Nimotop(R) (nimodipine) 30-mg Capsules
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Cerebral Vasospasm

Treatment is also needed to prevent delayed ischemic deficit associated with cerebral vasospasm, the narrowing of the large capacitance arteries at the base of the brain that leads to reduced perfusion of distal brain regions. Cerebral vasospasm has a delayed onset; it typically starts 3-5 days after the initial SAH, achieves maximal vessel narrowing at 5-14 days, and thereafter resolves gradually.1 Vasospasm appears due to the presence of blood in the CSF; oxyhemoglobin released by disintegrating erythrocytes may be the source of the substance(s) that interacts with the cerebral vasculature to produce arterial narrowing.2 The term vasospasm may be a misnomer, because the arterial narrowing may be secondary to structural changes of the cerebral blood vessels.3

More than half of SAH patients develop cerebral vasospasm, and approximately one-third develop symptomatic vasospasm, which is associated with neurologic signs and symptoms of ischemia.2

Of these latter patients, half progress to cerebral infarction and half recover without deficit. However, it is important to recognize that angiographic findings may not correlate with the patient's clinical presentation, because many asymptomatic patients develop significant vasospasm.3 Several factors appear associated with risk of ischemia; these include large volume of initial SAH, dehydration, use of antifibrinolytic agents, arterial hypotension, increased intracranial pressure, and reduced oxygen delivery.2
Oral nimodipine. Guidelines from the AHA Stroke Council indicate that "oral nimodipine is strongly recommended to reduce poor outcome related to vasospasm." These guidelines indicate that the value of other calcium antagonists, whether administered orally or intravenously, remains uncertain.1


Nimodipine Safety Considerations. Nimotop® (Nimodipine) must be given orally or administered via a nasogastric tube as described in the prescribing information.

DO NOT ADMINISTER NIMOTOP INTRAVENOUSLY OR BY OTHER PARENTERAL ROUTES. DEATHS AND SERIOUS, LIFE-THREATENING ADVERSE EVENTS HAVE OCCURRED WHEN THE CONTENTS OF NIMOTOP CAPSULES HAVE BEEN INJECTED PARENTERALLY

(See WARNINGS and DOSAGE AND ADMINISTRATION.)


In patients with SAH, Nimotop® controls damage with a low side effect profile.

Decreased blood pressure is the most common side effect, occurring in 4.4% of patients. Blood pressure should be monitored during therapy.4

Other side effects occurring at a low frequency of ≥1.0% include headache, nausea, and bradycardia.4

No clinically significant effects on hematologic factors, renal or hepatic function, or carbohydrate metabolism have been causally associated with oral nimodipine.4

Nimotop® does not appear to affect anesthetic management.5


"Triple-H" treatment. The efficacy of the "triple-H" therapy-hypertension, hypervolemia, and hemodilution- for cerebral vasospasm has not been demonstrated in controlled clinical trials.1,6 Nevertheless, several uncontrolled studies indicate that this treatment may aid in the resolution of deficits caused by vasospasm. Triple-H therapy is associated with significant risk, which includes heart failure, electrolyte imbalance, cerebral edema, and potential aneurysmal rupture, and therefore patients usually receive intensive care monitoring. Triple-H therapy is recommended for preventing and treating ischemic complications from vasospasm, with the aneurysm to be clipped surgically when possible.


Transluminal angioplasty. This technique is recommended for treatment of vasospasm in those patients who have failed conventional therapy.1 Several uncontrolled studies indicate that transluminal angioplasty provides neurologic improvement in patients who remain refractory to other treatments.




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Sources:
  1. Mayberg MR, Batjer HH, Dacey R et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke 1994;25:2315-2328.

  2. Weir B. Protection of the brain after aneurysmal rupture. Can J Neurol Sci 1995;22:177-186.

  3. Solomon RA, Fink ME. Current strategies for the management of aneurysmal subarachnoid hemorrhage. Arch Neurol 1987;44:769-774.

  4. Nimotop® (nimodipine) Capsules Prescribing Information December 2005

  5. Stullken EH, Johnston WE, Prough DS. Implications of nimodipine prophylaxis of cerebral vasospasm on anesthetic management during intracranial aneurysm clipping. J. Neurosurg. 1985; 62:200-205.

  6. Vermeulen M. Subarachnoid haemorrhage: diagnosis and treatment. J Neurol 1996;243:496-501.


DO NOT ADMINISTER NIMOTOP INTRAVENOUSLY OR BY OTHER PARENTERAL ROUTES. DEATHS AND SERIOUS, LIFE-THREATENING ADVERSE EVENTS HAVE OCCURRED WHEN THE CONTENTS OF NIMOTOP CAPSULES HAVE BEEN INJECTED PARENTERALLY

(See WARNINGS and DOSAGE AND ADMINISTRATION.)


 
  • In patients with SAH, Nimotop® controls damage with a low side effect profile.

  • Decreased blood pressure is the most common side effect, occurring in 4.4% of patients. Blood pressure should be monitored during therapy.1

  • Other side effects occurring at a low frequency of ≥1.0% include headache, nausea, and bradycardia.1

  • No clinically significant effects on hematologic factors, renal or hepatic function, or carbohydrate metabolism have been causally associated with oral nimodipine.1

  • Nimotop® does not appear to affect anesthetic management.2
 
Sources:
  1. Nimotop® (nimodipine) Capsules Prescribing Information December 2005

  2. Stullken EH, Johnston WE, Prough DS. Implications of nimodipine prophylaxis of cerebral vasospasm on anesthetic management during intracranial aneurysm clipping. J. Neurosurg. 1985; 62:200-205.



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