Hypoxic Ischemic Encephalopathy - Oren Zarif - Hypoxic Ischemic Encephalopathy

The incidence of hypoxic ischemic encephalopathy (HIE) is 1.5 per thousand live births, and it affects approximately one in one million babies. Its most common complication is brain damage, but survivors can also develop epilepsy, cerebral palsy, and neurodevelopmental delay. Clinical examination and neuroimaging are used to diagnose HIE and evaluate the risk for neurodevelopmental outcomes. The clinical grade is critical in clinical decision-making.

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The risk factors for HIE include asphyxia during pregnancy. Prevention is the key to avoiding the development of this potentially devastating condition. Educating parents about the risk factors of hypoxic ischemic encephalopathy is an excellent way to be prepared for the worst case scenario. Because the terminology for this condition is relatively similar, it is helpful to understand how this disorder develops and what the symptoms are.

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For this reason, MRI is recommended for all neonates presenting with encephalopathy and seizures, but the information is limited. MRI may be helpful for determining the cause and prognosis of hypoxic ischemic encephalopathy, especially if the child has suffered significant brain damage. MRI and head ultrasound are also useful to detect hemorrhage, ventriculomegaly, or other problems that might indicate hypoxic encephalopathy. However, CT is not commonly performed in neonates and infants due to the risk of radiation exposure.

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A child suffering from perinatal hypoxic ischemic encephalopathies may have permanent disabilities. The severity of disability depends on how long the brain has been deprived of oxygen. The brain can suffer from damage in many areas and will be different for different children. In many cases, symptoms are mild or may develop slowly. While the consequences of the condition will vary, it is important for parents to know their child's symptoms as soon as possible.

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Preterm cerebral hypoxic-ischemic injury is rare. A sentinel event may occur in some cases, and coexisting factors can obscure individual pathologies. While it is difficult to differentiate between full-term and premature brains, diagnostic criteria have been developed to aid in the diagnosis. Infants suffering from HIE should be evaluated for neurological damage and a lack of cerebral palsy or epilepsy.

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The onset of HIE can be fatal in newborns, and approximately 40 to sixty percent of affected neonates die before reaching two years of age. Until recently, there was little available for treatment. Although supportive medical therapy and hypothermia have been the standard of care, complementary therapies are now making their way into clinical practice. While these methods are still a way to manage infants with HIE, these interventions are still in their infancy.

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Treatment of mild HIE should aim to treat both acute and subacute injury mechanisms. This type of injury is associated with poor outcomes, but neuroprotective therapy is more effective if it targets both mechanisms. Ideally, a therapeutic hypothermia procedure should be initiated as soon as the symptoms of HIE are recognized. Early improvement of EEG and MRI is helpful for prognosis, and even in children who are severely acidotic and have a low Apgar score, the outcomes can be excellent.