How Long Will It Take To Recover From Patent Ductus Arteriosus & How Long Do The Symptoms Last?

In the US, the estimated incidence of patent ductus arteriosus in children born at term is around 0.02-0.006% of live births.1

The spontaneous closure of patent ductus arteriosus occurs in about 72-75% of premature infants <3 months.1

How Long Will It Take To Recover From Patent Ductus Arteriosus?

Normally, the functional closure of patent ductus arteriosus in infants born at term occurs by approximately 15 hours of life. However, anatomic closure occurs in several weeks. In functional closure, there is a tendency of the ductus arteriosus to reopen as it occurs by contraction of the muscular wall of the ductus, but in anatomic closure, the closure is permanent in which the closure occurs by the fibrous proliferation of the tissues.1

Spontaneous closure of the ductus arteriosus is also quite common in infants; however, spontaneous closure in infants >3 months is rare.

Spontaneous closure occurs in about 72-75% of premature infants <3 months. The closure rate with pharmacological therapy is around 80-92%.1

Minimal hospitalization is required after the treatment of patent ductus arteriosus. The patient can be discharged on the same day after catheter closure of the patent ductus arteriosus and for patients who undergo standard surgery with thoracotomy, the hospitalization is less than 3 days.1

How Long Do The Symptoms Of Patent Ductus Arteriosus Last?

The symptoms of patent ductus arteriosus may last depend on the viability of the ductus from infancy to adulthood if it goes undetected. The symptoms of patent ductus arteriosus are due to the delay in the closure of the ductus arteriosus. The patient may be asymptomatic to showing signs of congestive heart failure. The presenting symptoms may include increased heart rate, increased sweating, difficulty/inability feeding, weight loss of no weight gain, cough, lower respiratory tract infections, pneumonia, or atelectasis, failure to thrive during infancy, congestive heart failure, atrial arrhythmia, and cyanosis of the lower extremities.1

Usually, patent ductus arteriosus is associated with other cardiac anomalies, such as pulmonary atresia or coarctation, or interrupted aortic arch. Therefore, it is important to identify these abnormalities for additional management and the resolution of symptoms. It is important to close the defect due to concerns of infective endocarditis. Best results are obtained if the PDA is closed before the age of 3 years; however, the chances of pulmonary vascular resistance and pulmonary hypertension increases if the lesion is closed after the age of 3 years. The closure of ductus arteriosus does not reverse preexisting pulmonary vascular disease and premature infants with a significant PDA may develop bronchopulmonary dysplasia. Generally, after the closure of patent ductus arteriosus, there are no further symptoms or any cardiac sequelae.1

Patent ductus arteriosus (PDA) is considered a normal anatomical structure in fetal life that allows the blood to flow to other organs and structure bypassing the pulmonary circulation. Generally, the functional closure of ductus arteriosus occurs in the first 10-18 hours of life. However, the failure of closure of the ductus arteriosus after birth leads to patent ductus arteriosus, which is the communication between the aorta and the pulmonary artery resulting in the left-to-right shunt. The incidence of patent ductus arteriosus in the US children born at term is around 0.02-0.006% of live births. The incidence is 20-60% greater in premature children, low birth weight infants, perinatal asphyxia, and children born at high altitude. In the absence of any risk factors, females are twice more susceptible to PDA occurrence than males.1

Causes of Patent Ductus Arteriosus

There have been familial cases of patent ductus arteriosus, but no genetic cause has been determined yet. In some populations, it has been linked to a recessive trait labeled PDA1 on chromosome 12. Other causes include premature birth, teratogens (congenital rubella infection in the first trimester of pregnancy), maternal amphetamine or phenytoin use, fetal alcohol syndrome, low birth weight (LBW), high altitude and low atmospheric oxygen tension, prostaglandins, and hypoxia.1

The patency of PDA is maintained by the continuous production of prostaglandin E2 by the ductus and placenta. Early closure of the ductus during fetal life may lead to right heart failure.1

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