hypokalemia
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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
- distal renal tubular acidosis (RTA-1)
- hypomagnesemia causes loss of potassium into the urine[3] through the collecting tubule
- alcoholism frequently associated with hypomagnesemia[9]
- proton pump inhibitors are associated with hypomagnesemia[3]
- gastrointestinal
- gastrointestinal (GI) loss of K+
- vomiting[3]
- diarrhea through upregulation of K+ channels in the colon
- villous adenoma
- fistula
- laxative abuse
- decreased dietary intake
- starvation
- clay ingestion
- gastrointestinal (GI) loss of K+
- intracellular shift of K+
- insensible losses
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
- smooth muscle dysfunction
- renal failure
- renal tubular dysfunction
- glucose intolerance[3]
- 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
- high blood pressure: excess glucocorticoids, mineralocorticoids (urine Cl- generally > 40 meq/L)
- 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[3]
- urine Cl- > 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[3]
- > 20 meq/L suggests renal origin
- serum Mg+2: may be low[3]
- blood gas: pH
- metabolic alkalosis
- vomiting, NG suction, diarrhea, previous diuretics
- metabolic alkalosis
* 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[3]
- increased prominence of U wave
- ventricular arrhythmias
- severe hypokalemia
- in patients taking digoxin
Complications
- exacerbation of digitalis toxicity
- glucose intolerance from impaired insulin secretion
Management
- fatal arrhythmias may occur in patients taking digoxin even if hypokalemia is mild
- oral KCl (first resort)
- intravenous KCl*, potassium phosphate
- normal saline for chloride-reponsive hypokalemic metabolic alkalosis with low urine chloride
- potassium sparing diuretics*
- 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[3]
* no advantage to potassium acetate; acetate may exacerbate metabolic alkalosis[10]
* use of K+ sparing diuretics questioned[10]
More general terms
Additional terms
References
- ↑ Harrison's Principles of Internal Medicine, 13th ed. Companion Handbook, Isselbacher et al (eds), McGraw-Hill Inc. NY, 1995, pg 831
- ↑ Saunders Manual of Medical Practice, Rakel (ed), WB Saunders, Philadelphia, 1996, pg 674-676
- ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 Medical Knowledge Self Assessment Program (MKSAP) 11, 14, 15, 16, 18, 19. American College of Physicians, Philadelphia 1998, 2006, 2009, 2012, 2018, 2021.
Medical Knowledge Self Assessment Program (MKSAP) 19 Board Basics. An Enhancement to MKSAP19. American College of Physicians, Philadelphia 2022 - ↑ Sandle GI, Hunter M. Apical potassium (BK) channels and enhanced potassium secretion in human colon. QJM. 2010 Feb;103(2):85-9. PMID: https://www.ncbi.nlm.nih.gov/pubmed/19892809
- ↑ Unwin RJ, Luft FC, Shirley DG. Pathophysiology and management of hypokalemia: a clinical perspective. Nat Rev Nephrol. 2011 Feb;7(2):75-84. PMID: https://www.ncbi.nlm.nih.gov/pubmed/21278718
- ↑ Shin HS. Value of the measurement of urinary chloride in hypokalaemic metabolic alkalosis. PMID: https://www.ncbi.nlm.nih.gov/pubmed/20377781
- ↑ Berl T, Rastegar A. A patient with severe hyponatremia and hypokalemia: osmotic demyelination following potassium repletion. Am J Kidney Dis. 2010 Apr;55(4):742-8. PMID: https://www.ncbi.nlm.nih.gov/pubmed/20338465
- ↑ Medford-Davis L, Rafique Z. Derangements of potassium. Emerg Med Clin North Am. 2014 May;32(2):329-47. Review. PMID: https://www.ncbi.nlm.nih.gov/pubmed/24766936
- ↑ 9.0 9.1 Elisaf M; Liberopoulos E; Bairaktari E; Siamopoulos K Hypokalaemia in alcoholic patients. Drug Alcohol Rev. 2002; 21(1):73-6 PMID: https://www.ncbi.nlm.nih.gov/pubmed/12189007 https://reference.medscape.com/medline/abstract/12189007
- ↑ 10.0 10.1 10.2 NEJM Knowledge+ Endocrinology
- ↑ Palmer BF, Clegg DJ. Physiology and pathophysiology of potassium homeostasis: core curriculum 2019. Am J Kidney Dis. 2019;74:682-695. PMID: https://www.ncbi.nlm.nih.gov/pubmed/31227226