Management of acute hyperkalaemia: evidence, practice and pitfalls

Acute hyperkalaemia is a medical emergency requiring rapid clinical evaluation.Point-of-care blood gas analysis may overestimate serum potassium concentration and should be confirmed with a laboratory sample unless urgent treatment is required.When ECG (electrocardiogram) changes are present, immediate cardiac protection is a priority.Current guidelines recommend administering intravenous 10% calcium gluconate to restore cardiac conduction velocity.Intravenous insulin rapidly shifts potassium into cells.It is given with intravenous dextrose to reduce the risk of hypoglycaemia.A reduced insulin dose can be considered in patients with significant kidney dysfunction.Salbutamol shifts potassium into cells and has a synergistic effect with insulin.Nebulised salbutamol administration offers similar efficacy to intravenous delivery with fewer adverse effects.The routine use of intravenous sodium bicarbonate or oral potassium binders is not recommended for immediate lowering of serum potassium in acute hyperkalaemia.Sodium bicarbonate should be reserved as an adjunctive treatment for patients with concurrent metabolic acidosis.Post-acute care focuses on addressing reversible triggers and, once hyperkalaemia resolves, restarting important drugs that can increase potassium concentrations, if their benefit outweighs the risk (e.g.renin-angiotensin-aldosterone system inhibitors).adrenal disease and the use of drugs that may increase serum potassium concentrations (Box 1).2,3 Assessment Although there is no universally accepted definition of hyperkalaemia severity, the Kidney Disease: Improving Global Outcomes (KDIGO) group stratifies risk according to the absolute potassium concentration and the presence or absence of electrocardiogram (ECG) changes (Figure 1). 4 Potassium sample types and pseudohyperkalaemiaPotassium concentrations can be measured via point-of-care blood gas analysis (BGA) or laboratory samples.The results from these are not directly interchangeable because BGA measures whole-blood concentrations whereas laboratory serum samples require clotting, which releases potassium from platelets and leucocytes.Consequently, laboratory serum potassium concentrations are typically 0.2 to 0.3 mmol/L higher than matched BGA results.5 BGA does not detect pseudohyperkalaemia (falsely raised potassium concentrations), which can be caused by haemolysis of the sample, severe thrombocytosis, This article provides an overview of the acute management of moderate to severe hyperkalaemia, summarising current evidence and highlighting practical considerations for clinicians.The management of chronic hyperkalaemia is not addressed. Risk factors for hyperkalaemiaKidney impairment is the major risk factor for developing acute hyperkalaemia, especially a glomerular filtration rate below approximately 15 mL/min. 1 Additional risk factors include diabetes,