Acute Pulmonary Thromboembolism and Deep Vein Thrombosis during the Medical Treatment of Acute Aortic Dissection was Successfully Treated by the Combination of Inferior Vena Cava Filter Installation and Anti-Coagulant Therapy: A Case Report

Abstract

A 71-year-old woman was admitted with Stanford type A acute aortic dissection (AAD). Computed tomography (CT) revealed thrombosis of the false lumen, and we planned to treat medically. She developed transient pleural effusion and hypoxemia, which persisted despite her pleural effusion disappeared. We performed CT and found a large thrombus in the pulmonary artery and femoral vein. We administered low doseunfractionated heparin and installed a retrievable inferior vena cava fi lter, which caused the thrombus in the pulmonary artery to disappeared without exacerbating AAD. Our strategy seems to be suitable for acute pulmonary thromboembolism that occurs during the treatment of AAD.Keywords: acute aortic dissection, acute pulmonary thromboembolism, deep vein thrombosis auscultation, respiratory sounds were clear, and no murmurs were detected. A laboratory examination demonstrated a white blood cell count of 12100/µL, a hemoglobin concentration of 13.0 mg/dL, and a platelet count of 22.9 × 10 4 /µL. Blood biochemical tests produced normal results, including an aspartate aminotransferase level of 17 IU/L, an alanine aminotransferase concentration of 15 IU/L, a creatinine kinase concentration of 71 IU/L, and a creatinine level of 0.58 mg/dL. A troponin T test produced negative results. However, a coagulation test showed that the patient's D-dimer (60.9 µg/mL) levels were markedly elevated. Electrocardiography revealed a normal sinus rhythm, and did not detect any signifi cant ST-T wave changes (Fig. 1). Chest radiography demonstrated mediastinal widening, but no pleural effusion was observed (Fig. 2). Contrast-enhanced computed tomography (CT) depicted an acute aortic dissection (AAD), which extended from the ascending aorta to the common iliac artery (Fig. 3). A transthoracic echocardiographic examination did not detect any aortic regurgitation, pericardial effusion, or dilatation of right heart. So, we diagnosed the patient with a Stanford type A AAD. As complete thrombosis of the aortic false lumen was achieved on admission, the patient was treated with antihypertensive agents.The clinical course of the patient's AAD was good, and she underwent rehabilitation according to the program recommended by the appropriate treatment guidelines. 1) However, transient pleural effusion was showed to develop on chest radiography of day 4, and we considered that this would reduce the patient's oxygen saturation level. Although the pleural effusion subsequently disappeared on chest radiography of day 12, the patient's oxygen saturation level remained low (about 85%) in room air. Rehabilitation did not progress because of hypoxemia, and sometimes she walked only in the room with oxygen Case ReportA 71-year-old woman with a history of hypertension suffered a 2-hour episode of sudden severe back pain and visited our hospital. Her height was 160 cm and her weight was 70 kg. Her blood pressure was 170/90 mmHg in both arms, her heart rate was 55 beats per minute, and her oxygen saturation level was 100% in room air. On 36

Deep vein thrombosis and pulmonary embolism in a patient with acute type B aortic dissection: a case report

“…In our case thrombolytic therapy was contraindicated and the convenience for the application of LMWH was uncertain. The vena cava filter should be a treatment option to prevent pulmonary embolism in such cases [10]. However in our case acute pulmonary embolism was present from the time of the DVT diagnosis.…”

“…It was suggested that during aortic dissection hypercoagulability may be triggered as a self-defence and this may cause thromboembolism [10]. VTE is a miscellaneous entity in the presence of acute aortic dissection therefore the anticoagulant or the thrombolytic therapy essential for the treatment of VTE may cause recanalization of the false lumen of the aorta.…”

“…VTE is a miscellaneous entity in the presence of acute aortic dissection therefore the anticoagulant or the thrombolytic therapy essential for the treatment of VTE may cause recanalization of the false lumen of the aorta. At the meantime the tear may be expanded proximally or distally and the false lumen may turn into a devastating hematoma ending in a poor outcome for the patient [10]. On the other hand in a hypercoagulable circumstance, the pulmonary thromboembolism with or without DVT is a life threatening status which should be treated promptly.…”