What is the treatment for subarachnoid hemorrhage?

Treatment for Subarachnoid Hemorrhage

The cornerstone of subarachnoid hemorrhage (SAH) management includes early aneurysm obliteration, oral nimodipine administration, maintenance of euvolemia, and cerebrospinal fluid diversion for hydrocephalus. 1, 2

Initial Management

• Rapid assessment of clinical severity using validated scales (Hunt and Hess, World Federation of Neurological Surgeons) is essential as it is the most useful indicator of outcome 2
• Transfer to high-volume centers with experienced cerebrovascular surgeons, endovascular specialists, and multidisciplinary neurocritical care services improves outcomes 3
• Blood pressure should be controlled with a titratable agent to balance the risk of stroke, hypertension-related rebleeding, and maintenance of cerebral perfusion pressure 2

Specific Treatments

Aneurysm Management

• Surgical clipping or endovascular coiling of the ruptured aneurysm should be performed as early as feasible to reduce the rate of rebleeding 2, 3
• For patients with ruptured aneurysms amenable to both techniques, endovascular coiling should be considered as the first option 3
• Complete obliteration of the aneurysm is recommended whenever possible 3
• The timing of surgery is critical, as rebleeding risk increases with time (0-3 days: 5.7%; 4-6 days: 9.4%; 7-10 days: 12.7%; 11-14 days: 13.9%; 15-32 days: 21.5%) 2
• "Ultraearly rebleeding" (within 24 hours of initial SAH) occurs in up to 15% of cases, with 70% happening within 2 hours of the initial SAH 2

Prevention of Delayed Cerebral Ischemia (DCI)

• Oral nimodipine must be administered at a dose of 60 mg every 4 hours for 21 consecutive days, starting within 96 hours of hemorrhage onset 1, 4
• Nimodipine improves neurological outcomes but does not prevent cerebral vasospasm itself 1, 5, 6
• The recommended dosing is two 30 mg capsules every 4 hours for 21 consecutive days, preferably not less than one hour before or two hours after meals 4
• If the capsule cannot be swallowed (e.g., during surgery or if the patient is unconscious), extract the contents with a syringe and administer orally or via nasogastric tube 4
• Maintenance of euvolemia and normal circulating blood volume is recommended to prevent DCI 1, 3
• Prophylactic hypervolemia or triple-H therapy is not recommended as initial treatment 3
• For symptomatic vasospasm, triple-H therapy (hypertension, hypervolemia, hemodilution) is a reasonable approach 1
• Cerebral angioplasty and/or selective intra-arterial vasodilator therapy may be used after, together with, or in place of triple-H therapy, depending on the clinical scenario 1

Management of Hydrocephalus

• Acute symptomatic hydrocephalus (occurs in 20-30% of patients) should be managed by cerebrospinal fluid diversion via external ventricular drainage (EVD) or lumbar drainage, depending on the clinical scenario 1
• Chronic symptomatic hydrocephalus (occurs in 8.9-48% of patients) should be treated with permanent cerebrospinal fluid diversion 1
• Weaning EVD over >24 hours does not appear to be effective in reducing the need for ventricular shunting 1
• Routine fenestration of the lamina terminalis is not useful for reducing the rate of shunt-dependent hydrocephalus 1

Seizure Management

• Routine prophylactic anticonvulsants are not recommended for all patients with SAH 3
• Patients treated with endovascular coiling have a lower incidence of seizures compared to those treated with surgical clipping 3

Monitoring and Complications

• Transcranial Doppler ultrasonography can be used to monitor for vasospasm development 3
• The risk of arterial hypotension with nimodipine requires close monitoring, especially in higher-grade SAH patients 7
• Nimodipine dosage often needs to be reduced or discontinued due to hypotension, with only 57.2% of patients able to receive the full intended dose 7
• Oral nimodipine solution causes drops in blood pressure more frequently than tablets, though plasma levels are similar 7

Common Pitfalls and Considerations

• Misdiagnosis is common in SAH (up to 12% of cases), and high suspicion should be maintained with acute severe headache 2
• Hypervolemia is potentially harmful and associated with excess morbidity; euvolemia should be the target 3
• Nimodipine can cause hypotension requiring dosage reduction or discontinuation, particularly in patients with higher-grade SAH 7
• Patients with liver dysfunction may require reduced nimodipine dosing (30 mg every 4 hours) due to increased bioavailability and reduced clearance 4
• Grapefruit juice should be avoided during nimodipine therapy due to drug interactions 4