Subarachnoid Haemorrhage

Meet the patient

A 52-year-old woman lifting groceries at 4pm drops to her knees: a headache that went from nothing to "the worst pain of my life" inside a minute — occipital, radiating down the neck, with one vomit. She is alert but photophobic at 90 minutes; neck stiffness is not there yet, and that empty early exam is exactly the trap.[1][4]

The question that decides her next hour decides every SAH: is this the thunderclap I must not miss? A thunderclap headache is SAH until proven otherwise — CT first, LP if the scan is negative or stale, and secure the aneurysm before it re-ruptures. This topic is the ward-round answer to that patient.[1][11]

What SAH actually is — blood where CSF should be

SAH is blood in the wrong compartment, and it is a neurological emergency. Bleeding fills the subarachnoid space between the arachnoid and the pia — where CSF should circulate — and it is the third commonest stroke subtype after ischaemic stroke and intracerebral haemorrhage. It is only about 5 percent of strokes but a disproportionate share of stroke death and disability because it strikes younger people (mean age 50 to 55 years) and steals productive decades.[1][2]

The defining symptom is the thunderclap headache — maximum intensity within one minute. That single feature is the cornerstone of the disease: a thunderclap is SAH until proven otherwise. The discipline of the job is to take every sudden severe headache seriously, scan at once, and tap if the scan is negative or stale. The penalty for missing it is final — an unsecured aneurysm re-ruptures, and rebleeding carries about 70 percent mortality.[1][11]

Two parallel, clock-driven objectives govern everything that follows. First, prevent rebleeding by obliterating the aneurysm, ideally within 24 hours — the killer of the first day. Second, prevent delayed cerebral ischaemia, the vasospasm-driven injury of days 4 to 14 — the killer of the second week. Blood pressure control, nimodipine, ventricular drainage, and sodium correction all exist to serve these two objectives.[2][7]

Classification — cause, site, and severity

Three axes sort every SAH: what bled, where it bled, and how sick the patient looks. Together they set prognosis and treatment.[1]

By cause, aneurysmal rupture dominates — about 85 percent of spontaneous SAH. Perimesencephalic non-aneurysmal SAH (PNSAH) is roughly 10 percent and runs a strikingly benign course; extension of an intracerebral haemorrhage (hypertensive or AVM) into the ventricles and subarachnoid space makes up the rest.[1][2]

By site, saccular aneurysms arise at Circle of Willis bifurcations where the muscularis media and internal elastic lamina are naturally deficient. The anterior communicating artery (ACom) is the commonest at roughly 30 percent, then the internal carotid or posterior communicating artery (PCom) at 25 percent, the middle cerebral artery (MCA) bifurcation at 20 percent, and the basilar tip or vertebrobasilar circulation at 7 to 10 percent. The site predicts the deficit: a third-nerve palsy points to PCom, paraparesis and abulia to ACom, and a hemiparesis or aphasia to MCA.[1][6]

By severity, two scales are in routine use at the bedside. The Hunt and Hess grade (1968) is symptom-based; the WFNS grade (1988) is built on the GCS plus a motor deficit. Both predict outcome and are recorded at first contact and on any change. The Fisher scale grades the CT blood burden and predicts vasospasm — all three are reproduced verbatim in Investigations because examiners expect the components stated exactly.[6][10]

Who bleeds — epidemiology and the screenable risks

SAH is rarer than ischaemic stroke but kills a younger patient. Annual incidence is about 6 to 10 per 100,000, higher in Finland and Japan (around 20 per 100,000), and falling over recent decades as smoking drops, blood pressure improves, and unruptured aneurysms are found earlier. About 10 to 15 percent die before reaching hospital, and 30-day mortality is around 30 percent; a further 10 to 20 percent of survivors stay functionally dependent.[1][2]

The modifiable risks, in order of impact, are hypertension, smoking, alcohol, and sympathomimetics. Hypertension is the strongest; smoking is dose-dependent and synergistic with hypertension; cocaine and amphetamines produce acute blood-pressure surges that rupture the aneurysm in the moment.[1][6]

The non-modifiable and genetic risks are deliberately tested in exams. Age peaks at 40 to 60; female sex raises risk about 1.6-fold after 55; and two or more first-degree relatives with aneurysmal SAH confer a 2 to 4-fold risk and are an indication for screening.[1][7]

Autosomal dominant polycystic kidney disease (ADPKD) is the one to name first. About 5 to 10 percent of ADPKD patients harbour an intracranial aneurysm, and all ADPKD patients should be screened with MRA — as should anyone with two or more first-degree relatives who have bled. The vascular type of Ehlers-Danlos (type IV, type III collagen), Marfan (fibrillin-1), neurofibromatosis type 1, and fibromuscular dysplasia all weaken the arterial wall and belong on the same list.[1][7]

For an incidental unruptured aneurysm, rupture risk tracks size, site, and shape. Small (under 7 mm) anterior-circulation aneurysms in a patient without prior SAH carry a low annual risk; larger aneurysms, posterior-circulation sites (especially PCom and basilar tip), symptomatic aneurysms, and those with a daughter lobe or documented growth carry higher risks that warrant repair.[6][7]

Why the aneurysm ruptures — pathophysiology in four moves

A berry aneurysm is a wall defect at a bifurcation, polished open by years of haemodynamic load. At Circle of Willis apices the muscularis media and internal elastic lamina are physiologically deficient, so the intima carries the full wall stress. Sustained shear injures the endothelium, fragments the elastic lamina, depletes smooth muscle, and the intima bulges into a saccular pouch — often with a narrow neck and an asymmetric daughter sac that is the usual point of rupture.[1]

Rupture happens during a transient blood-pressure surge — exertion, straining, coitus, emotional stress. Blood leaves the aneurysm under systemic arterial pressure into the subarachnoid space, and three things follow in seconds.[1]

First, intracranial pressure spikes — often approaching diastolic blood pressure — so cerebral perfusion pressure (CPP equals MAP minus ICP) collapses, producing the brief loss of consciousness at the moment of rupture. Second, blood irritates the meninges, generating neck stiffness, photophobia, and a positive Kernig sign over the following hours. Third, a massive catecholamine surge stuns the myocardium — troponin rises, the QT prolongs, and the ECG shows the diffuse T-wave inversion called "cerebral T waves".[2][11]

The most consequential secondary event is delayed cerebral ischaemia (DCI), days 4 to 14, peak 7 to 8. It is the leading cause of preventable death and disability. Breakdown of subarachnoid blood releases oxyhaemoglobin, which depletes nitric oxide, releases the vasoconstrictor endothelin-1, generates free radicals, and activates protein kinase C — together producing sustained large-vessel vasospasm (visible on angiography in 30 to 70 percent, peaking at days 7 to 8). Vasospasm alone does not explain DCI: microvascular dysfunction, cortical spreading depolarisations, microthrombosis, and autoregulatory failure all contribute.[2][11]

Two further complications flow straight from the bleed. Hydrocephalus arises because blood blocks CSF reabsorption at the arachnoid granulations (a communicating hydrocephalus) or because intraventricular clot obstructs the aqueduct or fourth ventricle (an obstructive hydrocephalus). Hyponatraemia in roughly 30 to 40 percent is most often cerebral salt wasting — natriuretic-peptide-driven volume depletion with high urine sodium — rather than SIADH, and that distinction is one of the most heavily examined points in the disease.[2][11]

The thunderclap at the bedside — clinical presentation

The cardinal symptom is the thunderclap: sudden onset, maximum intensity within one minute. Patients reach for the same words — "the worst headache of my life", "like being kicked in the back of the head", "an explosion". It is classically occipital or suboccipital but may be diffuse, and it persists for hours to days. Reported by 75 to 95 percent, it is the single most important symptom in medicine to take seriously: no thunderclap may be dismissed as migraine without excluding SAH.[1][4]

The classic trap: neck stiffness is absent in the first hour. Meningism — neck stiffness, photophobia, positive Kernig and Brudzinski — appears only at 3 to 12 hours as blood irritates the meninges. A thunderclap with a soft neck at 90 minutes is still SAH until excluded; the empty early exam is the danger. Nausea and vomiting (about 75 percent, sometimes projectile at onset), a brief loss of consciousness at the moment of rupture (about half, from the ICP surge), and seizures at onset (10 to 20 percent, from cortical irritation) round out the acute picture.[1][11]

Focal deficits localise the aneurysm. A third-nerve palsy — ptosis, a dilated pupil, the eye deviated "down and out" — indicates a PCom aneurysm compressing the oculomotor nerve. Lower-limb-dominant weakness and abulia point to ACom; a hemiparesis or aphasia to MCA.[1][6]

Two atypical presentations are examined deliberately because they are missed. The sentinel (warning) bleed is a minor leak days to weeks before the catastrophic rupture, presenting as a sudden but resolving headache — missed in about half of cases and dismissed as migraine; recognising it lets you intervene before the major rupture. Terson syndrome — vitreous or preretinal haemorrhage on fundoscopy from ICP transmitted along the optic nerve sheath — occurs in 15 to 20 percent, signals a larger bleed and a worse prognosis: always examine the fundi in any thunderclap headache.[1][11]

In the elderly the headache may be muted or absent — the patient presents with confusion, a fall, or coma after a collapse, and the trap is to call it a simple fall. In pregnancy and the puerperium SAH is a leading non-obstetric cause of maternal death; any thunderclap in pregnancy is SAH (alongside pre-eclampsia, HELLP, and cerebral venous sinus thrombosis) until proven otherwise.[2]

The mimics — exclude SAH first, then name the rest

The job is not to name the mimic; it is to exclude SAH first. Any headache that is sudden, maximal within a minute, exertional, "worst ever", or paired with neck stiffness, vomiting, loss of consciousness or a focal deficit — in anyone over 40, pregnant, or anticoagulated — mandates CT and LP if needed.[1][5]

Which single feature most reliably separates SAH from its mimics?

The tempo of onset. SAH reaches maximum intensity within one minute; migraine builds over minutes to hours; meningitis evolves over hours; thunderclap headache of any cause (SAH included) shares the sudden onset — which is why primary thunderclap headache is a diagnosis of exclusion only after CT ± LP have excluded SAH.[1][4]

The ward-round assessment — onset time, GCS, fundi

The onset-to-peak time is the single most discriminating historical detail. A focused assessment combines a precise history of onset, vital signs, the GCS, meningeal signs, a cranial-nerve and focal exam, and fundoscopy. A thunderclap maximal within one minute is SAH until excluded regardless of the rest of the exam.[1][5]

Record the GCS at first contact and repeat it often — a drop of one point mandates urgent reassessment and CT. It is the cornerstone of WFNS grading and ongoing monitoring. Vital signs typically show acute hypertension from the sympathetic surge (which does not by itself mean chronic hypertension). Meningeal signs appear from 3 to 12 hours and may be absent early. Fundoscopy checks for Terson syndrome and the papilloedema of raised ICP.[1]

The Ottawa SAH Rule is the rule-OUT decision aid for the alert, neurologically intact patient. It guides imaging in patients whose non-traumatic headache peaked within one hour, and it is used to decide who does and does not need a CT.[5]

Severity is graded at the bedside with Hunt and Hess and WFNS (reproduced in Investigations), and the general exam hunts for the complications as they arise: hydrocephalus (depressed consciousness with rising BP and falling heart rate — the Cushing response), rebleeding (sudden deterioration), and vasospasm (a new focal deficit or confusion at days 4 to 14).[6][10]

Investigations — CT, LP, CTA, DSA

First test — non-contrast CT brain

The non-contrast CT brain is the first and most important investigation. Performed within 6 hours of onset on a modern third-generation scanner it has a sensitivity of about 100 percent (95 percent confidence interval 97 to 100) — supporting a CT-first approach without mandatory LP when the scan is that early.[4]

The blood of SAH lies in the basal cisterns, the Sylvian fissure, the interhemispheric fissure, and the cortical sulci as hyperdense material. The CT also shows intracerebral or intraventricular extension, hydrocephalus, mass effect, and often the aneurysm's location from the blood pattern. Because CT sensitivity falls steeply with time — about 85 percent at 24 hours, 50 percent at one week, 30 percent at two weeks — a negative CT done more than 6 hours after onset does not exclude SAH; the next step is a lumbar puncture.[1][4]

Lumbar puncture — xanthochromia

The LP is done when the CT is negative but suspicion persists — ideally at 6 to 12 hours, preferably 12. The delay lets red-cell lysis generate bilirubin. Opening pressure is raised. The decisive finding is xanthochromia — a yellow CSF supernatant from bilirubin, the in-vivo breakdown product of haemoglobin, absent in a traumatic tap (where the supernatant stays colourless). Xanthochromia appears from about 12 hours, peaks at 48 hours, persists about two weeks, and is best confirmed by spectrophotometry. Comparing red cells in the first and third bottles helps tell true SAH (similar counts) from a traumatic tap (falling counts).[1][4]

Why does xanthochromia take hours to appear — and why is a 'blood-stained' CSF not enough?

Because bilirubin is generated by red-cell lysis in vivo, which takes several hours after the bleed. A blood-stained CSF sampled immediately could be a traumatic tap (the needle hitting a vessel). The yellow supernatant (bilirubin) — confirmed by spectrophotometry, and stable from 12 hours to about 2 weeks — is the signature of true SAH.[1]

Vessel imaging — CTA and DSA

Once SAH is confirmed, CT angiography is the next step. CTA identifies the aneurysm — size, neck, location — and guides coiling versus clipping, with 95 to 98 percent sensitivity for aneurysms over 3 mm. Digital subtraction angiography (DSA) remains the gold standard (about 99 percent) and is reserved for a negative or inconclusive CTA where the blood pattern still suggests an aneurysm, and for planning and performing endovascular treatment. A perimesencephalic non-aneurysmal SAH is confirmed by a negative DSA in the characteristic CT pattern.[1][6]

[1]

Severity scales reproduced verbatim

The named scales are reproduced exactly as examiners expect them. Hunt and Hess (1968) and WFNS (1988) grade clinical severity and predict outcome; the Fisher scale grades the CT blood burden and predicts vasospasm.[6][10]

Hunt and Hess grade (I–V): [1]

WFNS grade (based on GCS and motor deficit): [1]

Fisher scale (CT blood burden): [1]

Bloods and surveillance

Bloods, troponin, ECG, and transcranial Doppler are the surveillance backbone. Full blood count, urea and electrolytes (watch the sodium), coagulation, glucose, liver function, and group-and-save or crossmatch. Troponin and an ECG detect the neurogenic stunned myocardium — a troponin rise with QT prolongation and the "cerebral T waves" of diffuse T-wave inversion. Transcranial Doppler from about day 3: a rising middle cerebral artery velocity (over 120 cm/s, or a Lindegaard ratio above 3 to separate vasospasm from hyperaemia) heralds vasospasm. EEG is reserved for suspected seizures or unexplained depressed consciousness.[2][11]

The first hour — the resuscitation bundle

[1]

Resuscitation follows ABCDE with two parallel time-critical objectives: prevent rebleeding (the killer of the first 24 hours) and prevent DCI (the killer of days 4 to 14). Protect the airway in the comatose patient — intubate and ventilate if the GCS is 8 or lower — give oxygen to keep the saturation at or above 94 percent, and avoid both hypotension and hypoxia, which worsen secondary brain injury.[6][11]

[1]

Blood pressure before the aneurysm is secured lowers rebleed risk without sacrificing perfusion. A common target is a systolic blood pressure below 160 mmHg (or a mean arterial pressure below 110) with a titratable agent. After the aneurysm is secured the target is liberalised to maintain perfusion, and may be raised deliberately if vasospasm develops.[6][7]

The four pillars of definitive management

Definitive management stands on four pillars: secure the aneurysm, nimodipine, hydrocephalus and raised ICP, and systemic complications. The first two fight rebleeding and DCI directly; the last two keep the brain alive long enough for the drugs and the clip to work.[6][7]

Pillar 1 — secure the aneurysm

Obliterate the aneurysm ideally within 24 hours, by coiling or clipping. Endovascular coiling packs the aneurysm with detachable platinum coils delivered by catheter angiography; surgical clipping places a clip across the neck at craniotomy. The landmark International Subarachnoid Aneurysm Trial (ISAT) made coiling the preferred treatment for aneurysms suitable for either approach.[3][6]

Anatomy, patient, and local expertise choose the technique. MCA bifurcation and wide-necked aneurysms often favour clipping; posterior circulation and elderly patients favour coiling. Flow-diverting stents suit complex aneurysms. Until the aneurysm is secured the patient stays at high rebleeding risk — and rebleeding carries about 70 percent mortality — hence the urgency.[3][11]

Pillar 2 — nimodipine, the only drug that works

Nimodipine is the only drug proven to improve outcome after SAH. A dihydropyridine calcium-channel blocker, it is given to all patients with aneurysmal SAH regardless of grade — 60 mg orally (or via nasogastric tube) every 4 hours for 21 days, started within 4 days of the bleed.[8][9]

[1]

The named trap: giving the full 21 days is non-negotiable. The benefit is neuroprotection, not angiographic spasm reversal — so do not stop early because the patient looks well, and do not be swayed by the negative trials. Magnesium (MASH-II) and simvastatin (STASH) both failed to improve outcome — nimodipine remains the only proven pharmacotherapy.[9]

Pillar 3 — hydrocephalus and raised ICP

An EVD is inserted for acute obstructive hydrocephalus, intraventricular blood blocking CSF flow, or deteriorating consciousness with ventriculomegaly. A lumbar drain or serial LPs may be used for communicating hydrocephalus, and about 10 to 20 percent develop chronic symptomatic hydrocephalus needing a ventriculoperitoneal (VP) shunt. General ICP measures — head of bed 30 degrees, normocapnia, sedation, osmotic therapy (mannitol or hypertonic saline) — run in parallel.[6][11]

Pillar 4 — systemic complications

Keep the brain out of trouble while it recovers. DVT prophylaxis begins with compression stockings, with low-molecular-weight heparin added after the aneurysm is secured (typically more than 24 hours after). Normoglycaemia, normothermia, and treating anaemia (transfusion threshold generally a haemoglobin of 80 to 90 g/L) each matter — hyperglycaemia, fever, and anaemia are independently linked to poor outcome. Early enteral nutrition and stress-ulcer prophylaxis complete the bundle.[2][11]

Treating vasospasm when it occurs

When DCI strikes at days 4 to 14, restore cerebral perfusion — but only after the aneurysm is secured. Modern euvolaemic hypertensive therapy maintains euvolaemia and induces hypertension (raising the systolic BP to 160 to 200 mmHg with vasopressors such as noradrenaline). Raising the pressure against an unsecured aneurysm invites rebleeding. This replaced the older "triple-H" therapy (hypervolaemia, haemodilution, hypertension), which caused pulmonary oedema, hyponatraemia, and haemorrhage. Refractory cases move to intra-arterial vasodilators (milrinone, verapamil) or balloon angioplasty.[2][7]

Subtypes and scenarios that change the plan

Perimesencephalic non-aneurysmal SAH is the exception examiners love — the SAH that is not dangerous. Blood is confined to the perimesencephalic and prepontine cisterns, no aneurysm is found on DSA, the patient is usually well, and the outcome is excellent with vasospasm rare; nimodipine is often still given for caution. At the other extreme, high-grade SAH (WFNS IV to V) was once treated palliatively, but modern series show aggressive early management secures functional independence in a meaningful proportion of survivors — justify maximal initial therapy before any limitation decision.[2][10]

Complications by clock — the timeline that runs SAH

The complications follow a predictable timeline, and recognising them is the core of neurocritical care. Rebleeding owns the first day, early brain injury and hydrocephalus the next three, vasospasm the second week, and chronic hydrocephalus with cognitive and mood sequelae the months that follow.[1]

[1]

The sodium trap — cerebral salt wasting versus SIADH

The classic trap: never fluid restrict hyponatraemia after SAH — it is cerebral salt wasting. Low sodium after SAH is most often cerebral salt wasting, a volume-depleted state driven by natriuretic-peptide release — not SIADH, which is volume-replete or expanded. The two are separated by volume status, and the treatment diverges: fluid restriction (right for SIADH) is dangerous in cerebral salt wasting because it worsens hypovolaemia, provokes vasospasm, and threatens cerebral ischaemia.[2][11]

[1]

How SAH patients die — the preventable list

Five errors account for most preventable deaths, and each is examinable. Name them in the order a patient is harmed.[1][11]

• Dismissing a thunderclap as migraine — the cardinal error; the headache that is "first or worst" is SAH until excluded.
• No LP after a negative CT done more than 6 hours after onset — the CT sensitivity has already fallen; only xanthochromia closes the gap.
• Fluid restricting the hyponatraemia — cerebral salt wasting worsens into vasospasm and cerebral ischaemia.
• Not giving the full 21 days of nimodipine — the only drug that works, stopped early.
• Attributing early deterioration to "expected" decline — when the real cause is rebleeding, hydrocephalus, or vasospasm, each mandating an urgent CT.[1][4][9][11]

Prognosis and disposition

About 10 to 15 percent die before reaching hospital, and 30-day mortality is around 30 percent. A further 10 to 20 percent of survivors stay functionally dependent. Outcomes have improved over decades with better diagnosis, early aneurysm repair, nimodipine, and centralised neurocritical care.[1][2]

Poor outcome is predicted by a high clinical grade (Hunt and Hess or WFNS IV to V), older age, a large aneurysm (over 10 mm), a posterior-circulation site, rebleeding, intraventricular blood or hydrocephalus, a thick subarachnoid clot (high Fisher), symptomatic vasospasm, hyperglycaemia, fever, anaemia, and hypotension. Good outcome is predicted by a low WFNS grade (I to II), a small aneurysm, an anterior-circulation site, early securing, no vasospasm, younger age, and management in a high-volume centre.[6][10]

Vasospasm and DCI are the leading cause of preventable death and disability — which is why nimodipine prophylaxis and vigilant surveillance through days 4 to 14 are non-negotiable. Even patients judged to have a "good outcome" often carry subtle cognitive deficits (attention, executive function, processing speed), fatigue, and depression — only about 30 to 50 percent return to their previous work without restriction. Perimesencephalic non-aneurysmal SAH is the exception, with vasospasm rare and prognosis excellent.[2]

Disposition is a neurosciences ICU through days 0 to 14 (the vasospasm window), then a step-down ward and rehabilitation, with outpatient follow-up for cognition and mood and surveillance angiography for coiled aneurysms (slightly higher late rebleed risk, may recur).[3][7]

Special populations

Pregnancy and the puerperium — a thunderclap is SAH until excluded. SAH is a leading non-obstetric cause of maternal death; the differential is pre-eclampsia, HELLP, and cerebral venous sinus thrombosis. Management is multidisciplinary; coiling is preferred where feasible (avoids craniotomy), nimodipine is given (the maternal vasospasm risk outweighs theoretical teratogenicity), and excessive blood-pressure drops are avoided.[2]

The elderly present atypically — confusion, a fall, less prominent headache — and have higher complication rates. Coiling is preferred when feasible, outcomes are worse, but age alone does not justify withholding aggressive therapy.[1]

The anticoagulated patient has a higher rebleeding risk and worse outcome — reverse urgently as part of resuscitation: prothrombin complex concentrate plus vitamin K for warfarin, idarucizumab for dabigatran, andexanet alfa for anti-Xa DOACs.[1]

ADPKD — screen all with MRA; two or more first-degree relatives with SAH is also a screening indication. Marfan syndrome, the vascular type of Ehlers-Danlos (type IV), neurofibromatosis type 1, and fibromuscular dysplasia round out the associations.[1][7]

Incidental unruptured aneurysms are managed by size, site, and patient factors. Small (under 7 mm) anterior-circulation aneurysms in a patient without prior SAH carry a low annual rupture risk and may be observed; larger, posterior-circulation, symptomatic, or growing aneurysms warrant repair.[6]

The evidence — the trials that built the pathway

Three landmark contributions anchor the evidence base. ISAT (Molyneux 2002) made coiling the preferred treatment for aneurysms suitable for both techniques. The nimodipine story begins with Allen (1983) and is consolidated by the Dorhout Mees Cochrane review (2007), which confirmed oral nimodipine reduces poor outcome with a relative risk of 0.67 and a number-needed-to-treat of about 19 — making nimodipine the only drug proven to improve outcome after SAH.[3][8][9]

[1]

The diagnostic evidence is Perry's. Perry (2011, BMJ) showed modern CT within 6 hours of onset has about 100 percent sensitivity; Perry (2017, CMAJ) validated the Ottawa SAH Rule (sensitivity about 100 percent) for ruling out SAH in alert, neurologically intact patients.[4][5]

The guidelines are the AHA/ASA Connolly 2012 guideline, now superseded by the AHA/ASA Hoh 2023 guideline — the current framework endorsing early aneurysm repair, oral nimodipine, euvolaemic hypertensive therapy for DCI, and centralisation to high-volume centres.[6][7]

The negative trials matter because examiners test them. MASH-II (Dorhout Mees 2012) showed magnesium sulphate did not improve outcome; STASH (Kirkman 2014) showed simvastatin did not improve outcome. Both remind you that, despite decades of trials, nimodipine is the only pharmacotherapy proven to help.[9]

The mantra, and the exam pearls

Hold three things and every SAH answer slots into place: the thunderclap, the CT-then-LP rule, and the four pillars. The mnemonic and the recap below are the last-minute viva armoury.[1]

[1]

The mantra: Thunderclap is SAH until proven otherwise — CT first, LP if negative; secure the aneurysm early, nimodipine for 21 days, never restrict fluids.[1][8][11]

Exam application bank (NEET-PG / INICET)

One-line answer

Subarachnoid haemorrhage is bleeding into the subarachnoid space, usually from a ruptured intracranial aneurysm (85 percent), presenting with a thunderclap headache (maximal within 1 minute) with neck stiffness, photophobia, vomiting, depressed consciousness and sometimes seizures. Diagnose with CT brain (about 100 percent sensitive within 6 hours); if the CT is negative or over 6 hours old, LP for xanthochromia. Secure the aneurysm within 24 hours (coiling preferred over clipping, ISAT), give nimodipine 60 mg every 4 hours for 21 days, and never fluid restrict the hyponatraemia — it is cerebral salt wasting.[1][4][3]

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Name the defining symptom and its time criterion, the first investigation, and the first treatment step with dose and route.[1]

Stem 2 — Unstable or complicated. List the red flags that force immediate resuscitation, imaging, theatre, or ICU — and what you do in the first 15 minutes.[6]

Stem 3 — Atypical group. Elderly, pregnant, anticoagulated: how the presentation and the thresholds change, and what you must not miss.[2]

Stem 4 — Differential trap. Name the three closest mimics of a thunderclap and one discriminator for each.[1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU or ICU or theatre, and what follow-up is mandatory.[7]

Rapid viva checklist

1. Definition and classification
2. Pathophysiology chain
3. Bedside signs and criteria
4. Score with exact components (Hunt and Hess, WFNS, Fisher)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline or trial name if classic
10. Three exam traps[1]

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG or INICET questions on subarachnoid haemorrhage.[1]

Ward-round test — three stems, thirty seconds each

Stem 1 — the thunderclap sent home (answer)

A 48-year-old man presents an hour after a sudden occipital "explosion" headache, maximal within a minute, with one vomit. The CT at 90 minutes is reported as normal; he is discharged as a migraine. He collapses at home 10 hours later — a rebleed. What was missed, and what should have happened? Model: A thunderclap headache is SAH until proven otherwise. A CT done within 6 hours on a modern scanner is about 100 percent sensitive — but the discipline is to finish the work-up: when the CT is negative but suspicion persists, or the CT is more than 6 hours old, perform an LP for xanthochromia (bilirubin, from 12 hours, peaks at 48 hours, lasts about 2 weeks) before discharge. Discharging a thunderclap as migraine without an LP is the cardinal preventable error; the unsecured aneurysm then re-ruptures, and rebleeding carries about 70 percent mortality.[1][4][11]

Stem 2 — day 7, new weakness and low sodium (answer)

Seven days after a coiled anterior communicating aneurysm, the patient develops a right hemiparesis and confusion; sodium is 128 mmol/L with high urine sodium and signs of volume depletion. The nurse has started fluid restriction. Two questions: what is the neurological event, and what is wrong with the sodium plan? Model: The neurological event is delayed cerebral ischaemia from vasospasm — days 4 to 14, peak 7 to 8, the leading cause of preventable death and disability. The aneurysm is secured, so treat with euvolaemic hypertensive therapy (induce systolic BP 160 to 200 mmHg with noradrenaline) and ensure nimodipine is running for the full 21 days. The sodium plan is wrong: hyponatraemia after SAH is usually cerebral salt wasting (hypovolaemic), not SIADH — fluid restriction is dangerous, worsens vasospasm, and threatens cerebral ischaemia. Give hypertonic saline with volume replacement, consider fludrocortisone, and distinguish the two by volume status.[2][7][11]

Stem 3 — CT negative at 18 hours (answer)

A 35-year-old has a thunderclap headache maximal within one minute. The non-contrast CT at 18 hours is normal. The registrar wants to discharge with analgesia. What is the next step, and why? Model: Do not discharge. CT sensitivity falls steeply with time — about 85 percent at 24 hours, 50 percent at one week — so a normal CT at 18 hours does not exclude SAH. The next step is a lumbar puncture for xanthochromia: a yellow CSF supernatant from bilirubin (generated in vivo by red-cell lysis, confirmed by spectrophotometry, present from 12 hours to about 2 weeks), with a raised opening pressure. A traumatic tap leaves a colourless supernatant and falling red-cell counts between bottles. Only a negative LP at the right interval closes the case.[1][4]

References

1. [1]Macdonald RL, Schweizer TA. Spontaneous subarachnoid haemorrhage Lancet, 2017.PMID 27637674
2. [2]Claassen J, Park S. Spontaneous subarachnoid haemorrhage Lancet, 2022.PMID 35985353
3. [3]Molyneux A, Kerr R, Stratton I, et al. International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised trial Lancet, 2002.PMID 12414200
4. [4]Perry JJ, Stiell IG, Sivilotti ML, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study BMJ, 2011.PMID 21768192
5. [5]Perry JJ, Sivilotti MLA, Sutherland J, et al. Validation of the Ottawa Subarachnoid Hemorrhage Rule in patients with acute headache CMAJ, 2017.PMID 29133539
6. [6]Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association Stroke, 2012.PMID 22556195
7. [7]Hoh BL, Ko NU, Amin-Hanjani S, et al. 2023 Guideline for the Management of Patients With Aneurysmal Subarachnoid Hemorrhage: A Guideline From the American Heart Association/American Stroke Association Stroke, 2023.PMID 37212182
8. [8]Allen GS, Ahn HS, Preziosi TJ, et al. Cerebral arterial spasm--a controlled trial of nimodipine in patients with subarachnoid hemorrhage N Engl J Med, 1983.PMID 6338383
9. [9]Dorhout Mees SM, Rinkel GJ, Feigin VL, et al. Calcium antagonists for aneurysmal subarachnoid haemorrhage Cochrane Database Syst Rev, 2007.PMID 17636626
10. [10]Ironside N, Buell TJ, Chen CJ, et al. High-Grade Aneurysmal Subarachnoid Hemorrhage: Predictors of Functional Outcome World Neurosurg, 2019.PMID 30735864
11. [11]Busl KM, Bogossian EG, Claassen J, et al. Beyond the bleed: complications after aneurysmal subarachnoid hemorrhage. Pathophysiology, clinical implications, and management strategies: a review Crit Care, 2025.PMID 41029753