Diversity Elements on Maternal Fetal Medicine (MFM) Fellowship Websites: Opportunity for Improvement in Recruitment and Representation.

Background: There has been a fundamental shift in recruitment of medical students and trainees into residency and fellowship programs during the Covid 19 pandemic.1 Historically, websites for medical trainees demonstrate a lack of explicit focus on diversity, equity, and inclusion. 2-7 Diversity has positive associations of improving healthcare team performance, patient care, and even financial goals.8 A lack of diversity may negatively impact patient care.9 Directed recruitment of underrepresented in medicine applicants has proven successful to increase diversity within training programs. Department websites have a more prominent role in virtual recruitment since the beginning of the COVID pandemic. Features on these websites may be utilized to attract underrepresented in medicine applicants and increase diversity in a field. Objective: To analyze Maternal Fetal Medicine fellowship websites for presence of diversity elements important to those people who are underrepresented in medicine. Study Design: Fellowship websites were accessed summer of 2021. They were analyzed for presence of twelve website elements that demonstrate commitment to diversity, including: 1) nondiscrimination statement; 2) diversity and inclusion message; 3) diversity specific language; 4) resources for trainees; 5) community demographics; 6-7) personalized biographies of faculty or fellows; 8-9) individual photographs of faculty or fellows; 10) photos or biographies of alumni; 11) diversity publications and; 12) department statistics. Program size, region, and location were collected. Self-reported underrepresented in medicine data on residency programs was extracted from the National Graduate Medical Education Survey from 2019. Programs were dichotomized into 6+ diversity elements. Nonparametric, chi-square and Fisher's exact were used for analysis. Results: Fellowship programs were analyzed (excluding military/fetal surgery, n = 91/94). Websites included a mean of 4.1± 2.5 diversity elements. Most featured fewer than 6 elements (n =75, 82.4%). When dichotomized to 6+ diversity elements, larger faculty size was the only significant factor (p=0.01). The majority of programs had fewer than 12 faculty members (n=54, 59.3%) and only 9.3% of those programs had 6 or more diversity elements. By contrast, among programs with more than 12 faculty, 29.7% had 6 or more diversity elements. Faculty photos, fellow photos, and diversity publications were the most commonly featured items (92.4%, 68.1%, and 49.5%, respectively). Mean rate of underrepresented in medicine was 18.8% ± 11.3% and no significant associations were noted. There was a non-significant difference in diversity elements in the West United States with a mean of 5.3±2.2 diversity elements, compared to 3.7±2 in the South. Conclusion: Fellowship websites convey information for trainees, especially in an era of virtual recruitment. This study highlights opportunities for directed improvements of websites for features which URIM medical trainees have identified as important.

Neutrophil gelatinase-associated lipocalin as a predictor of pre-eclampsia: A systematic review and meta-analysis.

BACKGROUND: Protein neutrophil gelatinase-associated lipocalin (NGAL) has been associated with kidney injury and inflammatory conditions. In particular, several studies have found an association between maternal blood and urine levels and the development of pre-eclampsia. OBJECTIVES: To examine whether maternal blood and urine levels of NGAL are good predictors of pre-eclampsia. SEARCH STRATEGY: The authors searched MEDLINE databases via PubMed, Embase, Scopus, Scielo, Google Scholar, PROSPERO International Prospective Register of Systematic Reviews, and the Cochrane Central Register of Controlled Trials. SELECTION CRITERIA: The authors included case-control observational clinical studies comparing protein levels of NGAL in serum and urine in women with pre-eclampsia with uncomplicated pregnancies. Only studies where the collection of blood or urine was peformed before the occurrence of pre-eclampsia were selected. DATA COLLECTION AND ANALYSIS: The primary outcome was the difference in NGAL levels in blood or urine between women with and without pre-eclampsia. RESULTS: Seven studies in total were included: five studies measuring NGAL in blood and two in urine. Regarding the serum studies, 315 patients were included as cases and 540 as controls. Higher NGAL in maternal blood during all three trimesters together was associated with pre-eclampsia; the standardized mean difference was 1.15 ng/mL (95% confidence interval, 0.92-1.39; P < 0.01). Regarding the urine studies, 39 patients were included as cases and 220 as controls. There was no statistically significant difference between patients with pre-eclampsia and controls regarding urine NGAL. CONCLUSIONS: NGAL in maternal blood is higher in patients who later develop pre-eclampsia compared with controls and could be used as a potential predicting test in the routine clinical setting.

Glanzmann's thrombasthenia during pregnancy complicated by large subchorionic hematoma managed with antifibrinolytics, human leukocyte antigen-matched platelet transfusion, and primary cesarean delivery: a case report.

A 29-year-old primipara with Glanzmann's thrombasthenia presented for prenatal care at 8 weeks of gestation. Pregnancy remained uncomplicated until 22 weeks of gestation when a subchorionic hematoma, measuring 5.8 × 4.1 × 6.7 cm, was diagnosed and managed outpatient. At 28 weeks of gestation, the subchorionic hematoma was significantly expanding to 11 × 13 × 3.7 cm (∼30% of the placental surface). The patient was admitted for antepartum surveillance and steroid treatment. Fetal and maternal status were reassuring. At 36 weeks of gestation, there was active extravasation from the subchorionic hematoma, prompting interdisciplinary discussion with neonatal intensive care unit, blood bank, pharmacy, anesthesia, hematology, and the patient regarding her options. Immediate delivery risked platelet sensitization because of unavailable human leukocyte antigen-matched platelets. The patient opted for medical management with aminocaproic acid. At 37 weeks of gestation, she underwent a scheduled cesarean delivery. Human leukocyte antigen-matched platelets and additional aminocaproic acid were administered preoperatively. Intrapartum hemorrhage of 1200cc was controlled with uterotonics in addition to the above measures. Antifibrinolytics were continued. The neonate had an uncomplicated postpartum course. The patient had symptomatic anemia on postoperative day 1, which prompted red blood cell transfusion. Discharge was delayed until postoperative day 6 to further monitor her bleeding; oral antifibrinolytics were continued for 2 weeks. This case adds to the growing use of adjuvant medications, including antifibrinolytics such as aminocaproic acid and tranexamic acid, to reduce the reliance on platelet transfusion. This is critical for maintaining a favorable response to platelet transfusions and minimizing the risk of fetal neonatal alloimmune thrombocytopenia in current and subsequent pregnancies among women with lifelong bleeding disorders.

Cesarean Delivery with External Negative Pressure Dressing System: A Retrospective Cohort Study.

Objective To determine whether the use of external negative pressure dressing system (ENPDS) can reduce the incidence of wound complications after cesarean delivery (CD) compared with traditional dressings. Methods Retrospective review of all patients undergoing CD between November 2011 and March 2013. Information was collected on demographics, body mass index (BMI), duration of labor, pre- and postnatal infections, incision and dressing type, and postoperative course. Comparisons were made between traditional dressing and an external negative pressure dressing system. Results Of 970 patients included in the study, wound complications occurred in 50 patients (5.2%). Comparisons of ENPDS ( n = 103) and traditional dressing ( n = 867) groups revealed higher wound complications for ENPDS with odds ratio (OR) 3.37 and confidence interval (CI) 1.68 to 6.39. ENPDS was more commonly used in patients with BMI > 30 and preexisting diabetes. After controlling for BMI and pregestational diabetes in logistic regression analysis, ENPDS was equivalent to traditional dressing for risk of wound complications with an adjusted OR 2.76 (CI 0.97 to 7.84), with a trend toward more wound complications with ENPDS. Wound separation also tended to be more common in ENPDS group versus traditional dressing with an adjusted OR 2.66 (CI 0.87 to 8.12), although this result did not reach significance. Conclusion ENPDS is equivalent to traditional dressing for preventing wound complications after controlling for the higher-risk population selected for its use. In particular, wound separation appears to occur more frequently in women treated with ENPDS versus traditional dressing and should be regarded as a potential hazard of the system.

The association between social stressors and home smoking rules among women with infants in the United States.

OBJECTIVES: We examined the role of social stressors on home-smoking rules (HSRs) among women with infants in the United States, with attention on the moderating role of smoking status and depression. METHODS: We analyzed data for 118 062 women with recent births in the United States who participated in the Pregnancy Risk Assessment Monitoring System (2004-2010), which is a population-based surveillance data set. We fit multinomial logistic models to predict the odds of partial or no HSRs by a cumulative index of prenatal social stressors. RESULTS: Compared with those with no stressors, mothers with high levels of social stressors had 2.5 times higher odds of partial or no HSRs. Smokers in the 1-2, 3-5, and ≥ 6 stressor categories were 9.0%, 9.6%, and 10.8% more likely to have partial or no HSRs, respectively. Under the highest levels of stress (≥ 6), nonsmokers were almost as likely as smokers to have partial or no HSRs. In addition, the effects of stress on HSRs were more pronounced for nonsmoker, nondepressed mothers. CONCLUSIONS: Increases in social stressors represented an important risk factor for partial or no HSRs and might have potential negative implications for infants.

Breastfeeding in obstetrics residency: exploring maternal and colleague resident perspectives.

BACKGROUND: Pregnancy is becoming more common in residency, and about 80% of residents are female. This leads to questions of breastfeeding, work demands, and perception of burden by colleagues. This study was designed to assess experiences of (1) breastfeeding obstetrics residents and (2) their colleagues. MATERIALS AND METHODS: This was a cross-sectional study of obstetrics and gynecology residents. Residents were categorized into experience with or no experience with breastfeeding to determine differences. RESULTS: Responses were obtained from 404 residents in obstetrics. Breastfeeding is common, with 90% of residents knowing a breastfeeding resident and 22% of residents reporting personal experience with breastfeeding. Breastfeeding residents (n=89) felt support from their faculty and fellow residents. More than one in three breastfeeding mothers felt they placed extra demands on colleagues, despite 80% of colleagues reporting that they did not feel that breastfeeding colleagues placed extra demands. A breastfeeding policy was important to 85% of residents, but only 7% believed their program had one. Two-thirds of breastfeeding residents struggled with low milk supply and stopped breastfeeding early. CONCLUSIONS: Despite high levels of perceived support from faculty/fellow residents, breastfeeding residents struggle with low milk supply and work demands that lead to early discontinuation.

Additive inhibitory effects of progesterone and sodium nitroprusside on uterine contractility during pregnancy.

Progesterone (P4) and nitric oxide (NO) suppress uterine contractility (CTX). This study compares the effects of P4 to sodium nitroprusside (SNP, an NO donor) and their combination on human CTX of term/preterm and labor/nonlabor tissues. Uterine tissues (n = 128) from women (n = 28) undergoing Cesarean were suspended in organ baths. Tissues (n ≥ 6/group) were treated with vehicle, P4, SNP, or combinations. A subset of tissues (n ≥ 2/group) from term/preterm ± labor and nonpregnant patients was analyzed with P4 alone. Analysis of variance (ANOVA) was used for statistical differences (P < .05). The combination of P4 with SNP significantly suppresses CTX (% inhibition of -127.1 ± 14.5) to the levels lower than with either P4 (-20.1 ± 8.6) or SNP alone (-72.0 ± 11.2). Suppression of P4 is similar in term, preterm, and nonpregnant tissues, with increased sensitivity in laboring tissues. This indicates that P4 or SNP alone may be used for preterm labor and their combination may be more successful.

Role of the renin-angiotensin system in the systemic microvascular inflammation of alveolar hypoxia.

Alveolar hypoxia (AH) induces widespread systemic inflammation. Previous studies have shown dissociation between microvascular Po(2) and inflammation. Furthermore, plasma from AH rats (PAHR) induces mast cell (MC) activation, inflammation, and vasoconstriction in normoxic cremasters, while plasma from normoxic rats does not produce these responses. These results suggest that inflammation of AH is triggered by a blood-carried agent. This study investigated the involvement of the renin-angiotensin system (RAS) in the inflammation of AH. Both an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin II (ANG II) receptor blocker (ANG II RB) inhibited the leukocyte-endothelial adherence produced by AH, as well as the inflammation produced by PAHR in normoxic rat cremasters. MC stabilization with cromolyn blocked the effects of PAHR but not those of topical ANG II on normoxic cremasters, suggesting ANG II generation via MC activation by PAHR. This was supported by the observation that ACE inhibition and ANG II RB blocked the leukocyte-endothelial adherence produced by the MC secretagogue compound 48/80. These results suggest that the intermediary agent contained in PAHR activates MC and stimulates the RAS, leading to inflammation, and imply an RAS role in AH-induced inflammation.

Plasma from conscious hypoxic rats stimulates leukocyte-endothelial interactions in normoxic cremaster venules.

Systemic hypoxia results in rapid increases in leukocyte-endothelial adherence (LEA) and emigration, vascular permeability, and mast cell activation in several microcirculations. Observations in cremaster muscle suggest that this response is initiated by a mediator released from a distant site (Dix R, Orth T, Allen JA, Wood JG, and Gonzalez NC. J Appl Physiol 95: 2495-2502, 2003). The present experiments in rat cremaster muscle tested the hypothesis that, if a circulating mediator triggers hypoxia-induced inflammation, then plasma from hypoxic rats should elicit LEA in normoxic cremaster venules. Plasma from conscious donor rats breathing 10% O2-90% N2 for 5 min was applied topically to the cremaster of normoxic anesthetized rats. In this and all other groups described below, the donor plasma had attained normoxic PO2 when applied to the cremaster. LEA (leukocytes/100-microm venule) increased from 2.7 +/- 0.8 to 12.3 +/- 2.4, and venular shear rate and arteriolar diameter decreased to 79 +/- 9% (P < 0.05, n = 6) and 77 +/- 5% of control (P < 0.05, n = 5), respectively, 10 min after application of plasma from hypoxic donors. The decrease in venular shear rate was exclusively due to a reduction of venular blood flow, secondary to the upstream arteriolar vasoconstriction. Plasma from normoxic donors had no effects. Plasma from blood equilibrated in vitro for 5 min with 5% CO2-95% N2 did not alter LEA or shear rate of normoxic cremasters, suggesting that the putative mediator does not originate in blood cells. The effects of plasma from hypoxic rats persisted when the donors were pretreated with the mast cell stabilizer cromolyn, which prevents hypoxia-induced LEA. This suggests that the effects of hypoxic plasma are not due to inflammatory mediators released by adherent leukocytes in the donor rat. There was a positive correlation between LEA and mast cell degranulation observed histologically. These results support the idea that systemic hypoxia produces the release of a substance transported by the circulation that initiates the microvascular inflammation.

Exercise training prevents the inflammatory response to hypoxia in cremaster venules.

Systemic hypoxia produces microvascular inflammation in several tissues, including skeletal muscle. Exercise training (ET) has been shown to reduce the inflammatory component of several diseases. Alternatively, ET could influence hypoxia-induced inflammation by improving tissue oxygenation or increasing mechanical antiadhesive forces at the leukocyte-endothelial interface. The effect of 5 wk of treadmill ET on hypoxia-induced microvascular inflammation was studied in the cremaster microcirculation of rats using intravital microscopy. In untrained rats, hypoxia (arterial Po(2) = 32.3 +/- 2.1 Torr) increased leukocyte-endothelial adherence from 2.3 +/- 0.4 to 10.2 +/- 0.3 leukocytes per 100 microm of venule (P < 0.05) and was accompanied by extravasation of FITC-labeled albumin after 4 h of hypoxia (extra-/intravascular fluorescence intensity ratio = 0.50 +/- 0.07). These responses were attenuated in ET (leukocyte adherence was 1.5 +/- 0.4 during normoxia and 1.8 +/- 0.7 leukocytes per 100 mum venule after 10 min of hypoxia; extra-/intravascular fluorescence intensity ratio = 0.11 +/- 0.02; P < 0.05 vs. untrained) despite similar reductions of arterial (32.4 +/- 1.8 Torr) and microvascular Po(2) (measured with an oxyphor-quenching method) in both groups. Shear rate decreased during hypoxia to similar extents in ET and untrained rats. In addition, circulating blood leukocyte count was similar in ET and untrained rats. The effects of ET on hypoxia-induced leukocyte-endothelial adherence remained up to 4 wk after discontinuing training. Thus ET attenuated hypoxia-induced inflammation despite similar effects of hypoxia on tissue Po(2), venular shear rate, and circulating leukocyte count.

Activation of mast cells by systemic hypoxia, but not by local hypoxia, mediates increased leukocyte-endothelial adherence in cremaster venules.

Systemic hypoxia, produced by lowering inspired Po2, induces a rapid inflammation in several microcirculations, including cremaster muscle. Mast cell activation is a necessary element of this response. Selective reduction of cremaster microvascular Po2 (PmO2) with normal systemic arterial Po2 (PaO2; cremaster hypoxia/systemic normoxia), however, does not elicit increased leukocyte-endothelial adherence (LEA) in cremaster venules. This could be due to a short time of leukocyte exposure to the hypoxic cremaster environment. Conversely, LEA increases when PaO2 is lowered, while cremaster PmO2 remains high (cremaster normoxia/systemic hypoxia). An alternative explanation of these results is that a mediator released from a central site during systemic hypoxia initiates the inflammatory cascade. We hypothesized that if this is the case, cremaster mast cells would be activated during cremaster normoxia/systemic hypoxia, but not during cremaster hypoxia/systemic normoxia. The microcirculation of rat cremaster muscles was visualized by using intravital microscopy. Cremaster PmO2 was measured with a phosphorescence quenching method. Cremaster hypoxia/systemic normoxia (PmO2 7 +/- 1 Torr, PaO2 87 +/- 2 Torr) did not increase LEA; however, topical application of the mast cell activator compound 48/80 under these conditions did increase LEA. The effect of compound 48/80 on LEA was blocked by topical cromolyn, a mast cell stabilizer. LEA increased during cremaster normoxia/systemic hypoxia, (PmO2 64 +/- 5 Torr, PaO2 33 +/- 2 Torr); this increase was blocked by topical cromolyn. The results suggest that mast cell stimulation occurs only when PaO2 is reduced, independent of cremaster PmO2, and support the idea of a mediator that is released during systemic hypoxia and initiates the inflammatory cascade.