Cerebrovascular Surgery: AVMs, Moyamoya, and Stroke Revascularisation

Quick Answer

What are the critical anaesthetic principles for cerebrovascular surgery?

Cerebrovascular surgery (AVM resection, Moyamoya bypass, stroke revascularisation) requires meticulous haemodynamic control to maintain cerebral perfusion while avoiding catastrophic complications. Key principles:

1. AVM surgery - Manage "steal" (pre-resection) and "normal perfusion pressure breakthrough" (post-resection); maintain CPP 70-80 mmHg; controlled hypotension only if surgeon requests
2. Moyamoya disease - Maintain normotension to hyperperfusion; avoid hypotension (stroke risk); CO2 management critical; postoperative hypertension management
3. Stroke revascularisation (EC-IC bypass) - Similar to Moyamoya - preserve CPP; avoid hypercapnia (steal); normoglycaemia; seizure prophylaxis
4. Monitoring - Arterial line, BIS, SSEPs, MEPs for critical cases
5. Positioning - Head-up 15° to reduce venous bleeding; careful neck positioning
6. Emergency preparedness - Blood products, cell saver, intralipid for local anaesthetic toxicity, emergency bypass plan

Clinical Pearl: The most dangerous phase in AVM surgery is immediately after resection when the "normal perfusion pressure breakthrough" phenomenon can cause catastrophic oedema and haemorrhage. The brain that was chronically hypoperfused due to steal is suddenly exposed to normal systemic pressures and loses autoregulatory capacity.

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Clinical Overview

Epidemiology

Cerebrovascular pathology:

Australian context:

• 30-40 cerebrovascular bypass procedures annually in major centres
• AVM surgery concentrated in state neurosurgical centres (Sydney, Melbourne, Brisbane, Perth)
• Moyamoya disease less common in Caucasian populations but increasing recognition

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Arteriovenous Malformation (AVM) Surgery

Pathophysiology

AVM characteristics:

Spetzler-Martin grading system:

Grades: I-VI (VI = unresectable/untreatable)

• Grade I-III: Favourable surgical risk
• Grade IV-V: High surgical morbidity (consider radiosurgery/endovascular)

Steal Phenomenon (Pre-resection)

Mechanism:

• High-flow AVM acts as low-resistance shunt
• Blood preferentially flows to AVM rather than normal brain
• Perinidal brain chronically hypoperfused
• Chronic hypoperfusion causes maximal vasodilation
• Autoregulatory curve shifted to lower pressures

Anaesthetic implications:

• Normal or slightly reduced MAP acceptable
• Hypotension dangerous (further reduces perfusion to at-risk brain)
• Hypercapnia dangerous (vasodilation worsens steal)
• Target: Normotension, normocapnia (PaCO2 35-40 mmHg)

Normal Perfusion Pressure Breakthrough (NPPB)

Mechanism (post-resection):

• After AVM removal, blood redirected to previously hypoperfused brain
• Chronic maximal vasodilation means no autoregulatory reserve
• Brain unable to constrict in response to normal pressures
• Hyperperfusion causes oedema and haemorrhage
• Occurs minutes to hours after resection

Clinical presentation:

• Massive brain swelling ("brain rock")
• Venous oozing despite good surgical haemostasis
• Haemorrhage from fragile vessels
• Delayed postoperative oedema/haemorrhage

Risk factors:

• Large AVM size
• High-flow fistula
• Deep venous drainage
• Long-standing AVM
• Perinidal ischaemia on imaging

Prevention and management:

Perioperative Management

Preoperative:

Intraoperative anaesthetic technique:

Critical phases:

Controlled hypotension (if used):

• Agent: Labetalol, esmolol, remifentanil, SNP
• Target: MAP 50-60 mmHg or 20% below baseline
• Timing: After dural opening but before critical dissection
• Contraindications: Contralateral stenosis, aneurysm on other vessels, cardiac disease
• Risks: Cerebral ischaemia, myocardial ischaemia, renal impairment

Emergency management:

• Massive haemorrhage protocol
• Cell salvage if available
• Mannitol 0.5-1 g/kg for brain swelling
• Thiopentone 3-5 mg/kg for refractory swelling
• Consider temporary clip application

Postoperative:

• ICU monitoring
• BP control: Target MAP 20% below baseline for 24-48 hours [5]
• Seizure prophylaxis (phenytoin/levetiracetam)
• Serial CT imaging
• Delayed neurological deterioration: CT immediately (suspect haemorrhage/oedema)

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Moyamoya Disease

Pathophysiology

Definition:

• Chronic progressive stenosis of terminal ICA and proximal ACA/MCA
• Collateral vessel development at base of brain ("puff of smoke" on angiography)
• Compensatory vessels fragile and prone to bleeding
• Results in chronic ischaemia with risk of stroke or haemorrhage

Types:

Suzuki stages (angio):

• Stage 1: Narrowing of ICA bifurcation
• Stage 2: Initiation of Moyamoya vessels
• Stage 3: Intensification of Moyamoya vessels
• Stage 4: Minimisation of Moyamoya vessels
• Stage 5: Reduction of Moyamoya vessels
• Stage 6: Disappearance (only ECA collaterals)

Surgical Revascularisation

Techniques:

Indications for surgery:

• TIA or stroke with haemodynamic insufficiency
• Progressive symptoms
• Failed medical therapy
• Cognitive decline in children

Perioperative Management

Critical principle: MAINTAIN CEREBRAL PERFUSION AT ALL COSTS

The Moyamoya brain has:

• Fixed cerebrovascular resistance (maximally dilated)
• Loss of autoregulation
• Flow-dependent perfusion (pressure-passive)
• Extreme sensitivity to hypotension

Preoperative:

Intraoperative management:

Specific techniques:

SSEPs monitoring:

• Mandatory for direct bypass procedures
• Warning criteria: >50% amplitude reduction or >10% latency increase
• Respond immediately if changes: increase BP, check PaCO2, check clip position

Emergency protocol for SSEP loss:

1. Increase MAP by 20% (phenylephrine, metaraminol)
2. Check PaCO2 (maintain 35-40)
3. Check temperature (maintain normothermia)
4. Request surgeon check clips/patency
5. Consider thiopentone/propofol for neuroprotection
6. If persistent: consider bypass revision

Fluid management:

• Maintain euvolaemia
• Isotonic crystalloids
• Avoid glucose-containing solutions unless hypoglycaemic
• Slight positive fluid balance acceptable

Postoperative:

• ICU monitoring
• BP: Slight hypertension permitted (up to 20% above baseline)
• AVOID HYPOTENSION - greatest stroke risk period
• Continue aspirin (unless bleeding concern)
• Hyperperfusion syndrome: Risk in 20-40% [6]
  • Presents with headache, seizures, focal deficits
  • CT perfusion shows hyperperfusion
  • Managed with BP control (not too aggressive), hydration

Hyperperfusion Syndrome

Definition:

• Excessive CBF through new bypass
• Occurs 3-10 days postoperatively
• 20-40% incidence after direct bypass [6]

Risk factors:

• Poor preoperative collateral circulation
• Intraoperative temporary clip time >30 minutes
• Old age
• Preoperative ischaemic symptoms

Clinical features:

• Headache (most common)
• Focal neurological deficits
• Seizures
• Intracerebral haemorrhage (most serious)

Management:

• BP control (reduce 20-30% below preoperative baseline)
• Osmotherapy if oedema
• Seizure control
• Antiplatelet therapy (continued despite haemorrhage risk - paradoxical but necessary)

Clinical Pearl: The hyperperfusion syndrome risk is the reason we allow slight hypertension intraoperatively and immediately postoperatively, but then gradually normalise BP over 48-72 hours. Too rapid BP reduction risks bypass occlusion; too slow risks hyperperfusion haemorrhage.

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Stroke Revascularisation (EC-IC Bypass)

Indications

Current indications (limited after EC/IC bypass study):

Preoperative evaluation:

• PET with acetazolamide challenge
• BOLD MRI with CO2 or acetazolamide
• Xenon CT
• SPECT
• Transcranial Doppler with CO2 reactivity

Surgical Technique

Direct bypass:

• STA-MCA (superficial temporal artery to middle cerebral artery)
• Occipital artery to PCA (for posterior circulation)
• Other variants

Anaesthetic considerations:

• Identical to Moyamoya principles
• Maintain perfusion pressure
• Normocapnia
• SSEP monitoring essential
• Temporary clip tolerance 30-60 minutes

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Evoked Potential Monitoring

Somatosensory Evoked Potentials (SSEPs)

Principle:

• Stimulate peripheral nerve (median, tibial)
• Record cortical response
• Monitor dorsal column/medial lemniscus pathway

Anaesthetic effects:

Optimal anaesthetic for SSEPs:

• TIVA with propofol + remifentanil
• <0.5 MAC volatile if volatile used
• No nitrous oxide
• Stable temperature (hypothermia increases latency)

Warning criteria:

• 50% amplitude reduction

• 10% latency prolongation

• Persistent changes >10 minutes

Motor Evoked Potentials (MEPs)

Principle:

• Transcranial electrical stimulation of motor cortex
• Record compound muscle action potential (CMAP) from target muscles
• Monitor corticospinal tract

Anaesthetic considerations:

• Cannot use muscle relaxants (need muscle response)
• Volatile agents depress MEPs (>0.5 MAC unreliable)
• Propofol acceptable at moderate doses
• Ketamine enhances MEPs
• Etomidate enhances MEPs

Optimal technique:

• TIVA with propofol + remifentanil
• No volatile agents
• No NMBA (orTOF count 2-3 if absolutely needed)
• Train-of-four monitoring essential

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Complications and Management

Air Embolism

Risk:

• Open venous sinuses
• Head-up position
• Low CVP
• Open dural veins

Recognition:

• Sudden EtCO2 drop (>2 mmHg)
• Oxygen desaturation
• Hypotension
• Mill-wheel murmur (rare)
• Cardiac arrhythmias

Management:

Prevention:

• Trendelenburg position during risk periods
• Maintain adequate intravascular volume
• Avoid hypocapnia (reduces venous pressure)

Seizures

Risk factors:

• Cortical stimulation
• Previous seizures
• Haemorrhage
• Cortical irritation

Management:

• Cold saline irrigation
• Propofol 0.5-1 mg/kg
• Midazolam 2-5 mg
• Loading with anticonvulsant if persistent

Cerebral Oedema

Causes:

• NPPB (AVM)
• Manipulation/irritation
• Prolonged retraction
• Venous outflow obstruction

Management:

• Mannitol 0.25-0.5 g/kg
• 3% hypertonic saline 3-5 mL/kg
• Head elevation
• Brief hyperventilation (temporary only)
• Barbiturate coma if refractory
• Decompressive craniectomy (surgical option)

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Indigenous Health Considerations

Aboriginal and Torres Strait Islander Patients

Access challenges:

Specific considerations:

Cultural considerations:

1. Family involvement - Extended family often want to be present for major surgery
2. Decision-making - May need to consult with multiple family members
3. Fear of surgery - Need clear explanation of procedure and risks
4. Aftercare - Ensure understanding of antiplatelet therapy importance (bypass patients)

Māori Health (Aotearoa New Zealand)

Cerebrovascular disease burden:

Cultural considerations:

Te Tiriti obligations:

• Equity of access to cerebrovascular surgery
• Culturally safe care
• Māori health workforce development
• Reduced health disparities in stroke outcomes

Practical approaches:

1. Preoperative - Māori Health Worker involvement; whānau hui if appropriate
2. Surgery - Keep whānau informed; allow presence when possible
3. Recovery - Whānau-supported rehabilitation
4. Follow-up - Telehealth; coordination with Māori health providers

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ANZCA Final Examination Focus

High-Yield Topics

Written examination:

Viva scenarios:

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Assessment Content

SAQ 1: Normal Perfusion Pressure Breakthrough (20 marks)

Question:

A 28-year-old woman is undergoing surgical resection of a large (6 cm) Spetzler-Martin Grade IV frontal AVM. She has had preoperative embolisation. During dissection of the AVM nidus, the surgeon reports significant brain swelling and diffuse venous oozing immediately following ligation of the main draining vein.

a) What is the likely diagnosis and underlying pathophysiology? (6 marks)

b) What are the risk factors for this complication? (4 marks)

c) Outline your immediate anaesthetic and pharmacological management. (6 marks)

d) What postoperative measures are required to prevent delayed complications? (4 marks)

Model Answer:

a) Diagnosis and Pathophysiology (6 marks):

Diagnosis (2 marks):

• Normal Perfusion Pressure Breakthrough (NPPB) phenomenon
• Also known as "cerebral hyperperfusion syndrome" or "perfusion breakthrough"

Pathophysiology (4 marks):

• Pre-resection: AVM creates low-resistance shunt causing "steal" from surrounding brain
• Perinidal brain chronically hypoperfused; autoregulatory vessels maximally dilated
• Chronic hypoperfusion shifts autoregulatory curve to lower pressures; loss of autoregulatory reserve
• Post-resection: Blood flow redirected to previously hypoperfused brain at normal systemic pressures
• Brain unable to autoregulate; hyperperfusion causes vasogenic oedema and haemorrhage
• Occurs minutes to hours after AVM elimination

b) Risk Factors (4 marks):

• Large AVM size (>6 cm) - higher flow, more significant steal
• High-flow fistula component
• Deep venous drainage (venous congestion risk)
• Long-standing AVM (chronicity of steal)
• Absence of preoperative embolisation (higher flow)
• Multiple feeding arteries from different territories
• Perinidal ischaemia on preoperative imaging
• High Spetzler-Martin grade (III-V)

c) Immediate Management (6 marks):

Haemodynamic (2 marks):

• Reduce MAP by 20-30% below baseline immediately
• Agents: Labetalol 10-20 mg IV, esmolol infusion, SNP if rapid titration needed
• Target MAP 60-70 mmHg (if no contraindications)

Pharmacological (2 marks):

• Mannitol 0.5-1 g/kg IV to reduce brain volume
• Consider thiopentone 3-5 mg/kg or propofol 1-2 mg/kg for burst suppression if refractory swelling
• Brief hyperventilation to PaCO2 30-35 mmHg (temporary measure only)

Surgical communication (1 mark):

• Inform surgeon of blood pressure reduction
• Request application of additional haemostatic agents
• May need temporary ventricular drain if CSF compartment compromised

Monitoring (1 mark):

• Ensure adequate anaesthetic depth
• Check temperature (avoid hyperthermia)
• Consider jugular venous bulb saturation if available

d) Postoperative Measures (4 marks):

Blood pressure control (2 marks):

• Maintain MAP 20% below preoperative baseline for 24-48 hours
• ICU admission with arterial line
• Nicardipine or labetalol infusion as needed
• Gradual normalisation after 48 hours

Monitoring and prophylaxis (2 marks):

• Serial neurological examinations
• CT at 24 hours and if any deterioration
• Seizure prophylaxis (phenytoin or levetiracetam)
• Avoid hypertension triggers (pain, nausea, anxiety)
• Osmotherapy if ongoing oedema

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SAQ 2: Moyamoya Disease Anaesthesia (20 marks)

Question:

A 16-year-old female with Moyamoya disease is scheduled for direct STA-MCA bypass surgery. She has had two previous TIAs and has poor collateral circulation on imaging.

a) What are the fundamental pathophysiological principles of Moyamoya disease that dictate anaesthetic management? (6 marks)

b) Outline your specific targets for the following physiological parameters during surgery, with rationale: i) Blood pressure (3 marks) ii) PaCO2 (3 marks) iii) Temperature (2 marks)

c) What monitoring is essential for this procedure, and how would you respond to concerning changes? (6 marks)

Model Answer:

a) Pathophysiological Principles (6 marks):

Primary pathology (3 marks):

• Progressive stenosis of terminal ICA and proximal ACA/MCA
• Formation of fragile collateral vessels at base of brain ("puff of smoke")
• Chronic ischaemia due to inadequate perfusion
• Risk of completed stroke or intracranial haemorrhage

Haemodynamic consequences (3 marks):

• Maximally dilated cerebral vessels to maintain perfusion
• Loss of autoregulatory capacity (autoregulatory curve flattened)
• Pressure-passive cerebral circulation (CBF directly proportional to CPP)
• Extreme vulnerability to hypotension (causes immediate ischaemia)
• Fixed cerebrovascular resistance - no compensatory vasodilation possible
• Both hypercapnia (steal) and hypocapnia (ischaemia) dangerous

b) Physiological Targets (8 marks):

i) Blood pressure (3 marks):

• Target: Normotension to mild hypertension (maintain at baseline or 10-20% above)
• Rationale: Brain has no autoregulatory reserve; perfusion entirely pressure-dependent
• Hypotension causes immediate critical ischaemia and stroke
• During temporary clipping: Accept MAP up to 20% above baseline
• Avoid any period of hypotension (induction, positioning, blood loss)

ii) PaCO2 (3 marks):

• Target: Strict normocapnia 35-40 mmHg
• Rationale:
  • Hypercapnia causes vasodilation in normal brain, creating "steal" from Moyamoya territories
  • Hypocapnia causes vasoconstriction; Moyamoya brain cannot compensate → ischaemia
• Most critical parameter to control
• EtCO2 monitoring with frequent correlation to PaCO2

iii) Temperature (2 marks):

• Target: Normothermia 36-37°C
• Rationale:
  • Hypothermia shifts oxyhaemoglobin dissociation curve left (reduces O2 delivery)
  • Hyperthermia increases metabolic demand
  • Maintain tight control to optimise oxygen delivery

c) Monitoring and Response (6 marks):

Essential monitoring (3 marks):

• Arterial line (preferably contralateral radial or femoral): Continuous BP, ABGs
• BIS/entropy: Ensure adequate depth, avoid burst suppression
• Somatosensory evoked potentials (SSEPs): Monitor cortical perfusion (mandatory)
• Motor evoked potentials (MEPs) if available
• Temperature probe
• Urine output (maintain >0.5 mL/kg/hr)
• Train-of-four if any muscle relaxation used

Response to SSEP changes (3 marks):

• Warning criteria: >50% amplitude reduction or >10% latency increase
• Immediate steps:
  1. Increase MAP by 20% (phenylephrine 50-100 mcg bolus or infusion)
  2. Check arterial blood gas (ensure PaCO2 35-40, PaO2 >100)
  3. Check temperature (ensure 36-37°C)
  4. Inform surgeon to check temporary clip position/patency
  5. Consider thiopentone 3-5 mg/kg for neuroprotection
  6. If changes persist >5-10 minutes: request surgeon release temporary clip or check bypass patency

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Viva Scenario: AVM Surgery Haemodynamic Management

Scenario:

You are anaesthetising a 35-year-old man for resection of a large parietal AVM. The surgeon requests controlled hypotension during dissection of the deep arterial feeders.

Examiner: "What are your concerns about controlled hypotension in this case, and how would you implement it?"

Candidate Response:

"I have several concerns about controlled hypotension in AVM surgery:

First, the timing is critical. During the pre-resection phase when the AVM is still patent, there is a 'steal' phenomenon where blood preferentially flows to the low-resistance AVM rather than the surrounding brain. The perinidal brain is chronically hypoperfused and has maximally dilated vessels. If I reduce blood pressure during this phase, I risk critically compromising perfusion to the already ischemic perinidal brain, potentially causing infarction.

Second, there's the normal perfusion pressure breakthrough risk post-resection. While controlled hypotension is actually beneficial after the AVM is removed to prevent NPPB, doing it before resection is dangerous.

Third, I need to consider any contraindications:

• Contralateral carotid stenosis or occlusion would make hypotension extremely dangerous
• Associated aneurysms on feeding arteries might rupture if hypotension masks their inflow
• Significant cardiac disease or cerebrovascular disease in the patient

My approach would be:

1. Discuss with surgeon: Clarify exact timing requested. I would strongly prefer to maintain normotension (MAP 70-80 mmHg) during pre-resection phase, and only implement controlled hypotension AFTER the AVM is resected to prevent NPPB.

2. If hypotension absolutely required intraoperatively:

   • Use short-acting agents for rapid reversibility
   • Remifentanil infusion (0.2-0.3 mcg/kg/min) - reduces BP via sympatholysis, rapidly reversible
   • Esmolol infusion (50-300 mcg/kg/min) - titratable beta-blockade
   • Avoid long-acting agents (labetalol large boluses, deep volatile anaesthesia)

3. Targets:

   • MAP 60-65 mmHg (approximately 20% reduction)
   • Not lower than 50 mmHg
   • Maintain for shortest possible time

4. Monitoring:

   • Arterial line for beat-to-beat monitoring
   • Consider jugular venous oximetry if available
   • BIS to ensure adequate depth (avoid excessive anaesthesia contributing to hypotension)
   • SSEPs if eloquent area nearby

5. Reversal:

   • Immediately reversible agents
   • Phenylephrine/ephedrine available for rapid restoration of BP
   • Volume loading ready

6. Post-resection:

   • This is when controlled hypotension is truly beneficial
   • Maintain MAP 20% below baseline for 24-48 hours
   • ICU with arterial line and infusion (nicardipine/labetalol)"

Examiner: "What agents would you avoid for controlled hypotension in this situation and why?"

Candidate:

"I would avoid several agents:

1. Sodium nitroprusside (SNP) - While very effective and titratable, it crosses the blood-brain barrier and can cause cerebral vasodilation, which is undesirable in AVM surgery. It also raises ICP. If I had to use it, I'd use it only briefly for precise control.

2. Deep volatile anaesthesia - High concentrations (>1 MAC) suppress SSEPs and MEPs if we're monitoring, and impair autoregulation. Not precise enough for controlled hypotension.

3. Large bolus doses of labetalol - While I might use small incremental doses (10-20 mg), large boluses (50-100 mg) have a long duration and are not easily reversible if the surgeon suddenly needs normal pressure.

4. Nitroglycerine - Similar concerns to SNP about cerebral vasodilation, though less potent. More appropriate for coronary vasodilation than neurosurgery.

My preference is for remifentanil-based technique because:

• Context-insensitive half-time - rapidly reversible regardless of infusion duration
• Sympatholysis rather than direct vasodilation
• Minimal effect on cerebral autoregulation
• No accumulation
• Can be combined with propofol TIVA for smooth anaesthesia

I would also ensure the patient is adequately anaesthetised before manipulating blood pressure, as light anaesthesia causing sympathetic stimulation can make hypotension difficult to achieve."

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