This is defined as a plasma level below 0.7 mmol/L. As it is not predominantly an extracellular ion, this may not clearly reflect total body levels. In the case of plasma hypomagnesaemia, total body levels will often also be low. It is a common abnormality in hospital, particularly in critical care where it may be a high as 60-65% of patients.
Hypomagnesaemia primarily arises from increased GI or renal losses. As there is limited ability to mobilise the body stores (in the bone) this can lead to plasma levels dropping fairly quickly. Other mechanisms may include impaired absorption and saponification.
Aetiology
GI Losses/Impaired absorption
Diarrhoea (acute and chronic)
Malabsorption syndromes
Vomiting (less common than with diarrhoea)
PPIs
Familial
Small bowel bypass surgery
Renal Losses
Diuretics
Loop
Thiazide
Other drugs
Aminoglycosides
Digoxin
Cisplatin
Amphotericin
Alcohol
Hypervolaemia (reduced sodium reuptake)
Poorly controlled diabetes
Post transplant
Tubular dysfunction pathology
Hypercalcaemia
Familial
Presentation
It will usually be alongside another problem e.g. critical illness, although may be a primary problem. However, it often is accompanied by other biochemical derangement:
Hypokalaemia
Hypocalcaemia
Metabolic alkalosis
The depletion can affect multiple systems. CNS:
Weakness
Tremor
Tetany
Seizures
Movement disorder
Delirium
Depressed GCS
CVS
Widening QRS (mod)
Peaked T waves (mod)
Wide PR (severe)
Atrial/ventricular arrhythmias (severe)
Promotes digoxin toxicity
Metabolic
Hypokalaemia
Hypocalcaemia
Hypoparathyroidism/PTH resistance
Insulin resistance
Management
This essentially involves replacement of the deficit. The urgency will impact on the rapidity of replacement:
Emergency - 10-20 mmol IV immediately, then 40 mmol IV over 4h
Urgent - 40 mmol initially IV. Can step down
Non-urgent - 15 mmol/day - usually enterally
Caution should be taken in cases of IV administration (especially when rapid) as may cause hypotension and bradycardia. Monitoring of levels is also essential given the potential for toxicity. The development of absence of deep tendon reflexes is often used as a rapid clinical assessment of toxicity in cases where it may develop (e.g. preeclampsia treatment protocols).
Links & References
Watson, V. Vaughan, R. Magnesium and the anaesthetist. CEPD Review. 2001.