- 65% of body magnesium in mineral phase of skeleton, 34% in intracellular
space and 1% in ECF
- serum Mg 0.8-1.2 mmol/l. 55% in ionized form.
- homeostasis maintained principally by renal and gastroenterological
- dietary Mg obtained from green leafy vegetables, grain products and dairy
products. Absorption is related to dietary Mg availability (the smaller the
amount presented to the small bowel the higher the proportion absorbed), plasma
Mg, oral Ca intake and vitamin D
- kidney is primary affector of serum Mg. Diffusable Mg is filtered at the
glomerulus. 10-20% is reabsorbed in proximal tubules, 60-70% in the thick
ascending limb of loop of Henle and 5-10% in the distal loop with a resulting
5-10% fractional excretion.
- serum Mg levels directly affect tubular transport of Mg. High levels decrease
effective net absorption with a resulting increase in fractional excretion. Low
levels have the opposite effect.
- inhibition of sodium reabsorption in proximal tubule (eg by diuretics or fluid
loading) inhibits Mg reabsorption
- hypercalcaemia inhibits tubular reabsorption, possibly by an as-yet
unelucidated shared transport mechanism.
- PTH probably directly enhances tubular Mg reabsorption although this effect is
usually overshadowed by the hypercalcaemia present.
- end result of all these mechanisms is a reasonable resistance of the body to
hypermagnesaemia in the presence of normal renal function.
- usually iatrogenic and is frequently seen in conjunction with renal failure
Renal: creatinine clearance < 30ml/min
Non renal: iatrogenic - much more likely to occur in the presence of renal
Both: excessive Mg in diasylate
Effects are essentially those of a calcium channel blocker combined with a
membrane stabilizer. (Mg binds to many Ca binding sites and therefore blocks the
effect of Ca in a number of enzyme systems). Serum concentrations of at least 2
mmol/l are necessary to produce clinical effects.
delayed interventricular conduction
first and second degree AV block
> 12.5 mmol/l
complete AV block
- hypotension: usually only transient. Except in severe toxicity or following
rapid parenteral administration of MgSO4 hypermagnesaemia does not usually
produce a profound reduction in SVR.
- myocardial contractility is probably not affected by mild to moderate
- varying degrees neuromuscular block by decreasing impulse transmission
across the neuromuscular junction
- decrease in post-synaptic membrane responsiveness and an increase in the
threshold for axonal excitation also occur
- one of the earliest clinically noticeable signs of Mg toxicity is diminution
of deep tendon reflexes. Becomes apparent at levels > 2 mmol/l. almost always
antecedes more significant symptoms
- hypoventilation due to respiratory muscle paralysis
- somnolence and coma at very high levels
- prolonged administration of parenteral Mg lowers serum Ca. ? by impairment
of peripheral effects of parathormone
- may impair clotting
- determine cause and stop administration if iatrogenic
- if haemodynamically stable, no evidence of respiratory depression and reflexes
present simply observe for further symptoms and maintain urine output
- if reflexes diminished treat with saline diuresis or loop diuretics. If
symptoms persist or in massive overdose this should be followed by dialysis with
Mg free diasylate +/- prolonged IV calcium (15 mg/kg as gluconate over 4 hours).
- cardiac arrest or resp. depression: calcium gluconate 1g over 3 mins
- malabsorption syndromes
- GI fistulae
- short-bowel syndrome
- prolonged NG suction
- parenteral nutrition
- diuretic phase ATN
- carbenicillin, ticarcillin
- amphotericin B
- neuro: confusion, irritability, delirium tremens, fits
- often associated with resistant hypokalaemia and hypocalcaemia
- treat underlying cause
- IV MgSO4 10 mmol. over 5 min followed by 20-60 mmol/day
© Charles Gomersall December 1999