Acute management of hyperkalemia involves various interventions, including the intravenous administration of calcium salts or drugs that affect the cellular distribution of K+, and definitive measures to remove K+ from the body. The effects of interventions that alter the distribution of K+ usually occur within a short period of time (<1h), but they do not affect total body K+ levels. Definitive therapy for hyperkalemia in patients with a net positive K+ balance necessitates the removal of K+ from the body.
Explore below to learn more about the different treatments for hyperkalemia.
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+.
Intravenous administration of 10 units of regular insulin with 50 g of glucose can help prevent hypoglycemia
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. Experimental studies suggest that the sorbitol added to sodium polystyrene sulphonate is the main exacerbating factor for colonic necrosis. However, some case reports suggest that polystyrene sulphonate derivatives administered without sorbitol can also cause gastrointestinal toxicity.
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.
Visit the organizations below for more information on K+-rich foods and strategies to establish a better dietary routine.
The most vexing clinical problem is the management of hyperkalemia in patients receiving RAAS inhibitors, as the known beneficial effects of these agents on both kidney function and cardiovascular disease makes their discontinuation undesirable. Nonetheless, discontinuation rates of these agents remain very high in patients with CKD.