[Intraventricular hemorrhage in premature neonates: etiopathogenesis, detection and prevention]

Although the incidence of intra-periventricular hemorrhage has reduced in recent years, the increasing survival rates for the very low birth babies indicates that the lesion remains to be a big problem. Neuropathologic base of IVH-PVH is subependimal bleeding into germinal matrix, with consecutive dilatation of lateral ventricles and possible development of germinal matrix destruction, posthemorrhagic hydrocephalus and periventricular hemorrhagic infarction. Pathogenesis of IVH-PVH is multifactorial with participation of intravascular, vascular and extravascular factors. Detection of IVH-PVH and its neuropathologic consequences has been facilitated greatly by the introduction of real-time cranial ultrasonography. Long-time prognosis relates to the mechanisms of brain injury, i.e. presence of hypoxic-ischemic injury, posthemorrhagic hydrocephalus and periventricular hemorrhagic infarction. Extensive parenchymal lesions are associated with frequent subsequent motor, less frequent cognitive deficits. Prevention of IVH-PVH remains the most important goal. That includes prenatal interventions, such as prevention of premature birth, transportation of the premature infant "in utero", prenatal administration of phenobarbital and K-vitamin and optimal management of labor and delivery. Postnatal interventions include careful newborn resuscitation, correction of fluctuating cerebral blood velocity, correction of hemodynamic disturbances and pharmacologic interventions. Postnatal administration of different medicaments (phenobarbital, indomethacin, ethamsylate and vitamin E), have showed inconsistent results in reduction of IVH-PVH, thus there is no pharmacologic agent yet to be recommended for routine use in premature infants.