Hypoxic-Ischemic Encephalopathy Overview
Hypoxic-Ischemic Encephalopathy or HIE is also called perinatal asphyxia and is a serious condition of the newborn and is a result of a lack of oxygen and blood flow to the brain that happens before, during, or after the delivery. The exact timing of the injury is unknown, and the cause can be multi-factorial. HIE can result in long-term neurological consequences. Worldwide, 23% of babies born with HIE die early. They are classified as either mild, moderate, or severe.
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Hypoxia is present when the oxygen level in the fetal blood circulation decreases. The initial compensatory response to hypoxia is an increase in fetal blood pressure and blood flow to the brain. If the hypoxia does not improve, the blood pressure drops which results in a decreased blood flow to the brain known as ischemia. Unlike adults, fetal blood pressure changes result in more dramatic changes in the blood flow to the brain. As the cells of the fetal brain are deprived of oxygen and energy, the brain temperature drops which increases neurotransmitters such as gamma-aminobutyric acid transaminase (GABA). This is a protective response to minimize asphyxia. However, a cascade of events eventually determines whether the brain can be revived or damages minimized. The many chemical responses result in the accumulation of toxins which damage brain cells and can result in cellular death. Calcium levels increase inside the cell which causes more damage. The early developing neurons of the baby are uniquely susceptible to lack of oxygen and blood flow. Free radicals are produced which causes more oxidative or inflammatory damage. This is what produces the long-term learning and memory problems in infants with HIE.
When the infant is resuscitated, and blood flow to the brain is improved, more free radicals develop, and the fetal anti-oxidative response is too weak to repair the damage. When free radicals combine with nitric oxide, another chemical which is a result of inflammation, a highly toxic oxidant causes more damage to the stressed brain cells. Nitric oxide plays an important role in HIE because it is very neurotoxic and can be overproduced for another 4-7 days after the initial instance. Secondary damage occurs in the fetal brain if interventions are not performed within 6 hours of the initial instance. The duration of this delayed phase of brain injury is correlated with adverse neurodevelopment outcomes.
Additional Factors
Severe intrauterine growth restriction, nutritional aspects of the brain, pre-existing brain defects, and the frequency and severity of the seizures that result all influence the final outcome after a hypoxic-ischemic event.