Implementation of an Enhanced Recovery after Surgery Pathway to Reduce Inpatient Opioid Consumption after Cesarean Delivery.

OBJECTIVE: Opioid prescription after cesarean delivery is excessive and can lead to chronic opioid use disorder. We assessed the impact of an enhanced recovery after surgery (ERAS) pathway on inpatient opioid consumption after cesarean delivery. STUDY DESIGN: An ERAS pathway was implemented as a quality improvement initiative in December 2019. Preintervention (PRE) data were collected from March to May 2019 to assess baseline opioid consumption. Postintervention (POST) data were collected from January to March 2020. The primary outcome was inpatient postoperative opioid consumption in morphine milligram equivalents (MME). Secondary outcomes included the consumption of any opioids, postpartum length of stay, and opioid prescription at discharge. RESULTS: A total of 92 women were in the PRE group and 91 were in the POST group. Inpatient opioid consumption decreased by 87.3% from PRE to POST, from 124.7 (interquartile range [IQR]: 10-181.6) MME to 15.8 (IQR: 0-75) MME (p < 0.001). There was no difference in median postpartum length of stay (3.4 days PRE vs. 3.3 days POST; p = 0.12). The proportion of women who did not consume any opioids increased by 75.4% from PRE to POST (p = 0.02). The proportion of women discharged with an opioid prescription decreased by 25.6% from PRE to POST (p = 0.007), despite no formal change to prescribing practices. After adjustment for differences in race/ethnicity and gravidity, there was still a reduction in total inpatient opioid consumption (p < 0.001) and an increase in the proportion of women not consuming any opioids (adjusted relative risk (RR): 2.14, 95% confidence interval [CI]: 1.18-3.87), but the difference in rate of prescription of opioids at discharge was no longer statistically significant (adjusted RR: 0.70, 95% CI: 0.48-1.02). CONCLUSION: Adoption of an ERAS pathway for cesarean delivery resulted in a marked reduction in inpatient opioid consumption. Such a pathway can be implemented across institutions and may be a powerful tool in combating the opioid epidemic. KEY POINTS: · ERAS after cesarean reduces inpatient opioid consumption.. · ERAS after cesarean increases the proportion of women not consuming any opioids.. · This pathway can be feasibly adopted elsewhere..

Update on Prenatal Laboratory Screening: Joint Commission Required Elements.

The Centers for Disease Control and Prevention, the American College of Obstetricians and Gynecologists, and the American Academy of Pediatrics recommend routine screening for pregnant women for evidence of infection with human immunodeficiency virus, hepatitis B and syphilis, and vaginal-rectal colonization with group B Streptococcus For each of these pathogens, there are important opportunities to provide maternal treatment, prevent vertical transmission of the pathogen during the prenatal or intrapartum periods, and/or administer neonatal treatment immediately after birth. Such prevention and/or treatment measures are critical to limiting maternal and neonatal morbidity; however, this is dependent on recognition of maternal disease status. A significant number of women in the United States receive either inadequate prenatal care or inadequate screening for these pathogens. The time of admission to labor and delivery units represents an important opportunity to detect at-risk pregnant women and infants. To optimize both maternal and neonatal health, the Joint Commission issued new guidance effective July 1, 2018, mandating documentation of maternal disease status for these pathogens in the maternal medical record and documentation of positive results in the newborn medical record. Immediate peripartum testing for women with inadequate screening is also required. These measures should allow for timely interventions to improve maternal health and ideally to prevent perinatal disease transmission to the newborn.

A competitive stapled peptide screen identifies a selective small molecule that overcomes MCL-1-dependent leukemia cell survival.

Cancer cells hijack BCL-2 family survival proteins to suppress the death effectors and thereby enforce an immortal state. This is accomplished biochemically by an antiapoptotic surface groove that neutralizes the proapoptotic BH3 α helix of death proteins. Antiapoptotic MCL-1 in particular has emerged as a ubiquitous resistance factor in cancer. Although targeting the BCL-2 antiapoptotic subclass effectively restores the death pathway in BCL-2-dependent cancer, the development of molecules tailored to the binding specificity of MCL-1 has lagged. We previously discovered that a hydrocarbon-stapled MCL-1 BH3 helix is an exquisitely selective MCL-1 antagonist. By deploying this unique reagent in a competitive screen, we identified an MCL-1 inhibitor molecule that selectively targets the BH3-binding groove of MCL-1, neutralizes its biochemical lock-hold on apoptosis, and induces caspase activation and leukemia cell death in the specific context of MCL-1 dependence.