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Obstet Gynecol Clin N Am 32 (2005) 287 296

Chorioamnionitis and Labor

Rodney K. Edwards, MD, MS
Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, University of Florida College of Medicine, PO Box 100294, 1600 Southwest Archer Road, Gainesville, FL 32610-0294, USA

Chorioamnionitis is a puerperal infection that may be defined clinically or histologically. It also exists in a subclinical form. This entity may complicate labor at term and is believed to play a causative role in many cases of spontaneous preterm delivery. Dysfunctional labor, an increased need for cesarean delivery, and infection-related problems are maternal complications associated with chorioamnionitis. Appropriate treatment of patients with clinical chorioamnionitis includes delivery and the administration of broad-spectrum antibiotics as soon as possible after diagnosis. This article focuses primarily on the effects of chorioamnionitis on the progress of labor and the clinical management of the infection. The epidemiology and pathogenesis of this infection are reviewed. Although the associated maternal and neonatal outcomes are addressed, detailed discussion of these associations is the subject of other reviews.

Definitions, incidence, and risk factors The term chorioamnionitis, strictly defined, refers to inflammation or infection of the placenta and of the chorion and the amnion (the fetal membranes). The term may refer to a histologic, subclinical, or clinical diagnosis. Synonyms for clinical chorioamnionitis include intra-amniotic infection and amnionitis. Histologic chorioamnionitis is defined by infiltration of the fetal membranes with polymorphonuclear leukocytes, and it occurs far more frequently than does clinically evident infection [1]. Most cases of histologic chorioamnionitis

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Table 1 Independent risk factors for clinical chorioamnionitis Risk factor Nulliparity Duration of labor Duration of ROM Internal fetal monitors Number of vaginal examinations Soper et al, [3]
a a a a

Newton et al, [4]

a a a

Abbreviation: ROM, rupture of membranes. a Independent risk factor by logistic regression analysis.

occur in cases in which there were no clinical signs or symptoms of infection. This diagnosis can be made in up to 20% of term deliveries and more than 50% of preterm deliveries. In contrast, clinical chorioamnionitis occurs in 1% to 2% of term and 5% to 10% of preterm deliveries [2]. The incidence may be higher in the setting of prolonged rupture of the membranes. Risk factors that often are cited as being associated with clinical chorioamnionitis include young age, low socioeconomic status, nulliparity, long labor, extended duration of ruptured membranes, multiple vaginal examinations, prolonged internal fetal monitoring, bacterial vaginosis, colonization with group B streptococci, and meconiumstained amniotic fluid. Table 1 lists the risk factors that were independently associated with this infection in prospective studies conducted at two tertiary care medical centers [3,4].

Microbiology and pathogenesis Most cases of chorioamnionitis are ascending in origin, with organisms from the vagina gaining access into the upper genital tract through the cervix. A few cases, however, are caused either by hematogenous spread or invasive procedures, such as amniocentesis. The infection is polymicrobial in nature. The organisms most commonly isolated from the amniotic fluid of patients with clinical chorioamnionitis are mycoplasmas such as Mycoplasma hominis and Ureaplasma urealyticum, anaerobic Gram-negative bacilli, such as those of the genera Bacteroides and Prevotella, coliforms such as Escherichia coli, anaerobic streptococci, and group B streptococci [57]. Table 2 summarizes the results from one study that evaluated the distribution of microorganisms isolated from the amniotic fluid of 408 patients with chorioamnionitis. Note that in keeping with the contention that this infection is polymicrobial, the total number of isolates is much larger than the total number of patients. Supporting ascension from the vagina as the source of most cases of chorioamnionitis, organisms isolated from subjects in this and similar studies are found in the bowel flora or in cases of bacterial vaginosis.

chorioamnionitis and labor Table 2 Micro-organisms isolated from 408 patients with chorioamnionitis Organism Ureaplasma urealyticum Mycoplasma hominis Bacteroides bivius Gardnerella vaginalis Group B streptococci Peptostreptococci Escherichia coli Fusobacterium species Enterococci Other aerobic Gram-negative rods Bacteroides fragilis Total isolates Number of isolates 193 125 120 99 60 38 33 23 22 21 14 748


Patients (%) 47 31 29 24 15 9 8 6 5 5 3

Data from Sperling RS, Newton E, Gibbs RS. Intra-amniotic infection in low-birth-weight infants. J Infect Dis 1988;157:1137.

Chorioamnionitis may result in or occur in conjunction with infection or inflammation of other gestational tissues. These sites include the decidua (deciduitis), placental villi (villitis), and the umbilical cord (funisitis). Chorioamnionitis also may result in maternal or fetal bacteremia. In the small percentage of cases that are caused by hematogenous spread, bacteremia actually may precede and cause the infection of the placenta and fetal membranes. As stated earlier, however, hematogenously acquired chorioamnionitis is unusual.

Making the diagnosis Histologic chorioamnionitis occurs with a much higher incidence than clinical chorioamnionitis. Consequently, the occurrence of these two entities correlates poorly [1]. The diagnosis of histologic chorioamnionitis is made based on identification of polymorphonuclear leukocytes on pathologic examination of the placenta and fetal membranes. Its diagnosis has little value in the prospective clinical management of patients. The clinical criteria used to make the diagnosis of clinical chorioamnionitis include maternal fever, maternal tachycardia, fetal tachycardia, uterine tenderness, and foul-smelling amniotic fluid [2]. Different centers have different requirements for making this clinical diagnosis. At the University of Florida, we require a temperature of at least 388C and one or more of the previously mentioned criteria. Other researchers have published different diagnostic criteria. Gibbs et al [7], in their prospective studies, defined intra-amniotic infection on the basis of a temperature of at least 37.88C (1008 F) and two or more of the following additional criteria: maternal tachycardia, fetal tachycardia, uterine tenderness, foul odor of the amniotic fluid, and maternal leukocytosis.



Maternal leukocytosis supportsbut is not required to make the diagnosis ofclinical chorioamnionitis. A mild leukocytosis can be associated with labor or with pregnancy itself; however, a peripheral white blood cell count of more than 15,000 is suspicious for infection. Leukocytosis particularly is consistent with infection if a left shift (ie, an increase in the proportion of neutrophils, especially immature forms) is present. One caveat is that the recent administration of corticosteroids may cause a mild leukocytosis. The increase will be caused by demarginated mature neutrophils, however, and the presence of immature forms still would suggest infection. For cases in which the diagnosis is in doubt or when a diagnosis of subclinical chorioamnionitis is sought, amniocentesis may provide useful information. Tests that commonly are performed on amniotic fluid in an attempt to diagnose subclinical chorioamnionitis include leukocyte esterase (on a urine dipstick), glucose, Gram stain, and culture. Of the tests that can be performed rapidly, amniotic fluid glucose is the one that is the most specific for predicting a positive amniotic fluid culture [8]. Amniotic fluid interleukin-6 is even more sensitive and specific [9,10]. The test usually is not available, however, except in a research setting. Studies that use polymerase chain reaction directed against the common bacterial ribosomal subunit have demonstrated that amniotic fluid culture probably is an unsatisfactory gold standard for detection of subclinical chorioamnionitis, because many more patients in preterm labor with intact membranes have organisms detectable in the amniotic fluid by polymerase chain reaction than by culture [11].

Effects on the progress of labor In the 1980s, studies were conducted that evaluated the characteristics of labor in patients with chorioamnionitis. Duff et al [12] evaluated patients who developed clinical chorioamnionitis after entering labor spontaneously. Seventyfive percent of the patients in that study had decreased uterine contractility, and despite oxytocin augmentation, 34% required cesarean delivery because of failure to progress in labor. As compared with their uninfected counterparts, even patients with subclinical chorioamnionitis seem to have poorer uterine contractility. Silver et al [13] found that patients with positive amniotic fluid cultures but no clinical signs or symptoms of infection required higher doses of oxytocin to achieve adequate uterine activity. Many patients with chorioamnionitis, perhaps as many as 75%, require oxytocin augmentation [3,12]. When this diagnosis is made, dysfunctional labor and the need for oxytocin augmentation should be anticipated. Whether chorioamnionitis is a result of or results in protracted labor is a difficult question. At least one study suggested that the former is true, however. Satin et al [14] conducted a case-control study that demonstrated that patients with chorioamnionitis diagnosed before oxytocin augmentation had shorter

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intervals from initiation of oxytocin to delivery than did uninfected controls. The cesarean delivery rate was not increased in that infected subgroup. In contrast, when chorioamnionitis was diagnosed after oxytocin augmentation had begun, the interval from oxytocin initiation until delivery was significantly longer than in the uninfected controls, and the cesarean delivery rate was increased by a factor of 4 (40% versus 10%; P b 0.001). Mark et al [15] conducted a cohort study to evaluate the relationship between clinical chorioamnionitis and abnormal uterine function, including labor abnormalities, cesarean delivery, and postpartum hemorrhage. In their study, as in the others cited previously, chorioamnionitis was associated with an increased likelihood of labor abnormalities and cesarean delivery. After multivariate analysis, the chorioamnionitis group was 50% (95% confidence interval 20, 80) more likely to have a postpartum hemorrhage after cesarean and 80% (95% confidence interval 50, 110) more likely to have a postpartum hemorrhage after vaginal delivery. When making the diagnosis of clinical chorioamnionitis, a clinician should anticipate suboptimal uterine contractility before and after delivery. Many cases of preterm labor, particularly if remote from term, are related to infection or inflammation. Clinically evident or subclinical chorioamnionitis is the most frequent identifiable cause of preterm labor. Preterm labor may have a different mechanism than labor at term. In myometrial cell culture, prolonged exposure to interleukin-1 has been shown to decrease the production of inositol triphosphate by myometrial cell and to decrease intracellular calcium [16]. The number of oxytocin receptors on the surface of the myometrial cells is decreased by a factor of 10 with such prolonged pro-inflammatory stimulation [17]. In the setting of chorioamnionitis, labor probably is not as much associated with oxytocin as it is with prostaglandins produced by cyclo-oxygenase-2 in response to the pro-inflammatory stimulus. The results of these basic science experiments also may explain partially the increased rate of labor abnormalities that are encountered in the setting of chorioamnionitis.

Management For the most part, the management of patients with clinical chorioamnionitis centers on effecting delivery and administering broad-spectrum antibiotics. Although there does not seem to be a need for an arbitrary time limit from diagnosis to delivery [18], as discussed in the previous section, the rate of cesarean delivery increases in patients with this infection. The most widely studied regimen for the treatment of chorioamnionitis is the combination of gentamicin (Garamycin), 1.5 mg/kg intravenously every 8 hours, plus either ampicillin (Omnipen; Principen), 2 g intravenously every 6 hours, or aqueous penicillin G, 5 million U intravenously every 6 hours [19,20]. A drug to provide enhanced coverage of anaerobic bacteria should be added for patients who undergo cesarean delivery. Appropriate choices include clinda-



mycin (Cleocin) or metronidazole (Flagyl). In some clinical settings, singleagent treatments may be more cost effective or more desirable because of other considerations. Reasonable choices include extended-spectrum penicillins or cephalosporins, such piperacillin-tazobactam (Zosyn) or cefotetan (Cefotan) [19]. Antibiotic therapy should be initiated as soon as possible after the diagnosis of chorioamnionitis is made. In the past, there was concern about such an approach resulting in false-negative neonatal blood cultures that would complicate decision making in the care of the neonate. The available evidence clearly shows an advantage of intrapartum treatment over immediate postpartum treatment of chorioamnionitis, however. In 1987, Sperling et al [21] published a cohort study that evaluated 257 mother-infant pairs. Intrapartum or postpartum treatment was left to the discretion of the treating physician. As would be expected, the group that received intrapartum treatment had a longer diagnosis to delivery interval (4.7 versus 1.9 hours; P b 0.001). The rate of neonatal sepsis was significantly lower in that group (2.8 versus 19.6%; P b 0.001), however, and there was a trend toward a lower rate of sepsis-related neonatal mortality (0.9 versus 4.3%; P = 0.15). The following year, Gilstrap et al [22] published a similar retrospective study of 312 women with chorioamnionitis. They demonstrated a lower rate of neonatal bacteremia in the group that received antibiotics intrapartum rather than immediately postpartum (1.5 versus 5.7%; P = 0.06). Finally, Gibbs et al [23] conducted a randomized, nonblinded trial of intrapartum compared with immediate postpartum treatment of chorioamnionitis. They used a combination of ampicillin plus gentamicin, and they added clindamycin to the regimen for patients who underwent cesarean delivery. The results of the study were so dramatic that the trial was halted prematurely by its data safety monitoring board after enrollment of only 45 patients because of ethical issues of withholding treatment of future enrollees who would be randomized to the postpartum treatment group. There were no cases of neonatal sepsis in the intrapartum treatment group, compared with a rate of 21% in the postpartum treatment group (P = 0.03). The maximum maternal temperature in the postpartum period also was lower with intrapartum treatment. Based on the results of these three studies, it seems clear that treatment for chorioamnionitis should be started intrapartum as soon as possible after the diagnosis of chorioamnionitis is made. Such an approach results in decreased rates of neonatal infection and improved maternal outcome and is not associated with any increase in delayed neonatal sepsis. The duration of maternal antibiotic therapy necessary in the postpartum period for women who were diagnosed with chorioamnionitis intrapartum traditionally has been thought to be 48 to 72 hours [19,24]. This recommendation primarily was based on expert opinion (level III evidence), however, and recent investigators have challenged the need for prolonged antibiotic therapy in the postpartum period. Chapman and Owen [25] conducted a randomized clinical trial that involved women with chorioamnionitis who delivered vaginally. During labor, women

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received a combination of ampicillin and gentamicin. At the time of delivery, subjects were randomized to receive either a single 2-g dose of cefotetan or this same dose every 12 hours for 48 hours. The study was not powered to detect a difference in treatment failure between groups. In the single and multiple dose groups, respectively, the treatment failure rate was 11% compared with 3.7% (P = 0.27). The single-dose regimen was associated with shorter mean maternal postpartum hospital stays, however (33 versus 57 hours; P b 0.001). Turnquest et al [26] published a randomized clinical trial that involved women with chorioamnionitis who underwent cesarean delivery. All patients received intrapartum ampicillin. Preoperatively, they received doses of gentamicin plus clindamycin. Postpartum, patients were randomized to receive no additional antibiotics or gentamicin and clindamycin every 8 hours for 24 hours. Although this study also was underpowered to detect a difference in treatment failure rate between groups, the rates were 14.8% and 21.8% for the no antibiotics and the antibiotics groups, respectively. To address this issue more definitively, we conducted a randomized clinical trial of an abbreviated postpartum antibiotic regimen for patients with chorioamnionitis that was sufficiently powered to address treatment failure as the primary outcome [27]. Women with vaginal and cesarean deliveries were included. The intrapartum treatment regimen was ampicillin and gentamicin. Patients who delivered vaginally received either the next scheduled dose of both drugs or continued ampicillin and gentamicin until afebrile and asymptomatic for at least 24 hours postpartum. Patients who underwent cesarean delivery received a dose of clindamycin at the time of umbilical cord clamping. Patients who were randomized to the abbreviated treatment regimen received no additional doses of clindamycin but did receive the next scheduled dose each of ampicillin and gentamicin. The other group of subjects received all three drugs until afebrile and asymptomatic for at least 24 hours postpartum. We defined treatment failure as one postpartum temperature at or above 398C or two temperatures, at least 4 hours apart, of at least 38.48C. For the short and long course groups, respectively, the rates of treatment failure were 4.6% compared with 3.5% (P = 0.64). Infection-related complications were rare and did not differ between groups. A short course of antibiotics seems to be sufficient postpartum therapy for women with chorioamnionitis.

Maternal and neonatal outcomes Maternal bacteremia is an uncommon complication of clinical chorioamnionitis and occurs in less than 10% of cases [20]. Because bacteremia is infrequent and the infection is treated with broad-spectrum antibiotics, performing blood cultures is not necessary in the routine care of patients with chorioamnionitis. Operations performed in an infected surgical field (eg, cesarean delivery of a patient with clinical chorioamnionitis) are associated with an increased likelihood of complications. Fortunately, however, wound infections oc-



cur in fewer than 10% of cases, and pelvic abscess is rare with the use of perioperative anti-anaerobic antibiotics [27]. It is well established that there are increased rates of bacteremia, clinical sepsis, and mortality in infants born to women with chorioamnionitis. The rates of these complications decrease significantly with the prompt administration of maternal antibiotics intrapartum. Other neonatal complications associated with chorioamnionitis have been appreciated more recently, however. Grether and Nelson [28] published a case-control study of infants with birth weights of at least 2500 g. Clinical chorioamnionitis was associated with an odds ratio of 9.3 for cerebral palsy. Infection also was linked to low Apgar scores, hypotension, the need for resuscitation at the time of delivery, and neonatal seizures. Another group of investigators reported that in a cohort of infants with birth weights between 500 and 1500 g, after adjusting for other factors, clinical chorioamnionitis was associated with a threefold increased risk of intraventricular hemorrhage, periventricular leukomalacia, and seizures within the first 24 hours of birth [29]. Periventricular leukomalacia is the radiographic finding most closely linked to the later development of cerebral palsy. Evidence exists that this association between chorioamnionitis and adverse neurologic outcome in the neonate is caused by the inflammatory response. In a cohort of women with preterm labor but without the clinical diagnosis of chorioamnionitis, Yoon et al [30] found that increased amniotic fluid levels of pro-inflammatory cytokines (tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6) were associated with a four- to sixfold increased risk of cystic periventricular leukomalacia. The same group reported that the presence of funisitis or increased amniotic fluid levels of interleukin-6 and interleukin-8 all had adjusted odds ratios of 5 to 7 for the clinical diagnosis of cerebral palsy in the child at the age of 3 years [31].

Summary Clinical chorioamnionitis occurs in 1% to 2% of term and up to 15% of preterm deliveries. The incidence of histologic chorioamnionitis is much higher than that of clinically diagnosed infection, and the correlation between these entities is poor. Most cases of chorioamnionitis are caused by organisms ascending into the uterus from the lower genital tract. The pathogens involved in this polymicrobial bacterial infection primarily are mycoplasmas, anaerobes, coliforms, and group B streptococci. The infection primarily is diagnosed clinically. In selected situations, however, amniocentesis may be useful in uncovering subclinical cases of chorioamnionitis. When chorioamnionitis is diagnosed, dysfunctional labor and the need for oxytocin augmentation should be anticipated. Broad-spectrum antibiotics should be started at the time of diagnosis; such an approach improves maternal and neonatal outcome. Anti-anaerobic coverage is needed after ce-

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sarean delivery, but a short course of antibiotics is sufficient for postpartum treatment of patients with chorioamnionitis. Despite appropriate therapy, recent evidence has demonstrated that even subclinical chorioamnionitis is associated with neonatal complications. These complications include not only infection but also intraventricular hemorrhage, periventricular leukomalacia, and the development of cerebral palsy.

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[20] Newton ER. Chorioamnionitis and intraamniotic infection. Clin Obstet Gynecol 1993;36: 795 808. [21] Sperling RS, Ramamurthy RS, Gibbs RS. A comparison of intrapartum versus immediate postpartum treatment of intraamniotic infection. Obstet Gynecol 1987;70:861 5. [22] Gilstrap LC, Leveno KJ, Cox SM, et al. Intrapartum treatment of acute chorioamnionitis: impact on neonatal sepsis. Am J Obstet Gynecol 1988;159:579 83. [23] Gibbs RS, Dinsmoor MJ, Newton ER, et al. A randomized trial of intrapartum versus postpartum treatment of women with intraamniotic infection. Obstet Gynecol 1988;72:823 8. [24] Gilstrap LC, Cox SM. Acute chorioamnionitis. Obstet Gynecol Clin N Am 1989;16:373 9. [25] Chapman SJ, Owen J. Randomized trial of single-dose versus multiple-dose cefotetan for the postpartum treatment of intrapartum chorioamnionitis. Am J Obstet Gynecol 1997;177: 831 4. [26] Turnquest MA, How HY, Cook CR, et al. Chorioamnionitis: is continuation of antibiotic therapy necessary after cesarean section? Am J Obstet Gynecol 1998;179:1261 6. [27] Edwards RK, Duff P. Single additional dose postpartum therapy for women with chorioamnionitis. Obstet Gynecol 2003;102:957 61. [28] Grether JK, Nelson KB. Maternal infection and cerebral palsy in infants of normal birth weight. JAMA 1997;278:207 11. [29] Alexander JM, Gilstrap LC, Cox SM, et al. Clinical chorioamnionitis and the prognosis for very low birth weight infants. Obstet Gynecol 1998;91:725 9. [30] Yoon BH, Jun JK, Romero R, et al. Amniotic fluid inflammatory cytokines (interleukin-6, interleukin-1beta, and tumor necrosis factor-alpha), neonatal brain white matter lesions, and cerebral palsy. Am J Obstet Gynecol 1997;177:19 26. [31] Yoon BH, Romero R, Park JS, et al. Fetal exposure to an intra-amniotic inflammation and the development of cerebral palsy at the age of three years. Am J Obstet Gynecol 2000; 182:675 81.