Chorioamnionitis and neonatal morbidity: current perspectives

Abstract

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.

Retrospective study 2005–2015 of all cases of fetal death occurred at ≥23 gestational weeks, in Friuli Venezia Giulia, Italy

“…We believe this aspect is also important to give a just and dutiful answer to the couple that suffered this dramatic event, which in our population occurred after 30 weeks of gestation in 72% of the cases, when the chances of newborn survival increase significantly with good intensive care, and after 36 weeks in 34% of cases, meaning at term. Some 88% of IUFD cases recorded in this study occurred in the antepartum period and this figure is in line with what was reported by other works carried out in high-income countries, where 90% of deaths in utero occur precisely in this period and are often associated with preventable risk factors, such as obesity, smoking, failure to identify pregnancies at risk [6,[27][28][29][30][31][32][33][34][35]. Therefore, being able to understand the cause of death in utero would allow addressing the available resources more appropriately to combat the etiological factors on which it is possible to implement concrete prevention.…”

“…Consideration must be made on the high frequency of cases in which a condition of chorioamnionitis (11%) had occurred, a share that is certainly higher than the values reported in the literature for this pathology and that is usually estimated in the range of 1-4% [32,33]. Chorioamnionitis was defined by the association of clinical signs of maternal inflammation with fetal tachycardia.…”

Effect of preeclampsia and premature rupture of membrane on neonatal birth weight and length by gestational age: A retrospective study in China

“…[ 17 ] The term intrauterine infection refers to different clinical or pathological conditions characterized by an infectious or inflammatory process that affects the chorioamniotic membranes, amniotic fluid, umbilical cord (funisitis), and eventually the fetus. [ 18 ] Intrauterine infection is one of the significant intrinsic causes of IUGR, since in intrauterine infection, the umbilical cord also gets infected which causes uteroplacental insufficiency which further reduces the transportation of nutrients and oxygen and ultimately results in poor fetal growth during pregnancy. [ 19 ] The findings that PROM has a significant adverse impact on neonatal birth weights and birth length by all gestational weeks, which indicate that it may be due to intrauterine infection of neonates, but unfortunately, we are missing the data regarding intrauterine infection in our study.…”

Chorioamnionitis and Its Fetal Effects

“…23 Amniyon kavitesi, normalde steril kabul edilmekle birlikte son yıllarda plasentanın kendine özgü florası olduğu da artık bilinmekte ve bu vajinal/servikal mikrobiyal floranın değişerek patolojik bakterinin ortaya çıkabileceği görüşü de ağırlık kazanmaktadır. [24][25][26][27][28] İNFLAMASYON NASIL OLUYOR?…”

“…Fetal kortizol seviyesi yükselmekte ve bakteriler ve/veya onların endotoksinlerine yanıt olarak interlökin (IL)-1, IL-6, IL-8, tümör nekrozis faktör-α (TNFα), MMP gibi sitokin/kemokin artışı, lökosit adez-yon moleküllerinin upregülasyonu ile fetal sellüler ve humoral immün aktivasyonu ortaya çıkmaktadır. 9,24,[29][30][31][32]…”