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NiinaMatikainen

Hyperkalaemia

Essentials

  • The symptoms of hyperkalaemia vary from asymptomatic to life-threatening cardiac arrhythmias.
  • The cause of hyperkalaemia may be a shift of potassium from the intracellular to the extracellular space, a disturbance in renal excretion or pseudohyperkalaemia.
  • Monitor serum potassium in patients using potassium preparations or drugs affecting the renin-angiotensin-aldosterone (RAA) system (potassium-sparing diuretics, ACE inhibitors or ATR blockers).
  • By preventing and treating hyperkalaemia, the aim is to continue the use of prognosis-improving RAAS inhibitors with the highest tolerable dose in patients with diseases such as cardiac or renal failure.
  • Haemolysis in the test tube, thrombocytosis or leucocytosis may cause pseudohyperkalaemia. Prolonged tourniquet use and fist clenching during blood sampling may cause local acidosis and hyperkalaemia.

Reference values

  • The reference values vary between laboratories and depending on the age of the patient. Do not confuse these with decision-making values. In this article, the normal plasma potassium is considered to be 3.3-4.9 mmol/l (HUSLAB, Finland). Check local reference and decision-making values.

Aetiology Aldosterone Receptor Antagonists Spironolactone and Eplerenone for Congestive Heart Failure, Aldosterone Antagonists for Preventing the Progression of Chronic Kidney Disease

  • Very rarely hyperkalaemia is caused by excessive intake of potassium. The cause is usually a shift of potassium from the intracellular to the extracellular space, a disturbance in renal excretion or a combination of these. Remember to exclude pseudohyperkalaemia that may result from in vitro haemolysis, thrombocytosis, leucocytosis or from acidosis caused by prolonged tourniquet use during blood collection.
  • Renal damage
    • Hyperkalaemia is often present in acute renal failure.
    • In chronic renal failure plasma potassium usually remains within the reference limits for a long time because of compensatory mechanisms. Furthermore, patients have become adapted to the higher than normal potassium concentration without ECG changes or clinical heart symptoms.
    • Remember obstructive uropathy and anuria as causes for hyperkalaemia.
  • Diuretics
    • Spironolactone may cause severe hyperkalaemia, particularly if the patient has renal failure or is taking ACE inhibitors, ATR blockers or potassium.
    • Other potassium-sparing diuretics (amiloride, triamterene) are usually combined with a thiazide or furosemide. Even these preparations may cause hyperkalaemia if the patient has renal failure.
  • ACE inhibitors and ATR blockers
    • Plasma potassium increases slightly. In the elderly the increase may be clinically significant if the patient has renal disease. Persons with diabetes may also be susceptible. In the case of a mild increase in a patient in whom the medication is indicated it is sufficient to monitor the potassium concentration.
  • Other drugs causing hyperkalaemia include a combination of ATR blocker and neprilysin, NSAIDs in renal disease, heparin, cyclosporin, tacrolimus, trimethoprim and lithium, and more rarely beta blockers and suxamethonium.
  • Insulin deficiency
    • Ketoacidosis
    • Hyperosmolar hyperglycaemic state
  • Severe systemic diseases resulting in acidosis
    • Acute circulatory failure
    • Tissue hypoxia
  • Extensive tissue destruction
    • Rather extensive trauma and burns
    • Rhabdomyolysis
  • Addison's disease
    • Hyperkalaemia together with dark skin pigmentation, low blood pressure and many systemic symptoms Addison's Disease and other Conditions Inducing Hypocortisolism. Caused by lack of mineralocorticoid effect.
    • Hyporeninemic hypoaldosteronism associated with diabetes, HIV, lupus, amyloidosis, digitalis intoxication and lead poisoning are rare causes of hyperkalaemia.

Symptoms

  • ECG
    • High T waves at plasma potassium concentrations in the range 5.5-6 mmol/l
    • As hyperkalaemia becomes more severe, up to 7-8 mmol/l, the QRS complex widens, ST segment is depressed, PR interval lengthens and P waves disappear.
    • There is a risk of ventricular fibrillation and asystole.
  • Muscle weakness, symptoms of paresis and paraesthesia
    • Similar to hypokalaemia

Treatment Emergency Interventions for Hyperkalaemia

  • The underlying cause or condition behind hyperkalaemia should always be treated as effectively and quickly as possible in addition to the symptomatic treatment.
  • To treat incipient hyperkalaemia or to prevent recurrence
    • In all patients
      • Start a low-potassium diet
      • Correct hypovolaemia, and
      • Discontinue any drugs possibly causing hyperkalaemia, such as NSAIDs, provided they are not prognostically relevant.
    • Start a thiazide or loop diuretic or increase its dose, if such medication is indicated.
    • Intensify dialysis treatment.
  • Urgent treatment is indicated if symptoms of muscle weakness or arrhythmia, new ECG changes consistent with hyperkalaemia, acute renal failure or some other acute condition (trauma, tumour lysis, haemorrhage, etc.) is detected.
    • Plasma potassium should be monitored for a few hours to 24 hours.

Acute symptomatic hyperkalaemia (P-K > 5.5-6.5 mmol/l)

  • As above, and if deemed necessary give a cation exchanger (patiromer, sodium zirconium cyclosilicate or, if these are not available, sodium polystyrene sulfonate). The efficacy in acute hyperkalaemia has not been studied.
  • In severe hyperkalaemia consider the following
    • Only in acidotic patients: infuse 50-100 ml of 7.5% sodium bicarbonate intravenously over 5 minutes. Repeat after 10-15 minutes if necessary.
    • Infuse glucose with insulin: infuse 200-500 ml of 10% glucose with 5 units/100 ml (1 unit/2 g of glucose) of rapid-acting or very rapid-acting insulin over 30-60 min. After insulin administration, infusion should be continued with 5% glucose in order to prevent hypoglycaemia.
    • Calcium gluconate antagonizes the cardiac effects of potassium (Calciumgluconat B. Braun® 100 mg/ml, 10 ml slowly i.v.). Digitalized patients should be treated with extreme caution. Note! The drug must not be administered via the same route as NaHCO3 (calcium carbonate will precipitate).
    • NaCl fluid therapy and furosemide (20-40 mg i.v.)
    • Beta-2 agonists (e.g. salbutamol) shift potassium into cells (with tachycardia as an adverse effect).
    • If necessary, haemo- or peritoneal dialysis, especially if the patient has renal failure or rhabdomyolysis

Chronic asymptomatic hyperkalaemia (K HASH(0x2f830d0) 5.5-6.5 mmol/l)

  • Usually no hurry to treat
  • Mostly due to renal failure and/or treatment with RAAS inhibitors
  • Active treatment of hyperkalaemia and monitoring of K levels are used to maintain or restart treatment with RAAS inhibitors and to define the highest tolerated dose.
  • Furosemide is the treatment of choice if hyperkalaemia is caused by severe renal failure.
  • Bicarbonate should be given for patients with acidosis.
  • A cation exchanger (patiromer, sodium zirconium cyclosilicate or, if these are not available, sodium polystyrene sulfonate)

References

  • Mount DB. Treatment and prevention of hyperkalemia in adults. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com/contents/treatment-and-prevention-of-hyperkalemia-in-adults (referenced 2.1.2023).
  • Ferreira JP, Butler J, Rossignol P, et al. Abnormalities of Potassium in Heart Failure: JACC State-of-the-Art Review. J Am Coll Cardiol 2020;75(22):2836-2850 [PubMed]
  • Sterns RH, Grieff M, Bernstein PL. Treatment of hyperkalemia: something old, something new. Kidney Int 2016;89(3):546-54 [PubMed]
  • Kovesdy CP. Management of Hyperkalemia: An Update for the Internist. Am J Med 2015;128(12):1281-7 [PubMed]
  • Medford-Davis L, Rafique Z. Derangements of potassium. Emerg Med Clin North Am 2014;32(2):329-47 [PubMed]

Evidence Summaries ⬆