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Hypoxic Ischemic Encephalopathy - Oren Zarif - Hypoxic Ischemic Encephalopathy


The incidence of hypoxic ischemic encephalopathies (HIE) is around one in every 1,000 live births. Those who survive this condition may have neurological disabilities, such as cerebral palsy and epilepsy, and are at increased risk of Cerebral Palsy in the later years. However, even mild cases may disappear within 24 hours, so it's important to monitor the patient and assess his or her condition.

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Neuroimaging techniques can help diagnose hypoxic ischemic encephalopathic diseases. These include diffusion-weighted imaging (DWI) and MR spectroscopy. To diagnose HIE, however, a doctor must first suspect it. Parents can watch their children for symptoms and consult a physician. Clinical observation can also help determine the extent of the disorder, and cognitive development is often assessed.

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In cases of severe hypoxia and ischemia, a process known as necrosis occurs. This process causes cellular death, and exacerbates the inflammation. It may also result in the formation of scar tissue. In addition to necrosis, two other processes contribute to HIE. One of these is apoptosis, in which cells undergo programmed cell death. During the late stages of hypoxic ischemic encephalopathy, brain cells begin to shrink, preserve their cellular membranes, and eventually die.

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Although HIE is fairly rare, there are a number of factors that may cause it. During pregnancy, during delivery, and immediately after delivery, many factors can cause the condition. Some of these factors are not known, but they are associated with prolonged reductions of cerebral blood flow in the newborn. In addition to severe prematurity and severe lung or heart disease, there are also congenital brain malformations, infections, and low blood pressure in the baby.

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Seizures are common in infants with significant HIE. Seizures increase with the severity and duration of hypoxia-ischemia. Several studies have suggested that seizure activity is associated with adverse neurodevelopment. Moreover, repetitive seizures in infants should be managed with EEG techniques. If a child suffers from HIE, the seizure activity should be monitored closely and treated if possible.

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If the baby is not delivering enough blood to the brain, he or she will suffer from perinatal hypoxic-ischemic encephalopathy. As the baby is devoid of oxygen, his or her brain cells will die. In severe cases, the baby may be severely disabled. In most cases, the baby will not survive, but there are also rare cases of full-term newborns.

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A neonatal rat model of HIE has been developed. This model enables clinicians to analyze the brains of newborns with the disease. Early recognition of the condition will facilitate earlier diagnosis and treatment, which is usually supportive. But early recognition of HIE may help reduce the severity of neurological consequences. It may be beneficial to consider neonatal hypothermia as a potential therapy for perinatal hypoxia.

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Although early intervention is essential, medical providers can only make limited predictions about neurodevelopmental outcomes. Apgar scores and umbilical artery blood gas determinations are of limited value in predicting neurodevelopmental outcomes in children with HIE. However, the degree of encephalopathy is a valid indicator of the child's development. Some children with mild encephalopathy go on to develop with no neurodevelopmental disabilities, while others have more severe disability.

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Therapeutic hypothermia is a commonly used therapy for HIE. It reduces cerebral injury and infarct size, and it improves hippocampal structure. The effects of therapeutic hypothermia can also be seen in pediatric patients. It is important to start the treatment before the child experiences delayed energy failure or develops excitatory features. Early treatment improves survival and decreases disability rates of perinatal HIE survivors.

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