Hayashi N, Hirayama T, Udagawa A, Daimon W, Ohata M
Nihon University Memorial Critical Care and Emergency Center, Tokyo, Japan.
Acta Neurochir Suppl (Wien). 1994;60:541-3. doi: 10.1007/978-3-7091-9334-1_149.
Cerebral hypothermia treatment of critical brain injury patients was studied based on the management and control of cerebral thermo-pooling, synaptic excitation, hypermetabolic demand, and the systemic critical condition of the metabolic reserve. The initial pathophysiological changes after trauma included a progressive increase in brain tissue temperature. Such cerebral thermo-pooling, which reached a maximum of 43.8 degrees C, can change or damage the vascular proteins directly. The brain tissue temperature was influenced by four factors: 1. the cerebral metabolism, 2. the systemic excess energy metabolism, 3. the CPP that carries the systemic energy to the brain tissue, and 4. the cerebral blood flow that leads to washout of brain tissue temperature. Mild cerebral hypothermia (32-33 degrees C) managed by the whole body compartment cooling technique in the critical conditions of diffuse brain injury patients (GCS < 4) produced a good recovery in 8 of 10 patients. Continuous monitoring of the jugular venous oxygen saturation and BTT/TMT was effective for evaluating cerebral ischemia and oxygen metabolic disturbances even during cerebral hypothermia treatment.
基于对脑热池、突触兴奋、高代谢需求以及代谢储备的全身危急状况的管理和控制，对重症脑损伤患者进行了亚低温治疗研究。创伤后的初始病理生理变化包括脑组织温度的逐渐升高。这种脑热池最高可达43.8摄氏度，可直接改变或损伤血管蛋白。脑组织温度受四个因素影响：1. 脑代谢；2. 全身能量代谢过剩；3. 将全身能量输送到脑组织的脑灌注压；4. 导致脑组织温度消散的脑血流量。在弥漫性脑损伤患者（格拉斯哥昏迷评分<4）的危急情况下，采用全身腔室降温技术进行轻度亚低温治疗（32 - 33摄氏度），10例患者中有8例恢复良好。即使在亚低温治疗期间，持续监测颈静脉血氧饱和度和脑温/体温也有助于评估脑缺血和氧代谢紊乱。
