Perinatal asphyxia occurs when blood flow or gas exchange to or from the fetus is disrupted immediately before, during, or after birth. This condition can lead to severe systemic and neurological complications due to reduced oxygen and blood supply to vital organs, including the brain, heart, liver, and muscles. When placental (prenatal) or pulmonary (postnatal) gas exchange is compromised, partial (hypoxia) or complete (anoxia) oxygen deprivation occurs, causing progressive hypoxemia and hypercapnia. If severe, this oxygen deficit triggers anaerobic metabolism and lactic acidosis. Neonatal hypoxic-ischemic encephalopathy (HIE) specifically refers to the neurological damage resulting from perinatal asphyxia and ischemia.
A neonatal hypoxic event can present with:
Metabolic acidosis
Base deficit
Low Apgar scores
Presence of multiple organ-system failure
Clinical evidence of encephalopathy, including hypotonia, abnormal oculomotor or pupillary movements, weak or absent suck, apnea, hyperpnea, or clinical seizures
Neurologic findings that cannot be attributed to other causes such as inborn errors of metabolism, genetic disorders, congenital neurologic disorders, or medication effects
Characteristic findings on magnetic resonance imaging (MRI).
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