Patent ductus arteriosus

Common symptoms include:

• dyspnea (shortness of breath)

Signs include:

• tachycardia (a heart rate exceeding the normal resting rate)
• continuous "machine-like" (also described as "rolling-thunder" and "to-and-fro") heart murmur (usually from aorta to pulmonary artery, with higher flow during systole and lower flow during diastole)
• cardiomegaly (enlarged heart, reflecting ventricular dilation and volume overload)
• left subclavicular thrill
• bounding pulse
• widened pulse pressure
• increased cardiac output
• increased systolic pressure
• poor growth[1]
• differential cyanosis, i.e. cyanosis of the lower extremities but not of the upper body.

Patients 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. [2]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.

Known risk factors include:

• Preterm birth
• Congenital rubella syndrome
• Chromosomal abnormalities (e.g., Down syndrome)
• Genetic conditions such as Loeys–Dietz syndrome (would also present with other heart defects), Wiedemann–Steiner syndrome, and CHARGE syndrome.

Phonocardiograms from normal and abnormal heart sounds

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.[3]

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.

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  Illustration of Patent Ductus Arteriosus
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  Patent ductus arteriosus
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  An echocardiogram of a stented persisting ductus arteriosus: One can see the aortic arch and the stent leaving. The pulmonary artery is not seen.
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  An echocardiogram of a coiled persisting ductus arteriosus: One can see the aortic arch, the pulmonary artery, and the coil between them.

Some evidence suggests that 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. Indomethacin treatment in premature infants also may reduce the need for surgical intervention.[4] Administering ibuprofen probably helps to prevent PDA and reduce the need for surgery but it probably increases the risk of kidney complications.[5]

Symptomatic PDA can be treated with both surgical and non-surgical methods.[6]

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.

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.[15]

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.

• George Alexander Gibson

• Patent Ductus Arteriosus Causes from US Department of Health and Human Services
• Patent Ductus Arteriosus from Merck
• Patent ductus arteriosus information for parents.