For hospitalized patients with mild hyperkalemia, using a higher dose of sodium polystyrene sulfonate (SPS) results in greater reductions in serum potassium, with minimal risk of subsequent hypokalemia, a new study suggests.
Despite routine use of SPS in treating hyperkalemia, previous research has not revealed an optimal dosing strategy. To provide clinicians with some guidance, a team headed by Mielen Mistry, BScPhm, ACPR, a clinical pharmacist at Kingston General Hospital in Ontario, Canada, reviewed the medical records of 118 in-patients who received sorbitol-free SPS at Ottawa Hospital 2010–2014. The investigators evaluated both oral and rectal SPS at doses of 15g, 30g, and 60g oral and 30g rectal. The study excluded patients receiving dialysis or other hyperkalemia treatments around the time of SPS therapy. The researchers measured potassium levels within 12 hours before and after SPS, accounting for the drug’s slow onset and duration of action.
According to results published in Annals of Pharmacotherapy, serum potassium levels decreased by 0.39, 0.69, and 0.91 mEq/L following 15g, 30g, and 60g oral doses of SPS, respectively. The 30g rectal dose lowered potassium by just 0.22 mEq/L. Interestingly, factors such as concurrent administration with a stimulant laxative, did not alter SPS dose-response.
Half of patients receiving oral SPS at 15g had persistent hyperkalemia compared with 23% of the 60g group. All patients in the rectal SPS group remained hyperkalemic. None of the patients experienced post-treatment hypokalemia.
“The results of this study support the use of a single 60g oral dose of SPS to treat a mild hyperkalemic episode, without concern for post-dose hypokalemia,” Mistry told Renal & Urology News. The 60g dose potentially prevents the need for repeat, smaller doses of SPS and multiple blood draws. For moderate to severe hyperkalemia (defined as potassium levels above 6 mEq/L), Mistry discouraged the use of SPS as monotherapy in favor of alternative approaches.
As rectal SPS showed limited efficacy, using an alternative strategy in NPO patients, such as an intravenous bolus of insulin/dextrose or sodium bicarbonate seems warranted, according to Mistry. The hypothesis is the decrease in response may be due to the resin not reaching far enough to have sustained contact with potassium in the lumen of the gastrointestinal tract.
Greater reductions in potassium from oral SPS have been reported in previous studies, such as a 2011 study published in the Journal of Hospital Medicine by Chad Kessler, MD, and colleagues. The differences may be due to the timing of the post-dose potassium measurement (an average 10 hours in the 2011 study and 6.5 hours in this study). In addition, the 2011 study did not consider the influence of stopping hyperkalemia-precipitating agents.
Among the limitations, the current study did not account for some factors that could affect SPS response, such as excretion of the resin, diarrhea, vomiting, edema, and fluid shifting.