Abstract

A patent ductus arteriosus (PDA) results from the failure of the ductus arteriosus to close within 72 hours after birth. In most neonates, a PDA can lead to significant morbidities and often warrants pharmacologic intervention for closure. Common pharmacologic interventions include indomethacin, ibuprofen, and acetaminophen. In cases of ductal-dependent congenital heart defects (CHDs), such as hypoplastic left heart syndrome, it is imperative to keep the ductus arteriosus patent to maintain adequate pulmonary or systemic circulation until surgical intervention can be performed. The only proven pharmacologic agent used for this indication is prostaglandin E1 (PGE1) commonly in the form of intravenous alprostadil. This case report describes a neonate with multiple cardiac and genetic anomalies that required increased alprostadil infusion after exposure to rectal and oral acetaminophen. The patient initially presented with a large PDA on echocardiogram (ECHO); however, after an incidental finding of a small PDA on ECHO, the administration of as needed rectal acetaminophen was discontinued out of concern for its effects on patency. After a few days of increased prostaglandin therapy and 2 reassuring ECHO results, the patient was given oral acetaminophen on an as needed basis. Within 24 hours of restarting the acetaminophen, the repeated ECHO showed a reduction in PDA and flow. In patients with ductal-dependent cardiac lesions, it is important to maintain PDA patency and, therefore, introducing a medication with antiprostaglandin properties should be avoided.

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