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 •
c san
Principles and
Practice of
Surgery
Principles and
Practice of

Surgery
7th Edition

Edited by

O. James Garden
CBE BSc MB ChB MD FRCS(Glas) FRCS(Ed) FRCP(Ed)
FRACS(Hon) FRCSCan(Hon) FACS(Hon) FRCS(Hon)
FCSHK(Hon) FRCSI(Hon)
Regius Professor of Clinical Surgery,
Clinical Surgery, University of Edinburgh;
Honorary Consultant Hepatobiliary
and pancreatic Surgeon,
Royal Infirmary of Edinburgh, UK

Rowan W. Parks
MB BCh BAO MD FRCSI FRCS(Ed)
Professor of Surgical Sciences,
Clinical Surgery, University of Edinburgh;
Honorary Consultant Hepatobiliary and Pancreatic
Surgeon, Royal Infirmary of Edinburgh, UK

Edinburgh London New York Oxford Philadelphia St Louis Sydney Toronto 2018
© 2018 Elsevier Ltd. All rights reserved.

No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including
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This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be
noted herein).

First edition 1985

Second edition 1991
Third edition 1995
Fourth edition 2002
Fifth edition 2007
Sixth edition 2012
Seventh edition 2018

ISBN 978-0-7020-6859-1
IE 978-0-7020-6858-4
Inkling 978-0-7020-6856-0

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A catalogue record for this book is available from the British Library

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A catalog record for this book is available from the Library of Congress

Notices
Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding,
changes in research methods, professional practices, or medical treatment may become necessary.

Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information,
methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own
safety and the safety of others, including parties for whom they have a professional responsibility.

To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury
and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any
methods, products, instructions, or ideas contained in the material herein.

Printed in China
Last digit is the print number: 9 8 7 6 5 4 3 2 1

Senior Content Strategist: Laurence Hunter

Senior Content Development Specialist: Ailsa Laing / Trinity Hutton
Project Manager: Andrew Riley
Illustration Manager: Nichole Beard
Illustrators: Gillian Lee and Barking Dog Illustrators
 Contents
Preface vii
Acknowledgements viii
Contributors ix
International Advisory Board xi

SECTION 1 PRINCIPLES OF PERIOPERATIVE CARE 1

1. Metabolic response to injury, fluid and electrolyte balance and shock 3

Stuart McKechnie, Timothy Walsh
2. Transfusion of blood components and plasma products 29
Rachel H.A. Green, Marc L. Turner
3. Nutritional support in surgical patients 40
Gordon L. Carlson, Ken Fearon†
4. Infections and antibiotics 48
Savita Gossain, Peter M. Hawkey
5. Ethics, preoperative considerations, anaesthesia and analgesia 60
Ewen M. Harrison, Michael A. Gillies
6. Principles of the surgical management of cancer 86
Mark A. Potter
7. Trauma and multiple injury 98
Euan J. Dickson
8. Practical procedures and patient investigation 112
Damian James Mole
9. Postoperative care and complications 128
Pawanindra Lal
10. Evidence-based practice and professional development 137
Steven Anderson, Siun Walsh, Arnie D.K. Hill

SECTION 2 GASTROINTESTINAL SURGERY 145

11. The abdominal wall and hernia 147

Andrew de Beaux
12. The acute abdomen 159
Simon Paterson-Brown

†
Deceased
vi • CONTENTS

13. The oesophagus, stomach and duodenum 179

Richard Hardwick
14. The liver and biliary tract 206
Saxon Connor
15. The pancreas and spleen 233
C. Ross Carter, Colin McKay
16. The small and large intestine 252
Malcolm G. Dunlop
17. The anorectum 283
Farhat Din

SECTION 3 SURGICAL SPECIALTIES 299

18. Plastic surgery including common skin and subcutaneous lesions 301
Patrick Addison
19. The breast 326
J. Michael Dixon
20. Endocrine surgery 351
Sonia Wakelin
21. Vascular and endovascular surgery 375
Hanafiah Harunarashid
22. Cardiothoracic surgery 409
Robert R. Jeffrey
23. Urological surgery 429
Grant D. Stewart
24. Neurosurgery 461
Lynn Myles, Paul M. Brennan
25. Transplantation surgery 487
Lorna Marson, John Forsythe
26. Ear, nose and throat surgery 502
Janet Wilson
27. Orthopaedic surgery 528
John C. McKinley, Issaq Ahmed

Appendix Laboratory reference ranges 548

Index 551

This seventh edition of Principles and Practice of Surgery builds
on the success and popularity of previous editions and its com-
panion volume Davidson’s Principles and Practice of Medicine.
Many medical schools now deliver undergraduate curricula which
focus principally on ensuring generic knowledge and skills, but the
continuing success of Principles and Practice of Surgery over the
last 30 years indicates that there remains a need for a textbook
which is relevant to current surgical practice. This text provides
a ready source of information for the medical student, for the
recently qualified doctor on the surgical ward and for the surgical
trainee who requires an up to date overview of the management
approach to surgical pathology. The content is patient focused
and reflects the fact that surgery is often as much about resusci-
tation and when not to operate as trying to intervene to deliver a
better outcome. This book should guide the student and trainee
through the core surgical topics which will be encountered within
an integrated undergraduate curriculum, in the early years of sur-
gical training and in subsequent clinical practice.
Although it might seem that surgical practice has remained fairly
constant in recent years, there have been considerable develop-
ments, and sufficient evidence has become available to merit a
Preface
number of chapters undergoing significant change. We have also
taken into account feedback on the presentation of some of the
contents. The format of chapters has been made more consistent
and evidence based practice has been highlighted where appro-
priate. A global focus has been maintained throughout. It is our
intention that this edition is relevant to doctors and surgeons prac-
tising worldwide and a balanced approach has been taken to the
presentation where appropriate to ensure that variations in prac-
tice are identified. The contributions of our internationally-based
contributors and advisors have ensured the book’s contents
are fit for purpose in those parts of the world where disease pat-
terns and management approaches may differ.
We very much hope that this edition continues the tradition and
high standards set by our predecessors and that the revised
content and presentation of the seventh edition satisfies the
needs of tomorrow’s doctors.
OJG, RWP
Edinburgh, 2018
Acknowledgements
We are indebted for the past contributions from former authors who step down with the arrival of this new edition. They include
Sunil Agarwal, Derek Alderson, Andrew W. Bradbury, Ari George Chacko, Trevor J. Cleveland, Steven M. Finney, Pranay Gaikwad,
Roy John Korula, Thomas W. J. Lennard, Dermot W. McKeown, Douglas McWhinnie, Rachel E. Melhado, M. J. Paul, Colin E.
Robertson, Venkatramani Sitaram, Laurence H. Stewart, Sumit Sural, Anubhav Vindal, James D. Watson and Ian R. Whittle.
We would also particularly wish to acknowledge the outstanding contributions made over the years to past editions and to this
new edition by our colleague, Ken Fearon, whose death during the preparation of this edition has cast a shadow over British and
international surgery.
We have benefited greatly from the strong editorial support of Professors Andrew Bradbury and John Forsythe over past editions
and wish them well as they move on to new phases of their careers. We remain indebted to the founders of this book, Professors
Sir Patrick Forrest, Sir David Carter and the late Mr Ian Macleod, who established the reputation of the textbook in its early years
with students and doctors around the world.
We are grateful to Laurence Hunter of Elsevier for his encouragement and enthusiasm and to Ailsa Laing for keeping our contributors
and the editorial team in line during all stages of publication. As always, this has not been easy!

Patrick Addison BSc(Hons) MBChB MD FRCS(Plast)
Consultant Plastic Surgeon, St John’s Hospital, Livingston;
Consultant Plastic Surgeon, Royal Hospital for Sick Children,
Edinburgh, UK
Issaq Ahmed FRCS(Ed, Tr&Orth)
Consultant Orthopaedic and Trauma Surgeon, Department
of Orthopaedic Surgery, Royal Infirmary of Edinburgh,
Edinburgh, UK
Steven Anderson MB BAO BCh
Department of Surgery, Beaumont Hospital, Dublin, Ireland
Paul M. Brennan BMedSci(Hons) MBBChir PhD FRCS(SN)
Department of Clinical Neurosciences, University of Edinburgh,
Western General Hospital, Edinburgh, UK
Gordon L. Carlson BSc MBChB MD FRCS FRCS(Gen)
FRCS(Ed)
Professor of Surgery, Salford Royal NHS Foundation Trust,
Salford, UK
C. Ross Carter MD FRCS
West of Scotland Pancreatic Unit, Glasgow Royal Infirmary,
Glasgow, UK
Saxon Connor MBChB FRACS
Hepatobiliary Surgeon, Department of General Surgery,
Canterbury District Health Board, Christchurch, New Zealand
Andrew de Beaux MBChB FRCS MD
General and Upper GI Surgeon, Department of Surgery, Royal
Infirmary of Edinburgh, Edinburgh, UK
Euan J. Dickson MBChB MD FRCS
Consultant Surgeon, West of Scotland Pancreatic Unit, Glasgow
Royal Infirmary, Glasgow, UK
Farhat Din BSc MBChB MD FRCS
Senior Lecturer, Academic Coloproctology, Western General
Hospital, Edinburgh, UK
Contributors
J. Michael Dixon BSc(Hons) MBChB MD FRCS FRCS(Ed)
FRCP(Ed, Hon)
Professor of Surgery, Breakthrough Research Unit, Western
General Hospital, Edinburgh; Consultant Surgeon, Edinburgh
Breast Unit, Western General Hospital, Edinburgh; Clinical Lead,
Breast Cancer Now Research Unit, Western General Hospital,
Edinburgh, UK
Malcolm G. Dunlop MD FRCS FRSE FMedSci
Professor of Coloproctology, University of Edinburgh, Edinburgh,
UK
John Forsythe MBBS MD FRCS(Ed) FRCS(Eng) FEBS(Hon)
Consultant Transplant and Endocrine Surgeon, Transplant Unit,
Royal Infirmary of Edinburgh; Honorary Professor, Clinical
Surgery, University of Edinburgh, UK
Michael A. Gillies MD
Consultant and Honorary Reader in Anaesthesia, Critical Care
and Pain Medicine, Royal Infirmary of Edinburgh, Edinburgh, UK
Savita Gossain BSc MBBS FRCPath
Consultant Microbiologist, Public Health Laboratory Birmingham,
Heart of England NHS Trust, Birmingham, UK
Rachel H. A. Green MBChB FRCPath BMedBiolFRCP
Associate Medical Director, Scottish National Blood Transfusion
Service, Glasgow; Associate Medical Director, Diagnostics
Directorate, Greater Glasgow and Clyde Health Board, UK
Richard Hardwick MBBS MD FRCS
Consultant Upper GI Surgeon, Cambridge Oesophagogastric
Centre, Addenbrooke’s Hospital, Cambridge, UK
Ewen M. Harrison MBChB MSc PhD FRCS
Senior Lecturer, Clinical Surgery, University of Edinburgh;
Consultant HPB Surgeon, Royal Infirmary of Edinburgh,
Edinburgh, UK
x • CONTRIBUTORS

Hanafiah Harunarashid BScMed MBChB FRCS(Ed)
FRCS(Ire) FRCS(Gen) AM(Mal)
Director, Advanced Surgical Skills Centre, Associate Professor,
Consultant Vascular and Endovascular Surgeon, Department of
Surgery, Universiti Kebangsaan Malaysia, Kuala Lumpur
Peter M. Hawkey BSc DSc MBBS MD FRCPath
Professor of Clinical and Public Health Bacteriology, Honorary
Consultant, Heart of England Foundation Trust; HPA West
Midlands Regional Microbiologist, University of Birmingham, UK
Arnie D. K. Hill MBBCh MCh FRCSI
Professor of Surgery, Department of Surgery, Beaumont Hospital,
Dublin; Head of School of Medicine, Royal College of Surgeons of
Ireland, Dublin, Ireland
Robert R. Jeffrey BSc(Hons) MBChB FRCSEd FRCPEd
FRCSGlas FETCS
Honorary Senior Lecturer, Department of Surgery University of
Edinburgh, Edinburgh, UK
Pawanindra Lal MS DNB FCLS FRCS(Ed) FRCS(Glasg)
FRCS(Eng) FACS
Director Professor of Surgery, Consultant Laparoscopic
Gastro-intestinal, Oncology and Bariatric Surgeon, Chairman,
Division of Minimal Access Surgery, Head of Clinical Skills Centre,
Maulana Azad Medical College (University of Delhi) & Associated
Lok Nayak Hospital, New Delhi
Lorna Marson MBBS MD FRCS(Eng) FRCS(Ed) FRCP(Ed)
Reader in Transplant Surgery, Clinical Sciences (Surgery),
University of Edinburgh, Edinburgh, UK
Colin McKay MBChB MD FRCS
Consultant Pancreatic Surgeon, West of Scotland Pancreatic
Unit, Glasgow Royal Infirmary, Glasgow, UK
Stuart McKechnie MBChB BSc(Hons) FRCA DICM
FFICM PhD
Consultant in Intensive Care Medicine and Anaesthetics, John
Radcliffe Hospital, Oxford, UK
Lynn Myles MBChB BCS(Hons) MD FRCS(SN)
Consultant Neurosurgeon, Western General Hospital, Edinburgh,
and Royal Hospital for Sick Children, Edinburgh, UK
Simon Paterson-Brown MBBS MPhil MS FRCS(Ed)
FRCS(Eng) FCS(HK)
Consultant General and Upper Gastro-Intestinal Surgeon,
General Surgery, Royal Infirmary of Edinburgh, Edinburgh, UK
Mark A. Potter BSc MBChB MD FRCS FRCS(Ed)
Consultant Surgeon and Honorary Senior Lecturer, Department
of Colorectal Surgery, Western General Hospital, Edinburgh, UK
Grant D. Stewart BSc(Hons) FRCS(Ed, Urol) MBChB PhD
University Lecturer in Urological Surgery, Academic Urology
Group, University of Cambridge; Honorary Consultant Urological
Surgeon, Department of Urology, Addenbrooke’s Hospital,
Cambridge; Honorary Senior Clinical Lecturer, University of
Edinburgh, Edinburgh, UK
Marc L. Turner MB ChB PhD
Medical Director, Scottish National Blood Transfusion Service,
Edinburgh, UK
Sonia Wakelin MBChB BSc(Hons) PhD
Consultant Surgeon, Royal Infirmary of Edinburgh, Edinburgh, UK
Siun Walsh MB BAO BCh MD
Department of Surgery, Beaumont Hospital, Dublin, Ireland
Timothy Walsh BSc(Hons) MBChB(Hons) FRCP FRCA
FFICM MRes MD
Chair of Critical Care, Anaesthesia and Pain Medicine, University
of Edinburgh, UK
Janet Wilson BSc MD FRCSEd FRCSEng
FRCSLT(Hon)
Professor of Otolaryngology Head and Neck Surgery, Newcastle
University, Newcastle upon Tyne, UK

John C. McKinley BMSc MBChB FRCS

Orthopaedic Consultant, Royal Infirmary of Edinburgh,
Edinburgh, UK

Damian James Mole BMedSci MBChB PhD FRCS

Senior Clinical Lecturer and Honorary Consultant Surgeon,
University of Edinburgh; Senior Clinical Lecturer, MRC Centre for
Inflammation Research, University of Edinburgh, Edinburgh, UK
 International Advisory Board
Ewen M. Harrison MBChB MSc PhD FRCS
Senior Lecturer, Clinical Surgery, University of Edinburgh;
Consultant HPB Surgeon, Royal Infirmary of Edinburgh,
Edinburgh, UK
Hanafiah Harunarashid BScMed MBChB FRCS(Ed)
FRCS(Ire) FRCS(Gen) AM(Mal)
Director, Advanced Surgical Skills Centre, Associate Professor,
Consultant Vascular and Endovascular Surgeon, Department of
Surgery, Universiti Kebangsaan Malaysia, Kuala Lumpur
Arnie D. K. Hill MBBCh MCh FRCSI
Professor of Surgery, Department of Surgery, Beaumont Hospital,
Dublin; Head of School of Medicine, Royal College of Surgeons
Ireland, Dublin, Ireland
PawanIndiara Lal MS DNB FCLS FRCS(Ed) FRCS(Glasg)
FRCS(Eng) FACS
Director Professor of Surgery, Consultant Laparoscopic
Gastro-intestinal, Oncology and Bariatric Surgeon, Chairman,
Division of Minimal Access Surgery, Head of Clinical Skills Centre,
Maulana Azad Medical College (University of Delhi) & Associated
Lok Nayak Hospital, New Delhi
Venkatramani Sitaram MBBS MS FRCS(Glas)
Former Professor of Surgery, Christian Medical College and
Hospital, Vellore, India
Martin D. Smith MBBCh FCS (SA) Cert GIT (Surg) FEBS
Professor of Surgery, Department of Surgery, University of the
Witwatersrand, Johannesburg, South Africa
 Section 1
Principles of perioperative care
Metabolic response to injury, fluid and electrolyte balance and shock 3
Transfusion of blood components and plasma products 29
Nutritional support in surgical patients 40
Infections and antibiotics 48
Ethics, preoperative considerations, anaesthesia and analgesia 60
Principles of the surgical management of cancer 86
Trauma and multiple injury 98
Practical procedures and patient investigation 112
Postoperative care and complications 128
Evidence-based practice and professional development 137
 Stuart McKechnie
Timothy Walsh
Metabolic response to
injury, fluid and electrolyte
balance and shock
Chapter contents
The metabolic response to injury 3
Fluid and electrolyte balance 9
The metabolic response to injury
To increase the chances of surviving injury, all animals have a com-
plex set of mechanisms that act locally and systemically to restore
the body to its preinjury condition. While these mechanisms are vital
for survival in the wild, in the context of surgical injury they can be
harmful. By minimizing and manipulating the metabolic response to
injury, surgical mortality, morbidity and recovery times can be
greatly improved. An understanding of the metabolic response to
injury is therefore fundamental to modern surgical practice. Reduc-
tion of the metabolic (or stress) response to surgery has improved
clinical outcomes in surgical patients.
Features of the metabolic response to injury
Historically, the response to injury was divided into two phases:
‘ebb’ and ‘flow’. In the ebb phase during the first few hours after
injury, patients were cold and hypotensive (shocked). When intra-
venous fluids and blood transfusion became available, this shock
was sometimes found to be reversible and in other cases irrevers-
ible. If the individual survived the ebb phase, patients entered the
flow phase, which was divided into two parts. The initial catabolic
flow phase lasted about a week and was characterised by a high
metabolic rate, breakdown of proteins and fats, a net loss of
body nitrogen (negative nitrogen balance) and weight loss. Over
2–4 weeks, there then followed the anabolic flow phase during
which protein and fat stores were restored and weight gain occurred
(positive nitrogen balance). Modern understanding of the metabolic
response to injury is still based on these general principles.
Factors mediating the metabolic response
to injury
The metabolic response is a complex interaction between many
body systems.
1
Shock 18
The acute inflammatory response
Inflammatory cells and cytokines are the principal mediators of the
acute inflammatory response. Physical damage to tissues results
in local activation of cells such as macrophages that release a vari-
ety of cytokines (Table 1.1). Some of these, such as interleukin-
8 (IL-8), attract large numbers of circulating macrophages and
neutrophils to the site of injury. Others, such as tumour necrosis
factor alpha (TNF-α), IL-1 and IL-6, activate these inflammatory
cells, enabling them to clear dead tissue and kill bacteria. Although
these cytokines are produced and act locally (paracrine action),
their release into the circulation initiates some of the systemic fea-
tures of the metabolic response, such as fever (IL-1) and the
acute-phase protein response (IL-6, see later) (endocrine action).
Other proinflammatory (prostaglandins, kinins, complement, pro-
teases and free radicals) and antiinflammatory substances such
as antioxidants (e.g., glutathione, and vitamins A and C), protease
inhibitors (e.g., α2-macroglobulin) and IL-10 are also released
(Fig. 1.1). The clinical condition of the patient depends on the
extent to which the inflammation remains localised as well as
the balance between these pro- and antiinflammatory processes.
The endothelium and blood vessels
The expression of adhesion molecules upon the endothelium
leads to leucocyte adhesion and transmigration (Fig. 1.1).
Increased local blood flow due to vasodilatation, secondary to
the release of kinins, prostaglandins and nitric oxide (NO), as well
as increased capillary permeability, increases the delivery of
inflammatory cells, oxygen and nutrient substrates important for
healing. Colloid particles (principally albumin) leak into injured tis-
sues, resulting in oedema.
The exposure of tissue factor promotes coagulation, which,
together with platelet activation, decreases haemorrhage but
at the risk of causing thrombosis and tissue ischaemia. If the
inflammatory process becomes generalised, widespread micro-
circulatory thrombosis can result in disseminated intravascular
coagulation (DIC).
4 • METABOLIC RESPONSE TO INJURY, FLUID AND ELECTROLYTE BALANCE AND SHOCK

and the lateral spinothalamic tract, and further mediate the met-
Table 1.1 Cytokines involved in the acute inflammatory
abolic response in two important ways:
response
Cytokine Relevant actions 1. Activation of the sympathetic nervous system leads to the
release of noradrenaline from sympathetic nerve fibre endings
TNF-α Proinflammatory; release of leucocytes by bone marrow; and adrenaline from the adrenal medulla, resulting in
activation of leucocytes and endothelial cells
tachycardia, increased cardiac output, and changes in
IL-1 Fever; T-cell and macrophage activation carbohydrate, fat and protein metabolism (see later).
IL-6 Growth and differentiation of lymphocytes; activation of the Interventions that reduce sympathetic stimulation, such as
acute-phase protein response epidural or spinal anaesthesia, may attenuate these changes.
IL-8 Chemotactic for neutrophils and T cells 2. Stimulation of pituitary hormone release (see later).

IL-10 Inhibits immune function

IL, Interleukin; TNF, tumour necrosis factor.
Afferent nerve impulses and sympathetic
activation
Tissue injury and inflammation lead to impulses in afferent pain
fibres that reach the thalamus via the dorsal horn of the spinal cord
The endocrine response to surgery
Surgery leads to complex changes in the endocrine mechanisms
that maintain the body’s fluid balance and substrate metabolism,
with changes occurring to the circulating concentrations of many
hormones following injury (Table 1.2). This occurs either as a result
of direct gland stimulation or because of changes in feedback
mechanisms.

Bacterial invasion
Macrophage activation
• Phagocytosis
• Cytokine release Stimulation of afferent
• Prostanoid release nerve impulses
• Protease release Haemorrhage into
injured tissue Plasma cascades activated
Neutrophil accumulation • Coagulation/platelets
• Phagocytosis • Complement
• Cytokine release
• Protease release

Neutrophil–endothelial
cell adherence and
neutrophil migration
Fluid and protein leak
Endothelial activation • Tissue oedema
• Vasodilatation
• Increased capillary
permeability
Fig. 1.1 Key events occurring at the site of tissue injury.

Table 1.2 Hormonal changes in response to surgery and trauma

Pituitary Adrenal Pancreatic Others

" Secretion Growth hormone Adrenaline Glucagon Renin

Adrenocorticotrophic hormone Cortisol Angiotensin
Prolactin Aldosterone
Antidiuretic hormone/arginine vasopressin
Unchanged Thyroid-stimulating – – –
hormone
Luteinizing hormone
Follicle-stimulating
hormone
# Secretion – – Insulin Testosterone
Oestrogen
Thyroid
hormones
 The metabolic response to injury • 5

Consequences of the metabolic Table 1.3 Causes of fluid loss following surgery and
trauma
1
response to injury
Nature of fluid Mechanism Contributing factors
Hypovolaemia Blood Haemorrhage Site and magnitude of
Reduced circulating volume often characterises moderate to tissue injury
Poor surgical haemostasis
severe injury, and can occur for a number of reasons (Table 1.3):
Abnormal coagulation
• Loss of blood, electrolyte-containing fluid or water.
• Sequestration of protein-rich fluid into the interstitial Electrolyte- Vomiting Anaesthesia/analgesia
containing (e.g., opioids)
space, traditionally termed ‘third-space loss’, due to
fluids Obstruction or ileus
increased vascular permeability. This typically lasts Nasogastric drainage Ileus
24–48 hours, with the extent (many litres) and duration Gastric surgery
(weeks or even months) of this loss dependent on the Diarrhoea Antibiotic-related infection
type and severity of tissue injury. For example, it is Enteral feeding
greater following burns, infection or ischaemia– Sweating Pyrexia
reperfusion injury. Water Evaporation Prolonged exposure of
viscera during surgery
Plasma-like Capillary leak/ Acute inflammatory
1.1 Summary fluid sequestration in response
tissues Infection
Factors mediating the metabolic response to injury Burns
The acute inflammatory response Ischaemia–reperfusion
Inflammatory cells (macrophages, monocytes, neutrophils) syndrome
Proinflammatory cytokines and other inflammatory mediators
Endothelium Aldosterone secretion from the adrenal cortex is increased by:
Endothelial cell activation • Activation of the renin–angiotensin system. Renin is released
Adhesion of inflammatory cells from afferent arteriolar cells in the kidney in response to
Vasodilatation reduced blood pressure, tubuloglomerular feedback
Increased permeability
(signalling via the macula densa of the distal renal tubules in
Nervous system response to changes in electrolyte concentration) and
Afferent nerve stimulation and sympathetic nervous system activation activation of the renal sympathetic nerves. Renin converts
Endocrine circulating angiotensinogen to angiotensin (AT)-I. AT-I is
Increased secretion of stress hormones converted by angiotensin-converting enzyme (ACE) in
Decreased secretion of anabolic hormones plasma and tissues (particularly the lungs) to AT-II, which
Bacterial infection causes arteriolar vasoconstriction and aldosterone
secretion.
• Increased adrenocorticotropic hormone (ACTH) secretion by
the anterior pituitary in response to hypovolaemia and
Decreased circulating volume will reduce oxygen and nutrient
hypotension via afferent nerve impulses from stretch
delivery, and so increase healing and recovery times. The neuro-
receptors in the atria, aorta and carotid arteries. ACTH
endocrine responses to hypovolaemia attempt to restore normo-
secretion is also increased by ADH.
volaemia and maintain perfusion to vital organs.
• Direct stimulation of the adrenal cortex by hyponatraemia or
hyperkalaemia.
Fluid-conserving measures Aldosterone increases the reabsorption of both sodium and water
Oliguria, together with sodium and water retention – primarily by distal renal tubular cells with the simultaneous excretion of
due to the release of antidiuretic hormone (ADH) and aldoste- hydrogen and potassium ions into the urine.
rone – is common after major surgery or injury, and may persist Increased ADH and aldosterone secretion following injury usually
even after normal circulating volume has been restored lasts 48–72 hours, during which time urine volume is reduced and
(Fig. 1.2). osmolality increased. Typically, urinary sodium excretion decreases
Secretion of ADH from the posterior pituitary is increased in to 10–20 mmol/24 hours (normal 50–80 mmol/24 hours) and
response to: potassium excretion increases to >100 mmol/24 hours (normal
50–80 mmol/24 hours). Despite this, hypokalaemia is relatively rare
• Afferent nerve impulses from the site of injury
because of a net efflux of potassium from cells. This typical pattern
• Atrial stretch receptors (responding to reduced volume) and
may be modified by fluid and electrolyte administration.
the aortic and carotid baroreceptors (responding to reduced
pressure) Blood flow–conserving measures
• Increased plasma osmolality (principally the result of an Hypovolaemia reduces cardiac preload, which leads to a fall in
increase in sodium ions) detected by hypothalamic cardiac output and a decrease in blood flow to the tissues and
osmoreceptors organs. Increased sympathetic activity results in a compensatory
• Input from higher centres in the brain (responding to pain, increase in cardiac output, peripheral vasoconstriction and a rise
emotion and anxiety). in blood pressure. Together with intrinsic organ autoregulation,
ADH promotes the retention of free water (without electrolytes) by these mechanisms act to try to ensure adequate tissue perfusion
cells of the distal renal tubules and collecting ducts. (Fig. 1.3).
6 • METABOLIC RESPONSE TO INJURY, FLUID AND ELECTROLYTE BALANCE AND SHOCK

Anterior pituitary:
Secretes ACTH

ACTH actions:
• Stimulation of aldosterone
secretion by adrenal cortex
Kidney juxtaglomerular
apparatus (JGA):
Secretes renin
Adrenal gland cortex:
Secretes aldosterone
Renin–angiotensin system

Renin (JGA)
Aldosterone actions:
• Na+ and water retention Angiotensinogen Angiotensin I
from distal renal tubules
• Negative feedback on Angiotensin-
anterior pituitary converting enzyme

Angiotensin II

Angiotensin II actions:
• Stimulates aldosterone
secretion
• Stimulates thirst centres
in brain
• Potent vasoconstrictor

Fig. 1.2 The renin–angiotensin–aldosterone system. ACTH, Adrenocorticotrophic hormone.

Pituitary
Hypothalamus ACTH
Pyrexia Antidiuretic hormone

Adrenal gland
Aldosterone
Cardiovascular system Cortisol
Sympathetic activation Adrenaline (ephinephrine)
Tachycardia

Kidney
Renin–angiotensin system
activation
Liver Na+ reabsorption
Glycogenolysis K+ reabsorption
Gluconeogenesis Urine volumes
Lipolysis Poor erythropoietin response
Ketone body production to anaemia
Acute-phase protein release
Pancreas
Insulin release
Site of injury/surgery Glucagon release
Inflammation
Oedema Skeletal muscle
Endothelial activation Muscle breakdown
Blood flow Release of amino acids into
Afferent nerve stimulation circulation

Bone marrow
Impaired red cell production

Fig. 1.3 Summary of metabolic responses to surgery and trauma.

 The metabolic response to injury • 7

metabolic activity might appear to be of limited utility (e.g.,

1.2 Summary
Urinary changes in metabolic response to injury
# Urine volume secondary to " ADH and aldosterone release
# Urinary sodium and " urinary potassium secondary to " aldosterone
release
" Urinary osmolality
" Urinary nitrogen excretion due to the catabolic response to injury.
Increased energy metabolism and substrate
cycling
The body requires energy to undertake physical work, generate
heat (thermogenesis) and to meet basal metabolic requirements.
Basal metabolic rate (BMR) comprises the energy required for
maintenance of membrane polarisation, substrate absorption
and utilisation, and the mechanical work of the heart and respira-
tory systems.
Although physical work usually decreases following surgery
due to inactivity, overall energy expenditure may rise by 50%
due to increased thermogenesis and BMR (Fig. 1.4).
Thermogenesis
Patients are frequently pyrexial for 24–48 hours following injury (or
infection) because proinflammatory cytokines (principally IL-1)
reset temperature-regulating centres in the hypothalamus. BMR
increases by about 10% for each 1°C increase in body
temperature.
Basal metabolic rate
Injury leads to increased turnover in protein, carbohydrate and
fat metabolism (see below). Whilst some of the increased
glucose–lactate cycling and simultaneous synthesis and degra- 1
dation of triglycerides), it has probably evolved to allow the body
to respond quickly to altering demands during times of extreme
stress.
Catabolism and starvation
Catabolism is the breakdown of complex substances to the con-
stituent parts (glucose, amino acids and fatty acids) that form
substrates for metabolic pathways. Starvation occurs when
intake is less than metabolic demand. Catabolism and starvation
usually occur simultaneously following severe injury or major sur-
gery, with the clinical picture being determined by whichever
predominates.
Catabolism
Carbohydrate, protein and fat catabolism is mediated by the
increase in circulating catecholamines and proinflammatory cyto-
kines, as well as the hormonal changes observed following
surgery.
Carbohydrate metabolism
Catecholamines and glucagon stimulate glycogenolysis in the
liver, leading to the production of glucose and rapid glycogen
depletion. Gluconeogenesis, the conversion of noncarbohydrate
substrates (lactate, amino acids, glycerol) into glucose, occurs
simultaneously. Catecholamines suppress insulin secretion, and
changes in the insulin receptor and intracellular signal pathways
also result in a state of insulin resistance. The net result is hyper-
glycaemia and impaired cellular glucose uptake. While this pro-
vides glucose for the inflammatory and repair processes, severe
hyperglycaemia may increase morbidity and mortality in surgical
patients, and glucose levels should be controlled in the perioper-
ative setting.

Physical work 15% Fat metabolism

Physical work 25%
Thermogenesis 10%
Basal metabolic
rate 65%
Healthy sedentary
70 kg man
• Total energy expenditure
about 1800 kcal/day
Fig. 1.4 Components of body energy expenditure in health and
following surgery.
Thermogenesis 15%
Basal metabolic
rate 70%
24 hours following major
surgery
• Total energy expenditure
increased 10–30%
• Relative reduction in physical
work due to inactivity
• Thermogenesis/heat energy
increased by mild pyrexia
• Basal metabolic rate increased
by raised enzyme and ion
pump activity and increased
cardiac work
Catecholamines, glucagon, cortisol and growth hormone all acti-
vate triglyceride lipases in adipose tissue, leading to the break-
down of triglycerides into glycerol and free fatty acids (FFAs)
(lipolysis). Glycerol is a substrate for gluconeogenesis and FFAs
can be metabolised in most tissues to form ATP. The brain is
unable to use FFAs for energy production and almost exclusively
metabolises glucose. However, the liver can convert FFAs into
ketone bodies that the brain can use when glucose is less
available.
Protein metabolism
Skeletal muscle is broken down, releasing amino acids into the
circulation. Amino acid metabolism is complex, but glucogenic
amino acids (e.g., alanine, glycine and cysteine) can be utilised
by the liver as a substrate for gluconeogenesis, producing glucose
for re-export, while others are metabolised to pyruvate, acetyl
coenzyme-A (acetyl-CoA) or intermediates in the Krebs cycle.
Amino acids are also used in the liver as substrate for the
‘acute-phase protein response’. This response involves increased
production of one group of proteins (positive acute-phase
proteins) and decreased production of another (negative acute-
phase proteins) (Table 1.4). The acute-phase response is
mediated by proinflammatory cytokines (notably IL-1, IL-6 and
TNF-α), and although its function is not fully understood, it is
thought to play a central role in host defence and the promotion
of healing.
8 • METABOLIC RESPONSE TO INJURY, FLUID AND ELECTROLYTE BALANCE AND SHOCK
Table 1.4 The acute-phase protein response
Positive acute-phase proteins (increase after injury)
• C-reactive protein
• Haptoglobins
• Ferritin
• Fibrinogen
• α1-antitrypsin
• α2-macroglobulin
• Plasminogen
Negative acute-phase proteins (decrease after injury)
• Albumin
• Transferrin
The mechanisms mediating muscle catabolism are incom-
pletely understood, but inflammatory mediators and hormones
(e.g., cortisol) released as part of the metabolic response to injury
appear to play a central role. Minor surgery, with minimal meta-
bolic response, is usually accompanied by little muscle catabo-
lism. Major tissue injury is often associated with marked
catabolism and loss of skeletal muscle, especially when factors
enhancing the metabolic response (e.g., sepsis) are also present.
In health, the normal dietary intake of protein is 80–120 g per day
(equivalent to 12–20 g nitrogen). Approximately 2 g of nitrogen are
lost in faeces and 10–18 g in urine each day, mainly in the form of
urea. During catabolism, nitrogen intake is often reduced but
urinary losses increase markedly, reaching 20–30 g/day in patients
with severe trauma, sepsis or burns. Following uncomplicated
surgery, this negative nitrogen balance usually lasts 5–8 days,
but in patients with sepsis, burns or conditions associated with
prolonged inflammation (e.g., acute pancreatitis) it may persist
for many weeks. Feeding cannot reverse severe catabolism and
negative nitrogen balance, but the provision of protein and calories
can attenuate the process. Even patients undergoing uncom-
plicated abdominal surgery can lose 600 g muscle protein (1 g
of protein is equivalent to 5 g muscle), amounting to 6% of total
body protein. This is usually regained within 3 months.
Starvation
This occurs following trauma and surgery for several reasons:
• Reduced nutritional intake because of the illness requiring
treatment
• Fasting prior to surgery
• Fasting after surgery, especially to the gastrointestinal tract
• Loss of appetite associated with illness.
The response of the body to starvation can be described in two
phases (Table 1.5).
Acute starvation is characterised by glycogenolysis and
gluconeogenesis in the liver releasing glucose for cerebral
energy metabolism. Lipolysis releases FFAs for oxidation by
Table 1.5 A comparison of nitrogen and energy losses in a catabolic state and starvationa
Catabolic state
Nitrogen loss (g/day) 20–25
Energy expenditure (kcal/day) 2200–2500
a
Values are approximate and relate to a 70-kg man.
other tissues and glycerol, a substrate for gluconeogenesis.
These processes can sustain the normal energy requirements
of the body (1800 kcal/day for a 70-kg adult) for
approximately 10 hours.
Chronic starvation is initially associated with muscle catabolism
and the release of amino acids, which are converted to glucose
in the liver, which also converts FFAs to ketone bodies. As
described above, the brain adapts to utilise ketones rather than
glucose, and this allows greater dependency on fat
metabolism, so reducing muscle protein and nitrogen loss by
about 25%. Energy requirements fall to about 1500 kcal/day
and this ‘compensated starvation’ continues until fat stores are
depleted when the individual, often close to death, begins to
break down muscle again.
Changes in red blood cell synthesis and
coagulation
Anaemia is common after major surgery or trauma because of
bleeding, haemodilution following treatment with crystalloids or
colloids, and impaired red cell production in bone marrow
(because of low erythropoietin production by the kidney and
reduced iron availability due to increased ferritin and reduced
transferrin binding). Whether moderate anaemia confers a survival
benefit following injury remains unclear, but actively correcting
anaemia in nonbleeding patients after surgery or during critical ill-
ness does not improve outcomes. Evidence from clinical trials
suggests that blood transfusions to correct anaemia following
surgery are not required unless the haemoglobin concentration
has decreased to a concentration of <70–80 g/L.
Following tissue injury, the blood typically becomes hypercoa-
gulable and this can significantly increase the risk of thromboem-
bolism; reasons include:
• Endothelial cell injury and activation, with subsequent
activation of coagulation cascades
• Platelet activation in response to circulating mediators (e.g.,
adrenaline and cytokines)
• Venous stasis secondary to dehydration and/or immobility
• Increased concentrations of circulating procoagulant factors
(e.g., fibrinogen)
• Decreased concentrations of circulating anticoagulants (e.g.,
protein C).
Anabolism
Anabolism involves regaining weight, restoring skeletal muscle
mass and replenishing fat stores. Anabolism is unlikely to occur
until the processes associated with catabolism, such as the
release of proinflammatory mediators, have subsided. This point
is often temporally associated with obvious clinical improvement
in patients, who feel subjectively better and regain their appetite.
Hormones contributing to this process include insulin, growth
hormone, insulin-like growth factors, androgens and the
Acute starvation Compensated starvation
14 3
1800 1500
 Fluid and electrolyte balance • 9

17-ketosteroids. Adequate nutritional support and early mobilisa- of the metabolic response to surgery and injury are sum-
tion also appear to be important in promoting enhanced recovery marised in Table 1.6. 1
after surgery (ERAS).

1.3 Summary
Fluid and electrolyte balance
Physiological changes in catabolism In addition to reduced oral fluid intake in the perioperative period,
Carbohydrate metabolism fluid and electrolyte balance may be altered in the surgical patient
• " Glycogenolysis for several reasons:
• " Gluconeogenesis • ADH and aldosterone secretion, as described earlier
• Insulin resistance of tissues • Loss from the gastrointestinal tract (e.g., bowel preparation,
• Hyperglycaemia ileus, stomas, fistulae)
Fat metabolism • Insensible losses (e.g., sweating secondary to fever)
• " Lipolysis • ‘Third-space’ losses, as described earlier
• Free fatty acids used as energy substrate by tissues • Surgical drains
(except brain) • Medications (e.g., diuretics)
• Some conversion of free fatty acids to ketones in the liver (used • Underlying chronic illness (e.g., cardiac failure, portal
by brain)
hypertension)
• Glycerol converted to glucose in the liver
Careful monitoring of fluid balance and thoughtful replacement
Protein metabolism
of net fluid and electrolyte losses is therefore important in the
• " Skeletal muscle breakdown
• Amino acids converted to glucose in the liver and used as a substrate perioperative period.
for acute-phase proteins
• Negative nitrogen balance Normal water and electrolyte balance
Total energy expenditure is increased in proportion to injury severity
and other modifying factors. Water forms about 60% of total body weight in men and 55% in
women. Approximately two-thirds is intracellular, one-third extra-
Progressive reduction in fat and muscle mass until stimulus for cellular. Extracellular water is distributed between the plasma and
catabolism ends.
the interstitial space (Fig. 1.5A).
The differential distribution of ions (and water) across cell
membranes is essential for normal cellular function. The principal
Factors modifying the metabolic response
extracellular ions are sodium, chloride and bicarbonate, with
to injury the osmolality of extracellular fluid (ECF) (normally 275–295 mOs-
The magnitude of the metabolic response to injury depends mol/kg) determined primarily by sodium and chloride ion concen-
on a number of different factors (Table 1.6) and can be trations. The major intracellular ions are potassium, magnesium,
reduced through the use of minimally invasive techniques, phosphate and sulphate (Fig. 1.5B).
prevention of bleeding and hypothermia, prevention and The distribution of fluid between the intra- and extravascular
treatment of infection, and the use of local or regional anaes- compartments is dependent upon the oncotic pressure of plasma
thetic techniques. Factors that may influence the magnitude and the permeability of the endothelium, both of which may alter

Table 1.6 Factors associated with the magnitude of the metabolic response to injury
Factor Comment
Patient-related factors
Genetic predisposition Genotype determines changes in gene expression in response to injury and/or infection
Coexisting disease Cancer and/or pre-existing inflammatory disease may influence the metabolic response
Drug treatments Antiinflammatory or immunosuppressive therapy (e.g., steroids) may alter response
Nutritional status Malnourished patients have impaired immune function and/or important substrate deficiencies. Malnutrition prior to surgery
is associated with poor outcomes
Acute surgical/trauma-related factors
Severity of injury Greater tissue damage is associated with a greater metabolic response
Nature of injury Some types of tissue injury cause a disproportionate metabolic response (e.g., major burns)
Ischaemia–reperfusion Reperfusion of ischaemic tissues can trigger an injurious inflammatory cascade that further injures organs
injury
Temperature Extreme hypo- and hyperthermia modulate the metabolic response
Infection Infection is associated with an exaggerated response to injury. It can result in systemic inflammatory response syndrome,
sepsis or septic shock
Anaesthetic techniques The use of certain drugs, such as opioids, can reduce the release of stress hormones. Regional anaesthetic techniques
(epidural or spinal anaesthesia) can reduce the release of cortisol, adrenaline and other hormones, but has little effect on
cytokine responses
10 • METABOLIC RESPONSE TO INJURY, FLUID AND ELECTROLYTE BALANCE AND SHOCK

Intracellular
fluid
28 L

Total
2/3
Weight × 0.6 body water
42 L
1/3

Interstitial
Extracellular 3/4 fluid
fluid 10.5 L
14 L 1/4
Plasma 3.5 L

A 70 kg
ECF ICF mmol/l

200
Na+ HCO3

SO4
Mg++

Mg++
Ca++ 150
Others
K+
Protein Protein

HCO3

K+ 100

Na+

Cl– HPO4
50

B 0
Fig. 1.5 Distribution of fluid and electrolytes between the intracellular and extracellular fluid compartments. (A) Approximate water distribution in a 70-
kg man. (B) Cations and anions. ECF, Extracellular fluid; ICF, intracellular fluid.

following surgery, as described previously. Plasma oncotic pres-
sure is primarily determined by albumin.
The control of body water and electrolytes has been described
earlier. Aldosterone and ADH facilitate sodium and water retention
while atrial natriuretic peptide, released in response to hypervolae-
mia and atrial distension, stimulates sodium and water excretion.
In health (Table 1.7):
• 2500–3000 mL of fluid is lost every 24 hours from the kidneys
and gastrointestinal tract, and through evaporation from the
skin and respiratory tract
• Fluid losses are largely replaced through eating and drinking
• A further 200–300 mL of water is provided endogenously every
24 hours by the metabolic oxidation of carbohydrate and fat.
In adults, the normal daily maintenance fluid requirement is 20–
25 mL/kg (2000 mL/day). Newborn babies and children contain
proportionately more water than adults. The daily maintenance
fluid requirement at birth is about 75 mL/kg, increasing to
150 mL/kg during the first weeks of life. After the first month of life,
fluid requirements decrease and the ‘4/2/1’ formula can be used
to estimate maintenance fluid requirements: the first 10 kg of body
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