Infectious Diseases in and Gynecology 3:123-132 (1995) (C) 1995 Wiley-Liss, Inc.

Modern Management of Clinical

Thomas Westover and Robert A. Knuppel Division of Maternal-Fetal Medicine, Department of Obstetrics, Gynecology, and Reproductive Sciences, Robert Wood Johnson Medical School Peter's Medical Center, University of Medicine and Dentistry of New Jersey, New Brunswick, NJ

ABSTRACT

Clinical chorioamnionitis continues to contribute to fetal and maternal morbidity and mortality. Significant advances have been made in the last 20 years in understanding the pathophysiologic processes leading to chorioamnionitis. This review addresses the history, incidence, pathophysiol- ogy, host defenses, risk factors, diagnosis, and maternal and neonatal management of clinically evident chorioamnionitis. After a detailed review of the physiologic processes leading to clinical chorioamnionitis and sepsis, we present a modern management scheme designed to optimize peri- natal outcome for both mother and . (C) 1995 Wiley-Liss, Inc.

KEY WORDS Fever, amniotic infection, placenta, , intrauterine infection

ntrauterine infection, either antepartum or intra- tal ; and malodorous, purulent amniotic partum, continues to contribute to perinatal and fluid. Labor may or may not be present and the maternal morbidity and mortality. A number of membranes may or may not be ruptured. Any of terms have been used to describe this condition these physical findings may be absent depending on including clinical chorioamnionitis, intrapartum fe- the severity and duration of the infection, virulence ver, amnionitis, amniotic-fluid infection, and in- and inoculum size of the organism, integrity of the traamniotic infection. Unfortunately, these terms host defense mechanisms, and presence of masking have been used by different investigators to charac- factors such as regional anesthesia. The diagnosis terize 3 separate clinical processes: 1) histologic should be confirmed by histologic examination of chorioamnionitis in the absence of clinical symp- the placenta. The clinical usefulness of obtaining toms; 2) positive amniotic-fluid culture assessed at intrapartum amniotic-fluid cultures or placental the time of amniocentesis for preterm labor or pre- cultures after delivery remains unknown. In addi- mature rupture of the membranes; and 3) "clini- tion, the effect of intrapartum antibiotics on the cally evident" infection manifested by fever with success rate of amniotic-fluid or placental cultures localizing signs on physical examination. This re- remains unclear. However, if desired, the obstetri- view will address the history, incidence, patho- cian may, in the delivery room, manually separate physiology, host defenses, risk factors, diagnosis, the from the and obtain a culture of and management of intrauterine infection with an the fetal surface of the chorionic plate to optimize emphasis on "clinically evident" infection. the yield from placental cultures and minimize the Clinical chorioamnionitis is diagnosed in the isolation of contaminant vaginal flora. presence of clinical symptomatology: fever >3 8C The presence of histologic chorioamnionitis does accompanied by uterine tenderness; maternal or re- not imply that clinical chovioamnionitis was present

Address correspondence/reprint requests to Dr. Thomas Westover, Department of Obstetrics and Gynecology, Cooper Hospital, Three Cooper Plaza, Suite 211, Camden, NJ 08103. Received November 14, 1994 Review Article Accepted July 25, 1995 CHORIOAMNIONITIS WESTOVER AND KNUPPEL prior to delivery. Many authors have examined the 1-2%. Retrospective series at large indigent insti- frequency with which histologic chorioamnionitis tutions in the 1970s revealed a 0.5-0.8% incidence is found in febrile and afebrile parturients. In one of clinical chorioamnionitis. Conversely, 2 pro- of the largest prospectively evaluated series to date, spective series in the mid-1980s at teaching hospi- Mueller-Heubach et al. examined over 1,800 con- tals noted incidences of 4.2 and 10.5%. 5,6 It is secutive singleton placentas in a blinded fashion. unclear if these reported differences reflect actual Standardized cuts of the chorionic plate were exam- changes in the incidence of the disease as a result of ined, but neither the membrane roll nor umbilical evolving obstetric practices (such as frequent inva- cord was examined. I--Iistologic chorioamnionitis sive fetal monitoring during the active manage- was present in 18% of the term deliveries vs. 32% ment of labor) or if they reflect the vagaries of of the preterm deliveries. Other series have noted disease detection in retrospective vs. prospective the incidences of histologic chorioamnionitis to be evaluations. The incidence of intrapartum chorio- 15%-80%, depending on the population and gesta- amnionitis varies according to the presence or ab- tional age studied and whether the sections were taken sence of a number of classically described risk fac- from the chorionic plate alone or from the chorion, tors such as socioeconomic status, parity, duration membrane roll, and umbilical cord. Grading classifi- of ruptured membranes and labor, presence of in- cations of the severity of the inflammatory infiltrate ternal fetal monitoring systems, gestational age at have also varied considerably. Therefore, no defini- delivery, number of vaginal examinations, and ab- tive conclusions can be made regarding the effect of normalities in labor progression (see Risk Factors placental histology on fetal or neonatal prognosis. below). However, 2 observations have been consistently noted Infrequently, clinical chorioamnionitis results in the literature: severe histologic chorioamnionitis is from an invasive procedure such as amniocentesis, infrequently found in afebrile gravidas and, if funisi- chorionic-villus sampling, cordocentesis, or cer- tis is present, severe chorioamnionitis will be found in clage. The risk of clinical infection after amniocen- the chorionic plate and membrane roll. tesis or chorionic-villus sampling is quite low, and large series have noted incidences of approximately HISTORICAL NOTES in 1,000 procedures. 7 These infections typically In 1962, Russell and Amadeus2 reviewed 131 con- lead to pregnancy loss at a pre-viable gestation. secutive cases of chorioamnionitis at a large obstet- More extensive and time-consuming procedures ric institution and noted a rate of such as cordocentesis and intravascular transfusion 3.8% secondary to sepsis. Gibbs and Locke, in a may be associated with infection rates of 1% to as review of maternal deaths in Texas from 1969- high as 5%.8 Elective prophylactic cerclage is gen- 1973, reported that 10 of 501 maternal deaths were erally considered to carry an infectious complica- secondary to chorioamnionitis. The Medical Society tion rate of 1-2%, while emergency cerclage place- of New Jersey Subcommittee on Maternal Mortality4 ment in the face of advanced cervical dilation and reviewed 115 maternal deaths for the years 1985- bulging membranes may be associated with rates of 1989 and noted no maternal deaths secondary to chori- clinical chorioamnionitis as high as 25%. 9'10 oamnionitis and sepsis during a period in which ap- proximately 500,000 live births were recorded. We PATHOPHYSIOLOGY have observed no maternal deaths in a series of over Clinical chorioamnionitis typically results from the 200 cases of clinical chorioamnionitis managed at our ascension of organisms from the vagina to the uter- tertiary-care institution from 1990-1994. It would ine cavity after rupture of the membranes. Occa- appear that advances in the understanding and man- sionally, infection may occur because of hematoge- agement of chorioamnionitis along with improve- nous dissemination of bacteria through the ments in critical-care medicine have led to decreases bloodstream. For example, Listeria monocytogenes in the case fatality ratio for chorioamnionitis. has been reported to result from a blood-borne infection after the ingestion of contaminated food. 11 INCIDENCE Even more rarely, bacterial infection with organ- Obstetric texts have stated in the past that the inci- isms such as Streptococcus pyogenes (group A strepto- dence of clinical chorioamnionitis is approximately coccus), Neisseria gonorrhoeae, Campylobacter, and

124 INFECTIOUS DISEASES IN OBSTETRICS AND GYNECOLOGY CHORIOAMNIONITIS WESTOVER AND KNUPPEL TABLE I. Distribution of microbes in 408 cases of could result in the generation of prostaglandins intraamniotic infection from the decidua or chorion and lead to uterine Microbe No. % contractions. Even though amniotic-fluid cultures are posi- Group B streptococci 60 15 tive for group B streptococci or E. coli in only 20% Enterococci 22 5 Escherichia coli 33 8 of patients with clinical chorioamnionitis, these 2 Gardnerella vaginalis 99 24 organisms account for two-thirds of maternal and Other aerobic gram-negative rods 21 5 neonatal bacteremia. 18 When either group B strep- Peptostreptococci 38 9 tococci or E. coli is present in the , Bacteroides bivius 120 29 Fusobacterium sp. 23 6 25-33% of the mothers or neonates will manifest Bacteroids fragilis 14 3 bacteremia. Rarely will anaerobic bacteria be found Mycoplasma hominis 125 31 in the maternal or neonatal bloodstream. It is un- Ureaplasma urealyticum 195 47 clear if the low incidence of anaerobic bacteremia aData from Gibbs et al. is reflects the true clinical state or greater difficulty in the laboratory in detecting these organisms. In addition to the initiation of labor, chorioam- Streptococcus pneumoniae may occur in the absence nionitis may lead to bacteremia, adult respiratory of labor or ruptured membranes if they ascend to distress syndrome (ARDS), disseminated intravas- the amniotic cavity, lz-14 It is unclear if these types cular coagulation (DIC), acute renal failure, or of infections reflect a subcategory of high-virulence septic shock secondary to the production of endo- organisms or an alteration in local or systemic host toxin and various humoral factors and cytokines factors. (Fig. 1). The elucidation of these humoral factors The bacterial composition of the amniotic fluid during the past 10 years has greatly increased our in clinical chorioamnionitis associated with rup- understanding of the pathogenesis of the sepsis syn- tured membranes appears to be polymicrobial. In drome. Arachidonic-acid metabolites such as the 1982, Gibbs et al. is reported the microbiologic leukotrienes, prostaglandins, and thromboxanes constituents of the amniotic fluid of patients with have complex effects on cellular physiology. clinical chorioamnionitis and matched controls. Thromboxane A2 has been shown to cause platelet Seventy percent of the patients with clinically evi- and neutrophil aggregation and activation, vaso- dent infection had >100 CFU/ml of virulent or- constriction of vascular beds, and bronchoconstric- ganisms compared with only 8% of the controls. tion. Prostacyclin has been shown to inhibit platelet The most common organisms noted were anaerobes adhesiveness, stimulate the release of cytokines, in- and group B streptococci. Gravett et al. 6 have hibit gastric-acid secretion, and relax smooth mus- noted similar findings. The distribution of organ- cle. 19 Increased levels of TNF and interleukin-1 isms in over 400 cases of chorioamnionitis can be are associated with increased mortality rates in sep- seen in Table 1. tic shock. Initial investigations into the use of anti- Interestingly, with chorioamnioni- cytokine antibodies in the management of sepsis tis resulting in the births of newborns <2,500 g have been encouraging. Randomized control trials have been noted to contain significantly higher fre- have shown improvements in survival when septic quencies of anaerobic organisms such as Bacteroides patients received anti-TNF antibody, interleukin-6 bivius and Fusobacterium than term controls but receptor antagonist, and anti-endotoxin antibod- similar frequencies of gram-negative enterics and ies. z However, these data must be considered pre- group B streptococci. One can speculate that these liminary, and further research is still needed. anaerobes may asymptomatically ascend to the uter- ine cavity and initiate preterm labor and delivery HOST DEFENSES through deciduitis and expression of humoral fac- It is unclear if amniotic fluid contains bacteriostatic tors such as tumor necrosis factor (TNF), interleu- or bacteriocidal substances. The simple empiric ob- kins, and other cytokines. Bejar et al. 17 have noted servation that clinical chorioamnionitis is an infre- that phospholipase A2 activity may be highest in quent event in patients with intact membranes led anaerobic isolates and that this resultant activity early investigators to presume that amniotic fluid

INFECTIOUS DISEASES IN OBSTETRICS AND GYNECOLOGY 25 CHORIOAMNIONITIS WESTOVER AND KNUPPEL

Endotoxin

Activation complement cascade

Immune complex formation Release of vasoactive substances Leukocyte migration and deposition Arachidonic acid and activation metabolites Free radicals Interleukins Tumor necrosis factor

Leaky capillaries Endothelial damage

Hypotension Hypoxemia Oliguria Disseminated intravascular coagulation

Shock (tissue hypoxia and )

Irreversible multiorgan failure/death

Fig. I. Pathophysiology of multiorgan failure in chorioamnionitis.

TABLE 2. Traditional risk factors for contains antibacterial agents. In addition, studies intraamniotic infection have demonstrated that a strong correlation exists between the degree of after pre- Duration of rupture of membranes Internal fetal monitoring term premature rupture of the membranes and clin- Number of vaginal examinations 21 ical chorioamnionitis. Investigators have at- Duration of labor tempted to document the presence of chemotactins, Young maternal age Low gravidity and parity a lysozymes, immunoglobulins, transferrin, and Low socioeconomic status zinc-peptide complex. None of these has conclu- Requirement of augmentation sively or repeatedly been shown to modify clinical inf'ection. 22 search (Tables 3 and 4). Their observation that RISK FACTORS most patients developing clinical chorioamnionitis The classically described risk factors for clinical entered high-risk categories for several hours prior chorioamnionitis are summarized in Table 2. In to the actual manifestation of chorioamnionitis is 6 5 1989, Soper et al. and Newton et al. prospec- especially intriguing, as intervention during the tively evaluated risk factors by multiple regression prodromal period could theoretically modify the analysis. Interestingly, several of the "established" infectious process. risk factors noted in Table 2 did not meet the criteria for independent risk status. The rates of DIAGNOSIS clinical chorioamnionitis were noted to be 4% and The diagnosis of clinical chorioamnionitis is sug- 10%, respectively, and these high rates may have gested by the presence of fever in a gravid patient contributed to the elimination of some factors clas- without evidence of urinary, respiratory, or other sically associated with clinical chorioamnionitis. localized infection. Ruptured membranes are typi- These investigators established probability curve cally present but are not essential for the diagnosis paradigms that may serve as models for future re- to be made. Most authors have noted that the fre-

INFECTIOUS DISEASES IN OBSTETRICS AND GYNECOLOGY CHORIOAMNIONITIS WESTOVER AND KNUPPEL

TABLE 3. Probability of intraamniotic infection maternal and fetal infection, an awareness of the given varying combinations of risk factors likelihood of vaginal delivery, an estimation of the Duration of anticipated timing of the delivery, and an anticipa- No. of ruptured Total tion of the postpartum and postnatal complications vaginal membranes labor in chorioamnionitis (Fig. 2). Though the risk of examinations (h) (h) Probability maternal death due to chorioamnionitis in modern 2 5.25 6.0 0.03 obstetrics is extremely low, the risk for significant 5 12.00 16.0 0.16 morbidity is real. As previously discussed, endo- 6 16.00 21.0 0.32 toxemia may result in endothelial damage and lead 8 21.75 29.0 0.63 to due to a leak 13 88.00 29.0 0.95 hypoxemia capillary syndrome. Bacteremia may lead to septic shock with resultant aData from Soper et al. ARDS, DIC, and acute renal failure. Close atten- tion must be paid to the volume status and clinical TABLE 4. Criteria predicting a probability of signs of disease progression such as hypotension, intraamniotic infection of 20./o or greater tachycardia, tachypnea, and oliguria. The manage- ment of these complications must be undertaken Internal Membrane with the appropriate critical-care consultation in an monitoring rupture (h) (h) intensive care setting where hemodynamic observa- tions and manipulations may be made. The inter- 0 with > 60 ested reader is directed to other works regarding with > 48 2 with > 36 the management of these conditions, as a descrip- 3 with > 28 tion of them is beyond the scope of this review. 4 with > 14 The initial laboratory assessment should include 5 with > 6 and urine CBC and 6 with > 6 blood cultures, differential, and serum chemistries including BUN and creati- aData from Newton et al. nine. Maternal blood cultures are recommended, as up to 10% of patients will exhibit bacteremia. 24 Coagulation studies should be performed if throm- quency of associated physical findings is low. I-Iauth bocytopenia or a bleeding diathesis is evident. Con- et al. 23 noted, in more than 100 cases of clinical tinuous fetal heart rate monitoring of all viable chorioamnionitis, that fever was present in >99%, should be initiated at the time of diagnosis. fetal tachycardia in 82%, maternal tachycardia in Fetal tachycardia may be a sign of fetal sepsis or 19%, uterine tenderness in 16%, and malodorous may simply reflect an appropriate cardiovascular amniotic fluid in 9%. The diagnosis is established response to endogenous maternal pyrogens such as clinically. Laboratory assessments such as leukocy- the interleukins and TNF. The loss of variability tosis with a left shift, increased C-reactive protein, typically seen at the fetal heart rate baselines of leukocyte esterase assays, and gas chromatography > 180 beats/min will prevent the obstetrician from are nonspecific, insensitive, or expensive and cum- making an accurate assessment of fetal acid base bersome, and therefore not clinically useful. Infre- status, and serial scalp samplings may be required quently, the diagnosis may be suggested in an afe- to document that acidosis is not developing. It has brile, laboring gravida by signs of fetal distress been hypothesized that cord-blood gases indicating such as fetal tachycardia and decreased variability. pre-acidosis or a mild metabolic acidosis may be a Rarely, the diagnosis will be made in an afebrile, marker for neonatal bacteremia, but investigators nonlaboring patient with intact membranes who testing this hypothesis have not been able to validate presents with decreased fetal movement and an ab- this theory, zs normal biophysical assessment. Infected fetuses can rapidly decompensate dur- ing labor. For example, at the time of the mother's MANAGEMENT presentation to the labor floor, the fetus may ex- The management of clinical chorioamnionitis must hibit a fetal heart tracing with normal variability, include an assessment of the clinical severity of the baseline, and periodic changes. After several hours

INFECTIOUS DISEASES IN OBSTETRICS AND GYNECOLOGY 27 CHORIOAMNIONITIS WESTOVER AND KNUPPEL

Assess clinical severity Estimation of timing Anticipation of of infection and mode of delivery postpartum complications

CBC with differential Intrapartum antibiotics Postpartum inpatient Serum chemistry Need for oxytocin antibiotics BUN, creatinine Delivery within 12 h Septic pelvic phlebitis Blood and urine cultures Ovarian vein thrombosis Coagulation studies Wound infection Endometritis Attention to volume Bacteremia status and vital signs Multiorgan failure Fetal heart rate analysis Outpatient antibiotics Cord blood gas $ Postnatal confirmation of clinical diagnosis

Placental histology

Placental culture

Fig. 2. Evaluation and management of clinical chorioamnionitis.

of labor, the fetus may manifest a new onset base- In addition, they noted that physiologic doses of line tachycardia with decreased variability but no oxytocin were unable to overcome this inhibitory decelerations. Thirty minutes later, persistent late effect. decelerations may be noted without a change in Once a diagnosis of clinical chorioamnionitis has variability. Sixty minutes after the first tracing, been established, delivery is indicated to remove there may be absent variability. At delivery or the infected fetus and placenta from the uterus and shortly thereafter, such a neonate may be septic, reduce the risk of sepsis to the fetus and mother. clinically depressed, and subsequently developmen- However, the optimal time frame in which to de- tally delayed. liver the fetus is unknown. Few data exist to de- Clinical chorioamnionitis has been associated scribe the most appropriate interval from either with an increased risk for abnormal labor progres- diagnosis to delivery or antibiotic administration to sion. z6 However, initial studies did not explain delivery. Although clinicians in the 1970s recom- whether the chorioamnionitis causes or results from mended that delivery be effected within 1-2 h after a protracted labor. Silver et al. 2v compared the the diagnosis, recent data have not supported this labor progress in afebrile, laboring nulliparas at recommendation. Gibbs et al. 29 studied 171 gravi- term with and without positive intraamniotic cul- das with clinical chorioamnionitis and noted no tures obtained through serial intrauterine pressure differences in the percentages of pregnancies with catheter aspirations. Nulliparas with persistent maternal or neonatal bacteremia when the diagno- high-virulent isolates (but no evidence of clinical sis-to-delivery intervals were arbitrarily broken into chorioamnionitis) had significantly lower cervical 4-h increments. However, < 10% of their fetuses dilation rates, despite a higher oxytocin infusion were delivered >12 h after the diagnosis. Hauth rate, and a higher cesarean delivery rate. They et al. 23 studied 103 gravidas with clinical chorio- suggested that the presence of high-virulence bacte- amnionitis in whom no differences in neonatal out- ria in the amniotic fluid predisposes to hypocon- come were noted when the diagnosis-to-delivery tractility and poor cervical dilation. In vitro evi- intervals were increased from h up to 10 h. dence to support this suggestion has been reported Again, however, only 2% of their patients were by Leek et al. 28 They noted that a number of dif- delivered after 10 h. It appears from the above data ferent bacterial isolates reduced or eradicated the that a diagnosis-to-delivery interval of up to 12 h is spontaneous motility of myometrial strips in vitro. not associated with increased neonatal morbidity

128 INFECTIOUS DISEASES IN OBSTETRICS AND GYNECOLOGY CHORIOAMNIONITIS WESTOVER AND KNUPPEL (assuming that the mother is receiving parenteral anaerobic neonatal sepsis has precluded the routine antibiotics). However, the risks to the fetus, if a use of intrapartum clindamycin or an equivalent delay beyond 12 h occurs, are simply unknown. In antibiotic. However, it is commonplace at our in- the only prospective, randomized control trial to stitution to add clindamycin during the intrapar- date regarding the therapeutic management of clin- turn period if the mother shows clinical signs of ical chorioamnionitis, Gibbs et al. 3 excluded pa- deterioration or high fever (temperature >39%). tients who were <4 cm dilated at the time of diag- The ideal antibiotic regimen for intrapartum usage nosis for fear of a prolonged labor course and is unknown at this time. Antibiotics cross the pla- resultant adverse perinatal outcome. centa in varying concentrations, but the measure- Until the late 1980s, no consensus of opinion ment of antibiotic levels in various maternal and existed as to the most opportune time to initiate fetal compartments suggests that ampicillin and gen- antibiotics after making the diagnosis of clinical tamycin have high cord blood/maternal blood ra- chorioamnionitis. Prior to this time, many obstetri- tios. In our institution, we typically administer cians chose to defer antibiotics until after the cord 2 g of ampicillin every 6 h and 100 mg of genta- was clamped so as not to interfere with the diagnosis mycin every 8 h (after a 120-mg loading dose) to and management of the neonate. Based on 2 retro- gravidas with suspected chorioamnionitis. We ad- spective studies and prospective study at large minister 900 mg of clindamycin every 8 h instead indigent institutions, popular opinion appears to of ampicillin if the patient reports a penicillin al- have changed. Sperling et al. 31 published a retro- lergy. Although ampicillin and gentamycin are con- spective examination of 257 term gravidas with sidered the "gold standard," newer broad-spectrum clinical chorioamnionitis and noted that the inci- agents such as ticarcillin or ampicillin-sulbactam dence of neonatal bacteremia was significantly lower demonstrate similar bacterial coverage. Neverthe- in newborns who received intrapartum antibiotics less, large series have not yet been reported to en- vs. those receiving antibiotics after cord clamping sure their clinical equivalence. (2.8% vs. 20%, respectively). Gilstrap et al. 2 Studies have repeatedly demonstrated that cesar- noted a similar trend but without statistical signifi- ean delivery increases the maternal morbidity in cance. In these retrospective studies, the patients clinical chorioamnionitis. Koh et al. 34 reported who did not receive antibiotics until after delivery a 43% incidence of endometritis after cesarean de- had significantly lower maximum temperatures and livery vs. only an 11% incidence after vaginal shorter diagnosis-to-delivery intervals. These facts delivery. Gogoi s reported that 13 of 14 maternal serve to confirm the efficacy of intrapartum treat- deaths as a result of chorioamnionitis occurred after ment, since the post-delivery treatment group cesarean delivery. Gravidas with clinical chorioam- should have had even lower neonatal sepsis rates. nionitis who are delivered abdominally are at in- The antibiotics used in these studies typically in- creased risk for postoperative peritonitis, postpar- cluded a penicillin or derivative (with or without tum endometritis, septic pelvic thrombophlebitis, an aminoglycoside) or a second-generation ceph- ovarian vein thrombosis, and wound infection. alosporin. Yonekura et al. z6 reported no difference in post- Gibbs et al. have published the only random- partum morbidity when comparing transperitoneal ized, controlled trial to date evaluating the useful- vs. extraperitoneal cesarean delivery. IV antibiotics ness of intrapartum antibiotics in the prevention of should be continued after cesarean delivery until neonatal sepsis. The trial was stopped after only fever has been absent for 24-48 h and the clinical half of the planned patients were enrolled because signs and symptoms are resolving. Additional an independent safety committee's interim analysis anaerobic coverage such as that obtained with clin- had noted statistically significant differences in the damycin or metronidazole should be added after rates of neonatal sepsis and pneumonia between the cord clamping if not previously administered dur- treated and untreated groups (0% vs. 33%). No ing the intrapartum period. This additional cover- differences in Apgar scores were noted. age is given to ensure adequate coverage of the Although no data exist to prove or disprove the anaerobic organisms traditionally associated with usefulness of anaerobic coverage during the intra- postpartum endometritis. The lower incidence of partum treatment of chorioamnionitis, the rarity of postpartum endometritis after a vaginal delivery

INFECTIOUS DISEASES IN OBSTETRICS AND GYNECOLOGY CHORIOAMNIONITIS WESTOVER AND KNUPPEL makes the need for the continuation of IV antibiot- a retrospective series of nearly 100 newborns posi- ics after vaginal delivery less certain. tive for early-onset group B streptococcal bactere- Recent studies have demonstrated that there may mia, 19% of these babies had received intrapartum be no need for a course of oral antibiotics after a antibiotics at a median age of 4 h prior to deliv- patient is discharged from the hospital in the case of ery. 45 Seventy-two percent of these newborns were an uncomplicated chorioamnionitis or endometri- born to mothers suspected of having chorioamnion- tis. 37'38 Gravidas presenting with bacteremia, im- itis. In addition, both the large data set from munosuppression, HIV positivity, concurrent Gilstrap et al. 2 and a small series from McDuffie wound or other infection, abscess, or septic pelvic et al. 46 suggest that intrapartum ampicillin may phlebitis have been excluded from these studies. result in neonatal sepsis due not to group B strepto- These patients deserve full courses of the tradition- coccus, but rather to more virulent and resistant ally described antibiotic regimens. organisms. Intrapartum chemoprophylaxis has The treatment of clinical chorioamnionitis in the never been to shown to prevent late-onset group B gravida with ruptured membranes using antibiotics streptococcal infection. alone and without an effort to deliver her poses The management of a term neonate delivered risks to both mother and fetus. However, the suc- through an infected uterus is controversial. Wiswell cessful eradication of clinical chorioamnionitis with- et a1.,47 in a survey of 75 teaching institutions, out delivery in gravidas with intact membranes and noted that only 30% of the respondents initiate listeriosis has been reported in all 3 trimesters. 39-41 therapy of the asymptomatic term neonate and only In the absence of symptoms of an upper respiratory 70% perform a laboratory or x-ray evaluation. At infection, we believe that the gravida presenting our institution, we evaluate the asymptomatic term with fever, a flu-like illness, and uterine contrac- neonate delivered through a clinically infected tions can be maintained on IV ampicillin until uterus with a CBC and blood culture immediately blood-culture negativity has been confirmed and after birth. Antibiotics are not begun if the mother listeriosis ruled out. Pregnant patients should avoid received intrapartum antibiotics unless the neonate the ingestion of raw meats, dairy products such as manifests signs of sepsis or the blood culture re- soft cheeses (brie or feta), and ready-to-eat pack- turns positive. Asymptomatic preterm newborns aged meats such as pats and sandwich meats. 42 are treated with a 7-10 day course of IV ampicillin and gentamycin for presumptive sepsis. Symptom- NEONATAL MANAGEMENT atic newborns (whether term or preterm) receive a Chorioamnionitis presents a number of threats to 10-21 day course depending on the infant's clinical the fetus and neonate. Sepsis rates of 1-6% are course and culture results. seen, and congenital pneumonia may be found in as many as 25% of neonates. 24'4 The mortality rate of neonatal septicemia has been described as 25- SUMMARY 5 0%, although more recent series have noted lower Clinical chorioamnionitis continues to be associated rates. Morales et al. 43 reported that mental and with significant neonatal and maternal morbidity physical development scores were not different in and mortality. Research during the last 20 years has preterm gestations complicated by chorioamnioni- enabled us to characterize the epidemiology and tis after controlling for ARDS, intraventricular molecular pathophysiology leading to this infec- hemorrhage, and birth weight. However, because tion. Unfortunately, we currently cannot establish premature newborns delivered through a clinically the diagnosis until the infection is clinically evi- infected uterus exhibit higher rates of ARDS and dent, resulting in alterations in the normal mater- intraventricular hemorrhage vs. gestational age- nal-fetal homeostasis. Current topics of research and weight-matched infants, their physical and de- include assessments of primary prevention such as velopmental scores and mortality rates will be worse vaccination with group B streptococcal antigen, than their noninfected counterparts. 44 early identification of at-risk parturients using clin- Although intrapartum antibiotics have been ical paradigms or rapid detection antigen assays, touted as a method of reducing the risk of neonatal and determination of the optimal type and mode of sepsis, they by no means reduce this risk to zero. In delivery of antibiotics.

130 INFECTIOUS DISEASES IN OBSTETRICS AND GYNECOLOGY CHORIOAMNIONITIS WESTOVER AND KNUPPEL

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