Calcium Imbalance

Calcium Imbalance

I. INTRODUCTION: Calcium (Ca), an extracellular and intracellular cation, has a normal serum range of 4.5 to 5.5 mEq/L or 9 to 11 mg/dl. Approximately, 99% of the body’s calcium is in bone and teeth. The other 1% is in tissue and intravascular fluid, of which half is bound to protein, mostly albumin, and the remaining half is free, ionized calcium. It has many functions in the body. It acts as a catalyst in the transmission and conduction of nerve impulses and stimulates the contraction of skeletal, smooth, and cardiac muscles. It maintains normal cellular permeability. Increased serum calcium levels decrease cellular permeability, and decreased serum calcium levels increase cellular permeability. It promotes coagulation of blood in all phases but mostly the prothrombin to thrombin phase. Calcium promotes absorption and utilization of vitamin B12. Finally, it promotes strong and durable bones and teeth. Calcium is excreted in the urine and feces. II. DISEASE ENTITY: A. Hypocalcemia •

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Cardiovascular complications: In severe cases, hypocalcemia may lead to arrhythmias, hypotension, and heart failure. Some patients may manifest digitalis insensitivity. Neurologic complications: In addition to acute seizures or tetany, hypocalcemia may lead to basal ganglia calcification, parkinsonism, hemiballisms, and choreoathetosis. Although some patients with hypocalcemia may improve with treatment, the calcification typically is not reversible. Hungry bone syndrome Surgical correction of primary or secondary hyperparathyroidism may be associated with severe hypocalcemia due to a rapid increase in bone remodeling. Hypocalcemia results if the rate of skeletal mineralization exceeds the rate of osteoclast-mediated bone resorption. A less severe picture is also observed after correction of thyrotoxicosis, after institution of vitamin D therapy

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for osteomalacia, and with tumors associated with bone formation (eg, prostate, breast, leukemia). Acute pancreatitis Pancreatitis can be associated with tetany and hypocalcemia. It is caused primarily by precipitation of calcium soaps in the abdominal cavity, but glucagon-stimulated calcitonin release and decreased PTH secretion may play a role. When the pancreas is damaged, free fatty acids are generated by the action of pancreatic lipase. Insoluble calcium salts are present in the pancreas, and the free fatty acids avidly chelate the salts, resulting in calcium deposition in the retroperitoneum. B. Hypercalcemia

• Hypercalcemia affects nearly every organ system in the body, but it particularly affects the CNS and kidneys. • Renal effects include nephrolithiasis from the hypercalciuria. Distal renal tubular acidosis may be observed, and the increase in urine pH and hypocitraturia also may contribute to stone disease. Nephrogenic diabetes insipidus occurs from medullary calcium deposition and inhibition of aquaporin-2, the argininevasopressin–regulated water channel. Renal function may decrease due to hypercalcemia-induced renal vasoconstriction or if hypercalcemia is prolonged from calcium deposition (nephrocalcinosis) and interstitial renal disease. • High calcium levels also affect the conducting system of the heart and cause cardiac arrhythmias. Calcium has a positive inotropic effect. Hypercalcemia also causes hypertension, presumably from renal dysfunction and direct vasoconstriction. • The GI manifestations of hypercalcemia include anorexia, nausea, vomiting, and constipation. Prolonged hypercalcemia tends to cause high gastrin levels, which may contribute to peptic ulcer disease and may lead to pancreatitis or the deposition of calcium in any soft tissue. This deposition of calcium is especially prevalent if phosphorous levels also are elevated, as in renal failure. III. PATHOPHYSIOLOGY

A. Hypocalcemia ( serum calcium level below 4.5 mEq/L or 8.5

mg/dl ) A lack of PTH results in inactivity of osteoclasts and a consequent fall in serum calcium levels. Nerve fibers become more and more excitable and may discharge spontaneously, causing muscles to twitch and to go into spasms or even tetany. Spasms of the muscles of the larynx interfere with respiration and may lead to death. During hypocalcemia, the bone is stimulated to release calcium, which makes the bone osteoporotic and subject to fracture. Hypocalcemia increases capillary permeability; causes neuromuscular excitability of skeletal, smooth, and cardiac muscles; and decreases blood coagulation, which results in bleeding. Severe hypocalcemia causes neuromuscular excitability that result in tetany. If it is untreated, convulsions and death can occur. Acute hypocalcemia may cause cardiac insufficiency and cardiac dysrhythmias. B. Hypercalcemia ( serum level over 5.5 mEq/L or 11 mg/dL )

Because calcium levels are increased, there is a lesser gradient between the cell and the serum. There is also an increased amount of calcium in the cell. Therefore, the threshold becomes more difficult to achieve and the cell membrane becomes refractory to depolarization. As a result, cardiac and smooth muscle activity is decreased. Calcium in the bloodstream impairs renal function and it precipitates as a salt, forming renal stones. Some cancer tumors destroy the bone, whereas others such as lung and breast cancers cause an ectopic PTH production. Hypophosphatemia is a complication of excessive PTH production that promotes calcium retention. A shortened QT segment and depressed T waves may be seen on ECG. IV. MEDICAL MANAGEMENT ( Diagnostic Tests ): A. Hypocalcemia

Medical management is focused on determining and correcting the cause of the hypocalcemia. Other medical management is dictated by the level of the serum calcium. Imaging Studies •

Skeletal x-rays •

Disorders associated with rickets or osteomalacia present with the pathognomonic Looser zones, better observed in the pubic ramus, upper femoral bone, and ribs. o Osteoblastic metastases from certain tumors (eg, breast, prostate, lung) can cause hypocalcemia. CT scan of the head may show basal ganglia calcification and extrapyramidal neurologic symptoms (in idiopathic hypoparathyroidism). o

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Other Tests •

Electrocardiogram (ECG): Hypocalcemia leads to a prolonged QT interval and severe ST abnormalities (see Media file 1).

Procedures •

Bone biopsy: If the diagnosis of osteomalacia is suspected, a bone biopsy can determine the final diagnosis.

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Parathyroidectomy (subtotal or total) may be indicated in certain patients with severe secondary hyperparathyroidism and renal osteodystrophy

B. Hypercalcemia Imaging Studies •

Chest radiographs always should be performed to help rule out lung cancer or sarcoidosis. Other radiographs should be

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considered to help evaluate for possible malignancies, metastases, or Paget disease. Mammograms should be considered to help rule out breast cancer, and CT scan and ultrasound should be considered to help rule out renal cancer. When a biochemical diagnosis of primary hyperparathyroidism is made, CT scan, ultrasound, MRI, and radionuclide imaging of the parathyroid gland may be helpful to assist with preoperative localization.

Other Tests •

Miscellaneous o Peripheral smear o Serum and urine immunofixation electrophoresis

Procedures •

Tissue histology o Biopsy of solid tumor o Biopsy of bone marrow

V. MEDICATION: A. Hypocalcemia Drug Category: Electrolytes Restores serum calcium levels. Calcium chloride delivers 3 times more elemental calcium than calcium gluconate. Drug Name Calcium chloride Description Ventricular fibrillation not associated with hyperkalemia, digitalis toxicity, hypercalcemia, renal insufficiency, or cardiac disease. Preferred when patient is in cardiac arrest and in other serious cases. Ten mL of calcium chloride 10% (1 g/10 mL) contain

272 mg of elemental calcium. Documented hypersensitivity; ventricular fibrillation Contraindica not associated with hyperkalemia; digitalis toxicity; tions hypercalcemia; renal insufficiency; cardiac disease Coadministration with digoxin may cause arrhythmias; with thiazides, may induce hypercalcemia; may antagonize effects of calcium channel blockers, Interactions especially verapamil; decreases effects of atenolol, tetracyclines, salicylates, fluoroquinolones, and sodium polystyrene sulfonate C - Fetal risk revealed in studies in animals but not Pregnancy established or not studied in humans; may use if benefits outweigh risk to fetus Drug Name Calcium carbonate (Oystercal, Caltrate) Indicated to restore and maintain normocalcemia when Description hypocalcemia is not severe enough to warrant rapid replacement. Documented hypersensitivity; renal calculi; Contraindicat hypercalcemia; hypophosphatemia; renal or cardiac ions disease; digitalis toxicity May decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; large Interactions intakes of dietary fiber may decrease calcium absorption and levels; calcium potentiates digitalis effects C - Fetal risk revealed in studies in animals but not Pregnancy established or not studied in humans; may use if benefits outweigh risk to fetus Drug Category: Vitamins Restore calcium levels in conditions associated with vitamin D deficiency. Vitamin D helps control hyperparathyroidism in patients with chronic renal failure and end-stage renal disease. Drug Name Calcitriol (Calcijex, Rocaltrol)

Increases calcium levels by promoting calcium absorption in intestines and calcium retention in Description kidneys. To prevent hyperparathyroidism, patients on dialysis may require higher doses, >1 mcg/d divided 23 times per wk. Contraindicat Documented hypersensitivity; hypercalcemia; ions malabsorption syndrome; hyperphosphatemia Cholestyramine and colestipol decrease absorption of Interactions calcitriol; magnesium-containing antacids and thiazide diuretics can increase calcitriol effects C - Fetal risk revealed in studies in animals but not Pregnancy established or not studied in humans; may use if benefits outweigh risk to fetus B. Hypercalcemia Drug Category: Bisphosphonates Inhibit bone reabsorption. Drug Name Pamidronate (Aredia) Used after initial hydration to inhibit bone reabsorption Description and maintain low serum calcium levels, especially in hypercalcemia of malignancy and Paget disease. Contraindica Documented hypersensitivity; hypocalcemia tions Interactions None reported Monitor hypercalcemia-related parameters (eg, serum levels of calcium, phosphate, magnesium, and potassium) once treatment begins; adequate intake of calcium and vitamin D are necessary to prevent severe Precautions hypocalcemia; caution when administering bisphosphonates in patients with active upper GI problems; do not coadminister with alendronate for osteoporosis in postmenopausal women

Drug Category: Antineoplastic drugs Some agents in this drug class can reduce bone turnover. Drug Name Gallium nitrate (Ganite) Available in the United States. Use should be limited to Description those with extensive experience in this field (ie, oncologists). Contraindica Documented hypersensitivity; renal failure tions Nephrotoxic effects increase when administered with Interactions amphotericin B or aminoglycosides Precautions Caution in renal failure Drug Category: Antidote, hypercalcemia agents Inhibit bone resorption and increase renal calcium excretion. Drug Name Calcitonin (Miacalcin, Osteocalcin) Lowers elevated serum calcium in patients with multiple myeloma, carcinoma, or primary hyperparathyroidism. Expect higher response when serum calcium levels are high. Description Onset of action is approximately 2 h following injection, and activity lasts for 6-8 h. May lower calcium levels for 5-8 d by approximately 9% if given q12h. IM route is preferred at multiple injection sites with dose > 2 mL. Contraindicat Documented hypersensitivity ions Interactions None reported Hypocalcemia may occur; examine urine sediment Precautions during prolonged therapy Drug Category: Glucocorticoids Inhibit cytokine release and have a direct cytolytic effect on some tumor cells.

Drug Name Prednisone (Deltasone, Orasone, Sterapred) Immunosuppressant for treatment of autoimmune disorders; may decrease inflammation by reversing Description increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and suppresses lymphocytes and antibody production. Documented hypersensitivity; viral infection, peptic Contraindicat ulcer disease, hepatic dysfunction, connective tissue ions infections, and fungal or tubercular skin infections; GI disease Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; Interactions phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, Precautions osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use Drug Category: Minerals Phosphate inhibits calcium absorption and promotes calcium deposition. Theorized to help bind dietary calcium, thus rendering it an unabsorbable calcium-phosphorous product, but used rarely. Drug Name Potassium phosphate (Neutra-Phos-K) Increases urinary pyrophosphate and complexes with calcium, thus decreasing urinary calcium level, while pyridoxine results in a reduction of urinary oxalate Description excretion. All dosage forms must be mixed in 6-8 oz of water. Never give IV. Never give if renal function is abnormal or if serum phosphorous levels are > 3 mg/dL.

Contraindicat Abnormal renal function, renal failure, serum ions phosphorous >4.5 mg/dL; IV administration Magnesium-containing and aluminum-containing antacids or sucralfate can act as phosphate binders Interactions and decrease serum phosphate levels; potassiumsparing diuretics, ACE inhibitors, and salt substitutes may increase serum phosphate levels Caution in patients with renal insufficiency and metabolic alkalosis; admixture of phosphate and Precautions calcium in IV fluids can result in calcium phosphate precipitation

VI. NURSING MANAGEMENT: A. Hypocalcemia The nurse should have a high index of suspicion for those clients at risk for hypocalcemia and present with clinical manifestations. If neuromuscular and cardiac symptoms are present, the hypocalcemic state is usually severe. Assessing the medications and diet of the client is taking is important. If the client is taking a digitalis preparation, administration of calcium will enhance the action of digitalis and may cause digitalis toxicity. The client’s diet may also give clues to hypocalcemia due to malnutrition or lack of calcium intake. Two tests used to check for increased neuromuscular excitability and tetany are the Trousseau’s sign and Chvostek’s sign. The Trousseau’s sign is carpopedal spasm. It is best elicited by inflating a blood pressure cuff on the upper arm for 1-5 minutes, constricting circulation. A positive test result is carpopedal spasm. The Chvostek’s sign is spasm of the muscles innervated by the facial nerve. It is best determined by tapping the client’s face lightly below the temple. Spasm of the face, lip or nose would indicate a positive for tetany. B. Hypercalcemia

The nurse should have a high index of suspicion for those clients at risk for hypercalcemia or with early symptoms of this disorder. When the nurse notes an elevated serum calcium level, the nurse should assess the client for signs and symptoms of neuromuscular and cardiac changes associated with hypercalcemia. An accurate nursing history may identify factors such as excessive use of calcium supplements or calcium-containing antacids that could cause a mild to moderate hypercalcemia. A drug history is important for determining whether the medications the client is taking could be affected by the hypercalcemic state. For example, an increased calcium level enhances the action of digitoxin; thus, digitalis toxicity may result. The client’s hydration status should be assessed for fluid volume depletion caused by hypercalcemia. ECG changes and the state of the client’s sensorium should be reported.