Department of Emergency Medicine, Monash Health , Melbourne , Australia.
Clin Toxicol (Phila). 2014 Jan;52(1):63-5. doi: 10.3109/15563650.2013.870343. Epub 2013 Dec 24.
Methylene blue inhibits the nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway, decreasing vasodilation and increasing responsiveness to vasopressors. It is reported to improve haemodynamics in distributive shock from various causes including septicaemia and post-cardiac surgery. Reports of use in overdose are limited. We describe the use of methylene blue to treat a case of refractory distributive shock following a mixed drug poisoning.
A 41-year-old male presented following reported ingestion of 18 g extended-release quetiapine, 10 g controlled-release carbamazepine, 240 mg fluoxetine, 35 g enteric-coated sodium valproate and 375 mg oxazepam. He was comatose and intubated on presentation. Progressive hypotension developed. Echocardiogram revealed a hyperdynamic left ventricle, suggesting distributive shock. The patient remained hypotensive despite intravenous fluid boluses, escalating vasopressor infusions. Arterial blood gas revealed metabolic acidaemia and high lactate. Methylene blue was administered as loading-dose of 1.5 mg/kg and continuous infusion (1.5 mg/kg/h for 12 h, then 0.75 mg/kg/h for 12 h) resulting in rapid improvement in haemodynamic parameters and weaning of vasopressors. Serum quetiapine concentration was 18600 ng/mL (30-160 ng/mL), collected at the time of peak toxicity.
Severe quetiapine poisoning produces hypotension primarily from alpha-adrenoreceptor antagonism. Methylene blue may have utility in the treatment of distributive shock resulting from poisoning refractory to standard vasopressor therapy.
亚甲蓝抑制一氧化氮-环鸟苷酸（NO-cGMP）途径，减少血管舒张并增加对血管加压药的反应性。据报道，它可改善败血症和心脏手术后等各种原因引起的分布性休克的血流动力学。关于过量使用的报道有限。我们描述了使用亚甲蓝治疗混合药物中毒后出现的难治性分布性休克的病例。
一名 41 岁男性，据报告摄入了 18 克缓释喹硫平、10 克控释卡马西平、240 毫克氟西汀、35 克肠溶性丙戊酸钠和 375 毫克奥沙西泮。他入院时昏迷并插管。逐渐出现低血压。超声心动图显示左心室高动力，提示分布性休克。尽管给予静脉输液和升压药输注，但患者仍持续低血压。动脉血气显示代谢性酸中毒和高乳酸血症。给予亚甲蓝负荷剂量 1.5mg/kg 和持续输注（12 小时内 1.5mg/kg/h，然后 12 小时内 0.75mg/kg/h），导致血流动力学参数迅速改善并停用升压药。在毒性高峰时采集的血清喹硫平浓度为 18600ng/mL（30-160ng/mL）。
严重的喹硫平中毒主要通过α-肾上腺素能受体拮抗作用导致低血压。对于对标准升压治疗耐药的中毒性分布性休克，亚甲蓝可能具有治疗作用。
