Savioli Gabriele, Gri Nicole, Ceresa Iride Francesca, Piccioni Andrea, Zanza Christian, Longhitano Yaroslava, Ricevuti Giovanni, Daccò Maurizio, Esposito Ciro, Candura Stefano M
Emergency Department, Fondazione IRCCS Policlinico San Matteo, 27100 Pavia, Italy.
Niguarda Cancer Center, ASST Grande Ospedale Metropolitano Niguarda, Piazza dell'Ospedale Maggiore, 3, 20162 Milano, Italy.
J Clin Med. 2024 Apr 23;13(9):2466. doi: 10.3390/jcm13092466.
Carbon monoxide poisoning remains a leading cause of accidental poisoning worldwide (both at home and at work), and it is also a cause of suicidal poisoning. Such poisoning can arise following prolonged exposure to low levels of CO or following brief exposure to high concentrations of the gas. In fact, despite exposure limits, high safety standards, and the availability of CO alarms, nearly 50,000 people in the United States visit the emergency department each year due to poisoning. Additionally, CO poisoning in the United States causes up to 500 deaths each year. Despite the widespread nature of this form of poisoning, known about for centuries and whose damage mechanisms have been recognized (or rather hypothesized about) since the 1800s, early recognition, especially of late complications, and treatment remain a medical challenge. A well-designed therapeutic diagnostic process is necessary so that indication for hyperbaric or normobaric therapy is correctly made and so that patients are followed up even after acute exposure to diagnose late complications early. Furthermore, it is necessary to consider that in the setting of emergency medicine, CO poisoning can be part of a differential diagnosis along with other more frequent conditions, making its recognition difficult. The last thirty years have been marked by a significant increase in knowledge regarding the toxicity of CO, as well as its functioning and its importance at physiological concentrations in mammalian systems. This review, taking into account the significant progress made in recent years, aims to reconsider the pathogenicity of CO, which is not trivially just poisonous to tissues. A revision of the paradigm, especially as regards treatment and sequelae, appears necessary, and new studies should focus on this new point of view.
一氧化碳中毒仍然是全球范围内(包括家庭和工作场所)意外中毒的主要原因,也是自杀性中毒的一个原因。这种中毒可能在长期接触低水平一氧化碳或短时间接触高浓度该气体后发生。事实上,尽管有接触限值、高安全标准以及一氧化碳报警器,但在美国,每年仍有近5万人因中毒前往急诊科就诊。此外,美国每年有多达500人死于一氧化碳中毒。尽管这种中毒形式很普遍,几个世纪以来就已为人所知,其损伤机制自19世纪以来就已被认识(或者更确切地说是被假设),但早期识别,尤其是对晚期并发症的识别以及治疗仍然是一项医学挑战。需要一个精心设计的治疗诊断过程,以便正确确定高压或常压治疗的适应症,并确保即使在急性接触后也对患者进行随访,以便早期诊断晚期并发症。此外,有必要考虑到,在急诊医学环境中,一氧化碳中毒可能是鉴别诊断的一部分,与其他更常见的病症一起,这使得其识别变得困难。在过去三十年里,关于一氧化碳毒性、其作用以及在哺乳动物系统生理浓度下的重要性的知识有了显著增加。本综述考虑到近年来取得的重大进展,旨在重新审视一氧化碳的致病性,一氧化碳对组织的毒害并非微不足道。似乎有必要对范式进行修订,尤其是在治疗和后遗症方面,新的研究应关注这一新观点。