L.S. originally presented at 42 years of age G-1, P1001, with an over one-year history of secondary infertility. L.S. and P.R. conceived their first child without delay and delivered via Caesarean section nearly 3 years prior. This delivery was complicated by post-partum hemorrhage and retained placental fragments requiring an emergent dilation and curettage (D&C). Her recovery after this intervention was unremarkable. She nursed for 1 year and had return of regular cyclic menses after weaning.
She had no other history of risk factors for infertility including STI’s, pelvic surgery or symptoms of endocrine dysfunction.
Our initial plan included routine ovarian reserve screening for L.S., a semen analysis for P.R. and an hysterosalpingogram (HSG). The latter was considered especially important in light of the post-partum D&C , as this is a know risk factor for intrauterine adhesions, also known as Asherman Syndrome.
L.S. presented at 7 days after a normal menstrual period for her HSG. A urine pregnancy test was negative in the HSG suite. The exam demonstrated a significant right-sided defect in the uterine cavity with non-filling of that tube, suggesting obstruction. The left tube was patent with normal features. The immediate presumptive diagnosis was intrauterine adhesions.
The following day, L.S. presented for a saline infusion sonogram to further delineate the mass seen at HSG. A urine pregnancy test was positive and transvaginal ultrasound demonstrated an intrauterine gestational sac with measurements consistent with a pregnancy of 5 weeks duration. Initial serum hCG concentration was 3772 IU with a progesterone concentration of 17.7 ng/dl.
At that time we reviewed the limited and largely historical data on inadvertent HSG during pregnancy. The iodinated contrast should be safe at the early gestational age at which she presented and the limited radiation from the fluoroscope would be expected to have an “all or nothing” effect on such an early gestation. Minimal embryonic development and no organ formation were expected to be present at that gestational age.
Complicating this picture was the high risk of spontaneous miscarriage due to age-associated aneuploidy at 42 years.
Serial ultrasounds demonstrated normal development and at approximately 9 weeks of pregnancy, L.S. was transferred to the care of her local Ob/Gyn. Non-invasive prenatal genetic testing and a level 2 obstetric sonogram were normal. Three weeks later, L.S. and P.R. relocated from metropolitan Washington, DC to Mexico City. Her only reported symptom was less fetal movement and greater maternal weight gain than in her prior pregnancy.
At approximately 25 weeks of pregnancy, 3 weeks after her last prenatal visit in the US, she presented for routine care in Mexico City. Evaluation at that time demonstrated acute, severe hydrops fetalis.
She was transferred back to the US for care. Multiple interventions failed to resolve the hydrops and at around 27 weeks an emergency caesarean section was performed for delivery of a female infant who could not be resuscitated, presumably due to pulmonary hypoplasia, and died shortly after .
A complete maternal evaluation was negative for any immunological or infectious factors could have led to the hydrops. An autopsy on the infant revealed no cardiac or other structural abnormalities. Their perinatologists have postulated a possible fetal lymphatic defect as the cause.
To our knowledge, this is the first report of this combination of events. Given the timing, the limited dose of radiation and the inert nature of the contrast, we can think of no mechanism of action for subsequent fetal disease but feel it is important to report this event to the community.
