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Subject: Magnesium (Mg)
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Mg is primarily an intracellular ion associated with GI absorption and renal excretion. At least 65–70% of Mg is in ionized state, and approximately 35% serum Mg is protein bound.
Normal range: 1.6–2.4 mg/dL.
Critical values: <1.0 and >4.9 mg/dL.
Diagnosis and monitoring of hypomagnesemia and hypermagnesemia, especially in renal failure or GI disorders
To monitor preeclampsia patients being treated with magnesium sulfate, although in most cases, monitoring clinical signs (respiratory rate and deep tendon reflexes) is adequate, and blood magnesium levels are not required
Iatrogenic (is usual cause; most often with impaired renal function).
Diuretics (e.g., furosemide >80 mg/day, thiazides)
Antacids or enemas containing Mg
Laxative and cathartic abuse
Mg for eclampsia or premature labor
Lithium carbonate intoxication
Renal failure (when GFR approaches 30 mL/minutes); in chronic renal failure, hypermagnesemia is inversely related to residual renal function. Increase is rarely observed with normal renal function.
Dehydration with diabetic coma before treatment
Addison disease and after adrenalectomy
Controlled DM in older patients
Accidental ingestion of large amount of sea water
Almost always GI or renal disturbance; chronic Mg deficiency produces hypocalcemia secondary to decreased production and effectiveness of PTH.
Malabsorption (e.g., sprue, small bowel resection, biliary and intestinal fistulas, abdominal irradiation, celiac disease, and other causes of steatorrhea; familial Mg malabsorption)
Abnormal loss of GI fluids (chronic ulcerative colitis, Crohn disease, villous adenoma, carcinoma of the colon, laxative abuse, prolonged aspiration of GI tract contents, vomiting)
Renal disease: a level >2 mEq/day in urine during hypomagnesemia indicates excessive renal loss.
Renal tubular acidosis
Diuretic phase of acute tubular necrosis
Diuretics (e.g., mercurials, ammonium chloride, thiazides, furosemide)
Antibiotics (e.g., aminoglycosides, gentamicin, tobramycin, carbenicillin, ticarcillin, amphotericin B)
Digitalis (in 20% of patients taking Digitalis)
Antineoplastic (e.g., cisplatin)
Cyclosporine: tubular losses due to ions or nutrients
Diuresis caused by glucose, urea, or mannitol
Extracellular fluid volume expansion
Primary renal Mg wasting
Prolonged parenteral fluid administration without Mg (usually >3 weeks)
Acute and chronic alcoholism and alcoholic cirrhosis
Starvation with metabolic acidosis
Kwashiorkor, protein–calorie malnutrition
Aldosteronism (primary and secondary)
Hyperparathyroidism and other causes of hypercalcemia
DM (in ≤39% of patients; caused by osmotic diuresis)
Third trimester of pregnancy
Insulin treatment of diabetic coma
Toxemia of pregnancy or eclampsia
Lytic tumors of bone
Active Paget disease of bone; caused by increased uptake by bone
Transfusion of citrated blood
Mg deficiency frequently coexists with other electrolyte abnormalities; it may cause apparently unexplained hypocalcemia and hypokalemia and should always be measured in such cases. About 40% of patients have coexisting hypokalemia.
About 90% of patients with high or low serum Mg levels are not clinically recognized; therefore, routine inclusion of Mg with electrolyte measurements has been suggested.
Digitalis sensitivity and toxicity frequently occur with hypomagnesemia.
Ionized Mg is decreased in only approximately 70% of critically ill patients with decreased total Mg.
Because deficiency can exist with normal or borderline serum Mg levels, a 24-hour urine test may be indicated by frequent concomitant disorders (coexist with other electrolyte abnormalities).
A 24-hour urine level <25 mg suggests Mg deficiency (in the absence of conditions or agents that promote magnesium excretion). If caused by renal loss, urine Mg should be >3.65–6 mg/day.
If level is <2.4 mg/day, collect a 24-hour urine sample during IV administration of 72 mg of MgCl2. Some 60–80% of the load is excreted by patients with normal Mg stores; <50% excretion suggests nonrenal Mg depletion.
Serum magnesium levels may remain normal even when total body stores of magnesium are depleted up to 20%.
Phylate, fatty acids, and an excess of phosphate impair Mg absorption
Hemolysis yields elevated results because levels in erythrocytes are two to three times higher than in serum.