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Abstract
Perinatal asphyxia is an insult to the fetus or newborn due to lack of oxygen (hypoxia) and/or lack of perfusion (ischemia) to various organs of sufficient magnitude and duration to produce more than fleeting functional and/ or biochemical changes.Asphyxia can occur before, during, or after birth due to various causes e.g.: maternal placental abruption, umbilical cord prolapse, anemia or shock to the newborn.Perinatal asphyxia can result in multisystem organ damage in a neonate, like kidneys (50%), central nervous system (28%), cardiovascular system (25%) lungs (23%) and hemostatic system although There are few studies published that describe hematologic sequelae of Perinatal asphyxia.In Egypt HIE is not an un-common health problem. It is one of the direct causes of infant mortality rate ranking only second to sepsis, the number one cause of mortality; it is defined as the abnormal neurobehavioral state in which the predominant pathogenic mechanism is impaired cerebral blood flow that may result in neonatal death or be manifested later as cerebral palsy or mental deficiency.Several systems have been created to measure the severity and monitor the progress of the encephalopathic signs and symptoms of HIE; The system Sarnat and Sarnat created in 1976 is still the most popular one, it classifies the degree of encephalopathy Stages I, II, and III according to the degree of injury mild, moderate, and severe encephalopathy respectively.Perinatal asphyxia alters the balance of hemostasis, resulting in abnormalities that may result in bleeding and thrombosis.Both large volumes of blood required for studies and challenges with parental consent in neonates provide barriers to large prospective studies.However, some hematologic and hemostatic sequelae have been described, including altered cellular components of whole blood, certain proteins, and increased activation of coagulation and platelets.Thrombocytopenia in the first five days of birth is characteristic of neonates who have experienced acute birth asphyxia and is incriminated in permanent neurologic impairment.Several pathophysiological mechanisms have been proposed for derangement in coagulation by these groups of babies. They tend to have decreased platelet survival and impaired platelet activation as well as aggregatory functions, because of hypoxaemia and acidosis associated with asphyxia.The aim of this study is to assess the hemostatic state in neonates suffering from perinatal asphyxia and its correlation with the clinical neurological assessment.This study was conducted upon 30 neonates admitted to neonatal intensive care units of Benha children Hospital (BENCH) during the period from April 2014 to September 2014. They fulfilled criteria of diagnosis of asphyxia, along with 20 gestational age and sex matched normal neonates as controls.Term and pre-term neonates with perinatal asphyxia were included in the study; asphyxiated neonates with congenital anomalies and/ or sepsis were excluded.All cases and controls were subjected to the following:1. Complete Maternal History. 2. Thorough Clinical Examination.3. Laboratory evaluation which include the followings:Complete blood count. Initial blood glucose.Blood gases and electrolytes (Na, K). Blood urea, Serum creatinine.Platelet count and function.Prothrombin time (PT).Partial thromboplastin time (PTT). Bleeding time (BT).Our results revealed that there was no significant difference between studied groups regarding gestational age, sex, or modes of delivery (p >0.05).In our study 33.3% of the asphyxiated neonates were males, while 66.7% were females; 36.7% of our patients delivered by vaginal delivery, while 63.3% of them delivered by cesarean section.Serum creatinine levels had been elevated significantly in asphyxiated neonates in comparison with control group (P<0.05).There was no significant difference between cases & controls regarding TLC, Hb% and HCT level (P > 0.05).The platelet count in asphyxiated newborns was highly significant lower than that of the controls. Also there was highly significant impairment in platelet functions (50% of asphyxiated group) mean ± SD 71.50±12.79 in relation to control group mean ± SD 82.40±4.38.The results of the present study revealed that PT, aPTT and Bleeding Time were significantly prolonged in group of cases compared to controles.Patients encountered in this study were further subdivided into three groups according to the staging system described by Sarnat and Sarnat (1976) into grade I HIE (4 patients), grade II HIE (12 patients), and grade III HIE (14 patients). On comparing these groups, we found that platelet count and function were lower in stage III in relation to stage I and II; also Pro-thrombin time, activated Partial thrombo-plastine, and Bleeding time were more prolonged in stage III in relation to other two stages.