|Symptoms||Weakness, confusion, decreased breathing rate|
|Causes||Kidney failure, treatment induced, tumor lysis syndrome, seizures, prolonged ischemia|
|Diagnostic method||Blood level > 1.1 mmol/L (2.6 mg/dL)|
|Differential diagnosis||Acute kidney failure, hypercalcemia, hyperkalemia, hypoparathyroidism, hypothyroidism, lithium toxicity, hemolysis, rhabdomyolysis|
|Treatment||Calcium chloride, intravenous normal saline with furosemide, hemodialysis|
Hypermagnesemia is an electrolyte disorder in which there is a high level of magnesium in the blood. Symptoms include weakness, confusion, decreased breathing rate, and decreased reflexes. Complications may include low blood pressure and cardiac arrest.
It is typically caused by kidney failure or is treatment induced such as from antacids that contain magnesium. Less common causes include tumor lysis syndrome, seizures, and prolonged ischemia. Diagnosis is based on a blood level greater than 1.1 mmol/L (2.6 mg/dL). It is severe if levels are greater than 2.9 mmol/L (7 mg/dL). Specific electrocardiogram (ECG) changes may be present.
Treatment involves stopping the magnesium a person is getting. Treatment when levels are very high include calcium chloride, intravenous normal saline with furosemide, and hemodialysis. Hypermagnesemia is uncommon. Rates may be as high as 10% among those in hospital.
Signs and symptoms
Abnormal heart rhythms and asystole are possible complications of hypermagnesemia related to the heart. Magnesium acts as a physiologic calcium blocker, which results in electrical conduction abnormalities within the heart.
Consequences related to serum concentration:
- 4.0 mEq/L decreased reflexes
- >5.0 mEq/L Prolonged atrioventricular conduction
- >10.0 mEq/L Complete heart block
- >13.0 mEq/L cardiac arrest
The therapeutic range for the prevention of the pre-eclampsic uterine contractions is: 4.0-7.0 mEq/L. As per Lu and Nightingale, serum Mg2+ concentrations associated with maternal toxicity (also neonate depression - hypotonia and low Apgar scores) are:
- 7.0-10.0 mEq/L - loss of patellar reflex
- 10.0-13.0 mEq/L - respiratory depression
- 15.0-25.0 mEq/L - altered atrioventricular conduction and (further) complete heart block
- >25.0 mEq/L - cardiac arrest
Kidney function plays a crucial role in the metabolism of magnesium. Of note, only approximately 10% of filtered magnesium is absorbed in the proximal tubule, whereas most of the filtered magnesium gets passively reabsorbed in the ascending limb of the loop of Henle. This factor is essential for the pathophysiology of kidney-related hypermagnesemia as along the loop of Henle, not only the volume of the filtrate gets reduced, but also the osmolarity decreases significantly (-66%), and consequently the solutes become less concentrated. Furthermore, this explains the high resorbent capacity of the kidney, which generally maintains magnesium equilibrium until the creatinine clearance falls below 20 ml/min. Thus, an increase in plasma magnesium levels is practically impossible to achieve with diet alone in conditions of perfect renal health. However, the odds of hypermagnesemia can increase by taking mega-doses of magnesium. The pathophysiology of hypermagnesemia related to excess laxative use is different. In this case, the huge amount of magnesium given through the digestive tract can lead to overwhelming the excretory mechanism, especially in cases with underlying subclinical kidney failure.
Magnesium works as a physiologic calcium blocker. Increased levels determine substantial electrophysiological and hemodynamic effects. Moreover, the potential concomitance of hyperkalemia increases the risk of abnormal heart rhythms and cardiac arrest. The neurologic manifestations are the result of the inhibition of acetylcholine release from the neuromuscular endplate due to increased extracellular magnesium levels.
Magnesium status depends on three organs: uptake in the intestine, storage in the bone, and excretion in the kidneys. Hypermagnesemia is therefore often due to problems in these organs, mostly intestine or kidney.
- Hemolysis, magnesium concentration in erythrocytes is approximately three times greater than in serum, therefore hemolysis can increase plasma magnesium. Hypermagnesemia is expected only in massive hemolysis.
- Chronic kidney disease, excretion of magnesium becomes impaired when creatinine clearance falls below 30 ml/min. However, hypermagnesemia is not a prominent feature of chronic kidney disease unless magnesium intake is increased.
- Other conditions that can predispose to mild hypermagnesemia are diabetic ketoacidosis, adrenal insufficiency, hypothyroidism, hyperparathyroidism and lithium intoxication.
Hypermagnesemia is diagnosed by measuring the concentration of magnesium in the blood. Concentrations of magnesium greater than 1.1 mmol/L are considered diagnostic.
People with normal kidney function (glomerular filtration rate (GFR) over 60 ml/min) and mild asymptomatic hypermagnesemia require no treatment except the removal of all sources of exogenous magnesium. One must consider that the half-time of elimination of magnesium is approximately 28 hours.
In more severe cases, close monitoring of the ECG, blood pressure, and neuromuscular function and early treatment are necessary:
Intravenous calcium gluconate or chloride [Dosage: 1 g in 2 to 5 min (repeatable over 5 minutes)]. The rationale is that the actions of magnesium in neuromuscular and cardiac function become antagonized by calcium. Intravenous normal saline (e.g., at 150 ml/hour)
Severe clinical conditions require increasing renal magnesium excretion through:
Intravenous loop diuretics (e.g., furosemide 1 mg/kg), or hemodialysis, when kidney function is impaired, or the patient is symptomatic from severe hypermagnesemia. This approach usually removes magnesium efficiently (up to 50% reduction after a 3- to 4-hour treatment). Dialysis can, however, increase the excretion of calcium by developing hypocalcemia, thus possibly worsening the symptoms and signs of hypermagnesaemia.
The use of diuretics must be associated with infusions of saline solutions to avoid further electrolyte disturbances (e.g., hypokalemia) and metabolic alkalosis. The clinician must perform serial measurements of calcium and magnesium. In association with electrolytic correction, it is often necessary to support cardiorespiratory activity. As a consequence, the treatment of this electrolyte disorder can frequently require intensive care unit (ICU) admission.
Particular clinical conditions require a specific approach. For instance, during the management of eclampsia, the magnesium infusion is stopped if urine output drops to less than 80 mL (in 4 hours), deep tendon reflexes are absent, or the respiratory rate is below 12 breaths/minute. A 10% calcium gluconate or chloride solution (10 mL intravenously repeatable over 5 minutes) can serve as an antidote.
Hypermagnesemia is an uncommon electrolyte disorder. It occurs in approximately 10 to 15% of hospitalized patients with renal failure. Furthermore, epidemiological data suggest that there is a significant prevalence of high levels of serum magnesium in selected healthy populations. For instance the overall prevalence of hypermagnesemia was 3.0%, especially in males in Iran. For instance high magnesium concentrations were typical in people with cardiovascular disease, and 2.3 mg/dL or higher values were associated with worse hospital mortality.
The prognosis of hypermagnesemia depends on magnesium values and on the clinical condition that induced hypermagnesemia. Values that are not excessively high (mild hypermagnesemia) and in the absence of triggering and aggravating conditions (e.g., renal insufficiency) are benign conditions. On the contrary, high values (severe hypermagnesemia) expose the patient to high risks and high mortality.
Severe hypermagnesemia (levels greater than 12 mmol/dL) can lead to cardiovascular complications (hypotension, and arrhythmias) and neurological disorder (confusion and lethargy). Higher values of serum magnesium (exceeding 15 mg/dL) can induce cardiorespiratory arrest and coma. 
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