I. Problem/Condition.

Magnesium plays a key role in adenosine triphosphate (ATP) metabolism, calcium and potassium regulation, and cardiac and neural conduction. Hypermagnesemia is rare in the setting of normal renal function given the kidney’s ability to decrease reabsorption when levels are increased. However, recent evidence suggests that even mild hypermagnesemia is associated with increased in-hospital mortality, and that the risk of mortality increases with increasing magnesium levels. Mild hypermagnesemia is classified as a serum magnesium level between 4 and 6 milliequivalents/liter (meq/L), with levels higher than that classified as severe.

II. Diagnostic Approach

A. What is the differential diagnosis for this problem?

There are two major differential diagnoses for hypermagnesemia; the most common is decreased kidney function, specifically a glomerular filtration rate (GFR) of less than 30 milliliters/minute (ml/min). The other major cause is excessive consumption and/or administration of magnesium-containing medications and supplements, such as laxatives, antacids, enemas, and the use of intravenous (IV) magnesium in patients with possible cardiac disease. In patients with chronic renal insufficiency, even a normal level of magnesium consumption can lead to elevated serum magnesium levels. Patients with normal renal function who develop hypermagnesemia will usually have an underlying bowel condition that contributes to decreased gut motility, leading to increased absorption of magnesium; possible underlying conditions include narcotic or anticholingeric use, inflammatory bowel diseases, and intestinal obstruction.

Less common causes of hypermagnesemia include the intravenous administration of magnesium in obstetric patients with preeclampsia, lithium use, and familial hypocalcuric hypercalcemia (see endocrine).

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

An initial approach to hypermagnesemia includes an assessment of renal function, a review of all medications and supplements taken by the patients, and an evaluation of possible bowel motility pathology. If this approach yields no cause, evaluation for the rarer causes listed above should be performed.

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

Patients with mild hypermagnesemia may report nausea, vomiting, facial flushing, difficulty urinating, and/or constipation. Severe hypermagnesemia may present with somnolence, flaccid paralysis, and respiratory depression. Magnesium levels should be checked in all patients with a history of renal insufficiency and in patients with gastrointestinal complaints requiring frequent use of antacids or laxatives.

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

Vital signs may show bradycardia, hypotension, and decreased respiratory rate; the first two signs can be seen even in patients with only mild hypermagnesemia. Patients with hypermagnesemia may also have decreased deep tendon reflexes.

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

Besides measurement of a patient’s serum magnesium level and GFR, other laboratory or radiographic tests are not useful in evaluation of the most common causes of hypermagnesemia.

If the hypermagnesemia is severe enough, regardless of the underlying cause, electrocardiogram (EKG) findings may include prolonged PR and QT intervals and wide QRS complexes. Severe hypermagnesemia may lead to complete heart block and cardiac arrest.

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

The cut-off for hypermagnesemia is generally considered to be above 2.3 meq/L; symptoms do not usually appear until the serum magnesium level reaches 4 meq/L.

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

It is unnecessary to measure an ionized magnesium level.

III. Management while the Diagnostic Process is Proceeding

A. Management of hypermagnesemia.

Mild hypermagnesemia in patients with a GFR > 30 ml/min can be managed conservatively with discontinuation of any offending substances and watchful waiting; if the cause of the hypermagnesemia was the intake of magnesium-containing medications or supplements, levels should return to normal within 24 hours. If desired, loop diuretics can speed up the process of normal renal magnesium excretion.

In patients with chronically or acutely decreased GFRs between 15-29 ml/min and only mild hypermagnesemia by serum levels or by symptoms, cessation of all magnesium-containing medications should be combined with administration of a loop diuretic and simultaneous normal saline (NS) infusion; for example, furosemide 20-40 milligrams (mg) IV every 4 hours and 0.9% NS at 150 milliliters/hour. The lower a patient’s GFR, the higher their necessary loop diuretic dose.

For symptomatic hypermagnesemia with hypotension or respiratory depression, regardless of GFR, hemodyalysis is often indicated; while preparing for dialysis, 100-200 mg IV elemental calcium should be given to temporarily reverse the effects of the hypermagnesemia on neuromuscular junctions. Lastly, unless the patient is completely anuric, administration of the loop diuretic and NS infusion as suggested in the previous paragraph is also indicated while awaiting dialysis.