OBJECTIVE:We sought to evaluate the frequency of, and factors associated with, the use of 3 evidence-based interventions: antenatal corticosteroids for fetal lung maturity, progesterone for prevention of recurrent preterm birth, and magnesium sulfate for fetal neuroprotection.STUDY DESIGN:A self-administered survey was conducted from January through May 2011 among obstetricians from 21 hospitals that included 30 questions regarding their knowledge, attitudes, and practice of the 3 evidence-based interventions and the 14-item short version of the Team Climate for Innovation survey. Frequency of use of each intervention was ascertained from an obstetrical cohort of women between January 2010 and February 2011.RESULTS:A total of 329 obstetricians (74% response rate) who managed 16,946 deliveries within the obstetrical cohort participated in the survey. More than 90% of obstetricians reported that they incorporated each intervention into routine practice. Actual frequency of administration in women eligible for the treatments was 93% for corticosteroids, 39% for progesterone, and 71% for magnesium sulfate. Provider satisfaction with quality of treatment evidence was 97% for corticosteroids, 82% for progesterone, and 57% for magnesium sulfate. Obstetricians perceived that barriers to treatment were most frequent for progesterone (76%), 30% for magnesium sulfate, and 17% for corticosteroids. Progesterone use was more frequent among patients whose provider reported the quality of the evidence was above average to excellent compared with poor to average (42% vs 25%, respectively; P < .001), and they were satisfied with their knowledge of the intervention (41% vs 28%; P = .02), and was less common among patients whose provider reported barriers to hospital or pharmacy drug delivery (31% vs 42%; P = .01). Corticosteroid administration was more common among patients who delivered at hospitals with 24 hours a day-7 days a week maternal-fetal medicine specialist coverage (93% vs 84%; P = .046), CONCLUSION: Obstetricians in Maternal-Fetal Medicine Units Network hospitals frequently use these evidence-based interventions; however, progesterone use was found to be related to their assessment of evidence quality. Neither progesterone nor the other interventions were associated with overall climate of innovation within a hospital as measured by the Team Climate for Innovation. National Institutes of Health Consensus Conference Statements may also have an impact on use; there is such a statement for antenatal corticosteroids but not for progesterone for preterm prevention or magnesium sulfate for fetal neuroprotection.
OBJECTIVE: We sought to extend our prior observations and histopathologically characterize key metabolic enzymes (CYP1A1) with markers of oxidative damage in the placental sections from smokers.STUDY DESIGN: Placental specimens were collected from term singleton deliveries from smokers (n = 10) and nonsmokers (n = 10) and subjected to a detailed histopathological examination. To quantify the extent of oxidative damage, masked score-graded (0-6) histopathology against 4-hydroxy-2-nonenal (4-HNE) and 8-hydroxydeoxyguanisine (8-OHdG) was performed. Minimal significance (P < .05) was determined with a Fisher's exact and a 2-tailed Student t test as appropriate.RESULTS: We observed a significant increase in the presence of syncytial knots in placentas from smokers (70% vs 10%, P = .02). These gross observations were accompanied by a significant aberrant placental aromatic hydrocarbon metabolism (increased CYP1A1, 4.4 vs 2.1, P = .002) in addition to evidence of oxidative damage (4-HNE 3.4 vs 1.1, P = .00005; 8-OHdG 4.9 vs 3.1, P = .0038).CONCLUSION: We observed a strong association between maternal tobacco use and aberrant placental metabolism, syncytial knot formation, and multiple markers of oxidative damage.
To determine whether the severity of placental vascular abnormalities in hypertensive disorders correlates with the severity of the condition. We retrospectively evaluated placental specimens from the surgical pathology repository at our institution. Inclusion criterion was hypertension in singleton gestation. We excluded cases that delivered at < 20 weeks of gestation, and those with a clinical diagnosis of chorioamnionitis. Hypertensive disorders were classified as mild or severe by ACOG criteria. Sections from the placentae were stained with hematoxylin & eosin and examined microscopically for relevant pathologic changes. Fisher′s exact test was used for statistical analysis (significance: P<0.05). 90 placentas were examined (25 from mild HTN and 65 from severe HTN). After adjusting for gestational age, placental weights were not significantly different between the 2 groups (P=0.91). The proportion of placental weights < 10%ile were similar between groups (2/25 and 10/65; P=0.49). Histological abnormalities were found in 22/25 (88.0%) of the mild HTN group and in 61/65 (93.8%) of the severe HTN group (P=0.39). The most common abnormality was placental infarction, which was found in 5/25 (20%) of the mild HTN group and in 30/65 (46.1%) of the severe HTN group (P=0.02). 2 (8%) in the mild HTN and 4 (6.1%) in the severe HTN had histological evidence of acute abruption (P=0.65). Decidual vasculopathy and ischemia were found in 17 (26.1%) cases of severe HTN and in 3 (12%) of the mild HTN (P=0.16). Advance villous maturation were found in 14 (21.3%) cases of severe HTN and in 3 (12%) of the mild HTN (P=0.75) Hypertensive disorders affecting pregnancy are associated with significant placental histopathology. Mild and severe hypertensive disorders lead to similar vascular abnormalities in the placenta. These abnormalities can significantly impair feto-placental perfusion equally between mild and severe conditions, resulting in fetal hypoxia or death.
To investigate the relationship between placental pathology and maternal clinical laboratory values in a well characterized series of stillbirths. 99 stillborn cases were examined. Placentas were examined, and full autopsies were performed on the stillborn infants. Clinical chemistry, hematology and coagulation panels were drawn on the mothers at the time of presentation. Placental pathology was compared between those with laboratory values within the normal ranges versus outside. Statistical analysis was conducted using SPSS to calculate relative risk (RR) and 95% confidence intervals (95%CI). Pathological evidence of infection (chorioamnionitis, chorionitis, deciduitis, funisitis) was noted in 47.5% of cases. Placental infarcts were observed in 15.2% of cases. These 2 findings were identified as the underlying cause of death in 18.2% of cases. Evidence of infections was higher in the group with elevated liver function tests (LFT) compared to patients whose LFTs were within normal limits (overall RR=2.55, 95%CI: 1.73-3.79). Subjects with elevated serum LDH also showed a higher frequency of infections in the placenta (RR=3.79, 95%CI: 2.38-6.02). Patients with elevated fibrinogen levels were also more likely to have placental infarcts (RR=5.33, 95%CI: 2.37-11.95) and evidence of infection (RR=1.92, 95%CI: 1.57-2.34). Patients with prothrombin time (PT) longer than normal showed a higher incidence of chorioamnionitis than patients with PT within normal limits (RR=1.75, 95%CI: 1.21-2.52), but there was no significant difference in the subjects with PT shorter than normal. Patients with lower PT showed a higher incidence of extensive placental infarcts compared to subjects in the reference range (RR=4.99, 95%CI: 3.04-8.21). We found a strong association between maternal laboratory abnormalities and placental pathologic changes identified as underlying or contributory to fetal death. In particular, hypercoagulative state was associated with placental infarcts, while hypocoagulative state was associated with evidence of infection.