Diagnosis

Hypermagnesemia

Serum Mg > 2,1 mg/dL / 0,9 mmol / 1,8 mEq/L.

Etiology

Cause [28d]

Pathophysiology [p6s]

  1. Magnesium is a physiologic calcium blocker, cofactor in hundreds of enzymatic reactions, critical to diverse molecular and catalytic processes, including energy transfer and maintenance of the genome [p6s][28d]

  2. Hypomagnesemia: associated with atherosclerosis and coronary artery disease [n8e]

  3. Hypermagnesemia inhibit the secretion of PTH --> hypocalcemia [sem]

  4. Distribution of magnesium: [pnf]

    • Bone: 60%

    • Extracellular: 1% (does not reflect total body stores.)

    • Intracellular: 39% (the second most common intracellular cation)

      • Muscle: 25-30%

      • Soft tissue: 10-15%

  5. Magnesium balance is determined by:

    • Dietary ingestion

    • Intestinal absorption

    • Bone and soft tissue deposition and efflux

    • Renal excretion and absorption

    • No hormone regulating (unlike calcium (PTH))

Complications [28d]

Epidemiology

Incidence per 100.000 [b91][p6s][n8e][nwi][nts][oow]

Epidemiology chart for Incidence

Prevalence per 100.000 [b91][p6s][n8e][nwi][nts][oow]

Epidemiology chart for Prevalence

Approach

Treatment

  1. Preserved renal function and mild asymptomatic hypermagnesemia (<7 mg/dL): [28d]

    • No treatment other than removal of exogenous magnesium

  2. Severe cases (>12 mg/dL): monitor ECG, blood pressure, and neuromuscular function

    • Saline IV (150 ml/hour)

    • Loop diuretics IV (Furosemide 1 mg/kg)

    • Calcium gluconate or chloride IV: 1 g in 5 min (repeatable over 5 minutes), counteracts neurologic/muscular manifestations

  3. If renal failure: Hemodialysis

Differential diagnoses

Acute renal failure, Adrenal insufficiency, Diabetic ketoacidosis, Drug side effects, Familial hypocalciuric hypercalcemia, Hemolysis, Hypercalcemia, Hyperkalemia, Hyperparathyroidism, Hypoparathyroidism, Hypothyroidism, Leukemia, Milk-alkali syndrome, Renal failure, Rhabdomyolysis


References

[1] Cascella M, Vaqar S. Hypermagnesemia. StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK549811/

[2] Adomako EA, Yu ASL. Magnesium Disorders: Core Curriculum 2024. Am J Kidney Dis. 2024 Jun;83(6):803-815.

[3] Syedmoradi L, Ghasemi A, Zahediasl S, Azizi F. Prevalence of hypo- and hypermagnesemia in an Iranian urban population. Ann Hum Biol. 2011 Mar;38(2):150-5.

[4] https://www.uptodate.com/contents/hypermagnesemia-causes-symptoms-and-treatment

[5] Felsenfeld AJ, Levine BS, Rodriguez M. Pathophysiology of Calcium, Phosphorus, and Magnesium Dysregulation in Chronic Kidney Disease. Semin Dial. 2015 Nov-Dec;28(6):564-77.

[6] Aal-Hamad AH, Al-Alawi AM, Kashoub MS, Falhammar H. Hypermagnesemia in Clinical Practice. Medicina (Kaunas). 2023 Jun 24;59(7):1190.

[7] Haider DG, Lindner G, Ahmad SS, Sauter T, Wolzt M, Leichtle AB, Fiedler GM, Exadaktylos AK, Fuhrmann V. Hypermagnesemia is a strong independent risk factor for mortality in critically ill patients: results from a cross-sectional study. Eur J Intern Med. 2015 Sep;26(7):504-7.

[8] Singhi SC, Singh J, Prasad R. Hypo- and hypermagnesemia in an Indian Pediatric Intensive Care Unit. J Trop Pediatr. 2003 Apr;49(2):99-103.

[9] Escuela MP, Guerra M, Añón JM, Martínez-Vizcaíno V, Zapatero MD, García-Jalón A, Celaya S. Total and ionized serum magnesium in critically ill patients. Intensive Care Med. 2005 Jan;31(1):151-6.

[10] http://emedicine.medscape.com/article/246489 (2014-01-02); [Medscape]

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