Subarachnoid Hemorrhage¶
Chapter 440 | Part 13: Neurologic Disorders · Part 13 – Neurologic Disorders · Chapter 440
Key Clinical Points¶
- Thunderclap headache is the hallmark of aneurysmal rupture; sudden onset is the most critical feature.
- Noncontrast CT identifies blood in >95% of cases within 72 h; lumbar puncture is indicated if CT is negative.
- Nimodipine (60 mg PO every 4 h) improves outcomes by preventing ischemic injury, not by reducing vasospasm risk.
- Rerupture of an untreated aneurysm occurs in ~30% of cases in the first month, peaking in the first 7 days.
- Delayed cerebral ischemia (DCI) occurs in ~30% of patients, typically peaking at 7 days post-hemorrhage.
- Hyponatremia (cerebral salt-wasting syndrome) is common in the first 2 weeks; free-water restriction is contraindicated.
- Modified Fisher Grade 4 (thick blood with intraventricular blood) carries a 40% risk of symptomatic vasospasm.
- Sentinel bleeds (small leaks) are high-risk indicators for imminent major hemorrhage.
- Developmental venous anomalies are benign and should be ignored if found incidentally.
- Saccural aneurysms in the anterior circulation account for ~89% of cases.
DEFINITION & OVERVIEW¶
• Definition: Subarachnoid hemorrhage (SAH) renders the brain critically ill from both primary and secondary brain insults. • Primary Causes: ◦ Rupture of a saccular aneurysm (most common cause excluding head trauma) ◦ Bleeding from a vascular malformation (AVM or dural arteriovenous fistula) ◦ Extension into the subarachnoid space from a primary intracerebral hemorrhage • Idiopathic SAH: ◦ Often localized to the perimesencephalic cisterns ◦ Generally benign; likely venous/capillary source; angiography is unrevealing.
ETIOLOGY & PATHOPHYYSOLOGY¶
• Saccular Aneurysms: ◦ Occur at the bifurcations of large- to medium-sized intracranial arteries ◦ ~89% occur in the anterior circulation (Circle of Willis) ◦ ~20% of patients have multiple aneurysms, often at mirror sites bilaterally ◦ Anatomy: Neck and dome structure are critical for planning treatment; rupture typically occurs at the dome where the wall thins to ≤0.5 mm. • Vasculopathy: ◦ Loss of internal elastic lamina at the base of the neck ◦ Media thins, and connective tissue replaces smooth-muscle cells • Pathophysiology of Rupture: ◦ Sudden rise in intracranial pressure (ICP) → potential for sudden loss of consciousness (in nearly half of patients) ◦ "Worst headache of my life" (sudden onset is the most important characteristic) ◦ Associated symptoms: Neck stiffness, vomiting, and potentially focal deficits (hemiparesis, aphasia, mental slowness). • Specific Clinical Signs of Expanding Aneurysms: ◦ 3rd nerve palsy + pupillary dilation → Posterior communicating artery/Internal carotid junction ◦ 6th nerve palsy → Cavernous sinus ◦ Visual field defects → Supraclinoid carotid or anterior cerebral artery (ACA) ◦ Occipital and posterior cervical pain → PICA or AICA ◦ Pain in eye/low temple → Middle cerebral artery (MCA) • Vascular Malformations: ◦ Arteriovenous Malformations (AVM): ◦ Rupture risk: ~2–4% per year (unruptured); up to 17% per year (previously ruptured) ◦ Symptomatic cerebral vasospasm is rare ◦ Large AVMs in MCA territory are most common ◦ Diagnosis: MRI > CT; Gold standard = conventional x-ray angiography ◦ Risk factors: Smaller lesions, deep venous drainage, venous outflow stenosis, intranidal aneurysms ◦ Developmental Venous Anomalies: ◦ Functional venous channels → No clinical significance; should be ignored ◦ Surgery may cause venous infarction ◦ May be associated with cavernous malformations (which do have bleeding risk) ◦ Capillary Telangiectasias: ◦ True capillary malformations in pons/deep white matter ◦ Rarely produce significant symptoms; no treatment options exist ◦ Associated with hereditary hemorrhagic telangiectasia ◦ Dural Arteriovenous Fistulas: ◦ Acquired connections (dural artery to dural sinus) ◦ Symptoms: Pulsatile tinnitus, headache ◦ Treatment: Surgical/endovascular techniques are usually curative ◦ May form because of trauma, but most are idiopathic. ◦ Cavernous Angiomas (Cavernous Malformations): ◦ Tufts of capillary sinusoids in deep white matter/brainstem ◦ Risk: 0.7–1.5% per year; higher if multiple or prior bleed ◦ Genetics: KRIT1, CCM2, PDCD10 ◦ Treatment: Surgery only for those near surface with prior bleeding or refractory seizures.
EPIDEMIOLOGY¶
• Prevalence: ~2% of adults harbor intracranial aneurysms (approx. 4 million in the US). • Incidence: 6–11 per 100,000 person-years → 25,000–30,000 cases annually in the US. • Risk Factors: 1.3 relative risk in women; increasing incidence with age. • Mortality/Morbidity: ◦ Overall mortality: ~35% ◦ One-third die immediately before hospital admission ◦ Over half of survivors have significant neurologic deficits (due to initial hemorrhage, delayed cerebral ischemia, or hydrocephalus).
CLINICAL FEATURES¶
• General Presentation: ◦ Most unruptured aneurysms are asymptomatic ◦ Rupture leads to decline in mental status and worsening headache• Sentinel Bleeds: ◦ Small ruptures/leaks → sudden unexplained headache → high suspicion for imminent major hemorrhage. • Delayed Neurologic Deficits (4 main causes): ◦ 1. Rerupture: ◦ Risk: ~30% in first month; peak in first 7 days ◦ Outcome: 50% mortality rate and poor outcome → early treatment is critical. ◦ 2. Hydrocephalus: ◦ Acute: Stupor/coma → managed with external ventricular drain ◦ Subacute: Progresses over days/weeks → drowsiness, slowed mentation ◦ Chronic: Weeks to months later → gait difficulty, incontinence. ◦ 3. Delayed Cerebral Ischemia (DCI): ◦ Cause: Vasospasm (narrowing of arteries) and inflammation from blood breakdown products ◦ Incidence: ~30% of patients; major cause of morbidity/death ◦ Timing: First appear 4–14 days post-hemorrhage (peak at 7 days) ◦ 4. Hyponatremia: ● Mechanism: Cerebral salt-wasting syndrome (mediated by ANP and BNP) → concurrent natriuresis and volume depletion ● Timing: Developur quickly in first 2 weeks; usually clears in 1–2 weeks ● Management: Do not use free-water restriction (risk of stroke).
DIFFERENTIAL DIAGNOSIS¶
• Thunderclap Headache: ◦ Can be a variant of migraine → requires definitive workup for aneurysm/intracranial pathology before concluding it is a migraine.
DIAGNOSTIC APPROACH¶
- Initial Imaging (Noncontrast CT): ◦ Timing: Within 72 h ◦ Sensitivity: >95% for visualizing blood ◦ Purpose: Identify location of aneurysm, identify cause of deficit, predict vasospasm risk.
- Lumbar Puncture: ◦ Indication: If CT is negative.
- Angiography (Gold Standard): ◦ Procedure: Four-vessel conventional x-ray angiography ◦ Purpose: Localize/define aneurysm anatomy, identify other unruptured aneurysms ◦ Timing: Can be performed at initial presentation to expedite treatment.
- Grading Scales: ◦ Clinical (Table 1): Hunt-Hess and WFNS scales used to predict outcome based on mental status, GCS, and motor deficits. ◦ Imaging (Table 2): Modified Fisher Grading System predicts risk of symptomatic vasospasm based on blood thickness (Note: "thick" is ≥1 mm). Grade 4 carries a 40% risk.
MANAGEMENT & TREATMENT¶
- Aneurysm Treatment: ◦ Surgical or endovascular techniques are typically curative for aneurysms and dural AV fistulas.
- Vasospasm Management: ◦ Nimodipine: 60 mg PO every 4 h → improves outcomes by preventing ischemic injury (not by reducing vasospasm risk). ◦ Induced Hypertension: ◦ Indication: Symptomatic patients with vasospasm ◦ Method: Plasma volume expansion and IV vasopressors (phenylephrine or norepinephrine) ◦ Note: Prophylactic use of induced hypertension is not recommended.
- Fluid Management: ◦ Goal: Target euvolemia; avoid hypervolemia and hypovolemia.
PROGNOSIS & COMPLICATIONS¶
• Vasospasm Risk Factors: ◦ Higher risk with larger volume of blood or thicker blood (Fisher Grade 3-4). ◦ Prediction: More reliable for MCA and ACA; less reliable for posterior circulation. • Complications: ◦ Rerupture: ~30% in first month, peak in first 7 days. ◦ Hydrocephalus: Can be acute (stupor/coma), subacute (drowsiness), or chronic (gait difficulty). ◦ Delayed Cerebral Ischemia: Occurs in ~30% of patients; major cause of morbidity and death. ◦ Hyponatremia: Common in first 2 weeks; risk of stroke if treated with free-water restriction.
KEY PEARLS & HIGH-YIELD POINTS¶
• Time is Brain: Early aneurysm repair prevents rerupture and allows for safer management of vasospasm. ◦ Nimodipine: Standard of care; 60 mg every 4 hours. ◦ Hyponatremia: Common in first 2 weeks; do NOT use free-water restriction. ◦ Fisher Scale: Grade 4 (thick blood + intraventricular) → 40% risk of symptomatic vasospasm. ◦ Sentinel Bleeds: Any sudden, unexplained headache should be treated as a potential SAH until proven otherwise.
Reference Tables¶
TABLE 440-1 Grading Scales for Subarachnoid Hemorrhage GRADE 1¶
Harrison's 22e, p.3459
| GRADE | HUNT-HESS SCALE | WORLD FEDERATION OF NEUROSURGICAL SOCIETIES (WFNS) SCALE |
|---|---|---|
| 1 | Asymptomatic, or minimal headache and slight nuchal rigidity. Normal mental status, no cranial nerve or motor findings |
GCSa score 15, no motor deficits |
| Moderate to severe headache, nuchal rigidity, normal mental status and motor function, may have cranial nerve deficit |
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| 3 | Somnolent, confused, may have cranial nerve or mild motor deficit |
GCS score 13–14, with motor deficits |
| Stupor, moderate to severe motor deficit, may have intermittent reflex posturing |
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| 5 | Coma, reflex posturing or flaccid | GCS score 3–6, with or without motor deficits |
TABLE 440-2 Modified Fisher Grading System for Prediction of Vasospasm Risk GRADE 0 1 2 3 4 Note: “Thin” is <1 mm…¶
Harrison's 22e, p.3460
| GRADE | CT SCAN FINDINGS | RISK OF SYMPTOMATIC VASOSPASM |
|---|---|---|
| 0 | No subarachnoid or intraventicular blood | 0% |
| Focal or diffuse thin subarachnoid blood without intraventricular blood |
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| 2 | Focal or diffuse thin subarachnoid blood with intraventricular blood |
33% |
| Focal or diffuse thick subarachnoid blood without intraventricular blood |
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| 4 | Focal or diffuse thick subarachnoid blood with intraventricular blood |
40% |