الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
perinatal hypoxic ischemic cerebral injury remains an important issue because it is the most clearly recognized cause of cerebral palsy. Most cases of hypoxic ischemic encephalopathy result from injury in the perinatal period secondary to intrauterine asphyxia, with disturbance of gas exchange across the placenta.
Objectives: The aim of the study was to evaluate clinical value of lactate measurements as predictor of short and long term outcome in hypoxic-ischemic neonates.
Patients and methods: The study was carried out in the neonatal intensive care unit, Obestetric hospital,Zagazig university during 2009-2010. The study included 40 cases divided into two groups; group I (20 full term hypoxic-ischemic neonates) and group II (20 preterm hypoxic-ischemic neonates), fulfilled the criteria of AAP, compared with 20 apparently healthy full term neonates, and 20 apparently healthy preterm neonates as a control groups with no obstetrical problems. Follow up of surviving asphyxiated neonates by neurodevelopmental assessment was done for period of six months.
Results: The result of the present study revealed: Statistically significant low Apgar score at 1 and 5 minute in hypoxic neonates compared to healthy neonates. Some risk factors associated with HIE were assessed among our patients and we found that diabetes mellitus and anemia were the most common matemal risk factors while preeclampsia and placenta previa were the most common obstetric factors in cases with HIE. Statistically significant correlation between grades of hypoxia and outcome, as with grade I all patients developed normal, while with grade III the patients either died or developed long term sequelae. Statistically significant higher mean plasma lactate level was found in hypoxic neonates compared to healthy neonates. Also non survivors had statistically significant higher mean plasma lactate level compared to survivors. Statistically significant higher mean plasma lactate level was found in survived hypoxic neonates who developed long term sequelae compared to survived hypoxic neonates who developed normal. Statistically significant higher mean plasma lactate level was found in hypoxic neonates with intractable convulsions, compared to those hypoxic neonates with infrequent attacks of convulsions. Statistically significant higher mean plasma lactate level was found in hypoxic neonates with IVH, compared to those hypoxic neonates without IVH. Statistically significant correlation between grades of hypoxia and mean plasmal lactate level. In full term hypoxic neonates, plasma lactate, NRBCs and total CK enzyme were reliable to predict hypoxia but plasmal lactate alone was able to assess the grade of hypoxia. In preterm hypoxic neonates plasma lactate, NRBCs and total CK enzyme were reliable to predict hypoxia while both plasma lactate and NRBCs were able to assess the grade of hypoxia.
Conclusion: from the results, it is found that, hypoxia leads to an increase in plasma lactate level, NRBCs count and total CK enzyme activity. Plasma lactate level, NRBCs count and total CK enzyme activity could be used as early predictors in diagnosis of hypoxic ischemic encephalopathy. Combined detection of plasma lactate level, NRBCs count and total CK activity in differentiation between grades of hypoxia gives us better sensitivity and specificity than each alone. Plasma lactate level could be used in predicting short and long term outcome in both full term and preterm hypoxic ischemic neonates.