Calcium imbalance
Calcium imbalance: Excerpt from Handbook of Diseases
Calcium plays an indispensable role in cell permeability, formation of bones and teeth, blood coagulation, transmission of nerve impulses, and normal muscle contraction. Nearly all (99%) of the body’s calcium is found in the bones. The remaining 1% exists in ionized form in serum, and it’s the maintenance of the 1% of ionized calcium in the serum that’s critical to healthy neurologic function.
The parathyroid glands regulate ionized calcium and determine its resorption into bone, absorption from the GI mucosa, and excretion in urine and stool. Severe calcium imbalance requires emergency treatment because a deficiency (hypocalcemia) can lead to tetany and seizures; an excess (hypercalcemia), to cardiac arrhythmias and coma.
Causes
Several factors can cause calcium imbalance.
Hypocalcemia
❑ Inadequate intake of calcium and vitamin D results in inhibited intestinal absorption of calcium.
❑ Hypoparathyroidism as a result of injury, disease, or surgery decreases or eliminates secretion of parathyroid hormone (PTH), which is necessary for calcium absorption and normal serum calcium levels.
❑ Malabsorption or loss of calcium from the GI tract can result from increased intestinal motility from severe diarrhea or laxative abuse. Malabsorption of calcium from the GI tract can also result from inadequate levels of vitamin D or PTH or a reduction in gastric acidity, which decreases the solubility of calcium salts.
❑ Severe infections or burns can lead to diseased and burned tissue trapping calcium from the extracellular fluid.
❑ Overcorrection of acidosis can lead to alkalosis, which causes decreased ionized calcium and induces symptoms of hypocalcemia.
❑ Pancreatic insufficiency may cause malabsorption of calcium and subsequent calcium loss in stool. In pancreatitis, participation of calcium ions in saponification contributes to calcium loss.
❑ Renal failure results in excessive excretion of calcium secondary to increased phosphate retention. Renal failure also results in loss of the active metabolite of vitamin D, which impairs calcium absorption.
❑ Hypomagnesemia causes decreased PTH secretion and blocks the peripheral action of that hormone.
Hypercalcemia
❑ Hyperparathyroidism increases serum calcium levels by promoting calcium absorption from the intestine, resorption from bone, and reabsorption from the kidneys.
❑ Hypervitaminosis D can promote increased absorption of calcium from the intestine.
❑ Tumors raise serum calcium levels by destroying bone or by releasing PTH or a PTH-like substance, osteoclast-activating factor, prostaglandins and, perhaps, a vitamin D–like sterol.
❑ Multiple fractures and prolonged immobilization release bone calcium and raise the serum calcium level.
❑ Multiple myeloma promotes loss of calcium from bone.
Other causes include milk-alkali syndrome, sarcoidosis, hyperthyroidism, adrenal insufficiency, and thiazide diuretics.
Signs and symptoms
Indications of calcium imbalance depend on the type of imbalance. (See Signs and symptoms of calcium imbalance.)
Hypocalcemia
A lack of calcium causes nerve fiber irritability and repetitive muscle spasms. Consequently, characteristic signs and symptoms of hypocalcemia include perioral paresthesia, twitching, carpopedal spasm, tetany, seizures and, possibly, cardiac arrhythmias. Although Chvostek’s and Trousseau’s signs are reliable indicators of hypocalcemia, they aren’t specific.
Hypercalcemia
Signs and symptoms of hypercalcemia include muscle weakness, decreased muscle tone, lethargy, anorexia, constipation, nausea, vomiting, dehydration, polydipsia, and polyuria. When calcium levels are greater than 3.2 mmol/L (13 mg/dL), calcification in kidneys, skin, vessels, lungs, heart, and stomach occurs and renal insufficiency may develop, especially if blood phosphate levels are normal or elevated due to impaired renal function. Severe hypercalcemia (serum levels that exceed 4.5 mmol/L or greater than 18 mg/dL) may produce cardiac arrhythmias and, eventually, coma.
Diagnosis
A serum calcium level below 4.5 mEq/L confirms hypocalcemia; a level above 5.5 mEq/L confirms hypercalcemia. (However, because about half of serum calcium is bound to albumin, changes in serum protein must be considered when interpreting serum calcium levels.)
In patients with hypercalcemia, urine test results show an increase in urine calcium precipitation. In those with hypocalcemia, an electrocardiogram (ECG) reveals a lengthened QT interval, a prolonged ST segment, and arrhythmias; in those with hypercalcemia, an ECG reveals a shortened QT interval and heart block.
Treatment
An acute imbalance requires immediate correction, followed by maintenance therapy and correction of the underlying cause.
Hypocalcemia
A mild calcium deficit may require nothing more than an adjustment in diet to allow adequate intake of calcium, vitamin D, and protein, possibly with oral calcium supplements. Acute hypocalcemia is an emergency that needs immediate correction by I.V. administration of calcium gluconate or calcium chloride.
Chronic hypocalcemia also requires vitamin D supplements to facilitate GI absorption of calcium. Although the amount of vitamin D in most multivitamin preparations is adequate to correct a mild deficiency, different forms of vitamin D are used for severe deficiency, including ergocalciferol (vitamin D2), cholecalciferol (vitamin D3), calcitriol, and dihydrotachysterol, a synthetic form of vitamin D2.
Hypercalcemia
Treatment of hypercalcemia primarily eliminates excess serum calcium through hydration with normal saline solution, which promotes calcium excretion in urine. Loop diuretics, such as ethacrynic acid and furosemide, also promote calcium excretion. (Because thiazide diuretics inhibit calcium excretion, they’re contraindicated in hypercalcemic patients.)
Corticosteroids, such as prednisone and hydrocortisone, are helpful in treating sarcoidosis, hypervitaminosis D, and certain tumors. Plicamycin can lower the serum calcium level and is especially effective against hypercalcemia secondary to certain tumors. Calcitonin may also be helpful in certain instances.
Sodium phosphate solution administered by mouth or by retention enema promotes calcium deposits in bone and inhibits its absorption from the GI tract.
Special considerations
Clinical tip If the patient is receiving massive transfusions of citrated blood or has chronic diarrhea, severe infection, or insufficient dietary intake of calcium or protein (common in elderly patients), monitor him for hypocalcemia.
If the patient has hypocalcemia:
❑ Monitor serum calcium levels every 12 to 24 hours; a calcium level below 4.5 mEq/L requires immediate attention. When giving calcium supplements, frequently check the pH level; an alkalotic state that exceeds 7.45 pH inhibits calcium ionization. Check for Chvostek’s and Trousseau’s signs.
❑ Slowly administer I.V. calcium gluconate in dextrose 5% in water (never in saline solution, which encourages renal calcium loss). Don’t add I.V. calcium gluconate to solutions containing bicarbonate; it will precipitate.
❑ When administering calcium solutions, watch for anorexia, nausea, and vomiting, which are signs of overcorrection of hypercalcemia.
❑ If the patient is receiving calcium chloride, watch for abdominal discomfort.
❑ If the patient is receiving a cardiac glycoside with large doses of oral calcium supplements, monitor him closely for a possible drug interaction; also watch for signs and symptoms of digitalis toxicity, including anorexia, nausea, vomiting, yellow vision, and cardiac arrhythmias. Administer an oral calcium supplement 1 to 1½ hours after meals or with milk.
❑ Observe seizure precautions for patients with severe hypocalcemia that may lead to seizures.
❑ Warn the patient not to overuse antacids because they may aggravate his condition.
❑ To prevent hypocalcemia, advise all patients (especially elderly ones) to eat foods rich in calcium, vitamin D, and protein, such as fortified milk and cheese, soybean products, and sardines. Explain how important calcium is for normal bone formation and blood coagulation. Discourage long-term use of laxatives.
If the patient has hypercalcemia:
❑ Monitor serum calcium levels frequently. If the serum calcium level exceeds 5.7 mEq/L, watch for cardiac arrhythmias. Increase fluid intake to dilute calcium in serum and urine and to prevent renal damage and dehydration.
❑ If the patient is receiving normal saline solution diuresis therapy, monitor him for signs of heart failure.
❑ Administer a loop diuretic (not a thiazide diuretic). Monitor intake and output, and check the urine for renal calculi and acidity. Provide acid-ash drinks, such as cranberry or prune juice, because calcium salts are more soluble in acid than in alkali.
❑ Frequently check the patient’s ECG and vital signs. If the patient is receiving a cardiac glycoside, watch for signs and symptoms of toxicity, such as anorexia, nausea, vomiting, and bradycardia (common with arrhythmia).
❑ If the patient has chronic hypercalcemia, handle him gently to prevent pathologic fractures.
❑ If the patient is bedridden, reposition him frequently, and encourage range-of-motion exercises to promote circulation and prevent urinary stasis and calcium loss from bone.
❑ To prevent recurrence, suggest a low-calcium diet and increased fluid intake.
Pictures
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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