Hypoxic Ischemic Encephalopathy - Oren Zarif - Hypoxic Ischemic Encephalopathy

The timing of injury is of utmost importance when designing therapies for hypoxic ischemic encephalopathies (HIE). This disease is not a simple one, as the intracellular mechanisms are complex and constantly evolve. In the latent stage, a majority of the surviving cells recover in part, providing an opportunity to intervene with therapies. Later in the disease, cell death occurs largely as a result of numerous intracellular mechanisms.

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Acute hypoxic ischemic encephalopathic insult sets in motion a series of intraneuronal events that may lead to cell death. Interestingly, multiple short seizures in animals do not lead to neuronal death, but rather morphological changes. Cognitive deficits are observed even in infants without clinically noticeable symptoms. Neuroimaging is an additional

diagnostic technique that helps in estimating the risk of neurodevelopmental outcomes.

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The underlying etiology of neonatal encephalopathy is not fully understood. However, most of these disorders are perinatal. While brain MRI and autopsy findings show a low proportion of prenatal injuries, 3% of neonates have non-hypoxic-ischemic encephalopathy. Currently, the most accurate way to determine the cause of neonatal encephalopathy is by observing the child for symptoms.

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Patients with HIE are classified according to their severity and the nature of their brain injury. The most common patterns include: none, watershed, punctate white matter lesions, arterial ischemic stroke, focal parenchymal lesion, and hippocampal injury. Lesions that fall outside these categories are classified as atypical. The severity of intraventricular hemorrhage and subarachnoid hemorrhage is also classified into mild/moderate and severe.

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Although perinatal hypoxia is rare, the long-term consequences are devastating. The effects range from mild behavioural deficits to severe neurologic complications, including cerebral palsy and mental retardation. Research continues to determine a treatment for hypoxic ischemic encephalopathy. A promising therapy is hypothermia. Future neuroprotective therapies for hypoxia sufferers are also being tested.

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There are several reasons why a premature baby may be at risk for HIE. Some are genetic, while others are caused by severe pulmonary disease, or both. Other conditions may also cause a baby to have an acidotic cord. Preterm babies with an acidotic cord can also be at risk. They may also show signs of severe hypoxia, including renal impairment and elevated creatinine and liver enzymes. Other risk factors include preterm birth, chorioamnioitis, and prolonged assisted ventilation.

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During pregnancy, asphyxia can cause brain damage. Pregnant women can be at risk for HIE if they had been exposed to the condition before they were pregnant. However, if the condition was detected during delivery, the infant's chances of surviving would have been much better. The earliest intervention will also reduce complications and minimize any related injuries. Although the exact cause of HIE remains unknown, many antecedents include severe prematurity, uterine rupture, or placenta previa. Low blood pressure in the baby may also be a contributing factor.

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After the acute exposure to hypoxic ischemia, the concentration of extracellular glutamate increases. This is due to glutamate receptor activation. Calcium from intracellular stores and influx through open receptor channels increases cytosolic calcium. These two factors trigger the activation of neuronal nitric oxide synthase and other enzymes, leading to degrading cellular lipids, proteins, and DNA. It further intensifies mitochondrial damage.

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While there is no cure for HIE, treatment methods include therapeutic hypothermia and body cooling. The goal of therapeutic hypothermia is to prevent the cascade effect and to slow the brain's cellular degradation. Treatments also include medication and therapy for children with HIE. Unfortunately, this condition is permanent, and the baby may require lifelong support. However, in many cases, medical professionals and parents can manage the symptoms of hypoxic ischemic encephalopathy.