What is Hypermagnesemia?

Hypermagnesemia occurs when the serum magnesium concentration exceeds the normal value, which means that Mg2 +> 1.25 mmoL / L in the blood. Except for a few iatrogenic factors that cause excessive magnesium entry into the body, most are due to decreased excretion due to renal dysfunction. Like hypomagnesemia, serum magnesium concentration is not a reliable indicator of magnesium increase, because 25% of magnesium in serum is bound to proteins, and this part of magnesium does not exert physiological effects. Magnesium ions are mainly in the cell, so when the body's magnesium content increases, serum magnesium can be within the normal range. However, in general, the degree of hypermagnesemia is consistent with the increase in magnesium in the body. Just as the kidneys have a certain delayed effect on the regulation of sodium ions, potassium ions, and bicarbonate ions, the regulation of the kidneys on magnesium does not play a significant role quickly. Therefore, a large number of intravenous magnesium preparations, if not monitored, severe hypermagnesemia can also occur. If renal dysfunction is combined and the regulating effect of the kidney is severely weakened, hypermagnesemia is prone to occur.

Basic Information

Visiting department: Nephrology
Common locations: kidney
Common causes: Reduced excretion due to renal dysfunction

Common symptoms: Early loss of appetite, nausea, vomiting, skin flushing, headache, dizziness; neuromuscular and circulatory changes when serum magnesium reaches 2 to 4 mmol per liter

Causes of hypermagnesemia

Acute or chronic renal failure is more common, but most patients with renal failure can still maintain normal or normal high levels of magnesium, and no symptoms caused by hypermagnesemia. If you take too much at one time (such as using antacids) or enter the body through other routes (such as intramuscular injection of magnesium sulfate, etc.), there may be obvious hypermagnesemia and symptoms. In addition, thyroxine can inhibit the reabsorption of magnesium in the renal tubules and promote the excretion of urinary magnesium, so hypermagnesemia can occur in patients with myxedema due to hypothyroidism. Aldosterone also has the effect of inhibiting renal magnesium reabsorption and promoting urinary magnesium excretion, so patients with Addison disease may have hypermagnesemia.

Clinical manifestations of hypermagnesemia

The clinical manifestations of hypermagnesemia are related to the magnitude and speed of serum magnesium elevation. Those who rise rapidly within a short period of time have more severe clinical symptoms. Generally, early manifestations include loss of appetite, nausea, vomiting, skin flushing, headache, dizziness, etc., due to Lack of specificity, easy to ignore, when the serum magnesium concentration reaches 2 ~ 4mmoL / L, obvious changes in the nerve-muscle and circulatory system can occur.

1. Neuro-muscular effects

Elevated serum magnesium ion can inhibit the release of nerve-muscle junctions and central nervous system acetylcholine, so it is manifested as respiratory muscle weakness and central inhibition. Generally, serum magnesium concentration has a certain relationship with clinical manifestations, that is, serum magnesium concentration> 3mmol / L When the tendon reflex weakens or disappears;> 4.8mmol / L, muscle weakness occurs, limb muscles are paralyzed, and respiratory failure can occur when breathing muscles are affected, and breathing stops;> 6mmol / L, severe central depression, Such as lethargy, stiffness, coma, etc.

2. Impact on the cardiovascular system

(1) The effect on the heart mainly manifests as the inhibition of autonomic cells, manifested as sinus bradycardia, and conduction block tissues in various conditions. As the autonomy of high normal cells decreases, the autonomy of low autonomic cells excites. Various arrhythmias occur.

(2) Effects on blood vessels Hypermagnesium can inhibit the release of acetylcholine from the presympathetic ganglion fibers, and correspondingly reduce the release of norepinephrine; of course, it also inhibits the release of acetylcholine from the parasympathetic nerve, but because the former is stronger, it appears as vascular smooth muscle Diastole, flushed skin, and decreased blood pressure.

3. Impact on the digestive system

Hyperglycemia inhibits the release of autonomic neurotransmitters and directly inhibits gastrointestinal smooth muscle. Patients can show abdominal distension, constipation, nausea, and vomiting.

4. Impact on the respiratory system

Severe hyperglycemia can reduce respiratory central excitability and respiratory muscle paralysis, leading to respiratory arrest.

Hypermagnesemia

Serum

Elevated magnesium concentration (serum magnesium> 1.25mmol / L) can directly diagnose hypermagnesemia.

2.24-hour urinary magnesium excretion

It is of great help in diagnosing the etiology. If the loss is reduced, it means that it is caused by renal factors, endocrine factors, metabolic factors, otherwise it is caused by increased intake or abnormal distribution.

3. ECG examination

Hypermagnesemia can occur with conduction block and bradycardia. Its ECG manifests as a prolonged PR interval, a widened QRS, and a prolonged QT interval. Because hypermagnesemia is often accompanied by hyperkalemia, high-point T waves can occur.

4.B-ultrasound

Early detection of organic changes in the kidneys.

Hypermagnesemia diagnosis

1. Serum Mg> 1.25mmol / L is hypermagnesemia

Most are due to decreased magnesium excretion caused by renal dysfunction, but the following special circumstances need to be taken into account: hypothyroidism, chronic adrenal insufficiency, increased renal tubular reabsorption of magnesium; excessive or long-term Take magnesium-containing antacids; hemolytic reactions, large area burns, severe trauma, and other tissue cells are destroyed, high levels of magnesium in the cells enter the blood; patients with mental illness take lithium for a long time; too much magnesium in cells during acidosis Swap outside the cell.

2. Slight increase in serum magnesium

Non-specific symptoms such as loss of appetite, nausea, skin flushing, and headache are easily ignored. Once serum Mg> 2mmol / L, it may cause respiratory depression and cardiac arrest.

Hypermagnesemia Treatment

Symptomatic treatment

(1) Use of calcium ions Because calcium has an antagonistic effect on magnesium, intravenous injection of 10% calcium gluconate or 10% calcium chloride can often relieve symptoms.

(2) General symptomatic treatment According to need, respiratory support therapy, booster therapy, and antiarrhythmic therapy can be used.

(3) Cholinesterase inhibitor hypermagnesemia can reduce the release of acetylcholine from nerve endings, and the use of cholinesterase inhibitors can reduce the destruction of acetylcholine, thereby reducing the decrease in excitability of the neuro-muscular junction caused by hypermagnesemia . Trial drugs include neostigmine and the like.

2. Reduce blood magnesium concentration

(1) Increase the excretion of urinary magnesium. Patients with normal renal function can properly add normal saline or glucose solution to correct dehydration, increase glomerular filtration excess, and accelerate the excretion of magnesium. On the basis of supplementing blood volume, the use of diuretics can increase urinary magnesium excretion. Combination of thiazide diuretics and tritium diuretics. But for those with obvious renal insufficiency, diuretics are ineffective.

(2) Hemodialysis The occurrence of hypermagnesemia in renal insufficiency is an indication for the application of dialysis therapy, because hypermagnesemia and hypercalcemia often occur in the presence of renal insufficiency, and the application of calcium treatment is inappropriate. But pay attention to the use of magnesium-free fluids during dialysis.

(3) Strict control of magnesium intake All magnesium-containing drugs must be stopped.