Clinical analysis of neonatal hypoxic-ischemic encephalopathy after intrauterine asphyxia with normal Apgar scores at birth / 中华围产医学杂志

ABSTRACT

Objective To analyse the associated clinical findings of newborn infants with HIE after intrauterine asphyxia with normal Apgar scores at birth and follow-up the neurologic sequelae. Methods 30 newborn infants admitted for HIE in Jan.to Dec. 2002 were analysed,they had(1)intra-uterine asphyxia with Apgar scores of 8～10 at birth,(2)with neurological symptoms on the first day after birth,(3)diseases of infection,genetics and metabolism,and deformity were ruled out,(4)with characteristic findings of HIE on cranial ultrasound examinations and CT scans. Results All of 30 newborn infants had signs of depression from the first day after birth,22 infants of them sometimes were irritable.17 cases (56.7%) with mild encephalopathy and 13 cases (43.3%) with moderate encephalopathy,none of severe case,compared with the infants who had HIE with birth asphyxia,there were no statistical difference. Less than 40% cases had elevated BUN and CKMB,hyponatremia,hypocalcemia,hypoglycemia,acidosis,etc The incidence of them were the same as the infants who had HIE with birth asphyxia. The findings of cranial ultrasound examinations were different between the acute and chronic hypoxic injury of intrauterine asphyxia Follow-up 28 infants at the mean age of (11.7?3.8) months. Except 1 case of cerebral palsy,all of them are normal intelligent infants. There were 4 cases of dilated lateral ventricle and 1 case of dilated 3rd ventricle at birth; 6 cases of dilated ventricles found in follow-up and 1 of them had cerebral palsy,all of those infants recovered at 12～19 months of age. Conclusion Newborn infants who had intrauterine asphyxia without birth asphyxia might suffer from HIE and cerebral palsy later. Cranial ultrasound examinations showed some of them had fetal brain damages. Therefore,intensive care of such infants,preventing and treating intrauterine asphyxia could decrease the morbidity of HIE.