In Utero Congestive Heart Failure Due to Maternal Indomethacin Treatment for Polyhydramnios and Premature Labour in a Fetus With Antenatal Closure of the Foramen Ovale

Abstract

A case of severe fetal congestive heart failure due to occlusion of the ductus arteriosus in a mother treated with indomethacin for polyhydramnios and premature contractions is described. Closure of the fetal foramen ovale that escaped detection by prenatal echocardiography was later demonstrated at neonatal autopsy. This case suggests that indomethacin treatment in a ductus‐dependent fetus may be hazardous. Therefore, careful surveillance of the fetus exposed to indomethacin in utero is warranted.

PREMATURE CLOSURE OF THE DUCTUS ARTERIOSUS: VARIABLE RESPONSE AMONG MONOZYGOTIC TWINS AFTERIN UTEROEXPOSURE TO INDOMETHACIN

“…In line with the suggestion made by Achiron et al [4] it seems that a predisposition is required that renders one twin more susceptible to developing hydrops than the other. In our two sets of monozygotic twins evidence of twin to twin transfusion was documented clinically and pathologically in the second case and pathologically in the first case.…”

“…Premature constriction creates right ventricular overload. The resultant pressure elevation causes tricuspid valve regurgitation, right ventricular failure, and pulmonary hypertension [4,12]. Fetal hydrops has also been reported following indomethacin treatment.…”

“…Fetal hydrops has also been reported following indomethacin treatment. Hallak et al [12] described a set of twins in which one became hydropic after in utero exposure to indomethacin; fetal hydrops had been reversed upon discontinuation of therapy; and pregnancy progressed to 37 weeks without further complication [4,12].…”

“…The associated side effect of constriction of the fetal ductus arteriosus was noted shortly thereafter, and indomethacin was quickly adopted in the management of neonates with persistent fetal circulation [2]. Other fetal and neonatal side effects of indomethacin exposure also have been reported, including renal insufficiency; altered platelet and neutrophil function; compromised blood flow in the mesenteric, renal, cerebral, and peripheral circulation; necrotizing enterocolitis; intracranial hemorrhage; tricuspid regurgitation; ventricular hypertrophy; and hydrops fetalis [2][3][4].…”

A Review of Findings in Fetal Cardiac Section Drawings

“…This will be associated with symmetric diagnoses of the first case. The possible causes include a hypoplastic left ventricle, as in hypoplastic left heart syndrome with aortic atresia, 21 early severe aortic stenosis or coarctation, 18 and early mitral stenosis or regurgitation, but also, there is an association with a left persistent superior vena cava, total anomalous pulmonary venous drainage, and premature closure of the ductus arteriosus [22][23][24] or foramen ovale. 25,26 Conversely, case 2 can represent a large right ventricle, and mostly the symmetric diagnoses of the first case plus a few originals must be considered.…”