TABLE 2318 Causes of Hypermagnesemia

PHYSIOLOGIC EFFECTS Hypermagnesemia only rarely produces symptoms. Mg2+ significantly decreases the transmission of neuromuscular messages and thus acts as a CNS depressant and decreases neuromuscular activity. An initial finding in hypermagnesemic patients is nausea that appears with serum levels greater than 2.0 meq/L. Somnolence may develop as levels approach 3.0 meq/L. Deep tendon reflexes tend to disappear at serum concentrations of 4.0 to 8.0 meq/L, and respiratory compromise or apnea is seen at higher levels, approximately 8.0 to 12.0 meq/L. Hypotension, heart block, or cardiac arrest may be seen with levels approaching 15.0 meq/L. ECG abnormalities such as prolonged PR and QT intervals and increased QRS duration may be seen at any level above 5.0 meq/L.

DIAGNOSIS Serum magnesium levels are usually diagnostic. The possibility of hypermagnesemia should be considered in patients with hyperkalemia or hypercalcemia. Hypermagnesemia should also be suspected in patients with renal failure, particularly in those who are taking magnesium-containing antacids, such as Maalox (see Ta_bie..2.3:18).

TREATMENT The only treatment available is the immediate cessation of Mg 2+ administration. If renal failure is not evident, dilution by IV fluids followed by furosemide (40 to 80 mg IV) may be helpful. In symptomatic patients, 1 ampule (10 mL of 10%) calcium gluconate or 5 mL of 10% IV CaCl2 (given over 5 to 10 min is appropriate). Patients with renal failure may benefit from dialysis against a decreased Mg 2+ bath that lowers serum Mg2+ levels. CHLORIDE (Cl-)

Alteration in serum chloride is seldom a primary disturbance. Chloride is a major extracellular anion that has the reciprocal power of increasing or decreasing in concentration whenever changes occur in the concentration of other anions. For example in non-anion-gap metabolic acidosis, the decrease in serum [HCO 3-] is replaced by Cl-. Cl- plays a major role in the maintenance of urinary output, ECF, acid-base, potassium balance, and normal anion gap. Cl - concentration is approximately 70 percent that of Na+ and is diffusable and active. [Cl-] should be between 95 and 105 meq/L. Cl- is easily absorbed in the intestine by active and passive transport coexistent with Na+ and HCO3-. Hydrogen and chloride ions are secreted into the gastric fluid while HCO 3- is transported into the bloodstream. Therefore, significant gastric loss of H + and Cl- from vomiting results in metabolic alkalosis. A total of 90 percent of Cl- is excreted through the kidney, with a small percentage (10 percent) secreted in sweat and stool.

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