Severity Of Neonatal Encephalopathy Research Articles

Early postnatal color Doppler changes in neonates receiving delivery room resuscitation with low 5 min Apgar score-a pilot study.

To evaluate the Doppler changes in the intracranial arteries of neonates exposed to perinatal hypoxic insult and compare it with normal neonates. Color Doppler of bilateral anterior and middle cerebral arteries was performed within 6 h of birth in 26 healthy neonates and 50 neonates who received delivery room resuscitation (DRR) for perinatal depression and had a 5 min Apgar score <7. Comparisons of resistive index (RI) and peak systolic velocity (PSV) were made between the (a) control group (b) patients with low 5 min Apgar score <7 who without clinical features of neonatal encephalopathy at 24 h (c) neonates with perinatal depression with a clinical evidence of disturbed neurological function at 24 h of birth and examination consistent with mild, moderate, or severe encephalopathy using modified Sarnat and Sarnat's classification. Significantly higher RI was observed in the neonates with to perinatal depression compared to the normal neonates. Significantly higher RI was seen in the patients with clinical features of neonatal encephalopathy (Group C) compared to group B. RI <0.6 and >0.82 was associated with severe neonatal encephalopathy. Differences in PSV were not statistically significant in the various groups. The study presents the changes in early cerebral Doppler parameters observed in neonates with low 5 min Apgar score following DRR compared to the normal neonates. We also present the relations of Doppler parameters with increasing severity of neonatal encephalopathy according to Sarnat classification.

Update on the current management of newborns with neonatal encephalopathy

Hypoxic-ischemic encephalopathy is a subtype of neonatal encephalopathy and a major contributor to global neonatal morbidity and mortality. Despite advances in obstetric and neonatal care there are still challenges in accurate determination of etiology of neonatal encephalopathy. Thus, identification of intrapartum risk factors and comprehensive evaluation of the neonate is important to determine the etiology and severity of neonatal encephalopathy. In developed countries, therapeutic hypothermia as a standard of care therapy for neonates with hypoxic-ischemic encephalopathy has proven to decrease incidence of death and neurodevelopmental disabilities, including cerebral palsy in surviving children. Advances in neuroimaging, brain monitoring modalities, and biomarkers of brain injury have improved the ability to diagnose, monitor, and treat newborns with encephalopathy. However, challenges remain in early identification of neonates at risk for hypoxic-ischemic brain injury, and determination of the timing and extent of brain injury. Using imaging studies such as Neonatal MRI and MR spectroscopy have proven to be most useful in predicting outcomes in infants with encephalopathy within the first week of life, although comprehensive neurodevelopmental assessments still remains the gold standard for determining long term outcomes. Future studies are needed to identify other newborns with encephalopathy that might benefit from therapeutic hypothermia and to determine the efficacy of other adjunctive neuroprotective strategies. This review focuses on newer evidence and advances in diagnoses and management of infants with neonatal encephalopathy, including novel therapies, as well as prognostication of outcomes to childhood.

Placental pathology is associated with severity of neonatal encephalopathy and adverse developmental outcomes following hypothermia

Although neonatal encephalopathy (NE) due to perinatal asphyxia accounts for a notable proportion of brain injury, the causal pathway remains largely unexplained. We sought to determine the association of placental pathology with: (1) severity of NE in the first 6 hours postnatal, and (2) abnormal neurodevelopmental outcomes (NDO) in neonates requiring hypothermia therapy. This is a retrospective cohort study of neonates ≥36 weeks' gestation born at Parkland Hospital, Dallas, TX, from January 2006 through November 2011 with NE. Placental histology was reviewed and validated by a pediatric pathologist blinded to outcomes. Abnormal NDO was defined as death or Bayley-III score of <85 at 18-24 months of age. Of 86,274 neonates ≥36 weeks' gestation, 120 had evidence of a combination of perinatal acidosis and NE. In all, 47 had mild NE and received no treatment, while 73 had moderate (n = 70) or severe (n = 3) NE and received systemic hypothermia. Nine neonates died and all survivors receiving hypothermia had a Bayley-III assessment at 22 ± 7 (SD) months of age. Chorioamnionitis with or without fetal response and patchy/diffuse chronic villitis were found to be independently associated with severity of NE (P < .001). Univariate logistic regression revealed an association with a diagnosis of major placental pathology (odds ratio, 3.5; 95% confidence interval, 1.1-11.4) and abnormal outcomes following cooling. Specifically, diffuse chronic villitis (odds ratio, 9.29; 95% confidence interval, 1.11-77.73) was the only individual predictor of abnormal NDO following hypothermia therapy. Placental inflammatory villitis appears to be a harbinger of abnormal outcomes in neonates with NE, spanning to the 18-24 month NDO.

PO-0431 Serum Vascular Endothelial Growth Factor (vegf) And Neonatal Encephalopathy

Background Pro-inflammatory cytokines in both cerebrospinal fluid (CSF) and serum have been associated with abnormal neurological findings following hypoxic-ischaemic injury. Vascular endothelial growth factor (VEGF) seems to have a neuroprotective effect in adult stroke and low levels correlate with poor outcomes. We aimed to establish a correlation between serum VEGF levels and the severity of Neonatal Encephalopathy (NE). Methods Multi-organ evaluation was carried out on infants with NE (n = 122) with a particular emphasis on neurological status and function including neuroimaging (MRI and Cranial Ultrasound) and placental pathology. Serial serum VEGF levels were measured by multiplex ELISA over the first week of life. Results Infants with NE (n = 73) had serum VEGF levels on days 1, 2 and 3 of life that decreased as the severity of NE increased (Grade 0: n = 9, Grade 1: n = 20, Grade 2: n = 37, Grade 3: n = 7). Infants with NE (n = 122) had an association between elevated serum VEGF levels on day 1 and histological chorioamnionitis (n = 24) (p = 0.025). The mean serum VEGF in those without chorioamnionitis was 570 ± 870pg/mL compared to 1144 ± 1129pg/mL in those with chorioamnionitis. Serial VEGF levels were significantly associated with cord anomalies (p Conclusions VEGF correlated with Histological Chorioamnionitis in NE and the severity of encephalopathy.

Determinants of Outcomes After Head Cooling for Neonatal Encephalopathy

The goal of this study was to evaluate the role of factors that may determine the efficacy of treatment with delayed head cooling and mild systemic hypothermia for neonatal encephalopathy. A total of 218 term infants with moderate to severe neonatal encephalopathy plus abnormal amplitude-integrated electroencephalographic recordings, assigned randomly to head cooling for 72 hours, starting within 6 hours after birth (with the rectal temperature maintained at 34.5 +/- 0.5 degrees C), or conventional care, were studied. Death or severe disability at 18 months of age was assessed in a multicenter, randomized, controlled study (the CoolCap trial). Treatment, lower encephalopathy grade, lower birth weight, greater amplitude-integrated electroencephalographic amplitude, absence of seizures, and higher Apgar score, but not gender or gestational age, were associated significantly with better outcomes. In a multivariate analysis, each of the individually predictive factors except for Apgar score remained predictive. There was a significant interaction between treatment and birth weight, categorized as > or =25th or <25th percentile for term, such that larger infants showed a lower frequency of favorable outcomes in the control group but greater improvement with cooling. For larger infants, the number needed to treat was 3.8. Pyrexia (> or =38 degrees C) in control infants was associated with adverse outcomes. Although there was a small correlation with birth weight, the adverse effect of greater birth weight in control infants remained significant after adjustment for pyrexia and severity of encephalopathy. Outcomes after hypothermic treatment were strongly influenced by the severity of neonatal encephalopathy. The protective effect of hypothermia was greater in larger infants.