1. Neuro

Question 1

a) What characteristic neurological changes occur immediately and in the first three months following
transection of the spinal cord at the fourth thoracic vertebra? (25%)

Answer 1

Question 2

b) What other clinical problems
may develop following this type
of injury? (40%)

Question 3

c) List the advantages of a
regional anaesthetic technique for
a cystoscopy in this patient. (20%)

Answer 3

> Avoids autonomic dysreflexia.
Avoids the need for intubation of a patient who may have previously had
a tracheostomy with its attendant complications, e.g. tracheal stenosis.
Avoids deterioration in lung function associated with general anaesthesia,
thus reducing the risk of postoperative respiratory complications.
Avoids opioid use with associated respiratory depression.
Reduces the risk of aspiration associated with delayed gastric emptying.
Avoidance of unopposed parasympathetic response to airway
instrumentation (bradycardia, cardiac arrest).

Question 4

d) Why and when may
suxamethonium be
contraindicated in a patient with
spinal injury? (15%)

Answer 4

Upregulation of nicotinic acetylcholine receptors in extrajunctional sites
results in massive potassium release with suxamethonium use.
This effect is seen between approximately 72 hours following injury and six
months.

Question 5

a) What are the symptoms
(10%) and signs (20%) of raised
intracranial pressure (ICP) in an
adult?

Answer 5

Symptoms:
> Headache: bursting, throbbing. Exacerbated by sneezing, exertion,
recumbency. Worse in morning after a period of recumbency, raised
PaCO2 associated with sleep, reduced CSF reabsorption.
> Vomiting.
> Visual disturbance.
Signs:
> Respiratory irregularity, Cheyne-Stokes breathing, neurogenic
hyperventilation due to tonsillar herniation.
> Cushing’s triad: hypertension with high pulse pressure, bradycardia and
associated irregular respirations.
> Eye signs: papilloedema, fundal haemorrhages, pupillary dilatation,
ptosis, impaired upward gaze (midbrain compression), abducens palsy.
> Progressive reduction in consciousness due to caudal displacement of
midbrain.

Question 6

b) Describe the physiological
principles underlying the
management of raised ICP. (40%)

Answer 6

The cranium is a closed compartment (Monroe–Kelly doctrine). The sum
of its contents (brain, CSF, blood, other) must therefore remain the same.
If the amount of one component increases, some compensation can
occur by reducing the amount of one of the other components. Once
these compensatory mechanisms are exhausted, ICP will rise, ultimately
causing pressure on the brain, herniation and thus direct tissue damage.
Physiological manipulation of the quantity of each of the components can
limit ICP rise.
> Reduce CSF: diuretics, mannitol, hypertonic saline, elevation of head of
bed 15–30 degrees, CSF drain.
> Reduce blood:
• Optimise venous drainage: avoid tight tube ties, head-up tilt
15–30 degrees, paralyse to reduce valsalva, treat seizures with
anticonvulsants, avoid excessive PEEP and peak airway pressures.
• Avoid excessive arterial flow: maintain PaO2, keep PaCO2 low-normal,
anaesthetise to reduce cerebral metabolic rate of oxygen (CMRO2)
and avoid pyrexia.
> Reduce brain: mannitol, avoid hyperglycaemia, avoid hypotonic fluid
administration.
> Reduce other: evacuate clot, excise tumour.
> Stop the cranium being a closed compartment: decompressive
craniectomy.
One of the main issues of a rising ICP is the impact it has on cerebral
perfusion pressure (CPP), according to the equation:
CPP M= − AP ICP o( , r JVP whichever is higher)
Therefore, in the early stages of rising ICP (before direct pressure brain
damage occurs), the effects can be mitigated by maintaining CPP through
manipulation of mean arterial pressure (MAP) and jugular venous pressure
(JVP).
> Maintain MAP: avoid dehydration and pyrexia, and use vasopressors to
target a MAP of 80 mm Hg (this value depends on ICP, which may not be
known).
> Reduce JVP: as previously, optimise venous drainage.

Question 7

c) What methods are used to
manage or prevent acute rises in
ICP? (30%)

Answer 7

Airway:
> Intubate.
Respiratory:
> Aim PaO2 >13 kPa and PaCO2 4.5–5 kPa, keep PEEP <15.
> Hyperventilation to PaCO2 4–4.5 kPa may be used for short time periods
in emergency situations with refractory intracranial hypertension.
Cardiovascular:
> 15–30-degree head-up tilt, tube ties not too tight/tape tube, head in
neutral position, increase sedation and paralyse if coughing or straining,
ensure that MAP >80 (depends on ICP, if being monitored).
Neurological:
> Adequate sedation to reduce CMRO2, treat seizures, treat pyrexia,
monitor for and manage hyperglycaemia (target 6–10 mmol/l).
Pharmacological:
> Mannitol 0.25–1 g/kg.
> Hypertonic saline 5% 2 ml/kg.
> Consideration of CSF drain, under expert guidance.
> Decompressive craniectomy in specialist centre.

Question 8

a) What is the cause of
acromegaly in this patient? (10%)

Answer 8

Hypersecretion of growth hormone from a pituitary adenoma.

Question 9

b) List the clinical features of
acromegaly of relevance to the
anaesthetist. (45%)

Answer 9

Airway:
> Large lips, macroglossia, macrognathia, thickening of pharyngeal tissues,
laryngeal stenosis. Possibility of difficult airway should be considered.
Respiratory:
> Obstructive sleep apnoea (OSA) with risk of hypoventilation and
respiratory failure postoperatively.
Cardiovascular:
> Hypertension, left ventricular hypertrophy, cardiomyopathy with diastolic
dysfunction, valvular regurgitation, ECG changes.
> Increased peripheral soft tissue deposition may make cannulation
difficult.
Neurological:
> Raised ICP (obstruction of the 3rd ventricle).
> Spinal cord compression. Meticulous care with padding and positioning
required.
> Peripheral neuropathies due to impingement by soft tissue or bony
overgrowth.
Endocrine:
> Diabetes mellitus. Blood glucose should be monitored and managed with
insulin intraoperatively if necessary.
Gastrointestinal:
> Increased risk of colonic polyps and cancer – may necessitate surgery.
Cutaneomusculoskeletal:
> Osteoarthritis, bony overgrowth around joints, limited movement. Care
with positioning and padding.
Renal:
> Renal dysfunction may impact on perioperative drug choices

Question 10

c) How do the surgical
requirements for this procedure
influence the conduct of the
anaesthesia? (45%)

Answer 10

Question 11

A 34-year-old man is scheduled for a posterior fossa tumour excision.
a) List patient positions that might be employed for this operation. (10%)

Answer 11

> Sitting.
Lateral.
Prone.
Supine.
Park bench

Question 12

b) What potential intraoperative
problems are associated with
posterior fossa craniotomy? (25%)

Answer 12

Surgery itself:
> Venous air embolism (VAE), paradoxical air embolism. Air entrainment
can happen whenever the venous sinuses are open, but the risk is
increased if the open sinuses are elevated, as occurs in e.g. sitting
position, thus increasing the pressure differential between them and
atmosphere further.
> Cardiovascular instability (hypo- or hypertension, brady- or tachycardia,
arrhythmia) due to stimulation of cranial nerve nuclei and other brainstem
structures.
> Bleeding, cerebellar haematoma.
> Brainstem damage: respiratory and cardiovascular centres and cranial
nerve nuclei.
> Long tract damage.
> CSF leak.
> Meningitis, wound infection.
Positioning:
Sitting:
• Airway: tube displacement, jugular venous obstruction due to flexed
neck causing laryngeal and tongue oedema.
• Cardiovascular: VAE, hypotension due to reduced venous return.
• Neurological: cord or brainstem ischaemia due to head flexion and
hypotension, sciatic nerve damage, pneumocephalus.
• Cutaneomusculoskeletal: compartment syndrome, lumbosacral
pressure sores.
Other positions:
• All other positions that involve moving the patient after induction
involve risk of tube dislodgement.
• Each position has its unique pressure points, elbow, knee, ankle
for lateral, genitalia and knees for prone. Also, each position has its
individual risks for nerve palsies, such as brachial plexus compression
in lateral position, brachial plexus stretch and ulnar nerve damage with
prone, brachial plexus stretch and common peroneal compression
with park bench.
• Prone position has the additional issues of reflux due to raised
intragastric pressure, decreased venous return, corneal damage,
central retinal artery occlusion, ischaemic optic neuropathy.

Question 13

c) What monitoring techniques can
specifically detect the presence
of venous air embolism during
surgery, and for each method
used, give the features that would
indicate the diagnosis? (40%)

Answer 13

Transoesophageal echo:
> Air in right-sided cardiac chambers. In the presence of patent foramen
ovale, it can detect air in the left heart also. Not necessarily suitable for
long operations where the head is flexed.
Precordial Doppler:
> Sound heard if air present in cardiac chambers.

Question 14

d) How would you manage a
significant venous air embolism in
this patient? (25%)

Answer 14

This is a medical emergency, and I would alert the theatre team, call
for help and adopt an ABC approach, assessing and managing issues
simultaneously. The aims of management are as follows:
> Prevent further air entry: flood site with saline, fluid load, lower patient so
that the surgical site is below the right atrium if possible, apply sustained
positive airway pressure until this is all achieved.
> Reduce size: stop nitrous oxide if it is being used, administer 100%
oxygen, aspirate air from right atrium via central line.
> Overcome mechanical obstruction: left lateral or Trendelenberg
positioning may help force bubble above the right ventricular outflow.
Inotropic support may be required. If the patient suffers cardiac arrest,
chest compressions may assist in dispersing the bubble

Question 15

A 64-year-old man is scheduled for a stereotactic brain biopsy. He is taking dual antiplatelet therapy
following the insertion of a drug-eluting coronary artery stent six months earlier.
a) Explain the issues that may arise from antiplatelet therapy in this patient. (30%)

Answer 15

If dual antiplatelet therapy (DAPT) continues, the patient is at very high risk
of bleeding as a result of the biopsy, into a closed skull, without access for
diathermy, with consequent pressure damage on surrounding structures
causing brain damage, obstruction of CSF drainage and seizures. Even
aspirin alone is associated with a significantly increased mortality risk in
neurosurgery. Excessive bleeding from the scalp may occur, but this is
unlikely to be a significant issue.
Premature cessation of DAPT renders patient at significant risk of in-stent
thrombosis, which carries a mortality of about 50%.
Cessation of ADP receptor antagonist may be associated with a rebound
phenomenon, which, in association with the stress response to surgery,
may render the patient at even higher risk of thrombosis than usual in the
perioperative period.

Question 16

b) Summarise the perioperative
strategies to minimise the above
issues. (40%

Answer 16

Multidisciplinary decision: cardiologist, anaesthetist, surgeon, patient.
The decision needs to balance the risks of premature cessation of DAPT
against the urgency of the biopsy. DAPT usually continues for one year after
insertion of a drug-eluting stent (DES) but factors that may increase the risk
of in-stent thrombosis and therefore mandate more prolonged DAPT include
impaired renal function, ejection fraction <30%, multiple overlapping stents,
stents at bifurcations, diabetes mellitus.
Options:
> Delay biopsy until planned time for DAPT has finished. Although one year
is usually the minimum duration for DAPT after DES, the risk of in-stent
thrombosis decreases after six months. This is only an option if the
indication for biopsy is not unduly urgent.
> Stop ADP receptor antagonist for an appropriate duration prior to
surgery but, ideally, continue aspirin if the surgeon and cardiologist
are in agreement that the risk of stopping the aspirin outweighs risk of
continuing (although the surgeon is unlikely to proceed with biopsy with
ongoing aspirin)
> Stop both ADP receptor antagonist and aspirin (a week) prior to surgery
if the surgeon and cardiologist are in agreement that the risks of bleeding
outweigh the risk of in-stent thrombosis. Restart aspirin as soon as
possible after surgery.
> Consideration of bridging with a short-acting GP IIb/IIIa inhibitor, starting
within 24 hours of stopping ADP receptor blocker, restarting after surgery
and then restarting ADP receptor antagonist the day after surgery if
satisfied with haemostasis. This is not, however, a licenced indication for
use of this drug.
> If the patient is deemed at high risk of in-stent thrombosis and the ADP
receptor antagonist +/− aspirin are to be discontinued, consideration
should be given to performing the biopsy in a centre with on-site 24-hour
interventional cardiology support to attempt to mitigate the severity of
any thrombosis that occurs.

Question 17

c) What are the specific
contraindications (15%) and
complications (15%) of a
stereotactic brain biopsy under
sedation?

Answer 17

Contraindications:
> Lesions too small to safely target.
> Coagulopathic patient.
> Highly vascular tumour or lesions that could possibly be vascular
malformations.
> Patient conditions causing inability to comply with procedure (difficulties
communicating, confusion, movement disorders).
Complications:
> Haemorrhage (and no direct access to the site for diathermy).
> Airway compromise in awake or asleep patient with poor access to
airway due to frame (if being used).
> Air embolism.
> Failure to obtain diagnostic specimen.
> Seizure.
> CNS infection

Question 18

A 54-year-old patient is admitted to the Emergency Department following a traumatic brain injury.
A CT scan reveals only cerebral oedema.
a) What is secondary brain injury and when is it likely to occur? (2 marks)

Answer 18

Primary brain injury occurs due to the initial insult, depends on the nature,
intensity and duration of impact. Macroscopically: fracture, contusion,
haematoma, cerebral oedema, diffuse brain injury. Microscopically: cell wall
disruption, increased membrane permeability disrupting ionic haemostasis.
Secondary brain injury is the deleterious changes that happen over hours
to days in the brain as a consequence of the initial injury, mediated by
inflammatory, neurogenic and vasogenic processes

Question 19

b) Outline the main physiological
and cellular changes associated
with secondary brain injury.
(7 marks)

Answer 19

> Primary injury (due to e.g. intracerebral bleeding) may exhaust the
compensatory capacity of the brain, leading to a raised ICP. Initially, as
one component in the closed compartment of the cranium increases
in size, it is compensated for by a reduction in another component
(intravascular blood or CSF). This is the Monroe–Kelly doctrine.
Ultimately, this compensation will reach its limit and ICP will start to rise.
This results in cerebral ischaemia and hypoxia.
Inflammation and local tissue damage cause excessive release of
excitatory neurotransmitters (excitotoxicity), resulting in calcium influx to
cells, cell oedema and death.
Dying cells release mediators (platelet activating factor, leukotrienes,
oxygen free radicals) that affect blood vessel permeability, resulting
in vasogenic fluid accumulation, raising ICP further, contributing to
hypoperfusion, cerebral ischaemia, and neurodegeneration.
Loss of cerebral autoregulation exacerbates cerebral oedema and raised
ICP.
Hypoxia, hypotension, hyper- or hypocapnia and hyper- or
hypoglycaemia will exacerbate secondary brain injury, worsen ability to
autoregulate, cause direct changes to brain tissue size and therefore
impact on ICP and perfusion, thus perpetuating a downward vicious
cycle.
Seizures will cause increased ICP, exacerbating poor cerebral perfusion
if untreated. Seizures will also lead to raised PaCO2 and reduced PaO2,
which will further decrease the brain’s autoregulatory capacity and
increase its metabolic demand

Question 20

c) How can secondary brain injury
be minimised in this patient?
(11 marks

Answer 20

I would assess and manage this patient simultaneously adopting an ABCDE
approach:
Airway:
> Intubate and control ventilation if:
• Unable to protect own airway.
• Loss of laryngeal reflexes.
• GCS less than 8.
• Hypoxic.
• Hypercarbic.
• Seizures.
> Cervical spine control with airway management: immobilise if
there is possibility of injury but ensure that collar does not obstruct
venous return.
Respiratory:
> Target PaO2 greater than 13 kPa, PaCO2 4.5–5.0 kPa.
> PEEP to maintain oxygenation, ideally less than 15 cm H2O.
> Oxygen saturation and etCO2 monitoring.
Cardiovascular:
> Cannulate.
> Maintain mean arterial pressure (MAP) greater than 80 mm Hg (higher if
ICP is raised) using isotonic fluids and vasopressors as necessary. Guide
with intra-arterial blood pressure (BP) monitoring.
> Head neutral, tube ties not too tight, 15–30 degree head-up tilt to
optimise venous return. Paralyse if coughing/straining on tube.
> Catheterisation to guide fluid balance.
Neurological:
> Target cerebral perfusion pressure >60 mm Hg, ICP less than 20 mm Hg
(if have capabilities of monitoring in this hospital).
> Sedate adequately to reduce CMRO2.
> Treat seizures.
> Maintain blood glucose 6–10 mmol/l.
> Treat any raised temperature (which raises CMRO2).
> Manipulation of ICP spikes:
• Temporising measures: hyperventilation, mannitol 0.25–1 g/kg, 5%
hypertonic saline 2 ml/kg (keep Na less than 155 mmol/l, plasma
osmolality less than 320 mOsm/l).
• Definitive: discuss with neurosurgical unit if ongoing coma, ongoing
confusion, seizures without recovery, progressive neurological
abnormality; consider transfer for decompressive craniectomy or other
neurosurgical intervention.
Exposure, environmental control:
> Seek other injuries causing blood loss, which may make maintaining
MAP or haemoglobin at adequate levels for brain perfusion a problem

Question 21

A 19-year-old patient has suffered a complete transection of the spinal cord at the first thoracic vertebral
level due to a fall, but has no other injuries.
a) Outline the sequence of neurological effects that may develop in the first three months following injury.
(6 marks)

Question 22

a) What is acromegaly? (2 marks)

Answer 22

> Acromegaly is the condition that results from excessive growth hormone
secretion after the growth plates have fused.
In this patient and 90% of cases, it results from hypersecretion from a
pituitary adenoma.
Occasionally, it may result from an ectopic pituitary adenoma near, but
not in, the sella turcica.
Rarely, it results from secretion of growth hormone releasing hormone or
growth hormone by lung, pancreatic or adrenal tumours.

Question 23

c) What other clinical
presentations of a pituitary
adenoma may be encountered?
(2 marks

Answer 23

Non-secretory presentation:
> Local pressure effects causing visual disturbance (bitemporal
hemianopia), headache.
> Raised intracranial pressure: cranial nerve palsies, hydrocephalus due to
3rd ventricle outflow blockage.
Hypersecretory presentation:
> Cushing’s disease: hypersecretion of adrenocorticotrophic hormone
(ACTH) resulting in fatigue, truncal obesity, striae, moon face, buffalo
hump, hypertension, glucose intolerance, hirsuitism, depression, anxiety.
> Hyperpituitarism: hypersecretion of any/all anterior pituitary hormones.
Hyposecretory presentation:
> Pituitary apoplexy: internal haemorrhage of the adenoma, or when
the adenoma outgrows its blood supply, causing tissue necrosis
and swelling. Therefore, there is loss of anterior pituitary hormones.
Symptoms include visual loss, sudden-onset headache, cardiovascular
instability.
> Central diabetes insipidus: a macroadenoma may cause damage to
posterior pituitary blood supply, thus (rarely) causing diabetes insipidus
with polyuria and polydipsia.
> Pituitary-related hypothyroidism: generally less severe than
hypothyroidism of thyroid origin.
> Adrenocortical insufficiency: again, not as severe as adrenocortical
insufficiency of adrenal origin

Question 24

a) What is Guillain–Barré syndrome
and what are its causes? (3 marks

Answer 24

What is Guillain–Barré?
> Acute, immune-mediated, pre-junctional, ascending demyelinating
polyneuropathy affecting sensory, motor and autonomic nerves.
What are its causes?
> Associated with respiratory or gastrointestinal infection (especially
Campylobacter) in preceding weeks.
> Autoimmune in nature – antibodies attack the myelin sheath or, more
rarely, the axon itself.

Question 25

b) What are the clinical features
of Guillain–Barré syndrome?
(6 marks)

Answer 25

Whenever you are describing a neurological condition, be clear in your mind
whether it is upper or lower motor neurone; whether it affects motor, sensory
or autonomic nerves; and whether the defect is of the axon, myelin sheath
or neuromuscular junction.
> Variable presentation depending on subtype; different forms associated
with immune attack on different parts of the neurone. Recovery is
variable, ranging from full recovery to relapsing, remitting form.
> Motor: typically ascending symmetrical weakness (flaccid, areflexic
paralysis), may ascend to involve respiratory muscles and also to cause
facial nerve palsies with bulbar weakness and opthalmoplegia.
> Sensory: ascending sensory impairment associated with pain.
> Autonomic: arrhythmias, labile BP, urinary retention, paralytic ileus,
hyperhydrosis, sudden death.
> Miller Fisher syndrome: this is a variant typified by ataxia, areflexia,
opthalmoplegia +/− weakness.

Question 26

c) List the investigations with
their findings that may be used to
support the diagnosis. (2 marks)

Answer 26

Blood tests:
> Variable, not specific or sensitive: low sodium, renal dysfunction, raised
ALT and GGT raised CK.
> Elevated ESR +/− CRP.
> Antiganglioside antibodies (antibodies against a component of the axon
itself, increased association with Campylobacter, worse prognosis) in 25%
> Serology for Campylobacter, CMV, EBV, HSV or Mycoplasma pneumoniae
may be positive.
> ABG may show development of respiratory failure.
Stool:
> GI infections, especially Campylobacter.
CT brain:
> Normal: to exclude other causes.
MRI spine:
> Selective anterior spinal nerve root enhancement with gadolinium.
Lumbar puncture:
> Normal cell count and glucose, elevated protein levels (although even this
may be normal early in the disease).
Nerve conduction studies:
> Depends on subtype: majority show demyelinating pattern, some show
axonal loss.
Respiratory function tests:
> Reduced vital capacity

Question 27

d) What are the specific
considerations when
anaesthetising a patient
recovering from Guillain–Barré
syndrome? (9 marks)

Answer 27

Back to the alphabet. Note that this is anaesthesia for a patient
RECOVERING from Guillain–Barré, not the initial management of the disease
process. However, a future question could ask about the anaesthetic
management of a patient at the time of initial diagnosis.
Airway:
> Bulbar weakness, poor cough, increased risk of aspiration. Intubation
required – consider need for rapid sequence induction.
> May still have tracheostomy in situ if still requiring ventilatory support or
assistance with secretion clearance.
Respiratory:
> Increased risk of pneumonia secondary to aspiration and poor ventilatory
function. Make full assessment of this – history, nature of secretions,
temperature, chest auscultation. Treat as required, delay non-urgent
surgery if necessary.
> Significantly reduced ventilatory capacity, assess likelihood of requiring
noninvasive or invasive ventilation postoperatively.
Cardiovascular:
> Autonomic instability, labile BP (with sensitivity to commonly used
vasoactive drugs), risk of arrhythmia. Invasive monitoring indicated
including cardiac output monitoring to guide fluid administration (ensure
full circulation as dehydration will exacerbate lability).
> Prolonged illness, multiple cannulations, access may be tricky.
Neurological:
> Neuropathic pain common – may already be on antineuropathic drugs
+/− opioid analgesia. Need to plan postoperative pain relief, involve acute
pain team.
Pharmacology:
> Suxamethonium: contraindicated due to risk of hyperkalaemia following
the development of extrajunctional nicotinic receptors.
> Non-depolarising neuromuscular blocking agents: increased sensitivity –
reduce dose.
> Opioids: increased sensitivity to respiratory depressant effect in the
presence of existing respiratory compromise, may already be taking
opioids and so dose adjustme
Haematology:
> Risk of deep vein thrombosis due to prolonged immobility – continuation
of thromboembolic deterrent stockings and pneumatic compression
devices and pharmacological prophylaxis (check timing if planning
neuraxial technique).
Cutaneomusculoskeletal:
> Prolonged illness may be associated with weight loss – care with
positioning and padding.
Renal:
> Check renal function – may dictate drug choices.nts may be necessary.