Hypomagnesemia

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Hypomagnesemia
Classification & external
resources

Magnesium

ICD-10 E83.4
ICD-9 275.2
DiseasesDB 6469
MedlinePlus 000315
med/3382
eMedicine emerg/274
ped/1122

The prefix hypo- means low (contrast with hyper-, meaning high). The middle magnes refers to
magnesium. The end portion of the word, -emia, means 'in the blood' (note, however, that
hypomagnesemia is usually indicative of a systemic magnesium deficit). Thus,
Hypomagnesemia is an electrolyte disturbance in which there is an abnormally low level of
magnesium in the blood. Usually a serum level less than 0.7 mmol/l is used as reference. It must
be noted that hypomagnesemia is not equal to magnesium deficiency. Hypomagnesemia can be
present without magnesium deficiency and vice versa.
It may result from a number of conditions including inadequate intake of magnesium, chronic
diarrhea, malabsorption, alcoholism, chronic stress, diuretic use and other disorders.

Contents

1 Homeostasis
2 Metabolism

3 Causes

4 Clinical Features

5 Investigations

6 Treatment
o

6.1 Arrhythmia

6.2 Obstetric

6.3 Electrolyte disturbances

6.4 Pulmonary

7 References

8 See also

9 External links

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. ATP, ADP, proteins 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, cocoaderivatives, nuts, wheat, seafood, and meat. It is resorbed through the small intestine, and to a
lesser degree in the 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 kidneys 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 inhibitor."
Lack of magnesium inhibits the release of parathyroid hormone, which can result in
hypoparathyroidism and 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:

o

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 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. aminoglycosides, amphotericin, pentamidine, gentamicin, tobramycin,

viomycin) block resorption in the loop of Henle. 30% of patients using these antibiotics
have hypomagnesemia,

other drugs
o

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

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
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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 tachyarrhythmia. 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-Kpump.
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 calciummediated 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.
Sumber: http://en.wikipedia.org/wiki/Hypomagnesemia