Whitelaw A, Mowinckel M C, Larsen M L, Røkås E, Abildgaard U
Department of Paediatrics, Aker University Hospital, Oslo, Norway.
Acta Paediatr. 1994 Mar;83(3):270-2. doi: 10.1111/j.1651-2227.1994.tb18092.x.
Failure to lyse multiple small blood clots in the cerebrospinal fluid (CSF) reabsorption pathways may be one of the mechanisms leading to posthaemorrhagic ventricular dilatation (PHVD). It has been suggested that intraventricular administration of streptokinase may resolve PHVD but it is not known whether such treatment produces an increase in fibrin degradation products in the CSF. Ventricular CSF was collected from six infants with PHVD before and during intraventricular treatment with streptokinase 1000 units/h. In all six infants, CSF D dimer increased during streptokinase treatment. Median D dimer before treatment was 1642 micrograms/l and during treatment 5440 micrograms/l (p < 0.05). Undetectable D dimer levels in plasma during streptokinase treatment ruled out the possibility that D dimer had merely diffused into the CSF. This augmentation of local fibrinolysis may have therapeutic potential. There was no evidence of systemic fibrinolysis.
脑脊液（CSF）重吸收途径中多个小血凝块未能溶解可能是导致出血后脑室扩张（PHVD）的机制之一。有人提出脑室内注射链激酶可能会缓解PHVD，但尚不清楚这种治疗是否会导致CSF中纤维蛋白降解产物增加。在6例PHVD婴儿脑室内以1000单位/小时的速度注射链激酶治疗前及治疗期间收集脑室CSF。在所有6例婴儿中，链激酶治疗期间CSF D-二聚体均升高。治疗前D-二聚体中位数为1642微克/升，治疗期间为5440微克/升（p<0.05）。链激酶治疗期间血浆中D-二聚体水平不可检测排除了D-二聚体仅仅扩散到CSF中的可能性。这种局部纤维蛋白溶解的增强可能具有治疗潜力。没有全身纤维蛋白溶解的证据。
