Propylene glycol toxicity following continuous etomidate infusion for the control of refractory cerebral edema.
Propylene glycol toxicity following continuous etomidate infusion for the control of refractory cerebral edema.
复制标题
连续输注依托咪酯控制难治性脑水肿后丙二醇的毒性。
作者：
Michael J. Levy;Margaret Aranda;V. Zelman;S. Giannotta
在创伤性或缺血性损害后，颅内压持续升高，已知会导致发病率和死亡率显著增加。由于巴比妥类药物的副作用包括低血压和延长恢复时间，已考虑使用短效麻醉剂来控制颅内压。依托咪酯持续输注可降低脑代谢，导致脑血流量继发减少，而脑灌流压变化不大。我们最初打算将20名患者随机分为一项研究方案，评估戊巴比妥或心脏保护剂依托咪酯对颅内压和心脏功能的影响。考虑到治疗的后遗症，我们只能随机选择7名内科治疗无效的脑水肿患者，接受依托咪酯或戊巴比妥的盲法治疗。接受依托咪酯治疗的3名患者出现肾损害(平均肌酐清除量低41毫升/分钟，范围37-44毫升/分钟)，最初出现在24小时。我们认为这是一种不良反应，可能与研究药物有关，研究停止了。每例患者静脉注射依托咪酯0.30 mg/kg诱导，然后0.02 mg/kg/min持续输注24-72小时。所有患者还接受地塞米松2 mg静脉注射，每6小时一次，以防止因依托咪酯抑制皮质醇合成而可能发生的肾上腺皮质功能不全。使用依托咪酯后，颅内压下降(平均为12毫米汞)。心脏参数保持不变(心输出量4.8±0.6升/分钟)。(摘要截断250字)
Continued elevations in Intracranial Pressure (ICP) following traumatic or ischemic compromise are known to cause markedly increased morbidity and mortality. Because of the side effects of barbiturates including hypotension and prolonged recovery time, the use of shorter-acting anesthetic agents to control ICP has been considered. Etomidate, when administered by continuous infusion, has been shown to decrease cerebral metabolism resulting in a secondary decrease in cerebral blood flow with minimal changes in cerebral perfusion pressure. We initially intended to randomize 20 patients prospectively into a study protocol that would assess the effects of either pentobarbital or the cardioprotective agent etomidate on ICP and cardiac performance. Given the sequelae of the therapy, we were only able to randomize seven patients with cerebral edema refractory to medical management to receive either etomidate or pentobarbital in a blinded fashion. Three patients who received etomidate developed renal compromise (mean low creatinine clearance 41 ml/min, range 37-44 ml/min) which was initially noted at 24 hours. We believed that this represented an adverse effect that was probably related to the study drug and the study was stopped. Each patient received a 0.30 mg/kg IV induction of etomidate and then 0.02 mg/kg/min continuous infusion for 24-72 hours titrated burst suppression. All patients also received dexamethasone 2 mg IV every six hours to prevent the adrenocortical insufficiency that might occur as a consequence of etomidate-induced suppression of cortisol synthesis. Intracranial pressure decreased (mean = 12mmHg) following the initiation of etomidate. Cardiac parameters remained unchanged (cardiac output 4.8 +/- .6 liters/min).(ABSTRACT TRUNCATED AT 250 WORDS)