过氧化氢中毒。

Barbara E Watt, Alex T Proudfoot, J Allister Vale
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Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. 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引用次数: 300

摘要

过氧化氢是一种氧化剂,用于许多家用产品,包括通用消毒剂,无氯漂白剂,织物去污剂,隐形眼镜消毒剂和染发剂,它是一些牙齿美白产品的组成部分。在工业上,过氧化氢的主要用途是在造纸和纸浆生产中作为漂白剂。过氧化氢在医学上已用于伤口冲洗和眼科和内窥镜器械的消毒。过氧化氢通过三个主要机制引起毒性:腐蚀损害、氧气形成和脂质过氧化。浓缩过氧化氢具有腐蚀性,接触可能导致局部组织损伤。摄入浓缩过氧化氢(>35%)也会产生大量氧气。当氧气释放量超过其在血液中的最大溶解度时,可能发生静脉或动脉气体栓塞。中枢神经系统损伤的机制被认为是动脉气体栓塞和随后的脑梗死。在封闭的体腔中快速产生氧气也会引起机械膨胀,并且有可能因氧气释放而导致空心内脏破裂。此外,吸收后的血管内泡沫会严重阻碍右心室输出,导致心输出量完全丧失。过氧化氢也可以通过脂质过氧化作用发挥直接的细胞毒性作用。摄入双氧水可能会刺激胃肠道,引起恶心、呕吐、吐血和口吐白沫;泡沫可能阻塞呼吸道或导致肺部误吸。胃胀痛和打嗝可能是由于胃中大量氧气的释放引起的。粘膜起泡和口咽烧伤在摄入浓缩溶液后很常见,喉痉挛和出血性胃炎也有报道。窦性心动过速、嗜睡、神志不清、昏迷、抽搐、喘鸣、会厌下狭窄、呼吸暂停、发绀和心肺骤停可能在摄入后几分钟内发生。氧气栓塞可引起多发性脑梗死。虽然大多数吸入性暴露只会引起咳嗽和短暂性呼吸困难,但吸入高浓度过氧化氢溶液会引起粘膜严重刺激和炎症,并伴有咳嗽和呼吸困难。暴露后24-72小时内可发生休克、昏迷和惊厥,并可发生肺水肿。使用过氧化氢溶液在封闭的体腔内冲洗伤口或在压力下因氧气栓塞而导致严重的毒性。皮肤接触后可能出现炎症、起泡和严重的皮肤损伤。眼睛接触3%的溶液可能会立即引起刺痛、刺激、流泪和视力模糊,但不太可能造成严重伤害。暴露于更浓的过氧化氢溶液(>10%)可能导致角膜溃疡或穿孔。由于过氧化氢会被过氧化氢酶迅速分解为氧气和水,因此不建议在摄入后进行肠道净化。如果胃胀痛,应通过胃管释放气体。对于摄入浓缩过氧化氢的患者,早期积极的气道管理至关重要,因为呼吸衰竭和骤停似乎是死亡的近因。如果有持续呕吐、吐血、明显口腔烧伤、严重腹痛、吞咽困难或喘鸣,应考虑内窥镜检查。高剂量的糖皮质激素被推荐用于喉水肿和肺水肿,但其价值尚未得到证实。对于危及生命的喉部水肿,可能需要气管插管,或罕见的气管造口术。被污染的皮肤应该用大量的水清洗。皮肤病变应按热烧伤处理;深度烧伤可能需要手术治疗。如果眼睛暴露,应立即用水或0.9%生理盐水彻底冲洗受影响的眼睛,至少10-15分钟。注射局部麻醉剂可以减少不适,并有助于更彻底的净化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hydrogen peroxide poisoning.

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.

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