rds-hie-ivh－全英班(編輯修改稿)
2025-02-13 11:18 本頁面
【文章內容簡介】 ? significant mortality and longterm morbidity permanent neurologic impairment (mental retardation, epilepsy and cerebral palsy) 37 Etiology ? Hypoxic factorsperinatal asphyxia, severe respiratory disease ? Ischemic factorssevere heart failure,severe bradycardia 38 Pathological changes ? Diffuse cerebral edema, necrosis and hemorrhage ? Term infants: necrosis of cerebral cortex,basal ganglia,thalamic nuclei ? Preterm infants: Periventricular hemorrhage (PVH) Intraventricular hemorrhage (IVH) Periventricular leukomalacia (PVL, 腦室周圍白質軟化 ) 39 Lesions of HIE 40 Pathogenesis Alteration of cerebral blood flow 41 Pathogenesis 2. Alteration of metabolism of brain tissue ? Hypoxia?anaerobic glycolysis↑ ? Na–KATPase pump insufficiency?cerebral edema ? Free radical formation ? Calcium influx ? Toxic effect of excitatory amino acids ? Neuronal apoptosis and necrosis 42 Clinical manifestation ?Altered level of consciousness Irritability– somnolence（嗜睡 〕 lethargy（昏睡 〕 a ?Muscle tone hypotonic or flaccid（肌力松軟 〕 ?Primary reflex diminish or disappear ?Seizures ?Increased intracranial pressure 43 Clinical manifestation 44 Diagnosis History: perinatal asphyxia ? Profound metabolic or mixed acidemia (pH 7) in an umbilical artery blood sample ? Persistence of an Apgar score of 03 for longer than 5 minutes Clinical manifestation ? Neonatal neurologic sequelae (eg, seizures, a, hypotonia) 45 Diagnosis Laboratory examination ? Cranial ultrasound ? CT scanning (decrease of tissue attenuation) ? MRI ? EEG abnormalities ? Biochemical markers (serum CKBB and plasma NSE?) 46 CT scanning of HIE 47 TreatmentI 1. Supportive care ? Maintain adequate ventilation PaO25070mmHg PaCO2 40mmHg ? maintain adequate tissue perfusion (normal HR,BP) ? correction of electrolyte and acidbase disorder ? correction of hypoglycemia ? correction of hypotension Dopamine and Dobutamine ? fluid therapy 6080ml/kg/d 48 TreatmentII seizures ? Sodium luminal (fir
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