INTRAVENTRICULAR HEMORRHAGE

Helene M. Lannon

Overview

Neonatal intracranial hemorrhage is a complication of premature birth. Intraventricular hemorrhage (IVH) is defined as bleeding in or around the ventricles of the brain with potential for extended bleeding into the white matter of the brain, periventricular leukomalacia (PVL). PVL is defined as injury and death of areas of white matter tissue around fluid-filled ventricles and usually results from an extension of IVH (Annibale, 2014). The incidence of IVH/PVL increases as birth weight and gestation decrease. Full-term infants rarely experience IVH, but may develop a subarachnoid hemorrhage as related to pregnancy risk factors or a complication of delivery. The most vulnerable infants are those born prematurely less than 34 weeks gestation, with a threefold risk for very-low-birth-weight infants (VLBW) born between 28 and 32 weeks gestation and of VLBW, 1,001 to 1,500 g (Blackburn, 2015). IVH may cause serious disabilities involving cognitive and motor deficits, vision, and hearing. The onset of IVH occurs in the majority of the time by 72 hours of life and 99.5% occur on day 7 of life (Annibale, 2014). Although the incidence of IVH has started to decline in recent years, IVH remains a significant cause of morbidity and mortality in premature infants (Annibale, 2014). Prevention of preterm birth is not always possible. Treatment after delivery depends on early diagnosis and demonstration of meticulous supportive nursing care.

Background

Brain formation and cerebral blood flow are factors that influence the incidence of IVH. Volpe (2009) notes that preterm infants are at risk for IVH because birth occurs during the time of peak brain synaptogenesis and developmental differentiation, with the migration of cells to match with specific receptor sites and organize the central nervous system. The subependymal germinal matrix (SEGM) is the prominent area of cell growth. It is an extremely vascularized area with high oxygen needs to nourish glial cell growth that strengthens membranes. It matures by 36 weeks of gestation (Blackburn, 2015).

After birth, cerebral blood flow increases to meet oxygen demands. A steady blood flow is maintained by the mechanism of autoregulation. Autoregulation is the ability to maintain cerebral blood flow regardless of changes in cerebral perfusion pressure from physiologic changes; cerebral vessels constrict when pressure rises and dilate when pressure decreases (Elser, Holditch-Davis, & Brandon, 2011). This mechanism is mature at term. However, in prematurity, flow is pressure-passive, and systemic blood pressure becomes the primary determinant of cerebral blood flow and pressure (Annibale, 2014). The absence of autoregulation or severe changes in cerebral blood flow is hypothesized to cause central nervous system IVH (Elser et al., 2011).

190Papile (2006) established the first grading system to define IVH that is used today. Classified as a small IVH are grades I and II. Grade I IVH is limited to the SEGM, often localized at the Foramen of Monroe. Grade II IVH has a partial filling of the lateral ventricle(s) without ventricular dilation. Grade III IVH includes ventricular hemorrhage with dilation. Severe grade IV IVH includes ventricular dilation with the parenchymal extension of blood into the cerebral tissue. Extension into the white matter of the brain is PVL that consists of ischemic lesions and multicystic encephalomalacia (Scher, 2013).

Mortality from severe IVH/PVL ranges from 27% to 50%. Low-grade I IVH usually resolves with only a 5% mortality rate, and grade II IVH has a 10% mortality rate (Annibale, 2014). Morbidity depends on the extension of the bleed. Approximately 25% to 30% of premature infants with grade I to II IVH will be discharged without major sequelae.

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