Subarachnoid Hemorrhage¶
Chapter 440 | Part 13: Neurologic Disorders
KEY CLINICAL POINTS¶
- SAH is most commonly caused by rupture of a saccular aneurysm (85% of cases), with other causes including AVMs, cavernous malformations, and traumatic injury.
- Hunt-Hess and WFNS grading systems predict outcomes: higher grades correlate with increased mortality (e.g., 60% mortality for WFNS Grade 5).
- Vasospasm is the leading cause of delayed cerebral ischemia, with modified Fisher scale grading CT findings to predict vasospasm risk (Grade 4: 40% risk).
- Endovascular coiling is preferred over surgical clipping for most aneurysms, with better short-term outcomes but similar long-term functional results.
- Hyponatremia (cerebral salt-wasting syndrome) is common after SAH and requires careful management to avoid osmotic demyelination.
1. DEFINITION & OVERVIEW¶
Subarachnoid hemorrhage (SAH) is acute bleeding into the subarachnoid space, most commonly from ruptured saccular aneurysms. It presents with sudden severe headache ("thunderclap headache") and is associated with high morbidity/mortality. SAH can also result from AVM rupture, cavernous malformations, or traumatic injury.
Table 440-1: Grading Scales for Subarachnoid Hemorrhage¶
| 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 | GCS score 15, no motor deficits |
| 2 | Moderate to severe headache, nuchal rigidity, normal mental status and motor function, may have cranial nerve deficit | GCS score 13–14, with motor deficits |
| 3 | Somnolent, confused, may have cranial nerve or mild motor deficit | GCS score 13–14, with motor deficits |
| 4 | Stupor, moderate to severe motor deficit, may have intermittent reflex posturing | GCS score 7–12, with or without motor deficits |
| 5 | Coma, reflex posturing or flaccid | GCS score 3–6, with or without motor deficits |
1.1 Pathophysiology¶
Ruptured saccular aneurysms cause bleeding into the subarachnoid space, leading to vasospasm, hydrocephalus, and cerebral ischemia. AVMs may bleed intraparenchymally or into the subarachnoid space, with risk of rebleeding and venous infarction. Cavernous malformations have a 0.7–1.5% annual bleeding risk.
1.2 Clinical Presentation¶
Classic presentation: sudden severe headache ("worst headache of my life"), neck stiffness, vomiting, and altered mental status. 10% present with loss of consciousness. 45% have severe headache with exertion. 50% have focal neurological deficits from hematoma or vasospasm.
2. EPIDEMIOLOGY¶
Incidence: 6–11 per 100,000 person-years in the US. 25,000–30,000 annual cases. 1.3x higher risk in women. 85% of SAH cases from ruptured saccular aneurysms. AVMs account for ~30% of SAH cases. Cavernous malformations: 0.7–1.5% annual bleeding risk. Risk factors: hypertension, smoking, family history, prior aneurysm rupture.
2.1 Demographics¶
Peak incidence in 55–65 years. Women more affected (1.3x risk). 20% of patients have multiple aneurysms. 5% of SAH cases are from giant aneurysms (>25 mm).
3. ETIOLOGY & PATHOPHYSIOLOGY¶
Primary cause: rupture of saccular aneurysms (85% of cases). Other causes: AVM rupture, cavernous malformations, traumatic injury, or mycotic aneurysms. Pathophysiology includes vasospasm, hydrocephalus, and cerebral ischemia. AVMs may cause venous infarction or steal syndrome.
Table 440-2: Modified Fisher Grading System for Prediction of Vasospasm Risk¶
| GRADE | CT SCAN FINDINGS | RISK OF SYMPTOMATIC VASOSPASM |
|---|---|---|
| 0 | No subarachnoid or intraventricular blood | 0% |
| 1 | Focal or diffuse thin subarachnoid blood without intraventricular blood | 24% |
| 2 | Focal or diffuse thin subarachnoid blood with intraventricular blood | 33% |
| 3 | Focal or diffuse thick subarachnoid blood without intraventricular blood | 33% |
| 4 | Focal or diffuse thick subarachnoid blood with intraventricular blood | 40% |
3.1 Aneurysm Pathophysiology¶
Saccular aneurysms form at arterial bifurcations. Rupture leads to subarachnoid hemorrhage, vasospasm, and rebleeding risk (20% in first 2 weeks, 30% in first month). Giant aneurysms (>25 mm) have 8–10% annual rupture risk.
3.2 Vasospasm Mechanisms¶
Vasospasm occurs due to direct effects of blood and its breakdown products on cerebral arteries. Risk factors: volume of subarachnoid blood, aneurysm location, and inflammatory mediators. 30% of patients develop delayed cerebral ischemia.
4. CLINICAL FEATURES¶
Classic presentation: sudden severe headache ("thunderclap headache"), neck stiffness, vomiting, and altered mental status. 10% present with loss of consciousness. 45% have severe headache with exertion. 50% have focal neurological deficits. 30% develop delayed cerebral ischemia.
4.1 Delayed Neurological Deficits¶
Rerupture (30% risk in first month), hydrocephalus (subacute/chronic), delayed cerebral ischemia (30% of patients), and hyponatremia (cerebral salt-wasting syndrome).
4.2 Complications¶
Hydrocephalus, vasospasm, cerebral infarction, rebleeding, and hyponatremia. 35% mortality rate for aneurysmal SAH, with 1/3 dying before hospital admission.
5. DIFFERENTIAL DIAGNOSIS¶
Headache of other causes (migraine, tension-type headache), intracerebral hemorrhage, cerebral infarction, meningitis, and subdural hematoma. Sentinel bleeds (small subarachnoid bleeds) may precede major hemorrhage.
5.1 Red Flags¶
Sudden severe headache, neck stiffness, vomiting, altered mental status, or focal neurological deficits. Presence of risk factors (hypertension, smoking, family history).
6. INVESTIGATIONS & DIAGNOSIS¶
Noncontrast CT (gold standard for initial diagnosis), lumbar puncture (if CT negative), CT angiography (for aneurysm localization), and conventional angiography (gold standard for aneurysm characterization).
6.1 Diagnostic Criteria¶
CT scan within 72 h detects 95% of SAH cases. Lumbar puncture confirms subarachnoid blood (xanthochromia peaks at 48 h). CT angiography identifies aneurysms and vasospasm.
6.2 Imaging Techniques¶
CT angiography (CTA) is preferred over conventional angiography for initial evaluation. Transcranial Doppler (TCD) monitors vasospasm. CT perfusion identifies reversible ischemia.
7. MANAGEMENT & TREATMENT¶
Immediate management: airway, blood pressure control (target systolic <160 mmHg), antifibrinolytic agents (aminocaproic acid), and anticoagulant reversal. Endovascular coiling vs surgical clipping based on aneurysm morphology. Nimodipine (60 mg PO q4h) for vasospasm prevention.
7.1 Medical Management¶
Blood pressure control, anticoagulant reversal, hyponatremia management, and prevention of secondary insults (e.g., DVT). Nimodipine reduces vasospasm risk but may cause hypotension.
7.2 Endovascular Treatment¶
Coiling via microcatheter with platinum coils. Flow-diverting stents and balloon-assisted coiling for complex aneurysms. Endovascular treatment reduces rebleeding risk but may increase delayed cerebral ischemia risk.
7.3 Surgical Treatment¶
Clipping via craniotomy for accessible aneurysms. Indicated for large AVMs causing steal syndrome or venous infarction. Risks include neurologic morbidity from brain retraction.
8. PROGNOSIS & COMPLICATIONS¶
Mortality: 35% for aneurysmal SAH, with 1/3 dying before hospital admission. 50% of survivors have significant neurologic deficits. Complications include vasospasm, hydrocephalus, rebleeding, and hyponatremia. 30% develop delayed cerebral ischemia.
8.1 Long-Term Outcomes¶
Cognitive and behavioral deficits in 50% of survivors. 10–20% require long-term follow-up for unruptured aneurysms. 30% of patients have poor functional outcomes at 1 year.
9. SPECIAL CONSIDERATIONS¶
Hyponatremia management: avoid free-water restriction, use hypertonic saline for severe cases. Anticoagulant reversal with vitamin K or reversal agents. DVT prophylaxis with heparin or compression stockings. Avoid anticonvulsants beyond 7 days unless seizures occur.
9.1 Pregnancy¶
SAH in pregnancy has higher maternal mortality (50–60%) due to increased bleeding risk. Cesarean delivery may be required for maternal stabilization.
9.2 Hyponatremia¶
Cerebral salt-wasting syndrome: 1–2 weeks duration. Avoid rapid correction of hyponatremia to prevent osmotic demyelination syndrome.
10. KEY POINTS & CLINICAL PEARLS¶
- SAH is a medical emergency with high mortality; immediate CT scan and lumbar puncture are critical. 2. Hunt-Hess/WFNS grading guides treatment decisions. 3. Nimodipine is first-line for vasospasm prevention. 4. Endovascular coiling is preferred over clipping for most aneurysms. 5. Hyponatremia management is critical to prevent osmotic demyelination.