Magnesium is one of the essential elements in the human body. Among the cations within cells, magnesium is second only to potassium in abundance. Magnesium is widely distributed in various tissues throughout the body, participating in numerous biological processes. It plays a role in maintaining muscle contractility and nerve excitability, and it activates many enzymes, promoting energy metabolism. The normal concentration of serum magnesium is 0.80 to 1.20 mmol/L. Its regulation is primarily managed by the kidneys, which excrete magnesium similarly to potassium. Even when serum magnesium levels decrease, the kidneys continue to excrete magnesium. Abnormalities in magnesium metabolism often occur in many diseases. When serum magnesium is less than 0.75 mmol/L, it is referred to as hypomagnesemia.

bubble_chart Etiology

Foods are rich in magnesium, and as long as the diet is normal, the body will not suffer from magnesium deficiency. Common causes include: a. Excessive loss from the digestive tract, as magnesium is absorbed in the small intestine and part of the colon. Severe diarrhea, steatorrhea, malabsorption, intestinal fistula, and extensive small intestine resection can all lead to hypomagnesemia; b. Excessive renal loss: such as chronic pyelonephritis, renal tubular acidosis, the polyuric phase of acute renal failure, or long-term use of loop diuretics, thiazides, and osmotic diuretics, which cause renal loss of magnesium and result in hypomagnesemia; c. Insufficient supplementation: in malnutrition, certain diseases with insufficient magnesium supplementation in nutritional support fluids, or even long-term use of magnesium-free solutions for treatment; d. Hyperthyroidism patients often have low blood magnesium and negative nitrogen balance, and primary hyperparathyroidism can cause symptomatic magnesium deficiency.

bubble_chart Clinical Manifestations

Early manifestations of magnesium deficiency often include anorexia, nausea, vomiting, weakness, and apathy. As magnesium deficiency worsens, symptoms such as memory impairment, nervous tension, irritability, confusion, dysphoria, restlessness, and athetoid movements may occur. Severe magnesium deficiency can lead to epileptic-like seizures. Since magnesium deficiency is often accompanied by potassium and calcium deficiencies, it is difficult to determine which symptoms are specifically caused by magnesium deficiency.

Additionally, hypomagnesemia can cause arrhythmias. Magnesium is an essential substance for activating Na⁺ K⁺ ATPase, and magnesium deficiency can lead to potassium loss in myocardial cells. On an electrocardiogram, this may manifest as prolonged PR and QT intervals, widened QRS complexes, ST segment depression, and widened, flattened, or inverted T waves. Occasionally, U waves may appear, which can be confused with hypokalemia or may be related to changes in serum potassium or calcium levels.

bubble_chart Diagnosis

The simplest method is to measure serum magnesium. However, the diagnosis of magnesium deficiency can sometimes be difficult, as normal serum magnesium levels do not rule out hypomagnesemia due to influences from pH, protein, and other factors.

For some patients with predisposing factors and presenting with hypomagnesemia, the symptoms can be hard to distinguish from hypokalemia. If there is no improvement after potassium supplementation, hypomagnesemia should be considered. Additionally, in patients experiencing convulsions suspected to be related to calcium deficiency, if convulsions persist after calcium injection, magnesium deficiency should also be suspected. Therefore, a comprehensive analysis of the patient's medical history is essential in clinical practice. When necessary, a magnesium loading test can be conducted, which is quite helpful in confirming the diagnosis of magnesium deficiency. In normal individuals, after intravenous infusion of magnesium chloride or magnesium sulfate at 0.25 mmol/kg, 90% of the infused amount is quickly excreted in the urine. However, in patients with hypomagnesemia, 40-80% of the infused magnesium can be retained in the body after the same amount of solution is administered, with as little as 0.5 mmol of magnesium excreted in the urine daily. The magnesium loading test is conducted as follows: collect all urine from the patient 24 hours before the test, then intravenously inject a solution of magnesium sulfate or magnesium chloride at 0.25 mmol/kg, and collect all urine again for 24 hours after the infusion. Measure the magnesium content in both urine samples and compare it with the amount intravenously administered.

For grade I magnesium deficiency, magnesium can be supplemented through diet or oral magnesium supplements. Magnesium oxide 250-500mg, 4 times a day, or magnesium hydroxide 200-300mg, 4 times a day can be administered. To avoid diarrhea, it can be used in combination with aluminum hydroxide gel. If oral administration is not tolerated or absorbed, magnesium can be administered via intramuscular injection, typically using 20-50% magnesium sulfate.

If hypomagnesemia is severe, presenting with hand and foot convulsions, seizure episodes, or arrhythmias, intravenous injection should be administered. The dosage is calculated as 0.5ml of 10% magnesium sulfate per kilogram of body weight. When administering magnesium intravenously, attention should be paid to the occurrence of acute magnesium toxicity to avoid causing cardiac arrest. Therefore, avoid excessive or rapid administration of magnesium. In case of magnesium toxicity, calcium gluconate or calcium chloride should be injected as an antidote.