sion is often unnecessary when such patients have a normal dietary pattern and when low doses of the diuretic are used. serum potassium should be checked periodically, however, and if hypokalemia occurs, dietary supplementation with potassium-containing foods may be adequate to control milder cases. in more severe cases, and if dose adjustment of the diuretic is ineffective or unwarranted, supplementation with potassium salts may be indicated.

sin converting enzyme (ace) inhibitors (e.g., captopril, enalapril) will produce some potassium retention by inhibiting aldosterone production. potassium supplements should be given to patients receiving ace inhibitors only with close monitoring. gastrointestinal lesions: solid oral dosage forms of potassium chloride can produce ulcerative and/or stenotic lesions of the gastrointestinal tract. based on spontaneous adverse reaction reports, enteric-coated preparations of potassium chloride are associated with an increased frequency of small bowel lesions (40-50 per 100,000 patient years) compared to extended-release wax matrix formulations (less than one per 100,000 patient years). because of the lack of extensive marketing experience with microencapsulated products, a comparison between such products and wax matrix or enteric-coated products is not available. potassium chloride extended-release tablets are wax matrix tablets formulated to provide an extended rate of release of potassium chloride and thus to minimize the possibility of high local concentration of potassium near the gastrointestinal wall. prospective trials have been conducted in normal human volunteers in which the upper gastrointestinal tract was evaluated by endoscopic inspection before and after one week of solid oral potassium chloride therapy. the ability of this model to predict events occurring in usual clinical practice is unknown. trials which approximated usual clinical practice did not reveal any clear differences between the wax matrix and microencapsulated dosage forms. in contrast, there was a higher incidence of gastric and duodenal lesions in subjects receiving a high dose of a wax matrix extended-release formulation under conditions which did not resemble usual or recommended clinical practice (i.e., 96 meq per day in divided doses of potassium chloride administered to fasted patients, in the presence of an anticholinergic drug to delay gastric emptying). the upper gastrointestinal lesions observed by endoscopy were asymptomatic and were not accompanied by evidence of bleeding (hemoccult testing). the relevance of these findings to the usual conditions (i.e., non-fasting, no anticholinergic agent, smaller doses) under which extended-release potassium chloride products are used is uncertain; epidemiologic studies have not identified an elevated risk, compared to microencapsulated products, for upper gastrointestinal lesions in patients receiving wax matrix formulations. potassium chloride extended-release tablets should be discontinued immediately and the possibility of ulceration, obstruction or perforation considered if severe vomiting, abdominal pain, distention or gastrointestinal bleeding occurs. metabolic acidosis: hypokalemia in patients with metabolic acidosis should be treated with an alkalinizing potassium salt such as potassium bicarbonate, potassium citrate, potassium acetate or potassium gluconate.

whole and never crushed, chewed, or sucked.

rate of potassium intake. such depletion usually develops slowly as a consequence of prolonged therapy with oral diuretics, primary or secondary hyperaldosteronism, diabetic ketoacidosis, severe diarrhea, or inadequate replacement of potassium in patients on prolonged parenteral nutrition. depletion can develop rapidly with severe diarrhea, especially if associated with vomiting. potassium depletion due to these causes is usually accompanied by a concomitant loss of chloride and is manifested by hypokalemia and metabolic alkalosis. potassium depletion may produce weakness, fatigue, disturbances of cardiac rhythm (primarily ectopic beats), prominent u-waves in the electrocardiogram and, in advanced cases, flaccid paralysis and/or impaired ability to concentrate urine. if potassium depletion associated with metabolic alkalosis cannot be managed by correcting the fundamental cause of the deficiency, e.g., where the patient requires long term diuretic therapy, supplemental potassium in the form of high potassium food or potassium chloride may be able to restore normal potassium levels. in rare circumstances (e.g., patients with renal tubular acidosis) potassium depletion may be associated with metabolic acidosis and hyperchloremia. in such patients potassium replacement should be accomplished with potassium salts other than the chloride, such as potassium bicarbonate, potassium citrate, potassium acetate or potassium gluconate. the potassium chloride in potassium chloride extended-release tablets is completely absorbed before it leaves the small intestine. the wax matrix is not absorbed and is excreted in the feces; in some instances the empty matrices may be noticeable in the stool. when the bioavailability of the potassium ion from the potassium chloride extended-release tablets is compared to that of a true solution the extent of absorption is similar. the extended-release properties of potassium chloride extended-release tablets are demonstrated by the finding that a significant increase in time is required for renal excretion of the first 50% of the potassium chloride extended-release tablets dose as compared to the solution. increased urinary potassium excretion is first observed 1 hour after administration of potassium chloride extended-release tablets, reaches a peak at 4 hours, and extends up to 8 hours. mean daily steady-state plasma levels of potassium following daily administration of potassium chloride extended-release tablets cannot be distinguished from those following administration of potassium chloride solution or from control plasma levels of potassium ion.