New Concepts in Hypoxic Ischemic Encephalopathy

The etiology of hypoxic ischemic encephalopathy (HIE) includethose circumstances that affect the cerebral blood flow in fetus andnewborn compressing oxygen supply to brain. It may develop in antepartum (20%) intrapartum and ante partum (35%) post partum (10%)periods. Ninety percent of asphyxia insults occur due to placentalinsufficiency. In post partum period, it is secondary due to pulmonary andcardiovascular or neurological insufficiency.The basis pathophysiology is the same of both full term and pretermhowever, the brain of preterm can develop periventricular white matterinjury in contrast to the brain of the fullterm and the post term the graywhite matter such as the parasagittal parietal cortex are more vulnerableto injury.The newborn brain is generally resistant to hypoxia, but the processof auto regulation is not. Thus, loss of auto regulation leads todevelopment of ischemia as a result of perinatal asphyxia.The fetus is quite capable of adjusting to episodes of hypoxemiawith a synchronized response which involves behavioral, cardiovascular,hormonal, autonomic, renal, hepatic, pulmonary, hematological,gastrointestinal, metabolic, and central nervous system. Sarnat and Sarnatin (1976) established three clinical categories of HIE.