Background: Oral nimodipine is administered to improve clinical outcome in patients with aneurysmal subarachnoid hemorrhage aSAH. In this study, clinical outcome in patients with and without oral nimodipine administration was assessed. Severity of initial aSAH and clinical status at admission Hunt and Hess was significantly higher in those receiving oral nimodipine. Conclusion: Oral nimodipine administration improved clinical outcome of patients after aSAH and should be administered routinely for such patients. One serious complication after aneurysmal subarachnoid hemorrhage aSAH is the incidence of symptomatic vasospasm 1. The thickness of the blood clot in the basal cisterns and the presence of intraventricular hemorrhage are the main risk factors for the development of DCI 6.

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WikiDoc is not a professional health care provider, nor is it a suitable replacement for a licensed healthcare provider. WikiDoc does not promote the administration of any medication or device that is not consistent with its labeling. Nimodipine is a Calcium Channel Blocker that is FDA approved for the treatment of improvement of neurological outcome by reducing the incidence and severity of ischemic deficits in patients with subarachnoid hemorrhage from ruptured intracranial berry aneurysms regardless of their post-ictus neurological condition. The concomitant use of nimodipine with strong inhibitors of CYP3A4 such as some macrolide antibiotics e. Moderate and weak inducers of CYP3A4 may also reduce the efficacy of nimodipine to a lesser extent. Patients on these should be closely monitored for lack of effectiveness, and a nimodipine dosage increase may be required. Moderate and weak CYP3A4 inhibitors include, for example: amprenavir, aprepitant, armodafinil, bosentan, efavirenz, etravirine, echinacea, modafinil, nafcillin, pioglitazone, prednisone and rufinamide. Blood Pressure: Nimodipine has the hemodynamic effects expected of a calcium channel blocker, although they are generally not marked. Nevertheless, blood pressure should be carefully monitored during treatment with nimodipine based on its known pharmacology and the known effects of calcium channel blockers. Hepatic Disease: The metabolism of nimodipine is decreased in patients with impaired hepatic function.

Aneurysmal subarachnoid hemorrhage is a significant cause of death and disability. However, hypotension is an adverse effect of nimodipine and is believed to prompt clinicians to prescribe an unproven, nonstandard nimodipine dosing regimen. The secondary objective was to determine factors associated with this dosage change. This retrospective cohort study evaluated participants receiving nimodipine for aneurysmal subarachnoid hemorrhage at a tertiary care teaching hospital between October and December A total of eligible patients were identified. For all of these patients, nimodipine 60 mg every 4 h was prescribed initially.

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It should be connected to a three-way stopcock using the infusion line provided. The three-way stopcock should be used to connect the Nimodipine polyethylene tube with the co-infusion line and the central catheter. Dosage: Recommended dose - Aneurysmal Subarachnoid Haemorrhage: For the first two hours of treatment 1 mg of Nimodipine, i. If it is well tolerated, the dose should be increased after two hours to 2 mg Nimodipine, i. Duration of treatment: Aneurysmal subarachnoid haemorrhage Intravenous treatment should begin as early as possible after neurological deficit occurs due to arterial spasm, post subarachnoid haemorrhage.

Nimodipine pharmacokinetics was investigated in 12 Chinese patients with acute subarachnoid haemorrhage receiving an IV infusion of 1. Eight survivors were given oral nimodipine 60 or 90 mg every 6h based on body weight, blood was sampled over 6 h and the plasma nimodipine level determined. In one very sick patient given crushed tablets by naso-gastric tube, the AUC was very low; in vitro studies indicated that adsorption of nimodipine by the tubing was unlikely to have been the cause. Rent this article via DeepDyve. New Trends Clin Neuropharmacol 3: Investigation of nimodipine pharmacokinetics in Chinese patients with acute subarachnoid haemorrhage.

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Nimodipine is a potent cerebral vasodilator that has been approved for use in relieving the vasospasm accompanying subarachnoid hemorrhage. From: Comprehensive Hypertension, Fargen, in Intracranial Aneurysms, Nimodipine, a calcium channel blocker of the dihydropyridine class, is often used in SAH patients to prevent symptomatic vasospasm and improve outcomes. Administering more than 5 mg dose is not recommended. Although considered safe, IA nimodipine has been associated with blood—brain barrier disruption Janardhan et al.

Table 1 Randomized controlled trials assessing neurologic outcomes after aneursymal Subarachnoid hemorrhage—completed nimotop 90 mg. Significantly less delayed cerebral ischemia in treatment group, no difference in angiographic vasospasm Petruk et al. Nimodipine did not significantly increase cerebral blood flow Mee et al. Poor GOS outcomes significantly reduced in nimodipine group at 3-months Pickard et al. More adverse effects in high-dose nicardipine group Haley et al. No significant difference in CT infarct.

Action And Clinical Pharmacology: Delayed neurologic deterioration secondary to cerebral ischemic deficits is believed to be a major determinant of outcome in patients who survive their initial subarachnoid hemorrhage SAH. Nimodipine is a calcium channel blocker of the dihydropyridine group. It appears to have a more marked effect on the cerebral circulation than on the peripheral circulation. Since it acts on the vascular smooth muscle tone by modifying the contractile process which is dependent upon the movement of extracellular calcium into the cells during depolarization, it was tested in patients with SAH in an effort to improve the neurologic outcome in these patients. A prospective, multicentre, randomized, double-blind placebo-controlled study was conducted with nimodipine in patients with traumatic head injuries in which traumatic subarachnoid hemorrhage tSAH was confirmed by computer tomography CT scanning. Within 12 hours of head injury, patients received either a sequential course of i.

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