Pediatric Hypermagnesemia Clinical Presentation

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

History

  • Symptoms of hypermagnesemia are nonspecific at lower levels (2-4 mEq/L) and may include the following:
    • Nausea
    • Vomiting
    • Flushing
    • Lethargy
    • Weakness
    • Dizziness
  • Higher levels may lead to a depressed sensorium, and cardiopulmonary arrest may occur at extreme levels (>10-15 mEq/L).
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Physical

  • Hypermagnesemia results in loss of deep-tendon reflexes at levels of 4-6 mEq/L. At magnesium levels of more than 5 mEq/L, CNS depression, which may range from drowsiness to coma, begins. Although concentrations of magnesium of more than 10 mEq/L lead to respiratory depression in adults, this may occur at much lower levels in the newborn.
  • Hypermagnesemia has a negative effect on heart rate.[7] Beginning with magnesium serum levels of 4.5 mEq/L, depression of sinoatrial node activity and atrial fibrillation may occur. Higher magnesium levels increase the P-R interval, widen the QRS complex, and can cause intraventricular conduction delays. Serum magnesium concentrations greater than 15 mEq/L can lead to complete heart block and asystole.
  • At varying levels (5-8 mEq/L), hypermagnesemia may produce vasodepression of vascular smooth muscle leading to systemic hypotension.
  • Although the absolute serum levels are important, the rate of rise is even more significant. For instance, a fast rise in serum level can produce cardiovascular symptoms more readily than can a slower rise in serum levels.
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Causes

  • Major predisposing factors for the development of hypermagnesemia include the following:
    • Renal failure (acute or chronic)
    • Iatrogenic over administration of magnesium (eg, antacids, cathartics)
    • Neonates born to mothers treated with magnesium sulfate for eclampsia
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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].

  3. Kaze Folefack F, Stoermann Chopard C. [Magnesium metabolism disturbances]. Rev Med Suisse. Mar 7 2007;3(101):605-6, 608, 610-1. [Medline].

  4. Moe SM. Disorders involving calcium, phosphorus, and magnesium. Prim Care. Jun 2008;35(2):215-37, v-vi. [Medline].

  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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