Nimotop: Targeted Cerebral Vasospasm Management Post-SAH

Nimotop

Product dosage: 30mg
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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 involves selective cerebral vasodilation, mitigating delayed cerebral ischemia—a leading cause of morbidity and mortality following SAH. Available in oral and liquid formulations, it is a cornerstone of neurocritical care protocols aimed at preserving cognitive and motor function during the vulnerable vasospasm period.

Features

• Active pharmaceutical ingredient: Nimodipine (30 mg per soft gelatin capsule)
• Pharmacologic class: Dihydropyridine calcium channel blocker
• High selectivity for cerebral arterial smooth muscle
• Formulation: Soft gelatin capsules for oral administration; also available in an intravenous formulation for hospital use (though oral administration is standard for the prophylactic course)
• 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 fecal (approx. 32%) as metabolites

Benefits

• Significantly reduces the risk of cerebral infarction and poor neurological outcome following aneurysmal subarachnoid hemorrhage.
• Provides targeted therapy to cerebral vasculature, helping to maintain blood flow to vulnerable brain regions during the high-risk period for vasospasm (typically days 4-14 post-bleed).
• Improves overall functional recovery, increasing the likelihood of patients returning to independent living.
• Offers a well-established safety and efficacy profile backed by decades of clinical use and research in neurocritical care.
• The oral capsule formulation facilitates continuation of therapy from the intensive care unit to step-down units and, potentially, discharge planning.

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 initiated within 96 hours of the onset of SAH and is continued for a period of 21 consecutive days. It is a standard component of post-SAH management protocols in conjunction with neurological monitoring, blood pressure management, and other supportive care measures. Its use is almost entirely within a hospitalized or closely monitored clinical setting.

Dosage and direction

The standard dosage for Nimotop is 60 mg (two 30 mg capsules) every 4 hours for 21 consecutive days.

• Administration: Oral administration. For patients who are unable to swallow solid oral dosage forms, the liquid contents of the capsule may be extracted using a syringe and administered via nasogastric (NG) tube. The capsule should be pierced, the contents withdrawn into a syringe, and then flushed through the NG tube with 30 mL of normal saline (0.9%).
• Timing: Doses should be administered precisely every 4 hours to maintain consistent plasma levels.
• Duration: Treatment should be continued for the full 21-day course, even if the patient is discharged from the hospital earlier. Patient and caregiver education on the importance of adherence is critical.
• Dosage in Hepatic Impairment: In patients with hepatic cirrhosis, the dosage should be reduced to 30 mg every 4 hours, with close monitoring of blood pressure and heart rate due to significantly increased bioavailability and the risk of hypotension.

Precautions

• Hypotension: Nimotop can cause hypotension, which may be particularly dangerous in the SAH population where cerebral perfusion pressure is critical. Blood pressure must be monitored frequently, especially during initiation of therapy and after any dosage increase.
• Liver Function: Patients with impaired liver function metabolize nimodipine more slowly, leading to higher plasma levels and an increased risk of adverse effects. Dose reduction is necessary, and liver function tests should be monitored.
• GI Perforation: There have been rare reports of gastrointestinal perforation associated with the administration of nimodipine in patients with recent brain injury. Use with caution in patients with a history of gastrointestinal disease or in those receiving corticosteroids or NSAIDs, which may increase the risk.
• CYP3A4 Inhibitors: Concomitant use with strong CYP3A4 inhibitors (e.g., some antifungals, macrolide antibiotics, HIV protease inhibitors) can dramatically increase nimodipine plasma concentrations, leading to severe hypotension and other adverse effects. This combination should be avoided.
• Pregnancy and Lactation: Nimodipine should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. It is not known whether nimodipine is excreted in human milk; a decision should be made whether to discontinue nursing or discontinue the drug.

Contraindications

• Known hypersensitivity to nimodipine, any other calcium channel blocker, or any component of the formulation.
• Concomitant use with strong inhibitors of CYP3A4 (e.g., ketoconazole, itraconazole, clarithromycin, ritonavir).
• Patients with cardiogenic shock or significant hypotension where a further drop in blood pressure would be clinically detrimental.

Possible side effect

The most common side effects are related to its vasodilatory effects and are generally dose-dependent.

• Very Common (>10%): Hypotension (low blood pressure).
• Common (1-10%): Headache, nausea, bradycardia (slow heart rate), diarrhea, rash, flushing (feeling of warmth), edema (swelling).
• Uncommon (0.1-1%): Tachycardia (fast heart rate), vomiting, gastrointestinal upset, drowsiness, dizziness.
• Rare (<0.1%): Gastrointestinal perforation, thrombocytopenia (low platelet count), leukopenia (low white blood cell count), increased liver enzymes, allergic reactions.

Drug interaction

Nimodipine is primarily metabolized by CYP3A4 and is highly protein-bound, making it susceptible to numerous interactions.

• Strong CYP3A4 Inhibitors (e.g., ketoconazole, itraconazole, clarithromycin, ritonavir, nefazodone): CONTRAINDICATED. Concomitant use can lead to a massive increase in nimodipine plasma levels, causing severe and potentially life-threatening hypotension.
• Moderate/Weak CYP3A4 Inhibitors (e.g., diltiazem, verapamil, erythromycin, fluconazole, grapefruit juice): May increase nimodipine concentrations. Use with caution and monitor for increased effects/toxicity (e.g., hypotension). Dose adjustment may be required.
• CYP3A4 Inducers (e.g., rifampin, phenytoin, carbamazepine, St. John’s Wort): May decrease nimodipine plasma concentrations, potentially reducing its efficacy. Consider alternative agents or monitor for reduced effect.
• Other Antihypertensives (e.g., beta-blockers, ACE inhibitors, other calcium channel blockers): Additive hypotensive effects. Blood pressure requires careful monitoring.
• Highly Protein-Bound Drugs (e.g., warfarin, phenytoin, NSAIDs): Theoretical potential for competition for protein-binding sites, though the clinical significance is likely low.

Missed dose

In the context of its critical 4-hour dosing schedule for SAH prophylaxis, missed doses are a significant concern.

• 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 double the dose to make up for the missed one.
• The dosing schedule should be re-established immediately.
• For patients on this critical therapy, healthcare providers should implement strict medication administration protocols (e.g., timed alarms, medication administration records) to minimize the risk of missed doses.

Overdose

Overdose would be expected to produce profound hypotension, bradycardia (or reflex tachycardia), and possibly cardiac arrest.

• Symptoms: Severe dizziness, syncope (fainting), marked palpitations, nausea, extreme lethargy, and profoundly low blood pressure.
• Management: There is no specific antidote for nimodipine overdose. Management is supportive and symptomatic.
  • Cardiovascular monitoring is essential.
  • Treat hypotension with intravenous fluids and vasopressors (e.g., norepinephrine, dopamine) as needed.
  • Atropine may be used for significant bradycardia.
  • Gastric lavage may be considered if ingestion was recent.
  • As nimodipine is highly protein-bound, dialysis is not likely to be effective.

Storage

• Store at room temperature between 20°C to 25°C (68°F to 77°F). Excursions are permitted between 15°C and 30°C (59°F and 86°F).
• Protect from light. Keep capsules in their original blister packaging until the moment of administration.
• Keep out of reach of children and pets.
• Do not use after the expiration date printed on the packaging.

Disclaimer

This information is for educational and informational purposes only and does not constitute medical advice. It is not a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician, neurologist, or other qualified health provider with any questions you may have regarding a medical condition or before starting or stopping any medication. Never disregard professional medical advice or delay in seeking it because of something you have read here. The content has been compiled from various sources but may not be comprehensive or fully up-to-date.

Reviews

• Neurocritical Care Consensus Guidelines: “Nimodipine remains a Class I, Level of Evidence A recommendation for all patients with aneurysmal subarachnoid hemorrhage to reduce the risk of poor neurological outcome from delayed cerebral ischemia.”
• Clinical Pharmacologist, Academic Medical Center: “It’s a niche drug, but within that niche, it’s irreplaceable. The 21-day oral course is a logistical challenge but the evidence for its benefit in functional outcomes is robust.”
• Neurosurgeon: “A cornerstone of our post-op SAH protocol. We see a tangible difference in the incidence of devastating strokes from vasospasm in patients who complete the full course.”
• ICU Pharmacist: “Requires vigilant monitoring for hypotension and careful review of the patient’s medication list to avoid dangerous CYP3A4 interactions. When managed correctly, it’s a powerful tool.”