Łopaciński Bogdan, Kołacinski Zbigniew, Winnicka Renata
Klinika Ostrych Zatruć, Instytutu Medycyny Pracy w Łodzi.
Przegl Lek. 2007;64(4-5):326-30.
Sodium azide poisonings occur very rarely. The mechanism of sodium azide toxic effect has not yet been fully explained. Despite the lack of an explicit procedure for the cases of sodium azide poisonings, in vitro tests and rare case reports suggest that treatment with antidotes for cyanide poisoning victims can be effective. This study describes two cases of suicidal sodium azide ingestion. Case 1. 30-year-old male ingested ca. 180 mg of sodium azide. On admission to hospital, within 4 hours from poisoning, the man complained of dizziness and anxiety. Physical examination revealed horizontal nystagmus, flapping tremor, HR 135/min. In laboratory tests, higher blood concentration of lactates (3 mmol/l) was detected, as well as lower potassium concentration (3.4 mmol/L) and increased transaminase activity (ALT 74 U/l, AST 90 U/l). Electrocardiographic tests showed a negative T wave in limb lead III. Other results were within normal. As the patient ingested a toxic dose of sodium azide, he was treated according to the therapy prescription for cyanide poisoning (amyl nitrite inhalation followed by intravenous administration of sodium nitrite and sodium thiosulphate). ECG record of the last day of hospitalization (7th day of treatment) showed negative T waves in lead III, V4-V6. He was discharged from hospital in good condition. Case 2.23-year-old male ingested 10 g of sodium azide 1.5 hours prior to admission to hospital. At the beginning, the patient's condition was good, but it changed to critical state within the first hours of hospitalization. He developed a deep coma, respiratory and circulatory insufficiency, metabolic acidosis, cardiac dysrrhythmias and anuria. Cardiac activity monitoring showed alternating tachycardia (140 beats per minute) and bradycardia (48 beats per minute), numerous additional supraventricular and ventricular extrasystoles and sinus dysrrhythmia. Cardiac arrest (asystolia) occurred twice, the second incident with fatal outcome. The patient received supportive therapy, he was also treated according to the therapy prescription for cyanide poisoning. Circulatory disturbances observed in both cases have been described in literature as symptoms of sodium azide poisoning. However, available literature data are scarce and lack systematization, most of them coming from several decades ago. The lack of patient's consent for detailed examination of circulatory system and liver made it impossible to gather further knowledge on the subject. The efficacy of treatment with antidotes for cyanide poisoning has not been unequivocally determined for this kind of intoxication.
叠氮化钠中毒极为罕见。叠氮化钠的毒性作用机制尚未完全阐明。尽管对于叠氮化钠中毒病例缺乏明确的治疗流程，但体外试验和罕见病例报告表明，对氰化物中毒患者使用解毒剂进行治疗可能有效。本研究描述了两例自杀性摄入叠氮化钠的病例。病例1：一名30岁男性摄入了约180毫克叠氮化钠。入院时，中毒后4小时内，该男子主诉头晕和焦虑。体格检查发现水平眼球震颤、扑翼样震颤，心率135次/分钟。实验室检查显示，血乳酸浓度升高（3毫摩尔/升），血钾浓度降低（3.4毫摩尔/升），转氨酶活性升高（谷丙转氨酶74国际单位/升，谷草转氨酶90国际单位/升）。心电图检查显示肢体导联III出现T波倒置。其他结果均正常。由于患者摄入了有毒剂量的叠氮化钠，按照氰化物中毒治疗方案进行治疗（吸入亚硝酸异戊酯，随后静脉注射亚硝酸钠和硫代硫酸钠）。住院最后一天（治疗第7天）的心电图记录显示导联III、V4 - V6出现T波倒置。患者康复出院。病例2：一名23岁男性在入院前1.5小时摄入了10克叠氮化钠。起初，患者情况良好，但在住院后的最初几个小时内病情转为危急状态。他陷入深度昏迷、出现呼吸和循环功能不全、代谢性酸中毒、心律失常和无尿。心脏活动监测显示交替出现心动过速（每分钟140次）和心动过缓（每分钟48次），还有许多额外的室上性和室性早搏以及窦性心律失常。心脏骤停（心搏停止）发生了两次，第二次导致死亡。患者接受了支持性治疗，也按照氰化物中毒治疗方案进行了治疗。两例病例中观察到的循环系统紊乱在文献中被描述为叠氮化钠中毒的症状。然而，现有的文献资料稀少且缺乏系统性，大多数来自几十年前。由于患者不同意对循环系统和肝脏进行详细检查，无法获取关于该主题的更多知识。对于这种中毒情况，氰化物中毒解毒剂治疗的疗效尚未明确确定。
