AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Hypokalemia is defined as a plasma potassium level of less than 3.5 mEq/L in children. It is frequently present in pediatric patients who are critically ill. Potassium is the most abundant intracellular cation and is necessary for maintaining a normal charge difference between intracellular and extracellular environments. Potassium homeostasis is integral to normal cellular function and is tightly regulated by specific ion-exchange pumps, primarily by cellular, membrane-bound, sodium-potassium adenosine triphosphatase (ATPase) pumps. Derangements of potassium regulation often lead to neuromuscular, gastrointestinal, and cardiac conduction abnormalities.

Pathophysiology

Hypokalemia may be due to a total body deficit of potassium, which may result from long-term inadequate intake, long-term diuretic or laxative use, and chronic diarrhea, hypomagnesemia, or hyperhidrosis. Acute causes of potassium depletion include diabetic ketoacidosis, severe gastrointestinal losses from vomiting and diarrhea, dialysis, and diuretic therapy. Hypokalemia may also be the manifestation of large potassium shifts from the extracellular to intracellular space, as seen with alkalosis, insulin, catecholamines, sympathomimetics, and hypothermia.

Other recognizable causes include renal tubular disorders, such as distal renal tubular acidosis, Bartter and Gitelman syndromes, periodic hypokalemic paralysis, hyperthyroidism, administration of beta2-adrenergic agents, and hyperaldosteronism. Other mineralocorticoid excess states that may cause hypokalemia include cystic fibrosis (with hyperaldosteronism from severe chloride and volume depletion), Cushing syndrome, and exogenous steroid administration.

Mortality/Morbidity

• Mortality is rare, except when hypokalemia is severe or occurs following cardiac surgery, when accompanied by arrhythmia, or in a patient who has underlying heart disease and requires digoxin therapy.
• Short-term morbidity is common and may include gastrointestinal hypomotility or ileus; cardiac dysrhythmia; QT prolongation; appearance of U waves that may mimic atrial flutter, T-wave flattening, or ST-segment depression; and muscle weakness or cramping.

Race

• Racial differences may be present in predisposing conditions such as Bartter syndrome, Gitelman syndrome, Conn syndrome (ie, hyperaldosteronism), Cushing syndrome, and familial hypokalemic paralysis. In addition, significant hypokalemia and hypokalemic paralysis develop in 2-8% of Asians with hyperthyroidism.

Sex

• No known sex predilection has been noted.

Age

• Viral gastrointestinal infections tend to be more common in infants and younger children. Younger children with emesis or diarrhea are at an increased risk of hypokalemia because the depletion of fluid volume and electrolytes from gastrointestinal loss is relatively higher than that in older children and adults.


• Insulin-dependent diabetes mellitus that results in diabetic ketoacidosis (with its inherent fluid and potassium loss) is more common in children. Excessive corticosteroid and mineralocorticoid secretion, as in Cushing and Conn syndromes, is a less common cause of hypokalemia in the pediatric patient. Periodic hypokalemic paralysis may appear in childhood or young adulthood, precipitated by rest after strenuous exercise, physical or metabolic stress (eg, exposure to cold, alcohol ingestion), a high-carbohydrate meal, or exposure to exogenous insulin or epinephrine. Hypokalemia due to hyperthyroidism is generally observed in adults.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• Hypokalemia due to excessive loss is usually accompanied by a history of gastrointestinal loss (emesis or diarrhea), urinary output, or sweating. This may be exacerbated by inadequate oral intake.
• Query about current or recent treatment with medications, including insulin, albuterol or other beta2-sympathomimetics, corticosteroids, diuretics, laxatives, enemas, or bowel-prep solutions.
• The patient may have had similar episodes in the past. Familial historical data may include surgery for pituitary or adrenal tumors or acute intermittent episodes of paralysis, with or without association with hyperthyroidism.

Physical

• Physical examination findings may frequently be within the reference range. Occasionally, muscle weakness is evident.


• Cardiac arrhythmias and acute respiratory failure from muscle paralysis are life-threatening complications that require immediate diagnosis.


• Cardiovascular examination findings may also be within normal limits. Occasionally, tachycardia with irregular beats may be heard. Severe hypokalemia may manifest as bradycardia with cardiovascular collapse.


• Hypoactive bowel sounds may suggest hypokalemic gastric hypomotility or ileus.

Causes

• Hypokalemia may be due to a total body deficit of potassium, which may occur chronically with the following:
• • Prolonged diuretic use
  • Inadequate potassium intake
  • Laxative use
  • Diarrhea
  • Hyperhidrosis
  • Hypomagnesemia

• Acute causes of potassium depletion include the following:
• • Diabetic ketoacidosis
  • Severe gastrointestinal losses from vomiting and diarrhea
  • Dialysis and diuretic therapy

• Hypokalemia may also be due to excessive potassium shifts from the extracellular to the intracellular space, as seen with the following:
  • Alkalosis

  • Insulin use

  • Catecholamine use

  • Sympathomimetic use

  • Hypothermia
• Other recognizable causes of hypokalemia include the following:
  • Renal tubular disorders, such as Bartter and Gitelman syndromes

  • Type I or classic distal tubular acidosis

  • Periodic hypokalemic paralysis

  • Hyperaldosteronism
• Other states of mineralocorticoid excess that may cause hypokalemia include the following:
• • Cystic fibrosis with hyperaldosteronism from severe chloride and volume depletion
  • Cushing syndrome
  • Exogenous steroid administration

• Other conditions that may cause hypokalemia include acute myelogenous, monomyeloblastic, or lymphoblastic leukemia.
• Drugs that may cause hypokalemia include the following:
• • Theophylline

  • Verapamil (with overdose)

  • High-dose penicillin

  • Ampicillin

  • Carbenicillin

  • Drugs associated with magnesium depletion, such as aminoglycosides, amphotericin B, and cisplatin

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Serum electrolyte tests: Screen for concurrent electrolyte abnormalities, which may affect treatment.


• Blood gas analysis
  
  
  • Assess acid-base status.
  
  
  • Alkalosis may induce hypokalemia, and treatment of acidosis may worsen existing hypokalemia.


• Drug screen (serum or urine)
• • Amphetamines and other sympathomimetic stimulants can cause hypokalemia.
  
  
  • Other drugs that can cause hypokalemia include verapamil (with overdose), theophylline, amphotericin B, aminoglycosides, and cisplatin.


• Serum adrenocorticotropic hormone (ACTH), cortisol, renin activity, and aldosterone tests: Evaluate for suspected Cushing, Conn, or adrenal hyperplasia syndromes, including 11-beta-hydroxylase deficiency.


• Simultaneous serum insulin and C-peptide tests: Because hyperinsulinism can cause transient hypokalemia, elevated serum insulin without appropriately elevated C-peptide suggests exogenous insulin administration, which may represent Münchhausen-by-proxy syndrome.

Imaging Studies

• MRI: Obtain a brain MRI if a brain or pituitary tumor is suspected as a cause of hypercortisolism.


• Ultrasonography and CT: Perform abdominal ultrasonography or CT scanning if an adrenal tumor or hyperplasia is suspected.

Other Tests

• Electrocardiography: Although ECG changes may be helpful if present, their absence should not be taken as reassurance of normal cardiac conduction. The ECG in hypokalemia may appear normal or may have only subtle findings immediately before clinically significant dysrhythmias.
• • Ventricular dysrhythmia
  • Prolongation of QT interval
  • ST-segment depression
  • T-wave flattening
  • Appearance of U waves
  • During therapy, monitor for changes associated with overcorrection and hyperkalemia, including a prolonged QRS, peaked T waves, bradyarrhythmia, sinus node dysfunction, and asystole.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

• Treatment depends on severity and etiology.


• Unlike hyponatremia, in which the total body sodium deficit can be readily estimated, serum potassium may not accurately reflect total body stores. Indeed, during diabetic ketoacidosis, serum potassium levels are usually initially elevated, even in the face of severe depletion of total body potassium. Correction of acidosis in diabetic ketoacidosis may cause a precipitous drop in serum potassium levels.


• Transient, asymptomatic, or mild hypokalemia may spontaneously resolve or may be treated with enteral potassium supplements.


• Symptomatic or severe hypokalemia should be corrected with a solution of intravenous potassium.

Surgical Care

• Except for excision of tumors leading to hypokalemia, management is nonsurgical.

Consultations

• After resolution, consultation with an endocrinologist, geneticist, or specialist in metabolic disease may be necessary to diagnose and manage predisposing conditions.
• Consultation with a dietitian may be helpful in cases of hypokalemia due to inadequate dietary intake.

Diet

• 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.
• Avoidance of specific foods (eg, licorice, which may have aldosteronelike activity) may also be necessary for high-risk individuals.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical therapy is aimed at potassium supplementation by the enteral (ie, oral or through feeding tubes) or parenteral route. Transient, asymptomatic, or mild hypokalemia may resolve spontaneously, or it may be treated using enteral potassium supplements. Symptomatic or severe hypokalemia should be corrected with intravenous potassium preparations.

Drug Category: Potassium supplements

These agents are used to restore body potassium storage. Electrolytes are used to correct disturbances in fluid and electrolyte homoeostasis or acid-base balance and to reestablish osmotic equilibrium of specific ions.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• After the initial phase of therapy is completed, focus further inpatient care on matching potassium intake to losses, periodic testing of serum potassium levels, and electrocardiographic monitoring for hypokalemia or hyperkalemia due to therapy.

• Alleviation of aggravating conditions, simplification of medication administration, and patient education form the basis of ongoing patient health and safety.

Further Outpatient Care

• If the condition is expected to persist beyond inpatient care, patients should receive follow-up medical care for home treatment.
• Additional medical follow-up must be obtained for associated medical conditions.

In/Out Patient Meds

• Other than potassium supplementation as described above, no additional medications are required.

Transfer

• Patients with severe or symptomatic hypokalemia require transfer to an ICU for intravenous potassium supplementation and continuous electrocardiographic monitoring.

Complications

• Hyperkalemia from excessive potassium replacement
• Cardiac dysrhythmia
• Gastric erosions
• Strictures

Prognosis

• With adequate control of potassium levels and resolution of any predisposing condition, prognosis is excellent.

Patient Education

• Patients should be educated in terms of predisposing conditions. The importance and risks involved with potassium supplementation and the warning signs of hypokalemia or overtreatment must be emphasized upon discharge from the hospital.
• Knowledge of cardiopulmonary resuscitation and education on timely access to emergency medical services may prevent morbidity or mortality.
• Ongoing communication is essential for reducing the risks and in therapy, especially in patients with chronic conditions associated with hypokalemia.
• For excellent patient education resources, visit eMedicine's Endocrine System Center. Also, see eMedicine's patient education article Low Potassium.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to adequately communicate the risks of treatment
• Failure to appropriately monitor patients receiving potassium supplementation for complications, especially patients with renal failure or patients receiving potassium-sparing diuretics or angiotensin-converting enzyme inhibitors
• Failure to follow serum potassium and other electrolyte concentrations during or after therapy
• Treating a patient on the basis of a low serum potassium value that is false because of a sampling or laboratory error (or failing to treat a patient with symptoms of actual hypokalemia because of an elevated serum potassium value that is false because of a sampling or laboratory error)

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Bevacqua JE. Diabetic ketoacidosis in the pediatric ICU. Crit Care Nurs Clin North Am. Dec 2005;17(4):341-7, x. [Medline].
• Clayton JA, Rodgers S, Blakey J, Avery A, Hall IP. Thiazide diuretic prescription and electrolyte abnormalities in primary care. Br J Clin Pharmacol. Jan 2006;61(1):87-95. [Medline].
• Jospe N, Forbes G. Fluids and electrolytes--clinical aspects. Pediatr Rev. Nov 1996;17(11):395-403; quiz 404. [Medline].
• Kumar PS, Deenadayalan M, Janakiraman L, Vijayakumar M. Neonatal Bartter syndrome. Indian Pediatr. Aug 2006;43(8):735-7. [Medline].
• Landau D. Potassium handling in health and disease: lessons from inherited tubulopathies. Pediatr Endocrinol Rev. Dec 2004;2(2):203-8. [Medline].
• Mueller PL, Jaimovich DG. Endocrine and Metabolic Emergencies. 1996:265-292, 492.
• Parr JR, Salama A, Sebire P. A survey of consultant practice: intravenous salbutamol or aminophylline for acute severe childhood asthma and awareness of potential hypokalaemia. Eur J Pediatr. May 2006;165(5):323-5. [Medline].
• Rodriguez-Soriano J. Bartter and related syndromes: the puzzle is almost solved. Pediatr Nephrol. May 1998;12(4):315-27. [Medline].
• Rose BD. Introduction to Disorders of Potassium Balance. 1989:715-756.
• Wiseman K. Index of suspicion. Case 3. Familial periodic paralysis. Pediatr Rev. Oct 1997;18(10):357, 359-60. [Medline].
• Wood EG, Lynch RE. Fluid and Electrolyte Balance. 1998:703-22.

Article Last Updated: Apr 13, 2007