eMedicine Specialties > Pediatrics: General Medicine > Endocrinology
Hypomagnesemia: Treatment & Medication
Updated: Sep 18, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
When an underlying cause of hypomagnesemia is identified, treatment should be directed toward correcting the problem, if possible.
If hypomagnesemia is mild (ie, serum magnesium levels >1.2 mEq/L) and the patient is asymptomatic, oral replacement is preferred. The exact dosage needed to correct magnesium deficiency is unknown and dosage amounts vary from patient to patient depending on the specific cause of hypomagnesemia and underlying renal function. For children, 10-20 mg of elemental magnesium per kg body weight given three or four times daily has been recommended.
In emergent cases (eg, seizures), intravenous infusion should be use. One regimen consists of 25-50 mg magnesium sulfate per kg body weight (maximum 2 g) given slowly. This dose can be repeated every 4-6 hours as needed or a continuous infusion of 100-200 mg magnesium sulfate per kg body weight per day can be given. Rapid intravenous administration can be life threatening. Risks involved with intravenous magnesium therapy include hypermagnesemia, hypocalcemia, and sudden hypotension.
Diet
Green vegetables such as spinach are good sources of magnesium because the chlorophyll molecule contains magnesium. Some legumes (beans and peas), nuts and seeds, and whole, unrefined grains are also good sources of magnesium.3
Medication
Treatment for hypomagnesemia depends on the degree of deficiency and the patient's clinical symptoms and signs. Therapy can be oral for patients with mild symptoms or intravenous for patients with severe symptoms or those unable to tolerate oral administration. Some patients with hypomagnesemia caused by renal magnesium wasting may benefit from certain diuretics that have magnesium sparing properties, such as spironolactone and amiloride.
Magnesium salts
Magnesium can be administered either orally in an oxide or gluconate form or parenterally as a sulfate salt.
Magnesium oxide
Treatment of magnesium deficiencies or magnesium depletion from malnutrition, restricted diet, alcoholism or magnesium-depleting drugs.
Adult
2000 mg/day divided tid-qid PO
Pediatric
65-130 mg/kg/day divided tid-qid PO
May decrease effects of benzodiazepines, chloroquine, corticosteroids, digoxin, H2 antagonists, hydantoins, nitrofurantoin, tetracyclines, iron salts, ticlopidine, phenothiazines, iron salts; increases the effects of dicoumarol, quinidine, and sulfonylureas
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Hypermagnesemia and toxicity may occur in renal impairment when >50 mEq magnesium is given qd due to decreased clearance of magnesium ion; approximately 5%-20% of PO administered magnesium salts can be systemically absorbed
Magnesium gluconate (Almora, Magonate)
500 mg contains 27 mg of elemental Mg.
Adult
500-1000 mg PO tid
Pediatric
10-20 mg/kg elemental Mg PO tid/qid; not to exceed 400 mg/d
Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may also worsen neuromuscular blockade seen with aminoglycosides, tubocurarine, vecuronium, succinylcholine; Mg may increase CNS effects and toxicity of CNS depressants, betamethasone, ritodrine
Documented hypersensitivity; heart block, myocardial damage; hepatitis
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Caution in renal failure; may alter cardiac conduction leading to heart block in digitalized patients; monitor respiratory rate, deep tendon reflex, and renal function when administered parenterally; caution when administering Mg dose since may produce significant hypertension or asystole; diarrhea is most common adverse effect
Magnesium sulfate
1 g contains 8.12 mEq of Mg (98 mg elemental Mg)
Adult
2 g IV solution over 20 min, then 1 g q6h until levels corrected
Pediatric
1 mEq/kg IV infused over 2-6 h on day 1, then half that amount over next 3 d
Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may also increase neuromuscular blockade seen with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants, betamethasone, and cardiotoxicity of ritodrine
Documented hypersensitivity; heart block, myocardial damage; hepatitis
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Mg may alter cardiac conduction leading to heart block in digitalized patients; monitor respiratory rate, deep tendon reflex, and renal function when electrolyte is administered parenterally; caution when administering Mg dose since may produce significant hypertension or asystole; dilute to 5-20% before IV administration; maximum concentration of 20%; rate of administration should be <1.5 mL of 10% solution or equivalent per min (150 mg/min with ECG monitoring); rapid IV administration can lead to cardiac dysrhythmias, hypotension, flushing, sweating, and/or sensation of warmth; in overdose, calcium gluconate, 10-20 mL IV of 10% solution, can be given as antidote for clinically significant hypermagnesemia; hypotension; hypocalcemia; respiratory depression; or venous irritation may occur
Diuretic, Potassium Sparing
Amiloride
Potassium-sparing diuretic that also has some mild hypocalciuric activity. Reduces the magnesium loss caused by thiazides. A pyrazine-carbonyl-guanidine that is chemically unrelated to other known antikaliuretic or diuretic agents. Potassium-conserving (antikaliuretic) drug that possesses weak (compared with thiazide diuretics) natriuretic, diuretic, antihypertensive, and hypocalciuric effects. In some clinical studies, its activity increased effects of thiazide diuretics. Amiloride is not an aldosterone antagonist, and its effects are observed even in the absence of aldosterone. Exerts potassium-sparing effect through inhibition of sodium reabsorption at distal convoluted tubule, cortical collecting tubule, and collecting duct. This decreases the net negative potential of the tubular lumen and reduces both potassium and hydrogen secretion and their subsequent excretion.
Amiloride usually begins to act within 2 h after an PO dose. Effect on electrolyte excretion reaches a peak between 6-10 h and lasts about 24 h. Peak plasma levels are obtained in 3-4 h and plasma half-life varies from 6-9 h. Not metabolized by liver; excreted unchanged by kidneys. About 50% of a dose of amiloride is excreted in urine and 40% in stool within 72 h. Has little effect on glomerular filtration rate or renal blood flow. Because liver does not metabolize amiloride HCl, drug accumulation is not anticipated in patients with hepatic dysfunction; however, accumulation can occur if hepatorenal syndrome develops.
Amiloride rarely should be used alone. Used as single agents, potassium-sparing diuretics, including amiloride, result in an increased risk of hyperkalemia (approximately 10% with amiloride). Should be used alone only when persistent hypokalemia has been documented and only with careful titration of the dose and close monitoring of serum electrolytes.
Adult
5-20 mg PO qd
Pediatric
<6 kg: Not established
6-20 kg: 0.625mg/kg/d PO (maximum dose 10 mg/day)
>20 kg: Administer as in adults
Concomitant therapy with potassium supplementation may increase serum potassium levels, if concomitant use of these agents indicated because of demonstrated hypokalemia, caution and monitor serum potassium frequently; lithium generally should not be given with diuretics because may reduce renal clearance and add a high risk of lithium toxicity; administration of nonsteroidal anti-inflammatory agents can reduce diuretic, natriuretic, and antihypertensive effects of loop, potassium-sparing, and thiazide diuretics, when used concomitantly, observe patient closely to determine if desired effect of diuretic
obtained; indomethacin and potassium-sparing diuretics, including amiloride, may be associated with increased serum potassium levels, consider potential effects on potassium kinetics and renal function
Documented hypersensitivity; elevated serum potassium levels, >5.5 mEq/L; impaired renal function, acute or chronic renal insufficiency, and evidence of diabetic nephropathy; monitor electrolytes closely if there is evidence of renal functional impairment, BUN >30 mg per 100 mL or serum creatinine levels >1.5 mg per 100 mL
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Potassium retention associated with use of an antikaliuretic agent accentuated in presence of renal impairment and may result in rapid development of hyperkalemia; monitor serum potassium level, mild hyperkalemia usually not associated with abnormal ECG
More on Hypomagnesemia |
| Overview: Hypomagnesemia |
| Differential Diagnoses & Workup: Hypomagnesemia |
 Treatment & Medication: Hypomagnesemia |
| Follow-up: Hypomagnesemia |
| Multimedia: Hypomagnesemia |
| References |
| Further Reading |
| « Previous Page | Next Page » |
References
Tong GM, Rude RK. Magnesium deficiency in critical illness. J Intensive Care Med. Jan-Feb 2005;20(1):3-17. [Medline].
Curiel-Garcia JA, Rodriguez-Moran M, Guerrero-Romero F. Hypomagnesemia and mortality in patients with type 2 diabetes. Magnes Res. Sep 2008;21(3):163-6. [Medline].
Guerrera MP, Volpe SL, Mao JJ. Therapeutic uses of magnesium. Am Fam Physician. Jul 15 2009;80(2):157-62. [Medline].
Naderi AS, Reilly RF Jr. Hereditary etiologies of hypomagnesemia. Nat Clin Pract Nephrol. Feb 2008;4(2):80-9. [Medline].
Agus ZS. Hypomagnesemia. J Am Soc Nephrol. Jul 1999;10(7):1616-22. [Medline].
Konrad M. Disorders of magnesium metabolism. In: Geary D, Shaefer F. Comprehensive Pediatric Nephrology. Philadelphia PA: Mosby Elsevier; 2008:461-475.
Martin KJ, Gonzalez EA, Slatopolsky E. Clinical Consequences and Management of Hypomagnesemia. J Am Soc Nephrol. Jan 30 2008;[Medline]. [Full Text].
[Best Evidence] Mouw DR, Latessa RA, Hickner J. Clinical inquiries. What are the causes of hypomagnesemia?. J Fam Pract. Feb 2005;54(2):174-6. [Medline]. [Full Text].
Rodriguez-Hernandez H, Gonzalez JL, Rodriguez-Moran M, Guerrero-Romero F. Hypomagnesemia, insulin resistance, and non-alcoholic steatohepatitis in obese subjects. Arch Med Res. Jul-Aug 2005;36(4):362-6. [Medline].
Topf JM, Murray PT. Hypomagnesemia and hypermagnesemia. Rev Endocr Metab Disord. May 2003;4(2):195-206. [Medline].
Further Reading
- Relevant clinical guidelines include the following:
- Atrial fibrillation
- Advanced life support: 2005 International Consensus Conference on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations
- Management of alcohol withdrawal delirium: An evidence-based practice guideline
- European Federation of Neurological Societies guidelines on management of neurological problems in liver transplantation
- Relevant clinical trials include the following:
- Related eMedicine topics include the following:
- Hypomagnesemia (Nephrology)
- Hypomagnesemia (Emergency Medicine)
- Hypoparathyroidism
- Hypermagnesemia
- Infant of Diabetic Mother
Keywords
hypomagnesemia, magnesium, Mg, infectious diarrhea, steatorrhea, inflammatory bowel disease, GI neoplasms, diabetic ketoacidosis, irritability, disorientation, depression, psychosis, treatment, diagnosis, low magnesium levels, treatment, diagnosis
