Hypomagnesemia: Difference between revisions

Jump to navigation Jump to search
← Older editNewer edit →
VisualWikitext
Charmaine Patel (talk | contribs)
nocaptcha
14,570 edits
No edit summary
Charmaine Patel (talk | contribs)
nocaptcha
14,570 edits
No edit summary
Line 18: Line 18:




==[[Homeostasis]]==
The body contains 21-28 grams of magnesium (1 mmol=2mEq=24.6 mg). Of this, 53% is located in [[bone]], 19% in non-muscular tissue, and 1% in [[extracellular fluid]]. For this reason, blood levels of magnesium are not an adequate means of establishing the total amount of available magnesium.
Most of the serum magnesium is bound to chelators, (i.e. [[Adenosine triphosphate|ATP]], [[Adenosine diphosphate|ADP]], [[protein]]s and [[citrate]]). Roughly 33% is bound to proteins, and 5-10% is not bound. This "free" magnesium is essential in regulating intracellular magnesium. Normal plasma Mg is 1.7-2.3 mg/dl (0.69-0.94 mmol/l). Of this 60% is free, 33% is bound to proteins, and less than 7% is bound to citrate, [[bicarbonate]] and [[phosphate]].


Magnesium is abundant in nature. It can be found in green vegetables, [[chlorophyll]], coca-derivatives, nuts, wheat, seafood, and meat. It is resorbed through the [[small intestine]], and to a lesser degree in the [[Colon (anatomy)|colon]]. The [[rectum]] and [[sigmoid colon]] can absorb magnesium. [[Hypermagnesemia]] has been reported after enemas containing magnesium. Forty percent of dietary magnesium is absorbed. Hypomagnesemia stimulates and hypermagnesemia inhibits this absorption.


The [[kidney]]s regulate the serum magnesium. About 2400 mg of magnesium passes through the kidneys, of which 5% (120 mg) is excreted through [[urine]]. The [[loop of Henle]] is the major site for Mg-homeostasis and 60% is resorbed.
Magnesium homeostasis comprises three systems: kidney, small intestine, and bone. In the acute phase of magnesium deficiency there is an increase in absorption in the distal small intestine and tubular resorption in the kidneys. When this condition persists serum magnesium drops and is corrected with magnesium from bone tissue. The level of intracellular magnesium is controlled through the reservoir in bone tissue.
==Metabolism==
Magnesium is a cofactor in more than 300 [[enzyme]] regulated reactions. Most importantly forming and using ATP, i.e. kinase. There is a direct effect on sodium- (Na), potassium- (K) and calcium (Ca)channels. It has several effects:
*Potassium channels are inhibited by magnesium. Hypomagnesemia results in increased [[efflux]] of intracellular Mg. The cell loses potassium which then is excreted by the kidneys, resulting in [[hypokalemia]].
*Release of calcium from the [[sarcoplasmic reticulum]] is inhibited by magnesium. Low levels of magnesium stimulate the release of calcium and thereby an intracellular level of calcium. This effect similar to calcium inhibitors makes it "nature's [[Calcium channel blocker|calcium inhibitor]]." Lack of magnesium inhibits the release of [[parathyroid hormone]], which can also result in [[hypocalcemia]]. Furthermore, it makes skeletal and muscle receptors less sensitive to parathyroid hormone.
*Through relaxation of bronchial smooth muscle it causes [[bronchodilation]].
*The neurological effects are:
**reducing electrical excitation
**blocking release of [[acetylcholine]]
**blocking N-methyl-D-aspartate, an excitatory [[neurotransmitter]] of the central nervous system.
==Causes==
Magnesium deficiency is not uncommon in hospitalized patients. Elevated levels of magnesium ([[hypermagnesemia]]), however, are nearly always [[iatrogenic]]. 10-20% of all [[hospital]] patients, and 60-65% of patient in the [[intensive care unit]] (ICU) have hypomagnesemia. Hypomagnesiemia is underdiagnosed, as testing for serum magnesium levels is not routine. Hypomagnesemia results in increased [[death|mortality]].
Low levels of magnesium in your blood may mean either there is not enough magnesium in the diet, the intestines are not absorbing enough magnesium or the kidneys are excreting too much magnesium. Deficiencies may be due to the following conditions:
* alcoholism. Hypomagnesemia occurs in 30% of [[alcohol abuse]] and 85% in [[delirium tremens]], due to [[malnutrition]] and chronic [[diarrhoea]]. Alcohol stimulates renal excretion of magnesium, which is also increased because of alcoholic [[ketoacidosis]], [[hypophosphatemia]] and [[hyperaldosteronism]] resulting from liver disease. Also hypomagnesemia is related to [[thiamine]] deficiency because magnesium is needed for transforming thiamine into thiamine pyrophosphate.
* diuretic use (the most common cause of hypomagnesemia)
* antibiotics (i.e. [[aminoglycoside]]s, [[amphotericin]], [[pentamidine]], [[gentamicin]], [[tobramycin]], [[viomycin]]) block resorption in the [[loop of Henle]]. 30% of patients using these antibiotics have hypomagnesemia,
* other drugs
** [[digitalis]], displaces magnesium into the cell
** adrenergics, displace magnesium into the cell
** [[cisplatin]], stimulates renal excretion
** [[ciclosporin]], stimulates renal excretion
* excess calcium
* increased levels of stress
* excess saturated fats
* excess [[coffee]] or [[tea]] intake
* excess phosphoric or carbonic acids (soda pop)
* insufficient water consumption
* excess salt
* excess sugar intake
* insufficient selenium
* insufficient vitamin D or sunlight exposure
* insufficient vitamin B6
* gastrointestinal causes: the distal tractus digestivus secretes high levels of magnesium. Therefore, secretory diarrhoea can cause hypomagnesemia. Thus,  [[Crohn's disease]], [[ulcerative colitis]], [[Whipple's disease]] and [[coeliac sprue]] can all cause hypomagnesemia.
* renal magnesium loss in [[Bartter's syndrome]], postobstructive diuresis, diuretic phase of acute tubular necrosis (ATN) and [[kidney transplant]]
* diabetes mellitus: 38% of diabetic outpatient clinic visits involve hypomagnesemia, probably through renal loss because of [[glycosuria]] or ketoaciduria.
* [[acute myocardial infarction]]: within the first 48 hours after a heart-attack 80% of patients have hypomagnesemia. This could be the result of an intracellular shift because of an increase in catecholamines.
* [[malabsorption]]
* milk diet in infants
* [[acute pancreatitis]]
* [[hydrogen fluoride]] poisoning


==Clinical Features==
==Clinical Features==

Revision as of 17:52, 20 September 2012

Hypomagnesemia
Magnesium
ICD-10 E83.4
ICD-9 275.2
DiseasesDB 6469
MedlinePlus 000315

Hypomagnesemia Microchapters

Home

Patient Information

Overview

Pathophysiology

Causes

Differentiating Hypomagnesemia from other Diseases

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Other Diagnostic Studies

Treatment

Medical Therapy

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Hypomagnesemia On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Hypomagnesemia

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Hypomagnesemia

CDC on Hypomagnesemia

Hypomagnesemia in the news

Blogs on Hypomagnesemia

Directions to Hospitals Treating Hypomagnesemia

Risk calculators and risk factors for Hypomagnesemia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Synonyms and keywords: Hypomagnesaemia; magnesium levels low (plasma or serum)




Clinical Features

Deficiency of magnesium causes weakness, muscle cramps, cardiac arrhythmia, increased irritability of the nervous system with tremors, athetosis, jerking, nystagmus and an extensor plantar reflex. In addition, there may be confusion, disorientation, hallucinations, depression, epileptic fits, hypertension, tachycardia and tetany.

Investigations

The diagnosis can be made by finding a plasma magnesium concentration of less than 0.7mmol/l. Since most magnesium is intracellular, a body deficit can be present with a normal plasma concentration. In addition to hypomagnesemia, up to 40% cases will also have hypocalcemia while in up to 60% of cases, hypokalemia will also be present. The ECG shows a prolonged QT interval.

Treatment

Treatment of hypomagnesemia depends on the degree of deficiency and the clinical effects. Oral replacement is appropriate for patients with mild symptoms, while intravenous replacement is indicated for patients with severe clinical effects. Intravenous magnesium sulphate (MgSO4) can be given in the following conditions:

Arrhythmia

Magnesium is needed for the adequate function of the Na+/K+-ATPase pumps in the cells of the heart. A lack of it depolarises and results in tachyarrythmia. Magnesium inhibits release of potassium, a lack of magnesium increases loss of potassium. Intracellular levels of potassium decrease and the cells depolarise. Digoxin increases this effect. Both digoxin and hypomagnesemia inhibit the Na-K-pump resulting in decreased intracellular potassium.

Magnesium intravenously helps in refractory arrhythmia, most notably torsade de pointes. Others are ventricular tachycardia, supraventricular tachycardia and atrial fibrillation.

The effect is based upon decreased excitability by depolarisation and the slowing down of electric signals in the AV-node. Magnesium is a negative inotrope as a result of decrease calcium influx and calcium release from intracellular storage. It is just as effective as verapamil. In myocardial infarction there is a functional lack of magnesium, suppletion will decrease mortality.

Obstetric

Most importantly pre-eclampsia. It has an indirect antithrombotic effect upon thrombocytes and the endothelial functions (increase in prostaglandin, decrease in thromboxane, decrease in angiotensin II), microvascular leakage and vasospasm through its function similar to calcium channel blockers.

Convulsions are the result of cerebral vasospasm. The vasodilatatory effect of magnesium seems to be the major mechanism.

Electrolyte disturbances

  • Hypokalemia: 42% of patients with hypokalemia also have hypomagnesemia, not responding to potassium supplementation. Magnesium is needed for the ATPase, Na-K-pump.
  • Hypocalcemia is present in 33% of patients in the intensive care unit, not responding to calcium supplementation. This is because of decreased function of the calcium pump, but also because of a decreased release of calcium by inhibition of parathyroid hormone release.

Pulmonary

Acute asthma, here there is a bronchodilatatory effect, probably by antagonizing a calcium-mediated constriction. Also, adrenergic stimulation, i.e. sympatheticomimetics used for treatment of asthma, might lower serum levels of magnesium, which must therefore be supplemented.

Sedation and anxiolytics may help in decreasing bronchoconstriction.

References

  1. Cecil Textbook of Medicine
  2. Harrison's Principles of Internal Medicine
  3. Intensive Care Medicine by Irwin and Rippe
  4. The ICU Book by Marino
  5. The Oxford Textbook of Medicine
  6. Saeed M.G. Al-Ghamdi, Eugene C. Cameron, MD and Roger A.L. Sutton, "Magnesium Deficiency: Pathophysiology And Clinical Overview", American Journal Of Kidney Diseases, 1994; 24 (5), 737-752.
  7. Delhumeau, J.C. Granry, J.P. Monrigal, F. Costerousse, "Indications Du Magnésium En Anesthésie-Réanimation", Annales Francaises D'Anesthésie Et De Réanimation, 1995; 14, 406-416.
  8. J. Durlach, V. Durlach, P. Bac, M. Bara and A. Gulet-Bara, "Magnesium And Therapeutics", Magnesium Research 1994; 7 (3-4), 313-328.
  9. Mark D. Faber, Warren L. Kupin, Charles W. Heilig and Robert G. Narins, "Common Fluid-Electrolyte and Acid-Base Problems In The Intensive Care Unit: Selected Issues", Seminars In Nephrology 1994; 14 (1), 8-22.
  10. Lee Goldman, J. Claude Bennett, Cecil's Textbook of Medicine, 21st Edition, 2000, 1137-1139.
  11. Paul L. Marino, The ICU Book, Second Edition 1998, Chapter 42, 660-672.
  12. A.E. Meinders, Professor of Internal Medicine at Leids Universitair Medisch Centrum, "Magnesium", Bij Intensive Care Patiënten
  13. R. Mills, M. Leadbeater and A. Ravalia, "Case Report: Intravenous Magnesium Sulphate In The Management Of Refractory Bronchospasm In A Ventilated Asthmatic", Anaesthesia, 1997; 52, 782-785.
  14. Michael A. Olerich, MD; Robert K. Rude, MD, "Should We Supplement Magnesium In Critically Ill Patients?", New Horizons, 1994; 2 (2),186-192.
  15. James G. Ramsay, MD, "Cardiac Management In The ICU", Chest, 1999; 115: 138S-144S.
  16. Richard A. Reinhart, MD, "Magnesium Deficiency: Recognition And Treatment In The Emergency Medicine Setting", American Journal Of Emergency Medicine, 1992; 10 (1), 76-83.
  17. Richard A. Reinhart, MD; Norman A. Desbiens, MD, "Hypomagnesemia In Patients Entering The ICU", Critical Care Medicine, 1985; 13 (6), 506-507.
  18. Elisabeth Ryzen, MD; Park W. Wagers, MD; Frederick R. Singer, MD; Robert K. Rude, MD, "Magnesium Deficiency In A Medical ICU Population", Critical Care Medicine, 1985; 13 (1), 19-21.
  19. Elisabeth Ryzen, MD, "Magnesium Homeostasis In Critically Ill Patients", Magnesium, 1998; 8, 201-212.
  20. Robert Whang, Edward M. Hampton and David D. Whang, "Magnesium Homeostasis And Clinical Disorders Of Magnesium Deficiency", The Annals Of Pharmacotherapy, 1994; 28, 220-226.
  21. Selenium deficiency as a cause of overload of iron and unbalanced distribution of other minerals

Related Chapters

External links

Template:Endocrine, nutritional and metabolic pathology

de:Magnesiummangel

Template:WikiDoc Sources

Retrieved from "https://www.wikidoc.org/index.php?title=Hypomagnesemia&oldid=746756"