Hypokalemia resident survival guide: Difference between revisions
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* Metabolic alkalosis (K+/H+ exchanger) | * [[Metabolic alkalosis]] (K+/H+ exchanger) | ||
* Insulin (activates Na+/K+ ATPase) | * [[Insulin]] (activates Na+/K+ ATPase) | ||
* Catecholamine (activates Na+/K+ ATPase) | * [[Catecholamine]] (activates Na+/K+ ATPase) | ||
* Hypokalemic thyrotoxic periodic paralysis | * [[Hypokalemic thyrotoxic periodic paralysis]] | ||
* Hypothermia | * [[Hypothermia]] | ||
* Chloroquine | * [[Chloroquine | ||
* Barium intoxication | * [[Barium]] intoxication | ||
* Cesium intoxication | * [[Cesium]] intoxication | ||
* Antipsychotic overdose | * [[Antipsychotic overdose]] | ||
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'''''Subject is normo or hypotensive'''''<br> | '''''Subject is normo or hypotensive'''''<br> | ||
''Associated with acidosis'' | ''Associated with acidosis'' | ||
* Diabetic ketoacidosis | * [[Diabetic ketoacidosis]] | ||
* Renal tubular acidosis type 1 | * [[Renal tubular acidosis type 1]] | ||
* Renal tubular acidosis type 2 | * [[Renal tubular acidosis type 2]] | ||
''Associated with alkalosis'' | ''Associated with alkalosis'' | ||
* Diuretics | * [[Diuretics]] | ||
* Vomiting (increase aldosterone) | * [[Vomiting]] (increase in [[aldosterone]]) | ||
* Bartter's syndrome (dysfunction of in loop of Henle) | * [[Bartter's syndrome]] (dysfunction of in loop of Henle) | ||
* Gitelman's syndrome (dysfunction in distal convoluted tubules) | * [[Gitelman's syndrome]] (dysfunction in distal convoluted tubules) | ||
* Hypomagnesemia | * [[Hypomagnesemia]] | ||
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'''''Subject is hypertensive'''''<br> | '''''Subject is hypertensive'''''<br> | ||
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* Conn's syndrome | * Conn's syndrome | ||
''Secondary hyperaldosteronism'' | ''Secondary hyperaldosteronism'' | ||
* Cushing's disease | * [[Cushing's disease]] | ||
* Congenital adrenal hyperplasia | * [[Congenital adrenal hyperplasia]] | ||
* Increased | * Increased [[mineralcorticoid]]s | ||
* Licorice ingestion | * Licorice ingestion | ||
* Liddle's | * [[Liddle's syndrome]] | ||
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''Associated with metabolic acidosis'' | ''Associated with metabolic acidosis'' | ||
* Diarrhea | * [[Diarrhea]] | ||
* Laxative abuse | * [[Laxative abuse]] | ||
* Villous adenoma | * [[Villous adenoma]] | ||
''Associated with metabolic alkalosis'' | ''Associated with metabolic alkalosis'' | ||
* Vomiting | * [[Vomiting]] | ||
* Nasogastric tube drainage | * [[Nasogastric tube]] drainage | ||
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* Megaloblastic anemia | * [[Megaloblastic anemia]] | ||
* Treatment of anemia | * Treatment of [[anemia]] | ||
* Crisis of AML | * Crisis of [[AML]] | ||
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* Tea and toast diet | * Tea and toast diet | ||
* Anorexia nervosa | * [[Anorexia nervosa]] | ||
* Alcoholism | * [[Alcoholism]] | ||
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Revision as of 22:27, 21 October 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]
Overview
Hypokalemia is defined as plasmapotassium levels less than 3.5 mEq/L. Hypokalemia may present as ileus, muscle cramps, rhabdomyolysis, and hypomagnesemia. EKG findings may include U wave, flat or inverted T waves, prolonged QT interval, and ventricular ectopy.
Causes
Life Threatening Causes
Life-threatening conditions which may result in death or permanent disability within 24 hours if left untreated. Severe hypokalemia may be life-threatening and must be treated as such irrespective of the underlying cause.
Common Causes
Shown below is a table summarizing the different pathophysiological processes that can lead to hypokalemia.
Trans-cellular shifts | Renal loss | GI loss | Increased hematopoiesis | Decreased intake of potassium | |
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Subject is normo or hypotensive Associated with alkalosis
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Subject is hypertensive
Secondary hyperaldosteronism
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Associated with metabolic acidosis Associated with metabolic alkalosis
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|
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Diagnostic Algorithm
Shown below is an algorithm depicting the possible laboratory findings and their interpretation.
Hypokalemia [K+] < 3.5 | |||||||||||||||||||||||||||||||||||||||||||||||
Order: ❑ 24 hours urinary K+ (UK) ❑ Transtubular potassium gradient (TTKG) | |||||||||||||||||||||||||||||||||||||||||||||||
UK > 25-30 mEq/L TTKG > 7 | UK < 25 mEq/L TTKG < 3 | ||||||||||||||||||||||||||||||||||||||||||||||
Renal loss of potassium | GI loss of potassium | ||||||||||||||||||||||||||||||||||||||||||||||
What is the blood pressure? | |||||||||||||||||||||||||||||||||||||||||||||||
Normal or ↓ | ↑ | ||||||||||||||||||||||||||||||||||||||||||||||
Check the acid/base status | Possible etiologies are: Primary aldosteronism Secondary aldosteronism Non aldosterone increase in mineralcorticoids | ||||||||||||||||||||||||||||||||||||||||||||||
Acidemia | Alkalemia | Variable | |||||||||||||||||||||||||||||||||||||||||||||
Check urinary chloride (UCl) | Hypomagnesemia | ↑ Aldosterone ↓ Renin | ↑ Aldosterone ↑ Renin | ↓ Aldosterone | |||||||||||||||||||||||||||||||||||||||||||
UCl < 20 | UCl > 20 | Primary aldosteronism | Secondary aldosteronism | Non aldosterone increase in mineralcorticoids | |||||||||||||||||||||||||||||||||||||||||||
Management
- Treat the underlying etiology.
- Dosages for potassium repletion are:
- PO: 40 mEq KCL Q 4-6 hours
- IV (if urgent): 10 mEq/hour KCL
- Recheck potassium levels in 2-4 hours.
- Provide IV hydration if necessary.
Do's
- Avoid excessive potassium repletion, particularly in the cases of transcellual shifts of potassium that can be reversed when the initial cause of hypokalemia is treated.
- Treat low magnesium blood concentration.
Dont's
- If hydration is needed, do not administer dextrose solutions because dextrose increases insulin which can causes intracellular shift of potassium, and further exacerbates hypokalemia.