Hypermagnesemia

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Hypermagnesemia
Mg-TableImage.png
Classification and external resources
Specialty endocrinology, disorder of magnesium metabolism[*]
ICD-10 E83.4
ICD-9-CM 275.2
DiseasesDB 6259
eMedicine med/3383 emerg/262 ped/1080

Hypermagnesemia is an electrolyte disturbance in which there is a high level of magnesium in the blood.[1] It is defined as a level greater than 1.1 mmol/L.[2] Symptoms include weakness, confusion, decreased breathing rate, and cardiac arrest.[2]

Hypermagnesemia can occur in kidney failure and those who are given magnesium salts or who take drugs that contain magnesium (e.g. some antacids and laxatives).[3] It is usually concurrent with other electrolyte disturbances such as a low blood calcium and/or high blood potassium level. Specific electrocardiogram (ECG) changes may be present.[2]

Treatment when levels are very high include calcium chloride, intravenous normal saline with furosemide, and hemodialysis.[2]

Hypermagnesemia occurs rarely because the kidney is very effective in excreting excess magnesium.

Signs and symptoms[edit]

Abnormal heart rhythms and asystole are possible complications of hypermagnesemia related to the heart. Magnesium acts as a physiologic calcium blocker, which results in electrical conduction abnormalities within the heart.

Clinical consequences related to serum concentration:

Note that the therapeutic range for the prevention of the pre-eclampsic uterine contractions is: 4.0-7.0 mEq/L.[4] As per Lu and Nightingale,[5] serum Mg2+ concentrations associated with maternal toxicity (also neonate depression - hypotonia and low Apgar scores) are:

  • 7.0-10.0 mEq/L - loss of patellar reflex
  • 10.0-13.0 mEq/L - respiratory depression
  • 15.0-25.0 mEq/L - altered atrioventricular conduction and (further) complete heart block
  • >25.0 mEq/L - cardiac arrest

Hypermagnesemia in kidney failure[edit]

An evaluation of 515 patients on hemodialysis demonstrated that serum magnesium concentration lower than 2.77 mg/dL (1.14 mmol/L) is a significant predictor for increased all-cause mortality. While the mean serum magnesium concentration of this study population (2.77 mg/dL or 1.14 mmol/L) would be considered indicative of mild hypermagnesemia in the healthy population, serum magnesium concentrations in hemodialysis patients may be optimal at a higher concentration, in view of better survival under hemodialysis conditions, without causing severe and symptomatic hypermagnesemia.[6] Consistently, lower magnesium levels were significantly associated with the presence of vascular calcification of the hand arteries in a study investigating 390 nondiabetic hemodialysis patients. These results suggest that higher serum magnesium concentrations may play an important protective role in the development of vascular calcification in hemodialysis patients.[7] Results from a longitudinal study with end-stage renal disease patients suggest that hypermagnesemia may retard the development of arterial calcifications in end-stage renal disease.[8] Significantly lower values of carotid intima-media thickness and aortic pulse wave velocity values, which are surrogate markers for vascular calcification, were observed in chronic kidney disease patients with high serum magnesium levels (0.90-1.32 mmol/L or 2.18-3.21 mg/dL) indicating a lower arteriosclerotic burden associated with a lower risk of cardiovascular events and mortality.[9] Consequently, CKD patients with mildly elevated magnesium levels could have a survival advantage over those with lower magnesium levels.[10]

Causes[edit]

Magnesium status depends on three organs: uptake in the intestine, storage in the bone and excretion in the kidneys. Hypermagnesemia is therefore often due to problems in these organs, mostly intestine or kidney.[11]

Predisposing conditions[edit]

Metabolism[edit]

For a detailed description of magnesium homeostasis and metabolism see hypomagnesemia.

Treatment[edit]

Prevention of hypermagnesemia usually is possible. In mild cases, withdrawing magnesium supplementation is often sufficient. In more severe cases the following treatments are used:

Definitive treatment of hypermagnesemia requires increasing renal magnesium excretion through:

  • Intravenous diuretics, in the presence of normal renal function
  • Dialysis, when kidney function is impaired and the patient is symptomatic from hypermagnesemia

References[edit]

  1. ^ "hypermagnesemia" at Dorland's Medical Dictionary
  2. ^ a b c d Soar, J; Perkins, GD; Abbas, G; Alfonzo, A; Barelli, A; Bierens, JJ; Brugger, H; Deakin, CD; Dunning, J; Georgiou, M; Handley, AJ; Lockey, DJ; Paal, P; Sandroni, C; Thies, KC; Zideman, DA; Nolan, JP (October 2010). "European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution.". Resuscitation. 81 (10): 1400–33. PMID 20956045. 
  3. ^ Romani, Andrea, M.P. (2013). "Chapter 3. Magnesium in Health and Disease". In Astrid Sigel; Helmut Sigel; Roland K. O. Sigel. Interrelations between Essential Metal Ions and Human Diseases. Metal Ions in Life Sciences. 13. Springer. pp. 49–79. doi:10.1007/978-94-007-7500-8_3. 
  4. ^ Pritchard JA. The use of the magnesium ion in the management of eclamptogenic toxemias. Surg Gynecol Obstet. 1955; 100:131–140
  5. ^ Lu JF,Nightingale CH. Magnesium sulfate in eclampsia and pre-eclampsia. Clin Pharmacokinet. 2000; 38:305–314
  6. ^ Ishimura E, Okuno S, Yamakawa T, et al. (2007). "Serum magnesium concentration is a significant predictor of mortality in maintenance hemodialysis patients" (PDF). Magnes Res. 20: 237–244. doi:10.1684/mrh.2007.0116. PMID 18271493. 
  7. ^ Ishimura E, Okuno S, Kitatani K, et al. (2007). "Significant association between the presence of peripheral vascular calcification and lower serum magnesium in hemodialysis patients". Clin Nephrol. 68: 222–227. doi:10.5414/cnp68222. PMID 17969489. 
  8. ^ Meema HE, Oreopoulos DG, Rapoport A (1987). "Serum magnesium level and arterial calcification in end-stage renal disease". Kidney Int. 32: 388–394. doi:10.1038/ki.1987.222. PMID 3669498. 
  9. ^ Salem S, Bruck H, Bahlmann FH, et al. (2012). "Relationship between magnesium and clinical biomarkers on inhibition of vascular calcification". Am J Nephrol. 35: 31–39. doi:10.1159/000334742. PMID 22179063. 
  10. ^ Massy ZA, Drüeke TB (2012). "Magnesium and outcomes in patients with chronic kidney disease: focus on vascular calcification, atherosclerosis, and survival" (PDF). Clin Kidney J. 5 (Suppl 1): i52–i61. doi:10.1093/ndtplus/sfr167. 
  11. ^ Jahnen-Dechent W, Ketteler M (2012). "Magnesium basics" (PDF). Clin Kidney J. 5 (Suppl 1): i3–i14. doi:10.1093/ndtplus/sfr163. 

External links[edit]