Patent ductus arteriosus (PDA) is the persistence of a normal fetal structure between the left pulmonary artery and the descending aorta. Persistence of this fetal structure beyond 10 days of life is considered abnormal.
For a related CME/CE activity, see CME/CE – A Newborn Presenting in Extremis.
The ductus is derived from the 6th aortic arch. From the 6th week of fetal life onwards, the ductus is responsible for most of the right ventricular outflow. It contributes to 60% of the total cardiac output throughout the fetal life. Only about 5-10% of its outflow passes through the lungs. The ductus arteriosus is an important structure in fetal development as it contributes to the flow of blood to the rest of the fetal organs and structure. Closure of the ductus before birth may lead to right heart failure. At birth, the ductus normally undergoes closure.
A PDA is variable in its presentation. It may be vary in size from small to large and may not be picked up based on physical exam at birth. The available retrospective data on the natural history of untreated patent ductus arteriosus are poor; however, complications can arise. Spontaneous ductal closure can occur without treatment.
Complications of untreated PDA include bacterial endocarditis, late congestive heart failure (CHF), and the development of pulmonary vascular obstructive disease. PDA can complicate other circulatory or ventilatory abnormalities.
PDA is the fifth or sixth most common congenital cardiac defect. It often is associated with other intracardiac structural defects.
PDA represents 5-10% of all congenital heart diseases, excluding those in premature infants. It occurs in approximately 8 of 1000 live premature births. In term infants, the incidence is about 1 in 2000 births. The female-to-male ratio is 2:1.
Morbidity and mortality rates are directly related to the flow volume through the ductus arteriosus.
A large patent ductus arteriosus may cause CHF; if left untreated for a long period, development of pulmonary vascular obstructive disease may occur. Occasionally, the ductus arteriosus patency can be intermittent.
It is estimated that left untreated, the mortality rate is 20% by age 20 years, 42% by age 45 years, and 60% mortality rate by age 60 years. An estimated 0.6% per year undergo spontaneous closure.
No data support a race predilection.
Females are 2-3 times more likely than males to develop PDA.
Patent ductus arteriosus is a common problem in premature infants and is less likely to be noted as gestational age increases to full term. Incidence ranges from 20% in premature infants older than 32 weeks’ gestation up to 60% in those younger than 28 weeks’ gestation.
Up to 30% of low birth weight infants (<2500 g) develop a patent ductus arteriosus.
Occasionally, an older child is referred with the late discovery of a typical ductus arteriosus murmur (eg, machinery or continuous murmur).
The history is variable depending on the size of the lesion and the coincident left-to-right shunting of blood through the pulmonary circulation.
When the ductus arteriosus is small, no symptoms are present.
A ductus arteriosus with a moderate-to-large left-to-right shunt may be associated with a hoarse cry, cough, lower respiratory tract infections, atelectasis, or pneumonia.
When the defect is large, CHF with dyspnea and poor weight gain or failure to thrive are the main presentations.
Bounding peripheral pulses and wide pulse pressure
Occasionally, with increased pulmonary artery pressure, accentuation of the pulmonic component of the second heart sound is heard.
A grade 1-4 of 6 continuous or machinery murmur is best heard at the upper left sternal border or left infraclavicular area.
An apical diastolic rumble with a large left to right shunt may be present.
Occasionally, auscultation of the PDA reveals numerous clicks or noises resembling shaking dice or a bag of rocks.
The murmur may be only a systolic ejection murmur, or it may be a crescendo/decrescendo systolic murmur that extends into diastole.
Low birth weight
Maternal rubella in the first trimester of pregnancy is thought to be a cause of the seasonal incidence of PDA.
High altitude and low atmospheric oxygen tension have been associated with persistence of the PDA.