Grout Sarah, Maue Danielle, Berrens Zachary, Swinger Nathan, Malin Stefan
Department of Pediatrics, Indiana University School of Medicine, Indianapolis, USA.
Department of Pediatrics, Division of Critical Care, Riley Hospital for Children, Indianapolis, USA.
Cureus. 2022 Mar 24;14(3):e23439. doi: 10.7759/cureus.23439. eCollection 2022 Mar.
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.
糖尿病酮症酸中毒（DKA）已知会导致全身钾耗竭，但在初次就诊时，很少有患者出现低钾血症，出现临床症状的患者更少。随着酸中毒的纠正以及胰岛素促使钾进入细胞内，测得的血清钾水平会下降，需要补充钾。这种现象已有充分描述，严重低钾血症需要延迟胰岛素治疗。关于脑水肿治疗导致钾排泄增加的性质描述较少。我们报告一例青少年男性，新发2型糖尿病，以DKA就诊，伴有脑水肿、高渗状态和低钾血症的体征。在开始胰岛素和脑水肿治疗后，尽管静脉大量补钾，其低钾血症仍恶化，最终导致室性心动过速和心脏骤停。在接下来的36小时内，患者接受了超过590毫当量（mEq）的钾。入院12天后出院，未遗留心脏骤停的后遗症。
