Ruptura prematura de membranas en nacimientos de pretérmino

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Abstract

La ruptura prematura de membranas de pretérmino ocurre en, aproximadamente, el 3% de los embarazos y numerosos aspectos vinculados a su manejo continúan siendo controversiales. El objetivo de esta actualización es revisar en forma detallada las estrategias destinadas a disminuir la morbilidad y mortalidad asociadas a esta situación clínica en las madres. Se discutirá la evidencia disponible acerca del uso en las madres de antibióticos, corticoides a distintas edades gestacionales, sulfato de magnesio como neuroprotector fetal, tocolíticos y el momento óptimo y la vía de finalización del embarazo. Asimismo, se incluyen los efectos de la ruptura prolongada de membranas en prematuros, la mortalidad y morbilidad de los recién nacidos en el corto y largo plazo, los perjuicios de la administración de antibióticos luego del nacimiento con las secuelas en el neurodesarrollo y la presencia de enfermedades crónicas a largo plazo.

Translated abstract

Preterm premature rupture of membranes occurs in around 3% of pregnancies, and several aspects related to its management are still controversial. The objective of this update is to provide a detailed review of strategies aimed at reducing morbidity and mortality associated with this maternal condition. We will discuss the available evidence regarding the maternal use of antibiotics, the use of corticosteroids according to gestational age, the use of magnesium sulphate for fetal neuroprotection, the use of tocolytic agents, and the best moment for and route of delivery. This review also covers the effects of prolonged preterm premature rupture of membranes, infant morbidity and mortality in the short and long term, the harmful effects of antibiotics after delivery, including the effects on neurodevelopment and the presence of longterm chronic diseases.

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Neurodevelopmental and growth impairment among extremely low-birth-weight infants with neonatal infection.

Barbara Stoll, Nellie I Hansen, Ira Adams-Chapman … (2004)

Neonatal infections are frequent complications of extremely low-birth-weight (ELBW) infants receiving intensive care. To determine if neonatal infections in ELBW infants are associated with increased risks of adverse neurodevelopmental and growth sequelae in early childhood. Infants weighing 401 to 1000 g at birth (born in 1993-2001) were enrolled in a prospectively collected very low-birth-weight registry at academic medical centers participating in the National Institute of Child Health and Human Development Neonatal Research Network. Neurodevelopmental and growth outcomes were assessed at a comprehensive follow-up visit at 18 to 22 months of corrected gestational age and compared by infection group. Eighty percent of survivors completed the follow-up visit and 6093 infants were studied. Registry data were used to classify infants by type of infection: uninfected (n = 2161), clinical infection alone (n = 1538), sepsis (n = 1922), sepsis and necrotizing enterocolitis (n = 279), or meningitis with or without sepsis (n = 193). Cognitive and neuromotor development, neurologic status, vision and hearing, and growth (weight, length, and head circumference) were assessed at follow-up. The majority of ELBW survivors (65%) had at least 1 infection during their hospitalization after birth. Compared with uninfected infants, those in each of the 4 infection groups were significantly more likely to have adverse neurodevelopmental outcomes at follow-up, including cerebral palsy (range of significant odds ratios [ORs], 1.4-1.7), low Bayley Scales of Infant Development II scores on the mental development index (ORs, 1.3-1.6) and psychomotor development index (ORs, 1.5-2.4), and vision impairment (ORs, 1.3-2.2). Infection in the neonatal period was also associated with impaired head growth, a known predictor of poor neurodevelopmental outcome. This large cohort study suggests that neonatal infections among ELBW infants are associated with poor neurodevelopmental and growth outcomes in early childhood. Additional studies are needed to elucidate the pathogenesis of brain injury in infants with infection so that novel interventions to improve these outcomes can be explored.

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Committee Opinion No. 713: Antenatal Corticosteroid Therapy for Fetal Maturation.

(2017)

Corticosteroid administration before anticipated preterm birth is one of the most important antenatal therapies available to improve newborn outcomes. A single course of corticosteroids is recommended for pregnant women between 24 0/7 weeks and 33 6/7 weeks of gestation who are at risk of preterm delivery within 7 days, including for those with ruptured membranes and multiple gestations. It also may be considered for pregnant women starting at 23 0/7 weeks of gestation who are at risk of preterm delivery within 7 days, based on a family's decision regarding resuscitation, irrespective of membrane rupture status and regardless of fetal number. Administration of betamethasone may be considered in pregnant women between 34 0/7 weeks and 36 6/7 weeks of gestation who are at risk of preterm birth within 7 days, and who have not received a previous course of antenatal corticosteroids. A single repeat course of antenatal corticosteroids should be considered in women who are less than 34 0/7 weeks of gestation who are at risk of preterm delivery within 7 days, and whose prior course of antenatal corticosteroids was administered more than 14 days previously. Rescue course corticosteroids could be provided as early as 7 days from the prior dose, if indicated by the clinical scenario. Continued surveillance of long-term outcomes after in utero corticosteroid exposure should be supported. Quality improvement strategies to optimize appropriate and timely antenatal corticosteroid administration are encouraged.

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Antibiotics associated with increased risk of new-onset Crohn's disease but not ulcerative colitis: a meta-analysis.

Ryan Ungaro, Charles Bernstein, Richard Gearry … (2014)

The objective of this study was to perform a meta-analysis investigating antibiotic exposure as a risk factor for developing inflammatory bowel disease (IBD).