Hypomagnesaemia is defined as a serum magnesium concentration < 0.7 mmol/L.
Hypomagnesaemia is a very common electrolyte disturbance that can be seen in up to 65% of intensive care unit patients.
Magnesium is commonly lost in the gastrointestinal tract and kidneys. Even small deficits in the net magnesium balance will lead to hypomagnesaemia. This is due to an inability to rapidly exchange between serum magnesium and the bony reserve.
The normal range of serum magnesium is 0.7-1.1 mmol/L. Hypomagnesaemia is defined as a serum concentration < 0.7 mmol/L, it is commonly found with other electrolyte derangement including hypokalaemia and hypocalcaemia.
Magnesium is principally absorbed from the intestines and excreted by the kidneys.
Magnesium is absorbed in the intestines and excreted in the kidney via urine. Bone is the main reservoir of magnesium in the body, but exchange with serum concentrations is not freely accessible.
The average daily intake of magnesium is 15 mmol, of which 5 mmol (one third) is absorbed and the rest is lost in the bowel. The principal site of absorption is the small bowel, but the colon can absorb a small amount.
The kidneys are the main site of magnesium excretion via the urine. An estimated 80% of serum magnesium is filtered at the glomerulus. From here the principal site of reabsorption is the Loop of Henle in the thick ascending limb.
Reabsorption of magnesium is by passive diffusion due to a favourable electrical gradient generated by the Na-K-2Cl cotransporter. Therefore, loop diuretics, which affect sodium and chloride reabsorption in the loop of Henle can affect magnesium reabsorption. Other diuretics such as thiazides also increase magnesium urinary excretion.
Other factors that influence magnesium reabsorption in the nephron include:
There are no major hormones that regulate magnesium and interaction with the magnesium stores in bone is slow. Therefore, a negative magnesium balance (e.g. from inadequate intake) quickly leads to hypomagnesaemia.
As magnesium is reliant on urinary excretion for clearance, a positive magnesium balance (e.g. intravenous infusion) in the context of renal impairment can lead to hypermagnesaemia.
Magnesium is predominantly lost from the gastrointestinal tract and kidneys.
The predominant cause of hypomagnesaemia is reduced dietary intake leading to a negative magnesium balance. This is commonly seen in alcoholic or severely malnourished patients.
Hypomagnesaemia may be seen in both vomiting and diarrhoea. Diarrhoeal losses account for more cases as the lower gastrointestinal content contains a higher concentration of magnesium.
Rarely, an inherited disorder of magnesium absorption may be the cause. This is autosomal recessive or X-linked recessive.
Hypomagnesaemia has been described in the chronic use of proton pump inhibitors (PPI) such as omeprazole. Hypomagnesaemia in the context of PPI use is much more common with concurrent diuretic use. PPIs are suspected to inhibit the magnesium transport receptor TRPM6.
There are multiple mechanisms by which magnesium can be lost in the urine:
Hypomagnesaemia is frequently asymptomatic and picked up on routine bloods ordered for inpatients.
In moderate-severe cases or in those with rapid changes to their serum magnesium features may include tremors, arrhythmias, convulsions and confusion.
Hypomagnesaemia can affect the myocardium leading to dangerous atrial and ventricular arrhythmias.
Features of hypocalcaemia may occur because it impairs the action of PTH. Hypomagnesaemia causes resistance to PTH and in severe cases reduces secretion.
Hypokalaemia is seen in 40-60% of patients with hypomagnesaemia. This can be due to shared aetiologies (e.g. diarrhoea and vomiting). It can also occur as normal levels of magnesium have an inhibitory effect on luminal potassium (ROMK) channels that prevent potassium efflux.
In the absence of magnesium replacement, potassium replacement may be attenuated.
The diagnosis of hypomagnesaemia is based on a serum magnesium concentration <0.7 mmol/L.
Hypomagnesaemia is a common finding on routine testing. Patients presenting with a suggestive aetiology (e.g. alcohol excess, malnutrition, diarrhoea) need magnesium testing.
Hypomagnesaemia commonly occurs with other electrolyte abnormalities so it is important to collect a full set of blood tests. Urinary magnesium collections can be used to determine between renal and gastrointestinal losses, but this is seldom completed in clinical practice.
Hypomagnesaemia typically causes an QT prolongation and increases the risk of atrial/ventricular ectopics, atrial tachycardias and polymorphic ventricular tachycardia.
The management of hypomagnesaemia involves oral or intravenous replacement.
It is important to determine and treat the underlying cause. This includes reviewing the medical history for any culprit medications. Usually short courses of replacement are enough to replace deficit, but more extended courses may be needed.
Common side-effects of oral magnesium replacement are abdominal discomfort and diarrhoea. Oral replacement may be poorly tolerated.
Intravenous doses of magnesium are needed for severe or symptomatic hypomagnesaemia (e.g. seizures, tetany, arrhythmias). Intravenous magnesium replacement requires cardiac monitoring, the duration of administration depends on hospital policy and the indication.
Patients unable to tolerate oral preparations usually require intravenous administration. Care should be taken in patients with reduced renal function as it can lead to hypermagnesaemia.
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