RESUMEN
BACKGROUND: Hypoxic Ischemic Encephalopathy (HIE) can lead to devastating consequences for the affected infant. Although therapeutic cooling benefits infants with moderate and severe HIE, differentiating mild from moderate-severe HIE may be challenging. The placenta reflects the fetal intrauterine environment and may reveal underlying processes that affect brain injury. AIM: To describe placental histopathology using the Amsterdam Placental Workshop Group Criteria in different grades of HIE. STUDY DESIGN: Retrospective cohort. SUBJECTS: Infants admitted to a tertiary care neonatal intensive care unit with a diagnosis of HIE between 2011 and 2016. OUTCOME MEASURE: Maternal and neonatal clinical variables and placental histopathology using the Amsterdam Placental Workshop Group Criteria were compared between mild and moderate-severe HIE. Mann-Whitney or t-test or ê2 were performed for bivariate associations as appropriate. To explain the relationship between placental pathology and severity of HIE odds ratios (ORs) and 95 % confidence intervals (CIs) were calculated using logistic regression models. RESULTS: Of the 73 infants in the study, 23 had mild and 50 moderate-sever HIE. There was no difference in maternal and neonatal characteristics except for sentinel events which were higher in the moderate- severe group. On placental histopathology, acute inflammation, including fetal inflammatory reaction (FIR) were significantly higher in the moderate-severe group. After adjusting for confounders, FIR remained significantly associated with moderate-severe HIE, ORs 6.29, 95 % CI 1.5-25. CONCLUSION: Our study demonstrates FIR in the placenta is associated with severity of HIE.
Asunto(s)
Lesiones Encefálicas , Hipotermia Inducida , Hipoxia-Isquemia Encefálica , Femenino , Humanos , Lactante , Recién Nacido , Embarazo , Lesiones Encefálicas/complicaciones , Hipoxia-Isquemia Encefálica/terapia , Placenta , Estudios RetrospectivosRESUMEN
BACKGROUND: The Neonatal Resuscitation Program (NRP) states that if adequate positive pressure ventilation (PPV) was given for a low heart rate (HR), the infant's HR should increase within the first 15 s of PPV. OBJECTIVE: To assess changes in HR in piglets with asphyxia-induced bradycardia. METHODS: Term newborn piglets (n=30) were anaesthetised, intubated, instrumented and exposed to 50 min normocapnic hypoxia followed by asphyxia. Asphyxia was achieved by clamping the tube until severe bradycardia (defined as HR at <25% of baseline). This was followed by 30 s adequate PPV and chest compression thereafter. Changes in HR during the 30 s of PPV were assessed and divided into four epochs (0-10 s, 5-15 s, 10-20 s and 20-30 s, respectively). RESULTS: Increase in HR >100/min was observed in 6/30 (20%) after 30 s of PPV. Within the epochs 0-10 s, 5-15 s or 10-20 s no piglet had an increase in HR >100/min. Additional 10/30 (33%) had a >10% increase in HR. CONCLUSION: In contrast to NRP recommendation, adequate PPV does not increase HR within 15 s after ventilation in piglets with asphyxia-induced bradycardia.