From Wikipedia, the free encyclopedia
Other namesMagnesium toxicity
SymptomsWeakness, confusion, decreased breathing rate[1]
ComplicationsCardiac arrest[1]
CausesKidney failure, treatment induced, tumor lysis syndrome, seizures, prolonged ischemia[1][2]
Diagnostic methodBlood level > 1.1 mmol/L (2.6 mg/dL)[1][3]
Differential diagnosisKidney failure, high blood calcium, high blood potassium, hypoparathyroidism, hypothyroidism, lithium toxicity, red blood cell breakdown, rhabdomyolysis[4]
TreatmentCalcium chloride, intravenous normal saline with furosemide, hemodialysis[1]

Hypermagnesemia is an electrolyte disorder in which there is a high level of magnesium in the blood.[3] Symptoms include weakness, confusion, decreased breathing rate, and decreased reflexes.[1][3] Complications may include low blood pressure and cardiac arrest.[1][5]

It is typically caused by kidney failure or is treatment-induced such as from antacids that contain magnesium.[1][6] Less common causes include tumor lysis syndrome, seizures, and prolonged ischemia.[2] Diagnosis is based on a blood level of magnesium greater than 1.1 mmol/L (2.6 mg/dL).[1][3] It is severe if levels are greater than 2.9 mmol/L (7 mg/dL).[5] Specific electrocardiogram (ECG) changes may be present.[1]

Treatment involves stopping the magnesium a person is getting.[2] Treatment when levels are very high include calcium chloride, intravenous normal saline with furosemide, and hemodialysis.[1] Hypermagnesemia is uncommon.[3] Rates among hospitalized patients in renal failure may be as high as 10%.[2]

Signs and symptoms[edit]

Symptoms include weakness, confusion, decreased breathing rate, and decreased reflexes.[1][3] As well as nausea, low blood pressure, low blood calcium,[7] abnormal heart rhythms and asystole, dizziness, and sleepiness.

Abnormal heart rhythms and asystole are possible complications of hypermagnesemia related to the heart.[8] Magnesium acts as a physiologic calcium blocker, which results in abnormalities of the electrical conduction system of the heart.

Consequences related to serum concentration:[9]: 281 

At magnesium levels about 4.5 mEq/L the stretch reflex is lost and with over 6.5 mEq/L respiratory failure may be observed. On ECG hypermagnesemia is mainly manifested by prolongation of PR and QRS intervals, T wave changes and AV block.[9]: 281 

The therapeutic range for the prevention of the pre-eclamptic uterine contractions is: 4.0–7.0 mEq/L.[10] As per Lu and Nightingale,[11] serum magnesium 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


Severe hypermagnesemia (levels greater than 12 mg/dL) can lead to cardiovascular complications (hypotension and arrhythmias) and neurological disorder (confusion and lethargy). Higher values of serum magnesium (exceeding 15 mg/dL) can induce cardiac arrest and coma. [4]


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 the intestine or kidney.[12]

Predisposing conditions[edit]


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


Hypermagnesemia is diagnosed by measuring the concentration of magnesium in the blood. Concentrations of magnesium greater than 1.1 mmol/L are considered diagnostic.[1]


People with normal kidney function (glomerular filtration rate (GFR) over 60 ml/min) and mild asymptomatic hypermagnesemia require no treatment except for the removal of all sources of exogenous magnesium. One must consider that the half-time of elimination of magnesium is approximately 28 hours.

In more severe cases, close monitoring of the ECG, blood pressure, and neuromuscular function and early treatment are necessary:

Intravenous calcium gluconate or calcium chloride since the actions of magnesium in neuromuscular and cardiac function become antagonized by calcium.

Severe clinical conditions require increasing renal magnesium excretion through:

Intravenous loop diuretics (e.g., furosemide), or hemodialysis, when kidney function is impaired, or the patient is symptomatic from severe hypermagnesemia. This approach usually removes magnesium efficiently (up to 50% reduction after a 3- to 4-hour treatment). Dialysis can, however, increase the excretion of calcium by developing hypocalcemia, thus possibly worsening the symptoms and signs of hypermagnesemia.

The use of diuretics must be associated with infusions of saline solutions to avoid further electrolyte disturbances (e.g., hypokalemia) and metabolic alkalosis. The clinician must perform serial measurements of calcium and magnesium. In association with electrolytic correction, it is often necessary to support cardiorespiratory activity. As a consequence, the treatment of this electrolyte disorder can frequently require intensive care unit (ICU) admission.

Particular clinical conditions require a specific approach. For instance, during the management of eclampsia, the magnesium infusion is stopped if urine output drops to less than 80 mL (in 4 hours), deep tendon reflexes are absent, or the respiratory rate is below 12 breaths/minute. A 10% calcium gluconate or chloride solution can serve as an antidote.[4]


The prognosis of hypermagnesemia depends on magnesium values and on the clinical condition that induced hypermagnesemia. Values that are not excessively high (mild hypermagnesemia) and in the absence of triggering and aggravating conditions (e.g., chronic kidney disease) are benign conditions. On the contrary, high values (severe hypermagnesemia) expose the patient to high risks and high mortality.[4]


Hypermagnesemia is an uncommon electrolyte disorder. It occurs in approximately 10 to 15% of hospitalized patients with renal failure. Furthermore, epidemiological data suggest that there is a significant prevalence of high levels of serum magnesium in selected healthy populations. For instance the overall prevalence of hypermagnesemia was 3.0%, especially in males in Iran. High magnesium concentrations were typical in people with cardiovascular disease, and 2.3 mg/dL or higher values were associated with worse hospital mortality.[4]


  1. ^ a b c d e f g h i j k l m 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.
  2. ^ a b c d Ronco, Claudio; Bellomo, Rinaldo; Kellum, John A.; Ricci, Zaccaria (2017). Critical Care Nephrology. Elsevier Health Sciences. p. 344. ISBN 9780323511995.
  3. ^ a b c d e f g "Hypermagnesemia". Merck Manuals Professional Edition. Retrieved 28 October 2018.
  4. ^ a b c d e Cascella M, Vaqar S (2020). "Hypermagnesemia". Statspearl. PMID 31747218. This article incorporates text available under the CC BY 4.0 license.
  5. ^ a b Lerma, Edgar V.; Nissenson, Allen R. (2011). Nephrology Secrets. Elsevier Health Sciences. p. 568. ISBN 978-0323081276.
  6. ^ Romani, Andrea, M.P. (2013). "Chapter 3. Magnesium in Health and Disease". In Astrid Sigel; Helmut Sigel; Roland K. O. Sigel (eds.). Interrelations between Essential Metal Ions and Human Diseases. Metal Ions in Life Sciences. Vol. 13. Springer. pp. 49–79. doi:10.1007/978-94-007-7500-8_3. PMID 24470089.{{cite book}}: CS1 maint: multiple names: authors list (link)
  7. ^ Cholst, IN; Steinberg, SF; Tropper, PJ; Fox, HE; Segre, GV; Bilezikian, JP (10 May 1984). "The influence of hypermagnesemia on serum calcium and parathyroid hormone levels in human subjects". New England Journal of Medicine. 310 (19): 1221–5. doi:10.1056/NEJM198405103101904. PMID 6709029.
  8. ^ Schelling, JR (January 2000). "Fatal hypermagnesemia". Clinical Nephrology. 53 (1): 61–5. PMID 10661484.
  9. ^ a b Advanced perioperative crisis management. Matthew D. McEvoy, Cory M. Furse. New York. 2017. ISBN 978-0-19-022648-0. OCLC 1007160054.{{cite book}}: CS1 maint: location missing publisher (link) CS1 maint: others (link)
  10. ^ Pritchard JA (1955). "The use of the magnesium ion in the management of eclamptogenic toxemias". Surg Gynecol Obstet. 100 (2): 131–140. PMID 13238166.
  11. ^ Lu JF, Nightingale CH (2000). "Magnesium sulfate in eclampsia and pre-eclampsia". Clin Pharmacokinet. 38 (4): 305–314. doi:10.2165/00003088-200038040-00002. PMID 10803454. S2CID 45298797.
  12. ^ Jahnen-Dechent W, Ketteler M (2012). "Magnesium basics". Clin Kidney J. 5 (Suppl 1): i3–i14. doi:10.1093/ndtplus/sfr163. PMC 4455825. PMID 26069819.

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