Hypoxic Ischemic Encephalopathy - Oren Zarif - Hypoxic Ischemic Encephalopathy
The mechanisms of hypoxic ischemic encephalopathies are unclear, but some recent research suggests that inflammatory mediators may play a role in the pathogenesis of brain injury. Animal studies have suggested that inflammatory mediators contribute to the damage in the brain caused by hypoxic ischemia. Although the role of inflammatory mediators is not clear, the delayed phase of the disorder seems to increase over the first 24 hours after an incident and resolves itself afterward. This is consistent with a link between the injury and adverse neurodevelopmental outcomes.
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Although the incidence of HIE is very low (1.5 per 1000 live births), there are several factors that increase the risk of developing it. One of these risk factors is asphyxia during pregnancy. Awareness of hypoxic-ischemic encephalopathy (HIE) risks may help parents to prepare. In addition to the risks of hypoxia, the condition is often diagnosed through clinical observation. Clinical symptoms, neurological development, and cognitive development may help determine the severity.
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If left untreated, HIE can lead to permanent brain damage and disability. Even mild cases can lead to Cerebral Palsy and other permanent conditions. However, some children recover without permanent damage. Although symptoms of HIE may disappear within 24 hours, the symptoms should be monitored to detect the disease as soon as possible. Once diagnosed, doctors may need to administer medications and monitoring to ensure the child is not suffering from permanent conditions.
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Although neonatal HIE is the most common type of HIE, it can be caused by other causes, such as infection, a specific metabolic syndrome, or even an alternative diagnosis. Because the condition can be life-threatening, the only treatment is to monitor the baby's brain function and make sure the symptoms do not deteriorate. In some cases, hypothermia may even help prevent death and improve the child's chances of survival.
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Regardless of the cause, an ischemic brain injury causes a cascade of intraneuronal events. Although there is evidence that multiple short seizures in infants may lead to cell death, it is unclear whether there is neuronal loss. However, morphologic changes are present in adult animals. A significant effect of multiple short seizures is reduced learning and a decreased seizure threshold in adulthood.
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It has also been reported that most cases of neonatal encephalopathy are caused by events during the prenatal period. However, brain MRI findings in neonates with encephalopathy indicate that 80% of the cases were perinatal. Only 3% of neonates had non-hypoxic ischemic encephalopathy. This is consistent with previous research, which suggests that the incidence of non-hypoxic encephalopathy is relatively low.
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The clinical pattern of hypoxic ischemic encephalopathies varies in infants with different stages of brain development at the time of the insult. Neuroimaging examinations include cranial ultrasonography, computed tomography, and magnetic resonance imaging. Magnetic resonance imaging reveals the presence of brain lesions, including periventricular leukomalacia. During severe hypoxia, infarctions occur in the brain stem and deep gray matter.
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HIE can occur during pregnancy and after delivery, and is associated with high morbidity. Up to one quarter of survivors will have recognizable motor and cognitive impairment after perinatal HIE. Several antecedents are known to increase the risk of HIE. Some of these include birth asphyxia, severe prematurity, and prolonged reduction in cerebral blood flow, such as placental abruption and hypotension. In rare cases, an undiagnosed HIE patient may have no known cause.
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Various studies have identified heart rate variability as an early biomarker of acute brain injury in patients with hypoxic ischemic encephalopathic (HIE). However, the evidence for this effect is heterogeneous, and further research is necessary. As a result, the current study aimed to systematically review current evidence regarding the relationship between HIE severity and HRV. These findings support the hypothesis that the heart rate variability may be an indicator of the severity of HIE in the brain.
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A common treatment for HIE is therapeutic hypothermia, a process that slows down the baby's metabolic rate. It also limits reperfusion injury. Reperfusion injury occurs when oxygenation is restored too quickly, causing more inflammation and the release of potentially toxic compounds. Therapeutic hypothermia stabilizes brain cells and limits the harmful effects of the inflammation. It is important to note that the damage to the brain is permanent, but there are several treatments available to help children recover from the condition.