BRASH Syndrome: A Rare Etiology of Cardiogenic Shock
Presenter
Steven Imburgio, MD, Jersey Shore University Medical Center, Neptune, NJ
Steven Imburgio, MD, Anne Marie Arcidiacono, MD, Lauren Klei, MD, Anmol Singh Johal, MD, Kylie Oppegaard, MD, Shuvendu Sen, MD, Mohammad Hossain, MD and Riple Hansalia, MD, Jersey Shore University Medical Center, Neptune, NJ
Title:
BRASH Syndrome: A Rare Etiology of Cardiogenic Shock Introduction:
BRASH syndrome is an acronym for a rare, and often underdiagnosed, constellation of clinical features including bradycardia, renal failure, atrioventricular (AV) nodal blockade, shock of cardiogenic nature, and hyperkalemia that can be seen in patients on AV nodal blocking medications. We present a case of BRASH syndrome involving severe cardiogenic shock requiring transfer to the cardiac intensive care unit (CICU) for life-sustaining interventions. Clinical Case:
A 63-year-old male with a past medical history of hypertension on Carvedilol 25 mg twice daily, type 2 diabetes mellitus, and stage 3b chronic kidney disease presented with a one-day history of vomiting and altered mental status. On admission, the patient had a temperature of 98.8° F, blood pressure of 69/36 mmHg, heart rate of 36 beats per minute, respiration rate of 16, and oxygen saturation of 96% on room air. Physical exam demonstrated lethargy, bradycardia, cold extremities, and signs of fluid overload including diffuse rales in all lung fields and pitting edema in the lower extremities. Electrocardiogram revealed junctional bradycardia at a rate of 36 beats per minute and a chest radiograph showed diffuse pulmonary congestion. Labs demonstrated signs of shock including elevated lactic acid of 3.7 mmol/L (Ref: 0.5-2.0 mmol/L), creatinine of 3.47 mg/dL from baseline of ~2 (Ref: 0.7-1.2), and transaminitis with aspartate transaminase of 72 U/L (Ref: 0-34 U/L) and alanine transaminase of 84 U/L (Ref: 10-49 U/L). Additionally, he had a potassium level of 6.7 mmol/L (Ref: 3.5-5.1 mmol/L). The patient was diagnosed with BRASH syndrome due to the combination of bradycardia, renal failure, AV nodal blockade, shock, and hyperkalemia. Given concern of cardiogenic shock in the setting of profound bradycardia, he was started on an intravenous Dopamine infusion and transferred to the CICU. He received emergent hemodialysis due to electrolyte abnormalities refractory to medical management. Following these interventions, a rapid improvement in mental status, vitals, and signs of end organ damage was observed. The patient was subsequently downgraded to the medical floors the following day. Discussion:
This case aims to bring awareness to the under-recognized diagnosis of BRASH syndrome as an etiology of cardiogenic shock. The proposed pathophysiology involves an insult such as dehydration, especially in elderly patients with preexisting kidney disease, which induces an acute kidney injury. The renal impairment causes both hyperkalemia and accumulation of AV nodal blocking medications like beta-blockers which act synergistically to produce significant bradycardia. This results in substantial cardiac shock, subsequently worsening renal perfusion and further fueling this vicious cycle. It is important for clinicians to not solely focus on any individual component of the pentad of clinical findings since there is often overlap with other medical conditions, but rather recognize the combination of features as a distinct entity. While BRASH syndrome can rapidly progress towards multi-system organ failure, our case demonstrates that immediate recognition of this diagnosis and initiation of advanced measures such as inotropic support and renal replacement therapy can reverse the underlying disease process and lead to a promising recovery for patients.