Carbon Monoxide Poisoning (Reprinted from the 2023 Hyperbaric Indications Manual 15th edition).

IF 0.7 4区 医学 Q4 MARINE & FRESHWATER BIOLOGY Undersea and Hyperbaric Medicine Pub Date : 2024-03-01
Lindell K Weaver
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Abstract

Despite established exposure limits and safety standards, and the availability of carbon monoxide (CO) alarms, each year an estimated 50,000 people in the United States visit emergency departments for CO poisoning. Carbon monoxide poisoning can occur from brief exposures to high levels of CO or from longer exposures to lower levels. If the CO exposure is sufficiently high, unconsciousness and death occur quickly, and without symptoms. With non-lethal exposures to CO, common symptoms include headaches, nausea and vomiting, dizziness, general malaise, and altered mental status. Some patients may have chest pain, shortness of breath, and myocardial ischemia, and may require mechanical ventilation and treatment of shock. Individuals poisoned by CO often develop brain injury. As with brain injury from non- CO causes such as traumatic brain injury, the clinical expression of brain injury caused by CO poisoning includes the domains of cognition, affect, neurological, and somatic. Common problems are neurological: imbalance, motor weakness, neuropathies, hearing loss, tinnitus, Parkinson's-like syndrome, vestibular, gaze, auditory processing, cognitive, anxiety and depression, posttraumatic stress, personality change, persistent headaches, dizziness, sleep problems, and others. In addition, some will have cardiac or other problems. While breathing oxygen hastens the removal of carboxyhemoglobin (COHb), hyperbaric oxygen (HBO2) hastens COHb elimination and favorably modulates inflammatory processes instigated by CO poisoning, an effect not observed with breathing normobaric oxygen. Hyperbaric oxygen improves mitochondrial function, inhibits lipid peroxidation transiently, impairs leukocyte adhesion to injured microvasculature, and reduces brain inflammation caused by CO-induced adduct formation of myelin basic protein. Based upon supportive randomized clinical trials in humans and considerable evidence from animal studies, HBO2 should be considered for all cases of acute symptomatic CO poisoning. Hyperbaric oxygen is indicated for CO poisoning complicated by cyanide poisoning, often concomitantly with smoke inhalation.

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一氧化碳中毒(转载自《2023 年高压氧适应症手册》第 15 版)。
尽管已经制定了一氧化碳接触限值和安全标准,而且一氧化碳(CO)报警器也已投入使用,但美国每年估计仍有 50,000 人因一氧化碳中毒而到急诊室就诊。一氧化碳中毒可能发生在短时间接触高浓度 CO 或长时间接触低浓度 CO 的情况下。如果接触的一氧化碳浓度足够高,很快就会失去知觉并死亡,而且没有任何症状。在接触一氧化碳不致命的情况下,常见症状包括头痛、恶心和呕吐、头晕、全身不适和精神状态改变。一些患者可能会出现胸痛、呼吸急促和心肌缺血,可能需要机械通气和休克治疗。一氧化碳中毒者通常会出现脑损伤。与创伤性脑损伤等非一氧化碳引起的脑损伤一样,一氧化碳中毒导致的脑损伤的临床表现包括认知、情感、神经和躯体等领域。常见的问题有神经系统问题:失衡、运动无力、神经病变、听力下降、耳鸣、帕金森样综合征、前庭、凝视、听觉处理、认知、焦虑和抑郁、创伤后应激、性格改变、持续性头痛、头晕、睡眠问题等。此外,有些人会出现心脏或其他问题。呼吸氧气可加速碳氧血红蛋白(COHb)的清除,而高压氧(HBO2)则可加速碳氧血红蛋白的清除,并对一氧化碳中毒引发的炎症过程产生有利的调节作用,这是呼吸常压氧所无法观察到的效果。高压氧可改善线粒体功能,短暂抑制脂质过氧化反应,降低白细胞对受损微血管的粘附性,并减轻因 CO 诱导的髓鞘碱性蛋白加合物形成而引起的脑部炎症。根据人体随机临床试验的支持性结果和动物实验的大量证据,所有急性症状性一氧化碳中毒病例都应考虑使用高压氧治疗。高压氧适用于并发氰化物中毒的一氧化碳中毒,通常与烟雾吸入同时进行。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Undersea and Hyperbaric Medicine
Undersea and Hyperbaric Medicine 医学-海洋与淡水生物学
CiteScore
1.60
自引率
11.10%
发文量
37
审稿时长
>12 weeks
期刊介绍: Undersea and Hyperbaric Medicine Journal accepts manuscripts for publication that are related to the areas of diving research and physiology, hyperbaric medicine and oxygen therapy, submarine medicine, naval medicine and clinical research related to the above topics. To be considered for UHM scientific papers must deal with significant and new research in an area related to biological, physical and clinical phenomena related to the above environments.
期刊最新文献
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