Hepatic Encephalopathy

Hepatic encephalopathy (HE) results from the failing liver's inability to clear gut-derived neurotoxins, primarily ammonia, from the portal circulation. In hepatic failure, portosystemic shunting allows ammonia to bypass the liver and enter the systemic circulation, crossing the blood-brain barrier where astrocytes convert it to glutamine via glutamine synthetase. Glutamine is osmotically active, causing astrocyte swelling (Alzheimer type II astrocytosis), disruption of astrocyte-neuron signaling, altered neurotransmission (increased GABAergic tone), cerebral edema, and increased intracranial pressure. HE is graded from minimal (subclinical, detected only by psychometric testing) through Grade I (mild confusion, sleep disturbance), Grade II (lethargy, asterixis, disorientation), Grade III (somnolence, marked confusion), to Grade IV (coma). Precipitating factors include GI bleeding, infection, constipation, dehydration, medications (sedatives, opioids), and excessive protein intake. The nurse monitors neurological status using the West Haven criteria, assesses for asterixis, administers lactulose titrated to 2-3 soft stools daily to promote fecal ammonia excretion, administers rifaximin to reduce ammonia-producing gut bacteria, monitors serum ammonia levels, implements fall and aspiration precautions, and identifies and communicates precipitating factors.