A Case of Carbon Monoxide Poisoning with Thrombus in the Heart: A Case Report

Abstract

Carbon monoxide is a nonirritant, odorless, colorless gas, and is lighter than air. It is an end product of the incomplete combustion of hydrocarbons. Its effects are most prominent in organs sensitive to oxygen deprivation, such as the heart, brain, and kidney. Carbon monoxide poisoning becomes more abundant in winter and at cold places. In Turkey, every year we see several deaths due to poisonous gas leaks from coal or wood stoves. Deaths particularly due to hypoxia-related central nervous system damage and ventricular dysrhythmias are observed. On the other hand, an association between thromboembolic accidents and carbon monoxide poisoning has been shown in literature. Thromboembolic accidents in the mesenteric, central nervous system, and extremities are reported. However, no atrial thrombus has been mentioned. In this study, a case of an atrial thrombus associated with carbon monoxide poisoning following a diagnosis of carbon monoxide poisoning and treatment in the emergency room is reported and the literature is revisited.

Carbon monoxide: Anticoagulant or procoagulant?

“…While a likely contributor to myocardial necrosis was hypoxia secondary to decreased oxyhemoglobin and increased COHb, the acute occurrence of coronary artery occlusion/thrombus [38][39][40] and coronary artery shunt thrombus [41] formation serve as evidence of an acute CO associated thrombophilic event. Even more impressive are the reports of acute intracardiac thrombus in the right atrium [42][43][44] or left ventricle [45] and pulmonary embolism [46] in patients with the diagnosis of acute CO poisoning;…”

“…In addition to these case reports and series [34][35][36][37][38][39][40][41][42][43][44][45] portraying a procoagulant feature of marked CO exposure, one recent article linked in vitro measures of coagulation with clinical CO poisoning in victims with COHb concentrations over 10% [47]. Compared to normal subjects, 48 CO poisoning victims (COHb=21.97.9%, meanSD) had significantly greater plasma concentrations of prothrombin fragment 1+2, plasminogen activator inhibitor-1 and tissue type plasminogen activator with normal fibrinogen concentrations [47].…”

“…Spectrophotometric measures of resistance to fibrinolysis also demonstrated that these CO poisoning victims had increased plasmatic resistance to fibrinolysis [47]. Taken as a whole, these aforementioned investigations potentially link CO exposure to thrombophilia [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46], with increased systemic thrombin generation and hypofibrinolysis being possible mechanisms by which CO were posited to mediate thrombotic events [47].…”

“…There is evidence that excessive CO exposure may result in decreased in vivo and in vitro hemostasis in humans and rodents [4][5][6][7][8][18][19][20][21][22][23], potentially by inhibition of platelet aggregation [9][10][11][12][13]15,16,[20][21][22][23]. However, there is also evidence that increased CO exposure can enhance platelet activation [14,17] and cause enhanced coagulation/decreased fibrinolysis in humans and other mammalian species [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][67][68][69][70]…”

The Effect of Carbon Monoxide Poisoning on Platelet Volume in Children

“…CO zehirlenmesinde trombotik olaylara yatkınlık olduğunu gösteren çalışmalar olmasına rağmen patofizyolojik mekanizma konusunda henüz yeterli bilgi yoktur. 10,11 Akut ya da süreğen hipoksi durumunda kemik iliğindeki megakaryositlerin proliferasyonu hızlanmakta ve işlevsel aktivitesi artmaktadır. Genç trombositlerin hem Akça Bicilioglu ve ark.…”