hypokalemia

Etiology

• renal
  • osmotic diuresis, i.e. diabetes mellitus
  • pharmacologic agents:
    • diuretics (most common cause)
    • amphotericin B
    • gentamicin
    • mineralocorticoids
    • glucocorticoids (some)
    • osmotic diuretics
    • tetracycline
    • theophylline
    • vitamin B12
    • carbenicillin
    • high dose penicillin
  • excessive mineralocorticoids
    • primary hyperaldosteronism (Conn's syndrome)
    • secondary hyperaldosteronism
      • Bartter's syndrome
      • Gitelman syndrome
      • renal artery stenosis
    • glucocorticoid excess
      • Cushing's disease
      • ectopic ACTH production
      • exogenous steroids
  • distal renal tubular acidosis (RTA-1)
  • hypomagnesemia causes loss of potassium into the urine through the collecting tubule
    • alcoholism frequently associated with hypomagnesemia
    • proton pump inhibitors are associated with hypomagnesemia
• gastrointestinal
  • gastrointestinal (GI) loss of K+
    • vomiting
    • diarrhea through upregulation of K+ channels in the colon
    • villous adenoma
    • fistula
    • laxative abuse
  • decreased dietary intake
    • starvation
    • clay ingestion
• intracellular shift of K+
  • metabolic alkalosis
  • pharmacologic agents
    • insulin
    • beta-adrenergic receptor agonists
    • ritodrine
    • theophylline
  • familial hypokalemic periodic paralysis
• insensible losses
  • sweating

Epidemiology

• 90% of hypertensive patients with hyperaldosteronism

Pathology

• alterations in action potential generation
  • skeletal muscle dysfunction
  • cardiac muscle dysfunction
• alterations in renal tubular function
• causes of renal potassium loss
  • increased urine flow or sodium delivery to distal nephron
  • increased mineralocorticoid activity

Clinical manifestations

• signs/symptoms depend upon acute vs chronic nature of hypokalemia
• musculoskeletal dysfunction
  • muscle weakness
  • flaccid paralysis (including respiratory paralysis)
  • hypotonia
  • hyporeflexia
  • rhabdomyolysis
• smooth muscle dysfunction
  • paralytic ileus with nausea
  • muscle cramps
• renal failure
• renal tubular dysfunction
  • polydipsia
  • polyuria
• glucose intolerance
• cardiac arrhythmias
  • sinus bradycardia
  • premature atrial beats
  • atrial tachycardia
  • AV block
  • junctional tachycardia
  • premature ventricular beat
  • ventricular tachycardia (especially in patients on digoxin)
  • ventricular fibrillation

Laboratory

• serum K+ < 3.5 meq/L
• increased serum glucose
  • hypokalemia impairs insulin secretion
• urine K+
  • > 20 meq/L suggests renal origin
    • urine Cl- > 20 meq/L
      • high blood pressure: excess glucocorticoids, mineralocorticoids (urine Cl- generally > 40 meq/L)
        • normal blood pressure: Bartter's syndrome, Gitelman's syndrome, current use of diuretics
        • renal tubular acidosis
    • urine Cl- < 20 meq/L suggests metabolic alkalosis
    • urine Na+ is generally < 20 meq/L with volume depletion but with metabolic alkalosis, Na+ accompanies bicarbonate excreted in the urine to maintain electroneutrality, thus becomes > 20 meq/L
  • < 20 meq/L non-renal origin
    • diarrhea, vomiting*, laxative abuse, villous adenoma
    • low potassium intake
  • urine potassium/creatinine < 13 meq/g identifies non-renal origin
• serum Mg+2: may be low
• blood gas: pH
  • metabolic alkalosis
    • vomiting, NG suction, diarrhea, previous diuretics

* urine K+ may be high or low with vomiting; check urine Cl-

Diagnostic procedures

• electrocardiogram (EKG)
  • flattening of T waves or inverted T waves
  • ST segment depression
  • QTc prolongation
  • tachycardia
  • increased prominence of U wave
  • ventricular arrhythmias
    • severe hypokalemia
    • in patients taking digoxin

Complications

• exacerbation of digitalis toxicity
• glucose intolerance from impaired insulin secretion
• excess risk for
  • 7-day mortality in hospitalized patients
  • intensive care admission
  • ventricular arrhythmia/cardiac arrest
• excess risk only when heart rate > 100/min & serum K+ < 3 mmol/L

Management

• fatal arrhythmias may occur in patients taking digoxin even if hypokalemia is mild
• oral KCl (first resort)
• intravenous KCl*, potassium phosphate
  • do not exceed 40 meq/L
  • do not exceed 20 meq/hr
  • EKG monitoring during rapid K+ infusion
  • total body K+ deficits ~ 200 meq for each 1 meq/L decrease in serum K+
• normal saline for chloride-reponsive hypokalemic metabolic alkalosis with low urine chloride
• potassium sparing diuretics*
  • amiloride
  • triamterene
  • spironolactone
• hypomagnesemia & magnesium deficiency MUST be corrected before K+ depletion can be corrected
• when hypokalemia is due to intracellular shift of K+ (see etiology), total body K+ is normal & K+ replacement may result in hyperkalemia

* no advantage to potassium acetate; acetate may exacerbate metabolic alkalosis

* use of K+ sparing diuretics questioned

More general terms

• electrolyte disorder
• sign/symptom

Additional terms

• potassium (K+) in serum/plasma

Patient information

hypokalemia patient information