Until recently, approved treatment options for hyperkalemia focused on emergent, intermediate, and maintenance interventions. Emergent treatments work within minutes by shifting K+ from the plasma space into the cell. After the serum K+ level is reduced to safe levels, experts recommend that treatment should focus on lowering total body K+ with intermediate or maintenance interventions.
Explore below to learn more about the different treatments for hyperkalemia.
A commonly used regimen to acutely treat life-threatening hyperkalemia is the intravenous administration of 10 units of regular insulin along with 25 g of glucose. Insulin works by redistributing K+ into the cells.
Calcium gluconate, administered parenterally, has the fastest onset of action among drugs used for the treatment of hyperkalemia and is used when ECG changes are present. It is administered to stabilize the myocardium; it lowers the threshold potential, thus counteracting the toxic effect of high K+.
β2 agonists can be administered intravenously, subcutaneously, or inhaled. They work by redistributing K+ to the intracellular space. The effect of β2 agonists is additive to that of insulin administration and they can be taken together. It should be noted that β2 agonists may be ineffective in up to 25% of patients when given by a nebulizer.
Sodium bicarbonate facilitates the movement of K+ from the plasma into the cell. However, due to the fact that sodium bicarbonate does not lower K+ in the absence of metabolic acidosis, experts no longer recommend this treatment except in patients with severe metabolic acidosis. In addition, this treatment generates a large sodium load, often a major factor limiting its use in patients with heart failure.
Loop or thiazide diuretics are sometimes used to prevent a rise in serum K+ by increasing the distal delivery of sodium and urine flow rate, effects that promote a kaliuresis.
According to KDOQI guidelines, thiazide diuretics given once daily are recommended in patients with GFR ≥30 mL/min/1.73 m2 (CKD stage 1-3), while loop diuretics given once or twice daily are recommended in patients with GFR <30 mL/min/1.73 m2 (CKD stage 4-5). However, it should be noted that, in general, patients with decreased kidney function may be relatively resistant to the effects of diuretics.
Diuretics have been associated with a number of adverse reactions. KDOQI guidelines recommend that patients being treated with diuretics should be monitored for volume depletion (for which heart failure patients are especially at risk), hypokalemia, and other electrolyte disorders (like hypomagnesemia and hyponatremia, which can cause lasting damage).
Furthermore, use of diuretics in some patients may be a risk because some complications that arise from their use are rare or idiosyncratic; their occurrence cannot be anticipated or prevented.
For patients who have persistent or severe hyperkalemia but very poor kidney function, such as stage 4 or 5 CKD, acute hemodialysis is the last course of action.
During hemodialysis, plasma K+ falls rapidly in the first hour and very little thereafter. If a 0-K dialysate is used, serum K+ may decrease by as much as 1.2 to 1.5 mEq/h. K+ concentrations show a rebound after dialysis is finished, and this rebound may require several hours to reach a plateau.
GI excretion is accomplished using SPS, which binds K+ in the colon in exchange for sodium. Warnings and Precautions were added to an SPS label in 2009 and 2011 due to cases of intestinal necrosis and other serious GI adverse events.
The National Kidney Disease Education Program supports dietary restriction of K+ for initial management of hyperkalemia in patients with CKD. While this strategy helps limit intake, it does not address any underlying kidney dysfunction that is reducing the excretion of K+.
Reproduced with permission from Weiner ID, Linas SL, Wingo CS. Disorders of Potassium Metabolism. In: Johnson R, Fluege J, Feehally J, eds. Comprehensive Clinical Nephrology. 4th ed. Philadelphia, PA: Saunders Elsevier; 2010:118-129.
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Identification and interruption of hyperkalemia-inducing medications (especially RAASi medications) is one of the guideline-recommended strategies for preventing recurrent episodes of elevated serum K+.
However, in patients treated with this strategy, a higher percentage of adverse outcomes or mortality was observed. Mortality was observed twice as frequently in patients who were discontinued from RAASi or were receiving a suboptimal dose irrespective of comorbidity status.
Until recently, the treatment paradigm for hyperkalemia has remained without major advances.1 However, as science evolves, the use of K+ binders to help patients chronically manage serum K+ is being explored on an ongoing basis.