Liu Yan-Cun, Zhou Zi-Kang, Yu Mu-Ming, Wang Li-Jun, Shou Song-Tao, Chai Yan-Fen
Department of Emergency Medicine, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Heliyon. 2024 Jun 4;10(11):e32407. doi: 10.1016/j.heliyon.2024.e32407. eCollection 2024 Jun 15.
Colchicine is a common therapeutic agent for inflammatory conditions such as gout, yet its narrow therapeutic range frequently results in cases of overdose and subsequent poisoning. Acute colchicine poisoning can be difficult to identify due to its nonspecific clinical manifestations, posing a diagnostic challenge for emergency physicians without a clear history of colchicine ingestion.
This report describes a tragic case of acute colchicine poisoning that resulted in three familial homicides. The patients presented with fever, abdominal pain, and diarrhea, which rapidly escalated to shock during their emergency department visits. Laboratory tests revealed a marked leukocytosis, mild elevation in procalcitonin (PCT), significantly elevated creatine kinase (CK) and CK-MB levels, and liver function abnormalities. Despite treatment with carbapenem antibiotics and aggressive fluid resuscitation, the patients' condition deteriorated, marked by a progressive decline in leukocytes and neutrophils. Initially misdiagnosed as septic shock, the ineffectiveness of the standard treatment protocols led to a fatal outcome for all three individuals.
Emergency physicians should consider acute colchicine poisoning as a differential diagnosis in patients presenting with shock and the following clinical indicators: (1) pronounced increase in peripheral leukocytes with a disproportionate rise in neutrophils; (2) discordance between the level of serum procalcitonin and the severity of presumed septic shock; (3) early increase in serum creatine kinase (CK) and CK-MB; (4) poor response to antibiotics and resuscitative efforts, accompanied by a continuous decrease in white blood cells and neutrophils. This case underscores the critical need for awareness of colchicine toxicity in the emergency setting, particularly when the clinical presentation mimics septic shock but fails to respond to standard treatments.
秋水仙碱是治疗痛风等炎症性疾病的常用药物,但其治疗窗狭窄,常导致过量用药及随后的中毒病例。急性秋水仙碱中毒因其临床表现不具特异性而难以识别,给无明确秋水仙碱摄入史的急诊科医生带来诊断挑战。
本报告描述了一例导致三起家庭凶杀案的急性秋水仙碱中毒悲剧病例。患者就诊时出现发热、腹痛和腹泻,在急诊科就诊期间迅速发展为休克。实验室检查显示白细胞显著增多、降钙素原(PCT)轻度升高、肌酸激酶(CK)和CK-MB水平显著升高以及肝功能异常。尽管使用了碳青霉烯类抗生素治疗并积极进行液体复苏,但患者病情仍恶化,表现为白细胞和中性粒细胞逐渐减少。最初被误诊为感染性休克,标准治疗方案无效导致三人全部死亡。
对于出现休克且有以下临床指标的患者,急诊科医生应考虑急性秋水仙碱中毒作为鉴别诊断:(1)外周白细胞显著增加且中性粒细胞不成比例升高;(2)血清降钙素原水平与假定的感染性休克严重程度不一致;(3)血清肌酸激酶(CK)和CK-MB早期升高;(4)对抗生素和复苏措施反应不佳,同时白细胞和中性粒细胞持续减少。本病例强调了在急诊环境中认识秋水仙碱毒性的迫切需要,特别是当临床表现类似感染性休克但对标准治疗无反应时。