Hypokalaemia, metabolic alkalosis, and hypernatraemia due to "massive" sodium penicillin therapy

Abstract

Hypokalaemia and metabolic alkalosis were seen in three patients and additionally hypernatraemia in two patients treated with 100 mega units of sodium penicillin G for subacute bacterial endocarditis. The hypernatraemia was probably due to the administration of insufficient fluid, while urinary potassium loss was an important factor in producing hypokalaemia and metabolic alkalosis after. Penicillin may promote urinary potassium excretion by acting as a non-reabsorbable anion.Potassium depletion during treatment with massive doses of sodium penicillin G may be prevented by concurrently administering potassium-sparing diuretics or by using the potassium salt of penicillin.