Hypermagnesemia

　　Acute or chronic renal failure is common, but generally, the blood magnesium levels in renal failure patients can still maintain normal or slightly elevated levels, and there are no symptoms caused by hypermagnesemia. If excessive intake occurs temporarily (such as the use of antacids) or excessive entry through other routes (such as intramuscular injection of magnesium sulfate), it may lead to significant hypermagnesemia and the appearance of symptoms. In addition, thyroxine can inhibit the reabsorption of magnesium by renal tubules and promote the excretion of urinary magnesium, so some patients with myxedema can develop hypermagnesemia. Aldosterone also has the effect of inhibiting the reabsorption of magnesium by renal tubules and promoting the excretion of urinary magnesium, so Addison's disease patients may have hypermagnesemia.

　　Common complications of this disease:

　　1. Disappearance of tendon reflexes.

　　2. Impaired cardiac conduction function.

　　3. Respiratory depression.

　　4. Cardiac arrest.

　　High magnesium levels can inhibit myocardial contractility, leading to cardiac insufficiency or cardiogenic shock. High concentrations of magnesium can inhibit atrioventricular and intraventricular conduction and reduce myocardial excitability, causing conduction block and bradycardia. Prolonged P-R interval and widened QRS complex can be seen on the ECG.

　　5. Effects on smooth muscle. Magnesium also has an inhibitory effect on smooth muscle. The inhibition of vascular smooth muscle in hypermagnesemia can cause dilation of small arteries and arterioles, leading to decreased peripheral resistance and a decrease in arterial blood pressure. The inhibition of visceral smooth muscle can cause symptoms such as belching, vomiting, constipation, and urinary retention.

　　Symptoms and signs of magnesium overload only appear when the serum magnesium concentration is > 2 mmol/L, mainly manifested as fatigue, weakness, disappearance of tendon reflexes, and blood pressure drop. As the serum magnesium concentration further increases, cardiac conduction function is impaired, and the ECG shows prolonged PR interval, widened QRS complex, and elevated T waves, similar to the changes in ECG of hyperkalemia. In the late stage, respiratory depression, drowsiness, and coma may occur, and even cardiac arrest.

　　Regularly check the serum magnesium concentration when using magnesium-containing drugs to avoid hypermagnesemia.

　　1. Prognosis

　　If hypermagnesemia is not diagnosed and treated in time, it can lead to acute or chronic renal insufficiency. It is necessary to monitor blood and urinary magnesium concentrations.

　　2. Prevention

　　After the diagnosis of hypermagnesemia is established, efforts should be made to find the cause. If it is caused by iatrogenic factors, the administration of magnesium-containing drugs or preparations should be immediately stopped.

　　Firstly, laboratory examinations

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

　　2. The 24-hour urinary magnesium excretion amount is of great help in diagnosing the cause. If the loss amount decreases, it indicates renal, endocrine, or metabolic factors, otherwise, it is due to increased intake or abnormal distribution.

　　Secondly, other auxiliary examinations

　　1. Electrocardiogram (ECG) examination shows conduction block and bradycardia. The ECG of hypermagnesemia is characterized by prolonged P-R interval, widened QRS complex, and prolonged Q-T interval. Since hypermagnesemia often accompanies hyperkalemia, high-tipped T waves may appear.

　　2. Ultrasound examination can help in early detection of renal organic changes.

　　What foods are good for hypermagnesemia patients to eat:

　　Eat more iron-rich foods, such as deep-sea fish, kelp, etc., followed by meat and eggs. Animal internal organs, such as liver, can also be eaten to supplement iron, but the liver in biological organisms is prone to accumulate toxins and is not suitable for long-term consumption (it's okay occasionally). Excessive magnesium can drink old tea or fluorinated tap water to make fluorine antagonize magnesium.

　　Calcium and magnesium have a significant antagonistic effect, and 10-20ml of 10% calcium gluconate or 5-10ml of 10% calcium chloride can be administered intravenously first to counteract the inhibition of magnesium on the heart and muscles, while actively correcting acidosis and dehydration. If the serum magnesium does not decrease or the symptoms do not improve, peritoneal dialysis or hemodialysis should be adopted as soon as possible.

　　First, symptomatic treatment

　　1. Use calcium ions:Due to the antagonistic effect of calcium on magnesium, intravenous injection of 10% calcium gluconate or 10% calcium chloride can often relieve symptoms, with the commonly used dose of the former being 10-20ml, and the latter 5-10ml, administered slowly.

　　2. General symptomatic treatment:Respiratory support therapy, antihypertensive therapy, and antiarrhythmic therapy can be used according to need.

　　3. Cholinesterase inhibitors:Hypermagnesemia can reduce the release of acetylcholine at the nerve endings, and the use of cholinesterase inhibitors can reduce the destruction of acetylcholine, thereby reducing the decrease in neuromuscular junction excitability caused by hypermagnesemia. Drugs that can be tried include neostigmine, etc.

　　Secondly, reduce blood magnesium concentration

　　1. Increase the excretion of urinary magnesium:Patients with normal renal function can appropriately supplement normal saline or glucose solution to correct dehydration, increase glomerular filtration rate, and accelerate the excretion of magnesium. On the basis of fluid resuscitation, the use of diuretics can increase the excretion of urinary magnesium. Thiazide diuretics and loop diuretics can be used together. However, for patients with obvious renal insufficiency, the use of diuretics is often ineffective.

　　2. Hemodialysis:Hypermagnesemia occurring in renal insufficiency is an indication for dialysis therapy because hypermagnesemia often coexists with hypercalcemia in renal insufficiency, and calcium treatment is not appropriate at this time. But note that magnesium-free fluid should be used during dialysis.

　　3. Strictly control the intake of magnesium:All magnesium-containing drugs must be discontinued.