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 found 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 combined with citrate or other organic ions.
Maintaining stable levels of ionized calcium in the serum is critical to 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.
Causes
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 reduces 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, laxative abuse, gastric or intestinal resection, or small bowel disease; from inadequate levels of vitamin D or PTH; or from a reduction in gastric acidity.
severe infections or burns, in which diseased or burned tissue traps calcium from the extracellular fluid
alkalosis, in which calcium forms a complex with bicarbonate, causing diminished levels of ionized calcium and inducing symptoms of hypocalcemia
pancreatic insufficiency, which may cause malabsorption of calcium and subsequent calcium loss in stool; in acute pancreatitis, hypocalcemia varies in degree with the disorder’s severity and is of unknown origin
renal failure or use of loop diuretics, resulting in excessive excretion of calcium
hypomagnesemia, which causes decreased PTH secretion and blocks the peripheral action of that hormone
hyperphosphatemia, which causes calcium levels to decrease as phosphorus levels rise
extensive administration of citrated blood, which may result in citrate binding with calcium
osteoblast metastasis, which is attributed to increased calcium influx into osteoblastic lesions
altered liver metabolism of vitamin D caused by hepatotoxic effects of drugs or chronic alcoholism.
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 may increase absorption of calcium from the intestine
Identifying calcium imbalance
Serum calcium levels help you identify a patient’s calcium imbalance.
To identify hypocalcemia, look for:
total serum calcium level less than 8.5 mg/dl
ionized serum calcium level less than 4.5 mg/dl.
To identify hypercalcemia, look for:
total serum calcium level greater than 11.0 mg/dl
ionized serum calcium level greater than 5.3 mg/dl.
Note: Because about one-half of serum calcium is bound to albumin, you must consider changes in serum protein levels when interpreting serum calcium levels.
multiple fractures and prolonged immobilization, which release bone calcium and raise the serum calcium level.
Other causes of hypercalcemia include milk-alkali syndrome, sarcoidosis, hyperthyroidism, adrenal insufficiency, thiazide diuretics, and excessive administration of calcium during cardiopulmonary arrest.
Complications
Severe hypocalcemia can lead to laryngeal spasm, seizures and, possibly, respiratory arrest. Cardiac arrhythmias may also occur.
In hypercalcemia, serum calcium levels greater than 13.5 mg/dl may cause coma and cardiac arrest. Hypercalcemia may also lead to renal calculi and bone demineralization (osteitis fibrose cystica).
Assessment
The history of a patient with hypocalcemia may disclose risk factors, such as hypothyroidism or renal failure. The patient may report digital and perioral paresthesia and muscle cramps. Inspection may reveal twitching, carpopedal spasm, tetany, and seizures. Auscultation sometimes detects cardiac arrhythmias. Also, a physical examination may uncover reliable indicators of hypocalcemia, including hyperactive reflexes, a positive Trousseau’s sign, and a positive Chvostek’s sign.
A patient with hypercalcemia may have a history of risk factors, such as excessive ingestion of vitamin D or prolonged immobilization. He may complain of lethargy, weakness, bone pain, anorexia, constipation, nausea, vomiting, and polyuria. Family members may report personality changes.
During assessment, the patient may appear confused or, in severe cases, comatose. Neuromuscular assessment may reveal weakness, with hyporeflexia and decreased muscle tone.
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