carbon monoxide ( co ) is a colorless , odorless , and nonirritant gas that is lighter than air , and it is a product of incomplete combustion of hydrocarbons.1 ) accidental , suicidal or homicidal intoxications with co have a long history . acute co poisoning is an important clinical problem and may lead large proportion of patients to fatal death . moreover , frequent neurologic and cardiovascular consequences have been described.2 - 4 ) the neurologic manifestations of co poisoning have been well described , and include headache , dizziness , weakness , nausea , and confusion.3)4 ) cardiac consequences have been reported , including arrhythmias and electrocardiographic alterations , acute myocardial infarction , pulmonary edema , and cardiogenic shock.5)6 ) among these , myocardial injury is common in patients with moderate to severe co poisoning,2 ) manifested as elevated cardiac biomarkers and the changes of regional wall motion abnormality in echocardiography.7 ) on the other hand , an association between thromboembolic accidents and co poisoning has been shown less frequently in the literatures.8 - 14 ) we report a co poisoning case complicated by intracardiac thrombus . a 24-year - old female patient with no preexisting disease was brought to the emergency unit for altered mentality due to suicidal exposure to co. the duration of the exposure was unclear . she showed a good general appearance , the level of consciousness was alert : glasgow coma scale was measuring up to 15 . vital signs were blood pressure of 132/101 mmhg , pulse rate of 87/min , respiration rate of 20/min and body temperature of 35.4. oxygen saturation measured using pulse oxymetry was 100% when 15 l / min oxygen was applied through a reservoir bag mask . she was 164 cm tall and weighed 50 kg , and her body mass index was 18.6 kg / m . lower and upper limb arterial and venous examination revealed normal circulation . in detailed system examinations , no pathological neurologic signs were detected . laboratory analyses revealed the following : white blood cells , 21200/l ; blood urea nitrogen , 17 mg / dl ; creatinine , 0.75 mg / dl , and blood glucose , 101 mg / dl , d - dimer 0.28 ug / ml . cardiac enzymes were elevated ( ck : 3306 u / l , ck - mb : 90.6 ng / ml , troponin i : 1.899 ng / ml , lactate dehydrogenase : 334 u / l ) . arterial blood gas was performed and revealed ph 7.40 , paco2 33 mmhg , pao2 380 mmhg , hco3 20 mmol / l , and the fraction of carboxyhemoglobin 16.0% ( reference range < 2% ) . pain was mainly retrosternal , lasted for several minutes , with no aggravating or relieving factors , and no change in position or respiration . coronary computed tomography ( ct ) angiography performed to rule out coronary artery disease revealed normal coronary artery . transthoracic echocardiography on the same day showed moderately reduced ejection fraction ( 42% ) , and akinesia of left ventricular apex . stress induced cardiomyopathy or ischemic insult of left anterior descending artery were suspected . during comprehensive echocardiographic examination , echogenic mass with multiple nodularity in right atrium ( ra ) was identified . the size measured about 30  15 mm , and it appeared to be attached to the junction of superior vena cava . transesophageal echocardiography and cardiac magnetic resonance imaging ( mri ) were requested for further characterization of the mass . in mid - esophageal 140 degree view the mass was highly mobile and oscillating up and down across the tricuspid valve throughout the cardiac cycle ( fig . the foremost diagnosis to exclude in this patient was intracardiac thrombus , and therefore we started anticoagulation therapy immediately . cardiac mri 1 day after anticoagulation therapy showed delayed enhancement suggestive of a thrombus , and an obvious reduction in size of the thrombus to 8 mm ( fig . , she was questioned concerning recent potential precipitating conditions , such as surgery , immobilization and use of medications including oral contraceptives . furthermore , she was evaluated for genetic and connective tissue disease leading to thrombophilic conditions . complete lower extremity ultrasound and abdominopelvic ct was conducted for suspicion of peripheral vein thrombosis and it demonstrated no thrombosis in other organs . the follow - up transthoracic echocardiogram was done on sixth day after anticoagulation , and showed no residual thrombus in the ra and normalized left ventricular ( lv ) systolic function ( fig . the patient has been free of symptoms and there have been no clinical features of neurologic or thromboembolic complications during the 3-months of follow - up . co poisoning has special impact on organs sensitive to oxygen deprivation such as the heart , brain , and kidney . myocardial injury assessed by ecg and cardiac enzyme elevation from moderate to severe co poisoning is common ( ~40% ) than expected.2 ) the proposed mechanism of global left ventricular dysfunction is tissue hypoxia and resultant myocardial stunning . the affinity of hemoglobin for co is more than 200 times greater than its affinity for oxygen , and competitive inhibition of oxygen release leads to tissue hypoxia.3 ) usually , the left ventricular dysfunction was transient and would be normalized with conventional treatment including high concentration of oxygen . in our case , left ventricular systolic dysfunction with regional wall motion abnormalities was associated with co poisoning and recovered with conventional therapy . in contrast , an association between thromboembolic accidents and co poisoning has been shown less commonly in the literatures . to our knowledge , this is the first korean case of acute co poisoning combined with ra thrombus formation . besides lv thrombus formation associated with transient apical ballooning of lv,15 ) there have been several reports regarding arterial and venous system thrombosis and related embolism including popliteal artery,8)9 ) superior sagittal sinus,10 ) vein of labbe,11 ) mesenteric artery,12 ) basillar trunk,13 ) and popliteal vein.14 ) a plausible explanation for thromboembolic events is the effect of co on platelets aggregation . co poisoning leads to some changes in blood vessel and co and nitric oxide exchange on platelet . disturbed mitochondrial mechanisms by no and its derivatives facilitate production of free oxygen radicals.16 ) oxidative stress enhanced by free oxygen radicals may lead to endothelial damage , and subsequent platelet aggregation.17 ) although the optimal therapy and duration of anticoagulation for co induced ra thrombus is still unknown , the use of anticoagulant therapy in the acute phase and until complete resolution of thrombus appears to be appropriate in patients with atrial thrombus.18)19 ) in conclusion , myocardial injury is common in co poisoning . thromboembolism could occur in cardiac chambers and peripheral vessels , although it was less frequent . therefore , patients presented with co poisoning should undergo echocardiographic examination followed by serial ecg and cardiac enzyme evaluation . careful examination should be performed for the assessment of intracardiac thrombus , in addition to the exact evaluation of ventricle function .
carbon monoxide is a nonirritant , odorless , colorless gas . 
 its effects are prominent in organs most sensitive to oxygen deprivation , such as the heart , brain , and kidney . 
 although less frequently , an association between thromboembolic events and carbon monoxide poisoning has been shown in the literatures . in this case , we report a case of atrial thrombus associated with carbon monoxide poisoning .