Patent ductus arteriosus
Other names	Persistent ductus arteriosus
Diagram of a cross-section through a heart with PDA
Specialty	Cardiac surgery,paediatrics
Symptoms	Shortness of breath,failure to thrive,tachycardia,heart murmur
Complications	Heart failure,Eisenmenger's syndrome,pulmonary hypertension
Causes	Idiopathic
Risk factors	Preterm birth,congenital rubella syndrome,chromosomal abnormalities,genetic conditions
Diagnostic method	Echocardiography,Doppler,X-ray
Prevention	Screening at birth, high index of suspicion in neonates at risk
Treatment	Nonsteroidal anti-inflammatory drugs (NSAIDs),surgery

Patent ductus arteriosus (PDA) is a medical condition in which theductus arteriosus fails to close afterbirth: this allows a portion of oxygenatedblood from the leftheart to flow back to the lungs from theaorta, which has a higherblood pressure, to thepulmonary 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 increasedwork of breathing andfailure to gain weight at a normal rate. With time, an uncorrected PDA usually leads topulmonary hypertension followed by right-sidedheart failure.

Theductus arteriosus is afetal 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 remainspatent (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 ashypoxia, and has a high occurrence inpremature newborns. Premature newborns are more likely to behypoxic and have PDA due to underdevelopment of the heart and lungs.

If the congenital defecttransposition 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 is inversely linked with gestational age and weight.^[2]

Common symptoms include:^{[citation needed]}

• dyspnea (shortness of breath)

Signs include:^{[citation needed]}

• 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 duringsystole and lower flow duringdiastole)
• cardiomegaly (enlarged heart, reflectingventricular dilation andvolume overload)
• left subclavicular thrill
• bounding pulse
• widenedpulse pressure
• increasedcardiac output
• increasedsystolic pressure
• poor growth^[3]
• differentialcyanosis, i.e. cyanosis of the lower extremities but not of the upper body.

People with patent ductus arteriosus typically present in good health, with normal respirations and heart rate. If the PDA is moderate or large, widenedpulse pressure and bounding peripheral pulses are frequently present, reflecting increased left ventricularstroke 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]

Knownrisk factors include:^[6]

• Preterm birth
• Congenital rubella syndrome
• Chromosomal abnormalities (e.g.,Down syndrome)
• Genetic conditions such asLoeys–Dietz syndrome (would also present with other heart defects),Wiedemann–Steiner syndrome, andCHARGE syndrome.
• Fetal alcohol spectrum disorder

PDA is usually diagnosed usingnoninvasive techniques.Echocardiography (in whichsound waves are used to capture the motion of the heart) and associatedDoppler studies are the primary methods of detecting PDA.Electrocardiography (ECG), in whichelectrodes are used to record theelectrical activity of the heart, is not particularly helpful as no specific rhythms or ECG patterns can be used to detect PDA.^[7]

A chestX-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 enlargedcardiac silhouette and increased blood flow to the lungs.^{[citation needed]}

• 
  Illustration of PDA
• 
  PDA
• 
  An echocardiogram of a stented persistingductus 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.

Some evidence suggests that intravenous NSAIDs, such asindomethacin, 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 ofkidney complications.^[9]

Symptomatic PDA can be treated with bothsurgical and non-surgical methods.^[10]

Neonates without adverse symptoms may simply be monitored asoutpatients.^{[citation needed]}

Surgically, the DA may be closed by ligation (though support in premature infants is mixed).^[11] This can either be performed manually and be tied shut, or with intravascular coils or plugs that leads to formation of athrombus in the DA.^{[citation needed]}

Devices developed byFranz Freudenthal block the blood vessel with woven structures ofnitinol wire.^[12] Newer procedures performed effectively in older, bigger children include catheter PDA occlusion and video-assisted thoracoscopic PDA clipping.^[13]

Becauseprostaglandin E2 is responsible for keeping the DA open, NSAIDs (which can inhibit prostaglandin synthesis) such asindomethacin or a special form ofibuprofen have been suggested as therapy to initiate PDA closure.^[3][14][15] Findings from a 2015 systematic review concluded that, for closure of a PDA in preterm and/or low birth weight infants, ibuprofen is as effective as indomethacin. It also causes fewer side effects (such as transientacute kidney injury) and reduces the risk ofnecrotising enterocolitis.^[16] The evidence supporting the effectiveness and safety of paracetamol (acetaminophen) is less clear.^[17] A review and meta-analysis showed thatparacetamol may be effective for closure of a PDA in preterm infants.^[18] A 2018network meta-analysis that compared indomethacin, paracetamol and ibuprofen at different doses and administration schemes among them found that a high dose of oral ibuprofen may offer the highest likelihood of closure in preterm infants.^[19][20][21] However, a 2020 (updated in 2025) systematic review found that early (≤7 days of life) or very early (≤72 hours of life) pharmacological treatment of symptomatic PDA does not reduce death or other poor clinical outcomes in preterm infants but instead increases their exposure to NSAIDS.^[22] Vasodilator therapy is suitable for people with Eisenmenger physiology. To assess improvement in people withEisenmenger physiology, close monitory of toe oxygen saturation is required, for there exists a chance of reversal after a successful right-to-left shunt^{[citation needed]}

Whileindometacin can be used to close a PDA, some neonates require their PDA be kept open. Keeping aductus arteriosus patent is indicated in neonates born with concurrent heart malformations, such astransposition of the great vessels. Drugs such asalprostadil, aPGE-1 analog, can be used to keep a PDA open until the primary defect is corrected surgically.^{[citation needed]}

If left untreated, the disease may progress from left-to-right shunt (acyanotic heart) to right-to-left shunt (cyanotic heart), calledEisenmenger's syndrome.Pulmonary hypertension is a potential long-term outcome, which may require a heart and/or lungtransplant. Another complication of PDA isintraventricular hemorrhage.^{[citation needed]}

Robert Edward Gross, MD performed the first successful ligation of a patent ductus arteriosus on a seven-year-old girl atChildren's Hospital Boston in 1938.^[23]

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.^{[citation needed]}

• 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.

• Congenital heart defects
• Neonatology

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