Hypokalaemia - an active contributor to hepatic encephalopathy?

Patients with cirrhosis are prone to electrolyte disorders, including hypokalaemia. The available evidence suggests that hypokalaemia facilitates hyperammonaemia and thus increases the risk for hepatic encephalopathy (HE). In case studies, plasma potassium decrements were followed by plasma ammonia increments and HE progression, which was reversed by potassium supplementation. The explanation to the hyperammonaemia may be that hypokalaemia both stimulates renal ammonia production and reduces hepatic ammonia elimination by urea synthesis. Further, hypokalaemia eases the entrance of the increased ammonia into the central nervous system because the lower potassium ion concentration favours the competition of NH4+ ions for potassium transporters across the blood brain barrier, and because hypokalaemia-induced metabolic alkalosis increases the amount of gaseous ammonia, which freely passes the barrier. Potassium depletion thus seems to be a mechanistic contributor to HE, supporting the clinical notion of routinely correcting low potassium in patients with cirrhosis.

Automated summary

Patients with cirrhosis are prone to electrolyte disorders, including hypokalaemia, which can lead to an increased risk of hepatic encephalopathy. Hypokalaemia stimulates renal ammonia production and reduces hepatic ammonia elimination, resulting in hyperammonaemia. Furthermore, hypokalaemia facilitates the entrance of ammonia into the central nervous system and increases the amount of gaseous ammonia passing the blood brain barrier. Correcting low potassium levels is crucial in the management of cirrhosis patients to prevent hepatic encephalopathy.