Hypokalemia resident survival guide: Difference between revisions
Rim Halaby (talk | contribs) |
Rim Halaby (talk | contribs) |
||
Line 37: | Line 37: | ||
* [[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) | ||
''Variable acid/base status'' | |||
* [[Hypomagnesemia]] | * [[Hypomagnesemia]] | ||
|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | | |style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | |
Revision as of 22:34, 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 plasma potassium concentration less than 3.5 mEq/L. Hypokalemia may present as ileus, muscle cramps, rhabdomyolysis, and polyuria. Electrocardiography 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 | |
|
Subject is normo or hypotensive Associated with alkalosis
Variable acid/base status |
Subject is hypertensive
Secondary hyperaldosteronism
|
Associated with metabolic acidosis Associated with metabolic alkalosis
|
|
|
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.