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العنوان
Umbilical Cord S100B Protein InNeonatal Hypoxic Ischemic Encephalopathy /
المؤلف
Elsisy, Amr Abd-Elhaleem Abd-Elhadi.
هيئة الاعداد
باحث / عمرو عبد الحليم عبد الهادى السيسى
مشرف / غادة محمد المشد
مشرف / داليا منير اللاهونى
مشرف / نجلاء فتحي برسيم
الموضوع
Pediatric - neurology. Newborn infants - Diseases.
تاريخ النشر
2017.
عدد الصفحات
187 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
طب الأطفال ، الفترة المحيطة بالولادة وصحة الطفل
تاريخ الإجازة
2/3/2017
مكان الإجازة
جامعة المنوفية - كلية الطب - طب الاطفال
الفهرس
Only 14 pages are availabe for public view

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Abstract

Perinatal cerebral hypoxia-ischemia remains a frequent cause of the chronic handicapping conditions of cerebral palsy, mental retardation, learning disability, and epilepsy. HIE is the abnormal neurological state occurring in a newborn infant following a significant hypoxic-ischemic insult. The insult may occur antenatally, intrapartum or less commonly postnatally.
The neonatal brain can have a lack of oxygen through two major pathogenetic mechanisms, hypoxemia, which is a diminished amount of oxygen in the blood supply, and ischemia, which is a diminished amount of blood perfusing the brain During the perinatal period hypoxemia or ischemia or both occur as a result of asphyxia, an impairment in the exchange of respiratory gases, oxygen and carbon dioxide.
The incidence of HIE in advanced countries is estimated to be 1.5 per 1,000 live births and in developing countries range from 2.3–26.5 per 1,000 live births.
Traditionally based on the severity of asphyxia and HIE, the children are described to have a mild, moderate or severe stage of HIE.
Mild HIE:
The infant have hyper alertness, mild distal flexion, normal or weak suckling, strong Moro reflex, mydriasis, tachycardia, no seizures, normal EEG.
Moderate HIE:
The infant is Lethargic or Obtunded (difficult to arouse), Strong distal flexion, Weak or absent suckling, Weak, incomplete Moro, miosis, Bradycardia, focal or multifocal Seizures and abnormal EEG.
Severe HIE:
The infant have Stupor or coma (cannot be aroused), Flaccid, Intermittent decerebration (extension), Absent Suckling , Absent Moro, Variable Pupils (often unequal, poor light reflex, fixed , dilated),Variable Heart rate, Frequent Seizures and abnormal EEG (Sarnat & Sarnat, 1976).
Accurate diagnosis relies on a combination of biomarkers suggestive of perinatal asphyxia as well as development of clinical symptoms of encephalopathy early after birth.
The aim of this study was to assess the patients of HIE and to establish a quick method that could be used to predict occurrence of HIE as early as possible to improve efficiency of short term prognosis of asphyxia in neonates by assessment of level of S100B protein in the cord blood.
Thirty full term neonates fulfilling criteria of asphyxia as well as twenty three full term healthy neonates, severed as control had enrolled in this study.
Cord Blood samples were collected as early as possible immediately after birth and used for measurement of S100B protein by ELISA.
Cord Blood samples also analyzed forarterial blood gases and blood films were done to search for nucleated RBCs (normoblasts). Summary Our results showed that, there was no significant difference between asphyxiated group and control group in terms of Gender, mode of delivery, weight and gestational age.
The median S100B protein level was statistically significantly higher in asphyxia group compared to control group. Within the asphyxia group, there was statistically significant difference between grade I, grade II and grade III HIE regarding the median S100B protein level where it was higher in grade III.
S100B protein was able to predict hypoxic ischemic encephalopathy early after labor and was able to assess the grade of hypoxia.