Emory University School of Medicine, Atlanta, Georgia; Georgia Poison Control Center, Atlanta, Georgia.
Emory University School of Medicine, Atlanta, Georgia.
J Emerg Med. 2020 Nov;59(5):e157-e162. doi: 10.1016/j.jemermed.2020.07.008. Epub 2020 Oct 1.
Cyanide (CN) toxicity commonly occurs during enclosed-space fires. Historically, the first step in treating CN toxicity utilized amyl nitrite and sodium nitrite to induce methemoglobinemia, which can be dangerous in this population. Hydroxocobalamin (OHCob), which binds to CN to form the nontoxic metabolite cyanocobalamin, is now the first-line antidote for CN toxicity, and has the advantage of not inducing methemoglobinemia.
A 62-year-old man presented to the Emergency Department (ED) after a house fire. He was intubated for respiratory distress and hypoxia with an initial carboxyhemoglobin of 1.3%, methemoglobin 0.3%, and anion gap 19. Eleven hours after presentation, his serum lactic acid was 9 mmol/L. Given his continued deterioration, 14 h after arrival he received OHCob 5 g i.v. for presumed CN toxicity. Methemoglobin concentration 4 min prior to OHCob administration was 0.7%, and 2 h after administration was 4.2%. This subsequently increased to 14.3% (16 h after OHCob administration) and peaked at 16.3% (47 h after OHCob administration), at which time he was administered a dose of methylene blue 50 mg i.v., 60 h after ED arrival. His methemoglobin concentrations fluctuated until a consistent downward trend starting at 92 h from ED arrival. He continued to deteriorate and expired on hospital day 5 with a methemoglobin concentration of approximately 6.0%. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: CN toxicity requires immediate recognition and treatment. The antidote, OHCob, is believed to not induce methemoglobinemia. However, this potential side effect must be considered by emergency physicians when treating suspected CN toxicity, especially if the patient does not improve after antidotal therapy.
氰化物（CN）中毒在封闭空间火灾中很常见。历史上，治疗 CN 毒性的第一步是使用亚硝酸戊酯和亚硝酸钠诱导高铁血红蛋白血症，这在该人群中可能很危险。羟钴胺（OHCob）可与 CN 结合形成无毒的代谢物氰钴胺，现在是 CN 毒性的一线解毒剂，并且具有不诱导高铁血红蛋白血症的优点。
一名 62 岁男性在一场房屋火灾后到急诊科就诊。他因呼吸窘迫和缺氧而被插管，初始碳氧血红蛋白为 1.3%，高铁血红蛋白 0.3%，阴离子间隙 19。就诊 11 小时后，他的血清乳酸为 9mmol/L。由于持续恶化，到达后 14 小时，他接受了 5g 静脉注射 OHCob，疑似 CN 毒性。OHCob 给药前 4 分钟的高铁血红蛋白浓度为 0.7%，给药后 2 小时为 4.2%。这随后增加到 14.3%（OHCob 给药后 16 小时），并在 47 小时达到峰值 16.3%（OHCob 给药后 47 小时），此时他接受了 50mg 静脉注射亚甲蓝剂量，在到达急诊科后 60 小时。他的高铁血红蛋白浓度波动，直到从急诊科到达后的 92 小时开始呈持续下降趋势。他继续恶化，在住院第 5 天死亡，高铁血红蛋白浓度约为 6.0%。
为什么急诊医生应该了解这一点？：CN 毒性需要立即识别和治疗。解毒剂 OHCob 被认为不会诱导高铁血红蛋白血症。然而，当治疗疑似 CN 毒性时，急诊医生必须考虑这种潜在的副作用，尤其是在解毒治疗后患者没有改善的情况下。
