Subarachnoid haemorrhage

Contents

Diagnosis

Clinical Presentation

  • Thunderclap headache: sudden onset, maximal within seconds — "worst headache of my life"
  • Neck stiffness (meningism), photophobia, nausea/vomiting
  • Sentinel headache in days–weeks before (30% of cases) — warning bleed
  • Focal deficits, coma, or sudden death in severe cases

Imaging

CT head (non-contrast):

  • Sensitivity ~98% within 6 hours of onset; falls to ~85–90% at 24h
  • Blood appears in basal cisterns, Sylvian fissures, or sulci
  • A negative CT does not exclude SAH if presentation is within 12 hours — LP required

Lumbar puncture:

  • Perform if CT negative and presentation within 12 hours of onset (later presentations have higher CT sensitivity)
  • Perform ≥12 hours after headache onset (allows bilirubin formation from haemoglobin breakdown)
  • Xanthochromia (yellow discolouration of CSF supernatant from bilirubin): key finding; spectrophotometry more sensitive than visual inspection; persists for up to 2 weeks
  • Elevated opening pressure; raised red cell count that does not diminish between bottles (vs traumatic tap, where it does)

CT angiography (CTA):

  • Sensitivity ~95% for aneurysm ≥5mm; first-line for aneurysm identification in confirmed SAH
  • Identifies aneurysm size, location, neck morphology (guides coiling vs clipping decision)

Digital subtraction angiography (DSA):

  • Gold standard; used when CTA is negative or equivocal, or pre-procedurally
  • ~5–10% of SAH has no identifiable cause even on formal angiography (perimesencephalic pattern — usually venous, benign prognosis)

Grading Systems

Hunt and Hess (Clinical Grade)

Grade Features
I Mild headache, subtle nuchal rigidity
II Moderate-severe headache, nuchal rigidity, cranial nerve palsy
III Drowsiness, confusion, mild focal deficit
IV Stupor, moderate-severe hemiparesis, early decerebrate signs
V Deep coma, decerebrate rigidity, moribund

Grades I–III: "good grade" — lower mortality; suitable for early aneurysm treatment.
Grades IV–V: "poor grade" — high mortality; management more complex; resuscitate and reassess.

WFNS Grading

Based on GCS and presence of motor deficit. Grade I (GCS 15) to Grade V (GCS 3–6).

Modified Fisher Scale (CT Grade — vasospasm risk)

mFS CT findings Vasospasm risk
0 No blood Low
1 Thin diffuse SAH, no IVH Moderate
2 Thin diffuse SAH + IVH High
3 Thick clot in cisterns/fissures, no IVH Highest
4 Thick clot + IVH High

mFS 3–4: highest DCI risk, requiring intensive monitoring.

Early Management

Immediate priorities

  1. Airway: intubate if GCS ≤8 or deteriorating; avoid hypoxia and hypercapnia
  2. Blood pressure: before aneurysm is secured, target SBP <160 mmHg (reduces rebleed risk without causing ischaemia); labetalol or nicardipine IV; avoid excessive hypotension
  3. Analgesia: paracetamol + opioids as required; avoid NSAIDs (antiplatelet effect)
  4. Bed rest, avoid Valsalva; stool softeners

Preventing rebleed

  • Highest rebleed risk: first 24 hours (5–10%)
  • Definitive prevention: secure the aneurysm as soon as possible (within 24h of ictus in good-grade patients)
  • Antifibrinolytics (tranexamic acid): short-term use (<72h, until aneurysm secured) may reduce rebleed but not improve outcome due to increased DCI risk; not recommended routinely

Nimodipine

  • 60 mg orally every 4 hours for 21 days — standard of care in all aneurysmal SAH
  • Reduces poor neurological outcome (not mortality) from vasospasm; evidence from multiple RCTs
  • Mechanism: L-type calcium channel blocker with relative cerebral selectivity; reduces vasospasm severity and possibly neuroprotection
  • Note: may cause hypotension (reduce dose to 30 mg if SBP falls <100 mmHg)

Hydrocephalus

  • Occurs in 20–30% of patients (obstructive or communicating)
  • Signs: deteriorating GCS, upward gaze palsy (Parinaud syndrome)
  • Treatment: external ventricular drain (EVD) for acute obstructive hydrocephalus; VP shunt for persistent communicating hydrocephalus

Securing the Aneurysm — Coiling vs Clipping

ISAT Trial (Molyneux et al, Lancet 2002)

  • Design: RCT, 2143 patients with aneurysmal SAH suitable for either coiling or clipping
  • Finding: endovascular coiling associated with significantly better 1-year outcome — dependency or death: 23.5% (coiling) vs 30.6% (clipping) — absolute risk reduction ~7%
  • Long-term follow-up: slightly higher rebleed rate after coiling; but overall favourable outcomes maintained
  • Implication: coiling is the preferred technique for aneurysms that are anatomically suitable for both approaches

Coiling vs Clipping — Key Differences

Feature Coiling Clipping
Access Endovascular (femoral approach) Open craniotomy
Recovery Faster Slower
Suitable for Most anterior circulation; morphology-dependent Wide-necked, complex aneurysms; posterior circulation (sometimes); accessible haematoma to evacuate
Rebleed risk Slightly higher long-term Lower (aneurysm excluded from circulation)
Radiological follow-up Required (MRA) Less frequently needed

The decision is made jointly by neurosurgery and interventional neuroradiology, based on aneurysm morphology, location, neck width, and patient factors.

Vasospasm and Delayed Cerebral Ischaemia (DCI)

Definitions

  • Vasospasm: narrowing of intracranial arteries on imaging
  • Delayed cerebral ischaemia (DCI): clinical deterioration attributable to ischaemia, occurring >72h post-ictus
  • Peak risk: days 4–14 post-ictus

Mechanism

Breakdown of subarachnoid blood → oxyhaeamoglobin → scavenges nitric oxide (NO) → loss of vasodilatory tone; endothelin-1 release → vasoconstriction; free radical damage to smooth muscle; cortical spreading depolarisations.

Diagnosis

  • Clinical: new neurological deficit or decline in GCS not explained by rebleed, hydrocephalus, or metabolic cause
  • Transcranial Doppler (TCD): ↑ mean MCA velocity >120 cm/s suggests vasospasm; Lindegaard ratio >3 (MCA:ICA velocity) more specific
  • CT/MR perfusion: identifies areas of reduced perfusion
  • DSA: definitive; allows concurrent intra-arterial treatment

Management

  • Nimodipine: prophylaxis (see above); does not reliably reverse established spasm but reduces DCI
  • Euvolaemia: maintain normal circulating volume; hypovolaemia worsens ischaemia
  • Induced hypertension: once aneurysm is secured, allow or induce hypertension (SBP 160–200 mmHg) to maintain CPP through narrowed vessels; noradrenaline or phenylephrine
  • Note: historical "triple-H therapy" (hypertension, hypervolaemia, haemodilution) — hypervolaemia and haemodilution are no longer recommended routinely; euvolaemia + induced hypertension is current practice
  • Intra-arterial vasodilators: nimodipine, papaverine, or verapamil via catheter; used for refractory vasospasm
  • Balloon angioplasty: mechanical dilation for severe proximal vessel spasm; used in specialist centres

Systemic Complications

Hyponatraemia

  • Common (30–40%); two distinct mechanisms:
    • SIADH (Syndrome of Inappropriate ADH): water retention; euvolaemic or mildly hypervolaemic; low serum osmolality; urine inappropriately concentrated; managed with fluid restriction (cautious — may worsen cerebral ischaemia)
    • Cerebral salt wasting (CSW): natriuresis with true sodium depletion; hypovolaemic; high urine sodium; managed with sodium and volume replacement (0.9% NaCl ± fludrocortisone)
  • Distinguishing SIADH from CSW is clinically difficult; in SAH, hyponatraemia + clinical hypovolaemia → favour CSW; aggressive fluid restriction is dangerous in SAH
  • Hyponatraemia in SAH worsens neurological outcome

Cardiac Complications

  • Troponin rise: 20–30% of patients; catecholamine-mediated myocyte injury from sympathetic surge at ictus
  • ECG changes: ST/T wave changes, deep T-wave inversions ("cerebral T-waves"), QT prolongation, U waves, pathological Q waves
  • Takotsubo (stress) cardiomyopathy: apical ballooning, LV dysfunction; occurs in ~5–8%; usually reversible
  • Neurogenic pulmonary oedema: sympathetically mediated pulmonary capillary leak; presents as acute pulmonary oedema without cardiac cause

Fever

  • Frequent; associated with worse neurological outcome
  • Infectious and non-infectious (central) causes; treat aggressively (target ≤37.5°C)

Viva Questions

1. A patient presents with thunderclap headache. CT is negative. How do you proceed?

A negative CT does not exclude SAH — sensitivity is ~98% within 6 hours but falls with time. If presentation is within 12 hours and CT is negative, perform lumbar puncture at least 12 hours after symptom onset. This allows bilirubin to form from haemoglobin breakdown, producing xanthochromia. Send CSF for spectrophotometry (more sensitive than visual inspection). Xanthochromia persists for up to 2 weeks. If LP is also negative and there are no other features, the diagnosis of SAH is effectively excluded. If the patient presents >12h after onset and CT is still the modality used, sensitivity improves — however, LP remains the definitive test to exclude SAH when there is clinical suspicion. If neither test is possible, or clinical suspicion remains very high despite negative tests, CT angiography to look for an underlying aneurysm may be appropriate in consultation with neurosurgery.

2. Explain the role of nimodipine in SAH and clarify what it does and does not prevent.

Nimodipine 60 mg every 4 hours for 21 days is standard care in all aneurysmal SAH. It is an L-type calcium channel blocker with relative cerebral selectivity. Evidence from multiple RCTs shows that nimodipine reduces poor neurological outcome — specifically dependency and death attributable to delayed cerebral ischaemia. Importantly, nimodipine does not reliably reduce the incidence of radiological vasospasm (arterial narrowing on imaging remains similar). Its benefit is thought to be neuroprotective at the cellular level (reducing calcium-mediated neuronal injury) rather than purely vasodilatory, and it may reduce DCI severity through cortical mechanisms. It does not clearly reduce mortality. The clinical implication is that nimodipine is given prophylactically for its neuroprotective and DCI-reducing effect, not as a vasodilator rescue therapy.

3. Describe delayed cerebral ischaemia — what causes it, when does it peak, and how is it managed?

Delayed cerebral ischaemia (DCI) is neurological deterioration due to ischaemia occurring >72h after SAH, peaking at days 4–14. It accounts for up to 30% of poor outcomes after aneurysmal SAH. The mechanism relates to breakdown of subarachnoid blood: oxyhaemoglobin scavenges nitric oxide (eliminating endothelium-derived vasodilatory tone), stimulates endothelin-1 release (vasoconstrictor), and causes free radical-mediated smooth muscle damage — together producing severe intracranial arterial vasoconstriction. Cortical spreading depolarisations also contribute. Clinically, new focal deficit, agitation, or declining GCS raises suspicion. Investigations: TCD (MCA velocity >120 cm/s, Lindegaard ratio >3), CT/MR perfusion, and DSA. Management: ensure aneurysm is secured; maintain euvolaemia; induce hypertension (SBP 160–200 mmHg) to drive flow through narrowed vessels (previously "triple-H" therapy — hypervolaemia and haemodilution are no longer recommended, as they carry risk without proven benefit); nimodipine prophylaxis ongoing; intra-arterial vasodilators or balloon angioplasty for refractory vasospasm in specialist centres.

4. A patient develops hyponatraemia (Na 128 mmol/L) on day 5 post-SAH. How do you manage it?

Hyponatraemia in SAH most commonly results from SIADH or cerebral salt wasting (CSW). The distinction is clinically important: SIADH is managed with fluid restriction, whereas CSW involves true sodium depletion and requires sodium and volume replacement. Distinguishing them requires clinical assessment of volume status: CSW patients are hypovolaemic (dry mucous membranes, negative fluid balance, raised urea, tachycardia), whereas SIADH patients are euvolaemic or mildly hypervolaemic. Urine sodium is elevated in both, making it unhelpful. In SAH specifically, the consequences of hypovolaemia are significant — it worsens DCI risk by reducing cerebral perfusion. For this reason, aggressive fluid restriction (standard SIADH treatment) is potentially dangerous in SAH and should be avoided or used very cautiously. In practice, I would treat conservatively with isotonic saline to maintain euvolaemia and correct hyponatraemia gradually (target correction <10–12 mmol/L/24h to avoid osmotic demyelination); consider fludrocortisone 100–400 mcg/day for CSW; hypertonic saline for severe symptomatic hyponatraemia (Na <125 with seizures or impaired consciousness). Liaise with neurosurgery/neurology for specialist input.