Chapter 7 Emergency
medicine and the
management of
trauma
Pathophysiology of trauma motility is reduced. Insulin production
Metabolic response to injury is reduced and glucagon production is
increased. Increased glycogenolysis increases
A similar metabolic response is seen blood sugar levels.
following trauma, burns, sepsis and surgery.
It involves both local and systemic reactions Acute phase response
with the extent of the response being Tissue injury results in cytokine release.
proportional to the severity of insult. An Important cytokines include tumour necrosis
appropriate response maintains homeostasis factor-alpha (TNF-a), interleukins (IL-1,
and allows wound healing to occur. An IL-2, IL-6), interferon and prostaglandins.
excessive response can produce a systemic Cytokines have mainly paracrine actions and
response. This can cause the systemic are important in regulating the inflammatory
inflammatory response syndrome (SIRS) response. Overflow of cytokines into systemic
and multiple organ dysfunction syndrome circulation is important factor in SIRS.
(MODS). Cytokines stimulate the production of acute
phase proteins such as C-reactive protein,
Initiation of response fibrinogen, complement C3 and haptoglobin.
Several factors can initiate the physiological Endocrine response
response to trauma and multiple The hypothalamus, pituitary, adrenal axis
simultaneous factors can have a synergistic is important in the endocrine response to
effect. Important factors are: trauma. Trauma increases ACTH and cortisol
production. Steroids have a permissive action
• Tissue injury in many metabolic responses. Catabolic
• Infection action increases protein breakdown. Insulin
• Hypovolaemia antagonism increases blood sugar levels.
• Hypoxia or hypercarbia Anti-inflammatory actions reduce vascular
permeability. Aldosterone increases sodium
Control of response reabsorption. Vasopressin increases water
reabsorption and produces vasoconstriction.
Four systems control the response to trauma: Histamine increases vascular permeability.
Total T4, total and free T3 levels are reduced.
• Sympathetic nervous system
• Acute phase response Vascular endothelium
• Endocrine response Nitric oxide production by the vascular
• Vascular endothelium endothelium produces vasodilatation.
Platelet activating factor (PAF) augments
Sympathetic nervous system the cytokine response. Prostaglandins
The sympathetic nervous system has direct produce vasodilatation and induce platelet
actions via the release of noradrenaline from aggregation.
sympathetic nerves and has indirect action
via the release of adrenaline from the adrenal Outcome of response
medulla. It produces cardiovascular, visceral
and metabolic actions. Blood is diverted from The inflammatory response produces
the skin and visceral organs. The heart rate clinically apparent local and systemic effects.
and myocardial contractility are increased.
Bronchodilation occurs and gastrointestinal
88 Chapter 7 Emergency medicine and the management of trauma
The local response is usually the cardinal mobile intensive care units often attend the
signs of inflammation. The systemic response scene of an accident. This has been described
includes: as ‘stay and play’.
• Increased ECF volume and hypovolaemia Initial action
• Increased vascular permeability and
Potential problems at the scene of an accident
oedema depend on the hostility of the environment,
• Early reduced urine output and increased the lack of familiarity with surroundings
and the presence of intrusive onlookers. It is
urine osmolality important to assess the ongoing safety of the
• Reduced ‘free’ water clearance emergency services and any casualties and if
• Late diuresis and increased sodium loss necessary, it is vital to make the accident site as
• Pyrexia in the absence of infection safe as possible before treating any casualties.
• Early reduction in metabolic rate It is important to determine the nature of the
• Late increased metabolism, negative accident and likely mechanism of injuries. At
road traffic accidents, the number, direction
nitrogen balance and weight loss and types of vehicles involved and the degree
• Lipolysis and ketosis of intrusion of damages vehicles should be
• Gluconeogenesis via amino acid assessed along with whether occupants were
wearing seatbelts.
breakdown
• Reduced serum albumin Important indicators of potential
• Hyponatraemia due to impaired sodium significant trauma are:
pump action • Penetrating injury to chest and abdomen
• Acid–base disturbance – usually a • Two or more proximal long bone fractures
• Burns involving more than 15% of body
metabolic alkalosis or acidosis
• Immunosuppression surface area
• Hypoxia and coagulopathy • Burns to face and airway
• Abnormal physiological variables
The inflammatory response can be limited by:
Evidence of high-energy impact include:
• Reducing the degree of trauma with
appropriate and careful surgery • Fall more than 6 m
• Crash speed greater than 20 mph
• Reducing infection with wound care and • Inward deformity of car of more than 0.6 m
antibiotics • Rearward displacement of front axle
• Ejection of passenger from vehicle
• Maintaining enteral nutrition • Rollover of vehicle
• Controlling pain • Death of another car occupant
• Correcting hypovolaemia • Pedestrian hit at great than 20 mph
• Correcting acid–base disturbance
• Correcting hypoxia Prehospital resuscitation
Initial assessment of the Prehospital resuscitation should follow
trauma patient the same principles as that in hospital but
Prehospital trauma care will need to be adapted to circumstances.
Airway management can be difficult but an
Epidemiology of trauma airway can usually be maintained with basic
measures. Intubation without anaesthesia
Trauma is the commonest cause of death in and rapid sequence induction is ill advised as
young adults. Road traffic accidents each year it can induce vomiting and raise intracranial
in UK result in 320,000 minor injuries, 40,000 pressure. The cervical spine should be
serious injuries and 3400 deaths. Up to 30% immobilised with a hard collar. Oxygen
of prehospital deaths may be preventable. should be given. Haemorrhage should be
Prehospital care is important. The philosophy controlled with direct pressure.
of prehospital care varies between countries.
In the USA, only basic resuscitation is
performed at the scene. This has been
described as ‘scoop and run’. In France,
Initial assessment of the trauma patient 89
If a casualty is entrapped it is important injury and is due to major neurological or
to ensure good venous access before vascular injury. Medical treatment can rarely
releasing him or her from the vehicle. Fluid improve the outcome for these patients. The
resuscitation should be give to maintain second peak occurs during the ‘golden hour’
a systolic blood pressure of 90 mmHg. If and is due to intracranial haematoma, major
venous access is difficult, consideration thoracic or abdominal injury. This time
should be given to ‘scoop and run’ rather period is the primary focus of intervention
than delay transfer. Analgesia can be for the Advanced Trauma Life Support
achieved with Entonox or ketamine. Entonox (ATLS) methodology. The third peak occurs
is contraindicated if there is a possibility after days or weeks and is due to sepsis and
of a pneumothorax or basal skull fracture. multiple organ failure. The assessment of
Extrication requires close co-ordination patients with major trauma should involve a
between medical and fire services. The primary survey and resuscitation, secondary
casualty should be ‘packaged for transport’. surgery and definitive treatment. The
This will require hard collar, head blocks, limb primary survey involves:
splints, scoop stretcher or a vacuum mattress.
• A = Airway and cervical spine
Major incident triage • B = Breathing
• C = Circulation and haemorrhage control
If faced with a large number of casualties, it • D = D ysfunction of the central nervous
is important to prioritise management. The
overall aim is to ‘do the most for the most’. system
Triage is the sorting of casualties by priority • E = Exposure
of treatment. Triage can be performed
rapidly by assessing ability to walk, airway, Primary survey and resuscitation
respiratory rate, pulse rate or capillary return. Airway and cervical spine
In a mass casualty situation it should be
performed by a ‘Triage officer’ who assesses In patients with major trauma, it is prudent
casualties without giving treatment. He or to assume that they have a cervical spine
she should divide patients into categories injury until proved otherwise. They should
according to the severity of the injuries be placed in a hard collar which should be
(Table 7.1). Casualties may be given a kept on until the cervical spine has been
coloured triage label to help with their ‘cleared’. If the patient can talk, then he or
subsequent management. she is able to maintain their own airway. If
the airway appears compromised, an initial
Clinical assessment and attempt should be made to improve it with
resuscitation a chin lift and by clearing the airway of any
foreign bodies. If a gag reflex is present,
Trauma deaths have a trimodal distribution. then consideration should be given to
The first peak occurs within minutes of insertion of a nasopharyngeal airway. If no
gag reflex is present, then the patient will
Category Definition Triage categories Treatment
P1 Life-threatening
P2 Urgent Colour Immediate
P3 Minor Red Urgent
P4 Dead Yellow Delayed
Green
Table 7.1 Triage categories White
90 Chapter 7 Emergency medicine and the management of trauma
need endotracheal intubation. If it proves Radiological investigations
impossible to intubate the patient, then
perform a cricothyroidotomy. Once a secure Plain radiographs play an important role in
airway has been achieved, 100% oxygen the primary evaluation of the unstable trauma
should be given through a Hudson mask. patient. For haemodynamically unstable
patients proceeding directly to surgery after
Breathing the primary survey, plain x-rays of the lateral
cervical spine, chest, and pelvis can detect
It is important to assess the position of life-threatening injuries that might otherwise
the trachea, respiratory rate and air entry. be missed. A chest x-ray should be obtained
If there is clinical evidence of a tension in patients with penetrating injuries of the
pneumothorax, then place a venous cannula chest, back, or abdomen. It the patient is
through the second intercostal space in the haemodynamically stable and a CT scan
mid-clavicular line on the affected side. If is indicated, then plain x-rays can often be
there is an open chest wound, seal it with an omitted.
occlusive dressing.
Airway and ventilation
Circulation and haemorrhage control
Airway assessment and management
It is important to check the pulse, capillary
return and state of neck veins. Identify any The patient should be asked a simple
exsanguinating haemorrhage and apply direct question. If he responds appropriately, the
pressure. Place two large calibre intravenous airway is patent, ventilation is intact and the
cannulas in the antecubital fossae and take brain is being adequately perfused. Agitation
venous blood for measurement of a full is often a sign of hypoxia. The aims of airway
blood count, electrolytes and a cross match. management are:
Take a sample for arterial blood gas analysis.
Boluses of intravenous fluids should be given • To secure an intact airway
and the patient should be attached to an • To protect a jeopardised airway
ECG monitor. A urinary catheter should be • To provide an airway when none is
inserted.
available
Dysfunction and exposure
These can be achieved with basic, advanced
Once problems related to the airway, and surgical techniques.
breathing, and circulation have been
addressed, it is necessary to perform a Basic life support
focused neurologic examination. The level
of consciousness should be rapidly assessed Foreign bodies should be removed from the
using AVPU method: mouth and oropharynx. Secretions and blood
should be removed with suction. The airway
• A = alert can usually be secured with a chin lift or jaw
• V = responding to voice thrust. An oropharyngeal or nasopharyngeal
• P = responding to pain airway may be required. Oxygen should be
• U = unresponsive delivered at a rate of 10–12 L/min. It should
be administered via a tight fitting mask with
This should be followed by recording of reservoir (e.g. Hudson mask). An FiO2 of 85%
the patient’s level of consciousness using should be achievable.
the Glasgow Coma Scale (GCS) score, and
assessments of pupillary size and reactivity, Advanced measures
gross motor function and sensation. The
patient should be fully undressed and other If a gag reflex is absent, endotracheal
signs of injury should be sought. Steps intubation is required. If no cervical spine
should be taken to avoid hypothermia. If fracture is suspected then orotracheal
hypothermia is identified then it should be intubation is preferred. If cervical spine
corrected. injury can not be excluded, then consider
nasotracheal intubation. The position of the
tube should be checked. Complications of
tracheal intubation include:
Initial assessment of the trauma patient 91
• Oesophageal intubation • Subglottic stenosis
• Intubation of right main bronchus • Mediastinal emphysema
• Failure of intubation
• Aspiration Ventilation
In a non-intubated patient, ventilation
Surgical airways can be achieved either mouth to mouth
If the patient is unable to be intubated, then using a face-mask. This is more efficient if
a surgical airway is required. There are few performed with a two person technique.
indications for an emergency tracheostomy. A One person maintains the face seal and the
surgical airway can be achieved with a needle other ventilates the patient. If endotracheal
or surgical cricothyroidotomy. intubation is required, it should be performed
with cricoid pressure. If rib fractures are
Needle cricothyroidotomy present, it is necessary to insert a chest drain
In a needle cricothyroidotomy, the on side of the injury to prevent a tension
cricothyroid membrane is punctured with pneumothorax.
a 12 or 14 Fr cannula. It is connected to an
oxygen supply via a Y connector. Oxygen is Hypovolaemic shock
supplied at a rate of 15 L/min. Jet insufflation
is achieved by occlusion of the Y connection. Clinical features
Insufflation is provided 1 second on and The clinical features of hypovolaemic
4 seconds off. Jet insufflation can result in shock depend on the extent of the blood
significant hypercarbia and should only be loss and the age of the patients. Signs
used for 30–40 minutes until a more secure of hypovolaemia include tachycardia,
airway can be achieved. a reduction in pulse pressure and
hypotension. In young fit patients, there
Surgical cricothyroidotomy can be significant hypovolaemia with
To create a surgical cricothyroidotomy, a few physical signs. Young patients can
small incision is made over the cricothyroid maintain an adequate blood pressure until
membrane. A 5 mm incision made in their physiological reserve is exhausted.
the cricothyroid membrane and a small At this point they can become profoundly
tracheostomy tube is inserted. Complications hypotensive. The grading of hypovolaemic
of surgical airways include: shock is shown in Table 7.2.
• Aspiration Fluid resuscitation
• Haemorrhage/haematoma
• Cellulitis Early intravascular volume replacement
• False passage is essential in trauma patients. The ideal
resuscitation fluid remains uncertain.
The grading of hypovolaemic shock
Grade Blood loss Clinical features
Grade 1 Up to 15%
Grade 2 15–30% Mild resting tachycardia
Moderate tachycardia, fall in pulse pressure, delayed
Grade 3 30–40% capillary return
Grade 4 40–50% Hypotension, tachycardia, low urine output
Profound hypotension
Table 7.2 The grading of hypovolaemic shock
92 Chapter 7 Emergency medicine and the management of trauma
Crystalloid versus colloid resuscitation replaced by yellow marrow after 5 years of
More than 40 randomised controlled trials age and therefore intraosseous infusion is
of crystalloid versus colloid resuscitation less effective in older children. The technique
have been published. None has shown the is generally safe with few complications.
use of either type of fluid to be associated Indications for intraosseous infusion include:
with a reduction in mortality. No single type
of colloid has been shown to be superior • Major trauma
another. Albumin solution may be associated • Extensive burns
with a slight increase in mortality. Colloids • Cardiopulmonary arrest
can more rapidly correct hypovolaemia. They • Septic shock
also maintain intravascular oncotic pressure.
Crystalloids require large volume but are Contraindications include ipsilateral lower
equally effective. They are cheaper and have limb fracture or vascular injury.
fewer adverse side effects.
Technique
Hypertonic solutions Intraosseous access is achieved with specially
Hypertonic solutions have been subjected to designed needles. A short shaft allows
recent intensive investigation. They can be used accurate placement within the medullary
to resuscitate patient rapidly with a reduced canal. The technique of intraosseous
volume of fluid and they may reduce cerebral needle insertion is shown in Figure 7.1. A
oedema in patients with severe head injuries. handle allows controlled pressure during
introduction. The needle is usually inserted
Packed red blood cells into the antero-medial border of tibia, 3 cm
Packed red blood cells provide the best below tibial tubercle. Correct placement can
volume expansion and oxygen carrying be checked by aspiration of bone marrow.
capacity. They do however need cross- Both fluids and drugs can be administered.
matching and are not immediately available. Fluid often needs to be administered under
Dilutional coagulopathy occurs with massive pressure. Once venous access is achieved the
transfusion. intraosseous needle should be removed.
Oxygen therapeutic agents Complications
The use of oxygen therapeutic agents is Complications of intraosseous needle
currently being investigated. The potential insertion are rare but needles are incorrectly
advantages over blood include that they placed or displaced in about 10% patients.
are free from potential viral contamination, Potential complications include:
have a longer shelf life and have universal
ABO compatibility. They have similar oxygen • Tibial fracture
carrying capacity to blood. Agents being • Compartment syndrome
studied include: • Fat embolism
• Skin necrosis
• Perflurocarbons • Osteomyelitis
• Human haemoglobin solutions
• Polymerised bovine haemoglobin Traumatic wounds
Gunshot and blast wounds
Intraosseous infusion
Gunshot and blast wounds are well known
Venous access can be difficult in the to military surgeons but are now increasingly
hypovolaemic child. If difficulty is seen in civilian practice. However, military
experienced, then the intraosseous route and civilian wounds differ in several key
can be used as an alternative. The medullary respects. Military wounds are often heavily
canal in a child has a good blood supply. contaminated with delays in treatment.
Drugs and fluids are absorbed into the venous Despite this, the same principles apply to
sinusoids of the red marrow. Red marrow is their treatment.
Technique of intraosseous needle insertion Traumatic wounds 93
Figure 7.1 Technique of
intraosseous needle insertion
Physical properties also tumble (yaw) within the wound. This
increases the presenting area of the bullet and
Penetrating missiles include both munition increases energy transfer. It can result in small
fragments and bullets. Often divided into entry and exit wounds but large wound cavity.
‘high’ and ‘low’ velocity. However, velocity Radial energy transfer can also cause indirect
per se is not important. The amount of fractures. Bullet and bone fragmentation
kinetic energy transferred to the tissues can cause secondary tracts and further
is the key factor. Kinetic energy transfer unpredictable damage.
depends on velocity, the presenting area of
the fragment and the mechanical properties Treatment
of tissue.
In the military environment, the standard
Munition fragments are usually small treatment of gunshot wounds has involved,
and numerous. They are of low velocity wound debridement, wound excision,
(100–500 m/s) and low energy (10–100 J). antibiotic prophylaxis with dressing change
They have poor tissue penetration. Injuries and delayed primary suture at 5 days.
are often numerous but are usually limited Similar wound management protocols
to the fragment track. Hand gun bullets are have been advocated by the Red Cross.
of low velocity (< 250 m/s) and low energy This approach may be modified in civilian
(200–300 J). Rifle bullets are high velocity environment.
(750–1000 m/s) and high energy (2–3 kJ). The
physiological effects depend on the degree of Abdominal stab wounds
energy transfer. If little energy is dissipated,
high velocity bullets can result in low energy Abdominal stab wounds cause less trauma
transfer wounds. than gunshot wounds and therefore the
associated morbidity and mortality is
Pathophysiology reduced. The upper abdomen is most
commonly involved, particularly the left
The effects of bullets can result from both upper quadrant. Peritoneal violation occurs
direct and indirect effects. In low energy in up 70% of abdominal stab wounds, but
transfer wounds, injury results from direct only half of those with peritoneal violation
effects along the bullet track. In high energy sustain an intra-abdominal injury requiring
transfer wounds, indirect effects are more perative intervention. The liver and small
important. Radial forces perpendicular to bowel are the commonest organs injured.
tract result in cavitation. This generates Multiple stab wounds are present in up
contusions and lacerations away from tract. to 20% of patients and 10% of abdominal
Negative pressure within the cavity can suck stab wounds enter the chest. Potential
in environmental contaminants. Rifle bullets
94 Chapter 7 Emergency medicine and the management of trauma
intrathoracic injuries include pneumothorax Compartment syndromes
and pericardial tamponade. Limb compartment syndromes
Clinical features The deep fascia envelops the limbs and
other fascial planes divide the limbs into
Assessment should gain knowledge of the compartments. The forearm has two fascial
implement used, its site of entry and likely compartments. The thigh has three fascial
track. Examination should look for signs of compartments. The lower limb has four
evisceration, haemorrhage and peritonitis. fascial compartments (Figure 7.2).
Digital exploration or probing of the wound
will determine whether the peritoneum has Compartment syndrome
been breached. A plain abdominal x-ray may
show signs of free gas but this investigation A compartment syndrome is a condition in
has limited sensitivity. Abdominal CT is which the circulation and function of the
better at assessing peritoneal penetration tissues within a closed space is compromised
and the extent of intra-abdominal injury. by an increase in pressure within the space.
The normal lower limb venous pressure is
Management up to 10 mmHg. Compartmental pressure
does not normally interfere with blood flow.
In the past surgical dictum mandated Swelling within a fascial compartment results
exploratory laparotomy for all patients with in increased intracompartmental pressure.
abdominal stab wounds. However, new Initial venous compromise may progress to
diagnostic techniques have rendered such reduced capillary flow. This exacerbates the
a dogmatic approach obsolete and reduced ischaemic insult and further increases the
the number of non-therapeutic laparotomies. compartment pressure. A vicious cycle of
Evisceration, hypovolaemia and peritonitis increasing pressures can be initiated. Arterial
are indications for a laparotomy without inflow is rarely reduced unless the pressure
the need for extensive investigation. If the exceed systolic blood pressure. If this occurs,
penetrating object is still in-situ, it should irreversible muscle ischaemia will occur within
remain so until after induction of anaesthesia. 6 to 12 hours. Surgical treatment within 6 hours
If there are no clinical or radiological signs of of onset usually results in a positive outcome.
bleeding or visceral perforation, then most
abdominal stab wounds can be managed Aetiology
conservatively. Patients should be actively
observed for 24–48 hours. Causes of compartment syndromes include:
Lower limb fascial compartments Figure 7.2 Lower limb fascial
compartments
Lateral Anterior
Tibia
Fibula
Deep Superficial
posterior posterior
Compartment syndromes 95
• Fractures (especially comminuted of disability. Decompression should not be
fractures) compromised by a desire for good cosmesis.
All compartments should be decompressed.
• Ischaemia–reperfusion injury All four compartments of the lower leg can
• Haemorrhage be decompressed through two incision. Skin
• Phlegmasia caerulea dolens incisions of about 15–20 cm in length are
• Intravenous or intra-arterial drug injection required. Timely surgery produces a good
• Soft-tissue injury functional outcome. Delayed surgery results
• Burns in muscle ischaemia and necrosis. Muscle
fibrosis produces the typical Volkmann’s
Clinical features ischaemic contracture.
Compartment syndromes are normally
seen within 48 hours of injury. Clinical Fat embolism
features include increasing pain despite
immobilisation of fracture, altered sensation Fat embolism is due to fat entering torn
in the distribution of nerves passing through venous channels at the site of a fracture.
the compartment, muscle swelling and Chylomicrons may also aggregate due to
tenderness and excessive pain on passive lipase release. Fat embolism presents with
movement. It is important to note that pyrexia, tachycardia, tachypnoea and reduced
peripheral pulses may still be present. consciousness. Patients may develop a
petechial rash. Clotting may be deranged
Pressure monitoring with features of disseminated intravascular
Intracompartmental pressure (ICP) can be coagulation. Arterial gases often show
measured by several means including: hypoxia and hypercapnia. Patients may
require ventilation. Mortality can be as high
• Wick catheter as 15%.
• Simple needle manometry
• Infusion techniques Abdominal compartment
• Pressure transducers syndrome
• Side-ported needles
An abdominal compartment syndrome occurs
The critical pressure for diagnosing a when the abdomen is subject to increased
compartment syndrome is unclear. Different intracompartmental pressure, usually defined
authors recommend surgical intervention if as a pressure above 20 mmHg. It is often the
the: result of retroperitoneal haemorrhage, trauma
or sepsis. Intraperitoneal or retroperitoneal
• Absolute ICP is greater than 30 mmHg fluid accumulation reduces the compliance of
• Difference between diastolic pressure and the abdominal wall. Once the abdominal wall
can no longer expand, any further fluid leaking
ICP is less than 30 mmHg into the tissue or peritoneum results in a rapid
• Difference between mean arterial pressure rise in the pressure. Increased intra-abdominal
pressure reduces blood flow to the abdominal
and ICP is less than 40 mmHg organs and impairs pulmonary, cardiovascular,
renal, and gastrointestinal function.
Management
Constricting casts and splints should be Clinical features
removed if there is any clinical suspicion
of a compartment syndrome. If there is no In the unconscious ventilated patient it
improvement, prompt fasciotomies are can be difficult to recognise. Clinically, it is
required. It is necessary to divide both the characterised by a reduce cardiac output,
skin and deep fascia for the whole length of increased central venous pressure, a fall
the compartment. Wounds should be left in urine output and the need to increase
open and may require delayed closure or skin ventilation pressures. Untreated it can lead
grafting at a later date. to multiple organ dysfunction and death.
The diagnosis can be confirmed by the
Fasciotomies
Several surgical approaches for fasciotomies
have been described. The goal is prevention
96 Chapter 7 Emergency medicine and the management of trauma
measurement of intra-abdominal pressure. vertical linear corneal abrasions. Eversion
This may be done using simple manometry of the upper eyelid with a cotton bud will
through a Foley catheter in the bladder. often show the foreign body. They can
be removed with a needle. Foreign body
Management sensation may persist for a while after
The development of an abdominal removal.
compartment syndrome can often be
anticipated. In these situations it often best Corneal abrasion
to leave the abdomen open. The abdomen
should not be closed under extreme tension. Corneal abrasions are often causes by twigs,
Exposed bowel can be covered with a fingernails and the edges of pieces of paper.
‘Bogota bag’ or vacuum-assisted temporary They causes intense pain and lacrimation.
abdominal closure can be performed. In The abrasion can be confirmed with the
those suspected of developing an abdominal aid of fluorescein. Antibiotic ointment and
compartment syndrome, the abdomen cycloplegic drops should be instilled into the
should be decompressed. However, sudden eye. A pad should be applied. Most abrasions
release of an abdominal compartment heal within 48 hours.
syndrome may lead to an ischaemia–
reperfusion injury causing acidosis, Blunt trauma
vasodilatation, cardiac dysfunction and
cardiac arrest. Blunt ophthalmic trauma can result in:
The eye – trauma and • Black eye
common infections • Subconjunctival haemorrhage
• Corneal abrasion
The eye is well-protected by the bony orbit • Traumatic mydriasis
and reflex closure of the eye lid. Corneal • Hyphaema
trauma is common but more major injuries to • Iridoialysis
eye and orbit are rare. • Concussion cataract
• Lens subluxation
Corneal foreign body • Retinal tear
• Vitreous haemorrhage
Corneal foreign bodies occur due to • Commotio retinae
fragments hitting the cornea at high speed. • Choroidal rupture
They often occur as a result of hammering or • Blow-out orbital fracture
drilling. Corneal foreign bodies usually causes
pain, photophobia and profuse lacrimation. Hyphaema
Local anaesthesia may be required in
order to examine the eye. The foreign body Hyphaema is blood in the anterior chamber
is often readily seen. If a metallic foreign of the eye. It is due to rupture of the iris
body is present for more than a few hours is blood vessels and presents with a reduction
often results in a ‘rust ring’. The object can in visual acuity. The red reflex is lost. Within
often be removed with sterile needle under a short period of time the blood settles and
local anaesthesia. Antibiotic ointment and produces a fluid level. Most hyphaema
cycloplegic drops should be instilled into the settle with conservative treatment. Surgical
eye. A pad should be applied. treatment may be required if the anterior
chamber is full of blood. Inadequate
Subtarsal foreign body treatment can result in glaucoma or blood-
staining of the cornea.
Foreign bodies occasionally become
embedded in the subtarsal conjunctiva Blow-out fracture
of the upper lid. They cause pain and
lacrimation. Examination may show fine, Posterior displacement of the globe raises the
orbital pressure. The orbit may then fractures
at its weakest point. This usually occurs at
the orbital floor and soft tissues herniates
The eye – trauma and common infections 97
into the maxillary sinus. Clinical features of reactions. Siderosis from iron causes staining
a blow-out fracture include, enophthalmos, of the iris, cataract formation and retinal
restriction of eye movement, especially on atrophy. Chalcosis from copper deposition
upward gaze and loss of sensation over the causes endophthalmitis and rapid visual loss.
region supplied by infra-orbital nerve. Sinus Ferrous foreign bodies can be removed with
x-ray will shows clouding of the affected sinus a powerful electromagnet. Non-magnetic
and may be able to identify herniated tissue. foreign bodies should be mechanically
CT scanning is able to more clearly define removed.
the extent and the site of injury. Surgical
correction is often required. Acute red eye
Penetrating injuries Common causes of an acute red eye include:
Penetrating injuries can result in: • Conjunctivitis
• Keratitis
• Corneoscleral lacerations • Iritis
• Intraocular foreign bodies • Acute glaucoma
• Sympathetic ophthalmitis • Episcleritis
• Scleritis
Intraocular foreign bodies
Chalazion
Intraocular foreign bodies are usually
caused by metal fragment hitting the eye at A chalazion is due to inflammation of the
high speed. The patient is usually aware of meibomian gland. It presents as a painless,
something having stuck the eye. In the early hard lump close to margin of eye lid. It
stages after the injury there is no significant is more common in the upper lid and
visual loss and the clinical signs may be easily can increases in size over days or weeks.
missed. An x-ray of the orbit is essential. Small lesions require no treatment. Large
Foreign body may also be identified on CT or symptomatic lesions can be incised and
ultrasound. Retained iron and copper foreign curetted. This can be performed under local
bodies can give rise to serious chemical anaesthesia via a conjunctival incision.
Chapter 8 Principles of
surgical oncology
Cell proliferation increasingly abnormal. It is a pre-malignant
condition.
In health, growth factors are made by one
cell type to stimulate another. In contrast, Neoplastic proliferation
malignant cells generate their own
stimulatory growth factors, losing negative Neoplasia is an abnormal, uncoordinated
feedback mechanisms. Positive feedback and excessive growth that persists after the
cycles can occur by alteration of growth initiating stimulus has been withdrawn.
factors, receptors or intracellular signaling Neoplastic proliferation is characterised by
pathways. Cell proliferation can be regarded being:
as neoplastic or non-neoplastic.
• Progressive
Non-neoplastic proliferation • Purposeless
• Regardless of surrounding tissues
There are several types of non-neoplastic • Not related to body needs
proliferation. • Parasitic
Hyperplasia Carcinogenesis
Hyperplasia is an increase in tissue or organ All cells have mechanisms for regulating
size due to cell proliferation (e.g. benign their growth, differentiation and death.
prostatic hyperplasia). Causes include Cancer develops when cells escape from the
chronic infection and increased hormonal normal control mechanism and proliferation
activity. is uncontrolled. Cells develop the ability
to invade and metastasise. Carcinogenesis
Hypertrophy is a multi-step process. Cells accumulate a
succession of gene mutations. Each mutation
Hypertrophy is an increase in tissue or organ overcomes natural anti-cancer defence
size due to enlargement of cell size (e.g. left mechanisms. Growth regulation is lost. Most
ventricular hypertrophy in hypertension). cancers result from a series of genetic errors.
There is no increase in cell number and it is
due to increased functional requirements. Cancer genes
Metaplasia Genes related to cancer development may
be divided into oncogenes and tumour
Metaplasia is a change of one type of suppressor genes. In health, the activity of
differentiated tissue to another (e.g. these genes is closely regulated. They allow
squamous metaplasia in the bronchial differentiated growth of normal tissues. In
epithelium). It is usually of the same class cancer, the balanced control of growth is lost.
of tissue but the new tissue type may be less
specialised. It occurs in both epithelial and Oncogenes
connective tissue and is often associated with Oncogenes are regulatory genes whose
hyperplasia. activity is abnormally increased after a
genetic alteration. Oncogene activation may
Dysplasia occur after chromosomal translocation, gene
amplification or mutation within a coding
Dysplasia is disordered cell development that sequence of an oncogene. Oncogenes act in
may accompany hyperplasia or dysplasia.
It is due to increased mitosis. Cells become
100 Chapter 8 Principles of surgical oncology
a dominant fashion. Examples of oncogenes tumour suppressor genes. The commonest
include: abnormality is in the BRCA 1 gene found
on long arm of chromosome 17. A mutation
• ras on chromosome 11 – mediates signal is seen in 50% of families with four or
transduction more affected members less than 60 years.
More than 100 BRCA mutations have been
• erbB2 on chromosome 7 – growth factor described. The highest carrier rate is in
receptor Ashkenazi Jews. If a patient is BRCA 1 positive
she has:
• src on chromosome 20 – tyrosine kinase
• myc on chromosome 8 – transcription • 50% risk of developing breast cancer by 50
years
factor
• 85% risk of developing breast cancer by 70
Tumour suppressor genes years
Tumour suppressor genes code for inhibitory • 70% risk of developing contralateral breast
proteins. There normal function is to prevent cancer
cell growth. In cancer, the suppressor
function is lost. Most tumour suppressor • 50% life time risk of developing ovarian
genes are recessive. Inactivation of tumour cancer
suppressor genes can occur by gene mutation
causing loss of the gene product, prevention Tumour markers
of binding of a gene product to its target site
or inactivation by other proteins. Examples of Tumour markers are molecules occurring
tumour suppressor genes include: in blood that are associated with cancer and
whose measurement or identification may
• Rb on chromosome 13 – control of cell be useful in patient diagnosis or clinical
cycle management. They are usually glycoproteins
detected by monoclonal antibodies. The
• p53 on chromosome 17 – DNA repair and ideal tumour marker would be present in the
apoptosis blood, undetectable in health, produced only
by malignant tissue, be organ specific and
• Bcl2 on chromosome 18 – apoptosis would have circulating levels proportional to
• APC on chromosome 5 – regulation of co- tumour mass. The ideal tumour marker does
not exist. Tumour markers can be used for:
transcriptional activators
• Screening for primary disease
Mutation of tumour suppressor genes is seen • Diagnosis of primary disease
in many familial cancers. • Monitoring response to treatment
• Establishing prognosis
• Rb – childhood retinoblastoma • Detection of recurrence
• p53 – Li–Fraumeni syndrome
• APC – familial colon cancer Commonly measured tumour markers include:
• BRCA1/2 – familial breast cancer
• CA-125 – ovary
Cancer genetics • CEA – colon, pancreas, stomach
• PSA – prostate
Several germline mutations have been shown • a-fetoprotein – teratoma, hepatoma
to increase cancer risk. More than 50 genetic • b-hCG – seminoma, choriocarcinoma
abnormalities have been identified. Most • CA19.9 – pancreas
are inherited in an autosomal dominant • CA15.3 – breast
fashion. Most genetic abnormalities involve
tumour suppressor genes. Hereditary cancer Epidemiology of
syndromes result from a germline mutation common cancer
in one copy of the suppressor gene. Somatic
mutation in the second copy of the gene There are more than 200 types of cancer,
results in the development of cancer. each with different causes, symptoms and
Breast cancer genetics
About 5% breast and ovarian cancers are due
to a germ-line mutation. The remaining 95%
are sporadic. The BRCA1 and BRCA 2 are
NHS Cancer Screening programmes 101
treatments. There are approximately 300,000 • The natural history of the disease should
new cases of cancer diagnosed in the UK each be well understood with a recognisable
year. Every 2 minutes someone is diagnosed early stage
with cancer and more than 1 in 3 people will
develop some form of cancer during their • A specific and sensitive test for the early
lifetime. Breast, lung, bowel and prostate detection of the disease must be available
cancers together account for over half of all
new cancers each year. Cancer can develop at • There should be good evidence that
any age, but is most common in older people. the screening test can result in reduced
More than 60% of cancers are diagnosed in mortality and morbidity in the targeted
people aged 65 and over. Approximately 1% population
of cancers occur in children, teenagers and
young adults. • The test must be acceptable, producing a
high participation rate
Overall, cancer incidence rates have
increased by more than a quarter since the • There should be suitable facilities for
late 1970s, but the rates have been fairly diagnosis and treatment of detected
stable since the late 1990s. Cancer incidence abnormalities
rates have risen by 16% in males and by 34%
in females. There have been increases in the • There should be appropriate treatment
incidence of renal cell, malignant melanoma, options
oral and endometrial cancers. Over the last
decade the incidence rate of stomach cancer • The benefits of screening should outweigh
has decreased by more than a quarter in both any adverse effects
sexes. Cervical and ovarian cancer have each
decreased by more than 10% and the lung • The benefit must be of an acceptable
cancer incidence rate in males decreased by financial cost
almost a fifth.
• The results of the implementation require
Prostate cancer has overtaken lung cancer audit to ensure they meet the above
as the commonest cancer diagnosed in men. criteria
The apparent incidence of prostate cancer
is rising due to the widespread use of PSA Bias within screening programmes
testing. Lung cancer is the second most
common cancer in men. The incidence of Various biases exist which can skew the
lung cancer in men is falling. Breast cancer apparent success of a screening programme:
is the commonest cancer in women and
accounts for 30% of all female cancer. The • Selection bias – patients select themselves
second commonest cancer in women is into one group by attending
colorectal cancer.
• Lead time bias – early detection appears
NHS cancer screening to improve survival by increasing the time
programmes from diagnosis to death, yet mortality is
unchanged. The patient is simply aware
Criteria for an effective that they have the disease for longer
screening programme
• Length bias – Slower growing better
To justify establishing a screening prognosis tumours are more likely to be
programme, the World Health Organization detected by screening
has recommended that the following criteria
be met: Sensitivity and specificity
• The disease screened for must be an A screening test can give a positive or negative
important problem result. It does not imply that the patient has
or does not have the disease. The test results
can be:
• True positive (TP) = A positive test result in
the presence of the disease
• True negative (TN) = A negative test result
in the absence of the disease
• False positive (FP) = A positive test result
in the absence of the disease
• False negative (FN) = A negative test result
in the presence of the disease
102 Chapter 8 Principles of surgical oncology
The sensitivity of a test is the ability of the test achieved nation wide coverage by 2010. If
to identify the disease in the presence of the offers screening by faecal occult blood (FOB)
disease (=TP/(TP + FN)). The specificity of a test testing every 2 years to all men and women
is the ability of the test to exclude the disease in aged 60 to 69. Patient with a positive result are
the absence of the disease (=TN/(TN + FP)). The invited for a colonoscopy. About 1 in 50 FOB
positive predictive value (PPV) is the probability tests are abnormal.
of a positive test reflecting the true presence of
the disease. The negative predictive value (NPV) Clinicopathological
is the probability of a negative test reflecting the staging of cancer
true absence of the disease.
Staging is the clinical or pathological
National heath service breast assessment of the extent of tumour spread.
screening programme Clinical staging is a preoperative assessment. It
is based on clinical, radiological and operative
The National Health Service Breast Screening information and is used to determine
Programme was introduced in 1988 following treatment offered to the patient. Pathological
the Forest Report in 1986. All women between staging is a postoperative assessment. It
50 and 70 years are invited for 3-yearly two- provides useful prognostic information.
view mammography. The age limit is being It allows decisions to be made regarding
extended from 47–73 years. If an abnormality adjuvant therapy and comparison of treatment
is seen on a mammogram women are recalled outcomes.
to a screening assessment clinic for a clinical
examination, further imaging and fine needle Staging systems
aspiration cytology or core biopsy as required.
About 70% of screen detected abnormalities The ideal staging system should be:
are shown to be of no clinical significance
following assessment. • Easy to use and remember
• Reproducible – not subject to inter or
National health service cervical
screening programme intra-observer variation
• Based on prognostically important
The National Health Service Cervical
Screening Programme was established in pathological factors
1988. Women are screened between 25 and
64 years, 25–49 every 3 years and 50–64 every TNM system
5 years. Cervical cells are obtained by either a
smear or brush. Brush samples are analysed The TNM system is based on the anatomical
by liquid based cytology. About 1:10 smear extent of spread:
tests are abnormal. Non-neoplastic causes of
an abnormal smear include: • T refers to the extent of primary tumour
• N refers to the extent of nodal metastases
• Infection • M refers to the presence or absence of
• Presence of blood or mucus
• Inadequate specimen distant metastases
• Poorly preserved specimen
Two classifications are described for each site:
Abnormal smears are reported as:
• Clinical classification (TNM)
• CIN 1 = Mild dyskariosis • Pathological classification (pTNM)
• CIN 2 = Moderate dyskariosis
• CIN 3 = Severe dyskariosis The TNM system is generally accepted but
does not recorded all factors (e.g. grade,
National health service bowel contiguous organ involvement) that are
cancer screening programme prognostically important.
The NHS Bowel Cancer Screening Programme T – primary tumour
started being rolled out in July 2006 and • Tx = Primary tumour can not be assessed
• To = No evidence of primary tumour
• Tis = Carcinoma in situ
• T1–4 = Increasing size and local extent of
primary tumour
Principles of cancer treatment 103
N – regional lymph nodes differentiated cells (e.g. muscle and nerves)
• Nx = Regional lymph nodes can not be are resistant to damage. The most significant
effects are seen in rapidly dividing cells
assessed (e.g. gut, bone marrow) and tumours. Acute
• N0 = No regional lymph node metastases toxicity occurs within days and depends on
• N1–3 = Increasing involvement of regional the overall treatment time. Acute toxicity
includes mucositis, bone marrow suppression
lymph nodes and skin reactions. Late toxicity occurs after
weeks or months and depends on total dose
M – distant metastases and fractionation. Late toxicity includes tissue
• Mx = Distant metastases can not be necrosis or fibrosis.
assessed Fractionation
• M0 = No distant metastases
• M1 = Distant metastases present A higher total dose of radiation can be given if
smaller repeated doses are administered. This
Principles of cancer allows a degree of repair of normal tissues.
treatment A high total dose increases the probability
Radiotherapy of tumour control. Hypofractionation is a
small number of large doses. Accelerated
Radiotherapy is the use of ionising radiation fractionation is a standard dose given over a
to treat malignancy. It attempts to deliver a short interval. Hyperfractionation is a large
measured radiation does to a defined tumour number of small doses.
volume, whilst limiting the dose to the
surrounding normal tissue. Radiotherapy may Uses of radiotherapy
be radical (with curative intent), palliative
or adjuvant. Brachytherapy is the use of Radiotherapy is used with curative intent and
intracavity irradiation. as the sole treatment in:
Physics • Head and neck cancers
• Carcinoma of the cervix
Radiation may be electromagnetic or • Seminomas
particulate. Linear accelerators are • Hodgkin’s and non-Hodgkin’s lymphomas
used to generate high energy x-rays • Bladder cancer
(electromagnetic) created by electrons • Early prostate cancer
hitting a fixed target. The depth of tissue • Early lung cancer
penetration depend on the x-ray voltage. 10– • Anal and skin cancer
125 KeV x-rays are absorbed by superficial • Medulloblastoma and other brain
tissues. 4–24 MV x-rays are absorbed in
deeper tissues. The use of MV x-rays reduces tumours
the risk of significant skin toxicity. High • Thyroid cancer
energy electrons may be used instead of
x-rays but electrons have limited tissue It is used as a component of multimodality
penetration. CT planning of radiotherapy therapy in:
fields reduces the radiation dose delivered to
normal tissue. • Breast cancer
• Rectal cancer
Biology • Soft tissue sarcomas
• Advanced head and neck cancers
Radiation damages DNA. It either causes direct • Whole body irradiation before bone
damage to DNA or acts via the production of
free radicals. Double-stranded DNA breaks marrow transplantation
and prevents cell replication, inducing cell
death. The tissue response depends on the It is used with palliative intent in:
degree of cellular differentiation. Terminally
• Pain – especially bone metastases
• Spinal cord compression
• Cerebral metastases
• Venous or lymphatic obstruction
104 Chapter 8 Principles of surgical oncology
Chemotherapy • DNA polymerase causing breakage of
single stranded DNA
The aims of chemotherapy are to selectively
destroy tumour cells whilst attempting • RNA synthesis by intercalating between
to minimise the toxicity on normal cells. DNA base pairs
This is achieved by the specific growth
characteristics of most tumours. • DNA synthesis by cross-linking DNA
strands
Mechanism of action
• Dihydrofolate reductase
A cell synthesising DNA goes through a • The metaphase of mitosis by binding to
regular cycle with different phases know as
the cell cycle (Figure 8.1) as follows: tubulin
• G0 is a resting phase outside the cell cycle Non-phase dependent drugs kill cells
• G1 is a phase of protein and RNA synthesis exponentially with increasing dose. They are
• S is a phase of DNA synthesis equally toxic for cell within the cell cycle or G0
• G2 is a phase of RNA synthesis phase. Examples include:
• M is mitosis
• Alkylating agents – cyclophosphamide,
Cells in G0 are resistant to the effects of cisplatin
cytotoxic drugs. The faster cells are growing
the more likely are that cytotoxic drugs are • 5 Fluorouracil
to ‘catch’ them. This also accounts for the • Anthracyclines – doxorubicin
toxicity that occurs on rapidly growing normal
tissues such as the gastrointestinal mucosa Phase dependent drugs kill cells at a lower
and bone marrow. Most drugs kill a fixed dose. They act within a specific phase of the
proportion of cells rather than fixed number. cell cycle. Examples include:
Large tumours are relatively unresponsive
to chemotherapy as more cells are in G0 and • Methotrexate
drug penetration is less reliable. • Vinca alkaloids – vincristine, vinblastine
Different drugs act at different phases Toxicity
of the cell cycle. As a result, combinations
of drugs are more likely to be effective. The Some general side effects occur with many
modes of action of chemotherapeutic agents cytotoxic agents and these include:
include inhibiting:
• Nausea and vomiting
• Bone marrow toxicity
• Gastrointestinal toxicity
• Alopecia
• Gonadal effects
• Hyperuricaemia
The cell cycle Figure 8.1 The cell cycle
M G0
G2 G1
G0 = resting phase
G1 = protein and RNA synthesis
S = DNA synthesis
S G2 = RNA synthesis
M = mitosis
Principles of cancer treatment 105
Specific side effects that are seen with certain • Selective oestrogen receptor modulators –
agents include: tamoxifen, raloxifene
• Pulmonary fibrosis – bleomycin • Aromatase inhibitors – anastrozole,
• Haemorrhagic cystitis – letrozole and exemestane
cyclophosphamide • Progestogens – megestrol acetate
• Cardiomyopathy – doxorubicin
• Hepatic damage – methotrexate Uses of hormonal treatment
• Skin pigmentation – 5-flurouracil
Hormonal treatment in breast cancer can be
Uses of chemotherapy used as adjuvant treatment or in metastatic
disease. In the adjuvant setting, tamoxifen or
Chemotherapy is used with curative intent in: an aromatase inhibitor are given for 5 years.
They have been shown to reduce the risk of
• Acute lymphoblastic leukaemia recurrence, reduce the risk of contralateral
• Germ cell tumours breast cancer and improve survival. In
• Choriocarcinoma patients with metastatic disease, the use of
• Hodgkin’s disease hormonal therapy depends on the ER status
• Wilms’ tumour of the tumour, the duration of disease-free
interval, the location of metastases, previous
A significant response to chemotherapy is therapy and the patient’s performance
seen in: status.
• Breast carcinoma Prostate cancer
• Ovarian carcinoma
• Lymphoma The aim of hormonal treatment in prostate
• Osteosarcoma cancer is to ablate androgen production.
About 80% of prostate cancers respond
Tumours that are poorly responsive to to medical or surgical androgen ablation.
chemotherapy include: Surgical ablation is by orchidectomy and
produces a rapid reduction in testosterone
• Pancreatic carcinoma levels. Medical ablation is reversible and the
• Melanoma effect may take several weeks to occur. The
• Soft tissue sarcomas side effects of androgen ablation include
• Colorectal carcinoma impotence, loss of libido, osteoporosis,
• Gastric carcinoma gynaecomastia and hot flushes. The site of
action of hormonal treatment are:
Hormonal treatment
• Pituitary gland – LH-RH analogues,
Hormonal treatment is used in that stilbeostrol, cyproterone acetate
management of several cancers. It usually
works by reducing steroid hormone • Adrenal gland – ketoconazole,
production. aminoglutethamide
Breast cancer • Prostate – flutamide, cyproterone acetate
• Testis – orchidectomy
The aim of hormonal treatment in breast
cancer is to reduce oestrogenic growth Uses of hormonal treatment
stimulation of cancer cells. Hormonal
treatment is effective in women with Androgen ablation is used in both the
oestrogen and/or progesterone receptor- neoadjuvant setting and in metastatic disease.
positive tumours. About 60% of breast In neoadjuvant setting is used in combination
cancers are ER positive and 80% of receptor- with external beam radiotherapy. LH-RH
positive tumours will respond to hormonal analogues are commonly used in metastatic
manipulation. The response in hormone disease. The median duration of response
receptor-negative tumours is minimal. The is about 18 months and about 20% patients
types of hormonal treatment include: achieve a response that may last several
years. The response can be measured by
• Ovarian ablation – surgical, LH–RH
analogues
106 Chapter 8 Principles of surgical oncology
assessing the PSA level. LH-RH analogues are Liverpool Care Pathway
give by monthly injection. The first injection
my induce LH-RH release, a rise in PSA and The Liverpool Care Pathway for the dying
worsening of symptoms. Cyproterone acetate patient was developed to transfer good
should be give for first 2 weeks of treatment to practice from the hospice model to other care
reduce this effect. settings such as hospitals. The key aims are to:
Palliative care • Discontinue or alter delivery of
medications
Principles of palliative care
• Discontinue interventions
Palliative care is the active, total management • Document cardiopulmonary resuscitation
of patients at a time when their disease is no
longer responsive to curative treatment and status
when control of pain (or other symptoms) • Deactivate implanted cardiac defibrillators
is of paramount importance. Dealing with • Discontinue inappropriate nursing
psychological, social and spiritual problems
is important. It affirms life and regards dying interventions
as normal. It neither hastens nor postpones • Communicate with the patient and assess
death. It perceives the patient and family
as a unit and creates a caring, comforting their insight
environment. It coordinates care and • Assess and meet religious and spiritual
provides relief from distressing symptoms.
It aims to maintain the independence of needs
the patient for as long as possible, provide • Keep the family informed
information and endeavours to reduce fear • Provided bereavement advice for relatives
and anxiety. It promotes an atmosphere
where an open and honest exchange of views Pain
can take place and helps the patient to come
to terms with impending death. It offers a Pain is the commonest and most feared
support system to the family to help them symptom associated with cancer. Chronic pain
cope with illness and bereavement. can be controlled in more than 80% of patients.
The WHO analgesia ladder (Figure 8.2) forms
the most common template for pain control
and consists of a ‘three-stepped ladder.’ With
increasing pain, increasing strength of analgesia
is required. On each step of the ladder the
maximum dose and frequency should be used.
The WHO analgesia ladder Figure 8.2 The WHO analgesia
ladder
Severe
Moderate
Mild
Paracetamol Codeine Morphine
Dihydrocodeine Diamorphine
Coproxamol
Co-analgesics
Principles of cancer treatment 107
Drugs should be prescribed on a regular basis antidepressants may have useful effect.
not ‘as required.’ Co-analgesic agents often Neurolytic blocks may be considered if the pain
have a synergistic effect and may increase the fails to respond to pharmacological agents.
efficacy of a particular analgesic agent.
Liver capsule pain
Control of pain
Liver capsule pain is often distressing and
Morphine non-steroidal anti-inflammatory drugs
Morphine is the most commonly used strong often have excellent additive effects in this
analgesic in palliative care. It should initially be situation. Steroids can reduce swelling,
prescribed as an immediate release preparation inflammation and pain. Dexamethasone is
(e.g. Oramorph) and can be given as required usually the drug of choice.
every 4 hours. The dose can be increased every
24 hours until pain is adequately controlled. Dyspnoea
Once pain has been controlled the total daily
dose can be calculated. Immediate release Dyspnoea is not always due to underlying
can then be substituted for delayed release malignancy and consideration should be
preparations. Immediate release preparations given to treatment of any underlying infection
can still be given for breakthrough pain. No or cardiac failure. Causes of breathlessness
ceiling exists for the maximum permissible related to malignancy include pleural
dose of morphine. Laxative should be effusion, lymphangitis carcinomatosis,
prescribed to prevent constipation. Patients intrapulmonary metastases and constricting
may also require an antiemetic. Complications chest wall disease. Aspiration of a pleural
of opiate analgesia include itch, hallucinations effusion often produces symptomatic
and dry mouth, but respiratory depression improvement. Pleurodesis with talc or
is rarely a problem. Physical dependence bleomycin is only effective if the pleural
may occur. Psychological dependence and effusion can be drained to dryness. A pleuro-
addiction are not a problem in the palliative peritoneal shunt may produce symptomatic
care setting. If the oral route is unavailable improvement. Steroids produce symptomatic
subcutaneous or percutaneous administration improvement in those with lymphangitis and
may be appropriate. intrapulmonary metastases. The respiratory
depressant effect of morphine will also
Co-analgesia reduce dyspnoea.
Co-analgesics have little intrinsic analgesic
activity but have additive effects to analgesic Nausea and vomiting
agents.
Nausea and vomiting is usually multifactorial
Non-steroid anti-inflammatory drugs may in origin and causes include, hypercalcaemia,
be useful in bone pain. Anticonvulsants and liver metastases, constipation, drug
antidepressants are useful in neuropathic side effects and intestinal obstruction.
pain. Steroids increase wellbeing and Metoclopramide, domperidone and
benzodiazepines reduce muscle spasm. cyclizine are useful if there is gastric stasis or
intestinal obstruction. 5-HT3 blockers (e.g.
Other symptoms ondansetron) are useful for chemotherapy-
induced nausea. Haloperidol is useful in
Bone pain morphine-induced nausea.
Bone pain is often well controlled with a single
fraction of radiotherapy and non-steroid Constipation
anti-inflammatory drugs may have useful
co-analgesic effect. Bisphosphonates reduce Treatment of constipation should be
osteoclastic activity and reduce bone pain. continuous and anticipatory. It is often a
predictable side effect of opiate analgesia. It
Neuropathic pain can be worsened by inactivity, dehydration
Neuropathic pain is often resistant and hypercalcaemia. Opiate-induced
to treatment. Anticonvulsants and constipation is best treated with compound
preparations containing both a stool softener
and stimulant (e.g. co-danthrusate).
Chapter 9 Cardiothoracic
surgery
Applied basic sciences and traverses the atrioventricular groove.
Anatomy of the heart It ends by anastomosing with the branches
of circumflex artery. Branches of the right
The heart is situated in the middle coronary artery supply the sino-atrial
mediastinum. It lies freely within the node and the left atrium. It also supplies
pericardium. It is pyramidal in shape with its the right marginal artery and the posterior
base lying posteriorly. The apex is anterio- interventricular artery, also known as
inferior and points to the left. The heart has posterior descending artery.
three surfaces. The strenocostal surface is
formed by the right atrium and ventricle ‘Dominance’ of the coronary circulation
and by parts of the left ventricle and atrium. Dominance of the coronary circulation
The diaphragmatic surface is formed by the arises from variation in the blood supply.
right and left ventricles. The base is formed Right dominance occurs when the posterior
by the left atrium. It is connected to the great interventricular artery arises from the right
vessels at the base. The atrioventricular coronary artery (80%). Left dominance
groove separates the right and left atrium occurs when the posterior interventricular
from the ventricles. The anterior and artery arises from left coronary artery (10%).
posterior interventricular grooves join Codominance occurs when the posterior
each other. Important lateral relations of interventricular artery is formed by both the
the heart include the phrenic nerves which right and left coronary arteries (10%).
run adjacent to the pericardium. Posterior
relations include the oesophagus, the Blood supply to the conducting
descending thoracic aorta, the azygos vein system of the heart
and the thoracic duct. The sino-atrial node is supplied by a branch
of the right coronary artery in 60% of the
Blood supply population. The atrio-ventricular node is
Left coronary artery supplied from the posterior interventricular
artery.
The left coronary artery arises from the left
posterior aortic sinus (Figure 9.1). It passes Venous drainage
behind the pulmonary trunk and then lies The coronary sinus receives most of the blood
under the left auricle. It divides into anterior from the heart. It lies in the posterior part of
interventricular and circumflex branches. the atrioventricular groove and opens into the
The anterior interventricular artery is also right atrium. It is a continuation of the great
known as the left anterior descending artery cardiac vein. Tributaries included the middle
and continues in the anterior interventricular and small cardiac veins. The anterior cardiac
groove. It anastomoses with the posterior vein opens directly into the right atrium. The
interventricular branch of the right coronary venae cordae minimae drain directly into the
artery and also gives the diagonal branch. chambers of the heart.
The circumflex artery winds (circumflexes)
around the left heart border. It passes in the Nerve supply
atrioventricular groove and anastomoses with
the right coronary artery. The sympathetic nerves supply of the heart
arises from the cervical and upper thoracic
Right coronary artery portions of the sympathetic chain through
the stellate ganglion. Afferent fibres run with
The right coronary artery arises from the the sympathetic fibres that conduct pain.
anterior aortic sinus. It passes between The parasympathetic supply is via the vagus
the pulmonary trunk and the right atrium
110 Chapter 9 Cardiothoracic surgery
The anatomy of the coronary arteries
Figure 9.1 The anatomy of the coronary arteries. (Reproduced from James S and Nelson K. Pocket Tutor ECG
Interpretation. London: JP Medical Ltd, 2011.)
nerves. The sympathetic and parasympathetic The atrioventricular bundle is also known
nerves form cardiac plexuses. The superficial as the Bundle of His. It is the only normal
cardiac plexus lies in front of the right pathway that connects the myocardium
pulmonary artery. The deep cardiac plexus of the atria and the ventricles. It descends
lies in front of the tracheal bifurcation. through the fibrous skeleton of the heart. At
the lower part of the membranous portion
Conduction system of the ventricular septum it divides into
two branches, one for each ventricle. The
The conduction system of the heart is by right bundle branch travels down the right
specialised muscle fibres. The sinoatrial (SA) ventricle wall. The left bundle branch travels
node is located in the wall of the right atrium down the left ventricular wall and splits into
just to the right of the opening to the superior anterior and posterior branches. Purkinje
vena cava. This node gives a spontaneous fibres cover the ventricle wall and ensure
impulse that spreads in all directions through that the whole of each ventricle contracts at
the myocardium of the atria and causes the once.
atrial muscle to contract. The atrioventricular
node is located on the lower part of the Pericardium
atrial septum, just above the tricuspid valve.
It is activated by the excitation wave that The pericardium is a made up of two
passes through the atria from the sinoatrial fibroserous layers that enclose the heart and
node. From this node the impulse moves to roots of the great vessels. The serous layer has
the atrioventricular bundle, from where it an inner visceral layer and outer parietal layer.
travels on down through the ventricles. Both layers are continuous around the great
Applied basic sciences 111
vessels and the pulmonary veins. This leads to Cardiac cycle
the formation of the two pericardial sinuses –
an oblique sinus and transverse sinus. These The cardiac cycle describes the events related
lie on the posterior surface of the heart. to the flow of blood through the heart during
one complete heartbeat. It has certain well-
Cardiac physiology described phases (Figure 9.3).
Myocyte action potential • Phase 1 – Atrial contraction
• Phase 2 – Isovolumetric ventricular
Normally, the SA node cells have the highest
rate of depolarisation. As a result, the SA node contraction
acts as the cardiac impulse generator. Cells of • Phase 3 – Rapid ventricular ejection
the SA node automatically depolarise slowly • Phase 4 – Reduced ventricular ejection
after each repolarisation. This is due to the • Phase 5 – Isovolumetric ventricular
gradual influx of calcium through T channels.
Once the threshold potential is reached, relaxation
sudden depolarisation results. This is due to • Phase 6 – Rapid ventricular filling
the rapid influx of sodium. Repolarisation is • Phase 7 – Reduced ventricular filling
brought about by the efflux of potassium. The
phases of the myocyte action potential are During atrial contraction, 25% of the
shown in Figure 9.2. ventricular filling occurs. The AV valves are
open and the aortic and pulmonary valves
The action potential spreads from SA closed. At the end of atrial contraction
node to other cells of the conducting system the AV valves close. During isovolumetric
and the myocytes. Its rapid spread between ventricular contraction, the ventricles
the myocytes is aided by the presence of contract as a closed chamber. The ventricular
gap junctions. As a result, the heart muscle pressure rapidly rises. At the end of
contracts as a syncytium. During the absolute isovolumetric ventricular contraction, the
refractory period, the myocyte cannot be aortic and pulmonary valves open. During
stimulated. This lasts from phase 1 through rapid ventricular ejection, ventricular
to the middle of phase 3. During the relative contraction continues and blood rapidly
refractory period, myocytes can be stimulated passes into the great vessels. About two-
only by a supranormal stimulus. This lasts thirds of the stroke volume is ejected in the
from when the absolute refractory period first one-third of systole. During reduced
ends until phase 4. ventricular ejection, ventricular contraction
continues but the outflow of blood reduces
as the ventricular pressure declines. At the
The myocyte action potential Figure 9.2 The myocyte action
potential. (Reproduced from
Phase 0 Phase 1 Phase 2 Phase 3 Phase 4 James S and Nelson K. Pocket
Sodium Potassium Calcium Calcium Na/K pump Tutor ECG Interpretation. London:
influx activation JP Medical Ltd, 2011.)
efflux influx efflux
+20 mV 1 2
0 mV
0 3 4
4 200 ms
–96 mV
112 Chapter 9 Cardiothoracic surgery
Seven phases of the cardiac cycle Figure 9.3 Seven phases of the
cardiac cycle. AP = Aortic pressure.
Systole Diastole LVP = Left ventricular pressure.
LAP = left atrial pressure. LVEDV
12 3 4 5 6 7 = Left ventricular end diastolic
120 Aortic volume. LVESV = Left ventricular
end systolic volume
pressure
Pressure (mmHg) 60 Left
arterial Left
pressure ventricular
pressure
0
Left ventricular volume 120 Left ventricular
(mL) end-diastolic
80 volume
40 S4 S1 S2 S3 Left
Sounds ventricular
end-systolic
volume
0 0.4 0.8
end of reduced ventricular ejection, the Cardiac function
aortic and pulmonary valves close. During
isovolumetric ventricular relaxation, the Measures of cardiac function that can directly
ventricles relax as closed chambers. When assessed include:
the ventricular pressures reduces to below
those in the great veins the AV valves open. • End diastolic volume
During rapid ventricular filling, blood flows • Stroke volume
into the ventricles from the atria. During • Ejection fraction
reduced ventricular filling the pressure • Cardiac output
difference between the atria and ventricle • Peripheral resistance
reduces and blood slowly keeps flowing into • Blood pressure
the ventricles. • Central venous pressure
• Pulmonary capillary wedge pressure
Heart sounds
Determinants of stroke volume
There are four heart sounds:
The stroke volume depends on several factors
• S1 – due to closure of the atrioventricular including:
valves
• Preload
• S2 – due to closure of the aortic and • Contractility
pulmonary valves • Afterload
• S3 – due to rapid ventricular filling Preload is a measure of how much the
• S4 – due to atrial contraction and blood myocyte is stretched before contraction. It
is represented by the end diastolic volume
flow into the ventricle
Applied basic sciences 113
or the end diastolic pressure. In the normal Anatomy of the lungs
heart, cardiac output is directly proportional
to preload. Contractility is a measure of the Pleurae
inherent ability of the myocyte to contract. It
can be increased by drugs such as digoxin and Each pleura has two parts. The parietal layer
catecholamines. Cardiac output is directly lines the thorax wall and the diaphragm.
proportional to the contractility. Afterload is The visceral layer covers the outer surface
the force against which the ventricle has to of each lung. They are continuous with each
contract. Peripheral resistance is a measure other at root of the lung. They are separated
of afterload and cardiac output is inversely by the pleural cavity containing a small
proportional to afterload. The Frank–Starling amount of pleural fluid. The pulmonary
curve (Figure 9.4) demonstrates that the ligaments at each lung root allow for
force of contraction of a myocyte is directly movement during respiration. The costal
proportional to its initial length up to a pleura is supplied by the intercostal nerves.
level, after which it reduces with any further The mediastinal pleura is supplied by the
increase in the initial length. phrenic nerves. The diaphragmatic pleura is
supplied by both the intercostal and phrenic
Regulation of blood pressure nerves.
Baroreceptors
Trachea and bronchi
Baroreceptors play an important role in the
day-to-day regulation of blood pressure, such The trachea has a fibroelastic wall with
as in response to postural changes. They are U-shaped hyaline cartilages. It begins below
located in the walls of carotid sinus and the the cricoid cartilage at the level of the C6
arch of the aorta. They are innervated by vertebra. It ends at the level of the sternal
glossopharyngeal nerve (ninth cranial nerve) angle at the level of the T4 vertebra. It lies
and stimulated by increased stretch that in the superior mediastinum. There are two
occurs following a rise in blood pressure. This bronchi. The right main bronchus is wider,
leads to inhibition of the vasomotor centre shorter and more vertical than the left. It
and hence a reduction in blood pressure. divides at the hilum of the right lung into
three branches. The left main bronchus is
Hormones and catecholamines longer and more horizontal and passes in
Renin–angiotensin, aldosterone, antidiuretic front of the oesophagus. It divides at the
hormone and catecholamines normally play hilum of the left lung into two branches.
a permissive role in the maintenance of blood
pressure but have a more important role in Lungs
blood pressure regulation in states of shock.
Each lung is conical in shape and is covered
The Frank–Starling curve by visceral pleura. They are attached to the
mediastinum by the root. The apex extends
Ventricular into the root of the neck. The base of the lung
perfomance overlies the dome of the diaphragm. The right
lung has three lobes – upper, middle and
End diastolic volume lower. The left lung has two lobes – upper and
lower. Each lobe of the lung is divided into
Figure 9.4 The Frank–Starling curve bronchopulmonary segments. Each receives
a segmental bronchus, artery and vein.
The blood supply of the bronchi and their
branches are from the bronchial arteries.
The bronchial arteries are direct branches of
the aorta. The bronchial veins drain into the
azygos and hemiazygos veins. Deoxygenated
blood enters each lung via the pulmonary
artery. Oxygenated blood leaves each lung
via the pulmonary vein. At each lung root is
114 Chapter 9 Cardiothoracic surgery
the pulmonary venous plexus. Sympathetic Oxygen and carbon dioxide
efferent fibres produce bronchodilatation. transport
Parasympathetic efferent fibres produce
bronchoconstriction. Haemoglobin
Respiratory physiology Haemoglobin consists of four polypeptide
chains joined to a porphyrin ring.
The thoracic cage is formed by the 12 Haemoglobin A1 consists of two α and
thoracic vertebrae, 12 ribs, the sternum and two β chains. The porphyrin ring contains
diaphragm. The top 10 ribs are attached iron. Only when the iron is in the ferrous
directly or indirectly to the sternum. Within (reduced) state does it binds with oxygen.
the thoracic cage are three compartments. Haemoglobin with ferric (oxidised) iron is
These are the two pleural cavities, each with known as methaemoglobin. It cannot take
a lung and the mediastinum, containing part in oxygen transport. Each haemoglobin
the heart. Gases enter and leave the lungs molecule can bind up to four molecules of
through the mouth and nose, the pharynx oxygen.
and larynx, the trachea, bronchi and
bronchioles. These tubes expand at their Oxygen is primarily transported bound
ends into alveoli, where gas exchange takes to haemoglobin. A small amount is
place. There are about 23 branchings which transported dissolved free in the plasma.
lead to a total of about 300 million alveoli. Haemoglobin bound to oxygen is known as
oxyhaemoglobin. One gram of haemoglobin
Respiratory mechanics can bind with 1.34 mL of oxygen. Therefore,
100 mL of plasma will have about 20 mL
Contracting the diaphragm or raising the of oxygen bound to haemoglobin. The
ribs expands the thoracic cavity. At rest, amount of oxygen bound to haemoglobin is
contraction of the diaphragm accounts expressed as oxygen saturation (SaO2). This
for most of inspiration. The diaphragm is is dependent upon the partial pressure of
supplied by phrenic nerve which originates oxygen (pO2).
from cervical spinal cord (C3–C5). The
external intercostal muscles also aid Oxygen dissociation curve
inspiration. At rest, expiration is mostly
passive and the lungs contract due to their The relationship between pO2 and SaO2 is
elasticity. During exercise, the internal expressed as the oxygen dissociation curve
intercostal muscles and other accessory (Figure 9.5). It is sigmoid in shape and
muscles aid expiration. They pull the ribs is due to facilitative binding of oxygen to
downward and inward, reducing the volume haemoglobin. Oxygen bound to haemoglobin
of the thoracic cavity. initially increases its affinity to bind further
oxygen. This facilitates further binding.
Pulmonary ventilation Haemoglobin has the least affinity for the
final oxygen molecule. This explains the
The total amount of air moved in and out of flattening of the curve with increasing pO2.
the lungs each minute depends upon the The p50 is the partial pressure of oxygen at
tidal volume (TV) and respiratory rate (RR). which 50% of the haemoglobin is saturated.
Pulmonary ventilation is the product of RR The p50 of adult haemoglobin is about
and TV. During exercise both RR and TV can 3.5 kPa.
be increased. The extra inspiration available
is called the inspiratory reserve volume The affinity of haemoglobin for oxygen
(IRV). The extra expiration, available is called is variable. When the affinity reduces, the
the expiratory reserve volume (ERV). After curve shifts to the right and the p50 increases.
maximum expiration some air is still present When the affinity increases the curve shifts to
in the lungs and is know as the residual the left and the p50 is reduced. The curve for
volume (RV). The maximum volume available haemoglobin in sickle cell anaemia is shifted
for breathing is the vital capacity (VC). Vital to the right. The curve for fetal haemoglobin is
capacity is the sum of IRV, TV and ERV. shifted to the left. Factors reducing the affinity
and thus shifting the curve to the right are:
Applied basic sciences 115
The oxygen dissociation curve Figure 9.5 The oxygen
dissociation curve. 2,3 BPG = 2,3
Biphosphoglycerate
% Saturation100 Decreased : Increased :
• temperature • temperature
• 2,3 BPG • 2,3 BPG
• CO2 • CO2
50 Half saturation
points
50 100
pO2 (mm Hg)
• An increase in pCO2 Carbon monoxide
• A reduction in pH The affinity of haemoglobin for carbon
• An increase in temperature monoxide is 250 times more than
• An increase in 2,3-biphosphoglycerate that towards oxygen. Its binding with
haemoglobin is competitive with oxygen.
Similarly, a reduction in these variables Carboxyhaemoglobin has a hyperbolic
results in an increase in the affinity of oxygen-dissociation curve
haemoglobin. Conditions which increase
the affinity of haemoglobin for oxygen, exist Transport of carbon dioxide
in the lungs. Therefore, oxygen gets bound
to haemoglobin. Conditions which reduce Carbon dioxide is 20 times more soluble in
the affinity of haemoglobin for oxygen, exist plasma than oxygen. It is transported in three
in peripheral tissues. Therefore, oxygen gets forms:
released from haemoglobin. The shift in the
dissociation curve due to changes in pCO2 is • Dissolved in plasma
known as the Bohr effect. • Bound to haemoglobin
• Bicarbonate ion
2,3-biphosphoglycerate
Haemoglobin combined with carbon dioxide
2,3-biphosphoglycerate (2,3-BPG) is a is known as carbaminohaemoglobin.
byproduct of anaerobic respiration. It The majority of carbon dioxide produced is
reduces the affinity of haemoglobin for transported as bicarbonate. Carbon dioxide
oxygen. Thus it shifts the oxygen dissociation diffuses into red cells and reacts with water to
curve to the right. Levels of 2,3-BPG increase produce bicarbonate and carbonic acid. This
in chronic hypoxia and thus more oxygen reaction is catalysed by the enzyme carbonic
is delivered to tissues. Levels of 2,3-BPG anhydrase. The bicarbonate produced inside
are reduced in stored blood. Thus oxygen red cells diffuses out into the plasma in
delivery to the tissues is sub-optimal with exchange with chloride ions. This is known as
transfused blood. Fetal haemoglobin is not chloride shift. Chloride moves into red cells
affected by 2,3-BPG. It has a higher affinity and bicarbonate moves out.
for oxygen than has maternal haemoglobin
and ensures transfer of oxygen across the Carbon dioxide equilibrium curve
placenta. Over the physiological concentrations of
carbon dioxide this curve is a straight line.
116 Chapter 9 Cardiothoracic surgery
The curve is shifted to the left in venous heat exchanger controls blood temperature.
blood. This improves carbon dioxide Surgery is often performed with 5–10°C of
transport and is known as Haldane effect. It hypothermia. A 40 mm filter removes air
occurs because deoxygenated haemoglobin bubbles. A pump returns blood into aorta
is a weaker acid and allows more carbon distal to a cross clamp. Suction is used to
dioxide to combine with haemoglobin. remove blood from operative field and this
is returned to the patient via the cardiotomy
Cardiac disease reservoir.
Cardiopulmonary bypass
Prolonged bypass induces cytokine
Cardiopulmonary bypass with the use of a activation and an inflammatory response. This
pump and oxygenator was first described results in red cell damage, haemoglobinuria,
in the 1950s. The components of a thrombocytopenia, clotting abnormalities.
cardiopulmonary bypass circuit are shown Reduced pulmonary gas exchange and
in Figure 9.6. A cannula is inserted into right cerebrovascular accidents.
atrium to drain the venous return. Venous
blood then passes into venous reservoir under Coronary artery surgery
gravity. It is oxygenated and CO2 is removed
by the use of a membrane oxygenator. A Pathology
Coronary artery disease is the commonest
cause of death in both men and women in
The components of a coronary artery by pass circuit
Aorta
Arterial line RA LA Cardiotomy suction
RV LV
Venous
resevoir
Arterial filter 12 Cardiotomy resevoir
Arterial pump Hot/ cold water
1 = Oxygenator Cardiotomy pump
2 = Heat exchanger
Figure 9.6 The components of a coronary artery bypass circuit. RA = Right atrium, LA = Left atrium, RV = Right
ventricle, LV = Left ventricle
Cardiac disease 117
the UK. It is progressive, generally begins in nitrates, b-blockers, statins and calcium-
childhood but manifests clinically in middle channel blockers. Revascularisation of
to late adult life. Atherosclerosis occurs in the the coronary arteries can be by either
proximal portions of the three main vessels percutaneous coronary intervention (PCI)
supplying the heart. The main treatable risk or coronary artery bypass surgery (CABG).
factors for coronary artery disease are: In the UK, about three times more patients
undergo PCI than CABG.
• Hypercholesterolaemia
• Hypertension Percutaneous coronary intervention
• Diabetes
• Smoking The use of PCI has increased dramatically
over recent years and has become one of the
Depending on the number of vessels most common medical interventions. PCI
involved, the patient is described as having describes a range of coronary interventions
double or triple vessel disease. The prognosis from angiography to angioplasty and stent
depends on both the number of vessels insertion. Indications for PCI include:
involved and left ventricular function.
• Acute ST elevation myocardial infarction
Clinical features (STEMI)
The symptoms of coronary artery disease • Non ST elevation acute coronary
vary widely. Some patients with mild disease syndrome
may present with clinically significant
symptoms and signs. Some patients with • Stable angina
advanced disease may have no symptoms • Mildly symptomatic patients with
and experience no functional impairment.
The spectrum of presentations includes: evidence of severe ischemia on
noninvasive testing
• Asymptomatic state
• Stable angina pectoris Contraindications to PCI include:
• Unstable angina
• Myocardial infarction • Left main stem stenosis in a patient who is
• Chronic ischaemic cardiomyopathy a surgical candidate
• Congestive heart failure
• Sudden cardiac arrest • Diffusely diseased small-caliber artery
• Other coronary anatomy not amenable to
Investigation
percutaneous intervention
An ECG will often show evidence of cardiac
ischaemia. Left ventricular function can Coronary artery bypass surgery
be assessed by measuring the ejection
fraction on echocardiography, coronary Coronary artery bypass surgery is indicated
angiography or multiple-gated acquisition for severe stenosis (>70%) with left main
(MUGA) scan. Coronary angiography allows stem or triple vessel disease. No improved
both confirmation of the diagnosis and survival has been shown in patients with
preoperative planning of the use of stents or single or double-vessel disease. Improved
the site of a coronary artery graft. survival is also seen in those with poor left
ventricular function. Similar survival is seen
Management in patients undergoing angioplasty for multi-
vessel disease. Patients at greatest risk have
The prevention and treatment of the most to gain from surgical intervention.
atherosclerosis requires control of the known Mortality risk can be estimated using
modifiable risk factors for the disease. This various scoring tools. Risk can be calculated
includes lifestyle changes and the medical by summating individual risk factors. The
treatment of hypertension, hyperlipidemia, Parsonnet score and Euroscore are the most
and diabetes mellitus. The mainstays of commonly used validated scoring system
pharmacologic therapy of angina includes (Table 9.1).
Choice of conduit The conduits for CABG
surgery can be either venous or arterial. Long
saphenous vein is easy to harvest by a second
surgeon and allows multiple grafts to be
118 Chapter 9 Cardiothoracic surgery
fashioned. Venous conduits have a patency occurs and angina recurs in 20% at 5 years and
rate of 60% at 10 years. The left internal 40% at 10 years.
mammary artery is often used to graft the left
anterior descending. Arterial conduits have a Valvular heart disease
patency rate of 90% at 10 years.
Aetiology
Surgery For CABG surgery, the chest is
entered via a median sternotomy and the The principal causes of valvular heart disease
left internal mammary artery is dissected. differ between Western and developing
The long saphenous vein can be harvested countries. Common causes include:
and prepared by second surgeon. The heart
is cannulated and the patient is placed on • Congenital valvular abnormalities
bypass. The aorta is cross clamped. Injury to (e.g. bicuspid aortic valve)
heart is reduced by cardioplegic solutions.
Cardioplegia can be either warm (37˚C) or • Infective endocarditis
cold (4˚C). Recent advances include off- • Rheumatic fever
pump coronary artery surgery and minimally • Degenerative valve disease
invasive direct coronary artery surgery. Both • Ischaemic heart disease
can avoid either bypass or median sternotomy.
Pathology
Complications The mortality rate following
CABG depends on the risk associated with Rheumatic fever results from immune-
patient groups but is generally around 2%. mediated inflammation of the heart valves.
The risk is higher in the acute or emergency It results from cross reaction between Group
setting. Complications of coronary artery A b haemolytic streptococcus and cardiac
bypass surgery included bleeding, atrial proteins. Valve disease results in either
fibrillation, wound infection, poor cardiac stenosis or incompetence. Stenosis causes
function and stroke. With time restenosis pressure load on the proximal chamber.
Incompetence causes volume load on
the proximal chamber. Thrombus may
form in the dilated left atrium resulting in
peripheral embolisation.
Risk changes as assed by the Parsonnet Score and Euroscore
Parsonnet Score Euroscore
Age greater than 70 years +7% Age – for each 5 years over 60 years +1%
Age greater than 75 years +12% Female sex +1%
Age greater than 80 years +20% Chronic respiratory disease +1%
Female sex +1% Extracardiac arteriopathy +2%
Hypertension +3% Neurological dysfunction +2%
Diabetes +3% Creatinine greater than 200 µmol/L +2%
Obesity +3% Previous cardiac surgery +3%
Good ejection fraction Nil Unstable angina +2%
Moderate ejection fraction +2% Recent myocardial infarction +2%
Poor ejection fraction +4% Good ejection fraction Nil
Moderate ejection fraction +1%
Poor ejection fraction +3%
Table 9.1 Risk changes as assed by the Parsonnet Score and Euroscore
Cardiac disease 119
Clinical features sudden death. Asymptomatic mitral stenosis
The clinical features of aortic, mitral and is well tolerated with greater than 50% 10-
tricuspid valve disease as follows: year survival. Medical management consists
of treatment of cardiac failure, digitalisation
Aortic stenosis if in atrial fibrillation and anticoagulation
• Angina pectoris if there is evidence of peripheral
• Syncopal episodes embolisation.
• Left ventricular failure
• Slow upstroke to arterial pulse Surgery
• Ejection systolic murmur in 2nd right
Surgery is usually performed through a
intercostal space median sternotomy. On cardiopulmonary
bypass with systemic hypothermia, the heart
Aortic regurgitation is arrested and protected with cardioplegic
• Congestive cardiac failure solution. Valves can be either repaired
• Increased pulse pressure or replaced. Valve repair results in better
• Water-hammer pulse haemodynamics and does not require long-
• Early diastolic murmur at left sternal edge term anticoagulation. Approximately 7000
patients per year undergo valve replacement
Mitral stenosis in the UK. The aortic valve is the commonest
• Pulmonary hypertension to be replaced.
• Paroxysmal nocturnal dyspnoea
• Atrial fibrillation Indications for aortic valve replacement
• Loud first heart sound include:
• Mid diastolic murmur at apex
• Symptomatic aortic stenosis
Mitral regurgitation • Asymptomatic aortic stenosis with
• Pulmonary oedema
• Apex beat displace laterally pressure gradient more than 50 mmHg
• Apical pansystolic murmur • Symptomatic aortic regurgitation
Tricuspid stenosis Indications for mitral valve replacement
• Fatigue and peripheral oedema include:
• Hepatomegaly and ascites
• Increased JVP with prominent a waves • Symptomatic mitral stenosis especially if
• Diastolic murmur at left sternal edge peripheral emboli
Tricuspid regurgitation • Mitral valve area less than 1 cm2
• Pulsatile hepatomegaly and ascites
• Right ventricular heave Prosthetic heart valves
• Prominent JVP with large v waves
• Pansystolic murmur at left sternal edge The principal types of replacement heart
valves are:
Investigation
Investigation of valvular heart disease • Heterografts – stented or unstented (e.g. pig)
will require, an ECG, chest x-ray and • Homografts
echocardiography. Cardiac catheterisation • Ball and cage (e.g. Starr–Edwards)
may be necessary to measure the • Tilting disc (e.g. Bjork–Shiley)
transvalvular pressure gradient.
Mechanical valves are readily available,
Management have good durability but require life-long
Few patients with symptomatic aortic anticoagulation. They are also at increased
stenosis survive 5 years and approximately risk of infective endocarditis. Heterografts
20% of symptomatic patients will suffer are readily available but have a limited
lifespan. The median survival of aortic
and mitral heterografts is 15 and 8 years,
respectively. They require a limited duration
of anticoagulation. Homografts are not readily
available and do not require anticoagulation.
The long-term outcome of homografts is
uncertain.
120 Chapter 9 Cardiothoracic surgery
Intra-aortic balloon pump Complications of an intra-aortic balloon
pump include:
Principles of action
• Limb ischaemia
Myocardial ischaemia can cause a fall in • Bleeding at insertion site
cardiac output and the coronary blood flow • Thromboembolism
may subsequently be reduced. Compensatory • Balloon leak
mechanisms may further reduce cardiac • Thrombocytopenia
output and coronary blood flow. Cardiac • Infection
performance can be improved by • Aortic dissection
optimisation of preload, afterload, heart rate,
contractility and myocardial oxygenation. Infective endocarditis
An intra-aortic balloon pump provides Infective endocarditis results from bacterial
haemodynamic support to the failing heart. infection of the endothelial surface of the
It works by increasing blood flow in the heart. It produces characteristic vegetations
coronary arteries and reducing the work of consisting of platelets, fibrin and bacteria.
the cardiac muscle. The balloon is inflated in Predisposing factors include:
diastole which increases diastolic coronary
artery perfusion pressure and increases • Rheumatic valve disease
myocardial oxygen delivery. The balloon is • Degenerative heart disease
deflated in systole which reduces impedance • Mitral valve prolapse
to left ventricular ejection and decreases • Congenital heart disease
myocardial oxygen demand. • Hypertrophic cardiomyopathy
• Intravenous drug abuse
Indications for the use of an intra-aortic • Prosthetic valve
balloon pump include:
Native-valve endocarditis often occurs as
• Perioperative myocardial ischaemia a complication of central venous catheter
• Acute mitral valve regurgitation infection. Prosthetic-valve endocarditis
• Postoperative low cardiac output states accounts for 10% cases of infective
• Preoperative use in high-risk coronary endocarditis. The greatest risk is during the first
6 months after surgery. MRSA is responsible for
artery surgery most cases seen in the first year.
• Refractory left ventricular failure
• Cardiogenic shock Microbiology
• Impending myocardial infarction
The relative proportions of infecting
Contraindications for the use of an intra- organisms depends on the underlying valve
aortic balloon pump include: disease. Native-valve endocarditis is usually
caused by:
• Severe aortic regurgitation
• Severe calcific aorto-iliac disease • viridans streptococci
• Severe peripheral vascular disease • Streptococcus bovis
• Aortic dissection • Staphylococcus aureus
• enterococci
Mechanics of the pump • Gram-negative coccobacilli
A catheter is inserted through the femoral Clinical features
artery using a Seldinger technique. The tip of
the balloon is placed about 2 cm distal to left The clinical presentation of endocarditis
subclavian artery. The balloon pump timing is can be varied. At one extreme there is acute
triggered from the ECG or arterial wave form. systemic toxicity with rapid progression to
Inflation occurs at the peak of the T wave at cardiac complications. At the other extreme
the end of systole. Deflation occurs just before there is an indolent low-grade febrile illness
the R wave. Correct timing of inflation and with minimal cardiac dysfunction. About 90%
deflation is essential for optimum diastolic patients have a fever and 85% have a murmur,
augmentation. Factors that reduce stroke usually that of underlying cardiac lesion.
volume also lower diastolic augmentation.
Cardiac disease 121
About 10–40% have a changing murmur. When empirical treatment is necessary,
Peripheral signs are rare. it is important to consider the risk factors
for certain organisms and local bacterial
Investigation resistance patterns. Microbiological
Almost 95% of patients will have positive investigation needs to determine the
blood cultures. Echocardiography allows antibiotic sensitivities and the minimum
visualisation of vegetations and the detection inhibitory concentrations. Indications for
of cardiac complications. Transthoracic surgical intervention include:
echocardiography has a low sensitivity
but high specificity. Transoesophageal • Moderate-to-severe heart failure as a result
echocardiography has a higher sensitivity. of valvular dysfunction
Duke’s Clinical Criteria • Partial dehiscence of a prosthetic valve
The diagnosis of infective endocarditis by the • Persistent bacteraemia despite optimal
Duke’s Clinical Criteria (Table 9.2) requires
the presence of: antimicrobial therapy
• Absence of effective bactericidal
• Two major criteria or
• One major and three minor criteria or treatment
• Five minor criteria • Fungal infective endocarditis
• Relapse of prosthetic-valve endocarditis
Management • Staphylococcus aureus prosthetic-valve
The optimal antibiotic therapy for infective
endocarditis depends on the infecting endocarditis
organism. Parenteral therapy is required
to ensure bactericidal concentrations. Aortic dissection
Aortic dissection is the commonest aortic
emergency. The incidence is twice that of
ruptured abdominal aortic aneurysm. It is
rare less than 40 years of age and is most
Duke’s Clinical Criteria for the diagnosis of infective endocarditis
Major criteria Minor criteria
Positive blood cultures
Evidence of endocardial involvement Predisposing heart condition or intravenous drug abuse
Fever (more than 38.0°C)
Vascular phenomenon
Major arterial emboli
Septic pulmonary infarcts
Mycotic aneurysm
Intracranial haemorrhage
Conjunctival haemorrhages
Immunological phenomenon
Glomerulonephritis
Osler nodes
Roth spots
Microbiological evidence (but less than major criteria)
Echocardiographic findings (but not meeting major
criteria)
Table 9.2 Duke’s Clinical Criteria for the diagnosis of infective endocarditis
122 Chapter 9 Cardiothoracic surgery
commonly seen between 50 and 70 years. The Clinical features
male:female ratio is equal and it is associated Aortic dissection usually presents with
with hypertension, Marfan’s syndrome and tearing chest pain radiating to the back,
bicuspid aortic valves. often associated with an episode of collapse.
Examination may show reduced or absent
Pathology peripheral pulses and a soft early diastolic
murmur. If aortic branches are occluded
An intimal tear results in blood splitting the there may clinical evidence of acute renal
aortic media. This produces a false lumen that failure, paraplegia, acute limb ischaemia,
can progress in an antegrade or retrograde cerebrovascular accident or an inferior
direction. Rupture can occur back into the myocardial infarction.
lumen or externally in to the pericardium or
mediastinum. External rupture often results in Investigation
fatal pericardial tamponade. The commonest A chest x-ray usually shows a widened
site of the intimal tear is within 2–3 cm of the mediastinum. The diagnosis can be confirmed
aortic valve. It is also seen in the descending by echocardiogram or CT scanning.
aorta distal to the left subclavian artery.
Dissection can result in occlusion of aortic Management
branches and the most commonly involved All patients require urgent management
are the renal, spinal, coronary or iliac arteries. of any associated hypertension. Type
A dissections usually require surgical
Classification intervention. Surgery is performed
via a median sternotomy and on
Two classifications systems are in common cardiopulmonary bypass. The dissection is
use (Figure 9.7). The Stanford classification excised and the aorta replaced with a graft.
divides dissections into Type A and B The aortic valve is preserved if possible.
depending on whether the ascending or An evolving CVA or established renal
descending aorta is involved. The DeBakey
divides dissections into Types I to III.
The Stanford and DeBakey Classification of Aortic Dissection
I II III
Type A Type B
Figure 9.7 The Stanford and DeBakey Classification of Aortic Dissection. Stanford classification = I, II, III.
DeBakey Classification = A and B
Thoracic disease 123
failure are contraindications to surgery. Indications for urgent thoracotomy are:
Without operation the prognosis for Type
A dissections is poor with about 40% dying • Chest drainage with more than 1500 mL or
within 24 hours and 80% dying within 2 more than 200 mL per hour
weeks. Operative mortality is approximately
25%. Type B dissections may be treated • Large unevacuated clotted haemothorax
without surgery but requires fastidious • Developing cardiac tamponade
blood pressure control. Surgery should be • Chest wall defect
considered if there is evidence of aortic • Massive air leak despite adequate drainage
expansion. Surgery for Type B dissections • Proven great vessel injury on angiography
is associated with significant risk of • Proven oesophageal injury
paraplegia. • Proven diaphragmatic laceration
• Traumatic septal or valvular injury of the
Thoracic disease
heart
Thoracic trauma
Haemothorax
Thoracic trauma accounts for only 5% of
admissions to a trauma centre but is second A haemothorax is common after both
only to head injury as the commonest cause penetrating and blunt trauma. Each pleural
of death. The mortality for isolated thoracic cavity can hold up to 3 litres of blood and 1
trauma is 5% but approaches 35% in those litre may easily accumulate before becoming
with concomitant abdominal or head injuries. apparent on a chest x-ray. About 90% of
cases of haemothorax are due to injury to
Chest injuries detected during the primary internal mammary or intercostal vessels. The
survey include: remaining 10% occur due to bleeding from
the pulmonary vasculature. The bleeding
• Airway obstruction usually stops when the lung is re-expanded
• Tension pneumothorax and most require no more than simple chest
• Open pneumothorax drainage.
• Massive haemothorax
• Flail chest Pericardial tamponade
• Cardiac tamponade
Pericardial tamponade is a major
Chest injuries detected during the secondary complication of penetrating chest trauma. A
survey include: haemopericardium prevents diastolic filling
of the heart. The classic signs of pericardial
• Pulmonary contusion tamponade are the Beck’s triad of:
• Myocardial contusion
• Aortic disruption • Hypotension
• Traumatic diaphragmatic hernia • Venous distension
• Tracheobronchial disruption • Muffled heart sounds
• Oesophageal disruption
Pericardial tamponade may be associated
Management of the unstable patient with pulsus paradoxus – an exaggerated
drop in systemic blood pressure during
Indications for an emergency room inspiration. A chest x-ray shows a globular
thoracotomy are: heart. An unstable patient requires urgent
thoracotomy. In a stable patient, the diagnosis
• Acute pericardial tamponade can be confirmed by echocardiography
unresponsive to cardiac massage or pericardiocentesis. Subxiphoid
pericardiotomy is both a diagnostic and
• Exsanguinating intra-thoracic therapeutic procedure.
haemorrhage
Cardiac stab wounds
• Intra-abdominal haemorrhage requiring
aortic cross clamping With cardiac stab wounds, the right side of the
heart is more commonly injured than the left.
• Need for internal cardiac massage
124 Chapter 9 Cardiothoracic surgery
Patients with a right ventricular wound are Treatment of a flail chest requires:
more like to survive than with left-sided injury.
The atria, inflow and outflow tracts may also • Adequate ventilation
be damaged. Patients usually present with • Humidified oxygen
pericardial tamponade and treatment consists • Adequate analgesia
of resuscitation and pericardiocentesis.
Stab wounds can be accessed via a median Consideration should be given to intubation
sternotomy and can be directly repaired and ventilation if:
without cardiopulmonary bypass. Teflon-
pledgeted prolene sutures are generally • Significant other injuries
used. • Respiratory rate more than 35 per min
• Partial pressure oxygen less than 8.0 kPa
Injuries to the great vessels • Partial pressure carbon dioxide greater
Injury to the great vessels should be than 6.6 kPa
suspected from the mechanism or site of • Vital capacity less than 12 mL/kg
penetrating injury. The patient usually • Right to left shunt of more than 15%
presents with shock or pericardial
tamponade. A chest x-ray may show: Operative fixation is not normally required.
• Widening of the mediastinum to greater Chest drains
than 8 cm
A chest drain is a conduit to remove air or
• Depression of the left main bronchus to fluid from the pleural cavity. The fluid can be
greater than 140 degrees blood, pus or a pleural effusion. It also allows
re-expansion of the underlying lung. It must
• Haematoma in the left apical area prevent entry of air or drained fluid back into
• Massive left haemothorax the chest. A chest drain must therefore have
• Deviation of oesophagus to the right three components:
• Loss of the aortic knob contour
• Loss of the paraspinal pleural stripe • An unobstructed chest drain
• A collecting container below chest level
Injury to the great vessels requires an • A one-way mechanism such as a water seal
emergency thoracotomy or sternotomy.
Injuries to the descending thoracic aorta or Heimlich valve
requires left anterior thoracotomy. Injuries
to the proximal aorta and proximal carotid Drainage occurs during expiration when the
arteries require median sternotomy. pleural pressure is positive. Fluid from within
pleural cavity drains into the water seal. Air
Flail chest also bubbles through water seal to the outside
world. The length of drain below the fluid
A flail chest is associated with multiple level is important. If greater than 2–3 cm,
rib fractures on the same side. The flail it increases the resistance to air drainage
segment does not have continuity with (Figure 9.8).
the remainder of the thoracic cage and
results in paradoxical chest wall movement Indications for chest drain insertion include:
with respiration. It is often associated
with an underlying pulmonary contusion. • Pneumothorax
Paradoxical movement results in impaired • Malignant pleural effusion
ventilation and the work of breathing is • Empyema and complicated
increased. Ventilation-perfusion mismatch
and arterio-venous shunting occurs. A chest parapneumonic pleural effusion
x-ray will show: • Traumatic haemopneumothorax
• Post thoracotomy, oesophagectomy and
• Multiple rib fractures
• Underlying lung contusion cardiac surgery
• Haemopneumothorax
• Other associated injuries Insertion
Unless performed in an emergency situation,
then a pre-procedure chest x-ray should be
performed. The drain is usually inserted under
local anaesthesia using an aseptic technique.
Thoracic disease 125
Principles of a chest drain provided there is no loculation of fluid within
pleural cavity. A large drain (28 Fr or above)
Figure 9.8 Principles of a chest drain. should be used to drain blood or pus. The
It should be inserted in the 5th intercostal space drain should be anchored and a purse-string
in the mid-axillary line. It should be inserted or Z-stitch inserted in anticipation of removal.
over the upper border of the rib to avoid the Complications of chest drains are shown in
intercostal vessels and nerves. Blunt dissection Table 9.3.
and insertion of a finger through the wound
should ensure that pleural cavity is entered. It Removal
used to be taught that to drain fluid it should
be inserted towards the base of pleural cavity A chest drain should be removed as soon
and to drain air it should be inserted towards as it has served it purpose. For a simple
the apex of the lung. It probably does not matter pneumothorax it can often be removed within
24 hours. To remove the drain, ask the patient
to perform a Valsalva manoeuvre and remove
drain at the height of expiration. The pre-
inserted purse-string or Z-stitch can then be
tied. A post-procedure chest x-ray should be
performed to exclude a pneumothorax.
Dos and don’ts of chest drains include:
• Avoid clamping of the drain as it can result
in a tension pneumothorax
• The drain should only be clamped when
changing the bottle
• Always keep the drain below the level of the
patient. If lifted above chest level contents
of drain can siphon back into chest
• If disconnection occurs reconnect and ask
the patient to cough
• If a persistent air leak occurs consider low
pressure suction
• Observe for post-expansion pulmonary
oedema
Complications of chest drains
Early Late
Haemothorax Blocked drain
Lung laceration Retained haemothorax
Diaphragm and abdominal cavity penetration Empyema
Bowel injury in the presence of unrecognised Pneumothorax after removal
diaphragmatic hernia
Tube placed subcutaneously
Tube inserted too far
Tube displaced
Table 9.3 Complications of chest drains
126 Chapter 9 Cardiothoracic surgery
Lung cancer • Chest pain
• Cachexia, fatigue, and loss of appetite
Epidemiology • Dysphonia
• Clubbing of the fingernails
Lung cancer is the leading cause of cancer- • Dysphagia
related deaths in the Western world. About
40,000 cases are diagnosed in the UK each Investigation
year resulting in 29,000 deaths. It is the
commonest malignancy in men and second Investigation of potential lung cancers
commonest malignancy in women. In the include imaging and endoscopy. Useful
1950s, the male:female ratio was 6:1 but radiological investigations include a
with decreasing male and increasing female chest x-ray, high-resolution thoracic CT,
incidence rates, the ratio is now almost equal. positron emission tomography and MRI.
Overall, 5-year survival is about 6%. Endoscopic and invasive procedures include
bronchoscopy, CT-guided percutaneous
Aetiology needle biopsy, mediastinoscopy and
endoscopic ultrasound.
Smoking is the primary risk factor and
is responsible for 85% cases in UK. The Staging of lung cancer:
incidence of lung cancer is related to the
number of cigarettes smoked. Other risk • Stage 1 – Tumour is found only in one lung
factors include: and has not spread to the lymph nodes
• Passive smoking • Stage 2 – Tumour is found only in one lung
• Environmental and occupational hazards and has spread to the lymph nodes
• Diet
• Genetic factors • Stage 3a – The tumour has spread to the
lymph nodes outside of the lung, including
Pathology the chest wall and diaphragm on the same
side as the cancer
Lung cancers can be classified as either
small cell (20%) or non-small cell (80%) • Stage 3b – The tumour has spread to the
carcinomas. The non-small cell tumours can lymph nodes on the opposite lung or in the
be subdivided into squamous cell carcinomas neck
(30%), adenocarcinomas (35%) and large
cell carcinomas (15%). Adenocarcinoma are • Stage 4 – The tumour has spread to other
found peripherally in the lung and lymph parts of the lungs or distant metastases
node metastases are common. Squamous present
cell carcinoma are found centrally near the
hilum or the major bronchi. They are often Management
locally invasive. Large cell tumours are
usually peripherally located. They are poorly The aims of evaluating a patient with
differentiated tumours and may cavitate. suspected lung cancer are to determine:
They spread early to distant sites. Small cell
tumours are usually centrally located. They • Cell type of the tumour
can produce neuroendocrine hormones and • Anatomical extent of the disease
may result in paraneoplastic syndromes. • Functional status of the patient
Clinical features Only surgery can cure non-small cell lung
cancer but only 25% patients have potentially
Symptoms that may suggest a diagnosis of resectable disease at presentation. If a patient
lung cancer include: is considered for surgical intervention,
preoperative assessment requires assessment
• Dyspnoea of:
• Haemoptysis
• Chronic coughing or change in regular • Pulmonary function
• Cardiac status
coughing pattern • Nutritional and performance status
• Wheezing
Pulmonary complications are the commonest
cause of postoperative morbidity and
mortality and assessment of respiratory
Thoracic disease 127
reserve is important. Pulmonary function mediastinal or pleural drains. Drains may
tests are essential before surgery. Full however block and a haemothorax may only
respiratory assessment includes: be detected on a chest x-ray. It can often
be treated conservatively with transfusion.
• Spirometry and peak flows Reoperation is required if:
• Estimation of transfer factor
• Postoperative lung function prediction • Rapid blood loss via chest drain
• Significant intrapleural collection on a
using anatomical equations
• Quantitative isotope perfusions scans chest x-ray
• Persistent hypovolaemia despite
An FEV1 and transfer factor less than 40%
places a patient in the high-risk group transfusion
• Hypoxia due to compression of the
Surgery
underlying lung
Lung resection is the best treatment for
Stage 1 and 2 disease. Most patients with Sputum retention and atelectasis
small-cell cancer are not suitable for
surgery. Five-year survival decreases with Failure to clear bronchial secretions can
the extent of the disease. The aims of surgery result in bronchial obstruction, atelectasis,
are complete resection of the tumour and lobar collapse and secondary pulmonary
intrapulmonary lymphatics. This can be infection. It usually presents with tachypnoea
achieved with: and hypoxia. Examination usually shows
reduced bilateral basal air entry. Prevention
• Pulmonary lobectomy is preferred to treatment. The risk of sputum
• Pneumonectomy retention can be reduced by:
• Sublobar resections
• Bronchoplastic resections • Preoperative cessation of smoking
• Adequate postoperative pain relief
The mortality from a lobectomy is 2–4%. The • Chest physiotherapy
mortality from pneumonectomy is 6–8% • Humidification of inspired oxygen
• Bronchodilator therapy
Thoracotomy • Early mobilisation after surgery
Thoracotomy allows access to the chest Treatment requires formal chest
cavity. The position of the incision depends physiotherapy. Mini-tracheostomy and
on the intended operation or procedure. suction may be required. Antibiotics should
Two different approaches exist – lateral be reserved for those with proven pneumonia.
thoracotomy or median sternotomy.
Lateral thoracotomy can be carried out in Air leak
three different positions – posterolateral,
anterolateral or lateral/axillary. Median Following lung resection, the residual lung
sternotomy allows access to the anterior tissue usually expands to fill the pleural
and superior mediastinum. The sternum is cavity. A raw area can result in an air leak into
divided with an oscillating or Gigli saw or the pleural cavity which presents as persist
Lebsche knife. Ooze from the bone marrow air leak or bubbling of a chest drain. It usually
may be stopped with bone wax. The sternum settles spontaneously over 2–3 days but
is usually closed with steel wire. may require suction to be applied to pleural
drains. Apposition of the lung to the parietal
Complications of thoracic pleura encourages efficient healing.
operations
Intrathoracic bleeding Bronchopleural fistula
Intrathoracic bleeding usually occurs from A bronchopleural fistula results from major
the lung parenchyma or bronchial vessels. air leak from a post-pneumonectomy
It may present with clinical features of bronchial stump. It is seen in about 2% of
hypovolaemia but is usually apparent from patients undergoing pneumonectomy. The
airway directly communicates with pleural
space. It usually occurs as a result of a leak
128 Chapter 9 Cardiothoracic surgery
from a suture line and is particularly seen epithelial lining and arise from rupture of the
in those with factors impairing wound alveolar wall. Apical blebs are found in 85%
healing. It most commonly occurs 7–10 of patients undergoing thoracotomy. The
days after surgery. It presents with sudden frequency of spontaneous pneumothorax
breathlessness and expectoration of increases after each episode and most
bloodstained fluid. The fluid is that which recurrences occur within 2 years of the initial
normally fills the postpneumonectomy space. event.
Emergency treatment consists of lying the Secondary spontaneous
patient with the operated side downwards. pneumothorax
Oxygen should be administered and a
pleural drain inserted. Thoracotomy and
repair of the fistula may be required. The Secondary spontaneous pneumothorax
repair may be reinforced with an omental accounts for 10–20% of spontaneous
pneumothoraces due to:
.ir/or intercostal muscle patch. A thoracoplasty
• Chronic obstructive pulmonary disease
may be necessary to obliterate the with bulla formation
postpneumonectomy space.
• Interstitial lung disease
sPneumothorax • Primary and metastatic neoplasms
sPneumothorax is the presence of air within the • Ehlers–Danlos syndrome
• Marfan’s syndrome
pleural space usually due to disruption of the
Traumatic pneumothorax
nparietal, visceral or mediastinal pleura. The
iaclassification of pneumothoraces is shown Traumatic pneumothorax results from
either blunt or penetrating trauma.
in Table 9.4. A tension pneumothorax occurs Tracheobronchial and oesophageal injuries
can cause both mediastinal emphysema and
rswhen the pleura forms a ‘one-way’ flap valve. a pneumothorax. Iatrogenic pneumothorax is
common and occurs after:
Tension pneumothorax is a medical emergency.
• Pneumonectomy
ePrimary spontaneous • Thoracocentesis
.ppneumothorax • High-pressure mechanical ventilation
• Subclavian venous cannulation
Primary spontaneous pneumothorax
usually occurs in healthy young adult men. Clinical features of pneumothorax
The predominant symptom is acute pleuritic
ipApproximately 85% of patients are less than chest pain. Dyspnoea results from pulmonary
40 years of age. The male:female ratio is
://v6:1 and in 10% of cases they are bilateral.
It usually occurs as result of rupture of an
acquired subpleural bleb. Blebs have no
http Classification of a pneumothorax
Spontaneous Traumatic
Primary – no identifiable pathology Blunt or penetrating thoracic trauma
Secondary – underlying pulmonary disorder Iatrogenic
Postoperative
Mechanical ventilation
Thoracocentesis
Central venous cannulation
Table 9.4 Classification of a pneumothorax
Thoracic disease 129
compression. Symptoms are proportional radiological size of the pneumothorax. Small
to the size of the pneumothorax and also asymptomatic pneumothoraces may simply be
depends on the degree of pulmonary followed up with serial chest x-rays. If drainage
reserve. Physical signs include tachypnoea is required, a chest drain should be inserted
with increased resonance and absent through the 5th intercostal space, just above
breath sounds on the affected side. In a the upper border of the rib. Blunt insertion
tension pneumothorax, the patient may be should be used and the position of the drain
hypotensive with acute respiratory distress, should be checked with a chest x-ray. It should
the trachea may be shifted away from the be connected to an underwater seal, placed
affected side and the neck veins may be below the level of the patient.
engorged. Tension pneumothorax is a clinical
diagnosis. In other cases the diagnosis can beTension pneumothorax
confirmed with a chest x-ray.
Prophylactic chest drains should be inserted in
.ir/Investigation patients with rib fractures prior to ventilation
to reduce the risk of a tension pneumothorax.
A chest x-ray will confirm the diagnosis Tension pneumothorax requires immediate
(Figure 9.9). This usually shows radiolucency needle aspiration. A canula should be inserted
anteriorly through the 2nd intercostal space
sand absence of the lung vascular markings on prior to chest drain placement.
sthe affected side. There may be mediastinal
Surgery
shift and the percentage volume of the
Surgery is required for a pneumothorax if an
npneumothorax can be calculated. The cause air leak persists for more than 10 days, there is
iaof the pneumothorax, such as fractured ribs,failure of lung re-expansion, or for a recurrent
spontaneous pneumothorax. The surgical
may also be visible. options include:
rsManagement • Partial pleurectomy
• Operative abrasion of pleural lining
Spontaneous pneumothorax • Resection of pulmonary bullae
eThe management of a spontaneous
.ppneumothorax depends the symptoms and the
http://vipChest x-ray showing a right spontaneous pneumothorax
Figure 9.9 Chest x-ray showing a
right spontaneous pneumothorax
130 Chapter 9 Cardiothoracic surgery
Poor-risk patients may benefit from chemical often multiloculated. Lung empyemas are
pleurodesis with tetracycline. also seen following oesophageal perforation
Pneumonia, lung abscess or rupture, blunt or penetrating thoracic
and empyema trauma, nasopharyngeal sepsis that has
spread to the chest and thoracic surgical
Lung abscess procedures. If the diagnosis is delayed, the
empyema will develop a thick, fibrous wall
Some patients with pneumonia develop focal making future management more difficult.
necrosis and a lung abscess. This particularly
occurs in patients with malignancy and Clinical features
malnutrition. It can also occur following An empyema usually presents with features
aspiration or inhalation of a foreign body. The of pneumonia that fails to improve with
diagnosis can be difficult. antibiotics. There is often pleuritic chest pain
and breathlessness. Examination may show
.ir/Clinical features features of pleural effusion.
Patients usually present with clinical features Investigation
of a pneumonia that fails to improve with A chest x-ray will show fluid within the
pleural cavity and a CT scan will confirm
santibiotics. They can develop pleuritic chest the diagnosis. Percutaneous aspiration will
provide microbiological samples for culture.
pain and haemoptysis. The volume of sputum
Management
sproduced may increase. Patients are usually Appropriate antibiotic therapy should be
nsystemically unwell with a swinging pyrexia. given based on sputum culture results. Pleural
drainage should be with adequate (28 Fr) chest
Examination usually shows signs of pneumonia. drain. Thoracoscopy may be required to break
down loculi. Decortication of the visceral
iaThe commonest complication is an empyema. and parietal pleura may be required to allow
lung expansion. Following surgery, adequate
The differential diagnosis includes: drainage is required. Pneumothorax is not a
risk due to the resulting pleural scarring.
rs• Primary lung neoplasm
Bronchiectasis
• Tuberculosis
Bronchiectasis is chronic bronchial
e• Aspergillosis dilatation with parenchymal infection and
an inflammatory reaction. It typically affects
• Lung cyst the basal segments of the lower lobes.
Acquired infections are the most common
.pInvestigation cause, typically when occurring in childhood.
Congenital causes include:
A chest x-ray may show a pulmonary cavity
• Cystic fibrosis
ipwith air/fluid level. CT scanning will confirm• Kartagener syndrome
• Various immunodeficiency disorders
the diagnosis if a chest x-ray is inconclusive. • Bronchopulmonary sequestration
://vBronchoscopy should be considered to
exclude a foreign body.
Management
ttpInitial management should include
appropriate antibiotic therapy based on
sputum culture results. Percutaneous
haspiration should be considered if the abscess
fails to improve with antibiotic therapy. For
abscesses greater than 5 cm diameter, open
drainage may be required. Thoracotomy
and lung resection should be considered in
complicated cases.
Empyema Clinical features
Empyema is defined as pus within a body The clinical features of bronchiectasis are
cavity. A lung empyema usually occurs recurrent pneumonia, a persistent cough and
secondary to pneumonia. The collection is copious foul smelling sputum. Haemoptysis
is common in adults but rare in children.
Thoracic disease 131
Investigation but 30% present with local symptoms related
A chest x-ray may show a typical ‘honeycomb’ to encroachment on adjacent structures.
pattern. Microbiological studies typically It may present with a cough, chest pain or
show Haemophilus influenza, Escherichia superior vena cava compression. About 20%
coli or Klebsiella as the causative agents. are identified during the investigation of
High resolution thoracic CT has replaced myaesthenia gravis.
bronchography as the investigation of choice. Investigation
Bronchoscopy may be required to rule out
Most thymomas are visible on chest x-ray and
an obstruction lesion and allow pulmonary
CT may be used to delineate the mass further.
lavage. Contrast-enhancement is useful in defining
vascularity and the extent of invasion. The
Management diagnosis can be confirmed by biopsy taken
Medical therapy is the primary approach, at anterior mediastinoscopy. The Masaoka
staging system is as follows:
.ir/using antibiotics, humidification and
• Stage 1 – Encapsulated tumour with no
bronchodilators. Surgical intervention is gross or microscopic invasion
indicated for:
• Stage 2 – Macroscopic invasion into
s• Failure of medical management mediastinal fat or pleura
• Persistent symptoms • Stage 3 – Invasion of pericardium, great
vessels or lung
s• Recurrent pneumonias
n• Haemoptysis • Stage 4 – Pleural or pericardial metastatic
spread
The ideal surgical candidate has unilateral
• Stage 5 – Lymphatic or haematogenous
iadisease confined to one lobe. Most patients spread
have bilateral disease. Surgery should be Management
rsreserved for localised disease, operating on Treatment depends on the stage of the
disease. Stage 1 disease can be managed
the worst side first. by complete surgical excision. Stages 2
and 3 disease requires surgical excision
eThymoma and postoperative radiotherapy. Stages 4
.pThe thymus is a lymphoid organ located in the and 5 disease requires surgical debulking,
radiotherapy and chemotherapy.
anterior mediastinum composed of epithelial
Thymectomy
ipcells and lymphocytes. It is responsible for
The initial management of most thymomas
maturation of cell-mediated immunity and is by surgery, usually performed via
a median sternotomy. Resection may
://vreaches maximum size at puberty. It regressesrequire excision en-bloc of any involved
in later life.
Pathology
ttpThymoma is the most common neoplasm
of the anterior mediastinum and accounts
for 25% of all mediastinal tumours. The peak
hincidence is between 40 and 50 years of
age. It originates from epithelial cells of the pericardium, pleura and phrenic nerves.
thymus gland. No clear aetiological factors If possible, damage to the phrenic nerves
have been defined. It is associated with the should be avoided. Clips should be placed
development of myaesthenia gravis. No clear to aide subsequent radiotherapy planning.
distinction between benign and malignant
Prognosis is worse for symptomatic
tumours exist. Malignant tumours can invade thymomas. The most important factor that
the vasculature and adjacent structures.
determines prognosis is invasion of adjacent
Death often occurs from cardiac tamponade
structures. Stage 1 disease is associated
or cardiorespiratory complications.
with greater than 90% 5-year survival. Stage
Clinical features 4 disease is associated with less than 25%
Almost 50% of thymomas are asymptomatic 5-year survival.
http://vip.persianss.ir/
Chapter 10 General
surgery
Abdominal trauma • Equivocal clinical examination
• Difficulty in assessing patient – alcohol,
Assessment of
abdominal trauma drugs, head injury etc
• Persistent hypotension despite adequate
Assessment of patients with abdominal
trauma can be difficult due to altered fluid resuscitation
sensorium (head injury, alcohol), altered • Multiple injuries
sensation (spinal cord injury) and injury • Stab wounds where the peritoneum is
to adjacent structures (pelvis, chest). The
pattern of injury will be different between breached
penetrating and blunt trauma. Indications for
laparotomy without extensive investigation Prior to the procedure, it is important to
include: ensure that a urinary catheter and nasogastric
tube are in place. Under local anaesthesia, a
• Unexplained shock sub-umbilical incision is made down to the
• Rigid silent abdomen linea alba. The peritoneum is incised and
• Evisceration a peritoneal dialysis catheter is inserted.
• Radiological evidence of intraperitoneal The catheter is aspirated and any free blood
or enteric contents is noted. If no blood is
gas aspirated, then 1 L of normal saline is infused
• Radiological evidence of ruptured and left in the peritoneal cavity for 3 minutes.
A drainage bag is attached to the catheter and
diaphragm the bag placed on the floor and allowed to
• Gunshot wounds drain. A 20 mL sample of the fluid is sent to
• Positive result on peritoneal lavage the laboratory for measurement of RBC, WCC
and microbiological examination. A positive
Imaging result is regarded as:
Either CT or ultrasound can be used for • Red cell count more than 100,000/mm3
the assessment of abdominal trauma. CT • White cell count more than 500/mm3
scanning is the preferred method but does • The presence of bile, bacteria or faecal
require the patient to be cardiovascularly
stable. Ultrasound has high specificity but material
low sensitivity for the detection of free fluid
or visceral damage. Focused assessment for Damage control surgery
the sonographic assessment of trauma (FAST)
is the use of ultrasound to rapidly assess for Following multiple trauma, a poor outcome
intraperitoneal fluid. The ultrasound probe is is seen in those with hypothermia,
placed on the right upper quadrant, left upper coagulopathy and severe acidosis. Prolonged
quadrant and suprapubic region to detect surgery can exacerbate these factors. As
fluid in the subphrenic or subhepatic spaces a result the concept of ‘damage control’
or pouch of Douglas in a hypotensive patient. surgery has been developed. Damage control
It can be used to confirm the likely need for surgery should be considered if a patient with
an emergency laparotomy. multiple trauma has an Injury Severity Score
greater than 25, core temperature less than 34
Peritoneal lavage degree or an arterial gas pH less than 7.1
With the more ready availability of abdominal Initial operation
CT scanning, then the use of peritoneal
lavage is falling. Indications for peritoneal The early surgical management of major
lavage include: abdominal trauma should aim to:
• Control haemorrhage with ligation of
vessels and packing
134 Chapter 10 General surgery
• Remove dead tissue occurs in the presence of lower rib fractures.
• Control contamination with clamps and It may become clinically apparent either early
or late after injury. Delayed presentation
stapling devices is usually due to rupture of a subcapsular
• Lavage the abdominal cavity haematoma. About 20% of splenic injuries
• Close the abdomen without tension occur inadvertently during other abdominal
operations. In some patients spontaneous
Options for temporary abdominal wound rupture can occur following trivial trauma.
closure include: In these situations, the spleen is invariably
abnormal due to other pathology such as
• Skin-closure only malaria or infectious mononucleosis.
• Plastic sheet or ‘Bogota bag’
• Absorbable mesh Clinical features
• Non-absorbable mesh with protection of The clinical features of splenic injury depend
on the extent of the blood loss and the presence
the underlying viscera of associated injuries. The clinical presentation
ranges from left upper quadrant pain with
Intensive care unit few clinical signs to shock and generalised
peritonitis. About 30–60% of patients have
Early surgery should be followed by a period of other associated intraperitoneal injuries.
stabilisation on the intensive care unit. During
this period the following should be addressed: Investigation
Abdominal ultrasound will often show
• Rewarming blood in the peritoneal cavity or a splenic
• Ventilation haematoma. Accurate definition of the extent
• Restoration of perfusion of splenic trauma requires a CT scan. The
• Correction of deranged biochemistry grading of splenic injuries is as follows:
• Commence enteral or parenteral nutrition
• Grade 1 – Minor subcapsular tear or
Second look laparotomy haematoma
A further planned re-laparotomy should take • Grade 2 – Parenchymal injury not
place at 24–48 hours to allow: extending to the hilum
• Removal of packs • Grade 3 – Major parenchymal injury
• Removal of dead tissue involving vessels and the hilum
• Definitive treatment of injuries
• Restoration of intestinal continuity • Grade 4 – Shattered spleen
• Closure of the musculofascial layers of the
Management
abdominal wall If the patient is cardiovascularly unstable,
they require resuscitation and early surgery.
This approach has been shown to be If the patient is cardiovascularly stable, then
associated with a reduced mortality. consideration can be given to CT scan and
if an isolated Grade 1 or 2 splenic injury is
Gastrointestinal injury identified, then consideration should be
given to conservative management.
Small bowel perforations can invariably be
primarily closed. The management of colonic Surgical options
perforations is more controversial. It used to
be common practice to excise the damaged The surgical management of splenic injuries
segment and fashion a proximal stoma. The can involve either splenectomy or splenic
perforation could also be exteriorised as repair. The main benefit of retaining the
a stoma. It is increasingly recognised that spleen is the prevention of overwhelming
primary repair of colonic injuries is safe and it post-splenectomy infection (OPSI). If splenic
is now the recommended method, especially conservation is attempted, it is necessary to
in the absence of significant contamination. preserve more than 20% of the spleen.
Splenic injury
Splenic injury can be either accidental or
iatrogenic. It is most commonly associated
with blunt abdominal trauma and often
Abdominal emergencies 135
Conservative management Primary peritonitis is diffuse bacterial
infection without loss of integrity of
Overall 20–40% of patients are suitable gastrointestinal tract. It often occurs in
for conservative management. In adolescent girls. Streptococcus pneumonia is
particular, children can often be managed the commonest organism involved. Secondary
conservatively as they have more low peritonitis is acute peritoneal infection
grade injuries and fewer multiple injuries. resulting from gastrointestinal perforation,
Patients require close cardiovascular and anastomotic dehiscence or infected
haematological monitoring preferably in a pancreatic necrosis. It often involves multiple
high dependency unit. Surgery is necessary organisms – both aerobes and anaerobes.
if the patient becomes hypovolaemic or they The commonest responsible organisms are
have a falling haematocrit. Approximately Escherichia coli and Bacteroides fragilis.
30% of patients fail conservative
management. Failure usually occurs Management
within the first 72 hours of injury. Failed
conservative management often results in The management of secondary peritonitis
splenectomy and it has been argued that, involves:
overall, more spleens can often be conserved
by early surgical intervention. If splenic • Elimination of the source of infection
conservation is successful, patients should • Reduction of bacterial contamination of
remain on bed rest for 72 hours, have limited
physical activity for 6 weeks and no contact the peritoneal cavity
sports for 6 months. • Prevention of persistent or recurrent intra-
Liver injury abdominal infection
The liver is the second most commonly These should be combined with fluid
injured organ in abdominal trauma, but resuscitation, antibiotics and intensive care
damage to the liver is the most common management. Source control can achieved
cause of death after abdominal injury. It is by closure or exteriorisation of perforation.
often associated with splenic injury and rib Bacterial contamination can be reduced by
fractures. CT is the investigation of choice aspiration of faecal matter and pus. Recurrent
allowing grading of the extent of injury and infection may be prevented by the used of
detection of associated injuries. In the past, drains, planned re-operations or leaving the
most of these injuries were treated surgically. wound open.
However, as many as 90% of liver injuries have
stopped bleeding by the time of operation. Peritoneal lavage
Angiography and embolisation may allow
conservative management that previously Peritoneal lavage with saline is often used
would have come to operation. during abdominal surgery, but its benefit is
unproven. Simple swabbing of pus from the
Abdominal emergencies peritoneal cavity may be of similar value. It
Peritonitis has been suggested that lavage may spread
infection or damage the peritoneal surface.
Intra-abdominal infection results in two There is no benefit of adding antibiotics to
major clinical manifestations. Early or diffuse lavage fluid. There is no benefit of adding
infection results in localised or generalised chlorhexidine or iodine to lavage fluid. If
peritonitis. Late and localised infections used, lavage with large volume of crystalloid
produce an intra-abdominal abscess. The solution probably has the best outcome.
pathophysiology depends on the competing
factors of bacterial virulence and host Intra-abdominal abscesses
defences. Bacterial peritonitis is classified as
primary or secondary. An intra-abdominal abscess may arise
following localisation of peritonitis,
gastrointestinal perforation, an anastomotic
leak or following haematogenous spread.
They develop in sites of gravitational drainage
such as the pelvis, subhepatic spaces,
subphrenic spaces and paracolic gutters.
136 Chapter 10 General surgery
Clinical features Pathology
Postoperative abscesses usually present Acute appendicitis usually arises secondary
at between 5 and 10 days after surgery. to obstruction of the appendicular lumen.
Following gastrointestinal surgery, an intra- Obstruction is usually caused by lymphoid
abdominal abscess should be suspected if hyperplasia or faecoliths. It can also occur as
there is an unexplained persistent or swinging a result of tumours or worms. Obstruction
pyrexia. It may also cause abdominal pain causes stasis and infection of the luminal
and diarrhoea. A mass may be present with contents. Increased pressure within the lumen
overlying erythema and tenderness. A pelvic causes venous congestion and thrombosis.
abscess may be palpable only on rectal Ischaemia can cause ulceration, necrosis and
examination. eventual perforation. The progression from
obstruction to perforation usually takes about
Management 72 hours. The degree of peritonitis depends
on the ability of the omentum and adjacent
A contrast-enhanced CT is probably the bowel loops to contain the infection.
investigation of choice. It will confirm the
presence of an abscess or collection and may Clinical features
delineate a gastrointestinal or anastomotic
leak. It may determine the possibility of The typical clinical features of appendicitis
percutaneous drainage. Operative drainage are well described but the presentation
may be required if the there is a multi- can be atypical. Patients often have central
locular abscess, there is no safe route for abdominal pain that migrates to right iliac
percutaneous drainage or if an abscess fossa. This may be associated with nausea,
recollects after percutaneous drainage. vomiting and anorexia. A low-grade pyrexia
Patients should receive antibiotic therapy and tachycardia may be present. Patients
guided by organism sensitivities. appear flushed with fetor oris. Abdominal
examination may show localised tenderness
Appendicitis in the right iliac fossa with signs of right iliac
fossa peritonism. Percussion tenderness
About 10% of the population will develop is a kinder sign of peritonism to elicit than
acute appendicitis at some stage in their lives. rebound tenderness. Rovsing’s sign is pain
The incidence of appendicitis is falling but in right iliac fossa during palpation in the left
70,000 appendicectomies are still performed iliac fossa. At the time of diagnosis, the rate
each year in the UK. The peak incidence is of perforation is about 20%. These patients
between 10 and 15 years of age. Appendicitis usually present with signs of generalised
is more common in men but appendicectomy peritonitis.
is performed more often in women. In about
10% of operations a normal appendix is Causes of right iliac fossa pain include:
removed. A woman is more likely to have
a normal appendix removed. The risk of • Appendicitis
perforation is highest at the extremes of age. • Urinary tract infection
• Non-specific abdominal pain
Anatomy • Pelvic inflammatory disease
• Renal colic
The appendix is about 5 cm long and arises • Ectopic pregnancy
from the caecum. Although the base has a • Constipation
fairly constant position, the tip can be located
in the pelvis, behind the caecum or in the Causes of a right iliac fossa mass include:
paracolic gutter. The anatomical position
of the appendix determines the clinical • Appendix mass
presentation of acute appendicitis. The • Crohn’s disease
appendix is lined by colonic epithelium and • Caecal carcinoma
the submucosa contains lymphoid follicles. • Mucocele of the gallbladder
These increase in number to a peak at 1–20 • Psoas abscess
years of age and then subsequently decline. • Pelvic kidney
• Ovarian cyst
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MRCS Applied Basic Science and Clinical Topics
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