Hypermagnesemia

Introduction to hypermagnesemia When the serum magnesium concentration exceeds the normal value, it is hypermagnesemia, and the blood [Mg2]>1.05mmoL/L or more. Except for a few iatrogenic factors, it leads to excessive magnesium in the body, and most of them are excreted due to renal dysfunction. Reduced, like hypomagnesemia, serum magnesium concentration is not a reliable indicator of magnesium increase, because 25% of magnesium in serum binds to protein, this part of magnesium does not exert physiological effects; magnesium ion is mainly in cells, so When the magnesium content of the body increases, the serum magnesium can be in the normal range, but in general, the degree of hypermagnesemia and the body magnesium increase is consistent. Just as the kidney has a certain delay on the regulation of sodium ions, potassium ions and bicarbonate ions, the regulation of magnesium by the kidneys does not play a significant role quickly. Therefore, a large number of intravenous magnesium preparations can be severely affected if not monitored. Hypermagnesemia, if combined with renal dysfunction, the renal regulation is severely weakened, it is prone to hypermagnesemia. basic knowledge The proportion of illness: 0.075% Susceptible people: no specific population Mode of infection: non-infectious Complications: cardiogenic shock

Cause of hypermagnesemia

(1) Causes of the disease

Acute or chronic renal failure is more common, but most patients with renal failure can still maintain normal or normal high blood levels, and no symptoms caused by hypermagnesemia, if excessive intake (such as the use of acid-resistant Agents or other ways to enter the body too much (such as intramuscular injection of magnesium sulfate, etc.), there may be obvious hypermagnesemia and symptoms, in addition, thyroxine can inhibit renal tubular magnesium reabsorption, promote urinary magnesium excretion, so Some patients with mucinous edema may develop hypermagnesemia, aldosterone also inhibits renal tubular magnesium reabsorption and promotes urinary magnesium excretion, so patients with Addison may have hypermagnesemia.

(two) pathogenesis

1. Reduction of magnesium excretion in the kidney: Magnesium mainly maintains the balance and stability of serum concentration through renal regulation. The urinary magnesium excretion in normal renal function is equivalent to 3% to 5% of glomerular filtration excess. When serum magnesium is elevated, the kidney The magnesium excretion ability can be significantly enhanced, generally does not occur hypermagnesemia, so hypermagnesemia is mainly seen in patients with impaired renal function.

(1) Acute renal insufficiency: mild hypermagnesemia may occur during oliguria of acute renal failure.

(2) Chronic renal insufficiency: When the glomerular filtration rate is less than 30ml/min, the blood magnesium is increased.

(3) severe hyponatremia: in severe hyponatremia, magnesium reabsorption in the proximal convoluted tubules, mild hypermagnesemia can occur.

(4) Endocrine disorders: abnormalities of certain hormone levels, such as thyroxine, adrenocortical hormone (mainly aldosterone) inhibit renal tubular reabsorption of magnesium, so hypermagnesemia can occur in patients with hypothyroidism or adrenal insufficiency Other hormones that promote renal tubular reabsorption of magnesium include parathyroid hormone, antidiuretic hormone, and glucagon.

(5) Reduction of extracellular fluid volume: If severe dehydration can lead to oliguria, the excretion of magnesium is reduced; at the same time, the reabsorption of magnesium by renal tubules is increased under low blood volume.

2. Excessive intake of magnesium or increased reabsorption of magnesium in the gastrointestinal tract

(1) excessive intake: generally caused by drugs, long-term oral magnesium-containing preparations, such as magnesium oxide, magnesium hydroxide, etc.; a large number of injections of magnesium preparations, such as a large number of magnesium sulfate treatment of eclampsia or pre-eclampsia.

(2) Increased gastrointestinal reabsorption: Vitamin D can increase the absorption of magnesium in the intestine. Patients with high doses of vitamin D may occasionally develop hypermagnesemia.

3. Distribution anomaly

(1) Mass destruction of tissue cells: Since magnesium is mainly present in cells, when a large amount of tissue is destroyed, a large amount of magnesium ions enter the blood and hypermagnesemia occurs, which is similar to the change of potassium ions, which is clinically common in hemolysis, large Area burns, severe trauma or surgical injury, skeletal muscle solubilization, etc.; also seen in cases of high catabolism.

(2) Magnesium ion transfer inside and outside normal cells: mainly seen in acidosis, when intracellular magnesium is transferred to the outside of the cell, hypermagnesemia occurs.

The difference between the two is mainly due to the fact that the former is the direct transfer of magnesium ions inside and outside the cell, while the latter is caused by the exchange of ions caused by acidosis.

Hypermagnesemia prevention

After the diagnosis of hypermagnesemia is established, the cause should be actively sought, if it is caused by iatrogenic factors. The application of magnesium-containing drugs or preparations should be stopped immediately.

Hypermagnesemia complications Complications cardiogenic shock

Hypermagnesemia can inhibit myocardial contractility, leading to cardiac insufficiency or cardiogenic shock.

Symptoms of hypermagnesemia Common symptoms Loss of appetite, bloating, constipation, nausea, blood pressure, respiratory depression, respiratory failure, arrhythmia, bradycardia

The clinical manifestations of hypermagnesemia are related to the amplitude and speed of serum magnesium elevation. The rapid clinical symptoms in a short period of time are severe, and the early manifestations are poor appetite, nausea, vomiting, skin flushing, headache, dizziness, etc. Due to the lack of specificity, it is easy to ignore. When the serum magnesium concentration reaches 2 ~ 4mmoL / L, there may be significant changes in the nerve-muscle and circulatory system.

1. Effects on nerves and muscles

Elevated serum magnesium ions can inhibit the release of neuro-muscle junctions and central nervous acetylcholine, so it is characterized by respiratory muscle weakness and central inhibition. In general, serum magnesium concentration has a certain relationship with clinical manifestations, ie serum magnesium concentration >3mmol/L When the sputum reflex is weakened or disappeared; >4.8mmol/L, muscle weakness occurs, muscles of the extremities are soft, and respiratory muscles may occur when respiratory muscles are affected. Respiratory arrest; >6mmol/L, severe central inhibition may occur. Such as lethargic, stupor, coma, etc., so when the vein is given magnesium, the speed can not be too fast, for patients who can not eat, it is best to input the daily magnesium output more evenly within 24h.

2. Impact on the cardiovascular system

(1) The effect on the heart: mainly manifested as the inhibition of autonomic cells, manifested as sinus bradycardia, conduction block in various cases, due to the decreased self-discipline of high normal cells, low self-regulatory cells, Various arrhythmias can occur.

(2) Effects on blood vessels: Hypermagnesium can inhibit the release of acetylcholine from the sympathetic preganglionic ganglia, and the release of corresponding norepinephrine is reduced; of course, the release of acetylcholine from the parasympathetic nerve is also inhibited, but because the former has a stronger effect, it is expressed as a blood vessel. Smooth muscle relaxation, skin flushing, and blood pressure drop.

3. Digestive system

Hypermagnesium inhibits the release of autonomic neurotransmitters and directly inhibits smooth muscles in the gastrointestinal tract. Patients may present with bloating, constipation, nausea, and vomiting.

4. Respiratory system

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

1. Serum [Mg2]>1.05mmol/L is hypermagnesemia: most of them are caused by reduced magnesium excretion due to renal dysfunction, but the following special circumstances need to be taken seriously:

1 hypothyroidism, chronic adrenal insufficiency, renal tubular reabsorption of magnesium increased;

2 excessive or long-term use of magnesium-containing antacids;

3 hemolysis reaction, large area burns, severe trauma and other tissue cells are destroyed, and high levels of magnesium in the cells enter the blood;

4 mental patients have long-term use of lithium;

5 In the case of acidosis, excessive intracellular magnesium is exchanged outside the cell.

2. The serum magnesium is mildly elevated, and there are non-specific symptoms such as loss of appetite, nausea, flushing of the skin, headache, etc., which are easily ignored. Once the serum [Mg2]>2mmol/L, it may cause respiratory depression and cardiac arrest.

Examination of hypermagnesemia

1. Increased serum magnesium concentration (sera magnesium > 1.25mmol / L) can directly diagnose hypermagnesemia.

2.24h urinary magnesium excretion: it is helpful for the diagnosis of the cause. If the loss is reduced, it indicates that it is caused by renal factors, endocrine factors and metabolic factors, otherwise it is caused by abnormal increase or distribution.

3. Electrocardiogram examination: conduction block and bradycardia, electrocardiogram of hypermagnesemia showed prolongation of PR interval, QRS widening and prolongation of QT interval, because high blood magnesium is often accompanied by hyperkalemia, it can appear high Sharp T wave.

4. B-ultrasound: early detection of renal organic changes.

Diagnosis and diagnosis of hypermagnesemia

Mild hypermagnesemia, symptoms and signs are often absent, easy to be ignored, for patients with magnesium, especially with renal insufficiency should pay attention to monitoring blood magnesium concentration, combined with uranium determination, primary basis Diagnosis and differential diagnosis of the disease.

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