Patent ductus arteriosus (PDA), one of the more common cardiac defects present at birth, is the persistence of an opening between the pulmonary artery and aorta.
This opening is as a result of failure of the physiological fetus ductus arteriosus to close, which normally occurs soon after birth. This hole causes high-pressure oxygenated blood from the aorta to mix with oxygen-depleted blood from the pulmonary artery.
As a consequence, significant strain is placed on the heart and pressure within the pulmonary arteries is dramatically increased.
Etiology and Pathophysiology
Often, PDA has no clear-cut cause; however, it is believed that genetic and environmental factors may be involved. During fetal development, a connection between the two major arteries leaving the heart (namely, the pulmonary artery and aorta) is imperative for the fetal circulation.
The ductus arteriosus functions as a shunt to divert blood away from the fetal lungs as they develop and oxygen is acquired directly from the mother’s circulation.
This shunt closes within three days after birth, but may take longer in premature babies.
The ductus arteriosus remains open during fetal development thanks to high levels of prostaglandins and low oxygen tension in the nonfunctional pulmonary system.
The placenta is a major source of fetal prostaglandins and its removal after birth allows for the lungs to expand and become metabolically active, providing for the breakdown of most prostaglandins.
This, in combination with increased pulmonary oxygen tension in healthy full-term infants, normally causes functional closure of the ductus arteriosus within 15 hours after birth.
Several studies have suggested that PDA occurs in premature babies due to the lungs being underdeveloped and poor metabolizers of prostaglandins.
Other risk factors that may be associated with PDA is a positive family history of cardiac defects, and genetically linked conditions like Down syndrome.
Maternal infection with German measles during pregnancy can cause damaging effects to the fetal heart and circulatory system and put the infant at greater risk of PDA.
Studies have also shown that children born at higher altitudes have an increased susceptibility to PDA.
Usually a small PDA does not cause any significant difficulties, but larger ones may cause a wide range of problems.
One such complication is pulmonary hypertension, which can cause irreversible damage to the lungs. Eisenmenger syndrome may develop as a result of a large PDA.
This syndrome occurs when the left-to-right shunting of blood causes the pulmonary arterial pressure to build up and reach systemic levels, which subsequently causes the direction of the flow of blood to become bi-directional. It can lead to congestive heart failure and sudden death.
Heart failure in PDA develops because of an excessive workload on the heart. It enlarges so much that the heart wall is weakened, such that the heart can no longer pump blood effectively.
The prognosis in such cases is extremely poor. In addition to this, PDA can cause damage to the lining of the pulmonary artery, which increases the risk of infectious endocarditis.
PDA in premature infants may cause more serious consequences than in those born at full term. These infants may have damage to other organs such as the intestines and kidneys due to reduced perfusion in these areas and increased flow through the lungs.