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Hypoxic Ischemic Encephalopathy - Oren Zarif - Hypoxic Ischemic Encephalopathy


There are numerous clinical signs of hypoxic ischemic encephalopathies, including seizures. A standard neurological examination can detect HIE in infants at 33-35 weeks of gestation. Clinical features of HIE are often masked by physiological immaturity, but low initial arterial pH is a subtle marker of hypoxic ischemia. Low initial arterial pH is associated with an abnormal cognitive outcome even in low-risk preterm infants.

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In severe cases of hypoxic ischemic encephalotoxicity, the brain is injured by reduced cerebral perfusion. The resulting damage causes cellular death and additional inflammation. This inflammation may result in scar tissue and further damage to the white matter. In addition, apoptosis, a programmed cell death, can result in decreased brain function. While hypoxia-ischemic encephalopathy may lead to death of brain cells, the damage is permanent.

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The most common causes of early neonatal mortality are prematurity, infections, and low birth weight. However, hypoxic ischemic encephalopathy is a significant contributor to early neonatal mortality. It also results in severe brain damage. Between twenty-five and thirty-five percent of asphyxiated infants die within the first few days, and an additional twenty-five percent develop neurological sequels. The consequences of such insults are substantial, both in terms of short and long-term costs and emotional toll.

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While neonatal HIE is the most common cause of hypoxic ischemic encephalopathy, the condition can also occur as a result of specific metabolic and genetic syndromes. The cause and severity of hypoxic ischemic encephalopathy depend on the length of time the brain is deprived of oxygen. It can be a mild condition or a chronic one requiring lifelong care.

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In neonatal infants, the pattern of hypoxic-ischemic brain injury differs based on the level of maturity at the time of the insult. A cranial ultrasonogram may show periventricular leukomalacia and a diffuse brain injury, while computed tomography or magnetic resonance imaging (MRI) may reveal cerebral hydrocephalus. However, magnetic resonance imaging is the most sensitive imaging modality for determining the pattern of brain injury.

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While some cases of HIE are mild and temporary, many cases of severe HIE have life-threatening consequences. These effects may include cerebral palsy, epilepsy, and developmental disabilities. A large percentage of babies with HIE also develop cerebral palsy, and their lifespan is similar to that of children with milder forms of the disease. When these effects are compounded, the symptoms may become permanent and interfere with the child's development.

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During acute HIE, there are various treatments available. Therapeutic hypothermia, for example, is commonly used to reduce brain injury and prevent the development of reperfusion injury, which occurs when normal oxygenation is restored too quickly. This rapid oxygenation leads to increased inflammation and the release of harmful compounds. Therefore, therapeutic hypothermia is an essential component of treatment for HIE. Although the effects of HIE may not be readily apparent until the patient develops mobility problems, neurological outcomes may improve with these treatments.

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Other causes of hypoxia include severe congenital heart disease, severe pulmonary disease, and excessive bleeding, which reduce blood flow to the brain. Some women also experience hypoxia during pregnancy. Acute shock can lead to reduced blood flow to the brain and severe anemia, reducing oxygen delivery to the brain. Drug-induced suppression is also a risk factor for HIE. Several pregnancy complications are linked to the development of HIE, and early diagnosis can help reduce the risk.

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The treatment for HIE in newborns involves cooling the body and brain to reduce the cascade effect of ischemia. This treatment can minimize a child's disability as they grow. Using therapeutic hypothermia requires that the treatment is provided within 6 hours of birth. However, some evidence suggests that therapy can be given as late as 24 hours after birth. These treatments should be considered an option when the baby is diagnosed with hypoxic ischemic encephalopathy.

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