Hypokalaemia Algorithm · Reasoning GP

Safety

Red Flags — Severe hypokalaemia, cardiac arrhythmias, paralysis

Done

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

Severe hypokalaemia K+ <2.5 Cardiac arrhythmia risk, muscle weakness, rhabdomyolysis → 999/Same-day hospital admission for IV potassium, cardiac monitoring

ECG changes U waves, T wave flattening, ST depression, prolonged PR, wide QRS, ventricular ectopics → 999 (life-threatening arrhythmia risk: VT, VF, torsades)

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

Digoxin toxicity Hypokalaemia + digoxin = arrhythmia (nausea, confusion, yellow vision, bradycardia, heart block) → 999 urgent digoxin level + cardiac monitoring

Rhabdomyolysis Muscle pain, dark urine, weakness, AKI (severe K+ depletion causes muscle breakdown) → Same-day bloods CK, U&Es, IV fluids

Symptomatic hypokalaemia Palpitations, chest pain, severe muscle weakness, cramps → Same-day assessment, ECG, urgent potassium replacement

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

Concurrent medications Diuretics + ACEi/ARB + hypokalaemia (paradoxical given ACEi raises K+, suggests severe depletion or renal pathology) → Urgent 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, give Digibind if severe. Never give calcium in digoxin toxicity (precipitates VF).

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+ 3.0-3.5): Often asymptomatic. Moderate (K+ 2.5-3.0): 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. 50% of patients on diuretics develop hypokalaemia.

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 (stool K+ 20-80 mmol/L). 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. Give magnesium sulfate IV if severe or oral magnesium if mild.

Diagnose

Classification — Severity and mechanism

Done

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

Mild (3.0-3.5)

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

Moderate (2.5-3.0)

Symptoms: Muscle weakness, cramps, fatigue, constipation, polyuria. ECG: May show U waves, T wave flattening. Management: Oral potassium, investigate cause, stop/reduce diuretic if possible. Monitor closely. 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: Urine K+ >20 mmol/day despite hypokalaemia = renal wasting.

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 exponential below 2.5 mmol/L. Every 0.5 mmol/L drop increases risk 2-fold.

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+ distinguishes renal from extrarenal: 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 (ARR >750 pmol/mU 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+ 3.0-3.5): U waves (after T wave), T wave flattening. Moderate (K+ 2.5-3.0): ST depression, prolonged PR, prominent U waves. Severe (K+ <2.5): Widened QRS, ventricular ectopics, VT. Do ECG if K+ <3.0 or symptomatic

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+ 3.0-3.5 (mild), 2.5-3.0 (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). Replace with magnesium sulfate IV or oral magnesium oxide.

Urinary potassium

Distinguishes renal from extrarenal causes. 24-hour urine K+ OR spot urine K+:creatinine ratio. <20 mmol/day: Extrarenal (GI losses, poor intake, intracellular shift). >20 mmol/day: Renal wasting (diuretics, Conn's, RTA). Not routine — do if cause unclear or diuretic stopped but K+ still low.

Acid-base status

Venous blood gas if available. 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 + hypokalaemia: Aldosterone:renin ratio (ARR) for Conn's syndrome. If Cushingoid features: 9am cortisol, overnight dexamethasone suppression test. If thyrotoxic features: TFTs (thyrotoxic periodic paralysis). Arrange via endocrinology if suspicion high.

ECG

Indications: K+ <3.0, symptomatic (palpitations, weakness), on digoxin, cardiac history. Findings: U waves, T wave flattening, ST depression, prolonged QT, ventricular ectopics. Action: If ECG changes present → urgent K+ replacement + cardiac monitoring.

Do NOT investigate

Mild hypokalaemia (K+ 3.0-3.5) on diuretics, asymptomatic, otherwise well → supplement K+, reduce diuretic, recheck in 1 week. Over-investigation (urinary K+, endocrine screen) unnecessary unless persistent despite treatment or red flags.

Magnesium MUST be checked — 40% of hypokalaemic patients have concurrent hypomagnesaemia. 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). ARR >750 pmol/mU (or 20 ng/dL per ng/mL/hr) suggests primary hyperaldosteronism. Confirmatory tests: saline suppression, fludrocortisone suppression. CT adrenals: adenoma (60%) or bilateral hyperplasia (40%). 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

K+ <2.5 mmol/L. ECG changes (U waves, ventricular ectopics, widened QRS). Symptomatic (muscle paralysis, palpitations, chest pain). Digoxin toxicity. Rhabdomyolysis. Requires IV potassium, cardiac monitoring, ICU if severe.

Same-day medical

K+ 2.5-3.0 + symptomatic (weakness, cramps). Unable to tolerate oral (vomiting). Dehydration + hypokalaemia. Requires IV fluids + potassium, monitoring, investigation.

Endocrinology

Hypertension + hypokalaemia (Conn's suspected — ARR raised). Cushingoid features. Thyrotoxic periodic paralysis (recurrent episodes weakness + hypokalaemia + hyperthyroidism). Unexplained persistent hypokalaemia off diuretics.

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+ 3.0-3.5) on diuretics, asymptomatic. Clear cause (vomiting, diarrhoea resolving). Management: Oral K+ replacement (Sando-K), dietary advice, reduce diuretic dose, recheck U&Es 1 week. Monitor closely.

IV potassium requires hospital — never give IV K+ in primary care. Maximum infusion rate 10 mmol/hour via peripheral line (20 mmol/hour via central line). Faster rates cause pain, phlebitis, cardiac arrest if bolus administered. Cardiac monitoring mandatory. Each 10 mmol IV raises serum K+ by ~0.1 mmol/L.

Conn's syndrome is treatable — if caused by aldosterone-secreting adenoma (60% cases), surgical adrenalectomy is curative (80% cure hypertension, 100% cure hypokalaemia). Bilateral hyperplasia (40% cases) treated with spironolactone (aldosterone antagonist). Missing Conn's = lifelong antihypertensives when surgery could cure.

Primary care manages mild cases — K+ 3.0-3.5 on diuretics, asymptomatic, obvious cause. Oral K+ supplementation (Sando-K 2 tablets BD = 24 mmol K+/day), reduce diuretic if possible, dietary advice (bananas, oranges, potatoes). 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+ 3.0-3.5), asymptomatic

Sando-K tablets Oral

2 tablets BD (each tablet = 12 mmol K+, total 48 mmol/day). Dissolve in water, take with food. Duration: 1-2 weeks then recheck. Adjust diuretic if cause.

Moderate (K+ 2.5-3.0), symptomatic

Sando-K 2 tablets TDS Oral

Total 72 mmol K+/day. Check U&Es after 48-72 hours. If K+ not rising or symptomatic worsens → admit for IV. Add Mg2+ if low.

Severe (K+ <2.5) or ECG changes

IV potassium chloride Hospital only

10-20 mmol/hour via central line (max 10 mmol/hr peripheral). Cardiac monitoring. Never IV bolus (cardiac arrest). Typical: 40 mmol in 1L NaCl 0.9% over 4 hours.

Step 1Sando-K 2 tablets BD — Effervescent tablets, dissolve in water (each = 12 mmol K+ + 8 mmol Cl-). Total 48 mmol K+/day. Take with food (GI irritation). Recheck U&Es 1 week.

Step 2Increase to TDS — If K+ not rising or symptomatic. Total 72 mmol/day. Check U&Es 48-72 hours. Warn: GI upset common (nausea, diarrhoea). Take with meals.

Step 3Add magnesium — If hypomagnesaemia (Mg2+ <0.7). Magnesium oxide 400mg BD or magnesium glycerophosphate (Magnaspartate) 1 sachet BD. Essential for K+ correction. Check Mg2+ with U&Es.

Step 4Potassium-sparing diuretic — If recurrent hypokalaemia on thiazide/loop. Add amiloride 5-10 mg OD or spironolactone 25-50 mg OD. Caution: monitor for hyperkalaemia (check U&Es 1 week). Avoid if CKD, ACEi/ARB.

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. Rate: Max 10 mmol/hr peripheral, 20 mmol/hr central. Typical: 40 mmol in 1L NaCl 0.9% over 4 hrs. 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 add K+-sparing (amiloride, spironolactone), OR switch to K+-sparing alone if heart failure controlled. Balance: fluid overload vs hypokalaemia.

Magnesium replacement

Essential if Mg2+ <0.7. Oral: Magnesium oxide 400mg BD (cheap) or magnesium glycerophosphate 1 sachet BD (better tolerated). IV: Magnesium sulfate 20 mmol (5g) in 500ml NaCl 0.9% over 4 hours (hospital only). Concurrent with K+ replacement.

Monitoring

Mild: Recheck U&Es 1 week. Moderate: Recheck 48-72 hours. Severe: Hospital monitoring 4-6 hourly. Caution: Overreplacement → hyperkalaemia (especially if renal impairment, ACEi/ARB, K+-sparing diuretics).

Oral replacement is slow but safe — each Sando-K tablet contains 12 mmol K+. Normal dietary K+ intake 60-100 mmol/day. Supplementing 48-72 mmol/day raises serum K+ by ~0.5 mmol/L over 3-5 days. GI upset common (nausea, diarrhoea) — take with meals, reduce dose if intolerable. Hyperkalaemia risk low with oral (body excretes excess).

IV potassium is high-risk — rapid infusion causes cardiac arrest (asystole, VF). Maximum safe rate 10 mmol/hour peripheral (20 mmol/hour central). Never give IV bolus. Each 10 mmol raises serum K+ by ~0.1 mmol/L. 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. Add to thiazide/loop rather than switching (synergistic effect). Caution: hyperkalaemia risk if CKD, ACEi/ARB. Monitor U&Es 1 week after starting.

Lifestyle

Dietary Potassium and Medication Review

Done

Increase dietary potassium intake and review medications to prevent recurrence.

High-potassium foods Bananas (12 mmol/banana), oranges (10 mmol), potatoes (15 mmol/medium), tomatoes, spinach, beans, lentils, nuts, dried fruit (apricots, raisins), avocado, fish (salmon, mackerel). Aim 60-100 mmol/day dietary K+.

Orange juice / tomato juice High K+ content (10-15 mmol/250ml glass). Practical daily source. Avoid if diabetic (sugar content). Fresh-squeezed better than concentrate (less sugar).

Low-sodium salt substitutes LoSalt, Pan Salt contain KCl instead of NaCl (13 mmol K+ per 1g). Use in cooking, on food. Cheap K+ supplement. CAUTION: Contraindicated if CKD, ACEi/ARB (hyperkalaemia risk).

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), NSAIDs (if on diuretics — synergistic K+ loss), steroids (if possible). Consider alternatives: thiazide-like (indapamide) → ACEi/ARB monotherapy for hypertension (K+-sparing).

Avoid excessive liquorice Contains glycyrrhizic acid (mimics aldosterone, causes K+ wasting). Found in liquorice sweets, herbal teas, aniseed drinks. Significant consumption (>50g/day) causes hypokalaemia + hypertension.

Alcohol moderation Alcohol excess causes K+ loss (vomiting, diarrhoea, poor nutrition, Mg2+ depletion). Limit to <14 units/week. 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 magnesium glycerophosphate (better tolerated).

Dietary K+ provides 60-100 mmol/day — adequate for maintenance once hypokalaemia corrected. Bananas (12 mmol each), oranges (10 mmol), potatoes (15 mmol medium) are richest sources. Fresh fruit/vegetables > processed foods (processing removes K+). Cooking leaches K+ into water — steam/roast > boil.

LoSalt is effective K+ supplement — 1g LoSalt contains 13 mmol K+ (vs 0 mmol in regular salt). Using 2-3g/day in cooking = 25-40 mmol K+ supplementation. Cheap (£2 for 350g vs £5 for Sando-K 100 tablets). CAUTION: Contraindicated in CKD (hyperkalaemia risk), ACEi/ARB users.

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 → increase Sando-K to TDS, check Mg2+. 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 → long-term Sando-K or add K+-sparing diuretic. Review medication list (stop laxatives, NSAIDs if possible).

3-monthly

Routine monitoring 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: Annual U&Es, 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, palpitations, syncope. 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, chest discomfort. 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 Sando-K 72 mmol/day + Mg2+ replacement + diuretic reduction = underlying pathology (Conn's, Bartter/Gitelman, RTA, VIPoma). Endocrine/nephrology investigation needed. Primary care has exhausted options.

Educational use. Pathway based on NICE CKS Hypokalaemia (2023), NHS Laboratory Medicine guidelines, British Society for Haematology. Always adapt to individual patient context and local biochemistry protocols.