Hypermagnesemia is a greater-than-normal serum concentration of magnesium. A serum magnesium level can appear falsely ele-vated when blood specimens are allowed to hemolyze or are drawn from an extremity with a tourniquet that was applied too tightly.
By far the most common cause of hypermagnesemia is renal failure. In fact, most patients with advanced renal failure have at least a slight elevation in serum magnesium levels. This condition is aggravated when such patients receive magnesium to control seizures or inadvertently take one of the many commercial antacids that contain magnesium salts.
Hypermagnesemia can occur in a patient with untreated di-abetic ketoacidosis when catabolism causes the release of cellu-lar magnesium that cannot be excreted because of profound fluid volume depletion and resulting oliguria. An excess of mag-nesium can also result from excessive magnesium administered to treat hypertension of pregnancy and to lower serum magne-sium levels. Increased serum magnesium levels can also occur in adrenocortical insufficiency, Addison’s disease, or hypother-mia. Excessive use of antacids (eg, Maalox, Riopan, Mylanta)and laxatives (Milk of Magnesia) also increases serum magne-sium levels.
Acute elevation of the serum magnesium level depresses the cen-tral nervous system as well as the peripheral neuromuscular junc-tion. At mildly elevated levels, there is a tendency for lowered blood pressure because of peripheral vasodilation. Nausea, vom-iting, soft tissue calcifications, facial flushing, and sensations of warmth may also occur. At higher magnesium concentrations, lethargy, difficulty speaking (dysarthria), and drowsiness can occur. Deep tendon reflexes are lost, and muscle weakness and paralysis may develop. The respiratory center is depressed when serum magnesium levels exceed 10 mEq/L (5 mmol/L). Coma, atrioventricular heart block, and cardiac arrest can occur when the serum magnesium level is greatly elevated and not treated.
On laboratory analysis, the serum magnesium level is greater than 2.5 mEq/L or 3.0 mg/dL (1.25 mmol/L). ECG findings may in-clude a prolonged PR interval, tall T waves, and a widened QRS. ECG findings demonstrate a prolonged QT interval and atrio-ventricular blocks.
Hypermagnesemia can be prevented by avoiding the administra-tion of magnesium to patients with renal failure and by carefully monitoring seriously ill patients who are receiving magnesium salts. In patients with severe hypermagnesemia, all parenteral and oral magnesium salts are discontinued. In emergencies, such as res-piratory depression or defective cardiac conduction, ventilatory support and IV calcium are indicated. In addition, hemodialysis with a magnesium-free dialysate can reduce the serum magnesium to a safe level within hours. Loop diuretics and 0.45% sodium chloride (half-strength saline) solution enhance magnesium ex-cretion in patients with adequate renal function. IV calcium glu-conate (10 mL of a 10% solution) antagonizes the neuromuscular effects of magnesium.
Patients at risk for hypermagnesemia are identified and assessed. When hypermagnesemia is suspected, the nurse monitors the vital signs, noting hypotension and shallow respirations. The nurse also observes for decreased patellar reflexes and changes in the level of consciousness. Medications that contain magnesium are not given to patients with renal failure or compromised renal function, and patients with renal failure are cautioned to check with their health care providers before taking over-the-counter medications. Caution is essential when preparing and administering magnesium-containing fluids parenterally because available parenteral mag-nesium solutions (eg, 2-mL ampules or 50-mL vials) differ in concentration.
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