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Hypoxic Ischemic Encephalopathy - Oren Zarif - Hypoxic Ischemic Encephalopathy


While the cause of hypoxic ischemic encephalopathic (HIE) is unknown, it is a condition where brain blood flow is interrupted. While this type of condition can affect the brain, it can also affect other organs. While the organs typically recover, the brain itself may never fully recover. The duration of the absence of oxygen determines how severe the damage is. Infants with HIE may have tense, floppy, and even feed poorly. Their developmental delays or organ dysfunction may be present as well.

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In addition to the neurodegeneration associated with HIE, infants with significant HIE are likely to experience seizures. Seizures tend to increase in severity with prolonged hypoxia-ischemia. Further, seizure activity has been associated with poor neurodevelopmental outcomes. Several studies have shown that repeated seizures can affect the brain and learning abilities of a child. Hence, treatment should include EEG techniques.

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Infants with mild hypoxic ischemic encephalopathic disease (HIE) are a growing risk factor for neonatal brain injury. A recent retrospective cohort study of infants who were hospitalized for hypoxia-related illness included MRIs of their brains. Two reviewers used a validated system to score the brain injury. Any discrepancies were resolved by consensus. In addition, the severity of MRI brain injury was assessed on a subset of MRIs performed before eight days of age.

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A neurologist should be consulted if an EEG tracing indicates this condition. An EEG interpretation should also be made by a clinical physiologist. A patient's prognosis will depend on the diagnosis. The earliest diagnosis of encephalopathy should be made possible as early treatment may improve outcomes. If the condition is diagnosed early, treatment will usually be supportive, rather than invasive.

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As the extent of hypoxic-ischemic brain injury increases, apoptosis results. Cells begin to swell and rupture, causing cellular death and additional inflammation. Both apoptosis and necrosis can damage the brain's white matter and lead to the formation of scar tissue. TH is an effective therapy for infants with moderate to severe HIE.

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Perinatal hypoxic ischemic encephalomy can lead to severe brain damage in newborns. The degree of disability depends on the length of time that the brain is deprived of oxygen. The condition occurs in one to three per thousand live full-term births. A majority of affected infants will develop severe neuropsychological sequelae, such as cerebral palsy, seizures, and visual motor dysfunction. A neonatal rat model is a useful model to simulate perinatal hypoxic ischemic encephalopathy.

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Neuroimaging examinations of neonates suffering from encephalopathy often demonstrate perinatal injuries. In 80% of cases, perinatal injuries are the cause. The cause of ischemic encephalopathy is not clear, but the HRV patterns reflect other etiologies. Fortunately, these encephalopathic conditions are often treatable by physicians and families. If you think you or your child may be suffering from HIE, contact a pediatrician.

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Despite the fact that HIE is relatively common and occurs in less than 5% of live births, it is still one of the leading causes of infant mortality in the U.S. every year. While the cause of HIE is not clear, a number of factors can be antecedents. Some of these include severe prematurity, severe lung disease, and infection. Moreover, perinatal HIE often results in cognitive and physical disability.

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In addition to resuscitation, therapeutic hypothermia is also effective in the treatment of HIE. Therapeutic hypothermia is administered to slow down the baby's metabolic rate and prevent reperfusion injury, which occurs when normal oxygenation is restored too quickly. Rapid oxygenation leads to increased inflammation, which releases more toxic chemicals. The effects of therapeutic hypothermia on children with HIE are not evident until the baby is older and has more mobility.

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