Implementation and Outcomes of a Model of Care for Placenta Accreta Spectrum in a Community-Based Private Practice.

OBJECTIVE: The aim of the study is to describe a model of care and outcomes for placenta accreta spectrum (PAS) implemented in the context of a community based non-academic health system. STUDY DESIGN: The program for management of PAS includes a multidisciplinary team approach with protocols for ultrasound assessment, diagnosis, and surgery. The program was implemented in the two largest private hospitals in the Twin Cities, Minnesota, United States. Maternal and fetal outcomes as well as cost were compared for histopathologic confirmed PAS cases before (2007-2014, n = 41) and after (2015-2017, n = 26) implementation of the PAS program. RESULTS: Implementation of the PAS program was associated with ICU admission reductions from 53.7 to 19.2%, p = 0.005; a decrease of 1,682 mL in mean estimated blood loss (EBL) (p = 0.061); a decrease in transfusion from 85.4 to 53.9% (p = 0.005). The PAS program also resulted in a (non-significant) decrease in both surgical complications from 48.8 to 38.5% (p = 0.408) and postoperative complications from 61.0 to 42.3% (p = 0.135). The total cost of care for PAS cases in the 3 years after implementation of the program decreased by 33%. CONCLUSION: The implementation of a model of care for PAS led by a perinatology practice at a large regional non-academic referral center resulted in reductions of ICU admissions, operating time, transfusion, selected surgical complications, overall postoperative complications, and cost. KEY POINTS: · Implementation of a PAS care model resulted in reduced ICU admissions from 53.7% to 19.2%.. · Patient safety increased by reducing blood loss, transfusions and postoperative complications.. · This model decreased operating time, as well as total cost of care by 33%..

Elevated plasma corticotrophin release factor levels and in utero meconium passage.

Intrauterine meconium (MEC) passage and aspiration may result in significant newborn morbidity, though there is little understanding of the physiologic mechanisms for MEC passage. We hypothesized that stress induces fetal MEC passage via corticotrophin releasing factor (CRF), a known mediator of colonic motility in adult rats. Pregnant rats at e22 were subjected to acute hypoxia or normoxia for 35 min, after which rats were anesthetized and fetuses operatively delivered. Amniotic fluid bilirubin and intestinal alkaline phosphatase were measured as markers for MEC passage, and fetal and maternal plasma CRF and corticosterone levels determined. Hypoxic stress induced defecation in all dams and provoked visible MEC passage in all fetuses. Amniotic fluid bilirubin content was significantly higher in hypoxic fetuses versus controls (1.064 +/- 0.101 versus 0.103 +/- 0.003 O.D. at 410 nm) and intestinal alkaline phosphatase was consistently elevated in MEC stained amniotic fluid. Hypoxia significantly increased plasma CRF (maternal, 82 +/- 5 to 196 +/- 14 pg/mL; fetal, 284 +/- 15 to 1523 +/- 185 pg/mL) and corticosterone (maternal, 417 +/- 50 to 1150 +/- 50 ng/mL; fetal, 96 +/- 5 to 182 +/- 10 ng/mL) compared with controls. In view of the known action of CRF in adult colonic motility, these results suggest that hypoxic stress-mediated MEC passage in term fetal rats is mediated by a CRF dependent pathway.

Meconium passage in utero: mechanisms, consequences, and management.

Meconium passage in newborn infants is a developmentally programmed event normally occurring within the first 24 to 48 hours after birth. Intrauterine meconium passage in near-term or term fetuses has been associated with fetomaternal stress factors and/or infection, whereas meconium passage in postterm pregnancies has been attributed to gastrointestinal maturation. Despite these clinical impressions, little information is available on the mechanism(s) underlying the normal meconium passage that occurs immediately after birth or during the intrauterine period of fetal development. Birth itself is a stressful process and it is possible that fetal stress-mediated biochemical events may regulate the meconium passage occurring either during labor or after birth. Aspiration of meconium during intrauterine life may result in or contribute to meconium aspiration syndrome (MAS), representing a continued leading cause of perinatal death. This article reviews aspects of meconium passage in utero, its consequences, and management.

Development of ovine fetal ileal motility: role of muscarinic receptor subtypes.

OBJECTIVE: In the preterm human fetus, immaturity of gastrointestinal (GI) motility contributes to impairment of oral feeding and an increased risk of necrotizing enterocolitis. In view of the limited knowledge of fetal GI motility development, and the primary role of the muscarinic system in adult GI motility, we examined the development of GI muscarinic receptor subtypes associated with ileal motility. STUDY DESIGN: Ovine term fetal, newborn, and pregnant adult ileal longitudinal muscle contractile responses to muscarinic agonists (bethanechol) and muscarinic nonspecific (atropine) and subtype specific-antagonists (M1-M4) were examined in organ baths. Immunohistochemical analysis of ileal muscle muscarinic receptor subtypes was correlated with contractile responses. RESULTS: Bethanechol induced a concentration-dependent ileal contraction at all 3 age groups. Adult ileal maximal tension was 2-fold higher than that of the fetus and newborn, while 50% effective concentration (EC(50)) was similar at all ages. Atropine (10(-6)mol/L) inhibited contractility in fetal (67%+/-7%), newborn (82%+/-5%), and adult (97%+/-2%) in an age-dependent manner. The M3 antagonist exhibited robust inhibition at all age groups while the M2 antagonist demonstrated enhanced inhibition in the fetus. Immunohistochemical analysis indicated coexpression of subtype receptors in fetal, newborn, and adult ileal smooth muscle with increasing expression with advancing age. CONCLUSION: These results demonstrate a specific developmental pattern of muscarinic receptor subtype expression. Knowledge and/or alterations of GI motility regulation may aid in the treatment of the preterm fetus or newborn.