Clinical Surgery by Alfred Cuscheri 2nd Edition

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Clinical Surgery

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Clinical Surgery SECOND EDITION

Alfred Cuschieri MD DM ChM FRSE FRCS(Ed) FRCS(Eng) FMedSci FIBiol FRCS(Glas) FRCS(I) FInst Mech(Eng) Professor of Surgery and Head of Department of Surgery and Molecular Oncology Ninewells Hospital and Medical School University of Dundee Honorary Consultant Gastrointestinal Surgeon Tayside University Hospitals NHS Trust and Acute Fife Hospitals NHS Trust

Pierce Grace MCh FRCS(I) FRCS Professor of Surgical Science University of Limerick Consultant Vascular Surgeon Mid-Western Regional Hospital Limerick

Ara Darzi KBE MD FRCS FACS FRCS(I) FRCPS(Glas) FMedSci Professor of Surgery and Head of Department Department of Surgical Oncology and Technology Imperial College of Science, Technology and Medicine St Mary’s Hospital Campus London

Neil Borley MB BS FRCS(Eng) MS Consultant Colorectal Surgeon Gloucestershire Hospitals NHS Trust Cheltenham General Hospital Cheltenham

David Rowley B.Med.Biol MD FCRS(Ed) FRCS(Eng) FRCPS(Glas) Head of Academic Department Ninewells Hospital and Medical School University of Dundee Director of Education Royal College of Surgeons of Edinburgh

Blackwell Science

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© 1996, 2003 by Blackwell Science Ltd a Blackwell Publishing company Blackwell Science, Inc., 350 Main Street, Malden, Massachusetts 02148-5020, USA Blackwell Publishing Ltd, 9600 Garsington Road, Oxford OX4 2DQ, UK Blackwell Science Asia Pty Ltd, 550 Swanston Street, Carlton, Victoria 3053, Australia The right of the Authors to be identified as the Authors of this Work has been asserted in accordance with the Copyright, Designs and Patents Act 1988. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher. First published in 1996 Reprinted 2001 Second edition 2003 Library of Congress Cataloging-in-Publication Data Clinical surgery / Alfred Cuschieri . . . [et al.]. — 2nd ed. p. ; cm. Includes index. ISBN 0-632-06394-7 1. Surgery. [DNLM: 1. Surgical Procedures, Operative. WO 500 C641 Cuschieri, Alfred. RD31 .C643 617—dc21

2003]

2003 2003000667

A catalogue record for this title is available from the British Library Set in 9.5/11.5pt Minion by Graphicraft Limited, Hong Kong Printed and bound in Italy by G. Canale & C. SpA, Turin Commissioning Editor: Vicky Noyes Managing Editor: Geraldine Jeffers Production Editor: Alice Emmott Production Controller: Kate Charman For further information on Blackwell Science, visit our website: http://www.blackwellpublishing.com

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Contents

Contributors, vi Preface, viii List of abbreviations, ix

20 21 22 23

Chest Trauma, 224 Musculoskeletal Trauma, 230 Soft-tissue Trauma, 248 Burns, 254

Part 1: Clinical Skills and Investigations 1 History-taking and Physical Examination, 1 2 Basic Clinical Procedures, 32 3 Principles of Investigation, 49 Part 2: Perioperative Care 4 Assessment of Patients for Surgery and Preoperative Medical Management, 62 5 Prophylaxis, 71 6 Transfusion of Blood and Blood Products, 79 7 Surgical Infection, 89 8 Pain Relief, 101 9 Complications following Surgery, 109 10 Rehabilitation, 120

Part 4: General Surgery 24 25 26 27 28 29 30 31 32 33 34 35 36

Part 3: The Management of Acute Surgical Illness and Trauma (A) Acute Surgical Illness Hypoxic States and Airway Obstruction, 127 Haemorrhage, Hypovolaemia and Shock, 136 Fluids, Electrolytes, pH Balance and Nutrition, 148 Acute Renal Failure, 159 The Acute Abdomen, 166 Systemic Inflammatory Response Syndrome, 181 Initial Management of the Severely Injured Patient, 188 18 Head Injury, 195 11 12 13 14 15 16 17

(B) Trauma 19 Abdominal Trauma, 210

Disorders of the Abdominal Wall, 269 Disorders of the Oesophagus, 276 Disorders of the Stomach and Duodenum, 301 Disorders of the Liver, 325 Disorders of the Biliary Tract, 343 Disorders of the Pancreas, 361 Disorders of the Spleen, 379 Disorders of the Small Intestine and Vermiform Appendix, 386 Disorders of the Colon and Rectum, 407 Disorders of the Breast, 428 Disorders of the Endocrine Glands, 441 Salivary Glands, 456 Skin and Adnexae, 464 Part 5: Specialist Surgery

37 38 39 40 41 42 43 44 45 46

Cardiovascular Disorders, 481 Pulmonary Disorders, 548 Genitourinary Disorders, 576 Neurosurgical Disorders, 619 Musculoskeletal Disorders, 641 Plastic and Reconstructive Surgery, 677 Ear, Nose and Throat Disorders, 713 Ophthalmic Disorders, 742 Principles of Transplantation, 759 Surgical Conditions in Neonates, Infants and Children, 771 Index, 793

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Contributors

Peter Butler Department of Plastic Surgery, Royal Free Hospital, Pond Street, London, NW3 2QG Author of Chapter 23 Co-author of Chapter 42

Paul Kinnear FRCS FRCOphth Consultant Ophthalmologist, Department of Ophthalmology, Charing Cross Hospital, Fulham Palace Road, London, W6 8RF Author of Chapter 44

Trottie Kirwan MB BChir Graham Haddock MBChB MD FRCS(Glas) FRCS(Ed) FRCS(Paed) Consultant Paediatric and Neonatal Surgeon, Department of Paediatric Surgery, Royal Hospital for Sick Children, Yorkhill, Glasgow, G3 8SJ

Consultant Anaesthetist, Chelsea & Westminster Hospital, 369 Fulham Road, London, SW10 9NH Co-author of Chapter 8

Graham Leese MD FRCP Author of Chapter 46

Ashok Handa FRCS FRCS(Ed) Clinical Tutor in Surgery and Honorary Consultant Surgeon, Nuffield Department of Surgery, John Radcliffe Hospital, Headley Way, Headington, Oxford, OX3 9DU Author of Chapter 45

Natasha Hidvegi MBBS Research Fellow, Department of Plastic Surgery, Royal Free Hospital, Pond Street, London, NW3 2QG Author of Chapter 42

Eamon Kavanagh MD FRCS(I) Department of Surgery, Mid-Western Regional Hospital, Dooradoyle, Limerick, Ireland Co-author of Chapters 3, 16, 35, 37

Michael Kerin MCh FRCS(I) FRCS(Ed) Lead Surgeon, National Breast Screening Programme, Mater Misericordiae Hospital, Eccles Street, Dublin 7, Ireland Author of Chapter 33

Consultant Physician, Ninewells Hospital and Medical School, Dundee, DD1 9SY Co-author of Chapter 34

Mervyn Maze MB ChB FRCP FRCA FMedSci Professor and Chair of Anaesthesia, Department of Anaesthetics and Intensive Care, Imperial College London; Director of Research and Development, Chelsea and Westminster NHS Healthcare Trust, 369 Fulham Road, London Co-author of Chapter 8

William Morrison MBChB FFAEM FRCP FRCS FRCA MRCGP DRCOG Accident and Emergency Consultant, Department of Accident & Emergency Medicine, Ninewells Hospital, Dundee, DD1 9SY Co-author of Chapter 17

Paraskevas Paraskeva FRCS Lecturer in Surgery, Department of Surgical Oncology and Technology, Imperial College London, St Mary’s Hospital, 10th Floor Queen Elizabeth the Queen Mother Wing, London, W2 1NY Author of Chapters 13, 20, 32 Co-author of Chapter 2

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Contributors

Peter Richards FRCS FRCPCH Department of Paediatric Neurosurgery, Radcliffe Infirmary, Woodstock Road, Oxford, OX2 6HE Author of Chapters 18, 40

Victoria Rose MD MRCS(Eng) Specialist Registrar, Department of Plastic Surgery, Royal Free Hospital, London, NW3 2QG Author of Chapter 42

David Smith MD FRCS(Ed) Consultant Surgeon and Honorary Senior Lecturer, Ninewells Hospital and Medical School, Dundee, DD1 9SY Author of Chapter 34

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Shawn St Peter MD Resident in Surgery, Mayo Clinic, Rochester, MN 55905, USA Co-author of Chapter 45

Janet Wilson MD FRCS(Ed) FRCS(Eng) Professor of Otolarnyngology, Head and Neck Surgery, University of Newcastle, Freeman Hospital, High Heaton, Newcastle upon Tyne, NE7 7DN Author of Chapter 43

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Preface

Clinical Surgery in its new edition is much more than a facelift. It is the outcome of a major collective effort based on regular meetings of the five editors with the publishers at which format, content and layout were discussed. Admittedly, completion of the second edition has taken longer than anticipated, but the delay has been worthwhile. Although the basic structure of the first edition has been retained, the rewrites, alterations and new material have been based on feedback from our readers specially commissioned by our publishers before work on the second edition commenced in earnest. The needs and comments expressed by students and house officers who took part in the feedback on each and every chapter (favourable or otherwise) were kept firmly in mind by the authors and editors during the redrafting process. Consequently, the editors are confident that all defects and criticisms have been met and the second edition has no serious shortcomings. In addition to this we have introduced some new features, which we regard as important in the continuous acquisition of medical and surgical knowledge that is based on reading, clinical observation and practice. Perhaps the most relevant of these are the Must know (core knowledge information), Must do (necessary clinical and humanistic skills) appropriate to each chapter. These provide evidence to the reader of landmark achievements of knowledge and goals in the learning process. When

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indicated, we have included references to evidence-based medical practice but shied away from any extensive bibliography. New material, previously not covered or dealt with in too superficial a manner in the first edition has been added or enhanced without a material increase in the size of the book. In achieving this, we have not sacrificed any of the good features of the book including the At A Glance boxes, which have been so popular as aides-mémoire with the medical undergraduates in particular. We trust the second edition of Clinical Surgery, like its predecessor, proves to be useful to students, house officers and senior house officers, that it will incite tham to consider a career in surgery, but if not, that they benefit as doctors from reading the book. If the second edition achieves the last, we as editors would be well pleased with the outcome of our work. We would like to thank Alice Emmott, Senior Production Editor, for her forbearance and tact and the entire team at Blackwell Publishing. Also, the authors, you all did a magnificent and expeditious job. Alfred Cuschieri Pierce Grace Ara Darzi Neil Borley David Rowley

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List of abbreviations

AAA ABI ACTH ADH ADL AF AFP AIDS ALT APACHE APTT ARDS ARF ASA AST ATLS ATN AVM AZT BCC BCG BPH CABG CARS CBV CDH CJD CMV CNS CO COPD COX CPAP CPK CPR CRP CSF CT CVP DIC 2,3-DPG DPL

abdominal aortic aneurysm ankle/brachial index adrenocorticotrophic hormone antidiuretic hormone activities of daily living atrial fibrillation α-fetoprotein acquired immunodeficiency syndrome alanine aminotransferase Acute Physiology and Chronic Health Evaluation activated partial thromboplastin time acute respiratory distress syndrome acute renal failure American Society of Anesthesiologists aspartate aminotransferase advanced trauma life support acute tubular necrosis arteriovenous malformation azidothymidine basal cell carcinoma bacillus Calmette-Guérin benign prostatic hypertrophy coronary artery bypass grafting compensatory anti-inflammatory response syndrome circulating blood volume congenital dislocation of the hip Creutzfeldt–Jakob disease cytomegalovirus; controlled mandatory ventilation central nervous system cardiac output chronic obstructive pulmonary disease cyclooxygenase continuous positive airways pressure creatine phosphokinase cardiopulmonary resuscitation C-reactive protein cerebrospinal fluid computed tomography central venous pressure disseminated intravascular coagulation 2,3-diphosphoglycerate diagnostic peritoneal lavage

DSA DTPA DVT EBV ECG EDTA EEG EMG ENT EPVF ERCP ESR ESRD ESWL EUS FAP FEV1 FFP Fio2 FVC GABA GFR GORD γ-GT GvHD HAFLOE HAV HBV HCC HCV HDL HDU HIV HLA HPP HR 5-HT HTLV ICP ICU IL INR IPSID ITP

digital subtraction arteriography diethylenetriaminepentaacetic acid deep vein thrombosis Epstein–Barr virus electrocardiogram, electrocardiography ethylenediaminetetraacetic acid electroencephalography electromyography ear, nose and throat extrapulmonary ventilatory failure endoscopic retrograde cholangiopancreatography erythrocyte sedimentation rate end-stage renal disease extracorporeal shock-wave lithotrispsy endoscopic ultrasonography familial adenomatous polyposis force expiratory volume in 1 s fresh frozen plasma fractional inspired oxygen concentration forced vital capacity γ-aminobutyric acid glomerular filtration rate gastro-oesophageal reflux disease γ-glutamyltransferase graft vs. host disease high-airflow oxygen enrichment hepatitis A virus hepatitis B virus hepatocellular carcinoma hepatitis C virus high-density lipoprotein high-dependency unit human immunodeficiency virus human leukocyte antigen human pancreatic polypeptide heart rate 5-hydroxytryptamine human T-cell leukaemia virus intracranial pressure intensive care unit interleukin international normalized ratio immunoproliferative small intestinal disease immune thrombocytopenic purpura ix

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List of Abbreviations

IVU JVP LDH LDL LHRH LOS LPS LSBO MALT MCH MCP MCV MEN MHC MNG MODS MRA MRCP MRI MRSA MUGA NGU NO NSAID OA OGD OPSI Paco2 Pao2 PCV PCWP PE PEEP PEFR PET PGL POSSUM

PPI PPV PSA PT

intravenous urogram jugular venous pressure, jugular venous pulse lactate dehydrogenase low-density lipoprotein luteinizing hormone-releasing hormone lower oesophageal sphincter lipopolysaccharide long-segment Barrett’s oesophagus mucosa-associated lymphoid tissue mean corpuscular haemoglobin metacarpophalangeal mean corpuscular volume multiple endocrine neoplasia major histocompatibility complex multinodular goitre multiple organ dysfunction syndrome magnetic resonance angiography magnetic resonance cholangiopancreatography magnetic resonance imaging methicillin-resistant Staphylococcus aureus multiple gated acquisition non-gonococcal urethritis nitric oxide non-steroidal anti-inflammatory drug oesophageal atresia oesophagogastroduodenoscopy overwhelming postsplenectomy infection partial pressure of arterial carbon dioxide partial pressure of arterial oxygen packed cell volume pulmonary capillary wedge pressure pulmonary embolism positive end-expiratory pressure peak expiratory flow rate positron emission tomography primary gastric lymphoma Physiological and Operative Severity Score for the enUmeration of Mortality and Morbidity proton pump inhibitor patent processus vaginalis prostate-specific antigen prothrombin time

PTH PUJ RA RBF RF RPLND RRT RTA SAH SBP SCC SIGN SIMV SIRS SLE SPECT SSBO SSEP SSI STD STN SV TENS TGF TIA TLC TNF TNM TOE TOF t-PA TPN TPO TRUS TSH TURP UTI VAC VC VIP VSD WCC WHO

parathyroid hormone pelviureteric junction rheumatoid arthritis renal blood flow radiofrequency retroperitoneal lymph node dissection renal replacement therapy road traffic accident subarachnoid haemorrhage spontaneous bacterial peritonitis squamous cell carcinoma Scottish Intercollegiate Guidelines Network synchronized intermittent mandatory ventilation systemic inflammatory response syndrome systemic lupus erythematosus single-photon emission computed tomography short-segment Barrett’s oesophagus somatosensory evoked potential surgical site infection sexually transmitted disease solitary thyroid nodule stroke volume transcutaneous electrical nerve stimulation transforming growth factor transient ischaemic attack total lung capacity tumour necrosis factor tumour, regional nodes, distant metastases transoesophageal echocardiography tracheo-oesophageal fistula tissue plasminogen activator total parenteral nutrition thyroid peroxidase transrectal ultrasound thyroid-stimulating hormone transurethral resection of the prostate urinary tract infection vacuum-assisted closure vital capacity vasoactive intestinal polypeptide ventricular septal defect white cell count World Health Organization

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History-taking and Physical Examination Introduction, 1 Clinical presentation, 1

The history, 2 Physical examination, 5

Must know Must do Must know Symptomatology and signs of common surgical disorders that present electively Presentation and physical findings of common surgical emergencies Must do Take histories of patients with surgical disorders: learn by experience how to establish rapport with patients Examine patients with surgical disorders: head and neck, chest, abdomen, limbs and genitalia Perform rectal examinations under supervision Acquire skill and experience in performing common clinical procedures, e.g. insertion of intravenous lines, insertion of nasogastric tubes, injections, setting up drips, catheterization of the urinary bladder (male and female) Examine the locomotor system of patients Attend outpatient general surgical clinics Attend fracture clinics

Introduction The mastery of clinical skills is different from knowing how the various clinical tasks are performed. This expertise has several components, including the ability to: communicate freely and efficiently with patients and colleagues; detect abnormal physical signs, e.g. an enlarged liver, rebound tenderness; recognize acute and life-threatening situations; perform common clinical procedures with proficiency; confirm normality when present. No amount of encyclopaedic knowledge gained from reading and lectures can ever impart clinical competence. The requirements for proficiency as a doctor are core knowledge of the common medical and surgical disorders and full clinical competence. Rare and obscure illnesses will be encountered by every clinician from time to time.

• • • • •

Examination of specific anatomical areas, 9

One needs only to be aware of these disorders since the competent doctor will recognize that the patient does not fit any of the common disease patterns and will seek advice or expert opinion.

Clinical presentation Patients may present in two ways: electively, with chronic symptoms of variable duration; or acutely, with life-threatening disorders. The pathways involved in management of the two are quite different. In the elective (cold) situation, the surgeon proceeds as shown in Table 1.1. If surgical treatment is required, the patient is usually put on the waiting list or is given a date for the operation at the time of the outpatient interview. A priority system based on disease severity is adopted in deciding which patients are operated on soon after the diagnosis is confirmed. Thus a patient with cancer takes precedence over a patient with an uncomplicated inguinal hernia. Cancer patients undergo a process of staging by appropriate investigations based on the TNM (tumour, regional nodes, distant metastases) system before the relevant treatment is selected. This staging process influences management in several ways. In some patients, the disease is found to be inoperable, when non-surgical treatment (chemotherapy, radiotherapy) may be employed. In others, the disease, though operable, is advanced and adjuvant therapy (endocrine, chemotherapy, radiotherapy) before or after surgery is needed in addition to surgical extirpation of the primary tumour. Staging (clinical and

• •

Table 1.1 Management of the elective patient. Establish the diagnosis and confirm it, whenever necessary, by the appropriate investigations Decide on the nature of the treatment required: surgical or medical Impart this information to the patient and carry out the treatment if the patient consents to this

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Table 1.2 Management of the acutely ill patient.

Table 1.4 Approach to history-taking.

Prompt diagnosis and assessment of the condition Resuscitation (Airway, Breathing, Circulation; see Chapters 11 and 12) Decision on treatment: emergency surgical intervention or conservative management with close clinical observation

Establish a rapport with the patient: introduce yourself, shake hands Initiate the process by asking the patient to tell you what made him or her seek medical advice Listen without interruption to the patient as he or she relates the history of the presenting complaint(s). During this process make a mental note of the key symptoms Wait for the answer before asking another question Obtain further details on specific symptoms, including duration, nature of severity and associations, by specific questions Briefly review the systems by key questions Obtain details of past medical history, including drug medication, surgical conditions, operations and exposure to general anaesthesia. Past medical incidents are important because they may relate to the patient’s current illness and may also influence management Obtain details of social history and habits, including alcohol consumption and smoking Obtain a brief family history

Table 1.3 Priorities in the management of the acutely injured patient. A B C D E

Airway Breathing Cardiovascular system Neurological Defects Exposure to detect all injuries

pathological) is also the best overall guide to prognosis in the individual patient. Acute patients are admitted as emergencies with lifethreatening disorders or trauma. The pathway of management in these patients is shown in Table 1.2. Frequently, resuscitation and diagnosis go hand in hand in the seriously ill or injured patient. Prompt and efficient resuscitation of seriously ill patients, which necessitates an understanding of the underlying pathophysiological mechanisms (see Chapters 11–16), is crucial to the survival of these patients. Not all acute conditions need surgical intervention and some are managed conservatively in the first instance, with recourse to surgery if progress is not made or the clinical condition deteriorates. The relief of acute pain by appropriate analgesia (see Chapter 8) is a very important part of the clinical management of acutely ill patients, whether they need emergency surgery or not. In the management of trauma victims, the priorities in order of precedence are shown in Table 1.3.

Table 1.5 Don’ts of history-taking. Do not interrupt the patient Do not use medical terminology Do not ask ambiguous or irrelevant questions Do not use leading questions in the first instance Do not be abrupt or impatient

to confirm. This provides a valid check of the accuracy of the history-taking process and is highly recommended until full proficiency in history-taking is obtained. The wrong information can be obtained if the technique is poor and the patient is confused by the interviewer. In this respect one should avoid the mistakes outlined in Table 1.5.

The history Much has been written about the technique of historytaking. For most individuals this is an acquired attribute. Basic to successful history-taking is the ability to establish a rapport with the patient, allowing him or her to relate the story (history) of the illness. In essence, history-taking is the art of conversation and requires a fine balance between listening and interjecting with relevant questions to clarify points and obtain details as the history unfolds (Table 1.4). In this process there are dos and don’ts. The only way a student can verify that an accurate history has been obtained is to summarize the information for the patient

Symptoms Patients can present with specific or non-specific symptoms or a combination of both. Specific symptoms are those that relate to disease in specific organs, e.g. difficulty with swallowing (dysphagia), indicating disorders of deglutition or organic narrowing of the oesophagus. Each system has its own specific symptoms, although there is considerable overlap (Table 1.6). Patients vary considerably in their clinical presentation. Although a few present with all the characteristic symptoms of a specific illness (classical presentation or ‘full-house’), in the majority of patients the history is not

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Table 1.6 Specific symptoms.

Table 1.7 Diagnostic clinical information on pain.

Nervous system: headache, nausea and vomiting, visual disturbances, motor defects (paralysis), incoordination, sensory loss and disturbances (paraesthesiae), altered levels of consciousness

Site Radiation Severity Nature Duration Relieving factors Aggravating factors Associations

Respiratory system: cough, expectoration, breathlessness, wheezing, chest pain, diminished exercise tolerance Cardiovascular system: loss of consciousness (syncope), breathlessness, diminished exercise tolerance, retrosternal chest pain, intermittent pain in limbs on walking (intermittent claudication), rest pain in the limbs, gangrene (necrosis of tissue) Hepatobiliary–pancreatic system: nausea and vomiting, pain, jaundice, itching, bleeding tendency, weight gain due to water retention, weight loss Gastrointestinal system: loss of appetite (anorexia), nausea and vomiting, difficulty in swallowing, indigestion, abdominal pain, altered bowel habit (diarrhoea and/or constipation), blood in vomit (haematemesis), passage of slime and fresh or altered blood in the faeces Genitourinary system: loin pain, fever, suprapubic pain, frequency, painful micturition (dysuria), micturition at night (nocturia), poor stream, dribbling and incontinence, blood in urine (haematuria), enlarged or tender testis

typical and the clinician has to decipher the situation. The ability to identify specific symptoms is one of the reasons for the increasing diagnostic efficiency that comes with clinical experience. Non-specific symptoms do not immediately give a clue to the diagnosis or site of disease. In this situation, a tentative diagnosis is made on the history as a whole. In this group of patients more reliance is placed on investigations in establishing the diagnosis.

Common important symptoms in general surgery Pain Pain is the most common and important symptom in surgical practice. (It used to be said with some truth that pain and blood were the only two events that brought patients quickly to the doctor.) Pain is universal and can be caused by benign or malignant disorders and elective or acute conditions. It is the symptom that is least commonly overlooked by patients, although the threshold for pain varies considerably from one person to another. The information required to establish the clinical significance of pain is shown in Table 1.7.

The most reliable way to obtain precise information on the location of pain is to ask the patient to point to the exact site of the pain and where it radiates. Pain may be localized or diffuse and can be referred. Localized pain is either musculoskeletal in origin or is indicative of disease, trauma or inflammation in the affected region. Pain may be referred to the corresponding sensory dermatome. This is exemplified by shoulder tip pain due to a subphrenic abscess causing irritation of the ipsilateral phrenic nerve. Types of pain Colicky pain is indicative of an obstructed hollow organ. It is griping in nature and fluctuates, with peaks of intensity followed by partial or complete relief before a further bout occurs. Colicky pain is always severe and makes the patient restless. The patient rolls about in agony, unable to find a comfortable position. It is usually accompanied by nausea and vomiting. Somatic pain, i.e. the severe pain due to inflammation of the parietal peritoneum from localized or general peritonitis, is aggravated by movement. The patient lies still and breathes shallowly to diminish abdominal wall excursion with respiration (e.g. perforated peptic ulcer) or assumes a position that releases tension on the abdominal musculature, i.e. draws the knees up, a posture often observed in patients with acute pancreatitis. The pain of acute peritonitis is also aggravated by coughing. Burning pain signifies mucosal injury/inflammation and is typified by the heartburn of reflux oesophagitis, the burning indigestion encountered in patients with peptic ulceration (see Chapter 26) and the dysuria that accompanies inflammation of the urinary bladder (cystitis; see Chapter 39). Intermittent claudication is the term used to signify cramp-like pain in the muscles of the lower limbs (usually calf, but may involve the thighs and gluteal regions) that develops with walking and subsides with rest, after which the patient can resume walking before the pain comes on again. It is caused by peripheral occlusive vascular disease (atherosclerosis), with a resultant defective blood supply

•

• •

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leading to the accumulation of metabolites such as lactic acid on exertion. The claudication distance (the distance the patient can walk before the onset of muscle cramps) reflects the severity of the peripheral vascular disease (see Chapter 37). Rest pain is a much more serious type of vascular pain. The patient experiences pain in the affected limb at rest. The pain is severe, constant and interrupts sleep. Some relief is obtained by dangling the affected limb over the edge of the bed. Rest pain denotes threatened viability of the limb and requires urgent vascular treatment to prevent the development of gangrene (see Chapter 37). Root pain is caused by irritation of the spinal dorsal roots and can be caused by compression (vertebral collapse) or direct malignant involvement. The pain radiates from the back around the body, usually on either side, in the distribution of the respective dermatomes. It is often accompanied by both sensory changes (paraesthesiae) and motor changes (muscle weakness/paralysis, bladder dysfunction). Pain due to inflammation, partial injury or neoplastic involvement of nerves or nerve roots is known as neuralgia. It is always severe, often intractable and requires special measures that may include neurosurgical intervention (see Chapter 40).

•

Indigestion Indigestion or dyspepsia are loosely defined words that denote epigastric discomfort or pain occurring either during fasting or during or after meals and indicate disease within the upper digestive and biliary tract. The practical problem encountered with these symptoms relates to the frequency with which normal individuals experience indigestion. One study has shown that 70% of people living in the UK experience episodes of indigestion and heartburn from time to time and reports from other western countries indicate a similar prevalence. The key issue in clinical practice is what constitutes abnormal indigestion. This is difficult to define and for this reason diagnosis of serious conditions, such as gastric cancer, is often delayed as the general practitioner usually prescribes medication designed to produce symptomatic relief. Meanwhile the tumour progresses and is often incurable by the time the diagnosis is made. Thus in most western countries 90% of all gastric cancers are advanced at the time of presentation. There are certain practical considerations related to dyspepsia that must never be overlooked and which require investigation by endoscopy rather than empirical symptomatic treatment (Table 1.8). From the symptomatic viewpoint, dyspepsia is often classified into: ulcer dyspepsia; reflux dyspepsia; malignant dyspepsia;

• • •

Table 1.8 Indications (‘alarm symptoms’) for upper gastrointestinal endoscopy. Frequent or persistent indigestion irrespective of age Indigestion accompanied by other gastrointestinal symptoms Indigestion with anorexia and/or weight loss Helicobacter pylori-negative dyspepsia Indigestion occurring for the first time in a patient above the age of 40 years

dyspepsia; • non-ulcer gallbladder dyspepsia. •

Dysphagia Dysphagia signifies inability to swallow and may be caused by motility disorders or organic disease that encroaches on the lumen of the oesophagus, such as stricture or neoplasm (see Chapter 25). This symptom always warrants urgent investigation by flexible endoscopy and a barium swallow. The difficulty in swallowing may be experienced in relation to liquids and solids. In some patients with inflammatory mucosal disease, the dysphagia is accompanied by pain. This symptom complex is known as odynophagia. Dysphagia due to organic disease is progressive and without treatment the patient may eventually be unable to swallow saliva due to complete occlusion of the oesophageal lumen. Dysphagia caused by motility disorders such as achalasia (see Chapter 25) may be intermittent. High dysphagia due to bulbar palsy or cricopharyngeal spasm is accompanied by spluttering and choking as the bolus, unable to negotiate the upper oesophageal sphincter, spills over into the larynx. In the presence of significant oesophageal occlusion, dysphagia is accompanied by regurgitation, which is passive and effortless as opposed to vomiting. In patients with dysphagia, spillage of retained food debris in the dilated oesophagus across the cricopharyngeus into the larynx may occur in the supine position during sleep, leading to aspiration and pneumonitis. This accounts for the chronic productive cough and fever encountered in patients with long-standing dysphagia.

Anorexia and weight loss Anorexia denotes loss of appetite. This may be due to an abnormal psychiatric state, e.g. anorexia nervosa, although in surgical patients loss of appetite is usually caused by malignant neoplasms, usually of the upper digestive tract and pancreas. Anorexia must be distinguished from fear of eating because of precipitation of symptoms or inability to eat consequent on a disordered swallowing mechanism

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from any cause. Anorexia is invariably accompanied by weight loss due to diminished protein–calorie intake. However, there are other causes of weight loss. Some malignant tumours are accompanied by the development of a catabolic state such that the weight loss is out of proportion to the reduced dietary intake (cachexia). Some patients lose weight because they are unable to assimilate ingested food. This may be the result of impaired digestion of foodstuffs (e.g. diminished pancreatic enzymes in chronic pancreatitis), reduced bile salt pool from any cause (malabsorption of fats), bacterial overgrowth, intrinsic disease of the small-bowel mucosa (coeliac disease, brush-border enzyme deficiencies), disorders affecting the small bowel (Crohn’s disease) or extensive resection of the small intestine (short gut syndrome).

Vomiting Vomiting is an active process, involving violent contractions of the abdominal musculature that forcibly expel the gastric contents in a retrograde fashion. During vomiting the lower oesophageal sphincter and the cricopharyngeus are reflexly opened and the glottis is closed. In surgical practice, vomiting may have a cerebral cause, such as raised intracranial pressure due to a space-occupying lesion. More commonly, however, it is the result of acute intra-abdominal disease or obstruction of hollow organs. Thus, nausea and vomiting may be a feature of such diverse conditions as acute appendicitis, acute gastritis (drug or alcohol induced), exacerbation of peptic ulceration, acute pancreatitis, renal and biliary colic. Vomiting is a predominant feature of an obstructed stomach (pyloric stenosis). The nature of the vomit is important. In obstructions proximal to the pylorus, the vomit does not contain bile. Vomiting of blood (haematemesis) is encountered in bleeding lesions of the lower oesophagus, stomach and duodenum. The blood may be fresh or dark and ‘coffeeground’ in appearance as a result of digestion by hydrochloric acid and pepsin in the stomach. In pyloric stenosis, the vomit often contains portions of food that the patient had ingested several hours, sometimes days, beforehand. In some of these patients, the vomiting may be selfinduced in an effort to relieve the upper abdominal discomfort caused by a distended stomach. Vomiting in the unconscious state (e.g. head injury, alcoholic stupor and during recovery from general anaesthesia) is particularly dangerous in view of the distinct possibility of inhalation of vomit into the tracheobronchial tree, with severe pulmonary damage and the development of acute (formerly referred to as adult) respiratory distress syndrome (see Chapters 11 and 38).

Vomiting is a major clinical presentation of acute smallbowel obstruction (Chapters 15 and 31), where it is accompanied by variable abdominal distension and constipation.

Altered bowel habit Strictly speaking, this term is applied to patients with previously regular bowel habits who suddenly develop constipation, diarrhoea or diarrhoea alternating with constipation. This is a feature of some but not all patients who develop a colonic neoplasm in the left colon or upper rectum. The difficulty lies in establishing what was normal for the patient beforehand. Because of the diminished dietary intake of fibre in western countries, constipation and low-bulk stools are undoubtedly very common, as are disorders of colonic transit (diverticular disease, slowtransit constipation). There is also a tendency towards constipation with increasing age. In patients with rectal or lower sigmoid carcinoma, the constipation may also be accompanied by a feeling of incomplete evacuation after defecation. This is often referred to as tenesmus. Other symptomatic accompaniments in these patients include the passage of mucus and rectal bleeding, which is mixed with the motion. Bloody diarrhoea is a feature of colonic inflammatory bowel disease and infective colitis. Diarrhoea may also signify the presence of colonic motility disorders, exemplified by irritable bowel syndrome. This common obscure condition can also present with constipation. Foul-smelling diarrhoea that floats and is difficult to flush away is encountered in malabsorption. Because the faeces contains a large amount of fat, the term steatorrhoea is often used in this condition. Passage of foul-smelling tar-like liquid or solid motion (melaena) indicates a proximal source of bleeding in the gastrointestinal tract.

Physical examination General principles Physical examination must be thorough and efficient without being overdone and exhausting to the patient. Whichever system or anatomical region is examined, the process relies on four skills, i.e. inspection, palpation, percussion and auscultation, and is designed to elicit the appropriate clinical signs. Whereas examination of the various systems is crucial to the management of patients with medical disorders, in surgical practice physical examination is more commonly focused on anatomical regions (head and neck, ear, nose and throat, breasts, abdomen and limbs), although assessment of the respiratory, cardiovascular and renal systems is often also necessary. Certain vital signs such as temperature, blood pressure,

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pulse rate, pulse volume and respiratory rate are performed routinely in all but minor cases.

to outline the size or margins of an organ, one should percuss from the resonant to the dull area. The point where the note changes marks the margin of the organ.

Inspection Inspection requires a trained eye actively to detect abnormalities. Inspection consists of a detailed and systematic scrutiny of the anatomical region and entails close observation of abnormal movements of the parietes and body contour, as well as surface abnormalities (scars, surface lesions, lumps, bulges) and complexion of the skin, lips, conjunctival membranes and sclera. Good lighting is essential, particularly for the detection of abnormal discoloration (pallor, cyanosis, jaundice).

Palpation Palpation relies on the tactile sense organs in the fingers to outline surface irregularities, tension of the abdominal walls, lumps and enlarged organs. The exercise should be carried out by a relaxed warm hand and should be conducted gently and in an orderly fashion. In general, the more you press, the less you feel, and worse still, the patient is hurt.

Percussion Percussion is very useful for establishing the consistency of a swelling or organ. Thus a solid lump or organ is dull to percussion. A fluid-containing cyst or body cavity (peritoneal, thoracic) is stony dull to percussion. For the same reason a distended urinary bladder is detected as a localized dull swelling in the suprapubic region. By contrast, air-containing organs (normal ventilated lung, air-containing hollow abdominal viscera) are resonant on percussion (much like a drum). When using percussion

Regional lymph nodes

Edge

Floor (what you see at the bottom of the ulcer, e.g. granulation tissue)

Base (tissue under the ulcer, e.g. muscle, bone)

Auscultation Auscultation with the stethoscope requires considerable experience to recognize the normal from the abnormal, and is used to examine the lungs (normal and adventitial breath sounds), heart sounds and murmurs, abdominal bowel sounds, and bruits over stenotic or dilated segments (aneurysms) of arteries.

Examination of an ulcer An ulcer is defined as an area of discontinuity of the surface epithelium and may occur internally (mucosal) or externally, when it involves the skin and subcutaneous tissues. Ulceration has a varied aetiology and ulcers may be benign or malignant in nature. In establishing the nature of an ulcer, certain characteristics are important, including the site of the ulcer, its floor, and its base and edges (Fig. 1.1). The history is also important and often provides useful diagnostic clues. The duration of the ulcer, history of trauma and the presence or absence of pain are all relevant.

Floor of an ulcer The floor of an ulcer is made up of fibrovascular granulation tissue. If this consists of healthy pink granulations, the ulcer has an excellent chance of healing. By contrast, healing is compromised if the floor is covered by grey slough and pale granulation tissue, e.g. neuropathic or trophic ulcers. These are deep penetrating ulcers found on pressure areas of the feet in patients with absent or

Sloping

Venous ulcer

Punched out

Neuropathic

Undetermined

Decubitus

Rolling

Basal cell ca.

Everted

Squamous ca.

Figure 1.1 Anatomy of an ulcer. The important characteristics to establish with any ulcer are the site, size, shape, floor, base, edge, discharge, surrounding skin and regional lymph nodes.

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diminished sensation due to peripheral neuropathy from any cause (often diabetes). They are characteristically painless because of the anaesthesia involved in their aetiology, since they are attributable in part to repeated unrecognized trauma. Ischaemic ulcers have virtually no granulation tissue and may expose underlying structures such as tendons, muscles and periosteum. They usually require limb revascularization (by arterial surgery to restore blood flow to the limb) and sometimes skin grafting.

Base of an ulcer The base of an ulcer refers to the state of the tissues underneath and around the floor of the ulcer. If there is inflammatory involvement, the surrounding tissues feel indurated and the ulcer appears fixed and is tender. Fixation and induration may be the result of neoplastic infiltration of the deeper tissues if the ulcer is malignant. In this instance, fixation is not accompanied by tenderness.

Edge of an ulcer The edge of an ulcer is often indicative of the nature of the lesion. Sloping blue edges indicate advancing epithelium (over the red granulation tissue) and signify healing. Blue healing edges are often encountered in venous (gravitational) ulcers. Punched-out ulcers with sharp edges used to be characteristic of syphilis in the days before antibiotics. These have virtually disappeared from clinical practice nowadays and a more typical example of a punched-out ulcer is the neuropathic ulcer due to peripheral neuropathy, most commonly encountered in diabetic patients. Undermined edges are typical of decubitus ulcers (pressure sores) and tuberculous ulcers which, though rare in the West, are still common in developing countries. Decubitus ulcers are the result of poor medical and nursing care of patients confined to bed for prolonged periods as a result of illness or operation. These ulcers are caused by compression necrosis of the skin and subcutaneous tissues over pressure points: heels, sacral region, scapular region. Decubitus ulcers are largely preventable by ensuring clean soft bedding and frequent turning of these immobile patients. Rolled or everted edges are seen when central ulceration is accompanied by growth at the edges and are characteristic of malignant ulcers such as basal cell carcinoma (see Fig. 36.12) and squamous cell carcinoma (see Fig. 36.13) of the skin. Eversion of the edges is more prominent in squamous carcinomas than in basal cell lesions, where the edges are gently rolled and the floor is often encrusted.

• • •

•

Site of an ulcer The site of an ulcer may be a clue to the diagnosis. Examples of this include the predilection of basal cell lesions for the upper third of the face and forehead, occurrence of venous ulcers around the medial malleolus, frequency of ischaemic ulcers on the anterior aspect of the shin and dorsum of the foot, location of trophic ulcers on the sole of the forefoot (especially underneath the ball of the big toe) and common occurrence of decubitus ulcers in the sacral region.

Other characteristics While some ulcers are dry, a discharge is a common feature and may be thin and serosanguineous or thick and purulent if the ulcer is infected. If a discharge is present, a swab should be taken for culture and sensitivity testing. The regional lymph nodes are often enlarged due to infection, although the lymphadenopathy may be due to metastatic spread in the case of squamous cell carcinomas. If the nature of an ulcer remains in doubt after clinical examination, a biopsy with histological examination is essential. The biopsy taken is a wedge that includes a portion of the floor, the edge of the ulcer and adjacent normal skin.

Examination of a lump or swelling A lump may be visible on inspection or not be detected until palpation is carried out. The lump may be discrete and localized or be diffuse, when it is more properly designated a swelling. The important features that provide diagnostic information are site, anatomical plane, relationship to adjacent structures, temperature, tenderness, consistency, mobility, fluctuation, pulsatility (expansile, transmitted) and state of regional lymph nodes. In addition, specific lumps have additional characteristics that can be demonstrated by appropriate clinical tests.

Position, location, shape and size The first feature that should be noted is the position of the lump and its relationship to adjacent anatomical structures, the plane of location (subcutaneous, intramuscular, intra-abdominal, etc.). A lump that is superficial to a muscular compartment, e.g. situated in the subcutaneous plane, is rendered more prominent when the patient is made to contract the relevant muscles. By contrast, this manoeuvre makes a lump become less distinct on both inspection and palpation if the lesion lies within or beneath a muscular compartment. In subcutaneous swellings, it is often possible to ‘pinch’ the skin over the

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summit of the lesion. This cannot be achieved with intracutaneous lumps such as sebaceous cysts. During this stage of the examination, a note is also made of the shape and size (in two diameters) of the lump. Size is important in planning surgical excision and in the assessment of the effect of non-surgical therapy for inflammatory and neoplastic lesions.

Sensing fingers

Inflammatory characteristics Palpation of a lump should be carried out gently and, initially, the temperature of the lesion and the presence of any tenderness noted. Surface discoloration (erythema, bruising, etc.) should also be noted. An inflammatory swelling will be tender, hot, erythematous, indurated and oedematous. It is important to note, however, that some rapidly growing malignant neoplasms may exhibit an inflammatory appearance virtually indistinguishable from that caused by infective conditions. This is encountered most commonly in the breast, where differentiation between a breast abscess and inflammatory cancer may be difficult.

Mobility The mobility of a lump is tested in two planes at right angles to each other. For lumps situated over a muscle compartment, contraction of the muscle group is important before mobility is assessed since a lesion may be infiltrating the muscles and still appear to be mobile if the muscle is not contracted. Mobility does not designate a lump as benign. Indeed, many benign lumps exhibit limited mobility because of attachment of anatomical structures (e.g. ganglion, because of its attachment to tendons and joint capsule; goitre, because the thyroid is tethered to the trachea). The majority of neoplastic lesions are mobile in the early stages and become fixed only when they infiltrate surrounding tissues.

Consistency, dullness and resonance The feel or consistency of a lump is probably its most important clinical feature. It may be solid and hard (when the possibility of neoplasia arises), tense, soft, cystic, or pulsatile (vascular origin). Most enlarged lymph nodes feel rubbery. Solid and fluid-containing lumps are dull on percussion. Some swellings contain gas or gas-filled viscera, in which case they are resonant. A superficial fluid-containing cavity or collection is fluctuant. The test for fluctuation is simple and is illustrated in Fig. 1.2. Fluctuation is very useful for the detection of non-inflamed localized collections of fluid and blood. Generally speaking, cystic lumps and swellings are soft, although a tense cyst may feel hard. The benign

Mass

Displacing finger

Figure 1.2 Test for fluctuation. The index and middle finger of the left hand are placed in a V-shaped configuration on the mass and the index finger of the right hand is used to depress the summit of the mass repeatedly. If fluid is present, the pressure waves created are felt by the sensing left fingers. The test is applied twice, with the second attempt being at right angles to the first. Obviously inflamed and tender masses (e.g. abscesses) should not be subjected to fluctuation as this causes considerable pain.

tumour of fat (lipoma), which often presents as a subcutaneous lump, also fluctuates on testing. A fluid thrill may be present in some cystic swellings. This may be elicited by tapping one side of the swelling and detecting the transmitted percussion wave with the examining fingers placed on the opposite side of the swelling.

Transillumination Transillumination involves shining a light through a swelling to detect whether it transmits light brilliantly or not (Fig. 1.3). Transillumination is a function of the optical density of the component elements of the swelling. Thus a cyst containing clear fluid (e.g. hydrocele, cystic hygroma) transilluminates brilliantly, one containing opalescent fluid (spermatocele) less so. Fat (lipoma) and subcutaneous tissues also transilluminate to a varying extent.

Vascular swellings A swelling arising from an artery is usually the result of localized dilatation (aneurysm) and demonstrates expansile pulsation. The most common example encountered in clinical practice is abdominal aortic aneurysm, which must be palpated gently because of the risk of rupture. In superficial aneurysms, a vascular thrill caused by the turbulent flow in the aneurysm is felt on palpation. Some non-vascular (solid or cystic) lesions apposed to large arteries transmit arterial pulsations. The differentiation

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Roll of paper excludes external light

incompetence at the saphenofemoral junction), it forms a uniform bulge in the immediate subinguinal region and is known as a saphena varix. This swelling also exhibits a fluid thrill that is elicited by tapping the vein below the swelling and feeling the impulse with the fingers of the other hand placed over the varix.

Hernial swellings Pencil torch

Figure 1.3 Test for transillumination of a swelling. Transillumination is elicited by a pencil torch light and a hollow cylinder (made of rolled paper) placed on opposite sides of the swelling. If the swelling contains clear fluid, the light will be transmitted through the fluid and will be seen by the observer looking down the paper cylinder. The cylinder is used to exclude other light from the test region.

The characteristic features of hernial swellings (inguinal, paraumbilical and incisional) are increased prominence with a rise in intra-abdominal pressure (cough, contraction of abdominal musculature, erect posture) and an impulse, visible and palpable, when the patient coughs. There is one important exception to these observations: a femoral hernia usually presents as a subinguinal lump that does not have a cough impulse and does not change in size with change in posture.

Examination of specific anatomical areas Examination of the head and neck General aspects and inspection

Figure 1.4 To elicit expansile pulsation (i.e. an aneurysm) the index fingers are placed one on either side of the swelling. Separation of the two index fingers occurs synchronously with each systolic impulse.

between expansile and transmitted pulsations is important and requires bidigital palpation, with each index finger placed on either side of the swelling. If the lump is intrinsically pulsatile, the index fingers are separated with each systolic impulse (Fig. 1.4). Dilated (varicose) veins are obvious on inspection, especially with the patient standing up. When the proximal part of the long saphenous vein is dilated (due to

Examination of the head and neck begins with inspection. Lesions and abnormalities of bone structure and soft tissues of the face are obvious but lesions in the scalp are often not apparent except in bald males. Anatomically, the neck is divided into two triangles on either side of the midline (Fig. 1.5). Most abnormalities of the neck are visible as swellings. Size and location should be noted and confirmed later by palpation. Lumps attached to the trachea, e.g. thyroid swellings, move upwards (with the trachea) on swallowing. Central lumps attached to the hyoid bone, such as thyroglossal cysts, move upwards with both swallowing and protrusion of the tongue. The most common lump in the neck is due to cervical lymphadenopathy, which may be inflammatory but is often neoplastic (secondary carcinoma or lymphoma). The anatomical disposition of the cervical lymph nodes is shown in Fig. 1.6. An important feature of inspection of the head and neck relates to the venous drainage. Abnormal engorgement of the external jugular vein may be indicative of cardiac failure or circulatory overload. In patients with obstruction of the superior vena cava, usually caused by malignant lymphadenopathy in the superior mediastinum (primary or secondary), there is gross engorgement of the head and neck with prominent superficial veins, a congested suffused appearance and evidence of collateral pathways over the anterior chest wall. Surgical emphysema most commonly appears in the head and neck region as soft crepitant diffuse swelling. It is

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le Tra p e ziu

St e

line Mid

astoi d

d ib

r n om

Man

icle Clav

Figure 1.5 Anterior and posterior triangles of the neck. The boundaries of the anterior triangle are the midline, the anterior border of the sternomastoid muscle and the lower border of the mandible. The margins of the posterior triangle are the trapezius, the posterior border of the sternomastoid and the upper border of the clavicle. To determine whether an abnormality is in the anterior or posterior triangle, the sternomastoid muscle should be rendered tense by asking the patient to depress the chin against resistance.

Figure 1.7 Severe surgical emphysema of the head and neck. This patient was crushed in a lift shaft.

orbital regions. When marked, the resultant swelling leads to virtual occlusion of the eyelids (Fig. 1.7).

Palpation Pre auricular Post auricular Occipital nodes Submental Submandibular

Deep cervical or jugular chains (jugulodigastric node is part of this chain) Supraclavicular

Figure 1.6 Anatomical disposition of the cervical lymph nodes.

caused by escape of air from lacerations or perforation of the tracheobronchial tree or the oesophagus. The extravasated air tends to occupy and cause swelling of regions with lax tissue planes, such as the supraclavicular and peri-

Systematic palpation of the scalp is essential to detect lesions in this region. Parting of the hair over a lump identified by palpation enables closer inspection of the lesion. Scalp lesions superficial to the galea aponeurotica move with the scalp when the patient contracts the occipitofrontalis muscle. Lesions deep to this structure or those invading it and the subjacent pericranium are fixed. Palpation of the anterior triangles of the neck is carried out from the front, whereas palpation of the posterior triangles is best conducted from behind. The entire regions are covered and if an anterior lump is felt, the patient should be asked to swallow and any resulting displacement noted. The consistency of the lump is determined and fluctuation elicited if the swelling appears to be soft and cystic. Transillumination of a large cystic swelling in infants and children, if positive, confirms the presence of cystic hygroma (Fig. 1.8). Palpation of the neck must cover the lymph node groups, especially the deep cervical and the supraclavicular regions. The left supra-clavicular region is a common site for metastatic nodal disease from visceral cancer (oesophagus, stomach and pancreas). The

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Auscultation Auscultation is used if the swelling appears to be vascular and is most commonly applicable to patients with toxic enlargement of the thyroid gland (see Chapter 34). A systolic bruit is often present in patients with primary hyperthyroidism. Auscultation of the carotid vessels should be performed routinely in patients above the age of 50 years and is mandatory in patients with a history of fleeting blindness (amaurosis fugax) or recoverable attacks of muscle weakness or loss of consciousness. These symptoms are indicative of ‘minor strokes’, which are referred to as transient ischaemic attacks (TIAs) and are caused by emboli from atheromatous narrowing of the carotid vessels at the bifurcation into external and internal carotid branches. In these patients a carotid bruit is often heard on auscultation (see Chapter 37).

Cervical lymphadenopathy (a)

(b) Figure 1.8 (a, b) Large cystic hygromas both present at birth. Cystic hygromas are large disfiguring lymphangiomas that are treated by surgical excision.

carotid vessels must also be palpated for thrills, associated swellings and any aneurysmal dilatation.

Percussion Percussion is seldom employed in examination of the head and neck. It may provide useful information in swellings occupying or extending below the suprasternal notch, when percussion over the manubrium may elicit dullness, indicating probable retrosternal extension of the lump. This is most often encountered with swellings of the thyroid gland. However, it is an imprecise clinical test and is unreliable, especially in patients with chronic obstructive airways disease and emphysema.

Enlargement of the cervical lymph nodes may be due to infection or neoplastic infiltration. The latter may consist of secondary deposits from a primary tumour elsewhere in the body or be primary in nature, i.e. lymphoma. Infective conditions may be viral or bacterial, acute or chronic. Examples include tonsillitis, infectious mononucleosis, acquired immunodeficiency syndrome (AIDS), scalp infestations and cat-scratch fever. Pyogenic infections (usually staphylococcal in nature) may form large painful abscesses that require drainage. Cervical cellulitis due to streptococcal infection is fortunately rare nowadays. As the infection is confined by the deep cervical fascia, airway obstruction from pressure and laryngeal oedema can occur in these patients. Although rare in western countries, tuberculosis of the cervical lymph nodes (Mycobacterium tuberculosis) is common in developing countries and is encountered in the West in immigrant populations. Tuberculous cervical lymphadenopathy results in a collar-stud abscess (Fig. 1.9). In western countries infection is more commonly caused by atypical mycobacteria, also known as MOTT (mycobacteria other than typical tubercle). These infections are nowadays most often encountered in patients suffering from AIDS. Lymphomas The neck forms one of the most common sites for lymphoma, a primary tumour of lymph nodes. Lymphoma is classified into two broad categories, Hodgkin’s and nonHodgkin’s lymphoma, each category being subdivided into various types depending on the cell of origin of the tumour (T or B cell) and the degree of differentiation. When it arises in the neck, the tumour forms painless

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Deep cervical lymph nodes Skin

Periadenitis

Jugular vein

Glands matted together

Deep cervical fascia

Coagulative necrosis leads to collection of pus

Pus penetrates deep cervical fascia to produce collar stud abscess

Figure 1.9 Evolution of a collar-stud abscess. Initially, tuberculous lymph nodes are firm and discrete but as caseation (coagulative necrosis) progresses, the inflammatory process induces a marked periadenitis and the enlarged nodes become matted together. Eventually, the necrotic glands are converted into a collection of pus that burrows through the investing layer of the deep cervical fascia to form a superficial (subcutaneous) extension. This is referred to as a collar-stud abscess in view of the two localized collections superficial and deep to the investing layer of the deep cervical fascia. Although often tender, the superficial component of a collar-stud abscess is not accompanied by inflammatory changes of the overlying skin (as obtains with ordinary pyogenic abscesses). For this reason, it is often described as a cold abscess. Untreated, it ‘points’ and eventually erodes through the skin, forming single or multiple discharging sinuses.

non-tender swellings. The enlarged lymph nodes are discrete, firm and rubbery and may be located in either the anterior or posterior triangles. When enlarged nodes are discovered in the neck, a systematic palpation of other lymph node sites (axillary, inguinal) and palpation of the abdomen for enlarged liver and spleen are essential to determine whether the disease appears to be localized to one region or has disseminated. The patient may or may not have systemic symptoms such as malaise, intermittent fever and weight loss. The staging of lymphomas, necessary for outlining the treatment regimen, necessitates the performance of special investigations including radiology of the chest, computed tomography (CT), isotope bone scan and bone marrow biopsy. Within each stage, the absence or presence of systemic symptoms is designated by the letters A and B respectively. Metastatic cervical lymphadenopathy Overall, metastatic deposits in one or more cervical lymph nodes constitute the most common cause of a lump in the neck. The common sites of primary tumours that may present in this way are pharynx and larynx (squamous cell carcinomas), oral cavity (tongue, buccal mucosa), thyroid, bronchus, breast and upper digestive system (oesophagus, stomach, pancreas). The deposits may occur anywhere in the neck but the most common sites are the deep cervical and supraclavicular regions, especially on

Table 1.9 Management of enlarged cervical lymph node suspected of metastic tumour. Examination of other lymph node regions Full ear, nose and throat examination Chest X-ray Full blood count

the left side. Metastatic nodes are always hard in consistency and soon become fixed to surrounding tissues and matted together, although in early disease the enlarged nodes may be mobile on palpation. There is an important sequence of investigations whenever enlarged lymph nodes thought to be caused by secondary deposits are found in the neck, with no other apparent abnormality on complete physical examination. This is outlined in Table 1.9. It is very important that this protocol is followed before the lump is submitted to biopsy, since if the primary tumour is in the head and neck (usually squamous in nature), cervical block dissection of the enlarged lymph nodes is required together with excision of the primary. The success of this treatment is jeopardized if a preliminary excision biopsy of the involved nodes has been carried out.

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to determine the lower margin. If this cannot be felt, a retrosternal prolongation is likely. A large benign goitre with a retrosternal extension can give rise to pressure symptoms such as engorgement of the head and neck veins and stridor. These are accentuated when the patient elevates both upper arms above the head. Clinical assessment of thyroid status (euthyroid, hyperthyroid or hypothyroid) is an integral part of the examination of a patient with thyroid enlargement (see Chapter 34).

Enlargement of the salivary glands

Figure 1.10 Large malignant goitre in an elderly man.

Thyroid swellings Thyroid swellings are designated by the general term goitre and move on swallowing. Enlargement of the thyroid gland may be unilateral or diffuse and bilateral. If a discrete lesion is located in the isthmus of the gland, it presents as a midline swelling; otherwise the majority of unilateral swellings are lateral or anterolateral. They are commonly solid but may be cystic. Diffuse multinodular enlargement (nodular goitre) is common and associated with iodine deficiency. In some disorders such as primary hyperthyroidism the thyroid is uniformly enlarged with a smooth surface. A discrete solitary nodule in an otherwise normal thyroid should always raise suspicion of malignancy (papillary or follicular neoplasm) and must be accompanied by a systematic palpation of the neck to exclude or confirm associated lymphadenopathy (see Chapter 34). However, the anaplastic cancers encountered in older patients present as diffuse infiltrative enlargement of the thyroid gland (Fig. 1.10). Because of fixation to surrounding tissue, the mass does not move with swallowing and may be accompanied by features indicative of tracheal compression (dyspnoea and stridor) and involvement of the recurrent laryngeal nerve (hoarseness). The position of the trachea should be checked in all patients with thyroid enlargement, and with large swellings the inferior part of the mass is palpated carefully

There are four major salivary glands: two parotid and two submandibular. The parotid gland has been likened to ‘a lump of bread dough poured over an egg whisk’, the dough representing the glandular tissue and the egg whisk the branches of the facial nerve. The gland occupies and extends over the hollow between the masseter muscle anteriorly and the sternomastoid posteriorly (see Fig. 35.3a). It is covered with a dense parotid fascia, deep to which are attached the parotid lymph nodes. The submandibular gland overlies the mylohyoid muscle under the ramus of the mandible. The posterior part of the gland bends around the posterior border of the mylohyoid and then gives rise to the submandibular duct, which runs on the floor of the mouth to open at the frenulum of the tongue. The lingual nerve, the submaxillary ganglion and the hypoglossal nerve are situated close to the deeper part of the gland (see Fig. 35.1a). In practice, enlargement most commonly affects the parotid gland, followed by the submandibular gland. Although swellings of the salivary glands may be due to viral infections (e.g. mumps parotitis), in surgical practice the enlargement is most commonly caused by calculous disease blocking the ductal drainage system (submandibular more commonly than parotid) or by tumours (predominantly mixed parotid tumours). Enlargements of the submandibular gland appear as swellings in the submandibular triangle. In contrast, parotid swellings occur within a large inverted triangular area with boundaries extending from the tragus of the ear to the anterior border of the mandibular ramus and the gap between the mastoid process and the angle of the mandible inferiorly. Swellings caused by infection and stones obstructing the salivary duct are painful and tender, whereas tumours are painless and non-tender (see Chapter 35).

Face, oral cavity and scalp Inspection forms an important part of the examination. The facial expression describes the mood of the patient and, with practice, the physician can rapidly establish anxiety, depression, introversion and mania. Inspection

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of the skin and mucosal surfaces, conjunctivae and buccal mucosae identifies pallor (anaemia), central cyanosis (deoxygenation of the blood and polycythaemia) and abnormal pigmentation. The yellowish discoloration in jaundiced patients is obvious on inspection but minor grades of icterus are identified by examination of the sclera in a good light. Other features of hepatic disease include muscle wasting, bruising, spider naevi found in the territory of the superior vena cava, and yellowishwhite periocular fatty deposits (xanthelasma) encountered in certain hyperlipidaemic states. The mucosal lining of the lips and buccal mucosa may exhibit areas of pigmentation in certain disorders. The most common ulcers of the lips are viral lesions (herpes simplex), which often accompany debility and infections of the upper respiratory tract and occur as painful lesions at the angle of the mouth. Malignant ulcers of the lip are squamous cell lesions that present as painless persistent ulcers, usually on the lower lip (Fig. 1.11a). Spread is to the submental and submandibular lymph node groups in the first instance. Basal cell carcinomas (rodent ulcers) are much more frequent and occur in elderly patients, predominantly in the upper third of the face and scalp above the maxillary line (Fig. 1.11b,c). The other common malignant tumour encountered in the face and scalp is malignant melanoma (Fig. 1.12), of which there are various types. Malignant melanomas occur as pigmented lesions over a wide age range and are prevalent in fair-skinned individuals exposed to sunshine (see Chapter 36). The buccal cavity is examined for gingival hypertrophy (often drug induced), inflammation (gingivitis) and tumours of the gums, and for lesions (ulcers, thickenings and fissures) of the tongue and buccal mucosa. Oral and mucocutaneous candidiasis (infestation by Candida albicans) is encountered in debilitated individuals and may complicate antibiotic therapy. The infection causes a very sore mouth and throat and may extend to the oesophagus. The affected mucosa is red and covered with white adherent patches. The pharynx can be inspected directly or indirectly with a laryngeal mirror and light source. Ulcers of the tongue should always be viewed with suspicion. While some are traumatic (caused by a jagged tooth or ill-fitting dentures) or aphthous in nature, a significant percentage prove to be malignant. As approximately one-third of cancers of the tongue occur on the undersurface or on the lateral edge of the posterior third of the tongue, examination should include elevation of the organ for inspection of the inferior surface and protrusion forwards and laterally (to either side), while the appropriate angle of the mouth is retracted to enable adequate inspection or the posterior part of the lateral borders.

(a)

(b)

(c) Figure 1.11 (a) Squamous carcinoma on the lower lip of an inveterate pipe smoker. (b) Early basal cell carcinoma on the forehead. At this stage treatment is straightforward and the prognosis is excellent. (c) A neglected basal cell carcinoma on the side of the head involving the ear and a large area of the scalp. Treatment is now extremely difficult and it may not be possible to remove the lesion completely.

The most common swelling of the scalp is a sebaceous cyst, which is a retention cyst of a hair follicle. Sebaceous cysts are often multiple (Fig. 1.13). They are round in shape and always attached to the skin. Their contents are

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diffuse and cyclical, with pain and tenderness before and during menstrual periods (cyclical pronounced mastalgia), or localized to a specific area with or without a palpable lesion at this site (trigger-point mastalgia). Nipple discharge may occur alone or in association with other symptoms (e.g. lump or pain). The nature and colour of the discharge vary but when blood-stained, nipple discharge signifies the presence of a duct papilloma or carcinoma. The examination of the breasts should always include palpation of the neck and both axillae for lymph node enlargement.

Inspection Figure 1.12 Malignant melanoma on the leg of a ‘sun worshipper’.

Figure 1.13 Sebaceous cysts are often multiple.

cheesy in nature and on palpation they are firm and nonfluctuant. Sometimes, a punctum can be identified in the centre of the lesion. They become painful and swollen if infected, when they discharge pus and then resolve, although recurrence of the swelling is frequent.

This necessitates removal of clothing to the waist and therefore requires privacy and the presence of a nurse. Inspection is carried out in two postures. 1 The breasts are initially inspected with the patient sitting up straight and the arms by the side facing the doctor. At this stage one is assessing size, contour of breast mounds, surface abnormalities and the state and direction of the nipples. A certain amount of disparity in breast size is quite common and normal, but the nipples should point in the same direction. Inversion of the nipples is frequently encountered and may be normal or due to benign disease (usually bilateral retraction) or an underlying cancer (unilateral retraction). The skin over a breast abscess is red, shiny and oedematous. However, a similar appearance is encountered in patients with inflammatory breast cancer (mastitis carcinosa). The thickening of the skin in these patients is due to oedema secondary to cutaneous lymphatic permeation, the pitted appearance simulating orange skin a hence the term peau d’orange. 2 The patient is then asked to lift her upper arms above her head. This manoeuvre normally results in uplifting of the breasts with diminished protrusion of the nipples, although the surface contour of the breast mounds should remain smooth and convex. Dimpling or localized depression or obvious inversion of the nipple is indicative of an underlying malignant mass that is causing tethering of the superficial tissues.

Examination of the breasts The common breast complaints in females are discovery of a lump (benign or malignant), pain (mastalgia) and nipple discharge. In males, the most common ailment is unilateral or bilateral hypertrophy (gynaecomastia), which may be idiopathic (postpubertal), drug induced or secondary to certain disorders, e.g. liver disease. Undoubtedly the most important presentation is a palpable lump, in view of the frequency of breast carcinoma, which now affects 1 in 12 females in western countries. Breast pain is a very common complaint and may be either

Palpation of the breast The unaffected breast is palpated first. The patient must be comfortable in the sitting or semirecumbent position, with her elbows resting on the couch and the arms on her flanks. Palpation of the breast is carried out with the flat of the hand gently compressing the breast tissue against the chest wall (Fig. 1.14). It starts in the areolar region and covers, in a systematic manner, the entire breast, including the axillary tail. If a lump is found, its position is noted but the general palpation is continued

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Figure 1.14 Palpation of the breast is carried out with the flat of the hand gently compressing the breast tissue against the chest wall.

to determine whether any other lumps are present. Normal breast tissue feels soft and smooth. However, in many adult females, the breasts have a nodular lumpy consistency and the distinction between normal and abnormal may be difficult and requires considerable experience. Pathological diffuse thickening may be localized or generalized.

Palpation of an identified breast lump If a lump is identified during the general palpation, the following information is essential: tenderness, position, size, consistency, margins, mobility and involvement of adjacent structures and tissues. A breast abscess is exquisitely tender. Tenderness is also encountered in mammary duct ectasia, Mondor’s disease (thrombophlebitis of the subcutaneous breast veins) and traumatic fat necrosis of the breast. In terms of precise location of a lump, the breast is divided into the areolar region and four quadrants: upper inner, upper outer, lower outer, lower inner (see Fig. 14.1). The size of the lump is best measured by callipers in two directions. Size is one of the variables used in the staging of cancer of the breast. Breast cancer feels firm to hard, is not tender and has indistinct margins. In contrast, benign lesions (fibroadenomas, breast cysts) are firm, smooth and always mobile. Fibroadenoma is very mobile and tends to slip away from the examining finger and for this reason has been described as a ‘breast mouse’. The mobility of a lump is tested in relation to both the overlying skin and the underlying pectoralis major fascia and muscle. Tethering or fixation of the lump to the underlying pectoral muscles is determined after the patient is asked to contract the ipsilateral pec-

Figure 1.15 Palpation of the axilla is carried out from in front of the patient who is either in the semirecumbent or sitting position. The patient’s upper arm is supported on the examiner’s arm during the palpation.

toralis major muscle by pressing on her hips with her hand. Involvement of the superficial breast tissue varies from tethering, such that the skin and subadjacent breast parenchyma cannot be rolled over the mass, to actual involvement with puckering of the skin, ulceration and fungation.

Palpation of the axillae and neck Examination of the breasts is incomplete without careful palpation of both axillae and neck for palpable lymph nodes, which could represent metastatic disease. Palpation of the axilla is carried out from in front of the patient, who is either in the semirecumbent or sitting position. The patient’s upper arm is supported on the examiner’s arm during the palpation (Fig. 1.15), which must be carried out in an orderly fashion, starting at the apex of the axillae followed by the medial (chest) wall, anterior wall (pectoral muscles) and posterior wall (over the subscapularis muscle). If palpable lymph nodes are present, their number and mobility or otherwise are noted (see Chapter 43).

Examination of the abdomen An abdominal examination consists of several parts: examination of the abdomen, examination of the inguinal region, examination of the scrotum and testes, and rectal examination.

Abdominal examination Good examination of the abdomen entails certain requirements, such as a well-lit room to detect skin colour changes and a warm environment to prevent shivering,

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which results in contractions of the abdominal wall and thereby interferes with palpation of the abdomen. If the patient is in a multibed unit, curtains are drawn around the bed for privacy during the examination. The patient is examined supine with one pillow beneath the head and a sheet or blanket covering the pubic region and the lower limbs. Patients with an acute abdomen are often more comfortable with the legs drawn up as this relieves tension on the anterior abdominal musculature. No attempt must be made to straighten their lower limbs as this will exacerbate the pain and limit the scope of the examination. Right-handed individuals should examine patients from the right side of the bed and left-handed individuals from the other side. Ideally, the patient’s abdomen should be at the level of the examiner’s elbow. This is achieved either by elevating the bed to the right level or by the examiner bending. Surface anatomy The various quadrants described in anatomical textbooks are not practical because of considerable overlap. A better subdivision for clinical purposes is shown in Fig. 13.1, which has the following components: four quadrants (right and left upper quadrants and right and left iliac fossae), epigastric, periumbilical (or central), suprapubic and two flank (or loin) regions. The important cutaneous landmarks on the anterior aspect are the costal margins, xiphoid process, umbilicus, anterior iliac spine, pubic tubercle, symphysis pubis and the inguinal ligament (Fig. 1.16). The useful cutaneous landmarks on the posterior aspect are the tip of the 11th rib (the 12th rib is not usually palpable), the ridge of the paraspinal muscles (erector spinae), the vertebral spinous processes and the iliac crest. Inspection Inspection should cover the following: abdominal wall movement; contour of the abdomen; surface markings and abnormalities; hernial defects.

• • • •

movement and contour In normal individuals, the anterior abdominal wall moves passively with respiration (expands with inspiration and recedes with expiration). This movement is abolished or considerably reduced in patients with an acute abdomen, where the abdominal muscular walls are in spasm. The contour of the anterolateral abdominal wall and the flank provides useful information in both the elective and emergency situations. In normal individuals in the supine position, the abdomen is flat, although it may be scaphoid in thin people; the contour of the flank is flat in

Anterior superior iliac spine

Inferior epigastric artery Superficial inguinal ring

Inguinal ligament Deep inguinal ring

Spermatic cord

Nerve Artery Vein Canal

Pubic symphysis

Lacunar ligament

Femoral

Pubic tubercle Figure 1.16 Anatomy of the inguinal canal. The midpoint of the inguinal ligament between the anterior superior iliac spine and the pubic tubercle marks the site of the internal or deep inguinal ring, whereas the midinguinal point between the anterior superior iliac spine and the pubic symphysis locates the superficial femoral artery as it emerges below the inguinal ligament. The important structures below the inguinal ligament, from the lateral to medial aspect, are the femoral nerve, femoral artery, femoral vein and the femoral ring, which is bordered medially by the lacunar ligament and laterally by the femoral vein.

males and concave in females. Bulging of the flanks and abdominal distension are encountered in obesity, ascites, pregnancy and intestinal obstruction. surface markings and abnormalities These include the following: previous operation scars (normal, keloid, pitted due to previous infection); skin lesions; scratch marks (in jaundice); striae (previous pregnancy or obesity); bruising or staining of the skin of the abdomen, e.g. flank in acute pancreatitis (Turner’s sign), periumbilical staining due to haemoperitoneum (Cullen’s sign); obvious swellings; dilated abdominal wall veins (obstruction or compression of the inferior vena cava); previously constructed ostomies (colostomy, ileostomy); abnormal pulsations (abdominal aortic aneurysm).

• • • • • • • • •

hernial defects Herniation may occur through natural orifices such as the inguinal or femoral canal (see Chapter 24) or through weaknesses in the anterior abdominal wall such as beside

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the umbilical cicatrix (paraumbilical hernia) or through a poorly healed surgical wound (incisional hernia). During inspection with the patient in the supine position, an unobstructed hernia appears as a momentary bulge when the intra-abdominal pressure is raised by asking the patient to cough or tense the abdominal muscles. In some patients atrophy of the recti abdominis muscles together with their separation from each other results in a central abdominal bulging defect. This is most commonly seen in multiparous females but is also encountered in males and is referred to as divarication of the recti or ventral hernia. An irreducible hernia (one that is stuck in the parietes) or an obstructed hernia appears as a constant bulge that cannot be reduced by either the patient or the doctor. The demonstration of an incisional or ventral hernia is best achieved simply by asking the patient to lift his or her head (without support from the upper arms) from the pillow. This raises the abdominal pressure and produces a distinctive bulge. The same effect can be achieved by asking the patient to lift the lower limbs off the bed (see Fig. 24.9). Palpation Palpation is the most important aspect of the physical examination of the abdomen. Various techniques are used: light palpation, deep palpation, palpation of specific organs (liver and spleen), bimanual palpation (kidneys and retroperitoneum) and palpation of a fluid thrill. general principles Aside from ensuring that the patient is in a comfortable supine position, palpation must be carried out gently with warm hands and in a systematic fashion from quadrant to quadrant. Long fingernails, by digging into the patient’s skin, impair the ability to conduct the examination. A common mistake made by the inexperienced is to hurry the palpation (flitting palpation). The hand should not be transferred to another region until the doctor has registered whether the area concerned feels normal or not. Light palpation (Fig. 1.17) is conducted before deep palpation. In general, the more one presses the abdominal wall, the less one feels for two reasons. First, the tactile sensation is diminished with constant sustained pressure. Second, clumsy deep palpation hurts the patient and induces spasm of the abdominal muscular walls. The technique used varies with the state of the abdomen: acute or non-acute. acute abdomen These patients are acutely ill, usually in considerable pain and some may be in shock from dehydration/ hypovolaemia (see Chapter 12). The primary concern is therefore resuscitation and relief of pain by intravenous

Figure 1.17 Light palpation of the abdomen is best performed by a doctor in the sitting or kneeling position so that the examiner’s arm is comfortable and level with the anterior abdominal wall. Palpation should proceed in an orderly fashion around the quadrants of the abdomen, always starting diametrically opposite the area of interest (e.g. if the patient has right iliac fossa pain, start in the left upper quadrant). Note that the patient is exposed from the nipple line to mid-thigh.

opiates. Both these measures must precede palpation of the abdomen. Opiates should be administered via the intravenous route, especially in shocked patients, since the peripheral shutdown greatly reduces uptake of the drug by the circulation when administered via the intramuscular route. Relief of pain is not only kind and humane but also facilitates the conduct of the examination by increasing patient comfort and allaying anxiety. The belief that analgesia may mask physical signs is completely unfounded. The abdominal palpation of patients with an acute abdomen must be conducted with the utmost gentleness and is primarily designed to establish the presence of reflex spasm of the abdominal muscles (guarding and rigidity) and the presence, extent and location of abdominal tenderness. In the presence of peritoneal irritation due to infection or escape of gastrointestinal contents (e.g. perforated peptic ulcer), both the visceral and the parietal peritoneum become inflamed (peritonitis). The localized pain and tenderness and the resulting spasm of the overlying abdominal muscles are due to stimulation of the somatic nerves supplying the abdominal parietes. When the abdominal wall is depressed by palpation, the pain is enhanced over the inflamed area. Moreover, the pain is intensified further as the pressure from the fingers is released. This is known as rebound tenderness. The test, although valuable, must be elicited with the minimum of suffering possible. In the vast majority of patients, simple coughing will induce pain in the affected region and this is equivalent to eliciting rebound tenderness by light palpation. In others, gentle percussion by the right hand on the

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the enlargement of organs (liver, spleen and kidneys) and the presence of any intra-abdominal masses.

Figure 1.18 Technique of deep palpation using two hands.

examiner’s left fingers (placed on the abdominal wall) can elicit the sign. In any event, deep palpation must never be practised in these patients. The extent of spasm of the abdominal musculature varies from increased tension of the abdominal wall (guarding) to board-like rigidity. To some extent, the degree of rigidity depends on the state of the individual patient’s musculature. Thus, elderly patients with atrophic muscles may not exhibit significant rigidity despite an established generalized peritonitis, although they will always experience tenderness with rebound during the examination. In contrast, the abdomen of a previously fit athletic male patient with a perforated ulcer will be board-like in most instances. Physical signs, including guarding and rebound tenderness, may be abrogated by drugs (especially steroids), old age and immunosuppression from any cause. Thus, a high index of suspicion must be kept in these groups of patients. non-acute abdomen Light palpation is used in the first instance and suffices for most patients. The technique entails using a slightly cupped hand that is warm and relaxed (almost dead weight), with the terminal phalanges gently depressing the anterior abdominal. The sensitivity and ability to feel lumps and normal organs increase with practice and experience, for which there is no substitute. Deep palpation is necessary in obese individuals and patients with welldeveloped abdominal musculature. The best technique entails the use of both hands: the left on the abdominal wall (the sensing hand) is overlapped and depressed by the right hand (Fig. 1.18). Again, as little force as is necessary is applied. Some clinicians perform deep palpation using one hand. Palpation of the abdomen in the non-acute situation is designed to detect the presence of tenderness,

specific organs Liver and gallbladder. The lower edge of the liver is just palpable in most normal individuals with the tips of the fingers pointing upwards, starting in the right lower quadrant and moving up towards the right costal margin. Normally, a distinct smooth edge is felt that moves and becomes more prominent with inspiration. The substance of the liver lies underneath the thoracic cage and its upper margin is therefore impalpable; however, its position can be identified by percussion (see later). When the liver enlarges as a result of disease, the anterior superior surface becomes palpable as a firm mass extending from the right hypochondrium to the epigastric region. Normally, the gallbladder is not palpable. When enlarged, as in patients with cancer of the head of the pancreas (see Chapter 29), it is felt as a round smooth swelling that moves with respiration in the right hypochondrium along the midclavicular line. Spleen. This has to be enlarged to one-and-a-half to twice its normal size (splenomegaly) before it can be felt. As the spleen enlarges medially and inferiorly, it projects for a varying distance below the left costal margin towards the right lower quadrant. Palpation of the spleen requires elevation of the left lower ribcage and flank as the abdomen is palpated with the right hand starting in the right iliac fossa (Fig. 1.19a). When uncertainty remains as to whether a spleen is palpable or not, the patient should be positioned in the right semiprone position as this results in anterior displacement of the organ (Fig. 1.19b). Palpation of the spleen should be carried out during inspiration because the diaphragm pushes the organ downwards, rendering it more accessible to the tips of the fingers. In some enlarged spleens a distinct notch is palpable along the anterior margin, but this is by no means universal. Kidneys. The kidneys are examined by the technique of bimanual palpation shown in Fig. 1.20. For the right kidney, the left hand is placed beneath the right flank and the right hand is placed anteriorly. The left hand is used to lift the retroperitoneal contents and thereby trap the mass or kidney between the two hands. The kidneys are not palpable in health, although in thin patients the lower poles may be felt occasionally. On the right side, an enlarged kidney has to be differentiated from a mass in the hepatic flexure or enlarged liver. On the left, the differentiation is between an enlarged spleen and mass in the descending colon. intra-abdominal masses Distinction between intra-abdominal masses and swellings within the abdominal wall is achieved by asking the

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Table 1.10 Palpable abdominal masses.

(a)

(b)

Mass in RUQ: cancer of the hepatic flexure, enlarged gallbladder, enlarged right kidney Mass in RUQ extending to the epigastrium: hepatomegaly Mass in the epigastric region: liver, gastric cancer, abdominal aortic aneursym Mass in LUQ: splenomegaly, cancer of the descending colon, swelling in tail of pancreas, enlarged left kidney Mass in the periumbilical region: paraumbilical hernia, cancer of the transverse colon, tumour deposit from visceral neoplasm (Sister Mary Joseph’s nodule) Mass in LLQ: constipation (faecal scybala), cancer of the descending colon Mass in the suprapubic region: distended urinary bladder, pregnancy, ovarian cyst Mass in RLQ: appendiceal disease, cancer of the ascending colon, Crohn’s disease of the terminal ileum Mass in the inguinal region: hernia, enlarged lymph node (inflammatory, lymphoma, secondary tumour deposit), saphena varix, aneurysm LLQ, left lower quadrant; LUQ, left upper quadrant; RLQ, right lower quadrant; RUQ, right upper quadrant;.

Figure 1.19 (a) Palpation of the spleen requires elevation of the left lower ribcage and flank as the abdomen is palpated with the right hand starting in the right iliac fossa. (b) When uncertainty remains as to whether a spleen is palpable, the patient should be positioned in the right semiprone position, as this results in anterior displacement of the organ.

Figure 1.20 The kidneys are examined by the technique of bimanual palpation. The technique for examining the left kidney is shown here.

patient to contract the abdominal muscles. This accentuates intramural masses and renders intra-abdominal swellings less distinct or impalpable. The most important clue to the nature of a swelling within the abdomen is the site (Table 1.10). Other important features include presence of tenderness over the mass (denotes an inflammatory component), mobility with palpation, movement with respiration and consistency. Percussion Percussion is best regarded as an adjunct to palpation. It is used to determine the presence of tenderness, to estimate the size of an enlarged organ or mass, and to distinguish gaseous distension of hollow organs from an excessive amount of fluid in the peritoneal cavity (ascites), both of which cause generalized abdominal distension. The technique consists of gentle tapping with the right fingers (and a relaxed right wrist) on the index and middle finger of the left hand placed on the area to be percussed. A resonant note is obtained over a hollow organ distended with air (dilated stomach, colon, etc.) whereas a dull note is elicited over a solid organ (e.g. liver) or mass and fluidfilled cavities (e.g. distended urinary bladder, intraabdominal cyst, ascites). Liver. The objective is to determine the size of the liver. The upper margin is defined first. This is normally situated at the level of the sixth rib in the midclavicular line

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but may be displaced downwards in patients with obstructive airways disease (emphysema) and in asthenic patients whose liver is loosely attached and ptotic. To determine the upper margin of the liver, percussion is started on the right anterior chest wall at the fourth intercostal space. A resonant note (due to aerated lung parenchyma) is obtained initially. This changes to relative dullness as the upper margin of the liver (still overlapped by lung) is reached. A few centimetres further down the percussion note becomes dull and remains so until the lower margin of the liver is reached. The normal anterior span of the liver varies with body size and ranges from 11 to 15 cm in males and 9 to 13 cm in females. Auscultation Auscultation of the abdomen is performed with the diaphragm end-piece of the stethoscope. It is used to listen for bowel sounds, bruits and venous hums and succussion splashes. An adequate technique is required to avoid spurious sounds caused by movement of the stethoscope over the abdominal wall, particularly in hairy individuals. During auscultation the diaphragm must be held absolutely still. bowel sounds The normal bowel sounds are difficult to describe and indeed exhibit a wide range of frequency, intensity and pitch. They are caused by peristaltic activity. In mechanical intestinal obstruction (see Chapter 15), they become hyperactive due to the enhanced peristaltic activity proximal to the obstruction and can be heard as loud rushes coincident with episodes of colicky abdominal pain. Absent bowel sounds (during a 2-min period of auscultation) indicate loss of peristaltic activity and are encountered in adynamic ileus from any cause. In some of these patients, particularly those with hugely distended small intestine, tinkling sounds are heard. These result from the passive movement of fluid contents inside the cavernous intestinal loops. bruits Most bruits are heard in the midline between the xiphoid process and the umbilicus. They are caused by aneurysms (aorta, splenic artery) or stenosis (renal artery). A soft hum may be heard over the liver in portal hypertension and large vascular hepatic tumours, including hepatomas. A friction rub may be audible over the splenic region along the lower part of the left costal margin in patients with splenic infarct or perisplenitis. succussion splash The stomach becomes distended with fluid (ingested liquid, saliva and gastric juice) when the pylorus is ob-

Figure 1.21 Technique of palpation of a fluid thrill. The right hand is placed flat on one side of the distended region and the swelling is tapped by the fingers of the left hand. This action produces sets of waves in the fluid (much like the ripples in a pool) that are felt by the right hand. The fluid thrill is accentuated if an assistant (or the patient) compresses the swelling with the edge of one hand.

structed by tumour or cicatricial stenosis. The distended stomach gives rise to a dull fullness in the epigastrium. When the diaphragm of the stethoscope is placed medial to the left costal margin and the patient is shaken from side to side by the lower ribcage, a splashing sound (succussion splash) is heard that is pathognomonic of this condition. The test must, however, be carried out after a 4-h fast. Examination of the abdomen for ascites Ascites, the pathological accumulation of an excessive amount of fluid in the peritoneal cavity, causes abdominal distension that is dull to percussion. Similar findings on physical examination may be caused by large cysts that usually arise from the pelvis and are ovarian in origin, although some large cysts arise in the small-bowel mesentery. As distinct from large cysts, ascites is always accompanied by bulging of the flanks and the patient often has an everted umbilicus due to the formation of an umbilical hernia. Both specific palpation and percussion techniques are used to identify large cysts and differentiate one from the other. The technique of palpation of a fluid thrill, which establishes the presence of fluid, is illustrated in Fig. 1.21. The presence of ascites can only be established clinically by the detection of shifting dullness (Fig. 1.22).

Examination of inguinal region The inguinal region is a site of common pathology: hernia

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01 Direction of percussion from resonant (centre) to dull (flank)

Point when change occurred when patient was flat B A

A' Patient supine

A Point where note changes from resonant to dull

A' B' Patient turned 45° to the left

Figure 1.22 Tests for shifting dullness. In the supine–lateral position test, the abdomen is percussed from the umbilicus laterally in either direction and the line where resonance is replaced by dullness (A–A′) is marked on either side. The patient is then rolled 45° on to one side and the abdomen percussed again, when (as a result of fluid displacement by gravity) the level of dullness is seen to have shifted closer to the umbilicus on the dependent side (B–B′). This test is always positive when the ascites is accompanied by distension of the abdomen but may be negative or equivocal if the amount of fluid is less than 1500 mL. When doubt persists, the knee– elbow–supine test, which is more sensitive, is performed. The patient is first asked to assume the prone position for several seconds and then to elevate the trunk off the bed by assuming the knee–elbow position. Percussion reveals dullness around the central region of the abdomen, extending to the flanks. The lateral borders of the dullness are marked on either side. The patient is then turned to the supine position when the previous dull region becomes resonant.

formation, lymph node enlargement, etc. The important anatomical landmarks are described in Fig. 1.16. Inguinal lymph nodes are disposed both along the inguinal ligament (oblique) and vertically along the femoral vessels. They drain the lower abdominal wall, the genitalia, perineal region and the lower limbs (Fig. 1.23).

Figure 1.23 Massive metastatic inguinal lymph node deposits.

Inguinal herniae arise above the inguinal ligament and emerge through the external ring medial to the pubic tubercle. By contrast, a femoral hernia exits through the femoral canal below the inguinal ligament and lateral to the pubic tubercle. Inguinal herniae are anatomically classified into direct (weakness through the posterior wall made up of the transversalis fascia and conjoint tendon) and indirect, where the hernia enters the inguinal canal through the internal ring and courses down obliquely through the canal before it exits through the external ring. As it enlarges, an indirect inguinal hernia descends into the scrotum (inguinoscrotal hernia), which a direct hernia never does. The examination for suspected hernia commences with inspection of the patient in the standing position, when a bulge may be seen. This will become more prominent if the patient coughs. The hand is then placed over the lump and the patient is asked to cough again, when a cough impulse is felt. This establishes the diagnosis. It is important that both inguinal regions are examined for cough impulse as inguinal herniae are often bilateral. The patient is then placed in the supine position. If the hernia disappears spontaneously in this position, it is likely to be of the direct variety. Otherwise an attempt is made to reduce the hernia. If this is unsuccessful, the hernia is labelled as irreducible. This stage is accompanied by a significant increase in the risk of obstruction and strangulation (see Chapter 24). A femoral hernia is usually not reducible and may not transmit a cough impulse. It forms a tense globular subcutaneous swelling below the inguinal ligament and lateral to the pubic tubercle and is sometimes difficult to differentiate from an enlarged lymph node (see Fig. 24.9).

Examination of the scrotum and external genitalia In surgical practice this is usually confined to examination

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Figure 1.24 ‘Can I get above it?’ The first objective with any scrotal swelling is to determine whether one can get above it by approximating the tips of the two hands above the upper limit of the swelling.

of the male genitalia, since females with disorders of this region are managed by gynaecologists. The examination is best performed with the patient in the supine position. Phimosis (narrowing of the preputial orifice such that the prepuce cannot be retracted over the glans) is common in uncircumcised males and often causes infection (balanitis) and meatal stricture. The majority of penile tumours are confined to the glans penis and this region should always be inspected in patients with a history of bloodstained discharge. Initially one should establish that the patient has two palpable testes. If only one testis is palpable, palpation of the groin may reveal an ectopic testis (usually in infants and children). The impalpable testis may of course be in the inguinal canal or the abdominal cavity (undescended testis). Scrotal swellings may originate from disease of the testis and epididymis and their coverings or result from a swelling (an indirect inguinal hernia) that descends to, and in time occupies, the scrotum. Thus the first objective with any scrotal swelling is to determine whether one can get above it by approximating the tips of the two hands above the upper limit of the swelling (Fig. 1.24). If the examiner is unable to establish this, the swelling is inguinoscrotal and caused by a large indirect inguinal hernia.

The common swellings encountered in the scrotum are hydrocele, inflammation of the testis and epididymis (epididymo-orchitis), and tumours of the testis (seminomas and teratomas). Torsion of the testis presents acutely with a very painful tender swelling and may be very difficult to distinguish from epididymo-orchitis. A hydrocele is a collection of fluid in the tunica vaginalis and therefore surrounds the testis, which thus becomes difficult to palpate. The swelling caused by a hydrocele is smooth and uniform, fluctuates and is brilliantly transilluminable. Cysts of the epididymis (multiloculated epididymal cyst, spermatocele) are not surrounded by fluid and for this reason are felt as swellings above and behind the testis, which is also easily palpable in this situation. Because of the septation, multiloculated epididymal cysts have a characteristic ‘Chinese lantern’ appearance on transillumination. Testicular tumours form heavy painless swellings of the testis and may be surrounded by a lax secondary hydrocele that does not, however, obscure their presence. When suspected, palpation of testicular tumours should be gentle to minimize the risk of dissemination of these malignant tumours. As the lymphatic spread from these tumours goes straight to the para-aortic lymph nodes, palpation of the abdomen for masses on either side of the umbilicus should be conducted.

Rectal examination Examination of the abdomen is incomplete without a rectal examination. For this purpose, the patient is most commonly positioned in the left lateral decubitus position, although some prefer the knee–chest position. Inspection The examination starts with inspection of the perineum for external skin tags, perianal inflammation, sinuses, fissures, induration medial to the ischial tuberosity (base of the ischiorectal fossa). Digital examination Digital examination of the rectum is performed in both the elective situation and patients with an acute abdomen. The actual rectal examination is carried out with a lubricated gloved hand. The tip of the index finger is placed inside the anal canal and directed initially towards the umbilicus before turning posteriorly towards the sacral concavity. Deep rectal tenderness is encountered in acute appendicitis, salpingitis and peritonitis. A ballooned empty rectum may be found in patients with small-bowel obstruction. Alternatively, in patients with large-bowel obstruction due to severe constipation, a mass of impacted faeces is encountered.

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Figure 1.26 Gangrene of great toe in an elderly patient with peripheral vascular disease who presented with rest pain.

Figure 1.25 Varicose veins.

In the elective situation, the rectal walls (anterior, lateral and posterior) are first felt for mucosal lesions (polypoidal growths, ulcers, etc.). The prostate gland is examined through the anterior wall. Normally, it should be possible to move the rectal wall over the prostate gland. The median sulcus between the two lobes of the prostate gland is also palpable. In benign disease the prostate may be enlarged or fibrotic, whereas in cancer of the prostate the gland feels craggy with loss of the normal outline and infiltration of the anterior rectal wall. No other structure should be palpable through the rectal walls. Ovaries and tubes are felt laterally only when enlarged and pathological. Tumour deposits in the pelvic peritoneum may be felt as a hard shelf anteriorly. When the digital examination is complete, the glove is inspected for the presence of blood and a Haemoccult test performed before the glove is discarded.

Examination of the limbs Aside from tumours (skin, soft tissues and bone), the limbs are examined for disorders of the locomotor system (see Chapters 37, 40 & 41), the peripheral nervous system (see Chapter 40) and the vascular system (see Chapter 37). Detailed descriptions of the clinical examination of the limb are given in these chapters. Common conditions

Figure 1.27 Primary lymphoedema of the legs in a 28-yearold man.

include varicose veins (Fig. 1.25) and peripheral vascular disease due to acute or chronic vascular insufficiency (Fig. 1.26). Lymphoedema, which is caused by primary (Fig. 1.27) or secondary disorders of the lymphatics (e.g. after radical surgery or radiotherapy), is less frequent. Peripheral nerve injury is a relatively common complication of trauma and produces characteristic clinical signs (discussed in detail in Chapter 40).

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Orthopaedic examination Examination of the hip Look: for scars, muscle wasting or any other skin changes such as psoriasis which may be associated with underlying joint disease. Observe how the patient walks – their gait. Many patients with hip disease have a short stride and limp with either an adduction deformity, dipping of the pelvis due to poor abductor muscle function or a combination of these two. This characteristic style of walking is sometimes summarized as an 'antalgic' gait. Feel: there is little to feel around the hip but it helps to know the surface marking of the femoral head. It lies halfway on a line between the anterior superior iliac spine and the symphysis pubis and approximately 2–3 cm more distal to this midpoint. Is the shortening (a) above or (b) below the knee.

Measure leg length: true length (a) from medial malleolus to anterior superior iliac spine. (b) Apparent length from medial malleolus to xyphisternum. Apparent shortening is caused by postral differences such as adduction deformity, pelvic tilt or spinal curvature.

(a)

(b) (b)

Move: First place the hip in a neutral position. In normal lying down the hip is slightly flexed to compensate for lumbar lordosis (a), by flexing the opposite hip the lordosis is removed by tilting the pelvis and then the hip lies in neither flexion or extension. This is known as Thomas' manoeuvre. If there is any hip deformity this test will reveal it (b). (a)

(b)

Having confirmed a neutral position we can now examine flexion, extension, abduction and adduction and internal and external rotation. Abduction: hold the pelvis with your non-moving hand. When the pelvis begins to move then further abduction is caused by spinal and pelvic tilt, not true hip motion.

Adduction

Internal rotation: although it is easier to elicit rotation in flexion of the hip, most functional rotation during gait occurs in the extended hip and so it is in extension we test this motion.

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Examination of the knee Look: for scars – accidental or surgical and uninfected or infected. Feel: for tenderness (unlikely in this joint as it is well covered with muscle). Move: the knee into its anatomical range. The knee can flex and extend and has limited rotation in association with flexion and extension. All other movements are abnormal and suggest instability of the joint. Look for wasting. Feel the joint line and associated anatomical features (a). Move in flexion (b) and ensure extension is full (c). Ensure the knee is intrinsically stable in flexion (d). (a)

(b)

(c)

(d)

Examination of the spine The spine can move depending on the anatomical region. In the cervical spine: most rotation occurs between occiput, atlas and axis. In the dorsal spine there is little movement because of the ribs. The lumbar spine flexes and extends with a small degree of rotation. The sacrum is fixed and joins spine to pelvic girdle. The examination consists of movement and examination of the nervous tissues associated with the spine. Examining flexion in the lumbar spine: choose an arbitary point near the top of the lumbar spine and hold a tape measure in place. Note the measure to a point such as the underwear waistband. Ask the patient to bend. Flexion of the lumbar spine can be measured in cms. This technique separates hip flexion from spinal motion.

Separate lateral flexion from pelvic tilt by feeling for pelvic motion with hands on the iliac spines.

Do a neurological examination of the lower limb myotomes and dermatomes concentrating on L4, 5 and S1. Nerve root Myotome Dermatome L4 Inversion Inner calf L5 Hallux extension Dorsum foot S1 Hallux flexion Outer border foot Reflexes Knee L2/3 Ankle L5/S1

Having established spinal movements do a neurological examination. First test straight leg raising to see whether the sciatic nerve is irritable or not. Ask the patient to lift the leg straight and then pull the foot upward to stretch the nerve. Pain right up the leg is a positive stretch test.

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Examination of the elbow and forearm Look: first observe the natural valgus posture and full extension (a). The elbow will flex until the hand touches the shoulder.

Rest the arm on a surface and test pronation (b) and supination (c). (b)

(a)

(c)

Examination of the hand in brief Look: at the posture of the hand. Notice how the fingers naturally curl and the thumb is at right angles to the fingers.

The intrinsic muscles extend and adduct and abduct the phalanges.

Move the joints systematically whilst thinking of the nerve supply. First examine the long extrinsic flexors: the profundus is a mass action muscle and so all are allowed to move whilst each tendon is tested.

The superficialis tendons each have a muscle belly. So by holding all the other fingers we isolate the tendons to the finger being examined. The superficialis flexes the proximal inter-phalangeal joint.

Adduction is also measured in extension. A piece of paper (or even better a ten pound note) will test how well the patient can grip in extension using intrinsic muscle power only. Extension of the metacarpo-phalangeal joints occurs through long finger extensors whch also aid in wrist extension. Don't forget sensation. Volar radial side is median, volar and palmar one and a half fingers are ulnar and the rest of the back is radial

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Examination of the foot and ankle Look: at the foot from the front and the back. Observe the arches, which denote normal posture. Observe the natural vagus orientation of the heel relative to the leg. Make sure you check the skin for rashes such as fungus and check the peripheral circulation.

To examine plantar and dorsiflexion at the ankle observe the motion whilst grasping the heel to exclude midfoot movement.

The mid-foot contributes to supination and pronation as well as dorsi- and plantarflexion of the foot complex.

Examine the hind-foot by moving the foot about the heel with the heel held in neutral to dorsiflexion so as to hold the talus in the mortise of the ankle joint. Now the subtalar joint will supinate and pronate the foot.

Clinical skills at a glance Definitions Symptom: a subjective perception (e.g. pain, nausea) suggesting a bodily defect, malfunction or disease. It is experienced only by the patient and cannot be perceived by others Sign: an objective indicator of disease (e.g. a lump, an enlarged liver) Medical history: the record of everything that is relevant to the patient’s health. The components of a standard medical history are presenting complaint, history of presenting complaint, assessment of risk factors, past medical history, social history, family history and systems review Physical examination: a structured process whereby the physician attempts to elicit physical signs in a patient by observation, palpation, percussion and auscultation History Common important symptoms in general surgery Pain • Site

• Radiation • Severity • Nature • Duration • Relieving factors • Aggravating factors • Associations Different types of pain: • Colicky pain: obstruction of a hollow organ, e.g. biliary, intestinal or ureteric colic • Somatic pain: inflammation of parietal peritoneum, e.g. peritonitis • Burning pain: mucosal injury, e.g. heartburn/reflux oesophagitis • Intermittent claudication: muscle ischaemia during exercise, e.g. peripheral vascular disease • Rest pain: critical limb ischaemia, e.g. peripheral vascular disease • Root pain: irritation of nerve roots, e.g. prolapsed intervertebral disc

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Indigestion/dyspepsia Types: • Peptic ulcer • Reflux • Malignancy • Non-ulcer • Gallbladder Indications for upper gastrointestinal endoscopy: • Frequent or persistent dyspepsia • Indigestion accompanied by other gastrointestinal symptoms • Indigestion with anorexia or weight loss • Helicobacter pylori-negative dyspepsia • First-onset indigestion in patient > 40 years Dysphagia • Indicates obstruction or motility disorder of the oesophagus • Should always be investigated • Painful dysphagia is called odynophagia Anorexia and weight loss • Often an indication of malignancy Vomiting • Frequency: gastroenteritis causes frequent vomiting • Does vomit contain bile? No bile in patients with pyloric stenosis • Does vomit contain food particles? Old food present in pyloric stenosis • Does vomit contain fresh blood? Blood that appears after the onset of forceful vomiting indicates an oesophageal tear • Does vomit contain ‘coffee grounds’ (blood partially digested by HCl and pepsin in the stomach)? • Are there other symptoms/signs (pain, nausea, constipation, headache, jaundice)? Altered bowel habit • Constipation or diarrhoea or both • Feeling of incomplete evacuation after defecation (tenesmus) • Blood per rectum should always be investigated • Foul-smelling diarrhoea that floats (steatorrhoea) indicates malabsorption • Foul-smelling dark tar-like motion (melaena) indicates proximal gastrointestinal tract bleeding

Physical examination General principles Examination of system or anatomical region using: • Inspection • Palpation • Percussion • Auscultation Specific examination Ulcer (area of discontinuity of normal surface epithelium) • Site: where is it? • Size: measure diameter in two dimensions • Shape: round, irregular? • Floor: what you see in the ulcer • Base: what is underneath the ulcer • Edge: sloping, punched out, undermined, rolled, everted? • Surrounding skin: inflamed? • Regional lymph nodes: enlarged? Lump/swelling • Site: where is it anatomically? • Plane of location: skin, subcutaneous tissue, muscle, bone, body cavity? • Size: measure diameter in two dimensions • Shape: is there a characteristic shape? • Inflammation: pain, redness, swelling, heat? • Mobility: does it move? Test in two planes • Consistency: solid, hard (?neoplasm), tense, soft, cystic, pulsatile? • Transillumination: positive indicates fluid, negative indicates no fluid Vascular swellings • Aneurysm (abnormal dilatation of an artery to more than 1.5 times normal diameter) (a) Expansile pulsation: bidigital examination in two planes (b) May be thrill on palpation • Saphena varix (varicose vein in proximal long saphenous vein) (a) Disappears on lying down (b) Fluid thrill may be elicited Hernial swellings (inguinal, paraumbilical, incisional) • Increase in size when intra-abdominal pressure is raised • Visible and palpable impulse on coughing (except femoral hernia: no impulse and do not reduce on lying down)

Abdominal wall movement Contour Surface markings Abnormalities Hernial orifices

Warm hands: yours not the patient’s! Light palpation followed by deep Acute abdomen: presence, extent, location of guarding or rigidity Non-acute abdomen: tenderness, organomegaly (liver and gallbladder, spleen, kidney), intra-abdominal masses (contraction of abdominal muscles accentuates intramural masses and de-accentuates intra-abdominal masses)

Use flat of hand Systematic: areola, four quadrants, axillary tail If lump detected: location, size, consistency, mobility in relation to skin and underlying muscle • Firm/hard, non-tender, indistinct margins: malignant • Firm, smooth, mobile: benign

Abdomen

Arms by side Arms over head Examine contour of breast, dimpling, skin changes, e.g. peau d’orange Nipple: retraction, discharge

Breasts

Lump(s) Lymph nodes Thyroid Trachea Transilluminate* large swelling (?cystic hygroma) Surgical emphysema feels like broken egg shells

Palpate apex, medial (chest) wall, anterior (pectoralis major) wall, posterior (subscapularis) wall Assess mobility

Swellings (?move with swallowing) Veins (?engorged) Surgical emphysema Jaundice, anaemia, cyanosis Facial asymmetry (?VII nerve palsy)

Head and neck (face, scalp, neck)

Palpation

Not used in axillary examination

Not used in breast examination

Carotid Thyroid (may hear a systolic murmur over the thyroid in advanced thyrotoxicosis)

Auscultation

Adjunct to palpation Bowel sounds: present, Determine tenderness, size increased, decreased, of enlarged organ or mass, tinkling distinguish liquid from gas Bruit (renal stenosis, Percuss from resonant to dull aneurysm), venous hum Ascites: fluid thrill and (liver tumour, portal shifting dullness hypertension) Succussion splash: splashing sound heard over stomach on shaking patient from side to side (pyloric stenosis)

Not used in axillary examination

Not used in breast examination

Not used often in neck May be useful for detecting large retrosternal goitre

Percussion

Axilla (always examine ?Mass visible as part of breast examination)

Inspection

Anatomical area

Examination of specific anatomical areas

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Patient standing Look for bulge in inguinal region More prominent on coughing (indicates inguinal hernia) Patient supine

Penis: phimosis (narrowing of preputial orifice), meatal stricture, balanitis (infection of prepuce), carcinoma of glans Scrotum: look for swelling, unilateral or bilateral

Lateral decubitus position Inspect perineum for skin tags, perianal inflammation, sinuses, fissures

Inguinal region

Scrotum and external genitalia

Anus and rectum

Percussion

Lubricated glove Use index finger for examination Gentle pressure on anus towards umbilicus. Then turn finger posteriorly into rectum. Examine anterior (prostate), posterior (sacrum) medial and lateral walls (ovaries and fallopian tubes may be palpable if pathological). Normally should not feel any structure other than prostate Tenderness: peritonitis, salpingitis, appendicitis Empty rectum: intestinal obstruction Rectum loaded with faeces: constipation Prostate: median sulcus between two lobes. Benign enlargement is smooth. Malignancy is hard, craggy and may be quite small

Are there two testes? If only one check external ring area Swelling: can you get above it (in scrotum) or is it coming down from inguinal region (indirect hernia)? Scrotal swellings: hydrocele (transilluminates* brilliantly), epididymal cysts (‘Chinese lantern’ on transillumination), epididymoorchitis (very tender), torsion of testis or appendix testis (also very tender), tumours (painless lump ± hydrocele)

Not used in examination of scrotum and testis

Palpate groin lump Not used in examination Determine position in relation to pubic of hernia tubercle: lump above and medial (inguinal hernia); lump below and lateral (femoral hernia, no cough impulse with femoral hernia) Lump disappears: direct inguinal hernia Lump persists: probably indirect. Is it reducible? Femoral herniae are never reducible Differential: lymphadenopathy

Palpation

Not used in examination of scrotum and testis

May hear bowel sounds over hernia

Auscultation

History-taking and Physical Examination Chapter 1

* Method of transillumination: place one end of a roll of paper against the swelling/scrotum and, while looking through the other end of the roll, apply a light to the swelling/scrotum adjacent to where the roll is applied. A brilliant suffusion of light indicates the presence of fluid.

Inspection

Anatomical area

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Basic Clinical Procedures 01 Introduction, 32 General principles, 32 Consent to treatment, 33 Aseptic technique, 34 Scrubbing up, 34 Gowning, 34 Donning gloves, 35

Local anaesthetics, 35 Performing a simple interrupted suture, 35 Excising a lesion, 36 Maintaining the airway, 36 Basic thoracic procedures, 38 Urinary catheterization, 40

Must know Must do Must know The medical and legal basis of informed consent Principles of sterile technique, scrubbing up and gowning Principles of airway management Must do Suture a minor skin wound Perform a male and female urinary catheterization Perform peripheral venous cannulation Perform peripheral arterial blood sampling under supervision Perform a nasogastric tube insertion Observe a chest tube insertion Observe a central venous line insertion Observe an upper gastrointestinal endoscopy Observe a rigid and flexible sigmoidoscopy

Introduction In many realms of surgical practice you will be called upon to perform procedures on your patients in the ward, in the emergency department as well as in the operating theatre. In patients who are conscious it is imperative to appreciate the importance of fully explaining the procedure and why the patient should have it. As with all skills, clinical procedures require practice. Often it is not appropriate to practise on patients at the start of your training; however, the development of medical simulations in the form of bench-top and computer models can now assist the learning process, so that the surgeon is familiar with a procedure before using it in clinical practice. Many medical schools now require an assessment of clinical skills in the form of objective structured clinical examinations (OSCEs). This chapter gives a step-by-step guide to performing 32

Rectal examination, 41 Taking blood from a patient, 42 Insertion of an intravenous cannula, 43 Arterial blood gas sampling, 45 Nasogastric tubes, 47 Diagnostic peritoneal lavage, 47

many of these skills along with their indications and possible complications.

General principles When performing any clinical procedure you should follow the principles listed below. 1 Always be courteous to the patients and the staff on the ward. 2 Confirm that the procedure you have been asked to do is in fact indicated. This may involve taking a history and examining the patient, as well as referring to medical notes and talking to ward staff. An excellent example is where you are asked to catheterize a man with urinary retention, where it would be wise to take a history and palpate for a bladder. 3 Explain to the patient what is about to happen in plain English in a private environment. Good communication about what you are going to do will relax the patient and makes performing the procedure easier. Obtaining verbal consent for some ward procedures and written consent for others is an important aspect of modern medical practice and is discussed later. 4 Gather all the pieces of equipment you require for the task before you start. Do not assume someone will do it for you. 5 You may need an assistant for some procedures (e.g. to pass things to you when sterile) or to act as a chaperone. 6 Make sure the surroundings are as private as the environment will allow. 7 If the procedure requires sterile conditions, first unwrap your sterile pack and open any necessary items onto it, then scrub up and don gloves. 8 Try to talk to your patient throughout the procedure. 9 When the procedure is finished make sure the patient understands what has happened and is not suffering any discomfort. Always cover your patients and never leave them exposed to the rest of the ward.

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10 Make sure you have personally disposed of any sharp items you have used and removed any rubbish you have created. 11 Finally, communicate what you have done to the nursing staff along with any instructions. Then document your findings, procedure and instructions in the medical notes.

Consent to treatment The role of the doctor is to advise the patient as to the best course of treatment within the clinical scenario presented – you cannot force treatment on any patient. It is important to appreciate that forcing treatment on a patient without their expressed consent amounts to assault and could result in litigation. It is also pertinent to remember that the majority of complaints to hospital trusts about clinical staff are directly related to poor communication. Patients should always have procedures explained to them as fully as possible, and to aid this many hospitals use patient information leaflets, the internet and even videos. Modern hospital care revolves around multidisciplinary teams, and occasionally the help of a specialist nurse practitioner eases the process of gaining consent. The consent a patient gives should always be informed consent, i.e. after you have thoroughly explained the procedure and its associated complications. It is always wise at the end of the consenting process to ask the patient if they have understood what you have said and if they have any further questions. Table 2.1 summarizes the consenting process. 1 Expressed consent is what we commonly think of as consent and can be written or verbal. For minor procedures such as taking blood or inserting a urinary catheter, verbal consent is sufficient. For more involved procedures such as surgery and endoscopy, written consent is required. It is always wise to document your discussion with the patient in the medical notes, especially if the procedure is complex. 2 Implied consent is a verbal agreement to undergo a medical procedure that should not have associated risks. A good example is a patient agreeing to undergo physical examination. No other person can give consent on behalf of a competent adult; however, emergency life-saving procedures can be performed as long as there is agreement among senior medical staff and the proposed measures comply with hospital policy.

The mentally ill If a patient is detained under the Mental Health Act, only treatment immediately necessary to preserve life can be performed without consent; otherwise, no one can give or withhold consent on behalf of a mentally incapacitated

Table 2.1 The process of obtaining informed consent 1 Introduce yourself to the patient 2 Ask the patient how much they understand about their diagnosis and proposed investigations and treatments 3 Re-emphasize the diagnosis and the natural history of the disease with and without treatment 4 Give the options available for treatment 5 Explain the purpose of a proposed investigation or treatment 6 Describe the likely benefits and probability of success 7 Describe any possible adverse effects 8 Explain the procedure using diagrams and patient information sheets 9 The help of another healthcare professional may aid the process 10 Ask the patient if they have understood what you have said and if they have any questions 11 Answer all questions honestly; if you cannot answer them, get someone who can 12 A person seeking consent from a patient should be suitably trained in the procedure in question, and should have knowledge of the procedure and its risks 13 Make sure the patient reads the consent form and signs it 14 Make sure you have signed the form and printed your name

patient. If the patient is unwilling to have treatment, then it should not be performed. Mentally ill patients have exactly the same rights as other patients.

Children Even in minors, simple bedside procedures can be performed with verbal consent, usually with the parent either present or aware that the procedures may happen. For more involved procedures, written consent is required from a parent or guardian for children under the age of 16. If a child refuses a treatment, a parent can still sign the consent to authorize treatment if it is in the child’s best interest.

Jehovah’s Witnesses These patients can cause significant dilemmas when their treatment requires the use of blood products. Surgeons must decide if they wish to proceed with the treatment within the boundaries set by the patient’s beliefs. If surgery is to be offered and blood products withheld, then patients must be fully counselled as to the possible dangers of their actions and must sign a specially prepared consent form noting all this. All discussion must be clearly documented in the notes. After discussion with the patient, the

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management plan should be communicated to all staff responsible for the patient.

Aseptic technique Aseptic technique is the maintenance of a sterile field throughout a particular procedure. In clinical procedures there are usually two sterile fields: the work surface and the patient. A sterile work surface is achieved by ensuring that: 1 base of work surface is clean (usually a trolley); 2 outer wrap of dressing pack and all required items are intact and in date; 3 inner part of dressing pack is wrapped in sterile paper; 4 hands are clean and hand-washing facilities/alcohol rub is available. Note that alcohol rub is a suitable alternative to hand washing if hands are clean. It may also be used immediately prior to gloving with sterile gloves. Procedure 1 Peel apart and remove dressing pack from outer wrap. 2 Open pack by handling from corners only. If possible undo first two paper folds at both sides and then open third fold away from you. The final fold will present the pack in the centre of a sterile wrapping (sterile field). It is important that only sterile items should be placed on the sterile work surface. Equipment must not be touched until hands have been cleaned and sterile gloves applied. 3 Add all other sterile goods to sterile work field. 4 Wash hands/use alcohol rub and apply sterile gloves using open method of application. 5 Request cleaning solution and any other solutions from assistant, e.g. sterile water/saline. Prepare dressing towel and prepare local anaesthetic for administration if necessary. If injecting local anaesthetic, it may be preferable to administer the drug before preparing the dressing pack in order to allow time for it to work. Clean hand–dirty hand principle This method is designed to reduce the possibility of contamination of the work surface to ensure that the hand in closest contact with the patient never touches the work field. It is achieved by placing the trolley closest to the clean hand (usually the dominant hand) and by passing items from the clean hand to the dirty hand without touching fingers/forceps. The clean hand/forceps is usually above the dirty hand/forceps when passing swabs, etc. to reduce the possibility of contamination. Choice of antiseptic cleansing agent The cleansing agent of choice must take into account wound/operative site and patient allergies. The most common solutions used are povidone iodine or chlorhexidinebased preparations. Antiseptics with an aqueous base are

suitable for most procedures. Alcohol-based solutions are generally used in specific circumstances, most commonly orthopaedics where there is little risk of the solution coming into contact with delicate membranes. Clean the patient methodically in one direction and discard used swab in clinical waste bag (yellow). Use a new swab each time until area and surrounding skin is thoroughly cleaned.

Scrubbing up Prior to scrubbing up you should have opened your gown and on to that opened your gloves. 1 Turn on taps until water is a comfortable temperature. Use elbow control taps if possible. Avoid excessive water pressure so that water does not splash off your arms while scrubbing. 2 Position hands upwards and higher than your elbows to encourage excess water to fall from the elbow into the sink. Wet hands and forearms from fingertips to elbows. 3 Using your preferred ‘scrub solution’ wash hands and forearms thoroughly for 1 min. Pay special attention to areas around the base of the thumb, between the fingers and the wrist areas, as these are often neglected or missed. Rinse again from fingertips to elbows. 4 Using a nailbrush, scrub each fingernail in turn on both hands with chosen scrub solution. The total time for this is 1 min. Rinse nails thoroughly. 5 Wash hands up to wrists only, with preferred solution. Pay special attention to each finger, web spaces, and base of thumb, palm and back of each hand. 6 Rinse thoroughly from fingertips to elbows, being especially careful not to get wet. A wet scrub suit will subsequently contaminate a sterile gown. 7 Dry both hands using the towels provided with the sterile gown. Ensure hands and forearms are dried from fingertips to elbows.

Gowning 1 Pick up the sterile gown with both hands. Identify yoke of neck to ensure that the gown is the right way up. 2 Step away from the trolley into an area where it is safe to open the gown without risk of touching an object or wall and thus contaminating the gown. 3 With the inside of the gown towards you, open it up by allowing it to drop downwards gently. 4 Slide hands and arms into the ‘arm holes’ of the gown by advancing the gown slowly up your arms. Do not be tempted to put the gown on to your shoulders as contamination of the sleeves could occur. 5 If gloves are to be donned using the closed technique, keep your hands inside the sleeves of the gown. If using the open technique, advance your hands out of the sleeves.

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6 An assistant will bring the gown on to your shoulders by touching the inside of the gown only. The assistant will also secure the ties at the back of the gown. 7 Ensure the section at the back of the gown is secured using the tapes on the side.

Donning gloves Closed method 1 With hands still inside sleeve of sterile gown, place thumb across palm of hand with palm facing upwards. 2 Pick up either glove and place it onto upturned palm. Ensure that the thumb of the glove is placed on top of thumb of hand and that the fingers of the glove are facing up your own arm towards your body. 3 Hold one side of glove cuff with sleeved hand and the other side with the free hand. 4 Bring glove over top of fingers and push fingers up into the glove. Using the free hand pull glove down onto your sleeved hand. 5 Once the glove is fairly secure, pull sleeve of gown downwards towards your body so that your hand advances from the sleeve of gown into the glove. 6 Position glove until it is comfortable. Do not allow the cuff of the gown to protrude from the glove as this area is not waterproof. 7 Repeat same procedure for other glove.

facilitating the use of higher doses of anaesthetic. Never use adrenaline when injecting into tissue supplied by an end artery (fingers, toes, ears, nose, penis). Doing so may cause ischaemia and is indefensible. 2 Explain to your patient that the anaesthetic will take away all pain but that they will still feel pressure. 3 Draw up the anaesthetic into a syringe using a green needle. Change to an orange needle for injecting. 4 Clean the skin, insert the needle with the bevel facing upwards and inject slowly, keeping the needle moving as you do so. 5 In the case of a skin lesion, remember to infiltrate deep to the lesion as well as all round it. 6 Allow several minutes for the anaesthetic to take effect before starting the procedure. 7 Document the type and amount of agent used, including whether it contained adrenaline.

Performing a simple interrupted suture (Fig. 2.1) 1 Select and open a suitable suture, wash your hands, put on sterile gloves and clean the wound. Table 2.2 shows how sutures are classified.

Correct

Excise

Open method 1 Pick up either glove from packet by touching only the inside of the cuff of the glove, which should be folded back upon it. 2 Advance hand into glove with the aid of your other hand, remembering to only touch the inside of the glove. 3 Using already gloved hand, pick up the other glove by touching only the outside of the glove at the cuffed area. 4 Advance ungloved hand into glove and with the aid of the other hand ensure that it is comfortable. 5 When turning cuff area down be careful that accidental contamination does not occur.

Undermine

Wide undermining

Closure without tension Incorrect

Jagged laceration

Local anaesthetics 1 Choose a local anaesthetic preparation. Lidocaine 1% is suitable for most purposes, although bupivacaine can also be used and has a longer action. You must be aware of the safe levels of anaesthetic to give to a patient: in adults, approximately 3 mg/kg of plain 1% lidocaine and 2 mg/kg of bupivacaine. The addition of 1 : 200 000 adrenaline to these anaesthetics causes vasoconstriction and decreases their systemic absorption, leading to longer effect and

Wide, untidy scar Figure 2.1 Performing a simple interrupted suture.

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Table 2.2 Classification of sutures and needles

Natural

Synthetic

Absorbable

Non-absorbable

Absorbable

Non-absorbable

Catgut Chromic catgut

Silk

Polyglycolic acid (Dexon) Polyglactin (Vicryl) Polydiaoxanone (PDS)

Nylon (monfilament) Polypropylene (monofilament) Mersilene (braided polyester)

Suture size

Needle types

10/0 9/0 Smallest

8/0

7/0

6/0

5/0

4/0

3/0

Shape

Point

Curved: quarter/half circle Straight J-shaped

Cutting Reverse cutting Tapered Round bodied Blunt

2 Grasp the needle with the tip of the needle holder, twothirds of the way from the needle’s point to where the suture is attached. 3 Steadying the skin with dissecting forceps, take a bite through the full thickness of the wound edge with the needle. The needle should follow the line of its curvature as it passes through the tissue. 4 Remove the needle and remount it in the needle holder before taking a corresponding bite on the other side of the wound. 5 Do not touch the needle with your fingers or you may cause a needlestick injury. Hold it with toothed forceps while repositioning it in the needle holder. 6 Pull the suture through until only a short free end protrudes. 7 Tie a reef knot, ensuring that the knot is not too tight. 8 Cut both ends of the suture, but not so short that they will be difficult to identify during removal. 9 The wound should be dressed and advice given to the patient about care of the wound and when sutures should be removed (Table 2.3).

2/0

1/0

4 5 Largest

Excising a lesion 1 Mark a 2-mm margin around the lesion. This will provide adequate removal if the lesion turns out to be malignant. 2 Design an elliptical incision that encompasses the lesion. The ratio of length to width should be 3 : 1. Ensure that the long axis lies parallel to the line of relaxed skin tension (Langer’s lines, Fig. 2.2). Mark the incision with a felt pen. 3 Infiltrate with local anaesthetic. 4 Holding the scalpel blade at right angles to the skin, make a decisive incision along the marked lines. 5 Ensure that the incision is adequate in all three dimensions. 6 Remove the lesion and send to histology. 7 Close the wound with interrupted sutures.

Maintaining the airway Maintenance of an airway is a basic skill that all doctors should know. It is a life-saving procedure and always comes first in many treatment algorithms.

Table 2.3 When sutures should be removed*

Simple manoeuvres and airways Head and face: 3–5 days Arms and hands: 7–10 days Chest: 7–10 days Abdomen: 7–10 days Lower limb/feet: 10–14 days * Patients on long-term immunosuppressive drugs may require longer before sutures are removed.

Maintaining the airway first involves removal of debris and vomitus from the mouth. Then either a chin lift or jaw thrust should be performed; in this position the patient can be adequately ventilated. The use of simple airway adjuncts can also aid maintenance of an airway. The two most common airways are the oropharyngeal (Guedel) and nasopharyngeal. Oropharyngeal airways come in a

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Figure 2.3 Laryngeal mask airway.

an associated inflatable cuff that lies over the entrance to the larynx like a cup. Under direction a laryngeal mask is easily positioned and is kept in place by inflation of the cuff. Despite this cuff, a laryngeal mask is not a definitive airway because it does not protect the patient from aspiration. However, it is an effective method of ventilating the patient and is particularly useful in day-case surgery.

Figure 2.2 Langer’s lines.

variety of sizes; the most appropriate for the patient is found by measuring the distance from the angle of the mouth to the angle of the jaw. They are inserted upside down and twisted so that the airway does not impinge on the palate. Nasopharyngeal airways have a similar function but are inserted through the nostrils.

How to insert a laryngeal mask (Fig. 2.3) 1 Select laryngeal mask size 3 for women and 4 for men. 2 The cuff is deflated and lubricated. 3 The patient’s head is extended and the cuff pushed over the back of the tongue. 4 The cuff is inflated. 5 Correct placement is confirmed by adequate bilateral expansion of the lungs and bilateral breath sounds.

Endotracheal intubation Mask ventilation If the patient has a stable airway, high-flow oxygen can be provided by means of a rebreathing bag. If the patient needs to ventilated and an endotracheal tube cannot be inserted, the patient can be ventilated using a bag and mask (Ambu bag). With this procedure it is very important to establish a good position for ventilation, i.e. chin lift and jaw thrust, and to ensure that there is a good seal between the mask and the patient’s face.

Invasive airways If a more secure airway is necessary, then invasive devices are required.

Laryngeal mask This device is a recent development in airway management. It consists of a tube for ventilating the patient, with

Intubating the patient with an endotracheal tube is an example of a definitive airway because it not only facilitates adequate ventilation but also protects the lungs from aspiration when the balloon is inflated. The method is indicated in: cardiorespiratory resuscitation; surgery where aspiration is a risk; elective ventilation patients transferred to intensive care; patients who cannot protect or maintain the airway, e.g. unconsciousness following head injury.

• • • •

How to insert an endotracheal tube (Fig. 2.4) 1 Pre-oxygenate the patient using a bag and mask. 2 Tilt the patient’s head back into full extension. 3 Insert the blade of the laryngoscope into the mouth to the right of the midline and sweep the tongue to the left. 4 Advance the instrument into the vallecula and lift up. Take care not to rock on the teeth.

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Figure 2.4 Endotracheal intubation.

Thyroid cartilage Cricothyroid membrane Cricoid cartilage Thyroid isthmus

Figure 2.5 Site of a surgical cricothyroidotomy.

5 Take an appropriately sized lubricated endotracheal tube (7–8.5 for women, 8–9.5 for men) and when the vocal cords are visible insert the tube through them. 6 Inflate the cuff on the endotracheal tube. 7 Attach to a ventilation bag. 8 Check the tube is in the correct position by inspecting the chest for symmetrical rising, bilateral breath sounds and absence of bubbling in the stomach. 9 Secure the tube with a tie. 10 Attach the patient to the ventilator.

Cricothyroidotomy In an emergency situation when an airway cannot be established by any of the methods described, the quickest, easiest and safest way to proceed is to perform a cricothyroidotomy. In this procedure, access to the airway is gained via the cricothyroid membrane. Access can be achieved using a large needle (needle cricothyroidotomy) or via an incision (surgical cricothyroidotomy) (Fig. 2.5). Needle cricothyroidotomy is easier to perform and is more useful in paediatric cases; however, the technique has the disad-

vantage that the patient has to be connected to an oxygen jet insufflator. This causes the patient to retain carbon dioxide as a jet insufflator is not a means of ventilation. Surgical cricothyroidotomy allows the placement of a definitive airway into the trachea, thereby facilitating adequate ventilation and protection of the patient’s airway.

Basic thoracic procedures Tube thoracostomy The insertion of a chest tube into the pleural space is another life-saving procedure that may be performed on the ward or more commonly in the emergency department. Chest tubes are also inserted in a more elective fashion at the end of cardiac or thoracic surgery. In general the reasons for placing a chest tube into the pleural cavity are to: drain air from a pneumothorax; drain blood from a haemothorax; drain fluid from a pleural effusion; drain pus from an empyema.

• • • •

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6 6

5 6 7

7 Figure 2.6 Insertion of a chest drain.

How to insert a chest tube Equipment Chest tube (size 28–36F) Sterile pack and antiseptic Scalpel Sterile gloves Two heavy silk sutures Local anaesthetic Long curved haemostat Tube clamps Drainage tubing and bottle Dressing tape

• • • • • • • • • •

Procedure When inserting the chest tube on the ward this can be safely achieved by approaching the chest through the sixth intercostal space, slightly anterior to the midaxillary line on the affected side. A chest tube can be inserted through the second intercostal space in the midclavicular line, but is more difficult to do, more inconvenient for the patient and leaves significant visible scarring. 1 Explain the procedure fully to the patient as it can be uncomfortable. 2 Position the patient in a recumbent position with the arm on the affected side placed behind the head. Then prepare the skin with antiseptic.

3 Infiltrate the area with local anaesthetic, including deep into the track where the chest tube is going to pass. 4 Make a 3-cm incision along the line of the sixth or seventh rib, down to the bone. 5 Take the long curved haemostat and tunnel upwards towards the fifth intercostal space; continue dissecting through the intercostal muscles at this point. 6 Continue dissecting with the haemostat until a loss of resistance is felt when the pleural space is entered. 7 Remove the clamp and insert a finger through the track into the pleural cavity and sweep around the entry site to remove any adhesions tethering the lung (Fig. 2.6). 8 Take the chest tube, remove the trocar and discard, attach the long haemostat to the end of the tube and push it through the track into the pleural cavity. 9 For drainage of air, place the tube in the apex of the cavity; for fluid or pus, the drain may need to be directed basally. Occasionally, two tubes may be required. 10 Suture the drain to the skin with the heavy silk suture. Also place a pursestring suture, which will be used to close the entry site when the drain is removed. 11 Attach the drain to the drainage tubing and the bottle with underwater seal mechanism. 12 Apply an occlusive dressing around the tube and attach the drainage system to gentle suction.

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13 The patient should be sent for a chest X-ray to confirm position and to check for lung re-expansion.

Needle thoracocentesis The two main indications for performing a needle thoracocentesis on the ward are to drain air and to drain fluid.

Draining air The main indication for draining air with a needle is a tension pneumothorax, where the procedure will save the patient’s life. If tension pneumothorax is suspected, a large-bore cannula is inserted into the second intercostal space in the midclavicular line. This will decompress the pleural space and convert a tension pneumothorax into a simple pneumothorax, until a formal chest tube is inserted.

Draining fluid Occasionally a large pleural effusion can lead to respiratory distress on the ward. Removal of the fluid helps respiration and also allows a sample of the fluid to be analysed in order to identify the cause of its accumulation. Equipment Large-bore cannula Local anaesthetic Three-way tap 50-mL syringe Collecting jug

• • • • •

Procedure 1 After explaining the procedure to the patient, position them so they are sitting forward over a pillow. 2 Mark the site of entry in the posterior intercostal spaces; the level is determined by the size of the effusion. 3 Infiltrate the area with local anaesthetic. 4 Insert the cannula at 90° to the skin, until a loss of resistance is felt. 5 Attach a three-way tap to the end of the cannula and aspirate the fluid with the syringe. When it is full, close the three-way tap so that fluid can be emptied into the jug. 6 Continue this process until fluid is drained. Drainage of fluid should not exceed 1000 mL in one sitting to avoid massive sudden mediastinal shift and subsequent pulmonary oedema. 7 The needle is removed and an occlusive dressing applied. 8 A chest X-ray should be taken. 9 The fluid drained should be sent for cytology, biochemistry (protein estimation) and bacteriological culture.

Urinary catheterization Commonly patients are catheterized in order to relieve urinary obstruction and for monitoring purposes, e.g. in shock or after surgery. Catheters are also used in the unconscious and immobile patient. It is also important to remember that catheterization can be short term, as is usual, or longer term, e.g. incontinence.

How to insert a urinary catheter into the male Equipment Catheter size 14 or 16 Fr (catheters can be made of either latex or silicon and can also have an additional port for irrigation) Catheter bag Catheterization pack Sterile saline Lidocaine gel (with introducer nozzle) Water to inflate catheter balloon Sterile gloves

• • • • • • •

Procedure 1 Confirm the diagnosis and explain to the patient what you are about to do and why. At all times ensure that the patient knows what is happening. 2 Choose an appropriately sized Foley catheter and check the capacity of its balloon. 3 Gather all the materials you will need. 4 Open the pack onto a trolley. Then open all the other items onto the sterile field, being careful to avoid contaminating it. 5 Roll up your sleeves (if necessary), wash your hands carefully and put on sterile gloves. 6 Prepare a sterile paper drape by cutting a hole with scissors. 7 Grasp the penis gently but firmly with a swab held in your non-dominant hand. Clean the penis with a single pass of each lotion-soaked swab, moving from meatus towards the perineum (Fig. 2.7). 8 Pass the drape over the penis, thereby providing a sterile field. 9 Gently insert the nozzle of the anaesthetic gel into the meatus and firmly squeeze the tube. Gently press the penile urethra to stop the gel oozing out. Wait several minutes for the anaesthetic to take effect. 10 Open the catheter’s inner covering but ensure that the tip does not become unsterile. Insert it gently into the meatus and feed it steadily in. Position a receiver under the free end of the catheter. Only when urine flows out is it safe to inflate the balloon with the specified amount of fluid.

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5 Insert the catheter as in step 10 above but remembering that the female urethra is much shorter than its male counterpart. 6 Follow steps 10–13 of the male catheterization procedure (see above).

Suprapubic catheterization

Figure 2.7 Technique for insertion of a urinary catheter.

11 Attach the catheter to the leg bag, ensuring that the bag’s emptying port (if present) is in the ‘off’ position. Failure to do this will lead to urine-soaked clothes. 12 Remove the drape. 13 Ensure that the prepuce (if present) is pulled down over the glans. Failure to do this may result in a painful paraphimosis. 14 Clear away all debris. Ensure your patient is comfortable and that you have written up the necessary instructions for the ward staff.

How to insert a urinary catheter into the female Remember that it may be difficult to identify the external urethral orifice in the female, especially if the tissues are swollen. It is surprisingly easy to pass a catheter into the vagina instead of the urethra. Only by seeing urine flow through the catheter can you be sure that you have performed the procedure correctly. 1 Follow steps 1–6 of the male catheterization procedure (see above). 2 Swab the perineum, holding each lotion-soaked swab in your non-dominant hand and swabbing from urethra to anus. 3 Cover the perineum with a fenestrated drape. 4 Identify the external urethral orifice and insert local anaesthetic gel. Wait for this to take effect.

As the bladder enlarges it fills a space between the abdominal wall and the peritoneum, thereby facilitating its puncture. Rather than being a second-line treatment after urinary catheterization, the suprapubic route is favoured by many urologists because the prostate is not damaged prior to treatment. There are different types of suprapubic introducing sets, although the procedure is the same. 1 The presence and position of the bladder is confirmed by clinical examination. 2 The skin two fingers’ width above the pubic symphysis is infiltrated with local anaesthetic. 3 A small incision is made above the symphysis pubis. 4 An introducing trocar, incorporating either a sheath or the catheter itself, is pushed into the bladder. 5 This is confirmed by the loss of resistance and the aspiration of urine. 6 For catheters introduced with a trocar and sheath, a standard Foley catheter is inserted into the bladder and the sheath removed. 7 Non-Foley catheters are secured with sutures to the skin. 8 The advantage of the Foley catheter is that a tract will form between the bladder and the skin, which allows easy change of catheter if it is required long term. 9 A sample of urine is taken for analysis and the catheter attached to the bag.

Rectal examination Digital rectal examination Equipment Gloves Lubricating jelly Swabs

• • •

Procedure 1 Ensure that the patient knows what you are going to do and why. Arrange for a chaperone to be present. 2 Place your patient in the left lateral position, with knees pulled up towards the chin and the back near the edge of the couch (Fig. 2.8). 3 Put on gloves and have lubricating jelly and a paper tissue within easy reach.

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light source is inserted into the anal canal pointing toward the umbilicus. The obturator is removed and the anal mucosa visualized. Syringes and banding devices to treat haemorrhoids can then be passed through its lumen.

Rigid sigmoidoscopy

Figure 2.8 Position of the patient for a digital rectal examination.

4 Lift the patient’s right buttock with your left hand and inspect the anus carefully, using a good light. 5 Put a little jelly on the pad of your right index finger. 6 Explain to your patient that they will feel pressure and probably a feeling like wanting to empty their bowels. 7 Place your finger on the anus. Do not force it in but wait patiently until you feel the sphincter relax. 8 Gently pass your finger through the anus, trying to form a mental picture of the anatomy as you do so. Watch your patient’s face throughout the procedure to detect if you are causing pain. 9 Gently insert your whole finger and sweep round the rectum systematically, feeling for abnormalities in the lumen, the rectal wall, the perirectal tissues and beyond. 10 To feel the prostate, sink down on one knee and pronate your wrist. Identify the prostate gland and assess its size and hardness and whether you can feel the midline sulcus. 11 In a female patient you will usually feel the cervix anteriorly. This is normal. 12 Remove your finger and examine the glove for traces of stool, mucus or blood. 13 Wipe any gel from the anus and perineum. 14 Ensure that your patient is comfortable and covered.

Proctoscopy A proctoscope is used to visualize the anal canal but can also be used to facilitate biopsies of the mucosa and is commonly used for the therapy of haemorrhoids. Following a digital rectal examination and with the patient in the left lateral position, the proctoscope with attached

The rigid sigmoidoscope is used to visualize the rectum primarily and occasionally the lower sigmoid colon. Sigmoidoscopes are available in reusable and disposable types; they are approximately 30 cm in length. For the sigmoidoscope to be used effectively requires the attachment of a lens and light source at the operator end of the device. Also to facilitate visualization, air is pumped through the sigmoidoscope to open the collapsed bowel using a bellows. 1 After explaining the procedure, the patient is placed in the left lateral position and a digital rectal examination is performed. 2 The lubricated sigmoidoscope is then gently inserted into the anus pointing towards the umbilicus. The obturator is then removed and air is passed through the tube into the anus to facilitate navigation. The sigmoidoscope should only be advanced into areas with a visible lumen otherwise there is a risk of perforation. 3 Inspect the mucosa for lesions, vascularity and friability and note at what distance from the anal verge these occur. 4 Any suspicious lesions can be biopsied with a long biopsy forceps passed through the lumen of the tube. 5 Note the extent of your examination in centimetres and withdraw the scope gently, inspecting as you go. 6 Release any insufflated air and wipe the patient.

Taking blood from a patient When taking blood you must obviously know which tests are required. This means that you must use the correct bottle with the correct additive for different tests. The chart on page 43 shows the colour coding of different bottles and their use. Equipment Blood-taking device (vacutainers, syringe, butterfly) Tourniquet Alcohol swab Cottonwool ball Plaster Blood forms

• • • • • •

Procedure 1 Complete the blood forms for the tests required. 2 Gather your equipment; a vacutainer system is described here.

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Blood collection tubes (Vacutainer system) EDTA liquid

Forms calcium salts to remove calcium

Haematology (FBC) and blood bank (crossmatch): gently invert bottle after filling to prevent clotting and platelet clumping

Sodium citrate

Forms calcium salts to remove calcium

Coagulation tests (INR), full draw required

Plasma separating Anticoagulates with tube (PST) with lithium heparin; plasma is lithium heparin separated with PST gel at the bottom of the tube

Chemistries

None

Serum separator tube (SST) contains a gel at the bottom to separate blood from serum on centrifugation

Chemistries, Immunology and Serology

None

Blood clots, and the serum Chemistries, Immunology and is separated by Serology, some blood bank centrifugation profiles

Sodium fluoride and potassium oxalate

Antiglycolytic agent For glucose levels preserves glucose for up to five days

Sodium citrate (buffered)

Forms calcium salts to remove calcium

Erythrocyte Sedimentation Rate (ESR)

Correct order of draw (as recommended by the National Committee for Clinical Laboratory Standards, 1991 Guidelines Reference H3A3) • Blood culture (Bacteriology) • Plain or serum (no additives) • Coagulation profiles • Other additive tubes, e.g. EDTA, lithium heparin, glucose

3 Introduce yourself to the patient and explain what you are going to do and why. 4 Attach the tourniquet to the upper arm of the patient and ask them to open and close their hand. 5 Select a vein; usually the antecubital fossa is the best. Also make sure you are not taking blood from an arm that has an intravenous drip running into it. 6 Assemble the vacutainers. 7 Swab the selected vein with the alcohol swab. 8 Warn the patient you are about to start and insert the needle at 30° to the skin. 9 Insert a bottle into the vacutainer barrel; if the needle is in the vein, the bottle will fill with blood. If not, adjust the needle. 10 Fill all the bottles required. 11 Remove tourniquet.

12 Place cottonwool ball over needle and withdraw it rom the skin; the patient should apply pressure for 5 min. 13 Dispose of sharps. 14 Label bottles fully with name, hospital number, date of birth and date of sample. Place them with the completed forms in a bag for transfer to the laboratory. 15 Apply a small plaster to the patient’s arm.

Insertion of an intravenous cannula Equipment Intravenous cannula (for sizes refer below): blue, 22G (very small) pink, 20G (small) green, 18G (average) grey, 16G (large) brown, 14G (very large)

•

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• Tourniquet flush or intravenous fluid with giving set • Saline Securing dressing • Sharps bin • Procedure 1 Gather your equipment, introduce yourself to the patient and explain what you are about to do. 2 Apply a tourniquet to upper arm and ask the patient to open and close their hand. 3 Select a vein that is palpable and straight; if the cannula is for long-term use, it is best situated away from joints, e.g. lower forearm cephalic vein. In an emergency, select a large-bore cannula in an antecubital fossa vein. 4 Take the cannula, remove the sheath, open the wings and introduce the needle into the vein at 30° to the skin. Once the needle is in the vein there will be a visible flashback in the barrel of the needle. 5 Slide the cannula into the vein over the needle while removing the needle. 6 Remove the tourniquet, remove the needle and put white cap on the end of the cannula. 7 Dispose of sharps. 8 Apply a dressing to the cannula. 9 Flush the cannula with saline. 10 Eliminate any air bubbles from the giving set of the intravenous fluid and then attach it to the cannula. 11 Set infusion rate and note time infusion started.

Venous cut-down If emergency intravenous access is required and no other sites are available, then a venous cut-down can be performed. The most consistent and easily accessible large vein is the long saphenous vein; alternative sites include the antecubital fossa and the wrist. Aseptic technique should be used. 1 Infiltrate the skin with local anaesthetic. 2 A transverse incision is made 1 cm above and anterior to the medial malleolus. 3 The vein is gently dissected out; to control the vein, two ligatures are passed under it. 4 The distal ligature is tied; the other is left untied until a cannula is inserted. 5 A large-bore cannula is inserted through the skin and into the vein; the proximal ligature is then tied to keep the cannula in place. 6 The skin is closed and the cannula secured with a further suture and a dressing.

of central venous pressure; • measurement infusion of irritant drugs, e.g. amiodarone, dopamine, • streptokinase; of parenteral nutrition; • infusion measurement of pulmonary artery wedge pressure; • infusion of chemotherapeutic agents; • placement of pacing wires. • It is important to note that although fluids can obviously be given through a central line, it is not the method of choice if fluid needs to be infused quickly as central lines tend to be long and thin. Central venous access may be required for a short period of time or for longer-term therapy such as chemotherapy. If long-term central venous access is required, then a tunnelled central line should be inserted (e.g. Hickman line). Non-tunnelled central lines are changed every 7 days to minimize infection.

Insertion of the central line In general, most clinicians approach the central veins from either above or below the clavicle (Fig. 2.9). In the supraclavicular approach the preferred vein to cannulate is the right internal jugular vein because it is easily accessible, has a straight path to the right atrium and possible injury to the thoracic duct is eliminated. Also, with the supraclavicular approach there is less risk of damaging the pleural cap and causing a pneumothorax. Hence it should be the method of choice for the less experienced practitioner. The infraclavicular or subclavian approach tends to be used by more experienced practitioners. However, there is an increased risk of pneumothorax and should not be used in patients with clotting abnormalities as it is difficult to stem bleeding from the subclavian vein if haemorrhage occurs. Nevertheless, this approach makes nursing care of the central line easier and is more comfortable for the patient.

Central venous cannulation Access to the central veins is a common requirement in modern practice and is important for:

Figure 2.9 Insertion of a central venous cannula: internal jugular approach.

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Equipment Central line set: central venous catheter syringes introducing wire Saline Local anaesthetic Suture material Antiseptic Transparent dressing Giving set Sterile pack Sterile gloves

• • • • • • • • •

cannulation needles scalpel blade track dilator

Procedure 1 You will need an assistant for this procedure to pass you items while you are sterile; the maintenance of sterility is extremely important, especially when placing lines on the ward. 2 Explain the procedure to the patient. 3 Remove the pillows from under the head and tilt the patient 30° head down. Some patients may not tolerate this, especially those in heart failure. 4 Place a bag of fluids under the right shoulder to bring the vessels forward. 5 Expose the area and turn the patient’s head to the left. 6 Scrub and don sterile gloves. With patient in position paint the area where you are going to insert the central line with antiseptic. 7 Inject local anaesthetic into the skin and deeper tissues at the cannulation site. internal jugular approach (Fig. 2.9) The right internal jugular vein runs from the base of the skull anterolaterally in the carotid sheath below the sternomastoid muscle to meet the innominate vein and thence into the superior vena cava. The vein can be approached either high or low. In the high approach, the landmark for cannulation is half distance along a line between the sternal head of the clavicle and the mastoid, and lateral to the sternomastoid muscle. Enter the skin with a needle connected to a syringe with saline. Advance the needle deep to the sternomastoid and point towards the suprasternal notch until you freely aspirate blood. In the low approach to the vein, the landmark is the triangle formed by the sternal and clavicular heads of the sternomastoid; the vein lies between them. subclavian approach (Fig. 2.10) In this approach, the entry point of the needle should be 3 cm below the midpoint of the clavicle, with the needle angled towards the jugular notch. Occasionally, the needle may abut against the clavicular periosteum; this will be painful, so it is important to anaesthetize down to the clav-

Figure 2.10 Insertion of a central venous cannula: subclavian approach.

icle. If the clavicle is encountered, then gentle downward pressure should be applied to the needle to help it enter the vein. seldinger technique The Seldinger technique is common to whichever method of insertion is used. After the vein has been cannulated, a flexible wire with a leading J end is inserted into the needle and fed through the vein towards the right atrium. Electrocardiographic monitoring helps gauge whether the wire has been inserted too far and is impinging on the myocardium. When the wire has been placed, the needle is removed over the top of it. The track formed by the wire is then dilated by making a small incision over the wire and placing a dilating device over it. The central venous catheter is then fed into the vein over the wire; the wire is removed through the cannula. The cannula is aspirated and flushed with saline to check it is working, is sutured in place and a transparent dressing applied, and a giving set attached to the line. Once the patient has received a chest X-ray to check position and exclude a pneumothorax, the line can then be used. The complications of central line insertion are shown in the box below. Complications of central line insertion Immediate Haemorrhage Misplacement Pneumothorax Early Infection Blockage Late Scarring Myocardial damage

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point that is recorded as the CVP. A normal CVP is approximately 5 cm H2O. If the patient is hypovolaemic, right atrial pressure will be lower thereby allowing more fluid from the manometer to run into the heart, leading to low or even negative CVP values. When there is heart failure the opposite occurs and the CVP remains high.

Arterial blood gas sampling Femoral artery Equipment Arterial blood gas syringe with heparin Alcohol swab Swab 1% lidocaine local anaesthetic Syringe and blue needle for anaesthetic

• • • • • Figure 2.11 Measurement of central venous pressure using a manometer.

Measuring central venous pressure (Fig. 2.11) Monitoring of central venous pressure (CVP) is commonly required in patients who need intensive fluid management or who may have circulatory failure. The CVP can be measured using a transducer or a water manometer. It is essential that you are competent at measuring the CVP, commonly performed in the ward using a manometer. A giving set, three-way tap and manometer are attached to the central venous catheter. The manometer is attached to a drip stand that has a scale in centimetres and a side arm with a spirit level. The CVP must be referred to the level of the right atrium; this is called the zero point and must be the same for all subsequent readings. With the patient lying flat, the zero point is indicated by aligning the spirit level with the sternal angle; alternatively the point where this level crosses the midaxillary line can be used. The zero point should be marked on the scale with a permanent marker. To measure the CVP the manometer is primed with fluid from a reservoir bag, the zero point is set and the manometer levelled. The three-way tap is then opened to allow fluid to run into the patient. The fluid level fluctuates with the respiratory cycle, but will settle around a

Procedure 1 The patient should be supine with the groin and leg extended and slightly abducted. 2 Locate the femoral artery, halfway between the anterior superior iliac spine and pubic symphysis, 2 cm below the inguinal ligament. 3 Clean the skin directly over the artery with an alcohol swab. 4 Raise a bleb of local anaesthetic. 5 Fix the artery between two fingers while inserting heparinized syringe and needle at 90° to skin. 6 Slowly advance the needle until there is free flow into syringe. 7 Withdraw needle and apply pressure for 5 min. 8 Cap the syringe and place in ice if immediate analysis is not possible.

Radial artery Equipment Arterial blood gas syringe with heparin Alcohol swab Swab 1% lidocaine local anaesthetic Syringe and blue needle for anaesthetic

• • • • •

Procedure 1 Before the procedure perform the Allen test. 2 Occlude both ulnar and radial arteries digitally and allow the veins to drain all the blood. 3 Release the ulnar artery while keeping the radial artery compressed. 4 Hand colour should return in less than 5 s, indicating that there is sufficient collateral blood flow from the ulnar artery.

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Figure 2.12 Insertion of a nasogastric tube.

5 If the patient fails the Allen test, radial artery sampling should not be attempted. If the test is successful, place patient in supine position with wrist and thumb extended. 6 Place a rolled-up hand towel under the dorsal surface of the wrist. 7 Palpate the radial artery. 8 Clean the skin proximal to the wrist joint. 9 Using a 25G needle, raise a small bleb of local anaesthetic at the proposed entry site. 10 Insert the needle of a heparin-coated 2-mL syringe at 60–90° through the skin, ensuring avoidance of air in the syringe. 11 Palpate the radial artery proximally, using it to guide direction of the needle. 12 Arterial blood pressure will fill the syringe automatically. 13 Withdraw the needle and apply pressure for 5 min. Cap the syringe and place in ice if immediate analysis is not possible.

Nasogastric tubes Tubes inserted into the stomach via the nose are used for either drainage or feeding. The most commonly used nasogastric tubes are of the drainage type, are made of plastic and are called Ryle’s tubes. Tubes used for feeding, which are likely to be in place for a longer period of time, are thinner and made of silicon, which is softer and hence more comfortable for the patient and blocks less readily. It is very important to remember that passage of a nasogastric tube is contraindicated in patients with a head injury because of the risk of passing the tube through a fractured cribriform plate into the brain. If drainage of the stomach is required, an orogastric tube can be passed.

Insertion of a drainage tube Equipment Nasogastric tube made stiffer by storing in refrigerator Lubricating jelly Bladder syringe Drainage bag Securing tape Litmus paper

• • • • • •

Procedure 1 Explain to the patient that the procedure is not particularly pleasant and insertion of the tube may cause them to retch. 2 Inspect the nose for any obvious deformities. 3 Lubricate the tube. 4 Insert the tube into nostril pointing towards the occiput (Fig. 2.12). 5 Ask the patient to swallow, and as they do advance the tube. 6 To check the tube is in the stomach aspirate contents and test for acidity with litmus. Alternatively instil 30 mL of air with the bladder syringe and auscultate the epigastrium for bubbling. 7 Secure the tube to the nose and attach a drainage bag.

Insertion of a feeding tube Insertion of a feeding tube is similar to that described above, except that feeding tubes have a wire within them as they have insufficient rigidity for insertion into the stomach. An X-ray is taken of the epigastrium to check the position of the wire. When in the correct position the wire is removed, leaving the feeding tube in place.

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Diagnostic peritoneal lavage The main indication for performing diagnostic peritoneal lavage (DPL) is in a trauma situation where a haemodynamically unstable patient is suspected of haemorrhaging into the peritoneal cavity. Prior to starting the procedure the patient must have a stable airway, an orogastric or nasogastric tube placed in the stomach and a urinary catheter passed to drain the bladder after a normal digital rectal examination. Equipment Minor operation pack (must have retractors) Scalpel size 10 Heavy absorbable sutures Local anaesthetic Peritoneal dialysis catheter 1 L bag of normal saline

• • • • • •

Procedure 1 Scrub up as for a regular surgical procedure and don gown and gloves.

2 Prepare the abdomen with antiseptic and drape the patient. 3 You may need to infiltrate some anaesthetic into the skin infraumbilically, depending on the patient’s level of consciousness. 4 Make a 3-cm incision below the umbilicus in the midline and dissect down to the linea alba. 5 Divide the linea alba and place two sutures, one on each edge. 6 Insert the peritoneal dialysis catheter; aspiration of frank blood, faeces, urine or bile is a positive DPL and the patient requires a laparotomy. 7 If aspiration is negative, run 1 L of warmed normal saline into the abdomen. Then place the infusion bag on the floor to allow the fluid to drain back from the peritoneal cavity. 8 A positive DPL is indicated by a red blood cell count of greater than 100 000/mL or a white cell count of more than 500/mL, a raised amylase and the presence of bacteria. 9 The fascia is closed by tying the stay sutures together, and skin is closed with nylon sutures.

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Introduction, 49 Blood investigations, 50

Microbiology, 52 Imaging, 52

Must know Must do Must know Principles, values and uses of screening Indications and implications of commonly used investigations Cost and risk–benefit ratio of common investigations Normal values for commonly used laboratory tests Selective use of expensive imaging investigations Selective use of invasive investigations Must do Examine a blood film from an anaemic patient Examine a blood film from a patient suffering from a major surgical infection Examine a urine specimen from a patient with obstructive jaundice Visit the radiology department to witness a CT scan being performed Observe duplex scan (colour flow Doppler) examination of the carotid arteries Look down an endoscope in use

Introduction Throughout this book reference is made to investigations carried out in patients suspected of having various surgical disorders. Although specific investigations provide valuable information, their indiscriminate use constitutes bad practice; not only is it wasteful of resources but it may also put patients and staff at risk (e.g. contrast media may induce anaphylaxis). The risk to the patient correlates with the degree of invasiveness of the procedure and a spectrum of risk exists. This ranges from no risk when the examination is entirely non-invasive and has no known harmful adverse effects (e.g. ultrasonography) to considerable risk with invasive procedures (e.g. arterial puncture during arteriography may result in serious complications). In addition, there are risks to the staff, for example handling contaminated blood exposes staff to the risk

Endoscopy, 58 Measurement of function, 60

of disease transmission (such as hepatitis and acquired immunodeficiency syndrome, AIDS) and radiography staff have to be vigilant about exposure to radiation. Investigations may be classified into a number of large groups (Table 3.1). A key investigation is one that confirms or excludes a strongly suspected diagnosis and is always necessary, e.g. gastroscopy in a patient with a history suggestive of upper gastrointestinal bleeding. In contrast, routine or baseline haematological and biochemical tests are performed before surgery to establish normality or to obtain baselines. However, the ordering of baseline investigations, though widespread in hospital practice, is wasteful of resources and is gradually being replaced by selective testing based on clinical findings. One study found abnormalities on routine testing in only 0.4% of asymptomatic patients undergoing surgery. Thus, asymptomatic healthy young patients may have surgery without any investigations, while specific tests should be ordered on the basis of the clinical preoperative evaluation (including urinalysis). For example, urea and electrolytes are indicated when there is evidence of water and electrolyte depletion or renal disease, in elderly patients or in patients taking diuretics. A preoperative chest X-ray is indicated only in patients with cardiorespiratory disease or symptoms, in the elderly, in smokers, in patients with possible pulmonary metastases and in recent immigrants from countries where tuberculosis is still endemic.

Screening Investigations may be used for general population screening of common conditions or may be directed towards subpopulations known to be at increased risk of developing a condition. Before an investigation can be used as a screening tool, it is desirable that a number of criteria should be fulfilled. 1 The disease should be relatively common and have serious sequelae. 2 The condition should be identifiable at a stage where intervention is effective.

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Table 3.1 Investigations commonly used in the assessment of patients. Blood investigations Haematology Biochemistry Blood gas analysis Immunology Microbiology Imaging X-rays Barium studies Water-soluble contrast studies Cholecystography and cholangiography Intravenous urography, cystography Arteriography Venography Myelography Computed tomography Magnetic resonance imaging Ultrasound Nuclear medicine studies Endoscopy Function tests Pulmonary function Oesophageal motility Urodynamics Anorectal manometry Nerve conduction studies Vascular ECG Holter monitoring Echocardiography Duplex scanning Plethysmography Ankle/brachial pressure index

3 The investigation should be non-invasive and acceptable to patients to ensure good compliance. 4 The investigation used should identify all affected individuals (sensitivity) and avoid mistaken diagnosis in unaffected individuals (specificity). 5 The investigation should be relatively inexpensive. Few screening investigations fulfil all these criteria. The limitations of a particular investigation are quoted as the false-positive rate (mistaken diagnosis in unaffected individuals) and the false-negative rate (failure to identify all affected individuals). In some cases, there is debate as to whether earlier identification of the disease process

makes any difference to overall outcome, e.g. prostate cancer. The proof that is necessary can only be provided through randomized controlled trials of a screening procedure. Examples of screening investigations include mammography for women over 50 years of age, cervical smears for all sexually active women, prostate-specific antigen for prostate cancer, colonoscopy for relatives of patients with colorectal cancer, ultrasonography of the abdominal aorta for relatives of patients with aneurysms.

Blood investigations Haematology The standard investigation performed to assess the status of the elements in blood is the full blood count. The information derived from this investigation is given in the box below. Full blood count, normal values Haemoglobin Packed cell volume (PCV) (haematocrit) Red cell count Mean corpuscular volume (MCV) Mean corpuscular haemoglobin (MCH) White cell count (WCC) Platelet count

Male Female Male Female Male Female

12.5–16.5 g/dL × 109/L 11.5–15.5 g/dL × 109/L 0.42–0.53 0.39–0.45 4.4–6.5 × 1012/L 3.9–5.6 × 1012/L 80–96 fL 27–31 pg 4–10 × 109/L 150–400 × 109/L

Haemoglobin Haemoglobin is reduced in anaemia and elevated in dehydration and polycythaemia. Most ‘surgical’ anaemias are due to chronic blood loss (e.g. oesophagitis, carcinoma of the caecum) and are described as microcytic (mean corpuscular volume or MCV < 80 fL) and hypochromic (mean corpuscular haemoglobin or MCH < 25 pg). However, a macrocytic picture (MCV > 96 fL) may be seen in anaemias following gastrectomy (due to loss of intrinsic factor) or in patients with ileal disease (e.g. Crohn’s disease) or after ileal resection. Polycythaemia may be primary (haemoglobin > 18 g/dL), with elevation of haematocrit (> 0.55), white cell count (> 12 × 109/L) and platelets (> 650 × 109/L), or secondary due to hypoxia or increased erythropoietin production in renal disease.

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White cell count

Disseminated intravascular coagulation

The white cell count (WCC) is often measured in surgical patients. A raised WCC is commonly due to the presence of excessive numbers of neutrophils (neutrophilia/ leukocytosis) as a result of acute bacterial infections, haemorrhage or tissue necrosis. Rarely, an infection is so severe that white cell production is decreased, leading to a reduced WCC (neutropenia/leukopenia). Raised lymphocyte counts should alert one to the possibility of viral infections or leukaemias, while reduced lymphocyte levels are seen with AIDS, radiation and chemotherapy.

If extensive intravascular clotting occurs (e.g. in sepsis), the coagulation factors are consumed and the PT and APTT are prolonged. The vast amounts of fibrin formed in the coagulation process are broken down into fibrin degradation products, the levels of which are elevated in the serum and urine. Blood grouping and cross-matching for transfusion are frequently required in surgical patients. Transfusion of blood may be hazardous and should not be undertaken lightly. This subject is discussed fully in Chapter 37.

Platelets Increased platelet numbers (thrombocytosis) are seen after haemorrhage and especially after splenectomy. Thrombocytopenia (low platelet count) may be due to an autoimmune process (idiopathic thrombocytopenic purpura), hypersplenism secondary to splenomegaly, or drug reactions (e.g. heparin-induced thrombocytopenia).

Bone marrow examination Occasionally, patients are seen who have a combination of anaemia, leukopenia and thrombocytopenia. This is referred to as pancytopenia. This may be induced by drugs or result from marrow destruction (e.g. by tumour infiltration) and is diagnosed by bone marrow examination.

Tests for clotting Bleeding is arrested by vessel constriction, development of a platelet plug and activation of the clotting cascade (see Chapter 37). The three investigations routinely used to assess clotting are the platelet count (deficiencies cause purpura), the prothrombin time (PT) and the activated partial thromboplastin time (APTT). 1 The PT measures the extrinsic pathway and factors VII, X and V. It is prolonged in vitamin K deficiency and is used to monitor anticoagulation with warfarin. The normal PT is 12–15 s. The result of the PT in patients is now expressed as the international normalized ratio (INR), which is derived by dividing the patient’s PT by an international reference standard (e.g. if a patient’s PT is 30 s and the standard is 12 s, then the INR is 30/12 = 2.5). 2 The APTT measures deficiencies of factors V, VII–XI and XII (the intrinsic pathway) and is used to monitor anticoagulation with heparin. The APTT is prolonged in haemophiliacs.

Biochemistry Measurement of various biochemical parameters is frequently performed in surgical patients. It is important to note that some assays (e.g. potassium, lactate dehydrogenase) may be limited by haemolysis or clotting of the blood sample because of difficult venepuncture or a delay in transport to the laboratory. Calcium assay depends on the amount bound to albumin and therefore the value obtained must be corrected depending on the albumin level. The main biochemical tests performed and the normal range of values are listed in the box below. Similarly, blood gases are frequently measured to assess the acid– base balance of surgical patients. Acid–base disorders are closely allied to electrolyte disorders and both are discussed fully in Chapter 13. Normal serum biochemistry values Sodium Potassium Urea Creatinine Glucose Calcium Phosphate Bicarbonate Uric acid Total protein Albumin Bilirubin Osmolality

135–146 mmol/L 3.5–5.0 mmol/L 2.5–6.7 mmol/L 60 –120 µmol/L 4.0–7.0 mmol/L 2.2–2.6 mmol/L 0.8–1.4 mmol/L 22–30 mmol/L 0.18 –0.42 mmol/L 62–80 g/L 34 – 48 g/L < 17 µmol/L 280–296 mosmol/L

Enzymes Alkaline phosphatase Aspartate aminotransferase (AST) Alanine aminotransferase (ALT) Lactate dehydrogenase (LDH) Creatine phosphokinase (CPK)

25–120 U/L 10 –40 U/L 5–30 U/L 40 –125 U/L 24 –195 U/L

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Immunological tests Antibodies Antibodies are generated in response to extrinsic antigens (e.g. microorganisms, environmental allergens) or intrinsic antigens (autoantibodies). Measurement of serum autoantibody levels is often required in surgical patients. These tests are usually requested as an autoantibody screen (see box below). Antibodies identified in autoimmune diseases Figure 3.1 Dipstix used for urinalysis. Disease Graves’ disease # Hashimoto’s thyroiditis $ Pernicious anaemia Addison’s disease Diabetes mellitus Connective tissue disease Biliary cirrhosis Chronic active hepatitis Coeliac disease # Crohn’s disease $ Rheumatoid arthritis

Antibodies produced Thyroglobulin Thyroid microsomal antigen Gastric parietal cell Adrenal Pancreatic islet cell Antinuclear (ANA) Mitochondrial Smooth muscle Reticulin Anti-IgG antibody

Acute-phase proteins The levels of a number of plasma proteins increase rapidly in response to infection or tissue injury. These include a1antitrypsin, fibrinogen and C-reactive protein (CRP). CRP is frequently measured in surgical patients and is useful in the diagnosis of bacterial infections (when its level rises) and in following the progress of inflammatory conditions such as pancreatitis and Crohn’s disease. Serum albumin can be considered a negative acute-phase protein, as levels fall in response to inflammation.

performed to confirm or refute this diagnosis. If haematuria is present on urinalysis, formal microscopy of the urine should be performed. The presence of nitrates or protein is an indication for urine culture. Samples for urine culture are obtained as midstream specimens (see Chapter 39). Blood cultures should be obtained in all patients with suspected infection where the source is not obvious and in all patients with rigors. A blood culture is obtained by venepuncture. Following sterilization of the skin with alcohol, 10 ml of blood is withdrawn into a syringe. The blood is then decanted from the syringe into two sterile culture bottles, one for aerobic culture and one for anaerobic culture. A new needle is placed on the syringe and the top of the bottle is swabbed with alcohol prior to decanting the blood sample.

Imaging Details of the various imaging techniques used to investigate specific systems are given in the relevant chapters. Only the principles underlying the specific imaging techniques are given here.

Microbiology In patients with a suspected bacterial infection, cultures should be obtained before starting antibiotic therapy. If the source of infection is suspected, then the appropriate culture should be obtained (e.g. wound exudate in an infected wound). If the source is unclear, urine, blood and sputum cultures should be obtained and central venous lines removed and cultured. Urinalysis should be performed on all patients entering hospital. This is a quick dipstick test that identifies the presence of glucose, blood and protein in the urine (Fig. 3.1). The presence of glucose should alert one to the possibility of diabetes and a blood sugar test should be

Radiography X-rays were discovered by Wilhelm Roentgen in 1895 and were almost immediately applied to medicine (see box below). X-rays are generated by passing an electric current through a vacuum tube. The quality and quantity of X-rays produced are determined by the electrical potential (measured in kilovolts, kV) applied to the tube and the electrical energy (measured in milliampere seconds, mA·s) passed through it. The X-rays produced diverge uniformly from the tube so that the area covered is directly proportional to the square of the distance travelled.

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Roentgen discovers X-rays

Wilhelm Roentgen (1845 –1923) was professor of physics at Würzburg. He was interested in phosphorescence of metallic salts exposed to light. In November 1895, he performed an experiment that involved passing an electrical current through a vacuum tube. While the current was passing through the tube he noticed that a screen 2 m away gave off a greenish glow and on further investigation found that the screen had been painted with barium platinocyanide, a phosphorescent substance. He deduced that something given off by the tube was affecting the screen. He did some more experiments and found that the invisible (X) rays coming from the tube could pass through solid materials, e.g. wood. He also observed that when the rays were passed through his hand an image of the bones of his hand appeared on a photographic plate. He presented his findings to the Wurzburg Medical Society in December 1895. His discovery, surprisingly, was almost immediately taken up by the medical profession and Roentgen received the Nobel prize for physics in 1901.

Plain film radiography When an X-ray beam passes through tissues it is differentially attenuated by the various structures present. The absorption of X-rays by tissues depends on the atomic number of the principal substance of which the tissue is composed. Thus, bone (containing calcium and other radiopaque salts) absorbs considerably more X-rays than surrounding tissues (e.g. muscle or lung). This variable absorption produces a shadow on an X-ray plate that reflects tissue composition and structure (Fig. 3.2) and it is this phenomenon that forms the basis of plain film radiography. Bone density can also be assessed by measuring the amount of x-irradiation absorbed by the bones. This is the basis of DXA (dual X-ray absorptiometry) scanning which is used for diagnosing osteoporosis.

Figure 3.2 A chest radiograph. The basis of plain film radiography is that differential absorption of X-rays by tissues produces a shadow on a sensitized plate. The resulting image is called a radiograph, not an X-ray!

Contrast media Contrast media are substances introduced into the body to enhance the differences in absorption and thereby delineate a particular tissue. Contrast material may have either a high atomic number and provide positive contrast (e.g. barium sulphate, organic iodine compounds) or a low atomic number and provide negative contrast (e.g. gases such as air). In some situations both positive and negative contrast materials are used together, e.g. in a double-contrast barium enema both barium sulphate and air are used to outline the colon (Fig. 3.3). Water-soluble contrast such as Gastrograffin gives lower-quality defini-

Figure 3.3 Double-contrast barium enema. Both barium (positive contrast) and air (negative contrast) are passed into the colon per rectum to enhance the quality of the image obtained.

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Figure 3.4 Digital subtraction fluorography. Digital subtraction angiogram of the aorta and iliac arteries in a patient with peripheral vascular disease. Note the catheter in the left iliac artery and the stenosis in the right iliac artery (arrowed).

tion but is safer than barium when gastrointestinal perforation is a possibility.

Figure 3.5 Tomogram of a chest lesion showing cavitation and calcification due to active pulmonary tuberculosis.

Subtraction techniques Subtraction techniques are now widely used to obtain enhanced images with lower concentrations of parenterally administered contrast media. In the subtraction technique, a positive-image radiograph is obtained first. Contrast material is then injected and a second identical negative image obtained. The two images are then superimposed; the positive and negative images common to both radiographs cancel out, leaving only the negative image of the injected contrast material. The modern technique is called digital subtraction fluorography. The analogue images are converted to digital signals and held in computer memory. The computer mixes, subtracts and manipulates the images to give the optimum detail. The image is reconverted to analogue form and displayed on a screen (Fig. 3.4).

Tomography Tomography is a technique whereby a structure in a preselected plane, such as a kidney, is highlighted radiographically by causing blurring of the images from the tissues anterior and posterior to the preselected plane. The simplest way to achieve this effect is by moving the tube and film in opposite directions while the patient remains stationary so that only the images of the prese-

lected plane remain sharp. Tomography has been superseded by computed tomography (CT) and is seldom used now (Fig. 3.5).

Computed tomography CT uses tomography to produce cross-sectional images of the body. A large number of images taken in different directions by a CT scanner (Fig. 3.6a) are fed into a computer, which constructs the cross-sectional image. The system is very sensitive, so that small differences in tissue density can be recognized and a very detailed two-dimensional picture constructed (Fig. 3.6b). It is possible to construct three-dimensional CT images of structures so that complex anatomy can be interpreted with ease (Fig. 3.6c). In conventional CT scanning, ‘slices’ of the body are obtained at 1-cm intervals by a camera that rotates around the patient at each 1-cm level. A newer, faster technique, known as helical or spiral CT scanning, produces a continuous image as the camera spirals around the patient. Reconstructed images of the colon have aroused much interest as they allow virtual reality ‘fly-through’ images of the entire colon that have been shown to be accurate in detecting polyps and tumours. CT colonography (virtual colonoscopy) still requires a full bowel preparation.

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(a)

Figure 3.7 Doppler probe. (b)

body tissues reflect the sound waves as echoes. The echoes are returned to the transducer disc and converted into electrical impulses, which can be converted into images. The images can be displayed in various ways: A-mode or amplitude-modulated scan; M-mode or motion scan; B-mode or brightness-modulated scan; real-time or two-dimensional scan. Most diagnostic scanning now uses B-mode or real-time scanning. M-mode scanning is used (with pulsed Doppler and real-time scanning) in echocardiography. Ultrasound scanning is routinely used for imaging of thyroid, breast, biliary tract, liver, kidneys, uterus and ovaries and is a good first-line investigation for the assessment of any abdominal mass. Ultrasound is increasingly used as a diagnostic tool in the emergency trauma setting to detect intraperitoneal haemorrhage. A miniaturized laparoscopic ultrasound probe may also be used for intraoperative staging of tumours or to aid localization of hepatic metastases for radiofrequency thermoablation. The Doppler effect is the change in frequency of a sound due to the movement of the source of the sound relative to the observer. Simple Doppler probes (Fig. 3.7) can be used to detect arterial or venous blood flow, while pulsed Doppler probes, which emit short bursts or pulses of ultrasound, are very useful in cardiology for the detection

• • • •

(c) Figure 3.6 (a) CT scanner: as the patient passes through the scanner several images in different directions are accumulated and a computer constructs a cross-sectional image. (b) CT scan of the abdomen: the image is viewed from ‘below’. In this case a tumour of the left kidney can be seen. (c) Three-dimensional CT scan of the upper abdomen showing the aorta, both kidneys and the spleen.

Ultrasonography Ultrasonography is a diagnostic technique that uses highfrequency sound waves to generate an image. Ultrasound is generated in pulses from a special transducer disc when a voltage is placed across it. The interfaces of different

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(a)

Figure 3.9 Radionuclide scan: isotope bone scans. The image on the left is normal while the image on the right shows multiple ‘hotspots’ indicating metastatic disease.

(b) Figure 3.8 (a) Duplex scanner being used to obtain scan of carotid artery. (b) Colour duplex scan of carotid arteries: blood flowing in one direction appears red/orange in colour, whereas turbulence producing disrupted or reversed flow appears blue; CCA, common carotid artery; ECA, external carotid artery; ICA, internal carotid artery.

of shunts and in the assessment of valvular heart disease. Pulsed Doppler is also combined with real-time scanning in duplex scanners (Fig. 3.8), which are used to assess flow and anatomy in peripheral vessels, especially the carotid.

Radionuclide imaging (scintigraphy) Radionuclide imaging uses a special radiation detector (gamma-camera) to depict the distribution of an administered isotope within an organ or the whole body (Fig. 3.9). Radionuclide imaging is mainly used to measure function but it can also demonstrate anatomy. Several radionuclide tests are now available, but all conform to the principle that an injected, inhaled or ingested pharmaceutical compound labelled with a suitable radionuclide is

concentrated in the organ under review and the emitted radiation is detected by the gamma-camera. Areas of increased or decreased activity are thus easily detected. Technetium 99m (99mTc) is an ideal radionuclide because it emits only γ radiation, has a single energy peak, is readily available, has a half-life of 6 h and is suitable for many investigations (e.g. brain, thyroid, bone, kidney, adrenal glands). It is also used in the form of a radiocolloid to perform lymphoscintigraphy, which aids in identifying the sentinel lymph node draining breast tumours and melanomas (Fig. 3.10). Other isotopes used are krypton (81mKr) for ventilation studies, iodine 131 (131I) for thyroid studies and gallium 67 (67Ga), which is used to locate abscesses and tumours. Patients are sometimes concerned that they are being given a radioactive material. The radiation dose is usually less than an equivalent radiological investigation but as the isotope is excreted by the body, tissues other than the tissue under examination are exposed to some radiation. Radionuclide examinations should be avoided in lactating mothers as the radionuclide will be excreted into the breast milk.

Positron emission tomography Positron emission tomography (PET) is a diagnostic imaging technique used to study metabolic activity in tissues, e.g. to assess the vascularity of a brain tumour. In a

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PET scan, a low-dose radionuclide produced by a cyclotron is coupled to glucose and injected intravenously. The radionuclide emits positively charged electrons (positrons) that are annihilated thus producing photons, which are detected by the scanner. The PET scanner, which rotates around the patient, detects the photon emissions from the radioactive sugar. Highly malignant tumours consume glucose at a higher rate than normal brain. These differences can be detected and displayed as a dynamic image. PET scanning has particular applications in neurology in conditions such as epilepsy, brain tumours and dementia. It also has applications in cardiology and oncology.

Magnetic resonance imaging

Figure 3.10 The sentinel node is defined as the first lymph node that drains lymph from a primary tumour. It may be identified by injecting a radiocolloid (e.g. technetium rhenium sulphide) on the morning of surgery at multiple points around the periphery of a tumour, in this case a lower limb melanoma. A lymphoscintigram identifies the nodal basin (e.g. axillary or inguinal) containing the sentinel node. A second injection of blue dye (e.g. Lymphazurin) at the time of operation allows the accurate identification of the correct node by visualization of a blue node, which is also ‘hot’ as determined by a handheld gamma probe. This can be performed through a very small incision. The benefit of identifying the sentinel node is that if there is no evidence of metastatic tumour in this node, then there is a 95% probability that the other nodes are also clear. This allows the pathologist to concentrate carefully on a small amount of tissue rather than sampling from a large number of nodes. It also allows many patients to avoid the morbidity of block dissection of lymph nodes.

Magnetic resonance imaging (MRI) is a diagnostic technique based on the principle that an externally applied magnetic field causes protons in tissues to align in the direction of the magnetic field. By applying a second smaller magnetic field, in the form of a radiofrequency (RF) pulse, perpendicular to the main magnetic field, the alignment of the protons is changed. When the RF pulse is stopped, the protons return to equilibrium and in so doing produce another RF signal. This is the magnetic resonance signal, which is amplified and transformed by computer into images. The process whereby protons give off energy is called relaxation. This process is characterized by two time constants: T1 refers to the time for the protons to return to their original state of equilibrium; T2 refers to the time for the protons to become out of phase with each other. Protons in different tissues (water, fat, muscle) have different T1 and T2 relaxation times and this difference is utilized for image contrast. Certain scanning parameters can be changed to enhance differences in T1 or T2 times. This is referred to as weighting, e.g. T1-weighted images are used to demonstrate neural tissues (Fig. 3.11). Intravenous contrast such as gadolinium principally affects T1-weighted scans, as a main effect of added contrast is to shorten the T1 relaxation time. Magnetic resonance angiography (MRA) provides angiographic data without the need for catheter insertion. MRA images are acquired by exploiting the differences between stationary tissues that have been saturated with RF pulses and unsaturated blood that flows into the saturated area from outside the excited section. Two slightly different techniques, called time of flight and phase contrast, are used to acquire the images. Gadolinium is used to enhance MRA images. MRA is especially useful in assessing patients with suspected neurological disease (Fig. 3.12). Magnetic resonance cholangiopancreatography (MRCP) is useful in non-invasive assessment of

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(a)

Figure 3.12 Magnetic resonance angiography demonstrating the circle of Willis.

(b) Figure 3.11 Magnetic resonance scan: (a) T1-weighted image; (b) T2-weighted image.

complex biliary and pancreatic pathology and in many cases may obviate the need for the more invasive procedure of endoscopic retrograde cholangiopancreatography (ERCP). T2-weighted images produce a high signal from bile because it is a relatively static fluid with a long T2 time (Fig. 3.13). MRI has brought its own hazards. Patients (or staff) with pacemakers should not go near an MRI scanner. There have been horror stories of scissors and scalpels flying into the centre of the scanner and injuring patients. Credit cards should also be kept at a safe distance.

Figure 3.13 Magnetic resonance cholangiopancreatography showing gallbladder full of gallstones and a dilated common bile duct containing a stone. Right and left hepatic and cystic ducts are also shown.

Endoscopy Doctors have been trying to peer inside their patients’ bodies for centuries (open your mouth, please!) but only in the last 150 years have instruments been developed that allow them to achieve this aim with any degree of precision (e.g. the first electrically lighted cystoscope was developed by Max Nitze in 1877, but fully flexible endoscopes for gastroscopy were not available until the late 1960s). Today several types of scope are available, not only for examining the inside of the body but also for facilitating endoscopic surgical operations.

Rigid scopes Scopes are of two kinds: rigid and flexible. Rigid scopes are simply straight tubes through which light is passed from an external source into the part of the body under examination. The simplest are proctoscopes (used to illuminate the anal canal) and rigid sigmoidoscopes (for examining the rectum and sigmoid colon; Fig. 3.14). Rigid bronchoscopes and oesophagoscopes are rarely used now but occasionally a rigid scope is employed to examine the mediastinum (mediastinoscope). Rigid cystoscopy is used

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Figure 3.14 Proctoscope and rigid sigmoidoscope. Figure 3.16 Oesophagogastroduodenoscopy using a videoendoscope.

with controls and an eyepiece; • aa head flexible shaft with a manoeuvrable tip; and • an external light source. • The head is connected to the light source via a connect-

Figure 3.15 Diagnostic laparoscopy.

regularly and a rigid scope with a resecting wire and irrigating channels (resectoscope) is used to perform transurethral prostatectomy or resection of bladder tumours. The scopes used for laparoscopy and arthroscopy are also rigid. Laparoscopy (‘keyhole surgery’) is facilitated by the insufflation of the peritoneal cavity with CO2, a noncombustible gas. Although CO2 is systemically absorbed during the procedure, the advantages of reduced postoperative pain far outweigh any potentially deleterious effects of hypercapnia. A single camera port and a number of operating ports are placed, through which specially designed instruments are used to manipulate the intraabdominal contents. Laparoscopy is a useful diagnostic tool for acute abdominal pain and for the preoperative staging of oesophageal and pancreatic tumours (Fig. 3.15).

Flexible scopes Flexible endoscopes are complex pieces of equipment consisting of:

ing flexible shaft, which also contains tubes supplying air insufflation, suction and irrigation to the scope. The light from a high-intensity light source is transmitted down the scope via fibreoptic light bundles. This illuminates the body cavity being inspected. The image generated is transmitted up the scope via fibreoptics to the eye-piece or, more recently, via a charge-coupled device to a television monitor. This is known as videoendoscopy (Fig. 3.16). Flexible endoscopes are used to examine the bronchial tree (bronchoscopy), upper gastrointestinal tract (oesophagogastroduodenoscopy, OGD; Fig. 3.16), biliary and pancreatic ducts (ERCP), sigmoid colon (flexible sigmoidoscopy), entire colon (colonoscopy), urethra and bladder (flexible cystoscopy), and the lumina of blood vessels (angioscopy). Most flexible scopes also have working channels incorporated into them that facilitate the passage of a variety of instruments: biopsy forceps for obtaining specimens for histology; brushes for obtaining specimens for cytology; flexible needles for injection of sclerosants or drugs (e.g. adrenaline) to stop bleeding from varices or ulcers; heater probes and laser fibres to stop bleeding from ulcers; snares for removing polyps; graspers for removing foreign bodies; papillotome for dividing the papilla of Vater; wire baskets for removing stones, e.g. from the biliary tract, and self-expanding stents for placing across oesophageal or biliary strictures. Endoscopic ultrasound probes are useful in staging rectal, oesophageal and periampullary tumours and are

• • • • • • • •

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Part 1 Clinical Skills and Investigations

Table 3.2 Investigations commonly used to assess physiological function. Respiratory system Pulmonary function tests Peak expiratory flow rate Spirometry Blood gas analysis Cardiovascular system Tests of heart function Echocardiography Electrocardiography Resting ECG Exercise ECG Holter monitoring Investigations of peripheral vascular disease Doppler velocimetry Ankle pressure measurement Ankle/brachial pressure index Segmental pressure measurement Waveform analysis Exercise response Plethysmography Pulse volume recording Digital plethysmography Duplex colour ultrasonography Gastrointestinal tract Tests of oesophageal function Oesophageal manometry pH studies Tests of gastric function Pentagastrin test Tests of anorectal function Electromyography Anorectal manometry Defecating proctography Genitourinary tract Urodynamics Uroflowmetry Cystometry Urethral pressure profile Nervous system Tests of central nervous system function Electroencephalography Somatosensory evoked potential Tests of peripheral nerve function Nerve conduction studies Electromyography

very effective in localizing small pancreatic tumours such as insulinomas. Transoesophageal echocardiography is more sensitive than conventional transthoracic echocardiography in detecting valvular vegetations in bacterial endocarditis and atheroma of the great vessels in patients with cerebral emboli. Most gastrointestinal endoscopy is now performed in purpose-designed endoscopy units. Formal written consent should be obtained prior to endoscopy. Patients have to starve before upper gastrointestinal endoscopy and bowel preparation is required before colonoscopy. Pharyngeal anaesthesia is given to patients before OGD or ERCP and most patients require sedation (midazolam and diazepam are the commonly administered sedatives). Patients having colonoscopy also require sedation, usually with a benzodiazepine and an opiate. Sedated patients should be monitored with electrocardiography (ECG), frequent blood pressure estimation and pulse oximetry. The antagonists for benzodiazepines (flumazenil) and opiates (naloxone) should be immediately available when performing endoscopy. Specific endoscopic investigations are discussed in the relevant chapters of this book.

Measurement of function Many investigations are undertaken to measure how well a system is functioning or to detect abnormalities in the function of an organ or structure. Clearly, some laboratory investigations (e.g. creatinine clearance for assessment of renal function, thyroid function tests) and many imaging techniques (e.g. renal scanning) achieve this aim. However, specific investigations have been developed to assess function in most of the body’s major systems. These are discussed in the relevant chapters but are listed briefly in Table 3.2.

Evidence-based medicine http://www.nlm.nih.gov/research/visible/visible_human. html United States National Library of Medicine Visible Human Project: a collection of three-dimensional CT and MRI representations of normal human anatomy. http://www.biosound.com/images.html A corporate website featuring ultrasonic images and links to other resources. http://mphsun.mph.ed.ac.uk/ University of Edinburgh Department of Medical Physics and Medical Engineering: this website features virtual colonoscopy among other images and movies. http://www.laparoscopy.com Interactive multimedia website featuring images and movies of laparoscopic operations.

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Principles of investigation at a glance Basic principles A key investigation is one that confirms or excludes a strongly suspected diagnosis and is always necessary. The risk to the patient correlates with the degree of invasiveness of the procedure; informed consent must be obtained for any procedure. Routine preoperative investigation is often unnecessary and is being replaced by selective testing based on the clinical history or examination. Screening is the examination of apparently healthy people to identify those with a particular disease at an early stage, e.g. breast cancer.

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Blood investigations Full blood count. A microcytic hypochromic anaemia is usually due to iron deficiency and should always raise the possibility of occult gastrointestinal blood loss. The leukocyte count is often raised in acute surgical conditions. Thrombocytopenia may be autoimmune or due to hypersplenism or massive transfusion and may cause bleeding problems during or following surgery. Coagulation screen. This is important in patients on anticoagulant drugs and in those who may have a bleeding disorder, e.g. liver failure. Biochemistry. Baseline biochemistry screens can sometimes reveal asymptomatic conditions, e.g. primary hyperparathyroidism. Some biochemical assays (e.g. potassium, LDH) may be limited by haemolysis or clotting of the blood sample because of difficult venepuncture or a delay in transport to the laboratory. Autoantibody screen. Autoantibodies are often present in the sera of patients with autoimmune conditions and may identify reasons for surgical problems, e.g. failure of a leg ulcer to heal in a patient with rheumatoid arthritis.

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Microbiology A septic screen consists of the collection of samples of blood, urine, sputum, wound swabs and sometimes stool for culture and sensitivity. Antibiotic sensitivity is important because it directs the use of drugs with a narrow spectrum of activity, thus avoiding the antibiotic resistance that develops from the indiscriminate use of broad-spectrum antibiotics. Imaging Radiography. When an X-ray beam passes through tissues it is differentially absorbed depending on the composition of the tissue. This variable absorption produces a shadow on an X-ray plate and forms the basis of plain film radiography. Contrast media are substances introduced into the body to enhance the differences in absorption and thereby delineate a particular tissue. Water-soluble contrast such as Gastrograffin gives lower-quality definition but is safer than barium when gastrointestinal perforation is a possibility. Parenterally administered contrast media may cause allergic reactions or renal failure in susceptible patients. Subtraction techniques are now widely used to obtain enhanced images with lower concentrations of contrast (e.g. digital subtraction angiography). CT uses tomography to produce cross-sectional images of the body. Spiral CT scanning

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produces high-quality reconstructed images, as in virtual colonoscopy. Ultrasonography uses high-frequency sound waves to generate an image. Ultrasound scanning is routinely used for imaging of thyroid, breast, biliary tract, liver, kidneys, uterus and ovaries and is a good first-line investigation for the assessment of any abdominal mass. The Doppler effect is the change in frequency of a sound due to the movement of the source of the sound relative to the observer. Pulsed Doppler is combined with real-time scanning in duplex scanners, which are used to assess flow and anatomy in peripheral vessels, especially the carotid. Radionuclide imaging uses a special radiation detector (γ-camera) to depict the distribution of an administered isotope within an organ or the whole body. Technetium 99m (99mTc) has a half-life of 6 h and is suitable for many investigations (e.g. brain, thyroid, bone, kidney, adrenal glands). It is also used in the form of a radiocolloid to perform lymphoscintigraphy, which aids in identifying the sentinel lymph node draining breast tumours and melanomas. MRI is based on the principle that an externally applied magnetic field causes protons in tissues to align in the direction of the magnetic field. MRA is a technique that provides angiographic data without the need for catheter insertion. MRCP is useful in non-invasive assessment of complex biliary and pancreatic pathology.

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Endoscopy Rigid scopes are simply straight tubes through which light is passed from an external source into the part of the body under examination. Examples are the proctoscope, rigid sigmoidoscope, mediastinoscope, resectoscope, laparoscope and arthroscope. Flexible scopes utilize fibreoptics to give better-quality imaging that can be displayed on a video monitor. Examples are the gastroscope, colonoscope, cystoscope, bronchoscope and angioscope. They may contain side channels to insert instruments for diagnostic or therapeutic procedures, e.g. biopsy, ERCP sphincterotomy.

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Measurement of function Specific investigations have been developed to assess function in most of the body’s major systems. These vary in invasiveness from the ECG to anorectal manometry, and in length of time from the peak expiratory flow rate (seconds) to 24-h oesophageal pH monitoring. Criteria for population screening The disease should be relatively common and have serious sequelae. The condition should be identifiable at a stage where intervention is effective. The investigation should be non-invasive and acceptable to patients to ensure good compliance. The investigation used should identify all affected individuals (sensitivity) and avoid mistaken diagnosis in unaffected individuals (specificity). There should be a proven treatment for the disease. The investigation should be relatively inexpensive.

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Part 2 Perioperative Care

Assessment of Patients for Surgery and Preoperative Medical Management

Goals of preoperative assessment, 62

Methods of assessment, 63

Must know Must do

Must know Concept of preparation for surgery as a balance of risks Effects of commonly encountered coexisting medical conditions on clinical outcome after surgery Principles of clinical assessment and investigation to gauge operative risk Must do Follow at least one patient from preoperative assessment through to discharge from hospital Follow at least one diabetic through preoperative management prior to general anaesthesia

Calculating risk, 68

Patient selection Patient selection is the overall process of assessment and risk comparison that allows the surgeon to make a decision regarding the suitability of a patient for a given operation. Previously, there was very little selection involved in the decision to operate, particularly in life-threatening conditions such as bleeding peptic ulcers. Today, there is a greater understanding of the mortality and morbidity associated with surgery. Surgeons, physicians, patients and relatives are all much more aware of the risks involved. This is especially true in elective surgery such as organ transplantation, where the point at which surgical risk is outweighed by the risk of medical management is becoming much better understood. In order to offer the best ‘patient selection’, the use of careful perioperative assessment is crucial.

Goals of preoperative assessment Good preoperative assessment of patients is a fundamental requirement of the practice of surgery. Surgery is always a process associated with risks. One of the essential tasks of a surgeon is to make well-founded, accurate assessments of how the risks entailed in performing surgery are balanced by the risks of not doing so (Fig. 4.1). Crucial to this process is to obtain a clear and detailed picture of the status of the patient and what risks, known and unknown, are present. The goals of preoperative assessment can be summarized as shown in the box below.

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To assess the risk of surgery vs. non-surgical treatments in order to allow a choice of treatments to be offered and informed consent about a given operation to be obtained To assess the extent of known disease present in the patient in order to allow appropriate treatment to be employed preoperatively and postoperatively To identify unknown or hidden diseases (risks) in order to allow prophylactic treatment that might reduce the risk and allow planning for management of potential complications if the risk is fixed

Patient with: Hypertension Angina Abdominal aortic aneurysm Op

Risk of stroke Risk of acute MI Risk of graft failure Risk of per-op embolus

No op

Risk of embolism Risk of aneurysm rupture

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Figure 4.1 Preoperative assessment involves balancing the risks of not operating against those of surgery.

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Methods of assessment There are several ways to approach the assessment of patients.

Assessment of the patient pathway One way of performing the assessment is to examine the key areas where risk may arise during the patient’s path through the process of surgery. Preoperative, e.g. immobility leading to the development of silent deep vein thrombosis (DVT), jaundice leading to bleeding disorders, chronic bleeding from colorectal cancer causing anaemia. Perianaesthetic, e.g. unstable asthma causing bronchospasm under general anaesthesia, rheumatoid disease causing difficult intubation, bleeding disorders with increased risk of haemorrhage. Postoperative, e.g. occult ischaemic heart disease leading to acute myocardial infarction, chronic pulmonary disease leading to consolidation, intrinsic renal disease predisposing to acute renal failure. This approach is useful as a checklist to help identify risky situations that might not otherwise be recognized. It is suited to medical records that are based on the problemoriented approach, since identified medical problems can readily be seen in the context of how they might affect the patient during the operative period. It has the disadvantage that unforeseen or occult risks may not be identified unless a systems-based approach is also used. A similar approach to assessment of the patient is to consider each area of medical and nursing care and assess the possible problems. Anaesthesiology, e.g. unstable asthma causing bronchospasm under general anaesthesia, rheumatoid disease causing difficult intubation, chronic bleeding from colorectal cancer causing anaemia. Nursing, e.g. rheumatoid disease leading to poor mobility and risk of developing DVT, poor eyesight causing problems with stoma care. Surgeon, e.g. bleeding disorders with increased risk of haemorrhage. This approach has many of the same advantages and disadvantages as the ‘pathway’ system.

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System assessments An alternative to the methods desribed above is to consider the systems of the body and evaluate each separately. This is also valuable because it will help uncover unsuspected problems that are potentially life-threatening. Broadly, assessment of systems is carried out using the principles of history-taking and examination (see Chapter 1). Several principles still apply.

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Most problems can be identified and a guide to severity obtained by a good history and clinical examination. Investigations should be used to clarify areas of uncertainty and suspicion or to give more quantitative information about identified problems. They are not an excuse for poor basic clinical assessment. The most useful investigations are often those that give functional information, e.g. blood gases are far more informative than the erect chest X-ray in a patient with chronic obstructive pulmonary disease (COPD). Nobody can be expert in the assessment of all medical problems related to surgery. The opinion of specialist physicians and anaesthetists is always useful in difficult or uncertain situations.

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Cardiac Ischaemic heart disease Ischaemic heart disease (known and unsuspected) still represents the single most dangerous risk factor for the development of perioperative complications. Although the absolute mortality from cardiac causes has been reduced in recent years by advances in understanding of the changes in haemodynamics caused by surgery and by advances in anaesthetic techniques, perioperative myocardial ischaemia is still a common cause of problems. Several scoring schemes exist for the assessment of cardiac disease on the basis of clinical findings (e.g. Goldman cardiac index, Detsky cardiac score). These give values to cardiac factors such as history of recent myocardial infarction, presence of added heart sounds, etc. and derive a total score that is then stratified into ‘bands’ of risk. management It is rare to be able to reverse established coronary disease in order to improve the patient’s status but the prevention of risk means ensuring that optimal prophylaxis is used. Elective surgery should always be delayed until 6 months after a myocardial infarction and never undertaken in situations where symptoms of angina are poorly controlled or unstable. Antiplatelet therapy may be appropriate unless contraindicated by the surgery to be performed. It is vital to ensure that patients do not become excessively dehydrated or overhydrated directly before the operation because this can result in unpredictable alterations in coronary and vital organ perfusion under general anaesthesia.

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Arrhythmias The most common and potentially most dangerous arrhythmia encountered in surgical patients is atrial fibrillation

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(AF). Chronic AF predisposes to mural thrombosis, with the risk of arterial embolism causing stroke or other organ infarction. Acute AF may be provoked in susceptible individuals by surgical stress, mild hypoxia or dehydration, which are often seen postoperatively. Generally, complex arrhythmias are best managed by cardiologists to prevent the risk of perioperative complications, although it is also necessary to be aware of the likelihood that patients may be on anticoagulants because of abnormal cardiac rhythms.

Left ventricular failure Poor left ventricular function is often an underrecognized condition in preoperative patients. Moderate restrictions in exercise tolerance may reflect poor cardiac reserve rather than chest disease or ‘old age’. Many anaesthetic agents may cause depression of myocardial function and the significant swings in fluid balance around the time of surgery can cause acute pulmonary oedema very rapidly in patients with poor left ventricular reserve. management Correction of anaemia, optimization of diuretic therapy and avoidance of negatively ionotropic drugs may help to improve left ventricular function. Patients with limited cardiac reserve need close monitoring of fluid balance preoperatively and postoperatively in order to avoid large or rapid shifts.

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Cardiac investigations Electrocardiography (ECG) is useful in patients with a possible history of ischaemia as a screening tool for previous myocardial infarction. Unfortunately it is normal in up to 60% of patients with occult ischaemic heart disease. It may also show evidence of global ischaemia (ST segment abnormalities) and may clarify the presence of arrhythmias. It should be performed in any patient with a history of cardiac disease and in those over the age of 55 as a screening test for occult disease. 24-h ECG: only useful for patients suspected of having major but paroxysmal arrhythmias. Exercise ECG: relatively simple and easy to perform but a coarse test for reversible coronary ischaemia and gives a gross test of cardiac reserve. Echocardiography: transthoracic echocardiography may give an indication of poor left ventricular function by showing hypokinesia but is imprecise. Transoesophageal echocardiography using Doppler flow assessment has been used to estimate cardiac output (left ventricular output) but is moderately invasive and is only available in some institutions. Nuclear cardiography: the assessment of cardiac function using radiolabelled blood, e.g. multiple uptake gated

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acquisition (MUGA) scans, has provided a relatively noninvasive and highly accurate method of assessing cardiac function at rest and in response to physical stress. For high-risk patients, MUGA and similar scans can provide some of the most accurate assessments of cardiac risk in elective surgery but require specialist investigation services and are expensive to perform.

Respiratory Obstructive lung disease Smoking is the single biggest cause of perioperative respiratory morbidity. It is most commonly manifest as COPD. Frequently patients may have moderately severe COPD with relatively few clinical symptoms or signs, especially if they have an inactive lifestyle due to other disease. COPD may affect the patient in several different ways: reduced gas exchange, leading to chronic hypoxia and much reduced pulmonary reserve postoperatively; reduced airway clearance for secretions, increasing the risk of mucus plugging, segmental collapse and subsequent consolidation; reduced lung compliance, causing increased difficulties maintaining ventilation under anaesthesia. In addition to direct lung effects, smoking has the added consequence of impairing the intrinsic pulmonary immune system, while nicotine increases myocardial oxygen demand and carbon monoxide in circulating blood reduces oxygen-carrying capacity.

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Respiratory investigations Chest X-ray: only rarely of use in the assessment of respiratory disease. Radiographically normal lungs may exhibit profoundly abnormal tests of function. Arterial blood gases: probably the most useful bedside test. Provide a direct picture of the degree of impairment of gas exchange and a useful benchmark against which to monitor progress. Peak expiratory flow rate: a simple and reproducible test for obstructive lung disease, most useful in reversible conditions such as asthma. It allows day-to-day monitoring of status and the effects of treatment. Lung function tests: full spirometry and gas exchange coefficients are rarely useful in the routine assessment of preoperative patients. In those with severe or atypical lung disease, they can give an accurate picture of the extent of disease and pulmonary reserve.

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Management Wherever practical, smokers should aim to stop smoking for a full 6 weeks prior to surgery to allow the temporary effects on mucus and tracheobronchial cilia to wear off.

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The most important management of respiratory disease is preventive. Reversible obstructive disease should be aggressively treated by inhaled or nebulized bronchodilators preoperatively. Physiotherapy should be started preoperatively and continued immediately the patient is able to cooperate in active exercises. Adequate hydration helps prevent viscid secretions and helps mouth-breathing. Adequate analgesia is critical. For ventilation to be effective and to allow coughing and physiotherapy to work, control of pain, particularly from abdominal and thoracic incisions, should be good. Up to 85% of patients on surgical wards may become hypoxaemic after abdominal surgery, most without obvious signs.

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Endocrine Adrenal disorders Adrenocortical disease is uncommon in surgical patients. Most abnormalities are due to iatrogenic steroid administration causing adrenocortical suppression. This rarely causes any biochemical abnormalities associated with endogenous steroid excess (Cushing’s syndrome) but is a source of risk because of inadequate stress response immediately postoperatively. Patients on long-term systemic steroids (other than low-dose treatment) should be considered for postoperative supplementation in the form of intravenous hydrocortisone. This may need to continue for several days or weeks postoperatively. Diabetes mellitus The assessment of patients with diabetes mellitus revolves around two issues: identification of the extent and severity of diabeticrelated organ system diseases; establishment of adequate control of glucose levels perioperatively.

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complications Diabetes can affect most organ systems of the body, often with little in the way of clinical signs until significant reduction in reserve or function. This is even true in relatively ‘young’ diabetics, who may develop complications 10 or 20 years before they might do in non-diabetics. Typical complications that may lead to perioperative problems include the following. Renal: reduced glomerular filtration rate (GFR), with increased risk of drug toxicity and acute renal failure. Vascular: occult small-vessel vascular disease leading to increased risk of pressure sores, peripheral arterial disease and intestinal ischaemia.

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Cardiac: silent myocardial ischaemia with increased risk of infarction. Immunocompromise: increased risk of superficial and deep infections. Ketoacidosis: inadequate insulin availability under conditions of stress may lead to acute diabetic ketoacidosis with associated high morbidity and mortality. management Preoperative investigation of long-standing diabetic patients should include routine screening for renal, liver and vascular disease. The rule is to suspect occult disease even in the young. Perioperative care should be tailored to the individual patient. The extent and duration of surgery as well as the type of diabetes (insulin-dependent or non-insulindependent) determines which regimen is best. If there is doubt, liaison between surgeon, anaesthetist and diabetologist is essential. Broadly, patients can be managed using the guidelines shown in the box below.

Management strategies for diabetics undergoing surgery Diet control only Unlikely to need additional insulin but may require close monitoring of blood sugar, particularly during long operations or during recovery after bowel surgery. Oral hypoglycaemic agents Long-acting oral hypoglycaemic agents should be stopped in advance of all but minor or short day-case surgery. Oral therapy should be stopped on the day of surgery and blood sugar level monitored. For inpatient surgery, close monitoring of blood sugar may be necessary until the patient is able to start oral diet again. For major abdominal surgery or where control is poor, consider switching to an insulin sliding scale during the perioperative period. Insulin-dependent diabetes May be possible to simply omit the morning dose of insulin on the day of surgery for minor or day-case procedures with close monitoring of blood sugar. Prolonged starvation or major procedures usually require an insulin infusion to control blood sugar. A sliding scale is safer and more reliable than a fixed-rate insulin/dextrose ‘drip’ and should be monitored by regular blood sugar measurements. Normal insulin regimens can be reintroduced when the patient is eating a normal diet.

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Haemostasis

Thrombophilias Most patients with a history of thromboembolic disease do not have an inherited or acquired thrombophilia. Although protein C or protein S deficiency and factor V Leiden mutation are being increasingly identified as a cause of atypical, familial or recurrent thrombosis, routine screening for them is not indicated in the majority of patients. Obesity, immobility, underlying malignancy and drugs such as the oral contraceptive pill are of much greater relevance in surgical practice. The risk of thrombosis (and hence embolism) can be divided into three groups. Low: no adverse risk factors, minor or intermediate surgery where early mobilization is expected (inguinal hernia repair). Medium: risk factors such as obesity or smoking or surgery where mobilization may be delayed (e.g. laparotomy, open cholecystectomy). High: multiple adverse risk factors, a history of recurrent DVT/pulmonary embolism (PE) or major surgery associated with high risk of thrombosis (e.g. pelvic exenteration).

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management Reversible risks should be removed wherever possible, e.g. stopping the combined oral contraceptive pill 4 weeks prior to major surgery. Patients at low risk require no specific prophylaxis. Patients at medium risk may be managed with lowdose chemoprophylaxis (heparin or similar) and mechanical prophylaxis (compression stockings). Patients at high risk should have mechanical prophylaxis and be considered for high-dose chemoprophylaxis or low-dose anticoagulation.

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Bleeding disorders Bleeding disorders in surgical patients fall into four groups and the management of each depends on both the cause and extent of the operation planned. Inherited disorders: the haemophilias and congenital platelet disorder syndromes are usually well known prior to surgery. Management involves the replacement of appropriate clotting factors or blood constituents and should be done in close conjunction with the patient’s regular haematologist. Warfarin/non-steroidal anti-inflammatory drugs (NSAIDs): a careful history will reveal therapeutic anticoagulation but it is often easily overlooked. Management depends on the indication for the anticoagulation. Life-threatening risks, such as mechanical mitral valves, must remain anticoagulated and surgery either performed

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under heparin anticoagulation or with close attention to haemostasis. Less absolute indications, such as prophylaxis against stroke in patients with AF, may be temporarily reversed to allow the operation to proceed. Liver disease: often associated with abnormalities of clotting (see later); any patient with clinical liver impairment should be considered for treatment of clotting disorders. Systemic inflammatory response syndrome/massive transfusion: both associated with profound and wide-spread abnormalities of clotting. Prophylactic replacement of clotting factors and platelets may need to be considered in either situation.

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Gastrointestinal disorders Liver disease The assessment of chronic liver disease can be extremely complex, reflecting the liver’s role in a wide range of synthetic and metabolic processes. problems and their management Consideration should be given to several broad areas when assessing and managing patients with liver disease prior to surgery. Failure or abnormalities of the normal biosynthetic and regulatory pathways of the liver Deficiencies of clotting factors III, VII, IX and X as well as abnormalities of platelet function leading to prolonged bleeding times and the risk of spontaneous bleeding: always check clotting studies and be prepared to give vitamin K supplements as well as clotting factors if necessary. Hypoalbuminaemia promoting the formation of oedema and making the regulation of circulating fluid volume more difficult: hypoalbuminaemia is difficult to correct with simple albumin infusions. Always be careful with fluid infusions to prevent gross tissue oedema and monitor the amount of sodium given in intravenous fluids. Reduced cellular and humoral immunity. Poor transmetabolism of endogenous waste products causing toxin-induced renal failure (hepatorenal syndrome): the best way to protect renal function is to ensure a high GFR during periods of sepsis and surgical stress. This means ensuring that patients are adequately hydrated and passing good volumes of urine (if necessary by using small amounts of osmotic diuretic).

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Presence of potential surgical difficulties, e.g. portal hypertensive disease causing distended veins in the abdominal viscera.

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Effect of decreased liver metabolism on anaesthetic agents, analgesics and other drugs. Prolonged effects and increased adverse effects of drugs normally metabolized by the liver need to be borne in mind. Use the British National Formulary to check which drugs undergo mainly hepatic metabolism and avoid hepatotoxic drugs. Associated problems in those suffering liver disease. This is particularly true of alcoholic liver disease, where chronic malnutrition may cause hypovitaminoses, alcohol dependency can give rise to acute withdrawal symptoms during hospital admission, and the chronic adverse effects of alcohol can disturb normal sleep patterns or responses to surgical stress. Be prepared to give intravenous vitamin supplements and start a course of withdrawal therapy for those with ongoing alcohol dependency. Avoid strong sedatives as they may produce bizarre effects and make assessment of the patient difficult, especially in the postoperative period. Intestinal obstruction Intestinal obstruction is mainly an exercise in fluid balance management. Assessment should concentrate on estimation of total fluid loss from the extracellular fluid space, depletion of sodium and potassium ions and the extent of any resultant acid–base imbalance. It is a good rule of thumb that the extent of fluid loss is often 50% greater than that estimated by gauging recorded losses. There may be many litres of fluid present in the bowel lumen that are lost to the circulation but not apparent. management Fluid losses in obstruction are mostly in the form of sodium and chloride ions, with additional loss of potassium ions. Acid–base imbalance results from total body depletion of these ions and will almost always correct spontaneously provided the fluid and electrolyte imbalances are treated. Gross dehydration should be corrected promptly but not too rapidly as sudden swings in extracellular fluid volume, especially if accompanied by rapid changes in sodium concentration, can cause cellular oedema and damage particularly in the young and elderly.

Nutrition Nutrition is a major factor in the assessment of surgical patients. Obesity (‘overnutrition’) is associated with an increased risk of respiratory complications, associated cardiovascular disease, diabetes and DVT due to immobility postoperatively. Malnutrition is often less well recognized than obesity but can have profound effects on healing and recovery following surgery. It is particularly prevalent in

the elderly and those with malignancy, and is often difficult to identify. How to assess The assessment of nutritional status ranges from simple and readily reproducible bedside tests to complex and specialist biochemical investigations. The following are the commonly used bedside tests. Body weight (percentage body weight lost): a relatively poor index since it is easily affected by simple dehydration and often reported inaccurately. Body mass index (weight/height2): most useful as an assessment of mild to moderate obesity. Triceps skinfold thickness: measured using springloaded callipers. Gives a reliable and reproducible measure related to the amount of subcutaneous fat. Grip strength: measured using a spring-loaded hand grip. Gives an imprecise indirect assessment of muscle mass, most sensitive at detecting mild malnutrition. The most useful biochemical tests include the following. Serum albumin (corrected): only of use in malnutrition. Often unreliable because it is affected by renal, hepatic and other diseases. When low in the presence of apparent malnutrition, acts as a good marker of status. It is slow to fall in response to real stresses and is slow to recover with treatment. Serum transferrin: difficult to measure but a much more sensitive measure of liver protein production (nutritional status).

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How to correct Obesity is difficult to correct: to reduce the risks associated with obesity may take months of weight reduction. It is only feasible for strictly elective surgery (e.g. hernia repair), particularly where the success of the surgery may partly depend on the body habitus of the patient. In overweight patients, particular attention should be paid to the risk of thromboembolism and respiratory complications caused by poor chest movements and general lack of mobility. Additional measures may be necessary, e.g. higher dose thromboprophylaxis. Malnutrition is not easy to address either. It may be impractical to delay surgery to allow correction of nutrition or surgery may be impossible while the cause is untreated (e.g. chronic sepsis or malignancy). Preoperative ‘hyperalimentation’ or protein–calorie supplementation has been shown to reduce the risk of some surgery, and most surgeons would advocate an aggressive policy towards supporting the nutrition of patients before and immediately after surgery. Generally, supplying additional nutrition is best considered via the normal alimentary route wherever possible, including:

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diet supplements; • high-protein/high-calorie fine-bore nasogastric tube feeding at night; • percutaneous gastrostomy feeding. •

young diabetics may have occult impairment in several body systems and are prone to complications that occur more readily and which are potentially more severe.

Role of total parenteral nutrition Total parenteral nutrition (TPN) or other parenteral methods of delivering nutritional support have significant problems. These are associated with the risk of intravenous line sepsis, venous thrombosis, embolism, liver cell injury, metabolic disturbances and other complications. However, it is the only way to deliver nutrition in circumstances where the gut is either inaccessible or nonfunctional. TPN is usually reserved for situations where enteral feeding is not possible or feasible and where nutritional support is likely to be necessary for 7 days or more.

Elderly The elderly are at greater risk for several reasons. With age, the normal physiological reserve inherent in most organ systems is eroded, even in the absence of identifiable disease (e.g. reduced forced vital capacity, reduced GFR). Coronary and peripheral arterial disease is common even if not clinically evident and further reductions in blood flow caused by surgical stresses can trigger major cardiovascular complications. Multiple organ disease is common and thus polypharmacy is also common. This increases the risk of drug interactions and adverse effects when anaesthetic and surgical drugs are added to existing medications.

High-risk groups Some groups are particularly prone to high operative risks due to severe or multiple organ disease. Neonates and small infants The physiological reserve of infants is low and the effects of abnormalities in one system often affect many other body systems. Diabetics The extent of organ involvement in diabetes has been discussed earlier but it is worth remembering that even

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Calculating risk Understanding and managing risk is the reason for preoperative assessment. Quantifying that risk is often difficult and surgeons and anaesthetists employ several systems of assessment in an attempt to categorize patient risk. It is not possible to predict the risk for a given patient in a particular circumstance but the box below shows examples of systems that assess risk for groups of patients.

Systems of risk assessment in surgery American Society of Anesthesiologists (ASA) This is a global scale offering five broad categories. 1 Fit with no obvious physical or psychological abnormality 2 Mild to moderate systemic disturbance that does not amount to a threat to life or significantly limit the patient (e.g. well-controlled diabetes) 3 Moderate to severe systemic disease that places significant limitations on the patient (e.g. uncontrolled diabetes, established diabetic nephropathy) 4 Severe systemic disturbance that is incapacitating or a threat to life (e.g. diabetic renal failure and coronary disease) 5 Life-threatening disease that is likely to be fatal with or without an operation (e.g. ruptured aortic aneurysm)

POSSUM (Per-Operative System for the Surgical enUmeration of Mortality) This is a mathematical equation that scores factors relating to the patient and the operation and adjusts them to produce a figure for the estimated probability of death. Several versions exist with minor modifications (p-POSSUM, v-POSSUM). Many have been tested and shown to be fairly accurate, although most overestimate risk in very safe conditions (e.g. elective hernia repairs) and underestimate risk in high-risk situations (e.g. the very old, the very young, multiple comorbiditiy). Factors used in POSSUM scoring include: Age Cardiac history Respiratory history Systolic blood pressure Heart rate Glasgow Coma Scale

Serum Na+ Serum K+ Serum urea White blood count Haemoglobin ECG

Size of operation Number of operations Surgery for cancer Peritoneal soiling Blood loss Operation severity

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Key points

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The role of assessment is to provide information on risk, define and reduce the extent of known risks, and discover unknown risks Liaise early with anaesthetists and medical specialists to help select appropriate investigations and treatment Target investigations rather than use ‘routine’ testing The most useful investigations are often those providing dynamic functional information Elderly patients often have hidden multiple organ disease

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Diabetics may develop significant multiple organ dysfunction even in young adulthood Beware occult coronary artery disease Remember the effects of common drugs such as the combined oral contraceptive pill Consider nutrition: it is an underdiagnosed problem Do not forget the role of the professions allied to medicine: rehabilitation and recovery begins before surgery

02 Assessment of patients for surgery and preoperative medical management at a glance Definition Preoperative assessment: a process that provides information on risk, defines and reduces the extent of known risks, and discovers unknown risks in a patient prior to surgery Goals of preoperative assessment Assess risk of surgery vs. risk of medical or no treatment Document extent of known disease Discover unknown disease Plan prophylactic or definitive treatment of comorbid conditions that might complicate or adversely affect surgery Patient selection: based on the best available evidence and the preoperative assessment, the patient is given the facts about an operation (success rate and complications) and advised whether they would or would not be a suitable candidate for that operation. Only after this can the patient make an informed choice Identify high-risk groups and calculate risk using ASA or POSSUM systems

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Methods of assessment Assessment based on patient pathway Preoperative Perianaesthetic Postoperative

• • •

System assessment (most commonly used) Cardiac Respiratory Endocrine Haemostasis Gastrointestinal Nutrition

• • • • • •

Principles of system assessment A good history and clinical examination will uncover most problems

•

• • •

Investigations should be used to confirm or quantify clinical findings The most useful investigations are those that give functional information Ask the experts (anaesthetist or physician) if a difficult problem is encountered Details of system assessment Cardiac Ischaemic heart disease Risk can be calculated clinically using Goldman cardiac index or Detsky cardiac score Elective surgery should be delayed until 6 months after myocardial infarction

• •

Arrhythmia Patients may be on anticoagulants because of an arrhythmia

•

Left ventricular failure Avoid negative inotropes and monitor fluid balance

•

Respiratory COPD Patient must stop smoking! Physiotherapy should be started preoperatively Adequate analgesia should be given: patients in pain will not cough Adequate hydration should be maintained: prevents viscid secretions

• • • •

Endocrine Steroids Patients on long-term steroids may need i.v. hydrocortisone postoperatively

•

Diabetes mellitus Control blood glucose levels perioperatively

•

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Diet controlled Monitor blood sugar, unlikely to require insulin

•

Oral hypoglycaemic agents Stop oral therapy on the day of surgery, monitor blood sugar For major surgery may need i.v. dextrose/insulin sliding scale

Intestinal obstruction Causes major fluid, sodium and potassium loss, and acid–base disorders (usually metabolic acidosis) depending on the level of obstruction Losses are generally 50% greater than recorded losses because of fluid sequestration in the bowel lumen

Insulin-dependent diabetes Omit morning dose of insulin, monitor blood sugar Commence sliding scale insulin infusion Use sliding scale to adjust insulin dose Haemostasis Thrombophilias Risk factors: obesity, immobility, smoking, age > 40 years, malignant disease, history of DVT/PE, known thrombophilia (protein C or protein S deficiency, factor V Leiden mutation), oral contraceptive pill, major surgical operation Low risk: no specific prophylaxis Medium risk: low-dose chemoprophylaxis (heparin), mechanical prophylaxis (compression stockings) High risk: mechanical prophylaxis, high-dose chemoprophylaxis, low-dose anticoagulation

Reduced metabolism of anaesthetic agents, analgesics and other drugs

• •

Nutrition Obesity Increased risk of respiratory and cardiovascular disease, DVT, diabetes, infection

•

Malnutrition Often not recognized. Results in poor healing and delayed recovery

• • •

Assessment Body weight: not a good index of nutritional status Body mass index (weight/height2): useful assessment of obesity Triceps skinfold thickness: reliable measure of subcutaneous fat Grip strength: indirect assessment of muscle mass, detects mild malnutrition Serum albumin: useful in assessing malnutrition but may be affected by disease Serum transferrin: difficult to measure but sensitive marker of nutritional status

Bleeding disorders Inherited disorders Warfarin/NSAIDs Liver disease

• • •

Gastrointestinal disorders Liver disease Bleeding disorders Hypoalbuminaemia Reduced cellular and humoral immunity Poor metabolism of endogenous waste products: hepatorenal syndrome

• • • •

Evidence-based medicine Prytherch, D.R., Whiteley, M.S., Higgins, B., Weaver, P.C., Prout, W.G. & Powell, S.J. (1998) POSSUM and Portsmouth POSSUM for predicting mortality. Physiological and Operative Severity Score for the enUmeration of Mortality and morbidity. Br J Surg 85, 1217–20.

• • • • • • •

Management Attention should be given to prophylaxis Nutritional support essential before and after surgery: alimentary route is preferable

• •

http://www.asahq.org American Society of Anesthesiologists website. http://www.rcoa.ac.uk/publications.htm Royal College of Anaesthestists publications/guidelines website. http://www.ncepod.org.uk National Confidential Enquiry into Peri-Operative Deaths website.

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Prophylaxis

Introduction, 71

Principles of prophylaxis, 71

Must know Must do Must know Principles of prophylaxis for common medical and surgical disorders including common cancers Principles of prophylaxis for surgical complications Must do Participate in the prophylaxis used in a patient undergoing elective major surgery for cancer Participate in the prophylaxis used in a patient undergoing emergency surgery for an acute abdomen

Introduction Prophylaxis (i.e. prevention) is always better than cure. Thus a careful assessment of the relative risks of complications and their prevention is an important consideration in preoperative planning. Once the diagnosis has been made and the indications for surgery established in the individual patient, the potential benefits of the operation must be offset against the risks of the procedure for the individual patient. In some patients, the risks factors (from comorbid cardiovascular or respiratory disease, etc.) are such as to preclude surgical intervention. The second category of risk relates to complications that may occur during and after surgery and general anaesthesia. The occurrence of these can be minimized or avoided by careful planning, anticipation and the institution of specific prophylactic measures. The prophylactic measures themselves must carry minimum risks to the patients and their benefits must outweigh any risks by a significant margin. In this respect, drugs used for prophylaxis must carry a high therapeutic ratio (benefit greatly exceeds adverse effects). Clinicians should also give consideration to their own protection and that of their colleagues. Infectious disorders may be transmitted from patients to doctors and vice versa. Many viral disorders, including hepatitis (A, B, C) and acquired immunodeficiency syndrome (AIDS), are included in this category. Clinicians who contract

Specific prophylaxis, 71

AIDS or whose serology (antibody/antigen profile) indicates risk of transmission of viral hepatitis are not allowed to practise clinical medicine. Health workers in most hospitals are now immunized against hepatitis B.

Principles of prophylaxis Medical prophylaxis is based on a number of considerations. The risk of certain complications varies from procedure to procedure and may be influenced by prior medication, including oral contraception in females. To be maximally effective, prophylactic measures must be started before the operation or procedure and be continued until the risk period has passed. For example, prophylactic heparin used to prevent postoperative venous thromboembolism must be started preoperatively and be continued at least until the patient is discharged from hospital. The prophylactic measure/device/drug must be effective and carry very little risk of itself. Specific prophylaxis is used to prevent complications that are relatively common, e.g. antibiotics after elective bowel surgery. Specific prophylaxis is also used for complications that are relatively rare but have serious consequences including death if and when they occur.

• •

• • •

Specific prophylaxis Prophylaxis for postoperative surgical infections Several measures have been introduced over the years to reduce postoperative infection. No surgical wound is completely sterile but provided bacterial counts are kept low, the body’s normal immune system will cope with the small inoculum and prevent infection. The following measures are known to reduce infection rates: laparoscopic vs. open operations; skin cleansing/disinfection; filtering of the air in the operating room; surgical masks and impervious surgical microfibre gowns; prophylactic antibiotics.

• • • • •

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Infection related to a surgical operation is referred to as a surgical site infection (SSI) and may be superficial or deep or associated with an organ/space.

Table 5.1 Site-specific organ/space surgical site infections in the surgical specialties (from Scottish Intercollegiate Guidelines Network, www.sign.ac.uk).

Superficial SSI. Defined as infection occurring within 30 days of the operation that involves only skin and subcutaneous tissues of the incision and at least one of the following: purulent discharge with or without laboratory confirmation; bacteria isolated from culture of wound; clinical signs (any one or more of pain/tenderness, localized swelling, redness, heat); diagnosis of superficial SSI by attending surgeon.

Arterial or venous infection Breast abscess or mastitis Disc space Ear, mastoid Endocarditis Eye, other than conjunctivitis Gastrointestinal tract Intra-abdominal Intracranial, brain abscess or dura Joint or bursa Meningitis or ventriculitis Myocarditis or pericarditis Oral cavity Osteomyelitis Other infections of lower respiratory tract (e.g. abscess or empyema) Sinusitis Spinal abscess without meningitis Upper respiratory tract

• • • •

Deep incisional SSI. Defined as infection occurring within 30 days after operation if no implant is left in place or within 1 year if implant is in place, and the infection appears to be related to the operation and the infection involves deep soft tissues (e.g. fascial and muscle layers) and at least one of the following: purulent discharge from deep incision but not from organ/space component of the surgical site; deep incision dehisces spontaneously or is deliberately opened by surgeon to evacuate pus; clinical signs (one or more of fever > 38 °C, localized pain, tenderness); abscess/other evidence of deep infection; diagnosis by attending surgeon.

• • • • •

Organ/space SSI. Defined as infection occurring within 30 days after operation if no implant is in place or within 1 year if implant is in place and the infection appears to be related to the operation and involves any part of the anatomy (e.g. organs or spaces) other than the incision, which was opened or manipulated during the operation and one of the following: purulent discharge from a drain into the organ/space; organisms isolated from an aseptically obtained culture of fluid or tissues in organ/space; abscess or other evidence of infection involving organ/space found on direct examination, during reoperation or by histopathological or radiological examination; diagnosis by attending surgeon.

• • • •

The classification of organ/space SSI in surgical practice (excluding gynaecology) proposed by the Scottish Intercollegiate Guidelines Network (SIGN) is shown in Table 5.1. In general the risk of SSI is determined by the nature of the operation as outlined in Table 5.2. The benefit of antibiotic prophylaxis is related to the severity of the consequences of SSI. Thus antibiotic prophylaxis reduces postoperative mortality after colectomy

with anastomosis and long-term morbidity after hip replacement surgery. Antibiotic prophylaxis also reduces hospital stay and therefore the costs. The disadvantages of antibiotic prophylaxis cannot be overlooked and include: antibiotic-associated colitis due to Clostridium difficile; emergence of antibiotic-resistant bacteria, e.g. methicillin-resistant Staphylococcus aureus (MRSA); immediate hypersensitivity and other organ-specific toxicity, e.g. renal failure, liver damage and cholestasis, nerve damage, etc. Patients who give a history of anaphylaxis or urticaria or rash immediately after penicillin or cephalosporin therapy are at risk of immediate hypersensitivity to penicillins and should therefore not receive antibiotic prophylaxis with any β-lactam antibiotic. The principles governing antibiotic prophylaxis include the following: used if there is a significant risk of SSI; used if the consequences of an SSI are severe; used if randomized prospective trials have confirmed efficacy; antibiotics used must cover the common pathogens and are administered intravenously; prophylaxis should be started within 30 min of induction of anaesthesia; single dose of antibiotic for prophylactic use is the same as would be used therapeutically;

• • •

• • • • • •

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Table 5.2 Incidence of superficial and deep surgical site infection (SSI) in relation to type of operation. Type of operation

Definition

Examples

Clean

Operations that do not involve gastrointestinal, genitourinary or respiratory tracts, no infection present

Thyroidectomy

Clean-contaminated

Operations that involve gastrointestinal, genitourinary or respiratory tracts with minimal or no obvious contamination

Gastrectomy

Contaminated/dirty

Significant spillage, spontaneous or during operations on gastrointestinal tract, operations in presence of infection

Bowel perforation Drainage of abscess

•

additional dose is administered if there is blood loss exceeding 1500 mL or the operation is very prolonged (> 3 h). The recommended indications for prophylactic antibiotics as outlined by the SIGN guidelines for elective surgery are shown in Table 5.3. Each hospital has its own specific antibiotic policy that mandates which antibiotics are used for prophylaxis and which for first-line treatment of community and hospital-acquired infections.

Prevention of hospital-acquired infections Hospital-acquired infections with resistant organisms, e.g. MRSA, cause significant morbidity and mortality and add considerably to the cost of care. In addition to the risk to the individuals who contract them, there is the added concern of spread to other patients. In severe outbreaks, whole wards may need to be closed. Hospital-acquired infections occur in all specialties, including the intensive care unit where the major concern relates to ventilator pneumonia caused by resistant Gram-positive and Gramnegative bacteria. The principles governing prevention of these infections are based on sound common sense and include: strict adherence to hospital antibiotic practice; always washing hands after examining a patient; strict aseptic care of intravenous lines; isolation of infected cases. Patients with established MRSA infections are nursed in a separate room and require specialist bacteriological advice about the antibiotic treatment needed. All attending staff (medical and nursing) should wear protective clothing (plastic apron and gloves) that is discarded in a designated container immediately the patient is seen. This is followed by thorough disinfection of the hands with alcohol.

• • • •

Average incidence of SSI

> 20%

Prophylaxis following trauma All open wounds are contaminated by microorganisms and debris, such as bits of clothing, soil, grit, etc. The addition of soft tissue injury, including ischaemic muscle, further reduces the tissue oxygen tension, thus favouring anaerobic infection. Of particular concern are spore-bearing Gram-positive organisms, including clostridia that may cause gas gangrene (Clostridium welchii) or tetanus (Clostridium tetani). Other organisms may be present in particular situations, e.g. human bites may produce serious mixed infections. Most patients have received active tetanus immunization in childhood, although few have subsequent booster injections in adult life. If active immunization has not been administered in the last 5 years, a booster toxoid injection should be given. In previously non-immunized patients and in the presence of gross contamination of the wound, passive immunity with human antitetanus globulin should be administered. First-line treatment of all open wounds includes surgical exploration and removal of dead tissue (débridement). This is followed by primary suture closure unless the wound is grossly contaminated and there has been a delay of several hours before presentation, when delayed closure after initial formation of granulation tissue is practised. Wounds exposing fractured bones (compound fractures) require urgent treatment to deal with the fracture and provide soft tissue cover as well as systemic antibiotic therapy.

Prophylaxis of deep vein thrombosis The importance of deep vein thrombosis (DVT) is stressed by the fact that 1% of patients admitted to general hospitals die from pulmonary embolism (PE) and most fatal emboli result from postoperative DVT. The Thrombo-embolic

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Table 5.3 Recommended indications for prophylactic antibiotics based on published randomized controlled trials (from Scottish Intercollegiate Guidelines Network). Cardiothoracic operations/procedures Cardiac pacemaker insertion Coronary artery bypass grafting Pulmonary resection

Gastrointestinal surgery Colorectal surgery Appendicectomy Open biliary surgery Breast surgery Endoscopic gastrostomy Gastroduodenal surgery Oesophageal surgery Small bowel surgery Mesh hernia repair including laparoscopic

Recommended Recommended Recommended Highly recommended Recommended Recommended Recommended Recommended Recommended Recommended Recommended Recommended

Neurosurgery Craniotomy Cerebrospinal fluid shunt

Recommended Recommended

Orthopaedic surgery Total hip replacement Prosthetic knee joint replacement Close fracture fixation Hip fracture repair Spinal surgery Insertion of prosthetic device

Highly recommended Highly recommended Recommended Recommended Recommended Recommended

Urology Transurethral prostate biopsy Shock-wave lithotripsy Transurethral resection of prostate

Recommended Recommended Recommended

Vascular surgery Lower limb amputation Vascular surgery of abdomen and lower limb

Table 5.4 Risk factors for deep vein thrombosis. Age (> 40 years) Prior history of deep vein thrombosis Surgery Trauma Sepsis (particularly with endotoxin) Recumbency/immobilization Obesity Malignancy Heart disease Pregnancy Oestrogen administration Inflammatory bowel disease Blood disorders Thrombocytosis Polycythaemia Antithrombin III deficiency Fibrinolytic deficiencies

Mechanical prophylaxis Mechanical measures aim at diminishing venous stasis in the legs. Such measures include elevation of the foot of the bed by 10–15° and the use of compression stockings (properly called antithrombotic rather than antiembolic). Pneumatic-graded sequential compression devices have been shown to inhibit venous stasis and enhance fibrinolytic activity. Electrical stimulation of calf muscles has also been used peroperatively. One of the most important prophylactic measures is early ambulation postoperatively a this does not include sitting in a chair!

Pharmacological prophylaxis Recommended Recommended

Risk Factors (THRiFT) Consensus Group recommends that prophylaxis should be given to patients (according to the degree of risk for DVT), at least until discharge from hospital. Adequate methods of prophylaxis for DVT are available and their use saves lives. All patients aged over 40 and those with the risk factors listed in Table 5.4 should have prophylaxis for DVT. General prophylactic measures include adequate hydration, mobilization preoperatively and postoperatively, and avoidance of oestrogen therapy for 6 weeks prior to elective surgery. Specific measures are aimed at reducing venous stasis by mechanical techniques and countering hypercoagulability pharmacologically.

Three agents have been used for prophylaxis of DVT: warfarin, dextran and heparin. Aspirin, which inhibits platelet aggregation, does not prevent postoperative venous thrombosis. Warfarin sodium This is an effective prophylactic oral antithrombotic agent and its use reduces the incidence of DVT and PE. It acts by inhibiting the synthesis of vitamin K-dependent coagulation factors (II, VII, IX, X; see Fig. 37.35). However, because of its delay in action and slow reversal in the event of bleeding, warfarin has not found much favour with surgeons as a prophylactic anticoagulant. Recently, minidose warfarin (1 mg/day without laboratory control) has been used successfully for prophylaxis in gynaecology. Dextran 70 Dextran 70 in 500 mL of 5% dextrose, given as an intra-

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venous infusion at the time of operation and for 2 days postoperatively, reduces proximal vein thrombosis and PE. Low-molecular-weight dextran interferes with platelet function and fibrin polymerization (see Fig. 37.35) and is associated with less bleeding than heparin. It is used extensively in elective orthopaedic surgery, especially hip arthroplasty. Subcutaneous heparin Low-dose or minidose heparin is the most widely used agent for prophylaxis of DVT. In 1975, Kakkar showed that subcutaneous minidose heparin reduced the incidence of DVT from 24.6 to 7.7%. Heparin acts by accelerating antithrombin III inhibition of activated factor X (see Fig. 37.35). The prophylactic regimen consists of 5000 units administered 2 h preoperatively followed by 5000 units every 8 –12 h postoperatively. There are exceptions to the start time. Thus when an epidural block is considered for postoperative analgesia, most anaesthetists prefer to delay the first dose of heparin until the epidural catheter has been placed. Low-molecular-weight heparins constitute an alternative to unfractionated heparin and may have some advantages (single daily injection, low cost, fewer haemorrhagic adverse effects). Heparin (5000 units) in combination with dihydroergotamine (0.5 mg), which increases venous flow by constricting capacitance vessels, has also been used for prophylaxis of venous thrombosis and this combination reduces the incidence of wound haematoma.

02 Figure 5.1 Large decubitus ulcer in sacral region.

patients; • diabetic patients with peripheral vascular disease; • patients with impaired cutaneous sensation; • patients with rheumatoid arthritis; • patients with spinal cord injury. • Pressure sores are entirely preventable by careful skin care and hygiene and frequent turning of the patient. Patients at risk may be nursed on special pneumatic mattresses. Once established, pressure sores are treated by débridement (removal of slough), ensuring adequate drainage of pus and daily dressings with zinc lotion to encourage formation of healthy granulation tissue. Plastic surgical treatment by flap advancement may be necessary for large defects once the infection has been controlled.

Prevention of pressure sores Patients lying immobile in bed for long periods are at risk of developing pressure sores (bedsores, decubitus ulcers). These occur at points where the patient’s own weight causes prolonged and excessive pressure, leading to diminished tissue perfusion and ischaemic necrosis of the skin and subcutaneous tissues often extending to the underlying bone. The lesion starts as a red dusky discoloration that ulcerates rapidly and extends deeply and laterally beneath the skin margins in a matter of days (Fig. 5.1). When large, decubitus ulcers cause considerable morbidity from infection and a protein-losing catabolic state. They are also slow to heal and may require extensive plastic surgery. Common sites include: buttocks and sacral region; skin over greater trochanters; heels. All patients immobile for long periods are at risk; however, some patient groups are especially prone: the elderly; incontinent patients; patients on steroids;

• • • • • •

Prevention of chest problems Postoperative ventilation and functional lung volumes are impaired largely because of pain, with reduction of chest wall and diaphragmatic movements that, together with the excessive bronchial secretion after general anaesthesia (bronchorrhoea) and diminished efficacy of coughing, cause de-aeration of the alveoli. This leads to patchy collapse and bronchopneumonic consolidation if infection supervenes. The patients at risk of postoperative pulmonary collapse/infection and consolidation are: cigarette smokers; patients with chronic obstructive pulmonary disease (COPD); obese patients. Smokers need to give up smoking for at least 3 months before improvement in their pulmonary function can be expected. Thus short-term abstinence immediately before surgery is of doubtful value. Selected patients with chronic obstructive airways disease may benefit from bronchodilators, usually administered by aerosol inhalation. Deep breathing exercises under the direction of a physiotherapist

• • •

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and incentive spirometry for some days before surgery are beneficial. One of the most important prophylactic measures is effective pain relief without depression of the respiratory centre. For this reason epidural block is used extensively after major abdominal and abdominothoracic operations. Early detection of patchy basal collapse and vigorous postoperative chest physiotherapy/incentive spirometry may prevent pneumonic consolidation.

Prevention of acute renal failure

Those at risk include: jaundiced patients undergoing surgery; patients with liver disease; patients undergoing cardiopulmonary bypass and aortic surgery; patients with blood volume deficits. The important prophylactic measures include: prompt correction of any blood volume deficits; preoperative hydration in jaundiced patients; induction of natriuresis by mannitol or loop diuretics at the start of the operation in jaundiced patients; hourly urine output (bladder catheter); avoidance of nephrotoxic drugs/antibiotics; renal-dose dopamine if urine output falls persistently below 30 mL/h despite volume replacement; Renal failure and its treatment are dealt with in Chapter 14.

• • • • • • • • • •

Prevention of stress ulceration Stress ulceration is rare nowadays but is encountered in patients who sustain severe trauma (especially burns) or undergo major surgery (including neurosurgery). The ulceration may consist of a single ulcer in the duodenum (known as Curling’s ulcer) or, more usually, multiple erosions involving the gastric antrum and body of the stomach (erosive gastritis). Prevention is by suppression of gastric acid secretion using intravenous histamine H2 blockers or proton pump inhibitors or by protection

of the mucosa using agents such as sucralfate. The stress ulceration may cause severe gastrointestinal bleeding, which is initially controlled by conservative measures including flexible endoscopic control. Rarely, surgery (truncal vagotomy and antrectomy) may be needed if bleeding persists.

Protection against AIDS and hepatitis There is no doubt that doctors and nurses risk acquiring hepatitis (especially hepatitis B infection) and AIDS, but the risk is small especially if suitable precautions are taken against accidental injury with ‘sharps’ during surgery and injection of, or procurement of blood samples from, infected patients. Likewise, infected doctors have been known to transmit disease to their patients. In most instances this has been hepatitis B and C. The infectivity of human immunodeficiency virus (HIV) is much less than that of hepatitis B virus; thus transmission of HIV requires direct inoculation by a ‘sharps’ injury contaminated with the virus. The following precautions are necessary in relation to patients known to be HIV-positive or infected with or carrying hepatitis. Strict protocol to avoid ‘sharps’ injuries: no sharp instrument is handed from person to person. The item is placed in an intermediate container for subsequent careful disposal. Double gloving. Avoidance of spillage of blood and body secretions. Labelling suspect blood specimens as high risk so that laboratory staff are alerted when handling the specimen. Disinfection of any spillage by gluteraldehyde. Use of disposable equipment/aprons and impermeable gowns. Disposal of all used disposable items and clinical waste by incineration after bagging in clearly marked rip-proof containers. All healthcare workers, including medical students, are now vaccinated against hepatitis.

• • • • • • •

Prophylaxis at a glance Definition Prophylaxis: the process whereby disease or complications are prevented by protective measures. Principles of surgical prophylaxis • Risk of complications varies from procedure to procedure • Prophylactic measures must be started before the operation or procedure and be continued until the risk period has passed

• Prophylactic measure/device/drug must be effective and carry very little risk of itself • Specific prophylaxis is used to prevent common complications or rare complications that are catastrophic if they occur Surgical infection Measures that reduce infection rates • Laparoscopy

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• Skin cleansing/disinfection • Filtering of the operating theatre air • Surgical masks and impervious surgical microfibre gowns • Prophylactic antibiotics Surgical site infections • Superficial SSI: infection occurring within 30 days of the operation that involves only skin and subcutaneous tissues of the incision • Deep incisional SSI: infection occurring within 30 days after operation if no implant is left in place or within 1 year if implant is in place • Organ/space SSI: infection occurring within 30 days after operation if no implant is in place or within 1 year if implant is in place and the infection involves any part of the anatomy other than the incision • In general the risk of an SSI is determined by the nature of the operation (see Table 5.2). Hospital-acquired infection (MRSA) • Strict adherence to hospital antibiotic practice • Always wash hands after examining patients • Strict aseptic care of intravenous lines • Isolation of infected cases Trauma • Risk of anaerobic infection, especially with contaminated wounds or after human bite • Clostridial infection: gas gangrene (Clostridium welchii ) or tetanus (Clostridium tetani ) • If no active immunization within 5 years, give booster tetanus toxoid injection • If never immunized or gross contamination present, give human antitetanus globulin Deep vein thrombosis • 1% of patients admitted to general hospitals die from PE • Most fatal emboli result from postoperative DVT • Risk factors for DVT: age > 40 years, previous DVT, surgery, trauma, sepsis, immobility, obesity, malignancy, oestrogen General measures • Adequate hydration • Mobilization preoperatively and postoperatively • Avoidance of oestrogen therapy Specific measures Mechanical prophylaxis • Elevation of foot of bed by 10 –15° • Compression stockings • Pneumatic-graded sequential compression devices • Electrical stimulation of calf muscles • Early postoperative ambulation

Pharmacological prophylaxis • Warfarin sodium: effective in preventing DVT. Acts by inhibiting synthesis of vitamin K-dependent coagulation factors (II, VII, IX, X). Cumbersome to use • Dextran 70: administered i.v. in 500 mL of 5% dextrose at time of operation and for 2 days postoperatively. Interferes with platelet function and fibrin polymerization • Subcutaneous heparin: low-dose or minidose heparin is the most widely used agent for DVT prophylaxis. Acts by accelerating antithrombin III inhibition of activated factor X. Give 5000 units 2 h preoperatively plus 5000 units every 8 –12 h postoperatively. Low-molecular-weight heparins are a popular alternative • Note that aspirin does not prevent postoperative venous thrombosis Respiratory problems Postoperative lung function impaired by • Pain • Reduction of chest wall movement • Reduction of diaphragmatic movement • Bronchorrhoea, decreased ciliary motion • Diminished efficacy of coughing Effects • De-aeration of the alveoli • Patchy collapse • Bronchopneumonia Patients at risk • Cigarette smokers • Patients with COPD • Obese patients Perioperative care • Aerosol bronchodilators for patients with COPD • Deep breathing exercises and incentive spirometry preoperatively • Effective pain relief without depression of the respiratory centre, e.g. epidural block • Vigorous postoperative chest physiotherapy and incentive spirometry Acute renal failure Patients at risk • Jaundiced patients • Patients with liver disease • Patients undergoing cardiopulmonary bypass and aortic surgery • Patients with blood volume deficits Prophylactic measures • Prompt correction of volume deficits • Preoperative hydration in jaundice

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• Induction of natriuresis by mannitol or loop diuretic at

• Considerable morbidity from infection and protein-losing

start of operation in jaundiced patients • Hourly urine output (bladder catheter) • Avoid nephrotoxic drugs/antibiotics • Renal-dose dopamine if urine output < 30 mL/h despite volume replacement

catabolic state

Stress ulceration Patients at risk • Severe trauma (especially burns) • Major surgery (including neurosurgery)

Type of ulcer • Erosive gastritis (common) • Single duodenal ulcer (Curling’s ulcer) Management • Suppression of gastric acid secretion • Proton pump inhibitors (e.g. omeprazole) • Mucosal protective agents (e.g. sucralfate) If gastrointestinal bleeding • Conservative treatment initially • Rarely, surgery required Pressure sores • Immobile patients at risk • Pressure of patient’s own weight leads to ischaemic necrosis of tissues

Evidence-based medicine Scottish Intercollegiate Guidelines Network (2000) Antibiotic Prophylaxis in Surgery. www.sign.ac.uk. Thrombo-embolic Risk Factors (THRiFT) Consensus Group (1992) Risk of and prophylaxis for venous

Common sites • Buttocks and sacral region • Skin over greater trochanters • Heels Prevention • Careful skin care and hygiene • Frequent turning of patients • Nurse at-risk patients on pneumatic mattresses Treatment • Débridement (removal of slough) and drainage of pus • Daily dressings with zinc lotion to encourage granulation tissue • Plastic surgical treatment by flap advancement in some patients AIDS and hepatitis • Generally to protect staff from injury with contaminated material • Strict protocol to avoid ‘sharps’ injuries • Correct disposal of all used items and clinical waste • Vaccination of health workers against hepatitis

thromboembolism in hospital patients. Br Med J 305, 567–74. National Guideline Clearinghouse, www.guideline.gov. A very useful public resource for evidence-based clinical practice guidelines including prophylaxis.

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Transfusion of Blood and Blood Products Introduction, 79 Good transfusion practice, 79

Blood and plasma products, 81

Must know Must do Must know Commonly used blood products, synthetic colloids and crystalloid solutions Indications for blood component transfusions Complications of blood component transfusions Complications of synthetic colloid and crystalloid infusions Must do Be involved in the resuscitation of a patient with hypovolaemic shock Be involved in the management of a patient with irondeficiency anaemia Be involved in the resuscitation of a patient with severe dehydration See a patient undergoing a blood product transfusion

Introduction In the UK, all blood and plasma products are derived from voluntary non-remunerated donors aged 18 –65 years. In accordance with the policy of the Department of Health, donors are carefully selected and all donations are tested for known markers of disease. Currently these are syphilis, human immunodeficiency virus (HIV)-1, HIV-2, hepatitis B virus (HBV) and hepatitis C virus (HCV). Sterilization of other transmitting agents not detected by donor screening is not guaranteed. Thus the risk of disease transmission though very low cannot be ignored. The current concern is with the recently identified hepatitis G virus and the prion protein responsible for new variant Creutzfeldt–Jakob disease (CJD).

Good transfusion practice Modern blood transfusion is based on the intravenous administration of those components of blood that are deficient in a particular patient rather than transfusion of whole blood. This practice ensures the safe economic use

Adverse effects of transfusion, 83

of blood products and increases the therapeutic scope. Thus a single blood donation may be used for treating a variety of disorders. The blood products available in the majority of hospitals are shown in Table 6.1. Safe blood transfusion depends on: careful selection of donors; quality assurance testing of blood and blood products prepared and issued by transfusion centres; blood grouping, antibody screening and cross-matching;

• • •

Table 6.1 Blood products available for therapy. Red cell preparations* Whole blood Red cell concentrate Leukocyte-poor red cell concentrate Frozen red cells (not available generally) Autologous blood Platelets* Random donor pooled Single-donor apheresis Human leukocyte antigen-matched Cross-matched Plasma components Plasma protein fraction (5% albumin in buffered saline) Salt-poor human albumin (25%) Fresh frozen plasma (plasma + all clotting factors)* Cryoprecipitate (factor VIII, von Willebrand factor, fibrinogen)* Factor VIII concentrate Factor VIIa Factors II, IX, X Factor VII von Willebrand factor Antithrombin III Intravenous IgG Human normal IgG Specific hyperimmune IgG (Rh anti-D, tetanus, etc.) Fibrin sealant (glue) * ABO compatibility essential.

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blood ordering policies; • standardized strict guidelines for administration and monitoring of • patients receiving blood products; • local and central reporting of adverse effects when encountered.

It is a medicolegal requirement within the UK that details of any blood component infusion are fully documented in the patient’s case notes, including: indication; date/time of issue, donation number; ordering physician; duration of infusion; who gave the infusion and who checked it prior to administration; time the infusion was commenced. The written procedures for infusing blood and blood components are issued by the hospital blood transfusion department, and hospital management is responsible for ensuring that the written procedures are updated and made available to all staff (medical and nursing) who may have to administer transfusions. Two blood samples (clotted and anticoagulated in ethylenediaminetetraacetic acid, EDTA) are sent with the completed request form to the blood transfusion department once the decision is taken that the patient needs a transfusion. The patient’s red cells are grouped for ABO and Rh(D). The antibody screen is carried out on all the serum samples to detect the presence in the recipient of any clinically important antibody that would haemolyse the transfused cells. Cross-matching entails testing the red cells from the donor units against the patient’s serum. The final step in the safe administration of blood is the verification by two people that the information on the transfusion request form, the labels on the unit of blood and the patient identification (from case notes and wrist band) all agree. This remains the weakest link in the safety chain and most deaths from blood transfusion are related to misappropriation. It should be noted that there is no medical or surgical condition that justifies the transfusion of less than 2 units of blood.

• • • • • •

Elective situation Blood tariffs Unnecessary ordering of cross-matched blood constitutes bad practice and is wasteful of a limited resource. Many operations do not usually require perioperative blood transfusion; others may do and some incur a need for red cells as a matter of routine. Nowadays, blood for elective surgery is ordered in accordance with the ‘blood tariff’ policy. This is based on the average requirement of a par-

ticular operation. Type and screen (group and hold, group and save) is all that is required for operations that do not usually require blood. The patient’s serum is kept in the blood transfusion laboratory for 7 days. Should blood be required, cross-matched red cell units can be available in 15 min.

Haemoglobin transfusion thresholds Patients do not require a preoperative blood transfusion unless the haemoglobin is less than 8 g/dL. The exceptions to this rule are patients with cardiovascular disease or those expected to have covert cardiovascular disease (elderly patients and patients with peripheral vascular disease). These patients are likely to benefit and thus require a blood transfusion when their haemoglobin falls below 9 g/dL.

Blood-sparing strategies These should be considered in all patients who might require a blood transfusion, especially: Jehovah’s Witnesses; patients with multiple antibodies; patients with serious anxieties about the transfusion of allogeneic blood. Blood-sparing strategies that are commonly used include: preoperative autologous blood donation (predeposit); erythropoietin; acute normovolaemic haemodilution; antifibrinolytic drugs; cell salvage.

• • • • • • • •

Preoperative autologous blood donation The benefit of autologous, as distinct from allogeneic, transfusion is the elimination of disease transmission and allergic and incompatible reactions (other than procedural errors). It should only be offered when it is possible to guarantee admission and operative dates and is targeted to patients who are to undergo elective surgery where blood will be lost and whose haemoglobin at presentation is 11.0–14.5 g/dL in males and 13.5–14.5 g/dL in females. The experience with predeposit in the UK has been disappointing because of the limitations of the National Health Service. It is more expensive than allogeneic blood transfusion. In addition, the blood is wasted if the patient does not need perioperative transfusion as it cannot be administered to other patients; if the patient requires blood in excess of the predeposited units, all possible advantage is lost. Thus a balance must be struck between collecting enough units to minimize allogeneic exposure and wastage.

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Erythropoietin This hormone is produced and secreted by the kidneys and regulates erythropoiesis. Recombinant human erythropoietins (α and β) are widely used in the anaemia associated with renal failure and as a blood-sparing strategy in patients undergoing major surgery. It is administered subcutaneously (600 units/kg) three times weekly and on the day of surgery and is preferably accompanied by oral/intravenous iron therapy. Erythropoietin is used to counteract blood loss in: patients scheduled for major surgery under 70 years of age with a presenting haemoglobin < 13 g/dL; patients scheduled for major surgery who refuse allogeneic blood transfusion; Jehovah’s Witnesses. The risk of erythropoietin therapy is deep vein thrombosis, especially if the haemoglobin exceeds 13 g/dL. A 500-mL venesection is necessary whenever erythropoietin induces the patient’s haematocrit to rise above 0.5. Patients on erythropoietin should have their haematocrit checked weekly.

• • •

Acute normovolaemic haemodilution Immediately before surgery, usually following induction, 1000 mL of blood are removed with replacement of blood volume by crystalloids (with monitoring of central venous pressure). The blood is given to the patient if and when it is needed during or after surgery. Acute normovolaemic haemodilution is useful in fit patients if: a substantial blood loss is anticipated during surgery; the patient’s initial haemoglobin is high; a relatively low target haemoglobin is acceptable.

• • •

Antifibrinolytic drugs These include aprotinin (a kallikrein inhibitor) and tranexamic acid (ε-aminocaproic acid). They are recommended for patients undergoing cardiac surgery that carries a high risk of transfusion, such as: repeat cardiac operations; multiple valve replacements; thoracic aortic operations; patients on aspirin therapy; anticipated long bypass times. Antifibrinolytic drugs are acceptable to Jehovah’s Witnesses.

• • • • •

Intraoperative blood salvage This includes automated blood salvage using the cell saver equipment (Haemonetics) and the more simple manual systems for storage and reinfusion of red cells as exemplified by the Solcotrans autologous collection system. Both techniques are only applicable to clean operative sites without bacterial, bowel or tumour cell contamina-

Figure 6.1 Cell saver.

tion. The Haemonetics cell saver system (Fig. 6.1) is a completely automated device that aspirates, anticoagulates and filters the extravasated blood from the operative field. The red cells are then washed before being transfused in a packed cell volume of 0.5. This system is used extensively during liver transplantation and in Jehovah’s Witnesses undergoing major surgery.

Blood and plasma products Stored whole blood Whole blood is only indicated for the treatment of acute haemorrhage; hypovolaemia is accompanied by an acute reduction in red cell mass, resulting in impaired oxygencarrying capacity at a time when tissue perfusion is compromised. Even in this situation, its use must be reserved for those patients with substantial blood loss and a haematocrit of 0.3 or less after volume replacement with crystalloids and plasma expanders. Stored blood has a number of unwanted features: citrate anticoagulant; an acid pH (6.6–6.8); high levels of K+ (from the stored red blood cells); ammonia (from erythrocyte adenosine);

• • • •

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•

reduced red-cell 2,3-diphosphoglycerate (2,3-DPG), which leads to impaired release of oxygen from oxyhaemoglobin). The use of stored whole blood is declining rapidly because of increasing demand for individual blood products and for economic reasons.

Red cell concentrates

Packed red cells have the same oxygen-carrying capacity of blood but a lower volume. They are thus ideal for the treatment of anaemic patients, who invariably have a normal blood volume and are at risk from circulatory overload. Even so, unless the anaemia is severe and symptomatic, transfusion is no substitute for haematinic (promotion of blood production) therapy and is only indicated in patients who: do not respond to haematinic treatment (refractory anaemia); are unable to adapt to the reduced oxygen-carrying capacity of the blood and exhibit signs of incipient cardiovascular failure; require urgent surgery. Up to 10% of patients develop alloimmunization to leukocyte antigens, usually after repeated red cell infusions. The antibodies cause severe febrile reactions, which can only be prevented by the use of leukocyte-poor red cell concentrates.

• • •

Table 6.2 Indications for platelet transfusion. Surgical Bleeding and thrombocytopenia Limited cover for operative interventions where platelet count < 40 × 109/L Platelet dysfunction Acute disseminated intravascular coagulation (with fresh frozen plasma) Massive blood transfusion (washout thrombocytopenia) Post cardiac bypass platelet loss and/or dysfunction Medical Marrow-suppressed patients (intensive chemotherapy) Aplastic anaemia

lets and determine platelet survival after transfusion. These HLAs lead to alloimmunization in patients requiring repeated platelet transfusions. The antibodies generated cause rapid destruction of the transfused platelets and account for the progressive inefficacy of repeated transfusions. For these patients, HLA-matched platelet concentrates are needed. The indications for platelet transfusions are shown in Table 6.2. In surgical practice, platelet transfusions are most commonly used to stop bleeding in thrombocytopenic patients, to cover surgery if the platelet count is below 40 × 109/L and in patients with platelet dysfunction.

Frozen red cells The use of cryoprotective agents such as glycerol or hydroxyethyl starch allows satisfactory storage of red cells at – 80 to –196 °C (mechanical freezing or liquid nitrogen storage) for long periods (up to 10 years). This method of storage removes leukocytes, platelets and any viral particles, thereby reducing the incidence of both transmission of viral disease and alloimmunization to leukocyte and platelet antigens. Red cells recovered from a frozen bank are of particular value to patients on renal dialysis programmes, those with refractory anaemias, and those with rare cell types and complex antibody mixtures. However, frozen red cells are very expensive and impractical for most patients.

Platelet concentrates Platelet concentrates can be obtained by centrifugation of blood from several donors or by plateletpheresis of a single donation. Because of the variable but significant contamination with red cells, platelet concentrates have to be obtained from ABO/Rh-compatible donors. Some human leukocyte antigens (HLAs) are expressed on plate-

Plasma products These are produced from voluntary donors and are used for a variety of purposes. As coagulation factors for specific deficiency states, either to stop spontaneous bleeding or cover an operation/ intervention in a patient with such a deficiency, e.g. haemophilia A (congenital factor VIII deficiency). To provide passive immunity to non-immunized individuals exposed to a serious infective agent (viral or bacterial), e.g. human tetanus immunoglobulin. In the prophylaxis of haemolytic disease of the newborn due to Rhesus incompatibility and sensitization of Rh(D)-negative women. In the management of autoimmune thrombocytopenic purpura. High-dose intravenous human immunoglobulin can produce remissions of varying duration. IgG is also used to treat acute haemorrhage due to this condition when conventional therapies have failed and to cover patients with idiopathic thrombocytopenic purpura requiring surgery including elective splenectomy. As volume replacement fluid (ALBA 4.5%) and as plasma volume expander and short-term management in

• • • •

•

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hypoproteinaemic patients (Human Albumin Solution 20%). The most common fraction used in surgical practice is fresh frozen plasma (FFP). Each unit is obtained from a single donation and consists of 200 –300 mL of plasma with 40 – 60 mL of citrate anticoagulant nutrient mixture. FFP is used in the following clinical situations. To correct isolated deficiencies of plasma proteins, e.g. factor II, V, VII, X, XI, XIII, pseudocholinesterase, antithrombin III and C1 esterase inhibitor. To reverse oral anticoagulation with warfarin/coumarin compounds if prothrombin complex concentrate is not available. Normally, reversal of anticoagulant is indicated in the presence of bleeding. To provide haemostatic support and to cover operations/interventions in patients with liver disease, major hepatic resections and severe liver injuries. To replace factors consumed by the pathological process in the treatment of patients with disseminated intravascular coagulation (DIC). In patients who develop a bleeding diathesis after largevolume blood transfusion. In this situation, however, platelet transfusion is more commonly needed first. In the treatment of thrombotic thrombocytopenic purpura, where FFP is usually combined with plasma exchange. Cryoprecipitate (factor VIII, von Willebrand factor, fibrinogen) is used in haemophilia, von Willebrand’s disease and fibrinogen deficiency. However, because of the risk of transmitted infection, cryoprecipitate is now used much less for haemophilia. Factor VIII concentrate is preferred as it is safer and gives a more certain dose. Factor IX concentrate is indicated to arrest acute bleeding and cover operative interventions in patients with Christmas disease. Factor VIII and IX therapy requires expert guidance.

• • • • • •

Adverse effects of transfusion Blood transfusion is nowadays very safe, the overall risk of an adverse outcome being 1 in 12 000. The mechanisms of transfusion reactions are varied, depending on the cause. Hence the complications of transfusion are usually classified according to aetiology; they may also be either acute or delayed (Table 6.3).

It is recommended that every patient is monitored closely during the first 15–30 min of the infusion of each unit of blood. This enables early detection of the clinical manifestations of severe acute reaction due to incompatibility or bacterial infection, at which point the infusion is stopped and the necessary action taken.

Table 6.3 Complications of transfusion. Acute Non-haemolytic reactions Pyrogenic (febrile) reactions Hypersensitivity Haemolytic reactions Metabolic, respiratory and haemostatic complications Circulatory overload Septic shock (bacterially infected units) Delayed Delayed haemolytic Infective Bacterial: brucellosis, syphilis Helminthic: filariasis Protozoal: babesiosis, Chagas’ disease, kala-azar, malaria, trypanosomiasis, toxoplasmosis Rikettsial: relapsing fever, Rocky Mountain spotted fever Viral: B19, CMV, EBV, HIV-1, HIV-2, HTLV-1, HTLV-2, hepatitis, yellow fever Sensitization/alloimmunization Haemolytic disease of the newborn Immune suppression (increased infective risk) Post-transfusion purpura Platelet refractoriness Transfusion iron overload (haemosiderosis) Graft vs. host disease CMV, cytomegalovirus; EBV, Epstein–Barr virus; HIV, human immunodeficiency virus; HTLV, human T-cell leukaemia virus.

Acute reactions Acute non-haemolytic reactions The routine establishment of quality control in the manufacture of both intravenous fluids and disposable giving sets has virtually eliminated pyrogenic reactions. Pyrexia following blood transfusion is nowadays the result of alloimmunization to leukocyte and platelet antigens in patients requiring repeated blood transfusions. This is the commonest cause of severe febrile reactions. Although the reaction is usually self-limiting and benign, the transfusion must be stopped to exclude the possibility of a more serious haemolytic reaction. Febrile reactions in alloimmunized patients can be prevented by using red cell concentrates, from which most of the other formed elements have been removed (leukocytes, platelets, soluble histocompatibility antigens). Other non-haemolytic reactions include severe immediate hypersensitivity reactions and mild allergic or anaphylactoid reactions. The causes of these reactions are rarely established. The reaction results in the release of vasoactive peptides and activation of complement.

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Severe anaphylaxis is a rare (1 in 20 000 transfusions) but potentially fatal reaction. Occasionally, it is caused by antibodies to IgA in patients who have extremely low plasma levels of this immunoglobulin. Whatever the cause, anaphylaxis results in the release of vasoactive peptides and activation of complement, with the development of profound hypotension, laryngeal spasm and/or bronchospasm, and cutaneous flushing. Anaphylaxis is treated with: immediate termination of the transfusion; intravenous crystalloids; maintenance of airway and administration of oxygen; adrenaline (0.5 –1.0 mg i.m.); intravenous antihistamines and salbutamol. The adrenaline dose is repeated, if necessary every 10 min, depending on the improvement in blood pressure and pulse. Chlorpheniramine 10 –20 mg is administered by slow intravenous injection after the adrenaline treatment and is continued for 24 – 48 h. Salbutamol is administered by nebulizer. Severe anaphylaxis can only be predicted in patients with low serum IgA. If possible, transfusion should be avoided in these patients.

• • • • •

Acute haemolytic reactions These reactions are usually the result of ABO incompatibility due to human error at the bedside (blood given to the wrong patient) or in the laboratory (faulty crossmatching). The transfused cells react with the patient’s own anti-A or anti-B antibodies or other alloantibodies to red cell antigens. Incompatible blood transfusion is a serious complication and carries an average mortality of 3%, but is higher if more than 200 mL of incompatible blood are administered. The reaction is usually most severe if group A red cells are administered to a group O patient. The syndrome is caused by the release of the polypeptide products of complement in the plasma, which cause contraction of smooth muscle and degranulation of mast cells with release of vasoactive peptides (bradykinin and serotonin). Procoagulant substances are released from the stroma of lysed red cells. Together with antigen–antibody complexes, these initiate DIC. The clinical features in the conscious patient include: pain at the infusion site and along the vein; facial burning; chest and back pain; fever; rigors and vomiting; restlessness and dyspnoea; flushed facies; hypotension; oozing from vascular access sites and wounds.

• • • • • • • • •

Table 6.4 Investigation of an acute haemolytic transfusion episode. Report incident to the blood transfusion department Establish that the unit of blood had been issued to the patient who received it Obtain fresh samples of patient’s blood (clotted and in EDTA) for repeat cross-matching and serological testing Send the unit of blood to the blood transfusion department for culture and further investigation Obtain further blood samples from the patient for clincial chemistry (electrolytes, urea, free haemoglobin) and coagulation screen Discuss any further transfusion requirements with the blood transfusion officer EDTA, ethylenediaminetetraacetic acid.

The only manifestations of incompatible blood transfusion in unconscious or anaesthetized patients are sudden hypotension and bleeding due to DIC. The extensive intravascular haemolysis results in haemoglobinaemia and haemoglobinuria. Oliguria rapidly supervenes and progresses to acute renal failure. The differential diagnosis is between incompatibility and the infusion of bacterially contaminated blood. The management entails: immediate recognition, with cessation of the transfusion and replacement of the giving set; adequate hydration by intravenous infusion of crystalloids; attempts at forced diuresis, with intravenous largedose furosemide (150 mg). If furosemide fails, a 20% solution of mannitol (100 mL) is administered. If diuresis is obtained, a high urine output (100 mL/h) is maintained by large-volume crystalloid infusions. Often, however, these patients progress to acute renal failure necessitating haemodialysis. The other problems that require immediate support are bleeding from DIC (blood component therapy guided by clinical state and coagulation screen) and hyperkalaemia. Intravenous glucose–insulin (50 mL 50% glucose + 10 units of insulin) is administered if the serum K+ rises above 6.0 mmol/L. This is followed by an intravenous infusion of 10% glucose containing 10 units of insulin over a period of 4 h. After the initial resuscitation is completed, investigation of such an incident is essential (Table 6.4). Acute haemolytic reactions with a similar picture may arise from acute haemolysis caused by preformed antibodies in the patient’s blood as a result of alloimmunization to minor blood group antigens in the donated unit. These may be encountered in patients requiring repeated blood transfusions. Delayed haemolytic transfusion reactions are rare but can occur in patients whose level of

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antibodies to the blood group antigen is so low that it escapes detection by the pretransfusion screen. Following transfusion, the secondary immune response raises the antibody titre to a level that results in the delayed destruction of the transfused cells. Thus the manifestations, which include fever, falling haemoglobin, jaundice and haemoglobinuria, appear some 5 –10 days after the transfusion. Delayed haemolytic transfusion reactions are seldom fatal.

Transfusion-related acute lung injury This is one cause of acute respiratory distress syndrome (ARDS) and was previously thought to result from pulmonary microvascular occlusion by microaggregates of platelets, leukocytes and fibrin (50 –200 µm), which are known to be present in stored blood. For this reason microaggregate filters were recommended for transfusions using in excess of 5 units of blood. A more definite cause is donor blood containing antibodies to the patient’s leukocytes (nearly always donations from multiparous women). Following transfusion, the patient develops fever, increasing breathlessness, non-productive cough and hypoxaemia. The chest X-ray shows the typical features of ARDS, with perihilar infiltrates leading to a whiteout in severe cases.

Metabolic, haemostatic and respiratory complications These complications are confined to patients who, because of severe haemorrhage, receive a massive blood transfusion of stored blood. Massive blood transfusion is defined as a volume equivalent to or exceeding the patient’s own blood volume transfused within 12 h. Apart from being cold (4 °C), stored blood has an acid pH, contains citrate anticoagulant, has elevated plasma potassium and ammonia and reduced 2,3-DPG. The metabolic consequences therefore include the following. Hypothermia may lead to cardiac arrhythmias, including ventricular fibrillation and asystole. For this reason, blood warming is necessary if the transfusion rate exceeds 50 mL/min. Unfortunately, heating coils increase the resistance of the giving circuit; nonetheless, their use is essential in these patients. Acidosis. Increased affinity of oxyhaemoglobin for oxygen, which is thus not readily released to the tissues, thereby contributing to defective tissue oxygen uptake. However, increased oxygen affinity reverses after transfusion. Citrate intoxication is due to the chelation of ionized calcium, which may result in prolongation of the QT interval. However, this does not usually affect cardiac

• • • •

function and ionized calcium levels rapidly return to normal after the transfusion as the excess citrate is metabolized and excreted. Thus the use of supplemental calcium is not justified, particularly as it may itself give rise to arrhythmias. Hyperkalaemia is seldom a problem because excess plasma K+ enters the red blood cells with warming to body temperature. However, it is a consideration in patients with acidosis and renal failure when calcium is administered as the physiological antidote. Stored blood is deficient in platelets and labile clotting factors (V and VIII). For this reason, massive transfusion of stored blood induces a dilution of labile clotting factors in addition to a moderate thrombocytopenia. The deficiency of labile clotting factors can be circumvented by the administration of 2 units of FFP for every 8 units of blood. The transfusion-related thrombocytopenia is seldom significant and can usually be ignored.

• •

Circulatory overload Circulatory overload is encountered in the transfusion of anaemic patients, particularly those with severe and longstanding anaemia. These patients must be transfused very slowly and only with packed cells (with or without concomitant diuretic therapy). In some patients, an exchange transfusion has to be carried out to avoid severe congestive failure.

Transfusion of bacterially contaminated/ infected blood This disastrous complication is fortunately rare in the UK (1 in 400 000 transfusions). The majority have been associated with platelet transfusions. The pathogens are usually cold-growing strains of Pseudomonas fluorescens or Yersinia enterocolitica. Skin organisms such as staphylococci can proliferate in platelet concentrates stored at 20–22 °C. The clinical picture is similar to that of ABOincompatible blood transfusion reaction. Despite aggressive supportive therapy, the mortality is high and averages 60%.

Delayed reactions Transmission of infectious disease A wide spectrum of infectious disease can be transmitted by the transfusion of blood and blood products, although the modern practice of screening blood donors and heat treatment of blood protein products means the risk is extremely small (1 in 105–106). Post-transfusion levels of HIV, human T-cell leukaemia virus (HTLV), HBV and

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HCV are extremely low and the risk of their transmission is minimal compared with other risks. Hepatitis A can very occasionally be transmitted by blood products. Hepatitis G has been recently identified; currently, this can only be done by gene amplification technology and there is no screening test. It is not known whether hepatitis G can cause serious disease and whether the existing plasma fractionation and heat treatments inactivate it, though this is thought likely. The other concern relates to transmission of new variant CJD but as yet no cases have been documented. Human parvovirus B19 may not be inactivated by current plasma fractionation and heat treatments. It causes depressed erythropoiesis in some patients. HTLV-related disease following transfusion is extremely rare in the UK and for this reason donors are not screened for HTLV-1 or HTLV-2 infection. However the prevalence of HTLV-1 is high in some countries, notably Japan and the Caribbean. HTLV-1 causes neurological disease and a rare form of adult T-cell leukaemia, usually many years after the transfusion. Current concern relates to infection by the prion protein responsible for new variant CJD by donors harbouring the infection but showing no sign of the disease. Cytomegalovirus (CMV) is a problem because 50% of UK donors have antibody to CMV, although fortunately only a fraction of antibody-positive donations transmit the virus. Post-transfusion CMV is important in premature infants born to CMV antibody-negative mothers and in CMV-negative recipients of bone marrow allografts from CMV seronegative donors. These patients should receive CMV-negative products or leukocyte-depleted blood components. The HIV problem has been largely resolved with donor selection and testing.

Immune suppression There is no doubt about the immunosuppressive effect of blood transfusion; indeed prior to the introduction of cyclosporin, transfusion before renal transplantation was

employed specifically to improve graft survival. The use of cyclosporin has made this procedure unnecessary. In the context of general surgery, perioperative blood transfusion has undoubted undesirable consequences because of its immunosuppressive effect (which is additive to the immunosuppression produced by operative trauma). Aside from the risk of circulatory overload, perioperative blood transfusion enhances the risk of infective complications (proven) and may increase recurrence rate and reduce disease-free survival in patients after extirpative surgery for cancer. The latter, however, remains unproven.

Transfusion haemosiderosis Iron overload of the monocyte–macrophage system is caused by repeated red cell transfusions over many years. This becomes significant after 100 units have been administered, when the liver, pancreas, myocardium and endocrine glands become damaged. It is especially a problem in childhood anaemias (e.g. thalassaemia) and in patients with chronic refractory anaemia. Iron overload is reduced in these patients by iron chelation therapy with desferrioxamine.

Graft vs. host disease Graft vs. host disease (GvHD) is a rare but usually fatal complication that occurs mainly in immunodeficient patients, e.g. recipients of allogeneic marrow transplants and fetuses receiving intrauterine transfusions. However, GvHD has also been documented in immunocompetent patients after transfusion of blood from a relative. The disease is caused by T lymphocytes and starts some 4–30 days after the transfusion. The patient develops a high fever, a diffuse erythematous skin rash progressing to erythroderma and desquamation, gastrointestinal symptoms, severe hepatic dysfunction and pancytopenia. GvHD is prevented by administering γ-irradiated cellular components to immunodeficient patients. Similarly, blood donated from relatives should be γ-irradiated.

Transfusion of blood and blood products at a glance Definitions Blood: a complex fluid vital for life that is circulated around the body in arteries and veins by the pumping action of the heart Plasma: the fluid component of circulating blood in which the formed elements such as erythrocytes, leukocytes and platelets are suspended

Stored whole blood: blood from which no constituent has been removed Red cell concentrates (packed red cells): solutions of erythrocytes obtained from blood after the plasma has been removed. They also contain some white cells Platelet concentrates: solutions containing platelets that are frequently derived from several donors

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Fresh frozen plasma: plasma prepared from the supernatant liquid obtained by centrifugation of one donation of whole blood Cross-matching: process where the red cells from the donor are tested against the serum from the recipient Blood bank: a refrigerated store where donated blood is kept for up to 3 weeks until required for transfusion Transfusion: replacement of lost blood by blood or blood products usually donated by another person (i.e. an allograft) Good transfusion practice 1 Careful selection of donors 2 Test donated blood for known markers of disease (syphilis, HIV-1, HIV-2, HBV, HCV) 3 Standardized blood grouping, antibody screening and cross-matching techniques

4 Standardized blood ordering policy 5 Strict guidelines for administration and monitoring of blood products (a) Use blood tariffs for elective operations (most do not need blood at all) (b) Do not transfuse unless there is a clear indication to do so (c) Transfuse the required blood component rather than whole blood (d) Use blood-sparing strategies: (i) Preoperative autologous donation (ii) Erythropoietin (iii) Acute normovolaemic haemodilution (iv) Antifibrinolytic drugs (v) Cell salvage 6 Full documentation of transfusion in patient’s case notes 7 Local and central reporting of adverse effects

Blood and plasma products Some indications

Problems

Blood products Stored whole blood

Acute haemorrhage

Red cell concentrates

Refractory anaemia

Frozen red cells

Patients on renal dialysis, rare cell types and complex antibody mixtures

Citrate anticoagulant Acid pH (6.6 –6.8) High levels of K+ Ammonia (from red cell adenosine) Reduced 2,3-DPG 10% of patients develop alloimmunization to leukocyte antigens Very expensive and impractical for most patients

Platelet concentrates

Stop bleeding in thrombocytopenic patients To cover surgery if platelet count < 40 × 109/L

Alloimmunization leads to progressive inefficiency of repeated transfusion

Reversal of anticoagulant Correct isolated plasma protein deficiency Treatment of DIC Treatment of burns Haemophilia, von Willebrand’s disease, fibrinogen deficiency

Allergic reactions ARDS

Haemophilia

Allergic reactions Hyperfibrinogenaemia after massive doses (now rare) Allergic reactions

Plasma products Fresh frozen plasma

Cryoprecipitate (factor VIII, von Willebrand factor, fibrinogen) Factor VIII concentrate

Factor IX concentrate

Acute bleeding and perioperatively in Christmas disease

Risk of transmitted infection

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Adverse effects of transfusion

Acute reactions

Cause

Treatment

Acute non-haemolytic reactions

Alloimmunization to leukocytes commonest cause of pyrexia Immediate hypersensitivity reactions cause anaphylaxis: hypotension, laryngeal spasm ± bronchospasm, cutaneous flushing

Immediate termination of transfusion Treat anaphylaxis by: • i.v. crystalloids • maintain airway and O2 • adrenaline (0.5 –1 mg i.m.) • i.v. antihistamine (chlorpheniramine) • salbutamol nebulizer

Acute haemolytic reactions

ABO incompatibility usually caused by human error Pain at infusion site and along vein, chest and back pain, flushing, rigors and vomiting, dyspnoea, hypotension, restlessness. Evidence of DIC

• Immediate termination of transfusion • Replace giving set • i.v. crystalloids • Forced diuresis with furosemide (150 mg) ± mannitol (100 mL, 20%), haemodialysis • Treat hyperkalaemia (dextrose 50% + 10 units insulin if K+ > 6.0 mmol/L) • Treat DIC • Investigate incident fully later

Transfusion-related lung injury

Donor blood antibodies reacting with patient’s leukocytes lead to ARDS

Respiratory support. May need ventilation with positive end-expiratory pressure (PEEP)

Metabolic, haemostatic and respiratory complications

Massive transfusion volume (≥ patient’s blood volume over 12 h)

• Hypothermia: transfuse warm blood • Metabolic acidosis: may need NaHCO3 • Impaired release of O2 from RBCs: self-limiting, no therapy • Citrate intoxication causing hypocalcaemia: self-limiting, no therapy • Hyperkalaemia: seldom a serious problem • Platelet and clotting factor deficiency: give 2 units FFP for every 8 units of blood

Circulatory overload

Seen with transfusion of anaemia

Use only RBC concentrates, diuretic therapy

Transfusion of bacterially contaminated (infected) blood

Rare. Usually after platelet transfusion. Pseudomonas fluorescens, Yersinia enterocolitica

Full resuscitation and management in ICU for septic shock. Despite therapy, mortality is 60%

Delayed reactions

Comment

Transmission of infectious disease

A wide spectrum of infectious disease can be transmitted by blood (product) transfusion. Risk is very small. See text for details Perioperative blood transfusion enhances risk of infection (proven) and may adversely affect outcome in cancer (not proven) Iron overload of the monocyte/macrophage system occurs after 100 units of blood or red cells have been transfused over a number of years. Iron chelation with desferrioxamine may help Immunologically competent transfused cells attack the host environment. May occur when immunodeficient patients are transfused. Rare but fatal

Immune suppression Transfusion haemosiderosis

Graft vs. host disease

Evidence-based medicine McClelland, D.B.L. (1996) Handbook of Transfusion, 2nd edn. HMSO, London.

Scottish Intercollegiate Guidelines Network (SIGN). Perioperative Blood Transfusion for Elective Surgery.

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Surgical Infection

Introduction, 89 Pathophysiology of infection, 89 Management of surgical infections, 91

Specific surgical infections, 93 Postoperative infection, 95

Must know Must do Must know Community vs. hospital-acquired infections Types of surgical infections Infective complications of surgery Must do Visit the radiology department to see percutaneous radiologically guided drainage of an abscess See patients with a superficial surgical site infection (SSI) Under supervision, remove stitches from an SSI in a postoperative wound to achieve drainage of pus

Viral diseases of surgical importance, 97 Principles of antibiotic therapy, 98

from which Borrelia vincentii and various bacteria are isolated, are common in some parts of the world. Most of this chapter is devoted to the problem of bacterial infection.

Pathophysiology of infection Like the rich and the poor, microorganisms are always with (and within) us, but for most of the time we coexist happily with them. Infection occurs when microorganisms in sufficient numbers and virulence (i.e. with an innate capacity to cause disease either by invasion or toxin production) breach the body’s defensive barriers and initiate an inflammatory response.

Establishing an infection

Introduction Surgeons encounter infection in two ways: (i) patients present with an infection that requires surgical treatment, e.g. drainage of an abscess; or (ii) infection complicates a surgical procedure, e.g. wound infection. This problem was almost universal prior to the development of aseptic surgery in the last century and, despite our more sophisticated understanding of the nature of infection and an arsenal of antimicrobial agents, infection remains a major surgical problem today. An infection acquired in hospital is called a nosocomial infection. Most surgical infection is due to bacterial and, more rarely, fungal infection. Viruses, such as human immunodeficiency virus (HIV) and hepatitis B and C virus, are important to surgeons because they may cause disorders that require surgical treatment, e.g. transplantation of liver for fulminant/chronic liver failure, splenectomy for acquired immunodeficiency syndrome (AIDS)-related purpura. In addition, of course, there is the problem of disease transmission, especially with hepatitis B infection. Spirochaetal diseases rarely come to the attention of surgeons now, although noma and tropical phagedenic ulcer,

Generally, various combinations of three elements are important for bacterial infection.

An inoculum of bacteria The numbers of a bacterium required to establish an infection depends on the virulence of that bacterium. Relatively small numbers of a very virulent organism (e.g. β-haemolytic Streptococcus) or large numbers of organisms with low virulence (e.g. Staphylococcus epidermidis) may cause an infection. However, in most established surgical infections there are 100 000 organisms per millilitre of exudate, gram of tissue or square millimetre of infected surface area. A single organism or mixtures of organisms can establish an infection and synergistic infections can be particularly severe (e.g. Vincent’s angina, caused by Gram-negative anaerobic Fusobacterium species and the spirochaete Borrelia vincentii). The elements of aseptic surgery (i.e. sterilization of instruments and drapes, skin preparation with antiseptics such as povidone-iodine, wearing of special clothing in theatre) were introduced to reduce the size of any potential inoculum that might enter the body via the wounds made during surgery. It is almost impossible to create a germ-free surgical environment.

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Physical barriers Biochemical/humoral Skin Acute phase proteins Mucus membranes Complement Cilia Antibodies Gastric HCl Interferon Tears Host defence systems Urine Sweat

Cellular Neutrophils Macrophages Natural killer cells B-lymphocytes T-lymphocytes

Figure 7.1 Elements of the immune system that counter bacterial infection.

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Enzymes (e.g. haemolysins, streptokinase, hyaluronidase) help the organism become established. Exotoxins are proteins released from the intact bacterial cell wall of (mostly) Gram-positive bacteria. They spread via the bloodstream or in some cases (e.g. tetanus) via nerves. Exotoxins produce ill effects both at the site of infection and remote sites. In tetanus (see later) the bacteria stay in the wound but the clinical features of the disease are caused by the action of the exotoxin. (Diphtheria produces its ill effects in a similar manner.) Exotoxins can be attenuated with formaldehyde so that they lose their toxicity but retain their antigenicity. The attenuated toxin is called toxoid and is used as a vaccine. Endotoxins are composed of lipopolysaccharide (LPS) in the bacterial cell wall of Gram-negative bacteria. They are liberated only on the death of the bacterium. LPS stimulates macrophages and endothelial cells to release cytokines, which mediate the inflammatory response and play an important role in the pathogenesis of septic shock (see Chapter 16).

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Natural history of infection A ‘bacteria-friendly’ environment We know from bacteriology that bacteria grow best in culture media that contain water, electrolytes, carbohydrate, protein digests and blood; some also like air (aerobes), some do not (anaerobes). Any in vivo situation that provides these elements will facilitate bacterial growth and infection. Thus patients with diabetes mellitus, whose tissues contain excess amounts of glucose, are more prone to infection than non-diabetics. Accumulations of blood or serum, e.g. in surgical wounds or after trauma, and ischaemic or necrotic tissues are all likely to promote bacterial growth.

Diminished host resistance The complicated systems that protect us from a hostile environment are summarized in Fig. 7.1. Anything that reduces the host’s resistance will allow an infection to become established, even with a relatively small inoculum. During an operation the physical barriers are breached but the risk of infection is greatly increased if the host is also immunocompromised (e.g. if the patient has AIDS). Patients who are malnourished, have malignancy or are taking steroids or other immunosuppressive agents are more susceptible to bacterial infections.

Bacterial secretions Bacteria cause some of their ill effects by releasing various compounds.

Prior to the introduction of antibiotics, little could be done to halt the progress of an infection and a patient’s survival depended on the ability of his or her immune system to deal with the invading organism (see box below). It is the body’s reaction to an invading microorganism that produces the classical inflammatory response resulting in the clinical features of infection: rubor (redness); tumor (swelling); dolor (pain); calor (heat). In acute infection these clinical features may be accompanied by a swinging pyrexia, leukocytosis, raised C-reactive protein and, if the infection spreads, bacteraemia (see Chapter 16). Following an acute inflammatory response a number of outcomes are possible.

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Resolution. If tissue damage is minimal, the inflammatory response settles completely and the tissue returns to normal. Spreading infection. An infection may spread from its initial site: by direct spread into adjacent tissues; along tissue planes, e.g. tendon sheaths; via the lymphatic channels, producing the characteristic red lines of lymphangitis and enlarged tender lymph nodes (acute lymphadenitis); or via the bloodstream, causing bacteraemia (presence of bacteria in the blood) or septicaemia (presence of propagating organisms in the blood).

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The tragedy of Ignaz Semmelweis (1818–1865) and puerperal sepsis Throughout history young mothers frequently died from infection (puerperal fever) following childbirth. Ignaz Semmelweis, a Hungarian doctor working in Vienna in the 1840s, noticed that the maternal death rate in one of the two maternity wards of the Allgemeines Krankenhaus was 10% compared with only 3% in the other. He observed that the first ward was run by doctors and that frequently medical students would come to this ward straight from the autopsy room and perform vaginal examinations on the women in labour. The second ward was run by midwives who paid a lot of attention to personal cleanliness. Medical students did not come to this ward. Semmelweis conducted some animal experiments in which he transmitted fatal puerperal sepsis to rabbits by introducing into the rabbit’s vagina pus he had obtained from women dying from puerperal fever. The use of chlorinated lime prevented the sepsis. On the maternity ward he introduced a programme of compulsory hand washing with chlorinated lime and immediately reduced the mortality rate to 3%. Thus he performed a very important piece of research: he identified a problem, he tested his hypothesis in the laboratory and applied his solution to patients, resulting in considerable reduction in mortality. Was Semmelweis hailed as a hero and given a medal? He was dismissed from his post and forgotten. He returned to Budapest where he published a little-read monograph on puerperal fever and its prophylaxis. In 1865 he was committed to a mental institution and died shortly thereafter.

Figure 7.2 Abscess on the right side of the neck.

cause most of their damage by chronic inflammation, e.g. Mycobacterium tuberculosis.

Management of surgical infections Prevention of infection

Abscess formation. An abscess is defined as a localized collection of pus. Pus is composed of neutrophils, exudate and bacteria. The common pus-producing (pyogenic) organisms are Staphylococcus aureus, Streptococcus pyogenes, Escherichia coli and Bacteroides. An abscess that is not drained surgically may discharge spontaneously (e.g. through the skin) and resolve or it may lead to septicaemia and death (Fig. 7.2). Organization. Following acute inflammation with tissue damage or drainage of an abscess, repair of the tissues is achieved by organization, formation of granulation tissue and fibrosis. Chronic inflammation. If the agent causing injury persists in the tissues (e.g. foreign body), a chronic inflammatory response is established. Such responses are characterized histologically by macrophages and giant cells and often the presence of granulomas. Certain microorganisms

Several prophylactic measures are now available to prevent infection. These are discussed fully in Chapter 5.

Management of established infection Diagnosis The presence of an infection will be suspected from the clinical picture. Wherever possible, infected material should be obtained for culture before commencing antibiotics. Swabs should be obtained from infected skin lesions and discharging wounds. Material from deepseated infections (e.g. subphrenic abscess) may be obtained by needle aspiration, possibly using computed tomography (CT) or ultrasound imaging to guide the needle. The tips of infected intravenous lines should be cultured and blood cultures obtained in anyone with an unknown pyrexia. Urine and sputum should be cultured as appropriate.

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Antibiotics The use of antibiotics has revolutionized the management of surgical infection and, where possible, antibiotics should be administered on the basis of the culture results. However, until the culture result becomes available, treat-

ment should be given on the basis of the most likely organisms present. A Gram stain of the material sent for culture will usually give a clue as to what is present (e.g. Grampositive cocci, Gram-negative bacilli) and an appropriate antibiotic may be chosen.

Surgical infection in general at a glance Definitions

Infection: the process whereby organisms (e.g. bacteria, viruses, fungi) capable of causing disease gain access and cause injury or damage to the body or its tissues Pus: a yellow/green foul-smelling viscous fluid containing dead leukocytes, bacteria, tissue and protein Abscess: localized collection of pus, usually surrounded by an intense inflammatory reaction Cellulitis: a spreading infection of subcutaneous tissue Pathophysiology of bacterial infection Establishing a bacterial infection requires • An inoculum of bacteria (usually 100 000 organisms per millilitre of exudate, gram of tissue or square millimetre of infected surface area) • A bacteria-friendly environment (water, electrolytes, carbohydrate, protein digests, blood) • Diminished host resistance to infection (impaired physical barriers, reduced biochemical/humoral response, reduced cellular response) Bacterial secretions Bacteria cause some of their ill effects by releasing: • Enzymes (e.g. haemolysin, streptokinase, hyaluronidase) • Exotoxin (released from intact bacteria, mostly Grampositive, e.g. tetanus, diphtheria) • Endotoxin (LPS released from cell wall on death of bacterium) Natural history of infection • Inflammatory response is established: rubor (redness), tumor (swelling), dolor (pain), calor (heat) • Resolution: inflammatory reaction settles and infection disappears • Spreading infection: (a) Direct to adjacent tissues (b) Along tissue planes (c) Via lymphatic system (lymphangitis) (d) Via bloodstream • Abscess formation: localized collection of pus • Organization: granulation tissue, fibrosis, scarring • Chronic infection: persistence of organism in tissues elicits chronic inflammatory response

Management of surgical infection Preventive measures • Short operations • Skin cleansing with antibacterial chemicals and detergents (patient’s, surgeons’s and nurse’s skin) • Filtering of air in operating theatre • Occlusive surgical masks and gowns • Prophylactic antibiotics: (a) Should be bacteriocidal (b) Should have high tissue levels at time of contamination (c) One preoperative dose given 1 h prior to surgery should suffice (d) Should be given to patients with implanted prosthetic materials, e.g. heart valves, vascular grafts, joint prostheses Wound classification • Rate of infection related to type of wound: clean, cleancontaminated, dirty (see Chapter 5) Management of established infection Diagnosis • Made by culture of appropriate specimens (pus, urine, sputum, blood, CSF, stool) Antibiotics • Prescribe on basis of culture results and ‘most likely organism’ while waiting for results • Certain antibiotics are reserved for serious infections • Therapeutic monitoring of drug levels may be required, e.g. with aminoglycosides • Synergistic combinations may be required in some infections, e.g. aminoglycoside, cephalosporin and metronidazole for faecal peritonitis • In serious infections seek advice from clinical bacteriologist • Barrier nursing and isolation of patients with methicillinresistant Staphylococcus aureus or vancomycin-resistant enterococcus Drainage • Surgical or radiological drainage is the most important treatment modality for an abscess

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Drainage Drainage is essential once an abscess has become established and antibiotics play only a secondary role in the management. Traditionally all abscesses were drained surgically but nowadays many, including intra-abdominal abscesses, are drained percutaneously by interventional radiology techniques with CT or ultrasound guidance. Irrespective of approach, radiological or surgical, the principle is the same: the pus should be removed and a track established for free drainage.

Specific surgical infections Figure 7.3 Cellulitis from an infected intravenous line.

Cellulitis Cellulitis is defined as an infection of the subcutaneous tissues. Two distinct types are recognized.

Acute pyogenic cellulitis Acute pyogenic cellulitis is the common type of cellulitis and is caused by Streptococcus pyogenes. It presents as a spreading infection (facilitated by streptokinase and hyaluronidase) of the skin and subcutaneous tissues (Fig. 7.3). It is characterized by a dark-red skin discoloration, heat and oedema and is often associated with lymphangitis and lymphadenopathy (see earlier). The most virulent form of this streptococcal infection is called erysipelas, which most frequently affects the face, producing a characteristic butterfly erythema. Erysipelas is a rarely seen condition today. Treatment consists of immobilization, elevation of the affected part and intravenous antibiotics (penicillin or erythromycin).

Anaerobic cellulitis This type of cellulitis is much more sinister and fortunately rare. It is known as the ‘flesh-eating’ infection (Meleney’s gangrene) and is caused not by a single organism but by a combination of aerobes (Streptococcus pyogenes, Staphylococcus aureus, Escherichia coli, Proteus, Klebsiella, Pseudomonas aeruginosa) and anaerobes (Bacteroides, anaerobic cocci, Clostridium). These act synergistically to cause extensive tissue destruction and death. Two clinical syndromes are recognized in this type of infection. Progressive bacterial synergistic gangrene, in which the skin becomes dark red and purple with areas of necrosis. This infection classically arose around infected closed wounds (e.g. abdominal wound) or a stoma but can complicate a simple abrasion. It spreads very rapidly and a whole limb can be involved in a few hours. When it affects

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the penoscrotal region it is called Fournier’s gangrene (see Chapter 36). Necrotizing fasciitis is a deep cellulitis affecting the fascial planes. Initially the overlying skin is relatively normal while the necrotic process proceeds underneath. The patient becomes extremely toxic and later the skin becomes painful, red and necrotic as it is deprived of its blood supply. Treatment of anaerobic cellulitis includes surgery to remove the necrotic tissue, appropriate antibiotics depending on sensitivity (e.g. combinations of flucloxacillin, benzylpenicillin, cephalosporins, erythromycin or gentamicin for the aerobes and metronidazole for the anaerobes) and systemic support in an intensive care unit (see Chapter 7). The mortality from anaerobic cellulitis is high.

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Staphylococcal infections Staphylococci are Gram-positive organisms that cause a spectrum of skin infections (boils, styes, carbuncles, abscesses and sycosis barbae) as well as osteomyelitis and deeper abscesses (e.g. breast abscess). The pathogenic species is Staphylococcus aureus. Staphylococci are normal skin commensals; Staph. epidermidis is found on all skin and rarely causes disease. Some 10–30% of the population carry Staph. aureus in the nares or perineum. A boil (furuncle) is a skin abscess that involves a hair follicle and its associated gland. Boils are found commonly on the face, neck and axilla. Treatment is by incision and drainage and better hygiene. Systemic antibiotics are not indicated. A stye is a self-limited staphylococcal infection of the eyelash follicles. A carbuncle is a serious infection characterized by an area of subcutaneous necrosis with a honeycomb of small abscesses. It is particularly common in diabetics and can

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02 Figure 7.4 Carbuncle.

cause considerable disability. Treatment is with antibiotics and, rarely, surgery (Fig. 7.4). Sycosis barbae is a staphylococcal infection of the shaving area caused by minor trauma made by a razor. This is one of the few conditions that should be treated with topical antibiotics. Most strains of staphylococci are now resistant to penicillin as a result of their ability to produce an enzyme (β-lactamase) that breaks the β-lactam ring of the penicillin molecule. However, penicillinase-resistant antibiotics (e.g. flucloxacillin) remain effective against most species and are the first line of treatment for staphylococcal infections. In recent years a species of Staphylococcus has been identified (usually in hospitals) that is resistant to most antibiotics. This is called methicillin-resistant Staphylococcus aureus (MRSA) and radical measures (e.g. patient isolation, barrier nursing, ward closure and disinfection) have to be taken when it is isolated to prevent its spread throughout a unit.

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Hidradenitis Hidradenitis suppurativa is an infection of the apocrine glands in the skin. It is common in the axilla and the groin. Irritation by deodorants and excessive sweating have been implicated as precipitating factors. The patient presents with multiple tender swellings under the arm or in the groin; these enlarge and discharge pus. Unless the area is kept very clean, recurrence is common and often surgery is required to excise the involved skin (Fig. 7.5).

Tetanus Tetanus is a clostridial infection caused by Clostridium tetani. This is now a rare infection in the western world due to universal vaccination but is an important cause of death in the developing world. The infection is estab-

Figure 7.5 Hidradenitis suppurativa affecting the axilla.

lished when a penetrating wound, often of a minor nature, is contaminated by soil or animal manure containing C. tetani spores. In anaerobic conditions the spores germinate to produce bacilli that form an exotoxin. The bacteria are confined to the wound but produce their ill effects via the exotoxin, which is absorbed at the motor nerve endings and travels via the nerves to the anterior horn cells. The exotoxin is composed of two elements. A neurotoxin acts on neuromuscular end-organs, producing spastic contractions and trismus (lockjaw), spasm of the facial muscles (risus sardonicus), rigidity and generalized convulsions so severe that only the patient’s heels and head touch the bed (opisthotonus). Death, when it occurs, is due to asphyxia from spasm of the respiratory muscles and cardiovascular complications. A haemolytic toxin lyses red blood cells.

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Management Tetanus prophylaxis Prevention is the ideal and in the UK active immunization with tetanus toxoid is administered to all children as part of the triple vaccine during the first year of life, with a booster dose at 5 years and at the end of schooling. If a patient presents to a casualty department with a potentially contaminated wound and has previously been

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fully immunized, then a booster dose of tetanus toxoid is administered. If a patient has not been vaccinated or is unsure of status, passive immunization with human antitetanus immunoglobulin is given and a full course of active immunization with toxoid is commenced. Treatment Antibiotics (penicillins) are administered to eliminate the contaminating organisms in a potentially infected wound. In an established case, artificial ventilation with muscle relaxation is required and antitetanus immunoglobulin is administered in large doses. Antibiotics should be given to destroy the bacteria and prevent further toxin production.

Gas gangrene Gas gangrene, the scourge of all wounded soldiers since men began to assault each other, is rare in civilian practice. Occasionally gas gangrene follows operations such as amputation for lower limb ischaemia. It is a spreading gangrene of the muscles accompanied by oedema, blackening of the tissues, crepitus (from gas production), profound toxaemia and shock. It is caused by contamination of extensive necrotic wounds with soil or animal manure containing clostridial species (Clostridium perfringens, 65% of cases; C. novyi, 30%; C. septicum, 15%) that secrete powerful toxins. The toxins produce further tissue destruction and anaerobic conditions that enhance the spread of the infection. There is usually a foul-smelling discharge. Treatment consists of wide excision or amputation of all necrotic and ischaemic tissue with free drainage and high-dose antibiotic therapy, including penicillin and metronidazole. Hyperbaric oxygen may be helpful in some cases and should be administered if available. Antitoxin has been used in military practice but with little benefit. The outlook for patients with this condition is still grim.

indicate bacteraemia/viraemia and always necessitate blood culture in addition to physical examination. A flushed appearance with a hyperdynamic circulation is also indicative of a bacteraemia and usually signifies the early stages of septic shock. Intermittent pyrexia is indicative of an abscess. If a patient develops a temperature in the postoperative period, the following are necessary in all patients: physical examination of the lungs, wound, calves and urine. In addition most would advise a chest X-ray. Laboratory tests (white blood cell count, total and differential) and culture screen (sputum, urine, blood and wound) are undertaken on a selective basis in patients with fever that: persists beyond the first 24 h; recurs after a period without fever (intermittent); arises after the first 24 h; is accompanied by rigors, haemodynamic change or chest/abdominal signs. Postoperative infections are most frequently seen in surgical wounds, the abdominal cavity, chest, urinary tract and catheter sites. Clinically, infection may present as cellulitis or abscess formation. Local symptoms and signs are pain, tenderness, swelling and heat. Systemic signs are fever, rigors and malaise. Uncontrolled infection may spread to the bloodstream, producing septicaemia and septic shock.

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Wound infections The incidence of wound infection depends on whether the wound was initially clean, clean-contaminated or contaminated/dirty (see Table 5.2). A mild infection may present as no more than a cellulitis with pain, tenderness, swelling and redness and may subside with rest and antibiotics. However, most wound infections progress to abscess formation and require incision and drainage. The wound should be left open and secondary suture employed when the infection has subsided.

Intra-abdominal infections

Postoperative infection Pyrexia Pyrexia is a common feature of postoperative infections, although it may be absent in immunologically compromised patients. Its important features are: time of onset; degree of pyrexia and type (persistent, intermittent); accompaniments, particularly rigors (shivering) and haemodynamic change. Most early postoperative fevers are due to noninfectious causes, particularly pulmonary collapse. Rigors

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Postoperative intra-abdominal infections present in one of two ways.

Generalized peritonitis Generalized peritonitis is usually a preoperative event but may also occur postoperatively (e.g. due to suture line dehiscence in gastrointestinal surgery). Postoperative peritonitis is a polymicrobial infection commonly caused by Escherichia coli, Klebsiella, Proteus, Streptococcus faecalis and Bacteroides. The rapid spread of infection throughout the peritoneal cavity is a consequence of the virulence of

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the organisms, diminished host resistance and the failure to wall off the infection and confine it locally with omentum, loops of intestine and fibrinous deposits. Clinical features include pain, rigidity and absence of bowel sounds. Fever and leukocytosis are present and septic shock rapidly supervenes. Treatment consists of intravenous fluids for resuscitation, elimination of the source of infection (e.g. closure of perforated viscus), removal of necrotic material and appropriate therapy.

Intra-abdominal abscess

Intra-abdominal abscess can arise in the following groups of patients. Patients undergoing a major operation involving the alimentary tract: abscess due to contamination at the time of surgery or suture line dehiscence/leakage. Critically ill patients: abscess due to failure of intraperitoneal host defences and gut barrier function, with translocation of intraluminal bacteria into the peritoneal cavity (tertiary peritonitis). Patients with acute abdominal conditions requiring emergency operations, e.g. trauma, perforated viscus, severe gangrenous perforated appendicitis: these patients have a 6 –10% risk of developing intra-abdominal abscesses. Signs and symptoms of abdominal abscess usually arise 5 –10 days postoperatively and include intermittent fever, localized tenderness and absent bowel sounds. In some instances the abscess is palpable abdominally or rectally (pelvic collection). Persistent drainage from an abdominal wound infection that has been opened indicates that this is being fed from an intra-abdominal site. Patients with intra-abdominal abscess may develop signs of sepsis, such as hypotension, hyperdynamic circulation, respiratory distress and other features of multiple organ failure/ systemic inflammatory response syndrome (SIRS). Diagnosis is nowadays based on ultrasound scanning and especially CT; both are usually performed successively. CT provides more detailed information on the precise location and anatomy of the abscess cavity. CTguided drainage is now used as the first line of treatment in these patients, with surgery being reserved for large multiloculated abscesses containing a large amount of slough. However, in many cases a surgical approach is necessary in order to deal with the underlying pathology (e.g. perforated viscus) or to divert the faecal stream (i.e. create a stoma). Systemic antibiotics are indicated to forestall the systemic effects of bacteraemia that may occur before, during or after the abscess drainage. In the past, laparotomy was recommended in all septic patients even when imaging tests failed to show any localized intra-abdominal collection, on the premise that

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detection and evacuation of an abscess was followed by improvement in some patients. This view is now not generally accepted, as the majority of patients with SIRS do not have an intra-abdominal focus of infection. The current consensus is that laparotomy is used selectively in patients in the early stages of the disease, especially those in whom the organ failure was precipitated by intraabdominal infection in the first instance, i.e. detection of residual collections. Laparotomy is not indicated in patients in the late hypodynamic decompensated stage of the disease unless there are specific signs of intraabdominal infection.

Respiratory infection Pulmonary infection is common after surgery. Factors that predispose to postoperative respiratory infection include the following. Pre-existing pulmonary disease, e.g. chronic obstructive airways disease. Smoking: causes thick mucus production and ciliary dysfunction. Starvation and fluid restriction prior to surgery: leads to dehydration. Anaesthesia: paralyses respiratory epithelial ciliary activity. Postoperative pain: makes deep breathing and coughing difficult and predisposes to atelectasis. Preventive measures include vigorous preoperative physiotherapy with incentive spirometry, cessation of smoking and postponement of surgery in the presence of acute infection. Physiotherapy and antibiotics are the mainstay of treatment for an established infection, with bronchoscopy and bronchial aspiration for atelectasis. Minitracheostomy may be helpful when regular bronchial toilet is needed (see also Chapters 11 & 38).

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Urinary tract infection Postoperative urinary tract infection is commonly related to the presence of urinary catheters. Catheterization of the urinary bladder should be employed only when necessary and should be discontinued as soon as possible. A strict sterile technique should be observed during catheterization and a closed system used for drainage. Culture of the urine and appropriate antibiotic therapy should be employed when infection occurs. Symptoms include dysuria and frequency and, sometimes, the onset of incontinence. Loin pain and tenderness are only found in patients with severe upper urinary tract infections. The specific diagnosis of urinary infection is made with the recovery of more than 105 organisms per millilitre of urine. The most common organisms cultured in nosocomial

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urinary infections are Escherichia coli, Pseudomonas aeruginosa and coagulase-negative Staphylococcus spp. (see Chapter 39).

Intravenous central-line infection Avoidance of intravenous central-line sepsis is achieved by strict aseptic technique during the insertion of the catheter and careful maintenance of the line, with removal after a limited time. It is important to avoid using central lines for administration of drugs. Similarly, in patients receiving parenteral nutrition, all the nutritional requirements should be provided in a single bag that is infused over a 24-h period. Once the bag has been prepared in the pharmacy, nothing should be added to it. Sepsis is manifested by pyrexia and sometimes rigors. Central-line infection is encountered in 3–5% of patients who have monitoring lines in place and those receiving parenteral nutrition. Fever in such patients is an indication for inspection of the puncture site for signs of inflammation and for changing the line. For temporary lines, removal and replacement to another site are indicated. Replacement over a guide wire may permit preservation of a valuable access site. Permanent lines may occasionally be salvaged temporarily by a course of systemic antibiotics. However, if signs of infection have not resolved completely within 48 h, the catheter should be removed. The tip of all removed catheters should be cultured. The presence of more than 15 colonies is indicative of line infection. Episodes of line sepsis can be prevented by meticulous attention to cleanliness of nutrition support lines.

Infection of implanted prosthetic material Infection is an ever-present risk when prosthetic material/ implants are used, e.g. synthetic mesh for hernia repair, vascular grafts, joint prostheses, cardiac valves. Infected aortic grafts may present with life-threatening haemorrhage or acute aorto-enteric fistula. In nearly all instances, removal of the implant is necessary to control infection. Implanted devices such as pacemakers are removed and replaced at another site and the patient given systemic antibiotics. Infected vascular grafts are removed and the new prosthesis is usually tunnelled through uncontaminated tissue (extra-anatomical bypass), e.g. axillo-bifemoral graft for infected abdominal aortic graft. In some patients, the threat to life or anticipated disability may prohibit removal of the implant, e.g. infected thoracic aortic graft. Irrigation of the infected area with antibiotic solutions, in addition to systemic antibiotics, may alleviate the problem temporarily but does not provide permanent control of the infection.

Pseudomembranous enterocolitis Pseudomembranous enterocolitis is an infection caused by Clostridium difficile. It is seen in postoperative patients who have received antibiotics (cephalosporins, ampicillin) and is characterized by diarrhoea, abdominal discomfort, leukocytosis and the presence of a typical (pseudomembranous) membrane in the colon. The infection develops because antibiotics alter the normal flora, allowing the overgrowth of C. difficile, a normal bowel organism in 5% of people. Clostridium difficile produces an enterotoxin responsible for most of the gut symptoms. Treatment consists of withdrawing current antibiotics and giving oral vancomycin or metronidazole, to which C. difficile is sensitive.

Viral diseases of surgical importance Hepatitis B and C Hepatitis B is a viral infection that causes hepatitis. It is spread by infected blood products (e.g. among intravenous drug abusers) or secretions (sexual contact). Healthcare workers, especially those who handle blood products, are at high risk of contracting hepatitis B. The symptoms of hepatitis are fever, malaise, anorexia, nausea, vomiting and upper abdominal discomfort. The patient becomes jaundiced with a hepatitic picture (cholestasis with elevated enzymes; see Chapter 27). There are three hepatitis B antigens: a surface antigen (HBsAg), which appears in the blood at 6 weeks; an internal antigen (HBeAg), which is present from 6 weeks to 3 months and indicates high infectivity; a core antigen (HBcAg), which is usually found only in the liver. The majority of patients require supportive treatment only. Spontaneous recovery is usual, although a minority of patients (5%) become carriers, with persistent HBsAg in the blood, and may progress to chronic hepatitis and hepatocellular carcinoma. High-risk groups (including healthcare workers) should be vaccinated against hepatitis B. This is achieved with three injections of recombinant HBsAg. Hepatitis C is also transmitted parenterally from contaminated blood products and is clinically similar to hepatitis B.

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AIDS AIDS is caused by HIV. First recognized in 1981, the virus is transmitted by sexual contact or by direct injection from contaminated syringes or blood products. Although the

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majority of cases have been reported in homosexual men, intravenous drug abusers and haemophiliacs, the incidence among heterosexual women and men is increasing at the greatest rate in certain African countries. Symptoms of HIV infection are absent in early cases; however, those infected commonly go on to develop weight loss, night sweats and pyrexia. Generalized lymphadenopathy, oral candidiasis and Kaposi’s sarcoma are also seen. The disease causes a decrease in T-helper lymphocytes and an abnormal decrease in the ratio of T-helper to T-suppressor cells, making patients more susceptible to opportunistic infections, including Pneumocystis pneumonia, toxoplasmosis and cryptococcal meningitis. Testing of HIV infection utilizes the enzymelinked immunosorbent assay and the Western blot test, which together have greater than 99% sensitivity and specificity. Treatment with azidothymidine (AZT) has been shown to benefit some patients with HIV infection. Although no cure or vaccine is presently available, AZT helps slow the progression of the disease in some patients. All members of the healthcare profession must be aware of the rapidly growing incidence of this disease and practise universal precautions when dealing with all patients to eliminate direct contact with blood and secretions. This is the most appropriate strategy to prevent transmission of the virus.

Principles of antibiotic therapy Antibiotics are rarely used as the sole agents to eradicate surgical infections; usually they constitute adjuvant treatment to surgery, e.g. excision of the infecting focus, drainage of abscesses, débridement, lavage of infected serous cavities. The use of antibiotics as prophylactic agents to cover certain operations is well established and of proven value. The adverse effects of antibiotics, particularly the emergence of resistant strains of organisms, limit their overall usefulness particularly in critically ill patients. The following are the principles governing antibiotic therapy in hospital practice. Each hospital has its own drug formulary that includes an antibiotic policy (first-line antibiotics to be used for specific conditions) based on cost efficacy, pharmacokinetic properties and the hospital’s known resistant species. This policy covers both treatment of established infections and the use of specific antibiotics for prophylaxis of infection in patients undergoing surgery. Certain antibiotics are kept in reserve for serious infections.

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For established infections, the sensitivity of the organisms cultured to antibiotics is performed routinely and the first-line antibiotic regimen used may need to be changed accordingly. For certain antibiotics, therapeutic drug monitoring is necessary to (i) establish adequate serum concentrations and (ii) identify potentially lethal concentrations. This applies to aminoglycosides (gentamicin, netilmicin, tobramycin, vancomycin) and flucytosine. The desirable levels of aminoglycosides vary according to the nature and severity of the infection. Dose adjustment is essential in patients with renal impairment, when advice should be sought from the clinical pharmacist. In some infections synergistic combinations of antibiotics are used, e.g. aminoglycoside combined with penicillin for treatment of certain staphylococcal or enterococcal infections, and with ticarcillin for enhanced activity against Pseudomonas spp. For surgical patients, the traditional treatment of potentially life-threatening infections (e.g. pneumonia, suppurative cholangitis, peritonitis, burn sepsis) has been with combinations of aminoglycosides and other drugs such as cephalosporins, clindamycin and metronidazole. Infected collections negate antibiotic activity due to changes in tissue pH, oxygen tension, levels of magnesium and calcium, and the production by various organisms of substances that inactivate antibiotics, e.g. β-lactamase that inactivates penicillin. Thus drainage and débridement will improve antibiotic effectiveness as well as reduce the bacterial inoculum. In serious infections in critically ill patients, discussion/advice from the hospital clinical bacteriologist is essential. Special nursing measures and isolation are essential for patients infected with MRSA. Additional measures for enhancing antibiotic action include: altering body fluid pH, e.g. urine; delaying excretion of the drug, e.g. use of probenecid with penicillin; changing the route of administration, e.g. intravenous from oral; increasing the dose of antibiotic (effective with cephalosporins), which can be achieved by increasing the absolute dose or the total dose (increase duration of therapy), or by reducing the dosing interval; using substances that block bacterial-inactivating enzymes, e.g. clavulanic acid.

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Specific surgical infections at a glance Cellulitis • Acute pyogenic cellulitis (Streptococcus pyogenes): erysipelas (face) is most virulent form • Anaerobic cellulitis: combination of aerobic and anaerobic organisms. Two forms clinically: (a) Progressive bacterial synergistic gangrene (including Fournier’s gangrene) (b) Necrotizing fasciitis Staphylococcal infections (Staphylococcus aureus, Staphylococcus epidermidis) • Furuncle (boil): skin abscess involving hair follicle • Stye: infection of eyelash follicle • Carbuncle: subcutaneous necrosis with network of small abscesses • Sycosis barbae: infection of shaving area caused by infected razor • Hidradenitis suppurativa: infection of apocrine glands in skin (axilla, groin) Tetanus (Clostridium tetani) • Penetrating dirty wounds • Most symptoms caused by exotoxin, which is absorbed by motor nerve endings and migrates to anterior horn cells: (a) Spastic contractions and trismus (lockjaw) (b) Spasm of facial muscles (risus sardonicus) (c) Rigidity and extensor convulsions (opisthotonus) Standard tetanus prophylaxis in the UK • Tetanus toxoid is given during first year of life as part of triple vaccine. Booster at 5 years and end of schooling • Presentation with potentially contaminated wound plus previous full immunization: booster dose of tetanus toxoid given • Presentation with potentially contaminated wound without previous immunization: passive immunization with human antitetanus immunoglobulin and full course of active immunization commenced Gas gangrene • Clostridial infection caused by C. perfringens (65%), C. novyi (30%), C. septicum (15%) • Contamination of necrotic wounds with soil containing clostridia. • Spreading gangrene of muscles, with crepitus from gas formation, toxaemia and shock Postoperative infections Diagnosis Pyrexia is a common sign of infection. A mildly raised temperature is normal in the early postoperative period, indicating response to major surgery. If pyrexia develops:

Note • Time of onset (first 24 h usually atelectasis) • Degree and type: (a) Low persistent: low-grade infectivity or inflammatory process (b) Intermittent: abscess ± rigors or haemodynamic change (bacteraemia/septicaemia) Check • Lungs (atelectasis/pneumonia) • Wound (infection) • Calves (deep vein thrombosis) • Urine (infection) • Intravenous or central lines Do • Septic screen: (a) Urine specimen (b) Sputum sample (c) Swabs of wounds or cannulae (d) Blood cultures • Chest X-ray (± other imaging as indicated, e.g. abdominal ultrasound or CT scan if peritonitis present) Give • Antibiotics on basis of ‘most likely organism’ (refine treatment when septic screen results available) Treat • Cause as appropriate, e.g. remove infected cannula, drain abscess surgically or radiologically, give chest physiotherapy and respiratory support, deal with anastomotic dehiscence Wound infections • Incidence depends on wound classification (see Chapter 5) • Mild infections may settle with antibiotics but most need wound to be opened and drained Intra-abdominal infections Generalized peritonitis • Pain, rigidity, absence of bowel sounds • Causative organisms: Escherichia coli, Klebsiella, Proteus, Streptococcus faecalis, Bacteroides • Resuscitation, broad-spectrum antibiotics, laparotomy and deal with cause Intra-abdominal abscess • Intermittent pyrexia, localized tenderness ± evidence of bacteraemia/septicaemia 5–10 days post operation • Diagnosis by ultrasound or CT • Treatment: drainage, either radiologically guided or surgical

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Respiratory infections Predisposing factors • Pre-existing pulmonary disease • Smoking • Starvation and fluid restriction • Anaesthesia • Postoperative pain

Intravenous central-line infection Prevention • Use sterile technique when inserting line • Do not use line for giving intravenous drugs or taking blood samples • Use single-bag parenteral nutrition given over 24 h • Never add anything to the bag

Prevention • Preoperative physiotherapy • Incentive spirometry • Stop smoking

Diagnosis • Fever in patient with central line

Treatment • Physiotherapy and appropriate antibiotics Urinary tract infections • Often related to urinary catheter • Only catheterize when necessary • Use sterile technique and closed drainage • Treat with antibiotic on basis of urine culture

Treatment • Remove the line, send tip of catheter for culture, antibiotics Pseudomembranous enterocolitis • Caused by Clostridium difficile • Seen in patients who have been on antibiotics • Presents with diarrhoea, abdominal discomfort, leukocytosis, pseudomembranous membrane in colon • Treatment: stop current antibiotics, oral vancomycin or metronidazole

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Pain Relief

Introduction, 101 Benefits of treating acute pain, 101 Reasons for inadequate pain control, 101 Factors affecting postoperative pain, 101

Assessment of pain, 102 Selection of appropriate analgesic drugs, 102 Regular monitoring and recording, 105 Opioids, 105

Non-steroidal anti-inflammatory drugs, 106 Local and regional analgesia, 106 Non-drug analgesia, 107

02 Must know Must do Must know Principles and practicalities of relief of acute and chronic pain World Health Organization analgesia ladder Commonly used analgesics for control of acute pain, their dosage, details of administration and adverse effects Must do Attend pain clinic Follow the postoperative pain management of patients undergoing major open abdominal surgery for cancer Observe an epidural catheter being inserted for postoperative epidural analgesia and its subsequent management

Introduction Surgery usually involves damage to tissues, and after surgery 30 –70% of patients have moderate or severe pain. The pain of surgery is nociceptive (i.e. it is caused by tissue damage and is transmitted by normal physiological pathways), is acute and of short duration, and subsides when the damaged tissues heal. This type of pain serves an important protective function in ordinary life, although it is unpleasant and damaging postoperatively; it is usually amenable to treatment with common analgesics.

Benefits of treating acute pain The primary reason for trying to control pain after surgery is to relieve the suffering of patients since ‘It is the basic duty of all health care professionals to relieve pain and the most important indication for the treatment of pain after surgery is humanitarian’ (Royal College of Surgeons Report on Pain after Surgery 1990). Effective pain control

can attenuate the stress response to surgery, improves respiratory function, enables patients to cooperate with physiotherapy, and promotes better mobility. Reduction in postoperative complications and better mobility permit earlier discharge and produce cost savings. Early and aggressive treatment of acute pain may prevent the development of chronic postoperative pain.

Reasons for inadequate pain control Audit by acute pain teams shows that postoperative pain can nearly always be controlled with conventional analgesic drugs and that suboptimal use of these drugs is a very common cause of inadequate pain control. Pain is widely underestimated by doctors and nurses and is underreported by patients, who expect to be in pain and do not want to bother staff. Doctors often write inadequate prescriptions and nurses administer less analgesia than prescribed because of fear of adverse effects (such as respiratory depression) or mistaken beliefs that analgesia hampers assessment of physical signs or leads to drug addiction. Patients themselves may prefer to suffer pain rather than the adverse effects of the drugs. Analgesia is often prescribed rigidly despite the variability of patients’ requirements. Analgesia p.r.n. requires patients to be in pain before they receive analgesics.

Factors affecting postoperative pain Patients exhibit wide variation in the degree of pain suffered and the analgesia required because of differences in surgery and among individuals. The site of surgery affects pain. Movement in damaged tissue causes pain, e.g. thoracic and upper abdominal incisions are very painful because of the movement of breathing. Surgical procedures in regions that are densely innervated (e.g. the hands) may be disproportionately painful. The type of surgery, the size of the wound, whether tissue fibres are cut or separated, and surgical technique 101

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all affect postoperative pain. Swelling in a confined space (e.g. after a total knee replacement) causes pain. Patient factors that affect pain and analgesia include physical and emotional condition, cultural background, age, reason for and outcome of surgery, and ability to sleep. Additionally there may be genetic factors that modulate tolerance to pain.

Assessment of pain

Regular assessment of pain scores improves the effectiveness of analgesia. Only the patient has real knowledge of the pain, and whenever possible assessment should ask specifically about pain and be self-reported by the patient. The assessment should be recorded quantitatively in the chart and repeated regularly. Better pain control is achieved if pain is recorded both at rest and during movement.

Methods of pain assessment

•

A categorical rating scale is commonly used in clinical practice. Patients rate their pain as none, slight, moderate, severe, very severe. A visual analogue scale is often used in acute pain research. The patient marks a point on a 10-cm line where 0 cm represents no pain and 10 cm the worst imaginable pain.

•

Freed

• •

A verbal numerical rating scale asks patients to score their pain out of 10 or 100. Techniques using pictures of faces, colours or a ladder to represent levels of pain may be useful, particularly in children or patients with chronic pain. Behavioural and physiological scoring systems can be used for patients who are not able to give an assessment of pain, e.g. babies, patients on ventilators and the demented. Multifactorial scales are used in chronic pain clinics and as research tools.

• •

Selection of appropriate analgesic drugs The World Health Organization (WHO) analgesia ladder (Fig. 8.1) is a method for prescribing analgesic drugs: each step on the ladder indicates the appropriate type of analgesic for a particular level of pain. Patients are assessed with regard to the severity of pain anticipated and their condition and a step on the ladder is selected. Thus patients suffering discomfort should be given a simple analgesic such as paracetamol, with the addition of other non-opioids (e.g. non-steroidal anti-inflammatory drugs) and weak opioids (e.g. codeine) for more intense pain. For severe acute pain, the most effective treatment is a strong opioid such as morphine (Table 8.1).

om fro

pain Opioi d for m ± No n-o oderate to sever ± Adj pioid e pai uvan n t

Pain p

ersistin

g or in

creasin Opioi g df ± No or mild to n-opi m odera oid ± Adj te pa uvant in Pain p

ersistin

g or in

Nonop ± Ad ioid juvan t

creasin

g 1

Pain

Figure 8.1 World Health Organization analgesia ladder.

60 mg p.o./i.m. (4–6 h) 30 mg p.o./i.m. (4–6 h)

50 mg p.o./p.r. (8 h) 400 mg p.o. (4–6 h) 50–100 mg p.o. (12 h) 10 mg p.o. (6 h) 10 mg i.v. first dose then 10–30 mg (4–6 h) Max. 90 mg/day for max. 2 days

12.5 mg p.o. (12–24 h)

50–100 mg p.o./i.m./i.v. (4–6 h)

1 g p.o., max. 4 g/day (4–6 h)

600–900 mg p.o. (4–6 h)

Buprenorphine

Codeine Dyhydrocodeine

Diclofenac Ibuprofen Ketoprofen Ketorolac

Rofecoxib

Tramadol

Paracetamol

Aspirin

Inhibition of COX

Inhibition of COX in CNS

Weak opioid agonist, actions at adrenergic and serotonin receptors

COX-2 specific NSAID

NSAIDs: inhibition of COX

Weak opioid agonists

Mixed opioid receptor agonist/antagonist

Opioid receptor agonists

Mechanism of action

Weak analgesia, anti-inflammatory, antipyretic

Weak analgesia, antipyretic

Moderate analgesia

Analgesia, as other NSAIDs

Moderate analgesia, anti-inflammatory, antipyretic

Moderate analgesia

Strong analgesia, sedation, euphoria

Effects

As for NSAIDs

None at therapeutic doses

Nausea, confusion in the elderly, rarely fits

May have less gastrointestinal and platelet effect

Gastrointestinal irritation, renal dysfunction, platelet dysfunction, bronchospasm

Constipation

As other opioids

Respiratory depression, sedation, dysphoria, nausea, constipation, tolerance

Adverse effects

As for NSAIDs. May cause Reye’s syndrome, contraindicated in children < 16 years old

Causes liver failure in toxic doses

All adverse effects more likely with bolus i.v. injection

As other NSAIDs, except reduced GI and bleeding risk

Known intolerance, risk of gastrointestinal ulcer, renal risk, hypovolaemia, elderly patients, immediately after major surgery, coagulation abnormality, caution in asthma

Poor bowel function

May antagonize other opioids Only partly reversed by naloxone

Respiratory failure, altered conscious level, cumulation in renal failure

Contraindications and cautions

Pain Relief Chapter 8

CNS, central nervous system; COX, cyclooxygenase; NSAID, non-steroidal anti-inflammatory drug.

200– 400 µg s.l. (6–8 h)

Pethidine Diamorphine Oxycodone

Dose (duration of action)

5 –15 mg i.m. (3–4 h) 10–20 mg p.o. (4–6 h) 50–150 mg i.m. (2 h) 5–10 mg i.m. (3–4 h) 5–15 mg p.o. (4 h)

Morphine

Drug

Table 8.1 Commonly used analgesics.

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CHELSEA & WESTMINSTER HOSPITAL ACUTE PAIN SERVICE

PATIENT CONTROLLED ANALGESIA CHART Standard morphine solution: 100mg in 50ml NaCl 0.9% (= 2mg/ml)

Morphine 100mg in 50ml

Loading dose (if required): 5-10mg (= 2.5-5ml)

. . . . . . . . . . . . . . . . . . . . . . mg

PCA: No background infusion Bolus 1mg (= 0.5ml) Lockout 5 minutes

............................ Anaesth. sign for APS protocol PCA

Anaesthetist prescribing and setting machine Signed: Time: Date:

Recovery Nurse handing over to Ward Nurse Signed: Signed: Time: Date:

GENERAL INSTRUCTIONS • Pump settings must be checked and signed for at each handover • A dedicated line for the PCA should be used. Alternatively an anti-reflux valve may be used • Monitoring: HR, BP, RR, Sedation, Pain and Nausea Scores 15min for 1 hour; 30min for 1 hour; 4 hourly when stable • Oximetry and apnoea monitor if indicated • No additional opiods should be prescribed. However, if patient is in pain, a re-loading dose should be given in increments, IV by a doctor or the APS nurse. PCA should be used to maintain analgesia, not to establish it. • If respiratory rate is < 8 and /or patient is unrousable, STOP INFUSION, GIVE OXYGEN, CALL APS ANAESTHETIST (bleep 0100) Date Time Resp. rate O2 sats. Sedation Score Nausea Score Pain Score PCA given Pump checked ( ) RN sign. Date Time Resp. rate O2 sats. Sedation Score Nausea Score Pain Score PCA given Pump checked ( ) RN sign. Pain Score: 0 None 1 Mild pain 2 Moderate pain 3 Severe pain 4 Unbearable pain

Sedation Score: 0 Awake 1 Dozing 2 Asleep 3 Unrousable

Nausea: 0 No nausea 1 Nausea 2 Vomiting Figure 8.2 Postoperative monitoring chart.

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Pain Relief Chapter 8

A combination of different drugs improves the effectiveness of analgesia; by using smaller doses of each drug, adverse effects are reduced. If repeated doses of analgesia are required they should be given regularly, so that each dose is given before the effect of the previous one wears off. Analgesics have adverse effects and contraindications to their use should be followed. The common adverse effects of analgesics should be prevented by using adjuvant treatments such as antiemetics and laxatives. It is prudent to use a small range of analgesics that are familiar to all staff.

Regular monitoring and recording Regular reassessment of pain scores and vital signs in order to detect adverse effects of treatment early is essential to ensure effective and safe pain management. Adequate monitoring allows the maximum safe dose of analgesia to be given and thus permits maximum benefit to the patient. For every patient at risk of acute pain, basic monitoring includes regular recording of the pain score as well as routine physiological parameters: heart rate, respiratory rate, blood pressure and temperature. For patients on opioids there should be in addition regular monitoring of sedation score, nausea score and cumulative dose of analgesia. Pulse oximetry should be considered (Fig. 8.2). Patients receiving epidural analgesia require regular recording of heart rate, respiratory rate, blood pressure, temperature, pain score, sedation score and nausea score. In addition, the height of the epidural sensory block, the degree of motor block and the cumulative dose of epidural drugs are recorded. The catheter insertion site and the condition of potential pressure sore areas are reviewed regularly.

Opioids Opioids are the most effective drugs available for the treatment of severe acute pain. Morphine is still the most widely used; other opioids have similar actions and adverse effects.

Intravenous bolus For severe acute pain, intravenous morphine gives rapid pain relief and enables evaluation of the patient’s individual requirement. A dose of 5 –10 mg should be titrated slowly until the patient is comfortable, without excessive sedation or respiratory depression.

105

Intermittent intramuscular injection Traditionally morphine has been given intramuscularly as required postoperatively. This method is very effective when used optimally, but frequently in practice patients are in pain because of delay in giving repeated doses. Blood levels of drug may swing between excessive (with adverse effects) after injection and inadequate (with pain) before the next injection.

Intravenous infusion A constant-rate infusion overcomes the problems of variable blood levels and delays in administration of intramuscular morphine. If given by a single-rate infusion, a steady-state blood level is only obtained after about four half-lives so a loading dose is needed to establish analgesia. A maintenance infusion is then adjusted according to the patient’s response. With a device that continues to infuse at a steady rate regardless of the effect on the patient, there is a risk of inadvertent overdose and regular monitoring is crucial. This technique is especially suitable for patients in the intensive care unit, high-dependency unit or terminal care.

Patient-controlled analgesia Patient-controlled analgesia is a technique where the patient self-administers a small dose of drug when necessary. A loading dose is given to establish analgesia; the bolus dose, which the device supplies when the patient presses the button, is usually 1–2 mg morphine. The lock-out time, the period during which the device will not supply another dose, is usually set at 5–10 min. This prevents multiple dosing and means that each dose can only be given when the previous one has had time to take effect. Background continuous infusions are not advisable for most adult patients: there is no improvement in pain control but adverse effects are increased.

Advantages

•

Each individual can maintain the blood level of drug that gives the best analgesia for the least adverse effects. The analgesic dose can be varied to meet fluctuating pain levels. The drug is only given on demand, so that if the patient becomes sedated administration stops. This makes the technique safer than continuous infusion but does not obviate the need for careful monitoring.

• •

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Disadvantages

Topical

•

Local anaesthetic can be applied as a gel, e.g. for venepuncture in children, and after transurethral and eye surgery.

The patient needs to be intellectually, emotionally and physically able to use the device, and to be taught how to use it. The equipment is expensive.

•

Oral

Morphine can be given by mouth and this route is suitable for patients whose gastrointestinal function is normal and whose requirement for analgesia is stable. However, bioavailability can be quite variable and oral morphine is inappropriate for sick patients or immediately following major surgery. The oral dose is usually about twice the intramuscular dose for the same patient, and is adjusted according to clinical response.

Non-steroidal anti-inflammatory drugs Non-steroidal anti-inflammatory drugs (NSAIDs) reduce prostaglandin synthesis by inhibition of cyclooxygenase. Because prostaglandins are involved in so many physiological processes, NSAIDs have a variety of actions and adverse effects. These actions include inhibition of peripheral nociceptor sensitivity and of inflammation, which is a frequent cause of pain. NSAIDs also reduce fever. NSAIDs are very effective drugs for moderate pain and do not cause nausea, sedation, respiratory depression or depression of bowel function. They are widely used for analgesia after minor and intermediate surgery. They can also be used in combination with opioids for treatment of severe pain; this combination has an ‘opioid-sparing effect’ that reduces the requirement for opioid and diminishes opioid-related adverse effects. Major adverse effects include renal dysfunction, gastric irritation, platelet inhibition and bronchospasm. NSAIDs should not be used for patients at risk of adverse effects. The incidence and significance of adverse effects are greater in the elderly and immediately after major surgery.

Local and regional analgesia Local anaesthetics are often used in the operating theatre and may be continued for postoperative pain relief. The duration of action of commonly used local anaesthetics ranges from 2 to 6 h; for longer-lasting analgesia, repeated injections or continuous infusion is necessary.

Nerve block A single injection is often used in the operating theatre. Repeated injections postoperatively are impractical, but a catheter may be sited for regular administration.

Epidural analgesia Epidural analgesia may be given as a single dose in the operating theatre or a catheter may be left in the epidural space for repeat bolus administrations or continuous infusion. The most commonly used drugs are a combination of local anaesthetic and an opioid. Epidural analgesia has the following effects. Sensory block provides very high quality analgesia, with much less risk of the sedation, respiratory depression and nausea associated with systemic opioids. Sympathetic block causes vasodilatation and may result in hypotension if the block extends to levels involving sympathetic outflow (T1–L2), particularly if there is coexisting hypovolaemia. Motor block may cause weakness.

• • •

Advantages

•

Excellent analgesia can be achieved without the use of systemic opioids, and the patient feels comfortable and well. Mobilization is improved and patients can cough and cooperate with physiotherapy. This is particularly useful for patients with respiratory disease, and following upper abdominal and thoracic surgery.

•

Disadvantages fails if the catheter is displaced. • Analgesia A high level of specialist care and monitoring is • required. • Complications include severe headache if there is accidental dural puncture (about 1% of epidurals), excessive motor block, hypotension, urinary retention and pressure sores.

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Pain Relief Chapter 8

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• • • • • • • • • •

Non-drug analgesia

Effective pain relief reduces the incidence of postoperative complications Most postoperative pain can be controlled effectively by optimal use of common analgesics People vary widely in their analgesic requirements Pain control is improved by regular assessment Regular combination therapy gives the best pain relief for the least adverse effects Regular monitoring is essential for safe analgesia Opioids are the gold standard of care for severe acute pain NSAIDs are effective for moderate pain or as co-therapy for severe pain Regional analgesia is effective and needs careful management The approach of staff to patients may have a profound effect on pain and suffering

Methods of relieving pain that do not involve drugs should always be considered. The painful stimulus may be reduced by immobilization (e.g. a fracture) or careful mobilization (e.g. low back pain). Inflammation and oedema may be reduced by elevation and ice packs. Non-painful stimulation such as heat or transcutaneous nerve stimulation reduces ‘trafficking’ of pain signals in the spinal cord. Above all, pain and suffering may be reduced by the attitude of staff. Fear, anger, sadness and bewilderment make pain worse and should be treated by listening to the patient, explaining the planned treatment clearly, and approaching patients and their families in a friendly, respectful and sympathetic manner.

Pain relief at a glance Definitions Pain is an unpleasant localized sensation caused by the stimulation of sensory nerve endings called nociceptors, which are stimulated by the release of prostaglandins and other chemical mediators released from cells damaged by injury or inflammation. Adverse effects of untreated pain Psychological Suffering Anxiety Depression Anger

• • • •

Stress response Sympathetic activation: hypertension, tachycardia, vasoconstriction Increased risk of myocardial infarction, stroke, renal failure Gastric ulceration, gastric stasis Metabolic: muscle loss, sodium and water retention, hyperglycaemia

• • • •

Immobility Chest infection Venous thrombosis Pressure sores Delayed recovery

• • • •

Development of chronic pain

Reasons for inadequate pain control Suboptimal use of analgesics Underestimated by doctors and nurses Underreported by patients Fear of adverse effects of analgesics Philosophy that patient must be in pain before they can have analgesia

• • • • •

Factors affecting postoperative pain Site of surgery: chest, upper abdomen, hand very painful Type of surgery: size of wound, postoperative swelling Patient factors: physical, emotional, cultural, age

• • •

Pain assessment Regular assessment of pain scores and vital signs is essential for effective and safe pain management Categorical rating: none, slight, moderate, severe, very severe Visual analogue scale: patient marks a point on a 10-cm line where 0 cm represents no pain and 10 cm worst imaginable pain Verbal numeral rating: score pain out of 10 or 100 Behavioural and physiological scoring systems Multifactorial scales

• • • • • •

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Analgesia ladder Level of pain

Analgesic

Method of administration

Adverse effects

Discomfort Increasing pain

Simple analgesic, e.g. paracetamol Simple analgesic ± non-opioid (NSAID) ± adjuvant Strong opioids (morphine)

Oral Oral, suppository

Liver damage with overdosage Renal dysfunction, gastric irritation, platelet inhibition, bronchospasm Nausea and vomiting, constipation, drowsiness, respiratory depression, hypotension

Severe acute pain

Oral, i.v. bolus, i.m. bolus, i.v. infusion, patientcontrolled analgesia

Other types of analgesia Local Topical gel (lidocaine) Nerve block either by injection or via catheter

• •

Regional Epidural either by single injection in theatre or via catheter Epidural analgesia achieved by combination of local anaesthetic (bupivacaine) + opioid

• •

Evidence-based medicine Rowbotham & Macintyre (2003) Clinical Pain Management: Acute Pain. Arnold, London. McQuay, H., Moore, A. & Justins, D. (1997) Treating acute pain in hospital. Br Med J 314, 1531. http://www.jr2.ox.ac.uk/bandolier/booth/painpag/ Oxford pain internet site.

Non-drug analgesia Immobilization, e.g. for fractures Elevation and ice packs, e.g. for inflammation Heat (reduces trafficking of pain signals) Transcutaneous nerve stimulation (reduces trafficking of pain signals) Attitude of staff

• • • • •

Australian National Health and Medical Research Council (1999) Acute Pain Management: Scientific Evidence. Full text on website http://www.health. gov.au/nhmrc/publications/ Handbook for choosing and using drugs: British National Formulary (latest edition).

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Complications following Surgery Classification of complications, 109

Common clinical presentations, 109

Common or important problems, 114

when faced by real clinical problems in actual patients. Several of these common clinical presentations are discussed below.

Must know Must do Must know Causes, diagnosis and principles of management of common postoperative complications Hospital antibiotic policies Must do Examine chest radiographs of postoperative pneumonia and pleural effusion Follow up patients with chest infection, pulmonary embolism and intra-abdominal abscess Wear antithrombosis stockings for one day Participate in postoperative intravenous fluid management in a patient after major gastrointestinal operation

Common clinical presentations Low urine output (oligo-anuria) Urine output is of prime concern in the postoperative management of patients and several points should be borne in mind when assessing the rate of urine formation in a given patient. Urine output is used as a reflection of glomerular filtration rate (GFR), which is itself a reflection of renal blood flow (RBF) and hence the overall hydration status of the patient. Surgery produces the ‘stress response’ and hence tends to lower urine volume below the normal rate for a given patient. Many factors other than RBF may affect GFR and hence urine output. Urine output (and GFR) should be corrected for body weight. As a rule of thumb, a minimum acceptable urine output is 0.5 mL/kg per h. When assessing a patient with a low or apparently zero urine output it is important to be methodical; one approach is given in Fig. 9.1. It is important to act

• •

Classification of complications Classically, complications can be divided into the cause (specific to the surgery performed or general to any surgery) and the time period in which they arise (immediate, early and late) (Table 9.1). Many of the complications have specific investigations and treatments (see section Common or important problems). This approach to classification provides a useful way of ensuring important complications are not forgotten but does not often help

• • •

Table 9.1 Complications of a bowel resection for colon cancer. Immediate

Early

Late

Specific to the operation

Intraoperative haemorrhage

Wound infection Anastomotic breakdown Intra-abdominal abscess

Adhesion-related problems Anastomotic stricture Wound hernia

General to the anaesthesia

Perioperative myocardial infarction Anaphylactic reaction

Pulmonary collapse Deep vein thrombosis Cannula phlebitis Urinary tract infection

Pulmonary embolism

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Patient reported as oligo-anuric

If not catheterised do so and check for urinary retention If catheterised - flush catheter to exclude blockage

Real oligo/anuria

Check for low cardiac output

Assess for signs of hypovolemia

Treat causes of low cardiac output (e.g. arrhythmias)

Trial of fluid challenge bolus up to 5mL/kg per L

Consider ITU support

If fails consider further fluid challenge monitored by central venous catheter

Figure 9.1 Diagnostic algorithm for oligo-anuria.

promptly on a genuinely low or absent urine output; prolonged problems with poor renal perfusion can rapidly lead to acute tubular damage and necrosis and eventually to established acute renal failure.

Fluid challenges in oliguria The role of a fluid challenge is to assess whether the oliguria is due to simple hypovolemia. The principles of a fluid challenge are: that it should reflect the volume of fluid by which the circulation is anticipated to be depleted; the fluid should be given over a short period of time and the response assessed over the next hour or so; the fluid used is less important than choosing the correct volume and giving it over the correct time span a normal saline is as good as any other fluid for a challenge. Great care should be taken when deciding to give a fluid challenge. An assessment needs to be made of the cardiac function of the patient. Those with poor cardiac output or cardiac reserve (such as those with known ischaemic heart disease, known pulmonary hypertension or the elderly) are much more likely to develop acute pulmonary oedema with a prompt fluid challenge. Do not repeat a fluid challenge unless there is good reason to believe the patient is grossly hypovolaemic. If it is felt that further challenges are appropriate, monitoring of the central

• • •

venous pressure (CVP) response to the challenges may be necessary.

Advanced therapies Furosemide High-ceiling loop diuretics such as furosemide may have a role in preventing the establishment of renal damage in oligo-anuria. They work not only by reducing sodium reabsorption and so causing a diuresis but also have an effect on RBF by promoting increased flow in the renal cortex. Provided a patient has a properly restored circulating fluid volume, doses of furosemide may help promote the re-establishment of urine flow. High-dose furosemide infusions are usually reserved for the intensive care setting or with specialist advice. Dopamine The kidney contains dopaminergic receptors and it has been suggested that low-dose dopamine infusions would activate these receptors to increase RBF without affecting other systems. It is more likely that dopamine infusions promote RBF through a general stimulation of the cardiovascular system (inotropic and chronotropic effects) rather than an isolated renal effect. Their role is to support renal function in established acute or prerenal failure. Renal support In cases where renal function does not improve with prompt restoration of the circulating volume and attempts to restore renal function by diuretics or inotropes, it may be necessary to provide renal support until renal function returns spontaneously (which may be prolonged). Methods to replace or support renal function include haemofiltration, haemodialysis and haemodiafiltration. The main indications for providing renal support are: failure to excrete water causing fluid overload; failure to excrete potassium causing hyperkalaemia; rising serum urea to toxic levels; failure to autoregulate acid–base balance.

• • • •

Confusion Confusion is common on surgical wards. As patients get older and are admitted nearer to the time of surgery, simply being in hospital and waking up following a major operation and anaesthetic are causes for confusion, especially in the elderly. However, confusion should never be treated as a simple matter of disorientation until the major causes have been considered and eliminated. These causes can be remembered by the acronym ‘DAM Hypos’ (Table 9.2). Never treat confusion with sedatives unless the cause is certain, however appealing it may be to have the patient

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Complications following Surgery Chapter 9

Table 9.2 Common causes of confusion in the postoperative patient.

Pyrexia A raised temperature is the single most common finding on a surgical ward. A mildly raised temperature is a normal part of the early postoperative response to major surgery. However, the development of a temperature following surgery should always be cause for concern. The likely cause varies according to when the temperature appears. The most common causes are shown in Fig. 9.2. The form of the temperature chart can also give important clues as to the cause (Fig. 9.3). As ever, a high swinging temperature suggests a collection of pus, either in a body cavity (e.g. pelvic abscess, subphrenic abscess or empyema) or within a body organ (e.g. gallbladder empyema, pyometria, renal abscess). A low-grade ‘grumbling’ temperature suggests a low-grade infective or inflammatory process (e.g. deep vein thrombosis or cannula-related sepsis).

Drugs Anaesthetic agents Analgesics (opiates) Normal drugs being given Normal drugs not being given Acute systemic infections Wound infections Anastomotic leak Chest infection Metabolic disturbances Hypokalaemia/hyperkalaemia Hyponatraemia/hypernatraemia Hypoglycaemia/hyperglycaemia Fluid overload Alcohol withdrawal Hypotension Occult haemorrhage Inadequate fluid infusion Low cardiac output (arrhythmias, myocardial ischaemia, pulmonary embolism)

Management of postoperative pyrexia A thorough assessment of the patient, including a brief history and physical examination, is necessary. If a likely source is identified, then specimens should be taken wherever possible to identify the causative organism (e.g. wound swabs for a wound infection). If the patient is not unwell and the cause is a minor infection, it may be appropriate to withhold antibiotics until the cause is known. If the patient is unwell or the cause is considered potentially serious, antibiotics (oral or intravenous) should be started using a ‘best guess’ as to the likely causative organism (e.g.

Hypoxia

quiet and undisturbed for the benefit of other patients, the nurses and the doctors. A simple guide is ‘Check the vitals, check the bloods, check the drug chart and check the abdomen’.

Risk of causing pyrexia Operation 0

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Intra-operative Drug related Blood transfusion

Early post-op (3-5) • Wound infection • Respiratory infection • Cannula sepsis

Immediate post-op (1-3) • Release of inflammatory mediators • Respiratory collapse • UTI

Figure 9.2 Causes of postoperative pyrexia according to time of appearance.

12 13 14 Day post-op Delayed post-op (5-12) • Wound breakdown • Anastomotic leakage • Abscess formation • DVT

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DATE TIME 41˚

.00 .00 .00 .30 .00 .00 2.10 1.007.002.006.301.205.456.002.056.001.006.209.457.009.30 6.00 0.006.302.00 6.008.406.05 2.006.006.405.00 6.001.00 15 18 20 21 09 11 1 1 2 0 1 1 0 1 1 2 0 0 1 1 0 1 1 2 0 0 1 2 0 1 1 0 1 2

TEMPERATURE

40˚

39˚ 38˚ 37˚ 36˚ 35˚

Figure 9.3 Patient observation chart showing pyrexia caused by an intraabdominal abscess.

34˚

POSTOPERATIVE HYPOXIA Opiates ( Cough) Anaesthetics ( Production Cough) Anticholinergics ( Sticky Cilial action)

Smoking ( Production Cilial action)

N2O/O2 more soluble than O2/N2 GASES ABSORBED

Secretion blocking airways

Collapse

COPD Age Inhaled anaesthetics

100% O2 prior to extubation very soluble

Absorption collapse

(Shunting Available lung) Dynamic collapse

Supine position

Abdominal pain Recumbent position ( Depth Cough)

Hypoxia

Hypoventilation

Anaesthetic agents

Opiates Alcohol ( Deep breaths Rate)

Figure 9.4 Causes of postoperative hypoxia.

an antistaphylococcal antibiotic for significant cannularelated sepsis). If the cause is unclear, it is usual to collect a ‘septic screen’ from the patient. This includes a urine sample, sputum sample, swabs of any suspicious wounds or cannulae, chest X-ray and blood cultures. For patients who have had recent abdominal surgery where an intraabdominal cause is suspected, contrast-enhanced com-

puted tomography (CT) of the abdomen is often requested urgently. If the patient is unwell and the cause is unknown, then it is best to start broad-spectrum intravenous antibiotics with a view to refining treatment once the results of the screen are known. If the diagnosis appears to be deep venous thrombosis, anticoagulation should be discussed with the surgical team. A good guide is to remember that intra-abdominal

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complications may first manifest only with pyrexia and a high index of suspicion should be maintained for complications of the surgery itself.

Hypoxia Postoperative hypoxia is more common than documented, especially in patients who have had major thoracic or abdominal surgery. The cause may be multifactorial (Fig. 9.4). There are two key factors in the management of postoperative hypoxia. 1 Have a low index of suspicion. Mild confusion, mild hypotension and slight tachycardia may be the only signs of quite profound hypoxia. If in doubt, check for hypoxia and treat it. 2 Concentrate on the mechanics and basic physiology of ventilation first. Adequate analgesia, proper patient positioning, humidified oxygen and physiotherapy (active and passive) are the mainstays of treatment.

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Chest radiography and antibiotics Both chest radiography and antibiotics for ‘chest infection’ have a limited role in the management of postoperative hypoxia. The patchy small airway collapse that is a common cause after major surgery is rarely visualized on the chest radiograph and there may be frank consolidation present that is not seen. Chest X-ray is useful where pneumothorax or pleural effusions are suspected as contributory factors. Most postoperative respiratory problems are not due to classical ‘pneumonia’ of any type. Provided the collapse and hypoventilation that underlies many problems is treated, any infectious element usually resolves spontaneously. Systemic antibiotics should be reserved for cases where there is a strong suspicion of established lobar consolidation or where the patient shows signs of systemic sepsis.

Complications following surgery at a glance Definitions Complication: an additional disorder or problem arising in the course, or as a result, of a disease, injury or abnormality Oliguria: an abnormally small amount of urine (< 400 mL/day) Anuria: no urine passed in a day Confusion: a state of disorientation arising from loss of contact with reality, disturbance of memory, hallucination or dementia Pyrexia (fever): an elevation of the body temperature, taken in the mouth, above 37 °C Hypoxia: a deficiency of oxygen in the tissues

Common presentations indicating a postoperative complication Low urinary output (see also Chapter 14) • Minimal acceptable urinary output is 0.5 mL/kg per h (30 mL/h for most adults) • Low urine output reflects GFR, which reflects RBF, which reflects arterial blood pressure and general level of hydration Management • Low urinary output: catheterize patient to confirm. True oliguria tested by fluid challenge (5 mL/kg per h) • Signs of hypovolaemia present (tachycardia, low blood pressure): tested by fluid challenge (5 mL/kg per h) • No response to fluid challenge: place central line to monitor CVP ± transfer to HDU/ICU • May need diuretics, inotropes or renal support (haemofiltration, haemodialysis, haemodiafiltration)

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Confusion Common after surgery particularly in the elderly. Seek and treat cause. Don’t just give sedation! • Drugs (a) Anaesthetic agents (b) Analgesics especially opiates (c) Normal drugs: administered/not being administered (d) Alcohol withdrawal • Metabolic (a) Hypokalaemia/hyperkalaemia (b) Hyponatraemia/hypernatraemia (c) Hypoglycaemia/hyperglycaemia (d) Fluid overload • Hypoxia • Infections (a) Chest (b) Wounds (c) Intra-abdominal (d) Urine • Hypotension (a) Haemorrhage (b) Dehydration (c) Low cardiac output (arrhythmias, myocardial infarction, pulmonary embolism) Assessment of a confused patient • Check vitals • Check chest

• Check abdomen • Check drugs • Check urine • Check bloods Pyrexia (see also Chapter 7) • Pyrexia is a common sign of infection • A mildly raised temperature is normal in the early postoperative period, indicating response to major surgery • If pyrexia develops follow ‘Note, Check, Do, Give, Treat’ scheme outlined in Chapter 7 Hypoxia (see also Chapter 11) • Common after surgery, especially thoracic or upper abdominal surgery • Mild confusion, mild hypotension and slight tachycardia may be only clinical features • Check and monitor hypoxia with pulse oximetry • Treatment should concentrate on restoring normal ventilation: (a) Adequate analgesia (b) Proper patient positioning (c) Humidified oxygen (d) Physiotherapy (active and passive) • Chest X-ray and antibiotics have a limited role

Common or important problems

Peritonitis

Postoperative complications involving some common problems are covered in other chapters (blood transfusion, Chapter 6; surgical infections, Chapter 7).

When a leak occurs at an intra-abdominal anastomosis and there is failure to control the spread of leaking contents by surrounding tissues or omental fat, peritonitis usually ensues. The clinical picture is typically one of a patient becoming rapidly unwell, with a rising tachycardia, fever, hypotension and increasing abdominal pain. The abdomen may be difficult to assess, particularly if the patient is in the early postoperative period when abdominal examination is uncomfortable (other than patients having epidural analgesia). The absence of obvious clinical peritonitis should not dissuade the surgeon from the diagnosis of a leaking anastomosis. Free gas on the chest radiograph may be an unreliable sign in the early period because gas is usually seen up to 3 days after laparotomy; however, a large volume of free gas appearing much later than this is often diagnostic of a major problem. On investigation, neutrophilia and

Anastomotic leak Leakage from any kind of intestinal, biliary or urinary anastomosis is a relatively rare but potentially lifethreatening complication. The possibility of the presence of a leak should be borne in mind in all patients who have an anastomosis and in whom progress is not as expected or who show signs of sepsis not otherwise explained. A leak may manifest in several distinct clinical scenarios and may occur at any time following surgery, although most often it is diagnosed between days 4 and 14 postoperatively.

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metabolic acidosis are typically, but not necessarily, present. Management The principles of management are as follows. Stabilize the patient and maintain the cardiovascular and respiratory systems. Patients should have good intravenous access established and usually require fluid resuscitation to support the cardiovascular system. High-dose oxygen and monitoring of vital signs, urine output and oxygen saturation should be started. Begin treatment for presumed systemic sepsis. Highdose intravenous antibiotics are usually given on the basis of ‘most likely organism’. In the case of bowel surgery, this must include antibiotics active against Gram-negative and anaerobic organisms. Reoperate to control the leak in the quickest, most effective way. Once the patient is stable, urgent surgery is required for definitive treatment of the leak. This usually means control of the leak by exteriorizing the ends of the anastomosis, insertion of a drain or, rarely, repair of the leak. Once a leaking anastomosis and peritonitis have been diagnosed, treatment must be begun immediately, if necessary with the help of the intensive care unit, as peritonitis carries one of the highest rates of morbidity and mortality of any complication.

• • •

Intra-abdominal abscess Frequently, a small leak may be contained by the surrounding body tissues or the adherence of the omentum to the site. This prevents widespread contamination by the leak but may result in the formation of a local abscess. The abscess is commonly, but not always, found in the region of the anastomosis (e.g. pelvic abscess following surgery on the rectum). The clinical picture tends to be one of a high swinging fever and associated variable tachycardia, localized abdominal pain and poor postoperative progress. The location of the abscess may also give rise to symptoms (e.g. rectal pain and mucous discharge with a pelvic abscess, chest and shoulder tip pain with a subphrenic abscess). Neutrophilia and metabolic acidosis are also frequent findings on investigation. The chest radiograph may occasionally show an air–fluid level in a subphrenic abscess. Where an intra-abdominal abscess is suspected, the investigation of choice is contrast-enhanced CT. Management The management of the patient depends on the clinical picture. If the patient is very unwell and the degree of sepsis caused by the abscess is severe, then treatment should be

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the same as for patients with a leak and peritonitis. If the degree of sepsis is not severe, most abscesses will resolve with percutaneous drainage and antibiotic treatment. The most common method of drainage is CT- or ultrasoundguided drain insertion under local anaesthetic. Occasionally, open surgical drainage may be necessary where the abscess is surrounded by other organs or is inaccessible. In the case of a pelvic abscess, drainage can sometimes be made through the wall of the rectum or through the anastomosis, avoiding an external drain of any kind.

Enteric fistula A leak may occasionally present with the formation of a fistula (usually between the leaking point and the surgical wound or drain hole). This most often represents a small leak and abscess formation that has escaped detection and which ‘points’ through the tissue planes opened up by the surgery as the ‘path of least resistance’. The clinical picture is typically the development of an erythematous, apparently infected area of wound or drain site that begins to discharge pus and then bowel contents, bile or urine. On close review the patient is often seen to have had a low-grade temperature and signs of infection prior to the development of the fistula. Patients who develop a fistula are rarely severely septic. Although it signifies a leak, this is almost always contained by the body tissues directing the fistula outwards. Management If the patient shows signs of peritonitis or gross sepsis, then management should be as for peritonitis. If not, the principles of management of a postoperative fistula are as follows. Drain any associated abscesses that will prevent healing of the fistula. Where these are present, CT- or ultrasoundguided drainage is employed. Ensure the fistula can drain properly at the exit point, i.e. the wound is draining freely (e.g. into a stoma bag). Maintain fluid balance and nutrition during the healing. Initially this means support with intravenous fluids but may also mean intravenous nutrition if the fistula is large or slow to heal. Provided that there is no obstruction to the bowel or source of the fistula, the fistula will close spontaneously.

• • • •

Wound complications Wound infection Superficial wound infection may occur after any sort of surgery, the risk of infection being related to many factors. An increase in wound infection rates is seen with

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increasing length of time spent in hospital prior to surgery, emergency or urgent surgery vs. elective surgery, malnutrition or immunosuppression of the patient, and surgery that involves opening body viscera (e.g. bowel or biliary tract) or surgery for septic indications (e.g. acute diverticulitis). The most common source of infection is the skin flora of the patient (e.g. Staphylococcus aureus). Another common cause is contamination with organisms from the site of surgery (e.g. Escherichia coli from bowel cases). The infection usually presents with a low-grade temperature and a painful erythematous wound with a purulent discharge. It can often be managed by simply allowing the infection to drain freely by opening the infected area of the wound and cleaning the site with antiseptic solution. Only for large or deep infections are antibiotics required. A wound infection is nowadays categorized as a superficial surgical site infection.

Wound dehiscence Breakdown of the deeper layers (fascia and muscle) of a wound may be due to infection but may also represent problems with poor healing and/or poor surgical suturing technique. Nowadays, abdominal wounds rarely dehisce. This complication is more common in the elderly and the chronically ill or malnourished patient. The first sign is often a high volume of clear, strawcoloured, serous discharge from the wound, indicating that the deeper tissue layers are no longer in close contact and this allows peritoneal fluid to leak out. If the skin and subcutaneous layers also break down, the patient is left with omentum or loops of bowel protruding into the wound. Although this is often a dramatic and very distressing occurrence for the patient, it is actually not particularly dangerous. Provided there is no strangulation of the bowel loops in the wound, repair can be left until the next suitable operating slot. The wound should be dressed with soft swabs and an occlusive dressing to prevent excessive fluid losses from the exposed bowel. Wound breakdown after thoracic, neck or limb surgery is much less common and rarely needs a return visit to theatre for repair.

Wound hernia A late complication of abdominal surgery is the development of incisional wound hernia. This may be the consequence of early partial wound dehiscence but is more often the result of chronic failure of the tissues of the scar. It is more common in the obese patient or patients with risk factors for other hernias such as chronic cough (see Chapter 24).

Other infections (see also Chapter 7) Cannula-related sepsis Cannula-related sepsis is the most common complication suffered by patients on surgical wards. Although the majority of infections are trivial, a proportion can develop a nasty local cellulitis and a small proportion go on to develop septicaemia as a result. In the UK every year patients die from septicaemia, infective endocarditis and metastatic abscesses originating from cannula-related infections. Most of these infections can be prevented by simple measures related to good hygiene and sensible practice. Cannulae should be inserted under clean conditions and properly dressed to avoid contamination. Intravenous infusions should be changed only as necessary to reduce the risk of contamination of the cannula. Cannulae should be changed regularly rather than waiting for signs of sepsis to develop in a cannula that has been present for many days.

• • •

Urinary infection The urinary tract is often instrumented or catheterized in surgical patients. The urethral orifices are notoriously rich in bacterial flora and, once introduced, the lower urinary tract in particular is prone to the development of infection in a short period of time. Ascending infection involving the upper renal tract and kidney is uncommon but can cause major complications. As a rule, catheters should be used only when strictly necessary, inserted as aseptically as possible and removed at the first suitable opportunity. As soon as signs of urinary infection are present, any catheter should be removed if possible and the patient treated by promotion of an active diuresis as well as oral antibiotics that are concentrated in the urine.

Intestinal obstruction (see also Chapter 23) Mechanical Mechanical intestinal obstruction is uncommon as an early complication following surgery. Certain procedures have a particular risk of mechanical obstruction (e.g. after intestinal stoma formation, following abdominoperineal excision of the rectum), although most mechanical intestinal obstruction following surgery occurs as a late complication due to adhesions (see later). The majority of postoperative mechanical obstructions resolve spontaneously, although reoperation is occasionally required when a loop of bowel is trapped in a suture.

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Paralytic Paralysis of the gastrointestinal tract, particularly the small bowel, may occur after any operation, not just those involving opening of the abdomen. Many factors may contribute to the development of postoperative ileus, including handling of the bowel, procedures on the bowel itself, anaesthetic drugs (especially epidural anaesthetics), analgesics such as opiates, electrolyte imbalances and underlying endocrine abnormalities such as thyroid disease. The principles of management are: maintain adequate fluid and electrolyte balance, correcting any initial abnormalities that might be contributing to the cause; rest the gastrointestinal tract with nil-by-mouth or the insertion of a nasogastric tube if the patient is vomiting; remove any drugs that might be contributing to the cause; maintain the nutritional requirements of the patient by parenteral methods only when the ileus is persistent or when prolonged periods without oral nutrition are expected. Most cases of postoperative paralysis resolve spontaneously and there is little role for drugs that promote gastrointestinal motility.

• • • •

Fluid and electrolyte imbalance (see also Chapter 13) Fluid and electrolyte disturbances following surgery may occur for several reasons. Inappropriate administration of fluid replacement therapy by the medical staff, causing excessive or insufficient infusion of sodium, potassium or water. Excessive losses of electrolytes, particularly sodium and potassium, due to nasogastric tubes, high intestinal stoma outputs, intestinal fistulae, diuretics or other drugs. Intrinsic renal disease exacerbated by surgery or administered drugs. The consequences of imbalances can include paralytic ileus, persisting nausea and vomiting, metabolic acidosis or alkalosis, confusion or even convulsions (especially in the susceptible such as the elderly and very young).

• • •

Thromboembolic disease Deep vein thrombosis Up to 20% of patients undergoing major surgery and in hospital longer than 7 days may develop deep vein thrombosis (DVT). The risk is highest in women using the contraceptive pill and those undergoing major pelvic surgery. The majority of these will not be clinically apparent and only 1% or so of patients will develop life-threatening

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complications such as pulmonary embolism. Prophylaxis for DVT is now a recognized part of routine preoperative care for most patients undergoing emergency or major surgery (see Chapter 5). Postoperatively, the signs of DVT (see Chapter 28) may be masked, especially in patients undergoing major lower limb orthopaedic surgery, and it is necessary to have a high index of suspicion. The diagnosis is usually made postoperatively by a combination of duplex ultrasound scanning of the above-knee venous system, serum D-dimer FDP levels and occasionally venography. Patients in whom anticoagulation is not contraindicated because of their surgery should receive standard full anticoagulation, initially with heparin.

Pulmonary embolism Postoperative pulmonary embolism may present as chest pain, dyspnoea, hypoxia, confusion or even an unexplained persistent tachycardia or pyrexia. The classic signs of haemoptysis and sudden-onset dyspnoea together with electrocardiographic changes are present in only a few patients postoperatively. The chest X-ray is usually unhelpful and a ventilation–perfusion scan often inappropriate. Recent advances in scanning technology make CT pulmonary angiography a very sensitive and specific test where the diagnosis is seriously considered.

Adhesions Adhesions may form in body cavities (pleura and peritoneum) normally lubricated by only a thin film of serous fluid. Any inflammatory insult may provoke a reaction in the mesothelial lining of the cavity, with formation of a fibrinous membrane that tends to stick the mesothelial surfaces together. These thin, ‘filmy’, fibrinous adhesions are common after any insult such as infection (e.g. underlying pneumonia or appendicitis) or surgical transgression of the cavity (e.g. after pneumonectomy or uncomplicated bowel surgery). Fibrinous adhesions usually resolve with no lasting effect after 6–8 weeks. A proportion of patients have an apparent underlying predisposition for these adhesions to heal by organization and fibrosis, with the result that much more dense fibrotic adhesions form between mesothelial layers. In the abdomen these bands of tissue may form between or over loops of small bowel in particular. In some cases, despite the presence of fibrous adhesions, there are no clinical symptoms. In others they may lead to ‘kinking’ or compression of small-bowel loops, causing obstruction and even infarction of the blood supply. Such complications may occur shortly after the adhesions form, within months of surgery, or many years after.

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Factors related to the formation of adhesions include: unknown patient genetic factors; presence of infection or gross inflammation at the time of surgery; use of powdered (starch) surgical gloves; use of biological suture materials (which provoke a strong tissue reaction); cooling of intestinal loops.

• • • • •

Management of adhesional obstruction (see also Chapters 15, 31)

The principles of management of adhesional obstruction are the same as for any other cause, namely: maintenance of fluid and electrolyte balance; rest of the gastrointestinal tract; prevention of complications; surgery when appropriate. The diagnosis of obstruction caused by adhesions is one of exclusion and even in patients with previous abdominal surgery, other causes of mechanical obstruction should be considered before assuming adhesions as the cause. Surgery for adhesions should generally be avoided, since in those patients prone to their formation, adhesions are likely following any operation for their division and the surgery may be prolonged and fraught with complications. Surgery is generally indicated only where complications have developed (e.g. intestinal ischaemia is suspected) or the obstruction is failing to resolve with a reasonable period of conservative management.

• • • •

Key points

• • •

Oligo-anuria is an acute surgical emergency: work methodically to identify the cause and treat it promptly Confusion should never be treated by sedatives until all major causes have been excluded In postoperative infections, target antibiotics to the cause whenever possible and use broad-spectrum treatment as a last resort Suspect occult hypoxia in patients following abdominal and thoracic surgery and treat them with simple measures aimed at restoring normal physiology Suspected peritonitis due to anastomotic leak is a surgical emergency and requires urgent resuscitation and treatment Most anastomotic leaks that result in intra-abdominal abscesses can be managed non-operatively Cannula-related sepsis is a very common complication that is potentially serious and, occasionally, life-threatening Postoperative obstruction is usually paralytic and rarely needs surgery Beware electrolyte imbalances in patients with nasogastric tubes or intestinal stomas All patients on a surgical ward are at risk of deep vein thrombosis

• • • • • • •

Common surgical complications at a glance Definitions Wound dehiscence: a process where the deep layers of an abdominal wound burst and viscera protrude on to the abdomen Paralytic (adynamic ileus): temporary failure of gut peristalsis, resulting in failure of onward movement of bowel content, vomiting, distension and absent bowel sounds Adhesions: Abnormal fibrous bands found in the pleuroperitoneal cavities that develop following an inflammatory insult, resulting in an abnormal connection between bodily parts that are normally separate Anastomotic leak • Leakage from any anastomosis (intestinal, biliary or urinary) is rare but potentially life-threatening • Usually occurs 4 –14 days postoperatively

Presentations • Peritonitis: resuscitate and reoperate • Intra-abdominal abscess: drain abscess either radiologically or surgically • Enteric fistula: control; may close spontaneously Wound problems (wound infection, see Chapter 7) Superficial wound infection • Common • Treatment: drainage (open the wound), culture the pus and give antibiotics Wound dehiscence • Uncommon • Treatment: reassure patient, occlusive dressing, resuture wound Wound (incisional) hernia • Late failure of wound • May need surgical repair

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Other infections Cannula-related sepsis • Careful aseptic technique for insertion of cannulae • Change infusions only as necessary • Re-site cannulae regularly

Factors related to adhesion formation • Genetic (unknown) • Infection/inflammation at time of surgery • Use of powdered (starch) surgical gloves • Use of biological suture materials

Urinary infection • Only use catheters when strictly necessary • Aseptic technique for insertion • Remove at earliest opportunity

Management Non-operative • ‘Rest’ gastrointestinal tract: nasogastric tube • Maintain fluid and electrolyte balance • Exclude other causes of obstruction

Intestinal obstruction Mechanical • Uncommon in early postoperative period • Usually due to adhesions and appears during first 2 years after surgery Paralytic (adynamic) ileus Occurs immediately postoperatively Predisposing factors • Bowel handling • Bowel operations • Anaesthetic agents (epidural drugs) • Analgesics (opiates) • Electrolyte imbalance (low K+, Ca2+, Mg2+) • Endocrine abnormality (thyroid disease) • Infection shock injury Management • Maintain fluid and electrolyte balance • ‘Rest’ gastrointestinal tract: nil-by-mouth or nasogastric tube • Discontinue potentially exacerbating drugs • If prolonged, give parenteral nutrition Adhesions • Any inflammatory process in the pleuroperitoneal cavity causes a fibrinous membrane to develop that sticks two mesothelial surfaces together (e.g. pleura to lung, peritoneum to bowel, bowel to bowel) • They are common and develop after any surgery to the pleuroperitoneal cavity. In some people they develop into dense fibrous bands and may lead to obstruction or gangrene by ensnaring the bowel • Problems occur in about 10% of patients after abdominal surgery • Adhesions are the most common cause of intestinal obstruction

Evidence-based medicine Royal College of Surgeons of England Care of the Critically Ill Surgical Patient, course manual.

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Surgery (avoid if possible as it creates more adhesions) • If obstruction not resolving after a few days • If peritonism develops Fluid and electrolyte imbalance (see also Chapter 15) Causes • Inappropriate (too much or too little) administration of water, Na+ or K+ • Excessive losses of electrolytes from nasogastric tubes, high intestinal fistula, diuretics • Renal disease Consequences • Nausea and vomiting • Paralytic ileus • Metabolic acidosis or alkalosis • Confusion • Convulsions Thromboembolic disease (see Chapter 29) Deep vein thrombosis • May develop in up to 20% of patients undergoing major surgery and in hospital for > 7 days • Risk highest in women on contraceptive pill and patients having pelvic surgery • Prophylaxis mandatory for patients undergoing major surgery (see Chapter 5) • Full anticoagulation with low-molecular-weight heparin initially and warfarin for 6 months Pulmonary embolism • Chest pain, dyspnoea, hypoxia, confusion, unexplained tachycardia or pyrexia • Full anticoagulation with low-molecular-weight heparin initially and warfarin for 6 months

http://www.rcoa.ac.uk/publications.htm of Anaesthetists audit publications

Royal College

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Rehabilitation

Introduction, 120

Principles of rehabilitation, 120

02 Must know Must do Must know Principles underlying rehabilitation of patients after recovery from disease, operation or injury Must do Attend physiotherapy department Attend prosthetic/orthotic department Talk with stoma therapist Attend multidisciplinary meeting concerned with rehabilitation/continued care of a patient known to you

Introduction Rehabilitation is the process whereby a patient is actively helped to return to a maximum potential lifestyle a physical, mental and social a after illness, accident or surgery. All patients undergoing surgery or suffering illness need some form of rehabilitation. The vast majority conduct this process themselves with no specific help from the medical/surgical/paramedical team, e.g. a young car mechanic following appendicectomy for acute appendicitis will gradually reintroduce himself to work and his leisure activities. For other patients, the need for rehabilitation is more obvious and is critical for their ability to achieve an optimum level of ‘lifestyle’. The work of rehabilitation is carried out by all members of the medical, nursing and paramedical team and may include specialists in both the hospital and the community. Initially rehabilitation starts in hospital but rapidly progresses to rehabilitation in the community. Ultimately, rehabilitation takes place in an environment most suited to the patient, preferably at home. Rehabilitation may be carried out by individual medical or surgical specialties. However, specialists in rehabilitation medicine provide a professional and cost-effective approach and may save time and effort through their expertise. 120

Specific problems of rehabilitation, 122

Principles of rehabilitation Rehabilitation should begin as soon as possible and potential disabilities should be anticipated. Disability may be either: primary, i.e. directly due to the disease or injury (e.g. direct trauma, amputation, stroke); or secondary, i.e. as a complication of the disease or injury (e.g. muscle atrophy, joint contractures, decubitus ulcers, depression). For patients undergoing elective treatment, planning for the potential rehabilitation needs of the patient should ideally form part of the pretreatment assessment so that the correct specialists can be involved in the patient’s care as soon as appropriate. Rehabilitation is a team effort and often demands the services and enthusiasm of many groups and individuals to be effective (Fig. 10.1). The aim of the team must be to prepare a plan of action culminating not in the patient’s discharge from hospital but in the restoration of as normal a lifestyle as practical. However, rehabilitation should not be overly ambitious and limitations set by disability must be appreciated. The setting of unrealistic and overoptimistic goals is as counterproductive as setting no goals at all.

• •

Physiotherapy Physiotherapists use a variety of techniques to prevent patients developing complications, to relieve pain and to enhance physical activity. These techniques include the following. Chest physiotherapy: deep-breathing exercises, incentive spirometry, coughing, chest percussion. Muscle exercise and re-education: active and passive exercises, stretching, joint movements. Electrotherapy may be used to stimulate denervated muscles. Walking: teaching patients to stand and walk, initially with support (physiotherapists, parallel bars, walker frames, crutches, stick) and then without support, progressing to walking up stairs.

• • •

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Dieticians Doctors

Nurses

Stoma therapists

Prosthetists

Occupational therapists

Psychologists

The Patient

Patient's family

Social workers

District nurses

Speech therapists

General physiotherapists

Psychiatrists Specialist physiotherapists (e.g. hand)

General practitioners

Figure 10.1 Contributors to the rehabilitation process.

•

• •

Pain relief: both heat (superficial and deep) and cold are used to relieve pain. Transcutaneous electrical nerve stimulation (TENS) is also commonly used in the management of chronic pain. Massage may be combined with heat to reduce oedema and relax muscle tension. Ultraviolet therapy: some decubitus ulcers (pressure sores) respond favourably to ultraviolet light. Hydrotherapy: helps to relieve pain, reduce muscle spasm and induce relaxation.

provide splints and other prostheses to facilitate independent daily living; give emotional and motivational support to patients during rehabilitation.

Occupational therapy

• •

The aims of occupational therapy are to: assist in increasing the physical rehabilitation of the patient; assess and maximize the patient’s ability to perform daily activities, including self-care, mobility and communication, known as activities of daily living (ADL);

• •

Social services The social services should be contacted as early as possible so that the particular care required for a given patient will be available when the patient is ready for discharge from hospital. The social worker will: inform the patient what services are available; evaluate which services are appropriate for a patient, e.g. whether the patient should go home and be provided with meals on wheels, home help and district nursing or be offered supervised accommodation; coordinate the provision of services for the patient; and maximize financial benefits for the patient.

• •

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Rehabilitation in general at a glance Definition Rehabilitation: the process whereby a patient is actively helped to return to a maximum potential lifestyle (physical, mental and social) after illness, accident or surgery

General points • All patients undergoing surgery or suffering illness need some form of rehabilitation • Rehabilitation is carried out by doctors, nurses and paramedics in both the hospital and the community • Rehabilitation takes place in an environment most suited to the patient, preferably at home • Specialists in rehabilitation medicine provide a professional and cost-effective approach and may save time and effort through their expertise Principles of rehabilitation • Planning for the potential rehabilitation needs to start early, preferably before treatment • Potential disabilities should be anticipated: (a) Primary disability: due to the disease or injury (b) Secondary disability: due to a complication of the disease or injury • Rehabilitation is a team effort • Prepare a plan of action culminating in the restoration to as normal a lifestyle as practical • Setting unrealistic or overoptimistic goals is as counterproductive as setting no goals at all

Specific problems of rehabilitation Musculoskeletal disorders Rehabilitation of the musculoskeletal system may be viewed as the recovery from trauma caused by chance accident or surgery. In both cases the needs of the whole patient and family must be catered for and must, if possible, span the whole of the subject’s lifestyle, including pastimes and work.

Physiotherapy • Prevents complications • Relieves pain • Enhances physical activity Techniques • Chest physiotherapy • Muscle exercise and re-education • Electrotherapy to stimulate denervated muscles • Standing and walking • Pain relief: heat, cold, electrical stimulation (TENS), massage • Ultraviolet light (for some decubitus ulcers) • Hydrotherapy Occupational therapy • Assist in increasing the physical rehabilitation of the patient • Assess and maximize the patient’s ability to perform ADL • Provide splints and other prostheses to facilitate independent daily living • Give emotional and motivational support to patients during rehabilitation Social services • Inform the patient what services are available • Evaluate which services will be appropriate for the patient • Coordinate the provision of services for the patient • Maximize financial benefits for the patient

Generally, patients are taught simple exercises that they can perform at home, with supervision at outpatient follow-up. While in hospital an attitude of progress towards recovery must be engendered from the first day, otherwise regression to a dependent state rapidly becomes established. Specialist physiotherapy is particularly important in areas such as hand and upper limb injury/surgery, as loss of function is both rapid and debilitating but can be reversed by appropriate therapy.

Multiple injuries Isolated injuries Whatever the cause (trauma, musculoskeletal disease or surgery), the principles of isolated musculoskeletal rehabilitation are the same: pain relief to allow early mobilization; active and passive physiotherapy to preserve/regain range of movement; occupational therapy to encourage adaptation of function.

• • •

Multiple injuries are more problematic and often associated with head injury so that rehabilitation needs to be instituted as soon as medical and surgical management permits. In these cases commitment of large resources may be required to ensure optimal recovery. For example, following a head injury that may have involved many months in bed, vigorous physiotherapy will be required to re-establish motor function, speech therapy may be required to re-establish the patient’s ability to speak and

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occupational therapy to help the patient back to independent living. Careful psychological examination is also essential because the presence of psychological disturbance is often underestimated unless a full assessment is performed. The long-term effects of head injury can be one of the most difficult areas in rehabilitation as behaviour and personality changes may make reintegration into the community very difficult.

Gastrointestinal disorders Intestinal stomas Patients in whom stomas have been created have specific concerns and needs and require expert advice concerning the management of the stoma. Patients are often concerned about leakage, odour and, in the case of colostomies, noisy expulsion of gas. Ileostomies may also be associated with skin irritation and preventive measures need to be taken to avoid dermatitis. Particularly for young patients, the psychosexual implications of even a temporary stoma are extremely important and should be addressed with care. Meeting other young people with a stoma may be an excellent way of allaying fears about their ‘body image’ and self-esteem. If the stoma is created electively, then the skin can be marked preoperatively and the stoma placed in the optimal site for the patient. Postoperatively, the patient should be encouraged to take charge of stoma care as soon as practicable. Most hospitals now have a stoma nurse or therapist dedicated to dealing with patients who have stomas. A wide variety of appliances are now available that attach securely to the abdominal wall, do not leak and do not allow any malodorous gas to escape (Fig. 10.2). The stoma therapist will help the patient choose the most suitable appliance and give dietary advice. A number of ‘ostomy’ support groups also exist that provide assistance to patients with stomas. Most patients learn to manage their stoma very efficiently and live ‘normal’ lives.

Neurological disorders Following head injury, stroke, paraplegia or extensive neurological deficits, patients require intensive rehabilitation to allow them to achieve their maximum potential. They often require extensive early and late rehabilitation, such as: chest care (to avoid infection); protection of pressure areas; assistance with bladder and bowel function; assistance with or modification of feeding; assistance with mobilization (including active and passive physiotherapy); speech therapy.

• • • • • •

Figure 10.2 Range of stoma appliances available.

Patients and their relatives also need constant support and encouragement.

Cardiovascular disorders Peripheral arterial disease Rehabilitation for peripheral arterial disease and its surgery begins almost immediately after diagnosis. Common areas where rehabilitation can be of considerable importance include: provision of mobility aids; alteration of home layout to avoid the necessity of climbing many flights of stairs repeatedly; exercise classes and exercise programmes; smoking cessation programmes. Following reconstructive surgery or surgery for arterial ulcers, early physiotherapy and mobilization may be undertaken in hospital in order to maximize the benefit of increased exercise capacity.

• • • •

Venous disease One area where early rehabilitation and physiotherapy can be of great assistance in minimizing the effects of disease is following deep vein thrombosis (DVT), particularly extensive iliofemoral thrombosis. Active mobilization and physiotherapy can reduce the effects of leg swelling and stiffness associated with extensive DVT and may help reduce the risk of development of long-term postphlebitic limb syndrome.

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Part 2 Perioperative Care

Transplantation

Amputation

Transplant recipients have to come to terms with a lifelong commitment to continued medical care and intervention. Early after transplantation the problems of the continuing medical care and drug therapy may be balanced by the euphoria of a successful transplant, and psychological support of the patient may need to include balancing unrealistic expectations of future progress. Encouraging an independent lifestyle is important, particularly taking responsibility for ongoing drug treatment and medical follow-up. Long-term rehabilitation may include support for the patient during reintroduction to work. Psychological rehabilitation may also be necessary for those patients in whom the transplant fails. Profound grief, anger and resentment may occur that can interfere with the patient’s recovery.

Following amputation, patients have to cope with very specific problems; this group of patients presents an ideal model to illustrate all aspects of rehabilitation. The trauma of the surgery has profound psychological effects on the individual concerned. For the traumatic amputee there has been no warning or preparation prior to limb loss. The majority of these patients are young and following the accident there may be considerable anguish, disbelief and despair at the amputation and the perceived problems that may follow. The initial postoperative period requires considerable care and understanding and should be handled by experienced staff. Full explanations must include realistic consideration of likely outcome and description of the rehabilitation process that is to follow. In contrast, the elderly vascular amputee has usually had a period of pain and suffering prior to surgery. The patient will have often chosen amputation as a means of relieving the severe pain of an ischaemic limb. Counselling patients preoperatively is extremely valuable and should wherever possible be undertaken by experienced staff. In addition, relatives need to be included in these discussions as their understanding and reassurance can help the patient overcome the natural fear of the future. The expertise of the rehabilitation team and the facilities at its disposal can affect the ultimate success of the rehabilitation process. The rehabilitation team caring for the amputee (of whatever age) must be a closely integrated group of professionals who work together. Nursing staff: provide day-to-day care of the patient, with particular attention to pressure areas and care of the stump. Physiotherapist: provides assessment of early mobilization of the patient: (a) chest physiotherapy to avoid chest infections; (b) early mobility to avoid DVT, including use of early walking aids; (c) mobility with a prosthesis. Prosthetist: manufacture, fitting and maintenance of artificial limbs. Occupational therapist: teaching aids to daily living skills and assessment of home circumstances, including domiciliary visits at home with the patient. Social workers: arrange domiciliary services (e.g. home help, meals-on-wheels) and may help with financial matters. General practitioner: continuing care once discharge has occurred. District nurses: nursing in a home situation. The whole team should meet regularly to discuss the patient’s progress and decide on realistic goals that the patient can achieve. Patients should be involved in the discussion so that they are aware of what is to be achieved.

Malignancy Rehabilitation following surgery for malignancy may involve many aspects.

Psychological A diagnosis of malignancy often precipitates a profound reaction that can be a mixture of grief, anger, resentment and helplessness. After the initial diagnosis and medical problems have been addressed, this reaction can greatly affect the patient’s ability to recover from the effects of treatment and achieve a ‘normal’ lifestyle. Support from nurses, specialist nurses, general practitioners, palliative care specialists and psychologists may all be necessary to help the patient come to terms with the diagnosis.

Physical Depending on the site of the primary or secondary tumour(s) and the nature of any surgery performed, there may be many physical limitations for which rehabilitation is important. Feeding and nutrition, e.g. following oesophageal or gastric surgery the patient requires the advice of dieticians, speech therapists, stoma therapists. Mobility and ADL, e.g. general debility and limitations imposed by systemic malignancy requiring alterations to the home environment, home aids, social support. Chest physiotherapy: following pulmonary or intrathoracic oesophageal surgery. Speech therapy: following laryngeal or upper oesophageal surgery. Stoma therapy: following some types of surgery for abdominal malignancy.

• • • • •

• • • • • • •

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Family members also need to be kept aware of progress and of problems as they arise. As the rehabilitation process proceeds, the goals may need to be modified in the light of progress.

Work In the case of a young amputee, the return to work can be an important issue. The social worker and occupational therapist can give initial guidelines and discussion with the employer can be helpful. In a situation where return to the former work is not possible, the patient is referred to the disablement employment adviser, who has a statutory responsibility to advise on retraining programmes and potential employers. Local charitable organizations may also offer employment advice.

Social reintegration The amputee may initially feel isolated and handicapped by surgery. Family and friends play a vital role in encour-

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aging the patient to reintegrate. A range of clubs and societies (e.g. National Association for Limbless Disabled) exist to help amputees. To encourage this reintegration, rapid discharge home is important but should only be undertaken once prosthetic fitting has been completed and the occupational therapist has assessed the patient’s home. If discharged too early, demoralization of both patients and relatives can reduce the ability to achieve full potential.

Follow-up The patient needs to remain in lifelong contact with a limb-fitting centre for the maintenance and provision of prostheses. Regular reviews are initially necessary as the stump matures and the patient adapts to the new situation. The review clinics act as both a stump and prosthetic review but also as an opportunity for open discussion on how the patient is managing at home. In this way, shortfalls in service provision and the identification of areas in which help can be provided are assessed.

Specific problems of rehabilitation at a glance Musculoskeletal disorders Isolated injuries • Pain relief to allow early mobilization • Active and passive physiotherapy to preserve/regain range of movement • Occupational therapy to encourage adaptation of function Multiple injuries • Rehabilitation needs to be instituted as soon as medical and surgical management permits • Commitment of large resources may be required to ensure optimal recovery Gastrointestinal disorders Intestinal stomas Patient concerns • Leakage • Odour • Noisy expulsion of gas • Skin irritation • Psychosexual concerns • Body image issues Management • Create stoma in optimal site • Patient should be encouraged to take charge of stoma care

• Stoma therapist • Choose the most suitable appliance • Give dietary advice • ‘Ostomy’ support groups Neurological disorders • Chest care (to avoid infection) • Protection of pressure areas • Assistance with bladder and bowel function • Assistance with or modification of feeding • Assistance with mobilization (including active and passive physiotherapy) • Speech therapy • Constant support and encouragement for patient and family Cardiovascular disorders Peripheral arterial disease • Smoking cessation programmes • Exercise classes and exercise programmes • Mobility aids/alteration of home layout Venous disease • Active mobilization and physiotherapy after DVT • Bandaging, mobilization and active ankle exercises with venous ulcers

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Amputation Traumatic amputee • No warning prior to limb loss • Young patients • Anguish, disbelief and despair Vascular amputee • Pain and suffering prior to amputation • Elderly patients • Amputation may be a great relief

Malignancy Psychological • Grief, anger, resentment and helplessness

Physical • Feeding and nutrition • Chest physiotherapy • Speech therapy • Stoma therapy • Mobility and ADL Transplantation • Psychological support: (a) Deal with unrealistic expectations of future progress (b) Graft failure may lead to grief, anger and resentment • Encourage an independent lifestyle • Encourage responsibility for continuing drug treatment and medical follow-up

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Hypoxic States and Airway Obstruction Introduction, 127 Causes of acute hypoxia, 127 Clinical features of hypoxia, 129

Principles of treatment of the hypoxic patient, 129 Oxygen therapy, 131

Mechanical ventilation, 132 Pulse oximetry, 133

Table 11.1 Causes of hypoxia.

Must know Must do Must know Cause and management of acute hypoxia Immediate and supportive management of the hypoxic patient Clinical features and diagnosis of acute hypoxia Principles and practicalities of airway control Oxygen therapy Indications for mechanical ventilation Must do Visit the intensive care unit to learn about types of ventilatory support Become familiar with the various oxygen masks, humidifiers, and pulse oximetry equipment Observe endotracheal intubation Observe percutaneous tracheostomy Assist/observe patients undergoing CPR

Introduction The general term for lack of oxygen is hypoxia while the specific term for lack of oxygen in the arterial blood is hypoxaemia. Hypoxia may be acute or chronic. Acute hypoxia is immediately life-threatening if left uncorrected for more than a few minutes. Acute hypoxia causes cardiac arrest and severe cerebral impairment, leading to brain death or gross permanent mental disability should the patient survive. Thus acute hypoxia is seldom seen in isolation and usually requires cardiopulmonary resuscitation (CPR). Chronic hypoxia is seen in chronic obstructive or restrictive lung disease (see also Chapter 38). The causes of hypoxia are listed in Table 11.1.

Hypoxic hypoxia Decreased PO2 in inspired air (high altitude) Hypoventilation Depression of respiratory centre (head injuries, opiates, cerebrovascular accident) Shallow respirations due to pain (after chest or upper abdominal surgery, pleurisy) Airway obstruction (foreign body, aspiration) Increased airway resistance (asthma, emphysema) Large pneumothorax (trauma, rupture of emphysematous bulla) Alveolar–capillary diffusion block Decreased alveolar membrane area (pneumonia, pulmonary congestion) Fibrosis of alveolar or pulmonary capillary walls (pulmonary fibrosis) Abnormal ventilation–perfusion ratio Perfusion of unventilated alveoli (atelectasis) Ventilation of underperfused alveoli (pulmonary embolism) Shunting of venous blood into arterial circulation (cyanotic congenital heart disease) Anaemic hypoxia Anaemias (hypoxia is worse on exercise) Carbon monoxide poisoning (binds to haemoglobin to produce carboxyhaemoglobin, which cannot release oxygen) Stagnant hypoxia During shock, slow circulation to the tissues produces hypoxia and damage (e.g. renal failure) Histotoxic hypoxia Inhibition of the cytochrome oxidase system in the tissues (cyanide poisoning)

Impaired level of consciousness

Causes of acute hypoxia The two most important causes of sudden hypoxia are impaired level of consciousness and aspiration.

Impaired level of consciousness from any cause (e.g. head injury, sedation, cerebrovascular accident) can be accompanied by depression of the respiratory centre 127

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Mandible

Uvula Pharynx Epiglottis

Genioglossus muscle (a)

(diminished ventilatory drive). Loss of consciousness is also accompanied by loss of the protective gag and cough reflexes such that aspiration of foreign material into the bronchopulmonary tree is likely. In addition, the tongue musculature is relaxed and the neck muscles fail to lift the base of the tongue from the posterior pharyngeal wall. If the patient’s head is in the flexed or mid-position, acute obstruction of the upper airway supervenes. Hypopharyngeal obstruction by this mechanism is the commonest cause of hypoxia encountered in clinical practice. This type of upper-airway obstruction is commonly seen after head injuries with loss of consciousness (Fig. 11.1).

Aspiration Aspiration of blood, vomit or gastric juice will result in severe laryngospasm in the stuporous or lightly comatose patient. In addition, and irrespective of the degree of coma, it causes lower-airway obstruction by a combination of bronchospasm, excessive bronchial secretions and mucosal oedema. If the aspirated fluid is irritant (e.g. gastric juice), it often progresses to pulmonary oedema and acute respiratory distress syndrome (ARDS; see Fig. 38.21). Aspiration syndromes are discussed fully in Chapter 38.

03 (b)

Acute cardiorespiratory disease

•

Community-acquired pneumonia and hospitalacquired/ventilator-associated pneumonia (see Chapter 38). Imbalance between alveolar ventilation and perfusion, i.e. there is a mismatch of blood and airflow to the lungs (e.g. pulmonary collapse and pulmonary embolism). Right-to-left shunting (blood returns to the left heart without being oxygenated). Impairment of gaseous diffusion due to thickening of the alveolar–capillary interface between blood and inspired air. Defective extrapulmonary ventilation due to diminished central (cerebral) ventilatory drive or disease/ trauma limiting effective chest wall and diaphragmatic movement. Important medical disorders accompanied by hypoxaemia are heart failure, severe lobar pneumonia and status asthmaticus.

• • •

(c)

Figure 11.1 Upper-airway obstruction. (a) The tongue is normally lifted forwards in the mouth by the action of the genioglossi muscles, which are attached to the inner surface of the symphysis of the mandible. (b) If the patient is unconscious or has a fracture of the mandible, the tongue may fall back into the pharynx and cause airway obstruction. Flexion of the head causes more narrowing of the pharynx, exacerbating the situation. (c) The triple-airway manoeuvre is used to correct the resulting airway obstruction: the neck is extended, the mandible is displaced forwards and the mouth opened.

• •

Traumatic chest injuries These include certain types of pneumothorax and injuries to the pulmonary parenchyma (see Chapter 38).

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Facial fractures Occlusion of the laryngeal orifice by the prolapsed tongue is particularly prone to occur in patients with fractures of the body of the mandible. The upper airway may also be compromised directly by fractures of the middle third of the face, when the maxillae are driven backwards over the laryngeal orifice.

Extrinsic upper-airway compression Thyroid disease Extrinsic compression of the upper airway in patients with thyroid disease may occur in several ways. Bleeding inside a thyroid nodule may result in rapid enlargement with compression of the trachea, especially if it occurs in a retrosternal thyroid, as the rigid boundary of the thoracic inlet cannot accommodate the sudden increase in volume. Tracheal compression is also encountered in advanced thyroid cancer (especially of the anaplastic variety), in the late stages of Reidel’s thyroiditis (due to fibrous contracture) and after thyroidectomy (due to postoperative bleeding with clot compression underneath the strap muscles). If, as rarely happens nowadays, both recurrent laryngeal nerves are damaged during thyroid surgery, severe asphyxia is encountered when the endotracheal tube is removed because the paralysed vocal cords become opposed in the midline and occlude the laryngeal orifice.

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raclavicular spaces. Stridor is an inspiratory whooping sound that indicates partial obstruction of the trachea (intrinsic or extrinsic). Apnoea (defined as cessation of breathing in the expiratory position) is the most serious clinical situation and demands immediate active intervention (see below).

Physical examination 1 Examine the patient and ensure that there is no obstruction to the airway. 2 Determine the presence or absence of pulse (femoral or carotid). If the patient is apnoeic and there is no pulse, full CPR should be instituted immediately (see below). 3 If spontaneous respiration is present, the essential physical examination is assessment of the respiratory system (see Chapter11). Briefly, this should include: (a) inspection of the chest wall: for injuries, expansion and paradoxical movement, i.e. chest wall moves in with inspiration and out with expiration; (b) auscultation of both lung fields: for air entry to both lungs, abnormal breath sounds (crepitations, bronchial breathing); (c) percussion: if air entry is absent, this will determine whether the affected hemithorax is hyperresonant (air in pleural cavity), dull (pneumonic consolidation) or stony dull (fluid).

Investigations Malignancy Extrinsic compression from secondary tumour deposits or lymphomas in the mediastinum is usually part of the superior vena cava compression syndrome. In addition to the respiratory difficulties, there is marked congestion of the upper half of the body. When due to lymphomas, rapid relief is obtained by appropriate urgent therapy with chemotherapy and radiotherapy. Endovascular stents are also used to relieve superior vena cava compression syndrome.

Clinical features of hypoxia Symptoms If the patient is unconscious, the only reliable clinical manifestations of hypoxia are central cyanosis, abnormal respiration (rapid, slow, apnoea, gasping) and hypotension. Complete airway obstruction leads to asphyxia and cardiac arrest within 5–10 min. Incomplete airway obstruction in the unconscious patient is noisy (rattling, stridor). The conscious hypoxic patient is cyanosed, anxious, restless, sweating and often confused. Accessory muscles of respiration are recruited, with indrawing of the sup-

The most important immediate investigation is blood gas analysis of a femoral arterial blood sample. With respiratory failure the blood gases will indicate respiratory acidosis, but if there has been significant anoxia to the tissues (e.g. cardiac arrest) there will also be a metabolic acidosis due to accumulation of lactic acid (see Chapter 13). A portable chest radiograph should also be obtained. It is imperative that the hypoxic patient is never sent to the radiological department for the chest X-ray. Other investigations such as portable electrocardiography (ECG) are needed in the event of cardiac arrest.

Principles of treatment of the hypoxic patient The principles underlying basic life support in the immediate management of the acutely hypoxic patient are: A airway control; B breathing support; C circulatory support; D determine the cause. Once the critical situation has been controlled, the underlying cause must be treated.

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sequence is to tilt the patient’s head backwards and inflate the lung by mouth-to-mouth ventilation. If this meets with an obstruction, the patient’s mouth is closed and mouth-to-nose ventilation is tried. After an airway has been introduced one can change to mouth-to-airway ventilation.

Self-refilling bag-valve unit (Fig. 11.4)

Figure 11.2 Oropharyngeal and nasopharyngeal airways.

Airway control

In the non-intubated patient, experience is required for the efficient use of this equipment with a mask. Once the patient has been intubated, the bag-valve unit is particularly effective for maintaining oxygenation. It permits respiration during both spontaneous and artificial ventilation. The unit consists of a self-refilling bag with an inlet valve to which an oxygen cylinder is attached, and has a non-rebreathing valve at the mask or endotracheal tube.

The first measure is to correct hypopharyngeal obstruction. This is achieved by the triple-airway manoeuvre: 1 extension of the neck; 2 forwards displacement of the mandible; 3 opening the mouth (see Fig. 11.1c). Next, any secretions or fluid (vomit, blood) in the mouth or pharynx are removed by suction, intraoral foreign bodies including dentures are removed, and a nasopharyngeal or oropharyngeal airway (Fig. 11.2) is inserted if the patient is unconscious. If the upper airway is blocked, a laryngoscopic examination is performed to clear the pharynx and rapidly assess the situation. Then an endotracheal tube is passed or, if this fails, a cricothyroidotomy or minitracheostomy is performed (Fig. 11.3). Usually senior staff are available for this contingency. The Heimlich manoeuvre is a first-aid procedure used to relieve upper-airway obstruction caused classically by inhalation of a bolus of food, the so-called café coronary syndrome. Standing behind the patient, place your arms around the patient’s upper abdomen and, clasping your hands together, firmly force upwards under the ribs. In this way the air in the chest is compressed and, with luck, the foreign body will be expelled from the upper airway.

Circulatory support

Breathing support

Having resuscitated the patient, the specific condition that led to the hypoxic arrest must be treated, e.g. correction of maxillary fractures, pharmacological treatment of heart failure or asthma, antibiotics for pneumonia, etc. If the apnoea is thought to result from opioid-induced depression of the respiratory centre, naloxone hydrochloride is administered intravenously. In patients who aspirate gastrointestinal contents, acid damage to the lung with the development of ARDS is likely (see Chapter 38). These patients are given antibiotics and vigorous physiotherapy. If ARDS develops, the patient will require ventilation.

Mouth-to-mouth breathing support Expired air contains 16–18% oxygen and, when delivered adequately to the apnoeic patient via mouth-to-mouth or mouth-to-nose ventilation, achieves an arterial Po2 (Pao2) of 10 kPa or 75 mmHg (normal 13.3 kPa or 100 mmHg) if the patient’s lungs are normal. Mouth-to-mouth breathing is commenced immediately and continued until oxygen delivery systems can be brought to the scene. The practical

Circulatory support involves external cardiac massage for cardiac arrest and the insertion of adequate intravenous lines for volume replacement and drug administration. For external cardiac massage the patient is placed supine on a hard surface. The aim is to compress the heart between the sternum and the spine, thereby forcing blood from the heart and producing a circulation. It is important to feel the femoral or carotid pulse during CPR to ensure that an adequate circulation is being produced. External cardiac massage is performed by placing the heel of one hand, with the other hand on top, over the lower half of the sternum. With the arms extended the sternum is pressed down and then released at a rate of about 60 times per minute. Excessive force should be avoided, as there is a risk of fracturing the ribs. External cardiac massage must be coordinated with ventilation, with one respiration being given for every five compressions. CPR must not be interrupted for more than 10 s. An algorithm for the use of drugs and defibrillation during CPR is given in Fig. 11.5.

Correction of underlying abnormality

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Thyroid cartilage Cricoid cartilage Sandbag

Tracheal rings (c)

(a)

(b)

Figure 11.3 Minitracheostomy. (a) The head is extended and a small sandbag placed between the shoulder blades. The cricothyroid membrane is identified between the thyroid and cricoid cartilages. The overlying skin and cricothyroid membrane are infiltrated with local anaesthetic and a few drops of anaesthetic are flushed into the trachea. A transverse stab incision is made through the skin and subcutaneous tissue and the cricothyroid membrane is punctured. (b) An introducer is then passed through the wound into the trachea and over this the minitracheostomy tube (internal diameter 4 mm) is passed. The introducer is removed and the minitracheostomy tube is secured. A minitracheostomy allows for very effective aspiration of sputum in postoperative patients and may obviate the need for intubation and ventilation. (c) The equipment required to perform a minitracheostomy.

Oxygen therapy Oxygen is often administered by mask to patients who are hypoxic but breathing spontaneously. A number of different types of mask are available. Oxygen is usually administered via masks that do not deliver a constant known percentage of oxygen to the patient; this is due to the variable dilution of oxygen in the mask by inspired air. Examples of these types of mask are the Mary Catteral (MC) and the Hudson, which administer oxygen concentrations ranging from 35 to 60%. Unless there is additional lung pathology, 35% oxygen is adequate for ensuring normal Pao2 and oxygen toxicity is unlikely if less than 60% oxygen is administered. When more accurate oxygen administration is needed, a high-airflow oxygen enrichment (HAFLOE) mask such as the Ventimask is used (Fig. 11.6). Several models are available that are capable of administering oxygen in defined concentrations ranging from 24 to 60%. Accurate masks delivering low inspired oxygen concentrations are essential for patients with chronic lung

•

• •

Figure 11.4 Self-refilling bag-valve unit consists of a self-refilling bag with an inlet valve to which an oxygen cylinder is attached and a non-rebreathing valve at the mask or endotracheal tube.

disease who have lost normal ventilatory control and depend on moderate hypoxaemia to stimulate the respiratory centre. Such patients require enough oxygen to avoid serious hypoxaemia but not so much that the Pao2 reaches

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ECG

Electromechanical dissociation (EMD)

Ventricular fibrillation (VF)

VF cannot be excluded

Adrenaline 1 mg IV Give specific therapy for: Hypovolaemia Pneumothorax Cardiac tamponade Pulmonary embolism Consider calcium chloride 10 ml of 10% for: Hyperkalaemia Hypocalcaemia Calcium antagonists

Defibrillate 200 J Defibrillate 200 J Defibrillate 360 J Adrenaline 1 mg IV Defibrillate 360 J Lignocaine 100 mg IV Repeated defibrillations 360 J Consider: different paddle positions different defibrillator other antiarrhythmic drugs

Asystole

VF can be excluded

Adrenaline 1 mg IV Atropine 2 mg IV Consider pacing if p waves or any other electricity present

Continue CPR for 2 min after each drug and do not interrupt for more than 10 s except for defibrillation. If resuscitation is prolonged give 1 mg of adrenaline IV every 5 min and consider giving 50 mmol of 8.4% bicarbonate or according to blood gases

Figure 11.5 Algorithm for drug therapy and the use of defibrillation during cardiopulmonary resuscitation (CPR).

inspired air–oxygen mixture. In addition, ciliary activity is lost. This further exacerbates the retention of bronchial secretions. Humidification is best achieved by blower humidifiers of the heated water or ultrasonic type. When oxygen is administered in very high concentrations, oxygen toxicity may occur. In practice this is only seen in ventilated patients breathing > 60% oxygen for more than 24 h. The manifestations of oxygen toxicity are lung damage, blindness from retrolental fibroplasia (seen in premature babies) and epilepsy.

•

Mechanical ventilation Figure 11.6 Ventimask.

the normal range, as this would result in apnoea due to loss of the respiratory drive. When longer oxygen therapy is needed, humidification is necessary, especially in patients who are mouthbreathers or who have sputum retention. Otherwise, tracheal secretions become inspissated by the cold dry

•

The decision to perform tracheal intubation and ventilation is based on the clinical criteria shown in Table 11.2. Ventilatory support usually involves the application of intermittent positive pressure via an endotracheal tube or tracheostomy. Regular aspiration of secretions and physiotherapy is required. The underlying condition needs to be treated while the lung is supported. The endotracheal tube acts as a conduit for infection, and ventilator-associated pneumonia is a common problem.

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Table 11.2 Clinical indications for tracheal intubation and mechanical ventilation. SaO2 < 90% on > 60% oxygen Respiratory arrest or rate < 8/min Tachypnoea > 35/min Fatigue Agitation, confusion, refusal of oxygen mask Diminished conscious level Airway obstruction or impairment Rising PaCO2 Worsening respiratory acidosis

Types of mechanical ventilation Controlled mandatory ventilation (CMV): this is the •classic form of ventilation and the most basic. A preset tidal volume is delivered at a preset rate, regardless of any patient effort. The patient may ‘fight the ventilator’ and require deep sedation or muscle relaxation. Traditionally, tidal volumes of 10 mL/kg are used and patients are ventilated to normocarbia. There is now an increasing awareness of the potential of ventilator damage to the lung (barotrauma) in those patients with severe respiratory failure (see below). Synchronized intermittent mandatory ventilation (SIMV): a preset tidal volume is delivered synchronized with the patient’s respiratory effort. In the absence of effort, the breath is given after a set time lapse known as the SIMV period. Between mandatory breaths the patient is free to breathe through the ventilator circuit. Pressure support: when patient effort is detected, the machine applies a preset pressure to the airway thus assisting inspiration. As the lungs fill, the flow decreases and the inspiratory phase is terminated. In the absence of patient effort no ventilation occurs; thus it is only suitable for patients with adequate respiratory drive. Pressure-control ventilation: positive airway pressure is applied at a fixed rate. Patient effort is not required or sensed. The tidal volume depends on the resistance and compliance of the tubing, airways and lungs. Pressurecontrol ventilation is used in paediatric practice to compensate for variable leaks around uncuffed endotracheal tubes and in severe respiratory failure to limit barotrauma. Positive end-expiratory pressure (PEEP): this is an adjunct to positive pressure ventilation. The airway pressure is never allowed to fall to zero, thus splinting the alveoli open in expiration. This aids recruitment of lung and improves matching of ventilation and perfusion. This is useful in any condition where the alveoli are prone to collapse, as in ARDS. Excessive PEEP can reduce cardiac output and blood pressure by raising intrathoracic pressure.

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Continuous positive airways pressure (CPAP): this is •effectively PEEP without positive pressure ventilation. The patient breathes spontaneously without assistance, but gains the benefit of airway splinting. It is used either via an endotracheal tube when the patient has been weaned from ventilatory support but is not ready for extubation or through a tight-fitting facemask as an alternative or precursor to intubation and ventilation. When the patient recovers from respiratory failure, the functional inspired oxygen concentration (Fio2) can be reduced. When it is below 50%, weaning from ventilation can be considered. Any muscle relaxants are stopped and sedation is reduced to encourage respiratory effort. After a short period of ventilation it may be possible to rapidly convert to spontaneous breathing and extubate the patient, but usually a process of weaning is required. Respiratory support is gradually reduced until the patient is performing the work of breathing.

Pulse oximetry Pulse oximetry is a method for continuously measuring oxygen saturation. A small device placed on a digit estimates arterial oxygen saturation (Sao2) by calculating relative absorption of light from two light-emitting diodes at different wavelengths. The process is repeated many times a second, and the non-pulsatile (non-arterial) component subtracted. The Sao2 is displayed on a screen (Fig. 11.7).

• •

(a)

•

(b) Figure 11.7 Pulse oximeter: (a) a small device placed on a digit detects blood flow by transillumination and plethysmography; (b) oxygen saturation and pulse rate are displayed continuously on a small screen.

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Pulse oximetry is very useful in detecting hypoxic episodes during intubation and extubation, during the recovery period after surgery, especially in elderly and obese patients prone to hypoxaemia, and during gastrointestinal

endoscopy. However, movement, peripheral vasoconstriction and the presence of carboxyhaemoglobin can produce inaccurate readings.

Hypoxia at a glance Definitions Hypoxia: lack of oxygen (usually meaning lack of oxygen delivery to tissues or cells) Hypoxaemia: lack of oxygen in arterial blood Apnoea: cessation of breathing in expiration Common causes of hypoxia Acute hypoxia • Impaired level of consciousness • Aspiration

Postoperative causes • CNS depression, e.g. post anaesthesia • Airway obstruction, e.g. aspiration of blood or vomit • Poor ventilation, e.g. abdominal pain, mechanical disruption to ventilation • Loss of functioning lung, e.g. ventilation–perfusion mismatch (pulmonary embolism, pneumothorax, collapse/ consolidation) General causes • CNS depression, e.g. opiates, cerebrovascular accident, head injury • Airway obstruction, e.g. facial fractures, aspiration of blood or vomit, thyroid disease or cervical malignancy • Poor ventilation, e.g. pleural effusions, neuromuscular failure • Loss of functioning lung, e.g. ventilation–perfusion mismatch (pulmonary embolism, pneumothorax, collapse/consolidation), right-to-left pulmonary shunt, traumatic chest injury Key points • During the first 48 h following upper abdominal surgery, 80% of patients are hypoxic. Have a high index of suspicion and treat prophylactically • Adequate analgesia is more important than the sedative effects of opiates: ensure good analgesia in all postoperative patients • Ensure the dynamics of respiration are adequate: upright position, abdominal support, humidified oxygen • Acutely confused (elderly) patients on a surgical ward are hypoxic until proven otherwise • Pulse oximetry SaO2 values < 85% equate to PaO2 < 8 kPa and are unreliable in patients with poor peripheral perfusion

Clinical features In the unconscious patient • Central cyanosis • Abnormal respirations • Hypotension In the conscious patient • Central cyanosis • Anxiety, restlessness and confusion • Tachypnoea • Tachycardia, arrhythmias, atrial fibrillation (AF) and hypotension Investigations • Pulse oximetry: SaO2 guide to arterial oxygenation • Arterial blood gases (PCO2, PO2); pH and base excess for respiratory acidosis, metabolic acidosis later • Chest radiograph: collapse/pneumothorax/consolidation/ pleural effusion • ECG: atrial fibrillation Essential management Airway control • Triple-airway manoeuvre, suction secretions, clear oropharynx • Consider endotracheal intubation in CNS depression/ exhausted patients (rising PCO2), neuromuscular failure • Consider surgical airway (cricothyroidotomy/ minitracheostomy) in facial trauma, upper-airway obstruction Breathing • Position patient upright • Adequate analgesia • Supplemental oxygen: mask/bag/ventilation • Support respiratory physiology: physiotherapy, humidified gases, encourage coughing, bronchodilators Circulatory support • Maintain cardiac output • Ensure adequate fluid resuscitation Determine and treat the cause Oxygen therapy • Mask that delivers 30–60% oxygen diluted with inspired air (MC or Hudson mask) • HAFLOE delivers oxygen in defined concentrations from 24 to 60%

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• Humidification required for longer-term therapy • Beware of toxicity in ventilated patients breathing > 60% oxygen for 24 h Mechanical ventilation

• CMV: ventilator delivers a preset tidal volume at a preset rate regardless of what the patient does • SIMV: ventilator delivers a preset volume synchronous with the patient’s respiratory effort. If the patient does not attempt to breathe, a breath is given after a set time lapse • Pressure support ventilator applies a preset pressure to the airway, assisting patient-generated inspiration • Pressure-control ventilation: positive airway pressure is applied with a fixed rate regardless of patient. Used in

Evidence-based medicine Copeland, G.P., Jones, D. & Walters, M. (1991) POSSUM: a scoring system for surgical audit. Br J Surg 78, 356– 360.

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paediatrics to compensate for leaks around uncuffed endotracheal tubes • PEEP: ventilator never allows airway pressure to fall to zero, thus keeping the alveoli open in expiration • CPAP: this is PEEP without positive pressure ventilation. Airway pressure is maintained above zero but the patient breathes spontaneously. It is often given via a tight-fitting mask around the mouth and nose Pulse oximetry A method of continuous measurement of SaO2 based on calculating relative absorption of light from two lightemitting diodes at different wavelengths

Knaus, W.A., Draper, E.A., Wagner, D.P. & Zimmerman, J.E. (1985) APACHE II: a severity of disease classification system. Crit Care Med 13, 818–829.

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Haemorrhage, Hypovolaemia and Shock Introduction, 136 Classification of shock, 136

Clinical features, 138 Assessment and treatment of shock, 138

Must know Must do

Must know Clinical features and management of the various types of shock Assessment and monitoring of patients in shock Complications of shock and their management Causes and management of upper gastrointestinal haemorrhage Causes and management of lower gastrointestinal haemorrhage Must do See and follow patients admitted with upper gastrointestinal bleeding Help in the resuscitation of patients with hypovolaemic shock Observe and follow patients admitted with lower gastrointestinal bleeding Observe upper gastrointestinal endoscopy performed to stop bleeding peptic ulcer Observe a flexible sigmoidoscopy Observe a colonoscopy Observe an emergency coeliac axis/mesenteric angiogram Perform faecal occult blood in patients with hypochromic microcytic anaemia Become familiar with the interpretation of small bowel enema and colonic barium enema If possible, observe an enteroscopy

Introduction Shock may be defined as acute circulatory failure with inadequate or inappropriate perfusion resulting in generalized cellular hypoxia. Inadequate tissue perfusion for whatever reason causes cellular hypoxia, thereby precipitating a number of intracellular reactions and a cytokine cascade, culminating in a metabolic acidosis. The latter, by altering vascular permeability, creates a vicious circle: there are increasing plasma losses from the circulation 136

Complications of shock, 141 Gastrointestinal haemorrhage, 142

with reducing cardiac output (CO) and further acidosis, so that the state of shock becomes irreversible.

Classification of shock The pathophysiological changes that occur in shock are summarized in Fig. 12.1.

Hypovolaemic shock Hypovolaemia is defined as a reduced circulating blood volume (CBV = 70 mL/kg in an adult; 80 mL/kg in infants) and can be either true or apparent. True hypovolaemia results from contraction of CBV as a result of: loss of blood due to haemorrhage; loss of plasma due to burns; dehydration from deficits of water and saline. Apparent hypovolaemia ensues because of increased vascular capacity, usually due to loss of peripheral resistance in the muscular arterioles (sepsis, adrenal insufficiency, anaphylaxis, neurogenic factors). However, in some of these conditions (e.g. sepsis) the situation is more complex as the increased capillary permeability induces intravascular fluid losses into the interstitial space.

• • •

Response to hypovolaemia The adverse effects of hypovolaemia are the result of inadequate CO and hence inadequate cellular perfusion. Overall CO is determined by stroke volume (SV) and heart rate (HR): CO = SV × HR. In a young fit adult at rest, each ventricle fills during diastole to reach an enddiastolic volume of 120 mL. With each ventricular contraction (systole), 70 mL is ejected from each ventricle. This amount is known as the ejection fraction, which is normally 60% of the volume present in each ventricle at the end of diastole. In accordance with Starling’s law, the more the heart fills during diastole, the greater the volume expelled with each beat (SR), although the ejection fraction remains fairly constant. CO is then determined by the following factors.

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137

Activation of renin angiotensin system Production of angiotensin and aldosterone Vasoconstriction, Na & H2O retention Sympatho-adrenal response Sympathetic nervous activity Adrenaline (noradrenaline) Vasoconstriction, tachycardia cardiac output

Neuroendocrine/ endocrine responses ACTH, GH, ADH β endorphins & encephalins Cortisol, glucagon Blood sugar, Na & H2O retention

SHOCK

Cellular changes Anaerobic metabolism Lactic acidosis Loss of Na/K pump Cellular oedema Cell death

Microcirculatory responses Prostaglandin release Membrane phospholipids

Inadequate tissue perfusion Sequestration of fluid Build up of lactic acid & CO2

Arachidonic acid Prostaglandins & thromboxane

Leucotrienes

Figure 12.1 Shock, regardless of cause, initiates a series of pathophysiological changes aimed at protecting the organism and preserving its vital functions.

Preload (i.e. venous filling/venous return) is reduced •significantly in hypovolaemia. Cardiac contractility: diminished in hypovolaemia •because of reduced end-diastolic filling/volume of the ventricles (and thus stretch of the cardiac muscle fibres). Afterload (i.e. peripheral arterial resistance) acts as an impediment to cardiac ejection; thus a reduced afterload tends to favour an increase in CO but only in the presence of an adequate CBV. In the hypovolaemic patient, peripheral resistance is initially increased (sympathetic and adrenal response) so that the percentage fall in blood pressure is always an underestimate of the drop in CO. Heart rate: within limits, tachycardia increases CO, although extreme heart rates reduce output by diminishing ventricular filling and coronary artery nutrient blood flow to the myocardium. The response of an individual to blood loss varies considerably. Indeed there are young healthy individuals who, by virtue of the intense vasoconstriction they can mount in response to volume deficits, can lose as much as 25% of CBV without any significant change in arterial blood pressure. The response is influenced by age, dura-

•

tion and severity of injury, pre-existing myocardial disease, anaemia, and associated trauma. In the accident victim, the additional trauma alters the neuroendocrine and metabolic response. Thus trauma victims with mild to moderate hypovolaemia may have a normal or even elevated CO, and may be normotensive or even hypertensive after the accident.

Cardiogenic shock Cardiogenic shock signifies central pump failure. It is most commonly seen after major myocardial infarction but is also encountered in ventricular arrhythmias (pump action ineffective), interruption of ventricular outflow by massive pulmonary embolus, and cardiac tamponade usually caused by direct penetrating injuries to the myocardium, where subsequent haemorrhage into the pericardial sac prevents adequate filling of the ventricles during diastole. Cardiogenic shock is characterized by profound hypotension and distended neck veins. It carries a high mortality even with prompt and energetic treatment.

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Septic shock Septic shock may arise as a consequence of Gram-positive or Gram-negative infection (more usually the latter) in the urinary, biliary or gastrointestinal tracts. Shock results from the action of bacterial endotoxins and exotoxins on the cardiovascular system. The presence of vasoactive cytokines gives rise to greatly increased capillary permeability and peripheral vasodilatation. Large quantities of fluid leak out of the circulation and the increased vascular capacity causes a relative hypovolaemia. A myocardial-depressant factor may be released from hypoxic cells that restricts CO. The common bacteria involved are Escherichia coli, Proteus, Pseudomonas and Bacteroides. Fungal infections are increasingly seen in patients on broad-spectrum antibiotics and in patients who are immunologically suppressed (see Chapter 16).

Fig. 12.1). The tachycardia attempts to compensate for the low CO and the peripheral vasoconstriction attempts to redistribute the intravascular volume. The change in intracellular metabolism from aerobic respiration via the Kreb’s cycle to anaerobic respiration with lactic acid production produces a metabolic acidosis that provokes compensatory hyperventilation. Oliguria is due to the reduction in renal blood flow. In the early stages of septic shock the patient may present a different picture, with warm flushed skin and bounding pulse. This is due to endotoxin-induced vasodilatation that is unresponsive to catecholamines and the reduced peripheral resistance is accompanied by an increased CO. This phase is temporary, however, and soon reverts to the low-output state with increased peripheral resistance.

End-stage Anaphylaxis

Anaphylactic shock occurs when a hypersensitive patient is exposed to an antigen to which he or she has previously been sensitized. The binding of antigen and antibody releases histamine, components of complement, cytokines and other vasoactive substances that cause vasodilatation, increased capillary permeability and bronchoconstriction; this interferes further with the already impaired oxygenation. Common causes of anaphylactic shock are drugs such as penicillin and co-amoxiclav and radiological contrast media.

Clinical features The clinical features of shock are summarized in Table 12.1. Patients in hypovolaemic or cardiogenic shock are pale, cold and sweating. The pulse is fast and weak. The blood pressure is low and there is oliguria. These clinical manifestations are due to the intense sympathetic and adrenal activity with release of catecholamines (see

The failing circulation is unable to provide the major organs with an adequate supply of oxygen and progressive cerebral hypoxia is manifested by agitation and restlessness, followed by confusion and coma. Diminished coronary blood flow leads to progressive heart failure, which may be aggravated by myocardial-depressant factor and hypoxia. The fall in renal blood flow diminishes the glomerular filtration rate (GFR) and induces oliguria, leading to acute tubular necrosis (see Chapter 14).

Assessment and treatment of shock Patients in shock require invasive monitoring and vigorous treatment, which is usually performed in the accident and emergency department, the operating theatre or the intensive care unit (and sometimes in all three!). Details of the type of monitoring performed on patients in the intensive care unit are given in Chapter 16. However, a summary of the assessment of the shocked patient is given here. Usually, assessment and treatment are performed concurrently.

Table 12.1 Clinical features of shock: all patients experience hypotension, tachycardia, dyspnoea, oliguria and restlessness to some degree.

Skin colour Sweating Temperature Capillary refill Central venous pressure Mental status

Hypovolaemic

Cardiogenic

Septic

Anaphylactic

Pale Present Cold Slow Low Restless

Pale Present Cold Slow High Quiet

Flushed Absent Warm Rapid Low Drowsy

Urticarial rash Absent Warm Normal or rapid Low Variable

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Assessment

•

Clinical assessment includes pulse rate, blood pressure, respiratory rate and temperature. A rapid clinical examination may provide some clues to the underlying cause, whether it be haemorrhage, anaphylaxis, sepsis or cardiac insufficiency. An electrocardiogram (ECG) provides evidence of cardiac status and may be helpful in identifying pulmonary embolus also. However, the classical ECG findings (Swave in lead I and Q-waves and inverted T-waves in lead III: S1QT3) are found in only 10–20% of patients with pulmonary embolus (see Chapter 38). Venous blood samples are used for measuring haemoglobin, haematocrit, urea and electrolytes, and cardiac enzymes. Grouping and cross-matching are done if haemorrhage is the underlying problem. If sepsis is suspected, a blood sample is taken for aerobic and anerobic blood culture. Urine output should be documented hourly after insertion of a urinary catheter. Central venous pressure (CVP) is used to monitor CBV. However, changes in blood volume may be absolute or relative, depending on whether the patient is suffering from haemorrhage, fluid loss, sepsis or anaphylaxis. CVP may also reflect intrinsic myocardial disease in right ventricular failure or, more commonly, the pulmonary hypertension induced by left ventricular failure. Its interpretation may therefore be difficult and misleading and must be carried out in conjunction with other evidence. Blood gas analysis and arterial pH provide important information on arterial Po2 and Pco2. Patients in shock usually have a metabolic acidosis due to accumulation of lactic acid, the main product of anaerobic metabolism (see Chapter 12).

• • • • • •

•

Treatment The aim of treatment is to: resuscitate the patient and improve tissue perfusion and delivery of oxygen to the cells to maintain aerobic respiration; deal with the cause of shock, e.g. stop bleeding, treat infection; prevent and treat complications of shock.

• • •

Resuscitation

•

Ensure that the airway is clear, breathing is spontaneous and adequate, and the patient has a circulation (ABC; see Chapter 11, p. 129). Provision of 100% oxygen via a facemask is immediately helpful (see Chapter 11).

•

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•

Blood or plasma is given as indicated as soon as available, e.g. blood for haemorrhagic shock, plasma for burns. Hypovolaemia Management of the hypovolaemic patient entails: detection of the hypovolaemia, its cause and severity; arrest of haemorrhage; establishment of good intravenous access with largebore peripheral cannulae (two if hypovolaemia is severe); replacement of the deficit; repeat clinical observations and monitoring of the patient. In hypovolaemic shock, restoration of CBV must be carried out as quickly as possible. Crystalloid solutions (e.g. Ringer’s lactate solution) are ideal in situations where water and sodium loss is predominant and serve as initial treatment in haemorrhagic shock. Colloid solutions, e.g. hydroxyethyl starch, gelatins (Haemaccel), remain longer in the circulation and draw extracellular fluid into the circulation by osmotic pressure. The administration of intravenous crystalloid or colloid should be monitored by CVP and urine output.

• • • • •

detection of hypovolaemia, its cause and severity Diagnosis and assessment is based on clinical measures including careful history, clinical examination, estimation of observed losses, haemodynamic measurements (HR, pulse volume, arterial and venous pressures, haematocrit) and indices of tissue perfusion (nail-bed capillary refill, peripheral skin temperature, urine output, level of consciousness). The severity of hypovolaemia correlates with the volume lost and is reflected in the clinical signs. In general, contraction of CBV by more than 25% (1.5 L) is regarded as severe hypovolaemia. The severity of the hypovolaemia is much more difficult to assess clinically when the hypovolaemia is secondary to deficits of water and saline. In these instances, careful reappraisal of the fluid balance charts allows the best estimate of the losses incurred. monitoring of the hypovolaemic patient The primary objectives of monitoring are to ensure that CBV has been replaced and that tissue perfusion has been restored to normal. In the unstable patient, monitoring also provides early signs of either renewed bleeding or cardiac decompensation and thus the need for inotropic support. Basic monitoring of the otherwise stable patient who recovers quickly with volume replacement includes the following. Arterial blood pressure, core temperature and pulse rate. CVP: if values are equivocal, the effect of a fluid challenge (100–200 mL over 2–3 min) on CVP will determine

• •

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whether the patient is still hypovolaemic (CVP remains unchanged or may even drop as the vasoconstriction subsides) or is likely to be overloaded (sharp elevation of CVP). Hourly urine output: an output > 30 mL/h indicates adequate renal perfusion. Pulse oximetry: preferably one that also displays the pulse plethysmogram in addition to percentage oxygen saturation. More intensive monitoring is required in cardiovascularly unstable patients, including those who sustain major trauma. This includes the following (in addition to the above). Insertion of radial artery cannula for continuous monitoring of arterial pressure and to obtain samples for blood gas analysis. Core–peripheral temperature gradient: useful noninvasive indicator of peripheral perfusion. Insertion of pulmonary artery flotation catheter (Swan–Ganz catheter) allows monitoring of right atrial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, measurement of CO (by thermodilution), and sampling of mixed venous blood for oxygen saturation (Sv¯o2). A number of important derived variables can be obtained from these measurements in conjunction with the results of blood gas analysis, including pulmonary vascular resistance, systemic vascular resistance, oxygen extraction ratio and systemic oxygen consumption.

• •

• • •

Cardiogenic shock The aim of treatment is to improve CO without increasing excessively the workload on the heart, which might further compromise the coronary circulation. Patients should have complete bedrest and be monitored in a coronary care unit. Pain relief should be achieved with diamorphine or morphine. If the patient has had a myocardial infarction, thrombolytic therapy in the form of streptokinase or recombinant tissue plasminogen activator should be administered as well as aspirin. If the patient is in heart failure, diuretics (e.g. furosemide 40 mg), nitrates, angiotensin-converting enzyme inhibitors, cardiac glycosides and dopexamine may be indicated. Arrhythmias must be avoided and controlled (Table 12.2). Septicaemic shock Septicaemic shock is commonly seen in surgical practice. The source of infection may arise de novo from a perforated viscus or may be due to postoperative complications (e.g. abscess, leaking anastomosis). Treatment is aimed at controlling infection and improving the hypovolaemic state caused by endotoxin-induced peripheral vasodilata-

Table 12.2 Management of common arrhythmias seen after myocardial infarction. Arrhythmia

Treatment

Supraventricular tachycardia

Carotid massage Adenosine DC cardioversion

Atrial flutter or fibrillation

Digoxin Verapamil Amiodarone DC cardioversion

Complete heart block

Atropine Cardiac pacing

Ventricular arrhythmias

Lidocaine infusion Bretylium

Ventricular tachycardia

CPR DC cardioversion

CPR, cardiopulmonary resuscitation; DC, direct current.

tion. The latter is improved by the administration of colloid solutions, the volume of which is monitored by CVP and urine output. Blood cultures should always be carried out before antibiotic administration so that the sensitivity of the responsible organisms may be determined. In the interim a combination of penicillin, aminoglycoside and metronidazole should be effective against the most common organisms. The use of inotropes is often indicated in severely ill septic patients to maintain CO and preserve vital functions. The most frequently used inotropes are listed in Table 12.3. These drugs are very potent, however, and should only be used in an intensive care setting and in conjunction with the treatment of abnormalities that may impair cardiac performance, e.g. hypoxia, acidosis, hypocalcaemia. Intravenous hydrocortisone has been advocated in the treatment of septic shock but its use is controversial. Anaphylactic shock Anaphylactic shock may be precipitated as a response to an antigen to which the individual has been previously sensitized. The release of histamine and other vasoactive amines causes widespread vasodilatation, with increased capillary permeability. Bronchoconstriction is also a prominent feature that further exacerbates the tissue anoxia. The common causes of anaphylactic shock in hospital practice are the administration of radiological contrast media and intravenous drugs, e.g. penicillin. While most insect bites produce no more than a mild local hypersensi-

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Table 12.3 Inotropic agents frequently used in patients with shock. Dopamine Low-dose: peripheral resistance falls secondary to dilatation of splanchnic and renal vasculature. Renal and hepatic blood flow increase. Renal-protective effect High-dose: causes noradrenaline release, leading to vasoconstriction and loss of renal-protective effect Dobutamine Reduces systemic resistance and improves cardiac performance. Possibly has better inotropic effect than dopamine Dopexamine β2-Adrenergic agonist and dopamine receptor agonist: Increased heart rate Increased cardiac index Increased cardiac output Decreased peripheral resistance No vasoconstriction Adrenaline Low-dose: β2-adrenergic agonist effects High-dose: α-adrenergic agonist effects: Vasoconstriction Decreased renal blood flow Peripheral gangrene Noradrenaline α-Adrenergic agonist effects

tivity, wasp and bee stings may produce full-blown anaphylactic shock with circulatory collapse in some people. Treatment consists of: intravenous fluids to compensate for the relative hypovolaemia produced by widespread capillary vasodilatation; intramuscular administration of adrenaline to improve CO and induce vasoconstriction; antihistamines to block the histamine receptors (for details see Chapter 6). Specific treatment such as penicillinase is used if the anaphylactic reaction is due to penicillin.

• • •

Complications of shock Apart from the profound effects on the cardiovascular system, shock may precipitate acute respiratory failure, acute renal failure, disseminated intravascular coagulation (DIC) or, more rarely, hepatic failure. Severely ill patients may develop systemic inflammatory response

141

syndrome, which often results in multiple system organ failure (also known as multiple organ dysfunction syndrome) and, ultimately, death (see Chapter 16).

Disseminated intravascular coagulation DIC is a major complication of septic shock. In this condition the various factors involved in the clotting mechanism are activated and widespread intravascular coagulation takes place, with consequent depletion of clotting factors, including platelets. Profuse spontaneous haemorrhage is then paradoxically produced and bleeding from operation sites may be uncontrollable. If the condition is suspected, diagnosis is confirmed by the high level of fibrin degradation products present in the serum. Intravenous heparin is administered to control the coagulation and the normal clotting factors are restored by giving fresh frozen plasma and platelets.

Stress ulceration Severe haemorrhage may occur from multiple gastric erosions in critically ill patients. The erosions are secondary to mucosal ischaemia, which is caused by hypotension or the effects of endotoxin. Alteration in mucosal permeability allows back-diffusion of H+, which stimulates excess acid secretion. Administration of antacids to raise the gastric pH to 7 may be of help; H2-receptor antagonists have also been used, although their efficacy remains unproven. However, the elevation of pH may allow bacterial colonization of the stomach from the oropharynx, where Gram-negative colonization is common in seriously ill patients. To avoid bacterial overgrowth, cytoprotection with sucralfate has been used as an alternative to raising the pH.

Acute respiratory failure Severe respiratory problems may develop after successful resuscitation of the shocked patient. The so-called shock lung syndrome may be associated with a variety of abnormalities, including sepsis, fat embolism, massive blood transfusion, oxygen toxicity and DIC. The varied aetiology has prompted the term ‘acute respiratory distress syndrome’ (ARDS) to cover all these conditions. Increasing evidence implicates activated white cells (e.g. by endotoxin via the complement system in the case of Gram-negative septicaemia) as the mediators of ARDS. The activated white blood cells release free radicals and hydrolytic enzymes that damage the endothelium of lung capillaries. The result is that the lungs become very oedematous; fibrin and microaggregates collect in the

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interstitial spaces around the alveoli and capillaries, thus reducing efficient gas exchange (see also Chapter 38). Clinically, respiration becomes more rapid, the Pao2 falls significantly, even when the patient is breathing high concentrations of oxygen, and the increased respiration lowers the Pco2, producing a respiratory alkalosis. Chest radiographs may change from normal to complete ‘whiteout’ over a 24-h period. Treatment is mainly supportive and aimed at preserving adequate Pao2. Intermittent positive-pressure ventilation is necessary if Pao2 falls below 8 kPa. If intermittent positive-pressure ventilation fails to maintain adequate oxygenation, positive endexpiratory pressure of between 5 and 15 cm H2O is used (see Chapter 11). Other measures to reduce oedema (e.g. maintaining plasma osmotic pressure by gastrointestinal or intravenous feeding and the administration of intravenous albumin, and the judicious use of diuretics) are important. Steroids and antibiotics are of doubtful value.

Acute renal failure

The commonest cause of acute renal failure in the surgical patient is a fall in GFR as a consequence of hypovolaemic shock. This is clinically manifest as oliguria with a daily urine output of between 400 and 700 mL, i.e. less than 20 mL/h. When oliguria becomes established, fluid intake must be severely restricted and electrolyte concentrations carefully monitored. The blood urea will rise rapidly and serum K+ tends to rise to dangerous levels, which can cause cardiac arrhythmias or cardiac arrest. A severe metabolic acidosis develops (see Chapter 13). Fluid administration is restricted to 400 mL/day plus known losses. A rising K+ may be controlled by giving intravenous glucose and insulin, calcium gluconate or ion-exchange resins. Sodium bicarbonate is used to control the metabolic acidosis. In most cases of acute renal failure some form of dialysis is necessary during the acute tubular necrosis phase. Peritoneal dialysis has the advantage of being a simple technique but haemodialysis is more efficient. At the end of the oliguric phase, assuming that acute tubular necrosis rather than acute cortical necrosis is the problem, the diuretic phase commences, during which large quantities of unconcentrated urine are passed and very high losses of Na+ and K+ may occur, which need careful management (see Chapter 14).

Acute hepatic failure Rarely, severe shock may bring about acute hepatic failure. Encephalopathy, jaundice and coagulation disorders may supervene, with progressive coma and respiratory failure. Treatment is mainly supportive and the mortality

is very high. Hepatic failure is discussed fully in Chapter 27.

Prognosis The prognosis of patients with two or more system failures is poor. Each organ failure carries a mortality of about 30%. However, these mortality rates are additive, so that patients with three or more system failures have mortality rates of 90–95%.

Gastrointestinal haemorrhage This is one of the most common clinical presentations in gastroenterological and general surgical wards. The causes, by topographical site in the gut, are outlined in Table 12.4. From a clinical standpoint, patients present with: iron-deficiency anaemia due to chronic occult blood loss with positive faecal occult blood, e.g. gastric cancer, right colon cancer; minor episodes of blood loss, e.g. rectal tumours, inflammatory bowel disease, etc.; acute gastrointestinal bleeding with hypovolaemic shock; recurrent obscure gastrointestinal bleeding.

• • • •

Acute upper gastrointestinal bleeding There are marked regional differences in the incidence even within a country. Thus in the UK, Aberdeen has a much higher incidence (116 per 100 000) compared with Oxford (47 per 100 000). The causes of upper gastrointestinal bleeding in descending order of frequency are outlined in Table 12.5. In 20%, the diagnosis is not clear despite upper gastrointestinal endoscopy at presentation because: there is too much blood in the stomach to permit adequate inspection; the lesion is missed; the lesion has healed; the source of bleeding is outwith the stomach and proximal duodenum.

• • • •

Bleeding due to aspirin and non-steroidal anti-inflammatory drugs All these drugs cause peptic ulcers in the stomach and duodenum. Aspirin increases the risks for both gastric and duodenal ulcers two to four times and accounts for 1 in 10 ulcer bleeds in patients aged over 60 years. The nonaspirin non-steroidal anti-inflammatory drugs (NSAIDs), such as fenbufen, benoxaprofen, indomethacin, ibuprofen and piroxicam, carry a higher risk of peptic ulceration

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Table 12.4 Causes of gastrointestinal bleeding by site. Foregut Ulcers: usually drug induced Oesophageal varices Gastritis Peptic ulcer: duodenal, gastric Tumours: adenoma, smooth muscle, lymphoma Vascular anomalies Hereditary telangiectasia Anastomotic suture line: postoperative Mallory–Weiss syndrome Trauma: including iatrogenic Haemobilia Chronic pancreatitis: aneurysms, sectorial portal hypertension Midgut Colorectal tumours/polyps Small bowel tumours Vascular anomalies: right colon and small bowel Hereditary telangiectasia Peutz–Jeghers polyps Jejunal diverticula Meckel’s diverticulum: infants and children Aorto-enteric fistula: patients with aortic grafts Crohn’s disease Anastomotic suture line: postoperative Portal hypertension: includes bleeding from stomal varices Hindgut Inflammatory bowel disease Diverticular disease Angiodysplasia Ischaemic colitis Trauma Endometriosis Anastomotic suture line: postoperative Portal hypertension Haemorrhoids

than aspirin and account for 20% of all bleeding ulcers in patients aged over 60 years. In the UK, 12 000 emergency upper gastrointestinal hospital admissions per annum (perforation, bleeding, acute pain) are caused by NSAIDs, with 2230 deaths. Overall, 30% of ulcer bleeds in patients above 60 years of age are due to aspirin or non-aspirin NSAIDs. Aspirin and the NSAIDs act by inhibiting cyclooxygenase (COX) and thus the synthesis of prostaglandins. There are two isoforms of COX: COX-1 and COX-2. COX-1 is always present and is responsible for most of the physiological prostaglandin production involved in cytoprotection, especially of the gastric mucosa. In contrast, COX-2 is involved in the synthesis of prostaglandins that mediate the inflammatory response (including joint inflammation). Thus specific inhibitors of COX-2 suppress the inflammatory response while preserving the cytoprotective function of COX-1. COX-2 inhibitors such as meloxicam have decreased gastrointestinal toxicity but are less effective in pain relief.

Clinical presentation The majority of patients are admitted as emergencies with: haematemesis (blood in vomit), which may be bright red or altered to look like ‘coffee grounds’ because of HCl digestion; or melaena (blood in stool), usually altered foul-smelling blood; or both. Severity of upper gastrointestinal bleeding determines the presence and extent of hypovolaemia. Mild: no significant hypovolaemia (includes anaemic patients). Moderate: hypovolaemia that responds to volume replacement (crystalloids and blood); thereafter the patient remains stable. Severe: active continued major bleeding that renders resuscitation with transfused blood difficult, or recurrent major bleeding after successful resuscitation from the initial bleed. Although this classification is useful in dictating management, the category can change after initial assessment from mild to severe. Thus complacency must be avoided and repeat clinical monitoring is essential even in patients with mild upper gastrointestinal haemorrhage. This situation is best exemplified by the patient who develops an aorto-enteric fistula after aortic replacement by prosthetic graft. The initial (secondary) bleeds may appear trivial yet are warning manifestations of an impending catastrophic haemorrhage that is often fatal. Persistent bleeding is diagnosed when the patient requires 8 units (> 60 years) or 12 units (< 60 years) or more over a 48-h period to

• • • • • •

Table 12.5 Causes of upper gastrointestinal bleeding. Disease category

Frequency (%)

Duodenal ulcer Gastric ulcer Oesophagitis and ulcer Acute gastric lesions Mallory–Weiss syndrome Oesophageal varices Gastric cancer Diagnosis unclear

29 22 12 7 7 5 2 15

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Table 12.6 Techniques for endoscopic control of upper gastrointestinal bleeding. Injection therapy: vasopressors, sclerosants, thrombin, mixtures Banding: alternative to injection sclerotherapy for oesophageal varices H-F electrocoagulation: unipolar, bipolar, argon ion plasma coagulation Heater probe Photocoagulation (gas vapour lasers, diode array lasers) Non-contact (laser beam) Contact (with sapphire tip)

niques, e.g. adrenaline injection therapy plus electrocoagulation or photocoagulation, is used and is reported to be beneficial by allowing a clearer target for the endoscopist and reducing the heat-sink effect when thermal energy is applied. Indications for surgical treatment Patients with exsanguinating haemorrhage. Elderly patients (> 60 years): if more than 4 units of blood are necessary during the initial resuscitation on admission, patient has one recurrence of bleeding after initial endoscopic control of bleeding, and persistent bleeding requires 8 units of blood within 48 h. Younger patients (< 60 years): if 8 or more units of blood are required during the initial resuscitation and persistent bleeding requires 12 units of blood over a 48-h period.

• • •

maintain the haemoglobin at 10 g/dL. In addition to the severity of the bleed, the patient must be examined for stigmata of chronic liver disease, which may indicate variceal haemorrhage. Examination of the cardiovascular and respiratory systems is necessary with appropriate investigations (chest X-ray and ECG). Significant cardiac and respiratory disease are important determinants of morbidity and mortality and influence the approach used to control bleeding.

Management Diagnosis is based on upper gastrointestinal endoscopy carried out within 24 h of admission in haemodynamically stable patients and following resuscitation. All patients with acute upper gastrointestinal haemorrhage should have a joint consultation by a surgeon and gastroenterologist soon after admission. Patients with severe continued bleeding require surgery concomitantly with volume replacement through two large infusion cannulae. The hypovolaemia is corrected with blood and colloids/ crystalloids and a catheter is inserted in the urinary bladder for hourly measurement of the urine output. A Salem sump nasogastric tube is inserted and hourly clinical observations commenced: pulse, blood pressure, CVP; pulse oximetry; urine output.

• • •

Endoscopic treatment Control of bleeding in the majority of patients is achieved by interventional flexible endoscopic techniques carried out in a dedicated endoscopy suite with the necessary cardiovascular monitoring. The endoscopic techniques used for visible vessels and active bleeding are classified as thermal, electrocoagulation, photocoagulation and injection therapy (Table 12.6). Sometimes, a combination of tech-

Lower gastrointestinal bleeding Unlike upper gastrointestinal bleeding, the vast majority of patients present electively, and only a minority are admitted as emergencies for massive bleeding and signs of hypovolaemia. In many cases such bleeding stops spontaneously; if it does not, it requires emergency treatment. The commonest cause of massive rectal bleeding is diverticular disease, although the bleeding may originate from vascular lesions of the colon or small bowel and from more proximal lesions, especially posterior duodenal ulcers.

Management In massive rectal bleeding the priority is resuscitation, but investigation must proceed promptly during the resuscitation. The first step must be to exclude bleeding haemorrhoids by means of proctoscopy, and this should be followed by upper gastrointestinal endoscopy. If these are negative, urgent mesenteric angiography may locate the bleeding point. For intermittent bleeding with negative angiography, radionuclide-labelled red cell scanning may be used. The patient’s own red cells are labelled with 51Cr and reinjected so that a gamma-camera can be used to localize pooling of blood in the intestine. Surgical treatment is usually required for massive rectal bleeding, with resection of the appropriate segment of colon or small bowel after attempts at preoperative localization. Occasionally, it is necessary to proceed to laparotomy because of the severity of the bleeding. In this case, intraoperative colonoscopy with on-table antegrade colonic lavage is performed to locate the bleeding lesion. If this proves unsuccessful, colectomy and ileostomy are performed, preserving the rectal stump for later reanastomosis.

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Haemorrhage, hypovolaemia and shock at a glance Definition Shock: a state of acute inadequate or inappropriate tissue perfusion resulting in generalized cellular hypoxia and dysfunction Classification of shock Hypovolaemic True hypovolaemia is due to contraction of circulating blood volume: • Blood loss (ruptured abdominal aortic aneurysm, upper gastrointestinal bleed, multiple fractures, etc.) • Plasma loss (burns, pancreatitis) • Extracellular fluid losses (vomiting, diarrhoea, intestinal fistula) Apparent hypovolaemia is a result of increased vascular capacity due to loss of peripheral resistance in muscular arterioles: • Sepsis • Adrenal insufficiency • Anaphylaxis • Neurogenic Sympathoadrenal response Activation of renin–angiotensin system Neuroendocrine response

Microcirculatory response Cellular phospholipid injury

Cellular changes

Cardiogenic • Myocardial infarction • Arrhythmias (atrial fibrillation, ventricular tachycardia, atrial flutter) • Pulmonary embolus • Cardiac tamponade • Valve disease Septic • Gram-negative, less often Gram-positive, infections Anaphylactic/distributive • Release of vasoactive substances when a sensitized individual is exposed to the appropriate antigen Pathophysiological response to shock Regardless of cause, shock produces a series of changes aimed at protecting the organism and preserving its vital functions

Sympathetic discharge (Nor)adrenaline release Angiotensin Aldosterone Adrenocorticotrophic hormone, growth hormone b-endorphins Cortisol, glucagon Inadequate perfusion Arachidonic acid Prostaglandins Leukotrienes Anaerobic metabolism

Clinical features Hypovolaemic and cardiogenic shock • Pallor, coldness, sweating and restlessness • Tachycardia, weak pulse, low blood pressure and oliguria Septic shock • Initially, warm flushed skin and bounding pulse • Later, confusion and low-output picture Investigation and management Principles of management • Identify the cause early and begin treatment quickly

Vasoconstriction Tachycardia, increased CO Vasoconstriction Na+ and H2O retention Na+ and H2O retention Pain relief Elevated blood sugar Fluid sequestered, acidosis Increased permeability Neutrophil activation Lactic acidosis Loss of Na+/K+ pump Cellular oedema and death

• Shock in surgical patients is often overlooked: unwell, confused, restless patients may well be shocked • Unless a cardiogenic cause is obvious, treat shock with urgent fluid resuscitation • Worsening clinical status despite adequate volume replacement suggests the need for intensive care Details of management • Resuscitate patient, ABC, give 100% O2 via mask • Establish good i.v. access and set up CVP line (possibly Swan–Ganz catheter as well) • Start i.v. infusion, usually crystalloid initially

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• Monitor pulse, blood pressure, temperature, respiratory rate and hourly urinary output via catheter • ECG, cardiac enzymes, echocardiography • Haemoglobin, haematocrit, urea and electrolytes, creatinine • Group and cross-match blood: haemorrhage • Arterial blood gases • Blood cultures: sepsis Complications • Acute renal failure (acute tubular necrosis) • ARDS • DIC • Systemic inflammatory response syndrome (may ensue if shock not corrected) • Acute hepatic failure • Stress ulceration

Summary of management • Airway and breathing: give 100% O2, position patient upright, consider ventilatory support if necessary • Circulation: ensure good i.v. access, urinary catheter, monitor cardiac rate and rhythm • Deal with the cause of the shock, e.g. stop the bleeding, drain the abscess, remove the source of the anaphylactic antigen, etc.

Gastrointestinal haemorrhage Definitions Gastrointestinal haemorrhage is defined as loss of blood (which may be acute or chronic) from the gastrointestinal tract anywhere from the mouth to the anus

Anaphylactic

Cardiogenic

Septic

Hypovolaemic

i.v. fluids i.v. adrenaline i.v. antihistamines i.v. hydrocortisone

Optimize rate and rhythm (e.g. cardioversion, drugs) Optimize preload (e.g. adequate volume, diuretics) Optimize afterload (e.g. vasoconstrictors/dilators) Optimize cardiac function (e.g. thrombolytic therapy, inotropes, assist devices)

Fluids to restore circulating volume Antibiotics or surgery Support cardiac function (e.g. inotropes)

Identify and arrest losses (may include surgery) Restore circulating volume (crystalloids, colloids or blood) Support cardiac function

Causes Anatomical site

Pathology

Mouth and pharynx Oesophagus Stomach Duodenum Small bowel Colon Rectum Anus

Carcinoma, trauma Oesophagitis, varices, peptic ulcer disease (PUD), Mallory–Weiss syndrome, carcinoma Gastritis, PUD, carcinoma (leiomyoma, lymphoma, Dieulafoy lesion, hereditary telangiectasia) PUD (periampullary carcinoma, aortoduodenal fistula, haemobilia) Meckel’s diverticulum, intussusception, enteritis (infection, radiation, Crohn’s), ischaemia, tumours Angiodysplasia, polyps/carcinoma, diverticular disease, inflammatory bowel disease, ischaemia Polyps/carcinoma, proctitis, solitary rectal ulcer, trauma Haemorrhoids, fissure-in-ano, carcinoma, perianal Crohn’s disease

Aspirin and the NSAIDS Aspirin and the NSAIDs inhibit the enzyme cyclooxygenase (COX). COX exists as two isoforms: COX-1 (responsible for physiological prostaglandin production) and COX-2 (mediates production of prostaglandins involved in inflammation). Specific COX-2 inhibitors suppress inflammation while preserving cytoprotective function of COX-1

• Aspirin use is the cause of 10% of all peptic ulcers in patients aged 60 years and over • NSAID use is the cause of 20% of all peptic ulcers in patients aged 60 years and over • In the UK, 12 000 patients are admitted with upper gastrointestinal pathology related to NSAID use annually • Of these patients, 2230 (18.5%) die

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Presentations • Iron-deficiency anaemia due to chronic blood loss, e.g. gastric or caecal carcinoma • Minor episodes of blood loss, e.g. rectal tumours, ulcerative colitis • Acute major gastrointestinal bleeding (haematemesis or rectal bleeding) with hypovolaemic shock, e.g. duodenal ulcer, angiodysplasia • Recurrent obscure bleeding, e.g. Meckel’s diverticulum Management Upper gastrointestinal haemorrhage (heamatemesis, melaena or both) • Secure airway, breathing and circulation, insert two largebore i.v. cannulae, insert urinary catheter • Send bloods for group and cross-match, full blood count, urea and electrolytes, creatinine • Give i.v. fluids: crystalloids to begin and then blood if necessary • Monitor pulse, blood pressure (CVP if patient is shocked), pulse oximetry, urinary output • Assess severity: (a) Mild: no hypovolaemia (b) Moderate: hypovolaemia that responds to volume replacement, patient remains stable (c) Severe: active continued major bleeding requiring continuous resuscitation or recurrent major bleed • Arrange diagnostic upper gastrointestinal endoscopy (see table below) within 24 h (sooner if bleed is severe) Indications for surgery • Exsanguinating haemorrhage • > 60 years: (a) ≥ 4 units on initial resuscitation (b) one recurrent bleed after initial endoscopic control (c) persistent bleeding requiring 8 units in 48 h • < 60 years (a) ≥ 8 units on initial resuscitation (b) persistent bleeding requiring 12 units in 48 h Lower gastrointestinal haemorrhage (rectal bleeding) • Most patients are elderly, bleeding is usually not severe and frequently stops spontaneously

147

• Massive haemorrhage with hypovolaemia: initial resuscitation is the same as for upper gastrointestinal haemorrhage. Investigation proceeds with resuscitation: (a) Proctoscopy: exclude haemorrhoids (b) Colonoscopy: often difficult to see anything because of blood (c) Upper gastrointestinal endoscopy: bleeding may be from a duodenal ulcer (d) Mesenteric angiography (e) Radiolabelled red blood cell scanning Indications for surgery: continued bleeding • Remove segment of bowel containing ‘bleeder’ if known from preoperative investigation • If source unknown, perform laparotomy with intraoperative colonoscopy to try and identify ‘bleeder’. If source still cannot be found, a total colectomy may be needed Iron-deficient anaemia and obscure haemorrhage These need to be investigated thoroughly to find the cause. Examination may include upper and lower gastrointestinal endoscopy, contrast studies of the whole bowel, nuclear medicine studies, laparoscopy with or without laparotomy

Should be performed within 24 h in appropriately equipped unit Will give the diagnosis in 80% of patients Will miss the diagnosis in 20% because: Large amounts of blood in stomach obscure the view Lesion is missed Lesion has healed Source of bleeding is more distal than the duodenum Can be used to control the bleeding by: Injection therapy: vasopressors, sclerosants, thrombin, mixtures Banding: oesophageal varices H-F electrocoagulation Heater probe Photocoagulation

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Fluids, Electrolytes, pH Balance and Nutrition Introduction, 148 Fluid and electrolytes, 148

Acid–base balance, 152

Must know Must do

Must know Composition and distribution of fluids and electrolytes in healthy subjects Clinical features, diagnosis and management of fluid and electrolyte disorders Clinical features, diagnosis and management of disorders of acid–base balance Clinical features, diagnosis and management of nutritional disorders Common crystalloid and colloid solutions used in surgical wards At least one enteral feeding regimen Core knowledge of parenteral feeding and its complications

Nutrition, 155

to comprise three spaces: the intracellular and extracellular spaces, which are physiological; and the ‘third space’, representing fluid accumulation in disease leading to dehydration, which is pathological (Fig. 13.1). The intracellular compartment is the largest fluid compartment, with a volume of 22–30 L. The extracellular compartment is composed of the plasma or intravascular compartment (3 L) and the interstitial space (10–12 L). Normally, there is a continuous bidirectional movement of water between the plasma and the interstitial fluid across the capillary bed. This movement is governed by the hydrostatic pressure at the arteriolar end of the capillary and the oncotic pressure of plasma at the venular extremity. The exchange of fluid across the capillary membrane is, of course, essential for the supply of nutrients and oxygen to the tissues and the elimination of waste products of metabolism.

Must do Participate in the fluid and electrolyte management of patients after major surgery Undertake clinical nutritional assessment of patients Calculate the body mass index of patients Observe and follow patients on parenteral nutrition Observe and follow patients on enteral nutrition

Introduction Surgical illness and operative intervention disrupt homeostasis and lead to changes in fluid, electrolyte and acid– base balance. A grasp of the surgical physiology involved is vital for understanding the principles of preoperative and postoperative care. The monitoring and alteration of fluid and acid–base status comprise the principal aspects of the care of surgical patients.

Fluid and electrolytes Distribution Water constitutes approximately 70% of lean tissue mass, the value varying with age, sex and patient circumstances. In general, fluid distribution in a patient can be considered 148

Connective tissue 3L

Plasma 3L

Interstitial fluid 10L

Intracellular fluid 24L

Na+

K+

Bone 3L

Pathological – 3rd space

Figure 13.1 Extracellular and intracellular compartments of the body in a 70-kg man.

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Table 13.1 Daily requirements of a normal 70-kg man. Input

Volume (mL)

Output

Volume (mL)

Oral liquids Water in food Water of oxidation

1500 1000 300

Urine Stool Lungs Skin

1500 300 500 500

Total

2800

149

resuscitation. • Postoperative Electrolyte disorders. • Thus patients not eating or drinking must be provided with their daily requirements, i.e. 2.5–3 L of water, 100 mmol Na+ and 60 mmol K+.

Types of fluids

2800 Crystalloids Normal saline Dextrose saline Hartmann’s solution

The osmolality (total particle concentration) is the same in all the fluid compartments and is normally 280– 295 mosmol/kg H2O. In contrast, the electrolyte composition of the intracellular compartment is very different from that of plasma and interstitial fluid. The main cation [positively charged atom attracted to a negative electrode (cathode)] in the plasma is Na+ and the accompanying anions [negatively charged atoms attracted to a positive electrode (anode)] are Cl– and HCO3–. In the normal state, plasma electrolytes account for the majority of plasma osmolality and there is a good correlation between the plasma concentration of Na+ and plasma osmolality, i.e. a high plasma Na+ signifies hyperosmolality and vice versa. In certain pathological states, the osmolality may also be elevated by the accumulation of large amounts of organic solutes, e.g. excess urea in renal failure and excess glucose in uncontrolled diabetes mellitus.

On the wards you will mainly use crystalloids to provide the normal daily requirement and replace additional losses. Three major types of fluid are used: 0.9% sodium chloride, dextrose saline and 5% dextrose. The composition of these fluids is shown below. 1 L 0.9% sodium chloride contains 153 mmol NaCl. 1 L dextrose saline contains 31 mmol NaCl + 40 g dextrose. 1 L 5% dextrose contains 50 g dextrose. Potassium can be added to these solutions in the form of potassium chloride (KCl).

Fluid and electrolyte balance

Fluid replacement regimens

Table 13.1 shows the inputs and outputs of 70-kg man in homeostasis. As a rule of thumb, the daily (24-h) requirements of an average subject are 100 mmol (2 mmol/kg) Na+ and 60 mmol (1 mmol/kg) K+.

There are two major regimens used (Fig. 13.2a,b). If the patient is also losing additional fluid (e.g. vomiting, nasogastric tube, ileostomy), then this volume must also be measured and replaced over and above the normal requirements using normal saline. Fluid status is judged by examination of the patient every day: check for signs of dehydration; check blood pressure and pulse; examine the abdomen and chest; check the ankles for oedema. The fluid balance chart should be examined to determine the patient’s fluid input and output. The hourly urine output is a good guide to fluid status; urine output should not fall below 30 mL/h. In most cases, the urine output falls because the patient is volume depleted.

Intravenous fluid therapy During your time on the wards you will always see patients on drips; when you are a house officer, you will be responsible for siting the drip and managing the fluids from day to day. Intravenous fluid therapy is used extensively in surgery; indeed it is of vital importance that patients are adequately resuscitated prior to surgery, especially in the emergency situation. The indications for fluid therapy are as follows. Preoperative resuscitation, e.g. before emergency surgery, elective surgery in a jaundiced patient. Replacement of abnormal losses, e.g. vomiting, diarrhoea, ileostomy bags. Provision of normal daily requirements if patient is nil by mouth.

• • •

Colloids Natural, e.g. blood, albumin Synthetic, e.g. gelatin-based infusions

• • •

• • • •

Other fluids encountered in practice

•

Hartmann’s solution is the replacement fluid favoured by anaesthetists because it is a physiological mixture of

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0.9% NaCl + 20 mmol KCl

5% Dextrose + 20 mmol KCl

Assessment of adequacy of resuscitation

• • • •

Clinical history and observations: pulse, blood pressure, skin turgor. Urine output: oliguria defined as < 0.5 mL/kg per h Central venous pressure (CVP) or pulmonary capillary wedge pressure. Response of urine output or CVP to fluid challenge: (a) 200–250 mL bolus of colloid administered as quickly as possible; (b) response in CVP or urine output should be seen within minutes; (c) size and duration of the CVP response rather than actual value recorded is more important.

(a) Dextrose saline + 20 mmol KCl

Dextrose saline + 20 mmol KCl

(b)

Figure 13.2 (a) Regimen for the normal daily fluid requirement that includes 1 L of 0.9% sodium chloride and 2 L of 5% dextrose with KCl added to each bag. (b) An alternative prescription of the normal daily fluid requirement in the form of 3 L of dextrose-saline with added KCl.

ions and water: 1 L Hartmann’s solution contains 2 mmol Ca2+, 5 mmol K+, 29 mmol HCO3–, 110 mmol Cl– and 131 mmol Na+. All the solutions described so far have been crystalloids and are not confined to the intravascular compartment. On occasions, for example if a patient is shocked due to haemorrhage, fluid replacement of the intravascular compartment is essential. In these circumstances, gelatin colloid solutions are used. These are solutions of saline and gelatin: 1 L synthetic colloid contains 35 g gelatin, 6.25 mmol Ca2+, 145 mmol Cl– and 145 mmol Na+. Because gelatin has a high molecular weight, it is confined to the intravascular compartment and thus acts as a plasma expander.

•

Fluid and electrolyte disturbances Water Water intoxication This condition is rare and is caused by the administration of excessive amounts of 5% dextrose, especially in the presence of impaired renal function. Occasionally, it is associated with excessive secretion of antidiuretic hormone (ADH). There is an expansion of the intracellular and extracellular fluid compartments, a low serum Na+ and widespread oedema. Irritability, drowsiness, convulsions and coma may occur. Treatment is by water restriction and sometimes administration of hypertonic saline. Water depletion Inadequate intake of water leads to dehydration and raised plasma Na+ (hypernatraemia), with a rise in the osmolality of body fluids. Despite increased reabsorption of water by the kidneys, there is contraction of both the extracellular and intracellular fluid compartments. Clinically there is thirst, drowsiness and coma. Treatment consists of slow intravenous replacement with hypotonic saline solution. Rapid intravenous infusion with 5% dextrose is contraindicated as it will cause water intoxication with coma and convulsions.

Sodium Hypernatraemia Hypernatraemia may be due to excessive administration of Na+ (usually iatrogenic from infusion of excessive amounts of Na+ in intravenous fluids) or dehydration due to decreased fluid intake or water loss. The osmotic pressure of the extracellular fluid rises and the clinical picture is similar to that of water depletion (see above). Rarely, hypernatraemia is caused by primary hyperaldosteronism (Conn’s syndrome, see Chapter 34). If the serum Na+ rises above 160 mmol/L, hypernatraemic encephalopathy may

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Table 13.2 Inappropriate antidiuretic hormone secretion. Cranial Head injury, e.g. base of skull fracture Cerebral metastases Peripheral Carcinoma of the lung Bronchial carcinoid Tuberculosis Pneumonia Prostatic carcinoma Pancreatic carcinoma Lymphomas

and sunken eyeballs. If Na+ levels decrease below 110 mmol/L, convulsions and coma may ensue. Therapy for hyponatraemia is directed at the underlying cause. Losses of Na+ can be replaced by increasing Na+ intake without increasing daily fluid intake (e.g. giving normal saline continuously); water retention should be treated by fluid restriction.

Potassium

occur. Treatment of hypernatraemia is by slow intravenous replacement with hypotonic saline solution. Hyponatraemia Deficiency of Na+ is the most common acute biochemical disturbance encountered in surgical practice. The common causes of hyponatraemia (i.e. serum Na+ < 130 mmol/L) are listed below. Na+-rich losses from the gastrointestinal tract, e.g. vomiting, diarrhoea, intestinal obstruction. Renal Na+ loss, e.g. Addison’s disease. Diuretic use, particularly those that promote natriuresis, e.g. furosemide and the thiazide diuretics. Prolonged infusion of dextrose 5% alone. Transurethral resection of the prostate (TURP). Cardiac failure and cirrhosis of the liver. Inappropriate ADH secretion (Table 13.2). In its most usual mild form, hyponatraemia is asymptomatic. When plasma Na+ falls below 120 mmol/L patients become confused. There is severe contraction of the extracellular fluid compartment, with hypovolaemia, poor venous filling, oliguria, dry skin with loss of turgor

• • • • • • •

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Hyperkalaemia An elevated serum K+ is encountered in acidotic, hypoxic and ischaemic states. In these conditions K+ is released from cells. However, the most common cause of hyperkalaemia is K+ retention due to renal failure. Clinically, hyperkalaemia is associated with diarrhoea, colicky abdominal pain and peaked T waves on the electrocardiogram (ECG) (Fig. 13.3). Irrespective of cause, a serum K+ concentration above 6 mmol/L may precipitate a cardiac arrest (usually ventricular fibrillation). The treatment of hyperkalaemia entails correction of the underlying cause, together with measures designed to reduce the level of plasma K+: administration of intravenous calcium gluconate or sodium bicarbonate or insulin and glucose (the latter two act by promoting the movement of K+ into cells); administration of the cation-exchange resin calcium resonium by mouth or as an enema is also effective in removing excess body K+; severe hyperkalaemia associated with renal failure is an indication for dialysis.

• • •

Hypokalaemia A low serum K+ is encountered in pyloric stenosis, high jejunal obstructions, liver failure and diarrhoea from any cause. Rarely, hypokalaemia is caused by primary hyperaldosteronism (Conn’s syndrome). Clinically, hypokalaemia is characterized by lethargy, muscle weakness,

U T

Figure 13.3 Typical ECG changes associated with hyperkalaemia and hypokalaemia.

Hyperkalaemia showing peaked T waves

Hypokalaemia with prolonged P-R interval, T-wave inversion and U-waves

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adynamic ileus and life-threatening ventricular arrhythmias that may progress to cardiac arrest in asystole. The ECG shows a prolonged PR interval, T-wave inversion and classical U waves. Hypokalaemia is always accompanied by a metabolic alkalosis (see later). This is due to increased reabsorption of HCO3– and excretion of H+ from the proximal tubules of the kidney. The correction of hypokalaemia has to be done gradually. If hypokalaemia is severe, intravenous KCl in a concentration of not more than 40 mmol/L may be administered. Such therapy should be monitored by ECG as severe cardiac arrhythmias may be encountered and require temporary interruption of the infusion.

Calcium

The normal range of total calcium concentration is 2.2– 2.6 mmol/L. Calcium is usually bound to albumin, and the levels of both calcium and albumin should be measured together. (To correct for low serum albumin, 0.025 should be added to the serum calcium for every 1 g/L that the albumin is lower than 40 g/L.) The box below summarizes the common causes of hypocalcaemia and hypercalcaemia. Hypercalcaemia Hypercalcaemia is usually asymptomatic below a serum concentration of 3.5 mmol/L. Above this level, clinical

Common causes of hypocalcaemia and hypercalcaemia Hypercalcaemia Absorption induced Vitamin D excess Milk alkali syndrome Sarcoidosis Drugs, e.g. thiazides

Hypocalcaemia Hypoproteinaemia Vitamin D deficiency Parathyroidectomy Acute pancreatitis Medullary carcinoma of thyroid Idiopathic

Bone disease Secondary tumour deposits Myeloma Lymphoma Paget’s disease Endocrine Hyperparathyroidism Ectopic parathyroid hormone (PTH) production Thyrotoxicosis Addison’s disease

features include muscle weakness, lassitude, drowsiness and hyperreflexia. Anxiety and mania may develop, with coma as a terminal event. Polyuria and polydipsia indicate impaired renal concentration. Nausea, vomiting, constipation and peptic ulceration may also occur. Treatment is directed at dealing with the underlying cause, although rapid reduction of serum calcium levels can be achieved by hydration with saline, calciuresis with diuretics (furosemide), steroids and specific drugs, e.g. mithramycin, calcitonin, ethylenediaminetetraacetic acid (EDTA) and bisphosphonates. Hypocalcaemia Hypocalcaemia (serum Ca2+ < 2 mmol/L) results in a dramatic clinical picture characterized by tetany. In its mildest form, there may be paraesthesiae and muscle cramps. The full-blown picture is characterized by hyperexcitability of the nervous system, most commonly expressed as carpopedal spasm. This consists of severe tonic contractions of the muscles of the hand; the fingers are bunched together and flexed at the metacarpophalangeal joints and the wrist is acutely flexed (main d’accoucheur). Similarly, the toes are flexed and the ankle joint acutely plantar flexed. Latent tetany may be demonstrated by Chvostek’s sign (tapping over the facial nerve induces twitching of the facial muscles) and Trousseau’s sign (carpal spasm induced by inflating a sphygmomanometer cuff above systolic pressure). Acute hypocalcaemia is treated by slow intravenous infusion of calcium gluconate (10% solution).

Acid–base balance The pH is the negative logarithm of the hydrogen ion (H+) concentration in the body fluids. Maintenance of a blood pH between 7.37 and 7.42 is essential for normal metabolic activity. As normal metabolism results in the generation of acids (e.g. lactic acid), particularly during physical exertion, efficient compensatory mechanisms are invoked to prevent any significant deviations in the pH. These compensatory mechanisms include those listed below. Buffer systems: intracellular buffers are proteins and phosphates while blood buffers are bicarbonate and haemoglobin. Lungs: overall regulation of pH consists of immediate buffering of acid metabolites, followed by pulmonary excretion of H+ as water and carbon dioxide (CO2). Kidneys: renal regulation of pH is achieved mostly by retention or excretion of HCO3–. The lungs and kidneys act in concert such that in the presence of mild renal impairment, increased acid removal is achieved by the lungs and vice versa.

• • •

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Fluid and electrolytes at a glance Definitions Homeostasis: the self-regulating feedback process that maintains internal stability in biological systems such as the human body Mole: the amount of a substance that contains the same number of elementary particles (atom, ion, molecule) as there are atoms in 0.012 kg of carbon 12 Osmole: the standard unit of osmotic pressure (= molecular weight of dissolved substance in grams divided by number of particles into which the molecule dissociates in solution). Serum osmolality indicates the concentration of solutes in the serum and is expressed as milliosmoles per kilogram of water. The normal osmolality of body fluids is 280–295 mosmol/kg H2O

anion is a negatively charged ion that has gained an electron, e.g. Cl–, HCO3– Fluid and electrolyte distribution and daily requirements Fluid compartment

Volume (L)

Main cation

Extracellular Intravascular Interstitial Intracellular

3 10–12 22–30

Na+ Na+ K+

Daily requirements Water: 2.5–3 L Na+: 2 mmol /kg (~ 100 mmol) K+: 1 mmol/kg (~ 60 mmol)

Ion: an electrically charged atom. A cation is a positively charged atom that has lost an electron, e.g. Na+, K+. An Fluid therapy

Indications

Types of fluid

Composition (per L)

Preoperative resuscitation Replacement of abnormal losses Provide normal daily requirements Correct electrolyte disorders

Crystalloids Normal saline Dextrose 5% Dextrose-saline Sodium lactate (Hartmann’s solution) Colloids Natural: blood, albumin Synthetic (Gelofusine, Haemaccel)

Typical daily fluid replacement regimens Regimen 1 • 1 L 0.9% NaCl + 20 mmol K+ over 8 h plus

153 mmol NaCl 50 g glucose 31 mmol NaCl + 40 g glucose 131 mmol Na+ + 5 mmol K+ + 2 mmol Ca2+ + 29 mmol HCO3– (as lactate) + 111 mmol Cl–

35 g gelatin + 145 mmol Na+ + 145 mmol Cl– + 6.25 mmol Ca2+

• 2 L 5% dextrose + 40 mmol K+ each litre over 8 h Regimen 2 • 3 L dextrose-saline + 60 mmol K+ over 8 h

Fluid and electrolyte disturbances Disturbance

Cause

Findings

Treatment

Water intoxication

Excess administration of 5% dextrose Excess secretion of ADH

Oedema, confusion, coma, convulsions, low serum Na+

Water restriction Rarely hypertonic saline is given

Water depletion

Inadequate intake of water

Thirst, drowsiness, coma, oliguria Raised serum Na+, urea and haematocrit

Slow i.v. replacement with hypotonic saline solution

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Disturbance

Cause

Findings

Treatment

Hypernatraemia

Dehydration Iatrogenic: excess i.v. saline Primary hyperaldosteronism (Conn’s syndrome)

Similar to water depletion Serum Na+ > 160 mmol/L causes hypernatraemic encephalopathy

Slow i.v. replacement with hypotonic saline solution

Hyponatraemia (most common disturbance seen in surgical practice)

GI: vomiting, diarrhoea Renal: Addison’s disease Diuretics: furosemide Excess i.v. 5% dextrose TURP Cardiac failure, cirrhosis Inappropriate ADH secretion

Na+ < 130 mmol/L: asymptomatic Na+ < 120 mmol/L: confusion, contraction of ECF space, oliguria, hypovolaemia, dry skin, loss of turgor, sunken eyeballs Na+ < 110 mmol: convulsions, coma

Treat the cause Give daily fluid requirement as i.v. normal saline Rarely hypertonic saline is given Water retention treated by fluid restriction

Hyperkalaemia

Renal failure Acidosis, hypoxia, ischaemia

Diarrhoea, colicky abdominal pain, peaked T waves on ECG K+ > 6 mmol/L: cardiac arrest (VF)

Treat the cause Give i.v. calcium gluconate or NaHCO3, i.v. insulin and dextrose Give calcium resonium p.o. or p.r. Dialysis

Hypokalaemia

Pyloric stenosis High jejunal obstruction Liver failure Diarrhoea Primary hyperaldosteronism (Conn’s syndrome)

Lethargy, muscle weakness, ileus Prolonged PR interval, T-wave inversion, U waves on ECG Cardiac arrest (asystole) Metabolic alkalosis

Replace K+ gradually If severe give KCl i.v. (≤ 40 mmol/L) Monitor ECG for arrhythmias during therapy

Hypercalcaemia

Absorption induced Excess vitamin D, sarcoidosis, milk alkali syndrome, drugs Bone disease Bony metastases, myeloma, lymphoma, Paget’s disease Endocrine Hyperparathyroidism, ectopic PTH production, Addison’s disease, thyrotoxicosis

Muscle weakness, lassitude, drowsiness, hyperreflexia Polydipsia, polyuria Nausea, vomiting, peptic ulceration Anxiety, mania, coma (terminal)

Treat the cause Hydration with saline Calciuresis (furosemide) Steroids Specific drugs, e.g. mithramycin, EDTA, calcitonin, bisphosphonates

Hypocalcaemia

Hypoproteinaemia Vitamin D deficiency Parathyroidectomy Acute pancreatitis Thyroid medullary carcinoma Idiopathic

Tetany: paraesthesiae, muscle cramps, carpopedal spasm, Chvostek’s (face) and Trousseau’s (hand/foot) signs

Slow i.v. infusion of 10% calcium gluconate solution

ECF, extracellular fluid; GI, gastrointestinal; VF, ventricular fibrillation.

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Acidosis/alkalosis

Blood gas changes

Certain disease states overwhelm these homeostatic mechanisms and result in significant accumulation of acid or base, with corresponding deviations from normal pH. Acidaemia occurs when the pH falls below 7.36 and alkalaemia when the pH exceeds 7.44. Acidaemia, which signifies an excess of unbuffered H+ in the blood and body fluids, is the more common disorder of acid–base balance. The compensatory mechanisms of the body try to normalize the pH in these situations and are reflected in changes in the blood gas analysis, from which the diagnosis of acidosis (tendency to low pH) and alkalosis (tendency to high pH) is made (see box below).

The blood gas analysis also provides the clinician with information about the metabolic or respiratory origin of the acid–base disturbance in an individual patient. This distinction is based on the relationship between the changes in pH and Paco2. When the pH change occurs in the opposite direction to Paco2 (i.e. pH down and Paco2 up), the underlying cause is respiratory impairment. In contrast, in metabolic disturbances, the pH change occurs in the same direction as the Paco2 (alkalosis, both up; acidosis, both down). The base excess is derived from the difference between the patient’s standard bicarbonate and the normal mean and is a good indicator of metabolic disturbances. A base deficit of –5 to –10 mmol/L is present with metabolic acidosis (this is sometimes confusingly expressed as a ‘base excess of –5 to –10 mmol/L’). With metabolic alkalosis, there is a base excess of +5 to +10 mmol/L. Thus from the blood gas analysis it is possible to calculate whether the patient is acidotic or alkalotic and whether the abnormality is metabolic or respiratory.

Common causes of acidosis and alkalosis and the blood gas findings typical of each abnormality Metabolic acidosis Causes Hypoxic causes Lactic acidosis Non-hypoxic causes Ketoacidosis Excess HCO3– loss Renal failure Drugs (e.g. salicylates)

Metabolic alkalosis Causes Excess H+ loss Nasogastric suction Vomiting Hypokalaemia Excess alkali NaHCO3 ingestion Diuretics Excess citrate

Blood gas picture pH < 7.36 (H+ > 44 nmol/L) PaCO2 < 4.7 kPa HCO3– < 18 mmol/L Base excess < –5 mmol/L

Blood gas picture pH > 7.44 (H+ < 36 nmol/L) PaCO2 > 6.0 kPa HCO3– > 32 mmol/L Base excess > +5 mmol/L

Respiratory acidosis Causes Decreased CO2 excretion Hypoventilation Ventilation–perfusion mismatch Airway obstruction Increased CO2 excretion Hypermetabolism

Respiratory alkalosis Causes Hyperventilation Apprehension Hysteria CNS injury Mechanical ventilation

Blood gas picture pH < 7.38 (H+ > 44 nmol/L) PaCO2 > 5.7 kPa HCO3– 22 mmol/L Base excess –2 mmol/L

Blood gas picture pH > 7.42 (H+ < 36 nmol/L) PaCO2 < 5.3 kPa HCO3– 22 mmol/L Base excess +2 mmol/L

Nutrition Malnutrition is recognized as an important factor affecting the outcome of many surgical patients. A malnourished patient has a significantly impaired immune system, delayed wound healing and reduced strength that manifests itself as decreased ventilatory function. Modern management of surgical patients places increasing importance on adequate nutrition. The current areas of intense discussion are when and how nutrition should be administered and how it changes outcome.

Nutritional assessment of the surgical patient (Fig. 13.4) Previously, the assessment of nutritional status was performed from the end of the bed by observing the patient’s general condition. This may still be useful, although there are more objective assessment parameters that can be used. 1 Clinical findings: history and examination, regular weights, body mass index. 2 Anthropometric measurements: skinfold thickness (e.g. triceps, iliac crest), arm circumference, grip strength. 3 Blood tests: serum albumin, serum transferrin, lymphocyte count.

Nutritional requirements As with fluid requirements, the nutritional status and the requirements of the patient will change according to the state of health. In the surgical patient the aim is to prevent

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pH balance at a glance Definitions pH: negative logarithm to the base of 10 of the free hydrogen ion concentration [H+] in moles per litre (pH = –log[H+] ). It is expressed as a positive number that describes the acidity or alkalinity of a chemical solution on a scale of 0 (acidic) to 14 (alkaline). The normal pH of body fluids is maintained between 7.3 and 7.5 Acidosis: accumulation of H+ ions in the extracellular fluid resulting in a fall of pH below 7.36

Alkalosis: accumulation of base in the extracellular fluid resulting in an elevation of pH above 7.44 Buffer system: one that keeps the concentration of H+ relatively constant. Intracellular H+ buffers are proteins and phosphates; H+ buffers in blood are HCO3– and haemoglobin. The lungs (by excreting H+ as H2O and CO2) and the kidneys (by retaining or excreting HCO3– ) also control H+ levels and thereby the pH

Acid–base disturbance

Causes

Blood gas picture

Treatment

Metabolic acidosis

Lactic acidosis Ketoacidosis Excess HCO3– loss Renal failure Drugs

pH < 7.36 PaCO2 < 4.7 kPa HCO3– < 18 mmol/L Base excess < –5 mmol/L

Treat underlying cause Sodium bicarbonate

Metabolic alkalosis

H+ loss Nasogastric suction Vomiting Hypokalaemia Excess alkali NaHCO3 ingestion Diuretics Excess citrate

pH > 7.44 PaCO2 > 6.0 kPa HCO3– > 32 mmol/L Base excess > +5 mmol/L

Treat underlying cause Isotonic sodium chloride i.v. and correction of hypokalaemia if present

Respiratory acidosis

Hypoventilation Ventilation–perfusion mismatch Airway obstruction Hypermetabolism

pH < 7.38 PaCO2 < 5.7 kPa HCO3– 22 mmol/L Base excess –2 mmol/L

Treat underlying cause

Respiratory alkalosis

Hyperventilation Apprehension Hysteria CNS injury Rapid-rate mechanical ventilation

pH > 7.42 PaCO2 > 5.3 kPa HCO3– 22 mmol/L Base excess +2 mmol/L

Treat underlying cause

depletion of protein stores as a result of increased catabolism, which can lead to a negative nitrogen balance. The average carbohydrate stores are depleted in 24 h, while protein and fat stores are depleted over the following month. The daily calorie requirement for an adult is approximately 25–35 kcal/kg (105–147 kJ/kg); younger patients require higher calories per kilogram than older ones. However in some patients, e.g. those with severe burns, calorie requirements may increase by 100% above basal resting values. The protein requirement for an adult is 1–1.5 g/kg

daily; since 6.25 g of protein provide 1 g of nitrogen, the average nitrogen requirement is approximately 12 g/day.

Delivery of nutritional therapy Enteral nutrition Enteral nutrition is preferred for the patient unable to maintain an adequate oral intake but who has a functioning gastrointestinal tract that can be used safely. Early

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Evaluation of the patient

Mild/moderate malnutrition

Moderate/severe malnutrition

Oral feeding is possible? Yes No Oral supplements

Does the GI tract function? Yes

Finebore feeding tube Gastrostomy Jejunostomy

No Peripheral TPN Central line TPN Tunnelled central line TPN

Figure 13.4 Overview of surgical nutrition.

enteral nutrition has been advocated in order to preserve intestinal structure and the role of the intestine in immune function. The absence of enteral feeding is related to villous and cellular atrophy. Enteral feeding can be done initially by providing supplement drinks. If this is not sufficient, then an elemental diet can be given through a fine-bore nasogastric tube placed directly into the stomach or small bowel. These types of feeds (e.g. Osmolite) provide approximately 1912 kcal (8000 kJ) of energy plus about 70 g of protein in 2–3 L. Types of feed Polymeric (near-normal composition). These contain intact proteins, starches and long-chain fatty acids. They are useful in patients who have a functioning stomach and normal digestive capacity. Disease specific. These are feeds tailored to meet the requirements of specific diseases, e.g. feeds for patients with liver disease are deficient in branched-chain amino acids, which can exacerbate encephaolopathy. Elemental. These are chemically defined feeds that contain simple amino acids, oligosaccharides and monosaccharides. These require minimal digestion and are useful in patients with intestinal fistulae but are far from palatable.

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Methods of administration Apart from oral supplementation, enteral feed can be delivered through enteral tubes. Enteral nutrition can also be given via: gastrostomy: surgical or endoscopic (percutaneous endoscopic gastrostomy); jejunostomy: surgical.

• •

Indications Long-term feeding Dysphagia, e.g. stricture, stroke Chronic disease, e.g. neoplasia Malnutrition Sepsis Burns Major surgery Coma/ICU

• • • • • • • •

Complications Diarrhoea and vomiting Malposition or blocking of tube Feed intolerance Electrolyte imbalance Aspiration

• • • • •

Total parenteral nutrition Total parenteral nutrition (TPN) can be given via a large peripheral vein or a central venous channel. Indications Severe malnutrition Inability to swallow, e.g. oesophageal tumour Prolonged obstruction, high-output fistula Sepsis Burns where upper gastrointestinal tract is severely damaged Severe pancreatitis Prolonged ileus Short bowel syndrome Severe Crohn’s disease

• • • • • • • • •

Complications Pneumothorax/haemothorax Cardiac tamponade Sepsis, e.g. Staphylococcus epidermidis, Candida, Pseudomonas Mineral overload Reactive hypoglycaemia Vitamin and mineral deficiencies

• • • • • •

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Nutrition at a glance Definitions Nutrition: the process of utilizing exogenous substances for the production of energy and the synthesis of new tissue

• Weight measurement • Body mass index

Food: any substance that can be used by the body to produce energy or some essential nutrient

Anthropomorphic • Skinfold thickness • Arm circumference • Grip strength

Adverse surgical effects of poor nutrition • Impaired immunity • Delayed wound healing • Decreased respiratory function • Reduced muscle strength

Blood tests • Serum albumin • Serum transferrin • Lymphocyte count

Methods of assessing nutritional status Clinical • History and examination

Daily nutritional requirements • Calories 25–35 kcal/kg (105 –147 kJ /kg) • Protein 1–1.5 g/kg • Nitrogen 12 g

Delivery of nutrition Type

Enteral Polymeric: near-normal Disease specific: tailored for patients with specific diseases Elemental: requires minimal digestion Total parenteral nutrition

Administration

Indications

Complications

Orally Gastrostomy Jejunostomy

Long-term feeding Dysphagia: stricture, stroke Chronic disease: neoplasia Malnutrition Sepsis/burns/major surgery Coma/ICU

Diarrhoea and vomiting Malposition or blocking of feeding tube Intolerance to feed Electrolyte imbalance Aspiration ± pneumonia

Central line via internal jugular or subclavian vein

Severe malnutrition Inability to swallow Prolonged intestinal obstruction/ileus High-output intestinal fistula Sepsis Burns involving upper gastrointestinal tract Severe pancreatitis Short bowel syndrome Severe Crohn’s disease

Pneumothorax Haemothorax Cardiac tamponade Line sepsis Mineral overload Reactive hypoglycaemia Vitamin deficiency Mineral deficiency

Evidence-based medicine Halperin, M.L. & Goldstein, M.B. (1999) Fluid, Electrolyte and Acid–Base Physiology: A Problem-based Approach, 3rd edn. W.B. Saunders. Lefever Kee, J. & Paulanka, B.J. (1999) Fluids and Electrolytes with Clinical Applications: A Programmed Approach. Thompson Learning.

Pestana, C. (2000) Fluids and Electrolytes in the Surgical Patient. Lippincott, Williams & Wilkins. http://www.virtual-anaesthesia-textbook.com http://www.medstudents.com.br http://www.family.georgetown.edu http://www.familypracticenotebook.com

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Acute Renal Failure

Introduction, 159 Classification, 159

Pathophysiology, 159 Clinical features, 160

Must know Must do Must know Causes, types and management of ARF List of commonly used drugs, including antibiotics and analgesics, known to cause renal damage Principles of renal replacement therapy Must do Clerk patients with chronic renal disease/failure Follow patients being treated for ARF Become familiar with the biochemistry of renal failure Become proficient in catheterizing male and female patients Observe patients undergoing haemodialysis and haemofiltration Observe cadaveric-donor and living-donor-related renal transplantation

Management, 161 Prognosis, 163

types of renal failure usually encountered following surgery. The causes of prerenal ARF are shown in Table 14.1. Prerenal ARF can progress to ATN (intrinsic ARF) if the underlying cause is not reversed promptly, although instrinsic ARF may arise directly from other causes (shown in Table 14.2). Postrenal failure, which results from obstruction to urinary flow, is categorized as obstructive uropathy (see Chapter 39). When the kidney is obstructed, glomerular function does not cease completely because the filtrate is reabsorbed by the renal lymphatics and veins. Unrelieved, obstruction leads to ischaemic renal damage mediated by vasoactive hormones including renin, angiotensin, endothelin, etc. Return to useful function depends on duration/degree of obstruction and the presence/absence of infection above the obstruction. Following relief of obstruction, recovery of tubular function lags behind restoration of glomerular filtration rate (GFR), resulting in a diuresis.

Introduction

Pathophysiology

Acute renal failure (ARF) is defined as the rapid onset of renal impairment resulting in the accumulation of nitrogenous waste products, i.e. urea and creatinine, within the body. The process may become irreversible because of: pre-existing renal damage (acute-on-chronic renal failure); irreversible damage; delays in treatment. Acute tubular necrosis (ATN) is used to denote ARF where there is intrinsic but reversible damage to the kidney. ARF commonly presents with sudden anuria (no urine) or oliguria (< 400 mL/day). However, non-oliguric renal failure may also occur and is recognized by a persistently rising serum creatinine level in the presence of normal output of urine.

ARF may occur as a consequence of shock. The reduction in circulating blood volume produces a significant decrease in renal blood flow, which may fall to one-third of its normal level. The GFR is correspondingly reduced and the patient becomes oliguric, producing only 400 – 700 mL of urine per 24 h, or less than 20 mL/h. When oligaemic states cause a reduction in renal blood flow, additional changes take place. There is a diversion of blood from the renal cortex and this exacerbates the situation by causing a further reduction in GFR. If the impairment in renal blood flow is of brief duration and blood volume is restored rapidly, the condition can be reversed and normal urine output resumed, although sometimes there is a lapse of some hours before this takes place. A more prolonged ischaemic insult causes ATN, with oliguria persisting for 1 to 3 or 4 weeks, followed by a period of diuresis when large volumes of dilute urine are passed each day. More profound ischaemia gives rise to cortical necrosis, an irreversible condition requiring renal dialysis and eventually renal transplant.

• • •

Classification Renal failure may be classified into prerenal, intrinsic and postrenal (Fig. 14.1). Prerenal oliguria and ATN are the

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Prerenal failure Caused by reduced renal perfusion No renal parenchymal damage Rapidly reversed with fluid therapy

Intrinsic renal failure Caused by renal ischaemia secondary to hypovolaemic or endotoxic shock Caused by nephrotoxins e.g. aminoglycosides, ethylene glycol, myoglobin Renal parenchymal damage (acute tubular necrosis) occurs Is recoverable following oliguric and diuretic phases

Postrenal failure

Caused by obstruction to urinary flow in the urinary tract Exacerbated by the presence of infection If unrelieved parenchymal damage can occur Figure 14.1 Classification of renal failure.

Table 14.1 Aetiology of prerenal acute renal failure. Reduced cardiac output Acute myocardial infarction Cardiac arrest Cardiac failure Significant valvular disease Cardiac tamponade Depleted circulating volume Sepsis Haemorrhage Hypoalbuminaemia Depleted extracellular fluid volume Loss from gastrointestinal tract with diarrhoea, vomiting Loss from urinary tract due to excessive diuresis Loss from skin/body surface associated with sweating and burns Vascular disease Renal artery thrombosis/embolism

Once ARF becomes established, serious water and electrolyte disturbances occur. During the oliguric phase, water retention with a relatively low Na+ may precipitate cardiac failure, accompanied by pulmonary and systemic oedema. The degree of dyspnoea may be sufficiently severe to warrant ventilatory support. Inability to excrete K+ leads to dangerously high plasma levels, which may give rise to arrhythmias and, if uncontrolled, to cardiac arrest. Retention of H+ ions precipitates metabolic acidosis. At first, hyperventilation and respiratory alkalosis compensate for this but these mechanisms eventually fail and the pH of the blood falls rapidly. This phase may be exacerbated by respiratory failure and a developing lactic acidosis. Both the blood urea and serum creatinine levels progressively increase and calcium levels may fall.

Clinical features

•

Dyspnoea is a frequent problem and in some patients respiratory failure may require intermittent positivepressure ventilation (see Chapter 38). The respiratory problems are due to fluid retention, with fluid overload giving rise to pulmonary as well as systemic oedema.

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Table 14.2 Aetiology of intrinsic acute renal failure. Inadequate/delayed treatment of prerenal acute renal failure Most common cause in surgical practice Ischaemia and toxin Hypercalcaemia Hepatorenal syndrome Toxins Aminoglycosides, cephalosporins, paracetamol, salicylates, paraquat, etc. Tubular obstruction Light-chain deposition in myeloma Myoglobinuria (muscle injury, snake bite, heroin, barbiturates) Haemoglobinuria (mismatched blood, nitrofurantoin) Acute interstitial nephritis Antibiotics: penicillin, cephalosporins, co-trimoxazole, vancomycin, rifampicin NSAIDs: mefenamic acid, indomethacin, ibuprofen Diuretics: thiazides, furosemide Other drugs: sulfasalazine, allopurinol, gold, phenytoin Infections: infectious mononucleosis, measles, Legionnaire’s disease, etc. Vascular (endothelial damage) Vasculitis Haemolytic–uraemic syndrome Disseminated intravascular coagulation Accelerated hypertension Primary glomerulonephritis Renal involvement secondary to systemic disease Infection: bacterial endocarditis Shunt nephritis: associated with ventriculoatrial shunts Hepatitis B-associated nephritis Diabetes Vasculitis: Henoch–Schönlein purpura, systemic lupus erythematosus, polyarteritis nodosa, etc. NSAIDs, non-steroidal anti-inflammatory drugs.

Metabolic acidosis (see Chapter 13) and pulmonary infection may contribute further to the respiratory difficulties. Hypertension may also be a consequence of fluid overload and retention of K+ may give rise to arrhythmias. Gastrointestinal symptoms range from nausea and vomiting due to water intoxication to hiccups and diarrhoea, which frequently accompany uraemia. Stress ulceration and gastric erosions are common with ARF following shock, and gastrointestinal haemorrhage may be severe. Cerebral oedema and toxic metabolites cause confusion, drowsiness and eventually coma.

• • •

161

•

A progressive anaemia may develop and coagulation defects may occur. Disseminated intravascular coagulation is a not uncommon development. Finally, there is a generalized impairment of the immune system, increasing the risk of serious infection, which is probably the commonest cause of death in ARF. The indiscriminate use of antibiotics exacerbates this risk by promoting the development of resistant strains of pathogenic bacteria.

•

Management Prevention ARF may be prevented by careful attention to preoperative fluid balance, proper monitoring of the patient peroperatively and avoidance of hypotension and sepsis. Patients at risk of developing renal failure, e.g. those with obstructive jaundice, should have an intravenous infusion established the night before surgery so that they are well hydrated. Remember that patients are starved prior to surgery and will not be allowed oral fluids for about 12 h (but often longer) before surgery. Patients undergoing major surgery should have a urinary catheter for hourly measurement of urine ouput during surgery and in the postoperative period. A central venous line and arterial line are usually inserted by the anaesthetist for haemodynamic monitoring. Some drugs may help to avoid renal failure in certain situations. Dopamine, which at low doses (< 5 µg/kg per min) induces vasodilatation and increased renal perfusion, is frequently given to at-risk patients in an attempt to preserve renal function. Mannitol, an osmotic diuretic, may also protect renal function in some patients, such as those with obstructive jaundice or those at risk of rhabdomyolysis (e.g. following arterial embolectomy). Patients receiving known nephrotoxic drugs should have their renal function monitored regularly. In the case of aminoglycosides, plasma concentrations should be measured 1 h after intramuscular or intravenous administration and just prior to the administration of the next dose. This ensures that excessive and subtherapeutic doses are avoided. For gentamicin, the peak level should not exceed 10 mg/L, while the trough level should be less than 2 mg/L.

Conservative treatment Identification and correction/removal of the cause is essential and any sepsis treated with a third-generation cephalosporin in the first instance. In oliguric patients with adequate circulating volume, intravenous diuretic is administered and may promote a diuresis. Removal of obstruction is necessary in obstructive anuria. The

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Table 14.3 Treatment of hyperkalaemia. 1 10–20 mL of 10% calcium gluconate or chloride i.v.: has no effect on the serum potassium concentration but stabilizes the myocardial membrane 2 50 mL of 50% dextrose i.v. with 10 units of soluble insulin: drives potassium into the cells and should be started directly after step 1 3 200–300 mL of 1.4% sodium bicarbonate i.v.: drives potassium into cells and helps to correct the acidosis of acute renal failure. However, the fluid load necessary makes use of this agent less desirable in hyperkalaemic acute renal failure 4 Calcium resonium 15 g three times daily orally or by enema: binds potassium in the gut and releases calcium in exchange. Unlike the other actions listed this can control the serum potassium for hours to days 5 Dialysis: should be implemented if there is severe hyperkalaemia and/or the patient requires dialysis for other reasons, e.g. fluid overload

conservative management of intrinsic renal failure is only possible when the patient’s condition is not so severe as to warrant immediate renal replacement therapy (RRT). Conservative management consists of: restriction of fluid intake to cover daily estimated losses (insensible perspiration and stools); restriction of first-class protein to 30 g/day to reduce nausea and anorexia; restriction of potassium intake to 20 mmol/day to minimize risk of hyperkalaemia; correction of biochemical abnormalities; maintenance of adequate nutrition, including parenteral nutrition (if required). Hyperkalaemia is the most serious biochemical abnormality since it can cause cardiac arrhythmias and sudden death. Prompt detection and treatment are thus essential (Table 14.3).

• • • • •

Renal replacement therapy Abnormalities of potassium, calcium and phosphate can be corrected by the various forms of RRT using dialysate or replacement solutions. The indications for RRT are: uraemia (significant retention of nitrogenous waste products with associated clinical signs); metabolic acidosis; hyperkalaemia; significant fluid overload.

• • • •

Type of therapy Treatment for the majority of patients with ARF requires adequate vascular access, most commonly achieved using

the internal jugular vein with subclavian or femoral vein as lesser alternatives. The use of the subclavian route carries an increased risk of pneumothorax and venous stenosis. The femoral route is only suitable for short periods because of the high infection rate. Temporary lines may have a single, double or triple lumen. Double- and triplelumen lines are associated with improved clearance of uraemic toxins, and the triple-lumen line allows administration of intravenous therapy without interfering with RRT. The choice is between the following. Haemodialysis: efficient small-molecule and volume removal. Haemofiltration: removes large molecules and volume by convection. Haemodiafiltration: combination of haemodialysis and haemofiltration. Haemofiltration uses a highly permeable synthetic membrane and negative pressure in the dialysate compartment of the dialyser without dialysate flowing such that up to 80 L of fluid are removed from the patient in a 4-h session. Solute removal is by ‘convection’, or passive flow of solute with water. The desired proportion of the filtrate is replaced by infusion usually from preprepared sterile bags of replacement fluid. Convection allows greater removal of solutes in the ‘middle molecular’ range (110–500 Da) but is less efficient at the smaller end of the molecular spectrum, which contains most of the lifethreatening compounds (Fig. 14.2). Haemodialysis is based on diffusion across a semipermeable membrane porous to molecules under 500 Da. It thus exhibits high efficiency with regard to smallmolecule and volume removal and is cost-effective but relies on well-trained personnel (Fig. 14.3). The combination of these two techniques is called haemodiafiltration. With this modality, the benefits of diffusion and convection are combined in a dialysis circuit similar to that used for haemofiltration but with dialysis fluid being pumped round the dialysate circuit. Venovenous haemofiltration requires at least a doublelumen venous line and relies on a pumped system to create a gradient across the filter and hence a filtrate from the patient. If the patient is normotensive, it is possible to use an arterial and venous line to create the pressure gradient across the filter line (arteriovenous haemofiltration), thus removing the need for a pump in the circuit. The choice between these types of support is normally decided by the renal physician and intensivist. All three modalities of RRT can be performed on an intermittent or continuous basis. Haemofiltration and haemodiafiltration are of great value in unstable patients with ARF and in the elderly with cardiac failure and severe arteriosclerosis. Patients with uncomplicated ARF whose cardiovascular system is stable are usually treated with intermittent

• • •

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Blood from patient 30–150 ml/min

Blood to patient

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need for rapid removal of water-soluble substances such as potassium, myoglobin and drugs.

Heparin

Nutritional management

Pump Ultrafiltrate 600 ml/hr

Replacement fluid 450 ml/hr

Figure 14.2 Haemofiltration. In a haemofiltration circuit, blood passes across a filtration membrane. Ultrafiltration rates of 600 mL/h are usual, removing toxins and fluid with a clearance of 10 mL/h. In the intensive care unit, many patients with acute renal failure are managed with continuous venovenous haemofiltration, which requires the use of a pump.

Blood from patient 300 ml/min

Blood to patient

Heparin Pump

(a)

Dialysis fluid 500 ml/min

Nutrition for patients with ARF is extremely important. All patients with dialysis-dependent ARF have higher nutritional requirements than normal, especially if the ARF arises as a complication of other severe illness. These patients have a relative insulin-resistant state, low triiodothyronine, decreased testosterone and increased energy expenditure above expected resting levels. Hyperglycaemia (insulin resistance) is not uncommon and glucose oxidation forms a smaller component of total energy consumption. Lipid and protein metabolism is also disturbed, with increased plasma triglycerides and increased protein catabolism. RRT adds a further strain. Whilst the glucose in haemofiltration fluids provides a large number of calories, amino acids are lost during RRT. The haemodynamic state of the patient may restrict the ability to supply the patient’s nutritional requirements. Patients with ARF have the same daily requirements as other acutely sick patients, i.e. a caloric intake of 35 kcal/kg (147 kJ/kg) body weight and nitrogen 1.2 g/kg body weight, with the ratio between glucose and lipid in the non-protein part of the diet being 70/30.

Diuretic phase As ARF resolves there is often a diuretic phase. This occurs because although filtration is restored, the concentrating ability of the recovering tubules has not. During this phase there is a risk of dehydration. The excessive fluid loss (as much as 20 L/day) must be replaced intravenously until the tubules are able to concentrate the urine. High urinary volumes such as these are unlikely to persist for more than a few days. The diuretic phase of renal failure may last several weeks to months but is usually shorter if patients do not become anuric or severely oliguric. (b) Figure 14.3 (a) Haemodialysis. In a haemodialysis circuit, blood and dialysis fluid circulate in a countercurrent fashion separated by a semipermeable membrane. Blood flow rates of 100–300 mL/min are usual and patients undergo haemodialysis for 3–5 h three times per week. Creatinine clearances are 100–150 mL/min during dialysis or 5 –10 mL/min when calculated for a week. (b) Patient undergoing haemodialysis.

techniques, whereas more unstable patients, in whom fluid removal is more difficult, benefit from continuous therapies. Continuous treatment is especially useful for patients with cerebral oedema or hypoxia. Intermittent haemodialysis is the treatment of choice when there is a

Prognosis The prognosis of ARF depends on the underlying aetiology. The overall mortality has not changed materially during the past three decades and averages 50%. However, the mortality rate associated with certain categories of ARF has improved, e.g. ARF associated with trauma and obstetric disorders. Comorbid disease influences the outcome: ARF in patients nursed in intensive care units has an overall mortality of 70%. For all patients if there is associated failure of one other system the overall patient survival is less than 30% and failure of two systems reduces survival further to less than 10%. Increasing age also impacts adversely on survival.

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Acute renal failure at a glance Definitions Acute renal failure: a sudden deterioration in renal function such that neither kidney is capable of excreting the waste products (e.g. urea, creatinine, potassium) that accumulate in the blood. It is fatal unless treated Anuria: no urine passed Oliguria: urine levels of < 0.5 mL/kg per h passed. Nonoliguric renal failure is characterized by a persistently rising serum creatinine level in the presence of normal output of urine

Classification Prerenal failure (failure to perfuse kidney with blood) • Reduced cardiac output: acute myocardial infarction, cardiac arrest, significant valvular heart disease, cardiac tamponade • Depleted circulating volume: haemorrhage, sepsis, hypoalbuminaemia • Depleted extracellular fluid volume: (a) Gastrointestinal loss: diarrhoea, vomiting (b) Genitourinary loss: diuresis (c) Loss from skin, body surface, peritoneum: sweating/burns/peritonitis • Vascular disease: renal artery thrombosis or embolism Intrinsic renal failure (damage to parenchyma of kidney) • Inadequate/delayed treatment of prerenal failure leading to acute tubular necrosis. (commonest surgical cause) • Ischaemia and toxin: hypercalcaemia, hepatorenal syndrome • Nephrotoxins: aminoglycosides, cephalosporins, paracetamol, salicylates, paraquat • Tubular obstruction: myeloma (light-chain deposition), myoglobinuria, haemoglobinuria • Nephritis: acute glomerulonephritis, pyelonephritis, drugs (antibiotics, NSAIDs, diuretics, sulfasalazine, allopurinol, gold), diabetes mellitus • Vascular endothelial damage: vasculitis, haemolytic– uraemic syndrome, disseminated intravascular coagulation, accelerated hypertension

Outcome Depends on duration of renal impairment: • Short: full recovery • Intermediate: ATN (oliguric phase for 1–3 weeks followed by diuretic phase) • Prolonged: no recovery; requires long-term dialysis and/or renal transplantation Fluid and electrolyte imbalance • Water retention may precipitate congestive cardiac failure with pulmonary and systemic oedema • K+ retention causes hyperkalaemia, leading to arrhythmias and cardiac arrest • H+ retention causes metabolic acidosis. Serum urea and creatinine levels rise, Ca2+ falls Clinical features Specific to the cause • Hypovolaemia: cool peripheries, tachycardia, confusion, restlessness, dry mucous membranes Oliguric phase (may last hours/days/weeks) • Oliguria • Uraemia: (a) dyspnoea, confusion, drowsiness, coma (b) nausea, vomiting, hiccups, diarrhoea (c) anaemia, coagulopathy, gastrointestinal haemorrhage • Fluid retention: hypervolaemia, hypertension • Hyperkalaemia: arrhythmias • Acidosis: metabolic • Anaemia Polyuric (recovery) phase (may last days/weeks) • Polyuria: hypovolaemia, hypotension • Hyponatraemia • Hypokalaemia

Postrenal failure (obstruction to outflow of urine from kidney) • Urinary tract obstruction, e.g. prostatic hypertrophy • Obstructing renal calculi

Investigations • Urinalysis • Urea and electrolytes (especially K+) • Creatinine • ECG/chest X-ray • Arterial blood gases: (a) Normal PO2 (b) Low pH: metabolic acidosis (c) Low PCO2: compensatory respiratory alkalosis (d) High base deficit: metabolic acidosis

Pathophysiology Shock → reduction in circulating blood volume → decreased renal blood flow by 60% → decreased GFR → shunting of blood from renal cortex → oliguria

Management General • Oliguria in a surgical patient is an emergency and the cause must be identified and treated promptly

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• Prompt correction of prerenal causes may prevent the development of established renal failure • Ensure the oliguric patient is normovolaemic as far as possible before starting diuretics or other therapies • Do not use large blind fluid challenges, especially in the elderly; if necessary use a CVP line • Established renal failure requires specialist support as electrolyte and fluid imbalances can be rapid in onset and difficult to manage Prevention • Keep at-risk patients (e.g. obstructive jaundice) well hydrated preoperatively and peroperatively • Protect renal function in selected patients with drugs such as dopamine and mannitol • Monitor renal function regularly in patients on nephrotoxic drugs (e.g. gentamicin) Identification • Exclude urinary retention as a cause of anuria by catheterization • Correct hypovolaemia as far as possible. Use appropriate fluid boluses, if necessary guided by CVP • A trial of bolus high-dose loop diuretics may be appropriate in a normovolaemic patient • Dopamine infusions may be necessary but suggest the need for HDU or ITU care Treatment of established renal failure Conservative • Maintain fluid and electrolyte balance: (a) Water intake: 400 mL/day plus measured losses (b) Na+ intake: limited to replace loss only (c) K+ intake: nil (dextrose and insulin and/or ionexchange resins required to control hyperkalaemia)

Evidence-based medicine Renal Association (1997) Treatment of Adult Patients with Renal Failure. Recommended Standards and Audit Measures, 2nd edn. Royal College of Physicians, London.

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(d) Diet: high calorie, low protein (30 g/day) in a small volume of fluid (e) Acidosis: sodium bicarbonate Treat any infection

Renal replacement therapy (requires placement of double- or triple-lumen central venous line) • Indications: hyperkalaemia, uraemia, metabolic acidosis, fluid overload • Types of RRT (a) Haemofiltration: removes large molecules and volume by convection (b) Haemodialysis: efficient small-molecule and volume removal (c) Haemodiafiltration: combination of haemofiltration and haemodialysis • Nutrition: patients with ARF have the same requirements as other sick patients: (a) Calories: 35 kcal/kg (147 kJ /kg) body weight daily (b) Nitrogen: 1.2 g/kg body weight daily (c) Glucose : lipid ratio 70/30 Diuretic phase • Replace fluid losses (up to 20 L/day) until renal tubules are able to concentrate the urine Treatment of hyperkalaemia • 10 –20 mL calcium gluconate or calcium chloride i.v.: stabilizes myocardial membrane • 50 mL 50% dextrose + 10 units soluble insulin i.v.: promotes migration of K+ into cells • 200 –300 mL NaHCO3 i.v.: promotes migration of K+ into cells and helps to correct metabolic acidosis • Calcium resonium 15 g t.d.s. orally or by enema: binds K+ in the gut, releases calcium in exchange • Dialysis: implement if hyperkalaemia is severe.

Scottish Intercollegiate Guidelines Network (SIGN) (1997) Investigation of Asymptomatic Microscopic Haematuria in Adults. SIGN publication 17, Edinburgh. Scottish Intercollegiate Guidelines Network (SIGN) (1997) Investigation of Asymptomatic Proteinuria in Adults. SIGN publication 18, Edinburgh.

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The Acute Abdomen

Introduction, 166 Aetiology, 166 Investigations, 167

Peritonitis, 168 Haemoperitoneum, 171 Intestinal obstruction, 172

Must know Must do

Must know Clinical features of patients with acute abdomen Clinical features and management of patients with acute appendicitis Clinical features and management of patients with primary and secondary peritonitis Causes, types, clinical features and management of intestinal obstruction Complications that develop in patients with acute abdomen Must do See patients with acute abdomen and generalized peritonitis and follow their management See patients with small and large bowel obstruction and follow their management Familiarize yourself with the antibiotic policy used in the management of patients with acute abdomen Learn to detect free gas under the diaphragm on the PA chest film in patients with gastrointestinal perforation Insert a nasogastric tube in a patient with intestinal obstruction Learn to examine hernial orifices to exclude strangulated external abdominal herniae Observe an emergency appendicectomy Observe an emergency laparotomy for acute abdomen

Introduction The collective term acute abdomen is used to describe a group of acute life-threatening intra-abdominal conditions (including pelvic) that require emergency hospital admission and often emergency surgical intervention. Early recognition, adequate resuscitation and prompt treatment are necessary for recovery of these patients from potentially fatal conditions. 166

Complications, 177 Intestinal pseudo-obstruction, 178

Aetiology (see Table 15.1) The causes of an acute abdomen fall into four main categories: inflammatory; traumatic; obstructive; vascular.

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Inflammatory The inflammatory intraperitoneal conditions originate as either acute inflammations of specific regions of the gastrointestinal tract (e.g. acute appendicitis, acute diverticulitis) or primary perforations of the gastrointestinal tract as a consequence of either benign disease (e.g. perforated duodenal ulcer) or malignant tumours (perforated gastric lymphoma, caecal carcinoma, etc.). Anastomotic leakage following resections with primary anastomosis of parts of the gastrointestinal tract is the most common cause of the postoperative acute abdomen. All the conditions in

Table 15.1 Acute abdomen: disease processes. Inflammatory Secondary bacterial peritonitis: localized, generalized Primary bacterial peritonitis: generalized Tertiary peritonitis: generalized, very poor prognosis Traumatic Injury to solid organs: acute intra-abdominal bleeding Peritonitis secondary to intestinal injury Obstructive Acute intestinal obstruction (small bowel) Chronic intestinal obstruction (colonic) Vascular Mesenteric infarction Strangulated external/internal herniae Volvulus (small or large intestine)

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this category invariably lead to a localized or generalized bacterial peritonitis that is usually polymicrobial (caused by several bacteria). Some infections of the peritoneal cavity are primary de novo; in contrast these much rarer infections are caused by a single organism, usually Streptococcus pneumoniae.

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in this category. Fortunately most aortic aneurysms do not sustain frank rupture but leak into the retroperitoneal tissues. Thus the bleeding is contained initially and this accounts for survival with emergency therapy in some of these patients (see Chapter 37).

Investigations Traumatic Intra-abdominal injuries may be due to blunt or penetrating abdominal trauma (see Chapter 19). When solid organs such as the liver and spleen are involved, the clinical picture is dominated by acute hypovolaemia due to massive internal haemorrhage. In contrast, when the pancreas or gastrointestinal tract is traumatized, the symptoms and signs are those of peritonitis. Another group relates to injuries sustained inadvertently during the course of any operation, e.g. bile duct and bowel injuries during laparoscopic cholecystectomy. These are referred to as iatrogenic injuries. Not infrequently, they are missed at operation and the injury declares itself clinically with fever, sepsis, peritonitis and fistulae. These injuries usually proceed to litigation and emphasize the importance of good technique and impeccable perioperative care.

Obstructive Obstructions of the gastrointestinal tract may involve the small intestine (acute) or the large bowel (chronic). The clinical picture of acute intestinal obstruction is dominated by vomiting, colicky abdominal pain and dehydration due to fluid and electrolyte losses, whereas chronic obstructions present with absolute constipation and marked abdominal distension. Unless the integrity of the wall of the obstructed bowel is compromised (as may happen in patients in whom the diagnosis is delayed or there is a primary adverse vascular event), there is no peritoneal contamination and therefore signs of peritonitis are absent.

It is axiomatic that: clinical assessment, relief of pain and resuscitation come before imaging tests; only investigations essential to the emergency management of the patient are carried out; no patient with acute abdomen should be left unattended (medically) in a radiology department. The basic investigations that are necessary in all patients with an acute abdomen are listed in Table 15.2. The essential blood investigations provide information on the following. Degree of hydration: osmolality, packed cell volume (PCV) and haemoglobin. Sepsis: white cell count (WCC), total and differential for leukocytosis; blood cultures (only in patients with rigors or shock without obvious blood loss). Urea and electrolyte imbalances. Chest X-ray is important, especially in the detection of free air under the diaphragm, which is always indicative of intestinal perforation or laceration (Fig. 15.1). Abdominal scout X-ray films for intestinal obstruction. In addition, there are a number of special investigations that may be carried out in patients admitted with blunt abdominal trauma or acute undiagnosed abdominal pain. These include ultrasound examination, abdominal computed tomography (CT), peritoneal lavage and laparoscopy. These tests are only performed in trauma patients if the cardiovascular system is stable, i.e. the patient is not shocked.

• • • • • • • •

Table 15.2 Investigations in patients with acute abdomen.

Vascular Acute intestinal ischaemia leading to infarction of segments of the gastrointestinal tract may be due to thrombotic or embolic occlusion of the mesenteric vessels, volvulus (twisting) of loops of small or large intestine, and external compression of the blood supply by bands or adhesions or the neck of external/internal herniae. Intestinal infarction is a serious condition that carries a high mortality. The clinical picture is dominated by severe pain, peritonitis, shock and, in some patients, rectal bleeding. Ruptured abdominal aortic aneurysm also comes

Essential Haemoglobin, white cell count, packed cell volume Urea, electrolytes and amylase Chest X-ray and abdominal scout films (erect/supine) Blood cultures for high fever and pyrexia Special Ultrasound and computed tomography Peritoneal lavage Mesenteric angiography Laparoscopy

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the laparoscopic findings. Emergency laparoscopy often resolves common diagnostic problems: Has the patient got acute appendicitis or acute pelvic adnexal disease (inflammatory, ruptured corpus luteum cyst or ectopic pregnancy)? Has the patient got mesenteric lymphadenitis (children)? Is there small bowel infarction? Has the patient sustained trauma to intra-abdominal organs (stab injuries of the abdomen)?

• • • •

Peritonitis Peritonitis is inflammation of the peritoneum. The peritonitis can be bacterial or chemical.

Figure 15.1 Perforated duodenal ulcer. Note presence of free air under the right diaphragm on the PA chest film.

Ultrasound examination and abdominal CT are both very useful in the detection of intraparenchymal haematomata, free fluid in the peritoneal cavity and localized inflammation, oedema and necrosis. Peritoneal lavage is carried out after the insertion of a peritoneal dialysis catheter in the immediate subumbilical region. If blood or blood-stained fluid emerges immediately through the catheter, the test is positive. Otherwise, 1 L of Hartmann’s solution is infused and then aspirated for examination. The test is considered positive if: red blood cells > 100 × 106/L; white blood cells > 500 × 103/L; amylase > 1100 U/L; or bile, bacteria or food particles are present. Peritoneal lavage is most commonly used in the diagnosis of suspected blunt intra-abdominal trauma. Its one disadvantage is a 15 –20% false-positive rate due to minor lesions, which stop bleeding and do not require laparotomy.

• • • •

Emergency laparoscopy is extremely valuable in patients with acute lower abdominal pain, especially in females of childbearing age. It is carried out in the operating theatre under general anaesthesia and thus precedes the emergency operation if this is indicated on the basis of

Bacterial peritonitis Bacterial peritonitis is divided into four types. 1 Secondary bacterial peritonitis: the majority of the morbid processes lead to a breach in the integrity of the wall of the gastrointestinal tract, with transmigration of intestinal bacteria to the peritoneal cavity or actual perforation with escape of intestinal contents and substantial contamination of the peritoneal space. The consequence is an acute secondary bacterial peritonitis. 2 Primary bacterial peritonitis: primary bacterial peritonitis is a much rarer condition that occurs in otherwise healthy people in the absence of surgery or trauma and is the result of primary infection of the peritoneal lining by streptococcal organisms, usually in children and adult females. 3 Spontaneous bacterial peritonitis: develops in chronically ill patients, e.g. cirrhotic patients with ascites, renal failure patients on peritoneal dialysis, nephrotic syndrome. 4 Tertiary peritonitis: occurs in intensive care patients and is defined as the persistence or recurrence of intraabdominal infection following apparently adequate therapy of secondary peritonitis. Patients who develop tertiary peritonitis have a significantly longer stay in the intensive care unit (ICU) and more advanced organ dysfunction reflected in higher ICU mortality than patients with uncomplicated secondary peritonitis. The most common infecting organisms in tertiary peritonitis are Enterococcus, Candida, Staphylococcus epidermidis and Enterobacter. These patients do not benefit from laparotomy, as the infection is diffuse and poorly localized. Tertiary peritonitis appears to be more a reflection than a cause of an adverse outcome. Chemical peritonitis In this instance the peritoneal inflammation is initially chemical in nature, e.g. early stages of perforated duodenal ulcer, extravasation of uninfected urine (bladder

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injuries) or bile (after biliary operations). However, if treatment is delayed, secondary infection supervenes within a few hours. Thus chemical peritonitis represents the initial clinical phase of extravasation of visceral contents into the peritoneal cavity and almost invariably merges into acute secondary bacterial peritonitis.

Clinical manifestations Irrespective of the exact aetiology, established peritonitis is usually accompanied by well-recognized systemic and local symptoms and signs.

Systemic manifestations These emanate from the presence of a serious infection: the patient looks ill and is toxic with a high metabolic rate, pyrexia, tachycardia and leukocytosis. If bacteria have invaded the bloodstream (bacteraemia, septicaemia), attacks of rigors (shivering) are encountered; the patient feels cold even though his or her temperature is elevated above 38 °C. The combination of fluid and electrolyte losses (vomit, fluid inside the oedematous intestinal loops and peritoneal exudate that is sequestrated) and the enhanced insensible loss caused by the pyrexia lead to dehydration with dry mouth, loss of skin turgor and collapse of the peripheral veins.

Local symptoms The pain of acute peritonitis is due to irritation of the somatic nerves supplying the parietal peritoneum. Its extent and exact location depend on whether the peritonitis is generalized or localized to a particular quadrant of the intra-abdominal cavity. It is always severe, constant and aggravated by movement (passive or active) and thus the patient lies still in the supine position and may at times draw up the knees to relax the abdominal musculature.

Local signs The local or abdominal signs are elicited by a methodical sequence of inspection, palpation, percussion and auscultation of the abdomen and digital rectal examination. Inspection On inspection of the normal abdomen, the abdominal wall is seen to move with respiration; it bulges with inspiration as the diaphragm descends. This normal excursion is often absent in patients with peritonitis as the abdominal muscles over the area of peritoneal inflammation undergo reflex spasm.

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Palpation The same phenomenon accounts for the tight feel of the abdominal musculature noted during light palpation and often referred to as guarding. When marked, the abdominal muscles actually feel rigid (rigidity), although descriptions of board-like rigidity are exaggerated and have conveyed the wrong impression that deep palpation is necessary to elicit this sign. In fact, deep palpation is absolutely contraindicated in all patients with acute abdomen as it serves no purpose other than to inflict severe pain on the patient and thereby lose his or her confidence. Tenderness on light palpation elicited over the affected region is a most useful and reliable sign. Rebound tenderness is experienced by the patient when the pressure of the palpating hand is released. Considerable store has been laid on this physical sign in the past. More recent studies have cast some doubt on its value in clinical practice. Certainly it must be elicited with great gentleness. Percussion A more humane way to evoke rebound tenderness is to tap the affected area gently or better still ask the patient to cough, which, by moving the inflamed viscera against the inflamed parietal peritoneum, reproduces the localized pain. Auscultation Auscultation of the abdomen in patients with peritonitis reveals a silent abdomen (no identifiable borborygmi) due to absence of the normal peristaltic activity. At times, tinkling bowel sounds may be heard. These are due to passive movement of fluid within dilated loops of inflamed gut and signify the presence of a paralytic ileus. Digital rectal examination No examination of a patient with an acute abdomen is complete without a rectal examination. Although this is best carried out in the left lateral position, if the patient is in severe pain it may be conducted in the supine posture with flexion and abduction of the hip joints. The specific findings on digital rectal examination may include pelvic tenderness, boggy swelling in the rectovesical pouch and tenderness caused by movement of the cervix in the female.

Treatment of secondary bacterial peritonitis Initial assessment and resuscitation The diagnosis is established clinically and with certain key laboratory investigations (urea, electrolytes, osmolality, haemoglobin, WCC, serum amylase) and chest X-ray (air

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Surgical treatment

Perforated acute appendicitis Gangrenous cholecystitis Perforated duodenal ulcer

Appendicectomy + peritoneal lavage Cholecystectomy + peritoneal lavage Suture closure + peritoneal lavage + postoperative eradication of Helicobacter pylori Biopsy + closure of ulcer + peritoneal lavage Drainage of localized pericolic abscess or colectomy for free + lavage Resection + lavage

Perforated gastric ulcer Perforated diverticulitis perforation Perforated gastrointestinal neoplasm

Table 15.3 Causes of peritonitis and their surgical treatment.

Cause of peritonitis

under the diaphragm). Pain relief is a priority and should precede clinical examination. Analgesic medication (opioid) is administered intramuscularly (intravenously if patient is shocked). The view that analgesia should be withheld initially in these patients because it may mask physical signs is incorrect. Aside from being unkind, it reduces patient cooperation and confidence. Blood samples are taken for blood grouping if the patient is to undergo surgical treatment following resuscitation.

Intravenous fluid therapy and nasogastric suction An intravenous line is set up for fluid and electrolyte replacement and all oral intake is stopped. A nasogastric tube is inserted and left draining continuously into a bag; the nursing staff check the patency of the tube by syringing and aspirating every hour.

Antibiotic therapy Antibiotics are administered in all patients with evidence of intra-abdominal sepsis. If the infection is thought to arise from the upper gastrointestinal or hepatobiliary tract, a cephalosporin (active against Gram-negative aerobes) is sufficient. However, if the peritonitis is generalized or the disease is thought to originate from the colon, additional cover for Gram-negative anaerobes must be provided. This usually entails the administration of metronidazole in addition to the cephalosporin or aminoglycoside. The exact antibiotic regimen may be changed in the individual patient subsequent to clinical progress, bacterial culture and sensitivity tests.

Observations If immediate surgery is not undertaken in any of these patients after they have been assessed by the more senior surgical staff, careful monitoring of their progress is

carried out, with measurement of pulse, temperature, blood pressure and urine output and repeated physical examination of the abdomen. Provided the patient is improving, conservative management is continued; if deterioration is observed or the condition remains static, then further special tests or exploratory laparotomy is carried out.

Surgical treatment Surgical treatment depends on the cause of the secondary bacterial peritonitis as established by laparotomy. The common acute intra-abdominal pathologies encountered and their treatment are shown in Table 15.3. The primary aim is to seal the perforation or remove the primary pathological source. This is followed by evacuation of pus with procurement of sample for culture, followed by abdominal lavage with several litres of warm isotonic saline. A perforated gastric ulcer must always be biopsied prior to closure because of the possibility of malignancy.

Primary bacterial peritonitis By definition, this occurs in healthy individuals and the infecting organism is of the Gram-positive type, most commonly Streptococcus pneumoniae and group A streptococci. The disease is encountered in children, adolescents and adult females, in whom it may follow childbirth or chest and urinary tract infection. In most instances, the infection is haematogenous. Infants and children usually present with acute abdominal pain, vomiting and fever, and abdominal signs indicative of peritoneal inflammation. Blood cultures may be positive. Treatment is with intravenous antibiotics in the first instance. Awareness of the condition is important as primary peritonitis is a rare condition, especially in children, and thus will be overlooked unless it is considered in the differential diagnosis of children presenting with an acute abdomen.

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The disease in adults is confined to females. Although the infection is commonly pneumococcal, instances of gonococcal peritonitis have been reported. The typical patients are usually young adolescent girls. Some cases are reported in association with acute (non-perforated) appendicitis. The patients become pyrexial and develop abdominal pain, diarrhoea and clinical signs of peritonitis. In addition to antibiotic therapy, laparotomy is usually necessary to remove pus and for abdominal lavage. Culture of vaginal swabs is usually positive for pneumococcus in patients who develop the condition after childbirth. The prognosis of primary peritonitis with early diagnosis and treatment (antibiotics and abdominal lavage) is good, with recovery of the vast majority of patients. As the infection is most commonly due to Streptococcus pneumoniae, the initial antibiotic should be Augmentin (amoxicillin + clavulanic acid).

Spontaneous bacterial peritonitis This carries a bad prognosis and has a definite mortality as a result of septic shock and multiorgan system failure. The groups of patients who are prone to develop spontaneous bacterial peritonitis (SBP) include: cirrhotic patients with ascites, Wilson’s disease, chronic active hepatitis; renal failure patients on chronic peritoneal dialysis; patients with nephrotic syndrome. These patients are all immunocompromised and exhibit reduced resistance to bacterial infection. The infecting organisms are often Gram-negative. About 30% of renal failure patients with SBP have no symptoms or signs directly referable to the abdomen. In other patients, the disease develops insidiously and localizing signs of peritonitis are minimal. The most common manifestations include abdominal pain, fever, tenderness and diminished or absent bowel sounds. The full-blown picture is accompanied by septic shock and is invariably fatal. Once suspected, a 100-mL specimen of ascitic fluid is taken for culture and Gram staining of the deposit after centrifugation and for measurement of polymorphonuclear cell count and pH. A polymorphonuclear cell count > 250 × 103/L and a pH < 7.37 are diagnostic and indicate the need for antibiotic therapy, even if the culture of the ascitic fluid is negative. A blood culture should also be taken. In cirrhotic patients, the condition is a bacterial infection of ascitic fluid. The reported incidence of SBP in cirrhotics with ascites averages 20%. Most of the infections are aerobic and 50 – 60% of cases are caused by Escherichia coli. The aetiology is thought to involve: bacterial translocation from the gut to mesenteric lymph nodes;

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depressed activity of the reticuloendothelial phagocytic system; decreased antimicrobial capacity of ascitic fluid (low levels of C3, opsonins and fibronectin). Diagnosis is based on clinical suspicion and analysis of ascitic fluid (WCC and culture in blood culture bottles). Treatment is with a third-generation cephalosporin. Despite documented cure of SBP, many patients (up to 30%) die during hospitalization from complications related to their end-stage liver disease. The long-term prognosis for patients with SBP is poor and they should be considered for liver transplantation. As in cirrhotic patients, SBP in patients on chronic peritoneal dialysis can be culture positive or negative. The infection is caused by either Gram-positive cocci or Gram-negative bacilli. It can also arise as a consequence of catheter-related infections (subcutaneous tunnel or catheter exit site). The standard primary treatment of SBP in patients undergoing chronic peritoneal dialysis is intraperitoneal netilmicin combined with intermittent intraperitoneal vancomycin.

Haemoperitoneum Haemoperitoneum is defined as free blood in the peritoneal cavity. It may arise from: intra-abdominal injuries, especially to solid organs; intra-abdominal operations; rupture of ectopic pregnancy; ruptured corpus luteum cyst; percutaneous interventions on the liver, e.g. core biopsy, transhepatic stenting; severe necrotizing pancreatitis; advanced peritoneal carcinomatosis; spontaneous rupture of primary liver tumour (rare); spontaneous rupture of an enlarged spleen (rare); spontaneous rupture of splenic aneurysm (rare). Fortunately, intraperitoneal abdominal aortic aneurysms tend to leak into the retroperitoneal tissues, forming a haematoma rather than a haemoperitoneum in the first instance.

• • • • • • • • • •

Clinical types In the clinical context, haemoperitoneum is best considered as falling into two categories: progressive and stable.

Progressive haemoperitoneum Progressive haemoperitoneum implies active continued intra-abdominal bleeding and is most commonly encountered with injuries to the solid organs (liver and spleen) or as an early complication after abdominal surgery. In

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times the patient complains of shoulder-tip pain when lying supine. This is the result of diaphragmatic irritation. In equivocal cases raising the foot of the bed, thereby encouraging any free blood present to flow into the subdiaphragmatic spaces, enhances shoulder tip-pain. The abdomen may be distended and may have a doughy feel. Shifting dullness can sometimes be elicited.

Treatment

Figure 15.2 Grey Turner’s sign in a patient with pancreatitis.

addition to obvious signs of hypovolaemic shock, there is progressive distension of the abdomen, which in severe injuries involving major vessels (e.g. hepatic veins) may become so tense as to obstruct venous return from the lower limbs. Postoperative bleeding is due either to slipping of a ligature on a blood vessel or reactionary bleeding or to oozing from raw surfaces (liver resections) or leaking arterial anastomosis. Reactionary bleeding occurs from cut small blood vessels that are missed at operation but which bleed subsequently as the blood pressure rises after recovery from surgery and anaesthesia. Bleeding from an arterial anastomosis may also be the result of infection. The signs and symptoms of progressive haemoperitoneum are dominated by the rapid loss of circulating blood volume, with the development of hypovolaemic shock. In this respect, the local abdominal signs, apart from increasing abdominal distension, are of minor importance. These patients only survive with prompt resuscitation and immediate surgical intervention.

Stable haemoperitoneum A stable haemoperitoneum implies that the lesion which caused the haemoperitoneum in the first instance is no longer actively bleeding. Given time, the blood may track along tissue planes to appear in the flank (Grey Turner sign, found in patients with necrotizing pancreatitis; Fig. 15.2) or the periumbilical region (Cullen’s sign, also found associated with necrotizing pancreatitis and rarely with missed ruptured ectopic pregnancy). The manifestations of patients with stable haemoperitoneum are not always clear-cut. The patient may appear clinically anaemic but this is best confirmed by haemoglobin estimation. Although free peritoneal blood acts as an irritant, the pain is not marked and tenderness is mild or absent. At

Progressive haemoperitoneum requires immediate surgical intervention with volume replacement (blood, colloids and crystalloids) during the surgery. Cross-matched blood should be available within 30 min in most hospitals nowadays and thus the need for transfusion of Group O Rh-negative non-cross-matched blood seldom if ever arises. The primary aim of the operation is to control the bleeding. Survival depends on this being achieved before substantial losses. In major liver injuries with massive bleeding that cannot be controlled at laparotomy, management is by packing of the entire supracolic compartment with gauze rolls and closure. The patient is re-explored 24 h later, when usually the condition has improved and control of bleeding by surgical means becomes feasible. Patients with stable haemoperitoneum should be investigated without delay and some will require urgent surgical treatment when the diagnosis is confirmed.

Intestinal obstruction Definitions and types Intestinal obstruction may be complete (total blockage of the lumen) or incomplete (partial blockage). It may present acutely with dramatic symptoms when the obstruction is situated at any point between the second part of the duodenum and the caecum (acute intestinal obstruction). Alternatively, the presentation may be more insidious, over several weeks, when the obstruction is located in the colon (chronic intestinal obstruction). If the blood supply to the obstructed segment is not jeopardized, the obstruction is referred to as simple or mechanical, in order to distinguish it from those obstructions in which the blood supply is compromised at an early stage (strangulating intestinal obstruction).

Aetiology and pathophysiology The various causes of mechanical intestinal obstructions can be grouped as extramural, intramural and intraluminal (Table 15.4).

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Table 15.4 Causes of mechanical intestinal obstruction. Extramural Adhesions, bands Herniae: external and internal Compression by tumours (nodal tumour deposits) Intramural Inflammatory disease: Crohn’s disease Tumours: carcinomas, lymphomas, etc. Strictures Intraluminal Faecal impaction Swallowed foreign bodies Bezoars Gallstone

•

Extramural obstructions. These are due to extrinsic compression of the walls of the gut by bands, adhesions or tumours (particularly secondary deposits in lymph nodes). Adhesive small-bowel obstruction secondary to previous peritonitis or surgical intervention is nowadays the most common cause of intestinal obstruction. Intramural obstructions. These are caused by lesions (neoplastic, inflammatory or cicatricial) arising from the wall of the intestine. The most common cause of this type of obstruction is carcinoma, usually of the colon. Intraluminal obstructions. Although intraluminal smallbowel obstructions are rare, chronic colonic intraluminal obstruction by impacted faeces in constipated elderly patients is quite common. The small-bowel lumen may be blocked by a swallowed object (children, mentally subnormal individuals) or a bolus composed of indigestible material (orange pith or hair bezoar, particularly in gastrectomized patients) or by a gallstone. The latter arises when a large gallstone in a chronically inflamed gallbladder that has become adherent to the duodenum erodes through the two organs by a process of pressure necrosis, thus entering the duodenum and becoming impacted lower down the small intestine, usually in the terminal ileum. The condition is known as gallstone ileus. By virtue of its origin it is always accompanied by a cholecystoduodenal fistula, which allows reflux of enteric contents and air into the biliary tract.

• •

Specific types Mechanical obstruction Following the onset of obstruction, the distal bowel empties to a collapsed state whereas the proximal bowel

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becomes hyperactive, with vigorous peristaltic contractions, in an effort to overcome the obstruction. These cluster contractions are the cause of the severe colicky abdominal pain experienced by these patients. Additionally, the bowel proximal to the obstruction dilates due to the accumulation of swallowed air and increased intestinal secretions. The interface between air and fluid in the dilated loops accounts for the fluid levels seen in the erect abdominal film of these patients. The wall of the obstructed gut becomes oedematous. This is the result of increased transudation across the capillary membrane as the venous drainage of the affected segments is impaired by the distension. The fluid and electrolytes that accumulate in the lumen of the obstructed bowel and within its wall are effectively lost (sequestrated third-space losses) and contribute (together with vomiting) to the fluid and electrolyte deficit in these patients. Bacterial overgrowth occurs within the obstructed loops of intestine. Unless the distension is relieved, there is progressive occlusion (by stretching) of the intestinal intramural vessels such that, untreated, a mechanical intestinal obstruction leads to ischaemia and eventually necrosis with perforation of the bowel.

Strangulating obstruction Here, in addition to the luminal obstruction, the viability of the gut is compromised because of impairment of its blood supply at an early stage. Common examples include strangulation caused by bands, adhesions and tight hernial sacs (strangulated herniae). There are special forms that merit separate attention, including intussusception, volvulus, closed-loop obstruction and mesenteric infarction. Intussusception This consists of telescoping of a loop of bowel inside itself (ileoileal, ileum inside ileum; ileocolic, ileum inside caecum or ascending colon; Fig. 15.3). It may or may not originate from a lead point, which is usually a swelling of the mucosa or submucosa (e.g. inflamed Peyer’s patch, mucosal adenoma, submucosal lipoma). Intussusception occurs most commonly in infants and children usually 3–18 months of age, but may be encountered in adults. The blood supply of the involved bowel is compromised at an early stage and unless the intussusception is reduced early (e.g. by barium enema or surgery), infarction and peritonitis supervene. Volvulus Volvulus is a 360° twist of a loop or loops of intestine. The rotation causes early obstruction of the vascular

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Figure 15.4 Plain abdominal X-ray showing a sigmoid volvulus. Figure 15.3 Diagram of ileocolic intussusception.

03 pedicle supplying the affected portion. Risk factors for small-bowel volvulus (which may affect the whole of the midgut) include adhesions or bands between the antimesenteric aspect of the bowel and the anterior abdominal wall and congenital malrotation of the gut. Volvulus of the sigmoid colon is encountered in the elderly, patients with chronic constipation and those with a redundant pelvic mesocolon (Fig. 15.4). Unless recognized early, volvulus leads to intestinal infarction, which often involves large segments of the gut. Closed-loop obstruction Although volvulus is an example of this type of obstruction, i.e. segment of the affected bowel closed at proximal and distal ends, the term ‘closed-loop obstruction’ is usually reserved for a complete obstruction of the left colon (usually by an annular carcinoma of the descending or sigmoid colon) in the presence of a competent ileocaecal valve. This prevents the proximal distended colon from decompressing into the small intestine. Meanwhile, smallbowel contents may continue to pass into the caecum through the one-way ileocaecal valve. The result is a rapid build-up of pressure in the colon, with the brunt being taken by the caecum, which becomes markedly distended to the point of ischaemia when it perforates, usually through a clear-cut hole (pistol-shot perforation). Mesenteric infarction In this serious condition, there is primary occlusion of the

Figure 15.5 Infarcted midgut.

blood supply to the intestine as a result of thrombotic or embolic disease of the mesenteric vessels. Most commonly, the superior mesenteric vessels are occluded, with infarction of the entire midgut from the level of the midduodenum to the junction of the proximal with the distal two-thirds of the transverse colon (long-loop infarction; Fig. 15.5). The condition, which affects patients who are elderly and suffer from cardiac and atheromatous vascular disease, is usually fatal. At times the extent of the infarction is less extensive, then resection may be followed by survival but the patient has insufficient small bowel for digestion and absorption and develops the short-gut syndrome. There is another type of small-bowel infarction encountered in patients with chronic hypoxia (chronic pulmonary disease, heart failure, etc.) and which is due

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to hypoperfusion. The ischaemia is patchy and the mesenteric vessels appear patent, the block occurring in the small intramural vessels of the intestine (microcirculation). This variant is known as non-occlusive mesenteric infarction. The same occlusive process may involve the vessels supplying the colon and lead to ischaemic colitis. This tends to affect predominantly the left colon and presents with a picture of acute inflammation not dissimilar from acute colonic diverticulitis. Fortunately the affected colon, although oedematous and inflamed, does not usually infarct and the process subsides with conservative management. However, a stricture of the left colon commonly situated just distal to the splenic flexure develops some weeks to months later.

Paralytic ileus This term is used to describe a syndrome in which intestinal obstruction is due to absence of the normal peristaltic contractions. The common abbreviation ‘ileus’ is incorrect as this word, which is of Greek derivation, means ‘to roll up’. Adynamic ileus is most commonly encountered after intra-abdominal surgery, when it is short-lived (few days) and often referred to as physiological ileus. The temporary cessation of intestinal motor activity is due to handling and exposure of the intestinal loops. On occasions, it is pathologically prolonged, when it is associated with postoperative intra-abdominal sepsis and fibrinous adhesion formation (postoperative ileus). In this setting the differentiation between mechanical and paralytic obstruction is difficult and often the clinical picture is mixed. Paralytic ileus may also be caused by spinal injuries and by the accumulation of retroperitoneal blood or irritant exudates that disturb the functional activity of the coeliac plexus and splanchnic nerves (retroperitoneal haematoma from renal injuries, ruptured abdominal aneurysms, acute pancreatitis, etc.). Haemoperitoneum may also be accompanied by some loss of intestinal peristaltic activity. Infective paralytic ileus is the most serious and is secondary to peritonitis from any cause.

Clinical features Symptoms The cardinal symptoms of mechanical bowel obstruction are: vomiting; colicky abdominal pain; abdominal distension; absolute constipation.

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Notwithstanding, the symptomatology may be varied and the clinical picture of acute small-bowel obstruction is quite different from that of chronic (colonic) obstruction. Vomiting is a marked feature of high small-bowel obstruction but is rarely encountered in colonic obstruction. Initially, the vomit consists of food followed by bile-stained fluid, which later becomes faeculent. This is caused by bacterial overgrowth in the obstructed small intestine. Vomiting, together with the sequestration of fluid in the dilated loops, rapidly leads to dehydration with significant water and electrolyte deficits, particularly Na+ and Cl–. The dehydration leads to raised PCV and prerenal azotaemia, with elevation of blood urea and reduced urine output. The pain in mechanical small-bowel obstruction is colicky in nature, situated in the centre of the abdomen around the umbilicus and accompanied by hyperperistaltic rushes that can easily be heard by the stethoscope. In colonic obstruction the pain is more of a discomfort and is situated in the suprapubic region. However, in the presence of closed-loop obstruction with marked caecal dilatation and impending perforation, localized pain is present in the right iliac fossa. Constant severe pain is ominous and indicates either infarction of the bowel or the onset of peritonitis. Paralytic ileus in itself is painless, except when secondary to peritonitis, when the pain is generalized and constant. Abdominal distension becomes progressively more marked the lower the obstruction is situated and may reach extreme degrees in low colonic obstruction and paralytic ileus. It is caused by accumulation of gas and fluid within the obstructed bowel. Following the onset of mechanical obstruction, the patient may have a bowel motion as the distal segment empties. Thereafter, there is absolute constipation (no passage of either flatus or faeces).

Physical signs The physical signs of intestinal obstruction are usually clear-cut. Dehydration is accompanied by loss of skin turgor. Pyrexia is mild unless there is infarction and peritonitis. Fluid and electrolyte losses cause a reduction of circulating blood volume with some hypotension and persistent tachycardia. The distended abdomen is resonant to percussion on the anterior aspect but is dull towards the flanks. Auscultation confirms the presence of excessive peristaltic activity (borborygmi) that coincide with attacks of colic. In paralytic ileus bowel sounds are not heard; instead these are replaced by tinkling high-pitched sounds due to passive movement of fluid within the dilated loops.

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Tenderness and rebound tenderness are indicative of ischaemic bowel or developing peritonitis (due to imminent or established perforation). They are usually accompanied by deterioration in the general condition of the patient and change in the character of the pain, which becomes severe and constant. Rectal examination in small-bowel obstruction usually confirms an empty rectum. In colonic obstruction the findings may be: empty rectum; gross faecal loading (in obstruction due to faecal impaction); low neoplasm can be palpated by the examining finger.

• • •

Investigations

The essential investigations in patients with intestinal obstruction are haemoglobin, PCV, WCC, urea and electrolytes, chest X-ray, plain erect and supine abdominal films. Both the haemoglobin and PCV are elevated because of haemoconcentration. The raised blood urea is the result of an element of prerenal failure due to the hypovolaemia. The WCC is usually normal or slightly elevated unless there is bowel infarction and/or peritonitis. The

(a)

serum Na+ and Cl– are low. Hyperkalaemia may be observed in patients with infarcted intestine. The chest radiograph shows an elevated diaphragm, which is secondary to the abdominal distension. In addition there may be free air underneath the right diaphragm in patients with infective paralytic ileus (secondary to intestinal perforation). The erect abdominal film is taken to outline air–fluid levels. These are multiple and centrally placed in a ladder fashion in small-bowel obstruction (Fig. 15.6a). In large-bowel obstruction they are less numerous and located in the flanks and suprapubic regions (Fig. 15.6b). The supine film is used to assess distension of the intestine and helps to differentiate small from large intestine. Dilated jejunum often exhibits parallel soft-tissue shadows that extend the whole width of the involved segment (due to the folds of the smallbowel mucosa, so-called valvulae conniventes; Fig. 15.6a), whereas in the obstructed colon the haustra cause crescentic soft-tissue shadows that do not traverse the entire width of the bowel (Fig. 15.6b). Also, the obstructed colon has a sacculated outline. The obstructed ileum is relatively featureless. Other investigations that may be necessary are contrast examinations (water-soluble contrast swallow and meal, gentle barium enema) and sigmoidoscopy.

(b)

Figure 15.6 (a) Valvulae conniventes. Supine film showing a dilated jejunum in mechanical small-bowel obstruction. The softtissue markings extend the whole length of the dilated segment. The obstructed ileum is relatively featureless. (b) Haustral softtissue markings in colonic obstruction. They do not extend across the whole width of the affected segment. Note the presence of air–fluid levels.

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Management The management of intestinal obstruction is based on four principles: decompression of the obstructed gut; replacement of fluid and electrolyte losses; special conservative measures in certain situations; surgical intervention.

• • • •

Decompression Although various long tubes were used in the past, decompression is nowadays achieved by the insertion of a nasogastric sump suction tube (Salem). This is aspirated at least every hour and left draining into a bag in the intervening periods. The daily aspirate is measured and the amount used in calculating the daily fluid and electrolyte requirements (see Chapter 13). If the intestinal obstruction responds to conservative management, the daily amount of aspirate gradually reduces and its nature changes to clear, often bile-stained fluid.

Fluid and electrolyte therapy Fluids and electrolytes are given through a peripheral venous line. As the major losses are water, sodium and chloride, the usual crystalloid solution consists of isotonic saline and 5% dextrose solution. Initially, large amounts are administered (1 L every 3– 4 h) to replace the losses. Thereafter, maintenance intravenous fluid therapy is continued until return of normal bowel function. The usual daily requirements of potassium (40 –120 mmol) are met by infusing 60 – 80 mmol of potassium chloride in divided doses over 24 h. If hypokalaemia is severe, up to 40 mmol may be infused over 1 h in 500 mL of fluid. It is important to remember that potassium must always be administered slowly and never given as a bolus injection because of the risk of cardiac arrhythmias and arrest.

Special conservative measures For certain types of intestinal obstruction, additional specific measures may result in rapid relief of the obstruction, thereby avoiding surgical intervention. Examples include the passage of a rectal tube or flexible sigmoidoscope to deflate a sigmoid volvulus, barium contrast enema to reduce an early intussusception in an infant and manual removal of faeces and/or oil retention enema to deal with obstruction caused by faecal impaction.

Assessment of progress It is important that the patient is assessed at frequent

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intervals to establish progress on conservative management. This is confirmed by relief of symptoms (vomiting and pain), improvement of the general condition and vital signs (pulse rate, temperature and blood pressure) and observations such as reduction in the amount of aspirate and abdominal girth and return of normal bowel sounds.

Surgical intervention This is undertaken if the following apply. The underlying disease needs surgical treatment (obstructed hernia, obstructing carcinoma, etc.). In this respect, intestinal obstruction due to adhesions often settles with conservative management and therefore is not initially treated surgically unless there is clinical evidence of strangulation. The patient does not improve with conservative treatment. There are signs of strangulation or peritonitis.

• • •

Complications The complications that may arise in patients with acute abdomen are outlined in Table 15.5. The acute complications develop early, usually during the same hospital admission. The most common is wound infection, which may be minor or major, i.e. requiring opening of the skin and subcutaneous tissue to drain the collection, necessary for healing by granulation (secondary intention). Some hospital-acquired infections (nosocomial) are more serious and can prove fatal, e.g. ventilator pneumonia. Hospitalacquired infections are often caused by resistant organisms, especially methicillin-resistant Staphylococcus aureus (MRSA). Aside from being difficult to treat, these

Table 15.5 Complications of acute abdomen. Acute (early) Nosocomial (hospital-acquired) infection: pneumonia, methicillin-resistant Staphylococcus aureus infection Wound infection Wound dehiscence Abscess formation Fistula formation External Internal Chronic (late) Incisional hernia Wound sinus Adhesions Recurrent small-bowel obstruction Bacterial overgrowth (blind loop)

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infections may be spread to other patients unless special precautions are taken: all MRSA-infected patients must be isolated; all staff attending patients must wear disposable plastic aprons and gloves (discarded in a special disposable bin for incineration); hands are washed with antiseptic soap and then disinfected with alcohol. Another serious early wound complication is total wound dehiscence, i.e. complete disruption of the abdominal wall. Often the skin edges remain approximated by the skin sutures but an obvious bulge is present in the subcutaneous layer with exudation of copious serosanguineous discharge. The treatment of wound dehiscence is immediate surgical intervention. The extravasated loops are washed and replaced in the peritoneal cavity and the abdominal wall closed in a single layer with large bites of non-absorbable sutures. Intra-abdominal abscesses may be located in the various compartments of the subphrenic region (on the right or left side), in the pelvis or between loops of small intestine. The systemic manifestations of intraperitoneal abscesses include malaise, weight loss, intermittent pyrexia and persistent leukocytosis. There may or may not be any localizing signs. A subphrenic abscess may cause shoulder-tip pain. Intraloop abscesses (often multiple) induce prolonged ileus and a pelvic abscess (most commonly encountered after a perforated appendicitis) causes rectal tenderness and diarrhoea. These abscesses are easily located by either ultrasound or CT examination and many are drained percutaneously, avoiding the need for surgical intervention. Intestinal fistulae may be external (enterocutaneous) or internal (between adjacent hollow viscera). Fistulae arise either from breakdown of an intestinal closure or anastomosis or because of delayed recognition or treatment of an intra-abdominal abscess, which then bursts, either between bowel and abdominal wall or between adjacent hollow viscera (e.g. colovesical fistula). An external high small-bowel fistula is a serious complication because most of the gastrointestinal secretions are lost through the fistulous opening (high-output fistula). As well as significant daily fluid and electrolyte losses, these fistulae lead to profound excoriation of the abdominal wall as this is digested by the activated pancreatic enzymes. These patients are managed by total parenteral nutrition and careful isolation of the fistulous discharge with the use of skin barriers and efficient sump suction drainage. Provided there is no distal obstruction or residual intra-abdominal abscess, the fistula usually heals with this conservative management. Colonic fistulae are much less serious and generally have a lower output. The same principles of management are adopted, except that nutrition is maintained enterally with low-residue or elemental diets.

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Chronic complications include: incisional herniae, usually in patients who develop a postoperative wound infection; formation of intraperitoneal adhesions; persistent wound sinus. Incisional hernias cause deformity and significant morbidity including strangulation. Thus if the patient is fit, repair is advocated. As the hernial defect is usually large, repair is carried out with a synthetic mesh as this carries the lowest incidence of recurrence. Intestinal adhesions cause considerable chronic disability because of recurrent attacks of small-bowel obstruction necessitating repeated hospital admissions and further surgical treatment. They are now the most common cause of intestinal obstruction. Currently several prophylactic treatments are being evaluated to reduce the formation of adhesions, e.g. intraperitoneal surfactant, Adept solution. Adhesions also cause chronic abdominal pain and may lead to the development of bacterial overgrowth (blind-loop syndrome) in the kinked small-bowel loops. The bacterial overgrowth results in malabsorption, anaemia and diarrhoea. A common chronic wound complication is the development of a persistent wound sinus. This is related to infection around a non-absorbable suture used in wound closure. Unless this is removed surgically, the sinus and the discharge persist, although one sinus may heal temporarily and then recur.

• • •

Intestinal pseudo-obstruction This is sometimes referred to as Ogilvie’s syndrome because he first described the condition in two patients with advanced cancer and involvement of the subdiaphragmatic autonomic plexus and postulated an imbalance between sympathetic and parasympathetic activity as the underlying cause. It is now thought to result from impairment of the reflex circuits within the enteric nervous system that ensure normal peristaltic progression. The syndrome is characterized by massive dilatation of the colon, suggesting distal organic colonic obstruction. This rare functional obstruction is usually encountered in elderly patients with severe extra-abdominal illness or injury (heart failure, sepsis, trauma, etc.). Other documented associations include chronic administration of hypnotics and sedatives, lead toxicity, hypothyroidism and various neurological disorders. The diagnosis is made by exclusion of organic disease. Air–fluid levels are often absent in this condition. Untreated the dilatation is progressive and when it exceeds 10 cm in the caecum, rupture with peritonitis may ensue. Treatment involves correction of the underlying cause, supportive management and decompression of the colon by passage of a rectal tube, sigmoidoscope or colonoscope.

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The acute abdomen at a glance Definitions Acute abdomen: describes a group of life-threatening intraabdominal conditions, characterized by peritonitis, that require emergency hospital admission ± surgery Peritonitis: inflammation of the peritoneum (bacterial or chemical) that is always serious Haemoperitoneum: the presence of free blood in the peritoneal cavity Complete intestinal obstruction: total blockage of the intestinal lumen. Incomplete intestinal obstruction denotes only a partial blockage. Obstruction may be acute (hours) or chronic (weeks), simple (mechanical) or strangulated (blood supply compromised). A closed-loop obstruction is an obstruction of the colon in the presence of a competent ileocaecal valve Causes Inflammatory • Acute inflammation of regions of the gastrointestinal tract • Anastomotic leakage • Secondary and primary peritonitis Traumatic • Blunt or penetrating trauma Obstructive • Small or large bowel Vascular • Thrombosis or embolus to mesenteric vessels • Volvulus and strangulated herniae • Adhesion or obstruction/infarction

• Spontaneous (seen in chronically ill): rare • Tertiary (ICU patients): uncommon Chemical • HCl (early perforated duodenal ulcer) • Extravasation of urine (ruptured bladder) • Bile (leak post cholecystectomy) • Amylase (pancreatitis) Clinical features Systemic features Illness, toxicity, pyrexia, tachycardia, leukocytosis, rigors (bacteraemia/septicaemia), dehydration, loss of skin turgor, collapse of peripheral veins Local symptoms Pain (localized to one quadrant or generalized), severe, constant, aggravated by movement (active, e.g. coughing; passive, e.g. palpation) Local signs • Inspection: loss of normal abdominal movement on respiration • Palpation: tenderness, guarding, rigidity, rebound tenderness (be gentle!) • Percussion: tenderness • Auscultation: silent abdomen • Digital rectal examination: may elicit pelvic tenderness, boggy swelling, cervical tenderness in female

Special • Ultrasound and CT • Peritoneal lavage • Mesenteric angiography • Laparoscopy/laparotomy

Management Secondary bacterial peritonitis • Resuscitate and investigate simultaneously • Pain relief is a priority and should precede clinical examination • Set up i.v. line and give crystalloids • Place nasogastric tube if vomiting • Give antibiotics: (a) If upper gastrointestinal pathology suspected, Gramnegative aerobe cover (b) If lower gastrointestinal pathology suspected, Gramnegative anaerobe cover • Observe pulse, temperature, blood pressure, urinary output • If unsure as to need for surgery, perform repeated physical examination ± special investigations • Surgical treatment indicated for definite deteriorating peritonitis

Peritonitis Bacterial • Secondary (from the gastrointestinal tract): common • Primary (streptococcal): rare

Primary bacterial peritonitis • Haematogenous spread of Gram-positive organisms (Streptococcus pneumoniae) to peritoneal cavity • Occurs in children and adult females

Investigations Essential • Haemoglobin, WCC, PCV • Urea, electrolytes, amylase • Chest X-ray, supine and erect abdominal X-ray • Blood cultures • Group and save ± cross-match

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• Treatment: antibiotics ± laparotomy to drain pus • Prognosis is good Spontaneous bacterial peritonitis • Occurs in immunocompromised patients: (a) Cirrhosis + ascites, Wilson’s disease, chronic active hepatitis (b) Chronic peritoneal dialysis (c) Nephrotic syndrome • Usually Gram-negative organisms • High risk of septic shock and multiorgan dysfunction syndrome • Poor prognosis Haemoperitoneum Some common causes • Intra-abdominal injuries (including iatrogenic) • Intra-abdominal operations • Ruptured ectopic pregnancy • Ruptured corpus luteum cyst • Retrograde menstrual flow • Necrotizing pancreatitis

Progressive type • Implies continued active intra-abdominal bleeding • Clinical features of hypovolaemia + abdominal distension • Requires prompt resuscitiation and surgery Stable type • Implies cessation of active bleeding • Clinical features of peritoneal irritation • (Abdominal ± shoulder-tip pain) • May settle but some require surgery Intestinal obstruction Causes • Extramural: adhesions, bands, volvulus, herniae (internal and external), compression by tumour (e.g. frozen pelvis) • Intramural: inflammatory bowel disease (Crohn’s disease), tumours (carcinoma, lymphoma), stricture, paralytic (adynamic) ileus • Intraluminal: faecal impaction, foreign bodies, bezoars, gallstone ileus Pathophysiology • Bowel distal to obstruction collapses • Bowel proximal to obstruction distends and becomes hyperactive. Distension is due to swallowed air and accumulating intestinal secretions • Bowel wall becomes oedematous. Fluid and electrolytes accumulate in the wall and the lumen (third-space loss) • Bacteria proliferate in the obstructed bowel • As the bowel distends, the intramural vessels become stretched and the blood supply is compromised leading to ischaemia and necrosis

Clinical features • Vomiting, colicky abdominal pain, abdominal distension, absolute constipation (i.e. neither faeces nor flatus) • Dehydration and loss of skin turgor • Hypotension and tachycardia • Abdominal distension and increased bowel sounds • Empty rectum on digital examination • Tenderness or rebound tenderness indicates peritonitis Investigations • Haemoglobin, PCV: elevated due to dehydration • WCC: normal or slightly elevated • Urea and electrolytes: urea elevated, Na+ and Cl– low • Chest X-ray: elevated diaphragm due to abdominal distension • Abdominal X-rays: erect film demonstrates air–fluid levels; supine gives clue as to whether obstruction is in small bowel (central distension/valvulae conniventes shadows cross entire width of lumen) or large bowel (peripheral distension/haustral shadows do not cross entire width of bowel). • Contrast studies, colonoscopy to show level of obstruction Management • Decompress the obstructed gut: pass a nasogastric tube • Replace fluid and electrolyte losses: give Ringer’s lactate or NaCl with K+ supplementation • Relieve the obstruction surgically if: (a) Underlying cause needs surgical treatment (e.g. hernia, colonic carcinoma) (b) Patient does not improve with conservative treatment, e.g. adhesion obstruction (c) There are signs of peritonitis or stangulation Complications Acute • Nosocomial infections: (a) Pneumonia (b) MRSA • Wound infection • Wound dehiscence • Abscess formation • Fistula formation: (a) External (b) Internal Chronic (late) • Wound sinus • Incisional hernia • Adhesions: (a) Recurrent small-bowel obstruction (b) Bacterial overgrowth (blind loop)

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Systemic Inflammatory Response Syndrome Introduction, 181 Pathophysiology, 181

Clinical features, 184 Management, 185

Must know Must do Must know Pathophysiology of SIRS Clinical features of MODS Must do Observe a patient with SIRS in an intensive care unit Look at a chest radiograph showing the features of ARDS

Introduction Over the last 30 years improvements in early resuscitation following major injury have meant that many very ill patients survive the initial traumatic insult (e.g. ruptured abdominal aortic aneurysm, road traffic accident) and are managed thereafter in intensive care units. Many of these patients subsequently develop a hypermetabolic state, similar to that seen with septic shock, that leads to sequential organ failure involving: lungs (acute respiratory distress syndrome, ARDS); kidneys (acute renal failure, ARF); gastrointestinal tract (liver failure, stress ulceration); central nervous system (confusion, encephalopathy); blood (disseminated intravascular coagulation, DIC); heart (cardiac depression). The response to injury that occurs in the body and leads to this hypermetabolic state is called systemic inflammatory response syndrome (SIRS) and the sequence of failing end-organs is referred to as multiple organ dysfunction syndrome (MODS). Despite advances in organ support with volume ventilators, nutritional support and haemodialysis, MODS remains the leading non-cardiac cause of death in surgical patients, with a mortality of approximately 50%. This condition places enormous strains on healthcare resources, as intensive care medicine is extremely dependent on new technology and high personnel costs.

• • • • • •

Prognosis, 186

The cost to society, however, runs much higher because these patients are often young productive individuals. Added to this is the knowledge that those who survive the initial insult without developing multiple organ failure would expect, in most cases, near-perfect rehabilitation and a normal life expectancy.

Pathophysiology The pathophysiology of SIRS/MODS is complex, although much research has focused on the role of the inflammatory response by cells of the immune system. It appears that one or more of many initiating factors (see below) causes a systemic hyperinflammatory response and it is the uncontrolled activity of this response that leads to organ failure (Fig. 16.1). A certain threshold level of injury is necessary for the development of SIRS, although this varies between individuals.

Initiating factors No single initiating factor for the hyperinflammatory response has been isolated but a few suspects have been identified. It is likely that the clinical syndrome of SIRS results from the interaction of a number of proposed initiating mechanisms. Infection has long been known to cause a systemic inflammatory response (i.e. septic shock) but the realization that many patients in ‘septic shock’ had no focus of infection led to the idea that other initiating factors could precipitate a similar syndrome. It would seem that the presence of large areas of damaged or necrotic tissue can mimic an infectious focus. Thus it appears that a common factor in the host response to severe tissue injury from different causes is the initiation of an acute inflammatory response. Multiple organ failure may be due to an overvigorous manifestation of this normally protective defence mechanism. Another view is that a shock toxin, thought to be a thrombogenic aminophospholipid that occurs only on the inner layer of all cell membranes, is liberated by cell

181

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Type of injury Severe haemorrhage with massive blood transfusion Trauma resulting in major tissue injury Large ischaemia-reperfusion injury A major burn A large inflammatory focus Severe infection with bacteraemia

MODS The lungs (ARDS) The kidneys (acute renal failure) The gastrointestinal tract (liver failure, stress ulceration) The central nervous system (confusion) The blood (DIC) The heart (cardiac depression)

Initiating factors Infection Macrophage-cytokine release Microvascular injury Gut injury (LPS)

Mediators of the inflammatory response TNF, IL-1, IL-6 Oxygen free radicals Activated neutrophils

Figure 16.1 Pathophysiology of systemic inflammatory response syndrome.

destruction. It causes DIC, which may obstruct the microcirculation of any and all organs producing MODS by microclots. These microclots may be lysed by plasminogen activator and circulation to the organs restored.

Infection Uncontrolled infection accounts for 50% of cases of MODS. Sepsis has been defined as the presence of microorganisms or their toxins (e.g. endotoxin) in the bloodstream together with the resultant host response. It has long been recognized that severe infection can lead to septic shock, with profound effects on haemodynamics and tissue perfusion. While most forms of circulatory shock induce cellular changes secondary to hypoxia, Gramnegative septic shock is associated with primary cellular dysfunction induced by bacterial endotoxins, which are composed of lipopolysaccharide (LPS) in the bacterial cell wall. LPS stimulates macrophages and endothelial cells to release cytokines that mediate the inflammatory response (Fig. 16.2). Gram-positive organisms (e.g. Staphylococcus aureus) release cytokines by adherence to macrophages, while their toxins act as superantigens that react directly with T cells, causing massive cytokine release (e.g. toxic shock syndrome).

Macrophage–cytokine release Tumour necrosis factor (TNF)-α is detected in the serum of most patients with SIRS. TNF is a principal mediator of the inflammatory response and is released with interleukin (IL)-1 and IL-6 from macrophages. It is thought that persistent stimulation of the release of these cytokines leads to the inflammatory response and tissue injury. Immune suppression and the compensatory anti-inflammatory response syndrome Early observations in patients with SIRS documented major defects in T-cell function, with a central defect in IL-2 (T-cell growth factor) production. This apparent paradox of immune suppression coexisting with immune hyperstimulation (macrophages) may be explained by a two-phase response to injury. One possibility is that an exaggerated inflammatory response to injury may be counterbalanced by the release of potent anti-inflammatory cytokines, including IL-4, IL-10 and transforming growth factor (TGF)-β. This is known as the compensatory antiinflammatory response syndrome (or CARS, a term used by Roger Bone who also coined the term SIRS). CARS may also be deleterious, resulting in opportunistic infection such as systemic candidiasis.

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Tumour necrosis factor Endotoxin (LPS)

IL-1 Pyrogen

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Membrane phospholipid

Phopholipase A2

Arachidonic acid Cyclo-oxygenase Prostacyclin Thromboxane

Lipoxygenase

Leukotrienes

Eicosanoids

Endothelial leak

Free radicals

Ischaemia–reperfusion may induce a systemic inflammatory response. Reperfusion of tissues after a period of ischaemia causes the release of toxic oxygen radicals (superoxide, O2–; hydrogen peroxide, H2O2; hydroxyl radical, OH–) that cause tissue damage by lipid peroxidation. The resulting endothelial damage causes release of cytokines, initiating a systemic inflammatory response and endorgan failure.

Gut injury The normal intestinal mucosa is an effective barrier against microorganisms and endotoxin. A number of adverse changes take place in the septic state that allow bacterial translocation (i.e. passage of bacteria from the gut to the systemic circulation) to occur. The nature of the microflora changes, especially in the presence of antibiotics, to a more pathogenic and more resistant pattern. Barrier function is lost through disappearance of tight junctions between epithelial cells, loss of mucus and increase in mucosal permeability. The Kupffer cells in the liver, which act as part of the

• • •

Microvascular thrombosis

DIC

Figure 16.2 Role of endotoxin in promoting an inflammatory response.

Microcirculatory injury

Ischaemia

reticuloendothelial system that provides the next line of defence, lose their filtering ability and allow bacteria and endotoxin to enter the portal and systemic circulations. Hepatocytes in the liver may also be damaged, with evidence of jaundice. Candida normally present in the gastrointestinal tract may migrate to the bloodstream and lungs, particularly when antibiotics are used. The gut has been called the ‘motor’ of SIRS/MODS because it provides a reservoir of bacteria and endotoxin that sustains the inflammatory response. The inflammatory response in turn causes further intestinal injury. The absorptive power of the gut may also be lost because of damage to intestinal villi. Whenever possible, enteral feeding (to avoid further mucosal atrophy) should be the preferred mode of nutritional support in SIRS. However, if enteral feeding cannot be sustained, intravenous feeding (total parenteral nutrition, TPN) with its additional hazards is necessary.

• •

Hyperinflammatory response The interaction between initiating factors (endotoxin, ischaemia–reperfusion, etc.) and the host-mediated response results in changes in cellular metabolism, with

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increased glucose and amino acid utilization. Mediators such as TNF (also called cachectin), IL-1 and IL-6 are released, resulting in a cascade of responses including: fever from endogenous pyrogen; priming of neutrophils to release reactive oxygen intermediates; promoting adherence of phagocytes to endothelium; activation of complement and release of prostaglandins and thromboxane A2. The mechanism by which the systemic inflammatory response causes end-organ failure is slowly being elucidated. The initial events occur at the microvascular endothelium. Thus, oxygen free radicals are released, neutrophil chemotactic factors are produced and surface adhesion molecules are expressed that enhance neutrophil adhesion and migration into the tissues. Further tissue damage is caused by release of destructive molecules from the trapped neutrophils (more oxygen radicals, elastase, collagenase and proteases). Tissue factor, which activates the extrinsic pathway of the coagulation system, is expressed on the cell surface of monocytes and endothelial cells. As a result, microthrombi are formed, interstitial oedema occurs and organ function deteriorates. Damage to cell membranes allows the free passage of calcium into the cell; this is toxic to mitochondrial function, with impairment of oxidative phosphorylation and ultimately cell death.

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Clinical features The patients at risk are those who have sustained a major biological insult, such as: severe haemorrhage requiring massive blood transfusion (e.g. liver trauma); trauma resulting in major tissue injury (e.g. crush injury); large ischaemia–reperfusion injury (e.g. reperfusion of a limb following embolectomy); major burn; large inflammatory focus (e.g. peritonitis, pancreatitis); severe infection with bacteraemia (e.g. ascending cholangitis). Typically the patient seems to do well following resuscitation but after 2 or 3 days develops the characteristic hypermetabolic picture. In the early phase, blood pressure remains normal, peripheral vascular resistance is lowered and there is an increase in cardiac output. Later, with the development of shock the blood pressure falls, peripheral resistance decreases further and cardiac output remains high. There is a metabolic acidosis with a compensatory respiratory alkalosis. Typically there will be a leukocytosis (or leukopenia), thrombocytopenia and hyperglycaemia. Finally, cardiac output decreases with a profound fall in blood pressure and exacerbation of the metabolic acidosis; oxygen consumption falls, indicating inadequate oxygen perfusion.

• • • • • •

Figure 16.3 Chest radiograph of a patient with acute respiratory distress syndrome.

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Table 16.1 Features of end-organ dysfunction.

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System

Features

Respiratory (ARDS)

Increasing minute ventilation Decreased pulmonary compliance Arterial hypoxaemia and hypercapnia Diffuse fluffy pulmonary infiltrates on chest radiograph

Renal (ARF)

Oliguria Rising urea and creatinine

Liver

Jaundice Decreased protein synthesis (hypoalbuminaemia, prolonged PT)

Gastrointestinal

Gastric stress ulceration Adynamic ileus Acalculous cholecystitis Pancreatitis

Haematology

Leukopenia Disseminated intravascular coagulation

Central nervous system

Confusion Decreasing Glasgow Coma Score

ARDS, adult respiratory distress syndrome; ARF, acute renal failure; PT, prothrombin time.

The diagnosis of SIRS is made when two or more of the following are present: tachycardia; tachypnoea or hyperventilation; and fever and leukocytosis. When two or more end-organs fail a diagnosis of MODS is made (Table 16.1).

• • •

Management The best form of therapy is prevention and every effort should be made during resuscitation to avoid hypotension and gross sepsis (e.g. during bowel surgery) and to ensure adequate oxygenation and urinary output. The general aims of therapy are to: treat infection; ensure adequate tissue oxygenation; maintain nutritional support; and minimize systemic inflammation. Management of the failure of the various end-organs must also be undertaken. This is largely supportive and is discussed in Chapters 11–15.

• • • •

Treat infection Eradication of the source of infection is a priority.

Removal of necrotic tissue or drainage of abscesses is essential. Nosocomial (hospital-acquired) infection must be prevented by aggressive physiotherapy, pulmonary toilet and care of central lines. Wounds must be kept clean and debrided, if necessary. Although no localized source of infection may be identifiable in SIRS, blood cultures are positive in one-third of patients. Antibiotic therapy is initiated on the basis of the most likely infecting organisms until the results of blood culture are available, when more specific antibiotic treatment can be initiated.

Adequate tissue oxygenation Circulatory support with intravenous fluids is important, with constant monitoring of urine output and pulmonary artery pressure. Diuretics may be required to maintain urinary output but should only be used when adequate hydration has been achieved. Inotropic support with adrenaline or noradrenaline is indicated in situations where despite adequate filling pressures cardiac output and perfusion pressure (mean arterial pressure, MAP) are inadequate. Ventilatory support may be necessary, with supplementary oxygen or mechanical ventilation in severe cases. Oxygen delivery must be high as SIRS is associated with increased consumption of oxygen.

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Nutrition Adequate nutrition is essential in the management of patients with SIRS. Nutritional support restores the barrier function of the gut and should thereby reduce bacterial translocation. Whenever possible, enteral feeding is preferred because the enterocyte receives its energy substrates primarily from the gut lumen. However, if enteral feeding cannot be sustained, intravenous feeding (TPN) is necessary. Immune modulation via the addition of l-arginine has been shown to be moderately beneficial in SIRS but has not gained widespread acceptance as yet.

Minimize the systemic inflammatory response

•

Corticosteroids have been used in the management of septic shock. However, their role is at best uncertain. A reduction in the damaging effects of the inflammatory response can be achieved with corticosteroids but only if given prior to the onset of sepsis so that the practical applications are limited. Generation of free oxygen radicals can be prevented by blocking the enzyme xanthine oxidase with allopurinol or by scavenging toxic radicals with superoxide dismutase. This has been shown to be beneficial in a number of experimental models and may be of future value in the clinical situation. Anti-TNF and anti-LPS monoclonal antibodies are among the newer approaches that show promise. They function by interrupting the inflammatory mediator cascade responsible for the persistent injurious response of the immune system to sepsis. However, results have been disappointing in the clinical setting. Other experimental treatments include IL-12 (restores

• • •

helper T-cell balance), the opioid receptor antagonist naloxone (counteracts β-endorphin release) and nonsteroidal anti-inflammatory agents (inhibit the arachidonic acid cascade). The majority of clinical trials in the area of SIRS have been disappointing because of the difficulty in translating therapies found to be successful in tightly controlled animal models to critically ill patients, who represent a very heterogeneous population. The first breakthrough in terms of improved survival was recently achieved in trials of recombinant activated protein C (an anticoagulant protein) in patients with septic shock. It is likely that further progress will be made only with increased understanding of the very complex mechanisms involved. In addition, there is recent evidence that biological variation in the host immune response to trauma and sepsis may have a genetic basis. Identification of those individuals who are likely to have a poor outcome may lead to more focused clinical trials of immunomodulatory agents.

Prognosis Overall, the prognosis for patients with SIRS remains poor. There are a number of factors that influence survival. Age: the very young and the very old have a poor outcome. Severity of the initial insult: the more severe the initial illness, the greater the chance of dying. Cardiac output: the ability to increase cardiac output during the hypermetabolic state is associated with better survival. Infection: identification of a septic source carries a better prognosis. End-organ failure: the more end-organs that fail, the worse the outlook. Patients with three or more end-organ failures rarely survive.

• • • • •

SIRS at a glance Definitions Systemic inflammatory response syndrome: a systemic inflammatory response characterized by the presence of two or more of the following: • hyperthermia > 38 °C or hypothermia < 36 °C • tachycardia > 90 beats/min. • tachypnoea > 20/min or PaCO2 < 4.3 kPa • neutrophilia > 12 × 109/L or neutropenia < 4 × 109/L Sepsis syndrome: a state of SIRS with proven infection Septic shock: sepsis with systemic shock not responsive to fluids

Multiple organ dysfunction syndrome: a state of derangement of physiology such that organ function cannot maintain homeostasis. Several organs may be involved: • lungs (ARDS); • kidneys (ARF); • gastrointestinal tract (liver failure, stress ulceration); • central nervous system (confusion); • blood (DIC); • heart (cardiac depression). Compensatory anti-inflammatory response syndrome: an anti-inflammatory response that counteracts the systemic inflammation of SIRS. CARS is characterized by the release

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of potent anti-inflammatory cytokines, including IL-4, IL-10 and TGF-b. It may also be deleterious, resulting in opportunistic infection such as systemic candidiasis. • TNF-a is both released by and activates macrophages and neutrophils. It is cytotoxic to endothelial cells and parenchymal cells of end-organs. There is no clear evidence for the efficacy of anti-TNF therapies in SIRS. • LPS released from Gram-negative bacterial cell walls activates macrophages via attachment of LPS-binding protein and activation of CD14 molecules on the cell surface. There is no proven value for anti-LPS antibody treatment. • IL-6 and IL-1b cause endothelial cell activation and damage. They promote complement and chemokine release. • High-dose intravenous steroids have little role in established SIRS (probably because of multiple pathways of activation). Steroids for early SIRS are unproven. • Platelet-activating factor (PAF): implicated particularly in acute pancreatitis. No proven role for anti-PAF antibody treatment. • Inducible nitric oxide synthase: synthesized by leukocytes, macrophages and Kupffer cells. It is active for up to 20 h and produces nitric oxide (NO) in nanomolar concentrations. NO is a potent vasodilator and a free radical scavenger. However, it can also form peroxynitrite (ONOO–), a free radical that may cause cellular damage. Common surgical causes SIRS is more common in surgical patients than is diagnosed.

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Common surgical causes of SIRS are:

• acute pancreatitis • perforated viscus with peritonitis • fulminant colitis • multiple trauma • massive blood transfusion • aspiration pneumonia • ischaemia–reperfusion injury Management Early treatment of SIRS may reduce the risk of MODS developing. The role of treatment is to eliminate any causative factor and support the cardiovascular and respiratory physiology until the patient can recover. • Treat infection • Ensure adequate tissue oxygenation • Maintain nutritional support • Minimize systemic inflammatory response • May be role for recombinant activated protein C Prognosis Overall mortality is 7% for SIRS, 14% for sepsis syndrome, 40% for established septic shock, and 90% for three-system failure. Factors predicting poor outcome: • very young and very old • severe initial insult • inability to increase cardiac output • inability to find septic source • multiple end-organ failure

Pathophysiology Initiating factor −−→ Infection: Gram-negative bacteria: endotoxin Gram-positive bacteria: exotoxin Macrophage cytokine release Microcirculatory injury Gut barrier failure

Systemic hyperinflammatory response Release of TNF-α, IL-1, IL-6

Evidence-based medicine Hardaway, R.M. (1998) Traumatic and septic shock alias post-traumatic critical illness. Br J Surg 85, 1473– 1479. Review of evidence supporting shock toxin hypothesis. http://www.ccforum.com/ Critical care forum of crit-

−−→

Common end pathway −−→ Endothelial cell activation Vasodilatation Capillary leak Intravascular coagulation

Clinical picture Tachycardia Tachypnoea Fever Leukocytosis

ical care and emergency medicine includes updates on clinical advances in the treatment of SIRS. http://www.aast.org American Association for the Surgery of Trauma website. http://www.emedicine.com/emerg/topic533.htm A comprehensive review of SIRS and sepsis with references.

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Initial Management of the Severely Injured Patient Introduction, 188 The golden hour, 188 Preparation, 188

Initial assessment, 189 Primary survey and resuscitation, 189

Must know Must do Must know Causes of death in injured patients Immediate resuscitation measures in injured patients Initial assessment of injured patients Neurological assessment Secondary survey of injured patients Principles underlying definitive care of injured patients

Must do Attend accident and emergency departments Observe initial management of severely injured patients Observe emergency operation for major orthopaedic, soft tissue and organ trauma Talk to paramedics who bring in severely injured patients

Introduction As a result of the chronic inability of humans to live at peace amongst themselves, their desire to go faster and further, and the increasing use of and illicit trade in mindaltering substances, there has emerged a modern epidemic a trauma. In the western world you are more likely to die as a result of trauma than any other cause in the first four decades of life. There is no doubt it would be preferable to prevent ‘accidents’ rather than deal with their often disastrous consequences but it is, and will remain, the responsibility of those who treat trauma victims within the ‘golden hour’ to ensure they have a clear understanding of the basic principles of resuscitation and a system that will not fail them in the acute situation.

The golden hour ‘The golden hour’ should not be taken as a literal 60 minutes, although the concept of a limited time period following 188

Secondary survey, 192 Definitive care, 192

injury where lives may be saved or lost is a valuable one. It has been documented that 30% of trauma deaths occurring in hospital might be prevented, the majority by early (within an hour) correction of hypoxia, replacement of circulating blood volume and arrest of continuing haemorrhage. Although the trimodal distribution of death (Fig. 17.1) is now thought to be more of a continuum, examination of its original form allows us to see where our efforts will be beneficial. The first peak of death is immediate (within minutes). These injuries affect vital structures (brainstem, upper spinal cord, great vessels including the heart) and death is probably inevitable. The second peak of deaths occurs in the first few hours: a substantial proportion of these are hypoxic and hypovolaemic deaths. The third peak occurs some weeks after the initial insult, probably in the intensive care unit (ICU), with death often due to multiorgan failure, which may have its origins in the hypoxic hypovolaemic phase. While we can have no effect on the first peak, our actions in the ‘golden hour’ may have a profound influence on subsequent mortality and morbidity.

Preparation Every hospital that receives severely injured patients must be prepared for that purpose. Some units are large enough to provide prehospital medical teams to support ambulance technicians and paramedics, while smaller emergency units may depend on summoning inpatient specialists to provide the initial reception of the patient on arrival at hospital. Whatever system prevails it is clear that each individual involved must know their role and that lines of communication are clearly established and understood. The resuscitation room should be appropriately equipped and the equipment should be checked at the beginning of every shift. Although there may be time for briefing of staff while waiting for the patient, individual roles should have been allocated at an earlier stage. Team members should have received appropriate training, understand what is expected of them and wear adequate

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Number of deaths

Immediate deaths (50%)

Early deaths (30%)

0 Figure 17.1 Trimodal distribution of death following trauma.

protective clothing. There should be a clear understanding of the dynamics of the team and the need to pass information to, and receive instruction from, the team leader.

Initial assessment It is clear that a system requiring a detailed history and examination to be carried out before any treatment is instituted would be inappropriate for the severely injured patient. A different approach is required whereby vital functions are rapidly assessed and secured before treatment priorities are established. The process is known as initial assessment and can be divided into: primary survey and resuscitation; secondary survey; definitive care. The importance of the primary survey cannot be overestimated. If life-threatening injuries are not identified and treated during this phase, then the quality of definitive care becomes irrelevant since the patient will not reach the operating theatre or the ICU.

• • •

Primary survey and resuscitation The primary survey and resuscitation phases are grouped together because the two proceed simultaneously. If a life-threatening injury is uncovered, then it is dealt with immediately. It is essential that the correct sequence is followed, although given adequate personnel in the trauma team a number of assessments and activities can take place simultaneously. The elements of the primary survey are:

2 Time (hours)

Late deaths (20%)

2 3 4 Time (weeks)

and cervical spine control; • airway breathing; • circulation and haemorrhage control; • disability/neurological impairment; • exposure. • The first contact must include talking to the patient. If the patient responds verbally and sensibly, he or she has already conveyed reassuring information about the state of the airway, breathing and circulation.

Airway and cervical spine control Patients who have been brought to hospital by ambulance and whose circumstances show the potential for cervical spine injury will almost certainly have had their spine immobilized. The initial approach to the patient should confirm that this is the case and that the equipment is correctly applied; this may have to be modified in the restless patient. Manual immobilization should be maintained until a semirigid collar, bolster splintage and tape or strapping is in place (Fig. 17.2). Airway management must proceed at the same time as the above, particularly if the patient has failed to provide a verbal response. Noisy respiration or evidence of trauma to the face or anterior neck should have raised awareness of a possible airway problem. The initial measures to clear the airway involve anterior displacement of the mandible. This pulls the tongue musculature from the posterior pharyngeal wall. While either a chin lift or jaw thrust are acceptable, care must be taken that the neck remains unmoved. The opportunity should be taken to look inside the oral cavity and suction applied

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Breathing

Figure 17.2 Trauma patient with spinal immobilization in place and receiving supplemental oxygen.

if there is evidence of blood or gastric contents. Dentures may also be removed. It is likely that if the airway requires manual methods to open it, then it will be jeopardized if manual support is withdrawn. There are a number of different options available at this stage, including oropharyngeal or nasopharyngeal airways. While these may be beneficial in the short term, they afford no protection for the lower airway. If there is doubt about the patient’s ability to maintain a clear unsoiled airway or if there is an absent gag reflex, then a definitive airway should be secured. This is achieved by endotracheal intubation with or without the use of induction and neuromuscular blocking agents. This is a procedure that requires skill and practice and has an incidence of complications even in experienced hands. Unless an individual has the ability to intubate, then the airway should be maintained by other methods until skilled assistance arrives. Attempts by the inexperienced will almost certainly result in oesophageal intubation, which if unrecognized will prove fatal. On rare occasions where there is severe disruption or swelling of the upper airway or it is not possible to intubate the trachea, a surgical airway is indicated. This is performed through the cricothyroid membrane. The area is relatively avascular and no significant structures are likely to be encountered during the procedure. A surgical cricothyroidotomy involves making an incision, forming an opening and then inserting a tube to maintain the opening. A needle cricothyroidotomy is performed by placing a cannula through the membrane, and attaching this to a high-flow oxygen source and a system for intermittently interrupting the gas flow. Once the airway is secured, all injured patients should receive oxygen. If the patient is breathing spontaneously, oxygen should be given via a mask with a reservoir that will deliver approximately 80% oxygen (Fig. 17.2).

The assessment of breathing should not commence until the airway has been secured. Attention should proceed downwards, with a check for tracheal deviation and inspection of neck veins before examination of all areas of the chest by inspection, palpation, percussion and auscultation. There are a number of traumatic conditions that present a threat to life in the immediate post-injury period and provided this logical and sequential approach to assessment of breathing and chest examination is adhered to, these will be uncovered as part of the primary survey. These conditions are: flail chest; open chest wound; massive haemothorax; tension pneumothorax; cardiac tamponade. The first two conditions should be picked up on inspection; the others give rise to findings that will be elicited if the above assessment is carried out. As the examination progresses certain conditions will be excluded while the presence of others may be proven. Students should consider what examination findings will be present in each of these clinical presentations. In tension pneumothorax, the intrathoracic pressure should be relieved by a needle thoracocentesis into the second intercostal space in the midclavicular line. A chest drain is required following the relief of pressure and this is positioned in the fifth intercostal space anterior to the midaxillary line. Massive haemothorax is treated with a chest drain inserted as above and cardiac tamponade may require a needle to be introduced into the pericardium from the xiphoid area. Open chest wounds can be covered with an occlusive dressing, which can function as a valve, but these patients must also have a chest drain inserted. Patients with flail chest require close observation and monitoring with supplemental oxygen and analgesia, although a proportion will require intubation and ventilation. The decision to carry this out at an early stage will be influenced by the severity of the underlying lung injury, the presence of other injuries and the premorbid state. Other less immediately life-threatening chest injuries will be revealed following the secondary survey and chest X-ray. Provided the conditions above have been dealt with, the primary survey progresses to management of circulation.

• • • • •

Circulation and haemorrhage control Provided the trauma team has adequate personnel, a number of tasks should occur simultaneously. An assessment of the patient’s skin colour and ‘feel’ and the capillary

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refill time should be carried out while monitoring is being attached to provide information on cardiac rate and rhythm, blood pressure and arterial oxygen saturation. If there is an identified source of bleeding, this should be controlled by direct pressure; with this in mind, staff should wear protective gloves and garments. While the classic signs of hypovolaemic shock (decreased systolic blood pressure and obvious tachycardia) are well known, these are late features that commonly only arise when at least one-third of the circulating blood volume is lost. The earlier, more subtle signs such as pallor, prolonged capillary refill and decreased pulse pressure must be sought so that early correction of blood loss can be guided. Two large-bore cannulae should be inserted in large veins, the obvious site for these being the antecubital fossae. Also available is the femoral vein just below the inguinal ligament, with the artery as a palpable landmark just lateral. If direct peripheral percutaneous cannulation is difficult or not achieved, venous cut-down may be attempted. Insertion of a central line is also an option but requires skilled personnel. There is the potential for making a critical situation worse if further bleeding is caused or a pneumothorax created. When vascular access is obtained, blood is drawn for routine haematological and biochemical analysis and cross-matching of blood. In the hypovolaemic patient, up to 2 L of warmed intravenous fluids (either colloids or crystalloids) are given while the patient is continually reassessed and monitored. The aim at this stage is to increase circulating volume so that the patient’s remaining red cells receive a wider distribution. If the patient remains unstable, then more circulating red cells are required and blood should be administered; whether this is with type-specific or O-negative blood will be dictated by the patient’s condition. During the correction of hypovolaemia signs of adequate replacement of blood loss and stabilization are sought. If this takes some time or is not happening, the resuscitator must be aware that blood loss is large or likely to be continuing. If that blood loss is not external, then it must be internal in one of three areas: the thorax, the abdomen (intraperitoneal or extraperitoneal) or the pelvic girdle. If surgical colleagues have not already been involved, they must be summoned immediately. Even if relative stability has been achieved, blood loss may continue at a slower rate and the patient must be continually reassessed and closely monitored. While hypovolaemia is the commonest type of ‘shock’ encountered in the trauma patient, it is not the only cause of a decrease in oxygen delivery to vital organs and tissues. Cardiogenic shock as a result of blunt or penetrating chest injury or myocardial infarction prior to an accident, neurogenic shock due to spinal cord injury, septic shock or

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even anaphylaxis may be present. These must be considered in all injured patients.

Disability A basic assessment of neurological status is carried out as part of the primary survey. The AVPU scale, now widely used, describes the patient as: Alert Responding to Verbal stimuli Responding to Painful stimuli Unresponsive. As well as giving an indication of the patient’s conscious level at any given moment, sequential assessment will indicate improvement or deterioration. In addition, the pupils are examined for size, reaction and any inequality. There is no purpose in carrying out even this basic neurological examination before hypoxia and hypovolaemia are corrected as any suboptimal response may be misinterpreted as a primary intracranial event rather than inadequate cerebral oxygenation. A detailed examination with formal assessment using the Glasgow Coma Scale takes place after the primary survey is completed.

• • • •

Exposure Before the primary survey is complete, the patient must be fully exposed and viewed from both front and back. Once this inspection has been carried out the patient should be covered to prevent heat loss. At this stage consideration is given to the insertion of a urinary catheter and gastric tube, provided there is no suspicion of urethral transection and rectal examination precedes passage of the catheter. Urinary output gives information on volume status and tissue perfusion, while a gastric tube allows decompression of the stomach and reduces the risk of aspiration. If there is the possibility of a base of skull fracture, the oral rather than the nasal route should be used. The presence of blood in urine or gastric aspirate indicates injury to the urinary or upper gastrointestinal tract and requires further investigation. At the end of the primary survey, X-rays of chest, pelvis and lateral cervical spine should be obtained in patients who have sustained blunt trauma. Further X-rays are obtained in the secondary survey. The primary survey is not complete until ABC has been secured and the patient is stable. This may not be achieved until the patient has undergone surgery to halt blood loss; if this is the case, the secondary survey should be carried out postoperatively. The importance of following the above system and repeating the primary survey in response to any deterioration in the patient’s condition cannot be overstated.

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Secondary survey During this phase of initial assessment, a head-to-toe examination is carried out. Unless this is done in a methodical fashion, injuries will be missed. A full neurological examination is a necessity and the Glasgow Coma Score should be determined and sequentially recorded. Further investigations and involvement of other specialists is dictated by examination findings, and the gradual piecing together of clinical information will lead to a plan of action. In addition, information should be obtained about how the patient sustained their injuries and their past medical history. If during the secondary survey there is any deterioration in the patient’s clinical condition, the priority is to revert to the primary survey and reassess airway, breathing and circulation. The patient must be closely monitored throughout all activities and should not be moved or subjected to diagnostic procedures outside the resuscitation room until stabilized.

Definitive care Once the initial assessment has been carried out, a plan should be formulated for the patient’s ongoing care. This may involve further investigation or transfer to the operating theatre for surgical intervention or to the ICU. There may be occasions when interhospital transfer is required. Before the patient leaves the resuscitation room a further re-evaluation should be carried out. Any equipment that might be required should be available in the form of a patient transfer kit. All patient records should be completed

• • • • • • • • • •

Trauma is the leading cause of death up to the age of 40 Major problems should be treated as they are identified Supplemental oxygen must be given to all trauma patients A cervical spine injury must be assumed in any patient with multiple injuries A lateral cervical spine X-ray must include the C7–T1 junction Most life-threatening chest injuries are treated by insertion of a tube or a needle and do not require surgery Hypotension and tachycardia may not be present until 30% of blood volume is lost The young and the elderly may have different physiological responses to injury The Glasgow Coma Scale has three parameters: eye opening, motor response and verbal response The severely injured patient must be constantly re-evaluated

and the results of all investigations documented. X-rays and cross-matched blood should go with the patient. It is essential that there is clear communication between the referring and the receiving staff to ensure that all relevant information is passed on and that care is continuous. The mode of transport should be appropriate and the accompanying staff of the same competence as were involved in the resuscitation. It is useful to have a checklist in the resuscitation room to confirm that all the criteria for a successful transfer have been fulfilled.

Initial management of the severely injured patient at a glance Definitions Trauma: any injury caused by a mechanical or physical agent The golden hour: a limited time period following injury when lives may be saved or lost depending on treatment given The golden hour 30% of trauma deaths in hospital might be prevented by early (within an hour) treatment including: • Correction of hypoxia • Cessation of haemorrhage • Restoration of circulating blood volume Death following injury is classically considered to have a trimodal distribution: • Death immediately (50%): vital structures injured (brainstem, upper spinal cord, heart, great vessels) • Death within a few hours (30%, reduced to 9% with

good immediate care): mostly due to hypoxia and hypovolaemia; these are the preventable deaths • Death weeks after injury (20%): (a) Multiorgan dysfunction syndrome secondary to systemic inflammatory response syndrome induced by injury (majority) (b) Raised intracranial pressure (c) Pulmonary embolism Management Preparation • Good paramedical staff to recover patient, commence resuscitation and transport patient safely to hospital • In hospital there should be a trained team with a recognized leader to deal with serious trauma. The team should comprise specialists in anaesthesia, orthopaedics, surgery and nursing

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• Fully equipped resuscitation room; equipment must be

• Draw and send blood for urgent cross-matching and

checked daily • Team members should wear protective clothing and roles and lines of communication should be clearly understood by all members

baseline haematological and biochemical analysis • If hypovolaemic give 2 L of warmed fluid (crystalloid or colloid) • If still unstable after initial fluid give blood (type-specific or O-negative if patient’s condition warrants) • Look for internal bleeding: thorax, abdomen, pelvis • Consider other causes of shock: cardiogenic, neurogenic, sepsis, anaphylaxis

Assessment of the injured patient Assessment and resuscitation are carried out simultaneously in a well-defined manner that has three elements: • Primary survey and resuscitation • Secondary survey • Definitive care Primary survey and resuscitation The primary survey follows a logical sequence of assessments (ABCDE), and if a life-threatening problem is uncovered during this assessment it is dealt with immediately A Airway and cervical spine control • Ensure airway is clear and give O2: (a) If patient talking freely, airway probably clear (b) Lift mandible anteriorly (make sure neck remains unmoved) (c) Suction oral cavity (d) Remove dentures (e) Place oropharyngeal or nasopharyngeal airway (f) Endotracheal intubation (no induction or muscle relaxant) (g) Cricothyroidotomy and minitracheostomy • Ensure spine is immobilized: (a) Already immobilized by paramedics (b) Manual in-line immobilization (c) Semirigid collar, bolster splintage and strapping B Breathing Once airway is secure, check for tracheal deviation and neck veins and examine all areas of chest by inspection, palpation, percussion and auscultation. Look for and treat: • Flail chest: intubation and positive-pressure ventilation • Open chest wound: cover with occlusive dressing and insert chest drain • Massive haemothorax: large-bore chest drain in fifth intercostal space, midaxillary line • Tension pneumothorax: needle thoracocentesis in second intercostal space, midclavicular line, then chest drain • Cardiac tamponade: needle aspiration via epigastric approach C Circulation and haemorrhage control • Assess skin colour and temperature while attaching pulse oximetry, blood pressure cuff and ECG leads • Apply direct pressure to any identified bleeding source • Insert two large-bore (size 14) cannulae in the antecubital fossae or the femoral vein • Insert a central line (jugular or subclavian) if appropriately skilled personnel are available

D Disability Basic assessment of neurological status: A alert V responding to verbal stimuli P responding to painful stimuli U unresponsive Pupils are examined for size, reaction, inequality E Exposure • Patient must be fully exposed and viewed from the front and the back At the end of the primary survey a urinary catheter and a nasogastric tube are placed and X-rays of chest, pelvis and lateral spine obtained. Once ABC has been secured and the patient is stable (which might be after an emergency laparotomy), a secondary survey can be carried out Secondary survey • Detailed head-to-toe examination of the patient • Neurological examination and determination of Glasgow Coma Score • ‘Tubes and fingers in every orifice’ • Further investigation as warranted by findings • Information regarding the injury • Past medical history • Continued monitoring of patient • Revert to primary survey if patient becomes unstable Definitive care A clear plan should be formulated regarding patient’s further care: • Further investigation • Transfer to operating theatre • Transfer to ICU/HDU • Interhospital transfer (e.g. to neurosurgical centre, burns unit) When transferring to another unit: • Ensure that appropriate transport and equipment to transfer the patient safely is available • Send all the documentation, X-rays and cross-matched blood with the patient • Communicate with the receiving unit • Remember the patient is the responsibility of the transferring unit until he or she physically reaches the receiving unit

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Evidence-based medicine American College of Surgeons Committee on Trauma (1997) Advanced Trauma Life Support for Physicians. American College of Surgeons, Chicago. Driscoll, P., Gwinnutt, C., Le Duc Jimmerson, C. & Goodall, O. (1993) Trauma Resuscitation: The Team Approach. Macmillan, London.

Robertson, C. & Redmond, A. (1994) The Management of Major Trauma. Oxford University Press, Oxford. Academic journals: Journal of Trauma, Emergency Medicine Journal http://www.baem.org.uk British Association of Accident and Emergency Medicine http://www.amtrauma.org American Trauma Society

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Head Injury

Introduction, 195 Pathology, 195 Classification, 197 Management, 197

Special problems, 201 Specific head injuries, 202 Intracranial haemorrhage, 204

Must know Must do Must know Differences between primary and secondary brain injury Classification of head injuries How to assess a patient with a head injury and to compute the Glasgow Coma Scale Understand the pathophysiology of raised intracranial pressure and its management Causes and treatment of intracranial haemorrhage Classification of facial fractures Must do Follow a patient with a severe head injury, including stay in the intensive care unit Follow a patient with a minor head injury Examine computed tomographic scans showing the different types of intracranial haemorrhage Talk to a professional involved in rehabilitation of a head injury patient

Introduction More than 1 million patients present to UK emergency departments every year as a result of a head injury, which is thus one of the most common conditions seen in hospital. The causes of head injury are many and varied, although it is common to see ‘head injury’ as the only description of the incident in hospital notes. Every effort must be made to discover its underlying cause, paying particular attention to: the likely speed of impact; any events that may have led to the injury (e.g. epilepsy, subarachnoid haemorrhage, alcohol consumption); any events after its occurrence (e.g. vomiting, epilepsy, talking).

• • •

Outcome from head injury, 206 Rehabilitation after head injury, 207 Spinal injury, 207

Pathology The brain within the skull is liable to injury when deceleration occurs, i.e. when the neck flexes, extends or rotates. As the brain moves within the cranial cavity, it may strike sharp objects such as the sphenoid wing and the frontal and occipital poles. In addition, points where the brain is tethered, such as the foramen magnum and the cranial nerves, are also potential sites of injury. Shaking of the brain when the skull moves at high speed therefore results in haemorrhage in the subarachnoid space and at the frontal, temporal and occipital poles and in tearing of nerves and vessels. This damage can occur without the head being struck, for example in a high-speed car crash or in a fall from a height in which the body decelerates rapidly. It may also be associated with direct damage from a blow or a penetrating wound.

Primary damage The impact from a direct blow to the head is absorbed by the scalp and the skull, which often fractures. The energy is then transmitted to the brain, damaging the tissue it strikes and causing brain movement within the skull. This damage occurring at the time of impact is called primary damage or concussion. Survival depends on the energy reaching the brain, which in turn depends on the velocity of impact (energy = 1/2m × v 2, where m is mass and v is velocity). Therefore hitting a brick wall at 70 mph (110 kph) will be fatal but a kick to the head playing rugby will probably not. Similarly, a shot from a high-velocity rifle will prove fatal but a shot from an air rifle will probably not. The mechanism is the same, the degree is different. Severe primary damage is characterized by coma from impact. The ability to talk, even a few simple words, after injury indicates that, whatever else may happen, the primary injury was not severe and the injury is theoretically survivable. 195

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Secondary damage Primary damage can be exacerbated by secondary damage (i.e. further insults to the damaged brain). These are important to understand as they can often be prevented and occasionally reversed, whereas nothing can be done about primary damage (except avoid the accident in the first place). The main secondary effects are respiratory complications, perfusion failure, intracranial haematoma, cerebral swelling, epilepsy, infection and hydrocephalus.

Respiratory complications Hypoxia, hypercarbia or obstruction to breathing will have disastrous effects on a damaged brain and can worsen the clinical picture dramatically. Head-injured patients are especially prone to respiratory problems because of lack of central drive, airway obstruction, haemothorax or pneumothorax and/or aspiration pneumonia. It cannot be overemphasized that the most important aspect of care in the head-injured patient is care of the chest.

Perfusion failure Perfusion failure will rapidly lead to cerebral ischaemia and a worsening of the clinical state. Head injury itself is rarely a cause of hypotension and other causes need to be investigated (e.g. ruptured spleen). Resuscitation must be rapid and patients with head injury accompanied by a systolic blood pressure of less than 60 mmHg for more than a few minutes rarely survive.

Intracerebral and acute subdural haematomata are usually associated with severe primary injury and carry a bad prognosis. In contrast, subacute subdural and extradural haematomata are often associated with little or no primary injury and bleed slowly over a few hours or days; removal before intracranial pressure (ICP) is excessive can lead to complete recovery.

Cerebral swelling If you sprain your ankle, it swells; if you injure your brain, it also swells. Because the brain is encased in a rigid box, cerebral swelling itself can cause damage by increasing ICP to levels at which cerebral perfusion fails. This leads to ischaemia, which in turn leads to more brain swelling and a further increase in ICP. This vicious circle tends to be worse in those with severe primary damage.

Epilepsy Fits are common in head injury and cause ischaemia while they are occurring. They must be stopped rapidly using intravenous diazepam in small doses, followed by phenytoin or valproate to prevent recurrence.

Infection The development of meningitis or an abscess after injury can reverse a good recovery and must be watched for and treated vigorously.

Hydrocephalus Intracranial haematomata Intracerebral, subdural and extradural haematomata occur and can lead to deterioration following head injury.

An absorptive hydrocephalus can occur during recovery and may slow or reverse recovery; however, it is relieved by shunting.

Head injury at a glance Definitions Head injury: the process whereby direct or decelerating trauma to the head results in skull and brain damage Primary brain injury: damage that occurs to the brain immediately as the result of the trauma Secondary brain injury: damage that develops later as a result of complications Epidemiology Head injury is very common: 1 million patients each year

present to accident and emergency departments in the UK with head injury and about 5000 patients die each year following head injuries Pathophysiology Direct blow • May cause damage to the brain at the site of the blow (coup injury) or to the side opposite the blow when the brain moves within the skull and hits the opposite wall (contrecoup injury).

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Rotation/deceleration • Neck flexion, extension or rotation results in the brain striking bony points within the skull (e.g. the wing of the sphenoid bone) • Severe rotation also causes shear injuries within the white matter of the brain and brainstem, causing axonal injury and intracerebral petechial haemorrhages Crush • Brain often remarkably spared direct injury unless severe (especially in children with elastic skulls) Missiles • Tend to cause loss of tissue with injury proportionate. Brain swelling less of a problem because the skull disruption automatically decompresses the brain • Degree of primary brain injury is directly related to the amount of force applied to the head • Secondary damage results from respiratory complications (hypoxia, hypercarbia, airway obstruction), hypovolaemic shock (head injury does not cause hypovolaemic shock: look for another cause), intracranial bleeding, cerebral oedema, epilepsy, infection, hydrocephalus

Eye opening Spontaneous To voice To pain No eye opening

Glasgow Coma Scale Provides a simple method of monitoring global CNS function over a period rather than a precise index of brain injury at any one time Investigations • Skull X-ray: AP, lateral and Towne’s views • CT/MRI: show contusions, haematomata, hydrocephalus, cerebral oedema

03 Best motor response

Alert and orientated Confused Inappropriate Incomprehensible No voice response

Classification There are four types of head injury. Trivial: little or no primary damage, no secondary effects. Apparently trivial but potentially fatal: little or no primary damage but underlying secondary effect (e.g. extradural haematoma). Apparently hopeless but potentially salvageable: moderate to severe but recoverable primary damage and avoidable or reversible secondary effects. Hopeless: overwhelming primary injury.

• • • •

Management The aims of management are to: recognize and treat those patients with apparently trivial but potentially fatal injuries at an early stage before brain damage occurs;

•

Clinical features • History of direct trauma to head or deceleration • Patient must be assessed fully for other injuries (full trauma survey) • Level of consciousness determined by GCS: fully conscious, GCS = 15; deep coma, GCS = 3 • Pupillary inequalities or abnormal light reflex indicate intracranial haemorrhage • Headache, nausea, vomiting, a falling pulse rate and rising blood pressure indicate cerebral oedema

Voice response 4 3 2 1

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5 4 3 2 1

Obeys commands Localizes pain Flexes to pain Abnormal flexion to pain Extends to pain No response to pain

6 5 4 3 2 1

• •

recognize those with hopeless injuries and to withdraw treatment at an early stage; treat those with potentially salvageable severe injuries adequately and rapidly minimize secondary effects and allow complete or partial recovery.

Trivial head injury If the patient is conscious, a history of the events leading up to the accident and subsequent to it is obtained. If the patient has sustained a period of unconsciousness, it is helpful to obtain corroboration of this from witnesses. Retrograde amnesia for events leading up to the accident is a significant factor in the history. The duration of unconsciousness and retrograde amnesia are indicative of the severity of the injury; if very transient and in the absence of other indications, they need not be a criterion for admission and further observation.

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Table 18.1 Society of British Neurological Surgeons’ guidelines for initial management of head injuries (1998).

Head injury

Patient fully conscious

Patient with impaired consciousness or neurological signs

Resuscitate

Is there an indication for SXR? No

Urgent CT scan

CT positive

Yes SXR

Patient in coma or deteriorating level of consciousness

SXR positive

CT negative

SXR negative Observation at home

Observation in hospital

Neurosurgical consultation /referral

Most general hospitals now have CT scanning available around the clock. The ability to transfer images electronically from the general hospital to the neurosurgical unit means that a neurosurgical opinion on a patient can be obtained and a treatment plan decided on without having to transfer the patient to the neurosurgical unit. In many cases care can be given in the general hospital ICU with remote neurosurgical input. Only those patients that require burr holes, craniotomy or intracranial pressure monitoring need be transferred to the neurosurgical unit.

The questions to be asked include the following. Does this patient need a skull radiograph? Do I need to admit this patient to hospital? Do I need to refer this patient to a neurosurgeon? These questions are easily answered by following guidelines laid down by a group of neurosurgeons under the auspices of the Kings Fund and first published by the Royal College of Surgeons in 1986. They have recently been updated and published in the British Journal of Neurosurgery (see Evidence-based medicine). The guidelines are shown in Table 18.1. The risk of a significant intracranial haematoma following head injury is 1 in 6000 among alert patients with no skull fracture, 1 in 120 among alert patients with a fracture and 1 in 4 among drowsy patients with a fracture. An admitted patient needs regular neurological observation. Patients who suffered no loss of consciousness or who had no more than retrograde amnesia or brief loss of consciousness may be allowed home if they remain stable for 24 h. Simple fractures are not an indication for continued hospital stay. Compound fractures, i.e. associated with open scalp wounds or basal fractures with otorrhoea or rhinorrhoea, will need a more prolonged hospital stay.

• • •

Indications for skull radiography* after recent head injury (A) Oriented patient History of loss of consciousness or amnesia Suspected penetrating injury Cerebrospinal fluid or blood loss from the nose or ear Scalp laceration (to bone or > 5 cm long), bruise or swelling Violent mechanism of injury Persistent headache or vomiting In a child, fall from a significant height (which depends in part on the age of the child) and/or on to a hard surface; tense fontanelle, suspected non-accidental injury (B) Patient with impaired consciousness or neurological signs All patients, unless urgent CT is performed Indications for admission to a general hospital (A) Oriented patient Skull fracture or suture diastasis Persisting neurological symptoms or signs Confusion or any other depression of the level of consciousness at the time of examination Difficulty in assessing the patient (e.g. due to alcohol, young age, epilepsy, attempted suicide) Inadequate social conditions or lack of responsible adult or relative Coexistence of other medical conditions (e.g. coagulation disorders) (B) All patients with impaired consciousness Indications for urgent CT scanning and/or neurosurgical consultation Coma, confusion or neurological signs persisting after resuscitation Deteriorating consciousness or progressive neurological signs Fractured skull in combination with: confusion or other impairment of consciousness epileptic seizure neurological symptoms or signs Open injury with: depressed compound fracture of skull vault fractured base of skull penetrating injury Unstable systemic state precluding transfer to neurosurgery Diagnosis uncertain Tense fontanelle or suture diastasis in a child Indications for neurosurgical consultation after CT scanning Abnormal CT scan High- or mixed-density intracranial lesion Midline shift Obliteration of third ventricle Relative dilatation of lateral ventricle(s) Obliteration of basal cisterns Intracranial air Subarachnoid or intraventricular haemorrhage CT scan normal but progress unsatisfactory * Skull radiography is not necessary if CT is to be performed.

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Figure 18.1 CT reconstruction of cervical spine C1/C2 fracture.

Traditionally prophylactic antibiotics have been given to these patients but are less commonly used nowadays. Persistent rhinorrhoea or otorrhoea requires surgical treatment to repair the skull base defect. Following head injury, patients also need to be normally hydrated not fluid-restricted. An intravenous infusion should be used if the patient is too sleepy to drink or is vomiting. The only other aspect of care is to deal carefully with any scalp wounds, remembering to: shave hair for at least 2 cm around the wound; remove foreign bodies; débride the skin edges; suture the scalp in a single layer, leaving stitches in for at least 7 days; use lidocaine with adrenaline to reduce bleeding.

• • • • •

Severe head injury A person with a severe head injury will invariably arrive unconscious in the emergency department and the injury may be just one aspect of multiple trauma. It is important to stabilize the airway, breathing, circulation and exclude cervical fractures before concentrating on the head injury (Fig. 18.1). The management of head trauma is essentially the same whatever the cause and consists of intubation and ventilation, resuscitation, a thorough examination, imaging and decisions on treatment.

Intubation and ventilation An unconscious patient with a head injury should be intubated to protect his or her airway. This usually involves sedation and paralysis and so ventilation will be required. There is no reason not to intubate. Traditional arguments against were that sedation prevented neurological monit-

oring of any deterioration and that intubation put at risk an unstable cervical spine. Nowadays, patients with severe head injuries undergo computed tomography (CT) so the first reason is less applicable and, although the cervical spine is also commonly involved in fatal head injuries, it is rarely injured in a survivable head injury. Having intubated and ventilated the patient, ensure the chest is moving properly, that there is no haemothorax or pneumothorax, and check blood gases to ensure adequate oxygenation.

Resuscitation Insert one or more large-bore cannulae, a central venous pressure line if necessary, and a urinary catheter. Make sure that the patient’s blood pressure and pulse are normal and that he or she has a good urine output. If there is bleeding, find its source and stop it. Stop any fits with intravenous diazepam and phenytoin.

Assess the level of consciousness Once the airway has been established and cardiovascular stability achieved, the next priority is to assess the level of consciousness. Response to verbal and painful stimuli provides a simple evaluation, although more objective analysis can be obtained by using the Glasgow Coma Scale (GCS) (Table 18.2). Any depression of consciousness is an indication for admission for observation. Confusion may arise if the patient has been taking alcohol or other drugs but this increases rather than diminishes the necessity for careful observation.

Thorough examination A full neurological and general examination is conducted to establish the presence or absence of focal neurological

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Table 18.2 Adult Glasgow Coma Scale. Score Eye opening Spontaneous To voice To pain No eye opening

4 3 2 1

Voice response Alert and orientated Confused Inappropriate Incomprehensible No voice response

5 4 3 2 1

Best motor response Obeys commands Localizes pain Flexes to pain Abnormal flexion to pain Extends to pain No response to pain

6 5 4 3 2 1

03 signs. Pupillary inequalities or abnormal response to light are indicative of intracranial haemorrhage. A falling pulse rate and rising blood pressure are also indicative of increasing ICP. In the conscious patient, nausea and vomiting may suggest rising ICP due to bleeding. In the unconscious or semicomatose patient, vomiting may lead to aspiration into the air passage. Look at every part of the body. Pay particular attention to puncture wounds and the possibility of a spinal fracture.

Imaging Accompanied by competent staff the patient should be imaged thoroughly. Skull (see Table 18.1), cervical spine (Fig. 18.2) and chest films are mandatory. If the patient has multiple injuries from a high-velocity injury, radiographs of the thoracic and lumbar spine, abdomen, pelvis and any suspected fractures should also be obtained. Nowadays, most multiple trauma patients will have CT of head, thorax and abdomen rather than radiography.

Treatment plan There is no point in moving an unstable patient to another hospital for neurosurgery unless the instability is purely neurological. It is better to perform laparotomy or thoracotomy before transfer to stop bleeding and then to

Figure 18.2 Radiograph of cervical spine showing fracture dislocation of the spine at C2/C3 level, so-called hangman’s fracture.

move the patient afterwards. Even if the patient is being transferred, spend a few minutes closing wounds and splinting fractures. Even if these procedures are crudely performed, it is better than not doing them at all, and they can be tidied up later. Frequently, patients who have suffered a serious head injury but do not have a neurosurgically remediable lesion (e.g. an extradural haematoma) are managed in the intensive care unit (ICU) of the admitting hospital. CT scanning is performed in the admitting hospital and the images are relayed electronically to the neurosurgical unit via an image link system. Based on the CT findings the neurosurgeons provide advice to the admitting hospital regarding treatment; these patients usually have some degree of cerebral oedema. Such a system reduces unnecessary transfers to the neurosurgical unit yet involves the neurosurgeons in the management of the patient’s head injury. Modern minimally invasive ICP monitors (e.g. Codman, Micro-sensor, Cimino) are being increasingly used in district general hospitals without neurosurgical facilities by anaesthetists or other surgeons.

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Transferring a neurosurgical patient Some patients will have to be transferred to a neurosurgical unit for treatment. Indications for transfer include contusions, haematomata or hydrocephalus seen on CT scanning. Unconscious patients do not travel well and care must be taken to ensure the safest journey. The patient must be stable before the journey starts because treatment of a deteriorating patient in a moving ambulance or helicopter is very difficult. The most experienced doctor available, preferably an anaesthetist, and a nurse should travel with the patient. Lines and tubes must be well secured before setting out and adequate supplies of paralysing agents, sedatives and fluids must be taken.

Neurosurgical management Neurosurgical management will depend on the CT findings. If a haematoma or hydrocephalus is evident, treatment with craniotomy or drainage is necessary. If no clots are shown, or after surgery, a decision must be made whether to ventilate the patient. Views differ about who should be ventilated; in the author’s practice, patients with respiratory problems or those at risk of developing them are ventilated to prevent hypoxia. Ventilation is also used along with sedation, diuretics and intermittent boluses of mannitol (an osmotic diuretic) to control ICP. Moderate hyperventilation works by reducing Pco2, which in turn reduces cerebral blood flow, although this mechanism tends to be effective for only 48–72 h. ICP monitoring is essential in these circumstances and is easily performed using a variety of methods. The most widely used technique is to insert a fine intraparenchymal wire sensor through a small twistdrill hole in the skull. The kits come prepacked with sensors and guarded drills and can be connected to the normal ICU monitoring systems (e.g. Codman, Microsensor, Cimino). Normal ICP is less than 10 mmHg. An ICP higher than 20 mmHg is worrying and needs to be treated; an ICP above 40 mmHg denotes severe problems and is rarely associated with a survivable injury. Note that these values apply to steady ICP levels. Coughing or chest physiotherapy may produce transient pressures of 60 mmHg or more but return to baseline when the stimulus stops. The patient is ventilated with full nursing care (Table 18.3) for periods determined at the onset of ventilation (e.g. 48 or 72 h). After this period, if there are no problems and the ICP is low, sedation is stopped to allow the patient to waken. If the process runs smoothly, all well and good; however, if the patient becomes distressed or the ICP increases excessively, ventilation should be restarted for another set period. As the patient begins to wake, he or she

201

Table 18.3 Nursing the unconscious patient. Elevate head 30°, turn patient frequently Monitor arterial blood pressure, blood gases, ICP, serum sodium, glucose and osmolality Endotracheal intubation, controlled ventilation Control ICP: ventilation, intermittent boluses of mannitol Enteral feeding, 2500 kcal/day (10 500 kJ/day) Ulcer prophylaxis: proton pump inhibitors ICP, intracranial pressure.

may be extubated as soon as the airway is secure. As soon as recovery begins, an active programme of physiotherapy, speech therapy and occupational therapy should be started to maximize rehabilitation.

Special problems Children Infants have a tendency to deteriorate dramatically after relatively minor injuries, becoming comatose and floppy and then recovering again rapidly (infant concussion syndrome). They also have a tendency to fit and may develop status epilepticus after minor trauma. Skull fracture and intracranial haematomata are less common in children than in adults. Non-accidental injury should always be borne in mind, especially when a child presents with acute subdural haematomata.

Depressed fracture In a depressed fracture, bone is driven inwards and may penetrate the dura. CT scanning will show whether the dura is lacerated. Scalp lacerations over a depressed fracture must be closed urgently and the patient given antibiotics. He or she may then be transferred at leisure to a neurosurgical unit where a decision can be made regarding wound exploration. If there is a suspicion that the dura is lacerated, the fracture is always explored, although the indication for exploring a slightly depressed fracture is usually only cosmetic (Fig. 18.3).

Missile injuries While high-velocity injuries are usually fatal, low-velocity injuries can be survivable. The patient should be resuscitated and transferred to neurosurgical care where the wound will invariably be explored to remove bone, skin and hair fragments. However, the missile itself can often be left undisturbed as the heat involved usually sterilizes it.

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Basal fractures Basal fractures may be accompanied by rhinorrhoea, periorbital haematoma and subconjunctival haemorrhage if the anterior cranial fossa is involved or otorrhoea if the middle cranial fossa is the site of injury. Subconjunctival haemorrhage, in which the blood tracks forwards from behind so that there is no posterior margin to the haematoma, is suggestive of anterior cranial fossa fracture. Direct injury to the eyeball produces a localized haematoma with visible margins. Periorbital bruising from direct injury is not confined by the orbicularis oculi, as is the case with intracranial (anterior fossa) injury.

Cerebrospinal fluid leak Cerebrospinal fluid (CSF) leaks occur through the nose or ear, or silently down the back of the throat. Most clear up spontaneously within 2 weeks. Only a tiny percentage need surgical exploration to close the dural tear. Most neurosurgeons now advocate no treatment for CSF leaks, although traditionally broad-spectrum antibiotics (e.g. ampicillin and flucloxacillin) were given.

(a)

Cervical spine injury

(b) Figure 18.3 (a) Skull radiograph showing depressed fracture and air within the skull. (b) CT scan showing large extradural haematoma in the right frontal area with compression of the ventricles.

Injury to the cervical spine may accompany a head injury and fractures and dislocations in this area are common after road traffic accidents and falls. If a patient complains of neck pain or weakness and/or numbness in the limbs or if there is loss of sphincter control, an injury to the cervical spine should be suspected. Precautions should be taken to prevent further damage. Extension and rotation of the neck should be prevented, preferably by halter traction. Skull callipers may be applied later. Sandbags may help prevent movement in the emergency situation. Collars should be maintained in position until radiography has been completed. Lateral radiographs of the cervical spine, including all seven cervical vertebrae, are done as soon as possible. Movement of the patient is especially hazardous: five individuals are needed to move the patient, keeping the head and neck immobile. Patients unconscious following a head injury should be assumed to have a cervical spine injury until proved otherwise by normal radiographs of the cervical spine (see Figs 18.1 & 18.2).

Other injuries Even relatively minor head trauma can be complicated by injuries to the eyes, facial skeleton, ears and cranial nerves. The cooperation of ophthalmic, ear, nose and throat, plastic and faciomaxillary surgeons is therefore needed. More serious head injury may also be complicated by cervical

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spine and carotid artery trauma, which may not be apparent at first.

septum, reduction is necessary to relieve the obstructed nasal passage.

Specific head injuries

Fracture of the zygoma

Skull fractures

Direct injury, such as a blow on the neck, may produce a depressed fracture of the zygoma. There are three common fracture sites: the arch, the region of the infraorbital foramen and the frontomalar suture. On examination, circumorbital ecchymosis is evident, with the bruising confined to an area within the orbital rim. Subconjunctival haemorrhage is also present without a posterior border. The cheek appears flattened and a bony step can be felt in the infraorbital rim, with an area of paraesthesia below that in the distribution of the infraorbital nerve. Diplopia may occur and the patient may have unilateral epistaxis. Movement of the mandible may be restricted. Diplopia is usually temporary due to bruising of the inferior rectus and inferior oblique muscles. However, if there is entrapment of the muscles in the fracture, the diplopia may persist and an inability to elevate the affected eye can be demonstrated. Blowout fractures of the orbit are due to direct trauma to the eye, with collapse of the orbital floor into the antrum. Entrapment of the inferior extraocular muscles may cause persistent diplopia. Zygomatic arch fracture should be elevated via a temporal incision within 10 days of the injury. An orbital blowout fracture requires elevation through the antrum or may need prosthetic replacement.

Skull vault Skull vault fractures, if linear and closed, do not of themselves require treatment and are more an indication of the severity of the trauma: attention is concentrated on the associated brain injury. Penetrating injuries may cause compound fractures, with pieces of bone and foreign bodies penetrating the meninges or the brain itself. These obviously require careful exploration and wound toilet. Depressed skull fractures may lacerate meninges or brain and pressure from a depressed fracture may cause traumatic epilepsy.

Base of skull Basal skull fractures have already been mentioned. They are usually anterior or middle cranial fossa fractures and may communicate with the exterior, with the risk of infection. Antibiotics should be given. In anterior cranial fossa fractures, persistent rhinorrhoea through the cribriform plate of the ethmoid may need formal repair.

Facial fractures Fractures of the maxilla Nasal bone fracture Nasal bone fractures are common and are accompanied by swelling, deformity and bleeding from the nose. Reduction is carried out to correct the deformity, although this is often delayed to allow resolution of swelling before reassessment for deformity. If there is dislocation of the

Figure 18.4 Le Fort classification of maxillary fractures.

Le Fort type I

Le Fort has separated fractures of the maxilla into three categories (Fig. 18.4). Le Fort I This fracture traverses the lower nasal septum and maxillary antrum, separating the dentoalveolar portion of the

III

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maxilla from the rest of the skull. The lower fragment is very mobile and dental occlusion is affected, giving an open bite.

Intracranial haemorrhage

Le Fort II In this higher-level fracture, the line of the fracture extends through the nasal bones and medial portion of the orbit. Epistaxis and rhinorrhoea may occur. Periorbital bruising and subconjunctival haemorrhage are evident. Malocclusion is present with an anterior open bite.

An extradural haemorrhage is almost invariably caused by trauma, the only other cause being postoperative. Usually the patient has received a relatively minor blow that causes little primary brain damage but which fractures the skull. Beneath the fracture a dural vessel, most commonly the middle meningeal artery, is torn and the bleeding strips away the dura from the inner table of the skull. Bleeding is rapid and an enlarging haematoma collects between the skull and the dura mater and compresses the underlying brain. The signs of increased ICP quickly develop, with a rise in blood pressure, a fall in pulse rate, a dilated pupil and focal neurological signs, which include paresis or paralysis of the limbs on the opposite side and Jacksonian epilepsy. The patient gradually sinks into a coma and will die from raised ICP if no action is taken. Evacuation of the haematoma can only be carried out completely by craniotomy. Burr-holes placed over the clot to release some of it may be a life-saving procedure if there is not sufficient time for transfer to a neurosurgical unit, but if appropriate predictive care of a head injury has been carried out such heroics should not be neccessary. The possibility of an extradural haematoma should be considered in all those with a skull fracture (other than the fully alert patient) and a CT scan performed before further deterioration occurs.

Le Fort III This is a very high fracture above the level of the zygomatic arch and including the whole maxilla, which is pushed downwards and backwards. There is extensive facial oedema and periorbital ecchymoses with subconjunctival haemorrhage. Involvement of the cribriform frontal sinuses in the line of the fracture gives rise to escape of CSF as rhinorrhoea.

Fractures of the mandible

These fractures often occur in two places, sometimes involving identical sites on both sides, sometimes involving quite different sites depending on the forces transmitted at the time of injury, e.g. a punch to the side of the jaw may cause a fracture through the premolar area on the side of the impact and a condylar fracture on the opposite side. The premolar area, angle of the jaw and the mandibular condyle are the common sites of fracture. The fracture is a compound fracture if it traverses a tooth socket, and the patient should accordingly be treated with antibiotics. Clinically, a patient who sustains a mandibular fracture has a defective bite. Because of the upward pull of masseter and pterygoid muscles on the posterior fragment, posterior dental occlusion occurs prematurely and anterior dental occlusion cannot be achieved. The anterior fragment tends to be pulled downwards and backwards by the digastric muscles, thus further preventing occlusion. Damage to the inferior alveolar nerve may occur as it runs from mandibular to mental foramen, causing anaesthesia or paraesthesia in the area. A sublingual haematoma develops and a step may be felt in the line of the mandible. Treatment is aimed at correcting the deranged dental occlusion and correcting the backward displacement of the horizontal ramus, which can obstruct the airway. As in any fracture, reduction with correct alignment of the fragments and immobilization achieves the desired result. Immobilization is achieved by fixing the upper and lower jaws together with cap splints or by direct wiring or plating of the fracture. Fixation for 4–6 weeks is usually required, except for unilateral condylar fractures where 10 days is deemed sufficient.

Extradural haemorrhage (Fig. 18.5 and Fig. 18.9)

Figure 18.5 Extradural haematoma. CT scan showing large extradural haematoma in the left temporoparietal area with compression of the ventricles.

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Acute subdural haematoma (Fig. 18.6 and Fig. 18.8) Acute subdural haemorrhage carries a poor prognosis as it is usually associated with severe primary injury. This type of intracranial bleeding is more common than extradural haemorrhage and tends to occur in elderly patients who sustain a head injury because of the increased mobility of the brain within the skull cavity. It is accompanied by cerebral laceration or contusion and the patient tends to be in a confused or unconscious state from the time of the injury. The bleeding is the result of tearing of thin-walled veins traversing the space between the arachnoid and dura mater. The patient’s neurological condition deteriorates progressively as the haematoma spreads. Even when the haematoma has been fully evacuated following craniotomy and incision of the dura mater, the patient may not fully recover because of the underlying brain injury or recovery may be slow.

Chronic subdural haematoma (Fig. 18.7) Figure 18.6 Acute subdural haematoma. CT scan showing large subdural haematoma in the left occipitoparietal area with compression of the left ventricles.

Figure 18.7 Chronic subdural haematoma. MRI scan showing large chronic subdural haematoma surrounding the cerebral cortex.

Chronic subdural haemorrhage is seen in the elderly, alcoholics and infants. The most common cause in an infant is a non-accidental shaking injury and this possibility should always be considered. The condition develops over

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Table 18.4 Outcome from head injury related to Glasgow Coma Scale (GCS) on admission. Skull bone

Dura mater

GCS on admission (maximum score 15)

Mortality (%)

15 8–12 5 cm long), bruise or swelling • Violent mechanism of injury • Persistent headache or vomiting • In a child, fall from a significant height (depends in part on age of the child) and/or on to a hard surface; tense fontanelle, suspected non-accidental injury Patient with impaired consciousness or neurological signs • All patients, unless urgent CT is performed Indications for admission Oriented patient • Skull fracture or suture diastasis • Persisting neurological symptoms or signs • Confusion or any other depression of the level of consciousness at the time of examination • Difficulty in assessing the patient (e.g. due to alcohol, young age, epilepsy, attempted suicide) • Inadequate social conditions or lack of responsible adult or relative • Coexistence of other medical conditions (e.g. coagulation disorders) All patients with impaired consciousness Indications for urgent CT scanning ± neurosurgical consultation • Coma, confusion or neurological signs persisting after resuscitation • Deteriorating consciousness or progressive neurological signs • Fractured skull in combination with: (a) Confusion or other impairment of consciousness (b) Epileptic seizure (c) Neurological symptoms or signs

• Open injury with:

• • •

(a) Depressed compound fracture of skull vault (b) Fractured base of skull (c) Penetrating injury Unstable systemic state precluding transfer to neurosurgery Diagnosis uncertain Tense fontanelle or suture diastasis in a child

Indications for neurosurgical consultation after CT scanning Abnormal CT scan • High- or mixed-density intracranial lesion • Midline shift • Obliteration of third ventricle • Relative dilatation of lateral ventricle(s) • Obliteration of basal cisterns • Intracranial air • Subarachnoid or intraventricular haemorrhage CT scan normal but progress unsatisfactory Severe head injury • Patient will arrive unconscious at hospital. Head injury may be part of a multiple trauma • ABC: intubate and ventilate unconscious patients to protect airway and prevent secondary brain injury from hypoxia • Resuscitate patient and look for other injuries, especially if the patient is in shock. Head injury may be accompanied by cervical spine injury and the neck must be protected by a cervical collar in these patients • Treat life-threatening problems (e.g. ruptured spleen) and stabilize patient before transfer to neurosurgical unit. When transferring, ensure adequate medical supervision (anaesthetist + nurse) during transfer Complications Skull fractures • Indicate severity of injury • No specific treatment required unless compound, depressed or associated with chronic CSF loss (e.g. anterior cranial fossa basal skull fracture) Raised ICP • Trauma to the brain causes swelling but because the brain is encased in a rigid box (i.e. the skull) cerebral swelling results in raised ICP. If ICP rises above arterial blood pressure, cerebral perfusion fails. This leads to ischaemia, which in turn leads to more brain swelling and a further increase in ICP • ICP tends to be worse in those with severe primary damage

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• Ventilation is used with sedation, diuretics and intermittent boluses of mannitol (osmotic diuretic) to control ICP. Moderate hyperventilation reduces PCO2, which in turn reduces cerebral blood flow but this mechanism tends to be effective for only 48 –72 h • Monitoring is essential in patients with raised ICP: (a) Normal ICP < 10 mmHg (b) ICP > 20 mmHg is worrying and needs to be treated (c) ICP > 40 mmHg is severe and rarely associated with a survivable injury Intracranial haemorrhage • Extradural haemorrhage: tear in middle meningeal artery. Haematoma between skull and dura. Often a ‘lucid interval’ before signs of raised ICP ensue (falling pulse, rising blood pressure, ipsilateral pupillary dilatation, contralateral paresis or paralysis). Treatment is by evacuation of haematoma via burr-holes • Acute subdural haemorrhage: tearing of veins between arachnoid and dura mater. Usually seen in elderly. Progressive neurological deterioration. Treatment is by

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evacuation via craniotomy but even then recovery may be incomplete • Chronic subdural haematoma: tear in cortical vein. Haematoma enlarges slowly by absorption of CSF. Often the precipitating injury is trivial. Drowsiness and confusion, headache, hemiplegia. Treatment is by evacuation of the clot • Intracerebral haemorrhage: haemorrhage into brain substance causes irreversible damage. Efforts are made to avoid secondary injury by ensuring adequate oxygenation and nutrition Prognosis Related to level of consciousness on arrival in hospital GCS on admission

Mortality

15 8 –12 100 × 106/L; white blood cells > 500 × 103/L; amylase > 1100 U/L; the presence of bile, bacteria or food particles in the peritoneal effluent. The overall diagnostic accuracy of percutaneous peritoneal lavage in the detection of intra-abdominal trauma

• • • •

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of detecting intra-abdominal injury. Lesions of the liver and spleen give heterogeneous echo patterns. Haematomata appear as sonolucent (transparent) areas, while the presence of haemoperitoneum is identified by the crescent-moon sign. Computed tomography Contrast-enhanced CT scanning of the abdomen is used in the detection of abdominal injuries, provided the patient is haemodynamically stable (because the examination takes 45–60 min). It is particularly helpful in children where it is now the diagnostic procedure of choice. In children blunt abdominal injury, even with haemoperitoneum, is frequently treated non-operatively.

(a)

Angiography The use of angiography in the diagnosis of solid organ damage has declined since the introduction of CT, although it is still valuable in confirming significant active bleeding and major disruption of the vascular pedicle of an organ. Isotope scintigraphy was used to detect injury to the solid organs but has been largely superseded by CT and ultrasound scanning of the abdomen.

Antibiotics in abdominal trauma

(b) Figure 19.2 Equipment used for (a) peritoneal lavage and (b) diagnostic laparoscopy.

is 90%. One disadvantage of this test is the high falsepositive rate (15 –20%). This is due to minor lesions such as small lacerations that stop bleeding spontaneously by the time laparotomy is performed. Laparoscopy A small laparoscope (minilaparoscope) with an external diameter similar to that of the dialysis catheter can easily be inserted into the peritoneal cavity under intravenous sedation and local anaesthesia. Laparoscopy reliably excludes intra-abdominal injury and minor lacerations that do not require laparotomy (but which often yield a positive result with abdominal lavage). Laparoscopy is used in injured patients with stab wounds, a diminished level of consciousness and equivocal abdominal signs. The equipment used for peritoneal lavage and diagnostic laparoscopy is shown in Fig. 19.2. Ultrasonography Because haemoperitoneum and haematomata provide liquid–solid interfaces, high-resolution real-time ultrasonography is an extremely sensitive and accurate method

Systemic antibiotic therapy active against both aerobes and anaerobes is administered to patients with abdominal injuries. The risk factors for the development of infective complications are shock, missile/penetrating aetiology, colon injuries and old age. The most common causative aerobes are Enterococcus, Escherichia coli and Klebsiella pneumoniae, whereas the most commonly cultured anaerobes are Bacteroides species. The highest incidence of wound infection, abdominal abscess and mortality is encountered in colon injuries.

Specific intra-abdominal injuries Hepatic injuries Injuries to the liver include minor lacerations that do not require surgical treatment, moderately sized tears that need liver suture and severe injuries accompanied by extensive trauma to one or both lobes. The latter are lifethreatening because of haemorrhage and other associated injuries. Stable patients with minor injuries are treated conservatively in the first instance. These patients are best followed up by serial CT scanning to monitor resorption of haemoperitoneum and the pattern of healing of intrahepatic lesions. Surgical exploration is necessary if there is evidence of continued blood loss. Simple suture and resectional débridement are the two measures necessary

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for the control of bleeding due to moderate injuries. In major injuries with bleeding from the vena cava or hepatic veins, the supracolic compartment of the abdomen is packed with gauze rolls. This usually controls the bleeding and allows resuscitation and transfer to a specialized hepatobiliary unit for definitive treatment.

Splenic injuries Injuries to the spleen are usually sustained by blunt abdominal trauma: the spleen is the most commonly injured organ in RTAs. The injuries may consist of incomplete parenchymal tears, complete lacerations or severe fragmentation with avulsion of the hilar vessels. The clinical features of splenic injury include abdominal tenderness, hypotension and left lower rib fractures. Haematuria may be present. Left shoulder-tip pain, often stressed as a symptom of splenic injury, is in fact rare, being found in only 5% of patients. Associated chest injuries are very common. If in doubt, diagnosis can be confirmed by peritoneal lavage, minilaparoscopy or abdominal ultrasound scanning. The surgical management of splenic injuries varies. The emphasis in recent years has been on splenic preservation whenever possible because of the risk of overwhelming postsplenectomy infection by encapsulated organisms, particularly Streptococcus pneumoniae (see box). In this respect, splenic preservation is particularly indicated in children, who are more at risk of this complication than adults. Indeed, some of these children are managed conservatively in the first instance, surgery being undertaken only if there is evidence of continued or renewed bleeding. In those patients who require surgery because of active bleeding, splenic preservation (by special suturing and haemostatic techniques) is attempted only if the condition of the patient is stable and there is no contamination of the peritoneal cavity. Otherwise splenectomy is performed, in which case autotransplantation of splenic slices in omental pouches may be undertaken in an attempt to preserve splenic immune function. All patients undergoing splenectomy should be vaccinated.

Diaphragmatic injuries Injuries to the diaphragm are more commonly associated with abdominal than chest injuries. The majority follow RTAs but some are caused by crushing injuries and sharp localized blows such as a kick from a horse. The left diaphragm is more commonly injured than the right. Minor tears are usually unrecognized and may present several years later with incarcerated diaphragmatic hernia. More severe injuries are associated with multiple injuries and extensive herniation of the abdominal viscera a stomach,

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Protection for patients following splenectomy People who have had a splenectomy are at increased risk of severe infection. The risk is 12 times that expected in people with a normal spleen and children are the most vulnerable. The greatest period of risk is during the first 2 years after splenectomy but persists throughout life. The common pathogen is Streptococcus pneumoniae, although other bacteria with polysaccharide capsules (e.g. Haemophilus influenzae, Neisseria meningitidis) and malaria parasites also pose a significant risk. Patients who become infected may develop septicaemia with frightening speed and die within 24 h. Prophylaxis against infection is achieved by vaccination and antibiotics. Three vaccines are now recommended: pneumococcal vaccine, Haemophilus influenzae type b (Hib) vaccine, and meningococcal groups A and C vaccine. These should be administered prior to or soon after splenectomy. Antibiotic prophylaxis should be given to children until the age of 16 and to everyone for 2 years following splenectomy (e.g. amoxicillin 500 mg daily for adults, 250 mg daily for children; patients allergic to penicillin should be given erythromycin). Some physicians recommend lifelong antibiotic prophylaxis. Asplenic patients travelling to endemic malarial areas should take antimalarial chemoprophylaxis as well as the usual physical precautions against mosquitoes, e.g. insect repellents, screens at night, etc.

colon, omentum, small bowel and spleen on the left side and liver on the right. Massive herniation leads to mediastinal shift, which causes respiratory distress and hypotension due to reduced cardiac output.

Pancreatoduodenal injuries Injuries to the duodenum and head of the pancreas are more often due to penetrating than blunt abdominal trauma and usually give rise to peritonitis. Diagnosis is usually confirmed by peritoneal lavage, the effluent fluid from which will contain amylase. These are serious injuries and are accompanied by a high mortality and carry a substantial morbidity from the development of intra-abdominal sepsis and duodenal fistula. All these injuries require immediate surgical intervention. The vast majority of pancreatic fistulae that may complicate pancreatic injuries dry up within a short time following treatment with long-acting somatostatin, which has considerably simplified the management of this complication. Blunt injury to the upper abdomen may compress the pancreas against the vertebral column, leading to a traumatic pancreatitis and even transection.

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Small intestinal injuries

Intra-abdominal genitourinary trauma

Intestinal injury following blunt trauma may be due to: crushing of the intestinal loops between the vertebrae and anterior abdominal wall; a sudden increase in the intraluminal pressure of the bowel; tears at relatively fixed points along the attachment of the intestinal mesentery. Preoperative diagnosis can be established by peritoneal lavage. The small bowel is more commonly injured than the colon. Associated intra-abdominal injury, most commonly spleen or liver, is present in 40% of patients. Early diagnosis and prompt surgical intervention are the most important determinants of a successful outcome. Surgical treatment consists of resection of devitalized segments of bowel and primary anastomosis. This is followed by thorough saline/antibiotic lavage of the peritoneal cavity before closure of the abdomen. The skin and subcutaneous tissues are left unsutured and packed with acriflavine gauze. Delayed primary suture is undertaken 5–7 days later.

Approximately 10% of trauma patients seen in the accident and emergency department will have genitourinary trauma to a greater or lesser degree. Prior to catheter insertion the external urinary meatus must be examined for blood, which indicates the presence of urethral injury and the need for retrograde urethrography. When the catheter is passed, or if the patient voids spontaneously, the urine must be tested for blood immediately. Haematuria, gross or microscopic, is present in all patients with bladder or urethral injuries and in about 70% of patients with renal or ureteric injuries. In these patients retrograde cystography is performed prior to intravenous urography to rule out a bladder injury. Intravenous urography cannot reliably exclude a bladder injury. Where a renal injury is suspected, intravenous contrast should be injected once the intravenous lines have been erected. A plain abdominal film at the time of injection and 5, 10 and 15 min after injection will establish the presence of two kidneys, their function and any injury present. Urinary extravasation on these films indicates the need for nephrotomograms. It is essential to establish the number of functioning kidneys prior to any surgical exploration. If a CT scan is readily available, a contrast study will more thoroughly delineate renal injury than an intravenous urogram. In the case of renal injury with urine extravasation that is being managed conservatively, ultrasonography is a useful means of follow-up.

• • •

03 Colonic injuries Blunt injuries of the colon and rectum are rare and comprise 5% of all blunt injuries to the abdomen. As the force required to produce large-bowel injury needs to be considerable, associated injuries (e.g. liver, spleen, head, chest, pelvis and lower extremity) are common and adversely affect survival. The transverse colon is the most commonly affected segment, followed by the right colon, left colon and rectum. The lesions may consist of incomplete lacerations (seromuscular tears), haematoma or contusion with variable degrees of involvement of the adjacent mesentery or omentum, complete lacerations with faecal spillage and avulsion from the mesentery with full-thickness necrosis. The operative management depends on the severity of the injury. Minor injuries are closed with primary suture with or without proximal defunctioning colostomy, depending on the extent of faecal contamination and colonic loading (Fig. 19.3a). Severe injuries are excised with exteriorization of the two ends as a proximal endcolostomy and distal mucous fistula (Fig. 19.3b). Restoration of continuity is performed a few months later. Following the definitive repair, a thorough peritoneal lavage with saline is necessary before closure. As with small-bowel injuries, the skin and subcutaneous tissues are left unsutured and packed; secondary suture is performed 5–7 days later.

Renal injuries Injuries to the kidney are the most common injuries of the urinary system and account for approximately 50% of all genitourinary trauma. More than half these injuries involve patients under the age of 30 years and men are affected four times as frequently as women. Patients with renal abnormalities, such as hydronephrosis, are more prone to renal injury. Children are also at increased risk of renal injury because their kidneys are relatively larger than adults. Blunt trauma from RTAs and sporting mishaps account for 85% of renal injuries. Associated injury to other intra-abdominal organs occurs in approximately 40% of cases. Penetrating injury secondary to gunshot or stabbing occurs less frequently but associated organ injury occurs in approximately 80% of these patients. Highspeed vehicle collisions may result in major renal vascular injury due to rapid deceleration. Classification Renal injuries are classified as minor, major and vascular. Minor renal injury (85% of all cases). These injuries consist of renal contusion (bruising), subcapsular

•

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Loop colostomy

(a)

Figure 19.3 (a) Minor colonic injuries are closed with primary suture with or without proximal defunctioning colostomy depending on the extent of faecal soiling and colonic loading. (b) With major colonic injuries the injured colon is excised, the proximal end is exteriorized as an end-colostomy and the distal end exteriorized as a mucous fistula. Alternatively, the distal end may be closed and left intra-abdominally (Hartmann’s procedure).

Distal mucous fistula (alternatively this end may be closed – Hartmann's procedure)

(b)

haematoma or superficial lacerations of the cortex not involving the collecting system. Most instances of blunt trauma result in minor renal injuries and approximately 40% of penetrating trauma produces similar injuries. Major renal injury (14% of all cases). These injuries consist of deep lacerations and are associated with retroperitoneal and perinephric haematomata. If the laceration extends into the collecting system, urine extravasation with a perirenal urine collection (urinoma) results. In their severest form, deep renal lacerations may cause complete disruption of the kidney. Renal vascular injuries (1% of all cases). These uncommon but very serious injuries are more frequent with penetrating trauma. They range from intimal tears with subsequent renal artery thrombosis to avulsion of segmental arteries or veins to partial or complete avulsion of the main renal pedicle.

•

Proximal end colostomy (totally defunctioning)

Diagnosis Any penetrating injury to the flank should be suspected of causing renal injury, whether or not haematuria is present. Blunt injury associated with flank or abdominal tenderness, fractured lower ribs or vertebral transverse bodies or producing haematuria should be suspected of causing renal injury. It is important to remember that haematuria, gross or microscopic, only occurs in 70% of renal injuries and that the degree of haematuria does not correlate with the severity of the injury. A rapid deceleration injury should be suspected as a potential cause of renal vascular injuries. Intravenous urography is the key to diagnosis and staging. If urine extravasation is noted, nephrotomograms are required to delineate the injury further. If the patient is stable, a contrast CT scan may be the investigation of choice because it gives a greater degree of detail with respect to the renal injury and may also be used to assess possible associated organ injuries. If there is non-visualization of a kidney, renal vascular injury must be suspected and urgent arteriography is indicated.

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Treatment Minor renal injuries are managed conservatively by strict bedrest, antibiotics and monitoring of vital signs, haematocrit and the injured kidney. Patients with major renal injuries pose difficult management questions. Most cases can be managed conservatively as described without significant problems. Indications for surgical intervention are: signs of continued blood loss, such as falling haematocrit; increasing size of retroperitoneal or perinephric haematoma; and marked urine extravasation or vascular injury. The presence of associated organ injury may also call for surgical intervention. Smaller urinomas may be managed conservatively by frequent measurement using ultrasound examination to ensure decreasing size. Larger urinomas should be drained percutaneously and a urinoma that becomes infected (abscess) may require open surgical drainage. Where possible, exploration of renal injury due to blunt trauma should be avoided as the end-result is usually nephrectomy. In contrast, penetrating injuries almost always require surgical exploration.

• • •

Complications Bleeding at the time of injury and delayed bleeding within the first month of injury are important complications. In most cases bleeding ceases with conservative management but persistent bleeding or later heavy gross haematuria may require exploration. Urinomas and haematomas may result in fibrosis, leading to obstruction (hydronephrosis) that requires corrective surgery. Later complications include hypertension, arteriovenous fistula, hydronephrosis, stone formation, pyelonephritis and decreased function. For these reasons, careful follow-up of patients following renal trauma is necessary. Thus patients should have an intravenous urogram 6 months after injury and blood pressure should be monitored regularly for a year after injury.

• • •

Ureteric injuries Ureteric injuries are uncommon but their early recognition is critical as the nephrectomy rate may be as high as 30% when there is a delay in diagnosis. Most ureteric injuries are iatrogenic, with penetrating trauma the second most frequent cause. Blunt trauma to the ureter is rare and usually involves disruption of the ureteropelvic junction after rapid deceleration injuries; it occurs most frequently in children. The most common cause of iatrogenic injury is pelvic surgery, especially hysterectomy.

Surgery for carcinoma of the colon or rectum may be complicated by ureteric injury, especially where the tumour is extensive or ureteric abnormalities exist. Increasingly, endoscopic manipulation of stones with a basket or ureteroscope is being recognized as a potential cause of ureteral perforation or avulsion. Injury to the ureter may be recognized at the time of surgery or may present in the postoperative period as pyrexia, flank or lower quadrant pain, paralytic ileus or fistula. Haematuria, gross or microscopic, is present in 90% of cases but diagnosis rests on intravenous urography. Delayed excretion with hydronephrosis is the most common finding, although extravasation may also be noted. A retrograde ureterogram will demonstrate the exact site of the obstruction or extravasation. Early treatment is essential to preserve renal function. Stenting of ureteric repairs is an important determinant of a successful outcome. With prompt surgical intervention a satisfactory result can be anticipated in most cases.

Bladder injuries Bladder injury complicates 10–15% of cases of fractured pelvis. About 90% of bladder injuries are associated with pelvic fractures. Other causes include direct trauma to the lower abdomen in a patient with a full bladder, iatrogenic injuries (endoscopy and pelvic surgery), penetrating injuries and, very rarely, spontaneous rupture of an overdistended bladder. When the pelvis is fractured, fragments may perforate the bladder, resulting in extravasation of urine into the retropubic space (extraperitoneal rupture). If the bladder is full and subjected to trauma, the perforation occurs at the weakest point, i.e. the dome, with extravasation of urine into the peritoneal cavity (intraperitoneal rupture). Diagnosis There is a history of blunt abdominal trauma. The patient may be unable to urinate or, if voiding occurs, gross or microscopic haematuria will be apparent. On examination the patient may be shocked due to blood loss from the pelvic fracture or associated organ injury. An acute abdomen, i.e. pain, tenderness and guarding progressing to rigidity, suggests a perforated viscus or free intraperitoneal blood or urine. Urine must be obtained for testing. If haematuria is present, a urethral or bladder injury is likely but associated renal injuries may also coexist. For this reason all patients with haematuria after trauma must have an intravenous urogram (see box below). If the patient has not voided spontaneously, a catheter is passed after inspecting the external urinary meatus for blood. If blood is present at the meatus, a retrograde urethrogram is necessary to rule out urethral injury before proceed-

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Radiological investigations in the management of genitourinary trauma Plain abdominal radiography This will show fractures of the ribs or transverse processes of the vertebrae, indicating severe trauma and the possibility of associated renal injuries. Loss of renal outline, loss of psoas shadow, displacement of bowel gas suggesting a retroperitoneal haematoma or urinoma are other subtle manifestations of urinary tract injury. Pelvic fractures will also be seen and should raise the suspicion of bladder or urethral injuries. Retrograde urethrogram Prior to catheterization, the meatus should be inspected for blood. The presence of blood or difficulty in passing a catheter in the absence of blood at the meatus suggests a urethral injury and the need for a retrograde urethrogram. A size 12F Foley catheter is inserted to the fossa navicularis and the balloon inflated with 2–3 mL of water to hold the catheter in place; 20 mL of water-soluble contrast is gently injected through the catheter to outline the urethra. Retrograde cystography This is indicated in all patients with gross or microscopic haematuria on the voided or catheter specimen of urine. Contrast (300 mL) is infused through the catheter and a film of the distended bladder is taken. The bladder is allowed to drain by gravity and a second film is taken. This second picture is important in showing small amounts of extravasation. Intravenous urography After setting up the intravenous lines in a patient in whom renal injury is suspected, a bolus injection of contrast (2 mL/kg) is given. Films are taken at the time of injection and at 5-min intervals for 15–20 min. This investigation will establish the presence of two kidneys and their function. If urinary extravasation is present, nephrotomograms are necessary to delineate the degree of injury. If non-function is present, then absent perfusion due to a renal vascular injury must be considered and urgent arteriography is necessary. Computed tomography CT with intravenous contrast gives better definition of renal injuries than intravenous urography and may also assess the degree of associated intra-abdominal injuries. However, in the emergency situation intravenous urography suffices. Ultrasonography This investigation does not provide significant additional information in the immediate assessment of the trauma patient but it may be used to monitor patients with urinomas who are being managed conservatively.

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ing. If this is normal, a cystogram is performed by infusing 300 mL of constrast medium and taking an X-ray. A further exposure is taken after gravity drainage of the contrast through the catheter as small perforations may be missed on the full film. A cystogram may reveal compression of the bladder by pelvic haematoma (teardrop bladder) on the first film, with extravasation on the drainage film in extraperitoneal rupture. In intraperitoneal rupture, contrast will outline the loops of bowel. In patients with intraperitoneal rupture, serum urea rises with a normal creatinine level due to reabsorption of urea across the peritoneum. Recognition of bladder injury is important if mortality and morbidity are to be minimized. A fractured pelvis with haematuria indicates the need for urgent retrograde cystography. Treatment extraperitoneal rupture Very minor ruptures in patients who do not have infected urine may be treated conservatively by catheter drainage alone. However, careful observation is necessary as the pelvic haematoma may become infected, resulting in a pelvic abscess. For the majority of cases, urgent surgical intervention is indicated. The bladder is repaired transvesically by suturing the tear with absorbable sutures, inserting suprapubic and urethral catheters and placing a drain in the retropubic space. A small hole may be made in the peritoneal cavity to inspect the intra-abdominal fluid. If this is blood-stained, full laparotomy is required. Drainage is maintained for 10 days to 2 weeks and a cystogram is performed prior to removal of the suprapubic catheter. intraperitoneal rupture Intraperitoneal ruptures are approached transperitoneally. The bladder is drained by urethral and suprapubic catheters and the tear closed in layers with an absorbable suture. The peritoneal cavity is washed out to remove all urine and is also drained. Bladder integrity is checked by cystogram prior to removing the suprapubic catheter on the tenth postoperative day.

Penetrating abdominal trauma Stab wounds The vast majority of stab wounds are inflicted by knives and may be abdominal or thoracoabdominal. A high degree of suspicion of associated diaphragmatic laceration and pleuropulmonary injury is necessary in stab wounds of the upper abdomen as the direction of the knife thrust is often cephalad. Less commonly, stab wounds

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Figure 19.4 Impalement injury to the abdomen. Surprisingly, very little damage was caused by this injury. The caecum was perforated by the stake but the ureter and major vessels escaped injury. A right hemicolectomy was performed and the patient made an uneventful recovery.

03 occur from impalement injuries; these are usually serious and associated with major intra-abdominal trauma (Fig. 19.4). The management of abdominal stab wounds has changed in recent years to selective surgical intervention, depending on the clinical state of the patient, the nature of the wound and the results of specific investigations, i.e. peritoneal lavage or laparoscopy. The indications for laparotomy following a stab wound include: hypovolaemic shock; peritonitis; evisceration of viscera or omentum through the wound; gastrointestinal bleeding; free air on abdominal films. Wound exploration is useful in the management of the stable patient. In the absence of fascial penetration, wound toilet and primary suture are performed and the patient can usually be discharged from hospital after a short period of observation. Patients in whom wound exploration shows fascial penetration should have an abdominal lavage or laparoscopic examination followed by immediate laparotomy if indicated by the findings of either test.

• • • • •

Gunshot wounds Gunshot wounds are considerably more serious than stab

wounds and five times as lethal. Gunshot wounds to the abdomen are important because of their rising incidence worldwide and because they are accompanied by visceral injuries in the majority of cases. Some, especially those inflicted by high-velocity missiles, may not be initially accompanied by physical signs. For this reason all gunshot wounds of the abdomen should be explored, since physical examination and peritoneal lavage are unreliable in this situation. The propensity for visceral damage is directly related to the impact velocity and mass of the projectile. Thus, high-velocity missiles (usually from military weapons) impart a considerable amount of kinetic energy and produce extensive tissue damage, often remote from the site of injury. External contaminants are frequently introduced deep into the wounds caused by highvelocity missiles. Close-range use of the shotgun (favoured by bank robbers!) results in highly lethal injuries, with a reported mortality of 90% at a distance of less than 3 m.

Emergency laparotomy for abdominal injuries This must not be delayed unduly, particularly if volume replacement proves difficult, suggesting significant active intra-abdominal bleeding. An adequate reserve of crossmatched blood must be available to cover the procedure. Adequate intravenous lines capable of rapid acceleration of inflow must be in place before the patient is anaesthetized. Muscle relaxation causes a further fall in blood pressure as the tamponade effect of the abdominal wall is diminished, and this effect is entirely lost as the surgeon opens the abdomen. The operation is usually performed through a midline incision, as this can be readily extended from xiphoid to symphysis pubis and converted to a thoracoabdominal one when necessary. The first priority is control of haemorrhage. The next step concerns the operative treatment of hollow visceral injuries, especially those involving the colon, in order to minimize contamination. The abdominal exploration must be thorough, with a systematic inspection of all the quadrants and retroperitoneum (especially the second part of the duodenum) in order to avoid missed injuries. On completion, the peritoneal cavity is thoroughly lavaged with several litres of warm isotonic saline, especially in the presence of contamination from intestinal damage. Closure of the musculoaponeurotic layer of the abdominal wall is effected by absorbable monofilament material. The skin and subcutaneous tissues are left unsutured and the wound packed with acriflavine gauze if the peritoneal cavity has been contaminated by leakage of intestinal contents.

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Pelvic genitourinary injuries Urethral injuries Urethral injuries are uncommon and usually occur in men in association with straddle injuries or pelvic fractures with disruption of the pelvic ring. Urethral injuries are rare in women.

Injuries to the bulbar urethra These result from straddle injuries (e.g. falling astride a bicycle crossbar) or a direct kick to the perineum. Selfinstrumentation or iatrogenic instrumentation may occasionally be responsible for injury to the bulbar urethra. These injuries vary from a simple contusion or bruise of the urethra to laceration. In addition to the history of direct trauma, bleeding from the urethra and perineal haematoma will be evident. No attempt should be made to pass a urethral catheter under any circumstances. A retrograde urethrogram is indicated to delineate the severity of the injury. If the urethra is intact (no extravasation), a urethral catheter may be passed. If extravasation is present on the retrograde urethrogram, a laceration of the bulbar urethra has occurred. A percutaneous suprapubic catheter may be inserted in those patients in whom bladder injury is not suspected. The catheter is left in situ for 3 weeks and a micturating cystourethrogram is performed prior to its removal to ensure resolution of the injury. A urethral stricture may develop subsequently at the site of injury. If there is a possibility of associated bladder injury, then formal suprapubic cystostomy with inspection of the bladder and repair of any bladder laceration is necessary. Suprapubic drainage is maintained for 3 weeks and a voiding cystourethrogram performed prior to removal of the suprapubic catheter.

Injuries to the prostatomembranous urethra Injuries to this portion of the urethra usually result from blunt trauma, which causes pelvic fractures with disruption of the pelvic ring. Because of the nature of the trauma, bladder injuries are often also present. Patients complain of lower abdominal pain and are unable to void. On examination urethral bleeding with a large, often palpable, pelvic haematoma will be noted. Rectal examination may reveal superior displacement of the prostate (gland impalpable) due to complete disruption of the membranous urethra. A urethral catheter should not be passed under any circumstances. A retrograde urethrogram is urgently indicated. Free extravasation of contrast into the perivesical space indicates complete disruption of the membranous urethra. Incomplete disruption, which is less common, manifests as minor extravasation with some contrast

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material passing into the bladder. A urinary catheter should not be passed in these cases as it may convert an incomplete disruption into a complete one. The management of these injuries is somewhat controversial. However, most would agree that primary repair is a poor option because of the increased incidence of complications (stricture, impotence, incontinence) compared with delayed repair. Initial management consists of formal (i.e. operative) suprapubic cystostomy with inspection of the bladder for associated injuries. The suprapubic catheter is left in situ for 3 months, at which time a cystogram and urethrogram are performed to determine the extent of the resulting urethral stricture. The stricture is repaired by excision and anastomosis of the bulbar urethra to the apex of the prostate. This may be achieved through a perineal or transpubic approach. The suprapubic catheter is left in situ for a further month before repeating the radiological assessment of the urethra. Using this management protocol, complications occur in a small percentage of patients. Stricture at the anastomosis site occurs in approximately 5% of patients and can be dealt with by urethrotomy. Impotence may occur in 10–15% of patients. Incontinence after repair is uncommon and usually resolves slowly. In contrast, primary repair is associated with strictures in about 50%, impotence in 50% and incontinence in 30% of patients.

Penile injuries Most penile injuries result from accidents during sexual intercourse, resulting in a torn frenulum or fracture of the penile shaft. A torn frenulum presents as penile pain and bleeding after intercourse and is best dealt with by elongation of the frenulum (frenulopasty). Penile fractures occur due to bending during sexual intercourse, resulting in a large and painful haematoma. Surgical correction of the tear in the tunica albuginea minimizes future penile deformity. Penetrating injuries and avulsion injuries occur much less frequently.

Scrotal and testicular injury Blunt trauma to the scrotum may cause scrotal contusion alone or may also involve the testes. Abnormal testes, such as those with carcinoma, are more prone to trauma and this should be remembered when patients present with testicular injury after minimal trauma. In addition to the history of blunt trauma, examination will reveal a scrotal haematoma. Often the testis is impalpable and all such patients should have an urgent scrotal ultrasound. If ultrasonography confirms testicular injury, surgical exploration and repair are necessary. It is worthwhile noting that orchidectomy is a distinct possibility in these patients.

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Abdominal trauma at a glance Definitions Kinetic energy (KE): the capacity of a body or system to do work that arises from its motion. It is expressed as KE = 1/2m × v 2, where m is mass and v is velocity. Hence the speed of an object has a greater impact on the energy produced than the mass Impact force: the total kinetic energy transferred to the victim at the point of impact Strain: the physical deformity of the victim’s body produced by the impact force. There may be direct deformity, tensile strain (along longitudinal axis of victim) or shear strain (perpendicular to longitudinal axis of victim) Cavitation: a process whereby a layer or segment of tissue moves rapidly away from the point of impact, creating an actual cavity that collapses quickly as the energy dissipates into the tissues

Motor vehicle injuries • 40 people die every day in UK from accidents • Majority are RTAs • 25% have a blood alcohol level > 100 mg/L • Most victims are young • There is a huge financial cost in resuscitation, treatment, rehabilitation and lost years of productivity • Pedestrian RTA victims are often children, the elderly, and the inebriated Factors that influence severity of injury in RTAs • Size of car: smaller is worse • Position of victim in car • Morphology of victim: more weight is better • Use and type of restraint: three-point seat-belts, airbags • Type of RTA: (a) Lateral impact: least bad (b) Frontal impact: bad (c) Rollover and ejection: worst Classification and surgical anatomy of abdominal injuries Injuries may be: • Blunt: most common injury in civilian life, mostly RTAs • Penetrating:

(a) Low energy (knife): most survive with prompt treatment (b) High energy (gun): mortality (generally high) depends on bullet velocity, fragmentation, and severity and site of injury With respect to trauma, the abdomen is divided into four compartments: • Intrathoracic abdomen: liver, spleen, diaphragm, stomach • True abdomen: small and large intestine, pregnant uterus, distended bladder • Pelvic abdomen: sigmoid colon, rectum, small bowel loops, bladder, urethra, ovaries and uterus • Retroperitoneal space: kidneys and ureters, duodenum, pancreas, aorta, inferior vena cava Management 1 Resuscitate patient and perform primary and secondary surveys as described in Chapter 17 2 Deal with abdominal injury: (a) Unstable patient: surgery (b) Stable patient: ultrasound, CT, peritoneal lavage, diagnostic laparoscopy, then surgery if indicated 3 Antibiotics: give aerobic and anaerobic cover Peritoneal lavage Indications • Equivocal physical signs • Depressed level of consciousness • Spinal injury • Penetrating trauma below nipple line Technique • Under local anaesthetic aseptically, insert dialysis catheter into peritoneal cavity in midline below umbilicus • Infuse 1 L Ringer’s lactate solution and siphon out after 5–10 min • Positive if: (a) red blood cells > 100 × 106/L; (b) white blood cells > 500 × 103/L; (c) amylase > 1100 U/L; (d) presence of bile, bacteria or food particles in peritoneal effluent

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Specific injuries Site of injury (usual mechanism of injury) Type of injury

Treatment

Liver (blunt)

Minor laceration Moderate-sized tears Severe injury

Observe, serial CT, surgery if evidence of continued bleeding Laparotomy, liver suture, resectional débridement Laparotomy, ‘packing’, refer to hepatobiliary unit

Spleen (blunt)

Incomplete parenchymal tears Conservative management, especially in children Lacerations Splenic suturing and preservation if possible Fragmentation Splenectomy, vaccination against S. pneumoniae and H. influenzae

Diaphragm (blunt)

Traumatic rupture, usually left side

Early: laparotomy, reduce abdominal contents from chest and repair Late: presents as diaphragmatic hernia. Reduce and repair defect in diaphragm

Pancreas/duodenum (penetrating)

Blunt injury may fracture body of pancreas

Immediate surgery. May get duodenal or pancreatic fistula (treat with somatostatin). Very serious injuries with high mortality

Small intestine (blunt)

Crushing, tear from raised intraluminal pressure, tears at fixed points

Immediate surgery. Associated injury (spleen) in 40%. Resection of devitalized bowel with primary anastomosis. Stop mesenteric haemorrhage. Peritoneal lavage

Colon (rare, blunt and penetrating)

Minor injury Major injury

Immediate surgery. Primary closure ± proximal defunctioning colostomy/ileostomy. Peritoneal lavage Excision and exteriorization of two ends with reanastomosis at ~3 months

Kidney (blunt)

Minor injury (85%) Major injury (14%) Vascular (1%)

Conservative Conservative initially. Surgery only if continued blood loss, increasing haematoma, urine extravasation or vascular injury

Ureter (penetrating)

Usually iatrogenic (e.g. surgery for colorectal cancer)

If recognized immediately: repair with stenting (e.g. over ‘Double-J’ stent) If late diagnosis: attempt repair but high nephrectomy rate (30%)

Bladder (blunt) ± fractured pelvis

Extraperitoneal rupture Intraperitoneal rupture

Surgery and repair of bladder (absorbable sutures) + suprapubic and urinary catheters for ~14 days. Cystogram prior to catheter removal

Urethra (blunt)

Bulbar urethra (‘saddle injury’) Bleeding from urethra/perineal haematoma. Immediate retrograde Prostatomembranous urethra urethrogram: no extravasation, pass urinary catheter; (fractured pelvic ring) extravasation, insert suprapubic catheter for 3 weeks. May develop urethral stricture ± Bladder injury. Per rectum examination reveals upward displacement of prostate. Retrograde urethrogram. Cystostomy + suprapubic catheter for 3 months

Scrotum and testis (blunt)

Abnormal testes more prone to injury

Scrotal ultrasound: if testicular injury, explore and repair Orchidectomy sometimes required

Penis (blunt, during sexual activity)

Torn frenulum Fractured shaft

Frenuloplasty Surgical repair of tear in tunica albuginea

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Chest Trauma

Introduction, 224

Types of chest injury, 224

Must know Must do

Must know How to perform a primary survey of patients with chest injuries How to interpret a chest X-ray performed for suspected trauma Clinical features of major life-threatening chest injuries How to detect respiratory distress, pneumothorax and haemopneumothorax Indications for emergency thoracotomy for chest injuries Must do See patients with fractured ribs Observe and follow a patient with severe chest injuries Observe the insertion of an apical chest drain for pneumothorax Observe the insertion of a basal chest drain for haemothorax

impair breathing. The best example of this is after severe burns to the chest, causing an encircling eschar that impairs the respiratory excursions of the thoracic cage. In both the blunt and penetrating types of chest trauma the forces causing the trauma can be either low velocity or high velocity. It is obvious therefore that the mechanism of injury is important because it determines the extent and type of damage sustained. It should also be recognized that the mechanisms that cause injury to the chest are identical to those that cause injuries to the abdomen, and frequently patients with thoracic injuries also have abdominal involvement. An important example of this is a rib fracture on the left side that leads to splenic laceration. It must also be remembered that if a patient has been stabbed in the upper abdomen with a knife, frequently the upstroke of the attacker leads to diaphragmatic and thoracic injury despite an abdominal entry. The problems caused by thoracic trauma relate to the disruption of adequate gas exchange, leading to hypoxia, hypercarbia and acidosis. Other problems relate to shock secondary to disruption of major viscera in the chest.

Introduction

Types of chest injury

Chest injuries are common in civilian life, although the overall mortality is usually less than 10%. Many of the patients who die following thoracic trauma do so after reaching hospital, in the so-called ‘golden hour’ described in the advanced trauma life support (ATLS) guidelines, indicating that the majority of chest problems are under the treatable umbrella of most doctors. Moreover, less than 15% of chest injuries end up requiring a thoracotomy, with most being managed in the emergency department and on the ward. When considering trauma to the chest it is important to remember the anatomical structures present and how they could be damaged. Hence, viscera such as the lungs, heart and great vessels are at risk if the natural barrier of the ribcage is insufficient to prevent injury. In general, trauma to the chest can be considered to be either of the blunt type or the penetrating type. It is also important to remember that injuries to the chest can occur secondary to other traumatic processes and could significantly

As with all trauma, chest trauma should be managed according to the ATLS guidelines, which dictate that airway, breathing and circulation are examined sequentially, followed by disability and exposure of the patient. Following this primary survey and resuscitation of vital functions, a more detailed examination of the chest can occur followed by definitive care. It is therefore pertinent to divide the types of chest trauma into those encountered during the primary survey and those encountered during the secondary survey. The full spectrum of thoracic injuries is outlined in Table 20.1.

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Primary survey chest injuries Many of the problems that occur with trauma patients are secondary to thoracic cage trauma, the simplest example of which is fracture of a rib. The most common fractures are those of the lower ribs, usually the fifth to the ninth. Fractures of the lower ribs have significance because they

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Table 20.1 Spectrum of thoracic trauma. Chest wall trauma Fractured ribs Flail chest Fractured sternum Lungs and pleura Simple pneumothorax Tension pneumothorax Haemothorax Pulmonary contusion Pulmonary laceration Tracheobronchial disruption Cardiovascular injuries Cardiac trauma Aortic disruption

(a) (b)

Diaphragmatic injuries

can lacerate upper intra-abdominal viscera. It is also important to note that fractures of the upper four ribs, particularly the first rib, are indicative of extremely highvelocity trauma, as these ribs do not usually fracture because of their short, stout anatomy. Fractured ribs can also puncture the pleura and even the lung substance itself to cause a pneumothorax (see later). In more severe thoracic cage trauma, two or more consecutive ribs can be fractured in two or more places; this is the definition of a flail segment. A flail segment compromises a patient’s breathing because the fractured segment undergoes paradoxical movement on inspiration (segment moves inwards rather than outwards) and hence impedes ventilation of the ipsilateral lung (Fig. 20.1a,b). Invariably, the degree of trauma causing a flail segment is likely to lead to underlying lung contusion and even laceration. The consequences of rib fractures are treated individually. A simple rib fracture itself requires no specific treatment other than adequate analgesia. However, flail segments require specific therapy as well as adequate analgesia. This involves strapping of the segments and even positive pressure ventilation to compensate for poor oxygenation and to aid healing of the chest. Finally, the anterior thoracic wall can also undergo severe trauma when the sternum is fractured. The mechanism of injury is usually a severe impact on a solid structure, the most common example being a collision where a driver of a motor vehicle is thrown onto the steering column. As one can imagine, a fracture of the sternum produces intense, deep pain. However, it is the risk of injury to the mediastinum that causes the greatest concern. Patients with sternal fractures should always be admitted and observed, and electrocardiography (ECG)

Inspiration

Expiration

03 Figure 20.1 (a) Rib fractures leading to the development of a flail segment with paradoxical movement. (b) Paradoxical respiration can lead to embarrassment of gaseous exchange.

performed to look for electrical abnormalities. Cardiac enzymes should also be measured to ensure the myocardium has not sustained significant damage.

Pneumothorax A pneumothorax is defined as air entering the pleural cavity secondary to trauma (Fig. 20.2). It is the most common pleural-related problem that any doctor is likely to encounter in practice. Many pneumothoraces are caused by trauma, although it should be remembered that they can occur in association with other diseases, e.g. bullous disease of the lung secondary to emphysema. The entrance of air into the pleural cavity leads to the collapse of the lung on that side. Pneumothoraces may be caused by fractures of the ribs secondary to blunt trauma or by a penetrating injury (e.g. a knife). In general, a pneumothorax can be either a tension pneumothorax or a simple pneumothorax. A tension pneumothorax develops when a penetrating injury of the chest allows air from the external environment to enter the pleural cavity but not leave, the wound acting as a one-way valve. Eventually the accumulation of air in the pleural cavity displaces the mediastinum to the opposite side, thereby decreasing venous return and leading

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Air entering causing pressure

(a)

Air escaping from cannula

Figure 20.2 Chest X-ray showing a simple pneumothorax on the right and a lung contusion on the left.

to cardiac arrest that shows signs of electromechanical dissociation (Fig. 20.3a). A tension pneumothorax should be recognized at the time of the primary survey. The patient is typically short of breath and the trachea is displaced towards the side opposite the injury. The chest on the injured side also fails to expand and is hyperresonant to percussion. If, together with these findings, breath sounds are absent on the injured side, the patient should not proceed to chest X-ray. Immediate management is to relieve the build-up of air in the pleural cavity by decompression. A large-bore needle is inserted into the second intercostal space in the midaxillary line on the affected side. Successful decompression is heralded by a rush of air through the needle after insertion (Fig. 20.3b). This converts a tension pneumothorax into a simple pneumothorax. Simple pneumothoraces are those where there is a defect in the chest wall that allows air to enter and leave the pleural cavity, causing the lung to collapse. However, because air does not accumulate in the pleural cavity there is no deviation of the mediastinum as seen in a tension pneumothorax. The initial management of an open pneumothorax is prompt closure of the defect with a sterile occlusive dressing large enough to overlap the edges of the wound and taped securely on three sides. This works as a flutter valve, preventing air from entering the pleural cavity when the patient inhales but allowing air to leave when the patient exhales. Both types of pneumothoraces are definitively managed by the insertion of a chest tube to drain the air from the pleural cavity. The chest tube is traditionally inserted

(b)

Figure 20.3 (a) The mediastinal shift that occurs due to a tension pneumothorax. (b) Release of tension pneumothorax after insertion of a cannula into the right second intercostal space.

into the sixth intercostal space in the midaxillary line, the tube being aimed towards the apex of the lung. A tube of size 24F or greater is recommended. The tubing from the chest drain is attached to an underwater seal drainage system, where water in a bottle acts as an air lock. A negative pressure of approximately 5 mmHg may be attached to the system to aid adequate lung re-expansion (see Chapter 2). The majority of simple pneumothoraces resolve in days when the re-expanded lung adheres to the chest wall due to the secretion of fibrin. A drain tube should only be removed if there is cessation of bubbling in the drainage bottle, even with suction. When the lung is fully expanded, this lack of bubbling needs to have been present for at least a day. It is important to tie a second pursestring suture to allow adequate closure of the drain site. After drain removal, a chest X-ray should be taken to confirm continued lung expansion.

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Haemothorax Trauma to the chest can also lead to the accumulation of blood in the pleural space. This is the definition of a haemothorax. Haemothoraces are most commonly associated with laceration or disruption of the lung parenchyma and are obviously more common in penetrating than blunt injuries. Haemothoraces can be defined as small or massive. A massive haemothorax is one where there is rapid accumulation of more than 1 L of blood in the chest cavity. This is most commonly caused by disruption of the hilar vessels of the lung, and hence the problems experienced by the patient would be not only those of hypoxia but also those of hypovolaemia. A massive haemothorax is recognized clinically by hypoxia, decreasing blood pressure, and a chest where there may be obvious signs of trauma and on the ipsilateral side decreased expansion, decreased percussion note and decreased breath sounds. Initial management involves the insertion of a large-bore chest tube into the sixth intercostal space in the midaxillary line. If a massive haemothorax is suspected, the blood from the chest can be used for autotransfusion. The subsequent management of the patient depends on the volume of blood loss. If over 1 L is immediately drained from the thoracic cavity, the patient requires an early thoracotomy. If less than 1 L is drained, the patient can be managed expectantly, with the decision for surgery based on the rate of continuing blood loss. If the rate of blood loss is 200 mL/h over the subsequent 2– 4 h, the patient should be considered for surgery.

Figure 20.4 Site of insertion of a pericardiocentesis needle to decompress a cardiac tamponade.

inserted in the subxiphoid region and blood is evacuated. This procedure should always be performed under ECG monitoring. In very extreme situations, the thorax is opened and the pericardium evacuated (Fig. 20.4).

Secondary survey chest injuries Haemothoraces and pneumothoraces can also cause death during the secondary survey period. However, the occurrence and discovery of visceral injuries that were not obvious initially tend to dominate the secondary survey.

Cardiac tamponade Cardiac tamponade is the accumulation of fluid in the pericardial sac, which restricts the filling and contraction of the heart and leads to shock. If this fluid is blood, it can come from disruption of the great vessels or the heart itself, most commonly as a result of penetrating injuries, although severe blunt trauma can also be a cause. As little as 20 mL of blood can cause symptoms. Cardiac tamponade is often missed until later in the assessment, although three classic diagnostic features occur, namely elevation of jugular venous pressure (JVP), decline in blood pressure and muffled heart sounds (known as Beck’s triad). Additionally, the patient may demonstrate pulsus paradoxus and a rise in venous pressure with inspiration (also known as Kussmaul’s sign). Transthoracic echocardiography can help in confirming the diagnosis. However, the diagnosis is often made only when pericardiocentesis is performed in a last-ditch effort to relieve the cardiogenic shock. In this procedure, a long spinal needle is

Pulmonary contusion One of the most common and often unrecognized problems associated with severe chest trauma is pulmonary contusion. This potentially lethal injury can often display subtle signs, where significant portions of the lung fail to function and cause the patient to become markedly hypoxic. The patient’s injuries may often be sufficiently severe to require assisted ventilation and may also contribute to the development of adult respiratory distress syndrome (ARDS). More severe pulmonary injuries can lead to pulmonary laceration. However, this is most commonly observed with an associated fractured rib or secondary to penetrating trauma.

Aortic disruption Traumatic disruption of the aorta is a common cause of death after trauma that involves very rapid deceleration

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from great speeds, such as high-velocity road traffic accidents and falls from a great height. These patients are initially stable but continue to be hypotensive despite resuscitation, due to failure of the haematoma to contain the bleeding. There are usually few specific signs and symptoms. However, a high index of suspicion and a history of decelerating force will lead to inspection of the chest Xray for specific signs of mediastinal widening. Also, if the patient is stable, angiography and even CT scanning will help confirm the diagnosis. Immediate referral to a cardiothoracic surgeon is imperative if the patient is to survive.

Tracheobronchial disruption

Diaphragmatic injury

Oesophageal disruption

Injuries to the diaphragm can occur as a result of huge compressional forces that cause the diaphragm to be torn from its attachments or secondary to penetrating trauma. This type of injury is usually associated with abdominal injury as well. Diaphragmatic trauma is yet another injury that is often missed or diagnosed late. Some patients may present years later with herniation through previous diaphragmatic defects caused by trauma. On chest X-ray these injuries may be recognized by an elevated diaphragm and can be confirmed by inserting contrast into the oesophagus and observing a high stomach.

The oesophagus is most commonly traumatized by penetrating trauma. However, the oesophagus can tear due to forceful expulsion of contents from the stomach during huge impacts. This causes gastric contents and air to leak into the mediastinum, resulting in mediastinitis and air in the subcutaneous tissues of the neck, recognized as surgical emphysema. Patients may also develop a pneumothorax, usually more common on the left than the right. The diagnosis is confirmed when particulate gastric matter is recovered from the chest tube. Prompt diagnosis and repair produce the best results in these patients.

Injury to the trachea or major bronchi is uncommon and fatal if overlooked. Patients who suffer severe tracheobronchial disruption usually die at the scene of the accident. However, those with a more minor degree of disruption are frequently recognized by the fact that they have a pneumothorax with associated subcutaneous emphysema, the pneumothorax persisting despite chest tube drainage. Frequently, definitive surgery is required to correct the abnormality.

Chest trauma at a glance Definitions

Classification

Pneumothorax: the presence of air in the (normally potential) space between the visceral and parietal pleura in the chest cavity

• Type of injury: blunt or penetrating trauma • Mechanism of injury: high- or low-velocity injury

Tension pneumothorax: a life-threatening condition that results from the continuing accumulation of air in the pleural cavity such that mediastinal structures (especially the great veins) are compressed and displaced laterally, inhibiting venous return and resulting in decreased cardiac output and ultimately cardiac arrest Haemothorax: the presence of blood in the space between the visceral and parietal pleura in the chest cavity Flail chest: a segment of chest wall that moves paradoxically on respiration (inward movement on inspiration and outward movement on expiration) secondary to multiple rib fractures such that there are more than two rib fractures in two or more consecutive ribs Cardiac tamponade: abnormal compression of the heart as a result of the accumulation of fluid (e.g. blood) in the pericardial sac. A relatively small amount of fluid (~20 mL) can cause symptoms

Primary survey injuries • Fractured ribs • Flail chest • Fractured sternum • Pneumothorax • Tension pneumothorax • Haemothorax • Cardiac tamponade Secondary survey injuries • Pulmonary contusion • Aortic disruption • Diaphragmatic injury • Tracheobronchial disruption • Oesophageal disruption

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Clinical features and management Anatomical region

Injury

Clinical features

Management

Chest wall

Fractured ribs

Usually 6th to 9th ribs. Fracture of 1st rib indicates high-velocity trauma Paradoxical chest wall movement on respiration

Adequate analgesia Breathing exercises Adequate analgesia Strapping of flail segment Positive pressure ventilation Adequate analgesia Cardiac monitor Check cardiac enzymes

Flail chest

Lungs and pleura

Fractured sternum

Intense deep pain Look for cardiac injury

Simple pneumothorax

Dyspnoea Chest wall hyperresonant

Tension pneumothorax Dyspnoea Trachea deviated to opposite side Chest wall hyperresonant Cardiac arrest Open (sucking) pneumothorax Haemothorax

Massive (> 1 L) Small (< 1 L)

Pulmonary contusion or laceration Tracheobronchial disruption Cardiovascular Cardiac tamponade (cardiac trauma)

Aortic disruption

Miscellaneous

Open defect in chest wall Penetrating injury Decreased expansion, dull percussion, reduced breath sounds + Hypoxia and shock + Dyspnoea

Hypoxia ARDS Pneumothorax plus subcutaneous emphysema Persistent air leak from chest drain Elevated JVP Decreased blood pressure Muffled heart sounds Pulsus paradoxus Rise in JVP on inspiration (Kussmaul’s sign) History of rapid deceleration in high-velocity injury Hypotensive despite resuscitation

Venous injury

Rare History of penetrating injury Haemothorax

Oesophagus

Mediastinitis Subcutaneous emphysema in neck Sometimes hydropneumothorax (L > R) History of compression force on abdomen History of penetrating trauma

Diaphragm (rupture or penetration)

Chest X-ray Chest drain if > 5 –10% lung collapse (6th intercostal space midaxillary line) Do not perform chest X-ray to confirm diagnosis Insert large-bore needle into the chest (2nd intercostal space, midclavicular line) Then chest X-ray and chest drain Cover defect with sterile occlusive dressing taped down on three sides Insert large-bore chest drain If > 1 L blood discharges immediately, patient needs thoracotomy If < 1 L blood discharges immediately, observe If continuing blood loss of 200 mL/h, patient needs thoracotomy May need ventilation Surgical repair

Pericardiocentesis Sternotomy and drainage of pericardium (Open repair of heart injury)

Chest X-ray shows widened mediastinum Diagnosis confirmed with contrast-enhanced CT Open surgical repair Surgical repair

Urgent surgical repair Poor prognosis with mediastinitis

Often present late with herniation of stomach into chest Reduction of stomach into abdomen and open repair of diaphragm

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Musculoskeletal Trauma

Introduction, 230 History-taking after trauma, 230 Examination of the traumatized patient, 231

Investigation of fractures, 232 Management of fractures, 236 Complications of fractures, 240

Must know Must do

Must know How to take a concise basic history from a patient who has had an accident or from relevant witnesses Principles of assessment and resuscitation of the injured patient General principles of fracture and soft-tissue management Types of treatments available and the likely consequences for an individual patient such that you could answer sensible queries from the patient about what has happened or what may be about to happen How to manage pain and shock Common complications and consequences of injury or treatment Must do Attend the accident and emergency department to witness resuscitation/assessment of injured patients Attend fracture clinic Clerk patients in the orthopaedic wards recovering from major musculoskeletal trauma Observe open reduction and fixation of major limb fractures Attend rehabilitation sessions

Introduction Fractures are a common medical problem: most people have broken a bone or know someone who has. Bones are familiarly regarded as inert things that are important for body structure. In reality, however, bones are dynamic living tissues with a very rich blood and nerve supply. The immediate consequences of fracture therefore are severe pain and blood loss, and the strategy of early management is to minimize pain with splints and analgesics and to anticipate the effects of blood loss, i.e. hypovolaemic shock. In the longer term, the rich blood supply must be 230

Dislocations, 242 Common fractures and joint injuries, 243

re-established before bone will heal and so from the outset the state of the soft tissues becomes of central importance. Finally, it must be remembered that patients do not die from broken bones but from the results of associated injuries to the chest, head and abdomen and so fractures are not the first consideration when treating the injured patient.

History-taking after trauma There are two principal reasons for taking a careful history after trauma: clinical and medicolegal.

Clinical history Bones may be broken in many ways, including simple domestic accidents (the most common), high-velocity transport accidents and, more rarely, battle injuries. The following questions must be asked and answered (see box below). What happened? Once admitted to hospital, most fractures look the same whatever the mechanism of injury. However, there is a world of difference between a fracture caused by slipping off a step and a fracture caused by collision with a car; the first involves little energy transfer to the affected part of the body, while in the second a lot of energy is absorbed by the affected part. The amount of energy transferred to the body in an accident determines not only the bony injury but also the soft-tissue damage and the extent to which the blood supply is disrupted. Therefore, it is important to find out from the victim (direct history) and witnesses (collateral history) what exactly happened. How did it happen? How it happened can also help because injuries tend not to occur randomly but in some sort of pattern. For example, a pedestrian hit by a car tends to receive leg injuries from the bumper, pelvic and abdominal injuries from the bonnet and head injuries from the door pillar. Knowing something about these patterns permits the examiner to predict potential injuries.

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Where and when did it happen? It is also useful to know where and when it happened because a long delay between injury and treatment may limit therapeutic options. What was the patient like before it happened? Once the circumstances of the injury are appreciated, then the patient should have a full medical history taken. This is of course secondary to essential treatment required to protect the airway and control haemorrhage. It is important to establish as much as possible about the patient’s previous general medical state. Often medical conditions may be associated with an injury. For example, the patient may have had a fit or collapsed with a hypoglycaemic attack. In the elderly, presentation with a fracture may represent a fall secondary to a myocardial infarction or a cerebrovascular accident. Many patients with fractures will need an anaesthetic and so the state of the cardiovascular and respiratory system must be established. The last time the patient ate or drank should be confirmed so that surgery can be delayed, if possible, until the stomach is empty, so reducing the risk of aspiration of vomit. Who is the person? Finally, the social history is extremely important. This may be obtained after the immediate treatment of the fracture has been carried out or may be obtained from a relative. The status of patients before injury must be established. Where do they live and with whom? Do they have stairs to climb into the house or flat or within the home? Can the older patient go to relatives after any hospital stay to rehabilitate?

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possible. This is particularly important when it is realized that it is often months or years before one may be called to give an account of an accident. For all concerned, legible and complete notes are essential.

Examination of the traumatized patient (see Chapter 17) All patients need to have a full physical examination. Priorities should be established in the examination process as listed below. 1 Examine vital areas. 2 Examine injured areas. 3 Examine other areas at risk. 4 Do a general examination.

Vital areas For patients with multiple injuries, airway protection and cardiorespiratory viability take precedence over everything else. Ask a simple question such as ‘What is your name?’ If you get a sensible answer, then the patient is conscious with a good airway. However, for most patients with a single or few injuries, the examination will concentrate on the injured part and the fitness of the patient for anaesthetic.

Injured area

Taking a history

Examination of the fracture site

• • • • • •

The suspicion that a patient has sustained a fracture will have been raised from the history. The diagnosis should be confirmed by physical examination of the injured part and only rarely are radiographs needed to make the diagnosis. The signs of fracture are: deformity; tenderness; swelling; discoloration or bruising; loss of function; and crepitus. Crepitus is perceived as a grating or grinding of the broken bone ends, although this sign should not be purposefully elicited as it will cause intense pain to the patient (Fig. 21.1).

What happened? Was there a lot of violence involved or a simple fall? How did it happen? Can likely injuries be predicted from the patient’s description of the incident? Where and when? Did it happen recently or has the patient come late? To whom did it happen? How does the patient live? Will they need some help at home later? What was the patient like before the accident? Has this patient other medical problems? Has an adequate history been taken and recorded? As a responsible professional you may have to account for youself in the future

Medicolegal aspects Accidents have all sorts of consequences that affect the patient and the patient’s family. They often result in insurance claims and litigation, not infrequently directed at the doctors and nurses who cared for the patient immediately after the accident. It is important therefore to keep meticulous notes at the time or as soon after the event as

• • • • • •

Examination of the immediate vicinity of a fracture

•

The skin may be partially damaged and present with or subsequently develop blisters. Such skin is only partially viable and may not tolerate being incised as part of an

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Feel Tenderness See Deformity Discoloration Swelling Move (gently) Crepitus

Figure 21.1 The cardinal features of a common fracture.

operation. If the skin has been breached, the fracture is described as an open fracture (see below). The subcutaneous fat will almost certainly be damaged and later necrosis may cause reddening of the skin with firmness and tenderness; this is easily mistaken for infection. The surrounding muscle will be damaged to some degree, contributing to limb swelling. If swelling is severe, the patient may develop a full-blown compartment syndrome (see later and Chapter 17). Damage to major vessels is surprisingly rare, except in extensive open injuries where there has been a lot of direct violence. Certain specific fractures (supracondylar elbow fractures and dislocated knee) are sometimes accompanied by arterial damage. Vessels are also at risk from compression (see section Compartment syndrome) and from damage to the intima that could cause thrombosis and occlusion. The features of vascular trauma are described in Chapter 37. Complete or incomplete division of nerves is rare except in penetrating wounds, in association with severe open fractures or with major trauma (e.g. brachial plexus injury). However, stretching (or neuropraxia) is not uncommon. The nerves are sometimes stretched around deformed fragments and this is sometimes exacerbated by swelling.

•

• •

•

Other areas at risk Certain types of injury are classically associated with other specific injuries and the discovery of one injury should alert the examiner to the possibility of the associated injury. Head and spinal injuries. The possibility that a patient with a head injury also has a spinal injury should constantly be borne in mind. If a blow is sufficient to render a patient unconscious, then the same violence could have

•

broken the cervical spine, especially where it joins the head (at the atlas and axis) or where it joins the trunk (at the thoracocervical junction) (Fig. 21.2). If a patient is unconscious following a head injury, it is best to assume that he or she has a spinal injury until proven otherwise. Patients should be nursed with a collar and turned correctly (all in one piece and not twisted). Rib fractures and pneumothorax. The presence of fractured ribs should always raise the possibility of pneumothorax. The possibility of traumatic aortic dissection should be considered in a patient with a fractured left first rib following blunt trauma (see Chapter 20). Femoral and pelvic injuries. Pelvic injuries are sometimes seen in association with major long-bone injuries in the lower limb. Dislocation of a hip sometimes accompanies femoral fracture and ligamentous injuries to adjacent joints are always possible in any long-bone fracture. Small injuries with big injuries. It is wise to re-examine the patient on two or three occasions, including the next day, when small injuries are often discovered. It is often small injuries that lead to long-term problems: for example, it is extrememly unfortunate if a patient with a well-treated long-bone fracture is still not at work because of an unrecognized and untreated fracture of some metatarsals.

• • •

Examination of the traumatized patient

•

Is the patient conscious and responding sensibly? If not, resuscitation and airway protection take priority (ABC) If the injury is more localized, get the patient to show you where it hurts. Do not forget that some patients may be overwhelmed with pain in one area and forget a less sore injury elsewhere It is your job to examine the patient systematically to positively exclude injuries. It is easy to miss apparently minor injuries that become troublesome later Recognize associated injuries that commonly go together, e.g. ribs with pneumothorax, skull with neck, femur with pelvis Check the patient again on another occasion. You or the patient may have missed something When examining a limb always remind yourself about the areas at risk: skin, fat, muscle and tendon, bone, blood vessel, nerve, associated joints and ligaments

• • • • •

Investigation of fractures Fracture architecture Why is it important to describe the shape and degree of fragmentation of a fracture? In general, the shape of a

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03 (a)

(b) Figure 21.2 (a) This patient has an obvious fracture of the skull and is unconscious; (b) without careful examination and radiographic evaluation neck fractures such as these may be missed!

fracture reveals the amount of energy that has caused the damage and thus permits the correct treatment to be applied. In general, spiral fractures occur through twisting, which is a common low-energy mode of injury. Such injuries are usually associated with little soft-tissue damage and so the blood supply to the bone is preserved and therefore healing is unlikely to be a problem. In contrast, oblique and transverse fractures are caused by buckling or direct injury to the bone and involve a lot of energy, with soft-tissue stripping and damage to the blood supply. Such injuries require much consideration when the choice of treatment is being made. The types of fractures are summarized in Fig. 21.4.

Plain radiography of the injured area The radiograph must show the part under investigation and it must be of diagnostic quality. The responsibility for achieving this rests solely with the clinician ordering the film. Dark films are dangerous because vital information

may be missed. Equally, it is important to make sure the whole of the site of injury is included in the investigation and so it is safest to include the joint above and the joint below the area in question. Two films are usually taken at mutual right angles. Conventionally, an anteroposterior and a lateral view are taken. In this way, by always viewing conventional films the examiner recognizes deviations from normal patterns more easily. However, some injuries (e.g. of the hand) are best seen on oblique views. At least two views are needed to obtain a reasonably accurate impression of the extent of the fracture (Fig. 21.3). The radiographic features of a fracture include: lucencies at the site of fractures; discontinuity in the cortex or surface of a bone or joint. These features may be very obvious or quite subtle. The essence, however, is an index of suspicion and only rarely should the examiner be surprised by what is revealed by the radiograph (see box below).

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(a)

(b) Figure 21.3 (a) A nasty tibial plateau fracture as seen on (b) to be even nastier on an oblique film.

Transverse

Oblique

Spiral

Comminuted

Pathological

Butterfly fragment

Closed

Open

Greenstick

Figure 21.4 Fracture architecture.

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How to describe a fracture

• • • • • •

Which bone is broken and on which side? Is the fracture open or closed? Where on the bone is it broken? Intra-articular Mid-shaft Proximal or lower third What shape is the fracture? Spiral Oblique Transverse How many fragments? Simple Butterfly Comminuted Position of the distal fragment? Displacement: anterior–posterior, medial–lateral Angulation: anterior–posterior, varus–valgus Rotation: internal–external

Radiography of other areas

•

Other films may be taken where injury to other areas is contemplated (see above). For example, if the skull is fractured, it is wise to X-ray the cervical spine; this is mandatory if the patient is unconscious. If the patient is to have an anaesthetic, a chest film will help exclude a small pneumothorax that may become lethally significant if the patient is intubated and given positive-pressure ventilation. In multiple lower limb injuries, it is wise to take a radiograph of the pelvis. On occasions it is useful to take radiographs of the opposite normal limb. This is particularly so in children, where epiphyseal centres of ossification can produce confusing pictures, with many apparently free-floating ‘blobs’ of bone. A comparison with analogous films of the other side may reveal a displaced fragment, often lying in the joint. It is also useful sometimes to X-ray the patient on two separate occasions. For example, scaphoid fractures are frequently invisible on an initial radiograph, only to be revealed on a film taken 2 weeks later. This radio-opacity is caused by the hyperaemia in the surrounding bone that occurs in the acute inflammatory phase following fracture. The improvement in fracture image with time is almost certainly due to resolution of the hyperaemia (Fig. 21.5).

• • •

•

Tomography An alternative to waiting for radiolucency through areas of hyperaemia is to take tomograms. This is a radiographic

Figure 21.5 Special views are often required when a fracture is suspected. In this case an oblique view clearly shows that the scaphoid is fractured (left picture) but the fracture is not obvious on the conventional anteroposterior view (right picture).

technique where the X-ray beam and the film rotate around the limb so that only one point of the limb (the place that is potentially fractured) will be constantly in focus (see Chapter 3). In this way a detailed view of a small area of interest may reveal pathology. A good example is fracture of the odontoid peg, which is often lost among confusing shadows at the base of the skull.

Computed tomography Computed tomography (CT) is essentially an extension of ordinary tomography but scans are repeated thousands of times and assembled into a single image by a computer. This represents a section of the body a few millimetres thick, usually taken in the transverse plane. CT scans are most useful in determining the extent of an injury but are less useful in primary diagnosis. In detail they are of value in planning an operation or determining the stability of a fracture, e.g. the spine.

Magnetic resonance imaging Magnetic resonance imaging (MRI) works by aligning the body’s hydrogen atoms (protons) in a magnetic field and bombarding them with radiofrequency (RF) waves. The RF waves cause the hydrogen atoms to spin as they acquire energy. Removal of the RF waves causes the protons to release the energy they have acquired. This energy release is picked up by detectors and converted into a grey-scale image. Each tissue produces a characteristic signal; compact bone gives off little or no signal, while soft tissue generally gives a good signal. MRI therefore has little place in the management of most fractures but is important for the assessment of spinal cord and spine trauma (see also Chapter 3).

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Other investigations

Management of fractures

In acute injuries few investigations apart from the plain radiograph are necessary. Ultrasound of a joint may help in elucidating an effusion. When there is doubt, radioisotope bone scanning can help determine whether a bone is fractured. This is most useful about 2 weeks after the injury. It is a highly sensitive test but does not provide any information about the fracture except that it is there. A useful example is the scaphoid fracture, which may be seen on a second X-ray at 2 weeks but there can still be doubt. A negative scan is very positive reassurance in such a situation and may help to allay lingering clinical doubt.

How do fractures heal?

• •

Investigating fractures

• 03

Take a radiograph in two planes at right angles to each other to build up a mental three-dimensional image of the fracture If you cannot visualize the fracture adequately, take more films. Oblique films sometimes help If you still cannot see a fracture but suspect it clinically, do more tests. Your clinical judgement should always overrule negative investigations If you suspect associated injuries, use radiographs to exclude them: ribs–chest, skull–neck, femur–pelvis Sometimes it is necessary to take films on more than one occasion, e.g. scaphoid Use expensive tests specifically: CT for bones and joints, MRI and ultrasound for soft tissues, scintigraphy in specified circumstances

• • • • •

Week 1

Fracture

Week 2

Haematoma

Bone has a natural tendency to heal and, unlike any other connective tissue, has a remarkable repair mechanism that ultimately results in bone regeneration and structural integrity; it is literally ‘as good as new’. The pathology of fracture healing is summarized in Fig. 21.6. This remarkable process and its mechanism remain poorly understood but there are a number of points worth noting. Bones heal in the presence of some movement. This is clear from the example of broken ribs, which unite efficiently (albeit painfully) with prodigious external callus formation. It appears that movement stimulates union but the movement must be small and must not be in certain directions. Essentially, bones are stimulated by micromovement directed along their axis and heal least efficiently if subject to shearing forces or large movements. The converse also holds true: although bones will heal if there is no movement, they do so very slowly and by an entirely different process that does not utilize natural external callus formation. This alternative method of fracture healing appears to be similar to the normal remodelling processes of bone, which are slow but sure.

•

Immediate management Pain relief

•

Systemic pain relief for fractures requires the use of opiates given in adequate doses in combination with an antiemetic to offset the adverse effects of opiates. In

Week 3 +

Callus formation

Capillary invasion of haematoma Proliferation of osteogenic cells from the periosteum

Osteoblasts

New bone

Chondroblasts

Cartilage

Figure 21.6 The pathology of fracture healing.

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injured patients, intravenous rather than intramuscular opiates should be used. Clinicians, particularly when new, are often afraid to give adequate doses of opiates in the fear of affecting consciousness and clinical signs. In general, however, when serious head or visceral injury has been excluded, they may be used generously and early. Local anaesthetic nerve blocks are frequently effective. A femoral nerve block, for example, can remove the need for systemic drugs following femoral fracture, although the anxiolytic benefits of central nervous system agents should not be underestimated. Splintage can be applied to most fractures before arrival at hospital. This alone can relieve most intolerable pain. In general, a splint should encompass the joint above and below an injury. Simple expedients such as binding the arm to the chest, with or without a sling, or simply binding the legs together is often sufficient.

• •

Blood loss For most upper limb and peripheral lower limb fractures, blood loss is small and is tolerated even by the elderly. However, blood loss may be significant with major pelvic fractures (6+ units) and long-bone fractures, particularly the femur (2–3 units) and the tibia (1 unit). In general, all patients with long-bone injuries should be cross-matched for blood and a good-sized venous line established as soon as possible to ensure adequate resuscitation (see Chapter 6). For pelvic fractures two lines may be needed and a central venous line established to ensure transfusion is keeping up with loss.

Open fractures Open (or, less meaningfully, compound) fractures are serious injuries (Fig. 21.7). Considerable violence is required

to cause this type of injury and because there is a break in the skin, bacterial contamination of the bone occurs. The strategy of treatment is to clean the wounds as soon as possible and remove all dead tissue (débridement), thus preventing the development of infection. Open fractures are surgical emergencies and, provided the patient’s general condition permits, formal surgical wound débridement should be performed as soon as possible and preferably within 6 h of injury. Wounds must be left open, and closed either as a secondary procedure after a few days or left to heal spontaneously. Such patients all need supplementary broad-spectrum antibiotics and some form of tetanus prophylaxis, i.e. tetanus toxoid booster to those with a previous immunization record or human antitetanus globulin for those with no previous active immunity.

Definitive management The essential strategy of long-term fracture management must be to return patients to their preinjury level of function by the safest means. Functional requirements vary from individual to individual depending on many factors, including age, physical health and the patient’s occupation. For example, a fractured wrist in a frail elderly patient with poor osteoporotic bone might be managed differently from that in a young fit, right-handed craftsman. In the former, a less than ideal reduction under local anaesthesia might be acceptable, allowing for early discharge and early mobilization of the wrist; the young patient may be prepared to spend many months ensuring a perfect result because this is required for his longterm health and employment security. The basic goals of management are reduction, immobilization and rehabilitation.

Reduction In order to achieve acceptable function, a fracture should be reduced and held so that the anatomy of the bone is returned to as near normal as possible. If the fracture passes into a joint, then the anatomy should be restored accurately if acceptable function is to be achieved. If a fracture occurs through the shaft of a long bone, then it is desirable to return the anatomy to normal but the margin for error is much greater and something less than perfect is acceptable. Closed reduction may be achieved by traction on the distal fragment and relocation of that distal part on to the proximal fragment by manipulation (e.g. Colles fractures). In order to achieve a reduction, adequate analgesia must be given; this is achieved by general or regional anaesthesia. The manipulative procedure usually involves

• •

Figure 21.7 An open fracture undergoing surgery to clean the wound. An external fixator is in place.

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reversing the direction of the deforming force. If closed reduction is unsuccessful, then open reduction may be required, whereby the fracture site is opened surgically and the fragments are relocated directly under vision (e.g. unstable fracture of both forearm bones).

Holding Once the fracture is adequately realigned, then it must be held in the normal position until the bone has become strong enough to support itself (united) and then protected until it is strong enough to bear some load (consolidated). Methods of immobilizing fractures are listed below. Over a longer period of time the bone architecture will return to normal or near normal depending on how much displacement occurred during treatment; this process is known as remodelling.

Casting After the fracture has been manipulated, it may be held simply and effectively in a plaster of Paris cast until union occurs. The fracture must be held in a position that maintains it in three dimensions (tilt, twist and shift) and the cast must be the proper length. In order to ensure complete control of all dimensions of the fracture, it is necessary to control the joint above and below the fracture as otherwise joint movement may result in distortion in one or more dimensions. Plaster of Paris is relatively brittle, messy and very difficult to apply well. It is heavy and awkward, particularly in the elderly, and takes up to 3 days to dry fully. For these reasons, strong and light glass fibre and polyurethane resin materials have been developed. These are not as versatile as plaster of Paris and are better for secondary casts, which are applied after a week or two when the fracture swelling has settled (Fig. 21.8). Functional bracing Casts have a number of disadvantages: they are heavy, immobilize the joints and prevent access to the fracture site. The immobility imposed on a limb by a cast results in muscle wasting and joint stiffness. It is possible to overcome these disadvantages by the technique of functional bracing, i.e. freeing the joints while maintaining alignment at the fracture site. In order to maintain threedimensional control of the fracture, it is necessary to support the cast at the joints by a combination of accurate moulding and the provision of hinges, which permit motion in one direction, usually flexion and extension. Functional bracing is highly dependent on a very accurate fit and can be used only after a few weeks when the pain and swelling have settled. In practice, functional bracing is used in the management of fractures of the tibia and fibula.

Internal fixation Where accurate reduction and holding of fractures are required, internal fixation is performed. However, internal fixation is technically very demanding, has many complications and, most important of all, prevents natural healing. If fixation is to be used it can be achieved in a number of ways. Apposition. Once fractures are realigned, they may only need to be held in apposition for healing to proceed satisfactorily. This is particularly true in children. Apposition can be achieved simply by using semiflexible wires known as ‘K’ (for Kirschner) wires. They hold position without producing immobility and so healing occurs by natural callus formation. They can be left standing proud of the bone and can easily be pulled out once union is established and before consolidation. Interfragmentary compression is usually achieved by screws or occasionally by tension band wires. These achieve great accuracy and are particularly valuable in cancellous bone around joints. They are also useful in long bones, particularly in the upper limb, but in these situations extra support is required from an onlay device. Onlay devices are metal plates that are used to buttress weak structures around joints and to fix long bones in the upper limb. These very rigid systems inhibit natural bone union and, although they permit early movement, they ultimately delay healing and full load-bearing. Intramedullary or inlay devices are the most satisfactory method of fixation. They achieve alignment without unduly disturbing natural bone healing. They are a relatively inaccurate method of restoring anatomical position and so are not useful around joints. Their great strength makes them ideal devices for treating long-bone fractures, particularly in the lower limb.

•

• • •

External fixation When fractures are open and associated with extensive soft-tissue damage and contamination, neither plaster casting nor internal fixation is appropriate. Plaster splints are unsuitable because the wounds become inaccessible for inspection and dressing, while internal fixation is hazardous because of the very high risk of wound infection. A compromise solution is to apply an external fixation device, which consists of a strong metal rod (or series of rods) that runs parallel to the fractured bone and is attached to the bone by a series of pins. Such a device stabilizes the fracture and gives access to the soft tissues for dressings and secondary surgery such as skin grafting. A disadvantage of external fixators is the risk of infection at the pin sites. Traction Traction may be used to hold a fracture in a reduced

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(a)

(b)

(c)

(d) Figure 21.8 (a) A forearm midshaft fracture of radius and ulna; this may be treated in a plaster cast in children (b). (c) In adults it is usually plated following open reduction. (d) A tibia in a cast using modern resin materials. (e) Modern materials can be used to make sophisticated hinged casts that stabilise fractures but permit joint motion. A technique known as functional bracing.

(e)

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position. Traction is achieved by the application of a relatively small weight (4.5–7 kg) to a limb. The weight exerts a pull along the axis of the broken bone, thus stimulating muscle contraction. The increased muscle tone acts like a splint, holding the broken bone in the position achieved at reduction.

Rehabilitation Immobilization causes muscle atrophy and joint stiffness which, if not treated aggressively, may lead to contractures and post-traumatic syndromes (e.g. post-traumatic sympathetic dystrophy). Therefore, patients require intensive rehabilitation programmes to help them use their joints as soon as possible after the fracture, to exercise their muscles and begin to use and build up strength in the injured limb. Most of this work will be done under the supervision of physiotherapists and occupational therapists who work in close partnership with fracture surgeons (see also Chapter 10).

Treatment of fractures at a glance

•

Treat the pain and exclude the risk of serious blood loss. Most low-energy fractures are not associated with blood loss, but pelvic and long-bone fractures are, so calculate the potential blood loss Reduce the fracture: do this as simply and safely as possible. Restore function Hold the fracture in a functional position. This may mean using: (a) A cast (b) Doing an operation and inserting fixation devices such as nails, plates or screws (c) Applying external fixation where there is extensive soft-tissue damage (d) Using weights to apply gentle traction Rehabilitate the patient: work with the rest of the team of healthcare professionals including nurses, physiotherapists and occupational therapists

• •

•

tures or after internal fixation: it is notable that the most common cause of bone infection in the western world is surgery. Although infection may delay or prevent union, it is not inevitable that this will be so. Provided a fracture is held stable, it will unite despite infection. If there is movement and infection, then non-union is most likely. This phenomenon is poorly understood but if a fracture is infected, provided it is stable, it may be treated by drainage of pus and antibiotics until union has occurred.

Fat embolism After fracture of a long bone, a small number of patients (usually men under the age of 20) suffer from fat embolism characterized by an increasing degree of respiratory distress, leading to adult respiratory distress syndrome (see Chapter 20). The cause of fat embolism remains unclear. It was originally thought to be due to fat from the marrow of the fractured long bone precipitating in the lungs. However, an alternative view is that there is a breakdown of tissue fats to free fatty acids, which precipitate a pneumonitis. The symptoms (initially tachypnoea and mild confusion) usually commence within 2–5 days of injury. The patient may have a petechial rash on the chest, neck and conjunctiva but this is not a universal finding. Fat globules may be found in the urine and sputum and are occasionally seen in the retinal vessels on fundoscopy. Early diagnosis depends on a high index of suspicion and appropriate investigation. Blood gases will show a hypoxaemia (Pao2 4.7–6.7 kPa) and respiratory alkalosis (from hyperventilation) and a chest radiograph diffuse opacities that increase to complete ‘white-out’ over the following few days. In severe cases the respiratory distress increases to the point where positive-pressure ventilation and positive end-expiratory pressure are required (see Chapter 11), but even with this level of support the condition carries a significant mortality. Unfortunately, younger men are more prone to the full-blown syndrome. Early diagnosis and treatment with oxygen and chest physiotherapy are helpful.

Complications of fractures Early complications may occur either as a direct consequence of the injury or in association with the treatment. Late complications are generally related to the fracture but a few are unfortunately precipitated by treatment (or lack of it).

Infection Bone infection (osteomyelitis) may occur after open frac-

Renal failure Patients with massive soft-tissue injury who are trapped for prolonged periods, particularly where they are shocked or the trapped limbs are relatively ischaemic, are prone to develop acute tubular necrosis. Again the key is to recognize the possibility and be prepared to support such patients with renal dialysis. The cause is purported to be the release of myoglobin and this is found in abundance in the renal tubules (see Chapter 14).

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Compartment syndrome Compartment syndromes may occur in the upper and lower limbs following a fracture with excessive localized soft-tissue swelling. Classically it occurs in the forearm, where it leads to Volkmann’s ischaemic contracture, although any muscle compartment lined by a stout fascial sheath may be at risk (e.g. calf muscles). This condition is discussed more fully in Chapter 17.

Immobility After injury the injured part needs a short period of rest followed by motion to aid rehabilitation. The whole person does not need to be immobilized and patients must begin to move and rehabilitate as soon after the injury as possible. Injury results in negative nitrogen balance and patients will lose lean body mass. The effects can be minimized by early mobilization, which will also discourage disuse osteoporosis and the migration of calcium into the blood (which can precipitate renal stone formation).

Delayed union and non-union About 2% of all fractures fail to unite; this is known as non-union (Fig. 21.9). Delayed union is when fractures fail to unite within the expected time. If left to heal naturally, upper limb fractures heal in 6 weeks or so and lower limb fractures in 12 weeks. This rule of thumb is useful but must not be too strictly adhered to and will be modified depending on the degree of violence involved and how the fracture was treated. However, we may say that non-union is established at 20 weeks in the lower limb and 10 weeks in the upper. These are arbitrary but practical figures. Delayed union is even less specific and it is really a period between expected union and accepted non-union when the decision to intervene is contemplated. Non-union is most common in the tibia but may occur at any site. Why fractures demonstrate non-union is not fully understood but several factors have been implicated: excess movement; insufficient movement, e.g. rigid internal fixation; soft-tissue interposition; poor blood supply; infection; unstable fracture; excessive traction or separation of bone ends; intact fellow bone, e.g. fibula. Treatment of non-union relies on removing any underlying cause and then stimulating union. Stabilizing the fracture sufficiently and then adding bone graft seems to stimulate union but how bone graft does this remains

• • • • • • • •

Figure 21.9 Non-union occurs most commonly in the tibia. If a tibial fracture has failed to heal at 20 weeks, a diagnosis of non-union is made. On X-ray, the fracture is still visible and the bone ends are sclerosed.

an enigma. Bone graft is usually autologous, being taken from the iliac crest and placed next to the fracture. The graft contains cells and minerals and humoral factors that probably mediate the repair by activating the hitherto deficient mechanism.

Malunion Malunion implies that the fracture has been allowed to heal in a position that precludes normal function and usually implies failure of treatment or neglect. Regular review is the mainstay of fracture management and frequent radiological and clinical examination are essential to ensure that all is well.

Growth arrest Children have a great capacity to remodel malunited fractures but are not able to remodel rotatory deformities. However, if a fracture breaches the germinal layer of the epiphyseal growth plate, distorted bone growth may occur. These are rare injuries and difficult to manage. All parents of children with epiphyseal injuries must be warned of this possibility if misunderstandings are to be avoided.

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Complications These can be early or late and a direct consequence of the injury or associated with the treatment applied Early direct complications Specific to the fracture Infection in open fractures Associated stretching or crushing of nerves Very rarely, damage to a blood vessel or its lining causes thrombosis Compartment syndrome caused by localized swelling

• • • •

General All these general complications should be anticipated and are very rare Fat embolism Renal failure Unrecognized hypovolaemic shock Muscle wasting due to immobility

• • • • 03

Complications associated with treatment Infection of internally fixed fractures Surgical damage to vital structures such as nerves or blood vessels Compartment syndrome Pressure damage to skin or nerves from excessively tight bandages and splints

• • • •

(a)

Late bone complications Malunion due to poor supervision of healing Non-union usually associated with: (a) Excess movement (b) Insufficient movement (c) Poor local blood supply due to either anatomy (e.g. tibia) or a lot of trauma damage Growth arrest in children due to epiphyseal damage

• • •

(b)

Post-traumatic (reflex) sympathetic dystrophy This is a poorly understood syndrome characterized by persistent pain, swelling, hyperaesthesia, stiffness and disuse of a limb following an injury. If it persists, disuse osteoporosis may be seen on the radiograph. Treatment consists of physiotherapy with active and passive exercises and pain control. Chronic cases are extremely difficult to treat but pain clinics, vigorous rehabilitation and sympathectomy (in some patients) have been found to be helpful.

Dislocations Dislocations of joints are serious problems and notoriously painful (Fig. 21.10). Before the days of anaesthesia

Figure 21.10 (a) A dislocated shoulder. (b) This is clinically detectable due to the loss of normal shoulder conture.

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the reduction of a dislocated joint was exceptionally difficult because of the associated muscle spasm and the agony such a patient had to endure. Failure to reduce a joint was a serious consequence in terms of both pain and function. In modern times, reduction under anaesthesia ensures restoration of the joint surfaces. Nevertheless, dislocation is a potentially serious injury with long- and short-term consequences. In the immediate term, apart from pain and loss of function, adjacent nerves and blood vessels may be compressed and thus urgent reduction is important. In the medium term, the ligaments of the joint will be disrupted to some degree. Although these usually repair naturally after closed reduction, in some circumstances the joint can become chronically unstable. This is seen most frequently in the shoulder and less commonly at the ankle. In the long term, a dislocated joint may lose the blood supply to the bone, which results in avascular necrosis. Even without this complication, dislocated joints seem more prone to late arthritis, seen most commonly at the hip. The management of dislocation is first recognition and then assessment of the neurovascular status clinically, not least because it is essential to ensure that any nerve damage was present before treatment and not induced by manipulation. The joint is radiographed to ensure that there are no associated fractures that could be displaced further by the manipulation used to achieve reduction. Reduce the dislocation gently under sufficient anaesthesia to achieve muscle relaxation. Finally, hold the joint reduced in a position of function. Mobilise the joint gently as soon as pain permits but avoid full motion until ligaments have a chance to heal at 6 –10 weeks. Vascular problems need to be resolved immediately and continued features of ischaemia following reduction must be investigated to exclude vessel damage and thrombosis. Nerve lesions will not recover immediately, although most damage in association with dislocation is likely to be neuropraxia (see Chapter 22) and carries a good prognosis.

Common fractures and joint injuries It would be inappropriate to list all fractures but some are commoner than others and some case knowledge for all doctors is prudent. The principles of reduction and holding have been discussed previously and some of the holding methods available and in common use have been described. Most injuries are of low velocity and the majority of broken bones are treated non-operatively in splints. There are a number of different reasons why fractures are held in different ways: it is important to be accurate in reduction and holding so that function is maintained;

•

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• •

it is better for the general health of the patient, particularly when mobilization is paramount to good health; it is better to accept a less than perfect position and function in the interests of an individual’s overall well-being; it is more cost-effective for the health service or an individual to have internal fixation; in multiple injuries, internal fixation can be life-saving.

• •

Sometimes it is important to be accurate When fractures are near joints and the congruity of the articular surface is severely disrupted, an operation may be necessary to achieve both reduction and fixation. In general, mid-shaft long-bone fractures will tolerate some degree of incomplete reduction in terms of angulation and length and will remodel. However, any rotatory deformity along the long axis of the bone will not be remodelled. Growing children also exhibit excellent potential for remodelling, but again not for rotation. A good example of the need to be accurate is a fracture of both bones of the forearm. The radius articulates proximally and distally with the ulna and the two bones are further joined by a tough interosseous membrane. When the forearm is injured, both bones break or one bone breaks and either the proximal or distal joint dislocates. When both bones break, the angulation and shortening stop the ulna rotating as normal about the radius (Fig. 21.11). In adults, accuracy can only be assured by opening each fracture site and reducing the bones accurately under direct vision. Once reduced, holding with plates and screws protects the position until the soft tissues and then new bone consolidate the reduction. By holding the fracture firmly, the patient can immediately move the arm, thus restoring the important functional movements of pronation and supination as well as flexion and extension at the elbow and wrist. The disadvantages of fixation are that a closed fracture is now open and thus at risk of infection. Also by opening the fracture an already damaged blood supply is inevitably damaged further and will therefore take longer to become re-established. It is important to remember that no fracture will heal until blood supply is restored locally. Thus, although accurate reduction is achieved, union is delayed and infection becomes a risk. Bones fixed in this way do not heal by callus formation as described earlier but by slow remodelling across the fracture site, a process sometimes referred to as primary bone healing. In a way, when fractures are repaired a race is set up: will the fracture heal and the bone become strong before the fixation device fails through fatigue? It requires exacting surgical skill to achieve reliable results and thus fixation, although very effective when it works, should be reserved for particular

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(a)

(b)

Figure 21.12 The diagnosis of extrascapular fracture of the neck of the femur can be made from the end of the bed. The patient’s foot is externally rotated.

(c) Figure 21.11 (a) This fracture has been treated with a cast and good alignment has not been achieved. (b,c) This denotes how pronation and supination requires accurate rotation of the forearm bones. This is only possible if such fractures are fixed following accurate reduction.

situations, such as the need to be accurate. Even though the evidence in the scientific literature shows that forearm fractures in adults treated by internal fixation do better than those manipulated and placed in plaster, in this case the risks outweigh the benefits for most adults. This risk–benefit question must be considered every time a surgeon decides to fix a fracture.

Sometimes an operation is better for the patient’s general health Older people who injure themselves are vulnerable if

rested in bed too long. They may become disorientated in a new environment, are prone to chest and urinary infections and become rapidly susceptible to skin sores, muscle wasting and increasing osteoporosis. Older people are also more prone to falls for many reasons, such as poor eyesight and hearing, and have less adaptable cardiovascular and neurological function. Frequent falls, often but not always associated with osteoporosis, make older people particularly susceptible to fractures at the hip and wrist. A broken hip means loss of mobility and immediate exposure to all the risks mentioned above. Early restoration of mobility is a priority, otherwise the factors that precipitated the fall are magnified and the risk to health and life becomes acute. For this reason, operating on hip fractures has been demonstrated to improve the chance of survival after such injuries. Even with appropriate treatment, one in four old people die within a year or so of their injury, not from the fracture but from the precipitating factors and their consequences post surgery. Clearly the balance between risk and benefit is a fine one but in this case the decision is in favour of surgery. Any person admitted to hospital after a fall and who cannot walk should have hip fracture excluded clinically and if in any doubt radiologically (Fig. 21.12). There are two broad groups of hip fracture: those of the neck of the femur within the capsule of the joint (intracapsular) and

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those through the line of the greater and lesser trochanters outside the hip capsule (extracapsular). If the fracture is intracapsular, it may not heal because of disruption of the blood supply. The older the patient and the more displaced the fracture, the less likely it is to heal. If the fracture is extracapsular, it will heal but not in a functional position (the leg will shorten). In either case, operation is essential if the patient is to avoid the risks of being confined to bed. In younger intracapsular and all extracapsular fractures, reduction and internal fixation should be attempted as it is clearly better to have a healed normal hip than an artificial one if the state of the hip before fracture was otherwise normal. Any holding device needs to be strong enough to permit immediate mobilization of the patient. If the risk of failure of healing is high, then the head of the femur should be replaced with an artificial one. If the hip is otherwise healthy, it is quicker and safer to leave the natural acetabulum in place and perform a hemiarthroplasty. If the joint is arthritic, then a full replacement may be justified but this bigger operation carries more risk. The complications of surgery are infection, device failure in soft bone, or dislocation of the artificial joint component(s). These compound the problems that may have been associated with the fall, such as stroke or myocardial infarction. In general it is better to treat the fracture within a few days and then treat any underlying medical conditions if the patient is fit enough for anaesthesia. After surgery, early mobilization and rehabilitation is a vital step that requires a team approach involving physicians with a special interest in the elderly and the extensive network of healthcare professionals. The quality of the outcome is as much to do with good organization and teamwork as with good surgery.

Sometimes it is better to accept a less than perfect position The objective of all fracture treatment is to return patients to as normal function as possible using the safest method, in a reasonable period of time and at effective cost. Perfect function is sometimes not achieved because the damage is not entirely retrievable and because accurate reduction and effective holding can sometimes only be accomplished by exposing people to unnecessary risk. A good example of this is a common fracture of the distal radius named after an Irish surgeon, i.e. Colles fracture. Strictly speaking, a Colles fracture is a fracture of the distal 2 cm of the radius not involving the joint and results in dorsal angulation, posterior displacement and supination of the distal fragment; the fracture may include the tip of the ulna styloid but not the shaft of the ulna (Figs 21.13 & 21.14). It is commonly caused by a fall on to the out-

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Figure 21.13 Typical ‘dinner-fork’ deformity seen in a patient with a Colles fracture.

Figure 21.14 In a Colles fracture the radial fragment is shifted and tilted backwards and radially and impacted. There is usually also a fracture of the ulnar styloid.

stretched arm and may be produced by minimal force in older people with osteoporosis but requires more violence in young people with tougher bones. The resulting ‘dinner-fork’ deformity is unsightly and results in collapse of the radius such that wrist joint function becomes difficult and positioning of the hand for routine tasks is sufficiently impaired to threaten independent living in often frail older people. Ideally, the fracture would be routinely reduced and held until union using a cast. However, the presence of osteoporotic bone frequently indicates that the fracture cannot be effectively held without it later collapsing to the same position as that seen immediately after injury. In practice, all Colles fractures tend to collapse to some degree. However, aggressive intervention is not always required as this may mean prolonged and difficult surgery and the risk of hospitalization in frailer people. These patients may be better served by accepting a less than perfect result, provided the wrist is not painful and displacement not gross. In such circumstances, some help with rehabilitation to achieve

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acceptable activities of daily living may be a more pragmatic solution. In younger people, Colles fracture is a serious injury and requires a major investment in time and resources by the surgeon and the patient in order to restore long-term function. It is vital to appreciate that this is by no means a second-class service for one particular group just because they are old. On the contrary, it is about ensuring that treatment is tailor-made for the patient: we treat people with fractures, not just broken bones. Apart from malunion, the complications of Colles fracture include: acute compression of the median nerve, which may require operative intervention; late rupture of extensor tendons through attrition on displaced bone fragments; rare problems such as algodystrophy, which are seen more commonly at the wrist because wrist fractures are themselves very common. Management after fracture consists of ensuring that a reasonable level of function is maintained over the 4–6 weeks of splintage. This may require physiotherapy and encouragement from clinicians and carers to ensure that patients maintain a good range of upper limb function.

• • •

Sometimes an operation is more effective for the patient and the health service Fractures of major long bones such as the femur are potentially very serious injuries, especially if the fracture is open. Femoral fracture always implies that high energy transfer has occurred and soft-tissue damage will be extensive. However, the bone has a good blood supply and is surrounded by a large cuff of very vascular muscle. Provided bones can be held in alignment, the vast majority of even open femoral shaft fractures will heal with few complications. The issue is holding. Prior to the modern era of fracture fixation, patients with this injury were confined to bed on traction for many months. More recently, cast braces shortened the period of hospitalization but nonetheless was still 4 –6 weeks followed by up to 6 months of rehabilitation. Effectively, if all went well, a patient with a fractured femoral shaft would lose almost a year of normal life, threatening employment and disrupting family relationships. Intramedullary nailing, introduced during the Second World War and refined since the 1960s, has dramatically altered the pattern of post-fracture management and immeasurably improved quality of life for patients. Not

least, hospital stays for isolated fractures may be as short as 5 days, with minimum outpatient supervision being required and huge cost savings for healthcare providers. Complications following nailing include malposition, especially in rotation, infection and associated damage to structures such as nerves. Non-union sometimes occurs but is relatively rare in the femur. In contrast, although other bones can be nailed in this way, the risk–benefit ratio will be different. For example, in tibial fractures the bone is not cocooned in well-vascularized muscle and so complications such as infection and non-union are higher than in femoral fracture; thus alternatives to nailing, especially in lower-energy tibial fractures, are seen as viable techniques. In the upper limb, the humerus may be nailed but the vast majority of these injuries heal perfectly well with satisfactory function if treated with a simple sling or cast brace; surgery to the humerus carries a very high complication rate in terms of radial nerve palsy. As with all decision-making, surgeons must be certain that any intervention they contemplate is weighted heavily in favour of improved quality of life for the patient, with acceptable risk and reasonable cost. One other situation in this category is worth consideration. After pathological fracture following metastatic cancer, internal fixation is frequently deployed despite the severity of what is effectively a terminal illness. Fixation treats pain, permits nursing and medical management (mobilization, access to the fracture for adjuvant treatment such as radiotherapy) and improves the remaining quality of life for the individual.

Treating multiple injuries After serious accidents, when the subject may have many fractures and damage to other systems such as the gut or chest and head, the indications for fixation assume a different perspective. The evidence from the literature overwhelmingly supports early and aggressive fixation of all major fractures, especially to the long bones and the pelvis. Such operations are very demanding but are often essential to save the patient’s life. Multiple injuries treated conservatively lead to prolonged immobility, which is a major contributor to late death following injury. These major operations require massive resources in terms of intensive care, multidisciplinary teams, and highly skilled surgeons with regular experience of such operations. For these reasons, people involved in major injuries are best treated in regional centres supported by excellent mobile recovery services (paramedics and hospital-based retrieval teams).

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Musculoskeletal trauma at a glance Definitions Fracture: a break in the continuity of a bone; fractures may be transverse, oblique or spiral in shape Greenstick fracture: one in which only one side of the bone is fractured, the other simply bending (usually immature bones) Comminuted fracture: one in which there are more than two fragments of bone Complicated fracture: one in which some other structure is also damaged (e.g. a nerve or blood vessel) Compound fracture: one in which there is a break in the overlying skin (or bowel wall) with potential contamination of the bone ends Pathological fracture: fracture through a bone weakened by disease, e.g. metastasis Common causes Fractures occur when excessive force is applied to a normal bone or moderate force to a diseased bone, e.g. osteoporosis Clinical features Pain Loss of function Deformity, tenderness and swelling. Discoloration or bruising Crepitus (not to be elicited!)

• • • • •

Investigations Radiographs in two planes (look for lucencies and discontinuity in the cortex of the bone) Tomography, CT, MRI (rarely) Ultrasonography and radioisotope bone scanning

• • •

Management General Look for shock/haemorrhage and check ABC (see Chapter 17)

•

• • •

Always consider multiple injury in patients presenting with fractures Look for injury in other areas at risk (head and spine, ribs and pneumothorax, femoral and pelvic injury) Compound fractures are a surgical emergency and require appropriate measures to prevent infection, including tetanus prevention Always image the joints above and below a long-bone fracture

•

The fracture Immediate Relieve pain (i.v. opiates, nerve blocks, splints, traction) Establish good i.v. access and send blood for group and cross-match Open (compound) fractures require débridement, antibiotics and tetanus prophylaxis

• • •

Definitive Reduction (closed or open) Immobilization (casting, functional bracing, internal fixation, external fixation, traction) Rehabilitation (aim to restore patient to preinjury level of function with physiotherapy and occupational therapy)

• • •

Complications Early Blood loss Infection Fat embolism Deep vein thrombosis and pulmonary embolism Renal failure Compartment syndrome

• • • • • •

Late Non-union Delayed union Malunion Growth arrest Arthritis Post-traumatic sympathetic (reflex) dystrophy

• • • • • •

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Soft-tissue Trauma

Introduction, 248

Injuries to specific soft tissues, 248

Must know Must do

Must know Soft-tissue injuries can be minimized with simple treatment Principles of first aid for soft-tissue injuries How to diagnose soft-tissue injuries by careful examination of the injured patient. Some basic anatomical knowledge is required to achieve this, particularly with nerve injuries Not diagnosing apparently small and often remediable conditions can have serious social and economic consequences for patients Importance of prophylaxis against infection and tetanus in soft-tissue injuries Must do Visit the accident and emergency department to observe treatment of soft-tissue injuries Suture a minor laceration under vision Administer a tetanus toxoid booster injection

Introduction Although not usually life-threatening, soft-tissue injuries (i.e. injuries to ligaments, tendons, muscles and nerves) are important because they are common and result in morbidity for the patient and have important economic consequences through loss of work. Whenever the body receives a blow, the energy is transmitted through the softtissue layers and the bones to be dissipated as disruption, sound and heat. At low velocity such blows seldom break normal bones but will damage cells and tear soft tissues, causing bleeding followed by an acute inflammatory reaction. Acute inflammation is a physiological response to trauma and is associated with swelling, hyperaemia and pain. First aid consists of actions designed to reduce the effects of acute inflammation and to reduce pain. This may be achieved by applying: Rest, Ice,

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248

and • Compression Elevation. • Ice should be wrapped in a cotton towel before being applied to the injured area as direct contact with the skin may lead to thermal injury. Compression of an injured limb should be supervised and not prolonged or performed without elevation; care should be taken to avoid hindering the circulation (see also compartment syndrome, Chapter 17). Elevation of the affected limb above the heart requires the patient to lie down and have the limb raised or sit with the whole arm elevated (Fig. 22.1). These simple measures can be applied to any injury and can reduce swelling effectively, thus facilitating definitive treatment.

Pain relief The application of RICE, besides reducing swelling, will also help reduce pain. Simple oral analgesia often provides very effective pain relief and the anti-inflammatory properties of non-steroidal anti-inflammatory drugs (NSAIDs) make them particularly effective in soft-tissue injury. If used early and at relatively higher doses than normal, NSAIDs also help to reduce swelling and inflammation. Occasionally, opiates are required to provide pain relief. However, inordinate pain should alert the clinician to the possibility that some more serious condition such as a fracture or an impending compartment syndrome may have been missed.

Injuries to specific soft tissues Fat and skin Most superficial injuries to the fat and skin manifest themselves as bruising (ecchymosis) and blisters. The bruising may track along tissue planes but this is natural and simply an effect of gravity. Occasionally, fat necrosis causes an intense red reaction on the skin like an infection or cellulitis. If the patient is well and apyrexial, such reaction should not be treated with antibiotics. Haematomata in these layers may liquefy and cause fluid collections, which can be aspirated.

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Figure 22.1 Immediate treatment of soft-tissue injury consists of RICE (rest, ice, compression and elevation).

Muscle Dead muscle cells cannot regenerate. Healing following muscle injury is therefore by fibrosis, with compensatory hypertrophy of the surrounding muscle cells. However, deposition of fibrous tissue in muscle leads to stiffness. This process cannot be altered but early rehabilitation through movement will minimize stiffness and encourage muscle hypertrophy. Following muscle injury, physical therapy within the limits of pain should be instituted as soon as possible. Other techniques such as ultrasound may enhance recovery by dissipating the fibrous tissue.

Ligaments Incomplete ligament injuries are referred to as sprains. Complete injuries are known as ruptures or tears. A sprain is caused by rupture of some, but not all, of the fibres of a ligament. A sprain generally does not cause the associated joint to become unstable but will cause dysfunction through pain. It should also be appreciated that the proprioceptive function of the ligament will be disrupted and this adds to the problems of recovery. Sprains do not require surgical intervention and, following the application of the first-aid measures described above (RICE), recovery is encouraged by exercise – initially nonweight-bearing exercises, rapidly progressing to gradual loading. Most sprains recover in a few weeks depending on the severity of injury and individual requirements, e.g. an athlete may require longer to achieve a high level of performance. Ruptures may render a joint unstable and also proprioceptively insensitive in certain planes of movement. Complete ruptures often present with less severe pain than sprains, presumably because of the associated nerve damage. Surprisingly, surgical intervention is seldom required

•

except in specific cases (e.g. cruciate ligament injuries). If joint motion is controlled by splintage early in treatment, then most ligaments will heal spontaneously.

Tendons Tendon injuries generally arise from penetrating trauma, although they may be ruptured by excessive force. They occasionally rupture in middle and old age when subjected to normal forces. In these situations the tendon has undergone degenerative change due to either intrinsic collagen abnormalities or abnormal ‘wear’ against an osteophyte from an adjacent degenerative joint. Tendons usually require surgical repair, which can be technically challenging if function is to be restored. Postrepair physiotherapy to restore movement requires a balance between movement and a reduction in loading so that any repair is not damaged. Common penetrating injuries to tendons occur in the hand. Extensor injuries are relatively benign and can be repaired fairly easily by direct suture with strong absorbable materials. The local blood supply enables predictable healing. Flexor injuries are more complex because the tendons pass through tight synovial-lined tunnels in the palm and the fingers. The blood supply is more tenuous than in extensor tendons. This leads to the double challenge of needing accurate repair with minimal damage to any remaining blood supply. Such injuries need the attention of specialist surgeons. Whenever a hand sustains a cut, then tendon (and nerve) injury must be specifically excluded. Degenerative tendon injuries are commonly seen around the shoulder, affecting the tendon to the long head of biceps and the short tendinous sheath composed of the supraspinatus and infraspinatus muscles and the teres minor. Rotator cuff tears may occur through high-energy

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trauma but more commonly occur in association with degenerative changes in the glenohumeral and acromioclavicular joints. The patient may present with pain followed by loss of function (see painful arc syndrome, Chapter 21). Repair is technically difficult and sometimes all that may be done is to decompress the compromised tendon tissue by débriding degenerative osteophytes from around affected joints. This improves pain but unless the tear can be repaired there is no restoration of function.

Nerves

Stretching, crushing or cutting may injure nerves. Stretching or crushing may result in temporary loss of function. Such injuries may be associated with a fracture or a direct injury through pressure. Application of tight bandages or casts around a limb may cause nerve injury through pressure. It is important to document nerve injuries prior to treatment so that the relationship of the injury to the initial trauma is established and the clinician is not exposed to accusations that nerve injury has been caused by treatment.

Types of nerve injury

•

Neurotmesis is complete anatomical division of a nerve with Wallerian degeneration. The nerve tissue distal to the division degenerates and only the support cells survive. New nerve tissue grows back as a series of processes from the damaged cells and so recovery can be prolonged and is usually never completed. Mixed sensory and motor nerves have a particularly poor prognosis, while simple sensory nerves such as those found in the fingers are most likely to recover well. Tinel’s sign is used clinically to mark the level of nerve regeneration. The course of the nerve is percussed with a patella hammer from distally to proximally. A tingling sensation is felt when the level of regeneration is reached. Complete division of a mixed peripheral nerve results in motor, sensory, vasomotor, sudomotor and trophic symptoms in the anatomical distribution of the nerve. Electromyography is useful in identifying the paralysed muscle groups. Cutaneous sensation is usually lost only over the area of skin exclusively supplied by the nerve. For most sensory nerves this area is quite small, as much of the nerve territory is overlapped by supply from adjacent nerves. Destruction of a mixed nerve leads to vasomotor and trophic disturbances related to damage to sympathetic fibres. The anaesthetic skin is dry, does not produce sweat and, when injured, heals slowly. Oedema and cold sensitivity are also recognized. After complete division, recovery is enhanced by surgical repair using fine sutures

Table 22.1 Factors that adversely affect nerve recovery following injury. Older patients More proximal levels of nerve injury Injury caused by excessive trauma Injuries to mixed nerves Increasing distance between the nerve ends at the time of repair Need to use nerve graft in repair

and magnification. However, even with most careful surgery, results are often disappointing. Axonotmesis: an injury in which the connective tissue survives but most of the axons of the nerve are damaged and Wallerian degeneration occurs. These injuries produce symptoms similar to neurotmesis but their prognosis is better. Neuropraxia: a minimal lesion producing paralysis without peripheral nerve degeneration. The most common cause is pressure. As the nerve remains in continuity and tissue damage is incomplete, recovery occurs fairly rapidly. It is important that the muscles and joints in the distribution of the nerve distal to injury are kept mobile so that rehabilitation, once recovery is established, is feasible. The factors that influence recovery following nerve injury are summarized in Table 22.1.

• •

Specific nerve injuries Examination of all peripheral nerves can be considered under three headings: sensory loss, motor loss and trophic changes. An understanding of the anatomy of nerve supply is essential for understanding the lesions produced. The common upper limb nerve injuries are summarized in Table 22.2. Footdrop The common peroneal nerve may be compressed during medical management in situations where direct pressure may be applied to it. For example, a plaster cast may press on it or it may be subject to undue pressure while a patient is anaesthetized on the operating table. Of course because these potential hazards are recognized, then prevention by careful handling and padding to offer protection make these increasingly rare events. Occasionally the nerve may be stretched following major knee surgery or while treating fractures. In general, in all these cases, the nerve is likely to recover and the principle is to maintain passive motion and normal posture until the nerve recovers. The effect of footdrop, i.e. loss of peroneal muscle ability to produce dorsiflexion, makes the gait clumsy

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Table 22.2 Clinical features of some common upper limb peripheral nerve injuries. Cause

Motor

Sensory

Brachial plexus injury Complete Motor cycle accidents

Complete arm paralysis

Complete arm anaesthesia Muscle wasting

Upper (C4–C6; Motor cycle accident/ Erb/Duchenne) obstetric injury

Limb assumes ‘waiter’s tip’ position

Decreased sensation over outer upper arm

Muscle wasting

Lower (C7, C8, T1; Klumpke)

Paralysis of the small muscles of the hand (may be a Horner’s syndrome)

Sensory loss of inner side forearm and medial 31/2 fingers

Wasting of muscles in hand

Anaesthesia of a small area at base of thumb and index finger

Minimal wasting of long wrist extensors

Cervical rib/shoulder dislocation

Radial nerve injury (Fig. 22.2) Mid-shaft fracture of Wrist drop humerus ‘Saturday night’ palsy (falling asleep with arm draped over the back of a chair) Median nerve injury (Fig. 22.3) At the elbow Fracture of lower end of humerus Elbow dislocation At the wrist

Lacerations

Trophic

‘Pointing’ index finger Sensory loss over all Thenar eminence and ‘simian hand’ (loss palmar aspect and distal wasting of abduction and dorsal aspect of radial opposition of thumb) 31/2 fingers Simian hand

Sensory loss over all Thenar eminence palmar aspect and distal wasting dorsal aspect of radial 31/2 fingers

Ulnar nerve injury (Fig. 22.4) At the elbow Fracture of medial epicondyle of the humerus

Claw hand (main en griffe)

Palmar and dorsal medial 11/2 fingers

Wasting of all small muscles of the hand apart from the thenar eminence

At the wrist

Marked claw hand

Palmar and dorsal medial 11/2 fingers

Wasting of all small muscles of the hand apart from the thenar eminence

Lacerations

and inefficient. Classically, the patient has a high stepping knee gait to permit the floppy foot to come through during striding. Temporary splintage with a splint or orthosis will improve gait while the foot slowly recovers its functional power.

Figure 22.2 In radial nerve injury there is a characteristic wrist drop due to paralysis of the extensors of the wrist. There is only a very small area of anaesthesia at the base of the thumb and index finger as there is considerable sensory overlap from the median and ulnar nerves.

Wrist drop The wrist is extended by the radial nerve, which is prone to damage when the humerus is fractured. Radial nerve palsy or wrist drop is even commoner following operations to repair the humerus by open reduction and internal fixation. Closed injuries as described carry a good prognosis and the principle is as usual to maintain function with

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(a) Figure 22.3 In high median nerve lesions the flexors of the wrist and fingers will be paralysed, except those supplied by the ulnar nerve, i.e. flexor carpi ulnaris and the medial half of flexor digitorum profundus. Thus when the patient attempts to flex the fingers, the index finger remains extended (pointing sign). With high and low lesions there will be failure to abduct and oppose the thumb, resulting in a simian or ape-like hand. Wasting of the muscles of the thenar eminence will be pronounced in all median nerve lesions. There will be sensory loss to the palmar surface of the lateral 31/2 fingers and from the proximal interphalangeal joint distally on the dorsal surface of the same fingers.

03 splintage and therapy. In this case, a splint that maintains wrist extension and supports the metacarpophalangeal joints ensures the intrinsic muscles of the hand (supplied by ulnar and median nerves) continue to provide fine finger motion including finger extension. Physiotherapy is essential to provide the platform for recovery once nerve regeneration is established. Sciatic nerve injuries The sciatic nerve may be injured by penetrating trauma (e.g. an ‘intramuscular’ injection) or a posterior dislocation of the hip. There is paralysis of the hamstring muscles and all of the muscle groups below the knee. Only the muscles of the anterior compartment of the thigh are unaffected (as they are supplied by the femoral nerve). Sensory loss is also extensive, with complete anaesthesia below the knee except for a narrow strip along the medial side supplied by the long saphenous branch of the femoral nerve. The common peroneal branch of the sciatic nerve is at risk of injury as it winds around the neck of the fibula. Unfortunately, this nerve often suffers iatrogenic injury because of an excessively tight plaster cast or inadequate protection from pressure while the patient is under anaes-

(b) Figure 22.4 (a) Injury to the ulnar nerve produces a classical deformity known as claw hand or main en griffe. This occurs with both high and low lesions but the deformity is much more pronounced with low lesions. The clawed appearance results from the actions of the long extensors and flexors of the fingers. Wasting of all the small muscles of the hand (except the muscles of the thenar eminence) occurs and is seen most easily on the dorsum of the hand. (Weakness of the adductor pollicis accounts for Froment’s sign: if the patient holds a piece of paper between the thumb and fingers, the terminal phalanx of the thumb of the affected hand flexes due to the unopposed action of flexor pollicis longus.) Sensory loss is to the medial 11/2 fingers and affects both the dorsal and palmar surfaces. (b) A typical low ulnar nerve lesion: note the scar at the wrist.

thesia. Clinically, the patient has footdrop and anaesthesia on the dorsum of the foot. Most pressure-induced injuries are neuropraxias and as long as the paralysed part is managed carefully (by skin care, massage, passive joint movement and the use of spring-loaded ‘lively’ splints), a good outcome can be expected.

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Soft tissue trauma at a glance Definitions RICE: a mnemonic for Rest, Ice, Compression and Elevation, the mainstays of management of soft-tissue injuries Neurotmesis: complete anatomical division of a nerve with Wallerian degeneration Axonotmesis: a nerve injury that results in division of the axons but the connective tissues survive

Neuropraxia: a minimal nerve lesion producing paralysis without Wallerian degeneration Causalgia: a pain syndrome characterized by severe burning pain with autonomic and trophic (denotes nourishment, nutrition) changes that may accompany a partial mixed-nerve injury. It is often helped by sympathectomy

Soft tissue injuries Tissue

Type of injury

Treatment

Skin and fat

Ecchymosis (bruising) Fat necrosis Haematoma

RICE RICE RICE, aspirate if haematoma liquefies

Muscle

Tearing with healing by fibrosis

RICE with early movement ± ultrasound

Ligaments

Sprain (incomplete injury) Rupture (complete injury

RICE + exercise when pain allows Splintage, RICE, occasionally surgery, e.g. anterior cruciate ligament

Tendons

Penetrating trauma (hand, wrist) Rupture (degenerative change)

Surgical repair + physiotherapy

Nerves

Stretching, crushing or cutting

Neurotmesis: surgical repair Axonotmesis and neuropraxia: surgical repair not necessary. Maintain function while nerve recovers at rate of 1 mm/day. Recovery is usually excellent

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Burns

Introduction, 254 Epidemiology, 254 Pathophysiology, 254

Mechanisms of injury, 255 Initial management of major burns, 256

Must know Must do

Must know Pathophysiology of burns, including systemic response in major burns How to assess severity and depth of burns Indications for referral of patients to a major burns centre/department Principles of general and local management of burns Principles of intravenous fluid requirements in the severely burnt patient Principles of rehabilitation of burn victims Must do See patients with minor burns See at least one patient with a major burn, including any operative management, recovery and any subsequent plastic surgery Observe skin grafting for burns

Subsequent management of burn injury, 264 Rehabilitation, 266

scalding injuries. The elderly are at risk from scalds, contact and flame burns. Teenagers are often injured as a result of illicit activities involving accelerants or electrocution. The most common burns in adults are suffered by males aged between 17 and 30 years of age. These are mainly due to flame burns but also occur as a result of industrial accidents. Burn victims are often compromised by some other factor, such as alcoholism, epilepsy or psychiatric illness. All these problems need to be addressed when managing the patient.

Pathophysiology Burn injuries result in a local and systemic response.

Local response

Burn trauma represents one the most devastating conditions encountered in surgery. The correct treatment of these injuries is vital to ensure a favourable outcome and encompasses accurate assessment, careful resuscitation and precise surgical management. Much of the treatment of burns is controversial and the subject of debate. The aim of this chapter is to provide a framework for one method of managing a patient with major burns and to provide an overview of the complexities of dealing with these cases.

The three zones of a burn were described by Jackson in 1947 (Fig. 23.1). At the point of maximum damage there is a zone of coagulation. In this zone there is irreversible tissue loss due to coagulation of the constituent proteins. This is surrounded by a zone of stasis, characterized by decreased tissue perfusion. The tissue in this zone is potentially salvageable. The main aim of burns resuscitation is to increase tissue perfusion here and prevent any damage becoming irreversible. Additional insults, such as prolonged hypotension, infection or oedema, can convert this zone into an area of complete tissue loss. Finally, there is a zone of hyperaemia, where tissue perfusion is increased; this zone will invariably recover. In a burn wound, these zones are three-dimensional; loss of tissue in the zone of stasis will lead to the burn deepening.

Epidemiology

Systemic response

Every year in the UK there are 13,000 hospital admissions for burns and around 300 burn-related deaths. Burns tend to affect specific groups of the population, particularly the vulnerable: the young, the old and the debilitated. Children between the ages of 1 and 5 are at high risk from

The release of cytokines and other inflammatory mediators at the site of injury has a systemic effect once the burn reaches 30%. This systemic inflammatory response results in cardiovascular, respiratory, metabolic and immunological changes.

Introduction

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Zone of hyperaemia Zone of stasis Zone of coagulation

Epidermis

Dermis

Subcutaneous tissue Superficial

Mid-dermal

Figure 23.1 Jackson’s burn zones.

•

caused by hot bathing water. Scalds tend to cause superficial to superficial dermal burns (see later for burn depth assessment).

• •

Flame

Cardiovascular changes Increase in capillary permeability, leading to loss of proteins and fluids from the intravascular into the interstitial compartment. Peripheral and splanchnic vasoconstriction. Decreased myocardial contractility, possibly due to tumour necrosis factor α. These changes, coupled with fluid loss from the burn wound, result in systemic hypotension and end-organ hypoperfusion. Respiratory changes Bronchoconstriction secondary to inflammatory mediators. In severe burns, adult respiratory distress syndrome (ARDS) can occur.

• •

Metabolic changes Up to threefold increase in the basal metabolic rate. Splanchnic hypoperfusion. These two factors necessitate early and aggressive enteral feeding to decrease catabolism and maintain gut integrity.

• •

Immunological: non-specific downregulation of the immune response, affecting both cell-mediated and humoral pathways.

Mechanisms of injury Thermal injuries Scalds Of burns in children, 70% are caused by scalds. This type of burn also occurs frequently in the elderly. The common mechanisms are spillage of hot drinks/liquids or injuries

Flame burns comprise 50% of adult burns. They are often associated with inhalational injury and other concomitant trauma. Flame burns tend to be deep dermal or full thickness.

Contact In order to produce a burn by direct contact, the object touched must either have been very hot or the contact abnormally long. The latter is the more usual reason and these types of burns are commonly seen in epileptics, alcoholics and drug abusers. They are also seen in the elderly due to loss of consciousness; such a presentation requires a full investigation as to cause of the blackout. Contact burns tend to be deep dermal or full thickness.

Electrical injuries Of all admissions to burn units, 3–4% are due to electrocution injuries. An electric current will travel through the body from one point to another, creating ‘entry’ and ‘exit’ points. The tissue between these two areas can be damaged by the current. The amount of heat generated and hence the amount of tissue damaged in an electrical injury is equal to 0.24V 2 × R (where V is voltage and R is resistance). The voltage is therefore the main determinant of the degree of tissue damage, and it is logical to divide electrocution injuries into those caused by low-voltage domestic current and those caused by high-voltage currents. High-voltage injuries can be further divided into

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‘true’ high-tension injuries caused by high-voltage current passing through the body and ‘flash’ injuries caused by tangential exposure to a high-voltage current arc, where no current actually flows through the body. Domestic electricity: low voltages tend to cause small, deep contact burns at the exit and entry sites. The alternating nature of domestic current can interfere with the cardiac cycle, giving rise to arrhythmias. ‘True’ high-tension injuries (when voltage is 1000 V or greater). There is extensive tissue damage and often limb loss. There is usually a large amount of soft and bony tissue necrosis. Muscle damage gives rise to rhabdomyolysis and there is a significant incidence of renal failure with these injuries. This injury pattern needs more aggressive resuscitation and débridement than other burns. Contact with voltage greater than 70,000 V is invariably fatal. ‘Flash’ injury: in this scenario, there has been an arc of current from a high-tension voltage source. The heat from this arc can cause superficial flash burns to exposed body parts, typically the face and hands. However, clothing can also be set alight, giving rise to deeper burns. No current actually passes through the patient’s body. A particular concern after an electrical injury is the need for cardiac monitoring. There is good evidence that if the admission electrocardiogram (ECG) is normal and there is no history of loss of consciousness, then cardiac monitoring is not required. If there are ECG abnormalities or a loss of consciousness, then 24-h monitoring is advised.

• •

•

Chemical injuries Chemical injuries are usually the result of industrial accidents but may occur with household chemical products. These burns tend to be deep because the corrosive agent continues to cause coagulative necrosis until completely removed. Alkalis tend to penetrate deeper and cause worse burns than acids. Cement is a common cause of alkali burns (Fig. 23.2).

Certain industrial agents require specific treatments in addition to standard first aid. Hydrofluoric acid, widely used for glass etching and in the manufacture of circuit boards, is one of the more common culprits. It causes a continuing penetrating injury that is neutralized by calcium gluconate applied in a gel and/or injected into the affected tissues. The initial management of all chemical burns is the same irrespective of the agent. All contaminated clothing must be removed and the area thoroughly irrigated. This is often best achieved by showering the patient, which has been shown to limit the depth of the burn. Litmus paper can be used to confirm removal of alkali or acid. Eye injuries should be irrigated copiously and referred to an ophthalmologist.

Initial management of major burns The general approach to a major burn can be extrapolated to managing any burn. An accurate history and examination of the patient and the burn is vital. A systematic approach will ensure that key information is not missed.

History The history in a burn injury can give valuable information about the nature and extent of the burn. The likelihood of inhalational injury, depth of the burn and suspicion of other injuries can all be ascertained from a comprehensive history. The exact mechanism of injury and any prehospital treatment must be established. The key points are as follows. Exact time and mechanism of the injury: (a) Type of burn, i.e scald, flame, electrical, chemical. (b) How was the person put out? How long were they alight for? (c) What first aid was carried out? If cooling was performed, what with and for how long? Likelihood of concomitant injuries (i.e. fall from height, road traffic accident, explosion). Likelihood of inhalational injury: did the burn occur in an enclosed space? Scalding injuries: (a) What was the liquid? (b) If tea/coffee, was there milk in it? (c) Was there a solute in the liquid? This will raise the boiling temperature and result in a worse injury. Boiling rice is a common cause in the UK. Electrocution injuries: (a) What voltage? (b) Was there a flash/arcing? (c) Contact time. Chemical injuries: what chemical? Any suspicion of non-accidental injury?

• • • • •

Figure 23.2 Cement chemical burn.

• •

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Burns at a glance Definitions Burn: the response of the skin and subcutaneous tissues to thermal injury Partial-thickness burn: a burn that does not extend through all skin layers. Needle prick elicits bleeding and pain sensation Full-thickness burn: extends through all skin layers into the subcutaneous tissues. It destroys all sources of skin epithelial regrowth. No bleeding or pain on needle prick Deep dermal burn: extends through the epidermis and into, but not through, the deeper layers of the dermis. Needle prick elicits delayed bleeding and sensation of being touched but no pain Escharotomy: an emergency surgical procedure where the burnt tissue (eschar) of a circumferential full-thickness or deep dermal burn on a limb or on the chest is divided Epidemiology 13,000 burns and 300 burn deaths per annum in UK Children 1–5 years old: scalds Teenagers: flame, electrocution Adults (frequently males aged 17–30 years): flame burns, industrial accidents (flame, chemical, electrocution) Elderly: scalds, contact and flame burns

• • • • •

Pathophysiology Local response Zone of coagulation: coagulation necrosis, irreversible tissue loss

•

It is very important that the history be obtained at the point of admission. This may be the only time that a firsthand history is available because airway swelling may develop in the hours following injury and require intubation. A brief medical history should be taken (following the ‘AMPLE’ guidelines for ATLS).

Primary survey The initial management of a severely burnt patient is similar to that of any trauma patient. A modified ATLS primary survey is performed, with particular emphasis being placed on assessment of the airway and breathing. It is important that the burn injury does not distract from this sequential assessment, otherwise serious associated injuries may be missed.

• •

Zone of stasis: decreased tissue perfusion, potentially salvageable Zone of hyperaemia: increased tissue perfusion, invariably recovers Systemic response Mediated by cytokines and inflammatory mediators, present in burns of > 30% Cardiovascular: increased capillary permeability, vasoconstriction, decreased myocardial contractility Respiratory: bronchoconstriction, ARDS Metabolic: threefold increase in basal metabolic rate, splanchnic hypoperfusion Immunological: downregulation of both cell-mediated and humoral immune response

• • • •

Mechanism of injury Thermal injury: (a) Scalds: superficial, superficial dermal (b) Flame: deep dermal or full thickness, inhalation injury (c) Contact: deep dermal or full thickness Electrical injury: heat generated = 0.24V 2 × R, thus voltage main determinant of degree of injury (a) Low voltage (< 1000 V): deep contact burns at entry and exit sites (b) True high voltage (> 1000 V): current goes through body. Extensive soft tissue and bone necrosis (c) Flash high voltage (> 1000 V): current does not pass through body. ‘Flash’ burn from heat generated by current arc from high-tension source. Exposed parts of body affected (face, hands) Chemical burns: deep necrotic burns

• •

•

A: airway with cervical spine control An assessment must be made as to whether the airway is compromised or is at risk of compromise. The cervical spine should be protected unless it is definitely not injured. Inhalation of hot gases will result in a burn above the vocal cords; this burn will become oedematous over the course of hours, especially after fluid resuscitation has begun. Consequently, an airway that is patent on arrival may occlude after admission. Direct inspection of the oropharynx should be performed by a senior anaesthetist. If there is any concern about the patency of the airway, then intubation is the safest policy. However, unnecessary intubation and sedation could potentially worsen the patient’s condition, so the decision to intubate should be made carefully (Fig. 23.3 & Table 23.1).

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Table 23.2 Symptoms associated with different blood levels of carboxyhaemoglobin. Symptom 0 –10% 10 –20% 20 –30% 30 –40% 40 –50% > 50%

Minimal symptoms (normal level in heavy smokers) Nausea, headache Drowsiness, lethargy Confusion, agitation Coma, respiratory depression Death

Figure 23.3 Patient at high risk of inhalational injury. Table 23.1 Signs of inhalational injury and indications for intubation.

Signs of inhalational injury History of flame burns/burns in an enclosed space Full-thickness/deep dermal burns to the face, neck or upper torso Singed nasal hair Carbonaceous sputum/carbon particles in the oropharynx Indications for intubation Erythema/swelling of the oropharynx on direct visualization Change in voice, with hoarseness/harsh cough Stridor Dyspnoea

B: breathing All burn patients should receive 100% oxygen through a non-rebreathing mask on presentation. Breathing problems are considered as those that affect the respiratory system below the vocal cords. There are several mechanisms that can compromise respiration: mechanical restriction of ventilation; blast injury; smoke inhalation; carbon monoxide poisoning.

• • • •

Mechanical restriction of breathing Deep dermal or full-thickness circumferential burns of the chest can limit chest excursion and prevent aedequate ventilation. This requires immediate escaharotomy (see later). Blast injury If there has been a history of an explosion, blast lung can complicate ventilation. Penetrating injuries can cause

tension pneumothoraces and the blast itself can cause lung contusions and alveolar trauma and lead to ARDS. Smoke inhalation The products of combustion, though cooled by the time they reach the lungs, act as direct irritants to the lungs. This leads to bronchospasm, inflammation and bronchorrhoea. There is impaired function of type II pneumocytes and impaired ciliary action, both of which exacerbate the situation. The inflammatory exudate created is not cleared and atelectasis/pneumonia follows. The situation can be particularly severe in asthmatics. Noninvasive management can be attempted, with nebulizers and non-invasive positive-pressure ventilation with some positive end-expiratory pressure (PEEP). However, these patients may need a period of ventilation as this allows aedquate oxygenation and permits regular toiletting of the lungs. carboxyhaemoglobin Carbon monoxide binds haemoglobin with 40 times the affinity of oxygen. It also binds to other intracellular proteins, particularly the cytochrome oxygenase pathway. These two events lead to intracellular and extracellular hypoxia. The pulse oximeter will read spuriously high because it cannot differentiate between oxyhaemoglobin and carboxyhaemoglobin. However blood gases will reveal hypoxia, metabolic acidosis and raised carboxyhaemoglobin. The signs of carboxyhaemoglobinaemia are listed in Table 23.2. Treatment is with 100% oxygen as this displaces carbon monoxide from bound proteins six times faster than atmospheric oxygen. Patients with carboxyhaemoglobin levels greater than 25–30% should be ventilated. Hyperbaric therapy is rarely practical and has not been proven to be advantageous. It takes longer to shift the carbon monoxide from the cytochrome oxygenase pathway, so 100% oxygen should be continued until the metabolic acidosis has cleared.

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Figure 23.4 Escharotomies in upper limb.

C: circulation

Escharotomy

Intravenous access should be established with large-bore cannulae placed preferably through unburnt tissue. The peripheral circulation must be checked. Any deep or full-thickness circumferential extremity burns can act as a tourniquet, especially once oedema secondary to fluid resuscitation has begun. If there is any suspicion of decreased perfusion due to circumferential burns, the tissue must be released with escharotomies (see later). Profound hypovolaemia is not the normal initial response in a burn. If a patient is hypotensive, it is due to a delayed presentation, cardiogenic dysfunction or an occult source of blood loss (chest, abdomen, pelvis).

Any circumferential deep dermal or full-thickness burn on an extremity will not stretch as the underlying tissue swells due to burn wound oedema. This raises tissue pressure and can impair peripheral circulation but may only occur as fluid resuscitation causes oedema to develop. In addition, circumferential chest burns can limit chest excursion and impair ventilation. Both these situations require division of the burn eschar, a procedure known as escharotomy. Only the burnt tissue is divided, not any underlying fascia (differentiating this from a fasciotomy). Escharotomy is an emergency procedure that is performed at the bedside or in the trauma room. For extremities, incisions are made along the mid-lateral and/or medial aspects of the limbs, avoiding any underlying structures (Figs 23.4–23.6). For the chest, longitudinal incisions are made down each midclavicular line to the subcostal region. The lines are joined by a chevron incision running parallel to the subcostal margin. This creates a mobile breast-plate that moves with ventilation. Escharotomies are best performed with a cutting diathermy as they tend to bleed. They are then packed with Kaltostat and dressed with the burn.

D: neurological disability The patient’s score on the Glasgow Coma Scale should be assessed. Patients may be confused due to hypoxia or hypovolaemia.

E: exposure with environment control The whole patient should be examined (including the back) to obtain an accurate estimate of the burn area. It is very easy for the burn patient, especially children, to become hypothermic. This leads to hypoperfusion and deepening of the burn wound. The patient should be covered and warmed as soon as possible.

F: fluids The resuscitation regimen should be determined and begun. A urinary catheter should be placed.

Analgesia Superficial burns can be very painful and therefore intravenous morphine should be used as this can be easily titrated against pain and respiratory depression.

Figure 23.5 Escharotomies in lower limb.

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Front 18% Back 18%

9% 1%

Figure 23.6 Escharotomies in hand. 18% 18%

Investigations

The number of investigations will vary with the type of burn but most patients require: full blood count, haematocrit, urea and electrolytes; group and save/cross-match; microbiology swabs of burn wounds. Electrical injuries also require: 12-lead ECG; cardiac enzymes (high-tension injury). Inhalational injuries require: chest X-ray; arterial blood gases (can be useful in any burn because base excess is predictive of amount of resuscitation required). Any concomitant trauma requires its own investigations.

(Fig. 23.8) and can therefore give an accurate assessment of burns area in children. It is important that all of the burn is exposed and assessed. Pigmented skin can be difficult to assess and it may be necessary to remove all the loose epidermal layers in pigmented skin to get an idea of burn size.

Assessment of burn area

Assessment of burn depth

The assessment of burn area tends to be done badly, even by those who are expert at it. There are three commonly employed methods of estimating burn area and each has a role in different scenarios. When calculating the burn wound area, erythema should not be included. Erythema may take a few hours to fade so it is inevitable that some overestimation will occur if the burn is estimated acutely. Palmar surface: the surface area of the patient’s palm (i.e. not the fingers) is 0.8% (male) and 0.6% (female) of the total body surface area of the patient. Palmar surface area can be used to estimate relatively small burns (< 15%) or very large burns (> 85%, when unburnt skin is counted). For larger burns, it is inaccurate. Wallace rule of nines: this is a good quick way of estimating the area of medium to large burns in adults. The body is divided up into areas of 9% (Fig. 23.7) and the total burn area calculated. It is not accurate in children. Lund and Browder chart: if used correctly, this is the most accurate method. It is also the only chart that compensates for the variation in body shape with age

Burns are best classified into two groups by the amount of skin loss. Partial thickness: the burn does not extend through all skin layers. Full thickness: the burn extends through all skin layers into the subcutaneous tissues (Fig. 23.9). Partial-thickness burns can be further divided into superficial, superficial dermal and deep dermal. Superficial: the burn extends into the epidermis but not into the dermis (Fig. 23.10). Superficial dermal: the burn extends through the epidermis into the superficial layers of the dermis (Fig. 23.11). Deep dermal: the burn extends through the epidermis into the deeper layers of the dermis but not through the entire dermis (Fig. 23.12). In reality, most burns will be a mixture of different depths. The assessment of depth is important for planning because the more superficial burns will tend to heal spontaneously but deeper burns will need surgical intervention.

• • • • • • •

• • •

Figure 23.7 Wallace rule of nines.

• • • • •

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Lund and Browder charts A

Ignore simple erythema Superficial

11/2

Deep Region Head Neck Ant. trunk Post. trunk Right arm Left arm Buttocks Genitalia Right leg Left leg Total burn

11/2 21/2 21/2

11/2

11/2 B

13/4 13/4

Relative percentage of body surface area affected by growth Area A = 1/2 of Head B = 1/2 of one Thigh C = 1/2 of one Leg

Age 0 91/2 23/4 21/2

1 81/2 31/4 21/2

5 61/2 4 23/4

10 51/2 41/2 3

15 41/2 41/2 31/4

Figure 23.8 Lund and Browder chart.

Figure 23.10 Superficial burn: scald.

Figure 23.9 Full-thickness burn: flame.

Burn depth estimation is not necessary for estimating resuscitation formulae. The assessment of burn depth is very difficult. The history will give clues about the expected depth: a flash burn will probably be superficial and a flame burn that

Figure 23.11 Superficial dermal burn: scald.

Adult 31/2 43/4 31/2

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ideal dressing as it will cover the wound but not alter the physical appearance of the burn. This allows accurate evaluation by the burn team later on. Flamazine should not be used on a burn that is to be referred as it makes assessment of depth by appearance difficult. Other burns are dressed according to depth (see later).

Prognosis A rough estimate of prognosis can be given by adding the age of the patient to the percentage burn; this gives the percentage mortality. Inhalational injury increases mortality but it is arguable by how much. A decision should be made about whether resuscitation should be started or whether the patient should just be kept comfortable. Figure 23.12 Deep dermal burn: flame.

was not rapidly extinguished will probably be deep. There are three elements that should be assessed: bleeding, sensation and appearance. Bleeding. Test bleeding with a 21-gauge needle: brisk bleeding on a superficial prick means superficial/ superficial dermal; delayed bleeding on a deeper prick means deep dermal; no bleeding means full thickness.

• • •

Sensation. Test sensation with a needle (as for bleeding): pain means a superficial/superficial dermal burn; pin can be felt but is not painful means deep dermal; no sensation means full thickness.

• • •

Appearance. Though obvious, it can be hard to judge burn depth by appearance as the burn is often covered in soot or dirt. A red glistening wound that obviously blanches is superficial. A paler, drier, but blanching wound is partial thickness. A dry, leathery, hard wound is full thickness.

• • •

It must be remembered that a burn is a dynamic wound and depth will change depending on the success of resuscitation. Initial estimates need to be reviewed later. Once the burn’s surface area and depth have been estimated, the wound should be washed and any loose skin removed. Any blisters should be deroofed for ease of dressing. The burn should then be dressed. For an acute burn that is to be referred to a burn centre, clingfilm is an

Resuscitation regimens There is no ideal resuscitation regimen for burns and this is reflected by the continual change in the regimens in favour. It is vital to remember that all the fluid formulae are only guidelines. Their success relies on the adjustment of resuscitation against monitored physiological and investigative parameters. The main aim of these resuscitation formulae is to maintain tissue perfusion to the zone of stasis and prevent the burn deepening. This is not as easy as it sounds. Too little fluid will cause hypoperfusion; too much fluid will lead to oedema that will cause tissue hypoxia. There are some important overall concepts about fluid resuscitation in burn patients. The greatest amount of fluid loss occurs in the first 24 h. For the first 8–12 h, there is a general shift of fluid from the intravascular to interstitial fluid compartment. This was thought mainly due to increased capillary permeability but other factors have also been shown to play a role. This means that any fluid given in this period will rapidly leave the intravascular compartment. Therefore colloids have no advantage over crystalloids in maintaining circulatory volume. Indeed, colloids could exacerbate the situation because they will leak out into the interstitial space, where they will increase the oncotic pressure and increase the flow of fluid from the circulation. Rapid fluid boluses are also of no benefit as a rapid rise in intravascular hydrostatic pressure only drives more fluid out of the circulation. However, much protein is lost through the burn wound so there is a need to replace this oncotic loss. Therefore some regimens use some colloid after 8 h, when the loss of fluid from the intravascular space is decreasing. Burns greater than 15% in adults and 10% in children warrant formal resuscitation. Again, these are guidelines

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and some discretion can be used by experienced staff. The most commonly used formula at present is actually a pure crystalloid resuscitation formula, the Parkland formula, devised by Charlie Baxter. It has the advantages that it is easy to calculate and that the titration is against urine output. The fluid for the first 24 h is calculated as follows: 4 mL × percentage total burn surface area × weight in kg = total fluid requirement in 24 h. Half of the fluid is given in the first 8 h and half in the next 16 h. In children, maintenance fluid is required in addition, calculated by weight as: 4 mL/kg for 0 –10 kg + 2 mL/kg for 10 –20 kg + 1 mL/kg over 20 kg = rate in mL/h. The start point for the timing is the time of injury not the time of admission. Any fluid already given should be deducted from the amount of fluid required. The formula ends at 24 h. For the next 24 h, colloid is begun at a rate of 0.5 mL × percentage total burn surface area × weight (kg) and maintenance crystalloid is continued at a rate of 1.5 mL × total burn surface area × weight (kg). For example, a 25-year-old-man weighing 70 kg with a 30% flame burn is admitted at 16.00. His burn occurred at 15.00. He would need: 4 mL × 30% total burn surface area × 70 kg = 8400 mL in 24 h (4200 mL in first 8 h, 4200 mL over the next 16 h). If he has already received 1000 mL from the emergency services, he needs a further 3200 mL in the first 8 h post burn, i.e. by 23.00. If it is now 16.00, he needs 3200 mL over the next 7 h, then 4200 mL over the next 16 h. Therefore, until 23.00 he needs 3200/7 = 457 mL/ h. After 23.00 for the next 16 h he needs 4200/16 = 262.5 mL/ h. The maintenance fluid required for children is calculated as shown above. For example, a 24-kg child admitted with a resuscitation burn will need the following maintenance fluid: 4 mL/kg for first 10 kg (40 mL/h) + 2 mL/kg for next 10 kg (20 mL/h) + 1 mL/kg for next 4 kg (4 mL/h) = 64 mL/h. The maintenance fluid given is usually dextrose-saline. The end-point to aim for is a urine output of 0.5– 1 mL/kg per h in adults and 1–1.5 mL/kg per h in children. High-tension electrical injuries will need significantly more fluid (up to 9 mL/kg per percentage burn surface area in the first 24 h) and a higher urine output (1.5– 2 mL/kg per h). Inhalational injuries will also need more fluid. The most commonly used crystalloid is sodium lactate solution (known as Hartmann’s solution in the UK and

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Ringer-lactate in the USA). It comprises sodium chloride 0.6%, sodium lactate 0.25%, potassium chloride 0.04% and calcium chloride 0.027%. The colloid used is controversial. The Cochrane Report advised against the use of albumin but the review did not include many burn units and so may not be representative. Fresh frozen plasma is often used in children and albumin or a synthetic starch in adults. It should be emphasized that the above regimen is a guideline only and that resuscitation should not be guided purely by urine output. Other physiological parameters (pulse, blood pressure, respiratory rate) and investigations (haematocrit, plasma sodium, base excess) are useful for giving an indication of the resuscitation status of the patient. The regimens should not be followed slavishly but adjusted according to response. Fluid rate should be changed gradually, between 20 and 30%. Burn units will vary as to which resuscitation formula is used. It is best to contact the local burn unit and enquire how it wishes the patient to be resuscitated.

Referral to a burn unit The National Burn Care Review has set guidelines about which patients warrant referral to a burn unit. Burns are divided into complex burns (i.e. those that require specialist intervention) and non-complex burns (i.e. those that do not require immediate admission to a specialist unit). Complex burns should be referred automatically. A burn injury is more likely to be complex if associated with the following. Age: under 5 or over 60 years. Site: face, hands, perineum or feet (dermal/fullthickness loss) or any flexure (particularly the neck or axilla) or any circumferential dermal or full-thickness burn of the limbs, torso or neck. Inhalation injury: any significant injury, excluding pure carbon monoxide poisoning. Mechanism of injury: (a) chemical injury (> 5% total body surface area); (b) exposure to ionizing radiation; (c) high-pressure steam injury; (d) high-tension electrical injury; (e) hydrofluoric acid injury (> 1% total body surface area); (f) suspicion of non-accidental injury. Size (dermal/full-thickness loss): (a) paediatric (< 16 years old): > 5% total body surface area; (b) adult (16 years or over): > 10% total body surface area.

• • • •

•

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Coexisting conditions: any serious medical conditions (cardiac dysfunction, immunosuppression, pregnancy) or any associated injuries (fractures, head injuries, crush injuries). It is better to discuss all cases with the local burn unit as they will eventually be involved in the patient’s care.

•

Silver sulfadiazine (Flamazine) has good Gram-negative cover and keeps the wound moist and clean. It can be used on its own or with a gauze layer on top. Unfortunately it tends to macerate the wound and can make burn depth assessment difficult. It also requires frequent dressing changes, which can be uncomfortable for the patient.

Subsequent management of burn injury

Deep dermal/full thickness

Superficial/superficial dermal burns These heal spontaneously within 14 days unless there is secondary infection or the burn deepens. The aim is to provide a dressing that will keep the wound clean, create a suitable environment for healing and minimize pain. Various dressings are used.

Tulle gras (Jelonet, Bactigras)

The traditional method is to use tulle gras (Jelonet), either plain or containing an antiseptic solution such as chlorhexidine (Bactigras). This is adherent and can be difficult to remove once dried but provides a moist environment for healing. Gauze is placed over these wounds because they tend to exude fluid. The gauze may be changed as it soaks through but the tulle gras is usually left undisturbed for 5 days, unless there is concern about secondary infection.

Retention dressing (Hypafix) A novel way of dressing burns is to use an adhesive dressing such as Hypafix. This sticks to the wound and prevents any shear forces from disrupting healing. The dressing can be kept clean by showering. Gauze will also be required to absorb the initial exudate. The adhesive in the dressing is oil-based so the application of any kind of oil (typically olive oil) dissolves the adhesive and permits removal of the dressing without disturbing the healing burn.

Interface dressings (Biobrane, Transcyte) These bind to the raw epidermis and provide a semipermeable membrane that keeps the wound moist but prevents bacterial colonization. Transcyte has added growth factors that can accelerate wound healing. These dressings are only effective on superficial/superficial dermal burns and are expensive.

Topical antibacterial cream (Flamazine) Topical bacterial creams are a popular way of dressing.

Deep dermal and full-thickness burns will need surgical intervention. There has been a major change in the way burns are managed in the last 30 years. Initially, there was a reluctance to remove the burn wound early, as this caused additional trauma to the patient and ran the risk of removing tissue that might have healed if left undisturbed. Therefore deep burns were left until 3 weeks when all unhealed areas were excised and skin grafted. However, it was subsequently shown that early removal of the burn wound limited the systemic inflammatory response and improved outcome. In addition, tangential excision allowed burnt tissue to be shaved off in layers, leaving healthy tissue behind. The modern approach to major burns is to remove the burn wound as soon as possible before the patient becomes unwell (< 48 h), resurface the burn and start rehabilitation. This allows faster healing, limits the stress from the burn wound and is associated with improved mortality. The only innovation to this approach is the use of topical agents that bind to damaged proteins in the wound and inhibit the inflammatory response that the burn causes, e.g. cerium nitrate/silver sulfadiazine cream (Flammcerium). It is useful for large burns because it allows staged excision or for burns in the elderly who may need optimizing prior to surgery.

Surgery Tangential excision involves shaving the burnt tissue off the healthy unburnt tissue below. This can be performed with a skin graft knife, Goulian hand-held blade for small areas or a mechanical dermatome. This approach is a team effort and requires skilled anaesthesia, as the patients cools down rapidly and blood loss can be large and dramatic. Infiltration of the burn and any skin donor sites with 1 in 1,000,000 adrenaline is effective at reducing blood loss, as is the use of tourniquets when excising burns on extremities. If the burn affects all the subcutaneous tissues, excision at the fascial layer can be performed (fascial excision). This leads to less blood loss but results in a poor cosmetic result with marked contour defects. Depending on the skill of the team and the stability of the patient, burns of up to 50% can be excised in one session.

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Skin allografts Cadaveric skin can be used as a temporary biological dressing. The storage solution decreases the antigenicity of the skin and the burn patient is relatively immunosuppressed, so the graft is not rejected for a few weeks. This may allow autograft donor sites time to heal for regrafting.

Figure 23.13 Meshed skin graft.

Skin xenografts Porcine skin can also be used as a temporary biological dressing. Synthetic skin There is much research being directed at creating artificial skin. Integra is the most commonly used variety and consists of an artificial neodermis and a silicone top layer. Once placed on the burn wound, the neodermis is vascularized over the course of a few weeks. The silicone layer is removed and a thin skin autograft placed on top. The use of Integra has allowed the rapid débridement and resurfacing of very large burns. Unfortunately it is prone to infection and can lead to hypertrophic scarring. Its overall usefulness in major burns is still being evaluated.

Figure 23.14 Healing meshed skin graft.

Resurfacing Excising the burn wound is only part of the battle. The main challenge is to resurface the excised wound. There are various approaches to this. Skin autografts If the burn wound is less than 50% of total body surface area, then it can be covered with the patient’s own skin (autograft). Split skin grafts are taken from unburnt areas and are usually meshed (i.e. have slit perforations placed in them) (Figs 23.13 & 23.14). This helps any exudate beneath the graft to ooze out and also allows the graft to be stretched to cover a larger area. The standard mesh ratio is 1 : 1.5. Wider meshing can cover a larger area but leaves bigger interstices to fill in. Meshed skin grafts heal with the mesh pattern visible so tend not to be used on the face. The grafts are secured with staples or tissue adhesive and then dressed. It is important to prevent shearing forces from disrupting the grafts so joints may be temporarily splinted. In very large burns there may not be enough unburnt skin to provide autograft to cover the burn wound. Various alternatives to autografts are available.

Cultured skin An alternative approach is to grow the patient’s own skin in culture. A small skin biopsy is taken on the day of admission and within 2–3 weeks sheets or suspensions of keratinocytes are available. Unfortunately, these keratinocytes are very delicate and are vulnerable to infection and shearing forces. The delay in culture is also a major drawback but this may be resolved in the future. However, cultured keratinocytes can be useful when used in conjunction with autografts, for filling in the interstices in a widely meshed skin graft.

Nutritional support The systemic response to a burn injury leads to a threefold increase in the basal metabolic rate. It is not possible for the patient to maintain an adequate calorie and protein intake by eating and hyperalimentation is required. Adequate nutrition is essential for ensuring wound healing and preventing gastrointestinal complications. Resuscitation burns should have a nasogastric or nasojejunal tube placed and enteral feeding commenced. There are various formulae for estimating the caloric requirements. The Curreri formula is commonly used (daily requirement = 25 kcal/kg + 40 kcal/percentage burn). Trace elements must also be measured and replaced. For the above reasons, it is obvious that a dietician is an important member of the burn team.

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Microbiological support Burn wound sepsis is a major problem. Infection can deepen a burn wound as well as worsening the general condition of the patient. Prophylactic antibiotics are of no benefit and may worsen the situation by selecting resistant bacterial strains. The best policy is strict wound care and repeated and regular wound cultures. Evidence of invasive infection should be treated with short courses of highdose antibiotics to which the organism is sensitive. Topical agents can also be useful in decreasing the bacterial load. Organisms of particular concern include the βhaemolytic streptococci Lancefield group A, C and G. Skin grafts are particularly vulnerable to these organisms and grafting should not be performed on a wound colonized with them. Intravascular lines are associated with high infection rates in burn patients and so should be used sparingly.

Non-accidental injury

Of paediatric burns, 3–5% are due to non-accidental injury. As with other non-accidental injuries, the history and the pattern of injury may arouse suspicion. History Delayed presentation. No explanation given for the burn. Implausible explanation for the burn. Inconsistency between age of the burn and age given by the history.

• • • •

Injury pattern Obvious pattern from cigarettes, lighters, irons. No splash-marks in a scald injury: a child falling into a bath will splash; one that is placed into it may not. ‘Tide-line’ of scald: if the child is put into the fetal position, do the burns line up (i.e. what position was the child in when he/she was burned)? ‘Doughnut sign’: an area of spared skin surrounded by scald. If a child is forcibly held down in a bath of hot water, the part in contact with the bottom of the bath (e.g. the heels or buttocks) will not burn but the tissue around will.

• • • •

Any suspicion of non-accidental injury should lead to

immediate admission of the child to hospital, irrespective of how trivial the burn injury is, and the notification of social services. It should be remembered that the injury does not have to be deliberately caused for social services to intervene; inadequate supervision of children mandates their involvement.

Rehabilitation There is no starting point for rehabilitation because it blends into the acute management phase. Physiotherapy is important initially for treating pulmonary problems and later for mobilizing the patient and regaining strength. Occupational therapists carry out much of the scar management for the patient. There is significant psychological trauma in a burn injury and a clinical psychologist has an important role in helping the patient come to terms with what has happened. Managing a burn patient is truly a team task and requires close cooperation between the various disciplines. Only if all members of the team work together will the patient have a good outcome.

Scar management Hypertrophic scars are a major problem in children, pigmented skin and burns that take a long time to heal. There are several ways of preventing hypertrophy. Direct pressure on the scar can keep it flat. This can be achieved with adhesive tape, pressure garments or masks for facial burns. Silicone can also prevent hypertrophic scars and is applied as either a gel or a tape. Finally, direct steroid injections can cause a hypertrophic scar to involute, although these are painful and require general anaesthesia in children.

Secondary reconstruction Secondary surgery addresses functional and cosmetic issues. The most common secondary procedure preformed is contracture release. This can be due to either the scar contracting or, in the case of children, the patient growing. Local flaps with or without tissue expansion or full-thickness skin grafts are often used. Minor cosmetic adjustments can have major psychological benefits for a patient and should be performed.

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Assessment and management of burns at a glance History Exact time, cause and mechanism Concomitant injuries Inhalational injury Non-accidental injury

• • • •

Primary survey A: airway (above vocal cords) Evidence of inhalational injury Flame burns/enclosed space Burns to face, neck, upper torso Singed nasal hair Carbonaceous sputum

• • • •

Intubate if: Erythema/oedema in oropharynx Voice change with hoarseness/harsh cough Stridor Dyspnoea

• • • •

B: breathing (below vocal cords) Mechanical restriction: circumferential chest burns. Treatment: escharotomy Blast injury: lung contusion and alveolar trauma Smoke inhalation: bronchospasm, bronchorrhoea, inflammation, ciliary failure, atelectasis, pneumonia Carboxyhaemoglobin: CO binds haemoglobin and cytochrome oxygenase pathway proteins, extracellular and intracellular hypoxia, spurious readings on pulse oximetry, metabolic acidosis. Treatment: 100% O2

• • • •

C: circulation If profound hypovolaemia is present, look for cause other than burn Circumferential full-thicknes limb burns require escharotomy

• •

D: neurological disability Score on Glasgow Coma Scale may be abnormal due to hypoxia/hypovolaemia

•

E: exposure Examine whole patient including back Cover patient to keep warm

• •

F: fluids Determine and commence fluid regimen, place urinary catheter

•

Monitor pulse, blood pressure, temperature, urinary output, give adequate analgesia i.v., consider nasogastric tube Give i.v. fluids according to Muir–Barclay formula: (%burn × weight in kg)/2 = one aliquot of fluid Give six aliquots of fluid over first 36 h in 4, 4, 4, 6, 6, 12 h sequence from time of burn Crystalloid (Ringer’s lactate) and colloid (albumin or plasma) solutions are used

• • •

Pain relief Superficial burns are very painful so give i.v. morphine

•

Nutritional support Increased metabolic rate requires hyperalimentation with enteral feeding Daily caloric requirement is 25 kcal/kg + 40 kcal/ %burn

• •

Antibiotics Prophylactic antibiotics are not indicated Strict wound care and regular wound cultures required Invasive infection treated with short courses of high-dose antibiotic Give tetanus prophylaxis

• • • •

Investigations Full blood count and haematocrit Urea and electrolytes Group and save/cross-match Swabs from burn for microbiology If inhalation suspected: chest X-ray; arterial blood gases, CO estimation ECG/cardiac enzymes with electrical burns

• • • • • •

Burn assessment Generally poorly done Erythema is not included in calculation

• •

Methods for assessing area of burn Palmar surface: area of patient’s palm (no fingers!) = 0.8% (male) and 0.6% (female) of total body surface area. Useful for calculating small (< 15%) burns Wallace rule of nines: head 9%, torso front 18%, torso back 18%, right upper limb 9%, left upper limb 9%, right lower limb 18%, left lower limb 18%, perineum 1% Lund and Browder chart: widely available and very accurate

• • •

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Methods for assessing depth of burn Response to needle prick Burn depth

Bleeding

Sensation

Appearance

Superficial Deep dermal Full thickness

Brisk Delayed None

Pain Touch but no pain None

Red, glistening, blanches Pale, not moist, blanches Dry, leathery, hard

Referral to burn unit Age < 5 or > 60 years Site: face, hands, feet, perineum, flexure (neck/axilla/groin), circumferential Inhalational injury Mechanism: chemical (> 5% total body surface area), ionizing radiation, high-pressure steam, high-tension electrical, hydrofluoric acid (> 1% total body surface area), non-accidental injury Size: paediatric (age < 16 years), > 5% total body surface area; adult > 10% total body surface area Coexisting medical conditions or associated injuries

• • • •

• •

Management Superficial Heals spontaneously in 14 days Needs dressing (tulle gras, retention dressing, interface dressing, topical antibacterial cream) to keep wound clean

• •

Deep dermal/full thickness Excise burn wound as soon as possible after resuscitation (usually < 48 h after burn) Resurface wound with: (a) Skin autograft (patient’s own skin, possible if burn < 50% total body surface area) (b) Skin allograft (cadaver skin as temporary biological dressing) (c) Skin xenograft (porcine skin as temporary biological dressing) (d) Synthetic skin (artificial neodermis and silicone top layer) (e) Cultured skin (culture patient’s own skin)

• •

Rehabilitation Physiotherapy (pulmonary problems and mobilization) Occupational therapy (contractures) Clinical psychology (psychological trauma)

• • •

Complications Immediate Compartment syndrome from circumferential burns: limb burns leading to limb ischaemia, thoracic burns leading to hypoxia from restrictive respiratory failure Prevent by urgent escharotomy

• •

Early Hyperkalaemia (from cytolysis in large burns): treat with insulin and dextrose Acute renal failure (combination of hypovolaemia, sepsis, tissue toxins): prevent by aggressive early resuscitation, ensuring high GFR with fluid loading and diuretics, treat sepsis Infection (beware Streptococcus): treat established infection (106 organisms in wound biopsy) with systemic antibiotics Stress ulceration (Curling’s ulcer): prevent with antacid or histamine H2-blocker

• • • •

Late Contractures

•

Prognosis Age of patient + %burn = %mortality (e.g. 60 year old + 40% burn = 100% mortality) Mortality increased with inhalational burn

• •

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Disorders of the Abdominal Wall Introduction, 269 Swellings in the wall, 269

Common abdominal herniae, 269

Must know Must do Must know Surface anatomy of common external abdominal herniae Clinical symptoms and signs of common external abdominal herniae and their complications Complications of external abdominal herniae Principles of operative management of common external abdominal herniae Must do Examine patients with inguinal, femoral, paraumbilical and incisional herniae Observe elective repair operations for external abdominal herniae Follow the management of patient(s) admitted as emergency with obstructed/incarcerated external abdominal hernia

Introduction Disorders of the abdominal wall are commonplace in surgical practice. The majority of problems encountered are in the form of herniation, with inguinal herniae forming a significant bulk of outpatient referrals and theatre operating time.

Swellings in the wall Haematoma of rectus sheath A haematoma of the rectus sheath presents as a swelling in the anterior abdominal wall, usually below the umbilicus, and is associated with sudden abdominal wall strain such as sneezing or coughing. This causes a tear in a branch of the inferior epigastric artery and the rapid formation of a haematoma. Clinically, the patient experiences severe abdominal pain with nausea and vomiting accompanied by pyrexia and leukocytosis. The abdominal wall swelling is tender and takes several weeks to resolve. No interven-

Unusual herniae, 274

tion is needed if the diagnosis is certain. If not, the haematoma should be evacuated and the artery ligated.

Desmoid tumour These slow-growing non-metastasizing tumours arise from the rectus abdominis muscles and may attain a very large size. The histology of the tumour is variable and may resemble a low-grade fibrosarcoma. It is easily palpated and is rendered more prominent by contraction of the abdominal muscles. It may be associated with Gardner’s syndrome and may be related to childbirth injuries.

Common abdominal herniae A hernia is defined as the protrusion of a viscus or part of a viscus through an abnormal opening. Herniae may occur in the brain (e.g. after head injury), in muscle through its fascial covering, internally in the abdomen (internal hernia) or externally through a weak normal opening (inguinal and femoral herniae) or an abnormal opening (e.g. incisional hernia) in the abdominal wall. The common external abdominal herniae are presented here (Table 24.1; Figs 24.1 & 24.2).

Inguinal hernia Inguinal hernia is a common complaint, occurring mostly in men. It is twice as frequent as femoral hernia and in males more than 90% of herniae are inguinal. Inguinal herniae may occur at any age. In children they are generally associated with developmental disorders such as persistent processus vaginalis or testicular maldescent. Inguinal hernia is also common in young adult males and this is also related to a congenital defect such as a persistent processus, which may be precipitated from potential to actual existence by physical effort (Fig. 24.3).

Anatomy Inguinal canal The anterior wall of the inguinal canal is formed by the aponeurosis of the external oblique and in its lateral half 269

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Table 24.1 Common abdominal herniae and their management.

Site of defect

Treatment

Umbilicus Just above umbilicus Midline between umbilicus and xiphisternum

Observe Surgical repair (Mayo) Surgical repair

Inguinal Indirect

Deep inguinal ring

Direct Femoral

Posterior wall Femoral canal

Incisional

Previous abdominal wound

Infant: herniotomy only Adult: herniotomy/herniorrhaphy (Sholdice, Darn; occasionally truss) Herniorrhaphy Surgical repair (femoral, Lotheissen, McEvedy) Surgical repair (occasionally Marlex mesh)

Umbilical Paraumbilical Epigastric

Figure 24.2 Femoral (right), inguinal (left) paraumbilical and incisional herniae in one patient. Courtesy of Mr K. Mealy.

Figure 24.1 Diagram of common herniae: incisional, periumbilical, indirect inguinoscrotal (right), direct inguinal and femoral (left).

by the internal oblique and transversus abdominis muscles. The floor of the canal is formed by the inguinal ligament and the roof of the canal by the conjoint tendon, which consists of the fused inferior borders of internal oblique and transversalis abdominis. The posterior wall of the canal consists of the transversalis fascia, with a portion of the medial end formed by the insertion of the conjoint tendon (Fig. 24.4a). At its lateral end the transversalis fascia is penetrated at the deep inguinal ring by the spermatic cord, with the

Figure 24.3 Inguinal hernia.

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Clinical features

Internal oblique Aponeurosis of external oblique Transversus abdominis

Inguinal ligament Spermatic cord

(a)

Inguinal ligament

Femoral artery Femoral vein Femoral canal Lacunar ligament

An indirect inguinal hernia occurs when a sac develops by emerging through the deep inguinal ring and passing through the inguinal canal in the spermatic cord adjacent to the vas deferens and surrounded by the coverings of the cord. The sac, if sufficiently large, may emerge through the external inguinal ring or descend into the scrotum. It may contain omentum or small bowel and has the potential to become irreducible and strangulated. On examination an indirect inguinal hernia is detectable above and medial to the pubic tubercle. The latter may be detected by palpating laterally along the pubic ramus or by invaginating the scrotum in the male, when it can be felt underneath and just lateral to the spermatic cord. Unless incarcerated, an inguinal hernia has an impulse on coughing and, if reducible, can be controlled by pressure over the internal inguinal ring, which is situated at the mid-inguinal point 1 cm above the pulsation of the femoral artery. A direct inguinal hernia occurs as a result of a weakness in the transversalis fascia and is common in the elderly because of aetiological factors such as chronic cough, chronic strain during micturition due to prostatic hypertrophy, or chronic constipation. A direct hernia usually appears as a diffuse bulge that cannot be controlled by pressure over the internal ring. It is above and lateral to the pubic tubercle and does not enter the scrotum. A direct inguinal hernia has a wide neck, in contrast to the narrow neck of an indirect hernia. In consequence, a direct hernia is much less likely to strangulate.

Strangulation (b) Figure 24.4 Anatomy of (a) the inguinal and (b) the femoral canal.

inferior epigastric artery passing upwards and medial to it. Thus an indirect inguinal hernia as it emerges through the deep ring within the spermatic cord has the conjoint tendon laterally and above it, the inferior epigastric artery medially and the inguinal ligament inferiorly. Femoral canal The femoral canal is bounded anteriorly by the inguinal ligament, posteriorly by the fascia over the pectineus muscle, medially by the lacunar ligament and laterally by the femoral vein. The canal often contains a named lymph gland (of Cloquet; Fig. 24.4b).

Strangulation of an inguinal hernia develops when constriction occurs at the neck of the sac, cutting off the blood supply of the contents. Initially the venous blood supply is obstructed. This causes swelling of the contents (omentum or bowel) and eventually a combination of oedema and constriction interrupts the arterial blood supply and gangrene supervenes in the strangulated loop (Fig. 24.5). These changes are accompanied by severe local pain, with irreducibility of the hernia and tenderness. The symptoms of small-bowel obstruction are also evident, with colicky abdominal pain, nausea and vomiting. When the hernia first becomes obstructed it is possible to reduce it by manipulation. It is important, however, to ensure that the hernia is not reduced en masse into the abdominal cavity with the contents still strangulated by the constricting neck of the sac. An irreducible hernia per se does not indicate strangulation and may be incarcerated with an adequate blood supply but completely irreducible.

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(a)

Figure 24.5 Strangulated photograph).

inguinal

hernia

(operative

Management

Ideally, all inguinal herniae should be repaired by elective surgical operation. Surgery is usually performed under general anaesthesia but local or regional anaesthesia is also used. Surgical repair classically consists of two elements: excision of the hernial sac (herniotomy) and repair or buttressing of the weakness in the posterior inguinal canal (herniorrhaphy). In infants (always indirect herniae), the internal and external rings are superimposed and only a herniotomy is required for effective treatment. Laparoscopic repair of adult inguinal herniae is also performed by some surgeons. Complications of hernia repair include the following. Haematoma: may be in the wound or scrotum. Acute urinary retention: this frequently follows bilateral repair. Wound infection: this should be rare as hernia repair is a clean operation, but in practice infection occurs in 5–8%. Chronic pain: trapping of the ilioinguinal nerve. Testicular pain and swelling followed by atrophy usually means that the repair is too tight and the testicular artery is compromised. Testicular atrophy will occur when the swelling subsides. Recurrence of hernia occurs in about 5% of patients but the rate is higher when surgical technique is poor. Occasionally a truss may be used to control an inguinal hernia if the patient is unfit for or refuses surgery. However, trusses are unsatisfactory, do not treat the hernia and the patient is still at risk of incarceration and strangulation.

• • • • • •

(b) Figure 24.6 Femoral hernia: (a) anterior and (b) lateral views.

Femoral hernia A femoral hernia emerges through the femoral canal and may be felt as a soft swelling below and lateral to the pubic tubercle (Fig. 24.6). It is a protrusion of peritoneum through the femoral canal, below which it emerges subcutaneously. It is usually a small sac and may contain omentum or small bowel. Because of its position below the inguinal ligament it must be distinguished from a saphena varix, which disappears on pressure or on lying down and has a cough impulse. It must also be distinguished from femoral artery aneurysm, enlarged lymph nodes or, on very rare occasions, a psoas abscess.

Strangulation Femoral herniae often strangulate. Because of their small size, femoral herniae do not provide local signs and symptoms comparable to inguinal hernia and the swelling of a strangulated femoral hernia may be impalpable. However, there is evidence of small-bowel obstruction and this should stimulate a careful search for a hernia.

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Figure 24.7 Congenital umbilical hernia.

Figure 24.8 Paraumbilical hernia.

Management Because femoral herniae are more likely to lead to strangulation than inguinal herniae, they should always be repaired without delay. A truss should not be used. Surgically, the hernia may be approached from below (femoral approach) or from above via the inguinal canal (Lotheissen approach) or via the rectus abdominis muscle (McEvedy approach). The contents of the sac are emptied, the sac is excised and the femoral canal is obliterated with three interrupted non-absorbable sutures.

versely with the upper flap overlapping the lower, thereby doubling the strength of the repair.

Epigastric hernia

True umbilical hernia is common in infants (especially in Africans) and is due to a persistent defect in the abdominal wall at the umbilicus. The majority close spontaneously and surgical closure is rarely necessary. Intervention is required in the unlikely event of strangulation or incarceration (Fig. 24.7).

These usually small but often quite painful swellings occur in the midline between xiphisternum and umbilicus. The swelling most frequently consists of herniation of extraperitoneal fat through a small defect in the linea alba. Sometimes it carries a peritoneal sac with it that may contain omentum but this is rare. Pain is localized to the site with tenderness on pressure, but it may also simulate the symptoms of peptic ulcer. Clinical examination reveals a tender swelling in the midline. Sometimes incarcerated fat becomes devascularized and necrotic. Treatment is surgical and may be carried out under local anaesthesia, enlarging the defect, excising the fat and suturing the defect with non-absorbable sutures.

Paraumbilical hernia

Incisional hernia

These herniae occur in obese adult women and are prone to strangulate. The defect occurs through the midline just above the umbilicus (Fig. 24.8). The sac may contain omentum or small intestine or both and, because of the narrow neck, strangulation is relatively common. With long-standing herniae, adhesions occur between the contents and the wall of the sac so that the hernia becomes irreducible. Strangulated herniae are repaired as an emergency. Long-standing herniae should be repaired electively. The Mayo repair is commonly used. With this technique the contents of the sac are freed from its walls and reduced. The sac is excised and the fascial defect is repaired trans-

This is a hernia that protrudes through a defect in an old abdominal wound. Wound infection predisposes to incisional hernia. The margins of the defect in the abdominal wall under the old incision can often be felt and the hernia is easily demonstrated by asking the supine patient to raise his or her head off the pillow (thus tensing the abdominal muscles; Fig. 24.9). An incisional hernia often contains bowel that is adherent to the peritoneal sac. Surgical repair requires excision of the sac and identification and apposition of the margins of the hernia. Occasionally, with a very large incisional hernia, it is not possible to bring the muscle edges together and a polypropylene mesh (Marlex) has to be inserted to close the abdominal wall defect.

Umbilical hernia

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•

Maydl’s hernia (hernia-en-W). In this rare form of inguinal hernia, two loops of intestine are incarcerated in the sac. The intervening loop of small intestine that remains in the abdominal cavity becomes strangulated by compression of its mesenteric vessels at the neck of the sac.

Richter’s hernia This is a variant of strangulated hernia. When a Richter’s hernia is present, only part of the circumference of the small bowel is strangulated. As a consequence, while the patient is still able to pass flatus, he or she experiences colicky abdominal pain and vomiting and radiological evidence of small-bowel obstruction is present. Figure 24.9 Large incisional hernia.

Spigelian hernia

Unusual herniae Inguinal variations hernia (hernia en glissade). Some inguinal her•niaeSliding are sliding herniae, i.e. retroperitoneal structures such as large bowel herniate into the inguinal canal and scrotum, dragging their overlying peritoneum with them. Thus the peritoneal sac itself is empty and the contents of the hernia lie behind the sac. These can often be quite difficult to repair. Littré’s hernia. This is an unusual hernia in which the sac of an inguinal hernia contains a Meckel’s diverticulum.

•

This is an interstitial hernia of the abdominal wall. The defect occurs at the lateral border of the rectus abdominis, emerging through a defect in the transversus and internal oblique fascia halfway between the umbilicus and the pubic symphysis. The swelling is diffuse and difficult to palpate as it is covered by the external oblique. It may be identified by its position above and medial to the location of an inguinal hernia.

Obturator, gluteal and lumbar herniae These are excessively rare herniae that occur with herniation through the obturator foramen and the gluteal and lumbar regions. It is likely that most doctors will never see any of them.

04 Abdominal herniae at a glance Definition Hernia: the protrusion of a viscus or part of a viscus through an abnormal opening in its coverings Types Common Umbilical/paraumbilical Inguinal (direct and indirect) Femoral Incisional

• • • •

Uncommon Epigastric Gluteal, lumbar, obturator

• •

Pathophysiology Defect in the abdominal wall may be congenital (e.g. umbilical hernia, femoral canal) or acquired (e.g. an incision) and is lined with peritoneum (the sac) Raised intra-abdominal pressure further weakens the defect, allowing some of the intra-abdominal contents (e.g. omentum, small-bowel loop) to migrate through the opening Entrapment of the contents in the sac leads to incarceration (unable to reduce contents) and possibly strangulation (blood supply to incarcerated contents is compromised)

• • •

Clinical features Patient presents with a lump over the site of the hernia

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Femoral herniae Femoral herniae are below and lateral to the pubic tubercle, usually flatten the groin crease and are 10 times more common in women than men Half present as a surgical emergency due to obstructed contents, and 50% of these will require small-bowel resection

• •

Inguinal herniae Inguinal herniae start off above and medial to the pubic tubercle but may descend broadly when larger; they usually accentuate the groin crease Most are benign and have a low risk of complications Indirect inguinal herniae can be controlled by digital pressure over the internal inguinal ring, may be narrownecked and are common in younger men (3% per annum present with complications) Direct inguinal herniae are poorly controlled by digital pressure, are often broad-necked and are commoner in older men (0.3% per annum strangulate)

• • • •

Incisional herniae Incisional herniae bulge and are usually broad-necked, poorly controlled by pressure and accentuated by tensing the recti Large chronic incisional herniae may contain much of the small bowel and may be irreducible/unrepairable due to the ‘loss of the right of abode in the abdomen’ of the contents

• •

True umbilical herniae Present from birth and are symmetrical defects in the umbilicus due to failure to close

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Paraumbilical herniae Develop due to an acquired defect in the periumbilical fascia

•

Management Assess the hernia for: (a) Severity of symptoms (b) Risk of complications (type, size of neck) (c) Ease of repair (size, location) (d) Likelihood of success (size, ‘loss of right of abode’) Assess the patient for fitness for surgery, impact of hernia on lifestyle (job, hobbies) Surgical repair is usually offered in suitable patients for: (a) Herniae at risk of complications whatever the symptoms (b) Herniae with previous symptoms of obstruction (c) Herniae at low risk of complications but symptoms interfering with lifestyle, etc. Principles of surgery: (a) Herniotomy: excision of the hernial sac (b) Herniorrhaphy: repair of the defect

• • • •

Complications of surgery Haematoma (wound or scrotal) Acute urinary retention Wound infection Chronic pain Testicular pain and swelling leading to testicular atrophy Hernia recurrence (about 5%)

• • • • • •

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Anatomy and physiology, 276 Symptoms of oesophageal disease, 277 Investigations, 278 Gastro-oesophageal reflux disease, 282 Benign oesophageal strictures, 286

Columnar metaplasia of the oesophagus (Barrett’s columnar epithelium), 288 Non-reflux oesophagitis, 288 Diaphragm, 289 Hiatus hernia, 290

Must know Must do Must know Symptoms and investigation of patients with oesophageal disease Principles of oesophageal function tests Medical, interventional and operative management of reflux disease and common oesophageal motility disorders Principles of management of oesophageal cancer

Must do Clerk a patient with dysphagia due to benign disease Follow the management of a patient with oesophageal cancer from time of diagnosis Attend sessions in the flexible endoscopy suite to observe upper gastrointestinal endoscopy for diagnosis of oesophageal disease and for stenting of inoperable oesophageal cancer Learn how to interpret a barium swallow

Anatomy and physiology The oesophagus is a muscular tube that transports food from the pharynx to the stomach. It is divided into three parts. Upper: extends from the cricopharyngeus to the level of the carina. Middle: extends from the level of the carina to halfway between the carina and the oesophagogastric junction. Lower: the remaining segment that joins the stomach. Clinically, the term ‘cardia’ is used to describe the junction between the oesophagus and stomach. It contains the squamocolumnar junction, which forms the serrated Zline that marks an abrupt change from the tough pale squamous epithelium of the oesophagus to the columnar epithelium of the stomach. A zone of junctional epithe-

• • •

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Oesophageal motility disorders, 291 Oesophageal diverticulae, 294 Sideropenic dysphagia (Paterson–Kelly or Plummer–Vinson syndrome), 295 Oesophageal perforations, 295 Tumour of the oesophagus, 296

lium is interposed between the squamous lining of the oesophagus and the gastric mucosa. The lower oesophagus is the most important site of communication between the portal and systemic venous systems in view of the development of varices in patients with portal hypertension. The lymphatics form extensive plexuses such that lymph flows long distances in the large submucosal plexus before passing through the muscular coat to the draining lymph nodes. These are grouped into three main tiers: the first lies alongside the oesophagus (para-oesophageal), the second is composed of mediastinal lymph nodes, and the third comprises the deep cervical, supraclavicular, tracheobronchial and coeliac nodes (from above downwards). In general, lymph drainage from the upper two-thirds of the oesophagus proceeds in a proximal direction, whereas the lower third drains distally to the subdiaphragmatic region and coeliac lymph nodes. Two nerve plexuses in the oesophageal wall (Meissner’s plexus in the submucosa, Auerbach’s plexus in the muscularis) form networks of ganglion cells, which receive axons from the vagus. Swallowing is coordinated by the swallowing centre in the medulla oblongata. This receives and coordinates sensory inputs from peripheral mechanoreceptors in the pharynx and oesophagus and sends motor impulses to the pharynx and upper oesophagus that initiate the swallowing reflex. The parasympathetic fibres to the oesophagus are predominantly motor and travel in the glossopharyngeal, vagus and recurrent laryngeal nerves to the myenteric plexus. The sympathetic nerve supply consists of preganglionic fibres derived from spinal cord segments T5 and T6. The postganglionic sympathetic fibres then reach the oesophagus as a periarterial plexus. The swallowing mechanism has three stages. 1 The first is voluntary and initiates the process. The food bolus is rolled posteriorly into the pharynx upwards and backwards against the palate by the tongue. 2 The pharyngeal stage is reflex. As food enters the pharynx it stimulates mechanoreceptors that trigger a series of

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automatic pharyngeal muscular contractions such that the soft palate is pulled upwards, preventing entry of food into the nasal cavities. The vocal cords adduct and the larynx is pulled upwards against the epiglottis, preventing passage of food into the trachea. The upward movement of the larynx enlarges the opening of the oesophagus and stimulates relaxation of the tonically active upper oesophageal sphincter (cricopharyngeus). The muscular wall of the pharynx then contracts from above downwards, propelling the food bolus into the oesophagus. 3 The oesophageal stage is also involuntary and propels food from the pharynx to the stomach by peristaltic waves. Primary oesophageal peristalsis is a continuation of the pharyngeal peristaltic wave and travels all the way from the pharynx to the stomach in approximately 8 s. If the primary peristaltic wave fails to move all the food into the stomach, secondary peristaltic waves result from distension of the oesophagus by the retained food and these continue until all the food empties into the stomach. Tertiary oesophageal contractions occur spontaneously and are non-propulsive. They are encountered in various oesophageal motility disorders but also occur in healthy individuals.

Symptoms of oesophageal disease The specific symptoms of oesophageal disease are dysphagia, regurgitation, odynophagia, chest pain and water brash.

Dysphagia Dysphagia is difficulty in swallowing or a sensation of food bolus arrest or delay. The patient feels the food sticking and often points to a particular site on the sternum. Dysphagia for solids implies significant disease, whereas dysphagia for liquids only is more likely to be of functional origin (oesophageal motility disorder), in which case it may be intermittent. Persistent and progressive dysphagia indicates mechanical narrowing of the oesophageal lumen and is usually associated with regurgitation. Eventually, the patient is unable to swallow saliva and exhibits constant drooling. Obstructive dysphagia is first experienced when 20–30% of the oesophageal lumen is lost; most patients usually present when 50% of the oesophageal lumen is compromised.

277

Regurgitation Regurgitation of gastric or oesophageal fluid into the throat accompanied by a sour taste is often postural and occurs predominantly in the supine position especially at night, with the regurgitated material staining the pillow. Postural regurgitation is a very common symptom of reflux disease. It is precipitated by meals and activities that raise intra-abdominal pressure, i.e. bending and straining. Regurgitation may also occur as an overflow of accumulated food in the oesophagus proximal to a stenosing lesion. This spillback into the pharynx and mouth at night may lead to aspiration pneumonitis.

Odynophagia This complaint consists of localized pain, usually in the lower sternal region, which occurs immediately on swallowing certain foods or liquids. It indicates oesophagitis. Hot drinks, acid citrus beverages, coffee and heavily spiced foods are among the most frequent dietary items that induce this symptom. It can be severe enough to condition patients not to eat or drink the offending item, or food in general. Odynophagia signifies mucosal damage by reflux, radiation, viral or fungal infections.

Heartburn This is the most common symptom of oesophageal disease and occurs in up to 50% of the population. It is due to reflux of gastric juice. Some patients complain of severe heartburn, yet on endoscopy there is little or no evidence of inflammation. These individuals may still have reflux in association with an abnormally sensitive oesophageal mucosa. Heartburn is often worsened by recumbency and increase in intra-abdominal pressure, and may follow fatty meals or alcoholic beverages. Heartburn is temporarily relieved by antacids.

Chest pain Oesophageal anterior chest pain consists of a tightening or gripping pain that closely simulates angina pectoris. Thus it may radiate to the back, jaw, arm and ear and may even be relieved by sublingual nitrates. This type of pain is commonly found in patients with reflux oesophagitis or oesophageal motility disorders.

Sensation of a substernal lump (globus)

Water brash

When this occurs during fasting it is termed ‘globus hystericus’. It is a neurotic symptom in patients with emotional instability but requires thorough examination to exclude organic disease.

This symptom is uncommon and is restricted to patients with reflux disease. It is due to excessive salivation, the mouth becoming full of fluid that has a salty taste and is clear and frothy.

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Table 25.1 Investigations for oesophageal disease. Test

Indications

Radiology

Chest radiograph Contrast swallow CT

Aspiration pneumonitis; oesophageal perforation, dysphagia, motility disorders; reflux disease, staging of malignant disease

Ultrasound

External Endoscopic

Diaphragmatic screening Staging of malignant disease

Radioisotope studies

Labelled liquid or solid bolus studies

Oesophageal transit, reflux disease

Endoscopy

Fibreoptic with biopsy, cytology

All patients with oesophageal symptoms, especially dysphagia

Physiological

Stationary and ambulatory manometry 24-h pH monitoring Bilitec

Pre-pH monitoring: reflux disease Oesophageal motility disorders: non-cardiac chest pain Alkaline reflux disease

Investigations These are outlined in Table 25.1.

Radiography

A chest radiograph is necessary in all patients admitted acutely with oesophageal symptoms in order to detect the following. Aspiration pneumonitis. Mediastinal widening from nodal involvement in patients with oesophageal tumours. Outline any soft-tissue shadows and fluid gas levels: intrathoracic stomach, achalasia. Mediastinal emphysema and/or pleural effusion: patients with oesophageal perforations or suture line dehiscence after an oesophagectomy. The standard contrast investigation is the barium swallow, which is particularly useful in the following. Patients with dysphagia from any cause. Patients with gastro-oesophageal reflux should have this investigation to determine the presence or absence of a hiatus hernia and to exclude oesophageal shortening. Patients with previous surgery to the oesophagus or oesophagogastric junction. Patients with known benign or malignant strictures about to undergo surgery or endoscopic therapeutic manoeuvres. Barium swallow is inaccurate for the detection of gastrooesophageal reflux. Its main value lies in the demonstration of an associated hiatus hernia and in detecting stricture formation (Fig. 25.1). A contrast swallow is an essential investigation in patients suspected of oesophageal perforation or leaking oesophageal anastomosis.

• • • • • • • •

Figure 25.1 Barium swallow showing irregular annular stricture in the middle third of the oesophagus that proved to be an annular carcinoma on endoscopy and biopsy.

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279

Ultrasound Endoscopic ultrasonography provides accurate staging of a tumour in terms of intramural involvement and enlargement of adjacent lymph nodes. Ultrasonically, five oesophageal layers can be distinguished. The first two layers correspond to the superficial and deep mucosa, the third layer to the submucosa, the fourth layer to the muscularis propria and the fifth layer to the adventitia (Fig. 25.3). Endoscopic ultrasound provides sufficient information on lymph nodes such that rounded, sharply demarcated, homogeneous, hypoechoic lymph nodes are most likely malignant.

Radioisotope studies Figure 25.2 CT cross-section showing oesophageal cancer abutting but not involving the descending thoracic aorta.

Computed tomography Computed tomography (CT) is very useful for the preoperative assessment of oesophageal malignancy (Fig. 25.2). It reliably assesses the extent of mural invasion and the size of the lesion. Aortic invasion can be predicted with accuracy if there is more than 90° contact. It is also used for the detection of distant metastases including pulmonary metastases but not small peritoneal deposits.

These are used to evaluate oesophageal transit of liquid and solid boluses in individuals with motility disorders. Standardized solid bolus tests are more reliable and the study is carried out with the patient in the erect position. The normal transit time for this test is 10 s. Special software can generate time vs. radioactivity curves and special techniques generate a condensed image that outlines the spatial transit of the labelled bolus. Prolonged transit times are encountered in oesophageal motility disorders. The condensed image shows a striking sinuous outline resulting from oscillations of the bolus in patients with achalasia and diffuse oesophageal spasm (Fig. 25.4).

Figure 25.3 Endoscopic ultrasound showing sequences of an oesophageal cancer extending by ‘pseudopodia’ into the adventitia/fat plane. Enlarged probably involved para-oesophageal lymph nodes are seen in top-right sequence.

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(a)

(c)

(b)

(d) Figure 25.4 Radiolabelled egg-white bolus transit studies: (a) overview; (b) normal transit; (c) step delay in a patient with nonspecific motility disorder; (d) oscillatory pattern in diffuse oesophageal spasm.

Endoscopy

Oesophageal manometry

Flexible endoscopy is essential in all patients with dysphagia. It provides direct visual information on the presence or absence of pathology. Both biopsy and brush cytology are used to confirm oesophageal malignancy. Endoscopic biopsies are also necessary in the diagnosis and histological grading of reflux oesophagitis and in the detection of Barrett’s epithelium and its surveillance in patients with long-standing reflux disease (Fig. 25.5).

This is used to measure the activity of the oesophageal musculature and oesophageal sphincters by recording intraluminal pressure profiles caused by contractions. Intraluminal pressure recording is carried out by a system of water-perfused catheters (Fig. 25.6) or by solid-state strain-gauge transducers built into catheters. The information obtained is analysed according to established criteria in order to diagnose oesophageal motility disorders. Prolonged ambulatory manometric studies are particularly useful for patients with non-cardiac chest pain who may have transient motility disturbances in the oesophagus.

Physiological tests These include manometry, pH monitoring and tests to assess bile reflux.

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Figure 25.5 Upper gastrointestinal endoscopy: pinkish red Barrett’s columnar mucosal change in a patient with gastrooesophageal reflux.

(a)

24-Hour pH monitoring This technique involves the transnasal placement of a pH measuring electrode in the lower oesophagus. The pH electrode monitors the changes in intra-oesophageal pH over 24 h, with the information stored in a portable logger (Fig. 25.7). A 24-h pH profile is thus obtained that provides information on frequency, duration and pattern of reflux episodes together with temporal correlation with symptoms. A reflux episode is defined as a pH drop to below pH 4. Specially designed software analyses the data in two ways. Reflux event analysis. All individual reflux episodes are identified and characterized: number, mean duration, number of long reflux events > 5 min, duration of the longest reflux episode. Cumulative oesophageal exposure analysis: depicts the frequency distribution of the oesophageal pH data for the erect and supine parts of the study as well as for the whole period of study. The indications for 24-h ambulatory pH monitoring are as follows. Definitive diagnosis of gastro-oesophageal reflux in patients who are sufficiently symptomatic to have warranted endoscopy but in whom endoscopy is normal. Investigation of patients suspected of having gastrooesophageal reflux as a cause of atypical symptoms, such as non-cardiac chest pain, respiratory and laryngeal symptoms, in whom the relevant investigations have been normal and to correlate such symptoms with reflux episodes. When established gastro-oesophageal reflux responds poorly to medical therapy and particularly when surgical treatment is contemplated.

•

(b) Figure 25.6 Perfusion manometry: (a) Arndorfer system; (b) multilumen catheter.

• • • •

Figure 25.7 Ambulatory 24-h pH logger.

24-Hour oesophageal bile monitoring (by spectrophotometry) This test uses an optical fibre sensor capable of detecting bilirubin in the oesophagus as a marker of

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enterogastro-oesophageal reflux. The ambulatory spectrophotometer transfers the signals to a data logger and a 24-h profile can be recorded. The data are then downloaded to a computer. It is important to use a standard diet that avoids coloured food substances and beverages during the test. The test is indicated in: patients with symptomatic gastro-oesophageal reflux with poor response to an adequate dose of proton pump inhibitor; patients with complications of gastro-oesophageal reflux disease such as Barrett’s metaplasia, strictures and ulcers; patients with reflux symptoms after gastrectomy.

Bernstein’s acid perfusion test

•

This detects oesophageal mucosal sensitivity to acid and is very useful in the determination of the oesophageal origin of chest pain. A nasogastric tube is positioned in the middle of the oesophagus. Infusion is initially started with isotonic saline and then switched to 0.1 m HCl without informing the patient.

•

Gastro-oesophageal reflux disease

•

Gastro-oesophageal reflux disease (GORD) is the most common upper gastrointestinal disorder in western

Oesophageal symptoms at a glance Definitions Dysphagia: difficulty with swallowing, which may be associated with ingestion of liquids, solids or both. Most causes of dysphagia are oesophageal in origin

•

Heartburn: an aching, burning sensation felt behind the lower part of the sternum, caused by reflux of acid from the stomach into the oesophagus

Extramural Pulsion diverticulum: intermittent symptoms, unexpected regurgitation External compression: mediastinal lymph nodes, left atrial hypertrophy, bronchial malignancy

Regurgitation: when fluid from the stomach flows back into the mouth producing a sour taste. It is frequently postural and indicates gastric reflux

Investigation of dysphagia Any new symptom of progressive dysphagia should be assumed to be a carcinoma until proven otherwise

Water brash: sudden secretion of a quantity of saliva into the mouth as a reflex response to reflux

Intramural Foreign body: acute distress, marked retrosternal discomfort, difficulty in swallowing saliva

Odynophagia: painful swallowing and usually indicates oesophagitis Causes of dysphagia Mural Carcinoma of the oesophagus: progressive, weight loss and anorexia, anaemia Reflux oesophagitis: preceded by heartburn, anaemia, nocturnal regurgitation Achalasia: liquids > solids, frequent regurgitation, recurrent chest infections due to aspiration, long history, younger patients or old age Tracheo-oesophageal fistula: recurrent chest infections, childhood (congenital), late adulthood (post trauma, deep X-ray therapy, malignancy) Caustic stricture: history of corrosive ingestion, chronic dysphagia Scleroderma: slow onset, skin and hair changes apparent Chagas’ disease: Trypanosoma cruzi, South America, arrhythmias, colonic dysmotility

• • • • • • •

• •

All patients Full blood count: anaemia more common with tumours than reflux Liver function tests: exclude hepatic disease

• •

Oesophagogastroduodenoscopy (OGD) Moderate risk Differentiates between tumour, reflux, stricture and achalasia Allows biopsy and possible treatment (e.g. placement of endoprosthesis)

• • •

Barium swallow Low risk Good for detecting fistula, reflux, high tumour, diverticulum ? Dysmotility: (a) Achalasia: video barium swallow (b) Neurogenic cause: oesophageal manometry ? Extrinsic compression: chest X-ray (AP and lateral)

• • • •

CT Chest and mediastinum

•

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countries. Minor gastro-oesophageal episodes occur in most people but they are short-lived and exposure of the lower oesophageal mucosa to acid pH < 4 does not exceed 5% in 24 h. Reflux in excess of this is considered pathological. In many patients the symptoms are mild and intermittent with no significant mucosal damage. In 10% of patients, the acid-induced mucosal injury causes oesophagitis, which may lead to further major complications such as: ulceration (bleeding); stricture/webs; columnar metaplasia (Barrett’s columnar epithelium); oesophageal shortening. Approximately 10% of patients with columnar metaplasia develop dysplasia in the metaplastic segment of the oesophagus.

• • • •

Pathophysiology The disease develops as a result of failure of the normal antireflux mechanisms, with chemical injury to the squamous lining of the oesophagus. The antireflux mechanisms include: competence of the lower oesophageal sphincter (LOS) ‘complex’;

•

Table 25.2 Effect on lower oesophageal sphincter pressure (high-pressure zone) by hormones, drugs and foodstuffs.

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clearance of refluxed material; • oesophageal mucosal resistance to the damaging effects of the • refluxate. The LOS is the single most important factor accounting for the competence of the gastro-oesophageal junction. Several drugs, hormones and food substances are known to influence the contractile activity of the LOS (Table 25.2). The normal resting pressure of the LOS is 10 – 25 mmHg. Temporary inhibition of the LOS occurs just prior to the arrival of a primary peristaltic wave induced by swallowing in order to allow entry of food into the stomach. The sphincter relaxes and contracts immediately the food bolus passes through. The length of the intra-abdominal segment of the oesophagus is another important factor in the competence of the LOS. The diaphragmatic crural mechanism exerts its antireflux effect mainly during deep inspiration or sudden increases in intra-abdominal pressure, e.g. coughing or sneezing. The acute angle of His is also thought to be important by providing an abrupt insertion of the oesophagus into the stomach. The mucosal rosette at the lower oesophagus provides substance for the valve and thus closure of the lumen when the LOS is contracted. Between 25 and 50% of patients with GORD have impaired peristaltic function.

Decrease pressure

Increase pressure

Glucagon Secretin Cholecystokinin Vasoactive intestinal peptide Gastric inhibitory polypeptide Progesterone Oestrogens Serotonin (N receptors) Histamine (H2 receptors) Enkephalins

Gastrin Motilin Bombesin Histamine (H1 receptors) Serotonin (M receptors)

Prostaglandins

E1, E2, A2

Drugs

Atropine Antihistamines Calcium blockers Ganglion blockers Tricyclic antidepressants

Metoclopramide Domperidone Cisapride Cholinergic drugs Anticholinesterases

Foodstuffs

Caffeine Fats Chocolate Alcohol

Protein meal

Other

Smoking

Hormones/peptides

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Aetiology The factors that promote reflux and damage include the following. Primary weakness of the smooth muscle of the LOS. Short length of the intra-abdominal segment of oesophagus. Defective hormonal and neural control of the sphincter: most commonly dietary induced and transient. Abnormally high number of transient LOS relaxations. Presence of a hiatus hernia. This results in a change of the pressure environment, shortening of the LOS and changes in the anatomy and reflexes of the gastric cardia. Approximately 50% of patients with reflux symptoms and 90% of patients with reflux oesophagitis have a hiatus hernia. However, many patients with a hiatus hernia are asymptomatic and 40 –50% have no oesophagitis. Delayed gastric emptying: present in up to 40% of patients with GORD. The principal components of the refluxate (gastric juice) are HCl and pepsins. Bile salts also produce severe mucosal damage. Clinically, pure acid and pepsin reflux occurs in 40% of patients and mixed reflux of gastric and duodenal juices occurs in 60% of patients. Pure alkaline reflux is uncommon and occurs after gastric resections.

• • • • •

•

Pathology The histological changes of early damage include widening of the basal layer and extension of the dermal papillae to more than two-thirds of the epithelium. With more

severe damage there is an accumulation of inflammatory cells and the epithelial thickness is reduced. The papillae become widened and extend to the surface, when superficial necrosis and ulceration supervene. These acute superficial ulcers heal without fibrosis. However, if the ulceration and inflammation reach the submucous layer or beyond, fibrosis ensues and the mucosa may undergo metaplasia to columnar epithelium (Barrett’s columnar epithelium). Infection with Helicobacter pylori protects against the development of GORD and its complications. This protective effect depends on the extent of Helicobacterinduced gastritis with reduction of acid secretion. Thus reflux oesophagitis may develop after therapy to eradicate H. pylori as gastric acid secretion returns to normal.

Clinical features The typical symptoms of GORD are heartburn, regurgitation and dysphagia. Symptoms are aggravated by posture and can be especially severe at night and after large meals and activities that increase intra-abdominal pressure, e.g. bending, stooping. Other symptoms include pain on swallowing hot or spicy foods (odynophagia) and water brash. Dysphagia may be due to spasm or oedema of the inflamed lower oesophagus, in which case it remits with improvement of the oesophagitis consequent on treatment. In some patients dysphagia may be secondary to a motility disorder or stricture formation. A scoring system introduced by DeMeester is useful for assessing the extent of symptomatic severity (Table 25.3). The severity of the disease is assessed by endoscopy (Table 25.4).

04 Symptoms

Grade

Description

Heartburn None Minimal Moderate Severe

0 1 2 3

No heartburn Occasional episodes Reason for medical visit Interference with daily activities

Regurgitation None Minimal Moderate Severe

0 1 2 3

No regurgitation Occasional episodes Predictable on position or straining Episodes of pulmonary aspiration with chronic nocturnal cough or recurrent pneumonitis

Dysphagia None Minimal Moderate Severe

0 1 2 3

No dysphagia Occasional episodes Requires fluids to clear Episode of meat impaction requiring medical treatment

Table 25.3 DeMeester’s scoring system for symptoms of gastro-oesophageal reflux.

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Table 25.4 Los Angeles classification of oesophagitis. Grade

Description

Grade A Grade B Grade C

One (or more) mucosal break no longer than 5 mm that does not extend between the tops of two mucosal folds One (or more) mucosal break more than 5 mm long that does not extend between the tops of two mucosal folds One (or more) mucosal break that is continuous between the tops of two or more mucosal folds but which involves less than 75% of the circumference One (or more) mucosal break that involves at least 75% of the oesophageal circumference

Grade D

Table 25.5 Drug therapy in gastro-oesophageal reflux disease. Drug class

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