Assessment of a multiprofessional training programme by in situ simulation in the maternity units of the Pays de Loire regional perinatal network.

INTRODUCTION: Initially dispensed in specialized simulation centers, simulation training has recently begun to take place directly in healthcare facilities, that is, in situ. The objective of this study is to assess the effect of training by in situ simulation in obstetrics. MATERIAL AND METHODS: The training program, dispensed over a 2-day period, took place in maternity units of the members of the Pays de la Loire perinatal network, Réseau Sécurité Naissance (Network Safety Birth). All participants received a learner satisfaction questionnaire to complete (5-point Likert-like scales). Then, at least 6 months later, each maternity ward received a general questionnaire to assess the effect of the training, as well as a second questionnaire specific to each institution, about the areas for improvement proposed by the teaching team after debriefings. RESULTS: The 14 establishments included in our study returned 375 satisfaction questionnaires. In all, 91.1 % were very satisfied and reported that the training met their expectations, and 99.7 % thought the program would have an impact on their professional practice. More than 94 % of the learners wanted more simulation sessions. Among the 14 facilities, 9 (64.3 %) returned their evaluation questionnaires. In 44.4 % of cases, they reported improvement in team cohesion and in team communication, while the others reported these elements remained stable. All maternity units reported that the training had a positive impact on their team, and that they would be interested in new training program with in situ simulation. DISCUSSION: Most participants clearly appreciated this training. In situ simulation training also led to the identification of areas for improvements, many of them accomplished, through the drafting of protocols or material modifications aimed at improving staff practices and therefore global patient care. There are many ways by which these training programs can be made sustainable, including the development of a new training program of in situ simulation or the creation of onsite simulation sessions on demand or by the professionals at each institution. CONCLUSION: This survey demonstrated the enthusiasm of healthcare professionals about in situ simulation. Moreover, overall improvement in team communication and cohesion was reported in the medium term (evaluation at more than 6 months). The interest of continuing these training sessions appears undeniable.

Effect of single and multiple courses of prenatal corticosteroids on 17-hydroxyprogesterone levels: implication for neonatal screening of congenital adrenal hyperplasia.

Measurement of 17-hydroxyprogesterone (17-OHP) from filter-paper blood is widely used to screen for congenital adrenal hyperplasia (CAH). However, in pregnancies with an expected preterm delivery, prenatal treatment with steroids to induce pulmonary maturation could suppress the fetal adrenals and interfere with this screening. In 160 infants who were born between 25 and 35 wk of gestation, we measured 17-OHP in filter-paper blood at 72-96 h and compared the values between those who had not received antenatal steroids (n=50) and those who had (n=110). A single course of steroids was two 12-mg injections of betamethasone given within a 24-h interval: 30 infants received a half single course, 45 received a full single course, and 35 received multiple courses. Results are expressed as medians (25th percentile; 75th percentile). Blood 17-OHP differed significantly among groups: 23.7 (14.2; 30.7) nmol/L, 26.1 (15.0; 50.1) nmol/L, 20.1 (13.8; 29.1) nmol/L, and 14.9 (9.5; 26.2) nmol/L (for, respectively, no steroid, half a single course, a full single course, and multiple courses; p <0.05, multiple comparisons with the Kruskal-Wallis test). However, only infants who were treated with multiple antenatal courses of steroids had lower blood 17-OHP than those who were untreated (p <0.05 with the Mann-Whitney U test). In multiple regression analysis, steroid treatment and intrauterine growth retardation were significant negative predictors of blood 17-OHP, whereas respiratory distress syndrome was a significant positive predictor (multiple R=0.50, p <0.001). Multiple courses of steroids in preterm infants decrease 17-OHP values by approximately 30% in filter-paper blood, thus raising the risk of false-negative results in screening programs for CAH.

Endocrine pancreas development in growth-retarded human fetuses.

Glucose intolerance in adults born with intrauterine growth retardation (IUGR) may involve peripheral insulin resistance and/or abnormal endocrine pancreas development during fetal life. We quantified insulin-containing cells in deceased human fetuses with IUGR (<10th percentile, n = 21) or normal growth (control fetuses, n = 15). Paraffin-embedded pancreatic tissues from fetuses older than 32 weeks were obtained from two fetopathology departments. Mean gestational age was 36 weeks in both groups. Tissues with lysis and those fetuses with defects, aneuploidy, or genetic abnormalities were excluded. For each subject, six pancreatic sections spaced evenly throughout the organ were immunostained with anti-insulin antibody. Total tissue and insulin-positive areas were measured by computer-assisted quantitative morphometry. Results were expressed in percentages. To evaluate islet morphogenesis, the percentages of beta-cells inside and outside islets were determined. Islet density was similar in the two groups (P = 0.86). The percentage of pancreatic area occupied by beta-cells (beta-cell fraction) was not correlated with gestational age (r = 0.06 and P = 0.97 in IUGR fetuses; r = 0.12 and P = 0.67 in control fetuses) or body weight (r = 0.16 and P = 0.47 in IUGR fetuses; r = 0.24 and P = 0.39 in control fetuses). Mean beta-cell fraction was 2.53% in the IUGR fetuses and 2.86% in the control fetuses (P = 0.47). The percentage of beta-cells located within islets was identical in the two groups (mean 35%). Our data militate against a primary developmental pancreatic abnormality in human IUGR, leaving peripheral insulin resistance as the most likely mechanism of glucose intolerance in adults born with IUGR.