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Calcium Imbalances

Hyper- and hypocalcemia can lead to life-threatening events.

This offering expires in 2 years: June 9, 2010

The goal of this continuing education offering is to provide nurses with current information on calcium imbalances. After reading this article, you will be able to:

1. Describe patient characteristics that increase the risk for calcium imbalances.

2. Relate pathophysiology of calcium imbalances to assessment findings.

3. Apply principles of collaborative management of patients with calcium imbalances to case studies.

You can earn 1 contact hour of continuing education credit in three ways: 1) For im-mediate results and certificate, go to Grade and certificate are available immediately after taking the online test. 2) Send this answer sheet (or a photocopy) along with the $8 fee (check or credit card) to ADVANCE for Nurses, Learning Scope, 2900 Horizon Dr., King of Prussia, PA 19406. 3) Fax the answer sheet to 610-278-1426. If faxing or mailing, allow 30 days to receive certificate or notice of failure. A certificate of credit will be awarded to participants who achieve a passing grade of 70 percent or better.

Merion Publications Inc. is an approved provider of continuing nursing education by the Pennsylvania State Nurses Association (No. 008-0-07), an accredited approver by the American Nurses Credentialing Center's Commission on Accreditation. Merion Publications Inc. is also approved as a provider by the California Board of Registered Nursing (No. 13230) and by the Florida Board of Nursing (No. 3298).


Calcium plays a major role in normal function of the neuromuscular, cardiovascular, renal and hematologic systems. A calcium imbalance can result in alteration in one or all of these systems and place patients who are acutely ill in a life-threatening situation.

Keys to providing effective nursing care for patients with calcium imbalances are:

  • monitoring patients at risk for hypocalcemia or hypercalcemia;
  • assessing for signs and symptoms related to calcium function; and
  • providing nursing care based on knowledge of the normal function of calcium and underlying pathophysiologies of calcium deficiencies.

Who's at Risk?

Hypocalcemia is identified by a total serum calcium level less than 8.5 mg/dL or an ionized (free) calcium less than 4.4 mg/dL. Common risk factors for low calcium can be found in patients who have had neck surgery or radiation, and those with renal failure, pancreatitis, rhabdomyolysis, magnesium deficiency or low albumin.

Patients with neck surgery or radiation are at risk because of potential injury to the parathyroid glands, small glands attached to the thyroid. The parathyroids produce parathyroid hormone (PTH) (see Figure 1). PTH regulates calcium balance through three mechanisms:

  • absorption of calcium via the gut from food;
  • reabsorption of calcium from the kidneys; and
  • absorption of calcium from bone.

If the parathyroid glands are destroyed or experience reduction in blood flow during surgery or via radiation to the neck, PTH is not available to correct low calcium levels in the serum.

Patients with renal failure cannot excrete phosphate, an electrolyte that has an inverse relationship with calcium. As phosphate levels rise in renal failure, calcium levels decrease to maintain the necessary relationship. Patients with renal failure, both acute and chronic, are at risk for hypocalcemia.

Pancreatitis causes calcium soaps to form in the peritoneum, resulting in hypocalcemia. Formation of calcium salts also may lead to hypocalcemia in rhabdomyolysis as the calcium salts are deposited in injured muscles.1

Low serum magnesium levels (normal 2-5 mg/dL) may result in hypocalcemia for patients who are acutely ill. Magnesium assists in PTH secretion and calcium use by the peripheral cells.

Patients with low albumin may have hypocalcemia reflected in total serum calcium. Normally, 40 percent of body calcium is bound to proteins as albumin. Patients with low albumin may have a low serum calcium level not reflective of the active or ionized calcium in their system. The measurement of ionized calcium is the best test of calcium balance in patients with low albumin.2Patients with hypercalcemia have a serum calcium level greater than 10.5 mg/dL or ionized calcium greater than 5.4 mg/dL. Common causes of hypercalcemia are hyperparathyroidism or malignancies that cause the release of calcium from the bone by tumor invasion.

Hyperparathyroidism causes high calcium levels by overproduction of PTH. When excess PTH is produced by overactive glands, calcium levels rise unchecked with resulting clinical manifestations of hypercalcemia.

Patients with chronic renal failure may develop hyperparathyroidism if elevated phosphate levels, due to lack of excretion of phosphate by the kidney, exist over months or years. Low calcium levels occur to maintain the normal inverse relationship of phosphate and calcium. The parathyroid glands hypertrophy in the patient with chronic hypocalcemia, leading to excess PTH production and hypercalcemia.

Malignancies, especially from breast and lung cancers as well as multiple myeloma, may invade bone, leading to release of calcium from the bone into the serum. These tumors also may produce a PTH-like protein that causes bone to release calcium, resulting in elevated calcium levels.3

Hypocalcemia Case Study

Mr. C is a 65-year-old patient who had subtotal thyroidectomy yesterday. This morning, he complains of pins and needles in his hands and feet and difficulty "getting my breath." His blood pressure is 90/60 with heart rate of 70.

Here are his labs:

  • calcium level = 7 mg/dL (8.5-10.5 mg/dL)
  • ionized calcium = 3 mg/dL (4.4-4.5 mg/dL)
  • albumin = 4.5 mg/dL (4.4 mg/dL)
  • phosphate = 4.0 mg/dL (3.0-4.5 mg/dL)
  • magnesium = 1.8 mg/dL (1.3-2.1 mEq/L)

Pulse ox is 87 percent on room air. During blood pressure measurement, Mr. C's hand develops a carpal spasm, indicating a Trousseau's sign.

Calcium levels less than 8.5 mg/dL in this case are related to lack of PTH to respond to low calcium levels. Low calcium levels would normally cause release of PTH, leading to increased absorption of calcium. This action would bring the calcium back to a normal range in the serum.

Serum albumin, phosphate and magnesium levels should be evaluated in the patient with hypocalcemia.4 Since 40 percent of calcium is bound to albumin, low albumin levels will result in low total erum calcium, but ionized calcium is usually normal (see Figure 2). Patients with elevated phosphate levels require phosphate control to normalize calcium. Correction of low magnesium may help correct low calcium as magnesium helps increase calcium absorption to the serum from the gut. All of Mr. C's levels of these key elements in calcium balance are normal.

In Mr. C's situation, the parathyroid glands are missing or injured due to surgery and cannot respond to lowered calcium. This common reason for hypocalcemia usually self-corrects 1-2 days after surgery as the parathyroid glands recover function.

Signs and symptoms of hypocalcemia are neuromuscular excitability and tetany, muscle contraction that does not stop. Low calcium levels allow neuromuscular cells to be depolarized unchecked. Trousseau's sign, carpopedal spasms during blood pressure cuff inflation, is a clinical sign of tetany. Laryngeal stridor and numbness and tingling around the mouth or in the extremities ("pins and needles") are signs of hypocalcemia. Seizures may develop if hypocalcemia is not reversed.

Hypocalcemia may cause decreased cardiac output and ECG changes. Mr. C's low blood pressure is a sign of insufficient calcium. Prolonged QT intervals in hypocalcemia may lead to ventricular tachycardia.

Hypercalcemia Presentation

Ms. X illustrates the most common risk factor for hypercalcemia, metastatic cancer in elders. Ms. X exhibits common signs and symptoms of calcium levels greater than 10.5 mg/dL or ionized calcium greater than 5.4 mg/dL. Life-threatening hypercalcemia occurs in patients with calcium levels greater than 14 mg/dL.

Ms. X is an 85-year-old admitted from home with increased confusion and lethargy. Her daughter says she has been making lots of urine and drinking lots until yesterday. Ms. X was diagnosed with lung cancer with bony metastases in the past year. She is afebrile with a heart rate of 110 and a BP of 100/60. Pulse ox is 90 percent on 2 L oxygen.

Lab values include:

  • total serum calcium = 15 mg/dL
  • ionized calcium = 7.8 mg/dL
  • albumin = 2.0 mg/dL
  • phosphate = 5.0 mg/dL
  • magnesium = 1.5 mg/dL
  • BUN = 46 mg/dL
  • creatinine = 1.5 mg/dL

Ms. X's elevated calcium level of 15 mg/dL is related to the release of calcium from the bone secondary to tumor invasion. Hypercalcemia leads to polyuria as the kidney attempts to excrete excess calcium. The polydipsia helps maintain urine flow and hydration state. Ms. X's decreased mental status resulted in dehydration and inability to maintain urine flow and calcium excretion. Note that Ms. X's magnesium and phosphate are normal, while her albumin is low. Her elevated BUN indicates dehydration.

Major assessment findings in hypercalcemia include altered level of consciousness, bradyarrhythmias including heart block, and gastrointestinal complaints of nausea and vomiting that increase the dehydrated state. The polyuria and polydipsia experienced by Ms. X occur as the calcium affects the kidney's ability to concentrate urine, leading to huge water losses. The water loss leads to dehydration and loss of the only way for the body to get rid of excess calcium. Ms. X has hypercalcemic crisis.

Management Approaches

Patients with hypocalcemia, such as Mr. C, require immediate intervention to prevent further deterioration. IV calcium administration in this setting is the treatment of choice. Calcium gluconate or calcium chloride may be prescribed in this situation of life-threatening symptoms. Oral calcium supplementation and a high-calcium diet would be used in a patient with chronic hypocalcemia.

Administration of oxygen to correct hypoxia, maintenance of the airway and cardiac monitoring until symptoms are relieved are key interventions.

Prevention of hypocalcemia symptoms in patients after thyroid surgery was the outcome of a randomized controlled trial undertaken by Kurukahvecioglu and colleagues.5The treatment group in this study received oral calcium and vitamin D supplementation after thyroid surgery. The result was decreased hypocalcemic symptoms and a shorter hospital stay for the treated group.

Phosphate binders for patients with renal failure nd magnesium replacement for patients with low magnesium are treatments of choice.6 hosphate binders lower serum phosphate, permitting calcium levels to return to near normal values.

Patients with hypercalcemia require volume expansion with normal saline as the first intervention. The saline will increase calcium excretion via the kidney and lower calcium. Furosemide causes calcium excretion when intravascular volume is repleted. Bisphosphonates, such as pamidronate continuous infusion for 24 hours, will decrease bone breakdown. Peak effect occurs over 2-4 days and may last for months. Calcitonin, given subcutaneously or intramuscularly, suppresses bone resorption in patients with hypercalcemia.

References for this article can be accessed at Click on Education, then References.

Joanne Konick-McMahan is a staff nurse at Pinnacle Health System, Harrisburg, PA, and nursing education advisor for the Pennsylvania State Board of Nursing. <% footer %>

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