Hyperkalemia Treatment & Management

Updated: May 18, 2017
  • Author: Eleanor Lederer, MD, FASN; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Approach Considerations

The aggressiveness of therapy for hyperkalemia is directly related to the rapidity with which the condition has developed, the absolute level of serum potassium, and the evidence of toxicity. The faster the rise in the potassium level, the higher it has reached; the greater the evidence of cardiotoxicity, the more aggressive therapy should be.

If the patient has only a moderate elevation in potassium level and no electrocardiographic (ECG) abnormalities, excretion can be increased by using a cation exchange resin or diuretics, and the source of excess potassium (eg, increased intake or inhibited excretion) can be corrected. [61]

In patients with severe hyperkalemia, treatment focuses on immediate stabilization of the myocardial cell membrane, rapid shifting of potassium to the intracellular space, and total body potassium elimination. In addition, all sources of exogenous potassium should be immediately discontinued; including intravenous (IV) and oral potassium supplementation, total parenteral nutrition, and any blood product transfusion. Drugs associated with hyperkalemia should also be discontinued (see Etiology). [62]

Definitive therapy is hemodialysis in patients with renal failure or when pharmacologic therapy is not sufficient. Any patient with significantly elevated potassium levels should undergo dialysis; pharmacologic therapy alone is not likely to bring about adequate reduction of potassium levels in a timely fashion.

After emergency management and stabilization of hyperkalemia, the patient should be hospitalized. Once the potassium level is restored to normal, the potassium-lowering therapies can be discontinued, and the serum potassium level can be monitored. Continuous cardiac monitoring should be maintained.

Further workup should be initiated to determine the inciting cause and to prevent future episodes. Such a workup should include evaluation of sources of potassium intake, causes for decreased renal excretion, and causes for decreased cell uptake of potassium. In most cases, all 3 of those etiologic factors contribute to hyperkalemia. It is particularly important to reevaluate the use of potassium supplements (including salt substitutes) in patients with renal insufficiency or in patients taking medications that impair renal excretion of potassium.


Initial Emergency Management

In the prehospital setting, a patient with known hyperkalemia or a patient with renal failure with suspected hyperkalemia should have IV access established and should be placed on a cardiac monitor. [21] In patients with hypotension or marked QRS widening, IV bicarbonate, calcium, and insulin given together with 50% dextrose may be appropriate (see Medication). If digoxin toxicity is suspected, avoid calcium; instead, give magnesium sulfate (2 g over 5 minutes) for patients with cardiac arrhythmias from digitalis toxicity.

In the emergency department (ED), perform continuous ECG monitoring with frequent vital sign checks when hyperkalemia is suspected or when laboratory values indicative of hyperkalemia are received. Measurement of potassium levels at least 1, 2, 4, 6, and 24 hours after identification and treatment of hyperkalemia is recommended. [62]

Discontinue any potassium-sparing drugs or dietary potassium. If the patient is taking digoxin, look for evidence of digitalis toxicity.

If the hyperkalemia is severe (potassium >7.0 mEq/L) or if the patient is symptomatic, begin treatment before diagnostic investigation of the underlying cause. Individualize treatment in accordance with the patient’s presentation, potassium level, and electrocardiographic findings. For example, patients with mild hyperkalemia may not need anything more than enhancement of potassium excretion.

Medications such as calcium, insulin, glucose, and sodium bicarbonate are temporizing measures. Definitive loss of excess potassium can be achieved only with cation exchange resins, dialysis, or increased renal excretion. Begin administration of a cation exchange resin soon after the other drugs have been administered.

Watch for overcorrection of potassium level. For example, in diabetic ketoacidosis (DKA) and many other types of metabolic acidosis, the extracellular potassium level is elevated, yet the patient may have a total body deficit of potassium. Once the clinician initiates therapy for DKA, the extracellular potassium level decreases spontaneously.


Pharmacologic Therapy and Dialysis

Medical treatment of hyperkalemia may be conveniently divided into discrete components. Although these different aspects of hyperkalemia treatment are listed sequentially below, in a step-by-step format, they generally are addressed simultaneously.

Step 1

The first step is to administer intravenous (IV) calcium to ameliorate cardiac toxicity, if present. Infuse calcium chloride or calcium gluconate (10 mL of a 10% solution over 2-3 minutes). Onset of action occurs within minutes; duration of action is 30 minutes to an hour. [63]

Step 2

The second step is to identify and remove sources of potassium intake. Discontinue oral and parenteral potassium supplements. Remove potassium-containing salt substitutes. Examine the patient’s diet. Change the diet to a low-potassium tube feed or a 2-g potassium ad-lib diet.

Step 3

The third step is to enhance potassium uptake by cells to decrease the serum concentration. IV glucose and insulin infusions are very effective in enhancing potassium uptake. A typical regimen is 10 U of regular insulin and 50 mL of dextrose 50% in water (D50W).The onset of action is within 20-30 minutes, and the duration is variable, ranging from 2 to 6 hours. Continuous infusions of insulin and glucose-containing IV fluids can be used for prolonged effect.

IV insulin (even when administered with dextrose) can cause hypoglycemia. Patients with acute kidney injury and chronic kidney disease are especially susceptible. Measure glucose and potassium levels every 2 hours. Continue monitoring glucose levels for at least 6 hours after administering insulin-glucose. [64]

A retrospective study by Pierce et al of 149 patients with low estimated glomerular filtration rate (eGFR) who received IV insulin for hyperkalemia found no significant difference in the rate of hypoglycemia (blood glucose ≤70 mg/dL) or severe hypoglycemia (<50 mg/dL) with 10 U versus 5 U of insulin. Rates of hypoglycemia in the 10-U and 5-U groups were 16.7% and 19.7%, respectively (P = 0.79). Rates of severe hypoglycemia were 8.9% and 7.0%, respectively (P = 0.90).  [65]

Correct metabolic acidosis with sodium bicarbonate. Because of the variable effect of different forms of metabolic acidosis on the serum potassium level, this therapeutic modality is less effective and less predictable in producing a hypokalemic response, especially in patients with chronic renal failure. Nonetheless, if the acidosis is severe, then a trial of parenteral sodium bicarbonate therapy is warranted.

Beta-adrenergic agonists also are quite effective but are perhaps somewhat more controversial and more likely to produce side effects. In the United States, the most commonly used preparation is nebulized albuterol. The dose for treating hyperkalemia, 10 mg, is substantially higher than the usual dose for the treatment of bronchospasm and requires the assistance of a respiratory therapist. The peak hypokalemic effect occurs at 90 minutes. This therapy is highly effective and is preferred to alkali therapy in patients with renal failure.

Parenteral isoproterenol and albuterol also decrease potassium. However, isoproterenol is not commonly used, and parenteral albuterol is not available in the United States. Some investigators have reported tachycardia and chest discomfort with the use of beta-agonist therapy for hyperkalemia. Discontinue beta-adrenergic antagonists.

Step 4

The fourth step is to increase potassium excretion from the body. Renal excretion is enhanced easily in patients with normal kidney function by administering IV saline accompanied by a loop diuretic (eg, furosemide). Discontinue potassium-sparing diuretics, angiotensin-converting enzyme (ACE) inhibitors, angiotensin-receptor blockers (ARBs), and other drugs that inhibit renal potassium excretion. Monitor volume status and aim to maintain euvolemia.

Renal excretion can be enhanced by administration of an aldosterone analogue, such as 9-alpha fluorohydrocortisone acetate. Fluorohydrocortisone is especially helpful in patients with hyporeninemia or hypoaldosteronism. It has been increasingly used in solid-organ transplant recipients who have chronic hyperkalemia from calcineurin inhibitor use. Usually, serum potassium returns to normal after about 48 hours. [66]

Sodium polystyrene sulfonate

Gastrointestinal (GI) excretion can be increased through the use of cation exchange resins such as sodium polystyrene sulfonate (SPS). SPS can be administered orally or rectally (as a retention enema). Because the major site of action for this drug is the colon, rectal administration is preferred for hyperkalemic emergencies. The effectiveness of SPS is enhanced if the enema can be retained for 1 hour.

SPS is not useful for acute control of hyperkalemia, because its effect on potassium is delayed for at least 2 hours, peaking at 4-6 hours. SPS can decrease serum potassium by 2 mEq/L.

Oral SPS is useful in patients with advanced renal failure who are not yet on dialysis or transplant candidates. One or more daily doses of 15 g can control mild to moderate hyperkalemia effectively, with little inconvenience to patients.

Although SPS has a long history of use for hyperkalemia, its safety and efficacy have been questioned. [64, 67, 68, 61] The US Food and Drug Administration (FDA) advises against its use in patients who do not have normal bowel function (eg, postoperative patients who have not had a bowel movement since their procedure) or those who are at risk for constipation or impaction. [69] SPS should be discontinued in patients who become constipated, and repeat doses should not be given to patients who have not passed a bowel movement.

In addition, the FDA cautions that giving SPS with sorbitol, an osmotic cathartic used to prevent fecal impaction from SPS and to speed delivery of resin to the colon, has been associated with cases of intestinal necrosis, some of them fatal. [69] Current evidence indicates that this serious side effect can occur with SPS even when preparation does not contain any sorbitol. [70]


Patiromer sorbitex calcium (Veltassa) is a nonabsorbed, cation exchange polymer that contains a calcium-sorbitol counterion. It increases fecal potassium excretion by binding potassium in the lumen of the GI tract. It is indicated for hyperkalemia. It should not be used as an emergency treatment for life-threatening hyperkalemia because of its delayed onset of action.

FDA approval of patiromer was based on the AMETHYST-DN trial. Results showed that among patients with hyperkalemia and diabetic kidney disease taking RAAS inhibitors, patiromer resulted in statistically significant decreases in serum potassium level after 4 weeks of treatment, lasting through 52 week. [71]

The OPAL-HK trial showed that patiromer was well tolerated, decreased serum K(+) , and, compared with placebo, reduced recurrent hyperkalemia in patients with chronic kidney disease (CKD) and heart failure who were hyperkalemic while taking renin-angiotensin-aldosterone system inhibitors (RAASi). In the study, patiromer was given to patients with CKD who were taking RAASi and had serum K(+) levels >5.1 mEq/L to <6.5 mEq/L (n=243) for 4 weeks. Patients whose K(+) levels were ≥3.8 mEq/L to <5.1 mEq/L at the end of week 4 entered an 8-week randomized withdrawal phase and were randomly assigned to continue patiromer or switch to placebo. [72]

The primary efficacy endpoint was the between-group difference in median change in the serum K(+) over the first 4 weeks of the withdrawal phase. The median increase in serum K(+) from baseline of the withdrawal phase was greater with placebo (n = 22) than patiromer (n = 27) (P < 0.001). Recurrent hyperkalemia (serum K(+) ≥5.5 mEq/L) occurred in 52% of patients on placebo and 8% of those on patiromer (P <0.001). [72]

Step 5

The fifth step is emergency dialysis; this is a final recourse for patients who are experiencing potentially lethal hyperkalemia that is unresponsive to more conservative measures or for patients who have complete renal failure. Initiation of dialysis can often take several hours; therefore, even if dialysis is contemplated, the other therapeutic modalities should be instituted as a bridge to dialysis.

The final step in the medical management of hyperkalemia is to determine the cause of hyperkalemia in order to prevent future episodes. This should include examination of the following:

  • Sources of potassium intake
  • Causes of decreased renal excretion
  • Causes for impaired cellular uptake

Surgical Therapy

Surgical intervention generally is not needed for the care of a patient with hyperkalemia. Patients with metabolic acidosis and consequent hyperkalemia due to ischemic gut obviously require exploration. Patients with hyperkalemia due to rhabdomyolysis may need surgical decompression of swollen, ischemic muscle compartments. Patients without end-stage renal disease who require hemodialysis for control of hyperkalemia require placement of a hemodialysis catheter for emergency dialysis. [73]

In patients with solid tumors, tumor debulking may be considered as a means of decreasing the risk of hyperkalemia from tumor lysis syndrome. [74]


Complications of Treatment

Complications of therapy include the following:

  • Failure to control hyperkalemia
  • Hypokalemia due to excessively aggressive therapy
  • Hypercalcemia due to excessive calcium administration
  • Hypocalcemia from excessive bicarbonate therapy
  • Chest discomfort or tachycardia due to beta-agonist therapy
  • Hypoglycemia or hyperglycemia complicating glucose and insulin administration
  • Metabolic alkalosis and tetany due to excessive sodium bicarbonate administration
  • Volume depletion, metabolic alkalosis, renal insufficiency, hypocalcemia, hypomagnesemia, and hypophosphatemia due to aggressive loop diuretic use
  • Colon perforation due to exchange resin administration

Treatment of pseudohyperkalemia may result in hypokalemia; thus, treatment of non–life-threatening hyperkalemia should be deferred pending verification of hyperkalemia.


Diet and Activity

A low-potassium diet containing 2 g of potassium is recommended so as to minimize potassium intake in patients at risk for hyperkalemia. In particular, potassium intake must be closely monitored (and possibly restricted) in patients with renal failure.

No restrictions on activity are necessary unless continuous monitoring for cardiotoxicity is required.



Inform patients at risk for hyperkalemia about dietary sources of potassium, including salt substitutes. Adjust the diet to decrease potassium dietary load. Adjust medications that predispose to or exacerbate hyperkalemia.

In a retrospective observational study of 27,355 patients with diabetes, Raebel et al concluded that potassium monitoring can reduce the incidence of serious hyperkalemia-associated adverse events in patients with diabetes and chronic kidney disease who are undergoing renin-angiotensin-aldosterone system inhibitor therapy. [16] The investigators found that for monitored patients with diabetes alone, the adjusted relative risk was 0.50, whereas for monitored patients who also had chronic kidney disease, the adjusted relative risk was 0.29.



For patients with severe hyperkalemia or renal failure, early consultation with a nephrologist for aid in implementing efficient therapy and plans for dialysis is highly recommended. In addition, these patients should be admitted to an intensive care unit (ICU).

Consultations with the following specialists may be necessary in cases of hyperkalemia that result from certain conditions or disease states:

  • Pediatric intensivist or neonatologist – For life-threatening hyperkalemia (hyperkalemia with ECG changes) in infants and children
  • Social services specialist – For hyperkalemia developing in children after unintentional ingestions or poisonings
  • Cardiologist - For emergency pacemaker placement in patients with refractory heart block
  • Hematologist/oncologist – For hyperkalemia resulting from tumor lysis syndrome
  • Nutritional support specialist - For hyperkalemia caused by renal failure, which requires close regulation of potassium and sodium intake
  • Endocrinologist – For suspected mineralocorticoid abnormalities (eg, congenital adrenal hyperplasia)

Long-Term Monitoring

For patients whose hyperkalemia resulted from a single, clearly defined episode (eg, acute exertional rhabdomyolysis or drug-induced hemolysis), infrequent monitoring of serum potassium generally suffices. However, for patients who have conditions or medications that will continue to predispose to hyperkalemia, more frequent monitoring of serum potassium is required. For patients at high risk, monthly measurements are indicated.

Continuing care relates to the disease process that led to the hyperkalemia. For patients who have recurrent or constant hyperkalemia (eg, those with diabetic nephropathy and type IV renal tubular acidosis), long-term therapy with an oral loop diuretic and SPS may be indicated. For pseudohypoaldosteronism type II, the treatment of choice is a thiazide diuretic.

The risk of severe hypoglycemia for patients with acute kidney injury or end-stage renal disease is heightened in patients with lower body weight and creatinine clearance. Sufficient dextrose in the patient’s treatment regimen can minimize the risk. [75] In patients with salt-wasting congenital adrenal hyperplasia, corticosteroid and mineralocorticoid supplementation are necessary.