Nimodipine for Subarachnoid Hemorrhage
Primary Recommendation
Administer nimodipine 60 mg orally every 4 hours for 21 consecutive days, starting within 96 hours of SAH onset, and maintain this regimen even if vasopressor support becomes necessary. 1, 2, 3
Dosing Protocol
- Standard dose: 60 mg (two 30 mg capsules) every 4 hours for 21 consecutive days 3
- Timing: Initiate within 96 hours of hemorrhage onset 2, 3
- Route: Oral administration, preferably 1 hour before or 2 hours after meals 3
- Avoid grapefruit juice during treatment as it interferes with CYP3A4 metabolism 3
Alternative Administration Methods
For patients unable to swallow (unconscious, perioperative):
- Pierce both ends of capsule with 18-gauge needle 3
- Extract contents with parenteral syringe 3
- Transfer to oral/enteral syringe labeled "Not for IV Use" 3
- Administer via nasogastric tube or PEG, followed by 30 mL normal saline flush 3
- Never administer intravenously - this can cause life-threatening hypotension requiring vasopressor support 3
Managing Hypotension
The American College of Cardiology recommends continuing nimodipine at standard dose even when vasopressors are required - concurrent vasopressor use is not a contraindication 1. This is critical because:
- Disruption of nimodipine therapy directly correlates with increased delayed cerebral ischemia (ρ=0.431, P<0.001) 1
- Attempt standard blood pressure support measures before considering dose reduction 1, 2
- Titrate vasopressors (typically noradrenaline) to maintain adequate cerebral perfusion pressure 1
- Maintain euvolemia, not hypervolemia, which increases complications 1, 2
Blood pressure drops occur commonly: 30% of patients experience >10% systolic blood pressure drop with IV formulation, 9% with oral administration 4. However, hypotensive episodes to <90 mmHg are rare with appropriate monitoring 4.
Dose Modifications (Use Sparingly)
Only reduce dose if standard interventions fail to manage hypotension 2:
- Reduce to 30 mg every 4 hours in patients with severe hepatic cirrhosis or unmanageable hypotension 3
- Monitor blood pressure and heart rate closely with dose reduction 3
- Consider temporary interruption only if blood pressure variability cannot be managed 2
Critical caveat: Real-world data shows only 33% of patients complete the full 21-day course at standard dosing 5, and dose reduction is associated with worse outcomes (OR 0.895, p=0.029) 6. The American Heart Association emphasizes that consistent administration without interruption is essential 1, 2.
Drug Interactions Requiring Dose Adjustment
- Strong CYP3A4 inhibitors: Contraindicated - do not use concurrently 3
- Strong CYP3A4 inducers: Generally avoid 3
- Moderate/weak CYP3A4 inhibitors: May require dose reduction if hypotension develops 3
- Moderate/weak CYP3A4 inducers: Monitor for lack of effectiveness; may need dose increase 3
Duration Considerations
The 21-day duration is evidence-based and should not be shortened arbitrarily 2, 3. While one retrospective study suggested 14 days might suffice for low-grade SAH patients (Hunt-Hess 1-2, GCS 15) 7, this contradicts guideline recommendations and the original trial data that established the 21-day standard 2, 3.
Common pitfall: 47% of patients in one series were discharged before day 21 without home nimodipine prescriptions 5 - ensure continuation after hospital discharge to complete the full 21-day course.
Evidence Base
The American Heart Association/American Stroke Association strongly recommends nimodipine based on meta-analysis of 16 trials involving 3,361 patients 8, 2. Nimodipine is the only FDA-approved medication proven to prevent delayed cerebral ischemia and improve functional outcomes after aneurysmal SAH 1, 2, 3. The mechanism extends beyond vasospasm reversal to include direct neuroprotective effects 2, 3.
Post-Aneurysm Securing Context
Once the aneurysm is secured (clipped or coiled), blood pressure can be safely augmented with vasopressors without rebleeding risk 1. This makes aggressive blood pressure support feasible while maintaining full-dose nimodipine, which is the optimal strategy for preventing delayed cerebral ischemia 1.