Calicum use in medical professionals by physicians

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1. Calcium • Normal serum calcium concentration is 8.5–10.5 mg/dL (total Ca2+ includesbound and unbound Ca2+), and normal ionized calcium is 4.4–5.3 mg/dL. • EC fluid contains less than 1% of the total body stores of Ca2+; 99% of totalbody stores of Ca2+ are in skeletal bone. • About half of Ca2+ in the EC compartment is bound to plasma proteins(primarily albumin). • The active form of Ca2+ is the unbound or ionized Ca2+.• Ionized Ca2+ is regulated by parathyroid hormone, phosphorus, vitamin D,and calcitonin.

2. Hypocalcemia • Causes : - chronic kidney disease –hypoparathyroidism -vitamin D deficiency–alcoholism – hyperphosphatemia -and in patients receiving large amounts ofblood products -or patients undergoing continuous renal replacementtherapy (CRRT [i.e., Ca2+ chelates with citrate used as anticoagulation inblood products or for plasmapheresis or CRRT.]) • Factors that cause an increase in EC Ca2+ binding to albumin (e.g.,metabolic alkalosis) can cause a reduction in plasma ionized Ca2+concentration. • A low serum albumin will cause a falsely low total serum calcium reading.

3. hypocalcemia • Signs and symptoms include tetany, muscle spasms, hypoactive reflexes,anxiety , hallucinations, lethargy, hypotension, and seizures. • Medications that cause hypocalcemia include loop diuretics, phenytoin,phenobarbital , corticosteroids, aminoglycosides antibiotics andacetazolamide . • Hypomagnesemia can also be related to hypocalcemia.

4. Treatment • Asymptomatic hypocalcemia associated with hypoalbuminemia is typicallyassociated with normal ionized Ca2+ concentrations and therefore does notrequire treatment. • Asymptomatic hypocalcemia can be treated with oral Ca2+ supplements ata dose of 2–4 g/day of elemental Ca2+ in divided doses; patients may alsorequire vitamin D supplementation. • Symptomatic hypocalcemia is treated with 200–300 mg of elemental Ca2+administered intravenously over 5–10 minutes; this is sometimes followedby a continuous infusion.

5. Treatment • Equivalent to 1 g of calcium chloride (273 mg of elemental Ca2+)administered through a central intravenous catheter; peripheraladministration of calcium chloride can result in severe limb ischemia. • Equivalent to 2–3 g of calcium gluconate (180–270 mg of elemental Ca2+);preferred for peripheral intravenous administration • Do not infuse Ca2+ at a rate faster than 60 mg of elemental Ca2+ perminute ; rapid administration, which is not recommended, is associated withhypotension , bradycardia, or asystole . • The duration of an intravenous dose of Ca2+ is ideally 1–2 hours. If acontinuous infusion is used, the rate should be 0.5–2 mg/kg/hour ofelemental Ca2+.

6. Hypercalcemia (>10.1 mg/dL) • Cancer and hyperparathyroidism are the most common causes of hypercalcemia . • Etiology of hyperparathyroidism is unclear but it affects women more than menespecially between 40-60 and 75% of patient have at least a single adenoma. • The most common tumors associated with hypercalcemia are lung, breast,multiple myeloma, head and neck, renal cell, and non-Hodgkin lymphoma. • Cancer-associated hypercalcemia results from increased bone resorption withcalcium release into the extracellular fluid; in addition, renal clearance of calcium isdecreased . • Some tumors cause direct bone destruction, resulting in osteolytic hypercalcemia.While Other tumors release parathyroid hormone–related protein (i.e., humoralhypercalcemia ).

7. Hypercalcemia • Hypercalcemia also occurs in Immobile patients due to increased resorptionof calcium, patients with kidney transplantation, Addison disease andphaechromocytoma . • Symptoms of hypercalcemia : Lethargy, confusion, anorexia, nausea,constipation , polyuria, and polydipsia • Multiple medications can cause hypercalcemia and include thiazide diuretics,estrogen , lithium, tamoxifen, vitamin A, vitamin D, ingestion of calcium withalkali and calcium supplements.

8. Treatment • Mild hypercalcemia (corrected calcium less than 12 mg/dL) may not warrantaggressive treatment. Hydration with normal saline followed by observationis an option in asymptomatic patients with chemotherapy-sensitive tumors(e.g., lymphoma, breast cancer). • Moderate hypercalcemia (corrected calcium 12–14 mg/dL) requires basictreatment of clinical symptoms with aggressive hydration. • Severe hypercalcemia (corrected calcium greater than 14 mg/ dL;symptomatic ) requires aggressive inpatient treatment.

9. Treatment • Hydration with normal saline about 3–6 L in 24 hours . • Loop diuretics may be administered after volume status has been correctedor to prevent fluid overload during hydration. •Thiazide diuretics are contraindicated in hypercalcemia because of theincrease in renal tubular calcium absorption. • Bisphosphonates bind to hydroxyapatite in calcified bone, which preventsdissolution by phosphatases and inhibits both normal and abnormal boneresorption . The onset of action is 3–4 days.

10. Treatment • Calcitonin (intramuscular formulation) inhibits the effects of parathyroidhormone and has a rapid-onset (though short-lived) hypocalcemic effect.May cause tachyphylaxis • Steroids may be used to lower calcium in patients with steroid-responsivetumors (lymphoma and myeloma). • Phosphate is reserved for patients who are both hypophosphatemic andhypercalcemic . Phosphate is seldom used because of the possibility ofcalcium and phosphate precipitation in soft tissue. • Dialysis may be needed in patients with hypercalcemia and renal failure.

11. Reference : ACCP2022