Causes — grouped by acid-base status
Sorting the causes by the accompanying acid-base picture is a useful exam approach:
Hypokalaemia with alkalosis
- Vomiting / nasogastric losses
- Diuretics (thiazides, loop)
- Conn's syndrome (primary hyperaldosteronism)
- Cushing's syndrome
Hypokalaemia with acidosis
- Diarrhoea
- Renal tubular acidosis (types 1 and 2)
- Acetazolamide
Also consider hypomagnesaemia (causes refractory hypokalaemia) and transcellular shift (insulin, salbutamol, alkalosis).
Clinical features
- Muscle weakness, cramps and, if severe, paralysis
- Cardiac arrhythmias — particularly with digoxin
- Constipation/ileus
- Polyuria (impaired concentrating ability)
ECG changes
- U waves
- Small or inverted T waves
- ST depression
- Prolonged PR and long QT
Management
- Replace potassium — oral where possible; IV for severe or symptomatic hypokalaemia, at a controlled rate with cardiac monitoring
- Correct magnesium — hypokalaemia is often refractory until hypomagnesaemia is treated
- Treat the underlying cause
MRCP-specific traps
- Refractory hypokalaemia — check and replace magnesium.
- Hypokalaemia plus hypertension and alkalosis suggests Conn's syndrome.
- Hypokalaemia potentiates digoxin toxicity.
Summary
Group hypokalaemia by acid-base status: with alkalosis (vomiting, diuretics, Conn's, Cushing's) or with acidosis (diarrhoea, renal tubular acidosis). Look for weakness and U waves on the ECG. Replace potassium (IV if severe) and always correct magnesium.
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