Diagnosis Of Chorioamnionitis Research Articles

Chorioamnionitis and cerebral palsy in term and near-term infants.

Half of all cases of cerebral palsy (CP) occur in term infants, for whom risk factors have not been clearly defined. Recent studies suggest a possible role of chorioamnionitis. To determine whether clinical chorioamnionitis increases the risk of CP in term and near-term infants. Case-control study nested within a cohort of 231 582 singleton infants born at 36 or more weeks' gestation between January 1, 1991, and December 31, 1998, in the Kaiser Permanente Medical Care Program, a managed care organization providing care for more than 3 million residents of northern California. Case patients were identified from electronic records and confirmed by chart review by a child neurologist, and comprised all children with moderate to severe spastic or dyskinetic CP not due to postnatal brain injury or developmental abnormalities (n = 109). Controls (n = 218) were randomly selected from the study population. Association between clinical chorioamnionitis and increased risk of CP in term and near-term infants. Most CP cases had hemiparesis (40%) or quadriparesis (38%); 87% had been diagnosed by a neurologist and 83% had undergone neuroimaging. Chorioamnionitis, considered present if a treating physician made a diagnosis of chorioamnionitis or endometritis clinically, was noted in 14% of cases and 4% of controls (odds ratio [OR], 3.8; 95% confidence interval [CI], 1.5-10.1; P =.001). Independent risk factors identified in multiple logistic regression included chorioamnionitis (OR, 4.1; 95% CI, 1.6-10.1), intrauterine growth restriction (OR, 4.0; 95% CI, 1.3-12.0), maternal black ethnicity (OR, 3.6; 95% CI, 1.4-9.3), maternal age older than 25 years (OR, 2.6; 95% CI, 1.3-5.2), and nulliparity (OR, 1.8; 95% CI, 1.0-3.0). The population-attributable fraction of chorioamnionitis for CP is 11%. Our data suggest that chorioamnionitis is an independent risk factor for CP among term and near-term infants.

Induction of hepatic granulopoiesis due to chorioamnionitis during the second trimester of development

Objective: To detect post mortem changes in fetal hematopoiesis consistent with infection from liver examination alone. Study design: We investigated the immunohistochemical expression of Glycophorin C, Neutrophilic elastase, and CD34, in the hepatic parenchyma from fetuses miscarried as a result of chorioamnionitis (caused by Chlamydia trachomatis) and correlated them with the equivalent from fetuses after voluntary abortion (gestational age: 16th, 20th, and 24th weeks). Results: A statistically significant difference was found in the Neutrophilic elastase positive cells to the advantage of cases with chorioamnionitis over voluntary abortions (24th week: P=0.0001, t-test) and also at the level of total hematopoiesis (20th and 24th week: P=0.041 and 0.004, respectively, t-test). There was no quantitative difference between the two settings at the level of erythropoiesis in the three examined periods. Conclusions: Fetal infection can be diagnosed from the liver alone. After detection of changes in fetal hematopoiesis indicative of infection, examination of additional specimens of placenta and membranes will document the diagnosis of chorioamnionitis.

The Association of Placental Abnormalities with Maternal and Neonatal Clinical Findings: A Retrospective Cohort Study

Objectives: (1) To determine the nature and extent of placental pathologic findings; (2) to associate placental pathologic findings with clinical indicators of infection; (3) to evaluate placental pathology in the context of the guidelines outlined by the College of American Pathologists (CAP).Methods: A retrospective cohort study, through review of maternal and neonatal charts and placental pathology, of 100 sequential pregnancies in which placentas were submitted to pathology. Data were examined using descriptive statistics, and proportional differences were compared using the chi-square test and Fisher’s exact test.Results: Overall, 75% of placentas submitted for pathology review had pathologic abnormalities. Fifty percent had findings consistent with inflammation, 38% had findings consistent with vascular abnormalities, and 18% had findings consistent with meconium. Fetal clinical indicators of infection were associated with placental findings of chorioamnionitis (p ≤ 0. 01), while maternal clinical indicators were not. Similarly, fetal clinical indicators were associated with placental findings of fetal inflammation (p ≤ 0. 025), whereas maternal indicators were not associated with placental findings of maternal inflammation. A diagnosis of chorioamnionitis in labour by the attending physician was associated with pathologic findings (p ≤ 0. 05). A CAP indication was found in 75% of the placentas. There was no difference in incidence of placental pathology between those placentas submitted with and without a CAP indication.Conclusion: Placental findings of inflammation or infection were associated with fetal clinical indicators of infection, but not with maternal indicators. Placental pathology is very useful in identifying undiagnosed maternal infection or inflammation.

Unexpected versus anticipated cystic periventricular leukomalacia.

The objective of this study is to contrast the clinical profile of premature infants who develop cystic periventricular leukomalacia (cPVL) following a severe hemodynamic event (anticipated) with infants whose cPVL is not preceded by such an event (unexpected). The study design is a Retrospective Cohort. The study setting is a Neonatal Intensive Care Unit. Infants born at a gestational age of 23-32 weeks received serial cranial ultrasounds to screen for cPVL. Infants were divided into two groups based upon whether or not they had experienced a hemodynamic event of sufficient severity to potentially cause cPVL. Details of the clinical profile of these two groups were compared. Cystic PVL occurred in 27 infants (2.1%). In 15 infants (56%) cPVL was antipicated as there was at least one severe preceding hemodynamic event. Twelve infants (44%) had not experienced such an event and the discovery of cPVL on routine cranial ultrasound was unexpected. These infants were more likely to have been born to mothers who had received tocolytics (67 versus 13%, p = 0.004), prenatal steroids (67 vs. 27%, p = 0.038), and intrapartum antibiotics (92 vs. 20%, p < 0.001) and were more likely to have been delivered more than 6 hours after arrival to the hospital (83 vs. 40%; p = 0.038) than infants whose cPVL was anticipated. The diagnosis of clinical chorioamnionitis was also more common in the group of infants whose cPVL was unexpected (50 vs. 13%, p = 0.038). Almost half (44%) of our cases of cPVL occurred unexpectedly in infants who did not appear to have an obvious cause, as they had not experienced a severe hemodynamic event. These infants were more commonly delivered to mothers who had been hospitalized long enough to have received a variety of prenatal therapies and more often had a diagnosis of chorioamnionitis.

Chorioamnionitis, not epidural analgesia, is associated with maternal fever during labour.

Maternal fever is associated with chorioamnionitis and has been linked to labour epidural analgesia (LEA). The purpose of this study was to determine possible associations between LEA and chorioamnionitis, maternal fever, operative delivery rate, and neonatal outcome. Data from 14,073 patients were entered into a database over a two-year period. From this database, 62 nulliparous parturients with clinical chorioamnionitis (amnionitis), but without LEA were identified (Group I). Two other groups who received LEA were matched for parity and gestation: Group II - LEA with concomitant amnionitis (n=50) and, Group III - LEA without concomitant amnionitis (n=201). The diagnosis of chorioamnionitis was confirmed by histologic examination. Results are expressed as mean +/- SD and analyzed at P <0.05 using ANOVA or Chi-square. No differences were noted among the groups in the operative delivery rate or Apgar scores at five minutes. The percentage of patients with maternal fever during labour (38.0 degrees C) with amnionitis was significantly less in Group III compared to the other groups (100% in both Groups I and II vs 1.0% in Group III; P=0.000). Likewise, Group III had a lower percentage of neonates with Apgar scores <7 at one minute (35.5% in Group I, 20.0% in Group II, 17.4% in Group III; P=0.010). The percentage of histologic chorioamnionitis was significantly higher in both amnionitis groups compared to Group III (67.7% in Group I, 56.0% in Group II, 4.0% in Group III; P=0.000). LEA without chorioamnionitis is not associated with maternal fever (38.0 degrees C), increased operative delivery rates or low Apgar scores.

Antenatal Corticosteroids and Placental Histology in Preterm Birth

To assess the effects of antenatal corticosteroid use on placental histopathology, we have reviewed a database of 463 consecutive non-anomalous singleton liveborns delivered at less than 32 weeks between April 1988 and December 1994, of which 280 received one or more doses of corticosteroids for promotion of fetal lung maturation. Patients were grouped by the number of corticosteroid doses received (analyzed as none, 1, 2 and 3 or more doses). Clinical and demographic factors were recorded prospectively. Placental histopathology was reviewed blinded to clinical factors except gestational age, and 42 distinct placental lesions were examined and scored for severity. Data were analyzed by contingency tables, one-way analysis of variance, and linear regression analysis. Among clinical variables, univariate analysis showed that the number of corticosteroid doses was significantly related to presence of labour prior to delivery, pre-eclampsia, premature rupture of membranes and clinical suspicion or diagnosis of chorioamnionitis. Using linear regression analysis with these clinical variables as confounders, increased number of doses of antenatal corticosteroids was related to increased severity of villous fibrosis and stromal mineralization, and fewer villous infarcts.

Elevations of group II phospholipase A2 concentrations in serum and amniotic fluid in association with preterm labor

Objective: The purpose of this study was to determine whether the elevation of secretory group II phospholipase A2 concentration in the serum and amniotic fluid in preterm labor is associated with intrauterine inflammation. Study Design: Serum and amniotic fluid were collected from women with preterm delivery (<37 weeks’ gestation; n = 38) and term delivery (n = 20). Phospholipase activity was measured with a highly sensitive system that was based on reverse-phase high-performance liquid chromatographic separation of 9-anthracenylmethyl derivatives of fatty acids released by phospholipase A2. The concentrations of immunoreactive isozymes (group I or II) of secretory phospholipase A2 were assayed with a radioimmunoassay kit with a monoclonal antibody against human pancreatic phospholipase A2 and splenic IIA phospholipase A2. Localization of immunoreactive group II phospholipase A2 in the amniotic membrane was determined by immunostaining visualized with the Vectastain ABC (Vector Laboratories, Inc, Burlingame, Calif) method. Results: Enzymatic activities of phospholipase A2 in the serum and amniotic fluid specimens obtained from patients in preterm labor with chorioamnionitis were significantly higher than those in specimens from patients in term labor. Significant elevations of phospholipase A2 activities were observed in patients with preterm labor without histologically evident chorioamnionitis. The activity of phospholipase A2 was clearly correlated with the concentration of the immunoreactive group II phospholipase A2. Group II phospholipase A2 was localized in amniotic cells obtained from patients with a pathologically determined diagnosis of chorioamnionitis. The predictive value for chorioamnionitis of the group II phospholipase A2 concentration was relatively higher than the predictive values of the concentrations of C-reactive protein and interleukins 6 and 8. Conclusion: Significant elevations of group II phospholipase A2 concentrations were detected in the serum and amniotic fluid of women with preterm labor. Group II phospholipase A2 concentration may be a useful indicator for preterm labor, and phospholipid metabolism is certainly activated both in preterm labor and in apparent inflammatory diseases. (Am J Obstet Gynecol 2000;183:1537-43.)

The value of interleukine 6 in the diagnosis of chorioamnionitis

The value of interleukine 6 in the diagnosis of chorioamnionitis

Chorioamnionitis: Is continuation of antibiotic therapy necessary after cesarean section?

Objective: Our purpose was to determine whether the continuation of antibiotics postoperatively after cesarean section in patients whose labors were complicated by chorioamnionitis would reduce the incidence of endometritis. Study Design: Patients with a clinical diagnosis of chorioamnionitis treated with ampicillin during labor and who required cesarean delivery for obstetric indications received preoperative intravenous clindamycin and gentamicin and were randomized into 2 groups. Group 1 received no scheduled postoperative antibiotics and group 2 continued to receive clindamycin 900 mg every 8 hours and gentamicin 1.5 mg/kg every 8 hours until afebrile for a minimum of 24 hours (temperature ≤100°F). Results: Sixty-one patients were randomized to group 1 and 55 patients were randomized to group 2. The duration of labor, the duration of membrane rupture, and the number of intrapartum vaginal examinations were statistically insignificant between the 2 groups. The mean duration of maternal postoperative hospital stay was 4 days for both groups. There were no statistically significant differences in the rate of endometritis for group 1, 9 of 61 (14.8%), versus group 2, 12 of 55 (21.8%), P = .32. Conclusions: In patients whose labors were complicated by chorioamnionitis and who underwent cesarean section, the continuation of preoperative clindamycin and gentamicin in the postoperative period did not reduce the risk of endometritis compared with a single preoperative dose. (Am J Obstet Gynecol 1998;179:1261-6.)

Chorioamnionitis: the association between clinical and histological diagnosis

Objective: To determine the association between clinical and histological diagnoses of chorioamnionitis. Methods: A retrospective 9-year review of hospital records for all perinatal deaths ( N = 804) occurring at a Western New York regional perinatal center between 1988 and 1996 was conducted. Information concerning clinical indicators of chorioamnionitis were recorded including: maternal fever, leukocytosis, uterine tenderness, foul smelling discharge, and fetal tachycardia. Histological examination of the placenta was conducted in 797 of 804 perinatal deaths and staged by a standardized method. Type and number of clinical signs and symptoms were correlated with severity of histologic grade to determine their relation. Results: Chorioamnionitis was diagnosed either clinically or histologically in 243 (30.5%) of 797 perinatal deaths. Of these, 72 cases (23.5%) occurred in the 307 fetal deaths and 171 (34.9%) occurred in the 490 neonatal deaths. Five cases were diagnosed only on autopsy. In 51 of 243 cases (21%) there was histologic confirmation of chorioamnionitis without any clinical indicators present. In 13 of 243 cases (5.4%) there were 1 or more clinical indicators of chorioamnionitis without histologic confirmation. Sensitivity and specificity for 1 or more clinical indicators was 77.8% and 97.7%, respectively. Conclusion: Chorioamnionitis was present in 30.5% of perinatal deaths in this cohort. Identification of one or more clinical signs or symptoms was found to be both a sensitive and specific screening method for a presumptive diagnosis of chorioamnionitis when using histologic confirmation as the gold standard.

Maternal Infection and Cerebral Palsy in Infants of Normal Birth Weight

Context. —Exposure to maternal or placental infection is related to risk of preterm birth and, in premature infants, of brain lesions predictive of cerebral palsy (CP). Few studies have investigated whether maternal infection is associated with risk of CP in children of normal birth weight. Objective. —To investigate maternal infection during the admission for delivery as a possible risk factor for CP in infants born weighing 2500 g or more. Design. —Population-based case-control study. Setting. —All hospitals in 4 northern California counties, 1983 through 1985. Participants. —A total of 46 children with disabling spastic CP who had no recognized prenatal brain lesions and 378 randomly selected control children weighing 2500 g or more at birth and surviving to age 3 years. Main Outcome Measures. —Disabling spastic CP and signs of neonatal morbidity. Results. —Maternal fever exceeding 38°C in labor was associated with increased risk of unexplained CP (odds ratio [OR], 9.3; 95% confidence interval [CI], 2.7-31.0), as was a clinical diagnosis of chorioamnionitis. One or more indicators of maternal infection were present in 2.9% of control children, 22% of children with CP (OR, 9.3; 95% CI, 3.7-23.0), and 37% of those with the spastic quadriplegic subtype of CP (OR, 19.0; 95% CI, 6.5-56.0). Newborns exposed to maternal infection, both cases and controls, had 5-minute Apgar scores below 6 more often than those unexposed. Among children with CP, those born to infected women were more often hypotensive, needed intubation, had neonatal seizures, and received a clinical diagnosis of hypoxic-ischemic encephalopathy. Conclusion. —Intrauterine exposure to maternal infection was associated with a marked increase in risk of CP in infants of normal birth weight. Maternal infection was also linked with low Apgar scores, other evidence of hypertension and need for resuscitation, and neonatal seizures—signs commonly attributed to birth asphyxia.

Letters to the Editor: Diagnosis of Chorioamnionitis

Letters to the Editor: Diagnosis of Chorioamnionitis

Letters to the Editor: Diagnosis of Chorioamnionitis

Letters to the Editor: Diagnosis of Chorioamnionitis

Maternal Infection and Cerebral Palsy in Infants of Normal Birth Weight

Exposure to maternal or placental infection is related to risk of preterm birth and, in premature infants, of brain lesions predictive of cerebral palsy (CP). Few studies have investigated whether maternal infection is associated with risk of CP in children of normal birth weight. To investigate maternal infection during the admission for delivery as a possible risk factor for CP in infants born weighing 2500 g or more. Population-based case-control study. All hospitals in 4 northern California counties, 1983 through 1985. A total of 46 children with disabling spastic CP who had no recognized prenatal brain lesions and 378 randomly selected control children weighing 2500 g or more at birth and surviving to age 3 years. Disabling spastic CP and signs of neonatal morbidity. Maternal fever exceeding 38 degrees C in labor was associated with increased risk of unexplained CP (odds ratio [OR], 9.3; 95% confidence interval [CI], 2.7-31.0), as was a clinical diagnosis of chorioamnionitis. One or more indicators of maternal infection were present in 2.9% of control children, 22% of children with CP (OR, 9.3; 95% CI, 3.7-23.0), and 37% of those with the spastic quadriplegic subtype of CP (OR, 19.0; 95% CI, 6.5-56.0). Newborns exposed to maternal infection, both cases and controls, had 5-minute Apgar scores below 6 more often than those unexposed. Among children with CP, those born to infected women were more often hypotensive, needed intubation, had neonatal seizures, and received a clinical diagnosis of hypoxic-ischemic encephalopathy. Intrauterine exposure to maternal infection was associated with a marked increase in risk of CP in infants of normal birth weight. Maternal infection was also linked with low Apgar scores, other evidence of hypotension [corrected] and need for resuscitation, and neonatal seizures-signs commonly attributed to birth asphyxia.

Fetal breathing movements within 24 hours of delivery in prematurity are related to histologic and clinical evidence of amnionitis.

Our objective was to determine the association of fetal breathing movements (FBM) within 24 hr of delivery, with the clinical diagnosis of chorioamnionitis and histologic evidence of severe acute amnionitis and umbilical-chorionic vasculitis in women delivering at < 32 weeks' gestation. We performed a cohort study of patients with singleton gestations delivered at < 32 weeks' following preterm labor with intact membranes and sonographically assessed biophysical profile within 24 hr of delivery (n = 111). Patients with FBM were compared with those without FBM, with regard to prevalence of clinical chorioamnionitis (CA) and histologic diagnosis of acute amnionitis and umbilical vasculitis. Maternal and neonatal charts were reviewed and the diagnosis of clinical CA made by previously established criteria. Histologic presence and extent of acute intrauterine inflammation was assessed and scored by a single pathologist blinded to clinical information. Results are presented as chi 2 values and odds ratios with 95% confidence intervals. Of the patients included in the study, FBM were absent in 56 and present in 55. The prevalence of CA was 13% (15 of 111), severe acute amnionitis 34% (38 of 111), and severe umbilical vasculitis 23% (26 of 111). Severe umbilical vasculitis was significantly less frequent in cases with FBM as compared to cases without FBM (15% [8 of 55] vs. 32% [18 of 56], p = 0.049). However, the difference in rate of CA (22% [12 of 55] vs. 34% [19 of 56], p = 0.22) and histologic severe amnionitis (29% [16 of 55] vs. 39% [22 of 56], p = 0.4) between cases with and without FBM was not significant. In the presence of preterm labor with intact membranes, absence of FBM had sensitivities of 73 and 72%, and specificities of 54 and 56% in the prediction of CA and histologic evidence of umbilical vasculitis, respectively. We conclude that absence of FBM is associated with histologic evidence of fetal inflammation in intrauterine infection in patients with preterm labor and intact membranes delivering at < 32 weeks. However, the low positive predictive value of absent FBM in predicting fetal inflammation in intrauterine infection should discourage the guidance of clinical management in patients < 32 weeks' gestation with preterm labor and intact membranes.

Letters to the Editor: Diagnosis of Chorioamnionitis

Letters to the Editor: Diagnosis of Chorioamnionitis

Incidence of Chorioamnionitis in Patients With Meconium‐stained Amniotic Fluid

Objective: The goal of this study was to determine if meconium staining of the amniotic fluid (MSAF) is a marker for chorioamnionitis. Methods: In a retrospective, case-control investigation, we studied 100 patients with MSAF. Each patient was matched with a control who delivered during the same period but did not have MSAF. Subjects and controls were matched for age, parity, gestational age, mode of delivery, duration of rupture of membranes (ROM), length of internal monitoring, and number of examinations before and after ROM. The incidence of chorioamnionitis in controls and study patients was compared. The diagnosis of chorioamnionitis was based on clinical examination. Results: Thirteen of the 200 patients [6.5%, 95% confidence interval (CI), 2.5–10.5%] developed chorioamnionitis. Of the 100 women with MSAF, 10 (10%, 95% CI, 4–16) were infected compared with only 3 controls (3%, 95% CI, 0–6, P = 0.04). The odds ratio (OR) for this comparison was 3.3, and the 95% CI was 1.02–10.63. Conclusions: MSAF is associated with an increased frequency of chorioamnionitis. Several factors could explain this association. Infection may cause fetal stress, leading to the release of meconium. MSAF may enhance the growth of bacteria by providing a rich medium of essential nutrients or growth stimulants. MSAF also may impair the host immune system so that chemotaxis or phagocytosis is diminished, thus allowing accelerated growth of microorganisms.

Management of premature rupture of membranes at term: Randomized trial

Objective: We hypothesize that expectant management in the presence of premature rupture of membranes at term would result in a lower cesarean birth rate with no increase in maternal, fetal, or neonatal infection.Study Design: Term patients who consented to the study were randomly allocated either to expectant management for 48 hours or to induction of labor 8 hours after premature rupture of membranes. Premature rupture of membranes was confirmed by sterile speculum examination of the vagina. Patients randomized to expectant management were transferred to antenatal care and were not examined vaginally until they went into labor. Patients randomized to induction of labor had induction with oxytocin 8 hours after premature rupture of membranes.Results: Two hundred sixty-two patients were randomized to the expectant management and induction of labor groups. The cesarean birth rate and the clinical diagnosis of postpartum endometritis was not significantly different in the two groups. Pathologic diagnosis of chorioamnionitis and funisitis, however, was significantly greater in the expectant management group (p < 0.05). Eight of the 15 babies with funisitis were admitted to the neonatal intensive care unit for therapy (two in the induction of labor group and six in the expectant management group, p < 0.05).Conclusion: Expectant management did not reduce the incidence of cesarean birth and increased the pathologic diagnosis of funisitis and newborn requirements for neonatal intensive care.

Chorioamnionitis: Association of Nonreassuring Fetal Heart‐rate Patterns and Interval From Diagnosis toDelivery on Neonatal Outcome

Objective: The purpose of this study was to determine whether selected fetal heart-rate (FHR) patterns and the interval from diagnosis to delivery in pregnancies complicated by chorioamnionitis could predict neonatal outcome. Methods: During a 6-month period, 217 consecutive patients with acute chorioamnionitis were prospectively identified in labor. Following delivery, the fetal monitor strips and hospital courses were reviewed for both the mother and neonate. Multiple logistic regression was used to analyze the presence of a nonreassuring FHR pattern and the effect on neonatal outcome. Fisher exact tests were used to analyze the time intervals from the diagnosis of chorioamnionitis to delivery and their significance on neonatal outcome parameters. Results: The overall incidence of chorioamnionitis in our population was 2.3%. None of the independent variables analyzed following the diagnosis of chorioamnionitis until delivery were significantly associated with an umbilical artery (Ua) pH < 7.20. There were no differences in cord pH, Apgar scores, sepsis, admission to special-care nursery, and oxygen requirements in neonates based on the duration of time from the diagnosis of chorioamnionitis to delivery in our study. None of the newborns had pathologic fetal acidemia (Ua pH < 7.00). None of the FHR patterns we identified after the diagnosis of acute chorioamnionitis were significantly associated with neonates with a Ua pH < 7.20. Conclusions: An interval from diagnosis to delivery of up to 12 h plays little if any role in neonatal outcome.

Investigation of the fetal pulmonary inflammatory reaction in chorioamnionitis, using an in situ Y chromosome marker.

Chorioamnionitis is a frequent finding in the placenta in second-trimester premature labor. Seventy-six archival perinatal and fetal autopsies between 15 and 28 weeks of gestation with a morphologic diagnosis of chorioamnionitis were reviewed. Of the 76 cases, 52 (68%) had inflammatory cells in the lungs, which is higher than the reported incidence of clinical infection in neonates with chorioamnionitis. In 23 cases there were peribronchial lymphocytic hyperplasia and neutrophils in the airspaces, in 8 there was a lesser degree of interstitial inflammation as well as luminal neutrophils, and in 21 (40%) there were neutrophils in the airspaces only. To determine whether the neutrophils in the airspaces in the latter were maternal or fetal in origin, the lung sections of seven male fetuses in the group were examined by in situ hybridization for the Y repeat probe pHY 2.1, together with appropriate controls. Two of the tests were technical failures. The remaining five, and the positive controls, showed positivity for pHY 2.1 in 70-86% of luminal neutrophils. We conclude that luminal neutrophils in fetal lungs in this situation are fetal in origin.