Emory University School of Medicine, Atlanta, GA, USA.
Florida/USVI Poison Information Center, Jacksonville, FL, USA.
Clin Toxicol (Phila). 2022 Sep;60(9):1012-1018. doi: 10.1080/15563650.2022.2072315. Epub 2022 May 12.
Historically, the first step in treating cyanide (CN) toxicity utilized antidotes to induce methemoglobinemia. This is concerning in patients who are already hypoxemic or have elevated carboxyhemoglobin. Hydroxocobalamin (OHCbl) is now the first-line antidote for CN toxicity and is not known to induce methemoglobinemia. We observed elevated methemoglobin (MetHb) levels in several patients treated with OHCbl and sought to investigate the incidence of MetHb formation following administration of OHCbl.
Chart review: A single-center, retrospective case series of patients who received 5 or 10 g of hydroxocobalamin from 01/01/2011 through 04/30/2019. Data was analyzed using descriptive statistics. study: Discarded blood was separated into whole blood and plasma samples. OHCbl and normal saline was added to reach 0×, 1×, 2×, and 4× peak therapeutic concentrations and analyzed at times 0, 2, and 4 h after administration.
Chart review Twenty-seven cases of OHCbl administration were identified. The median age was 53 years (IQR 38 - 64) and 20 (74.1%) were male. Exposure to a house fire or smoke inhalation was the reason for OHCbl administration in 21 (77.8%) patients. Five (18.5%) patients received 10 g of OHCbl while the rest received 5 g. Six (22.2%) patients developed methemoglobinemia, all after 5 g OHCbl administration; four had been exposed to fire and smoke, two received the medication for severe acidosis of unknown etiology not related to fire or smoke. The median peak level was 7.1% (IQR 2.2 - 16.4%) at a median time of 11.4 h post-administration. Two patients received methylene blue (MB), neither responded. Death occurred in 17 (63%) cases. study: We observed a dose dependent elevation in total hemoglobin but did not detect any increase in MetHb.
We observed a noteworthy temporal association between the formation of methemoglobinemia and the administration of hydroxocobalamin. This does not appear to be an artifact of the CO-oximeters. This could have profound implications for patients who are already hypoxemic or have impaired oxygen carrying capacity from carboxyhemoglobin.
历史上，治疗氰化物（CN）毒性的第一步是使用解毒剂诱导高铁血红蛋白血症。对于已经低氧血症或高碳氧血红蛋白的患者，这是令人担忧的。羟钴胺（OHCbl）现在是治疗 CN 毒性的一线解毒剂，并且不会引起高铁血红蛋白血症。我们观察到一些接受 OHCbl 治疗的患者高铁血红蛋白（MetHb）水平升高，并试图研究给予 OHCbl 后高铁血红蛋白形成的发生率。
图表回顾：2011 年 1 月 1 日至 2019 年 4 月 30 日期间，在一家中心接受 5 或 10g 羟钴胺的患者的单中心回顾性病例系列。使用描述性统计数据对数据进行分析。研究：分离出全血和血浆样本。加入 OHCbl 和生理盐水，达到 0×、1×、2×和 4×峰值治疗浓度，并在给药后 0、2 和 4 小时进行分析。
图表回顾：共确定 27 例 OHCbl 给药病例。中位年龄为 53 岁（IQR 38-64），20 例（74.1%）为男性。21 例（77.8%）患者因接触火灾或吸入烟雾而接受 OHCbl 治疗，5 例（18.5%）患者接受 10g OHCbl，其余患者接受 5g。6 例（22.2%）患者发生高铁血红蛋白血症，均在接受 5g OHCbl 给药后发生；4 例接触火灾和烟雾，2 例因不明病因的严重酸中毒接受药物治疗，与火灾或烟雾无关。给药后 11.4 小时中位时间内，高铁血红蛋白峰值中位水平为 7.1%（IQR 2.2-16.4%）。2 例患者接受亚甲蓝（MB）治疗，均无反应。17 例（63%）患者死亡。研究：我们观察到总血红蛋白的剂量依赖性升高，但未检测到高铁血红蛋白的任何增加。
我们观察到高铁血红蛋白血症的形成与羟钴胺的给药之间存在显著的时间关联。这似乎不是 CO- 分光光度计的人为因素。这可能对已经低氧血症或因碳氧血红蛋白而携氧能力受损的患者产生深远影响。
