SAH & Aneurysms
Subarachnoid Hemorrhage & Aneurysms
What You'll Learn
- Recognize the classic presentation of aneurysmal SAH — thunderclap headache, meningismus, and the sentinel headache concept
- Diagnostic algorithm: NCCT sensitivity by time → LP (xanthochromia) → CTA → DSA
- Hunt & Hess, WFNS, and Modified Fisher grading scales and their prognostic implications
- Aneurysm types, locations, associated conditions, and rupture risk factors
- Acute management: surgical clipping vs. endovascular coiling (ISAT, BRAT trials) and timing of intervention
- Vasospasm and delayed cerebral ischemia — timeline, monitoring (TCD, Lindegaard ratio), nimodipine, and rescue therapies
- Complications: rebleeding, hydrocephalus, hyponatremia (SIADH vs. CSW), cardiac injury, seizures
- Unruptured aneurysm management: ISUIA data, PHASES score, screening recommendations
HighYield Pearls
- Thunderclap “worst headache of my life”: sudden, peak in seconds, ± nuchal rigidity, photophobia, N/V, LOC — assume SAH until proven otherwise; CN III palsy with pupil involvement → PCom aneurysm
- Diagnostic algorithm: non-contrast head CT ≥95% sensitive within 6 h of onset → sensitivity falls after; if CT negative and clinical suspicion remains → LP for xanthochromia (spectrophotometry, optimal ≥12 h after bleed); then CTA, DSA gold standard for small/mycotic/dissecting aneurysms
- Sentinel headache in 30–50% days–weeks before rupture — warning leak; do NOT dismiss as migraine
- Saccular aneurysm distribution: A-com 30% > P-com 25% > MCA 20% > basilar tip 7% > PICA 3%; risk factors HTN, smoking, family hx, ADPKD, Ehlers-Danlos IV, FMD, coarctation
- Re-bleeding risk is highest in the first 24 h → secure aneurysm urgently (clip vs coil <24–72 h); pre-securing keep SBP <140–160; reverse anticoagulation; analgesia (avoid NSAIDs); short-course AED common practice (not routine prophylaxis)
- Clipping vs coiling (ISAT): coiling → lower disability at 1 year, favored for posterior circulation / narrow-neck / poor-grade SAH; clipping favored for wide-neck and MCA bifurcation; flow diverter (Pipeline) for giant/cavernous; balloon- or stent-assisted coiling for complex morphology
- Vasospasm / DCI days 4–14 (peak 7–10): oral nimodipine 60 mg q4h × 21 d improves outcomes (not vasospasm rate) — routine prophylaxis; clinical decline → CTA/CT perfusion → induced hypertension (Triple-H abandoned); refractory → intra-arterial calcium channel blockers / balloon angioplasty
- Hyponatremia: CSW vs SIADH — distinguish by VOLUME STATUS, not urine Na alone. CSW = hypovolemic (low BP, tachycardia, negative fluid balance) → hypertonic saline + NaCl tablets ± fludrocortisone; SIADH = euvolemic; AVOID fluid restriction in SAH (worsens vasospasm/DCI) — treat with hypertonic saline; SAH hyponatremia is most often CSW
- Hydrocephalus: communicating from arachnoid scarring → EVD acutely; ~20% need permanent VP shunt
- Perimesencephalic non-aneurysmal SAH: blood centered around midbrain/pons cisterns, negative CTA & DSA → benign course, minimal vasospasm risk, no recurrence — distinct entity; convexity (cortical) SAH in elderly → CAA (superficial siderosis); in younger → RCVS, vasculitis, dissection, AVM
- Unruptured aneurysm: use PHASES (a point score) to estimate 5-year rupture risk; consider repair based on size (often >7 mm, or lower threshold in posterior circulation / PCom), location, growth, irregular morphology, smoking, family history, age, comorbidity, and treatment risk — PHASES is a score, not a size.
🔍 Quick ReferencePresentation / scales · Imaging / etiology · Complications / treatment
Presentation / scales
- “Worst headache of my life” / thunderclap, peaks in seconds → aneurysmal SAH until proven otherwise
- Sentinel headache days–weeks before rupture (30–50%) → warning leak from saccular aneurysm
- CN III palsy with pupil involvement (down-and-out, mydriasis) → posterior communicating artery aneurysm
- Hunt-Hess (clinical 0–V; V = deep coma, decerebrate) → prognostic clinical scale
- Modified Fisher (CT — thick cisternal blood + IVH) → vasospasm risk stratification
- WFNS (GCS + motor deficit) → clinical severity grading
Imaging / etiology
- Hyperdense blood in basal cisterns / Sylvian fissure on NCCT → aneurysmal SAH
- Xanthochromia by spectrophotometry on LP ≥12 h after onset → confirms SAH when CT negative
- Blood centered around midbrain/pons cisterns, negative CTA/DSA → perimesencephalic non-aneurysmal SAH (benign)
- Convexity (cortical) SAH in elderly ± superficial siderosis → cerebral amyloid angiopathy
- Convexity SAH + thunderclap in younger / postpartum / sympathomimetic, “string-of-beads” CTA that resolves <12 wk (steroids worsen) → RCVS
- “String of beads” on carotid/intracranial angiography (non-RCVS) → fibromuscular dysplasia
- Bilateral renal cysts + intracranial aneurysm → ADPKD
- Distal MCA-branch aneurysm in endocarditis → mycotic aneurysm
Complications / treatment
- Nimodipine 60 mg PO q4h × 21 d → routine SAH prophylaxis — improves outcomes, not vasospasm rate
- Days 4–14 (peak 7–10) new deficit + elevated TCD velocities → vasospasm / delayed cerebral ischemia → induced hypertension, IA calcium channel blockers, balloon angioplasty
- Hyponatremia + hypovolemia + negative fluid balance + concentrated urine → cerebral salt wasting → hypertonic saline + NaCl tablets ± fludrocortisone (NEVER fluid restrict in SAH)
- Hyponatremia + euvolemia → SIADH — still treat with hypertonic saline in SAH (avoid free water, avoid fluid restriction)
- Progressive ventriculomegaly / declining mental status post-SAH → communicating hydrocephalus → EVD; ~20% need VP shunt
- ISAT trial → coiling lower 1-year disability vs clipping (esp. posterior circulation)
- Wide-neck / MCA bifurcation aneurysm → surgical clipping preferred
- Giant or cavernous ICA aneurysm → flow diverter (Pipeline)
- PHASES score (5-year rupture risk) + size >7 mm or lower threshold in posterior circulation/PCom, irregular morphology, smoker, family hx → consider repair of unruptured aneurysm
Epidemiology & Risk Factors
Incidence & Outcomes
- Incidence: ~9 per 100,000 person-years worldwide; higher in Finland and Japan (~20 per 100,000)
- Peak age: 50–60 years; female:male ratio ~1.6:1
- Case fatality rate: ~35% at 30 days; ~50% overall mortality (including pre-hospital deaths)
- ~12–15% of patients die before reaching hospital
- Of survivors, ~30% have moderate-to-severe disability; only ~33% achieve good functional recovery
- SAH accounts for ~5% of all strokes but disproportionate share of stroke-related lost productive life years (younger patients)
Risk Factors
Modifiable Risk Factors
- Cigarette smoking: Strongest modifiable risk factor; ~3–4× increased risk; dose-dependent; risk declines after cessation
- Hypertension: ~2.5× increased risk; promotes aneurysm formation, growth, and rupture
- Heavy alcohol consumption: ≥150 g/week (≥~10 drinks/week); binge drinking especially risky
- Cocaine and sympathomimetic drug use: Acute hypertensive surges → rupture; cocaine is a major risk factor in young patients
Non-Modifiable Risk Factors
- Family history: First-degree relative with SAH → 3–7× increased risk; two or more affected first-degree relatives → screening recommended
- Female sex: Especially post-menopausal (estrogen may be protective)
- Prior SAH: ~2% per year risk of new SAH from a different aneurysm
Associated Genetic & Connective Tissue Conditions
- Autosomal Dominant Polycystic Kidney Disease (ADPKD): ~8–12% harbor intracranial aneurysms (vs. 2–3% general population); screening recommended, especially with family history of SAH
- Ehlers-Danlos syndrome type IV (vascular type): Defective type III collagen → arterial fragility; aneurysms and dissections
- Fibromuscular dysplasia (FMD): ~7% have intracranial aneurysms; “string of beads” on angiography
- Coarctation of the aorta: Associated with intracranial aneurysms, possibly due to hemodynamic stress
- Marfan syndrome: Modest association with intracranial aneurysms (less strong than ADPKD or Ehlers-Danlos IV)
- Hereditary hemorrhagic telangiectasia (HHT): Associated with pulmonary AVMs and rarely cerebral aneurysms
💎 Board Pearl
ADPKD is the most commonly tested genetic association with intracranial aneurysms. Screen ADPKD patients with MRA if they have a family history of aneurysm/SAH. Smoking is the strongest modifiable risk factor — it promotes aneurysm formation AND rupture. Ehlers-Danlos type IV involves type III collagen (vascular, NOT skin hypermobility type).
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