Clinical Vascular

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 secondsaneurysmal 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 NCCTaneurysmal SAH
  • Xanthochromia by spectrophotometry on LP ≥12 h after onsetconfirms SAH when CT negative
  • Blood centered around midbrain/pons cisterns, negative CTA/DSAperimesencephalic non-aneurysmal SAH (benign)
  • Convexity (cortical) SAH in elderly ± superficial siderosiscerebral 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 aneurysmADPKD
  • Distal MCA-branch aneurysm in endocarditismycotic aneurysm
Complications / treatment
  • Nimodipine 60 mg PO q4h × 21 droutine SAH prophylaxis — improves outcomes, not vasospasm rate
  • Days 4–14 (peak 7–10) new deficit + elevated TCD velocitiesvasospasm / delayed cerebral ischemia → induced hypertension, IA calcium channel blockers, balloon angioplasty
  • Hyponatremia + hypovolemia + negative fluid balance + concentrated urinecerebral salt wasting → hypertonic saline + NaCl tablets ± fludrocortisone (NEVER fluid restrict in SAH)
  • Hyponatremia + euvolemiaSIADH — still treat with hypertonic saline in SAH (avoid free water, avoid fluid restriction)
  • Progressive ventriculomegaly / declining mental status post-SAHcommunicating hydrocephalus → EVD; ~20% need VP shunt
  • ISAT trialcoiling lower 1-year disability vs clipping (esp. posterior circulation)
  • Wide-neck / MCA bifurcation aneurysmsurgical clipping preferred
  • Giant or cavernous ICA aneurysmflow diverter (Pipeline)
  • PHASES score (5-year rupture risk) + size >7 mm or lower threshold in posterior circulation/PCom, irregular morphology, smoker, family hxconsider 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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