Delayed postpartum hemorrhage: a morphologic study of causes and their relation to other pregnancy disorders

To ascertain the various causes of delayed postpartum hemorrhage and to test whether subinvolution of the placental bed is associated with other pregnancy disorders for which defective maternal-fetal interaction has been implicated pathogenetically.

In a group of women presenting with postpartum hemorrhage following singleton pregnancies, tissue that had been submitted for histopathologic examination was reviewed morphologically to delineate the various causes of delayed postpartum hemorrhage. The stratified groups were analyzed for relationship to preeclampsia, fetal growth retardation (FGR), spontaneous abortion, placenta accreta, and retained placental fragments in previous pregnancies. Odds ratios (ORs) and their 95% confidence intervals (CIs) were calculated for each association.

One hundred sixty-nine cases were identified. Tissue obtained at curettage or, rarely, at hysterectomy could be categorized into seven pathologic groups: involution of the placental bed, subinvolution of the placental bed, retained placental fragments, endometritis, normal endometrium, normal decidua, or nondiagnostic tissue. Hyalinized fragments of uteroplacental (spiral) arteries that were either collapsed or completely thrombosed were seen in involution of the placental bed. Subinvolution of the placental bed was characterized by widely distended and patent residua of uteroplacental arteries with only partial occlusion by thrombosis. Women with retained placental fragments (OR 3.93, 95% CI 1.51-10.47), but not women with an involuted placental bed (OR 2.40, 95% CI 0.68-8.54) or subinvolution of the placental bed (OR 1.52, 95% CI 0.51-4.57), had increased incidences of preeclampsia, FGR, spontaneous abortion, or retained placenta in previous pregnancies when compared to women with endometritis, endometrium only, decidua only, or nondiagnostic tissue.

Retained placental fragments, reflecting placenta accreta, and subinvolution of the placental bed are important causes of delayed postpartum hemorrhage. The former is associated with an increased incidence, in prior pregnancies, of pregnancy complications that probably reflect aberrant maternal-trophoblastic interaction.