Hypercalcemia in Emergency Medicine 

Updated: Apr 11, 2018
Author: Thomas E Green, DO, MPH, MMM, CPE, FACEP, FACOEP; Chief Editor: Romesh Khardori, MD, PhD, FACP 


Practice Essentials

Hypercalcemia is a disorder that most commonly results from malignancy or primary hyperparathyroidism.[1, 2, 3, 4, 19, 20] Other, less common causes of elevated calcium include increased intake or absorption, granulomatous disease, immobilization, and thiazide diuretic use. However, the primary diagnostic approach should be to first rule out underlying malignancy and parathyroid disease.[5]

Hypercalcemic crisis does not have an exact definition, although marked elevation of serum calcium, usually more than 14 mg/dL, is associated with acute signs and symptoms of hypercalcemia. Treatment of the elevated calcium level may resolve the crisis.

The reference range of serum calcium levels varies among laboratories but generally is 8.7-10.4 mg/dL, with somewhat higher levels present in children. Approximately 50% of calcium is bound to protein, primarily albumin, and the remaining 50% is ionized and is in physiologic active form.[5]


When calcium levels are reported as abnormal, the first step is to measure the albumin level. The following is a common formula used in calculating a corrected calcium level[12] :

Corrected total calcium (mg/dL) = (measured total calcium mg/dL) + 0.8 (for every decrement in the serum albumin of 1 g/dL below the reference value [in many cases 4.1 g/dL]; subsequently, subtract 0.8 for every increment in the serum albumin of 1 g/dL above the reference value)

If the corrected serum calcium level still is not accurate, it is possible to measure the free calcium ion activity (ie, ionized calcium level).

Hypercalcemia may produce electrocardiographic abnormalities related to altered transmembrane potentials that affect conduction time.

After a diagnosis of hypercalcemia is established, the next step is to determine the cause. Initial testing is directed at malignancy, hyperparathyroidism, and hyperthyroidism, the most common causes of hypercalcemia.

Emergency department care

The initial step in the care of severely hypercalcemic patients is hydration and forced calciuresis. Because most of these patients are profoundly dehydrated, 0.9 normal saline is the crystalloid of choice for rehydration.

A loop diuretic (eg, furosemide) may be used with hydration to increase calcium excretion. This may also prevent volume overload during therapy.

Bisphosphates will inhibit osteoclast activity for up to a month. However, these agents may take 48-72 hours before reaching full therapeutic effect.[5]


Plasma calcium is maintained within the reference range by a complex interplay of 3 major hormones, parathyroid hormone (PTH), 1,25-dihydroxyvitamin D (ie, calcitriol), and calcitonin. These 3 hormones act primarily at bone, kidney, and small intestine sites to maintain appropriate calcium levels.

Calcium enters the body through the small intestine and eventually is excreted via the kidney. Bone can act as a storage depot. This entire system is controlled through a feedback loop; individual hormones respond as needed to increase or decrease the serum calcium concentration.

For hypercalcemia to develop, the normal calcium regulation system must be overwhelmed by an excess of PTH, calcitriol, some other serum factor that can mimic these hormones, or a huge calcium load.

Hypercalcemia can result from a multitude of disorders. The causes are divided into PTH-mediated hypercalcemia and non–PTH-mediated hypercalcemia.

PTH-mediated hypercalcemia

Primary hyperparathyroidism originally was the disease of "stones, bones, and abdominal groans." In most primary hyperparathyroidism cases, the calcium elevation is caused by increased intestinal calcium absorption. This is mediated by the PTH-induced calcitriol synthesis that enhances calcium absorption. The increase in serum calcium results in an increase in calcium filtration at the kidney. Because of PTH-mediated absorption of calcium at the distal tubule, less calcium is excreted than might be expected. Hypercalcemia of this disorder may remain mild for long periods because some parathyroid adenomas respond to the feedback generated by the elevated calcium levels.

Non–PTH-mediated hypercalcemia

Malignancy-associated hypercalcemia occurs in up to 20-30% of patients at some course within their disease. Most episodes occur with advanced disease and patients typically have a poor prognosis (with up to a 50% 30-day mortality). There are two generally recognized forms of this disorder, one in which hypercalcemia is the result of tumor secretion of a humoral factor (usually PTHrP) and one is the result of excessive bone metastases.[6] Common malignancies include multiple myeloma, breast cancer, or lung cancer. Multiple factors for osteolysis are responsible for this action, which is produced by or in response to the myeloma cells in the marrow. These are collectively referred to osteoclast-activating factors.[7]

Multiple endocrine neoplasia (MEN) are a group of disorders associated with hyperfunction of two or more endocrine glands and can be a cause of hypercalcemia (which may be milder and even asymptomatic). Finally, tamoxifen-linked hypercalcemia is hypercalcemia in association with the use of estrogen or antiestrogen therapy for therapy for carcinoma of the breast. The severity of hypercalcemia is variable, but it can be fatal. The mechanism by which tamoxifen and similar agents cause hypercalcemia is unclear but prostaglandins may be the main mediator of the response.[8] Other causes that are non-malignancy-related include milk-alkali syndrome (which involves large intake of calcium in association with volume contraction, systemic alkalosis and renal insufficiency) and medication-induced hypercalcemia (especially chronic lithium therapy).[6]

The emergency physician should be concerned about any patient with a history of cancer who presents with lethargy or altered mental status. Granulomatous disorders with high levels of calcitriol may be found in patients with sarcoidosis, berylliosis, tuberculosis, leprosy, coccidioidomycosis, and histoplasmosis.[4]



United States

Hypercalcemia is a fairly common metabolic emergency. Between 20-40% of patients with cancer develop hypercalcemia at some point in their disease (this may be decreasing with the use of bisphosphates, but data are lacking), and it is the most common serious electrolyte presenting in adults with malignancies.[9]

A study by Gastanaga et al estimated that between 2009 and 2013, 2.0-2.8% of all cancer patients in the United States were affected by hypercalcemia of malignancy, with the highest rates of such hypercalcemia found in multiple myeloma patients (7.5-10.2% between 2010 and 2012), and the lowest rates found in patients with prostate cancer (1.4-2.1% between 2011 and 2012).[10]

Primary hyperparathyroidism occurs in 25 per 100,000 persons in the general population and in 75 per 100,000 hospitalized patients. This condition is the most common cause of mild hypercalcemia, which can be treated on an outpatient basis. In the United States, more than 50,000 new cases occur each year.


A Scottish study, by McNeilly et al, estimated that in a general hospital setting, the rate of sustained hypercalcemia (hypercalcemia on 2 or more consecutive days) is 1 in 500 children, with the greatest frequency found in neonates. Etiologies varied with age among pediatric patients.[11]


Prognosis of hypercalcemia associated with malignancy is poor; the 1-year survival rate is 10-30%. In one study, 50% of patients died within 30 days of beginning treatment; 75% died within 3 months.

In a study by Ramos et al of patients with solid tumors suffering from malignancy-related hypercalcemia, univariable analysis showed significantly poorer survival in those with an Eastern Cooperative Oncology Group performance status of over 2, altered mental status, a C-reactive protein level above 30 mg/L, an albumin concentration of less than 2.5 g/dL, or a body mass index below 18 kg/m2.[22]

Prognosis related to many of the other causes of hypercalcemia can be excellent once the underlying disease is addressed.


The incidence of primary hyperparathyroidism is considerably higher in women. The annual incidence in women older than 65 years is 250 per 100,000.

Elevations in calcium levels related to cancer have no sex predominance.


The incidence of primary hyperparathyroidism increases with age.

The rate of malignancy and, thus, of malignancy-associated hypercalcemia increases with age.




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).[12]

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.[13, 14, 15]

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

These include the following:

  • 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 - Post–renal transplant and initiation of chronic hemodialysis

  • Miscellaneous - Immobilization, hypophosphatasia, primary infantile hyperparathyroidism, AIDS, and advanced chronic liver disease

A study by Meehan et al found that 26.2% of patients with bipolar disorder undergoing lithium treatment had hypercalcemia. Out of a study population consisting of patients with bipolar disorder being treated with lithium, patients with bipolar disorder not being treated with lithium, and controls, hypercalcemia occurred in 87 individuals, including 82 (94.3%) of those undergoing lithium therapy.[21]





Laboratory Studies

When calcium levels are reported as abnormal, the first step is to measure the albumin level. The following is a common formula used in calculating a corrected calcium level[12] :

Corrected total calcium (mg/dL) = (measured total calcium mg/dL) + 0.8 (for every decrement in the serum albumin of 1 g/dL below the reference value [in many cases 4.1 g/dL]; subsequently, subtract 0.8 for every increment in the serum albumin of 1 g/dL above the reference value)

If the corrected serum calcium level still is not accurate, it is possible to measure the free calcium ion activity (ie, ionized calcium level).

Other nonspecific laboratory abnormalities commonly found in patients with hypercalcemia result from disordered renal function. Patients commonly have significant azotemia at presentation.

Hypercalcemia may produce electrocardiographic abnormalities related to altered transmembrane potentials that affect conduction time. QT interval shortening is common, and, in some cases, the PR interval is prolonged. At very high levels, the QRS interval may lengthen, T waves may flatten or invert, and a variable degree of heart block may develop. Digoxin effects are amplified.

After a diagnosis of hypercalcemia is established, the next step is to determine the cause. Initial testing is directed at malignancy, hyperparathyroidism, and hyperthyroidism, the most common causes of hypercalcemia.

  • The measurement of circulating PTH in the serum is the most direct and sensitive measure of parathyroid gland function. A reference range is 2-6 mol/L. A nonsuppressed PTH level in the presence of hypercalcemia suggests a diagnosis of primary hyperparathyroidism. If the PTH level is suppressed in the face of an elevated calcium level, hyperparathyroidism is unlikely.

  • Parathyroid hormone-related peptide (PTHrP) is thought to mediate the hypercalcemia that develops with many malignancies. Assays to measure this peptide are available.[16]

  • Measurement of calcitriol is difficult but can be accomplished. This laboratory value is useful in diagnosing hypercalcemia secondary to a granulomatous disease such as sarcoidosis. It is often elevated in primary hyperparathyroidism.

  • Other electrolytes also may be disturbed in hypercalcemia. Serum phosphate levels tend to be low or normal in primary hyperparathyroidism and hypercalcemia of malignancy. Phospate levels are elevated in hypercalcemia secondary to vitamin D–related disorders or thyrotoxicosis. Serum chloride levels usually are higher than 102 mEq/L in hyperparathyroidism and less than this value in other forms of hypercalcemia.

A study by Balentine et al suggested that a large percentage of patients with hypercalcemia are not appropriately evaluated for hyperparathyroidism, while many of those who are diagnosed with hyperparathyroidism do not get a surgical referral. Looking at figures from a tertiary referral center, the investigators found that only 3200 (31%) of 10,432 patients with hypercalcemia underwent parathyroid hormone measurement, with a hypercalcemia diagnosis documented in just 2914 patients (28%) and a hyperparathyroidism diagnosis found in the medical records of 880 patients (8%). Of 2666 patients with classic hyperparathyroidism (ie, abnormal calcium and parathyroid hormone levels), only 592 (22%) received a surgical referral.[17]  

Imaging Studies

No imaging studies definitively diagnose hypercalcemia. However, the chest radiograph may reveal malignancy or granulomatous disease.[5]

Consider hypercalcemia in patients with multiple nonspecific complaints and an associated lung mass.

If laboratory evidence of primary hyperparathyroidism is present, CT scan of the head, MRI, ultrasound, or nuclear parathyroid scans may be helpful. Preoperative diagnostic imaging is essential in patients with previous neck surgery.



Prehospital Care

Prehospital care is primarily supportive with management of the ABCs. If a patient has a history of hypercalcemia and displays evidence of acute hypercalcemia, immediately begin IV hydration.

Emergency Department Care

The treatment of hypercalcemia depends on the level, the clinical presentation, and (if known) the underlying cause of the problem. In mild to moderate elevations of calcium, few treatment options may be available in the ED. A physical evaluation to help delineate the source of the elevation is always appropriate, as is a subsequent timely follow-up visit.

  • Initial goals of treatment

    • Assessment and maintenance of airway, breathing, and circulation (ABCs)

    • Stabilization and reduction of the calcium level

    • Adequate hydration

    • Increased urinary calcium excretion

    • Inhibition of osteoclast activity in the bone

    • Discontinuation of pharmacologic agents associated with hypercalcemia

    • Treatment of the underlying cause (when possible)

  • The initial step in the care of severely hypercalcemic patients is hydration and forced calciuresis. Because most of these patients are profoundly dehydrated, 0.9 normal saline is the crystalloid of choice for rehydration. Hydration helps decrease the calcium level through dilution. The expansion of extracellular volume also increases the renal calcium clearance. The rate of fluid therapy is based upon the following[5] :

    • Degree of hypercalcemia

    • Severity of dehydration

    • Ability of the patient to tolerate rehydration - Vigilance to prevent volume overload is critical.

    • Hydration is ineffective in patients with kidney failure because diuresis is impossible. Dialysis is necessary to correct hypercalcemia in patients with renal failure.

  • Loop diuretics

    • A loop diuretic (eg, furosemide) may be used with hydration to increase calcium excretion. This may also prevent volume overload during therapy.

    • In contrast to loop diuretics, avoid thiazide diuretics because they increase the reabsorption of calcium.

  • Bisphosphates - These agents will inhibit osteoclast activity for up to a month. However, these agents may take 48-72 hours before reaching full therapeutic effect.[5]


Patients with renal failure or heart failure may not be able to tolerate fluid hydration or some of the other medications. Patients in this group who present with severe elevations of calcium may require urgent dialysis. Consult a nephrologist immediately in such cases.

Patients with primary hyperparathyroidism may require surgery to eliminate the condition,[18] but surgery usually does not need to be performed on an urgent basis.

Patients with malignancy may require surgery, chemotherapy, or radiation treatment. Appropriate consultation should be undertaken.



Medication Summary

Several classifications of medications are used to treat elevations of serum calcium. Some can be used in acute life-threatening elevations, while others are used to help control calcium elevations after the acute event has been treated. Agents that help treat hypercalcemia include calcitonin, gallium nitrate, intravenous phosphate, bisphosphates, glucocorticoids, and calcimimetic agents.


Class Summary

These compounds are analogs of pyrophosphate that act by binding to hydroxyapatite in bone matrix, thereby inhibiting the dissolution of crystals. These agents prevent osteoclast attachment to bone matrix and interfere with osteoclast recruitment and viability.

Pamidronate (Aredia)

Mechanism of action is inhibition of normal and abnormal bone resorption; appears to inhibit bone resorption without inhibiting bone formation and mineralization. Potent agent that has several regimens for administration. Adverse effects of IV administration include mild transient increases in temperature, leukopenia, and mild reduction in serum phosphate levels. PO maintenance therapy is available after acute event has resolved, but this therapy is experimental. With acute hypercalcemia, all of these agents are effective; pamidronate may be preferable because of its potency and efficacy..

Zoledronic acid (Zometa)

Inhibits bone resorption, possibly by acting on osteoclasts or osteoclast precursors. Median duration of complete response (maintaining normalized calcium levels) and time to relapse reported as 32 and 30 d, respectively. Indicated for hypercalcemia of malignancy.

Etidronate (Didronel)

Reduces bone formation; does not appear to alter renal tubular reabsorption of calcium. Does not affect hypercalcemia in patients with hyperparathyroidism where increased calcium reabsorption may increase blood calcium levels. Response generally observed within first 48 h; more effective if patient is well hydrated before initial dose. If patient responds well before 7 d, therapy can be discontinued. Generally well tolerated; most common adverse effect is a transient elevation of serum creatinine and phosphorous. PO therapy is experimental and not always effective.

Antidote, Hypercalcemia

Class Summary

Inhibit RNA synthesis in osteoclasts and effective in treatment of hypercalcemia.

Calcitonin (Miacalcin, Cibacalcin, Calcimar)

A naturally occurring hormone that inhibits bone reabsorption and increases excretion of calcium. Most rapid onset of action of anticalcemic agents. Effects may be observed within a few hours with peak response at 12-24 h; because of short duration of action, other more potent but slower-acting agents should be started in patients with severe hypercalcemia. Salmon calcitonin is used most often and is more potent than human calcitonin. Action of this agent is short-lived. If elevation of calcium is severe, coadminister 1-2 doses with fluids and Lasix to provide a rapid, although limited, reduction of the calcium level.

Gallium nitrate (Ganite)

Works by inhibiting bone reabsorption and altering structure of bone crystals.

Exerts hypocalcemic effect, possibly by reducing bone resorption; performs well against other anticalcium agents but has slow onset of action.


No longer manufactured and distributed in the United States. Inhibits cellular ribonucleic acid (RNA) and enzymatic RNA synthesis. Possibly blocks hypercalcemic action of pharmacologic doses of vitamin D and may act on osteoclasts or block action of parathyroid hormone. Effect in lowering calcium is not related to tumoricidal activity.

Phosphate salts

Class Summary

Use of IV phosphate is very effective in lowering serum calcium levels most likely because of a precipitation phenomenon. Significant risk exists with use of this agent. This agent is reserved for hypercalcemia unresponsive to other agents.

Potassium phosphate

IV preparations are available as sodium or potassium phosphate (K2PO4). Response to IV serum phosphorus supplementation is highly variable and is associated with hyperphosphatemia.


Class Summary

While these agents do not treat hypercalcemia directly, they are useful for treating hypercalcemia caused by vitamin D toxicity, certain malignancies (eg, multiple myeloma, lymphoma), sarcoidosis, and other granulomatous diseases. These agents generally are not effective in patients with solid tumors or primary hyperparathyroidism. Several different glucocorticoids may be used.

Hydrocortisone (Cortef)

Mineralocorticoid activity and glucocorticoid effects; onset of activity is rapid. Significant number of adverse reactions for those on long-term steroids. In acute phase, few severe reactions present.

Calcimimetic Agent

Class Summary

Binds to and modulates the parathyroid calcium-sensing receptor, increases sensitivity to extracellular calcium, and reduces parathyroid hormone secretion.

Cinacalcet (Sensipar)

Directly lowers parathyroid hormone (PTH) levels by increasing sensitivity of calcium sensing receptor on chief cell of parathyroid gland to extracellular calcium. Also results in concomitant serum calcium decrease. Indicated for hypercalcemia with parathyroid carcinoma.



Further Outpatient Care

Patients with primary hyperparathyroidism who present with symptoms of severe or moderate elevations of calcium levels should be referred for parathyroidectomy. This referral may be urgent, depending on the severity of the hypercalcemia.

Patients with mild-to-moderate elevations of calcium who have no symptoms may be evaluated on an outpatient basis and usually are treated medically. For those patients with malignancy as the cause of their hypercalcemia, a cure may not be possible. The ideal scenario finds a treatable underlying cause for hypercalcemia and allows the physician to attend to this primary process. If this is accomplished, the patient may not need therapy for the hypercalcemia itself.

The drug regimen most appropriate for each individual depends on the cause of the elevation and usually is not managed by the ED physician. Patients may require ongoing treatment for calcium elevation. This type of treatment can be frustrating and difficult, and it is not always successful.

Further Inpatient Care

Serum calcium level generally responds to fluids and Lasix; however, this therapy has no effect on the principle pathologic process causing hypercalcemia. Additional therapy must be added to the temporizing treatment described above.

Treatment of the underlying disease must be addressed.


Transfer may be considered in a number of situations.

  • If a patient presents with severe hypercalcemia and renal failure, emergency dialysis is necessary. Consider transfer if this is unavailable at the initial treatment center.

  • If no intensivist or physician familiar with the inpatient treatment of hypercalcemia is available, consider transferring patients with normal kidney function who are being treated for severe hypercalcemia.


See the list below:

  • Avoid prolonged bedrest for patients known to have rapid bone turnover.

  • Consider elective surgical procedures for patients with Paget disease after therapy has been initiated for calcium elevation. Mobilize patients as quickly as possible to minimize bone loss.

  • Worsening hypercalcemia is common in patients with known metastatic disease who are too ill to ambulate. This should be anticipated and treated before the patient becomes symptomatic.

  • Patients at risk for hypercalcemia should have scheduled appointments with ongoing evaluation to monitor for development or progression of the disease.

  • Avoid salt restriction, diuretics, and other causes of volume depletion and dehydration in patients with active or potential hypercalcemia.


The prognosis of patients with hypercalcemia depends upon the etiology of the elevation.

  • Prognosis is very poor with malignancy that has progressed into development of hypercalcemia.

  • Prognosis is excellent when the underlying cause is treatable and treatment is initiated promptly.


Questions & Answers


What is hypercalcemia?

How is a hypercalcemic crisis defined?

What is the reference range of serum calcium?

What is the workup approach to hypercalcemia?

What is the treatment approach to hypercalcemia in the emergency department?

What is the physiology of normal plasma calcium regulation?

How does hypercalcemia develop?

What is the pathophysiology of parathyroid hormone (PTH)-mediated hypercalcemia?

What is the pathophysiology of hypercalcemia associated with malignancy?

What is the incidence of hypercalcemia among cancer patients in the US?

What is the incidence of hypercalcemia due to hyperparathyroidism in the US?

What is the international incidence of hypercalcemia in hospitalized pediatric patients?

What is the prognosis of hypercalcemia associated with malignancy?

What is the prognosis of hypercalcemia not associated with malignancy?

What are the sex-related demographics of hypercalcemia?

What are the age-related demographics of hypercalcemia?


How do the symptoms of hypercalcemia manifest?

What are the signs and symptoms of hypercalcemia?

Which patients with hypercalcemia are most likely to be symptomatic?

Why is hypercalcemia of malignancy difficult to detect?

Which symptoms of hypercalcemia are associated with hyperparathyroidism?

What are the physical findings in hypercalcemia?

Which nonspecific findings are associated with hypercalcemia?

Which corneal disease is associated with long-standing hypercalcemia?

What are the physical findings in hypercalcemia due to less common causes?

What are the different types of non-parathyroid hormone (PTH)-mediated hypercalcemia?

What are the main categories of hypercalcemia?

What causes parathyroid hormone (PTH)-mediated hypercalcemia?

What are the less common causes of hypercalcemia?


What are the differential diagnoses for Hypercalcemia in Emergency Medicine?


What formula is used to calculate a corrected calcium level in hypercalcemia?

What is the purpose of measuring the ionized calcium level in the workup of hypercalcemia?

Which nonspecific lab results are associated with hypercalcemia?

Which ECG abnormalities are associated with hypercalcemia?

What is the next step after the diagnosis of hypercalcemia is established?

How should patients with hypercalcemia be evaluated?

Which imaging studies are indicated in the workup of hypercalcemia?


What is included in the prehospital care of hypercalcemia?

Which factors determine the treatment of hypercalcemia in the ED?

What are the initial goals of treatment in hypercalcemia?

Which factors determine the rate of fluid therapy in the treatment of hypercalcemia?

What is the role of loop diuretics in the treatment of hypercalcemia?

What is the role of bisphosphates in the treatment of hypercalcemia?

What is specialist consultation indicated in the treatment of hypercalcemia?


Which medications are used in the treatment of hypercalcemia?

Which medications in the drug class Calcimimetic Agent are used in the treatment of Hypercalcemia in Emergency Medicine?

Which medications in the drug class Corticosteroids are used in the treatment of Hypercalcemia in Emergency Medicine?

Which medications in the drug class Phosphate salts are used in the treatment of Hypercalcemia in Emergency Medicine?

Which medications in the drug class Antidote, Hypercalcemia are used in the treatment of Hypercalcemia in Emergency Medicine?

Which medications in the drug class Bisphosphonates are used in the treatment of Hypercalcemia in Emergency Medicine?


What outpatient care is indicated for hypercalcemia?

How is the drug regimen for the treatment of hypercalcemia determined?

What is the inpatient care of hypercalcemia?

When is transfer indicated for patients with hypercalcemia?

How can hypercalcemia be prevented or minimized?

What is the prognosis of hypercalcemia?