IN 1968, Brunner and Frick reported severe metabolic alkalosis and hypokalemia in patients receiving large doses of penicillin G sodium.<sup>1</sup>It was suggested that penicillin promoted urinary potassium excretion by acting as a nonreabsorbable anion. Subsequently, correspondence in the medical literature implicated carbenicillin as another possible cause of hypokalemic alkalosis.<sup>2-4</sup>We report here the development of hypokalemia, hypochloremia, and metabolic alkalemia during the course of intravenous administration of carbenicillin disodium in a patient with pulmonary<i>Pseudomonas</i>infection. Serial arterial blood gas studies clearly demonstrated metabolic alkalosis in this patient. <h3>Report of a Case</h3> A 61-year-old woman had a recent thoracotomy and biopsy of a mass that demonstrated squamous cell carcinoma of the right upper lobe with metastases to the pleura and regional lymph nodes. After a week's course of postoperative radiation therapy, there was an onset of fever and a productive cough. Two sputum cultures were positive for