Therapeutic Hypothermia for Treatment of Neonatal Encephalopathy

Current Research and Nursing Care

Carmen K. Cederholm, BSN, RN, CCRN; C. Michael Cotten, MD, MHS

Disclosures

NAINR. 2014;14(2):77-81. 

In This Article

Pathophysiology

NE is a condition characterized by abnormal neurological function in the newborn period. Infants with NE may display an abnormal level of consciousness, altered muscle tone or reflexes, apnea or altered respirations, and sometimes seizures.[2,3] Hypoxic-ischemic encephalopathy (HIE) occurs when NE is the product of hypoxic-ischemic brain injury. HIE is the result of any event that causes decreased blood supply to the brain. Disturbed uteroplacental blood flow, placental abruption, tight or knotted nuchal cord, umbilical cord prolapse, and uterine rupture are risk factors.[3]

The disruption of blood flow and oxygen delivery that occurs in HIE causes a two phase reaction within the brain tissue that eventually causes brain injury.[3,4] Phase one, also known as primary energy failure, occurs when blood flow to the brain is disturbed and delivery of oxygen and other required substrates is impaired causing the brain to enter anaerobic metabolism.[4] Subsequently, brain tissue acidosis due to lactic acid buildup disrupts neuronal ability to maintain ionic balance, synthesize proteins, and regulate neurotransmitter release and reuptake.[5] One neurotransmitter in particular, glutamate, is a prominent excitatory neurotransmitter.[5] Buildup of excessive extracellular glutamate leads to a process called excitotoxicity where channels activated by glutamate remain open, causing persistent neuronal depolarization, allowing excess extracellular calcium into the cell resulting in cell death.[3,5,6]

Primary energy failure is relieved by the resolution of hypoxia-ischemia, leading to restoration of aerobic metabolism and reduced acidosis. However, reperfusion is followed by a secondary energy failure that usually occurs within 8–16 hours of primary failure.[5–7] Secondary energy failure is thought to be a product of mitochondrial damage, inflammation, the continued existence of surplus extracellular excitatory neurotransmitters, free radical damage, and oxidative injury culminating in premature neuronal apoptosis.[4–6] The timing and severity of secondary energy failure correlate with the severity of primary energy failure. Quicker onset and increased severity of secondary energy failure follow more severe primary failure.[5]

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