Subarachnoid haemorrhage (SAH) is bleeding into the subarachnoid space — the area between the arachnoid and pia mater membranes. 85% of spontaneous SAH results from ruptured intracranial aneurysm. Overall mortality is 25–50%; one-third die before reaching hospital.
Classic Presentation
"Worst headache of my life" + sudden onset = SAH until proven otherwise. Thunderclap headache — maximum severity at onset, within seconds. Any delay in diagnosis is potentially fatal.
Thunderclap headache: Sudden, severe, maximal within seconds — classic "hit over the head with a bat" description
Nausea and vomiting — very common
Neck stiffness (meningismus) — blood in CSF causes meningeal irritation; may be absent in early hours
Photophobia — meningeal irritation
Loss of consciousness — at onset (transient or sustained); indicates severe bleed
Up to 40% of SAH patients report a less severe "warning headache" days to weeks before the main bleed — minor leak from aneurysm before full rupture. This is critical to identify — prompt treatment can prevent the catastrophic main bleed. Nurses must ask about any unusual severe headache in preceding weeks.
Causes
Cause
Frequency
Ruptured intracranial aneurysm (berry/saccular)
85%
Arteriovenous malformation (AVM)
5–10%
Perimesencephalic (non-aneurysmal)
5–10%
Other (trauma, CVST, coagulopathy, cocaine)
<5%
Grading Scales
Hunt and Hess Grade
Grade
Clinical Features
Prognosis
I
Asymptomatic or mild headache, slight nuchal rigidity
Excellent (70% good outcome)
II
Moderate-severe headache, nuchal rigidity, no neurological deficit except CN palsy
Good (60%)
III
Drowsiness, confusion, mild focal deficit
Moderate (50%)
IV
Stupor, moderate-severe hemiparesis, early decerebrate posturing
Poor (20%)
V
Deep coma, decerebrate posturing, moribund appearance
Very poor (10%)
Fisher Grade (CT Classification)
Grade
CT Finding
Vasospasm Risk
1
No SAH on CT
Low
2
Diffuse thin SAH (<1 mm)
Low
3
Localised clot or thick SAH (>1 mm)
High
4
Intraventricular or intracerebral extension
High
Fisher grade 3 carries the highest vasospasm risk — critical nursing assessment window is days 4–14 after bleed.
Acute Management
Immediate Priorities
CT head (non-contrast): Hyperdense blood in basal cisterns — sensitivity 98% within 12 hours. After 12 hours sensitivity falls — LP needed if CT negative and clinical suspicion high
Lumbar puncture: If CT negative but clinical suspicion high — perform ≥12 hours after headache onset. Xanthochromia (yellow CSF) confirms SAH from bilirubin breakdown of haemoglobin
CT angiography: Identifies aneurysm location and morphology; guides neurosurgical/neurointerventional planning
Secure aneurysm: Endovascular coiling (preferred) or surgical clipping within 24–72 hours — prevents rebleeding (peak rebleed risk is first 24 hours: 15–20%)
Nimodipine: 60 mg orally (or via NGT) every 4 hours × 21 days — reduces cerebral vasospasm complications
Tranexamic acid: Short course (≤72 hrs) may reduce rebleeding risk before aneurysm secured — controversial
Cerebral Vasospasm
Vasospasm window: Days 4–14 post-bleed (peak Day 7). Occurs in 70% of SAH patients; clinical vasospasm (causing ischaemia) in 30%. Leading cause of morbidity and mortality in SAH survivors.
Recognising Vasospasm
New focal neurological deficit (contralateral hemiparesis, aphasia) after initial improvement
CT/MR perfusion: reduced perfusion in vasospasm territories
Nimodipine — Standard of Care
Nimodipine 60 mg every 4 hours orally × 21 days is the only proven treatment to reduce vasospasm-related complications. It is a calcium channel blocker that reduces smooth muscle contraction in cerebral arteries.
If patient cannot swallow: crush 60 mg tablet and flush via NG tube or use IV nimodipine (where available)
Monitor BP: nimodipine causes hypotension — hold if SBP <90; notify team
Do NOT miss doses — timing critical for vasospasm prevention
IV nimodipine: 1–2 mg/hr via central line (peripheral line causes burning)
Triple-H Therapy (Historical — Modified Approach)
Classic approach: Hypertension + Haemodilution + Hypervolaemia (Triple-H). Modern evidence supports euvolaemia + induced hypertension only (haemodilution shown to reduce O₂ delivery).
Euvolaemia: Prevent dehydration — cerebral salt wasting causes fluid and Na⁺ loss; replace with IV fluids (0.9% NaCl preferred; avoid hypotonic fluids)
Induced hypertension: If vasospasm confirmed — vasopressors (noradrenaline or phenylephrine) to raise MAP to 100–120 mmHg; increases cerebral perfusion pressure
Endovascular therapy: Intra-arterial verapamil or balloon angioplasty for refractory vasospasm
GCC-Specific Context
SAH in GCC
Hypertension: Poorly controlled hypertension is the primary modifiable risk factor for intracranial aneurysm rupture — GCC's high hypertension prevalence increases SAH risk
Smoking: Smoking is an independent risk factor for aneurysm formation and rupture — significant in GCC male population (shisha + cigarettes)
Consanguinity: Familial intracranial aneurysms cluster in some consanguineous GCC families — family screening CT angiography important when a first-degree relative has had SAH
Cocaine use: Increasingly recognised in GCC expatriate community — cocaine causes vasospasm, hypertension and aneurysm rupture; always screen for drug use in young SAH patients
GCC neuroscience centres: Certified neuro-intervention centres exist at KFSH&RC (Riyadh), Sheikh Khalifa Medical City (Abu Dhabi), SKMC, HMC (Doha) — transfer to these centres for coiling/clipping is critical
Exam Tips
"Worst headache of life" = SAH until proven otherwise
CT head first; LP if CT negative >12 hrs after onset (look for xanthochromia)
Nimodipine 60 mg every 4 hrs × 21 days — standard SAH treatment
Vasospasm window: Days 4–14 (peak Day 7)
Rebleed risk highest in first 24 hrs — urgent aneurysm securing
ECG changes in SAH are neurogenic — NOT always cardiac
Hyponatraemia in SAH: cerebral salt wasting (treat with IV NaCl) vs SIADH (fluid restriction)
Exam MCQs — DHA / SCFHS / QCHP
Q1. A 48-year-old patient presents with sudden onset "worst headache of my life" that began while straining at the gym. CT head is reported as "normal." What is the NEXT step?
✅ C — CT sensitivity for SAH falls from 98% at 12 hours to ~85% at 24 hours and continues declining. A negative CT does NOT exclude SAH. Lumbar puncture (LP) at ≥12 hours post-onset: xanthochromia (yellow CSF from bilirubin) confirms SAH. LP before 12 hours may show false-negative from red cell lysis not yet producing bilirubin.
Q2. A SAH patient is 6 days post-bleed. The nurse notes the patient has new left arm weakness that was not present yesterday. What is the MOST LIKELY cause?
✅ B — Day 6 is within the peak vasospasm window (Days 4–14). New focal neurological deficits after initial improvement = cerebral vasospasm until proven otherwise. Urgent TCD/CT perfusion needed. Start/optimise induced hypertension. Nimodipine must be continued. Rebleeding typically causes sudden deterioration with loss of consciousness, not gradual focal deficit.
Q3. A nurse is administering nimodipine 60 mg via nasogastric tube to a SAH patient. The patient's BP drops to 82/54 mmHg. What is the CORRECT action?
✅ B — Nimodipine causes dose-dependent hypotension. SBP <90 mmHg in SAH is dangerous — reduces cerebral perfusion pressure and can precipitate or worsen vasospasm ischaemia. Hold dose, notify team, fluid bolus and vasopressors if needed. Resume nimodipine at reduced dose when BP stable. Do NOT skip doses routinely — the benefit outweighs risk with close monitoring.
Q4. A SAH patient develops serum Na⁺ 125 mmol/L with high urine sodium (45 mmol/L) and signs of dehydration. What is the MOST LIKELY diagnosis and treatment?
✅ B — Cerebral salt wasting (CSW) in SAH: high urinary sodium + hypovolaemia (dehydration). Distinguished from SIADH by volume status — CSW is HYPOvolaemic, SIADH is EUvolaemic. Fluid restriction in CSW worsens hypovolaemia, reduces cerebral blood flow and WORSENS vasospasm risk. Treat with IV fluids (0.9% NaCl) ± fludrocortisone (reduces renal sodium loss).