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  • 1
    ISSN: 0942-0940
    Keywords: Cerebral vasospasm ; cerebral aneurysm ; calcium antagonist ; nicardipine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Calcium antagonists are currently most widely used for chronic cerebral vasospasm after aneurysmal subarachnoid haemorrhage (SAH). However, the vasodilatory effects of systemically administered calcium antagonists can be limited secondary to hypotension. We previously compared intrathecal and intravenous routes of administration of nicardipine. Intrathecal administration of nicardipine significantly dilated spastic basilar arteries on day 7 in a two-haemorrhage canine model of vasospasm. In the present communication, the effects of prophylactic, serial administration of intrathecal nicardipine on vasospasm was examined in 50 patients. Patients were classified as Fisher SAH group 3 and all had their aneurysms clipped within 3 days of SAH. Following placement of a cisternal drain, 2 mg of nicardipine was injected, three times each day for an average of 10 days. The control group consisted of 91 similar patients with cisternal drainage not treated with nicardipine. Intrathecal administration of nicardipine decreased the incidence of symptomatic vasospasm by 26%, angiographic vasospasm by 20% and increased good clinical outcome at one month after the haemorrhage by 15%. Postoperative angiograms revealed that patients in the nicardipine group showed less vasospasm of major cerebral arteries, near the tip of a drain in the basal cistern, but vasospasm in the A2 and M2 segments was not decreased. Radio-isotope cisternography suggested that nicardipine might not reach the subarachnoid space around A2 and M2 segments. Nine patients complained of headache probably secondary to nicardipine induced vasodilation. Two patients suffered from mengingitis, both were successfully treated. Intrathecal administration nicardipine appears to be effective in the treatment of vasospasm, but side effects were significant.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0942-0940
    Keywords: Cerebral vasospasm ; haemorrhagic infarction ; intracranial aneurysm ; normovolaemic induced hypertension therapy ; subarachnoid haemorrhage ; Swan-Ganz catheter
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We showed that normovolaemic induced hypertension therapy was effective in reducing ischaemic symptoms attributed to cerebral vasospasm in 41 patients after subarachnoid haemorrhage. By inducing hypertension to 25% to 50% above normal systolic arterial blood pressure, we observed that in 17 of 24 cases (71%) neurological deficits improved. In four cases of haemorrhagic infarction, the blood pressure rose to over 50% of systolic arterial pressure, and a low density area was confirmed on computerized tomography (CT) scan prior to vasospasm. Induced hypertension was therefore not considered when a low density area was revealed on CT scan. Restriction of fluid input is usually a factor in producing hypovolaemia after a neurosurgical operation. Intravascular volume expansion has been reported effective in reversing ischaemic deficits. However, according to Poiseuille's equation, increasing blood volume to a state of hypervolaemia can not enhance flow. The cerebral blood flow (CBF) was raised by increasing perfusion pressure, reducing viscosity, or increasing blood vessel diameter. Intravascular volume expansion elevates not only systemic arterial pressure, but also pulmonary artery wedge pressure over 18 mmHg and cardiac index over 2.2. Since pulmonary oedema and congestive heart failure may develop, one should monitor haemodynamic parameters with the Swan-Ganz catheter as a preventive measure. We emphasize that normovolaemic induced hypertension, maintaining haemodynamics subset 1 of the comparable haemodynamic subsets, is effective in raising perfusion pressure of CBF.
    Type of Medium: Electronic Resource
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