Petitjeans F, Leroy S, Pichot C, Geloen A, Ghignone M, Quintin L
Critical Care, Hôpital d'Instruction des Armées Desgenettes, Lyon, France.
Pediatric Emergency Medicine, Hôpital Avicenne, Paris-Bobigny, France.
Temperature (Austin). 2018 May 22;5(3):224-256. doi: 10.1080/23328940.2018.1453771. eCollection 2018.
During severe septic shock and/or severe acute respiratory distress syndrome (ARDS) patients present with a limited cardio-ventilatory reserve (low cardiac output and blood pressure, low mixed venous saturation, increased lactate, low PaO2/FiO2 ratio, etc.), especially when elderly patients or co-morbidities are considered. Rescue therapies (low dose steroids, adding vasopressin to noradrenaline, proning, almitrine, NO, extracorporeal membrane oxygenation, etc.) are complex. Fever, above 38.5-39.5°C, increases both the ventilatory (high respiratory drive: large tidal volume, high respiratory rate) and the metabolic (increased O2 consumption) demands, further limiting the cardio-ventilatory reserve. Some data (case reports, uncontrolled trial, small randomized prospective trials) suggest that control of elevated body temperature ("fever control") leading to normothermia (35.5-37°C) will lower both the ventilatory and metabolic demands: fever control should simplify critical care management when limited cardio-ventilatory reserve is at stake. Usually fever control is generated by a combination of general anesthesia ("analgo-sedation", light total intravenous anesthesia), antipyretics and cooling. However general anesthesia suppresses spontaneous ventilation, making the management more complex. At variance, alpha-2 agonists (clonidine, dexmedetomidine) administered immediately following tracheal intubation and controlled mandatory ventilation, with prior optimization of volemia and atrio-ventricular conduction, will reduce metabolic demand and facilitate normothermia. Furthermore, after a rigorous control of systemic acidosis, alpha-2 agonists will allow for accelerated emergence without delirium, early spontaneous ventilation, improved cardiac output and micro-circulation, lowered vasopressor requirements and inflammation. Rigorous prospective randomized trials are needed in subsets of patients with a high fever and spiraling toward refractory septic shock and/or presenting with severe ARDS.
在严重脓毒性休克和/或严重急性呼吸窘迫综合征(ARDS)期间,患者存在有限的心-肺储备(低心输出量和血压、低混合静脉血氧饱和度、乳酸增加、低动脉血氧分压/吸入氧分数值等),尤其是考虑到老年患者或合并症时。挽救治疗(低剂量类固醇、在去甲肾上腺素中添加血管加压素、俯卧位通气、烯丙哌三嗪、一氧化氮、体外膜肺氧合等)很复杂。体温高于38.5 - 39.5°C时,会增加通气需求(高呼吸驱动力:大潮气量、高呼吸频率)和代谢需求(氧消耗增加),进一步限制心-肺储备。一些数据(病例报告、非对照试验、小型随机前瞻性试验)表明,将体温控制在正常范围(35.5 - 37°C)可降低通气和代谢需求:当有限的心-肺储备受到威胁时,控制发热应能简化重症监护管理。通常通过全身麻醉(“镇痛镇静”、浅全静脉麻醉)、退烧药和降温联合来控制发热。然而,全身麻醉会抑制自主通气,使管理更加复杂。与之不同的是,在气管插管和控制强制通气后立即给予α-2激动剂(可乐定、右美托咪定),并预先优化血容量和房室传导,可降低代谢需求并促进体温正常化。此外,在严格控制全身酸中毒后,α-2激动剂可加速苏醒且无谵妄、早期自主通气、改善心输出量和微循环、降低血管升压药需求并减轻炎症。对于高热且病情逐渐发展为难治性脓毒性休克和/或患有严重ARDS的患者亚组,需要进行严格的前瞻性随机试验。