Hyperkalaemia

Clinical Cases

Causes of HYPERkalaemia

  • Serum potassium levels above the normal range (3.5-5.0 mmol/L)

1) Increased potassium intake (rare)

  • Oral (potassium supplements)
  • IV (transfusion of stored blood, supplement infusions)

2) Increased production

  • Tissue injury
    • Rhabdomyolysis, tumour lysis syndrome
    • Burns, ischaemia, haemolysis
    • Intense physical activity

3) Decreased renal excretion

  • Renal failure (ARF and CRF)
  • Aldosterone (Mineralocorticoid acting on collecting duct to reabsorb Na and excrete K and maintain intravascular volume)
    • Hypoaldosteronism, Addison’s, Chronic active hepatitis
  • Obstructive uropathy

4) Transcellular shift

  • Acidosis:
    • Metabolic acidosis (DKA, mineral acid overdose)
    • HYPERglycaemia
    • Respiratory acidosis

5) Fictitious (Pseudohyperkalaemia)

  • Laboratory error
  • Haemolysis of sample, clenched fist, ischaemic tourniquet
  • Leucocytosis, thrombocytosis

6) Drugs causing hyperkalaemia

  • Transcellular
    • Suxamethonium, Beta blockers, phenylephrine
  • Aldosterone inhibition
    • ACE inhibitors, Angiotensin II blockers
    • Heparin, spironolactone, Beta blockers
  • Increased aldosterone resistance (Trimethoprim, amiloride)
  • Inhibition Na/K/ATPase (Digoxin)
  • Potassium supplements and IV additives (Increase exogenous potassium)

Clinical

  • Muscle weakness
  • Lethargy
  • Ascending paralysis
  • Respiratory failure

Complications

Cardiac Arrhythmia

Correction

  1. Membrane stabilization
    • Calcium chloride/gluconate
  2. ECF – ICF shift
    • Sodium bicarbonate
    • Insulin/dextrose
    • Beta agonists (Salbutamol)
  3. Removal of K from body
    • Urine – Frusemide
    • Faeces – Resonium
    • Blood – Dialysis

Correction principles for hyperkalaemia

MILD (5-6mEq/L)

  • Diuretic-Frusemide
  • Calcium resonium- sodium polystyrene sulphate 100/gram.
    • PO or PR 6 hourly
    • Exchange resin with 1mmol K for every gram used.

MODERATE (6-7)

  • Glucose-insulin (10U insulin 50G dextrose)
    • IV over 20-30 mins
    • Decrease K 0.6-1.0
    • Onset 15mins duration 60 mins
  • Sodium bicarbonate (50ml 8.4% (50mEq/L) over 5 mins)
    • Increase alkalinity so reduce K
    • HCO3 increase causes extrusion of H from cells in return for K
    • Onset 5 mins duration 2 hrs
    • Especially in ARF with metabolic acidosis
  • Salbutamol (nebulised 20mg) (iv 500mcg or 5 mcg/kg NOT if IHD)
    • Additive effect in combination with insulin
    • Binds to B receptors and activate Na-K-ATPase to increase intracellular K

SEVERE (>7) (Toxic ECG changes)

  • Calcium
    • Calcium chloride (10%) 10ml iv 5 mins
    • Calcium Gluconate (10%) 20ml iv 5 mins
      • Antagonise toxic effects of K on the myocardium and lower the risk of VF
      • Immediate onset , duration 5 mins, but transient effect (30 minutes)
      • ALL patients with severe ECG changes
      • NOTE may potentiate digoxin toxicity
  • Dialysis most rapid and effective method

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