MRCS
Applied Basic Science
and Clinical Topics
http://vip.persianss.ir/
http://vip.persianss.ir/
MRCS
Applied Basic Science
and Clinical Topics
ianss.ir/Stephen Parker BSc DipMedEd MS FRCS (Gen)
Consultant General Surgeon
rsUniversity Hospitals of Coventry and
eWarwickshire NHS Trust
http://vip.pCoventry, UK
London • St Louis • Panama City • New Delhi
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Preface
MRCS Applied Basic Science and Clinical Topics has been written as a resource for candidates who are
preparing for postgraduate surgical examinations, in particular Parts A and B of the Intercollegiate
MRCS Examination. It has its foundation in my experience as a general surgical consultant with a
strong interest in medical education. The content has evolved over time, shaped by feedback from
previous candidates who have identified what they would have wanted when preparing for their
examinations.
The book aims to fill the gap between large surgical textbooks and smaller revision aids. This
has necessitated a selective approach to the topics included and the depth in which they are
.ir/discussed: the basic science topics have been chosen for their direct bearing on clinical practice
and the clinical topics are those commonly encountered both in the wards and in postgraduate
surgical examinations.
sEach chapter presents the basic science and clinical topics in a consistent format, in accordance
swith the MRCS syllabus. The clinical chapters aim to cover the whole breadth of surgical special-
ties at a level appropriate for the MRCS examination. Variations in surgical practice will inevitably
nmean that there will be disagreement with some of the views and recommendations that are
iapresented. In potentially contentious areas I have attempted to include opinions that are not too
extreme, are supported by current research evidence and will hopefully satisfy most examiners.
rsWithin the space available, the book cannot hope to be exhaustive. Nevertheless, I hope that it
will be a useful tool when working in and studying a particular surgical speciality, as well as serving
eas a revision tool and aide-mémoire immediately prior to the examinations.
.pStephen Parker BSc MS DipMedEd FRCS(Gen)
http://vip October2012
v
http://vip.persianss.ir/
Contents
Preface v
The MRCS examination xi
Glossary xii
Chapter 1 Professional skills in clinical practice 1
Duties of a doctor 1
Communication skills 1
2
.ir/Clinical governance 5
5
Ethics and the law
Medical litigation 7
rsianssChapter 2 7
Perioperative care 13
Preoperative assessment 15
Preparation for surgery 20
Principles of anaesthesia 22
Care of the patient under anaesthesia
Haematological problems in surgery 33
://vip.peChapter 3 33
Postoperative management and critical care 34
Autonomic nervous system 39
Pain 43
Metabolic and nutritional support 46
Postoperative complications
Principles of intensive care 55
ttpChapter 4 Surgical technique and technology 55
Surgical wounds 57
h Surgical technique
Surgical procedures 61
Chapter 5 Evidence-based surgical practice 67
Evidence-based medicine 67
Chapter 6 Surgical pathology and microbiology 73
Surgical pathology 73
Surgical microbiology 74
vii
Prevention of infection 83
Surgery in hepatitis and HIV carriers 84
Chapter 7 Emergency medicine and the management 87
of trauma
Pathophysiology of trauma 87
Initial assessment of the trauma patient 88
Traumatic wounds 92
Compartment syndromes 94
The eye – trauma and common infections 96
ianss.ir/Chapter 8
Principles of surgical oncology 99
Cell proliferation 99
Epidemiology of common cancer 100
NHS cancer screening programmes 101
Clinicopathological staging of cancer 102
Principles of cancer treatment 103
.persChapter 9
Cardiothoracic surgery 109
Applied basic sciences 109
Cardiac disease 116
Thoracic disease 123
ipChapter 10 General surgery
://vAbdominal trauma 133
133
Abdominal emergencies 135
Chapter 11 The abdominal wall
147
ttpApplied basic sciences 147
h Abdominal hernias 149
Intestinal fistulas 153
Chapter 12 Upper gastrointestinal surgery 155
Applied basic sciences 155
Oesophageal disease 159
Gastric disease 163
Chapter 13 Hepatobiliary and pancreatic surgery 169
Applied basic sciences 169
172
viii Hepatobiliary and pancreatic disease
Chapter 14 Colorectal surgery 189
Applied basic sciences 189
Colorectal disease 191
Perianal disease 201
Chapter 15 Breast disease 207
Applied basic sciences 207
Breast disease 207
Chapter 16 Endocrine surgery 221
221
.ir/Applied basic sciences 224
233
Thyroid and parathyroid disease 239
239
sPituitary and adrenal disease 243
sChapter 17 Vascular disease 254
260
nApplied basic sciences 264
iaArterial disease
rsVenous disease 269
269
Lymphatics and spleen 270
276
eRenal failure and transplantation 281
.pChapter 18 Otorhinolaryngology and head and 281
281
neck surgery
ipApplied basic sciences
://vEar, nose and throat disease
Salivary gland disease
ttpChapter 19 Paediatric surgery
Applied basic sciences
h Paediatric trauma
Correctable congenital abnormalities 282
Common paediatric surgical disorders 293
Orthopaedic disorders of infancy and childhood 300
Chapter 20 Plastic and reconstructive surgery 307
Applied basic sciences 307
Plastic surgery trauma 309
Pigmented skin lesions 315
ix
Chapter 21 Neurosurgery 323
Applied basic sciences 323
Neurosurgical trauma 325
Neurosurgical disorders 331
Chapter 22 Trauma and orthopaedic surgery 335
Applied basic sciences 335
Skeletal fractures 344
Degenerative and rheumatoid arthritis 351
354
.ir/Infections of bones and joints 357
359
Disorders of the upper limb 362
Disorders of the hand 363
364
sKnee injuries 364
365
Disorders of the foot 368
373
sOsteoporosis 373
nMetabolic bone disease 377
iaLocomotor pain 379
382
Bone tumours and amputations 385
388
rsChapter 23 Urology 392
eApplied basic sciences
.pUrological trauma 397
Urinary tract infections and calculi
ipHaematuria
://vUrinary tract obstruction
Pain and swelling in the scrotum
Aspects of pelvic surgery
httpIndex
x
The MRCS Examination
The Membership of the Royal College of Surgeons (MRCS) examination is a summative assessment
of candidates in the generality of surgery, whether in core surgical training or outside a training
programme. Its purpose is to determine that a trainee has acquired the knowledge, skills and
attributes required for the completion of core training and for those trainees following the
intercollegiate surgical curriculum programme, to determine their ability to progress to higher
specialist training. Passing the MRCS is mandatory to progress from ST2/CT2 to ST3/CT3.
Format of Part A
There is one 4-hour examination consisting of two 2-hour multiple choice question (MCQ) papers
that are sat consecutively. Paper 1 tests applied basic sciences and has single best answer (SBA)
questions. Paper 2 tests principles of surgery-in-general and has extended matching questions
(EMQs). Candidates score one mark for each correct answer. To pass Part A the overall pass mark
has to be met. The pass mark is set using a modified Angoff method. A score of at least 50% on
each paper has to be achieved. Candidates can have an unlimited number of attempts at this part.
Format of Part B
Part B is now in an objective structured clinical examination (OSCE) format. There are 16 stations
and four rest stations, each of 9 minutes. Candidates start at different points in the circuit. The
stations assess knowledge and skills in five main subject areas:
• Anatomy and surgical pathology
• Surgical skills and patient safety
• Communication skills
• Applied surgical science and critical care
• Clinical skills
Twelve stations test generic knowledge and are compulsory for all candidates. To allow for
differences in training, there are four speciality stations. Candidates select their speciality context
at the time of application. In each of the five subject areas, six domains are tested:
• Clinical knowledge
• Clinical skill
• Technical skill
• Communication
• Decision making and problem solving
• Organisation and planning
Most of the stations have surgeon examiners and all examiners must have completed a training
course. The marking scheme is a matrix in which the stations are marked using several domains.
There is a structured mark sheet for each station. The mark sheet includes a holistic judgement of
the candidate. Candidates must reach the overall pass mark set for Part B. They must also achieve
a minimum score in each of the domains. A variant of the contrasting groups method is used for
setting the overall mark.
xi
Glossary
AAA Abdominal aortic aneurysm CNS Central nervous system
ABPI Ankle brachial pressure index CO Cardiac output
ACE Angiotensin converting enzyme CPAP Constant positive airway pressure
ACTH Adrenocorticotrophic hormone CPP Cerebral perfusion pressure
ADH Antidiuretic hormone CRF Chronic renal failure
AF Atrial fibrillation CRP C reactive protein
AIDS Acquired immunodeficiency CSF Cerebrospinal fluid
CSOM Chronic secretary otitis media
syndrome CVA Cerebrovascular accident
ALI Acute limb ischaemia CVP Central venous pressure
ALI Acute lung injury
ALP Alkaline phosphatase DCIS Ductal carcinoma in situ
ANDI Aberrations of normal DIC Disseminated intravascular
development and involution coagulation
ANS Autonomic nervous system DIND Delayed ischaemic neurological
APACHE Acute Physiology and Chronic
deficit
Health Evaluation DIPJ Distal interphalangeal joint
APUD Amine precursor uptake DMSA Dimercaptosuccinic acid
DVT Deep vein thrombosis
decarboxylase
ARDS Acute respirator distress syndrome ECG Electrocardiogram
ARF Acute renal failure EGF Epidermal growth factor
ASA American Society of EMQ Extended matching question
EPSP Excitatory post synaptic potential
Anesthesiologists ERCP Endoscopic retrograde
ASD Atrial septal defect
ASI Acute serum conversion illness cholangiopancreatography
AST Aspartate transaminase ERV Expiratory reserve volume
ELISA Enzyme-linked immunosorbent
BE Base excess
BIPP Bismuth iodoform paraffin paste assay
BMI Body mass index ESR Erythrocyte sedimentation rate
BP Blood pressure ESWL Extracorporeal shockwave
BSA Body surface area
lithotripsy
CABG Coronary artery bypass graft EWS Early warning scoring system
CAPD Continuous ambulatory peritoneal
FAP Familial adenomatous polyposis
dialysis FAST Focused assessment with
CBD Common bile duct
CEA Carcino-embryonic antigen sonography for trauma
CHD Congenital heart disease FBC Full blood count
CI Cardiac index FEV Forced expiratory volume
CLI Chronic limb ischaemia FISH Fluorescence in situ hybridisation
xii
FNAC Fine need aspiration cytology MAC Minimal alveolar concentration
FOB Faecal occult blood MCH Mean corpuscular haemoglobin
FRC Functional residual capacity MCHC Mean corpuscular haemoglobin
FVC Forced vital capacity
concentration
GCS Glasgow coma score MCPJ Metacarpophalangeal joint
GIST Gastrointestinal stromal tumour MCQ Multiple choice question
GFR Glomerular filtration rate MCV Mean corpuscular volume
GMC General Medical Council MEN Multiple endocrine neoplasia
GORD Gastroesophageal reflux MI Myocardial infarction
GnRH Gonadotrophin-releasing hormone MIBG Metaiodobenzylguanidine
MODS Multiple organ dysfunction
HCC Hepatocellular carcinoma
HCV Hepatitis C virus syndrome
HDU High dependency unit MRA Magnetic resonance angiography
HIAA Hydroxyindolacetic acid MRCS Membership of the Royal College
HIV Human immunodeficiency virus
HNPCC Hereditary non-polyposis of Surgeons
MRSA Methicillin-resistant Staphylococcus
colorectal cancer
HRT Hormone replacement therapy aureus
MRI Magnetic resonance imaging
IC Inspiratory capacity MSH Melanocyte-stimulating hormone
ICP Intracranial pressure MSU Mid-stream urine
IGF Insulin-like growth factor MTPJ Metatarsophalangeal joint
IMA Inferior mesenteric artery MUGA Multiple-gated apposition
ILP Isolated limb perfusion
IPSP Inhibitory postsynaptic potential NCEPOD National Clinical Enquiry into
IRV Inspiratory reserve volume Perioperative Deaths
ISCP Intercollegiate Surgical Curriculum
NICE National Institute for Clinical
Programme Excellence
ISS Injury Severity Score
ITU Intensive therapy unit NPI Nottingham Prognostic Index
IUCD Intrauterine contraceptive devise NPV Negative predictive value
IVC Inferior vena cava NSAID Non-steroidal anti-inflammatory
IVU Intravenous urogram
drugs
OCP Oral contraceptive pill
OSCE Objective structured clinical
examination
KPPT Kaolin partial thromboplastic time PAF Platelet activating factor xiii
PCA Patient controlled analgesia
LCIS Lobular carcinoma in situ PCI Percutaneous coronary
LDL Low density lipoproteins
LFTs Liver function tests intervention
LMA Laryngeal mask airway PCR Polymerase chain reaction
LMWH Low molecular weight heparin PCV Packed cell volume
LSV Long saphenous vein PCWP Pulmonary capillary wedge
pressure
PDA Patent ductus arteriosus SPJ Saphenopopliteal junction
PDGF Platelet-derived growth factor SSV Short saphenous vein
PE Pulmonary embolus SV Stroke volume
PEG Percutaneous endoscopic SVR Systemic vascular resistance
gastroenterostomy TENS Transcutaneous electrical nerve
PEEP Positive end expiratory pressure stimulation
PGI Persistent generalised
TGF Transforming growth factor
lymphadenopathy TIA Transient ischaemic attack
PID Pelvic inflammatory disease TIPPS Transjugular intrahepatic portal
PIPJ Proximal interphalangeal joint
PONV Postoperative nausea and vomiting systemic shunt
POSSUM Physiological and Operative TLC Total lung capacity
TNF-α Tumour necrosis factor-α
Severity Score for the enUmeration TOF Trachea-oesophageal fistula
of Mortality and Morbidity TPN Total parenteral nutrition
PPD Purified protein derivative tPA Tissue plasminogen activator
PPV Positive predictive value TRH Thyrotrophin-releasing hormone
PT Prothrombin time TSH Thyroid-stimulating hormone
PTFE Polytetrafluoroethylene TV Tidal volume
PTH Parathyroid hormone
PUJ Pelviureteric junction U&E Urea and electrolytes
UTI Urinary tract infection
QoL Quality of life
RBC Red blood cell VF Ventricular fibrillation
RCT Randomised controlled trial VIP Vasoactive intestinal polypeptide
RES Reticulo-endothelial system VMA Vanillyl mandelic acid
RTS Revised Trauma Score VRE Vancomycin-resistant enterococcus
RV Residual volume VUR Vesicoureteric reflux
vWF von Willebrand factor
SBE Standard base excess
SFJ Saphenofemoral junction WCC White cell count
SIRS Systemic inflammatory response WHO World Health Organization
syndrome VC Vital capacity
SLE Systemic lupus erythematosus VSD Ventricular septal defect
SMA Superior mesenteric artery
xiv
Chapter 1 Professional
skills in clinical
practice
Duties of a doctor but also to share information within the
healthcare team. The benefits of effective
Patients must be able to trust doctors with communication include good working
their lives and wellbeing. To justify that trust, relationships and increased patient satisfaction.
the profession has a duty to maintain a good Effective communication may also increase
standard of practice and care and to show patient understanding of treatment, improve
respect for human life. In particular a doctor compliance and, in some cases, lead to
must: improved health. It engenders meaningful
and trusting relationships between healthcare
• Make the care of his or her patient their professionals and their patients.
first concern
Benefits for patients
• Treat every patient politely and
considerately The doctor–patient relationship is improved.
The doctor is better able to seek the relevant
• Respect patients’ dignity and privacy information and recognise the problems of
• Listen to patients and respect their views the patient by way of interaction and attentive
• Give patients information in a way that the listening. As a result, the patient’s problems
may be identified more accurately. Good
patient can understand communication helps the patient to recall
• Respect the rights of patients to be fully information and comply with treatment
instructions. It may improve patient health
involved in decisions about their care and outcomes. Better communication
• Keep his or her professional knowledge and dialogue, by means of reiteration and
repetition between doctor and patient, has a
and skills up to date beneficial effect in terms of promoting better
• Recognise the limits of his or her own emotional health, resolution of symptoms
and pain control. The overall quality of care
professional confidence may be improved by ensuring that patients’
• Be honest and trustworthy views and wishes are taken into account.
• Respect and protect confidential Good communication is likely to reduce the
incidence of clinical errors.
information
• Make sure that his or her personal beliefs Benefits for doctors
do not prejudice patient care Effective communication skills may relieve
• Act quickly to protect patients from risk if doctors of some of the pressures of dealing
with the difficult situations. Problematic
there are concerns to believe that he, she communication with patients is thought to
or a colleague may not be fit to practice contribute to emotional burn-out and low
• Avoid abusing their position as a doctor personal accomplishment in doctors, as well
• Work with colleagues in ways that best as high psychological morbidity. Being able to
serve patients’ interests communicate competently may also enhance
job satisfaction. Patients are less likely to
In all of these matters, doctors must never complain if doctors communicate well.
discriminate unfairly against their patients or
colleagues. They must always be prepared to
justify their actions.
Communication skills
Good communication is integral to medical
practice. Communication is important not
only in professional–patient interactions,
2 Chapter 1 Professional skills in clinical practice
Good communication skills expected of legal reasons. Records provide a means of
healthcare professional include the ability to: communication and record of events. Patient
records should be:
• Talk to patients, carers and colleagues
effectively and clearly, conveying and • Factual, consistent and accurate
receiving the intended message • Written as soon as possible after the event
• All entries should be dated and signed
• Enable patients and their carers to • The signature should clearly identify the
communicate effectively
author
• Listen effectively, especially when time is • Personal slur and value-judgment should
pressured
be avoided
• Identify potential communication
difficulties and work through solutions Clinical governance
• Understand the differing methods of Definition
communication used by individuals
Clinical governance is a framework
• Understand that there are differences in through which healthcare organisations are
communication signals between cultures accountable for maintaining and improving
the quality of their services, by creating an
• Cope in specific difficult circumstances environment in which excellence is allowed
• Understand how to use and receive non- to flourish. It embodies three key attributes:
verbal messages given by body language • Recognising high standards of care
• Utilise spoken, written and electronic • Transparent responsibility and
methods of communication accountability for standards
• Know when the information received • A constant dynamic of improvement
needs to be passed on to another person Clinical governance addresses those
or professional for action structures, systems and processes that assure
• Know and interpret the information the quality and accountability. It ensures
needed to be recorded on patients records, proper management of an organisation’s
writing discharge letters, copying letters to operation and delivery of service. Clinical
patients and gaining informed consent governance is composed of the following
• Recognise the need for further elements:
development to acquire specialist skills
• Education and training
Key tasks in communication with patients • Clinical effectiveness
include: • Research and development
• Openness
• Eliciting the patient’s main problems, • Risk management
the patients perception of these and the • Clinical audit
physical, emotional and social impact on
the patient and family Education and training
• Tailoring the information to what the It is no longer acceptable for any clinician
patient wants to know and checking their to abstain from continuing education after
understanding qualification. The continuing professional
development of clinicians is the responsibility
• Eliciting the patient’s reactions and their of the individual and his employer. It is the
main concerns professional duty of clinicians to remain up-
to-date.
• Determining how much the patient wants
to participate in decision making Clinical effectiveness
• Discussing the treatment options so that Clinical effectiveness is a measure of the
the patient understand the implications extent to which a particular intervention
• Maximising the chance that the patient
will follow the agreed treatment plan
Documentation and record
keeping
Accurate documentation and record
keeping is important for both clinical and
Clinical governance 3
works. The measure on its own is useful, but the effect of those that cannot be eliminated.
it is enhanced by considering whether the It establishes financial mechanisms to absorb
intervention is appropriate and whether it the consequences of the risks that remain.
represents value for money. In the modern Risk management involves consideration of:
health service, clinical practice needs to be
refined in the light of emerging evidence of • Risks to patients
effectiveness. It also has to consider aspects of • Risks to practitioners
efficiency and safety from the perspective of • Risks to the organisation
the patient.
Compliance with statutory regulations can
Research and development help to minimise risks to patients. This can
be further reduced by ensuring that systems
Good professional practice has always are regularly reviewed and questioned.
sought to change in the light of evidence Maintenance of medical ethical standards
from research. The time lag for introducing is also a key factor in maintaining patient
such change can be very long. Reducing and public safety and wellbeing. It is vital
the time lag and associated morbidity to ensure that clinicians work in a safe
requires emphasis not only on carrying out environment. Poor quality is a threat to any
and implementing research. Techniques organisation. They need to reduce their own
such as critical appraisal of the literature, risks by ensuring high quality employment
project management and the development practice, a safe environment and well-
of guidelines, protocols and implementation designed policies on public involvement.
strategies are all tools for promoting the
implementation of research practice. Risk management is essential to:
Openness • Providing a safe working environment
• Meeting the personal and professional
Poor performance and practice can too
often thrive behind closed doors. Processes responsibility to patients
which are open to public scrutiny, while • Complying with health and safety
respecting individual patient and practitioner
confidentiality are an essential part of quality legislation
assurance. Open proceedings and discussion • Reducing the risk of litigation
about clinical governance issues should
occur. Any organisation providing high Risks can be clinical or non-clinical. Once a
quality care has to show that it is meeting risk is identified it must be analysed:
the needs of the population it serves. Health
needs assessment and understanding the • How often it is likely to occur?
problems and aspirations of the community • What are the potential effects of managing
require the cooperation between healthcare
organisations, public health departments, the risk?
local authorities and community health • What are the potential effects if the risk is
councils. The system of clinical governance
brings together all the elements which seek to ignored?
promote quality of care. • How much is it likely to cost?
Risk management Consideration needs to be given to measures
to control the risk. It may be possible to totally
Risk management can be defined as a eliminate the risk. If it can not be eliminated,
proactive approach that addresses the various the risk should be minimised. Funding for
activities of an organisation. It identifies the risk management is part of every hospital’s
risks that exist and assesses each risk for the budget through the Clinical Negligence
potential frequency and severity. It eliminates Scheme for Trusts and existing liabilities
the risks that can be eliminated and reduces schemes.
Clinical audit
Clinical audit is the review of clinical
performance and the refining of clinical
practice as a result and the measurement of
performance against agreed standards. It is
a systematic, critical analysis of the quality
4 Chapter 1 Professional skills in clinical practice
of medical care, including the procedures • Implementation of change
used for diagnosis and treatment, to help to • Re-audit of clinical practice
provide reassurance that the best quality of
service is being achieved, having regard to Audit techniques include:
the available resources. Clinical audit is an
assessment of total care and can assess: • Basic clinical audit – throughput,
morbidity, mortality
• Structure – type of resources
• Process – what is done to patients • Incident review – critical incident reporting
• Outcome – the result of clinical • Clinical record review
• Criterion audit – retrospective analysis
interventions
judged against chosen criteria
Medical audit • Adverse occurrence screening
• Focused audit studies – specific outcome
Medical audit involves a systematic approach • Global audit – comparison between units
that highlights opportunities for improvement • National studies – e.g. National Confidential
and provides a mechanism for change. It is
not simply case presentations at morbidity Enquiry into Patient Outcome and Death
and mortality meetings. The audit cycle (NCEPOD)
(Figure 1.1) involves:
Comparative audit requires:
• Observation of existing practice
• The setting of standards • High quality data collection
• Comparison between observed and set • Relevant and valid measure of outcome
• Appropriate and valid measures of case mix
standards • A representative population
• Appropriate statistical analysis
The audit loop Figure 1.1 The audit loop
Choose topic
Agree standards
Intervene to promote Observe
change and observe current
practice
practice again
Assess conformity
to standards
Medical litigation 5
Ethics and the law • Industrial disease
• Sentence of death
The Coroner • Dependence on drugs or non-dependent
There are approximately 600,000 deaths per abuse of drugs
year in England and Wales. The cause of death • Lawful killing
is certified by the attending doctor in 75% • Open verdict
cases. Of the 150,000 deaths referred to the • Want of attention at birth
coroner, 60% are referred by doctors, 38% by • Unlawful killing
the police and 2% by the Registrar of Births, • Suicide
Marriages and Deaths. Initial investigations • Still birth
are conducted by coroner’s officers. They are • Attempted or self-induced abortion
often retired policemen. A death certificate
may be issued after discussion with a Medical litigation
coroner’s officers. Coroners hold inquests for
about 10% of deaths that they certify. Definition of negligence
Referral to the coroner For an allegation of negligence to succeed
claimant must prove:
A death should be referred to the coroner if:
• The defendant had a duty of care to the
• The cause of death is unknown claimant
• The deceased had not been seen by the
• There was a breach of the duty of care
certifying doctor either after death or • The claimant suffered actionable harm or
within 14 days of death
• The death was violent, unnatural or damage
suspicious • The damage was caused by the breach of
• The death may be due to an accident
• The death may be due to self-neglect or the duty of care
neglect by others
• The death may be due to an industrial Duty of care
disease or related to the deceased’s
employment All healthcare professional have a duty to
• The death may be due to an abortion become and remain competent. The level of
• The death occurred during an operation skill will depend on experience and seniority
or before recovery from the effects of an of the professional. If a senior delegates
anaesthetic responsibility to a junior he must be sure the
• The death may be due to suicide junior is competent. Otherwise he remains
• The death occurred during or shortly after responsible for any resulting error – vicarious
detention in police or prison custody liability. A breach of duty of care occurs if
the healthcare professional fails to reach
Role of the coroner the proficiency of his peers. This is known
as the Bolam test. It applies equally in
The Coroner’s Act 1988 defines when an treatment, diagnosis and advice. The breach
inquest should be held. Inquests are held in can be something done (commission) or
public and may involve a jury. The purpose of something not done (omission). A doctor can
an inquest is to determine: not be negligent if he acted in accordance
with relevant professional opinion and this
• Who is the deceased principle applies even if another doctor
• How, when and where he died would have adopted a different practice.
• Details of the cause of death Ignorance is not a defence for negligence.
Errors of clinical judgment (e.g. wrong
The coroner is not concerned with civil or diagnosis) often do not amount to negligence.
criminal liability. A coroner may record the
cause of death as: Actionable harm or damage
• Natural causes Actionable harm or damage is the disability,
• Accident/misadventure loss or injury suffered by the claimant.
6 Chapter 1 Professional skills in clinical practice
However negligent the defendant has been, brought, the solicitor issues a Letter of Claim.
the claimant must have suffered quantifiable A Letter of Response should be provided
harm. Quantifiable harm includes: within 3 months. If the case continues,
claim forms are raised by the solicitor and
• Loss of earnings submitted to the court.
• Reduced quality or quantity of life
• Disfigurement Civil Procedure Rules 1998
• Disability
• Mental anguish The Woolf report in 1994 noted that in
medical negligence cases there was a
There may also be an element of contributory disproportionate relationship between the
negligence. This occurs if the actions of the costs and the amounts awarded. There were
claimant is judged to have made the situation long delays in the settling of claims and
worse and can reduce the amount of damages unmeritorious cases were often pursued.
awarded. Clear-cut cases were defended longer than
should have been and success rate was
Causation lower than for any other personal injury
litigation. There was less co-operation
Causation is the link between actionable between opposing parties and 90% of litigants
harm and breach of duty of care. The harm were legally aided. Woolf has proposed
has to have occurred as a result of the actions case management by the courts, alternative
of the defendant. means of dispute resolution, court-based
experts and judges with specialist medical
Legal process knowledge. The future may include no-fault
compensation, early settlement using fixed
The burden of proof lies with the claimant. tariffs depending on the injury caused and
The standard of proof is the civil standard greater use of mediation to settle disputes.
of balance of probabilities. Actions must be
brought within 3 years. Different rules apply
for children and mentally ill. If a claim is
Chapter 2 Perioperative
care
Preoperative assessment Assessment of fitness
for surgery
Preoperative assessment aims to reduce
the morbidity and mortality associated ASA Grading
with surgery. It may prevent unnecessary Medical co-morbidity increases the risk
cancellations and reduce hospital stay. associated with anaesthesia and surgery. The
Evidence-based guidelines reduce the America Society of Anesthesiologists (ASA)
time and cost associated with unnecessary grade is the most commonly used system to
investigations. An effective preoperative grade co-morbidity. The ASA grade is as follows:
assessment process should inform the
patient of the proposed procedure and • 1 = N ormal healthy individual
allow informed consent for surgery to be • 2 = Mild systemic disease that does not
obtained. It should assess pre-existing
medical conditions and plan both the limit activity
preoperative and postoperative management • 3 = S evere systemic disease that limits
of these conditions. The issues that should be
addressed include: activity but is not incapacitating
• 4 = Incapacitating systemic disease which
• Time of admission and starving
instructions is constantly life-threatening
• 5 = M oribund, not expected to survive 24
• Management of usual medication
• Any specific preoperative preparation that hours with or without surgery
may be required ASA grade accurately predicts morbidity and
• Transport to theatre mortality. Over 50% of patients undergoing
• Any specific anaesthetic issues elective surgery are ASA grade 1. Operative
• Anticipated duration of surgery mortality for these patients is less than 1 in
• Likely recovery period 10,000.
• Need for drains and catheter
• Likely discharge date POSSUM Scoring
• Need for dressing change or specific POSSUM stands for Physiologic and
Operative Severity Score for the enUmeration
postoperative care of Mortality and Morbidity. It was developed
• Follow-up requirements in a general surgical population and has since
• Likely date of return to work or full activity been adapted for use in vascular, colorectal,
and oesophago-gastric patients. It is being
Important medical diseases that increase the increasingly ultilised in other specialties.
morbidity and mortality following surgery It uses 12 physiological and biochemical
include: variables, and six operative variables to give
an estimation of mortality risk.
• Ischaemic heart disease
• Congestive cardiac failure Elective surgery grades
• Hypertension The type of surgery is graded according to
• Cardiac arrhythmias the degree of stress it will cause. Different
• Chronic respiratory disease types of surgery carry different risks and need
• Diabetes mellitus differing levels of preoperative assessment.
• Endocrine dysfunction Elective surgery can be graded as follows:
• Chronic renal failure
• Nephrotic syndrome • Minor – e.g. excision of a skin lesion
• Obstructive jaundice • Intermediate – e.g. inguinal hernia repair
• Obesity • Major – e.g. hysterectomy
• Major plus – e.g. colonic resection
8 Chapter 2 Perioperative care
Preoperative investigations • Red – not required
• Amber – test to be considered
The main purpose of preoperative • Green – recommended
investigations is to provide additional
diagnostic and prognostic information with Indications for preoperative
the aim of: investigations
• Providing information that may confirm Chest x-ray
the appropriateness of the current course • All patients for major vascular surgery
of clinical management • Suspected malignancy
• Patients with cardiac or pulmonary disease
• Using the information to reduce the
possible harm to patients by altering their for grade 4 (major+) surgery
clinical management • Patients who have severe (ASA 3) cardiac
• Using the information to help assess the or pulmonary disease
risk to the patient and opening up the • Anticipated ICU admission
possibility of discussing potential increases
of risk with the patient ECG
• All patients aged 60 and over
• Predicting postoperative complications • All patients with cardiovascular disease,
• Establishing a baseline measurement for
including hypertension
later reference • All patients with severe (ASA 3) respiratory
The request for preoperative investigations or renal disease aged 40 and over
should be based on factors apparent from
the clinical assessment and the likelihood Echocardiography
of asymptomatic abnormalities. It should • Severe aortic or mitral stenosis
also take into consideration the severity • Severe left ventricular dysfunction
of the surgery contemplated. Preoperative • Cardiomyopathy
investigations rarely uncover unsuspected • Pulmonary hypertension
medical conditions. It is inefficient as a
means of screening for asymptomatic Full blood count
disease. Only 5% of patients have • All patients undergoing major (grade 3
abnormalities on investigations not predicted
by a clinical assessment. Only 0.1% of these or 4) surgery
investigations ever change the patient’s • Patients with severe (ASA 3) cardiac or
management. Over 70% of preoperative
investigations could be eliminated without respiratory disease
adverse effect. The National Institute for • Severe renal disease (creatinine > 200)
Clinical Excellence (NICE) has produced • Patients with a history of anaemia
guidelines on preoperative tests. These tests • Patients who require a cross match or
include:
group and save
• Chest x-ray • Patients with a bleeding disorder
• ECG • Patients with chronic inflammatory
• Echocardiography
• Full blood count conditions such as rheumatoid arthritis.
• Renal function
• Coagulation screen Renal function
• Glycosylated haemoglobin (HbA1c) • All patients with known or suspected renal
• Liver function
• Lung function tests dysfunction
• All patients with cardiac disease (including
The tests recommended are based on the age
of the patient, ASA grade and grade of the hypertension on treatment)
proposed surgery. Recommendations are • All patients on diuretic treatment
graded: • Patients with severe respiratory disease on
steroid or theophylline therapy
• All patients with diabetes
• All patients for major (grade 3 or 4) surgery
Preoperative assessment 9
Coagulation screen is called the expiratory reserve volume (ERV).
• Personal or family history of abnormal After maximum expiration, some air is still
present in the lungs and is known as the
bleeding residual volume (RV). The maximum volume
• Suspected liver dysfunction (cirrhosis, available for breathing is the vital capacity
(VC). Vital capacity is the sum of IRV, TV and
alcohol abuse, metastatic cancer) ERV.
• Current anticoagulant therapy
• Patients on haemodialysis Peak flow rates
Airway calibre can be assessed by peak
Glycosylated haemoglobin (HbA1c) flow measurements (Figure 2.2). Accurate
• Result within past 3 months for all diabetic assessment requires co-operation and
maximum voluntary effort of the patient. The
patients flow rates measured include:
• Current random blood glucose in known
• FVC = Forced vital capacity
or suspected diabetes • FEV1 = Forced expiratory volume in one
Liver function second
• Hepato-biliary or pancreatic disease
• Known alcohol abuse Absolute values depend on the height, weight,
• Major gastrointestinal surgery age, sex and race of the patient. The FEV1/
FVC ratio is a useful derived measurement.
Lung function Lung function can be classified as:
• Patients with severe (ASA 3) respiratory
• Normal
disease undergoing major surgery • Restrictive
• Obstructive
• Patients having scoliosis surgery
In restrictive lung disease, the FVC is reduced
• Asthmatics need a peak flow recorded but FEV1/FVC is normal. In obstructive lung
disease, the FVC is normal or reduced and
Tests of respiratory, cardiac FEV1/FVC is reduced.
and renal disease
Gas transfer
Respiratory function Arterial blood gases are the best measure
available for the measurement of gas transfer.
Lung function tests should be able to predict They also allow the assessment of ventilation/
the type and severity of any lung disease and perfusion mismatch. Important parameters to
correlate with the risk of complications and measure are:
postoperative mortality. Tests fall in to three
categories: • pH
• Partial pressure of oxygen
• Lung mechanics • Partial pressure of carbon dioxide
• Gas exchange
• Control of breathing Pulse oximetry gives an indirect estimate of
gas transfer. This technique may be unreliable
Useful radiological investigations include a in the presence of other medical problems
chest x-ray and high-resolution thoracic CT. (e.g. anaemia).
Arterial blood gases may provide additional
helpful information. Lung function tests allow Cardiac function
assessment of lung volumes, airway caliber
and gas transfer. Simple non-invasive and more complicated
invasive tests of cardiac function exist. Non-
Spirometry invasive tests include:
Lung volumes are assessed with spirometry
(Figure 2.1). The total amount of air moved • Chest x-ray
in and out of the lungs each minute depends • ECG
upon the tidal volume (TV) and respiratory • Echocardiography
rate (RR). Pulmonary ventilation is the • Exercise test
product of RR and TV. The extra inspiration
available is called the inspiratory reserve
volume (IRV). The extra expiration available
10 Chapter 2 Perioperative care
Respiratory volumes
Figure 2.1 Respiratory volumes. IC = Inspiratory capacity. IRV = Inspiratory reserve volume. TV = Tidal volume.
VC = Vital capacity. FRC = Functional residual capacity. RV = Residual volume. ERV = Expiratory reserve volume.
TLC = Total lung capacity. (Reproduced from Thillai M and Hattotuwa K. Pocket Tutor Understanding ABGs and
Lung Function Tests. London: JP Medical Ltd, 2012.)
Peak flow measurements Invasive tests include:
Volume (L) • Coronary angiography
• Thallium scanning
FEV1 FVC
Chest x-ray
01 Time (sec) Routine preoperative chest x-ray is not
recommended for all patients, but it is
Figure 2.2. Peak flow measurements. FVC = Forced indicated in the presence of cardiorespiratory
vital capacity. FEV1 = forced expiratory volume in symptoms or signs. Important signs
one second associated with increased cardiac morbidity
are cardiomegaly, pulmonary oedema or a
change in the cardiac outline characteristic of
specific diseases.
ECG
A resting ECG is normal in 25–50% of patients
with ischaemic heart disease. Characteristic
features of ischaemia or previous infarction may
be present. An exercise ECG provides a good
indication of the degree of cardiac reserve.
Preoperative assessment 11
24-hour ECG monitoring is useful in the • Non-diet controlled diabetes mellitus
detection and assessment of arrhythmias. • Age more than 70 years
• History of ventricular arrhythmia
Echocardiography
Can be performed percutaneously or via the Patients scoring zero are at low-risk, patients
transoesophageal route. Two-dimensional scoring one are intermediate risk and those
echocardiography allows assessment of scoring two or more are at high-risk. Low-
muscle mass, ventricular function, ejection risk patients require no further investigation.
fraction, end-diastolic and end-systolic Intermediate risk patients require an
volumes, valvular function and segmental exercise ECG and thallium scan. High-risk
defects. Doppler ultrasound allows patient should be considered for coronary
assessment of valvular flow and pressure angiography prior to major non-cardiac
gradients. surgery.
Nuclear medicine Revised cardiac risk index
Myocardial scintigraphy allows assessment One point is allocated for each of:
of myocardial perfusion. Radiolabelled
thallium is the commonest isotope used. • High-risk surgery
Areas of ischaemia or infarction appear as • Ischaemic heart disease
‘cold’ spots on the scan. Vasodilators can be • History of congestive heart failure
used to evaluate reversibility of ischaemia. • History of cerebrovascular disease
Radiolabelled albumin or red cells can be • Insulin therapy for diabetes mellitus
used to assess ejection fraction. Such dynamic • Renal impairment
studies are performed ‘gated’ to the ECG.
The risk of a major cardiac event during
Renal function surgery increases with the number of points
from 0.5% for zero points to 10% for more
Glomerular filtration rate is the gold standard than two points.
test of renal function. It can be calculated
by measuring creatinine clearance rate Myocardial infarction
but this requires 24-hour urine collection. Elective surgery should be deferred for 6
Serum creatinine allows a good estimate of months after a myocardial infarct. Risk factors
renal function. However the use of serum for postoperative myocardial re-infarction
creatinine may be inaccurate in patients with include:
obesity, oedema, pregnancy or ascites.
• Short time since previous infarct
Management of associated • Residual major coronary vessel disease
medical conditions • Prolonged or major surgery
• Impaired myocardial function
Some medical conditions increase the risk
associated with surgery. These need to be The risk of postoperative re-infarction after a
assessed preoperatively and where possible, previous myocardial infarct is 35% between 0
the patient’s condition optimised. and 3 months, 15% between 3 and 6 months
and 4% more than 6 months. Approximately
Cardiovascular disease 60% of postoperative myocardial infarcts
are silent. The mortality of re-infarction is
Several scoring systems exist for stratifying approximately 40%.
cardiac risk prior to non-cardiac surgery.
They are simple to use and identify patients in Hypertension
need of further investigation. In patients with hypertension, an assessment
is needed of the severity of hypertension and
Eagle index the presence of end organ damage. The risk
One point is allocated for each of: of cardiovascular morbidity is increased in
poorly controlled hypertension. Increased
• History of myocardial infarction of angina risk is present if the diastolic pressure is
• Q wave on preoperative ECG greater than 95 mmHg. Elective surgery
12 Chapter 2 Perioperative care
should be cancelled if diastolic pressure is measure of the degree of obesity. A patient’s
greater than 120 mmHg. BMI = Weight (kg)/height (m)2. The normal
BMI is 22–28. A BMI greater than 30
Respiratory disease equates to being significantly overweight.
A BMI greater than 40 equals morbid
Patients with lung disease are at increased obesity. Patients are at risk of numerous
risk of respiratory complications. The complications shown in Table 2.1.
complications include:
Diabetes mellitus
• Bronchospasm
• Atelectasis Pre- and perioperative management of
• Bronchopneumonia diabetic patients depends on the severity
• Hypoxaemia of the disease. Diet-controlled diabetics
• Respiratory failure require no specific precautions. The blood
• Pulmonary embolism sugar should be checked prior to surgery and
consideration given to a glucose–potassium–
In addition to routine preoperative insulin (GKI) infusion if more than
investigations, in patients with respiratory 12 mmol/L. Those patients on long acting
disease it is necessary to consider a chest sulphonylureas should stop them 48 hours
x-ray, spirometry and arterial blood gases. prior to surgery. Short acting agents should
A recent upper respiratory tract infection be omitted on the morning of operation. All
increases the risk postoperative chest oral hypoglycaemics can be recommenced
complications. Elective surgery should be when the patient is eating normally. A GKI
deferred for 2–4 weeks. infusion should be considered for non-insulin
dependent diabetics undergoing major
Smoking surgery. Insulin dependent diabetics should
Smoking doubles the risk of postoperative be placed early on an operating list and give
pulmonary complications. The increased a GKI infusion until eating normally. A GKI
risk persists for 3–4 months after infusion is made up with 15 units of insulin,
stopping smoking. Smoking increases 10 mmol potassium chloride and 500 mL 10%
blood carboxyhaemoglobin. Increased dextrose and infused at a rate dependent on
carboxyhaemoglobin persists for 12 hours the blood sugar level.
after the last cigarette.
Chronic renal failure
Obesity
Chronic renal failure affects multiple organ
Morbidity and mortality after all surgery is systems. Effects that need to be considered by
increased in the obese. The risk is increased both surgeons and anesthetists include:
even in the absence of other disease. The
Body Mass Index (BMI) is the best available
Complications associated with obesity
Cardiovascular Respiratory Other
Hypertension Difficult airway Gastro-oesophageal reflux
Ischaemic heart disease Difficult mechanical ventilation Abnormal liver function
Cerebrovascular disease Chronic hypoxaemia Insulin resistance and type 2 diabetes
Deep venous thrombosis Obstructive sleep apnoea Poor postoperative pain control
Difficult vascular access Pulmonary hypertension Unpredictable pharmacological response
Postoperative hypoxaemia
Table 2.1 Complications associated with obesity
Preparation for surgery 13
• Electrolyte disturbances information to determine what treatment
• Impaired acid–base balance that they are or are not willing to receive.
• Anaemia They have the right to decide not to undergo
• Coagulopathy a treatment even if this could adversely affect
• Impaired autonomic regulation the outcome or result in their death. Patients
• Protection of veins, shunts and fistula must be given sufficient information to
make these decisions. Obtaining informed
Preparation for surgery consent is not an isolated event. It involves a
continuing dialogue between the doctor and
Drugs patient.
Most medication can be continued in Types of consent
the perioperative period. A few drugs
need to be discontinued as they present Expressed consent can be oral or written. It is
either anaesthetic or surgical risks. Oral needed for most investigations or treatments
anticoagulation with warfarin is managed with risks attached. Implied consent is
according to the indication for its use. non-written and occurs when a patient
Patients with prosthetic heart valves need to co-operates with a particular action, such as
continue anticoagulation with therapeutic a physical examination or simple practical
doses of low molecular weight heparin. procedure. When obtaining consent, patients
Patients on warfarin for atrial fibrillation can should be informed of:
have their anticoagulation stopped prior to
surgery. Warfarin should be discontinued for • Details of the diagnosis and prognosis with
5 days prior to surgery but can be restarted and without treatment
the night following the operation.
• Uncertainties about the diagnosis
For minor surgery, there is no need to • Options available for treatment
stop either the oral contraceptive pill or • The purpose of a proposed investigation or
hormone replacement therapy. The oral
contraceptive pill increases the risk of venous treatment
thromboembolism four-fold and for major • The likely benefits and probability of
surgery patients should be informed of the
increased risk and an appropriate decision success
made. • Any possible side effects
• A reminder that the patients can change
Preoperative fasting
their mind at any stage
General anaesthesia increases the risk of • A reminder that the patients have the right
aspiration of gastric contents. Traditionally
patients have been starved since midnight to a second opinion
prior to elective surgery the following
morning. It is now known that clear fluids All questions should be answered honestly.
leave the stomach within 2 hours and that they Information should not be withheld that
do not increase the volume or acidity of gastric might influence the decision making process.
contents. For elective surgery, patients can Patients should not be coerced. The person
be allowed food and clear fluids until 6 and who obtains consent must be suitably trained
2 hours prior to their surgery, respectively. and qualified. They must have sufficient
For emergency surgery, oral intake should be knowledge of the proposed treatment and
restricted as many surgical emergencies are its risks. It is good practice for this to be the
associated with delayed gastric emptying. clinician providing the treatment.
Informed consent Specific problems
Patient autonomy must be respected at No-one else can make a decision on behalf
all times. They should be given sufficient of a competent adult. In an emergency, a
life-saving procedure can be performed
without consent. All actions must, however,
be justifiable to one’s peers. Advanced care
directives and living wills are legally binding
and should be followed.
14 Chapter 2 Perioperative care
Consent in children to make a decision have been taken without
success’. Every person should be presumed
At the age of 16 years a child can be presumed to be able to make their own decisions. One
to have the capacity to decide on treatment. can only take a decision for someone else
Below the age of 16 years, a child may have if all practical steps to help them to make a
the capacity to decide depending on their decision have been taken without success.
ability to understand what the treatment Incapacity is not based on the ability to make
involves (Gillick competence). If a competent a wise or sensible decision. To determine
child refuses treatment, a person with incapacity, it is necessary to consider whether
parental responsibility may authorise the person one is looking after is able to
treatment which is in the child’s best interests. understand the particular issue that they are
making a decision about. It is necessary to
Mental Capacity Act consider if they have:
In the UK, the Mental Capacity Act is • An impairment or disturbance in the
designed to protect people who can’t functioning of their mind or brain, and
make decisions for themselves or lack the
mental capacity to do so. This could be • An inability to make decisions
due to a mental health condition, a severe
learning difficulty, a brain injury, a stroke or A person is unable to make a decision if they
unconsciousness due to an anaesthetic or cannot:
sudden accident. The Act’s purpose is:
• Understand the information relevant to
• To allow adults to make as many decisions the decision
as they can for themselves
• Retain that information
• To enable adults to make advance • Use or weigh that information as part of
decisions about whether they would like
future medical treatment the process of making the decision, or
communicate the decision
• To allow adults to appoint, in advance of
losing mental capacity, another person to If, having taken all practical steps to assist
make decisions about personal welfare on someone, it is concluded that a decision
their behalf at a future date should be made for them, that decision must
be made in that person’s best interests. It is
• To allow decisions concerning personal essential to consider whether there is another
welfare and affairs to be made in the best way of making the decision which might not
interests of adults when they have not affect the person’s rights. The Mental Capacity
made any future plans and cannot make a Act sets out a checklist of things to consider
decision at the time when deciding what is in a person’s best
interests including:
• To ensure an NHS body or local authority
will appoint an independent mental • Do not make assumptions on the basis of
capacity advocate to support someone age, appearance, condition or behaviour
who cannot make a decision about serious
medical treatment when there are no • Consider all the relevant circumstances
family or friends to be consulted • Consider whether or when the person will
• To provide protection against legal have capacity to make the decision
liability for carers who have honestly and • Support the person’s participation in any
reasonably sought to act in the person’s
best interests acts or decisions made for them
• Do not make a decision about life-
• To provide clarity and safeguards around
research in relation to those who lack sustaining treatment ‘motivated by a
capacity. desire to bring about death’
• Consider the person’s expressed wishes
Under the Mental Capacity Act, a person and feelings, beliefs and values
is presumed to make their own decisions • Take into account the views of others with an
‘unless all practical steps to help him (or her) interest in the person’s welfare, their carers
and those appointed to act on their behalf
Principles of anaesthesia 15
Perioperative risk and improving communication within the
management team. Its routine use has been shown to
reduce the risk of complications and death.
We all take risks in everyday life. The degree
of risk taken depends on the perceived Principles of anaesthesia
benefit. Most decisions are made on previous Pharmacokinetics and
experiences. Risk assessment forms an pharmacodynamics
integral part of patient care. An assessment
needs to be made of the risks versus benefits Definitions
for an procedure performed. These will then
influence decisions made by the surgeon or Pharmacokinetics is the study of the bodily
the patient absorption, distribution, metabolism, and
excretion of drugs. Pharmacodynamics is the
Risk assessment models study of the biochemical and physiological
effects of drugs and their mechanisms of
Assessment of risk in surgery depends on action. Pharmacokinetics of a drug are
many factors. These involve knowledge of the: dependent on:
• Patient • Absorption into the body
• Disease • Distribution throughout the fluids and
• Co-morbidities
• Proposed surgery tissues of the body
• Physiological status • Metabolism and its daughter metabolites
• Excretion or elimination from the body
Risk assessment tools
First order kinetics
Decision making is rarely simple and straight
forward. Risk assessment tools have been With first order kinetics, a constant fraction
developed and are in common use to help of the drug in the body is eliminated per unit
assess risk. They include: time. The rate of elimination is proportional
to the amount of drug in the body. The
• Goldman Cardiac Risk Index majority of drugs are eliminated in this way.
• Parsonnet Score With drugs displaying first order kinetics
• POSSUM various properties can be defined:
• Injury Severity Score
• Revised Trauma score • The clearance is defined as the apparent
• APACHE I, II and III volume of plasma from which a drug is
entirely removed per unit time. It is usually
WHO Safe Surgery Check List expressed in proportion to body weight or
surface area.
In Western industrialised countries, major
complications are reported to occur following • The volume of distribution is the volume
about 15% of inpatient surgical procedures into which a drug appears to be uniformly
with permanent disability or death occurring distributed at the concentration measured
following 0.5% of operations. Some of this in plasma. It is usually a steady state
morbidity and mortality results from human volume of distribution equal to the
error and is preventable. The WHO Safe amount of drug in the body. Drugs that
Surgery Check List recommends a series of are lipid soluble have a high volume of
checks – Sign In, Time Out and Sign Out, distribution. Drugs that are lipid insoluble
be performed prior to, during and after any have a low volume of distribution.
surgical procedure. The aim of the use of the
checklist is to strengthen the commitment of • The half life is the time taken for the
clinical staff to address safety issues within plasma concentration of a drug to fall by
the surgical setting. This includes improving 50% when first-order kinetics are observed.
anaesthetic safety practices, ensuring correct Many drugs have an initial redistribution
site surgery, avoiding surgical site infections phase with a short half-life followed by an
elimination phase with a longer half-life.
16 Chapter 2 Perioperative care
• The bioavailability is the proportion of • Amnesia – benzodiazepines,
a dose of a specified drug preparation anticholinergics
entering the systemic circulation after
administration by a specified route. • Antiemetic – anticholinergics,
antihistamines, 5HT antagonists
Multicompartment models
• Antacid – alginates, proton pump
First order kinetics is often only displayed inhibitors
in drugs that are distributed around a single
compartment. The human body is more • Anti-autonomic – anticholinergics,
complex. It has several compartments – b-blockers
muscle, blood, brain fat etc. Some drugs
(induction anaesthetic agents) are initially • Adjuncts – bronchodilators, steroids
transported to organs with a rich blood
supply. After a few minute the agent Induction of anaesthesia
redistributes to other parts of the body.
Initially, the blood concentration rapidly Induction agents are usually administered
falls due to redistribution. Later, the blood intravenously. They are highly lipid soluble
concentration decreases more slowly due to and rapidly cross the blood–brain barrier.
metabolism or elimination of the drug. They are distributed to organs with a high
blood flow such as the brain. With falling
General anaesthesia blood levels they are rapidly redistributed. As
a result they have rapid onset and, without
General anaesthesia is a drug-induced state maintenance, have a rapid recovery.
of unresponsiveness and is usually achieved
by the use of a combination of agents. It has Thiopentone is a short-acting barbiturate
three phases: that was first used at Pearl Harbour in
1942. It depresses the myocardium and in
• Induction hypovolaemic patient can induce profound
• Maintenance hypotension. Propofol is now one of the
• Reversal and recovery most commonly used induction agents. It
has very short half-life and can also cause
Premedication hypotension. It can also be used as an
infusion for the maintenance of anaesthesia.
Is the administration of drugs prior to a Chemically, it is unrelated to barbiturates
general anaesthetic. It has three potentially and has largely replaced thiopentone for the
useful effects: induction of anaesthesia. Propofol has no
analgesic properties, so when used in the
• Anxiolysis maintenance of anaesthesia, opioids such as
• Reduced bronchial secretions fentanyl may be need to administered.
• Analgesia
Rapid-sequence induction
Anxiolysis, if needed, can be achieved with
either benzodiazepines or phenothiazines. Rapid-sequence induction involves the rapid
Opiate analgesics also have useful sedative induction of anaesthesia. Cricoid pressure
properties. Reduction of sections is not as is used to reduce the risk of aspiration.
important today with modern inhalational Pressure is released once tracheal intubation
agents. Ether was notorious for stimulating with a cuffed tube has been achieved. It
bronchial secretions. If required, secretions is achieved by the use of thiopentone and
can be reduced with hyoscine. It also suxamethonium and is used for patients
reduces salivation and prevents bradycardia. who are not fasted, have a history of
Analgesia is best achieved with strong opiates. gastro-oesophageal reflux, have intestinal
obstruction, pregnancy or intra-abdominal
Drugs used in premedication include: pathology that will delay gastric emptying.
• Anxiolysis – benzodiazepines, Endotracheal intubation
phenothiazines
Endotracheal intubation is the placement of
• Analgesia – opiates, non-steroids anti- a tube into the trachea to maintain a patient
inflammatories airway. Following insertion, air entry is
Principles of anaesthesia 17
confirmed by listening with a stethoscope The ideal inhalational anaesthetic agent
for breath sounds over each side of the chest
and by monitoring end tidal carbon dioxide The ideal inhalational anaesthetic agent
levels. The benefits of an endotracheal airway should have several properties. In its
include: preparation it should:
• Protection against aspiration and gastric • Be easily administered
insufflation • Have a boiling point above ambient
• More effective ventilation and oxygenation temperature
• Facilitation of suctioning • Have a low latent heat of vaporisation
• Delivery of anaesthetic and other drugs via • Be chemically stable with long shelf-life
• Be compatible with soda-lime, metals and
the endotracheal tube
plastics
Potential complications include: • Be non-flammable
• Be cheap
• Failed intubation and hypoxaemia
• Aspiration and post-intubation Its pharmacokinetic should be:
pneumonia • Low solubility
• Pneumothorax • Rapid onset, rapid offset, adjustable depth
• Trauma from the laryngoscope – teeth and • Minimal metabolism
• Predictable in all age groups
soft tissues
• Right mainstem intubation Its pharmacodynamic should be:
• Oesophageal intubation
• Hypotension and arrhythmias • High potency – allows high FiO2
• Vocal cord damage • High therapeutic index
• Analgesic
Laryngeal mask airway
The agent should have few adverse actions
The laryngeal mask airway (LMA) is an and have minimal toxicity. There should be no
alternative to the use of an endotracheal toxicity with chronic low-level exposure to staff.
tube. It consists of a tube with an inflatable
cuff that is inserted blindly into the pharynx, Anaesthesia is normally maintained with
forming a low-pressure seal around the inhaled volatile gases. They are lipid soluble
laryngeal inlet and permitting gentle positive hydrocarbons. They have high saturated
pressure ventilation. The apex of the mask, vapour pressures. Modern inhalational
with its open end pointing downwards agents are potent, non-inflammable and
toward the tongue, is pushed backwards non-explosive. The minimum alveolar
towards the uvula. The cuff follows the concentration (MAC) is the alveolar
natural bend of the oropharynx and is seated concentration required to keep 50% of
over the pyriform fossae. The advantages of population unresponsive. The adverse effects
an LMA is that it does not require the use of inhalational anaesthetics are shown in
of a laryngoscope or muscle relaxants and Table 2.2.
it provides an airway for spontaneous or
controlled ventilation that is well tolerated. Halothane
An LMA does not protect the lungs from
aspiration, making it unsuitable for patients Halothane is a potent anaesthetic but poor
at risk of this complication. analgesic agent (MAC = 0.75). It can be used
for gaseous induction in children. About 20%
Maintenance of anaesthesia is metabolised in the liver and it can cause
hepatic dysfunction. Occasionally it causes
Balanced anaesthesia has three aspects: severe hepatitis that can progress to liver
necrosis. It depresses myocardial contractility
• Hypnosis – suppression of consciousness and can induce arrhythmias.
• Analgesia – suppression of physiological
Isoflurane
responses to stimuli
• Relaxation – suppression of muscle tone Isoflurane is a potent anaesthetic but poor
analgesic agent (MAC = 1.05). It is less
and relaxation
18 Chapter 2 Perioperative care
Adverse effects of inhalational anaesthetic
Cardiovascular Respiratory Central nervous system Other
Decrease myocardial Depress ventilation Increase cerebral blood Decrease renal blood
contractility flow flow
Laryngospasm and
Reduce cardiac output airway obstruction Reduce cerebral Stimulate nausea and
metabolic rate vomiting
Decrease ventilatory
response to hypoxia
and hypercapnia
Bronchodilatation
Hypotension
Arrhythmias
.ir/Increase myocardial
sensitivity to
catecholamines
Increase risk of epilepsy Precipitate hepatitis
Increase intracranial
pressure
sTable 2.2 Adverse effects of inhalational anaesthetics
nscardiotoxic than halothane but causes greater
iarespiratory depression. It reduces peripheral approximately 1:7000 of population and is
due to pseudocholinesterase deficiency.
resistance and can cause a ‘coronary steal’. Malignant hyperpyrexia affects approximately
1:100,000 of population. It is due to increased
rsFew adverse effects have been reported. calcium influx and uncontrolled metabolism
and results in a rapid increase in body
Nitrous oxide temperature with increased PaCO2.
eNitrous oxide is a weak anaesthetic agent Non-depolarising agents (e.g. vecuronium)
.p(MAC = 103). It can not be used as an act over 2–3 minutes and the effects last for
30 minutes to 1 hour. They act as competitive
anaesthetic agent alone without causing antagonists of acetylcholine receptor and are
hypoxia. It is however a very potent analgesic used for intraoperative muscle relaxation.
ipagent. It is often used as a 50% N2O/50% Perioperative monitoring
O2 mixture known as Entonox. It is used in General anaesthesia removes the ability of a
patient to protect themselves. The safety and
://vanaesthesia mainly for its analgesic properties.physiological control of the patient becomes
the responsibility of the anaesthetist. The
Muscle relaxants anaesthetist needs to:
Muscle relaxants are either depolarising or
ttpnon-depolarising agents. Depolarising agents
(e.g. suxamethonium) act rapidly within
seconds and their effects last for approximately
h5 minutes. They are used during induction of
anaesthesia. Side effects include: • Maintain airway and oxygenation
• Histamine release producing a ‘scoline • Preserve circulation
rash’ • Prevent hypothermia
• Prevent injury
• Bradycardia • Monitor during anaesthesia
• Somatic pain resulting from fasciculation
• Hyperkalaemia Airway management
• Increased intraocular pressure
• Increased gastric pressure General anaesthesia removes muscle
tone. Without assistance the airway will
Persistent neuromuscular blockade can be compromised. Methods of maintaining
result in ‘scoline apnoea’. This affects airway include:
Principles of anaesthesia 19
• Manual methods (e.g. jaw thrust) provides information on myocardial
• Guedel airway ischaemia or infarction. ECG monitoring is
• Laryngeal mask essential for all patients and is of particular
• Endotracheal tube use in:
• Tracheostomy tube • All patients in ITU or HDU
Monitoring during anaesthesia • Patients with poor cardiac reserve
• Patients receiving vasoactive drugs
The continuous presence of an adequately • Patients with drug toxicity
trained anaesthetist is essential. Accurate • Monitoring of electrolyte disturbances
monitoring of vital signs is obligatory.
Facilities for cardiopulmonary resuscitation
should be immediately available. Monitoring Arterial pressure monitoring
of the following is considered essential for all
Invasive arterial pressure monitoring
.ir/patients: requires:
• Temperature • An arterial cannula
• Heart rate • A monitoring line
• A transducer
s• Blood pressure • A monitoring system
• ECG It provides information on systolic and
diastolic pressure and arterial waveform.
s• Oxygen content of inspiratory gas mix Complications and problems associated with
invasive monitoring include:
• End-tidal carbon dioxide
• Over and under dampening
n• Pulse oximetry • Incorrect zeroing
iaThe following may be considered for major • Haematoma
• Distal ischaemia
surgery: • Inadvertent drug injection
• Disconnection and haemorrhage
rs• Invasive blood pressure monitoring • Infection
• Central venous pressure Central venous pressure
e• Urine output Clinical assessment of jugular venous
pressure is unreliable. The central venous
Alarms should indicate oxygen supply failure system can be cannulated by the internal
jugular or subclavian routes to provide more
.pand ventilator disconnection. accurate information about central venous
ipInvasive and non-invasive pressure and intravascular volume. It also
allows assessment of the cardiac pre-load.
monitoring Complications of CVP lines include:
://vCardiac output is the ‘gold standard’ measure• Pneumothorax
of cardiovascular function. Measurement
normally requires invasive pressure
monitoring. Cardiovascular function can
ttphowever be assessed non-invasively with:
• Electrocardiogram
• Blood pressure
h• Central venous pressure
• Urine output • Arterial puncture
• Air embolism
Blood pressure can be monitored with a cuff • Infection
(intermittent) or arterial line (continuous)
and in the absence of vasoconstriction The site at which transducers are zeroed are
provides a good estimate of cardiac output. very variable. They also change with patient
movement. Therefore changes in pressure
The ECG rather than absolute values are important.
An electrocardiogram (ECG) provides The pressure response to a fluid bolus (e.g.
information on both heart rate and rhythm. 200 mL of colloid given as quickly as possible)
It also serves as a valuable monitor of give a good estimate of intravascular volume
electrolyte abnormalities. A 12-lead ECG status. A low CVP with a transient increase
20 Chapter 2 Perioperative care
with a fluid bolus indicates hypovolaemia. The derived haemodynamic data obtained
A high CVP with a persistent increase with a from a Swan–Ganz catheter includes:
fluid bolus indicates hypervolaemia. • Cardiac index
Cardiac output and left-sided pressures • Stroke volume
• Stroke volume index
If both ventricle are functioning normally,
• Systemic vascular resistance
cardiac pre-load will allow an assessment of
• Systemic vascular resistance index
cardiac output. However, in ischaemic heart
• Pulmonary vascular resistance index
disease or sepsis, left ventricular function
• Left ventricular stroke work index
can be reduced. Pulmonary hypertension
reduces right ventricular function. In these • Right ventricular stroke work index
situations, assessment of left heart pressures • Oxygen delivery
may be important. Also a more direct • Oxygen consumption
.ir/measure of cardiac output may be needed. Recovery from anaesthesia
Cardiac output can be measured either Recovery from anaesthesia should be
invasively with a pulmonary artery catheter monitored by a suitably trained nurse and it
or non-invasively using an oesophageal should occur in a properly equipped recovery
area. An anaesthetist should be immediately
sDoppler. available. Causes of failure to breath after
sSwan–Ganz catheter general anaesthesia include:
nA Swan–Ganz catheter is a balloon-tipped
iacatheter inserted through a central vein. It • Obstruction of the airway
• Central sedation due to opiates or
is floated through the right side of heart into
the pulmonary artery. The balloon allows anaesthetic agent
• Hypoxia
rs‘wedging’ in a branch of the pulmonary • Hypercarbia
• Hypocarbia due to overventilation
artery. The pressure recorded is known as • Persistent neuromuscular blockade
• Pneumothorax
ethe pulmonary capillary wedge pressure. • Circulatory failure leading to respiratory
It is a good estimate of left atrial pressure. arrest
.pThe tip of the catheter contains a thermistor.Care of the patient under
anaesthesia
The cardiac output can be measured using Thermoregulation
ipthermodilution principal. If blood pressure Mammals maintain a constant body
temperature. They are known as
and cardiac output are known then vascular homeotherms. Their body temperature
is usually above the environmental
://vresistance can be calculated. Complications
of a Swan–Ganz catheter include:
• Arrhythmias
• Knotting and misplacement
ttp• Cardiac valve trauma
• Pulmonary infarction
• Pulmonary artery rupture
h• Balloon rupture
• Catheter thrombosis or embolism temperature. Homeotherms have many
The primary haemodynamic data obtained advantages but do need a higher metabolic
from a Swan–Ganz catheter includes: rate.
• Heart rate Body temperature results from a balance
• Mean arterial pressure between production and heat loss. In a
• Central venous pressure balanced state, production and loss of heat
• Mean pulmonary artery pressure will be equal and the body temperature will
• Mean pulmonary artery occlusion be constant. Tight control of temperature is
essential for normal physiological functions.
pressure The core temperature is invariably higher
• Cardiac output then the skin temperature.
• Ventricular ejection fraction
Care of the patient under anaesthesia 21
Control of body temperature Perioperative hypothermia
Temperature is controlled by the Surgical patients are at risk of developing
hypothalamus. Control requires sensors, a hypothermia at any stage of the perioperative
control centre and effectors. Temperature pathway. Inadvertent perioperative
sensors are found throughout the body in hypothermia is a common but preventable
the skin, brain and other organs. There are complication of surgical procedures. It
two types of sensors that respond to hot and is associated with increased morbidity.
cold. The hypothalamus acts as a thermostat Hypothermia is defined as a patient core
and has a temperature set point. Effectors temperature of below 36.0°C. During the early
produce more heat (increased metabolic phase of anaesthesia, a patient’s temperature
rate, shivering, brown fat metabolism) or can easily fall. Reasons for this include:
change heat loss (blood vessel dilation or
constriction, erection of hair, curling up, • Loss of the behavioural response to cold
sweating). • Impairment of thermoregulatory heat-
The skin preserving mechanisms under general
anaesthesia
The skin is the primary organ for removal • Anaesthesia-induced peripheral
of metabolic heat. About 90% of heat is lost vasodilatation
through the skin. The remaining 10% is lost in • Patient getting cold while waiting for
urine and exhaled air. If the body temperature surgery on the ward
is too high, blood vessels in the skin can dilate
and increase blood flow by 150 times to lose It is important to prevent inadvertent
excess heat. In cold weather, blood vessels in perioperative hypothermia.
the skin will contract and reduce heat loss.
Heat loss is by: Perioperative care
• Radiation Patients should be informed that the hospital
• Conduction environment may be colder than their
• Convection own home and that staying warm before
• Sweating surgery will reduce the risk of postoperative
complications. They should bring additional
Newton’s law of cooling governs heat clothing, such as a dressing gown, a vest and
loss by radiation and conduction. Heat warm clothing. They should tell staff if they
loss = heat conductance x temperature feel cold at any time during their hospital
difference. The temperature difference = body stay. When using any device to measure
temperature – ambient temperature. patient temperature, healthcare professionals
Sweating can be used to lose enormous should be aware of, and carry out, any
amounts of heat. The heat of vaporisation adjustments that need to be made in order to
of water is about 580 calories/litre. If the obtain an estimate of core temperature.
ambient temperature is higher than the body
temperature, sweating is the only way heat Preoperative phase
can be lost. Sweat glands are activated by
nerves from the sympathetic nervous system. Each patient should be assessed for their risk
of inadvertent perioperative hypothermia.
Mechanisms of pyrexia Patients should be managed as higher risk if
any two of the following apply:
Fevers are caused by in increase in the
temperature set point – the thermostat has • ASA grade II to V
been set higher. Often caused by bacterial • Preoperative temperature below 36.0°C
toxins or inflammatory mediators, they act • Undergoing combined general and
directly on the hypothalamus. Fevers result
from either increased metabolism, reduced regional anaesthesia
heat conduction, or both. The benefits of a • Undergoing major or intermediate grade
fever are uncertain.
surgery
• At risk of cardiovascular complications
If the patient’s temperature is below 36.0°C,
forced air warming should be started
22 Chapter 2 Perioperative care
preoperatively on the ward and it should be positioning of the patient. The commonest
maintained throughout the intraoperative nerves affected are the ulnar and common
phase. peroneal nerves and the brachial plexus.
Predisposing factors include:
Intraoperative phase
• Medical conditions associated with a
The patient’s temperature should be neuropathy (e.g. diabetes mellitus)
measured and documented before induction
of anaesthesia. It should be repeated every 30 • Nerve ischaemia due to hypotension
minutes until the end of surgery. Induction • Local injections or direct nerve injury
of anaesthesia should not begin unless the • The use of a tourniquets
patient’s temperature is 36.0°C or above.
Intravenous fluids (500 mL or more) and Most nerve injuries are due to a neurapraxia.
blood products should be warmed to 37°C About 90% undergo complete recovery.
using a fluid warming device. Patients However about 10% are left with some
who are at higher risk of inadvertent residual weakness or sensory loss.
perioperative hypothermia and who are
having anaesthesia for less than 30 minutes Ulnar nerve injuries are caused by
should be warmed intraoperatively from positioning the arms along side the patient
induction of anaesthesia using a forced air in pronation. The nerve is compressed at
warming device. All patients who are having the elbow between the operating table and
anaesthesia for longer than 30 minutes medial epicondyle. Injury can be prevented
should be warmed intraoperatively from by positioning arms in supination. Brachial
induction of anaesthesia using a forced air plexus injuries are caused by excessive arm
warming device. abduction or external rotation and can be
prevented by avoiding more than 60° of
Postoperative phase abduction. Common peroneal nerve injuries
are caused by direct pressure on the nerve,
The patient’s temperature should be often with the legs in lithotomy position.
measured and documented on admission to The nerve can be compressed against the
the recovery room and then every 15 minutes. neck of the fibula. Injury can be prevented
Ward transfer should not be arranged unless by adequate padding of lithotomy poles. The
the patient’s temperature is 36.0°C or above. radial nerve can damaged by a tourniquet or
If the patient’s temperature is below 36.0°C, misplaced injection in the deltoid muscle.
they should be actively warmed using Injury can be prevented by adequate padding
forced air warming until they are discharged of any tourniquet used.
from the recovery room or until they are
comfortably warm. Haematological problems
in surgery
Prevention of injuries Function and components
of blood
General anesthesia removes many of the
bodies natural protective mechanisms. If Blood has both cellular and fluid
care is not taken, iatrogenic injuries are components. The cellular components make
possible. Many of these injuries can produce up 45% of the volume. The fluid component
lasting disability and can lead to litigation. makes up 55% of the volume.
Recognition of risks and prevention is
essential. Tissues at risk include nerves, eyes, Plasma
teeth and skin.
Plasma is the fluid component. Its normal
Nerve injuries pH is 7.35–7.45. About 90% is water and 10%
is solutes. Solutes include albumin (60%),
The incidence of nerve injuries during globulins (35%), fibrinogen, thrombin,
anaesthesia is unknown. However, in the hormones, cholesterol, nitrogenous wastes,
USA, they account for 15% of postoperative nutrients and electrolytes.
litigation claims. Most are due to careless
Haematological problems in surgery 23
Erythrocytes in haemoglobin, 30% is in ferritin and
haemosiderin and 3% is in myoglobin. Daily
Erythrocytes or red blood cells are biconcave dietary requirements are about 1 mg in a
discs. They are approximately 7.5 µm in man and 3 mg in a woman. An average diet
diameter. They are formed in the bone contains about 15 mg of iron daily, only
marrow and removed from circulation in 5–10% of which is absorbed. Absorption
the spleen and liver. They have no nuclei occurs in the ferrous (2+) form in the upper
or mitochondria. They have a life span of part of small intestine. Erythropoiesis
about 120 days. Normal red cell production occurs in the bone marrow. Iron is carried
requires iron, amino acids, vitamins and to the bone marrow by plasma transferrin.
hormones – erythropoietin. Reticulocytes are Iron is stored bound to ferritin and as
immature red blood cells. They account for haemosiderin.
1–2% of circulating red blood cells. Red cell
production is stimulated by haemorrhage, Ferritin
anaemia, hypoxia and increased oxygen
requirement. Ferritin is a water-soluble protein-iron
complex. It is made up of apoferritin and a
Leukocytes iron-phosphate-hydroxide core. About 20%
of its weight is iron. Synthesis is stimulated by
Leukocytes or white blood cells account for the presence of iron. Iron is in the ferric (3+)
1% of blood volume. They have both nuclei form.
and mitochondria. There are five types of
while blood cells as follows: Haemosiderin
• Neutrophils (40–70%) Haemosiderin is an insoluble protein–iron
• Lymphocytes (20–40%) complex. About 40% of its weight is iron. It is
• Monocytes (4–8%) formed by lysosomal digestion of ferritin.
• Basophils (1%)
• Eosinophils Transferrin
Neutrophils are responsible for phagocytosis Transferrin is a b-globulin that is synthesised
of bacteria. Eosinophils are involved in in the liver. It has a half-life of 8–10 days.
defence against parasites and in immune Each molecule binds two iron atoms and
complex destruction. Basophils release is normally only about 30% saturated.
histamine and produce chemotactic agents. Erythroblasts have transferrin receptors.
Monocytes are the precursors of tissue
macrophages. Lymphocytes are produce Dietary iron
in both lymph nodes and the spleen.
B lymphocytes produce antibodies. T Iron is present in food as ferric hydroxide
lymphocytes are involved in cell-mediated and ferric–protein complexes. Meat and
immunity. NK cells are lymphocytes that are liver are good sources of dietary iron. The
involved in immune surveillance. average Western diet contains 10–15 mg of
iron and 5–10% is absorbed in the duodenum
Platelets and jejunum. Absorption is increased in
pregnancy and iron-deficiency states. In a
Platelets are not true cells. They are fragments normal individual, the daily iron requirement
of cells known as megakaryocytes and are is 1–2 mg per day.
formed in the bone marrow and have a life
span of about 10 days. They have granules Iron absorption
that contain calcium, ADP, serotonin and
platelet derived growth factor. They have an Iron absorption is favoured by acid and
important role in blood coagulation. reducing agents and it is better absorbed
in the ferrous form. The amount of iron
Iron metabolism absorbed is controlled in the epithelial cells.
Excess iron forms ferritin and is shed with
The body contains about 5 g of iron. the cells into the gut lumen. Iron enters the
About 65% of the body’s iron is found plasma in the ferric form.
24 Chapter 2 Perioperative care
Iron transport The diagnosis of iron deficiency can be
based on:
Most iron is transported to the bone marrow
and is used mainly for erythropoiesis. It binds • Reduced haemoglobin (men < 13.5 g/dL,
to transferrin in the portal blood. About 6 g of women < 11.5 g/dL)
haemoglobin are produced each day and this
requires about 20 mg of iron. Total plasma • Reduced mean cell volume (< 76 fL)
iron turns over about seven times per day. • Reduced mean cell haemoglobin (< 27 pg)
• Reduced mean cell haemoglobin
Iron deficiency anaemia
concentration (< 300 g/L)
As the body has a limited ability to absorb • Blood film – microcytic, hypochromic red
iron and excess loss of iron through bleeding
is common, then iron deficiency is the cells
commonest cause of anaemia worldwide. It • Reduced serum ferritin (< 10 mg/L)
results in hypochromic and microcytic red • Reduced serum iron (men < 14 mmol/L,
blood cells. The diagnosis of iron deficiency
is usually straightforward. Determining the women < 11 mmol/L)
cause can be difficult. • Increased serum iron binding capacity
Clinical features (> 75 mmol/L)
The clinical features of iron deficiency
anaemia depend of the rate of onset. If the A diagnostic bone marrow examination is
onset is insidious, then symptoms are often rarely required.
few. The commonest symptoms are lethargy
and dyspnoea. Skin atrophy occurs in Other causes of a hypochromic microcytic
about 30% of patients. Nail changes include anaemia include:
koilonychia (spoon-shaped nails). Patients
may also develop angular stomatitis and • Anaemia of chronic disease
glossitis. Oesophageal and pharyngeal webs • Thalassaemia trait
may be seen. Examination should be directed • Sideroblastic anaemia
to identifying possible underlying causes.
Management
Causes of iron deficiency
The causes of iron deficiency anaemia The management of iron deficiency anaemia
include: relies on identification and management of
the underlying cause and iron replacement
• Increased blood loss – uterine, GI tract, therapy. Oral replacement with ferrous salts
urine is the preferred option. Preparations include
ferrous sulphate, fumarate and gluconate.
• Increased demands – prematurity, growth, They provide approximately 200 mg of iron
child-bearing per day. The side effects of iron supplements
include epigastric pain, constipation and
• Malabsorption – post-gastrectomy, coeliac diarrhoea. Effective treatment should
disease increase the haemoglobin concentration by
1 g/L/day and treatment should continue for
• Poor diet 3 months after a normal haemoglobin level
is achieved. Intravenous iron preparations
Investigation are available on a named patient basis but
The following investigations may be required: severe side effects (e.g. anaphylaxis) may
occur. Injections can result in skin staining
• Full blood count and blood film and arthralgia and should only be used when
examination patients can not tolerate oral preparations.
• Haematinic assays (serum ferritin, vitamin Sickle cell anaemia
B12 and folate)
Pathology
• Faecal occult bloods
• Mid-stream urine Sickle cell anaemia is an autosomal recessive
• Endoscopic or radiological studies of the disease. Normal haemoglobin has two
α and 2 β chains. In sickle cell disease
gastrointestinal tract a single amino acid substitution occurs
on the β chain. Valine is substituted for
Haematological problems in surgery 25
glutamic acid at position 6. Patients who • Intravenous fluids
are homozygous have sickle cell anaemia. • Adequate pain relief often with opiates
Patients who are heterozygous have sickle • Oxygen
cell trait. It is commonly seen in patients of • Early antibiotic therapy if suspected
Afro-Caribbean descent. The resulting Hb S is
less soluble than Hb A. When deoxygenated, infection
haemoglobin undergoes polymerisation
and forms characteristic sickle cells. The Painful crises
abnormal cells result in blockage of small Approximately 60% of patients with sickle
vessels and causes vaso-occlusive events. cell anaemia will have one episode per year.
Sickling may be precipitated by infection, Bony crises result from localised ischaemia.
fever, dehydration, cold or hypoxia. Avascular necrosis may occur. Treatment of
crises involves rest and analgesia. Abdominal
Clinical features crises present with pain, vomiting, distension
Patients with sickle cell anaemia have a and features of peritonism. About 40% of
chronic haemolytic anaemia with a high adolescents with sickle cell anaemia will have
reticulocyte count. They are at increased risk gallstones.
of infection by encapsulated bacteria. Acute
complications include: Anaemia
Worsening anaemia often presents with
• Painful crises tiredness and cardiac failure. It results from
• Worsening anaemia acute splenic sequestration or an aplastic
• Acute chest symptoms crisis. In both situations urgent transfusion
• Symptoms and signs of neurological or may be required.
ocular events Acute chest syndrome
• Priapism Patients present with chest pain, cough, fever
and tachypnoea accompanied by clinical
Investigation and radiological features of consolidation.
The diagnosis can be confirmed by: Chlamydia and Mycoplasma are important
causes of chest infections. Management
• Sickle solubility test requires parenteral antibiotic therapy.
• High performance liquid chromatography
Acute neurological events
Prevention of complications A stroke occurs in approximately 10% of
Patient and parent education of the risks patients before the age of 20 years. All acute
associated with sickle cell anaemia is neurological symptoms require investigation.
important. Patients need to avoid the cold and Acute stroke requires urgent exchange
dehydration. Antibiotic prophylaxis should transfusion.
be considered in children less than 5 years
of age. Usually phenoxymethylpenicillin is Priapism
the antibiotic of choice. Children should be Priapism occurs in about 20% of males
vaccinated with the pneumococcal vaccine. before the age of 20 years. If it lasts for more
than a few hours it can result in impotence.
Patients with sickle cell anaemia are at Blood should be aspirated from the corpora
high-risk of acute sickling complications cavernosa. Intra-cavernosal injection of an a
during general anaesthesia. They require agonist (e.g. phenylephrine) may be of benefit.
careful pre and perioperative management.
Preoperative transfusion may be required to Haemostasis
ensure a haemoglobin of 9–10 g/dL. During
surgery it is essential to avoid dehydration The haemostatic response has three
and hypoxia. Adequate intraoperative and elements:
postoperative pain relief is essential.
• Vasoconstriction
Management of complications • Platelet aggregation
Patients with suspected complications require: • Clotting cascade
26 Chapter 2 Perioperative care
Vasoconstriction Disorders of bleeding
and coagulation
Vasoconstriction occurs as a direct
result of vessel injury. It is enhanced by Coagulation tests
vasoconstricting elements released from
platelets. Pain can also result in reflex Prothrombin time
sympathetic vasoconstriction. The prothrombin time (PT) tests both
the extrinsic and common pathways.
Platelet aggregation Thromboplastin and calcium are added to
the patient’s plasma. The PT is expressed as a
Platelets are formed in the bone marrow ratio known as the International Normalised
from megakaryocytes. They contain the Ratio (INR). It is prolonged in:
contractile proteins actin and myosin. They
have no nucleus but contain endoplasmic • Warfarin treatment
reticulum and a Golgi apparatus that can • Liver disease
produce proteins. They contain mitochondria • Vitamin K deficiency
that can produce ATP and ADP. They can also • Disseminated intravascular coagulation
synthesis prostaglandins and thromboxane
A2. They have a half-life in the blood of 8 to Activated partial thromboplastin time
12 days. The activated partial thromboplastin time
(APPT) tests both the intrinsic and common
In response to tissue damage, platelets pathways. Kaolin is added to the patient
undergo a number of changes. Platelet plasma. It is prolonged in:
aggregation can result in a ‘platelet plug’.
Platelets adhere to damaged endothelium • Heparin treatment
(via von Willebrand factor). Aggregating • Haemophilia and factor deficiencies
platelets release arachadonic acid which is • Liver disease
converted to thromboxane A2 and calcium • Disseminated intravascular coagulation
mediated contraction of actin and myosin • Massive transfusion
results in degranulation. Release of ADP can • Lupus anticoagulant
induce further aggregation and release in a
positive feedback fashion. Thrombin time
The thrombin time tests the common
Clotting cascade pathway. Thrombin is added to patient
plasma. This converts fibrinogen into fibrin it
The clotting cascade has two semi- is prolonged in:
independent pathways (Figure 2.3). The
intrinsic pathway has all of its components • Heparin treatment
within blood. The extrinsic pathway is • Disseminated intravascular coagulation
triggered by extravascular tissue damage • Dysfibrinogenaemia
and is activated by exposure to a tissue
factor. Both pathways result in activation Bleeding time
of prothrombin (Factor II). The final The bleeding time measures capillary
common pathway converts fibrinogen to bleeding. It is prolonged in:
fibrin monomers. Polymerisation of fibrin
monomers results in the formation of long • Platelet disorders
fine strands held together by H-bonds. These • Vessel wall disorders
are then converted into covalent bonds
with stabilisation of the fibrin polymer. The Classification of bleeding disorders
intrinsic pathway is relatively slow (2–6
minutes). The extrinsic pathway is quite fast Bleeding diatheses can arise from disorders
(15 seconds). of the:
• Vessel wall
Haematological problems in surgery 27
The clotting cascade
Intrinsic pathway Prekallikrein C1- inhibitor
Kallikrein HK
HK
XII XIIa Anti- thrombin III
Ca2+
Extrinsic pathway
XI XIa TF
Ca2+ Ca2+
IX IXa VIIa VII
Ca2+
X Xa
Ca2+
Va II IIa Ca2+
Protein S Ca2+ XIII XIIIa
Protein C Fibrinogen Fibrin
Thrombomodulin
Fibrin polymer Fibrin clot
PAI-1, UK, SK, tPA
Plasmin Plasminogen
Figure 2.3 The clotting cascade (HK = High molecular weight kininogen. TF = Tissue factor. PAI-1 =
Plasminogen activator inhibitor-1. UK = Urokinase. SK = Streptokinase. tPA = Tisse plasminogen activator.)
• Platelets clotting disorder but one-third of patients
• Coagulation system have no family history.
A classification of bleeding disorders is shown Clinical features
in Table 2.3. Haemophilia usually presents in childhood
with prolonged haemorrhage after dental
Haemophilia extraction, recurrent haemarthroses or
muscle haematomas. Sub-periosteal
Haemophilia A is due to factor VIII deficiency. haematomas can result in haemophilic
Haemophilia B (Christmas disease) is due to pseudo-tumours. The clinical severity
factor IX deficiency. Haemophilia A affects
about 1 in 10,000 population. It is a sex-linked
28 Chapter 2 Perioperative care
Classification of bleeding disorders
Vessel wall Platelets Coagulation system
Hereditary haemorrhagic Congenital platelet disorders von Willebrand’s disease
telangiectasia Thrombocytopenia Factor VIII, IX deficiency
Ehlers–Danlos syndrome Myeloproliferative disorders Liver disease
Drugs (e.g. steroids) Drugs (e.g. aspirin) Anticoagulants
Sepsis Disseminated intravascular
Trauma coagulation
Vasculitis
Table 2.3 Classification of bleeding disorders
depends on the extent of the clotting factor (vWF). Haemostasis is impaired because of
deficiency. Patients with less than 1% clotting defective interaction between platelets and
factor activity have severe disease with the vessel wall. vWF mediates the adhesion of
life-threatening bleeding. Those with 1–5% platelets to sites of vascular injury and binds
activity have moderate disease with post- and stabilises the procoagulant protein factor
traumatic bleeding. Those with 5–20% activity VIII. Like haemophilia, it usually presents
have mild disease. with skin bruising, nose-bleeds, haematomas
and prolonged bleeding from trivial wounds.
Investigation Diagnosis is based on demonstrating a
Investigation will show the APPT to be deficiency of vWF. Treatment is usually with
prolonged. The PT is normal. The whole desmopressin.
blood coagulation time is prolonged and
Factor VIII levels are reduced. Recombinant factor VIIa
Treatment Factor VIIa is a trypsin-like serine protease.
Bleeding episodes are treated with factor It is an initiator of thrombin generation.
VIII replacement given as either factor VIII It acts via two pathways to activate Factor
concentrate or cryoprecipitate. Bleeding Xa. One pathway is at the site of tissue
is usually well-controlled if the factor VIII injury complexed with Tissue Factor. The
levels are raised to above 20% of normal. other pathway is on the platelet surface
Desmopressin will increase intrinsic factor independent of Tissue Factor. Tissue Factor
VIII levels. About 5-10% of patients develop is found in the subendothelial layer of the
antibodies to factor VIII which renders patients vascular wall and is not normally available
refractory to factor replacement therapy. to complex with Factor VIIa. Following
injury, the subendothelial layer is exposed
von Willebrand’s disease and Tissue Factor can bind to Factor VIIa.
Theoretically both mechanisms localise the
In 1926, Erik von Willebrand described a action of Factor VIIa to the site of trauma.
inherited bleeding disorder in a family from
the Aland Islands off the coast of Finland. Clinical uses
It is due to deficiency or dysfunction of a
protein termed the von Willebrand factor Recombinant Factor VIIa is licensed for use in
haemophiliacs with antibodies to Factor VIII.
Haematological problems in surgery 29
It may also be useful in trauma patients with • Human albumin 25%
massive blood loss. It significantly reduces • Cryoprecipitate
blood transfusion requirements in patients • Clotting factors – Factor VIII/IX
with blunt trauma and may also reduce the • Immunoglobulins
incidence of multi-organ failure.
Blood groups
Disseminated intravascular
coagulation ABO system
The ABO blood groups system consists of
Disseminated intravascular coagulation (DIC) three allelic genes – A, B and O. The A and
is due to widespread intravascular activation B genes control synthesis of enzymes that
of the clotting cascade. It causes a bleeding add carbohydrate residues to cell surface
tendency due to consumption of clotting glycoproteins. The O gene is an amorph and
factors. Patients present with bruising, does not transform the glycoprotein. Six
purpura and oozing from surgical wounds possible genotypes and four phenotypes exist.
and venepuncture sites. Causes include: Naturally occurring antibodies are found in
the serum of those lacking the corresponding
• Severe (usually Gram-negative or antigen. Blood group O is the universal donor.
meningococcal) infection Blood group AB is the universal recipient. A
summary of the ABO blood group system is
• Widespread mucin-secreting metastatic shown in Table 2.4.
adenocarcinoma
Rhesus system
• Hypovolaemic shock Rhesus antibodies are immune antibodies
• Burns requiring prior exposure during transfusion
• Transfusion reactions or pregnancy. About 85% of the population
• Eclampsia are rhesus positive and 90% of rhesus-
• Amniotic fluid embolus negative patients transfused with rhesus-
• Promyelocytic leukaemia positive blood will develop anti-D antibodies.
Investigation Cross matching
Investigation will show the APPT and PT Cross matching of blood requires three stages.
to be increased. Serum fibrinogen levels First, blood grouping is performed when the
will be reduced and fibrin degradation patient’s red cells are grouped for ABO and
products will be increased. There will be a Rhesus antigens. A serum test is performed
thrombocytopenia and Factor V and VIII to confirm the patient’s ABO group. Second,
activities will be reduced. antibody screening is carried out to detect
atypical red cell antibodies in the recipient’s
Management serum. Third, cross matching is performed to
Management of DIC involves fluid test the donor red cells against the patient’s
resuscitation and treatment of the underlying serum.
cause. The clotting abnormalities can
be corrected with fresh frozen plasma, Complications of blood transfusion
cryoprecipitate and platelet transfusion.
Complications of blood transfusion are rare.
Blood transfusion However, when they do occur they can be life-
threatening. They can be classified as early or
Blood products late (Table 2.5).
Blood products available include: Acute haemolytic or bacterial
transfusion reactions
• Whole blood Acute haemolysis or a reaction to bacterial
• Packed red cells contamination of blood can be difficult to
• Granulocyte concentrates
• Platelet concentrates
• Human plasma – fresh frozen plasma
• Plasma protein fraction
30 Chapter 2 Perioperative care
The ABO blood group system
Phenotype Genotype Antigens Antibodies Frequency (%)
O OO O Anti-A & B 46
A AA or AO A Anti-B 42
B BB or BO B Anti-A 9
AB AB AB None 3
Table 2.4 The ABO blood group system
Complications of blood transfusion shortness of breath and rigors. Examination
will show hypotension, oliguria and bleeding
Early from venepuncture sites. Urinalysis may show
Haemolytic reactions (immediate or delayed) haemoglobinuria.
Bacterial infections from contamination
Allergic reactions to white cells or platelets If acute haemolysis is suspected then the
Acute lung injury transfusion should be immediately stopped
Pyogenic reactions and the giving set removed. The unit of blood
Circulatory overload should be rechecked against the patient’s
Air embolism identity. Intravenous crystalloid should
Thrombophlebitis be given. Blood should be taken for a full
Citrate toxicity blood count, plasma haemoglobin, clotting,
Hyperkalaemia blood cultures and repeat grouping. Broad
Clotting abnormalities spectrum antibiotics should be given and the
urine output monitored.
Late
Infections – hepatitis or CMV Anaphylaxis
Iron overload
Immune sensitisation Anaphylaxis usually occurs soon after the
start of a transfusion and may be seen in IgA
Table 2.5 Complications of blood transfusion deficient patients reacting to transfused IgA.
The patient presents with circulatory collapse
differentiate on clinical grounds alone. It and bronchospasm. The transfusion should
may occur after infusion of a small volume be discontinued and the giving set removed.
of incompatible or infected blood and is The airway should be maintained and
associated with high morbidity and mortality. oxygen given. Adrenaline, chlorpheniramine,
In the unconscious patient, bleeding due and salbutamol should be administered.
to DIC may be the only sign. Most ABO If the patient is IgA deficient, any further
mismatched transfusions are due to human transfusion must be carefully planned.
error. The patient feels unwell and agitated.
Symptoms include back pain and pain at the Non-haemolytic transfusion
site of infusion. These may be associated with febrile reaction
Non-haemolytic transfusion febrile reactions
usually occur more than 30 minutes after the
start of a transfusion. Patient feels generally
well but may be shivering. Temperature
is usually less than 38.5°C and the blood
pressure is often normal. The transfusion
should be stopped and the possibility that
this may be a more significant reaction
Haematological problems in surgery 31
considered. The transfusion should be and reduces the risk of immunological
restarted at a slower rate. Consideration transfusion reactions. It also reduces the risk
should be given to the use of paracetamol. of postoperative immunosuppression seen
Hydrocortisone should not be routinely be with allogeneic transfusion. Collection is
used during a transfusion. expensive and time-consuming and it is only
suitable for elective surgery.
Transfusion-related acute lung injury
Intraoperative acute normovolaemic
Transfusion-related acute lung injury haemodilution
occurs following administration of plasma-
containing blood components. It is due With intraoperative acute normovolaemic
to interaction of donor antibodies with haemodilution, whole blood is removed
recipient white cells. The clinical picture at start of the operative procedure. Up to
is similar to the acute respiratory distress 1.5 litres of blood can be collected and
syndrome (ARDS) and occurs 30 minutes replaced with crystalloid or colloid solution.
to several days after transfusion. Clinical Few detrimental effects of acute anaemia
features include fever, cough and shortness have been demonstrated. The blood is
of breath. A chest x-ray shows perihilar stored in theatre at room temperature
shadowing and it should be treated as and it is re-infused during or immediately
ARDS. following surgery. It is cheaper than
predeposit transfusion. There is little risk of
Delayed haemolytic transfusion reaction administrative or clerical error. It is suitable
for elective or emergency surgery at which
Delayed haemolytic transfusion reaction considerable blood loss is anticipated.
occurs 5–10 days after transfusion. The
clinical features are usually minimal. The Intraoperative cell salvage
possibility should be considered if there
is unexplained pyrexia, jaundice or a drop With intraoperative cell salvage, shed blood is
in haemoglobin. Urinalysis may show collected from the operative field. The blood
urobilinogenuria. is anticoagulated with citrate or heparin and
filtered to remove debris and clots. Cells are
Autologous transfusion then washed with saline and concentrated
by centrifugation. The concentrate is
Autologous blood transfusion is the use of then reinfused. Large volumes of blood
the patient’s own blood. It is particularly can be salvaged. Salvaged blood is not
useful in elective surgery and accounts for haemostatically intact as both platelets and
about 5% of all transfusions performed in clotting factors are consumed. It is suitable
the USA. It is less commonly performed for use in cardiac, trauma, vascular and
in the UK. It reduces both the need for obstetric surgery. Its use is contraindicated
allogeneic blood transfusion and the risks of in contaminated operative fields and in the
postoperative complications (e.g. infection, presence of malignancy.
tumour recurrence). The three main
techniques are: Preoperative anaemia
• Predeposit transfusion Tissue oxygenation is dependent on arterial
• Intraoperative acute normovolaemic oxygen content, capillary blood flow and
the position on the oxygen dissociation
haemodilution curve. The haemoglobin concentration
• Intraoperative cell salvage affects all of these factors. Anaemia reduces
arterial oxygen content. Reduced plasma
Predeposit transfusion viscosity increases capillary blood flow.
Increased levels of 2,3 bisphosphoglycerate
For predeposit transfusion, blood collection shifts the oxygen dissociation curve to the
begins 3–5 weeks preoperatively. Between right.
2 and 4 units are often stored. The last unit
is should be collected more than 72 hours
before surgery. Predeposit transfusion
eliminates the risk of viral transmission
32 Chapter 2 Perioperative care
Both anaemia and polycythaemia increase of infection and increase the risk of tumour
postoperative mortality. A perioperative recurrence. If a blood transfusion is required,
haemoglobin concentration of approximately it should be given at least 2 days preoperatively
10 g/dL is ideal. Preoperative transfusion may as blood transfused immediately prior to
induce immunosuppression, increase the risk operation has reduced O2 carrying capacity.
Chapter 3 Postoperative
management and
critical care
Autonomic nervous system At each junction neurotransmitters are
released. The ANS has two divisions that
The autonomic nervous system (ANS) differ in anatomy and function.
controls the body’s internal environment and
is important in the process of homeostasis. Sympathetic nervous system
It controls the heart rate, blood pressure,
digestion, respiration, blood pH and other The sympathetic nerves arise from the
bodily functions. The functions of the thoracic and lumbar regions of the spinal
autonomic nervous system are summarised cord. The preganglionic nerves are short and
in Table 3.1. The control of the ANS is done synapse in paired ganglia adjacent to the
automatically below the conscious level. spinal cord. The adrenal medulla, technically
The hypothalamus has an important role in an endocrine gland, is functionally a
coordinating autonomic function. In the ANS part of the sympathetic nervous system.
there are two nerves between the central Acetylcholine is the neurotransmitter
nervous system (CNS) and the end organ. released from the preganglionic neurones.
The nerve cell bodies for the second nerve Noradrenaline is the neurotransmitter
are organised into ganglia. The ANS effects its released from the postganglionic neurones.
function via neural transmission as follows:
The sympathetic nervous system is the
• Central nervous system ‘fight or flight’ branch of the ANS. Emergency
• Preganglionic nerve situations are handled by the sympathetic
• Ganglion system. The sympathetic system increases
• Postganglionic nerve cardiac output and pulmonary ventilation,
• End organ diverts blood to the muscles, raises blood
glucose and slows down digestion, kidney
Functions of the autonomic nervous system
Eye Sympathetic Parasympathetic
Heart
Bronchioles Iris dilates Iris constricts
Bladder Increased heart rate Decreased heart rate
Bronchodilatation Bronchoconstriction
Intestine Sphincter constricts Sphincter dilates
Detrusor muscle relaxes Detrusor muscle constricts
Rectum Secretions decrease Secretions increase
Motility decreases Motility increases
Sphincter relaxes Sphincter constricts
Muscle wall contracts Muscle wall relaxes
Table 3.1 Functions of the autonomic nervous system
34 Chapter 3 Postoperative management and critical care
filtration and other functions not needed are found in autonomic ganglia. These
during emergencies. The adrenal medulla receptors are different to the nicotinic
behaves like a combined autonomic receptor found in neuromuscular junctions.
ganglion and postsynaptic sympathetic Muscarinic types are found on all organs with
nerve, It releases both adrenaline (80%) and parasympathetic innervation.
noradrenaline (20%).
Pain
Parasympathetic
nervous system Pain is an unpleasant sensory and emotional
experience associated with potential or actual
The parasympathetic nerves arise from tissue damage. It is a complex interaction of
the cranial and sacral regions of the CNS. sensory, emotional and behavioural factors.
The cranial nerves involved are III, VII, IX, Stimuli activate the nociceptive system
X. They have long preganglionic nerves which then conveys the information to the
which synapse at ganglia near or on the brain by an adaptable pathway. Pain is only
organs innervated. Acetylcholine is the experienced in the conscious brain.
neurotransmitter released from both the
pre- and postganglionic neurones. Types and physiology of pain
The parasympathetic nervous system is Somatic pain
the ‘rest and digest’ branch of the ANS. The
parasympathetic system promotes normal First pain
maintenance of the body. It increases First or ‘fast’ pain is a protective response
secretions and mobility of different parts which allows rapid withdrawal from a painful
of the digestive tract. It is also involved in stimulus. It occurs due to stimulation of high
urination and defecation. threshold thermo/mechanical receptors. The
information is transmitted by fast myelinated
Autonomic receptors A fibres. They enter the dorsal horn of
the spinal cord. Secondary fibres in the
There are multiple types of receptors in spinothalamic tract transmit the stimulus to
the autonomic nervous system. For the the posterior thalamic nuclei. Tertiary fibres
sympathetic system the major receptor transmit the stimuli to somatosensory post-
types are a and b receptors. These are central gyrus.
subdivided into α-1, α-2, β-1 and β-2. The
parasympathetic system has nicotinic and Secondary pain
muscarinic receptors. Secondary or ‘slow’ pain is responsible
for the delayed sensation of pain. It elicits
Receptors subtypes are not evenly behaviour to protect damaged tissue. It
distributed throughout the body. The initiates reflex responses such as tachycardia,
sympathetic and parasympathetic systems hypertension and increased respiratory rate.
often have opposing actions on the same organ. It is due to stimulation of high threshold
polymodal receptors. They respond
Adrenergic receptors are usually to mechanical, thermal and chemical
stimulated by noradrenaline or adrenaline. stimuli. The information is transmitted by
The α-1 receptor is found in the smooth slow unmyelinated C fibres which enter
muscle of arterioles and in the sphincter the dorsal horn. Secondary fibres in the
muscles of the gastrointestinal tract and palaeo-spinothalamic tract transmit the
bladder. The α -2 receptor is found in stimuli to the medial thalamic nuclei.
presynaptic nerves and other parts of the Collateral fibres transmit the stimulus to the
gastrointestinal tract. The β-1 receptor is the midbrain, medullary reticular formation
dominant type in the heart. The β-2 receptor and hypothalamus. Further information is
is found in the bronchioles of the lung and the transmitted to the forebrain limbic system.
muscles of the bladder.
Cholinergic receptors are usually
stimulated by acetylcholine. Nicotinic types
Pain 35
Visceral pain Postoperative pain control
There are fewer visceral nociceptors than Pain is a complex process influenced by both
somatic receptors and cortical mapping is physiological and psychological factors.
less concentrated. Therefore, visceral pain Management of postoperative pain has
is poorly localised. Visceral pain is also generally been shown to be inadequate.
qualitatively different due to progressive Adverse effects of postoperative pain include:
stimulation and summation. It may also be
referred to a site away from the source of • Respiratory – reduced cough, atelectasis,
stimulation. sputum retention and hypoxaemia
Physiology • Cardiovascular – increased myocardial
oxygen consumption and ischaemia
Peripheral activation
Most pain originates following tissue damage. • Gastrointestinal – decreased gastric
It is due to the local release of inflammatory emptying, reduced gut motility and
mediators. The mediators involved include: constipation
• Leukotrienes D4 and B4 • Genitourinary – urinary retention
• Bradykinin • Neuroendocrine – hyperglycaemia, protein
• Histamine
• 5HT catabolism and sodium retention
• Musculoskeletal – reduced mobility,
They activate or sensitise high threshold
nociceptors and results in primary pressure sores and increased risk of
hyperalgesia. venous thrombosis
• Psychological – anxiety and fatigue
Spinal level activation
Spinal level activation occurs in the Assessment of pain
dorsal horn of spinal cord. It is a complex
interaction between excitatory and inhibitory Pain is a subjective experience. Observer
interneurones. It also involves descending assessment of patient behaviour is unreliable.
inhibitory tracts in the spinal cord. The Pain should be assessed and recorded by
gate control theory (Figure 3.1) explains visual analogue scales, verbal numerical
the non-linear relation between injury reporting scale and categorical rating scales.
and response. It suggests that pain can
be ‘gated-out’ in the dorsal horn by other Management of pain
stimuli. The neurotransmitters involved are
excitatory amino acids and neuropeptides. Non-pharmacological methods of pain relief
Some neuropeptides increase nociception include:
(e.g. Substance P, bombesin, VIP). Other
neuropeptides reduce nociception (e.g. • Preoperative explanation and education
galanin, somatostatin, GABA). • Relaxation therapy
• Hypnosis
Supraspinal level activation • Cold or heat
Perception of pain is associated with activity • Splinting of wounds, etc.
in the thalamus and the primary and • Transcutaneous electrical nerve
secondary cortex. Various regions of the brain
are involved with descending inhibition. stimulation (TENS)
The stimuli originate at level of cortex and
thalamus and are mediated via relays in the Pharmacological methods of pain relief
brainstem and dorsal columns to the dorsal include:
horns. The mediators involved include
noradrenaline, 5HT and endogenous opioids. • Simple analgesia
• Non-steroidal anti-inflammatory agents
• Opiates
• Local anaesthetic agents
Simple analgesia
Paracetamol is a weak anti-inflammatory
agent. It modulates prostaglandin production
in the central nervous system. It can be
administered orally, intravenously or rectally.
It is best taken on a regular rather than ‘as
36 Chapter 3 Postoperative management and critical care
The gate control theory of pain Figure 3.1 The gate control theory
of pain
Spinal cord Ascending
pathways
Inhibitory
descending pathway
Fast Aβ fibres
Pain
Pain gate
Slow C fibres Inhibitory
spinal neuron
Aβ
fibres
Touch
required’ basis. Overdose results in hepatic is a prodrug rapidly hydrolysed to morphine
necrosis. It is often used in combination with and 6-monoacetyl-morphine. It is more lipid
weak opiates (e.g. dihydrocodeine). soluble than morphine with greater central
effects. Both act on µ receptors in the brain
Non-steroidal anti-inflammatory agents and spinal cord. µ 1 receptors are responsible
Non-steroidal anti-inflammatory agents for analgesia. µ 2 receptors are responsible
inhibit the enzyme cyclo-oxygenase. They for respiratory depression. The side effects
reduce prostaglandin, prostacyclin and of opiates include sedation, nausea and
thromboxane production. They also have a vomiting, vasodilatation and myocardial
weak central analgesic effect. They are often depression, pruritus, delayed gastric
used for their ‘opiate sparing’ effects. Side emptying, constipation and urinary retention.
effects include gastric irritation and peptic
ulceration, precipitation of bronchospasm in Morphine can be administered by several
asthmatics, impairment of renal function and routes. Intramuscular administration
platelet dysfunction and bleeding. produces peaks and troughs in both plasma
levels and pain relief. Subcutaneous infusion
Opiates is useful for chronic pain relief, particularly in
The most commonly used opiates are chronic pain and palliative care. Intravenous
diamorphine and morphine. Diamorphine injection is reliable but can produce both
sedation and respiratory depression. With