Failure of placental detachment in accreta placentation is associated with excessive fibrinoid deposition at the utero-placental interface.

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Analysis of 40 placenta accreta specimens revealed that excessive fibrinoid deposition at the utero-placental interface, rather than direct villous invasion, likely disrupts the physiological detachment site and causes failure of placental separation.

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This study analyzed histological specimens from 40 patients with placenta previa accreta and seven controls to investigate the pathophysiology of abnormal placental attachment. The researchers found that dense fibrinoid deposits were present at the utero-placental interface in the majority of accreta cases, whereas these deposits were absent in control samples. These findings suggest that excessive fibrinoid deposition, rather than true invasive villous tissue, may be responsible for the failure of placental detachment by distorting the Nitabuch membrane. This paper is centrally about placenta accreta spectrum disorders, which are distinct from endometriosis and adenomyosis; therefore, it does not explicitly discuss endometriosis or adenomyosis.

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Failure of placental detachment in accreta placentation is associated with excessive fibrinoid deposition at the utero-placental interface. Accepted version Peer-reviewed Repository URI Repository DOI Change log Abstract BACKGROUND: The main histopathologic diagnostic criteria for the diagnosis of placenta accreta for more than 80 years has been the finding of a direct attachment of the villous tissue to the superficial myometrium or adjacent to myometrial fibers without interposing decidua. There have been very few detailed histopathologic studies in pregnancies complicated by placenta accreta spectrum disorders and our understanding of the pathophysiology of the condition remains limited. OBJECTIVE: To prospectively evaluate the microscopic changes used in grading and to identify changes that might explain the abnormal placental tissue attachment. STUDY DESIGN: A total of 40 consecutive cesarean delivery hysterectomy specimens for placenta previa accreta at 32 to 37 weeks of gestation with at least 1 histologic slide showing deeply implanted villi were analyzed. Prenatal ultrasound examination included placental location, myometrial thickness, subplacental vascularity and lacunae. Macroscopic changes of the lower segment were recorded during surgery and areas of abnormal placental adherence were sampled for histology. In addition, 7 hysterectomy specimens with placenta in-situ from the Boyd Collection at 20.5 to 32.5 weeks were used as controls. RESULTS: All 40 patients had a history of at least 2 previous cesarean deliveries and presented with a mainly anterior placenta previa. Of note, 37 (92.5%) cases presented with increased subplacental vascularity, 31 (77.5%) cases with myometrial thinning and all with lacunae. Furthermore, 20 (50%) cases presented with subplacental hypervascularity, lacunae score of >3, and lacunae feeder vessels. Intraoperative findings included anterior lower segment wall increased vascularization in 36 (90.0%) cases and extended area of dehiscence in 18 (45.0%) cases. Immediate gross examination of hysterectomy specimens showed an abnormally attached areas involving up to 30% of the basal plate, starting at <2 cm from the dehiscence area in all cases. Histologic examination found deeply implanted villi in 86 (53.8%) samples with only 17 (10.6%) samples presenting with villous tissue reaching at least half the uterine wall thickness. There were no villi crossing the entire thickness of the uterine wall. There was microscopic evidence of myometrial scarification in all cases. Dense fibrinoid deposits, 0.5 to 2 mm thick, were found at the utero-placental interface in 119 (74.4%) of the 160 samples between the anchoring villi and the underlying uterine wall at the accreta areas and around all deeply implanted villi. In the control group, the Nitabuch stria and basal plate became discontinuous with advancing gestation and there was no evidence of fibrinoid deposition at these sites. CONCLUSION: Samples from accreta areas at delivery present with a thick fibrinoid deposition at the utero-placental interface on microscopic examination independently of deeply implanted villous tissue in the sample. These changes are associated with distortion of the Nitabuch membrane and might explain the loss of parts of the physiological site of detachment of the placenta from the uterine wall in placenta accreta spectrum. These findings indicate that accreta placentation is more than direct attachment of the villous tissue to the superficial myometrium and support the concept that accreta villous tissue is not truly invasive. Description Journal Title Conference Name Journal ISSN 1097-6868

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