Key result
Multimodal medical therapy reverses BRASH syndrome, normalizing renal function and potassium by Day 7.
Why the study?
BRASH syndrome is a frequently underdiagnosed condition resulting from a synergistic interaction between AV-nodal blockers and renal impairment that requires a high index of suspicion for early recognition and targeted intervention.
Case Report (n=1)
No
Early recognition of digoxin-associated BRASH syndrome and targeted medical management—including fluid resuscitation, hyperkalemia correction, and epinephrine infusion—can successfully reverse shock, renal failure, and high-grade AV block without requiring temporary pacing or hemodialysis.
Targeted therapy may reverse BRASH syndrome; leaves open confirmation in prospective studies.
BRASH syndrome (Bradycardia, Renal failure, AV-nodal blockade, Shock, and Hyperkalemia), a frequently underdiagnosed condition, arises from a synergistic, self-perpetuating interaction between atrioventricular-nodal blockers and renal impairment, often initiated by hypovolemia. Management requires a high index of suspicion, focusing on rapid correction of hyperkalemia, fluid resuscitation, and inotropic support. Early recognition is essential; timely, targeted intervention interrupts this vicious cycle and optimizes the clinical prognosis.
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Silwal et al. (2026) conducted a case report in BRASH syndrome (Bradycardia, Renal failure, AV-nodal blockade, Shock, and Hyperkalemia) (n=1). Digoxin discontinuation, fluid resuscitation, IV calcium gluconate, insulin with dextrose, nebulized salbutamol, and epinephrine infusion was evaluated on Clinical and laboratory resolution of BRASH syndrome. Digoxin withdrawal, fluid resuscitation, anti-hyperkalemic therapy, and epinephrine reversed BRASH syndrome by Day 7, normalizing creatinine (2.6 to 1.1 mg/dL) and potassium (6.2 to 4.0 mEq/L).
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