Hypokalemia

Descriptive text is not available for this imageBASICS

DESCRIPTION

  • Potassium (K+) is a major intracellular cation important in the body.
  • Distribution of total body K+ is 98% intracellular and 2% extracellular. This gradient is required for normal metabolism, growth, and maintenance of the transmembrane potential for excitable membranes.
  • Serum K+ levels are tightly regulated within a narrow range (generally 3.5 to 5 mEq/L in children and 4 to 5.5 mEq/L in infants depending on the laboratory). Small changes in serum K+ levels can have significant effects on excitability of cells.
  • Hypokalemia is defined as serum K+ <3.5 mEq/L and is graded according to level:
    • Mild hypokalemia (3 to 3.5 mEq/L)
    • Moderate hypokalemia (2.5 to 3 mEq/L)
    • Severe hypokalemia (<2.5 mEq/L)
  • Hypokalemia can be asymptomatic. However, symptoms are more likely to be observed if serum K+ is <3 mEq/L or if a rapid fall in serum K+ occurs.
  • Pseudohypokalemia, or a falsely low serum K+ measurement, can be due to uptake of K+ intracellularly into cells when blood samples are stored in warm temperatures and/or not processed immediately. This issue is particularly important in care settings where samples may be shipped without processing.

EPIDEMIOLOGY

Hypokalemia is common in the inpatient setting, and prevalence may be as high as 40% in critically ill children.

ETIOLOGY

  • External losses are the most common causes of hypokalemia in children. Examples include:
    • Diarrhea, laxatives, vomiting, nasogastric suctioning, pyloric stenosis, ileostomy, congenital chloride diarrhea, excessive sweating
  • Conditions associated with reduced intake include malnutrition and anorexia nervosa.
  • Hypokalemia due to renal losses can be further stratified by the presence (or absence) of hypertension:
    • Renal etiologies associated with normal blood pressure: RTA, diabetic ketoacidosis (due to osmotic diuresis), medications (diuretics, amphotericin B, aminoglycosides, cisplatin), Bartter syndrome, Gitelman syndrome, cystic fibrosis, hypomagnesemia, Fanconi syndrome, toluene intoxication
    • Renal etiologies associated with high blood pressure: congenital adrenal hyperplasia (17-α hydroxylase or 11-β hydroxylase deficiency), hyperaldosteronism, apparent mineralocorticoid excess (11-β hydroxysteroid dehydrogenase deficiency), Cushing syndrome, Liddle syndrome, renal artery stenosis, medications/herbs (mineralocorticoids, glucocorticoids, inhibition of 11-β hydroxysteroid dehydrogenase by licorice)
  • Hypokalemia due to transcellular shifts: β 2 agonists (albuterol), insulin, theophylline, alkalosis (metabolic or respiratory), hyperthyroidism, hypokalemic periodic paralysis, refeeding syndrome

RISK FACTORS

  • Malnutrition (more important in developing countries)
  • Eating disorders (particularly anorexia nervosa, especially in conjunction with laxative or diuretic abuse)
  • Conditions associated with increased stool losses (diarrhea, vomiting, loss of gastrointestinal [GI] fluid via surgical or tube drainage)

Genetics

Inherited disorders associated with low K+ include:

  • Bartter syndrome
  • Gitelman syndrome
  • Liddle syndrome
  • Syndrome of apparent mineralocorticoid excess
  • Hypokalemic periodic paralysis
  • Some types of congenital adrenal hyperplasia
  • Congenital chloride diarrhea
  • Cystic fibrosis
  • Renal tubular acidosis (RTA)

GENERAL PREVENTION

Prevention of malnutrition and checking serum K+ levels in high-risk patients (GI fluid losses, malnutrition, eating disorders, known inherited disorders) are the most important steps in preventing severe episodes.

PATHOPHYSIOLOGY

  • Mechanisms that account for low serum K+ levels include:
    • Reduced intake
    • Increased losses (GI, urinary, or skin)
    • Transcellular shifts (β 2-adrenergic receptor stimulation, insulin, alkalosis)

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