华中科技大学：《儿科学》课程PPT教学课件（讲稿，英文版）Intracranial Hemorrhage of the Newborn

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

Common Clinical signs/Symptoms Change of consciousness Abnormal eyes signs/movement Increased intracranial pressure Irregular respiratory pattern or apnea Changes of muscle tone Pupils signs Others: jaundice anemia, etc

Common Clinical Signs/Symptoms ➢ Change of consciousness ➢ Abnormal eyes signs/movement ➢ Increased intracranial pressure ➢ Irregular respiratory pattern or apnea ➢ Changes of muscle tone ➢ Pupils signs ➢ Others: jaundice, anemia, etc

Clinical Manifestation Most common symptoms are diminished or absent Moro reflex, poor muscle tone, lethargy, apnea and somnolence Often have a precipitous deterioration on the 2nd or 3rd days Periods of apnea, pallor, or cyanosis Failure to suck well Abnormal eye signs, fixed pupils A high-pitched, shrill cry Muscular twitching, convulsion, decreased muscle tone, or paralysis Metabolic acidosis, shock, decreased hematocrit Tense and bulging of fontanel Severe neurological depression or coma Asymptomatic periods or no clinical manifestations

Clinical Manifestation ➢ Most common symptoms are diminished or absent Moro reflex, poor muscle tone, lethargy, apnea and somnolence ➢ Often have a precipitous deterioration on the 2 nd or 3 rd days • Periods of apnea, pallor, or cyanosis • Failure to suck well • Abnormal eye signs, fixed pupils • A high-pitched, shrill cry • Muscular twitching, convulsion, decreased muscle tone, or paralysis • Metabolic acidosis, shock, decreased hematocrit • Tense and bulging of fontanel • Severe neurological depression or coma ➢ Asymptomatic periods or no clinical manifestations

Clinical Manifestation Periventriular Leukomalacia(PVL) Symmetric, non-hemorrhagic ischemic injury Often coexists with IVH Usually asymptomatic at early days Becoming spastic diplegia in later infancy when the neurologic sequelae of white matter necrosis become apparent Early echodense phase (3-10 days of life) Echolucent(cystic) phase(14-20 days of life)

Clinical Manifestation ➢ Periventriular Leukomalacia (PVL) • Symmetric, non-hemorrhagic ischemic injury • Often coexists with IVH • Usually asymptomatic at early days • Becoming spastic diplegia in later infancy when the neurologic sequelae of white matter necrosis become apparent • Early echodense phase (3~10 days of life) • Echolucent(cystic) phase (14~20 days of life)

Classification of Pvh/vi (Grading Mild(70%,40%I+30%Ⅲ Grade l: Isolated periventricular hemorrhage Grade lf: Intraventricular hemorrhage with normal ventricular size Moderate(20%) Grade lll: Intraventricular hemorrhage with acute ventriculardilation Severe(10%) Grade Iv: Intraventricular hemorrhage with parenchymal hemorrhage Papile La, J Pediatr 1978;92: 529-534

Classification of PVH/IVH (Grading) ➢ Mild (70%, 40% I + 30% II) • Grade I: Isolated periventricular hemorrhage • Grade II: Intraventricular hemorrhage with normal ventricular size ➢ Moderate (20%) • Grade III: Intraventricular hemorrhage with acute ventricular dilation ➢ Severe (10%) • Grade IV: Intraventricular hemorrhage with parenchymal hemorrhage Papile LA, J Pediatr 1978; 92:529~534

Diagnosis History Clinical manifestation Transfontanel cranial ultrasonography (real-time) Computed tomography (CT) Magnetic resonance imaging (MRD Magnetic resonance spectroscopy (MRS)

Diagnosis ➢ History ➢ Clinical manifestation ➢ Transfontanel cranial ultrasonography (real-time) ➢ Computed tomography (CT) ➢ Magnetic resonance imaging (MRI) ➢ Magnetic resonance spectroscopy (MRS)