Overview of Hypermagnesemia
Serum magnesium concentration exceeding the normal value is hypermagnesemia, refers to blood Mg2+>1.25 mmoL/L or more, in addition to a few medical factors lead to excessive magnesium into the body, most of them are due to renal dysfunction caused by reduced excretion, as in hypomagnesemia, serum magnesium concentration is not a reliable indicator of magnesium increase, because 25% of magnesium in the serum is bound to proteins, which do not play a physiologic The serum magnesium concentration is not a reliable indicator of increased magnesium because 25% of the serum magnesium is bound to proteins, and this portion of magnesium does not play a physiologic role; magnesium ions are mainly found in the cells, so serum magnesium can be within the normal range when magnesium levels increase in the body. However, in general, the degree of hypermagnesemia and increased body magnesium is consistent. Just as the kidney has a certain delayed effect on the regulation of sodium, potassium and bicarbonate ions, the regulation of magnesium by the kidney is not rapid to play a significant role, so a large number of intravenous application of magnesium preparations, if you do not pay attention to the monitoring, can also occur in severe hypermagnesemia, if the combination of renal dysfunction, the regulation of the kidney is seriously weakened, then it is easy to occur hypermagnesemia.
Etiology
Acute or chronic renal failure is common, but generally renal failure patients blood magnesium can still maintain most of the normal or normal high level, and there is no symptom caused by hypermagnesemia, if the momentary intake of excessive (such as the use of antacids) or through other routes to enter the body too much (for example, intramuscular injection of magnesium sulfate, etc.), it is possible to develop significant hypermagnesemia and symptoms. In addition, thyroxine can inhibit renal tubular magnesium reabsorption and promote urinary magnesium excretion, so some patients with hypothyroidism and mucous edema may develop hypermagnesemia, and aldosterone also has the effect of inhibiting renal tubular magnesium reabsorption and promoting urinary magnesium excretion, so patients with Addison’s disease may have hypermagnesemia.
Symptoms
The clinical manifestations of hypermagnesemia are related to the magnitude and speed of serum magnesium elevation, the rapid increase in a short period of time, the clinical symptoms are more serious, usually early manifestations of loss of appetite, nausea, vomiting, skin flushing, headache, dizziness, etc., due to the lack of specificity, easy to ignore, when the serum magnesium concentration reaches 2 ~ 4 mmoL / L, there can be obvious changes in the neuromuscular and circulatory system.
1.Effect on nerve-muscle
Elevated serum magnesium ion can inhibit the release of acetylcholine from nerve-muscle junction and central nervous system, so it is manifested as respiratory muscle weakness and central inhibitory state. Generally speaking, serum magnesium concentration has a certain relationship with the clinical manifestations, i.e., tendon reflexes will be weakened or disappeared when serum magnesium concentration is >3mmol/L; when it is >4.8mmol/L, muscle weakness will occur, limb muscle limpness will occur and respiratory failure and respiratory arrest will be caused when it affects respiratory muscles. Respiratory failure, respiratory arrest; >6mmol/L, severe central inhibition can occur, such as lethargy, rigor mortis, coma and so on.
2. Effects on cardiovascular system
(1) Effects on the heart Mainly manifested as the inhibitory effect of autoregulatory cells, manifested as sinus bradycardia, various cases of conduction block tissue, due to the decrease of autoregulation of high normal cells, low autoregulatory cell excitation, a variety of cardiac arrhythmias can occur.
(2) Effects on blood vessels High blood magnesium can inhibit the release of acetylcholine from the preganglionic fibers of the sympathetic nerves, and the corresponding release of norepinephrine is reduced; of course, it also inhibits the parasympathetic nerves from releasing acetylcholine, but since the former has a stronger effect, it is manifested as the vascular smooth muscle diastasis, flushing of the skin, and the drop of blood pressure.
3. Effects on digestive system
High blood magnesium inhibits the release of autonomic neurotransmitters and directly inhibits the smooth muscle of gastrointestinal tract, and patients may show abdominal distension, constipation, nausea, vomiting and so on.
4. Effects on respiratory system
Severe high blood magnesium can reduce the excitability of respiratory center and paralyze the respiratory muscles, leading to respiratory arrest.
Examination
1. Serum
Elevated magnesium concentration (serum magnesium>1.25mmol/L) can directly diagnose hypermagnesemia.
2. 24-hour urinary magnesium excretion
It is helpful to diagnose the etiology of the disease. If the loss decreases, it indicates that it is due to renal, endocrine and metabolic factors, otherwise it is due to increased uptake or abnormal distribution.
3.Electrocardiography
Conduction block and bradycardia can be seen in hypermagnesemia, and its electrocardiogram shows prolongation of P-R interval, widening of QRS and prolongation of Q-T interval, and because hypermagnesemia is often accompanied by hyperkalemia, hyperacute T-wave can be seen.
4.Ultrasound examination
Early detection of renal organic changes.
Diagnosis
1.Serum Mg2+＞1.25mmol/L is hypomagnesemia.
The vast majority is due to renal dysfunction resulting in decreased magnesium excretion, but the following special circumstances need to be taken into account: ① hypothyroidism, chronic hypoadrenocorticism, renal tubular magnesium reabsorption increases; ② once too much or long-term use of magnesium-containing antacids; ③ hemolytic reaction, extensive burns, severe trauma and other tissue cells are destroyed in large quantities, the high level of magnesium into the bloodstream; ④ psychiatric patients taking lithium over a long period of time; ④ patients with chronic lithium use; ④ patients with psychotic illnesses. Patients taking lithium for a long time; ⑤ Excessive exchange of intracellular magnesium to extracellular in acidosis.
2. Mild elevation of serum magnesium
Non-specific symptoms such as loss of appetite, nausea, skin flushing, headache, etc. are easy to be ignored. Once serum Mg2+＞2mmol/L, it may lead to respiratory depression and cardiac arrest.
Treatment
1. Symptomatic treatment
(1) Use of calcium ions Since calcium has an antagonistic effect on magnesium, intravenous injection of 10% calcium gluconate or 10% calcium chloride often relieves symptoms.
(2) General symptomatic treatment Respiratory support therapy, antihypertensive therapy, antiarrhythmic therapy, etc. can be used as needed.
(3) Cholinesterase inhibitor Hypermagnesemia can reduce the release of acetylcholine from the nerve endings, and the application of cholinesterase inhibitor can reduce the destruction of acetylcholine, thus reducing the excitability of the nerve-muscle junction caused by hypermagnesemia. The drugs that can be tried are neostigmine and so on.
2. Reduce blood magnesium concentration
(1) Increase urinary magnesium discharge Patients with normal renal function can supplement saline or glucose solution to correct dehydration, increase glomerular filtration, and accelerate the discharge of magnesium. On the basis of supplemental blood volume, the use of diuretics can increase urinary magnesium discharge. Thiazide diuretics and labeled diuretics can be combined. But for obvious renal insufficiency, the application of diuretics is ineffective.
(2) Hemodialysis Hypermagnesemia occurs in renal insufficiency, which is an indication for dialysis therapy, because hypermagnesemia and hypercalcemia often coexist in renal insufficiency, and it is inappropriate to apply calcium therapy at this time. However, pay attention to use magnesium-free fluid in dialysis.
(3) Strictly control the intake of magnesium, must stop using all magnesium-containing drugs.