Hyperkalemia (see OVERDOSAGE)
In patients with impaired mechanisms for excreting potassium, the administration
of potassium salts can produce hyperkalemia and cardiac arrest. This occurs
most commonly in patients given potassium by the intravenous route but may also
occur in patients given potassium orally. Potentially fatal hyperkalmia can
develop rapidly and be asymptomatic. The use of potassium salts in patients
with chronic renal disease, or any other condition which impairs potassium excretion,
requires particularly careful monitoring of the serum potassium concentration
and appropriate dosage adjustments.
Interaction with Potassium-Sparing Diuretics
Hypokalemia should not be treated by the concomitant administration of potassium salts and a potassium-sparing diuretic (e.g., spironolactone, triamterene, or amiloride), since the simultaneous administration of these agents can produce severe hyperkalemia.
Interaction with Angiotensin Converting Enzyme Inhibitors
Angiotensin 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.
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 sustained-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. Micro-K (potassium chloride extended-release) ® Extencaps®
and Micro-K (potassium chloride extended-release) ® 10 Extencaps® are microencapsulated capsules formulated
to provide a controlled rate of release of microencapsulated 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 controlled-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 controlled-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. Micro-K (potassium chloride extended-release) ® Extencaps® and
Micro-K (potassium chloride extended-release) ® 10 Extencaps® should be discontinued immediately and the possibility
of ulceration, obstruction or perforation considered if severe vomiting, abdominal
pain, distention, or gastrointestinal bleeding occur.
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.