Electrolyte (magnesium)
Magnesium is an essential mineral for muscle and nerve function. Magnesium sulfate is used in hospital, intravenously, mainly to prevent and treat seizures in pre-eclampsia and eclampsia (serious complications of pregnancy) and to replace magnesium when it is low.
Also known as: magnésio, magnesium, sulfato de magnésio, Epsom
Salbutamol + magnesium: additive hypokalaemia (the β2-agonist lowers potassium).
β2-agonists such as salbutamol activate the Na⁺/K⁺-ATPase pump and promote intracellular potassium uptake, causing transient hypokalaemia. Magnesium sulfate can also lower serum potassium and, at high concentrations, depresses neuromuscular and cardiac conduction. Together (a common situation in severe acute asthma, where both are used), hypokalaemia can be more pronounced and increase the risk of arrhythmias, especially in patients with cardiovascular disease or on digoxin. Serum potassium and ECG should be monitored during magnesium infusion in patients receiving high-dose β2-agonists, correcting hypokalaemia if needed.
Salbutamol + magnesium: additive hypokalaemia (the β2-agonist lowers potassium). Monitor serum potassium and ECG.
β2-agonists cause K+ shift into cells; combined with magnesium, hypokalaemia may be accentuated, especially at high doses.
Serum potassium.
Weakness, cramps, arrhythmias.
Monitor potassium at high doses or with prolonged use.
DailyMed (FDA) — approved Salbutamol label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=3236f82c-14e9-dfd4-e063-6294a90ac43d ; approved Magnesium sulfate label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=a5a9f565-639c-4b22-b9e5-718bac7cfcf3 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Ciprofloxacin + magnesium: chelation reduces fluoroquinolone absorption.
Magnesium, a divalent cation, forms insoluble chelates with fluoroquinolones in the gastrointestinal tract, reducing the oral bioavailability of ciprofloxacin and the risk of therapeutic failure in serious infections. The ciprofloxacin label recommends giving the antibiotic 2 hours before or 6 hours after magnesium-containing antacids or supplements (including magnesium laxatives). In hospitalised patients receiving oral/enteral magnesium sulfate and ciprofloxacin, check the administration times of both to ensure antibacterial efficacy.
Magnesium + ciprofloxacin: chelation with reduced absorption. Separate by 2–6 h.
Magnesium cations chelate ciprofloxacin in the gut.
Clinical response to antibiotic therapy.
Therapy failure.
Separate oral dosing by at least 2 hours.
DailyMed (FDA) — approved Ciprofloxacin label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=c527d138-e32c-418f-9573-a3d8a796279f ; approved Magnesium sulfate label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=a5a9f565-639c-4b22-b9e5-718bac7cfcf3 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Furosemide + magnesium: furosemide increases renal magnesium loss.
Loop diuretics (furosemide) increase renal excretion of magnesium (and potassium), potentially causing hypomagnesaemia in patients on prolonged or high-dose treatment. Hypomagnesaemia is clinically relevant in itself (weakness, tetany, arrhythmias) and because it potentiates digitalis toxicity and hypokalaemia. In patients receiving magnesium sulfate (infusion or oral replacement) with furosemide, monitor serum magnesium and potassium, correct deficits and periodically reassess the need for the diuretic and the replacement.
Furosemide + magnesium: furosemide increases renal magnesium loss — risk of hypomagnesaemia.
Loop diuretics increase urinary magnesium excretion; supplementation corrects the deficit but requires monitoring.
Serum magnesium and renal function.
Weakness, cramps, arrhythmias.
Monitor serum magnesium during supplementation in patients on diuretics.
DailyMed (FDA) — approved Furosemide label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=6d9caaab-d874-4cf1-b9fe-408452a18998 ; approved Magnesium sulfate label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=a5a9f565-639c-4b22-b9e5-718bac7cfcf3 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Digoxin + magnesium: electrolyte imbalance with risk of arrhythmias.
Digitalis toxicity is potentiated by hypomagnesaemia (and hypokalaemia); conversely, hypermagnesaemia — which can occur with rapid infusion or renal impairment — depresses cardiac conduction and can worsen atrioventricular block in patients on digoxin. In digitalised patients, keep serum magnesium and potassium in the normal range, correct deficits (magnesium is even used in the treatment of digitalis toxicity with hypomagnesaemia) and, if IV magnesium is given, infuse slowly with ECG and renal function monitoring.
Digoxin + magnesium: electrolyte imbalance (hypo/hypermagnesaemia) with risk of arrhythmias.
Hypomagnesaemia increases digoxin toxicity; intravenous magnesium sulfate is used in toxicity, but cardiac monitoring is required.
Serum magnesium and ECG.
Arrhythmias, weakness, tetany.
Monitor magnesium, potassium and heart rhythm.
DailyMed (FDA) — approved Digoxin label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=e61d2108-d871-44c0-b12a-2e61fbb56967 ; approved Magnesium sulfate label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=a5a9f565-639c-4b22-b9e5-718bac7cfcf3 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Aminoglycoside + magnesium: risk of neuromuscular blockade and additive nephrotoxicity.
Aminoglycosides (gentamicin) can cause neuromuscular blockade, especially in patients with myasthenia gravis, botulism or hypocalcaemia; magnesium at high concentrations also depresses neuromuscular transmission. Together, the risk of muscle weakness and respiratory depression increases. In addition, both can damage the kidney: nephrotoxicity is additive, and impaired renal function reduces clearance of both, raising levels even further. In patients receiving gentamicin and IV magnesium sulfate (e.g., pre-eclampsia with infection), monitor renal function, serum magnesium and aminoglycoside levels, and watch muscle strength and ventilation.
Aminoglycoside + magnesium: risk of neuromuscular blockade and additive nephrotoxicity.
Magnesium sulfate may potentiate aminoglycoside neuromuscular blockade; both may affect renal function.
Renal function, magnesium, neurological signs.
Weakness, respiratory depression, rising creatinine.
Monitor renal function and signs of muscle weakness during co-administration.
DailyMed (FDA) — approved Gentamicin label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=977180b3-a222-4282-d485-4a3217674305 ; approved Magnesium sulfate label: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=a5a9f565-639c-4b22-b9e5-718bac7cfcf3 — additional reference: Prontuário Terapêutico do INFARMED (11th ed., 2012)
Chronic alcohol use increases renal magnesium loss.
Moderate alcohol intake during magnesium supplementation.
EMC-UK (MHRA) — approved Magnesium sulfate SmPC: https://www.medicines.org.uk/emc/product/10502/smpc
Magnesium may worsen neuromuscular weakness in myasthenia.
Use with caution, especially intravenously, and watch muscle strength.
EMC-UK (MHRA) — approved Magnesium sulfate SmPC: https://www.medicines.org.uk/emc/product/10502/smpc
Magnesium accumulates in renal impairment, risking hypermagnesaemia.
Use with caution and monitor serum magnesium.
EMC-UK (MHRA) — approved Magnesium sulfate SmPC: https://www.medicines.org.uk/emc/product/10502/smpc
Magnesium sulfate is used in pregnancy (pre-eclampsia/eclampsia) only under clinical supervision.
Use only on indication with hospital monitoring.
Limited data in breastfeeding; use with caution.
No specific additional contraception.
EMC-UK (MHRA) — approved Magnesium sulfate SmPC: https://www.medicines.org.uk/emc/product/10502/smpc
Clinical and educational support tool. The information does not replace a medical prescription or the opinion of a qualified healthcare professional.
Magnesium is a cofactor for enzymatic reactions and important in neurochemical transmission and muscular excitability. The anticonvulsant and tocolytic effect depends on plasma concentration; clinical monitoring (reflexes, respiratory rate) is essential during infusion.
The magnesium ion (Mg²⁺) reduces acetylcholine release at the neuromuscular junction and antagonises the NMDA receptor, decreasing neuronal excitability and muscle contractility — the mechanism of the anticonvulsant (eclampsia) and tocolytic effect. At high doses it depresses the CNS and cardiovascular system.
After intravenous administration, magnesium is immediately absorbed (complete bioavailability). About 1–2% of total body magnesium is in the extracellular fluid; it is 30% bound to albumin.
Magnesium is not metabolised; it is excreted solely by the kidney, at a rate proportional to serum concentration and glomerular filtration. In renal impairment the dose should be reduced.
Serum half-life is about 4 hours after infusion; renal elimination adjusts rapidly. In patients with normal renal function, the excess is excreted within hours.
Medicines from the same therapeutic group (ATC classification) or the same pharmacological class.
