Diabetic Ketoacidosis With Refractory Hypokalemia Leading to Cardiac Arrest

Abstract

Diabetic ketoacidosis (DKA) is known to cause total body potassium depletion, but during initial presentation, very few patients are hypokalemic, and even fewer patients experience clinical effects. As the correction of acidosis and insulin drive potassium intracellularly, measured serum potassium levels decrease and require repletion. This phenomenon is well described, and severe hypokalemia necessitates delaying insulin therapy. Less well described is the kaliuretic nature of treatments of cerebral edema. We present a case of an adolescent male with new-onset type 2 diabetes who presented in DKA with signs of cerebral edema, hyperosmolarity, and hypokalemia. As insulin and cerebral edema therapy were initiated, his hypokalemia worsened despite significant IV repletion, eventually leading to ventricular tachycardia and cardiac arrest. Over the following 36 hours, the patient received >590 milliequivalents (mEq) of potassium. He was discharged home 12 days after admission without sequelae of his cardiac arrest.