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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. loss of P waves, hyperacute T waves and widened QRS<br>[[Image:EKG_hyperkalemia.gif|center| | {{familytree | | | C01 | | | | | | | | | | | C02 |C01=[[EKG]] changes, e.g. loss of P waves, hyperacute T waves and widened QRS<br>[[Image:EKG_hyperkalemia.gif|center|350px]]|C02=No changes in [[EKG]], stable patient}} | ||
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{{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 14:49, 26 July 2013
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Hyperkalemia Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Mahmoud Sakr, M.D. [2]
For hyperkalemia smart algorithm click here
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
Life Threatening Causes
Life-threatening causes include conditions which result in death or permanent disability within 24 hours if left untreated.
- Acute renal failure
- Adrenal insufficiency
- Diabetic ketoacidosis
- Large IV doses of calcium chloride or calcium gluconate
- Massive hemolysis
- Metabolic acidosis
- Rapid tissue necrosis
- Rhabdomyolysis
- Tumor lysis syndrome
Common Causes
- Pseudohyperkalemia
- Renal insufficiency
- Adrenal insufficiency
- Medications: ACE inhibitors, angiotensin receptor blockers, amiloride, spironolactone, NSAIDS, ciclosporin, tacrolimus, trimethoprim, pentamidine, succinylcholine
- Renal tubular acidosis type 4
- Iatrogenic
- Diabetic ketoacidosis
Management
Shown below is an algorithm summarizing the approach to hyperkalemia.
| High potassium level | |||||||||||||||||||||||||||||||||||||||||||||||||||
| R/O Pseudohyperkalemia Repeat potassium level | |||||||||||||||||||||||||||||||||||||||||||||||||||
| Check vital signs Stabilize the patient Order an EKG Concise history and physical exam | |||||||||||||||||||||||||||||||||||||||||||||||||||
| Assess EKG | |||||||||||||||||||||||||||||||||||||||||||||||||||
EKG changes, e.g. loss of P waves, hyperacute T waves and widened QRS | No changes in EKG, stable patient | ||||||||||||||||||||||||||||||||||||||||||||||||||
| 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
- Place the patient on a closely monitored bed for potential fatal arrhythmias, esp. with levels higher than 6.5.
- Repeat basic metabolic panels frequently.
- Stop 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.
- Consider consultation with nephrology.
Dont's
- Don't over use kayexalate, as it has been reported to cause colonic transmural necrosis.[1]
- Don't over treat with IV bicarbonate as it can lead to rebound metabolic alkalosis.
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.