Treatment of magnesium deficiency in hypomagnesaemia.
Treatment of magnesium deficiency where the oral route of administration may be inappropriate.
To prevent further seizures associated with eclampsia.

By intravenous infusion.
Adult, Children and the Elderly
35-50 mmol in 1 litre of 5% Glucose Intravenous Infusion or 0.9% w/v
Sodium Chloride Injection given over a period of 12 – 24 hours.
Patients with renal impairment, the dosage will need to be reduced.

Magnesium salts should be administered with caution to patients with impaired renal function;
appropriate reductions in dosage should be made (Refer to ‘Posology and Method of
Administration’ above).
Parenteral magnesium should be used with caution in individuals with myasthenia gravis, to
prevent an exacerbation of the condition or the precipitation of a myasthenic crisis. A riskbenefit
assessment should be performed in individual cases prior to initiation of treatment.
Magnesium sulfate should not be used in hepatic coma if there is risk of renal failure.
Serum calcium levels should be routinely monitored in patients receiving magnesium sulfate.

Muscle Relaxants: non-depolarising muscle relaxants such as tubocurarine are enhanced by
parenteral magnesium salts.
Calcium channel blockers such as nifedipine or nimodipine may rarely lead to a calcium ion
imbalance and could result in abnormal muscle function.
Nifedipine: profound hypotension was produced in two women who were given oral Nifedipine.
Magnesium salts should also be administered with caution to those receiving digitalis glycosides.
Parenteral administration of magnesium salts may enhance the effects of neuromuscular blocking
agents or of central nervous system depressants.
CNS Depressants: When barbiturates, opiates, general anaesthetics, or other
CNS depressants are administered concomitantly with magnesium sulfate, dosage of these agents
must be carefully adjusted because of the additive central depressant effects.
Antibacterials: The neuromuscular blocking effects of parenteral magnesium and
aminoglycoside antibacterials may be additive.
Magnesium may cause severe and unpredictable potentiation of neuromuscular blocking agents.
The muscle stimulating effects of Barium toxicity are reduced by magnesium.

Safety in human pregnancy has not been established, however, in the medical emergency of a
patient having Eclampsia, Magnesium Sulfate can be administered to relieve this condition,
which may be life threatening to both mother and baby.
As with all drugs it is not advisable to administer magnesium sulfate during pregnancy or
breastfeeding unless considered essential, and it must be administered under medical
supervision.
Magnesium crosses the placenta. When used in pregnant women, foetal heart rate should be
monitored and use within 2 hours of delivery should be avoided.
Magnesium sulfate can cause skeletal adverse effects when administered continuously for more
than 5 to 7 days to pregnant women. There are retrospective epidemiological studies and case
reports documenting fetal adverse effects including hypocalcaemia, skeletal demineralization,
osteopenia and other skeletal adverse effects with maternal administration of magnesium sulfate
for more than 5 to 7 days. The clinical significance of the observed effects is unknown.
If prolonged or repeated exposure to magnesium sulfate occurs during pregnancy monitoring of
neonates for abnormal calcium or magnesium levels and skeletal adverse effects should be
considered.

No studies on the effects on the ability to drive and use machines have been performed.

In patients with impaired renal function there may be sufficient accumulation to produce toxic
effects.
Excessive administration of magnesium leads to the development of hypermagnesaemia.
Symptoms of hypermagnesaemia may include nausea, vomiting, flushing of the skin, thirst,
hypotension due to peripheral vasodilatation, drowsiness, confusion, loss of tendon reflexes and

respiratory depression due to neuromuscular blockade, muscle weakness, respiratory depression,
cardiac arrhythmias, coma, and cardiac arrest.
Hypersensitivity reactions. Hypocalcaemia.
Metabolism and nutrition disorders
Electrolyte/fluid abnormalities (hypophosphataemia, hypertonic dehydration)
There have been isolated reports of maternal and fetal hypocalcaemia with high doses of
magnesium sulfate (see section 4.6).
Reporting of suspected adverse reactions
Reporting suspected adverse reactions after authorisation of the medicinal product is important.
It allows continued monitoring of the benefit/risk balance of the medicinal product.

The symptoms of progressive overdosage could be expected to be bradycardia, loss of deep
tendon reflexes, heart block, respiratory paralysis and finally cardiac arrest.
Treatment should include artificial respiration if necessary, intravenous calcium gluconate and
dialysis if renal function is reduced.

Pharmacotherapeutic group: Mineral Supplements,
ATC code: A12CC 02.
Magnesium is the second most abundant cation in intracellular fluid and is an essential body
electrolyte. Magnesium is a factor in a number of enzyme systems, and is involved in
neurochemical transmission and muscular excitability.
Parenterally administered magnesium sulfate exerts a depressant effect on the central nervous
system and acts peripherally to produce vasodilation.
Hypermagnesemia can cause the following ECG changes: prolonged PR, QRS and QT intervals.

The concentration of magnesium in plasma is normally tightly regulated in the range of 0.75-
0.95mmol/l.
Small and clinically irrelevant amounts are excreted in breast milk. The major excretory pathway
of magnesium is renal, and both oral and intravenous loads are rapidly eliminated in this way. In
renal impairment there may be accumulation of magnesium.
The potential for magnesium toxicity is greater in parenteral administration than with oral
dosing.
At plasma concentrations of up to 4mmol/l, the only adverse effect likely to be seen is flushing
due to peripheral vasodilatation. At about 4-5mmol/l, concentration-dependant toxicity is
heralded by loss of deep-tendon reflexes, then successively by hypotension, bradycardia and
ultimately neuromuscular blockade leading to respiratory arrest.
When given intravenously, Magnesium Sulfate has an immediate onset of action, and its duration
of activity is about 30mins.

This product has been available for many years and its side effects and clinical profile are wellunderstood,
therefore no further data is provided.

Water for Injection

The important possible interactions are listed below.
Alkali carbonates, bicarbonates and hydroxides, calcium, clindamycin phosphate, hydrocortisone
sodium succinate, phosphates, polymyxin B, procaine, salicylates and tartrates.
Streptomycin sulfate and tetramycin sulfate activity is inhibited by magnesium ions.

Do not store above 30° C.
Keep out of the sight and reach of children.

Colourless clear solution supplied in plastic ampoules containing10ml and 20ml.

None stated.