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Review
. 2017 Oct 7;3(1):47-55.
doi: 10.1016/j.ekir.2017.10.001. eCollection 2018 Jan.

Treatment of Severe Hyperkalemia: Confronting 4 Fallacies

J Gary Abuelo  1
Affiliations
Review

Treatment of Severe Hyperkalemia: Confronting 4 Fallacies

J Gary Abuelo. Kidney Int Rep. .

Abstract

Severe hyperkalemia is a medical emergency that can cause lethal arrhythmias. Successful management requires monitoring of the electrocardiogram and serum potassium concentrations, the prompt institution of therapies that work both synergistically and sequentially, and timely repeat dosing as necessary. It is of concern then that, based on questions about effectiveness and safety, many physicians no longer use 3 key modalities in the treatment of severe hyperkalemia: sodium bicarbonate, sodium polystyrene sulfonate (Kayexalate [Concordia Pharmaceuticals Inc., Oakville, ON, Canada], SPS [CMP Pharma, Farmville, NC]), and hemodialysis with low potassium dialysate. After reviewing older reports and newer information, I believe that these exclusions are ill advised. In this article, I briefly discuss the treatment of severe hyperkalemia and detail why these modalities are safe and effective and merit inclusion in the treatment of severe hyperkalemia.

Keywords: Kayexalate; colonic necrosis; low potassium dialysate; severe hyperkalemia; sodium bicarbonate; sodium polystyrene sulfonate.

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Figures

Figure 1
Figure 1
Sequential response of hyperkalemia to 4 therapies administered as initial management to a virtual hemodialysis patient. This patient missed a week of dialysis and presented to the hospital with muscle weakness, bradycardia, a serum potassium concentration of 8.5 mmol/l, bicarbonate concentration of 16 mmol/l, and an electrocardiogram (ECG) showing loss of P waves and a QRS in a sine-wave pattern. The ECG reverted to normal sinus rhythm after a second dose of calcium before there was a significant change in serum potassium level. The arteriovenous fistula was clotted. By the time vascular access was re-established and dialysis was performed, the serum potassium fell to a safe level (5.2 mmol/l).
Figure 2
Figure 2
Muscle cell uptake of potassium during therapy with sodium bicarbonate (NaHCO3). Functional coupling between sodium−hydrogen (Na+–H+) exchange and Na+, potassium (K+) adenosine triphosphatase (ATPase) (a) leads to apparent K+–H+ exchange, and between Na+–HCO3– cotransport and Na+, K+–ATPase (b) leads to apparent K+–HCO3– cotransport.
Figure 3
Figure 3
Plasma potassium concentration during and after dialysis.
See this image and copyright information in PMC

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