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Hyperkalemia Clinical Presentation

  • Author: Eleanor Lederer, MD, FASN; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Jan 11, 2016
 

History

Many individuals with hyperkalemia are asymptomatic. When present, the symptoms of hyperkalemia are nonspecific and predominantly related to muscular or cardiac function. The most common complaints are weakness and fatigue. Occasionally, a patient may complain of frank muscle paralysis or shortness of breath. Patients also may complain of palpitations or chest pain. Patients may report nausea, vomiting, and paresthesias. The history is most valuable in identifying conditions that may predispose to hyperkalemia.

When hyperkalemia is discovered, investigate potential pathophysiologic mechanisms. For excessive potassium intake, query patients about the following:

  • Eating disorders - Very unusual diets consisting almost exclusively of high-potassium foods, such as fruits (eg, bananas, oranges, or melons), dried fruits, raisins, fruit juices, nuts, and vegetables with little to no sodium
  • Heart-healthy diets - Very low–sodium and high-potassium diets recommended for patients with cardiac disease, hypertension, and diabetes mellitus
  • Use of potassium supplements in over-the-counter herbal supplements, sports drinks, dietary supplements such as noni ( Morinda citrifolia) juice, salt substitutes, or prescribed pharmacologic agents

Many patients with hypertension have heard the advice to eat a banana a day because the potassium in it reduces blood pressure. They may not realize that in the case of renal insufficiency and hypertension, this is potentially a life-threatening practice.

With hospitalized patients, review the medication list for potassium supplements or high-dose penicillin G potassium, and review the chart to determine whether the patient has received transfusions. With patients who have undergone cardiac surgery, consider the possibility of residual effects of cardioplegic solutions.

For decreased potassium excretion, query patients regarding a history of renal insufficiency or renal failure. In addition, elicit any history of diabetes mellitus, sickle cell disease or trait, or symptoms of lower urinary tract obstruction. These conditions predispose people to type IV renal tubular acidosis, also called hyperkalemic renal tubular acidosis. Type IV renal tubular acidosis also may accompany other tubulointerstitial disorders, such as polycystic kidney disease or amyloidosis.

Often, patients with type IV renal tubular acidosis have hyporeninemic hypoaldosteronism.[16, 17] One example is diabetes mellitus, where the relative volume overload leads to low renin.

Patients with ureteral diversion into the ileum can develop hyperkalemia due to reabsorption of secreted potassium.

Ask about the use of medications that impair renal potassium excretion, as follows:

  • Potassium-sparing diuretics, which are especially popular in the treatment of cirrhosis and chronic heart failure
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) [51]
  • Angiotensin-converting enzyme (ACE) inhibitors
  • The combination of spironolactone and ACE inhibitors [52]
  • Angiotensin-receptor blockers (ARBs)
  • Direct renin inhibitors (eg, aliskiren)
  • Cyclosporine or tacrolimus
  • Antibiotics (eg, pentamidine and trimethoprim-sulfamethoxazole) [53]
  • Epsilon-aminocaproic acid (EACA) [23]
  • Oral contraceptive agents, such as drosperinone

For a shift of potassium into the extracellular space, query patients about the following:

  • Recurrent episodes of flaccid paralysis
  • Presence of diabetes mellitus
  • Use of beta-blocker therapy (eg, for hypertension or angina)
  • Risk factors for rhabdomyolysis, such as heat stroke, chronic alcoholism, seizures, sudden excessive exertion (as in military recruits undergoing basic training), or use of medications that interfere with heat dissipation (eg, tricyclic antidepressants or anesthesia)
  • Risk factors for tumor lysis syndrome, such as ongoing treatment for widespread lymphoma, leukemia, or other large tumors
  • Risk factors for hemolysis, such as blood transfusion and sickle cell disease
  • Redistribution - Metabolic acidosis (diabetic ketoacidosis [DKA]) and catabolic states

Pediatric patients

In a previously well child with acute hyperkalemia, the history should focus on the following:

  • How the blood sample was obtained
  • Potassium intake or recent blood product transfusion
  • Risk factors for transcellular shift of potassium (acidosis) or tissue death or necrosis
  • Use of medication associated with hyperkalemia (by the child, other family members, pets, or household visitors)
  • Presence or signs of renal insufficiency

Specific questions may be focused on the following:

  • Urine output (last void or number of wet diapers) and fluid intake
  • Cola-colored urine (which may indicate acute glomerulonephritis)
  • Bloody stool (which may indicate hemolytic-uremic syndrome [HUS])
  • Drugs present in the household (or used by recent visitors), such as potassium preparations, digoxin, and diuretics
  • Any history of trauma (crush injuries) or thermal injury (burns)

Medical history, family history, and review of systems should be explored for any of the following:

  • Acute kidney injury or chronic kidney disease
  • Hypertension
  • Diabetes mellitus
  • Adrenogenital syndromes
  • Malignancy (tumor lysis syndrome)

The family history should include questions about the following:

  • Hyperkalemic periodic paralysis
  • Miscarriages
  • Deaths of very young siblings
  • Neuromuscular disorders
  • Malignant hyperthermia
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Physical Examination

In patients with hyperkalemia, vital signs generally are normal. Nonspecific findings can include muscle weakness, fatigue, and depression. Occasionally, cardiac examination may reveal extrasystoles, pauses, or bradycardia resulting from heart block or tachypnea resulting from respiratory muscle weakness. Skeletal muscle weakness and flaccid paralysis may be present, along with depressed or absent deep tendon reflexes. Patients with ileus may have hypoactive or absent bowel sounds.

In general, the results of the physical examination alone do not alert the physician to the diagnosis, except when severe bradycardia is present or muscle tenderness accompanies muscle weakness, suggesting rhabdomyolysis. However, when hyperkalemia has been recognized, evaluation of vital signs is essential for determining hemodynamic stability and identifying the presence of cardiac arrhythmias related to the hyperkalemia.[6]

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Contributor Information and Disclosures
Author

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

Disclosure: Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.

Coauthor(s)

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

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

Disclosure: Nothing to disclose.

Zygimantas C Alsauskas, MD Assistant Professor of Medicine, Division of Nephrology, Kidney Disease Program, University of Louisville School of Medicine

Zygimantas C Alsauskas, MD is a member of the following medical societies: American Society of Nephrology

Disclosure: Nothing to disclose.

Lina Mackelaite, MD Assistant Professor of Medicine, University of Louisville School of Medicine

Lina Mackelaite, MD is a member of the following medical societies: American Society of Hypertension, American Society of Nephrology, American Society of Transplantation, National Kidney Foundation

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, 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, International Society of Nephrology

Disclosure: Nothing to disclose.

Acknowledgements

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.

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.

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.

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 Heart Association, American Society of Nephrology, and Royal College of Physicians

Disclosure: Nothing to disclose.

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Widened QRS complexes in patient whose serum potassium level was 7.8 mEq/L.
ECG of patient with pretreatment potassium level of 7.8 mEq/L and widened QRS complexes after receiving 1 ampule of calcium chloride. Note narrowing of QRS complexes and reduction of T waves.
Hyperkalemia diagnosis and treatment flow chart.
Widened QRS complexes in hyperkalemia.
Table. Selected Factors Affecting Plasma Potassium
Factor Effect on Plasma K+ Mechanism
Aldosterone Decrease Increases sodium resorption, and increases K+ excretion
Insulin Decrease Stimulates K+ entry into cells by increasing sodium efflux (energy-dependent process)
Beta-adrenergic agents Decrease Increases skeletal muscle uptake of K+
Alpha-adrenergic agents Increase Impairs cellular K+ uptake
Acidosis (decreased pH) Increase Impairs cellular K+ uptake
Alkalosis (increased pH) Decrease Enhances cellular K+ uptake
Cell damage Increase Intracellular K+ release
Succinylcholine Increase Cell membrane depolarization
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