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Patent ductus arteriosus






The arterial duct is one of the fetal shunts and is closed in 3-4 days in 90% of term and ‘well’ premature babies. 
The duct closes in response to a rise in oxygen tension after birth and a fall in circulating prostaglandins. 


Patent ductus arteriosus (PDA) is seen in 50% of VLBW infants due to low oxygen tension, continuing high prostaglandin levels, or abnormal stimuli such as acidosis and expansion of the circulating volume.


Aorto-pulmonary shunting though the PDA causes high pulmonary blood flow, worsening RDS, cardiac failure and low diastolic pressure. 


PDA is a risk factor for intraventricular haemorrhage, necrotizing enterocolitis and CLD.


 PDA typically becomes symptomatic at 5-10 days as pulmonary vascular resistance falls; it presents with worsening respiratory function, bounding pulses, a continuous murmur and chest radiograph that shows cardiomegaly and increased lung shadowing.


 Diagnosis is confirmed by echocardiography. 


Conventional treatment for symptomatic PDA is fluid restriction, diuretics (furosemide) or medical closure with indomethacin or ibuprofen. Non-steroidal anti-inflammatory drugs (NSAIDs) may worsen renal function, and have been associated with gastrointestinal haemorrhage and perforation. These agents
are contraindicated in the presence of thrombocytopenia.


Surgical closure of symptomatic PDA is indicated for failed medical treatment or when NSAIDs are contraindicated.

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