Intraventricular hemorrhage

Background 1. Mechanism of hemorrhage a. Likely multifactorial

b. Lack of cerebral pressure autoregulation resulting in an inability to maintain relatively steady cerebral blood flow at a range of cerebral perfusion pressures i. Factors causing low cerebral blood flow: Hypotension, perinatal asphyxia ii. Factors causing increased cerebral blood flow: Hypertension, rapid infusion of fluid bolus, vasopressor therapy, pain, handling, hypercarbia iii. Factors causing elevated cerebral venous pressure: RDS, pneumothorax, pulmonary hemorrhage, positive pressure ventilation iv. Fluctuating cerebral blood flow is common in ventilated neonates who are out of synchrony with the ventilator. c. Excessive angiogenesis within the germinal matrix: VEGF (vascular endothelial growth factor) – Potent angiogenic factor d. Cytokines induce cyclooxygenase-2 production resulting in increased prostaglandin production, which causes vasodilatation that further affects cerebral pressure autoregulation. 2. Grades based on criteria by Papile and Volpe a. Grade I – Hemorrhage is limited to the germinal matrix. b. Grade II – Hemorrhage in the lateral ventricle, blood fills less than 50% of the ventricle c. Grade III – Hemorrhage in the lateral ventricle causing distension, blood fills more than 50% of the ventricle d. Grade IV – Hemorrhage into the surrounding parenchyma 3. Complications a. Periventricular leukomalacia b. Posthemorrhagic hydrocephalus – Up to 40% will require a ventriculoperitoneal shunt c. Cerebral palsy and/or mental retardation i. The risk for neonates with grade I or II IVH is similar to that for a premature neonate with a normal cranial ultrasonography and similar NICU course (i.e., experienced similar complications of prematurity). ii. Neonates with grade III or IV IVH have a 35%–50% and 75% increased risk of neurodevelopmental sequelae, respectively.