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Hypoxic Ischemic Encephalopathy - Oren Zarif - Hypoxic Ischemic Encephalopathy

Hypoxic ischemic encephalopathy (HIE) is a type of brain dysfunction caused by inadequate oxygenation of the brain. The brain receives oxygen from the mother through the umbilical cord. If the umbilical cord is compromised during pregnancy or delivery, the fetus can receive low oxygen levels and suffer an irreversible neurological condition. The effects of hypoxic ischemic encephalopathy can vary greatly among children, but the symptoms can range from mild to severe.

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The incidence of HIE is about one in every thousand live births. Some survivors may develop neurodevelopmental delay, cerebral palsy, epilepsy, and epilepsy. The severity of the effects is determined by the time in which the brain was without oxygen. Symptoms of HIE may include tense or floppy behavior, feeding problems, or signs of organ dysfunction. Some infants may also be born prematurely.

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The treatment of HIE is challenging, and it is estimated that forty to sixty percent of affected infants die before reaching adulthood. There has been little success in treating the underlying pathologic events of HIE, but recent advances in complementary therapies are making significant progress in clinical care. While the first phase of HIE treatment is based on supportive care, there are also experimental therapies to help alleviate the secondary injury.

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Neuroimaging techniques are essential to identify HIE, and the onset of the disease can affect the child's neurodevelopment. Newer techniques like diffusion-weighted imaging and MRI spectroscopy can help doctors identify the onset of the disease and assess its severity. In the meantime, parents can monitor symptoms and cognitive development to identify HIE as early as possible. They should also keep an eye out for other symptoms of the condition.

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A common underlying cause of the disorder is brain damage from hypoxic ischemia. The hypoxic-ischemic insult sets in motion a series of intraneuronal events. During this process, the brain may be damaged, resulting in cell death. However, the occurrence of multiple short seizures in newborn infants does not result in neuronal loss but rather in morphologic changes. The delayed phase of HIE is characterized by cortical activation and a decreased seizure threshold later in life.

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The final outcome of HIE is dependent on the initial insult, the effects of reperfusion injury, and apoptosis. These biochemical events take place after the initial insult has ended. The final outcome of the disease is determined by the initial insult, the extent of cell death, and the biochemical reactions that follow the hypoxic-ischemic injury. It is not clear which of these steps will ultimately result in death of the brain cells.

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The pathophysiology of HIE remains elusive. However, there is evidence that pregnancy and delivery are high-risk periods for cerebral vascular insults, such as premature delivery. Immature cerebral vasculature and increased white matter vulnerability also contribute to the risk of hypoxic ischemic encephalopathy in newborn infants. Additionally, oxidative stress and inflammation are important mediators in the development of HIE, and apoptosis most likely plays an important role. Apoptosis is a necessary process for brain development, and an aberrant process can result in severe neurodevelopmental consequences.

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Although the clinical manifestations of HIE are relatively subtle, they are consistent with the signs of an underlying disease - poor brain oxygenation. There is a risk of placental insufficiency during pregnancy, and fetal hypoxia may lead to intrauterine growth restriction. During pregnancy, the placenta and uterine contractions further reduce umbilical oxygenation, compromising fetal CNS and cardiovascular systems. The low Apgar scores of preterm babies may also indicate fetal depression.

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Thankfully, treatment for HIE can be found in a variety of ways. Therapeutic hypothermia, which involves cooling a newborn's body and brain, is an effective way to limit the effects of the disease on the brain. Combined with medication and therapy, this approach has been shown to improve outcomes in HIE and lessen the long-term consequences. When HIE is detected in infants, therapeutic hypothermia can be administered to slow the progression of the condition.

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