05. Hypokalemia

Definition: serum [K+] <3.5 mmol/L.

Etiology

  • Inadequate intake: this is rare and may be accompanied by signs of severe protein-calorie malnutrition. Average daily K+ intake is ~80 mEq/d and the kidney can reduce K+ excretion to <25 mEq/d, so there is a large range of intake across which K+ can be retained.
  • Intracellular shifts:  
    • Alkalemia.
    • Hypothermia: keep in mind when warming a patient after therapeutic hypothermia that serum K+ can rise rapidly.
    • Exogenous insulin/refeeding.
    • Catecholamines/β-agonists.
    • Treatment of anemia/neutropenia.
    • Hypokalemic periodic paralysis: rare; can be either congenital (related to Ca2+ channel or K+ channel mutation) or from thyrotoxicosis/hyperthyroidism.
  • Potassium loss: can be divided into renal and extrarenal (generally GI). See specific etiology in below tables. 

Renal causes of potassium loss

Cause

Associated blood pressure and acid/base

Excess mineralocorticoid activity:

  • Hyperaldosteronism
  • Cushing’s syndrome
  • Congenital syndrome of apparent mineralocorticoid excess
  • Excess licorice ingestion
  • Glucocorticoid remediable hyperaldosteronism
  • Liddle’s syndrome

High BP

Metabolic alkalosis
  • Diuretics
  • Bartter syndrome
  • Gitelman syndrome

Low/normal BP

Metabolic alkalosis
  • DKA
  • RTA Type I or II

Normal BP

Metabolic acidosis
  • Increased distal tubular flow (Fanconi syndrome, glucosuria)
  • Tubular toxins (amphotericin, cisplatin, aminoglycosides)
  • Impaired reabsorption (hypomagnesemia, non-reabsorbed anions)

Normal BP

 

Extrarenal causes of potassium loss

Cause

Acid/base

HCl loss and/or volume contraction: 

  • Vomiting (HCl loss leads to bicarbonaturia, causing K+ loss in urine due to electronegative tubular fluid. All GI losses will also increase RAAS if they reduce EABV)
  • Excess NGT output
  • Sweat

Metabolic alkalosis

Large volume stool output:

  • Diarrhea
  • Laxatives
  • Colostomy

Metabolic acidosis

Evaluation

  • Review medication list.
  • Basic labs:
    • Serum: BMP, Mg, osmolality; consider ABG/VBG for acid-base status.
    • Urine: urine electrolytes (Na, K, Cl), osmolality.
  • Distinguish renal from GI losses with urine K+.
    • How to measure urine K+ excretion:
      • Spot urine K/Cr ratio is often unreliable, but a K/Cr > 22 mEq/g suggests renal K+ wasting.
      • 24 hour urine collection is most helpful.
      • Transtubular potassium gradient (TTKG) is no longer recommended.
    • If inappropriately high urine K+ excretion, consider sending plasma renin activity and aldosterone levels.
      • High renin: suggests diuretics, GI losses, renovascular disease, reninoma (extremely rare).
      • Low renin and high aldosterone: primary hyperaldosteronism.
      • Low renin and low aldosterone: apparent (non-aldosterone) mineralocorticoid excess (e.g. licorice ingestion).
  • In severe hypokalemia, get an EKG. Changes include U-waves, shrunken/inverted T-waves, ST-depression, PR & QRS prolongation, and eventually V-Fib.

Management

  • Replete magnesium first if low (hypomagnesemia leads to K+ wasting).
  • Replete potassium to keep levels around 4 mEq/L.
    • Give about half the suggested dose of potassium in patients with decreased GFR.
    • See section Appendix C: Sliding Scales for detailed potassium supplementation.
    • Oral supplementation: first choice. Max 40 mEq; higher doses can cause stomach upset. Can give additional doses 2 hours apart. Caution in patients with peptic ulcer disease. 
    • IV KCl: usually infused no faster than 10 mEq/hr through a peripheral IV or 20 mEq/hr through a central line. If given too fast, can cause sclerosis of the veins and local pain for the patient.

Key Points

  • When evaluating hypokalemia, use the history to explore possible losses (renal vs. GI), shifts (pH, insulin, etc.), and intake. Get a full medication history. Then use the exam and data (e.g. blood pressure, serum pH, urine studies) to narrow down the mechanisms leading to hypokalemia.
  • Generally, replete potassium orally. Reduce the amount given if a patient has renal impairment.

 

Gennari FJ. Disorders of potassium homeostasis. Hypokalemia and hyperkalemia. Crit Care Clin 2002;18:273-288.

Halperin ML, Kamel KS. Potassium. Lancet 1998;352:135-140.

Reilly, Robert, Nephrology in 30 days. 2005.

Schaeffer TJ, Wolford RW.  Disorders of potassium. Emerg Clin N Am 2005;23:723-747.

Cheng S & Vijayan A (eds.) Nephrology Subspecialty Consult, 3rd addition. 2012.