Flynn Liam M C, Rhodes Jonathan, Andrews Peter J D
1 Center for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kindgom.
2 Department of Anesthesia and Critical Care, University of Edinburgh and NHS Lothian , Western General Hospital, Edinburgh, United Kingdom .
Ther Hypothermia Temp Manag. 2015 Sep;5(3):143-51. doi: 10.1089/ther.2015.0002. Epub 2015 May 19.
Traumatic brain injury (TBI) is a significant cause of disability and death and a huge economic burden throughout the world. Much of the morbidity associated with TBI is attributed to secondary brain injuries resulting in hypoxia and ischemia after the initial trauma. Intracranial hypertension and decreased partial brain oxygen tension (PbtO2) are targeted as potentially avoidable causes of morbidity. Therapeutic hypothermia (TH) may be an effective intervention to reduce intracranial pressure (ICP), but could also affect cerebral blood flow (CBF). This is a retrospective analysis of prospectively collected data from 17 patients admitted to the Western General Hospital, Edinburgh. Patients with an ICP >20 mmHg refractory to initial therapy were randomized to standard care or standard care and TH (intervention group) titrated between 32°C and 35°C to reduce ICP. ICP and PbtO2 were measured using the Licox system and core temperature was recorded through rectal thermometer. Data were analyzed at the hour before cooling, the first hour at target temperature, 2 consecutive hours at target temperature, and after 6 hours of hypothermia. There was a mean decrease in ICP of 4.3±1.6 mmHg (p<0.04) from 15.7 to 11.4 mmHg, from precooling to the first epoch of hypothermia in the intervention group (n=9) that was not seen in the control group (n=8). A decrease in ICP was maintained throughout all time periods. There was a mean decrease in PbtO2 of 7.8±3.1 mmHg (p<0.05) from 30.2 to 22.4 mmHg, from precooling to stable hypothermia, which was not seen in the control group. This research supports others in demonstrating a decrease in ICP with temperature, which could facilitate a reduction in the use of hyperosmolar agents or other stage II interventions. The decrease in PbtO2 is not below the suggested treatment threshold of 20 mmHg, but might indicate a decrease in CBF.
创伤性脑损伤（TBI）是导致全球残疾和死亡的重要原因，也是一项巨大的经济负担。与TBI相关的许多发病率归因于初始创伤后导致缺氧和缺血的继发性脑损伤。颅内高压和局部脑氧分压（PbtO2）降低被视为可能避免的发病原因。治疗性低温（TH）可能是降低颅内压（ICP）的有效干预措施，但也可能影响脑血流量（CBF）。这是一项对爱丁堡西部总医院收治的17例患者的前瞻性收集数据进行的回顾性分析。初始治疗难治的ICP>20 mmHg的患者被随机分为标准治疗组或标准治疗加TH组（干预组），将温度滴定至32°C至35°C以降低ICP。使用Licox系统测量ICP和PbtO2，并通过直肠温度计记录核心温度。在降温前1小时、目标温度下的第1小时、目标温度下连续2小时以及低温6小时后对数据进行分析。干预组（n = 9）从预冷到低温的第一个阶段，ICP平均下降4.3±1.6 mmHg（p<0.04），从15.7 mmHg降至11.4 mmHg，而对照组（n = 8）未观察到这种情况。在所有时间段内ICP均保持下降。从预冷到稳定低温，干预组PbtO2平均下降7.8±3.1 mmHg（p<0.05），从30.2 mmHg降至22.4 mmHg，对照组未观察到这种情况。这项研究与其他研究结果一致，表明随着温度降低ICP下降，这可能有助于减少高渗药物或其他II期干预措施的使用。PbtO2的下降未低于建议的20 mmHg治疗阈值，但可能表明CBF减少。
