Changes in Cerebral Blood Flow and Metabolism Related to the Presence of Subdural Hematoma

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Abstract
ACUTE SUBDURAL HEMATOMA (SDH) remains an important factor in head injury. 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 Virginia with severe closed-head injury between 1982 and 1990 were studied with Xenon-133 regional CBF measurement. Data were reviewed retrospectively with regard to the presence of SDH (n = 54). A comparison group consisted of patients with head injuries without mass lesions or midline shift on admission computed tomographic scans (n = 76). CBF measurements made in patients less than 16 years of age, with concurrent administrations of mannitol or vasopressors, or with cerebral perfusion pressure under 50 mm Hg were excluded. CBF measurements were made on multiple occasions during the first 6 days after injury, and in many instances, simultaneous determinations of cerebral arteriovenous oxygen difference (AVDO2) were made through sampling of jugular bulb and arterial oxygen content. Not all patients underwent CBF measurements on each day. Differences in mean CBF, CMRO2, and AVDO2 were evaluated on each day after injury with the application of Student's t-test for independent groups. Significant reductions in CBF were demonstrated in patients with SDH on Days 1 (P < 0.0005) and 2 (P < 0.01). CMRO2 differed notably on Days 1 (P < 0.005) and 2 (P < 0.05) in patients with SDH, but 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 covariance). CBF ≤ 18 ml/100 g/min (the threshold for infarction) occurred in 9% of patients with SDH within the first 24 hours, compared with none in those patients without mass lesions (P < 0.05 χ2). Mean PaCO2 values were compared, in which CBF was significantly reduced and no differences between groups could be demonstrated. These data demonstrate clear reductions in CBF that are paralleled by reduction in CMRO2 in the first 48 hours after injury in patients with SDH. These changes were not associated with increased AVDO2 in most patients. The lack of increased AVDO2 suggests that reductions in CBF may be related to diminished energy requirements or diminished ability for normal oxidative metabolism of the more severely injured brain.