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 who are in good neurological condition post-ictus (e.g., Hunt and Hess Grades I-III). Its primary mechanism of action is cerebroselective, exerting its effects predominantly on cerebral arteries to mitigate vasospasm, a common and serious complication following SAH. This expert-oriented guide provides a comprehensive, evidence-based overview of Nimotop, detailing its pharmacological profile, clinical application, and essential management protocols for healthcare professionals.

Features

• Active Pharmaceutical Ingredient: Nimodipine 30 mg
• Pharmacological Class: Dihydropyridine Calcium Channel Blocker
• Formulation: Oral soft gelatin capsules
• Bioavailability: Approximately 13% following oral administration due to significant first-pass metabolism
• Protein Binding: >95%
• Metabolism: Hepatic, via cytochrome P450 3A4 (CYP3A4)
• Elimination Half-life: Approximately 8-9 hours
• Excretion: Primarily renal (approx. 50%) and approximately 32% in feces

Benefits

• Reduces the incidence of cerebral infarction and severe neurological deficits secondary to cerebral vasospasm following aneurysmal subarachnoid hemorrhage.
• Demonstrates cerebroselectivity, preferentially dilating cerebral arteries over peripheral vessels, which helps minimize systemic hypotensive effects.
• May improve overall neurological outcome and functional recovery in patients who have experienced a subarachnoid hemorrhage.
• Supported by robust clinical trial data establishing its efficacy in reducing poor outcomes related to vasospasm when administered within 96 hours of the hemorrhage.
• The oral capsule formulation allows for continued treatment in both inpatient and carefully monitored outpatient settings.

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. It is not indicated for the treatment of high blood pressure outside of this specific cerebrovascular context. Its use is initiated within 96 hours of the onset of the hemorrhage and is typically continued for 21 consecutive days.

Dosage and direction

The standard dosage of Nimotop is 60 mg (two 30 mg capsules) every 4 hours for 21 consecutive days. Administration should commence within 96 hours of the subarachnoid hemorrhage.

Important Administration Instructions:

• Oral Route Only: Nimotop capsules are for oral administration only. The contents of the capsule must NOT be administered via nasogastric tube or any other parenteral route, as this has been associated with serious, including fatal, adverse events due to precipitous drops in blood pressure.
• Timing: Doses should be administered approximately every 4 hours. If a dose is missed, it should be skipped and the next dose taken at the scheduled time; the patient should not double the dose.
• For patients with hepatic impairment: A reduction in dose to 30 mg every 4 hours is recommended, with close monitoring of blood pressure.

Precautions

• Blood Pressure Monitoring: Nimotop can cause hypotension. Blood pressure should be monitored regularly during therapy, especially in patients with pre-existing hypotension or those on other antihypertensive agents.
• Liver Function: Patients with severe liver impairment require a reduced dosage (30 mg every 4 hours) and careful monitoring, as nimodipine is extensively metabolized by the liver.
• Grapefruit Juice: Patients should avoid consuming grapefruit or grapefruit juice, as it inhibits CYP3A4 metabolism and can significantly increase nimodipine plasma concentrations, leading to an enhanced hypotensive effect.
• CYP3A4 Inhibitors: Concomitant use with strong or moderate CYP3A4 inhibitors (e.g., some antifungals, macrolide antibiotics, antidepressants, protease inhibitors) may increase nimodipine levels. Consider dose reduction and monitor for increased effects.
• CYP3A4 Inducers: Concomitant use with strong CYP3A4 inducers (e.g., rifampin, carbamazepine, St. John’s Wort) may decrease nimodipine levels, potentially reducing its efficacy.

Contraindications

Nimotop is contraindicated in patients with:

• A 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 liver or kidney function, due to the high risk of significant interactions and adverse effects.

Possible side effect

The most common side effect associated with Nimotop is hypotension, which can be dose-related. Other possible adverse reactions include:

• Headache
• Nausea
• Gastrointestinal discomfort or diarrhea
• Bradycardia or tachycardia
• Peripheral edema
• Rash
• Dizziness or lightheadedness Less commonly, instances of ileus, thrombocytopenia, and elevated liver enzymes have been reported.

Drug interaction

Nimotop has a significant potential for drug-drug interactions, primarily mediated through its metabolism by the CYP3A4 enzyme system.

• Strong CYP3A4 Inhibitors (e.g., ketoconazole, itraconazole, clarithromycin): Can markedly increase nimodipine plasma concentrations. Concomitant use is generally not recommended. If unavoidable, close monitoring for hypotension and tachycardia is essential, and a dose reduction of Nimotop should be considered.
• Moderate CYP3A4 Inhibitors (e.g., diltiazem, verapamil, erythromycin): May increase nimodipine levels. Monitor blood pressure and heart rate closely.
• CYP3A4 Inducers (e.g., rifampin, phenytoin, carbamazepine, St. John’s Wort): Can significantly decrease nimodipine plasma concentrations, potentially rendering therapy subtherapeutic. Alternative agents should be considered.
• Other Antihypertensives (e.g., beta-blockers, ACE inhibitors, other calcium channel blockers): May have an additive hypotensive effect. Blood pressure requires vigilant monitoring.
• Grapefruit Juice: Contraindicated due to inhibition of CYP3A4.

Missed dose

If a dose is missed, the patient should skip that dose and take the next dose at the regularly scheduled time. The patient should not double the dose to make up for the missed one. Maintaining the strict 4-hour interval is more critical than catching up on a missed dose.

Overdose

Overdose with Nimodipine would be expected to manifest as significant, symptomatic hypotension and reflex tachycardia. Other symptoms could include bradycardia, dizziness, drowsiness, nausea, and gastrointestinal disturbances. Management: In case of suspected overdose, medical attention must be sought immediately. Treatment is primarily supportive and should include:

• Continuous monitoring of vital signs, especially blood pressure and ECG.
• Cardiovascular support, which may include placing the patient in the Trendelenburg position and administering intravenous fluids.
• For profound hypotension that is unresponsive to fluids, vasopressors (e.g., dopamine, norepinephrine) may be required. Calcium gluconate administration may be considered to counteract the effects of the calcium channel blocker.
• As Nimotop is highly protein-bound, dialysis is not likely to be of benefit.

Storage

• Store Nimotop capsules at controlled room temperature, 20°C to 25°C (68°F to 77°F).
• Excursions are permitted between 15°C and 30°C (59°F and 86°F).
• Keep the medication in its original container to protect it from light and moisture.
• Keep out of reach of children and pets.

Disclaimer

This information is intended for educational and informational purposes only for healthcare professionals and is not a substitute for professional medical advice, diagnosis, or treatment. The content provided is based on the manufacturer’s prescribing information and available clinical literature but may not encompass all possible uses, directions, precautions, or interactions. Always seek the advice of a qualified physician or other authorized health provider with any questions you may have regarding a medical condition or before starting any new treatment. Never disregard professional medical advice or delay in seeking it because of something you have read here.

Reviews

• The Nimodipine Study Group (1989): A pivotal randomized, double-blind, placebo-controlled trial demonstrated that oral nimodipine 60 mg every 4 hours significantly reduced the incidence of cerebral infarction and poor outcomes (death, vegetative survival, severe disability) from 33% to 22% in patients with aneurysmal subarachnoid hemorrhage.
• Pickard et al. (1989): The British Aneurysm Nimodipine Trial (BRANT) confirmed these findings, reporting a significant reduction in cerebral infarction with nimodipine treatment and establishing its role as a standard of care in this patient population.
• Clinical Consensus: Neurological and neurosurgical guidelines worldwide (including those from the American Heart Association/American Stroke Association) consistently recommend the use of nimodipine in patients with aneurysmal subarachnoid hemorrhage to reduce poor neurological outcomes caused by delayed cerebral ischemia. Its efficacy is well-established in the medical literature, though its precise mechanism beyond vasodilation (e.g., potential neuroprotective effects) continues to be an area of research.