Nonneoplastic placental conditions and abnormalities

Placental findings in specific conditions

Intrauterine fetal demise

Last author update: 1 October 2011
Last staff update: 27 October 2022 (update in progress)

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PubMed Search: Intrauterine fetal demise[title] placental[title]

Mandolin S. Ziadie, M.D.
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Cite this page: Ziadie MS. Intrauterine fetal demise. website. Accessed December 10th, 2022.
Definition / general
  • Intrauterine fetal demise that may be due to maternal factors (diabetes, preeclampsia, infection), placental abnormalities (vasculopathy, ischemia, infarction) or fetal anomalies (chromosomal disorders, congenital anomalies, Arch Pathol Lab Med 1976;100:367)
  • Chorioamnionitis, deciduitis or villitis may be present, thus warranting culture of the placenta
Recurrent fetal loss
  • Most common causes of intrauterine fetal death are genetic, infection, thrombotic disorders and autoimmune disease
  • Other causes include environmental (smoking, alcohol) and endocrine (diabetes)
  • Rate of occurrence varies based on gestational age
  • Early recurrent loss is generally due to genetic abnormalities; late loss is more often associated with infection / inflammation
  • First trimester: genetic (aneuploidy and other chromosomal abnormalities), thrombophilic and autoimmune
  • Second and third trimester: autoimmune (antiphospholipid syndrome), uterine anatomic abnormalities (polyps, leiomyomas, septae, cervical incompetence, etc.), maternal hypertension, thrombophilia and infection / inflammation
Gross description
  • Degree of maceration of the fetus and involution of the placenta are helpful indicators for the length of intrauterine demise
Microscopic (histologic) description
  • Microscopic changes are similar to those seen in fetal thrombotic vasculopathy (FTV) but are seen diffusely throughout the placenta
  • Early / recent demise ( > 24 - 48 hours) shows nuclear debris in blood vessels or villous vessels
  • This is followed by vascular septation in larger vessels with sequential changes in smaller vessels and terminal villi then villous fibrosis
  • Other nonspecific changes include calcification / increased mineralization of the trophoblastic basement membrane
Microscopic (histologic) images

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