What is the management of Subarachnoid Hemorrhage (SAH)?

Management of Subarachnoid Hemorrhage (SAH)

SAH is a medical emergency requiring immediate transfer to a high-volume center (>35 patients/year) with multidisciplinary neurovascular teams, early aneurysm securing (preferably by endovascular coiling), and administration of oral nimodipine 60 mg every 4 hours for 21 days starting within 96 hours of hemorrhage onset. 1, 2

Initial Assessment and Stabilization

Airway and Breathing Management

• Secure the airway immediately if consciousness is impaired using rapid sequence intubation with preoxygenation and pharmacological blunting of reflex dysrhythmia to avoid blood pressure spikes 3, 4
• Maintain appropriate oxygenation without hyperventilation, as hyperventilation worsens cerebral ischemia by causing vasoconstriction 4
• Place a nasogastric or orogastric tube after intubation to reduce aspiration risk 3

Clinical Severity Assessment

• Grade clinical severity immediately using validated scales (Hunt and Hess Scale, World Federation of Neurological Surgeons Scale, or Glasgow Coma Scale) as this is the most useful indicator of outcome 1, 2
• Document prognostic factors including age, preexisting hypertension, time of admission after SAH, and blood pressure at admission 3

Blood Pressure Control

• Control systolic blood pressure to <160 mmHg using titratable agents (such as nicardipine or labetalol) to prevent rebleeding while maintaining cerebral perfusion pressure 1, 4, 2
• Avoid rapid, large reductions in blood pressure as this may worsen cerebral perfusion in the setting of impaired autoregulation 4

Diagnostic Workup

Imaging

• Perform non-contrast head CT immediately as the first diagnostic test, which has high sensitivity for detecting SAH 3
• If CT is negative but clinical suspicion remains high, perform lumbar puncture for CSF analysis looking for xanthochromia and red blood cells 3
• Obtain selective catheter cerebral angiography (DSA) to document the presence and anatomic features of aneurysms as this remains the gold standard 3
• CTA may be considered when conventional angiography cannot be performed in a timely fashion, though it has limitations with small distal vessels and metal artifact from previous clips or coils 3
• If initial angiography shows no source, repeat DSA in 1-2 weeks as this identifies a previously unrecognized aneurysm in an additional 1-2% of cases 3

Definitive Aneurysm Treatment

Timing and Method

• Secure the ruptured aneurysm as early as feasible (ideally within 24 hours) to reduce the 15% risk of rebleeding in the first 24 hours, which carries extremely high mortality 1, 4, 2
• For aneurysms amenable to both techniques, endovascular coiling should be considered as the first option over surgical clipping, as it has been shown to improve outcomes in adequate clinical trials 3, 1, 2
• Complete obliteration of the aneurysm is recommended whenever possible 1, 2
• Patients treated with endovascular coiling have a lower incidence of seizures compared to those treated with surgical clipping 1

Prevention of Delayed Cerebral Ischemia (DCI)

Nimodipine Administration

• Administer oral nimodipine 60 mg every 4 hours for 21 consecutive days, starting within 96 hours of hemorrhage onset 1, 2, 5
• This is the only pharmacological therapy proven in randomized controlled trials to improve neurological outcomes and reduce severe deficits due to vasospasm 3, 5
• If the patient cannot swallow, make a hole in both ends of the capsule with an 18-gauge needle, extract contents into a syringe labeled "Not for IV Use," and administer via nasogastric tube followed by 30 mL normal saline flush 5
• Never administer nimodipine intravenously as this can cause fatal hypotension 5

Fluid Management

• Maintain euvolemia and normal circulating blood volume using goal-directed fluid management with crystalloid or colloid fluids 1, 4, 2
• Avoid prophylactic hypervolemia and triple-H therapy (hypertension, hypervolemia, hemodilution) as these increase complications without improving outcomes 1, 4, 2
• Avoid large volumes of hypotonic fluids and intravascular volume contraction 4

Treatment of Symptomatic DCI

• If DCI develops (presenting as new neurological deficits or decreased consciousness), induce hypertension as first-line therapy to increase cerebral perfusion 4, 2
• Elevate blood pressure using vasopressors (such as phenylephrine or norepinephrine) while maintaining euvolemia 4
• Consider endovascular therapies (intra-arterial vasodilators or angioplasty) if hypertension fails 4

Management of Hydrocephalus

• Treat acute symptomatic hydrocephalus with cerebrospinal fluid diversion using external ventricular drainage or lumbar drainage depending on the clinical scenario 1, 2
• Chronic symptomatic hydrocephalus requires permanent cerebrospinal fluid diversion (ventriculoperitoneal shunt) 1
• Weaning external ventricular drainage over >24 hours does not reduce the need for permanent shunting 1

Seizure Management

• Routine prophylactic anticonvulsants are not recommended for all patients with SAH 1
• Reserve anticonvulsant therapy for patients who have had a witnessed seizure or those at highest risk (such as those with cortical involvement or middle cerebral artery aneurysms) 1

Critical Care Management

Monitoring

• Implement invasive monitoring (intracranial pressure monitoring, brain tissue oxygen monitoring) in high-grade SAH patients with limited neurological examination 4
• Use transcranial Doppler ultrasonography to monitor for vasospasm development 1
• Perform cerebrovascular imaging after treatment and subsequent monitoring to identify aneurysm remnants, recurrence, or regrowth 1

Medical Complications

• Aggressively control fever to normothermia using antipyretics or advanced temperature modulation systems, as fever independently worsens cognitive outcomes 4, 2
• Perform careful glucose management with strict avoidance of hypoglycemia, as both hyperglycemia and hypoglycemia worsen outcomes 4, 2
• Consider packed red blood cell transfusion to treat anemia in patients at risk of cerebral ischemia, though transfusions have been associated with worse outcomes in some series 2
• Implement early identification and targeted treatment of heparin-induced thrombocytopenia and deep venous thrombosis 2
• In patients requiring mechanical ventilation for >24 hours, implement a standardized ICU care bundle to reduce duration of mechanical ventilation and hospital-acquired pneumonia 2

Transfer and Triage Considerations

• Transfer all SAH patients to high-volume centers (>35 patients/year) with dedicated neurocritical care units, experienced cerebrovascular neurosurgeons, endovascular specialists, and neurointensivists, as there is a strong positive correlation between hospital volume and outcome 3, 1, 4, 2, 6
• Avoid unnecessary on-scene delays during transfer 3

Common Pitfalls and Caveats

• SAH is frequently misdiagnosed—maintain high suspicion in any patient with acute onset of severe headache, even if neurologically intact 3, 1, 2
• Only 2% of sudden headaches are due to SAH, but missing the diagnosis significantly increases mortality and morbidity 3, 2
• Do not use statins or intravenous magnesium routinely as they are not recommended based on current evidence 4
• Hypervolemia is potentially harmful and associated with excess morbidity; euvolemia should be the target 1, 2
• Approximately 20-25% of cerebral angiograms performed for SAH will not indicate a source of bleeding initially, necessitating repeat imaging 3
• In patients with hepatic cirrhosis, reduce nimodipine dose to 30 mg every 4 hours due to increased bioavailability and risk of hypotension 5