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Hypokalemia Treatment & Management

  • Author: Eleanor Lederer, MD, FASN; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Oct 07, 2015
 

Approach Considerations

The treatment of hypokalemia has four facets, as follows:

  • Reduction of potassium losses
  • Replenishment of potassium stores
  • Evaluation for potential toxicities
  • Determination of the cause to prevent future episodes, if possible

Medications

Usually, oral potassium chloride is administered when potassium levels need to be replenished, as well as, in patients with ongoing potassium loss (eg, those on thiazide diuretics), when it must be maintained. Potassium-sparing diuretics are generally used only in patients with normal renal function who are prone to significant hypokalemia.

Angiotensin-converting enzyme (ACE) inhibitors, which inhibit renal potassium excretion, can ameliorate some of the hypokalemia that thiazide and loop diuretics can cause. However, ACE inhibitors can lead to lethal hyperkalemia in patients with renal insufficiency who are taking potassium supplements or potassium-sparing diuretics.

Surgical care

Generally, hypokalemia is a medical, not a surgical, condition. Surgical intervention is required only with certain etiologies, such as the following:

  • Renal artery stenosis
  • Adrenal adenoma
  • Intestinal obstruction producing massive vomiting
  • Villous adenoma
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Decreasing Potassium Losses

Measures to identify and stop ongoing losses of potassium include the following:

  • Discontinue diuretics/laxatives
  • Use potassium-sparing diuretics if diuretic therapy is required (eg, severe heart failure)
  • Treat diarrhea or vomiting
  • Administer H2 blockers to patients receiving nasogastric suction
  • Control hyperglycemia if glycosuria is present

Because of the risk associated with potassium replacement, alleviation of the cause of hypokalemia may be preferable to treatment, especially if hypokalemia is mild, asymptomatic, or transient and is likely to resolve without treatment. For example, patients with vomiting who are successfully treated with antiemetics may not require potassium replacement.

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Replenishment of Potassium

Replenishment of potassium is the second treatment step. For every 1 mEq/L decrease in serum potassium, the potassium deficit is approximately 200-400 mEq.

Bear in mind, however, that many factors in addition to the total body potassium stores contribute to the serum potassium concentration. Therefore, this calculation could either overestimate or underestimate the true potassium deficit. For example, do not overcorrect potassium in patients with periodic hypokalemic paralysis. This condition is caused by transcellular maldistribution, not by a true deficit.

Patients who have mild or moderate hypokalemia (potassium level of 2.5-3.5 mEq/L) are usually asymptomatic; if these patients have only minor symptoms, they may need only oral potassium replacement therapy. If cardiac arrhythmias or significant symptoms are present, then more aggressive therapy is warranted. This treatment is similar to the treatment of severe hypokalemia.

If the potassium level is less than 2.5 mEq/L, intravenous potassium should be given. Maintain close follow-up care, provide continuous ECG monitoring, and check serial potassium levels.

Higher dosages may increase the risk of cardiac complications. Many institutions have policies that limit the maximum amount of potassium that can be given per hour. Hospital admission or observation in the emergency department is indicated; replacement therapy takes more than a few hours.

The serum potassium level is difficult to replenish if the serum magnesium level is also low. Look to replace both.

Oral potassium is absorbed readily, and relatively large doses can be given safely. Oral administration is limited by patient tolerance because some individuals develop nausea or even gastrointestinal ulceration with enteral potassium formulations.

Intravenous potassium, which is less well tolerated because it can be highly irritating to veins, can be given only in relatively small doses, generally 10 mEq/h. Under close cardiac supervision in emergent circumstances, as much as 40 mEq/h can be administered through a central line. Oral and parenteral potassium can safely be used simultaneously.

Take ongoing potassium losses into consideration by measuring the volume and potassium concentration of body fluid losses. If the patient is severely hypokalemic, avoid glucose-containing parenteral fluids to prevent an insulin-induced shift of potassium into the cells. If the patient is acidotic, correct the potassium first to prevent an alkali-induced shift of potassium into the cells.

Evaluation for potential toxicities

Monitor for toxicity of hypokalemia, which generally is cardiac in nature. Monitor the patient if evidence of cardiac arrhythmias is observed, and institute very aggressive replacement parenterally under monitored conditions.

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Addressing the Cause of Hypokalemia

Determine the underlying cause of the patient’s hypokalemia to treat the condition and prevent further episodes. Again, history and physical examination findings clarify the cause in the vast majority of cases. Look for clues to the etiology (see Presentation and Workup). Inadequate intake as a cause of hypokalemia generally indicates abuse by self or others. Consider psychiatric evaluation for suspected alcoholism or an eating disorder. Consider referral to abuse authorities if neglect (particularly in the case of an elderly person) or abuse is suspected.

Tailor treatment to the individual patient. For example, if diuretics cannot be discontinued because of an underlying disorder such as heart failure, institute potassium-sparing therapies, such as a low-sodium diet, potassium-sparing diuretics, ACE inhibitors, and angiotensin receptor blockers.

The low-sodium diet and potassium-sparing diuretics limit the amount of sodium reabsorbed at the cortical collecting tubule, thus limiting the amount of potassium secreted. ACE inhibitors and angiotensin receptor blockers inhibit the release of aldosterone, thus blocking the kaliuretic effects of that hormone.

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Consultations

The following consultations may be appropriate, depending on clinical findings, for diagnosing and managing underlying conditions in patients with hypokalemia:

  • Renal specialist for evaluation of unexplained urine potassium losses suggested to be secondary to a tubular disorder
  • Endocrinologist if Cushing syndrome, primary hyperaldosteronism, glucocorticoid-remediable hypertension, or congenital adrenal hyperplasia is suggested
  • Psychiatrist or other mental health professional for alcoholism or eating disorders
  • Dietitian in cases of hypokalemia due to inadequate dietary intake
  • Surgeon for etiologies such as renal artery stenosis, adrenal adenoma, intestinal obstruction producing massive vomiting, and villous adenoma
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Transfer

Transfer generally is not required unless patients experience untreatable cardiac arrhythmias, digoxin toxicity, or paralysis and no facilities are available for monitoring. In general, even severe hypokalemia can be treated successfully in most medical centers.

Patients with severe or symptomatic hypokalemia require transfer to an intensive care unit for intravenous potassium supplementation and continuous ECG monitoring. Patients should be transferred only after any cardiac arrhythmias have been treated and the condition has been stabilized. Depending on the level of hypokalemia, an advanced cardiac life support (ACLS) ambulance should be used to allow continuous cardiac monitoring during transport.

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Diet and Activity

Dietary modification may be necessary for patients with excessive potassium losses (eg, diuretic or laxative use) or patients with hypokalemia who are at increased risk, such as those receiving digoxin. In general, a low-sodium and high-potassium diet is appropriate. Avoidance of specific foods (eg, licorice) may also be necessary for high-risk individuals.

Unless the patient has severe underlying cardiac disease, no activity restrictions are necessary in most cases. Instruct patients to discontinue exercise if muscle pain or cramps develop, because this may herald hypokalemia significant enough to produce rhabdomyolysis. Patients with hypokalemic periodic paralysis may need to modify exercise regimens to avoid periods of strenuous exercise.

Patients at risk for hypokalemia from sweat losses should have adequate potassium and fluid available during activities likely to result in significant sweating and should be given anticipatory guidance regarding symptoms of hypokalemia.

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Inpatient Care

Monitoring potassium levels and treatment

Inpatient care includes monitoring serum potassium levels every 1-3 hours and adjusting supplement doses as necessary. Recall that potassium can shift in and out of cells under several influences. Therefore, several determinations of serum potassium level after presumably adequate replacement are indicated to ensure that serum potassium levels achieve normalcy.

After potassium has been replenished, checking again for several days to determine whether potassium has stabilized or has started falling again is equally important. For example, if an individual presents with nausea, vomiting, and hypokalemia, the physician might understandably attribute the hypokalemia to the nausea and vomiting. However, if after replenishment the patient once again develops hypokalemia without nausea and vomiting, then considering other possible causes of hypokalemia is necessary.

Additionally, if a need for ongoing potassium supplementation is anticipated for the patient (eg, a patient on long-term diuresis for hypertension), then ensuring that the prescribed daily potassium supplement is adequate to maintain a normal serum potassium level is important.

Cardiac evaluation

Electrocardiographic (ECG) monitoring is imperative for severe hypokalemia (<2 mEq/L in otherwise healthy individuals or <3 mEq/L in patients with known or suspected cardiac disease). With a sudden shift of potassium into the cells (eg, with insulin therapy for diabetic ketoacidosis), even individuals with healthy hearts can develop lethal arrhythmias. Continuously monitor patients on digoxin or those with digoxin toxicity.

Further evaluation

Once a cause has been determined for hypokalemia and the condition has been treated as per the diagnosis, ensuring that treatment plans are adequate is imperative. Evaluate for more unusual secondary causes. If an unusual cause of hypokalemia is suggested, either by specific clinical features or failure to respond to initial therapy, evaluation can at least begin while the patient is hospitalized. However, evaluation often can be completed in an outpatient setting.

If covert diuretic or laxative use is suspected, establishing proof of this is best accomplished in the hospital, with patients in a relatively controlled environment. In this setting, 24-hour urine measurements of sodium and potassium excretion, measurement of serum potassium at frequent intervals, and supervision of intake and output are possible. Ongoing potassium losses in the face of a negative urine and serum screen for diuretics suggest another diagnosis.

If the patient has hypertension, then the next steps would be as follows:

  • Determine serum renin activity and aldosterone and cortisol levels
  • Obtain a 24-hour urine measurement for aldosterone, cortisol, sodium, and potassium
  • Consider an imaging study (eg, renal vascular Doppler, captopril renal scan, or computed tomography [CT] angiography) to investigate the possibility of renal artery stenosis; [45] perform a CT scan of the abdomen to investigate for a possible adrenal adenoma.

A high cortisol level suggests Cushing syndrome. Evaluate for pituitary or adrenal causes. If renin and aldosterone levels are both elevated, this points more strongly to renal artery stenosis. If the index of suspicion is high enough, perform a renal arteriogram and renal vein renin determination to look for significant renal artery stenosis as a cause of hypertension and hypokalemia.

A high aldosterone level with low renin activity suggests primary hyperaldosteronism. If the patient is hypertensive but the aldosterone level is low, this suggests one of the more unusual congenital forms of hypertension, such as Liddle syndrome, in which a mutation in the epithelial sodium channel produces uncontrollable sodium reabsorption or glucocorticoid-remediable hypertension. This scenario also could be produced by licorice ingestion or ingestion of a steroid with mineralocorticoid activity, such as prednisone or fludrocortisone.

If the patient is not hypertensive but has hypokalemic metabolic alkalosis, and diuretic use and bulimia have been excluded, then possibilities include Bartter syndrome and Gitelman syndrome. If patients have metabolic acidosis, the most common cause is diarrhea. If this is not present, then the most likely possibility is a distal renal tubular acidosis, as might be seen with amyloid or amphotericin use or with glue sniffing.

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Outpatient Care

For otherwise healthy patients undergoing what appears to be an acute episode, such as severe diarrhea, causing hypokalemia, no further follow-up care is required. For patients who are likely to develop hypokalemia again (eg, those requiring long-term diuretic therapy), periodic monitoring of serum potassium levels is essential. If not performed during hospitalization, then outpatient follow-up care with tests such as 24-hour urine cortisol and aldosterone is acceptable.

Patients taking drugs that can alter serum potassium levels require periodic follow-up care. The greater the number of medical problems and the greater the number of drugs, the more frequent the follow-up care should be. Failure to check potassium levels after alteration of 1 of these drugs could allow the patient to develop a lethal complication. Bear in mind that the combination of potassium supplements, ACE inhibitors, angiotensin receptor blockers, and potassium-sparing diuretics has the potential to produce severe hyperkalemia.

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Deterrence and Prevention

Some authors advocate the routine use of potassium supplementation in patients with congestive heart failure. Undoubtedly, most patients will require potassium supplementation because they will be taking loop diuretics. However, recall the caveats concerning the use of potassium supplements, ACE inhibitors, and potassium-sparing diuretics in patients with subclinical renal failure.

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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

Leslie Ford, MD Assistant Professor of Medicine, Kidney Disease Program, University of Louisville School of Medicine

Leslie Ford, MD is a member of the following medical societies: American Medical Association, American Society of Nephrology, and Kentucky Medical Association

Disclosure: Nothing to disclose.

James W Lohr, MD Fellowship Program Director, Professor, Department of Internal Medicine, Division of Nephrology, State University of New York at Buffalo

James W Lohr, MD is a member of the following medical societies: American College of Physicians, American Heart Association, 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 Reference 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: Genzyme Grant/research funds Other

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A model of transport mechanisms in the distal convoluted tubule. Sodium-chloride (NaCl) enters the cell via the apical thiazide-sensitive NCC and leaves the cell through the basolateral Cl− channel (ClC-Kb), and the Na+/K+-ATPase. Indicated also are the recently identified magnesium channel TRPM6 in the apical membrane, and a putative Na/Mg exchanger in the basolateral membrane. These transport mechanisms play a role in familial hypokalemia-hypomagnesemia or Gitelman syndrome.
 
 
 
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