Cerebral oxygenation in patients after severe head injury - Monitoring and effects of arterial hyperoxia on cerebral blood flow, metabolism, and intracranial pressure

Early impaired cerebral blood flow (CBF) after severe head injury (SHL) leads to poor brain tissue oxygen delivery and lactate accumulation. The purpose of this investigation was to elucidate the relationship between CBF, local dialysate lactate (lact(md)) and dialysate glucose (gluc(md)), and brain tissue oxygen levels (PtiO2) under arterial normoxia. The effect of increased brain tissue oxygenation due to high fractions of inspired oxygen (FiO(2)) on lact(md) and CBF was explored. A total of 47 patients with SHI were enrolled in this studies (Glasgow Coma Score [GCS] < 8). CBF was first assessed in 30 patients at one time point in the first 96 hours (27 +/- 28 hours) after SHI using stable xenon computed tomography (Xe-CT) (30% inspired xenon [FiXe] and 35% FiO(2)). In a second study, sequential double CBF measurements were performed in 7 patients with 35% FiO(2) and 60% FiO(2), respectively, with an interval of 30 minutes. In a subsequent study, 14 patients underwent normobaric hyperoxia by increasing FiO(2) from 35 +/- 5% to 60% and then 100% over a period of 6 hours. This was done to test the effect of normobaric hyperoxia on lact(md) and brain gluc(md), as measured by local microdialysis. Changes in p(ti)O(2) in response to changes in FiO(2) were analyzed by calculating the oxygen reactivity. Oxygen reactivity was then related to the 3-month outcome data The levels of lact(md) and gluc(md) under hyperoxia were compared with the baseline levels, measured at 35% FiO(2). Under normoxic conditions, there was a significant correlation between CBF and p(ti)O(2) (R = 0.7; P < .05). In the sequential double CBF study, however, FiO(2) was inversely correlated with CBF (P < .05). In the 14 patients undergoing the 6-hour 100% FiO(2) challenge, the mean PtiO2 levels increased to 353 (87% compared with baseline), although the mean lact(md) levels decreased by 38 +/- 16% (P < .05). The PtiO2 response to 100% FiO(2) (oxygen reactivity) was inversely correlated with outcome (P < .01). Monitoring PtiO2 after SHI provides valuable information about cerebral oxygenation and substrate delivery. Increasing arterial oxygen tension (PaO2) effectively increased PtiO2, and brain lact(md) was reduced by the same maneuver.