Key result
Prompt medical therapy and hemodialysis reverse severe BRASH syndrome lacking classic ECG changes.
Why the study?
Although BRASH syndrome represents a fully reversible cause of symptomatic bradycardia, it frequently goes unrecognized.
Case Report (n=1)
No
BRASH syndrome can present without classic ECG signs of hyperkalemia and requires prompt simultaneous management of hyperkalemia and AV nodal blockade to avoid unnecessary pacemaker implantation.
May prompt BRASH inclusion in unexplained bradycardia differentials; leaves open prospective validation of recognition criteria.
The term BRASH refers to a clinical constellation characterized by bradycardia, renal dysfunction, atrioventricular (AV) nodal-blocking medication exposure, shock, and hyperkalemia. Although the condition represents a fully reversible cause of symptomatic bradycardia, it frequently goes unrecognized. Prompt identification and a clear understanding of its underlying mechanisms are essential to avoid unnecessary procedures. The syndrome should be suspected when a patient presents with bradycardia in the setting of impaired kidney function and elevated serum potassium, particularly when there is recent or ongoing use of AV nodal-blocking agents. Early recognition is critical because effective management requires addressing each contributing factor simultaneously, rather than treating a single abnormality in isolation.
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Zuhri et al. (2025) conducted a case report in BRASH Syndrome (n=1). Diltiazem was evaluated. A 65-year-old woman presenting with BRASH syndrome due to diltiazem and severe hyperkalemia, notably lacking classic ECG changes, fully recovered following prompt medical management and hemodialysis.
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