Magnidown

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.

Hepatic encephalopathy, hepatic failure or renal failure.

Parenteral magnesium salts should generally be avoided in patients suffering from heart block.

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 risk-benefit assessment should be performed in individual cases prior to initiation of treatment.

Magnidown should not be used in hepatic coma if there is risk of renal failure.

Serum calcium levels should be routinely monitored in patients receiving Magnidown.

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.

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. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at: www.mhra.gov.uk/yellowcard.

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 Magnidown 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, Magnidown 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 well-understood, therefore no further data is provided.

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.

None stated