Overview
Subarachnoid Haemorrhage (SAH)
1. Clinical Overview
Summary
Subarachnoid haemorrhage (SAH) is bleeding into the subarachnoid space between the arachnoid and pia mater, most commonly caused by rupture of an intracranial aneurysm. It represents a neurological emergency with mortality of 30-50% and significant morbidity in survivors. The classic presentation is a thunderclap headache - the "worst headache of my life" reaching maximum intensity within seconds. [1,2]
Key Facts
- Incidence: 6-10 per 100,000 per year. Higher in Finland and Japan (approximately 20/100,000). [3]
- Peak Age: 50-60 years. Female predominance (1.6:1).
- Cause: Ruptured intracranial aneurysm (85%), Non-aneurysmal perimesencephalic (10%), Other (5%).
- Mortality: 30% pre-hospital, 50% at 30 days, 50% of survivors have permanent disability.
- Re-bleeding: 4% in first 24 hours, highest risk in first 6 hours.
- The Golden Window: Urgent diagnosis and treatment within 24 hours dramatically improves outcomes.
Clinical Pearls
The "Sentinel Headache": 30-50% of patients report a warning headache 2-8 weeks before major rupture. This represents minor leak (sentinel bleed) - often dismissed as migraine or tension headache. Missing this costs lives.
CT Sensitivity Declines Rapidly: CT sensitivity is 98% at 6 hours but drops to 50% by day 5. If clinical suspicion is high and CT is negative, lumbar puncture is MANDATORY. [4]
"The Worst Headache of My Life": This phrase should trigger immediate investigation for SAH. Absence of typical features does not exclude the diagnosis.
Nimodipine is NOT Neuroprotective: Nimodipine does not prevent vasospasm; it reduces ischaemic neurological deficit. The exact mechanism remains debated.
2. Epidemiology
Incidence and Demographics
- Global Incidence: 6-10 per 100,000 per year (Western countries).
- High-Incidence Regions: Finland (approximately 22/100,000), Japan (approximately 23/100,000).
- Sex Distribution: Female to male ratio 1.6:1.
- Age: Peak incidence 50-60 years; rare below 20 years.
- Seasonality: Slight increase in winter months (blood pressure variation).
Risk Factors with Relative Risk
| Risk Factor | Relative Risk | Modifiable? |
|---|---|---|
| Hypertension | 2.5x | Yes |
| Current Smoking | 3-4x | Yes |
| Excessive Alcohol | 2x (greater than 150g/week) | Yes |
| Family History (First-Degree) | 3-7x | No |
| Cocaine/Amphetamine Use | 5-10x | Yes |
| Autosomal Dominant PKD | 4-5x | No |
| Ehlers-Danlos Type IV | Increased | No |
| Fibromuscular Dysplasia | Increased | No |
| Previous SAH | 11x | No |
Aneurysm Prevalence
- Incidental Aneurysms: 2-3% of general population.
- Rupture Risk: 0.5-1% per year for most aneurysms; higher for larger aneurysms and posterior circulation.
- Most Common Locations: Anterior communicating artery (30%), Posterior communicating artery (25%), Middle cerebral artery (20%).
3. Pathophysiology
Step 1: Aneurysm Formation
- Hemodynamic Stress: Arterial bifurcations experience high wall shear stress.
- Structural Weakness: Deficiency in tunica media and internal elastic lamina.
- Risk Factors: Hypertension, smoking cause endothelial dysfunction and weakening.
- Growth: Progressive outpouching of vessel wall creating saccular (berry) aneurysm.
Step 2: Aneurysm Rupture
- Trigger: Often during physical exertion, straining, sexual intercourse.
- Hemodynamic Surge: Sudden blood pressure spike causes wall rupture at weakest point (dome).
- Blood Under Pressure: Arterial blood at 80-120 mmHg floods the subarachnoid space.
Step 3: Acute Phase (Minutes to Hours)
- Intracranial Pressure (ICP): Explosive rise in ICP approaching arterial pressure.
- Cerebral Perfusion: CPP = MAP - ICP. Brief global ischaemia causes loss of consciousness.
- Meningeal Irritation: Blood irritates meninges causing headache and neck stiffness.
- Clot Formation: Natural haemostasis may seal the rupture.
Step 4: Early Brain Injury (First 72 Hours)
- Oxidative Stress: Breakdown products of blood (iron, haemoglobin) cause free radical damage.
- Inflammation: Microglial activation and cytokine release.
- Blood-Brain Barrier Disruption: Oedema and further injury.
- Microvascular Dysfunction: Early contributor to poor outcomes.
Step 5: Delayed Cerebral Ischaemia (Days 3-14)
- Vasospasm: Arterial narrowing visible on angiography (approximately 70% of patients).
- Delayed Cerebral Ischaemia (DCI): Clinical deterioration from ischaemia (approximately 30%).
- Mechanism: Not simply mechanical spasm; includes microvascular dysfunction, cortical spreading depolarisation.
- Peak Risk: Days 7-10 post-bleed.
Step 6: Hydrocephalus Development
- Acute (10-30%): Blood clots obstruct CSF pathways; requires emergency EVD.
- Chronic (15-20%): Impaired CSF absorption at arachnoid granulations; may need VP shunt.
4. Clinical Presentation
Classic Presentation: Thunderclap Headache
Definition: Sudden-onset severe headache reaching maximum intensity within seconds to 5 minutes.
Symptoms by Frequency
| Symptom | Frequency | Mechanism |
|---|---|---|
| Thunderclap headache | 85-95% | Meningeal irritation |
| Nausea/Vomiting | 70-80% | ICP elevation, meningeal irritation |
| Loss of consciousness | 50% | Global cerebral hypoperfusion |
| Neck stiffness | 50-75% (delayed hours) | Meningism |
| Photophobia | 30-40% | Meningeal irritation |
| Seizure | 5-10% | Cortical irritation |
| Focal neurological deficit | 15-30% | Mass effect, ischaemia |
Atypical Presentations - The Diagnostic Traps
"Minor SAH": Some patients present with less severe headache (still different from usual). Sentinel bleeds are easily missed.
Red Flags - "The Don't Miss" Signs
- Thunderclap headache - SAH until proven otherwise.
- Any sudden severe headache unlike previous headaches.
- Headache with loss of consciousness - even if brief.
- Headache with neck stiffness - develops over hours.
- Headache with third nerve palsy (ptosis, dilated pupil) - PComA aneurysm.
- New headache in polycystic kidney disease patient.
- Headache triggered by exertion, sex, or straining.
Description
"Like being hit on the head with a bat", "Worst headache of my life", "Something popped in my head".
Location
Often occipital or generalised; may localise to aneurysm site.
Onset
During physical exertion (30-50%), at rest, during sex, straining, coughing.
5. Clinical Examination
Initial Assessment (ABCDE Approach)
Airway
- Protect airway if GCS 8 or below; intubate early.
Breathing
- Neurogenic pulmonary oedema in severe SAH.
Circulation
- Hypertension common (stress response); hypotension suggests severe injury.
Disability
- GCS score (critical for grading).
- Pupil response (third nerve palsy suggests PComA aneurysm).
- Focal neurological signs.
Clinical Grading Scales
World Federation of Neurosurgical Societies (WFNS) Grade
| Grade | GCS | Motor Deficit | Mortality |
|---|---|---|---|
| I | 15 | Absent | 5% |
| II | 13-14 | Absent | 9% |
| III | 13-14 | Present | 20% |
| IV | 7-12 | Present/Absent | 33% |
| V | 3-6 | Present/Absent | 70% |
Hunt and Hess Grade
| Grade | Clinical Features | Mortality |
|---|---|---|
| 1 | Asymptomatic or mild headache | 1% |
| 2 | Severe headache, neck stiffness, no deficit | 5% |
| 3 | Drowsy, confusion, mild deficit | 19% |
| 4 | Stupor, moderate-severe deficit | 42% |
| 5 | Deep coma, decerebrate | 77% |
Specific Signs
| Sign | Finding | Significance |
|---|---|---|
| Meningism | Neck stiffness, Kernig's, Brudzinski's | Blood irritating meninges |
| Subhyaloid haemorrhages | Blood tracking into eye (Terson syndrome) | High ICP, worse prognosis |
| Third nerve palsy | Ptosis, "down and out" pupil dilated | PComA aneurysm |
| Sixth nerve palsy | Abduction deficit | Raised ICP (false localising) |
| Papilloedema | Swollen disc | Raised ICP |
6. Investigations
Diagnostic Algorithm
THUNDERCLAP HEADACHE SUSPECTED SAH
↓
┌───────────────────────────────────────────┐
│ IMMEDIATE NON-CONTRAST CT HEAD │
│ (Sensitivity 98% within 6 hours) │
└───────────────────────────────────────────┘
↓
┌───────┴───────┐
↓ ↓
CT POSITIVE CT NEGATIVE
↓ ↓
SAH CONFIRMED LUMBAR PUNCTURE
↓ (After 12 hours post-onset)
CT Angiography ↓
┌─────┴─────┐
↓ ↓
Xanthochromia Negative
POSITIVE ↓
↓ Consider
SAH CONFIRMED alternatives
CT Head Without Contrast
- Timing Critical: 98% sensitive at less than 6 hours, 93% at 24 hours, 50% at 5 days. [5]
- Findings:
- Hyperdense blood in basal cisterns (star sign).
- Sylvian fissure blood (MCA aneurysm).
- Interhemispheric fissure (ACA/AComA aneurysm).
- Intraventricular blood (poorer prognosis).
- Modified Fisher Grade: Predicts vasospasm risk based on blood distribution.
Lumbar Puncture
- Indication: CT negative but clinical suspicion remains high.
- Timing: Wait until greater than 12 hours post-onset (time for xanthochromia to develop).
- Opening Pressure: Often elevated.
- CSF Analysis:
| Finding | SAH | Traumatic Tap |
|---|---|---|
| Red cells | Equal across 3 tubes | Decreasing count |
| Xanthochromia | Present (yellow) | Absent |
| Spectrophotometry | Bilirubin peak | Normal |
Xanthochromia: Yellow discoloration from bilirubin (breakdown of haemoglobin). Takes greater than 12 hours to develop. Gold standard is spectrophotometry.
CT Angiography (CTA)
- Sensitivity: 98% for aneurysms greater than 3mm.
- Timing: Perform immediately after SAH confirmed.
- Purpose: Identify aneurysm location, morphology, planning treatment.
Digital Subtraction Angiography (DSA)
- Gold Standard: For aneurysm detection.
- Indication: CTA negative but high suspicion, or treatment planning.
- Repeat DSA: If initial negative, repeat in 1-2 weeks (10% of aneurysms initially occult).
Modified Fisher Grade (Vasospasm Prediction)
| Grade | CT Findings | DCI Risk |
|---|---|---|
| 0 | No blood | - |
| 1 | Thin SAH, no IVH | 24% |
| 2 | Thin SAH with IVH | 33% |
| 3 | Thick SAH, no IVH | 33% |
| 4 | Thick SAH with IVH | 40% |
7. Management
Management Algorithm
SAH CONFIRMED ON CT
↓
┌─────────────────────────────────────────┐
│ IMMEDIATE MANAGEMENT │
│ - Protect airway (intubate if GCS≤8) │
│ - BP control (target SBP less than 160) │
│ - Analgesia (morphine) │
│ - Antiemetics │
│ - Nimodipine 60mg every 4 hours PO │
│ - Venous thromboprophylaxis │
└─────────────────────────────────────────┘
↓
CT ANGIOGRAPHY
↓
┌────────────┴────────────┐
↓ ↓
ANEURYSM FOUND NO ANEURYSM
↓ ↓
URGENT REFERRAL Repeat DSA
NEUROSURGERY Consider PMH
↓
┌─────────────────────────────────────────┐
│ ANEURYSM TREATMENT (within less than 72h) │
│ │
│ COILING (Endovascular) │
│ - First line for most aneurysms │
│ - ISAT trial showed better outcomes │
│ │
│ CLIPPING (Open Surgery) │
│ - MCA aneurysms, wide neck │
│ - Significant haematoma │
│ - Failed coiling │
└─────────────────────────────────────────┘
↓
POST-PROCEDURE CARE
↓
┌─────────────────────────────────────────┐
│ MONITOR FOR COMPLICATIONS │
│ - Vasospasm/DCI (days 4-14) │
│ - Hydrocephalus (acute and chronic) │
│ - Seizures │
│ - Hyponatraemia (SIADH/CSWS) │
└─────────────────────────────────────────┘
Immediate Resuscitation (First Hours)
Airway Protection
- Intubate if GCS 8 or below.
- Avoid hypoxia, hypercarbia (worsen ICP).
Blood Pressure Management
- Pre-Aneurysm Securing: Target SBP less than 160 mmHg to reduce re-bleeding risk.
- Agents: Labetalol, Nicardipine infusion.
- Avoid: Precipitous drops (risk of ischaemia).
Analgesia and Antiemetics
- Pain: IV Paracetamol, Morphine (titrated).
- Headache Uncontrolled: May indicate rebleed or hydrocephalus.
- Antiemetics: Ondansetron (avoid metoclopramide in neurosurgical patients).
Nimodipine - The Only Proven Medication
- Dose: 60mg every 4 hours orally (or 1-2mg/hr IV if unconscious).
- Duration: 21 days.
- Evidence: British Nimodipine Trial showed 34% reduction in poor outcomes. [6]
- Mechanism: Uncertain - likely improves microvascular function rather than preventing large vessel spasm.
- Side Effect: Hypotension (hold dose if SBP less than 100).
Aneurysm Treatment
Endovascular Coiling (First-Line for Most)
- Technique: Microcatheter via femoral artery, platinum coils deployed into aneurysm sac.
- Evidence: ISAT trial: Coiling superior to clipping for suitable aneurysms (23.7% vs 30.6% dead/dependent at 1 year). [7]
- Advantages: Less invasive, shorter ICU stay, lower morbidity.
- Limitations: Recanalization risk (15-20%), need for follow-up imaging.
Surgical Clipping
- Technique: Craniotomy, dissection to aneurysm neck, permanent titanium clip.
- Indications:
- MCA aneurysms (difficult endovascular access).
- Wide-neck aneurysms unsuitable for coiling.
- Associated haematoma requiring evacuation.
- Young patients (durability).
- Advantages: Definitive treatment, immediate haematoma evacuation.
Management of Complications
Vasospasm and Delayed Cerebral Ischaemia (DCI)
- Monitoring: Daily transcranial Doppler (TCD), clinical neuro obs.
- Prevention: Nimodipine, maintain euvolaemia.
- Treatment of DCI:
- Induced hypertension (target MAP 20% above baseline).
- IV fluids.
- Intra-arterial vasodilators (verapamil, nicardipine).
- Angioplasty for severe focal vasospasm.
Hydrocephalus
- Acute: External Ventricular Drain (EVD) - immediate CSF drainage.
- Chronic: VP Shunt if required (15-20% of survivors).
Seizures
- Prophylaxis: Levetiracetam for 7 days (controversial, not for all).
- Treatment: Standard anticonvulsants.
Hyponatraemia
| Condition | Mechanism | Treatment |
|---|---|---|
| SIADH | Excess ADH | Mild fluid restriction (avoid dehydration), Hypertonic saline if severe |
| CSWS | Natriuresis, volume depletion | Salt replacement, Fludrocortisone |
8. Complications
Acute Complications
| Complication | Timing | Incidence | Mechanism |
|---|---|---|---|
| Re-bleeding | 0-30 days | 4% first 24h | Clot lysis, persistent bleeding |
| Hydrocephalus | Hours-days | 20-30% | CSF obstruction |
| Seizures | First 24h | 5-10% | Cortical irritation |
| Cardiac | First 48h | 20-40% | Catecholamine surge |
| Neurogenic pulmonary oedema | First 24h | 2-8% | Sympathetic storm |
Delayed Complications
| Complication | Timing | Incidence | Management |
|---|---|---|---|
| Vasospasm | Days 4-14 | 70% (angiographic) | TCD monitoring, Triple-H |
| DCI | Days 4-14 | 30% | Induced hypertension, angioplasty |
| Chronic hydrocephalus | Weeks-months | 15-20% | VP shunt |
| Cognitive deficits | Long-term | 50% | Rehabilitation |
| Depression | Long-term | 20-40% | Screening, treatment |
Cardiac Complications
- Mechanism: Catecholamine surge causes myocardial stunning.
- ECG Changes: T-wave inversion, QT prolongation, ST changes (mimic ACS).
- Troponin: May be elevated (tako-tsubo).
- Arrhythmias: Common in severe SAH.
9. Prognosis and Outcomes
Mortality Statistics
- Pre-Hospital Death: 10-15%.
- 30-Day Mortality: 40-50%.
- 1-Year Mortality: 50-60%.
- Good Outcome (mRS 0-2): 50% of hospital survivors.
Prognostic Factors
Good Prognosis
- Low clinical grade (WFNS I-II).
- Younger age.
- Anterior circulation aneurysm.
- Early aneurysm treatment.
Poor Prognosis
- High clinical grade (WFNS IV-V).
- Thick SAH on CT.
- Intraventricular haemorrhage.
- Older age.
- Delayed treatment.
- Rebleeding.
Long-Term Sequelae
- Cognitive Deficits: Memory, executive function (50%).
- Fatigue: Persistent in 50-70%.
- Depression/Anxiety: 20-40%.
- Epilepsy: 5-10%.
- Return to Work: Only 50-70% at 1 year.
Screening for Unruptured Aneurysms
- Indications:
- Two or more first-degree relatives with SAH.
- Autosomal Dominant Polycystic Kidney Disease.
- Previous SAH (contralateral screening).
- Modality: MR Angiography.
- Frequency: Every 3-5 years if negative.
10. Evidence and Guidelines
Key Guidelines
| Guideline | Organisation | Key Points |
|---|---|---|
| AHA/ASA Guidelines 2023 | American Heart Association | Coiling preferred, Nimodipine 21 days, avoid hypotension |
| NICE NG128 | UK | Early specialist referral, CT within 12 hours of onset |
| Neurocritical Care Society | International | DCI monitoring, TCD protocols |
Landmark Trials
1. International Subarachnoid Aneurysm Trial (ISAT) 2002 [7]
- Question: Coiling vs clipping for ruptured aneurysms?
- N: 2,143 patients.
- Result: At 1 year, 23.7% dead/dependent with coiling vs 30.6% with clipping (RR 0.77).
- Impact: Established endovascular coiling as first-line treatment.
- PMID: 12414200.
2. British Nimodipine Trial 1989 [6]
- Question: Does nimodipine improve outcomes?
- N: 554 patients.
- Result: 34% reduction in poor outcomes at 3 months.
- Impact: Nimodipine became standard of care.
- PMID: 2493990.
3. CONSCIOUS Trials 2011
- Question: Does clazosentan (endothelin antagonist) improve outcomes?
- N: Over 1,000 patients.
- Result: Reduced vasospasm but no improvement in functional outcomes.
- Impact: Vasospasm alone is not primary driver of DCI.
- PMID: 21832227.
4. SAHIT Collaboration 2018
- Question: Predicting outcomes in SAH?
- N: Over 10,000 patients pooled.
- Result: Developed prognostic models.
- Impact: Better counselling for families.
- PMID: 29980622.
11. Patient and Layperson Explanation
What is a Subarachnoid Haemorrhage?
A subarachnoid haemorrhage (SAH) is bleeding around the brain. It usually happens when a weak spot in a blood vessel (called an aneurysm) bursts. The blood collects between the brain and the thin membranes that cover it.
What Causes It?
- Most commonly, rupture of a brain aneurysm (a balloon-like bulge in a blood vessel).
- Risk factors include high blood pressure, smoking, excessive alcohol, and family history.
What Are the Warning Signs?
- Sudden severe headache - often described as "the worst headache of my life" or "like being hit on the head".
- Headache reaching maximum intensity within seconds.
- Nausea and vomiting.
- Stiff neck (may develop hours later).
- Sensitivity to light.
- Loss of consciousness (sometimes brief).
- Confusion or drowsiness.
How is it Diagnosed?
- CT Scan: A brain scan that can show bleeding.
- Lumbar Puncture: If the CT is normal but suspicion is high, a sample of fluid from the spine is tested.
- CT Angiography: A scan to find the aneurysm.
How is it Treated?
- Emergency Care: Stabilising blood pressure and preventing further bleeding.
- Medication: Nimodipine tablets to reduce the risk of secondary brain damage.
- Fixing the Aneurysm: Either coiling (threading a small tube through blood vessels to block the aneurysm) or clipping (surgery to place a clip on the aneurysm).
What is the Recovery Like?
- Recovery varies widely depending on severity.
- Many people need weeks to months of rehabilitation.
- Fatigue, memory problems, and mood changes are common.
- About 50% of survivors make a good recovery.
When to Seek Emergency Help
- Any sudden severe headache that is different from previous headaches.
- Headache with neck stiffness, vomiting, or confusion.
- Collapse or loss of consciousness with headache.
Call 999/000/911 immediately - this is a medical emergency.
12. References
Primary Sources
- Macdonald RL, Schweizer TA. Spontaneous subarachnoid haemorrhage. Lancet. 2017;389:655-666. PMID: 27637674.
- Lawton MT, Vates GE. Subarachnoid Hemorrhage. N Engl J Med. 2017;377:257-266. PMID: 28723321.
- Etminan N, et al. Worldwide Incidence of Aneurysmal Subarachnoid Hemorrhage. Stroke. 2019;50:1205-1212. PMID: 31092157.
- 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. PMID: 21768192.
- Dubosh NM, et al. Sensitivity of Early Brain Computed Tomography. Ann Emerg Med. 2016;68:297-305. PMID: 26995676.
- Pickard JD, et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage. BMJ. 1989;298:636-642. PMID: 2493990.
- Molyneux A, et al. International Subarachnoid Aneurysm Trial (ISAT). Lancet. 2002;360:1267-1274. PMID: 12414200.
- Hemphill JC, et al. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage. Stroke. 2015;46:2032-2060. PMID: 26022637.
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