Magnesium status depends on three organs: uptake in the intestine, storage in the bone, and excretion in the kidneys. Hypermagnesemia is therefore often due to problems in these organs, mostly the intestine or kidney.
Predisposing conditions
Hemolysis, magnesium concentration in red blood cells is approximately three times greater than in serum, therefore hemolysis can increase plasma magnesium. Hypermagnesemia is expected only in massive hemolysis.
Chronic kidney disease, excretion of magnesium becomes impaired when creatinine clearance falls below 30 ml/min. However, hypermagnesemia is not a prominent feature of chronic kidney disease unless magnesium intake is increased.
Hypermagnesemia is diagnosed by measuring the concentration of magnesium in the blood. Concentrations of magnesium greater than 1.1 mmol/L are considered diagnostic.
Treatment
People with normal kidney function and mild asymptomatic hypermagnesemia require no treatment except for the removal of all sources of exogenous magnesium. One must consider that the half-time of elimination of magnesium is approximately 28 hours. In more severe cases, close monitoring of the ECG, blood pressure, and neuromuscular function and early treatment are necessary: Intravenous calcium gluconate or calcium chloride since the actions of magnesium in neuromuscular and cardiac function become antagonized by calcium. Severe clinical conditions require increasing renal magnesium excretion through: Intravenous loop diuretics, or hemodialysis, when kidney function is impaired, or the patient is symptomatic from severe hypermagnesemia. This approach usually removes magnesium efficiently. Dialysis can, however, increase the excretion of calcium by developing hypocalcemia, thus possibly worsening the symptoms and signs of hypermagnesemia. The use of diuretics must be associated with infusions of saline solutions to avoid further electrolyte disturbances and metabolic alkalosis. The clinician must perform serial measurements of calcium and magnesium. In association with electrolytic correction, it is often necessary to support cardiorespiratory activity. As a consequence, the treatment of this electrolyte disorder can frequently require intensive care unit admission. Particular clinical conditions require a specific approach. For instance, during the management of eclampsia, the magnesium infusion is stopped if urine output drops to less than 80 mL, deep tendon reflexes are absent, or the respiratory rate is below 12 breaths/minute. A 10% calcium gluconate or chloride solution can serve as an antidote.
Epidemiology
Hypermagnesemia is an uncommon electrolyte disorder. It occurs in approximately 10 to 15% of hospitalized patients with renal failure. Furthermore, epidemiological data suggest that there is a significant prevalence of high levels of serum magnesium in selected healthy populations. For instance the overall prevalence of hypermagnesemia was 3.0%, especially in males in Iran. For instance high magnesium concentrations were typical in people with cardiovascular disease, and 2.3 mg/dL or higher values were associated with worse hospital mortality.
Prognosis
The prognosis of hypermagnesemia depends on magnesium values and on the clinical condition that induced hypermagnesemia. Values that are not excessively high and in the absence of triggering and aggravating conditions are benign conditions. On the contrary, high values expose the patient to high risks and high mortality.
Complications
Severe hypermagnesemia can lead to cardiovascular complications and neurological disorder. Higher values of serum magnesium can induce cardiac arrest and coma.
