Cerebral lactate production in relation to intracranial pressure, cranial computed tomography findings, and outcome in patients with severe head injury.

Severe head injury is frequently associated with focal or global disturbances of cerebral blood flow and metabolism. Routine monitoring of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in these patients does not provide information about critically reduced local or global cerebral blood flow. Measurements of cerebral lactate difference, Lactate-Oxygen-Index (LOI) and cerebral oxygen extraction were evaluated for advanced monitoring by comparing these parameters with ICP, cranial computed tomography (CCT) findings, and outcome in a group of severely head-injured patients. In 21 patients with severe brain trauma (GCS < or = 8), arterial as well as jugular venous lactate levels and oxygen saturation were measured in vitro every 6 h after admission of patients to the intensive care unit (ICU) throughout the acute course of treatment. Arterial blood pressure, blood gases, and ICP were assessed by standard monitoring measurements. CCT was performed initially after admission of the patients to the hospital, during the acute period in the ICU, if indicated, and 10 to 14 days after trauma. Outcome was classified according to the Glasgow outcome scale (GOS) at six months after injury. Data were averaged in each patient for every day after trauma and over the entire monitoring period. Resulting values were tested for correlation by regression analysis. Additionally, the data of the group of patients with normal to minimally elevated mean ICP (ICP < 20 mmHg, n = 12) were compared to those of the patients with increased mean ICP (ICP > 20 mmHg, n = 9). The cerebral lactate difference in all patients on the day of trauma was significantly increased as compared to the later period (0.20 vs. 0.11-0.07 mmol/l, p < 0.05), but was not different with high or normal to minimally elevated ICP. In patients with intracranial hypertension, the cerebral lactate difference remained significantly increased from the first to the fifth day after injury, whereas it normalized in this period in the group with normal to minimally elevated ICP. Averaged over the acute course, patients with increased ICP had significantly higher mean lactate differences (0.18 +/- 0.16 vs. 0.067 +/- 0.025 mmol/l, p = 0.001) and higher mean LOIs (0.072 +/- 0.071 vs. 0.028 +/- 0.013, p = 0.011). There was a significant correlation of increased mean cerebral lactate difference to poor outcome (r = 0.46, p = 0.035). Cerebral oxygen extraction in all patients tended to increase on the day of trauma (36.7% vs. 29.2% to 31.5% during the subsequent course), but this difference was not significant. The initial degree of brain swelling, classified by CCT according to Marshall et al. (1991), showed no correlation with cerebral lactate differences, ICP, O2-extraction, or outcome. Neither was there a correlation of cerebral oxygen extraction to ICP nor to outcome. In conclusion, the severity of brain trauma and outcome of patients was reflected by increased cerebral lactate production. Unchanged values of global cerebral oxygen extraction suggest that the regulatory mechanisms of brain oxygen supply were not impaired by trauma. Measurements of cerebral lactate differences and brain oxygen extraction may contribute to advanced monitoring in severe head injury.