The rapid progression of the coronavirus disease 2019 (COVID-19) outbreak presented extraordinary challenges to the US health care system, particularly straining resources in hard hit areas such as the New York metropolitan region. As a result, major changes in the delivery of obstetrical care were urgently needed, while maintaining patient safety on our maternity units. As the largest health system in the region, with 10 hospitals providing obstetrical services, and delivering over 30,000 babies annually, we needed to respond to this crisis in an organized, deliberate fashion. Our hospital footprint for Obstetrics was dramatically reduced to make room for the rapidly increasing numbers of COVID-19 patients, and established guidelines were quickly modified to reduce potential staff and patient exposures. New communication strategies were developed to facilitate maternity care across our hospitals, with significantly limited resources in personnel, equipment, and space. The lessons learned from these unexpected challenges offered an opportunity to reassess the delivery of obstetrical care without compromising quality and safety. These lessons may well prove valuable after the peak of the crisis has passed.

Maternal obesity may program the fetus and increase the susceptibility of the offspring to adult diseases. Metformin crosses the placenta and has been associated with decreased inflammation and reversal of fatty liver in obese leptin-deficient mice. We investigated the effects of metformin on maternal and fetal lipid metabolism and hepatic inflammation using a rat model of diet-induced obesity during pregnancy. Female Wistar rats (6–7 weeks old) were fed normal or high calorie diets for 5 weeks. After mating with normal-diet fed males, half of the high calorie-fed dams received metformin (300 mg/kg, daily); dams (8 per group) continued diets through gestational day 19. Maternal and fetal livers and fetal brains were analyzed for fatty acids and for fatty acid metabolism-related gene expression. Data were analyzed by ANOVA followed by Dunnett’s post hoc testing. When compared to control-lean maternal livers, obesogenic-diet-exposed maternal livers showed significantly higher saturated fatty acids (14:0 and 16:0) and monounsaturated fatty acids (16:1n7 and 18:1n9) and lower polyunsaturated (18:2n6 and 20:4n6 [arachidonic acid]) and anti-inflammatory n3 polyunsaturated fatty acids (18:3n3 and 22:6n3 [docosahexaenoic acid]) (p < 0.05). Metformin did not affect diet-induced changes in maternal livers. Fetal livers exposed to the high calorie diet showed significantly increased saturated fatty acids (18:0) and monounsaturated fatty acids (18:1n9 and 18:1n7) and decreased polyunsaturated fatty acids (18:2n6, 20:4n6 and 22:6n3) and anti-inflammatory n3 polyunsaturated fatty acids, along with increased gene expression of fatty acid metabolism markers (Fasn, D5d, D6d, Scd1, Lxrα). Metformin significantly attenuated diet-induced inflammation and 18:1n9 and 22:6n3 in fetal livers, as well as n3 fatty acids (p < 0.05). Prenatal obesogenic diet exposure significantly increased fetal liver IFNγ levels (p < 0.05), which was reversed by maternal metformin treatment (p < 0.05). Consumption of a high calorie diet significantly affected maternal and fetal fatty acid metabolism. It reduced anti-inflammatory polyunsaturated fatty acids in maternal and fetal livers, altered gene expression of fatty acid metabolism markers, and induced inflammation in the fetal livers. Prenatal metformin attenuated some diet-induced fatty acid changes and inflammation in the fetal livers without affecting maternal livers, suggesting that maternal metformin may impact fetal/neonatal fatty acid/lipid metabolism.

Spontaneous spinal epidural abscess (SEA) is a rare infection of the central nervous system. We report a case of a 25‐year‐old G3 P0020 at 36 weeks of gestational age with history of intravenous drug abuse presenting with acute‐onset and severe back pain. Despite antibiotic therapy, pain worsened and she developed lower extremity weakness. Magnetic resonance imaging (MRI) revealed an SEA, and cesarean delivery was performed secondary to increasing weakness, followed by laminectomy (T9‐12) and decompression of epidural abscess. Postoperative course was complicated by a psoas muscle abscess and persistent SEA refractory to antibiotic therapy, requiring surgical reexploration and extended treatment with antibiotics. She was discharged home in stable condition and neonate did well with no resulting sequelae. Spinal epidural and psoas abscesses are rare and diagnosis is often delayed. Prompt recognition and treatment are necessary to prevent catastrophic neurologic consequences, and the diagnosis should be considered in pregnant patients presenting with back pain, especially in those with risk factors.