Hyperkalemia

 

• Background

  Definition and classification

  • Mild: K+ ≥5.5 mmol/L (some say 5.4).
  • Moderate: K+ ≥6.0 mmol/L.
  • Severe: K+ ≥6.5 mmol/L.

  Pathophysiology

  • ↑K+ in the serum (extracellular fluid, ECF) → ↓chemical gradient with intracellular fluid (ICF) → ↓K+ leakage from ICF → myocyte membrane depolarisation (inc. cardiac) → ↑excitability initially → later cells unable to repolarise fully so ↓excitability.
  • Other physiological effects: ↓NH4+ production, ↑insulin secretion.

  Causes

  ↓Excretion of K+:

  • Kidney failure – AKI or CKD – and its causes e.g. hypovolaemia, sepsis.
  • Drugs: spironolactone, amiloride, ACEi, A2RB, NSAIDs.
  • Addison's
  • Metabolic acidosis.
  • Gordon's syndrome.

  Movement of K+ from ICF→ECF:

  • Acidosis
  • Tissue damage: rhabdomyolysis (e.g. from trauma, intense exercise), tumour lysis syndrome.
  • Drugs: digoxin, mannitol, suxamethonium, β-blockers.

  ↑Intake of K+:

  • KCl (iatrogenic).
  • Salt substitutes.
  • Large blood transfusions.

  A false positive test, pseudohyperkalaemia, caused by:

  • Haemolysis e.g. from difficult venepuncture, wrong order of blood bottles.
  • Delayed analysis of blood sample.
  • ↑Platelets.

• Signs and symptoms

  CV:

  • May be asymptomatic but have ECG changes.
  • Arrhythmias: altered HR, palpitations, light-headed.

  Neurological:

  • Parasthesia
  • Flaccid weakness.
  • ↓Reflexes

• Investigations

  ↑K+ detected on U&E. Consider repeat testing (or VBG) if haemolysed sample suspected.

  Get ECG if K+ >6:

  • K+ >6.0: tented T, prolonged PR.
  • K+ >6.5: flattened or absent P, wide QRS, bradycardia, ST elevation.
  • K+ >8.0: even wider QRS, sine wave, VT.

  Other tests:

  • FBC to rule out pseudohyperkalaemia.
  • Blood gas may show acidosis. Will also give instant K+ reading.
  • Ca2+ and CK in suspected rhabdomyolysis.
  • Glucose if diabetic.
  • Digoxin levels if taking.

• Management

  Consider and treat underlying cause:

  • Stop drugs: ACEi, K+-sparing diuretics, NSAIDs.

  Mild (≥5.5 mmol/L) or moderate (≥6) and normal ECG:

  • Reduce dietary intake.
  • If moderate, consider insulin IV + glucose IV ± salbutamol nebs.
  • GI cation exchangers remove K+ from the body by binding it in GI tract: Calcium Resonium (calcium polystyrene sulfonate), Kayexalate (sodium polystyrene sulfonate), patiromer.

  Severe (≥6.5 mmol/L) or ECG changes is an emergency. Monitor ECG, K+, and glucose, and treat with CIGAR:

  1. Stabilize cardiac membrane if there are ECG changes: Calcium gluconate IV (commoner) or calcium chloride IV (more Ca2+ but needs central line as risk of irritation and tissue necrosis peripherally).
  2. Shift K+ into cells: Insulin IV and Glucose IV. Salbutamol nebs (Airway dilator) can be used as an adjunct.
  3. Remove K+ from body: furosemide or – if severe renal impairment – dialysis. GI cation exchangers are sometimes used though there is no evidence of efficacy for acute K+ lowering.

• Potassium physiology

  Distribution and role:

  • Major intracellular ion (98% of it is in ICF). ECF level is normally 3.5-5.5 mmol/L.
  • Important for resting membrane potential, maintaining cell size, and pH regulation.

  Moved into ICF (leading to ↓K+ in ECF) by:

  • Insulin
  • β-agonists, which upregulate Na+/K+ ATPase.
  • Aldosterone.
  • Alkalaemia, which causes H+ to move out of cell and K+ to move in via H+/K+ exchanger.

  Moved out of ICF (leading to ↑K+ in ECF) by:

  • ↑Osmolality
  • α-agonists and β-blockers.
  • Acidaemia
  • Intense exercise.

  Renal mechanisms:

  • α-intercalated cells in collecting duct exchange H+/K+, hence ↓ in one → compensation and ↓ in the other e.g. ↓K+ → metabolic alkalosis (and vice versa).
  • Synergistic with effect of cell membrane H+/K+ exchange.