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Magnesium deficiency occurs in up to 11% of hospitalized patients and 52% of
patients in coronary care units. The most common diagnoses in patients with acute
magnesium depletion are malignancy, chronic obstructive pulmonary disease, and
alcoholism; coronary artery disease (CAD) and bypass surgery are also often
associated with acute magnesium deficiency.
  Alcoholism, liver disease, diabetes mellitus, and carcinoma are most frequently

assoiated with chronic hypomagnesemia. The maintenance of body magnesium

stores within narrow limits is essential to cellular energy production. Depletion or

excess of body magnesium stores may have profound effects on cardiovascular
function. The normal range of serum magnesium is approximately 1.5 to 2.0 (±0.2)

mEq/L, which is maintained by the kidney, intestine, and bone.

I. Pathophysiology

   A. Decreased Magnesium Intake. Protein-calorie malnutrition, prolonged

      parenteral (Mg-free) fluid administration, and catabolic illness are common

      causes of hypomagnesemia.

   B. Gastrointestinal Losses of Magnesium. Gastrointestinal losses of Mg may

      result from prolonged nasogastric suction, laxative abuse, pancreatitis,

      extensive small bowel resection, short bowel syndromes, biliary and bowel

      fistulas, enteropathies, cholestatic liver disease, and malabsorption syndromes.
   C. Renal Losses of Magnesium

      1. Renal loss of Mg may occur secondary to renal tubular acidosis,
         glomerulonephritis, interstitial nephritis, or acute tubular necrosis.

      2. Hyperthyroidism, hypercalcemia, and hypophosphatemia may cause Mg

      3. Drugs Associated with Mg Loss. Diuretic agents (furosemide, thiazides)

         induce hypomagnesemia by increasing Mg excretion.                      Digitalis,

         aminoglycoside antibiotics, cyclosporine, methotrexate, amphotericin,
         pentamidine, ethanol, and calcium are associated with hypomagnesemia.

   D. Alterations in Magnesium Distribution

      1. Redistribution of circulating Mg occurs by extracellular to intracellular shifts,
             sequestration, hungry bone syndrome, or by acute administration of glucose,
             insulin, or amino acids.
         2. Mg depletion occurs during severe pancreatitis, large quantities of parenteral
             fluids, and pancreatitis-induced sequestration of Mg.
II. Clinical Manifestations of Hypomagnesemia

      A. Cardiovascular. Ventricular tachycardia, ventricular fibrillation, atrial fibrillation,

         multifocal atrial tachycardia, ventricular ectopic beats, hypertension,
         enhancement of digoxin-induced dysrhythmias, and cardiomyopathies.

      B. Neuromuscular findings may include positive Chvostek's and Trousseau's

         signs, tremors, myoclonic jerks, seizures and, eventually, coma.

      C. ECG Changes may include a spectrum of ventricular arrhythmias

         (extrasystoles,    tachycardia)    and    atrial   arrhythmias    (atrial   fibrillation,

         supraventricular tachycardia), as well as torsades de pointes. Prolonged PR
         and QT intervals, ST segment depression, T wave inversions, wide QRS

         complexes, and tall T waves may occur.

      D. Concomitant electrolyte abnormalities of sodium, potassium, calcium, or

         phosphate are common.

III. Clinical Evaluation

      A. Hypomagnesemia is diagnosed when the serum Mg is less than 0.7-0.8

         mMol/L. Symptoms of Mg deficiency occur when the serum Mg concentration

         is less than 0.5 mMol/L. 24-hour urine collection for magnesium is the first step
         in the evaluation of hypomagnesemia. In hypomagnesemic states, because of

         renal Mg loss, magnesium excretion exceeds 1.5-2.5 mMol/day.

      B. Low urinary Mg excretion (<1 mMol/day), with concomitant serum

         hypomagnesemia, suggests Mg deficiency due to decreased intake, nonrenal
         losses, or redistribution of Mg.
IV.      Treatment of Hypomagnesemia

      A. Asymptomatic Magnesium Deficiency

         1. In hospitalized patients, the daily Mg requirements can be provided through
             either a balanced diet, as oral Mg supplements (0.36-0.46 mEq/kg/day), or

             16-30 mEq/day in a parenteral nutrition formulation.

         2. Magnesium oxide is better absorbed and less likely to cause diarrhea than
             magnesium sulfate. Magnesium oxide preparations include Mag-Ox 400
     (240 mg elemental magnesium per 400 mg tablet) and Uro-Mag (84 mg
     elemental magnesium per 400 mg tablet).
B. Symptomatic Magnesium Deficiency

  1. Serum Mg #0.5 mMol/L requires IV Mg repletion with electrocardiographic
     and respiratory monitoring.
  2. Magnesium sulfate 1-6 gm of in 500 mL of D5W can be infused IV at 1
     gm/hr. An additional 6-9 gms of MgSO4 should be provided as intermittent
     bolus therapy or by continuous infusion over the next 24 hours. Parenteral

     MgSO4 (4 mMol/g) is more frequently used than MgCl2.

  3. States of severe Mg deficiency may require additional therapy over a number

     of days because of slow repletion of cellular Mg stores.

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