课件新生儿缺氧缺血脑病（hie） 七年制2010.pptVIP

HYPOXIC-ISCHEMIC ENCEPHALOPATHY Prof. Huimin Yu M.D. (俞惠民) Department of Pediatrics Zhejiang University School of Medicine DEFINITION HIE: Hypoxic-ischemic damage of the brain resulting from perinatal asphyxia; Brain dysfunction：encephalopathy Primary cause of permanent damage to CNS. ETIOLOGY Fetal asphyxia (80%-90%) Any process that Impairs maternal oxygenation Decreases blood flow from the mother to the placenta or from paecenta to the fetus Impairs gas exchange across the placenta or at the fetal tissure Increases fetal O2 requirement will exacerbate perinatal asphyxia ETIOLOGY Fetal asphyxia (80%-90%) Maternal Hypertension; Vascular disease; Diabetes; Drug use; Hypotension; Infection; Hypoxia from pulmonary, cardiac, or neurologic disease Placental or cordal Placental infarction or fibrosis; abruption; premature separation; insuficiency Cordal prolapse; entanglement; true knot; compression; abnormal vessels Fetal Hydrops; Infection; IUGR; Postterm ETIOLOGY Diseases after birth (10%) Severe anemia Severe CHD Shock Respiratory failure (central or peripheral) The problem Severe asphyxia: 2-4 per 1000 full-term births 20–50% mortality 25% of the survivors will exhibit permanent neuropsychological handicaps: Mental retardation Cerebral palsy Epilepsy Learning disability PATHOPHYSIOLOGY CBF changes due to cardiac dysfunction impairs of cerebrovascular autoregulation Abnormal metabolism of brain tissue Failure of energy metabolism Neurologic toxity of the excitory amino acid Ca++ influx Reperfution Oxygen free radicals Asphyxia increase in lactate ( pH ↓) hypoxia ↓ decreased ATP GS depletion ↓ ↓ cardiac output ↓cerebrovascular autoregulation ↓ ↓CBF ↓ faliure of ATP production ↓ impairs ion pumps (Na+-K+ ATPase) ↓ excitoxic amino acid (glutamate, NMDA) Ca++ influx ↓ open ion channels ↓ Na+, Cl- an