Hyperkalemia resident survival guide: Difference between revisions
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== Definition== | == Definition== | ||
[[Hyperkalemia]] is defined as a serum potassium concentration greater than 5.5 mEq/L in adults. Levels higher than 7 mEq/L can lead to significant hemodynamic compromise | [[Hyperkalemia]] is defined as a serum potassium concentration greater than 5.5 mEq/L in adults. Levels higher than 7 mEq/L can lead to significant hemodynamic compromise. | ||
==Causes== | ==Causes== | ||
*Hyperkalemia is most commonly caused by increased intake, impaired renal excretion, or rapid transcellular shift | *Hyperkalemia is most commonly caused by increased intake, impaired renal excretion, or rapid transcellular shift. | ||
===Life-Threatening Causes=== | ===Life-Threatening Causes=== | ||
Life-threatening here means a condition that can lead to death or permanent disability within 24 hours | Life-threatening here means a condition that can lead to death or permanent disability within 24 hours. | ||
* [[Acute | * [[Acute renal failure]] | ||
* [[Rhabdomyolysis]] | * [[Rhabdomyolysis]] | ||
* [[Rapid tissue necrosis]] | * [[Rapid tissue necrosis]] | ||
* [[Tumor | * [[Tumor lysis syndrome]] | ||
* [[Metabolic acidosis]], [[diabetic ketoacidosis]] | * [[Metabolic acidosis]], | ||
* [[Massive hemolysis]] | * [[diabetic ketoacidosis]] | ||
* [[Hemolysis|Massive hemolysis]] | |||
* large IV doses of [[Calcium chloride]] or [[calcium gluconate]] | * large IV doses of [[Calcium chloride]] or [[calcium gluconate]] | ||
* [[Adrenal insufficiency classification|Adrenal insufficiency]] | * [[Adrenal insufficiency classification|Adrenal insufficiency]] | ||
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*[[Renal insufficiency|acute or chronic renal failure]], (more common in acute) | *[[Renal insufficiency|acute or chronic renal failure]], (more common in acute) | ||
*[[Adrenal insufficiency]] | *[[Adrenal insufficiency]] | ||
* Medications; [[ACE inhibitor|ACE inhibitors]], [[ | * Medications; [[ACE inhibitor|ACE inhibitors]], [[angiotensin II receptor antagonist|angiotensin receptor blockers]], [[amiloride]],[[spironolactone]],[[NSAIDS]],[[ciclosporin]], [[tacrolimus]], [[trimethoprim]], [[pentamidine]], [[succinylcholine]] | ||
*[[RTA|Renal tubular acidosis]] (usually with type 4) | *[[RTA|Renal tubular acidosis]] (usually with type 4) | ||
* Iatrogenic | * [[Iatrogenic]] | ||
*[[diabetic ketoacidosis]] | *[[diabetic ketoacidosis]] | ||
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{{familytree | | | C01 | | | | | | | | | | | C02 |C01=EKG changes;e.g. hyperacute T waves, widened QRS,|C02=EKG not changed, patient stable}} | {{familytree | | | C01 | | | | | | | | | | | C02 |C01=EKG changes;e.g. hyperacute T waves, widened QRS,|C02=EKG not changed, patient stable}} | ||
{{familytree | | | |!| | | | | | | | | | | | |!|}} | {{familytree | | | |!| | | | | | | | | | | | |!|}} | ||
{{familytree | | | D01 | | | | | | | | | | | |!|| D01= | {{familytree | | | D01 | | | | | | | | | | | |!|| D01= Use rapidly acting transient agents,e.g [[Insulin]], [[Dextrose]], IV [[Calcium]]; with [[Ca gluconate]] generally preferred over [[Ca chloride]], inhaled [[beta2-adrenergic receptor agonist|Beta2 agonists]]}} | ||
{{familytree | | | | | | | | | | | | | | | | |!|}} | {{familytree | | | | | | | | | | | | | | | | |!|}} | ||
{{familytree | | | | | | | | | | |,|-|-|-|-|-|+|-|-|-|-|-|.|}} | {{familytree | | | | | | | | | | |,|-|-|-|-|-|+|-|-|-|-|-|.|}} | ||
{{familytree | | | | | | | | | | E01 | | | | E02 | | | | E03 |E01=Kayexalate, orally, and also can be given rectally in unconscious patients to avoid risks of aspiration'|E02=IV hydration|E03= stop potential causative medications }} | {{familytree | | | | | | | | | | E01 | | | | E02 | | | | E03 |E01=Kayexalate, orally, and also can be given rectally in unconscious patients to avoid risks of aspiration'|E02=IV hydration|E03= stop potential causative medications }} | ||
{{familytree | | | | | | | | | | | | | | | | |!| | | | | |!| | | }} | {{familytree | | | | | | | | | | | | | | | | |!| | | | | |!| | | }} | ||
{{familytree | | | | | | | | | | | | | | | | H01 | | | | H02 | |H01= | {{familytree | | | | | | | | | | | | | | | | H01 | | | | H02 | |H01= Use carefully in potential heart failure patients,<br> consider diuresis when clinically appropriate|H02= consult with nephrology for resistant and severe cases of hyperkalemia <br>may require urgent dialysis, yet rare}} | ||
{{familytree/end}} | {{familytree/end}} | ||
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==Do's and Don'ts== | ==Do's and Don'ts== | ||
* Place the patient on a closely monitored bed for potential fatal arrhythmias, esp. with levels higher than 6.5 | * Place the patient on a closely monitored bed for potential fatal arrhythmias, esp. with levels higher than 6.5. | ||
* Repeat basic metabolic panels frequently | * Repeat basic metabolic panels frequently. | ||
* Be ware when using [[kayexalate]], as it has been reported to cause colonic transmural necrosis<ref name="pmid3824154">{{cite journal| author=Lillemoe KD, Romolo JL, Hamilton SR, Pennington LR, Burdick JF, Williams GM| title=Intestinal necrosis due to sodium polystyrene (Kayexalate) in sorbitol enemas: clinical and experimental support for the hypothesis. | journal=Surgery | year= 1987 | volume= 101 | issue= 3 | pages= 267-72 | pmid=3824154 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3824154 }} </ref> | * Be ware when using [[kayexalate]], as it has been reported to cause colonic transmural necrosis.<ref name="pmid3824154">{{cite journal| author=Lillemoe KD, Romolo JL, Hamilton SR, Pennington LR, Burdick JF, Williams GM| title=Intestinal necrosis due to sodium polystyrene (Kayexalate) in sorbitol enemas: clinical and experimental support for the hypothesis. | journal=Surgery | year= 1987 | volume= 101 | issue= 3 | pages= 267-72 | pmid=3824154 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3824154 }} </ref> | ||
* Remove the offending medications that are associated with [[Hyperkalemia]] | * Remove the offending medications that are associated with [[Hyperkalemia]]. | ||
* Keep the patient well hydrated | * Keep the patient well hydrated. | ||
* Check levels of other [[electrolyte|electrolytes]] such as [[Magnesium]] and [[phosphorus]] as it may be abnormal as well. | * Check levels of other [[electrolyte|electrolytes]] such as [[Magnesium]] and [[phosphorus]] as it may be abnormal as well. | ||
* Avoid over treating with IV [[Bicarbonate]] as it may lead to rebound [[metabolic alkalosis]] | * Avoid over treating with IV [[Bicarbonate]] as it may lead to rebound [[metabolic alkalosis]]. | ||
* Consider consultation with [[nephrology]] | * Consider consultation with [[nephrology]]. | ||
==References== | ==References== |
Revision as of 19:10, 23 July 2013
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Mahmoud Sakr, M.D. [2]
Definition
Hyperkalemia is defined as a serum potassium concentration greater than 5.5 mEq/L in adults. Levels higher than 7 mEq/L can lead to significant hemodynamic compromise.
Causes
- Hyperkalemia is most commonly caused by increased intake, impaired renal excretion, or rapid transcellular shift.
Life-Threatening Causes
Life-threatening here means a condition that can lead to death or permanent disability within 24 hours.
- Acute renal failure
- Rhabdomyolysis
- Rapid tissue necrosis
- Tumor lysis syndrome
- Metabolic acidosis,
- diabetic ketoacidosis
- Massive hemolysis
- large IV doses of Calcium chloride or calcium gluconate
- Adrenal insufficiency
Common Causes
- Pseudoyperkalemia (consider rechecking the levels to confirm)
- acute or chronic renal failure, (more common in acute)
- Adrenal insufficiency
- Medications; ACE inhibitors, angiotensin receptor blockers, amiloride,spironolactone,NSAIDS,ciclosporin, tacrolimus, trimethoprim, pentamidine, succinylcholine
- Renal tubular acidosis (usually with type 4)
- Iatrogenic
- diabetic ketoacidosis
Management
Shown below is an algorithm summarizing the approach to hyperkalemia.
Check vital signs Stabilize the patient Order an EKG Concise history and physical exam | |||||||||||||||||||||||||||||||||||||||||||||||||||
Assess EKG | |||||||||||||||||||||||||||||||||||||||||||||||||||
EKG changes;e.g. hyperacute T waves, widened QRS, | EKG not changed, patient stable | ||||||||||||||||||||||||||||||||||||||||||||||||||
Use rapidly acting transient agents,e.g Insulin, Dextrose, IV Calcium; with Ca gluconate generally preferred over Ca chloride, inhaled Beta2 agonists | |||||||||||||||||||||||||||||||||||||||||||||||||||
Kayexalate, orally, and also can be given rectally in unconscious patients to avoid risks of aspiration' | IV hydration | stop potential causative medications | |||||||||||||||||||||||||||||||||||||||||||||||||
Use carefully in potential heart failure patients, consider diuresis when clinically appropriate | consult with nephrology for resistant and severe cases of hyperkalemia may require urgent dialysis, yet rare | ||||||||||||||||||||||||||||||||||||||||||||||||||
Do's and Don'ts
- Place the patient on a closely monitored bed for potential fatal arrhythmias, esp. with levels higher than 6.5.
- Repeat basic metabolic panels frequently.
- Be ware when using kayexalate, as it has been reported to cause colonic transmural necrosis.[1]
- Remove the offending medications that are associated with Hyperkalemia.
- Keep the patient well hydrated.
- Check levels of other electrolytes such as Magnesium and phosphorus as it may be abnormal as well.
- Avoid over treating with IV Bicarbonate as it may lead to rebound metabolic alkalosis.
- Consider consultation with nephrology.
References
- ↑ Lillemoe KD, Romolo JL, Hamilton SR, Pennington LR, Burdick JF, Williams GM (1987). "Intestinal necrosis due to sodium polystyrene (Kayexalate) in sorbitol enemas: clinical and experimental support for the hypothesis". Surgery. 101 (3): 267–72. PMID 3824154.