here are ive major categories of intracranial hemorrhage in the neonate (Volpe, 2008). Primay subarachnoid hemorrhage is more common in those born preterm and is frequently benign. Cerebelar hemorrhage is also more frequent in preterm neonates and is increasingly recognized as a cause of serious sequelae. Intraventricular hemorrhage IVH) is almost exclusively seen in preterm newborns, is relatively common, and can have serious efects. Subdural hemorrhages are more frequent in term newborns and can be serious. Miscelaneous intraparenchymal hemorrhage is also more frequent in those born at term and is of variable concern.
In preterm infants, the germinal matrix capillary network is fragile for several reasons. First, the subependymal germinal matrix provides poor support for the vessels coursing through it. Second, venous anatomy in this region causes stasis and congestion, which makes vessels susceptible to bursting if intravascular pressure rises. Third, vascular autoregulation is impaired in the preterm neonate (Matsuda, 2006; Verhagen, 2014).
If fragile capillaries in the germinal matrix rupture, blood escapes into surrounding tissues and may extend into the ventricular system and brain parenchyma. This type of hemorrhage is common in preterm neonates, especially those born before 32 weeks. However, it can also develop at later gestational ages and even in term neonates. Most hemorrhages develop within 72 hours of birth, but they have been observed as late as 24 days (Whitelaw, 20ll). Because IVH usually is recognized within 3 days of delivery, its genesis is often erroneously attributed to birth events. It is important to realize that prelabor IVH can also occur (Achiron, 1993; Nores, 1996).
The pathogenesis of IVH is multifactorial and includes hypoxic-ischemic events, carbon dioxide elevations, anatomical factors, blood pressure instability, coagulopathy, genetic factors, and many others (McCrea, 2008; Ment, 2016). Moreover, preterm birth is frequently associated with infection, which further predisposes to endothelial activation, platelet adherence, and thrombi (Redline, 2008). Respiratory distress and mechanical ventilation are commonly associated factors (Sarkar, 2009).
lmost half of hemorrhages are clinically silent. Most small germinal matrix hemorrhages and those confined to the cerebral ventricles resolve without impairment. But, nearly half do show some sign of neurological impairment (Patra, 2006). Survivors of extensive periventricularlintraventricular hemorrhage can have major neurodevelopmental handicaps (Mukerji, 2015). Large lesions can result in hydrocephalus or in degenerated cystic areas termed periventricular leukomalacia (PVL), discussed below. Importantly, the extent ofPVL correlates with CP risk (Bassan, 2006).
Ventricular hemorrhage incidences depends on gestational age at birth. From the Neonatal Research Network, approximately 65 percent of all neonates born before 28 weeks' gestation demonstrated some evidence of hemorrhage or PVL (Stoll, 2010). he incidence ranged from 60 percent in those born at 23 weeks to only 23 percent in those at 28 weeks. Importantly, grade IV intraventricular hemorrhage was documented in 21 percent of 23-week-old neonates but in only 3 percent of those at 28 weeks.
The severity of IVH can be assessed by neuroimaging studies.
Papile and coworkers (1978) devised the mostwidelyused grading scheme to quantiY the extent ofa lesion and estimate prognosis:
Grade I-hemorrhage limited to the germinal matrix
Grade Ill-hemorrhage with ventricular dilation