Prevalence, management, and outcomes of preterm prelabour rupture of the membranes of women in Canada.

OBJECTIVES: To determine the prevalence of preterm prelabour rupture of the membranes (PPROM) at Canadian university-affiliated perinatal referral centres, to assess the different management strategies, and to review neonatal outcomes. METHODS: Twelve Canadian university-affiliated perinatal referral centres provided information on their management of PPROM, and 9 participated in data collection to determine prevalence. All women presenting with PPROM during a 2-week period were observed until delivery, and obstetric and neonatal outcome data were subsequently obtained. The total number of deliveries in each centre was recorded for the same time period. We also determined the incidence of PPROM and the neonatal outcome for all women presenting with PPROM at the Kingston General Hospital from January 1999 to December 2001 by retrospective chart review. RESULTS: In the 9 academic centres, 27 women (1 with a twin pregnancy) presented with PPROM during the 2-week period. There were 1168 deliveries during the same time period, giving a prevalence of PPROM of 2.3%. Overall, 53% of placentas submitted for histopathology after PPROM demonstrated evidence of chorioamnionitis. In the retrospective chart review, we found 153 cases of confirmed PPROM from January 1999 to December 2001,an incidence of 2.8%. Clinical management in all centres was similar for most women who presented with PPROM prior to 34 weeks' gestation. Management after 34 weeks' gestation varied among the 12 centres, ranging from immediate induction of labour to expectant management and induction at a greater gestational age (GA). CONCLUSIONS: The increased neonatal morbidity associated with PPROM appears to be inversely related to GA. Increased risk of chorioamnionitis is related to increased time from PPROM to delivery.

Chorioamnionitis associated with Crohn's disease and azathioprine treatment: a case report.

This paper reports a case of S. constellatus chorioamnionitis in a pregnant Crohn's disease patient who was taking azathioprine. Chorioamnionitis is a major cause of perinatal morbidity. Azathioprine, an immunosuppressive antimetabolite, is widely used to treat inflammatory bowel disease. Streptococcus constellatus is a Gram-positive bacterium that has not previously been associated with chorioamnionitis. A high index of suspicion for chorioamnionitis and unusual pathogens should be maintained in the management of obstetric patients on immunosuppressive agents.

Cervical incompetence and the role of emergency cerclage.

OBJECTIVE: To evaluate the role of emergency cerclage for women who present with a dilated external cervical os and bulging or "hour-glassing" membranes. We examined overall experiences at Kingston General Hospital (KGH) from 2000 to 2004 and conducted a literature review for the period January 1, 1995, to December 31, 2004. METHODS: A search for cerclages placed by operators in Kingston revealed 12 pregnancies in the period between 2000 and 2004. We reviewed the charts for these women and for their infants. We conducted a literature review, using the terms "cerclage," "cervical," "emergent or emergency cerclage," "rescue cerclage," and "incompetent cervix," using an OVID interface to access MEDLINE records. We excluded articles in which the diagnosis of cervical incompetence was made using ultrasound, because its predictive value has not been shown in randomized trials. The most recent review of this type was carried out in 1995; since then, an additional 24 articles have been published that met our inclusion and exclusion criteria. RESULTS: The average time between cerclage placement and delivery at KGH was 7 weeks, which allowed for 10 of 13 infants (one twin pregnancy) to be born at 28 weeks or later. Three infants were born weighing under 1 kg; the 10 remaining infants weighed over 1 kg. Histological data are available for 12 placentas of the 13 infants delivered; 7 infants had a histological diagnosis of chorioamnionitis; none of the blood cultures from any of the infants post-delivery revealed septicemia. The literature review identified 638 women. Where reported, the average prolongation of the pregnancy was 7 weeks plus 1 day. This allowed for 60% of infants (range 26% to 80%) to be born after 28 weeks, with an average neonatal survival of over 70% (range 47.2% to 96%). Preterm premature rupture of membranes complicated an average of 29% of pregnancies (range 1% to 58%), and chorioamnionitis was reported in 5% to 80% of pregnancies. CONCLUSIONS: The KGH data collected and the data available in the literature suggest that emergency cerclage, under ideal circumstances, can significantly prolong pregnancy and increase the chance of viable pregnancy outcome. However, in counselling women about the potential therapeutic benefit of emergency cerclage, the increased risk of chorioamnionitis and its associated risk of fetal inflammatory brain injury, as well as the risk of extending a pregnancy from pre-viability to severe prematurity, should be discussed. A longer-term follow-up than has been carried out here is required for better elucidation of the effect of chorioamnionitis on those infants in childhood and beyond.

Antenatal steroids may reduce adverse neurological outcome following chorioamnionitis: neurodevelopmental outcome and chorioamnionitis in premature infants.

OBJECTIVE: To examine the effect of antenatal steroid exposure and in utero inflammation on the development of severe intraventricular haemorrhage, periventricular leukomalacia and long-term neurological outcome in infants less than 30 completed weeks gestation. METHOD: Infants less than 30 completed weeks gestation from January 1996 to July 2001 were identified from a prospectively managed database. Placental pathology was reviewed for the presence or absence of chorioamnionitis and funisitis. Infants were divided into three groups depending on the degree of exposure to fetal inflammation (no inflammation, chorioamnionitis only and chorioamnionitis and funisitis). Data relating to gestational age, birthweight, sex, antenatal steroid exposure, surfactant treatment, days of positive pressure ventilation and days of oxygen requirement were collected. Cerebral ultrasound studies were examined for evidence of intraventricular or intraparenchymal echodensity and periventricular leukomalacia. Long-term neurological outcome was assessed by neurological examination for cerebral palsy and by Griffiths Mental Developmental Assessment for general developmental quotient. RESULTS: Two hundred and twenty infants were identified. The mean gestational age was 27.7 weeks and the mean birthweight 1092 g. Seventy-two per cent of mothers had received a complete course of antenatal steroids. The risk of Grade III intraventricular haemorrhage or intraparenchymal echodensity was associated with exposure to in utero inflammation if a complete course of antenatal steroids had not been received (P = 0.002). This association did not exist if a complete course of antenatal steroids was given (P = 0.62). Fourteen infants had cerebral palsy (7%). The presence of cerebral palsy was also associated with in utero inflammation in the absence of complete antenatal steroid cover (P = 0.03) and not in the presence of complete cover (P = 0.59). The mean general developmental quotient on Griffiths Mental Developmental Assessment at 12 months or 3 years was not affected by exposure to in utero inflammation regardless of antenatal steroid exposure. CONCLUSION: Risk of intraventricular haemorrhage or intraparenchymal echodensity and cerebral palsy was associated with in utero inflammation in the absence of a complete course of antenatal steroids. A complete course of antenatal steroids appeared to extinguish any association between in utero inflammation and adverse neurological outcome.

The association between early tracheal colonization and bronchopulmonary dysplasia.

OBJECTIVE: To evaluate the relationship between early tracheal colonization and bronchopulmonary dysplasia (BPD). STUDY DESIGN: This is a retrospective cohort study which included 308 inborn neonates admitted to the newborn intensive care unit at the University of Miami Jackson Memorial Medical Center between January 1997 and December 2000 with birthweight 500 to 1000 g, who required mechanical ventilation on the first day of life. Chorioamnionitis was diagnosed by maternal symptoms and histopathopathology. Tracheal cultures were obtained immediately after tracheal intubation. BPD was diagnosed in neonates who had supplemental oxygen requirement for more than 28 days. Pearson's chi(2) and Logistic Regression Analysis were used to evaluate the relationship between chorioamnionitis, positive initial tracheal cultures and BPD, after adjusting for confounding variables. RESULTS: In patients with chorioamnionitis, the incidence of early positive tracheal cultures was 41% compared to 16% in those without chorioamnionitis, (p < 0.00001). In patients with birthweight 700 to 1000 g, a positive early tracheal culture increased the risk of BPD (OR = 2.42, CI 1.05 to 5.62, p < 0.05). CONCLUSION: Preterm infants exposed to chorioamnionitis have an increased incidence of early tracheal colonization. This early tracheal colonization may predispose them to develop BPD.

Antenatal associations with lung maturation and infection.

Chronic clinically unapparent chorioamnionitis is a common antenatal exposure for very preterm infants, and these infants have variable degrees of lung maturation and a high risk of developing bronchopulmonary dysplasia. Exposure of fetal sheep to intra-amniotic endotoxin or IL-1alpha induces chorioamnionitis and lung injury (decreased alveolarization and microvascular injury), which resolves to a phenotype of striking lung maturation (increased surfactant, improved gas exchange and lung mechanics). The immune responses of the fetus also are suppressed or induced (matured) in time and dose-dependent ways by either chorioamnionitis or antenatal corticosteroids. These experimental observations contribute to explanations of why preterm infants have variable degrees of lung maturation at birth and unpredictably develop bronchopulmonary dysplasia BPD.

Severe fetal placental vascular lesions in term infants with neurologic impairment.

OBJECTIVE: This study tests the hypothesis that placental disease can identify antepartum processes that either progress into the intrapartum period or predispose to intrapartum brain injury. STUDY DESIGN: Lesions that affect large fetal vessels were compared in the placentas of 125 neurologically impaired term infants who were the focus of clinical negligence litigation and 250 consecutive singleton deliveries of >/=36 weeks of gestation. RESULTS: One or more of 4 severe placental fetal vascular lesions (fetal thrombotic vasculopathy, chronic villitis with obliterative fetal vasculopathy, chorioamnionitis with severe fetal vasculitis, and meconium-associated fetal vascular necrosis) were found in 51% of index cases versus 10% of the comparison group ( P <.0001). Prevalence of these lesions in the 64 infants with cerebral palsy was 52% ( P <.0001). CONCLUSION: Severe fetal placental vascular lesions are correlated highly with neurologic impairment and cerebral palsy. Their nature, duration, and anatomic location make them strong candidates for the antepartum processes that place fetuses at risk for brain injury during the intrapartum period.

Septicemia in the first week of life in a Norwegian national cohort of extremely premature infants.

OBJECTIVES: To investigate the incidence, causes, predictors, and outcomes of septicemia in the first week of life in a national cohort of extremely premature infants. METHODS: A prospective study of survival of all infants with gestational age of <28 weeks or birth weight of <1000 g who were born in Norway in 1999-2000 was performed. Data on the maternal prenatal history, delivery, and neonatal course, including detailed information on episodes of microbiologically verified septicemia, were collected on predefined forms. Septicemia was reported in 2 groups, ie, episodes diagnosed on the day of delivery (ie, very early-onset septicemia [VEOS]) and episodes diagnosed from day 2 to day 7 of life (ie, early-onset septicemia [EOS]). Logistic regression models were used for the selection of variables for predictor analysis in each group. RESULTS: Of 462 included infants, VEOS occurred for 15 (32.5 per 1000 population) and EOS for 15 (35.5 per 1000 population). The most prevalent bacteria were Escherichia coli in VEOS (n = 9) and staphylococci (coagulase-negative staphylococci and Staphylococcus aureus) (n = 15) in EOS. Case fatality rates were 40% and 13%, respectively. Independent predictive factors for VEOS were clinical chorioamnionitis (odds ratio [OR]: 10.5; 95% confidence interval [CI]: 3.3-33.4) and high maternal age (OR: 1.2; 95% CI: 1.0-1.3), whereas not receiving systemic antibiotic therapy within 2 days of age (OR: 13.6; 95% CI: 3.7-50.2) and receiving nasal continuous positive airway pressure (n-CPAP) support at 24 hours of age (OR: 9.8; 95% CI: 2.5-38.4) independently predicted septicemia after the first day of life. CONCLUSIONS: Whereas vertically transmitted septicemia was dominated by Gram-negative bacteria, with predictors being exclusively of maternal origin, EOS was dominated by typically nosocomial flora, with n-CPAP treatment at 24 hours of age being a powerful predictor. Early n-CPAP treatment, as opposed to mechanical ventilation, as a powerful predictor of septicemia in the early neonatal period, even with adjustment for early systemic antibiotic treatment, is a new observation among extremely premature infants that warrants additional study.

Clinical characteristics of chronic lung disease without preceding respiratory distress syndrome in preterm infants.

BACKGROUND: Recently, the incidence of atypical presentation of chronic lung disease (CLD) that develops in infants without a history of preceding respiratory distress syndrome (RDS) is increasing. Therefore, the clinical characteristics of CLD without RDS in comparison with CLD with RDS were assessed. METHODS: Prospective cohort analysis was done from 117 very low-birthweight infants who were born in Seoul National University Hospital and survived more than 36 weeks postmenstrual age (PMA). RESULTS: Of the 117 infants analyzed, CLD developed in 44 infants (38%). Among these 44 infants, CLD with RDS developed in 27 infants (23%) and CLD without RDS developed in 17 infants (15%). Each type of CLD was subgrouped according to the presence of chorioamnionitis (CA): RDS(+)CA(+) CLD (n = 8) and RDS(+)CA(-) CLD (n = 19); and RDS(-)CA(+) CLD (n = 12) and RDS(-)CA(-) CLD (n = 5). There were no significant differences in the demographic characteristics between CLD with RDS and CLD without RDS. Chorioamnionitis was significantly more common in CLD without RDS, while patent ductus arteriosus was more common in CLD with RDS. Although the severity of initial respiratory failure was not greater than that of CLD with RDS, CLD without RDS showed a gradually increasing chronic oxygen requirement pattern. Chronic oxygen requirement pattern showed that infants with RDS(+)CA(+)CLD required the highest concentrations of oxygen not only initially but also thereafter until the 28th day of life and 36 weeks PMA. CONCLUSIONS: Although CLD without RDS was still less common than CLD with RDS, it comprised over a third of all cases of CLD in our study. Clinical characteristics and chronic oxygen requirement pattern of CLD without RDS seems to be less severe than those of CLD with RDS. Our data suggest that CLD without RDS may be developed by causes other than initial acute lung injury. Chorioamnionitis may be one of antecedents of CLD without RDS.

Maternal infection and risk of cerebral palsy in term and preterm infants.

OBJECTIVE: We tested the hypothesis that term and preterm infants exposed to maternal infection at the time of delivery are at increased risk of developing cerebral palsy (CP). STUDY DESIGN: A population-based case-control study was conducted using Washington State birth certificate data linked to hospital discharge data. Cases (688) were children

Benefit of antenatal glucocorticoids according to the cause of very premature birth.

In this observational study performed in a large cohort of very preterm singletons, respiratory outcome was found to be strongly dependent on the cause of premature delivery. Although less apparent in infants born to mothers with chorioamnionitis, exposure to antenatal glucocorticoids remained significantly associated with a decrease in the incidence of respiratory distress syndrome after adjustment for the main cause of premature birth.

Histologic chorioamnionitis: an occult marker of severe pulmonary hypertension in the term newborn.

OBJECTIVE: To determine whether the presence of histologic chorioamnionitis is associated with the severity of Persistent Pulmonary Hypertension of the Newborn (PPHN) as evidenced by the use of exogenous nitric oxide (iNO), high-frequency oscillatory ventilation (HFOV), extra-corporeal membrane oxygenation (ECMO) and/or death. METHODS: Retrospective chart review of term neonates > or =37 weeks gestation with PPHN. Placental pathology was reviewed. Primary outcome is the use of iNO. Secondary outcomes include the use of HFOV, ECMO and death. RESULTS: Over 2 years, 29 neonates fulfilled the entry criteria for the study. Interventions included iNO use n=14 (48%), HFOV n=7 (24%) and ECMO n=3 (10%); two neonates died. Histologic chorioamnionitis and/or funisitis was noted in 16 (55%) neonates. The presence of chorioamnionitis and/or funisitis (n=16) versus neither (n=13) was significantly associated with iNO use 11/16 (78%) versus 3/13 (22%) (p=0.02) and HFOV 7/16 (43%) versus 0/13 (0%) (p=0.008) but not to ECMO or death. CONCLUSION: The presence of histologic chorioamnionitis and/or funisitis is associated with more severe PPHN as indicated by the use of iNO as well as an increased requirement for more advanced respiratory support, that is, HFOV. The mechanism/s contributing to these findings are unclear.

Prolonged fetal bradycardia as the presenting clinical sign in Streptococcus agalactiae chorioamnionitis.

Group B Streptococcus remains a leading infectious cause of neonatal morbidity and mortality. We report a case of a 37 weeks' gestation infant with severe birth asphyxia, status epilepticus and GBS chorioamnionitis, in which a prolonged fetal bradycardia was the only prenatal clinical sign.

Are histopathologic chorioamnionitis and funisitis associated with metabolic acidosis in the preterm fetus?

OBJECTIVE: Perinatal infection increases the risk of neonatal neurologic injury. Our objective is to determine whether histologically confirmed chorioamnionitis and funisitis is associated with fetal metabolic acidosis. STUDY DESIGN: This is a retrospective cohort study of all infants 34 weeks or less born at a single tertiary hospital admitted to the neonatal intensive care unit (NICU) between April 1999 and September 2002. Maternal and neonatal records and placental pathology reports were reviewed. RESULTS: There were 392 infants at 23 to 34 weeks' gestational age admitted to the NICU during this period of whom 354 had placental pathology reported; 259 infants had umbilical cord gases available. These neonates were placed into 3 groups: group 1 (208 infants) had no signs of placental infection, group 2 (59 infants) had isolated chorioamnionitis, and group 3 (87 infants) had both chorioamnionitis and funisitis. The gestational age (30.2 +/- 2.8, 28.3 +/- 3.4, 27.8 +/- 2.8 weeks, P < .01) and birth weight (1358 +/- 520, 1242 +/- 547, 1103 +/- 381 g, P < .01) were significantly higher in group 1. There was an increase in neurologic morbidity in groups 2 and 3 (25.2%, 34.4%, 43.7%), which was not significant when corrected for gestational age. Groups 2 and 3 had a small but significant increase in umbilical arterial pH (7.25 +/- 0.10, 7.29 +/- 0.10, 7.30 +/- 0.08, P < .01) and base excess (-3.5 +/- 3.6, -2.2 +/- 3.6, -2.3 +/- 2.7 mmol/L, P = .02). When a single pathologist reviewed all placentas with any inflammation and staged them on the basis of the degree of the fetal inflammatory response, no relationship was found between the degree of fetal inflammation and umbilical arterial pH (stage 1, 7.27 +/- 0.09; stage 2, 7.30 +/- 0.09; stage 3, 7.30 +/- 0.08; P = .41) or base excess (stage 1, -2.82 +/- 3.47 mmol/L; stage 2, -1.95 +/- 3.17 mmol/L; stage 3, -2.23 +/- 3.07 mmol/L; P = .62). When stepwise multiple linear regression was performed, neither histologic chorioamnionitis nor histologic funisitis were associated with a change in umbilical cord pH or base excess. CONCLUSION: Intrauterine infection, as confirmed by histologic chorioamnionitis and funisitis, is not associated with fetal metabolic acidosis. Intrauterine infection may represent a nonhypoxic form of encephalopathy that produces neurologic morbidity by a mechanism independent of hypoxia-ischemia leading to metabolic acidosis.

Spleen depletion in neonatal sepsis and chorioamnionitis.

Neonatal sepsis and chorioamnionitis induce morphologic modifications and shrinkage of the thymus. We show fetal and neonatal morphologic modifications of the spleen in the same autopsy subjects as previously used to describe thymus shrinkage, including 10 preterm or full-term neonates who died of proven sepsis within 48 hours after birth and 20 fetuses spontaneously aborted because of extensive ascending chorioamnionitis. Control subjects included 10 fetuses from induced termination of pregnancy and 10 neonates who died suddenly during the perinatal period without evidence of chorioamnionitis. Spleen cell populations were studied by means of immunohistochemical analysis. Neonatal sepsis occurred with severe spleen depletion, involving both B and T lymphocytes (P < .001). Fetuses with chorioamnionitis also showed spleen cell depletion. These observations, to our knowledge not described before, indicate that preterm and term neonates show an inflammatory reaction similar to that of adult patients and that severe chorioamnionitis is associated with a nonspecific inflammatory response comparable to that of sepsis.

Development of a guinea pig model of chorioamnionitis and fetal brain injury.

OBJECTIVE: The purpose of this study was to develop a guinea pig model of chorioamnionitis to study the mechanisms that lead to fetal brain injury. Study design Pregnant guinea pigs at 70% gestation were inoculated intracervically with 1000 to 2500 colony-forming units of Escherichia coli. Guinea pigs were killed 2 to 3 days after bacterial inoculation. Maternal blood and fetal amniotic fluid samples were analyzed for proinflammatory cytokine tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 levels with the use of enzyme-linked immunosorbent assay kits. Fetal brains were stained for evidence of cell death with NeuroTacs stain. RESULTS: Of 34 maternal guinea pigs that were given an intracervical inoculation of E coli, 8 guinea pigs showed microbiologic evidence of chorioamnionitis in the amniotic fluid. Tumor necrosis factor-alpha and interleukin-6 were significantly higher (P<.05) in amniotic fluid samples that were obtained from sows that were subjected to intracervical inoculation with bacteria as compared with control animals (n=6 control maternal animals). These results were observed even if no bacteria were found subsequently on culture of the amniotic fluid from inoculated animals, which indicated that indirect exposure to infectious agents was sufficient to cause an elevated inflammatory response in the fetus. Levels of white matter injury were greater in fetuses that were exposed to bacterial infection in utero, as compared with control animals (P<.05). This result was found in the staining of periventricular and cortical white matter for the immunolabeling of activated caspase 3 and NeuroTacs staining for cells that exhibited evidence of apoptotic cell death (positive stain with evidence of karyorrhexis). CONCLUSION: Intracervical inoculation with E coli results in chorioamnionitis in guinea pigs that is associated with fetal brain injury.

Apoptosis and proliferation in lungs of human fetuses exposed to chorioamnionitis.

AIMS: To determine whether chorioamnionitis has an impact on the extent of apoptosis and proliferation in fetal lungs. Fetuses exposed to chorioamnionitis have an increased risk of aquiring lung tissue damage in utero. METHODS AND RESULTS: Lung tissue sections from 35 stillborn fetuses were used in this study. Chorioamnionitis-exposed fetuses were subdivided depending on whether pneumonia was diagnosed (n = 13) or not (n = 10); 12 unaffected fetuses served as controls. Apoptotic and proliferating cells were determined by in-situ terminal deoxytransferase-mediated dUTP nick end labelling (TUNEL) assay and by anti-Ki67 immunohistochemistry, and quantified. The median apoptotic index in lungs of chorioamnionitis-exposed fetuses increased 2.4-fold compared with chorioamnionitis-negative stillborn controls (P = 0.043) and rose 21.6-fold when chorioamnionitis-exposed fetuses additionally developed pneumonia (P < 0.001). Compared with the proliferation index of the control group (PI = 2.3), the median percentage of proliferating cells in the lungs of chorioamnionitis-exposed fetuses decreased (PI = 1.4) (P = 0.036), but increased 1.8-fold (P = 0.036) in fetal lungs of the chorioamnionitis/pneumonia group. By double labellings combining the TUNEL assay or the Ki67 antigen with cell marker proteins, we identified distal airway epithelial cells as the cell type undergoing apoptosis in chorioamnionitis-exposed fetal lungs, while epithelial, endothelial and smooth muscle cells proliferated. Immunolabellings of cleaved caspases -8 and -9 revealed that apoptosis is mediated via initiator caspase-8. CONCLUSION: Chorioamnionitis induces apoptosis of distal airway epithelial cells via the caspase-8 pathway and interferes with the normal proliferative activity of epithelial, endothelial, and smooth muscle cells in fetal lungs. Thus, apoptosis and proliferation are an important feature of chorioamnionitis-associated lung injury in utero.

The Maternal-Fetal Medicine Units cesarean registry: chorioamnionitis at term and its duration-relationship to outcomes.

OBJECTIVE: The purpose of this study was to evaluate the relationship between chorioamnionitis and its duration to adverse maternal, fetal, and neonatal outcomes. STUDY DESIGN: This was a 13-university center, prospective observational study. All women at term carrying a singleton gestation who underwent primary cesarean from January 1, 1999 to December 31, 2000 were eligible. Data abstraction was systematic and performed by trained research nurses. Selected adverse outcomes were compared between pregnancies with, and without, clinically diagnosed chorioamnionitis using relative risks (RRs) and 95% CIs. The duration of chorioamnionitis was stratified into 5 intervals (3-6 h,>6-9 h,>9-12 h, and>12 h), and respective outcomes compared by Mantel-Haenszel test for trend. Additionally, regression analysis was used to compute odds ratios (ORs) and 95% CIs for chorioamnionitis duration length as a continuous explanatory variable. RESULTS: 16,650 pregnancies were analyzed, 1965 (12%) with chorioamnionitis, which was associated with significantly increased risks of maternal blood transfusion, uterine atony, septic pelvic thrombophlebitis, and pelvic abscess (RR 2.3-3.7), as well as 5-minute Apgar

Chorioamnionitis/funisitis and the development of bronchopulmonary dysplasia.

OBJECTIVE: To examine the association between chorioamnionitis with or without funisitis and bronchopulmonary dysplasia in infants less than 30 completed weeks gestation given the current standards of antenatal steroid and surfactant use. METHODS: Infants included in the study were those delivered at less than 30 completed weeks gestation from January 1996 to July 2001, identified from a prospectively managed database. Placental pathology was reviewed for the presence or absence of chorioamnionitis and funisitis. Infants were divided into three groups depending on degree of exposure to fetal inflammation (no inflammation, chorioamnionitis only and chorioamnionitis and funisitis). Data relating to gestational age, sex, antenatal steroid exposure, surfactant treatment, days of positive pressure ventilation and days of oxygen required were collected. Bronchopulmonary dysplasia was defined as death due to respiratory failure or any oxygen requirement at 36 weeks postmenstrual age. RESULTS: Two hundred and forty-one infants were included in the study. The mean gestational age was 27.7 weeks and mean birthweight 1089 g. One hundred and sixty-one infants were not exposed to any in utero inflammation, 40 showed chorioamnionitis and 40 showed chorioamnionitis and funisitis. There was no significant difference between antenatal steroid and surfactant treatment between the three groups. There was no significant difference between the three groups in the development of bronchopulmonary dysplasia. Low gestational age was the most significant predictor of developing bronchopulmonary dysplasia. CONCLUSION: The risk of developing bronchopulmonary dysplasia is not increased following exposure to chorioamnionitis or funisitis in the context of current antenatal steroid and surfactant use. The most significant predictor for developing bronchopulmonary dysplasia is gestational age at the time of delivery.