Approach

Any condition that can cause hyperkalaemia (other than pseudohyperkalaemia) can increase serum potassium values sufficiently to result in life-threatening arrhythmias. The end-organ effects of potassium are more significant if hyperkalaemia has developed quickly.[72][73]

The management of hyperkalaemia and the urgency of initiating treatment is therefore dependant on:

  • The severity of hyperkalaemia (mild, moderate, or severe)

  • The rapidity of the rise in serum potassium (acute, chronic)

  • The clinical impact of hyperkalaemia (presence of ECG changes, symptoms, patient comorbidities).

The goals of acute management of hyperkalaemia are:[2]

  • Stabilisation of the cardiac membranes (options include intravenous calcium gluconate or calcium chloride)

  • Redistribution of potassium into cells (options include an insulin/glucose infusion and a nebulised beta-2 agonist, with or without sodium bicarbonate)

  • Elimination of potassium (options include cation-exchange resins/polymers, diuretics, and/or dialysis).

In addition, the underlying cause of the hyperkalaemia and any associated disorders (e.g., shock, hypovolaemia, heart failure, cause of acute kidney injury) should be addressed in all patients.[12]​ Renin-angiotensin-aldosterone system inhibitors (RAASi) should be withheld during acute intercurrent illness (e.g., sepsis, hypovolaemia, and/or acute kidney injury) at all severities of hyperkalaemia.[1]

The management of patients in cardiac arrest due to hyperkalaemia is not covered in this topic. See Cardiac arrest.

Severity of hyperkalaemia

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]

If hyperkalaemia-related changes are present on ECG, they may correlate with the severity and rate of rise of serum potassium.[1][4] 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 may often be normal in patients with hyperkalaemia.[12] It is important to note that relying on or expecting progressive ECG changes with increasing severity of hyperkalaemia may be misleading and potentially dangerous.[2] When treating hyperkalaemia it is therefore also important to also take into account the clinical impact of the disorder and the fluctuation in serum potassium levels.

For more detail on severity thresholds, see Criteria.

There is no clearly defined definition of chronic hyperkalaemia but the term is often used to reference persistent hyperkalaemia, which is most commonly found in patients in the community who have chronic kidney disease and/or receive RAASi.[1]

Acute hyperkalaemia with potentially life-threatening features

There is no definitive definition of hyperkalaemic emergency; determining whether emergency treatment is required is based on the severity of hyperkalaemia present, subjective clinical judgement, and ECG findings.​[1][3][12]

Initiate emergency management of hyperkalaemia on an urgent basis (before serum biochemistry is known if hyperkalaemia is suspected on clinical grounds/ECG findings) in patients with one or more of the following potentially life-threatening features:[1]

  • Severe hyperkalaemia (serum potassium ≥6.5 mmol/L [≥6.5 mEq/L])[4]

  • Moderate hyperkalaemia (serum potassium 6.0 to 6.4 mmol/L [6.0 to 6.4 mEq/L]) in addition to being clinically unwell or where a rapid rise in serum potassium is anticipated

  • Bradycardia with evidence of shock in the presence of renal failure and hyperkalaemia (which may be moderate)

  • Clinical signs and symptoms suggestive of hyperkalaemia (e.g., muscle weakness, cramps, or flaccid muscle paralysis)

  • ECG changes of hyperkalaemia (which may include cardiac conduction abnormalities [e.g., tall peaked T waves, disappearing P wave, widening of QRS] or arrhythmias [bradycardia, ventricular tachycardia]).[4]

In patients requiring emergency treatment for hyperkalaemia:

  • Seek expert help early[1][3]​​

    • This may include the involvement of a renal specialist if the patient has concurrent renal impairment

  • Administer rapidly-acting therapies to:[1][2][4][12]​​​[74][75]​​​​

    • Stabilise the myocardium and prevent or reverse dysrhythmias in the presence of ECG changes

    • Shift potassium intracellularly

  • Administer interventions that remove excess potassium from the body.[1][2]​​[4][12]

In addition:

  • Initiate continuous ECG monitoring (ideally in a higher-dependency setting), which should proceed until serum potassium values have been brought into a safe range and cardiotoxicity has resolved.[1][4]

  • Monitor serum potassium and serum glucose levels.[3][4]

    • Reassess hyperkalaemia every 2-4 hours as most temporising agents manifest their maximal effect within 2 hours, with effects wearing off at around 4 hours. At this point if serum potassium >6 mmol/L (>6 mEq/L), consider re-dosing with drugs and arranging haemodialysis.[2]

  • Consider emergency dialysis in patients with persistent ECG changes or those with an insufficient response to insulin/glucose and a beta-2 agonist. This will primarily be for patients with renal insufficiency.​[3]​​​​[4][12][76]

  • Prevent recurrence of hyperkalaemia.[3] This may include identifying and treating any underlying cause, management of risk factors, and patient education where relevant.

For management of patients in cardiac arrest due to hyperkalaemia, see Cardiac arrest.

Rapid-acting therapies to stabilise the myocardium

Give intravenous calcium (as calcium gluconate or calcium chloride) in patients with acute hyperkalaemia requiring emergency treatment in the presence of ECG changes consistent with cardiotoxicity.[1][2][3]​​​[4][12][76]​​ Note that this therapy does not lower serum potassium.

  • KDIGO states in its guideline on management of dyskalaemia in kidney diseases that it prefers the use of calcium gluconate to calcium chloride because the latter has been associated with skin necrosis.[4]

  • The UK Medicines and Healthcare products Regulatory Agency (MHRA) recommends calcium chloride in resuscitation circumstances (peri-arrest and cardiac arrest) and calcium gluconate for all other patients.[77]

  • The protective effect of calcium begins within minutes but is short-lived (30-60 minutes).[12] The dose can be repeated after 5 minutes if ECG changes persist or recur.[4]

  • Calcium should be avoided in patients with digoxin (digitalis) intoxication as it may worsen cardiotoxicity.

As the duration of effect of calcium is between 30 and 60 minutes, therapies to shift potassium into the cells or interventions to remove potassium from the body should be initiated as soon as possible after the first dose is given.[12]

Rapid-acting therapies to shift potassium intracellularly

Give an intravenous infusion of insulin/glucose and a nebulised beta-2 agonist (e.g., salbutamol) in patients with acute hyperkalaemia requiring emergency treatment with or without cardiotoxic changes on ECG.[1][2][3]​​[12]​​ This causes a shift of potassium into cells. 

Insulin/glucose and salbutamol has an additive effect reducing serum potassium by approximately 1.2 to 1.5 mmol/L (1.2 to 1.5 mEq/L).[15]​ Note that up to 40% of patients with end-stage kidney disease do not respond to beta-2 agonists, and therefore they should be given in combination with insulin/glucose.[1][78]​​​ 

  • Patients who receive insulin/glucose should undergo hourly blood glucose measurements for up to 6 hours in order to monitor for hypoglycaemia. Blood glucose monitoring is required for up to 12 hours after the infusion.[1]

  • Note that salbutamol can also be given intravenously; however, dosing and the safety profile of intravenous formulations are not established and the nebulised formulation is preferred.[2] The peak effect can be seen in 90 minutes with nebulisation and 30 minutes with intravenous administration.[79]

In addition, consider sodium bicarbonate for patients with concomitant metabolic acidosis, although data on its efficacy are conflicting and any benefits should be weighed against the impact of the additional fluid load and risk of hypernatraemia and metabolic alkalosis.[4][12]​ Note that the UK Kidney Association (UKKA; formerly the Renal Association) does not advocate the use of sodium bicarbonate in the management of acute hyperkalaemia.[1]

  • Isotonic sodium bicarbonate should be given in preference to hypertonic sodium bicarbonate.[80]

  • Studies do not support the use of sodium bicarbonate in hyperkalaemic patients when metabolic acidosis is not present.[81][82]

  • Sodium bicarbonate should not be used as the only treatment in acute treatment of hyperkalaemia due to its limited efficacy.[80][83][84]

Interventions to remove potassium from the body

Consider administration of an oral cation-exchange resin (e.g., sodium zirconium cyclosilicate) or cation-exchange polymer (e.g., patiromer) alongside the insulin/glucose infusion and nebulised beta-2 agonist.[1][2][4][12]​​​[85]​​​ These drugs bind potassium in the gastrointestinal tract, leading to an increase in faecal potassium excretion and a fall in serum potassium.

  • Oral potassium binders may play a role in the acute setting when administered in conjunction with rapid-acting therapies so that the onset action of the potassium binder follows the effect of acute treatments. The use of cation-exchange resins/polymers alongside standard therapies may prevent hyperkalaemia recurrence and the need for readministration of the standard acute therapies.[12]

  • In the US, sodium zirconium cyclosilicate and patiromer are not recommended as emergency treatments for life-threatening hyperkalaemia because of their delayed onset of action. However, in practice they are often used in the management of acute cases.[85][86]

  • In the UK (and some other countries), both drugs are recommended for use in the acute setting for life-threatening hyperkalaemia alongside standard care.​[85][86][87][88]

  • A large study is currently being undertaken to establish the role of patiromer in the acute treatment of hyperkalaemia.[89]​ 

  • Sodium zirconium cyclosilicate is preferred over patiromer in the acute setting because of its rapid onset of action.

Consider emergency dialysis in the following settings (seek expert help early):

  • Patients with end-stage renal failure (dialysis dependent) presenting with hyperkalaemia, as medical therapies will only temporise​[3][12][76]

  • Patients with acute kidney injury with severe hyperkalaemia if unresponsive to medical treatment​[3][12][76]

  • Severe hyperkalaemia in the presence of life-threatening ECG changes where more rapid control of hyperkalaemia may avoid cardiac arrest; vascular access will be required if the patient does not already have it[2] 

  • Patients in whom potassium level is rising rapidly (e.g., rhabdomyolysis).

Consider an intravenous loop diuretic (e.g., furosemide) in patients with hypervolaemia, unless the patient is anuric or has end-stage kidney disease.[2][4][12]​​ In the author’s opinion, a thiazide diuretic (e.g., chlorothiazide) may also be an option in patients with adequate renal function. In euvolaemic patients, concurrent saline infusion and diuretics can be administered to increase urine flow rate and thereby potassium excretion. Note, however, that the UKKA does not advocate the use of diuretics in the management of acute hyperkalaemia.[1]

  • Although there is little evidence to support the use of diuretics in acute hyperkalaemia, some guidelines state that they may be considered for use as an adjunct in patients with acute hyperkalaemia requiring emergency management.[2][4][12]​​​​

  • Ensure that the patient does not become volume depleted with diuretic therapy as dehydration will slow urine flow rate; as a result, potassium values may no longer drop with therapy and may even rise.

Patients with significant hyperglycaemia

In situations where the patient has significant hyperglycaemia, such as in diabetic ketoacidosis and hyperosmolar hyperglycaemic states, hyperkalaemia is due to movement of potassium out of the cells (although the total body potassium is reduced).

  • Administer insulin and fluids to cause intracellular shift of potassium, thereby correcting hyperkalaemia.[55]​ Consult your local protocols.

  • Treatment of the hyperglycaemia is required before the level of total body potassium depletion can be accurately gauged. See Hyperosmolar hypoglycaemic state and Diabetic ketoacidosis.

Acute hyperkalaemia without potentially life-threatening features

Patients with acute hyperkalaemia who do not meet the criteria for emergency treatment (i.e., patients with moderate hyperkalaemia who are not acutely unwell and do not have ECG changes, and patients with mild hyperkalaemia who are acutely unwell) do not require rapidly-acting therapies such as insulin/glucose, a nebulised beta-2 agonist, or treatment to stabilise the cardiac membrane. Instead, they require therapies that remove potassium from the body.[1][2]​​[12]

Arrange urgent dialysis for patients with hyperkalaemia receiving long-term haemodialysis.[1] Dialysis is the definitive treatment for hyperkalaemia in patients on long-term haemodialysis therapy.

  • Note that severe hyperkalaemia in this subset of patients should be treated as described above for patients requiring emergency treatment of hyperkalaemia if dialysis is not immediately available; if ECG changes associated with hyperkalaemia are present, intravenous calcium should be given alongside dialysis.[1]

Consider the use of oral cation-exchange resin/polymers in hospitalised patients with moderate hyperkalaemia who are not actively unwell.[85]

  • In the US, sodium zirconium cyclosilicate and patiromer are not recommended as acute treatment options because of their delayed onset of action. However, in practice they are often used in the management of acute cases.[85][86]

  • A large study is currently being undertaken to establish the role of patiromer in the acute treatment of hyperkalaemia.[89] 

  • When used in the acute setting, sodium zirconium cyclosilicate is preferred over patiromer because of its rapid onset of action.

  • In the UK (and some other countries), both drugs are recommended for use in the acute setting for life-threatening hyperkalaemia alongside standard care.​[85][86][87][88]

  • Also consider these drugs for patients with persistent moderate hyperkalaemia ≥6 mmol/L (≥6 mEq/L) with chronic kidney disease stage 3b-5 or heart failure who are not on dialysis, and who have previously not been able to take/or have been taking a reduced dose of a RAASi due to hyperkalaemia. Addition of these drugs may allow for reinstatement/continuation of RAASi.[1][87]​​[90][91]

​Consider an intravenous loop diuretic (with or without saline) for patients with adequate renal function (and who are not anuric) such as hospitalised patients with mild/moderate hyperkalaemia or patients who require optimisation prior to surgery (who are not actively unwell).[2][4][12]​​ Patients with moderate hyperkalaemia who are not acutely unwell may be considered for oral diuretic therapy.

  • In the author’s opinion, a thiazide diuretic (e.g., chlorothiazide) may also be an option in patients with adequate renal function.

In euvolaemic patients, concurrent saline infusion and diuretics can be administered to increase urine flow rate and thereby potassium excretion. Ensure that the patient does not become volume depleted with diuretic therapy as dehydration will slow urine flow rate; as a result, potassium values may no longer drop with therapy and may even rise. Note that the UKKA does not advocate the use of diuretics in the management of acute hyperkalaemia.[1]

Consider sodium bicarbonate in patients with metabolic acidosis who do not have volume overload.[4]

  • Also consider sodium bicarbonate for patients with chronic kidney disease (CKD) and a serum bicarbonate level <22 mmol/L (<22 mEq/L).[1]

  • Data on the efficacy of sodium bicarbonate are conflicting and any benefits should be weighed against the impact of the additional fluid load and risk of hypernatraemia and metabolic alkalosis.[4][12]

  • Studies do not support the use of sodium bicarbonate in patients with hyperkalaemia when metabolic acidosis is not present.[81][82]

Chronic hyperkalaemia

​Treatment in patients with chronic hyperkalaemia who present in the community should be guided by the severity of hyperkalaemia as well as the clinical condition of the patient:[1]

  • Admit all patients with confirmed severe hyperkalaemia (serum potassium ≥6.5 mmol/L [≥6.5 mEq/L]) in the community for urgent hospital assessment and management (treat as per patients requiring emergency management recommendation above)

  • Consider hospital admission for acutely unwell patients with confirmed mild hyperkalaemia (serum potassium 5.5 to 5.9 mmol/L [5.5 to 5.9 mEq/L]) or moderate hyperkalaemia (serum potassium 6.0 to 6.4 mmol/L [6.0 to 6.4 mEq/L]), particularly in the presence of an acute kidney injury. RAASi should be withheld during acute intercurrent illness (e.g., sepsis, hypovolaemia, and/or acute kidney injury) at all severities of hyperkalaemia.[1]

Patients with persistent mild hyperkalaemia (serum potassium 5.5 to 5.9 mmol/L [5.5 to 5.9 Eq/L]) or those with persistent moderate hyperkalaemia (6.0 to 6.4 mmol/L [6.0 to 6.4 Eq/L]) who are not acutely unwell may be managed in the community.[1] Management may include:[1]

  • Treatment of any underlying causes, including a drug history review (see below)

  • Review of dietary potassium intake

  • Methods to remove potassium from the body (e.g., initiation of cation-exchange resins/polymers and diuretics)

  • Treatment of metabolic acidosis.

Review of dietary potassium intake

Provide information to patients with chronic hyperkalaemia regarding dietary sources of potassium, and methods of reducing potassium intake via diet.[1][4]​​ Advise patients with end-stage kidney disease on dialysis that a low-potassium diet and compliance with dialysis are key in preventing hyperkalaemia.[1][13][14][15]​​

  • These patients should avoid periods of fasting, as this can lead to increased potassium movement out of the cells due to decreased insulin secretion and also causes resistance to beta-adrenergic stimulation of potassium uptake.[14][15] Note that this can also occur in haemodialysis patients who do not have diabetes.[14]

  • Patients on dialysis who have diabetes should also have their glycaemic control optimised to help prevent hyperkalaemia.[1]

Methods to remove potassium from the body

Consider sodium zirconium cyclosilicate or patiromer for patients with persistent moderate hyperkalaemia ≥6 mmol/L (≥6 mEq/L) with chronic kidney disease stage 3b-5 or heart failure who are not on dialysis, and who have previously not been able to take/or have been taking a reduced dose of RAASi due to hyperkalaemia. Addition of these drugs may allow for reinstatement/continuation of RAASi.[1][88][87]​​[90][91]​​ These drugs should be initiated in secondary care only and should be stopped if RAASi are discontinued.[1][87]

Consider a loop diuretic (e.g., furosemide) as an adjunct in patients with chronic mild to moderate hyperkalaemia who are not oliguric and are volume replete.[1] A thiazide diuretic (e.g., chlorothiazide) may also be an option in patients with adequate renal function.[1] Ensure that the patient does not become volume depleted with diuretic therapy as dehydration will slow urine flow rate; as a result, potassium values may no longer drop with therapy and may even rise.

Treatment of metabolic acidosis

Consider sodium bicarbonate for patients with hyperkalaemia and chronic kidney disease and metabolic acidosis (serum bicarbonate level <22 mmol/L [<22 mEq/L]).[1] Note that data on the efficacy of sodium bicarbonate are conflicting, and any benefits should be weighed against the impact of the additional fluid load and risk of hypernatraemia and metabolic alkalosis.[4][12] KDIGO notes that there is no evidence to support the correction of coincident acidosis in these patients.[4] Studies do not support the use of sodium bicarbonate in hyperkalaemic patients when metabolic acidosis is not present.[81][82]

Treatment of the underlying cause

​Address the underlying causes of hyperkalaemia in all patients presenting with hyperkalaemia, as well as any associated disorders.[1][4][12]​​​

Optimise existing drug therapies that may cause or contribute to hyperkalaemia - including treatment with RAASi, aldosterone antagonists, or trimethoprim.[1][4]​​​ RAASi should be withheld in all patients who are acutely unwell.[1]

Take into consideration that:

  • Hyperkalaemia associated with RAASi and aldosterone antagonists is dose-dependent and most significant when potassium is given concurrently, a potassium-enriched diet is being ingested, and a level of renal failure is present. If a patient is taking multiple RAASi or aldosterone antagonists, the risk of hyperkalaemia is significantly increased.[18][19][20]

  • The change in serum potassium associated with trimethoprim is also dose-dependent and greatest in older people, those with diabetes, and patients with renal insufficiency.

  • 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]

This list is not exhaustive and you should consult your local drug formulary for more information.

Other underlying causes of hyperkalaemia that that may need to be addressed include:

  • Shock. See Shock.

  • Hypovolaemia. See Volume depletion in adults. 

  • Heart failure.[1][2]​​[12][23]​​​ See Chronic heart failure.

  • Metabolic acidosis. See Assessment of metabolic acidosis. 

  • Digoxin toxicity. See Digoxin toxicity.

  • Mineralocorticoid deficiency. See Primary adrenal insufficiency.

  • Renal tubular acidosis.[66][67][68]​​ See Renal tubular acidosis.

  • Pseudohypoaldosteronism

  • Hypoaldosteronism or aldosterone resistance

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

  • Liver disease.[1][11]​​​​ See Assessment of liver dysfunction.

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

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

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