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Hypoxic Ischemic Encephalopathy - Oren Zarif - Hypoxic Ischemic Encephalopathy

Hypoxic ischemic encephalopathy, or HIE, is a neurological condition in which the brain does not receive enough oxygen during birth. The symptoms of the disease include motor and cognitive impairment, developmental delay, and epilepsy. The severity of the condition can be diagnosed when the child is three to four years old, although the exact cause of the disease remains unknown. Children with hypoxic ischemic encephalopathy often suffer from cerebral palsy as well.

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Hypoxic ischemic encephalopathy usually manifests as a diffuse brain injury. The duration and severity of the hypotension vary, depending on the stage of brain maturity. Imaging studies may include cranial ultrasonography and computed tomography. MRIs can reveal periventricular leukomalacia, germinal matrix hemorrhage, and hydrocephalus. Magnetic resonance imaging (MRI) is the most sensitive modality for evaluating patterns of brain injury.

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In addition to using neuroimaging to detect HIE, physicians can use heart rate variability (HRV) as a biomarker to monitor the condition. Stem cell therapy has shown positive results in improving cognitive function in children with moderate to severe hypoxic ischemic encephalopathy. Although more studies are needed to understand the mechanisms of hypoxic ischemic encephalopathy, TH is an effective treatment option for infants with moderate to severe cases.

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The mechanism of hypoxic ischemic brain injury is complex and largely unknown, but the underlying causes of the condition are remarkably similar, regardless of the cause of the traumatic event. The primary injury occurs when cerebral blood flow stops immediately after CA. Secondary injury occurs when cerebral blood flow resumes hours or days after the initial insult. Some factors implicated in secondary injury include microcirculatory dysfunction, impaired autoregulation, and hypoxemia.

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When the diagnosis of hypoxic ischemic encephalopathies is made, the infant's history must be detailed. In addition, there are additional conditions that may be responsible for the disease, including infections, genetic conditions, and inborn errors of metabolism. In neonates, fetal development should be monitored carefully, as alterations in craniofacial appearance can be indicative of prenatal onset of the disorder.

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The medical terms "hypoxia" and "ischemia" refer to reduced oxygen or blood supply to organs, and encephalopathy is the generalized disorder of brain function caused by inadequate blood flow. Perinatal encephalopathy can occur before, during, or after birth. In perinatal encephalopathy, blood and oxygen are reduced simultaneously in the brain. About three out of 1,000 babies will develop some type of perinatal encephalopathy.

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If a baby is born with suspected HIE, therapeutic hypothermia must be instituted immediately. A positive EEG and MRI show a good prognosis. A good outcome can be achieved even if the infant has low Apgar scores or severe acidosis. The newborn should be imaged within one week of birth and should receive anticoagulation if necessary. It should be noted that therapeutic hypothermia is not effective for all newborns with HIE.

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Moreover, the presence of other causes of encephalopathy can affect the outcome of the child's condition. Early diagnosis may affect the prognosis and can facilitate the onset of treatment in the child. Fortunately, treatment of this condition is supportive, with no known cure. For now, a more definitive diagnosis is required. However, it is unclear how to differentiate between infants with HIE and healthy newborns.

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Neonatal MRI is recommended for all neonates who have undergone a complication of severe hypothermia. MRI can reveal the etiology of the encephalopathy, determine the timing of the injury, and determine the prognosis. MRI can also reveal whether there is a link between hypothermia and a broader range of neurological deficits.

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Symptoms of the disorder include a pronounced acidotic cord and prolonged assisted ventilation. Other risk factors include severe congenital heart disease, pulmonary disease, and drug-induced suppression. The presence of an acidotic cord may also signal a hypoxic insult. In addition, high levels of creatinine and liver enzymes suggest a connection between the two conditions. Furthermore, fetal depression may occur as a result of low Apgar scores.

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Neurologic dysfunction is a key characteristic of HIE. After global cerebral ischemia, patients' level of consciousness declines. In humans, Rossen et al. demonstrated an acute decrease in consciousness within 10 seconds after a 600-mmHg CBF. Ischemic encephalopathy is also associated with ventricular fibrillation. Observational studies have demonstrated that the symptoms of HIE can manifest up to 20 seconds after ventricular fibrillation.

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Hypoxic ischemic encephalopathy (HIE) is a relatively rare condition and occurs in less than one-tenth of a percent of live births. However, it is an extremely serious condition that can lead to permanent brain damage in babies. It is estimated that fifteen to twenty percent of newborns with HIE will die within their first week of life, while 25% will be permanently handicapped. Many of these babies will have physical disabilities and cognitive impairment after suffering from HIE.

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