Raub J A, Mathieu-Nolf M, Hampson N B, Thom S R
National Center for Environmental Assessment, US Environmental Protection Agency, Research Triangle Park, NC 27711, USA.
Toxicology. 2000 Apr 7;145(1):1-14. doi: 10.1016/s0300-483x(99)00217-6.
Carbon monoxide (CO) may be the cause of more than one-half of the fatal poisonings reported in many countries; fatal cases also are grossly under-reported or misdiagnosed by medical professionals. Therefore, the precise number of individuals who have suffered from CO intoxication is not known. The health effects associated with exposure to CO range from the more subtle cardiovascular and neurobehavioral effects at low concentrations to unconsciousness and death after acute or chronic exposure to higher concentrations of CO. The morbidity and mortality resulting from the latter exposures are described briefly to complete the picture of CO exposure in present-day society. The symptoms, signs, and prognosis of acute CO poisoning correlate poorly with the level of carboxyhemoglobin (COHb) measured at the time of hospital admission; however, because CO poisoning is a diagnosis frequently overlooked, the importance of measuring COHb in suspicious settings cannot be overstated. The early symptoms (headache, dizziness, weakness, nausea, confusion, disorientation, and visual disturbances) also have to be emphasized, especially if they recur with a regular periodicity or in the same environment. Complications occur frequently in CO poisoning. Immediate death is most likely cardiac in origin because myocardial tissues are most sensitive to the hypoxic effects of CO. Severe poisoning results in marked hypotension, lethal arrhythmias, and electrocardiographic changes. Pulmonary edema may occur. Neurological manifestation of acute CO poisoning includes disorientation, confusion, and coma. Perhaps the most insidious effect of CO poisoning is the development of delayed neuropsychiatric impairment within 2-28 days after poisoning and the slow resolution of neurobehavioral consequences. Carbon monoxide poisoning during pregnancy results in high risk for the mother by increasing the short-term complication rate and for the fetus by causing fetal death, developmental disorders, and chronic cerebral lesions. In conclusion, CO poisoning occurs frequently; has severe consequences, including immediate death; involves complications and late sequelae; and often is overlooked. Efforts in prevention and in public and medical education should be encouraged.
在许多国家，一氧化碳（CO）可能是半数以上报告的致命中毒事件的原因；致命病例也常常未得到充分报告或被医学专业人员误诊。因此，一氧化碳中毒患者的确切人数尚不清楚。接触一氧化碳对健康的影响范围很广，从低浓度时较为隐匿的心血管和神经行为影响，到急性或慢性接触高浓度一氧化碳后的昏迷和死亡。本文简要描述了后者导致的发病和死亡情况，以全面呈现当今社会一氧化碳接触的全貌。急性一氧化碳中毒的症状、体征和预后与入院时测得的碳氧血红蛋白（COHb）水平相关性较差；然而，由于一氧化碳中毒是一种常被忽视的诊断，在可疑情况下测量碳氧血红蛋白的重要性再怎么强调也不为过。还必须强调早期症状（头痛、头晕、虚弱、恶心、意识模糊、定向障碍和视觉障碍），尤其是当这些症状有规律地反复出现或在同一环境中出现时。一氧化碳中毒时常会出现并发症。猝死最可能源于心脏，因为心肌组织对一氧化碳的缺氧作用最为敏感。严重中毒会导致明显的低血压、致命性心律失常和心电图改变。可能会发生肺水肿。急性一氧化碳中毒的神经表现包括定向障碍、意识模糊和昏迷。一氧化碳中毒最隐匿的影响可能是在中毒后2至28天内出现迟发性神经精神障碍，以及神经行为后果的缓慢恢复。孕期一氧化碳中毒会增加母亲的短期并发症风险，并导致胎儿死亡、发育障碍和慢性脑损伤，对胎儿构成高风险。总之，一氧化碳中毒很常见；会造成严重后果，包括猝死；会引发并发症和晚期后遗症；而且常常被忽视。应鼓励在预防以及公众和医学教育方面做出努力。
