Standardized Order Sets Do Not Eliminate Racial or Ethnic Inequities in Postpartum Pain Management.

Objective: To quantify the extent to which a standardized pain management order set reduced racial and ethnic inequities in post-cesarean pain evaluation and management. Methods: We conducted a retrospective cohort study to quantify racial and ethnic differences in pain evaluation and management before (July 2014-June 2016) and after implementation of a standardized post-cesarean order set (March 2017-February 2018). Electronic medical records were queried for pain scores >7/10, number of pain assessments, and opioid, nonsteroidal anti-inflammatory drug (NSAID), and acetaminophen doses. Outcomes were grouped into 0 to <24 and 24-48 h postpartum, and stratified by race/ethnicity (Hispanic, non-Hispanic Black [NHB], non-Hispanic White [NHW], Asian, and other), as documented in the electronic health record. Analyses included logistic regression for the categorical outcome of pain score >7 (severe pain), and linear regression, with propensity score adjustment. Main effect and interaction terms were used to calculate the difference-in-difference in pain process and outcome measures between the baseline and follow-up periods. Results: After order set implementation (N=888), severe pain remained more common among NHB patients (% pain scores >7 NHW vs. NHB 0 to <24 h: 22% vs. 33%, p=0.003; 24-48 h: 26% vs. 40%, p<0.001). Among all patients, pain management processes changed after implementation of the order set, with overall fewer assessments, less Opioids, and more nonopioid analgesics. However, racial and ethnic inequities in a number of assessments and in treatment were unchanged (all p for interaction >0.05), with the exception of a modest increase in NSAID doses 24-48 h postpartum for Hispanic patients. Conclusion: A standardized pain management order set reduced overall postpartum opioid use, but did not reduce racial and ethnic disparities in pain evaluation and management. Future work should investigate racial equity-focused education and interventions designed to eliminate disparities in pain management.

The association between maternal and paternal race and preterm birth.

BACKGROUND: Non-Hispanic black maternal race is a known risk factor for preterm birth. However, the contribution of paternal race is not as well established. OBJECTIVE: We sought to evaluate the risk of preterm birth among non-Hispanic black, non-Hispanic white, and mixed non-Hispanic black and non-Hispanic white dyads. STUDY DESIGN: This was a population-based cohort study of all live births in the United States from 2015 to 2017, using live birth records from the National Vital Statistics System. Singleton, nonanomalous infants whose live birth record included maternal and paternal self-reported race as either non-Hispanic white or non-Hispanic black were included. The primary outcome was preterm birth at <37 weeks' gestation; secondary outcomes included preterm birth at <34 and <28 weeks' gestation and delivery gestational age (as a continuous variable). Data were analyzed using chi-square, t test, analysis of variance, and logistic regression. A Kaplan-Meier survival curve was also generated. RESULTS: There were 11,809,599 live births during the study period; 4,008,622 births met the inclusion criteria. Of included births, 291,647 (7.3%) occurred at <37 weeks' gestation. Using the convention of maternal race first followed by paternal race, preterm birth at <37 weeks' gestation was most common among non-Hispanic black and non-Hispanic black dyads (n=70,987 [10.8%]), followed by non-Hispanic black and non-Hispanic white (n=3137 [9.5%]), non-Hispanic white and non-Hispanic black (n=9136 [8.3%]), and non-Hispanic white and non-Hispanic white dyads (n=209,387 [6.5%]; P<.001 for trend). Births at <34 weeks' (n=74,474) and <28 weeks' gestation (n=18,474) were also more common among non-Hispanic black and non-Hispanic black dyads. Specifically, 24,351 (3.7%) non-Hispanic black and non-Hispanic black, 1017 (3.1%) non-Hispanic black and non-Hispanic white, 2408 (2.2%) non-Hispanic white and non-Hispanic black, and 46,698 non-Hispanic white and non-Hispanic white dyads delivered at <34 weeks' gestation, and 7988 non-Hispanic black and non-Hispanic black (1.2%), 313 (1.0%) non-Hispanic black and non-Hispanic white, 584 (0.5%) non-Hispanic white and non-Hispanic black, and 9589 (0.3%) non-Hispanic white and non-Hispanic white dyads delivered at <28 weeks' gestation. Non-Hispanic white and non-Hispanic white dyads delivered at a mean 38.8± standard deviation of 1.7 weeks' gestation, although non-Hispanic white and non-Hispanic black, non-Hispanic black and non-Hispanic white, and non-Hispanic black and non-Hispanic black dyads delivered at 38.6±2.0, 38.5±2.3, and 38.3±2.4 weeks' gestation, respectively (P<.001). Adjusted odds ratios for the association between maternal or paternal race and preterm birth were highest for non-Hispanic black and non-Hispanic black dyads at each gestational age cutoff: adjusted odds ratio, 1.60 (95% confidence interval, 1.11-1.19) (<37 weeks' gestation); adjusted odds ratio, 2.47 (95% confidence interval, 2.41-2.53) (<34 weeks' gestation); and adjusted odds ratio, 4.22 (95% confidence interval, 4.04-4.41) (<28 weeks' gestation) compared with the non-Hispanic white referent group. Models adjusted for insurance status, chronic hypertension, tobacco use during pregnancy, history of previous preterm birth, and male fetus. In the Kaplan-Meier survival analysis, non-Hispanic black and non-Hispanic black dyads delivered the earliest across the range of delivery gestational ages compared with all other combinations of dyads. CONCLUSION: Non-Hispanic black paternal race is a risk factor for preterm birth and should be considered when evaluating maternal a priori risk of prematurity. Future research should investigate the mechanisms behind this finding, including determining the contribution of factors, such as racism, maternal and paternal genetics, and epigenetics to an individual's risk of preterm birth.

Association of chorioamnionitis and patent ductus arteriosus in a national U.S. cohort.

OBJECTIVE: To estimate the effect of clinical chorioamnionitis on the risk of patent ductus arteriosus (PDA). STUDY DESIGN: A secondary analysis of all deliveries >23 gestational weeks from the U.S. Consortium on Safe Labor (CSL) study. The primary exposure was a clinical diagnosis of chorioamnionitis, and the outcome was a diagnosis of PDA. Generalized estimating equations with estimated error variance for women with multiple deliveries were utilized. Models adjusted for age, race, region, delivery year, body mass index, infant sex, multiple gestation, mode of delivery, and antenatal corticosteroid exposure. RESULTS: Among 228,438 deliveries, a diagnosis of PDA was more frequent with chorioamnionitis exposure versus without (9.2% vs. 3.0%; OR: 3.25; 95% CI: 2.92-3.62). Chorioamnionitis was associated with higher adjusted odds of PDA (AOR: 2.18; 95% CI: 1.93-2.45). In sensitivity analyses, the association between chorioamnionitis and PDA held after adjustment for gestational age at delivery (AOR: 1.28; 95% CI: 1.13-1.44). CONCLUSIONS: Chorioamnionitis was associated with increased odds of PDA. Robust exposure and outcome ascertainment with careful assessment of confounding is needed to further investigate this epidemiologic association.

Racial Disparities in Prematurity Persist among Women of High Socioeconomic Status.

Objectives: Despite persistent racial disparities in preterm birth (PTB) in the US among non-Hispanic (NH) black women compared to NH white women, it remains controversial whether sociodemographic factors can explain these differences. We sought to evaluate whether disparities in PTB persist among NH black women with high socioeconomic status (SES). Study Design: We conducted a population-based cohort study of all live births in the US from 2015-2017 using birth certificate data from the National Vital Statistics System. We included singleton, non-anomalous live births among women who were of high SES (defined as having ≥ 16 years of education, private insurance, and not receiving Women, Infants and Children [WIC] benefits) and who identified as NH white, NH black, or 'mixed' NH black and white race. The primary outcome was PTB <37 weeks; secondary outcomes included PTB <34 and <28 weeks. In addition, analyses were repeated considering birthweight <2500g as a surrogate for preterm birth <37 weeks, birthweight <1500g as a surrogate for preterm birth <34 weeks, and birthweight <750g as a surrogate for preterm birth <28 weeks' gestation. Data were analyzed with chi-square, t-test, and logistic regression. Results: 2,170,686 live births met inclusion criteria, with 92.9% NH white, 6.7% NH black, and 0.4% both NH white and black race. Overall, 5.9% delivered <37, 1.3% <34, and 0.3 % <28 weeks. In unadjusted analyses of women with high SES, the PTB rate at each gestational age cutoff was higher for women of 'mixed' NH white and black race, and highest for women who were NH black only compared to women who were NH white only. In regression models we further adjusted for women with insurance and prenatal care their entire pregnancy, maternal race was associated with higher odds of PTB at each GA cutoff, with the highest odds observed at <28 weeks. Finally, in further adjustement analysis including only the 1,934,912 women who received prenatal care in the first trimester, findings were similar. Rates of preterm birth at each gestational age cutoff remained highest for women who identified as non-Hispanic black, intermediate for women identifying as both non-Hispanic black and white race, and lowest for non-Hispanic white women at <37 weeks (9.9% vs. 6.1% vs. 5.5%, respectively; p<0.001), <34 weeks (3.5% vs. 1.5% vs. 1.1%, respectively; p<0.001), and <28 weeks' gestation (1.2% vs. 0.4% vs. 0.2%, respectively, p<0.001). Conclusions: Even among college-educated women with private insurance who are not receiving WIC, racial disparities in prematurity persist. These national findings are consistent with prior studies that suggest factors other than socio-demographics are important in the underlying pathogenesis of PTB.