Hyperkalemia resident survival guide: Difference between revisions
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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}} | ||
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{{familytree | | | D01 | | | | | | | | | | | |!|| D01= use rapidly acting transient agents,e.g [[Insulin]], [[Dextrose]], IV [[calcium]], inhaled Beta2 agonists}} | {{familytree | | | D01 | | | | | | | | | | | |!|| D01= use rapidly acting transient agents,e.g [[Insulin]], [[Dextrose]], IV [[calcium]]; with [[Ca gluconate]] generally preferred over [[ca chloride]], inhaled Beta2 agonists}} | ||
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Revision as of 17:06, 23 July 2013
Resident Survival Guide |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; associate editor-in-chief: Mahmoud Sakr, M.D. [2]
Definition
Hyperkalemia is best 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
Common Causes
- Pseudoyperkalemia
- acute or chronic renal failure
- Adrenal insufficiency
- Medications; ACE inhibitors, Angiotensin receptor blockers, amiloride,spironolactone, NSAIDS,ciclosporin, Tacrolimus, Trimethoprim, Pentamidine, succinylcholine
- Renal tubular acidosis
- Iatrogenic
Life-Threatening Causes
- 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
Management
Please find below an algorithm that summarizes 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
- 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