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
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
calciumâ€“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
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
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.
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
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-tientâ€™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.