Department of Neuroscience, Section of Neurosurgery.
Department of Surgical Sciences/Anesthesia and Intensive Care, Uppsala University, Uppsala, Sweden.
J Neurosurg Anesthesiol. 2021 Oct 1;33(4):329-336. doi: 10.1097/ANA.0000000000000695.
Systemic hyperthermia is common after traumatic brain injury (TBI) and may induce secondary brain injury, although the pathophysiology is not fully understood. In this study, our aim was to determine the incidence and temporal course of hyperthermia after TBI and its relation to intracranial pressure dynamics, cerebral metabolism, and clinical outcomes.
This retrospective study included 115 TBI patients. Data from systemic physiology (body temperature, blood pressure, and arterial glucose), intracranial pressure dynamics (intracranial pressure, cerebral perfusion pressure, compliance, and pressure reactivity), and cerebral microdialysis (glucose, pyruvate, lactate, glycerol, glutamate, and urea) were analyzed during the first 10 days after injury.
Overall, 6% of patients did not have hyperthermia (T>38°C) during the first 10 days after injury, whereas 20% had hyperthermia for >50% of the time. Hyperthermia increased from 21% (±27%) of monitoring time on day 1 to 36% (±29%) on days 6 to 10 after injury. In univariate analyses, higher body temperature was not associated with higher intracranial pressure nor lower cerebral perfusion pressure, but was associated with lower cerebral glucose concentration (P=0.001) and higher percentage of lactate-pyruvate ratio>25 (P=0.02) on days 6 to 10 after injury. Higher body temperature and lower arterial glucose concentration were associated with lower cerebral glucose in a multiple linear regression analysis (P=0.02 for both). There was no association between hyperthermia and worse clinical outcomes.
Hyperthermia was most common between days 6 and 10 following TBI, and associated with disturbances in cerebral energy metabolism but not worse clinical outcome.
创伤性脑损伤（TBI）后常发生全身性发热，可能引发继发性脑损伤，但发病机制尚不完全清楚。本研究旨在确定 TBI 后发热的发生率和时间进程及其与颅内压动力学、脑代谢和临床结局的关系。
这是一项回顾性研究，共纳入 115 例 TBI 患者。分析伤后第 1 天至第 10 天期间全身生理学（体温、血压和动脉血糖）、颅内压动力学（颅内压、脑灌注压、顺应性和压力反应性）和脑微透析（葡萄糖、丙酮酸、乳酸、甘油、谷氨酸和尿素）的数据。
总体而言，伤后第 10 天内，6%的患者无发热（T>38°C），20%的患者发热>50%的时间。伤后第 1 天发热率为 21%（±27%），第 6 天至第 10 天增加至 36%（±29%）。单因素分析显示，体温升高与颅内压升高或脑灌注压降低无关，但与伤后第 6 天至第 10 天脑葡萄糖浓度降低（P=0.001）和乳酸-丙酮酸比值>25%的比例升高（P=0.02）相关。多元线性回归分析显示，体温升高和动脉血糖浓度降低与脑葡萄糖降低相关（两者 P 值均为 0.02）。发热与临床结局恶化无相关性。
TBI 后发热最常见于伤后第 6 天至第 10 天，与脑能量代谢紊乱相关，但与临床结局恶化无关。
