Common Aorto-Pulmonary Trunk: A Rare Congenital Defect

Abstract

A lad of eighteen was first seen on May 18, 1942. A congenital heart lesion had been diagnosed when he was a few weeks old, and though he was not then cyanosed at rest, he soon became blue and breathless on exertion, especially in cold weather. He had scarlet fever at the age of ten, but never rheumatism in any form. At the age of twelve, he was too breathless for any but short walks. He was unfit to play any games at school. A change had taken place six months before (October, 1941) when cyanosis became permanent and the dyspncea more distressing. There had been neither orthopncea nor cedema; he had never fainted, and he had not lost weight. Pain had started during these last months of increased dyspncea, and now constituted the greater complaint, though he was no complainer. On exertion it began in the left arm and if severe it affected the right. It was felt across the chest, especially on the left, but not in the back. Rest, especially if with warmth, relieved it, yet it might last 10 to 20 minutes once evoked by exertion, for it never began at rest. Palpitation was felt on emotion or exertion. There was a slight occasional cough.Examination.-He was a pleasant and fairly well-developed youth, with some cyanosis of the skin and moderate clubbing of the fingers and toes. The pulse was 70-80, and regular. The blood pressure was 125/100. A heaving apex beat was felt in the fifth space, two inches outside the nipple line. A long diastolic thrill was felt widely in the apical region, yet there was no thrill at the base. The first sound was snapping internal to the apex, and a thundering diastolic murmur was heard over the whole apical region, up to the fourth rib, though loudest internal to the apex. At the base the murmur was less loud; the basal second sound was just audible. There were no abnormal signs in the lungs or abdomen.The electrocardiogram (Fig. IA) showed a small R and a large S in all leads, and an isoelectric T in lead I. Two months later, three days before his death on July 18, 1942, T I was inverted (Fig. lB).Cardioscopy showed enlargement of the heart, mainly to the right, but with a single big rounded prominence on the left, in the region of the pulmonary artery and extending upwards to embrace the aortic area so that no aortic knob was visible. The right pulmonary artery was, however, not enlarged. In the right (I) oblique position, a barium swallow showed a combined aorto-pulmonary impression and no particular displacement of the left auricle. Radiographs by Major Peter Kerley are shown in Fig. 2 and 3.Course. A tentative diagnosis was made of patent ductus arteriosus with aneurysmal dilatation of the pulmonary artery, presumably combined with some other defect. This presumption seemed to preclude operation when this was considered because of the deterioration in his condition as already described. The physical signs by July 14, 1942 had altered as follows. Cyanosis was extreme, though he was not, even now, breathless at rest and could walk slowly in the street. The murmur had become more con...

Aorto-pulmonary Septal Defect with Patent Ductus Arteriosus and Death Due to Rupture of Dissecting Aneurysm of the Pulmonary Artery into the Pericardium

“…EMBRYOLOGY.-Shepherd, P a r k, and Kitchell (1944) Bain and Parkinson (1943) pointed out, there is no defect of the interventricular scptum or of the pulmonary or aortic valves. The defect is usually a centimetre or less above the pulmonary valves and thus distant from the site of the ductus.…”

“…There are notable exceptions where the defect is much larger. Dadds and Hoyle (1949) and Bain and Parkinson (1943) each report a defect which was over 5 cm. in the least diameter.…”

Truncus arteriosus communis with intact ventricular septum.

“…6.4 represents 'pure' truncus arteriosus communis with well-formed aorticopulmonary septum, embryologically, as exemplified by case 4 of Rosenquist et al (1976) and Fig. 6.5 truncus arteriosus communis with no aorticopulmonary septal defect, embryologically, but with ventricular septal defect, as exemplified by case 1 of Rosenquist et al (1976) The hearts described by Bain and Parkinson (1943), Van Praagh and Van Praagh (1965) and Daily et al (1975) are represented by Fig. 6.6.…”