Nimotop (nimodipine) is a calcium channel blocker specifically formulated for the improvement of neurological outcomes by reducing the incidence and severity of ischemic deficits in patients with subarachnoid hemorrhage (SAH) from ruptured congenital intracranial aneurysms. Its unique cerebroselective action targets cerebral arteries, making it a cornerstone in the prophylactic management of cerebral vasospasm, a common and serious complication following SAH. Administered orally, it is indicated for use in clinically stable patients, typically initiated within 96 hours of the hemorrhage. Its mechanism focuses on mitigating delayed cerebral ischemia, a primary contributor to morbidity and mortality in this patient population.

Features

• Active Pharmaceutical Ingredient: Nimodipine (30 mg per hard gelatin capsule)
• Pharmacologic Class: Dihydropyridine Calcium Channel Blocker
• Specialized Formulation: Optimized for cerebroselective vasodilation
• Administration Route: Oral (or via nasogastric tube if swallowing impaired)
• Standard Packaging: 100 capsules per bottle
• Bioavailability: High first-pass metabolism; approximately 13% oral bioavailability
• Protein Binding: >95%
• Metabolism: Hepatic, via cytochrome P450 3A4 (CYP3A4)
• Elimination Half-life: Approximately 8-9 hours
• Excretion: Primarily renal (approx. 50%) and fecal (approx. 32%) as metabolites

Benefits

• Reduces the incidence and severity of neurological deficits caused by cerebral vasospasm following subarachnoid hemorrhage.
• Improves overall neurological outcomes by helping to prevent delayed cerebral ischemia.
• Offers a targeted therapeutic approach with a primary effect on cerebral arteries rather than systemic vasculature.
• Provides a standardized, evidence-based prophylactic treatment protocol for a critical post-operative or post-hemorrhage period.
• Contributes to a potential reduction in long-term disability and improved functional recovery for survivors of SAH.

Common use

Nimotop is exclusively indicated for the improvement of neurological outcome by reducing the incidence and severity of ischemic deficits in patients with subarachnoid hemorrhage from ruptured congenital intracranial aneurysms who are in good neurological condition post-ictus (e.g., Hunt and Hess Grades I-III). Its use is prophylactic, aimed at preventing the secondary injury of cerebral vasospasm, which typically manifests 3 to 14 days after the initial bleed. It is not indicated for the treatment of high blood pressure outside of this specific neurovascular context.

Dosage and direction

The recommended dosage is 60 mg (two 30 mg capsules) every 4 hours for 21 consecutive days. Treatment should be initiated within 96 hours of the subarachnoid hemorrhage.

Administration Instructions:

• For alert patients: Administer orally with a generous amount of water. The capsules should be swallowed whole and not chewed, crushed, or divided.
• For patients with impaired swallowing: A hole may be carefully pierced at both ends of the capsule using an 18-gauge needle, and the contents may be extracted into a syringe. The liquid contents should then be emptied into the patient’s nasogastric (NG) tube funnel and washed down the tube with 30 mL of normal saline (0.9%).
• Dosing frequency must be strictly adhered to (q4h) to maintain stable therapeutic levels.
• If the capsule is not available, the intravenous formulation must be used; the oral solution should not be compounded from other nimodipine products.

Precautions

• Hypotension: Nimotop can cause hypotension, which may be more pronounced in patients with pre-existing low blood pressure or those who are volume-depleted. Blood pressure should be monitored regularly, especially during the initial dose titration period.
• Liver Impairment: Patients with severe liver dysfunction or cirrhosis may have significantly reduced clearance of nimodipine, leading to elevated plasma levels and an increased risk of adverse effects. Dose adjustment may be necessary; careful monitoring is advised.
• Gastrointestinal Perforation: There have been rare reports of gastrointestinal perforation associated with the administration of nimodipine capsules, particularly in patients with a history of diverticular disease, gastrointestinal tract malignancy, or recent bowel surgery. Use with caution in such patients.
• CYP3A4 Inhibitors: Concomitant use with strong inhibitors of the CYP3A4 enzyme system can drastically increase nimodipine plasma concentrations,potentiating its effects and side effects. Avoid concomitant use if possible.
• General Anesthesia: Calcium channel blockers may potentiate the effects of certain anesthetics and neuromuscular blocking agents. The anesthesiologist should be aware of nimodipine therapy.

Contraindications

• Known hypersensitivity to nimodipine, any other calcium channel blocker, or any component of the formulation.
• Concomitant administration with strong CYP3A4 inhibitors in patients with compromised CYP3A4 function (e.g., due to liver cirrhosis), due to the high risk of severe hypotension and other adverse reactions.
• Patients with cardiogenic shock or significant, uncompensated heart failure.

Possible side effect

The most common side effects are related to its pharmacological action as a vasodilator.

• Very Common (>10%): Decreased blood pressure (hypotension).
• Common (1-10%): Headache, nausea, bradycardia (slow heart rate), gastrointestinal upset (diarrhea, constipation), flushing, lightheadedness, edema (swelling), rash.
• Uncommon (0.1-1%): Tachycardia (fast heart rate), palpitations, drowsiness, sweating, vomiting.
• Rare (<0.1%): Gastrointestinal hemorrhage, thrombocytopenia, leukopenia, elevated liver enzymes, allergic reactions (e.g., urticaria, pruritus), depression.

Drug interaction

Nimodipine is primarily metabolized by CYP3A4. Co-administration with substances that affect this enzyme system can lead to significant interactions.

• Strong CYP3A4 Inhibitors (CONTRAINDICATED in specific populations): Drugs like ketoconazole, itraconazole, clarithromycin, ritonavir, and nefazodone can increase nimodipine plasma levels by over 10-fold, leading to severe hypotension and tachycardia. Avoid combination.
• CYP3A4 Inducers: Drugs like carbamazepine, phenytoin, phenobarbital, rifampin, and St. John’s Wort may decrease nimodipine plasma levels, potentially reducing its efficacy.
• Other Antihypertensives: Concomitant use with other blood pressure-lowering agents (e.g., beta-blockers, ACE inhibitors, other calcium channel blockers) may have an additive hypotensive effect.
• QT-Prolonging Agents: The potential for additive effects on QT interval prolongation exists, though the risk with nimodipine is considered low.
• Grapefruit Juice: Contains compounds that inhibit CYP3A4 and should be avoided during therapy as it can increase nimodipine bioavailability.

Missed dose

If a dose is missed, it should be taken as soon as it is remembered. However, if it is almost time for the next scheduled dose, the missed dose should be skipped. The patient should not take a double dose to make up for the missed one. It is critical to maintain the regular q4h schedule; frequent missed doses can compromise the prophylactic efficacy of the treatment regimen. The prescribing physician or neuroclinical pharmacist should be informed of the pattern of missed doses.

Overdose

Overdose would be expected to manifest as significant, pronounced pharmacological effects, primarily severe systemic hypotension and reflex tachycardia. Other symptoms could include bradycardia (especially with concomitant beta-blocker use), dizziness, drowsiness, confusion, and nausea.

Management:

• Provide supportive care with close monitoring of cardiac and respiratory function.
• Frequent blood pressure monitoring is essential.
• Treatment of hypotension should include placing the patient in the Trendelenburg position and administration of intravenous fluids. If these measures are inadequate, vasopressors (e.g., dopamine or norepinephrine) may be administered, with caution due to the risk of exacerbating cerebral vasospasm.
• Since nimodipine is highly protein-bound, dialysis is not likely to be of benefit.
• Gastric lavage may be considered if ingestion was recent.

Storage

• Store at controlled room temperature, 20°C to 25°C (68°F to 77°F).
• Protect from light and moisture. Keep the bottle tightly closed.
• Keep out of reach of children and pets.
• Do not use after the expiration date printed on the packaging.
• Do not transfer capsules to another container.

Disclaimer

This information is for educational and professional medical reference purposes only and is not a substitute for the professional judgment of a qualified healthcare practitioner in diagnosing and treating patients. The prescribing physician must rely upon their own professional knowledge and experience and a comprehensive assessment of the individual patient to determine appropriate diagnosis, treatment, and dosage. The information provided here is based on the product’s official prescribing information but may not be exhaustive. Please refer to the full local prescribing information for complete details on warnings, precautions, and adverse reactions.

Reviews

• “A foundational agent in our neuro-ICU protocol for aSAH. Its role in mitigating vasospasm is well-established in the literature. The dosing schedule is rigorous but necessary.” – Neurointensivist, Academic Medical Center
• “The transition to ensuring patients receive this medication on time, every 4 hours for 21 days, is a significant nursing challenge but one that is absolutely critical for positive patient outcomes. The NG tube administration method is straightforward.” – Neuroscience RN, BSN
• “While the evidence for nimodipine’s benefit is strongest in good-grade SAH patients, it remains a standard of care that we rarely deviate from. Monitoring for hypotension, especially in the elderly, is key.” – Vascular Neurologist
• “From a pharmacological standpoint, its cerebroselectivity, while not absolute, provides a valuable therapeutic window that other calcium channel blockers lack for this specific indication.” – Clinical Pharmacist, PharmD