RESUMEN
OBJECTIVE: The aim of this study was to assess neonatal and maternal adverse outcomes following expectant management of preterm prelabor rupture of membranes (PPROM) between 18 and 26 weeks and to identify maternal morbidity and prognostic factors for neonatal outcomes. METHODS: Data were collected from all pregnant women who presented PPROM between 18+0 and 26+0 weeks admitted into two tertiary centers in Brazil from 2005 to 2016. The neonatal adverse outcomes (mortality or the development of a severe morbidity) and maternal adverse outcomes were analyzed and compared among four groups (180/7 to 200/7 weeks, 20+1 to 220/7 weeks, 22+1 to 240/7 weeks and 24+1 to 260/7 weeks). A multiple logistic regression was performed for each predictor of neonatal adverse outcomes, and the area under the receiver operating characteristics curves for birth weight and gestational age at birth were calculated. RESULTS: Of the 101 women with PPROM during the study period, 97 fulfilled the eligible criteria. Among these patients, 30 (30.9%) had a miscarriage or stillbirth. Overall there were 67/97 (69.1%) livebirths, 45/97 newborns survived to discharge (46.3%), and 53/97 (54.6%) experienced severe neonatal adverse outcome. The median latency period was seven days, with 36 (37.1%) patients ending the pregnancy in 2-14 days. Among 29 patients with PPROM at 24+1 to 260/7 weeks, only 13 (44.8%) delivered between 2 and 14 days. Multivariate analysis has demonstrated that the independent predictor for adverse neonatal outcome was birthweight. The maternal morbidity was high; however, the expectant management did not increase the rate of severe maternal morbidity. CONCLUSIONS: PPROM between 18+0 and 26+0 weeks has high morbidity and mortality, and the only significant independent predictor of severe adverse neonatal outcomes is birthweight. Maternal morbidity is high, however, the expectant management is not increased by expectant management.
Asunto(s)
Rotura Prematura de Membranas Fetales , Resultado del Embarazo , Peso al Nacer , Femenino , Rotura Prematura de Membranas Fetales/epidemiología , Edad Gestacional , Humanos , Recién Nacido , Embarazo , Resultado del Embarazo/epidemiología , Segundo Trimestre del Embarazo , Estudios RetrospectivosRESUMEN
OBJECTIVES: To estimate the association between major types of congenital heart defects (CHD) and spontaneous preterm birth, and to assess the potential underlying mechanisms. STUDY DESIGN: This nationwide, registry-based study included a cohort of all singleton pregnancies in Denmark from 1997 to 2013. The association between CHD and spontaneous preterm birth was estimated by multivariable Cox regression, adjusted for potential confounders. The following potential mechanisms were examined: maternal genetics (sibling analyses), polyhydramnios, preterm prelabor rupture of membranes, preeclampsia, and indicators of fetal and placental growth. RESULTS: The study included 1 040 474 births. Compared with the general population, CHD was associated with an increased risk of spontaneous preterm birth, adjusted hazard ratio 2.1 (95% CI, 1.9-2.4). Several subtypes were associated with increased risks, including pulmonary stenosis combined with a septal defect, 5.2 (95% CI, 3.7-7.5); pulmonary stenosis or atresia, 3.1 (95% CI, 2.4-4.1); tetralogy of Fallot 2.5 (95% CI, 1.6-3.8); coarctation or interrupted aortic arch 2.2 (95% CI, 1.5-3.2); and hypoplastic left heart syndrome, 2.0 (95% CI, 1.0-4.1). Overall, preterm prelabor rupture of membranes mediated more than one-half of the association. Maternal genetics, polyhydramnios, or indicators of fetal or placental growth did not explain the reported associations. CONCLUSIONS: CHD, especially right ventricular outflow tract obstructions, were associated with an increased risk of spontaneous preterm birth. The risk was carried by the CHD and not by maternal genetics. Moreover, preterm prelabor rupture of membranes was identified as a potential underlying mechanism.
Asunto(s)
Cardiopatías Congénitas/epidemiología , Nacimiento Prematuro/epidemiología , Adulto , Estudios de Cohortes , Dinamarca/epidemiología , Femenino , Rotura Prematura de Membranas Fetales/epidemiología , Humanos , Masculino , Embarazo , Atresia Pulmonar/epidemiología , Estenosis de la Válvula Pulmonar/epidemiología , Sistema de Registros , RiesgoRESUMEN
OBJECTIVE DATA: Preterm prelabor rupture of membranes occurs in 3% of all pregnancies. Neonatal benefit is seen in uninfected women who do not deliver immediately after preterm prelabor rupture of membranes. The purpose of this study was to evaluate whether the administration of progestogens in singleton pregnancies prolongs pregnancy after preterm prelabor rupture of membranes. STUDY: Searches were performed in MEDLINE, OVID, Scopus, EMBASE, ClinicalTrials.gov, and the Cochrane Central Register of Controlled Trials with the use of a combination of keywords and text words related to "progesterone," "progestogen," "prematurity," and "preterm premature rupture of membranes" from the inception of the databases until January 2018. We included all randomized controlled trials of singleton gestations after preterm prelabor rupture of membranes that were randomized to either progestogens or control (either placebo or no treatment). Exclusion criteria were trials that included women who had contraindications to expectant management after preterm prelabor rupture of membranes (ie, chorioamnionitis, severe preeclampsia, and nonreassuring fetal status) and trials on multiple gestations. We planned to include all progestogens, including but not limited to 17-α hydroxyprogesterone caproate, and natural progesterone. STUDY APPRAISAL AND SYNTHESIS METHODS: The primary outcome was latency from randomization to delivery. Metaanalysis was performed with the use of the random effects model of DerSimonian and Laird to produce relative risk with 95% confidence interval. Analysis was performed for each mode of progestogen administration separately. RESULTS: Six randomized controlled trials (n=545 participants) were included. Four of the included trials assessed the efficacy of 17-α hydroxyprogesterone caproate; 1 trial assessed rectal progestogen, and 1 trial had 3 arms that compared 17-α hydroxyprogesterone caproate, rectal progestogen, and placebo. The mean gestational age at time randomization was 26.9 weeks in the 17-α hydroxyprogesterone caproate group and 27.3 weeks in the control group. 17-α Hydroxyprogesterone caproate administration was not found to prolong the latency period between randomization and delivery (mean difference, 0.11 days; 95% confidence interval, -3.30 to 3.53). There were no differences in mean gestational age at delivery, mode of delivery, or maternal or neonatal outcomes between the 2 groups. Similarly, there was no difference in latency for those women who received rectal progesterone (mean difference, 4.00 days; 95% confidence interval, -0.72 to 8.72). CONCLUSION: Progestogen administration does not prolong pregnancy in singleton gestations with preterm prelabor rupture of membranes.