The most appropriate treatment for lowering this patient's serum potassium level most quickly is intravenous glucose and insulin. He has end-stage kidney disease (ESKD) and presents with hyperkalemia and peaked T waves on electrocardiogram. Hyperkalemia is defined as a serum potassium level >5.0 mEq/L (5.0 mmol/L). Any level >6.0 mEq/L (6.0 mmol/L) can be life-threatening. Signs and symptoms are related to adverse effects of serum potassium on skeletal and cardiac muscle cell membranes, including muscle weakness and cardiac conduction and rhythm abnormalities. Intravenous calcium gluconate stabilizes the myocardium by lowering the threshold potential and is usually administered acutely to decrease the risk of arrhythmias; however, calcium does not have any effect on serum potassium levels. Major underlying causes of persistent hyperkalemia are disorders in which urine potassium excretion is impaired. The most common cause is chronic kidney disease with a glomerular filtration rate <20 mL/min/1.73 m2 or acute kidney injury. The appropriate treatment for reducing serum potassium quickly in this patient with ESKD and hyperkalemia is both insulin and glucose given intravenously to rapidly shift potassium intracellularly. Insulin effectively drives potassium into cells by increasing activity of the Na-K-ATPase pump in skeletal muscle. Glucose is given to counteract potential hypoglycemia associated with insulin therapy.
High-dose loop and thiazide diuretics increase kidney potassium loss, particularly when combined with saline hydration, in patients with normal kidney function or mild to moderate kidney failure. However, this effect is not immediate, and bumetanide would be ineffective in this patient with ESKD.
Intravenous sodium bicarbonate raises the serum pH and leads to a shift of potassium into cells as part of the buffering process. However, it has not been shown to be an effective or predictable method for producing a hypokalemic response, especially in patients with ESKD.
Oral sodium polystyrene sulfonate in sorbitol binds potassium in the colon in exchange for sodium. It is not useful for acute control of hyperkalemia because its effect on potassium is delayed for at least 2 hours and peaks at 4 to 6 hours. In addition, its effect on hyperkalemia is modest.