彩色多普勒能量图对新生儿缺氧缺血性脑病的观察

The observation of hypoxic ischemic encephalopathy in the neonates with color Doppler energy image

目的 探讨新生儿缺氧缺血性脑病 (HIE)脑血流的变化规律。方法 应用彩色多普勒能量图 (CDE)对 3 4例HIE患儿及 2 5例正常新生儿的大脑内侧面上部边缘血管网及脑动脉血流参数进行了对照观察。结果 在生后 2 4h内 ,HIE患儿脑血流灌注减少 ,大脑内侧面上部边缘小动脉血流直径缩小 ,网络稀疏 ,甚至难以显示 ;脑动脉流速较正常显著下降 ,阻力指数显著增高 (P <0 .0 1)。之后 ,除了 2例重度患儿持续“少灌注”状态而死亡外 ,其余患儿脑血流灌注开始增加 ,大脑内侧面上部边缘小动脉血流直径扩大 ,血管网络逐渐恢复 ,脑动脉流速增加 ,阻力指数下降。从 2 4～ 96h ,中重度患儿中有 9例呈现“多灌注”损伤表现 ,患儿病情及脑水肿声像图征象均加重 ,边缘小动脉血流直径及各流速参数亦大于正常 (P <0 .0 5 )。其余患儿则未观察到“多灌注”损伤表现。结论 用CDE监测HIE患儿大脑内侧面上部边缘血管网及脑动脉血流参数 ,对判断“少灌注”损伤有重要价值。对是否存在“多灌注”损伤 ,尚需结合临床表现及脑声像图综合判断 。

Objective To study the cerebral blood flow changes of neonates with hypoxic ischemic encephalopathy(HIE).Methods The arteriosum rete of upper border of medial surface of the cerebral hemisphere(ARUMS) and the blood flow parameters of cerebral arteries(CA) in 34 neonates with HIE and 25 health neonates were observed and compared by color Doppler energy image(CDE).Results The cerebral perfusion of neonates with HIE were decreased within 24 h after birth,the blood flow diameters of arteriolae of ARUMS were reduced,and the ARUMS were few and scattered,even it were hardly showed;The velocity of CA was decreased and resistance index(RI) was significantly rised compared with health neonates(P< 0.01 ).Afterwards,except for 2 severe cases,who were in continuous hypoperfusion and died,in the others,the cerebral perfusion started to be increased,the blood flow diameters of arteriolae of ARUMS were dilated,the ARUMS was recovered gradually, the velocity of CA was increased,and RI was decreased.From 24 to 96 h,9 cases in the moderate and severe groups show “luxury perfusion damage”:the condition and the ultrasonographic in brain edema sign of these cases became more severe,and the blood flow diameters of arteriolae of ARUMS and all of velocity parameters were also increased over normal(P< 0.05 ).But this phenomenon was not observed in other cases.Conclusions The monitoring ARUMS and blood flow parameters of CA of HIE by CDE is important in judging the “hypoperfusion damage”.But it had to combine clinical manifestation with brain ultrasonography to judge whether the “luxury perfusion damage” exists.