Pain 37
patient-controlled analgesia (PCA), morphine can be increased to 2 hours. The main toxicity
is administered intravenously but the patient is on central nervous and cardiovascular
determines their own analgesic requirement. systems. Plain lignocaine should be used for
A ‘lock-out’ period prevents accidental local anaesthesia in digits and appendages
overdose. It is a safe means of administration as adrenaline containing solutions can cause
as sedation occurs before respiratory tissue ischaemia.
depression.
Bupivacaine
Lipid soluble opiates (e.g. fentanyl) can
be used for spinal or epidural injection/ Bupivacaine is chemically related to
infusion. They produces good analgesia lignocaine but has a more prolonged onset
with reduced risk of side effects. Intrathecal and longer duration of action. It acts for 6–8
morphine administration is an attractive hours. Like lignocaine its main toxicity is
analgesic technique since the opioid is on the central nervous and cardiovascular
injected directly into the cerebrospinal fluid, systems. Its duration of action can also be
close to the structures of the central nervous prolonged by the addition of adrenaline
system where the opioid acts. The procedure
is simple, quick, and relatively low-risk. Spinal and epidural anaesthesia
Respiratory depression is however a major
safety concern. Spinal anaesthesia is the administration
of local anaesthetic or opiate into the
Local and regional anaesthesia cerebrospinal fluid (CSF) below the
termination of the spinal cord at L1. Epidural
Local anaesthetic agents act by reducing anaesthesia is the use of local anaesthetic or
membrane permeability to sodium. They opiate administration into the fatty epidural
act on the small unmyelinated C fibre before space. A single bolus dose, can produce good
large A fibres. Therefore, they reduce pain and anaesthesia for several hours. The use of
temperature sensation before touch and power. both requires an experienced anaesthetist
as complications are common and can be
Lignocaine life-threatening (Table 3.2). The quality of the
block is often better with a spinal anaesthetic.
Lignocaine is a weak base. At physiological Contraindications to spinal or epidural
pH, it is mainly ionised. It has a rapid onset anaesthesia are pre-existing neurological
but short duration of action. With the disease, known coagulopathy and sepsis.
addition of adrenaline, the duration of action
Complications of spinal and epidural anaesthesia
Immediate Characteristic Spinal Epidural
Early
Hypotension Common Less common
local anaesthetic toxicity Rare Occasional
High blockade Occasional Occasional
Urinary retention Common Less common
Headache 1–5% Never unless dural puncture
Local infection Almost never Uncommon
Meningism Uncommon Very rare
Epidural haematoma Almost never Very rare
Backache Common Common
Table 3.2 Complications of spinal and epidural anaesthesia
38 Chapter 3 Postoperative management and critical care
Postoperative epidural infusions Postoperative nausea
and vomiting
Postoperative epidural analgesia attenuates
the postoperative stress response, improves Postoperative nausea and vomiting
postoperative pain control, reduces the (PONV) may be the most unpleasant
incidence of postoperative pulmonary memory associated with a patient’s surgical
complications and allows the more rapid experience. PONV is common and in adults
return of gastrointestinal function. When its incidence has been estimated to be
used as part of an enhanced recovery approximately 25%. Prolonged vomiting can
programme it can shorten hospital stay. result in electrolyte imbalance, dehydration
and may prolong hospital stay. PONV can
Opioid alone epidurals allow opioid be induced by many physiological and
analgesia without sedation. There is no pathological factors, including drugs.
motor or sympathetic blockade. However
the quality of analgesia can be variable. Itch Nausea and vomiting is primarily
is a common side effect. Serious respiratory controlled by the vomiting centre. It is
depression can occur after stopping the located in the dorso-lateral reticular
infusion. formation of the medulla. This is an area
in the brainstem that integrates neural
Local anaesthetic alone epidural responses. Afferent stimuli arrive from
infusions have the potential for complete chemoreceptors and pressure receptors in
anaesthesia. They have no sedative effects the gut, from the CNS and from peripheral
or respiratory depression. However, pain receptors. Other sites of input include
sympathetic and motor blockade are the cerebral cortex, vestibular and cerebellar
common. Cardiovascular side effects can nuclei. Efferent impulses from this area
occur and the block occasionally is patchy influence other related brainstem nuclei
or unilateral. A combination of local including the chemoreceptor trigger zone
anaesthetic and opioid allows for synergy (CTZ). This is located in the area postrema
between the two mechanisms of action and of the 4th ventricle and is outside the blood–
the doses of both drugs can be reduced. brain barrier. The afferent and efferent
connections to the vomiting centre and CTZ
Hypotension are summarised in Figure 3.2.
The sympathetic outflow from the spinal cord Dopamine and 5-HT play an important
occurs between T1 and L2. It is blocked to role in the activity of the CTZ. 5-HT has an
varying degrees in both spinal and epidural important role in drug-induced emesis and
anaesthesia. The higher the block the greater 5-HT3 receptors appear to be an important
the degree of sympathetic blockade. In part in the mediation of nausea and vomiting
hypovolaemic patients, there is a greater risk induced by high doses of cytotoxic agents.
of hypotension. Hypotension during spinal Other neurotransmitters implicated in the
and epidural anaesthesia usually requires control of nausea and vomiting include
fluid resuscitation. acetylcholine and dopamine. Hence
anti-emetics act as antagonists to one or
Post spinal headache more of these neurotransmitters. These
include domperidone, metoclopramide,
A headache follows about 2% of spinal prochlorperazine, cyclizine, hyoscine and
anaesthetics and is usually due to a CSF leak. ondansetron. There is now great interest in
In most patients is settles after about 3 days. the use of combinations of anti-emetics to
The headache is characteristically occipital increase efficacy. There is increasing evidence
and is worse on standing and relieved by that combinations of different classes of
lying down. Initial treatment is with bed rest, antiemetics show improvements over
simple analgesia and fluids. If it persists, monotherapy.
a ‘blood-patch’ may be required when the
patient’s own blood is injected into epidural
space to seal the leak.
Metabolic and nutritional support 39
The afferent and efferent connections to the vomiting centre and chemoreceptor trigger zone
Higher centres
Vestibular input
Chemoreceptor trigger zone
• dopamine receptor D2
• 5 -hydroxtriptamine
receptor 5- HT3
Vomiting centre
• histamine receptor H1
• muscarinic acetylcholine receptor
• 5-hydroxytriptamine receptor 5- HT2
Peripheral circulation Vagal afferents
Figure 3.2 The afferent and efferent connections to the vomiting centre and chemoreceptor trigger zone
Metabolic and nutritional Maintenance requirements
support
Fluid and electrolyte Daily maintenance fluid requirements vary
management between individuals. For a 70 kg male it is
about 3 litres of water, 120 mmol sodium
For the ‘average’ 70 kg man, the total body and 70 mmol potassium. For a 40 kg
water is 42 litres. This represents about 60% woman it is 90 mmol sodium and 40 mmol
of the body weight. This is made up of 28 potassium. The daily maintenance fluid
litres in the intracellular and 14 litres in the requirements for children can be estimated
extracellular compartments. The plasma as follows:
volume is 3 litres and the extravascular
volume is 11 litres. The total body sodium • 0–10 kg is 100 mL/kg
is 4200 mmol of which 50% is in the • 10–20 kg is 1000 mL + 50 mL/kg for each kg
extracellular fluid compartment. The total
body potassium is 3500 mmol of which only more than 10
about 50 mmol is in the extracellular fluid • More than 20 kg is 1500 mL + 25 mL/kg for
compartment. The normal osmolality of
extracellular fluid is 280–295 mosmol/kg. each kg more than 20
When calculating fluid replacement for a
patient, it is necessary to consider: Pre-existing and on-going losses
• Maintenance requirements Pre-existing and ongoing losses can be rich in
• Pre-existing and ongoing losses electrolytes. Most ‘surgical ‘ pre-existing and
• Insensible losses ongoing losses are rich in sodium and should
be replaced with 0.9% saline. They include:
• Vomit and diarrhoea
• Nasogastric aspirate
• Stoma, drain and fistula output
40 Chapter 3 Postoperative management and critical care
Insensible losses They reduce plasma viscosity, reduce platelet
aggregation and have a risk of anaphylaxis.
Insensible losses occur via faeces (100 mL/ Gelatins are polydispersed polypeptides
day), the lungs (400 mL/day) and skin with a molecular weight of about 35 kDa.
(600 mL/day). Total insensible losses are They are rapidly lost from vascular space.
usually about 1 litre per day. Hydroxyethyl starch is a polydispersed
synthetic polysaccharide polymer derived
Fluid replacement therapy from amylopectin with a molecular weight in
the range 50 to 450 kDa. The large molecules
Fluids can be replaced with crystalloid are engulfed by the reticuloendothelial
or colloid solutions. There is no evidence system and their use may be associated with a
from RCTs that resuscitation with colloids bleeding diathesis.
reduces the risk of death, compared to
resuscitation with crystalloids, in patients Assessment of adequacy of
with trauma, burns or following surgery. resuscitation
Crystalloids are cheaper and are more
widely used. Clinical assessment and observations
will provide a rough guide to the need for
Crystalloids resuscitation. Tachycardia, hypotension and
reduced skin turgor are signs of dehydration.
The composition of different crystalloid In most situations, urine output is a good
solutions vary (Table 3.3). Normal saline estimate of the degree of hypovolaemia with
contains only sodium and chloride. oliguria defined as a urine output of less than
Hartmann’s solution has less chloride 0.5 mL/kg/hr. If doubt remains, then invasive
but also contains potassium, bicarbonate monitoring with an assessment of central
and calcium. Dextrose saline contains venous pressure may be required.
significantly less sodium and chloride in
relation to its volume than normal saline. The response of the urine output or central
venous pressure to a fluid challenge can be
Colloids used to assess the adequacy of resuscitation.
A fluid challenge should be regarded as a
Colloids can be either monodispersed with 200–250 mL bolus of colloid, administered
all molecules of similar molecular weight as quickly as possible. A response in the
or polydispersed with molecules having a central pressure or urine output should be
spread of molecular weights. The properties seen within minutes. A rapid rise followed
of commonly used colloid solutions is shown by a prompt fall suggests hypovolaemia. A
in Table 3.4. Albumin is monodispersed, rapid rise that is maintained suggests good
has a long half life and accounts for 60–80% intravascular volume replacement. The size
of normal plasma oncotic pressure. It has and duration of the response rather the actual
no adverse effect on coagulation. Dextrans values recorded are more important.
are polydispersed polysaccharides with a
molecular weight in the range of 10 to 90 kDa.
The composition of crystalloid solutions
Sodium (mmol/L) Hartmann’s Normal saline Dextrose saline
Chloride (mmol/L)
Potassium (mmol/L) 131 150 30
Bicarbonate (mmol/L) 111 150 30
Calcium (mmol/L) Nil Nil
5 Nil Nil
29 Nil Nil
2
Table 3.3 The composition of crystalloid solutions
Metabolic and nutritional support 41
The properties of colloid solutions
Gelatins (Haemaccel) Volume effect (%) Molecular weight (kDa) Half-life
4% Albumin 80 35 2–3 hours
Dextran 70 100 69 15 days
6% Hydroxyethyl starch 120 41 2–12 hours
100 70 17 days
Table 3.4 The properties of colloid solutions
Techniques of venous access • Seldinger technique
• Surgical cutdown
Peripheral venous access is required for
administration of fluids and drugs. Central Seldinger technique
venous access is required for parenteral
nutrition, monitoring of central venous There are four steps to the Seldinger
pressure, cardiac pacing and in patients with technique:
difficult peripheral access.
• Venepuncture is performed with an
Anatomy of venous access introducer needle
Central venous access can be via either the • A soft tipped guide wire is passed through
internal jugular or subclavian veins. The the needle and the needle removed
internal jugular vein is used more often and
right-sided access is preferred as the apical • A dilator is passed over the guide wire
pleura does not rise as high on the right and • The dilator is removed and the catheter is
it also avoids the thoracic duct found on the
left. The patient is positioned head down. passed over wire which is then removed
In the low approach, the triangle formed by
the two heads of sternomastoid and clavicle After insertion, a chest x-ray should be
is identified and the cannula is aimed down performed to check the position of catheter.
and lateral towards ipsilateral nipple. The Early complications of central venous
subclavian vein is usually approached from catherisation include:
below clavicle. The patient is positioned
head down. The needle is inserted below • Haemorrhage
the junction of medial two-third and lateral • Air embolus
one-third of the clavicle. The needle is aimed • Pneumothorax
towards the suprasternal notch, passing • Cardiac arrhythmias
immediately behind clavicle. The vein is • Pericardial tamponade
encountered after 4–5 cm. • Failed cannulation
Techniques Late complications of central venous
catherisation include:
Aseptic techniques should be used for all
cannulations. Local anaesthetic should be • Venous thrombosis
used for central catheters. Both success and • Infection
safety may be improved by using ultrasound
guidance. Techniques of gaining access Approximately 10% of central lines become
include: colonised with bacteria. About 2% of patients
in intensive care develop catheter-related
• Catheter over needle sepsis. Central line infections are usually
• Catheter through needle due to coagulase-negative staphylococcus
infection. They are occasionally due to
Candida and Staphylococcus aureus. The
incidence of infection can be significantly
reduced by aseptic techniques and adequate
care of lines. Closed systems should be used
42 Chapter 3 Postoperative management and critical care
at all times. Dedicated lines should be used be by a surgical gastrostomy or jejunostomy,
for parenteral nutrition. Antimicrobial coating percutaneous endoscopic gastrostomy or
of lines may reduce the risk of infection. needle catheter jejunostomy. Enteral feeding is
often started at a low rate of infusion and then
Venous cutdown increased. Complications of enteral feeding
Venous cutdown is useful for gaining access include malposition and blockage of the tube,
in shocked, hypovolaemic patients. The gastro-oesophageal reflux and feed intolerance.
commonest sites used are the long saphenous
vein at the ankle – 2 cm anterior to medial Parenteral nutrition
malleolus or the basilic vein and at the elbow
– 2.5 cm lateral to the medial epicondyle. At Intestinal failure can be defined as a
both sites, the vein is dissected and ligated reduction in the functioning gut mass to
distally. A small transverse venotomy is made. below the minimum necessary for adequate
The cannula is passed through the venotomy digestion and absorption of nutrients. It is
and secured. a useful concept for assessing the need for
parenteral nutrition which can be given by
Surgical nutrition either a peripheral or central line. Indications
for parenteral nutrition include:
Malnutrition is common in surgical patients
and results in: • Enterocutaneous fistulae
• Moderate or severe malnutrition
• Delayed wound healing • Acute pancreatitis
• Reduced ventilatory capacity • Abdominal sepsis
• Reduced immunity • Prolonged ileus
• Increased risk of infection • Major trauma and burns
• Severe inflammatory bowel disease
Nutritional assessment
Central parenteral nutrition is hyperosmolar
Weight loss of 10% and 30% should be and has a low pH. It is irritant to vessel walls.
regarded as mild and severe malnutrition, Typical feed contains the following in 2.5 L:
respectively. Useful anthropometric
measurements in the assessment of • 14 g nitrogen as L amino acids
nutritional status include triceps skin fold • 250 g glucose
thickness, mid-arm circumference and hand- • 500 mL 20% lipid emulsion
grip strength. • 100 mmol sodium
• 100 mmol potassium
Methods of nutritional support • 150 mmol chloride
• 15 mmol magnesium
Enteral nutrition • 13 mmol calcium
The gastrointestinal tract should be used for • 30 mmol phosphate
nutritional support if it is available. Prolonged • 0.4 mmol zinc
postoperative starvation is not required. Early • Water and fat soluble vitamins
enteral nutrition is associated with reduced • Trace elements
postoperative morbidity. Enteral feeding
prevents intestinal mucosal atrophy and Monitoring of parenteral nutrition
supports the gut-associated immunological
shield. It attenuates the hypermetabolic Feeding lines should only be used for that
response to injury and surgery. It is cheaper purpose. Drugs and blood products should
than parenteral nutrition and has fewer be given via a separate peripheral line or
complications. other channels on a multiple lumen central
line. About 5% of patients on total parenteral
Polymeric liquid diet is made up of nutrition develop metabolic derangement.
short peptides, medium chain triglycerides, Parenteral nutrition should be monitored:
polysaccharides, vitamins and trace elements.
Enteral feed can be taken orally or administered • Clinically – weight
via a nasogastric tube. Long-term feeding can • Biochemically twice weekly
• FBC, U+E, LFT
Postoperative complications 43
• Magnesium, calcium, zinc, phosphate • Chest x-ray
• Nitrogen balance • ECG
• Blood cultures on any sign of sepsis • Arterial blood gases
• Ventilation/perfusion scan
Metabolic complications of parenteral • Abdominal ultrasound or CT scan
nutrition include:
Wound dehiscence
• Hyponatraemia
• Hypokalaemia Wound dehiscence affects about 2% of
• Hyperchloraemia mid-line laparotomy wounds. It is a serious
• Trace element and folate deficiency complication with a mortality of up to 30%.
• Deranged LFTs It is due to failure of the wound closure
• Linoleic acid deficiency technique such as a broken suture, slipped
knot or inadequate muscle bites often in
Postoperative complications the presence of infection. It usually occurs
Postoperative pyrexia between 7 and 10 days after surgery and is
often heralded by a serosanguinous discharge
Pyrexia is a common problem seen after from the wound. Even if the dehiscence only
surgery. The underlying cause can often seems to affect part of the wound, it should be
be identified clinically depending on the assumed that the underlying defect involves
time since operation, the type of surgery the whole of the closure.
undertaken and associated clinical features.
Specific complications often occur at certain Management
times after an operation (Table 3.5). However,
the time scales should be regarded as a rough Opiate analgesia should be given and a
guide and not absolute rules. sterile dressing applied to the wound.
Fluid resuscitation may be required. An
Assessment early return to theatre is necessary and the
Adequate assessment requires a full history and wound should be resutured under general
examination, supplemented by investigations anaesthesia. The optimal technique is
as required. Respiratory complications are controversial. Interrupted or mass closure
often associated with breathlessness, cough with non-absorbable sutures is often
and chest pain. Wound infections may show used. The use of ‘deep tension’ sutures
erythema, purulent discharge or wound is controversial and is regarded by many
dehiscence. Abdominal pain, distension and as being almost obsolete as it is believed
ileus may suggest a collection or anastomotic to strangulate muscle and weaken the
leak. Calf pain and tenderness may suggest a closure. It is also painful and associated with
DVT. Useful investigations may include: increased risk of infection.
Timing of common postoperative complications
First 24 hours 24–72 hours 3–7 days 7–10 days
Systemic response Pulmonary atelectasis Chest infection Deep venous
trauma Chest infection Wound infection thrombosis
Intraperitoneal sepsis
Pre-existing infection Urinary tract infection Pulmonary embolus
Anastomotic leak
Table 3.5 Timing of common postoperative complications
44 Chapter 3 Postoperative management and critical care
Postoperative pulmonary in 15–20% of non-ventilated and 40–60%
complications of ventilated ITU patients. The organisms
responsible for hospital-acquired chest
Postoperative hypoxia infections include:
Postoperative hypoxia occurs due to a lack • Gram-negative bacteria (Pseudomonas
of alveolar ventilation or perfusion. Poor aeruginosa, Enterobacter)
alveolar ventilation can occur as a result of:
• Staphylococcus aureus
• Hypoventilation (airway obstruction, opiates) • Anaerobes
• Bronchospasm • Haemophilus influenzae
• Pneumothorax
• Arteriovenous shunting (collapse, There is no evidence that prophylactic
antibiotics reduce the risk of pneumonia.
atelectasis)
Aspiration pneumonitis
Poor alveolar perfusion can occur as a result of:
Aspiration of gastric contents results in a
• Ventilation–perfusion mismatch chemical pneumonitis. It is most commonly
(pulmonary embolism) seen in the apical segments of the right lower
lobe. If it is unrecognised or inadequately
• Impaired cardiac output treated, it can result in a secondary bacterial
• Decreased alveolar diffusion infection. Secondary infection is usually with
• Pneumonia Gram-negative and anaerobic organisms.
• Pulmonary oedema A chest x-ray of a patient with aspiration
pneumonitis is shown in Figure 3.3.
Atelectasis
Treatment
Hypoxaemia is often seen during the first 48 Immediate treatment of aspiration
hours after most major surgery. It occurs as should involve tilting the head of the
a result of a reduction in functional residual operating table down and sucking out the
capacity. Significant atelectasis is more pharynx. Consideration should be given
often seen in those with pre-existing lung to intubation and endotracheal suction.
disease, in those with upper rather than lower Prophylactic antibiotics should be given.
abdominal incisions, obese patients and There is no evidence that steroids reduce the
cigarette smokers. The basic mechanisms inflammatory response.
leading to atelectasis are an increase in the
volume of bronchial secretions, an increase in Other postoperative
viscosity of secretions and a reduction in tidal complications
volume and ability to cough.
Cardiovascular complications
Clinical features
Atelectasis usually presents as a postoperative Postoperative cardiovascular complications
pyrexia starting at about 48 hours after surgery. include:
It is often accompanied by tachycardia and
tachypnoea. Examination will show reduced • Hypotension
air entry, dullness on percussion and reduced • Hypovolaemia
breath sounds. A chest x-ray may show • Ventricular failure
consolidation and collapse. • Cardiogenic shock
• Arrhythmias
Treatment • Conduction defects
The management of atelectasis involves • Hypertension
intensive chest physiotherapy, nebulised
bronchodilators and appropriate antibiotics Perioperative arrhythmias can occur as result
for a possible associated infection. of:
Pneumonia • Physiological disturbances – acidosis,
hypercapnoea and hypoxaemia
Nosocomial pneumonia occurs in about 1%
of all patients admitted to hospital. It occurs • Electrolyte imbalance
• Vagal manoeuvres
Postoperative complications 45
A chest x-ray of a patient with aspiration pneumonitis Figure 3.3 A chest x-ray of
a patient with aspiration
pneumonitis
• Hypovolaemia Obstruction is the most likely diagnosis when
• Pathological disturbances – myocardial there is anuria.
ischaemia, pulmonary embolus Urinary tract infections
• Pharmacological agents
Approximately 10% of patients admitted to
Postoperative renal failure hospital have a urinary catheter inserted. The
risk of catheter-related infection depends on
Acute renal failure is commonly seen in the the age and sex of the patient, the duration
perioperative period and is associated with a of catheterisation and the indication for its
high morbidity and mortality. It is therefore use. Bacterial colonisation of catheters is
important to either prevent its occurrence or common. If a catheter is required for more
recognise its presence and treat it early. Causes than 2 weeks, 90% of patients will develop
of postoperative renal failure can be classified bacteriuria. The commonest organisms
as prerenal, renal or postrenal (Table 3.6). identified are enterobacter and enterococci.
Colonisation does not require treatment
Renal hypoperfusion from any cause unless the patient is systemically unwell.
makes the kidney concentrate urine, and Infection can be prevented by maintaining
decreases the urine output. Therefore, a closed drainage system, good infection
prerenal failure is not a failure per se but control standards and preventing the
a normal response to inadequate renal backflow of urine from the cather bag.
perfusion. Treating the precipitating
cause may reverse the renal dysfunction. Postoperative confusion
Direct renal injury may occur if there is a
superimposed insult such as exposure to a Postoperative confusion occurs in about 10%
nephrotoxic agent. Postrenal renal failure of postoperative patients. It is associated
occurs when there is obstruction to urine with increased morbidity and morality and
flow anywhere distal to the renal pelvis.
46 Chapter 3 Postoperative management and critical care
Causes of postoperative renal failure
Prerenal Renal Postrenal
Shock (hypovolaemia, Acute tubular necrosis Bladder outflow obstruction
cardiogenic, septic)
Glomerulonephritis Single ureter (calculus, tumour)
Renal artery disease Interstitial nephritis Both ureters (bladder
malignancy)
Table 3.6 Causes of postoperative renal failure
leads to increased duration of hospitalisation. All patients should have a clear diagnostic
Clinical features include a reduced level and monitoring plan documented
of consciousness, impaired thinking and on admission. Prompt recognition of
memory, perceptional abnormalities complications is essential. Patients often
and disturbances of emotion. Causes of require complex management and delay
postoperative confusion include: worsens outcome. Adequate and prompt
access to emergency operating theatres is
• Hypoxia – respiratory disease, cardiac essential.
failure, arrhythmia
The seniority of the staff involved a the
• Trauma – head injury patients management should be guided by a
• Infection – intracranial, extracranial risk assessment. High-risk surgical patients,
• Neoplasia – primary and secondary with a predicted hospital mortality of more
than 5% should have direct diagnostic, surgical,
cerebral tumours anaesthetic and critical care consultant input.
• Vitamin deficiency – thiamine (Wernicke Surgical procedures with a predicted mortality
of more than 10% should be performed under
encephalopathy), B12 deficiency the direct supervision of both a consultant
• Endocrine – hypothyroidism, surgeon and anaesthetist. Each patient should
have their risk of death re-assessed at the
hyperthyroidism, Addison’s disease end of surgery and the optimum location for
• Degenerative postoperative care determined. All high-risk
• Vascular – CVA, TIAs patients should be admitted to critical care.
• Drugs
• Metabolic derangement Outreach services
Principles of intensive care Outreach services are an essential component
of critical care services and have three
High-risk surgical patients essential objectives:
There is growing concern that high-risk • To assess potential admissions
surgical patients receive sub-optimal care • To enable discharges
which has important implications for both • To share critical care skills
the patient and the health economy. In the
UK, 170,000 patients undergo high-risk They often use Early Warning Scoring (EWS)
non-cardiac surgery each year. Of these, systems to identify sick patients, based on
100,000 will develop significant complications assessment of physiological dysfunction
resulting in 25,000 deaths. Each year, which trigger a clinical response. Various
emergency general surgical patients account validated early warning systems have been
for 14,000 admissions to intensive care in developed based on:
England and Wales and this group of patients
has a mortality rate of 25%. • Heart rate
• Blood pressure
It is important that hospitals formalise
pathways for unscheduled surgical care.
Principles of intensive care 47
• Respiratory rate • Cardiac – ECG and inotropic drugs
• Temperature • Hepatic – blood transfusion
• Conscious level • Neurological – intracranial pressure
Each observation is given a score. A normal monitoring
observation is scored zero. The greater the
physiological derangement the higher the Factors to be considered when assessing
score (Table 3.7). The sum of all parameters admission to ICU include:
scored gives a global ESW which should be
acted on as follows: • Diagnosis
• Severity of illness
• Low score – increased frequency of • Age
observation • Coexisting disease
• Physiological reserve
• Medium score – request appropriate • Prognosis
medical review • Availability of suitable treatment
• Response of treatment to date
• High score – request critical care • Recent cardiopulmonary arrest
assessment • Anticipated quality of life
• The patient’s wishes
Criteria for intensive care assessment include:
Sepsis and SIRS
• Threatened airway
• Respiratory arrest Sepsis is a clinical syndrome that complicates
• Respiratory rate more than 40 or less than severe infection. It is characterised by the
cardinal signs of inflammation occurring
8 breaths/min in tissues that are remote from the site
• Oxygen saturation less than 90% on more of infection. The systemic inflammatory
response syndrome (SIRS) is an identical
than 50% oxygen clinical syndrome that can arise from a
• Cardiac arrest number of aetiological triggers including:
• Pulse rate less than 40 or more than140
• Sepsis – bacterial, viral, fungal
beats/min • Hypovolaemic shock
• Systolic blood pressure less than 90 mmHg • Trauma
• Sudden fall in level of consciousness • Burns
• Repeated or prolonged seizures • Tissue ischaemia
• Rising arterial carbon dioxide tension with • Pancreatitis
respiratory acidosis Both sepsis and SIRS response can lead to
the multiple organ dysfunction syndrome
The indication for admission to ICU is
support of organ function including:
• Respiratory – ventilation/CPAP
• Renal – haemofiltration/haemodialysis
Physiological variables and scores of an early warning system
Heart rate (beats/min) 3 2 1 0 1 2 3
Mean BP (mmHg) < 70 < 40 41–50 51–100 101–110 111–130 > 130
Respiration rate 71–80 81–100 101–199
(breaths/min) < 8 15–20 > 200 > 30
Temperature 9–14 21–29
Consciousness level < 35 35.1–36.5 36.6–37.4 > 37.5
Awake Respond Respond No
to voice to pain response
Table 3.7 Physiological variables and scores of an early warning system
48 Chapter 3 Postoperative management and critical care
(MODS), which is the cause of the high • Interleukin-6
mortality associated with these syndromes. • Interleukin-8
The definitions of bacteraemia, SIRS, sepsis • Interleukin-10
and septic shock are shown in Table 3.8.
Clinical features
Bacterial infection is the commonest cause The cardiorespiratory effects include:
of sepsis with 50% and 40% of cases due to
Gram-negative and Gram-positive organisms, • Increased cardiac output
respectively. The incidence of both sepsis and • Decreased vascular resistance
SIRS is increasing as a result of advancing age, • Increased oxygen consumption
immunosuppression and multidrug-resistant • Fever or hypothermia
infection. Despite improvements in critical • Tachycardia
care, the mortality from SIRS, sepsis, severe • Tachypnoea
sepsis, and septic shock is 5%, 15%, 20%, and
50% respectively. The metabolic or haematological effects
include:
Pathophysiology
• Respiratory alkalosis
Sepsis and SIRS usually arises as a result of • Deranged liver function
failure of control of the inflammatory response. • Deranged renal function
The over-production of inflammatory • Altered white cell count and platelets
mediators, the under-production of anti- • Disseminated intravascular coagulation
inflammatory mediators and receptor
abnormalities appear to be important in Severe sepsis
both initiation and propagation of the
response. There is decreased destruction of Severe sepsis refers to sepsis plus at least one
inflammatory mediators and the production of of the following signs of hypoperfusion or
abnormal leukocytes. The major inflammatory organ dysfunction:
mediators involved in SIRS are:
• Areas of mottled skin
• Platelet activating factor • Capillary refilling requires 3 seconds or
• Tumour necrosis factor-a
• Interleukin-1 longer
• Urine output < 0.5 mL/kg for at least one
hour
• Lactate > 2 mmol/L
The definitions of SIRS, sepsis and septic shock
Bacteraemia Definition
SIRS
The presence of viable bacteria in the bloodstream
Sepsis
Severe SIRS The systemic inflammatory response to a variety of clinical insult manifest by
Septic shock two or more of the following:
Temperature > 38°C or < 36°
Heart rate > 90 bpm
Respiratory rate > 20 breaths per minute or PaCO2 > 4.3 kPa
White cell count > 12,000 or < 4000 per mm3
SIRS with documented infection
SIRS with documented infection and hypoperfusion, hypotension and organ
dysfunction
Sepsis with hypotension despite adequate fluid resuscitation
Table 3.8 The definitions of systemic inflammatory response syndrome (SIRS), sepsis and septic shock
Principles of intensive care 49
• Abrupt change in mental status the onset of hypotension increases the
• Abnormal electroencephalographic mortality associated with sepsis three-fold.
findings Respiratory support
• Platelet count < 100,000 platelets/mL
• Disseminated intravascular coagulation Oxygen delivery depends on:
• Acute lung injury or acute respiratory
• Cardiac output
distress syndrome (ARDS) • Haemoglobin concentration
• Cardiac dysfunction as defined by • Arterial oxygen saturation (SaO2)
• Arterial oxygen tension (PaO2)
echocardiography or direct measurement
of the cardiac index Pulse oximetry
MODS refers to progressive organ dysfunction Arterial oxygen saturation can be measured
in an acutely ill patient, such that homeostasis non-invasively using pulse oximetry. It
cannot be maintained without intervention. consists of two light emitting diodes of two
It is at the severe end of the severity of illness different wavelengths. The frequencies are
spectrum of both SIRS and sepsis. MODS in the red (660 nm) and infrared (940 nm)
can be classified as primary or secondary. spectrum. The monitor has one photodetector.
Primary MODS is the result of a well-defined The absorption spectrum of haemoglobin at
insult in which organ dysfunction occurs the two frequencies depends on the degree
early and can be directly attributable to of oxygenation and this allows calculation of
the insult itself. Secondary MODS is organ the oxygen saturation. The arterial component
failure that is not in direct response to the of the circulation is targeted by restricting
insult itself, but is a consequence of the host’s analysis to the signal that is pulsatile. Pulse
response. oximetry readings can be unreliable if there is:
Management • Intense vasoconstriction
• Jaundice
In the management of severe sepsis there are • Methaemoglobinaemia
two priorities:
Respiratory failure
• Prompt assessment and resuscitation
• Early control the source of sepsis Respiratory failure is used to describe
inadequate gas exchange with the result that
Prompt assessment has been aided by the arterial oxygen and/or carbon dioxide levels
development and uses of EWS systems. Blood cannot be maintained within their normal
should be taken for culture and measurement ranges. A fall in blood oxygenation is known
of the serum lactate. Oxygen, intravenous as hypoxaemia. A rise in arterial carbon
fluids and broad-spectrum antibiotics should dioxide levels is called hypercapnia. Patients
be administered. The effect of resuscitation with hypoxaemic respiratory failure (type 1)
should be closely monitored. These actions have reduced PaCO2 and reduced PaO2 and
can be summarised in the ‘sepsis six’: those with ventilatory respiratory failure (type
2) have increased PaCO2 and reduced PaO2.
• High flow oxygen Hypoxaemic failure can result from:
• Blood cultures
• Intravenous antibiotics within 1 hour • Low inspired oxygen partial pressure
• Fluid resuscitation • Alveolar hypoventilation
• Measurement of lactate and haemoglobin • Diffusion impairment
• Catheterise and monitor urine output • Ventilation to perfusion mismatch
• Right-to-left shunt
The control of sepsis in surgical patients often
requires radiological or surgical intervention. Ventilatory failure can result from:
This can be determined by the appropriate
use of radiological procedures. There is • Abnormalities of central respiratory drive
a progressive deterioration in outcome • Neuromuscular dysfunction
associated with increasing delay to source • Abnormalities of the chest wall
control. A delay of more than 12 hours after
50 Chapter 3 Postoperative management and critical care
• Abnormalities of the airway • Impaired venous return
• Abnormalities of the lung • Sodium and water retention
• Bronchopneumonia
Artificial ventilation
Acute respiratory distress
Artificial ventilation eliminates carbon syndrome
dioxide and improves oxygenation by
reducing respiratory work and oxygen Acute respiratory distress syndrome (ARDS)
consumption, administering a higher was first recognised in the 1960s. It was
inspired oxygen content (FiO2) and initially termed ‘adult’ respiratory distress
preventing or reversing atelectasis. syndrome but it is seen in both children and
adults. It occurs following many different
Indications for tracheal intubation include: inflammatory insults to the lungs. The causes
of ARDS are shown in Table 3.9.
• Facilitation of mechanical ventilation
• Protection from aspiration Pathology
• Facilitation of tracheobronchial suction Irrespective of the aetiology, the main
• Relief of upper airway obstruction pathological feature is diffuse alveolar damage.
Endothelial injury results in increased
Indications for mechanical ventilation permeability. Protein-rich exudate is found in
include: the alveoli. Neutrophils appear to be important
in the inflammatory process. Cytokines and
• Support in respiratory failure enzymes may be responsible for many of the
• Coma (head injury, drug overdose) features. Resolution of inflammation can occur
• Control of intracranial pressure but is usually associated with some degree of
• Reduction of metabolic demands pulmonary fibrosis.
• Allow muscle relaxation and facilitate
Clinical features
surgery ARDS is usually a progressive clinical
• Postoperative ventilation problem presenting with acute respiratory
failure. The hypoxaemia is often refractory
Most ventilators are volume/time-cycled with to increasing respiratory support. Lung
a pressure limit. They deliver a preset tidal compliance is reduced and hypoxaemia
volume irrespective of lung compliance. The persists. Resolution can occur and lung
pressure limit reduces the risk of over-inflation. function can return to normal. Overall
Possible modes in which they can be used are: mortality is approximately 50%.
• Controlled mechanical ventilation Diagnosis
• Assisted controlled or triggered ventilation Two conditions are now recognised, acute
• Intermittent mandatory ventilation lung injury (ALI) and ARDS. Both consist
• Pressure support of an acute lung injury with bilateral
pulmonary infiltrates on chest x-ray, a
Variables on a ventilator that can be preset or pulmonary capillary wedge pressure of less
altered include: than 18 mmHg and no evidence of left atrial
hypertension. In ALI the PaO2/FiO2 is less than
• Tidal volume 200 and in ARDS the PaO2/FiO2 is more than
• Ventilation rate 300.
• Inspiratory to expiratory ratio
• Flow waveform Management
• Partial pressure of inspired oxygen Supportive intensive care therapy is
• Pressure limit important. Sepsis should be treated with
• Positive end expiratory pressure (PEEP) appropriate antibiotics. Careful fluid balance
• Positive airway pressure (CPAP)
Complications of mechanical ventilation
include:
• Problems associated with endotracheal
tube – obstruction, misplacement
• Disconnection
• Barotrauma
Principles of intensive care 51
Direct lung injury The causes of ARDS
Pneumonia
Aspiration pneumonitis Indirect lung injury
Pulmonary contusion Sepsis
Fat embolism Trauma
Inhalational injury Cardiopulmonary bypass
Acute pancreatitis
Table 3.9 The causes of ARDS
is important and over hydration should The anion gap is the sum of the positive and
be avoided. The nutritional status should negative charges in the plasma. The cations
be addressed. Mechanical ventilation are sodium and potassium. The anions are
is important but the exact strategy is chloride, bicarbonate. The difference between
controversial. It is generally believed the two is the anion gap. If a metabolic
that ventilation with low tidal volumes is acidosis is due to anion excess the anion
beneficial. High tidal volumes can exacerbate gap is increased. If metabolic acidosis is
the lung injury. The role of positive end- due to bicarbonate loss the anion gap is
expiratory pressure is unclear. Inhaled nitric normal. Lactic acidosis and renal failure are
oxide or surfactant are of no proven benefit. associated with an increased anion gap.
Steroids may have some clinical effect.
Blood gas analysis
Acid–base balance A blood gas analyser measures:
pH is a logarithmic scale and the blood pH is • Partial pressure oxygen
normally maintained at 7.36–7.44. A change • Partial pressure carbon dioxide
in pH of 0.3 units is equivalent to a doubling • pH
of the hydrogen ion concentration. Blood
pH is maintained by biological buffering Other variables are derived using Henderson–
mechanisms involving proteins, bicarbonate Hasselbach equation and are summarised in
and haemoglobin. The relationship between Table 3.10.
serum pH and bicarbonate concentration
is described by the Henderson–Hasselbach Interpretation of results
equation. Compensatory mechanisms exist Blood gas results should be interpreted with
to compensate for changes in pH. Important knowledge of the patient’s clinical condition.
definitions include: It is important to check for the consistency
within the blood gas sample. To fully interpret
• Acidosis = a rise serum in hydrogen iron results it is important to:
concentration or fall in pH
• Look at the pH for the primary acid–base
• Alkalosis = a reduction in hydrogen iron disorder
concentration or rise in pH
• Assess a respiratory component by looking
• Respiratory acidosis = a fall in pH due to a at the partial pressure of carbon dioxide
rise in partial pressure of carbon dioxide
• Assess the metabolic component by
• Respiratory alkalosis = a rise in pH due to a looking at the base excess
fall in partial pressure of carbon dioxide
• Calculate the anion gap
• Metabolic acidosis = a fall in pH due to a
metabolic cause Lactic acidosis
• Metabolic alkalosis = a rise in pH due to a Metabolic acidosis is defined as a state of
metabolic cause decreased systemic pH resulting from either
52 Chapter 3 Postoperative management and critical care
a primary increase in hydrogen ion or a Shock
reduction in bicarbonate concentrations. In
the acute state, respiratory compensation of Shock is a pathological condition
acidosis occurs by hyperventilation resulting characterised by inadequate tissue perfusion
in a relative reduction in PaCO2. Chronically, reducing the delivery of oxygen and other
renal compensation occurs by means of essential nutrients to a level below that
reabsorption of bicarbonate. The underlying required for normal cellular activities.
aetiology of metabolic acidosis is classically Cellular injury and destruction may follow
categorised into those that cause an elevated and tissue and organ function deteriorate.
anion gap and those that do not. Lactic There is progressive cardiovascular collapse
acidosis, identified by a state of acidosis and resulting in:
an elevated plasma lactate concentration is
one type of anion gap metabolic acidosis. • Hypotension
• Hyperventilation
The normal blood lactate concentration • Reduced level of consciousness
is 0.5–1.0 mmol/L. Patients with a critical • Oliguria
illness can be considered to have normal
lactate concentrations of less than 2 mmol/L. The causes of shock include:
Hyperlactataemia is defined as a mild to
moderate persistent increase in blood • Hypovolaemia
lactate concentration without metabolic • Cardiogenic
acidosis. Lactic acidosis is characterised by • Septic shock
a persistently increased blood lactate levels • Anaphylaxis
in association with a metabolic acidosis.
Elevated lactate levels are a marker of Physiology of shock
inadequate tissue perfusion and should be
considered in relation the patient’s clinical Compensation
presentation. An elevated serum lactate alone Loss of effective circulating blood volume
cannot provide definitive confirmation of initiates reactive changes. Re-distribution of
disease presence, severity or prognosis. the circulating blood volume occurs. Perfusion
to the coronary and cerebral circulations
is maintained by autoregulation. Acute
hypovolaemia results in reduced central
Variables derived from a blood gas analyser
Temperature Normal value
pH 37°C
Partial pressure CO2 (pCO2) 7.36–7.44
Partial pressure O2 (pO2) 4.6–5.6 kPa
Bicarbonate 10.0–13.3 kPa
Total carbon dioxide 22 –26 mmol/L
Standard bicarbonate (SBC) 24–28 mmol/L
Base excess (BE) 22–26 mmol/L
Standard base excess (SBE) –2 to +2 mmol/L
Oxygen saturation –3 to +3 mmol/L
Haemoglobin >95%
11.5–16.5 g/dL
Table 3.10 Variables derived from a blood gas analyser
Principles of intensive care 53
venous pressure, cardiac filling and cardiac may need inotropic support. Some patients
output. Sympathetic stimulation causes require inotropes and vasopressor. Others
reduced splanchnic perfusion, cutaneous require inodilators to redistribute the blood
vasoconstriction and reduced renal perfusion. flow. The choice of inotrope depends on
The venous return is increased and myocardial their relative actions on the sympathetic
contractility is maintained. The renin/ nervous system.
angiotensin system is stimulated, antidiuretic
hormone is released and the urine output is Cardiogenic shock
reduced. If compensation is adequate, blood For patients who have low cardiac output
pressure is maintained and oxygen delivery to with high filling pressure and vascular
the essential tissues remains adequate. resistance, dobutamine is an inotrope that
reduces vascular resistance. Inodilators
Progression such as dopexamine are also useful. Pure
vasodilators such as nitrates or nitroprusside
If compensatory mechanisms are inadequate, also have a role.
ischaemia and hypoxia occur. Anaerobic
metabolism results in increased lactate High output states
production. Capillary permeability increases In severe cases of sepsis, vasodilatation is
and pulmonary oedema may occur resulting often resistant to the use of vasoconstrictors.
in ARDS. Renal hypoperfusion can result in The perfusion pressure can be restored with
acute tubular necrosis. noradrenaline. Dobutamine can be added
to increase cardiac output. Adrenaline
Irreversibility aggravates splanchnic ischaemia.
If compensatory mechanisms fail, then Acute renal failure
vasodilatation occurs and capillary
permeability is increased. Progressive tissue Acute renal failure is a reduction in renal
hypoxia occurs. When the systolic blood excretory or regulatory function resulting
pressure falls below about 50–60 mmHg, in the retention of waste products normally
reduced coronary circulation results in excreted by the kidney. A normal adult
myocardial ischaemia. Cerebral ischaemia urine output is about 0.5 mL/kg/hr. Renal
causes vasomotor depression and visceral failure can be anuric, oliguric or polyuric.
vasodilatation. Disseminated intravascular Biochemical changes of acute renal failure
coagulation occurs and water and electrolyte include:
disturbances develop.
• Hyponatraemia
Acute blood loss • Hyperkalaemia
• Hypocalcaemia
Following acute blood loss, the haemoglobin • Metabolic acidosis
and packed cell volume (PCV) remain normal
for the first 3–4 hours. Plasma volume then Management
expands and the haemoglobin and PCV fall, The management of acute renal failure is
associated with an increase in neutrophils to correct the precipitating cause. Most
and platelets. The reticulocyte count increases surgical patients are hypovolaemic and
on day 2 or 3 and this reaches a maximum require volume resuscitation. If there is
of 10–15% by day 8 to 10. Without treatment inadequate renal perfusion pressure then
haemoglobin begins to rise by day 7. consideration needs to be given to inotropic
support. Oxygen should be administered.
Cardiovascular support Consideration should be given to the use
of bicarbonate if the base excess is more
In all forms of shock, there is a need to re- than 10 or the arterial pH less than 7.
establish adequate cardiac output and tissue Hyperkalaemia requires urgent treatment if
perfusion. The aim is to achieve a mean the patient is:
arterial pressure of at least 80 mmHg. For
this to occur it requires preload optimisation
with volume replacement and patients
54 Chapter 3 Postoperative management and critical care
• Symptomatic APACHE II score
• ECG changes – increased PT interval,
The APACHE II score is a general measure of
tented T waves, ventricular tachycardia disease severity based on current physiologic
• Serum potassium more than 6 mmol/L measurements, age and previous health
condition. Scores range from 0 to 71 and with
Treatment options are: an increasing score there is an increasing
risk of hospital death. The APACHE II score is
• 10 mL 10% calcium gluconate made up of:
intravenously
• Acute physiology score
• 10 units actrapid in 50 mL 50% dextrose • Age points
• Salbutamol nebuliser • Chronic health points
• Calcium resonium 15–30 mg as required
POSSUM system
up to twice daily
The outcome of surgery depends on several
Physiological scoring systems factors including the physiological status
of the patient and the disease process
Patients admitted to intensive care form that requires surgical intervention. Raw
a heterogeneous population. They differ morbidity and mortality data can provide
in many respects including age, previous a biased picture. POSSUM stand for the
health status, reason for admission Physiological and Operative Severity Score
and severity of illness. All these factors for the enUmeration of Mortality. It allows
influence prognosis. Scoring system have risk-adjusted assessment of surgical quality
been developed to quantity this case mix. and accurately predicts 30-day morbidity
Scoring systems can be generic or specific and mortality. It is two-part scoring system
and can be used for audit, research and including a physiological assessment and
clinical management. Limitations and operative severity measure.
errors associated with their use include
missing data, observer error, inter-observer
variability and lead time bias.
Chapter 4 Surgical
technique and
technology
Surgical wounds fluid balance. This is achieved by both
Pathophysiology of migration and proliferation of epithelial
wound healing cells. Migration requires the presence of
granulation tissue. When epithelial cover is
Wound healing starts with an initial complete contact inhibition prevents further
vascular response. Vasoconstriction epithelial growth. Wound contraction can
occurs as a direct response to trauma. account for up to 80% reduction in wound
Exposed subendothelial tissue activates size. This occurs due to myofibroblasts in the
the coagulation and complement cascades. granulation tissue. Fibroplasia occurs due to
Platelet adhesion and aggregation causes procollagen production by fibroblasts. The
clot formation. Degranulation of platelets extracellular matrix contains fibronectin and
releases growth factors and chemotactic glycosaminoglycans. These regulate collagen
factors. An inflammatory response occurs synthesis and cellular differentiation.
due to histamine and 5HT release which Fibroplasia is accompanied by simultaneous
produces vasodilatation, increased capillary angiogenesis. Fibrous proliferation is
permeability and margination of neutrophils. followed by remodeling. Maximum collagen
production occurs at 20 days after injury
This is followed by a cellular response with and wound strength increases up to 3 to
migration of neutrophils, macrophages and 6 months. Initial collagen production is
lymphocytes. Macrophages produce growth disorganised. Remodelling lines it up with
factors leading to migration of fibroblast stresses in skin. The physiology of wound
and epithelial cells. This causes cellular healing is summarised in Figure 4.1.
proliferation with three components:
Important growth factors in wound
• Epithelialisation healing include:
• Contraction
• Fibroplasia • Platelet derived growth factors (PDGF)
• Insulin like growth factor (IGF-1)
The formation of an epithelial barrier is • Epidermal growth factor (EGF)
important to prevent infection and maintain • Transforming growth factor (TGF-β)
The phases of wound healing
Haemostasis Inflammation Proliferation Remodelling
Damaged vessels Neutrophils secrete Fibroblasts Fibroblasts
constrict factors proliferate secrete
collagen
Platelets Macrophages Epidermal cells Wound
aggregate remove debris migrate remodelling and
contraction
Leucocytes Capillary growth Granulation
migrate tissue forms
Figure 4.1 The phases of wound healing
56 Chapter 4 Surgical technique and technology
Factors that influence wound healing can be Keloid and hypertrophic scars
both systemic and local.
All scars become red and thickened during
Systemic factors include: the normal healing process. After several
months maturation results in flattening of the
• Age and sex wound. In some scars collagen formation is
• Nutrition excessive resulting in elevated and red scar.
• Vitamin and trace element deficiencies – If this process is confined to the area of the
wound the scar is described as hypertrophic.
vitamin C, vitamin A, zinc If it extends beyond the wound into normal
• Drugs – steroids, chemotherapy, tissue the scar is described as keloid scar.
Keloid scars are seen particularly in patients
immunosuppression of Afro-Caribbean origin and often affect the
• Systemic disease – diabetes, jaundice, presternal and deltoid areas. Treatment can
be difficult. Treatment options include:
malignancy
• Hypoxia • Intra-lesional steroid injections (e.g.
triamcinolone)
Local factors include:
• Compression dressings with elasticated
• Blood supply compression garments
• Infection
• Foreign bodies • Silastic gel therapy
• Surgical technique • Excision and radiotherapy
• Laser therapy
Scars and contractures
Principles of anastomoses
Factors that influence scar formation
include: Gastrointestinal anastomoses
• Individual genetic make up An anastomosis is a surgically created join
• Race between two hollow viscera or vessels
• Anatomical site in order to create a confluent channel.
• Wound tension Anastomoses can be fashioned in various
• Age ways including:
• Placement of incision
• Surgical technique • End-to-end
• End-to-side
To minimise the degree of postoperative • Side-to-side
scarring:
Any anastomotic technique is required to
• Incisions should run along Langer lines maintain apposition of the two sides of the
• The finest suture possible should be used anastomosis until collagen is laid down.
• Tension should be avoided Gastrointestinal anastomoses show serosal
• Sutures should be removed as soon as healing and require a good blood supply and
minimal tension. Anastomotic leak or failure
possible my occur if there is:
• Traumatic wounds should be clean and
• Distal obstruction
edges excised • Peri-anastomotic sepsis
• Exposure to sunlight should be avoided in • Peri-anastomotic haematoma
• Hypotension
the early postoperative period • Hypoxia
• Jaundice
Contractures result if scars shorten. They • Corticosteroids
are particularly seen in badly aligned scars • Uraemia
not corresponding to Langer lines. They
can reduce joint mobility and may require An anastomosis should promote primary
surgery such as a Z-plasty or skin graft to healing by accurate alignment and minimal
correct the deformity. Depressed scars occur disruption of the local vasculature. It should
if skin becomes attached to deep tissue. They
can be treated by the release of normal skin
from margins of scar. The scar can then de-
epithelialised and skin edges closed over the
top.
Surgical technique 57
incorporate a minimum amount of foreign Surgical technique
material. It should avoid implantation of Incisions
malignant cells and should not enhance the
risk of metachronous tumours. Incisions should allow access to the surgical
site and should:
Conventional methods of fashioning an
anastomosis is with sutures or staples. There • Be capable of extension if required
is no evidence to suggest that hand-sewn • Be secure when closed
are superior to stapled anastomoses. A ‘two • Have a low complication rate
layered’ technique is the classic method of • Be associated with minimal pain
gastrointestinal anastomosis. It requires the • Have a good cosmetic appearance when
use of an inner continuous all layer suture
and interrupted outer seromuscular suture. healed
It produces serosal apposition and mucosal
inversion. The inner layer was believed to be Various profiles of surgical blades are
haemostatic but may strangulates mucosa. available to optimise incisions (Figure 4.2).
A ‘single layered’ technique is the modern
teaching of gastrointestinal anastomoses. Wound closure
It requires an interrupted seromuscular
absorbable suture that incorporates a strong Wound closure is a matter of personal
submucosal layer. There should be minimal preference influenced by experience. Mass
damage to the submucosal vascular plexus. closure of midline abdominal incision is
the preferred technique using an ‘0’ or ‘1’
Stapled anastomoses can be fashioned non-absorbable monofilament suture.
side-to-side anastomosis with linear staplers About 1 cm bite should be placed 1 cm
or end-to-end with circular devices. Stapled apart. Applying ‘Jenkin’s Rule’, the suture
anastomoses may reduce radiologically length:wound length should be about 4:1.
detected anastomotic leaks but may be A no touch technique of needles should
associated with increased rate of anastomotic be used. The use of deep tension sutures is
strictures. controversial. Deep tension sutures offer no
extra security and often produce a painful
The use of drains around anastomoses is and cosmetically unacceptable scar. The use
controversial. There is no evidence that the of a ‘fat stitch’ reduces dead space but adds
use of a drain reduces the risk of anastomotic no strength to wound repair. There is no
leakage above pelvic brim. The presence evidence that the use of fat sutures reduces
of a drain may actually increase the risk of the risk of wound infection. The use of silk
leakage. sutures for skin closure should be avoided as
they increase risk of stitch abscesses. If there
The profiles of commonly used surgical blades
Figure 4.2 The profiles of commonly used surgical blades
58 Chapter 4 Surgical technique and technology
is concern about possible wound infection, • 5–0 = 0.10 mm
consideration should be given to leaving the • 4–0 = 0.15 mm
skin wound open. • 3–0 = 0.20 mm
• 2–0 = 0.30 mm
Sutures should be removed as early as • 0 = 0.35 mm
possible. On the head and face, limbs and • 1 = 0.40 mm
abdomen they should be removed at 5, 7 and • 2 = 0.5 mm
10 days respectively.
Suture materials and needles Needle points
The purpose of a suture is to hold a wound Five types of needle points are in common
together, in good apposition, until such time
as the natural healing process is sufficiently use and are shown in Figure 4.3:
well established to make the support from the
• Cutting needle
.ir/suture material unnecessary and redundant. • Reverse cutting needle
The ideal suture material should: • Round-body needle
• Taper cutting needle
• Have good handling characteristics • Blunt point needle
s• Not induce a significant tissue reaction Needles vary in their diameter and the
circumference of the curve as shown in
• Allow secure knots Figure 4.4.
s• Have adequate tensile strength Other techniques of wound closure
n• Not cut through tissue
SteriStrips are self adhesive tapes. They
• Be sterile can be used to reduce tension on a wound
and are particularly useful for superficial
ia• Be non-allergenic lacerations. Tension from the tapes can cause
skin blisters. Tissue adhesive is based on
• Be cheap cyanoacrylate monomer. It is simple and pain
free to use but wounds does need to be clean
rsThe choice of suture will depend on: and tension free.
• Properties of the suture material Wound dressings
e• Absorption rate The ‘ideal wound dressing’ should:
.p• Handling and knotting properties
• Maintain a moist environment at the
• Size of suture wound interface
• Type of needle
• Remove excess exudate without allowing
ipSuture characteristics ‘strike through’ to the surface of dressing
://vSuture materials vary in their physical
• Provide thermal insulation and
characteristics. Monofilament sutures (e.g. mechanical protection
polypropylene) are smooth. They slide well
in tissues but if handled inappropriately • Act as a barrier to micro-organisms
• Allow gaseous exchange
ttpthey can fracture. Multifilament sutures (e.g.
polyglactin) are braided. They have a greater
surface area. They are easier to handle and
hknot well. Some suture materials have a
‘memory’ and return to former shape when
• Be non-adherent and easily removed
tension is removed. Absorbable suture
without trauma
are broken down by either proteolysis or
• Leave no foreign material in the wound
hydrolysis. The rate of breakdown varies
• Be non-toxic, non-allergenic and non-
between individual suture materials. sensitising
Suture sizes Hydrocolloids
Sutures are sized by the USP (United States
Pharmacopoeia) scale. The available sizes Hydrocolloids are a matrix of cellulose and
and diameters are: other gel forming agents such as gelatin and
pectin. They form an occlusive dressing and
• 6–0 = 0.07 mm should be avoided if infection is a risk. This
Surgical technique 59
The common types of needle point Figure 4.3 The common types of
needle point
Round bodied
Cutting
Reverse cutting
Blunt point
.ir/Taper cutting
sThe common profiles of needle curves
s1/2 Circle 3/8 Circle 1/4 Circle J Shape
Figure 4.4 The common profiles
of needle curves
rsiantype of dressing promotes autolysis and aids
egranulation. It can remain in place for up to a Straight
week. Over-granulation can occur. Debriding agents
.pAlginates Debriding agents remove eschar and
ipAlginates are made from calcium and necrotic tissue. They do not maintain a moist
environment and need frequent changes.
sodium salts of alginic acid obtained form They damage granulation tissue and can
potentially delay healing.
://vseaweed. They are highly absorbent. They
Negative pressure topical dressings
are useful in medium to heavily exudating
wounds and form a gel in contact with Negative pressure topical dressings apply
wound exudates. pressure via a foam dressing. They remove
wound exudate and reduce extravascular
ttpFoam dressings and interstitial fluid. They improve blood
supply to the wound during the phase
Foam dressings are useful for moderately of inflammation. The mechanical effect
appears to stimulate cellular proliferation.
hexudating wounds. They prevents ‘strike
through’ of exudate to wound surface. They A polyurethane or polyvinyl-alcohol foam
deslough wounds by maintaining a moist dressing is cut to the shape of the wound.
environment. The foam is then covered with an adhesive
Hydrogels dressing with a small hole. A therapeutic
regulated accurate care (TRAC) pad is
Hydrogels have a high water content which applied over the hole and is connected to a
creates a moist wound surface. They debride negative pressure generator. The pressures
wounds by a combination of hydration and achieved at the TRAC pad–foam interface
promotion of autolysis. They will absorb light are regulated. A pressure of approximately
exudates but are not appropriate for heavily 125 mmHg is often used. Intermittent
exudating wounds. application of pressure may be advantageous.
60 Chapter 4 Surgical technique and technology
The dressings should be changed every 48–72 Diathermy can interfere with pacemaker
hours. Wounds suitable for negative pressure function. Arcing can occur with metal
topical dressings include those resulting from instruments and implants. Superficial burn
trauma, burns, pressure sores, leg ulcers and can occur if a spirit-based skin preparation is
infection. Contraindications include grossly used. A burn can occur under the indifferent
infected and bleeding wounds, malignancy electrode if the plate is not properly applied.
and exposed vessels and bowel. Channeling effects can occur if diathermy is
Diathermy used on a viscus with a narrow pedicle (e.g.
penis or testis).
Diathermy is the use of high frequency Bipolar diathermy
electrical current to produce heat. It is used
to either cut and destroy tissue or to produce With bipolar diathermy (Figure 4.6), the two
coagulation. Mains electricity is 50 Hz electrodes are combined in the instrument
(e.g. forceps) and the current passes between
.ir/and produces intense muscle and nerve the tips and not through the patient. The
advantage of bipolar diathermy is that the
activation. The electrical frequency used by electrical current does not pass through parts
diathermy is in the range of 300 kHz to 3 MHz. of the body which are not being treated. It is
The patient’s body forms part of the electrical possible to be much more precise with the
quantity of tissue being coagulated.
scircuit but the current has little effect on
smuscles and the myocardium. Lasers
nMonopolar diathermy
iaWith monopolar diathermy (Figure 4.5), Laser is an acronym for Light Amplification
by the Stimulated Emission of Radiation.
an electrical plate is placed on the patient Laser emissions vary and are:
rsand acts as an indifferent electrode. The • Collimated – parallel output beam results
in little energy loss
current passes between the instrument and
the indifferent electrode. As the surface area • Coherent – waves are all in phase resulting
in little loss of energy
eof the instrument is an order of magnitude
• Monochromic – all of the same wave
less than that of the plate, localised heating length
.pis produced at the tip of instrument and The effects of a laser depends on its
photochemical, photomechanical and
minimal heating effect is produced at the photothermal effects. Tissue penetration
increases with wavelength. Pulsing of output
ipindifferent electrode. The effects of diathermy can reduce thermal damage.
depend on the current intensity and wave-
://vform used. Coagulation is produced by
interrupted pulses of current (50–100/
second) and the use of a square wave-form.
Cutting is produced by continuous current in
ttpa sinus wave-form.
h Monopolar diathermy Figure 4.5 Monopolar diathermy
Monopolar
Bipolar diathermy Surgical procedures 61
Figure 4.6 Bipolar diathermy
Lasers are classified according to the Surgical procedures
amount of damage they can cause:
Day care surgery
• Class 1 – generally safe
• Class 2 – safe within the time of the blink During recent years, the duration of hospital
stay has been reduced. This has been
reflex associated with an expansion in the use of day
• Class 3 – cause blindness after short case surgery. Approximately 50% of elective
operations are now performed as day cases.
exposure from mirrored surfaces Potential benefits of day surgery include:
• Class 4 – unsafe even with reflection from
• Reduced disruption to patients’ normal lives
non-mirrored surfaces • Psychological benefit of avoiding
All medical lasers belong to class 4 and prolonged hospital stay
both patients and operators are required • Reduced morbidity including nosocomial
to wear goggles. The properties and uses of
different types of laser are shown in Table infections
4.1. Risks associated with the use of lasers • Reduced inpatient waiting lists
include excessive burning, scar formation, • Increased availability of inpatient beds
accidental skin exposure and corneal or • Reduced costs
retinal burns.
Properties and uses of different types of laser
Laser Wavelength (nm) Pulse length Uses
Carbon dioxide 10,600 Continuous Tissue cutting
Neodymium-YAG 1064 Continuous Coagulation
Neodymium-YAG 1064 10 ns Posterior capsulotomy
Ruby 694 100 µs Tattoo removal
Argon 488–514 Continuous Coagulation
Excimer 308 10 ns Photorefractive
keratotomy
Table 4.1 The properties and uses of different types of laser
62 Chapter 4 Surgical technique and technology
Safe day case surgery requires appropriate: Discharge criteria
• Patient selection Prior to discharge from the day case unit
• Operative procedures patients should:
• Anaesthetic techniques
• Have stable vital signs
Patient selection • Be alert and orientated
• Be comfortable/pain free
For day surgery patients should generally • Be able to walk
fulfill the following criteria: • Be able to tolerate oral fluids
• Have minimal nausea and vomiting
• Age less than 70 years
• ASA Grade 1 or 2 Adequate follow-up arrangements should
• BMI less than 30 be made. Patients should be provided with
• Availability of a responsible adult information sheets and have a contact
• Access to a telephone telephone number in case of problems.
• Live within an hour’s travelling time from
Endoscopic surgery and
the hospital laparoscopy
Appropriate patient selection requires close Minimal access surgery presents the
co-operation between surgeon, anaesthetist opportunity of reduced trauma associated
and day unit. Preoperative screening with access to body cavities without
should be performed. It can be carried compromising exposure of the operative field.
out by a questionnaire and/or in a nurse- Minimal access surgery can be performed
led assessment clinic. Patients requiring using the following approaches:
extensive preoperative investigation are not
suitable for day case surgery. • Laparoscopic
• Thoracoscopic
Operation selection • Endoluminal
• Intra-articular joint surgery
Operations suitable for day case surgery vary • Combined approaches
between specialties. The appropriateness
can be expanded by the facility for an The advantages of minimal access surgery are:
overnight stay. Generally operations should
be: • Less tissue trauma
• Less postoperative pain
• Short duration • Faster recovery
• Low incidence of postoperative • Fewer postoperative complications
• Better cosmesis
complications
• Not require blood transfusion The disadvantages of minimal access surgery
• Not require major postoperative analgesia are:
Laparoscopic surgery can be performed, • Lack of tactile feedback
usually with an overnight stay. Surgery should • Increased technical expertise required
be performed by an experienced surgeon. • Possible longer duration of surgery
There should be access to inpatient beds • Increased risk of iatrogenic injuries
should they be required. • Difficult removal of bulky organs
• More expensive
Day case anaesthesia
Pneumoperitoneum
The principles of anaesthesia are the same
as for inpatient care. It requires high quality Laparoscopic surgery invariably requires the
induction, maintenance and recovery. establishment of a pneumoperitoneum. The
The recovery should be free from side ideal gas for insufflation during laparoscopy
effects. Anaesthesia should be performed must have the following characteristics:
by an experienced anaesthetist. The use
of local anaesthetic techniques should be • Limited systemic absorption across the
encouraged. peritoneum
Surgical procedures 63
• Limited systemic effects when absorbed minutes). Multiple inflations or deflations
• Rapid excretion if absorbed should be avoided. Relative contraindications
• Incapable of supporting combustion to the use of tourniquets include:
• High solubility in blood
• Limited physiological effects with • Previous DVT or pulmonary embolus
• Arterial disease
intravascular systemic embolism • Vasculitic disorders
• Sickle cell anaemia
Carbon dioxide is the best gas available. A
pneumoperitoneum can be performed using Complications of tourniquet use include:
either a closed or open technique.
• Nerve injury
The closed technique involves the use • Vascular injury
of a Veress needle. It is a blind procedure • Postoperative embolic events
with the potential for complications. Major • Post-tourniquet syndrome
complications include visceral or vascular • Myoglobinuria
puncture. The needle is usually inserted at the • Increased blood viscosity
umbilicus and is aimed towards the pelvis. • Increased postoperative pain
Intraperitoneal placement can be checked • Tourniquet burns
by either a saline drop test or low-flow gas
insufflation. In an adult, insufflation of about Rubber tubing and surgical gloves are
3.5 litres of CO2 is required to establish an frequently used as tourniquets on fingers. This
adequate pneumoperitoneum usually with practice should be condemned as they can
a maximum pressure of 10–12 mmHg. The inadvertently be left on the digit at the end
primary port is then inserted blindly through of the procedure. Specific brightly coloured
the umbilicus and the secondary ports are digital tourniquets are now available.
placed under direct vision.
Surgical drains
The open (Hasson) technique for
establishing a pneumoperitoneum is Drains are often used to evacuate establish
associated with a reduced risk of visceral collections of pus, blood or other fluids (e.g.
injury. The primary port is inserted using a lymph) or to drain potential collections. Their
‘cut-down’ technique. A subumbilical incision use is contentious.
is made and stay sutures are inserted in to
the linea alba to provide counter traction. An Arguments for their use include:
incision is made in the linea alba and a finger
inserted through peritoneum to ensure that • Drainage of fluid removes potential
there are no adhesions. The primary port is sources of infection
then inserted under direct vision.
• Drains guard against further fluid
Tourniquets collections
Tourniquets are commonly used in surgical • They may allow the early detection of
practice to reduce blood loss in the operative anastomotic leaks or haemorrhage
field. When properly applied they provide
excellent haemostasis. When incorrectly • They leave a tract for potential collections
used, they can be dangerous. Cuff failure can to drain following removal
be disastrous with rapid systemic absorption
of drugs (e.g. local anaesthetics). Arguments against their use include:
The use of a tourniquet requires correct • The presence of a drain increases the risk
placement and connection. There should of infection
be adequate padding and the limb should
be exsanguinate before inflation. Their use • Tissue damage may be caused by
should involve minimal pressure (usually mechanical pressure or suction
100 mmHg above systolic blood pressure)
for minimal duration (no longer than 90 • Drains may induce an anastomotic leak
• Most abdominal drains become infected
within 24 hours
Types of drain
Most modern drains are made from an inert
silastic material. They induce minimal tissue
reaction. Older red rubber drains induce
64 Chapter 4 Surgical technique and technology
an intense tissue reaction allowing a tract • The diameter of the catheter (10 Fr to 24 Fr)
to form and have specific uses in modern • The number of channels (two or three)
surgical practice. In some situations this may • The size of the balloon (5 mL to 30 mL)
be useful (e.g. biliary T-tube). Drains can be • The shape of the tip
open or closed and can be active or passive.
Open drains include corrugated rubber or When using a catheter it should be of an
plastic sheets. The drain fluid collects into a appropriate size, inserted using an aseptic
gauze pad or stoma bag. Open drains can be technique and never with the use of force.
associated with an increased risk of infection. The balloon should not be inflated until urine
A closed drain consists of a tube draining into has been seen coming from the catheter.
a bag or bottle. Examples include chest and The residual volume should be recorded.
abdominal drains. With closed drains the A catheter introducer should not be used
risk of infection is reduced. Active drains are unless the operator has been trained in its
maintained under suction with either low or use. If difficulty is encountered inserting a
high pressure. Passive drains have no suction. urethral catheter consider a suprapubic route.
They function by the differential pressure The catheter should be removed as early as
between body cavities and the exterior. possible. Special catheters exist such as:
Nasogastric tubes • Gibbon catheters
• Nelaton catheters
Following abdominal surgery, • Tiemann catheters
gastrointestinal motility is reduced for a • Malecot catheters
variable period of time. Gastrointestinal
secretions accumulate in the stomach and Indications for a urinary catheter include:
proximal small bowel. This may result in
postoperative distension and vomiting • The management of acute urinary
and the risk of an aspiration pneumonia. retention or bladder outlet obstruction
Nasogastric tubes are often used to remove
fluid and secretions. There is little clinical • The measurement of urine output in a
evidence available to support their routine critically ill patient
use following elective gastrointestinal surgery
and they may actually increase the risk of • During surgery to assess fluid status
pulmonary complications. They are of proven • During and following specific surgeries of
value for gastrointestinal decompression
in intestinal obstruction and following the genitourinary tract
emergency abdominal surgery. Nasogastric • The management of haematuria associated
tubes are usually left on free drainage and
aspirated on an intermittent basis. They with clots
should be removed when the volume • The management of an immobilised patients
of nasogastric aspirate has reduced and • The management of patients with a
gastrointestinal motility has returned.
neurogenic bladder
Urinary catheters • Intravesical pharmacologic therapy
• Improved patient comfort for end of life care
A urinary catheter is a form of drain. It is • The management of patients with urinary
commonly used to alleviate or prevent
urinary retention or to monitor urine incontinence
output. It can be inserted transurethrally or
suprapubically. Catheters vary by: The only absolute contraindication to
the placement of a urethral catheter is
• The material from which they are made the presence of urethral injury. Relative
(latex, plastic, silastic, Teflon-coated) contraindications include a urtethral stricture
or recent urinary tract surgery.
• The length of the catheter (38 cm ‘male’ or
‘22 cm ‘female’) Complications of urethral catheterisation
include:
• Paraphimosis
• Blockage
• By-passing
• Infection
• Failure of balloon to deflate
• Urethral strictures
Surgical procedures 65
Suprapubic catherisation may be chosen to improve patient comfort,
dignity or convenience, and to prevent
Suprapubic catheterisation should be complications such as catheter-induced
used when urethral catheterisation is urethral injury. Insertion requires a palpable
contraindicated or where it is technically bladder. Complications include misplacement,
impossible to relieve urinary retention in both bleeding and bowel perforation.
acute and chronic conditions. In addition, it
Chapter 5 Evidence-based
surgical practice
Evidence-based medicine • Decision analyses
• Economic analyses
The primary purpose of any healthcare
system is to secure through the resources The strength of a study depends on its design.
available the greatest possible improvement A hierarchy of evidence (Table 5.1) exists with
to physical and mental health of the decreasing strength as follows:
population. To achieve this, decisions about
the delivery and provision of healthcare • Systematic review and meta-analysis
are increasingly being driven by evidence • Randomised controlled trials with
of clinical and cost-effectiveness as well
as systematic assessment of actual health definitive results
outcomes. Evidence-based medicine is • Randomised controlled trials with non-
the process of systematically reviewing,
appraising and using clinical research definitive results
findings to aid the delivery of optimum • Cohort studies
clinical care to patients. • Case–control studies
• Cross sectional surveys
Principles of research and • Case reports
clinical trials
Clinical trials
Primary research includes:
Purpose of clinical trials
• Animal or volunteer experiments
• Clinical trials Clinical trials conduct ‘human experiments’.
• Surveys Three fundamental principles apply:
Secondary research includes: • The trial must address a legitimate
question
• Systematic review and meta-analyses
• Guidelines • The patient must be informed and willing
to participate
• The patient may decline entry or withdraw
at any stage
Hierarchy of evidence
Level Description
Ia
Ib Evidence from a meta-analysis of randomised controlled trials
IIa Evidence from at least one randomised controlled trial
IIb Evidence from at least one well-designed controlled study without randomisation
III Evidence from at least one well-designed quasi-experimental study
Evidence from well-designed non-experimental descriptive studies such as comparative
IV studies, correlation studies or case studies
Evidence from expert committee reports or opinions or clinical experiences of respected
authorities
Table 5.1 Hierarchy of evidence
68 Chapter 5 Evidence-based surgical practice
Phase 1 study • Often imperfect randomisation
Phase 1 studies provide basic • Often not all eligible patients are randomised
pharmacological and toxicology information. • Failure to blind assessors to randomisation
They are not a test of therapeutic efficacy.
They can be performed on either on healthy status of patients
volunteers or patients whose disease has
progressed on all available treatments. Cohort studies
Phase 2 study Cohort studies compare groups exposed to
Phase 2 studies are used to identify the dose different factors who are followed up to see
range of a particular drug. The sample size whether there is a difference in outcome.
is small and patients usually have end-stage They are often used to study disease
disease. The study is not usually randomised aetiology and assess disease prognosis.
and drug combinations may be tested.
Case–control studies
Phase 3 study
Phase 3 studies are randomised and designed Case–control studies match patients with a
to compare the effects of different treatments. disease to controls. Data are then collected
One treatment option should be the best retrospectively to find a difference between
currently available. Outcome measures the groups.
usually include survival, disease-free survival,
response and toxicity. These studies usually Statistics
involve large numbers of patients.
Types of data
Phase 4 study
Phase 4 studies are less commonly used. Before data analysis can be performed it is
They are aimed at evaluating the long-term necessary to identify the type of data presented.
outcome of established therapies and are Data can be quantitative or categorical:
often regarded as a post-marketing study.
• Quantitative and continuous – e.g. height,
Randomised controlled trials weight, blood pressure
In randomised controlled trials (RCTs), • Quantitative and discrete – e.g. number of
participants are randomly allocated to one children
intervention or another. Both groups are
followed up for a specified period. The two • Categorical and ordinal – e.g. Grade of
groups are analysed in terms of outcome tumour
defined at the outset. If the groups are similar
at the outset then any difference should be • Categorical and nominal – e.g. Male/
due to the intervention. female, blood group
The advantages of RCTs are: Description of quantitative data
Data can be described by a ‘measure of location’
• Allow rigorous evaluation of a single
variable in a defined patient group • Median = mid point: 50% of variables
above and 50% of variables below
• Potentially eradicate bias by comparing
two (or more) identical groups • Mode = most common variable
• Mean = the average i.e. the sum of variable
• Allow for meta-analysis
divided by the number
The disadvantages of RCTs are:
Data can also be described by a ‘measure of
• Expensive and time consuming variation’
• Often have too few patients or too short a
• Range = distribution between maximum
follow-up period and minimum value
• Surrogate endpoints are often used in
• Interquartile range = distribution between
preference to clinical outcome measures first and third quartile
• Standard deviation = distribution
around mean in a ‘normally’ distributed
population
Data can be either be either normally
distributed (Figure 5.1) or can have a skewed
distribution, (Figure 5.2). With a normal
A normal distribution Evidence-based medicine 69
Mean Figure 5.1 A normal distribution.
SD = Standard deviation
Number
Mean ± SD (68%) Parameter
Mean ± 2SD (96%)
Mean ± 3SD (99.7%)
A skewed distribution Figure 5.2 A skewed distribution
Number Median
Interquartile range (75%) Parameter
Range (100%)
distribution the median equals the mean and whether a statistical hypothesis is true
68%, 95% and 99.7% of variable lies with one, would be to examine the entire population.
two and three standard deviations of the mean. Since that is often impractical, researchers
typically examine a random sample from the
Statistical hypothesis population. If sample data are not consistent
A statistical hypothesis is an assumption about with the statistical hypothesis, the hypothesis
a population parameter. This assumption may is rejected. There are two types of statistical
or may not be true. The best way to determine hypotheses.
70 Chapter 5 Evidence-based surgical practice
• Null hypothesis – is the hypothesis that statistical test can be selected. When
sample observations result purely from selecting an appropriate statistic test it is
chance necessary to decide whether the variables
are matched, paired or independent
• Alternative hypothesis – is the hypothesis and to define both the input and output
that sample observations are influenced by variables. Both variable can be categorical
some non-random cause or quantitative. Statistical tests for paired
or matched variables are shown in
Calculation of sample size Table 5.2. Appropriate statistical tests for
The sample size needed to test a hypothesis independent observations and categorical
depends on four factors: outcome variables are shown in Table 5.3.
Appropriate statistical tests for independent
• Expected difference in means between the observations and quantitative outcome
two groups variables are shown in Table 5.4.
• Variability of the data A test of a statistical hypothesis, where the
• Power of the study and the probability that region of rejection is on only one side of the
sampling distribution, is called a one-tailed
any difference is real (usually 90%) test. A test of a statistical hypothesis, where
• Level of significance accepted (usually 5%) the region of rejection is on both sides of the
sampling distribution, is called a two-tailed
Type I and Type II errors test.
A Type I error is rejection of null hypothesis
when it is in fact true: Quality of life
• No difference is present between the Diseases and their treatment have an
samples impact on patient wellbeing. Quality of life
(QoL) is a measure of an illness, disease
• The statistical method used identified a and its treatment on patient welfare. It has
difference dimensions beyond physical measures of
patients’ progress. No universal definition
A Type II error is rejection of null hypothesis of QoL exists. It has three fundamental
when difference between groups exists: characteristics:
• A difference is present between the samples • Multidimensional – physical, social,
• The statistical method used failed to psychological
identify it • Subjective
• Dynamic
Choice of statistical test
Quality of life assessment
Prior to analysing data it is necessary
to define the hypothesis being tested. QoL assessment is used to access progress
If no hypothesis is proposed then no of individual patients. In clinical trials it
is used to compare treatment options and
Statistical tests for paired or determine cost-effectiveness of treatment.
matched variables The instrument used must be:
Test • Valid – measure what it is supposed to
measure
Nominal McNemar
Wilcoxon • Reliable – produce consistent results
Ordinal Wilcoxon • Responsive – be able to detect changes
Quantitative
(non-normal) Paired t-test with time
Quantitative (normal)
QoL assessments can be either self-
Table 5.2 Statistical tests for paired or matched administered or by interview and can be
variables repeated on several occasions. Data are usually
collected using a structured questionnaire.
Evidence-based medicine 71
Statistical tests for independent observations and categorical outcome variables
Nominal Nominal Categorical Ordinal
Chi-squared or Fisher Chi-squared
Chi-squared or
Categorical Chi-squared Chi-squared Mann–Whitney
Kruskal–Wallis
Ordinal Mann–Whitney Spearman rank
Quantitative – discrete Logistic regression
Quantitative – non-normal Logistic regression
Quantitative – normal Logistic regression
Table 5.3 Statistical tests for independent observations and categorical outcome variables
Statistical tests for independent observations and quantitative outcome variables
Quantitative – discrete Quantitative – non-normal Quantitative – normal
Nominal Mann–Whitney Mann–Whitney or log-rank Student’s t-test
Categorical Kruskal–Wallis Kruskal–Wallis
Spearman rank Spearman rank ANOVA
Ordinal
Spearman rank Spearman rank Spearman rank or linear
Quantitative – regression
discrete Pearson or Spearmen rank
Quantitative – Spearman rank or linear
non-normal regression
Quantitative –
normal Pearson or Spearman rank
Linear regression Linear regression
Table 5.4 Statistical tests for independent observations and quantitative outcome variables
Different items on the questionnaire tap Specific instruments are used for specified
various dimensions of QoL. QoL instruments disease or condition. Several types exist
can be either generic or specific. including:
Generic instruments assess many • Domain specific (e.g. hospital anxiety and
dimensions and produce a global concept depression scales)
of QoL. Two types of generic questionnaires
exist: • Disease specific (e.g. EORTC QLQ-C30 for
cancer patients)
• Health profiles (e.g. SF-36)
• Health indices (e.g. Quality adjusted life • Population specific (e.g. children or elderly)
• Symptom specific (e.g. McGill pain
years)
questionnaire)
Chapter 6 Surgical
pathology and
microbiology
Surgical pathology Calcification
Necrosis Abnormal deposits of calcium salts occur in
two circumstances. Dystrophic calcification
Cells can be damaged by various processes is deposition of calcium that occurs when
including: necrotic tissue is not absorbed or tissues
undergo slow degeneration. Metastatic
• Reduced oxygen supply calcification occurs when serum calcium
• Physical agents is elevated for a long period of time. It is
• Chemical agents associated with increased calcium absorption
• Toxins due to high vitamin D levels, resorption
• Viruses of bone, mobilisation of calcium due to
• Abnormal immunological reactions parathyroid hormone excess and chronic renal
failure. Calcium is deposited in the arterial
Necrosis results from cell death. It results in walls, kidneys, lungs and stomach wall.
disintegration of the nucleus, cytoplasmic
organelles and the plasma membrane. Amyloid
Intracellular enzymes are released.
Necrosis is associated with visible changes Amyloid is abnormal protein that is
– coagulative or colliquative necrosis. In deposited in extracellular tissue. It occurs
coagulative necrosis the nucleus fades and around the basement membrane and
dissolves (karyolysis), becomes more dense capillaries and is resistant to degradation.
(pyknosis) and fragments (karyorrhexis). Two types of amyloidosis are recognised.
Primary amyloidosis is due to unknown
Apoptosis causes. Secondary amyloidosis is most
commonly due to:
Apoptosis is programmed cell death. It is
a physiological process and affects single • Tuberculosis
cells in a population of healthy cells. It is the • Pyogenic infection
mechanism of removing effete and abnormal • Rheumatoid arthritis
cells. Normal cells divide to replace lost cells. • Myeloma
There is no evidence of inflammation. It • Hodgkin’s disease
provides a balance between cell proliferation
and elimination. It is associated with Amyloidosis affects several organs including
maintenance of organ size in adults, organ the heart, intestinal tract and kidneys.
development and physiological atrophy or It results in atrophy due to pressure.
involution. Transudation of proteins occurs due to
increased permeability and is associated with
Atrophy vessel narrowing. Pathologically it can be
detected by Lugol’s iodine and Congo red dye.
Atrophy is a decrease in organ size due to With Congo red, tissues show apple green
a reduction in cell size or number. Causes fluorescence in polarised light.
include:
Hypersensitivity reactions
• Gradual diminution in blood supply
• Reduced functional activity Hypersensitivity reactions are exaggerated
• Interrupted nerve supply immunological response to an antigen by
• Endocrine deficiency a normal immune system. They require
• Pressure
74 Chapter 6 Surgical pathology and microbiology
previous exposure to the antigen. Four types Type III hypersensitivity
are recognised based on the mechanism
involved: Immune complex hypersensitivity can be
general or affect individual tissues. The
• Type I – anaphylactic reaction occurs several hours after exposure
• Type II – cytotoxic to antigen. It is mediated via soluble
• Type III – immune complex immune complexes and complement.
• Type IV – cell mediated or delayed Antibodies are of IgG class. Antigen can be
exogenous – bacteria, virus or parasites or
Various clinical conditions are associated endogenous. Examples include, systemic
with one or more type of reaction. lupus erythematosis and rheumatoid
arthritis.
Type I hypersensitivity
Type IV hypersensitivity
Immediate or anaphylactic hypersensitivity
reaction occurs within 10–15 minutes Cell mediated or delayed type
of exposure to an antigen. The extent of hypersensitivity reactions peak after
the reaction can range from mild to life- about 48 hours. They are mediated via T
threatening. Clinical features include lymphocytes, monocytes and macrophages
urticaria, conjunctivitis, rhinitis and with cytotoxic T cells causing direct damage.
bronchospasm. The reaction is mediated via T helper cells secrete cytokines that recruit
IgE. The main cellular component is the mast and activate macrophages. The major
cell or basophil. The reaction is amplified by lymphokines involved include monocyte
platelets and eosinophils. IgE is produced chemotactic factor, interleukin 2 and TNF-a.
in response to exposure to an antigen or Examples include many autoimmune
allergen. IgE binds to cell surface receptors on and infectious diseases (e.g. tuberculosis,
mast cells. Cross linking or receptors result in toxoplasmosis).
mast cell degranulation via a calcium influx.
Mediators released include: Surgical microbiology
• Histamine Abscesses
• Tryptase
• Kininogenase Superficial and deep abscesses
• Leukotriene B4
• Prostaglandin D2 An abscess is a collection of pus within soft
• Platelet activating factor tissues. It occurs when a host’s response
to infection is inadequate. Predisposing
Mast cell degranulation can also be factors include foreign bodies within
triggered by exercise, stress, chemicals the wound, haematoma formation and
and anaphylatoxins. Reaction to these ischaemia.
agents or stimuli is not mediated via IgE.
Treatment is by agents that block histamine Pathology
receptors, inhibit mast cell degranulation
and leukotriene receptor blockers. Examples An abscess contains bacteria, acute
include hay fever and drug allergies. inflammatory cells, protein exudate
and necrotic tissue. It is surrounded by
Type II hypersensitivity granulation tissue often called the ‘pyogenic
membrane’. The commonest organisms
Cytotoxic hypersensitivity affects various involved in superficial abscesses are
organs and tissues. Antigens are normally Staphylococcus aureus and Streptococcus
endogenous and reactions occurs in hours. pyogenes. The commonest organisms
It is mediated via IgM and IgG antibodies involved in deep abscesses are Gram-negative
and complement. Phagocytes and K cells species (e.g. Escherichia coli) and anaerobes
play a role. Examples include Goodpasture’s (e.g. Bacteroides).
syndrome and pemphigus.
Surgical microbiology 75
Clinical features psoas and iliacus muscles. The psoas lies
close to several abdominal structures and
Common superficial abscesses include organs (e.g. sigmoid colon, ureter, appendix)
infected sebaceous cysts, breast and pilonidal and infection in these structures can spread
abscesses. They show the cardinal features of to the muscles. The muscles also have a good
inflammation – calor, rubor, dolor, tumour blood supply predisposing to haematogenous
spread of infection.
• Heat
• Redness Aetiology
• Pain A psoas abscess can be classified as primary
• Swelling or secondary. A primary abscess occurs as a
result of haematogenous spread of infection
After a few days, superficial abscess become and is seen in conditions in which patients
fluctuant and often ‘point’. Deep abscesses are immunocompromised such as in diabetes
include diverticular, subphrenic and mellitus, intravenous drug abuse or renal
anastomotic leaks. Patients usually show failure.
signs of inflammation including a swinging
pyrexia, tachycardia and tachypnoea. Physical Secondary abscesses are associated with
signs are otherwise difficult to demonstrate. local pathology. Common causes include:
The site of an abscess may not be clinically
apparent. Radiological investigations are • Crohn’s disease
often required to make the diagnosis. • Diverticulitis
• Appendicitis
Treatment • Urinary tract infection
• Septic arthritis
All abscesses require adequate drainage • Femoral vessel cannulation
often under general anaesthesia.
Antibiotics have little to offer as tissue In developing countries, most psoas
penetration is usually poor and prolonged abscesses are primary. In Western countries,
antibiotic treatment can result in a chronic about 60% of abscesses are secondary.
inflammatory mass (an ‘antibioma’). Staphylococcus aureus is the commonest
Superficial abscesses are usually suitable for causative organism in primary abscess.
open drainage. For deep abscesses closed Gut-related organisms are the commonest
drainage may be attempted. cause of a secondary abscess. Tuberculosis
is a rare cause of psoas abscess in developed
Superficial abscesses can usually be countries.
drained through a cruciate incision. The
position of the incision should allow Clinical features
depended drainage. The loculi within The clinical features are non-specific and the
the abscess should be broken down and diagnosis may be delayed. Typical symptoms
necrotic tissue excised. Pus should be and signs include, flank, back or abdominal
sent for microbiology. A dressing should pain, fever, a limp, malaise and weight loss or
be inserted into the wound. Packing is a lump in the groin.
usually not required – it is painful and rarely
improves the outcome. Deep abscesses can Investigation
often be treated by ultrasound or CT guided The white cell count and inflammatory markers
aspiration, however, success can not always may be raised. A plain abdominal x-ray may be
be guaranteed. Percutaneous access may be normal. Ultrasound has limited use and has a
difficult because of the position of adjacent sensitivity of only 60%. CT is the gold standard
organs. Multiloculated abscesses may not investigation. MRI may be useful.
drain adequately and open drainage may be
required. Management
Management involves the use of appropriate
Psoas abcess antibiotics based on the likely cause and
The iliopsoas compartment is an
extraperitoneal space. It contains both the
76 Chapter 6 Surgical pathology and microbiology
drainage of the abscess, possibly by a it spreads slowly and often results in skin
percutaneous route. Antibiotics can be ulceration. It lacks the severe systemic toxicity
changed when sensitivities are known. seen with necrotising fasciitis. Treatment
Surgery may be more appropriate in should be with antibiotics including
secondary abscesses when the underlying benzylpenicillin. Surgical debridement of the
pathology may require surgical correction. affected area may be required.
Cellulitis Necrotising fascitis
Cellulitis is a spreading infection in the Necrotising fasciitis is usually seen in
subcutaneous tissue. It often occurs after a immunocompromised patients such as
skin abrasion or other similar minor trauma. diabetics, alcoholics or intravenous drug
It is usually due to infection with β haemolytic abusers. It occurs at several characteristic
Streptococcus or Staphylococcus aureus. Both sites including the limbs after cuts, abrasions
produce enzymes that degrade tissue and or bites, around postoperative abdominal
allow spread of infection. surgical wounds, in the perineum secondary
to anorectal sepsis or in the male genitalia
Clinical features (Fournier’s gangrene). It occurs as a result of
Cellulitis usually presents with a well- a polymicrobial infection involving facultative
demarcated area of inflammation. It is often aerobes, Streptococcal species or Escherichia
associated with malaise, fever and a raised coli and anaerobes. The exotoxins produced
white cell count. If not rapidly treated, it can by the organisms result in severe systemic
progress to lymphangitis and lymphadenitis. toxicity.
Localised areas of skin necrosis may occur.
Predisposing factors for infection include Clinical features
lymphoedema, venous stasis, diabetes
mellitus and surgical wounds. The early clinical features are often similar to
cellulitis but warning features include severe
Management pain – out of proportion to the clinical signs,
Treatment should be by rest and elevation systemic toxicity, cutaneous gangrene or
of the affected limb. Antibiotics may initially haemorrhagic fluid leaking from a wound.
be given orally but consideration should be Untreated, it rapidly progresses to multiple
given to intravenous administration if there organ failure and overall has a mortality of
is no early improvement. Benzylpenicillin about 30%. A plain x-ray may show gas in the
and flucloxacillin are usually the antibiotics subcutaneous tissue.
of choice.
Management
Necrotising soft tissue
infections Early and rapid treatment requires a high
degree of clinical suspicion. Patients should
Necrotising soft tissue infections are the result be managed in a high dependency unit as
of skin and subcutaneous infections with they will need vigorous fluid resuscitation
virulent bacteria. Bacterial toxins can cause and organ support. Early surgical
widespread skin and fascial necrosis. debridement is essential. Excision should
extend well into apparently normal tissue.
Meleney’s synergistic gangrene Amputation or fasciotomies may be required.
A defunctioning colostomy may be required
Meleney’s synergistic gangrene results from for perineal sepsis. Antibiotic cover should
synergistic infection affecting principally include benzylpenicillin, metronidazole and
the skin. It usually occurs around surgical gentamicin. Hyperbaric oxygen therapy may
wounds, stomas and cutaneous fistulae. It be of benefit.
is due to infection with both Staphylococcus
aureus and anaerobic streptococci. The Wound infection
initial clinical features are often initially
indistinguishable from cellulitis. However About 75% of nosocomial infections occur
in surgical patients. Most postoperative
Surgical microbiology 77
infections arise from the patient’s own • Staphylococcus aureus (17%)
bacterial flora. The commonest sites of • Enterococci (13%)
infection are the urinary tract (40%), wounds • Coagulase-negative staphylococci (12%)
(35%), the respiratory tract (15%) and • Escherichia coli (10%)
bacteraemia (5%). Wound contamination • Pseudomonas aeruginosa (8%)
can occur from direct inoculation from the • Enterobacter species (8%)
patient’s residual flora or skin contamination • Proteus mirabilis (4%)
from the surgeon’s hands, contaminated • Klebsiella pneumoniae (3%)
instruments, dressings, drains, catheters or • Candida species (2%)
intravenous lines. Airborne contamination
can occur from the skin and clothing of staff Prevention
or from air flow in the operating theatre or Exogenous methods of preventing wound
ward. Haematogenous spread can occur infections include:
from intravenous lines and sepsis at other
anatomical sites. • Sterilisation of instruments and sutures
• Positive pressure ventilation of operating
Definition
theatres
Wounds infections can be defined as: • Laminar air flow in high-risk areas
• Exclusion of staff with infections
• Surgical site infections
• Superficial incisional infections Endogenous methods of preventing wound
• Deep incisional infections infections include:
• Organ space infections
• Skin preparation
To meet the definition, surgical site infections • Mechanical bowel preparation
must occur within 30 days of surgery and • Antibiotic prophylaxis
the infection must involve only the skin • Good surgical technique
and subcutaneous tissue. There must be
either purulent discharge from a superficial Wound infection rates
infection or organisms isolated from
aseptically obtained wound culture. There The risk of wound infection varies with the
must also be signs of inflammation. Several type of surgery. Four categories of surgery
predisposing factors for wound infection are have been defined:
well-recognised (Table 6.1).
• Clean
Microbiology • Contaminated
• Clean-contaminated
Aerobic pathogens found in wound infections • Dirty
include:
A clean wound involves an incision though
non-inflamed tissue and the wound is
Predisposing factors to wound infection
General factors Local factors Microbiological contamination
Type and virulence of organism
Age, obesity, malnutrition Necrotic tissue Size of bacteriological dose
Endocrine and metabolic Foreign bodies
disorders Antibiotic resistance
Hypoxia, anaemia Tissue ischaemia
Malignant disease Haematoma formation
Immunosuppression Poor surgical technique
Table 6.1 Predisposing factors to wound infection
78 Chapter 6 Surgical pathology and microbiology
primarily closed. There is no breach in developing countries where it is seen in
aseptic technique and no viscus is opened. neonates (tetanus neonaturum) following the
Examples include mastectomy and hernia use of cow dung on the umbilicus.
repair and wound infection rates are
typically 1–2%. A clean-contaminated Microbiology
wound is created at emergency surgery or Tetanus is due to infection with Clostridium
by reoperation via a clean incision within tetani. This is a Gram-positive spore forming
7 days of the original surgery. A viscus may rod which on microscopy has a typical
be opened but no spillage of gut contents ‘drum-stick’ appearance with a terminal
has occurred. There can be a minor break spore. It is widely found in the environment
in aseptic technique. Examples include and soil. It is a strict anaerobe that produces
right hemicolectomy and cholecystectomy. a powerful exotoxin. The exotoxin is resistant
Infection rates are usually less than 10%. A to autoclaving. It is not antigenic and repeat
contaminated wound is one that is left open infection can occur. Infection produces few
or created by penetrating trauma less than signs of local inflammation.
4 hours old. A viscus may be opened with
inflammation or spillage of contents or there Pathogenesis
has been a major break in sterile technique.
Examples include appendicectomy and stab Germination of spores results in the release
wounds and infection rates are often about of the exotoxin. The toxin affects the nervous
15–20%. A dirty wound has the presence of system and reaches the central nervous
pus, intraperitoneal abscess formation or system via the peripheral nerves. It acts
visceral perforation. It can also be caused by on the presynaptic terminals of inhibitor
penetrating trauma more than 4 hours old. nerves and reduces the release of inhibitory
Examples include all perforated abdominal neurotransmitters (e.g. glycine). The excess
viscera and infection rates are often more activity of motor neurones produces muscle
than 40%. spasm.
Antibiotic prophylaxis Clinical features
Wound infection rates can be reduced with Facial muscle spasm produces trismus.
antibiotic prophylaxis. Prophylaxis is the use The typical facial appearance is often
of antibiotics to prevent infection. Treatment referred to as ‘risus sardonicus’. Back muscle
is their use to eradicate established sepsis. spasm produces opisthotonos. Eventually
Prophylaxis is important in surgery with a exhaustion and respiratory failure leads to
high incidence of postoperative infection death. The diagnosis is essentially clinical.
(e.g. colonic surgery) or where infection Differentiating between contamination and
would be disastrous (e.g. prosthetic valves). infection on wound swabs is difficult.
It is necessary to consider the use of an
appropriate antibiotic based on likely Treatment
bacteria, tissue penetration and the timing
and duration of administration. Antibiotics Tetanus can be prevented by active
are usually administrated intravenously at immunisation with tetanus toxoid with
induction of anaesthesia and often involves a booster every 5–10 years, adequate
only one or a limited number of doses to wound toilet of contaminated wounds and
cover the period of risk. passive immunisation with hyperimmune
immunoglobulin in those at risk. In
Tetanus suspected cases, treatment should involve
passive immunisation with anti-tetanus
Less than 100 cases of tetanus are reported immunoglobulin, adequate wound
each year in the UK. It develops following debridement, intravenous benzylpenicillin
a deep or penetrating wound in a relatively and intensive care support. Despite the use of
avascular area. It is more prevalent in intensive care, the mortality associated with
tetanus is about 50%.
Surgical microbiology 79
Gas gangrene organisms responsible are usually sensitive
to penicillin. Hyperbaric oxygen may
Clostridial spores are widely distributed in be helpful. Benzylpenicillin antibiotic
the environment. They may enter traumatic prophylaxis should be considered in those
or surgical wounds. Contamination may with contaminated wounds or in diabetics
also occur from the patient’s own faecal undergoing elective peripheral vascular
flora. surgery.
Microbiology Pseudomembranous colitis
Gas gangrene results from the following
clostridial species: Pseudomembranous colitis is due colonic
infection with Clostridium difficile. It is a
• Clostridium welchii Gram-positive anaerobic bacillus. It was not
• Clostridium oedematiens identified until 1953 because it was ‘difficult’
• Clostridium septicum to culture. Spores are commonly found in the
hospital environment.
Microscopy of wound exudate shows Gram-
positive bacilli. They are rectangular in shape Pathophysiology
without spore formation. Anaerobic culture
on blood agar show haemolytic colonies Normal stool contains more than 500
(Clostridium welchii) and a ‘stormy’ clot reaction different bacteria at a concentration of 1012
with litmus milk. Clostridium welchii also shows per gram. Antibiotic therapy can change
a positive Nagler reaction (Figure 6.1) due to a the faecal flora. Broad-spectrum antibiotics
lecithinase reaction of a exotoxin. are the main culprits and particular
problems are seen with lincomycin
Clinical features and clindamycin – but these are rarely
Patients with gas gangrene are generally toxic used. Changes in the faecal flora allow
and unwell. They often have features of shock, colonisation by C. difficile transmitted by
jaundice, haemolysis or acute renal failure. the faecal–oral route. Exotoxins produced
Local signs of gas gangrene include myositis by bacteria are cytotoxic. They act via cell
or myonecrosis, gas formation with palpable membrane receptors and produce mucosal
crepitus and mottled discolouration of the inflammation and cell damage. If severe
overlying skin. A plain x-ray often shows gas infection occurs, epithelial necrosis follows
in the subcutaneous tissue and fascial plains. and a pseudomembrane is formed. This
Failure of recognition often results in rapid consists of mucin, fibrin, leukocytes and
deterioration. cellular debris. Approximately 50% of
neonates are transient healthy carriers of C.
Treatment difficile. Only 1% of adults are asymptomatic
Patients usually require vigorous carriers. About 10% patients on antibiotics
resuscitation and early surgery. Debridement develop diarrhoea but only 1% develop
or amputation should be considered to pseudomembranous colitis.
remove the affected tissue or limb. The
The Nagler reaction on an agar plate Figure 6.1 The Nagler reaction on
an agar plate
Lines of clostridial Opacification due to
innoculation lecinthase activity of
alpha toxin
Antitoxin on No antitoxin on this
this side of plate side of plate
80 Chapter 6 Surgical pathology and microbiology
Clinical features Post-primary tuberculosis
The spectrum of symptomatic disease is Post-primary tuberculosis occurs in
wide and includes mild diarrhoea, colitis adolescence or adult life. It is due to
without pseudomembrane formation, reactivation of infection or repeat exposure
pseudomembranous colitis and fulminant and results in more significant symptoms.
colitis. Diagnosis of C. difficile infection is Reactivation may be associated with
confirmed by the detection of the toxin in the immunosuppression (e.g. drugs or HIV
stool. infection). Pulmonary infection accounts for
70% of cases of post-primary tuberculosis.
Treatment It usually affects the apices of either the
upper or lower lobes. Cavitation of infection
Asymptomatic carriers require no active into the bronchial tree results in ‘open’
treatment. Those with mild diarrhoea should tuberculosis. Clinical features include cough,
have their antibiotics stopped. If colitis is haemoptysis, malaise, weight loss and night
present, then active treatment with oral sweats. Infection of lymph glands results in
antibiotics is required. Metronidazole is discrete, firm and painless lymphadenopathy.
first line therapy. Vancomycin is second Confluence of infected glands can result in a
line therapy. Symptoms usually improve ‘cold’ abscess. Infection of the urinary tract
within 72 hours but it may take 10 days for can cause haematuria and ‘sterile pyuria’.
diarrhoea to stop. About 10% of patients
relapse after initial treatment due to either Investigation
failure of eradication or re-infection.
Pseudomembranous colitis requires Large volume specimens of sputum or urine
aggressive resuscitation and treatment. should be collected, preferably in the early
If fulminant colitis occurs with toxic morning. Repeated samples may be required.
megacolon or perforation, surgery will be
required. Microbiology
Tuberculosis If mycobacterial infection is suspected,
then samples should be submitted for a
Tuberculosis is common throughout the Ziehl–Neelsen stain. Mycobacteria appear
world. It causes significant morbidity and as red acid-alcohol fast organisms. The
mortality, particularly in Africa and Asia. organisms also fluoresce with auramine
Over 10,000 cases per year occur in UK and staining. Negative microscopy does not
it accounts for 1000 deaths mainly in the exclude tuberculosis. Mycobacteria can be
immigrant Asian population. It is usually due difficult to culture. To confirm or exclude
to infection with Mycobacterium tuberculosis a diagnosis, one needs to collect adequate
or Mycobacterium bovis. and relevant specimens (e.g. early morning
urine ×3), concentrate the specimen (e.g.
Primary tuberculosis centrifugation), decontaminate the specimen
to remove other organisms (e.g. Petroff
Primary tuberculosis is usually a respiratory method). The material should be cultured
infection that occurs in childhood. Infection on Lowenstein–Jensen method at 35–37°
results in a sub-pleural Ghon focus and for at least 6 weeks to confirm that any
mediastinal lymphadenopathy. This if mycobacteria cultures are pathological.
often regarded to as the primary complex.
Symptoms are often few and resolution of Histology
infection usually occurs. Complications of
primary tuberculosis include haematogenous Histological examination shows evidence
spread causing miliary tuberculosis affecting of a delayed hypersensitivity reaction.
the lungs, bones, joints, meninges or direct The classical appearance is of caseating
pulmonary spread resulting in tuberculosis necrosis. Tuberculous follicles consist of
bronchopneumonia. central caseous necrosis, surrounded by
Surgical microbiology 81
lymphocytes, multi-nucleate giant cells and on blood agar. Microscopically, it is Gram-
epitheloid macrophages. Organisms may be positive and forms clusters on solid media.
identified within the macrophages. There is increasing spread of clones resistant
to b-lactam antibiotics (e.g. MRSA).
Skin tests
Staphylococcus aureus produces skin and
A delayed hypersensitivity skin reaction soft tissue infections including impetigo,
can be used to diagnose tuberculosis. The folliculitis and cellulitis. Deeper infections
two commonest tests are the Mantoux and may occur after trauma or surgery. Metastatic
Heaf test. In the Mantoux test, 0.1 mL of infection may result in endocarditis,
purified protein derivative (PPD) is injected pericarditis, osteomyelitis and lung abscesses.
intradermally. A positive reaction is a papule Treatment is with anti-staphylococcal
of more than 5 mm diameter at 72 hours. In antibiotics (e.g. flucloxacillin). In MRSA,
the Heaf test, PPD is placed on the skin. A vancomycin is the treatment of choice.
gun is used to produce multiple punctures.
A positive reaction is more than four papules Coagulase-negative staphylococci
at the puncture sites at 72 hours. Positive
skin tests are indicative of active infection or Staphylococcus epidermidis and
previous BCG vaccination. Staphylococcus saprophyticus are
the commonest human pathogens.
Management Staphylococcus epidermidis is a common
cause of nosocomial bacteraemia, often
First line chemotherapeutic agents are associated with indwelling catheters and
rifampicin, isoniazid and ethambutol. They prosthetic materials. It is a common cause
are given as ‘triple therapy’ for the first 2 of prosthetic valve endocarditis. It is often
months until sensitivities are available. multiple antibiotic resistant. Treatment may
Rifampicin and isoniazid are then usually require removal of the line or prosthesis.
continued for a further 7 months. Less than
5% of organisms are resistant to first-line Streptococcal infections
agents. Second line treatment includes
pyrazinamide. Streptococci are Gram-positive cocci. More
than 30 species have been identified. On solid
Staphylococcal and media they grow in pairs or chains. They are
streptococcal infections catalase negative. b-haemolytic streptococci
are classified according to their Lancefield
Staphylococcal infections group. The following are human pathogens
More than 30 staphylococcal species exist. • Strep. pyogenes (group A streptococcus)
All are part of the normal skin and mucous • Group C and G streptococci
membrane flora. They are either coagulase- • Strep. pneumoniae (pneumococcus)
positive or negative. The most important • Group B streptococcus
coagulase-positive species is Staphylococcus • viridans group streptococci
aureus. • Enterococcus
Staphylococcus aureus Streptococcus pyogenes
About 30% of adults carry Staphylococcus Streptococcus pyogenes is an important
aureus in the anterior nares of their nose. human pathogen. It causes various
Carriers transfer the organism to skin cutaneous and systemic infections including
allowing a portal of entry. The organism streptococcal pharyngitis, scarlet fever,
has several putative determinants of rheumatic fever and post-streptococcal
pathogenicity including cell wall constituents, glomerulonephritis. The bacterium is
cell surface proteins, toxins (e.g. haemolysins sensitive to penicillin.
and leukocidins) and enzymes (e.g.
coagulase, protease, hyaluronidase). The Streptococcus pneumoniae
organism is both aerobic and anaerobic
Streptococcus pneumoniae is a common
bacterial pathogen. It is found in the
82 Chapter 6 Surgical pathology and microbiology
nasopharynx of 20% of adults. On a personnel may be carriers. It is often found
Gram-stain it appears as a diplococcus. on the inguinal, perineal or axillary skin and
It is a-haemolytic on blood agar. It is a anterior nares. It can be spread by hand,
common cause of localised and systemic usually of healthcare workers. Risk factors for
infections including otitis media, sinusitis, colonisation of patients include:
meningitis, pneumonia, endocarditis and
osteomyelitis. Infection can be prevented • Advanced age
by the pneumococcal vaccine. Resistance to • Male gender
penicillin is increasing worldwide. • Previous hospitalisation
• Length of hospitalisation
Viridans group streptococci • Stay in intensive care
• Chronic medical illness
The viridans group of streptococci are • Prior and prolonged antibiotic therapy
a diverse group of organisms. They are • Presence and size of a wound
respiratory, gastrointestinal and oral cavity • Exposure to colonised or infected patient
commensals. Infection usually occurs in • Presence of invasive indwelling device
immunocompromised hosts. The principal
virulence trait is to adhere to cardiac valves Clinical features
and cause endocarditis. It accounts for
30–40% of cases of endocarditis. Most occur The clinical presentation of MRSA infection
in patients with valvular heart disease. is as:
Other risk factors include prosthetic heart
valves and intravenous drug abuse. Most • Pneumonia
viridans streptococcal species are sensitive to • Surgical site infections
penicillin. • Line sepsis
• Intra-abdominal infections
Enterococcus species • Osteomyelitis
• Toxic shock syndrome
Enterococci are facultative anaerobes.
They are common commensal of the Microbiology
gastrointestinal tract. They are significant
cause of nosocomial infection including Staphylococcus aureus is a Gram-positive
urinary tract infections, endocarditis and coccus which forms clusters on culture
intra-abdominal infection. Risk factors for medium. Methicillin resistance is mediated
infection include severe underlying disease, by the mecA gene which encodes a single
previous surgery, previous antibiotic therapy, additional penicillin binding protein
renal failure and the presence of vascular or PBP2a. Expression of mecA can be either
urinary catheters. Mortality from enterococcal constitutive or inducible. The risk of
infection is high. They are intrinsically colonisation and infection of patients can be
resistant to b-lactams and aminoglycosides. reduced by strict infection control measures
They can also acquire resistance to including:
vancomycin. Management of vancomycin-
resistant enterococcus is difficult. • Screening of patients and staff
• Hand washing
Methicillin resistant • Use of gowns and gloves
Staphylococcus aureus • Topical antimicrobials
• Isolation of patients
Methicillin resistant Staphylococcus aureus • Environmental cleaning
(MRSA) is a major nosocomial pathogen.
It causes severe morbidity and mortality Management
worldwide. It is endemic in many European
and American hospitals where 40% of Vancomycin is the antibiotic of choice.
nosocomial Staphylococcus aureus infections Teicoplanin may be used if the isolate is
are methicillin resistant. Many inpatients are resistant to vancomycin. Linezolid is new
colonised or infected and up to 25% hospital class of antimicrobial agent active against
MRSA and VRE. Quinupristin and dalfopristin
are also newer alternatives.
Prevention of infection 83
Prevention of infection forming organisms. It is effective against both
Principles of asepsis Gram-positive and Gram-negative organisms.
and antisepsis It is rapidly inactivated by organic material
such as blood. Patient skin sensitivity is
Antisepsis is the use of chemical solutions occasionally a problem. Chlorhexidine may
for disinfection. It involves the removal of be more effective than iodine at reducing
transient microorganisms from the skin and a wound infections.
reduction in the resident flora. Asepsis is the
complete absence of infectious organisms. Surgical preparation
Aseptic techniques are those aimed at
minimising infection. Asepsis usually involves Preoperative washing with bactericidal
the use of sterile instruments and a gloved no agent eliminates transient skin flora. A brush
touch technique. should be used on the nails but not on the
skin and should only be performed once
Preoperative skin preparation in a surgical session. The scrub time makes
little difference to the incidence of wound
The bacterial flora of the patient is the infections. Most surgical gloves are made
principle source of surgical wound infection. of latex and are disposable and single-use.
It is important that focal sources of sepsis About 50% of gloves are punctured during
should be treated prior to elective surgery. In surgery. Glove perforation increases the
patients with active infection, consideration risk of wound infection by a factor of five.
should be given to delaying surgery. Double gloving affords better protection to
Preoperative showering with an antiseptic the surgeon. Face masks protect the surgeon
solution does not reduce wound infections but not the patient. There is no evidence
that masks reduce the incidence of wound
Skin shaving infections.
Skin shaving is aesthetic and makes surgery, Sterilisation and disinfection
suturing and dressing removal easier. Wound
infection rates are lowest when when skin- Sterilisation
shaving is performed immediately prior to
surgery. Infection rate increases from 1% to Sterilisation is the removal of viable
5% if performed more than 12 hours prior to microorganisms including spores and viruses.
surgery. Abrasions can cause colonisation It can be achieved by the use of:
which can lead to wound infection. The
use of clippers or depilatory creams reduce • Autoclaves
infection rates to less than 1%. • Hot air ovens
• Ethylene oxide
Skin preparation • Low-temperature steam and formaldehyde
• Sporicidal chemicals
70% isopropyl alcohol acts by denaturing • Irradiation
proteins. It is bactericidal but short acting. • Gas plasma
It is effective against both Gram-positive
and Gram-negative organisms. It is also Autoclaves and hot air ovens
fungicidal and virucidal. 0.5% chlorhexidine
is a quaternary ammonium compound that Autoclaves use steam under pressure at high
acts by disrupting the bacterial cell wall. temperature. To be effective against viruses
It is bactericidal but does not kill spore and spore-forming bacteria, it is necessary to
forming organisms. It is persistent and has have steam in direct contact with the material
a long duration of action (up to 6 hours). and for a vacuum to be created. To ensure
It is more effective against Gram-positive sterilisation, it is necessary to autoclave for 3
organisms. 70% povidone–iodine acts by minutes at 134°C or 15 minutes at 121°C.
oxidation/substitution of free iodine. It is Performance can be checked by colour
both bactericidal and active against spore changes on indicator tape. Autoclaves are
highly effective and inexpensive but are not
suitable for heat-sensitive objects. Hot ovens
84 Chapter 6 Surgical pathology and microbiology
are inefficient compared to autoclaves. They organisms are highly sensitive where as
require temperatures of 160°C for 2 hours or clostridial and mycobacterial species are
180°C for 30 minutes. very resistant. Disinfectants are suitable for
Ethylene oxide heat-sensitive items but are less effective
than heat. Chemicals used for disinfection
Ethylene oxide is highly-penetrative gas that include:
is active against bacteria, spores and viruses. • Clear soluble phenolics
Unfortunately, it is also flammable, toxic • Hypochlorites
and expensive and leaves toxic residue on • Alcohols
sterilised items. Instruments therefore need • Quaternary ammonium compounds
to be stored for prolonged period before use.
It is suitable for sterilisation of heat-sensitiveSurgery in hepatitis and
items. HIV carriers
Hepatitis B
.ir/Sporicidal chemicals
The hepatitis B virus is a single-stranded
Sporicidal chemicals are often used DNA virus. It consists of 42 nm Dane particle
as disinfectants but can also sterilise (HbsAg) and 22 nm core (HbcAg). The
hepatitis B surface antigen (HbsAg) is also
sinstruments if used for prolonged period. know as the Australia antigen. The virus also
sThey are inexpensive and suitable for heat- contains the hepatitis B ‘e’ antigen (HbeAg).
The body produces antibodies to the surface
sensitive items. They are toxic and irritant. antigen (HbsAb).
n2% Glutaraldehyde is the most widely used In the UK, the prevalence of HbsAg
ialiquid sporicidal chemical. Most bacteria positivity is about 1–2% and is seen
particularly in drug addicts, homosexuals,
and viruses are killed within 10 minutes but dialysis patients and occasionally medical
spores can survive several hours. staff. In Asia, Middle East and South
America the prevalence of HbsAg positivity is
rsIrradiation between 20–30%. It is transmitted by vertical
eGamma rays and accelerated electrons are transmission, inoculation, oral and sexual
contact. The incubation period is between 6
excellent at sterilisation and are used as an weeks and 6 months. The period of infectivity
is from 6 weeks, before the onset of symptoms
.pindustrial rather than hospital-based method and possibly indefinitely after. About 10% of
infected patients become chronic carriers.
of sterilisation. The risk of chronic infection varies with age at
which infection is acquired and is greatest in
ipDisinfection young children.
://vDisinfection is a reduction in the number of
viable organisms. It can be achieved by:
• Low-temperature steam
• Boiling water
ttp• Chemical disinfectants
Low-temperature steam
hMost bacteria and viruses are killed by
exposure to moist heat. This is usually Clinical features
achieved with dry saturated steam at 73°C
for greater than 10 minutes. It is effective and There are three common clinical pictures:
reliable and suitable for instrument with a • Acute hepatitis with clinical recovery
lumen but is not suitable for heat-sensitive • Acute fulminating hepatitis leading to death
items. • Chronic active hepatitis with risk of
Chemical disinfectants cirrhosis and hepatocellular carcinoma
Chemical disinfectants destroy micro- Serological results
organisms by chemical or physicochemical HbsAg positivity is the first indicator of
means. Different organisms vary in their infection and is seen throughout the course of
sensitivity to disinfectants. Gram-positive
Surgery in hepatitis and HIV carriers 85
the disease. Persistence is a marker of failure was isolated in 1983. In 1984, a serological test
to clear infection. HbsAb positivity is a marker for antibodies to the virus became available.
of protection due to either previous infection About 30–50% of HIV positive patients are
or immunisation. HbeAg positivity is closely unaware of their infection. HIV is a treatable
associated with infectivity of the patient. disease. Where therapy is available, infected
Prevention of infection individuals have the same rate of death as
aged-matched uninfected controls.
It is important to avoid contact with the virus. Immunology
It requires care with needles and body fluids.
After a needle stick injury from a high-risk HIV is a double-stranded RNA retrovirus that
patient, hyperimmune anti-hepatitis B IgG
should be given, ideally within 24–48 hours attaches to human immune cells through the
after exposure and repeated at 1 month. All CD4 molecule. It produces DNA by the use of
the enzyme reverse transcriptase. DNA is then
.ir/paramedical staff should be immunised. incorporated into host cells. The incorporated
viral DNA produces new viral components
Hepatitis B vaccine should be given and which are spliced and assembled using a viral
repeated at 1 and 6 months. A HbsAb levels protease. HIV infection results in widespread
of more than 1000 μ/L indicates an adequate immunological dysfunction. It results in a fall
in CD4 lymphocytes, monocytes and antigen-
sresponse and confers protection for up to 5 presenting cells. Immunological dysfunction
syears . results in opportunistic infections and
nHepatitis C increases the risk of malignancy. The virus is
iaThe hepatitis C virus (HCV) is a small, transmitted in bodily fluids by:
enveloped, single-stranded RNA virus. The • Heterosexual intercourse
• Homosexual intercourse
rsinfection is often asymptomatic, but chronic • Blood transfusions
• Intravenous drug abuse
infection can occur. The HCV is spread by • Perinatal transmission
blood-to-blood contact. The virus persists in
Natural history
ethe liver in about 85% of those infected. During
Up to 3 months after infection, there is often
the first 12 weeks after infection with HCV, most an asymptomatic viraemia and patients are
infective during this period. The ELISA test for
.ppeople suffer no symptoms. For those who do, HIV antibodies is negative. At seroconversion
an acute seroconversion illness (ASI) can
the main manifestations of acute infection are occur and may be followed by persistent
generalised lymphadenopathy (PGI).
ipgenerally mild and vague, and rarely point to Progression to symptomatic disease occurs
within several years. AIDS develops within 5
a specific diagnosis of hepatitis C. The HCV is to 10 years. AIDS is diagnosed by the presence
://vusually detectable in the blood by PCR within 1
to 3 weeks after infection, and antibodies to the
virus are generally detectable soon after that.
Chronic hepatitis C is defined as infection with
ttpthe hepatitis C virus persisting for more than
6 months. Clinically, it is often asymptomatic,
and it is mostly discovered accidentally,
hfollowing the investigation of elevated liver
enzyme levels. One-third of untreated patients of an AIDS indicator disease with a positive
will progress to cirrhosis within 20 years.
HIV test. The median survival with AIDS is 5
Treatment is generally recommended for
years. The virological, serological and clinical
patients with proven hepatitis C virus infection response to HIV infection is shown in Figure
and persistently abnormal liver function
6.2. AIDS indicator diseases include:
tests. Current treatment is a combination of
interferon-a-2a and the antiviral drug ribavirin. • Multiple recurrent bacterial infections
• Tracheal or bronchial candidiasis
HIV infection • Invasive cervical carcinoma
• Extrapulmonary or disseminated
Acquired immunodeficiency syndrome (AIDS)
was first recognised in the USA in the 1970s coccidioidomycosis
and the human immunodeficiency virus (HIV) • Cryptosporidiosis
• Cytomegalovirus retinitis
86 Chapter 6 Surgical pathology and microbiology
The virological, serological and clinical response to HIV Figure 6.2 The virological,
serological and clinical
Seroconversion response to human
immunodeficiency virus
Window Latent stage Symptomatic AIDS infection. AIDS = Acquired
period stage immunodeficiency syndrome
ss.ir/Plasma viraemia
nCD4 lymphocyte count
iaAntibody response
HIV-specific cytotoxic T lymphocyte response
ers• HIV encephalopathy
.p• Disseminated or extrapulmonary • Osteomyelitis
• Septic arthritis
histoplasmosis • Epididymo-orchitis
• Pelvic inflammatory disease
ip• Kaposi’s sarcoma • Appendicitis
• Lymphoma Management
://v• Disseminated mycobacteriosis HIV therapies are available that prevent
virus entry into cells, inhibit the viral reverse
• Pneumocystis carinii pneumonia transcriptase and viral protease. Combination
• Progressive multifocal therapy with anti-HIV drugs inhibits viral
replication, reduces viraemia to undetectable
leukoencephalopathy levels, leads to reconstitution of immune
dysfunction and prevents opportunistic
ttp• Cerebral toxoplasmosis disease. Stopping therapy often leads to re-
emergence of the viraemia.
Sites of pyogenic infections in AIDS include:
• Thoracic empyema
h• Anorectal abscesses
• Skin boils, carbuncles and cellulitis
• Necrotising fasciitis
• Pyomyositis
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MRCS Applied Basic Science and Clinical Topics
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