Hypermagnesemia
Classification & external resources
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| Magnesium
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| ICD-10
| E83.4
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| ICD-9
| 275.2
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| DiseasesDB
| 6259
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| eMedicine
| med/3383 emerg/262 ped/1080
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Hypermagnesemia is an electrolyte disturbance in which there is an abnormally elevated level of magnesium in the blood. Usually this results in excess of magnesium in the body.
Hypermagnesemia occurs rarely because the kidney is very effective in excreting excess magnesium. It usually develops only in people with kidney failure who are given magnesium salts or who take drugs that contain magnesium (e.g. some antacids and laxatives). It is usually concurrent with hypercalcemia and/or hyperkalemia.
Additional recommended knowledge
Metabolism
For a detailed description of magnesium homeostasis and metabolism see hypomagnesemia.
Symptoms
- Weakness, nausea and vomiting
- Hypotension
- Impaired breathing
- Arrhythmia and asystole, most prominent cardiac symptoms are due to conduction delays, since magnesium acts as physiologic calcium blocker.
Clinical consequences related to serumconcentration:
- 4.0 mEq/l hyporeflexia
- >5.0 mEq/l Prolonged atrioventricular conduction
- >10.0 mEq/l Complete heart block
- >13.0 mEq/l Cardiac arrest
Causes
Since magnesium is excreted through the kidneys, renal failure can result in hypermagnesemia. The most important cause however is suppletion.
Predisposing conditions
- 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.
- Renal 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, hyperparathyroidism and lithium intoxication.
Therapy
Prevention of hypermagnesemia usually is possible. In mild cases, withdrawing magnesium suppletion is often sufficient. In more severe cases the following treatments are used:
Definitive treatment of hypermagnesemia requires increasing renal magnesium excretion through:
- Intravenous diuretics, in the presence of normal renal function
- Dialysis, when kidney function is impaired and the patient is symptomatic from hypermagnesemia
| Metabolic pathology / Inborn error of metabolism (E70-90, 270-279) |
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| Amino acid | Aromatic (Phenylketonuria, Alkaptonuria, Ochronosis, Tyrosinemia, Albinism, Histidinemia) - Organic acidemias (Maple syrup urine disease, Propionic acidemia, Methylmalonic acidemia, Isovaleric acidemia, 3-Methylcrotonyl-CoA carboxylase deficiency) - Transport (Cystinuria, Cystinosis, Hartnup disease, Fanconi syndrome, Oculocerebrorenal syndrome) - Sulfur (Homocystinuria, Cystathioninuria) - Urea cycle disorder (N-Acetylglutamate synthase deficiency, Carbamoyl phosphate synthetase I deficiency, Ornithine transcarbamylase deficiency, Citrullinemia, Argininosuccinic aciduria, Hyperammonemia) - Glutaric acidemia type 1 - Hyperprolinemia - Sarcosinemia |
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| Carbohydrate | Lactose intolerance - Glycogen storage disease (type I, type II, type III, type IV, type V, type VI, type VII) - fructose metabolism (Fructose intolerance, Fructose bisphosphatase deficiency, Essential fructosuria) - galactose metabolism (Galactosemia, Galactose-1-phosphate uridylyltransferase galactosemia, Galactokinase deficiency) - other intestinal carbohydrate absorption (Glucose-galactose malabsorption, Sucrose intolerance) - pyruvate metabolism and gluconeogenesis (PCD, PDHA) -
Pentosuria - Renal glycosuria |
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| Lipid storage | Sphingolipidoses/Gangliosidoses: GM2 gangliosidoses (Sandhoff disease, Tay-Sachs disease) - GM1 gangliosidoses - Mucolipidosis type IV - Gaucher's disease - Niemann-Pick disease - Farber disease - Fabry's disease - Metachromatic leukodystrophy - Krabbe disease
Neuronal ceroid lipofuscinosis (Batten disease) - Cerebrotendineous xanthomatosis - Cholesteryl ester storage disease (Wolman disease) |
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| Fatty acid metabolism | Lipoprotein/lipidemias: Hyperlipidemia - Hypercholesterolemia - Familial hypercholesterolemia - Xanthoma - Combined hyperlipidemia - Lecithin cholesterol acyltransferase deficiency - Tangier disease - Abetalipoproteinemia
Fatty acid: Adrenoleukodystrophy - Acyl-coA dehydrogenase (Short-chain, Medium-chain, Long-chain 3-hydroxy, Very long-chain) - Carnitine (Primary, I, II) |
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| Mineral | Cu Wilson's disease/Menkes disease - Fe Haemochromatosis - Zn Acrodermatitis enteropathica - PO43�' Hypophosphatemia/Hypophosphatasia - Mg2+ Hypermagnesemia/Hypomagnesemia - Ca2+ Hypercalcaemia/Hypocalcaemia/Disorders of calcium metabolism |
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Fluid, electrolyte
and acid-base balance | Electrolyte disturbance - Na+ Hypernatremia/Hyponatremia - Acidosis (Metabolic, Respiratory, Lactic) - Alkalosis (Metabolic, Respiratory) - Mixed disorder of acid-base balance - H2O Dehydration/Hypervolemia - K+ Hypokalemia/Hyperkalemia - Cl�' Hyperchloremia/Hypochloremia |
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| Purine and pyrimidine | Hyperuricemia - Lesch-Nyhan syndrome - Xanthinuria |
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| Porphyrin | Acute intermittent, Gunther's, Cutanea tarda, Erythropoietic, Hepatoerythropoietic, Hereditary copro-, Variegate |
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| Bilirubin | Unconjugated (Lucey-Driscoll syndrome, Gilbert's syndrome, Crigler-Najjar syndrome) - Conjugated (Dubin-Johnson syndrome, Rotor syndrome) |
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| Glycosaminoglycan | Mucopolysaccharidosis - 1:Hurler/Hunter - 3:Sanfilippo - 4:Morquio - 6:Maroteaux-Lamy - 7:Sly |
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| Glycoprotein | Mucolipidosis - I-cell disease - Pseudo-Hurler polydystrophy - Aspartylglucosaminuria - Fucosidosis - Alpha-mannosidosis - Sialidosis |
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| Other | Alpha 1-antitrypsin deficiency - Cystic fibrosis - Amyloidosis (Familial Mediterranean fever) - Acatalasia |
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