Key Facts

Hypokalaemia is one of the most common electrolyte abnormalities encountered in clinical practice. It ranges from an incidental finding to a medical emergency requiring urgent treatment.

Epidemiology

• Present in up to 20% of hospitalised patients
• 50% of patients on thiazide or loop diuretics develop hypokalaemia
• Common in eating disorders (bulimia nervosa)
• More common in elderly and those with chronic disease

Aetiology

Increased losses:

• Renal: loop diuretics, thiazides, mineralocorticoid excess (Conn), Cushing, renal tubular acidosis, hypomagnesaemia
• GI: vomiting, diarrhoea, laxative abuse, ileostomy

Intracellular shift:

• Insulin (endogenous or exogenous)
• Beta-2 agonists (salbutamol)
• Alkalosis (for every 0.1 rise in pH, K falls by ~0.3 mmol/L)
• Refeeding syndrome

Inadequate intake:

• Malnutrition, anorexia nervosa

Pathophysiology

• Potassium is the major intracellular cation (98% intracellular)
• Hypokalaemia hyperpolarises cell membranes → impaired electrical excitability in cardiac and skeletal muscle
• Cardiac effects: delayed repolarisation, increased automaticity → arrhythmias
• Renal effects: impaired concentrating ability → polyuria
• Metabolic effects: impaired insulin secretion, metabolic alkalosis

Mild Hypokalaemia (3.0-3.5 mmol/L)

• Often asymptomatic
• Mild fatigue, muscle cramps

Moderate Hypokalaemia (2.5-3.0 mmol/L)

• Muscle weakness (proximal)
• Constipation (smooth muscle dysfunction)
• Cramps, myalgia
• Polyuria, polydipsia (nephrogenic DI)

Severe Hypokalaemia (<2.5 mmol/L)

• Cardiac arrhythmias: ventricular tachycardia, ventricular fibrillation, torsades de pointes
• Ascending paralysis (can mimic Guillain-Barré)
• Respiratory failure (diaphragmatic weakness)
• Rhabdomyolysis
• Paralytic ileus

Red Flags

• ECG changes (flattened T waves, U waves, prolonged QT, ST depression) → urgent correction needed
• Severe hypokalaemia (<2.5 mmol/L) → cardiac monitoring
• Concurrent digoxin therapy → hypokalaemia potentiates digoxin toxicity
• Hypokalaemia + hypertension → consider Conn syndrome, Cushing, renal artery stenosis

Bedside

• ECG: essential in all patients – look for flattened T waves, U waves, ST depression, prolonged QT
• Assess for muscle weakness, ileus

Bloods

• Serum potassium: confirm and grade severity (repeat if haemolysed sample suspected)
• Serum magnesium: always check – hypomagnesaemia makes hypokalaemia refractory
• U&Es: renal function, sodium, bicarbonate
• Arterial blood gas: acid-base status (metabolic alkalosis common)
• Serum bicarbonate: elevated in metabolic alkalosis
• Glucose: insulin effect on potassium

Urine

• Spot urine potassium: <20 mmol/L suggests extrarenal loss (GI); >20 mmol/L suggests renal loss
• Urine potassium:creatinine ratio: more accurate than spot potassium
• Transtubular potassium gradient (TTKG): >7 suggests renal potassium wasting

Special Tests

• Aldosterone:renin ratio (ARR): if hypertensive with hypokalaemia (screen for Conn syndrome)
• 24-hour urinary cortisol: if Cushing suspected
• Plasma renin activity: helps differentiate causes of mineralocorticoid excess

Mild Hypokalaemia (3.0-3.5 mmol/L)

• Oral replacement is usually sufficient:
  • Sando-K (potassium chloride 12 mmol per tablet): 2 tablets TDS
  • Kay-Cee-L syrup (1 mmol/mL): 20-40 mmol daily
  • Potassium-rich diet: bananas, oranges, potatoes, spinach
• Address underlying cause (reduce diuretic dose, add potassium-sparing diuretic)

Moderate to Severe Hypokalaemia (<3.0 mmol/L or symptomatic)

• IV potassium chloride replacement:
  • Maximum rate: 20 mmol/hour via central line (10 mmol/hour via peripheral – max concentration 40 mmol/L)
  • Usually given as 20-40 mmol KCl in 1L 0.9% NaCl over 2-4 hours
  • Never give potassium IV bolus (risk of cardiac arrest)
  • Cardiac monitoring essential for rates >10 mmol/hour
• Correct magnesium first or simultaneously: IV magnesium sulphate 20 mmol (5g) over 6-12 hours
• Recheck K every 2-4 hours during IV replacement

Specific Situations

• Diuretic-induced: add amiloride 5-10mg or spironolactone 25-50mg, or switch to potassium-sparing diuretic
• Digoxin therapy: maintain K >4.0 mmol/L (hypokalaemia increases digoxin toxicity)
• Conn syndrome: spironolactone 100-400mg daily or surgical adrenalectomy
• Refeeding syndrome: aggressive K, Mg, phosphate replacement with caloric restriction

Referral Criteria

• Refractory hypokalaemia → investigate for Conn syndrome, Cushing, Bartter/Gitelman
• Severe hypokalaemia with arrhythmias → critical care
• Recurrent hypokalaemia with hypertension → endocrinology

• Mild hypokalaemia has excellent prognosis with correction of underlying cause
• Severe hypokalaemia (<2.5 mmol/L) is life-threatening due to arrhythmia risk
• Hypokalaemia in acute MI doubles mortality
• Digoxin toxicity is potentiated by hypokalaemia – can be fatal
• Chronic mild hypokalaemia is associated with increased risk of glucose intolerance and hypertension
• Most drug-induced hypokalaemia is readily reversible with dose adjustment or supplementation

ECG Changes in Hypokalaemia (progressive)

Potassium Replacement Guide

Causes by Acid-Base Status