A 52-year-old woman is brought to the emergency department by her husband. She was washing dishes when she suddenly screamed and collapsed. Her husband reports she said it was "the worst headache of her life" before losing consciousness briefly. She has now regained consciousness but is confused and photophobic.
Vitals: BP 178/102 mmHg, HR 88 bpm, RR 18, SpO2 97% on room air, Temp 37.2°C
Examination: GCS 13 (E3V4M6). Neck stiffness present. Kernig's sign positive. Pupils equal and reactive, 3mm bilaterally. No focal neurological deficit.
What is the most likely diagnosis? How would you investigate and manage this patient?
What is Subarachnoid Haemorrhage?
Subarachnoid haemorrhage (SAH) is bleeding into the subarachnoid space — the area between the arachnoid and pia mater membranes that surrounds the brain and spinal cord. This space normally contains cerebrospinal fluid (CSF); when blood enters it, the consequences are immediate and potentially fatal.
SAH accounts for approximately 5% of all strokes but carries a disproportionate mortality — up to 45% of patients die within 30 days, and of those who survive, up to 50% are left with significant neurological disability. Early recognition and rapid management are therefore critical.
Incidence: approximately 6–8 per 100,000 population per year globally. Peak age: 55–60 years. Women are affected more than men. Risk factors include hypertension, smoking, heavy alcohol use, family history, and connective tissue disorders (e.g. Marfan syndrome, polycystic kidney disease).
Causes
The cause determines management and prognosis. The most important distinction is between aneurysmal and non-aneurysmal SAH:
| Cause | Proportion | Key Feature |
|---|---|---|
| Ruptured intracranial aneurysm | ~80% | Most common; highest rebleed risk; requires urgent neurosurgical intervention |
| Perimesencephalic (non-aneurysmal) | ~10% | Benign pattern on CT; venous origin; excellent prognosis |
| Arteriovenous malformation (AVM) | ~5% | More common in younger patients |
| Trauma | ~4% | History of head injury; different management |
| Other (vasculitis, tumour, cocaine) | ~1% | Rare; always consider in young patients |
Clinical Presentation
The Thunderclap Headache
The hallmark of SAH is the thunderclap headache — a sudden-onset, severe headache that reaches maximum intensity within seconds to minutes. Patients classically describe it as "the worst headache of my life" — a phrase you must take seriously every single time you hear it.
This headache is caused by sudden raised ICP and direct meningeal irritation from blood in the subarachnoid space. It is often occipital but can be global. Associated features include:
Classic Presenting Features
- Thunderclap headache — sudden onset, maximal within 60 seconds, severe
- Meningism — neck stiffness, photophobia, phonophobia (takes 6–12 hours to develop fully)
- Kernig's sign — inability to extend the knee when the hip is flexed at 90°
- Brudzinski's sign — involuntary flexion of the knees when the neck is flexed
- Loss of consciousness — occurs in ~50% at ictus due to sudden ICP spike
- Focal neurology — CN III palsy suggests posterior communicating artery aneurysm; focal deficits suggest intracerebral extension
- Subhyaloid haemorrhages — flame-shaped haemorrhages on fundoscopy, pathognomonic when present
"Worst headache of my life" = SAH until proven otherwise. Do not attribute it to tension headache, migraine, or hypertension without a CT head and — if CT is negative — a lumbar puncture. Missing SAH is one of the most litigated diagnoses in emergency medicine.
Grading Systems
Two grading systems are used routinely in SAH. Both predict prognosis and guide management decisions.
World Federation of Neurological Surgeons (WFNS) Grade — Clinical
| Grade | GCS | Motor Deficit | Prognosis |
|---|---|---|---|
| I | 15 | Absent | Excellent |
| II | 13–14 | Absent | Good |
| III | 13–14 | Present | Fair |
| IV | 7–12 | Present or absent | Poor |
| V | 3–6 | Present or absent | Very poor |
Fisher Grade — Radiological (CT findings)
| Grade | CT Appearance | Vasospasm Risk |
|---|---|---|
| 1 | No blood detected | Low |
| 2 | Diffuse thin SAH (<1mm) | Low |
| 3 | Localised clot or thick SAH (>1mm) | HIGH |
| 4 | Intracerebral or intraventricular blood | Low |
Our patient has GCS 13 with no motor deficit — WFNS Grade II. This is a good-grade SAH with a reasonable prognosis if managed promptly.
Investigation
Key Investigations
Investigation Checklist
- CT head (non-contrast): First-line. Blood appears hyperdense in the basal cisterns. Sensitivity ~98% within 6 hours, drops to ~90% at 24 hours.
- Lumbar puncture: If CT negative but suspicion high — must be done at least 12 hours after headache onset to allow xanthochromia to develop. Xanthochromia (yellow CSF on spectrophotometry) is diagnostic.
- CT Angiography (CTA): Once SAH confirmed — identifies aneurysm in ~90% of cases. Faster than formal angiography and widely available.
- Digital Subtraction Angiography (DSA): Gold standard for aneurysm characterisation — used when CTA is inconclusive or before endovascular treatment.
- Bloods: FBC, U&E, coagulation, group & save, glucose. ECG (SAH causes cardiac changes — tall T waves, prolonged QT).
Management
Immediate — First Hour
The priorities in the first hour are stabilisation, preventing rebleed, and urgent transfer to a neurosurgical unit.
Immediate Management
- Airway: Protect if GCS ≤8. Early intubation if deteriorating.
- Blood pressure: Target systolic <160 mmHg to reduce rebleed risk before aneurysm is secured. Avoid hypotension — maintains cerebral perfusion pressure.
- Analgesia: IV paracetamol and opioids for headache. Avoid NSAIDs (antiplatelet effect).
- Nimodipine: 60mg orally every 4 hours for 21 days — reduces cerebral vasospasm and improves neurological outcome. Start immediately.
- Strict bed rest: Minimise stimulation, dim lights, quiet environment.
- Neurosurgical referral: Urgent — all confirmed SAH needs specialist input.
- Avoid: Anticoagulants, antiplatelets, excessive IV fluids.
Definitive — Securing the Aneurysm
The most dangerous complication of aneurysmal SAH is rebleeding — which occurs in up to 15% within 24 hours and carries 70% mortality. The aneurysm must be secured as early as possible, ideally within 24–72 hours.
Two methods are used:
| Method | How | Best For | Trade-off |
|---|---|---|---|
| Endovascular coiling | Catheter through groin → coils packed into aneurysm sac → thrombosis | Most aneurysms — now preferred method globally | Higher recanalization rate; needs follow-up imaging |
| Surgical clipping | Craniotomy → titanium clip across aneurysm neck | Complex neck anatomy; MCA aneurysms; large haematoma needing evacuation | Higher surgical risk; more definitive long-term |
Complications to Watch For
The Major Complications
- Rebleeding (Day 0–3): Most lethal complication. Prevented by early aneurysm securing and blood pressure control. Presents as sudden deterioration in GCS.
- Cerebral vasospasm (Day 4–14): Delayed ischaemic neurological deficit from arterial spasm. Treat with nimodipine, maintain euvolaemia, consider endovascular intervention. Fisher Grade 3 = highest risk.
- Hydrocephalus (acute or delayed): Blood in CSF pathways obstructs drainage. Acute: external ventricular drain. Delayed: ventriculoperitoneal shunt.
- Hyponatraemia: From cerebral salt wasting or SIADH. Monitor sodium daily. Treat with careful fluid management — avoid fluid restriction.
- Seizures: Occur in ~10%. Prophylactic antiepileptics controversial — treat seizures if they occur.
- Cardiac complications: Neurogenic stunned myocardium, arrhythmias, ECG changes. Monitor with serial ECGs and troponin.
Our patient had an urgent CT head showing hyperdense blood in the basal cisterns — confirmed SAH. CT angiography identified a 7mm posterior communicating artery aneurysm. She was started on nimodipine, blood pressure controlled to systolic <160 mmHg, and transferred to the neurosurgical unit. She underwent successful endovascular coiling within 18 hours. At 3-month follow-up her GCS was 15 with no neurological deficit — an excellent outcome for WFNS Grade II SAH.
Summary — Key Points
1. Thunderclap headache = SAH until proven otherwise — never dismiss "worst headache of life."
2. CT head within 6 hours is 98% sensitive — if negative, LP at 12 hours looking for xanthochromia.
3. 80% caused by ruptured intracranial aneurysm — CTA to find the source.
4. Start nimodipine immediately — 60mg every 4 hours for 21 days — reduces vasospasm.
5. Secure the aneurysm within 24–72 hours — coiling preferred; clipping for complex anatomy.
6. Watch for the big four complications: rebleed, vasospasm, hydrocephalus, hyponatraemia.
References
- Connolly ES et al. Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage. Stroke. 2012;43(6):1711–1737.
- Steiner T et al. European Stroke Organization Guidelines for the Management of Intracranial Aneurysms and Subarachnoid Haemorrhage. Cerebrovasc Dis. 2013;35(2):93–112.
- van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid haemorrhage. Lancet. 2007;369(9558):306–318.
- Perry JJ et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage. BMJ. 2011;343:d4277.
- Molyneux AJ et al. International Subarachnoid Aneurysm Trial (ISAT). Lancet. 2002;360(9342):1267–1274.
