Search

in infants with asphyxia Cristina Plevani, Ilaria Pozzi, Anna Locatelli, Silvia Malguzzi, Gaia Kullmann, Maddalena Incerti, Giuseppe Paterlini MBBM Foundation, University of Milano-Bicocca, Obstetrics and Gynecology, Monza, Italy, MBBM Foundation, San Gerardo Hospital, Neonatology, Monza, Italy OBJECTIVE: Hypoxic-ischemic encephalopathy (HIE) occurs in the first days of life in asphyxiated term neonates. Our objective is to identify markers predictive of moderate-severe HIE and long term adverse neurodevelopmental outcome (ANDO) among neonates with asphyxia. STUDY DESIGN: All term asphyxiated neonates (umbilical artery (UA) pH 7.0 or base excess (BE) -16 or Apgar 5 at 5 min or need of intubation or prolonged resuscitation at birth) inborn between January 2004 and June 2011 were prospectively admitted to a clinical and instrumental monitoring protocol and at least 12 months follow-up. Data on antenatal, intrapartum risk factors, placental histology and neonatal outcome were collected. HIE was defined as mild, moderate and severe according to modified SarnatSOR 145) and UA BE (p 0.04; OR 0.7) were independently related to moderate-severe HIE and ANDO. CONCLUSION: Among neonates with asphyxia, the risk of developing moderate-severe HIE or ANDO is predicted by perinatal factors, i.e. need for intubation and UA BE. Neither antenatal and intrapartum risk factors nor placental histology are helpful to identify these outcomes.

BORN WITH INTRAUTERINE INFECTION? ANNA LOCATELLI, MARIANNA ANDREANI, FRANCESCA ASSI, AGNESE PIZZARDI, SILVIA MALGUZZI, ALESSANDRO GHIDINI, University of Milano-Bicocca, Obstetrics and Gynecology, Monza, Italy, University of Milano-Bicocca, Neonatology, Monza, Italy OBJECTIVE: Intrauterine infection (II) is a risk factor for cerebral lesions (CL), and part of the damage seems to be attributed to the immune fetal response. We have evaluated which factor have an effect on neonatal ultrasonographic (US) evidence of CL in the presence of histological or clinical evidence of II. STUDY DESIGN: From a cohort of 567 consecutive singleton neonates born after preterm delivery at 24.0-31.6 weeks from 1/1993 to 12/2006 we selected 180 infants with histological and/or clinical evidence of II. Obstetric (gestational age, pregnancy complications, use of steroids and antibiotic, fetal distress, mode of delivery) and neonatal (sex, weight, Apgar score, pH, neonatal complications) were evaluated in reference to evidence of neonatal severe US CL, defined as IVH grade 3-4 and/or PVL. Excluded were stillbirths and congenital anomalies. Logistic regression analysis was used to control for confounders with P 0.05 considered significant. RESULTS: Table 1 Logistic regression analysis demonstrated that evidence of neonatal severe US CL is independently associated with antenatal administration of corticosteroids (OR 0.3, 95% CI 0.11, 0.88, P 0.03) and occurrence of abruptio placentae (OR 5.4, 95% CI 1.4, 20.7, P 0.02)

OBJECTIVE: The purpose of this study was to investigate the significance of preterm acidosis and its risk factors. STUDY DESIGN: From a cohort of 786 consecutive singleton neonates who were born after spontaneous or iatrogenic preterm delivery at 24.0-33.6 weeks of gestation from January 1993 to December 2005 with an evaluation of umbilical artery pH at delivery, we extracted demographic, obstetric, neonatal, and placental histologic variables and related them to umbilical artery evidence of fetal acidemia, which was defined as pH < 7.10. Excluded were stillbirths and neonates with major congenital anomalies. Fetal distress was defined as nonreassuring fetal hearth rate tracing or biophysical profile or appearance of thick meconium at delivery. Statistical analysis included 1-way analysis of variance and logistic regression with a probability value of