Annen Eva, Girard Thierry, Urwyler Albert
Department of Anesthesia and Intensive Care Medicine, University Hospital Basel, Switzerland.
Clin Pract. 2012 Sep 3;2(3):e79. doi: 10.4081/cp.2012.e79. eCollection 2012 May 29.
We present the case of a 7-year old boy with traumatic brain injury who received propofol during 38 h. Thirty-six hours after cessation of propofol infusion asystole occurred. After immediate mechanical and medical resuscitation, unreactive dilated pupils were observed. The following computed tomography scan revealed a generalized brain edema with transtentorial herniation. Prolonged bradyarrhythmia, rhabdomyolysis, and peracute renal failure were observed. Despite immediate craniectomy, barbiturate treatment, hemofiltration, and recovery of appropriate cardiac function, the patient died four days after discontinuation of propofol. In this case, metabolic acidosis, cardiac failure, rhabdomyolysis, and renal failure are in accordance with the symptoms of propofol infusion syndrome (PRIS), while seizure, brain edema, and transtentorial herniation could be caused by traumatic brain injury. However, it may be assumed that the entire clinical picture was caused by PRIS. This view could be explained by a common loss of function of ryanodine receptors in patients presenting with PRIS.
我们报告一例7岁创伤性脑损伤男孩，其在38小时内接受了丙泊酚治疗。丙泊酚输注停止36小时后发生心搏停止。立即进行机械和药物复苏后，观察到瞳孔散大且无反应。随后的计算机断层扫描显示广泛性脑水肿伴小脑幕切迹疝。观察到持续性缓慢性心律失常、横纹肌溶解和急性肾衰竭。尽管立即进行了颅骨切除术、巴比妥类药物治疗、血液滤过并恢复了适当的心功能，但患者在丙泊酚停用四天后死亡。在本病例中，代谢性酸中毒、心力衰竭、横纹肌溶解和肾衰竭符合丙泊酚输注综合征（PRIS）的症状，而癫痫发作、脑水肿和小脑幕切迹疝可能由创伤性脑损伤引起。然而，可以推测整个临床情况是由PRIS所致。这一观点可以通过PRIS患者中兰尼碱受体的共同功能丧失来解释。
