Magnesium Deficiency Algorithm

Safety

Red Flags — Severe Hypomagnesaemia & Life-Threatening Arrhythmias

Done

Torsades de pointes, ventricular or haemodynamically significant arrhythmia, or significant QT prolongation with hypomagnesaemia → 999 / immediate hospital transfer regardless of the exact Mg value. Torsades is managed per the resuscitation/acute-care algorithm: IV magnesium (ERC 2025: 8 mmol over 10 minutes, repeated once if necessary), correction of potassium and removal of QT-prolonging causes.

Seizure, tetany or severe neuromuscular symptoms with hypomagnesaemia → 999 regardless of the exact Mg value. IV magnesium in hospital per the local acute protocol (non-eclamptic seizure regimens differ from obstetric ones). Refractory hypocalcaemia always check Mg (hypomagnesaemia prevents PTH release).

Hypomagnesaemia + concurrent hypokalaemia not responding to potassium replacement Refractory hypokalaemia — Mg is essential for renal K⁺ retention (Na/K-ATPase cofactor). Hypokalaemia will not correct until Mg is repleted. Always check Mg when K⁺ is persistently low despite supplementation. Refractory hypokalaemia or hypocalcaemia with hypomagnesaemia → immediate same-day hospital transfer (999 if arrhythmia, significant QT prolongation, seizure, tetany, syncope, or respiratory or swallowing weakness).

Hypomagnesaemia + hypocalcaemia + tetany Severe Mg depletion causes functional hypoparathyroidism (Mg required for PTH secretion and PTH end-organ action). Chvostek and Trousseau signs positive. Correct Mg first — calcium supplementation alone will be ineffective.

Severe hypomagnesaemia in a patient on cisplatin, amphotericin, or aminoglycosides Drug-induced renal Mg wasting (mechanisms vary between drugs). Replacement during the treatment course is directed by the prescribing specialist team. Oncology/renal liaison.

Hypomagnesaemia + muscle weakness + dysphagia + respiratory muscle involvement Neuromuscular manifestations of severe Mg deficiency — respiratory failure risk. → 999 / immediate transfer. IV Mg in hospital. Monitor respiratory function.

Syncope or collapse with suspected electrolyte-related arrhythmia → 999 / immediate hospital transfer.

Severe (Mg <0.5 mmol/L, NHS SPS) or symptomatic hypomagnesaemia Same-day hospital assessment (999 if any feature above). IV magnesium replacement should be undertaken in hospital or another appropriately equipped setting with ECG, blood pressure, renal-function and electrolyte monitoring. It is not a routine GP-treatment procedure.

Hypomagnesaemia + AKI, eGFR <30, dialysis, oliguria, inability to take or absorb oral treatment, or suspected refeeding syndrome Same-day hospital assessment — magnesium is renally excreted and can accumulate; refeeding needs NICE CG32 management.

Magnesium is the second most abundant intracellular cation after potassium and is a cofactor for over 300 enzymatic reactions, including ATP synthesis, DNA/RNA synthesis, protein synthesis, and virtually all reactions involving ATP. Serum magnesium represents only approximately 1% of total body magnesium — the vast majority is intracellular or in bone. This means that serum magnesium can be normal even when significant intracellular deficiency exists, and conversely, serum magnesium can be low in the context of a severe total body deficit. The clinical implication: a patient with a serum Mg of 0.65 mmol/L (mildly low) but with persistent symptoms (muscle cramps, fatigue, palpitations) and risk factors for depletion (PPI use, alcohol, malabsorption) may have significant total body Mg deficiency that is not captured by the serum level. The refractory hypokalaemia principle is one of the most clinically important relationships in electrolyte physiology: magnesium is required as a cofactor for the Na/K-ATPase pump that maintains intracellular potassium. Without adequate magnesium, potassium leaks out of cells into the urine through the ROMK channel in the distal tubule. Any patient with persistent hypokalaemia despite adequate potassium supplementation must have their serum magnesium checked — treating the hypomagnesaemia is the prerequisite for correcting the hypokalaemia.

Diagnose

Causes of Hypomagnesaemia

Done

GI loss or impaired absorption

Chronic diarrhoea (IBD, coeliac, short bowel, laxative abuse) · Malabsorption syndromes · Proton pump inhibitors (PPIs — associated with impaired intestinal Mg absorption; risk mainly with prolonged use) · Alcohol (combined: reduced intake + malabsorption + renal wasting) · Post-gastric bypass · Prolonged nasogastric suction

Renal losses

Drugs: loop diuretics (furosemide — inhibit thick ascending limb Mg reabsorption), thiazides (milder), aminoglycosides, cisplatin, amphotericin, ciclosporin, tacrolimus, foscarnet (mechanisms vary) · Diabetes with marked glycosuria (increased urinary Mg loss) · Primary aldosteronism (aldosterone promotes renal Mg wasting) · Gitelman syndrome (genetic renal tubular defect — hypomagnesaemia + hypokalaemia + hypocalciuria + metabolic alkalosis) · Bartter syndrome

Reduced intake

Alcohol dependence (combined effect: poor diet + vomiting + diarrhoea + renal wasting from alcohol) · Prolonged IV fluids without Mg supplementation · Critical illness/ICU · Eating disorders

Redistribution

Refeeding syndrome (phosphate and Mg shift intracellularly on insulin release when nutrition restarted after starvation) · Post-parathyroidectomy (hungry bone syndrome) · Acute pancreatitis (Mg deposits in peripancreatic fat necrosis)

Drug-related causes

PPIs (GI absorption) · Loop and thiazide diuretics · Cisplatin, aminoglycosides, amphotericin B, calcineurin inhibitors (ciclosporin, tacrolimus), foscarnet (renal wasting) · Laxative excess · Review all medicines in persistent or recurrent hypomagnesaemia. Note: hypoalbuminaemia alters measured total Mg rather than directly causing urinary loss.

PPI-induced hypomagnesaemia is an important and under-recognised cause of hypomagnesaemia in primary care. The mechanism is not fully established — impaired intestinal magnesium absorption is thought to be involved (possibly including reduced TRPM6/TRPM7-mediated transport). The risk increases with: dose (omeprazole 40 mg > 20 mg), duration (reported after as little as 3 months, most cases after about 1 year — MHRA), concomitant diuretics (additive renal loss), and older age. The MHRA Drug Safety Update (April 2012) advised considering measuring magnesium before starting a PPI and periodically during prolonged treatment, especially with digoxin or other drugs that lower magnesium (such as diuretics). Consider periodic serum magnesium in prolonged PPI treatment, with frequency determined by risk; monitor more closely with diuretics/digoxin or previous hypomagnesaemia. If hypomagnesaemia is confirmed on PPI therapy: review the indication and use the lowest effective dose; step down or stop where appropriate (an H2-receptor antagonist may be considered depending on the indication). Long-term PPI may still be appropriate (Barrett's oesophagus, severe oesophagitis, high-risk gastroprotection) — then continue with oral Mg replacement. The hypomagnesaemia resolves within weeks of PPI discontinuation in most cases.

Diagnose

Assessment — Symptoms, Examination & Investigations

Done

Symptoms (often non-specific at mild-moderate deficiency)

Muscle symptoms: cramps (especially nocturnal leg cramps), tremor, weakness, fatigue · Neuromuscular: tetany (Chvostek and Trousseau signs), paraesthesiae · Cardiac: palpitations, arrhythmias (particularly AF and VT — Mg stabilises cardiac membranes) · Neurological: anxiety, irritability, confusion, depression · Chronic: osteoporosis (Mg required for bone mineralisation and PTH regulation) · Red-flag: syncope, seizure, dysphagia, respiratory weakness · Often asymptomatic at Mg 0.5–0.7 mmol/L

Examination

Chvostek sign: tap facial nerve anterior to ear → ipsilateral facial muscle twitch (non-specific — can be positive in people with normal magnesium). Trousseau sign: inflate BP cuff above systolic × 3 min → carpal spasm (more specific for hypocalcaemia/hypomagnesaemia). Tremor, muscle fasciculations. BP (hypertension — Mg is a physiological calcium channel blocker). ECG: prolonged QT, PR prolongation, widened QRS, T-wave flattening.

Investigations

Serum Mg (hypomagnesaemia <0.7 mmol/L — use the lab reference range; repeat if unexpected or clinically discordant) · U&Es, creatinine/eGFR (check before any replacement) · Albumin · Serum K⁺ + Na⁺ (hypokalaemia often co-exists) · Serum Ca²⁺ + adjusted Ca (hypocalcaemia from hypomagnesaemia) · ECG (if Mg substantially low, symptoms, hypokalaemia, QT-prolonging medication or cardiac disease) · Serum phosphate (refeeding) · eGFR (renal Mg wasting vs retention) · Glucose/HbA1c (where clinically relevant) · Medication review · assess diarrhoea, vomiting, malabsorption, alcohol use, nutritional risk and laxative excess · Coeliac serology (consider if chronic diarrhoea, iron deficiency, weight loss or suspected malabsorption) · Urinary Mg (24h or FEMg) (consider if persistent and unexplained after stopping or reviewing causative medicines; >1 mmol/24h suggests renal wasting, <1 mmol/24h GI loss or poor intake — interpret with renal function and context)

Fractional excretion of Mg (FEMg)

FEMg = (urine Mg × serum Cr) / (0.7 × serum Mg × urine Cr) × 100. FEMg >4% suggests renal Mg wasting; <2% suggests an extra-renal cause (GI loss, poor intake). Not a standalone diagnostic test — less reliable in CKD, after recent Mg replacement, with changing renal function or low Mg intake. The 0.7 factor approximates the ultrafilterable fraction of plasma Mg; follow local laboratory practice and specialist advice (specialist-level test rather than routine GP algorithm).

The 24-hour urine magnesium test can help distinguish renal from extra-renal causes of persistent unexplained hypomagnesaemia — it directly measures how much magnesium the kidney is excreting. In hypomagnesaemia due to GI loss or inadequate intake, the kidney appropriately conserves magnesium (urine Mg <1 mmol/24h = appropriate renal conservation). In hypomagnesaemia due to renal wasting (loop diuretics, cisplatin, aminoglycosides, Gitelman syndrome, primary aldosteronism), the kidney inappropriately excretes magnesium despite low serum levels (urine Mg >1 mmol/24h = renal wasting). This distinction guides management: renal wasting requires addressing the cause (reviewing the diuretic indication, stopping a nephrotoxic drug where possible, treating aldosteronism) in addition to replacement; GI loss requires treating the GI condition + supplementation. The fractional excretion of Mg (FEMg) is a spot urine alternative that does not require a 24-hour collection; both must be interpreted with renal function and clinical context, and are less reliable in CKD, after recent replacement or with changing renal function.

Diagnose

Severity & Clinical Consequences

Done

Severity classification

Hypomagnesaemia is generally defined as serum magnesium below 0.7 mmol/L. Clinical risk depends on the absolute concentration, rate of fall, symptoms, ECG findings, associated hypokalaemia/hypocalcaemia and renal function. Mild: ~0.5–0.7 mmol/L — often asymptomatic; oral replacement if stable without concerning features; address cause. Severe: <0.5 mmol/L, or symptomatic — particularly with neurological or cardiac manifestations; same-day hospital assessment, IV in hospital if symptomatic or oral treatment unsuitable (999 if arrhythmia, significant QT prolongation, seizure, tetany, syncope, or respiratory or swallowing weakness) (NHS SPS).

Cardiac consequences

QT prolongation → torsades de pointes (polymorphic VT) → ventricular fibrillation. AF: Mg depletion is a risk factor for AF and increases rate control difficulty, but magnesium is not the universal first-line treatment for AF (adjunct only in selected acute-care settings). Torsades: manage per the resuscitation/acute-care algorithm — IV magnesium (ERC 2025: 8 mmol over 10 minutes, repeat once if necessary), correct potassium, remove QT-prolonging causes. Mg stabilises cardiac membrane potential by competing with calcium at voltage-gated channels.

Bone consequences

Mg deficiency impairs: PTH secretion (Mg required for PTH granule release), PTH receptor sensitivity, and 25-OH-D → 1,25-OH-D conversion (renal activation of vitamin D). Long-term Mg deficiency may contribute to reduced bone health through these mechanisms; this is not an indication for Mg supplements without documented hypomagnesaemia.

Metabolic consequences

Low Mg is associated with insulin resistance and hypertension, largely in observational studies. Optimise diabetes control, nutrition and alcohol intake where relevant. Do not prescribe magnesium solely to improve glycaemic control or prevent diabetes unless hypomagnesaemia is documented or there is a specialist indication.

The torsades de pointes-magnesium connection is one of the most important pharmacological relationships in acute medicine — torsades de pointes (TdP) is a potentially lethal polymorphic ventricular tachycardia associated with QT prolongation (the twisted points pattern on ECG where QRS complexes appear to twist around the isoelectric line). TdP is managed according to the resuscitation/acute-care algorithm regardless of the serum magnesium level: IV magnesium sulfate 8 mmol (2 g) over 10 minutes, repeated once if necessary (ERC 2025), with correction of potassium and removal of QT-prolonging causes. The mechanism: magnesium blocks the cardiac L-type calcium channel and stabilises the cardiac action potential. GPs must know this for two reasons: (1) any patient on QT-prolonging drugs (antipsychotics, antifungals, antimalarials, methadone, many antiarrhythmics) who is also at risk of hypomagnesaemia (PPI, diuretics, alcohol, diarrhoea) has compounded QT prolongation risk — serum Mg should be checked and maintained in the normal range; (2) GPs must not prescribe QT-prolonging drugs to patients with known hypomagnesaemia without correcting the Mg first.

Refer

Referral Pathways

Done

999 / Same-day hospital

Call 999 / arrange immediate hospital transfer for: torsades de pointes, ventricular arrhythmia or haemodynamically significant arrhythmia · syncope or collapse with suspected electrolyte-related arrhythmia · seizure, tetany or severe neuromuscular symptoms · respiratory muscle weakness, dysphagia or respiratory depression · hypomagnesaemia with significant QT prolongation. Same-day hospital assessment for severe (Mg <0.5 mmol/L) or symptomatic hypomagnesaemia, or refractory hypokalaemia/hypocalcaemia. Same-day hospital assessment also for AKI/eGFR <30/dialysis, inability to take or absorb oral treatment, or suspected refeeding syndrome.

Nephrology

Suspected Gitelman syndrome (young patient, recurrent hypomagnesaemia + hypokalaemia + hypocalciuria + metabolic alkalosis) · Persistent renal Mg wasting not explained by drugs · Bartter syndrome · Unexplained, persistent, recurrent or familial hypomagnesaemia, or with hypokalaemic metabolic alkalosis · Before replacement in CKD 4–5, AKI, dialysis or kidney transplant (SPS)

Gastroenterology

Hypomagnesaemia from malabsorption not yet investigated (coeliac, IBD) · Post-bariatric surgery (complex nutritional support)

Endocrinology

Primary aldosteronism with Mg wasting · Unexplained persistent hypomagnesaemia

Same-day hospital / dietetics

Suspected or high-risk refeeding syndrome requires same-day hospital/dietetic assessment. Do not manage severe malnutrition or refeeding risk using an isolated magnesium replacement plan. Follow NICE CG32 and the local nutrition-support pathway.

Obstetrics

Confirmed hypomagnesaemia in pregnancy — manage with the obstetric team, particularly if symptomatic, severe or requiring parenteral treatment

GP management

Mild (~0.5–0.7 mmol/L), no concerning symptoms, stable, eGFR ≥30: oral replacement per the local formulary + address cause; recheck after about 7 days (SPS). PPI-related: review indication, lowest effective dose, periodic Mg by risk. Dietary advice (supportive). Amiloride only for persistent renal Mg wasting with specialist advice or a clear local protocol.

Gitelman syndrome is an important differential diagnosis in young patients with recurrent or unexplained hypomagnesaemia — it is an autosomal recessive tubular disorder (SLC12A3 gene — thiazide-sensitive Na/Cl cotransporter) causing: hypomagnesaemia (always present), hypokalaemia, hypocalciuria (low urine calcium — distinguishes from Bartter syndrome), and metabolic alkalosis. It is often discovered incidentally on routine bloods in young adults, but can present with: muscle weakness, cramps, tetany, fatigue, and palpitations. The diagnosis should be suspected in any patient under 40 with unexplained hypomagnesaemia + hypokalaemia + metabolic alkalosis, particularly if the urine calcium is low. The treatment: lifelong oral magnesium supplementation (product per specialist advice and local formulary) + dietary salt and potassium supplementation. Amiloride (potassium-sparing diuretic that also reduces renal Mg wasting) may be used as an adjunct under specialist supervision, monitoring potassium, eGFR and blood pressure. Nephrology referral for genetic confirmation and management optimisation.

Treat

Magnesium Replacement — Oral (Primary Care) & IV (Hospital Only)

Done

Mild deficiency Oral (asymptomatic)

Oral Mg per the local formulary: e.g. magnesium aspartate 10 mmol sachets or magnesium glycerophosphate 4 mmol (97.2 mg) chewable tablets 1–2 TDS

For asymptomatic or mildly symptomatic hypomagnesaemia in stable patients. Glycerophosphate (alternative, particularly where tolerated or a lower dose is required) — Magnesium 4 mmol Chewable Tablets SPC: tablets chewed; contraindicated in severe renal impairment (GFR <30 mL/min) and hyperphosphataemia (contains phosphate); contains sorbitol, sodium and sucrose; diarrhoea and hypermagnesaemia are important adverse effects. No significant bioavailability differences between oral salts (SPS) — choose by formulary, tolerability and response. Start with a tolerated dose in divided doses with food; titrate to serum Mg and GI tolerance; diarrhoea is dose-limiting. Check eGFR first, and the SPC for renal contraindications, excipients and drug-interaction intervals. Recheck Mg, K⁺, Ca²⁺ and renal function after about 7 days (SPS).

Moderate deficiency Oral or IV

Oral titrated to response if stable; otherwise hospital

Mg <0.5 mmol/L is severe (NHS SPS) — same-day hospital assessment. If oral treatment cannot be taken or absorbed: same-day hospital assessment. IM magnesium is painful and not for routine general practice — reserved for specialist/hospital circumstances where IV access is unavailable.

Severe deficiency / arrhythmia IV (hospital)

IV MgSO₄ — hospital, per local acute protocol

No single universal IV regimen in a GP guide — follow the local acute medical, emergency medicine or electrolyte-replacement protocol (SPS: initial dose commonly 1–5 g (4–20 mmol), further doses guided by repeat levels). Confirm the formulation and calculate the dose in mmol of elemental magnesium; dilute concentrated magnesium sulfate before IV use (20% or less — SPC); monitor ECG where severe symptoms, arrhythmia or QT prolongation; monitor Mg, K⁺, Ca²⁺, renal function, BP and clinical status; reduce or avoid in AKI, eGFR <30, dialysis or severe renal impairment, with specialist advice. Torsades: resuscitation algorithm (ERC 2025: 8 mmol over 10 min, repeat once if needed).

Renal wasting — prevention

Amiloride — specialist advice only

Consider amiloride only for persistent renal magnesium wasting after review of the indication for the causative diuretic and with specialist advice or a clear local protocol. Not for all diuretic-associated hypomagnesaemia — serious hyperkalaemia risk, especially in heart failure, CKD, older adults, diabetes, or with ACE inhibitors, ARBs, MRAs or potassium supplements. Monitor potassium, creatinine/eGFR and blood pressure shortly after initiation and after dose changes.

PPI-related — switch or supplement

Review PPI indication and dose

Use the lowest effective dose; step down or stop where the indication allows (an H2-receptor antagonist may be considered depending on the indication — not a routine switch). Long-term PPI may still be appropriate (Barrett's oesophagus, severe oesophagitis, high-risk gastroprotection) — continue with oral Mg and periodic Mg monitoring by risk. If hypomagnesaemia persists despite tolerated oral replacement, review adherence, diarrhoea, renal losses and all causative medicines. If the PPI cannot be withdrawn because of a strong indication, discuss with gastroenterology, renal medicine or acute medicine. Recurrent parenteral replacement is a specialist decision.

Choosing an oral magnesium preparation: there are no significant differences in bioavailability between oral magnesium salts (SPS), so choose according to the local formulary, tolerability and response. Glycerophosphate is often well tolerated in practice. All oral salts can cause dose-dependent osmotic diarrhoea — which can worsen hypomagnesaemia if the cause is GI. Licensed 4 mmol chewable tablets (for example Neomag) are available on FP10 prescription. Magnesium oxide is not recommended here unless a specific current product and its local prescribing status are checked — it is not necessarily cheaper, absorption is variable and diarrhoea is common. The dosing principle: start at the lower end of the dose range and titrate up based on serum Mg response and GI tolerability. Diarrhoea is dose-limiting. IV replacement for severe or symptomatic deficiency, or when oral treatment cannot be taken or absorbed, is a hospital treatment following the local acute protocol.

Treat

Addressing Underlying Causes

Done

PPI review and rationalisation

NICE CG184 (dyspepsia and GORD in adults) advises using the lowest effective PPI dose and offering people on long-term treatment an annual review with a trial of step-down or stopping. In hypomagnesaemia: review the indication and attempt step-down or stopping where appropriate (an H2-receptor antagonist may be considered depending on the indication). If the PPI must continue: lowest effective dose + oral Mg + periodic serum Mg with frequency by risk (MHRA). Document indication for ongoing PPI (Barrett's oesophagus, severe oesophagitis, high-risk/NSAID gastroprotection — valid long-term indications; non-specific dyspepsia — step-down trial appropriate). Add Mg monitoring to medication review template.

Diuretic optimisation

Loop diuretics (furosemide, bumetanide) can cause significant Mg wasting. Review the indication and use the lowest effective dose. Do not switch a loop diuretic to a thiazide solely to reduce magnesium loss — the choice depends on the indication, volume status, heart failure, blood pressure and renal function. Consider amiloride only for persistent renal Mg wasting after review of the causative diuretic, with specialist advice or a clear local protocol; monitor K⁺, creatinine/eGFR and BP shortly after starting and after dose changes. Check Mg according to clinical risk rather than routinely 6-monthly in every patient on a loop diuretic.

Alcohol — Mg depletion mechanism

Alcohol causes Mg depletion through: direct toxic effect on renal tubules (Mg wasting), poor dietary intake, vomiting, diarrhoea, and nutritional deficiency. Abstinence is the most effective intervention. Assess magnesium, potassium, phosphate, calcium, glucose, renal function and nutritional risk in patients with significant alcohol dependence, withdrawal, vomiting or malnutrition. Treat confirmed or clinically suspected hypomagnesaemia according to severity and local acute-care guidance. Give thiamine in accordance with the alcohol-withdrawal/refeeding protocol; thiamine and magnesium are separate treatments (Pabrinex does not contain Mg).

Diabetes and Mg

Diabetes with marked glycosuria can increase urinary Mg loss. Optimise diabetes control, nutrition and alcohol intake where relevant. Do not prescribe magnesium solely to improve glycaemic control or prevent diabetes unless hypomagnesaemia is documented or there is a specialist indication.

Next steps: see Harmful drinking and alcohol dependence · PPI prescribing · Chronic kidney disease

The alcohol withdrawal protocol and magnesium connection is important for GPs managing inpatient or outpatient alcohol detoxification — standard chlordiazepoxide CIWA protocols do not include magnesium supplementation, but Mg deficiency is common in alcohol dependence and may contribute to withdrawal symptoms (tremor, anxiety, seizures, cardiac arrhythmias). IV Pabrinex (which contains thiamine, riboflavin, pyridoxine, nicotinamide, and ascorbic acid) does not contain magnesium. Magnesium replacement should be based on the magnesium result, symptoms and clinical context — not every patient undergoing alcohol withdrawal requires IV magnesium. Treat confirmed or clinically suspected hypomagnesaemia according to severity and local acute-care guidance; thiamine and magnesium are separate treatments.

Lifestyle

Dietary Sources, Prevention & Long-Term Management

Done

Dietary magnesium-rich foods High Mg content: dark leafy greens (spinach about 80 mg/100g), seeds (pumpkin seeds 534 mg/100g — highest), nuts (almonds 270 mg/100g, cashews), legumes (black beans 60 mg/100g, lentils), wholegrains (brown rice, oats, quinoa), dark chocolate (64 mg per 30g), fish (mackerel, salmon), bananas (27 mg each). UK RNI: 300 mg/day (men), 270 mg/day (women). Dietary advice is supportive, not a treatment for clinically significant deficiency.

PPI review and Mg monitoring Review the indication and dose of every long-term PPI; use the lowest effective dose. Consider Mg measurement before and periodically during prolonged therapy (MHRA), particularly with diuretics, digoxin, previous hypomagnesaemia, CKD, diarrhoea or malabsorption, or other Mg-wasting medicines; repeat according to risk and previous result. Code Mg result in clinical record. If Mg persistently low: PPI step-down attempt where the indication allows, or oral Mg supplementation. Document PPI indication at every annual review — many patients continue PPIs for years without a current indication.

Diuretic monitoring Monitor electrolytes according to the diuretic indication; check Mg according to clinical risk (symptoms, hypokalaemia, digoxin, previous hypomagnesaemia) rather than routine 6-monthly Mg in every patient. Amiloride only for persistent renal Mg wasting, with specialist advice or a clear local protocol. Advise Mg-rich diet (particularly nuts, seeds, wholegrains) alongside diuretic therapy.

Alcohol moderation Alcohol <14 units/week (UK CMO guidance). Assess Mg, K⁺, phosphate, Ca²⁺, glucose, renal function and nutritional risk in significant alcohol dependence, withdrawal, vomiting or malnutrition; treat documented hypomagnesaemia, not nonspecific symptoms — and treat alcohol use disorder. AUDIT-C screening at every relevant GP review.

Cramps and Mg Do not prescribe magnesium to treat nonspecific or exercise-related cramps unless hypomagnesaemia is documented or there is a specialist indication. A balanced diet including Mg-rich foods is reasonable supportive advice.

Diabetes and Mg Optimise diabetes control, nutrition and alcohol intake where relevant. Check Mg if symptoms, marked glycosuria, diuretics or other risk factors. Do not prescribe magnesium solely to improve glycaemic control or prevent diabetes unless hypomagnesaemia is documented or there is a specialist indication.

Pre-eclampsia and obstetric Mg use IV MgSO₄ is the standard treatment for eclampsia and severe pre-eclampsia in the UK (Magpie Trial evidence). Pregnancy: manage confirmed hypomagnesaemia in conjunction with the obstetric team, particularly if symptomatic, severe or requiring parenteral treatment. Do not use serum magnesium thresholds from this guide to direct obstetric magnesium sulfate therapy for pre-eclampsia/eclampsia. Prolonged maternal magnesium sulfate (more than 5–7 days) has potential fetal/neonatal skeletal and calcium effects (SPC). Breastfeeding: oral magnesium glycerophosphate is compatible according to its SPC, but check the individual product information; parenteral magnesium only where clinically indicated and under medical supervision.

Osteoporosis connection Long-term hypomagnesaemia contributes to osteoporosis through multiple mechanisms (reduced PTH function, impaired vitamin D activation, direct effects on osteoblasts). Do not prescribe magnesium to prevent osteoporosis unless hypomagnesaemia is documented or there is a specialist indication; dietary advice is supportive.

The dietary magnesium insufficiency across the UK population is a genuine public health concern — NDNS (National Diet and Nutrition Survey) data consistently shows that a significant proportion of UK adults have magnesium intakes below the lower reference nutrient intake (LRNI), with older adults, adolescent girls, and people with low socioeconomic status particularly affected. Dietary advice is reasonable and supportive, but do not prescribe magnesium solely to improve glycaemic control, prevent diabetes, treat nonspecific cramps or prevent osteoporosis unless hypomagnesaemia is documented or there is a specialist indication.

Safety

Follow-Up & Safety-Netting

Done

On oral Mg supplementation

After starting or changing oral replacement: Mg, K⁺, Ca²⁺ and renal function after about 7 days (SPS), or sooner if symptoms are significant. If substantially abnormal, persistent or on a high dose: repeat at 1–4 weeks according to clinical risk. Once stable: every 3–6 months if the cause persists or still on supplementation (SPC); otherwise review clinically and repeat if symptoms or risk factors recur. CKD, frailty, recurrent abnormalities or interacting medicines: monitor more frequently. Aim for the laboratory reference range, with correction of associated K⁺ and Ca²⁺. In transient deficiency, treatment can usually stop shortly after normalisation; continue longer if the cause persists (SPS).

PPI-related Mg deficiency monitoring

Periodic serum magnesium monitoring should be considered in prolonged PPI treatment, with frequency determined by risk; monitor more closely if combined with diuretics/digoxin or if previous hypomagnesaemia has occurred. If Mg stays low despite tolerated oral replacement: review adherence, diarrhoea, renal losses and all causative medicines; reattempt step-down where the indication allows. If the PPI cannot be withdrawn because of a strong indication, discuss with gastroenterology, renal medicine or acute medicine. Recurrent parenteral replacement is a specialist decision.

After IV Mg infusion (hospital)

Repeat Mg, K⁺, Ca²⁺ and renal function per the hospital protocol. Renal function (IV Mg requires adequate renal function for excretion — accumulation risk in CKD). Arrange oral Mg continuation on discharge. Address root cause before discharge.

Return immediately

Palpitations with dizziness, fainting or collapse in a patient with known hypomagnesaemia → 999 · New muscle weakness + dysphagia + breathlessness → respiratory Mg toxicity or deterioration → 999 · Seizure, tetany, syncope or collapse → 999

Same-day review

Serum Mg <0.5 (severe, NHS SPS), with or without symptoms → same-day hospital assessment, ECG and concurrent electrolytes (IV only in hospital) · Persistent hypokalaemia despite adequate K⁺ replacement → check Mg urgently

The interaction between hypomagnesaemia and digoxin toxicity is a crucial prescribing safety point — magnesium deficiency increases myocardial sensitivity to digoxin toxicity. Hypomagnesaemia reduces Na/K-ATPase activity in cardiomyocytes, which is the same enzyme inhibited by digoxin. The combined inhibition from Mg deficiency + digoxin leads to: increased intracellular calcium (the toxic mechanism of digoxin toxicity) at lower digoxin concentrations than usual. This means a patient with hypomagnesaemia can develop digoxin toxicity at serum digoxin levels considered therapeutic in a normomagnesaemic patient. GPs prescribing digoxin to patients who are also on loop diuretics or PPIs (Mg-depleting) must monitor serum Mg regularly and maintain it in the normal range. Any patient on digoxin presenting with nausea, visual disturbances, bradyarrhythmia, or altered cognition should have serum digoxin level AND serum Mg measured simultaneously.