CALCIUM EXCESS (HYPERCALCEMIA)
Hypercalcemia (excess of calcium in the plasma) is a dangerous imbalance when severe; in fact, hypercalcemic crisis has a mor-tality rate as high as 50% if not treated promptly.
The most common causes of hypercalcemia are malignancies and hyperparathyroidism. Malignant tumors can produce hyper-calcemia by a variety of mechanisms. The excessive PTH secretion associated with hyperparathyroidism causes increased release of calcium from the bones and increased intestinal and renal ab-sorption of calcium. Calcifications of soft tissue occur when the calcium–phosphorus product exceeds 70 (serum calcium [mg/dL] x serum phosphorus [mg/dL]) (Marx, 2000).
Bone mineral is lost during immobilization, sometimes caus-ing elevation of total (and especially ionized) calcium in the bloodstream. Symptomatic hypercalcemia from immobiliza-tion, however, is rare; when it does occur, it is virtually limited to people with high calcium turnover rates (eg, adolescents dur-ing a growth spurt). Most cases of hypercalcemia secondary to immobility occur after severe or multiple fractures or spinal cord injury.
Thiazide diuretics may cause a slight elevation in serum calcium levels because they potentiate the action of PTH on the kidneys, reducing urinary calcium excretion. The milk-alkali syndrome can occur in patients with peptic ulcer treated for a prolonged period with milk and alkaline antacids, particularly calcium carbonate. Vitamin A and D intoxication, as well as the use of lithium, can cause calcium excess.
As a rule, the symptoms of hypercalcemia are proportional to the degree of elevation of the serum calcium level. Hypercalcemia re-duces neuromuscular excitability because it suppresses activity at the myoneural junction. Symptoms such as muscle weakness, in-coordination, anorexia, and constipation may be due to decreased tone in smooth and striated muscle. Cardiac standstill can occur when the serum calcium level is about 18 mg/dL (4.5 mmol/L). The inotropic effect of digitalis is enhanced by calcium; therefore, digitalis toxicity is aggravated by hypercalcemia.
Anorexia, nausea, vomiting, and constipation are common symptoms of hypercalcemia. Dehydration occurs with nausea, vomiting, anorexia, and calcium reabsorption at the proximal renal tubule. Abdominal and bone pain may also be present. Abdominal distention and paralytic ileus may complicate severe hypercalcemic crisis. Excessive urination due to disturbed renal tubular function produced by hypercalcemia may be present. Se-vere thirst may occur secondary to the polyuria caused by the high solute (calcium) load. Patients with chronic hypercalcemia may develop symptoms similar to those of peptic ulcer because hypercalcemia increases the secretion of acid and pepsin by the stomach.
Confusion, impaired memory, slurred speech, lethargy, acute psychotic behavior, or coma may occur. The more severe symp-toms tend to appear when the serum calcium level is approxi-mately 16 mg/dL (4 mmol/L) or above. However, some patients become profoundly disturbed with serum calcium levels of only 12 mg/dL (3 mmol/L). These symptoms resolve as serum calcium levels return to normal after treatment.
Hypercalcemic crisis refers to an acute rise in the serum cal-cium level to 17 mg/dL (4.3 mmol/L) or higher. Severe thirst and polyuria are characteristically present. Other findings may in-clude muscle weakness, intractable nausea, abdominal cramps, obstipation (very severe constipation) or diarrhea, peptic ulcer symptoms, and bone pain. Lethargy, confusion, and coma may also occur. This condition is very dangerous and may result in cardiac arrest.
The serum calcium level is greater than 10.5 mg/dL (2.6 mmol/L). Cardiovascular changes may include a variety of dysrhythmias and shortening of the QT interval and ST segment. The PR interval is sometimes prolonged. The double-antibody PTH test may be used to differentiate between primary hyperparathy-roidism and malignancy as a cause of hypercalcemia: PTH levels are increased in primary or secondary hyperparathyroidism and suppressed in malignancy. X-rays may reveal the presence of osteoporosis, bone cavitation, or urinary calculi. The Sulkowitch urine test analyzes the amount of calcium in the urine; in hyper-calcemia, dense precipitation is observed due to hypercalciuria.
Therapeutic aims in hypercalcemia include decreasing the serum calcium level and reversing the process causing hypercalcemia. Treating the underlying cause (eg, chemotherapy for a malig-nancy or partial parathyroidectomy for hyperparathyroidism) is essential.
General measures include administering fluids to dilute serum calcium and promote its excretion by the kidneys, mobilizing the patient, and restricting dietary calcium intake. IV administration of 0.9% sodium chloride solution temporarily dilutes the serum calcium level and increases urinary calcium excretion by inhibit-ing tubular reabsorption of calcium. Administering IV phosphate can cause a reciprocal drop in serum calcium. Furosemide (Lasix) is often used in conjunction with administration of a saline solu-tion; in addition to causing diuresis, furosemide increases calcium excretion.
Calcitonin can be used to lower the serum calcium level and is particularly useful for patients with heart disease or renal failure who cannot tolerate large sodium loads. Calcitonin reduces bone resorption, increases the deposit of calcium and phosphorus in the bones, and increases urinary excretion of calcium and phos-phorus. Although available in several forms, calcitonin derivedfrom salmon is commonly used. Skin testing for allergy to salmon calcitonin is necessary before the hormone is administered. Sys-temic allergic reactions are possible since this hormone is a pro-tein; resistance to the medication may develop later because of antibody formation. Calcitonin is administered by intramuscular injection rather than subcutaneously because patients with hyper-calcemia have poor perfusion of subcutaneous tissue.
For patients with cancer, treatment is directed at controlling the condition by surgery, chemotherapy, or radiation therapy. Corti-costeroids may be used to decrease bone turnover and tubular re-absorption for patients with sarcoidosis, myelomas, lymphomas, and leukemias; patients with solid tumors are less responsive. The bisphosphonates inhibit osteoclast activity. Pamidronate (Aredia) is the most potent of these agents and is given IV; it causes a tran-sient, mild pyrexia, decreased white blood cell count, and myalgia. Etidronate (Didronel) is another bisphosphonate that is given IV, but its action is slower. Mithramycin, a cytotoxic antibiotic, in-hibits bone resorption and thus lowers the serum calcium level. This agent must be used cautiously because it has significant side effects, including thrombocytopenia, nephrotoxicity, rebound hypercalcemia when discontinued, and hepatotoxicity. Inorganic phosphate salts can be administered orally or by nasogastric tube (in the form of Phospho-Soda or Neutra-Phos), rectally (as reten-tion enemas), or IV. IV phosphate therapy is used with extreme caution in the treatment of hypercalcemia because it can cause se-vere calcification in various tissues, hypotension, tetany, and acute renal failure.
It is important to monitor for hypercalcemia in patients at risk. Interventions such as increasing patient mobility and encourag-ing fluids can help prevent hypercalcemia, or at least minimize its severity. Hospitalized patients at risk for hypercalcemia are en-couraged to ambulate as soon as possible; outpatients and those cared for in their homes are informed of the importance of fre-quent ambulation.
When encouraging oral fluids, the nurse considers the pa-tient’s likes and dislikes. Fluids containing sodium should be ad-ministered unless contraindicated by other conditions, because sodium favors calcium excretion. Patients are encouraged to drink 3 to 4 quarts of fluid daily. Adequate fiber should be provided in the diet to offset the tendency for constipation. Safety precautions are taken, as necessary, when mental symptoms of hypercalcemia are present. The patient and family are informed that these men-tal changes are reversible with treatment. Increased calcium po-tentiates the effects of digitalis; therefore, the patient is assessed for signs and symptoms of digitalis toxicity. ECG changes (pre-mature ventricular contractions, paroxysmal atrial tachycardia, and heart block) can occur; therefore, the cardiac rate and rhythm are monitored for any abnormalities.
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