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Beta-Blocker and Calcium Channel Blocker Toxicity With BRASH Syndrome: A Case Report
Adolfo Martinez1, Niket Shah1,2, Andrew Kim1
1Internal Medicine, Michigan State University, East Lansing, USA.
Abstract:
Atrioventricular (AV) nodal blockers have a wide variety of medical uses, including the management of hypertension and cardiac arrhythmias. Like any other drug, they can carry side effects and toxicity. We present a case of a patient with a constellation of findings consistent with bradycardia, renal failure, AV nodal blockade, shock, and hyperkalemia (BRASH) syndrome. A 75-year-old female with a history of paroxysmal atrial fibrillation and heart failure with preserved ejection fraction presented to the hospital with shortness of breath. She was discharged two weeks prior to the presentation from another hospital after being treated for atrial fibrillation with a rapid ventricular response. She was discharged on metoprolol and diltiazem. Upon presentation to the hospital, the patient was noted to be bradycardic and hypotensive with blood work notable for acute kidney injury and hyperkalemia, consistent with BRASH syndrome. She received a dose of intravenous (IV) glucagon followed by infusion and received epinephrine infusion. Once clinically stable, she was discharged with her home dose of metoprolol and a reduced dose of diltiazem with a close follow-up with cardiology. Early recognition of BRASH syndrome as a unique clinical entity rather than different pathologic conditions is important to improve morbidity and mortality in these patients.
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