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Jan 2015, Vol 3, Issue 1
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Original Article
A Retrospective Study of Placenta Creta: A Six Year Experience and Histopathological Insights
Hamide Sayar1, Esma Gurbuz1, Emel Canaz2, Nurten Seringec3, Deniz Cemgil Arikan2, Harun Ciralik1
1Department of Pathology, Faculty of Medicine, Kahramanmaras Sutcu Imam University, Kahramanmaras, Turkey
2Department of Obstetrics and Gynecology, Faculty of Medicine, Kahramanmaras Sutcu Imam University, Kahramanmaras, Turkey
3Department of Physiology, Kahramanmaras Sutcu İmam University Faculty of Medicine, Kahramanmaras, Turkey

IJWHR 2015; 3: 067-071
DOI: 10.15296/ijwhr.2015.11
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Keywords : Placenta Accreta, Placenta Increta, Placenta Percreta, Cesarean Section
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Abstract
Objectives: The aims of this study were to describe the histopathological findings of placenta creta samples obtained over a six year period and to report the obstetric conditions related to the histopathologic findings.

Materials and Methods: Pathology records from gravid hysterectomies performed due to placenta creta from 2006 to 2012 were reviewed. We evaluated the decidual layer, percent of multinucleation, and depth of invasion of Interstitial Trophoblasts (ITs) at the implantation site. Spiral arteries were also assessed to determine the degree of remodeling.

Results: During the study period, 20 cases of placenta creta occurred: 3 (15%) were placenta accreta, 7 (35%) were placenta increta, and 10 (50%) were placenta percreta. In 25% of cases, vessels had no remodeling at all, whereas 45% had partially remodeled vessels, and 30% completely remodeled vessels. The proportion of incomplete or complete physiological changes in the vascular wall did not significantly differ between the different subtypes of creta (P=0.68). Depth of IT invasion varied significantly between the groups (accreta 1.30±0.17 mm, increta 3.56±1.12 mm, and percreta 2.00±1.31 mm, P=0.011). The number of multinucleated trophoblasts in the placenta accreta and increta were higher than those in placenta percreta cases. A history of Cesarean Section (CS) was present in 80% of the patients. All cases with placenta percreta (N=10) had undergone more than two previous CSs. Placenta previa was identified in four cases (20%).

Conclusion: Uterine damage caused by CSs results in poor decidualization, abnormal trophoblastic invasion, incomplete vascular remodeling, fewer multinuclei trophoblasts and deep infiltrative pathology.

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