Subarachnoid haemorrhage

Surgical approach (aneurysmal SAH: securing the aneurysm)

Two main definitive strategies: endovascular coiling or surgical clipping (choice depends on aneurysm anatomy, patient factors, local expertise)
- Coiling: femoral/radial arterial access → cerebral angiography → microcatheter into aneurysm → deploy coils (± stent/balloon assistance) → confirm occlusion
- Clipping: craniotomy (often pterional) → microsurgical dissection to aneurysm neck → temporary clip sometimes → permanent clip across neck → confirm flow in parent vessels (Doppler/ICG) → close
Adjunct/complication procedures
- External ventricular drain (EVD) for acute hydrocephalus / raised ICP
- Decompressive craniectomy (rare; malignant cerebral oedema/infarction)

Anaesthetic management (for aneurysm securing: coiling or clipping)

Type of anaesthesia: General anaesthesia is standard (immobility, airway control, tight BP/CO2 control). Regional not appropriate.
Airway: ETT (cuffed). SGA generally inappropriate (need controlled ventilation, neurophysiology, potential for sudden deterioration).
Duration: coiling often 2–4 h; clipping often 4–8 h (variable with complexity, vasospasm, intra-op rupture).
Pain: coiling = low/moderate (groin/radial access, headache); clipping = high (craniotomy) → multimodal analgesia, avoid oversedation post-op.
Core goals: prevent rebleeding, maintain cerebral perfusion, avoid secondary brain injury (hypoxia, hypercapnia, hypotension, hyperthermia, hypo/hyperglycaemia).
Monitoring: invasive arterial line pre-induction; large-bore IV access; consider CVC if vasoactive infusions likely; temperature; urine output; neuromonitoring as per centre (EEG/SSEP for clipping).
BP strategy: before securing aneurysm avoid hypertension (rebleed risk) but ensure CPP; after securing treat vasospasm with induced hypertension if needed (centre-specific).
Ventilation: normocapnia (PaCO2 ~4.5–5.0 kPa). Hyperventilation only short-term rescue for acute ICP crises.
Fluids: aim euvolaemia; isotonic crystalloids; avoid hypotonic fluids; avoid routine hypervolaemia. Manage sodium carefully (risk SIADH/CSW).
Drugs: nimodipine (vasospasm prophylaxis) often causes hypotension—anticipate vasopressors. Avoid large BP surges at laryngoscopy/extubation.
Emergencies: intra-op rupture (sudden hypertension/bradycardia, blood in field, rising ICP) → immediate BP reduction, deepen anaesthesia, hyperventilate briefly, give mannitol/hypertonic saline if requested, communicate and prepare massive transfusion.
Post-op: aim early neuro assessment if safe; ICU/HDU. Extubate if stable, normothermic, good gas exchange, controlled BP, no major brain swelling/bleed.

Definition and key concepts

Subarachnoid haemorrhage = bleeding into the subarachnoid space (between arachnoid and pia), mixing with CSF.
Causes: aneurysmal (~80–85% of spontaneous SAH), non-aneurysmal/perimesencephalic, AVM, trauma, anticoagulation/bleeding diathesis, pituitary apoplexy (can mimic).
Major early threats: rebleeding, raised ICP, hydrocephalus, seizures, cardiopulmonary complications; later threat: delayed cerebral ischaemia (DCI) from vasospasm and microcirculatory dysfunction.

Epidemiology and risk factors

Incidence ~6–10 per 100,000/year (varies by population). High morbidity/mortality; many deaths occur before hospital.
Risk factors: hypertension, smoking, excess alcohol, sympathomimetics (e.g., cocaine), family history, connective tissue disorders (e.g., Ehlers-Danlos), polycystic kidney disease.

Clinical presentation and examination

Symptoms: thunderclap headache (max intensity within 1 min), neck stiffness/photophobia, vomiting, collapse/syncope, seizures, focal deficits, reduced consciousness.
Signs: meningism, reduced GCS, cranial nerve palsies (e.g., III palsy with posterior communicating aneurysm), retinal/subhyaloid haemorrhage (Terson syndrome).
Cardiorespiratory: neurogenic stunned myocardium, arrhythmias, pulmonary oedema (neurogenic), aspiration risk.

Diagnosis: investigations and interpretation

First-line: non-contrast CT head (highest sensitivity early; declines with time).
- If CT negative but suspicion high: LP for xanthochromia (after appropriate timing) and RBCs; consider CTA/MRA depending on pathway.
Identify source: CT angiography ± digital subtraction angiography (DSA) (gold standard) to define aneurysm/AVM and plan treatment.
Baseline labs: FBC, U&E (Na+), coagulation, group & save/crossmatch, glucose; ECG and troponin if indicated.

Grading and prognostication (learn the common scales)

WFNS grade (based on GCS + focal deficit): correlates with outcome and guides urgency/ICU needs.
- I: GCS 15, no deficit; II: GCS 13–14, no deficit; III: GCS 13–14 with deficit; IV: GCS 7–12; V: GCS 3–6.
Hunt & Hess (clinical severity) used historically; still encountered in exams.
Fisher / modified Fisher (CT blood burden) predicts vasospasm/DCI risk (more blood and intraventricular blood = higher risk).

Immediate management in ED/ICU (before aneurysm secured)

Priorities: A–E, treat hypoxia/hypercapnia, secure airway if low GCS/aspiration risk, manage seizures, analgesia/antiemesis, control BP, reverse anticoagulation, urgent neurosurgical/neurointerventional referral.
Blood pressure: avoid extremes. Aim to reduce rebleed risk while maintaining CPP (local targets vary; commonly treat marked hypertension). Use titratable agents (e.g., labetalol, nicardipine) and avoid sudden drops.
Nimodipine: give early unless contraindicated (reduces poor outcome from DCI; not a direct antispasm guarantee). Watch for hypotension.
Hydrocephalus/raised ICP: head up 30°, neutral neck, analgesia/sedation as needed, maintain normocapnia; urgent EVD if obstructive hydrocephalus/deterioration.
Anticoagulation/antiplatelets: reverse where appropriate (vitamin K + PCC for warfarin; specific reversal agents if available; consider platelet transfusion/DDAVP case-by-case). Liaise with neurosurgery/interventional team.
Avoid: hypotonic fluids, hypoglycaemia, hyperthermia; treat fever aggressively.

Definitive treatment: securing the aneurysm

Aim to secure aneurysm early (often within 24–72 h depending on grade and logistics) to reduce rebleeding risk and allow more aggressive treatment of vasospasm.
Coiling vs clipping: coiling less invasive and often preferred for suitable aneurysms; clipping may be preferred for certain morphologies, wide necks, associated haematoma requiring evacuation, or when endovascular not feasible.

Anaesthetic considerations: pre-op assessment

Assess neurological status (baseline GCS, focal deficits), CT findings (hydrocephalus, mass effect), and timing since bleed (rebleed risk highest early).
Cardiac assessment: ECG changes common; consider echo if haemodynamic instability, troponin rise, pulmonary oedema (neurogenic stunned myocardium).
Optimise physiology: oxygenation, Hb, glucose, temperature, sodium; treat aspiration risk (RSI considerations).
Discuss with neuroradiology/neurosurgery: BP targets, heparinisation plan (coiling often uses heparin), need for burst suppression/temporary clipping, anticipated rupture risk, post-op ventilation plan.

Anaesthetic technique: induction and maintenance (key exam points)

Induction: smooth, avoid coughing/straining and hypertension. Consider opioid + propofol/etomidate (if unstable) + rocuronium. Lidocaine/esmolol/remifentanil can blunt response.
Ventilation: controlled ventilation with normocapnia; avoid hypoxia. Use PEEP cautiously if ICP concerns but prioritise oxygenation.
Maintenance: TIVA (propofol/remifentanil) or volatile-based; both acceptable. Prioritise stable haemodynamics and rapid wake-up if planned.
BP management: titrate vasopressors/inotropes (phenylephrine/metaraminol/noradrenaline) to maintain CPP; avoid hypertensive surges pre-securing; after securing, induced hypertension may be used for DCI (consult team).
Anticoagulation during coiling: systemic heparin may be used after access/initial coil placement; be prepared for reversal (protamine) if rupture occurs (team-dependent).
Brain relaxation for clipping: optimise venous drainage (head position), normocapnia, consider mannitol/hypertonic saline if requested, avoid excessive fluids and high CVP.
Temperature: maintain normothermia (hypothermia not routine neuroprotection).

Post-op and ICU care

Destination usually ICU/HDU. Key aims: frequent neuro obs, BP control, nimodipine continuation, euvolaemia, normoxia/normocapnia, normothermia, glucose control, DVT prophylaxis when safe.
Detect and treat complications: DCI/vasospasm, hydrocephalus, seizures, electrolyte disturbances, cardiopulmonary complications, rebleed.
Analgesia: regular paracetamol ± opioids carefully titrated; avoid masking neuro deterioration; treat nausea/vomiting to avoid ICP/BP surges.

Complications and their management (high-yield)

Rebleeding: highest risk early; catastrophic. Prevent with early aneurysm securing and BP control; avoid agitation/coughing; treat coagulopathy.
Delayed cerebral ischaemia (DCI) / vasospasm (often days 3–14, peak ~days 5–10): new neuro deficit or reduced consciousness not explained by other causes.
- Prevention: nimodipine; maintain euvolaemia; avoid hypotension.
- Treatment: induced hypertension (common first-line once aneurysm secured), optimise Hb/oxygenation, treat fever; consider endovascular therapy (intra-arterial vasodilators, angioplasty) in refractory cases.
Hydrocephalus: acute (obstructive) or chronic communicating; treat with EVD/VP shunt. Watch for reduced GCS, headache, vomiting, papilloedema.
Electrolyte disorders: hyponatraemia common (SIADH vs cerebral salt wasting). Manage based on volume status; avoid rapid correction; consider hypertonic saline if severe/symptomatic.
Seizures: treat promptly; prophylaxis is centre-specific (more likely with cortical involvement, intraparenchymal haematoma, post-clipping).
Cardiac: ECG changes, troponin rise, LV dysfunction (Takotsubo-like), arrhythmias; manage as heart failure/ACS mimic but recognise neurogenic cause; avoid fluid overload if pulmonary oedema.
Neurogenic pulmonary oedema: supportive ventilation, treat catecholamine surge/afterload, careful fluid balance.

Differential diagnosis of thunderclap headache (viva list)

SAH (aneurysmal/non-aneurysmal), cervical artery dissection, cerebral venous sinus thrombosis, reversible cerebral vasoconstriction syndrome (RCVS), intracerebral haemorrhage, meningitis/encephalitis, pituitary apoplexy, acute glaucoma, migraine (diagnosis of exclusion).

You are called to ED: 45-year-old with sudden worst headache, vomiting, photophobia. Talk through your initial management and priorities.

Structure as A–E, prevent secondary brain injury, and expedite definitive care.

A: assess airway; if reduced GCS/aspiration risk → RSI with haemodynamic control; C-spine not routine unless trauma.
B: oxygenation/ventilation; aim normoxia and normocapnia; treat pulmonary oedema/aspiration.
C: IV access, ECG, treat arrhythmias; avoid hypotension; manage hypertension with titratable agents avoiding sudden drops; send bloods incl. coagulation and group & save.
D: neuro exam (GCS, pupils, focal deficits), glucose, treat seizures, analgesia/antiemesis; head up 30°, neutral neck.
E: temperature control; avoid hyperthermia; urgent CT head ± CTA; early neurosurgery/neurointerventional referral; start nimodipine if SAH suspected/confirmed and haemodynamics allow.

CT head is negative but suspicion of SAH remains high. What next and why?

Know the diagnostic pathway and the rationale for LP/xanthochromia.

Reassess pre-test probability and timing from onset; consider CTA (many pathways now use CTA early).
If CT negative and suspicion persists → LP to look for xanthochromia and persistent RBCs (distinguish from traumatic tap).
Explain: CT sensitivity declines with time; xanthochromia indicates breakdown products in CSF consistent with SAH.
If LP/CTA suggests aneurysm → DSA to define anatomy and plan coiling/clipping.

Describe WFNS grading and how it influences anaesthetic/ICU planning.

Examiners want the scale and practical implications.

WFNS uses GCS and presence of focal neurological deficit (I to V).
Higher grade (IV–V): higher risk of airway compromise, aspiration, haemodynamic instability, raised ICP → likely intubation/ventilation, invasive monitoring, ICU.
Lower grade (I–II): may tolerate early securing with planned early extubation and close neuro monitoring.

What are your anaesthetic goals for aneurysm coiling in a patient with unsecured SAH?

Focus on preventing rebleed and maintaining cerebral perfusion while enabling the procedure.

Smooth induction and emergence: avoid coughing/straining and hypertensive surges (rebleed risk).
Maintain CPP: avoid hypotension; treat nimodipine-related hypotension with vasopressors.
Normocapnia and normoxia; avoid hyperventilation except short rescue for acute ICP rise.
Anticipate heparinisation; plan for rapid reversal if rupture occurs; ensure blood available.
Rapid wake-up if feasible for immediate neuro assessment; plan ICU/HDU bed.

During clipping, the surgeon requests 'brain relaxation'. What do you do and what are the pitfalls?

Give a stepwise approach and show awareness of consequences.

Check basics: head position/venous drainage (neutral neck, avoid tight ties), adequate anaesthesia, normocapnia, treat hypertension.
Osmotherapy if requested: mannitol (diuresis, hypotension risk) or hypertonic saline (Na+ rise, volume expansion).
CSF drainage if EVD/ventricular access available (surgeon/neurosurgeon).
Pitfalls: excessive hyperventilation → cerebral ischaemia; hypotension after mannitol; fluid overload increasing brain swelling; hypovolaemia reducing CPP.

Intra-operative aneurysm rupture: how would you recognise it and what immediate actions do you take?

This is a classic FRCA neuroanaesthesia scenario.

Recognition: sudden surgical field bleeding; abrupt haemodynamic change (often hypertension then hypotension), rising ICP, bradycardia, sudden drop in ETCO2 if major haemorrhage.
Immediate actions: call it out; deepen anaesthesia; ensure 100% O2; brief hyperventilation; rapidly control BP per surgeon request (often lower to facilitate clip control) while maintaining perfusion.
Give osmotherapy if requested; prepare blood products; activate massive transfusion if needed; correct coagulopathy.
If heparinised (coiling) consider protamine after discussion; anticipate post-op ICU and possible non-wake-up scan.

What is delayed cerebral ischaemia (DCI) and how is it managed in ICU once the aneurysm is secured?

Differentiate DCI from angiographic vasospasm and list pragmatic management.

Definition: new focal deficit or drop in consciousness lasting >1 h not explained by other causes (e.g., hydrocephalus, seizure, metabolic). Often associated with vasospasm days 3–14.
Initial steps: exclude other causes (CT/CTA/CTP, check EVD patency, electrolytes, infection, seizures).
Treatment: induced hypertension (vasopressors) to improve cerebral blood flow; maintain euvolaemia; optimise oxygenation and Hb; continue nimodipine if tolerated.
Refractory cases: endovascular therapy (angioplasty for proximal spasm; intra-arterial vasodilators).

A SAH patient becomes drowsy on day 2 with headache and vomiting. Give a differential and immediate management.

Show you can prioritise reversible causes early.

Differential: hydrocephalus, rebleed, seizure/non-convulsive status, electrolyte disturbance (hyponatraemia), infection, sedative/opioid effect, early DCI (less common day 2 but possible).
Immediate management: A–E; check glucose, pupils; urgent CT head; review EVD if present; treat seizures; correct sodium/volume status; ensure BP supports CPP.

Hyponatraemia after SAH: outline causes, how to distinguish them, and management principles.

Common FRCA viva topic: SIADH vs cerebral salt wasting (CSW).

Causes: SIADH (euvolaemic/hypervolaemic hyponatraemia) and CSW (hypovolaemic hyponatraemia due to renal sodium loss).
Distinguish: assess volume status (clinical, UO, haemodynamics), urine sodium/osmolality; CSW typically high urine Na with hypovolaemia and high UO.
Management: avoid hypotonic fluids; treat symptomatic/severe with hypertonic saline carefully; SIADH may need fluid restriction (but caution in SAH where euvolaemia is important); CSW needs volume and sodium replacement (± fludrocortisone in some protocols).
Avoid rapid correction to prevent osmotic demyelination.

What ECG/cardiac abnormalities occur after SAH and what are the anaesthetic implications?

Demonstrate awareness of neuro-cardiac interactions.

Findings: QT prolongation, ST/T changes, U waves, arrhythmias; troponin rise; LV systolic dysfunction (neurogenic stunned myocardium/Takotsubo-like).
Implications: higher risk of peri-induction hypotension/arrhythmias; consider echo; cautious fluid strategy if pulmonary oedema; vasopressor/inotrope support may be required.

Outline a safe extubation strategy after aneurysm securing.

Examiners want criteria and how to avoid BP/ICP surges.

Extubate if: haemodynamically stable, normothermic, adequate ventilation/oxygenation, acceptable ICP/brain swelling, no major intra-op complication, obeying commands or appropriate neurological baseline.
Plan: smooth emergence (opioid/remifentanil tail, lidocaine, antiemetics), avoid coughing/straining; ensure BP targets met; have rescue plan (reintubation, ICU).
If not extubating: reasons include poor grade SAH, pulmonary oedema, ongoing vasospasm therapy, significant brain swelling/bleed, need for imaging/ICU optimisation.