Along with addressing underlying causes, the treatment options for hyperkalemia consist of dietary restriction, pharmacotherapy, and hemodialysis. Asymptomatic patients with mild hyperkalemia may be managed with dietary education and careful monitoring of potassium concentration. A loop diuretic may be added to increase urinary potassium elimination. For patients unable to tolerate loop diuretics, a cation-exchange resin like sodium polystyrene sulfonate (SPS) may be administered orally or rectally. In patients with severe hyperkalemia or acute ECG changes, intravenous calcium is administered for stabilization of the cardiac membrane and hemodynamics. Calcium gluconate is preferred over calcium chloride due to an increased risk of tissue necrosis with the chloride salt if extravasation occurs. Concomitantly, an additional therapy should be instituted to shift potassium intracellularly and attain a serum potassium concentration <5.5 mEq/L. Sodium bicarbonate, insulin and dextrose, and albuterol are available options. Comorbid disease processes may influence the choice of therapy. Sodium bicarbonate is advantageous for patients with concomitant metabolic acidosis; however, the effects on potassium-lowering are significantly delayed in patients with advanced renal insufficiency. Additionally, renal patients are at increased risk of sodium and volume overload. Insulin and dextrose administration does not adversely impact volume status, but blood glucose levels must be monitored carefully. Beta-agonists have a dual mechanism for lowering potassium by stimulating the Na+-K+-ATPase pump and stimulating increased secretion of pancreatic insulin, but the effects can be unpredictable secondary to variable bioavailability of inhaled agents. Finally, excess potassium is removed from the body with diuretics, a resin binder, or hemodialysis.27,28 Dosing information and utility of available therapies for potassium disorders is described in Tables 34-6 and 34-7.
Adverse effects associated with treatment of hyperkalemia include hypo- or hyperglycemia from administration of insulin and dextrose, SPS-induced diarrhea, cardiac excitability from albuterol, volume depletion or electrolyte abnormalities following diuretic therapy, and hypercalcemia from intravenous calcium. Additionally, skin necrosis may occur if calcium extravasates.
During emergent treatment, the serum potassium concentration should be evaluated hourly, and ECG monitored continuously until the serum concentration is <5 mEq/L and ECG changes have resolved. Patients who receive SPS and are asymptomatic should have serum potassium concentrations obtained within 4 hours to guide the need for readministration.