The Consequences of Chorioamnionitis: Preterm Birth and Effects on Development

Journal Reading Oleh: Dessy Esa S (030.08.074) Pembimbing: dr. Arie W, Sp.OG

Kepaniteraan Klinik Ilmu Penyakit Kandungan dan Kebidanan RSAL Mintohardjo Periode 13 Januari 2014 – 22 Maret 2014

Preterm Birth a major cause of perinatal mortality and long-term morbidity. Chorioamnionitis is a common cause of preterm birth. .

retinal. and renal outcomes observed in preterm infants exposed to chorioamnionitis .This paper outlines clinical and experimental studies have improved our current understanding of the mechanisms responsible for chorioamnionitisinduced preterm birth explores the cellular and physiological mechanisms underlying poor cardiorespiratory. neural.

Moderate preterm births  between 32 and 33 weeks and 6 days of gestation Infants born very preterm  before 32 completed weeks Infants born extremely preterm  before 28 completed weeks of gestation .infants born preterm  before 37 completed weeks of gestation. Late preterm births include infants  between 34 and 36 weeks and 6 days of gestation.

The World Health Organisation estimates there are 15 million preterm births globally and 1 million direct fatalities annually .

• (ii) multiple pregnancy. • (iv) preterm prelabour rupture of membranes.. including the following: • (i) spontaneous preterm labour. • (v) hypertensive disorders of pregnancy (e. preeclampsia).g. • (iii) assisted reproduction. cervical incompetence. • (vii) antepartum haemorrhage.Etiology of Preterm Birth There are a number of known contributors to premature birth [19]. .g. uterine malformations). • (ix) intrauterine inflammation/Chorioamnionitis. • (viii) miscellaneous (e.. • (vi) intrauterine growth restriction.

24] a conservative estimate due to the difficulty associated with detecting chorioamnionitis using conventional culture techniques .The incidence of intrauterine inflammationges tational age(majority of extremely preterm births and 16% of preterm births at 34 weeks) [21. 22] Microbiological studies indicate that intrauterin inflammation approximately 25–40% of all preterm births [20. 23.

Chorioamnionitis Clinical maternal fever. leukocytosis. tachycardia. uterine tenderness. clinical chorioamnionitis is usually diagnosed after attempting to delay preterm delivery or with preterm prolonged rupture of the fetal membranes . Highly virulent organisms likely cause clinical chorioamnionitis Before 30 weeks of gestation. and preterm rupture of membranes Diagnose most commonly made during labour near or at term.

which is considered the most common manifestation and is defined histologically by inflammation of the chorion. Deliveries prior to 30 weeks of gestation are typically associated with histological chorioamnionitis Histological chorioamnionitis • Histological diagnosis occurs after delivery and is based on a semiquantitative assessment of inflammatory cells in the chorioamniotic .Histological chorioamnionitis • chorioamnionitis can be subclinical. amnion. Histological chorioamnionitis • organisms considered to be of low virulence. and placenta.

Clinical FIRS is defined by a fetal plasma [interleukin-6] >11 pg/mL [32].The majority of fetuses exposed to chorioamnionitis develop a systemic inflammatory response known as the fetal inflammatory response syndrome (FIRS) [30. whilst subclinical FIRS is defined histologically by funisitis and fetal vasculitis [31] . 31]. FIRS can itself be categorised as clinical or subclinical. This is due to the fetus being in direct contact with infected amniotic fluid and/or inflammatory cell transfer from the uteroplacental circulation.

LPS is capable of inducing an inflammatory cascade (which is the dominant feature of clinical and subclinical chorioamnionitis). derived from the outer cell wall of gram negative bacteria. in the absence of bacterial infection . Intrauterine inflammation can be produced in experimental animals by exposing the fetus to lipopolysaccharide (LPS).Animal Models of Chorioamnionitis/Intrauterine Inflammation.

The consequences of this experimental intervention mimic the most severe forms of clinical chorioamnionitis. .injection of LPS into the cervix  high-grade placental inflammationassociated with a maternal systemic inflammatory response moderate to high rates of fetal loss [34–37].

and.Intravenous Sheep maternal pyrexia. fetal death [46] Mice . and increased uterine contractility Rodents maternal systemic inflammatory systemic and placental response that causes inflammation and placental altered placental inflammation.Intraperitoneal . septicaemia. FIRS vascular function [43–45]. in some cases.

Chorioamnionitis Causes an Inflammatory Cascade That Leads to Preterm Birth .

IL-1𝛼 . IL-1𝛽. and tumour necrosis factor-𝛼 (TNF 𝛼) within the decidua and the fetal membranes) prostaglandins neutrophil chemotaxis. IL-8.PRETERM LABOUR Bacteria that invade the choriodecidual space endotoxins and exotoxins Toll-like receptors (TLRs) on the surface of leukocytes. and activation stimulate uterine contractions synthesis and release of metalloprotea ses cervical ripening and degrade the chorioamniotic membranes causing them to rupture . and trophoblast cells Cytokines & Chemokines((IL)-6. epithelial. infiltration. and dendritic.

which stimulates placental prostaglandin synthesis and myometrial contractility [69]. .Prostaglandins produced in the amnion are normally inactivated by prostaglandin dehydrogenase released by the chorionic tissue. Increased CRH causes the fetal adrenal glands to increase cortisol production. Infection of the chorion inhibits the activity of prostaglandin dehydrogenase. thus preventing prostaglandins reaching the myometrium and causing uterine contractions [23]. In human pregnancies affected by chorioamnionitis. thereby allowing prostaglandins to reach the myometrium and cause premature contractions [68]. FIRS increases the production of corticotrophin releasing hormone (CRH) from both the fetal hypothalamus and the placenta [23] .

epidemiological.SUMMARY • Available clinical. • Improved antenatal screening for chorioamnionitis and identification of effective treatment strategies for preterm infants exposed to intrauterine inflammation will likely provide a better prognosis for infants at risk of multiple organ disease as a result of exposure to inflammation before birth. . and experimental data indicate that chorioamnionitis plays a significant role in predisposing the preterm infant to multiple organ disease.


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