目的　分析宫内缺氧所致Apgar评分正常的新生儿缺氧缺血性脑病 (HIE)的临床特点及随访结果。　方法　 2 0 0 2年 1月～ 12月我院收治的足月新生儿HIE 88例中 ,选择诊断为宫内缺氧所致HIE 30例进行分析。其诊断符合以下条件 :(1)有宫内缺氧史 ,出生Apgar评分 8～ 10分 ;(2 )生后早期出现神经症状 ;(3)排除感染、遗传代谢及畸形等神经系统疾病 ;(4)头颅B超或CT有HIE特征性改变。　结果　本组病例生后第 1天起均表现有轻度抑制症状 ,其中 2 2例间歇出现兴奋症状。临床症状属轻度者 17例 (5 7% ) ,中度 13例 (43% ) ,无一例重度 ,与出生时有窒息的 5 8例HIE比较差异无显著性。本组有不足 4 0 %病例有血尿素氮 (BUN)增高 ,低钠、低钙、低糖血症 ,代谢性酸中毒等并发症 ,与出生有窒息的HIE比较也基本一致。分别分析了单纯急性及慢性缺氧病例的B超改变 ,发现两者有所不同。本组随访 2 8例 ,出院后平均 (11.7± 3.8)个月 ,除一例脑瘫外 ,余体格、智能发育正常。B超复查 2 0例 ,出生时侧脑室扩大 4例、第 3脑室扩大 1例均恢复正常 ;出生时脑室不大 ,随访中出现脑室扩大者 6例 ,其中 1例为脑瘫 ,余者均恢复正常。　结论　胎儿有宫内缺氧史 ,新生儿出生时虽无窒息 ,但仍可发生HIE ,头颅B超可见有胎儿期脑损害 ,个别 Objective To analyze the clinical features and follow-up results of neonatal hypoxic-ischemic encephalopathy (HIE) with normal Apgar score caused by intrauterine hypoxia. Methods From January to December 2002, 88 neonates with full-term neonates admitted to our hospital were enrolled in the study. Thirty patients with HIE induced by intrauterine hypoxia were selected for analysis. The diagnosis meets the following conditions: (1) a history of intrauterine hypoxia, birth Apgar score of 8 to 10 points; (2) neurological symptoms early in life; (3) exclude infection, genetic metabolism and deformities and other nervous system diseases; 4) B-head or CT have HIE characteristic changes. Results The patients in this group showed mild symptoms on the first day after birth, of which 22 cases showed excitatory symptoms intermittently. The clinical symptoms were mild in 17 cases (57%) and moderate in 13 cases (43%), with no severe cases. There was no significant difference in 58 cases with asphyxia at birth. Less than 40% of cases in this group have increased blood urea nitrogen (BUN), hyponatremia, hypocalcemia, hypoglycemia, metabolic acidosis and other complications, compared with the birth of asphyxia HIE basically the same. The changes of B-mode in acute and chronic hypoxia cases were analyzed separately and found to be different. This group was followed up 28 cases, an average of (11.7 ± 3.8) months after discharge, except for one case of cerebral palsy, I physically and mentally normal development. B-ultrasound 20 cases, 4 cases of lateral ventricle expansion at birth, the third ventricle enlarged in 1 case were returned to normal; ventricular small at birth, there were 6 cases of ventricular enlargement at follow-up, of which 1 case of cerebral palsy, the rest were recovered normal. Conclusions The fetus has a history of intrauterine hypoxia. Although there is no asphyxia at birth, the fetus may still develop HIE. Brain damage may occur during fetal B-