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• It is defined as measured serum k+ of > 5.5. mEq/L.

• The most common cause is factitious hyperkalemia due to intracellular potassium caused by hemolysis during phlebotomy.

• Clinical manifestation of hyperkalemia usually result from disordered membrane potential.

• Cardiac manifestation are the most serious .

• ECG changes :

  • 6.5 -7.5 mEq/L: Prolonged PR interval, tall peaked waves, short QT interval

  • 7.5 – 8.0 mEq/L: Flattening of the p wave, QRS Widening.

  • >8 mEq/L : QRS complex degrading into a sinusoidal pattern.

  
  Note the ECG changes in a patietn presented with acute renal failure. ECG shows flattening of P waves and widenening of QRS with Tall tented T waves.

Note the reappearance of P wave , reduction of height of T waves in the precordial leads & normal QRS duration after correction of potassium with medical measures.

• Cardiac dysarrythmia such as ventricular fibrillation , complete heart block, & asystole may occur.
  

• Other symptoms include neuromuscular dysfunctional weakness, paresthesia, areflexia, ascending paralysis and GI signs.

ETIOLOGY

• PSEUDOHYPERKALEMIA

  • Tourniquet use

  • Hemolysis

  • Leukocytosis

  • Thrombocytosis

• Intra to Extracellular potassium shift

  • Acidosis

  • Heavy exercise

  • β- blockade

  • Insulin deficiency

  • Digitalis intoxication

  • Hyperkalemic periodic paralysis

• Potassium load

  • Potassium supplement : food , iv , potassium containing drugs.

  • Transfusion of aged blood

  • Hemolysis

  • GI Bleeding

  • Cell destruction after chemotherapy

  • Rhabdomyolysis / crush injury

  • Extensive tissue necrosis

• Decreased potassium excretion

  • Renal failure

  • Drug : potassium sparing diuretics, β blocker , NSAID'S , ACE Inhibitors.

  • Aldosterone deficiency

  • Selective defect in renal potassium excretion: Pseudohypoaldosteronism , SLE, Sickle cell disease, Obstructive uropathy , renal transplantation, Type IV renal tubular acidosis.

TREATMENT

1. Membrane stabilisation :

• Calcium gluconate:

  • Calcium rises the action potential threshold and reduces excitability without changing the resting membrane potential. By restoring the difference the resting and threshold potential, calcium reverses the depolarisation blockade caused by hyperkalemia.

  • Inj 10% calcium gluconate 10- 20 ml IV over 2 -3 min. (Calcium chloride 3 – 4 ml IV)

  • The effect of the infusion starts in 1 – 3 minutes and last for 30 -60 minutes.

  • The dose should be repeated if there is no change in ECG findings.

2. Intracellular shift of K+

• GI Bolus :

  • 10 U of regular IV insulin is followed by 50 ml of 50 % Dextrose.

  • The effect begins in 10 -20 minutes, peaks at 30 -60 minutes and lasts for 4 – 6hours.

 Note Sine wave pattern, where QRS complex is degraded following hyperkalemia in a patient with acute renal failure, note reversal of changes in the below ECG tracing. Second  ECG even though it shows normal QRS complex P wave is still flattened indicating persistence of hyperkalemia.

• Salbutamol nebulisation :

  • 10 – 20 mg of salbitamol in 4ml NS is inhaled for 10 minutes.

  • Effect starts at 30 minutes, reaches its peak at 90 minute and last for 2 – 6 hours.

  • Salbutamol and insulin with glucose have an additive effect on plasma potassium concentration.

  • However 20% of patients with end stage renal disease are resistant to beta agonist therapy, hence the should not be used without insulin.

• Sodium bicarbonate

• Sodium bicarbonate has no role in the routine treatment of hyperklemia.

• It is reserved for patients with concomitant hyperkalemia and metabolic acidosis.

3. Removal or excretion of K+ from the body

• Diuretics

  • Furosemide : 40mg IV

• Sodium polystyrene sulfate

  • They exchange sodium for potassium ions in the GI tract and increases the fecal excretion of potassium ions.

  • : 25 – 50 gm PO OR PR. Duration of action 4 -6 hrs.

  • It is given as suspension with sorbitol to avoid constipation.

  • Adverse effect : Intestinal necrosis

• Hemodialysis.

What is transtubular pottasium gradient?

• Transtubular potassium gradient is a rapid and simple test designed to evaluate the driving force for net K+ secretions. TTKG is useful to diagnose K+ disorders, as it differentiate renal from non renal causes of hypo/hyperkalemia.

• TTKG = ([urine K+] x serum osmolality) / ([serum K+] x urine osmolality)

• Uk &Pk stands for urine & plasma potassium.

• Uosm & Posm stands for urinary & potassium osmolality.

• Normal value : 8- 9

• Low value :<3 is suggestive of renal conservation of K+ (Poor intake, diarrhoea) or impaired secretion of K+ in patients with hyperkalemia (eg: Hypoaldosteronism)

• High value: >10 is suggestive of increased urinary secretion of potassium.

Note :

• Giving calcium will increase the threshold potential ; actually it normalize the threshold level for excitation.

• Calcium gluconate should not be used in digitalis toxicity as it may precipitate arrythmia.

Updated on 28/11/2014

Reference

• Harrison

• Tintinalli

• Zirconium cyclosilicate for treatment of hyperkalemia ; JAMA 2014.