Department of Anesthesiology and Reanimation, University of Health Sciences, Derince Training and Research Hospital, Kocaeli, Turkey; Formerly: Department of Anesthesiology and Reanimation, Kocaeli State Hospital, Kocaeli, Turkey.
Department of Anesthesiology and Reanimation, Hitit University, Erol Olcok Training and Research Hospital, Corum, Turkey.
Neurocirugia (Astur : Engl Ed). 2020 Sep-Oct;31(5):216-222. doi: 10.1016/j.neucir.2019.12.003. Epub 2020 Mar 4.
To evaluate the incidence of severe potassium disturbances during barbiturate coma therapy in patients with severe traumatic brain injury (TBI), and the characteristics of these patients.
The study comprised 37 patients with severe TBI who were treated for barbiturate coma between 2015 and 2017 in level 3 intensive care units of two hospitals.
No potassium disturbance occurred in 14 patients. Seventeen patients developed mild-moderate hypokalemia (2.6-3.5mEq/L), and 6 patients developed severe hypokalemia (<2.5mEq/L) following the induction of barbiturate therapy. The incidence of mild-to-severe barbiturate-induced hypokalemia was 62.2% and the rate of severe hypokalemia was 16.2%. The mean potassium supply per day during thiopentone therapy was statistically significantly different between patients with mild-to-moderate hypokalemic and those with severe hypokalemic (p<0.001). Four of 6 patients with severe hypokalemia developed rebound hyperkalemia exceeding 6mEq/L following the cessation of barbiturate infusion. The nadir potassium concentration was 1.5mEq/L and the highest value was 6.8mEq/L. The mean time to reach nadir potassium concentrations was 2.8 days. The mortality rate of the 6 patients was 66.7%. Of the 2 survivors of severe hypokalemia, the Glasgow Outcome Scale (GOS) on discharge and the extended GOS one year after the trauma were 5 and 8 respectively.
Severe hypokalemia refractory to medical treatment and rebound hyperkalemia is a serious adverse effect of thiopentone coma therapy in patients with severe TBI. Excessive and aggressive potassium replacement during the barbiturate-induced hypokalemia period must be avoided. Weaning barbiturate treatment over time may be advantageous in the management of severe serum potassium disturbances.
评估严重颅脑损伤（TBI）患者行巴比妥类药物昏迷治疗期间严重钾紊乱的发生率，并分析这些患者的特点。
本研究纳入了 2015 年至 2017 年期间在 2 家医院的 3 级重症监护病房接受巴比妥类药物昏迷治疗的 37 例严重 TBI 患者。
14 例患者未发生钾紊乱。17 例患者出现轻-中度低钾血症（2.6-3.5mEq/L），6 例患者在诱导行巴比妥类药物治疗后发生严重低钾血症（<2.5mEq/L）。轻-重度巴比妥类药物诱导性低钾血症的发生率为 62.2%，严重低钾血症的发生率为 16.2%。戊巴比妥治疗期间，每天钾的供给量在轻-中度低钾血症患者与重度低钾血症患者之间有显著统计学差异（p<0.001）。6 例重度低钾血症患者中有 4 例在停止输注巴比妥类药物后出现钾浓度超过 6mEq/L 的反弹性高钾血症。最低血钾浓度为 1.5mEq/L，最高值为 6.8mEq/L。达到最低血钾浓度的平均时间为 2.8 天。6 例患者的死亡率为 66.7%。2 例重度低钾血症幸存者，出院时格拉斯哥预后评分（GOS）和创伤后 1 年扩展 GOS 分别为 5 分和 8 分。
严重 TBI 患者行戊巴比妥昏迷治疗时，严重低钾血症且对治疗抵抗、出现反弹性高钾血症是一种严重的不良反应。在巴比妥类药物诱导性低钾血症期间，应避免过度和激进的补钾。随着时间的推移逐渐减少巴比妥类药物治疗可能有利于严重血清钾紊乱的管理。
