Calcium chloride Disease Interactions

Calcium chloride is acidifying. Therapy with calcium chloride should be administered cautiously in patients with or predisposed to acidosis, including those with renal disease, cor pulmonale, severe respiratory obstruction, or respiratory failure. Calcium chloride should not be administered as therapy for hypocalcemia in patients with acidosis associated with renal failure. Clinical monitoring of acid/base balance and calcium concentrations is necessary during calcium chloride therapy.

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Calcium chloride injection is contraindicated in patients with ventricular fibrillation, asystole and electromechanical dissociation.

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Elevated serum concentrations of calcium and phosphate can exceed the solubility level and result in calcium- phosphate precipitates that deposit in vascular and renal systems as well as other soft tissues of the body. Therapy with calcium should be administered with extreme caution in patients with hyperphosphatemia (hypoparathyroidism or severe renal impairment). Administration of oral calcium acetate or calcium carbonate, in addition to providing calcium, complexes phosphates within the GI tract. These complexes are eliminated in the feces. Clinical monitoring of serum calcium and phosphate concentrations is necessary.

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Calcium is involved in cardiac muscle contraction and electrical impulse conduction. Therapy with calcium salt formulations (particularly IV) should be administered cautiously to patients with cardiac disease. Patients receiving cardiac glycosides and concomitant IV calcium may experience arrhythmias. Therapy with IV calcium should be administered slowly and at reduced dosages in patients with cardiac disease.

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Absorption of oral calcium formulations may be altered and elimination of calcium by the kidney decreased with renal impairment. Hyperphosphatemia occurs during renal failure. Calcium acetate or calcium carbonate, in addition to providing calcium, complexes phosphates within the GI tract. Calcium carbonate can partially correct metabolic acidosis associated with chronic renal failure. Clinical monitoring of renal function and serum calcium and phosphate concentrations is necessary.

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Hypercalciuria, with or without hypercalcemia, may occasionally occur in patients with sarcoidosis. Elevated calcium levels may result from increased intestinal absorption of calcium, which is related to the extrarenal production of vitamin D by mononuclear phagocytes present within the sarcoid granuloma. Therapy with calcium salts should be administered cautiously and only if necessary in patients with sarcoidosis.

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Calcium chloride may lead to tissue necrosis and calcinosis cutis in patients with local trauma due to increase in local calcium levels. To reduce the risk of tissue necrosis, administer this drug slowly through a small needle into a large vein. Avoid extravasation or accidental injection into perivascular tissues. If it occurs, stop the infusion immediately and treat the area as needed.

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Calcium chloride injection in patients with renal dysfunction may increase the risk of calcium-phosphorus product. Patients with renal dysfunction are at higher risk of aluminum toxicity. In these patients, it is recommended to begin with the lowest dose within the approved range. Serum calcium levels should be monitored frequently, based on the severity of renal dysfunction and the risk of a high calcium-phosphorus product.

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