Clinical Chorioamnionitis and the Prognosis for Very Low Birth Weight Infants

Alexander, J.; Gilstrap, Larry C.; Cox, Susan M.; McIntire, Donald; Leveno, Kenneth J.

doi:10.1097/00006250-199805000-00016

Cited by 45 publications

(54 citation statements)

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“…However, BPD remains a major chronic pulmonary complication in small preterm infants. In previous studies, antenatal inflammation has been shown to increase the risk of BPD (2)(3)(4)(5), although ironically antenatal inflammation may improve pulmonary function during the immediate neonatal period (6). Furthermore, in infants who subsequently develop BPD, we have reported increased levels of inflammatory biochemical factors in serum and tracheal aspirate at birth, thus implicating inflammation in the development of BPD (7,8).…”

mentioning

confidence: 76%

“…Chorioamnionitis has shown to be associated with an increased BPD prevalence (2,4,5), which suggests that antenatal infection and/or inflammation amplify postnatal lung injury. In preterm lambs and baboons, the intra-amniotic administration of endotoxin or Ureaplasma urealyticum was found to decrease alveolarization or alter developmental signaling in the immature lung (11,12,16).…”

Section: Discussionmentioning

confidence: 99%

“…This phenomenon has also been reported in cases of human antenatal infection and/or inflammation (2,4 -6). These conditions have been reported to reduce the risk of RDS and improve surfactant production and gas exchange (2,6), but paradoxically to increase the prevalence of BPD (2,4,5).…”

Section: Discussionmentioning

confidence: 99%

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Bronchopulmonary Dysplasia in a Rat Model Induced by Intra-amniotic Inflammation and Postnatal Hyperoxia: Morphometric Aspects

et al. 2009

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Antenatal inflammation is a known risk factor of bronchopulmonary dysplasia. The authors hypothesized that lipopolysaccharide (LPS) administration amplifies hyperoxia-induced lung injury in neonatal rats. LPS (0.5 or 1.0 g) or normal saline was injected into the amniotic sacs of pregnant rats at 20 d gestation (term 22.5 d). After birth, rats were exposed to 85% oxygen or room air for 1 or 2 wk. Morphometric analysis of lungs was performed on 14 d. One week of hyperoxia without LPS administration resulted in modest lung injury. LPS at 0.5 g alone did not alter lung morphology, but amplified the effect of 1 wk of hyperoxia resulting in marked inhibition of alveolarization (airspaces were enlarged and alveolar surface areas further reduced). LPS at 1.0 g independently induced modest lung injury and also amplified the effect of 1 wk of hyperoxia. However, this sensitizing effect of LPS was not observed in rats subjected to 2 wks of hyperoxia, which in itself caused extensive lung injury (possibly masking the effect of LPS). The authors concluded that intra-amniotic LPS sensitizes neonatal rat lungs, and thus, amplifies the hyperoxia-induced inhibition of alveolarization. (Pediatr Res 65: 323-327, 2009) T he pathophysiology of bronchopulmonary dysplasia (BPD) has evolved from its classical form following the introduction of antenatal glucocorticoid, surfactant replacement therapy, and gentler ventilatory support (1). However, BPD remains a major chronic pulmonary complication in small preterm infants. In previous studies, antenatal inflammation has been shown to increase the risk of BPD (2-5), although ironically antenatal inflammation may improve pulmonary function during the immediate neonatal period (6). Furthermore, in infants who subsequently develop BPD, we have reported increased levels of inflammatory biochemical factors in serum and tracheal aspirate at birth, thus implicating inflammation in the development of BPD (7,8). In addition, prolonged hyperoxic exposure has been found to lead to BPD in clinical and animal studies, but much remains to be determined concerning the role of antenatal inflammation in the development of BPD. Recently, Van Marter et al. (4) reported that mechanically ventilated preterm infants with chorioamnionitis or postnatally acquired sepsis showed a several fold increase in the prevalence of BPD compared with mechanically ventilated preterm infants without these complications. Ikegami and Jobe (9) suggested that endotoxin had a sensitizing effect after observing that fetal sheep exposed to intraamniotic endotoxin showed further increased proinflammatory responses to mechanical ventilation. Jobe (10) subsequently suggested antenatal inflammation has a sensitizing effect and that it increases the incidence and severity of BPD when neonates are exposed to oxygen and mechanical ventilation. A number of animal models of BPD have been devised (9,11,12), but to date this concept that antenatal inflammation increases susceptibility to lung injury by hyperoxia has not been demonst...

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Section: Discussionmentioning

confidence: 99%

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Bronchopulmonary Dysplasia in a Rat Model Induced by Intra-amniotic Inflammation and Postnatal Hyperoxia: Morphometric Aspects

et al. 2009

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“…Most studies in this field have revealed a positive association between both CCA and HCA and the risk of an earlyonset neonatal sepsis (EONS), 11,[54][55][56][57][58][59][60] and this association persists after adjusting for GA, birth weight (BW), and other confounders. Fetal infection is the most advanced stage of an ascending intrauterine infection, and bacteremia have been detected in 33% of fetuses with positive AF cultures, in contrast to only 4% of fetuses with AF negative cultures.…”

Section: Infection-related Complicationsmentioning

confidence: 99%

Chorioamnionitis and neonatal morbidity: current perspectives

Henríquez¹,

Rodrigo²

2017

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Abstract:The term chorioamnionitis (CA) is commonly used to refer to different clinical or pathological conditions characterized by an infectious and/or inflammatory process that affects primarily the chorioamniotic membranes, but also the amniotic fluid, vessels of the chorionic plate, and, eventually, the umbilical cord (funisitis) and the fetus. Its incidence is higher at lower gestational ages, and the main mechanism is believed to be the ascending bacterial infection from the maternal genital tract. It can be diagnosed by clinical criteria, amniotic fluid examination for inflammatory mediators, and/or isolation of microorganisms, or by histopathological examination of the placenta. CA is an important cause of stillbirth and is related to an increased incidence of premature rupture of membranes, preterm delivery, and adverse maternal and neonatal outcomes such as early-onset neonatal sepsis and necrotizing enterocolitis. An independent causal association to other neonatal morbidities is more controversial. The heterogeneity in the diagnostic criteria and in the operative definitions for morbidity makes comparison of studies difficult, and results are inconsistent. In addition, the intensity and duration of the process are usually not considered. For all these reasons, evidence-based recommendations for the management of mother and infant under these circumstances are difficult to establish, and clinical practice varies widely.

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“…Improvements in survival have made it necessary to investigate causes of death other than immaturity for the infant of BW <751 g. For example, amniotic fluid infection can be responsible for premature delivery and for death of the infant due to congenital pneumonia. 43 A recent study of causes of death from our hospital that included infants from period 4 has shown that congenital infection as a cause of death in the ELBW infant peaked at GA 24 weeks and between BW 600 and 700 g. 44 Hack and Fanaroff 28 are the only authors to report survival data who also present causes of death for infants of BW <751 g. They found 34% of the deaths of these extremely premature infants due to amniotic fluid infection syndrome, compared to 27% in our study of ELBW infants. Without autopsy and study of the placenta, these deaths would likely be attributed to immaturity or RDS rather than infection.…”

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confidence: 99%