C M Salafia1, A Ghidini, D M Sherer, J C Pezzullo. 1. Department of Pathology and Obstetrics, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York, USA. Salafiacm@aol.com
Abstract
OBJECTIVE: To evaluate whether fetal heart rate (FHR) patterns obtained in nonstress testing within 24 hours of delivery in patients with preterm delivery were associated with histologic acute infection, and if so, whether the associations are with maternal as opposed to fetal acute inflammation (acute amnionitis versus acute umbilical vasculitis). METHODS: The data set included 351 consecutive patients delivering from 22 to 32 weeks' gestation (excluding cases of preeclampsia; nonhypertensive abruption; stillbirth; fetal structural and karyotypic anomalies; Rh isoimmunization and hydrops fetalis; and maternal diabetes and hypertension). Severe variable decelerations were defined as FHR < 70 beats per minute lasting > 60 seconds, and decreased fetal heart variability included both reduced beat-to-beat variability and long-term heart rate cyclicity. Amniotic fluid volume was graded sonographically as part of a fetal biophysical profile. Acute inflammation of amnion (indicative of maternal inflammation) and umbilical cord (fetal inflammation) were scored by a single pathologist blinded to clinical data. RESULTS: Severe FHR variable decelerations were directly related to acute amnionitis (P = .012) and acute umbilical vasculitis (P = .0013). In preterm labor, decreased FHR variability was related to acute amnionitis (P = .005). All observations were independent of amniotic fluid volume or use of tocolytic agents. CONCLUSIONS: Severe variable decelerations and decreased FHR variability at < 32 weeks' gestation are related to histologic evidence of acute inflammation.
OBJECTIVE: To evaluate whether fetal heart rate (FHR) patterns obtained in nonstress testing within 24 hours of delivery in patients with preterm delivery were associated with histologic acute infection, and if so, whether the associations are with maternal as opposed to fetal acute inflammation (acute amnionitis versus acute umbilical vasculitis). METHODS: The data set included 351 consecutive patients delivering from 22 to 32 weeks' gestation (excluding cases of preeclampsia; nonhypertensive abruption; stillbirth; fetal structural and karyotypic anomalies; Rh isoimmunization and hydrops fetalis; and maternal diabetes and hypertension). Severe variable decelerations were defined as FHR < 70 beats per minute lasting > 60 seconds, and decreased fetal heart variability included both reduced beat-to-beat variability and long-term heart rate cyclicity. Amniotic fluid volume was graded sonographically as part of a fetal biophysical profile. Acute inflammation of amnion (indicative of maternal inflammation) and umbilical cord (fetal inflammation) were scored by a single pathologist blinded to clinical data. RESULTS: Severe FHR variable decelerations were directly related to acute amnionitis (P = .012) and acute umbilical vasculitis (P = .0013). In preterm labor, decreased FHR variability was related to acute amnionitis (P = .005). All observations were independent of amniotic fluid volume or use of tocolytic agents. CONCLUSIONS: Severe variable decelerations and decreased FHR variability at < 32 weeks' gestation are related to histologic evidence of acute inflammation.
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