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Chapter: Medical Surgical Nursing: Fluid and Electrolytes: Balance and Distribution

Calcium Deficit (Hypocalcemia)

Hypocalcemia (lower-than-normal serum concentration of cal-cium) occurs in a variety of clinical situations.

CALCIUM DEFICIT (HYPOCALCEMIA)

 

Hypocalcemia (lower-than-normal serum concentration of cal-cium) occurs in a variety of clinical situations. A patient may have a total body calcium deficit (as in osteoporosis) but a normal serum calcium level. Elderly people with osteoporosis, who spend an increased amount of time in bed, are at increased risk for hypo-calcemia as bed rest increases bone resorption.

Several factors can cause hypocalcemia. Primary hypopara-thyroidism results in this disturbance, as does surgical hypo-parathyroidism. The latter is far more common. Not only is hypocalcemia associated with thyroid and parathyroid surgery, but it can also occur after radical neck dissection and is most likely in the first 24 to 48 hours after surgery. Transient hypo-calcemia can occur with massive administration of citrated blood (as in exchange transfusions in newborns), because citrate can combine with ionized calcium and temporarily remove it from the circulation.

 

Inflammation of the pancreas causes the breakdown of pro-teins and lipids. It is thought that calcium ions combine with the fatty acids released by lipolysis, forming soaps. As a result of this process, hypocalcemia occurs and is common in pancreatitis. It has also been suggested that hypocalcemia might be related to ex-cessive secretion of glucagon from the inflamed pancreas, result-ing in increased secretion of calcitonin (a hormone that lowers serum calcium).

 

Hypocalcemia is common in patients with renal failure be-cause these patients frequently have elevated serum phosphate levels. Hyperphosphatemia usually causes a reciprocal drop in the serum calcium level. Other causes of hypocalcemia include inadequate vitamin D consumption, magnesium deficiency, me-dullary thyroid carcinoma, low serum albumin levels, alkalosis, and alcohol abuse. Medications predisposing to hypocalcemia in-clude aluminum-containing antacids, aminoglycosides, caffeine, cisplatin, corticosteroids, mithramycin, phosphates, isoniazid, and loop diuretics.

 

Osteoporosis is associated with prolonged low intake of cal-cium and represents a total body calcium deficit, even though serum calcium levels are usually normal. This disorder occurs in millions of Americans and is most common in postmenopausal women. It is characterized by loss of bone mass, causing bones to become porous and brittle and therefore susceptible to fracture.

Clinical Manifestations

Tetany is the most characteristic manifestation of hypocalcemia and hypomagnesemia. Tetany refers to the entire symptom com-plex induced by increased neural excitability. These symptoms are due to spontaneous discharges of both sensory and motor fibers in peripheral nerves. Sensations of tingling may occur in the tips of the fingers, around the mouth, and less commonly in the feet. Spasms of the muscles of the extremities and face may occur. Pain may develop as a result of these spasms.

 

Trousseau’s sign (Fig. 14-6) can be elicited by inflating a blood pressure cuff on the upper arm to about 20 mm Hg above systolic pressure; within 2 to 5 minutes, carpopedal spasm (an adducted thumb, flexed wrist and metacarpophalangeal joints, extended in-terphalangeal joints with fingers together) will occur as ischemia of the ulnar nerve develops. Chvostek’s sign consists of twitching of muscles supplied by the facial nerve when the nerve is tapped about 2 cm anterior to the earlobe, just below the zygomatic arch.


 

Seizures may occur because hypocalcemia increases irritability of the central nervous system as well as of the peripheral nerves. Other changes associated with hypocalcemia include mental changes such as depression, impaired memory, confusion, delir-ium, and even hallucinations. A prolonged QT interval is seen on the ECG due to prolongation of the ST segment; a form of ven-tricular tachycardia called torsades de pointes may occur.

Assessment and Diagnostic Findings

When evaluating serum calcium levels, one must consider several other variables, such as the serum albumin level and arterial pH. Because abnormalities in serum albumin levels may affect inter-pretation of the serum calcium level, it may be necessary to cal-culate the corrected serum calcium if the serum albumin level is abnormal. For every decrease in serum albumin of 1 g/dL below 4 g/dL, the total serum calcium level is underestimated by ap-proximately 0.8 mg/dL. The following is a quick method to cal-culate the corrected serum calcium level:


An example of the calculations needed to obtain the corrected total serum calcium level is as follows:

 

A patient’s reported serum albumin level is 2.5 g/dL; the re-ported serum calcium level is 10.5 mg/dL.

 

The decrease in serum albumin level from normal level (difference from normal albumin of 4 g/dL) is calculated: 4 g/dL 2.5 g/dL = 1.5 g/dL

 

The following ratio is calculated:

 

0.8 mg/dL: 1 g/dL = ?mg/dL: 1.5 mg/dL

               = 0.8 mg × 1.5

               = 1.2 mg/dL calcium

Add 1.2 to 10.5 mg (reported serum calcium level) to ob-tain the corrected total serum calcium level of 11.7 mg/dL. 1.2 + 10.5 mg = 11.7 mg/dL

 

Clinicians often ignore a low serum calcium level in the pres-ence of a similarly low serum albumin level. The ionized cal-cium level is usually normal in patients with reduced total serum calcium levels and concomitant hypoalbuminemia. When the arterial pH increases (alkalosis), more calcium becomes bound to protein. As a result, the ionized portion decreases. Symptoms of hypocalcemia may occur with alkalosis. Acidosis (low pH) has the opposite effect—that is, less calcium is bound to protein and thus more exists in the ionized form. However, relatively small changes in serum calcium levels occur in these acid–base abnormalities.

Ideally, the laboratory should measure the ionized level of cal-cium. In many laboratories, however, only the total calcium level is reported; thus, concentration of the ionized fraction must be estimated by simultaneous measurement of the serum albumin level. PTH levels are decreased in hypoparathyroidism. Magne-sium and phosphorus levels need to be assessed to identify possible causes of decreased calcium.

 

Medical Management

Acute symptomatic hypocalcemia is life-threatening and re-quires prompt treatment with IV administration of calcium (Marx, 2000). Parenteral calcium salts include calcium gluco-nate, calcium chloride, and calcium gluceptate. Although cal-cium chloride produces a significantly higher ionized calcium level than calcium gluconate, it is not used as often because it is more irritating and can cause sloughing of tissue if it infiltrates. Too-rapid IV administration of calcium can cause cardiac arrest, preceded by bradycardia. IV calcium administration is particu-larly dangerous in patients receiving digitalis-derived medica-tions because calcium ions exert an effect similar to that of digitalis and can cause digitalis toxicity, with adverse cardiac ef-fects. IV calcium should be diluted in D5W and given as a slow IV bolus or a slow IV infusion using a volumetric infusion pump. The IV site must be observed often for any evidence of infiltra-tion because of the risk for sloughing of tissues with calcium in-fusions. A 0.9% sodium chloride solution should not be used with calcium because it will increase renal calcium loss. Solu-tions containing phosphates or bicarbonate should not be used with calcium because they will cause precipitation when cal-cium is added. The nurse must clarify with the physician which calcium salt to administer, because calcium gluconate yields 4.5 mEq of calcium and calcium chloride provides 13.6 mEq of calcium. Calcium can cause postural hypotension; therefore, the patient is kept in bed for IV replacement and blood pressure is monitored.

 

Vitamin D therapy may be instituted to increase calcium absorption from the GI tract. Aluminum hydroxide, calcium acetate, or calcium carbonate antacids may be prescribed to decrease elevated phosphorus levels before treating hypocal-cemia for the patient with chronic renal failure. Increasing the dietary intake of calcium to at least 1,000 to 1,500 mg/day in the adult is recommended (eg, milk products; green, leafy veg-etables; canned salmon; sardines; fresh oysters). Because hypo-magnesemia can also cause tetany, if the tetany responds to IV calcium, then a low magnesium level is explored as a possible cause in chronic renal failure.

Nursing Management

It is important to observe for hypocalcemia in patients at risk. Seizure precautions are initiated when hypocalcemia is severe. The status of the airway is closely monitored because laryngeal stridor can occur. Safety precautions are taken, as indicated, if confusion is present.

 

People at high risk for osteoporosis are instructed about the need for adequate dietary calcium intake; if not consumed in the diet, calcium supplements should be considered. Also, the value of regular weight-bearing exercise in decreasing bone loss should be emphasized, as should the effect of medications on calcium bal-ance. For example, alcohol and caffeine in high doses inhibit cal-cium absorption, and moderate cigarette smoking increases urinary calcium excretion. Additional teaching topics may involve discus-sion of medications such as alendronate (Fosamax), risedronate (Actonel), raloxifene (Evista), and calcitonin to reduce the rate of bone loss. Teaching also addresses strategies to reduce risk for falls.

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Medical Surgical Nursing: Fluid and Electrolytes: Balance and Distribution : Calcium Deficit (Hypocalcemia) |


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