Hypoxic Ischemic Encephalopathy - Oren Zarif - Hypoxic Ischemic Encephalopathy

Among the many neurological conditions resulting from birth asphyxia, hypoxic ischemic encephalopathic (HIE) can result in permanent brain damage. Children with the disorder can be at risk of permanent disabilities, including Cerebral Palsy. While symptoms can clear up within 24 hours, if they remain, they should be evaluated and treated by a doctor. There are many possible causes for HIE, including premature delivery and other problems that occur shortly after birth.

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Although perinatal hypoxic-ischemic encephalopathy is rare, it is important to recognize the signs and symptoms of the disorder. A neonate who develops this condition should undergo an MRI as soon as possible. MRI can help determine if the underlying condition is associated with seizures or hypoxic-ischemic brain injury. The findings from these scans can also be useful in guiding therapy.

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Seizures are a common symptom of moderate or severe HIE. Seizures increase with hypoxia-ischemia severity. Repetitive seizures are associated with adverse neurodevelopmental outcomes. A recent meta-analysis of five studies found that phenobarbital treatment did not increase the risk of death or severe neurodevelopmental disabilities. The drug also has a potential for side effects, including toxic effects on brain growth and a negative impact on cognition in immature animals.

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Hypoxic ischemic encephalopathy is a serious birth complication. Forty to sixty percent of affected infants die within two years. It is not yet known which factors cause the condition, but the underlying pathologic events are largely caused by impaired cerebral blood flow and oxygen delivery to the brain. While supportive medical therapy has been the standard of care for infants with HIE, complementary therapies are quickly making their way into clinical practice.

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Symptoms of HIE include changes in consciousness, depressed primitive reflexes, seizures, and altered mental status. The severity of the condition is categorized based on the worst degree of encephalopathy noted on serial examinations. Severity is associated with a high mortality rate, and up to one-quarter of survivors show recognizable motor and cognitive impairment. Certain risk factors are associated with HIE, including birth asphyxia and prolonged reduction of cerebral blood flow. However, many cases of HIE do not have a clear history of asphyxia.

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Hypoxic ischemic encephalopathy occurs when oxygen and blood flow to the brain are limited during delivery. The effects of HIE may range from mild to severe and depend on the length of time the baby was deprived of oxygen. It occurs during pregnancy and the immediate postnatal period. There are a number of possible causes for the condition, but the most common is birth asphyxia, which can occur in three out of every thousand deliveries.

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The first step in diagnosis is MRI. This imaging test is important because it enables the doctors to determine the etiology of HIE and its prognosis. An MRI will help determine the exact degree of brain damage, timing, and location of the injury. MRIs of the brain can provide important prognostic information, as well as reveal unusual findings. A child with HIE may also exhibit a watershed pattern of injury that may be associated with a favorable outcome.

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Preterm babies with an acidotic cord are considered hypoxic. The presence of elevated creatinine and liver enzymes, renal impairment, and prolonged assisted ventilation are all indicative of a hypoxic insult. Low Apgar scores are another symptom, which indicates an underlying condition. In addition, the fetus may suffer from intrauterine growth restriction. Further, uterine contractions may further reduce umbilical oxygenation, affecting the fetal CNS and cardiovascular system. As a result, the fetus may develop fetal depression.

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The final pathway in cerebral brain death is a mismatch between the blood supply and oxidative metabolism. Regardless of the instigating event, the final pathway leading to cerebral brain death will result in similar cell death. The extent of cell death will depend on the severity of the initial insult. The secondary energy failure phase begins six to 48 h after the initial insult. This may be the cause of a delayed diagnosis of hypoxic ischemic encephalopathy.