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PubMed2003

Pulmonary fluorodeoxyglucose uptake in infants of very low birth weight with and without intrauterine inflammation.

OBJECTIVE: We compared early pulmonary (18)fluorodeoxyglucose ((18)FDG) uptake in infants who had very low birth weight with and without exposure to intrauterine inflammation by using positron emission tomography (PET). A secondary goal was to correlate (18)FDG uptake with later death or bronchopulmonary dysplasia. METHODS: Within 72 hours of birth, 22 singleton infants between 25 and 30 weeks of gestation had a thoracic PET scan after intravenous (18)FDG. Influx constants (K(i)) for (18)FDG were determined. Placental histology assessed exposure to intrauterine inflammation. RESULTS: Chorioamnionitis was found in 13 infants. Seven of these infants also had evidence of funisitis. No inflammation was detected in the remaining nine infants. Median (minimum, maximum) thoracic K(I) was 0.008 (0.006, 0.011) mL/min/mL in infants with funisitis, 0.006 (0.002, 0.008) in infants with chorioamnionitis only, and 0.006 (0.001, 0.015) in infants with no evidence of intrauterine inflammation (P=.16). No relation was found between K(i) and later death or bronchopulmonary dysplasia. Cord blood interleukin-6 was elevated in newborns with placental inflammation (P=.014). CONCLUSION: Early thoracic PET scanning for metabolically active inflammatory cells does not differ between infants with and without exposure to intrauterine inflammation. Evidence of early intrapulmonary sequestration of inflammatory cells in some infants without chorioamnionitis points to the complex etiology of postnatal inflammation.

Bronchopulmonary Dysplasia↗
PubMed2005

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.

Cerebral Palsy↗
PubMed2004

Chorionic plate vessels as an origin of amniotic fluid neutrophils.

The present study was conducted to investigate the potential anatomical source of amniotic fluid neutrophils. Microdissection of neutrophils from the chorioamnion of the fetal membranes and the amnion of the chorionic plates of 10 preterm placentas with acute chorioamnionitis was performed and the genotypes of the neutrophils were compared with those of the mother and fetus using polymerase chain reaction of nine autosomal STR loci. In separate analyses, we reviewed eight cases of fetal autopsies with increased amniotic fluid neutrophils for the presence of neutrophils in the alveoli, and also analyzed the relationship between the amniotic fluid white blood cell (WBC) count and the histological pattern of placental inflammation. The genotypes of all of the neutrophils found in the chorioamnion of the fetal membrane matched those of the mother (n = 10). The genotypes of neutrophils found in the chorionic plate were of mixed maternal and fetal origin (n = 4). In the autopsy series of the fetuses with amniotic fluid WBC (n = 8), only five cases showed neutrophils in the alveolar space, while all the placentas had chorioamnionitis. There was no significant difference in amniotic fluid WBC count between the cases with or without acute membranitis, while among the cases with placental inflammation, those with inflammation of the chorionic plate had a significantly higher amniotic fluid WBC count than both the membranitis-only cases (P < 0.001) and the membranitis and funisitis cases (P < 0.05). These results imply that fetal vasculature at the chorionic plate is the main source of amniotic fluid neutrophils, especially in the cases without funisitis.

Adult↗
PubMed1977

Placental abnormalities in victims of the sudden infant death syndrome.

Placentas from 79 victims of the sudden infant death syndrome (SIDS) were compared with placentas from 30,640 controls who survived in a search for evidences of infections or other disorders that might have damaged the SIDS victims before birth. Placentas from the SIDS victims had an increased frequency of acute funisitis, acute chorioamnionitis, lymphocytic infiltration of the decidua and macrophages in the fetal membranes. The acute funisitis and chorioamnionitis were associated with preterm deliveries and were probably related to amniotic fluid bacterial infections which are a common cause of premature delivery.

Bacterial Infections↗
PubMed2006

Myelopoiesis in the liver of stillborns with evidence of intrauterine infection.

CONTEXT: Chorioamnionitis is the maternal and fetal response to an ascending intrauterine infection. The fetal response is manifested by funisitis and chorionic vasculitis, or as neutrophils within pulmonary spaces. Human hematopoiesis occurs in the liver primarily during the 6th to 22nd weeks of gestation. OBJECTIVE: To establish the relationship between the presence of an intrauterine infection and the degree of fetal hepatic myelopoiesis in second- and third-trimester fetuses. DESIGN: Liver and lungs from 49 fetal autopsies, 20 to 41 weeks of gestational age, and their associated placentas and membranes were analyzed for evidence of intrauterine infection and hepatic myelopoiesis. Hematoxylin-eosin-stained sections from fixed tissues were evaluated for the presence of amnionic fluid infection, defined by the presence of acute chorioamnionitis or funisitis. The degree of portal hematopoiesis, myelopoiesis and intra-alveolar neutrophils was assessed semiquantitatively with hematoxylin-eosin-stained sections and immunohistochemically with antimyeloperoxidase. The Kruskal-Wallis 1-way analysis of variance and the Wilcoxon-Mann-Whitney test were used to determine the significance of any observed difference. RESULTS: The degree of portal and lobular myelopoiesis was significantly greater with the presence of inflammation in both the membranes and umbilical cord, and correlated with the presence of intra-alveolar neutrophils (P < .001). A high correlation between the hematoxylin-eosin and immunohistochemistry assessment of myeloid cells was noted. CONCLUSIONS: There is increased portal and lobular myelopoiesis in 20-week to 41-week gestational age fetal livers that is associated with intrauterine ascending infection. The presence of increased portal or lobular myelopoiesis suggests the presence of an active fetal response to an intrauterine ascending infection.

Adult↗
PubMedDate not supplied

Mycoplasma hominis: a placental pathogen?

Current information on the role played by Mycoplasma hominis in placental inflammation was reviewed. M. hominis is associated with chorioamnionitis and funisitis, but the clinical significance of this association in not clear. Further research on the role of the organism in perinatal disease is needed. Meanwhile, in a gravely ill infant with a history of prolonged rupture of the placental membranes, chorioamnionitis, and funisitis, M. hominis should probably be considered a potential pathogen, cultures for this organism should be performed, and therapy with an antibiotic regimen effective against M. hominis should be instituted.

Amnion↗
PubMed1975

Congenital cutaneous candidiasis.

Two cases of congenital cutaneous candidiasis are presented in order to call attention to this rarely recognized and infrequently reported condition. Clinical features and appropriate cultures are useful in differentiating the lesions from other more common dermatoses of the neonatal period. Microscopic examination of the placenta may disclose fungal funisitis or chorioamnionitis, thus defining the congenital nature of the disease. Topical antifungal therapy is sufficient unless systemic candidiasis is present. No evidence of impaired immunological responsiveness was found in the two infants.

Candidiasis, Cutaneous↗
PubMed2002

Spontaneous prolonged hypertonic uterine contractions (essential uterine hypertonus) and a possible infective etiology.

The management of a pregnant woman presenting with prolonged hypertonic uterine contractions (essential uterine hypertonus) and mildly elevated temperature at term is described. Histology of the placenta, cord and membranes, following delivery, revealed evidence of chorioamnionitis, funisitis and deciduitis. Our findings raise the possibility that essential uterine hypertonus may have an infective or inflammatory component to its etiology.

Adult↗
PubMedDate not supplied

Amniotic infection syndrome: nosology and reproducibility of placental reaction patterns.

Clinically responsive placental examination seeks to provide useful information regarding the etiology, prognosis, and recurrence risk of pregnancy disorders. The purpose of this study was to assemble and validate a complete set of the placental reaction patterns seen with amniotic fluid infection in the hope that this might provide a standardized diagnostic framework useful for practicing pathologists. Study cases (14 with amniotic fluid infection, 6 controls) were reviewed blindly by six pathologists after agreement on a standard set of diagnostic criteria. After analysis of initial results, criteria were refined and a second, overlapping set of cases were reviewed. Majority vote served as the gold standard. Grading and staging of maternal and fetal inflammatory responses was found to be more reproducible using a two- versus three-tiered grading system than a three- versus five-tiered staging system (overall agreement 81% vs. 71%). Sensitivity, specificity, and efficiency for individual observations ranged from 67-100% (24/30 > 90%). Reproducibility was measured by unweighted kappa values and interpreted as follows: < 0.2, poor; 0.2-0.6, fair/moderate; > 0.6, substantial. Kappa values for the 12 lesions evaluated in 20 cases by the six pathologists were: acute chorioamnionitis/maternal inflammatory response (any, 0.93; severe 0.76; advanced stage, 0.49); chronic (subacute) chorioamnionitis (0.25); acute chorioamnionitis/fetal inflammatory response (any, 0.90; severe, 0.55; advanced stage, 0.52); chorionic vessel thrombi (0.37); peripheral funisitis (0.84); acute villitis (0.90); acute intervillositis/intervillous abscesses (0.65), and decidual plasma cells (0.30). Adoption of this clearly defined, clinically relevant, and pathologically reproducible terminology could enhance clinicopathologic correlation and provide a framework for future clinical research.

Adult↗
PubMedDate not supplied

Differences among acute, subacute, and chronic chorioamnionitis based on levels of inflammation-associated proteins in cord blood.

The serum concentration of inflammation-associated proteins and several complement components in the cord blood of 215 newborns with and without chorioamnionitis (CAM), who were delivered between 17 and 42 weeks of gestation, were measured. We investigated the relationship of levels of serum proteins to acute, subacute, and chronic CAM, and to subacute necrotizing funisitis (SNF). Complement components C3d, C3, and C4 levels increased in subacute CAM (P = 0. 0002, P = 0.0007, P = 0.0029, respectively), whereas factor B increased in each type of CAM (P = 0.0001, P = 0.0009, P = 0.0004, respectively). Among the immunoglobulins, IgG levels were unrelated to the presence or type of CAM, IgM levels increased in subacute CAM (P < 0.0001), and IgA levels increased in chronic CAM (P < 0.0001). Among the acute phase reactants (APR), haptoglobin and C-reactive protein (CRP) levels increased in acute (P < 0.0001, P = 0.0022, respectively) and chronic CAM (P = 0.0035, P = 0.0345, respectively), whereas orosomucoid levels increased in chronic CAM (P = 0.0003). IL-6 levels increased in acute (P = 0.0011) and subacute (P = 0. 0475) CAM. C3d (P = 0.0063), C3 (P = 0.0289), C4 (P = 0.0491), and IgM (P < 0.0001) levels were increased in SNF. These findings suggest that the histologic distinction of acute, subacute, and chronic CAM is a useful indicator of the inflammatory mediator status of the infants. The infants with SNF may have ended their initial active inflammatory states, but they still have subacute immune activation.

Acute Disease↗
PubMedDate not supplied

Effects of cocaine on the placenta.

Adverse perinatal outcomes of gravidas using cocaine is well documented, but the effects on the placenta have been difficult to elucidate due to confounding factors such as concurrent use of other drugs. This study compares pathologic findings of 26 placentas from women who used only cocaine during pregnancy with findings from 26 controls. All women were from a similar socioeconomic class and were controlled for gestational age and tobacco use. None of the cocaine placentas were from women whose toxicology screens were positive for drugs other than cocaine. In the 26 cocaine placentas, there was 1 infarct, 3 chronic villitis, and 1 segmental fibrosis, with none present in the controls. In the control group, there was 1 decidual vasculopathy and 1 thrombus in a maternal vessel, but none were in the cocaine placentas. Each group had 1 thrombus in a fetal vessel. The study group showed 6 cases of chorioamnionitis and 1 funisitis; the control group had 10 and 4 cases, respectively. None of the above or seven other features showed a statistically significant difference between the cases and controls. Cocaine is a potent vasoconstrictive agent that blocks re-uptake of norepinephrine at the adrenergic nerve terminals. Our study suggests that cocaine does not cause an increased incidence of any of the 15 clearly recognizable placental features examined.

Adult↗
PubMed1992

The relationship between acute inflammatory lesions of the preterm placenta and amniotic fluid microbiology.

OBJECTIVE: Our objective was to determine the relationship between microbial invasion of the amniotic cavity and the presence and severity of acute inflammatory lesions in the placenta. STUDY DESIGN: Placental histologic and amniotic fluid microbiologic studies were performed in 92 consecutive patients who were admitted with preterm labor and intact membranes and delivered within 48 hours after amniocentesis. RESULTS: The prevalence of a positive amniotic fluid culture was 38% (35 of 92). There was a strong association between the presence and severity of inflammation in the amnion, chorion-decidua, umbilical cord, and chorionic plate and the results of the amniotic fluid culture (p less than 0.0001 for each tissue section). Three patterns of inflammation of the chorion-decidua were identified: marginating, nonmarginating, and a mixed pattern. The marginating and the mixed patterns of inflammation were strongly associated with the presence of a positive amniotic fluid culture. Acute inflammation of the chorionic plate was the most sensitive indicator of a microbial invasion of the amniotic cavity (sensitivity 96.6%), and funisitis and umbilical vasculitis had the highest specificity (85.7%). CONCLUSION: The presence of acute inflammatory lesions of the chorioamniotic membranes can serve as a marker of microbial invasion of the amniotic cavity.

Amnion↗
PubMed1993

Expectant management of preterm prelabour rupture of membranes--the significance of oligohydramnios at presentation.

In a retrospective study, the relationship between oligohydramnios (largest amniotic fluid pocket less than 2 x 2 cm) at the time of presentation and the outcome of expectant management of patients with preterm (< 35 weeks) prelabour rupture of membranes (PROM) was examined in 62 patients admitted with a confirmed diagnosis and in the absence of complications or established labour. There were no differences in the maternal age, incidence of multiparity, or additional complications between patients without (Group 1, n = 24) and with (Group 2, n = 38) oligohydramnios. However in Group 2, 44.7% of the patients developed PROM before 28 weeks and 63.2% were delivered within 48 h of assessment, in contrast to 20.8% (P < 0.05) and 12.5% (P < 0.001), respectively, in Group 1. Group 2 patients had a higher incidence of histological chorioamnionitis (55.3% vs. 29.3%, P < 0.05) and funisitis (44.7% vs. 16.7%, P < 0.02), an earlier mean gestation at delivery (29.1 +/- 2.8 weeks vs. 31.5 +/- 2.0 weeks, P < 0.001) and lower birth weight (1373 +/- 467 g vs. 1856 +/- 496 g, P < 0.001). Our results indicate that oligohydramnios at presentation of preterm PROM is an unfavourable prognostic sign in the expectant management of these pregnancies.

Adolescent↗
PubMed2004

A fetal response to chorioamnionitis is associated with early survival after preterm birth.

OBJECTIVE: The purpose of this study was to determine, in a large preterm cohort (20-34 completed weeks of gestation), the incidence of histologic chorioamnionitis and the incidence of a histologic fetal response to chorioamnionitis (umbilical vasculitis with or without funisitis) in neonatal survivors (to 28 days) and perinatal deaths. STUDY DESIGN: Placental histopathology was reviewed (n=3928 reports). In a subset of this cohort (n=2076 reports), evidence of a histologic fetal response was compared in neonatal survivors and perinatal deaths. RESULTS: The incidence of histologic chorioamnionitis ranged from 66% at 20 to 24 weeks of gestation (n=261 neonates) to 16% at 34 weeks (n=770 neonates). The overall incidence was 31% (n=3928 neonates). At 25 to 29 weeks of gestation, neonatal survivors had a higher incidence of histologic chorioamnionitis (P=.02; 95% CI, 1.02-1.21). In addition, neonatal survivors had a higher incidence of a histologic fetal response to chorioamnionitis at 25 to 29 weeks of gestation (P=.01; 95%CI, 0.33-0.86) and 30 to 34 weeks of gestation (P=.02; 95%CI, 0.18-0.85). CONCLUSION: Histologic chorioamnionitis is inversely related to gestational age. Both histologic chorioamnionitis and a histologic fetal response to chorioamnionitis were observed to be more common in preterm survivors of the neonatal period.

Australia↗
PubMed2005

Chorioamnionitis with a fetal inflammatory response is associated with higher neonatal mortality, morbidity, and resource use than chorioamnionitis displaying a maternal inflammatory response only.

OBJECTIVE: This study was undertaken to evaluate whether the proximity of infection of the chorion/amnion and fetal vessels affects neonatal outcomes. STUDY DESIGN: We examined all (n=2012) infants admitted to the British Columbia's Children's Hospital Neonatal Intensive Care Unit, from January 1996 to October 1997. We included infants with a placental examination (n=1296), and stratified those with histologic chorioamnionitis into cases displaying a maternal inflammatory response only and cases also displaying a fetal inflammatory response (funisitis and/or fetal surface vessel angiitis). RESULTS: Histologic evidence of chorioamnionitis was present in 31% of placentas. Of those, 38% exhibited maternal inflammation only, whereas 62% also exhibited fetal inflammation. Neonatal mortality (9.2% vs 7.2%), morbidity, and resource use were significantly (P < .05) higher when fetal inflammation was present compared with when only maternal inflammation was present. CONCLUSION: Chorioamnionitis with a fetal inflammatory response is associated with higher neonatal mortality, morbidity, and resource use than when only a maternal inflammatory response is present.

Chorioamnionitis↗
PubMed2006

Preterm histologic chorioamnionitis: impact on cord gas and pH values and neonatal outcome.

OBJECTIVE: The purpose of this study was to further delineate the impact of preterm chorioamnionitis on a spectrum of neonatal outcomes using a large tertiary hospital population. STUDY DESIGN: The perinatal/neonatal and placental pathology databases of St. Joseph's Health Care, London, Ontario, Canada, were used to obtain the umbilical cord gas and pH values, incidence of adverse neonatal outcomes, patient demographics, and placental pathology reports for all preterm (25 to 34 weeks of gestation), singleton, liveborn infants with no major anomalies who were delivered with spontaneous onset of labor or for suspected chorioamnionitis between November 1, 1995, and October 31, 2003. Patient groupings on the basis of placental inflammation and clinical chorioamnionitis were studied by a comparison of mean values and incidences for those neonatal outcomes that were available from the database with the use of linear and logistic regression analysis and controlling for potentially confounding variables. RESULTS: There were 660 infants who met the inclusion criteria and had placental pathology available of whom 368 (56%) had no placental inflammation, 114 (17%) had placental chorioamnionitis, and 178 (27%) had placental funisitis. Umbilical cord partial pressure oxygen and base excess values were generally higher in the placental inflammation/clinical chorioamnionitis groups, in keeping with enhanced oxygen delivery and an overall decrease in the metabolic contribution to acidosis attributed to altered lactate metabolism in these infants. After adjusting for confounders (primarily differences in gestational age), the incidence of respiratory distress syndrome was significantly decreased in the placental inflammation/clinical chorioamnionitis groups, in keeping with cytokine-induced synthesis of surfactant proteins in these infants. Although the incidence of bronchopulmonary dysplasia, intraventricular hemorrhage, and periventricular leukomalacia was generally unchanged among the groups studied, that for intraventricular hemorrhage and periventricular leukomalacia was lowest in the placental inflammation/no clinical chorioamnionitis patients and highest in the placental inflammation/clinical chorioamnionitis patients, suggesting a differential effect of clinical chorioamnionitis for these outcomes. CONCLUSION: Overall, infants born preterm with intrauterine infection were better oxygenated and showed less metabolic acidosis at birth and had incidences of respiratory distress syndrome and intraventricular hemorrhage, which were variably lower. Although there are likely threshold levels of inflammatory cytokines that do give rise to adverse outcome, a minimal level of cytokines may also be beneficial for the transition at birth from intrauterine to extrauterine existence when preterm pending the circumstances (ie, exposure to antenatal steroids) and emphasizing the complex relationship among preterm birth, infection, and adverse neonatal outcome.

Acidosis↗
PubMed2006

Intra- and interobserver agreement and statistical clustering of placental histopathologic features relevant to preterm birth.

OBJECTIVE: Many previous studies of agreement in identifying placental histopathologic lesions have been based on small sample sizes, and none has examined whether individual histologic features cluster robustly together within and between observers. STUDY DESIGN: We studied 767 placental specimens from case-control studies of preterm birth and preeclampsia nested within a prospective cohort of pregnant women recruited from 4 large Montreal maternity hospitals. The specimens were fixed, embedded, stained, and examined using a standardized protocol; a 10% random sample (n = 81) was then blindly reexamined at least 6 months later by the same pathologist and a second pathologist. RESULTS: Intra- and interobserver agreement were high (kappa > or = 0.50) for membrane inflammation, funisitis, and umbilical cord vasculitis, and these 3 features were robustly clustered statistically, consistent with an underlying mechanism of ascending infection. Agreement and clustering were also high or moderate for features of placental underperfusion: infarction, decidual vasculopathy, and syncytial knotting. CONCLUSION: Our results should help researchers to interpret future findings relating placental histopathology to preterm birth, preeclampsia, and other adverse pregnancy outcomes, and to their etiologic determinants and causal pathways.

Case-Control Studies↗
PubMed2004

Placental fetal thrombotic vasculopathy is associated with neonatal encephalopathy.

Neonatal encephalopathy (NE) remains an important cause of morbidity and mortality in the term infant, and many cases have an antepartum, rather than an intrapartum, etiology. Chronic processes such as thrombosis result in changes in the placenta. We sought to determine whether histopathological examination of the placenta in cases of NE, focusing on these changes, could identify significant antenatal processes that are not recognized by clinical assessment alone. Infants born at term with NE were identified retrospectively over a 12-year period. Placental tissue from deliveries during the study period was available for reexamination. Controls were selected from a cohort of 1000 consecutive deliveries on which clinical and pathological data were collected as part of an earlier study. Bivariate and multivariate analyses of clinical and pathological factors for cases and controls were used to test for an independent association with NE. Clinical and placental data was collected on 93 cases of NE and 387 controls. The placental features of fetal thrombotic vasculopathy (FTV), funisitis (signifying a fetal response to infection), and accelerated villous maturation were independently associated with NE. Of the clinical factors studied, meconium-stained liquor and abnormal cardiotocograph were independently associated. There were no independently associated clinical antenatal factors. Placental features of infection, thrombosis, and disturbed uteroplacental flow are significant independent factors in the etiology of NE in this study. Acute and chronic features suggest that NE may result from acute stress in an already compromised infant. The absence of significant clinical antenatal factors supports the value of placental examination in the investigation of infants with NE.

Adolescent↗