Applying Cerebral Hypothermia and Brain Oxygen Monitoring in Treating Severe Traumatic Brain Injury

BACKGROUND: Severe traumatic brain injury (TBI) was to be one of the major health problems encountered in modern medicine and had an incalculable socioeconomic impact. The initial cerebral damage after acute brain injury is often exacerbated by postischemic hyperthermia and worsens the outcome. Hypothermia is one of the current therapies designed to combat this deleterious effect. The brain tissue oxygen (PtiO2)-guided cerebral perfusion pressure (CPP) management was successfully reduced because of cerebral hypoxic episodes following TBI. MATERIALS AND METHODS: Forty-five patients with severe TBI whose Glasgow Coma Scale (GCS) score ranged between 4 and 8 during September 2006 and August 2007 were enrolled in China Medical University Hospital, Taichung, Taiwan. One patient with a GCS score of 3 was excluded for poor outcome. These patients were randomized into three groups. Group A (16 patients) was intracranial pressure/cerebral perfusion pressure (ICP/CPP)-guided management only, Group B (15 patients) was ICP/CPP guided with mild hypothermia, and Group C (14 patients) was combined mild hypothermia and PtiO2 guided with CPP management on patients with severe TBI. All patients were treated with ICP/CPP management (ICP <20 mm Hg, CPP >60 mm Hg). However, the group with PtiO2 monitoring was required to raise the PtiO2 above 20 mm Hg. Length of intensive care unit stay, ICP, PtiO2, Glasgow Outcome Scale (GOS) score, mortality, and complications were analyzed. RESULTS: The ICP values progressively increased in the first 3 days but showed smaller changes in hypothermia groups (Groups B and C) and were significantly lower than those of the normothermia group (Group A) at the same time point. We also found out that the averaged ICP were significantly related to days and the daily variations [measured as (daily observation - daily group mean)(2)] of ICP were shown to the significantly different among three treatment groups after the third posttraumatic day. The values of PtiO2 in Group C tended to rise when the ICP decreased were also observed. A favorable outcome is divided by the result of GOS scores. The percentage of favorable neurologic outcome was 50% in the normothermia group, 60% in the hypothermia-only group, and 71.4% in the PtiO2 group, with statistical significance. The percentage of mortality was 12.5% in the normothermia group, 6.7% in the hypothermia-only group, and 8.5% in the PtiO2 group, without statistical significance in three groups. Complications included pulmonary infections, peptic ulcer, and leukocytopenia (43.8% in the normothermia group, 55.6% in the hypothermia-only group, and 50% in the PtiO2 group). CONCLUSIONS: Therapeutic mild hypothermia combined with PtiO2-guided CPP/ICP management allows reducing elevated ICP before 24 hours after injury, and daily variations of ICP were shown to be significantly different among the three treatment groups after the third posttraumatic day. It means that the hypothermia groups may reduce the ICP earlier and inhibit the elicitation of acute inflammation after cerebral contusion. Our data also provided evidence that early treatment that lowers PtiO2 may improve the outcome and seems the best medical treatment method in these three groups. We concluded that therapeutic mild hypothermia combined with PtiO2-guided CPP/ICP management provides beneficial effects when treating TBI, and a multicenter randomized trial needs to be undertaken.