One hot summer evening, sweating away in the gym, I stumbled across a pearl from Scott Weingert's EMCrit podcast. His podcasts are full of many gems, but for a third year medical student, most of them are neither practical at the moment nor within my comprehension. His "Is Kayexelate Useless?" episode picked apart the evidence behind our utilization of this binding resin in hyperkalemia. I found this useful as an overeager medical student, recently unbound by the restraints of the classroom and ready to save some lives on the wards....or check labs and write SOAP notes all day.
Nevertheless, I eagerly attempted to apply the information garnered from this podcast when I was pimped on hyperkalemia a few days later. My attending stated that over his years in clinical medicine, he has witnessed sodium polystyrene sulfonate (kayexelate, SPS) work. I made it my mission to ask nearly every general practitioner about their experience with SPS. Until today, I had only heard positive things about the effect of SPS in hyperkalemia. The general sentiment was something akin to: "Well, I started Kayexelate and by the next day their potassium decreased from 7 to 4." What about all of the other therapies that were simultaneously started (or stopped)? Today, however, my attending made rotating for a month in nephrology worthwhile when he stated he thought people still used SPS due to habit and dogma.
So why do we still use SPS for hyperkalemia? It's probably a reflex, something that was taught and has become an unquestioned standard practice. Also, since there is a paucity of evidence on SPS in terms of harm (although SPS with sorbitol is clearly BAD for the bowel), it's probably something that gives us reassurance that at least we've done something. According to the evidence base, diuretics aren't much better than SPS in decreasing potassium and we all want to do something to feel like we're actively helping our patients.
Problems with the evidence: The evidence base for SPS in hyperkalemia is meager and results from a 1961 article in the NEJM. Unfortunately, I was unable to read the article and there is no abstract, save a meager 100 word preview, available online. However, the study was small and didn't actually measure the excretion of potassium other than measuring the serum potassium level in the patients some 24 hours later.
Problems with the resins: SPS with sorbitol can cause colonic necrosis, which can be nasty. Also, we don't even know if SPS works for hyperkalemia.
Efficacy of the resins: A 2010 article in the J Am Soc Nephrol by Sterns et sl is pretty convincing that there is really no evidence that SPS increases fecal loss of potassium thus leading us to inquire, what good is the drug doing?
So what do we do?
In an emergency-
- First line management for hyperkalemia is still to ensure that the heart is protected, as hyperkalemia causes a depolarization of the cardiac membrane resting potential. If there are ECG changes that are scary...like a widened QRS, then give calcium gluconate 1000 mg via IV push over 2-3 minutes. You can give calcium chloride 500-1000 mg but from what I understand, this burns pretty bad so it shouldn't be given through a peripheral line.
- Calcium chloride contains much more elemental calcium, but due to aforementioned reasons, calcium gluconate may be a better bet if you don't have central access.
- Monitor the patient's cardiac status and dose again in 5 minutes if the ECG still looks bad.
- Don't give in bicarbonate solutions because you'll end up with Calcium Carbonate precipitation
- Calcium works within minutes but the effects will wear off within the hour
- Insulin + glucose. The insulin (usually 10 U in 500 mL of D10 over 1 hour) will drive the potassium into cells. The glucose will prevent you from having to deal with a hypoglycemic patient (Unless the patient's glucose is already over 250)
- Results in a 0.5 mEq-1.2 mEq lowering of potassium which will occur within an hour and persist for 4-6 hours
- B2 adrenergic agonists: Theoretically, these should work just as we memorized during our first two years of medical school. I have no experience using these (which isn't saying much since I have no experience at...anything) and I've been somewhat dismissed when I've mentioned these while hanging out in our ED. UpToDate recommends the possiblity of using albuterol in patients an addendum to the insulin/glucose therapy. Just remember that albuterol can make people jumpy and tachycardic.
- Sodium Bicarbonate: This is for the sick patients with a bad metabolic acidosis. The effect on the serum potassium is suggested to be mild (maybe 0.5 mEq) although it is does increase the bicarbonate in an individual with metabolic acidosis.
Fix the cause?
- RAAS inhibitors (spironolactone, eplerenone, etc)
- Urinary Tract Obstruction
Long Term Treatment? So now that the patient is not in imminent danger of a life threatening arrhythmia, how do we get rid of the excess potassium?
- Loop/thiazide diuretics (furosemide, torsemide, hydrochlorothiazide, etc). These, along with gentle saline hydration, are probably most effective chronically.
- Dialyze if the patient has ESRD, extreme hyperkalemia, or has a crush injury or another mechanism of severe tissue breakdown (which will release potassium as well as other toxins into the blood)
- Sterns RH, et al. Ion-exchange resins for the treatment of hyperkalemia: are they safe and effective? J Am Soc Nephrol. 2010 May;21(5):733-5. doi: 10.1681/ASN.2010010079. Epub 2010 Feb 18.
- Lens XM, Montoliu J, Cases A, Campistol JM, Revert L "Treatment of hyperkalaemia in renal failure: salbutamol v. insulin. Nephrol Dial Transplant." 1989;4(3):228.
- David B Mount. "Treatment and Prevention of Hyperkalemia." February 15, 2011 Accessed at http://www.uptodate.com.ezproxylocal.library.nova.edu/contents/treatment-and-prevention-of-hyperkalemia?source=search_result&search=kayexelate&selectedTitle=4~26#H15