Patients with symptomatic magnesium depletion can present in many ways. The major clinical manifestations include neuromuscular and cardiovascular manifestations and other electrolyte abnormalities. Specific signs and symptoms are outlined below.

Neuromuscular Manifestations

• Tremors
• Tetany, including positive Trousseau and Chvostek signs, muscle spasms, muscle cramps
• Seizures
• Vertical nystagmus
• Apathy
• Delirium
• Coma

Cardiovascular Manifestations

• Electrocardiogram changes, including widening of the QRS complex, peaked T waves, prolongation of the PR interval
• Atrial and ventricular premature systoles
• Atrial fibrillation
• Ventricular arrhythmias, including torsades de pointes
• Cardiac ischemia

Other Electrolyte and Hormone Abnormalities

• Hypocalcemia
• Hypoparathyroidism
• Hypokalemia

It is recommended to check the following in a patient suspected of having hypomagnesemia:

• Serum magnesium, phosphate, calcium level
• Basic metabolic panel, including serum creatinine/kidney function, glucose levels
• Electrocardiogram

Once hypomagnesemia is confirmed, the etiology usually can be obtained from the history. If unsure, the distinction between gastrointestinal losses and renal losses can be made by measuring the 24-hour urinary magnesium excretion. In addition, one can calculate the fractional excretion of magnesium (on a random urine specimen) with the following formula where U” and “P” refer to the urine and plasma concentrations of magnesium (Mg) and creatinine (Cr). 

• FE = [ U x P ]/[ (0.7 x P) x U ] x 100 

If the fractional excretion of magnesium is above 2% in someone with normal renal function, the hypomagnesemia is likely secondary to renal magnesium wasting from drugs such as diuretics, aminoglycosides, or cisplatin.

The treatment of patients with hypomagnesemia is based on a patient’s kidney function, the severity of their symptoms, and their hemodynamic stability. If a patient is hemodynamically unstable in an acute hospital setting, 1 to 2 grams of magnesium sulfate can be given in about 15 minutes. For symptomatic, severe hypomagnesemia in a stable patient, 1 to 2 grams of magnesium sulfate can be given over one hour. Non-emergent repletion of the adult patient is generally 4 to 8 grams of magnesium sulfate given slowly over 12 to 24 hours. In pediatric patients, the dose is 25 to 50 mg/kg (with a maximum of 2 grams).[9][10]

For an asymptomatic patient who is not hospitalized and can tolerate medications by mouth, sustained-release oral replacement should be tried first.

After repletion, serum electrolyte levels must be rechecked (whether in an inpatient or outpatient setting) to ensure that the treatment was effective. Although serum magnesium levels rise quickly with treatment, intracellular magnesium takes longer to replete. Thus, patients with normal renal function should try to continue magnesium repletion for two days after the level normalizes.

Use caution in repleting magnesium in patients with abnormal kidney function (defined as creatinine clearance less than 30 mL/min/1.73 m2). These patients are at risk of hypermagnesemia. Studies recommend reducing the magnesium dose by 50% and closely monitoring magnesium levels in these patients. 

The underlying cause of persistent hypomagnesemia should be addressed and treated. For example, if a patient is consistently having low levels of the electrolyte due to renal losses, they may benefit from amiloride, a potassium- and magnesium-sparing diuretic.

Always check for other electrolyte abnormalities when suspecting or treating hypomagnesemia. Low levels of magnesium can, in turn, cause low levels of potassium and/or calcium as well. Furthermore, many other electrolyte and hormonal abnormalities can present with similar symptoms.

Prognosis depends on the underlying cause of the hypomagnesemia. Patients with hypomagnesemia from an identifiable cause have a good prognosis for complete recovery.

It is important to treat hypomagnesemia. Dangerously low levels of magnesium have the potential to cause fatal cardiac arrhythmias, such as torsades de pointes (polymorphous ventricular tachycardia with marked QT prolongation). Moreover, hypomagnesemia in patients with acute myocardial infarction puts them at higher risk of ventricular arrhythmias within the first 24 hours.

Consider consulting a nephrologist if suspecting an inherited tubular disorder or in a patient in which magnesium levels are difficult to regulate. If a patient has a cardiac arrhythmia from magnesium deficiency, cardiology can be consulted, and the patient should be monitored closely on a telemetry floor or critical care unit.

Patients with hypomagnesemia should be encouraged to eat the following foods:

• Green vegetables, such as spinach
• Beans
• Peas
• Nuts
• Seeds
• Unrefined grains

Magnesium deficiency is commonly encountered in clinical practice. The key is to find the primary cause. Asymptomatic patients can be managed with supplements prescribed as outpatients. Symptomatic patients need admission and parenteral magnesium. The prognosis for most patients with a reversible cause is excellent.

Clinicians, nurses, and pharmacists must coordinate care to find a rapid resolution to magnesium deficiency. This often involves education of the patient, family, and a team approach from the health practitioners.