RESUMO
A 76-year-old man was evaluated in our emergency department (ED) for right toe swelling and pain. His initial ED workup revealed volume overload, uncontrolled hypertension, slow atrial fibrillation, refractory hypokalemia, mixed metabolic alkalosis and respiratory acidosis, with a normal plasma pH, and hypernatremia. His medical chart revealed long standing hyperkalemia and metabolic acidosis, related to his diabetic kidney disease. We hypothesized that a short course of daily SPS ingestion (Sodium Polystyrene Sulfonate, "Kayexalate") was the sole etiology for the compound electrolyte abnormalities and the electrolyte "flip flop". SPS ingestion can cause hypokalemia by excessive potassium binding in the gut. SPS exchanging potassium for sodium caused excessive sodium retention leading to hypernatremia, hypertension and volume overload. Volume overload worsened his chronic obstructive sleep apnea and yielded respiratory acidosis. Finally hypokalemia by itself was the main trigger for generation and maintenance of metabolic alkalosis. Urinary electrolytes, and renin and aldosterone levels taken at the ED ruled out primary aldosteronism and renal potassium and hydrogen loss. The patient's potassium was replenished by both PO and IV routes. He was treated for his volume overload and hypertension with furosemide. Spironolactone and amiloride, potassium sparing diuretics, were cautiously given only during his hypokalemic phase. His plasma sodium and potassium levels, blood pressure and volume status gradually improved. "Kayexalate" effect should be suspected in a patient presenting with unexplained hypokalemia and alkalosis, accompanied by volume overload rather than volume depletion, developing shortly after SPS ingestion. ED doctors should specifically ask CKD or ESRD patients on SPS, as it otherwise can skip the medication reconciliation process.