REASONING GP · Clinical algorithm · Quick reference

Hypokalaemia in adults — triage and diagnostic approach

A result on a screen, usually from a diuretic or vomiting. Set urgency from the level, the ECG and the drugs together — then check the magnesium, because without it the potassium will not correct.

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AdultsLab resultK⁺ below 3.5v1.0 · Sep 2026

Core rule. K⁺ below 2.5 mmol/L is a medical emergency, as is any level with ECG changes, arrhythmia, weakness or paralysis, or any hypokalaemia in a patient on digoxin — digoxin toxicity is precipitated at levels that would otherwise be tolerated. 2.5–2.9 needs same-day assessment; 3.0–3.4 in a well patient can be managed in primary care. Two things are forgotten every time: check the magnesium (hypokalaemia will not correct while magnesium is low) and ask about vomiting, laxatives and diuretic misuse — the cause is often not on the prescription list.

On seeing the result: is this an emergency now? Arrange emergency admission — 999 or immediate discussion with the acute team

K⁺ below 2.5 mmol/L, however well the patient seems · any ECG change — flattened or inverted T waves, ST depression, prominent U waves, long QT, ventricular ectopics or arrhythmia · palpitations, syncope or cardiac arrest · profound muscle weakness, flaccid paralysis, ileus or difficulty breathing · rhabdomyolysis (severe muscle pain, dark urine) · any hypokalaemia on digoxin, or digoxin toxicity features (nausea, visual change, confusion, bradycardia) · K⁺ below 3.0 with vomiting or diarrhoea that cannot be replaced orally · suspected DKA or thyrotoxic periodic paralysis. Do the ECG if it does not delay transfer, and hand over the potassium, the magnesium, the drug list and the fluid losses.

Before anything else: how urgent, and what is the mechanism? Level and ECG set the destination; the mechanism decides the treatment

Urgency by level and ECG

Below 2.5, or any ECG change, weakness or digoxin: emergency admission for IV replacement and monitoring. 2.5–2.9: ECG today and same-day assessment. 3.0–3.4: primary care if asymptomatic, well, eating and drinking, not on digoxin. Oral replacement is safe; IV is a hospital decision.

Always check alongside

Magnesium — hypomagnesaemia causes renal potassium wasting and makes the potassium refractory; correct it or the replacement fails. Also sodium, bicarbonate, calcium, glucose, creatinine and eGFR, and the blood pressure.

Drugs — the usual cause

Thiazide and loop diuretics (the commonest by far) · corticosteroids and fludrocortisone · beta₂ agonists, theophylline · insulin · laxatives · amphotericin, aminoglycosides, cisplatin · PPIs via hypomagnesaemia · liquorice and carbenoxolone.

Losses — ask directly

Vomiting or diarrhoea; self-induced vomiting, laxative or diuretic misuse — ask in every young or normotensive patient without an obvious cause. Alcohol excess and refeeding. Poor intake in frailty. Ileostomy or fistula output. Sweating and heat.

Red-flag screen: trigger → concern → destination → what to do before handover One row is enough; do not add up reassuring features

Trigger / red flag	Leading concern · destination	Do now · do not delay
K⁺ below 2.5 mmol/L, whatever the symptoms; or any ECG change at any level — flat or inverted T waves, ST depression, U waves, long QT, ectopics or arrhythmia.	Risk of ventricular arrhythmia — needs IV potassium with cardiac monitoring Emergency admission now	Oral replacement is not enough and outpatient rechecking is not safe. 12-lead ECG if it does not delay transfer; a normal ECG does not make a K⁺ below 2.5 safe. Send the magnesium with the sample and say on the handover whether it is known. Stop the diuretic, the beta₂ agonist and any laxative now, and list what was stopped.
Any hypokalaemia in a patient taking digoxin, or digoxin toxicity features — nausea and vomiting, visual disturbance, confusion, bradycardia or new arrhythmia.	Digoxin toxicity precipitated by hypokalaemia Emergency admission now	Hypokalaemia sensitises the myocardium to digoxin, so a level tolerated by others is dangerous here — admit even at 3.0–3.4 if there are any toxicity features. Send a digoxin level via the acute route rather than the community. Withhold the next digoxin dose and the diuretic, and say so on the handover.
Neuromuscular compromise: profound weakness, flaccid paralysis, absent reflexes, ileus or abdominal distension, respiratory difficulty; or rhabdomyolysis — severe muscle pain, dark urine.	Hypokalaemic paralysis · respiratory muscle failure · rhabdomyolysis Emergency admission now	Assess power, reflexes and bowel sounds, and whether the patient can complete a sentence. Check CK via the acute route. Thyrotoxic periodic paralysis in a young Asian man with sudden weakness is a recognised presentation — send the patient in and check TFTs there.
K⁺ 2.5–2.9 mmol/L, or ongoing vomiting, diarrhoea or high-output stoma that oral replacement cannot keep up with, or a patient not eating and drinking.	Moderate hypokalaemia with continuing losses — needs assessment today ECG today and same-day clinical assessment	ECG the same day, not "at the next appointment". Check magnesium, sodium, creatinine and glucose today. Stop or hold the diuretic. Where losses continue, or vomiting prevents oral potassium, the patient needs IV replacement — refer rather than escalating the oral dose. Repeat U&E within 24–48 hours.
Hypokalaemia with hypertension, especially if resistant to two or three agents, in someone under 40, or with a low or normal bicarbonate; or an adrenal incidentaloma.	Primary hyperaldosteronism (Conn's) · Cushing's · renal artery stenosis Same-day advice if severe; otherwise investigate before starting more antihypertensives	NG136 says to consider specialist investigation for people under 40 with hypertension, and hypokalaemia with hypertension is the classic pointer to a secondary cause. Measure the aldosterone–renin ratio before adding further drugs, and take endocrine advice on which drugs must be stopped first (MRAs and, where possible, beta-blockers and ACE inhibitors distort the result). Do not simply replace the potassium and add a fourth antihypertensive.
Hypokalaemia with a metabolic acidosis (low bicarbonate, normal anion gap), or with a low magnesium, low calcium, low phosphate or nephrocalcinosis.	Renal tubular acidosis · Fanconi · Gitelman or Bartter · drug-induced tubulopathy Same-day bloods; nephrology advice if persistent	Hypokalaemia with acidosis points to RTA, while hypokalaemia with alkalosis points to vomiting, diuretics or mineralocorticoid excess — the bicarbonate divides the differential, so always look at it. Check magnesium, calcium and phosphate. Review amphotericin, aminoglycosides, cisplatin and long-term PPIs.
Suspected eating disorder, or laxative or diuretic misuse: unexplained hypokalaemia with a normal blood pressure, dental erosion, parotid swelling, callus on the knuckles, low BMI, or a metabolic alkalosis with no prescribed diuretic.	Bulimia nervosa or anorexia nervosa · purging behaviour · refeeding risk Same-day medical and eating-disorder assessment if K⁺ below 3.0, bradycardic or rapidly losing weight	Ask directly and without judgement about vomiting, laxatives and diuretics — this is the commonest cause of unexplained hypokalaemia in a young, normotensive patient and it will not appear on the repeat-prescription screen. Use the MEED guidance (Medical Emergencies in Eating Disorders): potassium below 3.0, bradycardia, postural drop or a rapid weight fall are physical-risk criteria for urgent medical assessment. Replacing potassium without addressing the purging simply repeats the result, and refeeding without monitoring risks a further fall.
Unexplained hypokalaemia with systemic features: weight loss, new or worsening hypertension with proximal weakness, striae, bruising, hyperglycaemia; or hypokalaemia with a metabolic alkalosis and a raised bicarbonate in a smoker.	Ectopic ACTH — small-cell lung cancer · Cushing's syndrome Urgent chest X-ray within 2 weeks where there is any respiratory or smoking history · NICE NG12	Severe hypokalaemic alkalosis with new hypertension, proximal weakness and hyperglycaemia is the ectopic-ACTH picture and is often the first sign of a small-cell lung cancer. Hypokalaemia is not itself an NG12 criterion, but an urgent CXR within 2 weeks applies where there are unexplained respiratory symptoms, weight loss or a smoking history (NG12) — arrange it alongside endocrine advice, and refer urgently if the film is abnormal.

Trigger / red flag

Leading concern · destination

Do now · do not delay

K⁺ below 2.5 mmol/L, whatever the symptoms; or any ECG change at any level — flat or inverted T waves, ST depression, U waves, long QT, ectopics or arrhythmia.

Risk of ventricular arrhythmia — needs IV potassium with cardiac monitoring
Emergency admission now

Oral replacement is not enough and outpatient rechecking is not safe. 12-lead ECG if it does not delay transfer; a normal ECG does not make a K⁺ below 2.5 safe. Send the magnesium with the sample and say on the handover whether it is known. Stop the diuretic, the beta₂ agonist and any laxative now, and list what was stopped.

Any hypokalaemia in a patient taking digoxin, or digoxin toxicity features — nausea and vomiting, visual disturbance, confusion, bradycardia or new arrhythmia.

Digoxin toxicity precipitated by hypokalaemia
Emergency admission now

Hypokalaemia sensitises the myocardium to digoxin, so a level tolerated by others is dangerous here — admit even at 3.0–3.4 if there are any toxicity features. Send a digoxin level via the acute route rather than the community. Withhold the next digoxin dose and the diuretic, and say so on the handover.

Neuromuscular compromise: profound weakness, flaccid paralysis, absent reflexes, ileus or abdominal distension, respiratory difficulty; or rhabdomyolysis — severe muscle pain, dark urine.

Hypokalaemic paralysis · respiratory muscle failure · rhabdomyolysis
Emergency admission now

Assess power, reflexes and bowel sounds, and whether the patient can complete a sentence. Check CK via the acute route. Thyrotoxic periodic paralysis in a young Asian man with sudden weakness is a recognised presentation — send the patient in and check TFTs there.

K⁺ 2.5–2.9 mmol/L, or ongoing vomiting, diarrhoea or high-output stoma that oral replacement cannot keep up with, or a patient not eating and drinking.

Moderate hypokalaemia with continuing losses — needs assessment today
ECG today and same-day clinical assessment

ECG the same day, not "at the next appointment". Check magnesium, sodium, creatinine and glucose today. Stop or hold the diuretic. Where losses continue, or vomiting prevents oral potassium, the patient needs IV replacement — refer rather than escalating the oral dose. Repeat U&E within 24–48 hours.

Hypokalaemia with hypertension, especially if resistant to two or three agents, in someone under 40, or with a low or normal bicarbonate; or an adrenal incidentaloma.

Primary hyperaldosteronism (Conn's) · Cushing's · renal artery stenosis
Same-day advice if severe; otherwise investigate before starting more antihypertensives

NG136 says to consider specialist investigation for people under 40 with hypertension, and hypokalaemia with hypertension is the classic pointer to a secondary cause. Measure the aldosterone–renin ratio before adding further drugs, and take endocrine advice on which drugs must be stopped first (MRAs and, where possible, beta-blockers and ACE inhibitors distort the result). Do not simply replace the potassium and add a fourth antihypertensive.

Hypokalaemia with a metabolic acidosis (low bicarbonate, normal anion gap), or with a low magnesium, low calcium, low phosphate or nephrocalcinosis.

Renal tubular acidosis · Fanconi · Gitelman or Bartter · drug-induced tubulopathy
Same-day bloods; nephrology advice if persistent

Hypokalaemia with acidosis points to RTA, while hypokalaemia with alkalosis points to vomiting, diuretics or mineralocorticoid excess — the bicarbonate divides the differential, so always look at it. Check magnesium, calcium and phosphate. Review amphotericin, aminoglycosides, cisplatin and long-term PPIs.

Suspected eating disorder, or laxative or diuretic misuse: unexplained hypokalaemia with a normal blood pressure, dental erosion, parotid swelling, callus on the knuckles, low BMI, or a metabolic alkalosis with no prescribed diuretic.

Bulimia nervosa or anorexia nervosa · purging behaviour · refeeding risk
Same-day medical and eating-disorder assessment if K⁺ below 3.0, bradycardic or rapidly losing weight

Ask directly and without judgement about vomiting, laxatives and diuretics — this is the commonest cause of unexplained hypokalaemia in a young, normotensive patient and it will not appear on the repeat-prescription screen. Use the MEED guidance (Medical Emergencies in Eating Disorders): potassium below 3.0, bradycardia, postural drop or a rapid weight fall are physical-risk criteria for urgent medical assessment. Replacing potassium without addressing the purging simply repeats the result, and refeeding without monitoring risks a further fall.

Unexplained hypokalaemia with systemic features: weight loss, new or worsening hypertension with proximal weakness, striae, bruising, hyperglycaemia; or hypokalaemia with a metabolic alkalosis and a raised bicarbonate in a smoker.

Ectopic ACTH — small-cell lung cancer · Cushing's syndrome
Urgent chest X-ray within 2 weeks where there is any respiratory or smoking history · NICE NG12

Severe hypokalaemic alkalosis with new hypertension, proximal weakness and hyperglycaemia is the ectopic-ACTH picture and is often the first sign of a small-cell lung cancer. Hypokalaemia is not itself an NG12 criterion, but an urgent CXR within 2 weeks applies where there are unexplained respiratory symptoms, weight loss or a smoking history (NG12) — arrange it alongside endocrine advice, and refer urgently if the film is abnormal.

Safety rule. Wellness is not reassurance and a normal ECG does not make a low potassium safe. A potassium that will not correct despite replacement is a magnesium problem until the magnesium has been checked. Hypokalaemia on digoxin is dangerous at any level. If a row applies and the safe destination is unavailable, escalate rather than recheck.

Colour is semantic: red = emergency now · amber = same-day assessment · blue = define/assess · green = primary-care management · purple = uncertain / specialist route (including 2WW). Continued on page 2: examination and tests, classification, cause classifier, routine referral, primary-care management, endpoint.

REASONING GP · Hypokalaemia in adults — triage and diagnostic approach

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Assessment and investigation A result reviewed remotely still needs an ECG and a face-to-face assessment below 3.0

ECG — what to look for

Flattened or inverted T waves, ST depression, prominent U waves, prolonged QT, ventricular ectopics, and any tachyarrhythmia. Long QT plus hypokalaemia plus a QT-prolonging drug is a torsades risk.

Clinical assessment

Blood pressure (hypokalaemia with hypertension changes the pathway), volume status and postural drop, pulse and rhythm, muscle power and reflexes, bowel sounds, BMI and weight trend. Look for dental erosion, parotid swelling and knuckle callus.

Bloods

Magnesium — always; plus sodium, bicarbonate, calcium, phosphate, glucose, creatinine and eGFR, FBC. Consider TFTs, digoxin level, CK; aldosterone–renin ratio where there is hypertension; urinary potassium and a spot urine chloride where the cause is unclear.

Do not do

Do not replace potassium without checking magnesium. Do not give IV potassium in the community. Do not add a fourth antihypertensive before the aldosterone–renin ratio. Do not recheck at 2 weeks below 3.0. Do not accept "diuretic" in a normotensive young patient with alkalosis.

Classify: three exits, not two "On a diuretic" is a mechanism, not a complete answer

Emergency or same-day

K⁺ below 2.5, any ECG change, weakness or paralysis, digoxin, continuing losses, or 2.5–2.9 needing assessment today. Output: destination, potassium and magnesium with previous values, ECG findings, drugs stopped with the time.

Mild, manageable in primary care

K⁺ 3.0–3.4, asymptomatic, well, eating and drinking, not on digoxin, normal ECG, cause identified. Output: cause, replacement started, magnesium result, repeat date, escalation thresholds.

Unclassified or recurrent

Persistent or recurrent despite replacement, hypokalaemia with hypertension or acidosis, no cause found, or suspected purging. Output: state the uncertainty, take the §6 route, name the reviewer and timeframe.

Cause classifier: use the bicarbonate and the blood pressure to divide it Only once the urgency is settled

Renal loss — drugs, and GI loss

Drugs (commonest in primary care): thiazide and loop diuretics, corticosteroids, fludrocortisone, amphotericin, aminoglycosides, cisplatin — normal or raised BP with alkalosis. GI: vomiting, diarrhoea, laxative misuse, high-output stoma or fistula. Vomiting gives a metabolic alkalosis with a low urine chloride; diarrhoea and laxatives give a normal or low bicarbonate.

Transcellular shift

Insulin (including DKA treatment), beta₂ agonists and theophylline, alkalosis, refeeding syndrome, thyrotoxic periodic paralysis. Total body potassium may be normal — it corrects as the driver is treated, and over-replacement then causes rebound hyperkalaemia.

Mineralocorticoid excess

Hypokalaemia with hypertension and alkalosis: primary hyperaldosteronism (Conn's), Cushing's, ectopic ACTH, renal artery stenosis, liquorice. Measure the aldosterone–renin ratio before adding antihypertensives; under 40 with hypertension warrants specialist investigation (NG136).

Renal tubular disorders

With acidosis: renal tubular acidosis (types 1 and 2), Fanconi syndrome. With alkalosis and a normal BP: Gitelman or Bartter — consider in a young normotensive patient with a low magnesium and persistent hypokalaemia after purging has been excluded.

Hypomagnesaemia

Causes renal potassium wasting and makes hypokalaemia refractory to replacement. Think diuretics, alcohol, diarrhoea, long-term PPIs, poor intake. Correct it alongside the potassium, not afterwards — the single most common reason replacement appears to fail.

Do not conclude by default

"It's the diuretic" in a young normotensive patient with alkalosis — ask about purging. "Poor intake" when the BP is high — measure the aldosterone–renin ratio. "Refractory" before the magnesium is checked. Never treat the potassium alone when sodium, bicarbonate or calcium is also abnormal.

Refer or seek advice routinely from this consultation Not same-day — the cases that leave by letter; §7 is what primary care does today

Hypokalaemia with hypertension, or resistant hypertension, or hypertension under 40 → endocrinology or a hypertension clinic with the aldosterone–renin ratio already sent (NG136) · persistent or recurrent hypokalaemia despite replacement and a corrected magnesium → nephrology or endocrinology · suspected renal tubular acidosis, Gitelman or Bartter → nephrology · suspected eating disorder or purging → the eating-disorder service, with the MEED physical-risk parameters in the referral (NG69) · hypokalaemia in a patient who needs their diuretic → cardiology advice on a potassium-sparing agent rather than long-term supplements · suspected Cushing's or ectopic ACTH → urgent endocrinology alongside the NG12 chest X-ray.

The only decisions that belong in this consultation What primary care manages today — mild hypokalaemia in a well patient

Correct the magnesium first, or the potassium will not rise

Check magnesium in every case and replace it alongside the potassium, not afterwards — oral magnesium where mild, specialist or IV where severe or symptomatic. A potassium that fails to correct on adequate replacement almost always has an uncorrected low magnesium behind it.

Oral potassium replacement

For K⁺ 3.0–3.4 in a well patient: oral potassium chloride (for example Sando-K or a modified-release preparation) at the BNF dose, with food and plenty of fluid to reduce gastric irritation. Caution or avoid in renal impairment, and never combine with a potassium-sparing diuretic or an ACE inhibitor without a plan and a recheck. Supplements are a bridge while the cause is fixed, not a long-term answer.

Review the drugs, and treat the loss

Drugs: reduce or stop the thiazide or loop diuretic where possible, or switch to or add a potassium-sparing agent; review corticosteroids, beta₂ agonists, theophylline and laxatives; stop liquorice. Where a diuretic must continue, plan the monitoring rather than the supplement. Loss: rehydrate and treat vomiting or diarrhoea, withholding the diuretic during the illness with sick-day rules. Potassium-rich foods help mild cases but will not correct a level below 3.0 alone.

Recheck and the escalation rule — write it down

Repeat U&E and magnesium within 3–7 days of starting replacement or changing a drug. Tell the patient and the record what triggers what: below 2.5, any ECG change, weakness, or hypokalaemia on digoxin → emergency admission; 2.5–2.9 → same-day assessment. Name who is checking the result.

What not to do

Do not manage a potassium below 2.5 in the community. Do not give IV potassium in primary care. Do not continue supplements indefinitely without addressing the cause. Do not replace potassium in significant renal impairment without advice. Do not file a low potassium as "on a diuretic" with no magnesium and no plan.

Endpoint and documentation Finish with one of four conclusions

1 · Emergency

Admission arranged; potassium and magnesium with previous values, ECG findings, power and reflexes, digoxin status, fluid losses, drugs stopped with the time.

2 · Same-day

ECG done and assessment arranged today; magnesium sent; the question being answered (losses, hypertension, acidosis); diuretic held; repeat within 24–48 hours; who was spoken to.

3 · Mild, managed

Level, cause, magnesium and BP recorded; replacement and drug changes made; repeat date booked and escalation thresholds written in the record and told to the patient; named reviewer.

4 · Unclassified or recurrent

Uncertainty stated; §6 referral sent with the aldosterone–renin ratio or MEED parameters, with date; interim replacement plan and sick-day rules; review owner and timeframe.

Why primary-care management is safe today, in one line: K⁺ is 3.0–3.4 · asymptomatic, well, eating and drinking · not on digoxin · ECG normal where indicated · magnesium checked and corrected · blood pressure normal, or a secondary cause already being investigated · bicarbonate, sodium and calcium reviewed · cause identified and acted on · repeat booked within 3–7 days with a named reviewer and written escalation thresholds. Safety-net wording: contact us or 111 the same day if you develop palpitations, feel faint or black out, notice new muscle weakness or cramps, cannot keep fluids down, or your vomiting or diarrhoea continues; and come for the repeat blood test even if you feel well — a low potassium often causes no symptoms until it affects the heart.

Remote and result-handling limitation. A potassium below 3.0 cannot be managed on the telephone: it needs an ECG and a face-to-face assessment the same day. Convert to face-to-face or emergency assessment where an ECG cannot be obtained today, vomiting prevents oral replacement, the patient takes digoxin, there is any weakness, or the result arrives out of hours with no one able to act — a critical potassium must never sit in an inbox overnight.

Clinical decision support only; follow local acute-transfer, renal and prescribing policies and check doses against the current BNF. Source hierarchy: NICE guidelines and CKS first, then BNF/MHRA for doses and safety, then national specialty guidance. Sources: NICE NG136 Hypertension in adults · NG203 Chronic kidney disease · NG148 Acute kidney injury · NG69 Eating disorders · NG12 Suspected cancer (May 2025) · CG32 Nutrition support (refeeding) · NICE CKS Hypokalaemia, Hypertension, Eating disorders · RCPsych CR233 Medical Emergencies in Eating Disorders (MEED) · UK Kidney Association · BNF · MHRA. Review after any guidance or medicines-safety update, otherwise every 6 months. © Reasoning GP · gpreasoning.uk