Hypokalemia: Difference between revisions

(Created page with "==Background== Low = <3.5meq/L Low! = <2.5meq/L ==Diagnosis== Symptoms: 1) CNS (weakness, cramps, hyporeflexia) 2) GI (ileaus) 3) CV (dysrhythmia, dig tox, U waves, S...")
 
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==Background==
==Background==
*Hypokalemia is one of the most common electrolyte derangements
*While mild-moderate hypokalemia can be asymptomatic or mildly symptomatic, severe hypokalemia can be fatal
*Potassium is predominantly intracellular; important in maintaining cell membrane potential, especially in cardiac/nerve/muscle tissue
*While the renal and endocrine systems regulate total body potassium, transient physiologic shifts can greatly alter measured serum potassium


==Clinical Features==
*Central nervous system
**[[Weakness]] or [[Numbness]]
**[[myalgia|Cramps]]
**Hyporeflexia
*Gastrointestinal
**[[Ileus]]
**[[Nausea and vomiting]]
*Renal
**[[Metabolic alkalosis]]
*Cardiovascular
**[[PACs]]/[[PVCs]]
**[[ACLS: Bradycardia|Bradycardia]] or [[atrial tachycardia|atrial]]/[[junctional tachycardia]]
**[[Atrial fibrillation]]
**[[AV block]]
**[[Tachycardia (wide)|Ventricular tachycardia]], [[Adult pulseless arrest|Ventricular fibrillation]]


Low = <3.5meq/L


Low! = <2.5meq/L
==Differential Diagnosis<ref>In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. McGraw-Hill; Accessed November 29, 2020. https://accessmedicine.mhmedical.com/content.aspx?bookid=1658&sectionid=109381281</ref>==
[[File:Hypokalemia.png|thumb|Differential diagnosis of hypokalemia]]
===Intracellular Shift===
*Alkalosis (each 0.10 rise in pH causes 0.5 decrease)
*[[Insulin]]
*[[Beta agonists]]
*[[Hypokalemic periodic paralysis]]


===Decreased intake===
*Special diets or those low in potassium
*Chronic [[alcohol Abuse|alcohol abuse]]
*Fasting
*Eating disorders


==Diagnosis==
===Increased loss===
*GI
**[[Vomiting]], [[diarrhea]], fistula
*Renal
**[[Diuretics]], especially loop and thiazide diuretics
**Osmotic diuresis (late-presenting [[Diabetic ketoacidosis|DKA]])
**Hyperaldosteronism
**[[Renal tubular acidosis]]
**[[Hypercalcemia]]
**[[Hypomagnesemia]]
*Increased sweat loss
**Heavy exercise
**Heat stroke
**Fever


===Drugs===
*Barium
*Catecholamines
*Glycyrrhizin (licorice extract)
*[[Insulin]]
*L-dopa
*[[Lithium toxicity|Lithium]]
*[[Penicillins]]
*[[Quinine]]
*[[Theophylline]], methylxanthines (e.g. [[caffeine]])


Symptoms:
===Other===
*Acute leukemia and lymphomas
*Recovery from megaloblastic anemia
*Hypothermia (accidental or induced)


1) CNS (weakness, cramps, hyporeflexia)
==Evaluation==
*Serum potassium level is diagnostic
**Normal = 3.5-5meq/L
**Moderate hypokalemia = between 2.5 and 3.0 meq/L. Severe hypokalemia = <2.5meq/L
*Always check magnesium
**Na+/K+ ATPase pump requires Mg to function, therefore low Mg can lead to refractory hypoK
*Obtain [[ECG]]. Suggestive findings include:
**[[ST segment depression]] or flattened or inverted [[T wave]]
**U wave (V4-V6)  
**[[QT prolongation]]
**[[Premature ventricular contraction]], other ectopy, or any new arrhythmia
*Careful review of medication list


2) GI (ileaus)


3) CV (dysrhythmia, dig tox, U waves, ST depression, prolonged QT)
[[Image:ECG Hypokalemia.jpg]]


4) Renal (met alkalosis)
==Management==
*Potassium repletion (PO or IV)
**Every 10mEq KCl → serum K ↑ ~0.1mEq/L
**PO preferred; if symptomatic or level is <2.5, both oral and IV should be given
**Note: Administration of KCl during an ongoing intracellular shift can lead to rebound hyperkalemia when the shift reverses
**Potassium chloride is usually preferred; other forms of potassium salts (potassium bicarbonate, potassium phosphate) increases serum potassium slower<ref>Cohn JN, Kowey PR, Whelton PK, Prisant LM. New guidelines for potassium replacement in clinical practice: a contemporary review by the National Council on Potassium in Clinical Practice. Arch Intern Med. 2000 Sep 11;160(16):2429-36. doi: 10.1001/archinte.160.16.2429. PMID: 10979053.</ref>
**Consider repeating chem panel 3-4 hrs later to check for response; check faster if giving at a faster rate
*Oral potassium
**Inexpensive, well-tolerated, and rapidly absorbed
**Consider giving 20 mEq q3hr or 40 mEq PO q6hr
**KCl tablet (elixir form available but has poor taste)
**K-Dur (extended release tablet) is large and may be difficult to swallow
**If sending patient home can also increase food intake of potassium as an alternative or supplementing potassium tablets. Printable table that can be given to the patient available at this reference: <ref>[https://www.mayoclinic.org/drugs-supplements/potassium-supplement-oral-route-parenteral-route/description/drg-20070753?p=1 Potassium Supplement (Oral Route, Parenteral Route) from Mayo Clinic]</ref>.
*Intravenous potassium
**Must be given in dilute solutions at slow rate (10 mEq/hour) to minimize side effects (burning/phlebitis) and cardiac toxicity
***If needing to infuse at 20 mEq/hr, consider infusion via central line or two peripheral lines
**Consider runs of 10 mEq in 100 mL of water, each administered over 1 hr. Or 40-60 mEq in a 1000 mL bag, administered at a rate appropriate to type of IV access
**Do not replete with dextrose-containing solutions since dextrose-induced insulin release can worsen hypokalemia
**Continuous tele is recommended for both the underlying hypokalemia and the potassium administration
*Also treat [[Hypomagnesemia]] if present
*Re-check ECG after treatment <ref>Slovis, Corey. "Electrolyte Emergencies". Presentation.</ref>
*Hypokalemia in acute or recent [[myocardial infarction]] places patients at much higher risk for [[ventricular fibrillation]]<ref>Goyal A et al. Serum Potassium Levels and Mortality in Acute Myocardial Infarction. JAMA. 2012;307(2):157-164.</ref>
**Previous studies and many professional organizations recommend maintaining K between 4.0 - 5.0 mEq/L in MI patients
**However, more recent studies suggest 3.5 - 4.5 mEq/L results in the lowest mortality


==DDX==
A. Shift
    1) Increased pH
    2) B-agonist, inuslin
B. Reduced intake
C. Increased loss
    1) Renal
          i) Primary (hyperaldos, osmotic diuresis)
          ii) Secondary (*diuretics, malignant HTN, renal art stenosis)
          iii) Misc (licorice, hyperCa, Mg def, RTA, leukemia)
          iv) Drugs (PCN, lithium, L-dopa, theophyline)
    2) GI Loss (v/d/fistula)
==Treatment==
20meq/h KCl IV or PO
(every 10meq should inc serum by ~0.1meq/L)
*treat hypomag if present
==Source ==
2/7/06 DONALDSON (adapted from Tintinalli)


==Disposition==
*Based on underlying cause
*One admission criteria is potassium less than 3.0 meq/L and a QTc that is close to or more than 500 msec. <ref>[https://www.emrap.org/episode/emrap2018august/electrolyte EM:RAP 2018 August Electrolyte Emergencies - Part 1 - All Things Potassium]</ref>


==See Also==
*[[Electrolyte Abnormalities (Main)]]
*[[Hypokalemic periodic paralysis]]
*[[Hyperkalemia]]


==External Links==
*[https://emcrit.org/ibcc/hypokalemia/ IBCC Hypokalemia]
*[http://ddxof.com/electrolyte-abnormalities/ DDxOf: Differential Diagnosis of Electrolyte Abnormalities]


==References==
<references/>
[[Category:FEN]]
[[Category:FEN]]

Latest revision as of 03:09, 6 August 2025

Background

  • Hypokalemia is one of the most common electrolyte derangements
  • While mild-moderate hypokalemia can be asymptomatic or mildly symptomatic, severe hypokalemia can be fatal
  • Potassium is predominantly intracellular; important in maintaining cell membrane potential, especially in cardiac/nerve/muscle tissue
  • While the renal and endocrine systems regulate total body potassium, transient physiologic shifts can greatly alter measured serum potassium

Clinical Features


Differential Diagnosis[1]

Differential diagnosis of hypokalemia

Intracellular Shift

Decreased intake

  • Special diets or those low in potassium
  • Chronic alcohol abuse
  • Fasting
  • Eating disorders

Increased loss

Drugs

Other

  • Acute leukemia and lymphomas
  • Recovery from megaloblastic anemia
  • Hypothermia (accidental or induced)

Evaluation

  • Serum potassium level is diagnostic
    • Normal = 3.5-5meq/L
    • Moderate hypokalemia = between 2.5 and 3.0 meq/L. Severe hypokalemia = <2.5meq/L
  • Always check magnesium
    • Na+/K+ ATPase pump requires Mg to function, therefore low Mg can lead to refractory hypoK
  • Obtain ECG. Suggestive findings include:
  • Careful review of medication list


ECG Hypokalemia.jpg

Management

  • Potassium repletion (PO or IV)
    • Every 10mEq KCl → serum K ↑ ~0.1mEq/L
    • PO preferred; if symptomatic or level is <2.5, both oral and IV should be given
    • Note: Administration of KCl during an ongoing intracellular shift can lead to rebound hyperkalemia when the shift reverses
    • Potassium chloride is usually preferred; other forms of potassium salts (potassium bicarbonate, potassium phosphate) increases serum potassium slower[2]
    • Consider repeating chem panel 3-4 hrs later to check for response; check faster if giving at a faster rate
  • Oral potassium
    • Inexpensive, well-tolerated, and rapidly absorbed
    • Consider giving 20 mEq q3hr or 40 mEq PO q6hr
    • KCl tablet (elixir form available but has poor taste)
    • K-Dur (extended release tablet) is large and may be difficult to swallow
    • If sending patient home can also increase food intake of potassium as an alternative or supplementing potassium tablets. Printable table that can be given to the patient available at this reference: [3].
  • Intravenous potassium
    • Must be given in dilute solutions at slow rate (10 mEq/hour) to minimize side effects (burning/phlebitis) and cardiac toxicity
      • If needing to infuse at 20 mEq/hr, consider infusion via central line or two peripheral lines
    • Consider runs of 10 mEq in 100 mL of water, each administered over 1 hr. Or 40-60 mEq in a 1000 mL bag, administered at a rate appropriate to type of IV access
    • Do not replete with dextrose-containing solutions since dextrose-induced insulin release can worsen hypokalemia
    • Continuous tele is recommended for both the underlying hypokalemia and the potassium administration
  • Also treat Hypomagnesemia if present
  • Re-check ECG after treatment [4]
  • Hypokalemia in acute or recent myocardial infarction places patients at much higher risk for ventricular fibrillation[5]
    • Previous studies and many professional organizations recommend maintaining K between 4.0 - 5.0 mEq/L in MI patients
    • However, more recent studies suggest 3.5 - 4.5 mEq/L results in the lowest mortality


Disposition

  • Based on underlying cause
  • One admission criteria is potassium less than 3.0 meq/L and a QTc that is close to or more than 500 msec. [6]

See Also

External Links

References

  1. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. McGraw-Hill; Accessed November 29, 2020. https://accessmedicine.mhmedical.com/content.aspx?bookid=1658&sectionid=109381281
  2. Cohn JN, Kowey PR, Whelton PK, Prisant LM. New guidelines for potassium replacement in clinical practice: a contemporary review by the National Council on Potassium in Clinical Practice. Arch Intern Med. 2000 Sep 11;160(16):2429-36. doi: 10.1001/archinte.160.16.2429. PMID: 10979053.
  3. Potassium Supplement (Oral Route, Parenteral Route) from Mayo Clinic
  4. Slovis, Corey. "Electrolyte Emergencies". Presentation.
  5. Goyal A et al. Serum Potassium Levels and Mortality in Acute Myocardial Infarction. JAMA. 2012;307(2):157-164.
  6. EM:RAP 2018 August Electrolyte Emergencies - Part 1 - All Things Potassium