Fu Mingjie, Zhao Jie, Li Zhitao, Zhao He, Lu Anwei
Department of Surgical Intensive Care Unit, First Affiliated Hospital, College of Medicine, Zhejiang University.
Department of Anesthesiology, Hangzhou Red Cross Hospital, Hangzhou, Zhejiang Province, P.R. China.
Medicine (Baltimore). 2019 Jul;98(30):e16580. doi: 10.1097/MD.0000000000016580.
Colchicine can inhibit cell division and intracellular transport in affected organs by fixing intracellular tubulin and preventing its polymerization into microtubules. A lethal dose of colchicine is considered to be 0.8 mg/kg. The wide distribution of colchicine through 70% of the body following an overdose makes it difficult to eliminate.
A 56-year-old man with a clear history of colchicine overdose was admitted to our hospital nearly 40 hours after taking 12 mg (0.17 mg/kg) of colchicine. He had a history of gout and chronic kidney disease. As the disease progressed, he showed most of the clinical manifestations and pathological features of colchicine overdose.
Colchicine overdose was clear, with symptoms of multiple organ failure including primary gastrointestinal failure, bone marrow hematopoietic inhibition, rhabdomyolysis, cardiac damage, hepatocyte damage. The patient developed secondary septic shock, renal failure, circulatory failure, and respiratory failure. We performed continuous renal replacement therapy and gastric lavage, and administered norepinephrine, frozen plasma, proton-pump inhibitors, adenosylmethionine, antibiotics, granulocyte colony stimulating factor, and total parenteral nutrition.
The patient rapidly developed complete hematopoietic function inhibition, gastrointestinal failure, and cardiac damage 32 hours after admission. Sustained severe infection and circulatory instability caused a progressive deterioration of respiratory function. Tracheal intubation was performed but the patient continued to deteriorate, and death occurred approximately 132 hours after admission.
Excessive colchicine levels cause continuous organ damage due to extensive tissue distribution, eventually leading to multiple organ failure. Colchicine metabolism is delayed in patients with liver or kidney dysfunction, and even a low dose of colchicine may result in poisoning in these individuals. Early diagnosis and reduction of colchicine levels is critical to improve prognosis, and colchicine poisoning should be considered in patients with poor liver or kidney function even when the ingested dose is low.
秋水仙碱可通过固定细胞内微管蛋白并阻止其聚合成微管,从而抑制受影响器官中的细胞分裂和细胞内运输。秋水仙碱的致死剂量被认为是0.8毫克/千克。过量服用后,秋水仙碱在全身70%的组织中广泛分布,难以清除。
一名56岁男性,有明确的秋水仙碱过量服用史,在服用12毫克(0.17毫克/千克)秋水仙碱近40小时后入院。他有痛风和慢性肾脏病病史。随着病情进展,他出现了秋水仙碱过量的大多数临床表现和病理特征。
秋水仙碱过量明确,出现多器官功能衰竭症状,包括原发性胃肠功能衰竭、骨髓造血抑制、横纹肌溶解、心脏损害、肝细胞损害。患者继发感染性休克、肾衰竭、循环衰竭和呼吸衰竭。我们进行了持续肾脏替代治疗和洗胃,并给予去甲肾上腺素、冰冻血浆、质子泵抑制剂、腺苷蛋氨酸、抗生素、粒细胞集落刺激因子和全胃肠外营养。
患者入院32小时后迅速出现完全造血功能抑制、胃肠功能衰竭和心脏损害。持续的严重感染和循环不稳定导致呼吸功能逐渐恶化。进行了气管插管,但患者仍持续恶化,入院后约132小时死亡。
秋水仙碱水平过高会因广泛的组织分布导致持续的器官损害,最终导致多器官功能衰竭。肝或肾功能不全患者秋水仙碱代谢延迟,即使低剂量秋水仙碱也可能导致这些个体中毒。早期诊断和降低秋水仙碱水平对改善预后至关重要,即使摄入剂量低,肝或肾功能差的患者也应考虑秋水仙碱中毒。