Hypoxic Ischemic Encephalopathy - Oren Zarif - Hypoxic Ischemic Encephalopathy

Although the incidence of hypoxic ischemic encephalopathies (HIE) is relatively low, it is a serious neurological condition affecting infants. Survivors may experience neurological impairment including cognitive impairment, cerebral palsy, or epilepsy. There are several neuropathological varieties of HIE, and the major one is selective neuronal necrosis. The latter is characterized by widespread distribution and is rare in isolation. The topography of neuronal injury is determined by the type of insult and gestational age.

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The symptoms of HIE may include epilepsy, motor impairment, cognitive impairment, and developmental delay. At birth, the symptoms can be detected; however, the exact cause is not known. The condition can also result from problems with the child after birth, including premature birth and other complications that could affect the baby. Although the exact cause of HIE has not yet been established, a child with cerebral palsy is likely to develop the condition.

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The neuronal damage associated with HIE is a complex process. The initial insult and the effects of reperfusion injury and apoptosis all influence the final damage. Once the brain begins to die, the subsequent events of cell death are responsible for the cognitive and neurodevelopmental impairment. The effects of the condition may be permanent or temporary. In either case, it is crucial to diagnose hypoxic ischemic encephalopathy as early as possible.

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Preterm infants with HIE are at a higher risk for neurological impairment and death. It is estimated that approximately one out of every eight live births results in an infant with HIE. While there are no definitive treatments for HIE, supportive care and hypothermia have become the standard of care. Hypothermia and other complementary therapies have a role in managing this neurological condition. The best way to diagnose hypoxic ischemic encephalopathy in preterm infants is by observing the symptoms.

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The basic pattern of hypoxic ischemic encephalopathic infants can be observed with neuropathology. Infants with perinatal asphyxia show pontosubicular neuronal injury. A dominant lesion may be found in the cerebral white matter. About 15 percent of these infants exhibit a dominant abnormality. Symptoms may include loss of consciousness, muscle control, and reflexes.

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This condition occurs when the brain does not receive enough blood and oxygen during labor. It can cause permanent brain damage and disability. The degree of disability depends on the length of oxygen deprivation and the area of the brain affected. It occurs most often in full-term infants, but can affect preterm and premature infants as well. Depending on the cause, the effects of hypoxic ischemic encephalopathy may range from mild to severe disability.

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The outcome of HIE depends on the severity of encephalopathy and areas of the brain affected by the trauma. Moderate and severe encephalopathy is associated with an extensive range of cognitive impairment. MRI is helpful in assessing prognosis. Infants with severe HIE may show signs of organ dysfunction or development delay. Even if the condition is detected early enough, it may not be easy to determine how severe the brain injury is.

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HIE is fairly common, occurring in one to six babies per thousand live births. It is associated with a high mortality rate and a significant amount of morbidity. Up to a quarter of survivors show recognizable motor and cognitive impairment. There are some known risk factors, such as asphyxia at birth or a prolonged reduction of cerebral blood flow during labor and delivery. However, many cases of HIE are not linked to an asphyxia-related cause.

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After the initial compensatory adjustment to an asphyxial event, the CBF falls. This is because the body fails to produce adequate compensatory mechanisms. The cerebral blood flow is then redistributed to vital organs. The redistribution of CBF to the brain occurs through the adrenal glands. Additionally, the release of epinephrine is associated with increased blood pressure. The outcome of asphyxia is often irreversible.

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If there is no definitive diagnosis, the treatment of HIE is largely based on preventing further brain damage. Therapeutic hypothermia, or body cooling, is an effective treatment. It slows the cellular decay and damage that occurs in the brain. The goal is to minimize the long-term effects of HIE on a child's brain. While therapeutic hypothermia does not cure the condition, it does slow its progression. The treatment of HIE is divided into two stages: immediate hospital management and long-term care.