Christopher P. Coppola, Alfred P. Kennedy, Jr. and Ronald J. Scorpio (eds.)Pediatric Surgery2014Diagnosis and Treatment10.1007/978-3-319-04340-1_80
© Springer International Publishing Switzerland 2014
Patent Ductus Arteriosus Ligation
(1)
Department of Pediatric Cardiothoracic Surgery, Janet Weis Children’s Hospital, 100 N. Academy Av. MC 27-10, Danville, PA 17822, USA
Abstract
Patent ductus arteriosus (PDA) is an abnormal communication between the aorta and the pulmonary artery. It occurs in 1 in 2,000 term births but it can be present in over 70% of infant born at or prior to 32 weeks.. There is a female predominance.
Patent ductus arteriosus (PDA) is an abnormal communication between the aorta and the pulmonary artery. It occurs in 1 in 2,000 term births but it can be present in over 70 % of infants born at or prior to 32 weeks. There is a female predominance.
1.
Pathophysiology:
(a)
Embryology [1]:
(i)
The PDA originates from the left sixth aortic arch. It is rarely absent or dual.
(ii)
The circulation in-utero differs markedly from postnatal circulation. Gas exchange occurs in the placenta, which receives blood from the umbilical arteries. Oxygenated blood then returns through the ductus venosus, which joins the inferior vena cava at the level of the hepatic veins. This blood is mixed with the venous return from the superior vena cava in the right atrium. Blood in the right atrium may be shunted across the foramen ovale to the left atrium, and through the left ventricle into the systemic circulation. Blood in the right atrium may also follow the right ventricle path and be pumped into the pulmonary artery. Patency of PDA in fetal life is maintained by regional and circulating prostaglandin. Pulmonary vascular resistance is very high in utero, and much of the blood pumped into the pulmonary artery returns through the PDA into the descending thoracic aorta. Because the PDA is large and communicates with the aorta, pressure in the pulmonary artery is the same as that in the aorta (systemic).
(iii)
After birth the umbilical cord is cut, thereby decreasing ductus venosus return to zero and causing the ductus venosus to constrict and obliterate. Pulmonary vascular resistance drops with expansion of the lungs, which causes pulmonary blood flow to increase. Because return to the left atrium is increased, left atrial pressure causes the foramen ovale to close. Increased oxygen partial pressure, decreased level of circulating prostaglandin and the interplay between circulating bradykinin, histamine, and catecholamines contribute on ductal constriction and, ultimately, its obliteration usually within 72 h from birth in terms neonates. Closure occurs with smooth muscle contraction of circular and longitudinal fibers within the media. Dense fibrous proliferation of the sub-intima permanently seals the lumen over 2–3 week period. The pulmonary and systemic circulations at this point become separate. In premature (less than 32 weeks) infants 88 % will close within the first 8 weeks.
(b)
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Anatomy and associated anomalies:
(i)
PDA usually arises from the upper descending thoracic aorta and attaches to the main pulmonary artery at the origin of the left pulmonary artery. However, its size, shape and location might be variable. Different locations include, but not limited, the undersurface of the right aortic arch to the right pulmonary artery, the Kommerell’s diverticulum in a vascular ring or the innominate/subclavian artery.
(ii)
The PDA is in close proximity with left recurrent laryngeal nerve.
(iii)
PDA may be associated with almost any congenital cardiac anomaly. One of the exceptions is tetralogy of Fallot with absent pulmonary valve where embryologically the PDA is absent in surviving fetuses.