THE RELATIONSHIP OF BLOOD VELOCITY AS MEASURED BY TRANSCRANIAL DOPPLER ULTRASONOGRAPHY TO CEREBRAL BLOOD-FLOW AS DETERMINED BY STABLE XENONCOMPUTED TOMOGRAPHIC STUDIES AFTER ANEURYSMAL SUBARACHNOID HEMORRHAGE

TRANSCRANIAL DOPPLER (TCD) ultrasonography is often used to guide the management of patients with subarachnoid hemorrhage (SAH). However, th e correlation between increased blood velocity as measured by TCD ultr asonography and angiographic vasospasm was established before the rout ine use of hypervolemia/hemodilution and administration of nimodipine and did not address blood flow. The relationship of blood velocity as measured by TCD ultrasonography and local cerebral blood flow (LCBF) i n SAH managed with these modalities is unknown. Patients presenting wi th aneurysmal SAH between January 1992 and September 1993 who underwen t TCD ultrasonography and xenon computed tomographic (Xe/CT) LCBF stud ies within 12 hours were retrospectively studied. Fifty patients under went a total of 94 paired studies, encompassing 709 vascular territori es. All were treated with nimodipine and hypervolemia/hemodilution. He matocrit, blood pressure, and partial carbon dioxide pressure were sim ilar at the time of TCD ultrasonography and Xe/CT measurement of LCBF. When LCBF in the middle cerebral artery (MCA) was less than or equal to 31 ml/100 g/min, the corresponding peak systolic velocity measured by TCD ultrasonography was 119 cm/s, whereas those >31 ml/100 g/min ha d a velocity of 169 cm/s (P = 0.006). High LCBF was associated with hi gh velocity in all vascular territories, reaching significance in all but the internal carotid artery. At the time of each study, 41 neurolo gical examinations were focal and 53 were nonfocal. The Xe/CT measurem ent of LCBF in the MCA contralateral to a deficit was significantly le ss than in territories without corresponding clinical deficits (P = 0. 01), whereas peak systolic velocities in the MCA were not significantl y different (P = 0.71). Territories with increases in blood velocity i n the MCA of >50 cm/s/24 h did not have statistically different LCBF ( P = 0.183). Our results suggest that increased blood velocity revealed by TCD ultrasonography correlates with increased LCBF and not with is chemia. No difference in LCBF was found in territories with and withou t rapid increases in blood velocity in the MCA. Furthermore, although focal neurological deficits corresponded with decreased contralateral LCBF in the MCA, increased velocity did not correlate with neurologica l findings. Therapeutic decisions based solely on blood velocity revea led by TCD ultrasonography might be inappropriate and potentially harm ful. Xe/CT studies of LCBF are useful in guiding the management of SAH .