|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)|
|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
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- Weakness, nausea and vomiting
- Impaired breathing
- Decreased respirations
- Low blood pressure
- Low blood calcium
- Abnormal heart rhythms and asystole
- Decreased or absent deep tendon reflexes
- Low heart rate
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.
Clinical 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
Note that 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
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.
- Kidney insufficiency, excretion of magnesium becomes impaired when creatinine clearance falls below 30 ml/min. However, hypermagnesemia is not a prominent feature of renal insufficiency 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.
Prevention of hypermagnesemia usually is possible. In mild cases, withdrawing magnesium supplementation is often sufficient. In more severe cases the following treatments are used:
- Intravenous calcium gluconate, because the actions of magnesium in neuromuscular and cardiac function are antagonized by calcium.
Definitive treatment of hypermagnesemia requires increasing renal magnesium excretion through:
- Intravenous diuretics, in the presence of normal kidney function
- Dialysis, when kidney function is impaired and the patient is symptomatic from hypermagnesemia
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