A nurse is reviewing statements made by a colleague about the medical management of a patient with hepatic encephalopathy receiving lactulose, rifaximin, and a protein-restricted diet. Which statement made by the nurse is incorrect?

Hepatic encephalopathy involves reversible neuropsychiatric impairment caused by porto-systemic shunting and liver failure. Accumulation of neurotoxic ammonia crosses the blood-brain barrier, causing astrocyte swelling and cerebral edema. Clinical manifestations include asterixis, fetor hepaticus, and altered consciousness levels. Rationale: A. Lactulose creates an acidic environment in the colon to convert ammonia into non-absorbable ammonium ions. This osmotic laxative ensures the rapid evacuation of nitrogenous wastes via the stool. It is the primary pharmacological intervention for improving cognitive function in cirrhotic patients. B. Chronic administration of osmotic laxatives frequently leads to significant fluid volume deficits. Excessive bowel movements cause the loss of potassium and sodium, potentially triggering profound hypokalemia or dehydration. Nurses must monitor metabolic panels closely to prevent secondary cardiac or neuromuscular complications. C. Rifaximin is a non-absorbable antibiotic that targets urease-producing bacteria within the intestinal lumen. It does not treat viral hepatitis or function as a systemic antimicrobial agent for hepatic tissue. Its sole purpose is decreasing the bacterial production of ammonia. D. Endogenous ammonia is a byproduct of the enzymatic breakdown of amino acids by gut flora. A temporary reduction in animal protein prevents the excessive accumulation of nitrogenous compounds that the liver cannot detoxify. This dietary modification remains a supportive strategy during acute exacerbations of the disease.