LOW BRAIN-TISSUE OXYGEN-PRESSURE - INCIDENCE AND CORRECTIVE THERAPIES

In 16 head injured patients, the monitoring of brain tissue oxygen pre ssure (ti-pO(2)) show 22 episodes of low ti-pO(2) (less than or equal to 12 mmHg). Mean episode duration was 16h. At time of the lowest ti-p O(2) value, cerebral perfusion pressure (CPP) was < 60 mmHg in 5 cases , 4 of them with impending brain death. Oxygen saturation values of th e jugular venous blood (svjO(2)) remained in the normal range (55-85 m mHg) in 12 cases and exceeded 85 mmHg in 3 cases, 2 of them with impen ding brain death. Lactate-oxygen index (LOD was normal (< 0.08) in 7/1 0 cases and at very high level (> 0.60) in 3 cases including 2 cases o f impending brain death. A first group of low ti-pO(2) episodes was cl early related to an insufficient CPP level (n = 73), comprising 4 case s of parallel decrease in CPP and ti-pO(2) until brain death, and 9 ca ses in which ti-pO(2) was restored along with a significant increase i n CPP (p < 0.001). In 5 patients, low ti-pO(2) episodes were due to an other cause: vasospasm (2 cases), hypoxemia, anemia and premature inte rruption of anesthesia. Appropriate treatments were effective in resto ring ti-pO(2) with no change in CPP In 4 patients, the cause of low ti -pO(2) was not identifiable and episodes resolved spontaneously. The r esults confirm the critical influence of CPP and ti-pO(2). Patients in whom elevation of CPP improved ti-pO(2) have normal range CPP during the episode. Optimal CPP should therefore be sometimes higher than rec ommended, ti-pO(2) monitoring appears a good method to define the opti mal CPP level in individual patient The duration of the artefactual pe riod after catheter placement is to clarify.