Magnesium (Mg) is essential for all enzyme processes involving adenosine triphosphate (ATP) and many enzymes involved in nucleic acid metabolism. It is required for thiamine metabolism, appears to stabilise the structure of DNA and RNA and is in some way related to calcium and potassium metabolism. The genetic mechanisms which control magnesium homeostasis are currently being researched.
It is involved in hormone production (most notably parathyroid hormone) and is implicated in neurotransmission. Changes in normal levels can thus have wide-sweeping effects on body function.
Magnesium is the 4th most common cation found in the body. Most is sequestered in bone cells, with only about 1% in the extracellular fluid. Normal plasma Mg concentration ranges from 0.70 to 1.05 mmol/L.
Plasma concentration is a reflection of the dietary intake of magnesium and of the ability of the kidneys and gastrointestinal tract to retain it. Because most magnesium is found intracellularly, the relationship between total body deficiency and plasma concentration is poor. However, in cases of severe deficiency, a reduction in plasma concentration can be seen.
This is defined as a level less than 0.7mmol/L. It may be seen in:
- Malabsorption syndromes.
- Protein-calorie malnutrition.
- Disorders of the parathyroid gland.
- Chronic alcoholism - secondary to alcohol-induced diuresis, malnutrition.
- Chronic diarrhoea.
- Patients on long-term proton pump inhibitors.
- Renal disorders causing reduced magnesium resorption - acute tubular necrosis, post-obstructive diuresis, renal tubular acidosis.
- Drugs - eg diuretics, cisplatin, fluoride poisoning.
- Diabetes (due to glucose-induced diuresis secondary to poor glucose control).
- Inherited forms exist.
- Miscellaneous - cirrhosis, pregnancy, excessive lactation.
American studies have reported that hypomagnesaemia occurs in 10-20% of hospitalised patients and 50-60% of patients in intensive care units. It is also very common in alcoholics (30-80%) and it occurs in 25% of diabetic outpatients.
Presentation of hypomagnesaemia
This may present with:
Investigations for hypomagnesaemia
- Serum magnesium should be arranged. It should be borne in mind, however, that the level may be normal in early mild deficiency because only a small amount of total body magnesium is extracellular. An ionised magnesium level would give a more accurate picture.
- Protein loss may affect the reading, as the majority of extracellular magnesium is protein-bound.
- Magnesium deficiency may be associated with hypocalcaemia, hypophosphataemia and hypokalaemia, so calcium, phosphate and potassium levels should all be checked.
- Glucose level should be checked due to the association with diabetes.
- ECG changes may include include ST segment depression; tall, peaked T waves; flat T waves or depression in the precordium; U waves; loss of voltage; PR prolongation; and widened QRS.
- Mild symptoms usually respond to oral replacement therapy with a magnesium salt (eg magnesium gluconate 500 mg/day = 27 mg elemental magnesium - orally for adults. In children, the dose is 3-6 mg elemental magnesium/kg/day orally).
- One study reported the successful treatment of hypocalcaemia secondary to hypomagnesaemia in an ileostomy patient by self-administered subcutaneous injections of magnesium.
- Severe depletion will require intravenous replacement with magnesium sulphate, 2-4 g of 50% solution (8.3-16.6 mmol) diluted in saline or dextrose intravenously (IV) over 30-60 minutes for adults: 0.5 mmol/kg IV on day 1; 0.25 mmol/kg/day over the next 3 days for children.
- 24-hour urinary magnesium excretion should be monitored to ensure response to treatment.
- Secondary causes should be treated and oral replacement continued if the cause cannot be corrected.
This is much less common that hypomagnesaemia. It is most frequently encountered in patients with renal failure, taking drugs containing magnesium and in patients on parenteral nutrition. Diuretics (particularly loop diuretics) may be a cause as may alcohol use and disorders associated with hypercalcaemia. It is also occasionally seen after hypothyroidism, adrenal insufficiency and prolonged laxative use.
There are no reliable figures for prevalence.
Presentation of hypermagnesaemia
The first changes (at 2.3-5.0 mmol/L) may be noted on an ECG and include depression of sinoatrial node activity and sometimes atrial fibrillation. At higher levels, the following may occur:
- Disappearance of deep tendon reflexes.
- Respiratory depression.
- Parkinson-like symptoms.
- Psychological changes.
- Seizures (rare).
- Cardiac arrest (at >6.0-7.5 mmol/L).
Investigations for hypermagnesaemia
- Atomic absorbance spectrophotometry (AAS) is the most specific technique available for measuring total serum magnesium.
- Hyperkalaemia and hypercalcaemia are often present and these levels should also be checked.
- Thyroid function tests and an early morning cortisol test should be performed if hypermagnesaemia is recalcitrant or recurrent.
- Hypermagnesaemia can be corrected using IV calcium. Calcium chloride (5 ml of a 10% solution) should be given IV over 30 seconds. The patient should be treated in an intensive care unit with regular ECG monitoring.
- If the patient has a normal urine output and renal function, magnesium loss can be enhanced using intravenous saline infusions and furosemide diuresis.
- Dialysis may be used for patients with:
- Renal insufficiency.
- Severe asymptomatic hypermagnesaemia (>4 mmol/L).
- Serious cardiovascular or neuromuscular symptoms irrespective of serum magnesium level.
- Non-magnesium-containing enemas may be used to enhance gastrointestinal loss.
- On discharge, the patient's ongoing medication regime should be reviewed to ensure that it does not include magnesium-containing laxatives or antacids.
Further reading & references
- Konrad M, Schlingmann KP, Gudermann T; Insights into the molecular nature of magnesium homeostasis. Am J Physiol Renal Physiol. 2004 Apr;286(4):F599-605.
- Alexander RT, Hoenderop JG, Bindels RJ; Molecular determinants of magnesium homeostasis: insights from human disease. J Am Soc Nephrol. 2008 Aug;19(8):1451-8. Epub 2008 Jun 18.
- Novello N et al; Hypomagnesemia, eMedicine, Jul 2010
- Fagan C, Phelan D; Severe convulsant hypomagnesaemia and short bowel syndrome. Anaesth Intensive Care. 2001 Jun;29(3):281-3.
- Turecky L, Kupcova V, Szantova M, et al; Serum magnesium levels in patients with alcoholic and non-alcoholic fatty liver. Bratisl Lek Listy. 2006;107(3):58-61.
- Cundy T, Dissanayake A; Severe hypomagnesaemia in long-term users of proton-pump inhibitors. Clin Endocrinol (Oxf). 2008 Jan 23;.
- Familial Hypomagnesaemia, Online Mendelian Inheritance in Man (OMIM)
- Ferry RJ; Hypermagnesemia, eMedicine, Jan 2010
- Hsieh CT, Liang JS, Peng SS, et al; Seizure associated with total parenteral nutrition-related hypermanganesemia. Pediatr Neurol. 2007 Mar;36(3):181-3.
- So M, Ito H, Sobue K, et al; Circulatory collapse caused by unnoticed hypermagnesemia in a hospitalized patient. J Anesth. 2007;21(2):273-6. Epub 2007 May 30.
|Original Author: Dr Laurence Knott||Current Version: Dr Laurence Knott|
|Last Checked: 22/06/2011||Document ID: 2413 Version: 23||© EMIS|
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