eMedicine Specialties > Nephrology > Acid-Base, Fluid, and Electrolyte Disorders

Hyperkalemia: Follow-up

Author: Eleanor Lederer, MD, Consulting Staff, Louisville VA Hospital; Professor of Medicine; Interim Chief of Nephrology; Director of Nephrology Training Program; Director, Metabolic Stone Clinic; Director of Outpatient Clinics, Kidney Disease Program, University of Louisville School of Medicine
Coauthor(s): Rosemary Ouseph, MD, Professor of Medicine, Director of Kidney Transplant, University of Louisville School of Medicine; Vibha Nayak, MD, Assistant Professor of Nephrology, Director of Home Dialysis, Kidney Disease Program, University of Louisville; Son Dinh, MD, Nephrologist, Southland Renal Medical Group, Inc
Contributor Information and Disclosures

Updated: Apr 7, 2009

Follow-up

Further Inpatient Care

  • Once the potassium level is restored to normal, the potassium-lowering therapies can be discontinued and the serum potassium level can be monitored.
  • Determine and address the cause for hyperkalemia, including an evaluation of sources of potassium intake, causes for decreased renal excretion, and causes for decreased cell uptake of potassium. Most cases of hyperkalemia are multifactorial, with elements of all 3 causalities contributing to the final picture. In particular, 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.

Further Outpatient Care

  • For patients who have a defined and finite reason for hyperkalemia, such as acute exertional rhabdomyolysis or drug-induced hemolysis, serum potassium can be monitored on an infrequent basis. However, for patients who have conditions or medications predisposing them to hyperkalemia and in whom hyperkalemia has developed, monitor serum potassium levels more frequently. Once monthly measurements are indicated for patients at high risk.
  • For patients who have recurrent or constant hyperkalemia, such as patients with diabetic nephropathy and type IV renal tubular acidosis, chronic therapy with an oral loop diuretic and Kayexalate may be indicated.

Inpatient & Outpatient Medications

  • Loop diuretics often offset mild hyperkalemia without producing significant volume depletion. Once daily furosemide is effective in patients with moderate hyperkalemia and type IV renal tubular acidosis.
  • Oral Kayexalate is useful in patients with advanced renal failure who are not yet on dialysis or transplant candidates. One or more doses of 15 g/d can control mild to moderate hyperkalemia effectively, with little inconvenience to patients.
  • Florinef 0.1 mg by mouth daily is a useful treatment in hyperkalemia associated with mild to moderate renal impairment.

Transfer

  • Transfer patients with severe cardiac toxicity (as recorded on ECG) to the intensive care unit for continuous monitoring and aggressive therapy.
  • If a patient needs hemodialysis for hyperkalemia, transfer to a facility with this capability may be required.

Deterrence/Prevention

  • Hyperkalemia is most effectively prevented through education of patients on the potential causes of hyperkalemia, on dietary sources, on medical conditions predisposing to hyperkalemia, and on contributing medications.
  • Additionally, repeated review of the patient's medications to identify potential interactions that can cause hyperkalemia is essential.
  • Some common clinical situations include the following:
    • Diabetic persons with mild nephropathy who are taking an angiotensin-converting enzyme inhibitor and are on a low-sodium diet
    • Patients with heart failure who are taking an angiotensin-converting enzyme inhibitor and spironolactone
    • Patients with chronic renal insufficiency placed on trimethoprim
    • Recipients of kidney transplants who are taking cyclosporin or tacrolimus and have an abnormal serum creatinine

Complications

  • Complications of hyperkalemia range from mild ECG changes to cardiac arrest. Weakness is common as well.
  • 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 Kayexalate administration

Prognosis

  • For patients with a defined and transient cause of hyperkalemia, the prognosis is excellent. However, patients who have ongoing risk factors for hyperkalemia are likely to develop recurrent episodes.

Patient Education

  • Inform patients regarding the following:
    • Dietary sources of potassium, including salt substitutes
    • Medications that impair renal excretion, including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, nonsteroidal anti-inflammatory drugs, and potassium-sparing diuretics
    • Clinical situations in which patients might be at risk for the development of hyperkalemia, which include volume depletion and acute renal insufficiency complicating gastrointestinal fluid losses; increasing doses of angiotensin-converting enzyme inhibitors or potassium-sparing diuretics; and addition of a medication that decreases renal excretion or cellular uptake in patients who already are taking such drugs.

Miscellaneous

Medicolegal Pitfalls

  • Checking the ECG of patients who are hyperkalemic to assess potential cardiac toxicity is imperative. ECG evidence of cardiac toxicity mandates treatment and monitoring of the serum potassium level.
  • Failure to document the stability of serum potassium after treatment is a potential pitfall in therapy. Often, when hyperkalemia is treated aggressively by several modalities, including diuresis, cation exchange resin, and glucose and insulin infusions, potassium can decrease markedly, only to rebound after therapy is discontinued. This is particularly likely in patients who have ongoing reasons for hyperkalemia, such as rhabdomyolysis or ingestion of a long-acting angiotensin-converting enzyme inhibitor.
  • If patients have been taking several drugs that contribute to hyperkalemia and they continue to require 1 or more of them, documenting the necessity of these drugs and documenting the education of patients regarding the risk of hyperkalemia is imperative.
 


More on Hyperkalemia

Overview: Hyperkalemia
Differential Diagnoses & Workup: Hyperkalemia
Treatment & Medication: Hyperkalemia
Follow-up: Hyperkalemia
Multimedia: Hyperkalemia
References
Further Reading
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Further Reading

Clinical guidelines:
Potassium in pre-dialysis patients. Caring for Australasians with Renal Impairment - Disease Specific Society. 2005 Dec. 6 pages. NGC:006168

The pharmacologic management of chronic heart failure. Department of Veterans Affairs - Federal Government Agency [U.S.]
Veterans Health Administration - Federal Government Agency [U.S.]. 2001 Feb (revised 2003 Aug). 45 pages. NGC:003566

Clinical trials:
Genetic Determinants of the Hypokalemic and Hyperglycemic Effect of Albuterol Inhalation
Inhibition of Aldosterone in Patients With Chronic Renal Disease

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Keywords

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Contributor Information and Disclosures

Author

Eleanor Lederer, MD, Consulting Staff, Louisville VA Hospital; Professor of Medicine; Interim Chief of Nephrology; Director of Nephrology Training Program; Director, Metabolic Stone Clinic; Director of Outpatient Clinics, Kidney Disease Program, University of Louisville School of Medicine
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: Nothing to disclose.

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.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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: Genzyme Grant/research funds Other

CME Editor

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 Osteopathic Internists, 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: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

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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