Description of the condition
Chorioamnionitis is an infection of the fetal membranes, amniotic fluid, and placenta and/or decidua during pregnancy and poses a significant risk to infant and maternal morbidity and mortality. It can also be referred to as intra-amniotic infection (IAI), amnionitis, and amniotic fluid infection (Incerpi 2010; Tita 2010).
Chorioamnionitis can be defined clinically or histologically. Clinical chorioamnionitis is estimated to occur in 1% to 2% of term and 5% to 10% of preterm births and histological chorioamnionitis is found in nearly 20% of term and 50% of preterm births (Incerpi 2010). The clinical definition of chorioamnionitis can vary but is best characterized as maternal fever (100.4 degrees Fahrenheit) that is not attributable to another cause and exhibits at least one of the following symptoms: maternal tachycardia, fetal tachycardia, uterine tenderness, maternal leukocytosis (white blood cell count greater than 15,000 mL) and amniotic fluid with a foul odor (Fishman 2012).
There are few diagnostic tests that are specific and sensitive, as well as safe for mother and infant, therefore, chorioamnionitis is primarily diagnosed through clinical signs and symptoms. A culture of the amniotic fluid obtained from an amniocentesis is the reference standard for diagnosis but it requires 48 hours for test results and there is insufficient evidence that it reduces maternal or neonatal morbidity. Blood cultures and vaginal swabs are other diagnostic tests for chorioamnionitis but the supportive evidence for both is limited and some recommendations suggest that vaginal swabs should not be used in cases of preterm prelabor rupture of membranes (Czikk 2011).
Like clinical chorioamnionitis, the case definition of histological chorioamnionitis varies between studies (Holzman 2007), but generally can be defined as acute inflammatory changes on the placenta's membrane roll and chorionic plate (Yoon 2001). Diagnosis is made based on microscopic examination of placental and chorioamnionic specimens (Tita 2010).
Chorioamnionitis is most frequently caused by bacteria ascending from the lower genital tract and is predominantly seen in instances of rupture of the membrane, but can occur in intact membranes (Fahey 2008). The infection can also be caused by blood-borne or transplacental infection, and transuterine infection from invasive procedures such as amniocentesis or chorionic villus sampling, but these routes tend to be less common (Edwards 2005; Fahey 2008).
Chorioamnionitis is generally a polymicrobial infection with most cases having two detectable pathogens but it can be caused by viral and in rare instances, fungal agents (Czikk 2011). The common organisms found in amniotic fluid are Mycoplasma hominis, Ureaplasma urealyticum ( Tita 2010) but other pathogens include Chlamydia trachomatis, Neisseria gonorrhoeae, Tichomonas vaginalis, anaerobic Gram-negative bacilli like Bacteroides and Gardnerella vaginalis, Escherichia coli, anaerobic streptococci and streptococci group B (Czikk 2011; Edwards 2005).
The differential diagnosis of chorioamnionitis includes epidural-associated fever and other extrauterine and non-infectious conditions. An epidural-associated fever may be considered for intrapartum patients with epidurals and a low grade fever but without maternal or fetal tachycardia or other clinical symptoms. Fever and abdominal pain are symptoms of extrauterine infectious including urinary tract infection, influenza, appendicitis and pneumonia. Abdominal pain without a fever may indicate a non-infectious condition including thrombophlebitis, round ligament pain, colitis, connective tissue disorder and placental abruption (Tita 2010).
Risk factors for developing chorioamnionitis include being in active labor for a long period of time, duration of rupture of membrane and internal monitoring (Newton 1989), meconium staining of amniotic fluid, a high number of digital vaginal examinations (Seaward 2005), nulliparity, African American ethnicity, smoking and alcohol or drug abuse, epidural anesthesia, bacterial vaginosis and colonization with group B streptococcus or Ureaplasma bacterium (Tita 2010).
Preventing chorioamnionitis is better than treatment and some interventions have been shown to reduce the incidence of chorioamnionitis (Gibbs 2004). A 53% reduction in maternal morbidity due to chorioamnionitis and endometritis was seen in term pregnancies receiving an active management of labor program compared with traditional management (López-Zeno 1992). For at-term pregnancies complicated by prelabor rupture of the membranes (PROM), management by immediate oxytocin induction compared with conservative management showed fewer cases of chorioamnionitis (Mozurkewich 1997) and for preterm pregnancies with PROM, the use of broad-spectrum antibiotics showed a decrease in chorioamnionitis (Kenyon 2010).
Description of the intervention
Some aspects of the timing of antibiotic therapy (intrapartum, postpartum, or combined intra- and postpartum), the antibiotic regimen, and the duration of antibiotic therapy have been evaluated in individual situations but not comprehensively (Fishman 2012). A previous Cochrane review (Hopkins 2002) identified two randomized controlled trials assessing the use of ampicillin and gentamicin for the treatment of intra-amniotic infection versus postpartum treatment and ampicillin/gentamicin/clindamycin versus ampicillin/gentamicin; none of the outcomes showed a statistically significant difference between the different interventions.
How the intervention might work
Treatment for chorioamnionitis is usually with antibiotics that can be administered intrapartum or immediately postpartum. Since the infection could be caused by a wide variety of organisms treatment with broad spectrum of antibiotics is needed. The typically standard of care is clindamycin for anaerobic and gram-positive bacteria and gentamicin for aerobic and gram-negative bacteria (Mtira 1997).
Why it is important to do this review
Chorioamnionitis is a common infection that affects both mother and infant. Infant complications associated with chorioamnionitis include early neonatal sepsis, pneumonia, meningitis (Incerpi 2010), asthma (Getahun 2010), cerebral palsy (Wu 2000), intraventricular hemorrhage (Edwards 2005), and periventricular leukomalacia (Edwards 2005; Rocha 2007). Although fetal complications are more common, chorioamnionitis can also result in maternal morbidity such as pelvic infection and septic shock (Incerpi 2010). The risk for cesarean delivery is two to three times higher in women who have chorioamnionitis as well as three to four times greater for endomyometritis, wound infection, pelvic abscess, bacteremia and postpartum hemorrhage (Tita 2010).
A Cochrane review was conducted 10 years ago to study the effects of maternal antibiotic regimens for intra-amniotic infection on maternal and perinatal morbidity and mortality (Hopkins 2002). The review identified two eligible studies and the conclusions were limited due to the small number of studies. A statistically significant difference was not seen in any of the outcomes and therefore the review was not able to make recommendations on timing of administration of the antibiotic treatment (intrapartum versus postpartum). Additionally, no Cochrane systematic review has evaluated studies in which antibiotic treatment for chorioamnionitis was given during the postpartum period. Currently, there is insufficient information to determine the most appropriate antimicrobial regimen for the treatment of intra-amniotic infection; whether antibiotics should be continued during the postpartum period, which antibiotic regimen, or what treatment duration should be used. This review will update the review with new references and expand the scope of the review to include antibiotic regimens during the postpartum period.