Monitoring of cerebral metabolism: non-ischemic impairment of oxidative metabolism following severe traumatic brain injury.

OBJECTIVE: To investigate and compare the respective dynamics of cerebral blood flow (CBF) and metabolism in response to changes in neurological condition and intracranial pressure (ICP) in severe traumatic brain injury (TBI).
METHODS: Eight-four patients with severe TBI were prospectively enrolled in this study. CBF was measured daily and global cerebral metabolic rates of oxygen (CMRO(2)), glucose (CMRGlc) and lactate (CMRLct) were calculated using arterial jugular differences. In addition, 33 patients had a second evaluation shortly after a significant change (>5 mmHg) in their ICP.
RESULTS: Eight hundred and ninety-four evaluations were collected during a period ranging between 1 and 12 days (mean: 5.1 +/- 2.6 days). CBF was moderately but significantly decreased. Oppositely, CMRO(2) was profoundly reduced with evidence for critical metabolic failure (<1.2 ml/100 g/min) in 30.5% whereas only 8.5% of CBF measurements were lower than 20 ml/100 g/min. Furthermore, in 78 instances of a dynamic assessment performed following ICP increase (n = 20) or decrease (n = 58), CMRO(2) but not CBF proved to be significantly and inversely affected by ICP fluctuations. Finally, CMRO(2) and CMRLct correlated with GCS score in contrast with CBF. Both CBF and metabolic indices, however, correlated with neurological outcome.
CONCLUSION: This study shows that cerebral metabolic failure following TBI is a common finding that is not of ischemic origin in most instances. Unlike frequently assumed, cerebral metabolism is not constrained within the narrow range of a static depression sustained for weeks but rather subject to significant variations in response to changes in ICP or neurological condition.