Placental CD34 immunohistochemistry in fetal vascular malperfusion in stillbirth

Abstract

Aim To assess the use of CD34 immunostaining in diagnosing of fetal vascular malperfusion (FVM) in stillborns. Methods We examined 25 independent clinical (pregnancy and fetal outcomes) and 48 placental phenotypes in 100 placentas of consecutive stillborns at ≥20 weeks of gestation. Group 1 comprised 34 cases with no distal villous FVM; Group 2 comprised 36 placentas with clustered distal villous FVM (sclerotic villi, hypovascularity, stromal vascular karyorrhexis, and/or mineralization) determined using hematoxylin–eosin staining not upgraded by CD34 immunostaining, and Group 3 comprised 30 placentas with FVM diagnosed or upgraded by CD34 immunostaining (distal villous endothelial fragmentation and/or villous hypovascularity). Results Diffuse villous lesions of fetal retention with various degrees were present in approximately 50% of the cases in all groups; however, histological evaluation for FVM was still possible in most stillborns. Abnormal clinical phenotypes were significantly less frequent than abnormal placental phenotypes of FVM (8.6% vs. 24%, respectively). Chronic hypoxic placental injury patterns, fetal blood erythroblastosis, some features of shallow placental implantation, and muscular FVM lesions were most common in Group 2. Only decidual arteriopathy (hypertrophic and or hyaline necrosis/atherosis) was most frequent in Group 3. Conclusion Most distal FVM lesions can be observed on hematoxylin–eosin placental slides only several days following the inciting event. CD34 immunostaining can reveal recent distal villous lesions of FVM featuring segmental villous endothelial fragmentation for de novo diagnosis or for upgrading FVM. Routine CD34 immunostaining has demonstrated FVM to be the major pattern of placental injury in stillborns.

Placental recent/on-going foetal vascular malperfusion with endothelial fragmentation is diagnostically equivalent to established distal villous lesions of foetal vascular malperfusion

“…Clustered linear basement membrane hemosiderosis, or speckled villous core staining, is a feature of FVM as opposed to diffuse deposition secondary to stillbirth because iron uptake by the placenta is an autonomous process, independent of the foetus, which continues after foetal death [36]. In stillbirth, FVM is the most common pattern of placental injury when CD34 immunostaining is applied [37]. When compared with H&E staining, the CD34 increased the sensitivity and/ or upgraded the FVM in stillbirths but not in livebirths, significantly improving the detection of focal or subtle findings of FVM in placental specimens, partic-…”