INTRODUCTION: Most clinical manifestations of aortic dissection are due to complications of either ischemic origin or wall rupture of pleural, pericardial, peritoneal or mediastinal cavity. Compression of other blood vessels such as pulmonary artery or superior vena cava is possible, but rarely occurs. CASE REPORT: A 60 year-old patient was admitted to hospital due to severe cyanosis and edema of the face, neck and upper thorax. Ten years ago, due to aortic insufficiency, aortic valve replacement with mechanical prosthesis (St. Jude) was performed. Diagnosis of superior vena cava syndrome was established on the basis of clinical examination, ECG and chest radiography. The etiology was confirmed by echocardiography indicating an enormous dissecting aneurysm of the ascending aorta, 9.2 cm in diameter. Lethal outcome followed 24 h after admission according to the type of electromechanical dissociation. DISCUSSION: The first case of superior vena cava syndrome was described by William Hunter in 1757. This severe disease is caused by tumors which compress or develop inside superior vena cava. In cases of rapid symptom occurrence, thrombosis or compression of vena due to hematoma (trauma, voluminous, dissecting aortic aneurysm) should be considered. Since symptoms of aortic dissection were absent (thoracic pain, aortic regurgitation, pulse asymmetry) the etiologic diagnosis of superior vena cava syndrome was confirmed by echocardiography. Surgical treatment of dissection provides repermeabilization of the superior vena cava and loss of symptoms. CONCLUSION: Superior vena cava syndrome is a rare and slightly known clinical manifestation of ascending aortic dissection. If symptoms rapidly occur, dissection should be considered, particularly in previously surgically treated patients.
INTRODUCTION: Most clinical manifestations of aortic dissection are due to complications of either ischemic origin or wall rupture of pleural, pericardial, peritoneal or mediastinal cavity. Compression of other blood vessels such as pulmonary artery or superior vena cava is possible, but rarely occurs. CASE REPORT: A 60 year-old patient was admitted to hospital due to severe cyanosis and edema of the face, neck and upper thorax. Ten years ago, due to aortic insufficiency, aortic valve replacement with mechanical prosthesis (St. Jude) was performed. Diagnosis of superior vena cava syndrome was established on the basis of clinical examination, ECG and chest radiography. The etiology was confirmed by echocardiography indicating an enormous dissecting aneurysm of the ascending aorta, 9.2 cm in diameter. Lethal outcome followed 24 h after admission according to the type of electromechanical dissociation. DISCUSSION: The first case of superior vena cava syndrome was described by William Hunter in 1757. This severe disease is caused by tumors which compress or develop inside superior vena cava. In cases of rapid symptom occurrence, thrombosis or compression of vena due to hematoma (trauma, voluminous, dissecting aortic aneurysm) should be considered. Since symptoms of aortic dissection were absent (thoracic pain, aortic regurgitation, pulse asymmetry) the etiologic diagnosis of superior vena cava syndrome was confirmed by echocardiography. Surgical treatment of dissection provides repermeabilization of the superior vena cava and loss of symptoms. CONCLUSION:Superior vena cava syndrome is a rare and slightly known clinical manifestation of ascending aortic dissection. If symptoms rapidly occur, dissection should be considered, particularly in previously surgically treated patients.