Evidence map›Paper›PMID 40995280›Full record

ArticleCureus2025

BRASH Phenomenon: A Case Report on the Dangerous Combination of Bradycardia, Acute Renal Failure, Atrioventricular Nodal Blockade, Shock, and Hyperkalemia.

Tetyana Okan, Azeem Arastu, Mehrdad Zarghami, Vidhi Patel, Uchenna Chinakwe, Zoran Lasic

Abstract readCase Reports
In one paragraph

Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Tetyana OkanInternal Medicine, Jamaica Hospital Medical Center, New York, USA.
Azeem ArastuInternal Medicine, Jamaica Hospital Medical Center, New York, USA.
Mehrdad ZarghamiInternal Medicine, Jamaica Hospital Medical Center, New York, USA.
Vidhi PatelInternal Medicine, Jamaica Hospital Medical Center, New York, USA.
Uchenna ChinakweInternal Medicine, Jamaica Hospital Medical Center, New York, USA.
Zoran LasicCardiology, Lenox Hill Hospital, New York, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

acute renal failureatrioventricular nodal blockersbradycardiabrash syndromecardiogenic shockdiagnosis of brash syndromehemodialysishyperkalemiamanagement of brash syndromeshock

Identifiers

PMID40995280
PMCPMC12456856

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