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Most common type of neonatal intracranial hemorrhage.
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Ischemia and reperfusion (e.g., following treatment of hypotension or hypovolemia)
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Impaired cerebral autoregulation
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Fluctuating cerebral blood flow
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↑ Cerebral blood flow (e.g., due to hypercarbia, volume expansion)
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↑ Cerebral venous pressure (e.g., with pneumothorax)
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Coagulation abnormalities
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Germinal matrix capillaries vulnerable to rupture: thin walls with large lumen
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Arterial development immature: acute transition from large vessels to a capillary network without gradual arborization
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Increased fibrinolytic activity
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Poor vascular support in cerebral tissue
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Grade I: Hemorrhage confined to the germinal matrix.
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Grade II: Hemorrhage within the lateral ventricle (10%-50% of ventricular area on sagittal view).
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Grade III: Hemorrhage within the lateral ventricle (>50% of ventricular area or distends ventricle).
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Periventricular hemorrhagic infarction (PHI)—parenchymal echodense lesion associated with large ipsilateral IVH; often referred to as Grade IV IVH.
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This venous infarction is caused by (usually) large IVH obstructing venous drainage of the periventricular white matter.
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Supportive care (including correction of coagulopathies, circulatory and respiratory support)
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Death may occur with catastrophic presentation of large bilateral IVH.
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There is a strong association between periventricular leukomalacia (PVL) and IVH. It is unknown to what degree the relationship is causal or whether the two entities develop in parallel because of common pathologic processes. There are data to suggest that IVH may exacerbate PVL, due to the presence of non-protein-bound iron in the CSF.7
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PHI often results in mild, moderate, or severe hemiplegia.
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Long-term cognitive impairments with school difficulties are frequent.
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Deficits in verbal learning and verbal memory particularly common.
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Sensory deficits (agnosia, tactile hypersensitivity, tactile hyposensitivity, dyspraxia) may also be associated with IVH.
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Risk of visual impairments (strabismus, optic atrophy, retinopathy of prematurity) is increased in the presence of IVH, particularly with PHI.
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PVD increases the likelihood of neurologic impairments and disabilities.
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Daily monitoring of head circumference, fontanelle, and serial head US examinations.
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Serial lumbar punctures (LPs) can be used to decrease ventricular volume ± increased intracranial pressure when there is evidence of rapidly progressive and/or persistent ventricular enlargement.
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Trials of fibrinolytics.
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A high-risk therapy called DRIFT (drainage, irrigation, and fibrinolytic therapy) was tested in an international randomized clinical trial. Although it did not significantly lower the need for shunt surgery, there was decreased mortality or risk of severe disability (54% vs. 71%) and decreased severe cognitive disability (31% vs. 59%) at 2 y.10 Due to high risks (e.g., secondary IVH), this therapy has not been widely adopted.
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Intraparenchymal hemorrhage (IPH) refers to bleeding into the brain parenchyma.
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Depends on the location and size of parenchymal injury
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Could include epilepsy and motor, cognitive, and/or sensory impairments
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Hemorrhage between the pial layer and cortical surface, most often around temporal lobe.
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Appears to be related to local trauma, e.g., with instrumented delivery.11
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On CT or MRI, appears as ribbon-like collections of blood following contours of gyri and sulci.
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Seizures most frequent presenting sign, babies often otherwise well-appearing.
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SDH and epidural hematoma most frequently related to trauma (e.g., birth trauma or nonaccidental injury) but epidural hematoma much less common.
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Small SDH related to birth: common and inconsequential.
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Rare causes of SDH are coagulation abnormalities and glutaric aciduria type 1.
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Both large SDH and epidural hematoma may present with signs of raised intracranial pressure.
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Lethargy, vomiting, bulging fontanel, increased head size, highpitched cry, irritability, feeding difficulties, seizures, or loss of consciousness.
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Characterized based on size, location, and age (i.e., acute, subacute, or chronic).
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Early surgical evacuation may be lifesaving for large hematomas with signs of raised intracranial pressure and significant neurologic compromise.
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Size, location, and age of SDH/epidural hematoma as well as the neurologic and medical condition of the patient determine the course of treatment and outcome.
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SGH may form because of preexisting risk factors (e.g., coagulopathy).
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Vacuum extraction predisposes a newborn toward subgaleal hemorrhage.
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SGH must be considered in any newborn with a scalp swelling and a falling hematocrit.
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In term babies, this subaponeurotic space may hold as much as 260 mL of blood.
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Death can result from exsanguination and hypovolemic shock, caused by massive bleeding into the subgaleal space.
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Close monitoring of vital signs, level of consciousness, hematocrit, blood gases, head circumference, and signs of tissue hypoperfusion is recommended.
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Coagulation studies should be performed in all newborns with a diagnosis of SGH.
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Very common, usually does not require treatment or diagnostic testing.
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Collection of blood beneath the periosteum.
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Limited by suture lines (if no associated skull fracture).
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Due to sliding/tearing forces during the birth process.
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More common with forceps and vacuum extraction.
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Generally benign, but if large, may exacerbate jaundice.
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Takes weeks to months to resolve (outer edges may calcify, so center may resolve initially, leaving a “crater”-like appearance).
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Large cephalohematomas may occur with coagulation abnormalities (vitamin K deficiency, factor 8 deficiency, etc.).
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Classical PVL consists of focal necrotic lesions and surrounding areas of gliosis, with cyst formation detectable typically 2 to 4 wk after birth.
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Both cystic and non-cystic forms are usually bilateral and symmetric.
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Histology shows microglial activation and loss of premyelinating oligodendrocytes.
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The periventricular white matter dorsolateral to the trigones and frontal horns of the lateral ventricles are areas most commonly affected by PVL.
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Recent MRI and neuropathology studies strongly suggest that cerebral neuronal structures, as well as cerebellum, are also frequently injured.14,15
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Gray matter injury may reflect damage to subplate neurons, which appears early in cortical development and directs projections of afferent and efferent thalamocortical neurons.16
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The reported incidence of cystic PVL has decreased over the past several years to ˜5% of very low birth weight newborns.
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Hypoxia-ischemia
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“Border zone” in the white matter between penetrating cortical arteries and deep lenticulostriate arteries is susceptible to ischemia during periods of hypotension.
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Inflammation
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Diffuse PVL.
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The importance of diffuse excessive high signal intensity (DEHSI) is unclear.
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Because of its high incidence in preterm newborns at term age, its absence after postmenstrual age of 50 weeks, and the sometimes normal neurologic outcome at a corrected age of 2 y, DEHSI may not be part of the spectrum of white matter injury, but rather a prematurity-related developmental phenomenon.20
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Recommended screening protocols suggest an initial cranial US within 3 to 5 d after birth, repeated at 7 to 10 & ˜30 days of age, and at 36-wk corrected gestational age and/or pre-discharge or term age equivalent.
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Depends on the severity and extent of PVL; however, rates of cognitive impairments, cerebral palsy or milder motor impairments, and visual perceptual or other sensory dysfunction are high.
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Cystic PVL tends to damage more medial fiber tracts that control lower extremity function, leading to spastic diplegia, where upper extremity spasticity/dysfunction is less severe.
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Extensive white matter involvement may result in quadriplegia and include facial weakness.
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Cognitive and/or behavioral deficits may be very specific, such as visuomotor and perceptual disabilities, constructional dyspraxia, or attention-deficit disorders.
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Attention deficits and impaired working memory may be associated with injury to the mediodorsal and reticular thalamic nuclei.15
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Punctate white matter lesions and ventricular dilatation are significantly associated with cognitive and psychomotor developmental delay, motor delay, and cerebral palsy.20
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Divided into three grades depending on severity23 (see Table 19.2).
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Intrapartum asphyxia with resultant hypoxic-ischemic encephalopathy
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Infection
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Drug exposure
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Perinatal arterial ischemic stroke
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Metabolic or other genetic disorders
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Brain malformation, epileptic encephalopathy
TABLE 19.2 Distinguishing Features of the Three Clinical Stages of Hypoxic-Ischemic Encephalopathy in the Full-Term Newborn | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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