Hyperkalaemia CCC

Clinical Cases

• Hyperkalaemia DDx
• Hyperkalaemia management
• Hyperkalemia Case Study

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