一氧化碳中毒。

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一氧化碳中毒。

Handb神经。2015;131:191 - 203。doi: 10.1016 / b978 - 0 - 444 - 62627 - 1.00024 x。

PubMed ID

26563790 (在PubMed

]

文摘

一氧化碳(CO)是一种无色,无味,无刺激性气体,占每年大量的CO中毒病例来自各种来源的碳氢化合物的不完全燃烧。这包括差功能加热系统,室内propane-powered叉车,燃烧室内燃烧木炭煤球,骑在皮卡,冰溜冰场使用propane-powered重修的机器,和汽油发电机没有在正确的位置。一旦公司吸入它与血红蛋白结合形成碳氧血红蛋白(COHb)氧亲和力200倍,导致减少携带氧气的能力和减少释放氧气到组织导致组织缺氧。缺血与CO中毒时出现意识丧失,伴有低血压和动脉缺血大脑的边境地区。除了绑定heme-containing蛋白质,许多公司破坏氧化代谢导致自由基的形成。曾经与CO中毒,低血压和无意识发生脂质过氧化和细胞凋亡。因为COHb半衰期较短,检查其他公司神经毒性的生物标志物反映炎症或神经损伤并没有表现出一致的结果。最初的症状与公司接触当COHb特异性的15 - 30%,也就是说,头痛、头晕、恶心、疲劳、和手灵巧度受损。然而缺血性心脏病患者可能经历胸痛和减少运动时间COHb水平在1%和9%之间。COHb水平在30%和70%之间导致意识丧失,最终死亡。 Following resolution of acute symptoms there may be a lucid interval of 2-40 days before the development of delayed neurologic sequelae (DNS), with diffuse demyelination in the brain accompanied by lethargy, behavior changes, forgetfulness, memory loss, and parkinsonian features. Seventy-five percent of patients with DNS recover within 1 year. Neuropsychologic abnormalities with chronic CO exposure are found even when magnetic resonance imaging (MRI) and magnetic resonance spectroscopy are normal. White-matter damage in the centrum semiovale and periventricular area and abnormalities in the globus pallidus are most commonly seen on MRI following CO exposure. Though not as common, toxic or ischemic peripheral neuropathies are associated with CO exposure in humans and animals. The cornerstone for treatment for CO poisoning is 100% oxygen using a tight-fitting mask for greater than 6 hours. The indications for treatment with hyperbaric oxygen to decrease the half-life of COHb remain controversial.

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一氧化碳