Pediatric Hypermagnesemia Medication

  • Author: Robert J Ferry Jr, MD; Chief Editor: Stephen Kemp, MD, PhD   more...
 
Updated: Jan 8, 2010
 

Medication Summary

Treatment depends on the degree of hypermagnesemia and the presence of symptoms. In patients with mildly increased levels, the source of magnesium may simply be removed. In patients with higher concentrations of magnesium or severe symptoms, other treatments are necessary. Reserve calcium for patients with life-threatening symptoms, such as arrhythmias or severe respiratory depression.

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Intravenous fluids

Class Summary

Dilution of the extracellular magnesium concentration is the rationale behind intravenous use. Fluids are used with diuretics to promote diuresis of magnesium by the kidneys.

0.9% sodium chloride (normal saline)

 

Isotonic fluid. Restores water and sodium chloride losses.

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Diuretics

Class Summary

These agents increase renal excretion of magnesium.

Furosemide (Lasix)

 

Increases excretion of water by interfering with chloride-binding cotransport system, which inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. Promotes loss of magnesium. Administer PO dose with food or milk to decrease stomach upset.

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Calcium

Class Summary

Calcium directly antagonizes the effects of magnesium.

Calcium chloride (10% sol)

 

Moderates nerve and muscle performance by regulating action potential excitation threshold. Dose expressed in calcium chloride, not elemental calcium. 1 g calcium chloride contains 270 mg elemental calcium.

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Contributor Information and Disclosures
Author

Robert J Ferry Jr, MD  Chief, Division of Pediatric Endocrinology and Metabolism, Le Bonheur Children's Hospital; Professor, Department of Pediatrics, University of Tennessee Health Science Center at Memphis; St. Jude Children's Research Hospital, Memphis, TN; Brigade Surgeon, 36th Sustainment Brigade, U.S. Army; Adjunct Professor, Pediatric Surgery Department, King Saud University, Riyadh, Saudi Arabia

Robert J Ferry Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Medical Association, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, Society for Pediatric Research, and Texas Pediatric Society

Disclosure: Nutropin Speakers Bureau Honoraria Speaking and teaching; Genotropin Speakers Bureau Honoraria Speaking and teaching; Eli Lilly & Co. Grant/research funds Independent contractor; MacroGenics, Inc. Grant/research funds Independent contractor; Ipsen, S.A. (formerly Tercica, Inc.) Grant/research funds Independent contractor; NovoNordisk SA Grant/research funds Independent contractor; Diamyd Independent contractor

Specialty Editor Board

Phyllis W Speiser, MD  Chief, Division of Pediatric Endocrinology, The Children's Hospital, North Shore LIJ Health System; Professor of Pediatrics, New York University School of Medicine

Phyllis W Speiser, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London)  Professor and Chair, First Department of Pediatrics, Athens University Medical School, Aghia Sophia Children's Hospital, Greece; UNESCO Chair on Adolescent Health Care, University of Athens, Athens, Greece

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) is a member of the following medical societies: American Academy of Pediatrics, American College of Endocrinology, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Merrily P M Poth, MD  Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences

Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Lawson-Wilkins Pediatric Endocrine Society

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD  Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas and Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

References
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  2. Musso CG. Magnesium metabolism in health and disease. Int Urol Nephrol. Mar 10 2009;[Medline].

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  5. Navarro-Gonzalez JF, Mora-Fernandez C, Garcia-Perez J. Clinical implications of disordered magnesium homeostasis in chronic renal failure and dialysis. Semin Dial. Jan-Feb 2009;22(1):37-44. [Medline].

  6. [Best Evidence] Ford AA, Wylie BJ, Waksmonski CA, Simpson LL. Maternal congenital cardiac disease: outcomes of pregnancy in a single tertiary care center. Obstet Gynecol. Oct 2008;112(4):828-33. [Medline].

  7. Corbi G, Acanfora D, Iannuzzi GL, et al. Hypermagnesemia predicts mortality in elderly with congestive heart disease: relationship with laxative and antacid use. Rejuvenation Res. Feb 2008;11(1):129-38. [Medline].

  8. Ali A, Walentik C, Mantych GJ, et al. Iatrogenic acute hypermagnesemia after total parenteral nutrition infusion mimicking septic shock syndrome: two case reports. Pediatrics. Jul 2003;112(1 Pt 1):e70-2. [Medline].

  9. Durham D, Worthley LI. Cardiac arrhythmias: diagnosis and management. The tachycardias. Crit Care Resusc. Mar 2002;4(1):35-53. [Medline].

  10. Henyan NN, Gillespie EL, White CM, et al. Impact of intravenous magnesium on post-cardiothoracic surgery atrial fibrillation and length of hospital stay: a meta-analysis. Ann Thorac Surg. Dec 2005;80(6):2402-6. [Medline].

  11. Jaing TH, Hung IJ, Chung HT, Lai CH, Liu WM, Chang KW. Acute hypermagnesemia: a rare complication of antacid administration after bone marrow transplantation. Clin Chim Acta. Dec 2002;326(1-2):201-3. [Medline].

  12. Knochel JP. Disorders of magnesium metabolism. In: Harrison's Principles of Internal Medicine. Vol 2. 1994:2187-2189.

  13. Kutsal E, Aydemir C, Eldes N, et al. Severe hypermagnesemia as a result of excessive cathartic ingestion in a child without renal failure. Pediatr Emerg Care. Aug 2007;23(8):570-2. [Medline].

  14. McGuire JK, Kulkarni MS, Baden HP. Fatal hypermagnesemia in a child treated with megavitamin/megamineral therapy. Pediatrics. Feb 2000;105(2):E18. [Medline].

  15. Nadler JL, Rude RK. Disorders of magnesium metabolism. Clinical Disorders of Fluid and Electrolyte Metabolism. Vol 24. 1995:623-637.

  16. Rude RK, Singer FR. Magnesium deficiency and excess. Ann Rev Med. 1981;32:245-259. [Medline].

  17. [Guideline] Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines [trunc]. Bethesda (MD): American College of Cardiology Foundation (ACCF); 2005 Aug. 82 p.

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(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. 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. 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.
 
 
 
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