Intraventricular hemorrhage

Intraventricular hemorrhage (IVH) is a major complication of prematurity. Despite the term referring to hemorrhage within the ventricle, it encompasses hemorrhage confined to the germinal matrix (grade I), extension to lateral ventricles without (grade II) or with (grade III) ventricular dilatation, and periventricular parenchymal hemorrhage (grade IV). Although periventricular hemorrhage (grade IV) may be considered as a separate entity ( ), for the purpose of this chapter, the original definition of IVH is used for all the four grades ( ). IVH affects approximately one-third of extremely preterm infants (<28 weeks’ gestation) ( ) and is a major risk factor for cerebral palsy, neurodevelopmental impairment, hydrocephalus, and mortality among these patients ( ; ).

Although IVH also occurs in term infants, preterm infants are particularly vulnerable due to structural and functional immaturity of the brain. In preterm infants, the site of hemorrhage is the germinal matrix ( Figs. 20.1 through 20.3 ). This is the site of active proliferation of future neuronal and glial cells and as such is a highly vascularized and metabolically active tissue ( ). Several characteristics of this vascular bed predispose it to hemorrhage. The capillary network consists of thin-walled, poorly supported fragile vessels ( ). It lies within an arterial end zone, which makes it particularly vulnerable to hypoperfusion–reperfusion injury ( ). The confluence of medullary, choroidal, and thalamostriate veins forms the terminal vein, which makes a U-turn going through the germinal matrix as it drains into internal cerebral vein, making it prone to congestion in case of large germinal matrix hemorrhage ( ; ). This venous congestion increases the risk of periventricular hemorrhagic infarction (grade IV, Figs. 20.4 and 20.5 ). Until its involution between 28 and 36 weeks’ gestation, the germinal matrix remains vulnerable to hemorrhage ( ; ).

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A head ultrasound image of a 2-day old preterm infant born at 25 weeks’ gestation. This is a left lateral sagittal view of the brain showing the caudate nucleus (A), thalamus (B), and choroid plexus (C). The arrows point to the caudothalamic groove. The absence of increased echogenicity anterior to the caudothalamic groove indicates absence of germinal matrix hemorrhage.

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A head ultrasound image of a 2-day-old preterm infant born at 25 weeks’ gestation (same as in Fig. 1). This is a right lateral sagittal view of the brain. The arrow points to an increased echogenicity anterior to the caudothalamic groove consistent with grade I IVH.

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A head ultrasound image of a 2-day-old preterm infant born at 25 weeks’ gestation (same as in Fig. 1). The arrow points to right grade I IVH.

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A head ultrasound image of a 1-day-old preterm infant born at 25 weeks’ gestation. This is a coronal view of the brain. The black arrow shows a right subependymal hemorrhage with possible extension hemorrhage into ventricular space without ventriculomegaly (likely grade II IVH). The white arrow points to germinal matrix hemorrhage with extension to left ventricle and possible periventricular involvement (likely grade IV).

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A head ultrasound image of a 1-day-old preterm infant born at 25 weeks’ gestation (same as in Fig. 4). This is a follow up coronal view on the 6th postnatal day. The bilateral periventricular echogenicity is consistent with hemorrhagic infarction (grade IV).

In addition to structural immaturity, the brain of preterm infants is also functionally immature. Cerebral blood flow (CBF) autoregulation, the ability to maintain CBF relatively constant despite fluctuations in blood pressure, is less robust in preterm infants and the autoregulatory plateau is quite narrow ( ; ; ). Therefore the brain of extremely preterm infants is prone to hypo- and hyperperfusion. Indeed, impairment of CBF autoregulation has been implicated in development of IVH among preterm infants ( ; ). Another functional immaturity of the brain that has recently been proposed is that the forebrain (including cortex, thalamus, and basal ganglia) does not have high-priority vascular bed in extremely preterm infants ( ). Therefore unlike the hindbrain, which vasodilates in case of hypoxia or low perfusion pressure, the forebrain of these patients may vasoconstrict. This immaturity of the forebrain vasculature can predispose the germinal matrix to hypoperfusion–reperfusion injury, which often precedes IVH.

Although vulnerability of immature brain is the key factor, pathogenesis of IVH is multifactorial and involves immaturity and/or maladaptation during the transitional period of other organs such as the heart and lungs. In addition, interventions aimed at supporting preterm infants surviving extrauterine life can increase the risk of IVH (see later). Further discussion of etiology, risk factors, pathophysiology, and clinical outcome of IVH is done through a case of twins born at 26 weeks’ gestation.