Magnesium (Mg2+)
BASICS
- Essential for cellular energy-dependent reactions involving ATP
- Important in the regulation of Ca2+ channel function
- Ionized Mg2+ is the active form
- Pathophysiology
- Approximately 99% of total Mg2+ is intracellular or bone deposited, with only 1% in extracellular fluid (serum)
- Approximately 60% of total Mg2+ is found in bone, 20% in muscle, and 20% in other soft tissues including the liver
- Approximately 70% of serum Mg2+ is ionized (active) while 30% is protein bound
- Extracellular Mg2+ depends on GI absorption renal excretion/reabsorption, and bone exchange, although Mg2+ is poorly mobilized from bone
- PTH increases Mg2+ absorption in the GI tract and resorption in the kidneys. Mg2+ renal reabsorption increases with activation of arginine vasopressin, β-adrenergic agonists, insulin, and PTH
- Renal reabsorption of Mg2+ decreases with hyperglycemia, hypercalcemia, hypermagnesemia, and hypophosphatemia
- Systems affected—neurologic; cardiovascular; gastrointestinal; musculoskeletal
- Clinical signs associated with hypomagnesemia are uncommon unless severe
- Clinical signs of hypermagnesemia are attributed to concurrent increases in other electrolytes
- Colic from ileus
- Weakness, muscle fasciculations, ataxia, seizures, and coma
- Severe hypomagnesemia can cause ventricular or supraventricular arrhythmias, or atrial fibrillation
- Hypomagnesemia and hypocalcemia can cause synchronous diaphragmatic flutter
- Anorexia
- Decreased GI absorption (e.g. infiltrative GI disease, enteritis)
- Renal loss (e.g. renal disease, diuretics, aminoglycoside administration)
- Prolonged exercise (i.e. loss through sweat)
- Sepsis/endotoxemia
- Lactation
- Hypersalivation
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS