Diagnosis of placental abruption: relationship between clinical and histopathological findings.

OBJECTIVE: We evaluated the extent to which histologic lesions bearing a diagnosis of abruption conform to a diagnosis based on established clinical criteria. We further examined the profile of chronic and acute histologic lesions associated with clinical abruption. METHODS: Data from the New Jersey-Placental Abruption Study - a multi-center, case-control study - were utilized to compare the clinical and histologic criteria for abruption. The study was based on 162 women with clinically diagnosed abruption and 173 controls. We examined the concordance between clinical indicators for abruption with those of a histopathological diagnosis. The clinical criteria for a diagnosis of abruption included (i) evidence of retroplacental clot(s); (ii) abruption diagnosed on prenatal ultrasound; or (iii) vaginal bleeding accompanied by nonreassuring fetal status or uterine hypertonicity. The pathological criteria for abruption diagnosis included hematoma, fibrin deposition, compressed villi, and hemosiderin-laden histiocytes in cases with older hematomas. Acute lesions included chorioamnionitis, funisitis, acute deciduitis, meconium stained membranes, villous stromal hemorrhage, and villous edema. Chronic lesions included chronic deciduitis, decidual necrosis, decidual vasculopathy, placental infarctions, villous mal-development (delayed or accelerated maturation), hemosiderin deposition, intervillous thrombus, and chronic villitis. RESULTS: Of clinically diagnosed cases, the sensitivity and specificity for a histologic confirmation of abruption were 30.2% and 100%, respectively. Presence of retroplacental clots remained the single most common finding (77.1%) among clinically diagnosed cases. Among the acute lesions, chorioamnionitis and funisitis were associated with abruption. The only chronic histologic lesion associated with abruption was placental infarctions. CONCLUSIONS: The concordance between clinical and pathologic criteria for abruption diagnosis is poor. The criteria for diagnosing a clinical abruption should include sonographic visualization of abruption, evidence of retroplacental clots, or vaginal bleeding accompanied by nonreassuring fetal status or uterine hypertonicity.

Changes in prepregnancy body mass index between pregnancies and risk of primary cesarean delivery.

OBJECTIVE: The objective of the study was to examine whether the risk and indications for primary cesarean in the second pregnancy are influenced by changes in prepregnancy body mass index (BMI) between pregnancies. STUDY DESIGN: We performed a cohort analysis using the Missouri maternally linked birth and infant death surveillance datasets (1989-1997), comprised of women with their first 2 consecutive live births (n = 113,789). BMI (kilograms per square meter) was categorized as underweight (less than 18.5 kg/m2), normal (18.5 to 24.9 kg/m2), overweight (25 to 29.9 kg/m2), and obese (30 kg/m2 or greater). Indications for primary cesarean were categorized as breech, dystocia, fetal distress, and others. Timing of primary cesarean was categorized as elective (prior to labor) and emergent (after initiation of labor). Adjusted odds ratio (OR) was used to quantify the associations between changes in prepregnancy BMI and indications for primary cesarean. RESULTS: The rate of primary cesarean in the second pregnancy was 9.2%. Compared with women with normal BMI in their first 2 pregnancies, women who increased their BMI between pregnancies had increased risk of primary cesarean for all indications. Women who remained obese or overweight in both pregnancies were at increased risk of primary cesarean following breech (OR 1.28 and 1.13, respectively); dystocia (OR 1.94 and 1.41, respectively); fetal distress (OR 1.43 and 1.26, respectively); others (OR 3.17 and 1.63, respectively); and elective (OR 2.31 and 1.43, respectively) and emergent (OR 1.66 and 1.30, respectively) cesarean section. Women who lowered their BMI from obese to overweight or overweight to normal between pregnancies had risks of primary cesarean comparable with those with normal BMI in both pregnancies. Any increase in BMI from underweight to overweight or obese between the first 2 pregnancies was associated with increased risk of primary cesarean (OR 1.20 to 3.04) in the second pregnancy. CONCLUSION: Increases in prepregnancy BMI between first 2 pregnancies from normal to obese is associated with increased risk of indications for primary cesarean. The association between being overweight or obese or increases in prepregnancy BMI between pregnancies and primary cesarean in the second pregnancy suggests that counseling women with regard to their high BMI may be beneficial.

Associations between 2 polymorphisms in the methylenetetrahydrofolate reductase gene and placental abruption.

OBJECTIVE: Heritable thrombophilias have been implicated as a potential cause of abruption by vascular disruption at the uteroplacental interface. Polymorphisms of the methylenetetrahydrofolate reductase (MTHFR) gene have been linked to vascular complications outside of pregnancy, which includes stroke. Given the underlying thrombotic nature of abruption, we hypothesized that polymorphisms in the MTHFR gene are associated with abruption. STUDY DESIGN: We examined 2 variants in MTHFR: 677C-->T and 1298A-->C in genomic DNA extracted from maternal blood from the New Jersey-Placental Abruption Study, an ongoing, multicenter case-controlled study. We identified 195 women with a clinical diagnosis of abruption (cases) and 189 control subjects who were matched on race/ethnicity and parity. We assessed allele and genotype frequencies and their associations with abruption risk after adjusting for confounders through multivariable logistic regression analysis. RESULTS: The wild-type allele (C) frequency of the 677C-->T variant of MTHFR among cases and control subjects was 69.0% and 64.3%, respectively; the wild-type allele (A) of the 1298A-->C variant was 75.9% and 79.4%, respectively. Distributions of the 677C-->T alleles among control subjects violated the Hardy-Weinberg equilibrium (P = .007); distributions of the 1298A-->C alleles were in equilibrium (P = .825). In comparison to the wild-type genotype (C/C), the homozygous mutant form (T/T) of 677C-->T was not associated with abruption (odds ratio, 0.60; 95% confidence interval [CI], 0.33-1.18). Similarly, the homozygous mutant form (C/C) of the 1298A-->C polymorphism was distributed equally between cases and control subjects (odds ratio, 2.28; 95% CI, 0.82-6.35). Plasma homocysteine and vitamin B12, but not folate, concentrations were elevated in cases compared with control subjects among women with the wild-type genotype of MTHFR 677C-->T (P = .039 for homocysteine; P = .048 for B12; P = .224 for folate). CONCLUSION: In this population, neither heterozygosity nor homozygosity for the 677C-->T and 1298A-->C variants in MTHFR was associated with placental abruption.

Polymorphisms in methionine synthase reductase and betaine-homocysteine S-methyltransferase genes: risk of placental abruption.

OBJECTIVES: Methionine synthase reductase (MTRR) and betaine-homocysteine S-methyltransferase (BHMT) are two enzymes that regulate homocysteine metabolism. Elevated homocysteine (hyperhomocysteinemia) is associated with adverse pregnancy outcomes and vascular disease. We assessed whether polymorphisms in MTRR (66A-->G; I22M) and BHMT (742G-->A; R239Q) were associated with abruption. We further evaluated whether homocysteine levels differed between cases and controls for MTRR and BHMT genotypes. METHODS: Data were derived from the New Jersey Placental Abruption Study (NJ-PAS)-an ongoing, multicenter, case-control study since August 2002. Women with a clinical diagnosis of abruption were recruited as incident cases (n=196), and controls (n=191) were matched to cases based on maternal race/ethnicity and parity. Total plasma homocysteine concentrations were evaluated in a subset of 136 cases and 136 controls. DNA was genotyped for the MTRR and BHMT polymorphisms. RESULTS: Frequencies of the minor allele of MTRR were 40.8% and 42.2% in cases and controls, respectively (adjusted OR 0.79, 95% CI 0.45, 1.40). The corresponding rates for BHMT were 33.9% and 31.7%, respectively (adjusted OR 1.93, 95% CI 0.99, 4.09). Distributions for the homozygous mutant form of MTRR were similar between cases and controls (OR 1.18, 95% CI 0.62, 2.24). The rate of homozygous mutant BHMT genotype was 2.8-fold (OR 2.82, 95% CI 1.84, 4.97) higher in cases than controls. Stratification of analyses based on maternal race did not reveal any patterns in association. CONCLUSIONS: In this population, there was an association between the homozygous mutant form of BHMT (742G-->A) polymorphism and increased risk for placental abruption.