Nimotop(R) (nimodipine) 30-mg Capsules
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About SAH

Epidemiology

Risk Factors

Clinical Manifestations

Diagnosis

Classification of SAH

Therapeutic Measures
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Epidemiology

Nontraumatic aneurysmal subarachnoid hemorrhage afflicts an estimated 30,000 people in the U.S. each year.1 Population-based studies suggest that SAH represents 5%-10% of all strokes.2 Approximately 25% of patients die from the immediate hemorrhage or as a consequence of secondary complications, and 50% of those patients who survive become seriously disabled.1 SAH is associated with a high degree of mortality and morbidity, part of which is caused by neurological deficits that are secondary to the initial hemorrhagic event. The estimated lifetime cost for annual cases of patients hospitalized with aneurysmal SAH in the U.S. is $1.75 billion.3

The incidence of SAH increases with age.4 It is higher among women than men,5 and may be higher among African Americans than Caucasians.2

In SAH, rupture of an intracranial aneurysm is the initial insult that causes bleeding, most frequently into the subarachnoid space and less commonly into the intravascular and intracerebral spaces.6 Bleeding may result in brain damage, decreased cerebral perfusion, brain shift and herniation, and hydrocephalus. Patients who survive the initial insult are at risk of secondary complications for the next three weeks, notably aneurysmal rebleeding and cerebral vasospasm.7

The rate of rebleeding is highest (4%) during the first 24 hours after the initial hemorrhage and declines to 1%-2% per day thereafter for the next 4 weeks. The early rebleeding appears in part due to acute arterial hypertension, which can develop in response to the patient's pain and fear.8

Angiograms show that cerebral vasospasm-the reversible narrowing of one or more of the cerebral arteries-frequently occurs between 4 days and 21 days after the SAH, but rarely during the first 96 hours.9 Severe arterial narrowing leads to delayed cerebral ischemia and infarction. The ninth day after hemorrhage marks the incidence peak for neurologic deficits, the risk for which is highest among patients who have large amounts of blood in the basal subarachnoid cisterns, as depicted by CT scan. Presumably, the arterial constriction is triggered by vasoactive substance(s) in the blood dots in the basal cisterns. A period of severe constriction could lead to morphologic changes in the walls of the cerebral arteries, which may cause them to remain narrowed without the continued presence of vasoactive substances. The area of the brain supplied by the affected artery then would experience ischemia.9

Both vasospasm and aneurysmal rebleeding, in addition to the effects produced by the initial hemorrhage, contribute to the delayed morbidity and mortality in SAH. About one-third of all SAH patients will experience cerebral vasospasm, and half of them will either die or develop severe neurologic deficits.10 There are circumstances-the ischemic penumbra-during which ionic homeostasis of brain tissue is maintained by low-level metabolism even though reduced blood flow has led to a loss of neuronal function. Neuronal damage can result whenever cerebral blood flow is reduced as the result of a hemodynamic insult known as cerebral ischemia.7 In the instance of delayed ischemic deficit even a marginal restoration of blood flow may restore neuronal function.11

Although the period of 7-10 days after the initial bleed appears to be the peak incidence of delayed ischemia, Pickard and colleagues found that in 554 SAH patients they studied, only 37% of all episodes of cerebral infarction occurred during this interval. They found that infarction could occur as soon as the first day and as late as the 40th day after the initial bleed.12

To reduce the effect of delayed neurologic events in the SAH patient, appropriate medical treatment must be provided early and continuously during the prolonged period when the patient is at risk-ie, for 21 continuous days after the onset of SAH.3

Back to About SAH Next: Risk Factors


Sources:
  1. AHA http://www.americanheart.org/presenter.jhtml?identifier=1192 (Copyright 2005 American Heart Association, Inc.)

  2. Ingall 1993, Weibers WO. Natural History of subarachnoid hemorrhage. In: Whisnant JP, ed. Stroke: Populations, Cohorts, and Clinical Trials. Boston, Mass: Butterworth-Heinemann Ltd; 1993:174-186.

  3. Weibers WO, Torner JC, Meissner MD. Impact of unruptured intracranial aneurysm on public health in the United States. Stroke 1992;23:1416-1419.

  4. King JT Jr. Epidemiology of aneurysmal subarachnoid hemorrhage. Neuroimag Clin North Am 1997; 7:659-668.

  5. Davis P. Stroke in women. Curr Opin Neurol 1994;7:36-40.

  6. Macdonald RL. Drug treatment of aneurysmal subarachnoid haemorrhage. CNS Drugs 1996;5:264-277.

  7. Weir B. Protection of the brain after aneurysmal rupture. Can J Neurol Sci 1995;22L177-186.

  8. Findlay JM. Current management of aneurysmal subarachnoid hemorrhage guidelines from the Canadian Neurosurgical Society. Can J Neurol Sci 1997;24:161-170.

  9. Allen GS. Role of calcium antagonists in cerebral arterial spasm. Am J Cardiol 1985;55:149B-153B.

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

  11. Mayer PL, Awad IA, Todor R, et al. Misdiagnosis of symptomatic cerebral aneurysm. Prevalence and correlation with outcome at four institutions. Stroke. 1996;27:1558-1563.

  12. Pickard JD, Murray GD, Illingworth F, et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid hemorrhage: British Aneurysm Nimodipine Trial. BMJ 1989;298:636-642.

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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The information provided on Bayer products is only intended for the United States audience. Regulatory requirements, regulations, laws, and distribution of information about drug products may vary from country to country. Product names and indications (product uses) also may be different in different countries. The prescribing information provided here is based on United States labeling and may not be appropriate outside of the US.