Harvard Medical Toxicology Program, Boston Children's Hospital, Boston, MA, USA.
Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Clin Toxicol (Phila). 2022 Jul;60(7):876-881. doi: 10.1080/15563650.2022.2042012. Epub 2022 Mar 4.
Thiocyanate can cause gastrointestinal, neurologic, and cardiovascular toxicity. Additionally, it interferes with multiple laboratory assays. We present a case of acute thiocyanate toxicity. A 17-year-old female presented with an intentional thiocyanate ingestion. Her course was notable for delirium, wide complex tachycardia, and presumed seizure activity with concurrent lactatemia, acidemia, and narrowing of her arterio-venous oxygen gradient. She received lipid emulsion therapy (LET). While hemodialysis was considered, she recovered without additional treatment. After resolution of her critical illness, a serum cyanide concentration was 0.21 mcg/mL. She had laboratory testing notable for hyperchloremia, hypocalcemia, hypokalemia, and an elevated salicylate concentration attributed to interference by thiocyanate. The thiocyanate was eliminated via first-order kinetics with a half-life of 61.6 hours. Thiocyanate poisoning may cause cardiac and neurologic toxicity. Laboratory evidence of impaired cellular respiration in this case suggests possible in vivo conversion to cyanide, however this is not proven. Cyanide antidotal treatment was not administered for this patient, however LET was given based on thiocyanate's lipophilicity. Hemodialysis is known to effectively remove thiocyanate from the blood, however the patient improved without it. The patient's laboratory derangements were due to thiocyanate interference with ion selective electrode and colorimetric analyzer technology. Thiocyanate can cause cardiac and neurologic toxicity, and interferes with several laboratory assays. Theoretically, LET and cyanide antidotal treatment may be useful, but this requires further investigation. Thiocyanate toxicity should be managed supportively, and hemodialysis may be used in severe cases.
氰化物可引起胃肠道、神经和心血管毒性。此外，它还会干扰多种实验室检测。我们报告了一例急性氰化物中毒。一名 17 岁女性因故意摄入氰化物而就诊。她的病程中出现谵妄、宽复合性心动过速，以及伴发乳酸性酸中毒、酸中毒和动静脉血氧梯度变窄的疑似癫痫发作。她接受了脂肪乳剂治疗（LET）。虽然考虑了血液透析，但她在没有其他治疗的情况下康复。在危急病况缓解后，血清氰化物浓度为 0.21 mcg/mL。她的实验室检测结果显著表现为高氯血症、低钙血症、低钾血症和水杨酸盐浓度升高，这归因于氰化物的干扰。氰化物通过一级动力学消除，半衰期为 61.6 小时。氰化物中毒可能导致心脏和神经毒性。该病例中细胞呼吸受损的实验室证据表明，体内可能转化为氰化物，但这尚未得到证实。未给予该患者氰化物解毒治疗，但鉴于氰化物的亲脂性，给予了 LET。已知血液透析可有效从血液中清除氰化物，但该患者未接受透析治疗即得到改善。患者的实验室异常是由于氰化物干扰离子选择性电极和比色分析器技术所致。氰化物可引起心脏和神经毒性，并干扰多种实验室检测。理论上，LET 和氰化物解毒治疗可能有用，但这需要进一步研究。氰化物中毒应支持性治疗，在严重情况下可使用血液透析。
