NephrologyTier 1Disease (DEADMAN)

Hypokalaemia

Description

K+ <3.5 mmol/L; severe <2.5 mmol/L
Reflects either transcellular shift or a true total-body deficit - management differs

Common - up to 20% of hospitalised patients, mostly diuretic-related
More clinically dangerous in patients with structural heart disease or on digoxin

Transcellular shift (no true deficit)

Insulin, beta-agonists (salbutamol), alkalosis, refeeding syndrome, hypothermia, periodic paralysis

Renal loss

Diuretics (loop, thiazide) - commonest cause overall
Mineralocorticoid excess - primary hyperaldosteronism, Cushing's, renin-secreting tumour, liquorice
Renal tubular acidosis type 1 (distal) and type 2 (proximal) - both cause hypokalaemia (type 4 causes hyperkalaemia)
Bartter syndrome (loop mimic), Gitelman syndrome (thiazide mimic) - both present with metabolic alkalosis
Magnesium depletion - impairs renal K+ conservation; hypokalaemia refractory to replacement until Mg2+ corrected

Extrarenal loss

Vomiting (also alkalosis + volume depletion -> secondary hyperaldosteronism worsens K+ loss), diarrhoea (usually with acidosis), laxative abuse, villous adenoma

Confirm and characterise

Repeat to exclude spurious result (haemolysis, delayed processing, marked leucocytosis)
Urine K+/creatinine or 24h urine K+ - distinguishes renal (inappropriately high) from extrarenal loss (appropriately low, kidney conserving K+)
Check Mg2+, VBG (acid-base pattern narrows the differential), BP (hypertension suggests mineralocorticoid excess)

ECG changes - correlate poorly with severity but assess if K+ <3.0 or symptomatic

Flattened/inverted T waves, U waves, ST depression, PR prolongation
Severe - arrhythmia, especially torsades de pointes, digoxin toxicity potentiated

Replacement

Oral replacement preferred if K+ >2.5-3.0 and asymptomatic
IV replacement if severe, symptomatic, ECG changes, or unable to tolerate oral
- Max peripheral IV rate ~10 mmol/h (up to 20 mmol/h with continuous cardiac monitoring via central line in critical care)
- Never as an IV push/bolus - fatal arrhythmia risk
Check and correct Mg2+ simultaneously - hypokalaemia will not correct with hypomagnesaemia untreated
Recheck K+ 2-4 hourly during active IV replacement

Treat the cause

Reduce/switch diuretic, add potassium-sparing agent (spironolactone, amiloride) if diuretic-induced and ongoing need
Investigate for mineralocorticoid excess if hypertensive + unprovoked hypokalaemia

Rhabdomyolysis (severe, prolonged hypokalaemia)
Ileus, muscle weakness/paralysis (periodic paralysis)
Nephrogenic diabetes insipidus (chronic hypokalaemia impairs urinary concentration)
Digoxin toxicity potentiation

Mild, easily corrected hypokalaemia - benign
Severe or refractory hypokalaemia - investigate for an underlying cause (RTA, mineralocorticoid excess, Bartter/Gitelman) rather than treating indefinitely with supplements alone
Recurrent hypokalaemia with hypertension warrants aldosterone:renin ratio testing

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