Placental Examination Reveals Umbilical Vein Thrombosis in 19-Week Demise
A 19-week intrauterine foetal demise caused by severe umbilical cord hypercoiling, umbilical venous thrombosis, and placental vascular compromise was documented in a case report. The female foetus, delivered vaginally without instrumentation, showed no external congenital anomalies or cardiac defects following an otherwise uneventful pregnancy. Post-mortem findings identified an umbilical cord with an excessive coiling density averaging approximately seven coils per 5-centimeter segment, well above the standard threshold for hypercoiling.
The pathological evaluation linked the fatal outcome to restricted blood flow and foetoplacental circulatory failure. The 190-gram placenta displayed focal calcification, infarction, and hemorrhage alongside a marginally inserted, three-vessel cord containing two arteries and one vein. Histological examinations confirmed thrombosis of the umbilical vein accompanied by dystrophic calcification. Additional microscopic findings revealed intraplacental embolic material, hyalinized avascular villi, and infarction, pointing to disrupted circulation between the mother and the developing foetus.
Clinical records indicated the pregnancy involved a 40-year-old patient with a gravida 5, para 2, and abortions 3 history. Prenatal genetic testing previously demonstrated a normal female foetal genotype (XX), and a recent anomaly scan reportedly showed normal foetal anatomy and growth. Maternal concern arose after a home Doppler device failed to detect foetal heart tones, prompting an ultrasound confirmation of intrauterine foetal demise at 19 weeks’ gestation.
Foetal measurements at autopsy included a crown-rump length of 15 cm, a crown-heel length of 21 cm, and a head circumference of 18 cm. The scalp exhibited marked congestion, cyanosis, and diffuse subgaleal hemorrhage, while the brain displayed edema and congestion consistent with a hypoxic-asphyxial terminal event. Sections from the scalp and skin over the shoulder showed dermal and subcutaneous edema alongside Grade 1 maceration with epidermal separation, aligning with an intrauterine demise duration of 6-12+ hours. The findings rule out primary congenital malformation syndromes and highlight an acquired vascular mechanism as the proximate cause of death.
Frequently Asked Questions About Cord Hypercoiling and Foetal Demise
What is the umbilical coiling index and how does it diagnose hypercoiling?
The umbilical coiling index (UCI) measures cord coiling by dividing the total number of complete vascular coils by the cord length in centimeters. Hypercoiling is generally defined as a UCI above the 90th percentile for gestational age, or more practically, when a cord exhibits an excessive coiling density of more than two to three coils per 5-centimeter segment.
How did researchers rule out genetic abnormalities in this case?
Prenatal genetic testing performed prior to the demise confirmed a normal female foetal genotype of XX. A recent anomaly scan showed normal foetal anatomy, and the post-mortem examination identified no external congenital anomalies or cardiac defects.
What specific placental lesions indicated foetal vascular malperfusion?
Histological sections of the placenta showed intraplacental embolic material, hyalinized avascular villi, and infarction. These features, combined with umbilical venous thrombosis and dystrophic calcification, demonstrated a severe and localized compromise in foetoplacental blood flow.
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