Treatment algorithm

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

ACUTE

acute hyperkalaemia with potentially life-threatening features

1st line – calcium

Back
ACUTE
|
acute hyperkalaemia with potentially life-threatening features
|
with ECG changes
1st line – 

calcium

Initiate emergency management of hyperkalaemia on an urgent basis (before serum biochemistry is known if hyperkalaemia is suspected on clinical grounds/ECG findings) in all patients with 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]).[1][4]​​​

Seek expert help early.[1][3]​​​​​ This may include the involvement of a renal specialist if the patient has concurrent renal impairment.

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

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

  • Kidney Disease: Improving Global Outcomes (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 two calcium salts are not equivalent in terms of calcium dose. Be alert to the risk of inadvertent underdosing if calcium gluconate is used instead of calcium chloride.[77]

  • The protective effect of calcium begins within minutes but is short-lived (30-60 minutes).[12] The dose can be repeated in 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] 

Primary options

calcium gluconate: consult local protocol for dose guidelines

More

OR

calcium chloride: consult local protocol for dose guidelines

More

Plus – insulin/glucose

Back
ACUTE
|
acute hyperkalaemia with potentially life-threatening features
|
with ECG changes
Plus – 

insulin/glucose

Treatment recommended for ALL patients in selected patient group

Give an intravenous infusion of insulin/glucose (in addition to salbutamol) according to local protocols.[1][2][3]​​[12]​​​​​ This causes a shift of potassium into cells.

Insulin/glucose (with 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]

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]

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. Consult your local protocols.

  • Treatment of the hyperglycaemia is required before the level of total body potassium depletion can be accurately gauged.

Primary options

insulin neutral: 5-10 units intravenously as a single dose

More

Plus – salbutamol

Back
ACUTE
|
acute hyperkalaemia with potentially life-threatening features
|
with ECG changes
Plus – 

salbutamol

Treatment recommended for ALL patients in selected patient group

Give a nebulised beta-2 agonist such as salbutamol (in addition to insulin/glucose).[1][2][3]​​[12]​​​​ This causes a shift of potassium into cells.

Note that up to 40% of patients with end-stage kidney disease do not respond to beta-2 agonists alone, and they should be used in combination with insulin/glucose.[1][78]​​​ 

Note that salbutamol can also be given intravenously; however, dosing and 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]

Primary options

salbutamol inhaled: 10-20 mg nebulised as a single dose

Plus – treatment of underlying cause

Back
ACUTE
|
acute hyperkalaemia with potentially life-threatening features
|
with ECG changes
Plus – 

treatment of underlying cause

Treatment recommended for ALL patients in selected patient group

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 renin-angiotensin-aldosterone system inhibitors (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, and Hypothermia

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

Consider – sodium bicarbonate

Back
ACUTE
|
acute hyperkalaemia with potentially life-threatening features
|
with ECG changes
Consider – 

sodium bicarbonate

Additional treatment recommended for SOME patients in selected patient group

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 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]

Primary options

sodium bicarbonate: consult local protocol for dose guidelines

Consider – cation-exchange resin/polymer

Back
ACUTE
|
acute hyperkalaemia with potentially life-threatening features
|
with ECG changes
Consider – 

cation-exchange resin/polymer

Additional treatment recommended for SOME patients in selected patient group

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.[1][2][4][12]​​​​[85]​​ 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.

Primary options

sodium zirconium cyclosilicate: 10 g orally three times daily for up to 48 hours initially, followed by 10 g once daily, adjust dose according to response and serum potassium levels (range 5 g every other day to 15 g once daily)

OR

patiromer: 8.4 g orally once daily initially, adjust dose according to response and serum potassium levels, maximum 25.2 g/day

Consider – emergency dialysis

Back
ACUTE
|
acute hyperkalaemia with potentially life-threatening features
|
with ECG changes
Consider – 

emergency dialysis

Additional treatment recommended for SOME patients in selected patient group

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 – diuretic

Back
ACUTE
|
acute hyperkalaemia with potentially life-threatening features
|
with ECG changes
Consider – 

diuretic

Additional treatment recommended for SOME patients in selected patient group

Consider an intravenous loop diuretic (e.g., furosemide) in patients with hypervolaemia, unless the patient is anuric, has severe volume depletion, 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 that the UK Kidney Association 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, they may be considered for use as adjuncts in a hyperkalaemic emergency.[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.

Primary options

furosemide: 20-40 mg intravenously initially, may increase by 20 mg every 2 hours according to response

Secondary options

chlorothiazide: 500-1000 mg intravenously once or twice daily

1st line – insulin/glucose

Back
ACUTE
|
acute hyperkalaemia with potentially life-threatening features
|
without ECG changes
1st line – 

insulin/glucose

Initiate emergency management of hyperkalaemia on an urgent basis (before serum biochemistry is known if hyperkalaemia is suspected on clinical grounds) 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 6.4mEq/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).

Give an intravenous infusion of insulin/glucose (in addition to salbutamol) according to local protocols.[1][2][3]​​​[12]​​​​​ This causes a shift of potassium into cells.

Insulin/glucose (with 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]

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]

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. Consult your local protocols.

  • Treatment of the hyperglycaemia is required before the level of total body potassium depletion can be accurately gauged.

Primary options

insulin neutral: 5-10 units intravenously as a single dose

More

Plus – salbutamol

Back
ACUTE
|
acute hyperkalaemia with potentially life-threatening features
|
without ECG changes
Plus – 

salbutamol

Treatment recommended for ALL patients in selected patient group

Give a nebulised beta-2 agonist such as salbutamol (in addition to insulin/glucose).[1][2][3]​​[12]​​​​ This causes a shift of potassium into cells.

Note that up to 40% of patients with end-stage kidney disease do not respond to beta-2 agonists alone, and they should be used in combination with insulin/glucose.[1][78]​​​

Note that salbutamol can also be given intravenously; however, dosing and 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]

Primary options

salbutamol inhaled: 10-20 mg nebulised as a single dose

Plus – treatment of underlying cause

Back
ACUTE
|
acute hyperkalaemia with potentially life-threatening features
|
without ECG changes
Plus – 

treatment of underlying cause

Treatment recommended for ALL patients in selected patient group

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 renin-angiotensin-aldosterone system inhibitors (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, and Hypothermia

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

Consider – sodium bicarbonate

Back
ACUTE
|
acute hyperkalaemia with potentially life-threatening features
|
without ECG changes
Consider – 

sodium bicarbonate

Additional treatment recommended for SOME patients in selected patient group

​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 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]

Primary options

sodium bicarbonate: consult local protocol for dose guidelines

Consider – cation-exchange resin/polymer

Back
ACUTE
|
acute hyperkalaemia with potentially life-threatening features
|
without ECG changes
Consider – 

cation-exchange resin/polymer

Additional treatment recommended for SOME patients in selected patient group

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.[1][2][4][12]​​​​[85]​​​ 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.

Primary options

sodium zirconium cyclosilicate: 10 g orally three times daily for up to 48 hours initially, followed by 10 g once daily, adjust dose according to response and serum potassium levels (range 5 g every other day to 15 g once daily)

OR

patiromer: 8.4 g orally once daily initially, adjust dose according to response and serum potassium levels, maximum 25.2 g/day

Consider – emergency dialysis

Back
ACUTE
|
acute hyperkalaemia with potentially life-threatening features
|
without ECG changes
Consider – 

emergency dialysis

Additional treatment recommended for SOME patients in selected patient group

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[12][3][76]

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

Back
ACUTE
|
acute hyperkalaemia with potentially life-threatening features
|
without ECG changes
Consider – 

diuretic

Additional treatment recommended for SOME patients in selected patient group

​Consider an intravenous loop diuretic (e.g., furosemide) in patients with hypervolaemia, unless the patient is anuric, has severe volume depletion, 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 that the UK Kidney Association 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, they may be considered for use as adjuncts in a hyperkalaemic emergency.[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.

Primary options

furosemide: 20-40 mg intravenously initially, may increase by 20 mg every 2 hours according to response

Secondary options

chlorothiazide: 500-1000 mg intravenously once or twice daily

acute hyperkalaemia without potentially life-threatening features

1st line – treatment of underlying cause

Back
ACUTE
|
acute hyperkalaemia without potentially life-threatening features
1st line – 

treatment of underlying cause

Patients without potentially life-threatening features who do not meet the criteria for emergency treatment of hyperkalaemia are those with moderate hyperkalaemia who are not acutely unwell and do not have ECG changes, and patients with mild hyperkalaemia who are acutely unwell. Patients with mild hyperkalaemia who are not acutely unwell should be managed as per patients with chronic hyperkalaemia.

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 renin-angiotensin-aldosterone system inhibitors (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)

  • 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]​​​ 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, and Hypothermia

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

Consider – cation-exchange resin/polymer

Back
ACUTE
|
acute hyperkalaemia without potentially life-threatening features
Consider – 

cation-exchange resin/polymer

Additional treatment recommended for SOME patients in selected patient group

Consider the use of oral cation-exchange resin/polymers in hospitalised patients with moderate hyperkalaemia who are not actively unwell.[85] These drugs bind potassium in the gastrointestinal tract, leading to an increase in faecal potassium excretion and a fall in serum potassium.

  • 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]

  • 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 renin-angiotensin-aldosterone system inhibitor (RAASi) due to hyperkalaemia. Addition of these drugs may allow for reinstatement/continuation of RAASi.[1][87][88][90][91]

Primary options

sodium zirconium cyclosilicate: 10 g orally three times daily for up to 48 hours initially, followed by 10 g once daily, adjust dose according to response and serum potassium levels (range 5 g every other day to 15 g once daily)

OR

patiromer: 8.4 g orally once daily initially, adjust dose according to response and serum potassium levels, maximum 25.2 g/day

Consider – diuretic

Back
ACUTE
|
acute hyperkalaemia without potentially life-threatening features
Consider – 

diuretic

Additional treatment recommended for SOME patients in selected patient group

Consider an intravenous loop diuretic (e.g., furosemide), with or without saline, for patients with adequate renal function (and 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. Note that the UK Kidney Association does not advocate the use of diuretics in the management of acute hyperkalaemia.[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.

Primary options

furosemide: 20-40 mg intravenously initially, may increase by 20 mg every 2 hours according to response; 20-80 mg orally initially, may increase by 20-40 mg every 6-8 hours according to response, maximum 600 mg/day

Secondary options

chlorothiazide: 500-1000 mg intravenously/orally once or twice daily

Consider – sodium bicarbonate

Back
ACUTE
|
acute hyperkalaemia without potentially life-threatening features
Consider – 

sodium bicarbonate

Additional treatment recommended for SOME patients in selected patient group

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 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]

Primary options

sodium bicarbonate: consult local protocol for dose guidelines

Consider – dialysis

Back
ACUTE
|
acute hyperkalaemia without potentially life-threatening features
Consider – 

dialysis

Additional treatment recommended for SOME patients in selected patient group

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

ONGOING

chronic hyperkalaemia

1st line – consider hospitalisation + treatment of underlying cause

Back
ONGOING
|
chronic hyperkalaemia
1st line – 

consider hospitalisation + treatment of underlying cause

There is no clearly defined definition of chronic hyperkalaemia, but the term is often used to reference persistent hyperkala​emia, which is most commonly found in patients in the community who have chronic kidney disease and/or receive renin-angiotensin-aldosterone system inhibitors (RAASi).​[1]

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

However, hospitalisation should be considered for certain patients.

  • 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.

  • 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]

  • See the Acute section for guidance on the management of these patients.

For patients who can be managed in the community, first 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, and Hypothermia

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

Plus – dietary potassium counselling

Back
ONGOING
|
chronic hyperkalaemia
Plus – 

dietary potassium counselling

Treatment recommended for ALL patients in selected patient group

Provide information to patients with chronic hyperkalaemia regarding dietary sources of potassium and methods of reducing potassium intake via diet.[1][4]​​​ Consider input from a renal dietitian in patients with stage 4 and 5 chronic kidney disease and those who receive renal replacement therapy, according to local protocol.[1]

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]

Consider – cation-exchange resin/polymer

Back
ONGOING
|
chronic hyperkalaemia
Consider – 

cation-exchange resin/polymer

Additional treatment recommended for SOME patients in selected patient group

Oral cation-exchange resins (e.g., sodium zirconium cyclosilicate) or cation-exchange polymers (e.g., patiromer) bind potassium in the gastrointestinal tract, leading to an increase in faecal potassium excretion and a fall in serum potassium.

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 renin-angiotensin-aldosterone system inhibitors (RAASi) due to hyperkalaemia. Addition of these drugs may allow for reinstatement/continuation of RAASi.[1][87][88]​​​​​[90][91]

These drugs should be initiated in secondary care only and should be stopped if RAASi are discontinued.[1]​​[87]​​

Primary options

sodium zirconium cyclosilicate: 10 g orally three times daily for up to 48 hours initially, followed by 10 g once daily, adjust dose according to response and serum potassium levels (range 5 g every other day to 15 g once daily)

OR

patiromer: 8.4 g orally once daily initially, adjust dose according to response and serum potassium levels, maximum 25.2 g/day

Consider – diuretic

Back
ONGOING
|
chronic hyperkalaemia
Consider – 

diuretic

Additional treatment recommended for SOME patients in selected patient group

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.

Primary options

furosemide: 20-80 mg orally initially, may increase by 20-40 mg every 6-8 hours according to response, maximum 600 mg/day

Secondary options

chlorothiazide: 500-1000 mg orally once or twice daily

Consider – sodium bicarbonate

Back
ONGOING
|
chronic hyperkalaemia
Consider – 

sodium bicarbonate

Additional treatment recommended for SOME patients in selected patient group

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]​ Kidney Disease: Improving Global Outcomes (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]

Primary options

sodium bicarbonate: consult local protocol for dose guidelines

back arrow

Choose a patient group to see our recommendations

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups. See disclaimer

Use of this content is subject to our disclaimer