Hypokalaemia

Hypokalaemia is a serum potassium below the reference range, graded as mild (3.0–3.4 mmol/L), moderate (2.5–2.9 mmol/L) and severe (<2.5 mmol/L).

It is among the commonest electrolyte abnormalities in hospital practice and is a well recognised precipitant of arrhythmia, particularly in patients on digoxin or with underlying cardiac disease.

Causes include renal loss (diuretics, particularly thiazides and loop diuretics, hyperaldosteronism, Cushing's syndrome, renal tubular acidosis, Bartter and Gitelman syndromes, hypomagnesaemia), gastrointestinal loss (vomiting, diarrhoea, laxative misuse, fistulae, villous adenoma), transcellular shift (insulin, beta-agonists, alkalosis, refeeding, thyrotoxic periodic paralysis) and, less commonly, inadequate intake alone.

• Frequently asymptomatic, particularly with mild or gradually developing hypokalaemia, and detected incidentally
• Neuromuscular: weakness (typically proximal and ascending), fatigue, cramps, myalgia, and in severe cases paralysis and respiratory muscle involvement
• Gastrointestinal: constipation, abdominal distension, and ileus
• Cardiac: palpitations and arrhythmia, with ECG changes including T wave flattening, ST depression, and prominent U waves, and, in severe cases, ventricular ectopics, ventricular tachycardia and torsades de pointes
• Renal: polyuria and polydipsia from a nephrogenic diabetes insipidus effect, and, in prolonged hypokalaemia, structural tubular changes
• Rhabdomyolysis in severe depletion

Symptoms correlate poorly with the absolute value, and severe weakness or arrhythmia can occur at levels that seem only moderately low, particularly if the fall has been rapid.

Correcting magnesium is the step most often missed and the commonest reason potassium replacement fails. Hypomagnesaemia promotes renal potassium wasting, and until magnesium is replaced, potassium will continue to be lost no matter how much is given. Check magnesium in every case of hypokalaemia, and replace it in parallel rather than sequentially.

Oral replacement is preferred where the patient is stable, tolerating oral intake, and the deficit is mild to moderate: potassium chloride, in divided doses, with the deficit typically being far larger than the serum value suggests (a fall of 1 mmol/L may represent a total body deficit of 200–400 mmol).

Intravenous replacement is indicated for severe hypokalaemia, symptomatic patients, arrhythmia, or where oral intake is not possible:

• Peripheral infusion should not exceed 10 mmol/hour and concentrations above 40 mmol/L are painful and sclerosing
• Faster rates (up to 20 mmol/hour) require central access and continuous cardiac monitoring, and are reserved for life-threatening hypokalaemia
• Never give potassium as a bolus or undiluted push — this is a well documented cause of fatal cardiac arrest
• Use saline rather than dextrose as the carrier where possible, since dextrose stimulates insulin release and drives potassium further into cells

Alongside:

• Recheck potassium regularly during replacement, at least every few hours during intravenous correction
• Identify and treat the cause: review diuretics, consider hyperaldosteronism in hypokalaemia with hypertension, and consider surreptitious vomiting or laxative use where the cause is unclear
• ECG monitoring for severe hypokalaemia
• In digoxin-treated patients, maintain potassium in the upper part of the reference range, since hypokalaemia potentiates digoxin toxicity

Referral: endocrinology if hyperaldosteronism or Cushing's syndrome is suspected; nephrology for renal tubular causes or recurrent unexplained hypokalaemia.