• T Rätsep and T Asser.
• Department of Neurology and Neurosurgery, University of Tartu, Estonia. tonu.ratsep@kliinikum.ee
• J. Neurosurg. 2001 Sep 1;95(3):393-401.

ObjectIn this study the authors evaluated the relative role of cerebral hemodynamic impairment (HDI) in the pathogenesis of delayed cerebral ischemia and poor clinical outcome after aneurysmal subarachnoid hemorrhage (SAH).MethodsCerebral hemodynamics were assessed daily with transcranial Doppler (TCD) ultrasonography in 55 consecutive patients with verified SAH. Hemodynamic impairment was defined as blood flow velocity (BFV) values consistent with vasospasm in conjunction with impaired autoregulatory vasodilation as evaluated using the transient hyperemic response tests in the middle cerebral arteries. A total of 1344 TCD examinations were performed, in which the evaluation of HDI was feasible during 80.9% and HDI was registered during 12% of the examinations. It was found that HDI occurred in 60% of patients and was frequently recorded in conjunction with severe vasospasm (p < 0.05) and a rapid increase of BFV values (p < 0.05). Detection of HDI was closely associated with the development of delayed ischemic brain damage after SAH (p < 0.05). Furthermore, because delayed ischemia was never observed in cases in which vasospasm had not led to the development of HDI, its occurrence increased significantly the likelihood of subsequent cerebral ischemia among the patients with vasospasm (p < 0.05). Detection of HDI was independently related to unfavorable clinical outcome according to Glasgow Outcome Scale at 6 months after SAH (p < 0.05).ConclusionsThe results showed that HDI is common after SAH and can be evaluated with TCD ultrasonography in routine clinical practice. Detection of HDI could be useful for identifying patients at high or low risk for delayed ischemic complications and unfavorable clinical outcome after SAH.

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