CEREBRAL HEMODYNAMICS IN SUBARACHNOID HEMORRHAGE EVALUATED BY TRANSCRANIAL DOPPLER SONOGRAPHY .1. RELIABILITY OF FLOW VELOCITIES IN CLINICAL MANAGEMENT

Citation
R. Laumer et al., CEREBRAL HEMODYNAMICS IN SUBARACHNOID HEMORRHAGE EVALUATED BY TRANSCRANIAL DOPPLER SONOGRAPHY .1. RELIABILITY OF FLOW VELOCITIES IN CLINICAL MANAGEMENT, Neurosurgery, 33(1), 1993, pp. 1-9
Citations number
36
Categorie Soggetti
Surgery,Neurosciences
Journal title
ISSN journal
0148396X
Volume
33
Issue
1
Year of publication
1993
Pages
1 - 9
Database
ISI
SICI code
0148-396X(1993)33:1<1:CHISHE>2.0.ZU;2-E
Abstract
DURING RECENT YEARS, the management of subarachnoid hemorrhage (SAH) h as changed, resulting in an increase in early operations and routine a dministration of nimodipine. Both influenced the indication for transc ranial Doppler sonography (TCD). Furthermore, investigations detected discrepancies between Doppler findings and neurological status. In a p rospective study, the reliability of TCD was investigated in patients with SAH treated with intravenously administered nimodipine. Patients with large hematomas were excluded. Neurological deficits immediately after surgery or within the first 48 hours were classified as not dela yed, and therefore not necessarily due to vasospasm. The most remarkab le points of this study are that there is no significant difference be tween the flow velocities for Hunt and Hess Grades I and II when compa red with those for Grade III, and that Grades IV and V seem to be affi liated with the lowest velocities. When the flow velocities of 11 pati ents who developed delayed ischemic deficits (DIDs) were compared with those of patients with no deficit, no significant difference was seen . A significant increase in velocity in the days before the onset of D ID was found only in 3 of 11 cases. Eight patients showed either const ant high or constant low velocities or even, in some cases, decreasing time courses. High flow velocities did not necessarily mean impending neurological deficits: 8 of 66 patients tolerated flow velocities ove r 200 cm/s. Therefore, it no longer seems to be justified to proclaim that TCD is able to predict neurological deficits, although it is doub tless able to detect vasospasm. In an additional series of 97 normal s ubjects, flow velocities were found to be higher than reported in the literature, but this fact seems to explain only a minor proportion of the discrepancies. The main difference between this series and older i nvestigations is the routine administration of nimodipine. In patients admitted within 48 hours after SAH (commonly no vasospasm) or with po or grade SAHs (commonly low flow velocities) TCD seems to have no valu e. Even in patients admitted later than 72 hours, the indication for T CD depends on the local management. If surgery is to be performed even in cases of asymptomatic vasospasm, the clinical value of TCD in case s of SAH is questionable.