Neonatal Hypoxic Ischemic Encephalopathy - Oren Zarif - Hypoxic Ischemic Encephalopathy
The incidence of hypoxic ischemic encephalopathies is estimated at 1.5 per 1000 live births. Affected children are at risk for developing a number of disabilities, including motor and cognitive impairment, epilepsy, and neurodevelopmental delay. These symptoms can develop during infancy or later in life. Clinical examination and MRIs are used to detect the disease and provide a degree of severity. Neuroimaging is often performed to further evaluate the severity of the condition and predict the risk for adverse neurodevelopmental outcomes.
The timing of the injury is essential for designing a treatment for HIE. Early intervention may be vital to reduce the severity of the disease and restore normal brain functioning.
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Treatments must consider the extent of hypoxic ischemic injury and any underlying disease. Many surviving cells partially recover in the latent phase, allowing the doctor to intervene with therapies. TH may be particularly beneficial in infants with moderate to severe cases of HIE.
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During HIE, the neuronal damage depends on the initial insult, the presence or absence of reperfusion injury, and the effects of apoptosis and other biochemical events. However, there is still much more to learn about the pathology of this disease. For example, it is still unclear how hypoxic ischemic encephalopathy may affect a child's learning and memory development.
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Neonatal diagnosis is important for HIE treatment, as it may lead to long-term brain damage. The disease affects 40-60% of infants and can cause significant neurodevelopmental disability. Primary energy failure in HIE is accompanied by impaired cerebral blood flow and oxygen delivery. In the past, the only treatment for HIE was supportive medical therapy. However, today complementary therapies are becoming clinically available, and are proving to be very beneficial for patients suffering from hypoxic ischemic encephalopathy.
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In neonatal HIE, diffuse hypoxic-ischemic brain injury is the cause of symptoms. The severity and duration of the hypoxia-ischemia episodes depend on the age of the infants at birth. Imaging techniques such as cranial ultrasonography and computed tomography (CT) are useful for diagnosis. Ct scans and computed tomography reveal signs of periventricular leukomalacia and germinal matrix hemorrhage and hydrocephalus. Magnetic resonance imaging (MRI) is the best method for assessing the pattern of brain damage.
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The symptoms of HIE are usually mild or moderate and can range from no noticeable to severe. The symptoms of Hypoxic Ischemic Encephalopathy are most often associated with pregnancy, but they can occur in premature infants as well. While the effects of HIE are temporary, the potential for permanent disability is severe. Hypoxic ischemic encephalopathy is also a leading cause of infant death in the U.S.
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Therapeutic hypothermia is one of the most commonly used treatments for HIE. The goal of therapeutic hypothermia is to slow the brain's metabolic rate and prevent reperfusion injury, which occurs when normal oxygenation is restored too rapidly. Reperfusion injury increases the risk of further inflammation and the release of harmful compounds. Therapeutic hypothermia stabilizes brain cells and limits the damaging inflammation. This treatment may be used in combination with other therapies.
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The most important aspect of early diagnosis is the prompt recognition of the first symptoms of hypoxic ischemic encephalopathic effects. An early diagnosis can exclude other causes of encephalopathy and enable earlier treatment. Treatment is supportive, but it may require surgical intervention. There are a few risk factors that should be addressed. If you suspect the presence of HIE, consult your physician immediately. So what are the symptoms and treatment of Hypoxic Ischemic Encephalopathy?