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Chorioamnionitis and neonatal encephalopathy in term infants with fetal acidemia: histopathologic correlations.

The aim of this study was to determine whether the presence or severity of histologic abnormalities of infection/inflammation such as chorioamnionitis, vasculitis, or funisitis confers an additional risk for neonatal encephalopathy in term infants delivered in the presence of severe fetal acidosis. The medical records as well as placental pathology of term infants (n = 51) born with a cord umbilical arterial pH <7.00 were reviewed. Abnormal outcome was predefined as Sarnat stage 2 or 3 neonatal encephalopathy in the first week of life or neonatal death as a consequence of severe brain injury. Consistent with prior data, the presence of severe fetal acidemia, a low 5-minute Apgar score, and need for cardiopulmonary resuscitation were significantly associated with neonatal encephalopathy. However, the presence of histologic chorioamnionitis had a poor predictive value and did not confer additional risk for the subsequent development of neonatal encephalopathy.

Acidosis↗

Umbilical arterial thrombosis with vascular wall necrosis: clinicopathologic findings of 11 cases.

Thrombosis of umbilical cord vessels is associated with a high perinatal mortality. Most cases are venous thrombi, arterial thrombi are uncommon. To clarify clinical and pathological features of this entity, we reviewed 11 cases with umbilical artery thrombosis. The gestational ages were 33-40 (mean 36.8) weeks. Three cases (38%) were associated with severe intrauterine growth retardation and two cases (25%) led to intrauterine fetal deaths. All cases had completely occlusive thrombi of one umbilical artery. The arteries with thrombosis demonstrated partial necrosis of vascular wall. The pathogenesis is unclear, but nine cases (82%) had cord abnormalities (long cord, peripheral cord insertion, short cord with twist, funisitis). This paper is the first report of clinical and pathological features of umbilical artery thrombosis. The results of this study confirm the clinical importance and unique histological findings of umbilical artery thrombosis. The recognition of umbilical artery thrombosis is necessary to establish the diagnosis and treatment of this condition.

Adult↗

Antenatal origin of neurologic damage in newborn infants. I. Preterm infants.

Currently, the diagnosis of white matter necrosis may be performed with echoencephalography when cysts are observed in the white matter adjacent to the lateral ventricles. One hundred twenty-seven infants with a gestational age less than 36 weeks (mean [+/- SE] gestational age = 31 +/- 3.2 weeks) were studied in the neonatal period with echoencephalography to determine the incidence of white matter necrosis and the perinatal variables associated with this complication. Twenty-three infants (18.3%) had white matter necrosis. Thirteen (10.3%) had cysts by day 3 (11 on day 1), indicating that the onset of white matter necrosis occurred antenatally. The incidence of antenatal white matter necrosis was inversely related to birth weight and was more frequent in infants weighing less than 1000 gm (19%). Stepwise logistic regression analysis of 31 antenatal variables showed that placental vascular anastomoses in multiple pregnancies, funisitis, and purulent amniotic fluid were the only complications associated with antenatal white matter necrosis. Follow-up neurologic evaluations were abnormal in four of six patients with antenatal white matter necrosis. The findings in this study focus attention on prenatal, rather than intrapartum and postnatal, factors as causative agents of neurologic morbidity and emphasize the importance of early and sequential evaluation of neonatal brain structures.

Cerebral Hemorrhage↗

Placental histopathology of congenital syphilis.

OBJECTIVE: To evaluate the contribution of placental histopathology to the diagnosis of congenital syphilis. METHODS: From January 1, 1986, through December 31, 1998, all pregnant women presenting to a large, urban Dallas County labor and delivery unit with untreated syphilis at delivery and who had placental evaluation performed were identified. Women were clinically staged, and the infants were evaluated for congenital syphilis using a standard protocol. Each placenta was evaluated by two independent pathologists. Histologic characteristics of the placenta related to congenital syphilis in live-born and stillborn infants were then analyzed. RESULTS: Sixty-seven women met the study criteria: 33 (49%) stillborn and 18 (27%) live-born infants with congenital syphilis, 15 (22%) uninfected live-born infants, and one uninfected stillborn fetus diagnosed by current criteria. There were no differences between the groups with regard to demographic characteristics, prenatal care, or stage of syphilis. Stillborn infants were more likely to deliver preterm (P <.001). Controlling for gestational age, histopathology revealed necrotizing funisitis, villous enlargement, and acute villitis associated with congenital syphilis. Erythroblastosis was more common in stillborn infants with congenital syphilis than all live-born infants (odds ratio 16, 95% confidence interval 1, 370). The addition of histologic evaluation to conventional diagnostic evaluations improved the detection rate for congenital syphilis from 67% to 89% in live-born infants, and 91% to 97% in stillborn infants. CONCLUSION: Our results show that histopathologic examination of the placenta is a valuable adjunct to the contemporary diagnostic criteria used to diagnose congenital syphilis.

Adolescent↗

Placental pathology in patients using cocaine: an observational study.

OBJECTIVE: Although retroplacental hemorrhage is a major cause of fetal death, its etiology often remains obscure. In some reports, cocaine use by pregnant women has been associated with retroplacental hemorrhage and clinical abruptio placentae. This study was designed to assess the occurrence of chorionic villus hemorrhage, an entity shown recently to be associated with retroplacental hemorrhage, in the placentas of cocaine users. METHODS: Twenty-nine placentas from cocaine users and 15 placentas from drug-free controls, as determined by questionnaire and urine toxicology screen, were examined prospectively, and pathological findings documented. The prevalence of retroplacental hemorrhage, chorionic villus hemorrhage, edema, chorioamnionitis, funisitis, infarction, fetal vessel thrombosis, and intervillus hemorrhage was examined in the two groups. RESULTS: Chorioamnionitis was the most frequent finding in both groups (58% of cocaine users, 66% of controls). Edema of moderate severity or greater was found only in the cocaine-using group (17%). The prevalence of chorionic villus hemorrhage among women using cocaine also was 17%. CONCLUSION: Cocaine use during pregnancy may be associated with chorionic villus hemorrhage and villus edema, even in the absence of clinical abruptio placentae. The relationship between abnormal placental morphology and adverse perinatal outcomes remains to be determined.

Adult↗

The inflammatory response in candidal chorioamnionitis.

Fetal infection with Candida organisms has not commonly been reported. Umbilical cords and placentas from 23 cases of chorioamnionitis collected over a nine-year period were examined by electron microscopy and immunoperoxidase staining. Gross features, especially of the umbilical cord, were distinctive and included the pale yellow plaques pathognomonic of candidal funisitis. Histopathologically, the lesions were found to be focal and subamniotic and were often embedded in a "fibrinoid" exudate and surrounded by inflammatory cells. In some cases the exudate and inflammatory cells were deposited in dense bands. Immunoperoxidase staining showed the lesions to contain IgG, IgM, and IgA, which probably originated in dense-staining plasmacytoid and immunoblastic cells in the inflammatory infiltrates. Additional findings in two fetal cases of giant cell pneumonitis suggested that the fetus can mount a brisk inflammatory and immune response to Candida organisms as early as 18 weeks' gestation and that mucosal exposure to this antigen can result in production of IgA by the lung.

Candidiasis↗

Intrauterine latent herpes simplex virus infection: II. Latent neonatal infection.

Herpes simplex virus (HSV, probably type 2) antigen has been detected in endometria and abortion tissue (companion paper) and in placentae, umbilical cords, and fetal and neonatal organs by avidin-biotin complex immunohistochemical studies. HSV cytologic abnormalities were not detected in any of the 12 normal and 64 abnormal cases analyzed, nor was HSV detected by culture or electron microscopy in selected cases. Antigen was present in single epithelial and, rarely, mesenchymal cells of various organs. Clinically unexplained fetal or neonatal problems associated with HSV antigen positivity included intrauterine death, fetal growth retardation, cystic brain degeneration, hydrops, interstitial pneumonitis, necrotizing enterocolitis, hepatitis, encephalitis, myocarditis, and renal failure. Maternal floor infarct of placenta and calcifying funisitis are the manifestations of intrauterine HSV infection in most cases. Maternal history of HSV infection was uncommon. It is concluded that intrauterine HSV infection may persist in the fetus and neonate in a latent fashion without cytologic abnormalities or detectable virus. This latent infection may be associated with intrauterine and neonatal death, organ damage, and neonatal disease.

Antigens, Viral↗

Inflammation of the lungs, umbilical cord and placenta associated with meconium passage in utero. Review of 123 autopsied cases.

It is uncertain how often the passage of meconium in utero is a response to some event causing fetal distress as opposed to being simply the physiologic functioning of a maturing intestinal tract. The extent to which meconium may produce injury or inflammation in pulmonary and placental tissues after intrauterine exposure is also unclear. This study was a retrospective review of 123 cases, 79 stillborn and 44 liveborn less than one month of age, autopsied at The Johns Hopkins Hospital, and showing histologic evidence of intrauterine meconium exposure by aspirated meconium or meconium macrophages in placental tissues. Of 55 cases with pulmonary inflammation, 13 (24%) had fetal pneumonia, 5 (9%) had postnatal bronchopneumonia, and 37 (67%) had inflammation secondary to meconium aspiration. There was inflammation of the umbilical cord in 31 (41%) of the 75 cases with available slides, 11 (15%) had funisitis associated with chorioamnionitis and 18 (58%) were secondary to meconium exposure. There were 19 cases with focal injury of cord vessels from meconium, two of which had cord ulceration. Inflammation of the membranes and chorionic plate was present in 24 (33%) of the 72 cases where it could be assessed, and was due to chorioamnionitis in 11 (46%) and to meconium in 13 (54%). In general, meconium-related inflammations was much less severe in the membranes than in the cord. There were 67 (54%) cases with definite or probable evidence of fetal distress. In 38 (48%) stillborns no cause of fetal death in utero was identified and in 18 (41%) liveborns there was no known prenatal problem. The results support the concept that meconium passage in utero may occur either as a response to fetal distress or as a physiologic process. Inflammation in the lung and placental tissues, and vascular injury in the umbilical cord may arise secondary to in utero exposure to meconium.

Female↗

[Maternofetal disseminated candidiasis and high-grade prematurity].

BACKGROUND: Despite the frequency of vaginal yeast colonization, serious candidiasis infections in pregnant patients or neonates remain rare. Four cases of disseminated congenital candidiasis in very preterm infants are reported. CASE REPORTS: Congenital Candida albicans infection has been diagnosed in four very preterm infants. In three cases, the mothers had intrauterine devices in place throughout pregnancy. A careful macroscopic examination of the umbilical cord and placenta after birth has allowed an early management strategy in three cases. In all cases, a serious infectious alveolitis occurred. A pronounced increase in white blood cells (> 50,000/mm3) and high levels of both segmented neutrophil and band cells, despite the frequent normality of the CRP, constituted other features. Infection was controlled by parenteral amphotericin B or fluconazole. In one case, serious thrombocytopenia occurred after the first amphotericin B injection requiring substitution for fluconazole. The outcome was unfavourable in two cases with an extensive periventricular leukomalacia. CONCLUSION: Congenital candidiasis in these four very preterm neonates has several features in common: intrauterine contraceptive device during pregnancy, characteristic chorioamnionitis and funisitis, high WBC count, infectious alveolitis. Fluconazole as alternative to amphotericine B therapy is proposed.

Adult↗

Intrauterine infection and the development of cerebral palsy.

Cerebral palsy is a serious motor disorder that appears in early life. The expectation that improved obstetrical and neonatal care would decrease the rate of this condition has not been realised. Recent evidence indicates that white matter brain lesions, often termed periventricular leukomalacia (PVL), are the most important identifiable risk factors for the development of cerebral palsy. The hypothesis under examination is that inflammatory cytokines released during the course of intrauterine infection play a central role in the genesis of preterm parturition, fetal PVL, and cerebral palsy. We examined the relationship between umbilical cord plasma concentrations of cytokines at birth and the occurrence of PVL in preterm gestation and demonstrated that umbilical cord plasma concentrations of interleukin (IL)-6 was a significant independent predictor of PVL-associated lesions. We also demonstrated that preterm neonates born to mothers with elevated amniotic fluid concentrations of pro-inflammatory cytokines were at increased risk for the subsequent development of PVL and cerebral palsy. Histological chorioamnionitis and congenital neonatal infection-related morbidity were more common in neonates with PVL than those without PVL in this study. We have also been able to induce PVL-like brain white matter lesions in the fetal rabbit after experimental ascending intrauterine infection. In support of this hypothesis, we were able to demonstrate overexpression of tumour necrosis factor-alpha and IL-6 in histological sections of neonatal brains with PVL. Moreover, the presence of funisitis, a histological counterpart of the fetal inflammatory response syndrome, and elevated concentrations of amniotic fluid IL-6 and IL-8 were strong and independent risk factors for the subsequent development of cerebral palsy at the age of 3 years in our recent study. Therefore, clinical and experimental data provide strong support for the hypothesis. There are significant implications of our findings. First, cytokine determinations in amniotic fluid provide information about the risk of PVL and cerebral palsy before birth. Second, the process responsible for some cases of PVL and cerebral palsy begins during intrauterine life, implying that effective strategies for the prevention of cerebral palsy associated with PVL must begin in utero.

Cerebral Palsy↗

Maternal antecedents for cerebral palsy in extremely preterm babies: a case-control study.

The study aimed to identify significant antenatal risk factors for cerebral palsy (CP) among extremely preterm infants with a matched case-control design. Infants born between 1989 and 1996 at 24 to 27 weeks' gestation who survived to hospital discharge were evaluated: 30 with a proven diagnosis of CP at 2 years corrected for prematurity and 120 control children matched for gestational age without CP. Information on maternal obstetric risk factors and medication was obtained. Matched analyses were performed and odds ratios (OR) and 95% confidence intervals (CI) were calculated. An antenatal diagnosis of intrauterine growth restriction was associated with an increased risk of CP (OR 6.6; 95% CI 1.8 to 25.2), while maternal administration of corticosteroids was associated with a reduced risk of CP (OR 0.4; 95% CI 0.1 to 0.98). A high rate of placental histopathology was achieved but no relation between clinical or histological chorioamnionitis or funisitis and CP was demonstrated. Maternal preeclampsia was not associated with a statistically significant reduction in the risk of CP. It is concluded that a reduced risk of CP in extremely preterm infants is associated with the antenatal use of corticosteroids.

Adrenal Cortex Hormones↗

Low blood pressure among very-low-birth-weight infants with fetal vessel inflammation.

OBJECTIVE: To test the hypothesis that fetal vessel inflammation (FVI: funisitis and/or fetal vasculitis) is associated with lower blood pressure (BP) over the first week of life and an increased risk of periventricular leukomalacia (PVL) among premature infants. STUDY DESIGN: A total of 255 infants born at <1350 g to normotensive mothers were stratified by gestational age (GA) and grouped by presence/absence of FVI on placental pathology. Daily highest (Hi) and lowest (Lo) systolic BP (BP(sys)), mean BP (BP(mn)) and diastolic BP (BP(dia)) over first 7 days of life were analyzed by repeated measures ANOVA and regression analysis. Cranial ultrasounds were obtained at 2 weeks of life. RESULTS: Infants > or =30 weeks gestation with FVI had lower HiBP(sys), HiBP(mn), HiBP(dia), LoBP(sys), LoBP(mn) and LoBP(dia) (p<0.001) than did infants without FVI. Infants with PVL (all < or =27 weeks gestation) had lower LoBP(mn) and LoBP(dia) (p<0.01) than controls. FVI did not increase the risk of PVL in these infants. CONCLUSION: FVI and PVL are associated with reduced BP over the first week of life.

Age Factors↗

The histologic fetoplacental inflammatory response in fatal perinatal group B-streptococcus infection.

OBJECTIVE: To determine the rate of histologic fetoplacental inflammation in fetuses and newborns with fatal perinatal Group B-Streptococcus (GBS) infection. STUDY DESIGN: Autopsy files (1990 to 2002) were searched for fetuses and newborns with GBS-positive post-mortem blood and/or lung cultures. The rate of histological fetoplacental inflammation in preterm (< 36 weeks gestational age) and term (> or =36 weeks) fetuses/infants was compared using chi(2) test. RESULTS: GBS infection was diagnosed in 4.9% (61/1236) of perinatal autopsies and was considered the exclusive cause of death in 58 cases (16 to 41 weeks gestation, median: 26 weeks). A total of 43 fetuses/infants (74%) were preterm, 24 (41%) were male and 33 (57%) stillborn. The histologic fetoplacental inflammatory response was age-dependent for the following variables: acute chorioamnionitis (seen in 67% of preterm vs 33% of term fetuses/infants, p < 0.05), multiple-vessel umbilical vasculitis (37 vs 7%, p < 0.05), funisitis (37 vs 13%, p < 0.05), and the presence of neutrophils in the gastrointestinal tract (35% vs none, p < 0.05). Neutrophils in the pulmonary airspaces (47 vs 33%) and pneumonia (16 vs 27%) were found with similar frequency in both groups. CONCLUSION: Histologic fetoplacental inflammation is a poor indicator of perinatal GBS infection; the sensitivity is 67% in preterm and 33% in term fetuses/newborns (overall sensitivity 59%). The higher rate of histologic inflammation in preterm fetuses/newborns suggests age-specific interactions between microorganism, host and placenta.

Chorioamnionitis↗

Methods to improve the reliability of histopathological diagnoses in the placenta.

The interobserver reliability of histopathological features in the placenta was examined. Two pathologists independently reviewed slides from 250 placentas. The pathologists were given a morphological description of the placenta, but were blinded to clinical status, gestational age and original diagnoses. A protocol for diagnosis and grading of features was first developed and pilot-tested. Definitions and criteria were refined and elaborated. A range of features was examined including inflammatory lesions, features indicative of reduced uterine blood flow and other miscellaneous histopathological changes. Weighted kappa coefficients were calculated. The effect of multiple features on reliability was examined by stratifying on the presence of a second feature and calculating stratum-specific kappa coefficients. Results indicated good to excellent agreement for diagnoses of chorioamnionitis, cord vasculitis, funisitis and villitis (kappa(w) range 0.70-0.83). Agreement between observers was more variable for the diagnosis of reduced uterine blood flow states. Excellent agreement was observed for the diagnosis of meconium staining of the placenta (kappaw = 0.79). In general, lower levels of agreement were observed for features in the presence of a second feature. Reproducible measures are a prerequisite to using placental histopathology for diagnostic and prognostic information. This study demonstrated reliable placental diagnoses can be achieved through a standardised protocol.

Clinical Protocols↗

Contemporary management of preterm premature rupture of membranes: determinants of latency and neonatal outcome.

Preterm premature rupture of membranes (PPROM) is responsible for 30% of neonatal morbidity and mortality in premature gestations. We sought to evaluate pregnancy outcomes in PPROM managed uniformly with antibiotics and steroids, and to determine what maternal factors influence latency. This was a retrospective analysis of 134 patients at 24 to 31.9 weeks with PPROM. Associations of maternal and pregnancy characteristics with latency were evaluated by chi-square for linear trend, nonparametric tests, or multivariable linear regression, as appropriate. Forty-three of 134 women (32%) had latencies greater than a week. Gestational age ( p < 0.001), admission white blood cell count ( p = 0.001), and amniotic fluid index ( p = 0.02) were independently predictive of latency. Histopathologic funisitis increased with pregnancy length. There were no fetal deaths or significant intraventricular hemorrhage past 28 weeks.

Adult↗

Interleukin 6 determinations in cervical fluid have diagnostic and prognostic value in preterm premature rupture of membranes.

OBJECTIVE: Our aim was to determine whether interleukin-6 concentrations in cervical fluid samples are of value in the identification of microbial invasion of the amniotic cavity, prediction of the duration of the latency period, and assessment of the risk of neonatal complications in preterm premature rupture of membranes. STUDY DESIGN: A cohort study was performed in 86 patients with preterm premature rupture of membranes. Amniotic fluid and cervical fluid were collected. Amniotic fluid was cultured for aerobic and anaerobic bacteria, as well as mycoplasmas. Interleukin 6 was measured by a sensitive and specific immunoassay. The receiver operating characteristic curve, logistic regression, and survival techniques were used for analysis. RESULTS: (1) Patients with a positive amniotic fluid culture had a significantly higher median cervical fluid interleukin 6 concentration than those with negative results (median, 528 pg/mL; range, 174-825 pg/mL; vs median, 169 pg/mL; range, 8-986 pg/mL; P <.0001). (2) A cervical fluid interleukin 6 concentration of >350 pg/mL had a sensitivity of 92% and a specificity of 78% in the identification of a positive amniotic fluid culture. (3) Patients with a cervical fluid interleukin 6 concentration of >350 pg/mL had a significantly shorter median interval to delivery and higher rate of funisitis, preterm delivery within 2 days and 7 days, and the occurrence of significant neonatal morbidity than did those with a cervical fluid interleukin 6 concentration of <350 pg/mL (P <.05 for each). (4) The increased perinatal morbidity remained significant after adjustment for gestational age (P <.05). (5) There was a strong correlation between cervical fluid concentrations and amniotic fluid concentrations of interleukin 6 (P <.001). CONCLUSION: Cervical fluid interleukin 6 determinations are of value in the assessment of the likelihood of microbial invasion of the amniotic cavity, impending preterm delivery, and the occurrence of significant neonatal complications in the setting of preterm premature rupture of membranes.

Amniotic Fluid↗

Umbilical arteritis and phlebitis mark different stages of the fetal inflammatory response.

OBJECTIVE: Funisitis, the inflammation of the umbilical cord determined by histologic examination of the placenta, is evidence of a fetal inflammatory response. The inflammatory process may involve the umbilical vein (phlebitis) and one or both umbilical arteries (arteritis) and extend into the Wharton's jelly. This study was conducted to examine whether the pattern of inflammation of the umbilical cord correlates with a biochemical marker of systemic fetal inflammation (umbilical cord plasma interleukin-6) and an adverse neonatal outcome. STUDY DESIGN: This cohort study included 636 cases of preterm delivery (<36 weeks) with or without inflammation of the umbilical cord. Umbilical cord blood was collected at the time of delivery. The aim of pathologic examination was to characterize the extent of umbilical cord inflammation and the involvement of the vein (phlebitis), the involvement of one or both arteries (arteritis), and the presence of inflammation of the Wharton's jelly. Umbilical cord plasma interleukin-6 concentrations were assayed by a sensitive and specific immunoassay. RESULTS: Neonates with umbilical arteritis had a significantly higher median concentration of cord plasma interleukin-6 (median, 111 pg/mL; range, 0.1-19,230 pg/mL) than those without umbilical arteritis (median, 22.5 pg/mL; range, 0.9-511.6 pg/mL; P <.05). Also, severe neonatal morbidity occurred more frequently in infants with arteritis than in those without arteritis (74% vs 50%; P <.05). And finally, the most severe form of inflammation, which involves both arteries, vein, and Wharton's jelly, was associated with the highest median concentration of plasma interleukin-6 observed in this study (median, 182.6 pg/mL; range, 0.1-7,400 pg/mL), whereas inflammation limited to the vein (phlebitis) was associated with a lower concentration of cord plasma interleukin-6 (median, 29.1 pg/mL; range, 0.9-511.6 pg/mL; P <.05). CONCLUSION: Neonates whose placenta demonstrates umbilical arteritis have higher concentrations of umbilical cord plasma interleukin-6 and higher rates of adverse outcome than those without umbilical arteritis.

Arteritis↗

Clinical significance of intra-amniotic inflammation in patients with preterm labor and intact membranes.

OBJECTIVE: The purpose of this study was to determine the frequency and clinical significance of intraamniotic inflammation in patients with preterm labor and intact membranes. STUDY DESIGN: Amniocentesis was performed in 206 patients with preterm labor and intact membranes. Amniotic fluid was cultured for aerobic and anaerobic bacteria and mycoplasmas. The diagnosis of intraamniotic inflammation was made in patients with a negative amniotic fluid culture on the basis of amniotic fluid concentrations of interleukin-6 (>2.6 ng/mL, derived from receiver operating characteristic curve analysis). Statistical analysis was conducted with contingency tables and survival techniques. RESULTS: Intra-amniotic inflammation (negative amniotic fluid culture but elevated amniotic fluid interleukin-6) was more common than intra-amniotic infection (positive amniotic fluid culture regardless of amniotic fluid interleukin-6 concentration; 21% [44/206 women] vs 10% [21/206 women]; P <.001). The amniocentesisto-delivery interval was significantly shorter in patients with intra-amniotic inflammation than in patients with a negative culture and without an inflammation (median, 20 hours [range, 0.1-2328 hours] vs median, 701 hours [range, 0.1-3252 hours], respectively; P <.0001). Spontaneous preterm delivery of <37 weeks was more frequent in patients with intra-amniotic inflammation than in those with a negative culture and without inflammation (98% vs 35%; P <.001). Patients with intra-amniotic inflammation had a significantly higher rate of adverse outcome than patients with a negative culture and without intra-amniotic inflammation. Adverse outcomes included clinical and histologic chorioamnionitis, funisitis, early preterm birth, and significant neonatal morbidity. There were no significant differences in the rate of adverse outcomes between patients with a negative culture but with intra-amniotic inflammation and patients with intra-amniotic infection (positive culture regardless of amniotic fluid interleukin-6 concentration). CONCLUSION: Intra-amniotic inflammation/infection complicates one third of the patients with preterm labor (32%; 65/206 women), and its presence is a risk factor for adverse outcome. The outcome of patients with microbiologically proven intra-amniotic infection is similar to that of patients with intra-amniotic inflammation and a negative amniotic fluid culture. We propose that the treatment of patients in preterm labor be based on the operational diagnosis of intra-amniotic inflammation rather than the diagnosis of intra-amniotic infection because the latter diagnosis cannot be undertaken rapidly.

Amniocentesis↗