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 hyperkalemia with potentially life-threatening features

1st line – calcium

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

calcium

Initiate emergency management of hyperkalemia on an urgent basis (before serum biochemistry is known if hyperkalemia is suspected on clinical grounds/ECG findings) in all patients with ECG changes of hyperkalemia (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 hyperkalemia see Cardiac arrest.

Give intravenous calcium (as calcium gluconate or calcium chloride) in patients with hyperkalemia 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 dyskalemia 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/dextrose

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

insulin/dextrose

Treatment recommended for ALL patients in selected patient group

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

Insulin/dextrose (with albuterol) has an additive effect, reducing serum potassium by approximately 1.2 to 1.5 mEq/L (1.2 to 1.5 mmol/L).[15]

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

In situations where the patient has significant hyperglycemia, such as in diabetic ketoacidosis and hyperosmolar hyperglycemic states, hyperkalemia 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 hyperkalemia. Consult your local protocols.

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

Primary options

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

More

Plus – albuterol

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

albuterol

Treatment recommended for ALL patients in selected patient group

Give a nebulized beta-2 agonist such as albuterol (in addition to insulin/dextrose).[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/dextrose.[1][78]​​ 

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

Primary options

albuterol inhaled: 10-20 mg nebulized as a single dose

Plus – treatment of underlying cause

Back
ACUTE
|
acute hyperkalemia 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 hyperkalemia in all patients presenting with hyperkalemia, as well as any associated disorders.[1][4]​​​​​[12]

Optimize existing drug therapies that may cause or contribute to hyperkalemia - 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 hyperkalemia 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 hyperkalemia 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 hyperkalemia, 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 (noncardioselective)[2]

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

  • Digoxin[2]

  • Heparin[2][38]

  • Isoflurane[4]

  • Lithium[2]

  • Mannitol[57]

  • Nonsteroidal anti-inflammatory drugs[2]

  • Penicillins[2]

  • Pentamidine[2]

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

  • Somatostatin[2]

  • Succinylcholine[2]

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

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

  • Shock, see Shock

  • Hypovolemia, see Volume depletion in adults

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

  • Metabolic acidosis, see Evaluation of metabolic acidosis.

  • Digoxin toxicity, see Digoxin toxicity.

  • Mineralocorticoid deficiency, see Primary adrenal insufficiency.

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

  • Pseudohypoaldosteronism

  • Hypoaldosteronism or aldosterone resistance

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

  • Liver disease, see Evaluation of liver dysfunction.[1][11]

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

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

Consider – sodium bicarbonate

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

sodium bicarbonate

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 hypernatremia and metabolic alkalosis.[4][12]​​ Note that the UK Kidney Association does not advocate the use of sodium bicarbonate in the management of acute hyperkalemia.[1]

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

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

  • Sodium bicarbonate should not be used as the only treatment in acute treatment of hyperkalemia 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 hyperkalemia with potentially life-threatening features
|
with ECG changes
Consider – 

cation-exchange resin/polymer

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/dextrose infusion and nebulized beta-2 agonist.[1][2]​​​[4][12][85]​​​​ These drugs bind potassium in the gastrointestinal tract, leading to an increase in fecal 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 hyperkalemia 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 hyperkalemia 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 hyperkalemia 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 hyperkalemia.[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 hyperkalemia with potentially life-threatening features
|
with ECG changes
Consider – 

emergency dialysis

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 hyperkalemia as medical therapies will only temporize[3][12][76]

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

  • Severe hyperkalemia in the presence of life-threatening ECG changes where more rapid control of hyperkalemia 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 hyperkalemia with potentially life-threatening features
|
with ECG changes
Consider – 

diuretic

Treatment recommended for SOME patients in selected patient group

Consider an intravenous loop diuretic (e.g., furosemide) in patients with hypervolemia, 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 euvolemic 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 hyperkalemia.[1]

  • Although there is little evidence to support the use of diuretics in acute hyperkalemia, they may be considered for use as adjuncts in a hyperkalemic 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/dextrose

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

insulin/dextrose

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

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

  • Moderate hyperkalemia (serum potassium 6.0 to 6.4mEq/L [6.0 to 6.4 mmol/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 hyperkalemia (which may be moderate)

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

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

Insulin/dextrose (with albuterol) has an additive effect, reducing serum potassium by approximately 1.2 to 1.5 mEq/L (1.2 to 1.5 mmol/L).[15]

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

In situations where the patient has significant hyperglycemia, such as in diabetic ketoacidosis and hyperosmolar hyperglycemic states, hyperkalemia 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 hyperkalemia. Consult your local protocols.

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

Primary options

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

More

Plus – albuterol

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

albuterol

Treatment recommended for ALL patients in selected patient group

Give a nebulized beta-2 agonist such as albuterol (in addition to insulin/dextrose).[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/dextrose.[1][78]​​ 

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

Primary options

albuterol inhaled: 10-20 mg nebulized as a single dose

Plus – treatment of underlying cause

Back
ACUTE
|
acute hyperkalemia 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 hyperkalemia in all patients presenting with hyperkalemia, as well as any associated disorders.[1][4]​​​​​[12]

Optimize existing drug therapies that may cause or contribute to hyperkalemia - 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:

  • Hyperkalemia 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 hyperkalemia is significantly increased.[18][19][20]

  • T​he 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 hyperkalemia, 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 (noncardioselective)[2]

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

  • Digoxin[2]

  • Heparin[2][38]

  • Isoflurane[4]

  • Lithium[2]

  • Mannitol[57]

  • Nonsteroidal anti-inflammatory drugs[2]

  • Penicillins[2]

  • Pentamidine[2]

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

  • Somatostatin[2]

  • Succinylcholine[2]​​​​​​

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

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

  • Shock, see Shock

  • Hypovolemia, see Volume depletion in adults

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

  • Metabolic acidosis, see Evaluation 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 Evaluation of liver dysfunction

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

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

Consider – sodium bicarbonate

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

sodium bicarbonate

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 hypernatremia and metabolic alkalosis.[4][12] Note that the UK Kidney Association does not advocate the use of sodium bicarbonate in the management of acute hyperkalemia.[1]

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

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

  • Sodium bicarbonate should not be used as the only treatment in acute treatment of hyperkalemia 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 hyperkalemia with potentially life-threatening features
|
without ECG changes
Consider – 

cation-exchange resin/polymer

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/dextrose infusion and nebulized beta-2 agonist.[1][2]​​​[4][12][85]​​​​ These drugs bind potassium in the gastrointestinal tract, leading to an increase in fecal 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 hyperkalemia 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 hyperkalemia 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 hyperkalemia 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 hyperkalemia.[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 hyperkalemia with potentially life-threatening features
|
without ECG changes
Consider – 

emergency dialysis

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 hyperkalemia as medical therapies will only temporize[12][3][76]

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

  • Severe hyperkalemia in the presence of life-threatening ECG changes where more rapid control of hyperkalemia 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 hyperkalemia with potentially life-threatening features
|
without ECG changes
Consider – 

diuretic

Treatment recommended for SOME patients in selected patient group

Consider an intravenous loop diuretic (e.g., furosemide) in patients with hypervolemia, 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 euvolemic 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 hyperkalemia.[1]

  • Although there is little evidence to support the use of diuretics in acute hyperkalemia, they may be considered for use as adjuncts in a hyperkalemic 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 hyperkalemia without potentially life-threatening features

1st line – treatment of underlying cause

Back
ACUTE
|
acute hyperkalemia 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 hyperkalemia are those with moderate hyperkalemia who are not acutely unwell and do not have ECG changes, and patients with mild hyperkalemia who are acutely unwell. Patients with mild hyperkalemia who are not acutely unwell should be managed as per patients with chronic hyperkalemia.

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

Optimize existing drug therapies that may cause or contribute to hyperkalemia - 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:

  • Hyperkalemia 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 hyperkalemia 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 hyperkalemia, 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[40]

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

  • Beta-blockers (noncardioselective)

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

  • Digoxin[2]

  • Heparin[2][38]

  • Isoflurane[4]

  • Lithium[2]

  • Mannitol[57]

  • Nonsteroidal anti-inflammatory drugs[2]

  • Penicillins[2]

  • Pentamidine[2]

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

  • Somatostatin[2]

  • Succinylcholine[2]​​​​​​​

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

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

  • Shock, see Shock

  • Hypovolemia, see Volume depletion in adults

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

  • Metabolic acidosis, see Evaluation 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 Evaluation of liver dysfunction

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

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

Consider – cation-exchange resin/polymer

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

cation-exchange resin/polymer

Treatment recommended for SOME patients in selected patient group

Consider the use of oral cation-exchange resin/polymers in hospitalized patients with moderate hyperkalemia who are not actively unwell.[85] These drugs bind potassium in the gastrointestinal tract, leading to an increase in fecal 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 hyperkalemia 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 hyperkalemia.[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 hyperkalemia alongside standard care.​​[85][86][87][88]

  • Also consider these drugs for patients with persistent moderate hyperkalemia ≥6 mEq/L (≥6 mmol/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 hyperkalemia. 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 hyperkalemia without potentially life-threatening features
Consider – 

diuretic

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 hospitalized patients with mild/moderate hyperkalemia or patients who require optimization prior to surgery (who are not actively unwell).[2][4][12]​​ Patients with moderate hyperkalemia 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 euvolemic 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 hyperkalemia.[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 hyperkalemia without potentially life-threatening features
Consider – 

sodium bicarbonate

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 hypernatremia and metabolic alkalosis.[4][12]​ Note that the UK Kidney Association does not advocate the use of sodium bicarbonate in the management of acute hyperkalemia.[1]

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

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

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

Primary options

sodium bicarbonate: consult local protocol for dose guidelines

Consider – dialysis

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ACUTE
|
acute hyperkalemia without potentially life-threatening features
Consider – 

dialysis

Treatment recommended for SOME patients in selected patient group

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

ONGOING

chronic hyperkalemia

1st line – consider hospitalization + treatment of underlying cause

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ONGOING
|
chronic hyperkalemia
1st line – 

consider hospitalization + treatment of underlying cause

​There is no clearly defined definition of chronic hyperkalemia, but the term is often used to reference persistent hyperkalemia, 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 hyperkalemia who present in the community should be guided by the severity of hyperkalemia as well as the clinical condition of the patient.[1] Patients with persistent mild hyperkalemia (serum potassium 5.5 to 5.9 mEq/L [5.5 to 5.9 mmol/L]) or those with persistent moderate hyperkalemia (6.0 to 6.4 mEq/L [6.0 to 6.4 mmol/L]) who are not acutely unwell may be managed in the community.[1]

However, hospitalization should be considered for certain patients.

  • Admit all patients with confirmed severe hyperkalemia (serum potassium ≥6.5 mEq/L [≥6.5 mmol/L]) in the community for urgent hospital assessment and management.

  • Consider hospital admission for acutely unwell patients with confirmed mild hyperkalemia (serum potassium 5.5 to 5.9 mEq/L [5.5 to 5.9 mmol/L]) or moderate hyperkalemia (serum potassium 6.0 to 6.4 mEq/L [6.0 to 6.4 mmol/L]), particularly in the presence of an acute kidney injury. RAASi should be withheld during acute intercurrent illness (e.g., sepsis, hypovolemia, and/or acute kidney injury) at all severities of hyperkalemia.[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 hyperkalemia in all patients presenting with hyperkalemia, as well as any associated disorders.[1][4][12]​​​​

Optimize existing drug therapies that may cause or contribute to hyperkalemia - 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:

  • Hyperkalemia 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 hyperkalemia 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.

Hyperkalemia 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 hyperkalemia 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 hyperkalemia, 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 (noncardioselective)[2]

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

  • Digoxin[2]

  • Heparin[2][38]

  • Isoflurane[4]

  • Lithium[2]

  • Mannitol[57]

  • Nonsteroidal anti-inflammatory drugs[2]

  • Penicillins[2]

  • Pentamidine[2]

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

  • Somatostatin[2]

  • Succinylcholine[2]​​​​​​

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

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

  • Shock, see Shock

  • Hypovolemia. See Volume depletion in adults

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

  • Metabolic acidosis, see Evaluation 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 Evaluation of liver dysfunction

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

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

Plus – dietary potassium counseling

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ONGOING
|
chronic hyperkalemia
Plus – 

dietary potassium counseling

Treatment recommended for ALL patients in selected patient group

Provide information to patients with chronic hyperkalemia 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 hyperkalemia.[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 hemodialysis patients who do not have diabetes.​[14]

  • Patients on dialysis who have diabetes should also have their glycemic control optimized to help prevent hyperkalemia.[1]

Consider – cation-exchange resin/polymer

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ONGOING
|
chronic hyperkalemia
Consider – 

cation-exchange resin/polymer

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 fecal potassium excretion and a fall in serum potassium.

Consider these drugs for patients with persistent moderate hyperkalemia ≥6 mEq/L (≥6 mmol/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 hyperkalemia. 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

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ONGOING
|
chronic hyperkalemia
Consider – 

diuretic

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 hyperkalemia 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 hyperkalemia
Consider – 

sodium bicarbonate

Treatment recommended for SOME patients in selected patient group

​Consider sodium bicarbonate for patients with hyperkalemia and chronic kidney disease and metabolic acidosis (serum bicarbonate level <22 mEq/L [<22 mmol/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 hypernatremia 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 hyperkalemic patients when metabolic acidosis is not present.​[81][82]

Primary options

sodium bicarbonate: consult local protocol for dose guidelines

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