新生儿颅内出血(intracranial hemorrhage of the newborn)

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1、Intracranial Hemorrhage of the Newborn ( ICH ),Contents mastered : The main causes of neonatal ICH The mechanism of PVH-IVH Classification and manifestation of PVH-IVH Diagnosis of neonatal ICH Prevention of neonatal ICH,A severe disease in neonate Related to perinatal asphyxia and trauma, and matur

2、ity of fetus There are four major types Subdural hemorrhage Primary subarachnoid hemorrhage Intracerebellar hemorrhage Periventricular-intraventricular hemorrhage (PVH-IVH),Introduction,Etiology and Epidemiology of ICH,Trauma (epidural, subdural, or subarachnoid) fetal head is too large compared wit

3、h the size of the pelvic outlet prolonged labor/breech or precipitant deliveries Delivery with mechanical assistance Asphyxia/Hypoxic-ischemic encephalopathy Maturity of neonate: germinal matrix, PVH/IVH for 20-30% infants with BW1500g,Primary hemorrhagic disturbance (subarachnoid or intracerebral)

4、DIC isoimmune thrombocytopenia neonatal vitamin K deficiency (maternal phenobarbital or phenytoin) Congenital vascular anormality Iatrogenic hemorrhage (sucktioning, infusing, ventilating),PVH / IVH,Most common neonatal intracranial hemorrhage Occurs primarily in premature infants Incidence is inver

5、sely proportional with birthweight: 6070% of 500- to 750-g infants, 1020% of 1000- to 1500-g infants Occasionally seen in near-term and term infants Rarely present at birth 50% on the 1st day, 8090% between birth and the 3rd day 2040% progress during the 1st week Delayed hemorrhage after the 1st wee

6、k in 1015% of the cases New-onset IVH is rare after the 1st month of life regardless of the birthweight,Pathogenesis of PVH / IVH,Gelatinous subependymal germinal matrix at periventricular area Embryonal neurons and fetal glial cells Immature blood vessels of germinal matrix: thin walls for their re

7、latively large size, lack of a muscularis layer Poor extravascular support: immature interendothelial junctions Predictive factors or events Prematurity, RDS, Hypoxic-ischemic or hypotensive injury, reperfusion, increased or decreased CBF, pneumothorax, hypervolemia, hypertension, etc,Pathogenesis o

8、f PVH / IVH,Intravascular factors Fluctuating cerebral blood flow, occurring prenatally or postnatally (related to pressure-passive cerebral circulation, mechanical ventilation, sucktion, infusion) Increasing of cerebral venous pressure (mechanical ventilation, rapid infusion or infusion of hyperosm

9、otic liquid) Platelet and coagulation disturbances (hypercoagulable state, vitamin K) Vascular factors Immature vessels in the germinal matrix Lack muscle and collagen, susceptible to rupture (germinal matrix) Vascular border zone with more mitochondria, more vulnerable to ischemia,Pathogenesis of P

10、VH / IVH,Extravascular factors No supportive stroma around the vessels Excessive fibrinokinase 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,Common Clinic

11、al Signs/Symptoms of ICH,Change of consciousness Abnormal eyes signs/movement Increased intracranial pressure Irregular respiratory pattern or apnea Change of muscle tone Pupils signs Others: jaundice, anemia, etc,Clinical Manifestation,Most common symptoms are diminished or absent Moro reflex, poor

12、 muscle tone, lethargy, apnea and somnolence Often have a precipitous deterioration on the 2nd or 3rd day Periods of apnea, pallor, or cyanosis Failure to suck Abnormal eye signs, fixed pupils A high-pitched, shrill cry Muscular twitching, convulsion, decreased muscle tone, or paralysis Metabolic ac

13、idosis, shock, decreased hematocrit Tenseness 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 asymptom

14、atic at early days Becoming spastic diplegia in later infancy when the neurologic sequelae of white matter necrosis become apparent Early echodense phase (310 days of life) Echolucent (cystic) phase (1420 days of life),Clinical Manifestation,PVH / IVH three clinical types Catastrophic Syndrome: very

15、 few clinical deterioration in minutes to hours, profound alteration in neurologic state, stupor or coma hypotension, apnea, bulging fontanel, drop in hematocrit, bradycardia, generalized tonic seizures, etc. Saltatory Syndrome: over hours to days Silent Syndrome: 60-70%, hemorrhages limited to the

16、germinal matrix area. no clinical manifestations whatever, and difficult to predict its presence by clinical criteria,Classification of PVH/IVH (Grading),Pathologic changes depended on amount of hemorrhage and are consistent to clinical features Mild (70%, 40% I + 30% II) Grade I: Isolated subependymal hemorrhage Grade II: Intraventricular hemorrhage with normal ventricular size Moderate (20%) Grade III: Intraventricular hemorrhage with acute ventricular dilation Severe (

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