• Mild – 3.0-3.5
  • Moderate – 2.5-3.0
  • Severe – <2.5

Aetiologies

  • can remember with the mnemonic Dr froM MIT:
    • Decreased intake (e.g. poor dietary intake, starvation)
    • Hypomagnesaemia which results in increased potassium loss
    • Mineralocorticoid excess
      • Cushing syndrome
      • Primary aldosteronism
      • Renal vascular hypertension
      • Renin producing tumour
      • Adrenogenital syndrome
      • Licorice excess
      • Bartter syndrome
      • Liddle syndrome
    • Increased loss
      • Drugs (digoxin, diuretics, laxatives, liquorice, steroids, antibiotics (carbapenems, gentamicin, amphortericin B))
      • Skin - profuse sweating, extensive burns
      • GI - diarrhoea, vomiting, ileostomy, intestinal fistula, villous adenoma, laxatives
      • Renal - tubular disorders, nephrogenic DI
      • Endocrine - hyperaldosteronism, Cushing syndrome, Conn syndrome
      • Dialysis - haemodialysis on low dialysate,peritoneal dialysis
    • Transcellular shift
      • Insulin/glucose therapy
      • Beta-agonists
      • Alkalosis: respiratory and metabolic
      • Hypokalaemic periodic paralysis

Clinical Features

  • Muscles - weakness (legs > arms), cramps, ileus, rhabdomyolysis
  • Cardiac conduction abnormalities
    • Dangerous arrhythmias are more common when hypokalaemia also occurs with QT prolonging drugs, digoxin toxicity, Hypomagnesaemia, coronary ischaemia

Assessment

History

  • fatigue
  • muscle cramps
  • weakness
  • constipation
  • rhabdomyolysis
  • ascending paralysis
  • respiratory failure
  • arrhythmias
  • symptoms more likely in pre-existing heart disease (IHD, CHF, LVH)
  • medications: cause of hypokalaemia and also anti-arrhythmics (sotalol → increased risk of arrhythmias)

Examination

Investigations

  • ECG
  • EUC
  • CMP
  • Digoxin level if on digoxin

Workup

  1. Most aetiologies are evident from history
  2. Assess magnesium level
  3. Check acid base status and measure urine potassium excretion

Management

  • Replace magnesium as fascilitates a more rapid correction of hyperkalaemia

  • For patients with hypokalaemia in the setting of essential diuretic use (e.g. heart failure) or hyperaldosteronism, a potassium-sparing diuretic is usually more effective than chronic potassium replacement
  • In stable patients, the maximum IV dose of potassium is 20 mmol/h
  • In unstable arrhythmias or when cardiac arrest is imminent use 2 mmol/min (20mmol total) for 10 minutes followed by 10 mmol over 5-10 minutes and magnesium 10mmol over 10 minutes
  • During cardiac arrest
    • Give a 5 mmol bolus, repeat as required
    • Give a 5 mmol bolus of IV magnesium sulfate, may repeat once, then 20 mmol over 4 h infusion
    • Stop precipitants: e.g. furosemide infusion, β-agonists (salbutamol), insulin without adequate and glucose-containing fluids (drives intracellular potassium shift)
    • Aim for potassium ≥ 4.0 mmol/L before discontinuing aggressive replacement
    • Consider beta-blockade (e.g. esmolol) is an emerging adjunct for refractory VF due to adrenergically driven arrhythmia (e.g. caffeine, salbutamol, thyroid storm)

Sources