M. Ross Bullock
Sandra Magnoni, Laura Ghisoni, Marco Locatelli, Mariangela Caimi, Angelo Colombo, Valerio Valeriani and Nino Stocchetti
Object. The authors investigated the effects of hyperoxia on brain tissue PO2 and on glucose metabolism in cerebral and adipose tissue after traumatic brain injury (TBI).
Methods. After 3 hours of ventilation with pure O2, 18 tests were performed on different days in eight comatose patients with TBI. Lactate, pyruvate, glucose, glutamate, and brain tissue PO2 were measured in the cerebral extracellular fluid (ECF) by using microdialysis. Analytes were also measured in the ECF of abdominal adipose tissue.
After 3 hours of increase in the fraction of inspired O2, brain tissue PO2 rose from the baseline value of 32.7 ± 18 to 122.6 ± 45.2 mm Hg (p < 0.0001), whereas brain lactate dropped from its baseline (3.21 ± 2.77 mmol/L), reaching its lowest value (2.90 ± 2.58 mmol/L) after 3 hours of hyperoxia (p < 0.01). Pyruvate dropped as well, from 153 ± 56 to 141 ± 56 µmol/L (p < 0.05), so the lactate/pyruvate ratio did not change. No significant changes were observed in glucose and glutamate. The arteriovenous difference in O2 content dropped, although not significantly, from a baseline of 4.52 ± 1.22 to 4.15 ± 0.76 ml/100 ml. The mean concentration of lactate in adipose tissue fell significantly as well (p < 0.01), but the lactate/pyruvate ratio did not change.
Conclusions. Hyperoxia slightly reduced lactate levels in brain tissue after TBI. The estimated redox status of the cells, however, did not change and cerebral O2 extraction seemed to be reduced. These data indicate that oxidation of glucose was not improved by hyperoxia in cerebral and adipose tissue, and might even be impaired.
Cristina Mattioli, Luigi Beretta, Simonetta Gerevini, Fabrizio Veglia, Giuseppe Citerio, Manuela Cormio and Nino Stocchetti
Object. The goal of this study was fourfold: 1) to determine the incidence of traumatic subarachnoid hemorrhage (tSAH) in patients with traumatic brain injury (TBI); 2) to verify agreement in the diagnosis of tSAH in a multicenter study; 3) to assess the incidence of tSAH on the outcome of the patient; and 4) to establish whether tSAH itself leads to an unfavorable outcome or whether it is a sign of major brain trauma associated with severe posttraumatic lesions.
Methods. Computerized tomography (CT) scans obtained in 169 head-injured patients on admission to 12 Italian intensive care units during a 3-month period were examined. The scans were collected for neuroradiological review and were used for the analysis together with data from a multicenter database (Neurolink).
A review committee found a high incidence of tSAH (61%) in patients with TBI and a moderate agreement among centers (K = 0.57). Significant associations were observed between the presence and grading of tSAH and patient outcomes, and between the presence of tSAH and the severity of the CT findings. Logistic regression analysis showed that the presence of tSAH and its grading alone do not assume statistical significance in the prediction of unfavorable outcome.
Conclusions. Traumatic SAH frequently occurs in patients with TBI, but it is difficult to detect and grade. Traumatic SAH is associated with more severe CT findings and a worse patient outcome.