Cerebral hemodynamic impairment after aneurysmal subarachnoid hemorrhage as evaluated using transcranial Doppler ultrasonography: relationship to delayed cerebral ischemia and clinical outcome
- 1 September 2001
- journal article
- research article
- Published by Journal of Neurosurgery Publishing Group (JNSPG) in Journal of Neurosurgery
- Vol. 95 (3) , 393-401
- https://doi.org/10.3171/jns.2001.95.3.0393
Abstract
Object. In 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). Methods. Cerebral 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). Conclusions. The 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.Keywords
This publication has 58 references indexed in Scilit:
- Effect of Acetazolamide Reactivity and Long-term Outcome in Patients With Major Cerebral Artery Occlusive DiseasesStroke, 1998
- Assessment of Cerebral Autoregulation Using Carotid Artery CompressionStroke, 1996
- Course of cerebrovascular reactivity in patients with carotid artery occlusions.Stroke, 1994
- Initial and recurrent bleeding are the major causes of death following subarachnoid hemorrhage.Stroke, 1994
- Prediction of symptomatic vasospasm after subarachnoid hemorrhage by rapidly increasing transcranial Doppler velocity and cerebral blood flow changes.Stroke, 1992
- Course of carotid artery occlusions with impaired cerebrovascular reactivity.Stroke, 1992
- Volume depletion and natriuresis in patients with a ruptured intracranial aneurysmAnnals of Neurology, 1985
- Hyponatremia and cerebral infarction in patients with ruptured intracranial aneurysms: Is fluid restriction harmful?Annals of Neurology, 1985
- Cerebral Vasospasm with Ruptured Saccular Aneurysm — The Clinical ManifestationsNeurosurgery, 1977
- Effects of subarachnoid hemorrhage on cerebral blood volume, blood flow, and oxygen utilization in humansJournal of Neurosurgery, 1977