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Hypoxic Ischemic Encephalopathy - Oren Zarif - Hypoxic Ischemic Encephalopathy

The incidence of hypoxic ischemic encephalopathies (HIE) is estimated at 1.5 cases per 1000 live births. In addition to its onset, hypoxic ischemic encephalopathy can lead to neurodevelopmental delay, epilepsy, or other complications in children. A clinical examination, Sarnat staging, and Thompson score are the primary means for grading HIE. Further, neuroimaging is often used to determine the risk of an adverse neurodevelopmental outcome. The clinical HIE grade is a crucial factor for decision-making.

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The most effective prevention is to eliminate the risk of asphyxia during pregnancy. Awareness of the risks of HIE and its risk factors will help parents prepare for the possibility of a baby developing the condition. While the terminology for HIE may be confusing, many of the underlying causes are similar and preventable. For example, hypoxic ischemia is a type of cerebral palsy, but the symptoms of it can be subtle.

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Hypoxic-ischemic encephalopathy is a devastating neurological disorder, resulting in long-term developmental disabilities and a high mortality rate. Fortunately, neuroprotective therapy is available to alleviate the symptoms and minimize the risk of permanent neurological damage. The goal of neuroprotective treatment for infants with HIE is to target both the acute and the subacute injury mechanisms. It's a rare but life-threatening condition.

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Seizures occur in many infants with significant HIE. These are typical symptoms of moderate and severe hypoxia-ischemia. Seizures tend to increase in frequency as the hypoxia-ischemia process goes on. Studies have linked prolonged seizures to an adverse neurodevelopmental outcome. Seizures that are repeated during this period may even go undetected. This is a crucial aspect of management of hypoxic ischemic encephalopathy in infants.

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While the exact pathophysiology of hypoxic ischemic encephalopathies (HIE) is not known, the most common time when infants are exposed to cerebral vascular insult is during labor and delivery. Both the brain's blood flow and the tissue's oxidative metabolism are impaired during this time. Several mediators have been implicated in the development of HIE, including inflammation, excitotoxicity, and oxidative stress. Most likely, apoptosis plays a significant role in neonatal brain injury. While apoptosis is essential for normal brain development, aberrant apoptosis puts infants at risk for neurodevelopmental disabilities.

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The extent of brain damage depends on the length of time that the blood supply was interrupted. Damage to other organs, including the brain, usually returns to normal after the event, but the brain may not recover completely. In such a case, the baby will be floppy or tense, may exhibit signs of organ dysfunction, and may be unable to feed. When HIE occurs, it can cause serious disability for the infant, including mental retardation, epilepsy, and cerebral palsy.

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As soon as the diagnosis of HIE is made, therapeutic hypothermia should be implemented immediately. The early improvement of EEG and MRI is prognostic. Even children with severe acidosis and low Apgar scores are at increased risk for this condition. But even with aggressive therapy and early diagnosis, good outcomes are possible. If a child develops HIE, he or she will require neuropsychological monitoring and treatment.

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A therapeutic hypothermia program should be commenced as soon as possible, especially before 6 hours of birth. However, it is vital to assess the grade of HIE before initiating hypothermia. There is good evidence that therapeutic hypothermia is neuroprotective. One study by Yamaguchi et al. showed that treatment with therapeutic hypothermia increased SDNN within the first six hours of delivery and decreased SDNN at 6 to 72 h.

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Preterm neonates with an acidotic cord are likely to have been exposed to a mild hypoxic insult during fetal development. However, in cases where the fetus is chronically hypoxic, intrauterine growth restriction may occur. Despite this, the neonate may not show traditional fetal distress symptoms such as a low Apgar score. Only a cordocentesis may confirm fetal hypoxia and lactic acidosis. Further, uterine contractions reduce umbilical oxygenation and damage the cardiovascular and CNS. Low Apgar scores are another sign of fetal depression.

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The emergence of heart rate variability (HRV) as a biomarker for acute brain injury has prompted further research on this topic. Although HRV is not a foolproof measure of hypoxia, it may be a valuable supplement to conventional methods. The current evidence on HRV is heterogeneous, but further studies are needed to determine its role in this condition. However, the authors acknowledge the support of the Victorian Government's Operational Infrastructure Support program.

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