Low brain tissue oxygen pressure: incidence and corrective therapies.

In 16 head injured patients, the monitoring of brain tissue oxygen pressure (ti-pO2) show 22 episodes of low ti-pO2 (< or = 12 mmHg). Mean episode duration was 16 h. At time of the lowest ti-pO2 value, cerebral perfusion pressure (CPP), was < 60 mmHg in 5 cases, 4 of them with impending brain death. Oxygen saturation values of the jugular venous blood (svjO2) remained in the normal range (55-85 mmHg) in 12 cases and exceeded 85 mmHg in 3 cases, 2 of them with impending brain death. Lactate-oxygen index (LOI) was normal (< 0.08) in 7/10 cases and at very high level (> 0.60) in 3 cases including 2 cases of impending brain death. A first group of low ti-pO2 episodes was clearly related to an insufficient CPP level (n = 13), comprising 4 cases of parallel decrease in CPP and ti-pO2 until brain death, and 9 cases in which ti-pO2 was restored along with a significant increase in CPP (p < 0.001). In 5 patients, low ti-pO2 episodes were due to another cause: vasospasm (2 cases), hypoxemia, anemia and premature interruption of anesthesia. Appropriate treatments were effective in restoring ti-pO2 with no change in CPP. In 4 patients, the cause of low ti-pO2 was not identifiable and episodes resolved spontaneously. The results confirm the critical influence of CPP and ti-pO2. Patients in whom elevation of CPP improved ti-pO2 have normal range CPP during the episode. Optimal CPP should therefore be sometimes higher than recommended. ti-pO2 monitoring appears a good method to define the optimal CPP level in individual patient. The duration of the artefactual period after catheter placement is to clarify.