A relatively common disorder of pregnancy.

Infection of amniotic fluid can result in endomyometritis.

Women with prolonged labor and ruptured membranes who have frequent pelvic examinations are at risk for amniotic fluid infection.

An inflammation of the fetal membranes, the amnion and chorion, due to a bacterial infection.

Usually results from bacteria ascending into the uterus from the vagina and is most often associated with prolonged labor.

Passage of bacteria occurs most commonly by retrograde or ascending infection from the lower genital tract from the cervix and vagina.

Hematogenous or transplacental passage of infectious agents and iatrogenic infection following amniocentesis or chorionic villous sampling are less common sources of infection.

The risk of its development increases with each vaginal examination performed in the final month of pregnancy, including during labor.

Risk factors include: long duration of membrane rupture, prolonged labor, nulliparity, African American ethnicity, multiple vaginal exams, meconium-stained amniotic fluid, smoking, alcohol and drug abuse, immune-compromised states, epidural anesthesia, colonization with group B streptococcus, bacterial vaginosis, sexually transmissible infections and and internal monitoring.

Associated with untreated Group B streptococcus bacteriuria.

Overall, 1–4% of all births in the US are complicated by chorioamnionitis.

Twelve percent of primary cesarean births at term involve clinical chorioamnionitis, due to failure to progress usually after membrane rupture.

Chorioamnionitis clinically and histologically combined complicates as many as 40–70% of preterm births with premature membrane rupture or spontaneous labor and 1–13% of term births.

Frequency varies markedly by diagnostic criteria, specific risk factors and gestational age.

A risk factor for periventricular leukomalacia and prematurity.

A clinical diagnosis in the setting of maternal fever, uterine tenderness in the presence of confirmed premature rupture of membranes (PROM).

The key clinical findings associated with clinical chorioamnionitis include fever, uterine fundal tenderness, maternal tachycardia (>100/min), fetal tachycardia (>160/min) and purulent or foul amniotic fluid.

Maternal fever is the most important clinical sign.

Temperature > 100.4°F is considered abnormal in pregnancy. and if it persists more than 1h or any fever ≥101°F warrants evaluation and appropriate intervention.

Fever is present in 95–100% of cases, and its presence is required for the diagnosis.

Maternal tachycardia of >100 BPM) and fetal tachycardia >160 BPM occur frequently being reported in 50–80% and 40–70% of cases respectively.

The combination of maternal fever and maternal and/or fetal tachycardia are strongly suggestive of intrauterine infection.

Uterine fundal tenderness and a foul odor to the amniotic fluid occrs in only 4–25% of cases.

Maternal leucocytosis or the presence of a left shift supports the diagnosis.

Leucocytosis is reported in approximately 70–90% of cases of clinical disease.

Tests on amniotic fluid, obtained by amniocentesis, has been used for the diagnosis of chorioamnionitis.

Culture of amniotic fluid is the most reliable test but the results may not be available for up to 3 days.

Because of the invasive nature of amniocentesis it is not performed in the majority of cases, which occur during labor.

Amniocentesis to confirm clinically suspected chorioamnionitis may be performed to determine whether preterm delivery is warranted.

Amniocentesis is also used to identify subclinical chorioamnionitis in women with spontaneous preterm labor and preterm membrane rupture at early gestational ages.

Associated with significant maternal, perinatal, and long-term adverse outcomes.

Adverse maternal outcomes include postpartum infections and sepsis.

The presence of infectious agents in the chorioamnionitic membranes cause a maternal and fetal inflammatory response with the release of proinflammatory and inhibitory cytokines and chemokines.

The inflammatory response produces clinical chorioamnionitis, leads to prostaglandin release, ripening of the cervix, membrane injury and labor at term or premature birth at earlier gestational ages.

The fetal inflammatory response may induce cerebral white matter injury, with the development of cerebral palsy and other neurological deficits, risk of direct fetal infection and sepsis,

Adverse infant outcomes include stillbirth, premature birth, asphyxia, neonatal sepsis, neonatal shock, chronic lung disease, intraventricular hemorrhage and brain injury leading to cerebral palsy and other neurodevelopmental disabilities.

Can occur with intact membranes.

Chorioamnionitis with intact membranes common for genital mycoplasmas such as Ureaplasma species and Mycoplasma hominis, found in the lower genital tract of over 70% of women.

It is a polymicrobial infection most often due to ascending genital microbes with more than 65% of positive amniotic fluid cultures involving two or more organisms.

The genital mycoplasmas, Ureaplasma urealyticum and Mycoplasma hominis constitute the most frequently involved agents, occurring in up to 47% and 30%, respectively of cases of culture-confirmed cases.

These agents are commonly isolated from amniotic fluid in the setting of preterm birth or premature membrane rupture with or without clinical chorioamnionitis.

Genital mycoplasmas are found in the lower genital tract of over 70% of women, their presence in the upper genital tracts and chorioamnion of pregnant women is rare, less than 5%, the absence of labor or membrane rupture.

Other common agents include anaerobes such as Gardnerella vaginalis , 25%, and bacteroides, 30%, aerobes including Group B streptococcus 15%, and gram-negative rods including Escherichia coli.

Histologic chorioamnionitis at term is up to 3 times as frequent as clinical chorioamnionitis confirmed by amniotic fluid culture.

Cultures for genital mycoplasmas, the most common organisms associated with chorioamnionitis, are not very sensitive.

Rarely is hematogeneously spread, as may occur with Listeria monocytogenes.

Can be be diagnosed from a histologic examination of the fetal membranes showing infiltration of the chorion by neutrophils.

A more severe process involves subamniotic tissue and may have fetal membrane necrosis and/or abscess formation.

Severe disease may be accompanied by vasculitis of the umbilical blood vessels, and connective tissue can occur.

Chorioamnionitis in a previous pregnancy may not be associated with an increased risk in a subsequent pregnancies.

Preterm premature rupture of membranes is frequently due to subclinical chorioamnionitis.

Premature ROM at term, with membrane rupture at ≥37 weeks gestation but prior to onset of uterine contractions, occurs in 8% or less of term births, is also associated with an increased risk of chorioamnionitis.

Leads to a 2 to 3-fold increased risk for cesarean delivery.

Leads to a 2 to 4-fold increase in endomyometritis, wound infection, pelvic abscess, bacteremia and postpartum hemorrhage.

Postpartum hemorrhage as a result of chorioamnionitis is due to dysfunctional uterine muscle contractions as a result of inflammation.

Ten percent have positive blood cultures, most commonly involving Group B streptococcus and E. coli .

Multiorgan failure is. rarely encountered.

Fetal response to chorioamnionitis may lead to death, neonatal sepsis and numerous other postnatal complications.

The neonate may manifest adverse effects at or shortly after birth.

Neonatal pneumonia, sepsis and perinatal death occurs, in 4%, 8% and 2%, respectively of term deliveries associated with chorioamnionitis.

Respiratory distress occurs in 20% of neonates when chorioamnionitis is present.

Preterm infants have higher rates of complications than term infants, including perinatal death 25 vs. 6%, neonatal sepsis 28 vs. 6 %, pneumonia 20 vs. 3%, grades 3 or 4 intraventricular hemorrhage 24 vs. 8 % and respiratory distress 62 vs. 35%.

Associated with up to 40% of cases of early-onset neonatal sepsis.

Associated with a 4-fold increase in the frequency of cerebral palsy.

Rapid antibiotic therapy is essential to prevent both maternal and fetal complications.

Time -to-delivery after institution of antibiotic therapy does not affect morbidity.

Cesarean delivery to expedite delivery is not indicated unless there are other obstetric indications.

Antibiotic treatment consists of: multiple antibiotics including amoxicillin, gentamicin and metronidazole.

The frequency of neonatal sepsis is reduced by up to 80% with intrapartum antibiotic treatment.

Standard antibiotic regimen effectively treats >95% of maternal infections and reduces neonatal sepsis, despite not being optimal treatment for mycoplasma organisms, the most commonly associated agents associated with chorioamnionitis.

Macrolide antibiotics provide better coverage for mycoplasma.

Controlling maternal fever is important to prevent intrapartum period fetal acidosis and neonatal encephalopathy.

As preterm premature rupture of membranes (PPROM) is a major cause of clinical chorioamnionitis with up to 70% subsequently developing chorioamnionitis, prophylactic antibiotics, with ampicillin and erythromycin reduce neonatal death, chronic lung disease and cerebral abnormalities.

Antibiotics reduce the incidence of clinical or pathologic chorioamnionitis and neonatal sepsis and prolongs time-to-delivery among women with preterm membrane rupture, but not among those in active preterm labor with intact membranes.

The ORACLE II trial of antibiotics for women with spontaneous preterm labor (SPTL) with intact membranes was associated with an unexpected increase in cerebral palsy in infants.

Induction of labor and delivery for Preterm PROM (PPROM) after 34 weeks’ gestation is recommended.

Compared to expectant management, early delivery is associated with reduced maternal infection and need for neonatal intensive care without any increase in perinatal morbidity and mortality in the setting of PPROM.

With prolonged membrane rupture, longer than 18 hours at term, prophylactic antibiotics are not indicated if the mother is not colonized with GBS.

In the above circumstance if the maternal GBS is unknown then prophylactic antibiotics should be administered.

The use of intrapartum prophylactic antibiotics for meconium-stained fluid is associated with a reduction in the risk of chorioamnionitis.

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