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