A single maternal dose of intramuscular diclofenac at 35 weeks of gestation was associated with premature closure of the ductus arteriosus and severe biventricular hypertrophy in a term neonate.
Case Report (n=1)
No
Does maternal exposure to diclofenac during pregnancy cause premature closure of the ductus arteriosus in neonates?
A single dose of maternal diclofenac during the third trimester can cause premature closure of the fetal ductus arteriosus, leading to severe but reversible biventricular hypertrophy.
A male term neonate was admitted to the neonatal intensive care unit in the first hours of life with central cyanosis. Echocardiogram showed severe biventricular hypertrophy, markedly right-sided, tricuspid regurgitation, a patent foramen ovale and a closed ductus arteriosus (CDA). The mother recalled being treated with a single dose of intravenous diclofenac for low back pain 2 weeks earlier. The newborn was started on propranolol with symptomatic improvement and was discharged on day 10. At 1-month follow-up, he showed complete resolution of ventricular hypertrophy and suspended propranolol. In the literature, of the 22 cases of CDA after intrauterine exposure to diclofenac, 11 resolved in utero, 3 required ventilatory and inotropic support and 1 evolved to persistent pulmonary hypertension. In this case, a thorough anamnesis was key to identify the probable cause of an otherwise unexplained transient ventricular hypertrophy. This case also alerts to the fetal risks of non-steroidal anti-inflammatory drugs during the third trimester, requiring close monitoring.
Santos et al. (Tue,) conducted a case report in Premature closure of ductus arteriosus (n=1). Diclofenac was evaluated on Premature closure of ductus arteriosus and biventricular hypertrophy. A single maternal dose of intramuscular diclofenac at 35 weeks of gestation was associated with premature closure of the ductus arteriosus and severe biventricular hypertrophy in a term neonate.