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== | ||
*Serum potassium <3.5 mEq/L | |||
*Most common electrolyte abnormality encountered in clinical practice | |||
*Severity: | |||
**Mild: 3.0-3.5 mEq/L | |||
**Moderate: 2.5-3.0 mEq/L | |||
**Severe: <2.5 mEq/L (risk of arrhythmia, respiratory failure) | |||
*Every 1 mEq/L decrease in serum K represents ~200-400 mEq total body deficit | |||
===Causes=== | |||
*Decreased intake: malnutrition, anorexia, alcoholism | |||
*GI losses (most common): | |||
**Vomiting (metabolic alkalosis → renal K wasting) | |||
**Diarrhea (direct K loss) | |||
**NG suction, laxative abuse | |||
*Renal losses: | |||
**Diuretics (loops, thiazides — most common medication cause) | |||
**Hyperaldosteronism (primary or secondary) | |||
**[[Renal tubular acidosis]] (types 1 and 2) | |||
**Hypomagnesemia (impairs renal K conservation) | |||
**Osmotic diuresis ([[DKA]]) | |||
*Transcellular shift (K moves into cells): | |||
**Insulin (therapeutic or endogenous) | |||
**Beta-2 agonists (albuterol) | |||
**Alkalosis | |||
**Catecholamine surge, thyrotoxicosis | |||
**Hypothermia (shifts K intracellularly) | |||
==Clinical Features== | |||
*Often asymptomatic with mild hypokalemia | |||
*Muscle weakness (proximal > distal), cramps, myalgia | |||
*Ileus, constipation, nausea/vomiting | |||
*Rhabdomyolysis (severe hypokalemia) | |||
*Cardiac arrhythmias: | |||
**PACs, PVCs → atrial or ventricular [[tachycardia]] → torsades de pointes → VF | |||
**Potentiates [[digoxin toxicity]] | |||
===ECG Changes=== | |||
*Flattened T waves (earliest) | |||
*Prominent U waves (after T wave) | |||
*ST depression | |||
*Prolonged QT interval | |||
*T-U fusion (severe) | |||
==Differential Diagnosis== | |||
*Medication-induced (diuretics, insulin, albuterol) | |||
*GI losses (vomiting, diarrhea) | |||
*[[Diabetic ketoacidosis]] (total body K depleted despite possible normal level) | |||
*Hyperaldosteronism | |||
*[[Renal tubular acidosis]] | |||
*Hypomagnesemia | |||
*Bartter/Gitelman syndrome | |||
*Thyrotoxic periodic paralysis | |||
== | ==Evaluation== | ||
*ECG (look for U waves, flattened T waves, prolonged QT) | |||
*BMP: K level, bicarbonate (alkalosis?), glucose, creatinine | |||
*Magnesium level (hypokalemia refractory to replacement if Mg not corrected) | |||
*Calcium level (concurrent abnormalities) | |||
*Consider: urine K (spot urine K/Cr ratio or 24h K), urine chloride, TSH, cortisol/aldosterone if unexplained | |||
*Digoxin level if on digoxin (hypokalemia increases digoxin sensitivity) | |||
==Management== | |||
===Guiding Principles=== | |||
*Always check and replace magnesium first — hypokalemia is refractory to correction with concurrent hypomagnesemia | |||
*Oral replacement preferred when possible (better tolerated, less risky) | |||
*IV replacement for severe hypokalemia, ECG changes, or NPO patients | |||
===Mild Hypokalemia (3.0-3.5 mEq/L)=== | |||
*Oral KCl 20-40 mEq PO q2-4h (typical total dose 40-100 mEq/day) | |||
*Increase dietary potassium | |||
===Moderate Hypokalemia (2.5-3.0 mEq/L)=== | |||
*KCl 10-20 mEq/hr IV via peripheral line (max 40 mEq/L concentration peripherally) | |||
**Higher concentrations require central line | |||
*Max infusion rate: 10-20 mEq/hr (peripheral); up to 40 mEq/hr via central line with cardiac monitoring | |||
*Concurrent oral supplementation | |||
2) | ===Severe Hypokalemia (<2.5 mEq/L or ECG Changes)=== | ||
*Continuous cardiac monitoring | |||
*KCl 20-40 mEq/hr IV via central line | |||
*Magnesium sulfate 2g IV (if Mg not checked yet, give empirically) | |||
*Recheck K every 1-2 hours | |||
*May require 200+ mEq total replacement | |||
3 | ===Special Situations=== | ||
*[[DKA]]: K may be normal or elevated on presentation but total body stores are depleted | |||
**Replace K ''before or concurrent with insulin'' when K <5.3 | |||
**'''Do NOT start insulin if K <3.3''' — replace K to >3.3 first | |||
*[[Digoxin toxicity]]: maintain K >4.0 mEq/L | |||
*Refractory hypokalemia: check and replace magnesium<ref>Huang CL, Kuo E. Mechanism of hypokalemia in magnesium deficiency. J Am Soc Nephrol. 2007;18(10):2649-2652. PMID 17804670</ref>; consider amiloride or spironolactone | |||
==Disposition== | |||
*Admit if K <2.5, symptomatic, ECG changes, arrhythmia, or ongoing losses | |||
*Continuous telemetry for K <3.0 or ECG changes | |||
*Discharge if mild (3.0-3.5), asymptomatic, clear correctable cause, tolerated PO replacement, normal ECG | |||
*Close follow-up with recheck in 24-48 hours | |||
==See Also== | |||
*[[Hyperkalemia]] | |||
*[[Hypomagnesemia]] | |||
*[[Digoxin toxicity]] | |||
*[[Diabetic ketoacidosis]] | |||
*[[Electrolyte imbalances]] | |||
== | ==References== | ||
*Kardalas E, et al. Hypokalemia: a clinical update. ''Endocr Connect''. 2018;7(4):R135-R146. PMID 29540487 | |||
*Gennari FJ. Hypokalemia. ''N Engl J Med''. 1998;339(7):451-458. PMID 9700180 | |||
*Viera AJ, Wouk N. Potassium disorders: hypokalemia and hyperkalemia. ''Am Fam Physician''. 2015;92(6):487-495. PMID 26371733 | |||
*Crop MJ, et al. Role of magnesium in hypokalemia. ''Crit Care''. 2012;16(1):229. PMID 22866973 | |||
[[Category:Renal]] | |||
[[Category:Critical Care]] | |||
[[Category: | |||
Latest revision as of 10:06, 22 March 2026
Background
- Serum potassium <3.5 mEq/L
- Most common electrolyte abnormality encountered in clinical practice
- Severity:
- Mild: 3.0-3.5 mEq/L
- Moderate: 2.5-3.0 mEq/L
- Severe: <2.5 mEq/L (risk of arrhythmia, respiratory failure)
- Every 1 mEq/L decrease in serum K represents ~200-400 mEq total body deficit
Causes
- Decreased intake: malnutrition, anorexia, alcoholism
- GI losses (most common):
- Vomiting (metabolic alkalosis → renal K wasting)
- Diarrhea (direct K loss)
- NG suction, laxative abuse
- Renal losses:
- Diuretics (loops, thiazides — most common medication cause)
- Hyperaldosteronism (primary or secondary)
- Renal tubular acidosis (types 1 and 2)
- Hypomagnesemia (impairs renal K conservation)
- Osmotic diuresis (DKA)
- Transcellular shift (K moves into cells):
- Insulin (therapeutic or endogenous)
- Beta-2 agonists (albuterol)
- Alkalosis
- Catecholamine surge, thyrotoxicosis
- Hypothermia (shifts K intracellularly)
Clinical Features
- Often asymptomatic with mild hypokalemia
- Muscle weakness (proximal > distal), cramps, myalgia
- Ileus, constipation, nausea/vomiting
- Rhabdomyolysis (severe hypokalemia)
- Cardiac arrhythmias:
- PACs, PVCs → atrial or ventricular tachycardia → torsades de pointes → VF
- Potentiates digoxin toxicity
ECG Changes
- Flattened T waves (earliest)
- Prominent U waves (after T wave)
- ST depression
- Prolonged QT interval
- T-U fusion (severe)
Differential Diagnosis
- Medication-induced (diuretics, insulin, albuterol)
- GI losses (vomiting, diarrhea)
- Diabetic ketoacidosis (total body K depleted despite possible normal level)
- Hyperaldosteronism
- Renal tubular acidosis
- Hypomagnesemia
- Bartter/Gitelman syndrome
- Thyrotoxic periodic paralysis
Evaluation
- ECG (look for U waves, flattened T waves, prolonged QT)
- BMP: K level, bicarbonate (alkalosis?), glucose, creatinine
- Magnesium level (hypokalemia refractory to replacement if Mg not corrected)
- Calcium level (concurrent abnormalities)
- Consider: urine K (spot urine K/Cr ratio or 24h K), urine chloride, TSH, cortisol/aldosterone if unexplained
- Digoxin level if on digoxin (hypokalemia increases digoxin sensitivity)
Management
Guiding Principles
- Always check and replace magnesium first — hypokalemia is refractory to correction with concurrent hypomagnesemia
- Oral replacement preferred when possible (better tolerated, less risky)
- IV replacement for severe hypokalemia, ECG changes, or NPO patients
Mild Hypokalemia (3.0-3.5 mEq/L)
- Oral KCl 20-40 mEq PO q2-4h (typical total dose 40-100 mEq/day)
- Increase dietary potassium
Moderate Hypokalemia (2.5-3.0 mEq/L)
- KCl 10-20 mEq/hr IV via peripheral line (max 40 mEq/L concentration peripherally)
- Higher concentrations require central line
- Max infusion rate: 10-20 mEq/hr (peripheral); up to 40 mEq/hr via central line with cardiac monitoring
- Concurrent oral supplementation
Severe Hypokalemia (<2.5 mEq/L or ECG Changes)
- Continuous cardiac monitoring
- KCl 20-40 mEq/hr IV via central line
- Magnesium sulfate 2g IV (if Mg not checked yet, give empirically)
- Recheck K every 1-2 hours
- May require 200+ mEq total replacement
Special Situations
- DKA: K may be normal or elevated on presentation but total body stores are depleted
- Replace K before or concurrent with insulin when K <5.3
- Do NOT start insulin if K <3.3 — replace K to >3.3 first
- Digoxin toxicity: maintain K >4.0 mEq/L
- Refractory hypokalemia: check and replace magnesium[1]; consider amiloride or spironolactone
Disposition
- Admit if K <2.5, symptomatic, ECG changes, arrhythmia, or ongoing losses
- Continuous telemetry for K <3.0 or ECG changes
- Discharge if mild (3.0-3.5), asymptomatic, clear correctable cause, tolerated PO replacement, normal ECG
- Close follow-up with recheck in 24-48 hours
See Also
References
- Kardalas E, et al. Hypokalemia: a clinical update. Endocr Connect. 2018;7(4):R135-R146. PMID 29540487
- Gennari FJ. Hypokalemia. N Engl J Med. 1998;339(7):451-458. PMID 9700180
- Viera AJ, Wouk N. Potassium disorders: hypokalemia and hyperkalemia. Am Fam Physician. 2015;92(6):487-495. PMID 26371733
- Crop MJ, et al. Role of magnesium in hypokalemia. Crit Care. 2012;16(1):229. PMID 22866973
- ↑ Huang CL, Kuo E. Mechanism of hypokalemia in magnesium deficiency. J Am Soc Nephrol. 2007;18(10):2649-2652. PMID 17804670
