Hyperkalemia resident survival guide: Difference between revisions
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{{familytree | | | | | | | | | B01 | | | | | |B01=Assess [[EKG]]}} | {{familytree | | | | | | | | | B01 | | | | | |B01=Assess [[EKG]]}} | ||
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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= 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 | | | 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]]}} |
Revision as of 19:17, 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.