Hypermagnesemia

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Hypermagnesemia
Other namesMagnesium toxicity
Mg-TableImage.svg
Magnesium
Specialty Endocrinology
Symptoms Weakness, confusion, decreased breathing rate [1]
Complications Cardiac arrest [1]
Causes Kidney failure, treatment induced, tumor lysis syndrome, seizures, prolonged ischemia [1] [2]
Diagnostic method Blood level > 1.1 mmol/L (2.6 mg/dL) [1] [3]
Differential diagnosis Kidney failure, high blood calcium, high blood potassium, hypoparathyroidism, hypothyroidism, lithium toxicity, red blood cell breakdown, rhabdomyolysis [4]
Treatment Calcium chloride, intravenous normal saline with furosemide, hemodialysis [1]
FrequencyUncommon [3]

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. Hypermagnesemia can greatly increase the chances of adverse cardiovascular events. [1] [3] Complications may include low blood pressure and cardiac arrest. [1] [5]

Contents

It is typically caused by kidney failure or is treatment-induced such as from antacids or supplements 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

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.[ citation needed ]

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:[ citation needed ]

Complications

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]

Causes

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

Metabolism

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

Diagnosis

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]

Treatment

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]

Prognosis

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]

Epidemiology

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]

Related Research Articles

<span class="mw-page-title-main">Magnesium</span> Chemical element with atomic number 12 (Mg)

Magnesium is a chemical element; it has symbol Mg and atomic number 12. It is a shiny gray metal having a low density, low melting point and high chemical reactivity. Like the other alkaline earth metals it occurs naturally only in combination with other elements and almost always has an oxidation state of +2. It reacts readily with air to form a thin passivation coating of magnesium oxide that inhibits further corrosion of the metal. The free metal burns with a brilliant-white light. The metal is obtained mainly by electrolysis of magnesium salts obtained from brine. It is less dense than aluminium and is used primarily as a component in strong and lightweight alloys that contain aluminium.

<span class="mw-page-title-main">Parathyroid hormone</span> Mammalian protein found in humans

Parathyroid hormone (PTH), also called parathormone or parathyrin, is a peptide hormone secreted by the parathyroid glands that regulates the serum calcium concentration through its effects on bone, kidney, and intestine.

<span class="mw-page-title-main">Hypocalcemia</span> Low calcium levels in ones blood serum

Hypocalcemia is a medical condition characterized by low calcium levels in the blood serum. The normal range of blood calcium is typically between 2.1–2.6 mmol/L, while levels less than 2.1 mmol/L are defined as hypocalcemic. Mildly low levels that develop slowly often have no symptoms. Otherwise symptoms may include numbness, muscle spasms, seizures, confusion, or in extreme cases cardiac arrest.

Hypercalcemia, also spelled hypercalcaemia, is a high calcium (Ca2+) level in the blood serum. The normal range is 2.1–2.6 mmol/L (8.8–10.7 mg/dL, 4.3–5.2 mEq/L), with levels greater than 2.6 mmol/L defined as hypercalcemia. Those with a mild increase that has developed slowly typically have no symptoms. In those with greater levels or rapid onset, symptoms may include abdominal pain, bone pain, confusion, depression, weakness, kidney stones or an abnormal heart rhythm including cardiac arrest.

<span class="mw-page-title-main">Hyperkalemia</span> Excess potassium in the blood

Hyperkalemia is an elevated level of potassium (K+) in the blood. Normal potassium levels are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L) with levels above 5.5 mmol/L defined as hyperkalemia. Typically hyperkalemia does not cause symptoms. Occasionally when severe it can cause palpitations, muscle pain, muscle weakness, or numbness. Hyperkalemia can cause an abnormal heart rhythm which can result in cardiac arrest and death.

<span class="mw-page-title-main">Electrolyte imbalance</span> Abnormality in the concentration of electrolytes in the body

Electrolyte imbalance, or water-electrolyte imbalance, is an abnormality in the concentration of electrolytes in the body. Electrolytes play a vital role in maintaining homeostasis in the body. They help to regulate heart and neurological function, fluid balance, oxygen delivery, acid–base balance and much more. Electrolyte imbalances can develop by consuming too little or too much electrolyte as well as excreting too little or too much electrolyte. Examples of electrolytes include calcium, chloride, magnesium, phosphate, potassium, and sodium.

<span class="mw-page-title-main">Hypokalemia</span> Insufficient potassium in the blood

Hypokalemia is a low level of potassium (K+) in the blood serum. Mild low potassium does not typically cause symptoms. Symptoms may include feeling tired, leg cramps, weakness, and constipation. Low potassium also increases the risk of an abnormal heart rhythm, which is often too slow and can cause cardiac arrest.

Hypernatremia, also spelled hypernatraemia, is a high concentration of sodium in the blood. Early symptoms may include a strong feeling of thirst, weakness, nausea, and loss of appetite. Severe symptoms include confusion, muscle twitching, and bleeding in or around the brain. Normal serum sodium levels are 135–145 mmol/L. Hypernatremia is generally defined as a serum sodium level of more than 145 mmol/L. Severe symptoms typically only occur when levels are above 160 mmol/L.

The syndrome of inappropriate antidiuretic hormone secretion (SIADH), also known as the syndrome of inappropriate antidiuresis (SIAD), is characterized by a physiologically inappropriate release of antidiuretic hormone (ADH) either from the posterior pituitary gland, or an abnormal non-pituitary source. Unsuppressed ADH causes a physiologically inappropriate increase in solute-free water being reabsorbed by the tubules of the kidney to the venous circulation leading to hypotonic hyponatremia.

<span class="mw-page-title-main">Hypophosphatemia</span> Lack of phosphate in the blood

Hypophosphatemia is an electrolyte disorder in which there is a low level of phosphate in the blood. Symptoms may include weakness, trouble breathing, and loss of appetite. Complications may include seizures, coma, rhabdomyolysis, or softening of the bones.

<span class="mw-page-title-main">Metabolic acidosis</span> Imbalance in the bodys acid-base equilibrium

Metabolic acidosis is a serious electrolyte disorder characterized by an imbalance in the body's acid-base balance. Metabolic acidosis has three main root causes: increased acid production, loss of bicarbonate, and a reduced ability of the kidneys to excrete excess acids. Metabolic acidosis can lead to acidemia, which is defined as arterial blood pH that is lower than 7.35. Acidemia and acidosis are not mutually exclusive – pH and hydrogen ion concentrations also depend on the coexistence of other acid-base disorders; therefore, pH levels in people with metabolic acidosis can range from low to high.

<span class="mw-page-title-main">Gitelman syndrome</span> Genetic kidney disorder

Gitelman syndrome (GS) is an autosomal recessive kidney tubule disorder characterized by low blood levels of potassium and magnesium, decreased excretion of calcium in the urine, and elevated blood pH. It is the most frequent hereditary salt-losing tubulopathy. Gitelman syndrome is caused by disease-causing variants on both alleles of the SLC12A3 gene. The SLC12A3 gene encodes the thiazide-sensitive sodium-chloride cotransporter, which can be found in the distal convoluted tubule of the kidney.

<span class="mw-page-title-main">Ringer's lactate solution</span> Fluid used for resuscitation after blood loss

Ringer's lactate solution (RL), also known as sodium lactate solution,Lactated Ringer's (LR), and Hartmann's solution, is a mixture of sodium chloride, sodium lactate, potassium chloride, and calcium chloride in water. It is used for replacing fluids and electrolytes in those who have low blood volume or low blood pressure. It may also be used to treat metabolic acidosis and to wash the eye following a chemical burn. It is given by intravenous infusion or applied to the affected area.

Magnesium deficiency is an electrolyte disturbance in which there is a low level of magnesium in the body. Symptoms include tremor, poor coordination, muscle spasms, loss of appetite, personality changes, and nystagmus. Complications may include seizures or cardiac arrest such as from torsade de pointes. Those with low magnesium often have low potassium.

<span class="mw-page-title-main">Calcium gluconate</span> Chemical compound

Calcium gluconate is the calcium salt of gluconic acid and is used as a mineral supplement and medication. As a medication it is used by injection into a vein to treat low blood calcium, high blood potassium, and magnesium toxicity. Supplementation is generally only required when there is not enough calcium in the diet. Supplementation may be done to treat or prevent osteoporosis or rickets. It can also be taken by mouth but is not recommended for injection into a muscle.

<span class="mw-page-title-main">Multifocal atrial tachycardia</span> Fast heart rhythm associated with exacerbations of COPD

Multifocal atrial tachycardia (MAT) is an abnormal heart rhythm, specifically a type of supraventricular tachycardia, that is particularly common in older people and is associated with exacerbations of chronic obstructive pulmonary disease (COPD). Normally, the heart rate is controlled by a cluster of cells called the sinoatrial node. When a number of different clusters of cells outside the SA node take over control of the heart rate, and the rate exceeds 100 beats per minute, this is called multifocal atrial tachycardia.

<span class="mw-page-title-main">Digoxin toxicity</span> Medical condition

Digoxin toxicity, also known as digoxin poisoning, is a type of poisoning that occurs in people who take too much of the medication digoxin or eat plants such as foxglove that contain a similar substance. Symptoms are typically vague. They may include vomiting, loss of appetite, confusion, blurred vision, changes in color perception, and decreased energy. Potential complications include an irregular heartbeat, which can be either too fast or too slow.

Familial hypocalciuric hypercalcemia (FHH) is an inherited condition that can cause hypercalcemia, a serum calcium level typically above 10.2 mg/dL; although uncommon. It is also known as familial benign hypocalciuric hypercalcemia (FBHH) where there is usually a family history of hypercalcemia which is mild, a urine calcium to creatinine ratio <0.01, and urine calcium <200 mg/day (hypocalciuria).

<span class="mw-page-title-main">Sodium in biology</span> Use of sodium by organisms

Sodium ions are necessary in small amounts for some types of plants, but sodium as a nutrient is more generally needed in larger amounts by animals, due to their use of it for generation of nerve impulses and for maintenance of electrolyte balance and fluid balance. In animals, sodium ions are necessary for the aforementioned functions and for heart activity and certain metabolic functions. The health effects of salt reflect what happens when the body has too much or too little sodium. Characteristic concentrations of sodium in model organisms are: 10 mM in E. coli, 30 mM in budding yeast, 10 mM in mammalian cell and 100 mM in blood plasma.

Calcium acetate/magnesium carbonate is a fixed-dose combination drug that contains 110 mg calcium and 60 mg magnesium ions and is indicated as a phosphate binder for dialysis patients with hyperphosphataemia. It is registered by Fresenius Medical Care under the trade names Renepho (Belgium) and OsvaRen.

References

  1. 1 2 3 4 5 6 7 8 9 10 11 12 13 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. 1 2 3 4 Ronco, Claudio; Bellomo, Rinaldo; Kellum, John A.; Ricci, Zaccaria (2017). Critical Care Nephrology. Elsevier Health Sciences. p. 344. ISBN   9780323511995.
  3. 1 2 3 4 5 6 7 "Hypermagnesemia". Merck Manuals Professional Edition. Retrieved 28 October 2018.
  4. 1 2 3 4 5 Cascella M, Vaqar S (2020). "Hypermagnesemia". Statspearl. PMID   31747218. Creative Commons by small.svg  This article incorporates text available under the CC BY 4.0 license.
  5. 1 2 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. 1 2 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.