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The cause of meconium passage in utero is controversial, traditionally being considered evidence of fetal stress and hypoxia, and also associated with intra-amniotic inflammation/infection. It is now recognized to also occur in the absence of fetal stress. Autopsy studies have shown that many term stillborns (SB) have hypoxic/ischemic brain injury and other evidence of stress preceding the time period immediately before demise, including acute thymic involution (ATI); however, these findings, along with placental findings, have not been previously correlated with meconium-stained amniotic fluid (MSAF). 35 structurally normal singleton term SB (21 early term, 14 full/late term) with complete autopsies, including brain and placental examination, were identified. MSAF was visually identified at delivery and confirmed on the placental examination. Autopsy evaluation included brain injury and ATI. Placental evaluation included maternal and fetal vascular malperfusion and acute and chronic inflammatory lesions. Demographic and clinical features were compared. 18 (51%) SB had MSAF, and 17 (49%) had clear amniotic fluid (CAF). The was no significant difference in brain injury in the MSAF vs CAF group, including older gray matter injury (karyorrhexis) (67% vs 47%), recent gray matter injury (red neurons, but no karyorrhexis) (28% vs 35%), white matter injury (50% vs 29%), and hemorrhage (22% vs 24%). Severe ATI was more frequent in the MSAF vs CAF group (61% vs 24%,  p  = .04). There was no significant difference in placental lesions between groups, including acute maternal inflammation (39% vs 18%), acute fetal inflammation (6% vs 6%), fetal vascular malperfusion (11% vs 18%), maternal vascular malperfusion (39% vs 35%), and chronic inflammatory lesions (39% vs 29%). The MSAF group was more likely to be full/late term than early term (72% vs 28%), in contrast to the CAF group (6% vs 94%) ( p  = .0001). There was no difference in other clinical factors evaluated. 51% of term SB had MSAF, and, in contrast to the CAF group, these were significantly more likely to be full/late term. Brain injury was frequent in both MSAF and CAF groups, supporting hypoxia as the mechanism of demise in most of these SB. No placental lesions correlated with MSAF, including inflammation. This suggests that hypoxia is the cause of the MSAF in these SB, but that some additional biologic factor present in the full/late term SB, but not present in the early term SB, including possibly gastrointestinal maturation, is necessary for the meconium passage.

Does in utero meconium passage in term stillbirth correlate with autopsy and placental findings of hypoxia or inflammation?