Cytra-K Disease Interactions

The use of potassium citrate for management of renal tubular acidosis and renal stones is contraindicated in patients with active urinary tract infection caused by urea-splitting organisms. Its ability to increase urinary citrate may be attenuated by bacterial enzymatic degradation of citrate. Moreover, the rise in urinary pH resulting from potassium citrate therapy might promote further bacterial growth.

Administration of potassium salts in severe dehydration may predispose to renal impairment. Therapy with potassium salts should be administered cautiously in patients with acute dehydration (e.g., due to severe or prolonged diarrhea or heat stress). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

Administration of potassium salts may precipitate attacks in familial hyperkalemic periodic paralysis or paramyotonia congenita. Therapy with potassium preparations should be administered cautiously in patients with these conditions.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of potassium salts is contraindicated in patients with severe renal impairment characterized by oliguria, anuria, or azotemia. Since potassium is excreted by the kidney, the administration of potassium salts in such patients, particularly by the intravenous route, may produce hyperkalemia and cardiac arrhythmias or arrest. Therapy with potassium salts should be administered cautiously in patients with diminished renal function or other conditions which impairs potassium excretion (e.g. adrenal insufficiency). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

Alkalinizing agents act as proton acceptors and/or dissociate to provide bicarbonate ions. Elimination of bicarbonate is decreased in patients with renal impairment and can result in metabolic alkalosis. Symptoms of metabolic alkalosis include hyperirritability or tetany, arrhythmia, and/or seizures (altered pH = altered calcium), or lactic acidosis due to impaired oxygen release. Therapy with alkalinizing agents should be administered with extreme caution in patients with compromised renal function. Clinical monitoring of renal function, acid/base balance and electrolytes is recommended.

Hypokalemia in patients with metabolic or respiratory alkalosis should generally be treated with potassium chloride rather than an alkalinizing potassium salt (i.e. acetate, bicarbonate, citrate, or gluconate), since alkali therapy may exacerbate the condition. In addition, hypochloremia may accompany alkalosis, which is best treated with potassium chloride. Close monitoring of acid-base balance, serum electrolytes, electrocardiogram, and clinical status is recommended.