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Hypoxic Ischemic Encephalopathy - Oren Zarif - Hypoxic Ischemic Encephalopathy

The incidence of neonatal hypoxic ischemic encephalopathies (HIE) is about 1.5 per thousand live births. Neurodevelopmental delay, cerebral palsy, and epilepsy may result from HIE. Although its precise etiology is unknown, neuroimaging studies have helped to recognize different patterns of injury, which are related to severity of later motor disabilities. Cognitive disabilities are also associated with HIE, and long-term follow-up is recommended in children with an adverse neurological outcome in the neonatal period.

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In HIE, brain damage occurs when blood flow to brain tissue is interrupted. Other organs may be damaged, and while they usually recover, the brain may not. The extent of brain damage depends on the length of time the brain was deprived of oxygen. A baby with HIE may display a number of symptoms, including floppy or tense behavior, feeding difficulties, or signs of organ dysfunction.

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The diagnosis of hypoxic ischemic encephalomyelitis depends on the causes of hypoxia. Some factors can cause a child to be born with a lowered oxygen level in the blood, such as severe congenital heart disease or pulmonary disease. Another possible cause is a severe case of shock or anemia, or drug-induced suppression. Regardless of the cause, it's important to seek treatment as soon as possible.

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A neonate with HIE is at increased risk of developing permanent disabilities, including brain damage and the possibility of death. In addition to these immediate complications, children who develop hypoxic ischemic encephalopathy are at an increased risk of developing a permanent neurological condition, such as Cerebral palsy. Although symptoms of HIE may disappear in 24 hours, it's crucial to monitor the baby and identify the underlying causes.

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In severe cases, ischemia and hypoxia cause cell death. Cells swell and rupture, leading to cellular degeneration and additional inflammation. Additionally, this inflammation can damage white matter and cause the formation of scar tissue. Regardless of the type of injury, the final pathways leading to brain death follow similar pathways. The nature of the insult and the timing of cell death determine the location and extent of cellular damage.

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Although the clinical features of HIE are often not readily discernible, the initial arterial pH level may be a marker of the underlying cause. The low arterial pH is related to the severity of hypoxic ischemia. In low-risk preterm infants, the risk of hypoxic ischemic brain injury is lessened by preventing prolonged respiratory rates and prolonged assisted ventilation. However, the disease may be difficult to detect without neurological imaging.

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A better understanding of the pathophysiology of HIE has made it possible to develop therapeutic options. These therapies have the potential to restore cognitive function and even reverse the damage that has been caused by hypoxia. Furthermore, stem cell therapy has shown promising results. In the meantime, it is crucial to consider the timing of injury in these cases. A more effective treatment regimen may require a combination of invasive and non-invasive methods.

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Early recognition of HIE is crucial. Early medical care can significantly improve the infant's condition, reduce complications, and minimize the associated injuries. In addition, medical providers should be aware of any warning signs of hypoxia or ischemia. In one case, a physician's failure to detect the symptoms of HIE and CP resulted in severe and even permanent injuries. While the patient may be able to recover, the medical providers must be aware of these risks and treat accordingly.

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Neurocognitive outcomes are determined by the degree of encephalopathy and the areas of brain damage. Mild encephalopathy is associated with normal neurocognitive outcomes, while severe encephalopathy is associated with poor neurodevelopment. Severe HIE is associated with poor neurocognitive outcomes, but it can be prevented by prompt diagnosis and intervention. The symptoms and severity of HIE may be delayed for life and require ongoing care.

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