In February EMS World began a four-part look at electrolyte imbalances. This month we look at magnesium balance disorders.

Magnesium Balance Disorders

Magnesium is the fourth most common cation in the body and the second most abundant intracellular cation after potassium. Because of this, magnesium acts much like potassium, playing a vital role in many key metabolic pathways, including neurotransmission, the production of parathyroid hormone (PTH), hormone receptor binding, DNA and protein synthesis, and the sodium-potassium pump. Two-thirds of the magnesium in the body is found in an insoluble state in the bones, 31% in the ICF, and 1% in the serum. Of the 1% in the serum, 50% to 60% is ionized and physiologically available, 25% to 30% is protein bound, and 10% to 15% is combined with anions. The normal serum levels of magnesium are 1.5 to 2.5 mEq/L. A serum level less than 1.5 mEq/L is called hypomagnesemia, and a level greater than 2.5 mEq/L is called hypermagnesemia.

Control of magnesium is not well understood, but it is absorbed in the small intestine, and the kidneys are the primary regulator of magnesium concentration. It is excreted in the feces and urine. Magnesium is obtained through ingestion of fruits, vegetables, nuts, seeds, meats and fish.

Hypomagnesemia is a common electrolyte imbalance, and is often not recognized because it presents nonspecifically. Additionally other electrolyte imbalances, such as hyperkalemia and hypocalcemia, may coexist with hypomagnesemia, making its identification difficult. There are a wide variety of causes of hypomagnesemia (Figure 1), with the most common being malnutrition. This is particularly common in chronic alcoholic patients, who typically have poor nutritional intake, decreased pancreatic function, polyuria and increased GI losses. Hypomagnesemia should be considered in the alcoholic patient experiencing delirium tremens. Increased renal losses secondary to renal dysfunction or the use of thiazide and loop diuretics, as well as GI and endocrine disorders can also precipitate hypomagnesemia.

Clinical signs and symptoms of hypomagnesemia (Figure 2) are inconsistent and do not often correlate with actual serum magnesium levels. Conditions requiring emergency intervention generally present through the cardiovascular and neuromuscular systems at levels below 1.2 mEq/L. Cardiac dysrhythmias are associated with hypomagnesemia, as are EKG changes. However, these changes are nonspecific, as they may be secondary to existing hypokalemia.

In most instances treatment of hypomagnesemia in the prehospital setting is symptomatic and guided by the patient's presentation. If hypomagnesemia is suspected in the setting of life-threatening dysrhythmias, administration of 2 to 4 grams of 50% magnesium sulfate is appropriate, unless the patient has a history of renal insufficiency or preexisting atrioventricular block. Administration is via IV infusion over 30 to 60 minutes. Bolus administration of magnesium can result in bradycardias, cardiac conduction blocks and hypotension, as well as irritation and inflammation of the vein.

Hypermagnesemia is an uncommon condition. Patients with intact renal function will rarely, if ever, develop this condition secondary to the kidneys' ability to regulate magnesium levels. Renal dysfunction is the primary cause of hypermagnesemia, although often an increased intake of magnesium-containing compounds, such as antacids, is the cause. Although there are other causes of hypermagnesemia (see Figure 3), these remain rare without preexisting renal insufficiency.

Signs and symptoms of hypermagnesemia (Figure 4) correlate well with magnesium levels. An important factor associated with hypermagnesemia or the administration of magnesium is its cardiotoxicity. If magnesium is being administered in the prehospital setting, deep tendon reflexes (DTRs) can be used as a guide to toxicity. In general, DTRs diminish at 4.0 mEq/L, while cardiotoxicity and respiratory depression manifest between 9 and 10 mEq/L. Therefore, during the administration of magnesium, the DTRs should be evaluated whenever vital signs are evaluated. If the DTRs become diminished, hypermagnesemia must be considered, and the rate of magnesium administration slowed or stopped.

Most hypermagnesemic patients can be treated symptomatically via normal interventions in the prehospital setting. Recognition and appropriate transport are often all that is required. If the condition is secondary to the administration of magnesium, the rate should be reevaluated. Severe hypermagnesemia presenting with respiratory depression or cardiac conduction abnormalities may require more aggressive treatment to dilute magnesium levels, enhance elimination and promote the movement of magnesium to the ICF. Specific interventions include:

• Administration of normal saline to dilute the magnesium in the ECF and promote excretion by the kidneys;
• Administration of 20 to 80 mg of furosemide to promote the excretion of magnesium by the kidneys;
• Administration of 100 to 200 mg of a 10% solution of calcium to antagonize the neuromuscular and cardiovascular effects of magnesium. This may also be administered as an infusion at a rate of 2 to 4 mg/kg/hr.

Next month: Calcium Balance disorders.

Bibliography

Braunwald E, Fauci AS, Kasper DL, et al. Harrison's Principles of Internal Medicine, 15^th ed. New York, NY: McGraw-Hill, 2001.

Marx JM, Hockberger RS, Walls RM, et al. Rosen's Emergency Medicine: Concepts and Clinical Practice, 6^th ed. Philadelphia, PA: Mosby, 2006.

Tintinalli JE, Kelen GD, Stapczynski JS. Emergency Medicine: A Comprehensive Study Guide, 6^th ed. New York, NY: McGraw-Hill, 2004.

Robert Vroman, BS, NREMT-P, has been involved in all levels of EMS for almost 20 years, working with both rural and urban services as a provider and educator. He has a Bachelor’s degree in Emergency Medical Care from Western Carolina University, and is currently pursuing a Master’s of Education, specializing in Adult Education and Training at Colorado State University.