-The group agreed on sets of uniform sampling criteria, placental gross descriptors, pathologic terminologies, and diagnostic criteria. The terminology and microscopic descriptions for maternal vascular malperfusion, fetal vascular malperfusion, delayed villous maturation, patterns of ascending intrauterine infection, and villitis of unknown etiology were agreed upon. Topics requiring further discussion were highlighted. Ongoing developments in our understanding of the pathology of the placenta, scientific bases of the maternofetoplacental triad, and evolution of the clinical significance of defined lesions may necessitate further refinements of these consensus guidelines. The proposed structure will assist in international comparability of clinicopathologic and scientific studies and assist in refining the significance of lesions associated with adverse pregnancy and later health outcomes.

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Context.- A severe third wave of COVID-19 disease affected Ireland in the first 3 months of 2021. In this wave, 1 second trimester miscarriage and 6 stillbirths were observed in the Irish population due to placental insufficiency as a result of SARS-CoV-2 placentitis. This observation was at odds with the country's previous experience with COVID-19 disease in pregnant mothers. Objective.- To describe the clinical and pathological features of these pregnancy losses. Design.- Retrospective review of clinical and pathological data of cases of second trimester miscarriage, stillbirth or neonatal death identified by perinatal pathologists as being due to SARS-CoV-2 placentitis during the third wave of COVID-19 in Ireland. Results.- Clinical and pathological data was available for review in 6 pregnancies. Sequencing or genotyping of the virus identified SARS-CoV-2 Alpha (B.1.1.7) in all cases. Three of the 6 cases had maternal thrombocytopenia, while fetal growth restriction was not prominent suggesting a rapidly progressive placental disease. Conclusions.- The identification of SARS-CoV-2 Alpha in all these cases suggests that the emergence of the variant was associated with an increased risk of fetal death due to SARSCoV-2 placentitis when compared to the original virus. Maternal thrombocytopenia, may have potential as a clinical marker of placentitis but other inflammatory markers need investigation. Three of the 6 women had been assessed for reduced fetal movements in hospital some days before the fetal deaths actually occurred; this could suggest that there may be a window for intervention in some cases.

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Wilson-Mikity syndrome (WMS) is a disorder of uncertain origin. It is sometimes considered a variant of bronchopulmonary dysplasia (BPD), but it lacks the characteristic microscopic stigmata of destruction and fibrosis caused by the barotrauma and oxygen toxicity of ventilator support. Conventional clinical and autopsy studies of WMS have failed to identify the underlying pathophysiology. This study evaluated bombesin-containing pulmonary neuroendocrine (PNE) cells in eight WMS cases, seven cases of BPD, and five controls, using the immunoperoxidase technique. The PNE cells were quantified by established morphometric techniques. The percentage of airways containing PNE cells in WMS (mean, 85.56%) was similar to that in the controls (mean, 82.6%) but significantly greater than that in BPD (mean, 21.28%) (p < .001). Measurement of intraepithelial PNE cell cytoplasm within the bombesin-immunopositive airways demonstrated apparent PNE cell hyperplasia in both WMS and BPD. Prominent numbers of PNE cells were also present in the respiratory bronchioles and alveolar units in WMS. The increased PNE cells in WMS may reflect chronic hypoxia from hypoventilation and or autonomic dysfunction. The profile in BPD may reflect a similar pathophysiology but complicated by ventilator-induced injury to airway epithelium.