I. Problem/Condition.

Magnesium plays a key role in adenosine triphosphate (ATP) metabolism, calcium and potassium regulation and cardiac and neural conduction. Hypomagnesemia may occur due to either gastrointestinal or renal losses, and is a common finding among critically ill patients and patients with other electrolyte abnormalities.

II. Diagnostic Approach

A. What is the differential diagnosis for this problem?

Hypomagnesemia most commonly results from either urinary or gastrointestinal losses. Insufficient dietary intake of magnesium is rare with the exception of chronic alcohol abuse which may also directly inhibit tubular reabsorption of magnesium. More often, gastrointestinal losses may be seen in malabsorption due to chronic diarrhea, pancreatitis or bowel resection.

Excess urinary loss of magnesium occurs most often with diuretic use (both loop and thiazide), but may also be seen in post-obstructive diuresis, osmotic diuresis with uncontrolled hyperglycemia and more rarely in genetic deficiencies of tubular reabsorption such as Bartter’s and Gitleman’s Syndromes (see renal). A number of drugs including aminoglycosides, amphotericin B, cisplatin, cyclosporine and pentamidine may also cause tubular magnesium wasting. More unusual causes of hypomagnesemia include skin losses in burn victims and hungry bone syndrome after parathyroidectomy.

Continue Reading

B. Describe a diagnostic approach/method to the patient with this problem

Magnesium deficiency should be suspected in any patient presenting with malnutrion or malabsorption, excess urinary losses or known potassium or calcium abnormalities. The diagnosis can be confirmed with a serum magnesium level although this may not be reflective of overall body stores. If it is not clear whether magnesium losses are gastrointestinal or renal, rarely a 24-hour urinary magnesium excretion or fractional excretion of magnesium may be ordered. With gastrointestinal losses, the kidney is magnesium avid and urinary excretion will be low. High levels of magnesium excretion suggest tubular wasting.

1. Historical information important in the diagnosis of this problem.

Significant hypomagnesemia may present with nystagmus, vertigo, seizures and altered mental status. History to consider:

  • Does the patient have a history of diuretic use?

  • Is there a history of chronic diarrhea or bowel resection?

  • Does the patient have a history of chronic alcohol abuse?

2. Physical Examination maneuvers that are likely to be useful in diagnosing the cause of this problem.

Patients with hypomagnesemia may have tetany as well as positive Chvostek’s and Trousseau’s. These signs may be related to concomitant hypocalcemia, but may also occur despite normal calcium levels.

3. Laboratory, radiographic and other tests that are likely to be useful in diagnosing the cause of this problem.

Electrocardiography (EKG) changes with hypomagnesemia are similiar to those seem in hypokalemia- prolonged PR and QT intervals, ST depression and T wave inversions. Hypomagnesemia may cause arrhythmias such as supraventricular tachycardias and Torsade de Pointes.

C. Criteria for Diagnosing Each Diagnosis in the Method Above.

Mild hypomagnesemia is defined as between 1-1.5meq/L. Severe hypomagnesemia is considered at levels below 1meq/L.

D. Over-utilized or “wasted” diagnostic tests associated with the evaluation of this problem.

Magnesium levels do not need to be routinely ordered as part of the basic metabolic panel for every patient. Magnesium levels should be ordered for critically ill patients and for patients with risk factors such as diuretic use, malabsorption or renal insufficiency. It is unnecessary to directly measure an ionized magnesium level.

III. Management while the Diagnostic Process is Proceeding

A. Management of hypomagnesemia.

Mild hypomagnesemia may be treated with oral repletion. If the patient is asympomatic and lacks other electrolyte abnormalities, treatment may not be necessary. For symptomatic magnesium deficiency or for levels below 1meq/L, parental repletion is recommended in the form of magnesium chloride or magnesium sulfate.

Severe deficiency

Magnesium sulfate 8-12g IV over 24 hours, followed by 4-6g/day x 3 days

  • Magnesium chloride 50-100meq/day

  • Decrease rate by 50% for patients with reduced GFR

Mild deficiency
  • Oral magnesium salts (MgCl-, MgO, etc.) 2 tabs 2-3x/day

B. Common Pitfalls and Side-Effects of Management of this Clinical Problem

Magnesium sulfate contains significantly less magnesium than magnesium chloride and may aggravate hypocalcemia. Magnesium levels may improve immediately after infusion, but may subsequently decrease as the cation equilibrates with intracellular stores. Sustained treatment for several days may be necessary.