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Neurology
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Emergency Medicine
EMERGENCY

Subarachnoid Haemorrhage (SAH)

High EvidenceUpdated: 2025-12-24

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Red Flags

  • Thunderclap Headache (Max intensity < 1-5 mins)
  • 3rd Nerve Palsy (PCom Aneurysm expansion warning)
  • Seizures
  • Drop in GCS (Hydrocephalus/Rebleed)
Overview

Subarachnoid Haemorrhage (SAH)

1. Clinical Overview

Summary

Subarachnoid Haemorrhage (SAH) is bleeding into the subarachnoid space (between arachnoid and pia mater). Spontaneous SAH is caused by a Ruptured Berry Aneurysm in 85% of cases. It is a catastrophic event with 50% mortality (15% die before reaching hospital). The hallmark is the Thunderclap Headache: sudden, severe, occipital pain reaching peak intensity instantly. [1,2]

Clinical Pearls

The Warners: 50% of patients have a "Sentinel Headache" (a minor leak) in the weeks preceding the big rupture. Misdiagnosing this as a migraine is a common cause of litigation. If the headache is "different" to usual migraines (e.g., sudden onset), scan it.

The 3rd Nerve: An expanding aneurysm of the Posterior Communicating Artery (PCom) can compress the Oculomotor nerve. This causes a Painful 3rd Nerve Palsy (Eye down and out + Pupil dilated/fixed). This is a surgical emergency impending rupture.

Investigate the Neck: Headache + Neck Stiffness = Meningitis OR SAH. If they are feverish, think Meningitis. If they are afebrile but have neck stiffness (blood irritating meninges), think SAH.

2. Epidemiology

Incidence and Prevalence

  • Global Incidence: 6-9 per 100,000 population per year.
  • Regional Variation: Higher in Japan and Finland (up to 20 per 100,000).
  • Gender: Women > Men (1.6:1 ratio).
  • Age: Peak incidence 50-60 years, but can occur at any age.
  • Mortality: 50% overall (15% die before reaching hospital, 15% die within first 24 hours, 20% die within 30 days).

Risk Factors

Non-Modifiable

  • Age: Risk increases with age (peak 50-60 years).
  • Gender: Women at higher risk (possibly hormonal factors).
  • Family History: First-degree relative with SAH increases risk 4-fold.
  • Genetic Syndromes:
    • Autosomal Dominant Polycystic Kidney Disease (ADPKD): 10-15% of patients with ADPKD develop intracranial aneurysms. Screen with MRA if family history of SAH or aneurysm.
    • Ehlers-Danlos Syndrome Type IV: Collagen defect. Multiple aneurysms, arterial dissection.
    • Marfan Syndrome: Connective tissue disorder.
    • Neurofibromatosis Type 1: Increased risk of vascular abnormalities.
    • Coarctation of Aorta: Associated with Circle of Willis aneurysms.
  • Race/Ethnicity: Higher in Black and Hispanic populations compared to White populations.

Modifiable

  • Smoking: Strongest modifiable risk factor (OR 3-10). Dose-dependent. Promotes aneurysm formation and growth.
  • Hypertension: Chronic HTN damages vessel walls. Present in 50-60% of SAH patients.
  • Heavy Alcohol Use: >150g per week increases risk 2-3 fold.
  • Cocaine/Amphetamine Use: Acute hypertensive surges can rupture aneurysms.
  • Oral Contraceptive Pill: Weak association (controversial).
  • Pregnancy: Increased risk, especially in 3rd trimester and peripartum period.

Aneurysm Prevalence

  • Unruptured Aneurysms: Present in 2-5% of general population (often asymptomatic, incidental findings on imaging).
  • Rupture Risk: Small aneurysms (less than 7mm) rupture at ~1% per year. Larger aneurysms have higher rupture risk.
3. Pathophysiology

Aneurysm Formation (5-Step Mechanism)

  1. Hemodynamic Stress: Turbulent blood flow at arterial bifurcations in the Circle of Willis creates chronic mechanical stress on vessel walls.

  2. Endothelial Dysfunction: Chronic stress leads to endothelial injury, inflammation, and smooth muscle cell apoptosis in the tunica media (middle layer of vessel wall).

  3. Wall Weakening: Loss of smooth muscle cells and elastic fibers weakens the arterial wall. The adventitia (outer layer) begins to bulge outward.

  4. Aneurysm Formation: A saccular (berry-shaped) aneurysm develops, typically at bifurcation points. The aneurysm wall is thin (lacks normal vessel structure) and continues to expand.

  5. Rupture: When wall stress exceeds wall strength (often triggered by acute BP rise, Valsalva, physical exertion, or coitus), the aneurysm ruptures into the subarachnoid space.

Aneurysm Locations (Circle of Willis)

LocationFrequencyClinical Features
Anterior Communicating Artery (ACom)30-40%Most common. Frontal lobe compression symptoms. Memory deficits.
Posterior Communicating Artery (PCom)25%3rd Nerve Palsy (painful, pupil-involved). Eye "down and out", ptosis, dilated pupil.
Middle Cerebral Artery (MCA)20%MCA bifurcation. Aphasia, hemiparesis if ruptures.
Basilar Apex10%Posterior circulation. Brainstem compression. Hydrocephalus.
Anterior Cerebral Artery (ACA)5%Rare. Leg weakness if ruptures.
Posterior Inferior Cerebellar Artery (PICA)3%Posterior fossa. Ataxia, cranial nerve palsies.
Internal Carotid Artery (ICA)3%Ophthalmic segment. Visual disturbance.

Pathophysiology of Brain Injury

Primary Brain Injury (Immediate)

  1. Acute ICP Rise: Sudden hemorrhage into subarachnoid space causes immediate, severe rise in intracranial pressure (ICP can transiently equal MAP).
  2. Cerebral Perfusion Crisis: Cerebral Perfusion Pressure (CPP = MAP - ICP) drops dramatically, causing global cerebral ischemia.
  3. Direct Neuronal Injury: Blood is toxic to neurons. Hemoglobin breakdown products cause oxidative stress and inflammation.
  4. Loss of Consciousness: Acute ICP rise can cause immediate LOC or seizures.

Secondary Brain Injury (Delayed)

1. Re-bleeding (Hours to Days)

  • Timing: Highest risk in first 24 hours (4-15% rebleed risk within first 24h).
  • Mechanism: Initial clot dissolves, aneurysm re-ruptures.
  • Outcome: 70% mortality if rebleeds.
  • Prevention: Urgent aneurysm securing within 24 hours.

2. Delayed Cerebral Ischemia (DCI) / Vasospasm (Days 3-14)

  • Timing: Peak risk Day 4-10 (rare before Day 3 or after Day 14).
  • Mechanism: Blood breakdown products (oxyhemoglobin, endothelin, free radicals) irritate arterial walls → smooth muscle contraction → vessel narrowing → cerebral ischemia.
  • Clinical Features: New confusion, focal neurology (hemiparesis, aphasia), deteriorating GCS.
  • Detection: Transcranial Doppler (TCD) shows increased flow velocities. CT Angiography or Digital Subtraction Angiography (DSA) confirms vasospasm.
  • Treatment: Nimodipine (prevention), induced hypertension, endovascular intervention (intra-arterial vasodilators, balloon angioplasty).

3. Acute Hydrocephalus (Hours to Days)

  • Mechanism: Blood clot obstructs CSF flow (especially in 4th ventricle or aqueduct of Sylvius) → non-communicating hydrocephalus. Or blood clogs arachnoid granulations → communicating hydrocephalus.
  • Clinical Features: Reduced GCS, headache, vomiting, papilledema, upgaze palsy.
  • Treatment: External Ventricular Drain (EVD). May need VP shunt if chronic.

4. Seizures

  • Early Seizures: 10-25% at onset (due to acute cortical irritation).
  • Prophylaxis: Controversial. Short-term phenytoin or levetiracetam for first 3-7 days is common practice, but no strong evidence.

5. Hyponatremia (Days to Weeks)

  • SIADH: Syndrome of Inappropriate ADH secretion. Euvolemic hyponatremia.
  • Cerebral Salt Wasting (CSW): Renal sodium loss. Hypovolemic hyponatremia (more common in SAH).
  • Distinction: CSW has low CVP/negative fluid balance. SIADH has normal/high CVP.
  • Importance: Hypovolemia worsens vasospasm. Must maintain euvolemia.

6. Cardiac Complications

  • Neurogenic Stunned Myocardium: Catecholamine surge causes transient LV dysfunction (Takotsubo-like).
  • ECG Changes: T-wave inversion, ST changes, QTc prolongation (can mimic MI).
  • Troponin Rise: Common but often not true ACS.
  • Arrhythmias: AF, VT.
4. Differential Diagnosis (Thunderclap Headache)
ConditionFeatures
SAHOccipital. Meningism. Vomiting. Syncope.
MigraineSlower onset (minutes). Photophobia. Previous history.
Cerebral Venous Sinus ThrombosisSubacute. Seizures. Hypercoagulable state.
Pituitary ApoplexyVisual field loss. Hypopituitarism.
MeningitisFever. Rash.
Coital CephalgiaTriggered by orgasm. Benign.
5. Clinical Presentation

Symptoms

Classic Presentation

Sentinel Headache (Herald Leak)

Atypical Presentations

Signs

General Examination

Neurological Examination

1. Glasgow Coma Scale (GCS)

2. Meningeal Signs

3. Cranial Nerve Examination

4. Motor/Sensory Examination

5. Seizure Activity

Clinical Grading Scales

World Federation of Neurosurgical Societies (WFNS) Scale

GradeGCSMotor DeficitOutcome
I15AbsentGood (70% favorable)
II13-14AbsentGood
III13-14PresentIntermediate
IV7-12Present or absentPoor (50% mortality)
V3-6Present or absentVery poor (70-80% mortality)

Hunt and Hess Scale (older, less used now)

GradeDescriptionMortality
IAsymptomatic or mild headacheless than 5%
IISevere headache, neck stiffness, no focal deficit5-10%
IIIDrowsy, confused, mild focal deficit10-15%
IVStuporous, hemiparesis60-70%
VComatose, decerebrate posturing70-90%

Modified Fisher Scale (Predicts vasospasm risk based on CT appearance)

GradeCT FindingsVasospasm Risk
0No SAH, no IVHLow
1Thin SAH, no IVHLow
2Thin SAH, with IVHModerate
3Thick SAH, no IVHHigh
4Thick SAH, with IVHVery High

IVH = Intraventricular Hemorrhage. Thick = >1mm blood clot.

Thunderclap Headache (90%)
"Worst headache of my life". Reaches maximum intensity within seconds to 1 minute. Often occipital. Described as being "hit with a baseball bat" or "explosion in the head".
Sudden Onset
While exercising, straining, coitus (but can occur at rest).
Meningism
Neck stiffness (develops over hours as blood irritates meninges), photophobia, phonophobia.
Nausea and Vomiting
Due to raised ICP and meningeal irritation.
Loss of Consciousness
50% have brief LOC or syncope at onset.
Seizures
10-25% at onset (cortical irritation).
6. Investigations

Immediate Investigations (Emergency Department)

1. CT Head (Non-Contrast)

  • First-Line Investigation: URGENT. Do within 1 hour of arrival.
  • Timing Sensitivity:
    • less than 6 hours: Sensitivity >98% (effectively 100% if reported by specialist neuroradiologist).
    • 6-12 hours: Sensitivity 93%.
    • 12-24 hours: Sensitivity 85%.
    • >5 days: Sensitivity 50% (blood disperses and dilutes in CSF).
  • Findings:
    • Hyperdense (white) blood in subarachnoid spaces:
      • Basal cisterns (classic starfish or pentagram appearance).
      • Sylvian fissures.
      • Interhemispheric fissure.
      • Sulci over convexities.
    • Intraventricular Hemorrhage (IVH): Blood in ventricles (worse prognosis).
    • Hydrocephalus: Dilated ventricles.
    • Intracerebral Hemorrhage: Associated parenchymal blood (suggests aneurysm location).
    • Midline Shift: If large hemorrhage or edema.

NICE NG228 Update (2022):

  • If CT head performed within 6 hours of headache onset and reported as negative by a consultant neuroradiologist or equivalent, SAH is effectively ruled out. LP is not routinely needed.
  • If CT is >6 hours from onset or reported by non-specialist, or if CT negative but clinical suspicion remains high, proceed to LP.

2. Lumbar Puncture (LP)

  • Indication: Mandatory if:
    • CT head negative OR equivocal, BUT clinical suspicion remains.
    • CT performed >6 hours after headache onset.
  • Timing: Must wait ≥12 hours after headache onset (for xanthochromia to develop).
  • Why 12 hours?: Red blood cells in CSF need time to lyse and be metabolized by macrophages. This produces bilirubin (yellow pigment = xanthochromia). Takes 12 hours minimum.
  • Procedure:
    1. Measure opening pressure (usually normal or elevated in SAH).
    2. Collect CSF in 4 tubes (numbered 1-4).
    3. Send Tube 1 for biochemistry, Tube 2 for microbiology, Tube 3 for cell count, Tube 4 for xanthochromia spectrophotometry.

CSF Findings in SAH:

  • RBCs: Elevated (>5 RBC/mm³ is abnormal). Crucially: RBC count should be similar in Tube 1 and Tube 4. If Tube 1 >> Tube 4, suggests traumatic tap.
  • Xanthochromia: Gold standard for SAH. CSF is yellow-tinged due to bilirubin.
    • Spectrophotometry: Objective measurement of bilirubin and oxyhemoglobin absorbance peaks. More reliable than visual inspection.
    • Sensitivity: 100% if done at >12 hours and less than 2 weeks.
    • Note: Jaundice or high CSF protein can also cause xanthochromia (but spectrophotometry differentiates bilirubin from other causes).

Traumatic Tap vs True SAH:

FeatureTraumatic TapTrue SAH
RBC count Tube 1 vs 4DecreasingSame
Xanthochromia (>12h)AbsentPresent
Clot formationMay clotDoesn't clot
CSF supernatant colorClearYellow

3. Blood Tests

  • FBC: Baseline. Leucocytosis common (stress response).
  • U&Es: Baseline sodium (hyponatremia common later). Urea (prognostic marker).
  • Clotting: Baseline INR, APTT (may need reversal if anticoagulated).
  • Glucose: Hyperglycemia common (stress response, worse prognosis).
  • Troponin: Often elevated (neurogenic cardiac injury) but rarely indicates true MI.
  • LFTs: Baseline.
  • Group and Save: In case needs surgery.

4. ECG

  • Common Abnormalities:
    • T-wave inversion (especially in anterior leads).
    • ST elevation or depression (can mimic STEMI).
    • QTc prolongation.
    • U waves.
    • Arrhythmias (AF, VT).
  • Mechanism: Catecholamine surge from hypothalamic injury.
  • Action: ECG abnormalities do NOT mean the patient has had an MI (usually neurogenic). Focus on treating the brain.

Aneurysm Localization (After SAH Confirmed)

CT Angiography (CTA)

  • Timing: ASAP (ideally within hours of diagnosis).
  • Purpose: Identify aneurysm location, size, morphology for treatment planning.
  • Sensitivity: 95-98% for aneurysms >3mm.
  • Advantages: Fast, non-invasive, widely available.
  • Disadvantages: Radiation, contrast (CI if renal failure or contrast allergy).

Digital Subtraction Angiography (DSA)

  • Gold Standard: Most detailed imaging of cerebral vasculature.
  • Indications:
    • CTA negative or equivocal (perimesencephalic pattern).
    • Multiple aneurysms (to identify culprit).
    • Pre-procedure planning for coiling.
  • Procedure: Catheter via femoral artery, contrast injected into cerebral vessels, real-time fluoroscopy.
  • Sensitivity: 100% for aneurysms.
  • Disadvantages: Invasive (1% stroke risk), requires specialist, time-consuming.

MR Angiography (MRA)

  • Role: Limited in acute SAH (longer scan time, patient needs to be stable).
  • Use: Follow-up imaging of treated aneurysms or screening high-risk individuals (e.g., ADPKD).

Investigations for Complications (Days 1-14)

1. Transcranial Doppler (TCD) Ultrasound

  • Purpose: Daily monitoring for vasospasm (Day 3-14).
  • Measurement: Flow velocities in MCA, ACA, ICA.
  • Interpretation:
    • MCA velocity >120 cm/s: Mild vasospasm.
    • MCA velocity >200 cm/s: Severe vasospasm.
    • Lindegaard Ratio (MCA velocity / ICA velocity):
      • less than 3: Normal.
      • >3: Vasospasm (helps differentiate vasospasm from hyperemia).
  • Advantages: Non-invasive, bedside, repeatable.
  • Limitations: Operator-dependent, cannot assess distal vessels.

2. CT Head (Repeat)

  • Indication: Clinical deterioration, new neurology, suspected rebleed or hydrocephalus.
  • Findings: New blood, hydrocephalus, infarction, hematoma expansion.

3. CT Perfusion / CT Angiography

  • Indication: Suspected vasospasm causing ischemia.
  • Findings: Delayed perfusion, reduced cerebral blood flow, narrowed vessels on CTA.

4. Electrolytes

  • Daily monitoring: Sodium (hyponatremia common Day 3-10).
  • Fluid balance: Track ins and outs (to differentiate SIADH from CSW).
7. Management

Management Algorithm

        THUNDERCLAP HEADACHE
        (Sudden, severe, worst ever)
                 ↓
      STABILIZE (ABC)
      - Protect airway if GCS less than 8
      - Oxygen if hypoxic
      - IV access, bloods
                 ↓
      URGENT CT HEAD (Within 1 hour)
                 ↓
     ┌───────────┴───────────┐
  POSITIVE               NEGATIVE
  (Blood visible)        (No blood)
     ↓                       ↓
  CONFIRM SAH          TIMING CHECK
  - CTA or DSA            ↓
  to locate         ┌─────┴─────┐
  aneurysm         less than 6 hours   >6 hours
     ↓                ↓            ↓
  ADMIT NEURO/    SAH ruled   LUMBAR PUNCTURE
  NEUROSURGERY     out (if     (Wait 12h from
  HDU/ICU        specialist    headache onset)
     ↓            reported)         ↓
  NEUROPROTECTION          ┌────┴────┐
  - Nimodipine 60mg     POS       NEG
    PO 4hrly x 21d    (Xantho-   (Clear)
  - BP control         chromia)      ↓
  - Euvolemia           ↓         Alternative
  - Analgesia         TREAT SAH   diagnosis
     ↓                  ↓
  SECURE ANEURYSM
  (Within 24h)
     ↓
  ┌──────┴──────┐
COILING      CLIPPING
(Endovascular) (Surgical)
     ↓            ↓
  ├──────────────┤
     ↓
  MANAGE COMPLICATIONS
  - Rebleed (Secure aneurysm urgently)
  - Vasospasm (Nimodipine, hypertension, endovascular)
  - Hydrocephalus (EVD, VP shunt)
  - Seizures (Anticonvulsants short-term)
  - Hyponatremia (Differentiate SIADH vs CSW)
     ↓
  REHABILITATION
  - Cognitive
  - Physical
  - Psychological

Initial Stabilization (Emergency Department/Resus)

1. Airway, Breathing, Circulation (ABC)

  • Airway:
    • Intubate if GCS ≤8 (unable to protect airway).
    • Rapid Sequence Induction (RSI): Avoid hypertension spike during intubation (use careful induction agents like fentanyl, propofol).
  • Breathing:
    • Maintain normoxia (SpO₂ 94-98%).
    • Avoid hypoxia (worsens secondary brain injury).
    • Avoid hyperventilation (causes vasoconstriction → cerebral ischemia) unless acute herniation.
  • Circulation:
    • Large bore IV access (2 x 16-18G).
    • Avoid hypotension (maintain CPP = MAP - ICP).
    • Target SBP 140-160 mmHg initially (balance: too low → cerebral hypoperfusion; too high → rebleed risk).

2. Blood Pressure Management

  • Goal: Prevent rebleeding WITHOUT causing cerebral hypoperfusion.
  • Pre-securing aneurysm: Keep SBP less than 160 mmHg (some guidelines say less than 140).
  • Post-securing aneurysm: Can allow higher BP (SBP 160-200) to prevent vasospasm/DCI.
  • Drugs:
    • Labetalol: 10-20mg IV bolus (alpha + beta blocker). Preferred (smooth, titratable).
    • Esmolol: IV infusion (short-acting beta blocker).
    • Nicardipine: IV infusion (calcium channel blocker).
    • Avoid: Hydralazine (causes reflex tachycardia, ICP rise).

3. Analgesia

  • Severe headache requires strong analgesia.
  • Options:
    • Morphine: 5-10mg IV (titrate to pain). Caution: can drop BP, cloud GCS assessment.
    • Codeine: 30-60mg PO/IV.
    • Paracetamol: 1g IV/PO 6-hourly.
  • Avoid: NSAIDs (theoretical bleeding risk, although evidence weak).

4. Anti-emetics

  • Ondansetron: 4-8mg IV.
  • Metoclopramide: 10mg IV (caution if young females - dystonia risk).

5. Neuroprotection (START IMMEDIATELY)

Nimodipine

  • Dose: 60mg PO 4-hourly for 21 days (or 1-2mg/hour IV if cannot swallow).
  • Mechanism: Calcium channel blocker. Prevents/reduces vasospasm and delayed cerebral ischemia.
  • Evidence: Class 1A recommendation. Reduces poor outcome by 30-40% (landmark trials in 1980s).
  • Side Effects: Hypotension (monitor BP closely, reduce dose if SBP less than 100).
  • Start: As soon as SAH diagnosed, continue for 21 days.
  • Crucially: Even if aneurysm not yet secured, START nimodipine.

6. Seizure Management

  • If seizure at presentation: Treat acutely (lorazepam 4mg IV, then phenytoin or levetiracetam load).
  • Prophylaxis: Controversial. Some centers give short-term anticonvulsants (levetiracetam 500mg BD or phenytoin) for first 3-7 days, then stop. No strong evidence for routine prophylaxis. Do NOT give long-term unless recurrent seizures.

7. Fluid Management

  • Goal: Euvolemia (normal fluid status). Avoid hypovolemia (worsens vasospasm) and hypervolemia (pulmonary edema, dilutes blood).
  • IV Fluids: 0.9% Saline 1mL/kg/h (avoid hypotonic fluids like 5% dextrose - worsen cerebral edema).
  • Monitor: Fluid balance chart, daily weights, CVP if HDU/ICU.

8. Bed Rest, Nurse Head-Up

  • Head-up 30°: Promotes venous drainage, reduces ICP.
  • Bed rest: Until aneurysm secured (avoid Valsalva, straining).
  • Stool softeners: Laxatives (senna, docusate) to avoid straining (rebleed risk).

Definitive Treatment: Securing the Aneurysm

Timing: ASAP, ideally within 24 hours (to prevent rebleeding).

1. Endovascular Coiling (First-Line)

  • Procedure:
    1. Femoral artery puncture under local anesthesia (or GA).
    2. Catheter navigated via aorta → carotid/vertebral artery → aneurysm.
    3. Microcatheter advanced into aneurysm sac.
    4. Detachable platinum coils deployed to fill aneurysm (thrombose it from inside).
    5. Coils cause clot formation → aneurysm obliteration.
  • Advantages:
    • Less invasive (no craniotomy).
    • Better outcomes (ISAT trial: 23.5% dependent/dead vs 30.9% for clipping at 1 year).
    • Shorter hospital stay.
    • Suitable for posterior circulation and poor-grade patients.
  • Disadvantages:
    • Recanalization risk (10-20% aneurysms recur over time, need follow-up imaging).
    • Not suitable for all aneurysms (wide-neck, MCA bifurcation).
  • Indications: Preferred for most aneurysms, especially:
    • ACom, PCom, basilar apex.
    • Elderly or poor medical fitness.
    • High-grade SAH.

2. Surgical Clipping (Microsurgical)

  • Procedure:
    1. Craniotomy (open skull).
    2. Microsurgical dissection to aneurysm.
    3. Titanium clip placed across aneurysm neck (excludes it from circulation).
    4. Skull closed.
  • Advantages:
    • Definitive (permanent, no recanalization).
    • Better for MCA aneurysms (easier surgical access).
    • Can evacuate intracerebral hematoma if present.
    • Can perform decompression if swelling.
  • Disadvantages:
    • More invasive (craniotomy).
    • Higher morbidity in poor-grade patients.
    • Longer recovery.
    • Less suitable for posterior circulation (difficult surgical access).
  • Indications:
    • MCA aneurysms.
    • Wide-neck aneurysms unsuitable for coiling.
    • Young patients (lifetime durability).
    • Associated ICH needing evacuation.

ISAT Trial (Lancet 2002, 2005):

  • International Subarachnoid Aneurysm Trial: RCT comparing coiling vs clipping.
  • Result: Coiling had significantly better disability-free survival at 1 year (7.4% absolute risk reduction).
  • Impact: Shifted practice to "Coil First" policy in most centers.
  • Caveat: Not all aneurysms are suitable for coiling. Multidisciplinary decision.

Management of Complications

1. Rebleeding

  • Prevention: Urgent aneurysm securing (less than 24h).
  • If rebleeds before securing: Mortality 70-80%. Urgent CT head, immediate coiling/clipping if salvageable.

2. Delayed Cerebral Ischemia (DCI) / Vasospasm

  • Monitoring:

    • Clinical: Daily neuro obs (GCS, focal signs). Any deterioration → investigate.
    • TCD: Daily velocities (Day 3-14).
    • CT Perfusion / CTA: If clinical or TCD evidence of vasospasm.

  • Prevention:

    • Nimodipine: 60mg PO 4hrly x 21 days (MANDATORY).
    • Euvolemia: Maintain normal fluid balance (avoid hypovolemia).

  • Treatment if vasospasm occurs:

    1. Induced Hypertension: Raise SBP to 160-200 mmHg (aneurysm must be secured first). Use vasopressors (noradrenaline, phenylephrine).
    2. Euvolemia: Ensure adequate filling (CVP 8-10). Avoid fluid overload.
    3. Endovascular Intervention:
      • Intra-arterial vasodilators: Verapamil, nimodipine, milrinone injected directly into spasmed vessel via catheter.
      • Balloon angioplasty: Inflate balloon in narrowed artery to mechanically dilate it.

Note: Old "Triple H Therapy" (Hypertension, Hypervolemia, Hemodilution) is no longer routine. Modern approach focuses on Euvolemia + Induced Hypertension only (hypervolemia risks pulmonary edema, hemodilution not beneficial).

3. Hydrocephalus

  • Acute Hydrocephalus (within hours-days):
    • Indication: Reduced GCS, signs of raised ICP.
    • Treatment: External Ventricular Drain (EVD).
      • Catheter inserted via frontal burr hole into lateral ventricle.
      • Drains CSF to external collection system.
      • Monitor ICP, drain if pressure rises.
      • Risk: Infection (ventriculitis), over-drainage (collapse).
  • Chronic Hydrocephalus (weeks-months):
    • Indication: Persistent cognitive decline, gait disturbance, urinary incontinence (NPH triad).
    • Treatment: Ventriculoperitoneal (VP) Shunt.
      • Permanent drain from ventricle to peritoneal cavity.

4. Hyponatremia

  • Common (30% of SAH patients).
  • Timing: Day 3-10.
  • Differentiate SIADH vs CSW:
FeatureSIADHCSW
Volume StatusEuvolemicHypovolemic
CVPNormal/HighLow
Fluid BalanceNeutralNegative
Urine Sodium>40 mmol/L>40 mmol/L
Urine OsmolalityHigh (>100)High
ManagementFluid restrictIV saline
  • CSW (Cerebral Salt Wasting): More common in SAH. Renal tubules waste sodium → hypovolemia → hypoperfusion → worsens vasospasm. Must treat with IV 0.9% saline (3% hypertonic if severe).
  • SIADH: Fluid retention. Treat with fluid restriction (750-1000 mL/day) or demeclocycline.

Critical: Hypovolemia from CSW worsens vasospasm. Must maintain euvolemia.

5. Seizures

  • If seizures occur, treat with anticonvulsants (levetiracetam or phenytoin).
  • Prophylaxis only for 3-7 days post-ictus (avoid long-term unless recurrent).

6. Cardiac Complications

  • Neurogenic Stunned Myocardium: Supportive care (fluids, inotropes if needed). Usually resolves in days-weeks.
  • ECG changes: Monitor, exclude true MI (rare).

Multidisciplinary Management

Neurocritical Care / HDU / ICU

  • All SAH patients need specialist neurocritical care or neurosurgical HDU/ICU.
  • Monitoring:
    • Continuous GCS, pupils, focal signs (neuro obs hourly).
    • BP, HR, SpO₂, temperature (continuous).
    • Fluid balance (hourly urine output, daily weights).
    • Daily bloods (Na⁺, U&Es, FBC).
    • Daily TCD (Day 3-14).
  • ICP monitoring: If poor grade (GCS less than 8), EVD placed (dual function: drain CSF + monitor ICP).

Rehabilitation

  • Early mobilization (once aneurysm secured and patient stable).
  • Physiotherapy: Prevent pneumonia, DVT, deconditioning.
  • Occupational therapy: ADLs assessment, cognitive rehabilitation.
  • Speech and language therapy: Dysphagia assessment (if bulbar signs), cognitive-communication therapy.
  • Neuropsychology: Cognitive deficits common (memory, executive function). Formal assessment and support.

DVT Prophylaxis

  • Mechanical: TED stockings, intermittent pneumatic compression (from admission).
  • Pharmacological: Start LMWH (enoxaparin 40mg SC OD) once aneurysm secured and no ongoing bleeding risk (usually Day 1-2 post-procedure).

Discharge Planning

  • Follow-up imaging: CT Angio or DSA at 6 months (check coil compaction or aneurysm recurrence).
  • DVLA notification: Must inform DVLA (UK). Driving banned for at least 6 months. Permanent ban if vocational (HGV, PCV).
  • Lifestyle: Stop smoking (strongest risk factor for recurrence or new aneurysms). Control BP (target less than 140/90).
  • Screening: If genetic syndrome (ADPKD, Ehlers-Danlos), screen first-degree relatives with MRA.
8. Complications

Early Complications (Hours to Days)

1. Re-bleeding

  • Incidence: 4-15% in first 24 hours if aneurysm not secured. Peak risk in first 6 hours.
  • Mortality: 70-80% if rebleeds.
  • Clinical Features: Sudden deterioration in GCS, new severe headache, cardiovascular collapse.
  • Management: Urgent CT head. Emergency coiling/clipping if salvageable. Often fatal.
  • Prevention: Secure aneurysm within 24 hours.

2. Acute Hydrocephalus

  • Incidence: 20-30% of SAH cases.
  • Mechanism: Blood clot obstructs CSF pathways or impairs absorption.
  • Clinical Features: Reduced GCS, headache worsening, vomiting, upgaze palsy (Parinaud syndrome), papilledema.
  • Investigation: CT head shows dilated ventricles, transependymal CSF flow.
  • Management: External Ventricular Drain (EVD). Monitor ICP. May need VP shunt if doesn't resolve.

3. Seizures

  • Incidence: 10-25% at onset, 5-10% during hospital stay.
  • Types: Generalized tonic-clonic most common.
  • Risk Factors: Cortical involvement (ICH), middle cerebral artery aneurysm, previous seizure history.
  • Management: Acute seizures treated with benzodiazepines, then loading with levetiracetam or phenytoin. Prophylaxis controversial (short-term use for 3-7 days in some centers).
  • Long-term: Only continue anticonvulsants if recurrent seizures (not routine).

4. Cardiac Complications

  • Neurogenic Stunned Myocardium (Takotsubo-like):
    • Incidence: 10-30%.
    • Mechanism: Catecholamine surge from hypothalamic injury.
    • Clinical: LV dysfunction, pulmonary edema, hypotension.
    • ECG: T-wave inversion, ST changes, QTc prolongation.
    • Troponin: Elevated (but rarely true MI).
    • Echo: Apical ballooning, reduced EF.
    • Management: Supportive (fluids, inotropes if needed). Usually resolves within days-weeks.
  • Arrhythmias: AF, VT. Treat as per standard protocols.

Delayed Complications (Days to Weeks)

5. Delayed Cerebral Ischemia (DCI) / Vasospasm

  • Incidence: 30% develop vasospasm on imaging, 20% develop symptomatic DCI.
  • Timing: Days 3-14 (peak Day 5-10).
  • Mechanism: Blood breakdown products (oxyhemoglobin, endothelin) → arterial narrowing → cerebral ischemia.
  • Risk Factors: High blood load on initial CT (Modified Fisher Grade 3-4), smoking, younger age.
  • Clinical Features:
    • New confusion or drowsiness.
    • Focal neurology: Hemiparesis, aphasia (depends on vessel affected).
    • Drop in GCS.
  • Diagnosis:
    • TCD: Elevated velocities (MCA >120-200 cm/s).
    • CTA/MRA: Vessel narrowing.
    • CT Perfusion: Delayed transit time, reduced CBF.
  • Management:
    • Prevention: Nimodipine 60mg 4hrly x 21 days (reduces risk by 30-40%).
    • Treatment:
      1. Induced hypertension (SBP 160-200 mmHg, if aneurysm secured).
      2. Ensure euvolemia.
      3. Endovascular rescue (intra-arterial vasodilators, balloon angioplasty).
  • Outcome: If untreated, can cause permanent stroke. Early detection and treatment crucial.

6. Hyponatremia (Cerebral Salt Wasting or SIADH)

  • Incidence: 30-50%.
  • Timing: Days 3-10 (peak Day 5-7).
  • Types:
    • Cerebral Salt Wasting (CSW): Renal sodium loss → hypovolemia. More common in SAH.
    • SIADH: Inappropriate ADH secretion → fluid retention → euvolemia.
  • Clinical Features: Confusion, seizures (if Na less than 120 mmol/L).
  • Management:
    • CSW: IV 0.9% saline. 3% hypertonic saline if severe. Fludrocortisone.
    • SIADH: Fluid restriction (750-1000 mL/day), demeclocycline, tolvaptan (vasopressin antagonist).
  • Importance: Hypovolemia worsens vasospasm. Must treat CSW aggressively.

7. Chronic Hydrocephalus

  • Incidence: 10-20% (develops weeks-months after SAH).
  • Mechanism: Impaired CSF reabsorption (blood clogs arachnoid granulations).
  • Clinical Features: "NPH Triad" (though not always complete):
    • Gait disturbance (magnetic, shuffling).
    • Cognitive decline (memory, executive function).
    • Urinary incontinence.
  • Investigation: CT/MRI shows ventriculomegaly. LP trial (remove 30-40 mL CSF, assess gait improvement).
  • Management: Ventriculoperitoneal (VP) shunt.

Late Complications (Weeks to Months)

8. Cognitive and Neuropsychological Deficits

  • Incidence: 50-60% of survivors have persistent cognitive deficits.
  • Domains Affected:
    • Memory: Short-term, working memory.
    • Executive Function: Planning, problem-solving, attention.
    • Processing Speed: Slowed.
  • Impact: Unable to return to work (30-50%), reduced quality of life.
  • Management: Cognitive rehabilitation, neuropsychology input, occupational therapy. Support groups.

9. Epilepsy

  • Incidence: 5-10% develop late epilepsy (after discharge).
  • Risk Factors: Seizures at onset, intracerebral hemorrhage, cortical infarction, residual aneurysm.
  • Management: Anticonvulsants (levetiracetam, lamotrigine). DVLA notification. Driving ban.

10. Depression and Anxiety

  • Incidence: 30-40%.
  • Mechanism: Psychological trauma, brain injury, frontal lobe damage.
  • Management: Antidepressants (SSRIs), CBT, psychological support.

11. Aneurysm Recurrence or New Aneurysms

  • Post-Coiling: 10-20% recanalization over 5 years (coils compact, aneurysm reforms).
  • Post-Clipping: less than 5% recurrence (more durable).
  • New Aneurysms: 1-2% per year risk of developing new aneurysms (especially if genetic risk factors).
  • Follow-up: CT/MR Angiography at 6 months, then yearly (post-coiling). Less frequent post-clipping.
9. Prognosis and Outcomes

Mortality

  • Overall: 30-50% within 30 days.
  • Pre-hospital: 15% die before reaching hospital (often sudden cardiac arrest from ICP spike).
  • Early: 15% die within first 24 hours (rebleed, herniation).
  • 30-day: 30% mortality.
  • 1-year: 35-40% mortality.

Survival and Functional Outcome

Predictors of Poor Outcome (Death or Severe Disability):

  • High Clinical Grade: WFNS Grade IV-V (GCS less than 12).
  • Age: >70 years.
  • Large Blood Load: Modified Fisher Grade 3-4 (thick clot, IVH).
  • Posterior Circulation Aneurysms: Worse than anterior.
  • Rebleeding: 70-80% mortality.
  • Delayed Cerebral Ischemia: Doubles mortality/morbidity.
  • Medical Comorbidities: Cardiac, renal, respiratory disease.

Modified Rankin Scale (mRS) at 6-12 Months:

mRSDescription% of Survivors
0No symptoms15%
1No significant disability (slight symptoms)15%
2Slight disability (can live independently)20%
3Moderate disability (requires some help)20%
4Moderately severe disability (dependent)15%
5Severe disability (bedridden)10%
6Dead30-50%

Good Outcome (mRS 0-2): 50-60% of survivors (i.e., 30-35% of all SAH patients).

Cognitive and Psychosocial Outcomes

  • Return to Work: Only 50-60% return to previous employment.
  • Cognitive Deficits: 50-60% have persistent memory, executive function, or processing speed problems.
  • Depression: 30-40%.
  • Quality of Life: Reduced even in "good outcome" survivors.

Long-Term Prognosis

  • Recurrence: 1-2% per year risk of new aneurysm formation or treated aneurysm rebleed.
  • Life Expectancy: Reduced (especially if significant disability).
  • Need for Lifelong Follow-Up: Regular imaging, BP control, lifestyle modification.

Factors Improving Prognosis

  • Early Aneurysm Securing (less than 24h): Prevents rebleed.
  • Nimodipine: Reduces poor outcome by 30-40%.
  • Specialist Neurocritical Care: Better monitoring, early intervention for complications.
  • Rehabilitation: Intensive physio, OT, speech therapy improves functional outcomes.
10. Evidence and Guidelines

Key Guidelines

GuidelineOrganisationKey Recommendations
SAHNICE NG228 (2022)CT within 6h is adequate to rule out SAH (no LP needed if less than 6h and reported by neuroradiologist). Nimodipine for all.
AneurysmsAHA / ASACoiling preferred over Clipping (ISAT data).

Landmark Evidence

1. ISAT Trial (International Subarachnoid Aneurysm Trial)

  • Citation: Molyneux A, et al. Lancet. 2002;360(9342):1267-1274. PMID: 12414200
  • Design: Multicentre RCT comparing coiling vs clipping in 2143 patients.
  • Result: Coiling gave significantly better disability-free survival at 1 year (23.5% dependent/dead vs 30.9% for clipping). ARR 7.4% (p=0.0001).
  • Impact: Shifted practice to "Coil First" policy.

2. ISAT Long-Term Follow-Up

  • Citation: Molyneux AJ, et al. Lancet. 2005;366(9488):809-817. PMID: 16139655
  • Result: Coiling maintained advantage at 10 years. Rebleeding slightly higher (2.9% vs 0.9%) but overall outcome better.

3. Nimodipine Trials (1980s)

  • Citation: Pickard JD, et al. BMJ. 1989;298(6674):636-642. PMID: 2496789
  • Result: Nimodipine 60mg 4-hourly x 21 days reduced poor outcome by 30-40%.
  • Impact: Class I, Level A recommendation. Standard of care for all SAH patients.

4. Ottawa SAH Rule (Perry Rule)

  • Citation: Perry JJ, et al. JAMA. 2013;310(12):1248-1255. PMID: 24065011
  • Result: Clinical decision rule with 100% sensitivity for SAH.

5. Modified Fisher Scale

  • Citation: Frontera JA, et al. Neurosurgery. 2006;59(1):21-27. PMID: 16823296
  • Result: Grade 3-4 (thick SAH ± IVH) predicts 70-80% vasospasm risk.

6. Beyond Nimodipine Review

  • Citation: Luzzi S, et al. Neurosurg Rev. 2024. PMID: 38967704
  • Summary: Reviews emerging neuroprotection strategies (clazosentan, statins, magnesium) but nimodipine remains gold standard.
11. Patient and Layperson Explanation

What is a Subarachnoid Haemorrhage?

A subarachnoid haemorrhage is bleeding on the surface of the brain, in the space between the brain and the thin tissues covering it. Usually, it's caused by a weakness in a blood vessel wall (called an aneurysm) that balloons out and suddenly bursts, like a tire blowout.

Why is it so dangerous?

The bleeding is life-threatening for several reasons:

  1. Direct damage: The blood itself is toxic to brain cells.
  2. Pressure: Bleeding increases pressure inside the skull, crushing the brain.
  3. Delayed problems: Even if you survive the initial bleed, the blood irritates blood vessels for days afterwards, making them spasm (narrow). This can cause strokes 3-10 days later.

About half of people who have a subarachnoid haemorrhage die, and many survivors have permanent disabilities.

What is the "thunderclap headache"?

It's the hallmark symptom - a headache that comes on instantly, reaching maximum pain within seconds. People describe it as:

  • "The worst headache of my life"
  • "Being hit with a baseball bat"
  • "An explosion in my head"

It's different from migraines or tension headaches which build up gradually. Any sudden, severe headache like this is a medical emergency - call 999 immediately.

What is a "sentinel headache" or "warning leak"?

About half of people have a smaller "warning" headache days or weeks before the major bleed. This is a tiny leak from the aneurysm. If this warning is recognized and treated, the catastrophic rupture can be prevented. That's why any new, sudden, severe headache should be taken seriously, even if it seems to settle.

How is it diagnosed?

  1. CT scan of the head (urgent, within 1 hour). This shows the blood in about 98% of cases if done quickly.
  2. Lumbar puncture (spinal tap) if the CT doesn't show blood but doctors still suspect SAH. This is done 12 hours after the headache started (to allow breakdown products of blood to appear in the spinal fluid).

What is the treatment?

Immediate:

  1. Secure the aneurysm (within 24 hours) to stop re-bleeding, which is often fatal. This is done either by:

    • Coiling (preferred): A thin tube is threaded from the groin up to the brain, and tiny platinum coils are packed into the aneurysm to seal it off. No surgery needed.
    • Clipping: Open brain surgery to place a titanium clip across the aneurysm neck.

  2. Nimodipine medication: A calcium channel blocker tablet taken every 4 hours for 3 weeks. This prevents the blood vessels from going into spasm and reduces the chance of strokes. This is essential - it reduces disability/death by 30-40%.

Ongoing care (in intensive care):

  • Close monitoring for complications (vasospasm, brain swelling, fluid on the brain).
  • Blood pressure control.
  • Daily ultrasound checks of blood flow in the brain (days 3-14).
  • If blood vessels do spasm, treatment includes raising blood pressure or injecting drugs directly into the spasmed vessels.

What are the chances of recovery?

Unfortunately, outcomes are often poor:

  • 50% die (many before reaching hospital).
  • Of survivors:
    • About 50-60% make a good recovery (able to live independently).
    • 30-40% have permanent disabilities (weakness, memory problems, personality changes).
    • Many survivors cannot return to work.

What about long-term?

  • Rehabilitation: Months of physiotherapy, occupational therapy, and cognitive therapy.
  • Follow-up scans: To check the aneurysm hasn't reformed (especially after coiling).
  • Lifestyle changes: Stop smoking (biggest risk factor for new aneurysms), control blood pressure, avoid heavy alcohol.
  • Driving: Must notify DVLA. Usually banned for 6 months minimum.
  • Family screening: If you have certain genetic conditions (like polycystic kidney disease), family members may need screening for aneurysms.

Can it be prevented?

  • Primary prevention: Control blood pressure, stop smoking, avoid excessive alcohol and recreational drugs (cocaine, amphetamines).
  • Screening: Only recommended if:
    • You have polycystic kidney disease.
    • Two or more first-degree relatives have had SAH or aneurysms.
    • You have certain genetic conditions (Ehlers-Danlos, Marfan syndrome).
    • Screening is done with MR Angiography (MRA).

Key message for the public

Any sudden, severe, "worst ever" headache is an emergency. Call 999. Don't wait. Early treatment saves lives.

12. References

Primary Sources

  1. NICE. Subarachnoid haemorrhage caused by a ruptured aneurysm: diagnosis and management (NG228). 2022. Available: https://www.nice.org.uk/guidance/ng228

  2. 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;360(9342):1267-1274. PMID: 12414200

  3. Molyneux AJ, Kerr RS, Yu LM, et al. International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion. Lancet. 2005;366(9488):809-817. PMID: 16139655

  4. Pickard JD, Murray GD, Illingworth R, et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. BMJ. 1989;298(6674):636-642. PMID: 2496789

  5. Perry JJ, Stiell IG, Sivilotti ML, et al. Clinical decision rules to rule out subarachnoid hemorrhage for acute headache. JAMA. 2013;310(12):1248-1255. PMID: 24065011

  6. Frontera JA, Claassen J, Schmidt JM, et al. Prediction of symptomatic vasospasm after subarachnoid hemorrhage: the modified Fisher scale. Neurosurgery. 2006;59(1):21-27. PMID: 16823296

  7. 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;43(6):1711-1737. PMID: 22556195

  8. Neifert SN, Chapman EK, Martini ML, et al. Aneurysmal Subarachnoid Hemorrhage: the Last Decade. Transl Stroke Res. 2021;12(3):428-446. PMID: 33078345

  9. Luzzi S, Bektaşoğlu PK, Doğruel Y, et al. Beyond nimodipine: advanced neuroprotection strategies for aneurysmal subarachnoid hemorrhage vasospasm and delayed cerebral ischemia. Neurosurg Rev. 2024;47(1):407. PMID: 38967704

  10. Steiner T, Juvela S, Unterberg A, et al. European Stroke Organization guidelines for the management of intracranial aneurysms and subarachnoid haemorrhage. Cerebrovasc Dis. 2013;35(2):93-112. PMID: 24323712

  11. Petruk KC, West M, Mohr G, et al. Nimodipine treatment in poor-grade aneurysm patients. Results of a multicenter double-blind placebo-controlled trial. J Neurosurg. 1988;68(4):505-517. PMID: 3280747

  12. Muehlschlegel S. Subarachnoid Hemorrhage. Continuum (Minneap Minn). 2018;24(6):1623-1657. PMID: 30516599

  13. Lim WS, Smith DL, Wise MP, et al. British Thoracic Society community acquired pneumonia guideline and the NICE pneumonia guideline: how they fit together. Thorax. 2015;70(7):698-700. PMID: 25977290

  14. Geraldini F, De Cassai A, Diana P, et al. A Comparison Between Enteral and Intravenous Nimodipine in Subarachnoid Hemorrhage: A Systematic Review and Network Meta-Analysis. Neurocrit Care. 2022;37(2):535-544. PMID: 35419702

  15. Romenskaya T, Longhitano Y, Piccolella F, et al. Cerebral Vasospasm: Practical Review of Diagnosis and Management. Rev Recent Clin Trials. 2022;17(4):285-296. PMID: 35950252

  16. van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid haemorrhage. Lancet. 2007;369(9558):306-318. PMID: 17258671

  17. Lawton MT, Vates GE. Subarachnoid Hemorrhage. N Engl J Med. 2017;377(3):257-266. PMID: 28723334

  18. Diringer MN, Bleck TP, Claude Hemphill J 3rd, et al. Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society's Multidisciplinary Consensus Conference. Neurocrit Care. 2011;15(2):211-240. PMID: 21773873

  19. Suarez JI, Tarr RW, Selman WR. Aneurysmal subarachnoid hemorrhage. N Engl J Med. 2006;354(4):387-396. PMID: 16436770

  20. Macdonald RL, Schweizer TA. Spontaneous subarachnoid haemorrhage. Lancet. 2017;389(10069):655-666. PMID: 27637674

13. Examination Focus

Common Exam Questions

  1. Diagnosis: "What is the time window for LP in suspected SAH?"

    • Answer: Must wait ≥12 hours after headache onset to allow xanthochromia (bilirubin) to develop. Sensitivity 100% between 12 hours and 2 weeks.

  2. Pharmacology: "What drug prevents vasospasm in SAH?"

    • Answer: Nimodipine 60mg PO 4-hourly for 21 days. Calcium channel blocker. Reduces poor outcome by 30-40%. Class I, Level A recommendation.

  3. Anatomy: "Which aneurysm location causes a 3rd nerve palsy?"

    • Answer: Posterior Communicating Artery (PCom) aneurysm. Expanding aneurysm compresses oculomotor nerve → painful 3rd nerve palsy (ptosis, eye down-and-out, dilated fixed pupil). Surgical emergency.

  4. Genetics: "What renal condition is associated with SAH?"

    • Answer: Autosomal Dominant Polycystic Kidney Disease (ADPKD). 10-15% develop intracranial aneurysms. Screen first-degree relatives with MRA if family history of SAH/aneurysms.

  5. Imaging: "What is xanthochromia?"

    • Answer: Yellow discoloration of CSF due to bilirubin (breakdown product of hemoglobin from RBCs in CSF). Detected by spectrophotometry. Distinguishes true SAH from traumatic tap.

  6. Grading: "What is the WFNS scale?"

    • Answer: World Federation of Neurosurgical Societies scale. Grades SAH severity based on GCS and presence of motor deficit. Grade I (GCS 15) = good prognosis. Grade V (GCS 3-6) = 70-80% mortality.

  7. Complications: "What is delayed cerebral ischemia?"

    • Answer: Cerebral ischemia occurring days 3-14 after SAH (peak Day 5-10) due to vasospasm (blood breakdown products cause arterial narrowing). Presents with new confusion, focal neurology, or GCS drop. Prevented by nimodipine. Treated with induced hypertension ± endovascular rescue.

  8. Treatment: "ISAT trial findings?"

    • Answer: International Subarachnoid Aneurysm Trial. RCT comparing endovascular coiling vs surgical clipping. Coiling had better disability-free survival at 1 year (23.5% vs 30.9% dependent/dead). Established "coil first" policy.

  9. Investigation: "When can you avoid LP in suspected SAH?"

    • Answer: NICE NG228 (2022): If CT head performed within 6 hours of headache onset and reported as negative by specialist neuroradiologist, SAH is effectively ruled out. LP not needed.

  10. Monitoring: "What investigation monitors for vasospasm?"

    • Answer: Transcranial Doppler (TCD) ultrasound. Daily from Day 3-14. MCA velocity >120 cm/s suggests vasospasm. >200 cm/s = severe. Lindegaard ratio (MCA/ICA velocity) >3 confirms vasospasm (differentiates from hyperemia).

Viva Points

1. NICE NG228 Update (2022):

  • Crucial change: If CT head done less than 6 hours from headache onset and reported negative by consultant neuroradiologist, SAH is ruled out (no LP needed). Sensitivity >99%.
  • LP only if: CT >6h from onset, CT equivocal, or CT reported by non-specialist.
  • This reduces unnecessary LPs and speeds diagnosis.

2. Triple H Therapy (Historical vs Current):

  • Old practice: Hypertension, Hypervolemia, Hemodilution to treat/prevent vasospasm.
  • Current evidence: Hypervolemia and hemodilution are not beneficial (risk pulmonary edema, no outcome benefit).
  • Modern approach: Euvolemia (avoid hypovolemia) + Induced Hypertension (SBP 160-200 mmHg) if aneurysm secured. Endovascular rescue if refractory.

3. Nimodipine Mechanism:

  • Not just an anti-vasospasm drug. Has neuroprotective effects beyond preventing vessel narrowing.
  • Blocks calcium entry into neurons, reduces excitotoxicity.
  • Must start immediately, continue 21 days, even if aneurysm not yet secured.

4. Coiling vs Clipping Decision:

  • Coiling preferred (ISAT): Better outcomes, less invasive, suitable for posterior circulation, elderly, poor-grade patients.
  • Clipping indicated for: MCA aneurysms (surgical access easier), wide-neck aneurysms unsuitable for coiling, young patients (lifetime durability), associated ICH needing evacuation.
  • Rebleeding risk: Higher with coiling (2-3% vs less than 1%) but overall outcome still better. Requires long-term imaging follow-up.

5. Hyponatremia: SIADH vs CSW:

  • Both cause low sodium, but management is opposite.
  • SIADH: Euvolemic. Treat with fluid restriction.
  • CSW (Cerebral Salt Wasting): Hypovolemic (renal sodium loss). Treat with IV 0.9% saline or 3% hypertonic saline.
  • Importance: Hypovolemia worsens vasospasm. Must maintain euvolemia. In SAH, CSW is more common than SIADH.

6. Subhyaloid Hemorrhage (Terson Syndrome):

  • Retinal hemorrhage (between retina and vitreous) in 10-20% of SAH.
  • Looks like a fluid level on fundoscopy.
  • Mechanism: Acute ICP rise transmitted to optic nerve sheath → retinal vein rupture.
  • Clinical pearl: Always do fundoscopy in suspected SAH.

7. Sentinel Headache Litigation Risk:

  • 30-50% have "warning leak" days-weeks before major rupture.
  • Often misdiagnosed as migraine or tension headache.
  • Major cause of litigation if missed.
  • Action: Any new, sudden, severe headache that is "different" from usual → investigate (CT + LP).

8. Genetic Syndromes and Screening:

  • ADPKD: 10-15% have aneurysms. Screen with MRA if family Hx of SAH/aneurysms or if patient >30 years with hypertension.
  • Ehlers-Danlos Type IV: Collagen defect. Multiple aneurysms, arterial dissection.
  • First-degree relatives: Screen if 2+ relatives with SAH/aneurysms.

9. Re-bleeding Risk and Timing:

  • Highest risk: First 24 hours (4-15% rebleed). Peak in first 6 hours.
  • Mortality if rebleeds: 70-80%.
  • Prevention: Secure aneurysm ASAP (less than 24h). Avoid hypertension pre-securing (SBP less than 160).

10. Modified Fisher Scale:

  • Predicts vasospasm risk based on CT blood load.
  • Grade 3-4 (thick clot ± IVH): 70-80% develop vasospasm. Need intensive monitoring (daily TCD, close neuro obs).
  • Grade 0-2: less than 30% vasospasm risk.

Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.

Last updated: 2025-12-24

At a Glance

EvidenceHigh
Last Updated2025-12-24
Emergency Protocol

Red Flags

  • Thunderclap Headache (Max intensity < 1-5 mins)
  • 3rd Nerve Palsy (PCom Aneurysm expansion warning)
  • Seizures
  • Drop in GCS (Hydrocephalus/Rebleed)

Clinical Pearls

  • **Investigate the Neck**: Headache + Neck Stiffness = Meningitis OR SAH. If they are feverish, think Meningitis. If they are afebrile but have neck stiffness (blood irritating meninges), think SAH.
  • Tube 4, suggests traumatic tap.

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines