normally extracted from the portal blood by the liver, but when there is portal/systemic shunting and impaired hepatic metabolism, it reaches high concentration in the blood and adversely affects the brain. Theraputic measures that limit production of ammonia have therefore been developed.

Lactulose acts as an osmotic laxative to expedite clearance of potentially toxic substances from the gastrointestinal tract. In addition, colonic bacteria metabolise it to lactic and acetic acids which inhibit the growth of ammonia-producing organisms and, by lowering pH, reduce nonionic diffusion of ammonia (a basic substance) from the colon into the bloodstream. The correct dose is that which produces 2-4 soft acidic stools daily (usually 30-60 ml daily). Exceeding this dose can dehydrate the patient. As lactulose is intended for long-term use, there is no rational basis for giving it to patients after paracetamol overdose, as prophylaxis against hepatic encephalopathy.

Reduction of dietary protein reduces ammonia production and has long been used to prevent hepatic encephalopathy. Any potential benefit against encephalopathy must be tempered by the knowledge that most patients with severe liver disease are malnourished. Protein from vegetable sources is often better tolerated than animal-derived protein, at least in part due to its higher fibre content which accelerates transit through the gut.

Neomycin and metronidazole both inhibit urease-producing bacteria and are useful, but their long-term use is limited by toxicity.

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