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Hypercalcemia is caused by excessive release of calcium from bone, almost always from malignancy, hyperparathyroidism, thiazide-diuretic use, or excessive calcium intake.

Pathophysiology and Etiology

Most symptoms of hypercalcemia are present only when the serum cal-cium level is greater than 12 mg/dL and tend to be more severe if hyper-calcemia develops quickly. Causes of hyperhyper-calcemia include hyperparathyroidism, Paget’s disease, multiple fractures, and overuse of calcium-containing antacids. Patients with solid tumors that have metas-tasized, such as breast, prostate, and malignant melanomas, and hemato-logic tumors, such as lymphomas, acute leukemia, and myelomas, are also at risk for developing hypercalcemia.

Drugs that predispose an individual to hypercalcemia include cal-Nursing Points-of-Care: Hypocalcemia

Nursing assessments include:

1. Obtain history relative to potential causes of hypocalcemia, such as low-calcium diet, lack of vitamin D, low-protein diet, chronic diarrhea, or hormonal disorders.

2. Obtain history of drugs that could predispose the patient to hypocalcemia, such as furosemide (Lasix) or cortisone.

3. Assess for signs of hypocalcemia.

4. Obtain baseline values for serum calcium, ionized calcium serum albumin, and acid–base status.

Key nursing interventions include:

1. Taking safety precautions and preparing to adopt seizure pre-cautions if hypocalcemia is severe

2. Monitoring laboratory test results with emphasis on serum and ionized calcium

3. Monitoring ECGs for changes in pattern

4. Monitoring for irritation of subcutaneous tissue and tissue sloughing when calcium is given parenterally

5. Monitoring for signs of cardiac arrhythmias in patients receiv-ing digitalis and calcium supplements

6. Monitoring for hypocalcemia in patients receiving massive transfusion of citrated blood

cium salts, megadoses of vitamin A or D, thiazide diuretics (potentiate the action of PTH), androgens or estrogen for breast cancer therapy, I.V.

lipids, lithium, and tamoxifen.

Signs and Symptoms

Patients with hypercalcemia may experience neuromuscular symptoms such as muscle weakness, incoordination, lethargy, deep bone pain, flank pain, and pathologic fractures (caused by bone weakening). Other symp-toms include constipation, anorexia, nausea, vomiting, polyuria or poly-dipsia leading to uremia if not treated, and renal colic caused by stone formation. Patients taking digitalis must take calcium with extreme care because it can precipitate severe dysrhythmias.

Diagnostic Tests

■ Total serum calcium: May be more than 10.5 mg/dL.

■ Serum ionized calcium: Greater than 5.5 mg/dL

■ Serum parathyroid hormone: Increased levels in primary or sec-ondary hyperparathyroidism

■ Radiography: May reveal osteoporosis, bone cavitation, or urinary calculi.

Treatment and Management

Hypercalcemia should be treated according to the following guidelines:

1. Treat the patient’s underlying disease.

2. Administer saline diuresis. Fluids should be forced to help elimi-nate the source of the hypercalcemia. A solution of 0.45 percent NaCl or 0.9 percent NaCl I.V. dilutes the serum calcium level.

Rehydration is important to dilute the Ca^2⫹ion and promote renal excretion.

3. Give inorganic phosphate salts orally (Neutra-Phos) or rectally (Fleet Enema).

4. Provide hemodialysis or peritoneal dialysis to reduce serum cal-cium levels in life-threatening situations.

5. Use furosemide, 20 to 40 mg every 2 hours, to prevent volume overloading during saline administration.

6. Administer calcitonin, 4 to 8 U/kg intramuscularly or subcuta-neously every 6 to 12 hours. This will temporarily lower the serum calcium level by 1 to 3 mg/100 mL.

7. Give bisphosphonates to inhibit bone reabsorption. Pamidronate is effective, 60 to 90 mg in 1 L of 0.9 percent NaCl or 5 percent dex-trose in water is infused over 24 hours.

8. Administer plicamycin (mithramycin), which inhibits bone reab-sorption and reliably lowers serum calcium. It is used only in those with malignant hypercalcemia because of its toxicity. A single dose of 25 g/kg in 500 mL of 5 percent dextrose in water is infused intravenously over 4 to 6 hours (Phillips & Kuhn, 1999).

Magnesium (Mg

)

Normal Reference Value: 1.5 to 2.5 mEq/L

Physiologic Role

The physiologic role of magnesium includes:

■ Enzyme action

■ Regulation of neuromuscular activity (similar to calcium)

■ Regulation of electrolyte balance, including facilitating transport of sodium and potassium across cell membranes, influencing the uti-lization of calcium, potassium, and protein

Magnesium is a major intracellular electrolyte. The normal diet sup-plies approximately 25 mEq of magnesium. Approximately one third of

Nursing Points-of-Care: Hypercalcemia Nursing assessment includes:

1. Obtain a patient history of probable cause of hypercalcemia, such as cancer; excessive use of calcium supplements, antacids, or thiazide diuretics; or steroid therapy.

2. Assess for signs of hypercalcemia.

3. Obtain baseline values for serum calcium and serum phosphate.

4. Obtain baseline ECG.

5. Assess client’s fluid volume status and mental alertness.

Key nursing interventions include:

1. Monitoring changes in vital signs and laboratory tests 2. Encouraging the patient to drink 3 to 4 L of fluid per day 3. Encouraging the patient to consume fluids (e.g., cranberry or

prune juice) that promote urine acidity to help prevent forma-tion of renal calculi

4. Keeping accurate fluid intake and output records 5. Monitoring for digitalis toxicity

6. Handling the patient gently to prevent fractures 7. Encouraging the patient to avoid high-calcium foods

serum magnesium is bound to protein; the remaining two thirds exists as free cations. The same factors that regulate calcium balance have an influ-ence on magnesium balance. Magnesium balance is also affected by many of the same agents that decrease or influence potassium balance.

Magnesium acts directly on the myoneural junction and affects neu-romuscular irritability and contractility, possibly exerting a sedative effect. Magnesium acts as an activator for many enzymes and plays a role in both carbohydrate and protein metabolism. Magnesium affects the car-diovascular system, acting peripherally to produce vasodilation.

Imbalances in magnesium predispose the heart to ventricular dysrhyth-mias (Metheny, 2000).