Aim. Clinical and experimental studies have shown a reduction of cerebral blood flow (CBF) and metabolic alterations following traumatic brain injury (TBI). The incidence of ischemia and the meaning of post-traumatic metabolic alterations are still unclear. Methods. Revision of CBF and metabolic changes following TBI based on the literature and on our clinical experience. Results. Cerebral ischemia and metabolic alterations are part of the secondary insults/damage leading to an increased damage following TBI. Global ischemia occurs early following TBI as shown by CBF measurements and by greater values of arterio-jugular difference of oxygen (AJDO2) during the 1st 24 hours postinjury. Post-traumatic ischemia should be defined based on the relationships between CBF and on the metabolic requirements of the brain. Regional ischemia occurs more frequently than global ischemia as shown by regional monitoring of cerebral oxygenation. Following TBI there is a transient phase of increased glycolitic activity followed by a more prolonged phase of reduced metabolic rate of glucose (CMRglc) and oxygen (CMRO2). The extent of CMRO2 reduction is a marker of injury severity and it is associated with unforavorable outcome. Conclusion. Cerebral ischemia occurs following TBI and should he defined based on CBF value and the metabolic needs of the brain. Global monitoring of cerebral oxygenation adequacy should be combined with regional monitoring. The meaning of high AJDO2 values should be reconsidered: if they can highlights potential ischemia they are also showing a still living brain with a partially preserved oxygen extraction capability.
|Translated title of the contribution||Cerebral oxygen consumption and ischemia in traumatic brain injury|
|Number of pages||5|
|Publication status||Published - Apr 2004|
ASJC Scopus subject areas
- Anesthesiology and Pain Medicine