Fluids, Electrolytes, Acid-Base Disorders, and Nutrition Support

g/day orally

Kidney is primary route of elimination.

Magnesium status can influence calcium homeostasis (J Parenter Enteral Nutr 2004;28:133-41;

Annu Rev Med 1981;32:245-59).

Hypomagnesemia results in end-organ resistance to parathyroid hormone.

ii.

Hypomagnesemia may impair parathyroid hormone secretion.

iii.

Hypocalcemia will correct within 2 days after hypomagnesemia is corrected.

Definition: Corrected serum total calcium less than 8.5 mg/dL (non-ICU patients); ionized serum

calcium concentration less than 1.12 mmol/L

Signs and symptoms: Tingling, paresthesias, hyperactive deep tendon reflexes, tetany (Chvostek

and Trousseau signs), seizures, prolonged QT interval

Etiologies

Critical illness, surgery

ii.

Continuous renal replacement therapy (CRRT) and citrate anticoagulation

iii.

Massive blood transfusion (citrate in packed RBCs)

iv.

Hypomagnesemia

Hyperphosphatemia

vi.

Pancreatitis

vii.

Drugs (amphotericin B, cisplatin, cyclosporine, foscarnet, bisphosphonates, loop diuretics,

sodium bicarbonate, cinacalcet, fluoride poisoning)

viii.

Malabsorption

ix.

Hypoparathyroidism, hypothyroidism

CKD/AKI

xi.

Vitamin D deficiency

xii.

Severe alkalemia

J Parenter Enteral Nutr 2007;31:228-33; JPEN J Parenter Enteral Nutr 2005;29:436-4; Nutrition

2007;23:9-15).

Ionized Calcium

(mmol/L)

Calcium Gluconate

Calcium Chloride

Dosing

1–1.12

2 g (9.3 mEq) of in 100 mL for 2 hours

0.67 g (9.4 mEq) in 100-mL

solution over 1 h

≤ 0.99

4 g (18.6 mEq) of calcium gluconate in

100 or 250 mL for 4 hours

1.3 g (18.2 mEq) in 100 mL

over 1 h

aCalcium gluconate is the preferred method of repletion. Calcium chloride should be used (preferably) only in code situations, not for routine replacement therapy,

because the chloride salt contains about 2.5 times the amount of elemental calcium and can cause tissue necrosis when given peripherally in contrast to calcium

gluconate. In addition, calcium chloride should never be added to the PN solution unless there is no phosphate in the PN solution and the commercial amino acids used

in the PN solution do not contain phosphorus (some amino acid products do contain phosphate). A serum ionized calcium concentration determination should be repeated

several hours after completing the calcium infusion to allow equilibration (Nutrition 2007;23:9-15). More aggressive therapy may need to be considered for patients with

tetany or life-threatening cardiac arrhythmias caused by hypocalcemia.

bIntravenous calcium administration should be used with extreme caution in patients with severe hypokalemia or in those receiving digoxin or other digitalis alkaloids.

cAlways check the serum phosphorus concentration because hyperphosphatemia can induce hypocalcemia, given the metastatic precipitation of calcium phosphate in the

soft tissues and lungs (usually associated with renal disease).

dBoth calcium preparations are compatible with 0.9% NaCl and D5W.

eUse of a continuous infusion of calcium may be considered in some situations where severe and/or persistent hypocalcemia may occur. Examples include during

continuous renal replacement therapy and massive transfusion protocols where there may be concern for citrate-related toxicity. In these cases, 4 g of calcium gluconate

or chloride can be added to 1 L of solution and initiated at 50-100 mL/h. Further titrations should be made on the basis of repeat calcium concentrations (Endocr Connect.

2019;8(6):X1).

D5W = 5% dextrose in water; NaCl = sodium chloride.