Multimodal therapy including hemodialysis and MICRA leadless pacemaker implantation successfully managed a life-threatening case of BRASH syndrome in an 85-year-old female.
Case Report (n=1)
Early recognition and a multimodal approach, including hemodialysis and potentially pacemaker placement, are essential for managing the life-threatening synergistic cycle of BRASH syndrome.
Abstract BRASH syndrome (bradycardia, renal failure, AV nodal blockade, shock, and hyperkalemia) is a life-threatening but underrecognized condition triggered by a synergistic interaction between AV nodal blockers and renal dysfunction. Prompt diagnosis is essential to prevent irreversible organ damage. We present a case of BRASH syndrome in an elderly patient requiring intensive care unit admission, vasopressors, and dialysis. An 85-year-old female with a history of hypertension, esophageal cancer status post esophagectomy, chronic kidney disease (baseline creatinine 2.0 mg/dL), coronary artery disease post-coronary artery bypass graft, atrial fibrillation (on metoprolol succinate and apixaban), and hypothyroidism was admitted from a rehabilitation facility with dizziness and nausea. On arrival, she had profound sinus bradycardia, hypotension, and confusion. Workups were notable for potassium 7.0 mmol/L and creatinine 3.34 mg/dL. The patient was treated with insulin, calcium gluconate, albuterol, and IV fluids followed by atropine and glucagon to counteract beta blockade with limited response. She was admitted to the medical ICU and started on dopamine and norepinephrine. Despite fluid repletion and beta blocker discontinuation, her renal function continued to decline, requiring hemodialysis. Following dialysis, the patient’s potassium, renal function, and hemodynamics improved, and vasopressors were stopped. Six days into the patient's hospital course, she developed atrial fibrillation with rapid ventricular response. A MICRA leadless pacemaker was implanted to prevent further bradycardia-induced renal hypoperfusion, allowing safe resumption of metoprolol without recurrence of BRASH. BRASH syndrome is characterized by a synergistic cycle between AV nodal blockade, renal injury, and hyperkalemia requiring early recognition. Unlikely isolated hyperkalemia or beta-blocker toxicity, the synergism of BRASH leads to profound hemodynamic instability despite relatively mild hyperkalemia and beta-blocker dosage. An early multimodal approach to interrupt the cycle is essential. In our case, pacemaker placement additionally enabled rate control in atrial fibrillation while minimizing bradycardia. Clinicians must maintain a high index of suspicion for BRASH as its own clinical entity as prompt recognition and management may be lifesaving. This abstract is funded by: None
Liu et al. (Fri,) conducted a case report in BRASH syndrome (n=1). Multimodal therapy and MICRA leadless pacemaker was evaluated. Multimodal therapy including hemodialysis and MICRA leadless pacemaker implantation successfully managed a life-threatening case of BRASH syndrome in an 85-year-old female.