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Intraventricular streptokinase increases cerebrospinal fluid D dimer in preterm infants with posthaemorrhagic
A Whitelaw1, M C Mowinckel, M L Larsen
1Department of Paediatrics, Aker University Hospital, Oslo, Norway.
Insights
Intraventricular streptokinase treatment increased cerebrospinal fluid (CSF) D-dimer levels in infants with posthaemorrhagic ventricular dilatation (PHVD), indicating enhanced local fibrinolysis without systemic effects.
Area of Science:
- Neuroscience
- Biochemistry
- Pediatrics
Background:
- Posthaemorrhagic ventricular dilatation (PHVD) may result from unresolved blood clots in cerebrospinal fluid (CSF) pathways.
- Intraventricular streptokinase is proposed for PHVD treatment, but its effect on CSF fibrinolysis is unknown.
Purpose of the Study:
- To investigate whether intraventricular streptokinase increases fibrin degradation products in the CSF of infants with PHVD.
Main Methods:
- Ventricular CSF was collected from six infants with PHVD before and during intraventricular streptokinase (1000 units/h) infusion.
- CSF and plasma D-dimer levels were measured.
Main Results:
- All six infants showed increased CSF D-dimer levels during streptokinase treatment (median 1642 to 5440 µg/l, p < 0.05).
- Plasma D-dimer remained undetectable, suggesting local CSF fibrinolysis rather than systemic diffusion.
- No evidence of systemic fibrinolysis was observed.
Conclusions:
- Intraventricular streptokinase effectively increases local fibrinolysis within the CSF in infants with PHVD.
- This localized increase in fibrin degradation products suggests therapeutic potential for PHVD treatment.
Abstract:
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.