SVC syndrome complicated with acute PE in lung cancer: a cas
Superior vena cava (SVC) syndrome is relatively common in patients with malignancy, and it may lead to pulmonary thromboembolism. Published in the Journal of Cardiology Cases, the authors describe a case to caution physicians about its life-threatening complication, and to raise high degree of clinical suspicion for an early diagnosis of pulmonary thromboembolism after treatment of SVC syndrome.

A 63-year-old male patient presented himself with sudden onset of syncope at our emergency room. He had an underlying disease of extensive stage small cell lung cancer. He also complained of puffy face and progressive swelling of the right upper extremity. Electrocardiography revealed sinus tachycardia (Fig. 1). The result of chest X-ray (CXR) showed widening mediastinum and cardiomegaly.

Echocardiography revealed preserved left ventricle systolic function with moderate to severe tricuspid regurgitation. Color Doppler ultrasonography showed no evidence of deep vein thrombosis (DVT) of lower extremities. Chest computed tomography (CT) revealed several ill-defined mediastinal masses causing invasion, compression (Fig. 2A) and venous occlusion of superior vena cava (Fig. 2B). He received systemic chemotherapy with etoposide and cisplatin, and localized radiotherapy for lung cancer complicated with SVC syndrome.

His clinical symptoms of SVC syndrome were improved after several cycles of therapy. Unfortunately, he then complained of sudden onset of dyspnea and chest tightness about one week after chemo-radiotherapy. At that time, his vital signs revealed body temperature 36 °C, blood pressure 140/85 mm Hg, pulse rate 110 beats per minute, and respiratory rate 20 breaths per minute. SpO2 was about 72% under room-air condition. Physical examination demonstrated paradoxical respiratory movement and attenuated second heart sound. The value of serum D-dimer level was 0.63 mg/L (normal: <0.5 mg/L).

Blood arterial analysis showed SaO2: 75% and PaO2: 37.8 mm Hg. To compare with recent and previous 12 lead electrocardiogram and CXR, there was no significant difference. Chest CT was repeated, showing SVC recanalization and improvement of SVC syndrome (Fig. 2C). Additionally, low density of filling defect was located at the trunk of left pulmonary artery (Fig. 2D and E).

The values of serum protein C and protein S were 94% and 86% which were within normal limit. He received intravenous anticoagulant due to this acute pulmonary thromboembolism. His oxygenation and dyspneic condition were improved after anticoagulation use. Follow-up D-dimer level was 0.35 mg/L. Absence of right ventricle dysfunction or pulmonary hypertension was revealed by echocardiography.

After 48 h intravenous anticoagulant use, the anticoagulant was then shifted to rivaroxaban 15 mg twice daily for 3 weeks, followed by 20 mg once daily. SpO2 was about 96% under room-air condition about one month after acute pulmonary thromboembolism.

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