Catherine Y. Spong

Prioritizing posterior arm delivery during severe shoulder dystocia.

BACKGROUND Delivery of the posterior arm, or the Barnum maneuver, is at times used late in shoulder dystocia management algorithms, and is not often a first- or second-line management protocol. CASE A multiparous, diabetic patient, who was morbidly obese and had a residual obstetric brachial plexus injury, experienced a precipitous second stage of labor and severe shoulder dystocia. Attempts at the McRoberts maneuver with traction failed to deliver the fetus. In lieu of alternative maneuvers or continued attempts at traction, the posterior arm was delivered and the fetal trunk followed easily. CONCLUSION A geometric analysis reveals that using posterior arm delivery reduces the obstruction by more than a factor of two, relative to the McRoberts maneuver. We recommend earlier use of this maneuver during shoulder dystocia management.

The role of activity-dependent neuroprotective protein in a mouse model of fetal alcohol syndrome

OBJECTIVEnFetal alcohol syndrome (FAS) is the most common nongenetic cause of mental retardation. Peptides NAPVSIPQ (NAP) and SALLRSIPA (SAL), related to activity-dependent neuroprotective protein (ADNP), prevent alcohol-induced damage in a mouse model of FAS. Our objective was to characterize ADNP in this model to relate this protein to the mechanisms of damage and peptide neuroprotection.nnnSTUDY DESIGNnTimed, pregnant C57Bl6/J mice were treated on day 8. Groups were control, alcohol, peptide pretreatment, or peptide alone. Embryo and decidua were harvested at 6 and 24 hours and 10 days. To evaluate ADNP expression, real-time polymerase chain reaction was performed with results presented as the ratio of ADNP-to-glyceraldehyde-3-phosphate dehydrogenase (GAPDH) concentration. Analysis of variance was performed for overall comparisons with P<.05 considered significant.nnnRESULTSnAt 6 hours, there was no difference in ADNP between alcohol-exposed embryos compared with control embryos. At 24 hours, there was an increase in ADNP in alcohol-exposed embryos compared with controls (P<.001); these findings persisted at 10 days (P<.001). In the decidua at 6 hours, there was no difference between alcohol and control. At 24 hours, there was greater ADNP in alcohol-exposed decidua compared with controls (P<.001), which did not persist at 10 days (P=.97). Peptide pretreatment did not prevent the alcohol-induced increase in ADNP in embryo or decidua.nnnCONCLUSIONnAlcohol increased embryonic and decidual ADNP expression at 24 hours and it persisted in the embryo for 10 days. Because ADNP is a known neuroprotectant, these findings suggest that it may be released as a protective mechanism in FAS. Changes in the embryo were persistent suggesting that the embryo is more vulnerable to alcohol-induced damage than the mother.

Role of lamellar body count for the prediction of neonatal respiratory distress syndrome in non-diabetic pregnant women

ObjectiveLamellar body count is a new and fast technique to establish the presence of fetal lung maturity. We have assessed the predictive ability of lamellar body count for neonatal respiratory distress syndrome (RDS) in a non-diabetic population.Study designWe accessed a cohort of amniocenteses in non-diabetic women from 1998 to 2002 (n=102). Neonatal RDS was defined as need for surfactant, intubation, or continuous positive airway pressure (CPAP) in the setting of chest X-ray findings consistent with RDS. The predictive ability of lamellar body count was compared with those of lecithin/sphingomyelin (L/S) ratio and presence of phosphatidylglycerol (PG) using logistic regression analysis. The optimal threshold value of lamellar body count for prediction of neonatal RDS was established with receiver operating characteristic (ROC) curve analysis.ResultsLamellar body count ROC curve analysis identified a lamellar body count >37,000xa0μl−1 as optimal diagnostic threshold for diagnosis of lung maturity, having a negative predictive value of 98%. Lamellar body count and PG, but not L/S ratio, added significantly to the prediction of RDS.ConclusionsLamellar body count is a reliable predictor of fetal lung maturity in non-diabetic women and it can replace the L/S ratio.

Elevated second-trimester maternal serum hCG: a marker of inadequate angiogenesis.

Objective To measure angiogenin, a potent inducer of neovascularization and interleukin-6, as an indicator of acute inflammation, in second-trimester amniotic fluid of patients with elevated maternal serum hCG. Methods In this case-control study, 20 patients with elevated maternal serum hCG (at least 2.0 multiples of median) at triple screen were matched 2:1 with controls on the basis of year of amniocentesis, parity, and race. Inclusion criteria were 1) singleton gestation, 2) no evidence of anomalies, and 3) genetic amniocentesis. Amniotic fluid was immunoassayed for angiogenin and interleukin-6. The immunoassay sensitivity for angiogenin was 0.026 ng/mL, interassay coefficient of variation 4.6%, and infra-assay coefficient of variation 2.9%. For interleukin-6, the immunoassay sensitivity was 2.37 pg/mL, interassay coefficient of variation 2.7%, and intra-assay coefficient of variation 1.9%. Angiogenin and interleukin-6 values were normalized by using natural log transformation for statistical analysis. Statistical analysis included analysis of variance and stepwise regression, with P < .05 significant. Results After correcting (by multivariate regression) for gestational age at sampling and nulliparity, amniotic fluid angiogenin levels were significantly lower in the study subjects than in controls (26% ± 11% lower, P = .004), whereas the interleukin-6 levels did not change significantly (34% ± 40% lower, P = .3). Conclusion Amniotic fluid angiogenin levels are significantly lower in patients with elevated maternal serum hCG at triple screen, suggesting inadequate angiogenesis, but interleukin-6 values do not differ significantly.

Differential expression of c-fos in a mouse model of fetal alcohol syndrome ☆

OBJECTIVEnFetal alcohol syndrome (FAS) results in stillbirth, fetal growth restriction, and mental retardation with injury attributed to oxidative stress. Our objective was to identify signal transduction pathways expressed in a model of FAS and to quantify expression of c-fos, a gene in the stress signal pathway.nnnSTUDY DESIGNnTimed, pregnant C57Bl6/J mice were injected on E8 with saline solution or alcohol. RNA was extracted from decidua and embryo 6 and 24 hours later. Microarray analysis was used to screen gene pathways. Differential gene expression was confirmed using real-time polymerase chain reaction with results presented as the ratio of c-fos concentration to that of glyceraldehyde-3-phosphate dehydrogenase (GAPDH).nnnRESULTSnDifferential gene expression between alcohol and control was noted for stress signal pathway genes including c-fos. Real-time polymerase chain reaction demonstrated that c-fos messenger RNA expression was greater in the alcohol than control decidua at 6 hours after injection (P<.01). This effect persisted at 24 hours (P<.01). There was no difference in c-fos expression in embryos whose mothers received alcohol versus control after 6 hours (P=.12) or 24 hours (P=.89).nnnCONCLUSIONnAlcohol administration during pregnancy results in differential gene expression in the stress signal pathway, particularly in c-fos. C-fos expression in the decidua increases from 6 to 24 hours after alcohol injection, but does not change in the embryo, which may contribute to alcohol-induced damage in FAS.

Fetal growth after preterm premature rupture of membranes: Is it related to amniotic fluid volume?

Objective. Preterm premature rupture of membranes (PPROM) has been associated with an increased rate of fetal growth restriction (FGR). It is unknown whether impairment of fetal growth is mediated through external compression from decreased amniotic fluid volume or (an)other mechanism(s). Methods. Over a three-year period all patients with singleton pregnancies experiencing PPROM at <37 weeks lasting greater than 10 days, and who underwent serial sonograms to assess fetal biometry after PPROM, were included in the study. Patients were excluded for congenital anomalies or other inherent risk factors for abnormal fetal growth. Fetal abdominal circumference (AC) percentiles were compared between the first sonographic exam after PPROM and the last exam before delivery. The median amniotic fluid index between PPROM and delivery was correlated with the change in AC percentiles while controlling for the duration of PPROM. Statistical analysis utilized one-way analysis of variance and correlation; a p value of <0.05 was considered significant. Results. Twenty-two patients met our inclusion criteria with a mean duration (±SD) of PPROM of 58 days (±46). The median AFI during the PPROM period was not correlated with the change in AC percentiles after controlling for duration of PPROM (p = 0.49). Conclusions. The residual amniotic fluid volume after PPROM does not appear to correlate with fetal growth suggesting that the increased rate of FGR in PPROM is not secondary to oligohydramnios. We hypothesize that the intrauterine pathologic processes responsible for membrane rupture may also interfere with fetal growth.