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Distribution and Balance
Average body Mg content is about 1000 mmoles (14 mmoles / kg of body wt), of which ~50% resides in soft tissues and the remainder in bones. The extracellular space contains <1% of total body Mg. The plasma Mg level normally varies within a relatively wide range (1.5 - 2.5 mEq/L). Clinical laboratories typically measure total plasma Mg, of which ~30% is bound to plasma proteins, ~ 20% is complexed with such ions as phosphate and citrate, and ~50% exists in the ionized (physiologically active) state. Due to the relatively low protein binding, variations in the plasma protein level have little influence on the total plasma Mg concentration. This is unlike the case plasma calcium of which ~45% is protein-bound. To correct for low plasma protein levels:

Although serum Mg may not accurately reflect the overall body Mg balance, clinical symptoms of Mg deficiency correlate well with serum Mg. Levels < 1.0 mEq/L usually indicate significant total body Mg depletion. However, the severity of the symptoms among patients with similar degrees of hypomagnesemia vary widely. The so-called Mg retention test should not be used in patients with renal impairment or in transplant patients receiving cyclosporine or tacrolimus which cause urinary Mg wasting.
Mg balance is primarily a renal function (Mg intake does not appear to be regulated). The average diet provides 20 - 30 mEq daily, but the net absorption is only about 7 mEq. The kidneys normally excrete an equal amount in order to maintain Mg balance. However, in the presence of Mg deficiency urinary Mg excretion can be reduced to a minimum of about 2 mEq/day. Renal Mg reabsorption takes place primarily in the proximal tubule (30% of the filtered load) and the thick ascending limb of Henle's loop (65%). Overall renal reabsorption appears to be saturable, so that a higher Mg intake results in a proportional increase urinary excretion. For this reason, it is difficult for patients with normal renal function to develop hypermagnesemia.

Dietary Sources
Average diet provides a daily Mg intake ranging form ~17 to ~ 50 mEq ( 200 - 600 mg). Mg is ubiquitous in food, but it is particularly abundant in dairy products, bread and cereals, vegetables (specially the leafy types), meat, and nuts (specially almonds).

Symptoms of Hypomagnesemia

1. Neural and Neuromuscular:
   Neural and neuromuscular abnormalities are the most common clinical signs of hypomagnesemia. Lowered excitability threshold may be manifested as irritability, psychosis, esophageal spasms (leading to dysphagia), and convulsions. Neuromuscular manifestations include tremor, fasciculations, and tetany. The latter occurs almost exclusively in presence of hypocalcemia.
   Chronic, whole-body Mg depletion may be associated with lethargy, poor appetite, nausea, muscle cramps, paresthesias, and mental abnormalities (irritability, confusion, disorientation, etc.).
2. Cardiovascular
   • ECG changes: Prolonged PR & QT intervals and flattening of the T waves.
   • Ventricular dysrhythmias: Premature contractions, tachycardia, and fibrillation. These occur almost exclusively in patients receiving digoxin therapy because both digoxin and hypomagnesemia promote the loss of K from myocardial cells. Thus, hypomagnesemia, like hypokalemia, predisposes patients to digitalis toxicity.
3. Metabolic
   Although an acute fall in plasma Mg tends to stimulate the release of parathormone (PTH), chronic hypomagnesemia has the opposite effect, resulting in hypoparathyroidism and hypocalcemia. Also, hypomagnesemia is associated with target-tissue resistance to the actions of PTH. Correction of the hypocalcemia induced by Mg deficiency requires the repletion of Mg stores as an essential first step.

   Because Mg⁺⁺ is necessary for the activation of the Na-K-ATPase, Mg deficiency is almost always associated with intracellular K⁺ depletion. Also, Mg depletion induces renal K ⁺ loss possibly by inhibiting K ⁺ reabsorption in the proximal tubules. The hypokalemia associated with Mg deficiency can be corrected only through the administration of both ions.

Severe, symptomatic hypomagnesemia may be treated with magnesium sulfate (MgSO₄.7H₂O) given either IV or IM. In urgent cases (e.g., seizures) 2 grams of MgSO₄.7H₂O (16.3 mEq of Mg⁺⁺) may be given undiluted as iv push (1 mL / min) or diluted in 100 mL of D5W and infused over 10 - 20 min. Due to limitations in Mg retention and relatively slow equilibration with the intracellular pool, replenishment of the body's Mg stores should be carried out gradually over several days. A simple rule of thumb for a somewhat aggressive iv replacement protocol is:

Special attention must be paid to the patient's renal status and Mg level. The table below shows parenteral regimens suitable for less urgent cases involving adult patients with normal renal function.