ABSTRACT
BACKGROUND: The therapeutic effect of mild hypothermia in the treatment of severe brain injury has been recognized in spite of the poor understanding of its mechanism. Until now, no reports have been available to describe the changes in cerebral oxygen metabolism following serious brain and during mild hypothermia treatment.OBJETCIVE: To observe the patterns of cerebral oxygen metabolism changes during mild hypothermia treatment for severe brain injury, and explore the mechanism of the therapeutic effect of mild hypothermia.DESIGN: A clinical observation of factorial design.SETTING: Mild Hypothermia Treatment Center of Tianjin Huanhu Hospital.PARTICIPANTS: From August 1998 to January 2000, 13 patients with severe brain injury were treated in Mild Hypothermia Treatment Center of Tianjin Huanhu Hospital, including 11 males and 2 females aged 18-65 years. Diagnosis of brain contusion and laceration with subdural hematoma was established in 6 cases, epidural hematoma in 1 case, subarachnoid hemorrhage in 4 cases and diffuse axonal injury in 2 cases. Of these cases 7 were treated with conservative therapy, and 6 with internal/external decompression after surgical hematoma removal.METHODS: A blanket for controlling the body temperature was applied to induce whole-body hypothermia in the patients in the mild hypothermia treatment room with continuous intravenous infusion of chlorpromazine (100 mg), promethazine (100 mg) and atracurium besilate (400 mg) administered in 500 mL normal saline. Neurotrend-7TM multi-parameter monitoring system was used to for monitoring the dynamic changes of cerebral PO2,PCO2, pH and brain temperature to evaluate their changes after treatment.The correlation between cerebral oxygen metabolism and the scores of Glasgow Coma Scale was analyzed.MAIN OUTCOME MEASURES: Dynamic changes of cerebral PO2,PCO2, pH and brain temperature.RESULTS: All the 13 patients entered the final analysis. Eighteen hours after hypothermia, the PO2 [(2.23±1.29) kPa] was obviously increased in comparison with that before hypothermia [(1.29±0.57) kPa, t=2.449, P ＜ 0.05], and PCO2 exhibited significant decrease at hypothermia 6 hours to (7.32±0.92) kPa from the pre-treatment level of (7.75±1.07) kPa (t=2.446, P ＜ 0.05). Significant elevation of pH and descension of intracranial pressure occurred upon the achievement of hypothermia [7.06±0.15 vs 6.83±0.20 for pH, t=5.164, P ＜ 0.05;(2.03±1.01) vs (2.57±0.93) kPa for intracranial pressure, t=2.948, P ＜ 0.05].Six hours after hypothermia, the cerebral perfusion pressure was obviously higher than that before hypothermia [(9.40±1.80) vs (7.80±1.59) kPa, t=2.365,P ＜ 0.05]. PCO2 was found inversely correlated with Glasgow Outcome Scale (GOS) scores at 24 hours of hypothermia (r=-0.699, P ＜ 0.05). The variations of cerebral oxygen metabolism indices before and after mild hypothermia were positively correlated with GOS scores.CONCLUSION: Dynamic monitoring of cerebral oxygen metabolism is safe and effective, and may help in early detection of cerebral hypoxia and acidosis following severe brain injury. Mild hypothermia treatment can effectively alleviate hypoxia and acidosis following severe brain injury to improve the prognosis of the patients.