P684 Paradoxical cerebral infarction due to massive pulmonary embolism in extracorporeal cardiopulmonary resuscitation and surgical embolectomy
Authors: Shiota H , Kagawa E , Kato M , Oda N , Kunita E , Nagai M , Dote K 
Published: January 2020

Abstract

Introduction
Paradoxical cerebral infarction is a mechanism of acute ischemic stroke; however, definitive images to diagnose paradoxical embolism are not often obtained. We report a case of paradoxical cerebral embolism complicated with cardiac arrest due to massive pulmonary embolism.

Case report
A 40-year-old man presented due to sudden-onset chest pain, and was admitted to our hospital. He was restless and had cold sweat; we could not measure blood pressure. Electrocardiography showed wide QRS complex with right bundle branch block, and T wave inversion in leads V1 and III. Transthoracic echocardiography showed diffuse severe left ventricular hypokinesis, with slightly better inferior wall motion compared to other segments. Few minutes after arriving, he experienced cardiac arrest; chest compression was initiated. He was transported to the catheter laboratory, and veno-arterial extracorporeal membrane oxygenation was initiated subsequently. To diagnose the cause of arrest, we performed coronary angiography, which revealed no occluded coronary artery. Pulmonary angiograms showed bilateral proximal pulmonary artery occlusion with massive thrombi (panel A). Surgical embolectomy was performed after cardiac team discussion. After ICU admission post-surgery, pericardial effusion was increased, and the blood drained continuously from the chest tube; a large amount of blood transfusion was required. Reopen chest haemostasis was utilised. After the second ICU admission, anisocoria was observed; subsequent computed tomography showed low density and midline shift in almost the entire left cerebral hemisphere (Panel B). Carotid duplex ultrasound revealed a large thrombus saddled at the left carotid artery bifurcation (Panel C and D). We rechecked the transthoracic echocardiogram at arrival to reveal the cause of the cerebral infarction, which showed the thrombus to be at the ascending aorta (Panel E). We thought that the thrombi had moved from the lower limb to the right atrium. The massive pulmonary embolism increased the pulmonary artery and right atrial pressure, resulting in the lower pressure of the left atrium compared to that of the right atrium. The thrombi passed through the patent foramen ovale into the left atrium, moved into the left ventricle, and embolised the left internal carotid artery (Panel F). He expired due to severe neurologic injury from brain herniation.

Conclusion
In this case, although the pulmonary embolism was massive and led to cardiac arrest, the deteriorated haemodynamics improved by extracorporeal cardiopulmonary resuscitation and surgical embolectomy. However, we could not rescue the patient because of the severe neurological injury due to paradoxical embolism. Paradoxical cerebral infarction in pulmonary embolism is rare; however, we should pay careful attention to early detection of paradoxical cerebral infarction in pulmonary embolism and treatment for return of the patient to the former lifestyle.
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