Patent ductus arteriosus
Patent ductus arteriosus (PDA) is a medical condition in which the ductus arteriosus fails to close after birth: this allows a portion of oxygenated blood from the left heart to flow back to the lungs through the aorta, which has a higher blood pressure, to the pulmonary artery, which has a lower blood pressure. Symptoms are uncommon at birth and shortly thereafter, but later in the first year of life there is often the onset of an increased work of breathing and failure to gain weight at a normal rate. With time, an uncorrected PDA usually leads to pulmonary hypertension followed by right-sided heart failure.
Patent ductus arteriosus
Persistent ductus arteriosus
Screening at birth, high index of suspicion in neonates at risk
Nonsteroidal anti-inflammatory drugs (NSAIDs), surgery
The ductus arteriosus is a fetal blood vessel that normally closes soon after birth. This closure is caused by vessel constriction immediately after birth as circulation changes occur, followed by the occlusion of the vessel’s lumen in the following days.[1] In a PDA, the vessel does not close, but remains patent (open), resulting in an abnormal transmission of blood from the aorta to the pulmonary artery. PDA is common in newborns with persistent respiratory problems such as hypoxia, and has a high occurrence in premature newborns. Premature newborns are more likely to be hypoxic and have PDA due to underdevelopment of the heart and lungs.
If the congenital defect transposition of the great vessels is present in addition to a PDA, the PDA is not surgically closed since it is the only way that oxygenated blood can mix with deoxygenated blood. In these cases, prostaglandins are used to keep the PDA open, and NSAIDs are not administered until surgical correction of the two defects is completed.
In full-term newborns, PDA occurs in 1 in 2,000 births, and accounts for 5–10% of congenital heart disease cases. PDA occurs in 20–60% of all premature newborns, where its incidence inversely linked with gestational age and weight.[2]
Common symptoms include:
Signs include:
People with patent ductus arteriosus typically present in good health, with normal respirations and heart rate. If the PDA is moderate or large, widened pulse pressure and bounding peripheral pulses are frequently present, reflecting increased left ventricular stroke volume and diastolic run-off of blood into the (initially lower-resistance) pulmonary vascular bed.[4] Eisenmenger physiology is pulmonary hypertension due to a left-to-right shunt. Prominent suprasternal and carotid pulsations may be noted secondary to increased left ventricular stroke volume.[5]
Known risk factors include:[6]
Illustration of PDA
PDA
An echocardiogram of a stented persisting ductus arteriosus: One can see the aortic arch and the stent leaving. The pulmonary artery is not seen.
An echocardiogram of a coiled PDA: One can see the aortic arch, the pulmonary artery, and the coil between them.
PDA is usually diagnosed using noninvasive techniques. Echocardiography (in which sound waves are used to capture the motion of the heart) and associated Doppler studies are the primary methods of detecting PDA. Electrocardiography (ECG), in which electrodes are used to record the electrical activity of the heart, is not particularly helpful as no specific rhythms or ECG patterns can be used to detect PDA.[7]
A chest X-ray may be taken, which reveals overall heart size (as a reflection of the combined mass of the cardiac chambers) and the appearance of blood flow to the lungs. A small PDA most often accompanies a normal-sized heart and normal blood flow to the lungs. A large PDA generally accompanies an enlarged cardiac silhouette and increased blood flow to the lungs.
Prevention[edit]
Some evidence suggests that intravenous NSAIDs, such as indomethacin, administration on the first day of life to all preterm infants reduces the risk of developing a PDA and the complications associated with PDA.[8] Intravenous Indomethacin treatment in premature infants also may reduce the need for surgical intervention.[8] Administering ibuprofen probably helps to prevent PDA and reduce the need for surgery but it also likely increases the risk of kidney complications.[9]
Prognosis[edit]
If left untreated, the disease may progress from left-to-right shunt (acyanotic heart) to right-to-left shunt (cyanotic heart), called Eisenmenger's syndrome. Pulmonary hypertension is a potential long-term outcome, which may require a heart and/or lung transplant. Another complication of PDA is intraventricular hemorrhage.
History[edit]
Robert Edward Gross, MD performed the first successful ligation of a patent ductus arteriosus on a seven-year-old girl at Children's Hospital Boston in 1938.[23]
Adult[edit]
Since PDA is usually identified in infants, it is less common in adults, but it can have serious consequences, and is usually corrected surgically upon diagnosis.