Intracranial Hemorrhage of the Newborn
Intracranial Hemorrhage of the Newborn
Etiology and epidemiology ofice Trauma(epidural, subdural, or subarachnoid) fetal head is too large in proportion to the size of the pelvic outlet prolonged labor/breech or precipitate deliveries Mechanical assistance with delivery Asphyxia/Hypoxic ischemic encephalopathy Premature infants(peri-/intraventricular hemorrhage, PVH/IVH Primary hemorrhagic disturbance( subarachnoid or intracerebral) DIC isoimmune thrombocytopenia neonatal vitamin K deficiency(maternal phenobarbital or phenytoin) Congenital vascular anomaly latrogenic hemorrhage(sucktioning, infusing, ventilating
Etiology and Epidemiology of ICH ➢ Trauma (epidural,subdural, or subarachnoid) • fetal head is too large in proportion to the size of the pelvic outlet • prolonged labor/breech or precipitate deliveries • Mechanical assistance with delivery ➢ Asphyxia/Hypoxic ischemic encephalopathy ➢ Premature infants (peri-/intraventricularhemorrhage, PVH/IVH) ➢ Primary hemorrhagic disturbance (subarachnoid or intracerebral) • DIC • isoimmune thrombocytopenia • neonatal vitamin K deficiency (maternal phenobarbital or phenytoin) ➢ Congenital vascular anomaly ➢ Iatrogenic hemorrhage (sucktioning, infusing, ventilating)
ncidence ofp团团mH Most common neonatal intracranial hemorrhage Occurs primarily in premature infants Incidence increases with decreasing birthweight 60-70% of 500-to 750-g infants, 10-20% of 1000-to 1500-g infants Occasionally seen in near-term and term infants Rarely present at birth 50% occur on the ist day, 80-90% occur between birth and the 3rd day 20-40% progress during the 1st week Delayed hemorrhage may occur after the Ist week in 10-15% of the cases New-onset IVH is rare after the 1st month of life regardless of the birthweight
Incidence of PVH/IVH ➢ Most common neonatal intracranial hemorrhage ➢ Occurs primarily in premature infants • Incidence increases with decreasing birthweight: 60~70% of 500- to 750-g infants, 10~20% of 1000- to 1500-g infants ➢ Occasionally seen in near-term and term infants ➢ Rarely present at birth • 50% occur on the 1 st day, 80~90% occur between birth and the 3 rd day • 20~40% progress during the 1 st week • Delayed hemorrhage may occur after the 1 st week in 10~15% of the cases • New-onset IVH is rare after the 1 st month of life regardless of the birthweight
Pathogenesis of pvi/vH Gelatinous subependymal germinal matrix(periventricular) Embryonal neurons and fetal glial cells Immature blood vessels and y vascular area Poor tissue vascular support Predisposing factors or events Prematurity, RDS, Hypoxic-ischemic or hypotensive injury, reperfusion, ncreased or decreased CBF, pneumothorax, hypervolemia, hypertension, etc Periventricular leukomalacia(PVL Prenatal or neonatal ischemic or reperfusion injury Necrosis of the periventricular white matter Damage to the cortico-spinal fibers in the internal capsule
Pathogenesis of PVH/IVH ➢ Gelatinous subependymal germinal matrix (periventricular) • Embryonal neurons and fetal glial cells • Immature blood vessels and highly vascular area • Poor tissue vascular support ➢ Predisposing factors or events • Prematurity, RDS, Hypoxic-ischemic or hypotensive injury, reperfusion, increased or decreased CBF, pneumothorax, hypervolemia, hypertension, etc ➢ Periventricular leukomalacia (PVL) • Prenatal or neonatal ischemic or reperfusion injury • Necrosis of the periventricular white matter • Damage to the cortico-spinal fibers in the internal capsule
Pathogenesis of pvi/vH Intravascular factors Fluctuating cerebral blood flow (related to mechanics of ventilation) Increasing in CBF(pressure-passive cerebral circulation in premature infants Increases in cerebral venous pressure Decreases in CB F(occurring prenatally or postnatally) Platelet and coagulation disturbances(hypercoagulable state, vitamin K Vascular factors Immature vessels in the germinal matrix Lack muscle and collagen, susceptible to rupture Vascular border zone with more mitochondria, more vulnerable to ischemia Extravascular factors No supportive stroma around the vessels Excessive fibrinolytic activity
Pathogenesis of PVH/IVH ➢ Intravascular factors • Fluctuating cerebral blood flow (related to mechanics of ventilation) • Increasing in CBF (pressure-passive cerebral circulation in premature infants) • Increases in cerebral venous pressure • Decreasesin CBF (occurring prenatally or postnatally) • Platelet and coagulation disturbances (hypercoagulable state, vitamin K) ➢ Vascular factors • Immature vessels in the germinal matrix • Lack muscle and collagen, susceptible to rupture • Vascular border zone with more mitochondria, more vulnerable to ischemia ➢ Extravascular factors • No supportive stroma around the vessels • Excessive fibrinolytic activity