Antenatal and Perinatal Preventative Strategies for Intraventricular Hemorrhage

II -IntroductionIntraventricular hemorrhage (IVH) is a common complication of prematurity and is associated with significant morbidity and mortality.IVH risk increases with decreasing gestational age (GA); 30-32-week infants have an incidence rate of 0.5-2%, while 22-23-week infants have an incidence rate of 30-45% [1-3].Beyond gestational age, the risk of IVH reflects a multifactorial continuum spanning antenatal, perinatal, and early postnatal life, thereby defining multiple opportunities for prevention.More than 25% of all very low birth weight (VLBW; <1500 g) and up to 45% of extremely low birth weight (ELBW) infants are diagnosed with IVH [4].IVH is classified into mild IVH (i.e., grade I-II) and severe IVH (i.e., grade III or greater) based on cranial ultrasonography findings.Hemorrhage occupying <10% of the lateral ventricular area is grade I; 10-50% of the lateral ventricle area is grade II; >50% of the lateral ventricle area with acute ventricular dilatation is grade III; and periventricular hemorrhagic infarction (PVHI; previously referred to as grade IV IVH) [5].The predominant etiology of IVH is the fragility of the small germinal matrix blood vessels (GM, also termed the ganglionic eminence) located between the caudate nucleus and the thalamus at the level of the foramen of Monro, along with immaturity of cerebral autoregulation in preterm neonates.Blood vessel morphology in the neonatal germinal matrix differs from other cortical regions due to high metabolic demands from rapid precursor cell turnover.The germinal matrix is characterized by increased vascular density and area, and its vessels are more rounded rather than flattened, reflecting vascular immaturity [6,7].