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.

The ductus arteriosus is a

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]

Signs and symptoms

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 during systole and lower flow during diastole)
• ventricular dilation and volume overload
  )
• left subclavicular thrill
• bounding pulse
• widened pulse pressure
• increased cardiac output
• increased
  systolic pressure
• poor growth^[3]
• differential cyanosis, 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, widened

Known risk factors include:^[6]

• 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
  .
• Fetal Alcohol Spectrum Disorder

PDA is usually diagnosed using

• 
  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.

Prevention

Some evidence suggests that intravenous NSAIDs, such as

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

Conservative

Neonates without adverse symptoms may simply be monitored as

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 a thrombus in the DA.^{[citation needed]}

Devices developed by

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]

See also

• George Alexander Gibson

References