Doyle Andrew J, Meyer Joel, Breen Karen, Hunt Beverley J
Centre for Thrombosis & Haemophilia St Thomas' Hospital London UK.
Department of Intensive Care Medicine St Thomas' Hospital London UK.
Res Pract Thromb Haemost. 2020 Jun 14;4(5):829-834. doi: 10.1002/rth2.12360. eCollection 2020 Jul.
Coagulation changes, thrombosis, and hemorrhage have been described in patients following N-methyl-3,4-methylenedioxymethylamphetamine (MDMA) intoxication who subsequently developed serotonin syndrome and rhabdomyolysis. The clinical features and mechanism of this remain poorly described. We describe 5 sequential cases admitted to critical care due to severe recreational MDMA toxicity where coagulopathy occurred, and discuss key clinical issues. All patients presented with hyperpyrexia then developed subsequent rhabdomyolysis accompanied by a coagulopathy within 24 hours of presentation. This included a severe thrombocytopenia, prolonged coagulation times, grossly elevated D-dimer levels, and hypofibrogenemia. Multiorgan dysfunction was seen in all patients, including stroke in one patient and major hemorrhage in another. In 2 cases, low-dose low-molecular-weight heparin was used early after presentation, with no significant bleeding complications. Blood products usage was high but variable between the patients with lower use in those who received low-molecular-weight heparin early. Other treatments included intravascular therapeutic cooling, renal replacement therapy with large filter pores and cyprohepatidine. Current evidence suggests that in this group, rhabdomyolysis with subsequent myosin release may be a profound activator of coagulation leading to disseminated intravascular coagulation. Myosin-activated coagulation seems a potential cause of MDMA-related coagulopathy in the setting of rhabdomyolysis and serotonin syndrome. Further studies are needed to validate this and explore the use of low-molecular-weight heparin to reduce the clinical effects of this coagulopathy.
在N-甲基-3,4-亚甲基二氧甲基苯丙胺(摇头丸)中毒后继而出现血清素综合征和横纹肌溶解的患者中,已有凝血变化、血栓形成和出血的相关描述。但其临床特征和机制仍描述甚少。我们描述了5例因严重摇头丸中毒而入住重症监护病房并发生凝血病的连续病例,并讨论了关键的临床问题。所有患者均先出现高热,随后在就诊后24小时内出现横纹肌溶解并伴有凝血病。这包括严重血小板减少、凝血时间延长、D-二聚体水平显著升高和纤维蛋白原血症。所有患者均出现多器官功能障碍,其中1例患者发生中风,另1例患者发生大出血。2例患者在就诊后早期使用了低剂量低分子肝素,未出现明显出血并发症。血液制品的使用量很大,但患者之间存在差异,早期接受低分子肝素治疗的患者使用量较低。其他治疗包括血管内治疗性降温、使用大滤过孔径的肾脏替代疗法和赛庚啶。目前的证据表明,在这组患者中,横纹肌溶解及随后的肌球蛋白释放可能是凝血的一个重要激活因素,导致弥散性血管内凝血。肌球蛋白激活的凝血似乎是横纹肌溶解和血清素综合征背景下摇头丸相关凝血病的一个潜在原因。需要进一步研究来验证这一点,并探索使用低分子肝素以减轻这种凝血病的临床影响。