Lavinio A, Timofeev I, Nortje J, Outtrim J, Smielewski P, Gupta A, Hutchinson P J, Matta B F, Pickard J D, Menon D, Czosnyka M
Department of Clinical Neurosciences, Academic Neurosurgical Unit, Addenbrooke's Hospital, Cambridge, UK.
Br J Anaesth. 2007 Aug;99(2):237-44. doi: 10.1093/bja/aem118. Epub 2007 May 16.
Experimental evidence from a murine model of traumatic brain injury (TBI) suggests that hypothermia followed by fast rewarming may damage cerebral microcirculation. The effects of hypothermia and subsequent rewarming on cerebral vasoreactivity in human TBI are unknown.
This is a retrospective analysis of data acquired during a prospective, observational neuromonitoring and imaging data collection project. Brain temperature, intracranial pressure (ICP), and cerebrovascular pressure reactivity index (PRx) were continuously monitored.
Twenty-four TBI patients with refractory intracranial hypertension were cooled from 36.0 (0.9) to 34.2 (0.5) degrees C [mean (sd), P < 0.0001] in 3.9 (3.7) h. Induction of hypothermia [average duration 40 (45) h] significantly reduced ICP from 23.1 (3.6) to 18.3 (4.8) mm Hg (P < 0.05). Hypothermia did not impair cerebral vasoreactivity as average PRx changed non-significantly from 0.00 (0.21) to -0.01 (0.21). Slow rewarming up to 37.0 degrees C [rate of rewarming, 0.2 (0.2) degrees C h(-1)] did not increase ICP [18.6 (6.2) mm Hg] or PRx [0.06 (0.18)]. However, in 17 (70.1%) out of 24 patients, rewarming exceeded the brain temperature threshold of 37 degrees C. In these patients, the average brain temperature was allowed to increase to 37.8 (0.3) degrees C (P < 0.0001), ICP remained stable at 18.3 (8.0) mm Hg (P = 0.74), but average PRx increased to 0.32 (0.24) (P < 0.0001), indicating significant derangement in cerebrovascular reactivity. After rewarming, PRx correlated independently with brain temperature (R = 0.53; P < 0.05) and brain tissue O2 (R = 0.66; P < 0.01).
After moderate hypothermia, rewarming exceeding the 37 degrees C threshold is associated with a significant increase in average PRx, indicating temperature-dependent hyperaemic derangement of cerebrovascular reactivity.
创伤性脑损伤（TBI）小鼠模型的实验证据表明，低温后快速复温可能损害脑微循环。低温及随后的复温对人类TBI脑血管反应性的影响尚不清楚。
这是一项对前瞻性观察性神经监测和成像数据收集项目中获取的数据进行的回顾性分析。持续监测脑温、颅内压（ICP）和脑血管压力反应指数（PRx）。
24例难治性颅内高压的TBI患者在3.9（3.7）小时内从36.0（0.9）℃冷却至34.2（0.5）℃[平均值（标准差），P<0.0001]。低温诱导[平均持续时间40（45）小时]使ICP从23.1（3.6）显著降至18.3（4.8）mmHg（P<0.05）。低温并未损害脑血管反应性。因为平均PRx从0.00（0.21）至-0.01（0.21）无显著变化。缓慢复温至37.0℃[复温速率，0.2（约0.2）℃·h⁻¹]并未增加ICP[18.6（6.2）mmHg]或PRx[0.06（0.18）]。然而，24例患者中有17例（70.1%）复温超过了37℃的脑温阈值。在这些患者中，平均脑温升至37.8（0.3）℃（P<0.0001），ICP保持稳定在18.3（8.0）mmHg（P=0.74），但平均PRx升至0.32（0.24）（P<0.0001），表明脑血管反应性显著紊乱。复温后，PRx与脑温（R=0.53；P<0.05）和脑组织氧（R=0.66；P<0.01）独立相关。
中度低温后，复温超过37℃阈值与平均PRx显著增加相关，表明脑血管反应性存在温度依赖性充血紊乱。
