidence that

Pneumothorax  235 Box 16.5 

When to insert a chest drain

To patient

To air or wall suction regulator

Absolute indications n Pneumothorax (PNO) in ventilated patient n PNO in trauma patient who requires surgery n Haemothorax in trauma patient n Symptomatic PNO in patient with limited pulmonary reserve n PNO of any size prior to transfer of patient by air n PNO in stable patient prior to ambulance transfer if no doctor in attendance n Bilateral PNO n Obtunded patient with PNO Relative indications n PNO prior to ambulance transfer with doctor in attendance (provide equipment if no drainage!) n Small to moderate PNO in stable patient (other options are observation or aspiration) n Pleural effusions

suction may not be required for chest drains in the majority of cases and indeed that air leaks and chest drainage might resolve faster without suction. However, it is mandatory that all chest drains be attached to a device that allows air and fluid to escape freely from the pleural space without allowing air to enter into it. The most commonly used device is the underwater seal, which is illustrated in the single-bottle drainage system seen in Figure 16.2. This figure also illustrates double- and triplebottle systems. Commercially available chest drain collection systems are commonly three-bottle systems. To understand how the underwater seal works, imagine yourself with a drink and a straw. As long as the straw is in the drink and you are sucking on the straw the only way you can get air into your mouth is to either drink the glass dry or to remove the straw from the drink. So this underwater seal is a very simple, cheap and safe system as long as the drainage bottle is well below the patient (so as to prevent negative pleural pressure from ‘drinking the glass dry’) and the tube from the patient is below the level of the fluid (to ‘keep the straw in the drink’). If the tube entering the bottle is only 2 cm below the surface of the water, the resistance to air and fluid escaping from the chest into the drainage system is negligible and easily overcome during forced expiration and coughing. Another system of one-way valve that is commonly used is the Heimlich valve, illustrated in Figure 16.3. The inner tubing is made of very soft rubber (or some similar substance) so that it completely collapses and becomes airtight on inspiration but opens with almost no resistance to allow the free passage of air or fluid. It is imperative to ensure that a Heimlich valve is mounted correctly or it will rapidly produce a tension pneumothorax (see below). The standard chest drain should be placed in the 4th or 5th intercostal space in the midaxillary line and directed up to the apex of the chest along the posterior chest wall (see Ch. 11). Most drains placed by interventional radiologists are pigtail catheters. These can be remarkably effective, but in the author’s experience it is important to maintain their patency by irrigating them 1–2 times per day with 10–15 mL of sterile 0.9% saline solution.

To patient

To patient

To air or wall suction regulator

To air or wall suction regulator

Fig. 16.2  One-, two- and three-bottle drainage systems. In the one-bottle system the single bottle is both the collection chamber and the underwater seal. The drawback of this system is that the resistance to fluid and air escaping the chest increases as the bottle fills. Two-bottle systems have the collection chamber upstream from the underwater seal chamber. If suction is applied to the one- and two-bottle systems a wall-mounted suction regulator is required. In three-bottle systems a suctionregulating chamber is placed between the underwater seal chamber and the source of suction. Most commercially available drainage systems are three-bottle systems.

Criteria for drain removal – there is much variance in local custom. The common criteria to remove a drain are no air leak for 24 hours and drainage of less than 200 mL in 24 h.

PNEUMOTHORAX The definition of a pneumothorax (PNO) is when the pleural space contains air which separates the parietal and visceral pleura, preventing the lung from occupying its normal place in the pleural space.

Other lung tumours Principles of chest drainage Pneumothorax

16 

236  Chest and lungs ( 3 + 2 + 1) / 3 = 6 / 3 = 2; 2 × 10 = 20

Towards collection system or air

Towards patient

Soft, pliable reed valve

Hard case

Fig. 16.3  The Heimlich valve is a simple one-way valve device. A soft, pliable reed valve is placed in a rigid container. There is virtually no resistance to air and/or fluid escaping, but any relative depression on the patient side of the valve will cause the inner reed valve to collapse and seal off the passage through the valve.

a

so this is a 20% pneumothorax. Flying is contraindicated with a PNO because aeroplanes are only pressurised to around the equivalent of 2000 m in altitude. As pressure times volume equals a constant, the volume of the PNO will increase by 13 at this altitude with the attendant risk of tension.

Treatment There are three options: observation, aspiration and drainage. Small PNOs (35 History of diabetes regardless of duration BP >140 mmHg on two occasions Good: ≥50% Fair: 30–49% Poor: 80 years Second operation Third (or more) Inserted preoperatively Aneurysmectomy Within the 24 hours prior to surgery >24 hours prior to surgery but on same admission Dialysis dependent Acute structural defect, cardiogenic shock, acute renal failure Paraplegia, pacemaker, severe asthma, congenital heart disease in adult

1 3 3 3 0 2 4 7 12 20 5 10 2 5 10 5 10 10–50 2–10

Systolic pulmonary artery pressure < 60 mmHg Systolic pulmonary artery pressure ≥ 60 mmHg Aortic valve gradient < 120 mmHg Aortic valve gradient ≥120 mmHg

5 8 5 7 2 Operative mortality 1% 5% 9% 17% 31%

Operative risk Low Elevated risk Significant elevated risk High risk Very high risk

EUROscore risk stratification in cardiac surgery

Factor Patient-related factor Age Gender Chronic pulmonary disease Extracardiac arteriopathy Neurological dysfunction Previous cardiac surgery Serum creatinine Active endocarditis Critical preoperative state

Cardiac-related factor Unstable angina Left ventricular function Recent myocardial infarction Pulmonary hypertension Operation-related factor Emergency Other than isolated CABG Surgery on thoracic aorta Post-infarct septal rupture Cumulative EUROscore 0–2 3–5 >6

Definition

Score

Per 5 years or part thereof over 60 years Female Chronic bronchodilator or steroid use Claudication > 50% carotid stenosis Previous or planned surgery to limb arteries, carotids, abdominal aorta Affecting daily ambulation Pericardial cavity opened previously > 200 micromol/L On antibiotics at the time of surgery Ventilation before anaesthetic room Preop intra-aortic balloon Preop inotrope Preop renal failure

1 1 1

Requiring intravenous nitrates Moderate: ejection fraction 30–50% Poor: ejection fraction < 30% < 90 days Systolic pulmonary artery pressure ≥60 mmHg

2 1 3 2 2

Operated on before the next operating day Other cardiac procedure than, or in addition to, CABG Ascending, arch or descending aorta

2 2 3 4

Operative risk Low Medium High

Operative mortality is approximately same per cent as the EUROscore for each individual patient.

2 2 3 2 3

3

Heart failure  267 forwards or backwards. Retrograde extension goes back to the aortic valve, removing the commissural support and causing the valve to leak. It may also extend around the coronary arteries, usually the right, and thus mimic an inferior myocardial infarction. It may extend a variable distance antegradely, affecting the arch vessels, the blood supply to the spinal cord, the renal arteries, the coeliac axis and the femoral arteries. A variety of ischaemic syndromes may thus form part of the clinical presentation.

Classification Aortic dissections are classified according to their anatomical extent. The diagnostic watershed depends on whether the ascending aorta is involved. Type A dissections involve the ascending aorta, whereas Type B dissections are confined to the descending aorta (Fig. 17.9). Dissections are further classified as acute or chronic depending on the interval from onset to diagnosis, arbitrarily placed at 2 weeks. In Type A dissection 50% of patients are dead within 24 hours and 80% in 2 weeks. In general terms, Type A dissection is managed surgically to prevent the complications discussed (bearing in mind associated risks if there is neurological involvement), whereas Type B dissection is managed medically and only considered for surgery if there are any complications related to the dissection.

Operation Cardiopulmonary bypass is usually established with a femoral arterial cannula, but axillary artery cannulation is associated with less thromboembolism and a lower incidence of neurological damage. The patient is core-cooled on bypass, down

Type A

Type B

to 18°C, and a period of circulatory arrest is needed if the aortic arch is involved. Every effort is made to conserve the aortic valve. If there is dilatation of the aortic root, as occurs in Marfan’s syndrome, it is then necessary to replace the aortic root and the valve and to re-implant the coronaries. The hospital mortality for acute Type A dissections managed medically is over 90%, while the UK Cardiac Surgical Register reports a mortality of 10–15% for operated cases in the last 5 years. There is little doubt this group of patients stands the best chance of survival if the diagnosis is made promptly and they are referred for urgent surgery.

HEART FAILURE The number of patients with heart failure is reaching epidemic proportions in the Western world. In the UK there are approximately 100 000 new cases per year, and in the USA five times that number. Patients with end-stage heart failure may have a 1-year survival of 50%, and the figure is as low as 10% by 2 years. It is primarily a disease of the elderly and in 95% of cases is due to ischaemic heart disease. A minority of these are referred for conventional coronary artery surgery, provided a reasonable amount of viable myocardium can be demonstrated, as discussed earlier. The most effective treatment, but with limited availability, is heart transplantation.

Management Intra-aortic balloon pump The intra-aortic balloon pump (IABP) is a form of mechanical cardiac support. A balloon is introduced through the femoral artery and advanced to the descending aorta just beyond the origin of the subclavian artery. It is linked to an external console and is inflated in the diastolic phase of the cardiac cycle. The two principal effects of the IABP are increased coronary perfusion and reduction in the afterload for the heart during systole. The current indications for IABP use are shown in Box 17.4. A typical IABP set-up is shown in Figure 17.10a, b, and the arterial trace with the IABP counterpulsation in diastole is shown in Figure 17.10c.

Ventricular assist devices Current devices represent the results of 25 years of dedicated research, and were brought into clinical effect in the early 1990s. Most of the devices implanted to date have been

Box 17.4  n n n n n n n

Fig. 17.9  Stanford classification of aortic dissection. Type A dissections involve the ascending aorta, whereas Type B are confined to the descending aorta.

n n n

Indications for intra-aortic balloon pump

Refractory ventricular failure Cardiogenic shock Unstable refractory angina Impending infarction Mechanical complications due to acute myocardial infarction Ischaemia-related intractable ventricular arrhythmias Cardiac support for high-risk general surgical and coronary angiography/angioplasty patients Weaning from cardiopulmonary bypass Intra-operative pulsatile flow generation Support for failed angioplasty and valvuloplasty

Heart failure

17 

268  Cardiac surgery

a

b

Systole

Diastole

c 160 Diastolic augmentation coronary perfusion

mmHg

140 120

Unassisted systole

Assisted systole

100 80 60 40

Balloon inflation Unassisted aortic end diastolic pressure

Assisted aortic end diastolic pressure myocardial oxygen demand

Fig. 17.10  Use of intra-aortic balloon pump in heart failure: (a) positioning; (b) functioning; (c) arterial waveform variations.

first-generation pusher-plate pumps driven either pneumatically or electrically. Although the devices are implanted in the abdomen, they require external drivelines. Nevertheless, a substantial number of patients in Europe and North America have been successfully discharged home from hospital and have pursued an active life with these devices. The majority of these patients have been ‘bridged to transplantation’, but a few have been successfully ‘bridged to recovery’. In other words, some patients with non-ischaemic cardiomyopathy who have had a left ventricular assist device (LVAD) implanted for a number of months have, on later examination by echocardiography and intensive treadmill testing, shown remarkable recovery of their left ventricular function as a result of this prolonged period of unloading. These patients have then proceeded to have their devices removed at a subsequent operation. At the present time this is innovative treatment and the subject of intensive investigation.

Future developments The use of implantable ventricular assist devices is in its infancy. The treatment is labour-intensive and the devices are expensive. A recent randomised trial of implantable LVAD against optimal medical treatment for patients in severe heart failure revealed a 2-year survival of 23% for the LVAD group versus 8% for the medical group. These low figures indicate

how severely ill these patients were, but provide the background for future trials of chronic implantation. Some LVADs are illustrated in Figure 17.11.

Transplantation For details of organ retrieval and matching for transplantation see Chapter 13. The results of cardiac transplantation are now good enough for this to be used for patients with very severe cardiac conditions for which medical management can achieve nothing further. Indications for heart transplantation are: n

severe cardiomyopathy severe ischaemic heart disease, unsuitable for coronary bypass grafting or after repeated failure of that procedure n untreatable ventricular aneurysm n end-stage valve disease n severe congenital cardiac abnormalities but normal lungs. n

Positive criteria for recipient selection are: n

age under 50 no evidence of renal or hepatic dysfunction n no persistent causative problems (e.g. alcohol) n

Heart failure  269 a Aorta Outflow-valve housing Vent adapter and vent filter

External battery pack

Inflow-valve housing

Drive line

Prosthetic left ventricle

System controller

b

Skin line

c

d

PA

RA

RVAD

Ao

Apex

LVAD

Fig. 17.11  Ventricular assist devices: (a) Vented Electric HeartMate I; (b) HeartMate II; (c) Jarvik 2000; (d) Thoratec.

n

no major psychological difficulties no malignancy n no evidence of sepsis. n

In patients who comply with the above criteria, transplantation should be considered early. There is a significant mortality for those who have to wait for a transplant until their disease is in its end stages, with median survival of less than a year.

Operation The heart, including the pulmonary and aortic valves, is removed, leaving atrial cuffs to which the atria of the donor heart are then anastomosed (Fig. 17.12a). The operation is completed by joining the pulmonary vessels and the supra­ valvular aorta of the recipient to the transplant (Fig. 17.12b). Other anastomotic techniques involving bicaval anastomosis are also used.

17 

270  Cardiac surgery a

b

Fig. 17.12  The technique of cardiac transplantation.

Results These vary according to the selection of both donor and recipient and also between different centres. In general in the UK, survivals are: n

1 year – 85–90% 3 years – 80% n 5 years – 70%. n

Transplant activity is limited by two main factors: a shortage of donor organs and our inability to safely preserve the heart

in a clinical environment for more than 4 hours. The most common source of organs is relatively young patients (males < 55 years, females < 60) who meet the criteria for death due to brainstem injury. With improving road safety, the majority of deaths are due to intracranial haemorrhage. Unfortunately many of these donors have coronary artery disease or left ventricular hypertrophy, which makes their hearts unsuitable for donation. The recipients are very symptomatic with endstage heart failure due to idiopathic dilated cardiomyopathy or, more often, ischaemic heart disease.

Trauma to the heart and great vessels   271

TRAUMA TO THE HEART AND GREAT VESSELS Cardiac trauma and traumatic injury of the thoracic aorta is usually seen in the context of multiple injury and is often associated with head injury. The principles of trauma care are now well formulated as per ATLS guidelines.

Blunt cardiac injury The heart may be compressed between the sternum and the vertebral column. Compression forces may lead to rupture of the right ventricle, the septum or the atrio-ventricular valves. Rupture of one of the major cardiac chambers leads to tamponade and is usually fatal. Three patterns of injury are recognised amongst the survivors of cardiac compression injuries: n

Blunt trauma There are three patterns of cardiothoracic injury which may confront the trauma team: n

aortic rupture n myocardial contusion n rupture of a cardiac valve.

Rupture of the aorta Aortic rupture, termed aortic transection, results from a deceleration injury. The most common site for the tear is immediately distal to the origin of the left subclavian artery. The rupture involves the intima and media, and vascular continuity is maintained by the thin adventitia supported by the surrounding mediastinal tissues. This site is favoured for such an injury because it is at the boundary of a mobile arch and a tethered descending aorta. The relevant features on clinical examination are absent or weak femoral pulses and unequal blood pressure in the arms. Fluid in the left hemithorax can be missed or underestimated. An erect posterioranterior chest radiograph is usually impossible to obtain, and the surgeon may have to compromise with a supine anteroposterior film, which is more difficult to interpret because the cardiac shadow is enlarged and there are no fluid levels in the pleural space. In practice, if there is a haemothorax, the left pleural space may be a ‘white-out’ or it may have a ‘ground-glass’ appearance compared with the other side. However, a widened mediastinum should always raise the possibility of a transection. The diagnosis is confirmed by aortography, digital subtraction angiography or a CT scan. It is not always obvious, and there may be false-negative results. Once the suspicion has been raised, the problem may be an extremely difficult one. The condition is likely to prove fatal and requires emergency surgery, yet the process of transfer to a cardiothoracic unit is often hazardous and attention to other associated injuries such as splenic rupture may require attention first. In some patients the aortic injury is contained and they survive to appear many years later with a calcified false aneurysm. Operation is performed via a left thoracotomy. The mediastinum is featureless because of a spreading haematoma. Surgical options include direct suture with mobilisation of the aorta, but this requires time. However, usually an interposition graft is necessary. A shunt is inserted between the ascending and descending aorta in order to reduce the chance of spinal cord ischaemia during the period of aortic clamping. The use of a heparinised shunt avoids the need for systemic heparinisation, which may be an advantage in the presence of a head injury.

myocardial contusion ventricular false aneurysm n valve rupture. n

If the myocardium is contused but remains intact, the consequences are similar to those of myocardial infarction. ECG changes are common and may show Q waves or a generalised ST segment abnormality. Cardiac enzymes and troponin I will be elevated. The course is similar to that of a myocardial infarct and depends on the area of damage. Echocardiogram confirms abnormal ventricular wall motion and excludes any pericardial collection. If the myocardial injury is full-thickness, it may rupture slowly, be contained by pericardial adhesions and mature into a false aneurysm, usually of the left ventricle. This can be assessed and dealt with electively. If the rupture is sudden into the pericardium, it is likely to be fatal before the patient reaches hospital. Rupture of a heart valve is unusual and is likely to occur at the time of the injury. It is a difficult diagnosis to make on clinical grounds in the setting of multiple injury. An echocardiogram is the diagnostic procedure of choice. Surgical repair or replacement can usually be undertaken semi-electively the following day unless there is severe haemodynamic compromise which might necessitate emergency surgery.

Penetrating injuries to the heart Stab wounds to the heart present a wide spectrum of clinical pictures and can be a technical challenge to the emergency surgeon. Little history is available, but some idea of the length of the instrument and its direction is helpful. The site of the wound together with a relevant clinical history may enable the surgeon to anticipate the structures at risk. Two factors have to be considered: continuing haemorrhage and/ or presence of cardiac tamponade. If the diagnosis of tamponade is suspected clinically the neck veins will be engorged, and a subxiphoid incision immediately inferior to the xiphoid process is the easiest route to the pericardial cavity to relieve the tamponade and can be performed quickly without having to divide the sternum or perform a thoracotomy. The pressure–volume relationship of the pericardium space demonstrates hysteresis (Fig. 17.13). Therefore aspiration of as little as 50 mL of blood from the pericardial space in acute tamponade can greatly improve cardiac filling and thus the cardiac output. In a stable situation, echocardiography will confirm the presence of significant blood in the pericardial cavity. With ongoing bleeding or uncertainty regarding the source of bleeding, a full sternotomy is needed.

Trauma to the heart and great vessels

17 

272  Cardiac surgery Table 17.17

Aetiology and nature of congenital cardiac defects

Factor Maternal factors: Maternal virus infection (rubella)

Pressure

Maternal alcohol abuse Maternal drug and radiation treatment Genetic abnormalities: Down’s syndrome

Volume

Fig. 17.13  In cardiac tamponade the pressure–volume

Turner’s syndrome Marfan’s syndrome

relationship of the pericardial cavity shows hysteresis.

Bullet wounds to the heart When a bullet penetrates the thorax and pericardium, a cardiac wound is frequently produced. High-velocity missiles produce massive through and through injuries of the heart. Occasionally, a missile may penetrate a cardiac chamber and come to lie within it. Penetrating cardiac wounds are usually accompanied by wounds involving the pleural space, internal mammary vessels, lung and wounds of the liver and other abdominal viscera.

Operative management If there is a haemothorax, an intercostal drain should be inserted, preferably in the anterior to midaxillary line in the 4th or 5th intercostal space and definitely not below the 6th intercostal space in order to avoid passing below the diaphragm. If there is major cardiac or vascular injury, the drain will permit copious bleeding, and if the situation was previously balanced it may now become out of control and require urgent operation. Suction should not be applied to the drain, as it may lead to rapid exsanguinations. The most effective incision is a median sternotomy because all chambers of the heart and the ascending aorta can easily be reached. If a saw is not available, a left anterior thoracotomy via the 5th intercostal space will give excellent access to the left ventricle and left atrial appendage. A right anterior thoracotomy will allow access to the right atrium, interatrial groove and right ventricle. The left ventricle, with its thick walls, can be controlled with 3/0 atraumatic sutures, best placed as horizontal mattress sutures buttressed with autologous pericardium. As this is a semi-sterile operation it is best to avoid foreign material such as Teflon felt. The atria can be sutured directly or controlled with a side-biting clamp to allow more time. Bleeding from coronary arteries is a special problem. Small branches, well away from the interventricular and atrioventricular grooves can be oversewn. A hole in a larger branch should be controlled by taking delicate bites of epicardial fat on either side of the artery and using 5/0 or 6/0 sutures. In this way the haemorrhage can be stopped without occluding the artery. The pericardium can be left open, but drains should be placed in front of and behind the heart and connected via an underwater seal to suction.

DiGeorge syndrome Williams’ syndrome Uncertain

Outcome Persistent ductus arteriosus Pulmonary valve stenosis Pulmonary artery stenosis Septal defects Various Septal defects Tricuspid and mitral valve abnormalities Coarctation of aorta Dilatation of aortic ring Aortic incompetence Aortic aneurysm Interrupted aortic arch Supravalvular aortic stenosis Congenital aortic stenosis

CONGENITAL HEART DISEASE The surgery of congenital heart disease requires an appreciation of disordered three-dimensional anatomy and allows little room for error. Table 17.17 summarises some of the aetiologies of the common congenital cardiac anomalies. Congenital heart surgery is in most countries performed by a relatively small number of expert surgeons working in specialised units. In recent years the care of some congenital defects has been carried out by interventional radiologists. Examples of this are valvotomy for pulmonary stenosis, the use of clam-shell devices to close an atrial septal defect and some ventricular septal defects, and the use of coils to close off large collaterals prior to corrective surgery for pulmonary atresia. There is a very close working relationship between the paediatric cardiologist and surgeon. A functional classification is provided (Box 17.5) in which patients with congenital heart disease fall into one of four groups according to their pulmonary blood flow or vasculature. It is beyond the scope of this chapter to go into the details of individual conditions.

WORKING IN A MULTIDISCIPLINARY TEAM Over the last decade or so, it has become increasing clear that many of the pathologies affecting the heart as well as the great vessels within the thoracic cavity, primarily the aorta, are not the sole domain of cardiac surgery. Surgical solutions remain the gold standard and alternative approaches are benchmarked against the surgical results. Changes in the treatment of aortic stenosis, aneurysms of the aorta and even coronary artery disease will be used as an example to illustrate how treatment modalities on offer has changed of late and continues to change at a rapid pace.

Working in a multidisciplinary team  273 Box 17.5 

Functional classification of congenital heart disease

Normal pulmonary vasculature Without cyanosis n Right-sided obstruction – pulmonary valve stenosis – pulmonary artery stenosis n Left-sided obstruction – aortic stenosis – coarctation of aorta n Myocardial lesions – endocardial fibroelastosis – metabolic heart disease – coronary artery anomalies n Valve and vascular anomalies without shunt – idiopathic dilatation of pulmonary artery – vascular rings – aneurysm of sinus of Valsalva – Ebstein’s anomaly (without shunt) With cyanosis n Partial systemic venous drainage to left atrium n Ebstein’s anomaly (with shunt) Increased pulmonary vasculature Without cyanosis n Extracardiac left-to-right shunts – persistent ductus arteriosus – aortopulmonary window n Intracardiac left-to-right shunts – atrial septal defect – ventricular septal defect – partial anomalous pulmonary venous connection n Extracardiac to intracardiac shunts – ruptured sinus of Valsalva to RA or RV – coronary artery fistula to RA or RV With cyanosis n Bidirectional shunts (admixture lesions) – Transposition of the great vessels – Truncus arteriosus – Total anomalous pulmonary venous connection (supradiaphragmatic) – Double-outlet right ventricle without pulmonary stenosis – Atrioventricular septal defect – Single ventricle Decreased pulmonary vasculature n Tetralogy of Fallot n Tricuspid atresia n Transposition with pulmonary stenosis n Double-outlet right ventricle with pulmonary stenosis n Pulmonary atresia with ASD n Ebstein’s anomaly with ASD n Single ventricle with pulmonary stenosis Pulmonary venous obstruction Without cyanosis n Cor triatriatum n Mitral stenosis n Aortic stenosis n Coarctation of aorta n Stenosis of pulmonary veins With cyanosis n Hypoplastic left heart (mitral atresia, aortic atresia) n Anomalous pulmonary venous connection (infradiaphragmatic) ASD, atrial septal defect; RA, right atrium; RV, right ventricle.

Aortic stenosis The pathophysiology and surgical results for the treatment of aortic stenosis have already been discussed. Without any intervention the outcome in patients with symptomatic aortic stenosis is poor, with a 50% survival at 2–3 years. The results of surgical approach for aortic stenosis have been refined to an extent that isolated aortic valve replacement can be now undertaken with a mortality of around 1–2% universally with excellent medium- and long-term outcome from a functional and survival perspective. Nonetheless, a small but not insignificant group of patients remain a very high-risk population for conventional surgery as highlighted by various risk stratification models. Quite often the operative risks in this setting are increased due to the presence of comorbidities such as impaired pulmonary function, renal impairment, cerebrovascular disease and end-stage poor cardiac function in cases of very late presentation. Risks posed result from the anaesthesia and surgery as well as from the cardiopulmonary bypass required for conventional open-heart surgery. In an attempt to overcome these issues transcatheter aortic valve implantation (TAVI) has been developed to treat this high-risk group of patients with significant aortic stenosis. Biological valves are mounted on balloon-expandable metal stent and introduced either retrogradely through the femoral artery (exposed at the groin) or antegradely through the apex of the heart (exposed through a small anterior thoracotomy, usually in the 5th intercostal space). Once positioned in place within the stenosed native aortic valve, the stent is expanded using a balloon to enlarge the aortic orifice and has a new aortic valve implanted in place within the stent (Fig. 17.14a). TAVI has developed over the last decade or so. Initially it was reserved for use on compassionate grounds but the technology has developed to an extent and the early results have been promising such that this approach is now being used to treat patients at very high risk with conventional surgery (estimated operative mortality of the order of >20% or so). Nonetheless, there remains numerous challenges with regard to the changing stent technology, vascular access to implant the valve, and accurate positioning of the implanted valve. Despite the challenges faced, the early results are promising enough to recommend this approach to patients at very high risk with conventional open-heart surgery as general anaesthetic can be avoided if a femoral approach is taken for the TAVI and there is no need for cardiopulmonary bypass with both the transapical and the transfemoral approaches. The medium- and the long-term outlook remains uncertain at this stage and clearly only a biological valve can be implanted using this approach. The early enthusiasm for this approach has enabled a rapid growth in transcatheter valve implantation and time will tell with regards to its durability in the longer term when compared with a conventional surgical approach. There remains quite marked scepticism amongst some in the surgical fraternity that the risk models being used to justify the use of the transcatheter approach overestimates the risk of conventional surgery. Nonetheless, as the technology evolves, there is no doubt that the transcatheter valve will be established alongside conventional surgery to address aortic stenosis, although the boundaries between different approaches will change with time and indications for each approach will be redefined over time.

Congenital heart disease Working in a multidisciplinary team

17 

274  Cardiac surgery a

b Aorta

Inflated balloon deploying valve in stent Mitral valve

Valve within stent

Native aortic valve orifice

Apex of left ventricle

Fig. 17.14  Transapical and transfemoral catheter-based aortic valve implantation. (a) Insertion of an aortic valve prosthesis via the femoral artery. (b) Insertion of a prosthetic aortic valve via a left ventricle cardiotomy.

Aortic pathology The three main pathologies affecting the thoracic aorta are aneurysms, dissections and traumatic aortic transaction. Conventional surgical approaches to their treatment has been discussed elsewhere. However, the approach to all three of these pathologies has been greatly redefined over the last decade to an extent that endovascular approach to the aorta has become synonymous with thoracic aortic surgery as with abdominal aortic surgery. Multidisciplinary approach here involves interventional radiologist, cardiac surgeon and cardiologist in some groups and close liaison between the expertise of the individual specialties needs to be harnessed to optimise the outcome for this challenging group of patients. Descending thoracic aortic aneurysms can be treated relatively easily with a covered stent to exclude the aneurysmal segment of the aorta from circulation. The stents are introduced via the femoral artery and, once positioned, are expanded using a balloon. A prerequisite factor is the presence of satisfactory landing zones for the stent at either end of the aneurysmal segment of the aorta (Fig. 17.14b). The issue of excluding side branches of the aorta is rarely a major problem in addressing the descending aortic pathology. However, this approach has now been slowly expanded to address the aneurysms of the aortic arch and even the ascending aorta. The side branches in the form of arch vessels, i.e. the head and neck vessels from the aortic arch, pose a considerable challenge. However, this issue has been addressed by undertaking extra-anatomical bypasses to the cerebral and subclavian vessels prior to stenting the aneurysmal arch with a covered stent where the origins of the native arch vessels are excluded from circulation by

the covered stent (Fig. 17.14b). Although conceptually this approach is very attractive and the enthusiasts continue to push back the frontiers, many challenges remain, including stent migration, strut fracture, risk of infection to this large amount of foreign material exposed to blood within the circulation and ‘endoleak’ (continued communication between the endolumen and space outside the stent, between it and the native aortic wall). Similar approaches have been undertaken to address modern approaches to aortic dissection and transections, both extremely challenging surgical groups with a high operative mortality. The precise details of the treatment modalities are beyond the scope here. Suffice to say that in the setting of aortic transaction often seen in multiple injury a covered stent can be implanted across the site of injury/ breach of the aortic wall often covering and excluding the left subclavian artery. This has treated some critically ill patients with excellent early results. The approach to aortic dissection depends on the pathology. Type A aortic dissections are treated surgically because of the risk of proximal extension toward the aortic root, leading to aortic incompetence and coronary insufficiency. Type B aortic dissections only require intervention if there is malperfusion of the side branch, bleeding in the thoracic cavity or late aneurysm formation. In the cases where mal­ perfusion is identified, there may be a role for a percutaneous approach to fenestrate the dissection flap to perfuse the true and the false lumens. Lately there has been some interest in treating the dissection of the descending aorta with a covered stent at the site of the entry point of the dissection flap in order to reduce the risk of future aneurysm formation. Longterm data on this approach are lacking at present.

General comments  275 Coronary artery disease The surgical approach to coronary artery disease has already been discussed. However, the advent of drug eluting stents with significantly lower rates of restenosis compared with earlier bare metal stents or simple angioplasty alone has resulted in further challenges to surgery for coronary artery disease. Superiority of pedicled arterial grafts, i.e. pedicled left internal mammary artery grafted to the left anterior descending artery (LIMA to LAD), is well recognised with a >90–95% patency even after 20 years and remains the gold standard. Total arterial grafting is technically challenging and is not desirable in many patients. Therefore, what is in question is the continued use of vein grafts with a 50% patency at 10 years. The challenge posed by cardiologists to the surgical group has therefore been to address the problem of coronary artery disease in a ‘hybrid’ approach with LIMA to LAD performed surgically and to address other coronary lesions using a percutaneous approach using a drug eluting stent. The strengths of this argument are difficult to deny – especially as LIMA to LAD can be performed with a beating heart ‘off-pump’ technique, thereby avoiding the deleterious effects of the cardiopulmonary bypass and even more the fact that LIMA to LAD can be performed through a limited access approach using a left anterior mini thoracotomy or even totally thorasocopically. This area remains a very grey area where it is hoped that the cardiac surgeon and the interventional cardiologist continue to use evolving technology to look for better ways to advance the treatment of coronary artery disease, hopefully in collaboration with each other!

MINIMALLY INVASIVE CARDIAC SURGERY As with all other branches of surgery there is great enthusiasm for developing minimally invasive cardiac surgical procedures. For example, transcatheter stenting of thoracic aortic aneurysms (Fig. 17.15) avoids major open surgery. However, there are two aspects that need to be considered. First, there is the issue of anatomical invasiveness, i.e. size of the incision and the resultant trauma to the chest wall, and, secondly, the concept of physiological insult of the cardiopulmonary bypass. Each of these aspects will be considered below. Using coronary artery bypass surgery as a model pro­ cedure one can think of a conventional approach through full median sternotomy cardiopulmonary bypass with the heart arrested as the most invasive, gradually proceeding to a stage when the entire procedure could be undertaken thoracoscopically with the heart beating using an off-pump technique. Clearly there are several intermediate stages that are involved here and for all intracardiac procedures, i.e. the vast majority of valvular cases, cardiopulmonary bypass and arresting the heart are mandatory and hence the only scope for improvement is in the size of the incision. The vast majority of cardiac surgical operations are performed through a median sternotomy approach. The extensive size of the incision and the resulting trauma to the chest

wall is not only undesirable for cosmetic reasons but also has a deleterious effect on the respiratory function, postoperative pain, recovery time and possibly even blood loss. Upper partial sternotomy can be used for approaches to the aortic valve and ascending aorta and the mitral valve. Lower partial sternotomy is used for approaches to the mitral valve. Right anterior thoracotomy can be used for approaches to the aortic and the mitral valve and incisions can sometimes be kept very small (down to 4–5 cm in video-assisted cases). Employing a small incision has been shown to have improved functional outcome (cosmesis, quicker recovery time, less blood transfusion, reduced postoperative pain, reduced requirements for analgesia and improved patient satisfaction), although it is believed that the overall outcome in terms of mortality is no different to a conventional approach through a sternotomy. As a result, minimal access cardiac surgery has only been accepted in a limited way. The physiological insult of the cardiopulmonary bypass circuit must not be underestimated. The physiological response to the bypass circuit has already been discussed elsewhere. Although it is desirable to avoid the cardiopulmonary bypass circuit altogether, this is only really an option for coronary artery bypass surgery. Beating-heart off-pump coronary artery surgery has already been discussed. Suffice to say at present, except for certain indications, i.e. diseased ascending aorta, it is considered to be an equivalent mode of conducting CABG operations. It is recognised that technically it represents a higher level of complexity to undertake CABG in this manner with the resultant concerns over the quality and patency of the anastomosis. For intracardiac procedures, cardiopulmonary bypass is mandatory. Therefore improvements to the cardiopulmonary bypass circuit is highly desired by all cardiac surgeons to minimise the physiological insult to the patient. Improvements in the conduct and design of cardiopulmonary circuit have been alluded to earlier in the chapter and remain an area of great research interest.

GENERAL COMMENTS Access For cardiac surgery and transplantation, access is nearly always by a median sternotomy, although more limited (minimal access) approaches are being developed for all types of cardiac procedures. Clear benefits other than cosmesis remain to be proven when compared with conventional access through a full sternotomy and these have been highlighted elsewhere in the chapter.

Preoperative patient briefing Patients should be introduced to the recovery or intensive care unit and have its environment made familiar. Any special problems relating to individual operations should, as far as possible, be explained. Physiotherapy is begun, and the need for cooperation is emphasised.

ICU/recovery Most cardiac surgical patients now go through a specialised recovery/ICU area, requiring a stay of up to 24 hours. The

Minimally invasive cardiac surgery General comments

17 

276  Cardiac surgery a

b

Fig. 17.15  Stenting of descending and aortic arch aneurysms.

most complex patients may still require general ICU stay, as the recovery times are longer. On return to the ward, all patients are further monitored in a high-dependency area, and early mobilisation and physiotherapy are essential in helping patients become able to be discharged home within 1 week of operation. ICU/recovery monitoring involves: n n n n n n n n

continuous ECG, pulse and arterial and central venous pressure monitoring digital oxygenation saturation probe hourly measure of urine output (patient catheterised) hourly measure of peripheral and central temperature quarter-hourly, later hourly, measure of blood loss from chest drains frequent arterial blood gas measurements for Po2, Pco2, pH and acid–base balance controlled infusion pumps for fluid and drug administration general neurological assessment.

Ventilation Cardiac patients are ventilated until they are stable, rewarmed and are making good respiratory efforts with appropriately good arterial gases (usually 4–6 hours postoperatively). Thoracic patients are extubated in theatre and sat up early to encourage better respiratory mechanics. They are usually

managed in a general recovery area rather than fast-track or ICU.

Pain control Effective prevention of pain is of importance in all cardio­ thoracic surgery because it lessens the risk of postopera­ tive myocardial events, improves postoperative respiratory movements and increases the value of physiotherapy. Epidural analgesia and continuous opioid infusion controlled by the patient (PCA) are common methods which may be combined with local analgesia block of intercostal nerves at the time of thoracotomy.

Chest drainage All cardiac drains are connected to a closed underwater system to prevent an open pneumothorax occurring and to allow the lungs to maintain the normal negative intrathoracic pressure. Additionally, low-pressure suction is applied to encourage the release of air or blood from the operated site; this is particularly valuable after lung resection as suction helps the lung to seal its leaks by adhering to the chest wall.

Antithrombotic therapy For CABG, aspirin is commenced on day 1 and continued long term. For valve patients, warfarin is commenced on day 1, and INR is monitored daily until stabilised.

General comments  277 Long-term antithrombotic treatment depends on the procedure. After CABG with vein grafts, low-dose aspirin is necessary. Long-term secondary preventative strategy involves the use of cholesterol-lowering agents.

Return to full activities Most patients are able to return to work or full activities 2–3 months after a CABG. Convalescence after thoracic

procedures may be shorter, but this depends on the degree of respiratory reserve available. Secondary control of coronary risk factors is important in the long term. A statin drug is given to all hyperlipidaemic patients; hypertension and diabetes medication should be continued. Smoking must cease.

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18 

Oesophagus, stomach and duodenum

OESOPHAGUS

279

Oesophageal diverticula

283

Motility disorders

280 280 281 281

Oesophageal rupture and mucosal tear (Mallory–Weiss syndrome)

283

Cancer of the oesophagus

284

STOMACH AND DUODENUM Peptic ulcer disease

286 286

Gastroduodenal tumours

288

Hypermotility Hypomotility Achalasia

Gastro-oesophageal reflux disorders Hiatus hernia Reflux without abnormal anatomy

281 282 283

OESOPHAGUS Anatomical and physiological considerations The oesophagus is a muscular tube connecting the pharynx to the stomach, lined predominantly by squamous epithelium and guarded at both ends by sphincters. It lies anterior to the cervical vertebrae in the neck and in the posterior mediastinum in the chest and enters the abdomen through the oesophageal hiatus in the diaphragm. The last 2–3 cm are within the abdomen above the gastro-oesophageal junction with the stomach. The anatomical relationships between the oesophagus and the other mediastinal structures are illustrated in Figure 18.1. The mucosal lining of the oesophagus is pale grey and consists of squamous epithelium. The musculature of the upper two-thirds of the oesophagus is striated (though not under voluntary control) and that of the distal third is smooth. In contrast to most of the intraperitoneal gastrointestinal tract, the oesophagus is devoid of a serosal layer – a matter of some importance to the spread of malignant disease. For descriptive purposes, tumours are usually classifed as occurring in the upper, middle and lower thirds. The two sphincters are at the pharyngo-oesophageal junction (upper) and in the region of the oesophageal opening (hiatus) in the diaphragm. Both have intrinsic and extrinsic components. The upper intrinsic sphincter has the main function of preventing access of air to the oesophagus and working in conjunction with laryngeal closure during swallowing. It relaxes on initiation of the swallowing reflex, and the superior constrictor extrinsic component contracts to expel food or liquid into the oesophagus where a wave of peristalsis carries it downwards. Disorders of the upper sphincter are considered in Chapter 10. The lower intrinsic sphincter is the circular smooth muscle of the oesophagus, although anatomical as distinct from

physiological identification of a specific sphincter zone has proved difficult. Its role is to prevent gastro-oesophageal regurgitation, and it is normally closed but relaxes in response to the swallowing wave. Relaxation may fail in oesophageal motility disorders and low resting sphincter pressures are often seen in gastro-oesophageal reflux disease (GORD). The intrinsic sphincter is supplemented by the striated muscle of the right crus, which splits to embrace the lower end of the oesophagus, but it is probably involved only in keeping the gastro-oesophageal junction closed when intra-abdominal pressure is significantly increased as in straining. Another factor which prevents reflux from the stomach is the acute angle of insertion of the oesophagus into the stomach which brings the gastric and oesophageal walls in contact when intra-abdominal pressure rises. Anatomical disorders at the diaphragmatic hiatus reduce the efficacy of the intrinsic sphincter (see ‘Hiatus hernia’).

Clinical features of oesophageal disease Symptoms Dysphagia

Difficulty in swallowing may be: n

progressive when a lesion such as a malignant growth or a stricture reduces the size of the oesophageal lumen n non-progressive in disorders of function either of the whole oesophagus or at the lower sphincter. Progressive difficulty eventually goes on to total dysphagia when neither food, liquid nor the patient’s own saliva can be swallowed. This circumstance is an emergency. High grades of dysphagia are often associated with regurgitation into the pharynx and upper air passages and therefore with respiratory infection.

18 

280  Oesophagus, stomach and duodenum Endoscopy The flexible oesophago-gastroduodenoscope (see Ch. 4) is now often used as an alternative or complement to contrast radiology to achieve a diagnosis and has the advantage of being able to take tissue for histological examination. Endoscopic ultrasound is used to assess the T and N stage of oesophageal cancers.

Arch of aorta

Left bronchus Right bronchus

Manometry and oesophageal pH studies and impedence monitoring

Oesophagus Descending thoracic aorta

Stomach

Fig. 18.1  Anatomical relationships of the oesophagus. Pain Pain is ill-localised in the chest (often called substernal but more correctly retrosternal) and may accompany partial dysphagia from obstruction. It also occurs in motility disorders. Confusion with pain originating in heart muscle is common.

Heartburn Heartburn is a retrosternal sensation of discomfort and burning and may be a minor form of pain. It is the consequence of regurgitation from the stomach into the normally empty oesophagus. If there is considerable reflux, the patient may be conscious of the presence of liquid in the pharynx.

Signs The deep situation of the oesophagus usually makes specific clinical features entirely absent. Those which may accompany individual disorders are considered below.

Investigation Radiology n

Anteroposterior plain X-ray may occasionally show a broadening of the mediastinal shadow by a dilated oesophagus, but the finding is non-specific. An air–fluid level may be seen behind the heart if there is distal oesophageal obstruction. n Contrast radiology, usually with barium sulphate but in special circumstances with a water-soluble contrast medium, is the standard method of establishing both anatomical and functional abnormality. n CT scanning (and increasingly MRI) is used to assess tumours of the oesophagus giving information on the stage (T, N, M).

This investigation has an important role in the analysis of disorders of motility. In addition, similar equipment can be used for monitoring the acid level in the oesophagus in patients with suspected reflux. The technique is to place a pH sensor at the end of a tube in the lower oesophagus and to make continuous recordings over 24 hours. In normals there should be little change; however, in those with reflux of acid contents, the pH falls sporadically, particularly at night. The introduction of a capsule that can be temporarily fixed to the oesophageal mucosa at endoscopy (Bravo capsule) allows the measurement of oesophageal pH for up to 48 hours without the need for naso-oesophageal catheters. Measurements are transmitted wirelessly to an external receiver. Oesophageal impedence monitoring measures fluid and gas flows through the oesophagus by measuring electrical impedence using a catheter with multiple electrodes. In oesophageal transit tests this can be used to measure the clearance of a swallowed bolus, while in patients with suspected gastroesophageal reflux it can be used to measure reflux independent of its acidity.

MOTILITY DISORDERS Much has still to be learnt about these disorders, but a working classification is into those which involve: n

Hypermotility – chiefly diffuse spasm. Hypomotility – usually secondary to systemic sclerosis (scleroderma). n Sphincter dysfunction – especially the inability of the lower sphincter to relax (achalasia). n

HYPERMOTILITY

Diffuse oesophageal spasm Aetiology The cause is unknown and the condition is rare – or at least rarely recognised. There may well be a physiological link between this condition and achalasia (see below).

Clinical features The combination of intermittent, often quite severe, chest pain with dysphagia is characteristic. The condition may lead to investigation under a provisional diagnosis of angina pectoris.

Gastro-oesophageal reflux disorders  281 Investigation and management A contrast study shows exaggerated oesophageal contractions which may outline the gullet as a corkscrew. Oesophagoscopy is usually normal, but manometry shows exaggerated contractions. Drugs that reduce smooth muscle contraction (nitrates and calcium channel blockers such as nifedipine) occasionally help. Balloon dilatation is also an option, but in those with severe symptoms a long oesophageal myotomy in which all layers of muscle down to mucosa are divided may be required.

Nutcracker (super-squeeze) oesophagus It is uncertain whether this condition is a distinct entity. It is a common manometric finding in patients who present with chest pain which is of non-cardiac origin. The symptoms are the same as those for diffuse spasm, as is the management. However, surgical treatment is rarely required.

HYPOMOTILITY The only well-recognised disorder that causes hypomotility is systemic sclerosis – a condition of unknown cause. The muscle layer is replaced by fibrous tissue. The presence of the disease may be suspected from other features such as loss of mobility of the face and microvascular features, e.g. digital ischaemia.

Investigation and management Contrast radiology shows diminished peristalsis, and this can be confirmed by manometry. The treatment of hypomotility is that of the complications such as gastro-oesophageal reflux (see ‘Hiatus hernia’).

ACHALASIA This is commonly known as cardiospasm.

Aetiology In the great majority of patients the cause is unknown, but a similar clinical condition is found in South America as a result of infection with a protozoan organism Trypanosoma cruzi. The lower sphincter fails to relax in response to the peristaltic wave, and the bolus is partially retained in the oesophagus.

Clinicopathological features Dilatation and muscular hypertrophy occur above the lower sphincter. Histological examination shows loss of ganglion cells (see also ‘Hirschsprung’s disease’). In long-standing cases the oesophagus becomes elongated and its mucosa inflamed from stasis of food. The latter finding is a probable cause of the increased risk of the development of malignant change. There is not initially frank dysphagia but rather a slowing down of the normal rate of ingestion of food, so that at a meal the patient gets ‘left behind’. Obvious dysphagia ultimately develops with retrosternal discomfort, regurgitation

and weight loss. Onset of these symptoms in later life may lead to confusion between achalasia and carcinoma.

Investigation Endoscopy is essential and in older patients may show a secondary cause such as infiltration of the distal oesophagus by malignant disease. Contrast study confirms delay at the lower sphincter, although in early symptomatic patients the abnormality may be difficult to identify. Manometry shows incomplete relaxation of the lower sphincter in response to a swallow.

Management Medical treatment with muscle relaxants is usually unrewarding. The three effective methods are: n

Balloon dilatation, which leads to resolution of symptoms in 80% although it may have to be repeated and carries a small risk of oesophageal perforation. n Longitudinal myotomy of the gastro-oesophageal junction (known to surgeons as Heller’s operation) which can be done either at open operation or via a laparoscope or thoracoscope; some surgeons combine myotomy with an anti-reflux procedure. Surgical myotomy is associated with the risk of gastrooesophageal reflux but is otherwise a very satisfactory procedure. n Endoscopic injection of botulinum toxin into the oesophageal wall to paralyse the lower oesophageal sphincter is effective but lasts only for a few months. Repeated injections are possible.

GASTRO-OESOPHAGEAL REFLUX DISORDERS Features of reflux occur in association with many different oesophageal conditions, including most of the motility disturbances described above. However, reflux is particularly a symptom of abnormalities at the diaphragmatic hiatus.

Pathophysiological features If either acid or strongly alkaline (as may occur if there are large amounts of reflux from the duodenum) secretions reach the lower oesophagus, mucosal inflammation follows. Although this is mostly a superficial oesophagitis, there may be two consequences: Stricture – this is usually predominantly an inflammatory reaction in the mucosa and submucosa, but it can, if inflammation takes place, become a fibrous narrowing. n Metaplastic change – this leads to the development of gastric-type columnar epithelium in the lower oesophagus. This was first described by the British surgeon Norman Barrett and is, in consequence, often known as ‘Barrett’s oesophagus’. Its significance is that it is a remalignant lesion; adenocarcinoma of the lower oesophagus may develop at an estimated incidence of 0.5% per patient year. n

OESOPHAGUS Motility disorders Hypermotility Hypomotility Achalasia

Gastrooesophageal reflux disorders

18 

282  Oesophagus, stomach and duodenum

Clinical syndromes

Contrast radiography

There are two main causes:

The standard method of making the diagnosis is by barium swallow and meal (although some cynics say that a determined radiologist can identify a hiatus hernia in almost anyone). More often patients are now investigated by endoscopy.

n n

hiatus hernia with reflux reflux without abnormal anatomy.

HIATUS HERNIA There are two types of hiatus hernia: sliding and paraoesophageal. Occasionally these can be mixed (so-called type III). Although only the first is usually associated with reflux, both will be considered here.

Sliding hernia

Endoscopy Although it is not always easy to identify the oesophago­ gastric junction, this examination allows assessment of the severity of oesophagitis, and a tissue diagnosis by examination of a biopsy may be made in patients with Barrett’s oesophagus.

pH monitoring and impedence studies

The proximal stomach ascends into the chest through a lax or enlarged diaphragmatic opening, taking a circumferential cuff of peritoneum with it. The normally acute oesophago­ gastric angle is reduced, so that reflux is common even though the intrinsic lower sphincter is normal (Fig. 18.2a).

Oesophageal pH and, in some patients, impedence studies are useful in cases of diagnostic uncertainty and as a baseline measurement before surgical treatment.

Management The great majority of patients can be managed by medical measures for the control of reflux, including:

Aetiology Some examples of sliding hernia may be congenital but in most the cause is not established. Obesity, increase in abdominal contents (pregnancy) and ageing may be contributory factors.

Clinical features There is postural reflux, heartburn and occasionally some lower left chest pain. However, the latter should only be ascribed to a postulated or actual hiatus hernia with caution. Vague indigestion is rarely caused by a sliding hernia and must be explored clinically and by investigation for an underlying cause.

Investigation Patients with the recent onset of symptoms, particularly if they are elderly, should be investigated for possible oesophagogastric cancer.

n

weight loss in the obese sleeping with the head of the bed raised to avoid nocturnal reflux n alginate-containing antacids which are thought to reduce free liquid in the stomach and thus reduce the volume of reflux n acid reduction by H2-receptor antagonists (e.g. cimetidine or ranitidine) or proton pump inhibitors (e.g. omeprazole or lansoprazole). n

If these measures fail to control symptoms or the patient is not keen on long-term medication, then operation should be considered. However, it must be absolutely clear that the symptoms of which the patient complains are the consequence of the presence of gastro-oesophageal reflux, otherwise a dissatisfied patient will be the outcome. A surgical repair is now almost always carried out at laparoscopy. This involves: n n n

Cardio-oesophageal junction Hernial sac

Fig. 18.2  (a) The oesophagogastric anatomy in a sliding hiatus hernia. (b) The anatomy in a para-oesophageal hernia.

n n

reduction of the herniated stomach below the diaphragm removal of the circumferential peritoneal sac re-establishment of the oesophagogastric angle reduction of the intercrural space by suturing the crura together behind the oesophagus an anti-reflux procedure – often loosely called a fundoplication.

The fundus of the stomach is wrapped around the terminal oesophagus so that, as intra-abdominal pressure rises, the oesophagus is compressed (Fig. 18.3). One complication of such a procedure may occasionally be the inability to belch and, in consequence, bloating – a sensation of unrelieved fullness of the stomach. In addition, some patients experience postoperative dysphagia, which is usually transient. However, the outcome is usually good, and surgery should not be withheld provided the surgeon is satisfied with the relationship between the symptoms and the hernia – particularly given evidence from oesophageal pH monitoring.

Oesophageal rupture and mucosal tear (Mallory–Weiss syndrome)  283 Features of heartburn and dyspepsia are universal, with regurgitation of gastric contents in some.

Investigation Many patients are probably treated symptomatically in general practice without investigation. However, those with troublesome features should have a barium swallow and/or endoscopy. Ambulatory monitoring of lower oesophageal pH may establish that there is persistent reflux, and oesophageal manometry identifies those with a motility disorder.

Management Medical management as described above is often sufficient. For those with oesophagitis which is unresponsive to treatment (rare) and for patients who are not keen on long-term acid supression therapy, an anti-reflux operation should be considered.

OESOPHAGEAL DIVERTICULA Hypopharyngeal pouch is the most common of these. Other diverticula in lower parts of the oesophagus are rare.

Fig. 18.3  A fundoplication operation. The gastric fundus is wrapped around the abdominal oesophagus.

Para-oesophageal hernia Aetiology A discrete peritoneal sac occurs at the left lateral border of the oesophagus, and the fundus of the stomach rolls into this, sometimes carrying the oesophagogastric junction into the chest (Fig. 18.2b). More complicated examples may cause a twist of the whole stomach – a gastric volvulus.

Clinical features These patients are usually asymptomatic, although vague upper abdominal pain may occur. Incarceration going on to strangulation is not common but causes acute upper abdominal pain and what appears to be vomiting but is in fact total dysphagia. This occurrence – usually in elderly frail individuals – is a surgical emergency.

Management Unless the patient is unfit, para-oesophageal hernias should be repaired surgically because of the risk of strangulation. Usually this is done laparoscopically.

REFLUX WITHOUT ABNORMAL ANATOMY

Aetiology and clinical features Many patients have symptoms of reflux without any demonstrable anatomical abnormality. In some, obesity is a factor; others may have hyperchlorhydria with or without a demonstrable peptic ulcer. In the majority a definite cause is not identified.

OESOPHAGEAL RUPTURE AND MUCOSAL TEAR (MALLORY– WEISS SYNDROME) Aetiology Vomiting is usually a coordinated event. The stomach and diaphragm contract so that intragastric pressure is raised; the oesophageal sphincters then relax, as does the oesophagus as a whole, and the stomach content is ejected. However, this orderly course may not take place if: n n

vomiting is artificially induced, or the individual is confused – usually from excessive consumption of alcohol.

In such circumstances, intragastric pressure forces stomach contents into the distal oesophagus, dilating it. The oesophagus may rupture with emptying of stomach contents into the left pleural cavity. Because the relatively elastic muscle in the oesophageal wall has a greater capacity for stretch than does the folded mucosa and submucosa, quite often only these are split to produce a longitudinal mucosal tear at the oesophagogastric junction (Mallory–Weiss syndrome).

Oesophageal rupture Clinical features History Forceful vomiting may be recalled, but if there has been much intake of alcohol it is sometimes forgotten. Vomiting may also have been induced either in a glutton or in someone who is mentally disturbed with a history of excessive eating but with the paradoxical desire not to gain weight (bulimia). There will be sharp left-sided pleuritic pain.

Hiatus hernia Reflux without abnormal anatomy

Oesophageal diverticula Oesophageal rupture and mucosal tear (Mallory–Weiss syndrome)

18 

284  Oesophagus, stomach and duodenum

Physical findings The effect of gastric content within the chest is to rapidly produce signs of severe sepsis with fever and circulatory disturbance. A left pleural effusion is present. The course is downhill with all the features of systemic inflammatory response syndrome. Occasionally, however, the rupture is localised and the patient is less ill with localised pleural signs and features of sepsis which are less severe.

Management In early rupture, the oesophagus is exposed surgically and repaired. The area is drained and a gastrostomy is often done to drain gastric secretions, although whether this is effective is not established. Parenteral or enteral (jejunostomy) nutrition is used until healing is assured.

Mucosal tear (Mallory–Weiss syndrome) The presentation of this condition is with haematemesis, and it is therefore considered in Chapter 23.

CANCER OF THE OESOPHAGUS Epidemiology This condition is relatively rare in the Western world. However, studies have revealed a wide geographical variation with pockets of high incidence. For example, although the incidence in Europe overall is between 2 and 8 cases per 100 000 population, in some areas of northern France this figure may be as high as 30/100 000. In the Far East the incidence is in general much higher and may be between 100 and 150/100 000 in some provinces of China. Such a level warrants screening programmes within populations at high risk. Overall, the incidence is rising worldwide.

30 years ago the ratio was in the reverse direction. Metaplastic change in the oesophageal mucosa from squamous to columnar epithelium as a result of gastro-oesophageal reflux (Barrett’s oesophagus) predisposes to the development of adenocarcinoma. Endoscopic screening of all patients with significant reflux symptoms has been recommended to identify those with Barrett’s oesophagus. The magnitude of this risk varies, with dysplastic mucosal changes, intestinal metaplasia and length of Barrett’s mucosa all being factors which increase the chance of malignant change. Regular endoscopic surveillance with biopsy is indicated in such patients, particularly if risk factors are present, in an effort to detect early malignant change at a stage when curative treatment is possible.

Pathological features Nearly all lesions are a combination of narrowing and ulcer­ ation, although the extent of each varies. Spread takes place by: direct invasion first through the full thickness of the oesophageal wall and thence into adjacent structures such as the trachea or bronchi, the pericardium, chest wall and diaphragm. Once a fistula into the air passages has occurred, the condition is incurable and life expectation is short n submucosal infiltration both proximally and distally so that, if mucosal destruction is used as an indication of the extent of spread, there may be an underestimate of the extent of the growth n lymph node involvement in the mediastinum and, in distal lesions, around the stomach – the pattern is often not sequential. Upward spread in the mediastinum may produce a sentinel node in the supraclavicular fossa n the bloodstream – this is unusual in the early stages, but by the time of death up to 90% of patients may have distant metastases (liver, lung and brain). n

Aetiology Squamous carcinoma

Clinical features Symptoms

The wide geographical variation in incidence has been attributed to social and environmental factors. There appears to be a strong association between cigarette and alcohol consumption and the incidence of the disease. However, diet is probably of greatest importance. Three factors are recognised:

In early disease, for example those detected by endoscopic surveillance of patients with Barrett’s oesophagus, there may no symptoms. For others the mean duration of symptoms is 4–6 months but may be up to 3 years. To compound this, as is explained below, the average delay in presentation after their onset is 3–4 months. Early ill-defined symptoms. The lack of well-defined symptoms while the disease is developing is one reason why so few cases of oesophageal cancer are diagnosed while the condition is still in a pathologically early stage. There may be a feeling of something stuck in the oesophagus, although not necessarily after eating. Retrosternal discomfort, belching and dyspepsia are often elicited on detailed questioning but may have been discounted by the patient. Progressive dysphagia is the most common and important presenting symptom but may not be noticed until the oesophageal diameter is reduced by two-thirds. In the early stages, dysphagia is for solids only – particularly bulky foods such as meat and bread; only later is there difficulty with liquids. In the interim, most patients have simply

n

high intake of nitrosamines derived from nitrates used in food preservatives n low intake of both vitamin A and nicotinic acid n iron deficiency anaemia, a known associate of hypopharyngeal cancer but probably also a factor in cancer of the body of the oesophagus. Long-standing achalasia may lead to cancer, presumably because of stasis and mucosal irritation. The reported incidence is highly variable but may reach 2%.

Adenocarcinoma Cases of adenocarcinoma of the oesophagus now exceed those of squamous carcinoma in a ratio of 2 : 1, whereas

Cancer of the oesophagus  285 accommodated to their symptoms by dietary alteration such as avoiding solids. Regurgitation after eating may be misinterpreted as vomiting, and in consequence there may be delay until dysphagia is total (inability to swallow saliva). Weight loss. As dysphagia develops there is usually an associated dramatic decline in weight. More than 10–15% of the pre-illness weight may be lost over 4–6 weeks. Acute obstruction. A sudden acute obstruction may occasionally be precipitated in a symptomless patient by the impaction of a large (usually inadequately chewed) food bolus. For those patients who have developed an adenocarcinoma in an area of columnar metaplasia, a long history of heartburn suggestive of acid reflux may be elicited but is rarely volunteered. Pain is ominous and may indicate penetration of the tumour outside the wall of the oesophagus. Productive cough, particularly at night, may be produced either by aspiration of retained material into the respiratory tract or by the development of a malignant oesophagotracheal fistula. Hoarseness may mean involvement of the recurrent laryngeal nerve. Features of distant metastases can be the cause of presentation of a few patients.

n

concurrent dilatation and temporary relief of obstruction, although this is not usually performed.

However, it has some dangers, such as: n

perforation of a malignant or fibrotic stricture or diverticulum – flexible instruments make this unlikely unless dilatation of a stricture is undertaken n failure to detect a small lesion – though in experienced hands this is rare.

Further investigation Once the diagnosis is confirmed, further study is required to assess the stage of the disease and to determine the suitability of the patient for operative treatment.

Endoscopic ultrasound scanning (EUS) It is possible to obtain images from an ultrasound probe attached to an endoscope within the oesophagus which can accurately measure the depth of penetration of the growth into the oesophageal wall and assess involvement of mediastinal and perigastric lymph nodes.

Computed tomography

Signs Clinical examination of a patient with localised oesophageal cancer usually does not reveal any abnormalities other than evidence of recent weight loss. Total dysphagia is associated with signs of lack of water – reduced skin turgor and a coated furred tongue. A quarter of patients have palpable lymph­ adenopathy, which is usually in the supraclavicular region and is an indication of metastatic disease. Other signs of dissemination include hepatomegaly, jaundice, ascites, cardiac arrhythmias and features of pulmonary consolidation. Although the last may indicate advanced disease, respiratory infection may develop because of aspiration of oesophageal content.

Investigation Radiography Barium swallow has the advantages of: n n n n n n

simplicity relative lack of expense high sensitivity in diagnosis of a stricture, although this does not necessarily indicate that it is malignant accurate determination of the anatomical site definition of the anatomy of the stomach and duodenum – important for surgical planning creation of a ‘road map’ for endoscopy and thus a reduction in the risk of perforation, as well as indicating the level at which a lesion is likely to be found.

However, this investigation is often now omitted in favour of endoscopy.

Endoscopy This procedure is now usually done with a flexible instrument under local anaesthesia or sedation. It allows: n

biopsy and brush cytology for pathological confirmation of the type of cancer n assessment (partial) of the extent of the lesion

CT scan of both chest and abdomen may also detect metastases but is also helpful in determining the size of the primary and whether it is attached to surrounding structures. A fistula into the air passages may also be detected.

PET scanning PET scanning (FDG) is increasingly used to exclude distant metastatic disease in patients being considered for radical treatment (surgical resection or chemoradiotherapy). It may identify metastases not seen on other imaging modalities.

Screening The relative rarity of the condition in Western societies makes routine screening economically inappropriate, although it is indicated in high-risk groups such as those with Barrett’s oesophagus. However, in places where the incidence is high (such as China and Japan), routine flexible oesophagoscopy and/or obtaining oesophageal specimens for cytology are increasingly being recommended to detect early asymptomatic disease.

Management Endoscopic treatment For very early cancers (mucosal/submucosal involvement only) endoscopic therapy by submucosal resection (EMR) or radiofrequency ablation (RFA) may be considered, particularly in patients at high risk for operative treatment. Careful endoscopic follow-up is required because of the risk of local recurrence of cancer. These techniques and photodynamic ablative therapy (PDT) are also used for patients with high-grade dysplastic change within a Barrett’s oesophagus.

Surgical resection Surgical resection of oesophageal cancer is confined to patients with ‘operable’ disease – locally removable cancer and no detectable distant metastatic disease – who are considered fit enough for the major operation required.

Cancer of the oesophagus

18 

286  Oesophagus, stomach and duodenum

There is good evidence now that neoadjuvant chemotherapy, sometimes combined with radiotherapy, increases the frequency of complete cancer excision and significantly improves overall survival rates and disease-free interval. Such multimodal treatment is now standard practice apart from patients with very early stage disease (T1,N0,M0). Contraindications to surgery include: n

poor cardiovascular, pulmonary or renal function tracheo-oesophageal fistula n other evidence of advanced local disease n distant metastatic disease. n

The principles of resection with cure in mind are: n n

wide resection margins radical lymph node clearance within the chest and for distal growths at the oesophagogastric junction also in the upper abdomen.

The conventional method of resection is by open operation which may involve opening both the abdomen and thorax. However, two alternatives are now available: Trans-hiatal removal. The abdomen alone is opened and the oesophagus freed in the chest by blunt dissection through the diaphragmatic hiatus. Stomach (or colon) for reconstruction is then passed through the posterior medi­ astinum to the neck where it is anastomosed to the upper oesophagus through a cervical incision. This procedure is used by some surgeons for patients with Barrett’s oesophagus containing high-grade dysplasia and thus having a very high risk of developing adenocarcinoma. Minimal access surgical removal. The whole procedure can now be done by minimal access dissection within the

chest (thorascopy) and abdomen (laparoscopy), although there is little current evidence that this method is better than open operation.

Other methods of restoring swallowing In patients unsuitable for surgical treatment, other methods can be used to relieve dysphagia, as follows. Chemotherapy (e.g. with 5-fluorouracil [5-FU] and cisplatin), either alone or preferably in combination with radiotherapy, may lead to total disappearance of the local tumour in 30% of patients. Combined radiochemotherapy is used in some centres as primary radical treatment for squamous carcinoma. Resection in these cases is reserved for local recurrent or residual cancer. Endoscopic insertion of self-expanding metal endoprostheses – some of which are covered with a plastic membrane through the area of tumour stricturing and may provide palliation by improving swallowing. Covered stents can also be used to close fistulas between oesophagus and trachea. Local endoscopic destruction of the tumour by laser or argon-beam diathermy, which can be repeated.

Prognosis The outcome of resection depends on the stage of the growth. When tumour is confined to the mucosa, a 5-year survival of 80–90% is possible, but any further spread means a fall-off to less than 5% for growths that have penetrated the full thickness of the gullet. Combined regimens of resection and neoadjuvant combinations of radiotherapy and/or chemotherapy are producing improved results.

STOMACH AND DUODENUM PEPTIC ULCER DISEASE Surgeons are now mainly called on to treat the complications of this condition (Box 18.1), but to do so they require some understanding of the causative mechanisms responsible, the pathological changes and their effects.

Epidemiology Helicobacter pylori infection is now recognised as the main cause of peptic ulceration. There is a close association between peptic ulcer disease and poor socio-economic conditions and their consequences. Hence the condition is more Box 18.1  n

Indications for surgical intervention in peptic ulcer

Urgent complications – Bleeding (Ch. 23) – Perforation (Ch. 23) n Obstruction – usually by inflammation and fibrosis at the outflow of the stomach n Malignancy – gastric ‘ulcer’ (always a primary cancer which has been partially digested)

common in the developing rather than the developed world. Relevant factors may be tobacco and alcohol consumption, which tend to be higher amongst the poor and deprived. In duodenal ulcer, males outnumber females by a factor of 4, but gastric ulcer is equally distributed and its incidence increases with age.

Aetiology The discovery of Helicobacter pylori as a strong associate of peptic ulceration in both the stomach and duodenum, and the additional observation that its eradication can lead to cure, has made it clear that infection with this bacterium is the cause of peptic ulceration in most case. The mechanisms by which the organism exerts it effects, and particularly the way in which it causes the acid hypersecretion commonly seen in duodenal ulcer, are still uncertain. Moreover, there must be an idiosyncratic component to the H. pylori–ulcer diathesis because many people have H. pylori present without suffering a peptic ulcer. A relationship is also apparent between acute peptic ulceration and the consumption of non-steroidal antiinflammatory agents (NSAIDs). Patients, particularly the elderly, are increasingly being prescribed these drugs, and

Peptic ulcer disease  287 there is therefore a rising incidence of acute ulceration with complications such as perforation and haemorrhage. It is not clear whether the relationship implies a cause of peptic ulceration, but it seems more likely that NSAIDs upset the balance between mucosal regeneration and repair and therefore present a hazard for anyone who also has a peptic ulcer. Other antecedents of peptic ulcer which can have a bearing on management are shown in Table 18.1.

Anatomical and pathological features These features are of mucosal loss accompanied by chronic inflammation with varying amounts of fibrosis. An ulcer penetrates to a varying depth in the gastric or duodenal wall and may involve neighbouring organs such as the pancreas. Free perforation into the peritoneal cavity takes place when the rate of ulceration exceeds that of repair, and the final event is that the base of the ulcer becomes necrotic and gives way. An artery in the base may undergo fibrinoid necrosis of its media so that it becomes rigid and therefore more difficult for natural processes to close should bleeding take place; this is a more likely explanation of continued bleeding than the presence of atherosclerosis in the arteries of the gastric or duodenal wall, which is almost unknown. Gastric ulcers can occur anywhere but are most commonly found on the lesser curvature at the junction of antral and acid-secreting mucosa. It used to be thought that a benign gastric ulcer could undergo malignant change, but what appear to be instances of this are merely partial peptic digestion of a primary malignant tumour.

Clinical features Symptoms Both gastric and duodenal ulcers cause epigastric pain, and it is often difficult to distinguish one from the other, although it is often stated that patients with gastric ulcer have pain on eating and those with duodenal ulcer complain when they are hungry. Pain felt in or going through to the back can mean that the ulcer has penetrated into retroperitoneal structures such as the pancreas. Indigestion is often associated with the pain. Heartburn from acid-peptic reflux is common. Symptomatic episodes with temporary remissions which can last weeks or months are more characteristic of duodenal than gastric ulcer. In both, the symptoms are relieved by antacids. Vomiting is seen in gastric outflow obstruction (usually from a duodenal ulcer, although a pyloric channel gastric

Table 18.1

ulcer can also be the cause). Obstruction is the consequence of inflammatory oedema and/or fibrosis. In the first it subsides with effective anti-ulcer treatment; in the second it persists. The vomitus is usually free from bile and may contain partially digested food, recognisable as a meal taken a day or more before. Patients with gastric outflow obstruction often lose weight, but unless the obstruction is complete and vomiting profuse, they do not become dehydrated in that absorption of water and electrolyte still takes place across the gastric wall.

Signs In uncomplicated peptic ulcer, epigastric tenderness is the only feature, and even this is non-specific since a mild degree of tenderness can be present in normal people. Obstruction is associated with a succussion splash – a splashing sound heard upon gently rocking the patient’s abdomen to and fro. When obstruction is present, there may be signs of weight loss and of extracellular fluid volume deficiency with a lax dry skin and empty collapsed veins. Features of hypokalaemia such as drowsiness are the consequence of: n n

loss of hydrogen ions from the stomach compensatory renal excretion, first of sodium ions but later, and more importantly, of potassium ions.

Investigation Endoscopy The current initial investigation of the patient with indigestion which suggests peptic ulceration is by endoscopy, although, if this is the first episode, young patients (50

RESTRICTIVE PROCEDURES

The laparoscopic adjustable gastric band The adjustable gastric banding is a purely restrictive proce­ dure consisting of the placement of an inflatable prosthetic ring just below the gastroesophageal junction to create a small proximal gastric pouch (Fig. 19.1). The objective is to reduce food intake and to induce an early feeling of satiety. The band should therefore help to prevent overeating and decrease the overall daily calorie intake. The gastric band can be adjusted postoperatively by injecting or removing fluid from the band via a subcutaneous injection port. The first injection normally takes place 6 weeks after the band has been placed. The number of injections required varies between patients. Studies have shown that average weight

Fig. 19.1  Adjustable gastric banding. loss achieved is approximately 50–60% of excess body weight. There is, however, a large variation in results and adherence to dietary instructions and behavioural modifica­ tion is necessary to achieve good results. The specific com­ plications of gastric banding include gastric pouch dilatation, band slippage, gastric erosion, prosthesis infection, patient intolerance and subcutaneous port complications. The pro­ cedure is performed laparoscopically in the vast majority of cases.

The laparoscopic sleeve gastrectomy The sleeve gastrectomy (Fig. 19.2) is a restrictive operation that is increasingly used in super-obese patients (BMI > 50 kg/m2). It involves resection of the greater curve of the stomach, which is permanently removed. It has the advan­ tage of being technically easier than malabsorptive proce­ dures and avoids complications associated with foreign prostheses and anastomoses which may be more hazardous in super-obese patients. It also avoids malabsorptive com­ plications such as ‘dumping syndrome.’ Patients may still be considered for later conversion to a malabsorptive procedure if adequate weight loss is not achieved, though recent evi­ dence suggests it may offer an effective standalone proce­ dure. Specific complications include leakage from the gastric staple line, bleeding and gastric tube stricture.

COMBINED RESTRICTIVE/MALABSORPTIVE PROCEDURES

The laparoscopic gastric bypass The gastric bypass produces a restriction of food intake by creating a small gastric pouch and mild malabsorption by

Surgical options  295 Resected stomach

Definition and aetiology Epidemiology Management of obesity Surgical options Restrictive procedures

Gastric sleeve

Combined restrictive/ malabsorptive procedures

Pylorus

Summary

Excised stomach

Fig. 19.2  Sleeve gastrectomy. Bypassed small intestine Common channel Pouch

Fig. 19.4  Biliopancreatic diversion with duodenal switch.

Roux limb Bypassed small intestine

Bypassed portion of stomach

proximal jejunum. The base of the Roux limb is reconnected to the remaining portion of the small intestine forming a Y-shape. Reduced absorption of vitamins and minerals may be experienced. The gastric bypass is considered to be major surgery and involves making permanent changes to the digestive system. Specific complications of the gastric bypass include anastomotic leaks, internal hernias, and per­ nicious anaemia. Weight loss is rapid in the first year and maximum weight loss is achieved at 18 months to 2 years. Expected weight loss is approximately 65–70% of excess body weight. The procedure is performed laparoscopically in the majority of centres.

The biliopancreatic diversion with duodenal switch

Colon

Fig. 19.3  Roux-en-Y gastric bypass. bypassing the duodenum and the proximal jejunum (Fig. 19.3). After the stomach has been divided, the distal jejunum is connected to the gastric pouch. Food will travel from the pouch through this new connection called a Roux limb, bypassing the gastric remnant, the duodenum and the

The biliopancreatic diversion with duodenal switch is a mal­ absorptive procedure consisting of a vertical subtotal gast­ rectomy (sleeve gastrectomy) associated with a consistent reduction of the absorbing intestine (Fig. 19.4). The bile and pancreatic juice mix with the food in the distal small bowel segment called the common limb. The length of this common limb (usually between 50 and 100 cm) is critical in the absorption of sufficient protein, fat and fat-soluble vitamins. Specific complications include anastomotic leaks and mal­ nutrition, with diarrhoea and foul-smelling stools as frequent side-effects. Though the weight loss is substantial (70–75% of excess body weight), this procedure carries the highest mortality (1%) and is now the least commonly performed.

19 

296  Bariatric surgery

SUMMARY Bariatric surgery is a discipline that requires not only special­ ised surgical skills but also specific expertise in managing the morbidly obese patient. Obese patients are often complex, high-risk surgical candidates because of their underlying comorbidities. A comprehensive and structured programme is required to provide the safe and effective delivery of bariatric surgery. Surgery for obesity produces sustained significant weight loss for severely obese patients with consequent improvement or elimination of their obesityrelated comorbidities. The weight loss following bariatric surgery varies between patients and procedures. In contrast to medical therapies, weight loss is usually maintained for

many years. Plastic surgery may be later required to remove excess skin and recontour the body after successful weight loss (e.g. abdominoplasty).

FURTHER READING National Institute for Clinical Excellence 2006 Obesity: guidance on the prevention, identification, assessment and management of overweight and obesity in adults and children. Clinical Guidance n.43 Schauer PR, Shirmer, BD, Brethauer SA (eds) 2007 Minimally invasive bariatric surgery. Springer, New York Sjöström L, Narbro K, Sjöström CD et al 2007 Effects of bariatric surgery on mortality in Swedish obese subjects. New England Journal of Medicine 357:741–752

20 

Liver and biliary tree

Hepatic and biliary embryology and   anatomy

297

Hepatobiliary physiology

300

Jaundice

301

Non-neoplastic conditions of the liver

304 304 305 305 306

Congenital conditions Inborn errors of metabolism Hepatic trauma Liver infections

Neoplasms of the liver Benign tumours

307 307

HEPATIC AND BILIARY EMBRYOLOGY AND ANATOMY Embryology The hepatic diverticulum and hepatic primordia appear as an outgrowth of the distal foregut endothelium at stage 11 and grow into the septum transversum. Growth and proliferation lead to formation of the hepatic parenchyma, the biliary tree, gallbladder and extrahepatic bile ducts.

Clinical anatomy The liver lies below the diaphragm and extends across the upper abdomen. The liver is adherent to the under-surface of the diaphragm where the peritoneal covering of the liver reflects to form the coronary and triangular ligaments (Fig. 20.1). Ventrally the covering reflects to form the falciform ligament and in this runs the ligamentum teres hepatis which is the fibrosed remains of the fetal umbilical vein – which in intra-uterine life carries oxygenated blood from the placenta to the fetus. The vein runs along the undersurface of the liver to drain into the ductus venosus, between the caudate lobe and the left lateral section, to reach the inferior vena cava. Following birth, the umbilical vein fibroses and forms the round ligament lying in the falciform ligament. Recanalisation can occur in adult life if there is severe portal hypertension. The liver is unique in being nourished by a dual blood supply (Fig. 20.2). Blood flows to the liver from both the portal vein (80%) and the hepatic artery (20%). The portal vein carries blood returning from the GI tract and forms behind the head of the pancreas as a continuation of the superior

Malignant tumours

309

Gallstones (cholelithiasis)

311

Stones in the gallbladder: urgent management Common bile duct stones (choledocholithiasis): urgent management Stones in the small intestine: urgent management General management of gallstones

312 314 314 315

Acalculous cholecystitis

316

Gallbladder tumours

316

mesenteric vein and confluence with the splenic vein and then passes in the free edge of the lesser omentum to the liver hilum where it divides into a left and right branch. The hepatic artery usually arises from the celiac artery on the ventral surface of the aorta and passes to the right along the superior border of the pancreas to ascend in the free edge of the lesser omentum to the liver hilum where it divides into left and right branches. The bile duct also lies in the free edge of the lesser omentum. The triad of the bile duct, the portal vein branches and the arterial branches are enclosed in a fibrous (Glisson’s) sheath, which is a continuation of Glisson’s capsule that covers the liver. Venous drainage of the liver is through three central hepatic veins, right, middle and left, that have a very short extrahepatic length before reaching the IVC just below the diaphragm. There are a variable number of short veins draining directly into the retrohepatic IVC. The caudate lobe of the liver drains separately and directly into the IVC. In the Budd– Chiari syndrome, where there is thrombosis of the main hepatic veins, the caudate lobe can remain functional while the remaining liver undergoes necrosis. The caudate lobe may undergo compensatory hypertrophy.

Anatomical sectors Although the internal anatomy of the liver has been well known for many years the anatomic description of the internal structure of the liver has been confused for some time, partly because of the language used and partly because of two descriptive systems. In 2000 a single nomenclature was agreed. This anatomic description is based on the divisions of the artery and bile ducts and on this basis the liver is divided into two hemilivers, each supplied by a branch of the

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298  Liver and biliary tree Anterior view Right triangular ligament

Inferior vena cava Left triangular ligament

Bare area

Left lobe

Right lobe

Left and right coronary ligaments Falciform ligament Inferior view

Quadrate lobe

Gallbladder fossa

Hilus

Umbilical fissure

hepatic artery and the plane of separation between the right and left hemilivers lies along a virtual line (Cantlie’s line) drawn between the tip of the gallbladder fossa and the IVC (Fig. 20.3). Although this plane cannot be seen clinically, it is demonstrated on vascular cast studies. Thereafter, each hemiliver is subdivided into a medial and lateral section. In the right liver the medial and lateral sections are separated in the plane of the right hepatic vein and in the left liver the medial and lateral sections by the plane of the left hepatic vein. The arterial divisions further divide the liver into eight functional units called segments (of Couinaud), where segments 1–4 comprise the left hemiliver and 5–8 the right liver (Fig. 20.4). Segment 1 is also referred to as the caudate lobe. The arterial divisions allow each segment to be resected separately, if desired. Anatomically based resections derive their names from this description as hemihepatectomies, sectionectomies or segmentectomies. A non-anatomic resection is one that is performed across boundaries without regard for the segmental anatomy.

Bile collecting system – ducts and gallbladder The biliary collecting system   and extrahepatic bile ducts

Caudate lobe

Fig. 20.1  The anatomy of the liver. Anterior and inferior surface views.

The bile caniliculi around the hepatocytes unite to form intra­ lobular bile ductules, then interlobular ducts, and eventually converge to form the right and left hepatic ducts. The union of the left and right hepatic ducts forms the common hepatic duct and from the insertion point of the cystic duct the common bile duct lying in the free edge of the lesser omentum (Fig. 20.5). The common bile duct terminates at the ampulla of Vater adjacent to the termination of the pancreatic duct. The termination of each is guarded by a circular muscle forming the sphincter of Oddi. Although often described in illustrations, convergence of the ducts to form a single ostium in the ampulla of Vater is very unusual. A single common channel may lead to reflux of pancreatic juice into

Inferior vena cava

Left hepatic vein

Right hepatic vein Middle hepatic vein Right liver

Portal vein Hepatic artery

Left liver

Coeliac axis Splenic artery Splenic vein Aorta Superior mesenteric vein

Fig. 20.2  The blood supply to and drainage from the liver.

Hepatic and biliary embryology and anatomy  299 Hepatic and biliary embryology   and anatomy

Liver Right liver

Neck Body Common hepatic duct

Fundus

Calot's triangle Cystic duct

Hartmann's pouch

Sphincter of Oddi

Left liver

Common bile duct

Main pancreatic duct

Fig. 20.5  The anatomy of the gallbladder and biliary tract

Fig. 20.3  The right and left liver.

with Calot’s ‘triangle’ shown in blue.

8 7

2

4

1 3

6 5

Fig. 20.4  The segments of the liver, according to Couinaud.

the bile duct and of bile into the pancreatic duct. The former is thought to be a cause of choledochal cysts and the latter the cause of gallstone-induced pancreatitis (see below and ‘Pancreatitis’, Ch. 22). Unlike the liver parenchyma, the biliary system throughout is supplied only with arterial blood.

The gallbladder The gallbladder is a pear-shaped structure and variable in size but typically is the size of a small pear, although it can swell to enormous proportions in disease. The gallbladder sits on the underside of the liver in the gallbladder fossa and

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300  Liver and biliary tree Box 20.1 

Congenital abnormalities of the biliary tree

Gallbladder n Absence n Reduplication n Mesentery (floating gallbladder) n Phrygian cap (fundus of gallbladder folded or kinked upon body) Bile ducts n Obliteration n Low or otherwise abnormal entry of cystic duct into the common bile duct n Low junction of a right sectoral duct with common hepatic duct n Direct drainage of a bile duct into the gallbladder via the liver bed

thus between segments 4 and 5 (Fig. 20.5). Calot’s triangle marks the important landmarks in surgery of the gallbladder (Fig. 20.5). Sometimes it hangs off the underside of the liver on a mesentery and may undergo torsion. The gallbladder is described as having a fundus, body and neck and derives blood from the cystic artery, which is usually a branch of the right hepatic artery.

Anatomical variations As result of its complex development the biliary and arterial anatomy is highly variable and gives rise to difficulties and complications in surgery of the liver, gallbladder and bile ducts (Box 20.1). Injury to the bile duct during laparoscopic cholecystectomy remains a problem, with an incidence of about 1/500–1/1000 and is frequently due to misunderstanding of the anatomy at the time of operation. A major bile duct injury is a serious complication of this operation and requires specialist surgery to repair.

HEPATOBILIARY PHYSIOLOGY Hepatocellular functions are listed in Table 20.1.

Reticuloendothelial function Sixty-five percent of the reticuloendothelial system is within the liver, and it is responsible for filtering and destroying bacteria and their products that have been absorbed from the gut and for the removal of debris that results from the breakdown of intestinal cells. The hepatic reticuloendothelial cells also have similar functions in filtering blood that reaches them via the hepatic artery, but in this they are of less quantitative importance than the spleen (see Ch. 21).

Detoxification The liver detoxifies a variety of endogenous and exogenous substances (chiefly drugs) mainly by conjugating them into less active forms.

Intermediary metabolism Hepatocytes play a dominant role in metabolism and storage of basic foodstuffs:

Table 20.1

Hepatocellular functions Function

Hepatocellular component Nucleus Double contour, exchange with surrounding cytoplasm Mitochondria Energy provider from oxidative phosphorylation: ATP–ADP Rough endoplasmic Synthesis of albumin, other reticulum (RER) proteins, glycogenesis Smooth endoplasmic Detoxification, synthesis of bile reticulum (SER) acids and steroids (cholesterol) Peroxisomes Catabolism and biosynthesis Lysosomes Lytic function and deposit Golgi apparatus ‘Packing’ site of ingestion to be excreted Cytoskeleton Support of hepatocytes Sinusoidal cells Endothelial cells Kupffer cells Hepatic stellate cells (Ito cells) Pit cells

Barrier between sinusoids and space of Disse Highly mobile macrophage Storage of retinoids and fat Highly mobile, liver-specific natural killer lymphocytes

n

Carbohydrates are stored as glycogen and released in response to changes in blood sugar concentration to meet urgent energy needs. n Fats are metabolised – to ketone bodies – for energy transfer and release. Some special products, such as cholesterol, are synthesised. n Fat-soluble vitamins (A, D and K) are principally or exclusively stored in the liver. n The liver is the only source of albumin and alphaglobulin. Many other specialised proteins, such as clotting factors, are synthesised there. Operations on patients with liver disease and defective protein synthesis require management of deficiency states.

Excretory function The production, storage and release of bile into the duodenum is a fundamental function of the liver and has an impact on surgical practice because of: n n

gallstone formation the enterohepatic circulation of bile acids, which is of importance in the digestion and absorption of fat.

Bilirubin is a breakdown product of the cleavage of haem from red blood cells by the reticuloendothelial system. On release into the circulation it is unconjugated (fat-soluble) and transported in the plasma bound to albumin. On extraction from the plasma by the hepatocyte it is conjugated with glucuronide by the enzyme glucuronyl transferase to become water-soluble and is excreted continuously in the bile. Bacterial deconjugation in the colon produces stercobilin, which colours the faeces brown. If there is infection in the biliary tree, deconjugation may take place within it, and the bilirubin may aggregate to form stones (see ‘Oriental cholangiohepatitis’). Although bile is secreted continuously by the liver cells, one of its main functions is assisting in digestion. Under

Jaundice  301 physiological circumstances bile is intermittently released into the duodenum. Between meals, the gallbladder acts as a reservoir in which bile is concentrated from 5 to 20 times by removal of sodium and water. Release of bile into the duodenum begins shortly after the ingestion of food – in response to stimulation of the vagus. The main flow, which is accompanied by gallbladder contraction and relaxation of the sphincter of Oddi, takes place as the result of the secretion of cholecystokinin from the duodenal wall in response to the presence of fat in the lumen. Contraction of the gallbladder in this manner against an obstructing stone causes pain (biliary colic). In addition to concentrating bile, mucin is secreted from the gallbladder mucosa and this is believed to have a role in preventing stone formation.

JAUNDICE Jaundice is the clinical manifestation of an increased concentration of bilirubin in plasma, the normal upper limit of which is 17 µmol/L. When hepatic uptake and excretion are decreased, the excess bilirubin in plasma spills over into the interstitial space so that the tissues become stained yellow. A symptom that often accompanies jaundice is itching, but this is probably caused by bile salts rather than bilirubin. Jaundice is usually first detectable in the sclerae when the bilirubin levels in the plasma reach >35 µmol/L. As the hyperbilirubinaemia worsens the skin and mucous membranes also become stained yellow. It is important to distinguish between jaundice that occurs because of increased bilirubin production or because of a block to excretion at the hepatocyte or canaliculus (which usually requires medical management) and that caused by extrahepatic obstruction to bile drainage (which may need endoscopic, surgical or radiological intervention). Close cooperation between gastroenterological physicians, surgeons and radiologists is required to effectively manage such patients.

Classification of jaundice The classification of jaundice is outlined in Box 20.2.

Prehepatic This is a sequel to increased breakdown of red cells – haemolysis. The rate of production of bilirubin is sufficiently fast to saturate the uptake – conjugation mechanisms in the liver. The bilirubin in plasma is unconjugated and therefore is not excreted by the kidney, resulting in acholuric jaundice.

Box 20.2  n

Classification of jaundice

Prehepatic – haemolytic Hepatic – congenital defect of hepatocyte function – hepatocellular injury or infection n Posthepatic – obstruction to bile duct n

Hepatic (or hepatocellular) This, as its name implies, is caused by some disorder of the liver cell at the stages of uptake, conjugation or secretion of bilirubin, including also malfunction of the cells which line the bile canaliculi. Intrahepatic cholestasis occurs when there is a failure to excrete conjugated bilirubin into the cannuliculi within the liver, and it is a common occurrence in patients with hepatocellular jaundice. Jaundice may be caused by: n

Defective uptake occurs with mild intermittent jaundice in otherwise healthy individuals (Gilbert’s syndrome). n Congenital absence of glucuronyl transferase is associated with severe jaundice and early death (Crigler–Najjar syndrome). n Congenital impairment of excretion of conjugated bilirubin into the bile is known as the Dubin–Johnson– Rotor syndrome. All the above conditions are rare, apart from Gilbert’s syndrome. The common causes of hepatocellular jaundice are: n

viral diseases of the liver cell – hepatitis A, B, C, D and E n other hepatic infections n alcoholic liver disease n hepatotoxic drugs, such as the phenothiazines, which act mainly on the canalicular cells, but include many others with varied actions within cells.

Posthepatic This type of jaundice is often called obstructive or ‘surgical’ jaundice, which implies that the cause is a mechanical obstruction in the extrahepatic biliary tree (extrahepatic cholestasis). The term identifies those patients whose jaundice may be capable of relief by some form of mechanical intervention – either by surgery, endoscopy or interventional radiology. In these patients, the relatively intact hepatocyte conjugates bilirubin which is then released back into the plasma and excreted by the kidney so that the urine is dark and the stools pale. The same phenomenon occurs in patients with intrahepatic cholestasis caused by cannicular obstruction within the liver. Causes of extrahepatic cholestasis include: n

obstruction in the lumen of the biliary tree – gallstones obstruction in the wall of the ducts – biliary atresia; bile duct carcinoma (cholangiocarcinoma); postoperative stricture n extrinsic compression – pancreatitis; pancreatic tumour; secondary deposits in the hilar lymph nodes of the liver. n

Investigation Biochemical The three most useful measurements are the serum concentration of bilirubin, alkaline phosphatase and the transferases: n

Bilirubin. A raised level of plasma bilirubin indicates disruption of its normal passage from blood, through the hepatocyte and down the biliary collecting system into the duodenum. Serial measurements are helpful in following the course of hepatic or biliary disease.

Hepatobiliary physiology Jaundice

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302  Liver and biliary tree

Alkaline phosphatase. This substance is secreted predominantly from the cells of the collecting system, which proliferate in the presence of obstruction. A raised serum level in the presence of jaundice is therefore a good indicator of cholestasis – either extrahepatic or intrahepatic. The latter being caused by some drugs such as chlorpromazine and also seen in the later stages of viral hepatitis. n Transferases. These enzymes are constituents of the hepatocyte. If their serum levels are raised, the implication is that there is hepatocellular damage. Usually this is primary, within the hepatocyte, but, in long-standing extrahepatic obstruction, secondary interference with hepatocellular function may take place. n

The biochemical patterns of jaundice in hepatocellular and cholestasis including extrahepatic obstruction are shown in Table 20.2, although there can often be some overlap. Other measurements that may be of value in jaundice are: Albumin concentration. This gives a guide to the synthetic capacity of the liver and the nutritional state of the patient. n Clotting factors. These are synthesised in the liver. The most easily assessed is prothrombin. Vitamin K is a cofactor in its synthesis. Because the vitamin is fat-soluble and is therefore not well absorbed from the intestine in the absence of bile, its limited hepatic stores soon become exhausted. The hypoprothrombinaemia of jaundice responds to the administration of parenteral vitamin K provided hepatocyte function is preserved, as is nearly always the case when the jaundice is caused by obstruction. Measurement of the prothrombin time is therefore an essential preliminary before operation in a jaundiced patient. n Alpha-fetoprotein (AFP). See hepatocellular carcinoma, below. n Hepatitis virus markers. n

CT scanning CT scan has the advantage over ultrasound of providing more precise anatomical information and, unlike ultrasound, is unaffected by the presence of obesity or bowel gas. The image is enhanced with oral contrast medium to delineate the bowel and with an intravenous contrast agent to show vascular structures.

Cholecystography/cholangiography Magnetic resonance cholangiopancreatography (MRCP) now provides good images of the biliary and pancreatic ductal system, and this non-invasive method has replaced diagnostic ERCP and PTC. Percutaneous transhepatic cholangiography (PTC – Fig. 20.6) is achieved by introducing a fine needle (usually called a skinny or Chiba needle) through the substance of the liver into a bile duct. Success rates are reduced if the biliary system is not dilated. PTC is of particular value in determining the anatomical level and the nature of obstructing hilar lesions. Endoscopic retrograde cholangiopancreatography (ERCP – Fig. 20.7) similarly delineates the biliary tract but also can show the pancreatic ductal system. At both ERCP and PTC, bile may be aspirated for microbiological examination and cells may also be obtained for cytological assessment. Both procedures are usually now performed only for therapy, such as the placement of biliary stents to relieve obstruction or the removal of biliary stones by endoscopic sphincterotomy or dilatation of the sphincter of Oddi.

Arteriography Selective coeliac and superior mesenteric angiograms can show the abnormal circulation of a tumour (tumour blush – Fig. 20.8). The late-phase images of an angiogram

Imaging

Ultrasound Ultrasound scanning reliably detects a dilated ductal system and so helps to distinguish parenchymal liver disease from extrahepatic bile duct obstruction. The characteristic texture of the cirrhotic liver can also be identified. In addition, cysts, abscesses and tumours can be delineated, and guided fine-needle aspiration and biopsy (Ch. 4) are possible.

Table 20.2

Hepatocellular damage Cholestasis including extrahepatic biliary obstruction

Biochemical patterns of jaundice Alkaline phosphatase

Aspartate and alanine transferases

↑

↑↑↑

↑↑↑

↑

Fig. 20.6  A percutaneous transhepatic cholangiogram. The needle is seen coming from the patient’s right side. The common hepatic duct is obstructed by a tumour.

Jaundice  303 a

b

Fig. 20.7  An endoscopic retrograde cholangiopancreatogram showing the biliary ductal system with multiple bile duct stones. demonstrate the portal vein, and therefore neoplastic involvement of both arterial and venous vessels can be assessed. However, vascular reconstruction using CT or MRI images is comparable to direct angiography. Invasive angiography is now usually performed only as a precursor to embolisation.

Laparoscopy Laparoscopy permits direct visualisation of the liver and may be combined with laparoscopic ultrasound to provide both accurate staging and biopsy of diseased liver tissue. Because of the accuracy of modern staging imaging many surgeons do not use laparoscopy prior to resection. If laparoscopy is used it is normally performed immediately before planned laparotomy for liver resection.

Biopsy Percutaneous liver biopsy is an invasive procedure which is used in the diagnosis of diffuse liver disease or for confirmation of metastatic malignancy. Accuracy is increased when insertion of the needle for biopsy or liver cytology is guided by ultrasound, CT or at laparoscopy.

General management Preparation for liver surgery Surgical operations are usually major, and the preparations outlined in Chapter 5 must be followed in detail. Major

Fig. 20.8  (a) A tumour blush seen on hepatic angiography, and (b) the corresponding CT scan. Note that the arteries are displaced around the tumour.

resections may require specialised support for abnormalities in the clotting system and for postoperative nutrition by either the enteral or parenteral route (see Ch. 5).

The jaundiced patient Clotting

The most likely problem is vitamin K deficiency, which can be corrected by parenteral administration of the synthetic derivatives menadione or phytomenadione (K1). The synthesis of prothrombin, set in motion by restoring supplies of vitamin K, takes some hours, so the prothrombin time must, except in dire emergencies, be rechecked before operation is undertaken. In emergency cases fresh frozen plasma may be used to correct clotting.

Antibiotic prophylaxis Sepsis from organisms that originate in the GI tract is a major cause of death in the surgical management of jaundice, partly because of interference with hepatic reticuloendo­ thelial function. Prophylactic antibiotics against enteric

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304  Liver and biliary tree

organisms, such as cefuroxime or ciprofloxacin, are used routinely at the time of surgery or invasive procedures such as PTC and ERCP.

increased secretion of antidiuretic hormone on the distal tubule after operation; and also by administration of a low dose of inotrope which increases renal plasma flow and glomerular filtration rate.

Preliminary biliary decompression In a patient who will subsequently require an operation, liver function may be improved by biliary decompression which is done by one of the following methods: n

passing a catheter percutaneously into the liver substance and then into a bile duct at PTC n ERCP with or without dilatation of an obstructing lesion and insertion of biliary stent (plastic or expanding metal) or occasionally a nasobiliary drainage catheter (Fig. 20.9).

Hepatorenal syndrome This condition is probably one variant of the systemic inflammatory response syndrome (SIRS) in which renal and hepatic failure develop in response to severe injury or sepsis, especially if there is depression of the immune system. A patient with jaundice is particularly liable to develop acute kidney injury, and measures to prevent this include: n

adequate preoperative hydration avoidance of intraoperative hypotension n maintenance of high urine flow by the use of an osmotic diuretic (mannitol) which opposes the action of n

NON-NEOPLASTIC CONDITIONS OF THE LIVER CONGENITAL CONDITIONS

Biliary atresia Aetiology and pathological features The commonest cause of prolonged neonatal jaundice is extrahepatic biliary atresia. The cause is not known. There may be single or multiple points of obstruction, and the proximal ducts may dilate considerably. If not relieved, liver failure ultimately ensues with death in the first year of life, only a few infants surviving beyond 6 months.

Clinical features Mild jaundice is not uncommon in the neonatal period. However, persistence and progression beyond 2 weeks is definitely abnormal and then the distinction has to be made between obstruction and hepatitis. This can usually be achieved by the biochemical profile (Ch. 4) and ultrasound scanning.

Management There are two management options: n

For the majority, hepatic portoenterostomy (Kasai operation – Fig. 20.10) should be attempted within 60 days of birth; delay beyond this time is associated with the rapid development of intrahepatic fibrosis and a reduced chance of success. n When evidence of deteriorating liver function is apparent, liver transplantation should be considered (see Ch. 13).

Congenital cystic disease Cysts may be solitary or multiple. Multiple cysts are frequently associated with polycystic disease of the kidney (see Ch. 32).

Clinical features The cysts are often small, asymptomatic and found only incidentally either at laparotomy, during investigation of other problems, or at postmortem examination. Large cysts may present with pain in the right upper abdomen, which may radiate to the right shoulder and is believed to be caused by stretching of the liver capsule.

Management Fig. 20.9  Endoscopic insertion of a biliary stent over a guide wire.

In a few instances, percutaneous aspiration under image control is used but refilling of the cyst after needle aspiration Is common and so, occasionally, surgical decompression by fenestration or ‘de-roofing’ is required for the relief of

Non-neoplastic conditions of the liver  305 Non-neoplastic conditions of the liver Congenital conditions Inborn errors of metabolism Hepatic trauma

Fig. 20.10  The Kasai operation. A Roux-en-Y loop of jejunum is sutured to the hepatic hilum. symptoms. Rarely, in cases of multiple cysts located in the right or left liver, resection may be indicated. In patients showing multiple bilateral cysts with compromise of the quality of life and reduced functioning liver parenchyma, liver transplantation should be considered. In cases of polycystic liver and kidney disease associated with terminal renal insufficiency the therapy of choice is a combined liver and renal transplant.

Congenital cystic dilatation of the intrahepatic ducts (Caroli’s syndrome) This is a rare congenital but non-familial disorder with saccular dilatation of the intrahepatic ducts. The cause is not known. The syndrome is usually diffuse but is occasionally confined to one liver segment or lobe. In some cases there is associated renal tubular ectasia. Clinical features are of recurrent upper abdominal pain and cholangitis in childhood or early adult life. Cholangitis is treated with systemic antibiotics. Localised disease is susceptible to resection. Chronic cholangitis may lead to a secondary biliary cirrhosis. Bile duct carcinoma is described in some cases. Liver transplantation should be considered in patients presenting with a secondary biliary cirrhosis.

Choledochal cyst This term is used to describe dilatation of all or part of the extrahepatic biliary tree with or without associated cystic change of the intrahepatic bile ducts. Choledochal cysts are classified as follows:

n

Type I: cystic (Ia), segmental (Ib), or fusiform (Ic) dilatation of the extrahepatic bile duct n Type II: the cyst forms a diverticulum from the extrahepatic bile duct n Type III: cystic dilatation (choledochocele) of the distal common bile duct lying mostly within the duodenal wall n Type IV: type I associated with intrahepatic bile duct cysts. Types I and IV are usually associated with an anomalous biliary–pancreatic ductal junction which allows pancreatic juice to flow retrogradely into the biliary tree. These types of choledochal cyst in particular are associated with a much increased risk of cholangiocarcinoma (see below) development. Patients may present with upper abdominal pain and raised liver enzymes and amylase. Others are found incidentally on ultrasound scanning. Surgical excision of the cyst with hepaticojejunostomy Roux-en-Y is normally recommended.

INBORN ERRORS OF METABOLISM These are discussed in detail in Chapter 13 (see ‘Liver transplantation’).

HEPATIC TRAUMA The liver may be injured either by blunt or penetrating injury to the abdomen or chest. The commonest causes are road traffic accident (RTA), sporting injury, falls and violent aggression. In all cases there is a high probability of concomitant serious injury at other sites. Most liver injuries in the UK arise

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306  Liver and biliary tree

from blunt rather than penetrating trauma and this is in contrast to countries where gun crime is common.

Clinical features In blunt trauma the liver is the second most common site of injury within the abdomen, after the spleen, and is involved in about 50% of deaths from blunt abdominal trauma. Liver trauma complicates about 15–20% of blunt injuries to the abdomen and of these about half will have splenic trauma. The mechanism of the injury, a sudden compression of the liver between the ribs and the spine, disrupts the hepatic substance and results in a diversity of injury from contusions, subcapsular (contained beneath an intact Glissonian capsule) haematomas or lacerations. The surgical right side of the liver is far more likely to be injured and most blunt injuries involve segments 4, 6, 7 and 8. Associated gallbladder injury or portal triad injury is uncommon and occurs in about 5% of blunt injuries to the liver but is more common in penetrating injuries. Massive haemorrhage, bile leaks, and fistulae are not uncommon in portal triad injury and early mortality or longterm complications are more likely to occur. The risk of mortality from blunt abdominal trauma rises with the severity of the liver injury and with an increase in the number of other organs involved. Small injuries may not manifest any clinical signs. Larger injuries may show signs of volume loss but it is possible that even an extensive injury may be undetected clinically unless a complication results later.

Management While the clinical history and diligent clinical examination remain important in the management of abdominal trauma there is little evidence to support decision making based simply only clinical examination. The type of institution, the haemodynamic status of the patient and the availability of imaging are likely to determine whether imaging is useful in the individual management of blunt abdominal trauma. Immediate focused abdominal ultrasound and CT are both helpful. The sensitivity and specificity of CT imaging has been demonstrated to be high and CT can be used to classify the severity of injury (see Table 20.3), but is not necessarily a guide to management. The decision to operate is complex and includes an assessment of other intra-abdominal injuries. Surgeons have moved increasingly to a non-operative strategy in the management of both blunt and penetrating liver trauma. Most cases of grade I–III are likely to be haemodynamically stable and can be managed by a trauma service without a specialised liver unit. The survival should approach 100% in this setting. The more severe injuries should be transferred to the care of a specialist unit depending of course on the stability of the patient and other concomitant injuries that might take precedence. Even some high-grade injuries in stable patients can be managed non-operatively but complications such as re-bleeding, biloma, abscess, compartment syndrome or other event requiring intervention occur in about 15%. While re-bleeding tends to occur in the early days after injury, infective or biliary complications may not manifest themselves for weeks or months after injury. Injury grade IV or V and requirement for blood transfusion is predictive for a complication in the non-operatively managed patient. In the unstable patient

Table 20.3

Classification of liver injury

Grade

Injury

Description

I

Haematoma Laceration

II

Haematoma

Subcapsular 150 mg/L 48 h after admission: Clinical impression of severity Glasgow score 3 or more C-reactive protein >150 mg/L Persisting organ failure for 48 h Multiple or progressive organ failure

Imaging If an upright chest X-ray shows air under the diaphragm, then the cause of the acute abdomen is not pancreatitis but a gastrointestinal perforation, even if the serum amylase is elevated. A plain abdominal X-ray is not required in patients with a diagnosis of acute pancreatitis, but has often been performed and may show a sentinel dilated loop of small bowel overlying the pancreatic region (Fig. 22.3). Either X-ray may occasionally show calcified gallstones (15% of cases). CT may be useful in clinching the diagnosis by demonstrating a swollen gland with inflammatory changes in the surrounding tissues (Fig. 22.4) and identifying the underlying cause, particularly gallbladder stones, although these are better seen on ultrasound. Contrast enhanced CT scanning is also used at a later stage (usually after 72 hours) to assess the extent of pancreatic necrosis and the development of other complications (see below). It is indicated in patients with persisting organ failure, signs of sepsis or clinical deterioration – typically occurring 6–10 days after onset of acute pancreatitis.

Prognosis The severity of an attack of acute pancreatitis can be assessed in a number of ways (Table 22.3). These include: n

initial clinical condition single prognostic factor measurements such as CRP n multiple prognostic factor scoring systems. n

The Glasgow scoring system is widely used (Table 22.4). Measurements are made at presentation or within 48 hours of admission. The presence of three or more positive factors indicates a severe attack of acute pancreatitis; mortality is correlated with the number of positive factors. It is worth emphasising that hyperamylasaemia is not one of the predictive criteria. More recently the APACHE II score has been applied and gives a semi-continuous assessment of severity of pancreatitis, as it does of any acute surgical illness.

Mortality rates The overall mortality is 5–10%. Most patients (70%) have a mild attack with less than three positive prognostic criteria

Pancreatitis  333 Table 22.4

Factors which predict the severity of pancreatitis (Glasgow system)

Factor

Level

Age Leucocytosis Blood urea concentration

>55 years >15 × 109/L >16 mmol/L (no response to fluid administration) >10 mmol/L in the non-diabetic 100 IU/L 5 cm in greatest diameter No distant metastases Distant metastases

Polycythaemia Hypercalcaemia Raised alkaline phosphatase concentration Pyrexia Hypertension Amyloid deposition Peripheral neuropathy and myopathy

Table 33.2

N3 Circulating pyrogens Secretion of renin Unknown Unknown

T component of TNM staging of carcinoma of the kidney

Stage

Findings

T1a T1b T2 T3

Tumour 7 cm limited to kidney Tumour extends into major veins or invades adrenal or perinephric tissue but not beyond Gerota’s fascia Tumour invades beyond Gerota’s fascia

T4

N2

Prognosis For localised tumours, there is a 5-year survival of over 90%, but this falls in the presence of anaplastic histology, lymph node metastases and/or metastases to solid organs.

Adenocarcinoma Epidemiology and pathological features The peak incidence is in the fifth generation, and the condi­ tion is commoner in men. The tumour arises from the renal tubules, is usually well-encapsulated and contains areas of haemorrhage and necrosis. On histological examination, it consists of columnar or cuboidal cells with clear cytoplasm and dark nuclei. Spread is by local infiltration and chiefly by the blood to distant organs. Direct growth may take place into the renal vein and vena cava. Paraneoplastic syndromes may occur (Table 33.1).

Staging TNM staging is used, based on the preoperative investiga­ tions, operative findings and the histological examination of the excised tissues. T stages are shown in Table 33.2 and N and M stages in Table 33.3.

Clinical features Twenty percent of tumours are detected on ultrasound examination during the course of investigations for nonspecific symptoms or for features that suggest a paraneo­ plastic syndrome.

M0 M1

Symptoms Specific symptoms are not common, but there are some which are semi-specific: n

aching loin pain episodes of acute pain – caused by haemorrhage into the tumour and sometimes of sufficient severity for the patient to present as an emergency n haematuria (60%) n symptoms of paraneoplastic syndromes (Table 33.1) n pathological fracture. n

Signs A loin mass is the only finding unless there is clinical evi­ dence of distant metastases. By the time that the triad of loin pain, loin mass and haematuria is present, the tumour is usually advanced.

Investigation Urine Haematuria should be sought. Significant proteinuria may indicate involvement of the renal vein.

Blood Analysis should be done for any of the paraneoplastic syn­ dromes. Hypercalcaemia or a raised alkaline phosphatase does not necessarily imply metastatic disease.

Imaging Chest X-ray  may show typical ‘cannonball’ metastases. IVU  demonstrates a space-occupying lesion best seen in the nephrogram phase and also calyceal distortion. Ultrasonography can distinguish between a cyst and a solid tumour and is an effective way of identifying involve­ ment of the renal vein and the vena cava. CT scan  is the most precise way of staging the tumour (Tables 33.2 and 33.3; Fig. 33.8). Renal angiography  is less commonly used but is essential in bilateral tumours or a tumour in a solitary kidney.

Disorders of the kidney  571 Management

Stone disease

Surgery Radical nephrectomy is the primary treatment in the absence of metastatic disease. There is increasing utilisation of lapar­ oscopy both for removal of the whole kidney and more limited resections of small peripheral tumours. Large tumours and those with tumour tissue invading the renal vein or infe­ rior vena cava are not suitable for a laparoscopic approach.

Non-operative treatment In symptomatic patients who are unsuitable for surgical treat­ ment, embolisation of the renal artery is effective in control­ ling pain and haematuria. Radiotherapy to the primary tumour is ineffective but may help in reducing the pain of a bony metastasis. Endocrine therapy and chemotherapy are both ineffective. Newer treat­ ments for patients with metastatic disease include sunitinib (a tyrosine kinase inhibitir), bevacizumab (a vascular endothe­ lial growth factor inhibitor) and sorafenib (another tyrosine kinase inhibitor), which are showing improved effectiveness compared with previous treatment regimens.

Prognosis Seventy percent of those with T1 tumours survive for 5 years, and prolonged survival has been reported after removal of secondary deposits. However, there may be long intervals between the presentation of the primary and of metastases. Very rarely, secondary deposits may regress after removal of the primary. Nevertheless, very few patients who present with evidence of metastatic disease survive for more than 2 years.

Carcinoma of the renal pelvis Carcinoma of the renal pelvis accounts for 10% of all renal tumours, and may be bilateral in up to 25% of cases.

Aetiology and pathological features Ninety percent are derived from the transitional epithelium (urothelium) and are likely to be associated with similar tumours elsewhere in the urinary tract. However, urothelial tumours of the bladder are 60 times more common than those of the renal pelvis. The remaining 10% in the renal pelvis are squamous carcinomas – a consequence of meta­ plastic change – and are almost invariably associated with stones. The aetiological factors for transitional cell cancer are similar to those for the same lesion in the bladder.

Clinical features These are loin pain and haematuria.

Investigation Cytology Malignant urothelial cells may be present in the urine.

Imaging An IVU may show a filling defect in the calyces or renal pelvis (Fig. 33.18), which must be distinguished from a nonopaque renal calculus by ultrasound. CT scanning with and without intravenous contrast is required to provide further

Fig. 33.18  An IVU showing multiple transitional-cell carcinomas of the right renal pelvis.

information about the primary tumour and to exclude meta­ static disease.

Management Management is by removal of the kidney and ureter together with a cuff of bladder mucosa around the ureteric orifice. The reason for such radical surgery is the possibility of the occur­ rence of a further tumour; in the bladder it is simple to diag­ nose by cystoscopy, but the ureteric stump cannot be so easily examined. More conservative management has been attempted by endoscopic resection through a percutaneous nephrostomy tube, direct instrumentation of the ureter or instillation of chemotherapeutic agents directly into the renal pelvis.

Prognosis In localised transitional-cell tumours of the renal pelvis the outlook is good, but squamous-cell carcinoma of the renal pelvis has a poor prognosis.

STONE DISEASE

Epidemiology The incidence and site of occurrence of urinary stones vary in different parts of the world and in different parts of the UK. Renal stones are more common in affluent communities whereas bladder stones remain the common site in develop­ ing countries. In the UK, the incidence of upper urinary tract stones varies from 15 per 100 000 in the north of England (Burnley) to 47 per 100 000 in the south-east (Canterbury). There are similar differences in the type of stone between countries: uric acid stones make up only 5% of the total in the UK, but this rises to 40% in Israel.

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572  Urology

Aetiology In the majority of instances aetiology is unknown.

Metabolic disorders Conditions that alter the composition of the urine, chiefly (but not exclusively) to increase its calcium content, are shown in Box 33.7.

Other causes The commonest of these is infection with the urea-splitting organism Proteus. The result is the production of ammonia, an alkaline urine and triple phosphate stones (staghorn calculi) (see Fig. 33.2), which are a mixture of calcium, mag­ nesium and ammonium phosphate. Other factors are dehy­ dration and immobilisation.

Characteristics of stones These are given in Table 33.4.

Clinical features Symptoms These depend on the size and position of the stone and the presence or absence of infection. The patient may be asymp­ tomatic or give a history of occasional haematuria or dysuria. In cystine stone, there may be a family history, and in all stones there may have been previous episodes. A stone lodged at the neck of a calyx or at the pelviureteric junction causes renal colic, in which there are waves of increasing

pain in the loin often superimposed on a background of continuous nagging pain at the same site. Radiation down­ wards into the groin or scrotum is not common, in contrast to the symptoms of a stone in the ureter. The pain from a stone in the renal pelvis is continuous in the loin and often aggravated by movement.

Physical findings Tenderness may be found in the loin and is increased in severity if there is infection or obstruction when pyrexia is common.

Differential diagnosis Pain in stone disease is notorious for causing diagnostic confusion with other acute abdominal conditions, some of which require urgent surgical management (Box 33.8). There are two reasons for making as precise a diagnosis as possible: first, to undertake relief of pain when one of the alternative conditions is present and may mask the clinical features and compound the misdiagnosis; second, many substance abusers have learned the symptoms of renal colic in order to obtain analgesics or narcotics.

Investigation Any patient who has formed a renal stone stands a greater than 20% chance of producing another. It is important to identify metabolic or structural abnormalities because appro­ priate management may reduce the risk of recurrence.

Urine Box 33.7 

n

Culture and sensitivity, measurement of pH and screening for cystine. n Two 24-hour collections with the patient on a normal diet for measurement of calcium, uric acid, oxalate and citrate concentrations.

Metabolic causes of urinary tract stones

Hypercalcaemia and hypercalciuria n Hyperparathyroidism n Idiopathic hypercalciuria n Hypervitaminosis D n Disseminated malignant disease n Myeloma n Prolonged immobilisation n Sarcoidosis n Milk alkali syndrome n Cushing’s disease n Hyperthyroidism

Blood Concentrations of the following are measured: n n

Increase in other substances n Cystinuria (tubular transport defect for cystine, lysine, ornithine and arginine) n Xanthinuria n Primary hyperoxaluria n Secondary hyperoxaluria (ileostomy) n Hyperuricuria (gout; chemotherapy for leukaemia) n Indinavir therapy

Table 33.4

urea creatinine

Box 33.8 

Conditions which may mimic ureteric colic

n

Appendicitis Cholecystitis n Diverticulitis n Pyelonephritis n Leaking aortic aneurysm n

Characteristics of stones

Stone

Incidence

Colour

Appearance

Radio-opacity

Calcium oxalate (mulberry stone) Triple phosphatea (magnesium ammonium phosphate – struvite stone often causing a staghorn calculus) Uric acid Cystineb Xanthine

80% 10%

Pale yellow-brown Chalky white

Sharp projections Soft

Opaque Opaque

5% 2% Rare

Light brown Yellow-brown Yellow-brown

Facetted Smooth

Lucent Moderately opaque Lucent

a

Often associated with infection with urea-splitting organisms, e.g. Proteus. Often a family history and/or episodes of repeated stone formation.

b

Disorders of the ureter  573 n n n n n n

electrolytes total protein calcium alkaline phosphatase uric acid phosphate.

In a patient with a stone causing complete obstruction, the bladder urine may be sterile. Urine should then be obtained by the insertion of a percutaneous nephrostomy, which is almost certainly required for relief of obstruction.

Imaging A patient who presents with acute symptoms and signs and a suspected stone must have an urgent imaging. The use of CT with its ability to identify non-opaque stones is the inves­ tigation of choice. The diagnosis can be firmly established, the size of the stone determined, together with the degree of obstruction, the likelihood of the stone passing spontaneously, and the need for hospital admission.

Non-operative management Asymptomatic stone A small, asymptomatic, non-obstructing stone in an elderly, unfit patient can be left alone.

Acute episode The pain of renal colic is severe and is treated with intrave­ nous diclofenac and if necessary narcotic analgesics, and antispasmodics such as hyoscine. Stones less than 0.5 cm in diameter will usually pass spontaneously, and, if they are opaque, their progress can be assessed by repeated plain abdominal X-ray.

Oxalate stones The commonest abnormality detected is idiopathic hyper­ calciuria. A low-calcium diet and a high fluid intake to dilute urine calcium concentration is often recommended. However, it is usually unsuccessful in that tap water in many areas contains significant amounts of calcium and a reduction in dietary calcium intake leads to an increased intestinal absorption of oxalate. Attempts to reduce urine calcium excretion with ben­ drofluazide have only been shown to reduce calcium stone formation after prolonged periods of therapy. Sodium cellu­ lose phosphate decreases calcium excretion but is often unacceptable because of the foul diarrhoea it may cause.

Cystine stones Cystinuria is an inherited defect of amino acid transport involving cystine, ornithine, lysine and arginine. Cystine is relatively insoluble, particularly in acid urine, and this can lead to stone formation. Because its excretion is relatively constant, the stones can be both dissolved and prevented by maintaining a high fluid intake throughout the 24 hours and alkalinising the urine. The latter can be achieved with either sodium bicarbonate or potassium citrate, or a combi­ nation of both. If this fails, treatment with penicillamine, which produces a more soluble cystine–penicillamine complex, is sometimes successful. However, it may be

associated with the development of skin rashes and the nephrotic syndrome.

Disorders of the ureter

Uric acid stones

Congenital anatomical abnormalities

Uric acid is less soluble in acid urine and, as a result, patients with chronic diarrhoea or an ileostomy are more likely to produce uric acid stones. They can be dissolved or pre­ vented by increasing the fluid intake and alkalinisation of the urine. In addition, allopurinol (100 mg three times a day) should be given to those with an elevated serum level.

Triple phosphate stones The prevention of recurrent phosphate stones associated with infection is dependent on three factors: n

complete removal of the initial stone(s) correction of any anatomical abnormalities of urine drainage n maintenance of sterile urine. n

The last can be achieved with long-term low-dose antibiotic therapy. If this proves difficult, treatment with a urease inhibi­ tor (acetohydroxamic acid) should be considered.

Surgical management Indications for intervention Urgent percutaneous nephrostomy drainage is required when: n

fever does not resolve after 24 hours of appropriate antibiotic therapy in a patient with an obstructed kidney n severe pain persists in spite of the medical management outlined above. The nephrostomy track can be used at a later stage for endoscopic stone destruction or removal. An indwelling stent can be inserted to establish drainage down the ureter before treatment by lithotripsy (see below).

Intervention in persistent stone Major advances have been made in the management of stones over the past decade by techniques other than open operation. Destruction of the stone in situ can be done with: n

extracorporeal transcutaneous techniques (extracorporeal shock wave lithotripsy, ESWL) n direct application of shock waves or laser to the stone by a probe inserted endoscopically or percutaneously. Removal  can be percutaneously.

achieved

either

endoscopically

or

DISORDERS OF THE URETER CONGENITAL ANATOMICAL ABNORMALITIES

Ureteric duplication Incomplete duplication is much more common than com­ plete ureteric duplication and occurs in approximately 1% of

33 

574  Urology

individuals. Complete duplication is present in about 1 in every 500–600 individuals. The extent of incomplete ureteral duplication may vary from a bifid renal pelvis (which could be considered as a normal variant) to two separate ureters joining with each other at some point during their course. A complete duplication results in two separate ureters with two separate ureteric openings in the bladder. The orifice of the upper-segment ureter always enters the bladder more medial and caudal to the lower-segment orifice. The ureter from the lower part of the kidney is more likely to be associated with vesicoureteric reflux, as the orifice of this ureter is more lateral and cephalic. As the orifice of the ureter from the upper pole is more caudal, it can be located in an ectopic position which may open at the level of the bladder neck, urethra, vestibule or vagina and may result in either obstruc­ tion or incontinence.

Symptoms in infants and children are: n

abdominal mass urinary tract infection n haematuria n failure to thrive. n

Symptoms in adults are: n

intermittent loin pain sometimes associated with alcohol consumption n urinary infection n haematuria following mild trauma n symptoms of stones.

Signs In infants and children, the sole sign is abdominal mass. In adults, signs are:

Clinical features

n

Duplication of the ureters is commonly asymptomatic. Vesi­ coureteral reflux into the lower moiety can result in infection, haematuria or flank pain.

n

Management

loin tenderness rarely, abdominal mass n an incidental finding during the course of investigation for another condition.

Investigation

Asymptomatic duplications do not require any treatment. If one of the moieties of the kidney is non-functioning, a hemi­ nephroureterectomy is the procedure of choice. In cases of complete duplication, vesicoureteral reflux is managed in the usual way. An ectopic ureter can either be re-implanted or a heminephroureterectomy can be performed, depending on the function of that portion of the kidney.

To diagnose PUJ obstruction, both anatomical and func­ tional studies of the kidney are required. Anatomical informa­ tion of the kidney can be obtained by ultrasound examination. Ultrasound examination reveals dilatation of the pelvicalyceal system and also demonstrates the state of the renal cortex.

Congenital obstruction at the pelviureteric junction

IVU gives an indication of the anatomical as well as the functional state of the kidney (Fig. 33.5). IVU can also be combined with diuretic enhancement of urine flow by giving 40 mg furosemide (frusemide) intravenously. Following con­ trast and furosemide (frusemide) injection, if there is no increase of dilatation of the pelvicalyceal system and there is good washout of contrast, this indicates a non-obstructed system.

The pelviureteric junction (PUJ) is the most common site of obstruction in the upper urinary tract.

Aetiology In the congenital type, intrinsic abnormalities of the PUJ are the most common cause of obstruction. They result from an aperistaltic segment at the level of the PUJ, resulting in a functional obstruction to the passage of urine. In some cases, valve-like processes and polyps have been found. Extrinsic abnormalities are seen in about one-third of patients with PUJ obstruction. Aberrant vessels may cause obstruction, especially when they cross in front of the PUJ or when the ureter appears to be trapped between two such vessels. PUJ obstruction occurs in approximately 1 : 1500 births. It is more common in males and is bilateral in 5% of cases. Obstruction is acquired as a result of stricture formation following surgery for stones, trauma or tuberculosis.

Clinical features Symptoms The typical clinical presentation has changed since the advent of widespread antenatal sonographic screening. A significant number of babies with antenatal hydronephrosis are subsequently found to have a PUJ obstruction.

Intravenous urography with diuretic enhancement of urine flow

Nuclear isotope scan A prolonged excretory third phase occurs when there is pelvicalyceal dilatation. If furosemide (frusemide) is given, the counts may rise (obstructed) or fall (non-obstructed).

Management Broad options of management include: n n n n n n

observation surgical reconstruction percutaneous balloon dilatation retrograde balloon dilatation percutaneous incision (endopyelotomy) laparoscopic surgery.

Most PUJ obstructions are now discovered antenatally and hence are asymptomatic. Management is decided on the basis of anatomical and functional information provided by different scans. After birth, the kidneys are observed by repeated scanning with ultrasound and/or isotope renography.

Disorders of the ureter  575 Indications for surgery These are: n

deterioration of renal function worsening of renal dilatation n thinning of renal cortex n the presence of symptoms, pain, haematuria or infection. n

For primary PUJ obstruction, if operative intervention is required, surgical reconstruction is the method of choice. The percutaneous or retrograde dilatation/incision tech­ niques are usually reserved for secondary PUJ obstruction. The most common surgical technique is the Anderson– Hynes pyeloplasty which disconnects the pelvis from the ureter, reduces the size of the pelvis but requires re-anastomosis of the ureter to the pelvis. A Culp pyeloplasty is useful for those with a small extrarenal pelvis. Re-anastomosis of the ureter is not required (Fig. 33.19). Laparoscopic surgery is being increasingly utilised.

DISORDERS THAT MAY BE EITHER CONGENITAL OR ACQUIRED

Megaureter Aetiology The underlying cause of the congenital variety is the same as that of PUJ obstruction, but the muscular imbalance in megaureter is at the ureterovesical junction. The ureter

proximal to this becomes dilated and hypertrophied. The condition may be bilateral, and a secondary hydronephrosis may develop with the formation of stones. Secondary megaureter may be caused by schistosomia­ sis or bladder outflow obstruction.

Pathophysiology Classification on the basis of reflux and the presence of obstruction to flow is shown in Box 33.9 and is used to guide management. Very rarely, reflux and obstruction may coexist. A combination of ultrasound scanning, micturating cysto­ grams and renography permits appropriate categorisation.

Clinical features Symptoms of megaureter are: n

incidental finding during investigation for another condition n loin pain n urinary infection. Box 33.9 

Pathophysiological classification of megaureter

Congenital n Non-refluxing or refluxing n Non-obstructed or obstructed Secondary n Non-refluxing or refluxing n Non-obstructed or obstructed

a

b

Fig. 33.19  Pyeloplasty operations: (a) Anderson–Hynes; (b) Culp.

Disorders that may be either congenital or acquired

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576  Urology

Management Non-obstructed, non-refluxing megaureters do not require treatment. Congenitally obstructed megaureters should be re-­ implanted after the narrowing at the distal end has been removed. Those with reflux are treated along the lines of management of vesicoureteric reflux. A secondarily obstructed megaureter requires treatment of its cause.

rarely in an ectopic one. This usually involves the uppersegment ureter of a duplex system. They may become very large and occupy most of the available space in the bladder. A stone impacted in the lower end of the ureter is one cause.

Clinical features Some patients are asymptomatic. When symptoms do occur, they are usually secondary to complications, such as: n

Vesicoureteric reflux Aetiology and pathological features Primary reflux is the result of a defective valvular mechanism at the ureterovesical junction; when compared with a normal ureter, the intramural course is short and more horizontally directed. The condition is bilateral in 50%, and 90% of affected patients are female. There is a familial incidence. As the ureterovesical junction matures, reflux may cease spontaneously. Secondary reflux may occur because of bladder outlet or urethral obstruction or in neurogenic bladders. Inflammatory conditions of the bladder wall (schisto­ somiasis, tuberculosis) can hold the ureteric orifice open.

Clinical features In primary reflux, the onset is in the first decade. Symptoms may include fever, lethargy, anorexia, nausea and vomiting. There is often mild haematuria, but the main symptoms are those of recurrent urinary infections. Older children may complain of pain in the loin or on micturition. In secondary disease, the onset is later, and again symptoms of infection predominate. There are no specific signs.

Investigation Ultrasound  is often normal but may show ureteric dilatation or renal scarring. Micturating cystogram.  Cystoureteric reflux is best demon­ strated at the time of micturition (Fig. 33.7). Isotope scanning.  A DMSA scan can be used to identify current renal damage.

Management The majority of patients can be satisfactorily managed by antibiotic therapy. Long-term therapy to suppress infection is necessary up to the age of 6 years. The incidence of renal scarring after this age is very low. Surgical re-implantation of the ureter is indicated when medical management fails to suppress the development of new urinary infections or there is non-compliance with antibiotic treatment. The injection of inert, non-absorbable substances around the ureteric orifice to prevent reflux offers a non-surgical option to treat this condition.

Ureterocele Ureterocele is a cystic dilatation of the terminal portion of the ureter and may occur in either a normally placed ureter or

obstruction of the bladder outlet infection n loin pain. n

Signs are minimal. An ectopic ureterocele in a female may present as a vaginal tumour at birth or in childhood. Occa­ sionally they may present at the urethral meatus.

Diagnosis The diagnosis is made on an ultrasound which shows a rounded swelling in the bladder associated with a dilatation of the ureter – hydroureter.

Management Asymptomatic ureteroceles do not need treatment. If the ureter is dilated or there is a stone, the ureterocele can be transected endoscopically. The cut is made on the inferior surface because this makes reflux less likely. Ectopic uretero­ celes require a heminephroureterectomy.

ACQUIRED CONDITIONS

Ureteric injuries Aetiology Open injuries occur from gunshot or stabbing. A closed avul­ sion of the ureter from the renal pelvis may follow rapid deceleration. However, surgical injuries during abdominal or pelvic operations are the commonest cause. The ureter is at particular risk if it is displaced from its usual anatomical position by the condition under treatment. Operations most frequently associated with ureteric injuries are listed in Box 33.10.

Pathological features One or both ureters may be ligated. The kidney stops secret­ ing once the intraureteric pressure has risen to the filtration Box 33.10  Operations most frequently associated   with ureteric injuries

Gynaecological n Hysterectomy n Ovarian cystectomy n Repair of vesicovaginal fistula n Anterior colporrhaphy General surgery n Sigmoid colectomy n Abdominoperineal resection of the rectum n Repair of aortic aneurysm Urology n Excision of bladder diverticula n Ureterolithotomy n Ureteroscopy

Disorders of the ureter  577 pressure. In consequence, dilatation of the renal pelvis is mild and, if the condition goes untreated, atrophy of the kidney takes place. Less commonly the lumen is incom­ pletely obstructed by inclusion in a stitch, in which case the kidney continues to secrete and hydronephrosis devel­ ops often with accompanying infection. Alternatively, the ureter is divided or suffers a crushing injury. The latter may be ischaemic. Urine then leaks to the exterior or into the retroperitoneal tissues and, less commonly, the peritoneal cavity.

Clinical features The injury may be recognised at the time of surgery. If not, bilateral ligation will be recognised very soon. Leak usually presents around the fifth postoperative day but may be delayed for 10–14 days if it results from ureteric ischaemia. The features are: n n

n n

n

bilateral ligation – immediate postoperative anuria unilateral ligation – either absence of clinical features or, if there is proximal infection, fever and persistent loin pain division – urine appears from the drain, the wound or the vagina retroperitoneal leakage of sterile urine leads to abdominal distension secondary to ileus and intraperitoneal leakage to signs of free fluid in the peritoneal cavity retro- or intraperitoneal leakage of infected urine is associated with the features of peritonitis and generalised sepsis.

a

Investigation In the early stages of complete obstruction, an IVU shows a nephrographic effect – contrast medium outlines the whole kidney, but little change in radiodensity is seen in the renal pelvis or ureter. In incomplete obstruction or transsection, there is some delay in excretion, and ureteric dilatation on the side of the injury down to the site of damage is usually seen. If, however, this is not identified, retrograde ureterog­ raphy may help.

Management Prevention A CT scan should be done before any operation in which the ureters are at risk, particularly if there is the possibility of ureteric displacement.

Treatment The insertion of a ureteric stent may allow a small fistula to close. In critically ill patients, a temporary percutaneous nephrostomy is the procedure of choice to allow drainage of the obstructed and usually infected kidney. In all other instances, surgical repair is necessary, and complicated pro­ cedures may be required. If the injury is recognised at the time of surgery, ligatures should be removed, the crushed area resected, the cut ends should be spatulated and a primary anastomosis performed over a ureteric stent (Fig. 33.20b). Other techniques include: n

re-implantation of the damaged ureter into the bladder (Fig. 33.20d) n anastomosis of one ureter to the other (Fig. 33.20a)

b

Fig. 33.20  Techniques which may be used for repair of an injured ureter.

Acquired conditions

33 

578  Urology iii)

ii)

c i)

d i)

Fig. 33.20, continued

ii)

Disorders of the ureter  579 n n

replacement of the ureter by small intestine use of the bladder flap (Boari) to replace the damaged segment (Fig. 33.20c).

Retroperitoneal fibrosis Aetiology There are two forms: idiopathic and secondary. In the first, as its name implies, the cause is not known. Secondary retroperitoneal fibrosis may follow: n n n n n n

treatment with methysergide extravasation of urine retroperitoneal sepsis aortic or iliac aneurysms radiotherapy most commonly, retroperitoneal spread of malignant disease – cervix, ovary, testis, prostate and lymphomas.

Pathological features In the primary idiopathic form, one or both ureters become encased in and obstructed by a retroperitoneal plaque of fibrous tissue between the pelviureteric junction and the pelvic brim, although involvement may be more extensive.

Clinical features Symptoms are non-specific but include backache, low-grade fever and malaise, as well as those of hypertension, renal failure or anuria. The physical findings are also non-specific and related to the renal failure or hypertension.

Investigation ESR  is invariably raised.

pelviureteric junction, the pelvic brim where the ureter crosses the iliac vessels, and the intravesical termination.

Clinical features Ureteric stones almost always cause renal colic, and they account for one of the most frequent urological presentations in the Accident and Emergency Department.

Symptoms The patient is in severe pain which is intermittent and radiates from the loin to the groin and sometimes into the testicle, scrotum or labia. Vomiting frequently occurs and the patient is unable to find any comfortable position or to lie still. The urine is often bloodstained.

Signs Fever suggests the presence of a pyonephrosis. The abdomen is tender with slight guarding. An impacted stone may be complicated by paralytic ileus which produces a silent distended abdomen.

Investigation Urine Examination of the urine is carried out for red blood cells and bacterial culture.

Imaging A plain abdominal X-ray may show a calcified opacity lying in the course of the ureter. A CT scan should always be done urgently to confirm the diagnosis and to assess the degree of obstruction and the likelihood of the stone passing spon­ taneously; 90% of stones less than 0.5 cm in diameter will do so (Fig. 33.21).

Ultrasound  may show upper urinary tract dilatation. CT  scanning shows upper urinary tract dilatation, with medial deviation of one or both ureters, and is useful to define the extent of the retroperitoneal mass. Bilateral retrograde ureterography  often results in complete anuria from ureteric oedema and should be avoided.

Management Treatment is surgical. A definitive diagnosis of possible underlying causes can only be made by histological exami­ nation of tissue from the retroperitoneum, and ureterolysis can be done at the same time. To prevent recurrence of obstruction, both ureters are either wrapped in omentum or brought laterally and intraperitoneally to distance them from the fibrotic mass. Idiopathic retroperitoneal fibrosis does respond to treatment with steroids, but long-term therapy is required. A histological diagnosis to exclude retroperitoneal malignancy is not made unless therapy is preceded by surgi­ cal exploration.

Ureteric stone Aetiology and site of lodgement These stones originate in the kidney and migrate downwards. Arrest is likely at the three sites of relative narrowing: the

Fig. 33.21  An intravenous urogram showing clubbed calyces secondary to ureteric obstruction.

33 

580  Urology

Management Most patients are admitted to hospital for relief of pain, although the majority require only one parenteral injection of opiate. Antispasmodics and non-steroidal anti-inflammatory agents are effective thereafter.

Indications for intervention These are: n

evidence of infection recurrent or persistent pain n failure of the stone to progress downwards n deterioration of renal function determined by isotope scanning. n

Methods of intervention In an emergency, intervention is by either percutaneous nephrostomy or the passage of a ureteric stent to bypass the obstruction (Fig. 33.22). Definitive treatment is by: n

extraction – snaring small stones in the lower 5 cm of ureter in a basket passed up the ureter; or very rarely by open ureterolithotomy n extracorporeal destruction by shock wave lithotripsy n in-situ destruction with lithotripsy or laser via a ureteroscope.

Fig. 33.22  Double pigtail catheter providing drainage of the renal pelvis and stenting of the left ureter.

URINARY DIVERSION Decompression or drainage of the urinary tract is frequently employed in urological practice. It is now usually done under radiological control rather than at open operation.

Nephrostomy and pyelostomy In nephrostomy, a drainage tube is passed through the kidney substance into its pelvis; in pyelostomy the pelvis is intubated directly. Either procedure is most frequently employed to decompress and drain a kidney obstructed at the pelviureteric outflow. Decompression may also be needed after operations such as reconstruction of the pelvi­ ureteric junction. An external drainage bag can be avoided if it is possible to intubate an obstruction or suture line by placing a ureteric stent across it so that one end lies in the renal pelvis and the other in the bladder (Fig. 33.22). The technique is frequently used before lithotripsy, to prevent fragments of stone causing ureteric obstruction.

Other forms of urinary diversion Surgical diversion of urine to the exterior is required if the bladder is removed or is so congenitally deformed (exstro­ phy) or diseased that adequate function is impossible. Diver­ sion is most frequently achieved by using an isolated segment of ileum into which the ureters are implanted. The segment acts as a conduit to bring the urine to the abdominal wall (Fig. 33.23). Intestine can also be used to make a new

Fig. 33.23  An ileal conduit.

Urinary diversion  581 bladder with a continent external opening on the abdominal wall which the patient catheterises intermittently (cf. conti­ nent ileostomy). Rarely, the ureters may be implanted into the intact sigmoid colon. However, that technique often leads to ascending urinary infection and chronic pyelonephritis; and, because of reabsorption of urinary constituents from the

intestine, hyperchloraemic acidosis develops. Yet a further complication is the development of adenocarcinoma at the site of ureteric implantation. This procedure has now been superseded by the creation of a pouch in the sigmoid colon (Mainz II). This has a much lower incidence of complications.

THE LOWER URINARY TRACT Symptoms in the lower genitourinary tract Bladder pain This may be sharp or dull and is located in the midline of the lower abdomen. Rapid overdistension of a previously normal bladder causes severe pain, but if the distension is gradual over weeks or months, pain is absent.

Prostatic pain This is a dull ache which may be felt in the lower abdomen, the rectum, perineum and anterior thighs.

Urethral pain This is usually felt at the tip of the penis and ranges from a mere tickling discomfort to severe and sharp pain exacer­ bated by passing urine.

Scrotal pain Pain may be referred to the scrotum as in renal colic. Simi­ larly, pain arising from the scrotal contents may be referred to the groin or abdomen. Most scrotal pain is the result of stretching of the tunica albuginea; if this happens acutely, pain is severe, but slow distension, as in a tumour, causes a dragging sensation or a dull ache.

Disorders of micturition Increased frequency may occur during the day and the night (nocturia) and may be a response to an excess fluid intake or failure of the kidneys to concentrate the urine, as occurs in diabetes insipidus, hypercalcaemia, chronic kidney disease and diseases which produce a high solute load such as diabetes mellitus. Urological causes of increased frequency are: n

urinary infection incomplete bladder emptying n detrusor irritability n small bladder volume n bladder cancer. n

Dysuria.  The term describes a burning sensation during the passage of urine. It may occur throughout micturition or just at its end (terminal dysuria). Infection with inflammation of the urethra is the commonest cause. Strangury  is a repeated desire to pass urine but with little to show for it other than pain related to the urethra or the penile tip. Infection is likely.

Intermittency.  The urine stream is interrupted during micturi­ tion. The symptom is associated with bladder stones, urete­ roceles and benign prostatic obstruction. Hesitancy  is the need to wait before the urine stream begins. Prostatic obstruction to urine flow and stricture are causes. Incomplete emptying  is, as the phrase implies, a feeling that the bladder is not emptied at the end of micturition. Prostatic disease and detrusor dysfunction are possible causes. Terminal dribbling  is a progressive reduction in the rate of urine flow at the end of the urine stream and is associated with prostatic obstruction. Post-micturition dribbling  is leakage after the patient believes that micturition is complete and is associated with detrusor irritability, urethral diverticula or the failure to empty the urethra manually after micturition. Incontinence  is of five types (Box 33.11). Abnormal urine stream.  The stream may be: n n

slow – prostatic obstruction or detrusor insufficiency forked – often associated with a urethral stricture.

Examination A distended bladder is visible and palpable in most patients examined in the supine position. Dullness to percussion in the midline of the abdomen above the pubic symphysis nearly always means bladder distension in a male.

Box 33.11  Types of incontinence n n n

n

n

True – a fistula between the urinary tract and the exterior Giggle – in young girls, provoked by bouts of unre­ strained mirth Stress – leakage during a transient increase in abdominal pressure such as caused by coughing or laughing Urge – a desire to pass urine of such severity that the patient is unable to reach the toilet; it may be associ­ ated with urinary infection, bladder stones, detrusor instability or bladder cancer Dribbling or overflow – there is a continual loss of urine from a chronically distended bladder

Urinary diversion THE LOWER URINARY TRACT

33 

582  Urology

The external genitalia are often not examined, because of embarrassment. The foreskin, glans penis and urethral meatus must be examined for meatal stenosis, phimosis, anatomical abnormalities such as hypospadias, penile tumours and warts. The scrotal contents are examined with the patient both supine and standing to aid identification of a varicocele.

Rectal examination In the UK, it is traditional to examine the male in the left lateral position. The purpose is to identify abnormalities within the anal canal and rectum and to determine the size, contour and consistency of the prostate. A similar position is used in the female but is usually preceded by a vaginal examination with the patient supine and the knees flexed. In the latter, oestro­ genisation of the perineum, urethral prolapse, urethral diver­ ticula and gynaecological abnormalities of the vagina, cervix, uterus and its adnexa can be detected.

Investigation General Bacteriological and biochemical investigation for the upper urinary tract are also relevant to the lower tract.

Imaging

Urethrography Water-soluble contrast medium is introduced into the urethra via a catheter to outline urethral strictures, urethral diverticula and urethral injuries.

Ultrasonography Transabdominal, transurethral and transrectal routes are available (Fig. 33.24). The techniques provide precise infor­ mation on:

n

residual urine bladder tumours n prostatic size n nature of prostatic enlargement – benign or possibly malignant n staging prostatic cancer. n

Transrectal ultrasound (TRUS) guidance also improves the accuracy with which a prostatic biopsy is obtained when confirmation of malignant disease is required. CT and MRI are the most accurate way of assessing the depth of invasion of bladder and prostate cancer.

Bladder function Urinary flow rate

The patient voids into a device which records the rate of accumulation of the expelled urine (flow meter). The total voided, which should be greater than 150 mL, and the peak and mean flows are recorded (Fig. 33.25). A peak flow of less than 15 mL/s may indicate bladder outflow obstruction or detrusor failure.

Urodynamics The investigations are more invasive to the extent that ure­ thral catheterisation with a filling catheter and a pressure transducer is required. A further pressure transducer is placed in the rectum to measure intra-abdominal pressure. Subtraction of pressures recorded by the two catheters is done automatically and gives a true intravesical pres­ sure which is measured both during bladder filling and on micturition (Fig. 33.26). After micturition, residual volume is measured by emptying the bladder through the filling catheter.

Endoscopy A flexible cystoscope passed under local anaesthetic, or a small rigid cystoscope using sedation or general anaesthe­ sia, is used. The whole of the urethra and bladder can be examined and ureteric catheters passed.

Urine flow (mL/s)

30

20

Normal

10 Obstructed 0 Time

Fig. 33.24  Transrectal ultrasound scan showing benign

Fig. 33.25  Measurement of urinary flow rate using a flow

enlargement of the prostate.

meter.

Disorders and disease of the bladder   583 necessary to maintain continence. Urinary diversion and excision of the deformed bladder may be required. Conti­ nence can be achieved in 80% of cases.

Intravesical pressure (cm H2O)

100 Obstructed 50 Normal 0

Acute cystitis

VOIDS

100

In men, this is invariably bacterial and often associated with other bladder abnormalities such as outflow obstruction, foreign bodies, stones and tumours. In women, it is most commonly bacterial but may also be allergic or chemical. The agent responsible can easily ascend the short female urethra.

Unstable

50

INFECTIONS OF THE LOWER   URINARY TRACT

Clinical features

0 0

100

200

300

400

500

Volume (mL)

Fig. 33.26  Urodynamic pressure studies showing obstructed and unstable responses.

DISORDERS AND DISEASE OF THE BLADDER CONGENITAL ABNORMALITIES

Urachus Failure of the urachus to close results in a urachal fistula with leakage of urine from the umbilicus at birth. Persistence of the mid-part of the urachus produces an urachal cyst palpa­ ble in the midline below the umbilicus, which may undergo malignant change.

Exstrophy of the bladder (ectopia vesicae) Epidemiology and aetiology The incidence is approximately 1 : 50 000 live births, with 50% being male and 50% female. The cause is unknown. The bladder does not infold, so that its mucosa is exposed as a flat plate on the surface of the abdomen.

Pathological findings There is failure of development of the anterior wall of the urogenital sinus and of the lower abdominal wall. The abnor­ mality is associated with: n

wide separation of the symphysis pubis epispadias – failure of dorsal closure of the urethra n inguinal hernia n imperforate anus. n

A secondary problem is the development of adenocarcinoma if the exposed bladder mucosa remains untreated.

Management The bladder and penis are reconstructed in stages after a pelvic osteotomy to allow approximation of the symphysis pubis. The insertion of an artificial sphincter is usually

Frequency, dysuria, lower abdominal pain, strangury, hae­ maturia and pyrexia all occur to a varying degree. Mild suprapubic tenderness may be present, and the urethral meatus may be inflamed. Apart from these, specific signs are absent unless there is evidence of underlying disease.

Investigation Urine It is essential to send a urine specimen for culture and sen­ sitivity before antibiotic therapy is begun. In females, a high vaginal swab should be sent for analysis to exclude Candida, Trichomonas and other vaginal pathogens, because such infections may precipitate an attack of cystitis.

Imaging Patients who present with haematuria must have both an ultrasound and a cystoscopy, which are also indicated when the MSU shows no bacterial growth. Carcinoma in situ of the bladder may present with cystitis-like symptoms.

Management An episode requires a high fluid intake and antibiotic admin­ istration (e.g. amoxicillin), which may need to be modified once the results of urine culture and bacterial sensitivities are available. Seven days after the course of antibiotics, a further MSU and high vaginal swab should be obtained to ensure that bacteria have been eradicated. In women, it is essential to identify those who have developed Candida, because this needs to be treated to stop the development of a vicious cycle of cystitis → antibiotic administration → persistent Candida infection → further symptoms.

Chronic cystitis The cause is usually inadequate treatment and investigation of an acute attack. Postmenopausal women are prone to recurrent episodes of cystitis and can benefit from topical or systemic oestrogen replacement therapy. Ten percent of patients who receive pelvic irradiation suffer from haemor­ rhagic cystitis without bacterial infection. Most cases subside spontaneously during the 12–18 months after completion of therapy, although it may lead to bladder fibrosis with a small contracted bladder.

Disorders and disease of the bladder Congenital abnormalities Infections of the lower urinary tract

33 

584  Urology

Interstitial cystitis

Investigation

This occurs most frequently in women who have irritative voiding symptoms and negative urine cultures. Many develop severe bladder pain, frequency, urgency and incontinence.

Tuberculosis of the bladder In those who present with intractable symptoms that resem­ ble cystitis and have a sterile pyuria, repeated examinations of early morning urine should be carried out to identify the tubercle bacillus.

Management The treatment of contracted bladder is considered below.

Schistosomiasis (bilharzia) Epidemiology and aetiology The blood fluke Schistosoma haematobium is endemic in the Middle East and the Nile valley and other rivers and lakes of eastern and southern Africa. Human infestation is acquired by contact with infected water. Adult worms produce ova in the pelvic and vesical veins. The ova migrate through the bladder wall into the urine, which is passed into the irrigation ditches, where miracidia penetrate the water snail. These develop into cercaria which can pass through human skin and are carried to the pelvic venous plexuses where they develop into the adult fluke (Fig. 33.27).

Pathological features The eggs in the bladder wall cause an inflammatory reaction which goes on to fibrosis, calcification and secondary infec­ tion. Stone formation and squamous carcinoma are second­ ary consequences. The ureters may be involved directly or may become secondarily dilated because of the small, thickwalled and fibrotic bladder.

Clinical features In acute presentations, pyrexia, itching, dysuria, frequency and haematuria are seen. In those who are in a chronic state, frequency, haematuria and episodes of infection resistant to treatment are usual.

Hepatic cyst containing cercaria ruptures

Microcidia enter bullinus snail

Eggs can be identified in either the urine or on bladder biopsy.

Imaging Ultrasound may show dilated ureters, stone formation or a small contracted bladder. Cystoscopy.  There is a small bladder, and there may be small sandy patches around the ureteric orifices because of calcified granulomas. Areas of squamous malignancy may be obvious.

Management Medical treatment is with praziquantel. Surgery may be required to reconstruct the ureters and the small contracted bladder.

BLADDER TRAUMA Because of its anatomy, the bladder may rupture into either the peritoneal cavity or the extraperitoneal plane. The differ­ ences in cause between the two forms of rupture are sum­ marised in Box 33.12.

Intraperitoneal rupture Clinical features Symptoms Usually there is a history of injury. Patients with a very full bladder have often consumed large quantities of alcohol, and a clear history may be difficult to obtain. There is usually also severe lower abdominal pain – modified by the patient’s clinical state – and anuria.

Signs These are as follows: n

Symptoms

Cercaria

Urine examination and bladder biopsy

Penetrates skin of humans

Worms mature Eggs deposited in pelvic veins

Ova in the submucosa passed in the urine

Fig. 33.27  Life cycle of Schistosoma haematobium.

If the urine is sterile, increasing abdominal distension and discomfort n If the urine is infected, features of peritonitis n Attempted micturition results in the passage of a few millilitres of bloodstained urine n Urethral catheterisation is easy, but urine is not forthcoming, although there may be a little blood.

Box 33.12  Causes of bladder rupture

Intraperitoneal n Blunt abdominal trauma with a full bladder n Penetrating injury (rare) n Gross overdistension at endoscopy n During endoscopic surgery on the bladder vault Extraperitoneal n Fracture of the pelvis n Resection of prostate n Difficult lower abdominal surgery n During repair of a direct hernia with bladder in the medial aspect of the sac

Disorders and disease of the bladder   585 Management The abdomen is explored, the bladder laceration repaired and the bladder drained.

Extraperitoneal rupture

Chronic irritation may be caused by: n

schistosomiasis n exstrophy with persistent infection and physical trauma. Carcinogens include: n

tobacco smoke products of the chemical industry – aniline dyes, printing, rubber processing, pesticides.

Trauma is the only cause – a fracture of the pelvis, or during transurethral resection of the prostate or bladder tumours.

n

Clinical features

Because of the known association with the above industries, there are now regular surveillance programmes which use cytological examination of the urine. If a worker in an industry that is known to have a high risk develops bladder cancer, both the victim and dependents may be entitled to compensation.

There is a history of injury, either accidental or surgical. Symptoms are: n

lower abdominal pain, although this may be masked by the effects of pelvic fracture n inability to micturate or, at most, a few drops of bloodstained urine. Urine and blood extravasated into the perivesical space cause the following: n n

tender suprapubic thickening palpable mass (occasionally).

Management Extravasation of urine after transurethral resection of the prostate or of a bladder tumour usually responds to a period of urethral catheterisation. For severe injuries which are a consequence of pelvic fracture, suprapubic drainage of the bladder and drainage of the retropubic space are required.

BLADDER TUMOURS The bladder, like the rest of the urinary tract, is lined with transitional-cell epithelium and, because it acts as a store for urine and any carcinogens that may be present, it is the commonest site for the development of malignant urinary tract tumours. Benign tumours of the urothelium are exceed­ ingly rare, as are benign tumours of the bladder muscle. Rhabdomyosarcomas of the latter occur in childhood. However, the great majority of bladder tumours arise from the urothelium, 95% of which are transitional-cell lesions. Carcinoma in situ (CIS) refers to flat areas of epithelium composed of cells with anaplastic features and disorderly pattern of growth without extension into the bladder lumen. They are multicentric and commonly occur in association with obvious transitional-cell tumours. Squamous-cell tumours occur in schistosomiasis, and adenocarcinomas are the consequence of untreated bladder exstrophy or an urachal remnant.

Epidemiology For urothelial cancer there is a 5 : 1 male predominance, although the incidence in females is increasing and may be related to cigarette smoking. The highest incidence of bladder cancer is in the sixth and seventh decades.

Aetiology Chronic irritation and carcinogenic chemicals are associated with the development of the disease.

Clinical features Symptoms The great majority of patients present with painless haema­ turia. A small proportion have urinary infections. A few tumours are found coincidentally in patients who undergo a cystoscopy for other reasons. Advanced cases have lower abdominal pain, severe dysuria, strangury and incontinence of bloodstained urine. Similar irritative findings are found in patients with carcinoma in situ and must be distinguished from bacterial cystitis.

Signs Unless the disease is advanced, abnormalities are usually absent. A careful bimanual examination may reveal a mass in the bladder wall, but if the diagnosis is established by other means (usually endoscopically) then bimanual examination is better done under anaesthesia to stage the lesion.

Investigation Urothelial tumours are often multicentric. Any patient who presents with symptoms suggestive of a urothelial tumour requires full investigation of the urinary tract, which includes: n n

n n

n

n

n

n

urine microscopy and culture for evidence of haematuria and infection cytological examination of the urine – most likely to be positive in those with carcinoma in situ or welldifferentiated tumours assessment of renal function IVU used to be used to search for other tumours in the renal pelvis, ureter or bladder (Fig. 33.28), although small tumours were difficult to detect Ultrasound and CT scanning give additional information about the primary tumour stage and show other synchronous lesions or metastatic disease and are now used instead of IVU. endoscopic examination of the urethra and bladder; endoscopy identifies the number, position and macroscopic type of urethral or bladder tumours and obtains a biopsy for histological examination of both the tumours and apparently normal mucosa bimanual examination (rectum and abdomen in the male; vagina and abdomen in the female) to assess spread of tumour beyond the bladder wall chest X-ray and bone scan to seek distant metastases.

Bladder trauma Bladder tumours

33 

586  Urology Table 33.5

Stage

Histological findings

pT(CIS) pTa

Carcinoma in situ Papillary carcinoma with basement membrane intact Tumour has penetrated the basement membrane

pT1

Table 33.6

Findings

T2 T2a T2b T3a T3b

Superficial muscle is involved Through superficial muscle Into deep muscle Through deep bladder muscle into fat (microscopic) Extending beyond muscle into fat (macroscopic) but bladder still mobile Adjacent structures involved Fixed to pelvic wall

Table 33.7

defect in the right side of the bladder as a result of a tumour.

Local staging of bladder cancer that is no longer superficial

Stage

T4a T4b

Fig. 33.28  Intravenous urogram showing a large filling

Local staging of superficial bladder cancer from histological examination of the resected specimen

Nodal staging in bladder cancer

Stage

Findings

N0 N1 N2 N3

No nodes involved Single regional node 100). Management is with steroid therapy.

Gout Arthropathy with urate crystal deposition affects mostly men at the metacarpophalangeal joint of the big toe, although the knee is also a common additional site. Acute attacks may occur spontaneously or be precipitated by local trauma. Gout may also be secondary to myeloproliferative disorders with increased purine production or renal disease with reduced urate excretion. Urate crystals may also be deposited as tophi in soft tissues: the Achilles tendon, around joints, in bursae and on the pinna of the ear. The diagnosis is made by demonstrating the presence of urate crystals within the joint or soft tissues. Management includes treatment of the acute attack with NSAIDs and long-term prophylaxis with allopurinol to reduce uric acid production after the acute attack has settled.

MANAGEMENT OF ARTHRITIS Arthritis is rarely reversible, and treatment is directed at symptomatic relief and the preservation or restoration of function.

Operative When conservative measures have failed, surgical options need to be considered.

Arthroscopy A joint that is swollen and inflamed may benefit from an arthroscopic washout which removes inflammatory mediators and fragments of cartilage, although there is no evidence of benefit for this procedure in patients with uncomplicated osteoarthritis.

Synovectomy The role of synovectomy has reduced as more effective medical treatments for rheumatoid arthritis have become available. Surgical excision of the synovium or tendon sheath in rheumatoid arthritis can occasionally be beneficial. In the past it was done as an open procedure with con­ sequent considerable joint morbidity, but this has been replaced by arthroscopic synovectomy with special powered instruments.

Joint surgery Long-term or permanent relief of the symptoms of arthritis requires surgery on the bones of the affected joint. A variety of options are available (Table 34.4) and the choice depends on a number of factors, including:

Non-operative

age patient expectation n occupation n the joint affected.

Conservative measures are tried initially in patients with osteoarthritis. Pain relief with simple analgesics, NSAIDs or cyclo-oxygenase 2 (COX-2) selective inhibitors will be helpful. For patients with early rheumatoid arthritis, treatment with disease modifying anti-rheumatic drugs (DMARDs) provides

In the younger patient with osteoarthritis, prosthetic replacement (Table 34.5) is avoided, if possible, because of the limited lifespan of the prosthesis. The results of further replacements after initial failure (revision surgery) are not as good as those of the primary procedure, and with

Conservative management

n n

Infections  613 Table 34.4

Management of arthritis

Surgical options for an arthritic joint

Procedure

Effects

Example

Arthrodesis Excision

Stiff but pain-free joint Removal of one aspect of the joint may relieve pain; shortening of the limb beyond the resection Alteration of the line of load transmission to an unaffected part of the joint – now an infrequently performed procedure Excision of diseased joint surfaces and replacement of surfaces with metal and high-density polyethylene

Fusion of the lumbar spine, ankle or wrist Keller’s operation on the big toe for hallux valgus High tibial osteotomy for unicompartmental osteoarthritis of the knee Hip, knee and shoulder and other joints

Osteotomy Prosthetic replacement

Table 34.5

Types of joint replacement

Type

Nature

Comments

Examples

Constrained

Simple hinge

Elbow, wrist

Semi-constrained

Simple hinge, but some rotation possible Two independent parts so that stability depends on sound anchorage in bone and the soft tissues

Loosening because of inevitable rotational movement Still subject to loosening Most common type in use; highly satisfactory

Hip, knee, ankle, shoulder, elbow

Unconstrained

Elbow, wrist

In the knee, the replacement can be unicompartmental if one side only is affected; more usually, all three compartments are replaced.

each subsequent attempt the surgery becomes more challenging. Almost any joint in the arm or leg can be replaced. Usually the replacement consists of a metal component bearing on a high-density polyethylene surface. The prosthesis may be cemented into place with methyl-methacrylate bone cement or be uncemented, with the surface textured to encourage bone ingrowth. New surfaces include the use of hydroxyapatite (HA), which is the basic mineral of bone. With HA chemically bonded to the surface of the prosthesis, the patient’s bone can directly bind the implant. The first successful replacement was the hip joint developed by Charnley in the 1960s although previous attempts had been made to replace the hip as far back as the 1930s. The modern hip joint can be expected to last for 15–20 years but this depends upon:

present, the safest option is to remove all the foreign material, identify the infective agent and treat this vigorously. At a second procedure, it may then be possible to insert another prosthesis. Joint replacement surgery in rheumatoid arthritis carries particular risks. The immune response is altered, and infection rates are higher. At operation, the bones are often osteoporotic with an increased risk of intraoper­ ative fractures. When multiple joints are involved, the surgeon may be embarking on an extended programme of replacement.

n

Acute osteomyelitis

surgical experience state of the recipient bone n prosthesis design n stresses placed upon the implant n the materials used at the bearing surfaces – recent research has supported hard-on-hard articulation with ceramic-on-ceramic or metal-on-metal. n

Approximately 50 000 hips and 40 000 knees are implanted each year in the UK. Complications of joint replacement surgery include: n n

general complications of any major operation specific complications of the procedure, including intraoperative fractures, postoperative dislocations and fractures, infection of the implant and loosening.

Loosening may be secondary to infection or an aseptic mechanical process. If the prosthesis is mechanically loose, it can be removed and replaced, but when infection is

INFECTIONS Before the introduction of antibiotics, acute osteomyelitis was a common infection with a 50% mortality. In the Western world the condition has now become much less common – although the reason for this is not entirely clear – and fatalities are rare.

Aetiology Haematogenous Organisms transported by the bloodstream from a distant site lodge in the capillaries of bone (usually, but not always, the metaphysis of a long bone) and set up a focus. Their origin is usually not clear but occasionally there may be a distant infected focus, such as a boil. Localisation of the infection may be determined by a minor injury to the bone, although this is not well established in pathological terms. Individuals of any age may be infected but the condition is more common in children.

Infections

34 

614  Principles of orthopaedics

Exogenous Direct inoculation of bone from the outside takes place as a result of some surgical procedure or after an open fracture.

Pathological features Organisms In haematogenous osteomyelitis, the agent is most commonly Staphylococcus aureus (85%), now often penicillinresistant. Streptococcus pyogenes and Pseudomonas aeruginosa are other pus-producing organisms sometimes involved. Occasionally, Salmonella typhimurium is found either with or without an intestinal infection and is more common in patients with sickle cell disease. E. coli may infect the bones of neonates. Infection from without can be with any organism and is often mixed.

rarefaction. Later, dead bone and sequestra show up as sclerosis. Ultrasound  may identify a subperiosteal abscess. Radioisotope bone scan  shows increased activity after a few days but well before anything is seen on X-ray. MRI  is extremely sensitive in identifying intraosseous oedema and pus.

Blood examination White cell count, ESR and CRP  are raised. Blood culture  (before the administration of antibiotics) is positive in half of those with haematogenous osteomyelitis.

Management

Pathological course

Non-operative

In haematogenous osteomyelitis, a short period of intense inflammation is speedily followed by pus formation within the medulla. Because bone is not expandable, pressure rises rapidly with two effects:

High-dose intravenous antibiotics are begun immediately after a blood culture has been taken. The affected limb is elevated and splinted because this helps to relieve pain. Antibiotic therapy is continued until the ESR has returned to normal, which may take 6 weeks or longer.

n

pus is forced through the Haversian canals to reach the periosteum, so forming a subperiosteal abscess n blood vessels in the Haversian canals thrombose, and the bone dies; stripping of periosteum contributes to this infarction. Eventually, if treatment does not take place, pus breaks through the periosteum, tracks up to the skin surface and discharges to produce an infected sinus. There is dead bone in its depths which gradually separates to form a sequestrum. Exogenous infection does not usually pursue such an acute course, and damage to bone is less. However, it is often persistent and chronic.

Clinical features History There is often a history of minor trauma. The patient, usually a child, is unwell with a high pyrexia and – if old enough to voice this – a complaint of severe localised bone pain. The affected limb is held still (pseudoparalysis).

Physical findings Look: • redness and oedema may be seen over the affected metaphysis • the limb is held still. n Feel: • warmth at the affected site • focal bony tenderness – an important sign • fluctuant swelling overlying the bone n Move: • pain on movement. n

Investigation

Surgical If the patient fails to respond by speedy return of temperature to normal and relief of pain, or if there is a fluctuant abscess on presentation, then the site is explored. The periosteum is incised and the underlying bone drilled to drain and decompress the medullary cavity.

Complications Complications are: n n n n n

acute septic arthritis secondary to direct spread from adjacent bone pathological fracture through bone that is rarefied because of infection growth impairment from epiphyseal involvement chronicity because of dead bone chronic osteomyelitis.

Chronic osteomyelitis This condition occurs because of inadequate treatment of acute osteomyelitis, or it may complicate the management of an open fracture or the surgical treatment of a closed one. It is now rare in the UK.

Clinical features History There has usually been an episode of acute haematogenous osteomyelitis often followed by a discharging sinus. Evidence of infection is dormant for months or years with an occasional flare-up in which there is local pain and swelling with discharge of pus.

Imaging

Physical findings

Plain X-ray  is initially normal. Changes occur after 10–14 days, when the periosteum is lifted and there is local

There are often scars from old sinuses, one or more of which may still be open with a purulent discharge.

Infections  615 Investigation

Clinical features

Imaging

History

Plain X-ray shows grossly abnormal bone with areas of rarefaction and sclerosis. A sequestrum appears as a separate piece of dense bone lying within a cavity. Isotope bone scan may show increased activity although, if there is a sequestrum, reduced uptake is present in relation to it. CT may give useful information on the exact size and position of a sequestrum.

The patient complains of increasingly severe pain in the joint and is unwell with a high swinging pyrexia.

Examination of the blood This is usually unhelpful, but the ESR may be raised. Blood culture is negative except during a flare-up.

Management Non-operative Antibiotics are insufficient by themselves as they are unable to penetrate the dense soft-tissue fibrosis and the relatively ischaemic bone. The occasional flare-up can be managed with dry dressings until the sinus stops discharging.

Surgical The aim of surgery is to remove all dead bone and infected material. A chain of antibiotic impregnated beads can then be implanted in the cavity to give a very high but localised concentration of antibiotic.

Complications Complications are:

Physical findings Look for: • a red and swollen joint • immobility because of pain • rarely evidence of a local wound. n Feel for: • local warmth • local tenderness. n Move: • marked pain on movement. n

Investigation Imaging Plain X-ray is normal in the early stages. After 2–3 weeks, there is local rarefaction of the adjacent bone and loss of joint space. Still later, the necrosis of cartilage reduces the joint space still further. Finally, bony ankylosis can be seen.

Blood examination The white cell count, ESR and CRP are raised and blood culture may be positive.

Joint aspiration

Septic arthritis

This should always be done (before commencing antibiotics) and is both diagnostic and therapeutic. The aspirate is sent for culture. At the same time, the toxic content of the effusion can be reduced by washing out the joint cavity. The reduction of intra-articular pressure provides relief from pain.

Any joint may be affected but the common site is the knee and hip.

Management

n

pathological fracture n amyloidosis n squamous cell carcinoma in the sinus tract.

Aetiology Causes are: n

haematogenous spread from a distant focus of infection secondary to acute osteomyelitis n direct inoculation after trauma or surgery – the incidence after arthroscopy is less than 0.2%. n

Pathological features Organisms Staphylococcus aureus Streptococcus pyogenes n Neisseria gonorrhoeae. n n

Medical High-dose intravenous antibiotics are begun (flucloxacillin up to 8 g 6-hourly or clindamycin up to 1.2 g 6-hourly if allergic to penicillin), adjusted on the results of culture and continued until the ESR has returned to normal, which may take 6 weeks. The joint is rested.

Surgical Pus within a joint must be washed out as a matter of some urgency. This may be performed via an arthrotomy; however, some joints such as the knee, ankle, shoulder and elbow can easily be washed out through the arthroscope. This is simply because of the larger bore of the instrument, a more efficient form of aspiration.

Course The hyaline cartilage is destroyed by a combination of ischaemia and toxic enzymes released by white blood cells and bacteria. As with osteomyelitis, unchecked development of pus eventually ruptures the joint capsule, and discharge occurs through the skin. Such a damaged joint heals with either a fibrous or a bony ankylosis.

Complications Complications are: n

dislocation – in particular, the hip in children joint stiffness n secondary osteoarthritis. n

34 

616  Principles of orthopaedics Table 34.6

Bone tumours

Cell of origin

Benign

Intermediate

Malignant

Osteoblast Osteoclast

Osteoid osteoma

Osteoblastoma Giant-cell tumour (osteoclastoma)

Osteosarcoma

Chondroblast

Chondroma Osteochondroma Non-ossifying fibroma (unicameral bone cyst) Haemangioma

Fibroblast Vascular Marrow

BONE TUMOURS These are either primary or secondary. Primary tumours may be either benign or malignant, but some are in an intermediate group which, although showing locally invasive features, do not metastasise. A detailed classification is given in Table 34.6.

Chondrosarcoma Aneurysmal bone cyst Plasmacytoma

Table 34.7

Fibrosarcoma Haemangiosarcoma Ewing’s sarcoma Lymphoma Myeloma Leukaemia

Common sites of primary in secondary bone tumour

Site

Incidence (%)

Breast Prostate Bronchus Kidney Thyroid

35 30 10  5  2

Clinical features History When the tumour is secondary, there may be symptoms from the primary malignancy, although sometimes the first presentation is with bone pain or a pathological fracture. Pain is common and is localised at the site of the tumour. It is usually constant with no relieving factors and often worse at night. A lump may be noticed.

Physical findings A thorough general examination is required. Most bone tumours are secondary deposits, and so the common sites of a possible primary (breast, lung, prostate, thyroid and kidney) must be examined (Table 34.7): Look for a lump. Feel for: • a lump • local bony tenderness • crepitus under the fingers when there is a history of possible pathological fracture. n Move – possible abnormal movement in the presence of a pathological fracture. n n

Investigation

CT  is required to assess the local spread of malignant tumours and so to aid in the planning of surgery. The lungs are scanned for evidence of metastases. Biopsy  is essential for a histological diagnosis for all suspicious lesions.

Benign tumours These occur in young adults. They may be found in any bone; however, chondromas favour metacarpals, metatarsals and the phalanges.

Clinical features History Benign tumours are often without symptoms unless a pathological fracture occurs. Constant local pain often worse at night may be the presenting feature. In osteoid osteoma, relief is obtained from aspirin but not opioid analgesics. Local pressure symptoms is typical of osteochondromas.

Imaging

Physical findings

Plain X-ray  is always needed. Benign tumours have a sharp margin and the cortex is intact. By contrast, malignant growths are expansive with indistinct margins and destruction of the cortex. In osteosarcoma, new bone formation is seen – so-called ‘sun-ray spicules’.

n

Isotope scan  differentiates secondary deposits – which produce multiple areas of increased activity – from a primary tumour in which there is usually a solitary active area. MRI  is also useful for the assessment of local spread within the bone and adjacent soft tissues.

Look for any evidence of a fracture – chiefly deformity. Feel for: • a hard lump • localised bony tenderness • crepitus. n Test for unusual movement – indicative of a pathological fracture. n

Management If there are symptoms, curettage and bone grafting may be required. A pathological fracture through the tumour can lead to spontaneous cure.

Shoulder  617

Locally aggressive tumours

Fibrosarcoma

These tumours are not truly malignant, and metastatic spread is very rare. There is, however, local destruction, and there may be local recurrence after surgery.

This is a rare growth in the age range of 40–60 years and occurs at any site. Management is surgical, with wide excision or amputation. The outlook is poor, with a 5-year survival rate of about 30%.

Aneurysmal bone cysts

Ewing’s sarcoma

These are blood-filled cavities that usually occur in the spine and at the ends of long bones. On plain X-ray, the cyst is seen as an expansive lesion with thinning of the cortex. The management is curettage and bone grafting, which is usually curative. Radiotherapy may be required for recurrent lesions. Embolisation may represent optimal treatment for inaccessible lesions.

Giant-cell tumour (osteoclastoma) This occurs at the end of long bones in adults between the ages of 20 and 40 – the knee is a common site. There is local pain and possibly a pathological fracture. The X-ray appearance is that of a multiloculated lesion; the tumour extends up to the joint surface. Metastases are rare but can occur especially after local recurrence. Curettage with bone grafting is often followed by recurrence. The cavity should be filled with bone cement which sets by an exothermic reaction that is cytotoxic to residual tumour cells. Local recurrence necessitates wide excision and then either bone grafting or a prosthesis.

Malignant tumours These are rare – only 125 new osteosarcomas and 60 new chondrosarcomas a year in the UK. They spread via the bloodstream to the lungs and other sites.

Osteosarcoma This tumour occurs mainly in the young between the ages of 10 and 30 years. There is a second peak in the elderly in association with Paget’s disease of bone. The tumour occurs in the metaphyseal region of long bones, the knee being the most common site. Its management used to be by amputation, but now, with more effective chemotherapeutic agents and consequently a better prognosis, surgical resection is less radical. Excision of the affected bone and replacement with a custom-made or modular prosthesis now form the standard approach. Radiotherapy is usually reserved for inaccessible sites or for recurrence. With radical surgery and chemotherapy, there is a 90% survival at 1 year and over 50% at 3 years. Survival for more than 3 years means a probable cure.

Chondrosarcoma This occurs in an older age group than that of osteosarcoma: between 30 and 70 years. Tumours commonly involve the flat bones: scapula, ribs and pelvis. They vary widely in their degree of differentiation, from high-grade anaplastic to lowgrade with only slow growth. Their management is by wide local excision with bone grafting or reconstruction with a custom-made prosthesis. Radiotherapy is ineffective. The 5-year survival ranges from 20% to 80%, depending on size, location and histological grade.

This is a highly malignant tumour that affects children and adolescents of 5–20 years. Males are slightly more frequently affected. The common site is the diaphyseal region of long bones. The clinical features, in addition to local pain and a lump, may include general ill health and fever. The lump may be red and warm. Ewing’s sarcoma is often initially misdiagnosed as acute osteomyelitis. On the plain X-ray, a characteristic ‘onion peel’ appearance is typically seen. Management is by chemotherapy followed by surgical excision and radiotherapy. The outlook has been poor. However, with radical and aggressive treatment, survival rates are now approaching 50% or more at 5 years.

Plasmacytoma This condition is rare and consists of a mass of plasma cells in bone or soft tissue which may prove to be a focal manifestation of multiple myeloma. Isolated lesions may be excised followed by a course of radiotherapy.

Secondary tumours Secondary bone tumours are common: about 30% of patients who die of a malignancy have bone secondaries. Common sources of the primary growth are given in Table 34.7. The patients are often over 60, because of the nature of the primary. Any bone may be affected, but the skull, vertebrae, ribs and pelvis are common sites. On plain X-ray, most secondary tumours are osteolytic but bone deposits from carcinoma of the prostate and about 10% of breast cancers are osteosclerotic. Treatment which is appropriate for the primary – such as hormone manipulation in breast and prostate cancer and chemotherapy – may alleviate the symptoms of secondary deposits. The pain may respond to antiinflammatory drugs and local radiotherapy. Pathological fractures do not unite spontaneously and should therefore be internally fixed, by which quality of life is improved and nursing made easier, although life expectancy remains unchanged. Prophylactic internal fixation should be considered when there is: n

rapid increase in local pain destruction of 50% or more of shaft diameter in a long bone n a femoral lesion greater than 3 cm in diameter. n

SHOULDER The shoulder is the most mobile of all joints and, with the elbow, has the prime function of manoeuvring the hand to the best position required for function, particularly to the mouth.

Bone tumours Shoulder

34 

618  Principles of orthopaedics

General clinical features History Pain  is felt over the deltoid insertion in impingement syndromes (see below); at the front in arthritis; and at the top in acromioclavicular disorders. Radiation down the arm is common. Pain around the shoulder may also be the result of reference from other sites such as the heart, lung, diaphragm or cervical spine. Stiffness  is a common symptom in shoulder disease, and loss of function such as inability to brush the hair can be socially embarrassing. Trauma  frequently figures in the history and may cause fractures, dislocations or soft-tissue injury to the joint capsule, particularly the rotator cuff. Mechanical derangement  may be a presenting symptom, as in recurrent dislocation.

Physical findings Look for: • muscle wasting of the deltoid, biceps, supraspinatus and infraspinatus • scars – indications of previous injury or surgery • the contour of the shoulder – in dislocation, the normal rounded appearance is lost and the shoulder looks squared off because of the prominence of the acromion • winging of the scapula because of weakness of the serratus anterior muscle. n Feel for the belly of biceps during resisted elbow flexion – rupture of the long head of biceps tendon results in an abnormal contour of the muscle. n Move: • through the active and passive ranges (see Table 34.2) • note any painful arcs of movement during elevation of the arm – pain during mid-elevation is caused by subacromial impingement, but pain at full elevation is from an acromioclavicular disorder. n

Investigation Imaging Plain X-ray  is required, both an anteroposterior and an axillary view. This can show degenerative arthritis, loose bodies and abnormal calcification – usually in tendons. In recurrent dislocation, a defect (Hill–Sachs lesion) may be seen on the posterosuperior humeral head and is caused by repeated impingement of the rim of the glenoid on the humerus. Ultrasound scanning  is commonly used as the first investigation after plain X-rays. Arthrograms  were commonly performed and are still used where MRI is unavailable. Rotator cuff tears are demonstrated by leakage of contrast medium into the subacromial bursa. Alternatively the rotator cuff can be assessed by ultrasound scan.

CT and MRI  are of increasing value. A tear may be visualised, loose bodies seen and bicipital tendonitis can be diagnosed.

Arthroscopy The procedure is both a diagnostic tool and of therapeutic value. It is possible to repair tears in the labrum of the glenoid, to stabilise the shoulder in recurrent dislocation, to decompress the subacromial space, to repair rotator cuff, or SLAP (Superior Labrum from Anterior to Posterior at the point where the biceps tendon inserts on the labrum) lesions, synovectomy or release contractures and remove loose bodies.

ACROMIOCLAVICULAR DISORDERS

Acromioclavicular osteoarthritis Aetiology This condition is often secondary to trauma.

Clinical features History Pain is the usual feature often felt on the top of the shoulder in relation to the joint and aggravated by lifting the arm above the head or across the body.

Physical findings Look for: • prominence of the acromioclavicular joint • muscle wasting, in particular in the supraspinatus. n Feel for: • localised tenderness at the joint • crepitus on movement. n Test movement – pain is found when passive movement above shoulder level is attempted. n

Management Surgical excision of the outer end of the clavicle provides relief.

Rheumatoid arthritis The shoulder and acromioclavicular joint are often affected by rheumatoid arthritis. In addition to pain, there is often prominent swelling.

Management Non-operative Medical management of the disease is important and provides pain relief.

Surgical Excision of the outer end of the clavicle is performed.

SUBACROMIAL DISORDERS The subacromial bursa, the rotator cuff and the tendon of biceps lie between the acromion and the head of the humerus. Any one of these structures may become trapped between the two bones and cause pain.

Shoulder  619

Impingement This often affects the rotator cuff tendons of subscapularis and supraspinatus.

Clinical features A painful arc occurs on abduction of the humerus. On examination, the arc is confirmed and can be precisely defined. There is tenderness in the anterior cuff and signs of impingement are present. The most commonly used is the Hawkins sign where a forceful internal rotation on a forward flexed shoulder at 90° produces subacromial pain.

Management Non-operative Analgesics such as NSAIDs may help the local swelling to settle. Local steroid injection into the subacromial space is also helpful.

Surgical If symptoms fail to improve with conservative measures then surgery is advisable. The subacromial space is decompressed by excising the undersurface of the acromion as a wedge.

Rotator cuff tears There are two causes: n

acute injury as a result of trauma and seen with dislocations of the shoulder in the elderly n more commonly, chronic lesions from degeneration within the cuff.

Pathological features There is a spectrum of disorders that are interconnected and which range from superficial abrasions of the rotator cuff from impingement through incomplete (partial-thickness) tears to complete full-thickness ones. However, there is not inevitable progression from one to another. Other factors such as ischaemic degeneration within the cuff coupled with trauma may determine the extent of tear.

Clinical features History There may be a history of significant shoulder injury, but more usually there is chronic shoulder pain felt over the deltoid muscle, especially at one point of abduction. Adduction may also be difficult.

Physical findings Look for muscle wasting – especially in the supraspinatus. n Feel for localised tenderness along the lateral border of the acromion. n Test for shoulder movement – active movement, particularly abduction, is reduced but there is a full range of passive movement. n

Management Non-operative Partial tears of the cuff heal and the symptoms settle after resting the shoulder. Once acute symptoms have settled, a

graduated programme of rehabilitation is begun. Tears in the elderly should be managed conservatively; surgical repair in this age group is difficult, and severe stiffness after surgery is likely.

Surgical When symptoms fail to settle, then it is likely that the tear is complete. In the young, it should be repaired. The rotator cuff is exposed and repaired with interrupted sutures, which is now achieved by arthroscopic surgery, reducing morbidity. Very large tears may require grafts of fascia lata to close the defect.

Acute calcific tendonitis Deposition of calcium hydroxyapatite within the tendon of supraspinatus may occur for unknown reasons. There is a local inflammatory reaction.

Clinical features History The inflammation that takes place causes pain that is dull initially but over a few hours becomes increasingly severe. There is considerable muscle spasm, and a septic arthritis may be suspected, but the joint itself is not inflamed.

Physical findings Look for: • a pale, sweaty patient in severe pain • the arm held still by the side. n Feel for diffuse tenderness of the whole shoulder region. n Test for movement which will be resisted because of pain. n

Management Non-operative Rest, anti-inflammatory drugs and local anaesthetic injections may help.

Surgical Incising the tendon releases the calcific deposit. It squeezes out under pressure like toothpaste from a tube, and pain relief is immediate.

Adhesive capsulitis (frozen shoulder) This condition is characterised by increasing pain and relative immobility of the joint. It fundamentally is a contracture of the shoulder capsule. The aetiology is unknown, but there may be a history of minor trauma, and the disorder may also complicate other illnesses such as a myocardial infarct or pneumonia. Recent research has highlighted an association between adhesive capsulitis, insulin-dependent diabetes and Dupuytren’s contracture.

Clinical features Pain and stiffness are the only complaints. Joint movement is limited, and attempts to increase the range of passive movement cause pain. Over a period of about a year, the symptoms may gradually improve, and within 2 years the

Acromioclavicular disorders Subacromial disorders

34 

620  Principles of orthopaedics

shoulder may have returned to normal but sometimes the stiffness can be protracted.

Management Non-operative The mainstay of treatment is that resolution eventually takes place. Cautious physiotherapy is helpful, and steroid injections into the shoulder joint may also help during the painful phase.

Surgical When recovery is slow and stiffness persists, a manipulation under anaesthesia is often beneficial.

GLENOHUMERAL DISORDERS

Osteoarthritis This condition is uncommon and usually secondary to trauma. Pain is felt at the front of the joint and may radiate through to the posterior aspect. Conservative measures such as anti-inflammatory agents and steroid injections into the joint help in the early stages. Persistent disability requires: n

arthroscopy – the joint is washed out and any loose bodies are removed, which gives some relief for most patients n arthroplasty – replacement with a prosthesis; many designs are available but most consist of a metal humeral head and a high-density polyethylene glenoid n arthrodesis – fusion of the shoulder is rarely done except as a salvage procedure after failed joint replacement.

General clinical features History Stiffness is noticed early by patients because of difficulty in getting the hand to the mouth. n Pain is common and often aggravated by movement. n Locking is an occasional feature, particularly in degenerative disease. n Past trauma to the joint is not uncommon. n

Physical findings Look at: • the shape of the joint – compare with the other side • contour for swellings – a bursa, rheumatoid nodule or effusion • carrying angle of the arm in extension – normal is 8–10° of valgus. n Feel for: • crepitus • bony landmarks – two epicondyles and the olecranon: do they form an equilateral triangle with the elbow flexed (Fig. 34.3)? • effusion – best felt between the lateral epicondyle and the olecranon; the normal hollow is filled out by a soft swelling • radial head during pronation and supination – does it dislocate as the forearm moves? n Test for: • ulnar nerve function in the hand • movements – ask the patient to demonstrate the active range of movement; measure the passive range of movement (see Table 34.2). n

Rheumatoid arthritis The shoulder is commonly affected by this disease. Management is usually non-operative by treating the underlying condition and using intra-articular steroid injections. Surgical options are the same as for osteoarthritis.

Avascular necrosis of the humeral head This is much less common than the same condition in the femoral head. The causes and mechanisms are the same. Management is by treating any underlying cause and by the use of anti-inflammatory agents and physiotherapy. Surgical core decompression is indicated in early disease to arrest progress. In the late stages, when there has been collapse of the humeral head and secondary osteoarthritis has developed, an arthroplasty may be required.

ELBOW The elbow joint is a hinge that works in consort with the shoulder in positioning the hand.

Fig. 34.3  Equilateral triangle formed at the elbow by two epicondyles and the olecranon.

Hand and wrist  621 Investigation Imaging Plain X-ray is usually the only investigation required and can show old injuries, the presence of arthritis, loose bodies and subluxation of the radial head.

HAND AND WRIST

Nerve function

Loss of hand function is very disabling in that nearly all daily activities require the hands to a greater or lesser extent. The wrist, in conjunction with the elbow and shoulder, positions the hand in space while the fingers and thumb hold and manipulate.

If an ulnar nerve lesion is suspected, electromyography is required.

General clinical features History

Osteoarthritis Clinical features The condition is almost always secondary to trauma. Pain and stiffness are the common symptoms. Locking can sometimes occur.

Management Non-operative The usual initial – and often the only – treatment required consists of analgesia, local strapping and physiotherapy.

Surgical The indications for surgery are: n

symptomatic loose bodies which can be removed arthroscopically n ulnar neuritis – usually the consequence of a valgus deformity; this is treated by transposition of the nerve in front of the medial epicondyle. Fusion is indicated when there is failure of conservative treatment, with severe pain. The joint is fixed in a position of function that allows the hand to reach the mouth – about 100° of flexion. Total elbow replacement is possible, and the long-term results are less satisfactory in the joint with degenerative disease as compared with rheumatoid arthritis.

Rheumatoid arthritis The elbow is often involved in rheumatoid arthritis, and clinical features are of pain, swelling and stiffness.

Management Non-operative Most patients can be managed by control of the systemic disease and local measures including splints.

Operative If conservative measures are not sufficient, then there are a number of surgical options. Synovectomy can produce good relief of pain and is usually done through the arthroscope. n Excision of the radial head can reduce symptoms if this structure is particularly involved. n Fusion and replacement can both be considered. n

Pain  is often felt in the wrist but less commonly in the hand. Pain which originates in the hand may be felt across the wrist joint or be localised to a styloid process. In the fingers, it is usually related to pathological change in a joint. Pain at night which affects the hand and is associated with numbness is characteristic of compression of nerves in the carpal tunnel. Stiffness  in the wrist may not cause significant problems, but in the fingers it is an early complaint because it is so disabling. Swelling  in the hand or fingers is noticed early. Rings may become tight and so draw attention to the fingers. Paraesthesia  is usually in the distribution of a peripheral nerve. Weakness  is a common symptom in median or ulnar nerve lesions. Patients often complain of difficulty in fine finger movements such as in knitting or writing.

Physical findings Look for: • the position of the hand at rest – are the fingers in fixed flexion because of fascial contractures in the palm (Dupuytren’s contracture)? • finger deviation with ulnar drift as seen in the rheumatoid hand • muscle function in the hand – the thenar eminence may be atrophied in median nerve compression, and the hypothenar eminence and interossei in ulnar nerve compression • the pattern of any swelling at the joints of the fingers; Heberden’s nodes are seen at the distal interphalangeal joints in osteoarthritis. n Feel: • the palmar aponeurosis – thickened areas may indicate aponeurotic fibrosis • the skin – warmth and dryness are present if there is a peripheral nerve lesion. n Test: • sensation to light touch and pinprick and establish the distribution of any loss found • for crepitus at the wrist on movement • ulnar and median nerves for Tinel’s sign; this is often positive in fascial compression at the wrist or other causes of nerve excitability • active and passive ranges of movement (see Table 34.2). n

Glenohumeral disorders

Elbow Hand and wrist

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622  Principles of orthopaedics

Investigation

Non-operative

Imaging Plain X-ray is often needed and can confirm if a lump arises from bone. Arthritic change and its underlying cause can be demonstrated (see Table 34.3). Old trauma may be evident. Unusual conditions such as Kienbock’s disease (osteochondrosis of the lunate – often post-traumatic) or Madelung’s deformity (subluxation of the distal radioulnar joint, see below) can be confirmed.

Physiotherapy to conserve and improve hand function is essential. The occupational therapist can provide crucial aids to assist in the activities of daily living: modified cutlery with curved or flattened handles, special fasteners for clothes, and other devices may all preserve independence. Hand splints are often used. They rarely prevent deformity but do allow rheumatoid joints to be rested during an acute exacerbation of the disease.

Electromyography (EMG)

Surgical

If a peripheral nerve lesion is suspected, EMG is essential. It confirms the diagnosis and site of the lesion and may help to avoid unnecessary surgery.

Arthritis at the wrist At the wrist, osteoarthritis is often secondary to trauma. Rheumatoid arthritis also affects the wrist.

Clinical features

Various operative procedures are appropriate at different stages of the disease, but the potential problems of undertaking surgery should always be carefully discussed. Many badly deformed hands are still able to function usefully. Ruptured tendons should be repaired and, in rheumatoid arthritis, early synovectomy may delay destruction. In later stages, or in osteoarthritis, damaged joints may be replaced by Silastic implants. These correct deformities and relieve pain but rarely increase grip strength and some residual stiffness persists.

The symptoms are pain, stiffness and swelling. The swelling is often accompanied by deformity from a previous fracture. Crepitus may be felt.

Dupuytren’s contracture

Management Non-operative

This is a condition of the hand in which there is thickening and contraction of the palmar aponeurosis, which may be due to a local change in collagen metabolism.

Measures such as a removable wrist splint can relieve symptoms, as do mild analgesics.

Aetiology and pathological features

Surgical

The precise cause is not known, but there are nevertheless a number of well-recognised associated factors, including:

The indications for surgery are pain and incapacity which have failed to respond to non-operative measures, such as in the young adult with post-traumatic arthritis. Of the options available (see Table 34.4), fusion is the procedure of choice. The joint is removed and a bone graft inserted. A plate is normally required for stabilisation until the bone unites. Wrist joint replacement is technically feasible but remains controversial.

n n n n n n n

a family history male sex regular high consumption of alcohol insulin-dependent diabetes mellitus adhesive capsulitis phenytoin therapy trauma.

Arthritis of the hand

Contracture is bilateral in 45%; similar lesions in the plantar aponeurosis (Lederhosen’s disease) occur in 5%; and the penile fascia (Peyronie’s disease) is affected in 3%.

The distribution in the hand follows a pattern characteristic of the cause.

Clinical features

Clinical features Stiffness and deformity of the fingers are common symptoms. In rheumatoid arthritis, the hand deforms in a characteristic way. Progressive destruction of the metacarpophalangeal joints causes the fingers to drift to the ulnar side, and later there is subluxation at these joints. In addition, inflammatory tenosynovitis may lead to tendon rupture with one or more dropped (semi-immobile and flexed) fingers.

The condition usually develops at the base of the ring and little fingers. As the lesion progresses, the fingers gradually develop fixed flexion deformities, and the thumb web may also be involved.

Management Non-operative Although many measures have been tried, none is effective. The condition may be self-limiting but is usually progressive.

Management

Surgical

Because arthritis, in particular rheumatoid, is a continuing process, management varies with the stage of the disease. A series of procedures may be required as deformities develop and progress.

Five operations may be considered, and these are outlined in Table 34.8. The choice depends on the extent of the disease, the degree of disability and whether or not previous operations have been done.

Hand and wrist  623 Table 34.8

Operations for Dupuytren’s contracture of the palmar fascia

Procedure

Technique

Outcome

Percutaneous fasciotomy

Simple division of fibrous bands through percutaneous stab wounds Thickened areas are excised

Recurrence rates high and damage may occur to nerves and blood vessels Most common operation; successful in limited disease Potentially curative but high incidence of skin necrosis Curative but requires high skills

Selective fasciectomy Complete fasciectomy Complete fasciectomy and skin graft Amputation

Whole aponeurosis excised even if not obviously involved Aponeurosis excised together with the skin of the palm followed by split-skin grafting Removal of a single digit (usually little finger), severely contracted into the palm and interfering with hand function

Can be procedure of choice in special circumstances

Nerve entrapment syndromes These commonly affect the hand. Usually it is compression of the median nerve that gives rise to symptoms, but ulnar nerve entrapment at the elbow or occasionally the wrist can also occur.

Aetiology Median nerve compression  in the carpal tunnel is usually without an identifiable cause, but any abnormal structure within the tunnel can produce the condition. Examples are: n

wrist fracture – early from local haematoma and oedema or late because of a malunion and bony encroachment n ganglion within the carpal tunnel n tenosynovitis from rheumatoid arthritis or repetitive strain injury n changes in the interstitial space – obesity, diabetes mellitus, hypothyroidism, pregnancy, acromegaly and amyloidosis. Ulnar nerve compression  is usually at the elbow adjacent to the medial epicondyle of the humerus. There may not be an obvious cause, but a fracture which causes a valgus deformity of the elbow may attenuate the nerve. Compression at the wrist in the ulnar canal between the pisiform and the hook of the hamate is less common.

Clinical features History In median nerve compression – the characteristic carpal tunnel syndrome – there is often pain in the distribution of the median nerve, and this is frequently worse at night. Loss of grip and clumsiness in handling objects are other complaints. In ulnar nerve compression at the elbow there may be a past history of trauma in the region of the joint. Weakness and clumsiness of the hand are the chief complaints.

Fig. 34.4  Froment’s sign, positive in the patient’s left thumb.

angle. An elbow lesion also causes weakness of the ulnar half of flexor digitorum profundus, but flexor carpi ulnaris is weak only when the lesion is above the elbow. Wasting of the hypothenar and interosseous muscles is present (most noticeable in the first web space). The hand may appear flattened with the ring and metacarpophalangeal joints hyperextended because of lumbrical paralysis. Attempts to grip a sheet of paper between the thumb and index finger cause the trick movement of flexion of the distal phalanx of the thumb to compensate for the weak interossei (Froment’s sign – Fig. 34.4).

Management Non-operative Underlying causes at the wrist are treated. In pregnancy, the symptoms often resolve rapidly after delivery. Injections of steroid into the carpal tunnel may help in mild cases but should not be repeated more than twice or irreversible fibrosis may take place in the median nerve. Non-operative treatment of ulnar nerve problems usually fails.

Physical findings Median nerve.  Wasting of the thenar eminence and the first dorsal interosseous is seen. There is loss of sensation in the median nerve territory of lateral three and a half fingers. Ulnar nerve.  If the compression is at the elbow, evidence of elbow deformity may be apparent with an abnormal carrying

Surgical Median nerve.  Decompression of the median nerve by dividing the carpal ligament is a highly effective and simple procedure that can be carried out under local or general anaesthesia. Relief of symptoms is often immediate and any thenar wasting recovers with time.

34 

624  Principles of orthopaedics

Ulnar nerve.  For lesions with their cause at the elbow, the nerve is released in situ (releasing the nerve as it pierces the flexor carpi ulnaris distally and proximally the medial intermuscular septum) or rarely transposed to lie in front of the medial epicondyle after dividing the medial intermuscular septum which, if left intact, can chafe the nerve and cause persistent problems. At the wrist, the ulnar canal is explored and decompressed. Recovery is slow compared with the median nerve but symptoms do generally improve.

Ganglion

Management Surgical treatment is the only option. The sheath is incised to allow the tendon to move freely.

de Quervain’s syndrome Tenosynovitis of the tendon sheaths of extensor pollicis brevis and abductor pollicis longus may be the result of local trauma, but usually no cause is found. It is most frequent in middle-aged women.

Clinical features

Ganglions are tense cysts containing viscous, jelly-like material. They often occur on the dorsum of the wrist and are associated with joints or tendon sheaths. They are commonly found around the wrist and ankle but also occur in the hand and in the foot.

The symptoms are pain and weakness of the thumb. The sheath is palpably thickened and tender. Adducting and flexing the thumb and wrist (Finkelstein’s test) are painful.

Aetiology and pathological features

Non-operative

Many explanations have been advanced but none has been conclusively established. It is possible that they are derived from small extra-articular fragments of synovium and at times a communication with the underlying joint or tendon sheath can be demonstrated and this would certainly explain both their inspissated contents and their tendency to recur if incompletely removed.

Clinical features Symptoms are cosmetic only unless previous inadequate surgery has caused secondary problems. Signs are of a tense, fluctuant usually globular swelling deep to skin and incompletely mobile on the deep aspect because of attachment to a neighbouring joint or tendon sheath.

Management Non-operative An asymptomatic lesion which does not cause cosmetic embarrassment is best left alone. Traditional treatment has also included subcutaneous rupture – the family bible was often used as the weapon. More modern therapy consists of aspiration followed by steroid injection, but 15% or more recur.

Surgical Excision of the ganglion is effective provided the technique is meticulous and undertaken in a bloodless field.

Trigger finger The cause is unknown. There is localised thickening of a flexor tendon pulleys with associated narrowing of the sheath. The thickened part is then unable to pass smoothly under the entrance to the synovial sheath at the base of the finger.

Clinical features The patient recognises that the affected finger catches in flexion and straightens suddenly with assistance and a snap. The features can usually be produced to order.

Management Injection of steroid into the tendon sheath is often effective, but it is important that only the sheath (and not the tendon) is injected because the tendon may otherwise be weakened and rupture.

Surgical The tendon sheath is slit, so freeing up movement. The procedure is curative and that of choice if the condition is chronic.

Kienbock’s disease This condition is avascular necrosis of the lunate. In most instances the cause is unknown, but it may occasionally follow dislocation of the bone. The patient – a young adult – complains of local ache and stiffness at the wrist. There are no clinical findings except slight tenderness over the dorsum of the wrist.

Investigation and management Plain X-ray shows sclerosis of the lunate. As the condition progresses, there is fragmentation, and secondary osteo­ arthritis develops in the wrist joint. In the early stages a splint may help. Attempts have been made to revascularise the bone with part of the pronator quadratus muscle, but these have met with limited success. Other surgical options include: n

removal of the bone and insertion of a Silastic prosthesis n shortening of the radius to decompress the lunate n fusion if osteoarthritis is present.

Madelung’s deformity This is a growth disorder of the distal radial epiphysis. It becomes apparent after the age of 10 years and is more common in girls. The patient complains of a prominent lump alongside the ulnar styloid with stiffness at the wrist. Examination of the mother’s wrist often reveals the same deformity. There is some limitation of the range of movement.

Hip  625 Investigation and management Plain X-ray shows the distal radius to be shortened slightly and curved, with the lunate tending to sublux between the radius and ulna. The ulna is of normal length and therefore appears more prominent. Operations should be avoided if possible. Excision of a segment of distal ulna leaves a weak wrist. In gross deformity, elongation of the abnormal radius may improve the appearance and function of the wrist but is technically challenging.

flexion test). During abduction and adduction, a forearm across the pelvis prevents pelvic tilt.

Investigation Imaging Plain X-ray is usually sufficient to confirm a clinical diagnosis. n Isotope scan. In lytic lesions, there is increased uptake; avascular necrosis appears as a relatively dense area. n CT and MRI can help to determine the site or extent of bony and other damage in more detail. n

Blood examination

HIP General clinical features and examination History

In osteoarthritis, the ESR is normal and rheumatoid factor is absent. The reverse is usually true in rheumatoid arthritis.

Osteoarthritis

Pain  originating from the hip tends to be felt in the groin or thigh. It may be referred to the knee, particularly in children. Pain is worse at the end of the day and on weight-bearing. Nocturnal pain may cause much loss of sleep.

This condition is extremely common. Its treatment to relieve pain and restore mobility has been revolutionised by the development of prosthetic hip joints.

Past trauma.  In chronic disorders there may be a past history of trauma, e.g. fracture of the pelvis and dislocation or fracture-dislocation of the femur.

The factors that can contribute to the development of the condition have been discussed above. By far the most common is wear and tear on the joint in a population with an increased life expectancy – by the age of 80 years, 80–90% of hips show radiographic evidence of the condition. Women are more commonly affected than men (3 : 1). The condition can be unilateral or bilateral. More than 10% of unilateral instances become bilateral over 5–8 years.

Limp and gait.  Limp may be noticed by others or by the patient, and there may be increasing difficulty in walking. Causes may be: n

pain as the patient tries to protect the joint short leg n muscle weakness. n

For abnormal gaits associated with hip disorders, see Box 34.2.

Physical findings Look at: • skin for scars • the position of the hip – in established osteoarthritis the hip is in fixed flexion, internal rotation and adduction • gait; this can be protective (antalgic), Trendelenburg (abnormal abductor mechanism which included the hip joint fulcrum), short- or stiff-legged. n Feel: • for crepitus on movement • to measure leg length – from the anterior superior iliac spine to the medial malleolus. n Move: • to establish active range of movement • to measure the passive range of movement. n

The normal range is shown in Table 34.2. It is important to ensure that movement is taking place at the hip alone and not the pelvis as well. Fully flexing the other hip to abolish the normal lumbar lordosis demonstrates a fixed flexion deformity as the affected leg rises up off the examination couch. On flexion, a hand under the lumbar spine can feel when the pelvis starts to tilt (Thomas hip

Epidemiology and aetiology

Management Decisions on management depend on: n

the wishes of the patient age – although with modern techniques of surgery and anaesthesia, chronological age is rarely a bar to operation n general physical condition n degree of disability and its interaction with lifestyle. n

Non-operative Those with only minor symptoms can be managed by losing weight, physiotherapy, foam heel wedges, a walking stick and NSAIDs. Loss of 1 kg of body weight reduces the forces acting across the hip by roughly 3 kgf.

Surgical Surgery for osteoarthritis of the hip is now essentially joint replacement, although in the past there were other options (see Table 34.4). An osteotomy can provide short-term relief of pain, but a subsequent joint replacement may be difficult because of the altered anatomy. Excision is reserved for the infected hip replacement. The modern total hip replacement was introduced in 1961 and can be expected to last for at least 15–20 years. However, this depends on a number of factors, as described above. The chief causes of failure are: n n

infection, which should be less than 1% loosening without infection and recrudescence of pain.

Hip

34 

626  Principles of orthopaedics

Infection means that the prosthesis must be removed, although it may be possible to insert a replacement after the organism has been eliminated. Loosening without infection is treated by a revision procedure. A variety of surgical approaches to the hip are used, as shown in Table 34.9. Typical pre- and postoperative management is given in Clinical Box 34.1.

often poor, so that intraoperative fractures occur. Infection rates are higher than for replacement in OA. Nevertheless, hip replacement for RA has a definite place provided that the joint is the principal site of the problem and there is a good chance of restoring mobility.

Rheumatoid arthritis (RA)

In this condition, the femoral head becomes ischaemic and infarcts. As a result, there is structural weakness and collapse of the bone.

This is a systemic condition which is initially managed medically. The hip and knee are involved but, in particular, it affects the upper limbs and the feet. There are a number of problems encountered with hip joint replacement in the patient with RA. When, as is often the case, multiple joints are involved, rehabilitation may be difficult. Bone quality is

Osteonecrosis of the femoral head

Aetiology The underlying process is not fully understood. The following have been postulated: n

arterial insufficiency following a fracture or dislocation venous occlusion – a feature of Perthe’s disease n raised intraosseous pressure – possibly the cause in sickle cell disease, alcoholism, systemic steroids and decompression from high atmospheric pressure with the formation of gas bubbles (the bends in deep-sea divers). n

Table 34.9

Surgical approaches to the hip joint

Approach

Advantages

Disadvantages

Anterior/ anterolateral

Reduced risk of dislocation Sciatic nerve not at risk Faster and easier approach Muscle-splitting approach, so preserving muscle power Femoral nerve not at risk Improved access to femoral canal and acetabulum, especially in revision hip surgery

Increased muscle dissection Femoral nerve at risk Increased risk of dislocation Sciatic nerve at risk Increased risk of infection?

Posterior

✚

Clinical Box 34.1 

  Total hip replacement – pre- and postoperative management

Preoperative n Obtain adequate and up-to-date radiological images n Exclude intercurrent infection – Midstream urine sample – Skin infection and venous ulcers n MRSA swabs to groin and axilla to determine carrier status n Anaesthetic assessment n Group and save Postoperative n Abduction pillow for 24 hours, to minimise risks of dislocation n Early mobilisation n Low molecular weight heparin, dabigatran etexilate, fondaparinux sodium, or rivaroxaban continued for 4–5 weeks to reduce risks of venous thrombosis (unfractionated heparin in patients with renal failure) n Crutches or sticks to reduce risk of falling n In-patient stay for 4–7 days n Raised toilet seat for 6 weeks n Avoid low chairs for 6 weeks

Management Non-operative Treatment of any correctable underlying cause is instituted. Anti-inflammatory drugs are symptomatically helpful.

Surgical Surgery is often required to provide pain relief: n

core decompression – drilling a core of bone out of the femoral head and neck is thought to be effective by reducing the intraosseous pressure and improving venous drainage but is less helpful in later stages III or IV n arthroplasty is reserved for the late stages when there is collapse and secondary osteoarthritis.

Tuberculosis Aetiology and pathological manifestations The disease is now less common, although the incidence has recently increased in the poor and groups with immunosuppression from such causes as AIDS. The route of infection is haematogenous and the pathological features are the same as for tuberculosis in other organs – tissue destruction, abscess formation and fibrosis. Untreated, the joint progresses to fibrous ankylosis.

Clinical features As well as systemic symptoms of malaise and fever, local ones include a mild ache and limp. Initially, there is little to be found – only the features of an irritable hip. Later, there is marked muscle wasting, joint stiffness, pain and shortening. This chronic picture is in contrast to the acute, severe pattern of septic arthritis.

Investigation and management X-ray changes are of osteoporosis and, later, joint destruction.

Knee  627 As in septic arthritis, pus is drained, the organism is cultured to establish sensitivity to chemotherapy and appropriate anti-tuberculosis therapy begun. With these measures, damage can be limited. A hip that heals with ankylosis may require a raised shoe when walking is resumed. A painful joint may need to be arthrodesed. Arthroplasty is considered with caution because reactivation of the infection can occur.

KNEE General clinical features History Age.  Young adults commonly suffer injury in sport; their first presentation is often to general practitioners and casualty departments. In older individuals, the joint is more frequently affected by osteoarthritis, although injury may be a precipitating factor. In an acute event, the patient may be able to pinpoint the exact moment of injury. Pain.  Generalised or localised pain is a frequent symptom. The location is important because it may indicate the diagnosis. Generalised pain over the whole knee is a feature of arthritis and acute injury. In meniscal tears, pain is localised to the joint line, including posteriorly in the popliteal fossa. Collateral ligament sprains cause pain above or below the joint line. Anterior pain is a symptom of disorders of the patella such as chondromalacia. Such anterior pain is frequently worse when the knee is loaded in flexion – characteristically when going up or down stairs. Deficiency of the anterior cruciate ligament is often associated with a sensation of giving way; the pain is diffuse. Mechanism in injuries.  Commonly, there is a twisting injury, often with an associated tearing or popping sensation from the joint which is accompanied by pain. The patient may well fall to the ground and if playing a sport then has to stop. Swelling  may be immediate (within an hour) and implies an acute haemarthrosis (the usual causes are given in Table 34.10). Swelling delay for several hours suggests a meniscal injury. Arthritic knees are chronically swollen from either an effusion or thickened synovium. Locking and giving way  occur when the knee is unstable. Locking may fix the knee, usually in flexion, or it may unlock

Table 34.10

Causes of acute haemarthrosis of the knee

Lesiona

Percentage

Anterior cruciate ligament rupture Peripheral meniscal tear Collateral ligament injury Capsular tear Osteochondral fracture Posterior cruciate ligament rupture

39 26 13  9  7  6

a

Seventy percent have more than one lesion, 29% have only one lesion, and in 1% no cause is found.

with a pop or a click and indicates a bucket handle tear of the meniscus. The arthritic knee may also give way because of instability and may lock because of loose bodies trapped within.

Physical findings Look for: • swelling – by assessing contour • wasting of the quadriceps • position at rest – is the joint in fixed flexion or is there a varus or valgus deformity? • scars – previous arthroscopy portals can be missed unless examination is meticulous • abnormal skin colour. n Feel for: • swelling – if present, is it bone, boggy synovial thickening or fluid? • the presence of an effusion (see below) • altered temperature • the joint line – medially, laterally and in the popliteal fossa • local tenderness, which suggests a meniscal tear • tenderness over the femoral condyles when the knee is flexed; they may be tender when damaged, as occurs in arthritis • the patella – is it very mobile; when pushed laterally, does the patient flinch (such positive apprehension is seen with recurrent dislocation of the patella); is there tenderness on the retropatellar surface? • loose bodies which may shoot from under the fingers • crepitus when the joint is moved. n

Effusion  is diagnosed by two methods. The first, crossfluctuation, is the more sensitive of the two. The second, patellar tap, confirms a large effusion but may not be elicited with a small collection. Cross-fluctuation.  The suprapatellar pouch is emptied by placing one hand proximal to the patella, so pushing any fluid down into the main cavity of the joint. The hand stays in position and the medial and lateral sides are examined. In the normal knee, a soft hollow is seen, but this is absent with a large effusion. With a stroking motion of the other hand to the medial and lateral sides, fluid can be pushed across the joint. In the presence of an effusion, a soft swelling appears on the opposite side of the knee to the hand. Patellar tap.  The suprapatellar pouch is emptied as before and kept empty by leaving the hand above the patella. The other hand gently presses the patella down onto the underlying femoral condyles. There is a distinct feeling of the patella sinking down and coming to a sudden stop when it hits the condyles with a ‘tap’. Collateral ligament stability  is assessed with the knee in 20° of flexion. A varus strain is applied to test the lateral collateral ligament; a valgus strain for the medial collateral. Cruciate ligaments.  The integrity of the anterior cruciate is assessed by performing the Lachman test (Fig. 34.5), and the posterior cruciate by looking for ‘posterior sag’ (Fig. 34.6).

Knee

34 

628  Principles of orthopaedics of the patella should be about equal to the distance from the inferior pole of the patella to the tibial tuberosity. If it is less than this, then the patella is riding high (patella alta) which predisposes to dislocation. Skyline views show the patellofemoral joint and are taken with the knee flexed. The patella should be horizontal and centrally positioned within its trochlear groove. Tunnel views are taken with the knee flexed to 45° and provide a view of the intercondylar notch. They are useful if loose bodies are suspected. If an avulsion of the anterior cruciate is possible, then a small flake of bone torn off the tibial plateau may be seen. Weight-bearing films accentuate any loss of joint space and also show up varus/valgus deformities. Arthrography  can show meniscal and capsular tears. With the advent of MRI and diagnostic arthroscopy, its use is declining. CT  is not often used in the knee but can show arthritis, loose bodies and patella malalignment.

Fig. 34.5  Lachman’s test for integrity of the anterior cruciate.

MRI  can demonstrate meniscal and cruciate injuries. It is non-invasive and in most centres has replaced arthrography. Radioisotope scan  shows increased activity in degenerative conditions which may be localised to one compartment.

Meniscal injuries A meniscus trapped between the joint surfaces may tear. There are five main types of tear (Fig. 34.7). The dis­ tribution is: n

medial meniscus 70% lateral meniscus 25% n both 5%. n

Fig. 34.6  Posterior sag in a lesion of the posterior cruciate. Quadriceps wasting.  The circumference of the leg is measured on both sides at a fixed distance (usually 10 cm) above the upper border of the patella. Movement.  The patient is asked to walk. On bearing weight, does the knee go into a valgus or varus deformity? There may be an antalgic, short leg or stiff leg gait (see Box 34.2). The range of active movement is then assessed and compared with the passive range. Is it possible to get the knee to full extension, or is there a block? Finally, in a normal knee, the patella tracks evenly on the trochlear surface of the femur. Maltracking occurs when it is seen to sublux or dislocate laterally as the knee moves.

Investigation Imaging Plain X-ray  reveals any arthritis. Loose bodies may be seen, often in the intercondylar notch. On the lateral film, the length

The frequent involvement of the medial meniscus is because it is firmly adherent to the medial capsule and therefore less mobile than the lateral one.

Clinical features History There has usually been a painful twisting injury, often during sport. There may be an associated ‘pop’, ‘crack’ or tearing sensation within the joint and swelling quickly appears. Subsequently there is persistent swelling and a feeling of something catching. Occasionally the knee locks for some hours as the torn meniscus becomes lodged between the joint.

Physical findings Look for: • effusion • wasted quadriceps by comparison with the other side. n Feel for: • effusion • tenderness at the joint line. n

Knee  629

45%

12%

36%

Longitudinal split (= bucket handle tear)

Flap tear

Degenerate meniscus

3%

Radial split

3%

Horizontal split

Fig. 34.7  Types of meniscal tear in the knee.

n

Test movement for: • springy feel in a locked knee • McMurray’s test – with the knee at 90° of flexion, the tibia is rotated on the femur to try to trap the meniscal tear between the two bones; internal rotation of the tibia catches a lateral meniscus and external rotation the medial; in either event pain is felt at the joint line.

Management Non-operative When there is doubt about the diagnosis, then it is reasonable to treat the symptoms with a review in 2–3 weeks. In those with improvement, a graduated programme of knee rehabilitation is continued. When symptoms and signs persist, surgery should be considered.

Surgical When the clinical features are typical, then the management is surgical. Arthroscopy (see below) is both diagnostic and therapeutic – the tear can be seen and then either excised or repaired depending on the type of tear. Repairable tears are acute in the red zone (more vascular) of the meniscus near the periphery. After operation, it is vital that formal rehabilitation is undertaken to avoid further injury to the joint. This starts immediately with quadriceps exercises, and once the portals have healed, swimming, cycling and weight training of the muscles can begin. Only when all these activities are managed with ease is return to exercise which involves weight-bearing on the knee surface allowed (such as jogging, low-impact aerobics and, finally, contact or high-impact sporting activities).

Anterior cruciate ligament (ACL) injuries Mechanism and pathological features These injuries are sustained after a twisting and valgus strain is applied to the knee. Typically they are seen in the footballer who twists on the knee during a tackle on an opposing player. In women, the most common cause of ACL rupture is skiing. The medial collateral ligament and medial meniscus are often damaged at the same time. Hyperextension on its own can also produce an isolated ACL rupture. Occasionally, any of these mechanisms may avulse a fragment of bone at the insertion of the ACL onto the tibial plateau.

Clinical features Physical examination demonstrates only about 70% of ruptures of the ACL. The diagnosis is confirmed by MRI.

Management Non-operative The knee with a ruptured ACL can often be managed without resort to surgery. Intensive rehabilitation is used to strengthen the hamstring and quadricep muscles and improve proprioception at the knee. Swimming, cycling and weight training followed by gentle jogging can then be attempted. Change in lifestyle with withdrawal from some sports or other activities may be necessary. A brace can help to stabilise the knee. A large variety are available but all rely on firm strapping above and below the knee with metal or carbon fibre supports for tennis or skiing.

34 

630  Principles of orthopaedics

Surgical With effective non-operative management, surgery may often be avoided. If it is, urgent operation has no advantage over delayed repair. The only unequivocal indication for early repair is when a fragment of bone has been avulsed from the tibial plateau, in which case the fragment should be reattached with a screw. Delayed reconstruction may be required if the torn ACL continues to cause instability (giving way). Various methods to stabilise the knee have been used in the past, including an extra-articular reconstruction or use of synthetic intraarticular grafts however the current favoured surgical technique is an intra-articular reconstruction using either patellar tendon or hamstring tendons harvested from the patient’s knee.

Posterior cruciate ligament (PCL) injuries Rupture of the posterior cruciate is much less common than that of the ACL and is often not recognised. The tibia is forced posteriorly on the femoral condyles – as in a head-on car crash when the lower leg hits the dashboard.

Clinical features The functional instability after PCL rupture may be minimal, with the symptoms of pain, stiffness and an effusion only developing after degenerative changes in the knee have occurred. In an acute injury there is a tense haemarthrosis with perhaps soft-tissue abrasions on the front of the tibia.

Investigation and management Plain X-ray shows an effusion and sometimes a piece of bone that has been avulsed off the back of the tibia (PCL insertion). A change in lifestyle, including the form of sporting activity, may allow the patient to lead a near-normal life. An avulsed fragment should be exposed through the popliteal fossa and reattached. In a rupture with chronic problems, the indications for surgical treatment are the same as for repair of the ACL, and the methods are also similar.

over the front of the knee, which may feel unstable or give way. Minor swelling is noted over 24 hours.

Physical findings in acute dislocation Look for: • the patella on the lateral side of the knee • knee locked in flexion • effusion. n Feel for: • position of the bone to the lateral side • tenderness on the medial side of the patella after reduction • effusion. n Test for reducibility by applying firm pressure on the lateral side and simultaneously extending the knee; the bone may reduce with a ‘snap’. n

Investigation Plain X-ray shows the displacement. After reduction, patella alta (see below) may be seen. Skyline views are helpful and may reveal an osteochondral fracture that occurs as the patella dislocates over the lateral femoral condyle. In subluxation, X-rays may be normal or show patella alta (high riding patella).

Arthritis Arthritis of the knee is very common, and the usual form is osteoarthritis. Rheumatoid arthritis also occurs but less frequently. As in the hip, the management of this painful, disabling condition has been transformed by the development of prosthetic replacement.

Clinical features History Pain is the main complaint. Initially this is felt only after walking but later also at rest. Accompanying stiffness and swelling, initially intermittent but eventually permanent, occur. It is also common for the joint to lock because of loose bodies and painfully give way.

Physical findings

Recurrent dislocation of the patella The patella is a mobile sesamoid within the quadriceps tendon and is in a vulnerable position in front of the knee. True dislocation must be differentiated from maltracking in which there is painful subluxation.

Clinical features History Full dislocation.  The patella always dislocates laterally, and there is usually a history of direct trauma to the medial side, often during sport. The patient sees and feels the bone displaced, and the knee is locked in 30–40° of flexion. Anterior pain and rapid swelling develop.

Look for: • varus or valgus deformity with the patient standing • swelling. n Feel for: • effusion • tenderness at the joint lines and over the femoral condyles • crepitus. n Test for: • movement – fixed flexion deformity is common • collateral ligament laxity when there is varus or valgus deformity. n

Management Non-operative

Subluxation.  The patella is felt to ‘pop’ out of place, often during a turning movement. Pain is momentary and sharp

Weight loss, analgesics, physiotherapy, a walking stick and foam heel wedges all help in those with mild symptoms.

Ankle and foot  631 Surgical There are several surgical options. The choice depends on: n

wishes of the patient age n degree of disability. n

Arthroscopy  is a useful first step and allows the surgeon to assess the extent of the disorder. Debris in the joint is washed out and can provide pain relief for a year or more. Loose bodies can be removed and degenerative meniscal tears trimmed. In rheumatoid arthritis, an arthroscopic synovectomy is symptomatically useful in that synovial hypertrophy contributes to the inflammatory process. Osteotomy.  Often the medial compartment of the knee is affected by the arthritis but the lateral side is relatively spared. An osteotomy can be performed to realign the knee, and forces are transferred to the relatively healthy side. This procedure is of use in the younger patient and may provide 8–10 years of pain relief. Once the lateral side starts to wear, a knee replacement can be done. Total knee replacement.  Knee replacements with a hinge were inserted in the early 1950s, and later in that decade metal discs were interposed but with poor results. However, it was not until the early 1970s, with the development of dedicated instrumentation and unconstrained (no hinge) prostheses, that the results improved. ‘Unconstrained’ means that stability relies on the surrounding tissue tension to hold the two parts in correct alignment. A large variety of knee replacements are now available. These fall into three main groups as shown in Table 34.5. Arthrodesis.  This operation has largely been superseded by joint replacement. It can be a salvage procedure after joint replacement has failed. The knee is fused in a functional position of about 5–10° of flexion, which allows the limb to be swung through during the relevant phase of the gait cycle.

– cardiac or renal. In chronic instability, it is often localised at one or other malleolus. Trauma  is often an important factor. In addition to predisposing to chronic instability, it can also cause secondary osteoarthritis – the result of joint surface irregularity or of avascular necrosis in a fragment of a fractured talus.

Physical findings Look for: • swelling • scars. n Feel for: • localised tenderness in the malleoli • crepitus (gently) in the area as a whole • swelling – boggy synovial thickening, pitting oedema or an effusion within the joint • local warmth. n Move the ankle for: • walking – the gait (see Box 34.2) may attempt to avoid pain or there may be foot drop, which causes the toes to contact the ground when normally the heel should strike first; this gait is seen after injury to the sciatic nerve at the buttock, or the common peroneal nerve at the knee • active and passive range – the ankle joint is capable of both plantarflexion and dorsiflexion from a neutral position; inversion and eversion occur at the subtalar joint; the test is done by holding the lower leg with one hand and grasping the heel with the other so that the subtalar joint can then be moved separately • excessive movement – laxity of the collateral ligaments is detected on inversion and eversion; drawing the foot forwards and backwards on the lower leg may reveal subluxation. n

Investigation Imaging Plain X-ray may show arthritis or evidence of old trauma. When the history is one of instability, there may be localised arthritic changes at the malleolus with perhaps a loose body at the tip of the malleolus from an old avulsion fracture. Avascular necrosis of the talus results in sclerosis and collapse of the bone. If the history and examination suggest that the site of the problem is in the subtalar joint, it may be necessary to request plain films of this joint. n Stress X-ray is done by applying a valgus or varus strain to the joint while films are taken – when this is painful, general anaesthesia may be required. If there is significant instability, the talus may be shown to tilt within the mortice of the ankle joint. n Isotope bone scan may show an increase in activity in the ankle or subtalar joint or at a malleolus. In avascular necrosis of the talus, there is an area of reduced uptake. n CT or MRI confirm the presence of arthritis and are also helpful when avascular necrosis is suspected, as its extent can be clearly seen. n

ANKLE AND FOOT ANKLE

General clinical features History Pain  from the ankle joint is often felt as a band across its front. When there is a problem at the malleolus, the symptoms may be to one side or the other. Pain from the subtalar joint tends to be felt below the ankle and may radiate forward into the foot. Instability  is a sensation of unusual movement, usually from side to side, and is common because of the frequent exposure of the ankle to twisting strains. Swelling  around the ankle may be the consequence of local disease such as arthritis or of more general problems

Ankle and foot Ankle

34 

632  Principles of orthopaedics

Chronic instability This condition is better prevented than cured. The cause is an inversion or eversion injury that tears the collateral ligament which is put under stress.

Clinical features There is usually a history of the relevant injury. There is tenderness over the ligament just distal to the malleolus. Evidence of bruising is only present in the early stages.

Investigation and management Stress X-ray will demonstrate talar tilt, although this investigation may be difficult in the acute phase because of pain. In a patient with an acute injury in whom a diagnosis of a collateral tear has been made, the traditional treatment has been 3 weeks in a below-knee plaster cast to allow the ligament to heal. More recently, early intensive physiotherapy with proprioceptive training on a ‘wobble board’ (a board balanced on a ball) has been advocated, and the results are possibly better. In spite of adequate treatment, chronic instability may become established and is treated: non-operatively – which may be sufficient if the patient alters lifestyle, changes to a different sport or wears boots that support the ankle n surgically – a number of operations have been described; as well as reconstituting the affected ligament, further support is provided by using a local structure such as the tendon of peroneus brevis. The joint capsule may be shrunk with a thermal technique. n

Arthritis As a weight-bearing joint, the ankle is prone to osteoarthritis but much less commonly than the hip or the knee. The reason is unclear but may be in part because the ankle is essentially a hinge joint whereas at the hip and knee there is also rotation and therefore extra shear forces on the cartilage. Nevertheless, post-traumatic secondary osteoarthritis of the ankle is common in young adults involved in athletics. Involvement by rheumatoid arthritis is to a similar extent as the hip and knee.

Management Non-operative This is the most common method: a walking stick, firm boots to limit movement at the joint and anti-inflammatory drugs.

Surgical Operation is less satisfactory in the ankle than in the hip or knee; the options are fusion, providing a stiff painless joint, or arthroplasty. Prosthetic replacements are available but the long-term results are not as good as in the hip or knee.

FOOT Painful feet are common. The hazard of attempts at surgical management of an individual lesion is that it may merely

transfer the problem from one part of the foot to another and so never achieve a cure.

Clinical features History Pain is the usual presentation, most commonly localised to one point, but it may radiate, be worse on weight-bearing and be relieved by rest. There is often difficulty in finding shoes that can be worn without pain.

Physical findings The appearance of the foot can be the presenting feature. Look for: • shape, including any callosities and their site • the shoes and in what areas they show signs of wear – an indication of how load is being transferred • evidence of vascular insufficiency – the presence of peripheral vascular disease may contraindicate surgery on the foot. n Feel for: • local tenderness • pulses in the foot (dorsalis pedis and posterior tibial). n Move: • the midtarsal joint by holding the heel with one hand and the forefoot with the other • the toes – are any deformities correctable? n

Investigation Imaging Plain X-ray of the foot may be required so as to plan an operation. The presence of radiological evidence of arthritis may influence what procedure, if any, is performed. Films taken during weight-bearing may be useful.

Other investigations Pedobarography produces a pressure profile of the foot. However, the device is not widely available. It can confirm the areas of high pressure and can be used to assess the effect of surgical procedures. Most other investigations are usually not helpful. A very painful, red and swollen first metatarsophalangeal joint may raise the suspicion of gout.

Hallux valgus This is a progressive valgus deformity of the big toe. Once the toe starts to angulate, progression is inevitable because the pull of the tendons increases the deformity.

Aetiology A number of factors can be identified in the development of hallux valgus: n

family history sex – more common in females n age – tends to occur in the middle-aged; with the passage of time the foot tends to splay, so making any deforming forces worse n metatarsus primus varus – if the first metatarsal is in varus, there is a greater tendency for the big toe to go into valgus because of the pull of the extensor tendon n

Ankle and foot  633 n

shoes – modern shoes tend to be very tight at the toes, so forcing the big toe into valgus; hallux valgus rarely occurs in the unshod.

Metatarsalgia

Look for the deformity and the bunion. Feel for localised tenderness. n Test for movement, which is often reduced, and to find out if the valgus deformity is reducible.

In this condition, the distal foot is painful. The source of the pain is high pressure on the metatarsal heads as the patient walks. It is often associated with claw toes (see below), and as a result, instead of the toes sharing in weightbearing, all the weight is taken on the metatarsal heads. It can also occur when the foot has a high longitudinal arch (pes cavus) for either unknown reasons or in neuromuscular conditions such as cerebral palsy, spina bifida or Friedreich’s ataxia. Morton’s metatarsalgia (neuroma) is a specific condition in which there is an interdigital neuroma between the metatarsal heads. This is then irritated by the adjacent bones, so resulting in pain and sensory disturbance at the corresponding cleft.

Management

Management

Clinical features History There is cosmetic deformity and discomfort over the prominent bunion at the metatarsophalangeal joint. Inflammation occurs as this rubs on the shoes. Crossing of the first toe under or over the second and third increases discomfort.

Physical findings n n

Non-operative

Non-operative

In the elderly with poor peripheral blood flow, conservative management is best. Surgical shoes can be made to fit the foot, as opposed to the normal practice of squashing the deformed toe and foot into the shoe. Regular chiropody is important to care for the skin and nails.

A padded metatarsal bar fitted into the shoes to offload the metatarsal heads helps to spread the load across the foot. Surgical shoes may also be required to accommodate the foot comfortably.

Surgical

An oblique osteotomy of the metatarsal necks allows the heads of the metatarsals to ride up. It is important to divide the second, third and fourth metatarsals because operating on one alone is not sufficient. In Morton’s metatarsalgia, the affected space is explored and the neuroma excised. After operation, sensation is absent in the cleft.

Over 40 operations have been described for hallux valgus. A simple bunionectomy is usually not enough because the deformity will recur. When there is osteoarthritis at the joint, surgery is either an excisional arthroplasty (Keller’s) or joint replacement with a Silastic or ceramic implant. These relieve the pain and correct the deformity, but the joint is often stiffer than normal and, after a Keller’s procedure, the big toe is short. In the younger age group, surgery is directed at correcting the underlying deformity – the varus displacement of the first metatarsal. Various operations have been described to lateralise the head of the first metatarsal and therefore correct the deformity.

Hallux rigidus This condition of a stiff, painful big toe is caused by degenerative arthritis at the first metatarsophalangeal joint. During walking, the big toe is unable to extend as the foot rolls forwards to toe-off (see Table 34.1). This is painful.

Management Non-operative A rocker-bottom sole on the shoe allows the foot to roll forward more easily during walking. This is often cosmetically unacceptable and so is of use only in those unable to undergo an operation.

Surgical A dorsal cheilectomy is performed. This operation involves excision of the dorsal osteophytes and so allows a greater range of extension. Arthrodesis of the metatarsophalangeal joint provides good pain relief although the big toe will rest in a somewhat extended position. Other methods such as excisional arthroplasty may be useful in the frail or elderly population.

Surgical

Claw toes Toes hyperextended at the metatarsophalangeal joints and flexed at the interphalangeal joints are clawed and do not touch the ground. As a result, they rub on the shoes and callosities develop over the proximal interphalangeal joints. There is also a tendency to develop an associated metatarsalgia. The cause is usually unknown, but claw toes are seen in neuromuscular disorders such as spina bifida.

Management Non-operative Local measures such as felt pads and attention to footwear may be sufficient.

Surgical Fusion of the proximal interphalangeal joint allows the toe to straighten. This is usually done by excising the joint and then using a small wire to hold the toe straight for 6 weeks until the bone ends unite. A single, grossly deformed toe should be amputated.

Plantar fasciitis This is a painful condition of the heel caused by a localised area of inflammation of the plantar fascia at its origin from the os calcis. It is sometimes precipitated by local trauma or excessive weight-bearing.

Foot

34 

634  Principles of orthopaedics

Clinical features A relevant history of focal trauma may be obtained. Otherwise, the only complaint is of well-localised pain in the heel on weight-bearing. There is tenderness over the most prominent point of the calcaneus in the sole of the foot.

Table 34.11

Age ranges for paediatric hip conditions

Age

Condition

0–5 years 5–10 years 10–15 years

Congenital dislocation of the hip Perthe’s disease Slipped upper-femoral epiphysis

Investigation and management Plain X-ray may show a spur on the plantar aspect of the os calcis. Non-operative management with use of a cushioned heel wedge, night splints or local steroid injection is usually successful. Surgery to release the plantar fascia is occasionally required.

Developmental dysplasia of the hip The hip is unstable at birth either because of ligamentous laxity or because of dislocation out of an undeveloped (dysplastic) acetabular socket.

Epidemiology

Achilles tendonitis This is a similar condition to plantar fasciitis in which there is an area of local inflammation at the insertion of the Achilles tendon. It may be precipitated by local trauma or a new pair of shoes that rub on the heel. Treatment consists of a heel wedge to reduce the tension in the tendon and a local steroid injection to the tendon sheath. Surgery is occasionally required to incise the inflamed tendon sheath.

Freiberg’s disease This condition is of an unknown cause in which there is fragmentation and collapse of the second metatarsal head. It occurs in young adults, and there may be a history of local trauma. The enlarged metatarsal head produces local pressure symptoms and metatarsalgia. Treatment is conservative with felt pads to relieve pressure. Surgery is occasionally done to reduce the size of the metatarsal head.

Gout This is a medical condition which does not usually concern the orthopaedic surgeon, but patients may present initially to the A&E department or the orthopaedic clinic. The metatarsophalangeal joint is red, hot, swollen and extremely painful. There may be a precipitating history of minor trauma to the big toe, dietary excess, recent surgery or the use of drugs such as a thiazide diuretic. In the acute stage, the treatment is with NSAIDs. Prophylaxis with allopurinol may prevent recurrent attacks and should be undertaken if these are frequent.

PAEDIATRIC ORTHOPAEDICS HIP Problems with the hip are common. Patients present with a limp and pain which may be felt in the knee alone, and any child with knee pain must have his or her hip examined. Whereas trauma and infection can occur at any age, other conditions tend to occur within particular age brackets (Table 34.11).

The incidence is 15/1000 at birth but falls to 1.5/1000 at 6 weeks. The left side is affected in 60%, the right in 20% and the condition is bilateral in 20%.

Aetiology Genetic There may be a family history: n

affected sibling – 6% chance affected mother – 12% chance n affected sibling and mother – 35% chance. n

Sex It is more common in girls than in boys in a ratio of 9 : 1. This is probably because the girl fetus is more sensitive to the maternal hormone relaxin secreted during pregnancy.

Perinatal Associated factors are: n

first birth an extended breech presentation n coexistent talipes (see below) n any other congenital anomaly n oligohydramnios. n

Postnatal Wrapping the infant in extension and adduction can cause hip dislocation.

Clinical features History Often the condition is diagnosed at birth, as part of the routine postnatal check (clicky hips). Occasionally, the parents may notice asymmetry of the skin creases. In older children there is a history of abnormal gait (see Box 34.2).

Physical findings Look: • at the skin creases – there may be asymmetry of the gluteal creases but not if the condition is bilateral • for limited abduction in flexion • at the gait of an older child – it is a characteristic Trendelenburg gait. n Feel and move – the head may dislocate and relocate when Ortolani’s or Barlow’s tests are performed (Box 34.4); they must be done gently and not repeated, n

Paediatric orthopaedics  635 because avascular necrosis of the femoral head may result.

Investigation Plain X-ray.  Up to 15 signs can be identified on a plain X-ray of the pelvis. The common ones are shown in Figure 34.8. The ossification centre of the femoral head does not appear until the age of 5 months. For the acetabulum to develop normally, the femoral head must be within it. If not, it remains shallow with a large acetabular angle. Ultrasound.  In experienced hands, as well as being diagnostic, it is a useful screening technique. Under the age of 5 months, it is the investigation of choice to diagnose a dislocated hip. Arthrography  is required only for planning surgical correction in the older child.

Management The final result depends to a great extent on the age at which the diagnosis is made and treatment begun. If this is at birth, the developed hip is normal. The aim of treatment is to achieve a complete and stable reduction. Patients who are missed at birth may present late – up to the age of 3 or 4 years – and in these circumstances the outlook for good function is poor and treatment difficult.

Birth to 6 months A splint is used to hold the hip joint in approximately 60° of abduction and 90° of flexion. A variety is available, but the most common type used is the Pavlik harness. The splint is worn all the time until the acetabulum is seen to be developing normally. Box 34.4 

Special tests for developmental dysplasia of the hip

Six months to walking At this age, the hip is dislocated. Gentle traction is applied over a few weeks with progressive abduction (an adductor tenotomy may be required). The hip is then assessed under a general anaesthetic. If it is stable, a plaster of Paris hip spica is applied. If unstable or still dislocated, then an arthrogram is done which may show an inverted, thickened and folded acetabular labrum (limbus). This requires surgical removal to permit reduction.

The older child An open operation is required to remove the limbus (contracted acetabular labrum and capsule) which is in the way of reduction of the femoral head into its socket. At a later stage, femoral osteotomy may also be required. Over 7 years of age, there is a case for non-operative management and, when secondary osteoarthritis develops in adult life, a total hip replacement.

Perthe’s disease There is, in this condition, a variable degree of osteonecrosis of the femoral head.

Aetiology and pathological features The cause is essentially unknown. An effusion forms, perhaps as a result of minor trauma or a viral infection. Pressure within the joint rises and impairs venous return from the femoral head, which then undergoes avascular necrosis. The incidence is 1 : 9000, and the condition occurs four times more frequently in boys than in girls. It is bilateral in 10%. The degree of collapse of the femoral head and the subsequent secondary arthritis is such that, by the age of 45, nearly half require a hip replacement, and by 65, secondary osteoarthritis is evident in 86%.

Clinical features

Barlow’s test With the hips adducted and flexed to 90°, gentle pressure is applied along the femoral shaft to dislocate the head posteriorly

The age of onset is between 5 and 10 years with a limp and a complaint of a dull ache. There are few signs, but abduction in flexion is reduced.

Ortolani’s test The femoral head is dislocated as for Barlow’s test. The hips are then abducted and the head is felt to relocate with a ‘clunk’

Investigation Imaging Plain X-ray.  An effusion may be seen. As the condition progresses, the femoral head becomes increasingly sclerotic

1

2 4

1

3

2

3

4 DDH

Fig. 34.8  Common radiological features of the dislocated hip.

Normal

Acetabular angle: o should be 1 cm

III

Any size

Low velocity Minimal soft-tissue damage Low velocity Minimal soft-tissue damage High velocity or severe soft-tissue injury. Gross contamination as in military or agricultural injuries

0–10% >10%

Type III injuries are further subdivided into: IIIA – adequate cover of exposed bone still possible IIIB – wide periosteal stripping with possible devascularisation of bone IIIC – vascular (usually arterial) or nerve injury which requires repair. a

After Gustilo & Anderson.

Haematoma formation A fracture tears blood vessels in the surrounding soft tissue, periosteum and medulla. A haematoma forms around and between the ends of the bone. Osteocytes in the fractured ends are deprived of nutrition, and local cell death occurs. If a fragment of bone becomes completely detached from its blood supply, it undergoes avascular necrosis.

Cellular proliferation and organisation (inflammatory phase) The next stage is similar to that in healing soft tissues (see Ch. 2) – an acute inflammatory reaction with vasodilatation, plasma exudation and inward migration of acute inflammatory cells. The haematoma is replaced by granulation tissue with slender capillary loops in a loose connective tissue.

Fractures  641 Table 35.2

Causes of pathological fracture

Class

Example

Congenital Infection Metabolic

Osteogenesis imperfecta Chronic osteomyelitis Osteoporosis Osteomalacia Hyperparathyroidism Bone cyst Enchondroma Metastatic carcinoma (common are breast, kidney, prostate, thyroid, lung) Primary bone tumours (rare) Paget’s disease of bone

Benign neoplasms Malignant neoplasms

Other

1

Periosteum Dead bone Marrow Living bone Blood clot

2

3

Subperiosteal cellular proliferation Endosteal cellular proliferation Woven bone Cellular tissue Blood clot Dead bone being reabsorbed

4

Woven bone Marrow Lamellar bone

5

Marrow cavity reformed Lamellar bone

Fig. 35.2  Stages of fracture healing. Formation of callus Specialised cells invade the granulation tissue, including mesenchymal cells, fibroblasts and osteogenic precursor cells. These cells are derived from both local damaged tissue and the systemic circulation. The cells are stimulated to produce a randomly organised mass of fibrous tissue and cartilage, called soft callus, which provides an enveloping

Box 35.1 

Assessment of union of a fracture

Clinical n Absence of movement at the fracture site n Little or no tenderness on direct pressure over the fracture site n Little or no pain when the fracture site is stressed manually or by bearing weight through the limb Radiological* n Continuous callus seen spanning both sides of the fracture in 2 views *Radiological evidence usually occurs a few weeks after clinical evidence.

scaffold across the fracture, under the neighbouring periosteum and inside the medullary cavity. This callus is at first weak and flexible so that stressing the fracture at this stage is associated with some movement and pain. Soft callus is progressively replaced, from about 2 weeks onwards in a child and 3 weeks onwards in an adult long bone, by immature (or woven) bone, forming hard callus. With the progressive increase in hard callus, and thus mineral content, the callus becomes visible on radiographs and becomes increasingly stiff.

Union Once both surfaces of a fracture are connected by callus strong enough to hold the bone rigidly, union is said to have occurred. The practical assessment of union is summarised in Box 35.1. When the fracture is regarded as having united, external immobilisation should be discarded and the limb rehabilitated. As a rough guide, external splintage needs to be maintained for 4–8 weeks for fractures in cancellous bones and 6–12 weeks for fractures in long bones in adults. Fractures in children heal in approximately half these times.

Consolidation and remodelling In the months that follow, the immature woven bone is reorganised and replaced with mature, or lamellar, bone in a process called consolidation. This new bone is indistinguishable histologically from uninjured bone, with the bone laid down along lines of stress. Radiologically, the fracture line will be obliterated with clear bony trabeculae crossing it. The bone has returned to its original strength and the fracture is said to be consolidated. For several years later, the fusiform mass of healing bone is gradually removed and the bone’s shape is further refined along its whole length in response to the normal stresses across it. This process, called remodelling, is most remarkable in children (Fig. 35.3). Bony healing with callus formation does not always occur if a surgeon intervenes. The amount of callus produced is in direct response to the mobility of the fracture. Treatment options which give relative stability (see ‘Immobilisation’, below) will produce less callus than fractures left to heal naturally. The extreme of this occurs if the fracture is reduced and held rigidly with internal fixation; there is no movement and no gap for callus to fill. Instead, the bone heals by direct cortical healing, a process which resembles remodelling. The lack of callus formation can make radiological confirmation of union difficult.

Fractures

35 

642  Principles of management of fractures, spinal injuries

Fig. 35.3  Consolidation/remodelling of fracture site (left to right).

Clinical features History The history may throw light on the circumstances that led to the injury and the underlying causes. The following are of significance: n

An injury may have been caused by a simple mechanical fall but may be due to a fall secondary to a medical condition, such as cardiac or neurological problems. n Fracture after trivial injury or stresses within the normal range of physical exertion may indicate a pathological fracture, requiring careful investigation. n The way the injury was sustained should lead to a search for other skeletal injuries from the same cause; a fracture of the os calcis after a fall from a height may be accompanied by vertebral or hip injuries, and a knee injury in a front seat passenger in a head-on collision may be associated with a posterior dislocation of the hip. n Time since injury should be ascertained as accurately as possible because of its association with complications such as infection in an open fracture or with ischaemia distal to a vascular injury. Unless there is a neurological condition, a limb with a fracture is acutely painful and held as immobile as possible. However, there are circumstances in which a history cannot be obtained, such as unconsciousness or the overriding importance of other injuries; then the history of the injury obtained from others may be of importance.

Examination Swelling caused by haematoma formation and oedema is usually evident. n Deformity is seen in displaced fractures and is described anatomically as displacement of the distal fragment with respect to the proximal, e.g. anterior or posterior. Varus and valgus are terms also used, but in descriptions of fractures these are best avoided. n

n n

n

n

n

Abnormal mobility may be present but should be sought with gentleness. Crepitus is the grating sensation elicited on palpation as the broken ends of bone grind against each other with movement; it must not be deliberately elicited, as it causes intense pain. Skin integrity must always be assessed: abrasions or mild ischaemia may lead to later breakdown and infection of the fracture. Vascular perfusion and neurological function distal to the injury must be evaluated in all limb fractures. The presence of arterial pulses must be elicited and recorded. Sensation may be reduced in a glove and stocking manner in vascular insufficiency. Injury to peripheral nerves produces specific neurological deficiencies which must be tested for. Pelvic fractures may be associated with bladder and urethral injuries and disruption of the muscles of the pelvic floor. Examination for such accompanying injuries is essential.

Radiological investigation If a fracture is suspected, radiographs in two planes at right angles to each other (usually anteroposterior and lateral views) are initially taken and should include the whole length of the fractured bone including the joint above and below. Only in this way can the full extent of the injury and the associated bone injuries be detected (Fig. 35.4). In some circumstances, additional oblique or tangential views may be required. Computed tomography (CT) and magnetic resonance imaging (MRI) are valuable in the investigation of certain intra-articular fractures and specific fractures, such as of the pelvis and spine. Radioisotope bone scanning detects increased vascularity, which begins with the inflammatory phase of healing, and is useful in the diagnosis of fractures that are not immediately obvious on plain X-ray because of lack of displacement (e.g. fracture of the scaphoid).

Fractures  643 Box 35.3 

Methods of immobilisation of fractures

n

Fig. 35.4  Radiographic examination of a fracture. The X–ray is of a fracture of the ulna accompanied by anterior dislocation of the radial head at the elbow joint (Monteggia fracture–dislocation). The dislocation would not have been detected without an X-ray that included the elbow joint. Box 35.2 

Principles of fracture management: FRIAR

n

First aid and management of the whole patient – always Reduction – if necessary n Immobilisation – if necessary n Active movement of injured limb – as much as possible n Rehabilitation – always n

External splints – casts made of plaster of Paris or synthetic resins – specially designed splints n Continuous traction – applied to the distal fragment by skeletal pin or adhesive tape applied to the skin n Internal fixation – screws, plates and pins inserted at open operation n External fixation – a rigid bridging device held in place by bone pins either side of the fracture

fracture gradually overcomes the tension in the surrounding muscles and straightens the bone.

Open reduction Open reduction by operation is necessary when: n

closed reduction fails very accurate reduction is required, e.g. a fracture which involves a joint surface n the fracture has caused a vascular or (sometimes) a nerve injury. n

Principles of management The management of a patient with a fracture can be summarised by the mnemonic FRIAR (Box 35.2).

First aid and management   of the whole patient

The injured limb is opened surgically and the fracture manipulated under direct vision. It is then usually stabilised by internal fixation (see below).

Patients who have suffered violence sufficient to fracture part of their skeleton often have injuries to other systems, some which may be life-threatening. In the management of such multiply injured patients, priority should be given to the ABCs – Airway maintenance, Breathing and Circulation. The matter is considered in more detail in Chapter 3. Pain relief is also important and is discussed in Chapter 6.

Immobilisation

Reduction

Immobilisation is not always necessary, e.g. in fractures of the ribs or metatarsals. In some other injuries, relatively rigid immobilisation is essential if union is to occur, e.g. the shaft of the ulna. The methods of immobilisation are summarised in Box 35.3.

Reduction is the manipulation of the fractured bone to restore normal anatomy. In diaphyseal fractures it is to restore length, alignment and rotation and in intra-articular fractures to restore normal anatomy and perfect congruence of joint. Some fractures do not require reduction either because deformity is not present or because its nature is immaterial to the final functional result (e.g. many displaced clavicle fractures heal without functional deficit).

Closed reduction This is the preferred initial method. It can be carried out under general anaesthesia, regional anaesthesia or, in some instances, after injection of anaesthetic into the fracture haematoma. Reduction is achieved by: n

longitudinal traction which disimpacts any interlocked fragments n reversal of the forces that caused deformity. Reduction must be confirmed by radiography.

Mechanical traction This method may be used to gradually reduce fractures, such as of the spine or of the femur. The weight pulling on the

A fracture is held in reduction to: n

relieve pain prevent redisplacement of the fragments n avoid shearing movements at the fracture site which damage the delicate capillaries in callus and consequently interfere with the process of union. n

External splints Casts made from plaster of Paris (POP) or synthetic resins are, in most circumstances, the standard method. POP is commercially available as bandages coated with hemihydrated calcium sulphate which reacts with water to form a solid cast. Newer synthetic-resin materials are available which are stronger and lighter, but they are more expensive and harder to apply. When applying an external cast, a layer of cellulose padding is placed deep to the cast to prevent the plaster from sticking to the hairs and skin and to allow for expansion from swelling at the fracture site. Initial immobilisation should not be by completely encircling the limb; continued swelling within a rigid cast can lead to ischaemia distal to the fracture site – compartment syndrome (see below). In consequence, casts used on a newly injured limb are applied either as a slab on one aspect only held in place by a crepe

35 

644  Principles of management of fractures, spinal injuries

bandage or as a cylinder which is then immediately split longitudinally. Immobilisation of the adjacent joints above and below is usually necessary to stabilise a fracture managed in a cast but increases the risk of disuse muscle atrophy and joint stiffness. Any form of immobilisation inevitably causes some muscle atrophy and joint stiffness. The splint must be discarded as soon as union of the fracture is deemed to have occurred. In some long bone fractures, a hinge may be inserted in the splint (functional bracing) as union progresses.

a

Continuous traction This method is used when it is difficult to hold the bone reduced with an external splint because the fracture site is surrounded by soft tissue and/or because of absence of bony points above and below which can be used to gain purchase. Typical examples are fractures of the shaft of the femur and of the lower humerus. Traction of up to 2 kg may be applied with longitudinal adhesive strapping applied to the skin (skin traction) but a careful watch must be kept for skin damage, especially in the elderly and in patients on steroids. If more force is required, traction may be exerted through a pin inserted into the bone distal to the fracture site (skeletal traction). The pin site must be kept clean to prevent infection tracking down to the bone. Continuous traction confines the patient to bed and thus increases the risk of pressure sores, chest infection, disuse osteoporosis and other problems. It is therefore usually only used as a temporary measure until formal, usually surgical, immobilisation can be performed.

b

Internal fixation Internal fixation by open operation is used to secure reduction, to ensure it is maintained and to allow earlier mobility of the patient (Fig. 35.5). The advantages of earlier return of function, shorter hospital stay and quicker resumption of work or of pre-injury style of life have to be weighed against the risks of neurovascular damage, infection and of delaying healing by devascularisation of the bone. Unless the surgi­ cal team is experienced, closed means are preferable for simple fractures. Internal fixation is strongly indicated in patients with: n

multiple injuries pathological fractures n associated neurovascular injury n fractures where accurate reduction is required (e.g. those involving joints) n the need to avoid a long period of immobilisation in bed, e.g. an elderly patient with a fracture of the femur. n

Fig. 35.5  Open reduction and fixation. (a) Plate and screw fixation to the distal third of both radius and ulna. (b) Intramedullary nail fixation of a fracture of the distal third of the tibia.

External fixation This is mainly used in the management of open or infected fractures (see ‘Open fractures’, below). Pins are inserted through the skin into the fragments of bone and fixed rigidly to an external device such as a metal bar (Fig. 35.6). The skin overlying the fracture site can be dressed or grafted without disturbing the fracture.

Observation In the early stages after reduction and immobilisation, careful and repeated observation is required to detect insufficient

distal blood supply or a neurological injury. A tightly applied circular dressing which becomes soaked with blood and then dries may similarly impair the circulation (see also ‘Compartment syndrome’). Suggestive features include: n

persistent or increasing pain paraesthesia or tingling in digits n sluggish capillary return n cyanosis distal to the fracture (late finding) n absent pulses (late). n

Fractures  645 Box 35.4 

Complications of fracture

Early Local n Infection n Haemorrhage n Injury to other structures – arteries, nerves and viscera n Skin necrosis n Deep vein thrombosis n Compartment syndrome Systemic n Hypovolaemic shock n Fat embolism n Effects of prolonged immobilisation – chest infection, pressure sores, pulmonary embolism

Fig. 35.6  External fixation and management of type III open fracture.

Any of these requires removal of all dressings, external splints and casts so that the fracture site can be inspected and necessary remedial action undertaken.

Active movement and rehabilitation Rehabilitation starts immediately after treatment. The patient is asked to move the injured part as much as the method of fixation allows. This helps to: stimulate union decrease disuse osteoporosis n prevent muscle atrophy n minimise joint stiffness.

Late (delayed) Local n Malunion n Delayed union n Non-union n Muscle wasting n Joint stiffness n Osteoarthritis n Delayed tendon rupture n Tardy nerve palsy n Reflex sympathetic dystrophy n Myositis ossificans Systemic n Osteoporosis n Changes in lifestyle and psychological state

n n

All external splints are removed as soon as there is clinical evidence of union, and the patient is started on a supervised programme of active exercises to restore function (physiotherapy and/or occupational therapy).

Open fractures The communication of a fracture with the surface is a pathway along which bacteria can contaminate the fracture site and produce infection. Once bone is infected with pyogenic organisms, the inflammation tends to become chronic, especially if foreign material has been carried into the fracture site at the time of injury. Infection delays and may prevent union and, with some virulent infections such as clostridia (Ch. 9), may cause death. Open fractures are surgical emergencies and also represent significant soft-tissue damage where blood supply is also compromised, affecting healing potential. For first aid in all open injuries of bone, the wound is covered with a sterile dressing soaked in normal saline or aqueous iodine. Parenteral broad-spectrum antibiotic therapy is begun at once and attention paid to tetanus prophylaxis. In all open fractures, surgical debridement of the wound with removal of all devitalised tissue and foreign material as soon as possible is essential to prevent sepsis. If treatment on these lines is undertaken within 12 hours of injury, the incidence of sepsis is low. Therefore, internal fixation may be done safely by experienced surgeons operating in ideal conditions. In certain type III fractures, external trauma causes extensive skin and muscle damage, often with associated injuries to vessels and nerves. The incidence of sepsis is

high, and internal fixation is usually avoided in the first instance. After debridement of the wound, external fixation (Fig. 35.6) and repair of neurovascular structures is usually followed by many staged procedures to achieve skin cover. In the most severe of those injuries (a limb that has been avascular for more than 6 hours or one that has been severely crushed), an amputation both saves life and avoids a long period of invalidity which may have considerable psychological effects.

Complications In the great majority of fractures union proceeds according to expectation and function is fully restored. Complications do, however, occur and may be considered in two groups: early or delayed. In both, effects may be local or systemic (Box 35.4).

Infection This can occur in open fractures or in closed fractures treated by operation.

Haemorrhage Haemorrhage from the bone marrow, periosteum and surrounding soft tissues may not be immediately clinically obvious but can be considerable and cause significant reduction in blood volume. As a general rule, blood loss from adult fractures may be estimated as: n

pelvis: 2–3 L femur: 1–2 L n tibia or humerus: 0.5–1 L. n

Patients with open or pathological fractures bleed more profusely. Multiple fractures produce cumulative losses which,

35 

646  Principles of management of fractures, spinal injuries Table 35.3 Fracture

Nerve injury

Dislocation of the shoulder Shaft of humerus Injuries around the elbow Dislocation of the hip Injuries around the knee

Axillary nerve (30%) Radial (20%) Median, ulnar Sciatic (20%) Common peroneal

Box 35.5 

Fig. 35.7  Vascular injury as a consequence of fracture. A fracture of the surgical neck of the humerus has produced a spike that has injured the distal axillary artery, occlusion of which is shown on the arteriogram.

if unrecognised, are sufficient to cause hypovolaemic shock, which is a possible but preventable cause of death.

Arterial and venous injury This can occur in penetrating injuries such as a gunshot wound or from a spike of bone (Fig. 35.7). All types of injury occur. Some bony injuries are commonly associated with vascular damage – supracondylar fractures of the humerus contuse the brachial artery, and 50% of knee dislocations give rise to an intimal tear in the popliteal artery. Distal ischaemia may lead to: n n

nerve and muscle necrosis total limb death with gangrene, necessitating amputation.

The first line of treatment is to reposition the limb so as to correct gross deformity and remove all occlusive dressings. This may solve the problem but, if the signs of ischaemia do not disappear within 15 minutes, surgical intervention is necessary.

Deep venous thrombosis and pulmonary embolism These are common sequelae to many fractures, particularly in the elderly, and are discussed in Chapter 30.

Nerve damage Nerve palsies are common after high-energy-transfer (violent) injuries, and nerves are particularly vulnerable in fracture– dislocations. The common associations are given in Table 35.3.

Compartment syndrome This condition arises because the muscles, vessels and nerves in limbs are held within inelastic osseofascial compartments. Bleeding from a fracture increases the intracompartmental pressure and occludes the venous outflow and hence capillary inflow. The cells first become hypoxic and then swell. There is further rise in intracompartmental pressure and a vicious circle of hypoxia and further swelling ensues. The clinical features are summarised in Box 35.5.

Nerve injuries frequently associated with fractures and dislocations

Clinical features of compartment syndrome

Early symptoms n Increasing pain n Paraesthesia n Paresis Early signs n Pain on passive stretching of the muscle groups in the compartment n Palpably tense compartment n Pulses usually normal because arteries traversing the compartment are resistant to a rise in pressure within it Late symptoms n Numbness n Paralysis Late signs n Muscle contracture n Anaesthesia n Absence of arterial pulses

It is vital that compartment syndrome is detected early, well before the late signs and symptoms occur. Early detection is mainly clinical as seen by pain over and above that which can be explained by the injured part, stretch pain and a tense compartment. An intracompartmental pressure which differs from diastolic pressure by 30 mmHg or less is sufficient to impede capillary inflow, and irreversible damage to nerves and muscles occurs within a matter of 4–6 hours. The skin overlying the compartment is unaffected, but a dis­ abling contracture of the damaged muscles (Volkmann’s ischaemic contracture) may result as a late sequelae. Because of the risks of compartment syndrome, pain relief in fractures by the use of local nerve blocks is not recommended, as this may mask its early features. Vigilance in detection and prompt treatment are both vital. When a compartment syndrome is suspected, any cast and all dressings are removed. If symptoms do not improve immediately, the compartment is surgically decompressed by division of the overlying skin and fascia (open fasciotomy).

Fat embolism This is more common in patients with multiple fractures but may follow minor trauma. Its cause is not known: either fat from the marrow of the fractured bone enters the circulation and clogs capillaries or some as-yet unidentified factor causes chylomicrons in the bloodstream to aggregate. In either event, large fat globules are present in the bloodstream – on the right side of the heart in the pulmonary circulation and, perhaps aided by a subclinical patent foramen ovale, on the arterial side in the brain and skin. Clinically, a few days after injury the patient becomes increasingly confused, and

Fractures  647 develops tachypnoea and mild pyrexia. Skin petechiae may be seen, and laboratory investigations usually reveal a reduced Po2 and thrombocytopenia. Fat globules may be detected in the urine. Maintenance of oxygenation is of paramount importance and may require intubation and ventilatory support.

Pressure sores (decubitus ulcers) Sores occurring as a result of necrosis of skin over the heel, sacrum, ischium and hips are a real risk in patients confined to bed because of skeletal injury (or for other reasons), especially in the debilitated, the elderly and those with spinal cord injury. Prevention is by good nursing care and early mobilisation.

Malunion This follows imperfect reduction or redisplacement after satisfactory reduction and leads to cosmetic deformity and loss of function (Fig. 35.8). It is prevented by satisfactory primary management but, if established, may require complex corrective procedures.

Delayed union

Non-union This is diagnosed when healing has come to a halt before union has occurred (Fig. 35.9). Two broad types of exist: hypertrophic non-union and atrophic non-union. In hypertrophic cases the body has tried to heal the fracture but either too much movement is occurring between the bone ends or the bone ends are not in close contact. As a result the callus formed cannot bridge the gap. Radiographs show florid callus formation either side of the fracture but none bridging the gap. In atrophic non-union the body has not attempted to heal the fracture, commonly due to a lack of blood supply or infection. Radiologically the fracture edges have died back and there is little or no evidence of callus formation. The borderline between delayed union and non-union is often difficult to define, although the differentiation may be important for both the patient and the surgeon. Management is often complex and inevitably requires surgical intervention. In hypertrophic cases, more rigid (usually internal) fixation is required without excessive disturbance of the fracture; in atrophic non-union a direct operation on the fracture site is indicated with removal of sclerotic bone to increase the blood supply, bone grafting and rigid fixation.

Union is said to be delayed if the fracture has not united clinically or radiologically at a time when this would have been expected. The fracture may still continue to heal slowly until it unites and, provided there are not any adverse factors which require correction, a watching policy is adopted while making sure that optimum conditions for continued healing are present.

Fig. 35.9  Non-union. This fracture of the scaphoid has

Fig. 35.8  Malunion.

failed to unite. There is a radiological gap between the fragments which can be assumed to be filled with fibrous tissue. There is some, although not much, evidence of sclerosis.

35 

648  Principles of management of fractures, spinal injuries

Complex regional pain syndrome (CRPS) Type 1 This condition, otherwise known as reflex sympathetic dystrophy or Sudecks’s atrophy, presents at intervals of days or weeks after injury as: n n n n n n

disproportionate pain abnormal sensations (dysaesthesia) joint stiffness thickening of the soft tissues abnormal sweating loss of hair at the site of injury.

The hand, which is most commonly affected, is characteristically swollen, discoloured, painful, and exquisitely sensitive to touch. Tight plasters, bandages or splints, inactivity and dependence of the limb are common factors. The condition is largely preventable by holding the wrist and the digits in positions of function, by elevation of the part and by early active exercises. Use of the part is essential in treatment. There is a possible role for the post-ganglionic sympathetic efferent fibres in some cases.

Myositis ossificans This is heterotopic bone forming in the muscles around a fracture or injured joint. Movement is often restricted and painful. The most common site is the elbow, and the cause is possibly too early and too vigorous joint movement.

Fractures which involve articular surfaces If accurate reduction to obtain congruent surfaces is not achieved and maintained, secondary osteoarthritis can develop. Open reduction and internal rigid fixation are thus indicated. Early joint movement should be encouraged to reduce stiffness and (possibly) to promote the healing of articular cartilage.

Fractures in children The bones of children are more flexible, and incomplete fractures of the greenstick type (see Fig. 35.1) are common. Turnover of bone is more active in children, so that union occurs in approximately half the time taken in adult fractures. Remodelling in the plane of movement of the joints after a shaft fracture is usually so perfect that eventually the site is indistinguishable in radiographs (see Fig. 35.3). However, remodelling is incomplete in many situations, such as in varus or valgus deformities of the elbow and in rotational deformities of the forearm, and accurate reduction should be sought in these cases.

Epiphyseal displacement The growth plate (physis) between the epiphysis and metaphysis provides a relatively weak area which is often involved when forces are concentrated near the ends of the bone. Damage to the growth plate may result in arrest of growth and subsequent deformity. Accurate reduction is necessary.

Non-accidental injury (battering) This condition is part of child abuse and regrettably common. Suspicious features include a delay to take the child to

Fig. 35.10  Dislocation of the elbow. There is complete loss of joint apposition.

hospital, inadequate or inappropriate explanation of the injury, multiple bruises of differing ages, non-accidental burns and radiological evidence of previous injuries. A paediatrician should be involved from the outset.

JOINT INJURIES In dislocation (luxation) there is complete loss of contact of the articular joint surfaces (Fig. 35.10), and in subluxation there is partial loss of contact. Either may be combined with a fracture. The clinical features are the same as those of a fracture: n

pain deformity n loss of function. n

The diagnosis is confirmed by radiographs in two planes. The integrity of the surrounding nerves and vessels must be assessed clinically because of the relatively high incidence of associated damage. In addition, time factors are important: the risk of avascular necrosis of the femoral head after a traumatic posterior dislocation of the hip is directly proportional to the time interval between dislocation and reduction. Dislocations are therefore surgical emergencies. Treatment is usually by closed reduction; open reduction is rarely required.

SPINAL INJURIES Damage to the bony and ligamentous structures of the vertebral column as well as to the enclosed neural elements may occur in spinal injuries. During management it is important to prevent further injury, particularly to the spinal cord. For this purpose, spinal injuries are classified into two types: n

stable – the vertebral components will not be displaced by normal movements; an undamaged cord is not in danger

Spinal injuries  649 n

unstable – further displacement and damage to the cord may result from movement.

As in long bone fractures, the mechanism of injury may often produce particular injury types. For example, flexion injuries produce a crush fracture to the anterior vertebral body which is usually stable while axial compression may crush the entire vertebral body, often resulting in an unstable fracture. More complex injuries result from combined forces, and may result in fracture–dislocations. Cord injury without either fracture or dislocation may occur in the more elastic tissues of children or in the spondylitic spine of the elderly.

Clinical features History Suspicion of instability of the spine may be aroused from the mechanism of injury and, in a conscious patient, by complaints of pain, decreased muscle power and/or sensation and paraesthesiae. An unconscious accident victim should always be assumed to have a spinal injury until proven otherwise.

Physical findings Injuries to the neurological elements may be complete or incomplete; accurate neurological diagnosis is essential because recovery is more likely if some residual sensation or movement is detectable in the affected area.

Complete neurological lesions Complete neurological injury, such as a transection of the cord, causes complete permanent motor paralysis below the level of injury, with corresponding loss of sensation. It must be remembered that the level of the bony spinal injury may not correspond with the level of the neurological injury. Injuries to the lumbar vertebrae  will damage only the cauda equina and nerve roots and produce: n

flaccid paralysis and eventual wasting of the leg muscles n loss of sensation in the lower limbs n variable effects on the bowel and bladder, including loss of reflexes which initiate micturition and defecation tone.

Incomplete neurological lesions These may be the consequence of: n n

partial transection oedema and bleeding in relation to a spinal fracture or fracture–dislocation.

It is obviously of great importance to recognise that a lesion is incomplete in that efforts to prevent further injury must be rigorous. Although the neurological patterns may be complex, the preservation of any function distal to the established site of injury is an important initial finding; every care must be taken to preserve it. More-detailed neurological analysis can follow later.

Investigation Accurate imaging is essential. A frequent mistake is not to image the C7/T1 junction clearly, a common site for injury between the mobile cervical and the more-fixed thoracic vertebrae and also a difficult area to show on X-rays. If one fracture is found, the whole spine from the craniocervical junction to the lumbosacral articulation should be examined radiologically, as further fractures occur in 7% of patients. CT scanning may help visualize specific areas more clearly, demonstrate the extent of injury to the neural arch and the amount of bony neural canal impingement. MRI (Fig. 35.11) outlines the extent of spinal cord compression by bone or intervertebral disc and the type of injury that the cord has sustained, such as oedema or haemorrhage.

Management Management must start at the scene of the accident and may make the difference between recovery or lifelong para­ lysis. Paramedical staff are trained to apply rigid spinal support and to move patients only in a way that does not threaten further damage. The same must be the case for the surgical team.

Spinal shock Immediately after a severe spinal injury, a transient depression of all reflex activity is superimposed on the local neural damage due to cord concussion. There is a flaccid paralysis of all the distally supplied muscles and loss of all reflexes.

Complete lesions in the thoracic region  result in paraplegia (spastic paralysis of the legs) with: n

reflex spasms loss of sensation distal to the lesion n no voluntary control of bladder, bowel and sexual function, although automatic function is ultimately established. n

Injuries to the cervical region  lead to quadriplegia with: n n

partial or complete involvement of the arms and hands similar effects on organ function to paraplegia.

High cervical lesions  also lead to: n

phrenic nerve paralysis associated with respiratory failure which may cause immediate or later death n loss of the potential for an independent life.

Fig. 35.11  MRI of spinal cord compression. The image is viewed from below, and the posterior aspect of the spine is below. There is a filling defect which is compressing the spinal cord by about a third.

Joint injuries Spinal injuries

35 

650  Principles of management of fractures, spinal injuries

Recovery from spinal shock usually occurs within 24–72 hours and is first evident in men by return of the bulbocavernosus reflex (contraction of the external anal sphincter on stimulation of the glans penis). Identifying the end of spinal shock is important as further improvement in neurological function after this time is minimal.

Rehabilitation Return of the patient into society is best carried out by a multidisciplinary team working in a spinal injuries unit, and it is now feasible for most patients to achieve an independent and fulfilling life.

Neurogenic shock High thoracic or cervical injuries, resulting in transaction of the sympathetic pathways, may cause systemic vasodilatation, resulting in hypotension and paradoxical bradycardia. This is due to the unopposed parasympathetic action of the vagus nerve. Although hypovolaemic shock is far more common in the trauma situation, the presence of unexplained bradycardia in the shocked patient should be identified, as it may indicate a significant spinal injury and management of the shock will be modified.

Concomitant injuries Management of other life-threatening conditions, such as head, chest or abdominal trauma, must take precedence over the definitive management of the spinal injury. Reduction of displaced vertebrae is necessary to achieve bony alignment and decrease the distortion of the neural elements and their blood supply and can be achieved either by traction or by operation. Patients with incomplete lesions of the cord and fractures where the bone segments, vertebral disc or a haematoma within the vertebral canal narrow it by more than 50% do better if the canal is surgically decompressed early; the potential for recovery can be significant.

General management Skin

Rigorous attention must be given to the skin that is anaesthetic in an immobile limb. Alteration of position every 2 hours, cleanliness and avoidance of minor trauma are the best ways of avoiding pressure sores.

Bladder Initially in spinal shock there is acute retention and this should be relieved as soon as possible. Later, bladder ‘training’ is by intermittent catheterisation which ultimately results in micturition which can be predicted on the basis of time. A few patients may need a permanent indwelling urethral catheter.

Bowel Attention to diet and the use of aperients are started as early as possible.

Joint contractures These must be prevented by regular physiotherapy, and spasms can be controlled by skeletal muscle relaxants such as baclofen.

Mobilisation and fixation If the injury is confirmed to be stable, early mobilisation with appropriate orthotics is undertaken. Those with unstable injuries can be treated either by 6–12 weeks’ bed rest or by rigid fixation of the fracture to facilitate nursing and allow earlier rehabilitation.

PERIPHERAL NERVE INJURIES Transection of a major nerve trunk causes severe disability from paralysis, loss of sensation and sometimes pain. If untreated, atrophy and deformity of the injured part follow.

Pathological features The axons of peripheral nerves are cytoplasmic extensions of cell bodies located in the dorsal root ganglia (sensory) or the ventral horn of the spinal cord (motor). They are composed of axoplasm surrounded by a cell membrane. The axons are themselves enclosed in the sheath formed by Schwann cells and may or may not contain myelin. The peripheral nerves contain motor fibres (to end plates in skeletal muscle), sensory fibres (from organs and endings in skin, muscle, tendon and joint) and autonomic fibres (postganglionic sympathetic fibres) controlling the smooth muscle in blood vessels, sweat glands and in the hair follicles.

Types of injury Neurotmesis

This is division of a nerve trunk, and it causes well-defined changes both proximally and distally. Proximally, the axons die back for a distance of about 2 cm and the cell body enlarges with increase in RNA and protein. Sprouting of the divided axon at the division may be evident within a day. Distally, Wallerian degeneration occurs with lysis of axoplasm and fragmentation of myelin sheaths. If the nerve is not repaired, no recovery will occur. If the ends of the nerve are apposed, regenerating axons grow into the empty Schwann cell sheath at a rate of approximately 1 mm/day. However, haphazard matching of axonal sprouts with distal sensory receptors and motor units is inevitable. Recovery is therefore almost always incomplete. If the nerve ends are not in contact, the regenerating axons mingle with proliferating Schwann cells and fibroblasts to form a tangled mass – a neuroma – which may be painful. When the orderly sequence of regrowth into the distal stump is not achieved, with the passage of time the activity of the sprouting neurons diminishes, the distal endoneural tubes narrow and the brain forgets how to use the limb. The diagnosis and repair of nerve injuries are, consequently, a matter of urgency.

Axonotmesis In this type of injury there is damage to axons but the Schwann cell sheath remains intact. It may, for example, occur from traction on a nerve. Common examples of axonotmesis include many cases of radial palsy after fracture of shaft of humerus. Because the axon is disrupted, Wallerian degeneration occurs, but the potential for recovery is greater than in neurotmesis, as the sprouting neurons do not have

Peripheral nerve injuries  651 to bridge a gap in their sheaths. If the cause is removed, good recovery takes place with time and nerve repair is not required.

Neurapraxia In this type of injury, there is a physiological block to conduction but the axon is in anatomical continuity. A contusion is one cause – striking the ulnar nerve behind the medial epicondyle to cause the well-known ‘funny elbow’ is a good example. Function is temporarily absent, but Wallerian degeneration does not take place and, if the cause is removed, recovery is rapid. The classification given above into neurotmesis, axonotmesis and neurapraxia (described by Seddon) is useful, but it is important to realise that demarcation between different types is not always clear-cut in the individual case.

Clinical features Early recognition and prompt management of a nerve injury give the patient the best chance of restoring function.

History After a fracture or dislocation, or any penetrating injury that might conceivably have passed close to a nerve, the history should include specific questions about distal anaesthesia or loss of motor function, because these may not be appreciated by the patient who is more concerned with the bony or soft-tissue injury.

Physical findings A neurological examination for function of the nerves in the vicinity of all fractures, dislocations and lacerations must be done. The commonest reason for failing to detect a nerve injury is failure to suspect one and make a complete assessment. The critical step is to distinguish between nondegenerative and degenerative lesions. Non-degenerative lesions (neurapraxia).  Some sensation, e.g. for deep pressure, usually persists. Autonomic function – vasomotor and sudomotor control – is also usually intact. The nerve trunk distal to the injury continues to conduct because the axons beyond the injury are still nourished, and this can be established by electrodiagnostic testing. Spontaneous pain is uncommon. Degenerative lesions.  These follow axonotmesis or neurotmesis and cause a complete loss of all nerve function, including vasomotor and sudomotor control. In consequence, the skin innervated by the damaged nerve is red and dry. The nerve trunk distal to the injury conducts impulses only for the first 3 weeks until Wallerian degeneration has occurred. The difficulty lies in distinguishing between axonotmesis and neurotmesis. Only time or exposure of the nerve will ultimately be diagnostic. Where a fracture or dislocation has been caused by more than a moderate degree of violence and where there has been wide displacement of the skeletal fragments, then absence of function is assumed to be from rupture of the relevant nerve trunk. Similarly, where a laceration is present over the nerve or a surgeon has been operating in the vicinity, loss of function must be assumed to be from division.

Management It is better to explore too soon (even if the nerve is found to be intact) than too late. However, life-threatening injuries to the head, chest and abdomen take priority over nerve repair.

Nerve repair The ideal nerve repair should be performed as a primary procedure in an uncontaminated wound by an experienced surgeon and in an operating room with high-quality equipment and lighting. In contaminated wounds, repair is postponed for 3–4 weeks until either the wound is healed or infection has been controlled. Primary repair  is the suture of nerve stumps before a neuroma has had time to form, usually up to 2 weeks after the injury. It gives the best results. Secondary repair  is the later suture of nerve stumps in which a neuroma has formed and requires resection. It is done after any initial wound has healed and oedema and joint stiffness have resolved. Nerve grafting  is required when nerve tissue has been destroyed over a distance that makes direct repair impossible without tension. Nerves commonly used are the sural and the medial cutaneous nerve of the forearm which can be autotransplanted without significant loss of sensation. Nerve transfer  is sometimes indicated. For example, a fascicle from the ulnar nerve may be transferred into the stump of an irreparably damaged musculocutaneous nerve to restore biceps function, and the body learns to use this pathway.

Assessment of recovery ‘Tinel’s sign’ is valuable in the clinical detection of progress. Tinel’s sign indicates regenerating axons and it is not present in cases of neurapraxia (conduction block). Percussion along the course of a nerve from distal to proximal elicits painful paraesthesia when the area of regeneration is reached. Tinel’s sign is initially at the level of injury and advances distally with time. Rehabilitation should be started while recovery is awaited; the range of joint movement should be preserved and the anaesthetic skin protected.

Prognosis The outcome of nerve repair depends on: n n n

n n n

age delay between injury and repair type of lesion – a clean cut has a better prognosis than a crush injury, which in turn is better than a traction injury. Injuries associated with vascular injuries have a very poor prognosis nerve type size of the gap to be bridged surgical skill.

The two most important factors are the violence of injury, which defines the extent of damage to the nerve, and delay between injury and repair.

Peripheral nerve injuries Brachial plexus injuries

35 

652  Principles of management of fractures, spinal injuries Table 35.4

Classification of the obstetric brachial plexus palsya

Group

Nerves injured

Extent of paralysis

Natural course

I II III

C5, C6 C5, C6, C7 C5, C6, C7, C8, T1

Shoulder, elbow flexion Shoulder, elbow, wrist extension Complete

>90% recover completely 70% recover completely 50% recover completely. Residual defects usually affect the shoulder Few recover completely. 50% regain useful hand function

IV

C5, C6, C7, C8, T1 with Complete Horner’s sign Over 65% of all cases fall into Groups I and II

a

After Narakas.

BRACHIAL PLEXUS INJURIES Aetiology Brachial plexus injuries are amongst the most severe of all peripheral nerve lesions. They are usually caused by highenergy-transfer injuries, as in high-speed motorcycle accidents when there is violent distraction of forequarter from the trunk. Open wounds from bullets and other missiles or from knife attacks are increasingly seen. There are about 500 new cases every year in the UK. Life-threatening injuries to head, chest or abdomen are seen in 10%; the spine and spinal cord may be damaged in about 2%; there are fractures or fracture dislocations of long bones in 50%; the subclavian artery is ruptured in about 15%.

Pathological features The injury to the spinal nerves forming the brachial plexus may be pre-ganglionic or post-ganglionic. In pre-ganglionic injury the spinal nerve is separated from the spinal cord, and the level of rupture lies between the dorsal root ganglion and the cord. In post-ganglionic rupture the nerve trunk is torn apart, usually above the clavicle but also at varying levels below it.

Clinical features A severe lesion of the brachial plexus leads to extensive paralysis and loss of sensation. Pain is usually severe and it is characteristic of the pre-ganglionic injury. In one half of cases the injury to the brachial plexus is complete, so that all function in the upper limb is lost. In the remainder, spinal nerves survive, so that there is residual function, usually in the hand. Complete pre-ganglionic injury is seen in about 20% of the whole. A pre-ganglionic injury is suggested by: n n

n n n

a high-energy-transfer accident with violent distraction of the forequarter from the trunk severe pain – this is characteristic and it usually occurs on the day of injury. There are two patterns of pain. First is a constant, crushing burning bursting or tearing pain which is experienced within the anaesthetic hand. Next are convulsive shoots of ‘lightning like’ pain which course down the whole of the upper limb within the territory of the damaged nerve. The patient may experience up to 30 or 40 bursts of this convulsive pain every day sensory loss above the clavicle ipsilateral Bernard–Horner’s syndrome paralysis of serratus anterior and of the ipsilateral hemidiaphragm.

Management Other life-threatening injuries take priority in treatment. Plain radiographs of the neck, chest and shoulder, myelography, CT myelography and MR scanning are useful in diagnosis. Nerve conduction studies are valuable in describing the extent of the injury and in distinguishing between pre- and post-ganglionic injury. Repair of the ruptured nerves is urgently indicated. Preganglionic injuries may be treated by nerve transfer. There is growing interest in the concept of reconnecting the spinal cord to the peripheral nerves by means of interposed grafts in the pre-ganglionic injury. The process of rehabilitation is lengthy and is directed towards the relief of pain, the restoration of elements of function within the paralysed upper limb, and guiding the patient back to normal life, study and work.

The obstetric brachial plexus palsy (OBPP) There are approximately 300 new cases in the UK and Ireland every year, an incidence of about 1 : 2000 live births. There are two patterns (Table 35.4): n

Breech delivery is associated with severe bilateral lesions and paralysis of the phrenic nerves. These babies are small and are often premature. Breech delivery accounts for less than 10% of OBPP cases in the UK. n In cephalic delivery heavy babies and shorter, heavier mothers are at risk. Shoulder dystocia is recorded in about 60% of these cases. About 50% of the infants will make a complete spontaneous recovery, and 40% more will recover useful function. Exploration and repair of the brachial plexus may be con­ sidered in about 10% of the children. Posterior dislocation of the shoulder is the most significant and common of the secondary deformities in OBPP, occurring in about 25% of all cases. Abnormal posture of the shoulder and restriction of the range of lateral rotation are diagnostic features. FURTHER READING Hamblen DL, Simpson HR 2007 Adams’s outline of fractures, 12th edn. Churchill Livingstone, Edinburgh McRae R, Esser M 2008 Practical fracture management, 5th edn. Churchill Livingstone, Edinburgh O’Brien M 2010 Aids to the examination of the peripheral nervous system, 5th edn. Saunders Edinburgh Solomon L, Warwick D, Nayagam S (2005) Apley’s concise orthopaedics and trauma, 3rd edn. Hodder Arnold, London

36 

Principles of paediatric surgery

General principles

653

The inguinal region

661

Surgical pathology in children Conditions presenting with respiratory distress

654 654

Common abdominal masses in children

662

The newborn with intestinal obstruction

656

Tumours and the paediatric surgeon

663

Congenital abdominal wall defects

659

Disorders of genitalia

664

Disorders of the umbilicus

660

Principles of paediatric trauma

666

GENERAL PRINCIPLES What is paediatric surgery? Paediatric surgery involves a broad range of bodily systems and is the only surgical specialty defined by the age of the patient as well as the surgical condition. Patients range from children as young as 24 weeks premature weighing only 500 g up to late adolescence.

Assessing the paediatric surgical patient As with other branches of surgery and medicine the management of a paediatric surgical patient is fundamentally based on the ability to take an accurate history and perform a thorough clinical examination. Challenges lie in our patients who, unlike adults, are often unable and sometimes unwilling to allow such a process. History must often be extracted from those involved in the primary care of the child and examination techniques require skill and carefully applied strategies that develop with experience.

What are the main differences between adult surgery and paediatric surgery? n

n

n n

n

Surgical pathology is often related to congenital or inherited disorders as opposed to acquired conditions seen in adults such as atherosclerosis. Age-dependent physiological differences such as heart rate and blood pressure must be considered during assessment. Individual fluid and drug regimens are necessary as they are weight dependent. Children rely on the consent of others, usually parents, for permission to perform surgical procedures that they may require. The low incidences of many surgical conditions results in the transfer of many patients to regional centres for specialised anaesthetic and surgical management.

Principles of neonatal and paediatric transfer to a specialist centre The priorities in care during transfer are: n

temperature control nasogastric intubation to keep the stomach empty n airway protection, e.g. pharyngeal suction for oesophageal atresia (see below) and assisted ventilation via endotracheal tube for respiratory insufficiency n cardiorespiratory monitoring of pulse rate and oxygen saturation n intravenous fluids – to provide glucose and sodium; water overload must be avoided; fluid requirements are determined by the infant’s age and weight (Table 36.1). n

Temperature Hypothermia is minimised by the use of an incubator and a warming mattress and by an overhead heater in the operating theatre and anaesthetic room. The extremities are wrapped and the infant nursed in warm cotton wool covered by gauze (Gamgee), exposing only the operating field. Covering the abdomen with clear adhesive film decreases convection losses even further. Sick infants may be transferred between hospitals in a transport incubator with other support as detailed below.

Nasogastric intubation Whenever intestinal obstruction is suspected, a nasogastric tube large enough to keep the stomach empty (8–10 Fr) is essential to minimise the risk of aspiration of gastric contents into the respiratory tract. This should be kept on free drainage and regularly aspirated.

Cardiorespiratory monitoring Pulse rate and arterial oxygen saturation are sensitive indicators of how the infant is responding to the stresses of illness. Continuous records help to adjust respiratory support and fluid and electrolyte replacement.

36 

654  Principles of paediatric surgery Table 36.1

Fluids during first week of life

Day of life

Fluids (mL/kg per day)

Day Day Day Day

60 90 120 150

1, 2 3, 4 5, 6 7+

Table 36.2

3–10 kg 10–20 kg >20 kg

Guide to fluid maintenance volume in the infant and child according   to weight 100 mL/kg/d (4 mL/kg/h) 1000 mL/d + 50 mL/weight in kg less 10/d (40 mL/h + 2 mL/weight in kg less 10/h) 1500 mL/d + 25 mL/weight in kg less 20/d (60 mL/h + 1 mL/weight in kg less 20/h)

Fluid and electrolyte replacement To avoid hyponatremia this is best given as 0.9% saline with 5–10% glucose with 10 mmol of potassium added to each 500 mL bag. Close monitoring of serum electrolytes allows for volume adjustment. Maintenance fluid of 0.45% saline is acceptable though still hypotonic and must be considered in accordance with the physiological status of the patient. If the child is within the neonatal period (2 mL/kg/h is observed following intercostal drainage of a haemothorax.

Abdominal If bruising is discovered on a child’s abdomen following trauma, then it is likely that significant force has occurred. This may be as a direct blow or from restraint such as the seat or lap belt. Viscera such as the liver and spleen are less protected in the infant due to nature of rib cage shape and development and a high index of suspicion for visceral injury must be maintained. Splenic injury is common in children, though the majority of intrasplenic lacerations and haemorrhage will resolve if managed conservatively with bed rest and observation for 1–2 weeks. Deceleration injuries in road traffic accidents can affect hollow viscera such as the duodenum. CT with contrast is the preferred investigation. The mechanism of injury is the sudden visceral compression against the bony spine and shearing forces affecting retroperitoneal structures.

Assessment and management The Airway Breathing Circulation (ABC) principles of resuscitation apply to children as they do adults. Intravenous fluid

and pharmacotherapy, however, is weight based and each child must be considered on an individual basis. Within the trauma setting the primary concern is the airway together with cervical spine control. Once secured, the breathing is assessed and optimised, followed by support of the circulation. If the child is not breathing and there is no cardiac output, 5 rescue breaths are given prior to cardiac compression. Children require 30 chest compressions for every 2 breaths. Once resuscitation is successful, the neurological status of the patient is then assessed and the patient undergoes a full examination to complete the primary survey. The stabilised child can then undergo the secondary survey to look for additional injuries. The resuscitation of children in the UK should adhere to the guidelines set out by the advanced paediatric life support (APLS) group and this is mandatory training for all paediatric surgeons. FURTHER READING Holcomb GW, Murphy JP 2010 Ashcraft’s pediatric surgery, 5th edn. Saunders Elsevier, Philadelphia Spitz L, Coran A 2008 Operative paediatric surgery. Hodder Arnold, London Stringer MD, Oldham KT, Mouriquand PDE 2006 Pediatric surgery and urology: long-term outcomes. Cambridge University Press, Cambridge Thomas DFM, Duffy PG, Rickwood AMK 2008 Essentials of paediatric urology. Informa Healthcare, London

Principles of paediatric trauma

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37 

Ophthalmology in clinical surgery

Evaluation

669

Orbital pain

682

Ophthalmic injuries

672

Proptosis

682

Common symptoms of ocular disease

674 674 675 676 678 679 679 679 679

Epiphora

682

Ptosis

683

Anisocoria

683

The red eye

684

Diseases with ophthalmic   manifestations

685

Acute loss of acuity Subacute loss of acuity Gradual loss of acuity Transient loss of vision Loss of visual field Retinal detachment Neurological disease Visual distortion

The eye is a unique organ because of its specialised function. All ocular structures are transparent to allow the optimal focusing of light; therefore with appropriate instruments the ophthalmologist can examine all structures anterior to and including the retina without resort to special investigations. Moreover, the eye is a window to view the progression of systemic disease.

EVALUATION The non-ophthalmologist can make an effective assessment of the nature and urgency of a presentation from a detailed history and the use of equipment readily available in any Emergency Department or general practice rooms. Important symptoms and their possible causes are summarised in Table 37.1. Further details are given in the section on common symptoms and signs below. Important features of the examination are in Table 37.2.

Physical findings The items of equipment needed are: n

a Snellen chart of letters that reduce in size so that, to the eye, a letter from the 6 m line seen at 6 m should have the same size as a letter from the 3 m line seen at 3 m n bright pen torch n ophthalmoscope.

Visual acuity Distance.  The Snellen chart at 6 m is most commonly used with the subject wearing full refractive correction and bright ambient illumination. Interpretation of results is in Table 37.3.

Pinhole acuity.  If a refractive error is uncorrected, confusion may occur as to whether an intrinsic ocular disorder is responsible for poor vision. A pinhole only allows a central ray of light to pass through, undeviated by the eye’s focusing system onto the macula area, and therefore the significance of any refractive error is reduced. Pinhole acuity should be measured whenever the acuity, with or without refractive correction, is worse than 6/9.

Movements of the optic globe The ability to move both globes is tested by asking the eye to follow the examiner’s finger while keeping the head steady. The muscles responsible are illustrated in Figure 37.1.

Visual fields The confrontation method detects significant neurological field defects: 1. Test distance is approximately 1 m. 2. One eye each of both subject and examiner is occluded, which allows comparison between the visual field of the examiner and that of the subject. 3. The subject is asked to steadily fixate the examiner’s eye. 4. Finger counting is carried out in all four quadrants: superotemporal, inferotemporal, inferonasal and superonasal; it is best to present, in a static way, one, two or five fingers. A hemifield comparison is also made: 1. Similar distance to the confrontation method. 2. Controlled fixation of the subject on the examiner’s eye. 3. The examiner holds up both hands on either side of the vertical meridian and the subject is asked to compare their appearance – is one clearer or darker than the other?

37 

670  Ophthalmology in clinical surgery Table 37.1

Common symptoms of eye disease

Nature

Type

Causes

Pain

Ocular Referred

Visual disturbances

Distortion Photophobia Halos Flashing lights Floaters Acute visual loss Chronic visual loss Night blindness Monocular Binocular Red eye Proptosis Dry eye Watery eye

Uveitis, acute glaucoma Paranasal sinuses Dental Disease of the macula Uveitis, corneal disease Acute glaucoma Vitreous and retinal disorders, migraines Vitreous and retinal disorders Retinal, vascular and neurological disorders Media opacities, retinal, vascular and neurological disorders Retinal degeneration Cataract, refractive errors Extraocular muscle imbalance Conjunctivitis, episcleritis, uveitis, acute glaucoma Infection, thyroid eye disease Primary lacrimal failure, Sjögren’s syndrome Ocular irritation, blocked tear drainage

Double vision (diplopia) Altered appearance of the eye Lacrimal disturbance

Table 37.2

Ophthalmic examination

Property examined

Tests and abnormal findings

Visual acuity (normal = 6/6)

At distance At near Pinhole Confrontation Formal perimetry Misalignment of visual axis Nystagmus Unequal size (anisocoria) Distortion Reaction to light Response to accommodation Afferent pupil defect Redness Clarity Depth of anterior chamber Subjective hardness of globe Red reflex Optic disc Macula Retinal vessels

Visual field Ocular motility Pupil responses

Examination of anterior eye by torch Digital tonometry Fundoscopy

RSR

Table 37.3 Snellen acuity

Patient can see

At distance

6/60 6/36 6/24 6/18 6/12 6/9 6/6 6/5 CF HM PL

60 m line 36 m line 24 m line 18 m line 12 m line 9 m line 6 m line 5 m line To count fingers To detect hand movement To perceive light

6 m 6 m 6 m 6 m 6 m 6 m 6 m 6 m ×m ×m

LIO

RIO

RLR

Visual acuity

LSR

LLR

RMR LMR

RIR RSR = right superior rectus RLR = right lateral rectus

RSO

LSO

RIR = right inferior rectus RIO = right inferior oblique

Fig. 37.1  Movements of the optic globe and muscles responsible.

LIR RMR = right medial rectus RSO = right superior oblique

Evaluation  671 Finally a kinetic field test is done using a white hat-pin with a 5 mm diameter head. The pin is moved in from the periphery, and the point of first detection is recorded.

Appearance of external eye

Simple rules of interpretation of the acuity and field tests

n

The ‘rules of the road’ are: n

Lesions anterior to the chiasm affect one eye only. Lesions at the chiasm most usually damage the crossing nasal fibres from each eye to give rise to defects in the temporal fields on each side (bitemporal field defect). n Lesions posterior to the chiasm damage the temporal fibres from one eye plus the nasal fibres from the other eye to cause a homonymous defect (i.e. a defect affecting one visual hemifield). n

Pupil responses Abnormal responses are summarised in Table 37.4. Anisocoria is a visible difference between the pupil sizes of the two eyes, which may be a normal variation in about 20% of the population. Light reflex (parasympathetic) and pupillary constriction. If all pathways are intact, a light shone on one eye constricts both pupils at an equal rate and to a similar degree (direct and consensual reflexes).

Pupillary examination Procedure is described in Clinical Box 37.1.

Ocular motility The visual acuity must be known, to ensure that the subject can fixate on the targets presented. n

Observe for misalignment of the visual axis in the primary position, which can easily be determined by shining a torch light from 30 cm away and checking that the reflections on the corneas are central. n Is nystagmus (involuntary oscillations of the eyes) present? n Ask the subject to follow a target in the six different directions of gaze. n Is there a complaint of double vision?

Ocular adnexa (eyelids and periocular area): n

skin lesions inflammation n position of the eyelids – ptosis, retraction, entropion (lid margin turning in) or ectropion (lid margin turning out) n proptosis n general facial examination. Redness of the eye and opacities in the cornea can be easily seen with a torch. Fluorescein staining reveals areas of the cornea denuded of epithelium as bright yellow fluorescence when viewed with a blue light.

Digital tonometry Intraocular pressure is measured most accurately at the slit lamp using a tonometer. An estimate can be made by digital tonometry. The eyes are palpated through the closed lids over the upper outer angle of the orbit where the tarsal plate is thinnest. A hard eye indicates high pressure and, in the presence of a red, painful eye, may indicate acute angle closure glaucoma.

Fundoscopy The hand-held direct ophthalmoscope provides a magnified (×15) monocular view of the transparent ocular media (cornea, aqueous, lens and vitreous) and the fundus. The field of view is small, especially through an undilated pupil. The technique should be practised until one can reliably see the optic disc through an undilated pupil, as this forms an important part of any neurological examination. Technical points are described in Clinical Box 37.2. The examination starts with the ophthalmoscope 30 cm away from the subject and with observation of the red reflex which fills the pupil. It is formed by the reflection of light from the retina and is impaired by any obstruction to that light, e.g. cataract, vitreous haemorrhage. It proceeds

✚ n n n

Table 37.4

Abnormal responses of the pupil

Abnormality

Common causes

Dilatation

IIIrd nerve lesion Adie pupil (see text) Mydriatic drugs Iris trauma Horner’s syndrome Argyll–Robertson pupil Drugs: opiates, cholinergic Extrapyramidal disease (parkinsonism) Pineal tumour Damage to the anterior visual pathway up to the lateral geniculate nucleus

Constriction Failure of accommodation/ convergence Marcus–Gunn pupil

n

n

n

Clinical Box 37.1 

  Pupillary examination

Observe the sizes of both pupils in bright and dim illumination. Shine a bright torch in one eye and observe the direct and consensual light responses. A bright light shone into one eye will cause pupillary constriction in both eyes (direct and consensual light response). If there is an afferent defect on one side, e.g. a unilateral optic nerve lesion, then the stimulus to constriction when the light is shone on the affected side will be reduced relative to the response when light is shone on the normal side. When the torch is swung quickly across from one eye to the other, dwelling for a second on each, the pupils will dilate when light is shone on the affected side – paradoxical dilatation. The side that dilates is described as having a relative afferent pupillary defect (RAPD). This is a very important sign to elicit in the diagnosis of visual loss. Ask for fixation first on a distant target, then present a near target at 15 cm and observe the change in pupillary size as fixation is changed.

Evaluation

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672  Ophthalmology in clinical surgery

✚ n

n

n n

n

Clinical Box 37.2 

  Fundoscopy

Use a darkened room, ideally with both pupils dilated – common dilators (mydriatics) in adults are an anticholinergic (tropicamide 1%) and a sympathomimetic (phenylephrine 2.5%). Use your right eye to examine the subject’s right eye and your left for the subject’s left, which allows the instrument to be as close as possible to the subject’s pupil. The green/red free filter in the ophthalmoscope renders the blood vessels black and easier to view. An ophthalmoscope contains a sequential arrangement of lenses of different dioptric power which can be rotated clockwise (plus, convergent or black) to compensate for long sight, and anticlockwise (minus, divergent or red) to compensate for short sight in the subject. Refractive errors in the observer which normally require glasses can be dealt with by adjusting the diopter strength in the instrument or by keeping on corrective glasses.

n

n

n n n

n

inwards towards the pupil, with one hand on the patient’s forehead if necessary to steady the view. Features to note are the: optic disc macula n retinal vessels.

n

n n

The optic disc.  The margin should be sharp and the colour pink. A cup : disc ratio (the cup is the cavity in the centre of the disc) of 0.3 or less is considered normal but a large cup or asymmetry between the two eyes should lead to referral to an ophthalmologist for further investigation. The macula  is the area of central vision which lies approximately 1.5 disc diameters temporal to the optic disc. To examine it, the beam may be directed temporally or the subject asked to look directly at the light. The appearance is of a darker hue than the rest of the retina, with a central glistening area which is the reflection from the fovea – the centre of the macula. Retinal vessels.  Note the following: n

size: arteriolar attenuation (hypertension), venous dilatation (venous obstruction) n crossing over of the retinal vessels for signs of nipping (hypertension) n microaneurysms (diabetes).

OPHTHALMIC INJURIES Fortunately most injuries to the eye seen in the Emergency Department are superficial. The question is if and when an ophthalmologist needs to be involved: n

Any damage to the lacrimal drainage system which involves the lid margin. An ophthalmologist repairs the

lid margin to avoid notching and also determines any damage to lacrimal drainage. Blunt injuries. A history of considerable force, e.g. a punch, can cause effects to be transmitted deeper into the eye and should lead to consideration of referral. Blow-out fractures of the orbit. After a serious blunt injury with or without a fracture to the orbit, a thorough ocular examination is needed. A fracture can cause entrapment of extraocular muscles which can lead to double vision. Sinking of the globe into an enlarged orbital space created by the fracture has the same effect. Suspicion of penetrating injury or possible foreign body. See below. Chemical injury. Caustic chemicals, especially alkalis, can penetrate deeply. Contact lenses. Those with pain, with an acute red eye or with a visible corneal lesion have a high risk of keratitis and must be referred urgently. Recent intraocular procedures. Trauma may cause breakdown of fragile wounds, and infection may have a delayed presentation. Painful orbital swelling (orbital cellulitis). Particularly in a child, this is an ocular emergency, as the build-up of orbital pressure may compress the optic nerve.

General approach to ocular injuries Clinical features Complaints and history Special attention should be paid to: n

force applied, including direction and velocity what was being done at the time of injury – hammering, other industrial activities n possible nature of a foreign body. n

Physical findings Be suspicious of an undetected injury, particularly when other and apparently more obvious injuries are present either in the eye or elsewhere; an eyelid laceration can hide a perforated globe, which may in turn hide an intracranial injury.

Investigation Imaging is most important when a foreign body is suspected: orbital X-ray, CT or (if a non-radio-opaque object is suspected) ultrasound.

General management In a possible penetrating injury, check anti-tetanus status and bring up to date if necessary. (See below for individual injuries.)

Burns Aetiology Thermal injury in civilian practice is usually from molten metal. Rapid, reflex eye closure helps to limit the damage. Ultraviolet damage can arise from arc welding, sunlamps or

Ophthalmic injuries  673 prolonged exposure to high intensities of natural light (skiing or exploring without wearing sunglasses). Chemical burns are usually alkaline and have the devastating effect of saponifying lipid barriers so that they may penetrate into the anterior chamber.

Table 37.5

Structure involved

Immediate injury

Conjunctiva Cornea

Subconjunctival haemorrhage Abrasion Penetrating laceration Rupture, dialysis hyphaema Recession, dialysis Haemorrhage Commotio (bruising) Macular haemorrhage or hole Retinal tears/ dialysis Rupture Rupture Avulsion

Clinical features Extensive oedema in the lids and face after a thermal burn may limit examination and give the false impression of blindness until the swelling subsides. Repeated assessment is necessary.

Management Involvement of the lids in a thermal burn necessitates referral to an ophthalmologist for lid repair. Ultraviolet burns are usually self-limiting and require reassurance that vision will return, as well as pain relief. Chemical burns need copious irrigation with normal saline until the pH is returned to normal and urgent referral to an ophthalmologist to deal with the potentially serious consequences of corneal melt, glaucoma, cataract and phthisis (opacification and atrophy of the cornea).

Ophthalmic injuries

Effects of blunt trauma

Iris Ciliary body and angle Vitreous Retina

Choroid Sclera Optic nerve

Delayed injury

Glaucoma Hyoptony Macular hole Retinal detachment Subretinal membranes

Subretinal membranes Traumatic neuropathy

Orbital injuries More than 30% of patients who suffer blunt maxillofacial trauma sustain ocular injuries, of which 3% are blinding. More than 90% of the serious injuries result from midfacial, supraorbital and frontal sinus fractures; 4% of these cause optic nerve damage.

Clinical features History The history must include specific questions about: n

diplopia decreased vision n sensory deficits in the skin of the face n trismus n rhinorrhoea, which may indicate a compound fracture of the skull. n

Physical findings Assess: n

Fig. 37.2  Penetrating injury of the cornea with iris prolapse causing pupillary distortion, and secondary cataract.

Penetrating or perforating ocular injury

visual acuity pupil and pupil reactions n specific features – enophthalmos, subcutaneous emphysema, malar flattening and palpable steps in the orbital rim.

A penetrating injury causes cutting or tearing of the walls of the eye. A perforating injury is the same but with the addition of entry and exit wounds.

All orbital injuries should be examined by an ophthalmologist, and other specialties – maxillofacial and ear, nose and throat – should be involved as appropriate. CT is essential to plan surgical repair.

Suspicious appearances are:

n

Blunt ocular trauma Moderate to severe injury may cause immediate or delayed consequences (Table 37.5). All should be seen by an ophthalmologist.

Clinical features n

decreased visual acuity soft eye n distorted iris – a teardrop-shaped pupil points towards the site of the perforation (Fig. 37.2). n

Ocular foreign bodies Most foreign bodies in the eye are either trapped underneath the upper lid (subtarsal) or stuck in the cornea.

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674  Ophthalmology in clinical surgery

Management

COMMON SYMPTOMS OF OCULAR DISEASE

Removal is by the steps in Clinical Box 37.3.

Intraocular foreign bodies Aetiology These may be the consequence of a penetrating injury and can lodge in any part of the eye. Retrieval of foreign bodies from the eye, especially once they have lodged in the posterior segment, requires complicated vitrectomy techniques, often including lens extraction if a traumatic cataract has formed.

Visual loss may be a reduction of visual acuity (blurring) or loss of visual field, either partial or total. Unilateral symptoms are likely to be from lesions of the eye or the optic nerve; bilateral lesions commonly result from defects proximal to the optic chiasm – in the brain. A summary of visual loss is given in Table 37.6.

ACUTE LOSS OF ACUITY

Retinal artery occlusion Aetiology

✚

Clinical Box 37.3 

  Removal of a foreign body

1. Ensure the eye is well anaesthetised with several drops of topical preparation (e.g. tetracaine [amethocaine]) 2. Sit the patient at the slit lamp with a warning to keep the forehead firmly against the head rest 3. Instil a drop of fluorescein to stain any corneal abrasions and enhance the presence of subtarsal foreign bodies and errant contact lenses 4. Search systematically with a request to look up, down, right and left; evert the upper eyelid for the same purpose and remove foreign bodies with a sterile cotton bud 5. For a foreign body firmly embedded in the cornea, the ideal instrument is a blunt–tipped burr which can also effectively remove a rust ring which forms around some metallic objects; if this is not available, a green 18-gauge needle can be used with caution to scrape away the affected tissue 6. A 1–week course of topical antibiotic (e.g. chloramphenicol) is prescribed

Table 37.6

Central retinal artery occlusion (CRAO) typically occurs in the optic nerve just behind the visible optic nerve head and is usually the result of thrombosis of atheromatous vessels. Rarer causes include vasculitis. Branch retinal artery occlusions (BRAOs) are embolic – 80% are derived from atheromatous disease of the carotid arteries (Ch. 29). Less commonly, calcified material or cholesterol emboli may be released from other sites (valve vegetations and thrombi of cardiac origin). Emboli may be visualised on fundoscopy as white or yellow particles lodged at the bifurcations of the retinal arterioles.

Clinical features History When the central retinal artery is involved, the visual loss is sudden and painless, and the deficit is profound, with acuity usually reduced to counting fingers (CF) or worse, with even a loss of light perception.

Physical findings There is a relative afferent pupillary defect (impaired direct light response), and fundoscopy shows a pale retina with

Causes of visual loss Painful

Time course

Red eye

White eye

Painless (white eye)

Acute

Trauma

AION – arteritic

Subacute

Uveitis Orbital inflammation Acute glaucoma Uveitis

Optic neuritis

CRAO/ BRAO CRVO/BRVO AION – non–arteritic Wet ARMD Uveitis

Gradual

Transient

Migraine AION – arteritic

Optic nerve compression

Wet ARMD Dry ARMD Cataract Optic nerve compression Uveitis Chronic glaucoma Migraine TIA (amaurosis fugax) Syncope

AION, anterior ischaemic optic neuropathy; ARMD, age-related macular degeneration; BRAO, branch retinal artery occlusion; BRVO, branch retinal vein occlusion; CRAO, central retinal artery occlusion; CRVO, central retinal vein occlusion; TIA, transient ischaemic attack.

Common symptoms of ocular disease   675 attenuated vessels and a cherry red spot at the macula (Fig. 37.3). In around 20%, the macula receives its blood supply from the choroidal circulation via the cilioretinal artery, and, in these, a small island of central vision with variable retention of visual acuity may remain, but the loss of visual field greatly reduces function. BRAO affects vision and depends on the location of the vessel affected. A visual field defect (scotoma) results, and, when the macula is involved, there is reduced visual acuity. CRAO typically occurs in the optic nerve just behind the visible nerve head. The usual cause is atheroma with embolus of a fibrinoplatelet accumulation (Ch. 29) in the carotid bifurcation from atrial fibrillation or myocardial infarction, but vasculitis (including giant cell arteritis) is another possibility. Cardiovascular assessment is required. Emboli can be seen on fundoscopy as white or yellow particles lodged at bifurcations of the retinal arterioles (Fig. 37.4).

Retinal vein occlusion Aetiology Diabetes, hypertension and hyperlipidaemia are the major systemic risk factors.

History and findings Retinal vein occlusion is experienced as a sudden loss of vision of variable severity. Fundoscopy reveals dilated veins, haemorrhages and cotton wool spots in the affected area of retina. It may be localised, as in branch retinal vein occlusions, or involve all four retinal quadrants, often with disc swelling in a case of central retinal vein occlusion.

Anterior ischaemic optic neuropathy (AION) Aetiology This is an infarction of the optic nerve head because of closure of the ciliary arteries of supply. Two groups of patients can be identified: 50–60-year-olds and those aged >70 years. Members of the first group are likely to have cardiovascular risk factors such as hypertension and angina caused by thrombosis of atheromatous ciliary vessels. The over-70s may have arteritic AION, usually as a result of giantcell arteritis.

Clinical features A sudden visual loss results, which may be total or altitudinal (where the inferior or, less commonly, the superior half of the visual field in one eye is lost). Arteritic AION may be accompanied by symptoms of malaise, weight loss, muscle pains and stiffness, temporal headache and scalp tenderness, and jaw or tongue claudication. There is a relative afferent pupillary defect, and on fundoscopy a pale, swollen optic disc is seen.

Management All patients with acute visual loss thought to be of vascular origin should have an urgent ESR and immediate referral to an ophthalmologist if arteritis is suspected, because highdose systemic steroids may be required to prevent blindness from involvement of the other eye (see also transient visual loss – ‘stuttering amaurosis’).

Fig. 37.3  Central retinal artery occlusion with ‘cherry red spot’.

Fig. 37.4  Superior temporal branch retinal artery occlusion (see calcific embolus lodged in bifurcation of retinal arterioles), with cloudy retinal swelling in the distribution of the occluded vessel.

SUBACUTE LOSS OF ACUITY

Optic neuritis Visual loss which develops over a few hours to 2–3 days and which is associated with ocular pain exacerbated by ocular movements is characteristic of optic and retrobulbar neuritis. Loss of acuity is variable but may fall to an absence of perception of light. Colour desaturation (i.e. where colours are seen as being washed out) is a prominent early feature. There is a relative afferent pupillary defect and, if the intraocular optic nerve is affected, a swollen optic disc may be noted (Fig. 37.5). More commonly the inflammation is located in the intraorbital optic nerve and fundoscopy is normal (the patient sees nothing and the doctor sees nothing), and the condition is called retrobulbar neuritis. The most common cause is multiple sclerosis (MS), and patients tend therefore to be in the 20–40 year age group and are more often female. Enquiry and examination for symptoms or signs of previous neurological disease are essential and, if positive, confirm the diagnosis of multiple sclerosis.

Common symptoms of ocular disease Acute loss of acuity Subacute loss of acuity

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676  Ophthalmology in clinical surgery Reduction of ocular motility results either from IIIrd, IVth or VIth cranial nerve damage at the orbital apex or from direct mechanical restriction of ocular movement. Causes  to be considered are: n acute dysthyroid eye disease (Graves’ disease, see Ch. 32) n orbital cellulitis (usually secondary to paranasal sinus disease) n orbital pseudotumour (idiopathic orbital inflammation which mimics an orbital tumour).

Fig. 37.5  Papilloedema in benign intracranial hypertension.

Referral to an ophthalmologist or neurologist is indicated for confirmation of eye involvement.

Investigation and management In isolated optic or retrobulbar neuritis, the extent of investigation is controversial; some recommend a full work-up for signs of subclinical lesions elsewhere in order to make the diagnosis of MS; others feel that, because there is as yet no effective intervention, a ‘wait and see’ attitude should be adopted. Treatment is also controversial; intravenous corticosteroids shorten the acute episode but have no effect on the extent of final visual recovery or the ultimate prognosis.

Prognosis After visual loss, some degree of recovery always occurs. In most instances, this takes 4–6 weeks and is full or nearly so, although a small residual (subjective) defect is often present. Residual signs include red desaturation, a relative afferent pupillary defect and optic disc pallor, most marked temporally, which develops over a few weeks after an acute episode.

Optic nerve compression Lesions within the orbit may compress the optic nerve, especially if located posteriorly at the orbital apex where nerves and vessels are crowded together. Many such lesions result in gradual visual loss (see below). Orbital inflammatory disease may, however, be rapidly progressive and is an ophthalmic emergency.

Clinical features Symptoms include pain, visual loss and diplopia. Signs  are of: n reduced acuity n loss of colour vision n a relative afferent pupillary defect n proptosis n conjunctival chemosis.

Insidious, unilateral painless visual loss results from compression of the optic nerve by a slowly growing tumour. In children, this is most commonly an optic nerve glioma, sometimes seen as part of type 1 neurofibromatosis. In adults, usually women of 30–50 years, meningioma of the optic nerve sheath or sphenoid wing is most likely. Fundoscopy shows a pale and sometimes swollen optic disc. Tortuous abnormal vessels on the optic disc (retino­ choroidal shunts) are typical of a meningioma.

Management The patient should be referred to an ophthalmologist who, when the diagnosis is suspected, can confirm it by CT. Surgical excision often results in damage to the optic nerve. It may be indicated if the sight is already badly damaged and the tumour can be excised whole; otherwise, radiotherapy or observation alone may be preferred.

GRADUAL LOSS OF ACUITY Gradual diminution of visual acuity is one of the most common complaints encountered in ophthalmology. By contrast, gradual loss of visual field is rarely noticed by the patient – hence the need for screening programmes for chronic glaucoma. Field loss is usually noticed by the patient only when very extensive, because acuity is retained until late in the disease process.

Cataract A cataract is an opacity of the lens that interferes with vision (Fig. 37.6). Most are of the idiopathic senile type, and the prevalence increases with age. There are many other causes, which include: n

trauma uveitis n metabolic disorders (e.g. diabetes mellitus) n congenital. n

In those regions of the world where therapeutic resources are unavailable, cataract is the most common cause of blindness (visual acuity less than 3/60 in the better eye).

Clinical features Symptoms  include: n n

gradual blurring of vision change in the prescription for glasses – ‘second sight’ is the myopic shift induced by nuclear sclerotic cataract that may allow a presbyopic patient to resume reading

Common symptoms of ocular disease   677 Gradual loss of acuity

Fig. 37.6  Mature cataract.

Fig. 37.7  Age-related macular degeneration, with large confluent soft drusen. This eye is at high risk of visual loss from subretinal neovascularisation.

without reading glasses after previously having required them n glare – most marked in bright sunlight or when confronted by oncoming headlights while driving at night; this is typical of a posterior subcapsular cataract. A cataract is most easily identified as an obstruction of the red reflex during direct ophthalmoscopy.

Management Treatment is by extraction and insertion of a prosthetic intraocular lens once the reduction of vision is sufficient to interfere with lifestyle. The threshold for an operation is affected by individual visual needs – driving, occupation and hobbies. Cataract surgery is usually performed as a day case under local anaesthesia.

Macular degeneration Age-related macular degeneration (ARMD) is the most common cause of blindness (visual acuity of less than 3/60 in the better eye) in the developed world. It affects central vision, with reduction of visual acuity and sometimes formation of a central scotoma. There are two types: dry and wet.

Dry ARMD This is an idiopathic gradual loss of photoreceptors and retinal pigment epithelium in the macular area. Visual loss is gradual, mild to moderate in severity and usually symmetrical. Fundoscopy shows areas of hypo- and hyperpigmentation in the macula. There is no treatment to arrest the process. Management is directed at low-vision optical aids to make the most of what residual function exists. Registration as partially sighted or blind is valuable to increase help from community sources.

Wet ARMD Wet ARMD is again bilateral, although symptoms usually begin on one side. It tends to occur in a younger age group and results from the development of subretinal neovascular complexes: ‘membranes’ that leak serum and may bleed into the retina. Presentation is with more-rapid onset of poor vision; central scotomas and visual distortion (see below) are common. Fundoscopy (Fig. 37.7) may reveal dark red blood or grey subretinal elevation (fluid or subretinal membrane)

Fig. 37.8  Diabetic maculopathy. at the macula. Immediate referral to an ophthalmologist is required because treatment with anti-growth factor injected intravitreal can prevent blindness.

Macular oedema This is a complication of many ophthalmic disorders rather than a separate entity. It is the major cause of visual loss in diabetic retinopathy (Fig. 37.8) and may be the presenting feature of diabetes in non-insulin-dependent disease. Macular oedema may also be seen in ARMD, in uveitis, in hypertensive retinopathy (Fig. 37.9) and as a complication of intraocular surgery. Another relatively common cause is central serous retinopathy, an idiopathic condition seen most commonly in men of between 20 and 40 years. Choroidal fluid leaks through the macula to produce a localised serous retinal detachment, which presents with subacute onset of blurring and distortion of the central field characterised by micropsia (objects appear smaller than they actually are). In the great majority, the condition resolves spontaneously, usually within 1–6 months after the onset of symptoms.

Macular hole This is another degenerative disorder caused by an abnormal vitreoretinal adhesion at the macula which pulls out a circular fragment of retina. The disease is most common in women

37 

678  Ophthalmology in clinical surgery until the complications of secondary cataract and (often untreatable) cystoid macular oedema develop. For this reason all children with arthritis must have ophthalmic screening at regular intervals. Intermediate and posterior uveitis may cause gradual or subacute loss of vision, as a result of direct retinal damage, macular oedema or vitritis. The last of these causes a diffuse vitreous haze or floaters (below). All these conditions need specialist assessment. Management is often difficult but may involve periocular or systemic corticosteroids.

Fig. 37.9  Grade III hypertensive retinopathy. The concentration of exudates and haemorrhages in the peripapillary area is typical.

TRANSIENT LOSS OF VISION This is a common symptom. A careful history often allows benign conditions to be separated from more serious disease.

Syncope A fall in systemic blood pressure from whatever cause (e.g. Stokes–Adams attack, vasovagal response) can result in, initially, the loss of colour vision (grey-out) and subsequently all vision (blackout), as blood flow to the eyes decreases. Symptoms are bilateral and are usually accompanied by faintness, dizziness and palpitations. Provided blood flow is restored (e.g. by falling to a horizontal position), both general recovery and visual recovery are likely to be swift.

Fig. 37.10  Retinitis pigmentosa with classic bone spicule pigmentation. in the sixth and seventh decades of life and remains unilateral in 90%. The presenting features are similar to ARMD: visual distortion, reduced acuity and a central scotoma. On fundoscopy a small (approximately one-third of a disc diameter) red round hole over the fovea may be seen. Referral is indicated because surgical intervention may be possible.

Retinal dystrophies Gradual visual loss in younger patients is uncommon and always warrants ophthalmic referral. There are a large number of hereditary and sporadic retinal and macular dystrophies that may present with reduced acuity and colour or night blindness. Often the gross ophthalmoscopic appearance is normal. Retinitis pigmentosa is the best known of these conditions, in which case the classic mid-peripheral bone spicule pigmentation may indicate the diagnosis (Fig. 37.10).

Uveitis Acute uveitis (inflammation of the uvea, i.e. the iris [iritis], ciliary body [iridocyclitis] and choroid [posterior uveitis or choroiditis]) usually presents with a red eye and pain, but chronic uveitis may solely cause visual loss. Chronic anterior uveitis in juvenile rheumatoid arthritis may be asymptomatic

Migraine This is a familial vasospastic disorder that may cause neurological symptoms as a result of intracranial ischaemia, followed in most instances by headache which is thought to be the consequence of compensatory vasodilatation. The most common neurological disturbance is visual, with the appearance of jagged concentric black lines across the visual field (fortification spectra) and a scintillating scotoma. These sensations may last for around 30 minutes and are followed by a severe throbbing ipsilateral hemicranial headache, with debilitation and nausea present for up to several hours, followed by resolution and sleep. Migraine is, however, protean in its manifestations and should be included in the differential diagnosis of any transient visual disturbance, even without headache, especially in younger patients. If it occurs for the first time after the age of 50, the diagnosis must only be made with caution because an intracranial disorder is possible.

Transient ischaemic attack (TIA) (See also Ch. 29) A TIA that involves the central retinal artery circulation has the same cause as a branch retinal arterial occlusion, and those that affect the cerebral hemispheres (embolic disease) usually relate to atheroma of the extracranial carotid arteries. The patient typically describes a grey curtain moving horizontally upwards or downwards across the vision of one eye; it comes on over seconds to minutes and is likely to resolve within a few minutes (amaurosis fugax – fleeting blindness). Fundoscopy is often normal; alternatively, white/yellow refractile emboli may be visible within the retinal arterioles.

Common symptoms of ocular disease   679 Transient loss of vision

The significance of amaurosis fugax is the increased risk of retinal arterial occlusion or stroke. A full assessment is required (Ch. 29). A related symptom is stuttering amaurosis (repeated uniocular episodes of visual loss) which is an occasional precursor of permanent loss of vision in giant-cell arteritis.

Loss of visual field Retinal detachment Neurological disease Visual distortion

LOSS OF VISUAL FIELD Vascular All the vascular causes of acute loss of acuity described above can instead present as visual field loss, e.g. with a scotoma in BRAO and BRVO or altitudinal field loss in AION.

RETINAL DETACHMENT Retinal detachment may be traumatic; however, in the majority of cases it is spontaneous. The condition is more common in myopes.

Pathological and pathophysiological features Changes in the vitreous gel (posterior vitreous detachment) tear a hole in the retina and allow fluid from the vitreous to enter the subretinal space. The neurosensory retina separates from the underlying retinal pigment epithelium so that the detached area of retina ceases to function. The field defect which results mirrors the site of the detachment. Thus a superior detachment (the most common and rapidly progressive) produces an inferior-field defect, often referred to as a ‘shadow in the vision’.

Clinical features Symptoms Visual acuity is retained until the macula is involved in the detachment. This is important, because detachment that is surgically repaired when the macula is still on has a much better visual prognosis than when it has come off. Other symptoms include floaters and photopsia.

Physical findings The index of suspicion must be high – a myopic spectacle correction is easily detected by looking through the spectacle lens, when objects appear smaller. A monocular field defect is usually present. Visual acuity varies depending on the state of the macula. If more than a quarter of the retina has detached, there is a relative afferent pupillary defect. If the detachment is small, fundoscopy may be normal, especially if a direct ophthalmoscope through an undilated pupil is used, because this only affords a small field of view and the detachment starts peripherally. The detachment is seen as an elevated convex area of grey retina which moves with ocular movement and has a wrinkled surface (Fig. 37.11). Therefore, if the history is suggestive but the examination appears to be normal, a referral to an ophthalmologist for more detailed examination is important.

Management If central vision is retained at the time of diagnosis, detachment is an emergency. Treatment is surgical. It involves either an external approach with the application of a

Fig. 37.11  Retinal detachment.

compressive buckle to the outside of the eye, or an internal approach with removal of the vitreous gel and usually internal tamponade with gas or liquid. The aim is to oppose the detached retina and underlying retinal pigment epithelium. Adhesion between the two layers is then achieved by the use of laser or cryoprobe to create inflammation and scarring.

NEUROLOGICAL DISEASE Lesions of the retrochiasmal optic pathway result in bilateral hemianopic visual field defects that obey the vertical meridian. They can usually be easily detected by confrontation testing and must be specifically sought in all instances of apparently monocular visual loss because a positive finding excludes ocular disease as the cause. In a left homonymous hemianopia, for example, the nasal field defect in the right eye may not be noticed by the patient because it is overlapped by the retained nasal field of the left eye, and it may therefore present as an isolated loss of the left temporal visual field. Acute-onset hemianopic visual field loss is very likely to be cerebrovascular in origin – 80% of cases are caused by emboli from the extracranial carotid arteries (Ch. 29). Cardiovascular risk factors should therefore be assessed. Ophthalmic disease in multiple sclerosis is described later in this chapter.

VISUAL DISTORTION Visual distortion (metamorphopsia) is a symptom restricted to disorders that affect the macula, because it occurs when macular photoreceptors are displaced relative to each other. The result is disruption of macular representation of objects in the central visual field. Altered image size and reduced visual acuity result from the same mechanism. The formation of a fine membranous scar (epiretinal membrane) may cause metamorphopsia, as may macular oedema from any cause. Detection is easy by asking the patient to examine an Amsler chart, which is a regular grid of black lines on a white background, looked at from a distance of 30 cm. Typically there is distortion and blurring of the grid; the location of worst distortion corresponds to the site of the macular lesion. If an Amsler chart is not available, any straight

37 

680  Ophthalmology in clinical surgery

high-contrast edge will suffice; for example, ask if the edges of a window frame appear straight and regular.

Photopsia Photopsia refers to the sensation of light arising from nonlight stimuli. It may happen when mechanical forces act on the retina: either due to an external force (trauma), which can be transient, or secondary to intraocular disease which is more persistent. The two major intraocular causes are posterior vitreous detachment (see below) and retinal detachment. Mechanical photopsia are unformed visual sensations, as distinct from the structured visual sensations experienced as a result of neurological disease, such as migraine.

Floaters Floaters are dark spots seen moving in the visual field. They result from opacities within the vitreous gel casting a shadow on the retina, explaining their mobility.

Posterior vitreous detachment The vitreous gel is increasingly being recognised as a complex structure, rather than simply an amorphous gel, which is reflected in the degenerative changes that are seen in all eyes with increasing age. The gel collapses into itself in places to form denser spots and areas of increased gel mobility, which are of themselves sometimes large enough to be seen as floaters but are not of clinical significance. With further degeneration the volume of the vitreous gel decreases and the retrohyaloid space (the space between the vitreous and retina) is filled with aqueous. Movement of the eye will allow the liquid gel to strip the remaining vitreous away from the retina, to create a posterior vitreous detachment (PVD).

Clinical features Photopsia may be experienced during the development of a posterior vitreous detachment because of the traction on the retina when the gel collapses. The incidence of PVD increases with age. In the majority, it is annoying but not dangerous. Around 5%, however, sustain damage in the form of a retinal tear as a result of traction. Retinal tears are the major cause of retinal detachments because they allow the liquefied vitreous and/or aqueous to pass through the hole into the subretinal space and detach it from the retinal pigment epithelium.

Uveitis Chronic uveitis may lead to organised inflammatory reaction in the vitreous gel which the patient perceives as floaters. The eye is usually painless, and the condition may have been present for some time. Visual loss is common, but in intermediate uveitis/pars planitis, where only the region of the ciliary body is inflamed, visual acuity is usually normal, unless and until cystoid macular oedema supervenes.

Ocular pain While many disorders of the external eye produce ocular discomfort (e.g. conjunctivitis and blepharitis), ocular pain is less common and may indicate serious disease. It is helpful to elicit whether the pain feels superficial (sharp, scratching) or deep (aching, gnawing), as this sometimes distinguishes corneal from intraocular disease. Headache associated with visual symptoms occurs in migraine and giant-cell arteritis and should not be confused with ocular pain.

Corneal abrasion Defects in the corneal epithelium expose the underlying plexus of naked nerve terminals, cause severe, sharp pain, worse with lid movement, and excessive lacrimation.

Clinical features History There is usually a clear history of trauma to the eye, although sometimes an abrasion results from breakdown of healed epithelium at a site of previous injury. This recurrent corneal erosion syndrome has a characteristic pattern of pain on first opening the eyes in the morning, often preceded by shortlived episodes of pain and redness in the few days before the actual abrasion occurs.

Physical findings Abrasions are identified with guttae fluorescein 2% stain and cobalt blue light, which shows the abrasion as a fluorescent yellow-green area on the cornea (Fig. 37.12). A blue cover to a penlight torch can be used where a slit lamp is unavailable.

Retinal tear Clinical features of a retinal tear include floaters associated with photopsia, and impairment of visual acuity in the case of a larger vitreous haemorrhage. On fundoscopy the PVD and any vitreous blood may be seen as small, mobile, black spots in the red reflex. However, they are difficult to visualise with the direct ophthalmoscope. Management of suspected PVD or a retinal tear involves same-day referral to an ophthalmologist for thorough dilated indirect ophthalmoscopy. There is no treatment for the PVD, but retinal tears need laser or cryotherapy to seal the tear. Retinal detachments, if present, usually require operation.

Fig. 37.12  Fluorescein–stained dendritic ulcer (herpes simplex).

Common symptoms of ocular disease   681

Fig. 37.13  Soft contact lens in situ.

Fig. 37.14  Acute anterior uveitis (iritis) with ciliary flush and a fixed, oval pupil.

Management Treatment is with broad-spectrum antibiotic eye drops (usually chloramphenicol 0.5% four times a day for 5 days) with cycloplegia and/or an eye patch if the pain is severe. Simple abrasions do not need referral to an ophthalmologist but should be reviewed after 48 hours to confirm a reduction in size.

Keratitis Inflammation of the cornea is usually infective. Herpes virus infections and related immune keratitis are considered below. Most bacteria require a pre-existing epithelial defect to allow them to breach the cornea, but an important exception is Neisseria gonorrhoeae; hence the importance of urgent, aggressive treatment in ophthalmia neonatorum. Predisposing conditions include contact lenses (Fig. 37.13), a dry eye and the long-term use of eye drops that contain corticosteroids. Pain can be severe, partly because of the frequently present secondary uveitis. Suspected keratitis always needs urgent ophthalmic review.

Uveitis Acute anterior uveitis is inflammation of the iris and/or ciliary body. If only the iris is affected, it may also be called iritis or, if the ciliary body is also involved, iridocyclitis.

Aetiology There are many possible causes of acute anterior uveitis, including a number of associations with systemic disorders (e.g. HLA B27-positive arthropathies and sarcoidosis). How­ ever, in the majority a specific cause is not found.

Clinical features History Pain is usually moderate to severe, with photophobia, lacrimation and often reduction of vision.

Physical findings Redness is most marked around the cornea and typically has a violaceous hue. Miosis is present, and the pupil may also be fixed and irregular because of the formation of adhesions

between the iris and the lens – posterior synechiae (Fig. 37.14). In most, the condition is unilateral and should be strongly suspected in the presence of any unilateral, persistently painful red eye.

Management Uveitis always needs specialist attention, even when the diagnosis appears clear, because the efficacy of treatment and the presence of complications such as glaucoma can only be assessed by slit-lamp examination.

Glaucoma Glaucoma refers to a group of conditions characterised by retinal nerve fibre damage, resulting in typical optic disc changes (cupping) and visual field loss. There are many subgroups, most importantly acute and chronic glaucoma. Raised intraocular pressure is always a feature of acute glaucoma, and most cases of chronic glaucoma also have raised pressure, but to a lesser degree. Pain is not a feature of chronic open-angle glaucoma (the most common form). However, in acute angle closure glaucoma, the intraocular pressure rises rapidly and dramatically.

Clinical features of acute glaucoma The condition is more common with increasing age and is found predominantly in hyperopes (whose glasses magnify images seen through the lens). The patient is likely to be in distress, with severe pain, blurring of vision and halos around lights. The eye is intensely injected, with clouding of the cornea and a fixed semi-dilated pupil.

Management Immediate referral is necessary and urgent treatment to lower the pressure is required to alleviate the pain and prevent permanent visual loss due to pressure-induced damage to the retinal nerve fibres as they enter the optic nerve.

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682  Ophthalmology in clinical surgery

Episcleritis and scleritis Both these conditions present with a red eye and are immune-mediated.

Episcleritis This is a self-limiting condition characterised by ocular discomfort and diffuse or localised redness. It is rarely associated with underlying disease. If symptoms warrant treatment, a course of oral NSAIDs is usually effective.

Scleritis This is a much more serious condition that may lead to visual loss. Severe, constant, deep ocular pain is usual. The redness may be localised, diffuse or absent in posterior scleritis. An early ophthalmic opinion should be sought. Scleritis may occur in isolation, but is frequently associated with connective-tissue disorders (systemic lupus erythematosus, rheumatoid arthritis) or vasculitis.

Aetiology If a lesion is located within the retrobulbar space, bounded by the extraocular muscles (intraconal), the displacement is axial; if extraconal, then non-axial proptosis with mechanical strabismus ensues. Dysthyroid eye disease and idiopathic orbital inflammation (orbital pseudotumour), orbital cellulitis and other rarer conditions such as tuberculosis and sarcoidosis cause proptosis by increasing the volume of intraorbital fat and con­ nective tissue and also of the extraocular muscles. Tumours of all kinds may cause proptosis, as may vascular disease such as orbital varices and haemorrhagic cysts. Pulsatile proptosis with enlargement and injection of the conjunctival vessels is the hallmark of a carotid-cavernous fistula, in which the orbital venous system becomes arterialised as a result of an abnormal communication between the ophthalmic artery and the cavernous venous sinus.

EPIPHORA ORBITAL PAIN It is often very difficult clinically to differentiate between orbital and ocular pain because many describe ocular pain as coming from behind the eye and orbital pain is poorly localised. Orbital inflammatory conditions often lead to secondary scleritis, which adds ocular pain to the clinical picture. Associated features that lead to the suspicion of orbital disease as a cause include proptosis, ophthalmoplegia, ptosis and loss of corneal sensation.

Orbital inflammation Orbital cellulitis, dysthyroid eye disease and orbital pseudotumour have all been mentioned in the section on visual loss. The severity of pain, inflammatory signs or mass effects varies greatly.

Orbital malignancy Benign tumours generally present with painless gradual visual loss. Malignant tumours, however, often cause pain as a result of rapid growth or neuronal invasion, which is often associated with proptosis and ophthalmoplegia.

PROPTOSIS The orbit is bounded by bone on all sides except anteriorly. In consequence, any increase in the volume of the intraorbital contents can only be decompressed by forward displacement of the globe, which causes protrusion of the orbital contents – proptosis. Exophthalmos is a synonymous term but is usually reserved for dysthyroid eye disease (the most common cause of proptosis).

Epiphora (excessive production or running of tears) can be difficult to evaluate. Probably the most important question is: is it constant? Tearing which is only intermittent is unlikely to result from lacrimal duct obstruction. The diagnosis is best approached by considering where the problem may lie: Lacrimal gland.  Primary excessive activity of the gland is very rare but may be seen after injury to the facial nerve with aberrant regeneration (gustatory sweating). Secondary or reflex overactivity is much more common and can result from any painful ocular condition. For chronic epiphora, it is important to examine the lids and ocular surface for irritant lesions such as trichiasis (inturned lashes) and entropion (inturned lid). Eyelid.  Tears are moved across the eye from the superolat­ eral lacrimal gland to the inferomedial drainage system by a combination of gravity and the pumping action of the lids. The mechanism can be upset by ectropion, where the lid margin turns outwards away from the eye; tears spill over the edge and normal apposition of the lacrimal punctum to the pool of tears in the medial canthus is prevented. Even without ectropion, a flaccid orbicularis muscle can impair the pump mechanism and epiphora follows. These changes are commonly involutional in the elderly but may also be seen following VIIth nerve palsy or scarring of the skin of the lower lid. Lacrimal duct.  From the lacrimal punctae, tears drain via the canaliculi to the lacrimal sac and thence to the nasolacrimal duct and the nose. Obstruction at any of these sites causes epiphora. Congenital nasolacrimal duct obstruction affects up to 20% of neonates, but canalisation is completed spontaneously in over 90% by 1 year. When canalisation remains incomplete after this time, probing of the duct usually easily completes the process. In adults, stenosis may be traumatic, infective (e.g. herpes simplex conjunctivitis) or, most commonly, a gradual involutional change. Often a simple explanation of the cause of symptoms is all that is required;

Anisocoria  683 however, some require surgery, which can now often be done under local anaesthesia.

PTOSIS This is an abnormally low position of the upper eyelid which may be an isolated problem or the presenting feature of serious neurological disease. It should be differentiated from pseudoptosis, which is a relative ptosis because of contra­ lateral lid retraction. Ptosis is best considered initially in relation to age.

Congenital ptosis Infantile ptosis may be the outcome of any of the causes described under subsequent headings but is most commonly dystrophic with abnormal development of the levator muscle. The condition may be unilateral or bilateral. Any significant ptosis in a young child must be urgently referred because of the risk of occlusion amblyopia. This is a failure of development of the cerebral pathways serving the affected eye due to lack of stimulation during the critical period of development. The eye is physically normal, but processing of visual data from the eye is impaired. In infants, a week of occlusion may be significant; once a child is over around 7 years of age, amblyopia can neither develop nor be treated if present.

Adult Ptosis in adults of working age may result from a number of causes (Fig. 37.15). Diplopia, rapid muscle fatigue and muscle weakness should be specifically asked for and may indicate myasthenia gravis. The pupil and ocular movements must be examined specifically to look for the down-and-out globe position of a palsy of the IIIrd nerve. In those with diabetes or hypertension, this is commonly a microvascular event; however, the presence of a dilated pupil raises the possibility of an expanding aneurysm of the posterior communicating artery which must be investigated by neuroimaging. Trauma may also cause ptosis, which may not become evident until the initial swelling has died down.

The elderly The adult causes described above still apply in later life, but the most common cause is degeneration of the attachment of the levator palpebrae superioris aponeurosis to the lid. Five per cent of cataract operations precipitate the condition. There is a drooping upper lid with thin skin, and the horizontal upper lid crease lies high up on the lid. In spontaneous instances, the condition is bilateral but not necessarily symmetrical. Operation to reattach the aponeurosis to the lid tissues can be performed under local anaesthetic.

ANISOCORIA This is a visible difference in pupil size between the two eyes. It may be a normal variant (seen in 20% of the population at some time; pupillary reactions are normal) or pathological. Pathological causes can be divided into parasympathetic, tonic and sympathetic neurological causes and local (ocular) causes.

Parasympathetic palsy The innervation of the sphincter pupillae muscle which is responsible for constriction of the pupil (miosis) is by pre­ ganglionic parasympathetic axons in the oculomotor nerve with synapses in the ciliary ganglion. The fibres run on the superior border of the nerve within the subarachnoid space where they are vulnerable to compression by intracranial lesions, but their superficial location close to the pial blood vessels spares them from many vascular problems. In consequence, there are two types of lesion: a fixed dilated pupil (surgical) and a pupil-sparing IIIrd (medical).

Tonic (Adie) pupil This is a dilated pupil with light–near dissociation – the pupil fails to constrict in response to light but does so to accommodation (the near triad of miosis, accommodation and convergence). The lesion is in the ciliary ganglion and is thought to result from viral inflammation. The usual occurrence is in a young woman who presents with blurring of vision because of paresis of accommodation. Regeneration of the nerve results in the return of near vision, but the pupillary responses remain abnormal with a tonic (slow onset and prolonged duration) miosis, initially in response to near vision but which becomes permanent over a few years. The Holmes–Adie syndrome is the association of the tonic pupil with absence of deep tendon reflexes (e.g. knee jerks) which is seen in 60%.

Sympathetic palsy

Fig. 37.15  Right Horner’s syndrome: pupillary miosis and partial ptosis.

Horner’s syndrome is the triad of partial ptosis, miosis and anhidrosis resulting from a lesion in the sympathetic nervous system. The neuronal pathway originates with pre-ganglionic fibres in the hypothalamus, and then passes through the brainstem and spinal cord to exit in the anterior roots. They ascend in the sympathetic chain and synapse in the superior cervical ganglion. Post-ganglionic fibres pass from the ganglion into the cervical sympathetic chain and perivascular plexi, and thence to the orbit. Ptosis and miosis are seen in

Orbital pain Proptosis Epiphora Ptosis Anisocoria

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684  Ophthalmology in clinical surgery

all cases, whereas anhidrosis is absent with lesions affecting post-ganglionic fibres. Horner’s syndrome may be transient, as in neuralgic migraine/cluster headache where the neuronal plexus around the carotid artery is affected. Otherwise the lesion may be anywhere along the pathway described, and careful examination supplemented by imaging and pharmacological testing may be required to determine the cause. It is particularly important to examine the root of the neck for evidence of apical lung carcinoma (Pancoast’s syndrome).

Local causes Iris damage may result in an unreactive or poorly reactive pupil. Causes include trauma, uveitis and previous acute glaucoma. Pharmacological mydriasis is the commonest cause of an isolated unreactive pupil; usually the history is apparent, but unprescribed use of eye drops and accidental exposure to mydriatics (e.g. occupational) can also occur. Atropine, the longest-acting mydriatic, has a half-life of around 10 days.

THE RED EYE Red eye is an initially daunting matter when encountered in primary care or in the Emergency Department. Provided, however, that the main features of pain and visual symptoms are elicited, the most likely cause can be rapidly narrowed down as shown in Table 37.7 or, where features are suggestive of more serious disease, Box 37.1. Box 37.1 

Painless red eye with normal vision This can only be a subconjunctival haemorrhage (SCH), caused by the rupture of an episcleral vein and producing a bright red area over the sclera. Usually it is localised and the remaining conjunctiva can be seen to be normal; sometimes the bleed is more extensive, and swollen conjunctiva can prolapse through the palpebral fissure. SCHs may be caused by trauma, coughing and straining, clotting disorders or, rarely, hypertension. However, the great majority are spontaneous. Treatment is not required, and the discoloration fades over 1–2 weeks.

Uncomfortable red eye with normal vision Blepharitis This is a chronic inflammatory condition that affects the margins of the eyelid. It may be greasy (seborrhoeic) or crusting (staphylococcal), or a combination of both and can be associated with recurrent styes (Fig. 37.16). The complaint is of ocular discomfort, dryness and crusting of the lashes, most noticeable in the mornings. Conjunctival inflammation is mainly inferior from contact with the inflamed lower lid. The cornea may also become involved with a secondary conjunctivitis; more severe cases such as this are often seen in patients with acne rosacea. The main treatment is lid hygiene, with mechanical cleaning of the lid margin using a cotton bud dipped in a dilute solution of baby shampoo or bicarbonate of soda. Artificial tear drops may relieve the symptoms of dryness, and topical antibiotics are also often used initially to eliminate or reduce the load of staphylococci.

Features of the dangerous red eye

Symptoms n Severe pain n Photophobia n Loss of vision n Progression of symptoms Physical features n Reduced visual acuity n Unilateral n Intense injection High intraocular pressure n Corneal opacity, epithelial defect n Proptosis n Loss of red reflex At-risk individual n Neonate n Immunocompromise n Contact lenses

Table 37.7

Fig. 37.16  Acute infection of eyelash follicle (stye).

Causes of red eye Painless

Uncomfortable

Painful

Normal vision

Subconjunctival haemorrhage

Blepharitis Conjunctivitis Episcleritis

Reduced vision

None

Anterior uveitis Scleritis Keratitis (peri–peripheral) Anterior uveitis Posterior scleritis Central keratitis

Diseases with ophthalmic manifestations  685 Conjunctivitis This is a typical cause of ocular discomfort rather than pain which often begins in one eye but becomes bilateral within a few days. Discharge is an important feature: purulent or mucopurulent is typical in bacterial infection; mucopurulent in chlamydial; mucoid in allergic; and watery in viral (Fig. 37.17). In chlamydial and viral disease, there may be enlarged tender preauricular lymph nodes and conjunctival follicles, visible as small ‘rice grains’ in the inferior conjunctival fornices. Bacterial conjunctivitis  is commonly caused by Grampositive cocci, especially Staphylococcus aureus. Treatment is with a broad-spectrum topical antibiotic (e.g. chloramphenicol). Swabs are only required if the infection has not resolved within a week of effective treatment or if the condition is initially severe. Viral conjunctivitis  does not need treatment other than explanation and reassurance because the majority are mild and self-limiting. Adenovirus infection may be more severe, and the small proportion that develop keratitis (with visual disturbance and increased pain) require referral for specialist management. Chlamydial infection  is most commonly a sexually trans­ mitted disease in young adults and may be chronic and unilateral. Referral to an ophthalmologist is required for confirmation of the diagnosis. The genitourinary physician is also involved, in order to screen for sexual contacts for Chlamydia and other sexually transmitted diseases. Treatment includes topical and systemic tetracyclines.

Episcleritis See above.

Painful red eyes Scleritis, keratitis and uveitis are all possible causes of a painful red eye, and they are discussed above in the sections on visual loss, floaters and ocular pain.

DISEASES WITH OPHTHALMIC MANIFESTATIONS Acquired immune deficiency disease (AIDS) AIDS has a number of ophthalmic manifestations which include primary effects, opportunistic infections and tumours. Only the most important and common are described here. The high incidence of such conditions requires a low threshold for referral for specialist assessment.

Primary effects The HIV virus has a direct effect on the retinal vasculature, causing cotton wool spots and microaneurysms that are very similar to those seen in background diabetic retinopathy. The lesions are asymptomatic and resolve spontaneously, and treatment is not required.

Secondary infections Viral infections

Cytomegalovirus  is the major sight-threatening disease in HIV infection and is one of the defining illnesses of AIDS, rarely seen when the CD4 T-cell count is greater than 50 cells/µL. It occurs in approximately 30% of those with AIDS. The virus causes retinitis with white areas of retinal necrosis and often extensive retinal haemorrhages (the pizza-pie appearance). Vision is lost as a result of direct retinal destruction, secondary retinal detachment and optic nerve involvement. Treatment initially involves intravenous antiviral agents (ganciclovir is the current first-line agent), with long-term prophylaxis against relapses using intravenous oral or intraocular antivirals. The recent introduction of protease inhibitors as part of antiretroviral therapy (ART) has allowed lymphocyte counts to rise in some patients such that long-term prophylaxis can be safely stopped. Herpes simplex and varicella zoster  viruses may both cause acute fulminating retinitis with a very high incidence of visual loss.

Bacterial infections Staphylococcal blepharitis.  This is common in those with HIV (see also ‘Red eye’). Mycobacteria.  Tuberculous choroiditis may occur in isolation or with signs of disease elsewhere. Syphilis  has an increased frequency in AIDS because of both the impaired immunity and the common means of transmission. Uveitis is the most common manifestation.

Fungal infections Candida albicans  causes a severe uveitis. It is seen most often in intravenous drug abusers who use unsterilised needles (see Ch. 9).

Fig. 37.17  Viral conjunctivitis. The lids are swollen, the eyes are watering, red and uncomfortable.

Cryptococcus neoformans  can cause choroiditis in patients with cryptococcal meningitis.

The red eye Diseases with ophthalmic manifestations

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686  Ophthalmology in clinical surgery

Protozoal infections Toxoplasmosis.  In the immunocompromised, the condition differs from that in the healthy population by being acquired rather than congenital. Creamy white patches on the retina indicate active retinitis and cause visual loss by direct retinal damage. Systemic anti-protozoals are required to control the initial infection and are continued at a lower maintenance dose for life.

Tumours

a bull’s eye maculopathy which results in irreversible loss of visual acuity. The risk of this complication is much higher with chloroquine than with hydroxychloroquine and is doserelated. Typical dosage regimens of hydroxychloroquine are very unlikely to cause problems within 5 years of beginning the drug. Patients starting on these drugs have a baseline examination by the ophthalmologist and are then warned to stop the drug and seek ophthalmic advice should they subsequently develop visual symptoms or detect a scotoma when viewing an Amsler chart.

Kaposi sarcoma This is commonly seen on the eyelids or conjunctiva of AIDS patients and is a defining disease. It forms a dark red (or purple) firm mass which may be flat or elevated. In the conjunctiva it may resemble a subconjunctival haemorrhage and must be considered as a possible diagnosis for any such lesion, especially in the young, if persistent for more than 2 weeks.

Rheumatoid arthritis (RA)

Giant-cell arteritis (GCA) This multisystem disorder results in inflammation of mediumsized arteries with an internal elastic lamina. The terms ‘temporal’ and ‘cranial’ arteritis refer to the high incidence of involvement of the arteries of the head; systemic disease results in polymyalgia rheumatica. GCA is a disease of the elderly and is very rarely seen in those less than 50 years old.

Keratoconjunctivitis sicca

Clinical features

This is an example of secondary Sjögren’s syndrome, with autoimmune destruction of the lacrimal gland, which leads to dry eye symptoms and corneal damage. The symptoms are distressing and often difficult to control. The mainstay of treatment is ocular lubrication with artificial tears and ointments.

Symptoms

Scleritis and keratitis

Physical findings

Scleritis  in rheumatoid arthritis may be acute with a painful red eye and requires urgent referral to an ophthalmologist. More commonly it is chronic, without overt inflammation, eventual scleral thinning and exposure of the underlying uvea (scleromalacia perforans) which renders the eye vulnerable to minor trauma. There is no treatment for scleromalacia. Keratitis  may be painful, with a corneal opacity and conjunctival injection, or a painless non-inflammatory corneal melt which can result in corneal perforation. Again, urgent referral is required.

Iatrogenic disease Long-term steroid treatment (10 mg/day for more than a year) in rheumatoid arthritis commonly results in cataract.

Systemic lupus erythematosus Systemic lupus erythematosus (SLE), like RA, may be associated with secondary Sjögren’s syndrome. Small-vessel vasculitis may present as scleritis, corneal melt, retinal vasculitis or optic nerve infarction. Involvement of the retina or optic nerve implies central nervous system disease, which is a poor prognostic sign. Specialist management, with close liaison between ophthalmologist and rheumatologist, is required.

Iatrogenic disease Steroids are commonly used in SLE and, as with RA, may cause cataract. Chloroquine and hydroxychloroquine are used, particularly in the control of skin rashes, and can cause

The patient experiences temporal headache, scalp tenderness (even necrosis) and jaw and tongue claudication. General malaise is usual, and muscle stiffness and pain may be present. Visual loss is a late event but can be of sudden onset.

There are often no signs to support the diagnosis. Scalp tenderness on the side of the headache may be present. The ipsilateral superficial temporal artery just in front of the ear may be enlarged, tortuous, tender and non-pulsatile.

Investigation The erythrocyte sedimentation rate must be measured urgently. In GCA it is always elevated. Temporal artery biopsy is usually done to confirm the diagnosis; the histological findings are unaffected by up to a week of steroid treatment, so that treatment of suspected GCA must not be delayed until biopsy can be done.

Management Hospital admission is usual. Prednisolone 1 mg/kg per day is started orally immediately. If visual loss has occurred or appears imminent (‘stuttering amaurosis’), then a loading dose of intravenous hydrocortisone or methylprednisolone may be given. The dose is then gradually reduced according to the clinical response. The majority feel subjectively much better after 48 hours of treatment. Steroid therapy is continued at a low dose for around 2 years depending on ESR results.

Systemic candidiasis Candida albicans is a yeast-like organism commonly present as a commensal in the healthy gastrointestinal tract. Candidiasis only becomes an ophthalmic problem in immunocompromised patients (e.g. immunosuppressive

Diseases with ophthalmic manifestations  687 drugs, haematological malignancy and AIDS) or if the organism is directly introduced into the bloodstream by non-sterile i.v. drug abuse or the presence of indwelling catheters (especially hyperalimentation following bowel surgery).

Clinical features Blurring of vision and floaters are the main symptoms of candidal endophthalmitis, i.e. infective inflammation of the internal eye, including the vitreous gel. Pain with a red eye is less common. Vitreous inflammation may obscure the fundus; when it can be seen, there are usually elevated white chorioretinal lesions. The vitritis is frequently organised into localised masses – the string of pearls. In the minority who has associated anterior uveitis, there is ciliary injection and clouding of the anterior chamber.

Investigation and management Blood cultures for candidaemia and appropriate investigations to assess immunocompromise are required. Ocular investigation involves anterior chamber and vitreous sampling. Treatment is with vitrectomy and intravitreal and systemic antifungal agents.

Embolic disease Emboli which affect the visual system are most commonly thromboemboli and arise from the carotid vessels in the neck. Emboli may result in transient visual loss (transient ischaemic attack), sudden permanent visual loss (retinal artery occlusion) or visual field loss (cerebrovascular disease) (see common symptoms above and Ch. 29).

Graves’ disease This is an autoimmune disorder characterised by the production of thyroid-stimulating immunoglobulins (TSIs) that cause thyrotoxicosis (Ch. 32). Orbital inflammation – dysthyroid eye disease or thyroid ophthalmopathy – is associated. The orbital condition may occasionally be seen in those who are both clinically and biochemically euthyroid.

Physical findings In acute disease the conjunctiva are injected, particularly over the insertions of the horizontal recti muscles at 3 and 6 o’clock. There may be chemosis and swelling of the lids. Orbital inflammation increases the volume of the orbit which pushes the globes forwards and can lead to exposure of the cornea; downward movement of the upper eyelids may be restricted so that the sclera above the superior limbus becomes visible. This is most obvious in changing from up-gaze to down-gaze – lid lag. Lid retraction contributes to the staring look and to corneal exposure (Fig. 37.18). Nerve compression may reduce visual acuity, impair colour vision and cause a relative afferent pupillary defect. In the later stages, inflammation is replaced by fibrosis which restricts ocular movements. Any direction of squint may occur, but most commonly the limitations are in up-gaze and lateral gaze.

Management Management of the thyroid state is necessary (Ch. 32). In mild thyroid eye disease, treatment may not be needed. Artificial tears may be necessary to ease the ocular discomfort from corneal exposure. In more severe disease, immunosuppression with systemic corticosteroids or orbital irradiation may be nec­ essary. Surgical interventions include orbital decompression, strabismus correction and methods of lowering the retracted lids.

Multiple sclerosis This is an autoimmune disorder characterised by demyelinating inflammation within the central nervous system, with recurrent attacks in different locations. Ophthalmic presentations are common and include: n

Optic and retrobulbar neuritis. This is the most common ophthalmic complication, with around 70% having evidence of previous attacks. Optic neuritis may occur in isolation, but at least 50% of women and 25% of men with optic neuritis go on to develop MS. The

Pathological features Soft-tissue inflammation in and around the orbits may produce exophthalmos. If severe, the orbital contents, including the optic nerve, may be compressed and vision is lost. After 1–2 years, the acute inflammation tends to subside, leaving residual chronic fibrotic changes in the orbit and ocular muscles.

Clinical features Symptoms In the acute phase, sore red eyes are common. A ‘staring eyes’ appearance may cause self-embarrassment. When the condition is severe, reduced vision may be noted and, rarely, diplopia. If the condition reaches a chronic phase, diplopia and the poor appearance of exophthalmos and lid retraction are the main complaints.

Fig. 37.18  Dysthyroid eye disease, with exophthalmos and strabismus.

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688  Ophthalmology in clinical surgery

clinical features are described under ‘Loss of visual acuity’. n Ocular motility disorders. MS may affect individual nerves to cause paretic strabismus. Brainstem lesions of the medial longitudinal fasciculus cause internuclear ophthalmoplegia (INO – commonly bilateral) which affects horizontal gaze away from the side of the lesion so that the eye ipsilateral to the lesion fails to adduct across the midline, while the contralateral eye exhibits nystagmus. n Visual field defects. These are rarely seen but they are the result of a large demyelinating plaque which affects the optic radiations.

Fig. 37.19  Proliferative diabetic retinopathy, with new

Hypertension Hypertension can cause retinopathy, choroidopathy and optic neuropathy. The changes are most marked in the accelerated hypertension of pre-eclampsia or so-called malignant hypertension. The pathological changes in the eye are usually the consequence of ischaemia with tissue infarction or exudation from a compromised vascular endothelium. Retinopathy can be graded by the severity and duration of disease. In chronic disease (arteriosclerosis): n

Grade 1 – Grade 2 – n Grade 3 – crossings n Grade 4 – reflex and n

increased arteriolar light reflex deflection of veins at arteriovenous crossings arteriolar narrowing (nipping) at arteriovenous silver wiring of arterioles (increased light tortuosity of vessels).

In acute disease: n

Grade 1 – generalised arteriolar attenuation Grade 2 – focal arteriolar attenuation and deflection of veins at arteriovenous crossings n Grade 3 – hard exudates, flame-shaped haemorrhages and cotton wool spots with arteriolar narrowing (nipping) at arteriovenous crossings n Grade 4 – grade 3 changes plus silver wiring of arterioles and swelling of the optic disc.

vessels growing from the nasal side of the optic disc.

retinopathy, therefore all diabetic patients should be screened for retinopathy. Screening should begin 5 years from diagnosis or at 12 years of age (whichever is the later) in Type I diabetes and at diagnosis in Type II disease. Advanced diabetic eye disease is managed with vitreoretinal surgery and urgent referral is indicated.

Sarcoidosis The eye is (after the lungs and lymph nodes) the most common organ to be affected (20–30%) by this condition. Uveitis is the most common manifestation, and granulomatous inflammation can involve the retina and choroid to cause blindness. When this occurs there is a 30% incidence of central nervous system involvement. Granulomas can also affect the eyelid, conjunctiva and the lacrimal gland.

n

Grade 4 acute retinopathy is usually associated with encephalopathy and requires immediate referral for medical assessment. The fundal changes usually regress after the raised blood pressure has been corrected.

Diabetes Diabetic retinopathy is a potentially blinding disease and is the leading cause of registration for blindness in the working age population in the UK. It can occur in both Type I and Type II diabetes. Visual loss can occur as a result of macular damage (oedema or ischaemia), vitreous haemorrhage or retinal detachment. The latter two conditions result from proliferative retinopathy (Fig. 37.19) in which retinal ischaemia leads to abnormal neovascularisation. The incidence of retinopathy increases with duration of disease and is reduced by tight control of blood sugar and blood pressure. Argon laser treatment is effective in preventing visual loss from

Stevens–Johnson syndrome (erythema multiforme major) This is an acute, generally self-limiting mucocutaneous vesiculobullous disease which tends to affect young healthy individuals. It involves the conjunctiva in 90%, causing mucopurulent conjunctivitis. Lid scarring may follow and lead to misdirection of the eyelashes with corneal damage. In the acute phase, assessment by an ophthalmologist is necessary. Systemic treatment is generally with steroids.

Sickle cell disease Eye disease in the sickle haemoglobinopathies occurs in the SC and S-Thal forms but rarely in the SS form. The abnormal red blood cells cause vascular obstruction and infarction. The resulting ischaemia may lead to proliferation of abnormal new blood vessels, which may bleed to cause vitreous and retinal haemorrhages and retinal detachment. Once proliferative retinopathy has developed, there is a 3.4% 8-year incidence of visual loss, although the disease may be self-limiting. Most of the retinal changes occur in the retinal periphery, beyond the field of view of a direct ophthalmoscope. The disease is self-limiting but laser photocoagulation or vitreoretinal surgery is occasionally required.

Diseases with ophthalmic manifestations  689

Wegener’s granulomatosis This disease is characterised by necrotising granulomas of the upper respiratory tract. The eye can be affected by keratoconjunctivitis sicca, scleritis, corneal melt and orbital involvement. Treatment is by systemic immunosuppression, e.g. cyclophosphamide.

FURTHER READING Kanski J J, Bowling B 2011 Clinical ophthalmology: a systematic approach, 7th edn. Butterworth-Heinemann, Edinburgh Figures 37.2–37.19 are the copyright of St Mary’s Hospital, Imperial College Healthcare NHS Trust, London, UK

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38 

Principles of plastic surgery

Plastic surgery techniques Spontaneous wound healing Adjuncts to spontaneous wound healing Direct surgical wound closure Skin grafts Other types of graft materials Prostheses

691 692 692 692 694 696 696

Derived from the Greek ‘plastikos’ meaning to mould or to give shape the specialty of plastic surgery is perhaps more accurately described as one of reconstructive surgery. The lay person’s perception of plastic surgery is one of cosmetic surgery which represents merely a facet of the specialty, though aesthetic goals along with restoration of form and function underpin the basic principles of the specialty. Unlike other surgical specialties there is no specific territory of the body which is the monopoly of plastic surgery. Although a degree of subspecialisation has developed recently the plastic surgeon might be regarded as the last of the general surgeons in treating a great variety of problems in many sites (although in general, body cavities are excluded) by means of specialised ‘plastic surgery techniques’. Some of these techniques have been in use for many years – there are records of reconstructions of the nose with forehead flaps from India dating back 3000 years. The specialty only developed independently in the last 75 years, triggered specifically by mutilations from trench warfare in the First World War, although the increased mechanisation and high-speed travel of the 20th century have maintained the need for soft-tissue reconstruction. The demands on the specialty have been even greater as a result of the changing behaviour patterns and fashions of society. There has been a dramatic increase in sun-induced skin damage, including skin cancer, as a result of the burgeoning package holiday trade and the belief that a suntan is attractive. With greater emphasis on the merits of an improved physical appearance, the demand for aesthetic plastic surgery has also soared. The definition of plastic surgery from the Union Européenne de Médecins Spécialistes (UEMS) within the EU has therefore recently been modified as ‘surgery intended to restore form and function and to promote well being’. To simplify: the aetiology of defects requiring reconstruction are congenital or acquired, the acquired being either traumatic, degenerative or following tumour excision. Such defects may arise as a result of many different causes in sites all over the body, leading to considerable clinical overlap

Flaps Free tissue transfer Tissue expansion Ablative techniques Other reconstructive problems Aesthetic plastic or cosmetic surgery

697 697 698 698 698 702

whereby the plastic surgeon is the member of a team. But while plastic surgery may often be associated with sophisticated reconstructions, the plastic surgeon also manages the commonest tumours of infancy (vascular hamartomata), the commonest form of cancer (skin cancer), the commonest cause of admission to an emergency department (hand and soft-tissue injuries) and the commonest cause of prolonged morbidity in the elderly (chronic wounds and decubitus ulcers). Examples of types of problems involving the plastic surgeon are shown in Table 38.1. In practical terms, the commonest reconstruction required is the repair of a breach in the skin or a mucosal surface. However, the defect may extend deeper and involve other structures such as muscle, nerve, tendon and bone, and, where possible, these too will need to be corrected to enable full return of function.

PLASTIC SURGERY TECHNIQUES There has been an escalation of surgical technology in the last two decades, supported by advances in anaesthetic and monitoring techniques which have allowed a greater range of reconstructive options. Furthermore, development in instrument technology, including fibreoptics and microsurgery, has increased surgical safety and reliability. However, regardless of the rich choices available, the surgeon should opt for the simplest and safest surgery in the first instance, turning to more complex and potenti­ ally more hazardous procedures only when the simpler methods do not meet the reconstructive and occasionally aesthetic requirements. It is therefore helpful to have a mental picture of a ladder of surgical options (Fig. 38.1a), although recent developments have resulted in so many offshoots that the resulting plan resembles more closely a tree (Fig. 38.1b).

38 

692  Principles of plastic surgery Table 38.1

Types of problems involving the plastic surgeon

Aetiology of defect

Example

Congenital abnormality

Cleft lip and palate Congenital hand anomalies Lower limb soft-tissue loss Hand injury Extensive skin loss Skin cancer Intra-oral cancer excision and reconstruction Breast reconstruction following mastectomy Rheumatoid hand deformities

Trauma Burns Neoplasia

Degenerative processes

Highest risk

Complex Free flap

Regional flap

Local flap

Skin graft Primary closure

SPONTANEOUS WOUND HEALING Wound healing is a natural and spontaneous phenomenon which occurs irrespective of (and sometimes despite) the surgeon. Although the basic events of blood clotting, fibrin deposition, organisation and collagen synthesis have been observed for many years, the factors which initiate and control these processes are incompletely understood. The pattern of wound healing may be affected by sophisticated endocrine, pharmacological and physical manipulation, or simply by surgery, but the most important influence on open wounds is the nature in which they are dressed. Numerous dressings and topical agents are commercially available, sometimes making extravagant and unproven claims, but there is no evidence that any available dressings accelerate wound healing. They simply provide the optimal environment in which a wound can re-epithelialise. With this in mind, one should select well-tried and tested dressings which should also have the properties of being cheap and painless to apply and remove (Fig. 38.2). Some wounds will heal completely without surgical intervention. These not only include small wounds but also some large cavernous wounds as might be produced by abscess drainage or excision of a pilonidal sinus. Such wounds may be too heavily contaminated for surgical closure and often contract down surprisingly quickly, particularly if subjected to a negative pressure. When a wound fails to heal, adverse factors relating to the wound (local factors; Box 8.1) or to the patient (systemic factors; Box 8.2) need to be identified and, if possible, addressed. This is particularly true of chronic wounds if, following thorough debridement, healing is to be achieved.

ADJUNCTS TO SPONTANEOUS   WOUND HEALING Hyperbaric oxygen Improving tissue oxygen levels by intermittent inhalation of 100% oxygen in a hyperbaric chamber at pressures greater than at sea level (usually 2.2–2.4 atmospheres absolute) can be useful particularly in the treatment of chronic wounds. The positive effects on healing are observed at a cellular level such as enhanced fibroblast proliferation and collagen formation, improved microbial killing and neoangiogenesis.

Lowest risk

Simple

Secondary intention healing

The reconstructive ladder

Fig. 38.1a  The reconstructive ladder.

The practicalities of such treatment limits its widespread application.

VAC therapy Vacuum Assisted Closure (VAC®) therapy; KCI USA, San Antonio, TX) involves application of continuous or intermittent negative pressure to a wound through a non-adherent foam dressing via a closed system. Wound healing is assisted by reduction in bacterial load and interstitial fluid with improved angiogenesis and formation of granulation tissue. Suitable for large, deep wounds, it enables improved wound management and can occasionally convert a non-graftable bed into one that will accept a graft.

DIRECT SURGICAL WOUND CLOSURE The first choice for wound repair is direct closure by suture, a standard and common surgical procedure but one deserving attention to detail to enable the best possible scar. The wound should first be converted to an ellipse whose long axis lies in the same line as the local skin creases and perpendicular to the underlying muscle (failure to do so is likely to produce unsightly dog ears). The wound is sutured so that the edges are exactly matched and slightly everted while reducing any crushing damage of the tissues with the help of fine-toothed forceps or skin hooks. Tension and haematoma must be avoided at all costs by means of meticulous haemostasis and the support of buried intradermal sutures and adhesive tapes. However, the quality of the final scar is determined by the individual’s own wound-healing properties. It is unfortunate that a vigorous scar formation is not in the interests of a good cosmetic result. In some patients the normal equilibrium between collagen synthesis

Plastic surgery techniques  693

Skin

Plastic surgery techniques

Myocutaneous Muscle only With bone

Axial

Spontaneous wound healing Adjuncts to spontaneous wound healing

With nerve

Direct surgical wound closure

Free flaps Other

Fasciocutaneous

Breast

Myocutaneous

In situ Tissue expansion

Random pattern skin

Scalp

Ear

Other Stainless steel

Flap transfer Tendon rod

Vanadium

Titanium Tendon

Breast

Joint

Metals Silicones

Nerve

Bone

Osseo- Cartilage integrated Fat

Acrylic Fascia Flaps Synthetics

Direct wound closure

FullSplit- thickness thickness skin skin

Skin culture

Grafts

Argon

Hyperbaric oxygen

Dressings Lasers

Conservative treatment of wounds

Ablative techniques

Keratinocyte sheet

Composite skin substitute

Tunable dye

Ruby CO2 Dermabrasion Shave

Chemical peel Vacuum therapy

Fig. 38.1b Tree of reconstruction.

38 

694  Principles of plastic surgery Wound type Open

Sutured

Slough present

Infected

Clean

Remove sutures

Maintain sterility until physiologically sealed Dry gauze

Slough absent

Surgical debridement

Remove residual slough with dressings Dry eschar

Deslough mechanically 2 x day cotton gauze soaked with normal saline OR Rehydrate to promote autolysis Hydrogel dressing

Excess exudate

Reduce with alginate

Foul odour

Reduce with charcoal dressing Actisorb

Deep cavity

Vacuum Assisted Closure

Wound at risk of Gram -ve organisms (burns) including Pseudomonas

Silver sulfadiazine

Minimal granulation

Encourage bleeding: e.g. hypertonic saline

Normal wound activity

Alginate mesh dressing Paraffin gauze (may cause granulomas) Agents betadine or chlorhexidine (safest topical agents)

Excess granulation

Tri-Adcortyl ointment (not in children)

Fig. 38.2  Algorithmic flow chart showing choice and examples of dressings in different situations.

Table 38.2

Treatment of unsatisfactory scars

Treatment

Undesirable features of normal scars

Hypertrophic scars

Keloid scars

Pigmented scars

Stretch scars

Surgical revision Topical or intralesional Steroid Dermabrasion Injectable tissue filler External pressure with or without Silastic sheet Low-dose radiotherapy Cosmetic camouflage

Yes Rarely Yes Yes No No Yes

Yes Yes No No Yes No Yes

Very rarely Yes No No Yes Yes No

Yes No Yes No No No Yes

Yes No No Yes No No Yes

and degradation is disturbed. Instead of scar maturation occurring over a 12-month period, collagen may be produced in excess, resulting in a red, lumpy, hypertrophic scar. If there is extension into surrounding tissues a true keloid will result. The management of abnormal scarring following trauma or surgery is not entirely satisfactory, but the means available are charted (Table 38.2).

SKIN GRAFTS If a wound is too wide to be closed directly, grafting is the simplest method of repair. A skin graft is a sheet of skin harvested from elsewhere in the body and comprising either its epidermis and superficial dermis (split-thickness graft) or its entire thickness (full-thickness graft). The graft is

Plastic surgery techniques  695 Skin grafts

Good

Poor Nil Necrotic tissue

Denuded Cancellous Granulation Muscle cartilage bone tissue Fascia & cortical Paratendon Fat bone Periosteum Dermis

Fig. 38.3  Suitability of tissues to receive split skin grafts. completely detached from the body and, when applied to the wound, depends entirely on the underlying vascular bed for its nutrition by diffusion of metabolites for a few days before its revascularisation by the ingrowth of blood vessels. A skin graft will therefore only ‘take’ if applied to wounds which can supply the necessary environment. Graft loss can occur for several reasons: namely, haematoma beneath the graft (minimised by cutting slots [fenestrations] into the graft), infection, inadequate immobilisation of the graft to its bed permitting shear, positioning the graft on an unsuitable bed incapable of nourishing the graft (necrotic tissue, bare endochondral bone [without periosteum]), bare cartilage (without perichondrium), bare tendon (without paratenon), or technical error (placing the graft upside down!) The spectrum of ability of different tissues to receive a graft is shown in Figure 38.3. Most wounds older than 48 hours will be covered by granulation tissue, whose vascularity will be related to that of the underlying tissue.

a

b

Split-thickness skin grafts Split-thickness skin grafts are taken with either hand-held graft knives or by powered dermatomes, both of which cut the superficial layers of the skin 150–300 µm thick (Fig. 38.4). As a large number of epithelial remnants are left behind at the donor site, these will, in the same manner as a bad graze, heal within 2 weeks, provided they are kept free from infection. ‘Take’ also depends on stability of the graft. Shearing forces which disrupt ingrowing capillary loops must be avoided by immobilising the skin graft with the help of a tieover dressing or by sutures, staples or cyanoacrylate glue. This dressing is normally left intact for a period of 3–5 days to allow vascular ingrowth of the graft before it is inspected. Large areas of skin can thus be harvested, but as donor sites often heal with some alteration of pigmentation and occasionally with hypertrophic scars, the sites chosen should

Fig. 38.4  Harvesting a split-thickness skin graft.

be inconspicuous, such as the inner thigh or buttock. In the elderly who may have an attenuated dermis, the healing of these donor sites may be considerably delayed. The most acceptable donor site dressing is an alginate mesh, which should be left undisturbed for at least 10 days. The graft

38 

696  Principles of plastic surgery

donor site heals by re-epithelialisation from remnants of epithelium left in the donor site. The same donor site can be reused to supply further split skin graft providing sufficient dermis remains. The main disadvantage of split skin is that the final appearance is of a patch of unsightly scarring. Also, the wound continues to contract after graft application, which may lead to disabling contractures across joints and softtissue distortion of facial features. Although thin grafts take well, the thinner the graft the more aggressive the contracture. Given the limited donor sites available for resurfacing extensive defects (like major burns) and the potential morbidity of donor sites, the introduction of the graft mesher proved to be a bonus. The machine cuts slots into the split skin, which enables the graft to be stretched out like a string vest, thereby increasing the area of the original graft. The diamond-shaped slots permit any blood or serum to escape (which might otherwise lift the graft away from its bed), thus reducing the chance of graft failure. Once the graft has taken, each hole heals by secondary intention. However, the disadvantage is that the healed area is like a cobbled surface, implying that it is best suited to inconspicuous recipient beds. At best, split-thickness grafts must be regarded as ‘hole fillers’ for the repair of large skin defects.

Full-thickness skin grafts For smaller wounds in conspicuous areas, over joints or where scar contracture has produced deformity, a fullthickness graft is preferable. Although ‘take’ of these grafts is less predictable due to the greater volume of tissue requiring nourishment from the graft bed, they retain their original texture with little scarring and contracture, and are particularly suited to the face. However, the colour and texture of the standard postauricular graft is not ideal for all facial areas, and one should consider other donor sites such as redundant upper-eyelid skin, preauricular and supraclavicular skin to achieve optimum facial skin matching.

Cultured skin and skin substitutes Although not in common usage, there has been considerable clinical experience in the culture of keratinocytes isolated by trypsin from a small split skin graft. These are allowed to proliferate into large sheets of cells on a substrate of fibro­ blasts. However, such ultrathin layers of cells when applied as a graft are not sufficiently robust to withstand wear and tear and are subject to high infection rates with subsequent graft loss. These cultured epithelial autografts are seldom used alone for coverage. The fundamental problem is that replacement of epidermis alone (e.g. CEA) is insufficient for full-thickness defects and that the complex dermal structure cannot regenerate and be cultured in the same way. This has encouraged development of a wide range of skin substitutes for epidermal and dermal reconstruction that are employed particularly in the burns setting where large areas of skin loss require resurfacing. Some products contain specific growth factors designed to assist healing of chronic wounds:

– Biobrane® (Dow Hickman/Bertek Pharmaceuticals, Sugar Land, Texas, USA) – a Silastic sheet with nylon mesh seeded with porcine collagen and used principally for superficial partial-thickness skin loss. – Transcyte® (Advanced Tissue Sciences, Inc., La Jolla, California, USA) – silicone sheet on collagen-coated nylon mesh seeded with neonatal fibroblasts. – Integra (Integra Life Sciences, Plainsboro, New Jersey, USA) – a bilaminar sheet of bovine collagen and shark chondroitin 6-sulphate neodermis with an overlying Silastic sheet which is removed and replaced with thin split autograft following revascularisation of the neodermis at 3 weeks. – AlloDerm® (LifeCell, Woodlands, Texas, USA) – acellular cadaveric dermis requiring coverage with thin split autograft. The next logical step has been the development of a composite skin substitute which not only has an epithelial surface but also a tough adherent dermal layer, which raises the possibility of ‘off the shelf’ banks of skin.

OTHER TYPES OF GRAFT MATERIALS Other tissues available as free grafts for deep tissue defects, contour defects and functional restoration include bone, cartilage, nerve, tendon and fat. Bone is usually harvested from the ilium or rib and cartilage from the ear concha or the rib. For bridging gaps in nerves, a cutaneous nerve such as the sural nerve may be sacrificed, and for tendon reconstruction vestigial tendons such as palmaris longus and plantaris are used (fascia lata is a reasonable substitute in their absence). Other tissues such as muscle are used only occasionally as their survival is unpredictable. Fat harvested from any area of abundance can be reinjected to treat small to moderate contour defects. Autografts are preferable (in spite of potential problems at the donor site) on account of their more reliable long-term incorporation. Heterografts and xenografts have the disadvantages of the added expense of denaturing for the sake of reducing antigenicity, while also carrying the higher risk of infection and progressive absorption.

PROSTHESES Not only has an enormous range of implantable devices been designed in the last 20 years but also improvements in their composition has rendered them safer, with a lower implant failure rate. Silicone, the most commonly used implant material, is a polymer of silica and oxygen that can take on different physical characteristics from a thin oil to a hard block depending on its degree of polymerisation. It is relatively inert but after implantation, such as in a breast prosthesis or small joint replacement, is characteristically enveloped in a capsule of fibrous tissue of variable thickness lined with smooth meso­ thelium. An abnormally thick capsule may distort a breast prosthesis and, as yet, this phenomenon is unable to be predicted or prevented. Other materials used as a bone substitute, either to restore contour such as following loss of the calvarium or for skeletal replacement, include acrylic bone cement and (more

Plastic surgery techniques  697 commonly) metal such as stainless steel, chrome cobalt and titanium. The recent discovery that bone will produce a very tight bond on a molecular level with titanium even when the latter extends through skin or mucosa has generated ‘osseointegrated’ implants as studs on which artificial teeth and, more recently, external facial prostheses, such as a nose or ear, can be securely attached.

FLAPS Where a skin graft is impossible or a more durable construct is necessary, or indeed when aesthetics dictate, a defect should be resurfaced with a flap. A flap is a block of tissue which retains an attachment to the body, known as a pedicle, through which it receives its blood supply and innervation as required. An encyclopaedia of flaps have been described according to how they are moved, how they are composed and (of far greater importance) how they are vascularised. The earliest flaps were simply skin and subcutaneous fat designed without appreciation of the underlying blood supply (random pattern flaps), so that their length and mobility were restricted. More reliable and predictable flaps arose from understanding that the skin obtains its blood supply from three main sources: via direct cutaneous arteries, via perforating vessels of underlying muscles and via tributaries of the vascular plexus within the underlying deep fascia and fascial septa. This has led to the development of three different types of flap (Fig. 38.5). n

Axial pattern flaps have a known cutaneous artery which is included by orientating the flap in the same axis as the vessel, thereby enabling a long and versatile flap. The best-known example is the groin flap which has its base over the femoral vessels in the groin and extends laterally following the course of the superficial circumflex iliac artery. n Fasciocutaneous flaps are similar to skin flaps but also include deep fascia. These are normally used in the limb where there is a very definite layer of well-vascularised

deep fascia which permit a surviving length two to three times the length of the corresponding skin flap. n Muscle flaps usually include a polarised blood supply so that the axis of movement can only be at the site of axial arteriovenous penetration. Muscle flaps alone will require epithelial cover in the form of a skin graft; however, when the muscle is superficial it is possible to include the overlying skin as a ‘composite myocutaneous’ flap. Until a flap is incorporated within the defect, it needs to be nourished by an intact pedicle even if it bridges across intact skin. After this time the pedicle may be detached and discarded or returned to its original site. It follows that these flaps can only be transferred locally, although it is possible to transport them to distant sites by a series of staged and unreliable operations involving their inset into a ‘carrier’ such as the wrist. Flaps require a warm, tension-free environment until they become well healed. This requires observation to monitor satisfactory perfusion and freedom from haematoma.

FREE TISSUE TRANSFER As a result of advances in microsurgery, blood vessels as small as 1 mm can be successfully anastomosed. Thus, a new era of single-stage distant flap reconstruction became possible in which the flap is completely detached and its axial vessel is anastomosed to recipient vessels near the defect. Furthermore, this surgical technology obviates the need for multistaged procedures involving long inpatient stays. These ‘free flaps’ permit sophisticated reconstructions in either emergency or elective circumstances. The stages are as follows: 1. Elevation of the flap, islanding it on the vascular pedicle. 2. Preparation of the recipient bed and isolation of healthy recipient vessels (ideally performed by a second team of surgeons).

Deep fascia

Pedicle Random pattern flap

Muscle flap with skin graft

Fig. 38.5  The different types of flap.

Axial pattern flap

Fasciocutaneous flap

Myocutaneous flap

Exposed muscle

Other types of graft materials Prostheses Flaps Free tissue transfer

38 

698  Principles of plastic surgery

3. Detachment of the flap followed by anastomosis of donor to recipient vessels. 4. Inset of flap and closure of donor site. In the hands of an experienced microsurgeon supported by skilled anaesthesia (controlled, high peripheral perfusion is the key), a patency rate of 95% can be expected. Similar techniques are used in the reattachment of any traumatically amputated parts which must be brought swiftly to hospital, preferably cooled in a plastic bag lying within a second plastic bag filled with ice. If the vessels of the part and the recipient site are sufficiently healthy, one can safely proceed to replantation and revascularisation using an intervening vein graft, if necessary, to avoid any anastomotic tension.

Perforator flaps In order to limit the adverse effects of flap harvest (donor site morbidity), e.g. loss of one rectus abdominis muscle used in a TRAM (transverse rectus abdominis myocutaneous) flap, recent techniques have focused on sparing muscle by raising a block of tissue supplied by vessel branches that perforate the muscle and dissecting these ‘perforators’ back to the main pedicle. In the TRAM flap example, one or two perforators from the deep inferior epigastric artery are dissected from the main artery through the rectus abdominis muscle to the overlying abdominal integument (deep inferior epigastric perforator, or DIEP, flap). Many such perforator flaps have been described and their role within reconstructive surgery is becoming clearer.

TISSUE EXPANSION A tissue expander (which consists of an empty silicone balloon connected by a tube to a filler valve) is implanted subcutaneously adjacent to a defect at an initial operation. Over a period of weeks or months the expander is then inflated by serially injecting saline percutaneously into the filler valve, thereby distending the overlying skin. When enough skin has been generated the expander is removed and the surplus skin used for reconstruction. The great advantage is that the skin adjacent to the defect is most likely to match that of the area to be reconstructed, providing a good aesthetic match. This is particularly important in certain areas where the skin has very specific properties, such as the hair-bearing scalp. The method appears to be seductive in its simplicity, but in practice there is a 30–40% complication rate including infection, erosion of skin and extrusion. However, tissue expansion still has a place, particularly in breast reconstruction, and it is the treatment of choice in the reconstruction of the hair-bearing scalp (Fig. 38.6).

ABLATIVE TECHNIQUES In the restoration of normal form, surgical reconstruction may be unnecessary if the lesion concerned can be selectively destroyed. Rhinophyma (a condition characterised by massive hypertrophy of cutaneous sebaceous glands of the nose) is effectively treated by shaving alone. Deep epithelial remnants quickly re-epithelialise the surface of the nose. Dermabrasion is a similar technique in which minor irregulari-

ties of the skin such as post-acne scarring can be improved by abrading the superficial epidermo-dermal layers. However, the laser is the most sophisticated ablative tool. There are many types of medical laser, but those in plastic surgery differ in that they must be very selective in their tissue damage to leave the skin minimally unscarred. The treatment of the intradermal capillary haemangioma (or port wine stain) has been improved initially by an argon laser whose wavelength is similar to that absorbed by haemoglobin, so that abnormal vessels can thus be photocoagulated. However, this has been recently superseded by a tunable dye laser in which a dye is selected which has a wavelength even more specific for haemoglobin. In a similar manner the India ink pigment of amateur tattoos may be vapourised by the ruby laser which emits light of the appropriate wavelength.

OTHER RECONSTRUCTIVE PROBLEMS Other problems requiring reconstruction can broadly be divided into those of composite tissue loss and loss of function. In composite loss following the deep resection of a tumour, not only skin cover but also loss of mucosal surfaces and intervening tissue including skeletal support must be made good. Here the plastic surgeon is a member of a surgical team either in an excisional role but more commonly in a post-excisional, reconstructive role. Descriptions of specific reconstruction are beyond the scope of this chapter, but the specific aims of reconstruction will be considered for the major branches of the specialty.

Trauma Trauma has become a multidisciplinary specialty, and the plastic surgeon who cares for soft-tissue injuries must work as part of a team. Full assessment of the injured patient is essential, as other problems may take priority over the soft tissue. It is important to assess whether tissues are missing or simply displaced. The viability of remaining tissues is then determined and, if avascular such as amputated parts, their suitability for revascularisation. All debris and devitalised tissue must be removed without compromise to allow subsequent reconstruction. However, it is sometimes difficult to judge the viability of tissues, especially following injury when they are bruised and swollen. For example, the degloving injury, whereby skin is sheared from the underlying deep fascia, is notoriously difficult to accurately diagnose; the devitalisation of other tissues, notably fat, occurs some time after an apparently adequate wound toilet. Thus, if there is any doubt about tissue viability, the patient should be returned to theatre for second and third inspections of the wound with necrectomies and surgical toilet as necessary until a clean wound becomes apparent. It can then be closed with the techniques previously discussed.

Congenital abnormalities Birth defects result from failure of a variety of development processes, including formation, fusion, separation and

Plastic surgery techniques  699 a

Tissue expansion

b

Ablative techniques Other reconstructive problems

c

d

Fig. 38.6  Reconstruction of hair-bearing scalp. (a) Following a compound fracture of the right parietal bone with loss of the overlying scalp, a large scalp flap was used to repair this wound. The skin graft used to cover this flap’s donor site has left an obvious area of alopecia. (b) Following insertion and inflation of two tissue expanders. (c) At operation the expanders have been removed and scalp flaps have been raised in the expanded skin prior to excising the skin graft. (d) Six weeks after completion of the reconstruction.

regression of parts. Many abnormalities not only consist of a true shortage of tissues but also of an abnormal anatomy of the adjacent tissues. The treatment of many of these conditions may be started at a very young age, such as during the first few days of birth in the case of neonatal cleft repair. The essential goal is the restoration of as near normal function and appearance by the time the child starts primary school, and as little interference with schooling as possible by any further intervention. Surgery in infancy may interfere with growth of the operated part: thus while the timing of the procedure and meticulous technique are of obvious importance, there must also be

careful follow-up in order to monitor any untoward growth changes. Developments in anaesthesia, diagnostic imaging and neurosurgery have contributed towards safer and more precise correction of major craniofacial abnormalities. Although these conditions may produce very disfiguring abnormalities, they are not often life threatening, and therefore treatment can only be justified if the morbidity is acceptable. Contrary to other sites in the body, much of the facial skeleton can be mobilised, even if this involves devascularisation, and be expected to survive. Once the skeleton has been rigidly fixed in the correct position, possibly with the

38 

700  Principles of plastic surgery

addition of bone grafts, it is necessary to consider the correction of soft-tissue abnormalities. Craniofacial surgery has developed into a subspecialty in its own right involving a large team headed by plastic and neurosurgeons.

a

Breast reconstruction Despite recent trends towards the conservative management of breast cancer, there are still indications for mastectomy, and there will always be women requesting breast reconstruction. In its simplest terms, breast reconstruction requires the restoration of a skin envelope and the bulk with which to fill it. The former is achieved by a variety of flaps, including tissue expansion, and the latter by the bulk of the flap itself or by a silicone prosthetic implant. The restoration of a symmetrical breast with a natural ptosis and projection is sometimes impossible without surgical compromise involving a mastopexy (uplift) or reduction of the other breast. Over recent years there has been a trend, when the breast pathology allows, to perform a skin-sparing mastectomy and immediate breast reconstruction utilising the remaining breast skin. Good cosmetic results can be obtained, and this technique is commonly used in cases of ductal carcinoma in situ (Fig 38.7). Some patients will require a nipple–areolar reconstruction, which can be effected by a variety of local flaps or grafts taken either from the opposite nipple–areolar complex or skin from the upper inner aspect of the thigh.

Hand surgery Although the priority in hand surgery must always be function, the hand, like the face, is never normally covered, and aesthetics must also be borne in mind. The hand is a sophisticated sensate organ composed of highly specialised and compactly organised moving parts with little wasted space. Thus any surgical intervention should be designed to minimise postoperative oedema and scarring to avoid long-term compromise of function in terms of power, range of movement and sensation. Surgery of the hand is merely the start of treatment. Without dedicated postoperative treatment by physiotherapists, occupational therapists, orthotists and, in particular, the determination of the patient, even the most skilful surgery may result in an irreversibly stiff hand.

Burns Although the treatment of burns is performed by a multidisciplinary team the plastic surgeon is normally the main practitioner involved in the treatment of major burns. As with any major injury a primary survey must be performed and life-saving management begun. In the case of burns the sequence in Clinical Box 38.1 should be followed after first-aid measures to stop the burning process have been taken and the burn wound cooled. The initial treatment of patients with major burns is stabilisation by compensating the major fluid loss which will otherwise produce oligaemic shock. The weight of the patient and the extent of the burn, in terms of percentage of body

b

Fig. 38.7  Reconstruction of the right breast with a free TRAM flap following subcutaneous mastectomy. (a) Partial mastectomy defect resulting in asymmetry for volume with distortion of breast contour and nipple–areolar complex and prior to right subcutaneous mastectomy (including nipple–areolar complex) plus reconstruction with a free TRAM flap. (b) Postoperative result of free TRAM reconstruction of right breast (nipple position has been marked for nipple reconstruction using local flaps from TRAM flap skin paddle).

✚ A  B  C  D  E  F 

Clinical Box 38.1 

  Sequence in treatment of burns

Airway maintenance Breathing and ventilation Circulation Drip – instigate i.v. fluids Estimate burns size and depth Fluid resuscitation

surface area affected, needs to be assessed to determine the expected volume of fluid required to maintain satisfactory perfusion. In adults the rule of nines (see Fig. 10.4) is used to help in this assessment but, as the relative proportions of children differ, specific charts for children are available. Various formulae for fluid resuscitation have been devised based on the weight and percentage area of burn, using either crystalloid solutions such as Ringer’s lactate or colloid solutions such as plasma protein solution (PPS). In the UK for many years colloid resuscitation was favoured, but

Plastic surgery techniques  701 recently concern has been expressed that capillaries in the area of an extensive burn become so permeable that large molecules such as plasma proteins will pass into the extracellular space. In this situation colloid solutions confer no benefit over crystalloid solutions, and formulae employing the latter have become standard – such as the Parkland formula from Dallas, Texas. This requires a total volume replacement of approximately 4 mL Ringer’s lactate (Hartmann’s solution) per kg bodyweight per percentage total body surface burnt to be given in the first 24 hours postburn, of which one-half needs to be given within the first 8 hours. It is important to realise that these formulae are guides only and that the patient needs to be repeatedly assessed and the fluid resuscitation matched to clinical parameters such as urine output, haematocrit and blood pressure. The depth of the burn is also assessed to determine which areas are only superficially destroyed (i.e. deeper parts of the dermis are spared, implying spontaneous healing) or whether the damage is deeper and will require surgical excision. Further assessment is needed to determine whether excision should take place in the first few days

– reducing the risk of sepsis but increasing the risk of oligaemia – or at a later stage when oligaemia is less likely but septicaemia is a greater risk. In both instances the choice of graft is either whole or mesh split skin, or a combination of the two. In general burns over 15% body surface area in adults and 10% body surface area in children require intravenous resuscitation and would normally in the UK be transferred to regional burns units as soon as possible. The criteria for transfer to a regional burns unit are broad but include any inhalation injury, burns to difficult areas such as hands, perineum, and burns at extremes of age. As a result only small minor burns are managed outside the regional setting. Most deep burns will require intensive nursing care and, in particular, extensive dressings. Physiotherapy will be required to maintain joint mobility – particularly in the hand, which is often best dressed in a plastic bag to avoid the use of restrictive dressings. Once again, surgery is only the beginning; not infrequently the subsequent disfigurement and deformity from scarring and contracture involve the patient in multiple surgical procedures over many years.

a

b

c

d

Fig. 38.8  An example of complex intra-oral reconstructive surgery. (a) An advanced carcinoma of the floor of the mouth, invading the chin. (b) Defect following bilateral neck dissection and resection of chin skin, mandible from angle to angle, floor of mouth and anterior tongue. (c) Free flap raised for reconstruction. A fibular flap will reconstruct the mandible with some overlying skin, vascularised through its deep fascial attachment, which will replace the floor of mouth. Two osteotomies have been made in the bone, which has been plated in a design to conform with the resected mandible. (d) Four months following surgery there is good bony union. External skin cover was achieved with an axial skin flap from the upper chest (deltopectoral flap)

Aesthetic plastic or cosmetic surgery

38 

702  Principles of plastic surgery

Decubitus ulcers These wounds are caused by pressure necrosis of tissues in an immobilised and often debilitated patient. In those patients who are temporarily incapacitated and subsequently become ambulant, the prognosis is good and the defects can be managed conservatively. The majority of ulcers, however, occur in paraplegic patients in tissues over bony prominences subject to chronic pressure when a combination of poor-quality and insensate tissues, poor general nutrition and, occasionally, poor motivation exacerbate the situation. Management is directed to improving the nutritional status with the help of a dietician and excluding coexistent vascular disease. Continued pressure must be alleviated by regular turning of the patient, with mechanical assistance such as the low-air-loss bed. These patients are demanding of nursing time and require frequent dressings and repeated necrectomy. Eventually some of these wounds may heal spontaneously, though in many the resulting defect is of a size that can only be closed with a local flap. The surgery of decubitus ulcers can be expensive and time consuming and is inadvisable if measures cannot subsequently be taken to prevent any recurrence.

Head and neck surgery Reconstruction in the head and neck demands the highest possible standards and encapsulates all the principles of restoration of form, appearance and function. In the face the cosmetic result is all important and, with this in mind, the surgeon may well opt for a more complicated method of repair. However, prostheses are indicated when the defect may be beyond the scope of surgical reconstruction or the patient too frail for extensive surgery. The materials of the prosthesis together with the secure fixation with osseointegration or the new biological adhesives has initiated a new era in prosthetic rehabilitation. Conversely, intra-oral surgery demands the maintenance and restoration of function. Failure to adequately replace lost mucosal surfaces will produce tethering within the mouth, which is disastrous when it involves the tongue, resulting in interference with speech and swallowing. Thin and pliable flaps are ideal, as they drape the contours of the oral cavity.

In many flaps it is possible to include vascularised bone, which permits single-stage mandibular reconstruction. If part of the lip is resected, dynamic reconstitution of the oral sphincter should be achieved to prevent oral incontinence. An example of complex reconstruction in this region is shown in Figure 38.8.

AESTHETIC PLASTIC   OR COSMETIC SURGERY In cosmetic surgery there is no obvious surgical pathology. The source of distress may either be variants of normal appearance or the aftermath of normal ageing processes, often out of proportion to the degree of physical abnormality as perceived by others. It is therefore essential that the surgeon does not trivialise cosmetic surgery or impart his prejudices on patients, many of whom enjoy a dramatic improvement in the quality of their lives following appropriate treatment. Meticulous patient selection and detailed discussion of the treatment options are paramount, so that the potential benefits and harms can be fully understood. In no other form of surgery is the implementation of fully informed consent more important. In no other form of surgery is there such a thin line between success and failure; between a happy grateful patient and an unhappy, resentful and potentially litigious patient.

FURTHER READING Barret-Nerin J, Hemdon DN 2004 Principles and practice of burn surgery. Informa Healthcare, New York McGregor AD, McGregor IA 2000 Fundamental techniques of plastic surgery: and their surgical applications, 10th edn. Churchill Livingstone, London Settle JAD 1996 Principles and practice of burns management. Churchill Livingstone, Edinburgh Thorne CH, Bartlett SP, Beasley RW, Aston SJ, Gurtner GC 2006 Grabb and Smith’s plastic surgery, 6th edn. Lippincott Williams & Wilkins, Boston Warwick D, Dunn R, Melikyan E, Vadher J 2009 Oxford specialist handbooks in surgery – hand surgery. OUP, Oxford

39 

Skin disorders

INTRODUCTION

703

DISORDERS OF THE SKIN

707

Infections

707 707 709 710

Viral infections Bacterial infections Fungal infections

Tumours Benign tumours of the epidermis Other benign skin tumours Premalignant conditions of the epidermis Non-melanoma skin cancer Malignant melanoma Malignant tumours of the dermis Other malignancies of the skin

711 711 712 714 714 716 719 720

INTRODUCTION The most useful tool for diagnosing a skin complaint is skilful history-taking. The skin should be examined using the naked eye: the characteristics of the individual lesion(s) and their distribution are key to making the diagnosis. The whole skin surface must be examined even if the patient presents with an apparently solitary lesion, and careful consideration should be made of the need to examine the mucous membranes and the skin appendages, including nails and hair. It is also important to examine the regional lymph nodes draining the area of involvement, particularly in suspected neoplastic conditions. Most skin conditions examined in surgical practice are benign or malignant tumours. Other conditions encountered include inflammatory rashes, perhaps triggered by drugs or a physical stress such as surgery, so a broader understanding of dermatological conditions is essential.

Embryology and anatomy There are three layers to the skin (Fig. 39.1): n

epidermis dermis n subcutis. n

Epidermis The epidermis originates from the embryonic ectoderm, in contrast to the other two deeper layers which are of mesodermal origin. Some epidermal structures – the pilosebaceous unit and nail matrix (see below) – migrate inwards during development and are anatomically located in the dermis. Similarly, some cells of mesodermal origin, such as melanocytes which are of neural crest origin, migrate outwards to the epidermis and are located within the basal cell layer.

The interface between the epidermis and dermis is convoluted – the dermal projection of the epidermis is a rete peg and the upwardly projecting portion of the dermis is the papillary dermis (Fig. 39.2). Between the epidermis and dermis there is a basement membrane zone which is traversed by anchoring fibrils, which are important in adherence of the two structures.

Epidermal cells The keratinocyte  is the predominant cell of the epidermis. The epidermis is made up of stratified keratinising squamous epithelium the layers of which can be identified histologically and represent stages of the maturation of cell division of the keratinocytes. The cells mature progressively as they migrate from the basal layer towards the surface. Initially, in the basallayer keratinocytes, keratin filaments appear in the cytoplasm. As the cells mature further, the cytoplasm becomes progressively replaced by keratin – a structural protein which is surrounded by a phospholipid envelope that was the original cell membrane. As the cells with each division migrate towards the surface they flatten and by the time they reach the surface they form a laminated structure – the stratum corneum (Fig. 39.1) which serves as a physiological barrier to chemical and microbiological invasion from without, as well as fluid and salt loss from within. The epidermal transit time from the basal layer to stratum corneum is about 28 days. Disruption of this smooth transition occurs in inflammatory conditions of the epidermis such as psoriasis, and also as a result of actinic (sun-induced) damage to the basal cell – a process known as dyskeratosis which makes the affected epidermis unstable. Melanocytes  are cells of neural crest origin which produce the ultraviolet (UV) radiation-absorbing pigment melanin.

39 

704  Skin disorders

They are located along the basement membrane between the basal keratinocytes and have a dendritic shape with multiple root-like projections. Different racial groups have the same number of melanocytes, but there is a difference in the amount and type of melanin produced: Celtic races, for example, produce predominantly phaeomelanin, a yellowred pigment which gives poorer UV protection than brownblack eumelanin. Increased melanin production can be stimulated by UV light and the cytokines released by

Stratum corneum Granular cell layer

Prickle cell layer

Dermis Melanocyte

Basal cell layer Dermo–epidermal junction

Fig. 39.1  Structure of normal epidermis.

inflammatory processes. Melanocytes distribute their melanin granules to the surrounding basal cells through their dendrites. Once these granules are taken up by the basal cells, they are dispersed through the cytoplasm to absorb UV radiation, which protects the nuclei as well as deeper cells from UV damage. Thus melanin has a key role in preventing malignant change to basal cells and photodamage to the underlying collagen: individuals who produce phaeomelanin which is less photoprotective will burn rather than tan and are more vulnerable to developing UV-induced skin tumours and wrinkling. Immunocompetent cells  are of a number of classes: Langerhans cells are derived from bone marrow and are closely related to the macrophage. They are located just above the basal layer of keratinocytes in the so-called suprabasal layer. They express HLA receptors on their surface and are central to the presentation of antigens to other immunocompetent cells. They also, in their own right, release cytokines such as interleukin-2. Their prime importance is in immunosurveillance of the skin and mediation of the cutaneous immune response. Lymphocytes are present in small numbers in the normal epidermis – mainly T lymphocytes of both CD4 and CD8 subsets. The T lymphocytes are derived from the thymus, which also like the epidermis is of ectodermal origin, and it is believed that they migrate through the epidermis as part of their surveillance of immune function. The interaction between Langerhans cells and lymphocytes makes the epidermis an important component of the body’s immune system. This can be disturbed in some inflammatory conditions of the epidermis which are T-cell mediated: e.g.

Epidermis Papillary dermis

Sweat gland and duct Cutaneous nerve

Reticular dermis

Sebaceous gland Hair follicle

Subcutaneous fat

Fig. 39.2  Structure of normal skin.

Introduction  705 psoriasis in which T lymphocytes release lymphokines into the epidermis, resulting in keratinocyte proliferation. In the cell-mediated (type IV) reaction, such as that seen to adhesives used in wound dressings, the colophony allergen is presented by an antigen-presenting cell, such as a Langerhans cell, to a T lymphocyte, setting off the cascade of events which result in allergic contact eczema. The epidermal immune system may be suppressed in various ways. UV light can suppress type IV reactions in the skin. Some skin diseases such as atopic eczema are associated with local immunodeficiency and patients are prone to cutaneous infections with Staphylococcus aureus. The cutaneous immune system may also be suppressed during systemic diseases such as diabetes mellitus, HIV and leukaemia. Merkel cells  These, like melanocytes, are of mesodermal origin derived from the neural crest. They function as mechanoreceptors to help sense touch, and so are found particularly on the digital pads of the fingers.

Dermis The major component of the dermis is connective tissue composed mainly of collagen fibres within an amorphous ground substance. The papillary dermis is the uppermost layer of the dermis, intertwined with the rete ridges of the epidermis. Below this, the reticular dermis is less cellular and contains more densely packed collagen and elastic fibres (Fig. 39.2). The dermis contains blood vessels which derive from a deep vascular plexus, sweat glands, nerves, lymphatics, and muscle fibres associated with a pilosebaceous unit (see below).

n

apocrine glands occur in the intertriginous areas of the axillae and groin and also the scalp – their secretion is greasy.

Pilosebaceous units are a combination of a hair shaft, hair follicle and a sebaceous gland. Attached to the hair shaft are muscle fibres of the pili erector muscle. The keratin of the hair shaft is derived from a germinal layer of the hair bulb which lies deep in the dermis. The hair follicle is richly supplied by nerves and blood vessels. The sebaceous gland produces an oily secretion, sebum, which is discharged into the hair follicle via the pilosebaceous duct. Nail matrix produces the specialised keratin of the nail plate which grows out beneath the proximal nail fold (Fig. 39.3). The plate is closely adherent to the underlying nail bed. Melanocytes can be present in the nail matrix, causing linear pigmented striae within the nails, as well as providing a starting place for melanoma (see Fig. 39.23). On either side of the nail plate are the lateral nail folds. The nail plate can grow into the soft nail fold, giving rise to an ingrowing nail; if the nail folds become infected, this is termed paronychia (Fig. 39.4).

Subcutis The subcutis, which predominantly contains loose adipose tissue and elastin, serves to attach the skin to underlying muscle and bone as well as supplying it with blood vessels and nerves.

Proximal nail fold Cuticle Lunula

Dermal collagen  is produced by fibroblasts which lie between the collagen bundles. It forms a mesh-like network which provides a supportive framework for skin structures, and gives the skin strength and elasticity. Changes in collagen occur with ageing and from UV light, both of which make collagen less flexible and less able to provide support for other structures. Wrinkles result, and purpura may also follow from the increased fragility of blood vessels. Dermal blood vessels  arise from a deep arterial plexus which then subdivides and finally a capillary loop which supplies the dermal papillae. Blood then drains through a papillary venous network and back into the subcutaneous vessels.

Lateral nail fold Nail plate Nail bed Nail matrix

Fig. 39.3  Sagittal view of the nail anatomy.

Lymphatic channels  can be recognised within the dermis. Their obstruction or failure causes cutaneous lymphoedema. Dermal nerve fibres  are: n n

afferent for cutaneous sensation efferent vasomotor and also to the sweat glands, both of which help regulate body temperature; there is also a supply to the erector pili muscle.

Sweat glands  are of two types: n

eccrine glands are present throughout all skin and secrete an aqueous fluid

Fig. 39.4  Paronychia, showing loss of cuticle and swelling of nail fold.

INTRODUCTION

39 

706  Skin disorders

Principles of investigation: the biopsy Histological examination is required to confirm diagnosis, especially where there is doubt on clinical grounds. Small lesions may be completely excised (an excisional biopsy), larger ones may be removed initially in part (an incisional biopsy) before definitive therapy is decided on. When biopsying a rash, a relatively fresh representative lesion should be biopsied, and the biopsy should be taken across the edge of a lesion. It is important to provide adequate material for histological interpretation, which usually means a fullthickness biopsy including epidermis, dermis and a small amount of subcutis. Skin surgery is usually performed under local anaesthetic.

Full-thickness skin biopsies Any incision into collagen (i.e. through the dermis) leaves a scar on healing, and this inevitable consequence must be explained to the patient beforehand. Hypertrophic and keloid scarring is always a possibility, especially for surgery on the upper trunk and shoulders, and the risk is higher in patients with black skin tone. Full-thickness skin biopsies may be incisional or excisional, and a variety of techniques can be used including: n

Punch biopsy (Fig. 39.5). A small sharp tool, not dissimilar to an apple-corer is used to obtain a cylindrical sample of full-thickness skin. This technique

is often used to obtain an incisional biopsy for diagnostic purposes. Very small punch biopsies can heal well by secondary intention; otherwise, primary closure is achieved with sutures. n Ellipse biopsy (Fig. 39.6). Using a scalpel an ellipseshaped full-thickness biopsy is obtained of the skin. This technique is often used to perform excisional biopsies, e.g. of a melanoma, or when good-sized samples of the subcutis as well as the more superficial skin is required, e.g. in investigating inflammation of the fat. The wound is closed with sutures which are left in situ for 5–20 days dependent upon the site of the surgery and other wound-healing factors. For larger wound defects a variety of techniques are used to close wounds, including skin grafts and rotation flaps (Ch. 38).

Principles of therapy Neoplastic lesions must be excised without primary regard for the cosmetic outcome, and the sample submitted for histological examination to confirm the diagnosis and to check that the margins taken were adequate. For benign lesions, however, cosmesis must be given consideration. A variety of therapeutic surgical techniques may be used: punch and ellipse biopsies as above, and also these methods below which in experienced hands have the advantage of removing superficial skin lesions without damaging collagen.

Punch biopsy handle

Steel blade

Lesion to be biopsied Skin

Fig. 39.5  Punch biopsy technique: the sharp instrument is driven into the skin to obtain a cylindrical section of skin. Inset: the sample obtained is of full-thickness skin down to subcutis.

Infections  707 Curettage.  A ring or spoon-shaped curette is used to remove the epidermal lesion, by drawing the curette with pressure over the lesion, e.g. seborrhoeic keratoses.

DISORDERS OF THE SKIN Infections Viral infections

Shave biopsy.  A scalpel or razor blade is used to remove a superficial skin lesion in a single piece of unfragmented tissue, e.g. a benign intradermal melanocytic naevus which catches on clothing.

3

Skin lesion

Snip excision.  Sterile scissors are used to remove pedunculated skin lesions, e.g. skin tags. Haemostasis is then achieved to the resultant erosion using cautery, hyfrecation or chemically using topical aluminium chloride solution. Cryosurgery  can also be used to treat superficial lesions such as viral warts (see below) satisfactorily. Patients should be warned of the likelihood of pain and blistering after this treatment, and, especially in patients with pigmented skin types, of the risk of pigmentary changes. Injudicious use of this method may result in deeper tissue injuries, such as digital nerve or extensor tendon damage when used on the dorsal aspects of the fingers.

Ellipse-shaped excision margins

1 Fig. 39.6  Ellipse biopsy of skin showing the planned excision margins for a pigmented lesion, with the 3 : 1 ratio typically used to ensure a thin linear scar after suturing.

Lasers  can be used to treat benign vascular and pigmented lesions. The emission wavelength of the laser can be matched to the absorption spectrum of the pigment present, e.g. haemoglobin or melanin. Carbon dioxide lasers are more destructive, but give immediate haemostasis and vaporise a lesion; they have a role in ablative therapy especially.

DISORDERS OF THE SKIN The skin is the body’s largest organ – by weight, up to 15% of body mass. It is, along with the mucosal surface of the gastrointestinal tract, with which it is continuous, the interface between the external and internal environment and has a number of important functions in protection and in the maintenance of homeostasis. It is extensively exposed to agents which are actually or potentially noxious, including chemicals, carcinogens and pathogenic organisms. Also, it is at constant risk of physical trauma and subject to a large number of endogenous diseases such as eczema, lichen planus and psoriasis and may be involved in systemic problems such as vasculitis and granulomatous diseases (e.g. sarcoidosis). The prevalence of skin disorders is summarised in Box 39.1.

Box 39.1  n

Prevalence of skin disorders in the UK

Skin disease affects between 25% and 33% of the population at any given time n Skin disorders account for 15% of all consultations in general practice n The commonest skin disorders seen in general practice are eczema, acne, infections and psoriasis n Skin cancer accounts for 50% of the skin problem referrals from general practice to secondary care

INFECTIONS The skin is constantly exposed to infectious agents. Protection is afforded by the physical barrier of the stratum corneum and the very effective immunological barrier of the epidermis. Host defences may be breached as a result of: n

Physical injury, e.g. trauma or surgery to the skin Endogenous skin diseases, e.g. eczema or venous ulceration n Immunosuppression, e.g. HIV or leukaemia n Pathogenic organisms that are able to penetrate the normal skin defence mechanisms, e.g. fungal and candidal infection. n

VIRAL INFECTIONS

Human papillomaviruses These are a group of RNA viruses, and more than a hundred subtypes have been identified so far. The skin manifestation is a wart.

Epidemiology and aetiology Warts are common, and most people suffer infection at some stage. They are mostly prevalent in children, where

39 

708  Skin disorders

they are probably acquired from direct contact or from communal recreational facilities such as swimming pools. Genital (including perianal) warts are usually found in adults, and are most commonly, though not exclusively, acquired as a result of sexual intercourse so that they may coexist with other sexually transmitted infections.

History Cutaneous warts may present suddenly with rapid growth or more gradually creep up on their hosts over many weeks, even years. Itching may be a feature. Larger lesions can become painful, especially if they are on pressure points such as the heel or ball of the foot. Lesions can be of cosmetic concern when on exposed sites such as the hands or face.

treatment options for management of viral warts reflects the relatively poor efficacies of these individual treatments.

Keratolytic agents The use of local keratolytic agents such as salicylic acid paints for hand and foot warts remains the mainstay of therapy, particularly in children. Even when cure is not achieved the removal of excessive keratin helps to limit discomfort until resolution occurs.

Cryotherapy The application of liquid nitrogen can destroy the virusinfected tissue, which then sloughs off. Early resolution in individual lesions may follow, but there is a high rate of recurrence and treatment is painful.

Clinicopathological features

Curettage and other destructive measures

The virus infects the basal keratinocytes of the epidermis, resulting in increased proliferation of these cells. In stratified squamous epithelium this gives rise to hyperkeratosis and a hard wart is seen. The characteristics of a wart are loss of the normal dermatoglyphics of the skin and thrombosed capillaries that are seen as small black dots which bleed if the overlying hard skin is pared away (Fig. 39.7). On mucosal surfaces the wart is softer – a fleshy papilloma.

Immunotherapy

Management Prevention Vaccines have been produced against HPV subtypes 16 and 18, which together are associated with 70% of cervical cancers, and are also associated with many cases of anal cancer. Routine HPV immunisation of girls aged 9–14 years has been introduced in the UK and other countries. One currently available vaccine also protects against HPV types 6 and 11, which cause 90% of genital warts. These developments open up the future possibility of a vaccine against the HPV types (e.g. 1 and 2) more typically involved in cutaneous warts on the hands and feet.

Natural history Spontaneous resolution is the rule once natural immunity has developed, but this takes longer in adults than in children, so that infection can last for many years. The multiplicity of

Physical ablation of larger warts can be achieved by curettage, diathermy or laser therapy, but they also have significant recurrence rates.

Immunotherapy aims to stimulate the body’s immune system to effectively eliminate the virally infected cells, e.g. diphencyprone, a potent contact allergen which in expert hands is used to induce localised eczema associated with clearance of the warts; and imiquimod, a topical immune modulator which binds to cell-surface toll-like receptors resulting in the secretion of numerous pro-inflammatory cytokines including interferon-α, resulting in clearance of the warts.

Cytotoxic agents Podophyllin (a compound preparation which contains the agent podophyllotoxin) is particularly helpful in treating genital warts. Its application must be closely monitored, however, because it causes soreness and is teratogenic and therefore must not be used during pregnancy. Bleomycin has also been successfully used by injecting intralesionally.

Special problems with genital warts (syn. condylomata acuminatum) It is important when assessing a patient with genital warts to ensure that they have not also acquired any other sexually transmitted disease. In addition to podophyllin and imiquimod, these warts may be treated with physical destruction or excision under general anaesthesia. Excision has the benefit of providing histology as dysplasia and even squamous cell carcinoma may be present especially in immunocompromised patients.

Molluscum contagiosum Aetiology and pathological features

Fig. 39.7  Viral warts (verrucae) on the sole, demonstrating thrombosed capillaries which clinically appear as ‘black dots’.

This is caused by a pox virus. The individual lesions are smooth and dome-shaped, they have a characteristic central depression or umbilication and, if squeezed, a central white core can be expressed called the molluscum body. Florid molluscum contagiosum may occur in immuno­ suppressed patients, particularly those with HIV infection. When patients acquire immununity to the virus the lesions disappear.

Infections  709 Management Early resolution of individual lesions can be induced by minor trauma such as cryotherapy or superficial diathermy; imiquimod has also been used to good effect.

Herpes viruses There are two types of infection: n

Herpes simplex due to a number of subtypes of herpes simplex viruses (HSV) n Herpes zoster due to varicella-zoster virus (VZV). The distinction is summarised in Box 39.2.

Herpes simplex This condition can affect any area of the skin, however it is most commonly seen close to the mucous membranes of the lips in HSV type 1 and the genitalia in HSV type 2. The patient notices a prodromal tingling of the skin followed by the eruption of clusters of small vesicles. The active lesions are infectious, and surgeons need to take care to avoid direct contact, as this can result in a herpetic whitlow on a finger.

Herpes zoster This is caused by VZV; the primary widespread infection is chickenpox. The virus then lies dormant in the dorsal root ganglia of the CNS and is reactivated along peripheral nerves to produce vesicles and pustules in a dermatomal distribution, known as shingles or herpes zoster. Its relevance for surgeons is that herpes zoster can be triggered by stresses such as surgery. Additionally the prodromal phase, before the development of vesicles, gives rise to pain in the skin of the affected dermatome which may cause diagnostic difficulties by mimicking other nerve lesions such as sciatica, or an acute abdomen. Treatment with aciclovir or valaciclovir shortens attacks.

Box 39.2 

Herpes simplex and zoster

Herpes simplex n Subtype 1 – onset in childhood and usually orofacial n Subtype 2 – onset in adults and usually genital n Attacks may be precipitated by UV light, or an intercurrent illness, e.g. upper respiratory infection Herpes zoster n Caused by activation of dormant varicella-zoster (chickenpox) virus n Distribution is characteristically dermatomal and unilateral – more widespread infection suggests immunosuppression, e.g. HIV infection n Can present with unilateral abdominal pain before skin lesions appear n Rarely recurs but may be complicated in the long term by severe post-herpetic neuralgia n Antiviral drugs reduce the acute pain and duration of herpes zoster and should always be given

BACTERIAL INFECTIONS

Staphylococcal infections Aetiology, pathological features and management Staphylococcus aureus (SA) can cause primary skin infections such as impetigo, furunculosis and acute paronychia. Diabetic patients are particularly susceptible. Since the 1950s the majority of strains of S. aureus have been resistant to many commonly used antibiotics such as penicillin; from the mid-1990s there has been an increasing incidence of methicillin-resistant SA or MRSA such that it is now endemic in British hospitals. Community acquired MRSA infections are also increasingly seen. Panton–Valentine leukocidin (PVL) is a toxic substance produced by some strains of S. aureus which is associated with an increased ability to cause disease. This PVL SA remains relatively uncommon in the UK.

Impetigo This condition mainly affects the face and is much more common in children than in adults: presentation is as flaccid blisters underneath the stratum corneum which rupture early on, so giving rise to a raw eroded base. Impetigo is contagious, and infected children should be kept away from school. Swabs are taken to determine the antibiotic sensitivities of the organism. Both staphylococcal and streptococcal bacteria may cause the condition. If the lesions are localised, topical antibiotics such as fucidic acid or mupirocin are effective, dependent on sensitivities. If lesions are more widespread, they are treated with systemic flucloxacillin.

Furunculosis This term describes a group of conditions characterised by staphylococcal infection of the hair follicles. Staphylococcal folliculitis is a pyoderma localised to the hair follicle and can be either superficial or deep. A furuncle (boil) is a deepseated inflammatory nodule which develops around a hair follicle from a preceding, more superficial folliculitis. A carbuncle is a more-extensive and even deeper infiltrating inflammation which occurs in thick and inelastic skin – commonly on the back of the neck. The acute lesions of furunculosis are characterised by pain and tenderness of the infected area and soft tissue. Localisation of pus gives rise to abscesses. The natural history of the lesions is for the pus to discharge and this to be followed by resolution. Treatment of the early soft-tissue phase is with systemic antibiotics. If a deep abscess forms, then surgical drainage is indicated. Carbuncles and ecthyma represent infective gangrene of the deep tissues. The subcutaneous tissues become painful and indurated and drain to the surface through sinuses. Surgical debridement may be necessary, in addition to a course of antibiotics.

Paronychia This is the term given to inflammation of the nail fold. Infection is usually acquired through loss of the cuticle of the proximal nail fold, sometimes the consequence of a selfinflicted injury at manicure. Paronychia may be acute when caused by S. aureus infection, or chronic when the result of

Bacterial infections

39 

710  Skin disorders

Candida infection whose acquisition is difficult to determine (Fig. 39.4). Treatment is by surgical debridement – which may have to include the nail – under local anaesthetic.

Streptococcal infections Streptococcus pyogenes (beta-haemolytic streptococcus Lancefield group A) causes dermal infections of two types: n

erysipelas – infection in the deep dermis but not the subcutaneous tissues n cellulitis – full-thickness infection of the skin with involvement of the subcutaneous tissues. The presentation of both may be that of the systemic features of severe sepsis, with rigor and fever but without initial overt evidence of skin involvement. The earliest cutaneous sign is erythema. The leg and face are most commonly affected, although any site may be involved. The infection spreads through the tissue by the release of toxins, giving rise to a brawny erythema spreading across the skin with a sharp well-demarcated edge (Fig. 39.8). If left untreated, the infection will eventually resolve, but there is a significant mortality from overwhelming toxaemia and septicaemia. The treatment of choice for streptococcal cellulitis is bed rest with intravenous antibiotics. The majority of streptococci are sensitive to penicillin, and this is the agent of choice. The fever usually settles within 24–48 hours, and the erythema and swelling subside slowly. Streptococcal cellulitis can complicate chronic skin conditions such as venous leg ulceration (Ch. 30) and lymphoedema (Ch. 30). When this occurs, treatment with antibiotics may have to be prolonged to prevent early relapse.

Necrotising fasciitis Necrotising fasciitis is an acute and potentially life-threatening infection. It occurs in healthy individuals, often after mild trauma, usually on the leg. It may be caused by a single bacterium or a synergistic combination of different bacteria. The organisms commonly cultured include group A streptococcus, S. aureus (including MRSA), Vibrio vulnificus, Clostridium perfringens and Bacteroides fragilis. An illdefined erythema develops which rapidly becomes necrotic. The patient complains of severe pain and is found to have a high fever and the other features of systemic inflammatory

Fig. 39.8  Erysipelas, showing indurated red plaque spreading across face.

response out of proportion to the local skin findings. The infection spreads quickly in the fascial plane and involves both skin and subcutaneous tissues. Urgent CT or ultrasound scanning may confirm the diagnosis and help to define the extent of the disease, but these should not delay definitive surgical treatment. Urgent surgical wide debridement of the affected tissues is required together with intravenous antibiotics (e.g. linezolid with meropenem or piperacillin/ tazobactam). Antibiotic treatment may be modified once bacteriological culture results are available. Repeat operation is often performed within a few hours in case further tissue excision is required. Transfer to a plastic surgical unit for reconstructive surgery is usually required once the patient’s condition has improved.

Venous ulceration Ulceration in the gaiter area of the leg is common in patients with post-thrombotic venous hypertension and is also seen with advanced varicose veins. These ulcers may become secondarily infected and cause surrounding cellulitis. The condition and its treatment are described in detail in Chapter 30.

FUNGAL INFECTIONS

Superficial mycoses These infections are due to fungi that can only invade fully keratinised tissues. The clinical appearance depends on the severity of the inflammatory reaction to the fungi. When mild, the lesions are red and scaly; when severe, boggy areas of inflammation may arise; when present on the scalp or beard this is known as a kerion (Fig. 39.9). It is important to recognise this to prevent inappropriate surgical intervention as these lesions can best be treated medically with appropriate systemic antifungals. Mycological examination of the tissue

Fig. 39.9  Kerion in the beard area due to Trichophyton verrucosum. Treatment is with systemic antifungal therapy: this lesion resolved without scarring after treatment with oral terbinafine.

Tumours  711 conducted by direct microscopy is used to confirm the diagnosis.

TUMOURS The skin is exposed to chronic irritation and carcinogens. Tumours of the skin, as with any other tissue, can be benign or malignant. The latter may be primary or secondary. A number of premalignant conditions can be identified and are discussed below. Tumours that derive from the epidermis (ectodermal) have different clinical features from those of the dermis (mesodermal).

BENIGN TUMOURS OF THE EPIDERMIS

Seborrhoeic keratosis/wart (syn. basal cell papilloma) These lesions are common in the elderly.

Clinical features History These are rough lesions which may catch on clothing; this or other trauma may cause minor bleeding. The appearance is unattractive, and cosmetic distaste is a common reason for presentation.

Physical findings Raised, well-circumscribed lesions may occur anywhere on the body, although the trunk is the most common site. They are initially flat with varying amounts of pigmentation. The surface is waxy with superficial clefting and fissuring (Fig. 39.10).

Management The differential diagnosis of deeply pigmented papillomas from malignant melanoma can be difficult; if there is doubt, excision biopsy is indicated.

However, if the diagnosis is certain, shaving back the lesion or curettage and cautery give a satisfactory cosmetic result with the additional benefit of providing a specimen for histological confirmation of the diagnosis.

Skin tags These lesions are usually found in sites where skin surfaces rub together and the skin is therefore chronically irritated. There is a loose connective tissue core covered by epidermis which is variably pigmented. Skin tags are irritated by clothing and bleed as well as causing local symptoms in areas such as the skin surrounding the anus. Patients often present to request removal. The diagnosis is obvious to the naked eye. Management is by snip excision and cautery carried out under local anaesthetic.

Solar (actinic) keratoses These scaling red macular (flat) lesions occur on sun-exposed areas of the skin, often on a background of collagen damage known as solar elastosis. The basal epidermal cells are dysplastic: clinically this results in the skin surface changing from smooth to scaly with excessive keratin. Induration or pain can occurs if the lesion becomes invasive; progression to a squamous cell carcinoma may take place, although this is rare.

Management Isolated superficial lesions are dealt with by cryotherapy. If there is any induration, curettage and cautery are used and the fragments sent for histological examination. Where there is a high suspicion of squamous cell carcinoma lesions should be excised to avoid ambiguous histology. Close follow-up is indicated when the histological diagnosis is uncertain. Extensive areas of sun damage with multiple solar keratoses are better managed topically with application of cytotoxic creams such as 5-fluorouracil or immunomodulators such as imiquimod to stabilise the epithelium; this has to be done under close supervision.

Keratoacanthoma This lesion arises from squamous epithelium. It is most common on exposed areas of the body and is thought to result from minor trauma. As its name suggests, it has a central keratin plug with a surrounding collar of acanthotic thickened epidermis (Fig. 39.11).

Clinical features

Fig. 39.10  Large, deeply pigmented seborrhoeic keratosis with greasy, ceribriform surface. Close by, several smaller skin-coloured seborrhoeic keratoses may also be seen.

The lesion is characterised by rapid onset and growth. It then enters a static phase, which may last 3–4 months before spontaneous resolution. The appearance of the lesion by itself can be very difficult to distinguish from a squamous cell carcinoma (see below), although the latter usually grows progressively but less rapidly. The same difficulty also occurs on histological examination, but carcinoma always invades the deeper dermis. Treatment is by excision with a margin of

Fungal infections

Tumours Benign tumours of the epidermis

39 

712  Skin disorders n

Spitz naevus – reddish brown in colour, usually on the face or limbs of children and young adults; they are benign (but see below).

Most moles which are not present at birth will develop in the second or third decade. A Spitz naevus may undergo rapid growth and for this reason is often removed to exclude malignancy. Histological examination shows large cells which are pleomorphic and can be very difficult to distinguish from those of malignant melanoma. Skilled histological assessment is necessary.

Dermatofibroma Fig. 39.11  Keratoacanthoma on cheek, showing central keratin plug with surrounding acanthotic collar.

surrounding skin; if there is any remaining doubt about the diagnosis, careful follow-up is indicated.

OTHER BENIGN SKIN TUMOURS

Benign pigmented skin lesions Freckles (syn.ephelides) Freckles are areas of the epidermis where melanocytes produce more melanin, usually in response to ultraviolet light. The number of melanocytes is normal, and they are quite stable.

Lentigo (plural lentigines) Lentigines are areas of the epidermis where the number of melanocytes is increased and melanin production is excessive. They are found in areas of chronic sun exposure and hence are most common on the face, hands and shoulders. If seen in young patients, they are the sites of solar damage, and the patient should be advised against unnecessary exposure to the sun.

Melanocytic pigmented naevus   (plural naevi): ‘moles’ The term naevus is not necessarily confined to melanocytic skin lesions; it may equally refer to blood vessels (vascular naevi). The more correct generic term is a hamartoma. Essentially there is an abnormal collection of a normal skin constituent: in this case, melanocytes. Congenital melanocytic naevi are rare, often darkly pigmented and may be hairy or papillary. Melanocytic naevi may occur anywhere on the skin – including the nail bed, where they give rise to a linear pigmented stria. According to the clinical and histological features, melanocytic naevi can be subdivided into five types: n

junctional – at the dermo–epidermal interface (clinically brown and flat) n intradermal – entirely within the dermis (clinically skin-coloured and raised) n compound – features of both junctional and intradermal (clinically brown and raised) n blue – deep dermal with considerable pigmentation which gives rise to their colour (blue-black and flat)

This is a tumour (often multiple) of dermal connective tissue which contains histiocytes and is of unknown cause. There have been suggestions that they arise from insect bites as the lower leg is the most commonly affected site, and they are more common in women than in men. A small intradermal nodule is present. Pigmentation is usual, and the overlying epidermis is tethered to the lesion, giving a puckered appearance if the lesion is squeezed. As the lesion matures it changes from red-brown to pale, although often with a retained surrounding halo of pigmentation. A slow increase in size may occur, and excision may be necessary especially with the darker lesions, to exclude melanoma and establish the diagnosis with certainty.

Benign abnormalities of the blood vessels Haemangiomas are distinguished by the size of the blood vessel that is involved.

Pathological features Capillary haemangiomas are common and may give rise to salmon pink discoloration on the surface of the skin. The back of the neck is a common site. Other variants include the port wine stain on the face, which may be associated with ipsilateral intracranial haemangiomata, giving rise to epilepsy (Sturge–Weber syndrome). Strawberry naevi may appear in infancy and grow with age before resolving spontaneously by the early teens. Campbell de Morgan spots appear as small cherry papules on the trunk, are very common and of no significance, although they can become increasingly numerous with age and give rise to cosmetic embarrassment. Pyogenic granulomas are exuberant granulation tissue, an exaggerated healing response to minor trauma, and are usually found on the finger or the lip (Fig. 39.12). In spite of their name, the lesions are not infective in cause. They are friable and bleed readily. Glomus tumours appear as small vascular blebs on the skin. They have a generous nerve supply and are tender, especially if they occur within a confined space such as the nail bed.

Neurofibromas These are benign tumours of the fibroblasts of the nerve sheath. The usual presentation is a solitary lesion in the area of a peripheral nerve. On clinical examination they are soft and fleshy (Fig. 39.13).

Tumours  713

Cysts A cyst is an epithelium-lined cavity usually filled with thick products of epithelial secretion or of cell breakdown which have undergone degeneration. The most common type originates from the hair follicle.

Epidermoid and pilar cysts

Fig. 39.12  Pyogenic granuloma on finger, showing friable vascular tumour.

Fig. 39.13  Neurofibroma on wrist, showing soft fleshy

These are sometimes incorrectly termed sebaceous cysts. Epidermoid cysts have walls derived from the follicular infundibular epithelium, so they are found anywhere on the body where hair follicles occur. Many are solitary but multiple lesions occur. They range in size from a few millimetres to several centimetres. The cyst is located in the deep dermis but is connected to the superficial epithelium through the pilosebaceous duct. A blocked duct may be visible on the surface as a central black punctum. Clinically, they are soft and are mobile over deeper structures. Pilar cysts have walls derived from the outer root sheath of the hair follicle, and are almost invariably found on the scalp. Epidermoid and pilar cysts are not usually painful unless they are injured with disruption of the contents into the surrounding dermis, where they cause an intense inflammatory reaction. When this occurs, the area swells and becomes tender. Uninflamed cysts are excised; care must be taken that all abnormal epithelial elements are removed, or recurrence is likely. If the cyst has become inflamed, then the contents are best drained and the inflammation allowed to subside, at which point the whole cyst can be excised.

swelling.

Dermoid cysts Schwannomas are benign tumours arising from the Schwann cells around the peripheral nerves, are much firmer nodules than neurofibromas and are closely tethered to an identifiable nerve. Pressure on the tumour may cause pain in the area of distribution of the nerve, and excision has to be performed with great care. Some patients have multiple neurofibromas, which form part of the syndrome of neurofibromatosis with associated cafe-au-lait spots and axillary freckling. There are sometimes schwannomas of the larger cranial nerves and phaeochromocytoma. Two types of neurofibromatosis exist with identified mutations on chromosome 17q (neurofibromin protein, type 1) and 22q (merlin protein, type 2). They are both autosomal dominant, although there is a high spontaneous mutation rate seen in approximately 50% patients.

Congenital

These are rare and arise from abnormalities of development where epithelial remnants occur. They are found in lines of embryological fusion; the midline of the neck, the scalp and the face are common sites. The contents of the cysts include ectodermal structures of hair and sebaceous glands in addition to keratin.

Implantation dermoids In this condition, a usually insignificant injury drives a fragment of dermis into the subdermal layer from where its secretions cannot escape. The fingertip is the commonest site (e.g. rose gardeners), although they may occur at any site of injury.

Benign appendage tumours

Lipomas

Skin appendages, such as sweat glands and hair follicles, are a source of benign tumours. Non-specific tumours such as syringomata or trichofolliculomas are not usually diagnosed clinically but only retrospectively following excision of a nondescript skin nodule. A cylindroma is of hair follicle origin and gives rise to a fleshy nodule. They usually occur on the scalp and may become very large, giving rise to what in the past was labelled a turban tumour.

This is strictly a growth of fat deep to the skin proper. The overlying skin is normal, and the lump can be moved in relation to it. Fluctuation can be elicited, although the lesion is not cystic. The histological appearance is of a mass of adipose tissue with thin fibroid septa. The size varies, and penetration into muscles can occur. Treatment is by excision, particularly if the lipoma increases in size or becomes tender.

Other benign skin tumours

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714  Skin disorders

Fig. 39.15  Lentigo maligna on cheek, showing plaque with variation in pigmentation.

Paget’s disease of the nipple This is discussed in detail in Chapter 28.

Lentigo maligna Fig. 39.14  Bowen’s disease on leg, showing psoriasiform plaque.

PREMALIGNANT CONDITIONS   OF THE EPIDERMIS

Bowen’s disease This is characterised by a well-circumscribed scaly plaque (Fig. 39.14) most commonly on the lower legs although it can occur anywhere on the body including at the anus. The clinical appearance is similar to a solitary patch of psoriasis. Histological examination shows full-thickness epidermal dysplasia sometimes amounting to carcinoma in situ. The condition is potentially malignant although progression is slow.

This is a rare plaque-like condition which tends to develop in late middle age, most commonly on the cheek, and increases slowly in size with time. Initially the plaque is uniformly pigmented, but as the lesion develops, irregular pigmentation occurs which is the early superficial spreading phase of a malignant melanoma (Fig. 39.15). If left untreated, the melanoma advances and enters a deep invasive phase with the same risk of metastases as melanoma elsewhere.

Management Smaller lesions should be excised. There is a problem here with lesions that occupy a large surface area, and excision is not usually possible without grafting. A graft is unsightly, and the condition may be managed expectantly by close and regular follow-up. Action is taken if there is a change in appearance.

Management A variety of methods can be used to treat the condition, including curettage and cautery, the use of topical cytotoxic drugs, excision, cryotherapy, and sometimes superficial radiotherapy. The choice depends on the size of the lesion, its site and the age of the patient.

Leucoplakia In this condition, a fixed white plaque is seen on mucous membranes. The differential diagnosis is from lichen planus – a common inflammatory condition of the skin and mucous membranes – which has a more lace-like appearance, and Candida where the white plaques can be brushed off from the surface mucosa. Oral candidiasis usually occurs in immunocompromised patients, in diabetics or in those on systemic corticosteroid therapy. If there is any doubt, the plaque should be biopsied to exclude dysplasia and, if positive, the area ablated by cryotherapy or laser.

NON-MELANOMA SKIN CANCER

Classification There are two commoner clinical types of carcinoma, both of which arise from keratinocytes: n n

basal cell carcinoma squamous cell carcinoma.

A variety of factors predispose the epidermis towards these malignancies: n

exposure to the sun immunosuppression, e.g. from therapy to prevent rejection of organs n hereditary disorders, e.g. xeroderma pigmentosum, a condition of failure of DNA repair n

The annual incidence of non-melanoma skin cancer is increasing, and basal cell carcinoma is the more common.

Tumours  715

Basal cell carcinoma

Premalignant conditions of the epidermis

This generally arises in sites exposed to the sun. Ninety percent of lesions are on the face.

Non-melanoma skin cancer

Classification There are four clinical types: n

nodulocystic – the most common pigmented n superficial spreading n morphoeic or sclerotic. n

Pathological features Basal cell carcinomas cause local invasion and destruction of surrounding tissues. They penetrate into subcutaneous tissue and can erode into vital structures such as the orbit and brain. Histologically, the tumour cells have strongly basophilic nuclei and little cytoplasm. Cells at the periphery of the tumour give rise to a palisade pattern reminiscent of normal basal cells. Metastases are extremely rare.

Fig. 39.17  Pigmented basal cell carcinoma showing pigmentation of lesion.

Clinical features A nodulocystic lesion has fluid-filled spaces and initially presents as a small translucent or pearly nodule which eventually breaks down, usually as the result of minor trauma, to produce an ulcer – a rodent ulcer characterised by a rolled pearly edge with surface telangiectasia (Fig. 39.16). A pigmented form has characteristic pearly nodules around the edge (Fig. 39.17). Superficial spreading carcinoma is a scaly plaque, usually on the trunk, with epidermal atrophy; pearly translucent nodules can usually be seen around the periphery of the lesion (Fig. 39.18). Morphoeic or sclerotic lesions heal by fibrosis and scarring and may be multifocal; they do not look at all like cystic basal cell carcinomas, do not have pearly nodules but appear as a rather depressed plaque of sclerotic skin (Fig. 39.19).

Management It is important that the tumour is treated adequately on the first occasion to render recurrence unlikely. Treatment depends on the site and size of the lesions at the time of

Fig. 39.18  Superficial basal cell carcinoma on back, showing spreading flat, red plaque.

Fig. 39.16  Cystic basal cell carcinoma on temple,

Fig. 39.19  Sclerotic basal cell carcinoma on forehead

showing central breakdown and ulceration.

showing depressed white plaque.

39 

716  Skin disorders

diagnosis. Small lesions can be dealt with by curettage and cautery, although local excision is usually preferred to ensure there is a margin of clearance around the tumour. Larger lesions may require extensive reconstructive surgery or be treated by radiotherapy. Superficial lesions can be treated with topical immunomodulators such as imiquimod, topical chemotherapeutic agents such as 5-fluorouracil, photo­ dynamic therapy or cryotherapy.

eradicate the tumour. Most lesions are small, and local excision suffices. Problems can occur with larger lesions, where reconstruction by grafting or flap procedures (Ch. 38) may be necessary. Where extensive surgery seems likely, radiotherapy can be considered, although long-term sequelae include radiodermatitis, and an unattractive white, avascular scar may make this choice inappropriate for exposed areas such as the face. Tumours on the lip and ear must be treated vigorously from the outset.

Squamous cell carcinoma Aetiology and pathological features Older age groups than those with basal cell carcinoma are usually affected and lesions are also most commonly found on skin repeatedly exposed to ultraviolet light. Industrial carcinogens are also important in their development (ionising radiation, arsenic and chronic exposure to coal tar and mineral oils). They can also arise as a consequence of chronic inflammation, e.g. within chronic leg ulcers. Smokers are prone to squamous cell carcinomas of the lip. The origin of the tumour is within the epidermis, and the cells show some degree of maturation towards keratin formation. Occurrence may be de novo or in pre-existing skin lesions such as active solar keratoses, leucoplakia or Bowen’s disease. Squamous cell carcinoma invades the dermis and deeper tissues such as bone and cartilage. Metastasis to distant sites via both the lymphatics and the bloodstream takes place, although the second is usually a late and uncommon complication of the disease. Lesions of the lip (Fig. 39.20) and ear are prone to spread early.

Clinical features The usual presentation is with either an enlarging painless ulcer with a rolled indurated margin or a papillomatous appearance with areas of ulceration, bleeding or serous exudation from secondary infection on the surface. An unexplained area of ulceration or thickening of the lip must be biopsied at once to establish a diagnosis.

MALIGNANT MELANOMA (SYN. MELANOMA) This is a highly malignant tumour derived from melanocytes (Box 39.3).

Epidemiology and aetiology Malignant melanoma can arise de novo or from a pre-existing melanocytic naevus, especially a large congenital or atypical melanocytic naevus. Melanomas are rare in dark-skinned races and most common in fair-skinned people of Celtic origin. The highest incidence in the world is in northern and western Australia, perhaps because of the exposure of Northern hemisphere migrant ethnic groups to UV light for which their past genetic experience has not prepared them. The incidence of melanoma has been rising, because of the fashion of sun exposure for its perceived enhancement of lifestyle. In young adults its incidence is increasing more rapidly than for any other cancer, and for this age group it represents the second most common cancer (when nonmelanoma skin cancer is excluded). Over the last 40 years or so mortality rates for melanoma in Britain for men have continuously risen from around 1.2 to 3.1 per 100 000 of the population. In women, rates have also risen but less so: from 1.4 to 2.2 per 100 000. These figures reflect the rising melanoma incidence seen but are much less pronounced than the incidence figures would suggest, and this is thought to be due to more patients presenting at an earlier stage, with thinner melanomas.

Management Although metastases from squamous cell carcinoma of the skin are rare, there is a need for adequate local treatment to Box 39.3 

Malignant melanoma

n

UK incidence 19/100 000 per year Incidence has increased fourfold over the last 30 years – it is the most rapidly increasing malignancy in young adults n Risk factors include: – a family history of melanoma – previous melanoma – presence of a large number of moles (>100) – presence of atypical moles – significant ultraviolet exposure and burning – skin type I – affluencea n Prognosis of malignant melanoma is related to tumour thickness at the time of excision (Breslow thickness) n Adequate excision of primary tumour is most important aspect of surgical management n

a

Fig. 39.20  Squamous cell carcinoma on lower lip showing infiltrated keratinised lesion with ulceration.

Public awareness of significance of changes in moles is important to allow early detection and treatment.

Tumours  717 Pathological features All skin areas are vulnerable, although the most commonly affected sites are the lower extremities in women and the trunk) in men. Tumours may also arise in the choroid of the eye and in the oral mucosa. The classification of spread is dealt with below under ‘Management’. However, the pathways are: n

direct extension into the underlying dermis and thence to the subcutaneous tissues n satellite nodules – around the lesion and perhaps caused by tumour deposits lodging in the draining lymphatics n to regional lymph nodes n blood-borne to distant organs.

Clinical classification There are five clinical types of malignant melanoma:

n n

acral lentiginous melanoma (Fig. 39.23) amelanotic melanoma (Fig. 39.24) – a lesion where the malignant melanocytes are not producing melanin; this is uncommon.

Clinical features that suggest a melanoma Most patients present with a new skin lesion or a change in the character of a pre-existing naevus. The features are summarised in Box 39.4.

Other presentations Malignant melanoma can also present with metastases – localised lymph node enlargement or distant spread such as cerebral deposits.

Prophylaxis Public awareness campaigns are an important part of the management of the disease. Patients should be persuaded to check their skin regularly for moles that change and should

n

lentigo maligna superficial spreading melanoma (Fig. 39.21) n nodular melanoma (Fig. 39.22) n

Fig. 39.23  Acral melanoma spreading under nail.

Fig. 39.21  Superficial spreading malignant melanoma showing asymmetry, irregular border and variation in colour with raised nodule developing.

Fig. 39.22  Nodular malignant melanoma showing raised,

Fig. 39.24  Amelanotic malignant melanoma on neck,

deeply pigmented tumour.

showing raised, non-pigmented tumour.

Malignant melanoma (syn. melanoma)

39 

718  Skin disorders Box 39.4 

Changes in pigmented lesions indicative   of malignant melanoma

American Cancer Society checklist A  Asymmetry of lesion B  Irregular border C  Irregular colour D  Diameter >6 mm

Stratum corneum Granular cell layer Epidermis

Glasgow seven-point checklist Major features Minor features 1 2 3

Change in size Change in shape Change in colour

4 5 6 7 One major feature indicates

Diameter of lesion >7 mm Inflammation around lesion Bleeding of lesion Itch/altered sensation removal of lesion

Dermo–epidermal junction

A feature of both checklists is the presence of a changing lesion which identifies it as being different from other pigmented lesions on the patient.

then come early to their doctor if there is concern. Avoidance of unnecessary exposure to the sun by the use of hats, clothing and effective barrier creams is an important message to communicate to the public and should, in the long term, reduce the incidence of both malignant melanoma and other epidermal cancers. Patients with a greatly increased risk of melanoma are those with a giant (20 cm or more) congenital pigmented naevus and those with a strong family history of melanoma. Patients who have had a previous primary melanoma or who have >100 typical moles or >2 atypical moles have a moderately increased chance of developing melanoma. Individuals with fair skin and poor tanning ability or freckling should also be advised to take great care with sun avoidance and protection.

Management and prognosis Suspicious lesions Any questionable lesion on either history or physical examination must always be completely excised down to subcutis and sent for histological examination. A more difficult decision is when a patient presents with multiple naevi which are showing variation in the evenness of pigmentation within lesions and between lesions. Patients with this so-called ‘atypical naevus syndrome’ have a higher than normal risk of developing melanoma. They should be managed by careful photography of the lesions to act as a yardstick for future change. Any suspicious lesions should be excised and examined microscopically.

Establishing the diagnosis Initial management is by local full thickness skin excision. It is essential to have a clear peripheral and deep margin. The specimen is then assessed histologically to confirm the diagnosis and to assess depth of invasion. Histological classification is in two ways: n

Breslow thickness (which has become the widely adopted best criterion for assessment) – measurement of penetration of malignant cells in millimetres from the granular cell layer of the epidermis through to the deepest invading melanocyte (Fig. 39.25). Tumours less

Deepest invading malignant melanocyte

Dermis

Fig. 39.25  Breslow classification. The pathologist measures the thickness of the tumour in millimetres as the distance from the granular cell layer of the epidermis to the deepest invading melanoma cell.

Table 39.1

Clark’s classification of levels of malignant melanoma

Level

Definition

I II III

Lesion confined to epidermis (melanoma in situ) Invasion into upper (papillary) dermis Occupation and expansion of papillary dermis by melanoma cells Invasion into deeper (reticular) dermis Invasion into subcutaneous fat

IV V

Five-year survival figures fall steadily with deeper layers.

than 0.76 mm at the time of primary excision carry an excellent prognosis, but those that have penetrated further have a poorer prognosis proportionate to depth. Although the inverse relationship between thickness and survival is generally linear, there are occasional melanomas that do not follow the rule. Tumour thickness is the most important prognostic factor but others such as age, sex and size of lesion, metabolic rate, and tumour-infiltrating lymphocytes need to be considered. n Clark’s classification – grades the tumour on the depth within the dermis of malignant invasion (Table 39.1) TMN classification is also based on tumour thickness but includes other variables such as ulceration and mitotic rate (Table 39.2). Further excision can then be planned. Until recently, very wide excision with a skin graft was the normal practice, although recent experience suggests that this does not

Tumours  719 TNM staging of melanoma

Malignant tumours of the dermis

T stage T0 No evidence of primary tumor Tis Melanoma in situ (the tumor remains in the epidermis) T1a The melanoma is less than or equal to 1.0 mm thick, without ulceration and without any dermal mitoses (a mitotic rate of 0/mm2) T1b The melanoma is less than or equal to 1.0 mm thick. It is ulcerated and/or there is one or more dermal mitoses (a mitotic rate is equal to or greater than 1/mm2) T2a The melanoma is between 1.01 and 2.0 mm thick without ulceration T2b The melanoma is between 1.01 and 2.0 mm thick with ulceration T3a The melanoma is between 2.01 and 4.0 mm thick without ulceration T3b The melanoma is between 2.01 and 4.0 mm thick with ulceration T4a The melanoma is thicker than 4.0 mm without ulceration T4b The melanoma is thicker than 4.0 mm with ulceration N stage N0 No spread to nearby lymph nodes N1 Spread to 1 nearby lymph node N2 Spread to 2 or 3 nearby lymph nodes, or spread of melanoma to nearby skin or toward a nearby lymph node area (without reaching the lymph nodes) N3 Spread to 4 or more lymph nodes, or spread to lymph nodes that are clumped together, or spread of melanoma to nearby skin or toward a lymph node area and into the lymph node(s) M stage M0 No distant metastasis M1a Distant metastases to skin or subcutaneous (below the skin) tissue or distant lymph nodes M1b Metastases to lung M1c Metastases to other organs

Other malignancies of the skin

Table 39.2

improve the prognosis. Current practice for thin tumours is to excise with a 1 cm margin for each millimetre depth of invasion. Sentinel node biopsy is an important part of staging the tumour and is used in specialised melanoma centres for clinical trial work. It must be emphasised that malignant melanoma is a curable disease if treated early.

Thicker melanoma/metastases The prognosis is worse in patients with tumours of greater Breslow thickness. There is currently no standard additional treatment after surgical excision for patients whose tumour was of Breslow thickness 2 mm or more, or with surface ulceration. Such patients should be considered for clinical trials or given palliative treatment as appropriate.

Extensive local tumour Treatment is by wide excision including subcutaneous tissue down to the deep fascia. Evidence that this enhances survival is not established.

Satellite limb lesions Clinical control can be achieved by either chemotherapy (see below) or isolated limb perfusion of chemotherapy.

Fig. 39.26  Kaposi sarcoma showing purple nodule. Lymph node involvement Sentinel node biopsy, by which the local draining node is identified by injection of dye or radioisotope at the time of wide excision of the primary tumour and then removed for histological analysis, is helpful in assessing local node involvement. If positive, block dissection of the regional nodes is commonly performed. This helps prevent local recurrence and gives valuable prognostic information but its contribution to survival is unproven and it may cause lymphoedema in the limb with significant morbidity.

Chemotherapy and immunotherapy Local excision, without lymph node dissection but combined with cytotoxic agents (such as dacarbazene), has been used to lengthen the period to tumour relapse. Although some studies have shown that high-dose interferon can lengthen the recurrence-free period in a subset of patients with high-risk melanoma, other have not, and there is no evidence that it improves overall survival. Additionally the drug is associated with significant side-effects. B-RAF is a protein kinase involved in cell proliferation signalling. The gene which encodes this is commonly mutated in melanoma, resulting in the kinase becoming continuously active, leading to increasing cell proliferation and the development of cancer. Inhibitors of B-RAF kinase (and similarly targeted drugs) are currently in the research phase of development and offer hope for melanoma therapy in the future.

MALIGNANT TUMOURS OF THE DERMIS These are rare. The dermis is of mesodermal origin, and therefore malignant tumours are classified as sarcomas. They initially present as small nodules which increase in size and may become tender.

Kaposi sarcoma This is a type of haemangiosarcoma which used to be a relatively rare disease and was found most commonly as a small purple nodule usually on a lymphoedematous leg either of an elderly person of central European Jewish extraction or in sub-Saharan Africa. More recently, however, it has become recognised as an opportunistic tumour in immunosuppressed patients, especially those with HIV infections, in

39 

720  Skin disorders

association with herpes simplex virus type 8 infection. In this context there are a variety of clinical presentations. The most usual is that of a small purple nodule (Fig. 39.26), but a dusky purple plaque or with mucosal involvement is not uncommon. The treatment is usually surgical excision for small discrete lesions and radiotherapy for larger ones.

OTHER MALIGNANCIES OF THE SKIN

Lymphoma Most cutaneous lymphomas are T cell in origin and as they present with diffuse scaly plaques which may look like a cutaneous fungal infection (hence they are also known as mycosis fungoides) they rarely present to surgeons. B-cell lymphomas, however, may present with a solitary nodule or cluster of nodules, and the diagnosis is made on biopsy.

Secondary carcinoma The skin may be the site of distant spread of internal carcinoma. Sometimes solitary nodules arise in the skin that are the result of blood-borne metastases or direct involvement through the lymphatics. Biopsy of the lesion usually provides a clue to the site of the primary disorder. Solitary nodules may occur in cancers that are known to spread with single metastases such as thyroid and renal carcinoma.

Cutaneous signs of internal malignancy The skin is well recognised as a marker for non-metastatic signs of internal malignancy:

n

n n n n n n

n

pruritus may be a presenting feature of myeloproliferative malignancies, particularly in young people – polycythaemia vera, lymphoma deep jaundice from obstruction of the bile duct – carcinoma of the head of the pancreas increased pigmentation – ACTH secretion in carcinoma of the bronchus finger clubbing – colonic/bronchial carcinoma unusual annular erythemas such as erythema gyratum repens – carcinoma of the bronchus tylosis (diffuse keratinous thickening) with palmar plantar hyperkeratosis – carcinoma of the oesophagus acanthosis nigricans (a velvety papillomatous appearance in the intertriginous areas of the axillae and groin and around the neck) – upper gastrointestinal tumours acquired ichthyosis – any internal malignancy.

FURTHER READING Bolognia JL, Jorizzo JL, Rapini RP 2007 Dermatology, 2nd edn. Mosby Elsevier, St Louis Burns T, Breathnach S, Cox N, Griffiths CEM (eds) 2010 Rook’s textbook of dermatology, 8th edn. Wiley-Blackwell, Oxford Buxton PK, Morris-Jones R 2009 ABC of dermatology (ABC series), 5th edn. BMJ Books, London Calonje JE, Brenn T, Lazar AJ, McKee PH 2011 Pathology of the skin: with clinical correlations, 4th edn. Mosby Elsevier, Philadelphia Du Vivier A 2002 Atlas of clinical dermatology, 3rd edn. Churchill Livingstone, Edinburgh Wolff K, Johnson RA 2009 Fitzpatrick’s color atlas and synopsis of clinical dermatology, 6th edn. McGraw-Hill Medical, New York

40 

Surgery in the developing world

Introduction

721

Plastic surgery

730

General challenges of the environment

722

SYSTEMS REVIEW

728

General surgery

728 728

Burn injury Other injuries Advanced cancer Congenital deformity Conclusion

731 732 733 733 734

Infections

734

Some other specialties

736

The acute abdomen Specific causes of intestinal obstruction commonly seen in developing countries Hernia

728 730

INTRODUCTION Whilst there are some excellent surgical centres, the provision of healthcare in many developing countries is often rudimentary, with available expenditure greatly skewed towards the largest conurbations. For many isolated rural communities, secondary care is frequently non-existent (Box 40.1). While preventative medicine and primary care (e.g. mass immunisation programmes) are often supported by international organisations, secondary care (hospital-based) receives less attention. Millions of people do not have access to even basic surgical care. Against this backdrop, the impact of appropriately delivered primary surgery can be huge. For example, the impact of simple repair of an obstructed inguinal hernia, or the elective repair of a vesicovaginal fistula, can far exceed the value for money in quality life years delivered (including return to communal life and work) that is commonly assumed to accompany primary medical care. However, investment into the provision of surgical care in resource-poor nations lags unacceptably behind other domains of healthcare – notable the ‘big three’ well-resourced conditions of TB, HIV and malaria. There are signs that this discrepancy is now being recognised, but data describing the prevalence of surgically remediable disease and dysfunction is scarce, and good research urgently required.

Perspective for surgical visitors from developed countries A considerable challenge for the surgical visitor is the relevance of experience gained in highly technical surgical settings to resource-poor environments. Twenty-first-century developed surgery is highly technical and managed within narrow sub-specialties. In contrast, surgery in poor rural communities is usually delivered by the highly diverse skills

of a generalist working with little technical support. Surgeons are often called upon to undertake emergency obstetric and elective gynaecological operations in addition to general surgical procedures. In isolated areas they need experience in urology, orthopaedics, paediatric surgery, plastic procedures, neurosurgery and thoracic surgery. Many experienced surgical teams working in developing countries attest to the overwhelming importance of training and capacity-building in developing surgical resources for sustainable development in the longer term. Thus the ideal model for support from wealthier groups is to develop partnerships built on mutual respect, two-way learning from poor to rich and vice versa, with capacity-building a prime goal. The most valuable partnerships between developed and developing countries are multiprofessional. Long-term relationships flourish in contrast to short, one-off, visits, and longer-term exchanges of professionals are extremely beneficial. When such support does extend to short-term visits, such visitors must be prepared to empathise with local challenges faced by national colleagues working in developing countries, respect cultural differences, make an effort with the language and readily accept that they will probably receive more than they can give both professionally and personally. Not surprisingly, therefore, many surgeons from developed economies will attest to the impact of a surgical elective – undertaken whilst a medical student – on their career choice. Further into their career, surgeons may have opportunities to return to a developing country for varied periods of time. In the past the focus of these trips has been surgical service provision. In recent years, the focus of partnerships has shifted towards teaching and training, and the model of all forms of partnership between surgeons, surgical departments and institutions is now encouraged. It is beyond the remit of this chapter to discuss the specific management of all diseases that present to the surgeon. In fact, many of the diseases encountered are found in

40 

722  Surgery in the developing world

developed countries and have been discussed in previous chapters. The focus of this chapter will be on: n

understanding the multifactorial reasons for late and advanced surgical presentations n the difference in management of surgical disease n surgical presentations rarely seen in developed countries.

GENERAL CHALLENGES OF THE ENVIRONMENT

Poverty and low literacy rates Two indicators for health include the life expectancy at birth and the infant mortality rate (IMR). These indicators are influenced by the gross domestic product (GDP) and the percentage of GDP spent on health. Figure 40.1 shows the correlation between GDP per capita and infant mortality rates. In developing countries the percentage of GDP spent on education mirrors that spent on health, and adult literacy rates are consequently low. This impacts on public health awareness and health itself.

Lack of clean water and basic sanitation

Although there are many centres of excellence providing surgical care in the poorer developing nations, the overall provision of surgical care is low. This is a direct consequence of the many challenges faced by the population and healthcare workers, as set out in Box 40.2. At first glance these may not appear to be surgically relevant, but in fact they have a profound impact on surgical delivery.

This relates directly to poverty but deserves a separate mention, as its impact on health is so profound. Over twothirds of the population in the poorest countries are still without access to clean drinking water. Approximately 40% of the world’s population lack even basic sanitation. The

Box 40.2 

n n

Box 40.1  n n n n n

n

Statistics on surgery in the developing countries

Only 10% of all major surgery required is actually performed Only 2% of all minor surgery required is actually performed 10% of surgery requires specialist surgical training 40% of surgery requires postgraduate surgical training 50% of surgery requires minimal training

n n n n

Challenges to patients and healthcare workers   in developing countries

Poverty and low literacy rates Lack of clean water and basic sanitation Poor infrastructure, civil unrest, military conflict, distance from health centres and lack of patient transport Cultural practices and beliefs Poor health facilities and limited trained human resources Infectious diseases, malnutrition and the immunocompromised patient Problems in perioperative management

200

Liberia

160 Infant deaths/1000 live births

R2 = 0.90

Angola

180

140 Mozambique 120 100

Ethiopia

80

Swaziland Bangladesh

60

Zimbabwe

40

Egypt

20

Mexico Argentina

South Korea

Taiwan

Iceland

Norway

0 $0

$5000

$10 000

$15 000

$20 000

$25 000

$30 000

$35 000

Gross domestic product (GDP) per capita, in US dollars

Fig. 40.1  Infant mortality and GDP per capita (CIA Worldfactbook 2006).

$40 000

$45 000

General challenges of the environment   723 combination of poor hygiene, contaminated water and poor sanitation results in a heavy burden of infectious disease. The impact of this for surgeons will be discussed below. Waterborne diseases, spread by the faeco-oral route, are responsible for patients occupying half of the world’s hospital beds. Clean running water is frequently sporadic even within hospitals, adding further to the difficulties of providing a surgical service.

Poor infrastructure, civil unrest, military conflict, distance from health centres   and lack of patient transport Public health in any nation is a function not only of the system of delivery of basic healthcare services but also of the general state of the nation’s infrastructure. The developing world continues to struggle with inadequate delivery systems and poor infrastructure. Subsistence farmers who make up the rural poor may have some access to the limited service of a local health centre but this limited access might be completely confounded by inability to get transport to urban hospitals. Travel to health facilities incurs time away from their land (and therefore food supply as well as livelihood), and the financial obstacle may be insurmountable to a family. Travel by foot, bicycle, cart, bus or car may be impossible during rainy seasons when roads are impassable. Civil unrest and military conflict add to these difficulties by disrupting health service provision, destroying infrastructure and adding gross trauma to the burden of disease. Patients able to travel are frequently accompanied by relatives who need to remain with the patient to provide supportive care including food for themselves and the patient (Fig. 40.2).

Inadequate health facilities and limited trained human resources Not only are there limited numbers of health facilities in poor nations but also they may be poorly distributed within the country. In Nigeria, three-quarters of health facilities are in urban areas, where only 30% of the population live. Where hospitals do exist, standards may be poor. A survey undertaken by the World Bank revealed that of 15 publicly operated hospitals in Kenya, 40% of the buildings were in ‘poor and unsatisfactory condition’. Without reliable mains

Fig. 40.2  Patients, relatives and essentials!

electricity, hospitals require additional expensive equipment in order to function effectively (e.g. kerosene or solar fridges for maintaining the cold chain for vaccines). This is often unavailable. Phone and internet services may be non-existent or unreliable, reducing access to current literature and recent advances, second opinions/telemedical support and ongoing medical education – all of which improve isolated services. Surgeons frequently cope with only basic equipment (Fig. 40.3). Resources such as infusion lines, intravenous fluids, drugs and antibiotics are scarce. Surgical instruments are often old or of poor quality, demanding greater expertise from the isolated surgeon. Improvisation of instrumentation and dressings, together with and reuse of all materials, is an invaluable asset. Suture material is expensive and supplies may be erratic. As a result surgeons may have to compromise either with the type of needle or suture material they are using or by modifying their techniques. For instance, reusable needles may be preferred and knots tied with instruments rather than hands to save suture material. In the developed world, aspects of care managed by a clinical nurse specialist (CNS) are increasing to include many roles traditionally carried out by doctors (including surgical assistants). In many countries, nurses have carried out such extended surgical roles for many years. The ratio of medical staff to the general population is much lower than in developed nations; however, the spectrum of health workers carrying out surgical procedures is broader. Those involved in the care of surgical patients include: n

traditional healers health officers in rural health clinics n nurses and doctors in hospitals (district, regional and specialist) n visiting teams (e.g. Flying Eye Doctor). n

Provision of a surgical service is by no means limited to skills delivered by trained clinical staff. Limited human resources affect non-medical essential staff as well (e.g. store keeping, maintenance and accountancy). Inadequate staffing in these areas has a considerable impact on the general running of a hospital and especially affects the provision of specialist services. By way of example, a physician with no pharmacy might still run an out-patient clinic and give the patient a

Fig. 40.3  A theatre in East Africa.

Introduction General challenges of the environment

40 

724  Surgery in the developing world

script to buy medicine elsewhere, but a surgeon can do little without at least basic facilities.

Cultural practices and beliefs All societies have their fair share of diverse cultural, religious and personal beliefs, and some established attitudes can prevent individuals seeking medical intervention. These can result in increased morbidity and mortality and, not infreqently, the hospital is the last place for patients to seek help. Advice might be sought from traditional healers, which often leads to late presentation of established pathology. Surgeons are thus more likely to encounter patients in extremis with advanced disease. Figure 40.4 shows a patient who presented with surgical disease but had previously been ‘branded’ on the abdominal wall in order to exorcise the ‘evil spirits’. In sub-Saharan Africa female genital mutilation is still widely practised despite a growing effort to stop the practice. It is a cause of increased risk of morbidity during childbirth and also increases the risk of a stillbirth up to fourfold. Traditional herbal medicines are known to mimic surgical disease, for example by inducing an ileus complicating postoperative recovery.

Infectious disease, malnutrition   and the immunocompromised patient Of those patients who do present to the surgical team, many are malnourished and as a result have a degree of immunocompromise. Such a condition may also result from parasitic infestation and infectious disease such as HIV, tuberculosis and malaria. Specific surgical presentations relating to infections will be covered later. HIV.  The epidemic of HIV in developing countries is taking its toll on life and resources. In the last 10 years the estimated number of people living with HIV/AIDS has almost tripled, with Africa being the hardest hit region. About 28 million people are thought to be infected in sub-Saharan Africa alone, and 18 million deaths occur in the same region each

year. The second most affected area is South and SouthEast Asia. Pathology resulting from HIV infection is common. Figure 40.5 illustrates a patient with Kaposi sarcoma, a manifestation of advanced HIV. Challenges for the surgical team include: n

immunocompromised patients surgical presentations related to HIV n risks to staff from needlestick injury and mucous membrane contact n lack of antiretroviral prophylaxis after exposure. n

Malaria  kills 3000 children in Africa a day, as well as draining billions of dollars from the continent’s economy each year from lost work time and burden of care. Increasing drug resistance is a serious problem. Chronic malaria is a cause of massive splenomegaly that is associated with its own complications such as traumatic rupture and sepsis. Tuberculosis  remains a major global cause of death due to an infectious agent. Nearly one-third of the world population is infected with tuberculosis. Resurgence of the disease has occurred because of the increasing prevalence of immunocompromised patients, mainly with HIV. Drug-resistant strains have contributed to the problem. Malnutrition  can result from lack of calorific intake, protein, vitamins and/or trace elements. All these in the context of surgery predispose to higher risk of infection, slower healing, wound breakdown and wound dehiscence. Surgical patients who are malnourished need supplemental nutrition to aid healing. Perioperative nutrition (enteral and parenteral) in developed countries is often managed by specialist teams working in conjunction with the surgical team. Sustaining an adequate nutritional status can be a difficult (if not an impossible) task without the skill, knowledge and technological support usually associated with such team-based care.

Problems within perioperative management Regional or local anaesthesia is often preferred to general anaesthesia for safely and management logistic reasons. The only drugs available for such techniques are usually lido­ caine and bupivacaine. Oxygen supplies are often poor and piped oxygen scarce, making postoperative ventilation

Fig. 40.4  Patient whose abdominal wall has been branded to exorcise ‘evil spirits’.

Fig. 40.5  Kaposi sarcoma in a surgical patient.

General challenges of the environment   725 impossible. Opiates may be in scarce supply, and perioperative analgesia inadequate. Ketamine anaesthesia has been highly refined within poor settings, and good courses now exist to train in appropriate and relevant anaesthetic techniques (www.nda.ox.ac.uk/announcements/anaesthesia-indeveloping-countries). However, much investment is required for safer anaesthesia to become the norm in developing countries (Walker & Wilson, 2008). The ‘Lifebox’ safer surgery initiative aims, amongst a package of care for surgery, to ensure that pulse oximetry is available during every general anaesthetic. It is a new initiative that all surgeons in developing nations should be aware of (www.lifebox.org). Caring for critically ill surgical patients is a daunting task in the absence of specialised high-dependency and intensivecare units. Basic pathology tests measuring postoperative electrolytes may not be available, necessitating a different approach to patient care. Blood products are scarce, and their safety is often questioned. Other services including histology may be unavailable, with reliance on one or other of the extraordinarily valuable postal pathology services. The patient in Figure 40.6a underwent excision of a submandibular tumour (Fig. 40.6b), but unfortunately no histological diagnosis was possible. Figure 40.7 illustrates the lack of oncological and palliative care for a woman with local recurrence of breast carcinoma following a previous mastectomy. Stoma therapy in rural areas may not be possible, thus restricting surgical options.

a

Late presentation and advanced pathology As a result of these many challenges patients present in the elective and emergency setting with late and advanced pathology (Fig 40.8). The reasons for this are multifactorial and illustrated in Box 40.3.

b

Decision-making and advanced pathology Decision-making and good judgement are essential capabilities of surgeons worldwide. In developing countries, there may be added challenges often involving ethical dilemmas of when and when not to intervene because absent or inadequate resources might make the attendant risks of surgery greater. Managing advanced pathology in such areas with limited resources presents difficult questions. Elective surgery may be appropriately restricted in favour of life- or limb-saving surgery. Often a ‘wait-and-watch’ or conservative method of treatment can be preferable when the pathology is primarily of cosmetic significance only. It is imperative for surgeons to recognise that not all instances of grossly enlarged pathology require surgical resection. Very substantial salivary gland lumps are a classic example of this, and the morbidity attendant on unnecessary resection is the responsibility of the surgeon, who may wield considerable influence over the informed consent of a poorly educated patient. Rationalisation is important when deciding which pathology deserves scarce operative resources. A good example might be when dealing with a patient presenting with a goitre. A smaller goitre may, initially, appear innocent compared with an obvious larger thyroid mass. However, the

Fig. 40.6  (a) Submandibular tumour. (b) Resected specimen of the tumour. smaller one may extend retrosternally, with risk of the tracheal or oesophageal compression. This is illustrated in Figure 40.9, where only one patient was symptomatic. The social pressure to operate on gross paediatric pathology such as a large AV malformation (Fig. 40.10) may be hard to resist. Indeed, operative intervention may be appropriate after full consent, provided the attendant risks of surgery are fully acknowledged and understood by both patient and surgeon. However, such lesions are notoriously prone to unexpected clinical presentation, and wise judgement might advocate referral to whatever regional centre is available (despite what might be great waits or cost).

40 

726  Surgery in the developing world

Fig. 40.7  Recurrent breast carcinoma.

Fig. 40.9  Only one (second from right) among these patients with goitres was symptomatic.

Fig. 40.8  Obstructed inguinal hernia. Box 40.3 

n n n n n n

Emergency presentation of an obstructed   inguinal hernia

Fig. 40.10  Large arteriovenous malformation.

Inguinal hernia develops Absence of surgical care at the primary level, economic factors and social taboos lead to pathology being ignored Obstruction and surgical emergency (Fig. 40.8) Prolonged travel to surgical care leads to development of haemodynamic compromise, strangulation and sepsis Lack of trained surgical staff, technical equipment and nursing ability to look after critically ill surgical patient Multi-organ failure associated with preventable morbidity and mortality

Congenital and acquired orthopaedic pathology frequently present late, and patients may have significant disability. The fundamental question for the general surgeon outside a specialist centre to address is whether the functional outcome for the patient can and should be improved. This is sometimes much more important than cosmesis, which (as in the case of facial clefting) is likely to be far better addressed in the long term by waiting for specialist provision by referral or visiting team. Figure 40.11 illustrates a patient with chronic dislocation of the right hip and significant disability. Local resources were good, and operative intervention was undertaken. Conversely, Figure 40.12 illustrates a child with gross talipes equinovarus but remarkably good function despite appearance. Conservative management was followed. The management of congenital talipes has, in

Fig. 40.11  Chronic dislocated right hip. (By courtesy of Mr D Rajan, King’s College Hospital, London.)

General challenges of the environment   727 a

Fig. 40.12  Gross talipes equinovarus. (By courtesy of Mr D Rajan, King’s College Hospital, London.)

b

the great majority of cases, been radically transformed in recent years by the introduction of the Ponsetti method of conservative splinting and manipulation.

Surgery of the poor The example of obstetric fistulae There is probably no surgical pathology more illustrative of the plight of the isolated rural poor than the development of obstetric fistula from vagina to bladder and bowel in young women. Patients are often in their early teens, with cephalopelvic disproportion, and may have suffered an obstructed labour lasting many days, far from any medical help. Many women die in childbirth under these circumstances. If the mother survives and passes a macerated fetus, she may be left with a vesicovaginal fistula (VVF) and sometimes a rectovaginal fistula (RVF). Prolonged compression of the anterior vaginal wall, base of the bladder and urethra between the fetal head and the posterior surface of the pubis results in pressure necrosis and the development of a VVF. A similar process compressing the posterior vaginal wall and rectum between the fetal head and sacral promontory results in further necrosis and the development of an RVF. These women suffer constant incontinence of urine and/or faeces, leaving them wet, smelly, leading to social and psychological isolation (Fig. 40.13a). The complexity of the fistula repair varies

Fig. 40.13  (a) Patient with vesicovaginal fistula. (b) Simple vesicovaginal fistula. (By courtesy of Mr B Hancock, Manchester.)

40 

728  Surgery in the developing world

enormously. A simple mid-vaginal VVF (Fig. 40.13) can be simply repaired in two layers (occasionally interposing a transposed local fat flap) through the vagina. Other cases associated with far more extensive injuries and resultant

scarring require complex dissection and reconstruction. The overall success rate for repair in experienced hands is about 90%, and successful closure is one of the most lifetransforming procedures in the whole of surgery.

SYSTEMS REVIEW The pattern of surgical disease presentation varies enormously between the developed and less developed world. For example, appendicitis – although a common cause of acute abdominal pain in the West – is a rarer differential in many parts of sub-Saharan Africa. Inconsistencies in the prevalence of surgical diseases also occur between neighbouring countries. Hence, familiarity with the distribution of disease presentation to the local area is important. As mentioned previously, the diagnosis and management of surgical conditions presents the surgeon with specific challenges. Indeed, the lack of hospital and community resources available to diagnose and manage patients emphasises the importance of clinical skills and sound judgement. Described below are some of the conditions commonly encountered by surgeons practising in developing countries. The emphasis throughout this chapter is on the challenges that these pathologies present to the surgeon and on aspects of management that differ from those delivered in wealthier healthcare systems.

GENERAL SURGERY THE ACUTE ABDOMEN The most common procedure for the general surgeon is the drainage of abscesses. These are a consequence of inadequate hygiene, immunosuppression and malnutrition. Infections are frequently neglected, and abscesses of significant size and chronicity consequently have to be dealt with. In rural areas elective abdominal surgery is rarely performed; however, patients frequently present with acute abdominal pain. The initial management of patients with acute abdominal pain commences with resuscitation. It comprises: intravenous rehydration, correction of metabolic disorder, nasogastric aspiration, antibiotic treatment for sepsis and provision of analgesia. In contrast to the Western world, however, accurate preoperative diagnosis is often impossible in a developing country. In the absence of a definitive diagnosis, subsequent clinical management requires a pragmatic approach. In the first instance the surgeon must decide whether operative intervention is required. The general indications for operative intervention include conditions where a diagnosis has been made, e.g. perforated peptic ulcer that requires an operation. In addition, laparotomy is indicated in some circumstances when a diagnosis has not been secured and clinical improvement has not occurred despite resuscitation. In contrast, operations should be avoided for diagnosed abdominal conditions where surgery is not indicated and

also for undiagnosed abdominal pain where the patient is improving. In Uganda intestinal obstruction accounts for over 90% of all presentations with acute abdominal pain. The general causes of intestinal obstruction have been described in Chapter 24. The cardinal features of vomiting, colicky abdominal pain, distension and constipation should alert the surgeon to the likely diagnosis of obstruction. The generic diagnosis of obstruction, and the differentiation between small- and large-bowel obstruction, can generally be made with ease. The specific cause of obstruction can usually be identified from the history (e.g. adhesions if previous laparotomy). In other instances, a physical sign denotes the cause (e.g. an incarcerated hernia). The surgeon must be alert to physical signs that may represent pathology endemic to the area but not frequently seen in developed countries. For instance, in the obstructed patient, a mass in the right iliac fossa might represent ileocaecal tuberculosis rather than an appendix mass, the probable diagnosis in a Western country. In cases of simple obstruction, fluid and electrolyte resuscitation takes precedence over an operation. When closedloop or strangulated obstruction has occurred, aggressive rehydration is required as well as prompt operative intervention. Some causes of simple obstruction that resolve spontaneously on conservative treatment include: n

post-surgical adhesions a localised inflammatory mass (e.g. appendix mass or pyosalpinx) n a mass due to Ascaris worms. n

Non-operative management of obstruction should never be maintained if strangulation supervenes.

SPECIFIC CAUSES OF INTESTINAL OBSTRUCTION COMMONLY SEEN   IN DEVELOPING COUNTRIES

Sigmoid volvulus Aetiology and epidemiology The high-fibre diet consumed in underdeveloped countries produces a large residue in the colon. This results in colonic distension and also impacts on motility, facilitating volvulus formation. In contrast, this condition is relatively uncommon in the West, where diseases of a low-fibre diet, such as diverticular disease, predominate. In parts of East Africa, sigmoid volvulus commonly occurs in adult males.

Clinical features The condition may present acutely, but in many instances a history of subacute episodes can be elicited.

General surgery  729 The clinical features of large-bowel volvulus generally commence with constipation (for flatus), followed by increasing abdominal distension. The abdomen can distend to huge proportions, but often little pain is experienced and tenderness is minimal. This disparity between the patients’ apparent comfort and the abdominal signs is often striking. When available, abdominal radiography will classically display the ‘coffee-bean’ appearance of a sigmoid volvulus.

Caecal volvulus

Management

Management

Management of sigmoid volvulus depends largely on the type of volvulus that presents. In most instances, the volvulus is subacute and there is no impairment of intestinal blood supply. The aim should be to treat this group nonoperatively if possible. In acute cases, however, the mesenteric blood supply to the large bowel is impaired and septic shock can occur rapidly. These cases will require aggressive resuscitation as well as prompt intervention. In the first instance, decompression can be attempted with a sigmoidoscope and flatus tube. This technique is successful in 75% of cases. When successful, a flatus tube can be placed into the sigmoid colon to aid decompression and prevent recurrence. When successful decompression has been achieved an elective sigmoid colectomy should be considered as the incidence of recurrence is high. If, however, in the acute setting, the sigmoid decompression fails or there are signs of strangulation and gangrene, a laparotomy will be required. At operation, if the affected large bowel is viable, as in Figure 40.14, it requires untwisting with insertion of a rectal tube and/or suturing the colon to the abdominal wall to prevent further attacks. If the volvulus has strangulated, however, resection will be required. The surgical options depend largely on the condition of the patient and the technical ability of the surgeon. Much consideration is required prior to creating a stoma. Poverty and lack of specialist nursing staff makes successful stoma management unlikely. In this instance, however, when a sigmoid colon has required acute resection either a defunctioning transverse loop, end (Hartmann’s) or double-barrelled colostomy will be required.

Caecal volvulus in the absence of access to colonoscopy will almost always require a laparotomy. If the caecal volvulus can be untwisted and appears viable at operation a caecopexy procedure may be performed to anchor the caecum to the anterior abdominal wall. Alternatively a caecostomy with a Foley catheter passed through the anterior abdominal wall is fashioned. If, however, the bowel is not viable a right hemicolectomy will be required.

Caecal volvulus is rare in developed countries. In some instances the caecum, ascending colon and ileum are all free to rotate and undergo volvulus. The clinical presentation of this condition is much the same as that of an acute sigmoid volvulus. Plain abdominal radiographs may demonstrate a large gas shadow placed centrally with a suspicious absence of gas in the right lower quadrant.

Small-bowel volvulus Aetiology Volvulus of the small gut is encountered rarely in the developed world. When it does occur it is usually seen in infants as a result of intestinal malrotation or another congenital anomaly. In adults this condition is extremely rare and usually results from a ‘twist’ that has occurred around a fixed postsurgical adhesion. In contrast, however, small-bowel volvulus is seen frequently in developing countries in all age groups. The aetiology commonly arises from a congenital band which tethers the bowel from the posterior abdominal wall to a point a few centimetres proximal to the ileocaecal valve. In other cases post-surgical adhesions are to blame.

Clinical features and management The characteristic clinical features of small-bowel volvulus include the sudden onset of colicky abdominal pain, distension and vomiting. The impact of rapid cessation of blood flow to the bowel is profound. Over a short period of time haemodynamic instability supervenes secondary to hypovolaemia and sepsis. For this reason these patients require aggressive resuscitation with intravenous fluid and antibiotics. In theory, treatment is easy if the condition is detected early. In these cases ‘untwisting’ of the affected gut can be performed at laparotomy if irreversible bowel wall strangulation has not already occurred. In many cases small-bowel resection will be necessary, however. At the time of surgery, care must be taken not to rupture the affected bowel loop. Under these circumstances overall mortality rises to approximately 30%.

Adhesion obstruction

Fig. 40.14  Sigmoid volvulus.

Postoperative adhesions can cause intestinal obstruction many years following previous abdominal surgery. Management of obstruction that occurs secondary to adhesions virtually always affects the small bowel. Treatment for this form of obstruction is usually non-operative. Replacement of fluid and electrolyte losses as well as nasogastric

SYSTEMS REVIEW General surgery The acute abdomen Specific causes of intestinal obstruction commonly seen in developing countries

40 

730  Surgery in the developing world

decompression (drip and suck) forms the basis of management. The indications to discontinue non-operative treatment include signs of peritonism or sepsis. Under these circumstances the surgeon must suspect that bowel infarction has supervened.

Intussusception Epidemiology and aetiology Intussusception is rarely seen in adults in the developed world. In the developing world, however, it is encountered more frequently, although the condition still predominates in infants and young children. Telescoping of the ileum into the caecum (ileocaecal intussusception) is the type most commonly seen. In addition, adult caeco-colic, colo-colic and ileo-ileal intussusceptions are seen in parts of Nigeria and Uganda. Sometimes intussusception occurs secondary to a polyp or tumour acting as a lead-point but in many cases no specific cause is identifiable.

Clinical features The combination of colicky abdominal pain, bloody diarrhoea and an abdominal mass should alert the surgeon to the possibility of intussusception.

Management In children an intussusception will sometimes resolve spontaneously. This is not the case in adults. In developed countries it is sometimes possible to achieve reduction of an intussusception hydrostatically using contrast media. This is rarely possible in developing countries and should not be attempted without adequate access to surgical services. When an operation is required an attempt at manual reduction of the intussusception should be afforded. This is successful in approximately 80% of cases. When reduction is not possible, or the intussuscepted segment has strangulated, resection or exteriorisation of the affected bowel segment will be necessary.

Obstruction due to tuberculosis See below.

Obstruction due to Ascaris worms Aetiology Ingested Ascaris ova grow into worms within the gut lumen. Ascaris infestation is generally an indication of poor sanitation and consequently is seen frequently where poverty prevails. Only rarely is intestinal contamination so heavy that bowel obstruction occurs. Indeed, obstruction often follows an attempt at decontamination, as paralysis of the worms may result in a bolus and predispose towards complete blockage.

Clinical features A diagnosis of ascaris bowel obstruction may be considered when a child presents with a history of having passed worms rectally or having vomited them. In some cases an irregular mobile abdominal mass can be palpated.

Management When ascaris obstruction has been diagnosed, and there are no features of peritoneal irritation, conservative management should be instituted. This involves the administration of intravenous fluids and nasogastric decompression. Deworming with mebendazole should not be attempted until the obstruction has resolved, as there is a risk of aggravating the condition. In most instances non-operative treatment is successful and surgery is not required. In some cases, however, when the obstruction has failed to resolve, or perforation has occurred, a laparotomy is indicated. When surgery is required for uncomplicated obstruction, every attempt should be made to avoid enterotomy, and instead attempts should be made to break up the mass and milk the worms into the caecum from where they can be passed safely.

HERNIA A comprehensive account of the presentation, complications and management of inguinal hernias has been given in Chapter 27. Although inguinal hernias are commonly seen throughout the world, the presentation and management of this condition varies widely between developed and developing countries. Hernias often reach a gigantic size before treatment is sought. Size, in itself, is seldom the determinant for presentation; rather it is the negative impact of pain on work and earning capacity. Indeed, presentation is often delayed until complications such as incarceration or strangulation have supervened.

Management Standard treatment of inguinal hernias includes excision of the hernial sac (herniotomy) and repair of the abdominal wall defect (herniorrhaphy). The latter is achieved for inguinal hernia in developed countries by using a mesh which is fixed to the posterior wall of the inguinal canal. In developing countries, the technique generally requires modification. Certainly for large inguinoscrotal hernias, excision of the sac may require extensive dissection into the scrotum. Under these circumstances the sac can be divided once the contents have been reduced into the abdomen. The distal portion of the sac remains in situ in the scrotum. As a sterile mesh is expensive, repair of the posterior wall is usually achieved with the conventional Bassini or Shouldice procedures.

PLASTIC SURGERY Plastic surgery, or the surgery of reconstruction, is frequently neglected in the provision of comprehensive surgical care in developing countries. This is unfortunate, since at least 20% of the surgical case load of a hospital in rural Africa is likely to require plastic surgical methods as part or all of the management (Box 40.4). Plastic surgery frequently requires no more than basic surgical resources, with little of the specialised equipment that can be associated with other surgical disciplines. Its primary role is in restoring tissues to their

Plastic surgery  731 Box 40.4 

Main areas of plastic surgery in developing countries

Post trauma n Face n Hands n Lower limb, especially compound fractures n Urogenital n Skin, especially burns and degloving or crush Congenital anomaly n Face, especially clefting n Hands n Urogenital n Skin, especially lymphatic, vascular, tumours Cancer and sequelae n Skin n Facial n Sarcomas n Advanced cancers of many forms Soft-tissue infection n Hand infections n Necrotising fasciitis n Neglected infections, which may include bone ‘Difficult’ wounds n Overlying ‘privileged’ areas, or in diabetics, immunosuppressed patients, or following irradiation

normal form and function, thereby enabling the patient to feel more confident and function socially. Plastic surgery methodology (see Ch. 38) includes careful discipline for tissue handling, the use of grafts of all tissue types (which are transferred without their blood supply) and a wide repertoire of flaps (which are transferred with a nutrient blood supply). Basic principles include dealing adequately with the underlying pathology before reconstruction (which may follow immediately or be delayed) and not expecting grafted material to ‘take’ on sites which have exposed, dried bone or are otherwise denuded of nutrient supply for wound healing. Tissues which are raised for transfer must be mobilised with a clear understanding of the underlying blood supply, and put into the new position without tension, underlying blood or exudates, and with careful handling to avoid early damage or loss.

BURN INJURY It is outside the scope of this chapter to give a detailed account of burn management (see Ch. 10). Burn injury is one of the most commonly seen conditions in hospitals in the developing world, and is frequently neglected. Common causes include childhood scalds and falls into open fires used for cooking. Burns from petrol, electric shock and house fires are also remarkably common, and have been joined in many countries recently by conflict-related burns and acid burns following domestic violence. Burn injury is naturally more common where public health measures to control the use of volatile liquids and acids are less well organised. Likewise, poverty restricts cooking to open fires, and a reduction in severe burn injury usually follows significant periods of economic prosperity. The severity of a burn relates to its site and depth, and the mortality of given types increases with early childhood

✚ n n n

n n

n

Clinical Box 40.1 

  First aid in burns cases

Manage airway/ventilation if inhalational element is present Insert intravenous access line if burn >10% in adults, >6% in children Divide any circumferential full-thickness constricting burn immediately – so-called ‘escharotomy’, does not require anaesthetic Give appropriate analgesia Give fluids according to a regimen with which you are familiar – take great care not to fluid overload, especially in children Give tetanus prophylaxis

and also old age. Scalds treated rapidly with cold water may remain superficial depending upon the initial fluid temperature, and also whether secondary infection follows. They are usually treated locally, sometimes with traditional remedies, and do not constitute the main problem in developing-world hospitals. Most burns following flame injury, untreated scald, electrical injury and acid/alkali are full thickness, and should be assumed so unless proven otherwise. Minor burns do not require hospital admission, although relatively small-surfacearea burns of important areas (such as the hands or eyelids) should be given urgent priority because of the severe consequences of neglected treatment.

Immediate care Many burns cases in rural areas present late. In urban areas, however, they may arrive early, and require first aid. Initial assessment should include the following: n

Is there evidence of inhalational (smoke or toxic fume) injury? • singed nasal hairs • soot visible in back of throat • dyspnoea n What is the approximate body surface area of the burn? • ‘rule of nines’ in adults (see Ch.10); palm = 1%; children, the head and trunk have a higher proportion of surface area n What is the depth of the burn? • full thickness is insensate • superficial burns blister • history n Are any of the extremities circumferentially burnt, causing distal ischaemia? • tight leather-like band of burn, with blue or white hand/foot.

First aid See Clinical Box 40.1.

Burn management Consider early excision of full-thickness burns, before they become infected and can be grafted ‘cleanly’. Hand burns are usually best managed in plastic bags with some anti­ septic fluid, in order to maintain mobility. Eyelid burns must be managed urgently to prevent exposure of the corneas.

Hernia

Plastic surgery Burn injury

40 

732  Surgery in the developing world

Many hospitals in the developing world do not operate early on severe burns, because of the lack of facilities to undertake safe surgical excision with the inevitable fluid loss. This is unfortunate, since many of the later consequences of burn contracture and infection could be avoided if this were possible. If burns are to be dressed, areas which might be expected to heal should be dressed early with non-stick dressings and left intact for 4–5-day periods to prevent secondary contamination. Deeper burns are ideally dressed daily with silver sulfadiazine (Flamazine) or a hypertonic agent such as pure honey. There is no role for topical antibiotics. Facial burns can be covered with simple liquid paraffin for comfort and washed regularly. Regular washing with clean water is a cheap, comfortable and often life-saving action which reduces the overall bacterial concentration in the wound colonisation, thereby reducing the incidence of invasive cellulitis (which is the first cause of septicaemia in burns). Areas of up to 15% of body surface area burn can be excised and split skin grafted at one session, depending upon anaesthetic and postoperative support. Areas which often require more than a split skin graft include eyelids, exposed skull, tendons and nerves, and the neck. These may be best treated with flap cover or full-thickness grafting (difficult technique for large areas).

Longer-term management   and contracture prevention The paramount importance of splintage and mobilisation following burn injury cannot be overemphasised. Simple plastic rings fashioned from strips of suction tubing connected together and placed around the neck can prevent severe neck flexion contracture developing. Hands, which are not being used, must be splinted, usually with wrist extended, metacarpophalangeal joints flexed, and fingers straight. The social needs of badly burnt patients must also be addressed. Significant scarring and loss of function may often be unavoidable, and it is vital to begin to help the victim and their family early on in coming to terms with this, as well as planning for future occupation, and social reintegration.

Burn contracture Burn contractures present one of the most common and enduring images of disabling injury in the developing world (Fig. 40.15). The loss of function of limbs, and hands in particular, is all the more devastating to lives where physical function is an essential component in personal or family survival. These disabilities also influence future marriage prospects and social integration. Contracture release requires careful planning, and a certain amount of overall skin loss can be compensated for by mobilising adjacent tissue (such as in the versatile ‘Y to V plasty’ for dense linear flexion contractures). However, many contractures when released require the defect to be covered with additional skin, usually in the form of split graft. Thicker grafts are more difficult to get to ‘take’, and they leave poorly healing donor sites, but are most successful in preventing contracture relapse. Grafted areas must be splinted postoperatively until the joint has healed fully and is actively mobile.

Fig. 40.15  Burn contracture. When contracture release exposes major nerves, joints, or tendons, it is wise to attempt to cover these with local flaps of full-thickness tissue, and use split graft for the remaining areas. Contractures may often benefit from multiple operative releases and grafts, and the wise surgeon will anticipate this in taking care of available donor sites and careful attention to detail. Blood and exudates must be prevented from accumulating beneath the grafts, and this is usually best done by tying over dressings onto the graft in the early days.

OTHER INJURIES

Facial injuries Facial injuries are usually predominantly either bony or softtissue, although severe road accidents and conflict injuries are inevitably combined. The most severe mid-facial bony fracture (classified as the Le Fort III, or ‘craniofacial disjunction’) can compromise the airway, and first aid involves pulling the upper jaw firmly forward to disimpact the fracture and clear the airway. Most other fractures fall into welldescribed patterns and can be corrected electively. Soft-tissue facial injury in the developing world frequently involves loss of a major part, from animal or human bites, avulsion or weapon. It is not possible to describe all possible reconstructions, but two principles are essential: n

First, tissues such as the lip and nasal margin, the eyelid or the ear, are all irreplaceable, and therefore should be preserved if at all possible and only sacrificed if utterly destroyed or irredeemably damaged. Limited amounts of such remaining tissue should even be replaced, often contrary to the accepted teaching of surgical practice on wound debridement and toilet. n Second, most secondary, elective, reconstruction will involve flap mobilisation, with little role for ‘simple’ grafts or flaps. Such surgery is not complicated, but is usually best reserved for those with previous experience

Plastic surgery  733 rather than risking the production of additional scars in unfavourable places which is often seen following poor reconstruction.

Hand injuries Hand injuries require early wound care and washing, with preservation of all possible vital structures. The difficulties encountered with using dynamic splints following tendon repair in poor rural communities mean that tendon injuries are usually best given an attempt at primary repair and protected mobilisation (if fine instruments and suture materials are available). Flexor tendon injuries can have major long-lasting adverse effects on livelihood, and should always be managed with the best attention available for physiotherapy post surgery. Failing such a level of facilities, is the option of leaving the wound closed and treated with elective secondary tendon grafting at a later date (as was the case in major hand units up to about 30 years ago in developed health centres). Most bone injuries of the hand sustained in hot climates are best managed as conservatively as possible, using Kirchner wire fixation and pinning when necessary. There is an urgent need for many more dedicated hand injury treatment centres to be developed throughout poor countries, since this aspect of healthcare is ideally suited to management by skilled healthcare assistants and therapists (as has been shown clearly in India). It is also of greatest importance when livelihoods might be adversely affected by loss of hand function in manual labourers. The goal of all hand surgery is upgrading the injured or deformed hand to the best possible functional level.

Lower-limb injuries

health centres) may be painful, smelly and debilitating, with blood loss and suppuration. Such tumours may be of the breast, skin, thyroid, oropharynx, bladder, or other rarer conditions. In rural areas, other treatments, such as radiotherapy, chemotherapy and opiate analgesia are usually not available or a scarce resource. Surgical excision may often be the only reasonable option both for potential cure and for palliation if there is no hope of successful eradication. Major fungating cancers can present the surgeon with formidable problems in how to manage the resulting defect. Plastic surgery techniques are often able to deal with such tissue loss during the same operation, and can render cases operable which would otherwise be deemed not so. A common example is the use of the latissimus dorsi myocutaneous flap to cover massive anterior chest wall defects (including rib and pleural loss) following breast cancer excision.

CONGENITAL DEFORMITY Common congenital deformities which can be successfully reconstructed include facial clefts (approx 1 in 350 births in Asia, 1 in 650 births in Europe, 1 in 800 births in Africa), some urogenital defects (1 in 300 births) (Fig. 40.16) and hand anomalies. Cleft lip and palate in particular carries various stigmata: for example the speech disorder associated with unrepaired cleft palate is often thought to indicate mental deficiency (which it clearly does not). Since cleft repair is a method that is easily taught, but can produce very poor results in untrained hands, it should be confined to those with the relevant expertise. Most parts of the world now have either their own highly trained group of surgeons or are visited by one of the teams of volunteers who undertake such work.

Compound injuries of the lower limb can cause major disability, and are often treated with immediate below-knee amputation. In recent years, this amputation rate has been reduced by the introduction of a range of local, pedicled and distantly transferred (‘free’) flaps, which can be used to cover a carefully debrided and stabilised fracture site. Even complex injuries thus covered can subsequently be built up with cancellous bone grafting so long as an adequately vascularised soft-tissue ‘envelope’ has been created. The value of such lower-limb conservation has been challenged by some trauma authorities. However, the value of maintaining a viable limb without lifelong prosthetic requirements, to the rural communities of the developing world, cannot be overestimated. Such reconstructions are rarely indicated for the mangled and heavily contaminated landmine injury, and any major neurovascular loss (the so-called ‘Gustilo Grade 3c injury’) is usually an absolute indication for amputation in the developing world.

ADVANCED CANCER Much cancer in the developing world presents in an advanced stage. Clearly this may be terminal if metastatic disease is also present, but many tumours do not progress rapidly to such a stage before there has been advanced local tissue destruction. Neglected tumours (rarely seen in developed

Fig. 40.16  Ectopia vesicae.

Other injuries Advanced cancer Congenital deformity

40 

734  Surgery in the developing world CONCLUSION

Plastic techniques are versatile and overlap with many other disciplines. Thus, complex and difficult wounds encountered by trauma surgeons, gynaecologists, ENT, eye and neurosurgeons might all benefit from access to surgeons trained in reconstructive methodology. Such a repertoire does not have to be comprehensive, and there is a real role for the training of healthcare assistants with skills confined to wound care, simple grafting and local flap management. The numbers of people throughout the poor world with untreated wounds and injuries (especially in war-torn areas) is simply massive and is one of the most pressing public health needs in the world today.

INFECTIONS Many infections are disease entities that the visiting surgeon will not usually have encountered in regular practice. Unlike most surgery in developed countries which involves degenerative, malignant and traumatic conditions, surgery of sepsis and infection is proportionately much greater in developing nations. A description of common infections that often require surgical intervention follows.

Typhoid fever Pathophysiology During the second or third week of a typhoid illness, heavy gut contamination occurs through bilious excretion and bacteraemic spread. Typhoid (Salmonella typhi) colonises the lymphoid tissue of the jejunum, caecum, appendix and ascending colon. This leads to oedema and hyperplasia of the lymphoid follicles and may progress to ulceration and perforation.

Diagnosis The diagnosis of an intestinal typhoid perforation is often suggested by the clinical features of peritonitis in a region where the disease is known to be endemic. Blood cultures are positive in 80% of patients in the second week. At this time, stool and urine cultures also become positive in those that have not received antimicrobial treatment.

Management The surgical management of an intestinal perforation due to typhoid involves resuscitation and early laparotomy along with antimicrobial treatment. The perforation is usually found on the antimesenteric bowel border. Small perforations can be closed simply, but resection may be required for larger defects. The acutely ill patient with multiple perforations found at laparotomy might be best managed by simple ‘exteriorisation’ of the perforated area(s) and stabilisation of systemic disorder (with antimicrobial treatment) before definitive care of the bowel lesions as a delayed procedure. Acute cholecystitis due to typhoid infection is rare. Chronic cholecystitis due to Salmonella typhi can however perpetuate a carrier state where patients continue to excrete

microbes in the stool despite antimicrobial treatment. Cholecystectomy may be indicated for this group.

Abdominal tuberculosis Abdominal tuberculosis (TB) refers to mycobacterial infection of the gastrointestinal tract, mesenteric lymph nodes, peritoneum and omentum, as well as the liver and spleen. A recent resurgence of TB has occurred both in the West as well as the developing world as a result of the proliferation of HIV.

Pathophysiology Primary gastrointestinal infection occurs by ingestion of the bovine strain of Mycobacterium tuberculosis in milk. Secondary intestinal disease occurs from swallowing sputum infected with the bacteria. The terminal ileum and caecum are the most susceptible parts of the GI tract. The tubercle initially localises in the mucosal glands and, from there, spreads to Peyer’s patches, where ulceration, inflammation and/or sclerosis occur. The disease may extend to involve the peritoneum, producing widespread tuberculous deposits. The usual presentation involves a history of insidious ill health, abdominal pain and weight loss. In addition, an acute abdomen may result from peritonitis or obstruction depending on whether the ulcerative or inflammatory process has predominated.

Management Surgical treatment of intestinal TB is only indicated if gut complications, such as obstruction or peritonitis, have occurred. Otherwise, antituberculous chemotherapy is the mainstay of management.

Amoebiasis and amoebic liver abscess Pathophysiology Amoebiasis is caused by infestation with Entamoeba histolytica – a protozoal parasite. Approximately 10% of the world population have been infected, but many carriers remain asymptomatic. The active trophozoite subsists in the colon and, consequently, the disease is spread via the faeco-oral route. Amoebiasis exists in two forms: intestinal and extra­ intestinal. The intestinal form affects the large bowel, sparing the terminal ileum. The extraintestinal form affects the liver, lung, skin and brain.

Clinical features Clinical presentation may be insidious, but patients often present acutely with high fever, tenesmus and colicky abdominal pain associated with bloody diarrhoea (amoebic dysentery or colitis). Colonic perforation is accompanied by signs of peritonitis and shock. Operative treatment is not usually required but is indicated when perforation or severe bleeding has supervened.

Liver abscess Liver abscess is a potential complication of amoebic colitis (see Ch.19). The organ is affected by the portal spread of protozoa. Rupture of this abscess into the abdominal cavity

Infections  735 or into the pleural space is a life-threatening complication. Surgery is rarely needed for the treatment of amoebic liver abscesses, as most can be managed with metronidazole with or without needle aspiration.

Hydatid disease Pathophysiology and clinical features The liver is the commonest site of involvement for the tapeworm Echinococcus granulosus (see Ch. 19), although any organ can be affected. Ova are generally passed in the faeces of affected animal hosts, usually dogs, and consequently pass to humans via the faeco-oral route. The Echinococcus ova penetrate the intestine to pass into the portal circulation and thence to the liver. In the liver the ova develop into cysts and enlarge insidiously. Symptomatic patients may present with a history of vague abdominal pain, hepatomegaly, jaundice and fever.

Management Surgical management remains the mainstay of treatment for hepatic hydatid disease. Spillage of contents of the cyst should be avoided to prevent seeding. Surgical emergencies occur when rupture of the cyst occurs following trauma to an enlarged diseased liver. Medical treatment with albendazole is recommended perioperatively and for patients with disseminated disease.

Schistosomiasis (bilharzia) Three schistosomes produce human disease: Schistosoma haematobium, S. mansoni and S. japonicum. The latter is prevalent in the Far East, whereas the other species cause infection mostly in Africa and South America (see also Ch. 33).

Pathophysiology Cercaria represent the infective form of the parasite to humans. Snails act as vectors for the parasite. Human infection occurs following penetration of the skin by cercaria. The parasites then migrate to the liver and lungs via the venous system as schistosomules. Once mature, pairs of worms migrate to the mesenteric venules via the portal vein or to the bladder submucosa, where they replicate. The eggs can then leave the body in the faeces or urine by penetrating the intestinal or bladder wall. The larvae (miracidia) hatch once they enter fresh water, where they then infect host snails to perpetuate the cycle.

Clinical features The clinical features of schistosomal infection are widespread. Acute infection is generally heralded by an acute inflammatory response at the site of the invading cercaria. This is often termed ‘swimmers’ or ‘bathers’ itch. Within a few days of infection an acute febrile illness generally supervenes. The clinical features of acute infection include fever, myalgia, urticaria, eosinophilia, diarrhoea and cough. The clinical features of chronic schistosomal infestation depend mostly on the type of the schistosome involved. S. mansoni is the most prevalent schistosome in Africa and Latin America. It usually affects the colon, where it

causes erythema, ulceration and inflammatory pseudo­ polyps. In its progressive form, fibrosis and stricture formation supervene. Granulomatous hepatitis followed by portal hypertension can give rise to hepatosplenomegaly and oesophageal varices. Pulmonary schistosomiasis occurs as the schistosomules pass to the lungs. Chronic pulmonary infection leads to pulmonary hypertension and cor pulmonale. S. haematobium predominantly affects the urinary tract. It is most prevalent in Egypt and Middle Eastern countries. The presence of S. haematobium ova in 3000-year-old Egyptian mummies suggests that this disease was also prevalent in ancient times. Dysuria, haematuria and frequency result from the chronic inflammatory process that affects the urological system. In the latter stages, obstructive uropathy and chronic pyelonephritis supervene. Epidemiological studies suggest that schistosomal infection of the bladder is associated with both squamous cell and transitional cell cancer.

Diagnosis and management The diagnosis of schistosomal infection is often made on clinical grounds alone. Ova can, however, be detected in the stools and urine as well as on rectal biopsy. Antischistosomal chemotherapeutic agents include praziquantel and oxamniquine. In endemic areas reinfection occurs rapidly following treatment.

Tropical ulcer Tropical ulcer is common throughout the village communities in the tropics and subtropics.

Acute tropical ulcer Pathophysiology

Acute tropical ulcer results from a cutaneous synergistic bacterial infection usually following trivial injury to the leg below the knee. A combination of anaerobes and facultative aerobes have been implicated in the pathogenesis (Fusobacterium fusiforme and Borrelia vincentii ). Necrotising infection spreads within a few days until an area of demarcation is reached. Blistering of the skin with an area of central gangrene is usually surrounded by an area of cellulitis. Slough separation occurs early to reveal a bed of healthy granulation tissue surrounded by normal skin.

Differential diagnosis There are numerous causes of severe ulceration in tropical environments. In recent years, the widespread incidence of deeply necrosing ulcers from Mycobacterium ulcerans infection – the ‘Burulli ulcer’ – has been identified, and is the subject of a WHO Global Initiative to raise awareness and direct best practice in management (www.who.int/buruli/en/). Antimycotic therapy is essential first-line treatment for such ulcers, with surgery having a major role in debriding dead tissue, effecting viable cover for exposed vital structures, and managing contractures and disabling functional loss. Other causes of ulceration include other mycobacteria, cutaneous leishmaniasis (oriental sore), TB, leprosy, cutaneous anthrax, syphilitic gumma, and naturally causes such as venous stasis, and diabetic ulceration which are ubiquitous in presentation.

Conclusion

Infections

40 

736  Surgery in the developing world

Management Treatment of acute tropical ulcer might require prompt administration of intravenous systemic antibiotics with broad-spectrum cover. Unfortunately, most patients present at a later stage when skin necrosis is established. These patients may require antimicrobial treatment if persistent surrounding cellulitis is still present, as well as surgical debridement to remove non-viable tissue. Frequent washing with clean water and regular dressing changes then form the basis of local infection control. Small clean ulcers will heal spontaneously by epithelialisation from the ulcer edges. Larger ulcers (greater than 1–2 cm) can be encouraged to heal more rapidly with a split skin graft (meshed or perforated to encourage ‘take’ and allow exudate to escape).

Chronic tropical ulcer

Pathophysiology and differential diagnosis When acute tropical ulcers fail to heal they become chronic. The strict definition of a chronic tropical ulcer is an acute lesion that has become chronic; however, numerous disease processes produce identical lower-limb ulceration. These differential diagnoses (Box 40.5 – not exhaustive) can be difficult to distinguish from chronic tropical ulceration on clinical grounds alone. The chronic ulcer has a pale and scarred appearance and the ulcer base is usually adjacent to the tibial periosteum. Over an extended period, repeated fibrosis can lead to severe contracture formation. Most ulcers remain indolent over many years, with malnutrition often influencing adequate wound healing. Any significant change in ulcer size or associated pain may signal squamous cell malignant change (the development of a so-called ‘Marjolin’s ulcer’).

Management Treatment of chronic tropical ulceration comprises local infection control (usually by removal of dead tissue, copious washing and provision of skin cover). The latter is usually best achieved by shaving the ulcer down to a healthy bed, and covering with a split skin graft that has been perforated or meshed. The graft should be immobilised with a firm dressing while it ‘takes’ over 10–14 days, and supported with an external pressure dressing (such as Tubigrip) for several months after surgery.

Box 40.5  n n n n

n n n n

Differential diagnosis for chronic tropical ulceration

Syphilitic infection Yaws infection Mycobacterial ulceration Burulli ulcer – Tuberculosis – Leprosy Venous ulceration Arterial disease Diabetic ulceration Trauma

SOME OTHER SPECIALTIES Obstetrics and gynaecology Obstetricians and gynaecologists perform operations, yet in the developed world the specialty is a separate entity from other surgical disciplines. In developing countries, with obstetric specialists scarce, general surgeons are often called upon to perform emergency obstetric procedures and even elective gynaecological operations. Common O&G surgical procedures include: n

obstetric • caesarean section or symphysiotomy for obstructed labour, or in cases of pre-eclampsia/eclampsia • emergency hysterectomy or uterine repair for uterine rupture n gynaecological • bilateral tubal ligation • hysterectomy – abdominal and vaginal • ovarian cystectomy • vesicovaginal fistula repair.

Trauma and orthopaedics The most common cause of disability worldwide is trauma following road traffic injury (22.8%). War and civil unrest also results in a high volume of patients needing urgent treatment and thus stretching already scarce resources – with war and violence accounting for another 14.4 % of global injury. Disability as a long-term outcome of such injury is common, especially amongst those in poor countries where few have access to surgery, artificial limbs and rehabilitation. Recent global initiatives have attempted to address this urgent need. Primary Trauma Care is a comprehensive programme of appropriate methods and support for trauma delivery in resource-poor nations (www.nda.ox.ac.uk/ptc/) Provision of orthopaedic treatment in rural centres can be basic and is sometimes provided by a general surgeon. The most appropriate methods for fracture management might not be the more widely used internal fixation techniques adopted in developed hospitals with ultra-clean environments. The closed management of fractures using balanced traction and other well-established methods (Charnley 2007) may be. Serious complications of fractures such as malunion, delayed and non-union are common. This is illustrated in Figure 40.17, where a young man with non-union required hospital care for about 18 months. Immobilisation with such injury for long periods results in muscle atrophy, joint stiffness and possible further debilitation from pressure sore formation. Orthopaedic surgical procedures undertaken in poor environments are associated with a high incidence of complications, especially postoperative sepsis. Osteomyelitis (either primary or secondarily following compound fracture) is common and is difficult to erradicate without access to radical surgical excision, reconstruction (including soft-tissue transfer) and prolonged therapy with multiple antibiotics.

Ophthalmology It is estimated that blindness affects 37 million people worldwide (Table 40.1). Approximately three-quarters of all cases

Some other specialties  737 a

Table 40.1

WHO estimates of prevalence of blindness for different regions (2002)

Region

Prevalence of blindness

European region Americas SE Asia Africa Western Pacific region Eastern Mediterranean region World total

2.7 million 2.4 million 11.6 million 6.7 million 9.3 million 4.0 million 36.7 million

Table 40.2 b

Estimated causes of blindness worldwide (WHO 2010)

Cause

%

Cataract Glaucoma Macular degeneration Diabetic retinopathy Corneal opacities Childhood blindness Trachoma Onchocerciasis Others

48 12 9 5 5 4 4 1 12

a

b

Fig. 40.17  (a) Young patient with non-union of lowerlimb fracture. (b) X-ray of non-union.

Fig. 40.18  Trachoma: (a) subtarsal scarring in stage III; (b) corneal neovascularisation and scarring. (By courtesy of Mr D McHugh, King’s College Hospital, London.)

Some other specialties

40 

738  Surgery in the developing world

of blindness are preventable or amenable to cure. Data on the worldwide causes of visual loss are given in Table 40.2. Trachoma is present in epidemic proportions in many developing countries and accounts for a high proportion of preventable blindness. Figure 40.18a shows typical subtarsal scarring seen in stage III trachoma, and Figure 40.18b illustrates corneal neovascularisation and scarring.

FURTHER READING Charnley J 2007 The closed treatment of common fractures. Golden Jubilee edn. Cambridge University Press, Cambridge Walker IA, Wilson IH 2008 Anaesthesia in developing countries – a risk for patients. The Lancet 371: 968–969 Warrell DA, Cox TM, Firth JD (eds) 2010 Oxford textbook of medicine, 5th edn. Oxford University Press, Oxford World Health Organisation 2002 World Health Report, WHO, Geneva. Available online. Accessed 18 January 2011 www.who.int/ violence_injury_prevention/publications/road_traffic/world_report/

Index  739

Index Page numbers followed by “f” indicate figures, “t” indicate tables, and “b” indicate boxes.

A ABC, resuscitation, 133 abdomen acute see acute abdomen burst, 94 examination in critical illness, 131–132 guarding, 344 incisions, 60, 60f inspection in kidney disease, 558 masses in children, 662–663 pain, 341–344 rebound tenderness, 344 splenic rupture, 324 trauma, 667 tuberculosis, 734 abdominal aortic aneurysms (AAAs), 448–449, 462–465, 464b, 464f abdominal distension after incisional hernia repair, 411 intestinal obstruction, 355 abdominal pain and chest examination, 24 in intestinal obstruction, 355 abdominal tuberculosis, 734 abdominal wall closure, 106, 107f defects, congenital, 659–660 abdominal X-ray acute abdomen, 345 acute pancreatitis, 332 chronic pancreatitis, 335, 335f duodenal atresia/stenosis, 656 intestinal atresia, 657 intestinal obstruction, 355, 356f splenic rupture, 324 upper urinary tract, 560–561, 560f ureteric stones, 579 ablation androgen, 596 ovarian suppression and, 436–437 plastic surgery, 698 warts, 708 see also cryoablation; radiofrequency ablation ABO compatibility, 189–190 ABPI (ankle:brachial pressure index), 454 abscesses amoebic liver, 307, 734–735 anal, 394–396, 394f appendiceal, 346 breast, 419–420 crypt, 368, 368f drainage, 20, 116, 119 established, 122 intracranial, 524 intraperitoneal, 93, 93t lung, 243

parapharyngeal, 209, 209f perinephric, 566–567, 567f peritonsillar, 208–210, 209f pyogenic liver, 306–307 renal, 566 septal, 224 soft-tissue, 20–22 splenic, 321 absorbable sutures, 103–104 absorption large bowel, 365–366 small bowel, 354 acalculous cholecystitis, 313–314, 316 achalasia, oesophageal, 281 Achilles tendonitis, 634 ACL (anterior cruciate ligament) injuries, 629–630 acoustic neuroma, 222, 222f acquired hernias, 401 acquired immunity, 111–112 acquired immunodeficiency syndrome see HIV/AIDS acral lentiginous melanoma, 717, 717f acromegaly, 553, 553f acromioclavicular disorders, 618 ACTH (adrenocorticotrophic hormone), 545, 546t, 554 actinic keratoses, 711 active drains, 61 active movement, fractures, 645 activity energy expenditure (AEE), 83 acute abdomen, 341–345 causes, 342t definition, 341–345 developing countries, 728 gastrointestinal disturbances, 344 general clinical features, 341–344 investigation, 344–345 pain, 341–344 physical findings, 344 structured data sheets, 341, 343f adaptive immune system, 112 adenocarcinomas anal, 400 breast see breast cancer caecal, 382–383 gastric, 289 lung, 229 oesophageal, 284 renal, 570–571, 570t salivary glands, 208 small bowel, 364 ulcerative colitis complications, 369 adenoid cystic carcinomas breast, 427 salivary glands, 208 adenolymphoma, salivary glands, 208

adenomas adrenal, 546 adrenocortical, 546–547 gallbladder, 316 large bowel, 374–375, 375b, 375f liver, 308, 308f null-cell, 554 pituitary gland, 555 pleomorphic see pleomorphic adenoma small bowel, 364 thyroid gland, 555 thyrotrophic, 554 toxic solitary thyroid, 534 adenomatous polyps, 376 adenomyoma, gallbladder, 316 adenosine triphosphate (ATP), 133 ADH (antidiuretic hormone), 554 adhesions, 358, 358t, 729–730 adhesive capsulitis, 619–620 adhesives, wound closure, 105 Adie pupil, 683 adjuvant therapy, 181–182, 182t breast cancer, 435–437, 437t colorectal cancer, 379–381 timing of, 181–182 ADL (aids to daily living), 612 admissions unit, 10 adrenal cortex, 543–547 adrenal glands, 543–548, 544b tumours, 555 adrenal insufficiency, acute, 548, 548b adrenal medulla, 543–544, 547–548 adrenalectomy, 545–546 adrenaline, 150, 150b adrenocortical adenoma, 546–547 adrenocortical carcinoma, 546–547 adrenocorticotrophic hormone (ACTH), 545, 546t, 554 adult respiratory distress syndrome (ARDS), 138–139, 139b advanced pathology, developing countries, 725–727 Advanced Trauma Life Support (ATLS), 15 head injury, 22, 22b, 515 training, 4 aerodigestive tract, 201–212, 203f aesthetic plastic surgery, 702 AFP (alpha-fetoprotein), 243, 302 age breast cancer risk, 421–423, 421f of consent, 12–13 coronary artery disease risk, 253 knee disorders, 627 and wound healing, 100 age-related macular degeneration (ARMD), 677, 677f AIDS see HIV/AIDS aids to daily living (ADL), 612 AION (anterior ischaemic optic neuropathy), 675 air aspiration from pleura, 166

airway difficult, 71–72 management, 170–173, 171f emergency department, 15–16, 16b, 16f general anaesthesia, 69–70, 69f–70f, 71b obstruction acute, 210b management, 16b postoperative (thyroid or parathyroid surgery), 536b upper, 210–211 surgical, 171–173 (see also cricothyroidotomy; tracheostomy) airways pressure monitoring, in the critically ill, 136 ALARA principle, 29 albumin, 300, 302 alcohol consumption acute pancreatitis, 330 and anaesthesia, 67 chronic pancreatitis, 334 alcohol intoxication, 23–24 alemtuzumab, 192 alfentanil, 77, 145, 145t alkaline glutaraldehyde sterilisation, 56 alkaline phosphatase, 302, 610 alkylating agents, 182 allergic rhinitis, 225–226 allergies, 224 AlloDerm®, 696 allograft, 187 alpha-blockers, 547–548 alpha-fetoprotein (AFP), 243, 302 alpha-globulin, 300 amaurosis fugax, 473–474 amelanotic melanoma, 717, 717f American Society of Anesthesiologists (ASA), 68 amethonium, 145 Ametop, 72, 150 amino acids, 354 aminoglutethimide, 436 5-aminosalicylic acid (5-ASA), 369 amoebiasis, 734–735 amoebic liver abscess, 307, 734–735 amoxicillin, 118t amputation, 462, 468 anaemia, 558, 612 anaesthesia, 150 airway examination, 68, 68b assessment of medical fitness, 66–68 charting, 74–75 definition, 65–66 developing countries, 724–725 drugs used in, 76–78 examination under see examination under anaesthesia (EUA) existing medical treatment, 67 history, 65–66, 66b immediate preoperative preparation, 68–69

740  Index investigations, 68, 68t monitoring, 74–75 the anaesthetic machine, 75 the patient, 74–75, 74b, 74f postoperative care, 78–80 pre-assessment, 66 premedication, 69, 69t preoperative grading, 68, 68b preoperative preparation, 66–69 principles, 65–66 purpose, 65 recovery from, 78, 78b see also general anaesthesia; local anaesthesia; regional anaesthesia anaesthetic machine, 75, 75f anaesthetic mask, 69, 70f anal canal, 400 anal disorders, 385–400 causing pruritus ani, 397 clinical examination, 387–388 general considerations, 385–389 investigation, 388–389 symptoms, 387 anal intraepithelial neoplasia (AIN), 400 anal manometry, 399 anal margin, 400 anal polyps, 392 anal sepsis, 393–397 anal sphincters, 385, 386f, 397–398 analgesia after chest surgery, 245–246 cardiac surgery, 276 in critically ill patients, 144–145, 145t pancreatic cancer, 338 postoperative, 87–88 see also opioid analgesics analgesic agents, 77 anaplastic carcinoma, thyroid, 539–540 anastomotic false aneurysm, 465 Anderson-Hynes pyeloplasty, 575, 575f androgen ablation, 596 androgen suppression, 596 andrology, 604–606 aneurysmal bone cysts, 617 aneurysmal disease, 448–449, 452 management, 462–465 angiodysplasia, 351 angiofibroma, nasal, 227 angiogenesis, 98, 99t angiography arterial disease, 456, 456f coronary, 252 magnetic resonance, 46, 46f neurosurgery, 514 renal adenocarcinoma, 570 thoracic outlet syndrome, 471 vascular trauma, 477, 477f angioplasty, percutaneous transluminal coronary see percutaneous transluminal coronary angioplasty (PTCA) angiotensin I, 475 angiotensin II, 475 anisocoria, 683–684 ankle, 631–632 ankle:brachial pressure index (ABPI), 454 annular pancreas, 327 anorectal anomalies, 658, 658f see also anal disorders antalgic gait, 609b antegrade pyelography, 562 anterior cruciate ligament (ACL) injuries, 629–630 anterior ischaemic optic neuropathy (AION), 675

anterior triangle swellings, 201 anterolateral thoracotomy, 244–245 anti-arrhythmics, 67 antibiotic prophylaxis, 113–114, 113t choice of antibiotic, 113 dose and timing, 114 gangrene, 123b identification of patients at risk, 113 in the jaundiced patient, 303–304 long-term, 114 overwhelming postsplenectomy infection (OPSI), 325–326, 326t prosthesis infection, 90 respiratory complications, 92 route of administration, 114 tetanus, 123b wound infections, 89–90 wounds, 21 antibiotic therapy acquired infections, 119 acute pyelonephritis, 565 after chest surgery, 245 antimitotic, 183 common, and their uses, 118t cystitis, 583 infection management, 116 osteomyelitis, 614–615 selective decontamination, 117 septic arthritis, 615 septicaemia, 117 for specific infections, 119t urinary tract infection, 565 use of, 118–119 antibody-mediated immunity, 111–112 anticholinergics, 589 anticoagulant therapy after valvular surgery, 265 and anaesthesia, 67 cardiac surgery, 276–277 complications, 496 deep-vein thrombosis, 495–496 antidiuretic hormone (ADH), 554 anti-emetics, 78 antigen-presenting cells, 189, 189f anti-IL-2 receptor antibody, 191–192, 192t antimetabolites, 182–183 antimitotic antibiotics, 183 antioxidants, 135 antisepsis, 55, 109 antiseptics, 112 antistreptolysin (ASO), 610 antithrombotic therapy see anticoagulant therapy antithymocyte globulins (ATG), 191, 193 antithyroid agents, 535 antrostomy, 226 anuria, 558 anus anatomy, 385–389, 386f blood supply, 386 embryology, 385 epithelial lining, 385 fissure, 393, 394f lymphatic supply, 386 muscles, 385, 386f nerve supply, 385–386 physiology, 385–389 tumours, 400 see also entries beginning anal anxiolytics, 145t aorta acute transection, 17 pathology, 274 rupture, 271

aortic aneurysms, 274, 276f, 448–449, 452, 452f, 462–465, 464b, 464f–465f aortic dissection, 265–267, 267f, 274, 449 aortic regurgitation, 261 aortic stenosis, 260–261, 273–275, 274f aortobifemoral bypass graft, 468, 468f aorto-iliac disease, 458, 466–468, 468f APACHE II scoring system, 128, 129t, 332 apex beat, 131 apnoea, testing for, 146–147 apocrine sweat glands, 705 apparent pain, 342 appendicectomy, 346 appendicitis, acute, 345–346, 346f, 382 appendix, 381–383 abscess, 346 anatomy, 381–382 disease, 382 function, 382 histology, 381–382 mass, 346, 663 neuroendocrine tumours, 551 testes, 665 tumours, 382–383 aprons, 149 ARDS (adult respiratory distress syndrome), 138–139, 139b ARMD (age-related macular degeneration), 677, 677f aromatase inhibitors, 436 arterial anatomy, 446 arterial blood gases, 52, 136–137, 160–161, 160t arterial blood sampling, 158–161, 158f arterial disease, 443–479 future directions, 479 history, 451–453 investigations, 452–453 pathological features, 447–451 patient assessment, 451–456 physical findings, 452–453 techniques, 457–462 upper limb, 470–471 arterial endothelium, 446 arterial injury, fractures, 646 arterial narrowing (stenosis), 445, 454 arterial physiology, 443–445 abnormal, 445 arterial tree structure, 445 arterial wall compliance, 445 structure, 446, 446b arteriography jaundice, 302–303, 303f upper urinary tract, 562, 562f arteriosclerosis, 447–448 arteriovenous fistula, traumatic, 477–478, 569 arteriovenous malformations (AVMs), 351, 478–479, 725, 726f arteritis, 449–451, 450t arthritis, 610–613 management, 612–613 radiological appearances in, 609t arthrodesis arthritis, 631 osteoarthritis, 620 arthrography developmental dysplasia of the hip, 635 knee, 628

orthopaedics, 609 shoulder, 618 arthroplasty hallux valgus, 633 osteoarthritis, 620 osteonecrosis of the femoral head, 626 arthroscopy, 610 arthritis, 612, 631 meniscal injuries, 629 osteoarthritis, 620 shoulder, 618 arthrotomy, septic arthritis, 615 articular surface fractures, 648 artificial (hybrid) organ implantation, 187 ASA (American Society of Anesthesiologists), 68 Ascaris worms, 730 ascending venography, 488, 488f ascites, pancreatic, 336 asepsis, 109, 113, 149–150 Aspergillus spp., 242 aspiration cytology breast cancer, 431 malignant disease, 180 aspiration of stomach contents, 72 assisted spontaneous breathing (ASB), 139t astrocytomas, 518 ataxic gait, 609b ATG (antithymocyte globulins), 191, 193 atheroma, 447–448 atheromatous plaque, 448, 455 atherosclerosis and aneurysmal disease, 448–449 coronary artery, 252–258 renal artery, 475, 476t atherosclerotic occlusive disease, 447–448 atherosclerotic stenoses, 445 atonic bladder, 589 atracurium, 77, 145 atresia duodenal, 656–657, 656f intestinal, 657 atrioventricular (AV) node, 249 atrioventricular bundle, 249 atrophie blanche, 484 attico-antral disease, 219, 219f audiometry, 215–216, 216f auditory function see hearing audits, 3–4 auricle trauma, 216 auscultation abdomen, 344 intestinal obstruction, 355 kidney, 559 valvular heart disease, 260 auto transfusion, 457 autoantibodies, 534 autogenous tissue transfer, breast reconstruction, 440–441 autograft, 187 autologous vein prostheses, 457 autonomic neuropathy, diabetic foot, 470 autonomic rhinitis, 225 autonomy, 148 autosomal dominant polycystic renal disease, 564 autosomal recessive polycystic renal disease, 564 avascular necrosis of the humeral head, 620 of the lunate, 624 AVMs (arteriovenous malformations), 351, 478–479, 725, 726f axial pattern flaps, 697, 697f

Index  741 axillary lymph nodes, breast cancer, 423–424, 424t, 430f, 434, 434f axillary mini-thoracotomies, 244 axillary-subclavian vein thrombosis, 491–492 axonotmesis, 650–651 azathioprine, 191–192, 192t, 193b azoospermia, 605

B bacteraemia, 49, 116 bacteria infection see bacterial infection large bowel, 366 translocation, 117 see also microbiology; specific organisms bacterial infection conjunctivitis, 685 ophthalmic, in HIV, 685 salivary gland, 207 skin, 709–710 Bacteroides, 100 balance, 214 balanced anaesthesia, 65 balanoposthitis, 666 balloon angioplasty carotid artery disease, 474 critical limb ischaemia, 468 renal artery stenosis, 476 band ligation, haemorrhoids, 391, 392f bandaging leg ulcers, 506 barbiturates, 145t bariatric surgery, 7, 293–296 aetiology, 293 combined restrictive/ malabsorptive procedures, 294–295 definition, 293 epidemiology, 293 indications for, 294b management of obesity, 293 restrictive procedures, 294 surgical options, 293–295 barium enema colorectal cancer, 378 Crohn’s disease, 372, 372f diverticular disease, 373, 373f faecal incontinence, 399 ulcerative colitis, 369, 369f barium sulphate, 35, 36f–37f, 37t barium swallow, oesophageal cancer, 285 Barlow’s test, 635b Barrett’s oesophagus, 281, 284 basal cell papillomas, 711, 711f basal metabolic rate (BMR), 83 basal-cell carcinoma, 715–716, 715f bathers itch, 735 battering, 648 Behçet’s disease, 451 beneficence, 148 benign cystic swellings, cervical, 204 benign lymphoepithelial infiltration, salivary glands, 208 benign prostatic hyperplasia (BPH), 163–164, 591, 592f benzodiazepines, 78, 145t bereavement, 13–14 Bernoulli’s theorem, 443 beta-blockers, 67, 547–548 Bier’s block, 73 bilateral anterolateral thoracotomy with transverse sternotomy, 245 bilateral choanal atresia, 656

bilateral retrograde ureterography, 579 bile, 300–301 bile ducts, 298–300, 300b stones, 314–315 bile salt conversion, 376 bile stasis, 312 bilharzia, 584, 584f, 735 biliary atresia, 304 biliary colic, 312–313 biliary collecting system, 298–300, 299f biliary decompression, 304, 304f biliary stents, 304, 304f biliary tree, 297–317 anatomical variations, 300 congenital abnormalities, 300b biliopancreatic diversion with duodenal switch, 295, 295f bilirubin, 300–301 deconjugation, 312 increased secretion in bile, 312 bimanual examination bladder tumours, 585 see also rectal examination; vaginal examination Biobrane®, 696 biochemistry, 27–28, 27t gastrinoma, 550 insulinomas, 549 intestinal obstruction, 356 jaundice, 301–302, 302t pancreatic cancer, 337–338 peptic ulcer disease, 288 see also specific tests biological factors, wound healing, 100–101, 100b biological response to injury, 81 modification, 183 biopsy, 50–51, 50f bone tumours, 616 Crohn’s disease, 362 goitres, 533 jaundice, 303 malignant disease, 180 rectal, 388, 388f schistosomiasis, 584 skin, 706 thyroid gland, 532 Bismuth-Corlette classification, 317, 317b bispectral index (BIS) monitor, 75, 136 bladder conditioning, 589 congenital abnormalities, 583 disorders/diseases, 583–590 diverticula, 587, 587f examination, 581–582 exstrophy of the, 583, 660, 660f fistulae, 374, 587–588, 588t function tests, 582 incomplete emptying, 581 neuropathic, 588–589, 589f outflow obstruction, 663 pain, 581 in spinal injuries, 650 stones see urinary stones suprapubic drainage, 164–165 trauma, 584–585 tuberculosis, 584 tumours, 585–587 bleeding after thyroid surgery, 536 anal, 387, 389 arrest of (haemostasis), 102–103, 102f–103f, 104t post-splenectomy, 326 rectal, 381, 381b upper-gastrointestinal, 92–93, 346–351, 348b, 348t urinary catheterisation, 163

varicose veins, 485 wound healing, 97 see also haemorrhage blepharitis, 684–685, 684f blood disorders, 321, 323 fluidity within veins, 481 levels, 25–26 urinary see haematuria blood culture acute pyelonephritis, 565 infections, 115 orchitis, 602 osteomyelitis, 614 blood energy, 443–444 blood flow, 443 patterns of, 444, 444f phases of, 445 pulsatile nature of, 444 resistance to, 444 blood gas analysis pulmonary embolism, 502 see also arterial blood sampling blood loss non-traumatic causes of, 20 traumatic causes of, 20 see also haemorrhage blood pressure, 443–445 in acute cardiac tamponade, 18 in anaesthesia, 74 examination, arterial disease, 452 monitoring in the critically ill, 137 blood products, 457 blood tests acute abdomen, 344–345 acute cholecystitis, 313 acute pyelonephritis, 565 biliary colic, 312 hip, 625 hypersplenism, 322 infections, 115 intestinal obstruction, 356 orchitis, 602 orthopaedics, 610 osteomyelitis, 614–615 perinephric abscess, 567 Perthe’s disease, 636 phaeochromocytoma, 547 renal adenocarcinoma, 570 retroperitoneal fibrosis, 579 rheumatoid arthritis, 612 septic arthritis, 615 splenic rupture, 324 thyroid cancer, 539 urinary stones, 572–573 blood transfusion, 457 blood vessels, dermal, 705, 712 Bloom and Richardson grade, 426 blow-outs fractures of the orbit, 672 varicose veins, 486 blue naevus, 712 blunt trauma chest, 238 eyes, 672 heart and great vessels, 271 liver, 305–306 ocular, 673, 673t spleen, 323 vascular injuries, 476–477 B-lymphocytes, 111–112, 188, 189f B-mode ultrasound, 454, 454f body composition, 81 body mass index (BMI), 293, 294t body temperature control during operations, 59 monitoring in the critically ill, 138 paediatrics, 653

bone marrow function, hypersplenism, 322 bone metastases, 439 bone scanning ankle, 631 bone tumours, 616 osteomyelitis, 614–615 Perthe’s disease, 636 prostate cancer, 595, 595f bone tumours, 616–617, 616t bone wax, 104t boundary effects, blood flow, 444, 444f bowel function alteration, 387 intraluminal contrast agents, 35–37, 36f–37f, 37t preoperative preparation, 85, 113 regulation, 390 sounds, 131–132, 344 in spinal injuries, 650 Bowen’s disease, 714, 714f Bowie position, 58t bow-legs, 637 BPH (benign prostatic hyperplasia), 163–164, 591, 592f brachial artery, blood sampling, 159, 159f brachial plexus damage after breast surgery, 435 injuries, 59, 652, 652t brachytherapy, 182 brain traumatic injury, 514–518, 515b, 516f tumours, 518–519 see also entries beginning cerebral brainstem death, 146–147 diagnosis, 146–147 organ donation, 147 branch retinal artery occlusion (BRAO), 674, 675f branchial cyst, 204 BRAO (branch retinal artery occlusion), 674, 675f BRCA1/BRCA2, 421 breast conservation surgery, 434 reconstruction, 439–441, 440f–441f, 700, 700f breast cancer, 420–441 aetiology, 420–423, 421b, 421f, 421t, 423b clinical features, 427–428, 427t–428t, 428f clinicopathological features, 426–427, 426t developing countries, 725, 726f diagnosis, 428–432, 429f–431f, 430t epidemiology, 420 management, 432–437 advanced disease and special problems, 437–441 natural history, 423–424, 424t prevention, 425 prognosis, 424–425 screening, 425 staging, 424–425, 424t–425t breast disease, 415–441, 416f benign, 415–420, 416t infection, 420 lumps/lumpiness, 417–419 malignant see breast cancer nipple discharge, 419 pain, 415–417 trauma, 419–420 breast-feeding, 422

742  Index breathing management in the emergency department, 17–18 systems, 75 Breslow classification, 718, 718f bromocriptine, 552 bronchiectasis, 242–243 bronchodilators, 67 bronchogenic cysts, 243 bronchoscopy, 231–232 brushing, 50 Budd-Chiari syndrome, 308 Buerger’s disease, 451 bullet wounds, 272 bunionectomy, 633 bupivacaine, 150, 150t burns, 147, 147b, 147f contracture, 732, 732f developing countries, 731–732, 731b ocular, 672–673 plastic surgery, 700–701, 700b tetanus prophylaxis, 21 burns units, 128 burst abdomen, 94 butterfly fragment, fractures, 639 bypass surgery, arterial, 460, 461b coronary artery see coronary artery bypass grafting (CABG) critical limb ischaemia, 468–469

C CABG see coronary artery bypass grafting (CABG) cadaver grafts, 187 caecal adenocarcinoma, 382–383 caecal volvulus, 359, 729 caecum, 365 calcific tendonitis, acute, 619 calcitonin, 529, 540 calf perforating veins, 484–485 calf pump failure syndrome, 503–504 calf tenderness in deep-vein thrombosis, 494 calf thrombus, 495 callus formation, fractures, 641 caloric test, 216 Calot’s triangle, 299f Campbell de Morgan spots, 712 cancer see malignant disease; specific types/sites Candida infection, 124, 714 ocular, 686–687 in HIV, 685 cannulae, venous access, 151 capillary haemangiomas, 712 capnographs, 75 capsule endoscopy, 49 carbohydrate antigen 19-9 (CA 19-9), 338 carbohydrates, 300 14 CO2 breath test, 329 carboplatin, 183 carcinoembryonic antigen (CEA), 338, 378 carcinogenesis, 176–177 carcinoid syndrome, 551 carcinoid tumours see neuroendocrine tumours carcinoma in situ, 177 bladder, 585 breast, 426, 432–433 carcinomas adrenal, 545–546 adrenocortical, 546–547 colon, 378, 379f, 380b (see also colorectal cancer) invasive breast, 426–427 parathyroid glands, 543

penis, 600, 600f pituitary, 552, 554 rectal, 378–379, 380b, 380f (see also colorectal cancer) renal pelvis, 571, 571f secondary cutaneous, 720 ulcerative colitis complications, 369 cardiac catheterisation, 252 cardiac inotropes, 140, 140t cardiac output, 131 measurement, 157–158 monitoring in the critically ill, 137 cardiac surgery, 247–277 access, 275–277 anatomy, 249 antithrombotic therapy, 276–277 basic concepts, 247–249 chest drainage, 276 diagnostic procedures, 249–252 ICU/recovery, 275–276 minimally invasive, 275 multidisciplinary team, 272–275 pain control, 276 preoperative patient briefing, 275 return to full activities, 277 risk stratification, 265 ventilation, 276 see also specific procedures cardiac tamponade, 18, 168, 249, 259–260, 271, 272f cardiogenic shock, 133b–134b cardiopulmonary bypass (CPB), 247–249, 248f cardiopulmonary exercise testing (CPX), 52 cardiovascular system assessment in critical illness, 131 examination in arterial disease, 452–453 function tests, 51–52 medical fitness assessment, 66–67 monitoring in the critically ill, 137 in paediatrics, 653 therapeutics in the critically ill, 139–140 Care of Critically Ill Surgical Patient (CCrISP) course, 4 Caroli’s syndrome, 305 carotid artery disease, 473–474 carotid body tumour, 204, 474, 475f carotid endarterectomy (CEA), 474 carotid pulse, 260t casts, fractures, 643–644 cataract, 676–677, 677f catgut, 103–104 cauda equina compression, 522, 522b causation, wounds, 100 cavernous haemangioma, 308, 308f CD4+ cells, 189, 704–705 + CD8 cells, 189, 704–705 cefotaxime, 118t ceftazidime, 118t cefuroxime, 118t cell-mediated immunity, 112 cellular proliferation and organisation, fractures, 640 cellulitis, 119, 121–122 bacterial, 509 streptococcal, 710 varicose veins, 484 central nervous system (CNS) assessment and critical illness, 131

congenital anomalies, 520–521 disorders causing faecal incontinence, 398–399 medical fitness assessment, 67 metastases, 439 monitoring in the critically ill, 136 therapeutics in the critically ill, 141 tumours, 518t vasculitis, isolated, 451 central retinal artery occlusion (CRAO), 674, 675f central serous retinopathy, 677 central venous catheters, 154–158 common sites, 154 complications, 91–92, 157 equipment, 154 indications, 154 internal jugular vein, 156f post-cannulation checks, 156 procedure, 154–155 pulse-induced contour cardiac output (PiCCO) measurement, 158 right internal jugular vein, 156 subclavian vein, 155–156, 155f subcutaneous tunnelling, 157, 157f Swan-Ganz catheter, 157, 158f central venous pressure (CVP), 137 cephalosporins, 142 c-erbB2 receptors, breast cancer, 426, 435–436 cerebral haemorrhage, 519–520 cerebral injury, 141, 141b cerebral oedema, 141 cerebral perfusion pressure (CPP), 136 cerebrospinal fluid (CSF) circulation, 521, 521f leak, 222 overproduction, 522 cerebrovascular disease, 473–474 medical fitness assessment, 67 see also strokes cervical cystic lymphangioma, 655–656 cervical spine degenerative disease, 523 imaging in the trauma patient, 19, 19f injuries, 649 protection in the emergency department, 15–16 chemical injury, eyes, 672 chemodectoma, 204 chemotherapy, 182–183 brain tumours, 519 breast cancer, 435–437 colorectal cancer, 379–381 gastric cancer, 292 hydatid disease, 125 lung cancer, 233–234 malignant melanoma, 719 oesophageal cancer, 286 pancreatic cancer, 338–339 prostate cancer, 596 renal adenocarcinoma, 571 renal tuberculosis, 568 chest, 229–246 incisions, 244–245 physiotherapy, 245 postoperative care, 245–246 procedures, 165–169 trauma, 238–239, 666–667 chest drainage, 234–235, 235f cardiac surgery, 276 complications, 168 haemothorax, 17 Heimlich valve, 235, 236f indications, 235b insertion, 166–168, 167f, 235

postoperative care, 245–246 removal, 168 removal criteria, 235 tension pneumothorax, 17 underwater seal, 235 chest pain and abdominal examination, 24 pulmonary embolism, 501 chest X-ray acute abdomen, 345 acute pancreatitis, 332 bladder tumours, 585 cardiac disease, 250–251 haemothorax, 17 monitoring the respiratory system in the critically ill, 136 pulmonary embolism, 502 renal adenocarcinoma, 570 renal tuberculosis, 568 splenic rupture, 324 tension pneumothorax, 17 in trauma patients, 18–19 Chiari malformation, 521 child abuse, 648 child-bearing, breast cancer risk, 422 children, 653–667 brain tumours, 519 fractures, 648 general principles, 653–654 of Jehovah’s Witnesses, 13 organ transplantation, 198 orthopaedics, 634–637 surgical pathology, 654–656 urinary tract infection, 564–565, 565b see also neonates chin lift, 170, 171f chitin/chitosan dressings, 104t chlamydial infection, conjunctivitis, 685 chlorhexidine scrubbing up, 57 skin preparation, 56 choanal atresia, bilateral, 656 cholangiocarcinoma, 316–317 extrahepatic, 317, 317b intrahepatic, 310 cholangiography, 302, 302f–303f cholangitis, acute, 314 cholecystectomy, 315 en bloc, 316 cholecystitis in typhoid fever, 734 cholecystography, 302 cholecystokinin (CCK), 327 choledochal cyst, 305 choledocholithiasis, 314 cholestasis, extrahepatic, 301 cholesteatoma, 219 cholesterol coronary artery disease risk, 253 supersaturation, 312 cholesterosis, 316 chondrohamartomas, lung, 234 chondrosarcoma, 617 chronic pelvic pain syndrome, 591 chronic venous insufficiency, 503–504 Churg-Strauss arteritis, 451 Chvostek-Weiss sign, 536 chylothorax, 241–242 ciclosporin, 191–192, 192t, 193b ciprofloxacin, 118t circulation emergency department management, 18 postoperative complications, 90–91, 90b pulmonary embolism, 501–502 circumcision, 599, 666 cis-platinum, 183

Index  743 civil unrest, developing countries, 723 clam cystoplasty, 589 clarithromycin, 118t Clark’s classification, 718, 718t claw toes, 633 cleaning, 55b cleavage lines, 59, 59f cleft lip and palate, 733 clinical factors, wound healing, 100–101 clinical signs, postoperative, 86, 86t clipping, haemostasis, 102, 103f closed drains, 61 closed needle biopsy, 50–51, 50f closed reduction of fractures, 643 clostridial gangrene see gas gangrene Clostridium difficile, 92, 120–121 Clostridium perfringens, 122 Clostridium spp., wound contamination, 100 Clostridium tetani, 21, 123 clotting factors, 26–27, 302 coagulation, 97, 481, 482f in critically ill patients, 144 infrared see infrared coagulation in the jaundiced patient, 303 screen, 26 studies, pancreatic cancer, 337 thermal, 102 coagulopathies, 26 co-amoxiclav, 118t cocaine, 150 cochlear implants, 221–222, 221f coeliac disease, 364 coherent scattering, 28 cold sterilisation, 55–56, 56b colectomy colorectal cancer, 378, 379b–380b, 379f psychological effects of, 4 colitis, 367, 367b ischaemic, 372 see also ulcerative colitis collagen, 98 dermal, 705 wound healing, 99 collateral circulation, 445 collateral ligament stability, 627 colloid breast carcinoma, 427 colloids, 83, 700–701 colon see large bowel colonoscopy colorectal cancer, 378 diverticular disease, 373 faecal incontinence, 399 ulcerative colitis, 369 colorectal cancer, 376–381 aetiology, 376 clinical features, 377–378, 377b epidemiology, 376 intestinal obstruction, 357 investigation, 378 management, 378–381, 379f–380f, 380b metastatic, 310 pathological features, 376–377 screening, 377 staging, 377, 377f, 377t colorectal neuroendocrine tumours, 551 comminuted fracture, 639, 640f common bile duct, 298–299 stones, 314 common peroneal nerve injury, 59 communicating hydrocephalus, 521–522 compartment syndrome, 446, 646, 646b complement system, 111, 111t

complete neurological lesions, 649 complex regional pain syndrome (CRPS) type 1, 647f compound naevus, 712 compression, haemostasis, 102 compression hose deep-vein thrombosis, 496 leg ulcers, 506 varicose veins, 488, 489t compression sclerotherapy, 488–489, 489t Compton scattering, 28–29 computed tomography (CT), 30, 31f–34f acute abdomen, 345 acute appendicitis, 346 acute pancreatitis, 332 amoebic liver abscess, 307 ankle, 631 arterial disease, 455–456, 455f bladder fistulae, 588 bladder tumours, 585 bone tumours, 616 breast cancer, 431 cardiac disease, 251 chronic pancreatitis, 335 colorectal cancer, 378 comparison with other imaging techniques, 46t fractures, 642 gastric cancer, 292 hernias, 404 hip, 625 intestinal obstruction, 356 jaundice, 302 knee, 628 lung cancer, 231 neurosurgery, 513–514 oesophageal cancer, 285 oesophagus, 280 orthopaedics, 609 osteomyelitis, 615 pancreas, 329, 329t pancreatic cancer, 337 peptic ulcer disease, 288 perinephric abscess, 567, 567f pituitary tumours, 552, 552f pulmonary embolism, 502 renal adenocarcinoma, 570 renal trauma, 569 retroperitoneal fibrosis, 579 shoulder, 618 spinal injury, 649 splenic rupture, 324 testicular tumours, 603 in the trauma patient, 19 upper urinary tract, 562, 562f conduction system, 249 conductive hearing loss, 215 condylomata acuminata, 400, 708 confocal microscopy, 49 congenital abnormalities abdominal wall, 659–660 biliary tree, 300b bladder, 583 central nervous system, 520–521 in developing countries, 733, 733f diaphragmatic hernia, 655, 655f heart disease, 272, 272t, 273b hernias, 401 kidneys, 563–564 liver, 304–305 plastic surgery in, 698–700 umbilical hernia, 409 ureters, 573–575 urethra, 597, 597f congenital adrenal hyperplasia, 546

congenital cysts dermoid, 713 dilation of the intrahepatic ducts, 305 liver, 304–305 conjunctivitis, 685, 685f connective tissue disease Raynaud’s phenomenon, 473, 473b salivary gland swellings, 208 Conn’s syndrome, 544 consciousness assessment and critical illness, 131 assessment of level of, 513, 514b level of in head injury, 22 consent, 11–13, 149 consolidation, fractures, 641, 642f consolidative phase of wound healing, 97, 99 constipation, 355, 367, 367b contact lenses, 672, 681, 681f contamination, wounds, 100 continent ileostomy, 370, 371f continuous positive airways pressure (CPAP), 136, 139t continuous positive pressure ventilation (CPPV), 139t continuous traction, fractures, 644 continuous wave ultrasound deep-vein thrombosis, 494–495 varicose veins, 487–488 contractures burns, 732, 732f joint, 650 wound healing, 98 contrast studies, 30–37, 38f digital subtraction, 35–37 gastric cancer, 292 hiatus hernia, 282 intestinal obstruction, 356 intraluminal agents for the bowel, 35–37, 36f–37f, 37t intravascular contrast media, 31–35, 35t liver, 46–47 magnetic resonance imaging, 46–47 oesophageal cancer, 285 oesophagus, 280 peptic ulcer disease, 287–288 upper urinary tract, 560–561 see also entries beginning barium core biopsy breast cancer, 431 fibroadenosis, 418 thyroid gland, 532 core decompression, 626 corneal abrasion, 680–681, 680f corneal transplantation, 197–198 coronal synostosis, 521 coronary anatomy, 249 coronary angiography, 252 coronary arteries, 249, 250b, 250f coronary artery bypass grafting (CABG), 252 complications, 257–258 conduct of, 256–257, 257f conduits for, 255–256, 256t evidence for, 253–258 history, 252–253 indications, 253b results of, 257–258, 257t vs medical management, 253–257, 254f, 254t, 256b vs percutaneous transluminal coronary angioplasty, 254–255, 255t vs stenting, 255 coronary artery disease (CAD), 252–258 aetiology, 253 epidemiology, 253–258

management, 253, 256f (see also coronary artery bypass grafting (CABG)) pathology, 253 risk factors, 253 surgical approach, 275 corticosteroids immunosuppression, 191, 192t, 193b and wound healing, 101 cortisol, 545 deficiency, 546 cosmetic surgery, 702 co-trimoxazole, 118t country of birth, breast cancer risk, 421, 421t CPAP (continuous positive airways pressure), 136, 139t C-peptide, 549 CPPV (continuous positive pressure ventilation), 139t craniopharyngiomas, 518, 554 craniosynostosis, 521 craniotomy, brain tumours, 519 CRAO (central retinal artery occlusion), 674, 675f C-reactive protein (CRP), 610 creatinine, 137–138 creatinine clearance, 27, 559–563 crepitus, 642 cricothyroidotomy, 16, 16f, 171–172, 172f Crigler-Najjar syndrome, 301 critical arterial stenosis, 445 critical care units, 127–130 patient management, 128 scoring systems, 128–130, 129t critical illness, 127–148 aetiology, 132–135, 132f diagnosis, 132 ethical considerations, 148 examination, 130–132 history, 130–132, 130b monitoring, 135–138, 136b scoring systems, 128–130, 129t sequelae of intensive care treatment, 147–148 therapeutics, 138–145 Crohn’s disease, 361–362, 361f–362f, 364 anal manifestations, 396 and colorectal cancer, 376 large bowel, 371–372 cross-fluctuation, knee, 627 cross-infection, endoscopy complications, 49 cross-matching haematemesis, 348, 348b organ transplantation, 190 cruciate ligaments, 627, 628f, 629–630 crush fractures, 639, 640f cryoablation, prostate cancer, 596 cryosurgery, 707 cryotherapy, warts, 708 crypt abscess, 368, 368f Cryptococcus neoformans, 685 crystalloids, 83 CSF see cerebrospinal fluid (CSF) Culp pyeloplasty, 575, 575f cultural practices and beliefs, developing countries, 724, 724f culture blood, 115, 565 urine, 559, 565 cultured skin, 696 curettage, 707–708 Cushing’s disease, 553–554 Cushing’s syndrome, 545–546, 545b, 546f, 546t cutaneous fistula, 395

744  Index cyanosis, 17 cyclical breast pain, 416–417 cyclo-oxygenase 2 (COX-2) selective inhibitors, 612 cylindroma, 713 cystadenoma lymphomatosum, 208 cystadenomas, 339 cystic hygroma, 655–656 cystine stones, 572–573 cystitis acute, 583 chronic, 583 interstitial, 584 cystoscopy, 584 cysts aneurysmal bone, 617 branchial, 204 breast, 418–419 choledochal, 305 congenital see congenital cysts dermoid, 713 epidermoid, 713 epididymal, 602 mediastinal, 243 pancreatic, 339, 339t pilar, 713 renal, 564 splenic, 321 thyroglossal, 204, 204f, 528f cytokines infection, 112, 112t organ transplantation, 189 wound healing, 97–98, 99t cytology bladder tumours, 585 neck swellings, 203 renal pelvis carcinoma, 571 cytomegalovirus (CMV), 685 cytopenia, 325 cytotoxic therapy breast cancer, 435–437 warts, 708 see also chemotherapy

D dabigatran etexilate, 497 danazol, 417 day-case surgery, 9–10 recovery, 78 DBS (deep brain stimulation), 525 de Quervain’s syndrome, 624 de Quervain’s thyroiditis, 537 death certification, 13 due to surgery, 13–14 fear of, 184 risk of, 4 debridement, 101–102 decompression biliary, 304, 304f of the gastrointestinal tract, 88–89, 729 pancreatic, 338 decompressive craniectomy, 517 decubitus ulcers, 94, 647, 702 deep brain stimulation (DBS), 525 deep-vein thrombosis (DVT), 491–503 aetiology, 492–493 anatomical considerations, 492 axillary-subclavian vein thrombosis, 491–492 clinical features, 494 diagnosis, 494 epidemiology, 492–493 fracture complications, 646 investigation, 494–495 major antecedents, 492t management, 495–497, 495b–496b

pathological considerations, 493–494 prophylaxis, 496–497, 497t, 498f, 500f–501f pulmonary embolism in, 497–503 risk factors, 493, 493t defecation, 387 deformity, fractures, 642 degenerative valve disease, 259, 259t dehydration, 82 delayed primary closure, wounds, 101–102 delayed union of fractures, 647 dentures, airway obstruction, 15 depolarising muscle relaxants, 76 dermabrasion, 698 dermal collagen, 705 dermatofibroma, 712 dermis, 705 malignant tumours, 719–720 dermoid cysts, 713 desflurane, 76 destroyed lung, 242 detoxification, liver, 300 detrusor instability, 590 developing countries, 721–738 environmental challenges, 722–728 general surgery, 728–730 infections, 734–736 plastic surgery, 730–734 surgical visitors to, 721–722 systems review, 728–738 developmental dysplasia of the hip, 634–635, 635b, 635f deviated nasal septum, 225 diabetes insipidus, 554 diabetes mellitus and atherosclerotic occlusive disease, 447 coronary artery disease risk, 253 and infection, 111 medical fitness assessment, 67 ophthalmic manifestations, 688, 688f postoperative care in, 94–95 postoperative investigations, 86 and wound healing, 100 diabetic foot, 469–470 diabetic maculopathy/retinopathy, 677, 677f, 688, 688f diagnostic aspiration, pleura, 165 dialysis, 141 diamorphine, 77, 145, 145t diaphragm rupture, 239 diaphragmatic hernia, congenital, 655, 655f diastasis at the symphysis pubis, 18, 19f diathermy, 102, 103f diazoxide, 549 DIC (disseminated intravascular coagulation), 26–27, 144 diet breast cancer risk, 422 and colorectal cancer, 376 preoperative preparation, 85 ulcerative colitis, 368 Dieulafoy’s lesion, 351 diffuse nodular goitre, 531f diffuse oesophageal spasm, 280–281 digestion, 353–354 digital subtraction angiography (DSA), 456, 456f digital tonometry, 671 di-iodotyrosine (DIT), 528–529 dimercaptosuccinic acid (DMSA) renography, 565 direct inguinal hernia, 406

discharge anal, 387, 389 nasal, 223–224 nipple, 419, 430t disease modifying anti-rheumatic drugs (DMARDS), 612 disinfectants, 112–113 disinfection, 55b dislocation joint, 648, 648f patella, 630 shoulder, 618 disseminated intravascular coagulation (DIC), 26–27, 144 distance acuity, 669 disturbed blood flow, 444 DIT (di-iodotyrosine), 528–529 diuretics, 140–141 and anaesthesia, 67 diverticula bladder, 587, 587f oesophageal, 283 small bowel, 363 diverticular disease, 372–374 aetiology, 373–374 clinical features, 373 complications, 373 epidemiology, 373–374 investigation, 373, 373f management, 373 pathological features, 373 DLCO (transfer factor for CO), 233 DMSA (dimercaptosuccinic acid) renography, 565 DNA replication/repair/ transcription, 176 documentation, 149 see also records dominant hand, 608 Doppler effect, 39–41 Doppler examination, 39–41, 477 dorsal cheilectomy, 633 double balloon endoscopy, 49 double bubble sign, 656, 656f double gloving, 57 double-contrast studies, 35, 36f–37f drainage/drains, 60–61 abscess, 20, 116, 119 chest see chest drainage postoperative care, 88–89, 88t types of, 61, 61f see also specific types of drain drapes, 56 dressings, 106–107, 692, 694f drug reactions causing pruritus ani, 397 drug-induced salivary gland swelling, 208 dry age-related macular degeneration (ARMD), 677 dry heat sterilisation, 56 DSA (digital subtraction angiography), 456, 456f Dubin-Johnson-Rotor syndrome, 301 ductal carcinoma in situ (LCIS), 426, 432–433 Dukes staging, colorectal cancer, 377, 377f duodenal atresia/stenosis, 656–657, 656f duodenal neuroendocrine tumours, 551 duodenal ulcers, 287, 347, 349b, 350 duodenum, 286–292 Duplex ultrasound arterial disease, 454–455, 455f deep-vein thrombosis, 494

thoracic outlet syndrome, 471 varicose veins, 488 Dupuytren’s contracture, 622, 623t duty, 11 DVT see deep-vein thrombosis (DVT) dye test, bladder fistulae, 588 dying, fear of, 184 dysdynamic ileus, 359–363, 359t dysphagia, 279 oesophageal cancer, 284–285 sideropenic, 205 dyspnoea, pulmonary embolism, 501 dysthyroid eye disease, 682, 687, 687f dysuria, 581

E ear, 213–222 anatomy, 213–216, 214f clinical examination, 215, 215f common symptoms, 214–215 external, 213, 216–217 inner, 213, 220–222 investigations, 215–216 middle (tympanic cavity), 213, 217–220 physiology, 213–214 trauma, 222 early feeding, 142–143 early warning scores (EWS), 130, 130t eccrine sweat glands, 705 ECF (extracellular fluid), 81–82, 82f ECG see electrocardiography (ECG) Echinococcus granulosus, 125, 735 echocardiography, 41, 51 cardiac disease, 251 oesophageal atresia, 654 ECMO (extracorporeal membrane oxygenation), 139 ectopia vesicae, 583 ectopic pregnancy, 20 ectopic thyroid tissue, 532 ectropion, 682 eczema nipple, 428, 428t venous, 485 EEG see electroencephalography (EEG) efficacy of investigations, 25 effusion knee, 627 pleural see pleural effusions eGFR (estimated glomerular filtration rate), 559, 559b Ehlers-Danlos syndrome, 451 elastography, 43 elbow, 620–621 elderly patients, ptosis, 683 elective surgery, 8–9 electrical response audiometry, 216 electrocardiography (ECG), 51 in anaesthesia, 74 cardiac disease, 251 pulmonary embolism, 502 electroencephalography (EEG) monitoring in the critically ill, 136 neurosurgery, 514 phaeochromocytoma, 547 electrolytes absorption in the small bowel, 354 metabolism, 81–84, 82f, 82t paediatrics, 654, 654t serum, 27

Index  745 electromyography (EMG), 622 electronystagmography, 216 electrophysiology, 514 ELISA (enzyme-linked immunosorbent assay), 115 ELISPOT, 115 ellipse skin biopsy, 706, 707f embolectomy, 460–461, 461b embolisation arteriovenous malformations, 478–479 peptic ulcers, 349–350 embolism acute limb ischaemia, 471–472, 471t ocular, 687 pulmonary see pulmonary embolism (PE) emergency department, 15–24 apomorphisms in, 22–24 conditions commonly seen in, 20–22 imaging in the trauma patient, 18–19 life-saving procedures in, 15–18 urgent conditions causing hypovolaemic shock, 19–20 emergency surgery, 8, 10 EMG (electromyography), 622 EMLA, 72, 150 emphysema, 17, 244 empyema, 240–241 EMR (endoscopic mucosal resection), 49 encephaloceles, 520–521 endarterectomy, 460, 461f, 474 endocarditis, infective, 258, 258t, 263 endocrine analysis, infertility, 605 endocrine surgery, 527–555 choice of management, 528 diagnosis, 527–528 localisation of tumours, 527 principles, 527–528 rendering the patient into a safe physiological state, 527–528 see also specific glands endocrine therapy, prostate cancer, 596 endoluminal probes, ultrasound, 39, 41 endoluminal stents, 463–464, 464f endoluminal venous obliteration, 491 endolymph, 213 endolymphatic hydrops, 222 endoscopic mucosal resection (EMR), 49 endoscopic retrograde cholangiopancreatography (ERCP) chronic pancreatitis, 335, 335f jaundice, 302, 303f pancreas, 329–330, 338 endoscopic ultrasonography (EUS) gastric cancer, 292 oesophageal cancer, 285 pancreas, 329, 329t pancreatic cancer, 338 endoscopy, 35, 37t, 48–49 anal disorders, 388 bladder function, 582 bladder tumours, 585 complications, 49, 49b flexible instruments, 48 hiatus hernia, 282 neck swellings, 204 oesophageal cancer, 285–286 oesophageal varices, 350 oesophagus, 280

pancreas stenting, 338 pancreatic cancer, 338 peptic ulcer disease, 287 principles, 48–49 recent advances in gastrointestinal, 49 rigid instruments, 48 stenting, 49, 338 therapeutic, 49 upper gastrointestinal tract, 349 endotoxaemia, 116 endotracheal intubation, 16, 16f, 68, 68b, 70–71, 70f, 71b endovascular aneurysm repair (EVAR), 463–464, 464f end-tidal carbon dioxide, 136 energy expenditure, 83 energy requirements, 83, 83b, 143–144 enflurane, 76 Entamoeba histolytica, 734 enteral nutrition, 83, 142–143 enteric cysts, 243 enteric fistulae, 588 Enterobacter faecalis, 142 enterocutaneous fistula, 93, 93b entrapment, peripheral nerve, 524 environmental challenges in developing countries, 722–728 enzyme-linked immunosorbent assay (ELISA), 115 eosinophilia, 26 ependymomas, 518 ephelides, 712 epidermal cells, 703–705 epidermal growth factor (EGF), 435–436 epidermis, 703–705, 704f benign tumours, 711–712 premalignant conditions, 714 epidermoid cysts, 713 epididymis aspiration of the, 602 cysts, 602 epididymo-orchitis, 601–602 epidural anaesthesia, 73–74, 73f epigastric hernia, 410–411 epilepsy medical fitness assessment, 67 raised intracranial pressure, 515 epinephrine, 150, 150b epiphora, 682–683 epiphyseal displacement, 648 episcleritis, 682 epistaxis, 225 epithelial cells, 98 ERCP see endoscopic retrograde cholangiopancreatography (ERCP) erectile dysfunction, 605–606 erysipelas, 121–122, 710, 710f erythema multiforme major, 688 erythrocyte sedimentation rate (ESR), 610 erythromycin, 118t erythroplakia, 205 Escherichia coli, 92 ESR (erythrocyte sedimentation rate), 610 estimated glomerular filtration rate (eGFR), 559, 559b ethics critically ill patients, 148 issues for the surgeon, 10–14 ethmoidectomy, 226 ethyl chloride spray, 150 ethylene oxide sterilisation, 56 EUA (examination under anaesthesia), 388 European Convention of Human Rights, 11–12

European Working Time Directive (EWTD), 8 EUROscore, 265, 266t EUS see endoscopic ultrasonography (EUS) Eustachian tube, 213 euthyroid goitre, 533 evacuation proctography anal disorders, 388 EVAR (endovascular aneurysm repair), 463–464, 464f evening primrose oil, 417 evoked-potential monitoring, 136 Ewing’s sarcoma, 617 examination under anaesthesia (EUA), 388 excision biopsy, breast cancer, 431, 431f exercise after chest surgery, 246 exogenous osteomyelitis, 614 exomphalos, 659–660 exophthalmos, 682 explanation to patients, 149 exstrophy of the bladder, 583, 660, 660f extended field of view (FOV), ultrasonography, 42 external fixation of fractures, 644, 645f extra-abdominal pain, 342 extracellular fluid (ECF), 81–82, 82f extracorporeal membrane oxygenation (ECMO), 139 extradural haematoma, 517, 517f extrahepatic cholestasis, 301 extraperitoneal bladder rupture, 584b, 585 extrasphincteric fistula, 395 eye, 669–689 developing countries, 736–738, 737f, 737t disease, 674–682 common symptoms, 670t in Graves’ disease, 535, 535t diseases with ophthalmic manifestations, 685–689 evaluation, 669–672, 670t external appearance, 671 injuries, 672–674 pain, 680 protection, 57 see also entries beginning ocular eyelid, 682

F facial injuries, developing countries, 732–733 facial pain, 224 faecal elastase test, 329 faecal incontinence, 398–399, 398t faecal soiling, 387 faecaloma, 663 faeces, storage and evacuation, 366–367 false aneurysm, 465, 478, 478f false negatives, 26 familial adenomatous polyposis (FAP), 364, 375–376 fasciocutaneous flaps, 697, 697f fasciotomy, 477, 477f FAST (Focused Assessment with Sonography for Trauma) scan, 19 fat embolism, fracture complications, 646–647 fat necrosis, breast, 419 fat-free mass (FFM), 83 fats, 300 absorption in the small bowel, 354

female pubertal breast problems, 415 femoral artery, sampling, 159, 159f femoral head, osteonecrosis, 626 femoral hernia, 408–409, 408f–410f, 409t femorodistal bypass, 468–469, 469f fentanyl, 77, 145t fertility, breast cancer risk, 422 fetal therapy, 654 fever pyelonephritis, 557 swinging, 557 FFAs (free fatty acids), 83 fibre, dietary, 376 fibrin dressings, 104t fibrin sealants, 104t fibroadenoma, 418, 423 fibroadenosis, 418 fibroblasts, 98, 99t fibrolamellar hepatocellular carcinoma, 309–310 fibromuscular dysplasia, 475, 476t fibromuscular hyperplasia, 451 fibrosarcoma, 617 filariasis, 507 fine-needle aspiration cytology (FNAC) solitary thyroid nodule, 536 thyroid cancer, 539 thyroid gland, 532, 532t fine-needle aspiration (FNA), 50, 50b breast cancer, 431 fibroadenosis, 418 neck swellings, 202, 202f finger abscess, 20 in heart disease, 260t first aid, fractures, 643, 645 fissure in ano, 393, 394f fistulae anal, 394–396, 394f–395f bladder, 374, 587–588, 588t from bladder to gut, 588 causing faecal incontinence, 399 classification, 395 in diverticular disease, 374 enterocutaneous, 93, 93b formation, 395 gastric, 326 gastrocolic, 288 obstetric, 727–728, 727f pancreatic, 326 small bowel, 354 traumatic arteriovenous, 477–478 fistulography, anal disorders, 388 fits, 141 five-year survival, malignant disease, 183 flail chest, 18, 238 floaters, 680 flow meters, 75 flucloxacillin, 118t fluid aspiration from pleura, 166 fluid replacement, 82 burns, 700–701 fluid types, 83 ongoing losses, 82–83 paediatrics, 654, 654t pre-existing deficits, 82 fluorescein dilaurate test, 329 fluoroscopy detection, 29 FNA (fine-needle aspiration) see fine-needle aspiration (FNA) FNAC (fine-needle aspiration cytology) see fine-needle aspiration cytology (FNAC)

746  Index focal nodular hyperplasia (FNH), 308 Focused Assessment with Sonography for Trauma (FAST scan), 19 Foley catheter, 161, 162f follicular carcinoma, thyroid, 538 fondaparinux, 497 food, airway obstruction, 15 food bolus, 357 foot, 632–634 diabetic, 469–470 talipes, 637 foot drop, 609b forced expiratory volume in one second (FEV1), 52, 232–233 forced vital capacity (FVC), 52 foreign bodies ear, 216 intraocular, 674 nasal, 224 ocular, 672–674, 674b wound, 100 foreskin, 599, 666 formaldehyde sterilisation, 56 Foundation Trusts, 8 Fournier’s gangrene, 123, 123f fractures, 639–648 in children, 648 classification, 639–648, 640t clinical features, 642 complications, 645–648, 645b– 646b, 646f–647f, 646t diagnosis, 22–23 healing, 639–641, 641b, 641f–642f management, 643–645, 643b, 644f–645f nasal, 224 radiological investigation, 642, 643f rib, 238 types of, 639, 640f, 641t freckles, 712 free fatty acids (FFAs), 83 free radicals, 135 free skin flaps, 206 free tissue transfer, 697–698 Freiberg’s disease, 634 FRIAR, fractures, 643–645, 643b Froment’s sign, 623, 623f frontal sinus trephine, 226 fronto-ethmoidectomy, 226 frozen section biopsy, 51 frozen shoulder, 619–620 full blood count, 26, 26t infections, 115 full midline abdominal incision, 60 full thickness skin biopsies, 706, 706f–707f full-thickness skin grafts, 206, 694–696 fulminant colitis, 368 function tests, 51–52 see also specific organs functional magnetic resonance imaging (fMRI), 47 fundoplication, 282, 283f fundoscopy, 671–672, 672b fungal infections, 117 ophthalmic, in HIV, 685 skin, 710–711 furosemide, 140–141 furuncle, 217 furunculosis, 709

G gadolinium chelates, 46–47 gadolinium-based contrast agents, 46

gait, 625, 631 abnormal, 609b assessment, 608 phases of normal, 608t galactorrhoea, 419 gallbladder, 299–300, 299f, 300b tumours, 316–317 gallstone ileus, 314–315, 357 gallstones, 311–315 acute pancreatitis, 330 aetiology, 311–312 asymptomatic, 312, 315 clinical features, 312, 312b epidemiology, 311–312, 311t general management, 315 imaging, 312, 313f, 313t symptomatic, 312, 315 urgent management, 312–315 gamma knife, 519 gamma rays, 28, 28f gamma-linoleic acid, 417 ganglions, 624 gangrene, 122–123 clostridial see gas gangrene non-clostridial, 123, 123f prophylaxis, 123b Gardner’s syndrome, 364, 375 gas gangrene, 122–123 wound contamination, 100 gastrectomy, laparoscopic sleeve, 294, 295f gastric acid secretion, 288 gastric band, 294, 294f gastric bypass, 294–295, 295f gastric cancer, 288–292, 289f aetiology, 288–289 clinical features, 289–290 epidemiology, 288 investigation, 290–292 management, 291f, 292 pathological features, 289, 289f–290f prognosis, 292 screening, 290 staging, 289, 290t symptoms, 289–290, 290b gastric erosion, 350 gastric fistula, 326 gastric neuroendocrine tumours, 551 gastric outflow obstruction, 288 gastric ulcers, 142, 287, 347, 350 gastrin, 550 gastrinoma, 549–550 gastrocolic fistula, 288 gastroduodenal tumours, 288–292 gastroenteropancreatic tumours, 548–551 Gastrografin, 35–37 gastrointestinal neuroendocrine tumours, 551 gastrointestinal stromal tumours (GIST), 364 gastrointestinal tract decompression of the, 88–89, 729 medical fitness assessment, 67 monitoring in the critically ill, 137 postoperative complications, 92–93 stapling, 105 therapeutics in the critically ill, 141–144, 142t gastro-oesophageal reflux disorders, 281–283 without abnormal anatomy, 283 gastroschisis, 659, 659f Gaucher’s disease, 322 GCA (giant cell arteritis), 450, 686 GCS see Glasgow Coma Scale (GCS) gelatin foams, 104t

gender, breast cancer risk, 423 gene therapy, brain tumours, 519 general anaesthesia, 69–72 airway management, 69–70, 69f–70f, 71b complications, 71–72, 72b induction, 70–71, 71b, 76 maintenance, 71, 71b, 71f, 76 recovery, 71 General Medical Council (GMC), 11 genetics breast cancer risk, 421–422, 421t and colorectal cancer, 376 coronary artery disease risk, 253 genital disorders in children, 664–666 warts, 708 gentamicin, 118t germ cell tumours mediastinal, 243 testicular, 603–604, 603f GFR (glomerular filtration rate), 27, 559 giant cell arteritis (GCA), 450, 686 giant-cell bone tumours, 617 gigantism, 553 Gilbert’s syndrome, 301 GIST (gastrointestinal stromal tumours), 364 giving way, knee, 627 Glasgow Coma Scale (GCS), 22, 128–131, 131t, 513, 514b Glasgow scoring system, acute pancreatitis, 332, 333t glaucoma, 681 Gleason grade, prostate cancer, 594 glenohumeral disorders, 620 glomerular filtration, 141 glomerular filtration rate (GFR), 27, 559 glomus tumours, 712 gloves, 57, 149 double gloving, 57 glucagonoma, 549 glucose, 83 absorption in the small bowel, 354 in the critically ill, 144 monitoring, 94 replacement, 94–95 urinary, 27 glutaraldehyde cross-linked albumin, 104t glutaraldehyde sterilisation, 56 glycerol, 83 glycogen, 83 goggles, 57 goitre, 531f, 725, 726f diagnosis, 531 diffuse nodular, 531f non-toxic, 532–533 patient assessment, 530b toxic, 534–535 goitrogens, 532 gonadotrophin-producing tumours, 554 gout, 612, 634 gowns, 57 grafts see bypass surgery, arterial; skin grafts Gram-negative organisms, 90 Gram-staining, 115, 124 granulation tissue, 98–99 granulomas pyogenic, 712, 713f in tuberculosis, 124 umbilical, 660

Graves’ disease, 534–535, 534t–535t ophthalmic manifestations, 687, 687f great vessels, trauma, 271–272 greenstick fractures, 639, 640f Grey Turner’s sign, 331, 331f gridiron abdominal incision, 60, 60f groin swellings, 407, 409t, 661b see also inguinal hernia grommets, 218, 218f gross domestic product, 722, 722f growth factors, 98, 99t growth hormone excess, 553 guarding, abdominal, 344 gunshot wounds, 238 gut, vascular disturbances in, 360–361, 360b gynaecology, developing countries, 736–738

H HAART (highly active anti-retroviral treatment), 125 haemangioblastomas, 518 haemangioma, 478, 712 liver, 308, 308f haematemesis, 346–347, 347t–348t, 348b haematogenous osteomyelitis, 613–614 haematological investigations, 26–27 cardiac disease, 250–252 see also specific tests haematoma auricle, 216 cervical spine X-ray, 19 extradural, 517, 517f in fractures, 640 and infection, 111 intracerebral, 517 perianal, 392 septal, 224 subdural, 517–518, 517f traumatic, 21 haematopoiesis, 319 haematuria, 27, 558, 558b persistent, 569 haemodilution, 86 haemodynamics, valve disease, 259 haemoglobin levels, gastric cancer, 292 haemolytic anaemias, 321 haemoptysis, 239 pulmonary embolism, 501 haemorrhage cerebral, 519–520 in diverticular disease, 374 fractures, 645–646 postoperative, 86, 90–91 ulcerative colitis complications, 369 upper gastrointestinal, 92–93 vascular trauma, 477 haemorrhoidal artery ligation, 391 haemorrhoidectomy, 391–392 haemorrhoidopexy, 392 haemorrhoids, 389–392 aetiology, 389 classification, 389–392, 390t clinical features, 389–390 complications, 392 conditions related to, 390t definition, 389–392 management, 390–392, 391f–392f, 391t haemostasis, 102–103, 102f–103f, 104t haemothorax, 17, 238–239

Index  747 hallux rigidus, 633 hallux valgus, 632–633 haloperidol, 145t hamartomas, lung, 234 hand/arm cleaning (scrubbing up), 56–57 hands, 621–625 in heart disease, 260t injuries in developing countries, 733 plastic surgery, 700 Hashimoto’s thyroiditis, 537 Hawkins sign, 619 HCC (hepatocellular carcinoma), 309–310 HDU see high-dependency units (HDU) head injury, 21–22, 23f, 514–518, 515b, 516f plastic surgery, 702 positional testing, 216 health facilities, developing countries, 723–724 hearing, 213–216 loss, 215 sensorineural, 220–222 tests, 215–216, 216f hearing aids, 220–221 heart anatomy, 249 leaks from, 18 monitoring the left side of the, 137 transplantation, 190, 268–269, 270f trauma, 271–272 tumours, 265 heart failure, 139–140, 267–270 management, 267–270, 267b, 268f–269f right, 259, 259t heart sounds, 18 heartburn, 280 heart-lung transplantation, 190 heat sterilisation, 55–56, 56b Helicobacter pylori, 286, 288, 349–350 heparin, 495–497 heparin-induced thrombocytopenia, 496 hepatic artery embolisation, 309 hepatic jaundice, 301, 301b hepatitis B healthcare personnel protection, 114 high-risk patients, 57–58 hepatitis C, 57–58 hepatitis virus markers, 302 hepatocellular carcinoma (HCC), 309–310 hepatocytes, 300 hepatorenal syndrome, 304 HER2, 426, 435–436 herceptin, 437 hereditary non-polyposis colon cancer (HNPCC), 376 hereditary spherocytosis, 321 hernia, 401–414 aetiology, 401 anatomical features, 401–402, 402f classification, 401 clinical features, 403–404 complications, 402–403 congenital diaphragmatic, 655, 655f developing countries, 730 differential diagnosis, 404t epidemiology, 401–405 internal, small bowel, 358 investigation, 404 management, 404–405

natural history, 402–403 outcome, 405 relative frequency of anatomical features, 402t umbilical, 660 see also specific types hernia en glissade, 403, 403f hernia-en-W, 403, 403f herniography, 404 herniorrhaphy, 405, 730 herniotomy, 405, 730 herpes simplex virus, 685, 709, 709b herpes viruses, 709, 709b herpes zoster, 709, 709b hesitancy, urinary, 581 heterotopic graft, 187 heterotopic pancreas, 327 hiatus hernia, 282–283, 282f HIFU, prostate cancer, 596 high anterior triangle swellings, 201 high-dependency units (HDU), 127–130, 128b admission criteria, 128 highly active anti-retroviral treatment (HAART), 125 high-risk patients, 57–58 Hinchey classification, 374t hip, 625–627 dislocation, 726–727 paediatric orthopaedics, 634–637, 634t Hirschsprung’s disease, 657–658 histological grade of tumours, 180, 181t bladder tumours, 586 breast cancer, 424–425 HIV/AIDS, 125 developing countries, 724, 724f healthcare personnel protection, 114 high-risk patients, 57–58 ophthalmic manifestations, 685–689 small bowel neoplasia, 364 HLA (human leucocyte antigen), 188, 190 HNPCC (hereditary non-polyposis colon cancer), 376 hollow viscera perforation, 49 Homan’s sign, 494 horizontal abdominal incisions, 60 hormonal factors breast cancer risk, 422 slipped upper femoral epiphysis, 636 hormonal manipulation, breast cancer, 435–437 hormonal tests gastrinoma, 550 phaeochromocytoma, 547 hormone receptors, breast cancer, 435–436 hormone replacement therapy (HRT), 422 hormone therapy, prostate cancer, 595–596, 596f Horner’s syndrome, 683–684, 683f hospital-acquired infection, 100, 119, 119b prevention, 114 HPV (human papillomavirus), 707–708, 708f HRT (hormone replacement therapy), 422 human beta-chorionic gonadotrophin, 27 human immunodeficiency virus see HIV/AIDS human leucocyte antigen (HLA), 188, 190

human papillomaviruses (HPV), 707–708, 708f Human Rights Act 1998, 11–12 humeral head, avascular necrosis, 620 Hunterian perforator, 489–490 hydatid disease, 125, 297, 307 developing countries, 735 hydradenitis suppurativa, 397 hydrocele, 602, 661, 661f hydrocephalus, 521–522, 521f hydrocortisone, 546 hydronephrosis, 663 hygiene, developing countries, 722–723 hyperaldosteronism, primary, 544–545, 545f hyperbaric oxygen, 692 hypercalcaemia, 542–543, 542b, 542t hypercapnia, 141 hyperhidrosis, 461–462 hyperlipidaemia, 447–448 hypermotility, oesophageal, 280–281 hyperparathyroidism, 541–543 hyperplastic goitres, 532 hyperreflexic bladder, 589 hypersensitivity reactions, 91 hypersplenism, 320–323, 320t causes of, 320t investigation, 322–323 management, 323 splenectomy, 324–325 hypertension coronary artery disease risk, 253 ophthalmic manifestations, 688 hypertensive retinopathy, 677, 678f hyperthyroidism, 531 hypocalcaemia, 536, 537b hypocapnia, 141 hypomotility, oesophageal, 281 hyponatraemia, 27 hypoparathyroidism, 543 hypopharyngeal tumours, 205–206 hypospadias, 597, 597f, 666 hyposplenism, 320, 320b hypotension, 22, 131 hypothermia, 59 paediatrics, 653 use in cardiac surgery, 248 hypothyroid goitre, 533 hypothyroidism signs of, 530 symptoms, 530 hypovolaemic shock, 131 haemothorax, 17 management, 20b quantifying, 91, 91t splenic rupture, 324 in trauma, 134b urgent surgical conditions causing, 19–20 hypoxia, recovery period, 78 hysterectomy, psychological effects of, 4 hysteria, 24

I IABP (intra-aortic balloon pump), 267, 267b, 268f IBS (irritable bowel syndrome), 367 ICP see intracranial pressure (ICP) ICU see intensive care units (ICU) idiopathic hyperaldosteronism, 544 ileal conduit, urinary diversion, 580–581, 580f ileal pouch, 371, 371f

ileo-anal anastomosis, 371, 371f ileorectal anastomosis, 370, 371f ileostomy, 370, 370b, 370f–371f ileus, 359–363 gallstone, 314–315, 357 paralytic, 359–363, 359t iliofemoral vein thrombus, 495–496 imaging, 28–48 acute abdomen, 345 acute cholecystitis, 313 acute pancreatitis, 332, 332f acute pyelonephritis, 565 ankle, 631 biliary colic, 312 bone tumours, 616 breast, 430–431 chronic pancreatitis, 335 cystitis, 583 elbow, 621 fibroadenosis, 418 foot, 632 gastrinoma, 550 goitres, 533, 533f hand and wrist, 622 hernias, 404 hip, 625 infection, 116 intestinal obstruction, 355–356 jaundice, 302–303 knee, 628 lower urinary tract, 582 nephroblastoma, 569 nose and paranasal sinuses, 224 oesophagus, 280 orthopaedics, 609–610 osteomyelitis, 614–615 pancreas, 329–330, 329t pancreatic cancer, 337–338 perinephric abscess, 567 Perthe’s disease, 635–636 progression of malignant disease, 183, 183t pyogenic liver abscess, 307 renal adenocarcinoma, 570 renal pelvis carcinoma, 571 renal trauma, 569 renal tuberculosis, 568 requests for, 28 schistosomiasis, 584 septic arthritis, 615 shoulder, 618 solitary thyroid nodule, 536 splenic rupture, 324 testicular tumours, 603 thyroid cancer, 539 in the trauma patient, 18–19 upper urinary tract, 560–561 ureteric stones, 579, 579f urinary stones, 573 urinary tract infection, 565 varicose veins, 488, 488f see also specific modalities imipenem, 118t immobilisation of fractures, 643–644, 643b immune deficiency syndromes, 112 immune thrombocytopenic purpura (ITP), 321 immunity, 111–112 immunocompetent cells, 704–705 immunocompromised patients asepsis, 150 developing countries, 724 immunology nasal disease, 224 of organ transplantation, 188–189 spleen, 319 ulcerative colitis, 368 immunomodulation, 117

748  Index immunosuppression agents, 191–193, 192t clinical regimens, 192–193 complications, 193, 193b organ transplantation, 191–193 small bowel neoplasia, 364 immunotherapy malignant melanoma, 719 warts, 708 impedance audiometry, 215–216 impedence monitoring, oesophagus, 280, 282 impetigo, 709 impingement, shoulder, 619 implantation dermoids, 713 impotence, 605–606 incised wounds, 101 incision biopsy, breast cancer, 432 incisional hernia, 411–412 incisions, 59–60 abdominal, 60, 60f closure, 60 skin, 59 thoracic, 244–245 thoracoabdominal, 245 incomplete emptying, bladder, 581 incomplete neurological lesions, 649 incontinence faecal, 398–399, 398t urinary, 581, 581b, 590 indirect inguinal hernia, 406 induction, general anaesthesia, 70–71, 71b, 76 indwelling vascular catheters, 91–92 inertial energy losses, 444 infant mortality rate, 722, 722f infantile umbilical hernia, 409 infection control, 55–58, 112–114 operating department, 55–58, 55b patient protection, 113–114 protection for others, 114 infection(s), 109–125 acquired, 119t in acute pancreatitis, 334 and aneurysmal disease, 449 antisepsis and asepsis, 109 and atherosclerotic occlusive disease, 448 biology of, 110–112, 110f, 110t bone, 645 breast, 420 causing pruritus ani, 397 clinical features, 115 concomitant illnesses, 111 cost, 110 in critically ill patients, 144 developing countries, 724, 734–736 established, 121–125 fractures, 645–648 high-risk patients, 57–58 history, 109–110 host defences, 111–112 importance of, 109–110 incidence, 110 intracranial, 524–525 investigation of, 115–116 large bowel, 372 liver, 306–307 local host factors, 111 management, 116 morbidity and mortality, 110 neck space, 208–210 neonates, 654 organisms, 110–112 orthopaedics, 613–615 pulmonary, 242–243 raised intracranial pressure, 515 skin, 707–711 specific antibiotics for, 119t

splenomegaly in, 320–321, 323 wounds see wound infection see also specific infections; specific organisms infectious mononucleosis, 210 infective endocarditis, 258, 258t, 263 infective rhinosinusitis, 225–227 infertility, 604–605 inflamed hernia, 402–403 inflammation and aneurysmal disease, 448–449 and atherosclerotic occlusive disease, 448 in diverticular disease, 373–374 varicose veins, 484 inflammatory bowel disease, 367–372, 367b and colorectal cancer, 376 inflammatory breast carcinoma, 428, 438 inflammatory causes of intestinal obstruction, 357 inflammatory phase of wound healing, 97–98 informed consent, 11–13, 149, 536 infra-inguinal disease, 458, 460f, 467 infrared coagulation, haemorrhoids, 391 inguinal canal, 406, 406f inguinal hernia, 405–408 aetiology, 406 anatomy, 406, 406f in children, 661–662, 661f classification, 406, 406t clinical findings, 406–407 complications, 408 developing countries, 725, 726b, 726f management, 407–408 recurrent, 408 inguinal hydrocele, 661, 661f inhalational maintenance agents, 76 injection sclerotherapy, haemorrhoids, 390–391, 391f injury response, 81 Injury Severity Score (ISS), 128–130 innate immune system, 112 inotropes, cardiac, 140, 140t in-patient management, 9–10 instability ankle, 631–632 orthopaedic history, 607 insulinoma, 548–549 Integra, 696 intensive care units (ICU), 127–130, 128b admission criteria, 128 cardiac surgery, 275–276 sequelae of treatment in, 147–148 intercostal arteries, 17 intercostal nerve damage after breast surgery, 435 intermittency, urinary, 581 intermittent claudication, 453, 465–467 intermittent mandatory ventilation (IMV), 139t internal fixation of fractures, 644, 644f internal jugular vein, 156, 156f interparietal hernia, 412, 412f intersphincteric fistula, 395 interstitial cystitis, 584 intervertebral disc prolapse, 522

intestinal obstruction, 354–357 developing countries, 728–730 due to Ascaris worms, 730 extramural, 354b, 358–359 luminal, 354b, 357 mechanical, 354–359, 354b mural, 354b, 357 in newborns, 656–659 in-toeing, 637 intra-aortic balloon pump (IABP), 267, 267b, 268f intra-articular steroid injections, 612 intracerebral haematoma, 517 intracerebral haemorrhage, 519 intracranial bleeding, 22 intracranial haemorrhage, 519–520 intracranial infections, 524–525 intracranial pressure (ICP) monitoring in the critically ill, 136 raised, 141, 141b brain tumours, 518 causes of, 515 intradermal naevus, 712 intraductal papillary mucinous neoplasm (IPMN), 339 intrahepatic cholangiocarcinoma, 310 intranasal antrostomy, 226 intraocular pressure, 671 intraperitoneal abscess, 93, 93t intraperitoneal bladder rupture, 584–585, 584b intravascular contrast media, 31–35, 35t intra-vascular ultrasound (IVUS), 252 intravenous administration, antibiotic prophylaxis, 114 intravenous fluids, 82 paediatrics, 654 postoperative, 87, 87b see also fluid replacement intravenous induction agents, 76 intravenous regional anaesthesia, 73 intravenous urogram (IVU), 561–563, 561b, 561f bladder tumours, 585, 586f pelviureteric junction obstruction, 574 renal adenocarcinoma, 570 renal pelvis carcinoma, 571, 571f renal tuberculosis, 568, 568f intussusception, 662–663, 662b, 662f, 730 invasive breast carcinoma, 426–427 inverse ratio ventilation (IRV), 139t inverting papilloma, 227 investigation(s), 25–52 anaesthesia, 68, 68t efficacy, 25 neurosurgery, 513–514 objectives, 25–26 sensitivity, specificity, positive/ negative predictive values, 25–26 thyroid surgery, 536 see also specific diseases; specific techniques iodine, 528–529 deficiency, 532 dietary intake, 529 radioactive, 182, 535 total-body scanning, 539 iodine atoms, 34 125 I fibrinogen uptake tests, 494 iritis, 681, 681f

irradiation bladder fistulae, 588 breast cancer risk, 422 sterilisation, 56 see also radiotherapy irreducible hernia, 402, 404 irritable bowel syndrome (IBS), 367 ischaemia in infection, 111 limb see limb ischaemia vascular trauma, 477 visceral, 474–475 wound, 100 ischaemia-reperfusion injury, 446–447 ischaemic colitis, 372 ischaemic heart disease, 258 ischaemic valve disease, 259 ischiorectal abscess, 394 islet cell hyperplasia, 555 isoflurane, 76 isograft, 187 isotope scanning ankle, 631 bone tumours, 616 goitres, 533 hip, 625 orthopaedics, 610 osteomyelitis, 615 vesicoureteric reflux, 576 isovolaemic haemodilution, 457 ISS (Injury Severity Score), 128–130 ITP (immune thrombocytopenic purpura), 321 IVU see intravenous urogram (IVU) IVUS (intra-vascular ultrasound), 252

J jaundice, 301–304 classification, 301–304, 301b general management, 303–304, 304f investigation, 301–303 obstructive, 314, 338 and wound healing, 101 jaw thrust, 171 Jehovah’s Witnesses, 12–13 jejunal diverticula, 363 jejunal segmental transplant, 206 Jenkin’s rule, 94 jet insufflation, 16, 16f joint crease lines, 59 joint replacement, 612–613, 613t hallux valgus, 633 hip, 625–626, 626b, 626t knee, 631 joint(s) aspiration, septic arthritis, 615 contractures, spinal injury, 650 examination, 608–609 injuries, 648, 648f operation precautions, 58–59 movement, 609, 609t surgery, arthritis, 612–613, 613t jugular venous pressure, 131, 259–260, 260f jugular venous pulsation, 259–260 junctional naevus, 712 justice, 148

K Kaposi sarcoma, 234, 686, 719–720, 719f Kasabach-Merritt syndrome, 308 Kasai operation, 304, 305f Kawasaki disease, 451 keratinocytes, 98, 99t, 703

Index  749 keratitis, 681, 681f, 686 keratoacanthoma, 711–712, 712f keratoconjunctivitis sicca, 208, 686 keratolytic agents, warts, 708 kerion, 710–711, 710f ketamine, 76, 145, 145t kidneys, 557–581 abscess, 566 clinical examination, 558–559 congenital anatomical abnormalities, 563–564 cysts, 564 disorders, 563–573 symptoms arising from, 557–563 therapeutics in the critically ill, 140–141 transplantation, 191, 194, 194f–195f, 198 trauma, 568–569, 568b–569b tumours, 569–571 Kienbock’s disease, 624 Klippel-Trènauny-Weber syndrome, 478, 485–486 knee, 627–631 knock-knees, 637 meniscal injuries, 628–629, 629f Kocher’s incision, 60, 60f KUB (kidneys, ureters, bladder), 560

L laboratory investigations postoperative, 86–87, 87t pyogenic liver abscess, 307 labyrinthine nystagmus, 216 lacerated wounds, 101 Lachman test, 627, 628f lacrimal drainage system, 672 lacrimal duct, 682–683 lacrimal gland, 682–683 lactational breast abscess, 420 lactic acidosis, 133 LAD (left anterior descending) artery, 249 laminar blood flow, 444 Langerhans cells, 704 Langer’s lines, 59, 59f laparoscopic adjustable gastric band, 294, 294f laparoscopic sleeve gastrectomy, 294, 295f laparoscopy, 62 acute abdomen, 345 acute appendicitis, 346 colorectal cancer, 378 conversion to open exposure, 63 diagnostic, 62 gastric bypass, 294–295, 295f gastric cancer, 292 hernias, 404 hiatus hernia, 282 incisional hernia, 412 inguinal hernia, 407–408 jaundice, 303 pancreas, 329t, 330 pancreatic cancer, 338 therapeutic, 62 laparostomy, 106 laparotomy, 170, 245 Laplace’s law, 445 large bowel, 365–381 atresia, 657 cancer see colorectal cancer carcinoma, 378, 379f, 380b (see also colorectal cancer) functional disorders, 367–372 neoplasia, 374–381

obstruction, 359 (see also intestinal obstruction) physiology, 365–367, 366b structure, 365–367, 366f volvulus, 359 large vessel vasculitis, 450 large-cell lung carcinoma, 229–230 large-cell neuroendocrine lung carcinomas, 234 laryngeal mask airway, 70, 70f laryngeal tumours, 205–206 laryngoscopes, 70, 70f laser therapy, 698 gastric cancer, 292 prostate, 592 skin disorders, 707 late wounds, 101 lateral position, 58t LCA (left coronary artery), 249, 250b, 250f left anterior descending (LAD) artery, 249 left coronary artery (LCA), 249, 250b, 250f left ventricular function, 137 leg muscle pump, 483 legal issues, 10–14 lentigines, 712 lentigo maligna, 714, 714f leucoplakia, 205, 714 leukaemia, myeloid, 321 LH (luteinising hormone), 596 LHRH (luteinising hormonereleasing hormone), 596 lidocaine, 150 ligation, haemostasis, 102, 102f LIMA to LAD, 275 limb discolouration in deep-vein thrombosis, 494 limb ischaemia acute, 471–472, 471t, 472b chronic, 465–467 critical, 467–469, 467f sympathectomy, 461–462 limb length discrepancy, 609 limp, 625 lipid-lowering therapy, 448 lipodermatosclerosis, 484, 487, 487f lipomas, 364, 713 literacy, developing countries, 722–728 lithotomy, 58t liver, 297–317 abscess, 734–735 (see also amoebic liver abscess; pyogenic liver abscess) anatomical sectors, 297–298, 299f anatomical variations, 300 anatomy, 297–298, 298f–299f cancer, metastatic, 310–311 congenital conditions, 304–305 contrast agents, 46–47 detoxification, 300 embryology, 297 excretory function, 300–301, 300t function tests, acute pancreatitis, 332 infections, 306–307 intermediary metabolism, 300 metastases from colorectal cancer, 381 neoplasms, 307–311 non-neoplastic conditions, 304–307 physiology, 300–301 reticuloendothelial function, 300–301

transplantation, 190–191, 194–195, 195t, 196f trauma, 305–306, 306t living organ donors, 187, 191 Lloyd-Davies position, 58t LMWH (low-molecular-weight heparin), 495–497 lobular breast carcinoma, 427 lobular carcinoma in situ (LCIS), 426, 432–433 local anaesthesia, 65, 72–74 choice of, 150, 150t maximum safe doses, 72b mode of action, 72 toxicity, 72 locking elbow, 620 knee, 627 long bone fractures, 20 long saphenous vein (LSV), 457 loss of function, 607 low anterior triangle swellings, 201 lower limb deep-vein thrombosis, 492–497 deformities in children, 637 injuries in developing countries, 733 swellings, 509b venous physiology, 483 lower limb ulceration, 504–506, 710 aetiology, 504, 505t clinical features, 504–505, 505f, 505t diagnosis, 505 epidemiology, 504–506 management, 506 lower midline abdominal incision, 60 lower urinary tract, 581–606 infections, 583–584 symptoms (LUTS), 592 low-molecular-weight heparin (LMWH), 495–497 low-temperature steam sterilisation, 56 Ludwig’s angina, 122, 210, 210b lumbar canal stenosis, 522–523 lumbar hernia, 413–414, 413f lumbar puncture, 514 lumbar spine degenerative disease, 522–523 injuries, 649 lumpectomy, breast cancer, 433 lumps/lumpiness anal, 387 breast, 417–419, 427 Lundh meal, 328 lung cancer, 229–234 aetiology, 229 clinical features, 230 epidemiology, 229–234 pathological features, 229–230, 230b patient evaluation, 230–233 prognosis, 234 staging, 230, 231b treatment, 233–234 lung volume reduction surgery (LVRS), 244 lungs, 229–246 abscess, 243 contusions, 238 destroyed, 242 function tests, 51–52 infectious conditions, 242–243 metastases, 439 postoperative collapse, 92 stapling, 105 transplantation, 190, 244 trapped, 234 luteinising hormone (LH), 596

luteinising hormone-releasing hormone (LHRH), 596 LUTS (lower urinary tract symptoms), 592 LVRS (lung volume reduction surgery), 244 lymphadenopathy, 202, 506–507 lymphangioma, cervical cystic, 655–656 lymphangitis, 507 lymphatic channels, dermal, 705 lymphatic disorders, 506–509 lymphatic malignancy, 322–323 lymphatic spread of tumours, 178 lymphocytes, 188–189, 704–705 lymphoedema, 507–509 aetiology, 507–509 arm, after breast surgery, 435 bacterial cellulitis in, 509 classification, 507–509 clinical features, 507–508 investigation, 508 management, 508–509 pathological features, 507 pathophysiological features, 507 primary, 507–508 secondary, 507–508 lymphomas breast, 428 cutaneous, 720 diagnosis, 203 lung, 234 neck, 202–203, 206–207 presentation, 202 salivary glands, 208 small bowel, 364 testicular, 603 thyroid, 540 Lynch syndrome, 376

M McMurray’s test, 629 macrophages, 98, 99t, 111 macula, 672 degeneration, 677, 677f hole, 677–678 oedema, 677, 678f Madelung’s deformity, 624–625 magnetic resonance angiography (MRA), 46, 46f magnetic resonance arthrography, 46 magnetic resonance cholangiopancreatography (MRCP) chronic pancreatitis, 335 jaundice, 302 magnetic resonance imaging (MRI), 43–47 advantages and disadvantages, 46–47, 46f anal disorders, 388 ankle, 631 arterial disease, 456 bladder fistulae, 588 bone tumours, 616 breast cancer, 431 cardiac disease, 251–252 comparison with other imaging techniques, 46t, 47 detection and display, 43–46, 45f, 45t fractures, 642 hernias, 404 hip, 625 knee, 628 lung cancer, 231 neck swellings, 202 neurosurgery, 514 oesophagus, 280 orthopaedics, 610, 610f

750  Index osteomyelitis, 614 pancreas, 329, 329t pituitary tumours, 552 principles, 43, 44f prostate cancer, 594 safety, 46 shoulder, 618 spinal injury, 649, 649f thoracic outlet syndrome, 471 upper urinary tract, 562–563, 563b magnetic resonance spectroscopy, 47 magnification endoscopy, 49 maintenance, general anaesthesia, 71, 71b, 71f, 76 major histocompatibility complex (MHC), 188–189, 188f malabsorptive procedures, bariatric surgery, 294–295 malaise, 557 malaria, 724 maldescended testes, 603 male pubertal breast problems, 415 malignant disease, 175–185 adjuvant therapy, 181–182 aetiology, 175, 176t assessment of response to treatment, 183, 183t biology of, 176–179, 177f bladder fistulae caused by, 588 carcinogenesis and growth, 176–177 clinical features, 179, 180b cutaneous signs of internal, 720 in developing countries, 733 epidemiology, 175 examination, 179 history, 179 incidence, 175, 176t influence of biology on clinical course, 177, 177f invasion and metastasis, 177–179 investigation, 179–180 management, 179–184 non-operative therapy, 182–183 operative surgery, 181 orbital, 682 path to surgery, 9 prognosis, 180–181 screening, 184–185, 184t terminal care, 184 tumour staging, 180–181 malignant melanoma, 716–719, 716b aetiology, 716 epidemiology, 716 management, 718–719 pathological features, 717, 717f prognosis, 718–719 prophylaxis, 717–718 Mallory-Weiss syndrome, 283–284, 350–351 malnutrition in the critically ill, 143 developing countries, 724 and wound healing, 100 malrotation with volvulus, 657 malunion of fractures, 647, 647f mammary duct ectasia, 419 papilloma, 419 mammographic-guided needle biopsy, breast cancer, 432, 432f mammography, 417, 430 breast cancer screening, 425 fibroadenosis, 418 manganese compounds, 46–47

manometry anal, 399 oesophagus, 280 MAP (mean arterial pressure), 444 Marfan’s syndrome, 451 Marjolin’s ulcer, 484 mastectomy, 432–433, 438–441 psychological effects of, 4 mastitis, periductal, 420 mastoiditis, acute, 217–218 matrix metalloproteinases, 177 Maydl’s hernia, 403, 403f MCV (mean corpuscular volume), 26 mean arterial pressure (MAP), 444 mean corpuscular volume (MCV), 26 mechanical bowel preparation, 85 mechanical derangement, shoulder, 618 mechanical traction, fractures, 643 Meckel’s diverticulum, 353, 363, 363f meconium ileus, 657 median laparotomy, 245 median nerve compression, 623 median sternotomy, 245, 275 median sternotomy-median laparotomy, 245 median survival time, malignant disease, 183 mediastinoscopy, lung cancer, 231 mediastinum, 243–244 anatomy, 243 benign cystic lesions, 243 pathology, 243 signs and symptoms, 243 tumours, 243 medical fitness assessment, 66–68 medications and anaesthesia, 67 thyroid surgery, 536 medium sized vessel vasculitis, 451 medullary carcinoma breast, 427 thyroid, 539, 555 medulloblastomas, 518 megaureter, 575–576, 593b megestrol, 436 melaena, 346–347 melanocytes, 703–704 melanocytic pigmented naevi, 712 melanoma see malignant melanoma Meleney’s gangrene, 123 MEN see multiple endocrine neoplasia (MEN) menarche, breast cancer risk, 422 Ménière’s disease, 222 meningeal tumours, 518–519 meningiomas, 518–519 meningitis, 524 meningococcal septicaemia, 134b meniscal injuries, 628–629, 629f menopause, breast cancer risk, 422 menstrual cycle, breast pain, 416–417 Mental Capacity Act, 12 mental illness, consent in, 12 Merkel cells, 705 mesenteric ischaemia acute, 474–475 chronic, 475 mesh repair, inguinal hernia, 407–408 mesothelioma, malignant pleural, 240 metabolic acidosis, 133 metabolic disorders splenomegaly in, 322 and urinary stones, 572, 572b

metabolic effects of reperfusion injury, 446 metamorphopsia, 679–682 metastases, 177–179 bone, 439 breast cancer, 423–424, 438 central nervous system, 439 distribution of, 178 to the liver, 310–311, 381 lung and pleura, 439 from the lungs, 230–231 to the lungs, 240 malignant melanoma, 719 neuroendocrine tumours, 551 occult micrometastases, 178–179 routes of, 178, 178f–179f splenomegaly in, 322, 322f thyroid cancer, 538–539 metatarsalgia, 633 metatarsus primus varus, 632 meticillin, 118t meticillin-resistant Staphylococcus aureus (MRSA), 100, 121 metronidazole, 118t, 307 MEWS (Modified Early Warning Score), 86, 86t, 130, 130t MHC (major histocompatibility complex), 188–189, 188f microbiology, 27 anal disorders, 389, 389t empyema, 240 infections, 115 small bowel, 354 microfibrillar collagen, 104t micrognathia, 656 microscopy, 115 bladder tumours, 585 urine, 559 micturating cystourethrography, 562, 562f urinary tract infection, 565 vesicoureteric reflux, 576 micturition disorders, 164, 581 midazolam, 145, 145t midline submental swellings, 201 migraine, 678 Milan’s retropubic prostatectomy, 592 military conflict, developing countries, 723 minimal access surgery, 61–64, 62f advantages, 62 cardiac surgery, 275 conversion to open exposure, 63 disadvantages, 62–63 further advances (robotic surgery), 63–64, 63b oesophageal cancer, 286 stapling, 105 types of procedure, 62 minor procedures, 9–10 mitral regurgitation, 262–263 mitral stenosis, 261–262 mitral valvotomy, 262 mixed agglutination reaction (MAR) test, 605 MMF (mycophenolate mofetil), 191, 192t mobilisation, spinal injury, 650 Modified Early Warning Score (MEWS), 86, 86t, 130, 130t MODS (multiple organ dysfunction syndrome), 135 moles, 712 molluscum contagiosum, 708–709 monitoring critical illness, 135–138, 136b healthcare personnel injuries, 114 postoperative, 86, 86t–87t transplanted organs, 193–194

monoclonal antibodies, 183, 185, 191, 193 monoclonal anti-CD20 antibody, 192 monoclonal anti-CD25 antibody, 191 monoclonal anti-T-cell antibody (OKT3), 191, 193 monocytes, 99t mono-iodotyrosine (MIT), 528–529 morphine, 77, 79 Morton’s metatarsalgia (neuroma), 633 motility, small bowel, 353 motor neuropathy, diabetic foot, 470 mouth breathing, 223 movement disorders, 525 MRA (magnetic resonance angiography), 46, 46f MRCP see magnetic resonance cholangiopancreatography (MRCP) MRCS Diploma, 4 MRI see magnetic resonance imaging (MRI) MRSA (meticillin-resistant Staphylococcus aureus), 100, 121 MS (multiple sclerosis), 675, 687–688 mucin, 301 mucinous breast carcinoma, 427 mucinous cystadenocarcinoma, appendiceal, 382 mucinous cystadenomas, 339 mucocele, 314, 382 mucociliary clearance, 224 muco-epidermoid carcinomas, 208 multicystic kidney, 564 multidisciplinary team, 3, 272–275 multinodular goitre, 533 toxic, 534–535, 534t multiple cervical masses, 202 multiple endocrine neoplasia (MEN) type I, 554–555, 555t type II, 555 multiple organ dysfunction syndrome (MODS), 135 multiple sclerosis (MS), 675, 687–688 Münchhausen’s syndrome, 342 Murphy’s sign, 344 muscle flaps, 697, 697f muscle relaxants, general anaesthesia, 70–71, 71b, 76–77 myasthenia gravis, 243–244 mycobacteria, 685 Mycobacterium tuberculosis, 124 mycophenolate mofetil (MMF), 191, 192t myeloid leukaemia, 321 myelopathy, 523 myeloproliferative diseases, 321 myocardial infarction cardiogenic shock, 133b–134b postoperative, 91 myocardial perfusion scintigraphy, 251 myocardium, management in cardiac surgery, 248–249 myofibroblasts, 98 myoglobinuria, 446–447 myositis ossificans, 648 myxomas, 265

N naevi, 712 nail matrix, 705, 705f

Index  751 nails, 705, 705f naloxone, 138 nasal airway, 69–70 nasal polyps, 227 nasal septum, deviated, 225 nasal tumours, 205 nasogastric tubes, 88–89 equipment, 161 indications, 161 insertion, 161 paediatrics, 653 nasopharyngeal airway, 70f, 171 nasopharyngeal tube, 16, 16f natal cleft, 396–397 National Health Service (NHS), 8 National Training Number (NTN), 4 native valve endocarditis (NVE), 263 natural immunity, 111 natural orifice surgery, 63–64 Natural Orifice Transluminal Endoscopic Surgery (NOTES), 63–64 nausea, postoperative see postoperative nausea and vomiting (PONV) NEC (neonatal necrotising enterocolitis), 658–659 neck common surgical procedures, 211–212 plastic surgery, 702 swellings, 201–204, 202f–203f, 203t and upper aerodigestive tract, 201–212 veins in heart disease, 260t neck space infections, 208–210 necrosis avascular see avascular necrosis osteonecrosis, 626 pancreas, 334 necrotising fasciitis, 123, 123f, 710 needle aspiration, 116 see also fine-needle aspiration (FNA) needle biopsy intrahepatic cholangiocarcinoma, 310 malignant disease, 180 needles high-risk patients, 58 venous access, 151 wound closure, 103, 104f negative predictive values, 25–26 negligence, 11 Nelson’s syndrome, 554 neo-adjuvant therapy, 182t neonatal necrotising enterocolitis (NEC), 658–659 neonates infections in, 654 intestinal obstruction, 656–659 neostigmine, 360 nephrectomy, 569, 571 nephroblastoma, 569–570 in children, 663–664 nephrostomy ureteric stones, 580, 580f urinary diversion, 580–581, 580f urinary stones, 573 nerve block, 73, 76–77 nerve conduction studies, 471 nerve entrapment syndromes, 623–624 nerve fibres, dermal, 705 nerve function, elbow, 621 nerve grafting, 651 nerve injuries fracture complications, 646, 646t operation precautions, 58–59 thyroid surgery, 537

nerve repair, 651 nerve transfer, 651 nesidioblastosis, 548 neural crest, 543–544 neural crest cells, 544 neurapraxia, 651 neuroblastoma, 548 in children, 664 neuroendocrine tumours, 550–551 appendiceal, 382 lung, 230, 234 neurofibromas, 712–713, 713f brain, 518 small bowel, 364 neurogenic claudication, 453 neurogenic shock, spinal injuries, 650 neurological disease, visual symptoms, 679 neurological function, fractures, 642 neurological lesions complete, 649 incomplete, 649 neuromuscular blocking agents, 76–77 neuropathic bladder, 588–589, 589f neuropathy, diabetic foot, 470, 470f neurosurgery, 513–525 basic principles, 513–514 disorders treated, 514b examination, 513 history, 513 management of the unconscious patient, 513–514 neurotmesis, 650–651 neutrophilia, 26 neutrophils, 111 NHS (National Health Service), 8 nipple biopsy, breast cancer, 432 discharge, 419, 430t eczema, 428, 428t nitric oxide, 135 nitrites, urinary, 27 nitrous oxide, 76 no touch technique, 178, 179f nocturia, 581 nodular melanoma, 717, 717f non-absorbable sutures, 103–105 non-accidental injury, 648 non-clostridial gangrene, 123 non-communicating hydrocephalus, 522 non-compressible vessels, 454 non-cyclical breast pain, 417 non-depolarising muscle relaxants, 76 non-maleficence, 148 non-small-cell lung cancer (NSCLC), 229–230, 231b, 233 non-steroidal anti-inflammatory drugs (NSAIDs), 77, 245 arthritis, 612 haematemesis, 347 and peptic ulceration, 286–287 postoperative pain, 88 non-union of fractures, 647, 647f nose, 223–228 anatomy, 223–224, 223f discharge, 223–224 diseases, 223–227 obstruction, 223 physiology, 223 tumours, 227–228 see also entries beginning nasal

notes in the emergency Department, 22 postoperative orders, 85–89, 85b NOTES (Natural Orifice Transluminal Endoscopic Surgery), 63–64 Nottingham prognostic index (NPI), 435 NSAIDs see non-steroidal anti-inflammatory drugs (NSAIDs) NSCLC (non-small-cell lung cancer), 229–230, 231b, 233 nuclear isotope scan, 574 null-cell adenomas, 554 nutcracker oesophagus, 281 nutritional support, 143–144, 143f nystagmus, 216

O obesity, 7 aetiology, 293 breast cancer risk, 422 definition, 293, 294t epidemiology, 293, 294b management, 293, 294b (see also bariatric surgery) oblique abdominal incisions, 60 oblique fracture, 639, 640f obstetric brachial plexus palsy (OBPP), 652, 652t obstetrics, developing countries, 736–738 obstructed hernia, 402, 404–405 obstructive jaundice, 314, 338 obstructive sleep apnoea (OSA), 210–211 obturator hernia, 412–413, 413f occult micrometastases, 178–179 occupation, orthopaedic history, 608 octreotide, 549, 553 ocular motility, 671 ocular motility disorders, 688 odontoid peg fractures, 19 ODP (operating department practitioner), 54b oedema deep-vein thrombosis, 494 idiopathic scrotal, 665–666 macular, 677, 678f varicose veins, 484, 486–487 oesophageal varices, 347, 350 oesophagogastroscopy, 291 oesophagus, 279–286 anatomy, 279–280, 280f atresia with tracheooesophageal fistula, 654–655, 655f Barrett’s, 281, 284 cancer, 284–286 disease, 279–280 diverticula, 283 incomplete lower tear, 350–351 investigations, 280 motility disorders, 280–281 mucosal tear, 283–284 obstruction, 285 pH studies, 280 physiology, 279–280 rupture, 283–284 tumours, 205 oestrogen receptors, breast cancer, 426, 435–436 oligodendrogliomas, 518 oligospermia, 605 oliguria, 558 oncology see malignant disease one-stop clinics, 9

oophorectomy, 437 open access system, 9 open biopsy, 51 breast cancer, 431–432, 431f malignant disease, 180 open drains, 61 open fractures, 639, 640t, 645 open mesh repair, inguinal hernia, 407 open pneumothorax, 237–238 open reduction of fractures, 643, 644f open tracheostomy, 172–173 operating department, 53–55 design principles, 53 infection control, 55–58 layout, 54, 54f patient flow, 53–54 personnel, 54b structure, 54 supplies, 53 ventilation, 54–55 operating lists, 10 operating suite, 10 operating table, 58 operating team preparation, 56–57 operation field isolation, 56 ophthalmology see eye opioid analgesics, 77, 79, 80b, 88, 145, 145t OPSI (overwhelming postsplenectomy infection), 112, 319, 325–326, 326t optic disc, 672 optic globe movements, 669, 670f optic nerve compression, 676 optic neuritis, 675–676, 676f, 687–688 optical coherence tomography, 49 oral administration of antibiotic prophylaxis, 114 oral airway, 69–70, 70f oral cavity tumours, 205 oral contraceptive pill and anaesthesia, 67 breast cancer risk, 422 orbit cellulitis, 672 inflammation, 682 injuries, 673 malignancy, 682 pain, 682 orchidectomy, 596, 603 orchidopexy, 665 orchitis, 601–602 organ donation, 147, 187, 188b age range for donors, 191t contraindications to, 190 organ function in donors, 190–191 organ transplantation, 187–198 basic immunology, 188–189 in children, 198 complications, 193–194, 193t essential definitions, 187 exchange transplantation and desensitisation programs, 190 future of, 198 historical landmarks, 188b immunosuppression, 191–193 organ matching, 189–191 organ retrieval, 190–191, 192f rejection, 189 see also specific organs organisation of surgical services, 7–14 organisms load, 110 pathogenesis and virulence, 110–111 see also specific organisms

752  Index oropharyngeal airway, 16, 16f, 171 oropharyngeal tumours, 205 orthopaedics, 607–637 developing countries, 736, 737f examination, 607–608 history, 607–608 infections, 613–615 investigation, 609–610 paediatric, 634–637 terminology, 608b orthotopic graft, 187 Ortolani’s test, 635b OSA (obstructive sleep apnoea), 210–211 osmolality, 81–82 osmotic diuretics, 140–141 osteoarthritis, 610–611, 611b acromioclavicular, 618 ankle, 632 elbow, 621 glenohumeral joint, 620 hand, 622 hip, 625–626 knee, 630 radiological appearances in, 609t wrist, 622 osteochondritis, 417 osteoclastoma, 617 osteoma, 227 osteomyelitis acute, 613–615 chronic, 614–615 osteonecrosis of the femoral head, 626 osteosarcoma, 617 osteotomy, 631 otalgia, 214 otitis externa, 217 otitis media acute, 217–220 chronic suppurative, 218–219, 219f complications, 219, 219b, 220f with effusion, 218, 218f otosclerosis, 220 ovarian suppression and ablation, 436–437 ovarian tumours in children, 664 ovarian vein insufficiency, 485–486 overwhelming postsplenectomy infection (OPSI), 112, 319, 325–326, 326t oxalate stones, 573 oxidised cellulose, 104t oxycephaly, 521 oxygen delivery measurement, 140 methods of improving, 140 monitoring in the critically ill, 137 shock treatment, 133 oxyhaemoglobin dissociation curve, 74, 74f

P PABA test, 328 PaCO2, 160, 160t PAD (peripheral arterial disease), 448 paediatrics see children Paget’s disease, 428, 428t, 438 pain anal, 387, 390 ankle, 631 arising from urinary tract, 557–558 breast, 415–417, 427 deep-vein thrombosis, 494 disorders, 525

elbow, 620 foot, 632 hip, 625 knee, 627 localisation, 343–344 ocular, 680, 685 oesophageal, 280 orbital, 682 orthopaedic history, 607–608 parietal, 342 patterns, 343 perioperative, amputation, 462 postoperative see postoperative pain relief see analgesia shoulder, 618 varicose veins, 485 visceral, 342 wrist, 621 palliative therapy breast cancer, 439 critical limb ischaemia, 468 gastric cancer, 292 lung cancer, 233 pancreatic cancer, 338 palpation anal disorders, 387–388 intestinal obstruction, 355 kidney, 558 for peritoneal irritation, 344 pancreas, 327–339 anatomy, 327, 328f cysts, 339, 339t developmental anomalies, 327 embryology, 327–330 masses, 330 measurement of function, 328–329, 328b physiology, 327–328 transplantation, 191, 196, 197f tumours, 336–339 pancreas divisum, 327 pancreatic carcinoma, 336–339, 336b aetiology, 336, 336b clinical features, 337 diagnosis, 337 epidemiology, 336 investigation, 337–338 management, 338–339 pathological features, 336–337 prognosis, 339 pancreatic fistula, 326 pancreatic islet cell hyperplasia, 555 pancreatitis, 330–336 acute, 330, 330b aetiology, 330–331 clinical features, 331, 331f complications, 333–334, 333t diagnosis, 331 investigation, 331–333, 332f management, 333, 333b mortality rates, 332–333 pathological features, 330–331 prognosis, 332, 332t–333t causes of, 331t chronic, 334–336 aetiology, 334 clinical features, 334–335 complications, 336 imaging, 335, 335f investigation, 335 management, 335–336 pathological features, 334 classification, 330–334 pancreatoduodenectomy, 338 pancuronium, 77, 145 pansynostosis, 521 pantaloon hernia, 406 PaO2, 160, 160t

papillary carcinoma breast, 427 thyroid, 538 papilloma basal cell, 711, 711f inverting, 227 mammary duct, 419, 423 paracentesis, pericardial, 168–169, 169f paracetamol, 77 paradoxical breathing, 238 paraesthesia, hand and wrist, 621 paralytic ileus, 359–363, 359t paramedian abdominal incision, 60, 60f paranasal sinuses, 223–228 anatomy, 223–224, 223f diseases, 223–227 physiology, 223 tumours, 227–228 para-oesophageal hernia, 282f, 283 parapharyngeal abscess, 209, 209f parapharyngeal space, 209, 209f paraphimosis, 599, 666 parasites, 397 parasympathetic palsy, 683–684 parathyroid glands, 540–543 carcinoma, 543 hyperplasia, 555 localisation of abnormal, 542, 543f parathyroid hormone (PTH), 540–541 parathyroidectomy, 543 para-umbilical hernia, 409–410, 409f–410f parenteral fluids see intravenous fluids parenteral nutrition, 83, 142–144 complications, 144 parietal pain, 342 paronychia, 709–710 parotid swellings, 201, 202f parotitis acute, 94 bacterial, 207 viral, 207 Parsonnet score, 265, 266t passive drains, 61 passive incontinence, 398 patella, recurrent dislocation, 630 patellar tap, 627 pathological fractures, 639, 641t patient centred practice, 3 patient flow, operating department, 53–54 patient positioning, 58–59 airway management in general anaesthesia, 69, 69f common positions, 58t operating table, 58 precautions, 58–59 semi-prone, 16, 16f temperature control, 59 patient preparation for theatre, 84–85 patient well-being, malignant disease, 183, 184b patient-controlled analgesia (PCA), 79, 80f, 88 patients path to surgery, 8–9 PCA3, 594 PCA (patient-controlled analgesia), 79, 80f, 88 PCR (polymerase chain reaction), 115 PDA (posterior descending artery), 249 PE see pulmonary embolism (PE) peak systolic pressure (PSP), 445 peau d’orange skin appearance, 427, 428f

PEC (percutaneous endoscopic colostomy tubes), 399 pedicled skin flaps, 206 PEEP (positive end-expiratory pressure), 136, 139t pelvic congestion syndrome, 485–486 pelvic floor damage, faecal incontinence, 398 repair, 399 pelvis examination, acute abdomen, 344 fractures, 642 blood loss in, 20 imaging in the trauma patient, 18–19 pelviureteric junction (PUJ) obstruction, 574–575, 575f penetrating trauma chest, 238 eyes, 672 heart, 271–272 ocular, 673, 673f renal, 568–569 vascular injuries, 476–477 penicillin, 118t penis, 599–600 carcinoma, 600, 600f prostheses, 605 peptic ulcers, 286–288, 347, 349–350, 349b, 349t aetiology, 286–287, 287t anatomical features, 287 clinical features, 287 complications, 288 epidemiology, 286–288 indications for surgical intervention, 286b investigation, 287–288 management, 288 pathological features, 287 signs, 287 peptides absorption in the small bowel, 354 percussion intestinal obstruction, 355 kidney, 559 for peritoneal irritation, 344 percutaneous endoscopic colostomy tubes (PEC), 399 percutaneous tracheostomy, 173 percutaneous transhepatic cholangiography (PTC), 302, 302f percutaneous transluminal angioplasty (PTA), 458–459, 459f–460f limb ischaemia, 466 percutaneous transluminal coronary angioplasty (PTCA), 253–255, 255t perforation diverticular disease, 373, 374t gallbladder, 314 perforator flaps, 698 perforators, 482–485 perianal abscess, 394 perianal haematoma, 392 perianal warts, 400 pericardial paracentesis, 168–169, 169f periductal mastitis, 420 perineal hernia, 414, 414f perinephric abscess, 566–567, 567f perioperative management, 81–95 developing countries, 724–725 peripheral arterial disease (PAD), 448

Index  753 peripheral circulation, heart disease, 259, 260t peripheral nerve injuries, 650–651 peripheral nerve lesions, 524 peristalsis, 353 peritoneal lavage, 169–170, 170f peritonitis, 119 in diverticular disease, 373–374 peritonsillar abscess, 208–210, 209f peri-venous tissue changes, varicose veins, 484 personnel developing countries, 723–724 infection prevention, 114 operating department, 54b, 114 Perthe’s disease, 635–636 PET see positron emission tomography (PET) pethidine, 145, 145t Peutz-Jeghers syndrome, 364 Peyronie’s disease, 599–600, 600f Pfannenstiel abdominal incision, 60, 60f pH arterial blood gases, 160–161, 160t hiatus hernia, 282 studies, oesophageal, 280 phaeochromocytoma, 547–548, 547f phagocytic cells, 111 phantom pain, 462 phenoxybenzamine, 547–548 phimosis, 599, 666 phlegmasia alba dolens, 503 phlegmasia caerulea dolens, 494 phosphodiesterase inhibitors, 605 photoelectric effect, 28–29 photopsia, 680 phyllodes tumour, 418, 428, 428f physiological basis for surgical care, 81–84 physiological studies, anal disorders, 389 physiotherapy arthritis, 622 chest, 245 PiCCO (pulse-induced contour cardiac output) measurement, 158 pigmentation, varicose veins, 484 pilar cysts, 713 pilonidal disease, 396–397 pilosebaceous units, 705 pinhole acuity, 669 piperacillin, 118t pituitary gland, 551–554 adenomas, 555 complications of management of disorders, 554 pituitary tumours, 518, 552, 552f mixed, 554 plantar fasciitis, 633–634 plasma D-dimer, 502 plasmacytoma, 617 plastic surgery, 691–702 aesthetic/cosmetic, 702 developing countries, 730–734, 731b reconstructive ladder, 691, 692f–693f techniques, 691–702 platelets, 26, 97 pleomorphic adenoma, 208 plethysmography, 455 pleura, 239–242 abrasion, 237, 239–240 drainage, 165–166, 165f empyema, 240–241 metastases, 439 tumours, 240

pleural effusions, 239–242 malignant, 439 pleurectomy, 237, 239–240 pleurodesis, 237, 239–240 Plummer’s syndrome, 534, 534t pneumonectomy, 246 pneumonia, 240, 245 pneumoperitoneum, therapeutic, 405 pneumothorax, 235–238, 236f open, 237–238 secondary, 237–238 spontaneous primary, 236–237 tension see tension pneumothorax treatment, 236 PNMs (polymorphonuclear neutrophils), 97, 99t podophyllin, 708 polyarteritis nodosa, 451 polyclonal agents, 193 polycystic kidney disease, 564, 564f polyethylene glycol hydrogels, 104t polymerase chain reaction (PCR), 115 polymorphonuclear neutrophils (PNMs), 97, 99t polymyalgia rheumatica, 612 polyps large bowel, 374–376, 375b nasal, 227 PONV (postoperative nausea and vomiting), 78 popliteal aneurysm, 464–465 popliteal vein thrombus, 495–496 popliteo-pedal bypass, 468, 469f population screening, 184 porphyria, 322 portal hypertension, 321 portal pressure, lowering, 350 porters, 54b positive end-expiratory pressure (PEEP), 136, 139t positive predictive values, 25–26 positron emission tomography (PET), 47–48 cardiac disease, 252 gastric cancer, 292 lung cancer, 231 oesophageal cancer, 285 pancreas, 329t, 330 pancreatic cancer, 338 positron emission tomographycomputed tomography (PET-CT), 47–48 post-defecatory soiling, 397 posterior cruciate ligament (PCL) injuries, 630 posterior descending artery (PDA), 249 posterior triangle swellings, 202 posterior vitreous detachment, 679–680 posterolateral thoracotomy, 244 Post-graduate Medical Education and Training Board (PMETB), 4 posthepatic jaundice, 301, 301b postmicturition dribbling, 581 postmortem examination, 14 postnasal drip, 223–224 postoperative care after anaesthesia, 78–80 arterial disease, 458, 458b, 458f care pathway, 10 chest surgery, 245–246 postoperative nausea and vomiting (PONV), 78 postoperative pain, 78–80, 87–88, 88t chronic, 80 management, 79

methods of treating, 79, 79t patient-controlled analgesia see patient-controlled analgesia (PCA) reasons for treating, 79 postoperative period, 85–89 complications, 89–95 intravenous fluids, 87, 87b observations, 86–87, 86t–87t orders, 85–86, 85b pain and pain relief, 87–88, 88t tubes and drains, 88–89, 88t postphlebitic leg, 503–504 post-pneumonectomy, 246 postsplenectomy immunity, 112 potassium blood levels, 27 extracellular fluid, 81–82 intake, 82, 82t maintenance requirements, 82 poverty, 722–728 povidone-iodine scrubbing up, 57 skin preparation, 56 pox virus, 708 practical procedures, 149–173 see also specific procedures precordial examination, 261t predestination of blood, 457 prednisolone, 192 pregnancy and breast cancer, 423 goitre, 532 monitoring in the critically ill, 138 prehepatic jaundice, 301, 301b preliminaries, 149–150 premedication, 69, 69t prenatal diagnosis, 654 preoperative assessment, 84–85 anaesthesia, 66–69 arterial disease, 457–458, 457b patient preparation, 84–85 risk assessment, 84–85, 84b thyroid surgery, 536–537 pre-operative assessment clinics, 10 pressure sores, 94, 647, 702 pretibial area wounds, 21 priapism, 600, 600b prilocaine, 150 primary hernias, 401 primary wound healing, 97–101, 98f proctitis, 367, 367b proctocolectomy, 370, 370f proctography, evacuation, 388 proctoscopy, 388 profession of surgery, 3–5 progesterone receptors, breast cancer, 435–436 prognostic markers, 180–181 prolactinoma, 552 proliferative phase of wound healing, 97–98 prone jack-knife position, 58t prophylaxis antibiotic see antibiotic prophylaxis deep-vein thrombosis, 496–497, 497t, 498f, 500f–501f, 504 pulmonary embolism, 496–497, 498f, 500f–501f propofol, 76, 145, 145t proptosis, 682 prostaglandin E1, 605 prostate, 590–596 clinical assessment, 590 infections, 590–591 obstruction, 591–593 pain, 581

prostate cancer, 593–596 aetiology, 594 clinical features, 594 epidemiology, 593–596 investigation, 594–595 management, 595–596 pathological features, 594 prostatectomy, 592 post-prostatectomy failure of micturition, 164 prostate cancer, 596 urinary catheterisation in, 163–164 prostate-specific antigen (PSA), 594 prostatitis acute bacterial, 590–591 chronic bacterial, 591 prostheses heart valves, 263–264, 264t infection, 90, 120 penile, 605 in plastic surgery, 696–697 vascular, 457 prosthetic valve endocarditis (PVE), 263 protein, 144 protein electrophoresis, 610 Proteus spp., 572 proton pump inhibitors gastrinoma, 550 peptic ulceration, 349 protozoal infections, 686 prune belly syndrome, 660 pruritus ani, 387, 389, 397–398 PSA (prostate-specific antigen), 594 pseudocysts, pancreatic, 334, 336, 339, 339t pseudomembranous colitis, 120–121 pseudomembranous enterocolitis, 92–93 pseudo-obstruction, intestinal, 356, 360 psychodynamics, ulcerative colitis, 368 psychological considerations, breast cancer therapy, 438 psychological effects of surgery, 4 psychological preparation for theatre, 84–85 psychosocial problems causing pruritus ani, 397 PTA (percutaneous transluminal angioplasty), 458–459, 459f–460f, 466 PTC (percutaneous transhepatic cholangiography), 302, 302f PTCA (percutaneous transluminal coronary angioplasty), 253–255, 255t PTH (parathyroid hormone), 540–541 ptosis, 683, 683f pubertal problems breast, 415 goitre, 532 pulmonary artery catheter, 137 pulmonary embolism (PE) aetiology, 497 clinical features, 500–502 in deep-vein thrombosis, 497–503 diagnosis, 502 epidemiology, 498 fracture complications, 646 investigation, 502 management, 502–503, 503b pathological considerations, 498–500

754  Index physiological considerations, 498–500 postoperative, 91 prophylaxis, 496–497, 498f, 500f–501f recurrent, 503 pulmonary function tests, 232–233 pulmonary radioisotope ventilation/ perfusion (V/Q) scans, 502 pulp space abscesses, 20 pulse assessment in critical illness, 131 examination, 452–453 pulse oximetry, 74, 74f, 136 pulse-induced contour cardiac output (PiCCO) measurement, 158 pulsus paradoxus, 18 punch biopsy, 706, 706f pupils examination, 671, 671b responses, 671, 671t tonic, 683 pure tone audiometry, 215 PVE (prosthetic valve endocarditis), 263 pyelonephritis acute, 565 fever in, 557 pyeloplasty, 575, 575f pyelostomy, 580–581, 580f pyloric stenosis, 662 pylorus-preserving pancreatoduodenectomy, 338 pyogenic granulomas, 712, 713f pyogenic liver abscess, 306–307 pyrexia of unknown origin, 121

Q quadrantectomy, breast cancer, 433 quadriceps wasting, 628 quality of life (QOL), 128–130 quinsy, 208–210

R radial artery, sampling, 158–159, 158f radial head excision, 621 radial nerve injury, 59 radical antrostomy, 226 radiculopathy, 523 radio allergosorbent test (RAST), 224 radioactive implants, 182 radioactive iodine, 182, 535 radiofrequency ablation, metastatic liver cancer, 311 radioisotope studies, 47–48 advantages and disadvantages, 48 dynamic, 563 knee, 628 osteomyelitis, 614 principles, 47–48 prostate cancer, 595, 595f safety, 48 static, 563 upper urinary tract, 563, 563f radiological imaging, 28–38 fractures, 642, 643f interpretation, 37–38, 38f–42f physical basis, 28–29 see also imaging; specific modalities radionucleotide localisation (ROLL), breast cancer, 432

radionuclide investigation, cardiac disease, 251 radiotherapy, 182 acromegaly, 553 brain tumours, 519 breast cancer, 433–434 cervical tumours, 205 colorectal cancer, 381 effect on intestines, 363 lung cancer, 233–234 pancreatic cancer, 338–339 prostate cancer, 596 renal adenocarcinoma, 571 and wound healing, 101 rapamycin, 192, 192t Raynaud’s phenomenon, 462, 472–473 Raynaud’s syndrome, 473, 473b RCA (right coronary artery), 249, 250b, 250f, 610 rebound tenderness, 344 reconstructive ladder, 691, 692f–693f records, 22, 149 rectal administration of antibiotic prophylaxis, 114 rectal examination, 582 acute abdomen, 344 intestinal obstruction, 355 rectovaginal fistula, 727–728 rectum biopsy, 388, 388f bleeding, 381, 381b carcinoma, 378–379, 380b, 380f (see also colorectal cancer) recurrence, tumour, 184–185 recurrent inguinal hernia, 408 recurrent laryngeal nerve, 210 red blood cells dynamics, 323 gastric cancer, 292 maturation and destruction, 319 red eye, 684–685, 684b, 684f, 684t reducible hernia, 402 reduction of fractures, 643 reduction pneumoplasty, 244 REE (resting energy expenditure), 83 reflex sympathetic dystrophy see complex regional pain syndrome (CRPS) type 1 reflux, gastro-oesophageal see gastro-oesophageal reflux disorders reflux nephropathy, 566, 566f regional anaesthesia, 65, 72–74 advantages and disadvantages, 72b see also local anaesthesia regulation of surgical practice, 3–4 rehabilitation fractures, 645 spinal injury, 650 Reidel’s thyroiditis, 538 rejection, organ transplantation, 189 relatives, informing, 13 relaxants, 145 remifentanil, 77 remodeling phase of wound healing, 97, 99 remodelling, fractures, 641, 642f renal artery disease, 475–476, 475f aneurysm, 476 stenosis, 475–476, 475f, 476t renal failure therapeutics in the critically ill, 140–141 and wound healing, 101 renal function monitoring in the critically ill, 137 neuropathic bladder, 589

renal pelvis carcinoma, 571, 571f renal replacement, 141 renal stones, 571 see also urinary stones renal tuberculosis, 567–568, 568f renin, 475 renography, urinary tract infection, 565 renovascular hypertension, 475–476 reparative phase of wound healing, 97–98 reperfusion injury, 446–447 reporting healthcare personnel injuries, 114 resection breast, 434 gastric cancer, 291f, 292 lung, 232–233, 232f oesophageal cancer, 285–286 pancreatic, 338 resection margin, 181 respiratory distress in children, 654–656 respiratory failure in the critically ill, 138–139, 138b signs of, 130, 131t respiratory system infection, 120 medical fitness assessment, 66–67 monitoring in paediatrics, 653 monitoring in the critically ill, 136–137 perioperative period, 83–84 postoperative complications, 92, 92b pulmonary embolism, 502 therapeutics in the critically ill, 138–139 resting energy expenditure (REE), 83 restrictive operations, bariatric surgery, 294 resuscitation head injury, 515 pulmonary embolism, 502 retina detachment, 679, 679f dystrophies, 678, 678f tear, 680 vessels, 672 retinal artery occlusion, 674–675, 675f retinal vein occlusion, 675 retinitis pigmentosa, 678, 678f retrobulbar neuritis, 675–676, 687–688 retrograde ureterography, 561, 579 retroperitoneal fibrosis, 579 reverse Trendelenburg position, 58t Revised Trauma Score (RTS), 128–130 rhabdomyosarcoma, 585 rheumatic fever, 258–259 rheumatoid arthritis, 208, 611–612 acromioclavicular, 618 ankle, 632 elbow, 621 glenohumeral joint, 620 hand, 622 hip, 626 knee, 630 ocular manifestations, 686 wrist, 622 rheumatoid factor, 610, 612 rhinomanometry, 224 rhinophyma, 698 rhinosinusitis, 225–226 rib fracture, 238 Richter’s hernia, 403, 403f

right coronary artery (RCA), 249, 250b, 250f right heart failure, 259, 259t right subcostal abdominal incision, 60, 60f Rinne test, 215 risk assessment arterial disease, 453, 453b cardiac surgery, 265, 266t preoperative, 84–85, 84b rivaroxaban, 497 robotic surgery, 63–64, 63b Rockall risk score, 348, 348t rocuronium, 77 ROLL (radionucleotide localisation), breast cancer, 432 rotator cuff tears, 619 Royal Marsden Hospital Staging System, 603, 604t RTS (Revised Trauma Score), 128–130 runners, 54b rupture see specific organs

S sacral nerve stimulation (SNS), 399 safety magnetic resonance imaging, 46 radioisotope scanning, 48 ultrasonography, 43 X-rays, 29, 29t–30t sagittal synostosis, 521 salivary gland neoplastic diseases, 208 non-neoplastic diseases, 207–208 sanitation, developing countries, 722–723 sapheno-femoral ligation, 489–490, 490f sapheno-popliteal ligation, 489–490, 490f sarcoidosis, 688 satellite limb lesions, malignant melanoma, 719 scalp lacerations, 22 scars, 99, 692–694, 694t SCFAs (short-chain fatty acids), 366 schistosomiasis, 584, 584f developing countries, 735 Schroetter syndrome, 491–492 schwannomas, 518, 713 sciatic hernia, 414, 414f scissor gait, 609b scleritis, 682, 686 scleroderma, 451 sclerotherapy haemorrhoids, 390–391, 391f varicose veins, 488–489, 489t scraping, 50 screening, 52 abdominal aortic aneurysms, 463 breast cancer, 425 colorectal cancer, 377 definition, 25 gastric cancer, 290 malignant disease, 184–185, 184t oesophageal cancer, 285 for recurrence, 184–185 scrotum idiopathic oedema, 665–666 pain, 581 swelling, 602–604 scrub nurse, 54b scrubbing up, 56–57

Index  755 SDD (selective decontamination of the digestive tract), 117, 142 seborrhoeic keratosis, 711, 711f secondary hernias, 401 secretin, 327 sedation, 144–145, 145t seizures, 141, 518 selective decontamination of the digestive tract (SDD), 117, 142 selective oestrogen receptor modulators (SERMs), 436 semen analysis, 604–605, 604t seminomas, 243, 603–604, 604t semi-prone position, unconscious patient, 16, 16f sensitivity, investigations, 25–26 sensorineural hearing loss, 215, 220–222 sensory neuropathy, diabetic foot, 470 sentinel node biopsy breast disease, 434 malignant melanoma, 719 sepsis, 134–135 anal, 393–397, 394t postoperative, 91–92 septal haematoma and abscess, 224 septic arthritis, 615 septic shock, 134b septicaemia, 116–117, 117b, 134–135 meningococcal, 134b serial imaging of progression, malignant disease, 183, 183t SERMs (selective oestrogen receptor modulators), 436 serological examination amoebic liver abscess, 307 infections, 115 serous cystadenomas, 339 serum alkaline phosphatase, 560 serum amylase acute pancreatitis, 331–332 chronic pancreatitis, 335 serum calcium, 540–541, 543, 560 serum creatinine concentration, 27, 559–563 serum electrolytes, 27 serum lipase, 331 serum potassium, 27 serum prostate-specific antigen (PSA), 594 serum sodium, 27 serum urea concentration, 27, 559 sevoflurane, 76 shave biopsy, 707 shaving, 56 shin area wounds, 21 shock, 132–135 consequences, 133 examples of, 133–134 mechanisms, 132–133 responses, 133 treatment, 133 see also specific types short leg, 609b short-chain fatty acids (SCFAs), 366 shoulder, 617–620 shoulder stiffness after breast surgery, 435 shuffling gait, 609b sialadenitis, 207, 207f sialectasis, 207–208 sickle cell disease, 321 ophthalmic manifestations, 688 sideropenic dysphagia, 205 sigmoid volvulus, 359, 728–729, 729f

sigmoidoscopy anal disorders, 388 colorectal cancer, 378 ulcerative colitis, 369 sildenafil, 605 silhouette sign, 38, 42f silica, 507 silicone implants, 696 breast, 440, 440f SILS (single incision laparoscopic surgery), 63–64 single contrast studies, 35 single incision laparoscopic surgery (SILS), 63–64 single port surgery, 63–64 single-contrast studies, 36f single-photon emission computed tomography (SPECT), 47 sinoatrial (SA) node, 249 sinus rhythm, 249 sinus tumours, 205 sinusitis, 225–227, 226f sirolimus, 192 SIRS (systemic inflammatory response syndrome), 91, 117, 117f, 134–135 Sjögren’s disease, 208 Sjögren’s syndrome, 686 skin anatomy, 703–707, 704f biopsy, 706 changes in varicose veins, 484, 487, 487f disorders, 703–720 causing pruritus ani, 397 embryology, 703–707 infections, 707–711 integrity in fractures, 642 preparation, 56, 89, 113 in spinal injuries, 650 stapling, 105 substitutes, 696 therapy principles, 706–707 tumours, 711–720 skin appendages, benign tumours, 713 skin cancer melanoma see malignant melanoma non-melanoma, 714–716 skin flaps, 697, 697f breast reconstruction, 440, 440f free, 206 pedicled, 206 skin grafts, 694–696, 695f full-thickness, 206 materials, 696 split-thickness, 206 skin prick tests, 224 skin tags, 392, 711 skull base fracture, 222, 515b, 517 skull fracture, 517 SLE see systemic lupus erythematosus (SLE) sleeve gastrectomy, 294, 295f sleeve resection, 232, 232f sliding hernia, 403, 403f hiatus, 282, 282f slipped upper femoral epiphysis, 636–637, 636f slow-transit constipation, 367 small bowel, 353–364 anatomy, 353–354 atresia, 657 diverticula, 363 neoplasia, 363–364 neuroendocrine tumours, 551 obstruction, 359 (see also intestinal obstruction) physiology, 353–354 stones, 314–315

transplantation, 196–197, 197b, 197f volvulus, 359, 729 see also intestinal obstruction small vessel vasculitis, 451 small-cell lung carcinoma (SCC), 230, 234 smell tests, 224 smoking and anaesthesia, 67 and atherosclerotic occlusive disease, 447–448 cessation, 233 coronary artery disease risk, 253 and lung cancer, 229 Snellen chart, 669 snip excision, 707 SNS (sacral nerve stimulation), 399 sodium absorption in the large bowel, 365–366 blood levels, 27 extracellular fluid, 81–82 intake, 82, 82t maintenance requirements, 82 soft-tissue abscesses, 20–22 solar keratoses, 711 solid pseudopapillary tumours, 339 solitary cysts, kidney, 564 solitary thyroid nodule, 535–536 see also toxic solitary thyroid adenoma/nodule somatisation, 85 Specialist Registrars (SpRs), 4 specialities, surgical, 7 specificity, investigations, 25–26 SPECT (single-photon emission computed tomography), 47 spectacular injuries, 22 speech restoration, 206, 206f spermtoceles, 602 Spigelian hernia, 412 spinal anaesthesia, 73–74, 73f spinal cord tumours, 523t spinal shock, 649–650 spine compression, breast cancer, 439 degenerative disease, 522–523 dysraphism, 520 infection, 524–525 injuries, 648–650 tumours, 523 spiral fracture, 639, 640f spironolactone, 545 Spitz naevus, 712 spleen, 319–326 anatomy, 319 disorders, 320–324 haematological functions, 319 immunological functions, 319 physiological considerations, 319 postsplenectomy immunity, 112 ruptured, 323–324, 323f, 325f splenectomy, 324–326 complications, 326 immunological consequences of, 320 indications for, 323b preoperative management, 324–326, 325b procedure, 325–326 see also overwhelming postsplenectomy infection (OPSI) splenic abscess, 321 splenic cyst, 321 splenomegaly, 320–323 aetiology, 320–322 clinical features, 322

management, 323 physical findings, 322 splints, fractures, 643–644 split-thickness skin grafts, 206, 694–696, 695f spontaneous primary pneumothorax, 236–237 squamous carcinoma anal, 400 lung, 229 neck, 203 oesophageal, 284 salivary glands, 208 of the upper aerodigestive tract, 204–206 squamous-cell carcinoma, 716, 716f stab wounds chest, 238 heart, 271 staging of tumours, 180–181, 181b bladder tumours, 586, 586t breast cancer, 424, 424t colorectal cancer, 377, 377f, 377t gastric cancer, 289 histological grade, 180, 181t lung cancer, 230, 231b prostate cancer, 595, 595t renal adenocarcinoma, 570, 570t testicular tumours, 603, 604t see also specific staging systems stamping gait, 609b staphylococci antibiotic prophylaxis, 90 blepharitis, 685 lactational breast abscess, 420 skin infections, 709–710 Staphylococcus aureus, 709 stapled haemorrhoidectomy, 392 stapling, 105, 105t haemostasis, 102 high-risk patients, 58 star flower oil, 417 steam under pressure sterilisation, 56 steatorrhoea, 334–335 stents/stenting aortic aneurysms, 274, 276f biliary, 304, 304f coronary arteries, 253 endoluminal, 463–464, 464f endoscopy, 49, 338 oesophageal cancer, 286 vs coronary artery bypass grafting, 255 stereotaxy, 525 sterilisation, 55–58, 55b, 113 cold, 55–56, 56b heat, 55–56, 56b sternotomy, 245, 275 steroid injections, intra-articular, 612 steroid-dependent patients, postoperative care, 95 Stevens-Johnson syndrome, 688 stiff leg, 609b stiffness elbow, 620 hand and wrist, 621 orthopaedic history, 607 shoulder, 618 stomach, 286–292 contents, aspiration of, 72 see also entries beginning gastric stomas, 399 strangulated hernia, 402, 404–405 femoral, 409 umbilical, 410 strangury, urinary, 581

756  Index stratum corneum, 703 strawberry gallbladder, 316 strawberry naevi, 712 streptococci gangrene, 123 hospital-acquired infection, 100 skin infections, 710 Streptococcus pyogenes, 710 stress electrocardiography (ECG), 51 stress incontinence, 590 stress ulceration, 350 stress X-rays, 631 strictures in gastro-oesophageal reflux, 281 urethral, 598–599, 599b stricturoplasty, 362 strokes causes in open heart surgery, 257t medical fitness assessment, 67 styes, 684, 684f subacromial disorders, 618–620 subarachnoid haemorrhage (SAH), 519–520 subclavian vein, central venous catheterisation, 155–156, 155f subconjunctival haemorrhage (SCH), 684 subcutaneous infiltration, anaesthesia, 73 subcutaneous tunnelling, 157, 157f subcutis, 705 subdural haematoma, 517–518, 517f subluxation, patella, 630 submandibular gland bacterial infection, 207, 207f sialadenitis, 207, 207f swellings, 201 tumours, 725, 725f subungual haematoma, 21 succus entericus, 353–354 Sudeck’s atrophy see complex regional pain syndrome (CRPS) type 1 suffixes, commonly used, 54b sulfasalazine, 369 sulphonylurea, 549 superficial femoral vein thrombus, 495–496 superficial fistula, 395 superficial mycoses, 710–711, 710f superficial spreading melanoma, 717, 717f superficial veins distension, 494 superparamagnetic iron oxide particles (SPIO), 46–47 super-squeeze oesophagus, 281 supine position, 58t suppositories, 390 supraclavicular swellings, 202 supralevator abscess, 395 suprapubic bladder drainage, 164–165 suprasphincteric fistula, 395 surgeons, 3–5 surgery as an assault, 4 definition, 3 patients path to, 8–9 surgical airway, 171–173 see also cricothyroidotomy; tracheostomy surgical safety checklist, 53–54, 55f surgical services organisation, 7–14 Surgical Specialist Advisory Committees (SACs), 4 surgical specialities, 7

survival, malignant disease, 183 sutures, 103–105, 692 gauge, 105 materials, 105t suxamethonium, 76–77 swallowing difficulty see dysphagia Swan-Ganz catheters, 157, 158f sweat glands, 705 swellings anal, 387, 389 ankle, 631 brain, 515 in fractures, 642 groin, 407, 409t, 661b hand, 621 knee, 627 lower limb, 509b in the neck, 201–204, 202f–203f, 203t scrotal, 602–604 swimmers itch, 735 sympathectomy, 461–462, 468 sympathetic palsy, 683–684 sympathomimetics, 67 synchronised intermittent mandatory ventilation (SIMV), 139t syncope, 678 synergistic bacterial gangrene, 123 synovectomy arthritis, 612 rheumatoid arthritis, 621 synovial fluid investigation, 610 syphilis, 685 systemic inflammatory response syndrome (SIRS), 91, 117, 117f, 134–135 systemic lupus erythematosus (SLE), 451, 612 ophthalmic manifestations, 686 systemic sclerosis, 451

T TACE (transcatheter arterial chemo-embolisation), 309 tacrolimus, 191, 192t tadalafil, 605 Takayasu’s arteritis, 450 talipes, 637, 726–727, 727f tamoxifen, 417 breast cancer, 436 breast cancer prevention, 425 tamponade cardiac, 18 oesophageal varices, 350 tap test, 487 tapes, wound closure, 105 TAPP (trans-abdominal pre-peritoneal) hernia repair, 407 targeted screening, 184 TAVI (trans-catheter aortic valve implantation), 273, 274f TBI (traumatic brain injury), 514–518, 515b, 516f teamwork, 3, 8 teardrop appearance, 428, 428f tears, excessive, 682–683 technetium-labelled red cell ventriculography (MUGA), 51 teicoplanin, 118t telangiectasia, 489 telangiectatic carcinoma, 428 temporal arteritis, 450 temporal bone fracture, 222 tenosynovitis, 624 tensile strength recovery, wound healing, 99–100, 99f

tension pneumothorax, 17, 236–238, 237b, 237f relief of, 166, 166f teratomas, 603–604, 603b, 603f, 604t in children, 664, 664f terminal care, 13 terminal dribbling, urinary, 581 testes appendix, 665 torsion, 601, 665 tumours, 602–604 undescended, 600–602, 664–665, 665b testosterone, 596 tetanus, 123–124 prophylaxis, 21, 123b rates of, 21 wound contamination, 100 tetracycline, 118t thalassaemia, 321 thallium-201 (99mTc-sestamibi) perfusion scintigraphy, 51 theatre managers, 54b therapeutic aspiration, pleura, 165–166 therapeutic dressings, 107 Therapeutic Intervention Scoring System (TISS), 130 thermal coagulation, 102, 103f thermotherapy, prostatic obstruction, 592 thiopental (thiopentone), 76 thoracic degenerative disease, 523 thoracic incisions, 244–245 thoracic outlet syndrome, 470–471, 470f–471f thoracic spine injuries, 649 thoracic trauma, 666–667 thoraco-abdominal aortic aneurysm (TAAA), 465, 465f thoracoabdominal incisions, 245 thoracotomy, 244–245 aortic rupture, 271 haemothorax, 17 three/four dimensional images, ultrasonography, 43 thrombectomy, 469 thrombin, 104t thromboangiitis obliterans, 451 thrombocytopenia, 26 heparin-induced, 496 postoperative, 87 thrombocytosis, 26, 326 thrombolysis, 459–460 deep-vein thrombosis, 496 thrombosis in a graft, 469 thrombophlebitis, 481, 482f after venepuncture, 152 central venous, 92 superficial, 491, 494 thrombosis, 481, 482b, 482t, 491–504 acute limb ischaemia, 471–472, 471t in a graft, 469 haemorrhoids, 392 pathological features, 481–482 thymectomy, 243–244 thymomas, 243 thyroglobulin, 539 thyroglossal cyst, 204, 204f, 528f thyroid autoantibodies, 534 thyroid cancer, 538–540 differentiated, 538–539 imaging, 531–532 thyroid eye disease, 682, 687, 687f thyroid gland, 528–540 adenoma, 555 ectopic tissue, 532 embryology, 528–529, 528f evaluation of disease, 529–532

function tests, 531–534, 536 goitres see goitre histological features, 528 hyperactivity, 530 pathological features, 529 patient management, 536–537 physiological features, 528–529 solitary nodule, 535–536 surgical anatomy, 528, 529f thyroidectomy, 536, 536t Graves’ disease, 535 multinodular toxic goitre, 535 thyroiditis, 537–538 thyroid-stimulating hormone (TSH), 529, 531 thyroid-stimulating hormoneproducing adenomas, 554 thyrotoxic storm/crisis, 537 thyrotoxicosis, 534–535 clinical features, 530 management, 534–535 management of specific causes of, 535 thyrotrophic adenomas, 554 thyrotrophin-releasing hormone (TRH), 529 thyroxine, 528–529, 531 TIA (transient ischaemic attack), 678–679 tibial vein thrombus, 495–496 Tietze’s syndrome, 417 time, wounds, 100 Tinel’s sign, 651 tinnitus, 214 TIPS (transjugular intrahepatic portosystemic shunt), 350 tissue biopsy, 180 tissue death, infection, 111 tissue expansion, 698, 699f tissue harmonic imaging (THI), 39 tissue sampling, 50–51 see also specific techniques T-lymphocytes, 111–112, 704–705 in organ transplantation, 188–189, 189f TNM staging, 180, 181b bladder tumours, 586 breast cancer, 424, 424t colorectal cancer, 377, 377t gastric cancer, 289 lung cancer, 230, 231b malignant melanoma, 718, 719t prostate cancer, 595t renal adenocarcinoma, 570, 570t tobacco see smoking tomography, 30–38 computed see computed tomography (CT) contrast studies, 30–37 plain film, 30 tongue airway obstruction, 15–16 examination, 558 tonic pupil, 683 tonsillar swelling, 210 tonsillectomy, 211, 211b topical administration anaesthesia, 72 antibiotic prophylaxis, 114 topical haemostatic products, 103, 104t torsion, testicular, 601, 665 total body water, 81, 82f total energy expenditure (TEE), 83 total-body iodine scanning, 539 totally extra-peritoneal (TEP) hernia repair, 407 toxic megacolon, 368–369 toxic solitary thyroid adenoma/ nodule, 534–535 toxoplasmosis, 686 trace elements, 144

Index  757 tracheo-oesophageal fistula, oesophageal atresia with, 654–655, 655f tracheostomy, 172–173, 172f–173f, 211–212, 211f, 212b complications, 173 open, 172–173 percutaneous, 173 traction, fractures, 643–644 training, 4–5, 4f, 8 TRAM (transverse rectus abdominis myocutaneous) flap, 440–441, 440f, 698 tramadol, 77 trans-abdominal pre-peritoneal (TAPP) hernia repair, 407 trans-catheter aortic valve implantation (TAVI), 273, 274f transcatheter arterial chemoembolisation (TACE), 309 Transcyte®, 696 transferases, 302 trans-hiatal removal, oesophageal cancer, 286 transient ischaemic attack (TIA), 678–679 transjugular intrahepatic portosystemic shunt (TIPS), 350 transposed viscus, 206 transrectal ultrasound (TRUS), 582 transsphincteric fistula, 395 transumbilical laparoscopic surgery (TULA), 63–64 transurethral laser therapy of the prostate, 592 transurethral prostatectomy, 592 transurethral resection of the prostate (TURP), 592, 596 transverse abdominal incision, 60 transverse fracture, 639, 640f transverse rectus abdominis myocutaneous (TRAM) flap, 440–441, 440f, 698 trapped lung, 234 trash foot, 458, 458f trastuzumab, 437 trauma acute cardiac tamponade, 18 ankle, 631 arteriovenous fistula, 477–478 bladder, 584–585 breast, 419–420 breathing problems, 17–18 chest, 238–239 developing countries, 736 elbow, 620 in the emergency department, 15 head, 514–518, 515b, 516f heart and great vessels, 271–272 hip, 625 hypovolaemic shock, 134b liver, 305–306, 306t orthopaedic history, 607 paediatric, 666–667 peripheral nerves, 524 plastic surgery in, 698 renal, 568–569, 568b–569b secondary pneumothorax, 237–238 shoulder, 618 slipped upper femoral epiphysis, 636 ureteric, 576–579, 576b, 577f–578f urethral, 597–599, 598f vascular, 476–478, 477f traumatic brain injury (TBI), 514–518, 515b, 516f Trendelenburg gait, 609b

Trendelenburg position, 58t Trendelenburg test, 487, 487f trephine, 21 Trethowan’s line, 636, 636f TRH (thyrotrophin-releasing hormone), 529 triage, 15 tricuspid valve disease, 263 trigger finger, 624 triglycerides, 253 tri-iodothyronine, 528–529, 531 trimethoprim, 118t triple bubble sign, 657 triple phosphate stones, 573 TRISS, 128–130 trocars, 60 tropical diseases, splenomegaly in, 320 tropical ulcer, 735–736 acute, 735–736 chronic, 736, 736b Trousseau’s sign, 536 Truelove and Witts criteria, 368, 368t TRUS (transrectal ultrasound), 582 TSH (thyroid-stimulating hormone), 529, 531 tuberculosis, 124–125, 242 abdominal, 734 anal manifestations, 396 of the bladder, 584 developing countries, 724 hip, 626–627 intestinal, 362–363 renal, 567–568, 568f tubes postoperative care, 88–89, 88t see also specific tube types tubotympanic disease, 218–219 tubular breast carcinoma, 427 TULA (transumbilical laparoscopic surgery), 63–64 tumour doubling time, breast cancer, 423–424 tumour markers, 176, 185, 185t, 338, 603 tumour staging see staging of tumours tumours adrenal, 555 anal, 400 bladder, 585–587 bone, 616–617, 616t brain and meninges, 518–519 central nervous system, 518t endocrine, 527 gallbladder, 316–317 gastroduodenal, 288–292 gastroenteropancreatic, 548–551 gonadotrophin-producing, 554 heart, 265 intestinal obstruction, 357 large bowel, 374–381 liver, 307–311 ocular, in HIV, 686 paediatric, 663–664 pancreatic, 336–339 pituitary see pituitary tumours renal, 569–571 skin, 711–720 small bowel, 363–364 spinal, 523, 523t testicular, 602–604 virilising, 546–547 tuning fork tests, 215 turbulent blood flow, 444 TURP (transurethral resection of the prostate), 592, 596 tympanic cavity, 213, 217–220 tympanic membrane, 213, 215f typhoid fever, 734

U UICC (Union Internationale Contre le Cancer) staging, 289 ulcerative colitis, 367–371, 368b–369b, 368f–369f, 368t, 371f and colorectal cancer, 376 ulcers decubitus, 94, 647, 702 duodenal, 287, 347, 349b, 350 gastric, 142, 287, 347, 350 leg see lower limb ulceration peptic see peptic ulcers tropical see tropical ulcer varicose veins, 485 ulnar nerve compression, 623–624, 623f injury during operations, 59 ultrasonic instruments, 102 ultrasonography, 39–43 acute abdomen, 345 acute appendicitis, 346 acute cholecystitis, 313, 313f acute pyelonephritis, 565, 566f amoebic liver abscess, 307 anal disorders, 388 arterial disease, 453–455 biliary colic, 312, 313f bladder tumours, 585 breast cancer, 430–431 chronic pancreatitis, 335 comparison with other imaging techniques, 46t detection and display, 41–43, 43f developmental dysplasia of the hip, 635 Doppler effect, 39–41, 43f dynamic scanning, 42 faecal incontinence, 399 fibroadenosis, 418 gastric cancer, 292 goitres, 533 hernias, 404 intestinal obstruction, 356 intra-vascular, 252 jaundice, 302 lower urinary tract, 582, 582f nephroblastoma, 569 neuropathic bladder, 589 orchitis, 602 orthopaedics, 610 osteomyelitis, 614 pancreas, 329, 329t pancreatic cancer, 337 peptic ulcer disease, 288 perinephric abscess, 567 physical basis, 39–41 prostate cancer, 594 renal adenocarcinoma, 570 retroperitoneal fibrosis, 579 safety, 43 shoulder, 618 solitary thyroid nodule, 536 splenic rupture, 324 testicular torsion, 601 testicular tumours, 603 in the trauma patient, 19 upper urinary tract, 562 urinary tract infection, 565 vesicoureteric reflux, 576 ultrasound-guided biopsy, 432 umbilicus disorders, 660 granuloma, 660 hernia, 409–410, 409f, 660 unconscious patients consent in, 12 management, 513–514, 514b semi-prone position, 16, 16f undescended testes, 600–602, 664–665, 665b

undue influence, 13 Union Internationale Contre le Cancer (UICC) staging, 289 union of fractures, 641, 641b upper aerodigestive tract, 201–212, 203f upper limb arterial disease, 470–471 upper midline abdominal incision, 60, 60f upper urinary tract see kidneys; ureters upper-gastrointestinal bleeding, 92–93, 346–351, 347t–348t, 348b urachus, 583 urea, 137–138 ureteric colic, 572b ureterocele, 576 ureters, 557–581 clinical examination, 558–559 congenital anatomical abnormalities, 573–575 congenital obstruction at the pelviureteric junction, 574–575 disorders, 573–580 duplication, 573–574 injuries, 576–579, 576b, 577f–578f stones, 579–580, 579f symptoms arising from, 557–563 urethra, 597–599 congenital abnormalities, 597, 597f damage, 18, 19f drainage, 89 injury, 597–599, 598f pain, 581 stricture, 598–599, 599b urethral valves, 597, 597f urethrography, 18, 582 urge incontinence, 398 uric acid orthopaedics, 610 stones, 571, 573 urinalysis, 27 orchitis, 602 testicular torsion, 601 urinary catheterisation, 92, 161–165, 162f female, 164, 164f male, 161–164, 162f urinary diversion, 580–581, 580f, 589 urinary flow rate, 582, 582f urinary flow studies, 589 urinary retention, chronic, 163 urinary stones, 571–573, 572b, 572t urinary tract, postoperative complications, 92 urinary tract infection (UTI), 120, 564–568, 583–584 in children, 564–565, 565b urine abnormal stream, 581 culture, 565 examination, 559, 565, 568, 570, 572 output, 140–141 retention acute, 591, 593, 593b chronic, 592–593 urine examination acute abdomen, 344 cystitis, 583 incontinence, 590 neuropathic bladder, 589 schistosomiasis, 584 ureteric stones, 579

758  Index urodynamics, 582, 583f, 590 urological system assessment and critical illness, 132 monitoring in the critically ill, 137–138 uveitis, 678, 680–681, 681f

V VAC therapy, 692 vaccination healthcare personnel, 114 human papillomavirus, 708 vacuum erection devices, 605 vacuum suction biopsy, breast cancer, 431 Vacuum-Assisted Closure (VAC) therapy, 692 vaginal examination acute abdomen, 344 intestinal obstruction, 355 valve function tests, lower limb, 487, 487f valvular heart disease, 258–265 valvular surgery, 263–265, 264t vancomycin, 118t vaporisers, 75 vardenafil, 605 varicella zoster virus, 685 varicocele, 602 varicose veins, 482–491 aetiology, 483–484 anatomy, 482–491 bleeding, 485 classification, 483–484 clinical features, 485–487, 485t, 486f–487f epidemiology, 483 general examination, 487, 487f investigations, 487–488 management, 488–491, 489t, 490f, 491b primary, 483–484 secondary, 484 secondary effects, 484–485 variceal pattern, 485–487, 486f venous physiology in the lower limb, 483 vascular disease diabetic foot, 469–470, 470f visual field loss, 679 vascular disturbances in the gut, 360–361, 360b vascular impedance, 444 vascular injury, fractures, 646, 646f vascular perfusion, fractures, 642 vascular prostheses, 457 vascular trauma, 476–478, 477f vascular tumours, 204 vasculitis, 449–451, 450t vasointestinal peptide (VIP), 550 vasopressin, 554 vasospastic disorders, 472–473 vecuronium, 145 vein prostheses, 457 vencuronium, 77 venepuncture, 151–152, 152f venography deep-vein thrombosis, 494–495, 495f

thoracic outlet syndrome, 471 varicose veins, 488, 488f venous access, 150–158, 151b, 151f venous claudication, 453 venous cut-down, 152–154, 153f–154f venous disorders, 481–506 anatomical considerations, 481–482, 482f pathological features, 481–482, 482f physiological considerations, 481–482, 482f venous eczema, 485 venous insufficiency, chronic, 503–504 venous obliteration, endoluminal, 491 venous pressure and volume studies, 488 venous thrombosis, 481, 482b, 482f, 482t, 491–504 ventilation cardiac surgery, 276 methods of, 139, 139t see also breathing ventilation system, operating department, 54–55 ventilators, 75 ventilatory failure, 138, 138b ventricular assist devices, 267–268, 269f ventricular function, 252 verrucae, 708, 708f vertical abdominal incisions, 60 vertical nystagmus, 216 vertigo, 214–215, 222 vesicoureteric reflux, 576 vesicovaginal fistula, 587–588, 727–728, 727f vestibular function, 216 vestibular nystagmus, 216 video-assisted thoracoscopic surgery (VATS), 244–245 vinca alkaloids, 183 VIP (vasointestinal peptide), 550 VIPoma, 550, 550f viral conjunctivitis, 685, 685f viral infections salivary gland, 207 skin, 707–709 Virchow’s triad, 481, 482b, 482t virilising tumours, 546–547 virtual immobilisation, 63 virtual pneumocolon, 378 visceral angiography pancreas, 330 peptic ulcers, 349–350 visceral ischaemia, 474–475 visceral pain, 342 visceral perforation, 49 viscous energy losses, 444 visors, 57 visual acuity, 669, 670t, 671 visual distortion, 679–682 visual fields, 669–671 defects, 688 loss, 679 visual loss acute, 674–675, 674t gradual, 676–678

subacute, 675–676 transient, 678–679 vital signs, 86 vitamin D, 540–541, 541f vitamin deficiencies, 100 vitamin K deficiency, 303 vitamins, 144, 300 vitello-intestinal abnormalities, 353 vocal cord paralysis, 210–211 volvulus, 358–359, 728–729, 729f malrotation with, 657 vomiting in intestinal obstruction, 355 postoperative see postoperative nausea and vomiting (PONV) vulval varicosities, 485–486, 489

W walking aids, 608 wards, 128b warfarin, 495, 495b, 497 Warthin’s tumour, 208 warts, 400, 707–708, 708f, 711, 711f water absorption in the large bowel, 365–366 absorption in the small bowel, 354 developing countries, 722–723 maintenance requirements, 82 metabolism, 81–84, 82f, 82t water-soluble contrast media, 35–37 weakness hand and wrist, 621 orthopaedic history, 607 Weber test, 215 Wegener’s granulomatosis, 689 weight loss, 285, 557 weight reduction, arthritis management, 612 wet age-related macular degeneration (ARMD), 677 white blood cell count, 26 osteomyelitis, 614 postoperative, 86 white leg, 503 wide excision, breast cancer, 433 wide-bore core needle biopsy, breast cancer, 431 Wilms’ tumour, 569–570, 663–664 wound closure, 103–106 abdominal wall, 106, 107f direct surgical, 692–694 equipment, 103–105 simple, 106, 106f techniques, 105–106 wound healing primary, 97–101 clinical factors, 100–101 phases of, 97–99, 98f recovery of tensile strength, 99–100, 99f spontaneous, 692 adjuncts to, 692 wound infection, 100–101 after incisional hernia repair, 411

classification of risk of, 110t clinical features, 119 management, 101–102, 116b postoperative, 89–95 prevention, 101–102 wounds categories, 89 causation, 100 classification, 101 contamination, 100 dehiscence, 93–94, 94t management, 89, 101–107 minor, 21, 24 tetanus prophylaxis, 21 time, 100 wrist, 621–625

X xenograft, 187 X-rays acute abdomen, 345 acute pyelonephritis, 565 ankle, 631 bone tumours, 616 congenital diaphragmatic hernia, 655, 655f detection, 29 developmental dysplasia of the hip, 635 elbow, 621 foot, 632 fractures, 642, 643f goitres, 533, 533f hand and wrist, 622 hip, 625 interaction with matter, 28–29 knee, 628 oesophageal atresia, 654 oesophagus, 280 orthopaedics, 609–610, 609f, 609t osteoarthritis, 611 osteomyelitis, 614–615 pancreas, 329 perinephric abscess, 567 Perthe’s disease, 635–636 physical basis, 28–29, 28f pituitary tumours, 552 plain films, 29–30 renal trauma, 569 rheumatoid arthritis, 611 safety, 29, 29t–30t septic arthritis, 615 shoulder, 618 splenic rupture, 324 thoracic outlet syndrome, 471, 471f

Y Yankers sucker, airway obstruction, 15

Z Zollinger-Ellison syndrome, 549

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