The ductus arteriosus connects the pulmonary artery with the aorta, allowing blood to bypass the lungs. It usually stops functioning within 3-5 days of birth and closes entirely within the first three weeks of life.
Patent ductus arteriosus (PDA) occurs when it fails to close after birth. The reasons it fails to close are unclear.
Causes:
Much more common in premature babies
Can be related to a genetic condition e.g. Down's syndrome
Maternal conditions e.g. diabetes or rubella
Pathophysiology:
Prostaglandin E2 (produced by the placenta) keeps the ductus arteriosus open during pregnancy - levels fall following birth, resulting in closure
Pressure in aorta is higher than in the pulmonary vessels - blood flows across PDA from the aorta to the pulmonary artery - left to right shunt
Leads to pulmonary hypertension and right ventricular hypertrophy
Can then lead to left ventricular hypertrophy
Symptoms usually present 3-5 days after birth when the duct begins to close
Symptoms depend on the size of the lesion:
Small - asymptomatic
Moderate - congestive heart failure with failure to thrive
Large - poor feeding, severe failure to thrive, recurrent LRTI (preterm infants may experience failure to wean from ventilation)
Clinical features:
Palpate - palpable liver in heart failure, bounding pulses and wife pulse pressure
Auscultation - continuous machinery murmur typically heard at the upper left sternal border (best heard below the left clavicle), thrill at upper left sternal border
Investigations:
Echocardiogram and doppler (most useful)
CXR and EXG are less useful
Management:
Preterm - good probability of spontaneous closure - indomethacin/ibuprofen (inhibit prostaglandins)
Term - less likely to close spontaneously - closure - catheter closure or PDA ligation (thoracotomy)