Subarachnoid haemorrhage
Description
- Blood in the subarachnoid space - thunderclap headache + meningism +/- dec conscious state
- Non-traumatic SAH is aneurysmal until proven otherwise (trauma is the commonest cause of SAH overall)
Grading - do it on arrival, it drives prognosis
| WFNS | GCS | Focal deficit |
|---|---|---|
| I | 15 | No |
| II | 13-14 | No |
| III | 13-14 | Yes |
| IV | 7-12 | +/- |
| V | 3-6 | +/- |
- Hunt & Hess - clinical (I asymptomatic/mild headache -> V deep coma, decerebrate)
- Modified Fisher - CT blood volume; predicts delayed cerebral ischaemia, not rebleed
- Thick cisternal clot and intraventricular blood = highest DCI risk
Epidemiology
- ~6-9 per 100,000/yr; ~5% of all strokes but a disproportionate share of years of life lost
- Peak 45-60 yrs - young compared with other stroke
- F>M ~1.6:1
- Higher incidence in Finland and Japan; higher in Aboriginal and Torres Strait Islander Australians
- Unruptured intracranial aneurysms present in ~3% of adults
Aetiopathogenesis
Causes of non-traumatic SAH
- Ruptured saccular (berry) aneurysm ~80%
- Circle of Willis branch points: anterior communicating (~35%), posterior communicating (~30%), MCA bifurcation (~20%), posterior circulation (~10%)
- Perimesencephalic / non-aneurysmal (~10%) - blood confined around the midbrain, normal angiogram, excellent prognosis, no vasospasm; presumed venous
- AVM, dural AV fistula, cavernoma
- Arterial dissection (vertebral), mycotic aneurysm (endocarditis)
- Reversible cerebral vasoconstriction syndrome (RCVS) - convexity SAH, recurrent thunderclap, "sausage-string" vessels
- Cerebral venous sinus thrombosis; vasculitis; cocaine/amphetamine; pituitary apoplexy; coagulopathy
- Cerebral amyloid angiopathy - convexity SAH in the elderly
Aneurysm formation and rupture
- Haemodynamic stress at bifurcations + deficient tunica media -> outpouching
- Rupture -> abrupt inc ICP, dec cerebral perfusion pressure -> transient global ischaemia (loss of consciousness, "worst headache")
- Catecholamine surge -> neurogenic stunned myocardium, neurogenic pulmonary oedema, arrhythmia
- Blood breakdown products -> inflammation, cortical spreading depolarisation, microthrombosis and large-vessel vasospasm -> delayed cerebral ischaemia
Diagnosis
Clinical
- Thunderclap headache - maximal within 1 minute; "worst ever"; occipital/diffuse
- Vomiting, neck stiffness, photophobia, transient LOC, seizure (~7%)
- Terson syndrome - vitreous/subhyaloid retinal haemorrhage; look at the fundi
- Focal signs: CN III palsy with a fixed dilated pupil = posterior communicating aneurysm; monoparesis/abulia = ACom
- Sentinel ("warning") headache precedes SAH in ~10-40%, typically 2-8 weeks before
- *Never dismiss a first, worst or sudden headache - this is where SAH is missed*
Pathway
- A. Non-contrast CT brain immediately
- Sensitivity ~100% within 6 h of ictus on a modern scanner read by an experienced reporter -> LP can be omitted if CT is within 6 h and negative
- Falls to ~85% at 24 h and ~50% by day 5
- B. Lumbar puncture if CT negative and >6 h from onset
- Perform >=12 h after onset to allow oxyhaemoglobin -> bilirubin conversion
- Xanthochromia by spectrophotometry (standard in Australian laboratories) - distinguishes SAH from a traumatic tap
- Also: 3-tube red cell count not falling; raised opening pressure
- C. CT angiography once SAH confirmed - detects aneurysms >=3 mm with high sensitivity
- DSA remains the gold standard; repeat at 1-2 weeks if the first angiogram is negative in non-perimesencephalic patterns
Also do
- ECG and troponin - deep T inversion, long QT, "cerebral T waves"; neurogenic, do not take to the cath lab
- CXR (neurogenic pulmonary oedema), UEC (hyponatraemia), coagulation profile
- MRI/MRA if delayed presentation (FLAIR, SWI, T2*)
Management
A. Immediate - prevent rebleeding
- Urgent neurosurgical/neurointerventional referral and transfer to a comprehensive stroke or neurosurgical centre
- Secure the aneurysm within 24 h of diagnosis
- Endovascular coiling preferred over clipping where both are feasible (ISAT) - better disability-free survival; clipping favoured for large MCA aneurysms and large haematomas needing evacuation
- BP control until secured - avoid extremes; target systolic <160 mmHg, with a titratable agent (labetalol, GTN infusion)
- After securing, permissive hypertension is allowed
- Reverse anticoagulation immediately
- Analgesia, antiemetics, stool softeners, bed rest, quiet environment
- Short-course tranexamic acid is NOT recommended - the ULTRA trial showed no functional benefit
B. Prevent delayed cerebral ischaemia
- Nimodipine 60 mg PO every 4 h for 21 days - start immediately
- The only drug that improves neurological outcome in aneurysmal SAH
- *Works despite not reliably preventing angiographic vasospasm* - neuroprotective, not simply vasodilatory
- Hold/split the dose for hypotension rather than stopping; give NG if unable to swallow
- Maintain euvolaemia with isotonic fluid; monitor fluid balance and sodium daily
- *Prophylactic hypervolaemia and haemodilution ("triple-H") are obsolete and harmful - avoid both hypovolaemia and hypervolaemia*
- Avoid hypotension, hyponatraemia, fever, hyperglycaemia and anaemia
- Daily neurological observation + transcranial Doppler; CT perfusion or CTA if deterioration
C. Established delayed cerebral ischaemia
- New focal deficit or dec GCS at day 4-14 not explained by rebleed, hydrocephalus, seizure or metabolic cause
- Induced hypertension - stepwise vasopressor (noradrenaline) with the aneurysm secured, titrated to neurological response
- Add fluid only to restore euvolaemia
- Endovascular rescue if refractory - intra-arterial vasodilator (verapamil, milrinone, nimodipine) +/- balloon angioplasty for proximal spasm
D. Other complications
- Hydrocephalus - external ventricular drain for acute obstructive hydrocephalus; VP shunt in ~20% for chronic communicating hydrocephalus
- Seizures - treat clinical seizures; routine prophylaxis is not recommended
- Hyponatraemia - cerebral salt wasting (hypovolaemic, high urinary Na, high urine output) vs SIADH (euvolaemic)
- *Treat with saline and fludrocortisone, NOT fluid restriction* - dehydration precipitates DCI
- Cardiac: neurogenic stunned myocardium; DVT prophylaxis (mechanical until secured); fever workup and control
E. Long-term
- Smoking cessation and BP control - the two modifiable determinants of new aneurysm formation and recurrence
- Screening first-degree relatives if >=2 affected first-degree relatives, or ADPKD
- Cognitive, mood and fatigue assessment; driving and return-to-work advice
Associations
- Hypertension, smoking, heavy alcohol, sympathomimetics (cocaine, amphetamine)
- ADPKD (~10% harbour an aneurysm), Ehlers-Danlos type IV (vascular), Marfan, fibromuscular dysplasia, coarctation of the aorta
- Family history - risk up with >=2 affected first-degree relatives
- Female sex, post-menopausal state
- Bacterial endocarditis (mycotic aneurysm)
- Sickle cell disease
Natural history & complications
- Case fatality ~30-40%; ~10-15% die before reaching hospital
- ~1/3 of survivors remain dependent; cognitive impairment, fatigue and depression are common even in "good outcome" patients
- Perimesencephalic SAH: excellent prognosis, negligible rebleed or DCI risk
Aneurysm rupture risk factors
- Size >7 mm (risk rises steeply above this), posterior circulation location, irregular shape/daughter sac, documented growth
- Hypertension, current smoking, alcohol misuse, sympathomimetic drug use
- Black or Hispanic ethnicity; Finnish or Japanese ancestry
- Prior SAH from a different aneurysm; family history
- PHASES score aggregates these for unruptured aneurysms
Complications and their timing
| Timing | Complication |
|---|---|
| 0-72 h | Rebleeding - highest in the first 24 h; ~15% if unsecured, ~50% mortality. The reason for securing within 24 h |
| 0-72 h | Acute obstructive hydrocephalus; seizure; neurogenic pulmonary oedema; stunned myocardium |
| Day 4-14 | Vasospasm and delayed cerebral ischaemia - the peak is day 7-10 |
| Day 3-14 | Hyponatraemia (cerebral salt wasting > SIADH) |
| Weeks-months | Chronic communicating hydrocephalus, cognitive impairment, epilepsy, depression, endocrine (hypopituitarism) |
- DCI is a clinical syndrome and is not confined to the territory of any angiographic spasm - treat the patient, not the Doppler velocity
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