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Module 3 • Clinical Pharmacology
Fluids, Electrolytes, Acid-Base & Nutrition
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Fluids, Electrolytes, Acid-Base & Nutrition
Ashley Hawthorne ~3 min read Module 3 of 20
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Fluids, Electrolytes, Acid-Base Disorders, and Nutrition Support

D.Disorders of Magnesium Homeostasis
1

Magnesium homeostasis overview

99% intracellular (17% of total body content is in the muscle or in the skeleton)

Total body stores: Around 2000 mEq

Normal serum concentration: 1.8–2.4 mg/dL (about 30% bound to protein)

d.Average daily requirement: Around 24–32 mEq/day

Kidney is primary route of elimination (around 70% reabsorbed in ascending loop of Henle) and is

without any hormonal regulation of renal magnesium reabsorption.

Losses can be extensive with severe diarrhea or body fluid drainages (see Table 4).

Magnesium depletion can influence potassium and calcium homeostasis.

2Hypomagnesemia

Definition: Although the lower limit of normal for serum magnesium concentrations is 1.8 mg/

dL (1.5 mEq/L), most clinicians define significant hypomagnesemia as 1.5 mg/dL (1.3 mEq/L) or

less (Annu Rev Med 1981;32:245-59; Nutrition 1997;13:303-8). Many ICUs have a target serum

magnesium concentration greater than 2 mg/dL (1.8 mEq/L). Serum concentrations of magnesium

may be slightly falsely lowered in the presence of significant hypoalbuminemia (Annu Rev Med

1981;32:245-59; Nutrition 1997;13:303-8).

Signs and symptoms: Muscle weakness, cramping, paresthesias, Chvostek and Trousseau signs,

tetany, QT prolongation, hypokalemia, hypocalcemia

Etiologies:

GI losses (especially diarrhea) – Average stool loss of about 6 mEq/L; up to 10–12 mEq/L or

greater for secretory diarrheal losses

ii.

Alcohol abuse (increased renal excretion; impaired absorption; poor nutritional status of

patients with alcohol use disorder)

iii.

Sepsis/critical illness (increased urinary excretion – several factors)

iv.

Pancreatitis (partly attributable to calcium-magnesium soap formation in peritoneum)

Thermal injury/TBI (increased urinary excretion – several factors)

vi.

Drugs – Diuretics, amphotericin B, caspofungin, cyclosporin/tacrolimus, foscarnet,

pentamidine, piperacillin/tazobactam, cisplatin/carboplatin/ifosfamide/cetuximab, lactulose/

orlistat, aminoglycosides, and potentially long-term use of digoxin or proton pump inhibitors

vii.

Polyuria (osmotic agents, hypercalcemia, ureagenesis)

d.Estimating magnesium deficit: For a serum magnesium concentration of less than 1.5 mg/dL (1.3

mEq/L), a 1- to 2-mEq/kg deficit can be expected.

Treatment:

Treat the etiology (if possible). Be sure to treat magnesium deficiency at the same time or

before potassium therapy if the patient is also hypokalemic.

ii.

Successful treatment of hypomagnesemia usually takes 4–5 days of intravenous therapy.

Intramuscular magnesium therapy for replacement therapy is inadvisable given the limit on

volume per injection site with respect to dosage requirements and tissue irritation.

iii.

Intravenous magnesium sulfate 32–48 mEq/day (4–6 g/day) – Suggested to be sufficient to

maintain serum magnesium within 2–2.5 mg/dL for most magnesium-deficient patients (Crit

Care Med 1996;24:38-45; Annu Rev Med 1981;32:245-59)
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