Hyperkalemia Treatment & Management

  • Author: Eleanor Lederer, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Dec 16, 2011
 

Medical Care

Orient the medical care of patients with hyperkalemia toward 5 different aims.

  • Evaluation for potential toxicities
  • Decreasing potassium intake
  • Increasing potassium uptake into cells
  • Increasing potassium excretion
  • Determining the cause to prevent future episodes

Although explicated below in a step-by-step format, these different aspects of hyperkalemia treatment generally are addressed simultaneously. The aggressiveness of therapy is directly related to the rapidity with which hyperkalemia has developed, the absolute level of hyperkalemia, and the evidence of toxicity. The faster the rise of potassium, the higher the level, and the greater the evidence of cardiotoxicity, the more aggressive therapy should be.

The first step is to determine whether the hyperkalemia is producing life-threatening toxicity. Perform an ECG to look for cardiotoxicity. Administer intravenous calcium to ameliorate cardiac toxicity, if present.

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.

The third step is to enhance potassium uptake by cells to decrease the serum concentration.

Parenteral glucose and insulin infusions are very effective in enhancing potassium uptake. Although glucose stimulates insulin secretion, administration of glucose alone often is not as effective in this clinical situation. The onset of action is within 20-30 minutes, and the duration is variable, from 2-6 hours. Continuous infusions of insulin and glucose-containing intravenous fluids can be used for prolonged effect. Measure glucose and potassium every 2 hours.

Correct metabolic acidosis with sodium bicarbonate. This therapeutic modality is less effective and less predictable in producing a hypokalemic response, due to the variable effect of different forms of metabolic acidosis on the serum potassium level. This particularly is true 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. This therapy is highly effective and preferred over alkali therapy in patients with renal failure. Parenteral isoproterenol or albuterol also decrease potassium. However, isoproterenol is not used commonly, and parenteral albuterol is not available in the United States. Some investigators have reported tachycardia and chest discomfort using beta-agonist therapy for hyperkalemia. Discontinue beta-adrenergic antagonists.

The fourth step is to increase potassium excretion from the body. Renal excretion is enhanced easily in the individual with normal kidney function by the administration of parenteral saline accompanied by a loop diuretic, such as furosemide. Discontinue potassium-sparing diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, 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 (Florinef). Florinef especially is helpful in patients with hyporeninemia or hypoaldosteronism.

Gastrointestinal excretion can be increased by the use of cation exchange resins, such as Kayexalate. Kayexalate 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 this drug is enhanced if the enema can be retained for an hour.

Repeated enemas can be used but occasionally cause colon perforation.

The onset of action occurs within 2 hours and is long lasting. The serum potassium level can be decreased by 2 mEq/L with a single enema. Kayexalate administered orally also is quite effective if it is suspended in 70% sorbitol. However, a study by Sterns et al poses the concern that suspending Kayexalate may harm patients; therefore, other methods for management should be examined first.[29]

Emergency dialysis 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 often can take several hours; therefore, even if dialysis is contemplated, initiate the other modalities of therapy first.

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
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Surgical Care

Surgery 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 need placement of a hemodialysis catheter for emergent dialysis.[30]
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Consultations

  • For severe hyperkalemia, early consultation with a nephrologist for aid in efficient therapy and plans for dialysis is highly recommended.
  • For emergency pacemaker placement, the aid of a cardiologist may be required for patients with refractory heart block.
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Diet

A low-potassium diet with 2 g of potassium is recommended to minimize potassium intake.

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Activity

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

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Contributor Information and Disclosures
Author

Eleanor Lederer, MD  Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Dept of Veterans Affairs Grant/research funds Research

Coauthor(s)

Rosemary Ouseph, MD  Professor of Medicine, Director of Kidney Transplant, University of Louisville School of Medicine

Rosemary Ouseph, MD is a member of the following medical societies: American Society for Bone and Mineral Research, American Society of Nephrology, and American Society of Transplant Surgeons

Disclosure: Nothing to disclose.

Vibha Nayak, MD  Assistant Professor of Nephrology, Director of Home Dialysis, Kidney Disease Program, University of Louisville

Vibha Nayak, MD is a member of the following medical societies: American Society of Nephrology

Disclosure: Nothing to disclose.

Son Dinh, MD  Nephrologist, Southland Renal Medical Group, Inc

Son Dinh, MD is a member of the following medical societies: American Society of Nephrology and National Kidney Foundation

Disclosure: Nothing to disclose.

Specialty Editor Board

Anil Kumar Mandal, MD  Clinical Professor, Department of Internal Medicine, Division of Nephrology, University of Florida School of Medicine

Anil Kumar Mandal, MD is a member of the following medical societies: American College of Clinical Pharmacology, American College of Physicians, American Society of Nephrology, and Central Society for Clinical Research

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Christie P Thomas, MBBS, FRCP, FASN, FAHA  Professor, Department of Internal Medicine, Division of Nephrology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics

Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Heart Association, American Society of Nephrology, American Society of Transplantation, American Thoracic Society, International Society of Nephrology, and Royal College of Physicians

Disclosure: Nothing to disclose.

Rebecca J Schmidt, DO, FACP, FASN  Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine

Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association

Disclosure: Renal Ventures Ownership interest Other

Chief Editor

Vecihi Batuman, MD, FACP, FASN  Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology

Disclosure: Nothing to disclose.

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Peaked T waves on an electrocardiogram, as seen in hyperkalemia.
Widened QRS complexes in a patient whose serum potassium level was 7.8 mEq/L.
 
 
 
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