This topic has appeared as CRQs twice, though only features in the curriculum as 'principles of anaesthesia for...interventional procedures [including coiling of intracranial aneurysms]'.
Following the March 2020 CRQ (74% pass rate) the examiners gave only positive feedback(!).
There was a similar performance on the CRQ in September 2023 (72% pass rate), although marks were lost on 'causes and investigations of reduced neurological status post-op'.
Risk of rupture is related to aneurysm size; half of those with ruptured aneurysms have a risk factor such as hypertension or ischaemic heart disease
A sudden onset, occipital 'thunderclap' headache is characteristic
Caused by the raised ICP which occurs at rupture
Associated features include:
Nausea and vomiting
Meningism i.e. neck stiffness and photophobia
Confusion or agitation
Focal neurological deficits
Reduced consciousness (2/3rd by time of presentation)
Cardiac changes from catecholamine surge are common, including ECG changes, elevated cardiac enzymes and cardiogenic (or neurogenic) pulmonary oedema
At the more sinister end of the clinical spectrum, patients may have seizures or even cardiac arrest
ECG changes are often present:
Shortened PR
ST segment changes
T-wave inversion
Prolonged QTc
Cross-sectional imaging
Patients with a suspected diagnosis of SAH should have an urgent, non-contrast CT scan, which carries a 95 - 100% sensitivity on the first day
Patients with a negative CT scan should have a lumbar puncture 12hrs post-ictus
Measures CSF red cell count, bilirubin and xanthochromia
The gold standard for the detection of intracranial aneurysms is four-vessel digital subtraction angiography (DSA)
CT angiography, in comparison to DSA, is more rapid, less invasive and more readily available
Negative predictive value 82 - 96%
It has a lower sensitivity and specificity for small (<5mm) aneurysms
MR angiography may also be used
World Federation of Neurosurgeons (WFNS) grading
Grade
GCS
Motor deficit
I
15
Absent
II
13-14
Absent
III
13-14
Present
IV
7-12
Either
V
3-6
Either
Others
The (modified) Fisher scale for intracranial blood volume (<1mm or >1mm thickness) and distribution (SAH, IVH)
Classifies bleeds on a scale from I - IV
Grade IV corresponds to the highest risk of vasospasm
Grade corresponds to mortality/outcome
The Hunt & Hess grading scale is a clinical grading system
Medical management aims to prevent secondary brain injury, including that from complications such as vasospasm
This includes general neuroprotective measures such as:
Control of oxygenation and ventilation
Blood pressure control (see below)
Adequate sedation
Management of raised ICP
Prevention of hypo- or hyper-thermia; target a temperature of 36-37.5°C
Normoglycaemia; hyperglycaemia on admission, during surgery or within 72hrs of presentation is associated with unfavourable short- and long-term functional outcomes
Other measures include:
Emergency reversal of anticoagulation
Vasospasm prophylaxis; enteral nimodipine 60mg 4hrly for 21 days (or 30mg 2hrly to reduce effect on arterial BP if necessary)
Consider antifibrinolytic therapy may reduce the risk of rebleeding, but is not a consistent effect across trials and its use doesn't improve functional outcome
Blood pressure management
Avoid hypotension; aim for a MAP >65mmHg
Avoid large swings in blood pressure
Avoid hypertension; prior to the aneurysm being secured aim for:
SBP <160mmHg
MAP <110mmHg
Surgical management aims to prevent re-bleeding by occluding the aneurysm via either endovascular coiling or open surgical clipping
Surgical intervention should take place as soon as possible, ideally within 24hrs
The ISAT trial showed ruptured aneurysm coiling was more likely than clipping to result in independent survival at 1yr
Long-term follow-up of ISAT patients, however, revealed higher rates of delayed re-treatment in the coiled patients
Clipping may be required in the 5 - 15% of cases not amenable to coiling:
Aneurysm is wide-necked
Difficult angiographic arterial access inc. MCA
Failed coiling
Clipping takes 4-8hrs and alone carries a procedural mortality rate of 1-3%
Perioperative management of the patient undergoing surgery for aneurysmal subarachnoid haemorrhage
The principles apply whether patient is undergoing endovascular coiling, craniotomy and clipping, or other neurosurgical procedures e.g. EVD insertion
The goals are to:
Maintain CPP
Avoid sudden swings in ICP
Control the transmural pressure gradient (TMPG) of the aneurysm [ TMPG = MAP - ICP]
Provide optimal brain relaxation for surgery
Enable rapid awakening for neurological assessment
Minimise post-procedural pain, nausea and vomiting
Patients may not be capable of participating in assessment or consent processes
Thorough pre-operative assessment as standard, with a focus on:
Establishing and documenting patient's neurological status
Estimating ICP
Presence of systemic complications
Monitoring and access
AAGBI as standard
Arterial line routinely, pre-induction to enable fine control of BP at this time and transducer placed at level of external auditory meatus
± CVC for CVP and administration of vasopressors, electrolytes and mannitol
Core temperature monitoring; no role for hypothermia
± ICP monitoring
Use of neurophysiological monitoring e.g. MEP/SSEP does not improve outcome and has a poor predictive value
Jugular venous bulb monitoring is also not routinely used, it has not been shown to improve outcomes but may be used on an individual basis
Be mindful of the stimulating phases of the procedure will aid avoidance of gross haemodynamic instability or changes in ICP:
Laryngoscopy
Insertion of head pins
Raising bone flap
Periods of minimal stimulation and hypotension should be managed with vasopressor (rather than reducing depth of anaesthesia)
Induced hypothermia (33°C) did not show improved neurological outcome after craniotomy (IHAST trial) and leads to a higher incidence of bacteraemia
Ensure normoglycaemia
Brain relaxation
Brain relaxation is the process of creating an ideal volume of the intracranial contents in relationship to the capacity of the intracranial space, to:
Provide optimal operating conditions during open intracranial surgery
Improve patient outcome
Primary methods of brain relaxation
Head-up positioning
Hyperventilation to PaCO2 3.5 - 4.0kPa
Osmotherapy e.g. 0.25 - 1g/kg 20% mannitol over 20mins given post-induction
Furosemide
Bolus of IV anaesthetic e.g. thiopentone 500mg, propofol
CSF drainage
The presence of ventricular drains is beneficial as they provide the ability to monitor ICP ± drain CSF to control ICP or brain bulk
Care must be taken to avoid excessive CSF drainage, as this can cause brain sagging, cardiovascular instability and increase the TMPG of aneurysm walls
Intra-operative aneurysm rupture
May occur at any time during the procedure, particularly if there is sudden rise in TMPG due to either increased MAP or decreased ICP
It can lead to massive blood loss and high mortality
Management
Preferably temporary occlusion of proximal and distal arteries to allow surgical access and fixation
Maintenance of BP or increase to 10-20% above baseline
Replacement of lost blood
If no or difficult surgical access then transient decreases in MAP may facilitate orientation and clipping, but will compromise global CPP
Adenosine has been used to induce temporary cardiac standstill and facilitate aneurysm clip placement
Patients should be woken if possible to assess neurological function
WFNS Grade III - V patients may require a period of intubation first
Smooth, rapid emergence is ideal
New neurological deficits should prompt CT / CTA
Patients should be managed in higher care areas if available
Patients are typically hypertensive post-operatively and may need doses of anti-hypertensives or analgesics
Venous thromboembolism is common (4-24%) and patients should have appropriate prophylaxis
Mechanical in the first instance
Once aneurysm is secured, standard prophylaxis (e.g. enoxaparin 40mg OD) reduces risk of VTE and is not associated with bleeding risk
Ongoing glycaemic management to avoid hyperglycaemia
Improvements in early treatment mean that delayed neurological deterioration is now the main cause of death and disability post-SAH
Re-bleeding
Incidence 5 - 10% in first 72hrs
First 24hrs; 2-4%
After 24hrs; 1-2%
Occurs due to:
Sudden increases in aneurysm transmural pressure gradient (TMPG) e.g. due to fluctuating BP or ICP e.g. hypertension, coughing, EVD insertion
Respiratory failure is associated with higher treatment intensity, longer ICU stay, and poorer overall outcome
Vasospasm
See next section
Cerebral vasospasm is most likely to develop 3 - 12 days post-ictus, and can last up to two weeks
It occurs radiologically in 70% of patients
30 - 50% of these develop symptomatic cerebral ischaemia i.e. neurological deficits
Patients with SAH should receive enteral nimodipine 60mg 4hrly for 21 days as prophylaxis against vasospasm
Risk factors
Risk factors for vasospasm after SAH
Thick subarachnoid blood volume
Smoking
Cocaine use
Patient taking either SSRI's or statins
<50yrs age
Hypertension
ECG changes inc. LVH, QTc >450ms, ST depression
Diagnosis
Clinical i.e. onset of neurological deficits, reduced GCS
Radiological
CT angiography
Highly specific (85-95%) and sensitive (91%)
Tends to overestimate degree of stenosis
Transcranial Doppler ultrasound
Benefits from being non-invasive, so can be used for monitoring and diagnosis
High specificity but only moderate sensitivity
Operator dependent
Vasospasm present if flow velocities are high (>120cm/s), increasing (>50cm/s/day from baseline) or there is a high Lindegaard ratio (MCA:ICA flow velocity ratio >3)
CT perfusion
DSA remains the gold standard
Other
Continuous EEG monitoring
PbtO2 monitoring
Management
Early surgical securing of aneurysm
Euvolaemia
Hypertension with high MAP target e.g. 110 - 140mmHg