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Hypokalemia
Updated: Sep 21, 2009
Introduction
Background
Hypokalemia is generally defined as a serum potassium level of less than 3.5 mEq/L in children, although exact values for reference ranges of serum potassium are age-dependent, and vary among laboratories. It is frequently present in pediatric patients who are critically ill and reflects a total body deficiency of potassium or, more commonly, reflects conditions that promote the shift of extracellular potassium into the intracellular space.
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 may lead to neuromuscular, GI, and cardiac conduction abnormalities.
Prominent U waves after T waves in hypokalemia.
Pathophysiology
Hypokalemia may be due to a total body deficiency of potassium, which may result from prolonged inadequate intake, long-term diuretic or laxative use, and chronic diarrhea, hypomagnesemia, or hyperhidrosis. Acute causes of potassium depletion include diabetic ketoacidosis,1 severe GI losses due to 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 (including albuterol and other commonly-used beta2-adrenergic agonists), sympathomimetics, and hypothermia.
Other recognizable causes include renal tubular disorders, such as distal renal tubular acidosis, Bartter syndrome,2 and Gitelman syndrome, periodic hypokalemic paralysis, hyperthyroidism, 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. Excessive natural licorice consumption can also cause or exacerbate potassium loss due to inhibition of 11-betahydoxysteroid dehydrogenase, which leads to elevated endogenous mineralocorticoid activity.3
Mortality/Morbidity
Mortality is rare, except when hypokalemia is severe or occurs following cardiac surgery, when accompanied by arrhythmia, or in patients who have underlying heart disease and require digoxin therapy.
Short-term morbidity is common and may include GI 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.
Mortality and morbidity can also be related to treatment for hypokalemia with potassium supplementation, particularly if potassium is given in large doses or rapidly. 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.
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 GI 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 GI loss is relatively higher than that found 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 syndrome and Conn syndrome, 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 catecholamines (eg, epinephrine and albuterol). Hypokalemia due to hyperthyroidism is generally observed in adults.
Clinical
History
- Hypokalemia due to excessive loss is usually accompanied by a history of GI loss (emesis or diarrhea), urinary output, or sweating. This may be exacerbated by inadequate oral intake.
- Query about current or recent treatment with medications and herbal products (especially natural licorice), 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 GI 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 syndrome and Gitelman syndrome
- 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, including fludrocortisone and other mineralocorticoids
- Excessive licorice consumption
- Other conditions that may cause hypokalemia include acute myelogenous, monomyeloblastic, or lymphoblastic leukemia.
- Drugs that may commonly cause hypokalemia include the following:
- Furosemide, bumetanide, and other loop diuretics
- Methylxanthines (theophylline, aminophylline, caffeine)
- Verapamil (with overdose)
- Amphotericin B
- Quetiapine (particularly in overdose)
- Ampicillin, carbenicillin, high-dose penicillin
- Drugs associated with magnesium depletion, such as aminoglycosides, amphotericin B, and cisplatin
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References
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Further Reading
Keywords
hypokalemia, potassium deficiency, vomiting, dialysis, diarrhea, diuretics, alkalosis, insulin, catecholamines, sympathomimetics, hypothermia, renal tube disorders, distal renal tubular acidosis, Bartter syndrome, Gitelman syndrome, periodic hypokalemic paralysis, hyperthyroidism, beta2-adrenergic agents, hyperaldosteronism, cystic fibrosis, Cushing syndrome, exogenous steroid administration, GI hypomotility, GI ileus, cardiac dysrhythmia, QT prolongation, muscle weakness, muscle cramping, hypomagnesemia, hyperhidrosis, diabetic ketoacidosis, acute myelogenous leukemia, monomyeloblastic leukemia, lymphoblastic leukemia
