Cracking

CRACKING THE
MRCS Viva
CRACKING THE
MRCS Viva
A revision guide
Iain Au-Yong MA (Cantab) BMBCh(Oxon) MRCS(Ed)

Specialist Registrar, Department of Radiology, Queens Medical Centre and
Nottingham City Hospital, Nottingham, UK
Simon Howarth MA (Cantab) BMBCh MRCS(Eng) MRCS(Glas)

Honorary Specialist Registrar, Department of Neurosurgery, Cambridge University
Hospitals NHS Foundation Trust and Clinical Research Associate in Neuroimaging,
Department of Radiology, Cambridge University, Cambridge, UK
Tjun Tang MA (Cantab) MB BChir MRCS(Glas)

Specialist Registrar in General Surgery, Eastern Deanery; currently Research
Registrar in Neuroimaging, Departments of Radiology and Vascular Surgery,
Cambridge University Hospitals NHS Foundation Trust, and Cambridge University,
Cambridge, UK
Robert Sayers MD FRCS

Reader in Surgery, Department of Surgery, Vascular Surgery Group,
Leicester Royal Infirmary, Leicester, UK
Hodder Arnold
A MEMBER OF THE HODDER HEADLINE GROUP
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To Amy, for her endless patience and support.
IAY
To my Grandfather who guided me so well and whom I will miss so much.
SPSH
To Mummy and Papa for their love and tireless support over the years.
TT
To Patty
RS
Contents
Foreword xi
Preface xiii
Acknowledgements xv
Abbreviations xvii
PART 1: INTRODUCTION
1 Examination technique and useful tips 3
2 Diagrams and equations for the exam 7
PART 2: APPLIED SURGICAL ANATOMY

3 Abdominal aorta 13
4 Anal canal 15
5 Biliary tree and gallbladder 17
6 Blood supply to the heart 20
7 The diaphragm 22
8 The femoral triangle 24
9 Kidney 26
10 Liver 28
11 Median nerve 31
12 Pancreas 34
13 Phrenic and vagus nerves 36
14 Portal vein and portosystemic anastomoses 39
15 Radial nerve 41
16 Salivary glands 43
17 Stomach 46
18 Thyroid gland and parathyroid glands 49
19 The transpyloric plane of Addison 51
20 Triangles of the neck 53
21 Ulnar nerve 55
22 Ureter 58
PART 3: OPERATIVE SURGERY

23 Anorectal surgery 1: anal fissure and lateral sphincterotomy 63
24 Anorectal surgery 2: fistula in ano and pilonidal sinus 67
25 Anorectal surgery 3: injection sclerotherapy and
haemorrhoidectomy 73
26 Burr holes and lumbar puncture 78
27 Carotid endarterectomy 81
28 Carpal tunnel decompression 87
CONTENTS
29 Circumcision 91
30 Emergency splenectomy 94
31 Femoral and brachial embolectomy 98
32 Femoral hernia repair 102
33 Inguinal hernia repair 106
34 Laparoscopic cholecystectomy and laparoscopy 112
35 Long saphenous varicose vein surgery 117
36 Mastectomy, axillary dissection and breast reconstruction 120
37 Open appendicectomy 125
38 Orthopaedic related approaches and procedures 130
39 Perforated duodenal ulcer and exploratory laparotomy 135
40 Renal transplantation 140
41 Thyroidectomy 144
42 Tracheostomy 148
PART 4: APPLIED SURGICAL PATHOLOGY

43 Pathology definitions: helpful A–Z guide 155
44 Abscess and pus 158
45 Acute inflammation 161
46 Aneurysms 165
47 Asbestos 169
48 Ascites 172
49 Atherosclerosis 177
50 Breast cancer 182
51 Carcinogenesis 189
52 Cell cycle 194
53 Chronic inflammation 197
54 Colorectal cancer 200
55 Diverticula 210
56 Gastro-oesophageal reflux disease (GORD) and Barrett’s oesophagus 214
57 HIV and universal precautions in surgery 219
58 Hyperparathyroidism 224
59 Hyperplasia, hypertrophy and atrophy 227
60 Malignant melanoma 232
61 Portal hypertension 239
62 Thyroid cancer 244
63 Tumour markers 252
PART 5: PRINCIPLES OF SURGERY

64 Abdominal incisions 259
65 Amputation 265
viii
CONTENTS
66 Anastomosis and anastomotic leak 270

67 Antibiotics in surgery 275
68 Bowel preparation 280
69 Clinical governance 283
70 Day surgery 287
71 Diathermy 291
72 Drains in surgery 295
73 DVT prophylaxis and coagulation in surgery 297
74 The hip joint, neck of femur and sciatic nerve 303
75 Local anaesthetics 308
76 Operating theatre design and infection control 312
77 Screening in surgery 316
78 Skin grafting and flap reconstruction 320
79 Statistics and clinical trials 326
80 Stomas 330
81 Surgical sutures and needles 334
82 Tourniquets 339
83 Wound healing, scarring and reconstruction 342
PART 6: APPLIED SURGICAL PHYSIOLOGY

84 Acid–base balance 349
85 Action potential 353
86 Altitude 356
87 Blood pressure control 358
88 Calcium homoeostasis 362
89 Cardiac action potential 366
90 Cerebrospinal fluid and the blood–brain barrier 369
91 Control of respiration 373
92 Functions of the kidney I 376
93 Functions of the kidney II: fluid and electrolyte balance in
the kidney and the loop of Henle 377
94 Functions of the kidney III: endocrine functions of the kidney 381
95 Functions of the kidney IV: other functions 383
96 Functions of the liver 384
97 Functions of the stomach 388
98 Neuromuscular junction 391
99 Oxygen transport 394
100 Pituitary 397
101 Starling forces in the capillaries/oedema 401
102 Starling’s law of the heart and cardiovascular equations 403
103 Swallowing and oesophageal physiology 408
ix
CONTENTS
PART 7: CRITICAL CARE

104 Acute pancreatitis 413
105 Acute respiratory distress syndrome 419
106 Brain-stem death and transplantation 423
107 Burns 427
108 Compartment syndrome 433
109 Criteria for admission to the ITU and HDU 439
110 CVP lines and invasive monitoring 443
111 Fluid balance 452
112 Head injury and intracranial pressure 459
113 Inotropes 466
114 Intubation and ventilation 470
115 Nutrition 477
116 Oliguria and renal replacement 482
117 Pneumothorax 488
118 Pulse oximetry 491
119 Respiratory failure and respiratory function tests 495
120 Sedation 500
121 Sepsis and SIRS 505
122 Shock 510
123 Systemic response to surgery 514
Index 521
x
Foreword
This book is aptly entitled ‘Cracking the MRCS Viva’.
Most of us have been involved over the years in both taking exams and acting as
examiners and understand the problems that are faced by the examinee: what to
learn, what to say and most importantly what not to say. There is no book on the
market that can take the MRCS viva for you, however the authors of this volume
have done their best to do just that; they are all experienced at both taking exams
and being examiners and are therefore well qualified to set out the potential pitfalls
that may exist in viva situations. The book is divided into sections, beginning with
an introduction, which details useful tips on how to take a viva and sets out the
ways in which the candidate would do well. For example, do not lie and never get
angry seem obvious bits of advice but are terribly important. The sections that fol-
low on applied surgical anatomy, operative surgery, applied surgical pathology, prin-
ciples of surgery, applied surgical physiology and critical care are all set out in a
similar fashion and are extremely useful. I have always thought that passing a viva
in any examination depends upon a number of factors, which include presentation
(knowing what to say and what not to say), knowledge, composure, empathy with
the examiners, and some luck. This volume will educate you on how to do all of
these things and do them well. If you read this book and take note of the advice
given then the percentage influence of luck will be reduced considerably and the
pass rate for the exam undoubtedly increased. With the increased complexity of
examinations and the importance placed on the viva voce element of them, this
book is a must for all potential MRCS candidates because it not only tells you how
to behave in a viva but also gives you a very comprehensive list of possible viva ques-
tions related to each topic and then goes through the responses that are required in
some detail.
Sir Peter Bell
Emeritus Professor of Surgery
University of Leicester
Leicester
UK
Preface
The viva section of the MRCS exam is a difficult hurdle that many surgical trainees
find troublesome. There have hitherto been very few educational resources avail-
able to aid the trainee in preparing for this exam, and a lack of understanding of viva
technique and what is expected of the candidate has hindered many candidates’
efforts in the past.
Cracking the MRCS Viva provides a selection of common viva topics, all of which
have featured in the three collegiate exams. The authors consist of a team of regis-
trars who have all recently passed the MRCS exam at London, Edinburgh and
Glasgow, as well as a senior examiner for the current intercollegiate exam.
This book incorporates a novel layout, suggesting an exhaustive list of possible
questions related to each topic and a comprehensive accompanying text designed to
equip the candidate with a full knowledge of each topic. This is in contrast to the
style of many existing books that answer specific questions, which might not be
asked in the same manner in the actual exam.
There is also a novel and thorough system of cross-referencing throughout the
entire book so that all of the topics are cross-referenced to each other to enable ease
of use and to enable pairs or small groups of candidates to practise real-time viva
technique with each other.
The text is interspersed with boxes of example viva questions containing high-yield
facts on the topic, and key learning points are highlighted throughout.
The book incorporates an exhaustive list of simple to reproduce line diagrams for
the exam, as well as a list of important definitions that often constitute the opening
question of the viva, and are important to get exactly right to avoid the inevitable
examiners’ traps. We also present a list of commonly requested equations, and a sys-
tem for tackling all sorts of questions.
This book is not a comprehensive textbook, although each viva topic is considered
in some detail.
The authors sincerely hope that their logical approach to viva technique helps you
through what is no doubt a stressful experience, and arms you with the tools to do well.
IAY
SPSH
TT
RS
Acknowledgements
Thanks to Mr James R Seaward, MA(Cantab), MRCS(Eng), Registrar, Plastic Surgery,

Royal Devon and Exeter Hospital for his major contribution to the writing of this
manuscript.
We thank Sarah Burrows, Georgina Bentliff, Naomi Wilkinson and Francesca Naish
of Hodder Arnold Publishing, and would also like to acknowledge our families and
friends, without whose support this book would never have been published.
Abbreviations
1,25-DHCC 1,25-dihydroxycholecalciferol
5FU 5-fluorouracil
5-HIAA 5-hydroxyindoleacetic acid
!-hCG !-human chorionic gonadotrophin
A&E accident and emergency department
AAA abdominal aortic aneurysm
ABG arterial blood gas
ACEI angiotensin-converting enzyme inhibitor
ACS abdominal compartment syndrome
ACTH adrenocorticotrophic hormone
ADH antidiuretic hormone
AF atrial fibrillation
AFP "-fetoprotein
AIDS acquired immune deficiency syndrome
AP abdominoperineal
APER abdominoperineal excision of rectum
APTT activated partial thromboplastin time
ARDS acute respiratory disease syndrome
ARF acute renal failure
ASA American Society of Anesthesiologists
ASIS anterior superior iliac spine
AST aspartate transaminase
ATLS advanced trauma life support
ATN acute tubular necrosis
AV arteriovenous
BD twice daily
BERT bag for the endoscopic retrieval of tissue
BMI body mass index
BNF British National Formulary
BPH benign prostatic hyperplasia
BP blood pressure
BXO balanitis xerotica obliterans
CABG coronary artery bypass grafting
CAPD continuous ambulatory peritoneal dialysis
CC craniocaudal
CCA common carotid artery
CCK cholecystokinin
ABBREVIATIONS
CDK cyclin-dependent kinase

CEA carotid endarterectomy or carcinoembryonic antigen
CI confidence interval
CIN cervical intraepithelial neoplasia
CME continuing medical education
CMV cytomegalovirus
CNS central nervous system
CO cardiac output
COPD chronic obstructive pulmonary disease
CPAP continuous positive airway pressure
CPK creatine phosphokinase
CRF chronic renal failure
CPP cerebral perfusion pressure
CRH corticotrophin-releasing hormone
CRP C-reactive protein
CSF cerebrospinal fluid
CT computed tomography
CVA cerebrovascular accident
CVP central venous pressure
CVVH continuous venovenous haemofiltration
DCIS ductal carcinoma in situ
DHS dynamic hip screw
DIC disseminated intravascular coagulation
DIEP deep inferior epigastric perforator
DJ duodenojejunal
DPG 2,3-diphosphoglycerate
DRE digital rectal examination
DSA digital subtraction angiography
DVT deep vein thrombosis
ECA external carotid artery
ECF extracellular fluid
ECG electrocardiogram
EGF epidermal growth factor
ELND elective lymph node dissection
EPSP excitatory postsynaptic potential
ERCP endoscopic retrograde cholangiopancreatography
ESR erythrocyte sedimentation rate
ET endotracheal
EUA examination under anaesthetic
EVD external ventricular drain
FAP familial adenomatous polyposis coli
FBC full blood count
xviii
ABBREVIATIONS
FEV1 forced expiratory volume in 1 s

FGF fibroblast growth factor
FFP fresh frozen plasma
FNAC fine-needle aspiration cytology
FOB faecal occult blood
FRC functional residual capacity
FSH follicle-stimulating hormone
GABA #-aminobutyric acid
GCS Glasgow Coma Score
GI gastrointestinal
GH growth hormone
GIP gastric inhibitory peptide
GIT gastrointestinal tract
GMC General Medical Council
GnRH gonadotrophin-releasing hormone
GOJ gastro-oesophageal junction
GORD gastro-oesophageal reflux disease
GTN glyceryl trinitrate
HDL high-density lipoprotein
HDU high dependency unit
HEPA high efficiency particulate air
HIV human immunodeficiency virus
HNPCC hereditary non-polyposis colorectal carcinoma
HPV human papillomavirus
HR heart rate
HTLV-1 human T-cell leukaemia virus 1
IAP intra-abdominal pressure
ICA internal carotid artery
ICAM intercellular adhesion molecule
ICF intracellular fluid
ICP intracranial pressure
IGAP inferior gluteal artery perforator
IL interleukin
IHD ischaemic heart disease
IMHS intramedullary hip screw
INR international normalized ratio
IPPV intermittent positive-pressure ventilation
ITU intensive therapy unit
IV intravenous
IVC inferior vena cava
JVP jugular venous pulse
LCIS lobular carcinoma in situ
xix
ABBREVIATIONS
LDL low-density lipoprotein

LFT liver function test
LH luteinizing hormone
LDH lactate dehydrogenase
LIF left iliac fossa
LMM lentigo maligna melanoma
LMW low molecular weight
LOS lower oesophageal sphincter
LSV long saphenous vein
LVEDV left ventricular end-diastolic volume
MDT multidisciplinary team
MEN multiple endocrine neoplasia
MI myocardial infarction
MMPs matrix metalloproteinases
MODS multiple organ dysfunction syndrome
MRI magnetic resonance imaging
MRSA methicillin-resistant S. aureus
MSSA methicillin-sensitive S. aureus
NJT nasojejunal tube
NGT nasogastric tube
NHL non-Hodgkin’s lymphoma
NICE National Institute for Health and Clinical Excellence
NIPPV non-invasive positive-pressure ventilation
NM nodular melanoma
NMJ neuromuscular junction
NNT numbers needed to treat
NPC nasopharyngeal cancer
NPI Nottingham prognostic index
NSAID non-steroidal anti-inflammatory drug
OGD oesophagogastroduodenoscopy
OPSI overwhelming post-splenectomy infection
OPSS overwhelming post-splenectomy sepsis
ORIF open reduction and internal fixation
PA pulmonary artery
PAF platelet-activating factor
PAFC pulmonary artery flotation catheter
PAN polyarteritis nodosa
PAOP pulmonary artery occlusion pressure
PAWP pulmonary artery wedge pressure
PCA patient-controlled analgesia
PCT proximal convoluted tubule
PCO2 partial pressure of carbon dioxide
xx
ABBREVIATIONS
PCWB pulmonary capillary wedge pressure

PDGF platelet-derived growth factor
PDS polydioxanone sulphate
PE pulmonary embolus
PEEP positive end-expiratory pressure
PEG percutaneous endoscopic gastrostomy
PEJ percutaneous endoscopic jejunostomy
PIP peak inspiratory pressure
PO2 partial pressure of oxygen
PP pancreatic polypeptide
PPI proton pump inhibitor
PR per rectum
PSA prostate-specific antigen
PTFE polytetrafluoroethylene
PTH parathyroid hormone
PVS persistent vegetative state
RAP right atrial pressure
RCT randomized controlled trial
RIF right iliac fossa
RLN recurrent laryngeal nerve
RSD reflex sympathetic dystrophy
SFJ saphenofemoral junction
SGAP superior gluteal artery perforator
SIADH syndrome of inappropriate ADH secretion
SIMV simultaneous intermittent mechanical ventilation
SIRS systemic inflammatory response syndrome
SLE systemic lupus erythematosus
SLNB sentinel lymph node biopsy
SSM superficial spreading melanoma
SV stroke volume
SVR systemic vascular resistance
T3 triiodothyronine
T4 thyroxine
TAP transperitoneal
TB tuberculosis
TCD transcranial Doppler
TDS or t.d.s. three times daily
TEP total extraperitoneal
Tg thyroglobulin
TGF-! transforming growth factor !
TIA transient ischaemic attack
TIPSS transjugular intrahepatic portosystemic stent shunt
xxi
ABBREVIATIONS
TNF tumour necrosis factor

tPA tissue plasminogen activator
TPN total parenteral nutrition
TPR total peripheral resistance
TRH thyroid-releasing hormone
TRAM transverse rectus abdominis myocutaneous
TRUS transrectal ultrasonography
TSH thyroid-stimulating hormone
TV tidal volume
UC ulcerative colitis
U+Es urea and electrolytes
UICC Union Internationale Contre Le Cancer
UTI urinary tract infection
UV ultraviolet
VC vital capacity
VIP vasoactive intestinal polypeptide
VLDL very-low-density lipoprotein
V/Q ventilation/perfusion
VT ventricular tachycardia
VUJ vesicoureteric junction
WCC white cell count
WHO World Health Organization
WLE wide local excision
xxii
1
PART
INTRODUCTION
1 Examination technique and useful tips 3
2 Diagrams and equations for the exam 7
1 Examination technique and useful tips
WHEN DESCRIBING A CONDITION
Consider using the following headings:
Disease:
Definition:
Incidence: Common/Uncommon/Rare
Age:
Sex: M:F
Geography:
Aetiology and risk factors:
Pathogenesis:
Pathology: Macroscopic
Microscopic
Spread: e.g. tumour: haematogenous/lymphatic/local/transcoelomic
Where commonly?
Transmission route for infections
Presentation: Symptoms
Signs
Investigations:
Treatment:
Prognosis: 5- and 10-year survival rates depending on stage of disease
Mnemonic to remember
‘In A Surgeon’s Gown Even Physicians May Make Some Incredibly
Tentative Progress!’
In I Incidence
A A Age
Surgeon’s S Sex
Gown G Geography
Even (A)e Aetiology and risk factors
Physicians P Pathogenesis/Presentation (symptoms/signs)
May M Macroscopic (pathology)
Make M Microscopic (pathology)
Some S Spread
Incredibly I Investigations
Tentative T Treatment
Progress! P Prognosis
3
INTRODUCTION examination technique and useful tips
When working out causes to a condition use the surgical sieve.
Mnemonic to remember
‘INVITED MD’
I Infection
N Neoplasia
V Vascular
I Inflammatory/Idiopathic
T Traumatic
E Endocrine
D Degenerative
M Metabolic
D Drugs
Candidates are encouraged to start off by giving a definition if appropriate.
Example: What is Crohn’s disease?

‘Crohn’s disease is an inflammatory bowel disease of unknown aetiology, that
can affect any part of the bowel from the mouth to anus, and which is associ-
ated with a full thickness inflammation of the bowel wall.’
First impressions are vital in these vivas because there is a limited amount of time
to judge the candidate and most candidates are much alike. If you start well, the
examiner will pass you and you can then try to earn extra marks.
Try to keep talking to minimize the number of questions asked by the examiners.
By getting into the habit of doing this, you can steer the viva the way that you want
and try to pre-empt questions from the examiners!
Start broad and become more specific during your answer. Give examples along the
way to illustrate the principle or show your breadth of knowledge.
Example 1: ‘What can you tell me about the complications of gallstones?’

Answer: Many gallstones are asymptomatic
Complications can be divided into those:
• Within the gallbladder: common examples include:
• biliary colic (chat briefly)
• cholecystitis (ditto)
• mucocele
• empyema
4
• Within the biliary tree:

• obstructive jaundice
• ascending cholangitis
• pancreatitis
• Outside the gallbladder:
• gallstone ileus.
Rare but interesting complications include, for example, gallstone ileus or carcin-
oma of the gallbladder.
Example 2: see ‘Functions of the liver’, Chapter 96, page 384

Try to be a good undergraduate rather than a year 5 or 6 specialist registrar!
Pyramid principle
Stick to the basics first and work up! Try to be methodical as well as logical while
progressing through your answer. Examples:
1. Mention bedside and blood tests before CT/MRI!
2. When asked how to make a diagnosis always say ‘history, examination and
investigation’.
3. If the examiner is asking about a surgical emergency tell them that this is so
and start with ‘airway, breathing and circulation’ to show that you appreciate
the gravity of the problem and that you need to intervene promptly. Often you
need to mention that you would resuscitate the patient before surgery in the
operative surgery viva before detailing surgery.
4. When talking about tumours say benign, malignant, primary and secondary.
5. Try to avoid the ‘medical student syndrome’ and mentioning rare causes
before the more common ones. This greatly irritates the examiner! Try to put
important causes, such as cancers, high on the list too.
6. When talking about complications, discuss under the headings of immediate,
early and late’ and/or ‘general versus specific’.
7. With regards to operative surgery try using the headings ‘preoperative,
intraoperative and postoperative factors’.
8. In the operative surgery section don’t forget preoperative preparation and consent.
If you get stuck try to use the mnemonic mentioned on page 3 if asked about a partic-
ular condition or tumour, or the surgical sieve if you get stuck for causes of a condition.
For the surgical sieve, use the mnemonic ‘INVITED MD’ (infective, neoplastic, vascu-
lar, inflammatory, etc.).The surgical sieve is for looking for causes of something and the
surgeon’s gown is for describing a condition.
If you truly don’t know the answer, say so! What may happen is that the examiner
may suggest a line of reasoning to help you deduce the answer. If it is something very
common and obvious, say ‘of course!’ and everyone will know that you have just
5
forgotten in the stress of the exam. If it is something obscure, with any luck the
examiner will spend the next 2 minutes telling you about it!
Do not lie to the examiners! If they find out they will most probably fail you for
poor integrity or passing you off as unsafe and not knowing your limitations! Try to
avoid waffling because this does not go down well and gives the impression that you
do not know the answer and have not listened carefully to the question!
Several of the authors have said in their vivas: ‘Sir, I do not know the answer to your
question but using first principles I would deduce this … from this. etc.’
Never get angry or disagree with the examiner even if you know that you are right!
Look mainly at the examiner who is asking you the question but keep a regular eye on
the other examiner who may give you surprising non-verbal help or encouragement.
Don’t forget to have a sense of humour – remember that your pair of examiners
will be completely bored, having examined numerous candidates before you.
Remember the ‘KISS’ principle – ‘Keep It Simple Stupid!’
And avoid the ‘KICK’ principle – ‘Keep It Complicated and Knotty!’
6
2 Diagrams and equations that you should be
able to draw and write quickly for the
examination
TIPS
• These will be mainly for physiology and critical care vivas.
• Do not start drawing a graph if you are unable to label the axes and unable
to express the units that they are in. A graph without axes and units is
meaningless!
• Bring a blank piece of paper and pen with you into the exam. It looks
impressive if you can bring it out and start drawing to explain an answer!
Shows thought and organization!
DIAGRAMS
Physiology and critical care
Nerves and muscles
• Schematic diagram of a myelinated axon
• Action potential (cardiac and peripheral nervous)
• Sarcomere
• Neuromuscular junction.
Cardiovascular system
• Frank–Starling curve of the heart
• Cardiac cycle:
• jugular venous pulse (JVP): describe the ‘c’ wave, ‘a’ wave, ‘v’ wave, ‘x descent’
• arterial pressure waveform
• heart sounds
• Swan–Ganz catheter wedge trace
• Draw the compartments of the heart and what the pressures are within the
jugular vein, right atrium, right ventricle, pulmonary artery, left atrium, left
ventricle and aorta at rest
• Oxygen-dissociation curve: causes for a right and left shift; Bohr shift
• Myoglobin curve
• Fetal haemoglobin curve
• Cardiac action potential: explain on your diagram where the different ions
efflux and influx
7
INTRODUCTION diagrams and equations for the exam
• Starling’s law of flux: oedema

• need to know the oncotic, osmotic, capillary and hydrostatic pressures
• the pressure differences between the arterial and venous ends of a capillary
Respiratory system
• Static spirometry trace: label vital capacity (VC), tidal volume (TV), functional
residual capacity (FRC)
• Flow–volume loops for restrictive and obstructive airway disease:
• compliance curve in a stiff lung
• pressure–compliance curve in a mechanically ventilated patient
! !
• VA/Q profile in a standing patient
• Dead space versus a shunt
• PO2 – chemoreceptor firing
!
• graph showing VA versus PO2 (mmHg or kPa)
!
• graph showing VA versus PCO2 (mmHg or kPa).
Kidney
• Nephron (from glomerulus to collecting duct):
• what is absorbed where
• permeability of the different parts
• Concentration of sodium within the loop of Henle
• Describe the thin and thick portions of the loop of Henle
• The countercurrent exchange mechanism
• Functions of the glomerulus and Bowman’s capsule:
• proximal convoluted tubule or PCT
• distal convoluted tubule
• collecting duct
• Volumes of the various body fluid compartments.
Endocrinology
• Feedback loops: calcium metabolism flowchart.
Pathology and principles of surgery

• Audit and the feedback loop
• Cell cycle
• Anal fistulae.
Anatomy and operative surgery

• Surgical incisions
• Schematics of the different colonic resections along with blood supply
• Whipple’s procedure: the different anastomoses.
8
INTRODUCTION diagrams and equations for the exam
EQUATIONS
• Cardiac output:
CO " SV # HR
BP " SV # TPR
• Fick’s principle (for measurement of cardiac output)
• Blood flow
• Vascular resistance (Poiseuille–Hagen formula)
• Wall tension (Laplace’s law)
• Parkland’s formula or at least one formula for fluid replacement in burns
• Creatinine clearance (Cockcroft–Gault) equation
• Henderson–Hasselbalch equation
• Oxygen delivery and consumption equation.
9
2
PART
APPLIED SURGICAL ANATOMY

3 Abdominal aorta 13
4 Anal canal 15
5 Biliary tree and gallbladder 17
6 Blood supply to the heart 20
7 The diaphragm 22
8 The femoral triangle 24
9 Kidney 26
10 Liver 28
11 Median nerve 31
12 Pancreas 34
13 Phrenic and vagus nerves 36
14 Portal vein and portosystemic anastomoses 39
15 Radial nerve 41
16 Salivary glands 43
17 Stomach 46
18 Thyroid gland and parathyroid glands 49
19 The transpyloric plane of Addison 51
20 Triangles of the neck 53
21 Ulnar nerve 55
22 Ureter 58
3 Abdominal aorta
Possible viva questions related to this topic

What are the branches of the abdominal aorta?
In what order do they come off?
At what level does the aorta bifurcate?
Related topics
Topic Chapter Pages
Kidney 9 26
Aneurysms 46 165
LANDMARKS AND RELATIONS

The abdominal aorta starts at level T12 as it traverses the diaphragm. It passes
downwards in the midline in the retroperitoneum.
• Anterior relations: left renal vein, pancreas, lesser sac
• Posterior relations: anterior longitudinal ligament and vertebral bodies
• Right: cisterna chyli, thoracic duct, azygos vein
• Left: duodenojejunal (DJ) flexure.
It ends at L4, where it bifurcates into the common iliac arteries.
13
APPLIED SURGICAL ANATOMY abdominal aorta
BRANCHES
PAIRED BRANCHES (CRANIAL → CAUDAL) LEVEL SUPPLYING
Inferior phrenic artery T12 Adrenal gland and diaphragm
(inferior)
Adrenal artery T12 Adrenal gland
Renal artery L2 Kidneys, adrenal glands, ureter
Gonadal artery L2–3 Gonads, ureters
Lumbar arteries (four pairs) Segmental supply of lumbar
musculature
Iliac arteries (terminal branches) L4 Legs, pelvic viscera
Coeliac trunk T12 Foregut (oesophagus to second
part of the duodenum) plus liver,
spleen and pancreas
Superior mesenteric artery L1 Midgut (duodenum to two-thirds
along transverse colon)
Inferior mesenteric artery L3 Hindgut (transverse colon to
rectum)
Median sacral artery L4 Sacrum
14
4 Anal canal

What is the anatomy of the anal canal?
What is the embryology of the anal canal?
What are the differences between the anal canal above and the anal canal
below the dentate line?
How is faecal continence maintained?
What is the sequence of events in defecation?
Related topics
Topic Chapter Page

Anorectal surgery 3: injection 25 73
sclerotherapy and haemorrhoidectomy
EMBRYOLOGY
The gut starts off as an endoderm tube. The ectoderm invaginates and meets the
endoderm to form the anal canal. Hence, the distal half of the anal canal is ecto-
derm (proctodeum) derived and the proximal half is endoderm derived. This is
important in understanding the differences in characteristics of the two parts.
RELATIONS
• Posteriorly: anococcygeal body and coccyx
• Laterally: ischiorectal fossa
• Anterior: perineal body (both), penis (male), vagina (female).
STRUCTURE
The structure differs above and below the dentate line, which forms the embryo-
logical dividing line between ectoderm and endoderm.
This is a common MRCS question.
15
APPLIED SURGICAL ANATOMY anal canal
ABOVE BELOW
Lined by columnar epithelium Lined by squamous epithelium
Autonomic sensory nerve supply. Hence Somatically innervated inferior rectal
injections above the line are not painful and nerve
this is the target in haemorrhoidectomy
Sensitive to stretch Sensitive to pain/touch/temperature
Hindgut arterial supply – superior rectal Arterial supply is inferior rectal artery
artery from inferior mesenteric artery from internal pudendal artery
Venous drainage into inferior mesenteric Venous drainage into internal pudendal
vein (portal)a vein (systemic)
Lymphatic drainage follows the arterial Lymphatic drainage into internal
supply (superior rectal and inferior pudendal and internal iliac nodes
mesenteric nodes)
Anal columns are present No anal columns
a
Note that this is a site of a portosystemic anastomosis (see Portal vein and portosystemic anasto-
moses, Chapter 14). In portal hypertension varicosities can form here, resulting in rectal varices.
SPHINCTERS
The external sphincter is under voluntary control. It is divided into three parts: sub-
cutaneous, superficial and deep.
The puborectalis sling around the anal canal/lower rectum blends with this. This
sling causes the distal rectum to join the rectum at an acute angle. This mechanism
also helps to maintain continence.
The internal sphincter is under autonomic control. It forms an external muscle coat
at the upper end of the anal canal.
DEFECATION
Faeces arrive at the rectum from emptying of the distal large bowel, giving rise to
the urge to defecate. The intra-abdominal pressure rises with increase in diaphrag-
matic and abdominal muscle pressures. Anal sphincters now voluntarily relax and
the faeces are evacuated.
16
5 Biliary tree and gallbladder

What is the anatomy of the biliary tree?
What is a portal triad?
What is the anatomy of the porta hepatis?
What is Calot’s triangle?
What is Pringle’s manoeuvre?
Related topics
Topic Chapter Page

Portal vein and portosystemic anastomoses 14 39
Liver 10 28
Laparoscopic cholecystectomy and laparoscopy 34 112
DUCTS WITHIN THE SYSTEM

The biliary system is divided into intrahepatic and extrahepatic systems.
The biliary tree starts as bile canaliculi, which divide into bile ductules and small
interlobular tributaries of the bile ducts. These join each other to form larger ducts.
The right hepatic duct drains the right lobe of the liver and the left hepatic duct
drains the left lobe. These two ducts leave the liver at the porta hepatis to become
extrahepatic. They amalgamate to form the common hepatic duct. Distal to this it
accepts the cystic duct, and at this point it is called the common bile duct.
The common bile duct travels with the hepatic artery to its left and the portal vein
behind it in the free edge of the lesser omentum at the porta hepatis. At its most
distal aspect it accepts the pancreatic duct. The common bile duct terminates at
the sphincter of Oddi/ampulla of Vater. This structure is identified as a papilla in
the second part of the duodenum and is cannulated at endoscopic retrograde
cholangiopancreatography (ERCP).
The sphincter of Oddi opens into the medial aspect of the second part of the
duodenum.
RELATIONS OF THE COMMON BILE DUCT

• It is 8 cm in length.
17
APPLIED SURGICAL ANATOMY biliary tree and gallbladder
• It has a 6 mm upper limit of normal diameter, but gets 1mm larger every
10 years after the age of 60. It is also larger post-cholecystectomy.
• It travels in the free edge of the lesser omentum, in the porta hepatis, with and
to the right of the common hepatic artery; both of these structures are in front
of the portal vein (Fig. 5.1).
Liver
Hepatic
artery Lesser omentum
Portal vein (free border)
Stomach
Common bile duct
Figure 5.1
Example viva question

What is Pringle’s manoeuvre?
Pringle’s manoeuvre involves placing a clamp over the free edge of the
lesser omentum and occluding the vessels described above.
It is a useful, temporary measure for controlling heavy bleeding from the
liver, e.g. in trauma, by occluding the liver’s blood supply, because it can be
done quickly.
The common bile duct is divided into three parts:

1. First part: anterior to the opening of the lesser sac.
2. Second part: posterior to the first part of the duodenum.
3. Third part: posterior surface of the head of the pancreas.
18
APPLIED SURGICAL ANATOMY biliary tree and gallbladder

What is Calot’s triangle?
It is a triangle formed by the liver, common hepatic duct and cystic duct.
The cystic artery runs within it. It is important in identification of this
structure at dissection in a laparoscopic cholecystectomy (see
‘Laparoscopic cholecystectomy and laparoscopy’, Chapter 34, page 112).
HISTOLOGICAL LAYOUT OF BILIARY SYSTEM

The liver is divided into functional units, or lobules. At the periphery of each of
these are triads of tubes – bile ductule, terminal hepatic artery branch and terminal
portal vein tributary. These are the portal triads.
Each lobule has a central terminal hepatic venule.
Blood flows from the portal triad (portal vein and hepatic artery) and in the sinus-
oids to the central venule (from the periphery of the lobule to the centre). These
venules then transport blood to the hepatic vein.
Bile flows through the canaliculi in the opposite direction to the portal triads
peripherally.
GALLBLADDER
• Pear-shaped viscus
• Lined with columnar epithelium
• Contains some smooth muscle in the wall
• Can hold 50 mL bile
• Consists of fundus, body and neck
• Lies in the gallbladder fossa attached to ventral surface of the right lobe of the liver
• Neck is continuous with the cystic duct. There can be a small diverticulum at
this point, called Hartmann’s pouch. Stones can impact here.
Arterial supply
Cystic artery.
Venous drainage
Via small veins into the substance of the liver.
Lymphatic drainage
To cystic node in Calot’s triangle (see box above).
19
6 Blood supply to the heart

What is the arterial supply to the heart?
What is the origin of the coronary arteries?
Related topics
Topic Chapter Page

Blood pressure control 87 358
Starling’s law of the heart and cardiovascular equations 102 403
RIGHT CORONARY ARTERY

This arises from the right (anterior) aortic sinus and runs between the pulmonary
trunk and the right auricle.
It gives off a marginal branch at the junction of the posterior interventricular groove
and atrioventricular sulcus, and continues as the posterior interventricular artery.
The posterior interventricular artery continues in the interventricular groove and
anastomoses with the anterior interventricular artery. The marginal branch descends
over the front of the ventricle.
It supplies the right ventricle, sinoatrial node (60 per cent) and atrioventricular node,
and part of the left ventricle.
LEFT CORONARY ARTERY

This arises from the left (posterior) aortic sinus, and divides into the circumflex and
anterior interventricular (left anterior descending) artery on reaching the atrioven-
tricular groove.
The circumflex travels in the atrioventricular sulcus to anastomose with the right
coronary artery.
The anterior interventricular (left anterior descending) travels in the interventricular
groove to anastomose with the posterior interventricular artery.
20
APPLIED SURGICAL ANATOMY blood supply to the heart
The left coronary is larger than the right and supplies the left ventricle. The anasto-
moses are poor and in acute occlusion these arteries are functional end-arteries.
VENOUS DRAINAGE
All veins except for the anterior cardiac veins drain into the coronary sinus, which
opens into the posterior wall of the right atrium. The main tributaries are the great,
middle and small cardiac veins.
The great cardiac vein travels with the anterior interventricular artery and drains
into the left (proximal aspect of) coronary sinus.
The middle cardiac vein travels with the posterior interventricular artery and also
drains into the coronary sinus.
The small cardiac vein also drains into the coronary sinus proximally. The right
marginal vein travels along the inferior surface of the heart and drains into the small
cardiac vein.
The anterior cardiac veins run across the surface of the right ventricle and drain
directly into the right atrium.
21
7 The diaphragm

What openings of the diaphragm do you know? What goes through these
openings?
What are the origins and insertions of the diaphragm? What are its
functions?
What is the innervation of the diaphragm?
How does the diaphragm develop?
Related topics
Topic Chapter Page

Phrenic and vagus nerves 13 36
Key learning points

• Consists of peripheral muscular part and inserts via central tendon,
which fuses with the pericardium
• Bi-domed, reaching the fifth rib at its highest extent
• Two crura – sites of origin of the diaphragm:
• right crus originates in the first three lumbar vertebrae
• left crus arises from the first two lumbar vertebrae
• The right crus acts as a sling around the oesophagus and prevents reflux
• Medial and lateral arcuate ligaments are lateral to the crura and
contribute to the origin of the diaphragm
• Supplied by the phrenic nerve (‘C3, 4, 5 keeps the diaphragm alive’)
DEVELOPMENT
Develops from the septum transversum, pleuroperitoneal membranes, paraxial
mesoderm of the abdominal wall and oesophageal mesenchyme, all of which con-
tribute to it.
The septum transversum, which initially forms an embryonic partition between the
thorax and abdomen between embryonic weeks 5 and 7, eventually becomes the
central tendon.
The crura of the diaphragm are derived from foregut mesenchyme.
22
APPLIED SURGICAL ANATOMY the diaphragm
DIAPHRAGMATIC HERNIAS
These occur through persisting pleuroperitoneal communications (where the above
contributions fail to fuse).
A Morgagni hernia occurs anteriorly, through the foramen of Morgagni, pushing
into the anterior mediastinum.
A Bochdalek hernia herniates through the foramen of Bochdalek, posteriorly.
These can be diagnosed by computed tomography (CT).
Openings
Level Main structure passing through Other structures

T8 Inferior vena cava Right phrenic nerve
T10 Oesophagus Vagus (rhymes)
T12 Abdominal aorta Thoracic duct, azygos vein
Key learning points

Some aide-memoires for the vertebral levels
Vena cava has 8 letters and oesophagus has 10; abdomen aorta has 12.
Or CEA for the order (cava, oesophagus, aorta)
The subcostal nerve is transmitted under the lateral arcuate ligament.

The sympathetic chain passes behind the medial arcuate ligament.
The left phrenic nerve pierces the muscular portion of the diaphragm.
The greater, lesser and least splanchnic nerves pierce the crura of the diaphragm.
FUNCTIONS
• Main muscle of respiration
• Aids venous return to the heart (intermittent increased intra-abdominal
pressure on respiration)
• Straining – defecation and micturition
• Support to the vertebral column.
23
8 The femoral triangle

What are the boundaries of the femoral triangle?
What are the contents of the femoral triangle and their relations?
What are the contents of the femoral canal and what are its borders?
What are/draw me the borders of the femoral triangle(?)
Why is it important to know the relations of the femoral canal?
Related topics
Topic Chapter Page

Femoral hernia repair 32 102
Femoral and brachial embolectomy 31 98
Long saphenous varicose vein surgery 35 117
BOUNDARIES
• Superiorly: inguinal ligament
• Medially: medial border of adductor longus
• Laterally: medial border of sartorius
• Roof: fascia lata
• Floor (medial to lateral): adductor longus, adductor brevis, pectineus, iliopsoas.
24
APPLIED SURGICAL ANATOMY the femoral triangle
CONTENTS
Lateral
ASIS
Nerve
Artery
Ing
ui n
al l Vein
iga
me
nt
Y-fronts!
N Medial
E A
R R
V T V c tubercle
E E E P u bi
R I
Y N
Medial border
F
of sartorius E
M
O
R
A
L
C
A
N Medial border of
A adductor longus
L
Figure 8.1 Femoral canal is a space that allows the femoral vein to expand during increased
venous return, and contains only fat and a lymph node (Cloquet’s) draining the clitoris/penis.
(see Femoral hernia repair; Chapter 32, page 102) Anatomy mnemonic: NAVY (lateral to medial:
nerve, artery, vein, ‘Y fronts’).
NOTE that the nerve is not included within the femoral sheath. The canal, vein and
artery are, however. (The femoral branch of the genitofemoral nerve runs in the
sheath and pierces it anteriorly to supply skin overlaying the triangle.)
25
9 Kidney

Tell me about the anatomy of the kidney?
What are the relations of the kidney?
Describe the blood supply and lymphatic drainage of the kidney.
At what lumbar level do the renal hila lie?
Tell me about the development of the kidney. What common anomalies
do you know?
What is the clinical significance of the left-sided varicocele?
What are the important hilar structures and how are they arranged?
Related topics
Topic Chapter Page

Renal transplantation 40 140
Functions of the kidney I–IV 92–95 376–383
Fluid balance 111 452
Acid–base balance 84 349
Altitude 86 356
The transpyloric plane of Addison 19 51
OVERVIEW OF STRUCTURE
• Retroperitoneal organs, right lower than left on account of the liver; 12 !
6 ! 3 cm. The left hilum lies just above the transpyloric plane (L1) which
passes though the superior pole of the right kidney.
• Enclosed in fibrous capsule and embedded in renal fat, which is itself bounded
by Gerota’s fascia. This is attached to the renal pelvis but there is an inferior
opening, through which pus can track in renal disease.
• Divided into outer cortex and inner medulla. Cortex contains nephrons and the
medullary tissue contains collecting ducts and loops of Henle.
• Cortical pyramids lead into the papillae, which lead to calyces that drain into
the renal pelvis; this, in turn, leads to the ureter. Pyramids are separated by
columns of Bertin.
• Hilum of the kidney medially transmits vein, artery (! 2), ureter, artery (VAUA) –
this is the order from anterior to posterior.
26
APPLIED SURGICAL ANATOMY kidney
RELATIONS
• Posteriorly: diaphragm, quadratus lumborum muscle, psoas (medially);
subcostal, iliohypogastric and ilioinguinal nerves, eleventh and twelfth ribs
• Anteriorly: liver, second part of duodenum and hepatic flexure (right), spleen,
stomach, pancreas and splenic flexure (left).
• Superiorly: suprarenal glands, pleural reflection (also posterior to upper poles).
BLOOD SUPPLY AND LYMPHATIC DRAINAGE

Renal arteries bilaterally, branches of aorta, renal veins drain into the inferior vena
cava (IVC).

What is the clinical significance of a left varicocele?
The left testicular vein drains into the left renal vein (the right directly into
the IVC). A renal cell carcinoma can invade the renal vein and this will
lead to obstruction of the gonadal vein. The first presenting sign of this
may be a varicocele (these tumours may be silent) and these patients
should undergo renal ultrasonography.
Lymphatics follow the renal arteries to para-aortic lymph nodes.
NERVE SUPPLY
Autonomics from the renal sympathetic plexus are distributed via the renal vessels.
They mediate pain and vasomotor tone.
DEVELOPMENT AND ANOMALIES

The definitive kidney, or metanephros, is induced by the primitive ureteric bud (from
the mesonephric duct) to form from the sacral intermediate mesoderm. This happens
at day 32.
The ureteric bud itself is induced to branch by the metanephros. These branches
become the calyces.
The metanephros ascends from the sacral area to the lumbar region. Failure to ascend
results in a pelvic kidney. The kidneys may fuse during ascent and get ‘caught’ under
the inferior mesenteric artery and this leads to a horseshoe kidney.
27
10 Liver

What is the anatomy of the liver?
What do you know about liver segments?
How is the liver divided functionally and anatomically? Why does this
division differ?
Describe the development of the liver.
What surface markings are useful in preparing for a liver biopsy?
Related topics
Topic Chapter Page

Biliary tree and gallbladder 5 17
Systemic response to surgery 123 514
DEVELOPMENT OF THE LIVER

The liver develops embryologically as a ventral endoderm bud off the gut tube.
The gut tube has a dorsal and a ventral mesentery, which attach to the posterior and
anterior abdominal walls, respectively.
The liver forms within the ventral mesentery. The attachment of the ventral mesen-
tery to the anterior abdominal wall becomes the falciform ligament and the lesser
omentum attaches the liver to the gut tube (stomach). The free edge of the lesser
omentum is the point up to which the ventral mesentery involutes embryologically.
As the liver forms within the ventral mesentery, in adulthood, it is almost com-
pletely covered in peritoneum, with the exception of the bare area of the liver.
BLOOD SUPPLY
See also ‘Portal vein and portosystemic anastomoses’, Chapter 14, page 39.
The liver has a dual blood supply:
1. Portal system, which carries 70% of the blood to the liver. This carries the
products of digestion from the gut to the liver for metabolism.
28
APPLIED SURGICAL ANATOMY liver
Key learning points

• The liver is the largest gland in the body
• It lies in the right upper quadrant of the abdomen
• It is divided into two lobes, right and left at the level of the falciform
ligament. The caudate and quadrate lobes are included on the left side
• This is an anatomical division. The functional divide between left and
right is different and follows the blood supply. The dividing line between
the right and left lobes of liver functionally corresponds to a line drawn
down the middle of the gallbladder bed, which corresponds to the divide
between right and left hepatic artery/portal vein territories
• The liver is divided further (by clinicians and radiologists) into eight
segments. The caudate lobe is segment 1 and 2, 3 and 4 are in the left
lobe (anatomical), and 5, 6, 7 and 8 in the right lobe
• The portal vein and hepatic veins are used for division
• The gallbladder is attached to the undersurface of the right lobe of the liver
• Bile produced by liver hepatocytes drains into the biliary system
See ‘Biliary tree and gallbladder’, Chapter 5, page 17 for description of
histological arrangement of lobules and biliary anatomy.
2. Hepatic artery, which carries 30% and brings oxygenated blood to the liver.
Drainage is via the hepatic veins, which drain into the IVC.
Note that embryologically, venous blood bypasses the liver via the ductus venosus.
RELATIONS OF THE LIVER

• Superior: diaphragm
• Inferior: duodenum, stomach, gallbladder, hepatic flexure
• Posterior: right kidney and adrenal, retroperitoneum, oesophagus, aorta, IVC.
Surface markings
Upper border level is with the sixth rib in the midclavicular line. At the upper bor-
der of the liver, the percussion note changes from dull to resonant.
The normal liver span is less than 12.5 cm.
Mesenteric attachments and ligaments of the liver
• Falciform ligament: two-layered fold of peritoneum from umbilicus to superior
surface of liver, longitudinally.
29
APPLIED SURGICAL ANATOMY liver
• Coronary ligament: superiorly, the falciform ligament splits into its two layers;
the right becomes the coronary ligament.
• Left/right triangular: formed from the left layer of falciform ligament.
• Ligament: most extreme part of the coronary ligament is the right triangular
ligament.
• Lesser omentum: attached to lesser curve of the stomach and porta hepatis and
represents the ventral mesentery. Carries the portal vein, hepatic artery and bile
duct in its free edge.
• Ligamentum teres: obliterated umbilical vein. Joins left branch of portal vein in
porta hepatis (see ‘Portal vein and portosystemic anastomoses’, Chapter 14,
page 39).
• Ligamentum venosum: obliterated ductus venosus. Joins left branch of portal
vein to be attached to the superior vena cava.
LYMPHATICS
Liver produces one-third of body lymph.
The lymphatics pass through the porta hepatis nodes and thence to the coeliac
nodes.
NERVE SUPPLY
Coeliac plexus (sympathetic and parasympathetic).
FUNCTIONS
See ‘Functions of the liver’, Chapter 96, page 384.
30
11 Median nerve

What is the course of the median nerve?
What does the median nerve supply in the hand?
How would you test the function of this nerve clinically?
What are the consequences of dividing the median nerve at the level of
the carpal tunnel? Any differences in doing so in the arm?
Related topics
Topic Chapter Page

Carpal tunnel decompression 28 87
Ulnar nerve 21 55
COURSE
• Originates from C5, C6, C7, C8, T1 nerve roots
• Formed from the medial and lateral cords of the brachial plexus in the axilla
• Crosses in front of the brachial artery in the upper arm, having started medial
to it
• Enters the antecubital fossa and passes over coracobrachialis and brachialis.
Key learning point

The median nerve is medial to the brachial artery in the cubital fossa.
• Leaves the antecubital fossa by passing between two heads of pronator teres.
• Travels in the forearm between flexor digitorum superficialis and profundus.
• Gives off anterior interosseus nerve in the forearm. This runs in the forearm on
the interosseus membrane.
• Gives off palmar cutaneous branch just proximal to the wrist. This branch
enters the hand superficial to the flexor retinaculum.
• Enters the carpal tunnel where it divides into terminal branches, which supply
the hand.
31
APPLIED SURGICAL ANATOMY median nerve
MOTOR SUPPLY
• Flexors of the forearm: pronator teres, flexor carpi radialis, palmaris longus,
flexor digitorum superficialis.
• Anterior interosseus nerve supplies flexor pollicis longus and half of flexor
digitorum profundus (the other half supplied by ulnar nerve).
Intrinsic hand muscles

What is the nerve supply of the intrinsic muscles of the hand?
Mnemonic: the ulnar nerve supplies all except ‘LOAF’
Lumbricals (lateral two)
Opponens pollicis
Abductor pollicis brevis
Flexor pollicis brevis
Sensory supply
The nerve supplies the lateral three and a half fingers and lateral two-thirds of the
palm of the hand.
The palmar cutaneous branch supplies the lateral palmar skin. It is spared by divi-
sion of the median nerve at the carpal tunnel.
If the median nerve is divided in the upper arm, this is not spared and the whole
median nerve territory becomes insensate.
32
APPLIED SURGICAL ANATOMY median nerve
CLINICAL TESTS

What are the differences between dividing the median nerve at the elbow
and wrist?
Wrist
Cuts at the wrist or carpal tunnel syndrome are the most common lesions to
cause loss of nerve function at the wrist. This produces loss of motor function
of the small muscles of the hand as described above and sensory loss.
Signs of loss at the wrist
Sensory loss at lateral two-thirds of the hand and lateral three and a half
fingers (see notes above about superficial palmar branch).
Abductor pollicis brevis is the only muscle that will test pure median
nerve function (point patient’s thumb to ceiling with palm upwards and
test resisted abduction of the thumb – try to push the thumb down and
lateral from its base)
Look for thenar wasting in the hand (long-standing injury).
Signs specific to carpal tunnel syndrome
Tinel’s test: tap the carpal tunnel and the patient will experience an
electric shock sensation in the sensory distribution of the nerve.
Phalen’s test: forced flexion of the wrist produces the same symptoms. The
time to reproduce the symptoms is proportional to the severity of compression,
although nerve conduction studies are an adjunct to clinical examination.
Elbow
The long flexors (medial half of flexor digitorum profundus, flexor pollicis
longus) are lost in addition to the pronators (pronator teres) in lesions at
the elbow. Lesions may be produced by sharp trauma or occasionally
supracondylar fractures of the humerus.
Additional clinical signs of loss at the elbow
All of the above PLUS:
Hand held supinated, loss of pronation.
Loss of flexion of distal phalanx of thumb (flexor pollicis longus).
Ask the patient to make a fist and the index and middle fingers will remain
straight (loss of flexor digitorum profundus).
In prolonged lesions loss of muscle bulk in the flexor compartment of the
forearm.
33
12 Pancreas

Tell me about the anatomy of the pancreas?
What are the relations of the pancreas?
What are the blood supply and lymphatic drainage of the pancreas?
Tell me about the development of the pancreas and any abnormalities
that may arise as a result of developmental errors?
What is the accessory duct of Santorini and how is it derived?
Related topics
Topic Chapter Page

Acute pancreatitis 104 413
Emergency splenectomy 30 94
OVERVIEW OF STRUCTURE
• Exocrine and endocrine gland
• Retroperitoneal organ, crosses transpyloric plane (Chapter 19, page 51)
• Divided into head, body and tail
• Head lies within concavity of duodenum and pancreatic duct drains into
second part
• Tail lies in the lienorenal ligament and contacts the hilum of the spleen. It can
be damaged in a splenectomy, leading to fistula formation.
RELATIONS
• Posteriorly (right to left): common bile duct, portal vein, splenic vein, IVC,
aorta, superior mesenteric artery origin, left psoas muscle, left kidney and
adrenal, hilum of spleen.
• Anteriorly: transverse colon, transverse mesocolon, lesser sac, stomach.
BLOOD SUPPLY AND LYMPHATIC DRAINAGE

• Splenic artery and superior and inferior pancreaticoduodenal arteries
34
APPLIED SURGICAL ANATOMY pancreas
• Corresponding veins drain into portal system

• Lymphatics follow the arteries to coeliac and superior mesenteric nodes.
NERVE SUPPLY
Sympathetic and branches of the vagus.
DEVELOPMENT AND ANOMALIES

The pancreas forms by the fusion of dorsal and ventral pancreatic buds. Both arise
from the gut tube on day 26 at the level of the duodenum.
The ventral pancreatic bud migrates posteriorly around the duodenum and fuses
with the dorsal bud; it becomes the uncinate process.
Occasionally, there are two ventral buds and if these migrate in opposite directions
(anteriorly and posteriorly), this results in an annular pancreas.
The duct systems of the two buds becoming interconnected when the buds fuse.
The ventral pancreatic duct usually becomes the main pancreatic duct and the dor-
sal duct involutes. If the dorsal duct persists, it is called the accessory duct of
Santorini and it empties into the duodenum at a duodenal papilla.
35
13 Phrenic and vagus nerves

What is the course of the phrenic nerve?
What is the course of the vagus nerve?
What would be the effect on respiration of a spinal cord transection at C6?
Related topics
Topic Chapter Page

The diaphragm 7 22
PHRENIC NERVE
Provides motor and sensory supply to the diaphragm.
Course
RIGHT LEFT
Arises from anterior rami of C3–5 between scalenus medius and anterior
MRCS viva
Mnemonic: C3, 4, 5 keeps the diaphragm alive
Runs on scalenus anterior in the neck

Enters the thorax via the thoracic inlet, posterior to the subclavian vein
Travels anterior to the vagus
Travels lateral to the right brachiocephalic Crosses anterior to the aortic arch
vein and SVC (compare vagus)
On surface of fibrous pericardium Anterior to left pulmonary artery
Overlying right atrium, then IVC Lateral to left ventricle within
fibrous pericardium
Travels in front of the root of the lung
Pierces diaphragm Passes into abdominal cavity via
caval orifice
36
APPLIED SURGICAL ANATOMY phrenic and vagus nerves
Key learning point

Mnemonic: phrenic front

What would be the effect of a spinal cord transection at C6 on respiration?
The phrenic nerves, given off already at the level of C3–5 would be intact
and the patient’s diaphragm would not be paralysed. However, the
intercostals below would not be spared, leading to some difficulties with
ventilation despite sparing of the diaphragm itself. Chronically, immobility
and weakness of the chest wall could lead to lower respiratory tract
infections.
VAGUS NERVE
• Tenth cranial nerve (X)
• Visceral sensory and motor autonomic supply to most abdominal organs
• Also has motor branches to laryngeal muscles (superior and recurrent laryngeal
nerves).
Course
RIGHT LEFT
Fibres originate from medulla
Exit the cranium via the jugular foramen, forming two ganglia here
Passes down the neck in the carotid sheath (posteriorly) adjacent to oesophagus
Gives off superior, internal and external laryngeal branches in the neck
Passes into thoracic cavity via thoracic inlet behind the lung
Recurrent laryngeal nerve given off at Recurrent laryngeal nerve given off at
root of neck and hooks behind level of arch of aorta and hooks behind it
subclavian artery at level of ligamentum arteriosum
Travels behind the root of the lung (see above)
Travels behind oesophagus Travels in front of oesophagus
Travel into abdomen via oesophageal opening (T10) and forms oesophageal plexus
37
APPLIED SURGICAL ANATOMY phrenic and vagus nerves

What is the consequence of bilateral recurrent laryngeal nerve division?
This is a surgical emergency, because it would lead to adduction of both
the true vocal cords and hence acute airway obstruction. Surgical
cricothyroidotomy and tracheostomy are indicated. This is a rare complication
of thyroidectomy (see ‘Thyroidectomy’, Chapter 41, page 144).
38
14 Portal vein and portosystemic anastomoses

What is a portal system?
How is the portal vein formed?
What is the course of the hepatic portal vein?
Where are the portosystemic anastomoses?
What are the clinical effects of portal hypertension on the portosystemic
anastomoses?
Related topics
Topic Chapter Page

Liver 10 28
Pituitary 100 397

What is a portal circulation? Where in the body would you find one?
• Two sets of capillaries in series
• Seen in hepatic portal system described here, and in the pituitary
• The pituitary portal system starts as capillaries in the hypothalamus, and
ends as capillaries in the anterior pituitary gland. It carries releasing
hormones from the hypothalamus to the pituitary (see ‘Pituitary’,
Chapter 100, page 397).
HEPATIC PORTAL SYSTEM

This system begins as portal capillaries in the organs drained (gut organs) and ends
as capillaries within the liver.
Portal vein – anatomy and relations

• Formed behind the pancreatic neck by union of the superior mesenteric and
splenic veins at the level of L2, right of the midline
• Length 5 cm
39
APPLIED SURGICAL ANATOMY portal vein and portosystemic anastomoses
• Runs posterior to the first part of the duodenum

• Runs in the free edge of the lesser omentum into the porta hepatis, with and
posterior to the bile duct and hepatic artery.
Portosystemic anastomoses
These are areas where the portal capillaries are in continuation with systemic capil-
laries. Blood does not usually flow from portal to systemic; it flows preferentially to
the liver.
In portal hypertension, blood can flow from portal to systemic and these anasto-
moses become dilated, with clinical consequences:
Sites of anastomosis
Site Portal vessel Systemic vessel Clinical consequence

Lower third of Left gastric vein Azygos veins Oesophageal
oesophagus varices
Anal canal Superior rectal vein Middle/inferior Rectal varices
rectal veins
Umbilicus Paraumbilical veins Superficial anterior Caput medusae
abdominal wall veins
Retroperitoneal Colic and splenic veins Lumbar veins Retroperitoneal
bleeding
Bare area of liver Hepatic veins Phrenic veins
40
15 Radial nerve

What is the course of the radial nerve?
What is the effect of dividing the radial nerve?
What coexisting injuries would you be worried about if a patient suffers
a spiral fracture of the humerus?
Related topics
Topic Chapter Page

Median nerve 11 31
Ulnar nerve 21 55
COURSE
• C5–T1 nerve roots
• Arises from the posterior cord of the brachial plexus
• Posterior cutaneous nerve of the forearm is given off in the axilla
• Passes between the long and medial heads of triceps
• Passes adjacent to and in contact with the humerus in the spiral groove,
posteriorly, accompanied by the profunda vessels
• Pierces the anconeus muscle, supplying it
• Continues into antecubital fossa between brachialis and brachioradialis muscles.
It supplies the elbow joint
• Divides into deep and superficial branches in antecubital fossa
• The superficial radial nerve is sensory and supplies the hand
• The deep part is motor and continues into the forearm where it supplies the
extensors of the forearm.
MOTOR SUPPLY
Radial nerve
Triceps, brachialis (small part), brachioradialis.
Deep radial nerve
Extensors of the forearm: extensor digitorum, extensor digiti minimi, extensor carpi
ulnaris, abductor pollicis longus, extensor pollicis longus, extensor pollicis brevis,
extensor indicis.
41
APPLIED SURGICAL ANATOMY radial nerve
SENSORY SUPPLY
• Radial one and a half fingers dorsally
• Supplied by the superficial branch of the radial nerve
• Skin on the back of the posterior aspect of the forearm supplied by the
posterior cutaneous nerve of the forearm.
CLINICAL ASSESSMENT

What coexisting injuries would you be worried about if a patient suffers a
spiral fracture of the humerus?
The examiner is asking what the effects of division of the radial nerve are
at the level of the spiral groove.
Function of the superficial and deep branches of the radial nerve in the
forearm is lost. This leads to loss of sensation and muscle power. If the
radial nerve is divided the patient will suffer a wrist drop. This is caused by
paralysis of the extensors of the forearm, leading to unopposed action of
the flexors.
Loss of grip strength occurs because synergy of flexors and extensors is
required for gripping and the paralysis results in loss of this.
Paraesthesiae should be tested for over the first dorsal interosseus.
42
16 Salivary glands

What is the anatomy of the parotid and submandibular glands? Show me
their surface anatomy on this skull.
What structures are at risk in surgery of these glands?
Related topics
Topic Chapter Page

Triangles of the neck 20 53
PAROTID GLAND
Anatomy
• Paired glands
• Largest of the salivary glands
• Serous gland
• Wedge shaped
• Surrounded by connective tissue capsule (investing layer of deep cervical
fascia)
• Divided into superficial and deep lobes by the five divisions of the facial
nerve
• Overlies the angle of the mandible
• Superior margin extends behind the temporomandibular (TM) joint
• Anterior margin superficial to masseter muscle
• Deep part of gland between medial pterygoid and ramus of mandible
• Parotid duct from facial process of gland (anterior aspect) over masseter. Pierces
buccinator muscle; course is submucosal until it opens into a papilla opposite
the upper second molar tooth.
Contents – lateral to medial

• Facial nerve and branches
• Retromandibular vein
• External carotid artery
• Parotid lymph nodes.
43
APPLIED SURGICAL ANATOMY salivary glands
These structures are at risk at surgery. At superficial parotidectomy the facial nerve
is preserved and the plane that it forms between the superficial and deep parts of
the gland is dissected.
Blood supply
External carotid artery.
Lymphatic drainage
Parotid and deep cervical nodes.
SUBMANDIBULAR GLANDS
Anatomy
• Paired glands
• Mixture of serous and mucinous acini
• Connective tissue capsule, derived from the investing layer of deep cervical
fascia
• Consists of a superficial and deep part, in continuity with each other around the
posterior border of mylohyoid, which divides the two parts
• Superficial part lies within the digastric triangle (anterior triangle) (see
‘Triangles of the neck’, Chapter 20, page 53).
Relations
• Lateral: medial aspect of mandible, and below this, facial nerve (cervical) and
facial vein
• Medial: hyoglossus and styloglossus
• Anteriorly: anterior belly of digastric
• Posteriorly: stylohyoid, posterior belly of digastric, lingual and hypoglossal
nerves
• Superiorly: lingual nerve
• Inferiorly: hypoglossal nerve.
Submandibular duct (Wharton’s duct) emerges from the anterior aspect of the
gland, and travels lateral to the tongue in the submucosa; it is crossed twice by the
lingual nerve and opens into a papilla just lateral to the frenulum of the tongue.
Blood supply
Facial and lingual arteries.
Lymphatic drainage
Submandibular, deep cervical nodes.
44
APPLIED SURGICAL ANATOMY salivary glands
The marginal mandibular branch of the facial nerve is at risk in submandibular sur-
gery, so the incision is made low. The angle of the mouth will droop if the nerve is
divided at surgery.
SUBLINGUAL GLANDS
Anatomy
• Smallest of the three glands
• Paired glands
• Serous and mucinous acini, predominantly the latter
• Situated submucosally, beneath the floor of the mouth near the midline.
Relations
• Anterior: opposite gland
• Posterior: deep submandibular gland
• Medial: genioglossus, lingual nerve
• Lateral: mandible
• Inferior: mylohyoid muscle.
Several ducts open into the floor of the mouth, adjacent to the submandibular duct
opening.
45
17 Stomach

What are the different parts of the stomach?
What are attached to the lesser and greater curvatures of the stomach?
What are the anterior and posterior relations of the stomach?
What is the arterial blood supply to the stomach? What is the relevance
of knowing this in relation to performing an oesophagectomy?
What is the gastric innervation?
What are the results of denervation of the stomach?
Related topics
Topic Chapter Page

GORD and Barrett’s oesophagus 56 214
Vagus and phrenic nerves 13 36
STOMACH
Roughly J shaped. It consists of:
• Fundus
• Cardia
• Body
• Antrum
• Pylorus.
Relations
Anteriorly
• Abdominal wall
• Left costal margin
• Diaphragm
• Left lobe of the liver.
Posteriorly
• Lesser sac – this separates the stomach from the pancreas
• Transverse mesocolon
• Left colic flexure
• Upper pole of the left kidney
46
APPLIED SURGICAL ANATOMY stomach
• Left suprarenal gland

• Spleen and splenic artery.
Superiorly
• Left dome of the diaphragm.
The lesser omentum is attached along the lesser curvature of the stomach, the greater
omentum along the greater curvature. These omenta contain the vascular and lym-
phatic supply of the stomach.

What is the blood supply of the stomach?
• Left gastric artery – coeliac axis
• Right gastric artery – hepatic artery
• Right gastroepiploic artery – from the gastroduodenal branch of the
hepatic artery
• Left gastroepiploic artery – from the splenic artery
• Short gastric arteries – from the splenic artery.
Both sets of arteries anastomose with each other on their respective gastric
curvatures and then anastomose with the supply of the other curve.
During oesophagectomy, the short gastrics, left gastroepiploic and left gastric arter-
ies are divided to mobilize the upper part of the stomach, so that it can be pulled
up to form the neo-oesophagus. The stomach then derives its blood supply solely
from the right gastric and gastroepiploic arteries and their anastomoses.
Venous drainage
Corresponding veins drain into the portal system.
Lymphatic drainage
This accompanies its blood vessels. Stomach can be divided into three drainage
zones:
• Area I: superior two-thirds drains along left and right gastric vessels to aortic nodes.
• Area II: right two-thirds of the inferior third of the stomach drains along the
right gastroepiploic vessels to the subpyloric nodes and then to the aortic nodes.
• Area III: left third of the greater curvature drains along the short gastric arteries
and splenic vessels lying in the gastrosplenic and lienorenal ligaments, then via
the suprapancreatic nodes to the aortic group.
47
APPLIED SURGICAL ANATOMY stomach
Clinical implication
Extensive lymphatic drainage and technical difficulty of complete removal make
stomach cancer surgery difficult, with poor results. Involvement of the nodes
around the splenic vessels can be dealt with by removal of the spleen and the liga-
ments, body and tail of the pancreas; gastroepiploic lymph nodes are removed by
excising the greater omentum, but appreciate the difficulty of removing the lymph
nodes around the aorta and head of the pancreas!
Gastric innervation
The anterior and posterior vagi control motility and secretion.
They enter the abdomen through the oesophageal hiatus.
The anterior vagus lies close to the stomach wall. It supplies cardia and lesser curve,
and runs together with the left gastric artery. At this level, it is referred to the anter-
ior nerve of Latarget. It gives branches to the anterior stomach and a large hepatic
branch to the pyloric antrum.
The posterior vagal trunk runs down the back of the lesser omentum behind the
anterior trunk as the posterior nerve of Latarget. It supplies anterior and posterior
aspects of the body of the stomach. The bulk of the nerve forms the coeliac branch.
Truncal vagotomy was previously an operation for complicated peptic ulcer disease.
Truncal vagotomy of both trunks at the lower oesophagus reduces gastric secretion
and paralyses the pyloric antrum. Therefore it must be coupled with a drainage
procedure such as a pyloroplasty or gastrojejunostomy to avoid gastric stasis.
• Highly selective vagotomy divides the individual nerves as they supply the acid-
producing body and antrum, leaving the pylorus intact.
• Posterior truncal vagotomy leaves anterior pyloric nerves intact. It is coupled
with an anterior seromyotomy.
Vagotomy is a historical procedure, and these days it is very rarely performed.
48
18 Thyroid gland and parathyroid glands

What is the anatomy of the thyroid gland?
Describe the nerve supply of the thyroid gland.
What layers of the neck need to be divided at thyroidectomy?
What is the blood supply of the thyroid gland?
What are the positions of the parathyroids? Which are more constant?
What colour is a normal parathyroid?
How might a parathyroid be identified at surgery?
Plus questions related to thyroidectomy topic.
Related topics
Topic Chapter Page

Thyroidectomy 41 144
Phrenic and vagus nerves 13 36
Thyroid cancer 62 244
THYROID GLAND
Anatomy
• Has two lobes (right and left)
• Connected by a narrow central isthmus
• Pyramidal lobe sometimes presents projecting up from the isthmus
• Surrounded by sheath derived from pretracheal layer of deep cervical fascia
• Found in the anterior triangle of the neck
• Consists of follicular tissue (produces thyroxine or T4 and triiodothyronine or
T3) and medullary C-cells (produce calcitonin).
Relations
• Posterolateral: carotid sheath (common carotid artery, internal jugular vein,
vagus nerve)
• Anterolateral: strap muscles
49
APPLIED SURGICAL ANATOMY thyroid gland and parathyroid glands
• Medially: larynx, trachea, oesophagus, recurrent laryngeal nerve. Branch of

vagus nerve (in the groove between trachea and oesophagus) – see ‘Phrenic and
vagus nerves’, Chapter 13, page 36.
Blood supply
Important for the surgeon to know; commonly asked in vivas.
• Two arteries (superior, inferior)
• Three veins (superior, middle, inferior)
• Superior thyroid artery, branch of the external carotid artery
• Inferior thyroid artery, branch of the thyrocervical trunk, from the subclavian
artery
• Superior and middle thyroid veins drain into the internal jugular vein
• Inferior thyroid vein drains into the left brachiocephalic vein.
See ‘Thyroidectomy’, Chapter 41, page 144.
Lymphatic drainage
Deep cervical nodes.
Development
Embryologically, the thyroid gland descends embryologically from the foramen
cecum, which lies at the divide between the anterior two-thirds and the posterior
third of the tongue, guided by the thyroglossal duct, to its final position anterior to
the trachea.
The duct hooks behind the hyoid bone, which is important to remember in surgery
of thyroglossal cysts (remnants of the duct) because this part must be excised, with
the central part of the hyoid bone (Sistrunk’s operation).
PARATHYROID GLANDS
• Four in number
• Secrete parathyroid hormone (PTH) and mediate calcium homoeostasis (see
‘Calcium homoeostasis’, Chapter 88, page 362)
• Ochre in colour; can be stained by administration of methylene blue, which
stains them blue
• Two superior glands lie at the posterior border at the level of the mid-thyroid
• Two inferior glands are much more variable in position, at the inferior thyroid;
they can lie in the thyrothymic ligament or even the superior mediastinum
• Supplied by the superior and inferior thyroid arteries.
50
19 The transpyloric plane of Addison

What is the transpyloric plane?
At what level is the transpyloric plane found?
What are the surface markings for the transpyloric plane?
What structures are found in this plane?
What are the surface markings of the gallbladder?
What is the subcostal plane?
At what level does the abdominal aorta bifurcate?
What is the interrelationship of the common iliac artery, vein and distal
ureter?
What dermatome surrounds the umbilicus?
Related topics
Topic Chapter Page

Abdominal aorta 3 13
Kidney 9 26
Pancreas 12 34
Ureter 22 58
SURFACE MARKING OF THE GALLBLADDER

Level of the ninth costal cartilage in the midclavicular line.
THE SUBCOSTAL PLANE

This passes across the lower margins of the thoracic cage formed by the tenth costal
cartilage on each side.
It is also at the level of the third lumbar vertebra and at the level of the origin of the
inferior mesenteric artery.
51
APPLIED SURGICAL ANATOMY the transpyloric plane of Addison

What is the transpyloric plane?
The transpyloric plane of Addison is a plane perpendicular to a line
connecting the jugular notch and the pubic symphysis; it passes through
the body of L1 vertebra.
It is approximately halfway between the xiphisternum and umbilicus
Surface anatomy: a hand’s breadth below the xiphoid process
Structures found at this level: 12!
Important structures are found at this level, which is why it is frequently
asked about!
• Fundus of gallbladder (see ‘Biliary tree and gallbladder’, Chapter 5, page 17)
• Lower border of L1 vertebra
• Spinal cord ends
• Pylorus of stomach (see ‘Stomach’, Chapter 17, page 46)
• Neck of pancreas (see ‘Pancreas’, Chapter 12, page 34)
• Attachment of the transverse mesocolon
• Superior mesenteric artery branching off the aorta
• Portal vein formed from the superior mesenteric vein and splenic vein
(see ‘Portal vein and portosystemic anastomoses’, Chapter 14, page 39)
• Hilum of spleen
• Hilum of both kidneys and their vascular pedicles (see ‘Kidney’, Chapter 9,
page 26)
• Duodenojejunal (DJ) junction
TOPICS RELATED TO THE MAIN THEME

The abdominal aorta bifurcates at the level of the umbilicus or the fourth lumbar
vertebra slightly to the left of the midline (see ‘Abdominal aorta’, Chapter 3,
page 13).
The umbilicus is at the level of the L4 vertebra and its dermatome is T10.
The common iliac artery lies slightly anterior to the corresponding vein. The distal
ureter travels anterior to both these structures (see ‘Ureter’, Chapter 22, page 58).
52
20 Triangles of the neck

What are the triangles of the neck?
What are the borders of the triangles of the neck?
What are the contents of the triangles?
What is the surface anatomy of the anterior and posterior triangles of
the neck?
What structures could be damaged in a stabbing injury to the neck?
Related topics
Topic Chapter Page

Carotid endarterectomy 27 81
Tracheostomy 42 148
Salivary glands 16 43
TRIANGLES
• Posterior triangle
• Anterior triangle.
They are subdivided into: submental, digastric, carotid and muscular.
POSTERIOR TRIANGLE
Borders
• Anterior: posterior border of sternocleidomastoid
• Posterior: anterior border of trapezius
• Inferior: clavicle.
Contents
• Muscles (floor of triangle): splenius capitis, levator scapulae, scalenus medius
(scalenus anterior), (serratus anterior)
• Nerves: branches of cervical plexus, spinal accessory nerve (travels from one-
third of the way down posterior border of sternocleidomastoid to trapezius);
trunks of brachial plexus
• Other: lymph nodes (occipital/supraclavicular), subclavian artery. Transverse
cervical and suprascapular vessels.
53
APPLIED SURGICAL ANATOMY triangles of the neck
Key learning point

Mnemonic: the trunks are in the triangle – to remind you which part of the
brachial plexus is here.
ANTERIOR TRIANGLE
Borders of anterior triangle
• Midline
• Posterior border of sternocleidomastoid
• Ramus of mandible.
Subtriangles
• Carotid triangle: sternocleidomastoid, posterior belly of digastric, superior belly
of omohyoid. Key contents: common and external carotid artery.
• Digastric triangle: mandible, anterior and posterior bellies of digastric. Key
contents: submandibular gland (see ‘Salivary glands’, Chapter 16, page 43).
• Submental triangle: anterior bellies of digastric, body of hyoid. Key contents:
anterior jugular veins.
• Muscular triangle: sternocleidomastoid, superior belly of omohyoid, midline.
Key contents: larynx and trachea, thyroid gland and parathyroid glands (see
‘Thyroid gland and parathyroid glands’, Chapter 18, page 49).
Contents
• Muscle: suprahyoid muscles (digastric, stylohyoid, mylohyoid, geniohyoid)
• Strap muscles (thyrohyoid, sternothyroid, sternohyoid)
• Nerves: recurrent and external laryngeal nerves (from vagus nerve)
• Vagus nerve (in carotid sheath – see ‘Phrenic and vagus nerves’, Chapter 13,
page 36), ansa cervicalis, hypoglossal nerve
• Vessels: common carotid artery and bifurcation, branches of external; internal
jugular vein
• Other: thyroid gland, parathyroid glands, submandibular gland, trachea and
oesophagus.

What structures could be damaged in a stabbing injury to the neck?
This question requires the candidate to divide the neck into triangles, as
above, and then to go through each region methodically in terms of
structures (structures, muscles, nerves, arteries).
Mention the most important structures first.
54
21 Ulnar nerve

What is the course of the ulnar nerve?
What does the ulnar nerve supply in the hand?
How would you test the function of this nerve clinically?
What is the ulnar paradox?
What do the lumbricals do and how many are there?
What do the interossei do and how many are there?
How can you distinguish ulnar nerve injuries from other nerve injuries
by examining the hand?
Related topics
Topic Chapter Page

Radial nerve 15 41
Median nerve 11 31
COURSE
• Originates from C7, C8, T1 nerve roots
• Formed from medial cord of the brachial plexus in the axilla
• Runs between axillary artery and vein in the upper arm
• Lies on coracobrachialis in the arm, medial to the brachial artery
• Passes behind the medial epicondyle of the humerus
• Passes between the two heads of flexor carpi ulnaris, supplying it
• In the forearm it lies between flexor digitorum profundus and flexor carpi
ulnaris
• Passes superficial to the carpal tunnel
• Divides into terminal branches at the pisiform bone.
MOTOR SUPPLY
Forearm
Ulnar half of flexor digitorum profundus, flexor carpi ulnaris.
55
APPLIED SURGICAL ANATOMY ulnar nerve
Intrinsic hand muscles

Supplies all intrinsic muscles of the hand with four exceptions: ‘LOAF’ supplied by
median nerve – two lateral lumbricals, opponens pollicis, abductor pollicis brevis
and flexor pollicis brevis.

What is the ulnar paradox?
Division of the ulnar nerve at the wrist produces severely clawed ulnar fin-
gers as the lumbricals and interossei are lost. Flexor digitorum profundus
is intact, producing further flexion. In lesions at the elbow (a more ‘serious’
lesion, because more nerve is lost), flexor digitorum profundus is now
paralysed. Paradoxically, the claw hand is not as bad, because the extra
flexion of the ulnar two fingers that this muscle provides is lost.

What do the lumbricals do and how many are there?
There are four lumbrical muscles, the lateral two supplied by the median
nerve (see ‘Median nerve’, Chapter 11, page 31) and the medial two by the
ulnar nerve.
They originate from the flexor digitorum profundus tendons and insert
into the corresponding extensor expansion.
They flex the metacarpophalangeal joints and extend the interphalangeal
joints. They are responsible, in conjunction with the interossei, for coordinating
fine movements of the fingers such as writing or playing a musical instrument.

What do the interossei do and how many are there?
There are four palmar and four dorsal interossei.
They are supplied by the ulnar nerve.
Origin: metacarpal base.
Insertion: proximal phalanx base
The palmar interossei adduct the fingers and the dorsal interossei abduct.
Mnemonic: palmar adduct (PAD), dorsal abduct (DAB)
56
APPLIED SURGICAL ANATOMY ulnar nerve
SENSORY SUPPLY
The nerve supplies the medial one and a half fingers and medial third of the palm
of the hand.
CLINICAL TESTS
Wasting of the small muscles of the hand (particularly hypothenar eminence) in
longstanding lesions.
Test the interossei by asking the patient to grip a piece of paper between middle
and ring fingers, and try to remove the paper. Compare with the other side.
Froment’s sign: if a patient is asked to grip a piece of paper between the thumb and
lateral aspect of forefinger, he or she will flex as the thumb adductor is lost.
Test the sensory distribution.
57
22 Ureter

What is the course of the ureter?
What is the blood supply of the ureter?
What are the relations of the ureter and what structures cross it?
Trace the ureter’s course on a KUB abdominal film.
Where might stones be held up?
Related topics
Topic Chapter Page

Kidney 9 26
KEY FACTS
• Length 25 cm
• Lined by transitional epithelium (hence possible site of transitional cell
carcinoma)
• Blood supply superiorly by ureteric branch of renal artery and inferiorly by
superior vesical and gonadal artery; middle part supplied by aorta, gonadal and
iliac vessels
• Lymph drainage with the arteries, eventually to para-aortic nodes (superior part)
and iliac nodes (inferior part)
• Autonomic nerve supply, pain fibres accompany sympathetics.
58
APPLIED SURGICAL ANATOMY ureter
COURSE AND RELATIONS

RIGHT URETER LEFT URETER
Retroperitoneal
Descends on psoas major (adjacent to tip of vertebral transverse processes on KUB film)
Passes over the genitofemoral nerve and the gonadal vessels pass over it
Third part of duodenum anterior Lateral to the inferior mesenteric
vessels
Right colic, ileocolic and root of mesentery Left colic vessels anterior
anterior
Point of narrowing at pelviureteric junction, where it crosses the brim of the pelvis
Runs over external iliac artery and vein
Vas deferens in the male crosses over it
‘Water under the bridge’
Turns medially at the level of the ischial spine (key landmark on KUB film) and enters the
bladder inferolaterally
Second point of narrowing at point of entry to bladder – vesicoureteric junction or VUJ.
The two points of narrowing are the most common site of impaction of ureteric stones

Tell me the course of the ureter on this KUB film.
It passes down level with the tips of the transverse processes of the lumbar
vertebrae, commencing at the medial aspect of the kidney (outline seen on
KUB).
It turns medially at the level of the ischial spine. Point out the sites of
narrowing described above.
59
3
PART
OPERATIVE SURGERY
23 Anorectal surgery 1: anal fissure and lateral sphincterotomy 63
24 Anorectal surgery 2: fistula in ano and pilonidal sinus 67
25 Anorectal surgery 3: injection sclerotherapy and haemorrhoidectomy 73
26 Burr holes and lumbar puncture 78
27 Carotid endarterectomy 81
28 Carpal tunnel decompression 87
29 Circumcision 91
30 Emergency splenectomy 94
31 Femoral and brachial embolectomy 98
32 Femoral hernia repair 102
33 Inguinal hernia repair 106
34 Laparoscopic cholecystectomy and laparoscopy 112
35 Long saphenous varicose vein surgery 117
36 Mastectomy, axillary dissection and breast reconstruction 120
37 Open appendicectomy 125
38 Orthopaedic related approaches and procedures 130
39 Perforated duodenal ulcer and exploratory laparotomy 135
40 Renal transplantation 140
41 Thyroidectomy 144
42 Tracheostomy 148
23 Anorectal surgery 1: anal fissure and
lateral sphincterotomy

Examiner may show you a picture of an anal fissure and ask ‘what is the
diagnosis?’
In what positions are these normally found?
What are the most common causes of severe anal pain?
What is the differential diagnosis for anal fissure, especially if atypical in
location?
What is a sentinel pile?
How do you best diagnose an anal fissure?
How would you manage a patient with this problem?
What are the non-surgical treatment options for this condition?
Does it work?
How do you perform a lateral sphincterotomy and what are the main
complications?
Related topics
Topic Chapter Page
Anal canal 4 15
Fistula in ano and pilonidal sinus 24 67
Injection sclerotherapy and haemorrhoidectomy 25 73

What is an anal fissure?
An anal fissure is a longitudinal tear in the mucosa and skin of the lower
third of the anal canal.
ANAL FISSURE
• Common: seen in young adults – males ! females
• Peak incidence 20–30 years of age
63
OPERATIVE SURGERY anorectal surgery 1
• Constipation is thought to be the primary cause but there is actually no

evidence for this. The constipation could be the result of the fissure.
Underlying pathophysiology is local trauma → internal and external anal
sphincter dysfunction → ischaemia
• Anal fissures are the most common anal abnormalities in Crohn’s disease
• Most are posterior in the midline (90 per cent)
• Anterior (10 per cent) fissure more common in women, especially after
childbirth (vaginal delivery).
DIFFERENTIAL DIAGNOSIS OF SEVERE ANAL PAIN/ANAL FISSURE

• Acute fissure in ano
• Perianal haematoma
• Strangulated internal haemorrhoids
• Perianal and ischiorectal abscess
• Inflammatory bowel disease (IBD)
• Colorectal malignancy
• Proctalgia fugax (painful rectum).
SYMPTOMS AND SIGNS

Anal pain during or immediately after defecation as a result of sphincter spasm.
This can persist for up to an hour.
• Bright red bleeding per rectum – normally on the toilet paper on wiping
• Pruritus ani
• Watery discharge from anus
• Constipation
• There might be a history suggestive of cyclic fissuring and healing
• On examination, the fissure is usually concealed by anal spasm. Patient is in too
much pain even to let in a finger. However, you can sometimes see the white
circular fibres of the internal sphincter muscle at the base of the fissure. On
inspection you may see a small anal skin tag at the superficial end of the fissure
("sentinel tag). This suggests that the fissure is chronic.
The best way of diagnosing an anal fissure is by the history and visual inspection –
not by digital examination or proctoscopy!
CONSERVATIVE TREATMENT
• Conservative treatment is successful in up to 50 per cent of cases. Principle of
management is to reduce internal anal sphincter spasm: local anaesthetic gel
(good analgesia), GTN ointment cream (0.2 per cent TDS) for at least 4/52.
64
• GTN ointment thought to exert a local vasodilator effect and allow

healing.
• Patient advised to keep adequately hydrated, retain a high-fibre diet (also
thought to reduce the risk of recurrence) and be prescribed laxatives to keep
stool soft. Review in outpatients. Remember to advise using a glove for
application, otherwise it will get absorbed – warn patient of potential for
headaches. (If these occur, patient should be advised to discontinue use.)
• Can then try diltiazem cream (2 per cent BD) but some surgeons use this as a
first line option.
• Other options: botulinum toxin injection.
Key learning point

You should know the doses of the creams available:
GTN ointment cream (0.2 per cent TDS)
Diltiazem cream (2 per cent BD)
OPERATIVE SURGERY
Anal stretch
This is controversial – some think it causes uncontrolled disruption of the internal
anal sphincter and that reproducibility from one patient to the next is poor. High
rates of faecal incontinence have been reported.
Lateral sphincterotomy
• Indication: failed medical therapy (usually two courses of GTN 6/52 prescribed
before consideration)
• Usually leads to healing in 95 per cent cases after 4 weeks
• Performed under a general anaesthetic
• Patient is placed in the lithotomy position
• Per rectum examination, rigid sigmoidoscopy and proctoscopy performed to
confirm the diagnosis and rule out synchronous pathology
• Examine with Eisenhammer’s or Park’s retractor
• Internal sphincter muscle identified usually after developing a submucosal
plane with local anaesthetic
• Insert scissors into the intersphincteric space and enlarge
• Internal muscle fibres are cut usually to dentate line away and lateral to the
fissure
65
• Fissurotomy may be an added option

• Need to warn patient of risks of faecal and flatus incontinence and treatment
failure.

What are the complications of a lateral sphincterotomy?
Treatment failure (5 per cent)
Faecal incontinence (permanent in 5 per cent)
66
24 Anorectal surgery 2: fistula in ano and
pilonidal sinus

What is the difference between a fistula and a sinus?
How do you classify fistula in ano?
How would you excise a superficial fistula in ano?
What does Goodsall’s law state?
What are the features of a complex fistula?
What imaging modalities can help in defining complex fistulae?
How does a pilonidal sinus develop and where else can it occur?
How do these patients normally present?
What are the surgical options?
What is the Karydakis procedure?
Related topics
Topic Chapter Page
Anal canal 4 15
Anal fissure and lateral sphincterotomy 23 63
Injection sclerotherapy and haemorrhoidectomy 25 73
Key learning points

Definitions
A fistula is an abnormal communication between two epithelial-lined
surfaces.
Example: with a fistula in ano a communication exists between the
perianal skin and either the anal canal or the rectum
A sinus is a blind-ending tract communicating with an epithelial surface.
This may be normal (e.g. carotid sinus) or abnormal (e.g. pilonidal sinus).
67
FISTULA IN ANO
Causes
Most fistulae start as an abscess as a result of:
• Crohn’s disease
• Trauma
• Diabetes mellitus
• Infection: tuberculosis (TB) and HIV
• Carcinoma.
Classification (Fig. 24.1)
Ischiorectal
abscess
Lev
a tor Internal anal
ani sphincter
Puborectalis
External anal Dentate line

sphincter
Superficial
Trans- abscess Supra-
sphincteric Inter-
sphincteric
abscess sphincteric
abscess
abscess
Figure 24.1
• Superficial
• Intersphincteric
• Trans-sphincteric
• low
• high
• Suprasphincteric.
68
Key learning point

Goodsall’s law
This law states that, if an external opening lies anterior to an imaginary
transverse line with the patient in the lithotomy position, bisecting the anal
opening, its tract will pass directly into the anal canal, whereas, if the opening
lies posterior to this line, the tract will curve in a horseshoe manner towards
the internal opening by entering the anal canal in the midline posteriorly.
Aims of management
• Define anatomy – identification of the internal opening is the most important
determinant of successful treatment of fistula in ano.
• Effective drainage of sepsis (abscess and tracts)
• Eradication of source of sepsis
• Preservation of sphincter function
• Wound care.
Generally
• Superficial, intersphincteric and low trans-sphincteric fistulae (lie below
puborectalis) can be laid open and packed
• Suprasphincteric and high trans-sphincteric fistulae pass above the puborectalis
and should be treated by a seton suture because immediate laying open has a
high risk of faecal incontinence.
Procedure
• General anaesthetic; patient placed in lithotomy position.
• Examination under anaesthetic (EUA) and rigid sigmoidoscopy used to inspect
for internal openings of the fistula
• Pass a Lockhart–Mummery probe gently into the external fistulous opening and
note direction and depth in which the probe goes. Remember Goodsall’s law
when assessing the direction of the tract.
Superficial fistula
• If the probe passes superficially the tract is excised either with a knife or by
diathermy. The fistula is excised by directly cutting down on to the probe and if
necessary dividing the superficial fibres of the internal sphincter.
• Excise any overhanging skin on either side of the fistula to encourage healing by
granulation.
• Curette granulation tissue.
69
• Always send excised tissue for histology (look for cause).

• Apply an alginate dressing to raw area to aid haemostasis.
Deep fistula
• If the tract is deep it is likely to be complex and will require specialist colorectal
help. If no help is available to deal with a high fistula, insert a nylon seton to
aid drainage and allow reassessment at a later date.
• Endoanal ultrasonography and magnetic resonance imaging (MRI) can be
helpful in defining tracts when they are obscure or form part of a complex fistula.
• If anything more than a simple low fistula is present, the trainee should seek
expert assistance:
• A trans-sphincteric tract passes across the external sphincter to the
ischiorectal fossa. The internal opening is often at the level of the anal valves
• Identify internal opening with the proctoscope
• Probe the external opening
• Open the anal canal epithelium to the level of the internal opening
• If the tract is below or at the line of the anal valves, divide the muscle. If it is
above, insert a seton.
Setons
• A seton is a thread or suture that is passed along the fistula tract.
• Loose seton – tied loosely it acts as an effective drain and allows healing to occur
(50 per cent cases).
• Tight cutting seton – tied tightly it will slowly cut through the enclosed tissue.
The seton can be subsequently tightened every 2 weeks under local anaesthetic to
cut slowly through the enclosed sphincter muscle. This allows fibrosis to take
place behind, thus maintaining sphincter integrity.
Features of a complex fistula

• Recurrent episodes post-surgery
• Multiple external openings
• Induration felt above puborectalis muscle
• Probe from external opening passes upwards instead of to the anus
• Associated more with Crohn’s disease (Crohn’s perianal fistula).
PILONIDAL SINUS
Aetiology
There are two schools of thought:
• Congenital: a nest of hairs become enclosed as the skin closes over it. This
does not explain why the hairs found at the bottom of a pilonidal abscess are
demonstrably ‘scalp-type’ hairs. Hence this is not the current view.
70
• Acquired: chronic trauma allows a hair tip to penetrate the skin and the
rolling motion of the buttocks causes the hairs to burrow in. A deep natal cleft,
hairy area and occupations involving prolonged sitting also predispose to this
condition.
Also found in the finger webs of people in certain occupations: hairdressers and
sheepshearers. May be also seen in the umbilicus, axilla and perianal areas.
Presentation
• Asymptomatic
• Acute pilonidal abscess
• Chronic discharging sinus.
Management
Conservative
If the patient has midline pit disease and minimal symptoms, he or she can be man-
aged conservatively with good personal hygiene and regular removal of hairs.
Surgical
Indication
Persistent or recurrent pilonidal sinus.
Options
• Lay open wound and packing: completely excising pits and lateral tracks with
an elliptical excision. Wound should then be packed with a seaweed dressing.
• Primary closure: patient should be warned of wound breakdown and
dehiscence, because midline wounds are difficult to heal. Never attempt to
perform primary closure on purulent tissue.
• The Karydakis procedure is one of several types of operation for pilonidal
disease with the intent of primary closure. An advancement flap is created so
that the wound is brought away from the midline without being under tension
so that healing is improved. The natal cleft is also rendered shallow.
Preoperatively
• A phosphate enema is given to prevent early postoperative defecation.
Intravenous antibiotics (include anaerobic cover) are given at induction.
• The patient is placed prone on the table under general anaesthetic with the
buttocks strapped apart. The natal cleft area is shaved, prepared and draped,
and any areas of infection are covered.
• An asymmetrical (D-shaped) ellipse is marked on the skin to encompass both
the midline pits and the lateral sinus (wider part of the ellipse). Skin is incised
using diathermy according to the marked pattern and deepened to the
pre-sacral fascia. The block of tissue is excised.
71
• The restraining tapes are removed. Skin flaps are created so that both edges
can be approximated, achieving meticulous haemostasis with diathermy.
• Closure is with interrupted 1/0 Vicryl to fat and interrupted 1/0 nylon to skin.
A mini-vac is placed and secured beforehand to help close down the dead
space.
Postoperatively
• Drain reviewed and normally taken out at 24 hours
• Oral antibiotics are given for 5 days.
The patient is warned to lie on his or her side. No sitting for at least 5 days to pre-
vent excess tension on midline wound.
72
25 Anorectal surgery 3: injection sclerotherapy
and haemorrhoidectomy

What are haemorrhoids and what are their normal functions?
What are the common causes of pathological haemorrhoids?
How do you perform injection sclerotherapy for haemorrhoids?
What are the indications for performing a haemorrhoidectomy?
How do you perform a Milligan–Morgan open haemorrhoidectomy?
How do you distinguish the internal sphincter from the external sphincter?
What are the potential complications?
How would you treat thrombosed strangulated haemorrhoids?
What are you palpating for during a per rectal examination?
Related topics
Topic Chapter Page
Colorectal cancer 54 200
Anal fissure and lateral sphincterotomy 23 63
Fistula in ano and pilonidal sinus 24 67
HAEMORRHOIDS

What are haemorrhoids?
Haemorrhoids (piles) are engorged vascular cushions found within the
submucosa of the anal canal. They consist of a sacculated venous plexus
with a rich arterial supply supported by a fibromuscular connective tissue.
They normally contribute to:
• anal continence
• protection of the sphincter mechanism during defecation.
They are found at constant positions within the anal canal (3, 7 and
11 o’clock positions).
73
Common causes of pathological haemorrhoids

• Constipation (thought to produce shearing forces that lead to fragmentation of
the supporting fibromuscular matrix)
• Prolonged straining (thought to lead to engorgement of the anal cushions)
• Pregnancy
• Internal sphincter dysfunction.
Management
• Appropriate dietary and defecatory advice to prevent straining and constipation
• Asymptomatic: conservative
• Symptomatic: injection sclerotherapy or banding for primary and small
secondary haemorrhoids.

How do you inject haemorrhoids?
Injection sclerotherapy: outpatient setting
Warn the patient that the procedure may be painful, that he or she may
notice significant blood loss after the procedure for about 48 hours and
that repeat injections may be required.
Ask about nut allergy.
Left lateral position.
Position proctoscope within anal canal.
Visualize the groups of haemorrhoids and inject with 5 per cent phenol
in almond oil into the bases. Do not inject too close to the dentate line
because this can cause severe pain. Start with the lowest haemorrhoid first
so that any bleeding does not obstruct the view.
Watch till the superficial tissues blanch and swell. This is an indication that
the injection is in the correct plane.
Review in outpatients in 6 weeks.
HAEMORRHOIDECTOMY
Indication
Prolapsing third-degree haemorrhoids.
74
Milligan–Morgan technique advocated and can be performed as a day-case proced-

ure, although stapled anopexy can also be performed now with good results.
Open versus closed technique.
Preparation
• A preoperative phosphate enema should be given to allow an adequate
examination under anaesthetic to be performed.
• Patient is placed in the lithotomy or jack-knife position, slightly head down.
• Perform a per rectum examination (see below) and rigid sigmoidoscopy, and
visualize the anal canal and rectum with a proctoscope. Confirm the position of
the group of haemorrhoids by introducing a dry gauze swab into the anal canal
and gently withdrawing it.
• Insert an Eisenhammer’s retractor and assess which haemorrhoids need excision.
• Inject local anaesthetic into each skin bridge and external component of each
haemorrhoid to be excised. Apply Spencer–Wells forceps to the perianal skin
outside the mucocutaneous junction at the 3, 7 and 11 o’clock positions,
opposite the primary pile groups. Retract on these forceps to bring the
haemorrhoidal masses into view and reapply the forceps.
• Start with the most inferior haemorrhoid (7 o’clock group) because this
prevents blood clouding the operative field. Put the internal sphincter under
tension by inserting an index finger into the rectum while holding the forceps in
the palm of the hand.
• Mark out amount of haemorrhoid to be excised by scoring with the cutting
diathermy. This should bear a V- or U-shaped incision in the skin close to the
haemorrhoid.
• Excise the external component with coagulation diathermy.
• Extend dissection from the anal canal, separating the haemorrhoid from the
white fibres of the internal sphincter, with a combination of blunt (regular
sweeping motion pushing the subcutaneous tissue towards the anal canal, using
a piece of gauze) and sharp dissection. The external fibres look red.
• Some surgeons transfix the vascular pedicle with a 1/0 Vicryl suture, although
this is not the authors’ practice, because this has been attributed to causing
postoperative pain. If meticulous haemostasis is achieved gradually, the pedicle
can be transected without transfixion.
• Repeat the same procedure for the remaining haemorrhoidal groups, leaving
distinct skin bridges to avoid anal stenosis.
• If performing a closed technique, close skin bridges with 0 Vicryl.
• Achieve meticulous haemostasis because bleeding is the most common reason
for taking a patient back to theatre postoperatively.
• Insert metronidazole 500 mg and diclofenac suppositories along with a
soft petroleum jelly gauze or seaweed dressing into the anal canal. This is
75
partially to keep the mucocutaneous bridges flat against the internal

sphincter.
• The patient will naturally pass this gauze in 24 hours.
• Use blue gauze or perineal pad.
• Use a firm T bandage.
Postoperative advice
• Good oral analgesia (worse pain is the first bowel motion usually on day 7)
• Stool softeners
• 5/7 oral metronidazole
• Regular baths.
Key learning point

Principles
‘If it looks like a dahlia it’s sure to be a failure. If it looks like a clover
your worries are over!’
Don’t be too radical with your excisions; you can always come back and
repeat the operation. You cannot undo any damage to the internal or external
sphincters!
Thrombosed strangulated haemorrhoids, which may present as an emer-

gency, may be treated conservatively (analgesia, bed rest, elevated legs and
ice packs) or by immediate haemorrhoidectomy. One of the concerns per-
forming a haemorrhoidectomy on strangulated piles is sepsis.
Complications
• Pain ##
• Acute retention of urine (caused by postoperative pain)
• Reactionary haemorrhage (within 24 hours of surgery)
• Secondary bleeding is often the result of infection, which occurs on days 7 or 8
postoperatively
• Constipation and faecal impaction (resulting from pain)
• Faecal incontinence (damage to the sphincter mechanism)
• Perianal fistula formation
• Recurrence of the haemorrhoids
• Anal stenosis.
76

What are you palpating during a per rectum (PR) examination?
In males:
• Anterior: prostate gland, rectovesical pouch, vas deferens, seminal
vesicles, and bimanual palpation of the bladder
• Posterior: sacrum, coccyx, sympathetics and splanchnic vessels
• Laterally: ischial spines, obturator internus and Alcock’s canal
In females:
• Anterior: pouch of Douglas, uterus and vagina (posterior fornix)
• Posterior: sacrum and coccyx
• Laterally: ischial spines
Also examine for (can be bimanually):
• Rectal masses, e.g. rectal carcinoma (lower rectum)
• Acutely: pelvic appendix (mass)
• Blood, stool (superiorly)
77
26 Burr holes and lumbar puncture

How is a burr hole fashioned?
For what might a burr hole be used?
What are the complications of performing a burr hole?
At what level should a lumbar puncture be performed?
What are the principles of lumbar puncture?
What is a normal opening pressure?
What structures are traversed by the spinal needle during lumbar puncture
(from skin to deep)?
Related topics
Topic Chapter Page
Head injury and intracranial pressure 112 459

What might a burr hole be used for?
Burr holes are used for procedures that require limited intracranial access:
• Immediate relief of an acute extradural haematoma or acute subdural haema-
toma as a holding measure before performing a formal craniotomy procedure
• Treatment of chronic subdural haematoma
• Placement of a ventriculostomy catheter (external ventricular drain or EVD)
• Placement of an intraparenchymal pressure monitor (‘bolt’)
• Access for some stereotactic neurosurgery, including brain biopsy for
tumour pathology
• Burr holes can be used to allow insertion of a craniotome for the forma-
tion of a free bone flap in more extensive neurological operations.
POSITIONING A BURR HOLE

Principles of burr hole placement are away from major venous sinuses and air sinuses
and not overlying eloquent brain. The following are common sites for placement:
• Frontal (usually 1–2 cm in front of coronal suture in the midpupillary line to
avoid the primary motor cortex)
78
OPERATIVE SURGERY burr holes and lumbar puncture
• Parietal – overlying the parietal eminence

• Occipital
• Temporal (commonly used in the case of an acute extradural haematoma).
Technique
A classic technique for the fashioning a burr hole is described below, but this is rap-
idly being replaced with either a relatively wide twist–drill technique or the use of
a mechanical perforator (Midas Rex or similar):
• Position patient on horseshoe head cushion
• Check side on computed tomography (CT), which must be displayed in theatre
• Shave scalp and prepare it with alcohol solution
• Prepare skin and drape having marked midline and incision. Drape as if for a
craniotomy. Plan incision so that trauma flap could be raised if necessary
• Incision down to bone approximately 4 cm in length
• Use periosteal elevator to scrape back periosteum
• Insert small self-retaining retractor – this should stop all skin edge and galeal
bleeding
• Use the perforator attached to a Hudson brace to perforate the outer table of
the skull. Continue using the instrument until the inner table has just been
perforated and a small amount of shiny dura can be seen. A conical hole should
be the result (in the case of an extradural, at this stage dark clot and altered
blood should be expressed)
• Swap the perforator for the burr and widen the hole to its base without
damaging the underlying dura
• If subdural access is needed, score the dura with a no. 15 blade and pick up with
a dural hook. Cut onto the dural hook to fashion a cruciate opening of the dura
• Use monopolar diathermy to coagulate dural leaves
• Closure: 2/0 Vicryl to galea and clips or 3/0 nylon to skin.
Complications
• Extradural bleeding
• ‘Plunging’ and damage of underlying structures
• Infection: ventriculitis, subdural empyema
• Venous sinus damage and possible air embolism
• Cerebrospinal fluid (CSF) leak possible if dura opened.
LUMBAR PUNCTURE
Lumbar puncture should be performed below the level at which the spinal cord
ends (L1 in an adult, but lower in a child as a result of differential growth).
It allows the sampling of CSF and the measurement of the CSF pressure.
79
OPERATIVE SURGERY burr holes and lumbar puncture
Indications
CSF sampling
• Infection in bacterial or viral meningitis
• Xanthochromia in subarachnoid haemorrhage
• Cell count in suspected ventriculitis via EVD.
Pressure – diagnostic and treatment
Suspected raised intracranial pressure. Note that this must never be performed for
this indication unless CT reveals widely patent perimesencephalic cisterns and no
obvious mass effect. Inappropriate use of the technique in these cases can lead to
coning and death.
Technique
• Aseptic technique
• Skin preparation and drape
• Local anaesthetic infiltration 1 per cent lidocaine
• Midline approach usually at L3–4, L4–5 or L5–S1 interspace; spinal needle
directed at a cranial angle of 10–20°
• ‘Pop’ is often felt as the ligamentum flavum is traversed
• Remove stylet in spinal needle
• Allow CSF to drip from the needle – never aspirate
• Quickly place manometer on spinal needle and read off pressure on column of
CSF (normal opening pressure 5–10 cmH2O)
• Remove manometer and replace stylet once sufficient CSF has been expressed
• Remove spinal needle
• Patient should remain flat for at least 30 min to prevent a low pressure headache.

What structures are traversed by the spinal needle during lumbar puncture
(from skin to deep)?
• Skin
• Subcutaneous tissue
• Fat
• Supraspinous ligament
• Interspinous ligament
• Ligamentum flavum
• Epidural fat
• Dura
• Arachnoid into subarachnoid space
80
27 Carotid endarterectomy

What are the indications for performing a carotid endarterectomy (CEA)?
Are you aware of any trials that support CEA?
Which preoperative imaging modalities are commonly employed to
establish the diagnosis of carotid stenosis?
How do you perform a CEA?
What is a shunt and when is it used?
What are the potential complications of performing a CEA?
Which cranial nerves may be injured during a CEA?
How is the patient monitored perioperatively? What is transcranial
Doppler (TCD)?
Related topics
Topic Chapter Page
Atherosclerosis 49 177
Brain-stem death and transplantation 106 423
INDICATIONS
Large randomized trials have now provided reliable data identifying who should
undergo surgery.
Several thousand patients are randomized to surgery with appropriate medical ther-
apy or medical therapy alone.
North American Symptomatic Carotid Endarterectomy Trial (NASCET)

• CEA beneficial to patients with a symptomatic carotid stenosis with 70–99 per
cent (but not occlusion)
• Follow-up: 2-year risk of ipsilateral stroke reduced by CEA from 26 per cent
to 9 per cent (P $ 0.001)
• 30-day perioperative stroke and death rate was 5.8 per cent
• Numbers needed to treat (NNT) to prevent one ipsilateral stroke in
2 years " 6.
81
OPERATIVE SURGERY carotid endarterectomy
European Carotid Surgery Trial (ECST) – mirrored NASCET findings

• CEA reduced absolute stroke risk and death over 3 years from 21.9 per cent to
12.3 per cent (P $ 0.01)
• 30-day perioperative stroke and death rate was 7.5 per cent.
Recent data also suggest that maximum benefit is gained if CEA is done within
2 weeks of symptoms.
Asymptomatic patients (no focal symptoms within 6 months)

The Asymptomatic Carotid Atherosclerosis Study (ACAS)
• Recruited patients with 60–99 per cent stenosis
• 5-year rate of ipsilateral stroke and death twice as high in the control group
(11 per cent versus 5.1 per cent for CEA patients)
• 67 patients needed to have CEA to prevent one disabling stroke or death in 2 years!
Asymptomatic Carotid Surgery Trial (ACST)
• Patients allocated immediate versus delayed CEA
• Immediate CEA halved the net 5-year stroke risk from 12 to 6 per cent,
including the 3 per cent perioperative hazard, in asymptomatic patients aged
less than 75 years with a carotid stenosis of 70 per cent or more.
The trialists cautioned that, despite trial recommendations, either an inappropriate
selection of patients or technically poor surgery with a higher than 3 per cent com-
plication rate will obviate any benefit to the patient from intervention. CEA in a
selected subpopulation of asymptomatic patients should be considered as a long-
term (! 5 years) stroke prevention strategy.

Which patients benefit from CEA?
• Symptomatic patients with a ! 70 per cent carotid artery stenosis
• Asymptomatic patients aged less than 75 years with at least 70 per cent
carotid stenosis
• Other indications include lesser degrees of stenosis in symptomatic
individuals, who may have a dominant hemisphere largely supplied by
that artery and whose contralateral vessel is occluded
SURGICAL (CONVENTIONAL) TECHNIQUE

Preoperative considerations
• Preoperative assessment should include an up-to-date ($ 2 weeks) carotid
duplex. Digital subtraction angiography (DSA) can also be done
82
• Today, a magnetic resonance angiogram (MRA) is routinely performed

• Appropriate management of other co-morbidities: half deaths after CEA are the
result of cardiac disease
• Preoperative check of recurrent laryngeal and hypoglossal nerve function if
patient has undergone a previous CEA or thyroidectomy. Bilateral injury of
either nerve is fatal
• Symptomatic patients should also have a preoperative head CT or MRI because
$ 2 per cent patients have other significant brain pathology, including
malignant tumours (dangerous to operate on).
Procedure
• Usually performed under general anaesthetic
• Loupe magnification
• Head is extended and turned away from the side of operation and placed on a
rubber ring slightly head up
• Incision: centred over the anterior border of sternocleidomastoid muscle from ear
lobe to sternal notch, angling behind the ear if necessary for a high bifurcation
• Dissection continued down to the carotid bifurcation
• Dividing the common facial vein may be necessary for exposure
• Retract internal jugular vein laterally. Carotid vessels are controlled with slings,
although the authors do not subscribe to slinging the internal carotid artery
(ICA) because of the potential of dislodging thrombus
• Infiltrate carotid sinus with 1 per cent lidocaine to prevent reflex hypotension
and bradycardia
• Mobilize ICA 1 cm beyond the upper limit of the plaque
• Identify and conserve principal cranial nerves:
• vagus (X)
• hypoglossal (XII)
• glossopharyngeal (IX) – only with high dissections
• Systemic heparinization (5000 units)
• Apply soft clamps to distal ICA, common carotid artery (CCA) and external
carotid artery (ECA) in that order
• Make a longitudinal arteriotomy from the distal CCA across the plaque and into
the ICA beyond the stenosis using a no. 11 blade and Pott’s scissors
• A shunt may be required at this point if there is any evidence under local
anaesthetic of neurological hemispherical symptoms, or under general anaesthetic
of inadequate cross-flow on transcranial Doppler (TCD) or other measures of
cerebral blood flow.
• Enter endarterectomy plane using a Watson–Cheyne dissector
• It is conventional to divide the plaque first at the CCA aspect and then carefully
mobilize it up to the ICA, where it is cut transversely using micro-scissors to
avoid leaving an intimal flap
83
• Tack down any intimal flaps using fine interrupted Prolene sutures (6/0 or 7/0)
• Remove all loose intimal fragments
• Close arteriotomy either:
• primarily: running 6/0 Prolene suture
• patch (prosthetic or long saphenous vein)
• Before final couple of sutures flush with heparin saline
• Restore flow: ECA before ICA to minimize chances of embolization of any
loose material within the lumen or clot proximal to the CCA clamp.
Postoperatively
• Check for any neurological deficit
• Patient should be further monitored in a high dependency setting.
Perioperative monitoring
The principle of monitoring is to correct and/or prevent cerebral ischaemia before
onset of permanent neurological injury.
Transcranial Doppler is the most versatile and practical of available methods.
It can:
• Anticipate requirement and urgency for shunting
• Diagnose intraoperative embolization, thereby permitting early ICA clamping in
patients with unstable plaques
• Ensure optimal shunt function
• Can also detect postoperative hyperperfusion and monitor treatment response.
TCD uses a low frequency (2 MHz) pulsed-wave ultrasound beam directed through
the thin temporal bone.This permits insonation of the middle cerebral artery (MCA),
which receives 80 per cent of the ICA inflow.
The quality of the signal depends on the thickness of the cranium. An inaccessible
window is present in about 10 per cent of patients.
Neurological activity can be evaluated directly by performing a CEA under local
anaesthetic. This is a sensitive method of detecting clamp ischaemia and is the gold
standard in determining who needs a shunt, although it will not prevent thrombo-
embolic complications.
Shunt
This is a conduit, usually made of plastic, which diverts blood flow around the sur-
gically opened carotid artery while the endarterectomy is performed. A shunt is
used to ensure adequate cerebral perfusion.
• Routine versus selective use
84
Decision to use a shunt:

• Intraoperative assessment: temporary clamping of ICA under local anaesthetic
• Stump pressure measurement (back pressure of ICA after clamping): used to
assess the adequacy of cerebral perfusion (about 40 mmHg)
• TCD or other methods of cerebral blood flow monitoring.
SURGICAL COMPLICATIONS
Intraoperative
Cerebral ischaemia leading to neurological deficits in about 2 per cent.
• Embolization of debris during vessel manipulation
• Poor flushing technique after arteriotomy closure
• Hypotension or poor protection during cross-clamping.
Cranial nerve injuries
• Hypoglossal (XII)
• Vagus (X)
• Mandibular branch of the facial nerve (Ve)
• Spinal accessory nerve
• Glossopharyngeal nerve (IX) – more common after high carotid artery
dissections
• Superior laryngeal nerve (branch of vagus).
Overall rate of cranial nerve injury 8.6 per cent, although 92 per cent are transient
(NASCET findings).
Early
Thirty-day perioperative stroke and death rates between 5.8 and 7.3 per cent in
symptomatic individuals (NASCET # ECST data).
Asymptomatic patients % 2–4 per cent.
Medical problems
NASCET reported that about 10 per cent of surgical patients suffered a medical
complication within 30 days of the operation; 70 per cent were of short duration
and resulted in only 2.7 per cent of patients having prolonged stays.
Severe medical complications included:
• Myocardial infarction
• Arrhythmia
• Congestive cardiac failure
• Severe hypertension
• Severe hypotension.
85
Wound haematoma – large or rapidly expanding haematomas require urgent

re-exploration, because there is a risk of airway obstruction.
Hyperperfusion syndrome
• Uncommon but dangerous
• Hyperaemic cerebral perfusion can cause cerebral oedema and haemorrhagic
stroke
• Patients complains of a severe headache that improves with blood pressure
control.
Wound infection
Late
• False aneurysm formation
• Re-stenosis (wide range of 2–36!) – found to be lower if patch angioplasty is
employed to close arteriotomy.
86
28 Carpal tunnel decompression

What are the signs and symptoms of carpal tunnel syndrome?
What are the risk factors for developing carpal tunnel syndrome?
What other conditions should be excluded and what investigations
would you perform to establish a diagnosis?
What is the flexor retinaculum and what are its attachments?
What structures lie within the carpal tunnel?
What are the surgical options?
Where would you place your incision for carpal tunnel decompression?
Describe the surgical approach to carpal tunnel decompression.
How do you differentiate the median nerve from the flexor tendons?
How would you minimize sensory loss over the thenar eminence?
What are the possible surgical complications?
What is the predicted outcome?
Related topics
Topic Chapter Page
Median nerve 11 31
Tourniquets 82 339
Orthopaedic related approaches and procedures 38 130
The carpal tunnel is a space on the ventral surface of the wrist between the bony
gutter of the concave carpus and the overlying flexor retinaculum.
Carpal tunnel syndrome occurs when there is an increase in pressure within this
tunnel, leading to compression of the median nerve.
87
OPERATIVE SURGERY carpal tunnel decompression

What is the flexor retinaculum and what are its attachments?
The flexor retinaculum is a strong band of fibrous tissue attached to four
bony points on the volar aspect of the wrist. Its attachments are:
Laterally (radial): scaphoid tubercle, ridge of trapezium
Medially (ulnar): pisiform and hook of hamate
Contents of the carpal tunnel: think 11 structures – 10 tendons and 1 nerve:
• Median nerve (most superficial structure)
• Flexor digitorum superficialis & 4
• Flexor digitorum profundus & 4
• Flexor pollicis longus
• Flexor carpi radialis
RISK FACTORS
• Idiopathic (common)
• Obesity
• Rheumatoid arthritis
• Thyroid dysfunction
• Acromegaly
• Amyloid (infiltration of the flexor retinaculum)
• Pregnancy
• Ganglion
• Repetitive use of vibrating tools
• Tight bandaging and plaster immobilization – especially when the wrist is
immobilized in extreme flexion after a fracture
• Trauma – distal radius fractures.
SYMPTOMS AND SIGNS

• Patient typically wakes at night with burning pain, numbness or tingling in the
hand, typically relieved by hanging the arm out of bed and shaking it
• Pain and paraesthesiae in the distribution of the median nerve
• Wasting of the thenar muscles
• Signs: positive Tinel’s (tapping over the median nerve at the wrist reproduces
the tingling sensation) and Phalen’s (maximal flexion of wrist for 1 minute
exacerbates the symptoms, which are promptly relieved when the flexion is
88
discontinued). This is more important in clinical practice. Time to symptoms is

inversely proportional to the severity
• Preserved sensation over the thenar eminence.
DIFFERENTIAL DIAGNOSIS AND INVESTIGATIONS

• Symptoms and signs may mimic a C6–7 cervical spondylosis
• Cervical spine radiographs or magnetic resonance imaging (MRI) may
demonstrate degenerative changes, causing confusion
• Nerve conduction studies:
• sensory nerve velocities most helpful
• compare with ulnar nerve velocities
• MRI may be useful in identifying soft-tissue space-occupying lesions in the tunnel.
TREATMENT OPTIONS
Non-surgical
• Wrist splintage at night
• Hydrocortisone injections into the carpal tunnel, diuretics
• Correctable causes investigated and appropriately treated.
Surgical
• Carpal tunnel decompression:
• open
• endoscopic (Chow’s method) using a two-port technique. Thought to minimize
scarring, lower incidence of wound complications and allow earlier return to work.
SURGICAL PROCEDURE
Use an anterior (volar) approach.
Preoperative
• This operation can be done under a local (Bier’s block) anaesthetic, direct local
anaesthetic into the palm or general anaesthetic
• A tourniquet on the upper arm is mandatory for a bloodless operative field
• Arm is laid supine on the side table.
• Clean the forearm and fingers and drape the limb, but leave fingers and hand
exposed.
Perioperative
• Incision: longitudinal from distal flexor crease to transverse palmar crease. This
is in line with the radial border of the ring finger, avoiding damage to the palmar
cutaneous branch of the median nerve.
89
• Incision is deepened down through the longitudinal fibres of the palmar

aponeurosis to expose the transverse fibres of the flexor retinaculum.
• A small self-retaining retractor is placed.
• A MacDonald dissector is placed under the flexor retinaculum, which is then incised
longitudinally with a scalpel down to the retinaculum. This exposes the median nerve.
• Inadequate decompression and persistent symptoms can be a problem if the
proximal part of the retinaculum has not been adequately released where it
disappears under the skin in the proximal aspect of the wound. This should be
released with the Macdonald dissector along the surface of the median nerve
• In rheumatoid arthritis there may be an associated hypertrophic synovium
affecting the flexor tendons. Therefore, perform a flexor synovectomy by
stripping the synovium with a pair of fine bone nibblers.
Closure
• Deflate tourniquet
• Achieve meticulous haemostasis
• Close skin with interrupted Prolene sutures
• Apply compression bandaging
• Should be replaced with an adhesive dressing in 24 hours
• Elevation of hand recommended
• Early finger exercises encouraged
• Remove sutures at 10 days.
SURGICAL COMPLICATIONS
• Infection
• Haemorrhage
• Scar tenderness – can occur in up to 40 per cent of patients
• Nerve damage
• median nerve itself
• recurrent motor branch of the median nerve; this innervates the thenar
muscles. Division will cause wasting of these muscles and impede fine
movements of the hand
• palmar cutaneous branch of the median nerve; this supplies sensation to the
skin over the thenar eminence. Division will result in paraesthesiae
• Recurrent symptoms caused by inadequate decompression
• Scar formation – this is a high-risk area for keloid or hypertrophic scars
• Reflex sympathetic dystrophy (RSD).
PREDICTED OUTCOME
• Improvement in symptoms in 85 per cent of patients
• Thenar muscle wasting may resolve.
90
29 Circumcision

What are the indications for a circumcision?
What are the causes of a phimosis?
Describe your method of performing the operation.
Is there an alternative method in infants?
What methods of postoperative pain relief can be useful after circumcision?
What are the risks and complications of performing a circumcision?

What are the indications for a circumcision?
Medical versus religious.
Medical
• Phimosis
• Senile
• Balanitis xerotica obliterans (BXO)
• Squamous cell carcinoma of the prepuce
• Paraphimosis (irreducible)
• Recurrent urinary tract infections
• Recurrent balanitis
PHIMOSIS
• Congenital: as a result of congenital adhesions between the glans and foreskin; it
is not normally possible to retract the foreskin in the first year of life
• Acquired: commonly the result of BXO; can also be senile.
PROCEDURE
• Patient laid supine under general anaesthetic.
• The surgery is covered with intravenous antibiotics if there has been any
evidence of infection, e.g. balanitis.
91
OPERATIVE SURGERY circumcision
• Penile block performed.

• External genitalia prepared with aqueous antiseptic and draped accordingly.
• Prepuce retracted and glans beneath cleaned. Preputial adhesions freed using a
silver probe or artery forceps. If foreskin too tight to retract, a dorsal slit may
need to be performed.
• Two straight artery forceps placed side by side on the dorsum of the foreskin
and scissors used to divide the foreskin between the two clips to a level about
5 mm below the corona.
• The incision then carefully continued circumferentially by a freehand technique
in either direction around the penis, keeping about 5 mm below the corona until
the incisions meet at the frenulum.
• Frenulum picked up with another artery forceps and redundant skin excised.
• Frenulum and its artery transfixed or a box stitch used to create haemostasis.
Bleeding vessels along the way either clipped and tied with an undyed
dissolvable suture such as 3/0 Vicryl or coagulated with bipolar diathermy.
• After obtaining careful haemostasis, ridge of skin below the corona and free
edge of the foreskin remaining down the shaft opposed with interrupted
absorbable suture – in the authors’ experience Vicryl Rapide.
• Topical lidocaine (2 per cent) gel applied to the distal end of the penis.
• Penis loosely dressed in paraffin gauze and then dry gauze.
• Postoperative instructions would include a daily bath with good amount of
analgesia.
• In sexually active men, they should be warned to refrain from intercourse until
the wound is fully healed, which will take least 2–3 weeks.
• The foreskin should be sent for histology if BXO or carcinoma is suspected.
Postoperative analgesia
• All circumcisions should be performed with either a caudal or a penile block in
situ. This makes the postoperative period more comfortable.
• Insertion of a non-steroidal anti-inflammatory suppository just before the end of
the general anaesthetic will also give good analgesia for the first 12 hours.
• Oral analgesia can be used thereafter. Patients should not need an epidural or
patient-controlled analgesia (PCA).
INFANTS
Commercial devices such as the Plastibell (Hollister) instrument have been used
but have proved to be generally unsuccessful. The foreskin is freed and retracted.
The Plastibell is slipped over the glans penis and the foreskin ligated and divided in
the groove of the instrument. The foreskin is cut and removed.
92
OPERATIVE SURGERY circumcision

What are the complications?
• Infection
• Bleeding
• Haematoma
• Excision of too much skin
• Injury to the glans penis, degloving injury
• Breakdown of wound
• Urinary retention
• Psychological morbidity
• Urethrocutaneous fistula
• Meatal stenosis
• Ischaemia and necrosis of the distal part of the penis
• Need to repeat circumcision
93
30 Emergency splenectomy

What are the functions of the spleen?
How is the spleen commonly injured? What is the mechanism of injury?
What are the signs and symptoms of splenic injury?
What are the indications for performing an emergency splenectomy?
What are the principles of trauma splenectomy?
What are the possible complications?
What is overwhelming post-splenectomy infection (OPSI)?
What prophylaxis should be considered in all patients undergoing
splenectomy?
How should a patient be followed up after successful non-surgical treat-
ment of a splenic injury?
Related topics
Topic Chapter Page
Sepsis and SIRS 121 505
Antibiotics in surgery 67 275
FUNCTIONS OF THE SPLEEN

• Fetus: major site for haematopoiesis
• Childhood: produces Immunoglobulin M (IgM)
• Adult: acts as a filter – allows resident macrophages to remove abnormal
erythrocytes, cellular debris and encapsulated poorly opsonized bacteria.
INDICATIONS FOR EMERGENCY SPLENECTOMY

• Traumatic rupture: normally following road traffic accident (RTA) or violent
falls
• mechanism of injury: direct blunt force; deceleration and compression injuries
to the left side of the abdomen
• Spontaneous rupture: in enlargement.
94
OPERATIVE SURGERY emergency splenectomy
SIGNS AND SYMPTOMS OF SPLENIC INJURY

• Left upper quadrant pain (stretching of the splenic capsule)
• Peritonitis (from extravasated blood)
• Kehr’s sign: referred left shoulder tip pain resulting from diaphragmatic
irritation by extravasated blood
• Associated injuries, e.g. left-sided lower rib fractures and bruising.
INDICATIONS FOR OPERATIVE MANAGEMENT

Conservative management
May be possible in minor injury (grades I–III) and where there is no evidence of
haemodynamic instability.
Surgery indicated in:
• Haemodynamic instability or peritonitis
• Persistent coagulopathy and bleeding
• Additional intra-abdominal injury requiring surgical intervention
• Confounding injury: an additional injury that interferes with patient’s
monitoring, e.g. pelvic fracture with continuing bleeding
• Worsening pain and tenderness
• Severe splenic injury: grades IV # V.
PROCEDURE
• Patient is laid supine.
• Anaesthetic is general.
• Prepared and draped from nipple to groin.
• Intravenous penicillin (or suitable alternative in allergic individuals) given at
induction.
• A nasogastric tube should be placed because of the risk of acute gastric
distension after the procedure.
• Upper midline incision ('T-shaped extension).
• Check that spleen is the cause of the bleed and, if so, proceed with splenectomy
before inspecting the rest of the abdomen.
• Mobilize spleen and deliver it into the abdominal wound by dividing the
lienorenal ligament.
• Compress vascular pedicle between the finger and thumb.
• Enter lesser sac by dividing the greater omentum between ligatures.
• Palpate the splenic artery, which lies superior to the pancreas. Mobilize and
then ligate it with 0 Vicryl ties.
95
• Free the left colic flexure from the spleen.

• Free attachments to the diaphragm.
• Ligate and divide the gastrosplenic ligament along with the short gastric vessels.
• Double ligate and divide the splenic vessels but beware of the tail of the
pancreas.
• Pack the splenic bed and achieve haemostasis.
• A drain should be placed in the splenic bed and secured.
• Mass closure with looped 1/0 nylon or PDS.
COMPLICATIONS
• Chest infection
• Subphrenic abscess
• Bleeding
• Damage to adjacent structures:
• stomach
• splenic flexure of colon
• diaphragm
• pancreas: pancreatic fistula (damage to the pancreatic tail during ligation of
splenic vessels), so will be beneficial to drain – analyse drain fluid for grossly
elevated amylase
• Overwhelming post-splenectomy sepsis (OPSS): see below
• Small bowel obstruction: loops of small bowel may adhere to a raw area
underneath the diaphragm on the left side
• Acute gastric dilatation: hence importance of a nasogastric tube
• Development of splenunculi: splenic tissue shed during the operation may
undergo hypertrophy – no bad thing in the trauma setting!
• Infections: more prone to certain infections (see ‘Prophylaxis’ below)
• Malaria: more susceptible to the effects of malaria. Post-splenectomy patients
no longer have a spleen to sequester infected red blood cells and therefore
harbour a higher parasite load. These people should be advised not to visit
malaria endemic zones
• Thrombocytosis: usually after splenectomy for hypersplenism occurring in the
first 48 hours. There is usually a rise in white cell and platelet counts, often
confused with a picture of sepsis.
Overwhelming post-splenectomy sepsis (OPSS)
• Typically caused by encapsulated bacteria, the most common being:
• pneumococcal (50 per cent)
• meningococcal
• Escherichia coli
• Haemophilus influenzae
96
• Symptoms and signs are a flu-like prodromal illness followed by headache, fever,
malaise, coma, adrenal haemorrhage and circulatory collapse
• Affects 2 per cent of trauma splenectomies – OPSS is greatest if splenectomy
performed during infancy
• Occurs usually within 2 years of operation
• Mortality rate is high: 50–90 per cent
• Prevented primarily by immunization (see below).
PROPHYLAXIS
All elective and emergency patients undergoing splenectomy should receive
prophylactic immunization against:
• Haemophilus influenzae: Hibivax
• Streptococcus pneumoniae: Pneumovax
• Neisseria meningitidis strain C: Meningiovax.
In the emergency scenario this should be given postoperatively but not while the
patient is haemodynamically unstable because this can lead to further compromise.
Penicillin prophylaxis (or suitable alternative if allergic) should also be prescribed.
Duration is debatable. Some surgeons advocate lifelong prophylaxis whereas others
suggest a shorter interval of around 2 years, with a low threshold for antibiotic treat-
ment in the advent of any infection. Infants are recommended to continue to take
it until adulthood.
SUCCESSFUL CONSERVATIVE TREATMENT

Most patients who fail conservative management do so within 5 days.
If initial management is successful, obtain a follow-up ultrasound scan at 5 days to
document non-progression of splenic injury. A post-discharge CT scan is advised
6 weeks after injury to confirm complete healing. The patient should be advised to
refrain from contact sports for 3 months.
97
31 Femoral and brachial embolectomy

How do you perform a femoral embolectomy?
What surface landmarks are used to locate the femoral artery?
What are the boundaries of the femoral triangle?
What are the contents of the femoral triangle and their relationships?
What are the contents of the femoral canal and what are its borders?
When is a femoral embolectomy indicated?
What are the presenting features of acute critical ischaemia of the limb?
What are the causes of this problem?
How is thrombus distinguished from embolus in acute ischaemia?
How would you manage a patient with acute critical ischaemia of the
lower limb?
What are the complications associated with the vertical groin incision?
How would you approach performing a brachial embolectomy?
Related topics
Topic Chapter Page
The femoral triangle 8 24
ACUTE CRITICAL LIMB ISCHAEMIA
MRCS viva
What are the clinical features of acute critical limb ischaemia?
Learn the six ‘Ps’.
Sudden onset of:
Pain
Pallor
Pulselessness
Paraesthesiae
Paralysis
Perishing cold (poikilothermia)
98
OPERATIVE SURGERY femoral and brachial embolectomy
Causes
• Embolic: most commonly arise from the following sites:
• heart, either from left ventricular mural thrombus following an acute myocar-
dial infarction and congestive cardiac failure, or from the left atrium in atrial
fibrillation
• peripheral blood vessels: aortic or popliteal aneurysm, iliofemoral stenoses
• Acute thrombosis of an already atherosclerotic segment of artery.
It is often difficult to make the distinction between thrombosis and an embolus in
the lower limb.
Findings suggestive of embolus include:
• No prior history of vascular disease
• Normal contralateral leg circulation
• History of cardiac arrhythmia or recent myocardial infarction
• Patients with embolic disease who frequently have profound leg ischaemia
caused by the proximal nature of the occlusion (aortic or femoral bifurcation)
and the absence of developed collaterals
• Angiography is usually required to distinguish between the two.
Principles of management
• Medical treatment – liaise with medical colleagues
• Treat atrial fibrillation, e.g. with digoxin after confirmation with an ECG
• Treatment of arterial embolism – intravenous analgesia and heparinization
• Emergency angiogram ! thrombolysis (with streptokinase or tissue
plasminogen activator) if there are the facilities to do so
• This should be followed by heparinization and commencement of warfarin for
at least 6 months
• Further cardiac investigations such as an echocardiogram
• Surgical option would be femoral embolectomy.
The choice between the two therapies depends on the degree of the ischaemia.
Patients who have developed paralysis or paraesthesiae of the limb should proceed
promptly to embolectomy irrespective of the aetiology, because there may be sig-
nificant delay to reperfusion when the time that it takes for angiography and throm-
bolysis is taken into account.
Embolectomy is indicated in:
• Common femoral artery proximal to groin

• Brachial and axillary arteries.
More distal emboli can be treated by thrombolysis.
99
A non-viable limb should not be re-vascularized.

Patient should give consent for bypass grafting and amputation in case the leg
becomes unsalvageable.
FEMORAL EMBOLECTOMY
• Patient is fully heparinized.
• The anaesthetic is either local or general. Local is usually preferred considering
the likely number of other co-morbidities that the patient will have.
• The leg is cleaned and draped as appropriate but with the foot put into a
transparent sterile bag so that reperfusion can be assessed later.
• Vertical incision centred over the midpoint at the groin crease is made directly
over the artery. Landmarks: femoral artery lies at the midinguinal point –
midway between the anterior superior iliac spine and the pubic symphysis.
• Deepen incision over the artery by cutting through subcutaneous fat and staying
medial to sartorius. Expose femoral sheath. Incise it longitudinally to expose the
femoral artery.
• Pass a Lahey retractor posteriorly and sling the artery with sloupes such that
both proximal and distal control are achieved. The profunda femoris should
also be exposed and slung.
• A suitable size of Fogarty catheter is selected (size 3F or 4F femoral catheters)
and the balloon tested with saline.
• Arteriotomy is performed over the origin of the profunda – ideally transverse
because it reduces the risk of stenosis on closure.
• The uninflated catheter is passed proximally through the vessel beyond the
site of the clot. The balloon is inflated and the catheter withdrawn slowly
until the catheter is pulled out through the arteriotomy and the embolus
recovered.
• The assistant is asked to pull on the sloupes for haemostasis.
• This procedure is repeated proximally and distally until no further clot is
retrieved.
• The proximal and distal artery are flushed with heparinized saline.
• The arteriotomy is closed transversely with 4/0 Prolene sutures.
• A suction drain can be placed within the wound upon closure.
Complications associated with the vertical groin incision

• Wound infection
• Haematoma
• Lymphocoele/persistent lymph leak
• Flap necrosis and/or scarring.
100
Key learning points

Brachial embolectomy
The brachial artery may have to be exposed in order to dislodge an embolus
or for exploration after trauma.
Similar principles and procedure as a femoral embolectomy.
Medial approach
Incision made in the line of the artery along the medial edge of biceps
muscle. The basilic vein and the medial cutaneous nerve of the forearm are
superficial to the deep fascia at this level.
The deep fascia is divided and the inner fibres of the biceps muscle are
retracted upwards. The brachial artery should then be found lying on the
triceps muscle with the median nerve anterior to it.
Lying with the brachial artery are two venae comitantes.
Anterior (antecubital fossa) approach

Useful when it is deemed necessary to embolectomize the radial and
ulnar arteries separately. However, the brachial artery may bifurcate high
in the arm.
Sigmoid-shaped incision.
The distal end of the brachial artery lies in the antecubital fossa. By dividing
the bicipital aponeurosis the brachial artery is exposed, with the medial
cubital vein crossing it obliquely. The median nerve lies medial to the brachial
artery and the radial nerve lies inferior to the brachioradialis muscle.
Close the brachial artery with a vein patch or use a transverse incision.
101
32 Femoral hernia repair

What are the boundaries of the femoral canal?
Should all femoral hernias be repaired?
What are the differences between a femoral and an inguinal hernia?
What approaches do you know for a femoral hernia repair?
Which surgical approach would you use for a strangulated femoral
hernia? What layers would you need to go through?
Once you have exposed the femoral sac, what actions would you take?
If a piece of unviable bowel were to slip back into the abdomen and you
were unable to recover it, what action would you take?
What factors do you consider in determining the viability of bowel at the
time of a strangulated femoral hernia repair?
What important but inconsistent structure may be at risk in a femoral
hernia repair?
Related topics
Topic Chapter Page
Inguinal hernia repair 33 106

What are the boundaries of the femoral canal?
Medial: lacunar ligament
Lateral: femoral vein
Anterior: inguinal ligament
Posterior: pectineal ligament
• Generally a femoral hernia, if present, should be repaired promptly because it

has a narrow neck and is more likely to obstruct or strangulate than an inguinal
hernia. Exceptions can be made if the patient is frail and elderly and the hernia
has been an incidental finding
102
OPERATIVE SURGERY femoral hernia repair
• Fifty per cent strangulate within 1 month.

• More common in females because:
• the inguinal ligament makes wider angle with pubis in females
• enlargement of fat in middle age stretches the canal and this fat atrophies
later, leaving a larger canal
• pregnancy stretches transversalis fascia.

What are the differences between an inguinal and a femoral hernia?
Inguinal hernia Femoral hernia

Incidence In males and females More common in females
more common than than males (4:1)
femoral hernias
Obstruction and See above
strangulation Furthermore a femoral hernia is
more likely to strangulate with-
out obstructing (Richter’s hernia)
Position relative to Superior and medial Inferior and lateral
the pubic tubercle
Palpation Soft Firm
Percussion May be resonant Dull
Auscultation Bowel sounds Bowel sounds rarely heard
commonly heard
APPROACHES
Three approaches to the femoral canal have been described:
1. Low (Lockwood) used for elective repair:
• appropriate for non-strangulated hernias
• incision is 8–10 cm long in groin crease, below medial half of inguinal ligament.
2. Transinguinal/high (Lotheissen):
Rarely used today but is suitable for strangulated hernias, because it affords
suitable access for bowel resection but there is a risk of subsequent inguinal
hernia. Incision as for inguinal hernia, then expose inguinal canal and dislocate
spermatic cord laterally. Incise transversalis fascia as described in McEvedy’s
approach (below).
3. Extraperitoneal (McEvedy) – used for emergency repair.
103
Irrespective of approach, the following principles apply:

• Dissection and mobilization of the femoral sac
• Inspection and reduction of the sac contents
• Ligation of femoral sac
• Femoral hernia repair, which includes either approximation of the inguinal and
pectineal ligaments or insertion of a mesh plug into the femoral canal.
STRANGULATED FEMORAL HERNIA REPAIR

An extraperitoneal or McEvedy approach should be used because it gives better
control and access to inspect the affected loop of bowel and makes a bowel resec-
tion and anastomosis easier to perform if necessary.
Incision: vertical incision placed 2 cm above the medial third of the inguinal liga-
ment and extended proximally.
Go through:
• Skin
• Subcutaneous tissue
• Rectus sheath
• Rectus abdominis
• Transversalis fascia
• Peritoneum.
Divide inferior epigastric vessels:
• Hernia sac is held with two artery forceps and incised
• Bowel within hernia sac: bowel is drawn downwards and the ligamentous
margins of the sac neck are dilated with two fingers forming a wedge
• Bowel viability is then assessed
• Pay due attention to the constriction ring
• If there is doubt about bowel wall viability (see below), cover it with a warm
saline-soaked pack and re-examine in 5 mins. If the bowel is not viable after this
time, the affected segment is resected and anastomosed end to end with a one-
layer extramucosal technique
• If, at any stage, access were difficult or the affected loop of bowel were to fall
back into the abdomen and not be recoverable, you would perform a
laparotomy through a lower midline incision
• Return the sac contents into the abdomen
• Sac closed with an absorbable suture (2/0 Vicryl) and excised 1 cm distal to the
ligature
• Perform hernia repair by: approximating inguinal and pectineal ligaments using
interrupted non-absorbable monofilamentous suture (1/0 nylon). Three sutures
104
will usually suffice to narrow femoral ring. While this is done, care is taken to
protect and avoid constriction of the laterally placed femoral vein. The authors
personally dissect out the femoral vein before any repair because visualizing it
prevents injury and problems with compression
• An alternative method of repair is to fill the femoral canal with a plug of rolled
mesh, which may then be secured with sutures
• Closure:
• subcutaneous tissue with 2/0 Vicryl
• skin with 3/0 Monocryl.
Assessment of bowel viability

• Viable bowel " pink, visible peristalsis and mesenteric pulsation, sheen to
bowel wall
• Gangrenous bowel " green, black or purple colour with a malodour. There is
no visible mesenteric pulsation and the bowel wall would have lost its sheen.
In general, if there is any doubt about viability, it is best to resect it.
Key learning points

The accessory obturator artery
Present in 50 per cent of patients.
In 50 per cent it has an aberrant medial course running posterior to the
lacunar ligament.
Avoid dividing the lacunar ligament (the Hay–Groves manoeuvre) to
dilate the femoral canal in cases where you need more access to perform a
bowel resection. The authors would have a low threshold to converting to
a laparotomy if this were the case.
105
33 Inguinal hernia repair

What is a hernia?
What is a sliding hernia? What organs can be found within a sliding
hernia?
What are the boundaries of the inguinal canal?
What are the contents of the spermatic cord?
How would you perform an open (usually Liechtenstein) inguinal hernia
repair?
What postoperative complications should you warn the patient of?
What are the common sites of recurrence after an inguinal hernia repair?
How should a recurrent hernia be repaired?
What is the Shouldice repair?
Related topics
Topic Chapter Page
Abdominal incisions 64 259
Key learning point

Definition
A hernia is the abnormal protrusion of a viscus or part of a viscus through an
opening in the walls of its containing cavity into another body compartment.
TYPES
• Indirect (60 per cent) (lies lateral to the inferior epigastric artery)
• Direct (35 per cent) (lies medial to inferior epigastric artery)
• Pantaloon (5 per cent) (combined).
106
OPERATIVE SURGERY inguinal hernia repair
SLIDING HERNIA
A sliding hernia is formed when a retroperitoneal organ protrudes outside the abdom-
inal cavity in such a manner that the organ itself and a peritoneal surface constitute the
hernia sac.
Organs that can be found within a sliding hernia include:
• Colon
• Caecum
• Appendix
• Ovary
• Bladder
• Fallopian tubes and uterus (rare).
INDICATIONS FOR INGUINAL HERNIA REPAIR

• Symptomatic
• Incarcerated
• Strangulated.

What is the anatomy of the inguinal canal?
• 4 cm tunnel in the lower abdominal muscles
• Runs inferomedially between the deep and superficial inguinal rings
Boundaries
Anterior wall: external oblique # internal oblique for lateral third
Roof: conjoint tendon
Floor: inguinal ligament
Posterior wall: transversalis fascia and conjoint tendon
Contents
Male: spermatic cord
Female: round ligament
107

What is the spermatic cord?
Spermatic cord: extends from the deep inguinal ring to the posterosuperior
border of the testicle.
Contents
Think of 12 structures!
• Coverings:
• external spermatic fascia
• cremasteric fascia
• internal spermatic fascia
• Arteries:
• testicular
• artery to vas
• cremasteric
• Vas deferens
• Veins:
• pampiniform plexus
• Lymphatic vessels
• Nerves:
• genital branch of the genitofemoral nerve
• sympathetics
• Processus vaginalis.
The Royal College of Surgeons’ guidelines on hernia management suggest the

Liechtenstein repair or Shouldice technique for primary uncomplicated inguinal
hernias.
OPEN LIECHTENSTEIN REPAIR

• History and examination
• Exclude other causes of pain
• Gain informed consent
• Mark side
• Prophylactic antibiotics (particularly in an incarcerated hernia)
• Usually one shot of a broad-spectrum antibiotic, e.g. cefuroxime, at induction
will suffice
• General or local anaesthetic can be used
108
• Shave pubic hair and prepare skin and drape appropriately

• Incision: inguinal or skin crease
• Identify anterosuperior iliac spine (ASIS) and pubic tubercle
• Place inguinal incision 2 cm above and along medial two-thirds of inguinal
ligament. Do not incise skin lower than mid-inguinal point (surface marking of
deep inguinal ring)
• Ligate any large vessels with 2/0 Vicryl ties
• Divide Scarpa’s fascia and deepen incision to the external oblique aponeurosis.
Identify inguinal ligament and superficial inguinal ring
• Make a short fenestration in the line of the external oblique fibres. Beware: do
not make split too low, otherwise there will be difficulty in closing the
aponeurosis at the end of the operation
• Insert the scissors to separate the canal contents from the aponeurosis. This
reduces risk of damage to the ilioinguinal nerve
• Now enlarge the slit medially and laterally to open the inguinal canal to include
the superficial ring
• Apply forceps to each edge of the aponeurosis
• Apply self-retaining retractors
• Create ‘pockets’ above and below
• Identify and conserve the ilioinguinal nerve on the anterior aspect of the cord
• Mobilize the cord by dividing the mesentery just above and lateral to the pubic
tubercle (blunt dissection)
• Apply a hernia ring or piece of tape
• Move the cord downwards and laterally and divide the coverings along a line
just superior to it. This exposes the site of a direct hernia (medial to the
epigastric vessels) in the transversalis fascia
• Always exclude an indirect sac: open the spermatic fascia covering the cord.
Identify the sac and isolate it to the level of the deep ring
• Identify and conserve the vas deferens
• Open the sac and release the contents into the abdominal cavity. Beware of a
sliding hernia. Transfix (with 2/0 Vicryl) and divide the hernia sac
• Apply a polypropylene mesh – cut into a ‘fish’ shape to repair and reinforce the
weakened posterior wall
• The authors use a 2/0 Prolene suture on a J-shaped needle; the mesh should be
anchored to the pubic tubercle, the lower edge sutured to the inguinal ligament –
avoid including any external oblique fibres
• Overlap the lateral borders (‘fishtail’) around the cord (reconstruction of
the deep ring). Leave a slight gap of approximately 5 mm around the spermatic
cord
• Suture the lateral and superior borders of the mesh in place to the underlying
muscle using interrupted 2/0 Prolene. This should be ‘tension free’; otherwise
perform a Tanner slide
109
• Closure: infiltrate the wound in layers with local anaesthetic (make an effort to
block the ilioinguinal nerve – thought to reduce postoperative pain):
• 1/0 Vicryl to external oblique fascia
• 2/0 Vicryl to Scarpa’s fascia
• 3/0 Monocryl to skin; Steri-Strips
• Check ipsilateral testicle is drawn down to the bottom of the scrotum
• Postoperative advice: avoid heavy lifting for 6–8 weeks.
Key learning point

Hernia recurrence
Most commonplace is medial recurrence. Therefore, it is important to get
mesh far enough over to the midline.
Direct hernias often recur at the pubic tubercle and indirect hernias recur
at the internal ring.
Causes:
• Poorly placed or insufficient stitches
• Infection
• Poor tissue
• Poor collagen formation
• Surgical tension
SHOULDICE REPAIR
This was popularized at the Shouldice Clinic (Toronto) and is useful if repairing a
strangulated hernia when insertion of a mesh is not recommended as a result of
high risk of infection. This method double breasts the transversalis fascia and con-
joint tendon with four continuous lines of non-absorbable suture to reinforce the
posterior wall of the inguinal canal. The suture tract runs from the pubic tubercle to
a new internal ring and results in layered approximation of the conjoint tendon to
the inguinal ligament. In experienced hands, the reported incidence of recurrence is
1 per cent – lowest rate of recurrence for non-mesh repairs.
LAPAROSCOPIC REPAIR
This is indicated in bilateral inguinal hernias and recurrent hernias. The mesh is
stapled between the peritoneum and the fascia transversalis. The laparoscopic
approach is either transperitoneal (TAP) or total extraperitoneal (TEP).
110
COMPLICATIONS
General versus specific
Specific
• Wound:
• bruising and haematoma
• infection
• sinus formation
• Scrotal:
• ischaemic orchitis
• testicular atrophy
• hydrocoele
• damage to vas deferens – infertility
• Operation failure:
• recurrence (aim for 0.5 per cent 5-year recurrence rate)
• missed hernia (usually indirect)
• dehiscence
• Nerve injuries
• Must warn patient of risk of postoperative chronic pain (up to 30 per cent).
111
34 Laparoscopic cholecystectomy and
laparoscopy

What are the contraindications to performing a laparoscopic cholecystectomy?
What important risks should be explained to the patient in obtaining
consent for laparoscopic cholecystectomy?
What is Calot’s triangle and why it is important to identify this landmark?
What are the important steps in performing a laparoscopic cholecystectomy?
How many ports will you use?
How can you ensure that you are dividing the cystic artery rather than
the right hepatic artery?
When would you perform an intraoperative cholangiogram? Why should
it be encouraged?
How do you establish a pneumoperitoneum for laparoscopy?
What are the reported advantages of laparoscopic surgery over open
surgery? What are some of the disadvantages?
Related topics
Topic Chapter Page
DVT prophylaxis and coagulation in surgery 73 297
Functions of the liver 96 384
Liver 10 28
Currently in the UK 90 per cent of cholecystectomies are performed laparoscopically.
INFORMED CONSENT
Important risks associated with laparoscopic cholecystectomy include:
• Pain
• Haemorrhage
• Infection
• Common bile duct injury and possibility of jaundice
• Bowel injury requiring laparotomy
• Possibility of conversion to an open procedure (usually 1/40 – higher if previous
abdominal surgery because of adhesions).
112
OPERATIVE SURGERY laparoscopic cholecystectomy and laparoscopy
CONTRAINDICATIONS
Absolute
• Carcinoma of the gallbladder
• Severe chronic obstructive pulmonary disease (COPD)
• Bleeding diathesis
• Intraoperative:
• unexpected pathology, e.g. severe cholecystitis, portal varices
• inability to delineate anatomy safely
• uncontrollable bleeding
• adjacent organ damage.
Relative
• Liver: cirrhosis with portal hypertension
• Pregnancy
• Morbid obesity
• Previous abdominal surgery – adhesions causing difficult laparoscopic access and
progress
• Acute cholecystitis.
CALOT’S TRIANGLE
Borders are:
• Superiorly: inferior surface of the liver
• Laterally: cystic duct
• Medially: common hepatic duct.
Contents are:
• cystic artery – this is a branch of the right hepatic artery
• cystic lymph node.
It is important to identify and dissect out Calot’s triangle in order clearly to visualize
the cystic duct and artery so that both structures can be clipped and divided safely.
PRINCIPLES OF SURGERY
Preparation
• Warn patient of risks (above)
• Deep vein thrombosis (DVT) prophylaxis – venous stasis can be induced by the
reverse Trendelenburg position (see ‘DVT prophylaxis and coagulation in
surgery’, Chapter 73, page 297)
113
• Single-dose antibiotic prophylaxis has been shown to reduce wound infections

after cholecystectomy
• Anaesthetic is general
• Place patient on a radiolucent operating table in case an on-table cholangiogram
is required
• Skin preparation: nipple to suprapubic region
• Check and arrange leads and equipment
• Local anaesthetic is administered to the skin where the port sites are made.
Access
• Open Hasson technique is advocated by the surgical Royal Colleges because
closed Veress needle insertion is blind and thought to be less safe
• Infraumbilical incision
• Identify umbilical cicatrix and follow it down to the junction with the linea alba
and make an incision
• Insert a pair of McIndoe’s scissors and open the peritoneum. Introduce 10 mm
camera port without the sharp trocar under direct vision
• Create pneumoperitoneum by insufflating with carbon dioxide. Low pressure
and high flow indicate correct positioning of the port in the peritoneal cavity.
Aim for a pressure of 12–14 mmHg but this varies according to the body habitus
of the patient.
Dangers associated with high insufflation pressures

Respiratory
• Splinting of diaphragm leading to impaired gaseous exchange
• Risk spontaneous pneumothorax after higher inflation pressures by
anaesthetist to compensate for this.
Cardiovascular
• Reduced venous return leading to reduced cardiac output
• Reduced venous return increases risk of DVT (venous stasis).
Assessment
• Examine whole of abdominal cavity methodically
• Decide whether laparoscopic approach is feasible
• If so, insert the three remaining ports under direct vision:
• 10 mm epigastric (subxiphisternal) port – just to the right of the midline
• 5 mm midclavicular line port
• 5 mm anterior axillary line (5 cm below costal margin) port – parallel to umbilicus
• Tilt head upwards (reverse Trendelenburg’s position) and patient is rolled
towards operator (left side)
114
• Grasp fundus of gallbladder using a tissue-holding forceps via the most lateral
port and retract it in a cephalad direction over the liver. Ask the assistant to
hold. This minimizes the fold in the gallbladder infundibulum and brings Calot’s
triangle more clearly into view
• Pull gallbladder away from the liver by inferolateral traction on Hartmann’s
pouch. This aids identification of the cystic and common bile ducts by pulling
them out of alignment
• Start dissecting high on the neck of the gallbladder and proceed in a lateral to
medial direction, keeping close to the gallbladder until the anatomy is well defined.
The cystic duct node usually provides a useful starting point for the dissection
• Define and dissect out Calot’s triangle and its contents. Skeletonize the cystic duct
• Double clip the cystic duct and artery using a multiple clip applicator and
divide them. Follow cystic artery to the gallbladder wall to ensure that you have
not divided the right hepatic artery
• Obtain a cholangiogram as indicated:
• jaundice
• preoperative deranged liver function tests (LFTs)
• dilated common bile duct on preoperative ultrasonography
• Perform diathermy dissection of gallbladder off hepatic bed, keeping gallbladder
always on the stretch
• Remove gallbladder via the infraumbilical port ' BERT bag (for the endoscopic
retrieval of tissue)
• Lavage liver bed with warm physiological (0.9%) saline
• Secure haemostasis with hook or ball diathermy
• Consider drain
• Release pneumoperitoneum and watch the instruments carefully as you
withdraw them from the abdominal cavity
• 0 Vicryl stitch on a J needle to close umbilical and epigastric port sites
• Absorbable suture to skin.
OPERATIVE CHOLANGIOGRAPHY
Not all surgeons perform routine intraoperative cholangiography, although there
are good reasons why it should be encouraged. It can help:
• Define the anatomy
• Detect the presence of common bile duct stones
• Avoid further morbidity because ductal stones can be extracted using a
choledochoscope during the same operation. This avoids the need for a
postoperative ERCP (endoscopic retrograde cholangiopancreatography),
which has its own inherent risks including 1 per cent mortality rate
• Identify an injury.
115
LAPAROSCOPIC VERSUS OPEN SURGERY

Advantages
• Less traumatic for patients
• Reduced postoperative pain
• Improved cosmesis
• Faster postoperative recovery
• Reduced adhesion formation
• Shorter stay in hospital and quicker return to normal daily life.
Disadvantages
• Steep learning curve
• Inadvertent damage to surrounding structures as a result of limited field, e.g.
visceral injury.
116
35 Long saphenous varicose vein surgery

What are the indications for performing varicose vein surgery?
What tributaries of the long saphenous vein would you encounter during
a Trendelenburg procedure?
What is the course of the long saphenous vein in the lower leg?
How is the stripping of the long saphenous vein carried out?
What incision would you make to gain access to the saphenofemoral
junction during Trendelenburg’s operation?
How do you perform multiple phlebectomies of varicose veins?
What are the main complications of varicose veins?
Related topics
Topic Chapter Page
DEFINITION
Varicose veins are dilated tortuous superficial veins affecting the lower limb. Found
in distribution of the:
• long saphenous vein (most common)

• short saphenous vein.
AETIOLOGY
This is uncertain but an underlying weakness of the vein wall is likely.
INDICATIONS
The indications for varicose vein surgery are to prevent the complications from
developing or progressing. These are:
• Varicose eczema, lipodermatosclerosis and ulceration

• Bleeding
117
OPERATIVE SURGERY long saphenous varicose vein surgery
• Superficial thrombophlebitis
• Pain
• Calcification and periostitis
• Psychological complications
• Cosmetic reasons.
In most cases, do not operate if there is deep venous obstruction or incompetence.
It is mandatory to obtain a venous duplex scan preoperatively to map out the
venous incompetence.
LONG SAPHENOUS VARICOSE VEIN SURGERY

• Accurate marking of varicosities is essential before the operation. Come to an
agreement with the patient on which ones are to be removed.
• Place patient supine in the Trendelenburg position (30° head-down tilt). Legs
are placed straight but abducted, with both feet resting on the edges of a long
board at the lower end of the table.
• Make an oblique incision parallel to and below the inguinal ligament in the
groin crease over the saphenofemoral junction (SFJ). This is located 2 cm
lateral and below the pubic tubercle.
• Deepen incision through Scarpa’s fascia and insert a West self-retaining
retractor. The subcutaneous fatty tissue can be swept away with a swab to
expose the long saphenous vein (LSV) and its tributaries.
• Dissect out the LSV and follow it up to the SFJ.
• Dissect out and ligate all tributaries.
• It is important to display the femoral vein 1 cm above and below the SFJ in
order to prevent accidental division of it rather than the LSV.
• A double tie is used to ligate the LSV with 0 Vicryl flush with the SFJ, and
divide it such that there is a tuft of vein left at the SFJ to prevent the sutures
from falling off.
• Introduce a stripper distally and feed it down to a hand’s breath below the
knee.
• Make an incision over the tip of the stripper, deliver the vein, and tie and ligate
the distal LSV. Strip out the proximal part of the vein with gentle traction along
the long axis of the leg, applying some pressure over the tunnel as the stripper is
withdrawn. In the authors’ experience, this reduces the risk of haematoma and
bruising postoperatively.
• Perform multiple phlebectomies as agreed preoperatively with the patient:
• small vertical stab incisions are made over the varicosities; a loop of vein is
brought out through the stab incision by blunt dissection with an artery for-
ceps or a special fishhook
• the loop of vein is divided between two artery forceps
118
OPERATIVE SURGERY long saphenous varicose vein surgery
• using traction and rotation, the vein is pulled until it breaks

• bleeding is controlled by local pressure
• you may have to ask the anaesthetist to put the patient’s head down further to
reduce venous bleeding.
• Achieve haemostasis.
• Close the groin wound so that the SFJ is buried under opposed Scarpa’s fascia.
• The authors use a subcuticular skin closure in the groin wound and Steri-Strips
across the phlebectomy sites.
• A pressure dressing with wool crepe band or Velband is placed over the limb.
• One postoperative dose of subcutaneous heparin is given to reduce the risk of a
DVT.
• Patient is sent home, usually the same day, with usual varicose vein surgery
advice, including changing the dressing for a thromboembolic stocking on day 5.
The patients should be advised to keep this on for around 2 weeks.
• No follow-up is necessary.

What are the surface markings of the long saphenous vein?
Drains medial end of dorsal venous arch in the foot.
Passes anterior to the medial malleolus and ascends in company with the
saphenous nerve in the superficial fascia over the medial side of the leg.
Behind the knee, the LSV lies one hand’s breadth behind the medial
aspect of the patella.
It then passes along the medial aspect of the thigh through the lower part
of the saphenous opening in the cribiform fascia to join the femoral vein
2 cm below and lateral to the pubic tubercle (SFJ).
TRIBUTARIES OF THE LSV

There are commonly six:
1. Superficial inferior epigastric vein
2. Superficial external pudendal vein
3. Deep external pudendal vein
4. Superficial circumflex iliac vein
5. Anterolateral thigh vein
6. Posteromedial thigh vein.
119
36 Mastectomy, axillary dissection and
breast reconstruction

What is a mastectomy?
When would you perform a mastectomy?
What types of mastectomy do you know about?
What types of axillary clearance are there?
How would you perform an axillary dissection?
What is breast reconstruction?
What can be used to reconstruct a breast?
When should drains be removed post-mastectomy?
Related topics
Topic Chapter Page
Breast cancer 50 182
Wound healing, scarring and reconstruction 83 342
Skin grafting and flap reconstruction 78 320
Drains in surgery 72 295
Key learning point

Definitions
• Mastectomy: the surgical removal of all breast tissue of one breast
• Axillary clearance: the surgical excision of all axillary lymph nodes up to
a predetermined level
• Breast reconstruction: the use of material, either prosthetic or living, to
create a new breast mound
TYPES OF MASTECTOMY
• Subcutaneous: all breast tissue is removed but the overlying skin including the
nipple–areolar complex remains.
• Skin sparing: all breast tissue and the nipple–areolar complex are removed but
the overlying skin remains.
120
OPERATIVE SURGERY mastectomy, axillary dissection and breast reconstruction
• Simple (or total): all breast tissue and overlying skin is removed.
• Modified radical: all breast tissue, overlying skin and axillary lymph nodes are
removed.
• Radical: all breast tissue, overlying skin, pectoralis muscles and axillary lymph
nodes are removed. This is very rarely used any more.
INDICATIONS FOR MASTECTOMY

Therapeutic mastectomy for carcinoma of the breast
• Two or more tumours in separate areas of the breast
• Widespread DCIS (ductal carcinoma in situ)
• Subareolar tumour
• Large tumour relative to breast size
• High risk of further disease (BRCA-1/-2 positive)
• Previous irradation to breast
• When irradiation is contraindicated (e.g. early pregnancy)
• Patient preference.
Prophylactic mastectomy
• Strong family history for breast carcinoma
• To obtain optimal symmetry for reconstruction
• For peace of mind after mastectomy for carcinoma of the contralateral breast.
AXILLARY CLEARANCE LEVELS

The axilla is divided into three levels. These levels are defined by the inferior and
superior borders of pectoralis minor:
1. Level 1: axillary contents below pectoralis minor
2. Level 2: axillary contents up to upper border of pectoralis minor
3. Level 3: axillary contents to the outer border of the first rib.
A level 2 axillary clearance will take all nodes from levels 1 and 2. A level 3 clearance
will take nodes from levels 1, 2 and 3. Level 2 is most commonly performed and is
adequate clearance in almost all cases unless large apical nodes are present when
level 3 would be needed. Some surgeons will perform a level 3 clearance in the case
of metastatic melanoma (see ‘Malignant melanoma’, Chapter 60, page 232).
MODIFIED RADICAL MASTECTOMY

Preoperative considerations and management
• Check that a biopsy-proven diagnosis has been reached and that the side is
confirmed and marked
121
OPERATIVE SURGERY mastectomy, axillary dissection, and breast reconstruction
• Reconstruction should be offered to all women undergoing mastectomy

• The breast care nurse should have seen the patient preoperatively
• Multidisciplinary team (MDT) approach
• Group and save and routine preoperative bloods
• Careful, informed consent.
Mastectomy operation
• Place patient supine with the ipsilateral arm secured to an arm board
• Mark the limits of the breast
• Mark a transverse ellipse encompassing the nipple–areolar complex and the
lump and ensure that these wound edges will approximate
• Make a skin incision along the marked ellipse
• Elevate superior and inferior skin flaps between subcutaneous fat and breast fat
to the extents of the breast, as previously marked:
• ensure the flap thickness is adequate for skin viability but that no breast fat is
included in the flap
• handle the skin gently and use non-crushing instruments (e.g. skin hooks) to
avoid skin flap necrosis
• check the flap thickness regularly to avoid ‘buttonholing’
• At the upper and lower extents of the breast, dissect down towards the chest
wall to pectoralis fascia
• Dissect along the chest wall in the plane between pectoralis fascia and breast
tissue from medial to lateral in order to lift the breast from the chest wall. Leave
the axillary tail attached:
• ensure that large perforating vessels are ligated or cauterized before they are
cut to avoid retraction of cut vessels
• Identify the border of pectoralis major and clear the axillary tail
• Mark the specimen at the axillary tail and anteriorly
• Wash the cavity with water to eliminate any solitary tumour cells and
unvascularized fat globules
• Pack the cavity with saline-soaked gauze and change gloves.
Axillary clearance
• Extend the incision superolaterally to the anterior border of latissimus dorsi
• Identify the lateral border of pectoralis major and the anterior border of
latissimus dorsi, which form the anterior and posterior boundaries of the
clearance
• Dissect around the lateral border of pectoralis major to reach pectoralis minor
and retract this medially to visualize the level 2 axillary contents
• Continue your dissection superiorly to identify the axillary vein, the upper
boundary of the clearance. Dissect along and visualize the inferior border of this
vein along its whole length
122
OPERATIVE SURGERY mastectomy, axillary dissection and breast reconstruction
• Gently dissect the axillary contents away from the chest wall identifying:
• intercostobrachial nerve(s): these can be cut if necessary to facilitate clearance
but will result in numbness of the medial arm
• nerve to serratus anterior (posterior to the midaxillary line)
• nerve to latissimus dorsi
• subscapular vessels
• When all vessels and nerves have been identified, the axillary contents can be
removed
• Mark the specimen at the apex
• Insert two drains – one for the mastectomy flaps and one for the axilla
• Close the skin ensuring that any length discrepancy between the skin edges is
evenly distributed to avoid ‘dog ears’.
Postoperative
• Check Hb the next day
• Inspection of skin flaps for evidence of necrosis
• Drain management:
• a chart of daily drainage should be kept
• there is no consensus between specialties as to when drains should be
removed postoperatively. Many breast surgeons will remove drains when the
drain effluent becomes serous with little weight placed on volume of
drainage. This is in contrast to plastic surgeons who will often leave drains
until ! 30 mL drainage in a 24-hour period. The type of operation will obviously
have an impact on this decision with immediate reconstruction requiring more
cautious drain management.
RECONSTRUCTION
All women undergoing mastectomy should be offered breast reconstruction, the
goal of which is to create a mound to match the remaining natural breast.
There are three main types of reconstruction – prosthetic, autologous and a combin-
ation of the two. Any of these can be performed at the same time as mastectomy
(immediate reconstruction) or during a separate operation (delayed reconstruction).
Prosthetic reconstruction involves inserting an implant between the chest wall and
the pectoralis muscles, which can be either a fixed-volume silicone implant or an
expandable saline-filled implant, depending on the nature of the overlying skin and
the size of the desired reconstruction. Expanders are gradually filled with saline over
3–6 months and then removed and replaced with permanent fixed-volume implants.
A relatively recent development is a permanent expandable implant, which has an
outer fixed-volume silicone chamber and an inner expandable saline chamber. This
allows for tissue expansion and reconstruction in a one-stage procedure.
123
OPERATIVE SURGERY mastectomy, axillary dissection, and breast reconstruction
Autologous reconstruction involves moving tissue from elsewhere to the breast to

create a breast mound. Common donor sites are:
• The back (latissimus dorsi – muscle and skin)
• The abdomen (TRAM [transverse rectus abdominus myocutaneous] – muscle,
fat and skin; DIEP [deep inferior epigastric perforator] – fat and skin)
• The buttock (SGAP/IGAP [superior gluteal artery perforator/inferior gluteal
artery perforator] – fat and skin)
Combination reconstruction is generally used with a latissimus dorsi flap, when the
bulk of the muscle itself would not create an adequate mound to match the remain-
ing breast. An implant is inserted between the pectoralis muscles and transposed latis-
simus dorsi to increase the volume of the breast while overlying latissimus dorsi and
its skin paddle create a better texture and shape than prosthetic reconstruction alone.
124
37 Open appendicectomy
How would you prepare a patient for an open appendicectomy?
Why do you give intravenous antibiotics?
How would you perform an open appendicectomy?
What are the complications of an appendicectomy?
Where would you make your incision for an appendicectomy? What layers
do you go through to reach the peritoneum?
Do you bury the appendix stump?
When do you expect a difficult appendicectomy? What methods would
you employ before calling a senior colleague for help?
What would you do if the appendix were normal?
How would you manage an appendix mass? When would you operate?
Related topics
Topic Chapter Page
Abscess and pus 44 158
PREPARATION
• Full history and examination. Investigations: full blood count (FBC) and
C-reactive protein (CRP) ' imaging (ultrasonography or CT)
Prepare patient for theatre:
• Obtain informed consent including risk of wound infection, intra-abdominal
abscess/collection and possibility of a normal appendix
• Patient is kept nil by mouth, given intravenous fluids and antibiotics, the latter
ideally in the anaesthetic room before surgery
• Use cefuroxime (broad-spectrum) and metronidazole (anaerobic cover)
• Prophylactic antibiotics should be routinely given because the incidence of
wound and intra-abdominal infections is high after appendicitis
• Under general anaesthetic with an endotracheal tube, patient is placed supine
on the table. Abdomen is examined under anaesthetic – is there a mass? This
may help determine the best place for the incision
• The entire abdomen should be cleaned and draped to expose the right lower
quadrant including the right ASIS, umbilicus and midline.
125
OPERATIVE SURGERY open appendicectomy
PROCEDURE
• Incision: Lanz – centred over McBurney’s point (1⁄3 way from the ASIS to the
umbilicus) in Langer’s lines (better cosmesis). Gridiron is less good cosmetically
but enables easier extension of the wound
• Commence incision 1–2 cm medial to ASIS and continue it transversely
• A midline incision should be employed if the patient were elderly and there
may be a possibility of a caecal carcinoma
• Introduce a Norfolk and Norwich self-retaining retractor
• Peritoneum held up with two artery forceps and divided with a scalpel
• Care is taken not to damage any underlying loops of bowel
• Microbiology swab is taken of any peritoneal fluid for microscopy, culture and
sensitivity
• Inspect:
• caecum and small bowel for any other pathology, e.g. caecal neoplasm or
Meckel’s diverticulum
• in women inspect the ovaries and fallopian tubes – rule out pelvic inflamma-
tion, pelvic abscess or even an ectopic pregnancy (a preoperative #-hCG
[human chorionic gonadotrophin] should have been checked!)
• if all normal, proceed and mobilize caecum (most lateral structure in the peri-
toneum). Locate appendix by following the taenia to the base of the appendix.
If possible deliver appendix into the wound.

What layers do you go through to reach the peritoneum?
Layered incision through:
• Skin
• Fat
• Scarpa’s fascia
• Fat
• External oblique aponeurosis
• Internal oblique (muscle splitting incision with Langenbeck retractors)
• Transverse abdominis (muscle splitting incision with retractors)
• Transversalis fascia and peritoneum, which are fused
• Position:
• retrocaecal 62 per cent
• pelvic 34 per cent
• medial pre-ileal 1 per cent; post-ileal 0.5 per cent.
126
• Confirm diagnosis and begin mobilization of appendix. Hold appendix with a

pair of Babcock’s forceps and avoid perforating it
• The mesoappendix is divided between artery forceps and secured with 2/0
Vicryl ties to skeletonize the appendix and free it to its base
• A straight crushing clamp is applied across the base and replaced 5 mm distally.
After applying a 0 Vicryl tie in the form of a surgeon’s knot to the base, divide
the appendix flush to the clamp using a scalpel
• Diathermy is applied to the pouting mucosa of the appendix base to prevent
mucocele formation and reduce the bacterial load
• Ensure that the instruments used to divide the appendix are not used again so as
to avoid contamination
• The authors do not routinely apply a purse-string (in the form of a ‘Z’ stitch or
purse-string) to bury the stump. There is no evidence to suggest that routinely
burying the stump of the appendix reduces intra-abdominal infection, faecal
fistula formation or stump blow-out
• The abdomen is then washed out with warm saline and 10 per cent betadine
• If there is a pelvic collection, have a low threshold for inserting a drain and
carrying out a full pelvic lavage
• Achieve haemostasis
Key learning points

How to take out a difficult appendix
Commonly asked not only in the MRCS viva but also at general surgical
registrar interviews!
Expect a difficult operation if the history is long and if an appendix mass
is present.
The appendix is usually in a retrocaecal or pelvic position. Consider:
• Using your index finger of your dominant hand gradually to ‘winkle’ out
the appendix
• Removing the appendix retrogradely (base first)
• In a true retrocaecal appendix, the caecum can be mobilized by dividing
its lateral peritoneal attachments as for a right hemicolectomy
• Enlarging the incision by cutting the muscle. Don’t be afraid to do this
• Getting a good assistant to help retract for you
• In the presence of an abscess and being unable to find the appendix,
placing a large size Robinson drain into the abscess, washing out the
abdomen with saline and closing it
127
• Wound is closed in layers using absorbable sutures

• The authors use continuous 1/0 Vicryl to peritoneum and muscular layers with
2/0 Vicryl to the subcutaneous layer and 3/0 Monocryl to the skin
• If the patient had a perforated appendicitis he or she should continue to have
5 days of intravenous antibiotics postoperatively
• If the appendix were only inflamed (pre-perforation) one further dose should
suffice
• The appendix is routinely sent for histological confirmation (to exclude
carcinoid and carcinoma). Sometimes the appendix looks normal but
microscopically may be inflamed. The specimen should always be sent for
histological confirmation.

What would you do if the appendix were normal?
If the appendix were normal looking, I would need to search for other pos-
sible causes:
• In a woman, look at the right fallopian tube and ovary
• Inspect the terminal ileum and palpate for any thickening. This might
indicate Crohn’s ileitis or tuberculous ileitis depending on background
• The small bowel is run to examine for a Meckel’s diverticulum or for any
inflamed mesenteric lymph nodes (mesenteric adenitis)
• Palpate posterior abdominal wall, ascending colon, liver edge and gall-
bladder fundus (for cholecystitis). Look for bile-stained fluid suggesting a
perforated duodenal ulcer
• Inspect the large bowel (sigmoid diverticulitis)
• If there were an inflamed Meckel’s diverticulum this would need to be
resected with a short segment of adjacent normal bowel, and a primary
interrupted extramucosal anastomosis performed
COMPLICATIONS
General versus specific
Specific complications include:
• Wound infection
• Wound abscess
• Bleeding and haematoma
• Pelvic abscess and collection
128
• Peritonitis
• Keloid scar formation
• Peritoneal adhesions
• Increased incidence of right inguinal hernia (damage to ilioinguinal nerve)
• Incisional hernia (rare)
• Damage to other structures, e.g. small bowel, caecum (caecal fistula) and
fallopian tubes
• Normal appendix!

How do you manage an appendix mass?
An appendix mass is usually treated conservatively with bed rest and intra-
venous antibiotics. Serial examination to monitor the patient’s progress
carefully is important. An interval appendicectomy is usually performed at
6 weeks.
Indications for surgical intervention are:
• The mass becomes tender or enlarges
• The patient becomes toxic with a swinging pyrexia and tachycardia and
increasing white cell count (WCC and C-Reactive Protein (CRP))
• The patient develops signs of peritonitis, obstruction or paralytic ileus
129
38 Orthopaedic related approaches and
procedures

What are the typical features of a classic Colles’ fracture?
How would you reduce a Colles’ fracture?
What are the complications of a Colles’ fracture?
What is the clinical significance of the anatomical snuffbox?
What are the indications for performing an ORIF on a scaphoid fracture?
What are the steps involved?
How would you perform a DHS operation?
What common approaches to the hip/knee are you aware of ?
Related topics
Topic Chapter Page
The hip joint, neck of femur and sciatic nerve 74 303
REDUCTION OF A COLLES’ FRACTURE

A Colles’ fracture is a distal fracture of the radius that occurs in elderly, osteoporotic
patients. It usually results from a fall on to the outstretched hand and results in the
‘dinner fork’ deformity.
The fracture is:
• dorsally angulated
• impacted
• radially deviated
• associated with an avulsion of the ulnar styloid.
Complications
• Malunion
• Subluxation of the radioulnar joint
• Extensor pollicis longus tendon rupture
130
OPERATIVE SURGERY orthopaedic related approaches and procedures
• Joint stiffness
• Carpal tunnel syndrome
• Sudeck’s atrophy.
Reduction
• Disimpact the fracture by pulling and flexing the wrist dorsally
• Reduce the fracture by pushing the distal fracture in a volar direction with
ulnar deviation
• Set in plaster of Paris (POP).
OPEN REDUCTION AND INTERNAL FIXATION (ORIF) OF

SCAPHOID FRACTURE
Indications for surgery
• Non-union
• Freshly displaced fracture
• Trans-scaphoid perilunate dislocation.
Procedure
• Dorsal longitudinal incision
• Preserve radial artery
• Appraise need for a bone graft; if required harvest from iliac crest
• From distal to proximal:
• guide pilot drill
• use image intensifier (I/I) to view position
• Herbert screw fixation
• I/I to confirm position
• Set in POP.

What is the anatomical snuffbox?
Lateral border: two tendons
• abductor pollicis longus
• extensor pollicis brevis
Medial border: extensor pollicis longus
Floor: scaphoid bone
Contents: radial artery and nerve
131
Clinical significance
The scaphoid bone can be palpated in the snuffbox and is at risk in injuries that
involve force applied to the palmar surface of the outstretched hand. The scaphoid
is at risk of proximal avascular necrosis in fractures affecting the waist of the
scaphoid as a result of its end-arterial blood supply.
Any tenderness elicited in the snuffbox with the typical background history should
arouse suspicions of a scaphoid fracture and appropriate scaphoid radiological
views requested.
SURGICAL APPROACHES TO THE HIP

Anterior (Smith–Petersen) approach
Internervous plane between tensor fascia lata (superior gluteal nerve) and sartorius
(femoral nerve), then divide rectus femoris and anterior third of gluteus medius.
Used commonly in paediatric orthopaedic surgery to correct congenital dislocation

of the hip.
Lateral (Hardinge) approach

Patient is placed laterally on the table. A longitudinal incision is made 10 cm below
the greater trochanter and curved posteriorly.
Split tensor fascia lata, gluteus medius and minimus or detach them from the
greater trochanter.
Incision is then extended through vastus lateralis on to the anterior aspect of the
femur, which should expose the capsule of the hip joint.
Beware of the superior gluteal nerve.
Posterior approach
Skin incision is centred on the posterior part of the greater trochanter. Proximally
it is curved towards the posterosuperior iliac spine. After the subcutaneous tissue,
this involves splitting gluteus maximus and detaching piriformis, obturator inter-
nus and gemelli from the femur. This achieves access to the posterior capsule of the
hip joint.
Beware of the sciatic nerve.
132
DYNAMIC HIP SCREW (DHS) INSERTION

• General or spinal anaesthetic
• Broad-spectrum intravenous antibiotics at induction
• Patient placed supine on an orthopaedic traction table
• Reduce fracture by traction, abduction and internal rotation, and hold in place
using the traction table
• Check adequate reduction by using image intensifier
• Area is prepared and draped with a transparent polythene sheet
• Make a 15 cm longitudinal incision from greater trochanter down the thigh
• Layers traversed:
• skin
• subcutaneous fat
• fascia lata
• vastus lateralis to expose upper lateral femur
• Guidewire is passed across the fracture into the femoral head
• Use the jig to achieve an angle of 135° to the femoral shaft. Use the image
intensifier in two planes to check adequate placement
• Distance the screw needs to travel is measured accordingly and the path is
drilled over the guidewire
• The drill hole is tapped before the screw is inserted over the guidewire
• Use the image intensifier to check for a satisfactory position in the femoral head
(screw tip should abut the subchondral bone)
• Remove wire. Use the periosteal elevator to clear the lateral femur before
applying a five-hole buttress plate over the end of the DHS
• The plate is secured with screws through both cortices
• A check radiograph is performed before closing the wound in layers
• A suction drain should also be used.
APPROACH TO THE KNEE JOINT

Anteromedial approach
Longitudinal incision centred over the medial border of the quadriceps tendon. Start
8 cm proximal to the patella and extend distally.
Curve incision to the medial aspect of the patella and then return to midline infer-
iorly. Lower limit should be the tibial tuberosity.
The plane of dissection should be between vastus medialis and the quadriceps
tendon.
133
Expose capsule of joint by dividing the fascia.
Patella is reflected laterally and the knee flexed to obtain optimal views.
Lateral parapatellar approach

Incision parallel to the lateral edge of the patella 1–2 cm from it.
Divide extensor expansion, capsule and synovial membrane.
Avoid infrapatellar branch of saphenous nerve.
134
39 Perforated duodenal ulcer and
exploratory laparotomy

How would you perform an open repair of a perforated peptic ulcer?
What would your postoperative management be?
What is the differential diagnosis with the same clinical presentation?
Name four features of pneumoperitoneum on plain radiographs
What is the most common cause of free intra-abdominal gas?
Does the absence of air under the diaphragm on an erect chest radiograph
exclude a perforated peptic ulcer?
What conditions may mimic the appearance of a pneumoperitoneum?
How much free gas needs to be present to be detected on plain erect
chest radiograph?
What are the typical presenting features of a perforated peptic ulcer?
What do you understand by the term ‘right paracolic gutter phenomenon’?
How do you perform an exploratory laparotomy?
Related topics
Topic Chapter Page
CLINICAL FEATURES
Typically, perforated duodenal ulcers produce acute onset epigastric pain followed
by more generalized abdominal pain.
Sometimes right iliac fossa pain occurs as a result of duodenal–gastric contents
accumulating at this site under gravity. This can sometimes be confused with acute
appendicitis – ‘right paracolic phenomenon’.
The patient may also complain of right shoulder tip pain caused by referred pain
from diaphragmatic irritation.
Nausea is common but vomiting is uncommon.
The patient lies perfectly still with frequent shallow respirations. The diagnosis can
be made from the end of the bed.
135
OPERATIVE SURGERY perforated duodenal ulcer and exploratory laparotomy
Examination reveals a distended and ‘board-like’ abdomen as a result of involun-

tary contraction of rectus abdominis. There is a paucity/absence of bowel sounds.
Systemic signs include pyrexia, tachycardia, tachypnoea and a dry tongue.
Key learning points

Common topic to be asked alongside being shown erect chest and supine
abdominal radiographs.
Example
This erect chest radiograph and supine abdominal film were taken of a
34-year-old man with a 24-hour history of sudden-onset worsening gener-
alized abdominal pain.
What do these radiographs show?
Free air under the diaphragm
Visible falciform ligament
Rigler’s sign: both sides of the bowel wall are seen since air outside the
wall (free intraperitoneal air) acts as a contrast medium as it does
physiologically when inside the bowel.
What is the most likely diagnosis?
In a man of this age and with this history, the most likely diagnosis is a
perforated duodenal ulcer.
PREDISPOSING FACTORS
• Young men below the age of 50 years
• Smokers
• Drinking excess alcohol
• Steroids
• NSAID use.
Twenty per cent of cases have no prior history of peptic ulcer disease.
DIFFERENTIAL DIAGNOSIS
• Acute pancreatitis
• Acute cholecystitis
• Acute appendicitis
• Leaking abdominal aortic aneurysm
• Myocardial infarction.
136
CONDITIONS THAT MIMIC THE APPEARANCE OF A PNEUMOPERITONEUM

• Chilaiditi’s sign – presence of intestine (colon) between the liver and diaphragm
• Subphrenic abscess
• Basal atelectasis that mimics the contour of the hemidiaphragm
• Subdiaphragmatic fat
• Cysts in pneumatosis coli.
Pneumoperitoneum
The most common pathological cause of free intraperitoneal gas is a perforated pep-
tic ulcer.
It is possible to detect 1 mL of free air on an erect chest radiograph or decubitus view.
Features on a plain radiograph include:
• Free air under the diaphragm (erect chest radiograph)

• The falciform ligament of the liver
• The lateral wall of the large bowel – Rigler’s sign
• Air around the liver
• Free air in triangular shapes between loops of bowel.
The absence of subdiaphragmatic air on an erect chest radiograph does not exclude
a perforated peptic ulcer.
Approximately 10–30 per cent of cases do not demonstrate free intra-abdominal
gas. If in doubt request a lateral decubitus view because this is more sensitive at
picking up free air.
OTHER COMMON CAUSES OF VISCUS PERFORATION

• Perforated diverticular disease – normally free air is not detected because the
perforation gets sealed off and there is less air in the colon
• Appendix
• Malignant colonic tumour
• Gallbladder
• Small bowel (in obstruction).
PERFORATED PEPTIC ULCER REPAIR

If patient is aged over 60 years with multiple co-morbidities and a systolic blood
pressure $ 100 mmHg, consider conservative management with a strict nil-by-mouth
regimen and nasogastric tube insertion.
137
• Preoperative preparation includes fluid resuscitation, urinary catheter insertion

for strict input/output assessment, good pain control, broad-spectrum
antibiotics, strictly nil-by-mouth regimen with placement of a nasogastric
tube
• Under general anaesthetic (endotracheal intubation) patient is placed supine on
the table. Skin preparation includes the whole of the abdomen, as a perforated
colonic lesion cannot be ruled out
• Upper midline incision made from xiphisternum to umbilicus initially – can be
extended later if necessary
• Wound retraction using a self-retaining retractor or an assistant if required
• Careful assessment of stomach (especially lesser curvature) and duodenum is
made
• The perforated ulcer is identified. If gastric in nature, biopsy from edge is taken
and sent to histology to rule out malignancy
• Closure of the ulcer is made using an omental patch and interrupted parallel
absorbable sutures. The authors believe that primary closure of the ulcer is
technically unacceptable because there is bound to be tension on already friable
tissue and therefore technical failure ensues. The omental patch is positioned so
that it is placed right down into the ulcer cavity
• Peritoneal lavage is performed with warm physiological saline to include the
subphrenic spaces, paracolic gutters and pelvis
• The authors’ practice is to place a drain near the patch site, although this is
controversial
• Definitive treatment for the ulcer in the form of a truncal vagotomy and
drainage or partial gastrectomy is no longer performed
• Broad-spectrum antibiotics should be continued postoperatively for at least
5 days and then reviewed.
Variant scenarios
• If at laparotomy the surgeon cannot find a perforated peptic ulcer he would
explore all abdominal organs including the gallbladder and sigmoid colon.
Other causes for an acute abdomen should be excluded.
• For a bleeding perforated gastric ulcer, distal gastrectomy should be
performed.
• In a perforated anterior duodenal ulcer with a coexisting bleeding posterior
duodenal ulcer (‘kissing ulcers’), the author would insert non-absorbable
sutures at the base of the bleeding ulcer and close the anterior
gastroduodenotomy as a pyloroplasty.
138

How do you perform an exploratory laparotomy?
Methodical approach
Inspect and palpate:
1. Right lobe of liver, gallbladder, left lobe of liver, spleen
2. Diaphragmatic hiatus, abdominal oesophagus, stomach, duodenal bulb
3. Bile duct, right kidney, duodenal loop and transverse colon
4. Body and tail of pancreas, left kidney
5. Mesenteric root, superior mesenteric vessels, middle colic artery, aorta,
inferior mesenteric artery
6. Appendix, caecum, colon, rectum
7. Pelvis, uterus, fallopian tubes, bladder
8. Hernial orifices, iliac vessels
139
40 Renal transplantation

What are the indications for performing a renal transplantation?
What are the most common causes of end-stage renal failure?
What types of renal donors have you heard of ?
What are the principles of preparing a patient for renal transplantation?
How would you perform a renal transplant?
What are the operative principles of renal transplantation in adults?
What anastomoses are performed in a renal transplantation?
What are the possible complications?
How might you be aware that transplant rejection is occurring?
Outline the three main types of allograft rejection.
What are the indications for renal replacement therapy?
How can this be achieved?
Related topics
Topic Chapter Page
Brain-stem death 106 423
Kidney 9 26
Oliguria and renal replacement 116 482
Anastomosis and anastomotic leak 66 270
INDICATIONS
Renal transplantation has become a cost-effective, safe mode of treatment for end-
stage renal failure. Quality of life is improved considerably. The most common rea-
sons in the UK are:
• Hypertensive renal disease
• Glomerulonephritis
• Polycystic kidney disease
• Reflux pyelonephritis
• Congenital obstructive uropathies.
140
OPERATIVE SURGERY renal transplantation
DONOR TYPES
• Cadaveric (most common) or deceased donors. These can be divided into
brain-stem death donors who will become heart-beating donors (90 per cent of
solid organ donors) and donors who do not fulfil the brain-stem death criteria
(non-heart-beating cadavers)
• Living who can be related or unrelated to the recipient.
PREPARATION
• Careful consent
• Donor kidney retrieval – limit ischaemic time
• Antibiotics – usually co-amoxiclav (Augmentin)
• Immunosuppression (methylprednisolone) # calcineurin inhibitor
• Mannitol
• Cytotoxic cross-match
• Blood available (type matched) – usually for 2 units
• Work patients up for contraindications:
• cancer
• infections, e.g. need a urinary tract free of sepsis
• anatomical urological problems
• Correct metabolic abnormalities, e.g. hyperkalaemia
• Does the patient require dialysis preoperatively?
• Truly multidisciplinary approach.
PROCEDURE
• Prepare donor kidney under sterile conditions (usually at 4°C in theatre). This
involves assessment for damage, cleaning off excess fat and preparing renal vein
and artery for prompt anastomosis
• Lanz or hockey-stick incision (usually contralateral iliac fossa to the side where
the donor organ originated – heterotopic transplantation)
• Divide anterior abdominal wall muscles.
Extraperitoneal approach
• Identify and mobilize external iliac artery and vein and control with sloupes.
These vessels are clamped before anastomosis. Minimize disturbing the
surrounding lymphatic vessels – there is a risk of developing a postoperative
lymphocoele
• Remove the prepared donor artery from ice.
141
• Perform:
• end-to-side anastomosis between donor renal artery and external iliac artery
or internal iliac artery with 5/0 Prolene
• end-to-side anastomosis between donor renal vein and external iliac vein
• Remove clamps
• Secure haemostasis
• Fill bladder with physiological saline
• Spatulate end of ureter and anastomose to the dome of the bladder using 4/0
PDS and a submucosal tunnelling technique to prevent urinary reflux. Test the
anastomosis by refilling the bladder with saline
• When the three anastomoses have been performed, the renal pelvis is the most
anterior structure, then artery and the vein most posterior
• Take a renal biopsy (time 0 biopsy) for future baseline comparisons
• Wound closure in layers leaving a large silicone tube drain in situ.
POSTOPERATIVE CONSIDERATIONS
• Administer immunosuppressive regimen, e.g. steroids, ciclosporin, azathioprine
• Careful monitoring of urine output and fluid administration are essential in the
early postoperative period: the patient may be anuric, polyuric or producing
urine in a manner appropriate to the fluid balance.
COMPLICATIONS
• Bleeding
• Haematoma
• Delayed graft function – 20–30 per cent because of acute tubular necrosis
• Infection:
• immunosuppression increases susceptibility
• bacterial pathogens complicating any surgery
• opportunistic infections, e.g. cytomegalovirus (CMV)
• Ureteric leakage or stenosis
• Renal vein thrombosis
• Lymphocoele around kidney
• Rejection (see below)
• Increased risk of malignancy (lymphoma) because of immunosuppression.
FEATURES OF REJECTION
• Pyrexia
• Tenderness over the graft
• Reduction in urine output
142
• Weight gain
• Rising creatinine.
TYPES OF REJECTION
Hyperacute rejection
Recipient’s serum has preformed antibodies against the donor kidney’s antigens.
Antibodies adhere to the endothelium of the graft causing graft thrombosis and
infarction. This type of rejection is rapid – within minutes of surgery – and is pre-
vented by ABO matching and cross-matching tests. It is treated by graft nephrectomy.
Acute rejection
This is a T cell-mediated attack on the graft involving CD4 cells. It usually presents
within 3 months of transplantation and causes graft dysfunction. The diagnosis is con-
firmed with a biopsy of the graft and is treated by a short course of high-dose
immunosuppression with steroids or anti-lymphocyte antibodies.
Chronic rejection
This occurs usually ! 6 months after renal transplantation. It involves both the
humoral and cell-mediated arm of the immune response. Characteristic histological
features include glomerulosclerosis and intimal thickening of small arteries.
Non-immunological factors are also implicated including viral infection and drug
toxicity. Unfortunately it is not treatable or reversible.
Graft survival rates

Donor type 1-year survival rate (%) 5-year survival rate (%)
Cadaveric 85 65
Living related 90 80
143
41 Thyroidectomy

What are the indications for performing a thyroidectomy?
What incision would you make and what are your landmarks?
What layers are traversed in your approach to the thyroid gland?
What vessels need to be ligated during the operation and which set of
vessels should be ligated first to aid delivery of the gland into the surgical
field?
What are the important nerves to watch out for?
How would you perform a thyroid lobectomy/subtotal thyroidectomy?
What are the potential complications that should be told to the patient
while gaining informed consent?
What should be next to the patient’s bedside postoperatively? Under what
circumstance is this used and if this were to occur what else must you do?
Related topics
Topic Chapter Page
Hyperparathyroidism 58 224
Thyroid gland and parathyroid glands 18 49
INDICATIONS
• Malignancy: except anaplastic tumour or lymphoma
• Adenomas (fine-needle aspiration cannot often differentiate benign from
malignant)
• Thyrotoxicosis (failed medical management)
• Pressure symptoms: dyspnoea or dysphagia
• Cosmesis: large multinodular goitre.
PREOPERATIVE
• Vocal cord check with indirect laryngoscopy must be performed even if there is
no suspicion of recurrent laryngeal nerve (RLN) palsy
144
OPERATIVE SURGERY thyroidectomy
• Render thyrotoxic patients euthyroid with carbimazole and propranolol

• Informed consent (including hypothyroidism, risk to parathyroids and RLN)
• General anaesthetic
• Patient positioned supine with neck extended. Head ring and sandbags placed
in the interscapular region
• The neck is prepared and draped appropriately
• Transverse collar incision 2 cm above the sternal notch in Langer’s lines
• Extend incision as far laterally as the medial border of sternocleidomastoid and
deepen it through subcutaneous tissue and platysma
• Raise superior and inferior subplatysmal flaps above strap muscles using Allis
tissue forceps and a combination of sharp and blunt dissection. This process
should be continued superiorly to the upper border of the thyroid cartilage and
inferiorly to the sternal notch
• Position Joll’s self-retractor such that its clips are at the midpoint of the incision
• Identify the midline raphe between the strap muscles, incise the deep cervical
fascia, and extend incision superiorly and inferiorly to expose the thyroid gland.
Mobilize the medial border of sternocleidomastoid.

What layers are traversed in your approach to the thyroid gland?
• Skin
• Subcutaneous fat
• Platysma
• Deep investing fascia
• Strap muscles (sternohyoid and sternothyroid)
• Pretracheal fascia
• False sheath of connective tissue overlying the thyroid
• Isthmus of the thyroid gland
• Begin dissecting the plane between the strap muscles and the thyroid, working
out to the lateral lobe.
• Identify the middle thyroid vein; ligate and divide it with 2/0 Vicryl ties. Use
this to enable you to dislocate the lobe medially.
• Open the space between the thyroid gland, oesophagus and posterolateral neck
tissues (including vertebrae) to identify the recurrent laryngeal nerve (RLN).
The inferior thyroid artery often acts as a marker.
• Follow the RLN upwards to its point of entry close to the larynx. Now move
your body to face the patient’s head and draw the thyroid gland downwards to
aid identification of the superior pole vessels.
145
• It is advisable to secure the upper pole vessels initially because this will
facilitate delivery of the gland into the surgical field.
• Sweep sternothyroid away with a pledget and find the medial space between
the larynx and medial edge of the upper lobe. Make a window for entry here
and pass a Kocher’s grooved director through. Clip vessels individually using a
Lahey, staying close to the upper pole of the thyroid gland. This reduces the risk
of damage to the superior laryngeal nerve.
• Remember that the right upper pole is usually higher than the left. Now turn
towards the patient’s feet to deal with the inferior thyroid vein.
• Keep the RLN in view at all times. Isolate the inferior thyroid vessels, clip and
tie close to the thyroid gland to avoid damaging the parathyroid glands or their
blood supply from the inferior thyroid artery.
• Dissect the thyroid gland off the front of the trachea. Divide the ligament of
Berry, which is a strong ligament that attaches the posterior aspect of the
thyroid gland to the trachea.
• For a thyroid lobectomy, apply a heavy pair of forceps to the thyroid in the
midline, divide the thyroid and oversew the remaining lobe with an absorbable
suture. This removes the isthmus with the specimen.
• For a subtotal thyroidectomy, perform a similar mobilization of the other lobe,
divide the isthmus and work laterally, freeing the lobe from the trachea. Apply a
series of forceps to the lateral portions of the gland with the aim of leaving
5 cm3. Excise the thyroid with a scalpel and oversew the remnants with a
continuous absorbable suture (1/0 Vicryl) and attach it to the pretracheal fascia.
• Secure haemostasis using ligatures and ties (avoid diathermy – minimizes
damage to the laryngeal nerves and parathyroid glands) and insert a small
suction drain into the thyroid bed.
• Bring it out between the strap muscles. If the strap muscles were divided (usually
for a large goitre) repair them with an interrupted absorbable suture (1/0 Vicryl).
• Close the platysma with continuous 1/0 Vicryl.
• Use a subcuticular Prolene to skin (with beads) – reduces incidence of keloid
and hypertrophic scar formation compared with metal clips.
COMPLICATIONS
• Haemorrhage – potential for airway compromise
• Wound infection
• RLN palsy
• Superior laryngeal nerve palsy
• Hypothyroidism
• Hypocalcaemia secondary to parathyroid bruising or inadvertent removal
• Keloid scar
• Stitch granuloma.
146

What should be next to the patient’s bedside postoperatively? Under what
circumstance is this used and if this were to occur what else must you do?
Always have a pair of suture cutting scissors or clip removers by the
bedside in case the patient develops a haematoma causing a respiratory
obstruction. If this were to happen, the dressings should be removed and,
if a haematoma is seen, the sutures and clips should be removed immedi-
ately. Once the haematoma has been decompressed, the patient should be
taken back to theatre for formal exploration and closure of the wound. The
hospital cardiac arrest team should also be alerted promptly in case urgent
intubation is required.
147
42 Tracheostomy

What are the indications for a tracheostomy?
What types of tracheostomy have you heard of?
How do you perform a tracheostomy?
What layers do you go through to perform a tracheostomy?
What are the potential complications of performing a tracheostomy?
What is your postoperative management?
Which anatomical structure is at high risk of damage when performing a
tracheostomy on a child?
Related topics
Topic Chapter Page
Intubation and ventilation 114 470
TYPES
Elective versus emergency tracheostomy
Tracheostomy is not usually performed as an emergency procedure because it can-
not be performed as quickly and safely as a cricothyroidotomy.
Percutaneous tracheostomy
This avoids the need for the patient to go to theatre and be operated upon by a sur-
geon. This can be done in the intensive care setting under local anaesthetic whereby
a 14G cannula is inserted with a guidewire with subsequent serial dilatation. The
advantages include avoiding patient transfer and supposedly reduced incidence of
haemorrhage and infection.
Mini-tracheostomy
A small tracheostomy tube is placed through the cricothyroid membrane to aid
bronchial toileting and aspiration of secretions. This is not a definitive airway, because
the tube is not cuffed.
148
OPERATIVE SURGERY tracheostomy
INDICATIONS
Airway obstruction
• Congenital, e.g. laryngeal cysts, tracheo-oesophageal anomalies
• Trauma to larynx
• Infection: acute epiglottitis
• Head and neck tumours: tongue, larynx, pharynx and thyroid
• Facial fractures
• Bilateral vocal cord paralysis
• Sleep apnoea syndrome.
Respiratory insufficiency
• Long-term management of a ventilated patient (most common reason)
• Failed extubation in intensive care
• Chest injury (flail chest)
• Pulmonary disease.
Tracheostomy reduces upper airway dead space by 70 per cent.
Tracheobronchial tree protection

Temporary versus permanent.
• Trauma: burns to head and neck
• Coma: head injury, drug overdose
• Neurological problems: myasthenia gravis, multiple sclerosis
• Head and neck surgery: supraglottic laryngectomy.
(EMERGENCY) TRACHEOSTOMY
• Lie patient supine with neck extended
• Perform under general anaesthetic and intubation (elective cases)
• In emergency situations, give oxygen and inject local anaesthetic if there is time
• Vertical incision – from lower border of the thyroid cartilage in the midline to
the suprasternal notch (transverse incision 2 cm below cricoid cartilage in
elective cases)
• Deepen incision and extend between strap muscles
• Retract or divide thyroid isthmus
• Recheck size of cuffed tube to be placed
• Feel for first tracheal ring
• Try to identify the innominate vein. This structure is at high risk of damage
when performing a tracheostomy on a child, because it lies high on the
trachea
149
• Vertical incision through the second and third tracheal rings. Do not remove
the trachea cartilage in children because this can lead to tracheal collapse.
Damage to first tracheal ring may result in subglottic stenosis; lower placement
risks tracheo-innominate fistula
• The anaesthetist should be asked to withdraw the endotracheal tube to above
the incision and be ready to change the ventilator to the tracheostomy and then
withdraw the endotracheal tube
• Aspirate trachea
• Insert tracheal dilator or cuffed tube to secure airway
• Closure: skin edges closed loosely, tapes to secure tube.
POSTOPERATIVE MANAGEMENT
• Nurse upright
• Regular suction
• Humidified oxygen with 5–7 per cent carbon dioxide to prevent apnoea
• Mucolytic agents are sometimes employed
• Leave tube in place for 1 week before replacing it.

What layers do you go through when performing a tracheostomy?
Structures encountered (superficial inwards):
• Skin
• Superficial fascia
• Platysma
• Investing layer of cervical fascia (surrounds strap muscles)
• Pre-tracheal fascia
• Thyroid isthmus
• Trachea
150

What are the potential complications of performing a tracheostomy?
Complications
Immediate
• Asphyxia
• Pneumothorax
• Haemorrhage or haematoma
• Cricoid cartilage injury
• Damage to the oesophagus
Early
• Aspiration
• Obstruction
• Cellulitis
• Tracheitis
• Mucus plugging
• Malpositioned tube
• Creation of a false track
• Subcutaneous emphysema
Late
• Delayed haemorrhage – usually secondary to tracheo-innominate fistula
occurs "48 hours postoperatively
• Vocal cord palsy
• Atelectasis and bronchopneumonia
• Tracheocutaneous or tracheo-oesophageal fistula
• Subglottic stenosis
• Tracheomalacia
• Tracheal stenosis
• Difficult decannulation
151
4
PART
APPLIED SURGICAL PATHOLOGY

43 Pathology definitions: helpful A–Z guide 155
44 Abscess and pus 158
45 Acute inflammation 161
46 Aneurysms 165
47 Asbestos 169
48 Ascites 172
49 Atherosclerosis 177
50 Breast cancer 182
51 Carcinogenesis 189
52 Cell cycle 194
53 Chronic inflammation 197
54 Colorectal cancer 200
55 Diverticula 210
56 Gastro-oesophageal reflux disease (GORD) and Barrett’s oesophagus 214
57 HIV and universal precautions in surgery 219
58 Hyperparathyroidism 224
59 Hyperplasia, hypertrophy and atrophy 227
60 Malignant melanoma 232
61 Portal hypertension 239
62 Thyroid cancer 244
63 Tumour markers 252
43 Pathology definitions: helpful A–Z guide
Abscess Localized collection of pus, surrounded by a pyogenic membrane
Adenoma Benign glandular neoplasm
Aneurysm Abnormal permanent dilatation of a blood vessel or part of a
heart chamber
Apoptosis Programmed cell death
Atrophy Pathological or physiological reduction in size or number or both
of an organ or tissue
Carcinoma A malignant epithelial neoplasm
Cirrhosis Combination of widespread fibrosis and regenerative nodule
formation following necrosis of hepatic cells
Cyst Cavity with an epithelial lining and containing fluid or other
material
Cytokine Substances produced by one cell that influence the behaviour of
another, affecting intercellular communication
Cytotoxic Causing cell injury but not necessarily lethal
Differentiation Embryological: process by which a cell develops special
characteristics
Pathological: degree of morphological resemblance of a neoplasm
to its parent tissue
Diverticulum Abnormal hollow pouch communicating with the lumen of the
structure(s) from which it has arisen
Dysplasia Abnormal growth and differentiation of a tissue in epithelia –
often a feature of the early stages of neoplasia
Dystrophy Abnormal development or degeneration of a tissue
Ectasia Abnormal dilatation
Ectopic Tissue or substance in or from an inappropriate site (not
metastasis)
Effusion Abnormal collection of fluid in a body cavity
Embolus Fluid or solid mass mobile within a blood vessel and capable of
blocking its lumen
Empyema Cavity filled with pus
Endocrine Characteristic of cells producing hormones secreted into the
blood with distant effects
Endotoxin Toxin derived from disruption of the outer membrane of Gram-
negative bacteria
Erosion Loss of superficial layer or surface
Exophytic Tumour growing outwards from a surface usually because it
lacks invasive properties
Exotoxin Toxin secreted by living bacteria
Exudate Extravascular accumulation of protein-rich fluid as a result of
increased vascular permeability
Fibrosis Process of depositing excess collagen into tissue in attempted repair
Fistula Abnormal connection between two epithelial-lined surfaces
155
APPLIED SURGICAL PATHOLOGY definitions
Gangrene Bulk tissue necrosis. Dry ! sterile; wet ! bacterial putrefaction

Grade Degree of malignancy of a neoplasm (well, moderately or poorly
differentiated)
Granulation Newly formed connective tissue often found at the edge or base
tissue of ulcers and wounds, made up of capillaries, fibroblasts,
myofibroblasts and inflammatory cells embedded in mucin-rich
ground substance during healing
Granuloma An aggregate of epithelioid macrophages often including
giant cells
Haematoma Localized collection of blood or blood clot, usually within solid
tissue
Hamartoma Congenital tumour-like malformation comprising two or more
mature tissue elements normally present in the organ in which it
arises
Hernia Abnormal protrusion of an organ or part of it from one body
compartment to another
Hyperplasia Enlargement of an organ or tissue as a result of increased cell
numbers
Hypertrophy Enlargement of an organ or part of it as a result of increased cell
size
Infarction Death of a tissue as a result of insufficient blood supply
Ischaemia Inadequate blood supply to, or to part of, an organ
Malignant Condition with risk of morbidity and mortality, usually applied
to tumours
Metaplasia Reversible change in the character of a tissue from one mature
cell type to another
Metastasis Process by which a primary malignant neoplasm gives rise to
secondary tumours at distant sites, usually by lymphatic, vascular
or transcoelomic spread
Mucocele Mucus-filled cyst or hollow organ
Mutation Irreversible alteration in the base sequence of DNA, which may
occur spontaneously or in response to a mutagenic agent; may
result in the synthesis of an abnormal protein product
Necrosis Pathological cell or tissue death within a living organism
irrespective of cause
Neoplasm Abnormal or uncoordinated tissue growth persisting after
withdrawal of the initiating cause
Oedema Abnormal collection of fluid within or between cells
Oncogene A gene inappropriately, abnormally or excessively expressed in
tumours, the product of which is responsible for their
autonomous growth
Opsonin Factor which enhances the efficiency of phagocytosis because it
is recognized by receptor(s) on leukocytes; two major opsonins
are the Fc fragment of immunoglobulin G and a product of
complement, C3b
156
APPLIED SURGICAL PATHOLOGY definitions
Organization Natural process of tissue repair

Papilloma Benign neoplasm of non-glandular epithelium
Papillary Surface of a lesion characterized by numerous folds, fronds or
villous projections
Paracrine Characteristic of neighbouring cells of different types
influencing each other by secretion of cytokines, growth
factors or hormones
Pleomorphism Variation in size and shape, usually of nuclei and
characteristic of malignant neoplasms
Polymorphic Consisting of more than one cell type
Polyp Sessile or pedunculated protrusion from a body surface
Pseudocyst Cavity with a distinct wall but lacking an epithelial lining
containing fluid
Pseudomembrane False membrane consisting of inflammatory exudate rather
than epithelium
Putrefaction Decomposition or rotting of dead tissue as a result of
bacterial action, often accompanied by unpleasant odours
Repair Healing with replacement of lost tissue not necessarily by
similar tissue
Resolution Restoration of normality
Sarcoma Malignant connective tissue neoplasm
Sclerosis Hardening of a tissue often caused by excess deposition of
excess collagen
Serous Containing serum or a fluid resembling it
Sinus Blind-ending tract communicating with an epithelial surface –
can be normal or abnormal
Stenosis Narrowing of a lumen
Stoma Any normal, pathological or surgically constructed opening
between one hollow structure and another or the skin
Stroma Non-neoplastic reactive connective tissue within a neoplasm
Telangiectasia Dilated small blood vessels
Thrombus Solid mass of coagulated blood formed within the circulation
Ulcer Breach in epithelial surface with tissue loss
157
44 Abscess and pus

What is an abscess?
Give surgical examples of abscesses.
What tissue is the wall of an abscess characteristically composed of?
What is pus?
What are the possible sequelae of an abscess?
Related topics
Topic Chapter Page
Acute inflammation 45 161
Chronic inflammation 53 197
Open appendicectomy 37 125
Diverticula 55 210
Anorectal surgery 2: fistula in ano and pilonidal sinus 24 67

What is an abscess?
This is a common starting question, and it is important to get the definition
right because examiners can trip you up from the start. It is a good route
into a viva on abscesses, acute or chronic inflammation.
An abscess is a localized collection of pus surrounded by a pyogenic mem-
brane, which may occur as a consequence of acute inflammation.
This can lead to ‘what’s acute inflammation?’ (see ‘Acute inflammation’,
Chapter 45, page 161), or ‘tell me what the membrane consists of? Or
‘what’s pus?’.
The pyogenic membrane consists of fibrin, neutrophils, capillaries and
occasional fibroblasts.
Pus contains a mixture of dead and dying neutrophils and pathogens, cellu-
lar debris and globules of lipid.
The stimulus to acute inflammation is persistent, and often an infective
agent such as Staphylococcus aureus or Streptococcus pyogenes.
158
APPLIED SURGICAL PATHOLOGY abscess and pus
EXAMPLES OF ABSCESSES AND CAUSATIVE ORGANISMS

(THIS LIST IS NOT EXHAUSTIVE)
Pilonidal abscess
Arises from infection of a pre-existing pilonidal sinus. Gram-negative anaerobic
organisms and Bacteroides fragilis are often the cause.
Perianal abscess
Infection of hair follicles caused by Staphylococcus aureus. This organism is often
responsible for abscess formation wherever it causes disease; examples include lung
abscesses, psoas abscesses (see below), meningitis and brain abscesses, etc.
Appendix mass
A sequela of acute appendicitis. Caused by coliforms.
Liver abscess
May be caused by amoebae or coliforms.
Breast abscess
Caused by skin organisms such as S. aureus.
Psoas abscess
Caused by S. aureus, tuberculosis (TB) and other rarer causes.
Tuberculous abscess
This is a ‘cold’ abscess.
Subphrenic abscess
Usually post-abdominal surgery or perforated intra-abdominal viscus. Presents
with spiking temperature.
Perinephric abscess
A sequela of acute pyelonephritis.
Sterile abscess
Absence of micro-organisms. Causes include:
• Intramuscular injection of irritant agents such as paraldehyde (historical)

• Sterilization of a septic abscess by antimicrobials.
TREATMENT AND SEQUELAE

The appropriate treatment of most abscesses is surgical drainage. Antibiotics are
not effective because they do not penetrate the abscess, and antibiotic treatment
may lead to a chronic abscess.
159
APPLIED SURGICAL PATHOLOGY abscess and pus
Natural history of an abscess is to discharge itself through a line of least resistance.

Often abscesses point and then burst. This is seen in perianal abscesses that are not
drained surgically.
If incised and drained, an abscess may form a sinus tract (connection between the
abscess and the skin or a mucosal surface lined by epithelium). If the tract connects
two epithelial surfaces, a fistula results (see definitions in ‘Pathology definitions:
helpful A–Z guide’, Chapter 43, page 155).
Metastatic abscesses can result from haematogenous spread of the causative micro-
organism. An example includes liver abscesses secondary to appendicitis.
160
45 Acute inflammation

Define acute inflammation?
What cell types are involved in acute inflammation and at
what times?
What triggers acute inflammation?
What are the beneficial and harmful effects of acute inflammation?
What are the clinical features of acute inflammation?
What are neutrophils for?
What are the major differences between acute and chronic
inflammation?
What is complement? What does it do? What is its role in acute
inflammation?
What is a cytokine? What is a chemokine? What do they do?
Related topics
Topic Chapter Page
DEFINITION
• The cellular and vascular response to injury
• Short in duration
• Cellular and chemical components.
CAUSES
Injury by:
• Pathogens: bacteria, viruses, parasites
• Chemical agents: acids, alkalis
• Physical agents: heat, trauma, radiation
• Tissue death: infarction.
161
APPLIED SURGICAL PATHOLOGY acute inflammation
Key learning point

A viva on abscesses is an easy way into a discussion of acute inflammation and
vice versa, because an abscess is a sequela of acute inflammation (see below).
STAGES OF ACUTE INFLAMMATION

• Dilatation of local capillaries
• Increase in endothelial permeability
• Leakage of protein-rich fluid into the interstitial space, including fibrinogen
• Fibrinogen converted to fibrin, which forms a meshwork of fibrinous exudate
• Leukocyte margination to peripheries of capillaries and migration into the
interstitial space; mostly neutrophils
• Acute inflammation is mediated by chemicals, such as interleukins and
histamine, and proteins, such as the complement cascade (see below)
• Later on lymphocytes appear
• Lymphatics become dilated and carry the oedema fluid with pathogens to
lymph nodes, where lymphocytes contribute to the immune response.

What is complement? What is its role in acute inflammation?
Complement is a component of the innate immune system. It consists of
a cascade of proteins that result in the formation of a membrane attack
complex, which can destroy invading bacteria or recruit other cells to the
inflammatory response such as neutrophils (below). Their proteins can also
act as opsonins (see definition on page 156).
There are two main activating arms of the complement cascade. The classic
pathway consists of antigen–antibody complexes. The alternative pathway
is activated by contact with micro-organisms.
ROLE OF THE NEUTROPHIL

The predominant cell involved in acute inflammation is the leukocyte. Appears
early – the first cellular component to appear.
Attracted to the site of inflammation by inflammatory mediators (chemotaxis).
They can move.When they are recruited from blood vessels, they marginate, by adher-
ing to the vascular endothelium (the endothelium expresses more adhesion molecules
in response to cytokines), roll, pass between endothelial cells and emigrate into the
interstitial inflammatory exudate.
162
Phagocytosis of micro-organisms, with lysosomal and free radical degradation of

pathogens.
CHEMICAL MESSENGERS IN ACUTE INFLAMMATION

Acute inflammation requires several chemical messengers to enable cells to communi-
cate with each other and mediate the immune response. Cytokines are soluble, biologic-
ally active molecules secreted by cells that have a variety of effects on the function of
target cells. Chemokines cause the direct migration of target cells to the site of release.
Examples of cytokines include (non-exhaustive):
• Interleukin 1 (IL-1): neutrophil adhesion and vascular adhesion molecules
• Interleukin 2 (IL-2): proliferation, differentiation of B cells and natural killer
(NK) cells
• Tumour necrosis factor (TNF): causes fever and promotes inflammatory
response, neutrophil adhesion
• Interferon: activation of macrophages, NK cells
• Histamine: released early, vasodilatation and increased permeability.
MACROSCOPIC/CLINICAL FEATURES
Formulated by Celsus and summarized in Latin words:
• Rubor (redness), caused by increased flow in dilated capillaries
• Dolor (pain), caused by distortion of the local architecture and local release of
chemical mediators such as prostaglandins, which induce pain
• Calor (heat), caused by local vasodilatation
• Tumor (swelling), caused by extravasation of fluid
• Loss of function: caused by pain and swelling.
General features include fever, caused by chemical mediators such as interleukins
which change the set point for temperature homoeostasis.
BENEFICIAL EFFECTS OF ACUTE INFLAMMATION

• Dilution of bacterial toxin.
• Defence mechanisms are brought to the pathogen, such as neutrophils, which
can phagocytose, complement, which can cause cell lysis, and antibodies, which
facilitate cellular defence. Drugs and nutrients (for neutrophils) are also delivered.
• Increased drainage into the lymphatic system where antigens reach lymph nodes
to stimulate the immune response.
• Fibrin traps the pathogen in one place, where it can be attacked by the above
inflammatory components.
163
HARMFUL EFFECTS OF ACUTE INFLAMMATION

• Destruction of normal tissue (see below), particularly in autoimmune disease
such as rheumatoid arthritis
• The acute inflammatory response in certain parts of the body can cause lethal
swelling, e.g. acute epiglottitis and loss of the airway
• Hypersensitivity reactions (e.g. anaphylaxis and asthma).
OUTCOMES OF ACUTE INFLAMMATION

• Resolution: tissues restored to normal
• Chronic inflammation: if the causative agent is not removed
• Pus and abscess formation: a mixture of dead bacteria and neutrophils within
the affected tissues (see ‘Abscess and pus’, Chapter 44, page 158)
• Organization: tissues are replaced by granulation tissue.
164
46 Aneurysms

What is the definition of an aneurysm?
How would you classify aneurysms?
Where do they commonly occur?
How do aneurysms present?
What are their complications?
What are the important factors in deciding when to operate electively on
an abdominal aortic aneurysm?
How would you manage a patient who presented with a ruptured
abdominal aortic aneurysm?
Is screening for abdominal aortic aneurysms effective? Have you heard of
the MASS Trial?
Related topics
Topic Chapter Page
Screening in surgery 77 316
Key learning point

Definition: dilatation of part of an artery vessel or heart chamber by at least
100 per cent (" 50 per cent ! arteriomegaly).
CLASSIFICATION
• False: as a result of a traumatic breach of the wall with the sac made up from
the compressed surrounding tissue
• True: dilatation involving all layers of the wall.
By shape
• Fusiform: spindle shaped, involving whole of the circumference
• Saccular: small segment of wall ballooning as a result of localized weakness.
165
APPLIED SURGICAL PATHOLOGY aneurysms
By cause
Acquired versus congenital
• Acquired: normally caused by atherosclerosis
• Traumatic: e.g. popliteal artery aneurysms in horse-riders!
• Inflammatory: these rupture at a smaller diameter and can be very challenging at
surgery
• Mycotic: infective, e.g. caused by endocarditis; syphilis – typically saccular and
affecting the thoracic part of the aorta
• Connective tissue disorders: e.g. Marfan’s and Ehlers–Danlos syndromes.
The most common site is the abdominal aorta (2 per cent finding at postmortem
examination).
Abdominal aortic aneurysms (AAAs) often associated with aneurysmal dilatation
of the iliac, femoral and popliteal vessels.
Popliteal aneurysms: most common peripheral aneurysm and second most com-
mon type of aneurysm.
Splenic artery aneurysms: #1/10 000; four times more common in women, espe-
cially at child-bearing years. 25 per cent rupture, especially in the third trimester.
Associated with pancreatitis.
Intracranial ‘berry’ aneurysms: found at the junction of the limbs in the circle
of Willis.
Charcot–Bouchard aneurysms: microaneurysms in the brain as a result of
hypertension.
EPIDEMIOLOGY
• Incidence: increases with age, 5 per cent of over-50s; 15 per cent of over-80s
• Sex: male:female ! 6:1
• Family history: 12-fold risk for first-degree relatives affected
• Distribution: aneurysms caused by atherosclerosis found in the abdominal aorta;
30 per cent have iliac disease; 95 per cent infrarenal.
CLINICAL FEATURES
This depends on site. Seventy-five per cent are asymptomatic. Incidental finding
during screening or investigation of other problems
Berry aneurysms: rupture causes subarachnoid haemorrhage.
AAA: abdominal pain referred to the back (can be acute or chronic).
166
COMPLICATIONS OF AAA
• Rupture
• Thrombosis (causing lower limb ischaemia)
• Embolism
• Fistulation to bowel (aorto-enteric), to vena cava, renal vein
• Pressure effects on adjacent organs
• Death.
INVESTIGATIONS
• Chest radiograph (thoracic extension)
• ECG
• Echocardiogram: to aid in assessment of perioperative risk
• ESR (erythrocyte sedimentation rate): is there an inflammatory component?
• Urea and electrolytes (U!Es): preoperative renal failure is associated with
a poorer prognosis
• Ultrasonography: size
• Computed tomography (CT): to look at juxtarenal anatomy. Need to avoid
suprarenal clamping if at all possible. Also look at the distal extent of the
aneurysm – directs need for a bifurcated graft if iliac arteries are involved?
Key modality to diagnose rupture.
• May require a ‘stenting’ CT if endovascular repair considered
• Arteriography: multiple, rare aneurysms occurring with aberrant anatomy such
as horse-shoe kidneys. No longer used for assessment of aneurysm diameter.
MANAGEMENT ISSUES
Most important factor is the size of the aneurysm: repair all above 5.5 cm in diam-
eter (UK Small Aneurysm Trial).
Some surgeons would advocate repair at 6 cm in women because they are less prone
to rupture.
No benefit to repair of those sized 4–5.5 cm – operative mortality outweighs risk of
rupture. These patients should be enrolled on an annual ultrasonography screening
programme and operated on when they attain the requisite size:
• 5-year rupture rate: 25 per cent for " 5 cm
• Age limit for cut-off for surgery: 85 years, but need to consider patient on an
individual basis.
• Elective mortality rate: 1–5 per cent in regional centres
• Emergency mortality rate: up to 80 per cent!
167

Emergency question: the leaking aneurysm
Assess and resuscitate patient simultaneously – to stabilize patient
ABC protocol
Two large-bore cannulae into antecubital fossa veins – not central line
Intravenous fluids judiciously – maintain BP around 90–100 mmHg
Intravenous analgesia
Urinary catheter – with a urometer bag. Measure hourly urine outputs
because this is the most sensitive marker of tissue perfusion
Blood tests: FBC (full blood count), U$Es (urea and electrolytes), glucose,
amylase, LFTs (liver function tests), clotting screen
Cross-match 10 units of packed red blood cells $ 4 units of fresh frozen
plasma (FFP)
Contact senior member of surgical team
If patient stable, CT to confirm diagnosis
If any signs of being unstable, theatre
Contact anaesthetist and theatre staff ahead. Book an intensive care bed
Speak to the patient and relatives
SCREENING ISSUES
MASS Trial
Screening in AAAs is effective in certain groups of patients.
There is a definite survival benefit after screening for AAAs in men aged ! 65 years.
Below this age the data are less clear.
Screening in women does not seem to be effective.
168
47 Asbestos

What are the different forms of asbestos? Which one is the most common?
What types of asbestos cause disease?
What is the most important factor in the development of asbestosis?
In which occupations are people particular exposed to asbestos?
What happens to the asbestos fibres when they are inhaled?
What lung-related problems do asbestos cause?
Which type of asbestos is associated with the development of
mesothelioma? Why is this type of asbestos more pathogenic than the
other types?
Related topics
Topic Chapter Page
Respiratory failure and respiratory 119 495
function tests
Asbestos is a family of fibrous silicates.

It is used for insulation and the manufacture of brake linings and other friction
materials.
There are over 50 types. Only three are important in human disease, as follows.
Chrysotile
• Curled flexible serpentine mineral (long woolly fibres)
• White asbestos – accounts for 95 per cent of asbestos used in industry
• Associated with pulmonary fibrosis.
Crocidolite
• Brittle straight amphibole mineral (straight short fibres)
• Blue asbestos
• Associated with pulmonary fibrosis and malignant mesothelioma.
169
APPLIED SURGICAL PATHOLOGY asbestos
Amosite
• Brittle straight amphibole mineral (straight long fibres)
• Brown asbestos
• Associated with pulmonary fibrosis.
AT-RISK OCCUPATIONS
• Shipworkers
• Laggers and industrial plumbers
• Builders
• Workers in old institutions such as hospitals that had insulation installed more
than 50 years ago.
DISEASES CAUSED BY ASBESTOS

Malignant
• Mesothelioma of pleura, pericardium and peritoneum
• Bronchogenic carcinoma: usually bronchioloalveolar cell carcinoma; squamous
cell and adenocarcinoma also associated
Benign
• Asbestosis: fibrosing lung disease
• Pleural plaques: these can be mistaken for malignancy
• Pleural effusion.
PATHOGENESIS
• Important determining factor for the development of asbestosis is the amount of
dust inhaled
• Inhaled fibres that reach the alveoli are ingested by alveolar macrophages,
stimulating release of C5a and other chemoattractants
• Amphibole fibres, which are short and stiff, penetrate more deeply into the
lungs than the longer fibres of the other types of asbestos and hence are more
pathogenic
• Most of the inhaled asbestos is cleared by the macrophages; the rest reaches the
lung and lymphatics
• Some ingested fibres are coated by haemosiderin and glycoproteins to form
characteristic beaded, dumbbell-shaped, asbestos bodies.
Lung injury-related mechanisms and subsequent pulmonary fibrosis include:
• Release of lysozymes or toxic free radicals by macrophages recruited to the site
of the asbestos deposition
170
APPLIED SURGICAL PATHOLOGY asbestos
• Release of fibrogenic cytokines and growth factors by alveolar macrophages

after phagocytosis of the fibres
• Direct stimulation of fibroblast collagen synthesis by asbestos.
In addition to pulmonary fibrosis, asbestos induces pleural reaction manifested by:
• Benign effusions
• Fibrous pleural and fibrocalcific plaques.
This leads to alveolar obliteration with compensatory dilatation of intact
bronchioles.
171
48 Ascites

What are the causes of ascites?
What signs can be elicited in the patient?
What is ascites?
How is ascites formed?
How do you classify ascites?
Based on your understanding, how might liver cirrhosis cause ascites?
What tumours are particularly associated with malignant ascites?
What investigations can be carried out on ascitic fluid to ascertain the
cause of the ascites?
How would you perform an ascitic tap? What layers do you traverse?
What are the indications for the use of a shunt in the management
of ascites?
Related topics
Topic Chapter Page
Portal hypertension 61 239
Starling forces in the capillaries/oedema 101 401

What is ascites?
Ascites is an abnormal accumulation of fluid in the peritoneal cavity.
CLASSIFICATION AND CAUSES

Cirrhotic versus malignant versus pancreatic versus chylous.
Transudate (protein content # 30 g/L) versus exudate (protein content " 30 g/L).
172
APPLIED SURGICAL PATHOLOGY ascites
Transudate
Hydrostatic changes
This leads to increase in portal venous pressure:
• Cirrhosis: the transudate fluid mainly escapes through the capsule of the liver
• Right-sided cardiac failure
• Constrictive pericarditis
• Budd–Chiari syndrome
• Thoracic duct obstruction.
Plasma oncotic changes

• Liver failure with hypoproteinaemia
• Protein-losing enteropathy
• Starvation, cachexia
• Nephritic and nephrotic syndromes, renal failure.
Metabolic or endocrine changes

• Hypothyroidism
• Secondary hyperaldosteronism (though not in Conn’s syndrome).
Exudate
Inflammatory causes
These causes result in protein leakage:
• Peritonitis: bacterial and tuberculous

• Post-irradiation
• Talc granulomata
• Pseudomyxoma
• Peritoneal infiltration by carcinoma
• Severe uraemia
• Pancreatitis.
Iatrogenic
• Operative abdominal surgery: excess free fluid
• Continuous ambulatory peritoneal dialysis (CAPD).
FORMATION OF ASCITES
Fluid accumulation within the peritoneal cavity is dependent on regulating the inflow
and outflow of fluid. The most important factors are the inflow pressure, capillary
permeability, colloid osmotic pressure and lymphatic outflow capacity (see ‘Starling
forces in the capillaries/oedema’, Chapter 101, page 401).
173
Inflow is governed by venous pressure. There is a pressure gradient for peritoneal

fluid absorption, which is created by negative intrathoracic pressure generated during
the respiratory cycle. Outflow fluid is controlled primarily by the lymphatics. Ascites
forms where there is an imbalance of fluid movements. In ascites, raised venous
pressure is the cause of the inflow problem to the peritoneal cavity (portal hyper-
tension) and blocked lymphatics are the cause of the outflow problem.
Cirrhosis produces ascites by increasing both portal vascular resistance and splanch-
nic blood flow. These two factors act to create portal hypertension, which in turn leads
to increased visceral lymph formation. This increase in lymph production exceeds
absorption capacity and hence fluid accumulates in the peritoneal space. The
extracellular fluid (ECF) volume falls. The kidney responds by stimulating the renin–
aldosterone axis, leading to an increase in the ECF. This in turn leads to further
lymph formation and exacerbates the ascites.
INVESTIGATIONS ON ASCITIC FLUID

• Microscopy for bacteria, white cells and red cells
• Culture and sensitivity for TB and other bacteria
• Cytology for:
• involvement by metastatic or primary carcinoma
• involvement by lymphoma
• Biochemistry for:
• protein content
• amylase if pancreatitis is suspected
• Cytogenetics where appropriate.
TUMOURS ASSOCIATED WITH MALIGNANT ASCITES

• Ovary
• Breast
• Colon
• Pancreas
• Stomach
• Liver
• Lymphoma.
SPECIFIC TESTS FOR ASCITES

• Shifting dullness within the abdomen
• Fluid thrill
• Flank dullness within the abdomen.
174
ASCITIC TAP
• Perform under sterile conditions
• If ascites not clinically apparent or easy to locate, this procedure should be done
under ultrasound guidance to prevent visceral injuries
• Local anaesthetic infiltrated and site marked
• A narrow-gauge needle should be introduced first to check position before a
larger-gauge cannula is inserted into the abdomen
• Seldinger technique
• When in position a plastic tube can be connected to a urine bag in order to
collect the ascitic fluid.

What layers do you traverse when performing an ascitic tap?
Layers traversed:
• Skin
• Superficial fascia
• Scarpa’s fascia
• External oblique
• Internal oblique
• Transversalis fascia
• Extraperitoneal fat
• Parietal and visceral peritoneum
TREATMENT
• Mainstay of treatment of ascites is to treat the underlying cause
• Patient placed on a weight reduction programme
• Judicious use of diuretics
• Low-sodium, high-protein diet.
In diuretic-resistant ascites, shunting can be performed in a number of ways:
• Peritoneovenous shunting (Le Veen shunt): a subcutaneous Silastic catheter is
used to drain the fluid into the jugular vein.
• Denver shunt: this is a modification, adding a small subcutaneous pump that
can be compressed externally.
175
• Transjugular intrahepatic portosystemic stent shunt (TIPSS): this is a side-

to-side shunt stenting a channel between a branch of the portal vein and
hepatic vein.
Radiological techniques have now widely replaced the difficult surgically formed
shunt operations, e.g. selective splenorenal (Warren) shunt – anastomosis of the
distal (splenic side) splenic vein into the left renal vein with ligation of the left
gastric vein.
176
49 Atherosclerosis

What is atherosclerosis?
What are the mechanisms underlying the formation of the
atherosclerotic plaque?
What are the postulated mechanisms of plaque rupture?
What are the risk factors that contribute to the formation of atheroma?
At what sites is it most common for atheroma to develop?
What are the complications of atherosclerosis?
What symptoms can be caused by atheroma?
What therapeutic strategies are available for the treatment of
atherosclerosis?
Related topics
Topic Chapter Page
Aneurysms 46 165
DVT prophylaxis and coagulation 73 297
in surgery
DEFINITION
A pathological process of the vasculature beginning with endothelial dysfunction,
resulting in migration of macrophages across the endothelium, formation of foam cells
and a necrotic lipid core, and migration of vascular smooth muscle cells to form a
fibrous cap. This process ultimately results in stenosis of the vessel and rupture of
the cap can lead to thrombosis and possible infarction of the supplied tissue.
MECHANISMS OF PLAQUE FORMATION

• Endothelial dysfunction as a result of:
• loss of laminar blood flow in turbulent areas around bifurcations leading to
decreased wall sheer stress and direct endothelial cell changes.
• oxidative stress, e.g. free radicals from smoking
• possible infective cause: ? Chlamydia implicated
177
APPLIED SURGICAL PATHOLOGY atherosclerosis
• Low-density lipoprotein (LDL) becomes oxidized (ox-LDL) and damages

endothelium further – tight junctions are disrupted
• Macrophages migrate across endothelium by the interaction with selectins,
integrins and intercellular adhesion molecules (ICAMs)
• Macrophages ingest ox-LDL and become activated
• Some macrophages become foam cells and migrate to form a lipid core
• Plaque is stabilized by migration of vascular smooth muscle cells to form a
fibrous cap. Endothelial progenitor cells have also been shown to play an
important role in the formation of the cap. They are derived from the bone
marrow.
MECHANISMS OF PLAQUE RUPTURE

• Macrophages secrete enzymes to break down the collagen within the fibrous
cap (matrix metalloproteases or MMPs)
• Increased rate of apoptotic cell death within the cap, weakening it further
• Flow across a thinned fibrous cap causes biomechanical stress, which ultimately
leads to plaque rupture
• Lipid core is exposed to flowing blood
• Platelets adhere and the clotting cascade activated, causing a thrombosis (see
‘DVT prophylaxis and coagulation in surgery’, Chapter 73, page 297).
RISK FACTORS
• Smoking
• Hypertension
• Diabetes mellitus types 1 and 2
• Family history of atherosclerotic disease
• Increased cholesterol (specifically increased LDL and decreased high-density
lipoprotein or HDL).
178
Sites, symptoms and complications

Site Symptoms Complications
Aorta Pain from expanding aneurysm Aneurysm rupture
Claudication from occlusive Critical or acute limb ischaemia
aortoiliac disease
Distal embolic disease ‘trash
foot’ – particularly post-AAA
repair
Can be asymptomatic
Coronary arteries Angina Myocardial infarction

Coronary dissection % rare but can
occur after angioplasty & stenting
Carotid arteries Can be asymptomatic Cerebrovascular accident (stroke)

and cerebral Transient ischaemic Carotid aneurysm
vasculature attacks (TIAs) Hypoperfusion syndrome with
bilateral disease (rare)
Popliteal and Claudication Ulceration and critical limb

lower limb Distal embolization – ischaemia – may lead to amputation
vasculature painful gangrenous toes Distal embolization may lead
In situ thrombosis to gangrene of the toes
(particularly popliteal) Thrombosis of a popliteal
aneurysm may cause acute
limb ischaemia
Key learning point

Any question relating to the therapeutic options of atheroma is obviously
wide ranging. Try to structure and categorize your answer – this gives you
a few moments to think and also gives the examiner the impression that
you’re not about to reel off a badly constructed list of surgical options,
missing key medical points!
THERAPEUTIC OPTIONS
These depend on site and type of disease process (occlusive or aneurysmal) and can
be split into medical, surgical and radiological.
179
Occlusive disease
Medical
Secondary prevention
• Diet and pharmacological manipulation of LDL (e.g. statins) – recent
ASTEROID trial shows approximately 7 per cent reduction in atheroma
volume over 12 months in the high-dose statin group)
• Antihypertensives (especially angiotensin-converting enzyme inhibitors or
ACEIs and angiotensin II antagonists)
• Management of diabetes and strict blood sugar control
• Stop smoking and lifestyle modification.
Acute treatment
• High-dose aspirin (300 mg) for acute myocardial infarction (MI)
• Intravenous thrombolysis (e.g. streptokinase, tissue plasminogen activator or
tPA, recombinant tPA) for MI and cerebrovascular accident (CVA)
• Acute ' blocker and statin therapy for MI.
Symptom relief
For example, sympathectomy for foot pain in critical limb ischaemia.
Surgical (depends on site)
Lower limb/aorta
• Bypass grafting: anatomical versus extra-anatomical. Conduit can be vein, artery
or synthetic (e.g. Dacron for aorto-bifemoral, PTFE (polytetrafluoroethylene)
for femoral–distal bypass)
• Acute embolectomy for lower leg embolus.
Coronary arteries
Coronary artery bypass grafting (CABG).
Carotid arteries
Carotid endarterectomy (see ‘Carotid endarterectomy’, Chapter 27, page 81).
Radiological/cardiological intervention
Lower limb/aorta
• Angioplasty & stenting (can be subintimal for complete occlusion)
• Intra-arterial thrombolysis for acute thrombus in lower limb/upper limb
vasculature.
Coronary arteries
Angioplasty & stenting (sirolimus-eluting stents now used to prevent
re-stenosis).
Carotid arteries
Angioplasty $ stenting % relatively new treatment, no long-term follow-up.
180
Aneurysmal disease
Medical
Secondary prevention
• Low-dose aspirin (anti-platelet) and statins (the Heart Protection Study and
many studies since have shown a significant risk reduction in atheroma-related
ischaemic events after the administration of a long-term statin)
• Diet and pharmacological manipulation of LDL (e.g. statins)
• Antihypertensives (especially ACEs and angiotensin II antagonists)
• Management of diabetes and strict blood sugar control
• Smoking cessation and lifestyle modification.
Surgical and radiological
Aorta
• Surgery: AAA repair with Dacron graft
• Radiology: AAA stent.
Popliteal
• Surgery: bypass grafting and ligation of aneurysm
• Radiology: covered stent.
181
50 Breast cancer

What do you understand by the term ‘ductal carcinoma in situ’ or
‘DCIS’? How is it treated?
What would you do if you saw a patient with a breast lump in clinic?
What are the risk factors for breast carcinoma?
What is the management strategy for breast carcinoma?
What staging systems do you know?
How does breast cancer spread?
What adjuvant treatment is available for breast carcinoma and for whom
is it suitable?
What is the prognosis of the various types of breast cancer?
What is the Nottingham prognostic index?
What do you understand about Herceptin? What is its action?
Related topics
Topic Chapter Page
Cell cycle 52 194
Carcinogenesis 51 189
Mastectomy, axillary dissection 36 120
and breast reconstruction
DUCTAL CARCINOMA IN SITU

DCIS is a non-invasive precancerous process. It occurs most commonly in the 40 to
60 year olds and presents with a nipple discharge and/or mass. DCIS is usually uni-
lateral and, if left untreated, proceeds to invasive ductal carcinoma. There is a 25–50
per cent risk of breast cancer at 10–15 years. When DCIS recurs, 50 per cent will
be invasive tumours.
182
APPLIED SURGICAL PATHOLOGY breast cancer

What are the risk factors for breast carcinoma?
Breast cancer represents 20 per cent of all cancers in women. It is the most
common cause of death in women aged 35–55 years and there is a linear
increase in risk with an increase in age. One in seven women will eventually
develop breast carcinoma.
Risk factors
• Age: linear increase with age so older people more at risk
• Female sex (remember it can occur in men)
• Oestrogen exposure: early menarche, late menopause, oral contraceptive pill
• Nulliparous (early pregnancy is protective as is multiparity)
• Weight (in patients aged "55 years)
• Family history and genetic factors:
• BRCA-1 (2 per cent of all breast carcinomas) and BRCA-2
• relative risk ( 5 if multiple relatives affected
• relative risk ( 9 if first-degree relative with bilateral cancer
• Li–Fraumeni syndrome (increased risk of multiple primary cancers)
• Geography: high in North America and Europe, low in Africa and
south-east Asia
• Atypical hyperplasia
• Upper class " lower class
• Unmarried " married
• Jewish individuals and nuns have higher risk
LOBULAR CARCINOMA IN SITU

Lobular carcinoma in situ (LCIS) is found predominantly in premenopausal women.
It does not present as a mass and is often seen in biopsies. It is also often associated
with an infiltrating tumour, although not necessarily lobular carcinoma.
CLINICAL FEATURES AND ON EXAMINATION

• Painless breast lump: hard and irregular, fixed to underlying tissues (although
small T1a tumours are impalpable)
• Nipple discharge: blood-stained
• Pain is less common as is skin ulceration
• Nipple retraction, skin tethering
• Lymphadenopathy, limb oedema, satellite nodules
183
• Skin infiltration (chest, back and neck)

• Localized skin oedema (peau d’orange)
• Metastatic symptoms and signs: cachexia, ascites, jaundice, pathological
fractures, central nervous system (CNS) symptoms.
METHODS OF STAGING
There are three major clinical systems for staging: UICC (Union Internationale
Contre Le Cancer), Manchester and Columbia.
The UICC is the most comprehensive and relates to primary tumour, nodal disease
and systemic disease.
Key learning point

UICC system
T0 – subclinical
T1 – ) 2 cm
T2 – " 2 cm but # 5 cm
T3 – " 5 cm
T4 – any size with chest wall or skin invasion
N0 – no nodal disease
N1 – ipsilateral, mobile axillary node involvement
N2 – ipsilateral, fixed axillary node involvement
N3 – ipsilateral internal mammary node involvement
M0 – no distant metastases
M1 – distant metastases
PREDICTORS OF POOR OUTCOME

• Tumour size: the bigger the tumour, the worse the prognosis
• Tumour grade: Bloom and Richardson grading system based on histological
architecture – from grade 1 (well differentiated) to grade 3 (poorly
differentiated)
• Nodal involvement: five or more positive nodes on sampling; " 20 per cent
5-year survival rate
• Vascular invasion in primary tumour (tumour spreads haematogenously and via
the lymphatics)
• Multicentricity of primary tumour
• Oestrogen receptor positivity (predicts response to tamoxifen; negative is worse
prognosis).
184

How is a lump assessed in clinic?
Examination and investigation of a lump in the clinic
Triple assessment:
1 Clinical examination
2 Radiological assessment (mammography " 35 and ultrasonography
# 35 years)
3 Pathological (cytology or histology).
After a full examination, either fine-needle aspiration cytology (FNAC)
should be performed or a core biopsy (Trucut) taken. These investigations
have a preoperative diagnostic sensitivity of ! 95 per cent.
Tissue or cells are graded as below:
FNAC (cytology) Trucut (histology)
C1 inadequate B1 normal
C2 benign B2 benign
C3 equivocal B3 equivocal
C4 suspicious B4 suspicious
C5 malignant B5 malignant
NOTTINGHAM PROGNOSTIC INDEX (NPI)

This is based on tumour size (in centimetres), tumour grade (1–3) and nodal disease
status (1 ! no nodal involvement, 2 ! one to three nodes, 3 ! more than four nodes
or apical node)
NPI ! size ( 0.2 $ stage $ grade
If NPI # 3.4, 15-year survival rate is 90 per cent
If NPI " 5.4, 15-year survival rate is 8 per cent.
MANAGEMENT OF BREAST CANCER

• Multidisciplinary approach
• Treat local disease and axillary disease
• Can be split into surgical management of the breast and the axilla and systemic
medical management including hormonal therapy, chemotherapy and
radiotherapy.
185
Surgical management of the breast

• Breast-conserving operations are the norm where possible (wide local excision
or WLE instead of mastectomy)
• Clear resection margins of " 5 mm are required histologically
• Incomplete excision requires a further WLE or mastectomy
• Whole-breast radiotherapy is used for local disease control and to prevent local
recurrence after WLE, provided that margins are clear; given if local recurrence
risk is thought to be " 15 per cent
• Reconstruction may be immediate or delayed, depending on the tumour and
patient choice: immediate skin-sparing mastectomy and prosthesis or a free or
pedicled flap
• Delayed reconstruction with tissue expansion or a free or pedicled flap.
Management of the axilla

• Treated as a separate entity to the breast
• May be sampled or cleared
• Sampling provides essential diagnostic information although nodes may be missed
• Clearance can be split into three different levels:
• level 1: below pectoralis minor
• level 2: up to upper border of pectoralis minor
• level 3: to the outer border of the first rib
• As levels of clearance increase, risk of postoperative lymphoedema increases
• Sentinel node biopsy is a new technique aimed at identifying the first or
sentinel node draining the breast. It involves a combination of a radioactive
isotope (technetium) and a blue dye. It is still experimental but shows great
promise and will hopefully address the 60 per cent of women who are N0 and
do not need sampling
• Radiotherapy is used on the axilla if positive nodes are found on sampling. An
alternative is a level 2 clearance. If both radiotherapy and surgery are utilized,
the risk of lymphoedema goes up dramatically.
Systemic treatment
Can be given as primary method of treatment, although more usually given as adju-
vant therapy.
Split into hormonal therapy (e.g. tamoxifen) and chemotherapy. Specific chemo-
therapeutic regimens are beyond the scope of this topic and are unlikely to be
asked for:
• Adjuvant chemotherapy reduces mortality – absolute survival benefit rate at

10 years is approximately 8 per cent
• Chemotherapy reduces annual risk of death by 30 per cent for 10 years
186
• Evidence to suggest that goserelin (Zoladex) in combination with tamoxifen is

as effective as adjuvant chemotherapy in young women with poor prognosis
disease that is oestrogen receptor positive.

What do you understand about Herceptin? What is its action?
Herceptin or trastuzumab is a monoclonal antibody directed at human
epidermal growth factor 2 receptor (HER2) and prevents epidermal
growth factor from binding. Some breast tumours (about 20 per cent)
express this protein and, in these, Herceptin treatment appears to halt the
growth or shrink tumours. There is some evidence to suggest that it has a
synergistic effect with the chemotherapeutic agent paclitaxel and, given
1 year after chemotherapy in HER2-positive tumours, reduces the
recurrence rate by half.
Herceptin is now licensed for use in early breast cancer – the National
Institute for Health and Clinical Excellence (NICE) reported early in June
2006 about this indication.
RECURRENT DISEASE
• Local recurrence: treated by further WLE and/or radiotherapy if appropriate
• Regional recurrence: spread to axilla, brachial plexus, supraclavicular nodes –
axillary clearance/radiotherapy
• Distant metastases: bone, lungs, liver and brain. Can cause hypercalcaemia,
pleural effusion, hepatocellular jaundice, epilepsy and neurological symptoms.
Note that treatment can be palliative as well as curative:
• Bisphosphonates for hypercalcaemia and bone pain
• Analgesia
• Social and psychological support
• Palliative radiotherapy
• Blood transfusion for anaemia of chronic disease
• Resection for skin-ulcerating tumour
• Aspiration of pleural effusions and pleurodesis.
MANAGEMENT OF DCIS
• Of all cases of DCIS, 1 per cent is found to have positive nodal involvement
and therefore must represent small tumours not found at histology or screening.
187
• A third of all cases of DCIS go on to become invasive ductal carcinoma if left

untreated
• DCIS makes up 25 per cent of all screening-detected cancers
• Good prognosis in most cases but diffuse process and often requires total
mastectomy (5-year survival rate of 98 per cent)
• Localized DCIS (" 4 cm): treated by WLE & radiotherapy and tamoxifen
• Widespread and/or multifocal DCIS: treated by mastectomy & tamoxifen.
188
51 Carcinogenesis

What is carcinogenesis? What is oncogenesis?
How would you broadly divide the factors implicated in carcinogenesis?
What is the definition of a carcinogen?
What is a remote/proximate/ultimate carcinogen?
How do we classify carcinogens? Give examples in each category.
How do viruses induce malignancy? Give examples.
What types of genes have been implicated in carcinogenesis?
What are the differences in initiation, promotion and persistence?
What are oncogenes? Please give some examples.
What are tumour suppressor genes? Please give some examples.
What is Knudson’s ‘two-hit’ hypothesis?
Related topics
Topic Chapter Page
Cell cycle 52 194
Hypertrophy, hyperplasia and atrophy 59 227

What is carcinogenesis?
This is the process that results in the transformation of normal cells to
neoplastic cells, caused by permanent genetic alterations or mutations. It
applies only to malignant tumours.
Compare oncogenesis, which is the process that leads to the formation of
benign or malignant tumours.
Factors implicated in carcinogenesis are broadly divided into genetic and
environmental.
Carcinogen is an agent known to cause or suspected of causing cells to
transform and start dividing uncontrollably without their normal inhibitions,
eventually developing into neoplasms.
189
APPLIED SURGICAL PATHOLOGY carcinogenesis
TYPES OF CARCINOGENS
Chemical carcinogens
• Remote: precursor of a carcinogenic agent that may be found in food, the
environment, exposure to certain chemicals, infective organisms and physical
agents
• Proximate: metabolite(s) of a remote carcinogen that has some carcinogenic
potential but may be modified further in the body into an ultimate carcinogen
• Ultimate: active carcinogen that interacts with DNA and causes cancer.
Remote/proximate/ultimate carcinogen sequence: best example is "-naphthylamine.
Direct effect or after metabolic conversion. These carcinogens are usually hydro-
carbons, which form charged molecules called epoxides. Epoxides then bind to
DNA and RNA, causing a genetic mutation:
• Polycyclic aromatic hydrocarbons (tar) in smoke cause lung cancer
• Aromatic amines ("-naphthylamine – used in the rubber and dye industry):
converted to a carcinogen in the liver and thought to cause bladder cancer
• Nitrosamines: used in fertilizers, causing gastrointestinal tract cancers
• Azo dyes – in bladder and liver cancer.
Viral carcinogens
Some DNA and RNA viruses are oncogenic.
Directly: their integration into the host genome promotes over-activity of proto-
oncogenes (see below).
Indirectly: cause malignancy through diseases such as chronic hepatitis, which pre-
dispose to hepatocellular carcinoma.
DNA viruses
Human papillomavirus in cervical (HPV-16 and -18), anal and
oesophageal cancers
These viruses are seen in cervical intraepithelial neoplasia (CIN). The viral DNA is
integrated into the host cell DNA leading to over-expression of E6 and E7 viral pro-
teins. They bind to and inhibit p53 and Rb (see below). The transformation zone
(labile area where columnar epithelium undergoes metaplasia to squamous type) is
at the squamocolumnar junction.
Epstein–Barr virus – in Burkitt’s lymphoma and nasopharyngeal cancer (NPC)
This was discovered in cell cultures from Burkitt’s lymphoma.
It usually causes infectious mononucleosis but with a co-factor is oncogenic.
Epidemiological evidence suggests that the co-factor is malaria, which has a causal
link with NPC.
190
Hepatitis B and C
Strong association with hepatocellular carcinoma.
RNA viruses
• Human T-cell leukaemia virus (HTLV-1): in T-cell leukaemia and
lymphoma
• Human immunodeficiency virus (HIV): in Kaposi’s sarcoma.
Bacterial carcinogens
• Helicobacter pylori linked to gastric lymphoma and carcinoma
Radiant energy
• Non-ionizing radiation – ultraviolet (UV) light: malignant melanoma
• Ionizing radiation: leukaemia, skin and thyroid cancer.
Biological agents
• Hormones: oestrogens in breast and endometrial cancers
• Androgenic and anabolic steroids in hepatocellular carcinoma
• Mycotoxins: Aspergillus species (aflatoxin) in hepatocellular carcinoma
• Parasites:
• schistosomiasis in bladder cancer
• liver fluke in cholangiocarcinoma.
Other carcinogens
Industrial dusts
Asbestos: malignant mesothelioma and carcinoma of the lung (see ‘Asbestos’,
Metals
• Nickel: NPC and carcinoma of the lung
• Arsenic: skin cancer.
HOST FACTORS
• Race, e.g. breast cancer is less common in Africa
• Diet, e.g. fat and colorectal carcinoma
• Genetics
• Age
• Gender
• Pre-malignant lesions, e.g. polyps, chronic ulcerative colitis, hepatic cirrhosis
• Transplacental exposure, e.g. diethylstilbestrol and vaginal cancer in female
babies.
191
MULTI-STEP THEORY OF CARCINOGENESIS

Initiation refers to the induction of certain irreversible changes (mutations) in the
genome of the cells, which bestows neoplastic potential when appropriately stimu-
lated by promoting agents. Initiated cells are not transformed cells; they do not have
growth autonomy or unique phenotypic characteristics.
Promotion refers to the process of tumour induction in previously initiated cells by
chemicals called promoters. This stimulates clonal proliferation of the initiated cell.
Persistence is clonal proliferation of tumour cells that no longer require the pres-
ence of initiators or promoters.
ONCOGENES
A proto-oncogene is a cellular gene involved in normal regulation and differentiation
of cell growth. Most are growth factors or receptors. When they become mutated they
have altered and enhanced expression and become known as oncogenes. Oncogenes
are classified by the function of their gene products (oncoproteins).
Examples
• Bcl-2: involved with apoptosis
• Ras: signal transduction molecule involved in intracellular signalling
• Myc: nuclear binding protein involved in cell proliferation.
Mechanism of oncogene activation
• Translocation of an oncogene to a position adjacent to an actively translocated
gene (8 → 14 in Burkitt’s lymphoma)
• Point mutation
• Gene insertion resulting in the proximity of an oncogene to a promoter or
enhancing gene (retrovirus).
Abnormalities in oncogene expression may account for an increased risk of
carcinogenesis:
• Production of an excessive amount of oncoproteins
• Production of abnormally functioning oncoproteins
• Loss of usual growth inhibition – tumour suppressor genes.
Oncoproteins encourage cells to grow autonomously, have increased motility and
reduced cell–cell adhesion, all features of malignancy.
TUMOUR SUPPRESSOR GENES

These are recessive genes that encode proteins that inhibit cell proliferation. If
their function is disrupted, uncontrolled cell proliferation, and hence tumours, are
more likely to occur.
192
Examples
The p53 gene
This is the most common gene to be altered in human cancers (70 per cent of colon
cancers and one-third of breast cancers). It repairs damaged DNA before the S-phase
of the cell cycle by arresting the cell cycle in G1 until the damage is repaired. If the
damage cannot be repaired, it induces the cell to undergo apoptosis. Loss of function
causes:
• Mutations
• Binding of normal p53 proteins to proteins encoded by oncogenic DNA viruses.
Retinoblastoma ( Rb1 gene)
Patients with retinoblastoma usually have a hereditary germline mutation on chromo-
some 13. Therefore sporadic loss of the other gene as a result of mutation leads to
tumour development – Knudson’s ‘two-hit’ hypothesis. This states that both alleles
of the tumour suppressor gene need to be deleted or damaged for malignant trans-
formation to occur.
Key learning point

It is worthwhile knowing several examples of both tumour suppressor
genes and oncogenes because this question is frequently asked.
193
52 Cell cycle

What is the cell cycle and can you draw it?
Name some factors that influence the progression of the cell cycle.
What cell growth factors are important in wound healing and/or
inhibition?
What cell types are there?
Related Topics
Topic Chapter Page
Hypertrophy, hyperplasia and atrophy 59 227
DEFINITION
The cell cycle describes the progressive steps that a cell moves through in order that
DNA may be synthesized and cells may divide. It is made up of the following phases:
G0: resting phase – stable cells are held in G0
G1: first gap phase:
• main determinant of the cell cycle
• variable duration
• four options:
(1) recycle and embark on another round of DNA synthesis and mitosis
(2) decycle and move to G0 phase
(3) decycle and commit to terminal differentiation
(4) abort and undergo apoptosis.
If the cell cycle is permitted to advance beyond the restriction point, the cell must
complete the cycle and undergo mitosis (Fig. 52.1).
S: synthetic phase – DNA synthesis
G2: second gap phase
M: mitosis phase – nuclear and cytoplasmic division
194
APPLIED SURGICAL PATHOLOGY cell cycle
The S, G2 and M phases are usually of constant length. The G2 phase may vary
between cell types and species.
Example viva questions

Draw the cell cycle
M phase
G0 ! resting
G2 phase G1 phase
S phase Restriction point

(Rb gene)
Figure 52.1
MOLECULAR CONTROLS
These regulate the passage of cells through specific phases of the cell cycle. There
are two types: a cascade of protein phosphorylation pathways and checkpoints.
Cascade
The cascade involves cyclins and cyclin-dependent kinases. Cyclins are regulatory
proteins with concentrations that rise and fall during the cell cycle. They form com-
plexes with constitutively present protein kinases called cyclin-dependent kinases
(CDKs). Different combinations of cyclins and CDKs are associated with each of
the important transitions in the cell cycle.
Checkpoints
A set of checkpoints is present that monitor completion of the molecular events; if
necessary they delay progression to the next phase of the cycle.
These checkpoints provide a surveillance mechanism for ensuring that critical tran-
sitions in the cell cycle occur in the correct order and that important events are
completed with fidelity.
Examples
The gene p53 is activated in response to DNA damage and inhibits further pro-
gression through the cell cycle by increasing expression of a CDK inhibitor.
195
APPLIED SURGICAL PATHOLOGY cell cycle
Retinoblastoma (Rb) and related genes act at the restriction point, which holds the
cell in the G1 phase.
Growth factors involved in stimulating inflammation and repair

These are important in wound healing:
• Epidermal growth factor (EGF) from epithelial cells
• Fibroblast growth factor (FGF)
• Platelet-derived growth factor (PDGF) from * granules in platelets and
macrophages. It stimulates proliferation of epithelial cells in the epidermis with
the help of EGF. It also stimulates proliferation of myofibroblasts in the dermis
• Cytokines: TNF
• Transforming growth factor " (TGF-"): this stimulates the production of
collagen and fibronectin from myofibroblasts.
Growth factors involved in inhibition of inflammation and repair

• Interferon-*
• Heparin
• Prostaglandin E2.
Cell types
• Permanent: neurons, cardiac muscle
• Stable: liver, fibroblasts
• Labile: skin, blood, epithelium.
196
53 Chronic inflammation

Define chronic inflammation.
What cell types are involved in chronic inflammation and at what times?
What are the beneficial and harmful effects of chronic inflammation?
What are the clinical features of chronic inflammation?
Give some examples of chronic inflammation.
What happens in chronic peptic ulceration?
Related topics
Topic Chapter Page
DEFINITION
• Tissue response to persistent injury
• Long in duration
• Cellular components differ from acute inflammation.
CAUSES
• Foreign bodies (granulomata): surgical sutures
• Bacteria: TB
• Chronic abscess formation: osteomyelitis
• Transplant: chronic rejection
• Inflammatory bowel disease
• Progression from acute inflammation.
Key learning point

A viva on acute inflammation can easily lead into a viva on chronic inflam-
mation and a viva on abscesses can lead into discussion of both types of
inflammation.
197
APPLIED SURGICAL PATHOLOGY chronic inflammation
HISTOLOGICAL AND CELLULAR FEATURES OF CHRONIC INFLAMMATION

Compare with acute inflammation (‘Acute inflammation’, Chapter 45, page 161):
• The histological pattern is not as predictable as in acute inflammation, and
many of the features described below may coexist. There may be areas of
ongoing acute inflammation.
• Granulation tissue may be present, as may fibrosis. These reflect the tissue’s
attempts at repair.
• Lymphocytes predominate – they are recruited by macrophages and cytokines.
• Macrophages are also present. In granulomatous inflammation, they fuse to
form multinucleate Langhan’s giant cells, the presence of which is
microscopically diagnostic of graulomatous inflammation. They are important in
phagocytosis and antigen presentation.
• Plasma cells are also present: derived from B lymphocytes that migrate into
the area.

Describe what happens in a chronic peptic ulcer.
A breach in the stomach mucosa occurs.
Acute inflammation continues in the part of the ulcer in contact with acid
as the injury continues.
The base of the ulcer contains granulation tissue and fibrosis as attempts at
repair occur.
Role of the macrophage

• Derived from monocytes
• Phagocytosis and killing of pathogens by lysosomes, scavenging of debris
• Attracted by chemotaxis and produces cytokines
• Antigen presentation
• Formation of Langhan’s giant cells in granulomatous inflammation.
CLINICAL FEATURES
Fever is caused by the chemical mediators seen in acute inflammation, although it
is not as severe.
The predominant leukocytes present at the site of inflammation can be measured
in a FBC (lymphocytes, monocytes, eosinophils or neutrophils).
198
APPLIED SURGICAL PATHOLOGY chronic inflammation
Weight loss may occur because of the high metabolic rate required to maintain
cell division.
EFFECTS OF CHRONIC INFLAMMATION

• Secondary infection, e.g. in chronic epithelial injury
• Scarring
• Resolution (always some scarring)
• Secondary amyloidosis (rare) in rheumatoid arthritis and TB
• Local lymphadenopathy.
GRANULOMATOUS INFLAMMATION

What is a granuloma?
This is a common opening question in a pathology viva. Granulomatous
inflammation is commonly seen in surgical conditions – sutures, inflamma-
tory bowel disease, etc. and is also a good route into a viva on inflammation.
A granuloma is a collection of epithelioid (activated) macrophages. Granulomatous

inflammation is a form of chronic inflammation in which granulomata are seen
histologically.
Histologically, granulomatous inflammation is characterized by the presence of
epithelioid macrophages; these are so called because they resemble epithelial cells.
These macrophages can fuse to form multinucleate giant cells (Langhan’s cells),
which are sometimes present in granulomatous inflammation.
Some causes
Infections TB, leprosy
Chronic diseases Sarcoidosis, Wegener’s granulomatosis, inflammatory
bowel disease (Crohn’s disease)
Foreign bodies Surgical sutures
199
54 Colorectal cancer

How would you classify colonic tumours?
What are the risk factors for colorectal carcinoma?
What is the anatomical distribution of colorectal cancer?
How does colorectal carcinoma present clinically?
How is colorectal cancer staged?
What are the principles of management of colorectal cancer?
What is meant by the adenoma–carcinoma sequence?
What operations can be performed for colorectal cancer?
What is the prognosis after surgery for colorectal carcinoma?
What are the complications of surgery for colorectal carcinoma?
What are the advantages and disadvantages of pre- and postoperative
radiotherapy?
What are the indications for chemotherapy in colorectal cancer?
What is the risk of malignant transformation in ongoing ulcerative colitis?
Related topics
Topic Chapter Page
Antibiotics in surgery 67 275
Bowel preparation 68 280
Cell cycle 52 194
Stomas 80 330
DVT prophylaxis and coagulation in surgery 73 297
Tumour markers 63 252
Diverticula 55 210
DISTRIBUTION AND RELATIVE INCIDENCE

• Rectal 38 per cent
• Sigmoid 28 per cent
• Caecal 12 per cent
• Transverse colon 5.5 per cent
200
APPLIED SURGICAL PATHOLOGY colorectal cancer
• Ascending colon 5 per cent

• Descending colon 4 per cent
• Splenic flexure 3 per cent
• Hepatic flexure 2 per cent
• Anal 2 per cent
• Appendicular 0.5 per cent.

What are the risk factors for colorectal carcinoma?
Colorectal carcinoma is the second most common cancer causing death in
the UK with 20 000 new cases per year in the UK – 40 per cent rectal and
60 per cent colonic.
Three per cent of patients present with more than one tumour (! synchron-
ous tumours).
Risk factors
• Family history (although 75 per cent are sporadic)
• Adenomatous polyps (see ‘Adenoma–carcinoma sequence’ below)
• Familial adenomatous polyposis coli (FAP gene on chromosome
5q21)
• Hereditary non-polyposis colorectal carcinoma (HNPCC)
• Diet:
• low fibre intake (decreases gut transit time, increasing the time that poten-
tial carcinogens are exposed to the gut mucosa)
• high carbohydrate and fat intake (possibly favours bacteria that degrade
bile salts into carcinogens)
• high protein intake (particularly meat)
• low vitamin A, C and E intake
• Ulcerative colitis (UC): 1 per cent per year risk of malignant transform-
ation in ongoing colitis. After subtotal colectomy, the rectal stump still
requires surveillance, leading to most UC sufferers opting for a modified
panproctocolectomy and ileoanal pouch or end ileostomy
• Gardner’s syndrome
• Other hereditary mutations of tumour suppressor genes or proto-
oncogenes such as p53 and K-ras (see ‘Carcinogenesis’, Chapter 51,
page 189 and ‘Cell cycle’, Chapter 52, page 194)
• A previous colonic neoplasm increases the risk of a second tumour
(metachronous tumour)
201
CLINICAL FEATURES
Many tumours can be asymptomatic, with right-sided lesions being more likely to
be clinically silent than left-sided lesions.
Associated with primary tumour
• Change in bowel habit
• Weight loss
• Unexplained microcytic anaemia (iron deficiency)
• Faecal occult blood (FOB) positive
• Obstruction
• Mucus or altered blood per rectum (overt bleeding relatively uncommon in
colonic tumours, more common in rectal tumours)
• Tenesmus (a feeling of incomplete evacuation)
• Can present with perforation and an acute abdomen
• Can present with colovesical/colovaginal fistula (uncommon).
Associated with metastatic disease
• Jaundice, ascites and hepatomegaly from liver metastases
• Pleural effusion, recurrent chest infections from lung metastases
• Bone pain from bone metastases
• Lymphadenopathy.
Note that presentation of the primary tumour is often dependent on the site of the
tumour:
• Right sided: often clinically silent, iron deficiency anaemia, FOB positive,
mass & small bowel obstruction
• Left sided: fresh/altered blood and mucus per rectum, large bowel obstruction
• Rectal: tenesmus, incomplete evacuation, per rectum bleeding and mucus
• 30 per cent of cases present as an emergency and 20 per cent of all cases have
metastases at presentation.
PRINCIPLES OF MANAGEMENT
Diagnosis
• Bloods:
• FBC to look for microcytic anaemia
• U$Es and LFTs to look for any evidence of hepatic involvement or renal fail-
ure preoperatively
• Chest radiograph and ultrasonography of the liver & CT of the abdomen and
pelvis to exclude metastasis
• Flexible sigmoidoscopy can be used in elderly people, although a full
colonoscopy is the gold standard for diagnosis $ biopsy
202

How is colorectal cancer staged?
Classically colorectal tumours have been staged by the modified Dukes’
classification although TNM staging of cancer is becoming more standard
in the hands of specialist colorectal surgeons. The tumour’s stage deter-
mines the likely prognosis for the patient, but tumours cannot be staged
until the histology of the specimen has been performed. Thus, all fit
patients with no evidence of metastasis should be offered immediate surgery.
Modified Dukes’ classification

Based on the position of the tumour in relation to the muscularis propria
(NOT the muscularis mucosa):
Class Histology 5-year survival rate (%)
A Limited to muscularis propria 90–100

B Breaches the muscularis but does
not involve lymph nodes 75
C1 Some nodes $ve, apical node %ve 30–40
C2 Apical node $ve 25
D Evidence of metastases #15
TNM classification
TX Primary tumour cannot be assessed
T0 No primary tumour identified
Tis Carcinoma in situ (tumour limited to mucosa)
T1 Involvement of submucosa, but no penetration through muscularis
propria
T2 Invasion into, but not penetration through, muscularis propria
T3 Penetration through muscularis propria into subserosa (if present),
or pericolic fat, but not into peritoneal cavity or other organs
T4 Invasion of other organs or involvement of free peritoneal cavity
NX Nodal metastasis cannot be assessed
N0 No nodal metastasis
N1 One to three pericolic/perirectal nodes involved
N2 Four or more pericolic/perirectal nodes involved
MX Distant metastasis cannot be assessed
M0 No distant metastases
M1 Distant metastases
You will not be asked to repeat the TNM staging but you should at least
know Dukes’ classification and be aware that there are other systems.
203
• Barium enema is also a gold standard for diagnosis (although this does not give
a histological diagnosis, the classic ‘apple-core’ lesion appearance is diagnostic
of colorectal carcinoma)
• In frail patients who would not withstand an invasive investigation or bowel
preparation, CT colonography has been used, although this is not as sensitive or
specific a test as either colonoscopy or barium enema
• MRI of the pelvis is particularly good for local staging of rectal carcinoma
and assessing degree of invasion into the mesorectal fat surrounding the
rectum.
SPREAD
• Lymphatics: these run with the blood supply and drain to regional lymph nodes,
para-aortic nodes and then to the thoracic duct. Supraclavicular nodes can be
involved in advanced carcinoma.
• Blood borne: portal vein drains metastases to the liver. Thirty per cent of
patients have liver metastases at presentation. Lungs, adrenals, kidneys and
bones are other sites of spread.
• Transcoelomic: seeding of carcinoma throughout the peritoneal cavity; occurs in
10 per cent of cases after resection. Spread to ovaries results in ‘Krukenberg
tumours’.
OPERATIONS FOR COLORECTAL CANCER

Principles of surgery
• Bowel preparation if not obstructed (see ‘Bowel preparation’, Chapter 68,
page 280)
• Multidisciplinary approach: stoma nurse to counsel patient and site potential
stomas preoperatively. It is good practice to obtain consent for a stoma and
discuss the implications with the patient even in a planned primary
anastomosis
• Full anaesthetic assessment
• Epidural for pain relief if possible
• Prophylactic antibiotics (see ‘Antibiotics in surgery’, Chapter 67, page 275)
• In potentially curable cases, aim for wide resection margins along with regional
lymphatics. Rectal tumours should have a total mesorectal excision to decrease
risk of recurrence
• In incurable cases, minimize surgery and aim to prevent or treat obstruction
• Tension-free anastomosis (see ‘Anastomosis and anastomotic leak’, Chapter 66,
page 270)
204

What is meant by the adenoma–carcinoma sequence and what is the
evidence for it?
Most colonic carcinomas arise within adenomas and the accumulation of
about 5–10 stepwise mutations in tumour suppressor genes or oncogenes
over a lifetime results in cancer, e.g.
Tissue Mutation
Normal colonic endothelium APC
Small adenoma K-ras
Large adenoma smad4
Pre-malignant changes p53
Colorectal carcinoma E-cadherin – alters cell adhesion
Increasing aggressiveness and invasion
Evidence
• Distribution of cancers is similar to polyps
• FAP always proceeds to cancer
• Adenocarcinoma is seen histologically in adenomatous polyps
• Systematic removal of polyps reduces lifetime cancer risk
• Age incidence peaks for polyps about 5 years before carcinoma
• If anastomosis looks oedematous or bowel edges do not bleed well, consider a

loop ileostomy to allow the anastomosis to heal
• If primary anastomosis is not possible, consider a staged procedure, raising a
stoma in the first instance with the option of reversing it later.
Specific operations
Elective operations for non-obstructed tumours
• Right colonic tumour: right hemicolectomy with primary anastomosis
• Left colonic tumour: left hemicolectomy with primary anastomosis
• Transverse colonic tumour: extended right or left hemicolectomy
• Sigmoid colonic tumour: sigmoid colectomy
• High rectal tumours: anterior resection
• Low rectal tumours: some can be treated by anterior resection but usually
treated with an abdominoperineal (AP) excision and end-colostomy or
ileostomy. For palliative resection and small tumours with liver metastases,
transanal excision may be used.
205
Transanal stapling guns allow low primary anastomoses with only a small risk of
anastomotic leak.
Operations for obstructed tumours

Right-sided tumours are often suitable for a right hemicolectomy or extended right
hemicolectomy with primary anastomosis.
There are three approaches used for obstructed left-sided tumours.
Hartmann’s operation
Resection with oversewing of the rectal stump and fashioning of an end-
colostomy:
• Relieves obstruction and resects tumour
• No initial anastomosis
• Reversal possible but has 10 per cent mortality rate, so many patients end up
with a permanent colostomy.
• Modification with formation of a mucous fistula can simplify the reversal
operation and reduce the complication rate.
Primary resection and anastomosis

• Single procedure
• No stoma
• Anastomosis formed under suboptimal conditions – higher incidence of
anastomotic leak
• Loop ileostomy can be fashioned to allow the primary anastomosis to heal.
Reversal of this is a straightforward procedure
• On-table lavage and subtotal colectomy reduce incidence of sepsis.
Three-stage approach
Primary operation to relieve obstruction, second to resect tumour electively and
third to close a colostomy:
• Out of favour with most colorectal surgeons
• Cumulative mortality rate is 20 per cent
• 50 per cent patients never have colostomy closed.
Palliative surgery
• Resection of the primary tumour is the best palliation, simultaneously curing
obstruction and helping to prevent future obstruction.
• Bypass procedures many be of help in frail individuals with unresectable
tumours to prevent obstruction.
• Defunctioning colostomy/ileostomy in frail/elderly patients can relieve
obstruction.
206
• Stenting of rectal tumours can relieve low obstruction and is relatively

non-invasive.
• Local transanal excision may be of help in low rectal cancers.
• Other techniques for rectal cancer include laser treatment, contact irradiation
and electrocoagulation.
• Radiotherapy in rectal tumours and metastases (particularly bone) and
chemotherapy may offer some short-term benefit.
COMPLICATIONS OF COLORECTAL CANCER SURGERY

These can be divided into general and specific, early and late.
General
• Anaesthetic complications
• Cardiorespiratory: myocardial infarction, pulmonary embolus
• Deep vein thrombosis: leg, mesenteric (see ‘DVT prophylaxis and coagulation in
surgery’, Chapter 73, page 297)
• Postoperative renal failure.
Specific
Early
• Wound infection and/or dehiscence: reduced incidence with ‘clean’ operations
and the use of bowel preparation, prophylactic antibiotics and a meticulous
technique
• Urinary retention: cause by postoperative pain, denervation of the bladder or
prostatic obstruction
• Injury to ureters: can lead to urinary fistulae, pyonephrosis
• Injury to bladder: denervation or direct trauma during anterior resection
• Anastomotic leak: the most feared complication of the colorectal surgeon and
responsible for the major cause of postoperative morbidity and mortality along
with cardiorespiratory complications. Increased risk in low anastomoses and
emergency operations on unprepared bowel
• Postoperative ileus.
Late
• Anastomotic stricture
• Sexual dysfunction as a result of damage of the splanchnic nerves – more
common in rectal surgery than colonic surgery
• ‘Phantom rectum’ – present in 50 per cent of AP resections (an unpleasant
feeling of rectal discomfort despite the complete lack of the organ).
207

What are the advantages and disadvantages of pre- and postoperative
radiotherapy?
Radiotherapy
• Neither preoperative nor postoperative radiotherapy has been shown to
prolong survival or reduce distant metastases
• Both forms reduce local recurrence rates
Preoperative
• Can be used to attempt to downstage tumours, increasing the chance of
curative resection
• Compliance is high
• Irradiated bowel is all resected at surgery
• Patients may be included who do not require it and are found at lapar-
otomy to have earlier disease than was first thought
• Makes bowel friable and increases fibrosis in the mesorectum in rectal
surgery, making the planes more difficult to dissect and total mesorectal
excision more difficult
Postoperative
• Early disease excluded as pathology known
• Does not delay surgery
• Small bowel more likely to be in the field
• Prolonged course
• May be delayed by surgical complications
• Irradiated bowel is left in and may result in radiation colitis
• Compliance is lower as a result of postoperative morbidity
• Planes easier to dissect in total mesorectal excision
CHEMOTHERAPY IN COLORECTAL CANCER

• Improves survival in Dukes’ C tumours
• Not indicated in Dukes’ A tumours
• Controversy about role in Dukes’ B tumours
• currently being investigated in the QUASAR (Quick and Simple and Reliable)
trial
• QUASAR study to date has shown:
• 5-fluorouracil (5FU) and folinic acid are effective as adjuvant therapy
• high-dose folinic acid rescue confers no additional benefit
• the use of levimasole confers no additional benefit.
208
PRINCIPLES OF FOLLOW-UP FOR COLORECTAL CANCER

• Identification of recurrent disease:
• regular surveillance colonoscopy or barium enema to detect recurrence or
metachronous tumours
• carcinoembryonic antigen (CEA) is a tumour marker that can be used to pre-
dict recurrence (see ‘Tumour markers’, Chapter 63, page 252)
• follow-ups with ultrasonography or CT of the liver and pelvis are helpful and
have become standard level of care in many centres
• Check for postoperative complications
• Ensure appropriate adjuvant therapy.
209
55 Diverticula

What is the definition of a diverticulum?
What is the difference between a true and a false diverticulum? Give
examples.
What types of diverticula have you heard of?
What do you know about diverticular disease?
What are the complications of colonic diverticular disease?
How would you manage a patient who presents to the accident and
emergency department (A&E) with diverticulitis?
What is a Zenker’s diverticulum? Describe the relevant anatomy.
What is a Meckel’s diverticulum? How may it present?
What three surgical procedures may be used to deal with perforated
diverticular disease?
Which has the lowest operative mortality rate?
Related topics
Topic Chapter Pages
Stomas 80 330

What is a diverticulum?
A diverticulum is an abnormal outpouching of a hollow viscus into the
surrounding tissues.
CLASSIFICATION
1. True diverticulum: contains all layers of the wall of the viscus, e.g. Meckel’s
diverticulum
2. False diverticulum, only some layers present, e.g. colonic diverticulum (espe-
cially sigmoid colon).
Or classify by aetiology, so congenital (normally true in nature) versus acquired.
210
APPLIED SURGICAL PATHOLOGY diverticula
Key learning points

Meckel’s diverticulum
Rule of two: 2 per cent population; 2 inches long; 2 feet from the ileocaecal
valve along the antimesenteric border; remnant of the vitellointestinal duct
Zenker’s diverticulum
Pharyngeal pouch
Outpouching of pharyngeal mucosa through a gap between inferior con-
strictor and cricopharyngeus (Killian’s dehiscence)
Dehiscence is in midline but 90 per cent present on left side
Presentation: vomiting undigested food, halitosis and recurrent aspiration
pneumonia
Diagnosis with barium swallow; danger with OGD (oesophagogastroduo-
denoscopy) (perforation of pouch)
Surgery: laparoscopic versus open; staple off and invert pouch
DIVERTICULAR DISEASE
• Incidence: 60 per cent of 80 year olds
• Increasing in incidence (because of older population)
• Developed countries: associated with low-fibre diet.
Aetiology
Lack of fibre in the diet causes a raised intraluminal pressure, which in turn causes
outpouching of the colonic mucosa. Normally occurs at sites of weakness where
mesenteric blood vessels pass between muscles of the taeniae coli.
Distribution: sigmoid colon (45 per cent); sigmoid and descending colon (35 per cent);
10 per cent affect sigmoid, descending and transverse, 5 per cent pancolonic; caecum
(5 per cent).
Presentation
Usually presents with its complications:
• Diverticulosis: asymptomatic, altered bowel habit or abdominal pain
• Diverticulitis: $ inflammation
• Per rectal (PR) bleeding (usually in the absence of diverticulitis). Can be
localized, usually with mesenteric angiography
211
• Paracolic abscess: pyrexia and abdominal mass

• Peritonitis: faecal perforation of one of the diverticula
• Fistulae: to small bowel, large bowel, bladder (colovesical) present with
pneumaturia, faecaluria and chronic urinary tract infection or UTI
(polymicrobial); vagina (colovaginal), skin surface
• Stricture & obstruction.
Investigations in the acute setting

History
Left iliac fossa (LIF) pain, altered bowel habit, shivers/rigors, PR bleeding.
Examination
Pyrexia, dry, LIF tenderness.
Investigations
• FBC (raised WCC and neutrophilia)
• Urine microscopy: ?fistula; ?differential UTI
• Erect chest radiograph: ! supine abdominal film % perforation & suspected
obstruction
• Rigid sigmoidoscopy: to check that there is no tumour
• Barium enema: performed normally as an outpatient when pain has settled to
confirm the diagnosis and look at severity and site
• Ultrasonography: can demonstrate thickened colon and useful to exclude
localized collections
• CT is the investigation of choice if the pain does not settle. Good at picking up
intra-abdominal abscess, defining inflammatory masses and confirming diagnosis.
• Colonoscopy not usually recommended, especially in the acute setting – greater
risk of perforation. Also more challenging to the endoscopist in the presence of
many diverticula.
Management
Diverticulitis
Normally conservative with bowel rest.
Intravenous fluids
• Patient is normally dehydrated; cefuroxime and metronidazole for broad-
spectrum and anaerobic cover
• Begin with sips and build up when systemic symptoms start to settle
• Regular patient review.
Radiological
Percutaneous drainage of a collection/abscess under CT or ultrasonic guidance.
212
Surgery
For perforation or non-resolving episode of diverticulitis/abscess formation.
1-2-3 staged procedures

• Diverting colostomy and abscess drainage (first of three)
• Hartmann’s procedure (first of two)
• Resection with colonic wash-out and primary anastomosis (one stage).
Lowest operative mortality is with Hartmann’s procedure.
If a diverticular bleed is life threatening and cannot be localized with angiography,
the patient requires a subtotal colectomy with ileostomy or total colectomy with
ileorectal anastomosis.
213
56 Gastro-oesophageal reflux disease
(GORD) and Barrett’s oesophagus

What are the symptoms of GORD?
What is the difference between heartburn and GORD?
What is the aetiology of GORD? Is a hiatus hernia an essential component?
How do you diagnose GORD? What useful studies are there to
help you?
What are the complications of GORD?
What is the initial management of a patient suspected of having GORD?
What is the role of proton pump inhibitors (PPIs) in GORD?
When is surgery indicated? What is the goal of surgery? What procedures
can accomplish this?
What is Barrett’s oesophagus?
How would you manage a patient with a Barrett’s oesophagus?
Related topics
Topic Chapter Page
The diaphragm 7 22
Stomach 17 46

What is the difference between heartburn and GORD?
Heartburn is a lay term for mild, intermittent reflux of gastric content into
the oesophagus without tissue injury. It is relatively common among adults
(about 40 per cent).
GORD implies oesophagitis with varying degrees of erythema, oedema
and friability of the distal oesophageal mucosa.
214
APPLIED SURGICAL PATHOLOGY GORD and Barrett’s oesophagus
EPIDEMIOLOGY
• 7 per cent of normal individuals have GORD
• 5 per cent of sufferers go on to surgery
• Not all patients with GORD have a hiatus hernia and vice versa
• 50 per cent of those aged in their 50s have a hiatus hernia; a third of these
suffer with GORD.
AETIOLOGY
• Lower oesophageal sphincter (LOS) incompetence:
• normal is pressure of " 5 mmHg over a distance of 1 cm or more
• Gastric outlet obstruction: this increases acid reflux
• 50 per cent of GORD sufferers have an associated hiatus hernia.
• Defective oesophageal action, e.g. scleroderma, may act as a vicious cycle
because reflux can cause oesophageal dysfunction and may therefore predispose
to further reflux.
CLINICAL FEATURES
• Epigastric/retrosternal pain typically after meals or at night
• Pain is similar to angina (reflux may be exercise related)
• Reflux of food or gastric contents. This is effortless and occurs with bending.
Discomfort is relieved by standing or sitting
• Odynophagia, especially with hot food/drink
• Globus (lump in throat)
• Pulmonary aspiration: nocturnal coughing and hoarse voice.
DIAGNOSIS
• History and examination: effect of posture and antacids
• Upper gastrointestinal endoscopy (70 per cent specificity): shows changes
proximal to the squamocolumnar junction
• Biopsy (80 per cent specificity): ↑ eosinophils $ hyperplasia
• Barium swallow (60 per cent specificity): can diagnose reflux but frequently
cannot diagnose oesophagitis, although it can demonstrate other pathology
• Ambulatory 24-hour pH monitoring: gold standard and 90 per cent specific:
• antimony probe placed over gastro-oesophageal junction (GOJ) for 24 h
• diagnosis made if pH # 4 for " 1 per cent of time spent supine or if " 6 per
cent of time spent erect
• Oesophageal ! LOS manometry: used when an oesophageal motility disorder is
suspected and before any surgical intervention.
215
MANAGEMENT
Medical (90 per cent effective)
• Conservative: encourage weight loss (can be highly effective), avoid large meals
before bedtime, stop smoking, elevate the head of the bed 4–5 inches
(10–15 cm), change diet to avoid foods that are known to induce reflux, e.g.
chocolate and coffee, reduce alcohol intake
• Antacids for symptomatic relief
• Metoclopramide: increases LOS pressure and gastric emptying, but does not
relieve symptoms consistently in the absence of acid reduction
• H2-receptor blockers, e.g. ranitidine: 50 per cent of patients show significant
healing but only 10 per cent of such patients remained healed at 1 year
• PPIs, e.g. omeprazole:
• 80 per cent successful in healing severe erosive oesophagitis
• 70 per cent remained healed if they continue on this
• a concern with prolonged PPI use is hypergastrinaemia secondary to alkalin-
ization of the gastric antrum. Gastrin is known to be trophic to gastric
mucosa, which raised the fears of neoplasia, but this has not been borne out by
follow-up studies.
INDICATIONS FOR SURGERY

• Failed medical therapy: intractable disease, intolerance and allergy to
medications, non-compliance and recurrence of symptoms while on medication
• Complications: stricture, respiratory symptoms, dental erosions, pre-malignant
mucosal changes
• Patient preference: cost or lifestyle issues.
GOALS OF SURGERY
• Operations for GORD attempt to prevent reflux by mechanically increasing
LOS pressure and, in most procedures, to restore a sufficient length of distal
oesophagus to the high-pressure zone of the abdomen
• Hiatus hernia, when present, is simultaneously reduced.
PROCEDURES
• Nissen fundoplication (NF): fundus of stomach is mobilized and wrapped
around the oesophagus. The procedure alters the angle of the GOJ and
maintains the distal oesophagus within the abdomen. There is a 90 per cent
success rate.
216
• The Belsey mark IV operation: accomplishes same anatomical changes as NF

but is done via a thoracotomy.
• Hill repair: this restores the oesophagus to the abdomen by fixing the
fundoplicated OGJ to the median arcuate ligament of the diaphragm.
• Angelchick prosthesis: this is a silicone-filled collar placed around the distal
oesophagus within the abdominal cavity. It can increase dysphagia and the
prosthesis can migrate and cause erosion.
• Roux-en-Y procedure: for recurrent reflux, but there is associated high
morbidity and mortality.
COMPLICATIONS
Oesophageal stricture occurs in 10 per cent of patients and is treated by endo-
scopic dilatation using balloon dilators or bougies.
Haemorrhage (rare): suspect Barrett’s oesophagus (see below) or oesophageal can-
cer. Reflux does not cause anaemia so another cause should be sought.
BARRETT’S OESOPHAGUS
This is a pre-malignant condition. The relative risk of developing adenocarcinoma
of the oesophagus in patients with Barrett’s oesophagus is 50–100 times.
The normal surface epithelium of the oesophagus is mainly stratified squamous
epithelium. This becomes columnar lined at the level of the GOJ. If it occurs more
than 3 cm from the junction this is thought to be abnormal and is called a classic
Barrett’s oesophagus.
It is thought to occur via metaplasia (transformation of one differentiated cell type
into another). The stimulus is thought to be gastro-oesophageal reflux.
Shorter segments of metaplasia are also currently considered to be significant.
Barrett’s patients should receive permanent PPI therapy.
Treatment of Barrett’s oesophagus is controversial.
Few surgeons would advocate oesophagectomy for early dysplastic change. The dif-
ference between high-grade dysplasia and cancer is sometimes difficult and severe
dysplasia would warrant consideration of surgery in the setting of a multidiscipli-
nary team (MDT) meeting.
Most surgeons would advocate regular endoscopic surveillance once these changes
have been identified. If the patient were frail and elderly and not fit enough to
undergo oesophagectomy, repeat endoscopy would not be warranted.
The following are based on the British Society of Gastroenterology guidelines.
217
Patient should undergo endoscopic surveillance if:

• The length of Barrett’s oesophagus is ! 3 cm
• Intestinal metaplasia is found on histology
• The patient is fit for surgery if dysplasia is found and understands the need for
surveillance and surgery.
Surveillance endoscopy
Biopsy suspicious areas, then quadrantic biopsies every 2 cm from the tip of the
gastric folds to the squamous columnar junction.
Follow-up depends on histology.
No dysplasia
Three-yearly upper gastrointestinal (GI) endoscopy: discharge from surveillance if
co-morbidity or age rules out surgery.
Low-grade dysplasia
Treat with PPI to reduce inflammation and repeat upper GI endoscopy at 6 months
with quadrantic biopsies every 2 cm.
High-grade dysplasia
Discuss at upper gastrointestinal cancer MDT meeting for surgery.
218
57 Human immunodeficiency virus and
universal precautions in surgery

Who is at increased risk of acquiring HIV infection?
What is the mode of transmission of HIV? How can HIV be transmitted
from patients to theatre personnel?
What is the risk of transmission?
What precautions should be taken when operating on a patient who is
HIV positive?
How would you minimize the risk of transmission?
If in the event of exposure to contaminated body fluids or blood what
steps would you undertake?
What is the rationale for giving prophylactic medication?
What surgical conditions are more common in HIV-positive patients?
How long is the seroconversion process? What factors increase the risk of
seroconversion after a needle-stick injury?
What potential problems may arise from operating on HIV-positive
individuals?
Should patients undergoing surgery be routinely tested for HIV?
Justify your answer.
Related topics
Topic Chapter Pages
Operating theatre design and infection control 76 312
HUMAN IMMUNODEFICIENCY VIRUS

• There are 42 million HIV-positive people in the world, 65 000 in the UK.
• Retrovirus.
• Haematogenous or mucomucosal transmission.
• Transmission to healthcare workers by needle-stick injury with a hollow needle,
contamination of broken skin or contaminated fluid splashing into the eyes or
on to mucous membranes.
219
APPLIED SURGICAL PATHOLOGY HIV and universal precautions in surgery
• Mechanism: HIV binds to CD4 receptors in lymphocytes, replicates in the

nucleus and destroys T-helper cells, dendritic cells and macrophages. T-cell
depletion leads to immunodeficiency, including increased susceptibility to
opportunistic infections and neoplasms.
• AIDS-defining illness:
• development of neoplasia – Kaposi’s sarcoma, lymphoma
• unusual or opportunistic infection, e.g. Pneumocystis carinii pneumonia,
aspergillosis, candidiasis
• probable revision of definition to include HIV-positive people with # 200/mm3
T-helper cells (CD-4 count)
• 90 per cent 2-year mortality rate.
• Seroconversion: occurs in 85 per cent of cases within 3 months of infection. In
the other 15 per cent it may take up to 2 years to seroconvert. This
seroconversion window has implications for blood donation in that it is possible
to donate HIV-infected blood before antibody production has commenced,
thereby avoiding detection by antibody screening.
• Factors that increase the risk of seroconversion:
• large inoculum of infected blood, indicated by a deep injury, visible blood on
the device
• source patient with terminal disease
• procedures that entail needles directly placed into blood vessels.
HIGH-RISK GROUPS FOR HIV INFECTION

• Homosexual males
• Sexually active adults – incidence of HIV infection is now higher in
heterosexual than in homosexual males (Public Health Laboratory figures)
• Intravenous drug abusers
• People with haemophilia before October 1985
• Children of infected mothers
• Patients from endemic areas (Africa and south-east Asia)
Key learning points

Most of the questions on HIV can be applied to a hepatitis B or C viva
question.
Most of the principles for HIV can also be applied to hepatitis except for
the pathology.
HIV and hepatitis B and C viruses can coexist, so individuals with HIV
should be screened for antibodies for hepatitis B and C viruses.
220
RISK OF TRANSMISSION
Average risk of HIV infection after a single percutaneous inoculation is 0.3 per cent.
Risk is higher with conjunctival contamination compared with non-intact skin.
SURGICAL CONDITIONS IN CARRIERS OF HIV

• Common acute or elective surgical conditions, e.g. appendicitis, hernia. They can
present with atypical features, e.g. apyrexia and low WCC. This can make
diagnosis and management challenging. They are managed in the usual way
while taking special precautions (see below).
• Neoplasia: HIV carriers have a much higher incidence of cancer.
• Leukaemia and lymphoma.
• AIDS-related lymphoma may present in varied extranodal sites – perianally, as
an intracranial tumour or as an obstructing small bowel tumour.
• Human papillomavirus infection causes genital and anal warts. There is an
increased risk of developing anal, cervical and vulval cancers.
• Epstein–Barr virus infects B lymphocytes. Increased risk of developing
Hodgkin’s lymphoma and nasopharyngeal carcinoma.
• Herpes virus: associated with Kaposi’s sarcoma and multicentric Castleman’s
disease.
• HIV is a predisposing cause for development of a fistula in ano, anal fissure and
perianal sepsis.
• HIV salivary gland disease may require superficial parotidectomy to confirm
diagnosis.
Postoperatively, HIV-positive patients, particularly in the later stages of the disease,
are more prone to developing wound infections after surgery. Healing is comprom-
ised because of their immunocompromised state and there is a higher incidence
of anastomotic dehiscence (see ‘Anastomosis and anastomotic leak’, Chapter 66,
page 270).
PRECAUTIONS TO BE TAKEN
Theatre
• Routine universal precautions for all patients regardless of HIV or hepatitis
status because risk of infection is present in all patients
• Wear a facemask with visor or protective eyewear, an impermeable gown and
water-resistant footwear
• Keep cuts and abrasions covered
• Double glove – this reduces the contamination risk from glove penetration
221
• Reduce the number of people in theatre to a minimum:

• warn all theatre personnel to this ‘category 3’ risk and label all specimens
as such
• use of a surgical assistant only if strictly necessary
• Maximal use of disposable items including drapes; these should be bagged for
incineration after the procedure
• Careful disposal of clinical waste appropriately labelled as hazardous waste
• Limit use of sharps and use blunt needles where possible
• Safe handling of sharps between operators – use of a kidney dish
• Careful decontamination of theatre after surgery.
In the event of an exposure

• Affected area should be washed with copious amounts of water.
• Encourage open wounds to bleed.
• Report incident to occupational health for further advice or A&E out of hours.
Clinicians exposed to communicable viruses should report to the
Communicable Disease Surveillance Centre.
• Risk assessment:
• source patient may provide a sample for testing for hepatitis B or C; with
appropriate counselling and consent, the sample can be tested for HIV
• a sample is also taken from the affected staff member to be tested in the event
that he or she has any symptoms.
• Post-exposure prophylaxis is recommended for significant occupational
exposure or high-risk source patient. The rationale is that uptake of HIV and
processing of its antigen may take several hours or days, so there is a window for
therapeutic intervention after accidental exposure.
• Should be given within 1 hour of exposure.
• Giving zidovudine is associated with an 80 per cent reduction in the risk of HIV
infection.
• Triple therapy in the form of zidovudine, lamivudine and the protease inhibitor
indinavir is currently given for 6 months and may modify the clinical course of
the disease.
Should all patients before surgery undergo routine HIV testing?

In the authors’ opinion the answer is no.
Reasons
• All patients require formal consent for an HIV test. This slows down the process
of surgery. Some patients may not agree to the test.
• Added anxiety for the patient.
• The implications of a positive result would require appropriate counselling to
both the patient and the rest of family.
222
• Implications of a false-positive (distress to patient) or a false-negative result

(unduly reassuring to patient).
• Expense of testing.
• Time to conduct test.
• Delay of treatment.
HIV AND THE ACUTE ABDOMEN

• Bacterial enteritis: atypical mycobacterium, e.g. Mycobacterium avium-
intracellulare
• Viral enteritis: cytomegalovirus (CMV) infection of the colon causing toxic
megacolon
• Pancreatitis: related to CMV infection
• GI tract (GIT) haemorrhage: complication of Kaposi’s sarcoma
• GIT affected by lymphoma: classically non-Hodgkin’s lymphoma (NHL).
223
58 Hyperparathyroidism

How do you classify hyperparathyroidism?
What are the clinical manifestations of primary hyperparathyroidism?
What is the primary defect in primary hyperparathyroidism?
What is the effect on the circulating calcium concentration in primary/
secondary/tertiary hyperparathyroidism?
Related topics
Topic Chapter Page
Calcium homoeostasis 88 362
CHARACTERISTICS
• Prevalence of 1:1000
• Most common in the fifth and sixth decades of life
• Females : males ! 3:1
• Second most common cause of hypercalcaemia after malignancy
• Often an incidental finding.
CLASSIFICATION
Primary
• Single adenoma: 85 per cent
• microscopically: composed predominantly of chief cells arrayed in uniform
sheets, trabeculae or follicles
• Multiple adenomas: 5 per cent
• Diffuse hyperplasia of all four glands: 10 per cent
• microscopically: chief cell hyperplasia
• Parathyroid carcinoma: # 1 per cent
• difficult to distinguish from adenomas both grossly and microscopically.
Usually involves one gland and consists of grey–white irregular masses. Can
exceed 10 g in weight
• diagnosis of malignancy based on the presence of local invasion, metastases
or both.
224
APPLIED SURGICAL PATHOLOGY hyperparathyroidism
Sporadic: 95 per cent cases.

Inherited syndrome: multiple endocrine neoplasia (MEN) types I and IIa.
Secondary
Parathyroid glands’ response to hypocalcaemia from an underlying cause – usually
chronic renal failure. Hypocalcaemia is a result of the following.
In the kidneys
• Decreased metabolism of 1,25-dihydroxy-vitamin D
• Decreased renal resorption of calcium.
In the diet
• Decreased vitamin D ingestion.
Physiological
• Decreased exposure to sunlight, and therefore reduced production of
cholecalciferol in the skin.
• Vitamin D normally inhibits parathyroid hormone (PTH) production, so a
decrease in vitamin D causes secondary hyperparathyroidism.
Pregnancy
• Increased demands of calcium can lead to hypocalcaemia.
All glands are enlarged.
Tertiary
Chronic stimulation of all the parathyroid glands by hypocalcaemia in secondary
hyperparathyroidism eventually renders them autonomous, resulting in hypercal-
caemia. Such hypercalcaemia may manifest for the first time in a patient who has
received a renal transplant, and then becomes able to metabolize vitamin D nor-
mally. Occasionally an autonomous adenoma may develop.
DIAGNOSIS
Dependent on the finding of persistent hypercalcaemia in the presence of an inappro-
priately raised level of serum PTH.
CLINICAL MANIFESTATIONS OF PRIMARY HYPERPARATHYROIDISM

Symptoms and signs of hyperparathyroidism reflect the combined effects of increased
PTH secretion and subsequent hypercalcaemia. Multiple systems are involved.
225
APPLIED SURGICAL PATHOLOGY hyperparathyroidism
Key learning points

Remember:
‘Painful bones, renal stones, abdominal groans and psychic moans’
Bone disease: bone pain, secondary to bone fractures weakened by
osteoporosis
Renal disease: nephrocalcinosis and nephrolithiasis (renal stones) with
attendant pain and obstructive uropathy
Gastrointestinal disturbances: abdominal pain, constipation, nausea,
anorexia, peptic ulceration, acute pancreatitis and gallstones
CNS alterations: depression, lethargy, and eventually seizures
Neuromuscular abnormalities: weakness and fatigue
Cardiac manifestations: aortic and mitral valve calcifications
Biochemical abnormalities in hyperparathyroidism

[Ca2$]serum [PO43%]serum [PTH]serum
Primary hyperparathyroidism ↑ ↓ ↑ or →
Secondary hyperparathyroidism ↓ or → ↑ or → ↑
Tertiary hyperparathyroidism ↑ ↓ ↑
226
59 Hyperplasia, hypertrophy and atrophy

What do you understand by the terms ‘hyperplasia’ and ‘hypertrophy’?
Give examples.
Are they mutually exclusive?
How are hyperplasia and hypertrophy classified?
What is the definition of atrophy? Give examples.
What do you understand by the terms ‘aplasia’, ‘atresia’ and ‘hypoplasia’?
What are the differences between necrosis and apoptosis?
How is necrosis classified? Give examples.
Related topics
Topic Chapter Page
Cell cycle 52 194
DEFINITIONS
Hypertrophy
This is an increase in the size of a tissue or organ because of an increase in the size
of its cells.
Hyperplasia
This is an increase in the size of a tissue or organ because of an increase in the num-
ber of its cells. It can occur only in cells that are capable of DNA synthesis. Hence
nerve, cardiac and skeletal muscle cells undergo almost only pure hypertrophy
when stimulated by hormones or increased functional demand.
Autonomous hyperplasia
This is the increase in the number of cells in an organ or tissue but in the absence
of a demonstrable stimulus, e.g. in psoriasis and Paget’s disease of the bone.
Atrophy
This is a decrease in the size of the organ or tissue, as a result of a reduction in
either the size or the number of cells or both. The cells have diminished function
but are not dead.
227
APPLIED SURGICAL PATHOLOGY hyperplasia, hypertrophy and atrophy
Cells exhibit autophagy with the reduction of cell organelles and marked increase
in the number of autophagic vacuoles.
Components that resist digestion are converted to lipofuscin granules. This makes
the organ brown (‘brown atrophy’).
Examples
Hyperplasia Hypertrophy Atrophy

Physiological Hormonal: Skeletal and cardiac Thyroglossal duct
Breast in muscle to exercise Umbilical vessels
puberty/pregnancy Uterus – pregnancy Thymus – in early
Uterus – pregnancy adulthood
Thyroid in Endometrium and
puberty/pregnancy breast – old age
Bone marrow at altitude
Pituitary in pregnancy
Compensatory:
Liver after
hemi-hepatectomy
Pathological Over-stimulation Over-stimulation Loss of innervation
Thyroid – Graves’ Thyroid – Graves’ Ischaemia
disease disease
Prostate – benign Heart muscle in Lack of nutrition
prostatic hyperplasia aortic stenosis and (adipose)
hypertrophic
cardiomyopathy
Adrenals – Cushing’s Smooth muscle in Disuse – atrophy of
disease hypertension limb
Endometrium – Congenital Loss of hormone
excess oestrogen muscular stimulation – adrenal
dystrophies atrophy with reduced
ACTH secretion, e.g.
in hypophysectomy
Key learning points

Hyperplasia and hypertrophy are NOT mutually exclusive. They can both
occur in:
• Graves’ disease
• Adrenal hyperplasia
• Benign prostatic hyperplasia (BPH)
228
AGENESIS
This is the complete failure of an organ or tissue to develop in any way during fetal
development, e.g. failure of development of a pharyngeal pouch can result in the
thymus or parathyroid glands not developing.
APLASIA AND HYPOPLASIA

Aplasia
There is recognizable tissue that has failed to develop, e.g. MacLeod’s syndrome.
This is aplasia of a lobe of a lung, or part of a lobe of a child’s lung, with consequent
emphysema of the contralateral lung as a compensatory mechanism.
Hypoplasia
Failure of an organ or tissue to attain its proper size and state of function, although
there is an attempt at this. This follows the permanent loss of precursor cells in pro-
liferative tissues.
In hypoplasia the development has proceeded further but has not reached normal
maturity, i.e. a less severe form of aplasia, e.g. hypoplasia of the breast or amazia.
This is the absence of a breast with the nipple present. Ninety per cent have absent
or hypoplastic pectoral muscles.
Atresia is a form of aplasia but is the absence of an opening, usually of a hollow vis-
ceral organ such as the trachea, bile duct, oesophagus or intestine.
CELL DEATH
Necrosis is the sum of the morphological changes that follow abnormal death of
cells or tissues in a living organism. Two processes cause the basic morphological
changes of necrosis:
1. Denaturation of proteins
2. Enzymatic digestion of organelles.
Classification of necrosis
• Coagulative (structured): most tissues, e.g. heart, spleen, kidney and liver. Tissue
architecture maintained – protein denaturation " digestion.
• Caseous (unstructured): tissue architecture is lost, e.g. TB. Gross appearance
is of soft, cheesy, friable material. Microscopic appearance is amorphous
debris.
• Colliquative/liquefactive: CNS and localized bacterial infections (abscesses).
229
• Gangrene:
• dry: mummification of tissue without infection
• wet: necrosis where there is putrefaction caused by anaerobic bacteria.
• Fibrinoid.
• Fat:
• direct trauma: fat necrosis of the breast
• enzyme digestion: in pancreatitis.
Apoptosis
This is an energy-dependent process for deletion of unwanted individual cells –
‘programmed cell death’ – to balance mitosis in regulating the size and function of
the tissue/organ or to remove unwanted or defective cells with abnormal DNA.
Apoptosis may be:
• Physiological:
• thymus degeneration
• loss of tissue between digits during limb development
• hormone-dependent involution of tissues, e.g. endometrium and prostate in
the adult
• Pathological:
• tumours, e.g. Burkitt’s lymphoma
• graft rejection: damage to cells from viruses, irradiation and T lymphocytes.
230

What are the differences between necrosis and apoptosis?
Necrosis Apoptosis
Energy Independent Dependent
Inflammation Yes No
Physiological/ Always pathological Can be both
pathological
Cell membrane Fragmentation Integrity maintained
Involves Usually whole tissue Single cells
Morphological Eosinophilic, glassy Cell shrinkage
features and vacuolated cell
Nuclear changes: Chromatin condensation
and fragmentation
Pyknosis (small dense Cellular blebbing
nucleus)
Karyolysis (faint, dissolved Apoptotic bodies
nucleus)
Karyorrhexis Phagocytosis of
(nucleus broken apoptotic bodies by
into many clumps) healthy adjacent cells or
macrophages
Mitochondria swollen
Rupture of lysosomes
leading to autolysis
Dystrophic calcification
Form of cell Severity of injury Specificity of stimulus
death is
expressed by
231
60 Malignant melanoma

What is melanin? Describe its role?
What is the definition of a melanoma?
What are the predisposing factors in the development of malignant
melanoma?
What are the different subtypes?
Can you describe any systems that aid in the diagnosis of a suspicious
skin lesion?
What are the stages of tumour progression in malignant
melanoma?
What are surrounding lesions?
What are the factors assessed on an excision biopsy?
What are the systems used to grade this condition? Which gives the
better prognosis and why?
What are Clarke’s levels and the Breslow thickness?
What are the other indicators of prognosis?
What preventive aspects can be encouraged?
What are the treatment options available?
What is the role of adjuvant chemotherapy in the treatment of
malignant melanoma?
Related topics
Topic Chapter Page
Cell cycle 52 194
Melanin is a water-insoluble polymer. It is synthesized from tyrosine catalysed by

tyrosinase. It is found in melanosomes in melanocytes.
Melanin has two roles:
• Skin pigmentation
• Absorption of ultraviolet light to prevent skin damage.
232
APPLIED SURGICAL PATHOLOGY malignant melanoma
DEFINITION
Melanoma is a malignant neoplasm of epithelial melanocytes primarily arising in
the skin.
Other sites include the nasal cavities, retina and gastrointestinal mucosa.
PREDISPOSING FACTORS
Likely to be multi-factorial including:
• Excessive sun exposure: classically intermittent high-energy exposure compared
with continuous low-energy exposure (for basal and squamous cell carcinoma)
• Fair complexion $ prominent freckling tendency
• Presence of a changing mole on the skin
• Increased number of commonly acquired and dysplastic moles
• Family history of melanoma (2–10 per cent) and dysplastic naevi
• Albinism (lack of tyrosinase) and xeroderma pigmentosa.
More than 50 per cent of cases are believed to arise anew without a pre-existing
pigmented lesion.

What are the different subtypes of malignant melanoma?
• Superficial spreading melanoma (SSM)
• Lentigo maligna melanoma (LMM)
• Nodular melanoma (NM)
• Acral lentiginous melanoma – more common in dark-skinned individuals
• Amelanocytic melanoma
TUMOUR PROGRESSION
Five stages have been suggested:
1. Benign melanocytic naevi
2. Melanocytic naevi with architectural and cytological atypia (dysplastic naevi)
3. Primary malignant melanoma, radial growth phase
4. Primary malignant melanoma, vertical growth phase
5. Metastatic malignant melanoma.
Surrounding lesions are satellite nodules or in-transit metastatic deposits.
233

What systems do you know of that can aid in the diagnosis of a suspicious
skin lesion?
MacKie’s seven-point checklist
Major (carries 2 points each):
(a) Change in size
(b) Irregularity of pigmentation
(c) Irregularity of outline
(d) Diameter " 6 mm
Minor (carries 1 point each):
(e) Inflammation
(f) Oozing or bleeding
(g) Itch or altered sensation
Needs further evaluation in the presence of one major or if scores reach 3.
American ABCDE system
A – Asymmetry (opposite segments of the lesion are different)
B – Border (irregular representing coastline with bays and promontories,
elevation)
C – Colour variation
D – Diameter " 6 mm
E – Examination for other lesions
INFORMATION GAINED FROM AN EXCISIONAL BIOPSY

An excisional biopsy with adequate margins allows:
• Assessment of tumour depth (Breslow depth)
• Anatomical level of invasion (Clark’s level)
• Ulceration
• Presence of mitoses
• Lymphatic and vascular involvement
• Host response (tumour-infiltrating lymphocytes)
• Regression
• Immunohistochemical staining for lineage (S-100, homatropine
methylbromide 45) or proliferation markers (proliferating cell nuclear
antigen, Ki67).
234

What are Clarke’s levels and the Breslow thickness?
Clarke’s classification (level of invasion)
Level I: lesions involving only the epidermis (in situ melanoma); not
an invasive lesion
Level II: invasion of the papillary dermis, but does not reach the
papillary–reticular dermal interface
Level III: invasion fills and expands the papillary dermis, but does not
penetrate the reticular dermis
Level IV: invasion into the reticular dermis but not into the subcutaneous
tissue
Level V: invasion through the reticular dermis into the subcutaneous
tissue
The Breslow (depth) thickness of the lesion
Tumour thickness, as defined by the Breslow depth, is the most important
histological determinant of prognosis and is measured vertically in milli-
metres from the top of the granular layer (or base of superficial
ulceration) to the deepest point of tumour involvement. Increased
tumour thickness confers a higher metastatic potential and a poorer
prognosis.
5-year survival rate (%)

)0.75 mm 90
0.76–1.5 mm 80
1.5–4 mm 65
+4 mm 35
Breslow gives the better indication of prognosis.
In Clarke’s levels, the thicknesses of the papillary and reticular dermis vary
around the body: both are thin on the face but thick on the back.
OTHER PROGNOSTIC INDICATORS

• Male gender
• Increasing age
• Ulceration
• Site: in order of poor prognosis: lower limb, upper limb, trunk, head
and neck.
235
PREVENTION
The preventive aspects are:
• Adequate clothing
• UV-absorbent screens: UV radiation especially in the wavelength range
320–280 nm is the most carcinogenic
• Avoiding sunbathing and tanning salons: UV rays from tanning beds and
sunlamps are just as dangerous
• Avoid sun exposure, particularly for those patients at risk (albinism, xeroderma
pigmentosa)
• Local or systemic carotenoids (carotene, retinol, retinoids) prevent malignant
transformations; systemic retinoids are more effective
• Public education: regular skin check-ups and follow-ups are vital for early
detection.
PRINCIPLES OF SURGICAL MANAGEMENT

• Excision margin based on histological confirmation of tumour-free
margins:
• for melanoma in situ: 0.5 cm margin
• melanoma with Breslow thickness # 2 mm: 1 cm margin
• melanoma with Breslow thickness + 2.0 mm: 2 cm margin.
• Melanomas near a vital structure may require a reduced margin.
• Aggressive histological features may warrant a wider margin.
• Sites such as the fingers, toes, sole of the foot and ear need separate surgical
consideration.
• Elective lymph node dissection (ELND) is defined as the removal of regional
lymph nodes draining the site of the primary melanoma in the absence of any
clinical evidence of nodal metastases. This is a controversial point. Some studies
have shown increased prognosis but other studies have shown no statistical
difference.
• Sentinel lymph node biopsy (SLNB): this is based on the premise that the first
node draining a lymphatic basin (sentinel lymph node) would be expected to
predict the absence or presence of melanoma in that area. One per cent
isosulfan blue (Lymphazurin) dye is injected around the cutaneous lesion to
allow intraoperative localization of this sentinel lymph node. Alternatively, a
radioactive tracer, technetium-99, can also be injected at the lesion site. A
gamma probe is used to pinpoint the radiolabelled lymph node, which is then
removed for histopathological review. If no melanoma cells are found, no
further surgery is done. However, if the node does have involvement, the
remainder of the nodes in this area are removed.
236
• Determination of the status of the sentinel lymph node is relevant because:

• it has been shown to be an important independent prognostic factor, with a
positive result predictive of high risk of treatment failure
• it is a relatively low-risk procedure that can help identify high-risk patients
who might benefit from additional therapy such as selective complete
lymphadenectomy or adjuvant interferon-$-2b
• it provides a psychological benefit for the patient whose sentinel lymph node
biopsy does not reveal metastases.
ADJUVANT THERAPY: INTERFERON

• May improve the survival of patients with melanoma " 4 mm thick
• Diminishes the occurrence of metastases
• Prolongs the disease-free survival in patients with melanoma " 1.5 mm.
CHEMOTHERAPY
• Advanced stage III (unresectable regional metastases) or stage IV (distant
metastases).
• Dacarbazine remains the most active chemotherapeutic agent for the treatment
of advanced melanoma. The response rate is in the range of 10–20 per cent, and
patients with metastases in the skin, subcutaneous tissues or lymph nodes
respond most frequently.
• Other combination chemotherapy and biochemotherapy regimens could
achieve higher response rates, but do not appear to lead to durable remission.
BIOLOGICAL THERAPY
Therapy directed towards modulating or inducing the immune system against the
melanoma:
• Interleukin-2 (IL-2) as a single agent has been utilized in metastatic melanoma.

In one study, there was a complete response in 7 per cent of patients, which was
durable, with patients remaining disease free for up to 8 years after initiating
therapy.
• Another study also showed positive results treating patients with their own
tumour-infiltrating lymphocytes and IL-2.
• Monoclonal antibody therapies are still experimental and may be of potential
use in melanoma.
• Melanoma vaccines have been developed to stimulate a specific response
against melanoma-associated antigens. Vaccines are currently undergoing
clinical trials.
237
PERFUSION CHEMOTHERAPY
Isolated limb perfusion (ILP)
This involves isolating a limb from the systemic circulation with a tourniquet, using
arterial and venous cannulation, and infusing a chemotherapeutic agent by means
of a pump oxygenator, and then removing the medication from the limb. It has
been developed into the most effective method of treatment for local recurrent or
in-transit metastases of an extremity. Medications that are used for infusion include
melphalan, cisplatin and TNF-*.
Radiation
Radiotherapy is indicated in certain patients with stage IV disease, for the purpose
of palliation. Specific indications include brain metastases, pain associated with
bone metastases, and skin and subcutaneous metastases that are superficially
located.
238
61 Portal hypertension

What is portal hypertension?
What causes portal hypertension?
What is the underlying pathophysiology of this condition?
What are the common complications of portal venous hypertension?
What are the management options?
What is TIPPS?
How would you manage an acute oesophageal variceal bleed?
Related topics
Topic Chapter Page
Ascites 48 172
Starling’s law of the heart and 102 403
cardiovascular equations

What is portal hypertension?
Portal hypertension is defined as a portal venous pressure exceeding
10 mmHg.
PATHOPHYSIOLOGY
Increase in portal pressure is as a result of increased portal blood flow or increased
intrahepatic vascular resistance of cirrhosis.
Increased portal blood flow

Patients with liver cirrhosis are found to have systemic and splanchnic vasodilata-
tion as a result of a decrease in vascular tone. This is accompanied by hyperkinetic
blood flow in the splanchnic and systemic circulation.
239
APPLIED SURGICAL PATHOLOGY portal hypertension
Patients have warm, well-perfused extremities, bounding pulses and rapid heart
rate. The increase in blood flow through the splanchnic organs draining into the
portal venous system is a major contributor for the maintenance and aggravation of
portal hypertension.
Recent evidence has implicated circulating vasodilators, e.g. nitric oxide (NO). The
recognition of vasodilatation and hyperdynamic circulation has led to the ‘forward
flow theory’, which proposes that increased portal venous inflow plays a central role
in the pathogenesis of portal hypertension; this is independent of the increased
resistance in the portal venous and collateral circulation (‘backward flow theory’).
Increased intrahepatic vascular resistance of cirrhosis

Previously thought to be the result of fibrosis, scarring and regenerative nodule for-
mation. However, there is increasing evidence to suggest that this is more of a dynamic
process, whereby the intrahepatic vascular tone and resistance are modulated by
sinusoidal endothelial cells. Hepatic stellate cells located in the space of Disse are
contractile structures that have also been implicated in modifying intrahepatic vas-
cular resistance. Along with other extracellular matrix-producing cells, such as fibro-
blasts and myofibroblasts, present in the portal tract, they are thought to exert their
contractile effects under the influence of mediators such as NO and endothelin to
increase intrahepatic resistance.
Combination of both resistance to portal blood flow and increased portal blood
flow are now thought to play a central role in portal hypertension.
PRINCIPAL CAUSES
Pre-hepatic
• Portal vein thrombosis
• Portal vein compression by tumour.
Intrahepatic
• Cirrhosis
• Idiopathic (non-cirrhotic)
• Acute alcoholic hepatitis
• Congenital hepatic fibrosis.
Post-hepatic
• Budd–Chiari syndrome (hepatic vein thrombosis)
• Veno-occlusive disease
• Right heart failure
• Constrictive pericarditis.
240
COMPLICATIONS
• Haemorrhage from oesophageal varices (most common and dangerous)
• Hepatic encephalopathy
• Ascites
• Hypersplenism
• Rectal varices
• Hepatorenal syndrome (HRS)
• Spontaneous bacterial peritonitis
• Portal hypertensive gastropathy.
MANAGEMENT
Elective
Liver transplantation: established treatment and only cure for chronic progressive
liver disease and for complications of portal hypertension. Liver transplantation
should be performed before the onset of serious complications, e.g. encephalopathy
and hepatorenal syndrome.
Total portosystemic shunts

Non-selective shunts divert all portal blood flow into the systemic circulation and
decompress the entire portal system, producing a rapid decompression of varices
and relief of portal hypertension.
End-to-side shunt: the portal vein is ligated at the hepatic hilum and transected, and
the proximal end is anastomosed to the side of the inferior vena cava.
Main complication: 40 per cent incidence of encephalopathy and exacerbation of
underlying liver failure.
Selective shunts: designed for selective variceal decompression without portal diver-
sion, e.g. distal splenorenal (Warren) shunt involves anastomosing the splenic end of
the divided splenic vein to the left renal vein end to side. The spleen is left in place
and the left gastric vein, umbilical vein and other venous tributaries of the splenic
vein are all divided. This effectively excludes the gastrosplenic portal circulation
from the rest of the portal circulation. There is reduced hepatic encephalopathy
incidence with this method.
The Sugiura procedure

Reserved for patients with recalcitrant haemorrhage or patients who cannot undergo
a shunt operation because of portal vein thrombosis. Procedure involves:
• Splenectomy
• Devascularization of the stomach and lower oesophagus
241
• Oesophageal transection with a circular stapling device to disrupt flow to the

gastro-oesophageal varices.
This is a highly effective method in controlling active bleeding.
Transjugular intrahepatic portosystemic shunting (TIPSS)
This is an alternative to surgical shunting. It shunts portal blood across the liver into
the vena cava.
A guidewire introduced through the jugular vein is threaded through the liver and
forced into an intrahepatic branch of the portal vein. This track is balloon dilated and
held open with a metallic stent, creating a shunt that decompresses the portal system.
Use with caution because it can worsen an encephalopathy. Also it is only a temporary
measure – shunts usually stenose or thrombose within 1 year (50 per cent).

What is the management of acute variceal bleeding?
Effective resuscitation
Patients with massive haemorrhage should be considered for admission to
intensive care.
Early consideration for transfer to a specialist liver unit.
Two large-bore cannulae inserted into antecubital veins.
Obtain blood for grouping, cross-matching, FBC, clotting profile, elec-
trolytes, urea, creatinine, liver biochemistry and blood cultures.
Many patients have some degree of coagulopathy and thrombocytopenia.
These should be corrected with fresh frozen plasma, vitamin K injection
and platelet transfusion if platelet count # 50 000/mm3.
Upper gastrointestinal endoscopy is essential to establish an accurate diag-
nosis because 50 per cent patients with documented portal hypertension
and varices will have a non-variceal source of bleeding. Performed as soon
as resuscitation is adequate.
Endoscopic sclerotherapy or band ligation for control of active bleeding.
This arrests bleeding in 80 per cent of cases as well as reducing early
re-bleeding.
Pharmacological therapy: used in combination and while waiting for an
upper GI endoscopy. Works by causing splanchnic arterial constriction and
subsequent decrease in pressure and flow in the varices.
242
Vasopressin (0.4–0.8 U/min IV): efficacious in controlling bleeding and

reducing mortality.
Somatostatin (250 ,g IV bolus; then 250 ,g/h IV) and its synthetic ana-
logue octreotide decrease portal blood flow by selective splanchnic vaso-
constriction and are free from systemic side effects. Although effective in
controlling bleeding it has no effect on mortality.
Mechanical balloon tamponade with a Sengstaken–Blakemore tube. It
consists of a nasogastric tube with two large balloons at the distal end.
Two balloons – one in the oesophagus and one in the cardia – are blown
up to compress the varices. The tube position must be confirmed by radio-
graph before inflation of the balloons. The distal gastric balloon is inflated
with 250 mL of air and then pulled up tight against the gastro-oesophageal
junction. If the gastric balloon alone does not control the bleeding the
proximal oesophageal balloon is inflated to a pressure that equals portal
venous pressure (25 mmHg). The tube is deflated at 24 h and if bleeding
has stopped it is removed 48 h after insertion. If bleeding is not controlled
the tube is left inflated for a further 24 h after an interval of 1 h deflation.
Complications of balloon tamponade are ischaemic necrosis of the
oesophageal mucosa, oesophageal perforation and aspiration pneumonitis.
As a result of these complications, balloon tamponade should be used only
as a temporary measure.
TIPPS has been shown to be effective in controlling variceal bleeding in
more than 90 per cent of patients who continue to bleed after endoscopic
and vasoconstrictor therapy.
243
62 Thyroid cancer

What are the risk factors for thyroid cancer?
How would you investigate a thyroid mass in clinic?
What are the principles of management for thyroid cancer?
How can thyroid tumours be classified?
How is thyroid cancer staged?
How does thyroid cancer spread?
What percentage of thyroid tumours is secretory?
What are the disadvantages of fine-needle aspiration cytology and in
which particular type of thyroid tumour is this a problem?
If you have performed a hemi-thyroidectomy and the histology comes
back as papillary carcinoma, what extra management would you consider
for the patient?
What are multiple endocrine neoplasia (MEN) syndromes and which
specifically are associated with what type of thyroid cancer?
Related topics
Topic Chapter Page
Cell cycle 52 194
CLINICAL FEATURES
Systemic
• Patients are usually euthyroid – unusual to present as thyrotoxicosis. ‘Cold’
nodules (no isotope uptake and therefore not secretory) much more likely to
represent carcinoma than ‘hot’ nodules.
• May present like other goitres in the neck, but often growing more rapidly.
• Dysphagia may be present but uncommon (suggestive of an anaplastic tumour).
• Odynophagia is relatively common (pain on swallowing).
• Hoarse voice is suggestive of local invasion of the recurrent laryngeal nerve (see
‘Thyroid gland and parathyroid glands’, Chapter 18, page 49).
244
APPLIED SURGICAL PATHOLOGY thyroid cancer

What are the risk factors for thyroid cancer?
Thyroid cancer is the most common malignant endocrine tumour, but
represents only about 1 per cent of all malignancies.
• Every year there are about 900 new cases and 250 deaths
• Annual incidence is approximately 2 per 100 000 women and 1 per
100 000 men
• Affects those aged 25–65 years
Risk factors
• Radiation administered in infancy and childhood for benign conditions
of the head and neck (e.g. enlarged thymus, acne, or tonsillar or adenoidal
enlargement)
• Radiation exposure as a consequence of nuclear fallout
• History of goitre
• Family history of thyroid disease (particularly MEN syndromes and
papillary carcinomas)
• Female gender
• Asian race
• Deep cervical lymphadenopathy.

• Most commonly presents as a lump in the neck.
• Diarrhoea in medullary carcinoma.
CLASSIFICATION OF THYROID TUMOURS

If asked to classify thyroid tumours, always remember to start with benign and
don’t forget to include secondaries.
In terms of prognosis, a simpler classification of well-differentiated and poorly dif-
ferentiated can be used, although you should know the various types below.
Benign
Adenoma (follicular)
• Relatively rare
• Most functioning nodules are adenomas (Plummer’s syndrome)
• Most benign nodules are part of a multinodular goitre and are not true benign
adenomas.
245
Malignant
Primary (five main types)
Papillary carcinoma
• Most common type of thyroid malignancy
• 60 per cent of all thyroid cancers
• Most common in young adults and children
• Slow growing and metastasizes late
• Good prognosis
• Can be multifocal
• Histology: large epithelial cell nuclei – ‘orphan Annie’.
Follicular adenocarcinoma
• Most common in young and middle-aged adults
• Commonly associated with areas where endemic goitres are found
• Worse prognosis than papillary, although good prognosis if no invasion
• Haematogenous spread (lymphatic spread uncommon).
Anaplastic carcinoma
• Worst prognosis
• Occurs in elderly people
• Rapid local spread, often into trachea and oesophagus
• Early lymphatic spread
• Early haematogenous spread to lungs, bone and brain.
Medullary carcinoma
• Arises from parafollicular C cells of the thyroid and as a result may secrete
calcitonin as a tumour marker
• Can occur at any age
• Equal sex distribution
• Associated with other tumours (multiple endocrine neoplasia syndromes
MEN-IIa and -IIb – see later)
• Histology: amyloid found between tumour cells.
Lymphoma (very rare)

• Non-Hodgkin’s
• Associated with Hashimoto’s thyroiditis.
Secondary
• Direct invasion from adjacent anatomical structures (e.g. oesophagus,
larynx)
• Very rare site for blood-borne deposits.
246

How would you investigate a thyroid mass in clinic?
Similar to breast lumps, thyroid lumps arguably require a triple assessment
of clinical history and examination, radiological assessment and cytological
assessment.
Clinical history and examination

• Size and synchronicity of the mass
• Thyroid status of the patient (bloods should include calcitonin to rule
out medullary carcinoma as well as TSH (thyroid-stimulating hormone)
and thyroid autoantibody status)
• Evidence of systemic disease or local tumour infiltration
(see above)
• Assessment of any other similar masses (?multinodular goitre)
• Tethered to underlying structures?
• Moves up with swallowing?
• Associated lymphadenopathy (cervical/subclavian)?
• Vocal fold assessment (essential before surgery)
Radiological assessment
Ultrasound examination reveals whether the mass is solitary and guides
the FNAC. If not, then the diagnosis is likely to be multinodular goitre and
not carcinoma, particularly if the patient is not euthyroid.
Cytological assessment
FNAC is often ultrasound guided and gives an instant cytological diagno-
sis. It does not reveal histological architecture, however, and in the case of
follicular carcinoma is non-diagnostic because follicular cells may indicate
follicular adenoma (benign).
Other investigations
• Nuclear medicine examinations can look for a ‘hot’ nodule,
although they are of questionable use above the other clinical tests
available
• MRI and CT: when limits of the goitre cannot be determined, or for fixed
tumours or patients with haemoptysis. Note that iodinated material used
for CT contrast will reduce subsequent 131I uptake by thyroid tissue and
should be avoided if possible
• Chest radiograph: useful in assessing secondary disease
• Flow–volume loop: if upper airway obstruction is suspected
247
STAGING OF THYROID CANCER

TNM definitions for staging
Primary tumour (T)
All categories may be subdivided into (1) solitary tumour or (2) multifocal tumour
(the largest determines the classification).
TX: primary tumour cannot be assessed
T0: no evidence of primary tumour
T1: tumour ! 2 cm and limited to the thyroid
T2: tumour " 2 cm but ! 4 cm and limited to the thyroid
T3: tumour " 4 cm and limited to the thyroid, or any tumour with minimal extra-
thyroid extension (e.g. extension to strap muscles)
T4a: tumour of any size extending beyond the thyroid capsule to invade subcutaneous
soft tissues, larynx, trachea, oesophagus or recurrent laryngeal nerve
T4b: tumour invades prevertebral fascia or encases carotid artery or mediastinal
vessels
All anaplastic carcinomas are considered T4 tumours (and therefore have a worse
prognosis). The division of T4 in this case is whether or not the tumour is
resectable.
T4a: intrathyroidal anaplastic carcinoma – surgically resectable
T4b: extrathyroidal anaplastic carcinoma – surgically unresectable
Regional lymph nodes (N)

Regional lymph nodes are the central compartment, lateral cervical and upper
mediastinal lymph nodes.
NX: regional lymph nodes cannot be assessed
N0: no regional lymph node involvement
N1: regional lymph node involvement
N1a: metastasis to level VI (pretracheal, paratracheal and prelaryngeal/Delphian
lymph nodes)
N1b: metastasis to unilateral or bilateral cervical or superior mediastinal
lymph nodes
Distant metastases (M)

MX: distant metastasis cannot be assessed
M0: no distant metastasis
M1: distant metastasis
Although TNM staging is the recommended standard, there are different staging
systems based on groups with differing prognoses.
248
MANAGEMENT
• Well-differentiated tumours can be treated by a combination of:
• surgery (usually total or near-total thyroidectomy if tumour " 1 cm)
• thyroid suppression with thyroxine (T4)
• 131I (radio-iodine ablation)
• All new patients should be seen by a member of the multidisciplinary team
(MDT), and the treatment plan discussed
• Fine-needle aspiration cytology (FNAC) should be used in the planning of
surgery (see above)
• Most patients with tumours ! 1 cm in diameter should undergo near total or
total thyroidectomy with central node dissection
• Serum thyroglobulin (Tg) should be checked in all postoperative patients with
differentiated thyroid cancer
• Patients will normally start on triiodothyronine (T3) 20 #g t.d.s. (normal adult
dosage) after the operation (this should be stopped 2 weeks before radioiodine
therapy)
• The majority of patients with a tumour size ! 1 cm in diameter, should have 131I
ablation therapy
• Always exclude pregnancy and breast-feeding before administering radioactive
iodine
• Patients should be started on T4 3 days after 131I in a dose sufficient to suppress
TSH completely
• Reassessment with a post-ablation diagnostic scan (after stopping T4 for
4 weeks) is indicated 4–6 months after 131I ablation, although in low-risk
patients measurement of Tg alone may be adequate. If significant uptake of
the tracer is detectable, a further 131I therapy dose should be given and a
post-treatment scan performed. Following this the patient should restart T4
• If there is suspicion of residual disease, further scans should be carried out,
usually 6 months later.
• Recombinant human TSH (rhTSH) can be used instead of stopping T3 or T4 in
appropriate cases as decided by the MDT
• external beam radiotherapy is only occasionally used, for patients with T4
tumours (TNM staging – see above) or distant metastases.

If you have performed a hemi-thyroidectomy and the histology comes back as
papillary carcinoma what extra management would you consider for the
patient?
As papillary carcinoma can be multifocal, and if the patient was young
with a life-time follow-up, surgery to complete the thyroidectomy may be
considered in discussion with the patient.
249

What are MEN syndromes and which specifically is associated with
what type of thyroid cancer?
Multiple endocrine neoplasia syndromes
These are a group of inherited disorders (autosomal dominant) where
affected individuals develop tumours in two or more endocrine glands at
the same time, making the affected glands overactive. With several
endocrine systems being overactive, a diverse range of symptoms is seen.
They are broadly divided into three.
MEN type I (Wermer’s syndrome)
This is characterized by the coexistence of:
• Parathyroid tumours – 80–95 per cent of cases
• Pancreatic islet cell tumours (including gastrinomas, insulinomas,
glucagonomas, VIPomas and PPomas) – 80 per cent of cases
(VIP ! vasoactive intestinal polypeptide; PP ! pancreatic polypeptide)
• Anterior pituitary tumours (prolactin-, growth hormone- and ACTH-
secreting tumours and non-functioning tumours) – 50–71 per cent of
cases
More rarely tumours of the adrenal cortex, carcinoid tumours (special
tumours, often arising in the gut – described in their own section) and
lipomas (tumours of fat tissue) may also occur within MEN-I. It is NOT
associated with medullary carcinoma of the thyroid.
MEN type II
This is further subdivided into IIa and IIb, both of which include medullary
carcinoma of the thyroid:
• IIa (Sipple’s syndrome): the most common variant of MEN-II, with:
• medullary carcinoma of the thyroid – almost 100 per cent
• phaeochromocytoma – 50 per cent
• parathyroid tumours – 40–80 per cent
• IIb: this has no parathyroid involvement and is characterized by:
• medullary carcinoma of the thyroid – almost 100 per cent
• phaeochromocytoma
• marfanoid habitus
• mucosal neuromas
• medullated corneal nerve fibres
• megacolon
250
FOLLOW-UP
Clinical follow-up needs to be life-long because:
• The disease has a long natural history
• Late recurrences can occur, and these can be successfully treated
• Cure and prolonged survival are common, even after tumour recurrence
• Monitoring of treatment (TSH suppression, the consequences of
supraphysiological T4 replacement, treatment of hypocalcaemia)
• Life-long suppression of serum TSH level below normal (# 0.1 mU/L) is one of
the main components of treatment and requires monitoring
• Late side effects of 131I treatment should be monitored
• Surveillance for recurrence of disease is essential and is based on:
• annual clinical examination
• annual measurement of serum Tg and TSH
• diagnostic scanning when indicated (isotopic imaging and/or ultrasonography
or CT)
• Support and counselling are necessary, particularly in relation to pregnancy and
in familial medullary carcinoma and MEN syndromes.
251
63 Tumour markers

What is a tumour marker?
How are tumour markers classified?
Which tumour markers are characteristically found in testicular
tumours?
Give examples of enzymes, hormones and oncofetal antigens as tumour
markers.
What is PSA? How is it used clinically?
Can you give some examples of commonly used tumour markers in
clinical practice?
Name one example of a tumour marker that is used in the surveillance
of tumour progression.
Related topics
Topic Chapter Page

What is a tumour marker?
This is a tumour-derived or tumour-associated molecule found in the
blood or body fluids of a patient with neoplasia. It is directly related to the
presence of the neoplasm, disappears when the neoplasm is treated and
reappears when the neoplasm recurs.
FEATURES
• No tumour marker is pathognomonic
• Can aid in the diagnosis
• May be of value in determining response to a treatment
252
APPLIED SURGICAL PATHOLOGY tumour markers
• Most used as a surveillance tool to monitor for recurrence of the neoplasm

• Most are not stoichiometric – amount produced is not in direct proportion to
the tumour bulk, although there may be some evidence that carcinoembryonic
antigen (CEA) and prostate-specific antigen (PSA) are.
CLASSIFICATION
Classified in terms of biochemical structure and function:
• Hormones
• Enzymes
• Oncofetal antigens.
Hormones (examples)
Eutopic hormones
These are produced from tumours affecting endocrine organs:
• Pituitary tumour: produces ACTH, human growth hormone, prolactin
• Adrenal tumour: produces cortisol.
Ectopic hormones
These may be produced aberrantly from the tumour, which itself is not typically an
endocrine organ:
• Carcinoid tumours: produce 5-hydroxyindoleacetic acid (5-HIAA)
• Oat-cell lung tumours may produce ACTH and antidiuretic hormone (ADH)
• Neuroendocrine tumours.
Enzymes (examples)
Serine protease associated with semen. Normal function is to liquefy the ejaculate
enabling fertilization.
Prostatic acid phosphatase or PSA, produced by normal and malignant prostatic
ductal and acinar epithelial cells.
PSA is elevated in most patients with:
• Prostate carcinoma
• Benign prostatic hyperplasia
• Prostatitis
• After urinary retention
• After digital rectal examination (DRE)
• Urinary catheterization
253
• Used in combination with DRE, transrectal ultrasonography (TRUS) & biopsy

in the management of prostatic carcinoma for:
• diagnosis
• follow-up
• assessment of response to treatment.
The normal range for the serum PSA assay in men is # 4 ng/mL, although this varies
with age.
• PSA velocity: ! 0.75 ng/mL per year is associated with prostate carcinoma
• Prostatic carcinoma is associated with a lower free:total (F:T) PSA ratio.

Is PSA a good screening test for prostate carcinoma?
Yes No
Common disease $ major health problem High number of TRUS biopsies performed
Sensitive Not specific
Potential for cure if disease picked up early Poorly defined clinical outcome $ best
treatment for early disease unknown
Placental alkaline phosphatase: carcinoma of the bronchus, pancreas, colon and

germ cell neoplasms.
Oncofetal antigens (examples)

$-Fetoprotein (AFP): produced by primary liver tumours and testicular teratomas.
Also raised in non-neoplastic conditions:
• Liver cirrhosis
• Chronic hepatitis
• Pregnancy
• Neural tube defects.
CEA: normally produced by fetal gut, liver and pancreas.

It is elevated in 80 per cent of colorectal cancers. Twenty per cent of colonic neo-
plasms are non-expressors of the antigen.
This antigen is of value in estimating tumour burden in colorectal cancer and in
detecting recurrences after surgery
254
Also raised in carcinoma of the pancreas, stomach, ovaries and breast and, less con-
sistently, levels are elevated in non-neoplastic conditions, e.g. alcoholic cirrhosis,
hepatitis and ulcerative colitis
Not specific or sensitive enough to be used as a screening tool.
TESTICULAR TUMOUR MARKERS:

Teratoma: '-hCG, CEA, AFP.
Seminoma: placental alkaline phosphatase, sometimes '-hCG.
The measurement of serum levels of AFP is used to monitor the progress of testicu-
lar teratomas. A sample initially taken preoperatively, although not indicative of
tumour burden, is used as a guide with which the response to treatment may be
monitored. After orchidectomy, serum levels must be measured frequently until
they return to normal. Samples can then be taken less frequently and a rise may
indicate tumour recurrence, allowing instigation of further investigations.
OTHER TUMOUR MARKERS USED IN CLINICAL PRACTICE

• Ca 15-3: a glycoprotein occasionally elevated in breast carcinoma. Level is
related to the stage of breast cancer.
• Ca 19-9: a glycoprotein occasionally elevated in pancreatic and advanced
colorectal carcinoma.
• Thyroglobulin: elevated in some thyroid cancers.
• Calcitonin: raised in medullary thyroid carcinoma (see ‘Thyroid cancer’,
• Vanillylmandelic acid (VMA): produced by phaeochromocytomas and can be
detected in the urine.
255
5
PART
PRINCIPLES OF SURGERY
64 Abdominal incisions 259
65 Amputation 265
66 Anastomosis and anastomotic leak 270
67 Antibiotics in surgery 275
68 Bowel preparation 280
69 Clinical governance 283
70 Day surgery 287
71 Diathermy 291
72 Drains in surgery 295
73 DVT prophylaxis and coagulation in surgery 297
74 The hip joint, neck of femur and sciatic nerve 303
75 Local anaesthetics 308
76 Operating theatre design and infection control 312
77 Screening in surgery 316
78 Skin grafting and flap reconstruction 320
79 Statistics and clinical trials 326
80 Stomas 330
81 Surgical sutures and needles 334
82 Tourniquets 339
83 Wound healing, scarring and reconstruction 342
64 Abdominal incisions

What abdominal incisions are you aware of and what are their
advantages and disadvantages?
What is the ideal abdominal incision?
What are the factors to be considered while planning a surgical incision?
What are the advantages of transverse abdominal incisions?
What are the important principles regarding the closing of the abdominal
incision?
What is Jenkins’ rule?
What are the complications of abdominal incisions?
What are the differences between Lanz’s and McBurney’s incisions for
appendicectomy?
What are the different layers of the anterior abdominal wall that you go
through when performing a laparotomy?
Related topics
Topic Chapter Page
Anorectal surgery 1: anal fissure and lateral sphincterotomy 23 63
Anorectal surgery 3: injection sclerotherapy and haemorrhoidectomy 25 73
Burr holes and lumbar puncture 26 78
Circumcision 29 91
Mastectomy, axillary dissection and breast reconstruction 36 120
Perforated duodenal ulcer and exploratory laparotomy 39 135
Tracheostomy 42 148
259
PRINCIPLES OF SURGERY abdominal incisions
11 16
10
11
9 1
8 15
11
7 6 12
4 11, 18, 19 19
3 14
5 13
2 19
17
Figure 64.1
Incision Uses Notes

1. Midline Laparotomy See notes
2. Pfannenstiel’s Pelvic surgery Gynaecological surgery
3. McBurney’s Caecum/appendix Allows extension
4. Lanz’s Caecum/appendix Better cosmesis
5. Inguinal Inguinal and femoral hernia
6. Loin Upper renal tract Nephrectomy
7. Battle’s paramedian Laparotomy See notes
8. Transverse Right colon, biliary See notes
9. Kocher’s subcostal Open cholecystectomy Left side for splenectomy
10. Roof top Hepatobiliary, adrenal Good access
11. Port sites Laparoscopic cholecystectomy
12. Battle’s pararectal Colon, rectum Now abandoned as a
result of damage of
nerves on entering rectus
13. McEvedy’s (vertical) Femoral hernia Can extend to laparotomy
Femoral embolectomy Femoral vessels
14. Rutherford–Morrison Renal transplantation,
(hockey stick) difficult appendix
15. Gable (‘Mercedes Benz’) Liver transplantation,
hepatobiliary surgery
16. Thoracoabdominal Right: liver, portal vein
Left: oesophagus, stomach,
spleen, aorta
17. Groin crease Varicose veins, femoral hernia
18. Infraumbilical Umbilical and paraumbilical hernia
Laparoscopic camera port
19. Port sites Laparoscopic appendicectomy
260
PLANNING A SURGICAL INCISION

The following factors are important:
• Good access to site of operation

• Position: over lesion and away from bony prominences
• Adequate size
• Safety with consideration of underlying structures, nerves and blood vessels.
Normally made parallel to important structures
• Ease of access
• Speed of access
• Flexibility to extend the incision if needed
• Low incidence of complications such as incisional hernia
• Cosmesis: incisions should be made parallel to Langer’s lines – along natural
lines of tension – because they heal better and should be made perpendicular to
skin to avoid undermining, e.g. Pfannenstiel for pelvic surgery
• Presence of previous scars
• Nature of procedure, e.g. possible stoma
• Surgeon’s preference: should be familiar and comfortable with that incision for
that operation
• Shape of the abdomen, e.g. narrow costal angle
• Age of the patient, e.g. transverse incisions preferred in children.
TRANSVERSE INCISION
Advantages
• Better cosmesis
• Less postoperative pain
• Reduced incidence of postoperative chest infections
• Preferred incision in children to prevent scar puckering with subsequent
growth.
Disadvantages
• Division of red muscle involves more blood loss and postoperative pain
• Less secure closure than a longitudinal incision – higher incidence of incisional
hernia
• Longer to open and close
• Cannot be extended easily
• Limited access in adults to pelvic or subdiaphragmatic structures.
261
MIDLINE INCISION
Advantages
• Good access
• Easy to extend
• Quick to open and close
• Blood loss – relatively avascular.
Disadvantages
• More painful than transverse incisions because the incision is theoretically
cutting through more dermatomes
• Incision crosses Langer’s lines and therefore probable poorer cosmetic
appearance
• May cause bladder damage so essential to catheterize patient if performing a
laparotomy.
BATTLE’S PARAMEDIAN
• Muscle cutting so increased postoperative pain
• Used less widely today
• Takes longer to close
• Poor cosmetic result
• Can lead to infection in the rectus sheath
• Does not lend itself to closure by Jenkins’ rule
• Effective closure without strong sutures and low incidence of incisional hernia
rate – in the olden days used to be closed with catgut!
ABDOMINAL WOUND CLOSURE

• Mass closure is the present preferred method as opposed to layered closure,
followed in the past.
• The correct suture to be used: Prolene, nylon or PDS (polydioxanone), looped
or non-looped. Other absorbable sutures such as Vicryl or Monocryl are not
suitable for closing a laparotomy wound in an adult.
• The correct size: number 1; smaller sizes can cut through.
• The correct length: four times the length of the wound preferred (Jenkins’ rule
1976). It should definitely not be less than twice the length.
• The correct technique: large bites, taking care always to incorporate the rectus
sheath. The bites should be at least 1 cm from the edge of the sheath and 1 cm
apart.
262
• The correct tightness: the suture should be just tight enough to oppose the
margins together without gaps. It should not strangulate the tissues and render
them ischaemic.
• The correct knot technique: always perform square knots and use a surgeon’s
knot (double throw) and adequate number of knots for the suture being used.
COMPLICATIONS
Early
• Infection
• Bleeding/haematoma
• Necrosis of margins
• Wound dehiscence.
Late
• Incisional hernia
• Keloid formation or hypertrophic scar with poor cosmesis
• Suture sinus/granuloma
• Chronic pain caused by scar neuropathy.
APPENDICECTOMY SCARS
McBurney’s incision was the traditional incision for an appendicectomy. This is sited
over McBurney’s point, at right angles to the line joining the umbilicus and the
anterosuperior iliac spine.
Lanz’s incision is more cosmetic, being more transverse and along the skin crease. It
is usually shorter than McBurney’s incision.
The muscles are split and not cut in both incisions. If the muscles are cut it is called
a Rutherford–Morrison incision – rarely used today except for a heterotopic renal
transplantation or for a difficult appendicectomy.
263

What are the different layers of the anterior abdominal wall that you go
through when performing a laparotomy?
From surface inwards, the successive layers are:
Skin
Superficial fascia (comprising two layers)
• outer adipose layer
• inner fibroelastic layer (Scarpa’s fascia)
Musculoaponeurotic layer: comprises:
• rectus abdominis
• external oblique
• internal oblique
Transversalis fascia
Pre-peritoneal adipose layer
Parietal peritoneum
264
65 Amputation

What are the indications for lower limb amputation?
How would you decide the level of amputation?
How would you preoperatively assess and manage a patient undergoing
amputation?
How can you assess the blood supply before deciding on the level of
amputation?
What types of amputation are there?
What are the contraindications to performing a below-knee amputation?
What are the complications of performing a below-knee amputation?
Related topics
Topic Chapter Page
INDICATIONS
• Vascular:
• complications of peripheral vascular disease (85 per cent) – people with
diabetes (40 per cent)
• arteriovenous fistulae
• thromboangiitis obliterans
• Trauma (10 per cent):
• burns
• frostbite
• Malignant tumours (3 per cent), e.g. malignant melanoma
• Infection:
• osteomyelitis
• gas gangrene
• necrotizing fasciitis
• Congenital deformity
• Chronic pain
• ‘Useless’ limb, usually caused by neurological injury.
265
PRINCIPLES OF SURGERY amputation

What are the indications for performing an amputation?
Indications – think the three ‘D’s
Dead
• Acute ischaemia
• Unreconstructable critical ischaemia
Dangerous
• Crush injury
• Gas gangrene
• Necrotizing fasciitis
• Tumour
Damn nuisance
• Useless, insensate limb
CLASSIFICATION
Lower (97 per cent) versus upper (3 per cent) limb.
Major (most of limb removed) versus minor.
PREOPERATIVE WORK-UP AND ASSESSMENT

Multidisciplinary approach
• Anaesthetic team (patient normally has a high ASA grade with multiple
co-morbidities)
• Prosthetic specialist
• Nursing staff
• Physiotherapy
• Occupational therapy
• Psychologist.
Consent
Obtain consent to amputate more proximally than intended.
Assessment of level of amputation

This should include ability of patient to undergo successful rehabilitation:
• Energy expenditure with above-knee prosthesis ! below-knee prosthesis
• May limit patients with coexisting ischaemic heart disease (IHD)
266
• Above-knee or through-knee amputations generally better for wheelchair-bound

patients
• Below-knee stump more liable to decubitus ulceration so contraindicated in
bedbound individuals, and also those with a fixed flexion contracture ! 15°.
Level of amputation
This is influenced by:
• Viability of tissues and degree of tissue loss
• Severity and pattern of vascular disease, including consideration of previous
vascular grafts
• Previous orthopaedic prostheses
• Underlying pathology (ensure pathology available)
• Functional requirement
• Comfort
• Cosmetic appearance
• Preserve the knee joint and epiphysis in children.
Assessment of blood supply
Most surgeons rely on clinical judgement.
Unproven adjunctive tests include laser Doppler studies, transcutaneous measure-
ment of oxygenation and measurement of blood flow in the skin using isotopes.
Bony appraisal is assessed by taking plain radiographs.
Optimization
• Major amputation is high-risk surgery
• Patients are normally ASA grade III/IV
• Preoperative preparation to minimize perioperative complications would
include DVT (deep vein thrombosis) prophylaxis and antibiotic prophylaxis
• Urinary catheter to assess fluid management and allow ease of micturition while
bedbound.
267

What are the possible postoperative complications?
Remember early and late.
Early
• Stump haematoma
• Flap necrosis, infection
• Stump trauma from falls
• Wound-related pain
Late
• Neuroma formation
• Osteomyelitis
• Bony erosion
• Ulceration
• Ongoing ischaemia
• Phantom limb pain – good control with a combination of gabapentin and
amitriptyline
• Joint contractures
TYPES OF AMPUTATION
• Toe: most common; usually through proximal phalanx. Must not be performed
through the joint; exposes avascular cartilage and won’t heal.
• Ray: excision of toe through the metatarsal bone.
• Transmetatarsal: divided at mid-shaft level. Indicated for infection or gangrene
affecting several toes. Uses a TOTAL plantar flap. Provides excellent function
postoperatively.
• Midfoot: consider only in patients with correctable or absent ischaemia. Types
include Lisfranc (disarticulation between metatarsal and tarsal bones) and
Chopart (disarticulation of the talonavicular and calcaneocuboid joints). Main
disadvantage unpredictable healing rates and development of equinus deformity,
which limits ambulation.
• Ankle level (Syme and Pirogoff): rarely indicated in vascular practice today.
• Below-knee (Burgess long posterior flap and skew flap): randomized controlled
trial (RCT) comparing two – same healing, revision and successful ambulation
rates.
• Through-knee, e.g. Gritti–Stokes: useful if orthopaedic metalware in the femur
precluded above-knee amputation. Unpredictable healing of skin flaps.
• Above-knee.
268
• Hip disarticulation and hindquarter:

• malignant disease
• extensive trauma
• infection or gangrene
• non-healing high above-knee amputation.
SPECIFIC CONTRAINDICATIONS TO PERFORMING A BELOW-KNEE

AMPUTATION
• Specific indication for performing a higher amputation
• Fixed flexion deformity of knee
• Inability to leave a tibial stump of at least 7.5 cm
• Insufficient tissue for adequate healing
• Bedbound patients.
269
66 Anastomosis and anastomotic leak

What is the definition of an anastomosis?
How do bowel and vascular anastomoses differ?
What are the reasons for performing an anastomosis?
What are the principles of performing an ideal anastomosis?
What are the main risk factors for developing an anastomotic leak?
What are the signs of an anastomotic bowel leak? When do they typically
occur?
If an anastomotic bowel leak was found intraoperatively, what are the
different options available to the surgeon?
What would you do if the patient developed signs of an anastomotic leak
a few days after surgery and began to deteriorate?
What are the different anastomoses performed in a Whipple’s operation?
Related topics
Topic Chapter Page
Drains in surgery 72 295
Stomas 80 330
Surgical sutures and needles 81 234

What is the definition of an anastomosis?
Joining of two hollow organs or structures in order to re-establish a lumen
through which flow can continue.
AIMS OF AN ANASTOMOSIS
• To restore the continuity of a hollow organ, e.g. artery or bowel after removing
a diseased section of that organ
• To bypass an obstructed segment of an organ and divert flow through the
lumen distally
270
PRINCIPLES OF SURGERY anastomosis and anastomotic leak
• To restore inflow and outflow between a donor organ and the recipient body,
e.g. renal and liver transplantations.
BASIC PRINCIPLES OF ANASTOMOSIS

Any anastomosis requires:
• No tension
• A good blood supply
• Accurate apposition
• Good size approximation – avoid mismatch between the two ends
• Accurate suture technique, i.e. no holes or leaks
• Good surgical technique:
• do not perform anastomoses in ‘watershed’ areas
• perform adequate mobilization of the ends to be joined – avoids tension
• invert edges (bowel) to discourage leakage or evert edges to avoid risk of
lumen narrowing and intimal disruption (vascular)
• consider use of preoperative bowel preparation to prevent mechanical
damage to the join in bowel anastomosis
• prophylactic antibiotics – to cover appropriate organisms and minimize
infection
• consider the type of suture material: staples versus suture; absorbable versus
non-absorbable or continuous versus interrupted
• avoid strangulating the tissue on tying the knots: hand ties advisable
• single-layer versus two-layer in bowel anastomoses – ischaemia versus leak
rate. Perform technique with which you are familiar.
Bowel anastomosis
• Bowel anastomosis is performed usually using a 3/0 dissolvable monofilament
suture, e.g. PDS with an atraumatic round-bodied needle
• This should include the submucosa because this is the strongest layer
• Extramucosal inverting technique advised – discourages faecal or bile leakage
• Bowel can be joined together with either a continuous or an interrupted suture
technique
• Surgical Royal Colleges teach a single-layer, interrupted seromuscular technique
of sutures.
Vascular anastomosis
• Between arteries, veins, prosthetic material or combination of these
• Invariably performed with a non-absorbable monofilament suture, which moves
smoothly through the vessel wall, e.g. Prolene
271
• Vascular anastomoses are performed with a continuous suture technique to

ensure equal distribution of tension around the suture line
• Use small needles and suture strong enough to hold anastomosis
• Prophylactic antibiotics: to include staphylococcal cover
• Requires gentle handling: never hold between forceps!
• Inside-to-outside technique: prevents displacement and lifting up of
atherosclerotic plaques
• A vascular anastomosis aims to achieve eversion of the mucosa (see above).
ANASTOMOTIC LEAKS
Occurs when there is ischaemia of the two ends of the anastomosis – especially in
oesophageal and rectal surgery.
Predisposing factors
Patient factors
• Malnutrition
• Old age
• Malignancy
• Immunosuppression
• Steroids
• Radiotherapy
• Obesity.
Presentation factors
• Peritonitis
• Abscess
• Ileus
• Fistula
• Signs of sepsis.
Intraoperative factors
• Poor surgical technique
• Suture failure
• Stapler malfunction
• Disease process at the level of the anastomosis.
Postoperative factors
• Haematoma formation at the anastomotic line
• Infection.
272
Signs of an anastomotic bowel leak

Typically occurs around 7–10 days after surgery:
• Low-grade pyrexia: usually first sign
• Unexplained new-onset tachycardia or arrhythmia (usually atrial fibrillation)
• Other signs of sepsis, including rise in inflammatory markers
• Renal impairment
• Cardiac and respiratory problems
• Increasing abdominal pain and peritonism.
Checking for an anastomotic bowel leak (intraoperatively)

Typically performed after a low rectal anastomosis (low anterior resection):
• Examine the anastomotic doughnuts within the circular surgical stapler
carefully, making sure that they are complete and of a good size
• Air or fluid test: using a syringe or a rigid sigmoidoscope judiciously per
rectally
• Request a water-soluble contrast enema if worried postoperatively. This would
demonstrate the site and extent of any leak.
If a leak is found intraoperatively

Options include:
• Repair leak with further sutures
• Place a pelvic drain near the anastomosis "/#
• Carry out a defunctioning stoma to prevent faecal leakage and peritonitis and
hence pelvic sepsis. Defunctioning should not be deemed a failure by the
surgeon. Not performing one can put the patient at significant risk postopera-
tively if he or she develops an anastomotic leak. The current trend is to perform
a defunctioning loop ileostomy because it has the least morbidity associated
with it and is the easier stoma to close at a later date. Patients also find it easier
to manage a loop ileostomy compared with a loop colostomy.
Never perform an anastomosis in contaminated surroundings, e.g. perforated diver-
ticular disease leading to faecal peritonitis. The join is likely to break down.
If a leak develops postoperatively and the patient begins to deteriorate and has not
been defunctioned, he or she should be taken back promptly to theatre and an emer-
gency laparotomy performed. The surgeon should:
• Drain the resulting collection
• Perform the safe option, which is to take down the anastomosis and bring out
both ends as stomas, i.e. defunction the anastomosis
• Perform a full peritoneal lavage
273
• Place drains as appropriate

• Consider taking the patient to intensive care after discussion with anaesthetic
colleagues for ventilation or multisystem support, because the patient is likely to
be septic (see ‘Sepsis and SIRS’, Chapter 121, page 505).
WHIPPLE’S OPERATION
Procedure designed to resect the head of pancreas for carcinoma.
Roux-en-Y anastomosis performed; involves:
• Proximal loop of jejunum divided
• Distal end of divided loop anastomosed to stomach (gastrojejunostomy)
• Proximal end of divided loop anastomosed as an end-to-side anastomosis to the
jejunum further downstream (entero-enterostomy).
Other anastomoses performed are:
• Choledochojejunostomy
• Pancreaticojejunostomy.
As part of the operation, a cholecystectomy and a partial duodenectomy are also
performed.
274
67 Antibiotics in surgery

In what sort of operations should antibiotic prophylaxis be used?
What sorts of regimens are used for antibiotic prophylaxis?
Through what routes can antibiotics be used in surgery?
How should the choice of antibiotic be made?
What precautions and practices can be put into place to prevent the
transmission of MRSA?
Define ‘bactericidal’ and ‘bacteriostatic’, giving examples of antibiotics
from each class of agent.
What are the aims of antibiotic prophylaxis?
What is the mechanism of action of bactericidal antibiotics?
How do bacteria become resistant to antibiotics and what can surgeons
do to help prevent this?
What would be the antibiotic of choice for a Staphylococcus aureus infection?
What are the risks of giving elderly patients second- and third-generation
cephalosporins?
What are the definitions of narrow- and broad-spectrum antibiotics and
when should they be used?
Related topics
Topic Chapter Page
HIV and universal precautions in surgery 57 219
ROUTES, TIMING AND DURATION OF ADMINISTRATION

• Parenteral administration
• Before surgery to ensure effective tissue levels
• Postoperative antibiotics on their own do not prevent infection
• During a long operation, top-up doses may be given to maintain tissue levels of
the antibiotic
• Gentamicin in the wash for colonic on-table lavage, as well as in orthopaedic
cement, has proved useful
• Intrathecal vancomycin during cerebrospinal fluid (CSF) diversion procedures
has been shown to reduce the risk of postoperative shunt infection.
275
PRINCIPLES OF SURGERY antibiotics in surgery

What are the aims of antibiotic prophylaxis?
In what sort of operations should antibiotic prophylaxis be used?
Antibiotic prophylaxis is intended to reduce the risk of postoperative
infection without alteration of the normal flora.
It is required only when wound contamination is expected (e.g. colorectal
surgery) or when operations of a contaminated site might lead to bacter-
aemia (e.g. incision and drainage of a perianal abscess).
It is not required for ‘clean’ operations except:
• Where a vascular graft or prosthetic implant (e.g. total hip or knee
replacement) is used
• In patients with pre-existing valvular heart disease to decrease the risk of
infective endocarditis
• On an in-patient with pre-existing source of infection
• If an infection would have devastating or life-altering consequences (e.g.
all neurosurgical procedures)

Define bactericidal and bacteriostatic, giving examples of antibiotics from
each class of agent
Bactericidal: an antibiotic capable of lysing and killing bacteria (e.g. $-lactams,
vancomycin, aminoglycosides)
Bacteriostatic: an antibiotic capable of slowing or stopping the multiplication
of bacteria. Final elimination of pathogens depends on host cellular defence
mechanisms having an effective phagocytotic response (e.g. erythromycin)
MECHANISMS OF ACTION OF ANTIBIOTICS

Inhibition of cell wall synthesis
• Leads to bacterial lysis as a result of defective peptidoglycan molecules in the
cell wall
• Examples: $-lactams (e.g. penicillin, ampicillin, cephalosporins), vancomycin,
monobactams.
276
Inhibition of protein synthesis within the bacteria

Inhibition of:
• Transfer RNA (tRNA) via attachment of amino acids (tetracyclines,
bacteriostatic agents)
• Nuclear translocation (erythromycin [bacteriostatic at low concentrations],
chloramphenicol, fusidic acid [bactericidal at high concentrations])
• Messenger RNA (mRNA) attachment to ribosomes (aminoglycosides – bactericidal)
Inhibition of nucleic acid synthesis

• Decreased mRNA (e.g. rifampicin)
• Decreased RNA replication (e.g. quinolones, suphonamides, metronidazole).
Alteration of call membrane function

• Polymyxin: bactericidal action against Gram-negative bacteria.
BROAD-SPECTRUM VERSUS NARROW-SPECTRUM ANTIBIOTICS

Broad spectrum
• Often covers wide range of bacteria
• Useful for prophylaxis
• Tends to alter normal gut flora of the patient
• Can lead to complications such as Clostridium difficile enterocolitis (see below).
Narrow spectrum
• Covers many fewer types of bacteria
• Useful for prophylaxis if common infecting organisms are known but, otherwise,
better for use when treating a known infective organism
• Less likely to alter the normal gut flora of the patient
• Fewer complications such as C. difficile enterocolitis.
277

What precautions and practices can be put into place to prevent the
transmission of MRSA?
• Handwashing between patients is the single most important measure that
can be taken to curb the incidence of MRSA (meticillin-resistant S. aureus)
colonization in hospitals
• Many hospitals have instituted MRSA-only bays in wards and MRSA side
rooms
• Before examining a patient with MRSA, examination gloves and an
apron should be worn
• Stethoscopes should be disinfected between patients
• MRSA cases should be left for the end of a list or ensure that a thorough
cleaning of theatre occurs afterwards
• Barrier nursing
• Make it clear to theatre that the patient is MRSA
• The problem of resistant organisms has arisen, however, as a result of con-
tinued overuse of antibiotics, arguably particularly prophylactic antibiotics
A clinician can minimize this effect by ensuring appropriate use of prophy-
lactic antibiotics (see above) and compliance when a patient is prescribed a
full treatment dose of antibiotics – the patient must finish the course to
limit the risk of the formation of resistant organisms.
RISKS OF ANTIBIOTICS
One of the most feared risks of antibiotic prescription, particularly in elderly people, is
that of C. difficile enterocolitis. This occurs particularly after the intravenous adminis-
tration of a very broad-spectrum antibiotic such as a second- or third-generation
cephalosporin or classically co-amoxiclav (Augmentin). These antibiotics damage and
kill the natural protective commensal bacterial flora of the patient’s gut, allowing an
overgrowth of pathogenic bacteria.
Indeed, some centres will not allow a cephalosporin to be administered to someone
aged over 65 unless the infection is very severe (e.g. central nervous system or CNS
infection/overwhelming sepsis).
PRESENTATION OF ANTIBIOTIC-ASSOCIATED ENTEROCOLITIS

• Usually occurs in the first postoperative week
• Severe watery diarrhoea (can be bloody)
278
• Colonoscopy reveals mucosal inflammation and pseudomembranes

• Abdominal distension
• Shock secondary to profound fluid loss (see ‘Shock’, Chapter 122, page 510)
• Treatment is usually a course of oral metronidazole, although some strains that
are resistant will require oral vancomycin
• C. difficile toxin positive.

What would be the antibiotic of choice for a S. aureus infection?
Vancomycin is an excellent choice for an MRSA infection; indeed it is one
of a very few antibiotics that would be appropriate, although it is easy to
forget that not all S. aureus infections are MRSA!
For MSSA (meticillin-sensitive S. aureus) infection, flucloxacillin is a much
better option because its tissue penetration is better. Furthermore, the
appropriate use of vancomycin where it is not needed only increases the
chance of developing further strains of a vancomycin-resistant MRSA.
ANTIBIOTIC REGIMENS – EXAMPLES

• Clean procedures (e.g. varicose veins) – no prophylaxis
• Abdominal surgery with no expected contamination (e.g. cholecystectomy)
requires single-dose prophylaxis on induction only
• Procedures with a contaminated field (e.g. anterior resection, appendicectomy):
dose on induction and two further postoperative doses
• Wounds contaminated with skin flora need prophylaxis against staphylococcal
infection with 500 mg–1 g flucloxacillin intravenously
• Bowel procedures need broad-spectrum cover for Gram-positive, Gram-negative
organisms and anaerobes (an example regimen would be co-amoxiclav or a second-
or third-generation cephalosporin with metronidazole (for anaerobic cover)
• Biliary tract operations rarely involve a flora of anaerobes and, in this case, a
cephalosporin alone would be adequate prophylaxis.
• Despite being clean, orthopaedic implants and heart valve surgery require
prophylaxis because infection in either case is disastrous and potentially life
threatening (cefuroxime and gentamicin in the case of heart valves and
flucloxacillin and gentamicin in the case of orthopaedic implants).
279
68 Bowel preparation

What is the aim of preoperative bowel preparation?
What sorts of bowel preparation regimens are used?
How does Picolax work?
What are the complications of bowel preparation?
When should bowel preparations never be used?
What bowel preparations are used for left colon and right colon procedures,
respectively?
Is there any evidence to suggest that mechanical bowel preparation
with polyethyleneglycol reduces the incidence of anastomotic leak
postoperatively?
Related topics
Topic Chapter Page
Anorectal surgery 1–3 23–25 63, 67, 73
Shock 122 510
BOWEL PREPARATION REGIMENS

Large bowel surgery or colonoscopy
• Low residue diet 3 days before procedure
• Clear fluids 2 days before the procedure
• Bowel preparation sachet ! 2, 6 hours apart (usually sodium picosulphate or
other purgative) – patient is advised to continue drinking clear fluids during this
process. If unable to keep up with output, patient may go into hypovolaemic
shock and bowel preparation for elderly people may have to be in hospital while
on intravenous fluids
• Phosphate enema on the morning of surgery
• Intravenous fluid replacement is often required on admission.
280
PRINCIPLES OF SURGERY bowel preparation

What is the aim of preoperative bowel preparation?
The aim of preoperative bowel preparation is to reduce the incidence of
postoperative sepsis and other infective complications particularly after
large bowel surgery. It attempts to achieve this by reducing the overall
bacterial load within the gut before surgery.
There is no class I evidence to support the use the bowel preparation, and
indeed a relatively recent meta-analysis (see ‘Statistics and clinical trials’,
Chapter 79, page 326) looking at bowel preparation using propylethylene
glycol has shown no benefit and possibly an increased risk of postoperative
anastomotic leak.
The evidence has, thus far, failed to support the validity of preoperative
bowel preparation, although it is still a practice that is widely used in
general surgery.
There is no doubt that it has a role pre-colonoscopy to afford a much
better view of the whole bowel wall.
Sigmoidoscopy
• Phosphate enema on the morning of the procedure or at home the previous
evening.
Emergency large bowel resections

On-table ‘wash out’ or lavage may be used by some surgeons. This usually involves
making a small incision in the bowel wall and inserting a long Foley catheter or simi-
lar device through a caecostomy or appendicostomy, often distal to a soft clamp.
Infusion of warm saline with or without gentamicin can be used. Either the fluid is
allowed to drain out through the anus or, more commonly, the bowel is divided and
fluid escapes distally under controlled conditions (often through a large-bore efflu-
ent tube inserted into the bowel) with sterile saline-soaked gauze covering as much
of the operative field and wound edges as possible.
Anorectal surgery
• A glycerine suppository is often used preoperatively, although there is no
evidence of benefit for this.
• Some colorectal surgeons will perform a rectal wash-out (with Savlon or similar)
before making the primary anastomosis in an anterior resection.
281
PRINCIPLES OF SURGERY bowel preparation
Obstructed patients
As a general rule, preoperative bowel preparation should never be used in the case of
an obstructed patient for fear of perforation. Some surgeons may choose to use a phos-
phate or arachus oil enema for left-sided lesions, although there is no evidence in the
literature to support this practice.
SODIUM PICOSULPHATE (PICOLAX)

• Diphenylmethane derivative
• Stimulates myenteric plexus to increase the rate of peristalsis and decreases
transit time. This decreases the time for large bowel water absorption to take
place and results in very watery diarrhoea via two possible mechanisms:
• inhibition of the sodium pump (sodium/potassium adenosine triphosphatase
[Na"/K" ATPase]) preventing sodium transport across the gut wall and leading
to the accumulation of water and electrolytes in the gut lumen
• increased production of fluid in the intestine through cyclic adenosine
monophosphate (cAMP) and prostaglandins, which promote active secretory
processes in the intestinal mucosa.
COMPLICATIONS OF BOWEL PREPARATION

Systemic
• Water and electrolyte imbalance requiring intravenous fluids (see ‘Fluid
balance’, Chapter 111, page 452)
• Hypovolaemic shock (see ‘Shock’, Chapter 122, page 510)
• Cardiac arrhythmias as a result of electrolyte imbalance
• Death (reported in elderly people)
• Cramping pain
• Nausea and vomiting.
Local
Bowel perforation: large bolus of effluent builds up proximal to a luminal narrowing
or obstruction, leading to an increase in intraluminal pressure and subsequent perfor-
ation of an oedematous, ischaemic and friable gut wall.
282
69 Clinical governance

What is the definition of clinical governance?
What is audit?
What is an audit cycle?
What is the difference between audit and research?
What is meant by ‘closing the audit loop?’
Related topics
Topic Chapter Page
Statistics and clinical trials 79 326

What is the definition of clinical governance?
From the original paper on the subject by Scally and Donaldson in the BMJ:
‘A framework through which NHS organisations are accountable for
continually improving the quality of their services and safeguarding
high standards of care by creating an environment in which excellence
in clinical care will flourish.’
Clinical governance is a concept, introduced by the government in 1998, to re-structure

change within the NHS. It demands a fundamental change in the attitude and culture
of the NHS. The main difference under clinical governance is that a trust, and ultim-
ately the chief executive of that trust, is responsible for creating an environment in
which effective changes can be made to achieve high-quality care, and can be held
accountable if this is not provided.
For surgeons, clinical governance aims to ensure that:
• There are systems in place to monitor quality of clinical practice and that they
are functioning well
• Clinical practice is reviewed and improved as a result
• Surgeons continue to meet the national standards as issued by the professional
bodies.
283
PRINCIPLES OF SURGERY clinical governance
The areas covered by clinical governance are divided into seven pillars:
1. Clinical effectiveness (the degree to which the organization ensures that ‘best
practice’ is used):
• evidence-based medicine
• NICE (National Institute for Health and Clinical Excellence): this organisa-
tion appraises the evidence for and against funding new treatments and pro-
duces guidelines for best practice based on the available evidence.
2. Risk management (having systems to monitor and minimize risk to staff,
patients and visitors):
• incident and near-miss reporting
• health and safety
• complaints.
3. Clinical audit (the systematic critical analysis of the quality of clinical care).
4. Education and training (ensuring that support is available to enable staff to be
competent at their jobs and to develop their skills to be up to date).
• continuing professional development (revalidation and appraisal).
5. Staffing and staff management (recruitment and ensuring effective working
conditions).
6. Information use (systems in place to collect and analyse information on service
quality).
7. Patient experience and public involvement (ensuring individuals have a say in
their own treatment).
RESEARCH
Definition
‘The process of trying to find the truth.’
AUDIT
Definition
‘A process used by clinicians to improve patient care by assessing clinical prac-
tice, comparing against accepted standards and making changes if necessary.’
The audit cycle
• Collect data
• Assess conformity of data to a predetermined standard
• Feedback results
• Update standards if necessary
• Intervene to promote change
284
• Set standards
• ‘Close the loop’ and go back to collecting data.

What is the difference between audit and research?
Clinical audit is not research, but it does make use of research method-
ology in order to assess practice.
Although research and clinical audit are two distinct activities with differ-
ent purposes, they are interrelated in several ways:
• Research provides a basis for defining good-quality care for clinical audit
purposes
• Clinical audit can provide high-quality data for non-experimental evalu-
ative research
• Research into the effectiveness and cost-effectiveness of clinical audit is
needed
• Research needs to be audited to ensure that high-quality work is per-
formed (refer to www.corec.org.uk for more information on this)
Research Clinical audit

Aims to establish best practice Aim to see how close current practice is to
best practice and identify ways to bring the
two closer together
Designed to be replicated and validated by Specific to one particular patient group – the
other groups results are not transferable to other settings
Aims to generate new evidence/knowledge Aim to improve services
Usually initiated by researchers Usually initiated by service providers
Is theory driven Is practice based
Is often a single one-off study Is an ongoing process (see the audit cycle)
May involve randomization (see ‘Statistics Never involves randomization
and clinical trials’, Chapter 79, page 326)
May involve a placebo Never involves a placebo
May involve a novel treatment Never involves a completely novel treatment
Benefits of clinical audit

• Identifies and promotes good practice and can lead to improvements in service
delivery and outcomes for users
• Can provide the information that you need to show others that your service is
effective (and cost-effective) and thus ensure its development
• Provides opportunities for training and education
285
• Helps to ensure better use of resources and, therefore, increased efficiency

• Can improve working relationships, communication and liaison between staff,
between staff and service users, and between agencies
• The overall aim of clinical audit is to improve service user outcomes by
improving professional practice and the general quality of services delivered.
REVALIDATION AND APPRAISAL

• As part of the government’s commitment to delivering the quality agenda,
annual appraisal is being introduced for all doctors working in the NHS.
• Appraisal for consultants was launched in April 2001.
• Work is under way to roll out schemes for other groups of doctors, including
doctors in training, public health doctors and locum doctors.
• In effect, all NHS doctors (including GPs) will be discussing their practice with
their employer or a recognized NHS appraiser on an annual basis.
• Part of this appraisal process is a review of the evidence used to support the
standards set by good medical practice.
• During the development of appraisal, the General Medical Council (GMC)
made proposals to ‘revalidate’ all registered doctors. This means that every
5 years each doctor who wants to remain in practice must present evidence to
the GMC that he or she is competent in his or her field of practice and has kept
up to date (CME or continuing medical education points are essential to this
process).
• The appraisal system for NHS doctors is designed to support the process of
revalidation.
286
70 Day surgery

What is day surgery?
What are the criteria for consideration of day surgery?
What procedures are suitable for day surgery?
What are the advantages and disadvantages of day surgery?
What sort of instructions are patients who are undergoing day surgery given?
What are the contraindications to day surgery?
Related topics
Topic Chapter Page
Local anaesthetics 75 308
Key learning point

Day surgery
Procedures and operations performed on an elective non-resident basis but
that nevertheless require facilities for patient recovery.
The government has targeted 75 per cent of all elective surgery to be per-
formed on a day-case basis by the end of 2006!
CRITERIA FOR CONSIDERATION OF DAY SURGERY

• Patients must be ASA (American Society of Anesthesiologists) grade I or II
(i.e. fit and well)
• Patients must have body mass index (BMI) " 35
• Operations must be projected to be less than 1 hour
• Idea of day surgery must be acceptable to patient
• Pathology must be appropriate (i.e. no massive scrotal hernias, etc.)
• Patient must live close to day surgery unit (travel time % 1 hour)
• Patient must have friend or relative at home to look after the patient for 24–48
hours after surgery
• Patient must have a telephone at home.
287
PRINCIPLES OF SURGERY day surgery
PROCEDURES SUITABLE FOR DAY SURGERY

(These are based on the British Association of Day Surgery ‘trolley’ of procedures,
1999, of which 50 per cent should be suitable for day-case surgery.)
These procedures need to be relatively quick with a low complication rate. They can be
performed using local anaesthetic infiltration or a quick general anaesthetic but they
must not involve a spinal or epidural anaesthetic. Patient should not require strong opi-
oid analgesia postoperatively and oral analgesics should be sufficient.
General surgery
• OGD (oesophagogastroduodenoscopy)
• Colonoscopy
• Anal tag removal/haemorrhoidectomy
• Hernia repair (inguinal/femoral/umbilical/paraumbilical/epigastric)
• Varicose vein surgery
• Pilonidal sinus surgery
• Small breast lump excision.
ENT
• Direct pharyngoscopy and laryngoscopy
• Insertion of grommets
• Tonsillectomy.
Orthopaedics
• Arthroscopy (shoulder/knee)
• Trigger finger release
• Dupuytren’s contracture surgery
• Digit amputation
• Carpal tunnel release
• Ingrowing toenail surgery.
Ophthalmic surgery
• Cataract surgery
• Strabismus surgery (squint)
• Visual acuity correction surgery (LASIX, radial keratotomy).
Plastic surgery
• ‘Bat’ ears
• Breast augmentation
• Nipple and areola reconstruction
• Small contracture surgery (z-plasty, etc.).
288
Gynaecological surgery
• Dilatation and curettage
• Termination of pregnancy
• Laparoscopy and laparoscopic sterilization.
THE DAY SURGERY UNIT

These procedures should ideally be performed in a dedicated day surgery unit with its
own waiting lists, building, theatres and recovery area on the ground floor. Procedures
should be performed by an experienced consultant who is constantly audited to ensure
that complications remain low. In some cases an experienced senior registrar would be
acceptable. Patient satisfaction and adequacy of postoperative analgesia should be regu-
larly audited as well. A successful unit depends on day of surgery admission and nurse-
led discharge in many cases.
Advantages and disadvantages of day surgery

• Minimum time away from home
• Cost-effectiveness
• Less chance of operation being cancelled as a result of emergency work
• Inpatient beds released
• Arguably less chance of nosocomial infection
• Needs aftercare at home (friend or relative)
• Less opportunity for training in ‘bread and butter’ cases for juniors
• Inpatient admission can be required following an unexpected complication or
inadequate postoperative analgesia
Instructions given to patients

Patients must have full verbal and printed details giving a description of the surgical
problem, and outline of the surgery and other possible alternatives, pre-op instruc-
tions, post-op instructions and advice on when to return to work and/or follow-up
appointment or suture removal. A list of possible complications should also be given
along with anything that the patient should look out for at home that could indicate a
postoperative problem. The process of informed consent is exactly the same for day
surgery as for any other form of surgery.
Contraindications to day surgery

These can split up into surgical/anaesthetic and social.
Surgical/anaesthetic
• Unfit (ASA III or above)
• Operation longer than 1 hour
• Requires spinal or epidural analgesia
289
• Day surgery unacceptable to patient

• Patient is obese (BMI ! 35)
• Pathology too extensive to tackle as a day-case procedure.
Social
• Relative or friend unavailable to look after them for 24–48 hours
• No access to a lift in an upper floor flat or restricted access to a house; lack
of appropriate toilet facilities/bathroom
• Lives too far from day surgery unit.
290
71 Diathermy

What are the possible complications with using diathermy in theatre?
What different sorts of diathermy do you know?
How does diathermy work?
What different settings do you know for diathermy and how do they work?
Why does diathermy induce very little neuromuscular stimulation?
What is the difference between monopolar and bipolar diathermy?
What are the problems with using diathermy in patients with pacemakers?
Related topics
Topic Chapter Page
Surgical diathermy involves the passage of high-frequency alternating current between

two electrodes and through tissue. Where the local current density is the highest, a
large amount of heat is produced in the tissue, resulting in tissue destruction.
There are two main types: monopolar and bipolar.
Monopolar
Probably the most common sort, using a high-power generator (400 W). A current
is generated in the diathermy machine and passed to a hand-held electrode. At the
tip of this electrode, the current density is very high, resulting in very high tempera-
tures locally. The current then dissipates over a large amount of tissue to the patient
‘plate’ electrode – with a large surface area of at least 70 cm2, ensuring that the cur-
rent density at the plate is low, and thus causing minimal heating.
Bipolar
Here, the current is passed from one electrode to another across a small amount of
tissue. The two electrodes are usually incorporated into a pair of forceps with which
the surgeon can hold and coagulate tissue. As there is no need for a plate, bipolar
diathermy requires much less power (50 W). More commonly used in plastic surgery
and neurosurgery for very precise coagulation.
291
PRINCIPLES OF SURGERY diathermy
DIATHERMY SETTINGS
Cutting
Continuous output from the generator causes an arc to be struck between the active
electrode and the tissue in monopolar diathermy. Temperatures up to 1000°C are
produced and cellular water is instantly vaporized, causing tissue disruption without
much coagulation. This setting is not available in bipolar diathermy.
Coagulation
Pulsed output from the diathermy generator results in the sealing of blood vessels
with the minimum of tissue disruption.
Blend
Many machines have this setting for monopolar diathermy – a continuous output
with pulses to help coagulate as well as cut.
CAUSES OF DIATHERMY BURNS

Older earth-referenced machines
These are from ECG electrodes, metal drip stands or metal components of the oper-
ating table in contact with the patient’s skin. They provide other earths for the
diathermy machine and, as their surface area is relatively small, current density may
be high and severe burns will result. Modern isolated, as opposed to earth-referenced,
machines get around this problem by not needing an earth and using a tight frequency
range for the AC current, resulting in less earth current leakage.
Incorrect placement of patient plate (most common cause)

• Needs good contact with dry, shaved skin (no kinking because it reduces area)
• Contact surface must be at least 70 cm2 (minimal heating)
• Plate must be away from bony prominences and tissue with poor blood supply
(e.g. scar tissue) – poor heat distribution.
Careless technique
Failure to replace electrode in insulated quiver after use and use of spirit-based
skin preparation (use of diathermy without allowing sufficient time for the prep to
evaporate)
Use of diathermy on large bowel

Methane and hydrogen in large bowel can be explosive.
292
Use of monopolar on appendages (e.g. penis, digits or tissue pedicles)

Current is concentrated along the line of tissue pedicles and can cause tissue damage
far distant to the site of the electrode. In circumstances such as these where coagula-
tion is needed, bipolar should be used.
Used close to metallic implants (e.g. hip prostheses)

Current can be induced locally around metal implants, causing local heating and tissue
damage.
Active electrode not in view in laparoscopy

Diathermy should only be used in laparoscopy when the active electrode is fully in
view, along with the tissue that it is about to cut or coagulate. The electrode should
never be used ‘around the corner’.
Metal laparoscopic ports used with plastic insulator cuffs

The use of diathermy in this instance could set up a capacitance in the port and
local heating at the point where the port meets the skin. Thus laparoscopic ports
should always be made up of the appropriate components. Never ‘mix and match’.

Why does diathermy induce very little neuromuscular stimulation?
To produce profound neurostimulation, alternating current needs to be below
50 kHz. The mains electricity in the UK works at 50 Hz and a current of only
5–10 mA will cause painful muscle stimulation, whereas 80–100 mA across
the heart will result in ventricular fibrillation. Surgical diathermy involves
currents at 400 kHz–10 MHz and, with these frequencies, currents of up to
500 mA may be safely passed through the tissues.
DIATHERMY AND PACEMAKERS

There are two potential problems:
1. High frequency of the diathermy may result in induced currents in the logic
circuits of the pacemaker, resulting in potentially fatal arrhythmias.
2. Diathermy close to the box itself may result in currents travelling down the
pacemaker wires, leading to myocardial burns. This could either increase the
threshold or at worst cause cardiac arrest.
293
Thus, for any patients with a pacemaker:

• Discuss the case first with a cardiologist – type of box, type of pacing,
underlying arrhythmia, etc.
• Avoid diathermy completely if possible – if not, consider bipolar
• If monopolar must be used, use only for short bursts and place the patient’s
plate so that the current flows away from the pacemaker system. If any
arrhythmias are noted, stop all diathermy immediately.
294
72 Drains in surgery

What is the purpose of a surgical drain?
What are the complications associated with the use of drains in surgery?
What type of drains have you seen or heard about? Give examples.
Related topics
Topic Chapter Page
Ascites 48 172
Pneumothorax 117 488
INDICATIONS
• To exteriorize actual (e.g. radiologically placed drain for subphrenic abscess) or
potential collections of fluid in a wound
• To minimize dead space
• To divert fluid away from blockage or potential blockage, e.g. biliary T-tube and
suprapubic urinary catheter and protection of a healing anastomosis
• To decompress and allow air to escape (chest drain).
TYPES
• Open: these would be non-suction in nature, e.g. corrugated or Penrose drain
• Closed: suction versus non-suction (under the influence of gravity only)
• Suction: examples include sump, Redivac, firm multi-holed PVC, for skin flaps
• Non-suction (closed): examples include Robinson drain, T-tube, urinary (Foley)
catheter, chest drain, Blake drain
• Closed drain systems: advantage of reducing the risk of introducing
infection
• Suction drains provide the advantage of better drainage, but may damage
adjacent structures, e.g. bowel, which could precipitate a leak.
295
PRINCIPLES OF SURGERY drains in surgery
COMPLICATIONS
Immediate
• Air leak around a chest drain
• Pain: chest drain irritates the diaphragm, causing immobility and therefore its
potential complications
• Trauma at insertion and injury to surrounding structures during drainage or
placement, e.g. bowel injury as the result of an improperly placed ascitic drain.
Early
• Failure to drain adequately (incorrect placement, too small, blocked lumen)
• Fracture of drain
• Disconnection or removal postoperatively.
Late
• Infection: via the drain track
• Retraction of the drain into the wound: surgical removal may be required in this case
• Herniation, e.g. bowel at the drain site
• Fistula formation
• Bleeding: by erosion into a blood vessel – nasogastric tube causing a gastric ulcer
• Anastomotic leakage: direct damage to the anastomosis; prevent vascularization of
the anastomosis. However, if the anastomosis is not watertight a drain may be
useful to prevent the build-up of a collection, which may impede healing of, for
example, a urological or biliary anastomosis.
DRAINS USED IN SURGICAL PRACTICE

• Nasogastric tube: used to drain stomach air and fluid contents and to prevent
aspiration
• Chest drain: used to drain the pleural space – this is attached to an underwater
seal to prevent backflow from negative intrathoracic pressures
• Operative wound drain: used for an anticipated fluid collection in a closed
space; this prevents seroma formation, e.g. after an incisional hernia repair
• Pericardial drain: used after coronary artery bypass surgery
• Infected abscess: cavity drain (intra-abdominal).
296
73 DVT prophylaxis and coagulation in surgery

What do you understand by Virchow’s triad? How does this relate to
DVT prophylaxis in the surgical patient?
What regimen of DVT prophylaxis would you use for minor/major surgery?
What are the risk factors for DVT?
What is the definition of a thrombus? How does it differ from a clot?
What is the pathophysiology of the process of thrombosis?
How does heparin work?
What are the indications for intravenous heparin perioperatively?
How long before an operation should warfarin be stopped and which
patients need perioperative anticoagulation?
If a patient’s INR (international normalized ratio) is very high and the
patient is on warfarin but requires emergency, life-saving surgery such
as an abdominal aortic aneurysm repair, how would you reverse the
anticoagulation?
Related topics
Topic Chapter Page
Liver 10 28
Atherosclerosis 49 177

What is the definition of a thrombus? How does it differ from a clot?
Thrombus: a solid mass formed in flowing blood from blood constituents
Clot: a semi-solid mass formed in stationary blood from blood constituents.
It may be formed after death or outside the circulation
Pulmonary embolus (PE) accounts for 10–25 per cent of all postoperative inpatient
deaths. There are three major sources for this embolus:
1. DVT in the deep veins of the leg
2. Thrombosis in the mesenteric veins
3. Atrial fibrillation (AF) resulting in formation of right atrial thrombus (also
mural thrombus from myocardial damage).
297
PRINCIPLES OF SURGERY DVT prophylaxis and coagulation in surgery
In addition:
• At least 20 per cent patients with a DVT develop a post-thrombotic limb
• Most calf DVTs are clinically silent
• 80 per cent of calf DVTs lyse spontaneously without treatment
• 20 per cent of calf DVTs propagate to the thigh and have increased risk of PE.

What do you understand by Virchow’s triad?
Virchow’s triad
The three factors that contribute to the risk of thrombosis:
1. Damage to the vessel wall and vascular endothelium
2. Alterations in blood flow
3. Alterations in the constituents of the blood
Damage to the vessel wall and vascular endothelium
• Arterial: atherosclerosis (see ‘Atherosclerosis’, Chapter 49, page 177)
• Venous:
• damage to calf veins by direct pressure when in stirrups – therefore
patient positioning in long operations – crucial to reduce risk of DVT
• damage to femoral vein by distortion during hip replacement surgery
Alterations in blood flow
• Stasis and pooling of blood in leg veins in patients on bedrest
postoperatively – TED (thromboembolic deterrent) stockings are compres-
sion stockings that limit pooling of blood in the legs. Dynamic compression
of the legs during surgery has been shown to reduce the postoperative inci-
dence of DVT. Early postoperative mobilization is essential
• Immobility for long periods (including air travel)
• Stasis in the heart as a result of AF – if at all possible, AF should be car-
dioverted preoperatively or at the very least rate controlled
Alterations in the constituents of the blood
• Dehydration (increased viscosity) – ensure adequate fluid replacement
• Thrombocytosis (infection, asplenia, etc.) – important to treat all
postoperative infections promptly
• New platelets (increased platelet adhesion after surgery)
Thrombophilia (factor V Leiden, protein C/S deficiency, lupus anticoagu-
lant): these factors increase the risk of DVT postoperatively.
298
RISK FACTORS FOR DVT

• Age
• Previous DVT
• Pregnancy
• Obesity
• Surgery
• Varicose veins
• Pelvic disease
• Oral contraceptive pill
• Malignancy
• Immobility
• Thrombophilias.
CLINICAL FEATURES OF DVT

• Can be asymptomatic
• Warm, erythematous swollen leg
• Calf tenderness and pain
• Rise in skin temperature of leg
• Distended superficial veins
• Low–grade pyrexia at 7–8 days
• Doppler ultrasonography can be used for diagnosis of distal thrombosis
• Venography may be used to diagnose iliac vein thrombosis.
PATHOPHYSIOLOGY OF THROMBOSIS
• Platelets stick to damaged epithelium, releasing various mediators (e.g. platelet-
derived growth factor [PDGF])
• Fibrin and leukocytes adhere to platelets
• Fibrin network forms on this layer:
• clotting cascade (intrinsic system)
• activation of factor XII by contact with vascular endothelium
• thrombin catalyses fibrin formation from fibrinogen
• Second layer of platelets stick (alternate layers of fibrin network and platelets
form pathological ‘lines of Zahn’)
• Thrombus eventually occludes the lumen of the vein, creating stasis proximally
and promoting proximal propagation of the thrombus.
299
RISK STRATIFICATION ACCORDING TO PROCEDURES AND

RISK FACTORS
Patients are risk stratified into low-, moderate- and high-risk groups according to
their preoperative clinical condition, risk factors and type of operation.
Low risk
• Minor surgery (% 30 min) with no other risk factors other than age
• Major surgery (! 30 min), age % 40 years with no other risk factors
• Minor trauma or medical illness.
Moderate risk
• Major general, urological, gynaecological, cardiothoracic, vascular or neurological
surgery " age ! 40 years or other risk factor
• Major medical illness or malignancy
• Major trauma or major burns
• Minor surgery, trauma or illness in patients with previous DVT, PE or
thrombophilia.
High risk
• Fracture or major orthopaedic surgery of pelvis, hip or lower limb
• Major pelvic or abdominal surgery for neoplasia
• Major surgery, trauma or illness in patient with previous DVT, PE or proven
thrombophilia (see above)
• Major lower limb amputation.
UNTREATED EPIDEMIOLOGY OF DVT IN RISK GROUPS AND

RECOMMENDED REGIMENS
Group Calf DVT (%) Proximal DVT (%) Fatal PE (%)
Low risk % 10 %1 0.01

Moderate risk 10–40 1–10 0.1–1
High risk 40–80 10–30 1–10
300
High risk
• Graduated elastic anti-embolism stockings (e.g. Kendal TED)
• Unfractionated heparin 5000 U s.c. two or three times daily (there is evidence
that heparin given 8-hourly may be more effective than 12-hourly). Start on
admission or more than 2 hours before surgery (not in the case of epidural
insertion or removal) or
• low-molecular-weight heparin or
• adjusted-dose warfarin (INR 2–3) (not commonly used)
• Consider intermittent pneumatic compression of calves in theatre.
Moderate risk
• Graduated elastic anti-embolism stockings (e.g. Kendal TED) and/or
• low-dose unfractionated heparin 5000 U s.c. two or three times daily. Start on
admission or more than 2 hours before surgery (see above) or
• low-molecular-weight heparin (contact hospital pharmacy for available products
and dose).
Low risk
• Early mobilization.
Heparin
• Commonly used anticoagulant, available in unfractionated or low-molecular-
weight (LMW) forms
• Can be given intravenously or subcutaneously
• Acts by inhibition of factor X and binding anti-thrombin III
• Unfractionated heparin also acts significantly on factor II
• LMW heparin more specific to factor X and needs only to be given once daily. It
is more expensive than unfractionated heparin
• Intravenous heparin is reversed by intravenous protamine – standard procedure
in cardiothoracic surgery.
Warfarin
• Antagonizes the action of vitamin K in the liver and on the vitamin K-
dependent enzymes in the clotting cascade
• Reduces prothrombin and factors VII, IX and X
• Patients on warfarin are usually converted to some form of heparin
perioperatively to minimize bleeding risk and provide as much control as
possible to the surgeon.
301
INDICATIONS FOR INTRAVENOUS HEPARIN

With the advent of LMW heparin, indications for intravenous heparin are shrinking,
although it is still used in many centres. It is used where the anticoagulation needs to
be reversed quickly and cover with anticoagulant is important up to the last moment
(see below). The decision on whether or not to start intravenous heparin for warfarin
anticoagulation cover is based on the reason for the anticoagulation:
• AF is no longer considered an adequate reason for intravenous heparin, given its
difficulties and poor management of APTT (activated partial thromboplastin
time) ratios by juniors on the ward.
• Likewise, a metal aortic valve replacement is considered by many no longer to
require intravenous heparin cover because the risk of perioperative thrombosis
of the valve is tiny for anything up to 2 weeks after stopping warfarin.
• A metal mitral valve, however, has a higher risk of thrombosis and should be
covered perioperatively with intravenous heparin, bringing the patient in early
for the switch to take place on the ward.
• Intravenous heparin is also used in the context of vascular surgery, cardio-
thoracic surgery and interventional vascular radiology during procedures or
operations.

If a patient’s INR is very high and the patient is on warfarin but needs
emergency, life-saving surgery such as an abdominal aortic aneurysm
repair, how would you reverse the anticoagulation?
Although the use of intravenous vitamin K and/or fresh frozen plasma is
the classic way of reversing a wayward INR, it is not particularly efficient
or quick, often taking several hours to get the INR to a level where an
operation would become possible.
Thus, in concert with a haematologist, activated factor VII and factor IX
concentrate can both be given, which reverses the effect of warfarin almost
instantly. It is, however, very expensive, carries with it a small increased
risk of ischaemic sequelae, and should be used only in extremis such as the
situation above where any delay could be fatal.
302
74 The hip joint, neck of femur and sciatic nerve

What bone is this (femur) and from which side is it?
What is the blood supply to the head of femur?
Where does the hip joint capsule attach to the femur?
What are the ligaments of the hip joint?
What maintains the stability of the hip joint?
The sciatic nerve is derived from which nerve roots?
What is the surface marking of the sciatic nerve from the pelvis to knee?
What are the main branches of the sciatic nerve and what do they supply?
How do you classify fractures of the neck of femur and how does this
relate to management?
What are the possible complications of femoral neck fractures?
When is a neck of femur fracture an emergency?
Where does a prolapsed intervertebral disc normally occur?
What are the signs of an L5–S1 nerve root compression?
What does the patient typically present with?
Related topics
Topic Chapter Page
Orthopaedic approaches and procedures 38 130

How do you side a femur?
Helpful hints
Proximally: rounded head with a neck angled 125° to the femoral shaft.
Points upwards and medially
Distally: two femoral condyles. Note prominent adductor tubercle
proximal to medial condyle. Lateral condyle more prominent and acts as a
buttress to assist in preventing lateral dislocation of the patella
Anterior surface is smooth and convex. The junction between neck and
shaft is marked by the intertrochanteric line anteriorly
Posterior surface has the linea aspera (prominent ridge). Also note the
deep intercondylar notch that separates the two condyles
303
PRINCIPLES OF SURGERY the hip joint, neck of femur and sciatic nerve
BLOOD SUPPLY TO THE FEMORAL HEAD

Three sources
1. Through diaphysis
2. Retinacular branches from medial and lateral femoral circumflex arteries
(trochanteric anastomosis), which pass proximally within joint capsule to
anastomose at junction of neck and articular surface
3. Artery in the ligamentum teres (negligible in adults but essential in children,
when the femoral head is separated from the neck by the cartilage of the
epiphyseal line).
ANATOMY OF THE HIP JOINT

• Ball-and-socket primary synovial joint
• Ligamentum teres in fovea.
Capsule
The capsule of the hip joint is strong and attached to the acetabulum and the trans-
verse acetabular ligament. Anteriorly, it extends over the neck of the femur to the
intertrochanteric line. Posteriorly, it covers the neck only to halfway to the inter-
trochanteric crest.
Reflects back as the retinacular fibres which carry its blood supply.
• Blood supply: trochanteric (at greater trochanter) and cruciate (lesser
trochanter) anastomoses
• Three bursae: trochanteric, ischial and psoas bursae.
Stabilizing factors of the hip joint

Ligamentous, bony and muscular contributions.
Ligaments
Three ligaments support the capsule:
1. Iliofemoral: triangular ligament of Bigelow is the strongest. Arises from the
anteroinferior iliac spine and inserts Y shaped into the intertrochanteric line
2. Pubofemoral
3. Ischiofemoral: contributes little and is the weakest of the three ligaments.
Bony
Femoral head fits snugly into acetabulum. Deepened by the acetabular labrum.
304
Muscular
The short gluteal muscles, e.g. quadratus femoris and piriformis.
Gluteus minimus and medius are important stabilizers during weight bearing on
one leg; they act to prevent adduction rather than as pure abductors.
The hip joint is least stable in the flexed adducted position.
NECK OF FEMUR FRACTURES

Broadly divided into intracaspular and extracapsular.
Intracapsular (subcapital, cervical, basal–cervical)

These tend to disrupt the blood supply to the femoral head along the retinacular
fibres (see above). There is an increased risk of avascular necrosis of the head.
Garden classification for intracapsular fractures

This describes the degree of displacement at the fracture site:
Type I Incomplete fracture
Type II Complete but undisplaced fracture
Type III Complete fracture with partial displacement
Type IV Complete fracture with complete displacement
The degree of displacement of the fracture dictates surgical management:
• Undisplaced intracapsular fractures: internal fixation with two to three
cannulated parallel screws
• Displaced intracapsular fractures: hemiarthroplasty in elderly people, e.g.
simple unipolar prosthesis – Austin–Moore or Thompson
• Fit patients aged " 65 years should be treated by reduction and internal
fixation or considered for bipolar hemiarthroplasty.
Extracapsular (intertrochanteric, basal, subtrochanteric)

Distal to the insertion of the capsule through an area of well-vascularized bone.
Classification is based on the number of fragments produced by the fracture:
• Undisplaced (two part)
• Displaced (two part)
• Three part involving greater trochanter
• Three part involving lesser trochanter
• Four part
• Reverse obliquity.
305
Management depends on site and number of parts of fracture.

Dynamic hip screw (DHS) for intertrochanteric and basal fractures.
Subtrochanteric fractures with open reduction internal fixation with intramedullary
hip screw (IMHS) or DHS with medialization of the fracture.
Complications of femoral neck fractures

• Avascular necrosis: high risk in displaced fractures caused by disruption of the
blood supply; eventually the femoral head collapses, causing pain, loss of
function and progressive osteoarthritis
• Non-union
• Osteoarthritis
• Systemic: DVT, PE, chest infection, pressure sores.

When is a fractured neck of femur an emergency?
The benefit of preserving the femoral head in younger adults is much greater,
so biologically younger patients with displaced intracapsular fractures are
rushed into theatre for open reduction and fixation.
There is no evidence for this benefit and a wait of 48 hours will not prejudice
outcome of hip fracture surgery.
Prognosis
Neck of femur fractures normally occur in elderly people – a population with
extensive co-morbidity.
There is a 50 per cent risk of death within 6 months of a neck of femur fracture.
THE SCIATIC NERVE

Formed from the nerve roots of L4, L5 (lumbosacral trunk) and S1–3 (upper sacral
plexus).
Surface anatomy: midpoint between ischial tuberosity and greater trochanter down-
wards on the posterior thigh to the apex of the popliteal fossa.
Supplies the posterior compartment of the thigh.
Main branches
• Nerves to obturator internus and quadratus femoris: innervates the short
external rotators of the hip joint
306
• Common peroneal nerve: supplies muscles of the anterior (via deep peroneal
nerve) and peroneal (via superficial peroneal nerve) compartments of the lower
limb. Also supplies sensation to the anterolateral leg and dorsum of foot
• Tibial nerve: supplies the muscles of the posterior compartments (superficial
and deep) of the leg and sensation to the posterior region of the leg and sole of
the foot.

Where does a prolapsed intervertebral disc normally occur?
A tear in the annulus fibrosus allows herniation of the nucleus pulposus
and is usually secondary to a flexion–rotational injury.
The L4–5 and L5–S1 disc levels are most commonly affected.
Patients usually present with:
• Low back pain
• Pain in the leg in the L5–S1 nerve root distribution
• Limitation of straight-leg raise
• Positive sciatic stretch test
Signs of L5 nerve root compression:
• Decreased sensation in the L5 dermatome
• Weakness of extensor hallucis longus
• Weakness of dorsiflexion of the ankle
• Wasting of extensor digitorum brevis
Signs of S1 nerve root compression:
• Decreased sensation of S1 dermatome
• Weakness of plantarflexion of the ankle
• Weakness of eversion of the subtalar joint
• Absent or diminished ankle jerk
Lumbar ‘central disc’ prolapse causing cauda equina syndrome is rare but
is a surgical emergency.
Onset is sudden. Pain is felt in the back and radiates down the back of
both thighs and legs.
Numbness is in the same distribution, often extending into the soles of the
feet and perineum (saddle anaesthesia). Ankles, sphincters of the bowel
and bladder are weak or paralysed. There are absent ankle jerks. The patient
must go for immediate spinal decompression.
307
75 Local anaesthetics

Tell me the action of local anaesthetics.
How much anaesthetic is in a 1 per cent solution?
What are the different types of local anaesthetics?
What are the uses and complications of the various local anaesthetics?
How can local anaesthetics be administered?
What is the maximum dose of lidocaine 2 per cent that you could give a
70 kg man?
Why do local anaesthetics work less well in the presence of infection?
How does adrenaline mixed with local anaesthetic act and when should
it not be used?
What is Marcain Heavy?
Related topics
Topic Chapter Page
Action potential 85 353
Circumcision 29 91
Tracheostomy 42 148
308
PRINCIPLES OF SURGERY local anaesthetics
ACTION
Local anaesthetics are all sodium channel blockers of some sort. They cause reversible
blockade of motor and sensory nerves depending on type, concentration and site of
administration. They prevent influx of sodium in peripheral nerves, thus inhibiting
the propagation of the action potential.

How much anaesthetic is in a 1 per cent solution?
1 mL of a 1 per cent solution contains 10 mg of local anaesthetic. Likewise,
1 mL of 2 per cent contains 20 mg.
DIFFERENT TYPES
Ester class
Only cocaine still in frequent use for topical anaesthesia.
Amide class
• Lidocaine (formerly called lignocaine): short acting, usually available as 0.5 per
cent, 1 per cent and 2 per cent solutions
• Prilocaine: highest therapeutic index, safest agent for intravenous blockade.
• Bupivacaine: longer acting than lidocaine. Often used in epidurals. Levo-
bupivacaine now used extensively for local infiltration to minimize wound pain
postoperatively.
Maximum dose
Local (mg/kg) without Maximum dose (mg/kg)
anaesthetic adrenaline with adrenaline Common uses
Lidocaine 3 5 (infiltration) Local infiltration
Short-acting nerve blocks
Epidural top-ups
Bupivacaine 2 3 (do not use adrenaline Local
(Marcain) in spinals or epidurals!) infiltration (either alone or in
combination with lidocaine)
Epidurals
Spinals
Prilocaine 6 6 Regional nerve blocks
Bier’s block
309
Key learning point

Complications
Rather than remembering a long list, the complications of local anaesthet-
ics are all related to their membrane-stabilizing characteristics. These
effects are predominantly on the CNS and cardiovascular system:
CNS Cardiovascular system
Fitting Hypotension
Coma: leading to death (hypoxia) Cardiac arrhythmias
Acute cardiovascular collapse
ROUTES OF ADMINISTRATION
• Local infiltration
• ‘Field blocks’ and nerve blocks (e.g. femoral nerve block for neck of femur
fracture analgesia)
• Spinal anaesthesia: ‘one-off’, medium to short acting
• Epidural anaesthesia: longer acting, indwelling catheter; more problems with
potential infection
• Intravenous administration: most often used in a Bier’s block for manipulation
of a Colles’ fracture. Note that resuscitation facilities must be available in case
of cuff failure

What is the mechanism of hypotension in epidural and spinal anaesthesia
and what is the treatment?
The mechanism is blockade of the sympathetic outflow to the vasculature and
treatment is reduction of the epidural rate if possible, colloids to increase
blood volume and rarely vasoconstrictors, and potential complications.
CALCULATING THE MAXIMUM DOSE

Example
What are the maximum doses, with and without adrenaline (epinephrine), of 2 per
cent lidocaine that can be given to a 70 kg man?
• Maximum dose:
without # 3 mg/kg with # 5 mg/kg
310
• For a 70 kg man:
without & 3 ' 70 & 210 mg with & 5 ' 70 & 300 mg
• As 1 mL of 2 per cent solution contains 20 mg, for a 70 kg man:
without & 210/20 & 10.5 mL with & 300/20 & 15 mL
LOCAL ANAESTHETICS AND INFECTION

Infection promotes an acidic environment in the tissues with a great deal of anaerobic
metabolism. Local anaesthetics penetrate the cell membrane in an uncharged form. In
such an acidic environment the molecules become charged and cannot therefore pene-
trate the membrane and exert their effect.
Local anaesthetic infiltration can also spread cellulitis in the tissues.
LOCAL ANAESTHETICS AND ADRENALINE

Adrenaline is a vasoconstrictor; when mixed with local anaesthetics it:
• Increases the total dose of anaesthetic possible because it limits blood flow
though the tissue infiltrated, thus limiting clearance into the plasma.
• Local vasoconstriction can be useful surgically – blanching of the skin allows the
surgeon to see exactly where the anaesthetic has infiltrated and it provides a more
bloodless surgical field, particularly in highly vascular tissue such as the scalp.
• It must not be used near end-arteries, e.g. digital blocks and penile surgery.

What is Marcain Heavy?
This is bupivacaine prepared in a dextrose solution to increase its viscosity
and weight. It is used in spinal anaesthesia to keep the local anaesthetic
localized around the spinal cord for longer.
Care must be taken with its use in this context because patient positioning
is crucial. If the patient is too flat, a high concentration of bupivacaine can
gravitate to the high cervical cord and brain stem, causing problems with
respiration and maintenance of blood pressure (‘a total spinal’).
311
76 Operating theatre design and infection control

How would you best design an operating theatre suite?
Also what are the features of an operating theatre that promote an aseptic
environment?
What is the definition of asepsis?
What is aseptic technique?
What do you understand by the term ‘laminar flow’?
Describe how you would ‘scrub up’.
What antiseptics are commonly used to scrub up?
Describe clothing used in theatre to minimize infection risk to both
surgeon and patient.
What patient factors can be involved in reducing risk of postoperative
infection?
Related topics
Topic Chapter Page
HIV and universal precautions in surgery 57 219
Diathermy 71 291
Key learning point

Operating theatre design neatly leads on to infection control in a viva situ-
ation and allows you to show your knowledge of ideal theatre geography and
the various mechanisms and procedures designed to control infection risk.
OPERATING THEATRE DESIGN

• Theatres should ideally be situated away from the ground floor and main
hospital ‘traffic’ including the main entrance
• Theatres should be on the same level as the ITU (intensive therapy unit) and
surgical ward
• There should be a minimum distance from the operating theatre to A&E and
radiology (particularly CT, angiography suite and plain radiography)
312
PRINCIPLES OF SURGERY operating theatre design and infection control
• Sterile services within the unit

• Anaesthetic rooms adjacent to theatre
• Adequate room for storage and staff recreation
• Minimization of the number of people in theatre reduces the overall bacterial
load in the theatre air
• Theatres should be next to each other to minimize movement of staff and
equipment.
INFECTION CONTROL ZONES

• Outer zone: patient reception area
• Clean zone: between reception and theatre; no outside clothing
• Aseptic zone: within the theatre itself
• Dirty zone: disposal areas (sluice) and dirty corridors.
LAMINAR AIR FLOW AND POSITIVE PRESSURE SYSTEMS IN THEATRES

Airborne bacteria are thought to be a source of postoperative wound infection and
sepsis, now proven in the case of orthopaedic prosthetic joint implants.
Positive pressure ventilation systems use filtered air that enters via the ceiling in
theatre and leaves via the door flaps. There is a higher pressure in clean/ultra-clean
areas and lower in dirty areas, encouraging the flow of air and therefore any poten-
tial airborne pathogens from clean to dirty areas.
In the case of positive pressure systems, the number of complete air changes per
hour is a minimum of 20, but routine checks of bioload are not required.
Laminar flow is an upgraded version of positive pressure ventilation, ensuring lam-
inar or non-turbulent flow of air at approximately 300 air changes per hour. The air
is recirculated through a HEPA (high efficiency particulate air) filter.
Laminar flow has found particular favour in orthopaedics where the consequences
of prosthetic joint infection are disastrous. Laminar flow has been shown to reduce
the infection rate in orthopaedic theatres almost as much as getting the surgeons to
wear air-tight ‘space suits’.
ASEPSIS AND ASEPTIC TECHNIQUE

The term ‘asepsis’ refers to methods that prevent wound contamination by ensur-
ing that only sterile objects and fluids come into contact, and also by minimizing
the risk of airborne contamination. This should not be confused with ‘antisepsis’,
which is the use of solutions for disinfection (e.g. alcohol, chlorhexidine, iodine)
but does not necessarily imply sterility.
313
Thus, when describing an operation, the phrase ‘aseptic technique was used at all
times’ implies that the surgeon maintained strict asepsis towards the wound.
SCRUBBING UP
• 3- to 5-minute scrub at the beginning of the operating list using sterile, single
use sponges or polypropylene bristled brushes
• Water should run from ‘clean to dirty’ and therefore from fingertips to elbows
• Hands should be dried using single-use sterile towels, again from ‘clean to
dirty’
• Too much scrubbing causes skin abrasions and results in more bacteria being
brought to the skin surface
• After this, effective handwashing between cases should be all that is required.
SKIN ANTISEPTICS
• Chlorhexidine gluconate 4 per cent (Hibiscrub): broad spectrum and persists
with a cumulative effect
• Povidone–iodine (Betadine): used if surgeon is allergic to chlorhexidine. Less
prolonged effect than chlorhexidine.
CLOTHING IN THEATRE
• Gowns: woven cotton poor at preventing bacterial passage. Disposable, non-
woven PTFE (polytetrafluoroethylene), Goretex or tightly woven polycottons
are the ideal.
• Masks: no evidence to suggest that in standard abdominal procedures masks
decrease the risk of postoperative infection. They continue to be worn to
prevent risk of blood-borne viral transmission from the patient to the surgeon.
If worn, they should be single use and made of synthetic fibres containing filters
of polyester or polypropylene.
• Eye protection: as part of ‘universal precautions’, eye protection should be worn
to protect the surgeon from blood-borne viruses.
• Hair and beards must be covered at all times.
• Footwear: no obvious role in the spread of infection; need to protect from
sharps injury; boots in genitourinary surgery.
• Gloves: although improving, 20–30 per cent of all surgical gloves have
imperceptible holes in them by the end of an operation. Double gloving
improves this but at the expense of ‘feel’ and dexterity. Gloves should be single
use and sterilized by irradiation.
314
PATIENT FACTORS
• Short preoperative stay if possible to prevent nosocomial colonization
• Patient should be shaved in theatre and not on the ward because this increases
the risk of infection
• Ward blankets and clothing should be removed before entering theatre.
PREPARING THE SKIN

• Operation site and surrounding area should be cleaned using a sponge or swab
impregnated with detergent
• Skin is then prepared using an alcohol-based solution of chlorhexidine or
povidone–iodine. This should completely dry for adequate antisepsis. Care with
diathermy; alcohol should not be allowed to pool in the umbilicus or under the
perineum (see ‘Diathermy’, Chapter 71, page 291)
• Skin should be prepared from the cleanest area to the dirtiest area as with all
aspects of aseptic technique. Savlon (cetrimide and chlorhexidine) can be used
in perineal or vaginal antisepsis.
315
77 Screening in surgery

What do you understand by the term ‘screening’?
What are the desirable features of a screening programme?
What characteristics should a screening test have?
What do you understand by the terms ‘sensitivity’ and ‘specificity’?
What biases are associated with screening?
What are the potential advantages and disadvantages of screening for
cancer?
Related topics
Topic Chapter Page
Aneurysms 46 165
Statistics and clinical trials 79 326
Tumour markers 63 252

What is the definition of screening?
Screening is population testing of otherwise well and asymptomatic
individuals in order to identify a particular disease or its pre-morbid state.
This can be targeted at the whole population (breast cancer screening)
or at certain high-risk groups (patients with Barrett’s oesophagus for
oesophageal carcinoma). Screening tests are not usually diagnostic and
further investigations are required to establish the diagnosis.
DESIRABLE FEATURES OF A SCREENING PROGRAMME

Based on the guidelines of the World Health Organization (WHO):
• The disease being screened for should be an important health problem
• Natural history of the disease must be understood
316
PRINCIPLES OF SURGERY screening in surgery
• There should be a detectable early stage to the disease

• Treatment at the early stage should be of more benefit than at a later stage
• There should be a test available for detecting the early stage of the disease. The
test should be:
• sensitive (detects most cases, few false negatives)
• specific (few false positives)
• replicable
• safe
• acceptable screening test with a high compliance rate
• inexpensive
• Intervals for repeating the test should have been determined
• There should be adequate healthcare provision to manage the extra clinical
workload brought about by the screening
• Facilities for treatment must be available
• Benefit of reduced morbidity and mortality by detecting the disease earlier in its
course by screening.

What do you understand by the terms ‘sensitivity’ and ‘specificity’?
Sensitivity: the ability of the test to detect all the people who actually have
the disease, i.e. true positives. A high sensitivity is required so that large
numbers of people with the disease are not missed.
Specificity: the ability of the test to exclude the disease in those who actually
do not have it, i.e. few false positives. A high specificity is required so as not
to diagnose falsely or worry people who do not actually have the disease.
Biases associated with screening

Selection bias
Health-conscious individuals are likely to take part in screening programmes.
Length–time bias
Increased survival as a result of detection of slow-growing tumours with a better
prognosis.
Lead-time bias
Malignant tumours are likely to be picked up at an earlier stage and therefore lead
to increased survival time.
Diagnosis bias
This is the inclusion of individuals with pre-invasive conditions that would not have
generally progressed to invasive disease.
317
EXAMPLES OF SCREENING IN SURGERY

Cancer screening
Advantages
• Improved prognosis
• Less radical treatment regimens for early stage of the disease
• Reassurance to patients without pathology.
Disadvantages
• Treatment may not always alter the outcome and therefore patient will suffer
morbidity longer as a result of earlier diagnosis
• Screening test may be invasive and have associated complications
• False positives may lead to unnecessary treatment
• False negatives give false reassurance.
There are currently two national screening programmes available in the NHS.
Breast cancer
• Set up in 1988 following the Forrest Report
• All 50- to 70-year-old women invited for 3-yearly cycle of screening, although
those with a strong family history are screened earlier
• Women aged over 70 no longer receive an invitation but may request
screening
• Mammography is best screening tool available but detects only 95 per cent of
breast cancers
• Two views: craniocaudal (CC) and oblique views at each visit
• Abnormal mammogram initiates patient recall to specialist units for further
assessment and treatment
• 25 per cent of breast cancers are not palpable clinically
• NHS breast-screening programme is thought to save at least 300 lives a year and
this is likely to rise to 1250 by 2010, with the continued expansion and uptake of
the service. Overall breast cancer screening has been shown to reduce the mortality
rate by about 30 per cent in women aged over 50. However, there is some debate
about the effectiveness of the programme, with some of the decreased mortality
attributed to increased health awareness and treatments such as Tamoxifen.
Cervical cancer
• Cervical smear tests begin 3 years after commencement of sexual activity
• False-negative rate 10 per cent
• Labour intensive
• Compliance 80 per cent.
318
Colorectal cancer
Controversial; only in widespread use in the USA.
Main methods for screening are:
• Digital rectal examination (DRE)
• Rigid sigmoidoscopy
• Faecal occult blood (FOB)-positive patients undergo colonoscopy in the USA.
There is a low compliance rate and it is a costly exercise
• Serum tumour markers (CEA)
• Flexible sigmoidoscopy
• Colonoscopy
• Barium enema.
Better to screen for high-risk individuals for developing colorectal cancer, e.g.
• Long-standing ulcerative colitis
• Familial adenomatous polyposis coli
• Peutz–Jeghers syndrome
• Ureterosigmoidostomy
• Strong family history of colorectal cancer.
Abdominal aortic aneurysm

Not yet in place as a national screening programme but should be.
The Multicentre Aneurysm Screening Study (MASS) showed reduced mortality
from screening men over the age of 65 by a single abdominal ultrasound for abdom-
inal aortic aneurysms. Shown also to be cost-effective and give a better quality of
life. There was a high acceptance rate (80 per cent) in this study.
Prostate cancer
There is currently no national programme for screening for prostate cancer. There is
no definitive treatment available and there is the debate of using prostate-specific
antigen (PSA) as a screening tool (see ‘Tumour markers’, Chapter 63, page 252).
Stomach cancer
This is effectively performed in Japan with endoscopic surveillance.
Neonatal screening
In the form of postnatal checks, e.g. congenital dislocation of the hip, imperforate
anus and sexual abnormalities.
319
78 Skin grafting and flap reconstruction

What is a skin graft?
What are the differences between a split- and a full-thickness skin graft?
When would you use a skin graft?
From where would you harvest a skin graft?
Describe how you would harvest a split-skin graft.
Why do skin grafts fail?
What tissues do skin grafts not take on?
What is a flap?
How does a flap differ from a graft?
What are the principles of flap surgery?
How would you classify flaps?
How is the viability of a flap assessed?
What measures can be undertaken in the event of vascular compromise?
How is the donor site managed?
What complications need to be discussed with the patient before surgery?
Related topics
Topic Chapter Page
Burns 107 427
Key learning points

Definitions
A skin graft is a piece of skin transferred without a blood supply from a
donor site to reconstruct a defect
A flap is a volume of tissue transferred from a donor site to reconstruct a
defect while maintaining its own blood supply
A flap is dependent on its own blood supply. A graft is entirely dependent
on a vascular bed at the recipient site to establish a new blood supply
A pedicle is the attachment of a flap through which it receives its blood supply
320
PRINCIPLES OF SURGERY skin grafting and flap reconstruction
SKIN GRAFTS
Types of skin grafts
Skin grafts can be split thickness, full thickness, dermal or composite; they can also
be autografts, allografts or xenografts.
• Split thickness: epidermis and a thin layer of dermis
• Full thickness: epidermis and entire dermis
• Dermal: dermis only
• Composite: skin and an underlying structure (e.g. skin " cartilage from the ear).
Full thickness vs split thickness

Graft type Advantages of each type
Split thickness • More likely to ‘take’ – can survive longer by imbibition
• Less donor site scarring
• Suitable for larger grafts
• Can be meshed to cover a larger area
Full thickness • Better skin colour match
• Less contour defect
• More durable
• Less contracture of graft bed
• Adnexal structures are maintained (hair follicles, sweat glands)
Stages of graft take

• Adherence: a fibrin bond is formed between the graft and the bed.
• Imbibition: intracellular proteoglycans within the graft break down into smaller,
more osmotically active subunits. Interstitial fluid is absorbed, providing
nutrition to the graft, but causing graft swelling.
• Re-vascularization: ingrowth of vascular tissue into the graft differentiates into
afferent and efferent vessels, linking with graft vessels and restoring circulation.
Thicker grafts take longer to re-vascularize.
• Maturation: regeneration of appendages (hair follicles and sweat glands).
Re-innervation from graft edges.
Failure to take
Acute graft failure can occur as a result of the patient, the graft bed or the graft.
Although many factors can affect graft take, the three main causes for failure are
indicated in bold below:
• Shearing forces between graft and bed (disrupts re-vascularization)
• Graft separated from bed by seroma or haematoma
• Infection (especially beta-haemolytic streptococci)
321
• Unsuitable or avascular graft bed (poorly perfused tissues, exposed tendon,

cartilage, bone)
• Poor healing
• Poor graft handling
• Graft laid incorrectly.
Skin grafting technique
Graft type Common donor sites

Split-thickness skin graft • Thigh
• Abdomen
• Buttock
• Back
• Palm
Full-thickness skin graft • Groin crease
• Base of neck
• Pre-auricular
• Post-auricular
• Upper arm
• Upper eyelid
Split-thickness skin grafts are harvested with a dermatome, slicing a predetermined

thickness of skin from the donor site. This can be either a hand-held guarded knife
(e.g. Watson knife) or an air-powered dermatome (e.g. Zimmer air dermatome).
During graft harvest, the donor site is thoroughly lubricated with paraffin. An assist-
ant ensures that the site is flat by supporting the surrounding tissues and stretching
the area with a flat edge (e.g. a wooden board). The graft is harvested with the der-
matome and laid onto a flat board, and covered with a saline-soaked swab until ready
for use. The graft can be fenestrated, reducing the risk of fluid accumulating under the
graft, or meshed, allowing the graft to cover a larger area. Common mesh sizes are
1:1.5 and 1:3.
Full-thickness grafts are excised with a scalpel as an ellipse of skin, which is closed
directly. Any beads of subcutaneous fat are excised from the underside of the graft
and it is stored in a saline-soaked swab until ready for use. Full-thickness grafts can
also be fenestrated.
To minimize the chances of graft failure, haemostasis is achieved at the recipient
site to avoid development of a haematoma under the graft. The graft is laid onto the
bed, dermal (shiny) side down, and secured with a pressure dressing, reducing
shearing between the graft and the bed, and further reducing the likelihood of
haematoma or seroma under the graft.
322
Complications of skin grafts

• Partial or total graft failure
• Infection
• Bleeding
• Donor site pain and morbidity
• Need for further surgery.
FLAPS
Classification
Flaps can be classified in terms of the type of tissue transferred, the nature of the vas-
cular patterns of the tissues and the proximity to the defect requiring reconstruction.
Type of tissue
• Skin
• Fascia
• Fasciocutaneous
• Muscle
• Myocutaneous
• Bone/Osseocutaneous/Osseomyocutaneous
• Visceral (e.g. colon, small intestine, omentum)
• Innervated muscle flaps.
Vascular patterns
• Random pattern
• Axial pattern.
Random pattern flaps have no dominant blood supply. They rely on many unnamed
small vessels to provide a blood supply via the base of the flap. This limits the
length:breadth ratio to 1:1. Axial pattern flaps rely on a blood supply from a single
vessel or a group of recognized vessels, allowing flaps to be raised that are as long as
the vascular territory of their axial vessels.
Proximity to defect
• Local
• Distant
• Free.
A local flap is immediately adjacent to the defect and is transposed, advanced or
rotated into place. A distant flap remains attached to the body at the pedicle and
can be moved over a greater distance. A free flap is completely detached from the
body and regains a blood supply by microsurgical anastomosis of the vessels within
the pedicle to recipient vessels near the defect.
323
Flap failure and monitoring

Clinical evaluation is the best method of flap assessment:
• Flap colour (relative to skin adjacent to the donor site)
• Capillary refill time
• Skin turgor
• Skin temperature
• Bleeding after a pinprick or scratch test (avoid the pedicle)
• Hand-held Doppler ultrasonography
• Pulse oximetry
• Adhesive skin temperature probes.
Insufficient arterial supply – clinical signs

• Pallor
• Skin coolness
• Slow capillary refill ! 2 seconds
• Slow or absent bleeding on pinprick test
• No palpable pulse.
Insufficient venous outflow – clinical signs

• Blue to purple dusky hue
• Brisk capillary refill % 1 second
• Brisk dark blood on pinprick test
• Tense, swollen flap.
Factors leading to vascular compromise

• Tight dressings: loosen any tight dressings
• Tight sutures: release alternate/all sutures as necessary
• Pressure on the flap or pedicle from positioning: reposition the patient away
from the flap
• Haematoma impeding vascular in-/outflow: immediately release sutures and
return to theatre to evacuate the haematoma
• Vasoconstriction: avoid:
• dehydration – urine output % 1 mL/kg per h
• cold – ensure room is warmed
• nicotine
• caffeine
• pain – adequate analgesia
• Kinking of, or clot within, the flap pedicle: urgent return to theatre and consider
the use of local thrombolysis, dextran, heparin or aspirin.
Urgent re-exploration is essential if these fail to provide a rapid improvement.
324
Complications of flap surgery

• Partial or total flap failure
• Infection
• Bleeding and blood transfusion
• Anticoagulation requirements
• Donor site morbidity
• Need for re-exploration
• Reoperation for flap adjustment
• Anaesthetic complications of major surgery, including death.
325
79 Statistics and clinical trials

What types of clinical trial do you know?
What is meant by the power of a trial?
Define type I and type II statistical error.
What is meant by the sensitivity and specificity of a clinical test?
Which type of clinical trial has the most statistical power and why?
What is an odds ratio?
What is a 95 per cent confidence interval?
What is the difference between parametric and non-parametric statistics?
What is a meta-analysis and what is its purpose?
CLINICAL TRIAL TYPES

Clinical trials can be prospective or retrospective with the latter having a higher stat-
istical power than the former.
Observational cohort study

• Usually retrospective but can be prospective
• Observational investigation where a group of individuals with a specific disease
or characteristic are followed over a period of time to detect complications or
new events
• Comparisons may be made with a control group
• No interventions are normally applied to the participants.
Case–control study
• Usually retrospective but can be prospective
• Observational investigation in which characteristics of people with a condition
(cases) are compared with a selection of the population without the disease
(controls).
Cross-sectional study
• Usually retrospective
• A survey of the frequency of a disease or risk factor in a defined population at a
given time
326
PRINCIPLES OF SURGERY statistics and clinical trials
• Used to assess prevalence

• Cannot evaluate statistical hypotheses but can suggest statistical associations and
generate hypotheses.
Controlled trial
• Intervention under investigation is applied to one set of individuals
• Outcome compared with a similar group (the control group) not receiving that
particular treatment
• In drug trials the control group usually has a placebo, eliminating placebo effect
in the intervention group.
Randomized trial
• Participants are placed in a particular arm of the investigation in a random way,
rather than via the conscious choice of the investigator or participant
• Eliminates selection bias
• Ensures that confounding factors are spread evenly throughout the trial
groups.
Blinded (or masked) trial

• Either investigators or patient is unaware of treatment group to which the
participant has been assigned
• Eliminates assessment bias.
Double-blinded (double-masked) trial

• Both investigators and patient are unaware of treatment group to which the
patient has been assigned
• Eliminates both assessor and patient bias.

Which type of clinical trial has the most statistical power and why?
A double-blind randomized placebo-controlled trial has the most statistical
power by eliminating as much bias as possible and spreading confounding
factors evenly between the different trial arms. It ensures that statistical
samples come from truly random dataset, allowing the use of more powerful
statistics that make assumptions about randomization and population
distributions (see later).
327
STATISTICAL POWER AND P VALUES

Statistical power is defined as the ability of a study to demonstrate an association
or causal relationship between two variables, given that an association actually
exists. For example: 90 per cent power in a clinical trial means that the study has a
90 per cent chance of ending up with a p value " 0.05 in a statistical test if there
really is an important difference (e.g. 30 per cent versus 15 per cent mortality rate)
between treatment groups.
The p values
The probability (ranging from 0 to 1) that the results observed in a study (or more
extreme results) could have occurred by chance.
Convention dictates that we take a p value " 0.05 to indicate statistical signifi-
cance. It is worth bearing in mind that this could still mean that there is a 1 in 20
chance that a ‘statistically significant’ result could have occurred by chance!
The meta-analysis
Although not strictly a clinical trial, this is a study that attempts systematically to
merge the results from many clinical trials that are trying to answer the same clin-
ical question, in an attempt to increase the statistical power through an increase in
the overall number of cases.
STATISTICAL ERROR
Broadly statistical error can be divided into two: type I and type II errors.
Type I error
A true null hypothesis is incorrectly rejected (i.e. although there is no difference
between two groups, chance has shown there to be a statistical difference and the
null hypothesis is incorrectly rejected).
Type II error
Rejection of the alternative hypothesis when it is true (i.e. although there is a dif-
ference between two groups, it is determined that there is no difference).
The 95 per cent confidence intervals

This quantifies the uncertainty in measurement of a value. A 95 per cent confidence
interval (CI) gives a range in which there is a 95 per cent confidence that the unknown
value will lie within that range. Usually expressed as 95 per cent CI in clinical jour-
nals and gives much more information than a simple p value. Many high-impact fac-
tor journals now insist on the quotation of 95 per cent CIs.
328

What is meant by the sensitivity and specificity of a clinical test?
Sensitivity: the sensitivity of a test is the proportion of people with the dis-
ease who have a positive test result (the higher the sensitivity, the greater
the detection rate and the lower the false-negative rate)
Specificity: the specificity of the test is the proportion of people without
the disease who have a negative test (the higher the specificity, the lower
will be the false-positive rate)
Predictive value
• The positive predictive value of a test is the probability of a patient with
a positive test actually having a disease
• The negative predictive value is the probability of a patient with a nega-
tive test not having the disease
A confidence interval that includes 0 implies that the treatment effect is not statis-
tically significant.
Odds ratios in clinical trials

The ratio of the odds of having the target disorder in the experimental group relative
to the odds in favour of having the target disorder in the control group.
An odds ratio is calculated by dividing the odds in the treated or exposed group by
the odds in the control group.
Parametric and non-parametric statistics
For parametric statistics to be valid, they make an assumption that the groups being
compared are randomly sampled and conform to a normal distribution. Typical
examples of parametric statistics are Student t-tests and (2 (chi-squared) tests.
For non-parametric statistics to be valid, they make an assumption that the groups
being compared are randomly sampled, but they make no assumptions about the
distributions that they follow. Non-parametric statistics are not as statistically power-
ful as parametric statistics but are useful in circumstances where populations do not
conform to the normal distribution.
329
80 Stomas

What are the indications for forming a stoma?
What are the uses of a stoma?
How would you classify them further?
How would you prepare a patient who is going for surgery that will
involve formation of a stoma?
What are the principles of siting a stoma?
What are the potential complications of a stoma?
What are the differences between an ileostomy and a colostomy?
Why are ileotomies fashioned with a spout?
How would you rehabilitate a patient following creation of a stoma?
What is a mucous fistula?
Related topics
Topic Chapter Page
Diverticula 55 210
DEFINITION
A stoma is an artificial opening brought up on to the body surface.
INDICATIONS
• Decompression, e.g. caecostomy
• Exteriorization/drainage:
• perforated or contaminated bowel, e.g. distal abscesses/fistula
• permanent stoma, e.g. abdominal perineal excision of rectum (APER)
• Enteral feeding, e.g. percutaneous endoscopic gastrostomy (PEG) after
gastrointestinal (GI) surgery, in CNS disease or in coma
• Faecal stream diversion:
• protect a distal anastomosis: previously contaminated bowel; technical consid-
erations – low anterior resection or ileorectal anastomosis
• urinary diversion after a cystectomy
330
PRINCIPLES OF SURGERY stomas
• Diversion, e.g. pharyngostomy or oesophagostomy: to divert solids and liquids

in order to protect the bronchial tree in neonates with oesophageal atresia or
tracheo-oesophageal fistula
• Lavage: appendicostomy for large bowel washout.
CLASSIFICATION
Temporary
PEG tube, pharyngostomy, oesophagostomy, caecostomy, loop ileostomy or trans-
verse colostomy.
Permanent
End-colostomy after an abdominoperineal resection (APER), or end-ileostomy after
a panproctocolectomy.
PREOPERATIVE PREPARATION
• Psychosocial and physical preparation
• Informed consent with risk and benefits explained
• Use of a clinical nurse specialist in stoma care – who would also mark the site.
STOMA SITE
Generally:
• 5 cm away from umbilicus (not for PEG)
• Away from scars or skin creases
• Away from bony prominences or waistline of clothes
• Site that is easily accessible to the patient – not under a large fold of fat!
• Stoma must be within the rectus abdominis, otherwise parastomal herniation
will occur and obstruction and pain will ensue (not for PEG)
• Need to consider patient’s mobility and eyesight.
COMPLICATIONS
• General versus specific
• Technical versus general versus practical
• Immediate (% 24 hours), early (% 1 month) or late (! 1 month).
General
This is related to the underlying disease:
• Stoma diarrhoea: water and electrolyte imbalance, hypokalaemia
• Nutritional disorders: vitamin B deficiency, chronic microcytic/normochromic
anaemia
331
• Stones: both gallstones and renal stones are more common after an ileostomy
• Psychosexual
• Residual disease, e.g. Crohn’s disease and parastomal fistula, metastases.
Specific
• Ischaemia and gangrene
• Haemorrhage
• Retraction
• Prolapse/intusussception
• Parastomal hernia
• Stenosis – leads to constipation
• Skin excoriation.
PRACTICAL PROBLEMS:
• Odour: advice on hygiene, diet and deodorant sprays
• Flatus: improved with diet and special filters
• Skin problems
• Leakage: especially transverse loop colostomies.

What are the differences between an ileostomy and a colostomy?
Ileostomy Colostomy
Site Right iliac fossa (RIF) Left iliac fossa (LIF)
Surface Spout (prevents irritation of underlying skin) No spout
Flush with skin
Contents Watery – small bowel Faeculent
Effluent Continuous Intermittent
Permanent Panproctocolectomy APER
Temporary Loop ileostomy after low anterior resection Hartmann’s procedure
MUCOUS FISTULA
Used in similar circumstances to Hartmann’s procedure but, instead of dropping
the rectal stump back into the abdomen, it is brought out as a separate stoma,
which being an efferent limb produces only mucus. This makes the distal limb more
accessible when the bowel is later rejoined. Also performed in inflammatory bowel
surgery because of fear of rectal stump blow-out.
332
REHABILITATION
• Diet should be normal
• Bag should be changed once or twice a day (needs to be emptied more
frequently if urine or watery small bowel contents)
• Ileotomies should have a base plate under the bag changed every 5 days and the
bag changed daily
• Psychological and psychosexual support.
333
81 Surgical sutures and needles

What criteria would the ideal suture fulfil?
How do the characteristics of a suture material affect its behaviour?
What are the characteristics of natural versus synthetic suture materials?
What are the differences between monofilament and multifilament
sutures?
How would you classify sutures? Give examples of commonly used
sutures.
Name some examples of absorbable and non-absorbable sutures.
Describe some features of one of each.
What suture-related factors may lead to wound dehiscence?
When might you use clips instead of sutures?
Describe the type of needles in common surgical use and their
characteristics.
What are the various parts of a needle called?
CRITERIA OF AN IDEAL SUTURE

• Ease of handling
• Ease of knotting
• Knot securely without fraying
• Minimal tissue reaction
• Maintain tensile strength until it has served its purpose
• Provides effective duration of wound support appropriate to the tissue and
operation in question
• Narrow diameter to minimize tissue damage and scarring
• Unfavourable suture surface for bacterial colonization
• Inexpensive
• Easily sterilized
• Not electrolytic, carcinogenic or allogeneic and does not demonstrate capillary
action.
334
PRINCIPLES OF SURGERY surgical sutures and needles
Related topics
Topic Chapter Page
Circumcision 29 91
Tracheostomy 42 148
CLASSIFICATION
• Source: natural or synthetic
• Filament type: braided versus monofilament
• Absorbability.
Natural sutures
• Handle well and relatively inexpensive
• Unpredictable absorption
• Can incite tissue reaction and fibrosis
• Absorbed by enzymatic action. They can trap bacteria and set up a localized
infection because they are not monofilament. This can lead to wound sinus
formation.
335
Synthetic sutures
• Inert; absorbed by hydrolysis
• Predictable absorption and strength
• More difficult to handle.
Braided sutures
• Easier to handle and to perform knot tying
• Can create friction, more difficult to pass through tissue than monofilament, so
therefore more likely to incite more tissue reaction
• Infection can sit within the braids.
Monofilament sutures
• Glides more smoothly through the tissues and incites less tissue reaction
• More difficult to knot and handle than braided materials.

Give examples
Suture Type Description

Polyglactin (Vicryl) Synthetic Gives wound support for 30 days. Vicryl
Braided Rapide more rapidly degraded with wound
Absorbable support for 10 days
Polydioxanone (PDS) Synthetic Slowly hydrolysed (180 days). Good tensile

Monofilament strength for 56 days. Alternative to nylon for
Absorbable abdominal closure
Catgut Natural Rapidly hydrolysed

Absorbable 7–10 days wound support. Rarely used
today
Silk Natural Evokes marked tissue reaction. Encourages

Braided formation of suture sinuses and abscesses.
Non-absorbable Avoid in vascular anastomoses and skin
closure
Polypropylene Synthetic Slides well – good for vascular anastomoses,

(Prolene) Monofilament memory (difficult to handle and knot)
Non-absorbable
Nylon (Ethilon) Synthetic Loses 10–20 per cent tensile strength per
Monofilament year. Similar characteristics to Prolene but
Non-absorbable less memory
336
FACTORS INVOLVING THE SUTURE THAT CAN LEAD TO

WOUND DEHISCENCE
• Weak suture material or inappropriate choice
• Damage to suture by a surgical instrument
• Diathermy damage to the suture
• Poor surgical technique in knotting
• Wound under high tension that can lead to necrosis.
USE OF STAPLES
Staples confer only speed of application in wound closure. They are useful when
rapid wound closure is desirable or when the wound is large and suture closure
would be laborious. Also, if there is a high chance of infection, it may be easier to
remove staples rather than sutures to open up the wound.
TYPES OF SUTURE NEEDLES

Various parts are:
• Point
• Body
• Swage – for attachment to the suture.
Characteristics
Type of needle governed by the procedure, tissue, access, gauge of the suture and
surgeon’s preference. The body of the needle can be:
• Straight: used to suture skin wounds which are easily accessible; used by hand.
• Curved: ranging from 0.5 to 0.75 of the circumference; usually manipulated
with needle holder.
• Rounded: separates but does not cut tissue; this creates a watertight
suture line.
• J-shaped: used to approximate two tissues that are typically difficult to
access within a surgical wound, e.g. closure of umbilical port site after
laparoscopy.
• Round-bodied needle: this causes minimal tissue trauma so it is suitable for

fragile or delicate tissue, e.g. bowel anastomosis.
• Conventional cutting needle: triangular in cross-section with the cutting edge
on the concave side of the needle.
337
• Reverse cutting needle: for tough tissue; triangular cross-section with the cutting
edge on the convex side of the needle. This strengthens the needle and, with the
sharp edge on the outside of the curvature, protects tissue on the inside.
• Atraumatic or blunt needle: used for friable tissue, e.g. liver, spleen, kidney,
minimizing tissue trauma. This reduces the chance of an operative needle-stick
injury.
• Taper cut needle: provides effective initial tissue penetration.
338
82 Tourniquets

When would you use a tourniquet in surgery?
What are the contraindications for using a tourniquet?
What are the potential problems associated with tourniquet use? How
would you avoid them?
What are the complications of tourniquet use?
What size of tourniquet should you use and to what pressure should the
tourniquet be inflated?
For how long should you leave a tourniquet on?
Describe the procedure for application and removal of a tourniquet. Will
you ignore your anaesthetist when removing the tourniquet?
Related topics
Topic Chapter Page
Compartment syndrome 108 433
INDICATIONS FOR TOURNIQUET USE IN SURGERY

• To produce an effective bloodless surgical field; this facilitates the surgical
procedure and allows demonstration of important structures, e.g. median nerve
during carpal tunnel decompression
• To allow effective regional anaesthesia, e.g. during a Bier’s block, which requires
a double tourniquet
• To provide temporary haemostasis in the face of catastrophic and uncontrollable
blood loss when local pressure has failed
• Tourniquet test: to look for venous incompetence in the lower limb.
CONTRAINDICATIONS
All are relative contraindications:
• Crush injury
• Peripheral vascular disease
339
PRINCIPLES OF SURGERY tourniquets
• Pro-thrombotic states
• Sickle cell disease and trait
• Also generally avoid in elderly patients.
TOURNIQUET SIZE AND INFLATION PRESSURES

The size of tourniquet can be estimated by the cuff width approximating the diam-
eter of the limb plus 20 per cent.
A lower pressure is required to occlude the arterial circulation when using a wider
tourniquet.
There is no consensus regarding what pressure the tourniquet should be inflated to,
but ideally as low a pressure as will provide arterial and venous occlusion. A com-
mon recommendation is:
• Upper limb: 50 mmHg above normal systolic blood pressure
• Lower limb: 100 mmHg above normal systolic blood pressure.
SAFE TOURNIQUET ISCHAEMIC TIMES

There is no consensus on this subject either.
This needs to be considered in relation to the patient’s other co-morbidities and
problems. A long ischaemic time will not be safe for patients with known relative
ischaemia or injury.
Correct answer is as short as possible!
Ideally 90 minutes should not be exceeded.
Ischaemia time should not exceed 120 minutes without a 20-minute reperfusion time.
PRECAUTIONS WHEN USING A TOURNIQUET

• See above
• Neurovascular status should be documented before tourniquet application and
after removal
• Check monitor and cuff before applying to patient
• A well-covered area of the limb should be chosen – avoid joints for tourniquet
application; also avoid encroachment on surgical field
• The limb should be well padded with wool
• The tourniquet should have a width of at least half the limb circumference
• Limb exsanguination should be performed ideally with an Esmarch bandage or
rubber Rhys–Davies exsanguinator. This process can also be done by limb
340
PRINCIPLES OF SURGERY tourniquets
elevation for 2 minutes. Avoid expressive exsanguination in the presence of

tumour, infection or known DVT
• Note time of inflation and the surgeon should be informed every 30 minutes
of ischaemic time; note the time of deflation.
Always request the anaesthetist’s permission to deflate and remove the tourniquet.
During prolonged ischaemia, products of anaerobic metabolism accumulate in the
limb and are effectively excluded from the general circulation. When the tourni-
quet is released, there is not only a release of an acidotic blood load but also a gen-
eral decrease in cardiac afterload. In a patient with a limited cardiac reserve and
function this can precipitate cardiac arrhythmias and ischaemia.
COMPLICATIONS
Immediate
• Post-deflation bleeding: tourniquet deflation and meticulous haemostasis before
wound closure is one way of dealing with postoperative bleeding and
haematoma formation
• Cardiovascular collapse post-deflation: caused by afterload or reperfusion injury
• Muscle damage: rhabdomyolysis
• Skin necrosis
• Arterial damage: vascular endothelial injury and thrombosis (rare).
Early
• Venous congestion: caused by inadequate pressure
• Pressure neuropathy: not caused by ischaemia
• Pulmonary embolism (rare).
Late
• Post-tourniquet palsy.
341
83 Wound healing, scarring and reconstruction

How do wounds heal?
What factors influence the quality of a scar?
What are hypertrophic scars?
What is the difference between a hypertrophic and a keloid scar?
What is the reconstructive ladder?
How would you determine which reconstructive technique to consider?
Related topics
Topic Chapter Page
NORMAL WOUND HEALING

There are three phases of normal wound healing.
Inflammatory phase (days 0–4)

• Injury causes local bleeding
• Haemorrhage is limited by vasoconstriction, mediated by adrenaline,
thromboxane A2 and prostaglandin 2)
• Collagen, exposed by the injury and subsequent retraction of endothelial cells,
activates the clotting cascade and allows platelets to attach, forming a platelet
plug
• Platelets release platelet-derived growth factor (PDGF), fibronectin, fibrinogen
and von Willebrand’s factor, stabilizing the wound through clot formation
• Capillary vasodilatation occurs as a result of release of histamine, bradykinin,
prostaglandins and nitric oxide, allowing inflammatory cells to reach the wound
site
• Neutrophils scavenge for debris, débriding the wound, and help to kill bacteria
by oxidative burst mechanisms and opsonization; the neutrophil peak occurs at
24 hours after injury
342
PRINCIPLES OF SURGERY wound healing, scarring and reconstruction
• Monocytes enter the wound and become macrophages, which secrete numerous
enzymes and cytokines, including collagenases and elastases, to break down
injured tissues; and PDGF, macrophage-derived growth factors, interleukins,
tumour necrosis factor (TNF) and transforming growth factor $ (TGF-$) to
stimulate proliferation of fibroblasts, endothelial and smooth muscle cells
• Lymphocytes also enter the wound at day 3 and have a role in cellular immunity
and antibody production.
Proliferative phase (days 4–21)

• Angiogenesis, stimulated by TNF-), is the migration of endothelial cells to form
new capillaries within the wound bed
• Type III collagen is laid down by fibroblasts, attracted and activated by TGF-$
and PDGF. Total collagen content increases until day 21
• The combination of collagen deposition and angiogenesis forms granulation
tissue
• Epithelialization occurs by one of two mechanisms, depending on whether the
basement membrane has been breached. If the basement membrane is intact,
epithelial cells migrate upwards in the normal pattern, resulting in
epithelialization in 2–3 days. In a deeper wound, a single layer of epithelial cells
advances from the wound edges to cover the wound, which then stratifies when
cover is complete. Adnexal structures such as hair follicles and sweat glands can
also provide a source of cells for epithelialization.
Remodelling phase (days 21–360)

• During remodelling, collagen is reorganized; collagenases continue to break
down existing collagen while fibroblasts and myofibroblasts continue to
synthesize new collagen along lines of tension
• Type III collagen is replaced with type I collagen
• Water is removed from the scar, allowing collagen to cross-link
• Wound vascularity decreases
• Collagen cross-linkage allows increased scar strength, scar contracture and a
decreased scar thickness.
WOUND STRENGTH
Wounds have little strength during the inflammatory and proliferative phases of
wound healing. As remodelling occurs, wounds rapidly gain strength. At 6 weeks,
the wound is at 50 per cent of its final strength. Maximum strength, which is only
75 per cent of the pre-injury tissue strength, is achieved between 6 and 12 months
after the injury.
343
ABNORMAL SCARRING
Hypertrophic scars
• Raised, red, thickened scar
• Limited to the boundaries of the original scar
• Occurs soon after injury
• Related to wound tension and prolonged inflammatory phase of healing
• Common in wounds on the anterior chest and over shoulders
• Spontaneous regression over years.
Keloid scars
• Raised, red, thickened scar
• Extends beyond the original scar boundary
• Occurs months after injury
• No regression
• More common in dark skin colour
• Significant familial tendency
• Autoimmune phenomenon
• Worsens in pregnancy, resolves after menopause
• Worsened by surgery.
FACTORS INFLUENCING SCARRING

Patient factors
• Age: infants and elderly people scar well
• Skin type: Celtic skin types are more likely to form hypertrophic scars; dark-
skinned patients are more likely to form keloid scars
• Anatomical region: anterior midline, chest and shoulders scar poorly
• Concurrent morbidity: nutritional state, diabetes, wound infection
• Local tissue: oedema, previous radiotherapy, vascular insufficiency.
Surgical factors
• Atraumatic skin handling
• Eversion of wound edges: inversion places keratinised epidermis (dead material)
between healing surfaces
• Tension-free skin closure
• Clean, healthy wound edges
• Scar orientation: parallel to lines of relaxed skin tension
• Suture tension: over-tightening leads to pressure necrosis; under-tensioning can
lead to wound gaping and widening of scar
344
• Scar length: skin ellipse length should be at least four times the width to
minimize tension and avoid dog-ears
• Suture type: non-absorbable synthetic sutures cause least inflammation
• Timing of suture removal:
• 7 days or less leaves no stitch marks
• 14 days or more leaves stitch marks
• between these times depends on skin type and wound location.
THE RECONSTRUCTIVE LADDER

Closing wounds and repairing defects are fundamental surgical skills. There are many
techniques available for reconstruction and the reconstructive ladder is a useful sys-
tematic approach to the process of reconstructing a defect.As the ladder is descended,
surgery becomes more complex and risk to the patient increases. This approach of
considering simple techniques before complex techniques, allows defects to be recon-
structed with the least risk to patients (see ‘Skin grafting and flap reconstruction’,
Chapter 78, page 320):
• Allow to heal
• Primary closure
• Delayed primary closure
• Tissue expansion
• Split-thickness skin graft
• Full-thickness skin graft
• Local flap (a flap raised immediately next to the defect)
• Distant flap (a flap raised some distance from the defect, maintaining a vascular
supply through a pedicle)
• Free flap (a flap completely detached from the body and re-anastomosed to
vessels close to the defect).
345
6
PART
APPLIED SURGICAL PHYSIOLOGY

84 Acid–base balance 349
85 Action potential 353
86 Altitude 356
87 Blood pressure control 358
88 Calcium homoeostasis 362
89 Cardiac action potential 366
90 Cerebrospinal fluid and the blood–brain barrier 369
91 Control of respiration 373
92 Functions of the kidney I 376
93 Functions of the kidney II: fluid and electrolyte balance in the
kidney and the loop of Henle 377
94 Functions of the kidney III: endocrine functions of the kidney 381
95 Functions of the kidney IV: other functions 383
96 Functions of the liver 384
97 Functions of the stomach 388
98 Neuromuscular junction 391
99 Oxygen transport 394
100 Pituitary 397
101 Starling forces in the capillaries/oedema 401
102 Starling’s law of the heart and cardiovascular equations 403
103 Swallowing and oesophageal physiology 408
84 Acid–base balance

What is an acidosis? Give examples.
What is an alkalosis? Give examples.
How would this acidosis/alkalosis be compensated?
What are the harmful effects of acidosis?
What is the anion gap?
What is renal tubular acidosis?
Related Topics
Topic Chapter Page
Respiratory failure and respiratory function tests 119 495
Altitude 86 356
Criteria for admission to ITU and HDU 109 439
Key definitions
An acidosis (or acidaemia) is an excess of H! ions in the blood (buffered or
otherwise).
An alkalosis (alkalaemia) is a deficiency of H! ions in the blood (buffered or
otherwise).
Normal range of pH is 7.35–7.45.
Base excess (normal value 0) measures how far removed bicarbonate is from its
normal value.
A buffer is a weak acid, the presence of which prevents large fluctuations in the
concentration of H!. This text deals mainly with the bicarbonate/carbonic acid sys-
tem, but, in the urine, phosphate buffers H! ions.
Buffering in the blood

A small proportion of H! is buffered by haemoglobin and the plasma proteins, but
the majority is buffered by the bicarbonate/carbonic acid system.
H2O ! CO2 L H2CO3 L H! ! HCO3"
349
APPLIED SURGICAL PHYSIOLOGY acid–base balance
CO2 acts as an acid, because it pushes the equilibrium to the right and produces
more H!.
HCO3" acts as a base, because it pushes the equilibrium to the left and eliminates H!.
The equilibrium between bicarbonate and carbonic acid and the H! concentration
is referred to by the Henderson–Hasselbalch equilibrium:
pH # pK ! log[HCO3"]/[H2CO3]
where K # dissociation coefficient of carbonic acid.

The kidney is responsible for HCO3" homoeostasis (see ‘Functions of the kidney II’,
Chapter 93, page 377) and the lungs control CO2, enabling the pH to be tightly con-
trolled (discussed below).
Diagnosing blood gases: an algorithm

Step 1: what is the pH?
If ! 7.35, it is an acidosis.
If " 7.45, it is an alkalosis.
Step 2: what is the cause of this?

Acidoses
• If PCO2 $ 5.3 kPa, respiratory acidosis (high PCO2; retained CO2, which is an
acid)
• If HCO3" % 24 mmol/L, metabolic acidosis (high H!, low HCO3") (see above;
equilibrium pushed to left)
Alkaloses
• If PCO2 % 4.8 kPa, respiratory alkalosis (low PCO2, CO2 being lost)
• If HCO3" $ 28, metabolic alkalosis (low H!, therefore high HCO3")
(equilibrium to right).
Can use base excess quickly to diagnose metabolic alkalosis or acidosis in the clin-
ical setting (negative in acidosis, positive in alkalosis).
Note that the base excess is positive in a respiratory acidosis by the Henderson–
Hasselbalch equation. It refers to the amount of acid that should be added to the
solution to make it neutral.
Step 3: compensation?
This is more difficult. Respiratory causes are always compensated for by metabolic
change and metabolic causes are always compensated for by respiratory change.
350
In vivo, respiratory compensation is fast (breathe faster to eliminate CO2 [acid] or

slower to retain it) and metabolic compensation is slow (kidney buffers and excretes
or retains HCO3" [base]).
Compensated respiratory acidosis
HCO3" rises to try to correct high PCO2.
Compensated metabolic acidosis
PCO2 drops to try to correct high H!.
Compensated metabolic alkalosis
PCO2 rises to try to correct high HCO3".
Compensated respiratory alkalosis
HCO3" drops (eliminated by kidney) to try to correct low CO2 (acid) and hence
low H!.
Separate to acid–base analysis, but relevant to blood gases, is the assessment of the
patient’s oxygenation, which involves looking only at the PO2 and PCO2.
If the PO2 is ! 8 kPa, the patient has respiratory failure.
Assuming respiratory failure, if the PCO2 is % 6.7 kPa, this is called type 1 respira-
tory failure; if it is above this figure it is called type 2 respiratory failure.
Of course, these figures depend on the concentration of inspired oxygen – FIO2 – in
ventilated patients. The difference between the PO2 in the alveoli and arteries is
referred to as the alveolar–arterial or A–a gradient. As a guide, it should be no more
than 10, so the expected PAO2 can be calculated by subtracting 10 from the FIO2.
If the FIO2 is 50 kPa, the PAO2 should be no less than 40 kPa (see ‘Intubation and
ventilation’, Chapter 114, page 470).
CAUSES
Respiratory acidosis
Any cause of hypoventilation – cardiac arrest, COPD, pneumonia, asthma.
Metabolic acidosis (see ‘Anion gap’ below)

• Body produces too much acid – lactic acid – as a result of anaerobic respiration;
many forms of illness cause shock and hypoxia (e.g. severe sepsis). Important
surgical causes include pancreatitis (as a result of shock), ischaemic bowel
(shock) and crush injury
• Diabetic ketoacidosis (this is why these patients hyperventilate – they are trying
to compensate)
• Body cannot get rid of acid – renal failure
351
• Poisoning with acid (e.g. aspirin)

• Loss of bicarbonate (e.g. diarrhoea).
Respiratory alkalosis
Increased respiration (e.g. hyperventilation, PE).
Metabolic alkalosis
Loss of H! (e.g. vomiting).

What are the harmful effects of acidosis?
• Suboptimal enzyme action
• Depressed myocardial contractility/arrhythmias
• Decreased oxygen-carrying ability of haemoglobin
• Decreased response to vasopressor agents
• Hyperkalaemia and impaired potassium excretion
• Hyperventilation and exhaustion
ANION GAP
The anion gap is a calculation used to detect an unmeasured concentration of anion
(acid) in the blood.
It helps in the differential diagnosis of causes of a metabolic acidosis.
The number of anions and cations in the blood should be equal.
The main anions and cations (Na!, K!, HCO3", Cl") are measured when calculat-
ing the anion gap. So:
([Na!] ! [K!]) " ([Cl"] ! [HCO3"]) # [Unmeasured anions] "
[Unmeasured cations]
Normal range is 10–18 mmol/L because there are more unmeasured anions than
cations.
If the anion gap is increased, an unmeasured anion is present in the blood in increased
quantities.
Causes of metabolic acidosis with an increased anion gap include lactic acidosis,
ketoacidosis and salicylate poisoning.
Examples of causes of a metabolic acidosis with a normal anion gap include diar-
rhoea and renal tubular acidosis.
352
85 Action potential

Describe how an action potential is created and propagated?
Why is there a resting membrane potential and how is it maintained?
Define action potential.
What drugs affect the action potential?
What types of nerve do you know and how fast do they conduct?
What is the ‘all or nothing’ principle?
What is meant by the terms ‘threshold’ and ‘summation’?
What is the difference between skeletal and cardiac action potentials?
What drugs affect the action potential and how do they work?
Related topics
Topic Chapter Page
Neuromuscular junction 98 391
Cardiac action potential 89 366

What is the resting membrane potential and how is it generated and
maintained?
High sodium levels outside the cell (extracellular fluid) and high potas-
sium inside the cell.
This chemical gradient is maintained by the action of Na!/K! ATPase.
Both sets of ions try to cross the membrane and flow down their
concentration gradient, but this is limited by the formation of an electrical
gradient that occurs because they take their charge with them. This
potential (for each ion) is called the Nernst potential. It is also limited by
the fact that the cell membrane is impermeable to proteins, which are
also charged.
The overall resting potential is "70 mV in nerve (see Fig. 85.1).
353
APPLIED SURGICAL PHYSIOLOGY action potential
!30
Membrane potential (mV)

Na! in
K! out
Threshold
"70
Time
Figure 85.1
DEFINITION
An action potential is a rapid change in the membrane potential caused by influx
of positive ions, followed by a return to resting membrane potential caused by
efflux of positive ions; this leads to the generation of an electrical impulse that
enables signalling to occur in excitable tissue (nerve and muscle).
THE ACTION POTENTIAL

The initiating event for an action potential is depolarization of the membrane. The
membrane must be depolarized beyond a set threshold for this to occur.
In sensory nerves this is caused by activation by stimulus transducers (e.g. pressure
sensors, pain transduced by blind nerve endings). It can also by initiated by poten-
tials at synapses, or experimentally by applying a potential to the nerve directly.
Voltage-gated sodium channels open locally in response to this.
Sodium flows down its concentration gradient at this point, depolarizing the mem-
brane to about !40 mV (see Fig. 85.1, left).
The depolarization causes voltage-gated potassium channels in the membrane to open.
Potassium flows down its concentration gradient and the membrane repolarizes.
The potential propagates along the nerve as depolarization causes more and more
sodium channels to open.
The sodium channels close and become refractory, i.e. they cannot open for a time
period of 1 ms. This prevents the action potential from propagating backwards.
The changes in membrane potential are illustrated in Fig. 85.1 for a peripheral
nerve (left) and cardiac muscle (right). This diagram is often asked for in vivas.
354
APPLIED SURGICAL PHYSIOLOGY action potential

What is summation, and the ‘all or nothing’ principle?
As described above, the initiating event for an action potential is a stimulus
that depolarizes the membrane. Summation describes the process whereby
depolarizing stimuli can be added together (although the depolarizing
effect of this stimulus will be reduced), resulting in the generation of an
action potential if the threshold is reached.
The all or nothing principle refers to the action potential itself. Once the
threshold is reached, as described above, a positive feedback loop occurs
whereby all of the sodium and then the potassium channels in the area of
membrane excited become activated. An action potential must necessarily
involve all of the channels so it is an all or nothing phenomenon; there are
no weak or half-strength action potentials (in contrast to the depolarizing
potential responsible for their generation).
SALTATORY CONDUCTION
Some axons are coated with myelin, which does not conduct the impulse. There are
small interruptions to the myelin, called the nodes of Ranvier.
Conduction occurs only at these points and the current ‘jumps’ from node to node,
speeding up propagation. This process is called saltatory conduction, and explains
why, in myelinated fibres, such as in motor and large sensory neurons, the speed of
conduction is greater.
In smaller unmyelinated fibres, such as pain fibres, the speed of conduction is slower.
Axon diameter also affects the speed of conduction, with large diameters being faster.
DRUGS
The action potential is abolished by sodium channel blockers – this is how local anaes-
thetics work (see ‘Local anaesthetics’, Chapter 75, page 308 and ‘Neuromuscular
junction’ Chapter 98, page 391).
355
86 Altitude

What are the physiological changes that take place at altitude?
Related topics
Topic Chapter Page
Oxygen transport 99 394
Control of respiration 91 373
Cerebrospinal fluid and the blood–brain barrier 90 369
The topic is a good test of applied physiology and understanding across a variety of
topics.
PHYSIOLOGY AT ALTITUDE: THE PROBLEM

At altitude, the partial pressure of oxygen decreases, as does atmospheric pressure.
This leads to a number of physiological changes and resultant compensations. The
primary problem here is chronic hypoxia which leads to a drop in arterial PO2.
PHYSIOLOGICAL CHANGES
Altitude leads to a decrease in the arterial PO2.
Immediate changes
Respiratory and acid–base
Peripheral chemoreceptor detects a drop in PO2 which leads to a reflex tachypnoea and
increase in depth of respiration (see ‘Control of respiration, Chapter 91, page 373).
This, however, results in a respiratory alkalosis and its associated features (tingling
fingers, etc.). It also results in hypocapnia, which reduces the drive of the central
chemoreceptor (not desirable). This is compensated for in the short term by
removal of bicarbonate ions by the choroid plexus from the CSF.
Alkalosis has an adverse effect on oxygen delivery, because alkalosis shifts the
oxygen–haemoglobin dissociation curve to the left, thus making it more difficult for
356
APPLIED SURGICAL PHYSIOLOGY altitude
the haemoglobin to give up oxygen at the tissues at a given Po2 (see ‘Oxygen trans-
port’ Chapter 99, page 394).
Reduced humidity can lead to a dry cough.
Cardiovascular
Reflex tachycardia and cardiac output increase initially, via stimulation of the
peripheral chemoreceptors by hypoxia, to increase oxygen delivery to the tissues.
This settles with acclimatization.
Cerebral blood flow increases to increase delivery of oxygen to the brain.
Slow changes
Respiratory and acid–base
The alkalosis created by the tachypnoea is compensated for in the kidney by
increased excretion of HCO3" ions, a slow metabolic compensation.
Increased production of 2,3-diphosphoglycerate (DPG) compensates for the left
shift of the O2–haemoglobin dissociation curve and facilitates release of oxygen to
the tissues (see Fig. 99.1).
The chronic hypoxia leads to increased production of erythropoietin by the kidney,
which causes increased haemoglobin synthesis. This improves oxygen carriage, and
individuals chronically exposed to altitude become chronically polycythaemic (see
also ‘Oxygen transport’, Chapter 99, page 394).
There is a blunted response to hypoxia as the individual acclimatizes and the alka-
losis improves over time. There may also be an increase in the alveolar size and a
decrease in the thickness of the alveolar membranes, leading to more efficient gas
transfer.
Cardiovascular
Chronic hypoxia leads to pulmonary vasoconstriction and hypertension, and this can
lead to pulmonary oedema.
The alkalosis leads to cerebral vasoconstriction; intracranial pressure increases,
which can lead to cerebral oedema.
Blood viscosity increases at altitude.
Other medical problems
• Thrombosis
• Retinopathy
• Immunosuppression.
357
87 Blood pressure control

What is blood pressure?
How is blood pressure measured?
What factors determine arterial blood pressure?
What are the homoeostatic mechanisms that control blood pressure?
What are the causes of hypertension?
Tell me what homoeostatic mechanisms maintain blood pressure in the
face of acute haemorrhage?
Why do anaesthetists worry about blood pressure?
Related topics
Topic Chapter Page
Altitude 86 356
Shock 122 510
Inotropes 113 466
CVP lines and invasive monitoring 110 443
Portal hypertension 61 239
Key learning points

Some definitions
Arterial blood pressure: the systemic arterial pressure
Systolic blood pressure: maximum arterial pressure during cardiac systole
Diastolic blood pressure: minimum pressure during diastole
Pulse pressure: systolic minus diastolic value
Mean arterial pressure: diastolic pressure plus one-third pulse pressure
358
APPLIED SURGICAL PHYSIOLOGY blood pressure control
MEASUREMENT OF BLOOD PRESSURE

Manual versus invasive (via an arterial line).
Manual blood pressure is derived by listening to Korotkoff’s sounds (five different
sounds as the cuff is released).
Five phases
1. At systolic pressure the sound appears
2. Sounds become muffled
3. Reappears
4. Becomes softer
5. Disappears (diastolic blood pressure).
Invasive blood pressure monitoring gives a second-to-second indication of patients’

blood pressure, which is an advantage over serial manual readings (see ‘CVP lines
and invasive monitoring’, Chapter 110, page 443).
IMPORTANT RELATIONSHIPS
BP # CO $ SVR (Ohm’s law) (1)
CO # SV $ HR (2)
where BP is blood pressure, CO is cardiac output, HR is heart rate, SVR is systemic

vascular resistance, and SV is stroke volume.
Key learning point

Start a viva by writing these equations out on the paper provided and use
them to explain the physiology in a structured fashion
Cardiac output and systemic vascular resistance both have a direct bearing
on blood pressure. These two contributors can be explained separately in
the context of the question asked.
Cardiac output can be further broken down by the second equation.
Systemic vascular resistance is predominantly affected by the diameter of
the arterioles – the resistance vessels, with a calibre that can be quickly
controlled neurally or hormonally.
359
NEURAL HOMOEOSTATIC PATHWAYS

Blood pressure is monitored by baroreceptors (pressure receptors) in the aortic
arch and carotid sinus. Sensory information is carried to the brain via afferent glosso-
pharyngeal and vagal fibres. Integration takes place in the midbrain.
Efferent sympathetic fibres to the heart and arterioles make necessary alterations: if BP
is high, afferent firing increases and efferent sympathetic activity reflexly decreases.
This leads to vasodilatation and decrease in heart rate and force of contraction.
Arteriolar dilatation leads to a decrease in TPR (total peripheral resistance) and hence
a decrease in blood pressure (Eqn 1).
A decrease in stroke volume and heart rate lead to a decrease in blood pressure
(Eqns 2 and 1).
ENDOCRINE MECHANISMS
The blood vessels and heart, the main contributors to blood pressure, are also under
endocrine control.
Adrenaline (epinephrine) is released if there is a sustained decrease in mean arterial
pressure. This acts on &1-receptors in the arterioles and veins to increase TPR (Eqn 1)
and also on '1-receptors in the heart to increase the rate and force of contraction
(Eqns 2 and 1).
Loss of blood volume will lead to renal renin secretion, which ultimately leads to
angiotensin II secretion. This has a direct vasoconstrictor effect (Eqn 1) and leads to
aldosterone secretion, which causes sodium and fluid retention by the kidney. This
indirectly increases cardiac output (Eqn 2).

Tell me what homoeostatic mechanisms maintain blood pressure in the face
of acute haemorrhage?
Use the two equations above.
Baroreceptor pressure falls, leading to reflex increase in vasomotor and
cardiac sympathetic tone.
This leads to increased adrenaline secretion.
Renin is secreted by the kidney in response to decreased perfusion.
360
CAUSES
In hypertension, the set point for the above homoeostatic mechanisms is altered.
• 90 per cent essential (no cause found)
• Other endocrine causes: phaeochromocytoma, aldosteronoma, Cushing’s
disease, acromegaly
• Chronic renal failure.
361
88 Calcium homoeostasis

How is calcium homoeostasis maintained?
What are the different types of hyperparathyroidism?
What are the causes of hypercalcaemia?
How is a corrected calcium calculated and why would you do it?
How do hyper- and hypocalcaemia present?
How are hyper- and hypocalcaemia treated?
What are the functions of calcium?
What are the effects of pH on calcium metabolism?
Related Topics
Topic Chapter Page
Functions of the kidney II 93 377
KEY FACTS
• Over 99 per cent of total body calcium is stored in bone as hydroxyapatite; only
1 per cent is free
• Of this free calcium, 40 per cent is bound to serum albumin and 60 per cent is
free. It is only the unbound free calcium that is physiologically important
• Acidosis increases the amount of ionized calcium in the blood by dissolving
mineralized bone; the osteoclasts dissolve bone by this mechanism
• The functions of calcium include:
• muscle contraction
• cardiac action potential propagation
• constituent of bone and teeth
• enzymatic cofactor
• blood clotting
• Its intracellular release from stores (sarcoplasmic reticulum) is often responsible
for initiating cellular function, because physiologically there is very little
intracellular calcium
• It is also an intracellular second messenger.
362
APPLIED SURGICAL PHYSIOLOGY calcium homoeostasis

How do you correct the serum calcium?
The normal serum calcium level is 2.2–2.6 mmol/L. A normal albumin is
40 mmol/L. If the albumin level drops, the amount of free calcium rises
and, as this is the active calcium, an adjustment needs to be made under
these circumstances. For every 5 the albumin drops below 40 mmol/L, the
calcium level should be increased by 0.1 mmol/L.
This is important in hypoalbuminaemia in, for example, postoperative
undernourished patients in whom the uncorrected calcium may not
seem high.
CALCIUM HOMOEOSTASIS – HORMONES

Three hormones are responsible for keeping the serum calcium at this level within the
blood: parathyroid hormone (PTH), 1,25-dihydroxycholecalciferol (1,25-DHCC),
a metabolite of vitamin D, and calcitonin.
Parathyroid hormone
This hormone is the most important in the metabolism of calcium. It is a peptide
hormone, produced by the parathyroid glands. It is secreted in response to a
decrease in serum calcium, and high levels of serum calcium decrease its secretion
(a negative feedback loop; see Fig. 88.1).
It acts on osteoclasts that have PTH receptors, to increase resorption of bone and
release calcium into the blood. It also acts to increase the production of 1,25-DHCC
by the kidney, and increases secretion of phosphate by the kidney.
1,25-DHCC
This is a metabolite of vitamin D, which is obtained from the diet or action of UV
light on the skin. It is metabolized first in the liver to 25-hydroxycholecalciferol and
then in the kidney to produce the active hormone.
Its synthesis is potentiated by PTH, in the proximal tubule of the nephron. It causes
increased resorption of calcium from the gut (see Fig. 88.1).
Calcitonin
Not thought to be an important hormone physiologically. It is secreted by the
medullary (parafollicular) cells of the thyroid.
363
Fall in serum Ca2!
PTH secretion
1,25-DHCC
increases
increased
Phosphate
2! excretion Ca2! reabsorbed
Ca released
in kidney in gut (jejunum)
from bone
negative Serum Ca2! rises

feedback
Figure 88.1
It causes a decrease in serum calcium by inhibiting osteoclast function. It is secreted

abnormally in the medullary carcinoma of the thyroid, for which it is a tumour
marker.
HYPERCALCAEMIA
Clinical features
‘Stones, bones, abdominal groans, psychic moans.’
• Renal stones
• Bone pain
• Abdominal pain (gallstones and pancreatitis)
• Psychosis.
Causes include (mechanism in brackets) the following:
Common (80 per cent of all causes)
• Primary and tertiary hyperparathyroidism (see below)
• Malignancy (bone destruction).
Rarer
• Sarcoidosis (excess vitamin D)
• Myeloma (bone destruction)
• Thiazide diuretics
• Iatrogenic (excess administration of vitamin D)
• Milk alkali syndrome.
364
HYPOCALCAEMIA
Clinical features
• Paraesthesia
• Trousseau’s sign (twitching of facial muscles on tapping facial nerve) and
Chvostek’s sign (carpopedal spasm)
• Convulsions
• Tetany
• Rickets (may be a chronic association).
Causes include (mechanism in brackets):
• Parathyroidectomy (loss of PTH secretion)
• Thyroidectomy (transient, damage to parathyroids)
• Chronic renal failure (calcium loss)
• Massive blood transfusion (chelation of Ca2!)
• Vitamin D deficiency
• Pancreatitis.
HYPERPARATHYROIDISM
Primary
Caused by parathyroid adenomas and excessive PTH secretion.
Secondary
Caused by renal failure. PTH levels are high but calcium is being lost faster so
levels are low or normal.
Tertiary
Occurs in longstanding renal failure. The parathyroids become autonomous and
hyperplastic and behave like adenomas, secreting PTH autonomously. Calcium levels
become high again despite renal loss of calcium. Treatment is by parathyroidectomy
TREATMENT OF HYPERCALCAEMIA AND HYPOCALCAEMIA

Hypercalcaemia is an emergency, because it can cause arrhythmias. It is treated in the
short term by vigorous fluid resuscitation and administration of pamidronate, which
lowers the calcium levels. The cause should be sought and treated where possible.
Hypocalcaemia can be treated by administration of calcium or calcium-raising
preparations such as Calcichew (vitamin D derivative) and calcium gluconate.
365
89 Cardiac action potential

What makes the heart beat?
What are the functions of adrenaline?
What are the functions of atropine?
What drugs affect cardiac output or heart rate?
Talk about different types of muscle.
Related Topics
Topic Chapter Page
Neuromuscular junction 98 391
• The heart muscle has an intrinsic ability to beat.

• The heart acts as a functional syncytium, so that depolarization of a pacemaker
will rapidly lead to depolarization and contraction of the entire heart.
• All parts of the conducting apparatus are capable of pacing.
• The sinoatrial node does so because its intrinsic rate is fastest.
• In the absence of a pacemaker, other parts of the conducting system take over
(with a slower rate), e.g. in either complete AV block or ventricular escape,
the ventricles depolarize at a slower rate, which is why the patient’s heart
continues to beat in the absence of an atrial pacemaker, but a bradycardia is
present.
• In some arrhythmias, there is abnormal pacemaker function, e.g. in atrial
fibrillation (AF) there are multiple pacemakers that lead to fibrillation.
• The physiological resting heart rate is 90/min, which is slowed physiologically
by increasing vagal tone.
366
APPLIED SURGICAL PHYSIOLOGY cardiac action potential

Tell me how a transplanted heart functions
(A common MRCS question to make you think about the physiology.)
It has intrinsic rhythmicity, it is autonomically denervated, so there are no
direct effects of noradrenaline or acetylcholine (sympathetic and parasym-
pathetic neurotransmitters) but circulating hormones do (adrenaline – see
below) affect heart rate.

Draw the cardiac action potential for me. How does it differ from a somatic
action potential? Label the ion fluxes.
Ca2! in
Membrane potential (mV)
!30
K! out
Na! in
"70
Na leak
Time 300 ms
Figure 89.1
The cardiac action potential necessarily differs from that in somatic nerve or muscle.
• There is a constant sodium leak into the cell:
• this causes a gradual increase in the resting membrane potential; cardiac
myocytes derive their intrinsic rhythmicity from the presence of this sodium
leak, which is not present in other excitable cells
• when the membrane potential reaches threshold, voltage-gated sodium chan-
nels open, resulting in rapid depolarization as sodium flows down its concen-
tration gradient into the cell
• There is now an influx of calcium, which lengthens the cardiac action potential.
This period is the equivalent of the refractory period in somatic nerve.
367
APPLIED SURGICAL PHYSIOLOGY cardiac action potential
Key learning point

The influx of calcium prevents tetany, which occurs physiologically in
skeletal muscle but is obviously undesirable in cardiac muscle.
• Eventually, voltage-gated potassium channels open and potassium flows out of

the cell down a concentration gradient, repolarizing the cell membrane.
Key learning points

Drugs that affect the cardiac action potential – mechanism of action
• Adrenaline: this increases the rate of sodium leak, decreases the time
between action potentials and hence increases heart rate
• Acetylcholine: this decreases the rate of sodium leak, which has the
opposite effect to adrenaline, and hence slows down the heart rate
• Calcium channel blockers: these shorten the plateau phase of the action
potential and hence decrease the force of contraction of cardiac muscle.
Sodium channel blockers and calcium channel blockers can act as antiar-
rhythmics by decreasing the excitability of the cell membrane. They do not
affect the sodium depolarization, but prevent, for example, premature
beats because many of the channels are still blocked.
Don’t forget, CO # SV $ HR and the physiology of the cardiac action
potential can be used in discussions relating to Starling’s law and relationships
with respect to heart rate. (see ‘Starling’s law of the heart and cardiovascular
equations’, Chapter 102, page 403, and ‘Inotropes’, Chapter 113, page 466).
368
90 Cerebrospinal fluid and the
blood–brain barrier

What are the functions of the CSF?
Where is CSF produced?
Where does CSF flow and how is it resorbed?
What does normal CSF contain? How do its constituents change in
meningitis and subarachnoid haemorrhage?
How would you perform a lumbar puncture?
How does epidural and spinal anaesthesia work?
What is hydrocephalus? How is it classified?
Related Topics
Topic Chapter Page
CSF FLUX
Cerebrospinal fluid (CSF) is produced by the choroid plexus of the lateral, third
and fourth ventricles. It flows from the lateral ventricles to the third ventricle, and
then via the cerebral aqueduct into the fourth ventricle.
After this it flows into the subarachnoid space via the two foramina of Luschka
(lateral) and the single foramen of Magendie (midline). The fourth ventricle is dia-
mond shaped and its floor consists of pons and rostral brain stem, and the roof
includes the cerebellar peduncles. The caudal part of the roof contains an opening
into the cerebromedullary cistern and then into the subarachnoid space; this is the
foramen of Magendie. There are two lateral openings in the roof into the pontine
cistern and then into subarachnoid space (the foramina of Luschka). The basal cis-
terns (two described above) are dilated areas, here containing CSF.
CSF is reabsorbed by arachnoid villi/granulations of the venous sinuses, passively
under CSF pressure. Normal CSF pressure is 120–180 mmH2O.
There are 140 mL present in the adult, although four times this amount is produced
and resorbed each day.
369
APPLIED SURGICAL PHYSIOLOGY cerebrospinal fluid and blood–brain barrier
Choroid
plexus
Left lateral
ventricle
Foramen
of Monro
Third ventricle
Cerebral aqueduct
Fourth ventricle
Figure 90.1 Schematic anteroposterior view illustrating the ventricular system and CSF flux.
CONTENTS OF THE CSF

Normal CSF is crystal clear and contains:
• Water
• Protein: 0.15–0.45 g/L
• Glucose: 0.45–0.7 g/L
• Small numbers of white cells (leukocytes, neutrophils and monocytes)
% 5 white cells/mm3.
FUNCTION OF THE CSF

It acts as a shock absorber for the brain, bathing it in fluid. This is important, because
the brain is in the skull, which is fixed and hard.
It reduces the effective weight of the brain. It provides a route for excretion of waste
products from the brain.
It delivers glucose to the brain, and is important in its homoeostasis (e.g. ‘Acid–base
balance’, Chapter 84, page 349, and ‘Control of respiration’, Chapter 91, page 373).
370
ABNORMALITIES OF THE CSF

In meningitis
CSF samples are turbid in bacterial meningitis. The CSF contains several neutrophil
polymorphs and depleted glucose levels.
In subarachnoid haemorrhage there is xanthochromia (CSF looks yellow when
spun down in the lab).
Spinal and epidural anaesthesia
In spinal anaesthesia, a needle is passed into the subarachnoid space, below the level
at which the spinal cord ends (L1–2). The local anaesthetic is delivered directly to
the subarachnoid space where all the nerve roots are anaesthetized for a short time.
In epidural anaesthesia, the local anaesthetic is delivered to the epidural space, where
it remains for longer periods of time. This is why epidural block lasts for longer.
Hydrocephalus
This is an increase in CSF volume, usually resulting from impairment of absorption
of CSF. It is divided into obstructive and communicating:
Obstructive Communicating
Caused by a obstruction within the ventricular Obstruction outside the ventricular
system system
Tumours (primary, secondary), colloid cysts Subarachnoid haemorrhage (involve-
ment of arachnoid granulations)
Aqueductal stenosis (post-infective,
post-haemorrhage or congenital)
Aqueductal haematoma Excessive CSF production
Abscess High CSF protein content
Dandy–Walker syndrome (atresia of foramen of
Luschka or Magendie)
Note that normal pressure hydrocephalus (NPH) relates to the triad of dementia,
gait ataxia and incontinence, despite a ‘normal’ CSF pressure. It may be idiopathic,
or arise insidiously after a subarachnoid haemorrhage or meningitis. In actual fact,
studies show that NPH is usually associated with abnormal peaks of pressure that
oscillate throughout the day.
Diagnosed on computed tomography (CT) – dilated ventricular system.
Treated with ventriculoperitoneal shunting, third ventriculostomy ( treatment of
the cause (e.g. resection of an obstructing posterior fossa tumour).
371

How is raised intracranial pressure measured?
• Clinical assessment: headache, nausea and vomiting, papilloedema on
fundoscopy
• Lumbar puncture: although the CSF pressure can be measured during
this procedure, this is not routinely used because diagnostic lumbar
puncture is contraindicated in raised intracranial pressure (ICP) (see
‘Head injury and intracranial pressure’, Chapter 112, page 459)
• Ventricular catheter: a catheter is inserted into the anterior horn of the
lateral ventricle via a frontal burr hole to measure pressure directly.
A pressure $ 20 mmHg is moderately elevated and $ 40mm Hg is
severely elevated. It is used postoperatively and during treatment aimed
at reducing the ICP, where the CSF can be aspirated to reduce the overall
ICP (see ‘Head injury and intracranial pressure’, Chapter 112, page 459)
THE BLOOD–BRAIN BARRIER

The blood–brain barrier selectively controls the entry of substances into the extra-
cellular fluid of the CNS and the rate of their entry. This limits access of toxins but
also of immune mechanisms.
The blood–brain barrier is located in the smallest capillaries supplying the brain and
consists of tight junctions and transport mechanisms. Fat-soluble drugs (e.g.
diamorphine) cross quickly, and glucose and anaesthetic agents can also cross.
Hydrogen ions do not usually cross and this has implications for control of respir-
ation and acid–base balance (see ‘Acid–base balance’, Chapter 84, page 349).
The blood–brain barrier is absent in a number of areas:
• Median eminence of the hypothalamus where hypothalamic neurons release
hormones that act on the anterior pituitary into the portal system of capillaries.
• Posterior pituitary, where ADH- (antidiuretic hormone) and oxytocin-secreting
neurons secrete directly into the blood (see ‘Pituitary’, Chapter 100, page 397).
• Circumventricular organs adjacent to the third and fourth ventricles. This area
is adjacent to the chemotrigger zone.
The blood–brain barrier may be compromised in severely raised ICP and is often
disrupted in the context of aggressive intra-axial tumours.
372
91 Control of respiration

What types of respiratory failure do you know?
Why is pure oxygen contraindicated in patients with COPD (chronic
obstructive pulmonary disease)?
What are the roles of central and peripheral chemoreceptors in control-
ling respiration?
Tell me about how breathing is controlled?
What is the interrelationship of PaO2, PaCO2 and respiratory rate/minute
volume? Can you draw a graph?
What are the main sensors that maintain respiratory homoeostasis and
what is their relative importance?
What is the importance of the pH of CSF in control of respiration?
Related Topics
Topic Chapter Page
Respiratory failure and respiratory
function tests 119 495
CSF and blood–brain barrier 90 369
Altitude 86 356
SET-UP AND TERMINOLOGY

Homoeostasis is achieved by feedback systems that keep PO2 and PCO2 within tight
limits.
Sensors monitor levels and provide input to the respiratory centre if too low or high.
The respiratory centres control normal involuntary respiration. It can be overridden
voluntarily. They are in the brain stem (pons and medulla).
The effectors are the respiratory muscles that act to bring about change. The
respiratory centres control these effectors. They consist of diaphragm, intercostals
373
APPLIED SURGICAL PHYSIOLOGY control of respiration
and, where a greater respiratory effort is required, accessory muscles (abdominal,

serratus anterior, scalenus anterior, sternocleidomastoid, etc.).
RESPIRATORY CENTRES
These consist of the medullary respiratory, apneustic and pneumotaxic centres. Their
relationships are complex: they involuntarily produce a rhythmic respiratory cycle.
They can be overridden voluntarily by the cortex, when we breathe voluntarily.
SENSORS
Peripheral chemoreceptors
• The less important of the two sets of sensors
• They are situated in the carotid body and the aortic arch and receive a high
blood flow
• They primarily sense the PO2 and if this is low they increase afferent firing to
the respiratory centre, which reflexly beings about an increase in respiratory rate
and depth, and hence a return to normal PO2
• They are also, to a much lesser degree, sensitive to pH. This underpins the
increase in respiratory rate and depth seen in respiratory compensation of
metabolic acidosis (see ‘Acid–base balance’, Chapter 84, page 349).
Central chemoreceptors
• These are the most important sensors, and are situated on the ventral surface of
the medulla; they lie within the blood–brain barrier
• CO2 readily crosses the blood–brain barrier where it undergoes the conversion
H2O ! CO2 L H2CO3 L H! ! HCO3".
H! does not cross the blood–brain barrier, so changes in H! in the CSF equate
to a rise in PCO2
• They are sensitive to the level of H!, hence, indirectly, to CO2 in the CSF
• Therefore a rise in central H! (CO2) brings about a reflex increase in respiratory
rate and depth to reduce the PCO2
• If the PCO2 remains chronically high the central chemoreceptors reset their set
point for the ‘correct’ PCO2 at a higher level.
374
APPLIED SURGICAL PHYSIOLOGY control of respiration

Why is pure oxygen contraindicated in patients with COPD?
In COPD, the central chemoreceptors are chronically exposed to high
levels of CO2 as a result of poor gas exchange in the lungs. Hence, the set
point for PCO2 increases for the central chemoreceptors, and they no
longer respond to small changes in PCO2.
These patients therefore purely rely on hypoxia to stimulate the peripheral
chemoreceptors, which in turn stimulates the respiratory centres to
increase the drive to breathe.
If 100 per cent oxygen is given, there is no hypoxia to stimulate the
peripheral chemoreceptors and, because the central chemoreceptors also
no longer respond to a build-up of CO2 (as H!), the patient has no drive
to breathe.
Note that, in practice, however, it is more dangerous to leave the patient in
life-threatening hypoxia than to administer oxygen!
Effect of PACO2 and PAO2 on minute volume and respiratory rate

Respiratory rate
Respiratory rate
PACO2 PAO2
Figure 91.1
Figure 91.1 illustrates the relationship.

On a minute-to-minute basis, the PACO2 is proportional to the respiratory rate. This
is brought about by the central chemoreceptors.
The PAO2 brings about an increase in respiratory rate and minute volume only at
quite low values (6.5 kPa), this being effected by the peripheral chemoreceptors.
See ‘Altitude, Chapter 86, page 356 for another illustration of how it works.
375
92 Functions of the kidney I

What are the functions of the kidney?
What hormones does the kidney secrete?
What happens in renal failure?
How does the kidney act in electrolyte homoeostasis? (How does the
kidney handle Na!, K! and H! ions?)
How does the kidney conserve water?
How does the loop of Henle work? Draw a diagram to illustrate.
Related topics
Topic Chapter Page
Shock 122 510
Altitude 86 356
Pituitary 100 397

What are the functions of the kidney?
A common question in vivas and each function can lead into a separate
viva as can be seen by the numerous related topics. The key is dividing this
up into categories and having these ready, with an explanation of each. The
key functions are:
• Fluid balance and electrolyte homoeostasis (see Chapter 93, page 377)
• Acid–base balance (see Chapter 84, page 349)
• Nitrogen excretion, excretion of toxins and drugs (see Chapter 95, page 383)
• Endocrine functions (renin–angiotensin system, erythropoietin, ADH
system, calcium metabolism) (see Chapter 94, page 381).
376
93 Functions of the kidney II: fluid and electrolyte
balance in the kidney and loop of Henle
This is the kidney’s key function.
ELECTROLYTE BALANCE
Anatomy of the nephron (Fig. 93.1)
Bowman’s capsule
Distal
tubule
Proximal dilute
tubule
Collecting
Descending limb duct
loop of Henle
(water permeable) Medulla
concentrated
Ascending limb
loop of Henle
(water impermeable)
Figure 93.1
The blood is filtered at high pressure in the glomerulus; the large proteins and cells
remain in the blood and water, and solutes pass into the Bowman’s capsule and the
nephron; 170–180 L of plasma are filtered a day.
Several solutes are actively reabsorbed in the proximal tubule, including sodium,
glucose, calcium, phosphate and chloride. Water is also reabsorbed, as are amino
acids.
The renal medulla contains a gradient of sodium, which is most concentrated at the
centre and more dilute at the periphery. More sodium is pumped out actively at the
thick ascending limb of the loop of Henle to maintain the sodium gradient (see
below).
377
APPLIED SURGICAL PHYSIOLOGY functions of the kidney II
THE LOOP OF HENLE

Figure 93.2 explains how the sodium gradient is generated. The thin descending
limb of the loop of Henle is permeable to water and the thick ascending limb is not.
Sodium is pumped actively from the tubular fluid in the ascending limb of the loop
of Henle to the interstitium (at the centre of the loop in Fig. 93.2). Fluid moves
from left to right through the loop. The sequence of events is as follows (Fig. 93.2):
1. All concentrations are equal
2. Sodium is pumped out of the thick ascending limb
3. The increased concentration of sodium in the interstitium equilibrates with the
fluid in the descending limb
4. Fluid moves around the loop of Henle
5. Again, fluid is pumped from the thick ascending limb into the interstitium
6. The fluid concentrations equilibrate as before
7. The fluid moves once again.
A gradient has started to form. This is maintained by the sodium pumps and the
constant delivery of the sodium to the loop of Henle.
The fluid leaving the loop of Henle is very hypotonic because sodium has been
pumped away from it. Water is later reabsorbed through water channels (see
below) in the collecting system.
This sodium gradient, together with the countercurrent multiplier arrangement of
the loop of Henle and the blood supply, allows the urine to be concentrated, because
water follows sodium, the main anion in the blood. As the fluid filtered by the
Bowman’s capsule enters the loop of Henle and progresses through the permeable
descending limb, water enters the more concentrated interstitium by osmosis.
Sodium and chloride are reabsorbed here.

How do loop and thiazide diuretics work?
As water follows sodium, blocking of the sodium channels in the proximal
tubule, loop of Henle or distal tubule causes a diuresis (sodium not reab-
sorbed, so excreted with water); this is the basis of the action of different
types of diuretic.
In the loop of Henle, blocking of the sodium channels dissipates the
sodium gradient and the kidney cannot concentrate urine (loop diuretics
such as frusemide).
In the proximal tubule, if sodium reabsorption is blocked (thiazide diuretics
such as bendrofluazide) more water and sodium are excreted.
378
100 100 100 100 150 50
100 100 100 100 150 50
100 100
(1) Start (2) Pump
125 125 50 100 125 50
125 125 50 125 125 100
100 125
(3) Equilibrate (4) Move
100 150 25 125 125 25
125 175 50 150 150 50
125 125
(5) Pump (6) Equilibrate
100 125 50
125 150 125
150
(7) Move
Figure 93.2
379
DISTAL TUBULE
In the distal tubule, potassium is excreted under the control of aldosterone, in
exchange for sodium.
In the collecting duct, water is reabsorbed via water channels, the synthesis of
which is mediated by ADH. Some urea is passively reabsorbed, but the main con-
tents of the urine here are urea, sodium and water. These movements are summar-
ized in Fig. 93.3.
Na! out
K! in
Na!, glucose, Ca2!, PO43", Cl" out
Water out
Na! in
Cl" in
Some urea out

Urea, creatinine,
Na!, K! out
Figure 93.3
380
94 Functions of the kidney III: endocrine
functions of the kidney
Fluid balance is controlled by two main endocrine mechanisms:

1. The ADH system controls the tonicity of the blood.
2. The renin–angiotensin–aldosterone system controls the blood volume.
ADH SYSTEM: TONICITY OF THE BLOOD

The tonicity of the blood is sensed by cells in the lamina terminalis of the hypo-
thalamus and the magnocellular ADH-secreting neurons of the hypothalamo-
neurohypophyseal system (see ‘Pituitary’, Chapter 100, page 397).
If the blood becomes hypertonic (dehydration), these neurons become excited. This
causes the release of ADH from the posterior pituitary.
The site of action of ADH is the collecting duct of the nephron.
ADH causes the epithelial cells of the collecting duct to increase synthesis of water
channels, which results in increased water reabsorption and production of a con-
centrated urine.
The sodium gradient (see ‘Function of the kidney II, Chapter 93, page 377) is nec-
essary for this system to function.
THE RENIN–ANGIOTENSIN–ALDOSTERONE SYSTEM

This homoeostatic mechanism is mainly concerned with the regulation of blood
volume. This system will override the ADH system if there are conflicting interests
(i.e. low blood volume but dilute blood, as in haemorrhage).
Blood volume is sensed by blood pressure in the afferent arteriole of the juxta-
glomerular apparatus. A drop stimulates the production of the enzyme renin,
which converts circulating angiotensinogen to angiotensin I, which is in turn con-
verted to angiotensin II by angiotensin-converting enzyme in the lung.
Angiotensin II has a potent vasoconstrictor effect, which raises the blood pressure
in the face of hypovolaemia. It also causes increased secretion of aldosterone from
the adrenal cortex (zona glomerulosa).
Aldosterone causes sodium (and hence water) retention by the distal tubule of the
nephron, to increase blood volume. Its other function is potassium excretion.
381
APPLIED SURGICAL PHYSIOLOGY functions of the kidney III
This system overrides the ADH system, e.g. if renal perfusion is low, but the blood
is hypotonic. This makes sense because, in shock, it is more important to maintain
blood volume than to get rid of water from hypotonic blood (if the two coexist).
Erythropoietin is the other hormone that is secreted by the kidney. It causes
proliferation of erythrocytes in chronic hypoxia.
The kidney also metabolizes vitamin D derivatives, in the metabolism of calcium
(see ‘Calcium homoeostasis’, Chapter 88, page 362).
382
95 Functions of the kidney IV: other functions
ACID–BASE BALANCE
The kidney is important in compensating for acidosis or alkalosis produced by lung
disease (respiratory acidosis/alkalosis) – this is called metabolic compensation (see
‘Acid–base balance’, Chapter 84, page 349 for a more detailed discussion.)
The kidney achieves this by a complex system of buffers, which result in the excre-
tion of H! or HCO3". This is a slow process that occurs over days.
The pH of the urine must not fall below 4.5, and this is also achieved by the buffer-
ing system (see also ‘Acid–base balance, Chapter 84, page 349).
EXCRETION OF NITROGEN, TOXINS AND DRUGS

Urea and creatinine are excreted by the kidney, because most of these small waste
products of nitrogenous metabolism are not reabsorbed by the nephron. Many
drugs are excreted by the kidney.
There are two main routes of excretion:
1. Some drugs are filtered and not reabsorbed by the kidney. If such drugs are
highly polar, they can be trapped in the tubule (e.g. digoxin).
2. Drugs can also be actively secreted by the transporter systems in the proximal
tubule (examples include penicillins, morphine and salicylate).
383
96 Functions of the liver

What are the functions of the liver?
Tell me about liver function tests (LFTs)?
Tell me about what happens in starvation?
How are drugs metabolized here? What drugs interact with the metab-
olism of warfarin and how?
Related Topics
Topic Chapter Page
Liver 10 28

What are the functions of the liver?
A common question. The key is dividing this up into categories and having
these ready, with an explanation of each. The key functions are:
• Production of bile
• Protein, fat and carbohydrate metabolism
• Storage of glycogen and vitamins (A, D, E, K, B12)
• Detoxification of drugs, hormones and toxins
• Reticuloendothelial and haematopoietic (fetus) functions
PRODUCTION OF BILE
Bile is secreted by the hepatocytes and ducts add to its fluid content. About 1 L of
bile is produced per day.
It contains bile salts (cholate and chenodeoxycholate) and HCO3", as well as the
breakdown products of red cell metabolism such as conjugated bilirubin. These are
384
APPLIED SURGICAL PHYSIOLOGY functions of the liver
responsible for the digestion (emulsification) of lipids, which form micelles that
facilitate their absorption (mainly in the jejunum).
Bile produced by the liver flows into the gallbladder when not required (not down
the common bile duct because the sphincter of Oddi is closed).
When a fat-rich meal enters the duodenum, the gallbladder contracts and the
sphincter of Oddi relaxes to allow bile to reach the duodenum.
Most of the bile salts are reabsorbed in the terminal ileum where they are returned
via the portal circulation to the liver and recycled. This is called the enterohepatic
circulation and the bile salts are recycled six to eight times a day. Some bile salts are
lost in the faeces.
METABOLISM
Protein metabolism
The liver is responsible for gluconeogenesis (‘new glucose formation’), the synthe-
sis of glucose from other small molecules, such as amino acids. Muscle is broken
down in starvation to amino acids and transported to the liver for gluconeogenesis.
Protein is broken down in the liver to form nitrogenous waste products such as urea
via the urea cycle.
The liver is responsible for the synthesis of all non-essential amino acids. It is also
responsible for the synthesis of proteins, such as albumin, clotting factors and com-
plement proteins. For this reason, measurement of plasma albumin and clotting
(international normalized ratio or INR) constitute useful LFTs to look at synthetic
function; albumin decreases and clotting time increases if synthetic function is
deranged.
Fat metabolism
The liver is responsible for synthesis of transport proteins for fatty acids, and in star-
vation it synthesizes ketone bodies.
Very-low-density lipoprotein (VLDL) is a lipoprotein synthesized by the liver. Its
function is to transport fatty acids from the liver to the peripheral tissues for stor-
age. VLDLs are synthesized from chylomicron remnants after absorption by the
small bowel.
Fatty acids are cleaved to produce acetyl-CoA for the production of ATP.
In starvation, the brain requires glucose to function but can also metabolize ketone
bodies for energy. The liver can produce ketone bodies from fatty acids (which can-
not be used to produce glucose).
385
Carbohydrate metabolism
This occurs during gluconeogenesis (see above). In ‘times of plenty’, glucose is con-
verted into glycogen, for storage, a process termed ‘glycogenesis’. The breakdown of
glycogen to glucose takes place in the liver in early starvation (fasting), and is called
glycogenolysis.
STORAGE
The liver stores glycogen, vitamins A, D, E, K and B12, iron and copper.
Glycogen is a quick source of glucose in starvation as outlined above. It will last as

long as an overnight fast although other mechanisms are brought into play.
DETOXIFICATION
Peptide hormones (e.g. insulin) and steroid hormones (e.g. testosterone) are
degraded in the liver. The cytochrome P450 system is involved in their metabolism,
which includes increasing water solubility.
Drugs that increase or decrease the activity of the cytochrome P450 system may have
an effect on other drugs being administered concomitantly; this is a major source of
ADRs, and is particularly significant where the drugs being used have a narrow thera-
peutic window.

What drugs interact with warfarin and how?
Erythromycin inhibits the cytochrome P450 system and phenytoin
increases it, so warfarin, which is metabolized via this system, would have
its effects potentiated if administered together with erythromycin, and
reduced if administered with phenytoin. More details of such drugs are
available in the BNF.
RETICULOENDOTHELIAL AND FETAL

The liver has an erythropoietic function in the embryo. The Kupffer cells in the
sinusoids are responsible for removal of bacteria in the portal blood.
386

What is the role of the liver in starvation?
Early starvation: glycogenolysis and gluconeogenesis (muscle breakdown to
form amino acids).
Late starvation: breakdown of fatty acids.
Formation of ketone bodies, for use by the brain. Ketosis occurs when the
liver’s glycogen reserves are used up and the liver metabolizes fat to pro-
duce ketones. These are used as an energy source by respiring tissues, spar-
ing glucose for the brain, which relies on a proportion of glucose for
metabolism but can also use ketone bodies.
387
97 Functions of the stomach

What are the functions of the stomach?
How is acid production controlled?
What does the stomach secrete?
What are the effects of gastrectomy?
Related Topics
Topic Chapter Page
Stomach 17 46

What are the functions of the stomach?
The key is dividing this up into categories and having these ready, with an
explanation of each. The key functions are:
• Reservoir for food, mixing of food with gastric secretions to form chyme
• Endocrine function: secretion of gastrin
• Exocrine functions:
• production of acid – digestion of food and immune function
• enzyme production (pepsin) for protein digestion, intrinsic factor and
mucus
RESERVOIR AND MIXING FUNCTIONS

The stomach has highly distensible smooth muscle walls, which relax on the arrival
of a meal. Its volume can increase to 1.5 L without an increase in pressure.
The stomach undergoes peristaltic waves, which expel only a small amount of chyme
into the duodenum with each wave. These waves, generated by inherent electrical
activity in the smooth muscle of the stomach, combined with hormonal influences,
help to mix the stomach’s contents and produce chyme.
388
APPLIED SURGICAL PHYSIOLOGY functions of the stomach
ENDOCRINE FUNCTION
The stomach produces a hormone called gastrin (G cells of the antral mucosa).
This hormone is released in response to the cephalic phase controlling acid secre-
tion in the stomach.
Gastrin acts to increase the secretion of acid by the parietal cells in the stomach.
It also causes histamine release, which potentiates the release of acid.
H2-receptor blockers such as ranitidine and cimetidine reduce gastric acidity by

blocking this mechanism.
EXOCRINE FUNCTIONS
Acid secretion
• Two litres of HCl secreted per day
• Converts pepsinogen to pepsin, the active protease
• Converts ferric (Fe3!) iron to ferrous (Fe2!) for jejunal absorption
• Creates an acid environment in duodenum to facilitate iron and calcium
absorption
• Acid also provides innate immunity to infection.
There are three phases of control of acid secretion.
Cephalic phase
• Initiated by sight and smell of food
• Vagally mediated increase in acid production
• Stimulates gastrin secretion.
Gastric phase
• Food present in the stomach causes chemical and mechanical stimulation
• This causes further gastrin release, and reflexly (via vagal afferents and efferents)
increases acid secretion.
Intestinal phase
Duodenal distension and presence of degradation products bring about a reflex
decrease in acid secretion. Hormones released that mediate this include secretin,
gastric inhibitory peptide (GIP) and cholecystokinin (CCK).
The goblet cells in the stomach produce mucus, which lines the gastric mucosa and
prevents the formation of ulcers secondary to the acidity.
389
APPLIED SURGICAL PHYSIOLOGY functions of the stomach
INTRINSIC FACTOR
This is produced by the parietal cells. It binds to vitamin B12 in the stomach and is
necessary for its absorption in the terminal ileum.
Loss of the parietal cells and intrinsic factor by autoantibodies (pernicious anaemia)
or gastrectomy causes a lack of vitamin B12, an essential co-factor for red cell pro-
duction. This leads to megaloblastic anaemia.
Resection of the terminal ileum in, for example, Crohn’s disease has a similar effect.

Based on your knowledge of the functions of the stomach, what are the
effects of a total gastrectomy?
• Early dumping syndrome: food of high osmolarity, not mixed in the
stomach, causes rapid fluid shift and oligaemia. This causes fainting and
sweating from hypovolaemia
• Late dumping syndrome: caused by rebound hypoglycaemia, or high
insulin levels experienced after a high carbohydrate load is presented and
absorbed by the duodenum. Similar symptoms to above
• Pernicious anaemia (see above) and iron deficiency anaemia (see below)
• Early satiety: loss of reservoir function
• Bilious vomiting: loss of pyloric sphincter
• Hypocalcaemia and iron deficiency: hypochlorhydia (reduced HCl secre-
tion) interferes with the absorption of Ca2! and iron
• Gastric stump carcinoma: cancers occur at the gastrojejunal anastomosis
20 years or so after surgery. This may be a result of chronic irritation of
gastric mucosa by duodenal secretions
• Gallstones: caused by decreased gallbladder motility post-vagotomy
390
98 Neuromuscular junction

What happens at the neuromuscular junction (NMJ)?
How do paralysing agents work?
How are paralysing agents reversed?
What’s a synapse? Draw me one.
What do we mean by depolarizing and non-depolarizing blockers?
What is the molecular basis of myasthenia gravis and how is it diagnosed?
Related Topics
Topic Chapter Page
SEQUENCE OF EVENTS AT THE NMJ

The NMJ is the junction of an % motor nerve (somatic) terminal with the motor
end-plate (e.g. phrenic nerve on diaphragm).
The sequence of events at the neuromuscular junction is as follows:
• The action potential arrives at a motor nerve terminal
• This nerve terminal is depolarized
• Calcium enters the cell via voltage-gated calcium channels
• Acetylcholine-containing vesicles are mobilized on interaction with calcium and
exocytosis occurs; the acetylcholine is released into the NMJ
• Acetylcholine interacts with its receptor at the muscle end-plate, inducing an
excitatory post-synaptic potential (EPSP); it is broken down by
acetylcholinesterase in the nerve cleft
• The summation of EPSPs beyond threshold for the muscle induces an action
potential in muscle
• Excitation–contraction coupling occurs as the action potential is propagated
along muscle and causes release of calcium from the sarcoplasmic reticulum
within the muscle cell; Ca2! causes muscle contraction.
391
APPLIED SURGICAL PHYSIOLOGY neuromuscular junction
Nerve terminal
Acetylcholine
ACh vesicles
ACh
Acetylcholinesterase
ACh
Acetylcholine
receptors
Motor endplate
Figure 98.1 Diagrammatic representation of the neuromuscular junction.
DRUGS
Muscle relaxants
Suxamethonium
Short-acting muscle relaxant (lasts 5 minutes). Acts by mimicking acetylcholine but
it is hydrolysed much more slowly than acetylcholine, so a depolarizing block
occurs as the muscle becomes refractory. The depolarization is the reason that this
drug causes twitching in patients. Its action cannot be reversed. It does not compete
with acetylcholine for the receptor.
Vecuronium and atracurium

Derivatives of curare from the poison arrow frog. They are long-acting muscle relax-
ants and act by antagonizing the action of acetylcholine (competitively) through
action on its receptor. They do not produce depolarizing block so they can be
reversed.
Muscle relaxants aid the surgeon and the anaesthetist in control of the airway and
muscle tone of the patient, allowing the inspection of the abdominal contents and
the closure of a laparotomy without undue tension, and also allowing the abdom-
inal contents to fall back into the wound.
392
APPLIED SURGICAL PHYSIOLOGY neuromuscular junction
Neostigmine
An acetylcholinesterase inhibitor, neostigmine is applied when reversal of long-
acting block is desired. The resulting increased acetylcholine competes with these
agents for the receptor, relieving the block. It causes prolonged (4-hour) gut con-
traction and bradycardia (acetylcholine excess) so atropine (muscarinic blocker,
parasympathetic effect) is given in combination with it.

What is the molecular basis of myasthenia gravis and how is it diagnosed?
Antibody-mediated destruction of acetylcholine receptors.
This results in weakness and fatiguability of skeletal muscle (e.g. fatiguable
ptosis of eyelid clinically on prolonged upward gaze).
Edrophonium (Tensilon) is a short-acting acetylcholinesterase inhibitor,
and its administration briefly reverses the weakness, by increasing the
amount of available acetylcholine in the neuromuscular junction. This is
used as a diagnostic tool.
Thymectomy can be curative.
393
99 Oxygen transport

Draw the oxygen–haemoglobin dissociation curve?
What are the physiological advantages of its shape?
What would move the curve to the right or left?
What are the molecular properties of haemoglobin?
Why is carbon monoxide so toxic?
What molecules can haemoglobin carry?
How does a pulse oximeter work?
What determines oxygen delivery to the tissues?
Related Topics
Topic Chapter Page
HAEMOGLOBIN: THE MOLECULE

• Each molecule consists of four subunits (two &, two '), bound to a central
Fe2! ion
• Each subunit consists of a molecular group called haem, and a polypeptide chain
called globin
• Oxygen binds reversibly to haemoglobin; 97 per cent of oxygen in the blood is
carried this way, the remainder being dissolved
• Each subunit binds one oxygen molecule (each molecule binds four oxygen
molecules)
• Once one oxygen molecule has bound to the haemoglobin molecule, this
increases the affinity of the other sites for oxygen via a change in conformation
of the haemoglobin structure
• Haemoglobin also carries carbon dioxide, by combining reversibly with it to
form carbaminohaemoglobin, although the majority of CO2 combines with
H2O to form H! and HCO3" (see ‘Acid–base balance’, Chapter 84, page 349);
a small proportion is dissolved
• Haemoglobin may also combine reversibly with H! ions and buffer them
• It combines irreversibly with carbon monoxide to form carboxyhaemoglobin,
which is then no longer of any use for oxygen transport
394
APPLIED SURGICAL PHYSIOLOGY oxygen transport
• Carbon monoxide has a much higher affinity for haemoglobin than oxygen; this
is why carbon monoxide is so toxic
• Fetal haemoglobin has a higher affinity for oxygen than adult Hb, because the
globin chains are different (has two ) rather than ' subunits)
• Point mutations can occur, resulting in abnormal types of haemoglobin such as
HbS (sickle cell).
100
SaO2 (%)
50 Increasing PCO2,
[H!], 2,3-DPG, temp
(the Bohr effect)
5.3 10
PAO2 (kPa)
Figure 99.1
The relationship between arterial PO2 (the partial pressure of oxygen in the blood)
and oxygen saturation (percentage of haemoglobin molecules carrying oxygen) is a
sigmoid-shaped curve (Fig. 99.1).
The steep part of the curve corresponds to the fact that binding subsequent O2
molecules becomes easier after binding the first one and enables easy oxygenation
for small increases in PO2 as described above.
It also enables the haemoglobin to be released at low partial pressures of oxygen (as
in the tissues).
CHANGES IN AFFINITY FOR OXYGEN

The curve is shifted to the right in conditions that decrease its affinity for oxygen (it
takes a higher PO2 to produce the same saturation) – dotted curve on Fig. 99.1.
Such conditions include:
• Increasing CO2 concentration
• Increasing DPG concentration
• Increasing acidity
• Increasing temperature.
395
APPLIED SURGICAL PHYSIOLOGY oxygen transport

What factors shift the curve to the right?
This list may be difficult to remember under pressure. The way to
remember it is to remember that in the tissues, where the oxygen is to be
offloaded, the affinity of haemoglobin for oxygen needs to be reduced. So
an increased temperature (respiring tissue), acidity (lactic acidosis), CO2
concentration (produced by the tissues) and DPG (also produced by the
tissues) would all be expected to produce such a change.
Note that the fetal haemoglobin curve lies to the left of the adult curve because its
affinity for oxygen is higher as it takes oxygen away from maternal blood.

What factors determine oxygen delivery to the tissues?
This is determined by the oxygen delivery equation:
DO2 * [Hb] + SaO2 + CO + 1.34
1.34 # no. of millilitres of O2 carried by 1 g Hb
DO2 # oxygen delivery
CO # cardiac output
This is a useful equation to write in an exam, when faced with a hypoxic
patient to manage.
Improving any of the constituents of the equation will improve the
patient.
Cardiac output in surgical patient can often be improved by giving intra-
venous fluid (see Starling’s law of the heart and cardiovascular equations’
Oxygen saturation can be improved by putting the patient on high-flow
oxygen (see ‘Control of respiration’, Chapter 91, page 373).
The concentration of Hb may be improved by transfusion (remember that
the oxygen-carrying capacity of stored blood is limited).
396
100 Pituitary

How is the pituitary functionally and anatomically divided?
What hormones does the pituitary secrete?
How is pituitary secretion controlled?
What is Sheehan’s syndrome?
What are the physiological effects of hypophysectomy? What hormone
replacements are necessary?
How does the pituitary gland develop?
Describe the pituitary portal system.
Related Topics
Topic Chapter Page
Portal vein and portosystemic anastomosis 14 39
PITUITARY ANATOMY
The pituitary is divided, functionally and anatomically, into anterior and posterior.
The anterior part is also called the adenohypophysis, derived embryologically from
Rathke’s pouch – pharyngeal epithelium. The posterior part or neurohypophysis is
derived from hypothalamic tissue.
The pituitary stalk is called the infundibulum. It lies in the pituitary fossa and is infer-
ior to the hypothalamus.
The posterior pituitary consists of nerve terminals. The cell bodies of these nerves
are in the paraventricular and supraoptic nuclei of the hypothalamus, and this is
where the hormones are synthesized before release.
The anterior pituitary cells themselves synthesize hormones, which are under the
control of releasing hormones synthesized by the hypothalamus and released into
the portal system of capillaries (see ‘Portal vein and portosystemic anastomoses’,
The optic chiasm lies immediately anterior to the infundibulum. Tumours of the pitu-
itary affect the central fibres within the chiasma, producing a bitemporal hemianopia.
397
APPLIED SURGICAL PHYSIOLOGY pituitary
HORMONE SECRETION
Anterior pituitary
Hormone Site of action Action Controlling influence Pathologies
Growth Liver Hyperglycaemia GHRH secreted by Acromegaly
hormone Peripheral Secretion of insulin the hypothalamus is (epiphyses fused)
(GH) tissues growth factor I excitatory and Gigantism
(IGF-I), which somatostatin is Dwarfism
stimulates growth inhibitory
of unfused bone
Several anabolic
metabolic functions
Thyroid- Thyroid gland Promotes secretion Thyroid-releasing Hyper- and
stimulating of thyroxine (T4) and hormone (TRH) hypothyroidism
hormone triiodothyronine (T3) secreted by
(TSH) by the thyroid, and hypothalamus
increases their T3 and T4 feed back
synthesis negatively on the
pituitary
Prolactin Breast Promotes breast Dopamine produced Prolactinoma
development and by the hypothalamus
milk production has an inhibitory
effect
Adreno- Adrenal Promotes CRH (corticotrophin- Cushing’s disease,
corticotrophic cortex (zona secretion releasing hormone) Addison’s disease
hormone fasciculata) of cortisol and negative feed-
(ACTH) back by cortisol
Follicle- Gonads Promotes secretion Gonadotrophin-
stimulating of oestrogen and releasing hormone
hormone (FSH) progesterone in the (GnRH) by the
and luteinizing female, in a cyclical hypothalamus and
hormone (LH) fashion (menstrual complex feedback
cycle) and mechanisms by their
testosterone in target hormones
the male
398
Posterior pituitary
Hormone Site of action Action Controlling influence Pathology
Vasopressin Collecting duct Water retention Its release is increased Syndrome of
(antidiuretic of the nephron by increased tonicity of inappropriate
hormone or blood (dehydration), ADH secretion
ADH) which is sensed by the (SIADH),
lamina terminalis and diabetes
the neurons themselves insipidus
Oxytocin Uterus Initiation of Neural inputs from
Collecting duct parturition/ stretch receptors in
of the nephron uterine uterus
contraction
Smooth muscle Milk secretion Neural inputs from
cells in breast Water retention suckling child (breast) –
milk ejection reflex
IMPORTANT PATHOLOGIES
This section is not exhaustive.
Hypopituitarism
Causes
Hypophysectomy, pituitary adenoma, irradiation, Sheehan’s syndrome – pituitary
infarction following postpartum haemorrhage. Symptoms related to lack of hormones:
• Gonadotrophin: amenorrhoea, osteoporosis, loss of libido
• Corticosteroid: tiredness, postural hypotension, weight loss, hyponatraemia
• Androgen: impotence, loss of muscle and hair.
• Thyroid: constipation, weight gain, (hypothyroidism).
Diagnosis
Hormone levels (paired T4/TSH; Synacthen test).
Treatment
Hormone replacement – hydrocortisone, T4, testosterone/oestrogen and GH.
Pituitary tumours
Almost always benign adenomas; 35 per cent secrete prolactin, 20 per cent GH,
30 per cent non-functioning.
• Signs/symptoms: bitemporal hemianopia, hypopituitarism (above), headache
• Diagnosis: hormone tests and magnetic resonance imaging
399
• Treatment: dopamine agonists may shrink tumour; hypophysectomy (trans-

sphenoidal versus open); radiotherapy (usually for remnants or if unfit for
surgery).
Cushing’s syndrome
Called Cushing’s disease if secondary (pituitary ACTH hypersecretion).
Can be caused by adrenal cortical tumours (cortisol secreting) or ectopic ACTH
secretion (e.g. small-cell lung cancer), or iatrogenic (steroids).
• Signs/symptoms: glucocorticoid excess: weight gain with truncal obesity, muscle
weakness, depression, thin skin and bruising, hyperglycaemia
• Diagnosis: dexamethasone suppression test (to diagnose Cushing’s syndrome);
CT/magnetic resonance imaging (MRI) of adrenals/pituitary (localization) and
chest radiograph; inferior petrosal sinus sampling
• Treatment: adrenalectomy for tumours; hypophysectomy for pituitary lesions.
Acromegaly
Caused by hypersecretion of GH from a pituitary tumour.
• Signs/symptoms: as for pituitary tumour (above), proximal myopathy, carpal
tunnel syndrome, overgrowth of bones (prognathism, prominent supraorbital
ridges, large spade-shaped hands)
• Diagnosis:
• clinical to an extent, review past photographs as well as physical examination
• oral glucose tolerance test
• CT/MRI of pituitary
• Treatment: hypophysectomy ( radiotherapy.
400
101 Starling forces in the capillaries/oedema

What are the causes of oedema and how are they generated?
Tell me about/draw me a diagram of the Starling forces in the capillaries.
Why do patients with heart failure get oedema?
Related topics
Topic Chapter Page
Mastectomy, axillary dissections and breast reconstruction 36 120
STARLING FORCES IN THE CAPILLARIES

Lymphatics
Arterial end Venous end
32 15
40 20
20 15
Direction of bloodflow
Capillary
Figure 101.1
Figure 101.1 can be drawn in any viva question asking to explain the Starling forces
in the capillaries or mechanism for formation of oedema. Explanation of Fig. 101.1:
• Blood flows from the arterial end, through the capillary, to the venous end
• The hydrostatic pressure (generated by the pressure from the left ventricle) at
the arterial end is obviously higher
401
APPLIED SURGICAL PHYSIOLOGY Starling forces in the capillaries/oedema
• At the arterial end of the capillary (1), which is leaky to fluid, the hydrostatic
pressure exceeds the colloid oncotic pressure (this is the osmotic pull of the
large molecules in the blood, pulling any fluid pushed into the interstitial space
by hydrostatic pressure back into the capillary). Net movement of water here is
out of the capillary into the interstitial space
• At the venous end of the capillary (2), the colloid oncotic pressure now exceeds
the hydrostatic pressure and water is pulled back into the capillary. Hence the
Starling ‘filtration–reabsorption’ forces.
Any excess fluid in the interstitial space goes into the lymphatic system and is
returned to the circulation.
OEDEMA
The various causes of oedema can be explained using Fig. 101.1.
Increased leakiness of capillaries
• Occurs in burns, sepsis or acute respiratory disease syndrome (ARDS).
Increased hydrostatic pressure at the venous end
• This leads to increased hydrostatic pressure throughout the capillary and more
net movement of fluid into the interstitial space
• Occurs in DVT, venous hypertension (which often accompanies varicose veins
and ulcers), pelvic venous compression (by tumour), liver cirrhosis, renal cell
carcinoma infiltration and right-sided heart failure.
Decreased colloid oncotic pressure
• Basically any cause of hypoalbuminaemia
• Liver failure (lack of synthesis), increased loss: nephrotic syndrome, protein-
losing enteropathies, poor nutrition, etc.
Failure of lymphatic system to drain # lymphoedema
• Primary lymphoedema (unknown aetiology)
• Secondary lymphoedema: damage of the lymphatic system caused by surgery
(especially breast), radiotherapy or carcinoma.
Note that hypertension at the arterial end, according to this model, might be
expected to generate oedema, but does not.
402
102 Starling’s law of the heart and
cardiovascular equations

What is the effect on blood pressure of losing a litre of blood? What
mechanisms compensate?
What are the immediate cardiovascular effects of cross-clamping the
aorta in an aneurysm repair?
What are the cardiovascular effects of amputating the right leg?
What are the cardiovascular effects of standing up from a lying position?
Why would an anaesthetist be worried about a patient in heart block?
What are the cardiovascular effects of a Valsalva manoeuvre?
Related Topics
Topic Chapter Page
Inotropes 113 466
Altitude 86 356
Shock 122 510
Key learning point

This section will come up in some guise in almost every physiology and
critical care viva, and can be applied to all of the above questions. This
topic will provide a methodical approach to tackling such questions.
403
APPLIED SURGICAL PHYSIOLOGY Starling’s law of the heart
IMPORTANT RESTING VALUES

Stroke volume (SV): the amount of blood ejected by the left ventricle in one car-
diac cycle (70 mL).
Cardiac output (CO): the amount of blood ejected by the heart in 1 minute. If rest-
ing heart rate is also taken at 70: 70 + 70 # 4900, which is near enough 5000 or 5 L.
IMPORTANT RELATIONSHIPS
BP # CO + SVR (Ohm’s law) (1)
CO # SV + HR (2)
where SVR is systemic vascular resistance, HR heart rate and BP blood pressure.
Key learning point

On any question related to this topic, start by writing these equations out
on the paper provided and use them to explain the physiology and
responses (see examples below).
DETERMINANTS OF CARDIAC OUTPUT

Cardiac output is determined by three determinants: preload, contractility and
afterload on the heart.
Preload is determined by Starling’s law of the heart (see below).
Contractility is affected by disease, which affects the heart muscle or mechanics;
pathologies such as myocardial infarction, cardiomyopathy and pericardial effusion
will affect this. Sympathetic activity also increases contractility.
Afterload is determined by increased blood pressure or SVR or such pathologies as
aortic stenosis.
STARLING’S LAW OF THE HEART

Definition
The relationship between left ventricular end-diastolic volume (LVEDV) and
stroke volume (SV) in the heart, as shown in Fig. 102.1, which illustrates the rela-
tionship between LVEDV and SV.
404
Actin and myosin fibres

no longer overlap
CO Actin (thin)
SV
Myosin (thick)
Figure 102.2
LVEDV
CVP
JVP
PAWP
VRet
Figure 102.1 Figure 102.3
At low values of LVEDV, the amount ejected by the heart (SV) is proportional to the
degree that the actin and myosin fibres are stretched by the blood returning to the heart.
(Figure 102.2 shows one sarcomere: the myosin fibres are thick and the actin is thin).
Key learning point

Actin rhymes with thin
At the point at which the interdigitating fibres of actin and myosin in cardiac mus-
cle no longer overlap (Fig. 102.3, see arrow in Fig. 102.1), increasing LVEDV no
longer causes an increase in SV. This is because there are no longer strong cross-
bridges between the actin and myosin.
CO is SV in a unit time and the two are proportional, the relationship between CO
and LVEDV produces a similar graph.
Similarly, central venous pressure (CVP) and jugular venous pressure (JVP) are
measures of, and proportional to, LVEDV, as is pulmonary artery wedge pressure
(PAWP), so any of these could be placed on the x axis (as above). The importance
of this will become clear in the discussion below.
Figure 102.4 illustrates the effects of certain treatments on this curve, a commonly
asked MRCS viva question.
Intravenous fluid will increase the venous return, or JVP or CVP, so will move you
along Starling’s curve (see arrow).
405
CO
SV
LVEDV
CVP
JVP
PAWP
VRet
Figure 102.4
Inotropes increase the contractility of the heart. Giving an inotrope (or sympathetic
activation), or decreasing the afterload by giving a vasodilator such as GTN, will
move the patient to a higher curve (dashed line in Fig. 102.4), because the same
preload will now result in more blood ejected (or a higher stroke volume).
' Blockers or treatments that antagonize the sympathetic nervous system will
move the patient to a lower Starling’s curve (dotted line in Fig. 102.4) for the oppo-
site reason.

What are the cardiovascular effects of cross-clamping the aorta in
AAA repair?
1. CO # SV + HR
2. BP # CO + SVR
TPR increases markedly, pushing up blood pressure (2)
To compensate, there is a reflex bradycardia to reduce CO and hence BP (1)
406

What happens to your capillaries when you stand up/perform a Valsalva
manoeuvre?
1. CO # SV + HR
2. BP # CO + SVR
3. Draw Starling’s curve
Standing up leads to pooling of blood, and a decrease in venous return
This leads to a decrease in SV and hence CO (Starling’s curve)
This leads to a decrease in BP (2)
This drop in BP is sensed by the baroreceptors (see ‘Blood pressure
control’, Chapter 87, page 358) and there is a reflex constriction of the
capillaries and arterioles to maintain BP as the CO component of Eqn (2)
has dropped. There is also a reflex tachycardia (1), and an increase in
contractility caused by sympathetic activation of the heart.
A Valsalva manoeuvre (forced expiration against a closed glottis) causes
increased intrathoracic pressure and hence a decrease in venous return as
above.

Why would an anaesthetist be worried about a patient with heart block?
1. CO # SV + HR
2. BP # CO + SVR
3. Draw Starling’s curve
This question needs lateral thinking.
Induction agents cause vasodilatation and a decrease in SVR (2)
This causes the BP to drop (2)
To maintain reflexly the BP the SV and HR need to increase (1), but the
heart block prevents a reflex tachycardia.
See also ‘Blood pressure control’ Chapter 87, page 358 for discussion of
the effects of haemorrhage.
407
103 Swallowing and oesophageal physiology

What is the sequence of events in swallowing?
What sphincteric mechanisms are there in the lower oesophagus and
how is reflux normally prevented?
How is reflux investigated?
Related topics
Topic Chapter Page
Stomach 17 46
SWALLOWING
Oral phase
• Food is chewed and a bolus is formed, which is pushed to the posterior pharynx
by the tongue
• Here, afferent impulses in cranial nerves IX and X are transmitted to the
swallowing centre (medulla), which reflexly triggers swallowing via efferent
impulses in cranial nerves IX and X
• Respiration is also reflexly inhibited.
Pharyngeal phase
• The soft palate is pulled upward and palatopharyngeus helps to close the
nasopharynx and prevent reflux
• The true vocal folds are apposed and the larynx elevates. The bolus pushes
against the epiglottis to close the entrance to the respiratory tract and prevent
aspiration
• Upper oesophageal sphincter (cricopharyngeus muscle) relaxes
• The constrictor muscles (superior, middle, inferior) sequentially contract and
force the bolus down into the oesophagus.
Oesophageal phase
• Bolus is propelled along the oesophagus by a primary peristaltic wave behind
the bolus
408
APPLIED SURGICAL PHYSIOLOGY swallowing and oesophageal physiology
• Takes 9–10 seconds to traverse the oesophagus

• Secondary waves can occur if the bolus is not cleared
• Tertiary contractions are non-propulsive and their presence is pathological.
LOWER OESOPHAGEAL SPHINCTER

This is a physiological sphincter (there is no anatomical sphincter here), located at
the lower 2 cm of the oesophagus. It is an area of high pressure. Its function is to pre-
vent reflux of acid into the oesophagus. The factors preventing reflux are as follows:
• Acute angle of entry to the stomach acts like a valve
• Right crus of diaphragm acts as sling around the lower oesophagus
• Intra-abdominal pressure acts on segment of oesophagus below the diaphragm
• Mucosal folds act as a valve
• Lower oesophagus is normally contracted.
A degree of reflux occurs through this sphincter in normal individuals. However,
several factors can lead to disruption of this sphincter, and hence reflux:
• The upper stomach can herniate through the diaphragm (hiatus hernia)
• Increased intra-abdominal pressure in pregnancy or after a large meal can cause
reflux
• Some individuals have an incompetent lower sphincter.
See ‘GORD and Barrett’s oesophagus’, Chapter 56, page 214 for further discussion.
409
7
PART
CRITICAL CARE
104 Acute pancreatitis 413
105 Acute respiratory distress syndrome 419
106 Brain-stem death and transplantation 423
107 Burns 427
108 Compartment syndrome 433
109 Criteria for admission to the ITU and HDU 439
110 CVP lines and invasive monitoring 443
111 Fluid balance 452
112 Head injury and intracranial pressure 459
113 Inotropes 466
114 Intubation and ventilation 470
115 Nutrition 477
116 Oliguria and renal replacement 482
117 Pneumothorax 488
118 Pulse oximetry 491
119 Respiratory failure and respiratory function tests 495
120 Sedation 500
121 Sepsis and SIRS 505
122 Shock 510
123 Systemic response to surgery 514
104 Acute pancreatitis

What is pancreatitis?
What are the clinical features of pancreatitis?
What are the possible causes of pancreatitis?
How would you manage pancreatitis?
What are the complications of pancreatitis?
What scoring systems do you know of for pancreatitis and what use are they?
How useful is serum amylase in the diagnosis of acute pancreatitis?
What are the most important bedside tests in the context of pancreatitis?
What is a pancreatic pseudocyst?
Related topics
Topic Chapter Page
Shock 122 514
Nutrition 115 477
Acute respiratory distress syndrome 105 419
Clinical features
• Acute, severe abdominal pain; usually constant, epigastric and radiating into the
back, and relieved by sitting forwards
• Vomiting is early and profuse
• Patient usually shocked with rapid pulse, cyanosis
• Abnormal temperature: either subnormal or pyrexial
• Examination of the abdomen reveals generalized tenderness and usually
guarding with or without rebound
• 30 per cent of cases have mild jaundice as a result of oedema of the pancreatic
head obstructing the common bile duct
• After a severe attack, patient may develop a bluish discoloration in the loins
from extravasation of blood-stained pancreatic juice into the retroperitoneum
(Grey Turner’s sign)
413
CRITICAL CARE acute pancreatitis

What is pancreatitis?
Acute pancreatitis: acute inflammation of the pancreas is a common cause
of acute abdominal pain with considerable associated morbidity and
mortality. It can be divided into mild, moderate and severe, depending on
presentation.
A mnemonic to remember the causes of pancreatitis is GET SMASHED:
G: gallstones (probably the most common cause, impacted at the ampulla
of Vater and causing backwash of activated pancreatic enzymatic juice
into the parenchyma of the pancreas, leading to pancreatic autolysis
and haemorrhage)
E: ethanol (alcohol is a very common cause of pancreatitis and people
with alcohol problems often develop chronic pancreatitis after a number
of bouts acutely)
T: trauma
S: steroids
M: mumps (paramyxoviruses)
A: autoimmune (panarteritis nodosa or PAN, systemic lupus erythematosus
or SLE)
S: scorpion sting/snake bite!!
H: hypercalcaemia, hyperlipidaemia/hypertriglyceridaemia and hypothermia
E: ERCP (endoscopic retrograde cholangiopancreatography)
D: drugs (e.g. sulphonamides, frusemide, azathioprine, non-steroidal anti-
inflammatory drugs or NSAIDs)
Less common causes: carcinoma of the head of pancreas, pancreas divisum,
long common bile duct, fat necrosis, pregnancy, pancreatic ischaemia as a
result of bypass surgery.
• Bluish discoloration and bruising may occur in the periumbilical region

(Cullen’s sign).
Investigations
Tests confirm the diagnosis and utilize the criteria below to determine the severity.
In addition to arterial blood gases and venous sampling for amylase, liver function
tests (LFTs), full blood count (FBC) and urea and electrolytes (U+Es):
• ECG: flattened T waves or arrhythmias may cause confusion with cardiac
ischaemia.
414
• Abdominal radiograph: not usually helpful in acute pancreatitis but can show
pancreatic calcification in cases of acute-on-chronic pancreatitis. In some cases
a ‘sentinel loop’ of proximal jejunum may be seen to be dilated.
• Erect chest radiograph to exclude a perforation, which can present in a similar
manner.
• Ultrasonography: may show gallstones and/or dilated common bile duct and
pancreatic duct. Often gives poor views of the pancreas. Good for looking for
collections in the acute setting – can also be used to look for pleural effusions.
• Abdominal computed tomography (CT) is the investigation of choice for acute
pancreatitis but is not usually performed before 48 hours of onset of the
episode. Diagnostically, fat streaking is seen around the pancreas or fluid may be
seen in the lesser sac, and this may be confirmatory in cases where the serum
amylase is normal. Further, later imaging may reveal necrosis in the pancreas or
the formation of a pancreatic pseudocyst.
• Serum calcium: may well be lowered as a result of fat saponification, and may
lead to tetany and cardiac arrhythmias in severe cases.
ASSESSMENT OF PANCREATITIS SEVERITY

It is essential to perform arterial blood gas sampling in all patients with pancreatitis
to assess their acid–base status (see ‘Acid–base balance’, Chapter 84, page 349) and
to keep a regular check on their arterial PO2. Serum amylase is used as a diagnostic
criterion but, in 10 per cent of cases, it is normal, particularly in acute-on-chronic
pancreatitis, where there is a loss of acinar cell mass, or in severe pancreatitis with
pancreatic necrosis.
Scoring systems: two very well-known and used methods are the Ranson and the
Glasgow criteria.
Glasgow criteria for severe pancreatitis

The following criteria are assessed over the first 48 hours. Three or more indicate
severe pancreatitis with a high mortality:
• Age ! 55 years
• Hyperglycaemia (glucose ! 10 mmol/L in the absence of a history of diabetes)
• Leukocytosis (! 15 " 109/L)
• Urea ! 16 mmol/L after adequate rehydration
• PO2 # 8 kPa on arterial blood gases
• Calcium " 2.0 mmol/L
• Albumin " 32 g/L
• Lactate dehydrogenase (LDH) ! 600 IU/L
• Raised aspartate transaminase (AST) ! 100 IU/L.
415
Ranson’s criteria for pancreatitis

Ranson’s criteria on admission
• Age ! 55 years
• White blood cell count (WCC) ! 16 000/#L
• Glucose ! 11 mmol/L (! 200 mg/dL)
• Serum LDH ! 400 IU/L
• Serum AST ! 250 IU/L.
Ranson’s criteria after 48 hours of admission:
• Fall in haematocrit by more than 10 per cent
• Fluid sequestration of ! 6 L
• Hypocalcaemia (serum calcium # 1.0 mmol/L (# 8.0 mg/dL)
• Hypoxaemia (PO2 # 80 mmHg )
• Increase in urea to ! 1.98 mmol/L (! 5 mg/dL) after intravenous fluid hydration
• Hypoalbuminaemia (albumin # 32 g/L (# 3.2 g/dL) in the first 48 hours of
admission
• Base deficit of ! 4.
The prognostic implications of Ranson’s criteria are as follows:
Score 0–2: 2 per cent mortality rate
Score 7–8: 100 per cent mortality rate.
PATHOPHYSIOLOGY OF MARKERS OF SEVERITY

• Hypoxia: a result of acute respiratory distress syndrome (ARDS) and pleural
effusions.
• Hypocalcaemia: calcium is chelated after the saponfication of omental fat by
pancreatic lipases.
• Acidosis: anaerobic respiration of tissues as a result of poor perfusion leads to
a lactic acidosis.
• High urea: reflects dehydration.
• High WCC: acute inflammatory response and probable pancreatic necrosis $
supervening bacterial infection.
TREATMENT
This is largely conservative and non-surgical but aggressive, consisting of:
• Fluid resuscitation and replacement with either colloid or blood transfusion
to treat profound shock that can result from acute pancreatitis. Electrolyte
416
replacement is often required, with particular attention to potassium and calcium

if necessary. All patients should be catheterized and a urometer should be used to
produce a strict record of hourly urine output. Fluid sequestration can be very
severe in acute pancreatitis, requiring many litres of fluid replacement to keep up.
It is not uncommon for initial resuscitation volumes of an individual with acute
pancreatitis to be of the order of 10–15 L over several hours.
• Analgesia: pain relief with pethidine commonly. Morphine is said to produce
sphincter of Oddi spasm but there is little evidence to support this theory.
Patient-controlled analgesia (PCA) can be useful in this context.
• Antibiotics: if profound pyrexia, positive blood cultures or associated with
gallstones. Antibiotic of choice is imipenem (very broad spectrum with good
Gram-negative cover). Some centres use a second-generation cephalosporin and
metronidazole. Many clinicians will put all patients with acute pancreatitis on
antibiotics.
• Pancreas is rested by making the patient nil by mouth with a low threshold for
nasogastic aspiration to prevent vomiting. The bowel is also rested because
acute pancreatitis often results in a generalized ileus.
• Early liaison with the intensive therapy unit (ITU) to ensure that smooth
handover can occur if ventilatory support or inotropic support is required.
• H2-receptor prophylaxis many be used in the stomach with ranitidine or a
proton pump inhibitor (PPI).
• ERCP $ sphincterotomy performed early improves outcome in the case of
proven impacted gallstones at the ampulla. (Note that ERCP can itself worsen
or cause pancreatitis.)
• Surgery for the drainage of an abscess or pseudocyst. Exploratory laparotomy in
the context of acute pancreatitis massively increases mortality and should be
avoided.
• Late necrosectomy for débridement of a necrotic pancreas is sometimes
required in very severe cases.
• Nutrition: total parenteral nutrition (see ‘Nutrition’, Chapter 115, page 477) is
instituted in severe cases, although there is a move towards early enteral feeding
wherever possible. Drugs to reduce pancreatic secretion or enzyme activation
are of no proven benefit.
• After an attack of pancreatitis secondary to gallstones, cholecystectomy is
advised as an elective interval procedure.
COMPLICATIONS
These can be systemic or regional.
Systemic
• Death
417
• ARDS and acute lung injury (see ‘Acute respiratory distress syndrome’,
Chapter 105, page 419)
• Renal failure and/or multiple organ dysfunction syndrome (MODS) (see
‘Sepsis and SIRS’, Chapter 121, page 505).
Regional
• Abscess formation: seen best on abdominal CT with contrast; associated with
persistently raised WCC and swinging pyrexia
• Pseudocyst: persistently raised amylase and pain, usually in the second week,
presenting as an epigastric mass
• Gastrointestinal bleeding: acute gastric erosions or peptic ulceration
• Splenic artery pseudoaneurysm formation
• Venous thrombosis: splenic vein, superior mesenteric vein, portal vein
• Diabetes mellitus as a result of $-islet cell destruction.
418
105 Acute respiratory distress syndrome

What is the definition of ARDS?
What are the clinical features of ARDS?
What is the definition of lung compliance? What factors affect this?
What are the causes of ARDS?
What is the role of decreased surfactant and steroids in ARDS?
What pathological processes cause ARDS?
What are the treatment options for ARDS?
What is the prognosis with and without infection?
Related topics
Topic Chapter Page
Criteria for admission to the ITU and HDU 109 439
Acute pancreatitis 104 413

What is the definition of ARDS?
ARDS is a clinical syndrome of acute respiratory failure with non-cardiogenic
pulmonary oedema leading to decreased lung compliance and hypoxaemia
refractory to oxygen therapy. It is characterized by:
• Diffuse pulmonary infiltrates seen on chest radiograph

• A normal pulmonary artery wedge pressure (PAWP " 18 mmHg) –
important for excluding pulmonary oedema secondary to elevated left
atrial pressure
• PaO2/FiO2 ratio of # 26.6 kPa
419
CRITICAL CARE acute respiratory distress syndrome
DEFINITION OF LUNG COMPLIANCE

This is the change in volume of the lung per unit change in pressure; thus a lung
with low compliance will need greater pressure to inflate it than a highly compliant
lung.
CLINICAL FEATURES
• Dyspnoea
• Tachypnoea and increased work of breathing
• Hypoxia
• Bilateral diffuse infiltrates on chest radiograph
• No clinical evidence of a raised left atrial pressure.
CAUSES
• Sepsis
• Multiple trauma
• Aspiration
• Fat embolism
• Chest injury
• Burns (both skin and airway)
• Pancreatitis
• Massive transfusion
• Disseminated intravascular coagulation (DIC)
• Cardiopulmonary bypass.
PATHOLOGY
ARDS can be considered to be the respiratory component to the multiorgan effects
of the systemic inflammatory response syndrome or SIRS (see ‘Sepsis and SIRS’,
Chapter 121, page 505). An acute inflammatory response is seen with an immedi-
ate exudative phase, involving activated neutrophils and activated macrophages
secreting a number of cytokine mediators of acute inflammation, including inter-
leukin 6 (Il-6), tumour necrosis factor % (TNF%), proteases, prostaglandins and oxy-
gen radicals. In turn, the complement system is activated along with local activation
of the clotting cascades. This increases capillary permeability by local endothelial
injury, manifesting as a decrease of type II pneumocytes and reduced pulmonary
surfactant production. This reduces lung compliance further by increasing the force
required to open the alveoli.
420
A proliferative phase is seen some days later with a hyperplasia of both type II
pneumocytes and the local fibroblast population, leading to a progressive intersti-
tial fibrosis. This may persist even after the patient has recovered.
These pathological changes result in:
• Decreased lung compliance increasing work of breathing
• Increased local atelectasis leading to reduced functional residual capacity
.
• Increased shunt and ventilation–perfusion (V/Q) mismatch
• Increased pulmonary vascular resistance, as a result of pulmonary oedema
compressing the vessels, and local vasoconstriction,
. as a reaction to localized
hypoxia, in an effort to improve the V/Q mismatch
• Pulmonary hypertension can lead to right heart dysfunction.
PRINCIPLES OF MANAGEMENT
• Transfer to ITU
• Management of the initial causative factor (if known)
• Nutritional support (see ‘Nutrition’, Chapter 115, page 477)
• Mechanical ventilation to aid in oxygenation, decrease the work of breathing for
the patient and improve the clearance of CO2. High levels of positive end-
expiratory pressure (PEEP) can be used to splint open the stiff alveoli to
prevent collapse during the respiratory cycle and improve alveolar recruitment.
Note that high PEEP increases the risk of alveolar barotrauma
• Reversed inspiratory:expiratory (I:E) ratios to increase inspiratory phase at the
expense of the expiratory phase (may allow a moderate degree of hypercapnia)
• Prone ventilation: redistributes secretions, minimizes basal atelectasis with
.
regular turning and improves V/Q mismatch, thereby improving oxygenation
• Strict fluid management – low threshold for monitoring PAWP (using
Swan–Ganz catheterization) and ensure that patient does not develop
cardiogenic pulmonary oedema as a result of fluid overload
• Others: inhaled prostacyclin, nitrous oxide and steroids may be of help but are
unproven.
PROGNOSIS
Outcome usually poor:
• 50–60 per cent mortality rate overall
• 90 per cent mortality rate if associated with sepsis.
Morbidity can be a considerable problem with progressive interstitial fibrosis and
pulmonary hypertension being relatively common sequelae of ARDS.
421

What is the role of decreased surfactant and inhaled nitric oxide in ARDS?
Surfactant: there are, to date, no randomized controlled trials showing a mor-
tality benefit from the administration of exogenous surfactant in the adult
population. There are, however, a number of case series of its successful use
in the neonatal population.
Nitric oxide: in theory, inhaled nitric oxide acts as a potent local pulmonary
vasodilator, improving perfusion to better-ventilated areas of lung. There is,
however, no class 1 evidence to show any mortality benefit from its use.
422
106 Brain-stem death and transplantation

What is brain-stem death?
Why is brain-stem function important for life?
Why it is an important concept?
How is brain-stem death diagnosed?
What medical criteria need to be satisfied in order for a diagnosis of
brain-stem death to be valid?
Who can diagnose brain-stem death?
When should these cases be referred to the coroner?
What is the pathway to organ explantation and harvesting?
What is a persistent vegetative state? Does it constitute brain-stem
death?
Related topics
Topic Chapter Page
With the advent of transplantation medicine, brain-stem death has become an

important economic and resource-based concept, although the diagnosis also gives
important prognostic information to the relatives and treating doctors.

What is brain stem death?
The Department of Health working party on brain-stem death in 1998
defined it in these terms:
‘… irreversible loss of the capacity for consciousness, combined with
irreversible loss of the capacity to breathe. The irreversible cessation of
brain stem function (brain stem death) whether induced by intra-cranial
events or the result of extra-cranial phenomena, such as hypoxia, will
produce this clinical state and therefore brain stem death equates with
the death of the individual.’
423
CRITICAL CARE brain-stem death and transplantation
WHY IS BRAIN-STEM FUNCTION IMPORTANT?

The brain stem includes nuclei controlling the body’s major homoeostatic mechan-
isms including:
• Respiratory centres
• Cardiovascular centres (autonomics – particularly vagus nerve nuclei)
• Arousal centres (reticular activating system)
• & Cranial nerve nuclei IV–XII.
Loss of these nuclei is incompatible with life.
CRITERIA FOR BRAIN-STEM DEATH

All brain-stem reflexes are absent:
• The pupils are fixed and do not respond to light (mediated by cranial nerves II
and III).
• There is no corneal reflex (sensory Va, motor VII cranial nerves).
• The vestibulo-ocular reflexes are absent. (No eye movements are seen during or
following the slow injection of at least 50 mL of ice cold water over 1 minute
into each external auditory meatus in turn.) Clear access to the tympanic
membrane must be established by direct inspection and the head should be
flexed at 30°.
• No motor responses within the cranial nerve distribution (cranial nerves VII
and Vc) can be elicited by adequate stimulation of any somatic area. There is no
limb response to supraorbital pressure.
• There is no gag reflex (sensory IX, motor X cranial nerves) or reflex response to
bronchial stimulation by suction catheter placed down the trachea.
• No respiratory movements occur when the patient is disconnected from the
mechanical ventilator. During this test it is necessary for the arterial CO2 to
exceed the threshold for respiratory stimulation, i.e. the PaCO2 should reach
6.65 kPa. This should be ensured by measurement of the blood gases. If 6.65 kPa
is not reached as the patient becomes anoxic the test must be stopped: brain-
stem criteria are not met.
Note on the apnoea test

The patient may be moderately hypothermic, flaccid and with a depressed meta-
bolic rate such that the PaCO2 rises slowly during apnoea. Hypoxia during discon-
nection should be prevented by delivering oxygen at 6 L/min through a catheter in
the trachea. The patient should first be ventilated with 100 per cent oxygen for
10 min, then with 5 per cent CO2 in O2 for 5 min. The ventilator should then be
424
disconnected for 10 mins. During this period, O2 should be delivered through a

catheter at the carina.
Those patients with pre-existing chronic respiratory disease, who may be responsive
only to supranormal levels of CO2 and who depend upon hypoxic drive, are special
cases who should be managed in consultation with an expert in respiratory disease.
A number of medical criteria must be satisfied before brain-stem death testing is deemed
to be lawful and valid:
• No sedation (barbiturates and benzodiazepines can accumulate and need to be
stopped for some time before brain-stem testing can begin)
• No muscle relaxants (this must be confirmed by the use of a standard
neuromuscular stimulator on one of the limbs)
• Patient must be normothermic (hypothermia must be excluded)
• Patient must have normal electrolyte levels and be normoglycaemic
• Decerebrate or decorticate posturing is incompatible with brain-stem death
although true spinal-mediated reflexes may be compatible with the diagnosis.
The diagnosis of brain-stem death should be made by at least two medical practi-
tioners who have been registered for more than 5 years, are competent in this field
and are not members of the transplant team; at least one of the doctors should be a
consultant. Two sets of tests should always be performed; these may be carried out
by the two practitioners separately or together.
The timing between these two sets of tests will vary according to the pathology in
question and the individual situation but brain-stem death can be diagnosed only
after two full sets of criteria have been met.
ORGAN TRANSPLANTATION
If the patient is deemed to be a potential organ donor then the transplant coord-
inator for the unit should be contacted as soon as possible after the diagnosis of
brain-stem death. If they are contacted before the diagnosis is made, the patient’s
relatives should be informed of this. The transplant coordinator will ensure that
appropriate informed assent is gained from the relatives and that all virology, ser-
ology and tissue typing is performed appropriately after this (see ‘Renal transplant-
ation’, Chapter 40, page 140, for an example of this process).
DONOR CARDS
Although a signed donor card of the patient’s intentions is, by law, binding and
overrides any concerns voiced by the relatives, in practice organs are rarely har-
vested against the relative’s wishes.
425
PATHWAY TO TRANSPLANTATION
• Brain-stem death diagnosed
• ' Coroner informed
• Transplant coordinator involved
• Relatives consulted
• Blood tests, virology and serology, and other screening tests
• Donor must be screened for malignancy including glioblastoma
• ' Surgical and anaesthetic interventions to assess viability of organs (e.g.
Swan–Ganz catheterization is often performed if heart–lung or heart
explantation is expected)
• Organ harvesting by dedicated transplant team (heart–lung last).
INFORMING THE CORONER

In any case where the cause of brain-stem death is not clearly the result of natural
causes the coroner, coroner’s officer or, in Scotland, the procurator fiscal must be
consulted. The medical staff involved in the care of the patient ought to be the ones
who contact the coroner if this is necessary, although the transplant coordinator is
the person usually responsible for identifying who is in lawful possession of the
body and for obtaining the necessary authorization for organ removal.
PERSISTENT VEGETATIVE STATE

This should on no account be confused with brain-stem death. This is a state where
there is no evidence of higher brain function but brain-stem reflexes are intact.
There is much controversy about the definition and prognosis of persistent vegeta-
tive state (PVS) and there are reports of PVS being at least partially reversible in the
literature. Some functional brain studies have shown some of these patients to have
higher brain activity as a result of somatic stimuli despite no outward clinical evi-
dence of this.
426
107 Burns

How would you determine the area of a burn?
How would you determine the thickness of a burn?
Which burns patients need intravenous fluid resuscitation?
What is Parkland’s formula? How is it used?
Which burns patients need transfer to a regional burns centre?
How would you manage a patient with a 70 per cent burn?
What are the principles of escharotomy?
What are the complications of burns?
What sort of burns require skin grafting?
Related topics
Topic Chapter Page
BURN THICKNESS
Burns can be full thickness or partial thickness. The thickness of a burn is deter-
mined by the level of the dermis affected. Superficial partial-thickness burns involve
the epidermis and a thin layer of the dermis. Deep dermal burns are limited to, but
not involving the entire thickness of the dermis, and full-thickness burns involve the
entire thickness of the dermis and can also involve underlying structures.
427
CRITICAL CARE burns
Burn thickness Characteristics
Superficial partial thickness Blistering – note that erythema without blistering (e.g.
mild sunburn) is NOT counted as a burn
Colour – pink skin
Capillary return – blanches and refills rapidly
Pain – painful
No fixed (non-blanching) staining of skin
Soft skin
Deep dermal Colour – pink skin
Capillary return – blanches and refills
Pain – painful
Texture – soft skin
Some fixed (non-blanching) staining in tissues
Full thickness Colour – white or brown skin
Capillary return – none. Skin does not change colour
on pressure
Pain – painless
AREA OF A BURN
Accurate assessment of the area of a burn (measured as percentage of total body
surface area) is critical to acute burn management. There are three ways to deter-
mine the area:
1. Wallace’s rule of 9s: the body is divided into seven zones, each of which is
either 9 per cent or a multiple thereof. The head and each upper limb count as
9 per cent, the front of the torso, the back of the torso and each lower limb
count as 18 per cent. The genital area is the final 1 per cent, bringing the total
to 100 per cent.
2. Patient’s hand: a quick and easy method of calculating relatively small burns
is to use the patient’s hand area. The area of the closed palm is approximately
1 per cent of the total body surface area.
3. Lund and Browder charts: these charts give the most accurate estimations of
burn area. They also have the advantages of being able to correct for different
age groups (children have age-dependent head and limb proportions), and
they provide documentation of the burn for the patient’s notes.
BURNS MANAGEMENT
First aid at the scene
• Ensure your and the patient’s safety – remove any causative factors (e.g.
chemical burns, electrical burns)
428
CRITICAL CARE burns
• Remove any overlying or affected clothes, which can trap heat close to the skin
• Cool the burn in cold, running water up to 2 hours post-burn (avoid iced water
which can cause vasospasm and further compromise of perfusion).
Immediate management
Airway
Always check for signs of airway burns or inhalational injury, which can cause rapid
and dramatic airway oedema. Have a low threshold for an early anaesthetic opinion
and intubation. Mucosal oedema can occur up to 8 hours after the burn, so re-assess
regularly. Risk factors include:
• History of fire in enclosed space
• Soot around nostrils, in nose or mouth
• Singeing of nasal hairs
• Carbonaceous sputum
• Hoarseness
• Stridor or wheeze
• Drooling
• COHb ! 10 per cent.
Breathing
Ensure that adequate respiration can be achieved. Tracheal or pulmonary burns can
impair effective gas exchange (see ‘Acute respiratory distress syndrome’, Chapter
105, page 419). Full-thickness chest burns can impede chest wall expansion –
consider escharotomy.
Circulation
Fluid loss and shock are common in major burns. Early intravenous fluid resuscita-
tion is essential in management of any significant burn.
Then the next stages are:
• Remove any precipitating cause: dilute a caustic or acid burn with water
• Clean and cover the burn: aqueous chlorhexidine wound toilet and a Clingfilm
dressing
• Send blood for Hb, U+Es, albumin, COHb, blood gases, cross-match
• Beware of hypothermia.
Subsequent management and prognosis

• Goal is to minimize scarring and contractures causing loss of function:
• scarring occurs if burnt skin has not re-epithelialized by 2 weeks
• usually partial-thickness burns will heal by 2 weeks unless healing is delayed
by infection or concurrent morbidity
429
CRITICAL CARE burns
• Full-thickness burns and non-healing partial thickness burns require burn

excision down to healthy tissue
• Skin grafting may be required to cover areas of skin loss.
Late management
• Re-orientation of contractures to increase range of joint movement:
• Z-plasties
• local flaps
• Excision of contractures and reconstruction:
• split-thickness skin grafting
• tissue expansion
• synthetic dermal grafting (Integra)
• flap reconstruction.
INTRAVENOUS FLUID RESUSCITATION

Any burn ! 15 per cent in adults or ! 10 per cent in children requires intravenous
fluid resuscitation.The most common algorithm for resuscitation is Parkland’s formula.

What is Parkland’s formula? How is it used?
Parkland’s formula
Volume of crystalloid required (mL) ( 4 " % burn " Patient’s weight (kg)
This gives the volume of crystalloid needed for resuscitation within the
first 24 hours. Half is given in the first 8 hours and half in the subsequent
16 hours. If time has elapsed since the burn, initial fluid infusion rate
should be increased to meet the resuscitation deficit rapidly. Close moni-
toring of fluid balance is essential in these patients (see ‘Fluid balance’,
The Muir and Barclay formula was described for albumin as the resuscitation fluid.
It tends to give less fluid per unit time than Parkland’s formula favoured by the
British Burns Association, and is now little used.
National Burns Care Review guidelines recommend that the following patients be
transferred to a burns centre or burns unit:
• Adults with burns ! 15 per cent or 10 per cent with dermal loss
• Children with burns ! 5 per cent (note that not 10 per cent as required for
fluid resuscitation)
• Burns at extremes of age
430
CRITICAL CARE burns
• Airway burns or patients at risk of airway obstruction

• Facial burns
• Perineal burns
• Hand or feet burns
• Burns requiring escharotomy
• Other complex burns (burns in patients with significant associated injuries or
pre-existing medical conditions, chemical, radiation, high pressure or high
tension electrical burns and burns of flexures, especially the neck)
• When non-accidental burn injuries are suspected
• EXCEPT when specialist management of the burn is redundant (moving a
patient who will die from the burn away from friends and family causes
unnecessary additional distress).
SPECIFIC CONSIDERATIONS
• Acid or alkali burns: copious water irrigation until the burn area reaches pH 7.
Test repeatedly with appropriate litmus or universal indicator paper
• Hydrofluoric acid burns: apply calcium gluconate gel
• Electric burns: identify entry and exit wounds and consider that the entire tract
between these points will be burnt. Severe internal organ burns can occur with
even minor skin electrical burns
Key learning point

Escharotomy is the excision of burnt skin to relieve constriction.
It must be considered in circumferential burns or chest wall burns where con-
striction of overlying skin can cause compartment syndrome (see ‘Compart-
ment syndrome’, Chapter 108, page 433) or respiratory compromise (see
‘Respiratory failure and respiratory function tests’, Chapter 119, page 495).
Escharotomy is performed as an emergency and involves incisions down to
healthy tissue:
• In limbs: medial and lateral incisions that may need to be extended into
individual digits
• On chest wall: bilateral midclavicular incisions and two transverse incisions
to make the ‘noughts and crosses’ release
It may be required as an emergency procedure in the accident and emergency
department (A&E) resuscitation unit and may not reach theatre.
Consider combining escharotomy with fasciotomy if compartment syndrome
is suspected.
431
CRITICAL CARE burns
• Burns in children: consider non-accidental injury

• Circumferential burns: these can contract causing compartment syndrome.
Escharotomy may be required.
COMPLICATIONS OF BURNS
Early
• Death
• Renal failure
• Sepsis and DIC
• Infection
• Compartment syndrome
• ARDS.
Late
• Limb loss
• Scarring and contractures
• Cosmesis
• Chronic regional pain syndromes
• Functional disabilities.
432
108 Compartment syndrome

What is compartment syndrome?
What do you understand by the term ‘abdominal compartment syndrome’?
How do you measure the pressure in the abdominal compartment?
Where can compartment syndrome occur?
What are the clinical features of a compartment syndrome in the lower
limb?
What are the systemic consequences of a compartment syndrome?
Discuss the management of compartment syndrome.
What are the complications of compartment syndrome?
What are the causes of compartment syndrome?
Related topics
Topic Chapter Page
Shock 122 510
Burns 107 427

What is compartment syndrome?
A progressive condition in which the elevated tissue pressure within a
myofascial compartment exceeds the capillary pressure and compromises
blood flow to structures within that compartment.
It most commonly occurs in the fascial compartments of the limbs, although
an abdominal compartment syndrome is recognized where the intra-
abdominal pressure exceeds the capillary pressure within the abdominal
viscera, most notably the renal capillary bed.
433
CRITICAL CARE compartment syndrome
COMPARTMENT SYNDROME WITHIN A LIMB

This can result from factors that either increase the volume of the compartment
contents or decrease the volume of the compartment itself.
Increase in volume of compartment contents

• Large haematoma as the result of vascular injury or coagulopathy
• Haemorrhage and oedema after a fracture and soft tissue injury
• Swelling of muscle tissue post-ischaemic insult
• Limb compression.
Decrease in volume of compartment

• Overly constricting dressing or cast
• Full-thickness burns
• Closure of fascial defects after surgery.
The four compartments of the lower leg are most commonly affected, although
compartment syndrome can occur in the:
• shoulder
• arm
• forearm
• hand
• buttocks
• thigh
• foot.
Therefore, after orthopaedic surgery or vascular surgery to these areas, careful clinical
observation must be utilized to assess for a rise in compartment pressure.
Clinical signs of raised intracompartment pressure

Early signs
• Paraesthesia
• Pain on passive movement of distal joints
• Generalized pain in the limb
• Loss of distal sensation.
Late signs
• Obvious compartmental swelling
• Loss of muscle power
• Decreased pulse pressure or loss of pulse in distal limb (very late sign).
Muscle creatine phosphokinase (CPK) can be measured – massively elevated in
muscle necrosis.
434
It can be seen from the signs above that, in answer to this question, confusion with
the ‘pain, pale, paraesthetic, pulseless, perishingly cold’ description of the acutely
ischaemic limb is unwise! Indeed increasing pain associated with exacerbation of
pain on passive flexion and extension of distal joints is a sensitive test for early com-
partment syndrome.
If there is any doubt, pressure monitors can be placed in each compartment directly
to monitor the pressure, although the diagnosis is a clinical one with monitoring
only a confirmatory step.
A compartment pressure of 40 mmHg below the mean arterial pressure is enough
to cause compartment syndrome.
Management
Keep the patient nil by mouth if the diagnosis is suspected and measure the com-
partmental pressures if necessary.
Urgent decompressive fasciotomies to decompress the compartments (ensure that
all compartments are decompressed).
Urgent escharotomies in circumferential burns (see ‘Burns’, Chapter 107, page 427).
Formally split any orthopaedic plaster casts.
Wounds are left open and covered with saline-soaked gauze.
A re-look and exploration in 24–48 hours are usually necessary to excise any
necrotic tissue and débride the wounds. In extreme cases more than one re-look
may be necessary.
Closure of fasciotomies may well require skin grafting and early liaison with a plas-
tic surgeon should be the norm.
Complications
These can be divided into systemic and local.
Systemic (mostly as a result of muscle death)

• Rhabdomyolysis leading to myoglobinaemia and subsequent renal failure
• treated by prompt hydration and the maintenance of an alkaline urine using
sodium bicarbonate, provided that urine output is adequate (preventing
dissociation of myoglobin into more toxic metabolites)
• Shock as a result of massive peripheral vasodilatation (see ‘Shock’, Chapter 122,
page 510)
• Hyperkalaemia
• Hyperphosphataemia
• Hyperuricaemia
435
• Metabolic acidosis as a result of anaerobic respiration (see ‘Acid–base balance’,

• Death.
Local
• Chronic regional pain syndromes
• Contractures
• Muscle weakness
• Limb necrosis leading to requirement for amputation.
Note that early diagnosis and prompt treatment are the key to the prevention of com-
plications. A difference between compartmental pressure and mean arterial pressure
of just 30–40 mmHg for 15 min is enough to create functional changes in muscles and
nerves; 4–8 hours with this pressure difference can lead to ischaemic necrosis.
ABDOMINAL COMPARTMENT SYNDROME

What do you understand by the term ‘abdominal compartment syndrome?’
Abdominal compartment syndrome is defined as the adverse physiological
effects of increased intra-abdominal pressure (IAP). Prolonged, unrelieved,
increased IAP ! 20 mmHg can produce pulmonary compromise, renal
impairment, cardiac failure, shock and death.
Abdominal compartment syndrome (ACS) can be categorized into primary, sec-

ondary and chronic.
ACS occurs when the IAP is too high, similar to compartment syndrome in an
extremity. The three types of ACS have different and sometimes overlapping causes.
Primary (i.e. acute with abdominal pathology)

• Penetrating trauma
• Gastrointestinal haemorrhage
• Pancreatitis
• External compressing forces, such as debris from a motor vehicle collision or
after explosion of a large structure
• Pelvic fracture
• Rupture of abdominal aortic aneurysm
• Perforated peptic ulcer
• Closure of abdominal fascia in gastroschisis and exomphalos neonatally.
436
Secondary
Secondary ACS may occur in patients without an intra-abdominal injury, when
fluid accumulates in volumes sufficient to cause a rise in IAP.
• Sepsis
• Large areas of full-thickness burns
• Penetrating or blunt trauma without identifiable injury
• Postoperative
• Packing and primary fascial closure after emergency laparotomy
• Large-volume resuscitation.
Chronic
• Peritoneal dialysis
• Morbid obesity
• Cirrhosis
• Meigs’ syndrome (ovarian fibroma associated with ascites/pleural effusion).
Pathophysiology of abdominal compartment syndrome

Direct effects of compression on intra-abdominal and other viscera:
• Gut: compression of vasculature and portal system leads to thrombosis and
mucosal oedema, ultimately resulting in translocation of bacteria across the
mucosal wall and systemic sepsis; this causes more fluid secretion in the intra-
abdominal compartment and a further rise in pressure
• Kidneys: renal perfusion is impaired and urine output drops
• Liver: portal vein collapses along with the inferior vena cava (IVC), causing
congestion
• Respiratory: increased IAP makes it harder to breathe and ventilation becomes
more difficult
• Cardiac: rise in abdominal pressure causes CVP (central venous pressure) and
PAOP (pulmonary artery occlusion pressure) (see ‘CVP lines and invasive
monitoring’, Chapter 110, page 443) to rise despite a hypovolaemic state,
leading possibly to inadequate fluid resuscitation.
History
• Pancreatitis and/or alcohol abuse
• Emergency laparotomy
• NSAID use
• Melaena
• Syncope.
Signs and symptoms

• Abdominal pain – not always present and not always useful (particularly in
sedated and ventilated obtunded patients in the ITU!)
437
• Decreased urine output – a frequent and early sign of abdominal compartment

syndrome
• Melaena
• Progressively difficult ventilation
• Increased abdominal girth (not always easy to see).
Measurement of IAP is by the use of a Foley catheter introduced into the bladder;
50 mL saline is injected into it and then it is connected to a manometer to measure
intracystic pressure, which is thought to be a reflection of IAP.
Abdominal CT can be useful to look for radiological signs of raised pressure such as
collapsed IVC, bilateral inguinal hernias, and enhanced and thickened gut wall.
Management
• The best management of abdominal compartment syndrome is prevention and
early treatment of any intra-abdominal hypertension
• Consider avoiding primary closure in emergency laparotomies, which are at
high risk from abdominal compartment syndrome (extensive dead bowel, liver
lacerations and packing, necrosectomy for pancreatitis)
• Percutaneous drainage of fluid collections
• Laparoscopic decompression may be used in abdominal blunt trauma
• Laparostomy remains the mainstay of treatment in the UK.
Complications
These can be split into complications from the compartment syndrome and com-
plications from immediate decompression.
Direct complications from compartment syndrome
• Respiratory failure (increasing airway pressures and decreasing tidal volumes in
ventilated patients)
• Renal failure (see above)
• Bowel ischaemia and infarction
• Increased ICP
• Decreased cardiac output and refractory shock.
Complications from immediate decompression
• Massive and precipitous fall in blood pressure:
• caused partly by reperfusion syndrome with a fall in systemic vascular
resistance and partly by inadequate fluid resuscitation as a result of a falsely
elevated CVP (see above)
• extensive fluid resuscitation preceding decompression reduces the incidence
of refractory hypotension.
438
109 Criteria for admission to the ITU and HDU

What are the criteria for admission to the ITU?
What are the main differences between the ITU and the high dependency
unit (HDU)?
How do you go about making an ITU referral?
What investigations will be expected on making an ITU referral?
Do you know of any ITU scoring systems? What is the principle behind
them?
What is level 1, 2 and 3 care?
Related topics
Topic Chapter Page

What are the criteria for admission to the ITU?
A common question. The main criteria are set out below but the principles
here are that the ITU is the main place in the hospital for invasive ventilatory
support and the support of two or more failing organ systems (including
respiratory system).
In many hospitals, non-invasive ventilation such as continuous positive airway

pressure (CPAP) (see ‘Intubation and ventilation’, Chapter 114, page 470)
can be performed in an HDU setting.
439
CRITICAL CARE criteria for admission to the ITU and HDU
CRITERIA FOR ADMISSION TO THE ITU

• Patients requiring or likely to require advanced respiratory support (usually in
the form of endotracheal intubation and ventilation)
• Patients requiring support for two or more organ systems:
• respiratory: ventilation/CPAP
• renal: haemofiltration/haemodialysis
• cardiac: ECG monitoring and inotropic support
• hepatic: blood transfusion
• neurological: intracranial pressure monitoring
• Patients with chronic impairment of one or more systems sufficient to restrict
daily activities (co-morbidities ASA III and above) and who require support for
an acute, reversible failure of another organ system
• Patients who also require one-to-one nursing care.
CRITERIA FOR ADMISSION TO THE HDU

• Patients requiring support for a single failing organ system excluding those
requiring advanced respiratory support
• Patients who would benefit from more regular and detailed observation than
can be safely provided on a general ward
• Postoperative patients who need close observation and monitoring for longer
than a few hours.
DEFINITIONS OF SYSTEM FAILURES

Cardiovascular failure (see ‘Shock’, Chapter 122, page 510)
• Heart rate ! 140 beats/min
• Systolic blood pressure # 100 mmHg
• ' Cardiac arrest.
Respiratory failure (see ‘Intubation and ventilation’, Chapter 114, page 470)
• Airway compromise
• Respiratory rate ! 36 breaths/min
• SpO2 # 90 per cent on ! 40 per cent O2 (via non-rebreather O2 mask on the ward)
• ' Respiratory arrest.
Renal failure (see ‘Oliguria and renal replacement’, Chapter 116, page 482)
Urine output # 120 mL in 4 h with associated hyperkalaemia/acidosis.
Central nervous system (CNS) dysfunction
• Glasgow Coma Score (GCS) # 9 or a fall of 2 points
• Seizures, new or sustained ! 10 min (status epilepticus).
440
MAKING AN ITU REFERRAL

Differs between hospitals but either the senior house officer (SHO) or specialist regis-
trar usually makes referral directly to clinician on call for ITU specifically, registrar on
call for anaesthetics or consultant on call for ITU. History, pertinent examination find-
ings and laboratory tests/radiology/arterial blood gases will usually be required.
SIGNS AND INVESTIGATIONS
Respiratory failure
This cannot be adequately diagnosed without the use of arterial blood gas (ABG) and
this is a simple bedside test that should be performed in the case of all sick patients,
regardless of whether they appear to have respiratory compromise (see ‘Respiratory
failure and respiratory function tests’, Chapter 119, page 495).
Respiratory failure can be split into type I which is a failure of oxygenation and type
II which is a failure of ventilation:
• Type I: PaO2 # 8 kPa (PCO2 will be normal or low)
• Type II: PaCO2 ! 6.5 kPa and PaO2 # 8 kPa.
Note that normal PaO2 on air should be around 13 kPa, assuming normal lungs.
Subtract 10 from FiO2 (per cent) to obtain predicted PaO2 for that FiO2.
Severe respiratory failure is defined as one-third of the predicted value.
Thus, it is essential to know what FiO2 the patient is on when the ABG is taken.
Therefore, flow rate and type of mask must be recorded to determine the FiO2 (see
‘Intubation and ventilation’, Chapter 114, page 470, and ‘Acid–base balance’,
Circulatory failure
See ‘Shock’, Chapter 122, page 510 and ‘Inotropes’, Chapter 113, page 466.
To exclude compensated shock, all of the following should be fulfilled:
• Capillary refill # 10 s
• Patient not confused or thirsty
• Heart rate # 100 beats/min
• Mean arterial pressure (MAP) ! 80 mmHg (see ‘CVP lines and invasive
monitoring’, Chapter 110, page 443)
• Urine output ! 0.5 mL/kg per h
• Base excess # 2 (see ‘Acid–base balance’, Chapter 84, page 349)
• Normal CVP/PAWP: obviously not available on the ward but jugular venous
pressure (JVP) may be used as a non-invasive surrogate for ward assessment.
441
Oliguria
See ‘Oliguria and renal replacement therapy, Chapter 116, page 482.
• Urine output # 0.5 mL/kg per h
• Beware blocked catheters, diuretics and nephrotoxics on drug chart!
CNS
Basic assessment on the ward:
• Can the patient defend the airway and is there a cough reflex present?
• Is GCS # 7? Immediate intubation for airway protection
• Adequate ventilation? (Check PCO2)
• Clearing secretions?
• Is GCS deteriorating? (Fall by 2 points or more is significant)
• Presence of sepsis – confusion?
SCORING SYSTEMS IN ITU AND HDU

Various systems have been developed over the years in an attempt to quantify the
severity of a patient’s illness, the most widely used of which is the APACHE II
(Acute Physiology And Chronic Health Evaluation) system.
This is calculated by computer from data on a dozen physiological parameters (BP,
[Hb], etc.) + GCS. It is weighted for age, diagnosis and co-morbidities.

What is level 1, 2 and 3 care?
1 Acute postoperative care (excluding respiratory support)
2 HDU
3 ITU
442
110 CVP lines and invasive monitoring

How can blood pressure be monitored?
How do you assess the cardiovascular status of a patient?
What are the indications for central venous access?
What are the complications of central venous access?
Draw the CVP waveform and label the various components.
Is absolute CVP a useful measurement?
In what circumstances might CVP not represent overall filling?
How do you put in and take out a central line?
What are the indications for insertion of a pulmonary artery flotation
catheter (PAFC)?
Draw the trace of a PAFC as it passes though the heart and wedges.
What parameters can be measured and what parameters can be calcu-
lated from a PAFC (Swan–Ganz)?
What methods are there for measuring cardiac output in the intensive
care setting?
What do you understand by Fick’s principle?
How can an arterial waveform tell you about the patient’s fluid balance?
Related topics
Topic Chapter Page
Shock 122 510
Nutrition 115 477
443
CRITICAL CARE CVP lines and invasive monitoring

How can blood pressure be monitored?
Categorized into non-invasive and invasive measures:
Non-invasive
• Traditional sphygmomanometer
• intermittent, cumbersome and time-consuming
• non-invasive method is manual (using stethoscope)
• Dynamap system (still uses arm cuff but based on oscillometry)
• automatic, quicker, less time-consuming
• probably slightly less accurate than manual measurement
• intermittent but can be set to retake BP every minute
• Radial artery tonometry
• based on superficial pressure sensors and therefore highly positional
• new technology but may eventually replace an arterial line for short-term
monitoring (e.g. in local anaesthetic procedures such as carotid
endarterectomy)
• continuous monitoring, produces BP waveform as with an arterial line
• Finometer
• largely for research, based on measurement of ‘finger blood pressure’
Invasive
• Arterial line
• commonly a 20 G catheter inserted into the radial artery.
• invasive – risks of clotting of line, infection
• most accurate, continuous waveform
• allows accurate, beat-to-beat assessment of MAP and BP
• allows assessment of arterial waveform to see if it is ‘swinging’, indicating
underfilling (see ‘Fluid balance’, Chapter 111, page 452)
• allows regular aspiration of arterial blood for ABGs
ASSESSING THE CARDIOVASCULAR STATUS

Remember that in most cases, cardiovascular status is assessed clinically:
• Pulse:
• rate
• rhythm
• character (palpable radial suggests systolic ) 80 mmHg)
• Skin temperature (cold peripheries indicating poor peripheral perfusion)
444
• Skin colour (look for peripheral cyanosis, signs of early skin necrosis)
• Urine output (see ‘Fluid balance’, Chapter 111, page 452)
• Respiratory rate
• Mental status (evidence of brain perfusion, i.e. alert and coherent, confused,
obtunded, in coma).
FURTHER BEDSIDE TESTS AND OBSERVATIONS

• Pulse oximetry (see ‘Pulse oximetry’, Chapter 118, page 491)
• BP (as above)
• ECG
• ABGs: with particular attention to acid–base balance looking for any evidence
of a metabolic acidosis (see ‘Acid–base balance, Chapter 84, page 349).
CENTRAL VENOUS ACCESS

Indications
• Monitoring of CVP (see ‘Fluid balance’, Chapter 111, page 452)
• Passage of a pulmonary artery flotation catheter (Swan–Ganz)
• Infusion of inotropes and venosclerotic drugs centrally (usually via triple- or
quadruple-lumen CVP lines)
• Administration of total parenteral nutrition (TPN) (see ‘Nutrition’, Chapter 115,
page 477)
• Haemofiltration (large, double-lumen Vascath) (see ‘Oliguria and renal
replacement, Chapter 116, page 482)
• Insertion of pacing wire.

How do you put in and take out a central line?
Insertion
• Three standard approaches:
• internal jugular
• subclavian approach
• femoral (not usually the preferred route for most access – higher
incidence of deep venous thrombosis [DVT])
• Patient positioning:
• head down and turned to opposite side – particularly important in
underfilled patients to improve chances of cannulating the vein and
decrease the chances of an air embolism
• aseptic technique
445
• local infiltration with local anaesthetic

• prepare and drape the skin
• Seldinger technique the most common:
• or internal jugular: high or low approach.
– high: puncture the skin at the midpoint of the posterior border of
sternocleidomastoid with needle held at 30° to the skin, heading a
little laterally. Displace the internal carotid artery medially with a
finger. Continue, aspirating regularly until the vein is entered
– low: puncture the skin between the two heads of sternocleidomastoid –
careful, do not go too deep!
• for subclavian: puncture skin at a point between the lateral one-third
and medial two-thirds of the clavicle, heading for the sternoclavicular
joint ipsilaterally. ‘Walk’ the needle along the underside of the clavicle,
aspirating regularly until the vein is entered
• after the vein has been entered, pass the guidewire in through the
needle, checking that it advances freely – watch the ECG if you have
one and do not put the guidewire in too far!
• remove the needle and railroad dilators followed by the CVP line over
the guidewire (you will need to make a tiny incision in the skin to pass
the line dilator). Ensure that you don’t lose the guidewire when pushing
in the CVP line – keep some part of the wire in sight at all times
• after the line has been advanced to the required length (usually
15–20 cm), remove guidewire, ensure that line aspirates and flushes
freely through all lumina, and then suture in place
• chest radiograph to ensure that no pneumothorax has been caused and
that line is in the correct position (just above the right atrium)
Removing a central line
• Ensure that patient is flat/head down to prevent air embolus. Check that
clotting and platelets are normal. Remove line and immediately place a
dressing over the area. Send the tip for microbiology and culture
• Indwelling, tunnelled lines may need to removed in theatre as a larger
incision down to a retaining plastic cuff may be required
Complications of central venous access

• Line-related sepsis
• Problems associated with insertion:
• pneumothorax
• haemopneumothorax
• air embolus
446
• Damage to surrounding structures:

• arterial damage: puncture of carotid artery or cannulation of subclavian
artery, leading to false aneurysm formation, arteriovenous fistula or
haematoma
• cannulation of the thoracic duct
• Central venous thrombosis
• Catheter embolization
• Malposition of catheter (e.g. into neck veins from subclavian approach or into
contralateral vein)
• Cardiac complications:
• arrhythmias
• perforation of the right atrium.
THE CVP WAVEFORM
S1 S2
Figure 110.1
The a wave is caused by atrial contraction.
The x descent follows atrial relaxation.
The c wave is formed by the intrusion of the tricuspid valve leaflets into the atrium
at the start of ventricular systole.
The v wave is a measure of the venous return to the atrium. It marks the point of
ventricular systole but it is NOT caused by it.
The y descent occurs when the tricuspid valve opens and the atrium empties.
The waveform can be affected by various conditions:
• Atrial fibrillation (AF): absent a waves (lack of coordinated atrial contraction)
447
• Tricuspid regurgitation: large v wave caused by a jet of blood coming into the
atrium during ventricular systole as a result of an incompetent valve
• Tricuspid stenosis: large a wave caused by arteriovenous outflow obstruction.
Slow y descent results from slow atrial emptying
• Complete heart block: ‘cannon’ a waves caused by uncoordination of atria and
ventricles, leading to occasional contractions where the atrium contracts against
a closed tricuspid valve.

Is absolute CVP a useful measurement? In what circumstances might
CVP not represent overall filling?
Absolute CVP depends on ensuring that the patient is properly positioned
each time that it is measured (at 45° or at least the same angle for all
measurements with the transducer set at the same height.) It is not as
useful a clinical tool as the response of the CVP to a fluid challenge (see
‘Fluid balance’, Chapter 111, page 452).
In circumstances where the right heart is not functioning normally
(particularly in valvular heart disease) or the overall myocardial compliance
(e.g. right-sided heart failure or pulmonary hypertension) is affected, the
CVP may not give a true reflection of the patient’s filling. In these cases,
the parameter has to be considered in the light of other physiological
parameters and a PAFC may be considered.
THE PAFC (SWAN–GANZ)

This is a flow-directed catheter that is floated through the heart on an inflatable bal-
loon until it wedges in a branch of the pulmonary artery. When the balloon is
inflated, there is a continuous column of blood between the tip of the catheter and
the left atrium, so that the wedge pressure reflects left atrial pressure.
Indications
The indications for a PAFC are controversial and some clinicians believe that they
should not be used at all! There is ongoing research in this area and these devices
are likely eventually to be completely replaced by less invasive systems (see later).
• Measurement of the SVR (systemic vascular resistance) in septic shock, severe sepsis
or SIRS to guide inotrope management (see ‘Inotropes’, Chapter 113, page 466)
• Measurement of wedge pressure to guide fluid management in difficult cases
(severe sepsis and/or acute right heart failure)
448
• Post-cardiac surgery in cases of poor left ventricular function

• Multiorgan failure
• ARDS with or without concomitant pulmonary oedema
• Measurement of cardiac index and cardiac output in an ITU setting.
Insertion technique
Common approaches are internal jugular and subclavian as with all central venous
access. Once in the right atrium, the balloon is inflated to float through the tricus-
pid valve and into the right ventricle. The line is advanced through the right ven-
tricle, through the pulmonary valve and into the pulmonary artery. As it is advanced,
the balloon wedges in one of the branches of the pulmonary artery and the trace
become essentially flat (see below.)
As this line is indwelling, the balloon is kept deflated until a measurement of wedge
pressure is required.
Right atrium
(similar to CVP trace)
Right ventricle
Pulmonary artery
Wedged
Figure 110.2
Complications of PAFC insertion

• All central line insertion complications (see above)
• Cardiac arrhythmias:
• commonly atrial and ventricular ectopics
• can cause ventricular tachycardia, ventricular fibrillation and heart block in
irritable myocardium
• if encountered, balloon must be deflated before catheter is pulled back to
prevent valvular or myocardial damage
• Pulmonary artery rupture: usually presents as haemoptysis
• Pulmonary artery infarction: if balloon has been left up too long
449
• Pulmonary embolus from catheter tip

• Knotting of catheter.
Directly measured physiological parameters

• MAP
• Heart rate
• Cardiac output (measured by either thermodilution or indicator dilution
techniques – see below)
• Mean pulmonary artery pressure (MPAP)
• PAOP or PAWP
• Heart rate.
Derived physiological parameters

• Cardiac index (cardiac output/body surface area)
• Stroke volume
• SVR:
SVR ( (MAP * CVP)/CO " 80
• normal range 900–1400 dyn/s per cm%5
• Pulmonary vascular resistance (PVR):
PVR ( (MPAP * PAOP)/CO " 80
• normal range is 150–250 dyn/s per cm*5
• Indexed SVR and PVR (divided by body surface area)
• Oxygen delivery.
RA RV
15+30 15+30
0+8 0+8 5+15
Pulmonary
artery
80+140 80+140
60+90 0+10 5+10
Aorta
Pulmonary
LV LA vein
Figure 110.3 Schematic of pressures found within the heart and cardio-pulmonary circulation.
450

What methods are there for measuring cardiac output in the intensive care
setting? What do you understand by Fick’s principle?
Swan–Ganz (PAFC)
• Continuous cardiac output measurement is now available with the ther-
modilution technique and is based on Fick’s principle. A bolus of cold
saline is injected and a thermistor at the catheter tip measures the drop
in temperature of the blood. More modern systems use a small heater
coil some distance down the catheter and a thermistor at the tip
• Fick’s principle:
Classically described for oxygen consumption, it has been generalized to:
Organ blood flow/time ( Amount of marker taken up/Concentration

difference between supply and drainage
Thus, cardiac output is proportional to change in temperature of the
blood divided by time.
PiCCO
• Uses a thermodilution technique from cold fluid infused through a CVP
line and analysed via a modified arterial line containing a thermistor
• Commonly used in modern ITUs – allows continuous CO monitoring
LiDCO
• Uses principle of lithium dilution similar to Fick’s principle. Small doses
of lithium, as an indicator, are picked up by a lithium electrode in a
modified arterial line. CO is calculated from pulse contour analysis
Echo Doppler
• Measures blood flow in the aorta using an oesophageal probe. CO can be
derived from the Doppler waveform
Echocardiography
• Not a continuous technique and operator dependent but allows direct
visualization of the myocardium and an assessment of ejection fraction
451
111 Fluid balance

What are the daily maintenance requirements of common cations and
anions in a healthy 70 kg man?
How is body fluid homoeostasis achieved and regulated?
Discuss water balance in terms of intake and output in a healthy
individual.
What is the physiological consequence of dehydration?
What clinical measures do we have to assess fluid balance?
Discuss distribution of total body water with respect to intracellular and
extracellular compartments.
Discuss the ion composition of extracellular and intracellular fluid.
What’s in a bag of physiological (0.9%) saline?
What is Hartmann’s solution and what advantages does it have over
saline?
What is the difference between a colloid and a crystalloid? When might
you choose one over the other? Is there any evidence to support your
decision?
What is the osmolality of plasma? How would you calculate it roughly?
How can loss of extracellular fluid (ECF) volume be calculated?
How can loss of plasma volume be calculated?
What are the principles behind the prescription of fluid regimens for
maintenance and in the setting of an acutely unwell surgical patient?
What are the possible complications of giving a colloid?
Explain the effects of fluid resuscitation in terms of Starling’s curve and
explain how the CVP response to a fluid challenge is explained by the
curve.
Related topics
Topic Chapter Page
Shock 122 510
Functions of the kidney II: fluid and electrolyte 93 377
balance in the kidney
452
CRITICAL CARE fluid balance

What is in a bag of Hartmann’s solution, 0.9% (normal) saline and 5 per cent
dextrose?
Name of fluid Commonly Na' Cl* HCO3* K'

referred to as (all mmol/L)
NaCl (0.9 per cent) Normal (physiological) 150 150 – –
saline
Ringer’s lactate Hartmann’s 131 111 29 (as lactate) 5
Glucose (5 per cent) 5 per cent dextrose – – – –
BODY WATER
There is approximately 45 litres of total body water in a healthy 70 kg man. This is
split into extracellular and intracellular compartments:
• Intracellular: 30 litres in total
• Extracellular: 15 litres in total:
• lymph ( 1.5 litres
• transcellular ( 1.5 litres
• extracellular fluid proper ( 10 litres
• intravascular fluid (plasma) & 5 litres.
The transcellular compartment is separated by a layer of epithelium (e.g. CSF, gut
lumen). In some pathological processes, this space is increased and referred to as the
third space.
45 litres total body water
Intracellular Interstitial I
N
T
10 litres R
A
V
A
30 litres S
C
U
Lymph L
1.5 litres A
R
Transcellular 5
L
1.5 litres
Intracellular Extracellular
Figure 111.1
453
Ion composition of ECF and intracellular fluid (ICF)
Ion ECF (mmol/L) ICF (mmol/L)

Na& 135–145 4–10
K& 3.5–5.0 150
Ca2+ 1.0–1.25 0.001
Mg2+ 1.0 40
HCO3* 25 10
Cl* 95–105 15
PO43* 1.1 100
The distribution of the ECF between the plasma and the interstitial space is regu-
lated by the capillaries and lymphatics (see ‘Starling forces in the capillaries/
oedema’, Chapter 101, page 401).
WATER AND ELECTROLYTE BALANCE

As well as gastrointestinal intake of water, the human body makes approximately
350 mL water/day as a result of the oxidization of carbohydrates. This is known as
metabolic water and, added to approximately 1500 mL from drink and 750 mL
from food, makes up the average daily intake of 2600 mL.
Approximately 1000 mL of water are lost each day through the skin and the lungs;
1500 mL are lost in the urine and approximately 100 mL in the faeces, thus bal-
ancing the input and output.
More correctly, individual water requirements in a healthy individual are calculated
according to the patient’s weight and age. Thus, adults require about 30–40 mL/kg
per day, whereas children require relatively more:
• 0–10 kg: 4 mL/kg per h
• 10–20 kg: 40 mL/h & 2 mL/kg per h for each kg ! 10 kg
• ! 20 kg: 60 mL/h & 1 mL/kg per h for each kg ! 20 kg.
The average requirements of sodium and potassium are 1 mmol/kg per day of each. It
is particularly important to keep up with the potassium requirement because the kid-
ney is much more efficient at conserving sodium than potassium. Indeed, there is an
obligatory loss of potassium in both urine and faeces, and patients with diarrhoea or
polyuria can quickly become hypokalaemic. It should be noted that there is a consid-
erable intracellular potassium load and that there can be a steep fall in total body potas-
sium before it is noted as a fall in plasma potassium.
454
THE PHYSIOLOGY OF DEHYDRATION

See ‘Functions of the kidney II’, Chapter 93, page 377)
• One-fifth of the cardiac output is filtered by the kidney

• In dehydration, there is increased production of ADH by the neurohypophysis
(a direct effect by osmoreceptors in the hypothalamus)
• Leads to synthesis of more water channels in the distal collecting duct of the
kidney, leading in turn to increased H2O reabsorption and a concentrated urine
(see ‘Functions of the kidney II’, Chapter 93, page 377)
• Renin is produced by the juxtaglomerular apparatus in response to a decrease in
the afferent arteriolar pressure and decreased Na& delivery.
• Activation of the renin–angiotensin–angiotensin II axis leads to aldosterone
promoting Na' retention and K' excretion; angiotensin II is a potent
vasoconstrictor
• Two systems above achieve blood pressure homoeostasis.
ASSESSING FLUID BALANCE CLINICALLY

Bedside observations
• Pulse
• BP (including pulse width)
• Urine output (and assessment of bedside fluid chart)
• JVP
• Weight (particularly of relevance in renal patients)
• Peripheral capillary return
• Mental status
• Skin turgor
• Sunken eyes in dehydration
• Dry mouth in dehydration.
Invasive measurements
See ‘CVP lines and invasive monitoring’, Chapter 110, page 443).
• CVP and response to a fluid challenge: if inadequately filled, a patient’s CVP

will initially increase with a fluid bolus but rapidly fall again as the fluid
equilibrates between the intra- and extracellular compartments. If adequately
filled, the CVP will rise to a new level and be maintained at this level over time.
This can be explained in terms of Starling’s law of the heart (see ‘Starling’s law
of the heart and cardiovascular equations’, Chapter 102, page 403)
455
• PAWP: in some instances, this can be used as a surrogate for left atrial filling
pressure, particularly in instances where the function of the right side of the
heart is in doubt or where the peripheral vascular resistance is very low in an
acutely septic patient.
ASSESSMENT OF LOSS IN VOLUME OF PLASMA AND ECF

The key to this assessment is the plasma albumin concentration and the blood
haematocrit.
In the context of a loss in plasma volume, the plasma albumin concentration
remains constant but, as no erythrocytes have been lost, the blood haematocrit will
increase. The percentage loss of plasma volume can be calculated as below, where
H1 ( initial value of haematocrit and H2 ( value to which haematocrit rises.
Percentage fall in plasma volume ( 100 " {1 * [H1/(100 * H1)]
" [(100 *H2)]/H2}
In the context of a loss in ECF volume, the total albumin remains the same, although
the albumin concentration goes up. The percentage loss of ECF volume can be calcu-
lated as below, where A1 ( initial albumin concentration and A2 ( concentration of
albumin following dehydration.
Percentage fall in ECF volume ( (1 * [A1/A]) " 100
FLUID REPLACEMENT STRATEGIES

There are three factors to consider when prescribing fluid regimens:
1. Basic basal requirements of water and ions (as discussed above)
2. Continuing abnormal losses in addition to basal requirements
3. Correction of any pre-existing fluid or electrolyte deficit, and maintenance of
an adequate left atrial filling volume to maintain blood pressure, and therefore
tissue perfusion and peripheral oxygen delivery.
Basic requirements
An average 70 kg man requires 70 mmol/day of sodium and potassium and three
possible regimens are shown below:
1. 1 L 0.9% (normal) saline and 2000 mL 5 per cent dextrose (70 mmol Na&)
2. 2000 mL 5 per cent dextrose and 500 mL Hartmann’s (65.5 mmol Na&,
2.5 mmol K&)
3. 2500 mL dextrose saline (75 mmol Na&).
It should be noted that K' will need to be added to the above regimens and com-
monly now fluids are available with 20 mmol K& added to each bag. In the past,
456
ampoules of 20 mmol KCl in 10 mL were available to add to fluid bags, but unfor-
tunately these have been used in error as saline flushes, causing fatal arrhythmias.
Thus, concentrated KCl is now not routinely available on wards, although it is of
course still available as a controlled drug in an ITU/HDU setting.
It should never be given at a rate faster than 40 mmol/h.
Abnormal losses
A great deal of water is lost in an unwell patient, through the skin as a result of
pyrexia and through the lungs as a result of tachypnoea or ventilation with non-
humidified air. Two of the most common surgical conditions leading to massive
fluid and electrolyte deficits are pancreatitis (see ‘Acute pancreatitis’, Chapter 104,
page 413) and acute bowel obstruction.
The fluid secreted into the bowel and aspirated from the nasogastric tube is rich in
Na' and K' and therefore 0.9% (normal) saline with added K& should be used to
replace it. Inappropriate management with dextrose saline or 5 per cent dextrose
can lead to a rapid and profound hyponatraemia.
It is essential that an accurate input–output chart be kept in this type of patient and
that a daily positive or negative balance be calculated and recorded, taking into
account any insensible losses.
All too often, fluid management is careless and this can lead to both postoperative
and preoperative disasters.
Pre-existing fluid or electrolyte deficit

To assess this, the techniques described above are crucial to assess the fluid status of
the patient and their immediate electrolyte requirements (see ‘CVP lines and inva-
sive monitoring’, Chapter 110, page 443).
Postoperatively, for the first 36 hours there is sodium and water retention although
obligatory loss of potassium continues. Remember to check postoperative drains,
nasogastic tube aspirates, etc. and ensure that this loss is added to the input–output
chart and factored in when prescribing fluids.
TYPES OF COLLOIDS
• Blood
• HAS available in 4.5 per cent and 20 per cent
• Dextrans: 40 or 70 depending on molecular mass
• Gelatins: relatively short plasma half-life, e.g. Gelofusin, Haemaccel
• Starches, e.g. hetastarch or pentastarch – risk of coagulopathy.
457
COMPLICATIONS OF COLLOIDS
• Transmission of infection – particularly with blood and blood products
• Coagulopathy: Dextran 70, gelatins and starches can interfere with the clotting
cascade and platelet adhesion
• Anaphylaxis
• Worsening oedema (if capillary integrity is lost, larger molecules can leak into
the interstitial space taking water with it).
Key learning points

Colloids and crystalloids
Colloids: composed of large molecules with a molecular mass of ! 30 000
daltons (30 kDa). Can be natural or synthetic. Confined to the plasma for
longer.
Crystalloids: easily able to pass between compartments. Exert much less
osmotic pressure than colloids. Following the metabolism of dextrose,
5 per cent dextrose is distributed evenly as total body water.
A loss of plasma volume in the past has resulted in the use of human albu-
min solution (HAS) to replace the large protein content of plasma, providing
much of the osmotic pressure of the plasma. Not only is this expensive and
limited, but it has also been shown in many studies not actually to improve
outcome! Thus, colloids have been developed with osmotic activity, their
larger molecules attempting to hold water and sodium in the intravascular
space longer than crystalloids such as 0.9% (normal) saline.
Although controversial, most surgeons would use colloids to maintain
blood pressure and plasma volume in an acute situation, in an attempt to
keep volume in the intravascular compartment for longer. There is, however,
little evidence to suggest that colloid administration over crystalloid improves
overall outcome.
Five per cent dextrose is a poor choice for resuscitation in any setting because
the fluid is distributed as total body water between all compartments after
the metabolism of dextrose. Colloids are (in theory) confined for longer to the
intravascular space.
458
112 Head injury and intracranial pressure

You’re a general surgical registrar called to see a 28-year-old man who has
been in a road traffic accident (RTA) with a head injury.
How would you assess him?
His GCS falls to # 6 (E1 V1 M3). What would you do?
Right pupil becomes fixed and dilated. Why and what would you do?
Why does the pupil dilate in raised intracranial pressure (ICP)?
What now? How would you attempt to measure his ICP?
What is CPP (cerebral perfusion pressure)? Why is it useful? What is the
theory behind it?
What manoeuvres can be performed to control ICP and how do they
work?
What reversible factors could be responsible for a transient rise in ICP?
What do you understand by the Monro–Kellie doctrine?
Should you ever perform a lumbar puncture in head injury?
Related topics
Topic Chapter Page
CNP lines and invasive monitoring 110 443
RAISED ICP
Physiology
In order to understand the physiology of head injury, one must know the principles of
the Monro–Kellie doctrine: the brain is in a closed box, the skull. It contains three
things inside, namely blood, brain and CSF. The pressure in the head is related to the
balance among these three. If the brain volume increases, e.g. in cerebral oedema, in
order for the pressure to remain normal, one of the other two (blood and CSF) must
be decreased in volume.
459
CRITICAL CARE head injury and intracranial pressure
120
Cerebral blood flow is
100 constant across a
Cerebral blood flow

(mL /100 g per min)
physiological range
80
of blood pressures
60
40
20
0
0 50 100 150 200
Mean arterial pressure (mmHg)
Figure 112.1
100
Brain
ICP (mmHg)
Decompensation
50
Compensation
CSF
Blood
0
Intracranial Volume
Figure 112.2
Causes of raised ICP

Surgical
Infection
• Empyema.
Head injury
• Extradural haematoma: classic lucid interval; not necessarily associated with
cortical damage if evacuated in a timely manner; classically, an arterial injury
stripping pericranium away from the skull (mass effect increases ICP)
• Subdural haematoma: the result of tearing of dural bridging veins; indicates
underlying cortical damage (mass effect increases ICP)
• Subarachnoid haemorrhage: usually the result of direct contusional injury to
the brain and not the result of rupture of an underlying vascular malformation
(aneurysm/arteriovenous malformation) (blockage of arachnoid granulations
impairing CSF reabsorption, along with cerebral oedema, as a result of hypoxia
increases ICP)
460

What is CPP? Why is it useful? What is the theory behind it?
CPP ( mean arterial pressure (MAP) * ICP
where MAP & one-third of pulse pressure ' diastolic blood pressure
Thus, either decreasing ICP or increasing MAP should increase CPP. This
relationship holds true only for brain in which cerebral autoregulation is
lost, as in traumatic brain injury.
Write down these formulae in a viva when asked about factors that affect
ICP, e.g. in hyperventilation there is a decreased PCO2:
As an increase in PCO2 will cause vasodilatation, a decrease will cause

vasoconstriction, thus decreasing the cerebral blood volume and therefore
reducing ICP according to the Monro–Kellie doctrine (see above).
Similar questions could be devised for all factors that can affect ICP, e.g.
hydrocephalus involves an increase in the volume of CSF as a result of
obstruction, over-production or decreased absorption.
Caveats to the CPP model: although CPP is a useful concept, blood pres-
sure is not necessarily equivalent to blood flow or, even more fundamen-
tally, oxygen transfer and a tissue’s ability to utilize that oxygen. Thus,
brain may be ischaemic despite an adequate CPP of ! 70 mmHg.
• Contusions: the result of rapid deceleration of the brain against the inside of the
cranium (classically coup contre-coup). Bifrontal contusions common and likely
to evolve and swell, leading to a delayed drop in GCS. The initial CT scan
almost always underestimates the eventual size of contusions, leading to the
requirement for a low threshold for repeat imaging (contusions exert mass
effect as a result of blood and oedema to increase ICP)
• Diffuse axonal injury: this carries with it a poor prognosis and is a shearing of
the white matter against the grey matter, leading to significant fibre disruption
(increases ICP as a result of generalized cerebral oedema secondary to
parenchymal disruption).
Medical
• Electrolyte imbalance (cerebral oedema)
• Ischaemia (cerebrovascular accident or CVA)
• Infection: meningitis, cerebritis.
461
Symptoms of raised ICP

• Decreased conscious level (see below)
• Headache
• Nausea and vomiting.
A fall in GCS
• Pressure symptoms: evolving haematoma, evolving contusions (remember
classic lucid interval suggestive of extradural haematoma)
• Ischaemic cause: loss of autoregulation and decreased blood pressure may lead
to cerebral ischaemia
• Post-ictal: seizures are common after blunt head injury and can lead to a
temporary drop in GCS
• Remember metabolic causes: sudden hypoglycaemia in a patient with diabetes
can lead to a profound drop in GCS.
Signs of raised ICP

• A suddenly dilated pupil, unreactive to light is suggestive of a third nerve palsy.
Paralysis of lateral rectus (sixth nerve) leading to a defect in lateral gaze is also a
sign of raised ICP. This is a manifestation of a traction injury on the sixth nerve
because it has a long intracranial course.
• Fall in GCS usually a result of pressure on the brain stem (see other causes above).
• Papilloedema.

Why does the pupil dilate in raised ICP?
This occurs in raised ICP because the nerve is pushed against the free edge
of the tentorium and is a sign of impending tentorial herniation (coning).
The fibres that are damaged are the parasympathetics that travel with the
third nerve from the Edinger–Westphal nucleus in the midbrain to supply
sphincter pupillae, leading to unopposed sympathetic dilatation of the pupil.
Without a CT, in a suspected extradural haematoma, a burr hole would be
drilled on the same side as the pupil. However, in some cases the opposite
side can be dilated (false localizing sign).
CT signs
• Extradural: this respects the skull sutures because an extradural haematoma will
strip the pericranial dura away from the skull, classically creating a relatively
localized convex haematoma; often causes a midline shift
462
• Subdural: this does not respect skull sutures as with extradurals and will lie in a
relatively thin sheet of blood over the cortex. As this is the result of damage to
bridging veins, underlying cerebral damage usually leads to significant oedema
and midline shift
• Subarachnoid: blood is seen in the subarachnoid space, often in the
perimesencephalic cisterns and extending into the ventricles. Blood in the
ventricles increases the risk of hydrocephalus and a ‘full’ third ventricle along
with visible temporal horns are signs of this
• Midline shift: seen in many pathologies that result in mass effect; suggestive of
raised ICP if acute
• Grey/white differentiation: loss of grey/white differentiation on the CT is
suggestive of acute ischaemia.
MEASURING ICP
Invasive methods
• External ventricular drain (EVD) or ventriculostomy, passed into the anterior
horn of the lateral ventricle via usually a frontal burr hole, is still considered the
gold standard
• Brain parenchymal ICP transducer through a cranial access device (usually
referred to as ‘a bolt’)
• Subdural catheter: little used now and has been shown to correlate poorly with
‘actual’ ICP
• Palpation of a craniotomy flap when the bone is left out (obviously not very
accurate but can be a useful sign if there is no ICP monitor in situ).
Non-invasive methods
Not well validated but transcranial Doppler (TCD) can be used to measure veloci-
ties in the middle cerebral artery and derive a ‘pulsatility index’ that may correlate
with ICP.

What factors can cause a transient rise in ICP?
To answer this question, draw out the Monro–Kellie diagram and explain
that an increase in either cerebral blood volume, CSF or brain matter will
increase ICP. Transient factors to do this may include hypoventilation
(including PCO2) as a result of a mucus plug or migrated tracheostomy in
the ITU setting, traumatic hydocephalus or seizures. (There are of course
many others.)
463
MEDICAL MANAGEMENT OF RAISED ICP

Always remember ABC first!
Note that these are the factors that are most important when considering transfer
of the patient to a neurosurgical centre.
• Mannitol bolus (20 per cent) or hypertonic saline after discussion with
neurosurgeon
• Intubation if not protecting airway (remember ABC) and sedation
• Possibly load with phenytoin/use of benzodiazepines to control seizures
• Head up 30° (taking care to immobilize C-spine)
• Mild hypothermia
• An anaesthetist may aid with mild hyperventilation to keep the PCO2 around
4.5 kPa (dangerous if allowed to fall too low because this causes local cerebral
vasoconstriction and can lead to ischaemia)
• Increase CPP by increasing MAP with inotropes (dopamine, noradrenaline [care
as causes vasoconstriction], adrenaline) (see ‘Inotropes’, Chapter 113, page 466).
SURGICAL MANAGEMENT OF RAISED ICP

• External ventricular drain (EVD) to drain off CSF, so decreasing ICP transiently
• Surgical craniectomy $ evacuation of mass lesions
• Bifrontal craniectomy for intractably raised ICP.

Should you ever perform a lumbar puncture in head injury?
For the purposes of the viva, the answer to this question should be no!
A more correct answer is that lumbar puncture should not be performed
in the context of head injury unless an intracranial infection is suspected.
Furthermore, in the presence of a mass lesion with raised ICP, lumbar
puncture is absolutely contraindicated for fear of precipitating coning.
In rare cases, lumbar puncture is performed in head injury but only after a
CT to ensure no mass lesion and open basal cisterns.
ROLE OF IMAGING IN HEAD INJURY

Any drop in GCS initially warrants a CT of the head and any further deterioration
should result in repeat imaging. CT appearances of traumatic brain injury evolve
464
over time and must be monitored. Small subdurals and extradurals can easily
expand and contusions can evolve. Thus clinical vigilance and a very low threshold
for repeat imaging is required.
Currently there are no indications in traumatic brain injury for emergency magnetic
resonance imaging (MRI) because this is both costly and time-consuming, adding
little acute information in most cases. Contusions of the brain stem and posterior
fossa are better imaged with MRI but this information is prognostic on a more long-
term basis.
Key learning point

All questions related to ‘how should you manage’ and a clinical scenario
involving an acute patient should immediately result in ‘A, B, C’ and in this
case ‘D’ for disability. In advanced trauma life support (ATLS), the AVPU
score is taught but many surgeons will use the GCS (eyes/voice/movement).
465
113 Inotropes

What is an inotrope?
What different classes of inotropes do you know?
In what circumstances would you use adrenaline (epinephrine) and why?
How can inotropes be administered?
What monitoring is required if a patient is on inotropes?
Related topics
Topic Chapter Page
Starling’s law of the heart and cardiovascular 102 403
equations
Shock 122 510
DEFINITION
An inotrope is a drug that increases myocardial contractility and therefore shifts
Starling’s curve up (see ‘Starling’s law of the heart and cardiovascular equations’,
VASOACTIVE COMPOUNDS
These are drugs used artificially to support a failing or dysfunctional cardiovascular
system. Via their actions on various receptors, they affect either heart rate or force
of contraction, or alter systemic vascular resistance. Effects are predominantly
mediated by either %-, $1- or $2-receptors.
They are divided into the following groups:
• Inotropes: increase the force of contraction of the heart

• Pure chronotropes: increase heart rate
• Vasodilators
• Vasoconstrictors.
466
CRITICAL CARE inotropes
RECEPTORS, POSITION AND ACTION

• %-receptors: expressed in the vasculature; agonists cause vasoconstriction
• $1-receptors: expressed in the heart, agonists are positively chronotropic
(increase heart rate) and positively inotropic (increase force of contraction)
• $2: expressed predominantly in the vasculature; agonists cause vasodilatation.
Adrenaline
Actions on: (, )1, )2 – ‘dirty drug’.
Used at cardiac arrest and turns patient into ‘heart–brain preparation’ attempting
to spare the brain and myocardium from ischaemia by causing massive peripheral
vasoconstriction (( effects) and strong positive chronotropia ()1 effects).
Noradrenaline
Not an inotrope strictly because no increase in force of contraction.
Actions on: (.
• Causes peripheral vasoconstriction, so increasing SVR. An inotrope given in the

context of septic shock (see ‘Shock’, Chapter 122, page 510, and ‘Sepsis and
SIRS’, Chapter 121, page 505)
• Must be administered centrally
• At low doses, invasive arterial monitoring and urine output may be all that is
required. However, in the context of severe sepsis with high inotrope/multiple
inotrope requirements, some measure of SVR must be available to titrate the dose.
This can be derived from traditional Swan–Ganz (pulmonary artery or PA) catheter
measurements or, more commonly now, less invasive measures such as LidCo
(lithium dilution) (see ‘CVP lines and invasive monitoring’, Chapter 110, page 443).
Note that SVR is never directly measured but is derived from PA measurements in
the case of the PA catheter.
Dopamine
Actions on: D-receptors in the gut and kidney.
In small doses: renal arteries dilate, so increasing urinary output. Splanchnic blood
flow increases.
In medium doses: predominantly $1 effects resulting in a tachycardia and increased
force of contraction.
In large doses: predominantly % effects, causing peripheral vasoconstriction and an
increase in SVR.
467
Key learning point

Note that increasing evidence does not support the use of ‘low or renal dose’
dopamine in the context of a poor urinary output and failing cardiovascular
system as a renal-sparing inotrope, but it is still used in some units around
the country. You should be aware of the controversy surrounding its low
dose usage.
Many ITUs no longer use dopamine as their first-line inotrope and instead use more
selective dopamine derivatives, such as dobutamine or dopexamine.
Isoprenaline
Actions on: )1 and )2.
This affects the $-receptors in the heart, bronchi, skeletal muscle and gut vascula-
ture. It reduces the SVR by vasodilatation in the vascular beds of the skeletal
muscles, kidney and mesentery. It is positively chronotropic and inotropic so
increasing cardiac output.
Its strong $1 effects produce a tachycardia, however, and this limits its clinical
effectiveness.
Dobutamine
Actions on: predominantly )1 (with some $2 action)
A synthetic analogue of isoprenaline with its main advantage being that it causes less
of a tachycardia, so increasing its usefulness. The drug is used for cardiogenic shock on
cardiac care units because $2 action offloads the heart and $1 action increases force of
contraction.
Nitrates (vasodilators – not inotropes)

Actions: venodilatation.
In circumstances where the heart needs to be ‘offloaded’, such as pulmonary

oedema or left ventricular failure, nitrates can be used. Their action is to reduce
SVR and venodilate, thereby reducing both afterload and preload.
Note that, if arterial vasodilatation is required, hydralazine may be used (this of

course reduces afterload alone).
468
MONITORING AND CHOICE OF INOTROPE

The choice of inotrope will depend on the patient’s condition, and the specific physio-
logical parameters. Invasive monitoring is usually required with at least a urinary
catheter, an indwelling arterial line and some form of central venous access.
A measure of SVR, PA pressure and pulmonary capillary wedge pressure (PCWP) or
right atrial pressure (RAP) is often required. These can be measured (and derived, in
the case of SVR) from invasive PA catheters, less invasive PICCO or LidCo systems,
or even oesophageal Doppler measurements (see ‘CVP lines and invasive monitoring’,
469
114 Intubation and ventilation

What are the indications for intubation?
What apparatus can be used for endotracheal intubation? Describe the
technique for orotracheal intubation.
What is meant by ‘rapid sequence induction’?
How does cricoid pressure assist in rapid sequence induction?
What is the definition of anatomical and physiological dead space?
Draw a standard spirometry trace and label the key values.
How can oxygen be delivered to the patient?
What is a Venturi connector?
How does a reservoir bag increase the FiO2 given to a patient?
What modes of mechanical ventilation are available and what are their uses?
What do you understand by the term ‘CPAP’?
What is PEEP?
What are the complications of mechanical ventilation?
Related topics
Topic Chapter Page
Sedation 120 500
Pneumothorax 117 488
Tracheostomy 42 148
TYPES OF DEFINITIVE AIRWAY

• Endotracheal airways:
• orotracheal intubation – most commonly used
• nasotracheal intubation
• Laryngeal mask
470
CRITICAL CARE intubation and ventilation

What are the indications for intubation?
Endotracheal (ET) intubation is performed for the express purpose of
securing the airway. The use of an ET tube should prevent silent aspiration
with the cuff inflated.
Indications
• Apnoea and/or respiratory failure
• Protecting the airway from impending obstruction (e.g. burns/facial
oedema/facial trauma, low GCS)
• Protection from aspiration pneumonitis (e.g. in abdominal surgery)
• Head injury with risk of raised ICP and a need for tight control of PaCO2
• Inability to maintain an airway by less invasive methods
• Hypoxia refractory to oxygen therapy
• Vocal fold paralysis
• ET intubation is indicated in elective abdominal surgery
• Surgical airways:
• cricothyroidotomy
• tracheostomy (surgical or percutaneous) (see ‘Tracheostomy’, Chapter 42,
page 148).
METHODS OF OXYGEN DELIVERY

Oxygen delivery to the lungs depends on:
• Patent airway
• Concentration of inspired oxygen (FiO2)
• Adequate ventilation.
Patent airway
Although a definitive airway is often used in surgical practice, an obstructed airway
can be managed with escalating levels of invasive care:
• Chin lift and jaw thrust (as per ATLS): maintain patency of the upper airway
when the tongue has fallen back
• Guedel airway: not suitable for fully alert patients but useful for temporary bag-
and-mask ventilation of the unconscious patient before intubation. Situated
above the vocal folds so cannot prevent aspiration and can initiate the gag reflex
• Nasopharyngeal airway: more suitable for drowsy patients and less likely to
initiate the gag reflex than the Guedel airway. Contraindicated in facial trauma
and suspected base of skull fractures.
471

Describe the technique for orotracheal intubation.
Orotracheal intubation
• Check all equipment before starting: laryngoscope, suction, ET tube (size
7–8 for females and size 8–9 for males), Ambu bag and mask, oxygen
supply, muscle relaxant, intravenous sedation, intravenous access and
ensure that you have an assistant
• Preoxygenate the patient with 100 per cent O2 for several minutes – if
breathing on their own, hold the mask close to the face and allow them to
preoxygenate without sedation or muscle relaxation. In an acute setting,
give sedation and/or muscle relaxant before attempting to preoxygenate
• Allow a maximum of 30 seconds per insertion attempt
• Use laryngoscope directly to visualize the vocal folds and pass the ET
tube between them. In difficult intubations where an unobstructed view
of the folds cannot be achieved, the use of a bougie may be helpful, rail-
roading the tube on the bougie, having passed it between the folds
• Inflate cuff and check position of tube by auscultation of the lungs and epi-
gastrium. End-tidal CO2 monitors are also useful in verifying tube position
• Secure tube by tying in place with tapes (average length to teeth in
females is 21–23 cm, 23–25 cm in males)
Rapid sequence induction
This process involves the intubation of a patient with suspected gastric
contents:
• Recent meal
• Delayed gastric emptying: trauma, sepsis, gastroparesis
• Incompetent lower oesophageal sphincter: pregnancy, hiatus hernia
• After administration of the muscle relaxant, cricoid pressure is initiated by
the assistant. This collapses the oesophageal lumen behind and prevents
aspiration. The cricoid pressure is released only when the tube position has
been confirmed and the ET cuff inflated
Concentration of inspired oxygen

A simple Hudson mask delivers an unreliable FiO2 to the patient and its use should
be avoided in the acute setting if at all possible.
Venturi connectors are useful and reliable methods of delivering a relatively con-
stant FiO2 to a patient and rely on the Venturi effect.
The Venturi effect is a special case of Bernoulli’s principle, in the case of fluid flow or
airflow through a tube or pipe with a constriction in it. The fluid must speed up in the
472
restriction, reducing its pressure and producing a partial vacuum via Bernoulli’s effect.
This vacuum encourages air to mix with the oxygen flow at a set rate, thereby setting
the FiO2. It is essential, when using Venturi connectors, to ensure that the rate from the
wall is the same as that printed on the connector.
The most oxygen that can be delivered on the ward is through a reservoir bag. As the
flow of oxygen from the wall cannot match the minute volume of the patient, air mixes
with each breath around the sides of the Hudson mask and through the holes in it. A
mask with a reservoir bag must be close fitting and, with each breath, the extra air that
cannot be supplied by the wall is supplied by the 100 per cent oxygen in the reservoir
bag, thus increasing the FiO2. Despite this, a reservoir bag can still produce only around
a 60–70 per cent FiO2 as a result of imperfections in the fitting of the mask.
In the case of most modern mechanical ventilators, the FiO2 can be set through the
ventilator.

Draw a standard spirometry trace and label the key values.
IRV TLC
IC
Volume (L)
TV VC
ERV
FRC
RV
0
Time
Key :
IC Inspiratory capacity FRC Functional residual capacity
IRV Inspiratory reserve volume RV Residual volume
TV Tidal volume ERV Expiratory reserve volume
VC Vital capacity TLC Total lung capacity
Figure 114.1
473
ASSISTED VENTILATION
Assisted ventilation can be split into non-invasive and invasive ventilation.
Non-invasive ventilation
• CPAP (continuous positive airway pressure): delivered by an airtight mask over
the nose and mouth, which provides a continuous positive pressure in the
airways, thus splinting open alveoli and improving recruitment, reducing the
work of breathing
• Pressure support: can be delivered by a CPAP mask. Closely monitors the
airflow in the circuit and provides a positive pressure increase when it senses
that the patient wishes to take a breath. Used together with CPAP it can
drastically reduce the work of breathing and may be termed ‘BIPAP’ (bilevel
positive airway pressure).
Invasive ventilation
Invasive ventilation provides the most reliable way of providing a constant FiO2 to
the patient, along with reducing the anatomical dead space and in some cases
increasing the efficiency of ventilation.
• CPAP may be administered invasively.

• BIPAP and/or pressure support may be administered invasively.
• IPPV (intermittent positive-pressure ventilation) is an obligatory ventilatory
mode requiring apnoea. It is the most used form of ventilation in acute trauma
or surgery where patients are anaesthetized and paralysed at the same time.
• SIMV (simultaneous intermittent mechanical ventilation) allows
synchronization with any respiratory effort that the patient may make, but
guarantees a number of breaths per minute.

What is PEEP?
PEEP stands for positive end-expiratory pressure and is used to ensure a
positive pressure at the end of expiration, splinting open the alveoli and
preventing the usual alveolar collapse. This decreases the work of breath-
ing by obviating the initial force on inspiration required to open the alveoli
and overcome the surface tension of alveolar water.
High levels of PEEP increase the risk of barotrauma.
474
A further subdivision of invasive ventilation is pressure-controlled and volume-

controlled ventilation.
Volume controlled
A less sophisticated method of ventilation, this allows the user to set a tidal volume
that must be delivered regardless of the airway pressures involved, and thus
increase the risk or barotrauma to the lungs (see ‘Complications’ below). Pressure
limits can be used to help prevent this. Volume-controlled ventilation does provide
a constant minute volume.
Pressure controlled
A more sophisticated method of ventilation, it allows the user to set a peak inspira-
tory pressure (PIP). Inhalation occurs until this PIP is reached, after which passive
exhalation is allowed. The delivered volume with each respiration is dependent on
the pulmonary and thoracic compliance. A major advantage of pressure-controlled
ventilation is a decelerating inspiratory flow pattern, in which inspiratory flow
tapers off as the lung inflates. This usually results in a more homogeneous gas dis-
tribution throughout the lungs and a decrease in the incidence of barotrauma.
However, tidal volumes are not constant in this method of ventilation, although
mixed modes with volume-assured, pressure-controlled ventilation are now avail-
able on some ventilators.
Complications of mechanical ventilation

Pulmonary effects
• Barotrauma results in pulmonary interstitial emphysema, pneumomediastinum,
pneumoperitoneum, pneumothorax and/or tension pneumothorax. High peak
inflation pressures (! 40 cmH2O) are associated with an increased incidence of
barotrauma.
• Alveolar cellular dysfunction occurs with high airway pressures. The resultant
surfactant depletion leads to atelectasis, which requires further increases in
airway pressure to maintain lung volumes.
• High airway pressures result in alveolar over-distension (volutrauma), increased
microvascular permeability and parenchymal injury.
• High-inspired concentrations of oxygen (FiO2 ! 50 per cent) result in free-radical
formation and secondary cellular damage. These same high concentrations of
oxygen can lead to alveolar nitrogen washout and secondary absorption
atelectasis.
Cardiovascular effects
• Increased intrathoracic pressures result in a decrease in cardiac output as a
result of decreased venous return to the heart (see ‘Starling’s law of the heart
and cardiovascular equations’, Chapter 102, page 403), right ventricular
dysfunction and altered left ventricular distensibility.
475
• Exaggerated respiratory variation on the arterial pressure waveform (‘swinging

of the arterial line waveform’) is a clue that positive pressure ventilation is
significantly affecting venous return and cardiac output. In the absence of an
arterial line, a good pulse oximetry waveform can be equally instructive. A
reduction in the variation after volume loading confirms this effect (see ‘Fluid
balance’, Chapter 111, page 452).
Renal, hepatic and gastrointestinal effects
• Positive pressure ventilation is responsible for an overall decline in renal
function with decreased urine volume and sodium excretion.
• Hepatic function is adversely affected by decrease in cardiac output, increased
hepatic vascular resistance and elevated bile duct pressure.
• The gastric mucosa does not have autoregulatory capability. Thus, mucosal
ischaemia and secondary bleeding may result from a decrease in cardiac output
and increased gastric venous pressure.

What is the definition of anatomical and physiological dead space?
The dead space is the total volume of the parts of the lung and airways that
does not participate in gaseous exchange:
• Anatomical: mouth, nasopharynx, larynx, trachea and bronchi
• Physiological: diseased lung unable to perform gaseous
. . exchange (either
collapsed alveoli or poorly perfused alveoli, i.e. V/Q mismatch)
476
115 Nutrition

Why is nutrition important in the context of surgical disease?
How can nutrition be administered?
What are the clinical signs of malnutrition?
How can nutritional status be assessed?
What are the advantages of enteral feeding over total parenteral nutrition
(TPN)?
What are the complications of TPN?
What are the nutritional requirements of a 70 kg man before and after
elective surgery? What would happen to them if he developed a post-
operative pyrexia/sepsis?
How do severe burns affect nutritional requirements?
What trace elements are required and which are associated with wound
healing?
Related topics
Topic Chapter Page
NUTRITION IN SURGERY
In an elective context, the nutrition of a patient both pre- and postoperatively is cru-
cial. An undernourished patient will suffer from poor wound healing, a dampened
immune system and eventually organ dysfunction.
In an emergency context, the nutrition of an acutely unwell patient is even more
critical because ill, septic patients in a catabolic state have a much increased nutri-
tional requirement (see ‘Systemic response to surgery’, Chapter 123, page 574).
ASSESSMENT OF NUTRITIONAL STATUS

• History
• Examination
• Anthropometric and dynamometric measurements
477
CRITICAL CARE nutrition
• Biochemical assessment (e.g. albumin, liver function, U&Es)

• Immune function.
Key learning point

When asked how to assess the nutritional status of a patient, don’t jump to
the common answer ‘plasma albumin’, which has, in fact, been shown to
very poorly correlate with nutritional status. However, consistent drops in
plasma albumin in the context of acutely unwell patients have been shown
to correlate quite well with poor outcomes. (Note that this is not purely
attributable to nutrition.)
SIGNS OF MALNUTRITION
Early signs (loss of 15 per cent body weight)
Na& and water retention leading to peripheral oedema.
Severe signs (loss of ! 15 per cent body weight)
• Loss of muscle mass and fat
• Anaemia
• Diarrhoea.
Pre-terminal signs
• Decreased albumin synthesis and antibody production
• Poor wound healing (particularly zinc, magnesium and selenium trace elements
important)
• Acidosis
• Hyperkalaemia
• Decreased cough reflex – leading to possible pneumonia.
ENTERAL NUTRITION
This utilizes the GI tract and so a prerequisite for this type of nutrition is an intact
and functional gut. Methods of enteral feeding are:
• Oral
• Nasogastric tube (NGT) or nasojejunal tube (NJT)
• Percutaneous endoscopic gastrostomy (PEG)
• Percutaneous endoscopic jejunostomy (PEJ)
• Surgical jejunostomy.
478
Indications for enteral feeding

• Severe catabolic states (e.g. burns)
• Malnutrition pre-surgery
• Postoperative oesophagogastric surgery
• The unconscious patient
• Anorexic elderly patient with inadequate intake
• Mild-to-moderate GI disease (pancreatitis, short-gut syndrome, Crohn’s disease).
Monitoring
• Clinical
• Fluid balance
• Daily weights
• Electrolytes and twice-weekly trace elements.
Advantages over TPN

• Safer
• Cheaper
• Fewer complications
• Prevents atrophy of gut mucosa (occurs within 48 h of fasting)
• Continues to encourage adequate immunological barrier across gut mucosa
(IgA levels and intact endothelium).
Complications of enteral feeding

• Blockage/misplaced tube
• Aspiration (either silent or overt) and subsequent pneumonia
• Irritation of gut lining and ulceration/bleeding

What are the nutritional requirements of a 70 kg man before and after
surgery? How does this change if he develops a pyrexia or sepsis?
Normal nutritional requirements are approximately 30 kcal/kg, which
works out to roughly 2000 kcal in the 70 kg man.
Postoperatively this increases to 35 kcal/kg, and increases by a further
10 per cent per degree increase in temperature.
In the septic state, requirements go up further still to 40–45 kcal/kg and in
hypercatabolic states, such as severe burns, can rise to as high as 60 kcal/kg!
479
• Nausea and vomiting

• Diarrhoea
• Deranged LFTs
• ‘Re-feeding syndrome’ in patients who have not been fed for significant period
of time.
PPN AND TPN (PARTIAL OR TOTAL PARENTERAL NUTRITION)

This is delivery of nutrition via the intravenous route. Its advantages are that it does
not require an intact gastrointestinal system.
Indications
• Absolute or relative intestinal failure
• Hypercatabolic states
• Postoperative (in some selected cases – particularly with prolonged gastroparesis
and failure of absorption).

What does TPN contain?
TPN is made up for the individual patient and is changed according to
their individual requirements (e.g. more potassium, less lipids, etc.).
However, essentially TPN is a mixture of hypertonic sugars with fat emul-
sions, nitrogen, electrolytes, vitamins and trace elements:
• ! 50 per cent carbohydrates
• 30–40 per cent fat emulsions
• 1–2 g/kg by body weight per day of fat
• nitrogen: synthetic crystalline amino acid preparation in laevo form
• water: 30–35 mL/kg per day
• electrolytes: Na&, K&, Cl*, Ca2&, Mg2&, PO43*
• vitamins: A, D, E, K (fat soluble), B, C
MONITORING TPN
• Weight
• U&Es, glucose, FBC, LFTs
• Fluid balance
• Temperature and signs of sepsis
• Trace elements.
480
ROUTES OF ADMINISTRATION
This is usually via an indwelling central venous access device, be that a Hickman
line or simple non-tunnelled CVP line. TPN can be given by long/peripheral lines,
usually sited in the antecubital fossa.
COMPLICATIONS
• Line sepsis
• Metabolic derangement
• Na& retention, acidosis
• TPN jaundice
• Expense
• Venous access problems.
481
116 Oliguria and renal replacement

What are the common causes of postoperative oliguria?
What are the principles of management of oliguria?
What are the indications for renal replacement therapy?
What are the various varieties of renal replacement therapy?
What is the minimum acceptable urine output for a patient?
How would you classify acute renal failure?
What factors determine the urine output?
What is creatinine clearance? How can it be measured?
Related topics
Topic Chapter Page
Shock 122 510
Nutrition 115 477
ACUTE RENAL FAILURE AND CHRONIC RENAL FAILURE

Acute renal failure (ARF) is a relatively common postoperative surgical condition
and it in most cases a surgical disease as a result of shock from any cause (see
‘Shock’, Chapter 122, page 510) whereas chronic renal failure (CRF) is a medical
disease.
Factors that determine urine output

• Renal perfusion pressure (proportional to glomerular filtration rate or GFR)
• Renal tubular function
• Patent urinary tract
• Neurohormonal mechanisms affecting electrolyte and water retention (see
‘Function of the kidney II’, Chapter 93, page 377).
482
CRITICAL CARE oliguria and renal replacement

How would you classify acute renal failure?
Acute renal failure is a syndrome of rapidly deteriorating renal function.
There is no consensus as to its exact definition and over 30 different
definitions have been published.
One possible definition is: ‘Acute renal failure (ARF) is a syndrome
characterised by a rapid decline in glomerular filtration rate (hours to
days), retention of nitrogenous waste products, and perturbation of
extracellular fluid volume and electrolyte and acid–base homeostasis.’
Acute renal failure can be classified as:
• Pre-renal (haemodynamic instability, low cardiac output and hypotension
leading to low renal perfusion)
• Renal (parenchymal damage and glomerulonephritis)
• Post-renal (obstructive – stones, strictures, tumours in the wall of the
ureter, e.g. transitional cell carcinoma, iatrogenic [ligation of the ureters
intraoperative])

What is creatinine clearance? How can it be measured?
Definition: The inverse of the time constant that describes the removal rate
of creatinine from the body divided by its volume of distribution (or total
body water).
It is used as a surrogate for GFR but correctly is NOT the volume of
plasma cleared of creatinine per unit time. Thus:
CrCl ( (uCr " uV)/(sCr " 1440)
where: uCr ( urine creatinine concentration, uV ( volume of urine in

24 h, sCr ( serum creatinine concentration.
This method, known as ‘24-hour urine’ because required only in circum-
stances of altered protein intake or decreased body mass. In other cases,
the Cockcroft and Gault formula is usually sufficient:
• Altered protein intake – malnutrition, vegetarian diet, creatinine supple-
mentation
• Altered body mass – amputation, malnutrition or muscle wasting
483
DETERMINATION OF GFR AND CREATININE CLEARANCE

Clinically, the Cockcroft and Gault formula can be used to estimate the creatinine
clearance for a given patient and thus their GFR:
Male: GFR ( [(140 * Age) " (Weight)]/(sCr " 72)
Female: GFR ( [(140 * Age) " (Weight) " 0.85]/(sCr " 72).
Common causes of postoperative oliguria (" 30 mL/h or " 0.5 mL/kg per h in adults
and " 1.0 mL/kg per h in children)
• Stress response (see ‘Systemic response to surgery’, Chapter 123, page 514).
Sodium and water retained as a result of ADH, aldosterone and cortisol
secretion as a stress response
• Poor renal perfusion (pre-renal):
• hypotension as a result of underfilling (dehydration or inadequate fluid
replacement in patients nil by mouth) or continued blood loss
• low cardiac output state
• vasodilatation secondary to SIRS or septic shock (see ‘Sepsis and SIRS’,
• intra-abdominal compartment syndrome (see ‘Compartment syndrome’,
• Established acute tubular necrosis (ATN) (renal) from a bout of perioperative
hypotension
• Renal tract obstruction (post-renal) iatrogenic, blocked urinary catheter, stones,
extrinsic compression.
PRINCIPLES OF MANAGEMENT OF POSTOPERATIVE OLIGURIA

ARF as a result of ATN postoperatively is potentially fully reversible if caught in time.
It is therefore most important to exclude ATN as a cause of oliguria postoperatively.
• Obstruction must be excluded:

• urinary catheter flush $ replacement. Bladder scan can be useful to measure
the volume of urine in an obstructed bladder
• there are only two causes of anuria: one is a blocked catheter and the other
advanced ATN.
• Hypovolaemia should be excluded (see ‘Fluid balance’, Chapter 111, page 452).
• If necessary, a CVP line should be sited and response to a fluid challenge should
be assessed.
• Measure the patient’s urine osmolality. If the urine is isosmolar to plasma
(280–320 mosmol/L) this is suggestive of renal failure. Fluid should then be
restricted to 20 mL/h plus the previous hour’s output and a careful eye must be
484
placed on the serum potassium, treating above 6 mmol/L with an insulin and
dextrose infusion ' calcium resonium/calcium gluconate. ECG should be
performed to see if hyperkalaemia has associated ECG changes (peaked T
waves, etc.).
• Low threshold for liaising with ITU early.
• Check ABGs to monitor any development of a metabolic acidosis (see
‘Acid–base balance’, Chapter 84, page 349).
• Measure serum creatinine at least daily.
• Ensure that accurate fluid balance chart is kept and that urine osmolality and
electrolyte content are measured daily.
• Ensure that there are no nephrotoxic agents on the drug chart (e.g.
aminoglycosides and NSAIDs in particular).
• There is no evidence to suggest that so-called ‘renal dose’ dopamine improves
outcome or prevents renal failure.
• Consider inotropic support (see ‘Inotropes’, Chapter 113, page 466) and/or a
frusemide infusion (in HDU/ITU setting usually).
• Arrange ultrasonography of kidneys to exclude an obstructive cause.
RENAL REPLACEMENT THERAPIES

In an acute setting, renal replacement is indicated if:
• It is impossible to control the serum potassium with conventional measures
such as an insulin and dextrose infusion (hyperkalaemia ! 6 mmol/L)
• The patient is overloaded and in pulmonary oedema with the intention of
taking fluid off and creating a negative fluid balance
• There is a symptomatic uraemia (serum urea ! 30 mmol/L)
• There are signs of encephalopathy
• There is a profound metabolic acidosis (pH " 7.2)
• Hepatorenal syndrome is developing
• Serum creatinine is rising very steeply (although this is perhaps the most
controversial indication).
Methods of renal replacement

These can be continuous or intermittent and are broadly split into three categories.
Haemofiltration
• Continuous convection of molecules across a semipermeable membrane results
in removal of not only solutes but also fluid. This fluid is replaced with an
isotonic buffered solution. The technique is very useful in an ITU setting for
restoring fluid balance relatively quickly, and requires only one vascular access
port in its simplest venovenous configuration (usually in the femoral vein but
485
can be via a central line or surgical arteriovenous fistula in the case of chronic
patients)
• Good for fluid removal but not as efficient as haemodialysis in clearing smaller
molecules
• Continuous system.
Haemodialysis
• Blood interfaces with a dialysate across a semipermeable membrane, permitting
passage of molecules smaller than 5 kDa down a diffusion gradient
• Less good for fluid removal (see above)
• Continuous or intermittent.
Peritoneal dialysis
• No longer used in an acute setting
• Commonly used in patients with CRF
• Peritoneum and omentum becomes semipermeable membrane, dialysate is
infused into the abdominal cavity via a Tenckhoff indwelling catheter and is
drained off after several hours
• Slow and less efficient than either of above systems
• Does not require vascular access
• Spontaneous bacterial peritonitis a serious complication. Dialysate is infused
with broad-spectrum antibiotics to treat this condition.
Modalities of continuous renal replacement
These are categorized according to the vascular pattern utilized and the type of
replacement, either dialysis or filtration:
• Continuous venovenous haemofiltration (CVVH): flow is produced by roller
pumps. Patient needs good vascular access but one Vascath in the femoral vein is
common in ITU renal replacement strategies.
• Continuous arteriovenous haemofiltration: flow relies on patient’s arterial blood
pressure and is thus driven by the arteriovenous pressure difference. Less
commonly used in most ITUs.
• Continuous arteriovenous or venovenous haemodialysis.
• Haemodiafiltration: provides the best urea clearance by the combination of the
two techniques but can remove large volumes of fluid and needs careful
management to prevent the patient from becoming haemodynamically unstable.
Complications of renal replacement

These can be split into the following.
Infections
• Line sepsis
• Bacterial peritonitis in peritoneal dialysis.
486
Technical problems with the circuit

• Clotted circuit
• Loss of connection leading to air embolus
• Haemorrhage.
Systemic complications
• SIRS
• ARDS.
Complications as a result of fluid and electrolyte shifts
• Hypotension
• Disequilibrium syndrome: cerebral oedema following massive shifts in serum
osmolality after filtration of large numbers of urea molecules. Presents as
headache, nausea and vomiting, and occasionally seizures.
487
117 Pneumothorax

What is the definition of a pneumothorax?
What types of pneumothorax do you know of?
What cardiovascular changes occur in a ‘simple’ (open and closed)
pneumothorax versus a tension pneumothorax?
What is a tension pneumothorax and why is it universally fatal if left
untreated?
How should a pneumothorax be treated?
What are the causes of a pneumothorax?
Related topics
Topic Chapter Page
CVP lines and invasive ventilation 110 443
equations
DEFINITION
Abnormal air in the intrapleural space.
CLASSIFICATION OF PNEUMOTHORAX
• Closed (spontaneous)
• Open
• Tension.
Closed pneumothorax (spontaneous)

• Pressure within alveoli ! intrapleural pressure and if weakened alveolus
ruptures, and air passes from the lung into the intrapleural space until the
pressure in the two spaces equilibrates.
• The air will reabsorb if the source of the pneumothorax is sealed.
Clinical features
• SOB (shortness of breath)
• Chest pain (often pleuritic in nature)
488
CRITICAL CARE pneumothorax
• Tachycardia
• Reduced chest wall expansion on the affected side
• Hyperresonance on percussion of the affected side.
Causes
• Primary (no known cause – spontaneous)
• Rupture of bullae
• Marfan’s/Ehlers–Danlos syndrome and other connective tissue diseases
• Asthma
• Iatrogenic (e.g. CVP line, barotrauma with excessive ventilation)
• Blunt trauma.
Management
Twenty per cent of closed pneumothoraces do not require invasive management
and may be managed expectantly. Increasing the FiO2 of the patient will increase
the speed of reabsorption as nitrogen is replaced with oxygen in the intrapleural
space and this is reabsorbed faster.
Those patients who do require surgical management will require an intercostal
chest drain with an underwater seal. In a small number of cases, aspiration of the
pneumothorax may be sufficient.
Open pneumothorax
• Caused by penetrating trauma to the chest wall
• Enables air from the outside to communicate with air in the intrapleural space
• If hole in the chest wall is greater than the cross-sectional area of the
trachea/larynx, the mediastinum will shift to the contralateral side because air
will preferentially enter the hole.
Management
First the wound must be sealed either by surgical closure or temporarily by an occlu-
sive dressing, so converting the open pneumothorax to a closed pneumothorax. A
chest drain is then inserted. The danger in this is that, before the chest drain can be
inserted, the open pneumothorax may be converted to a tension pneumothorax.
Tension pneumothorax
• Occurs when the hole in the pleura is unsealed and a valve is formed which
allows air into the pleural space on inspiration but does not allow it to escape
on expiration
• Pressure in the intrapleural space therefore rises and the mediastinum is pushed
into the contralateral space in the chest cavity.
Management
This requires immediate needle decompression (without waiting for confirmatory
radiology) followed by a chest drain.
489
CRITICAL CARE pneumothorax

Why is a tension pneumothorax universally fatal if untreated?
As the intrapleural pressure rises and the mediastinum is further shifted
over to the opposite side of the chest cavity, so the high pressure reduces
venous return (Vret) and therefore cardiac output (CO). Eventually, Vret
falls to 0, so reducing CO to 0 and causing cardiac arrest. A heart that can-
not fill cannot empty!
INSERTION OF A CHEST DRAIN

• Unless an emergency, pre-procedure a chest radiograph should be performed
• Patient has arm fully abducted behind neck
• ‘Triangle of safety’ is identified (lateral border of pectoralis major, anterior border of
latissimus dorsi and a line superior to the horizontal level of the nipple)
• Skin is prepared and draped and local anaesthetic is infiltrated
• 3 cm incision in rib space (classically fifth intercostal space in the midaxillary line)
• Spencer–Wells forceps used to dissect tissue down to rib
• Chest wall and pleura breached above rib to avoid neurovascular bundle
• Drain is placed through track guided with forceps (never use a trocar!)
• Stitched in place with 1/0 silk and mattress suture or purse string inserted but
not tied in anticipation of removal
• Occlusive dressing placed around drain site
• Drain connected to underwater seal ' suction in some instances
• Chest radiograph to confirm drain position.
REMOVAL OF A CHEST DRAIN

• Remove in forced expiration
• Tie mattress suture/z-suture/purse-string suture
• Occlusive dressing over wound
• Chest radiograph post-procedure to check for pneumothorax.
490
118 Pulse oximetry

What is a pulse oximeter and what is it used for?
What are the principles of pulse oximetry?
What does pulse oximetry measure?
How does the SaO2 relate to PO2 on ABGs?
What other parameters need to be known to interpret a pulse oximeter
reading?
What are the pitfalls and sources of error in pulse oximetry?
In what circumstances might the percentage saturation be erroneously high?
What is methaemoglobin and how does its presence in the blood affect a
pulse oximeter?
Related topics
Topic Chapter Page
Altitude 86 356

How does pulse oximetry work?
Pulse oximetry is widely used in the postoperative surgical HDU patient.
It calculates the percentage oxygen saturation of the arterial blood (SaO2).
Oxygenated and deoxygenated haemoglobin optimally reflect different
wavelengths of incident light. Thus, the pulse oximeter uses two different
light-emitting diodes at two wavelengths:
• 660 nm (red light) – measures total amount of haemoglobin
• 940 nm (infrared or IR light) – measures oxygenated haemoglobin
Thus, a percentage of saturated haemoglobin can be calculated from a
ratio of the two.
491
CRITICAL CARE pulse oximetry
Probes are attached to either fingers or ear lobes and measure not only SaO2 but
also pulse rate, and estimate pulse volume in some cases.
PULSE OXIMETRY AND ABGs
Key learning point

FiO2 is key!
Note that either SaO2 or PaO2 is absolutely meaningless without know-
ledge of the concentration of inspired oxygen or oxygen flow (i.e. FiO2).
A saturation of 95 per cent on air may be considered reasonable but the

same saturations on high-flow oxygen with a non-rebreather reservoir bag
could indicate very poor gas transfer. Likewise, a PaO2 of 12.0 kPa on room
air would be considered normal but the same PaO2 on 100 per cent humidi-
fied O2 through an ET tube reflects severe respiratory failure.
Therefore, pulse oximetry does not assess ventilation and other tests such
as end-tidal CO2 and capnography should be used for this purpose.
What is the A–a gradient?
Put simply, the A–a gradient is a measure of how well oxygen is transferred
from the alveolus to the blood and is defined as:
A–a gradient ( PAO2 * PaO2
where PAO ( partial pressure of oxygen in the alveolus and PaO2 ( partial
pressure of oxygen in arterial blood.
PaO2 is obtained from ABGs and PAO2 is estimated from the alveolar gas
equation:
PAO2 ( [(760 *47 ) " FiO2 * PaCO2]/0.8
where FiO2 is expressed as a fraction.

A normal A–a gradient on air is estimated by:
(Age ' 10)/4.
A higher gradient indicates shunting and/or a ventilation–perfusion mismatch.
492
The delivery of oxygen to the tissues depends on three factors (see ‘Oxygen trans-
port’, Chapter 99, page 394):
1. Cardiac output
2. Haemoglobin concentration
3. Oxygen saturation (SaO2).
A drop in SaO2 can be picked up more quickly with pulse oximetry than clinical
observation for peripheral cyanosis (where SaO2 needs to drop to 60–70 per cent
before cyanosis is observed).
The PaO2 has a non-linear relationship to SaO2 (see ‘Oxygen dissociation curve’, in
‘Oxygen transport’, Chapter 99, page 394), although the two are often confused.
Remember that SaO2 can be normal despite a low PaO2 in acute pulmonary embolus,
reinforcing the need for ABGs in such a case.
PITFALLS AND SOURCES OF ERROR

• Cold peripheries and poor tissue perfusion can lead to an inability of the pulse
oximeter to get a reading
• Abnormal pulses such as atrial fibrillation and tricuspid regurgitation can affect
the reading because the signal is averaged over a number of heart beats
• Changes to Hb or pigments in the blood:
• CO poisoning in fire victims and smokers (this binds haemoglobin and
changes its light reflectance properties to that of oxyhaemoglobin; thus,
SaO2 is reported as erroneously high despite a low O2 saturation displaced by
the CO)
• bilirubin in high concentrations can have a similar effect but it causes the
pulse oximeter to underestimate the true SaO2
• methaemoglobinaemia (see below)
• Delay: SaO2 is calculated over a number of heart beats and so there is
approximately a 20-second lag between physiological values and SaO2
• Nail varnish: prevents penetration of light and must be removed preoperatively
• Electrical interference: diathermy
• High ambient light can interfere with the incident light from the pulse oximeter
• Movement/shivering can affect the signal
• Remember that pulse oximetry is not a measure of ventilation!
METHAEMOGLOBINAEMIA
Methaemoglobin (Met-Hb) has iron in a ferric state (Fe3') within the haem moi-
ety instead of the ferrous state (Fe2&) as in normal haemoglobin. The result of this
493
is that the Met-Hb molecule has a reduced oxygen-carrying capacity. This may be
a congenital problem with a deficiency of Met-Hb-reducing enzymes (NADH
methaemoglobin reductase) or an acquired problem as a result of nitrate pollution
in the water supply or use of the local anaesthetic agent prilocaine.
Treatment is by administration of a reducing agent such as methylene blue.
494
119 Respiratory failure and respiratory
function tests

What is the definition of respiratory failure?
How can it be classified?
Why is PCO2 normal or low in type I failure but high in type II failure?
What is the difference between type I and type II respiratory failure?
What are the principles of treatment of respiratory failure?
How is respiratory function measured?
Define the functional residual capacity (FRC). Name some factors that
increase and decrease it.
What parameters are affected in obstructive versus restrictive disease?
What is a flow–volume loop?
What do flow–volume loops look like in respiratory disease? Draw some
examples.
Related topics
Topic Chapter Page
Cerebrospinal fluid and the blood–brain barrier 90 369
CLINICAL SIGNS OF RESPIRATORY DISTRESS

A diagnosis of respiratory distress should be made on the following:
• Use of accessory muscles of respiration
• Tachypnoea
• Tachycardia
• Sweating
• Pulsus paradoxus
• Inability to speak full sentences
• Signs of CO2 retention.
495
CRITICAL CARE respiratory failure and respiratory function tests
Key learning point

Respiratory failure is when pulmonary gas exchange is sufficiently
impaired to cause hypoxaemia with or without hypercapnia.
That is, PaO2 " 8 kPa (60 mmHg) or PaCO2 ! 7 kPa (55 mmHg)
Normal ranges for an individual breathing air at sea level:
PaO2 &10.6–13.3 kPa, PaCO2 &4.7–6.0 kPa
Respiratory failure can be classified into two types.
Type I
A failure of oxygenation where PaO2 is low on ABG sampling but PaCO2 remains
normal or is slightly low. Examples:
.
• Pneumonia (V/Q mismatch) .
• Pulmonary embolism (V/Q mismatch)
• Cyanotic heart disease (right-to-left shunt)
.
• Pulmonary oedema (V/Q mismatch)
.
• Bronchiectasis and asthma (V/Q mismatch)
.
• ARDS (V/Q mismatch)
.
• Fibrosing alveolitis (V/Q mismatch).
Type II
A failure of ventilation where PaO2 is low and PaCO2 is abnormally high. Examples:
• COPD (chronic obstructive pulmonary disease)
• Chronic emphysema
• Chest wall deformities including flail chest trauma
• Respiratory muscle weakness (e.g. Guillain–Barré syndrome)
• Neuromuscular junction: myasthenia gravis
• Respiratory depression: opioids, barbiturates, head injury.
PATHOPHYSIOLOGY OF RESPIRATORY FAILURE

Type I
.
Pathology is the result of either a right-to-left shunt or a V/Q mismatch:
• Initial elevation of PaCO2 increases H+ in the CSF (see ‘Cerebrospinal fluid and
the blood–brain barrier’, Chapter 90, page 369) and stimulates the central
chemoreceptors to increase the respiratory rate
496
• Results in CO2 blown off maintaining PaCO2

• As the O2 dissociation curve is sigmoidal, increasing the ventilation does little to
the already low PaO2.
Type II
Pathology is the result of alveolar hypoventilation, leading to a progressive increase
in PCO2.
• No compensation of PaCO2 as a result of respiratory apparatus failure or a
resetting of the central chemoreceptors in the case of COPD, thereby tolerating
a higher PaCO2.
MANAGEMENT OF RESPIRATORY FAILURE

Remember A, B, C!
• Airway and breathing: ensure that the airway is patent and secure using ET
intubation if necessary
• Low threshold for assisted or mechanical ventilation
• Ensure adequate ventilation: progress from non-invasive ventilation such as
NIPPV (non-invasive positive-pressure ventilation) by mask to invasive
mechanical ventilation as required (see ‘Intubation and ventilation’, Chapter
114, page 470)
• Ensure adequate oxygenation: increase FiO2 and use humidified oxygen
• Antibiotics for underlying infective processes
• Management of other underlying causes (e.g. bronchodilators in asthma, chest
physiotherapy in bronchiectasis and cystic fibrosis)
• Regular airway management, e.g. suction of secretions and lavage if necessary
• FiO2 tailored to the results of regular ABG sampling
• Changing of mechanical ventilator parameters (such as PEEP, I:E ratio and
minute volume – see ‘Acute respiratory distress syndrome’, Chapter 105,
page 419 and ‘Intubation and ventilation’, Chapter 114, page 470).
INVESTIGATIONS FOR ASSESSING RESPIRATORY FUNCTION

Non-invasive
• Peak flow: bedside measure of respiratory muscle function and airway
resistance
• Pulse oximetry: estimates arterial oxygen saturation and is based on using two
wavelengths of light and the different reflective properties of oxyhaemoglobin
and deoxyhaemoglobin; depends on FiO2
497
• Capnography: end-tidal CO2 is measured as a marker of ventilatory function – a

facility available on all modern anaesthetic ventilators
• Spirometry: a measure of lung volumes and forced expiration (FEV1 – forced
expiratory volume in 1 s)
• Gas
. . transfer function: a measure of the diffusing capacity across the alveolus
• V/Q scanning and CT pulmonary angiography if pulmonary emboli are
suspected
• Echocardiography: assessment of PA pressure and right heart function in
pulmonary hypertension
• Other imaging modalities: plain radiology, CT and MRI.
Invasive
• ABGs: gold standard measurement of arterial oxygenation and PaCO2. Also
crucial for assessment of acid–base balance (see ‘Acid–base balance’, Chapter 84,
page 349)
• Bronchoscopy: for assessment of lesions and/or secretions; can be flexible or
rigid
• Lung biopsy: CT guided or open via thoracoscopic procedure or open
thoracotomy.
FUNCTIONAL RESIDUAL CAPACITY

This is the volume of gas remaining in the lungs after a quiet expiration (not forced.)
Factors increasing FRC
• Obstructive disease (e.g. asthma, bronchiectasis, COPD)
• Increasing PEEP – increases intrathoracic pressure.
Factors decreasing FRC

• Increasing age and body mass index (BMI)
• Limitation of lung inflation (e.g. pneumothorax, pleural effusion, empyema,
thoracic incision, interstitial lung disease, increased intra-abdominal pressure).
FLOW–VOLUME LOOPS IN OBSTRUCTIVE AND RESTRICTIVE

PULMONARY DISEASE
Plotting the relationship between airflow and lung volume over the respiratory
cycle gives an indication of the type of pulmonary disease. Obstructive diseases,
such as asthma, bronchiectasis and COPD, show an increase in the total lung cap-
acity and residual volume as a result of air trapping and hyperinflation.
498
Restrictive disease shows a reduction of all volumes because of an alteration in lung

parenchyma (e.g. idiopathic pulmonary fibrosis, fibrosing alveolitis), or a disease of
the pleura, chest wall (e.g. kyphoscoliosis) or neuromuscular apparatus as seen in
Fig. 119.1.
Restrictive
10.0 disease 10.0
7.5 7.5
Obstructive
E x p i r a ti o n
E x p i r a ti o n
5.0 5.0 disease
Total lung
capacity
Flow (L/s)
Flow (L/s)
2.5 2.5
0 0
Total lung
2.5 2.5 capacity
Residual
I n s p i r a ti o n
I n s p i r a ti o n
volume Residual
5.0 5.0 volume
7.5 7.5
10.0 10.0
7 6 5 4 3 2 1 7 6 5 4 3 2 1
Volume (L) Volume (L)

Normal flow loop
Figure 119.1
499
120 Sedation

What is a sedative? How do a sedative, an anxiolytic and an anaesthetic
differ?
What are the indications for sedatives in the acute setting?
What classes of sedatives are there and what is their action?
What sedatives are used in the ITU setting?
What sedative regimen would you use for minor procedures such as a
small fracture manipulation not requiring an anaesthetic?
What types of sedative reversal are there?
What are the complications of sedative use?
Should analgesia be withheld before initial examination of the acute
abdomen?
Related topics
Topic Chapter Page
Shock 122 510
INDICATIONS FOR SEDATION

Indications for sedation in surgery are many and varied although any invasive pro-
cedure can be made easier by some light sedation:
• Light sedation for minor procedures (e.g. manipulation of dislocations and
fractures, colonoscopy)
• Anxiolytic and light sedative can be used as a premedication before major
surgery
• Can be useful for a confused patient on the ward, although great care must be
taken to investigate the cause of the confusion (e.g. hypoxia, sepsis) and watch
for respiratory depression
• Sedation is mandatory (if patient is not in arrest) on ET intubation (see
‘Intubation and ventilation’, Chapter 114, page 470)
500
CRITICAL CARE sedation

What is a sedative? How do a sedative, an anxiolytic and an anaesthetic differ?
• Anxiolysis is relief of apprehension and uneasiness without alteration of
awareness
• Amnesia is loss of memory of an event or period and can be anterograde
or retrograde
• Sedation is depression of a patient’s awareness of the environment and
reduction of his or her responsiveness to external stimulation:
• conscious sedation is light sedation in which the patient maintains his or
her airway reflexes and ability to cooperate
• deep sedation is a more profound depression of the response to stimula-
tion in which airway reflexes are not maintained
• Analgesia is relief of pain without sedation or alteration of the state of
awareness (although analgesics may have a sedative effect)
• Anaesthesia is a state of unconsciousness
• After administration of neuromuscular blockers to paralyse the patient either

for intubation or in ventilatory modes that require paralysis, adequate sedation
is essential to prevent the patient from being aware of the paralysis. Further, in
ventilatory modes that do not accommodate the patient’s breathing effort (e.g.
intermittent positive-pressure ventilation or IPPV), if inadequately paralysed
and sedated, ventilation may be affected by ‘fighting against’ the ventilator
• An injured, stressed and uncooperative patient may benefit from sedation,
although care must be taken in the context of a head injury; sedation in this
context can help to decrease the acute physiological stress response (see
‘Systemic response to surgery’, Chapter 123, page 514)
• Sedation for MRI in children (must be done by paediatric anaesthetist).
CLASS OF SEDATIVE
Benzodiazepines (diazepam, lorazepam, midazolam)
The benzodiazepines act by stimulating GABA (,-aminobutyric acid) receptors in
the CNS. Stimulation of the receptor results in chloride influx, hyperpolarization
and decreased neuronal excitation. Actions include:
• Anxiolysis and sedation
• Amnesia (most profound with midazolam)
• Anticonvulsant
501
• No analgesic properties
• Respiratory and cardiovascular depression (much greater risk if administered
with centrally acting analgesic).
The major differences among the available agents concern the route of administra-
tion, time of onset, duration of action, mechanism of metabolism and accumulation
of metabolites. In non-intubated patients, they are titrated, starting at the lower end
of the range of recommended doses, followed by the administration of incremental
doses until the desired effect is achieved. These sedatives are also first-line agents for
acute seizure management.
Midazolam
• Most commonly used benzodiazepine for minor procedures
• Water soluble
• Short half-life
• Profound amnesic effect in many patients
• Rapid onset
• Metabolized by hepatic microsomal system, so suitable for use in renal failure
• In overdose can cause respiratory and cardiac depression
• All patients having midazolam sedation should have intravenous access and
pulse oximetry (see ‘Pulse oximetry, Chapter 118, page 491); ECG monitoring
and resuscitation facilities should be available (including flumazenil). Patients
should not drive or operate heavy machinery for 48 hours afterwards.
Lorazepam
• Water soluble
• Intermediate half-life
• Intermediate onset
• Suitable for infusion as little accumulation
• Cleared by hepatic conjugation.
Diazepam
• Not water soluble – usually prepared in glycerol
• Intermediate to long half-life
• Can be given intravenously, orally or rectally
• Good anticonvulsant acutely
• Hepatic metabolites are active and have long half-lives, so not suitable for
infusion.
Other sedatives: non-barbiturate and barbiturate

Non-barbiturates
Propofol
• Non-barbiturate sedative
502
• Substituted isopropyl phenol compound prepared in a 10 per cent lipid

emulsion (white emulsion)
• Anaesthetic induction agent: some short operations can be performed solely on
propofol without the use of a volatile agent
• Rapid onset and short half-life
• Clearance not affected by renal or hepatic dysfunction
• Respiratory and cardiovascular depressant
• Good agent for sedation in patients receiving mechanical ventilation
• Prolonged infusion in paediatrics is associated with lactic acidosis.
Etomidate
• Non-barbiturate imidazole
• Commonly used on rapid induction intubation alongside a muscle relaxant such
as suxamethonium
• Rapid onset of action and a short but dose-dependent duration of action
• Cardiovascular effects minimal
• Can be used as a short-term sedative for procedures
• Depresses adrenal cortex in the long term – not suitable for infusion.
Barbiturates
Barbiturates act on GABA-a receptors in the brain and are also respiratory and
cardiac depressants as with most sedative and induction agents. They are highly
addictive drugs.
Thiopental
• Commonly used induction agent
• Given in alkaline solution so irritant to the tissues if it extravasates
• Rapid onset and relatively short half-life
• If given in an infusion in the ITU (particularly in the treatment of intractably
raised ICP), it accumulates in the body’s fat stores so, when stopped, several
days must be given before any formal testing of brain or brain-stem function
• Negative inotrope.
Phenobarbital
• Older drug
• Used in the past as an induction agent
• Still used in some centres for intractable epilepsy and status epilepticus.
Opioids
Opioids are agents that induce systemic analgesia, some anxiolysis and mild sedation.
They do not induce amnesia of any significance. Examples: morphine, fentanyl.
• Main type of analgesic used in surgery
• Rapid onset and usually intermediate half-life
503
• Can cause respiratory depression in overdose

• Can be given intravenously, intramuscularly, intrathecally, transdermally or orally
in some cases
• Reversal using naloxone (see below)
• Given as titrated bolus in acute pain
• Commonly used in PCA
• Long-acting opioids (fentanyl patches or MST Continus) given in palliative care
or chronic pain.
Key learning point

Sedative reversal
There are two major sedative reversal drugs available for clinical use and they
are naloxone for opioid reversal and flumazenil for benzodiazepine reversal.
For this reason, many ITUs now use morphine and midazolam for sedation.
Naloxone
Naloxone is a competitive antagonist of the opioid class of drugs. The onset
of action after intravenous administration is rapid, with effects appearing
within 2–3 min. The duration of action is dose related. This antagonist may
have shorter duration of action compared with that of the longer-acting
opioids, and observation may be required with repeated dosing or an infusion
in some cases.
Flumazenil
Flumazenil is a competitive antagonist of the benzodiazepine class of
drugs. The onset of action is within 2 min of intravenous administration,
with peak effects within 10 min. The duration of action is dose related, but
it is typically shorter than that of longer-acting benzodiazepines. Repeat
dosing may be required.
Exercise caution in patients receiving long-term benzodiazepine therapy,
because seizures can occur.

Should analgesia be withheld before initial examination of the acute
abdomen?
Under no circumstances! There is no evidence to suggest that this is help-
ful and an uncooperative patient in pain is unlikely to allow a thorough
examination. There is evidence to suggest that more information may be
found from palpation after adequate analgesia than before it.
504
121 Sepsis and SIRS

What is the systemic inflammatory response syndrome?
How does it differ from sepsis?
What is the pathological process involved in SIRS?
What are its triggers?
Name some of the cytokines implicated in the development of SIRS.
What is MODS?
What are the possible treatments for MODS, SIRS and sepsis?
What is activated protein C? Who should receive it?
Why is fluid resuscitation alone usually ineffective in cases of severe sepsis?
Related topics
Topic Chapter Page
Shock 122 510
Nutrition 115 477
Inotropes 113 466

What is the systemic inflammatory response syndrome?
The systemic inflammatory response syndrome (SIRS) is defined by a
number of clinical criteria and is the body’s reaction to a critical illness
such as overwhelming infection or trauma (including surgery):
• Temperature ! 38°C or " 36°C

• Respiratory rate ! 20/min or PaCO2 " 4.3 kPa (32 mmHg)
• WCC ! 12 000 or " 4000/mL (or ! 10 per cent immature forms)
The concept of SIRS was introduced after it was noted that less than
50 per cent of patients showing signs of sepsis had positive blood cultures.
505
CRITICAL CARE sepsis and SIRS
Sepsis is defined as the body’s response to proven infection which includes two of
the clinical criteria for SIRS.
Severe sepsis is defined as sepsis with evidence of organ dysfunction.
Septic shock is defined as sepsis + hypotension with systolic # 90 mmHg or drop
in BP of ! 40 mmHg that is refractory to fluid replacement.
SEPSIS SYNDROME
This is a term that was coined in the original paper introducing the concept of SIRS.
It is defined as SIRS criteria plus clinical evidence of an infection site and with at
least one end-organ demonstrating inadequate perfusion or dysfunction, expressed
as poor or altered cerebral function, hypoxaemia, elevated plasma lactate or oliguria
(urine output # 30 mL/h or 0.5 mL/kg per h without corrective therapy).
SIRS
Split into three phases:
1. A localized injury in the body results in the activation of the local acute
inflammatory response. There is chemotaxis of neutrophils and macrophages
which themselves release inflammatory mediators (e.g. cytokines and proteases).
2. Systemic distribution of inflammatory mediators. Anti-inflammatory mediators
such as IL-10 are downregulated.
3. Massive cytokine release systemically causes endothelial dysfunction and
disruption of tight junctions, leading to leaky capillaries and subsequent
systemic sequelae: pyrexia, tachycardia, increased vascular permeability and
peripheral vasodilatation. A catabolic state ensues with reduced delivery of
oxygen to the tissues despite increased demand.
Triggers for SIRS
• Severe burns
• Multiple trauma (including surgery)
• Sepsis
• Acute pancreatitis
• Cardiopulmonary bypass.
Cytokines implicated in SIRS response

• IL-6 (involved in acute phase response)
• IL-10 (anti-inflammatory downregulated in SIRS)
• IL-8 (neutrophil chemotaxis)
• IL-1 (pyrogen that activates macrophages and T cells)
506
• TNF% (pyrogen that increases capillary permeability via the induction of nitric
oxide synthase & stimulates leukocytes)
• Platelet-activating factor or PAF (increases capillary permeability and activates
macrophages and T cells).

Why is fluid resuscitation alone usually ineffective in cases of severe sepsis?
Remember that the effects of sepsis are threefold:
• Vasodilatation
• Capillary leak after endothelial damage
• Myocardial depression (caused by an unknown toxin or cytokine)
These three factors dictate that fluid resuscitation alone will not solve the
problem. Vasoconstrictors and inotropic support are usually required (see
‘Inotropes’, Chapter 113, page 466).
MULTIPLE ORGAN DYSFUNCTION SYNDROME
Key learning point

This is defined as the presence of an acute, potentially reversible dysfunction
of two or more organ systems such that homoeostasis cannot be maintained
without intervention.
Multiple organ dysfunction syndrome (MODS) can be divided into:

1. Primary MODS: directly attributable to the initial insult
2. Secondary MODS (more common): failure is secondary to the effects of SIRS.
It is possible that there may be a latent period between the event triggering
SIRS and the onset of MODS.
Organ systems that can be involved in MODS

Any organ system can be involved.
Cardiovascular system
Initially a hyperdynamic state with decreased SVR as a result of massive systemic
vasodilatation and increase in capillary permeability. After this, myocardial depres-
sion may occur.
507
Respiratory system
ARDS is one of the potential components of MODS (see ‘Acute respiratory distress
syndrome’, Chapter 105, page 419).
Acute renal failure

This can occur as the result of acute tubular necrosis (see ‘Oliguria and renal
replacement’, Chapter 116, page 482) and is therefore potentially reversible.
Gut
Decreased absorption is associated with downregulation of secretory IgA. Bacteria
translocate across the deficient gut wall, perpetuating sepsis.
Liver
Deranged liver function and hepatocellular jaundice.
Blood
A coagulopathy can eventually lead to DIC.
Other systems include bone marrow failure giving a pancytopenia and neurological
disturbances including metabolic encephalopathy.
The mortality associated with MODS is directly related to the number of organs
affected. Failure of one organ (most commonly renal failure or respiratory failure)
has a mortality of about 10 per cent whereas renal failure and one other is around
70 per cent, with three or more organs at 95 per cent.
PRINCIPLES OF TREATMENT FOR MODS, SIRS AND SEPSIS

Always remember A, B, C!
• Removal of any precipitating cause and treatment of any underlying infection.
Antibiotic treatment is initially broad spectrum and empirical. This will be
changed depending on culture results and microbiological advice.
• Airway and breathing: ventilatory support for ARDS and respiratory failure.
• Circulation: intravenous fluids, invasive monitoring (arterial line, CVP ' PAFC)
and inotropic support to maintain cardiac index, noradrenaline to increase SVR,
MAP and organ perfusion, thereby maximizing oxygen delivery to the tissues.
• Renal support: maintain urine output and renal perfusion. Dopamine and
frusemide have been used to maintain renal perfusion but there is no evidence
that either of these improves outcome. Renal replacement is the mainstay of
renal support (haemofiltration, haemodialysis, haemodiafiltration).
• Nutritional support: in the presence of gut failure, parenteral feeding may be
necessary (see ‘Nutrition’, Chapter 115, page 477) to account for the body’s
massive calorific demands in MODS and SIRS.
508

What is activated protein C? Who should receive it?
Activated protein C modulates both inflammation and coagulation in
severe sepsis, and reduces mortality.
Activated protein C is an endogenous protein that promotes fibrinolysis
and inhibits thrombosis and inflammation. It is an important modulator of
the coagulation and inflammation associated with severe sepsis.
It is converted from its inactive precursor, protein C, by thrombin coupled to
thrombomodulin. The conversion of protein C to activated protein C may be
impaired during sepsis as a result of the downregulation of thrombomodulin
by inflammatory cytokines. (Reduced levels of protein C are found in most
patients with sepsis and are associated with an increased mortality.)
A large randomized controlled trial has confirmed the efficacy of activated
protein C. In patients with severe sepsis, an intravenous infusion for 96
hours is associated with a significant reduction in mortality. The use of this
drug is indicated if the patient has a systemic inflammatory response, at
least one organ dysfunction and known or suspected infection.
When using an infusion of activated protein C, it is important to monitor for
signs of bleeding, an important side effect of therapy with this compound.
The value of this agent in patients with multiorgan failure, or outside the
first 24 hours of injury, is unknown.
509
122 Shock

What is your definition of shock?
Tell me about the different types of shock.
What are the causes of the different types of shock?
How should the various types of shock be treated?
What are the mechanisms of the different types of shock?
Do you know any grading of hypovolaemic shock?
What is sepsis syndrome?
Related topics
Topic Chapter Page
Inotropes 113 466
DEFINITION
‘A sudden and generalised lack of perfusion and usually oxygenation of all of the
peripheral tissues and end organs, usually caused by cardiovascular collapse.’
CLINICAL FEATURES OF SHOCK

• Hypotension (systolic " 90 mmHg or drop of ! 40 mmHg)
• Decreased capillary refill
• Tachycardia
• Oliguria (see ‘Oliguria and renal replacement’, Chapter 116, page 482)
• Confusion and decreased level of consciousness
• Pyrexia and warm peripheries in septic shock (see ‘Sepsis and SIRS’, Chapter
121, page 505).
510
CRITICAL CARE shock
TYPES OF SHOCK
• Cardiogenic
• Hypovolaemic
• Anaphylactic
• Septic
• Spinal (evidence of spinal injury and no other reason for hypotension).
Cardiogenic shock
‘Pump failure causing circulatory collapse’
Causes
• Acute myocardial infarction (MI)
• Arrhythmias, e.g. ventricular fibrillation (VT), fast AF
• Tension pneumothorax
• Massive pulmonary embolus (PE)
• Cardiac tamponade.
Treatment
This should be aimed at resolution of the cause of the pump failure and is beyond the
scope of this topic. However, in broad terms, MIs should be thrombolysed or stented,
arrhythmias should be cardioverted, tension pneumothoraces should be decom-
pressed, massive PEs may be thrombolysed or undergo embolectomy, and cardiac tam-
ponade may be resolved by pericardiocentesis or may require cardiothoracic surgery
(e.g. pericardial window/repair of myocardial rupture).
Hypovolaemic shock
Haemorrhage
• Ruptured abdominal aortic aneurysm (AAA)
• Ruptured ectopic pregnancy
• Trauma (pelvic, long bones, splenic rupture, PA/aortic disruption, liver laceration)
• Upper/lower gastrointestinal (GI) bleeding (e.g. varices, duodenal ulcer eroded
into gastroduodenal artery, brisk bleeding from colonic neoplasm).
Loss of fluid
• Pancreatitis
• Intestinal obstruction
• High-output stoma (e.g. ileostomy)
• Iatrogenic, e.g. post-renal dialysis/haemofiltration.
Treatment
In this case treatment is largely aimed at stopping the plasma loss and replacing
appropriately with blood, crystalloids, colloids and clotting products if necessary.
511
CRITICAL CARE shock
Anaphylactic shock
Common allergies
• Drugs especially antibiotics (e.g. penicillin and radiological contrast agents)
• Foods (e.g. peanuts/shellfish)
• Medical equipment materials especially latex
• Insect bites/stings.
Treatment
Supportive treatment and cardiac support with adrenaline (epinephrine). Patients
who have an anaphylactic reaction to everyday substances such as foods should be
offered an EpiPen to carry around with them.

How do SIRS, sepsis and septic shock differ? What is sepsis syndrome?
See ‘Sepsis and SIRS’, Chapter 121, page 505
SIRS
Any two or more of the following:
Temperature ! 38°C or " 36°C
• Respiratory rate ! 20/min
• WCC ! 12 000 or " 4000/mL
Septic shock
Sepsis & hypotension with systolic BP # 90 mmHg or drop in BP of
! 40 mmHg that is refractory to fluid replacement. This relationship
should be clear in your mind when going into the exam.
Sepsis syndrome
This is a term that was coined in the original paper introducing the concept
of SIRS. It is defined as SIRS criteria plus clinical evidence of an infection
site, with at least one end-organ demonstrating inadequate perfusion or
dysfunction, expressed as poor or altered cerebral function, hypoxaemia
(PaO2 # 10 kPa), elevated plasma lactate or oliguria (urine output #
30 mL/h or 0.5 mL/kg per h without corrective therapy).
512
CRITICAL CARE shock
Septic shock
‘Hypotension complicating severe sepsis despite adequate fluid resuscitation.’
Commonly termed ‘warm shock’ as a result of the peripheral vasodilatation caused
by mast-cell degranulation from circulating endotoxin.
Treatment
This is with fluids until adequately filled, then vasoconstrictors such as noradren-
aline (norepinephrine) (see ‘Inotropes’, Chapter 113, page 466) should be used.
This will need to be given through central venous access (see ‘CVP lines and inva-
sive monitoring, Chapter 110, page 443) in an HDU/ITU setting (see ‘Criteria for
admission to the ITU/HDU, Chapter 109, page 439).
Classification of hypovolaemic shock
Class 1 Class 2 Class 3 Class 4

Volume loss (mL) 0–750 750–1500 1500–2000 >2000
Loss (%) 15 30 40 !40
Pulse (beats/min) #100 !100 !120 !140
BP Normal Normal Decreased Decreased
Pulse pressure Normal Decreased Decreased Decreased
Urine output (mL/h) !30 20–30 5–15 Anuric
Respiratory rate 14–20 20–30 30–40 !40

How much of the total plasma volume can be lost before the BP drops?
Up to 20 per cent of the entire plasma volume can be lost before seeing
significant physiological changes. Thus, a young and fit patient with a mild
tachycardia could already be in class 2 shock and already have lost over 1 L
of blood!
This relationship is even more important in the paediatric population
where children can lose even more before suddenly decompensating: thus
a tachycardia in a child in the context of a blunt abdominal injury must be
treated very seriously.
513
123 Systemic response to surgery

How does the body react to surgery?
What is the metabolic response to surgery?
How are lipids mobilized after trauma?
How is carbohydrate metabolism affected by trauma?
How is protein metabolism affected by trauma?
Why is urine output often low in the first 24 hours after surgery?
What happens to the metabolic rate after trauma or surgery?
How does the metabolic response to surgery affect the strategy for post
operative nutrition?
What do you understand by the ebb and flow phase after trauma to the
body?
What physiological systems are involved in the coordination of the stress
response?
What do glucocorticoids do?
Why might a metabolic alkalosis develop immediately after surgery?
How might the systemic response to surgery be minimized?
Related topics
Topic Chapter Page
Nutrition 115 477
equations
514
CRITICAL CARE systemic response to surgery

How does the body react to surgery?
Surgery is little more than highly controlled trauma. Thus, systems that are
activated after acute trauma are also activated after surgery:
• Sympathetic nervous system activation as a result of pain and hypovolaemia
leads to an increase in cardiovascular output via an increase in circulating
adrenaline (tachycardia) and noradrenaline (peripheral vasoconstriction).
Also aids activation of glycolysis in the liver and the renin–angiotensin–
aldosterone axis (see ‘Starling’s law of the heart and cardiovascular
equations’, Chapter 102, page 403, and ‘Functions of the kidney III’,
• Endocrine response: ACTH production is stimulated which, in turn, stimu-
lates glucocorticoid release – predominantly cortisol (see below)
• Acute phase response:
• cytokines released by circulating monocytes and lymphocytes
• kinins, interleukins, TNF and interferons likewise released; causes post-
operative fever and further increases metabolic demand
• ACTH release further enhanced
• clotting cascade activated
• serum levels of acute phase proteins increase (e.g. C-reactive protein or
CRP, fibrinogen, complement C3, ceruloplasmin and haptoglobin)
• liver downregulates albumin and transferrin production
• Vascular endothelium: highly complex system able to affect local vasomotor
tone (via nitric oxide or NO) and local coagulation; can affect systemic
response by modulation of platelet and leukocyte binding
Note that the six stress hormones in the response to surgery can be
remembered by ‘T, A, C, G. These are the bases in DNA!’:
T: trauma
A: ADH, aldosterone
C: cortisol, catecholamines
G: growth hormone, glucagon
METABOLISM AFTER SURGERY

Classically divided into ‘ebb and flow’ phases according to the metabolic rate:
• ‘Ebb’: reduced energy expenditure after injury for the first 24 hours and
therefore a reduction in the metabolic rate
515
• ‘Flow’: the metabolic rate increases dramatically and the catabolic ‘flow’ phase
can last many days with associated negative nitrogen balance and impaired
glucose tolerance.
Immediately after surgery, patients are nil by mouth and therefore starvation and the
response to trauma are both responsible for this catabolic state. There is increased heat
production in this phase, along with increased oxygen consumption and weight loss.
The overall duration and increase in metabolic rate in the ‘flow’ phase depend on the
type of stimulus:
• 10 per cent increase in elective surgical operations

• 50 per cent increase in polytrauma
• 200 per cent in major burns.
Once the ‘flow’ phase has begun, correction of the underlying stimulus (e.g. control-
ling infection, correcting hypovolaemia, controlling pain) will not rapidly reverse the
metabolic condition of the patient.
Finally, if recovery occurs, an anabolic phase occurs where the body replaces its fat
and glycogen reserves and synthesizes more protein.
Clearly this has a major implications for postoperative nutrition (see ‘Nutrition’,
Chapter 115, page 477), where calculated daily required nutrition must take into
account the extent and severity of the ‘flow’ metabolic phase of the patent.
Lipid metabolism
• Lipids are the principal source of energy after trauma
• Lipolysis stimulated by sympathetic nervous system, ACTH, cortisol, decreased
serum insulin levels and glucagons
• Ketones released and oxidized by all tissues except blood and brain
• Free fatty acids and glycerol undergo gluconeogenesis in the liver to provide
energy for all tissues.
Carbohydrate metabolism
• Insulin levels decrease and glucagon levels increase, mobilizing glycogen stores
and initiating glycolysis to create a transient hyperglycaemia. Increased
glucocorticoid levels also result in insulin resistance of the tissues, thereby
potentiating the effect.
• Glycolysis releases energy for obligate tissue (CNS, leukocytes and red blood
cells – cells that do not require insulin for glucose transport). This is a very
important mechanism because in a serious injury or after major surgery,
leukocytes can account for 70 per cent of all glucose uptake.
516
• Body glycogen stores can last for about 24 hours, after which blood glucose
must be maintained by other methods:
• gluconeogenesis of lipid breakdown products
• gluconeogenesis of amino acids mobilized from protein breakdown.
Protein metabolism
• Suppressed insulin levels encourage the release of amino acids from skeletal
muscle.
• A three- to fourfold increase in serum amino acids is usually required after
major trauma. The requirement reaches a peak at a week after injury,
although it may continue for many days after this. In the absence of a constant
exogenous supply of protein, the entire nitrogen requirement is gained from
the skeletal muscle. The extent of the nitrogen requirement is directly
proportional to the extent of injury (including trauma and sepsis) and the
muscle bulk.
• Major protein loss results in endothelial dysfunction and atrophy of the
intestinal mucosa, removing the barrier to translocation of pathogenic bacteria.
Thus, a loss of over 40 per cent body protein is usually fatal.
EFFECT ON RESPIRATION
• Pain causes splinting and hypoxia, leading to inadequate ventilation, basal
atelectasis and basal lung collapse
• Basal collapse increases risk of infection
• Hypoxia drives catabolic state and anaerobic respiration leading to a metabolic
acidosis (see ‘Acid–base balance’, Chapter 84, page 349).
MINIMIZATION OF THE SYSTEMIC RESPONSE TO SURGERY

Preoperative factors
• Minimize fear and stress (informed consent and clear, concise explanation,
premed anxiolytic if necessary) to reduce sympathetic activity
• Good, high protein load preoperative nutrition; enteral feeding if possible
before period of nil by mouth required for gastric emptying
• Correction and control of preoperative infection.
Operative factors
• Good tissue handling
• Minimally invasive surgery/minimal trauma
• Shorten duration of anaesthesia.
517

Why is urine output often low in the first 24 hours after surgery? Why might
a metabolic alkalosis develop immediately after trauma?
After trauma, the activation of the renin–angiotensin–aldosterone axis and
the increase in ADH secretion leads to a retention of sodium and water at
the expense of potassium (see ‘Functions of the kidney III’, Chapter 94,
page 381 and ‘Fluid balance’, Chapter 111, page 452).
Although the total body sodium may be elevated, a dilutional hyponatraemia
is not uncommon with an excess of serum ADH, leading to greater water
than sodium retention.
Furthermore, in catabolic cells with a degree of energy failure, sodium
pumps are impaired, so sodium tends to drift into cells and thereby further
decrease the plasma sodium concentration. This sodium and water reten-
tion leads to a low urine output (despite adequate filling) in the first
24 hours after surgery. Although the water retention lasts for only 24 hours,
the sodium retention may persist for much longer.
In many cases, postoperatively the patient may have an ileus, promoting
fluid extravasation into the gut lumen and intravascular depletion, leading
to dehydration and further compounding the low urine output state.
The most common acid–base imbalance is a metabolic alkalosis because
aldosterone promotes sodium retention at the expense of potassium. As
potassium is excreted, so are H+ ions in a co-transporter mechanism, leading
to an alkalosis.
In more severe trauma, a metabolic acidosis can result as a lactic acidosis
caused by poor tissue perfusion and anaerobic metabolism.
Postoperative factors
• Correction of hypovolaemia:
• prompt replacement of fluids and electrolytes (see ‘Fluid balance’, Chapter 111,
page 452)
• transfusion for haemorrhage if necessary
• colloids for plasma loss
• Correction of metabolic alkalosis/acidosis
• Control of postoperative infection:
• antibiotics (see ‘Antibiotics in surgery’, Chapter 67, page 275)
518
• enteral feeding as soon as possible to maintain gut mucosal barrier (see

‘Nutrition’, Chapter 115, page 477 and ‘Sepsis and SIRS’, Chapter 121,
page 505)
• débride wounds, drain pus, etc.
• Adequate and effective pain control (reduces sympathetic activation and
splinting/hypoxia and their effects)
• PCA if appropriate
• local and regional blocks – ideally given before surgical insult occurs
• epidurals/spinals
• Correction of hypoxia
• Increased arginine and glutamine intake can be helpful to improve nitrogen
balance, encourage weight gain, wound healing and immune function
• Trace elements such as zinc to improve wound healing and immune function.
519

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CRACKING THE

Iain Au-Yong MA (Cantab) BMBCh(Oxon) MRCS(Ed)

Simon Howarth MA (Cantab) BMBCh MRCS(Eng) MRCS(Glas)

Tjun Tang MA (Cantab) MB BChir MRCS(Glas)

Robert Sayers MD FRCS

No claim to original U.S. Government works

International Standard Book Number-13: 978-1-4441-1358-7 (eBook - PDF)

PART 2: APPLIED SURGICAL ANATOMY

PART 3: OPERATIVE SURGERY

PART 4: APPLIED SURGICAL PATHOLOGY

PART 5: PRINCIPLES OF SURGERY

66 Anastomosis and anastomotic leak 270

PART 6: APPLIED SURGICAL PHYSIOLOGY

PART 7: CRITICAL CARE

Thanks to Mr James R Seaward, MA(Cantab), MRCS(Eng), Registrar, Plastic Surgery,

CDK cyclin-dependent kinase

FEV1 forced expiratory volume in 1 s

LDL low-density lipoprotein

PCWB pulmonary capillary wedge pressure

TNF tumour necrosis factor

When working out causes to a condition use the surgical sieve.

Candidates are encouraged to start off by giving a definition if appropriate.

Example: What is Crohn’s disease?

Example 1: ‘What can you tell me about the complications of gallstones?’

• Within the biliary tree:

Example 2: see ‘Functions of the liver’, Chapter 96, page 384

• Starling’s law of flux: oedema

Pathology and principles of surgery

Anatomy and operative surgery

APPLIED SURGICAL ANATOMY

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LANDMARKS AND RELATIONS

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Topic Chapter Page

Possible viva questions related to this topic

Topic Chapter Page

DUCTS WITHIN THE SYSTEM

RELATIONS OF THE COMMON BILE DUCT

Common bile duct

Example viva question

The common bile duct is divided into three parts:

Example viva question

HISTOLOGICAL LAYOUT OF BILIARY SYSTEM

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Topic Chapter Page

RIGHT CORONARY ARTERY

LEFT CORONARY ARTERY

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Topic Chapter Page

Key learning points

Level Main structure passing through Other structures

Key learning points

The subcostal nerve is transmitted under the lateral arcuate ligament.

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Topic Chapter Page

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Topic Chapter Page

BLOOD SUPPLY AND LYMPHATIC DRAINAGE