Approach

​Most patients with hyperkalaemia are asymptomatic or have non-specific features only.​[1][2][12]​ However, be aware that some patients with significant hyperkalaemia may present with cardiac arrest, which is not covered in this topic.​[1][2][12]​ See Cardiac arrest.

A thorough history is key for a patient with suspected or confirmed hyperkalaemia in order to check for underlying causes and exclude pseudohyperkalaemia, spurious hyperkalaemia, and cellular redistribution of potassium.​​[1][2]

If hyperkalaemia is suspected, take the following key steps:

  1. Confirm elevation of potassium (potassium ≥5.5 mmol/L (≥5.5 mEq/L]) and severity of hyperkalaemia using serum potassium or blood gas measurement​​[1][2]

  2. Obtain an urgent 12-lead ECG in all hospitalised patients with a serum potassium ≥6.0 mmol/L (≥6.0 mEq/L; or use the threshold in your local protocol) to check for ECG changes that will determine the urgency and type of treatment​​[1][2]

  3. Check for kidney dysfunction and any other underlying causes of hyperkalaemia.​​[1][2]

History

The most common features of hyperkalaemia are weakness and generalised fatigue. Other common features are paraesthesia and muscle cramps. These may progress to flaccid muscle paralysis.[2] Occasionally a patient may describe:

  • Nausea and vomiting[2]

  • Diarrhoea[2]

  • Shortness of breath

  • Chest pain

  • Palpitations.

There may be features of the underlying precipitant of hyperkalaemia such as diarrhoea and vomiting, or infection, which can cause acute kidney injury.[1]

Elicit any key risk factors for hyperkalaemia.[1] Key risk factors include:

  • Kidney dysfunction (particularly end-stage kidney disease), including people receiving dialysis who are fasting or have missed dialysis[1][2][12][13][14][15]

  • Use of renin-angiotensin-aldosterone system inhibitors (RAASi), aldosterone antagonists, or trimethoprim​​[1]​​[2]​​[17][18][19][20][21][22][23][29]

  • Heart failure[1][2][12]​​[23]​​

  • Liver disease[1]

  • Tissue breakdown (e.g., rhabdomyolysis, trauma, tumour lysis syndrome, and severe hypothermia)[2][24][25][26]​​

  • Distal renal tubule defects that affect potassium excretion.[16]

Take a careful drug history. Ask about current drugs, any recent changes to drugs, and use of over-the-counter drugs or supplements (such as intake of high doses of potassium supplements).[1] Treatment with RAASi, aldosterone antagonists, or trimethoprim is strongly associated with hyperkalaemia.​​[1]​​[2]​​[17][18][19][20][21][22][23][29]​ However, many other drugs can cause hyperkalaemia, particularly when taken in combination with RAASi or aldosterone antagonists, and if there is concurrent kidney dysfunction. These include, but are not limited to:

  • Arginine[56]

  • Azole antifungals (e.g., ketoconazole)[2]

  • Beta-blockers (non-cardioselective)[2]

  • Calcineurin inhibitors (e.g., ciclosporin, tacrolimus)[4][40]​ 

  • Digoxin[2]

  • Heparin[2][38]​​

  • Isoflurane[4]

  • Lithium[2]

  • Mannitol[57]

  • Non-steroidal anti-inflammatory drugs[2]

  • Penicillins[2]

  • Pentamidine[2]

  • Potassium-sparing diuretics (e.g., amiloride, triamterene)[2]

  • Somatostatin[2]

  • Suxamethonium.[2]

In particular, certain drugs (e.g., mannitol, arginine, suxamethonium, digoxin) cause hyperkalaemia due to cellular redistribution. This list is not exhaustive and you should consult your local drug formulary for more information.

Physical examination

In general, there are no specific features on physical examination alone that lead to the diagnosis of hyperkalaemia. However, always be alert to the diagnosis if there is severe bradycardia, which results from heart block. Other features may include:

  • Extrasystoles and cardiac pauses

  • Tachypnoea, which is due to respiratory muscle weakness

  • Skeletal muscle weakness or flaccid muscle paralysis with depressed or absent deep tendon reflexes

  • Hypoactive or absent bowel sounds if ileus is present.

Initial investigations

Serum potassium

Order serum potassium in all patients.[12]​ In an emergency setting, measure potassium using arterial or venous blood gas while waiting for the results from formal laboratory measurement.[1]

There is no universally accepted definition of hyperkalaemia. However, many guidelines use a threshold of serum potassium ≥5.5 mmol/L (≥5.5 mEq/L) and the European Resuscitation Council classification of severity of hyperkalaemia, which is as follows:[1][2][3]

  • 5.5 to 5.9 mmol/L (5.5 to 5.9 mEq/L): mild

  • 6.0 to 6.4 mmol/L (6.0 to 6.4 mEq/L): moderate

  • ≥6.5 mmol/L (≥6.5 mEq/L): severe.

Note that Kidney Disease: Improving Global Outcomes (KDIGO) uses a similar scale but also adds ECG changes to categorise severity; according to the KDIGO scale, mild hyperkalaemia with ECG changes increases the severity level to moderate, and moderate hyperkalaemia with ECG changes increases the severity level to severe.[4]

It is useful to know whether serum or plasma was used for potassium measurement. Plasma potassium concentrations are on average usually 0.1 to 0.4 mmol/L (0.1 to 0.4 mEq/L) lower than serum levels due to release of potassium from platelets during coagulation.[1]

If serum potassium is elevated, exclude pseudohyperkalaemia (due to potassium released from blood cells during in vitro coagulation or errors in sample collection and/or storage) and cellular redistribution of potassium.[1][2]​​​ Assess the probability of these by reviewing the medical history (e.g., for diabetes, heart failure, chronic kidney disease), drug history, and other blood results (e.g., full blood count), as well as repeating the serum potassium level.[2] See Differentials.

12-lead ECG

Obtain an urgent 12-lead ECG in all hospitalised patients with a serum potassium level of ≥6.0 mmol/L (≥6 mEq/L; or use the threshold in your local protocol) to assess for changes associated with hyperkalaemia, which can help to determine the urgency and type of treatment required.[1]​ Note that the ECG is often normal in hyperkalaemia.[4][12]​​​ ECG changes may progress from peaked T waves to prolonged PR interval and progressive widening of QRS complex, followed by sine wave patterns, ventricular fibrillation, and asystole.[4]

If hyperkalaemia-related changes are present, they may correlate with the severity and rate of rise of serum potassium.[1]​ However, be aware that ECG changes are dependent on a variety of other factors (e.g., concurrent electrolyte abnormalities, acid-base status, prior cardiac injury), and relying on or expecting progressive ECG changes with increasing severity of hyperkalaemia may be misleading and potentially dangerous.[2]

[Figure caption and citation for the preceding image starts]: ECG changes in people with hyperkalaemiaBMJ 2009; 339:b4114. Copyright ©2009 by the BMJ Publishing Group [Citation ends].com.bmj.content.model.Caption@19f54677

Other blood tests

  • Renal chemistry (includes, in addition to potassium as discussed above, sodium, chloride, bicarbonate, urea, and creatinine): order to check for kidney dysfunction as a cause of hyperkalaemia, and to exclude cellular redistribution of potassium.

  • Plasma glucose: order to exclude hyperglycaemia, which causes cellular redistribution of potassium. This is useful in patients with known or suspected diabetes and when diabetic ketoacidosis is likely.

  • Serum calcium: order to check for hypocalcaemia as this will potentiate the toxicity of hyperkalaemia. Calcium will also be low in rhabdomyolysis, which is a cause of hyperkalaemia.

  • FBC: order (or review a recent FBC) if pseudohyperkalaemia is suspected to exclude a haematological disorder.[1]​ Hyperkalaemia in the setting of significantly elevated white cell count or platelet count with no obvious risk factor for hyperkalaemia indicates pseudohyperkalaemia.

Other investigations

Consider other investigations depending on the suspected underlying cause. These include:

  • Uric acid and phosphorus if tumour lysis syndrome is suspected.

  • Creatine kinase if rhabdomyolysis is suspected.[64][65]

  • Serum digoxin level if the patient is taking digoxin or if suicide is known to have been attempted with digoxin ingestion.

  • Cortisol and aldosterone levels if mineralocorticoid deficiency is suspected (e.g., primary adrenal insufficiency [Addison's disease]) and other potential causes of hyperkalaemia have been excluded. See Primary adrenal insufficiency.

  • Urine pH if renal tubular acidosis is suspected.[66][67][68]​ See Renal tubular acidosis.

  • Plasma renin activity if pseudohypoaldosteronism is suspected.

  • 24-hour urine potassium excretion to distinguish renal from extrarenal causes of hyperkalaemia.

  • Plasma and urine potassium and osmolality to calculate transtubular potassium gradient, if values from 24-hour urine potassium secretion are difficult to interpret or to identify impaired distal tubular secretion of potassium due to hypoaldosteronism or aldosterone resistance.

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