eMedicine Specialties > Emergency Medicine > Endocrine & Metabolic
Hypomagnesemia
Updated: Aug 18, 2009
Introduction
Background
Magnesium, the fourth most common cation in the body, has been the recent focus of much clinical and scholarly interest. Previously underappreciated, this ion is now established as a central electrolyte in a large number of cellular metabolic reactions, including DNA and protein synthesis, neurotransmission, and hormone-receptor binding. It is a component of GTPase and a cofactor for Na+/K+ –ATPase, adenylate cyclase, and phosphofructokinase. Magnesium also is necessary for the production of parathyroid hormone. Accordingly, magnesium deficiency has an effect on multiple body functions.
Magnesium is present in greatest concentration within the cell and is the second most abundant intracellular cation after potassium. The total body content of magnesium is 2000 mEq. The intracellular concentration of magnesium is 40 mEq/L, while the serum concentration is 1.5-2 mEq/L. Most of the body's magnesium is found in bone. Only 1% of the total body magnesium is extracellular. Of this amount, one half is ionized, and 25-30% is protein bound.
Magnesium, a component of chlorophyll, is absorbed in the small bowel by active and passive transport mechanisms. Absorption of dietary magnesium takes place mainly in the ileum. It is excreted in stool and urine, but regulation of serum magnesium is under renal control. Most renal reabsorption of magnesium occurs in the proximal tubule and the thick ascending limb of the loop of Henle. In hypomagnesemic patients, the kidney may excrete as little as 1 mEq/L of magnesium. Additionally, magnesium may be removed from bone stores in times of deficiency.
A: Magnesium reabsorption in the thick ascending limb of the loop of Henle. The driving force for the reabsorption against a concentration gradient is a lumen-positive voltage gradient generated by the reabsorption of NaCl. Terms: FHHNC (familial hypomagnesemia with hypercalciuria and nephrocalcinosis); ADH (autosomal-dominant hypocalcemia); FHH/NSHPT (familial hypomagnesemia/neonatal severe hyperparathyroidism). B: Magnesium reabsorption in the distal convoluted tubule. Active transcellular transport is mediated by an apical entry through a magnesium channel and a basolateral exit, presumably via a Na+/Mg2+ exchange mechanism. Terms: HSH (hypomagnesemia with secondary hypocalcemia); GS (Gitelman syndrome); IDH (isolated dominant hypomagnesemia). Source: Konrad M, Schlingmann KP, Gudermann T: Insights into the molecular nature of magnesium homeostasis. Am J Physiol Renal Physiol 2004; 286: F599-F605.
Pathophysiology
Clinical effects of hypomagnesemia are greatest in the CNS, neuromuscular, GI, and cardiac systems.
Frequency
United States
Risk of incidence is as follows:
- 2% in the general population
- 10-20% in hospitalized patients
- 50-60% in ICU patients
- 30-80% in alcoholics
- 25% in diabetic outpatients
Sex
Incidence is equal in males and females.
Age
Magnesium deficiency may contribute to many age-related diseases.1
Clinical
History
- Clues to the presence of hypomagnesemia can be found by obtaining a history of potential causes (see Causes).
- Historical complaints related to hypomagnesemia are nonspecific.
- Patients may report weakness, muscle cramping, or rapid heartbeats.
- Altered mental status may be present in severe cases. Less severe cases may result in vertigo, ataxia, depression, and seizure activity.
Physical
The primary clinical findings are neuromuscular irritability, CNS hyperexcitability, and cardiac arrhythmias. The severity of symptoms is not related directly to the magnesium level. The reference range for serum magnesium level is 1.8-3 mEq/L. Usually, patients become symptomatic at 1.8 mEq/L. However, the physical findings may not be present in all cases. In one study of patients who were severely depleted of magnesium, abnormal physical findings were present in only 2 of 21 patients.
- Neuromuscular irritability
- Hyperactive deep tendon reflexes
- Muscle cramps
- Muscle fibrillation
- Trousseau and Chvostek signs
- Dysarthria and dysphagia from esophageal dysmotility
- CNS hyperexcitability
- Irritability and combativeness
- Disorientation
- Psychosis
- Ataxia, vertigo, nystagmus, and seizures (at levels <1 mEq/L)
- Cardiac arrhythmias that may be caused by hypomagnesemia alone or concomitant hypokalemia result from decreased activity of ATPase.
- Paroxysmal atrial and ventricular dysrhythmias
- Repolarization alternans
- Neonates
- Apnea
- Weakness
- Seizures
- Jitteriness
Causes
The causes of hypomagnesemia are numerous. Most causes are related to renal and GI losses.- GI losses
- Malabsorption of magnesium in the ileum results in hypomagnesemia. Situations of decreased absorption include malabsorption syndromes (eg, celiac sprue), radiation injury to the bowel, bowel resection, or small bowel bypass.
- GI secretions in large amounts may cause hypomagnesemia. Upper GI secretions contain 1 mEq/L of magnesium, while lower GI secretions contain 15 mEq/L of magnesium. Significant losses of magnesium that result in hypomagnesemia may result from chronic diarrhea, laxative abuse, inflammatory bowel disease, or neoplasm.
- Malnutrition leads to hypomagnesemia when dietary intake of magnesium is low. Dietary sources include green vegetables, fruits, fish, fresh meat, and cereal. Alcoholics are classically hypomagnesemic in part due to poor nutrition.2 Diabetic patients who are not receiving magnesium supplements may have dietary deficiencies in magnesium.
- Renal losses from primary renal disorders or secondary causes (eg, drugs, hormones, osmotic load) may result in magnesium wasting and subsequent hypomagnesemia.
- Primary renal disorders cause hypomagnesemia by decreased tubular reabsorption of magnesium by the damaged kidneys. This condition occurs in the diuretic phase of acute tubular necrosis, postobstructive diuresis, and renal tubular acidosis.
- Drugs may cause magnesium wasting.
- Diuretics (eg, thiazide, loop diuretics) decrease the renal threshold for magnesium reabsorption in addition to wasting of potassium and calcium.
- Cisplatin causes dose-dependent kidney damage in 100% of patients receiving this drug.
- Pentamidine and some antibiotics also cause renal magnesium wasting.
- Fluoride poisoning similarly causes hypomagnesemia.
- Endocrine disorders may cause hypomagnesemia.
- Primary aldosteronism decreases magnesium levels by increasing renal flow.
- Hypoparathyroidism and hyperthyroidism may cause renal wasting.
- Osmotic diuresis results in magnesium loss in the kidney.
- Diabetic patients, especially those with poor glucose control, develop hypomagnesemia from a glucose-induced osmotic diuresis.
- Alcoholics become hypomagnesemic partially by an osmotic diuresis from alcohol. Urinary losses have been reported to be 2-3 times control values.
- Miscellaneous
- Extracellular volume expansion, as in cirrhosis or intravenous (IV) fluid administration, may decrease magnesium levels.
- Redistribution of magnesium into cells may cause lower magnesium levels. Insulin causes this effect.
- Excessive lactation may create a significant amount of magnesium loss.
- Hungry bone syndrome may lead to lower serum magnesium concentrations.
- Pregnant women have been found to be magnesium depleted, especially those women who experience preterm labor.
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References
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Monico EP, Bachman D, Anthony RG. Hypomagnesemia. Am J Emerg Med. Jul 1997;15(4):441-2. [Medline].
Nadler JL, Rude RK. Disorders of magnesium metabolism. In: Clinical Disorders of Fluid and Electrolyte Metabolism. Vol 24. 1995:623-36.
Stalnikowicz R. The significance of routine serum magnesium determination in the ED. Am J Emerg Med. Sep 2003;21(5):444-7. [Medline].
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Further Reading
Keywords
hypomagnesemia, low magnesium level, magnesium, electrolytes, parathyroid hormone, magnesium deficiency, magnesium malabsorption, celiac sprue, radiation injury to the bowel, bowel resection, small bowel bypass, chronic diarrhea, laxative abuse, inflammatory bowel disease, neoplasm, malnutrition, diabetes, primary renal disorders, acute tubular necrosis, postobstructive diuresis, renal tubular acidosis, diuretics, cisplatin, pentamidine, fluoride poisoning, primary aldosteronism, hypoparathyroidism, hyperthyroidism, osmotic diuresis, alcoholism, insulin, excessive lactation, hungry bone syndrome, hypokalemia, hypocalcemia, hypophosphatemia, magnesium supplements, ischemic heart disease
