Hypokalaemia Algorithm

Safety

Red Flags — Severe hypokalaemia, cardiac arrhythmias, paralysis

Done

Urgent exclusion of life-threatening complications of severe potassium depletion.

Severe hypokalaemia K+ <2.5 Urgent hospital assessment, usually admission for monitored replacement Same-day hospital. Emergency ambulance (999) if unstable, significant ECG abnormalities, arrhythmia, paralysis, respiratory compromise, syncope, chest pain or collapse.

Significant ECG abnormalities Arrhythmia, frequent ventricular ectopy, marked ST/T changes or prominent U waves (wide QRS is a late, serious sign) → Urgent hospital monitored replacement; 999 if arrhythmia or unstable. The ECG may be normal despite clinically important hypokalaemia.

Muscle paralysis Ascending weakness, respiratory muscle involvement, unable to walk → 999 (periodic paralysis, severe depletion, respiratory failure risk)

Digoxin Hypokalaemia increases arrhythmia risk on digoxin. ECG and urgent discussion with acute medicine/toxicology if palpitations, bradycardia, heart block, ventricular arrhythmia, syncope, confusion, vomiting or visual disturbance → Emergency hospital assessment now · 999 if unstable. Digoxin level where indicated (at least 6 h post-dose where possible) — do not delay treatment for it.

Rhabdomyolysis Muscle pain, dark urine, weakness, AKI (severe K+ depletion causes muscle breakdown) → Emergency hospital assessment · 999 if unstable — CK, U&Es and IV fluids in hospital

Symptomatic hypokalaemia Palpitations, severe muscle weakness, cramps → Same-day assessment, ECG, urgent potassium replacement. Chest pain, syncope or collapse → 999

Vomiting/diarrhoea + dehydration Severe GI losses, unable to tolerate oral, postural hypotension → Same-day (IV fluids + potassium needed)

ACE inhibitor / ARB + hypokalaemia Review, particularly if persistent or unexpected: assess renal function, bicarbonate, magnesium, adherence and concurrent diuretics. Escalate according to potassium level and clinical state rather than the drug combination alone. Review

Severe hypokalaemia (K+ <2.5) is life-threatening — causes ventricular arrhythmias (VT, VF, torsades de pointes), cardiac arrest, respiratory muscle paralysis. Risk exponential below 2.5 mmol/L. Requires urgent IV potassium replacement under cardiac monitoring. Oral replacement too slow in severe depletion.

ECG changes precede arrhythmias — U waves (most sensitive early sign), T wave flattening, ST depression appear at K+ <3.0. Below 2.5, ventricular ectopics, prolonged QT, widened QRS. Torsades de pointes (polymorphic VT) = cardiac arrest. ECG monitoring mandatory during IV replacement.

Digoxin toxicity amplified by hypokalaemia — low K+ increases digoxin binding to Na+/K+-ATPase, enhancing toxicity even at therapeutic digoxin levels. Presents with nausea, confusion, bradycardia, heart block, yellow vision. Check digoxin level urgently, digoxin-specific antibody fragments (DigiFab) if severe, via the acute team and toxicology advice. The old teaching that IV calcium always precipitates arrest in digoxin toxicity is not supported by recent evidence — any calcium decision belongs to the receiving team.

Diagnose

History — Medications, GI losses, dietary intake

Done

Identify cause through medication review, assessment of GI/renal losses, and dietary history.

Medications

Diuretics: Loop (furosemide, bumetanide) and thiazide (bendroflumethiazide, indapamide) cause kaliuresis. Laxatives: Chronic use (senna, bisacodyl). Steroids: Prednisolone, dexamethasone (mineralocorticoid effect). Insulin: Drives K+ intracellularly. Salbutamol: Beta-agonist (intracellular shift). Amphotericin, gentamicin (renal K+ wasting).

GI losses

Vomiting: Pyloric stenosis, hyperemesis, eating disorders (bulimia). Diarrhoea: Infective (cholera, norovirus), inflammatory (Crohn's, UC), laxative abuse. Stoma: Ileostomy, colostomy high output. VIPoma: Rare (watery diarrhoea, hypokalaemia, achlorhydria syndrome).

Dietary intake

Inadequate oral potassium rare as sole cause (found in tea/coffee/milk). At-risk: Eating disorders, alcohol excess (poor nutrition + diarrhoea + vomiting), elderly (poor diet, polypharmacy). Tea-and-toast diet with diuretics = classic combination.

Symptoms

Mild (K+ 3.0-3.4): Often asymptomatic. Moderate (K+ 2.5-2.9): Muscle weakness, cramps, fatigue, constipation, polyuria. Severe (K+ <2.5): Paralysis, arrhythmias, rhabdomyolysis. Cardiac: Palpitations, chest pain, syncope.

Renal losses

Diuretics (most common cause). Primary hyperaldosteronism (Conn's syndrome — hypertension + hypokalaemia). Renal tubular acidosis (RTA type 1, 2). Bartter/Gitelman syndrome (genetic, normotensive). Hypomagnesaemia (causes renal K+ wasting — check Mg2+).

Intracellular shift

Insulin therapy (DKA treatment). Beta-agonists (salbutamol, terbutaline). Alkalosis (respiratory or metabolic). Refeeding syndrome (anorexia, chronic malnutrition). Periodic paralysis (familial hypokalaemic, thyrotoxic).

PMH

Hypertension (Conn's syndrome, Cushing's), diabetes (DKA, insulin), eating disorders (purging, laxatives), CKD (RTA), thyrotoxicosis (periodic paralysis), alcohol excess.

Diuretics are the commonest cause — thiazides and loop diuretics cause kaliuresis (renal potassium loss). Thiazides inhibit NaCl reabsorption in distal tubule, increasing Na+ delivery to collecting duct → increased Na+/K+ exchange → K+ loss. Loop diuretics similar mechanism.

GI losses often underestimated — vomiting causes hypokalaemia via renal losses (not GI). Vomiting → volume depletion → aldosterone release → renal K+ wasting. Diarrhoea causes direct GI K+ loss. Chronic laxative abuse (bulimia, eating disorders) = important hidden cause.

Hypomagnesaemia causes refractory hypokalaemia — low Mg2+ impairs Na+/K+-ATPase, causing renal K+ wasting. Cannot correct K+ without correcting Mg2+ first. Check Mg2+ in all hypokalaemia, especially if resistant to oral K+ replacement. Correct clinically significant hypomagnesaemia concurrently, using the current local formulary/SPC for the preparation and dose; seek hospital advice for severe, symptomatic or IV magnesium replacement, especially in renal impairment. Magnesium replacement commonly causes diarrhoea, which may worsen potassium loss.

Diagnose

Classification — Severity and mechanism

Done

Classify by severity (determines urgency) and mechanism (directs investigation and treatment).

Mild (3.0-3.4)

Usually asymptomatic. Often incidental finding. Causes: Diuretics, poor diet, GI losses (mild). Management: Oral replacement, dietary advice, review diuretic dose. Primary care

Moderate (2.5-2.9)

Symptoms: Muscle weakness, cramps, fatigue, constipation, polyuria. ECG: May show U waves, T wave flattening. Management: ECG and clinical assessment the same day. Oral replacement only if well, able to absorb oral treatment, no significant ECG abnormality and reliable follow-up; same-day hospital assessment if symptomatic, vomiting, dehydrated, on digoxin, significant cardiac disease, renal impairment or potassium falling. Investigate cause, stop/reduce diuretic if possible. GP with close monitoring

Severe (<2.5)

Life-threatening. Arrhythmia risk, paralysis, rhabdomyolysis. ECG changes: U waves, ST depression, wide QRS, ventricular ectopics. Management: Hospital admission, IV potassium, cardiac monitoring. Medical emergency

Inadequate intake

Rare as sole cause (ubiquitous in diet). At-risk: Eating disorders, elderly tea-and-toast diet, alcohol excess. Management: Dietary advice, treat underlying (anorexia support, alcohol cessation). Usually coexists with other causes (diuretics, GI losses).

Increased GI losses

Vomiting, diarrhoea, laxatives, stoma, fistula. Diagnosis: History of GI symptoms. Management: Treat cause (antiemetics, rehydration, stop laxatives), oral K+ replacement, monitor U&Es.

Increased renal losses

Diuretics (most common), primary hyperaldosteronism (Conn's — hypertension + hypokalaemia + high aldosterone), Cushing's syndrome (cortisol excess), RTA, Bartter/Gitelman, hypomagnesaemia. Diagnosis: Urinary K+ above approximately 20 mmol/day during hypokalaemia suggests renal loss — difficult to interpret on diuretics or after recent replacement.

Intracellular shift

K+ moves into cells, total body K+ normal. Insulin, beta-agonists, alkalosis, refeeding, periodic paralysis, thyrotoxicosis. Diagnosis: Acute onset, appropriate trigger (insulin, salbutamol), normal/low urine K+. Management: Treat underlying, cautious K+ replacement (risk rebound hyperkalaemia).

Severity classification determines management setting — mild hypokalaemia managed in primary care with oral K+, severe requires hospital admission for IV replacement + monitoring. Risk of arrhythmia rises steeply below 2.5 mmol/L.

Mechanism classification directs investigation — GI losses (stop when vomiting/diarrhoea stops), renal losses (persistent, need investigation for Conn's/RTA), intracellular shift (transient, self-limiting). Urinary K+ helps distinguish renal from extrarenal (approximate thresholds, confounded by diuretics, recent replacement, renal impairment and collection): urine K+ <20 mmol/day = extrarenal (GI, poor intake, shift), >20 mmol/day = renal wasting (diuretics, Conn's, RTA).

Conn's syndrome prevalence 5-10% of hypertensive patients. Classically: hypertension + hypokalaemia + metabolic alkalosis. Aldosterone drives Na+ retention (hypertension) and K+ loss (hypokalaemia). Screen with aldosterone:renin ratio (a raised ARR, judged against the local laboratory's cut-off, suggests Conn's). CT adrenals to locate adenoma. Surgical cure possible.

Diagnose

Examination — Muscle strength, BP, signs of underlying cause

Done

Focus on neuromuscular examination, blood pressure, and signs of endocrine/renal disease.

Vital signs

BP (hypertension = Conn's, Cushing's), pulse (tachycardia, irregular if arrhythmia), postural BP drop (volume depletion from GI/renal losses), weight (malnutrition, eating disorder, cachexia).

Neuromuscular

Muscle strength: Proximal weakness (difficulty standing from squat, raising arms). Tone: Hypotonia (flaccid paralysis in severe cases). Reflexes: Reduced or absent. Respiratory: Tachypnoea, shallow breathing (respiratory muscle weakness). Paralysis: Ascending weakness, inability to walk.

Cardiovascular

Pulse (irregular if ectopics/AF), JVP (low if volume depleted), heart sounds (listen for murmurs, gallop), peripheral oedema (if heart failure or Conn's), capillary refill time.

Abdominal

Distension (ileus from severe hypokalaemia), bowel sounds (reduced/absent), tenderness, masses (VIPoma rare), stoma output (high output ileostomy). Examine for signs of Crohn's/IBD if diarrhoea.

Endocrine

Cushing's: Moon face, buffalo hump, abdominal striae, proximal myopathy, skin thinning. Thyrotoxicosis: Tremor, goitre, exophthalmos, tachycardia (periodic paralysis). Conn's: Hypertension, no specific signs.

Volume status

Dry mucous membranes, reduced skin turgor, postural hypotension, tachycardia (volume depletion from vomiting/diarrhoea/diuretics). Fluid overload rare (unless renal failure).

ECG

Early signs (K+ 3.0-3.4): U waves (after T wave), T wave flattening. Moderate (K+ 2.5-2.9): ST depression, prolonged PR, prominent U waves. Severe (K+ <2.5): Widened QRS, ventricular ectopics, VT. ECG if symptomatic, K+ <3.0, on digoxin or anti-arrhythmics, or significant cardiac disease

Muscle weakness is commonest symptom — affects proximal muscles first (difficulty standing, climbing stairs, lifting arms). Caused by hyperpolarisation of muscle cell membranes (low extracellular K+ increases K+ gradient). Severe cases progress to flaccid paralysis, respiratory failure. Reflexes absent (hypotonia).

Hypertension + hypokalaemia = Conn's until proven otherwise — primary hyperaldosteronism is underdiagnosed (5-10% of hypertensives). Aldosterone causes Na+ retention (hypertension) and K+ wasting (hypokalaemia). Classically K+ <3.5 with high-normal or elevated BP. Screen with aldosterone:renin ratio.

U waves are most sensitive ECG sign — small positive deflection after T wave, best seen in V2-V4. Appear when K+ <3.0. Mechanism: prolonged ventricular repolarisation. Progression: T wave flattening → ST depression → prolonged QT → widened QRS → ventricular ectopics → VT/VF. ECG mandatory if K+ <3.0 or symptomatic.

Diagnose

Investigations — U&Es, Mg2+, urinary potassium, endocrine screen

Done

Investigate to confirm hypokalaemia, assess severity, and identify underlying cause.

Repeat U&Es

Confirm hypokalaemia (pseudohypokalaemia if leukaemia — WBC consumes K+ in tube). Assess severity: K+ 3.0-3.4 (mild), 2.5-2.9 (moderate), <2.5 (severe). Concurrent abnormalities: Low Na+ (GI losses), high creatinine (CKD, dehydration), high glucose (DKA).

Magnesium

Always check Mg2+ — hypomagnesaemia causes refractory hypokalaemia (cannot correct K+ without correcting Mg2+). Normal: 0.7-1.0 mmol/L. Low Mg2+: Diuretics, diarrhoea, alcohol, PPI (chronic use). Correct clinically significant hypomagnesaemia concurrently, using the local formulary/SPC for preparation and dose; seek hospital advice for severe, symptomatic or IV replacement, especially in renal impairment.

Urinary potassium

If the cause is unclear or hypokalaemia persists after medication review, consider urinary potassium assessment (24-hour urine K+ or spot urine K+:creatinine ratio). Urinary potassium excretion above approximately 20 mmol/day during hypokalaemia suggests renal potassium loss, but results are difficult to interpret during diuretic therapy or recent potassium replacement — discuss with renal/endocrine services if equivocal. Not routine.

Acid-base status

Review bicarbonate on the U&Es. Obtain a venous blood gas when the patient is unwell, the bicarbonate is abnormal, DKA or RTA is suspected, or there is significant acid–base uncertainty. Metabolic alkalosis + hypokalaemia: Vomiting, diuretics, Conn's, Cushing's. Metabolic acidosis + hypokalaemia: Diarrhoea, RTA type 1 or 2, DKA. Interpretation: Alkalosis shifts K+ intracellularly (worsens hypokalaemia).

Endocrine screen

If hypertension + persistent or unexplained hypokalaemia: consider primary aldosteronism — correct potassium before ARR testing where possible, follow the laboratory/endocrine protocol on medication withdrawal or substitution, and do not interpret ARR without considering renin suppression, aldosterone concentration and medication effects. If convincing Cushingoid features: discuss testing with endocrinology — 1 mg overnight dexamethasone suppression test, late-night salivary cortisol or urinary free cortisol per local pathway. Do not use a 9 am cortisol to screen for Cushing's syndrome. Severe hypokalaemic alkalosis with rapid-onset hypertension, proximal weakness or hyperglycaemia (especially in a smoker): consider ectopic ACTH (e.g. small-cell lung cancer) — same-day endocrinology advice, and an urgent chest X-ray (within 2 weeks) if aged 40 or over and ever smoked with an unexplained symptom, or with 2 or more unexplained symptoms (cough, fatigue, breathlessness, chest pain, weight loss, appetite loss) (NICE NG12). If thyrotoxic features: TFTs (thyrotoxic periodic paralysis). Arrange via endocrinology if suspicion high.

ECG

Indications: symptomatic (palpitations, weakness), K+ <3.0, taking digoxin or anti-arrhythmic drugs, significant cardiac disease. Findings: U waves, T wave flattening, ST depression, prolonged QT, ventricular ectopics. Action: Significant ECG abnormalities or arrhythmia → urgent hospital assessment and monitored replacement. Prominent U waves may merge with the T wave (apparent QT/QU prolongation); a normal ECG does not exclude important hypokalaemia.

Proportionate investigation

In an otherwise well patient with stable K+ 3.0-3.4 and an obvious diuretic-related cause, extensive urinary or endocrine investigations are not usually required initially. Repeat U&Es including bicarbonate and magnesium, review the diuretic and reassess. Investigate further if persistent, recurrent, progressive, disproportionate to the treatment, or associated with hypertension, renal disease, acid–base disturbance or symptoms.

Magnesium MUST be checked — hypomagnesaemia commonly coexists with hypokalaemia. Low Mg2+ impairs cellular K+ uptake (Na+/K+-ATPase dysfunction) and increases renal K+ wasting. Hypokalaemia is refractory to treatment until Mg2+ corrected. Always replace Mg2+ first or concurrently.

Urinary K+ distinguishes pathophysiology — appropriate renal response to hypokalaemia is K+ conservation (urine K+ <20 mmol/day). If urine K+ >20 mmol/day despite hypokalaemia = inappropriate renal K+ wasting (diuretics, Conn's, Bartter/Gitelman, RTA). Guides investigation: extrarenal causes obvious (vomiting, diarrhoea), renal causes need endocrine/nephrology input.

Conn's syndrome screening if hypertension + hypokalaemia: aldosterone:renin ratio (ARR), after correcting potassium where possible (hypokalaemia can give a falsely negative result). A raised ARR, judged against the local laboratory's cut-off, suggests primary hyperaldosteronism. Confirmatory tests: saline suppression, fludrocortisone suppression. CT adrenals (with adrenal vein sampling to confirm laterality): unilateral adenoma (about one-third) or bilateral hyperplasia (about two-thirds). Adenoma → surgery curative. Hyperplasia → spironolactone.

Refer

Referral Criteria — When to escalate urgently

Done

Refer all severe hypokalaemia, symptomatic patients, ECG changes, and unclear/resistant cases.

999 / A&E

999: unstable, arrhythmia or significant ECG abnormality, paralysis or respiratory compromise, syncope, chest pain or collapse, suspected serious digoxin toxicity, rhabdomyolysis or significant AKI. K+ <2.5 mmol/L otherwise → urgent hospital assessment, usually admission for monitored replacement. Do not delay transfer for outpatient investigations.

Same-day medical

K+ 2.5-2.9 if symptomatic (weakness, cramps), on digoxin, significant cardiac disease, renal impairment or potassium falling. Unable to tolerate oral (vomiting). Dehydration + hypokalaemia. Requires IV fluids + potassium, monitoring, investigation.

Eating disorder

Suspected purging (unexplained hypokalaemia with normal BP, metabolic alkalosis and no prescribed diuretic, dental erosion, parotid swelling, knuckle callus, low BMI): ask directly and without judgement about vomiting, laxatives and diuretics. Assess physical risk using MEED (RCPsych CR233): K+ <2.5 (MEED red; 2.5–3.0 amber), bradycardia, postural drop or rapid weight loss → same-day medical assessment. Refer to the eating-disorder service (NICE NG69); replacing potassium without addressing purging repeats the result.

Endocrinology

Hypertension + hypokalaemia (Conn's suspected — ARR raised). Cushingoid features. Thyrotoxic periodic paralysis (recurrent episodes weakness + hypokalaemia + hyperthyroidism). Unexplained persistent hypokalaemia off diuretics. Suspected ectopic ACTH → same-day endocrinology advice plus NG12 chest X-ray (Step 5).

Nephrology

Renal tubular acidosis suspected (hypokalaemia + metabolic acidosis + normal anion gap). Bartter/Gitelman syndrome (young, normotensive, hypokalaemia + hypomagnesaemia + hypocalciuria). Refractory hypokalaemia despite K+ + Mg2+ replacement.

Primary care

Mild hypokalaemia (K+ 3.0-3.4) on diuretics, asymptomatic. Clear cause (vomiting, diarrhoea resolving). Management: Treat the cause, review the diuretic, oral potassium chloride if ongoing losses, cardiac risk or persistent hypokalaemia (individualised, local formulary), recheck U&Es and magnesium within about 1 week (sooner if high risk).

IV potassium requires hospital — never give IV K+ in primary care. Hospital protocols use premixed glucose-free solutions with a usual maximum rate of 10 mmol/hour; higher rates need specialist direction, an infusion pump, appropriate venous access and continuous cardiac monitoring. Never give potassium by IV bolus.

Conn's syndrome is treatable — if caused by an aldosterone-secreting adenoma (about one-third of cases), surgical adrenalectomy almost always corrects the hypokalaemia and improves blood pressure in most, normalising it in a substantial minority. Bilateral hyperplasia (about two-thirds of cases) is treated with spironolactone (aldosterone antagonist). Missing Conn's = lifelong antihypertensives when surgery could cure.

Primary care manages mild cases — K+ 3.0-3.4 on diuretics, asymptomatic, obvious cause. Oral potassium chloride individualised to level, renal function and ongoing losses (SPS: typically 24 mmol two or three times daily for mild), review diuretic, normal balanced diet. Recheck U&Es 1 week. If persistent or worsening → investigate/refer.

Treat

Potassium Replacement — Oral Sando-K, IV potassium if severe

Done

Replace potassium orally in mild-moderate cases, IV in severe/symptomatic cases (hospital only).

Mild (K+ 3.0-3.4), asymptomatic

Sando-K tablets Oral

Each tablet = 12 mmol K+. Typical adult dose 24 mmol (2 tablets) two or three times daily (SPS), individualised to potassium level, renal function, ongoing losses and local formulary; lower doses in CKD or changing renal function. Dissolve in water, take with or after food. Reassess at recheck rather than continuing automatically. Adjust diuretic if cause.

Moderate (K+ 2.5-2.9), well

Sando-K, if oral appropriate Oral

Typical 24–36 mmol three or four times daily (SPS) — only if well, able to absorb oral treatment, no significant ECG abnormality and reliable follow-up. Recheck within 24–72 hours. Symptomatic, vomiting, dehydrated, on digoxin, cardiac disease, renal impairment or falling K+ → same-day hospital assessment. Correct Mg2+ if low.

Severe (K+ <2.5) or ECG changes

IV potassium chloride Hospital only

Hospital-based: premixed glucose-free solutions under the local IV-electrolyte protocol (glucose-driven insulin release can lower K+ further). Usual maximum 10 mmol/hour; higher rates need specialist direction, an infusion pump, appropriate access and continuous cardiac monitoring. Never give potassium by IV bolus.

Step 1Oral potassium chloride (e.g. Sando-K) — Effervescent tablets, dissolve in water (each = 12 mmol K+ + 8 mmol Cl-). Dose by potassium level, renal function, ongoing losses and local formulary (SPS mild: 24 mmol two or three times daily); reduce in CKD or changing renal function; account for potassium in other preparations. Take with or after food; warn about nausea, diarrhoea and abdominal pain. Recheck U&Es and magnesium within about 1 week.

Step 2Review dose — If K+ not rising, check magnesium, adherence and ongoing losses before increasing (SPS moderate: 24–36 mmol three or four times daily); symptomatic → same-day assessment. Check U&Es within 24–72 hours. Warn: GI upset common (nausea, diarrhoea). Take with meals.

Step 3Correct magnesium — If clinically significant hypomagnesaemia, concurrently; preparation and dose per local formulary/SPC (oral magnesium commonly causes diarrhoea, which may worsen K+ loss); hospital advice if severe, symptomatic or IV needed, especially in renal impairment. Essential for K+ correction. Check Mg2+ with U&Es.

Step 4Potassium-sparing strategy — If hypokalaemia persists despite addressing the cause and replacing potassium/magnesium, discuss with the relevant specialist or follow the local formulary. Do not routinely start amiloride or spironolactone without checking renal function, reviewing interacting medicines (ACE inhibitors, ARBs, other potassium-raising drugs) and confirming the indication. If primary aldosteronism is suspected, obtain endocrine advice first — spironolactone interferes with diagnostic testing. NICE NG136: resistant-hypertension spironolactone only if K+ ≤4.5 mmol/L, with caution in reduced eGFR and electrolytes/renal function checked within 1 month.

Step 5Refer if refractory — Persistent hypokalaemia despite K+ + Mg2+ replacement and diuretic adjustment. Investigate for Conn's, RTA, Bartter/Gitelman. Endocrine/nephrology input.

IV potassium (hospital)

Indications: K+ <2.5, symptomatic, ECG changes, unable to tolerate oral. Fluids: premixed glucose-free solutions per local protocol (e.g. 40 mmol in 1L NaCl 0.9%) — glucose-driven insulin release can lower K+ further. Rate: usual maximum 10 mmol/hr; faster only with specialist direction, infusion pump, appropriate access and continuous cardiac monitoring. Never by IV bolus. Monitoring: Cardiac monitor, U&Es every 4-6 hrs. Never give in primary care

Diuretic adjustment

If cause is diuretic: Reduce dose (e.g. furosemide 80mg → 40mg, bendroflumethiazide 2.5mg → 1.25mg), OR discuss a potassium-sparing strategy with the relevant specialist/local formulary. Balance: fluid overload vs hypokalaemia.

Magnesium replacement

Correct clinically significant hypomagnesaemia concurrently — potassium may remain refractory until magnesium is corrected. Use the current local formulary/SPC for the preparation and dose; seek hospital advice for severe, symptomatic or IV replacement, especially in renal impairment. Oral magnesium commonly causes diarrhoea, which may worsen potassium loss.

Monitoring

Repeat testing according to potassium level, renal function, ongoing losses, ECG findings, treatment changes and comorbidities. Mild stable: recheck within 1 week after treatment or medication change. Moderate: generally within 24–72 hours. IV replacement: hospital monitoring. Caution: Overreplacement → hyperkalaemia (especially if renal impairment, ACEi/ARB, K+-sparing diuretics).

Next steps: see Eating disorders · Hypertension · Heart failure

Oral replacement is slow but safe — each Sando-K tablet contains 12 mmol K+. Dose is individualised to level, renal function and ongoing losses. GI upset common (nausea, diarrhoea) — take with meals, reduce dose if intolerable. Hyperkalaemia can still occur, particularly in CKD or with potassium-raising drugs.

IV potassium is high-risk — rapid infusion causes cardiac arrest (asystole, VF). Usual maximum rate 10 mmol/hour; rates above 20 mmol/hour require cardiac monitoring (SPS). Never give potassium by IV bolus. Cardiac monitoring mandatory. Extravasation causes tissue necrosis. Peripheral infusion painful (K+ irritates veins).

Potassium-sparing diuretics prevent recurrence — amiloride (epithelial Na+ channel blocker) and spironolactone (aldosterone antagonist) reduce K+ wasting while maintaining diuresis. Use is a specialist or local-formulary decision with the indication confirmed; spironolactone interferes with aldosterone–renin testing. Caution: hyperkalaemia risk if CKD, ACEi/ARB. Monitor U&Es 1 week after starting.

Lifestyle

Dietary Potassium and Medication Review

Done

Encourage a normal balanced diet and review medications to prevent recurrence.

Balanced diet Encourage a normal balanced diet including fruit and vegetables. Dietary potassium advice should be individualised and should not replace treatment of renal/GI losses or medication review. Avoid prescribing a fixed daily potassium target unless advised by a dietitian or specialist.

Salt substitutes — not a treatment Do not recommend potassium-containing salt substitutes (e.g. LoSalt) as potassium treatment — they can cause dangerous hyperkalaemia in CKD, heart failure, diabetes, or with ACE inhibitors, ARBs, MRAs, amiloride or other potassium-raising medicines. If a patient already uses one, review this if renal function deteriorates or potassium-raising medicines are started.

Reduce diuretic dose If hypokalaemia recurrent on diuretics: reduce dose (e.g. furosemide 80mg → 40mg OD), switch to alternate days, or stop if possible (if mild heart failure, well-controlled hypertension). Balance diuresis vs K+ depletion.

Review medications Stop/reduce: laxatives (if chronic use), steroids (if possible). Review NSAIDs, particularly with CKD, dehydration, heart failure, ACE inhibitor/ARB therapy or concurrent diuretics — stop or avoid where clinically inappropriate and offer an alternative. If a thiazide-like diuretic (indapamide) given for hypertension is the cause, review the antihypertensive choice in line with NICE NG136 (an ACE inhibitor or ARB tends to raise potassium).

Avoid excessive liquorice Contains glycyrrhizic acid (mimics aldosterone, causes K+ wasting). Found in liquorice sweets, herbal teas, aniseed drinks. Regular consumption can cause hypokalaemia + hypertension.

Alcohol moderation Alcohol excess causes K+ loss (vomiting, diarrhoea, poor nutrition, Mg2+ depletion). Keep within the UK Chief Medical Officers' low-risk guideline: no more than 14 units a week, spread over 3 or more days. Address alcohol dependency if present (brief intervention, refer alcohol services).

Treat underlying GI disease IBD (optimize medical therapy), coeliac (gluten-free diet), chronic diarrhoea (investigate cause). Eating disorders (bulimia) — laxative abuse, vomiting. Refer psychology/eating disorder services.

Educate on symptoms Muscle weakness, cramps, palpitations, constipation = hypokalaemia warning signs. Seek medical review if recurrent. Patients on diuretics should recognize risk and report symptoms early.

Medication compliance If on Sando-K: take regularly with food. Dissolve fully in water (reduces GI irritation). Do not chew tablets. If intolerant: try splitting dose (1 tablet QDS vs 2 BD), take with meals, or switch to potassium chloride oral solution (Kay-Cee-L; dose per NICE/SPC).

A normal balanced diet is usually adequate for maintenance once hypokalaemia is corrected and the cause treated — diet alone does not correct ongoing renal or GI losses.

Salt substitutes are not a potassium treatment — potassium-containing products can cause dangerous hyperkalaemia in CKD, heart failure, diabetes or with potassium-raising medicines.

Diuretic dose reduction often feasible — many patients started on high doses (furosemide 80-120mg) but only need 40mg maintenance. Trial dose reduction with close BP/fluid status monitoring. If mild heart failure well-controlled, consider stopping diuretic entirely (reduces K+ loss, polypharmacy).

Safety

Follow-Up — Monitor K+ levels, adjust treatment, prevent recurrence

Done

Regular monitoring of U&Es to ensure correction and prevent rebound hyperkalaemia.

1 week

Recheck U&Es after starting Sando-K or adjusting diuretic. Target K+ 3.5-5.0 mmol/L. If <3.0 still → check Mg2+, adherence and ongoing losses, and review dose and urgency. If >5.0 → stop Sando-K, reduce K+-sparing diuretic if on one. If 3.5-5.0 → continue current dose, recheck 1 month.

1 month

Repeat U&Es to confirm stable K+. If normalized → consider stopping Sando-K if dietary K+ adequate and diuretic dose reduced. If recurrent → investigate the cause; discuss a potassium-sparing strategy with the specialist/local formulary. Review medication list (stop laxatives; review NSAIDs).

3-monthly

Individualised monitoring (e.g. 3-monthly) if on long-term diuretics, K+ supplements, or K+-sparing diuretics. Check U&Es, adjust doses. Screen for hyperkalaemia (especially if CKD, ACEi/ARB added). Document in chronic disease register.

Annual review

Patients on diuretics: U&Es shortly after initiation or dose change and during intercurrent illness, then at individualised intervals — annual testing may be insufficient for high-risk patients or after changes in diuretic, RAAS-blocker or potassium-sparing treatment. BP, weight. Assess ongoing need for diuretic (can dose be reduced? can it be stopped?). Ensure dietary K+ adequate. Check compliance with K+ supplements if prescribed.

Safety-net 999

Severe muscle weakness (unable to walk, respiratory distress). Chest pain, syncope, or palpitations with feeling faint or breathless. Collapse, confusion (severe hypokalaemia → arrhythmia). Signs of rhabdomyolysis (dark urine, severe muscle pain).

Safety-net Same-day GP

Muscle cramps, weakness worsening despite K+ supplements. Palpitations without chest pain or faintness (chest pain → 999). Severe vomiting/diarrhoea (unable to take oral K+). New medications started that may affect K+ (ACEi, ARB, NSAIDs).

Re-refer if

Refractory hypokalaemia despite K+ + Mg2+ replacement and diuretic adjustment. Recurrent episodes without clear cause. Hypertension develops with hypokalaemia (Conn's). Hyperkalaemia on K+ supplements (? CKD, ? excessive supplementation).

Rebound hyperkalaemia is real risk — overreplacement with Sando-K + K+-sparing diuretics + ACEi/ARB = severe hyperkalaemia (K+ >6.0). Especially in CKD patients (reduced K+ excretion). Monitor U&Es 1 week after any change. Hyperkalaemia >6.5 is medical emergency (cardiac arrest risk).

Long-term K+ supplementation often unnecessary — once corrected and diuretic dose optimized, dietary K+ usually sufficient. Trial stopping Sando-K after 1-2 months if K+ stable and diet adequate. Recheck U&Es 1-2 weeks after stopping. Restart if K+ drops below 3.5.

Refractory hypokalaemia warrants specialist input — if K+ remains <3.5 despite appropriate oral replacement + Mg2+ replacement + diuretic reduction = underlying pathology (Conn's, Bartter/Gitelman, RTA, VIPoma). Endocrine/nephrology investigation needed. Primary care has exhausted options.