CHANGES IN CEREBRAL BLOOD-FLOW AND METABOLISM RELATED TO THE PRESENCEOF SUBDURAL-HEMATOMA

ACUTE SUBDURAL HEMATOMA (SDH) remains an important factor in head inju ry. The early effects of SDH on cerebral blood flow (CBF) and cerebral metabolic rate of oxygen consumption (CMRO2) in humans have not been clearly demonstrated. Patients admitted to the Medical College of Virg inia with severe closed-head injury between 1982 and 1990 were studied with Xenon-133 regional CBF measurement. Data were reviewed retrospec tively with regard to the presence of SDH (n = 54). A comparison group consisted of patients with head injuries without mass lesions or midl ine shift on admission computed tomographic scans (n = 76). CBF measur ements made in patients less than 16 years of age, with concurrent adm inistrations of mannitol or vasopressors, or with cerebral perfusion p ressure under 50 mm Hg were excluded. CBF measurements were made on mu ltiple occasions during the first 6 days after injury, and in many ins tances, simultaneous determinations of cerebral arteriovenous oxygen d ifference (AVDO2) were made through sampling of jugular bulb and arter ial oxygen content. Not all patients underwent CBF measurements on eac h day. Differences in mean CBF, CMRO2, and AVDO2 were evaluated on eac h day after injury with the application of Student's t-test for indepe ndent groups. Significant reductions in CBF were demonstrated in patie nts with SDH on Days 1 (P < 0.0005) and 2 (P < 0.01). CMRO2 differed n otably on Days 1 (P < 0.005) and 2 (P < 0.05) in patients with SDH, bu t when corrected for the lower Glasgow Coma Score in patients with SDH , the P values were only 0.07 and 0.12, respectively (analysis of cova riance). CBF less-than-or-equal-to 18 ml/100 g/min (the threshold for infarction) occurred in 9% of patients with SDH within the first 24 ho urs, compared with none in those patients without mass lesions (p < 0. 05 chi2). Mean PaCO2 values were compared, in which CBF was significan tly reduced and no differences between groups could be demonstrated. T hese data demonstrate clear reductions in CBF that are paralleled by r eduction in CMRO2 in the first 48 hours after injury in patients with SDH. These changes were not associated with increased AVDO2 in most pa tients. The lack of increased AVDO2 suggests that reductions in CBF ma y be related to diminished energy requirements or diminished ability f or normal oxidative metabolism of the more severely injured brain.