Hypomagnesemia medical therapy
|
Hypomagnesemia Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Hypomagnesemia medical therapy On the Web |
|
American Roentgen Ray Society Images of Hypomagnesemia medical therapy |
|
Risk calculators and risk factors for Hypomagnesemia medical therapy |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
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.
Medical Therapy
The use of magnesium replacement therapy has increased for unclear reasons[1].
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 depolarizes 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 depolarize. 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 depolarization 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, supplementation 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
- ↑ Kiberd BA, Tennankore KK, Daley CJ (2015). "Increases in intravenous magnesium use among hospitalized patients: an institution cross-sectional experience". Can J Kidney Health Dis. 2: 24. doi:10.1186/s40697-015-0056-7. PMC 4477498. PMID 26106483.