These results suggest that intraventricular bleeding may cause impairment of cerebrospinal fluid circulation but that the mass effect of clots distending the ventricle walls is the most important mechanism responsible for HVD. This model closely imitates several prominent features of human IVH and may therefore be a useful tool for preclinical assessment of the efficacy and safety of treatment with TPA.
Intraventricular haemorrhage (IVH) occurs in up to 50% of patients with primary intracerebral haemorrhage and aneurysmal subarachnoid haemorrhage. It is a significant and independent contributor to mortality and morbidity in these intracranial haemorrhages. Using a model of isolated IVH, we assessed the morphological changes induced by intraventricular bleeding and investigated the effects of intraventricular fibrinolytic treatment following IVH. IVH was induced in 32 pigs by intraventricular infusion of 10 ml autologous blood along with thrombin. The treatment group received an intraventricular injection of 1.5 mg (1 mg/ml) tissue plasminogen activator (tPA) following the injection of blood. The placebo group received the same volume of normal saline. Morphological examinations of the brains were carried out 7 days and 6 weeks following IVH. The ventricles were incompletely filled with blood and significantly enlarged in the placebo group 7 days after the IVH. In contrast, no residual intraventricular clots were visible in the animals treated with tPA, and the diameters of the lateral ventricles had returned to normal within 7 days. Marked losses of the ependymal covering of the ventricular walls were found in the placebo-treated animals, while the ependymal layer was largely intact in the animals treated with tPA. No haemorrhages induced by tPA were observed. The results indicate that intraventricularly administered tPA significantly enhances the lysis of intraventricular blood clots, accelerates the resolution of acute posthaemorrhagic hydrocephalus, and preserves the integrity of the ependymal layer.
The COP regulatory strategy for neonatal and infant CPB, based upon the 5% concentration of albumin in the priming and a COP target of 18 mmHg during bypass, better preserves the plasma albumin concentration within the physiological range and stabilizes the colloid pressure than the standard strategy (0.5 gkg(-1) albumin in the priming and bypass COP target at 15 mmHg). Nevertheless, only the lower postoperative plasma lactate concentration and the shorter duration of mechanical ventilation in the high COP group indicated the potential clinical benefit of this new strategy.
Routine use of conventional ultrafiltration during the cardiac surgery for patients with a bodyweight less than 10 kg was a safe technique that allowed us to achieve higher hematocrit levels at the end of the operation without additional transfusions of allogenic blood. On the other hand, ultrafiltration did not improve the clinical end points.
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