Body and Serum Potassium in Liver Disease

Abstract

Summary The hepatic coma syndrome is significantly associated with elevation of arterial ammonia and an alkaline extracellular pH, which were also related. By contrast, depletion of body potassium was not related to the presence of neuropsychiatric changes, nor could it be related to the presence of extracellular alkalosis. In sequential studies, improvement or deterioration in the electroencephalographic findings, arterial ammonia concentrations, and body stores of potassium usually coincided; these changes probably reflected nonspecific alterations in hepatic function, since no significant relationship in the degree of change was demonstrated. Changes in serum potassium were unrelated to those in the electroencephalogram and in body potassium. The administration of chlorothiazide by vein to patients with hepatic disease resulted in reduction in the urinary excretion and concentration of ammonia, with a simultaneous increase in arterial ammonia concentration, despite relatively trivial changes in urinary excretion of potassium. No change in fasting arterial ammonia concentrations was found when chlorothiazide was given by mouth in the f asting state, but higher arterial ammonium concentrations followed an ammonium chloride load when chlorothiazide was given simultaneously. This was consistent with additional ammonia entering the circulation as a result of administration of chlorothiazide, rather than with impairment of the peripheral utilization of ammonia. It is concluded that, in the majority of patients we studied, depletion of potassium had relatively little influence on clinical and biochemical changes in hepatic coma.