Is Cerebral Vasospasm still a Clinical Problem?
The first International Conference on Cerebral Vasospasm (ICCV) took place in Jackson (Mississippi) in 1972, and the second meeting in Amsterdam in 1979. At that time, ischemic deficits due to cerebral vasospasm (VSP) were a major clinical problem. The In
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Is Cerebral Vasospasm still a Clinical Problem? R. W. Seiler and R. Binggeli Department of Neurosurgery, University Hospital, Berne, Switzerland
The first International Conference on Cerebral Vasospasm (ICCV) took place in Jackson (Mississippi) in 1972, and the second meeting in Amsterdam in 1979. At that time, ischemic deficits due to cerebral vasospasm (VSP) were a major clinical problem. The International Cooperative Study on the Timing of Aneurysm Surgery evaluated the results of surgical and medical management in 3521 patients treated between 1980 and 1983. The results showed that 42,3% of all patients were dead or disabled, and the leading cause of death and disability was VSP which had been present in 33% of those patients [10], (Fig. 1). Around 1980, the anti fibrinolytic drug tranexamic acid was used for prevention of rebleedings. In a randomized study, it was found to be effective in reducing the number of rebleedings, but with a proportionally equal increase of ischemic deficits. The conclusion was that until some method can be found to minimize ischemic complications, tranexamic acid is of no benefit in patients with subarachnoid hemorrhage [24]. In 1967, Farhat and Schneider published their observation on the improvement of ischemic neurological deficits with increased systemic blood pressure [5]. In clinical vasospasm, regional cerebral blood flow (rCBF) is depressed and pressure autoregulation is impaired. Under these circumstances, rCBF is directly dependent on perfusion pressure. Despite this rationale, clinicians have been reluctant to use hypervolemia and vasopressors for fear of precipitating hemorrhagic infarction or rupture of un clipped aneurysms. In 1976, Kosnik and Hunt reported the reversal of delayed ischemic symptoms in 6 of 7 patients by the use of vasopressors and hypervolemia [12]. A larger series, published by Kassel et al. in 1982, reported on the response of 58 patients with ischemic deficits due to
vasospasm who were treated with intravascular volume expansion and induced arterial hypertension [11]. After these reports, hemodynamic therapy with careful fluid management to avoid hypovolemia and strict blood pressure limits to ensure adequate perfusion pressure became standard for the management of patients with subarachnoid hemorrhage. When the patients, despite these measures, become symptomatic, induced hypertension is now routinely used to try to reverse the ischemic deficit. In the 1980's, the calcium antagonist nimodipine was evaluated in several randomized studies, and its neuroprotective effect to reduce ischemic deficits after subarachnoid hemorrhage (SAH) was proven [1, 3, 15, 17, 18, 19] (Table 1). Combining hemodynamic therapy, nimodipine and early aneurysm operation, we were able to reduce the frequency of permanent ischemic deficits due to vasospasm to about 5% of all
Fig. \. Results of the International Cooperative Study, 1980- 1983. Clinical vasospasm permanently affected 13.5% of all patients and accounted for 33% of deaths and disability
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