{"id":33504,"date":"2023-12-08T20:55:01","date_gmt":"2023-12-08T20:55:01","guid":{"rendered":"https:\/\/todaysveterinarypractice.com\/?p=33504"},"modified":"2024-01-03T16:52:24","modified_gmt":"2024-01-03T16:52:24","slug":"a-practical-approach-to-hypercalcemia","status":"publish","type":"post","link":"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/internal-medicine\/a-practical-approach-to-hypercalcemia\/","title":{"rendered":"A Practical Approach to Hypercalcemia"},"content":{"rendered":"

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Abstract<\/strong><\/p>\n

Calcium is an important electrolyte and essential element for many cellular processes. This article provides a broad overview of calcium regulation and the development of hypercalcemia, as well as a practical approach to patients presenting with hypercalcemia, including initial stabilization of patients with severe hypercalcemia.<\/p>\n

Take-Home Points<\/strong><\/p>\n

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  • In patients with elevated total calcium, the first step in diagnosis is to verify hypercalcemia by measuring ionized calcium.<\/li>\n
  • Concurrent measurement and evaluation of serum phosphorus may provide further insight into the cause of hypercalcemia.<\/li>\n
  • If the cause of hypercalcemia remains elusive after a thorough history and physical examination, calcium hormone levels should be measured to ascertain whether the hypercalcemia is parathyroid dependent or independent.<\/li>\n
  • Clinical signs of hypercalcemia depend on the magnitude, rate of development, and duration of hypercalcemia as well as concurrent electrolyte and acid\u2013base disturbances.<\/li>\n
  • Overall, the most common causes of hypercalcemia in dogs and cats are nonpathologic and transient conditions.<\/li>\n
  • Medical therapy for persistent hypercalcemia is dictated by the systemic wellness of the patient, rate of rise of serum calcium concentration, and severity of hypercalcemia.<\/li>\n
  • No single treatment protocol effectively reduces serum ionized calcium concentrations, and each patient requires an individualized protocol until the cause of hypercalcemia can be determined. Definitive treatment involves treating or removing the underlying cause.<\/li>\n<\/ul>\n

    <\/div><\/div><\/p>\n

    Calcium is a vital electrolyte. It is essential for normal cell function, nerve conduction, muscle contraction (cardiac, skeletal, smooth), hormone secretion, and blood clotting, as well as skeletal support.1-3<\/sup> Ionized calcium (iCa), the biologically active form of calcium, is tightly regulated through the integrated actions of parathyroid hormone (PTH), 1,25-dihydroxyvitamin D3<\/sub>, and calcitonin.<\/span><\/p>\n

    Hypercalcemia develops when there is increased bone resorption, decreased renal excretion or increased gastrointestinal absorption of calcium, or increased serum binding of calcium to proteins\/complexes. The net result is a diverse array of clinical signs that depend on the severity and chronicity of the hypercalcemia. Severely hypercalcemic patients commonly demonstrate polyuria\/polydipsia<\/a>, anorexia, constipation, lethargy, and weakness.<\/span><\/p>\n

    The clinical workup for hypercalcemia initially encompasses a repeat confirmatory calcium measurement, thorough history, and meticulous physical examination. If the cause of hypercalcemia remains elusive, calcium hormone levels should be measured to ascertain whether the hypercalcemia is parathyroid dependent or independent. Further diagnostics depend on initial findings and may include thoracic radiography, advanced abdominal imaging, cervical ultrasound, and bone biopsy.<\/span><\/p>\n

    Initial treatment is symptomatic and supportive, aimed at diluting the iCa concentration through volume expansion with intravenous fluids and encouraging calciuresis. Other therapies include calciuretic diuretics (e.g., furosemide), bisphosphonates, and dietary modification. Unfortunately, no single treatment protocol effectively reduces serum iCa concentrations, with each patient requiring an individualized protocol until the cause of hypercalcemia can be determined. Definitive treatment involves treating or removing the underlying cause.<\/span><\/p>\n

    Overview of Calcium Physiology<\/h2>\n

    Most calcium in the body (99%) is stored in skeletal tissue as hydroxyapatite and is not immediately available. The remaining 1% is found intracellularly (0.9%) and extracellularly (0.1%). Extracellularly, calcium exists in 3 fractions: protein bound (approximately 35% to 40%), complexed (approximately 10%), and unbound (ionized) and biologically active (approximately 50% to 55%).4,5<\/sup><\/span><\/p>\n

    Blood iCa is maintained within a narrow range by complex, integrated interactions between phosphorus and 3 major hormones: PTH, calcitonin, and 1,25-dihydroxyvitamin D3<\/sub> (<\/span>FIGURE 1<\/b><\/span>). Calcium-sensing receptors in the parathyroid glands, thyroid, and kidney respond to disturbances in blood iCa by altering production of these hormones, which then act on specific cells in the bone, gastrointestinal tract, and kidney to restore calcium homeostasis. Disruptions of these normal homeostatic control mechanisms manifest as hypercalcemia or hypocalcemia.<\/span><\/p>\n

    \"\"<\/a><\/p>\n

    Definition of Hypercalcemia<\/h2>\n

    Hypercalcemia is defined as an elevation of serum total calcium (tCa) and\/or iCa above the following normal physiological ranges:<\/span><\/p>\n

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    • Adult dogs:<\/b> tCa, 9 to 11.5 mg\/dL (2.2 to 3.8\u00a0mmol\/L); iCa, 5 to 6 mg\/dL (1.2 to 1.5 mmol\/L)<\/li>\n
    • Adult cats:<\/b> tCa, 8 to 10.5 mg\/dL (2 to 2.6 mmol\/L); iCa, 4.5 to 5.5 mg\/dL (1.1 to 1.4 mmol\/L)<\/li>\n<\/ul>\n

      Young dogs and cats have serum iCa concentrations that are 0.1 to 0.4 mg\/dL higher than those reported in older animals.3<\/sup><\/span><\/p>\n

      Total Versus Ionized Calcium<\/h2>\n

      Historically, measuring tCa has been the most common method of assessing an animal\u2019s plasma or serum calcium level.7<\/sup> Total calcium measurements are reported in routine serum biochemistry panels and are easy to interpret. However, it is iCa, not tCa, that is responsible for deleterious biological effects. Total calcium elevation by itself is not harmful, as several conditions, such as hemolysis, bilirubinemia, and hyperlipidemia, may affect the measured accuracy of tCa, as may patient age, diet, and fasting.3<\/sup> Recent studies have investigated the utility of tCa to predict ionized hypercalcemia and concluded that tCa >12 mg\/dL in dogs and >11.8 mg\/dL in cats is very specific for ionized hypercalcemia.8,9<\/sup> Therefore, moderate to severe elevations in tCa should prompt clinicians to measure iCa. Ionized calcium serves as a better indicator of global physiological calcium status.10<\/sup><\/span><\/p>\n

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      Share this Today’s Veterinary Nurse<\/em> article on hypercalcemia with your team members<\/p>\n

      Hypercalcemia in Dogs: Emergent Care, Diagnostics, and Treatments<\/a><\/p><\/blockquote>\n