Multiple Small Pulmonary Arteriovenous Fistulas

THE ANTEMORTEM diagnosis of pulmonary arteriovenous fistula was made for the first time by Smith and Horton in 1939.1 The lesion was suspected from the appearance of the chest x-ray and subsequently proved by inj ection of contrast media into an arm vein with visualization of the abnormal vascular communication in the right lung. Since then many such lesions have been suspected from clinical findings and proved by angiocardiography. The classical clinical findings are cyanosis, polycythemia, clubbing of the digits, and murmurs over the lung fields in the absence of cardiac disease. Surgical excision has resulted in cure of the disease with disappearance of cyanosis and clubbing when the lesion or lesions are localized to one or two segments of a lung. The complications resulting from pulmonary arteriovenous fistulas, if untreated, include the following: 1. Rupture with massive hemorrhage.2 3 2. Cardiac decompensation.4 3. Cerebral thrombosis secondary to polycythemia.4 5 4. Cerebral emboli due to passage of emboli from the periphery through the fistulas.5 5. Brain abscess or meningoencephalitis, presumably secondary to septic emboli.5' 6 6. Impairment of cerebral function from chronic anoxemia.7 8 Cyanosis, polycythemia, and clubbing of the digits are found in patients in whom the pulmonary arteriovenous communications are of sufficient size or number to produce these findings. It is estimated that 5 Gm. of reduced hemoglobin per 100 ml. of blood or a right-to-left shunt of 20 per cent of the systemic cardiac output are necessary for cyanosis to be apparent clinically.4' 9 The presenee of even minimal shunting of venous blood into