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Hypercalcemia in Emergency Medicine Clinical Presentation

  • Author: Thomas E Green, DO, MPH, FACOEP, FACEP; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
Updated: Jul 08, 2014


Symptoms of hypercalcemia depend on the underlying cause of the disease, the time over which it develops (rapid increases in calcium cause more severe symptoms), and the overall physical health of the patient.

Mild elevations in calcium levels are usually asymptomatic and typically discovered on routine laboratory diagnostic testing (usually up to 11.5 mg/dL).[9]

As calcium levels increase, the following symptoms may occur:

  • Nausea
  • Vomiting
  • Alterations of mental status
  • Abdominal or flank pain (The workup of patients with a new kidney stone occasionally reveals an elevated calcium level.)
  • Constipation
  • Lethargy
  • Depression
  • Weakness and vague muscle/joint aches
  • Polyuria, polydipsia, nocturia
  • Headache
  • Confusion

Severe elevations in calcium levels may cause coma.

Elderly patients are more likely to be symptomatic from only moderate elevations of calcium levels.

Hypercalcemia of malignancy may lack many of the features commonly associated with hypercalcemia caused by hyperparathyroidism. In addition, the symptoms of elevated calcium level may overlap with the symptoms of the patient's malignancy.

Hypercalcemia associated with renal calculi, joint complaints, and ulcer disease is more likely to be caused by hyperparathyroidism.



Hypercalcemia has few physical examination findings specific to its diagnosis. Often it is the symptoms or signs of underlying malignancy that bring the patient with hypercalcemia to seek medical attention. The primary malignancy may be suggested by lung findings, skin changes, lymphadenopathy, or liver or spleen enlargement.

Hypercalcemia can produce a number of nonspecific findings, as follows:

  • Hypertension and bradycardia may be noted in patients with hypercalcemia, but this is nonspecific.
  • Abdominal examination may suggest pancreatitis or the possibility of an ulcer.
  • Patients with long-standing elevation of serum calcium may have proximal muscle weakness that is more prominent in the lower extremities; they also may have bony tenderness to palpation.
  • Hyperreflexia and tongue fasciculations may be present.
  • Anorexia or nausea may occur.
  • Polyuria and dehydration are common.
  • Lethargy, stupor, or even coma may be observed.

Long-standing hypercalcemia may cause band keratopathy, but this is rarely recognized in the ED.

If hypercalcemia is caused by sarcoidosis, vitamin D intoxication, or hyperthyroidism, patients may have physical examination findings suggestive of those diseases.



Hypercalcemia is divided into PTH-mediated hypercalcemia (primary hyperparathyroidism) and non–PTH-mediated hypercalcemia.[10, 11, 12]

PTH-mediated hypercalcemia is related to increased calcium absorption from the intestine.

Non–PTH-mediated hypercalcemia includes the following:

  • Hypercalcemia associated with malignancy: Unlike PTH-mediated hypercalcemia, the elevation of calcium that results from malignancy generally worsens until therapy is provided. Hypercalcemia caused by malignancy is the result of increased osteoclastic activity within the bone. This results from one or both of the mechanisms that follow:
    • Extensive localized bone destruction may result from osteolytic metastasis of solid tumors. Evidence indicates that many malignant cells may release local osteoclastic activating factors.
    • Increased calcium levels resulting from malignancy caused by a PTH-related protein (PTH-rp) is a second mechanism. This protein is a humeral factor that acts on the skeleton to increase bone reabsorption; it acts on the kidney to decrease excretion of calcium. The gene that produces this protein is present in many malignant tissues.
  • Granulomatous disorders: High levels of calcitriol may be found in patients with sarcoidosis and other granulomatous diseases. In these disorders, the increased level of calcitriol results from production within the macrophages, which constitute a large portion of some granulomas.
  • Iatrogenic: In some cases, elevation of calcium is a known adverse effect of appropriate dosage. In other cases, large ingestions must be taken to induce the increase in calcium levels. Obtain a complete review of current medications for patients presenting with hypercalcemia. Record any vitamin use.

Other causes of hypercalcemia

See the list below:

  • Neoplasms (nonparathyroid) - Metastasis to the bone from breast, multiple myeloma, and hematologic malignancies ( Breast cancer is one of the most common malignancies responsible for hypercalcemia.)
  • Nonmetastatic (humoral-induced) - Ovary, kidney, lung, head and neck, esophagus, cervix, lymphoproliferative disease, multiple endocrine neoplasia, pheochromocytoma, and hepatoma
  • Pharmacologic agents - Thiazide, calcium carbonate (antacid), hypervitaminosis D, hypervitaminosis A, lithium, milk-alkali syndrome, and theophylline toxicity
  • Endocrinopathies (nonparathyroid) - Hyperthyroidism, adrenal insufficiency, and pheochromocytoma
  • Familial hypocalciuric hypercalcemia
  • Tertiary hyperparathyroidism - Postrenal transplant and initiation of chronic hemodialysis
  • Miscellaneous - Immobilization, hypophosphatasia, primary infantile hyperparathyroidism, AIDS, and advanced chronic liver disease
Contributor Information and Disclosures

Thomas E Green, DO, MPH, FACOEP, FACEP Associate Dean for Clinical Affairs, Des Moines University College of Osteopathic Medicine; Attending Physician, Emergency Department, Emergency Practice Associates; Associate Professor of Emergency Medicine, Midwestern University, Chicago College of Osteopathic Medicine

Thomas E Green, DO, MPH, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Association for Physician Leadership, American Osteopathic Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Jeffrey L Arnold, MD, FACEP Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center

Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Physicians

Disclosure: Nothing to disclose.

Chief Editor

Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.

Additional Contributors

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.


Robin R Hemphill, MD, MPH Associate Professor, Director, Quality and Safety, Department of Emergency Medicine, Emory University School of Medicine

Robin R Hemphill, MD, MPH is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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