Hypermagnesemia is an electrolyte disturbance in which there is a high level of magnesium in the blood. It is defined as a level greater than 1.1 mmol/L. Symptoms include weakness, confusion, decreased breathing rate, and cardiac arrest.
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). 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.
Hypermagnesemia occurs rarely because the kidney is very effective in excreting excess magnesium.
Signs and symptoms
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- Weakness, nausea and vomiting
- Impaired breathing
- Decreased respirations
- Low blood pressure
- Low blood calcium
- Abnormal heart rhythms and asystole
- Decreased or absent deep tendon reflexes
- Low heart rate
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:
- 4.0 mEq/l decreased reflexes
- >5.0 mEq/l Prolonged atrioventricular conduction
- >10.0 mEq/l Complete heart block
- >13.0 mEq/l Cardiac arrest
Note that the therapeutic range for the prevention of the pre-eclampsic uterine contractions is: 4.0-7.0 mEq/L. As per Lu and Nightingale, 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
Results from a longitudinal study with end-stage renal disease suggest that hypermagnesemia may retard the development of arterial calcifications in end-stage renal disease. 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. Consequently, people with CKD with mildly elevated magnesium levels could have a survival advantage over those with lower magnesium levels.
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.
- Hemolysis, magnesium concentration in erythrocytes is approximately three times greater than in serum, therefore hemolysis can increase plasma magnesium. Hypermagnesemia is expected only in massive hemolysis.
- Kidney insufficiency, excretion of magnesium becomes impaired when creatinine clearance falls below 30 ml/min. However, hypermagnesemia is not a prominent feature of renal insufficiency unless magnesium intake is increased.
- Other conditions that can predispose to mild hypermagnesemia are diabetic ketoacidosis, adrenal insufficiency, hypothyroidism, hyperparathyroidism and lithium intoxication.
Hypermagnesemia is diagnosed by measuring the concentration of magnesium in the blood. Concentrations of magnesium greater than 1.1 mmol/L are considered diagnostic.
Prevention of hypermagnesemia usually is possible. In mild cases, withdrawing magnesium supplementation is often sufficient. In more severe cases the following treatments are used:
- Intravenous calcium gluconate, because the actions of magnesium in neuromuscular and cardiac function are antagonized by calcium.
Definitive treatment of hypermagnesemia requires increasing renal magnesium excretion through:
- Intravenous diuretics, in the presence of normal kidney function
- Dialysis, when kidney function is impaired and the patient is symptomatic from hypermagnesemia
- "hypermagnesemia" at Dorland's Medical Dictionary
- 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. doi:10.1016/j.resuscitation.2010.08.015. PMID 20956045.
- 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.
- Pritchard JA (1955). "The use of the magnesium ion in the management of eclamptogenic toxemias". Surg Gynecol Obstet. 100: 131–140.
- Lu JF, Nightingale CH (2000). "Magnesium sulfate in eclampsia and pre-eclampsia". Clin Pharmacokinet. 38: 305–314. doi:10.2165/00003088-200038040-00002. PMID 10803454.
- 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.
- 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.
- 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.
- Jahnen-Dechent W, Ketteler M (2012). "Magnesium basics" (PDF). Clin Kidney J. 5 (Suppl 1): i3–i14. doi:10.1093/ndtplus/sfr163.