hypomagnesaemia

introduction

magnesium is an important cation and often forgotten but low plasma levels may cause clinical effects, particularly severely low levels
unlike calcium, it is not under significant hormonal control and mobilisation of reserves from bone takes weeks

decreased intake:
- starvation
- anorexia nervosa / eating disorders
- alcohol abuse - 30-80% of alcoholics are deficient
- total parenteral nutrition
- ICU patients - 50-60% are deficient
- diabetics - 25% are deficient
- hospital inpatients - 10-20% are deficient
- general poor diet - 2% of population are deficient
GIT losses:
- diarrhoea
- vomiting
- NG suction
- GIT fistulae or stomas
- Hypomagnesemia with secondary hypocalcemia (HSH)
redistribution from extracellular to intracellular:
- Hungry bone syndrome
- Rx of diabetic ketoacidosis (DKA)
- alcohol withdrawal syndromes
- refeeding syndrome
- acute pancreatitis
increased renal excretion:
- diuretics
- some antibiotics such as aminoglycoside antibiotics
- proton pump inhibitors (PPIs)
- ethanol (alcohol and alcohol withdrawal)
- hypercalcaemia
- volume expansion
- primary hyperaldosteronism
- recovery phase of acute tubular necrosis
- postobstructive diuresis
- chronic metabolic acidosis results in renal magnesium wasting
- phosphate depletion (increases urinary magnesium excretion)
- colorectal cancer treatment with cetuximab/panitumumab (EGF receptor inhibitors)
- rare genetic disorders such as:
  - isolated dominant hypomagnesemia (IDH)
  - autosomal-dominant hypocalcemia with hypercalciuria (ADHH)
  - hypomagnesemia with secondary hypocalcemia (HSH) - early infancy
  - familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC)

in the presence of hypocalcaemia, tetany can occur during the administration of magnesium sulphate if calcium is not also supplemented, as ionized calcium levels can drop acutely from complexing of calcium with sulfate ions and increased urinary excretion
magnesium sulphate infusion also causes potassium excretion and may exacerbate hypokalaemia

an abrupt elevation in the plasma magnesium concentration by infusing magnesium sulphate will partially remove the stimulus for magnesium retention, and thus up to 50% of the infused magnesium will be excreted in the urine
magnesium is subject to slow equilibration between serum and the intracellular spaces and tissues, the serum magnesium level may appear artificially high if measured too soon after a magnesium dose is administered.
severe magnesium depletion requires sustained correction of the hypomagnesaemia, preferably by sustained-release oral preparations

Rx underlying cause
- those on diuretics which cannot be ceased, may benefit from use of a potassium-sparing diuretic as these increase magnesium reabsorption in the collecting tubule
if Mg < 0.4mM:
- Rx with iv magnesium sulphate as correction will take 7 days instead of 6 weeks as with oral supplements.
- One 5 mL ampoule of magnesium sulfate contains 10 mmol of magnesium ions.
- 10—20 mmol of magnesium ions can be given in 100 mL of 0.9% sodium chloride over 1—2 hours.
- hypomagnesemic-hypokalemic patient with ventricular arrhythmias:
  - 50mEq Mg over 8-24hrs, rpt x 1 prn to maintain plasma Mg > 0.4 mmol/L or 0.8 mEq/L
- Patients with renal insufficiency should have their doses decreased appropriately, be monitored closely for decreased deep tendon reflexes, and have their magnesium concentrations checked regularly.
- monitor calcium levels as sulphate anions however may bind calcium and aggravate existing [hypocalcaemia]].
oral magnesium supplements such as magnesium aspartate (1.66mmol Mg per tablet) ii-iv tablets per day in divided doses but risk of diarrhoea which will limit higher doses.