Hypoxic Ischemic Encephalopathy - Oren Zarif - Hypoxic Ischemic Encephalopathy
In some cases, children with HIE can develop cerebral palsy or even develop severe mental disability. It can also be caused by asphyxia during pregnancy. The best way to prevent hypoxic ischemic encephalopathy is to avoid asphyxia as much as possible. By understanding the symptoms and risk factors, parents can prepare themselves and their children for any eventuality. Hypoxic ischemic encephalopathy is also known as Stage I, II, and III.
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HIE is fairly common and occurs in between one and six per thousand live births. It is one of the leading causes of infant mortality in the United States. Almost one quarter of newborns who survive HIE will suffer some form of motor or cognitive disability. The causes of HIE are not completely understood, but known risk factors include severe prematurity, prolonged reduction in cerebral blood flow, and severe infections. However, many cases of HIE have no clear history of asphyxia.
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While the causes of HIE are still unknown, a child's condition will likely worsen over time. Cerebral palsy can affect a child's motor skills, cognitive abilities, and neurodevelopmental delay. At least sixty percent of those affected by HIE will develop severe disabilities, including cerebral palsy, epilepsy, and mental retardation. Although the underlying cause of HIE is unclear, it does lead to a heightened risk of cerebral palsy and epilepsy.
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The early recognition of HIE is crucial. Treatment should target both acute and subacute injury mechanisms. Early therapeutic hypothermia is key in this regard. MRI and EEG are prognostic indicators of a child's outcome. Children with severe acidosis and a low Apgar score may still have good outcomes. If the treatment is timely, the risk of severe disability is lessened.
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MRIs are recommended in infants with suspected hypoxic ischemic encephalopathic disease. Neuroimaging techniques are useful in identifying the cause of HIE and to determine whether the disease is progressive or reversible. If MRI is not enough, neuroimaging may help identify the presence of hypoxic-ischemic encephalopathy and assess whether the child is experiencing cognitive difficulties.
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One to three out of every thousand live-born babies may be born with this complication. Of those newborns who survive, approximately fifteen to twenty percent develop severe neuropsychological sequelae. In the postnatal period, more than half will develop cerebral palsy and visual motor dysfunction. Seizures and mental retardation may also be severe. Research on the prevention, diagnosis, and treatment of hypoxic ischemic encephalopathy is ongoing. While hypothermia is one promising therapy, further study of future neuroprotective strategies may be necessary.
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Several factors are thought to increase the risk of hypoxic ischemic encephalopathic disorders. Severe congenital heart disease, respiratory problems, and respiratory disorders all have the potential to produce hypoxic insults in newborns. In addition, a newborn with an acidotic cord may experience delayed acidosis, abnormal neurological examination, and elevated creatinine and liver enzymes.
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Asphyxiated infants are prone to seizures. These seizures may lead to significant functional injury and seizure burden. The optimal treatment plan is one that addresses the risk factors associated with seizures and other neurodevelopmental problems. When a child suffers from hypoxic ischemic encephalopathy, treatment is essential to prevent or delay the onset of seizures and its sequels. Acute ischemic encephalopathy can be fatal, and treatment options may involve surgery.
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In addition to the symptoms of hypoxic ischemic encephalopathic encephalopathy, patients with HIE may exhibit changes in consciousness, depressed primitive reflexes, or seizures. The severity of the encephalopathy is based on the worst degree observed on serial examinations and is associated with mortality. Severe HIE has a high mortality rate; moderate and mild cases have intermediate rates of mortality.
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The causes of hypoxic ischemic encephalopathic encephalopathy are still not clear, but it is known that a lack of blood supply leads to decreased cerebral perfusion, which in turn damages neurons. The reduction in cerebral blood flow and the disruption of oxidative metabolism is thought to be at the heart of this pathology. After restoration of blood flow, the brain begins to recover from the hypoxic ischemic insult. There is a period of time, which is known as the latent phase. After this, the second phase of hypoxic ischemic encephalopathy begins: the secondary energy failure phase.
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Optimal neonatal care involves active management of blood pressure and temperature. Optimal neonatal care will reduce fluctuations in brain perfusion, pressure passive circulation, and hypoglycemia, which can either cause de novo or exacerbate hypoxic ischemic injury. A good neonatal care team will be trained to recognize and prevent these risks and help ensure that neonates get the best care possible.