# Magnesium and Phosphate Disorders > Magnesium and phosphate disorders for NEET-PG Medicine: hypomagnesaemia, hypophosphataemia, refeeding syndrome, thiamine first and replacement strategies. - Canonical URL: https://prepelephant.com/topics/neet-pg/medicine/magnesium-and-phosphate-disorders - Exam / course: NEET-PG · Subject: Medicine - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-08 - Last updated: 2026-10-08 - Reference basis: Harrison's Principles of Internal Medicine; Davidson's Principles and Practice of Medicine; Brenner and Rector's The Kidney - How to cite: "Magnesium and Phosphate Disorders", PrepElephant, https://prepelephant.com/topics/neet-pg/medicine/magnesium-and-phosphate-disorders ## Direct answer Hypomagnesaemia, defined as serum magnesium below about 0.7 mmol/L, causes neuromuscular irritability, arrhythmia and refractory hypokalaemia or hypocalcaemia, while hypophosphataemia below about 0.8 mmol/L produces weakness, haemolysis and respiratory failure. Refeeding syndrome is the classic cause of an acute phosphate fall, because insulin drives phosphate into cells once feeding starts. Both are replaced intravenously in symptomatic or severe cases, and magnesium must be corrected before potassium can be restored in refractory states. ## What you must remember - **Hypomagnesaemia:** serum magnesium below about 0.7 mmol/L; the commonest causes are alcohol, loop and thiazide diuretics, long-term proton pump inhibitor use and diarrhoea. - **Neuromuscular signs:** tetany, positive Chvostek and Trousseau signs, tremor and seizures; torsades de pointes is the feared arrhythmia. - **Hypermagnesaemia:** mainly in renal failure with magnesium-containing antacids or laxatives; features are hyporeflexia, hypotension and respiratory depression, and calcium gluconate antagonises the effect. - **Hypophosphataemia:** serum phosphate below about 0.8 mmol/L; features include rhabdomyolysis, haemolysis, respiratory muscle weakness and encephalopathy. - **Refeeding syndrome:** insulin-driven shift of phosphate, potassium and magnesium into cells after nutrition starts in malnourished patients, prevented by slow feeding and thiamine given before glucose. - **Replacement:** intravenous magnesium sulphate for symptomatic or severe hypomagnesaemia; intravenous or oral phosphate for significant hypophosphataemia, with calcium monitored because rapid phosphate infusion can cause hypocalcaemia. - **Renal wasting:** magnesium loss in Gitelman syndrome and during prolonged diuretic use keeps levels low despite replacement. ## A malnourished alcoholic with a falling phosphate Consider a 45-year-old man with alcohol dependence, a body mass index of 15 and two weeks of little food intake, admitted with vomiting and weakness. Dextrose infusion was started in the emergency department, and within a day his potassium is 2.8 mmol/L, magnesium 0.5 mmol/L and phosphate 0.4 mmol/L. His ECG shows prolonged QT and his muscles are weak. 1. **Give thiamine:** Intravenous thiamine should come before any further glucose or feeding, because carbohydrate loading can precipitate Wernicke encephalopathy in a thiamine-depleted patient. 2. **Replace magnesium first:** Magnesium sulphate is replaced intravenously first, since low magnesium makes potassium and calcium correction ineffective. 3. **Replace potassium and phosphate:** Potassium and phosphate are then replaced, with phosphate given slowly and calcium checked because rapid infusion can drop calcium levels. 4. **Restart feeding cautiously:** Feeding is restarted at a low energy intake, with the highest-risk patients started at about 10 kcal/kg per day and advanced over several days. 5. **Monitor electrolytes:** Electrolytes are checked frequently, often twice daily at first, during the first week. High-risk features that prompt caution include a very low body mass index, little intake for more than ten days and low electrolytes before feeding. ## Where the examiner tries to catch you Several traps recur in magnesium and phosphate questions. - **Trap:** Persisting with potassium replacement in refractory hypokalaemia. — **Correct:** Potassium cannot be restored while magnesium is low, so magnesium must be replaced first, and a patient who keeps needing potassium is a candidate for magnesium deficiency or renal wasting. - **Trap:** Giving glucose before thiamine in the refeeding vignette. — **Correct:** The examiner expects thiamine to be named as the first drug, not glucose. - **Trap:** Trusting a normal serum magnesium. — **Correct:** Most magnesium lies inside cells, so serum levels underestimate total body deficits and a normal level does not exclude depletion. - **Trap:** Attributing every low phosphate to refeeding. — **Correct:** Primary hyperparathyroidism also lowers phosphate through renal wasting, which contrasts with the feeding-related fall. ## Frequently asked questions ### What is refeeding syndrome and which electrolytes fall in it? Refeeding syndrome is a metabolic complication in which nutrition restarted after prolonged starvation causes insulin-driven intracellular shifts. Phosphate, potassium and magnesium fall abruptly, and the effects include respiratory failure, cardiac arrhythmia, rhabdomyolysis and haemolysis, so monitoring electrolytes during the first days of feeding is essential. ### Why must thiamine be given before glucose in refeeding? Thiamine must be given before glucose because carbohydrate loading in a thiamine-depleted patient increases the demand for thiamine and can precipitate Wernicke encephalopathy. Giving thiamine first protects against this complication, which is especially important in alcohol-dependent or severely malnourished patients. ### Which drug classes cause hypomagnesaemia? Loop and thiazide diuretics, long-term proton pump inhibitors, aminoglycosides, calcineurin inhibitors such as tacrolimus, and cisplatin cause hypomagnesaemia. Chronic alcohol use and diarrhoea are also common causes, and in each case the renal or gastrointestinal loss needs to be identified and corrected. ### How is hypermagnesaemia treated? Hypermagnesaemia is treated by stopping all magnesium sources and giving intravenous calcium gluconate to antagonise the membrane and cardiac effects. In severe cases with respiratory depression, ventilatory support may be needed, and dialysis is used when renal failure prevents elimination. ### Why is refractory hypokalaemia treated by correcting magnesium? Refractory hypokalaemia is treated by correcting magnesium because low magnesium impairs the renal handling of potassium, so potassium keeps leaking out of cells and through the kidney. Potassium replacement alone fails until magnesium is restored, which is a classic clinical clue to combined deficiency.