Amnion nodosum (placenta)
PV bleeding 17 weeks into second pregnancy. Ultrasound confirmed fetal death in utero. Misoprostol-induced labor took place and the placenta was sent for examination. Macroscopic examination revealed a 40g relatively intact placenta showing no significant macroscopically-evident abnormalities. The fetus was morphologically unremarkable and fresh tissue was sent for genetic karyotyping.
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The membranes showed no significant acute inflammatory cell infiltrate that would indicate acute chorioamnionitis, however, as you can see from the images above, scattered clusters of intensely eosinophilic cellular material were present on the amniotic surface of the membranes. These clusters displayed varying degrees of degenerative change and appeared mostly amorphous and granular, but where more preserved, appeared to be partly composed of degenerate foetal squames. Careful inspection also revealed hemosiderin deposition (may not be seen in these images).
100x H&E (1): Degenerate material present on the amniotic surface of the membrane.
20x H&E: Low-power view showing slight prominence of eosinophilic material.
40x H&E: No significant inflammation.
100x H&E (2): Normal amnion interspersed with clusters of eosinophilic degenerate material.
200x H&E: Upon closer inspection, you can see variably preserved cells with rounded nuclei and more abundant eosinophilic cytoplasm, consistent with foetal squamous cells (squames).
Clinical Association: Severe oligohydramnios (associated with fetal renal agenesis, prolonged premature rupture of membranes - also higher percentage in mothers with gestational diabetes and pre-eclampsia).
Pathogenesis: There are a couple of ways that oligohydramnios is thought to result in amnion nodosum: firstly, that the concentrated amniotic fluid starts to adhere to the amniotic surface, causing degeneration of amniotic epithelium, and/or secondly, that in the context of reduced amniotic fluid volume, there is an increase in contact between the fetal and amniotic epithelium, causing erosion and resulting in fetal squames shedding and being incorporated into the eroded surface.
Other findings in this case: The placental disc also showed a mild diffuse chronic villitis without evidence of viral inclusions and chronic deciduitis along with changes consistent with uteroplacental malperfusion and fetal death in utero (prominent syncytial knots, decreased terminal villi showing sclerosis and loss of vessels and resultant increased intervillous space, intra-capillary karyorrhectic debris and obliteration of larger fetal vessels).
- 1. Adeniran AJ, Stanek J. Amnion nodosum revisited: clinicopathologic and placental correlations. Arch Pathol Lab Med, 2007 Dec;131(12):1829-33. Full article link (free access)