Abstract
Bradycardia, renal failure, AV nodal blockade, shock, and hyperkalemia (BRASH) syndrome is a rare medical phenomenon that includes the aforementioned symptoms. It can lead to multisystem organ failure, resulting in high mortality. We are reporting a case of BRASH syndrome in a 70-year-old female with a history of chronic kidney disease, severe rheumatic mitral stenosis and paroxysmal atrial fibrillation who presented to the emergency department after an episode of presyncope and worsening shortness of breath. The patient's home medications included carvedilol and apixaban (due to non-compliance with warfarin). Her initial blood pressure (BP) was 162/99 mmHg and heart rate (HR) 28 beats/min. EKG showed junctional bradycardia. After administration of atropine for symptomatic bradycardia and glucagon to reverse beta-blocker activity given poor response to initial atropine treatment, there was a transient improvement of HR to 43 beats/min. However, her BP decreased to 70/40 mmHg, requiring dopamine infusion. Laboratory findings showed significantly elevated blood urea nitrogen (BUN) at 114 mg/dL, creatinine at 12.4 mg/dL (baseline creatinine 6 mg/dL), and critical hyperkalemia of 7.9 mEq/L. These results prompted immediate treatment with intravenous calcium gluconate and an insulin-dextrose infusion, along with oral sodium zirconium cyclosilicate and albuterol nebulization. The patient was admitted to the intensive care unit for management of cardiogenic shock with refractory bradycardia and acute kidney injury with severe hyperkalemia requiring hemodialysis. She underwent urgent hemodialysis with resolution of hyperkalemia and improvement of HR to 68 beats/min and rhythm to sinus, thus, there was no need for pacemaker placement. She was discharged home with initiation of outpatient dialysis. Early recognition of BRASH syndrome is crucial because its management differs significantly from the standard Advanced Cardiovascular Life Support (ACLS) bradycardia algorithm. Unlike the standard approach, therapy for BRASH syndrome extends beyond atropine and electrolyte correction to potentially include hemodynamic vasopressor support, temporary transcutaneous pacing, and urgent renal replacement therapy.