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Introduction

  1. Pharmacology
    1. Calcium is a cation that is necessary for the normal functioning of a variety of enzymes and organ systems, including muscle and nerve tissue. Hypocalcemia, or a blockade of the effects of calcium, may cause muscle cramps, tetany, and ventricular fibrillation. Antagonism of calcium-dependent channels results in hypotension, bradycardia, and atrioventricular (AV) block.
    2. Calcium ions rapidly bind to fluoride ions, abolishing their toxic effects.
    3. Calcium may reverse the negative inotropic effects of calcium antagonists; however, depressed automaticity, AV nodal conduction velocity, and vasodilation caused by these agents may not respond to calcium administration.
    4. Calcium stabilizes cardiac cell membranes in hyperkalemic states.
    5. Calcium is a physiologic antagonist to the effects of hypermagnesemia.
  2. Indications
    1. Symptomatic hypocalcemia resulting from intoxication by fluoride, ethylene glycol, oxalate, or citrate anticoagulant found in banked blood products.
    2. Hydrofluoric acid exposure.
    3. Hypotension in the setting of calcium channel antagonist toxicity.
    4. Severe hyperkalemia with cardiac manifestations.
    5. Symptomatic hypermagnesemia.
  3. Contraindications
    1. Hypercalcemia except in the setting of calcium channel antagonist poisoning, in which hypercalcemia is desirable.
    2. Older textbooks list digoxin poisoning as a contraindication, but this warning is not supported by animal studies or human case reports.
    3. Note: Calcium chloride salt should not be used for intradermal, subcutaneous, or intra-arterial injection because it is highly concentrated and may cause further tissue damage. When given intravenously, use a central line or a secure, freely flowing, large peripheral venous line.
  4. Adverse effects
    1. Tissue irritation, particularly with calcium chloride salt; extravasation may cause local irritation or necrosis.
    2. Hypercalcemia, especially in patients with diminished renal function.
    3. Hypotension, bradycardia, syncope, and cardiac dysrhythmias caused by rapid intravenous administration.
    4. Neuromuscular weakness.
    5. Constipation caused by orally administered calcium salts.
    6. Use in pregnancy. FDA Category C (indeterminate). This does not preclude its acute, short-term use for a seriously symptomatic patient (Introduction).
  5. Drug or laboratory interactions
    1. Inotropic and dysrhythmogenic effects of digoxin and other cardiac glycosides may be potentiated by calcium, but this interaction appears largely theoretical, and animal studies have failed to demonstrate harm when calcium is used to treat severe hyperkalemia.
    2. A precipitate will form with solutions containing soluble salts of carbonates, phosphates, sulfates, and with sodium bicarbonate and various antibiotics.
  6. Dosage and method of administration. Note: A 10% solution of calcium chloride contains three times the amount of calcium ions per milliliter (27.2 mg/mL of elemental calcium) that a 10% solution of calcium gluconate contains (9 mg/mL of elemental calcium).
    1. Oral fluoride ingestion. Administer calcium-containing antacid (calcium carbonate) orally to complex fluoride ions.
    2. Symptomatic hypocalcemia, hyperkalemia. Give 20-30 mL (2-3 g) of 10% calcium gluconate (children: 0.3-0.4 mL/kg), or 5-10 mL (0.5-1 g) of 10% calcium chloride (children: 0.1-0.2 mL/kg), slowly IV over 5-10 minutes. Repeat as needed every 10-20 minutes.
    3. Calcium antagonist poisoning. May start with doses as described above. Typically, give an initial IV dose of 30 mL (3 g) of 10% calcium gluconate (children: 0.6 mL/kg or 60 mg/kg), or 10 mL (1 g) of 10% calcium chloride (children: 0.2 mL/kg or 20 mg/kg). High-dose calcium therapy has been reported to be effective in some cases of severe calcium channel blocker overdose. Corrected calcium concentrations of approximately 1.5-2 times normal have correlated with improved cardiac function. In the setting of calcium channel antagonist overdose, as much as 30 g of calcium gluconate has been given over 10 hours, resulting in a serum calcium concentration of 23.8 mg/dL, which was tolerated without adverse effect. However, not all patients will tolerate extreme elevations in serum calcium concentrations. Administer calcium in serial boluses or as a continuous infusion 0.6-1.5 mL/kg/h (60-150 mg/kg/h) of 10% calcium gluconate, or 0.2-0.5 mL/kg/h (20-50 mg/kg/h) of 10% calcium chloride, since bolus dosing briefly increases only ionized calcium levels. Serum calcium concentrations should be monitored every 1-2 hours during therapy with high-dose calcium.
    4. Dermal hydrofluoric acid exposure. For any exposure involving the hand or fingers, obtain immediate consultation from an experienced hand surgeon or medical toxicologist. Regardless of the specific therapy chosen, systemic opioid analgesics should be strongly considered as adjunctive therapy.
      1. Topical. Calcium concentrations for topical therapy have ranged from 2.5 to 33%; the optimal concentration has not been determined. In many industrial settings, a commercially available 2.5% calcium gluconate gel (Calgonate) is kept at the work site for rapid treatment of occupational exposures. A 2.5% gel may also be prepared in the emergency department by combining 1 g of calcium gluconate per 40 g (approximately 40 mL) of water-soluble base material (eg, Surgilube, K-Y Jelly). A 32.5% gel is made by compounding a slurry of ten 650-mg calcium carbonate tablets in 20 mL of water-soluble lubricant. For exposures involving the hand or fingers, place the gel in a large surgical latex glove serving as an occlusive dressing to maximize skin contact. Topical calcium gluconate treatment is much more effective if applied within 3 hours of the injury.
      2. For subcutaneous injection (when topical treatment fails to relieve pain), inject 5-10% calcium gluconate (not chloride) SC intralesionally and perifocally (0.5-1 mL/cm2 of affected skin), using a 27-gauge or smaller needle. This may be repeated two to three times at 1- to 2-hour intervals if pain is not relieved. No more than 0.5 mL should be injected into each digit.
      3. Bier block technique
        1. Establish distal IV access in the affected extremity (eg, dorsum of the hand).
        2. Exsanguinate the extremity by elevation for 5 minutes. Alternatively, an Esmarch bandage may be used by wrapping from the distal to the proximal extremity.
        3. Inflate a blood pressure cuff to just above systolic blood pressure. The arm can then be lowered or the bandage removed.
        4. With the cuff inflated, infuse 25-50 mL of a 2% calcium gluconate solution (10 mL of 10% calcium gluconate diluted with 40 mL of D5W) into the empty veins.
        5. After 20-25 minutes, slowly release the cuff over 3-5 minutes.
        6. Repeat if pain persists or use the intra-arterial infusion.
      4. For intra-arterial administration, dilute 10 mL of 10% calcium gluconate with 50 mL of D5W and infuse over 4 hours through either the brachial or the radial artery catheter. The patient should be monitored closely over the next 4-6 hours, and if pain recurs, a second infusion should be given. Some authors have reported 48-72 hours of continuous infusion.
    5. Other sites of hydrofluoric acid exposure
      1. Nebulized 2.5% calcium gluconate has been reported for cases of inhalational hydrofluoric acid exposure. Inhalational exposure should be considered with dermal exposures of more than 5% of the total body surface area. Add 1.5 mL of 10% calcium gluconate to 4.5 mL of sterile water to make a 2.5% solution.
      2. Ocular administration of 1% calcium gluconate solutions every 4-6 hours has been used for 24-48 hours but is of unproven efficacy compared with irrigation with saline or water. Higher concentrations of calcium gluconate may worsen corrosive injury to ocular structures. Ophthalmology consultation should be obtained.