Calcium Imbalance

What is Calcium Imbalance ?

Calcium plays an indispensable role in cell permeability, the formation of bones and teeth, blood coagulation, transmission of nerve impulses, and normal muscle contraction. Nearly all of the body's calcium is in the bones. The remaining exists in serum in three forms: ionized or free calcium (the only active, or available, calcium), calcium bound to protein, and calcium complexed with citrate or other organic ions.

Causes of Calcium Imbalance

Hypocalcemia may result from:

• inadequate intake of calcium and vitamin D. in which inadequate levels of vitamin D inhibit intestinal absorption of calcium
• hypoparathyroidism as a result of injury, disease, or surgery that 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, caused by 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, decreasing the solubility of calcium salts.)
• severe infections or burns, in which diseased and burned tissue traps calcium from the extracellular fluid
• alkalosis. in which calcium forms a complex with bicarbonate, causing decreased ionized calcium and inducing symptoms of hypocalcemia
• pancreatic insufficiency, which can cause malabsorption of calcium and subsequent calcium loss in stools (In acute pancreatitis, hypocalcemia varies in degree with the severity of the disorder. The exact cause of hypocalcemia in this instance is unknown).
• renal failure, resulting in excessive excretion of calcium (can also occur with the use of loop diuretics)
• hypomagnesemia, which causes decreased PTH secretion and blocks the peripheral action of that hormone
• hyperphosphatemia, which causes calcium levels to decrease as phosphorus levels increase
• extensive administration of citrated blood. which may result in citrate binding with calcium.

Hypercalcemia may result from:

• hyperparathyroidism, a primary cause. which increases serum calcium levels by promoting calcium absorption from the intestine, resorption from bone, and reabsorption from the kidneys
• hypervitaminosis D, which can promote increased absorption of calcium from the intestine
• some cancers, such as multiple myeloma, lymphoma, squamous cell carcinoma of the lung, and breast cancer, which 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, which release bone calcium and increase the serum calcium level.

Signs & Symptoms of Calcium Imbalance

If you have too little calcium, you may experience:

• Muscle spasms, twitching or cramps;
• Numbness and tingling in the arms, legs, hands and feet;
• Seizures;
• Irregular heartbeat;
• High blood pressure.

• Lethargy;
• Appetite loss;
• Vomiting and diarrhoea;
• Dehydration and thirst;
• Irregular heartbeat;
• Low blood pressure;
• Depression, delirium, confusion;
• Seizures or coma (worst cases only).

Diagnostic Tests

Total serum calcium levels are less than 8.5 mg/dl in hypocalcemia; greater than 10.5 mg/dl in hypercalcemia.

Ionized serum calcium levels less than 4.5 mg/dl confirm hypocalcemia; levels greater than 5.3 mg/dl confirm hypercalcemia. (Because about one-half of serum calcium is bound to albumin, changes in serum protein levels must be considered when interpreting serum calcium levels.)

Sulkowitch's urine test shows increased calcium precipitation in hypercalcemia.

Treatment

The aim of treatment is to correct acute imbalance, followed by maintenance therapy and correction of the underlying cause.

A patient with mild hypocalcemia may require only a diet adjustment 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, which is usually preferable to calcium chloride. If hypocalcemia is related to hypomagnesemia, magnesium replacement is necessary because hypocalcemia often doesn't respond to calcium therapy alone.

Patients with chronic hypocalcemia also require vitamin D supplements to facilitate GI calcium absorption. To correct mild deficiency, the amount of vitamin D in most multivitamin preparations is adequate. For severe deficiency, vitamin D is used in four forms: ergocalciferol (vitamin D2), cholecalciferol (vitamin D3), calcitriol, and dihydrotachysterol, a synthetic form of vitamin D2.

Treatment for patients with hypercalcemia that produces no symptoms may consist only of managing the underlying cause. Treatment of hypercalcemia that produces symptoms 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. (Thiazide diuretics are contraindicated in hypercalcemia because they inhibit calcium excretion.)

Corticosteroids, such as prednisone and hydrocortisone, are helpful in treating sarcoidosis, hypervitaminosis D, and certain tumors. Mithramycin can also lower serum calcium levels and is especially effective against hypercalcemia secondary to certain tumors. Calcitonin may also be helpful in certain instances. The administration of I.V. phosphates is potentially dangerous and is used only when other treatments prove ineffective.

Prevention Tips

• Eat a normal, balanced diet.
• Don’t drink more than 1 or 2 alcoholic drinks, if any, a day.
• Don’t use non-prescription antacids on a regular basis.