Location
Philadelphia, PA
Start Date
1-5-2024 1:00 PM
End Date
1-5-2024 4:00 PM
Description
INTRODUCTION
The ductus arteriosus (DA) is a cardiac structure present in utero, allowing for the bypass of the pulmonary circulation during fetal development. The DA closes within 24-48 hours of birth. DA patency is maintained in utero by a low oxygen gradient in the blood, endothelial NO production, and prostaglandins E1 and E21. Premature closure of the DA is a rare condition and can be idiopathic, a result of abnormal levels of circulating prostaglandins, or secondary to maternal ingestion of non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or polyphenol-rich foods2. Prenatal closure of the DA can lead to cardiovascular dysfunction, resulting in pulmonary hypertension, right heart failure, fetal hydrops, and fetal demise. Placental insufficiency can also predispose fetuses to premature ductal closure1.
METHODS
This case study was performed retrospectively using an autopsy report following intrauterine fetal demise. The diagnosis of prenatal DA closure is supported by the history of multiple exposures known to cause DA closure, including potential contributions from prostaglandin synthase-inhibiting medications. Permanent ductus response to NSAIDs remains limited prior to 31 weeks, with studies showing that from 24-32 weeks, fetal exposure to NSAIDs is often reversible with the removal of offending medication. While diagnosis can be made with sonography, it is often undiagnosed since most cases are subclinical3.
RESULTS
A 19-year-old G1P0 female at 35 weeks and 1 day gestation, with a past medical history of migraines, presented to the OB emergency department following an ultrasound where fetal heart tones were undetectable. Diagnosis of intrauterine fetal demise was confirmed in the OB ED. The pregnancy had been complicated by intrauterine fetal growth restriction and anemia in the third trimester. She was on prophylactic low-dose aspirin4. The patient was admitted for induction of labor and vaginally delivered a non-viable fetus at 35w2d. Upon inspection following delivery, the cord appeared to have multiple infarcts along its length and was thinner at the umbilical insertion on the infant. The family consented to an autopsy, which determined the cause of death to be a non-patent ductus arteriosus.
DISCUSSION
The cause of intrauterine fetal demise, in this case, was premature closure of the ductus arteriosus. Whether this was the result of maternal ingestion of NSAIDs, polyphenol-rich foods, or insufficient oxygen supply to the fetus secondary to maternal anemia is unclear at this time. Upon review of her prenatal records, nothing was identified as a cause of premature closure of the DA. While the patient was on low-dose aspirin prophylaxis, this is not known to be associated with ductal closure4. Idiopathic fetal ductal closure, without evidence of maternal use of ductal constrictive agents or structural cardiac defect5, is rare. The fetus had an atrial septal defect, but the heart defects typically associated with premature closure of the ductus arteriosus include Tetralogy of Fallot and a Truncus Arteriosus3. The patient had one postpartum follow-up and was doing well at the time. The ultimate cause of the premature closure of the DA remains unknown in this case.
Embargo Period
7-3-2024
Included in
Premature closure of the ductus arteriosus as a cause of intrauterine fetal demise: A case report
Philadelphia, PA
INTRODUCTION
The ductus arteriosus (DA) is a cardiac structure present in utero, allowing for the bypass of the pulmonary circulation during fetal development. The DA closes within 24-48 hours of birth. DA patency is maintained in utero by a low oxygen gradient in the blood, endothelial NO production, and prostaglandins E1 and E21. Premature closure of the DA is a rare condition and can be idiopathic, a result of abnormal levels of circulating prostaglandins, or secondary to maternal ingestion of non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or polyphenol-rich foods2. Prenatal closure of the DA can lead to cardiovascular dysfunction, resulting in pulmonary hypertension, right heart failure, fetal hydrops, and fetal demise. Placental insufficiency can also predispose fetuses to premature ductal closure1.
METHODS
This case study was performed retrospectively using an autopsy report following intrauterine fetal demise. The diagnosis of prenatal DA closure is supported by the history of multiple exposures known to cause DA closure, including potential contributions from prostaglandin synthase-inhibiting medications. Permanent ductus response to NSAIDs remains limited prior to 31 weeks, with studies showing that from 24-32 weeks, fetal exposure to NSAIDs is often reversible with the removal of offending medication. While diagnosis can be made with sonography, it is often undiagnosed since most cases are subclinical3.
RESULTS
A 19-year-old G1P0 female at 35 weeks and 1 day gestation, with a past medical history of migraines, presented to the OB emergency department following an ultrasound where fetal heart tones were undetectable. Diagnosis of intrauterine fetal demise was confirmed in the OB ED. The pregnancy had been complicated by intrauterine fetal growth restriction and anemia in the third trimester. She was on prophylactic low-dose aspirin4. The patient was admitted for induction of labor and vaginally delivered a non-viable fetus at 35w2d. Upon inspection following delivery, the cord appeared to have multiple infarcts along its length and was thinner at the umbilical insertion on the infant. The family consented to an autopsy, which determined the cause of death to be a non-patent ductus arteriosus.
DISCUSSION
The cause of intrauterine fetal demise, in this case, was premature closure of the ductus arteriosus. Whether this was the result of maternal ingestion of NSAIDs, polyphenol-rich foods, or insufficient oxygen supply to the fetus secondary to maternal anemia is unclear at this time. Upon review of her prenatal records, nothing was identified as a cause of premature closure of the DA. While the patient was on low-dose aspirin prophylaxis, this is not known to be associated with ductal closure4. Idiopathic fetal ductal closure, without evidence of maternal use of ductal constrictive agents or structural cardiac defect5, is rare. The fetus had an atrial septal defect, but the heart defects typically associated with premature closure of the ductus arteriosus include Tetralogy of Fallot and a Truncus Arteriosus3. The patient had one postpartum follow-up and was doing well at the time. The ultimate cause of the premature closure of the DA remains unknown in this case.