BRASH Syndrome: Shedding Light on a Lethal Yet Overlooked Clinical Entity

Document Type

Conference Proceeding

Publication Date

10-2024

Publication Title

Chest

Abstract

INTRODUCTION: BRASH syndrome is a rare yet frequently life-threatening disorder characterised by an acute renal injury that triggers a relentless cycle of bradycardia, hyperkalemia, hypotension, and deteriorating renal function particularly in patients taking AV nodal blocking agents. CASE PRESENTATION: A 63-year-old male with past medical history significant for hypertension, hyperlipidemia, coronary artery disease s/p remote PCI to RCA, was transferred from an outside hospital (OSH) after recent onset of gastrointestinal symptoms including diarrhea, nausea, and vomiting lasting for 4-5 days. Despite his symptoms, he continued taking his prescribed medications including metoprolol, metformin, olmesartan, and Jardiance. His heart rate of 30s and low blood pressure at home, prompted visit to the hospital. Initial laboratory results at OSH revealed elevated WBC(17K), aniongap(23), glucose 553, lactic acid(9.5), troponin(82), procalcitonin(6.18), potassium(5.6) and creatinine(4.47). VBGs showed metabolic acidosis. Despite attempts to increase heart rate with atropine, the patient remained bradycardic and required temporary transcutaneous pacing, arriving at the hospital with dopamine drip for persistent hypotension. Due to ongoing hypotension and shock, the patient was admitted to the ICU treated with antibiotics, vasopressors with suspicion of BRASH (Bradycardia, Renal failure, A-V block, Shock, and Hyperkalemia) syndrome versus septic shock. Although initially stabilised and off vasopressor support, persistent bradycardia leading to hypotension with EKG demonstrating complete heart block led to subsequent admission to the Coronary Care Unit (CCU), where he underwent placement of a permanent pacemaker. Due to troponin elevation, patient underwent echo which showed normal LVEF but new wall motion abnormalities of RV free wall. Subsequently, left cardiac catheterisation was performed demonstrating chronic RCA occlusion and mild LAD/LCx disease with plan to re-vascularise outpatient. Patient's clinical status and labs improved and he was discharged with close follow up recommendations. DISCUSSION: BRASH syndrome is a a relatively under-diagnosed but lifethreatening phenomen, associated with synergism between AV nodal blocking agents and hyperkalemia. Innocous stimuli like mild dehydration reduces renal perfusion especially if a patient is on an ACEI/ARBs leading to accumulation of beta-blockers and calcium channel blockers. This buildup worsens renal hypoperfusion, leading to increased cardiac depression and deteriorating renal function. Renal failure, in turn, worsens hyperkalemia, impairing drug excretion and intensifying the effects of AV nodal blockers. Although these drugs usually don't cause severe bradycardia at therapeutic levels, the combination of reduced renal clearance and hyperkalemia amplifies their impact. This cycle, often triggered by factors like hypovolemia or medications affecting the AV node, can escalate to shock and multiple-organ failure if not promptly identified. Our patient had decreased oral intake secondary to a GI symptoms and he continued to take his metoprolol and telmesartan. He presented with severe bradycardia that persisted despite improvement in electrolytes and renal function, ultimately requiring a pacemaker. CONCLUSIONS: It is prudent to include BRASH syndrome as a potential diagnosis for patients exhibiting bradycardia, acute kidney injury (AKI), hyperkalemia, and recent intake of AV nodal-blocking agents, for guiding early and appropriate management.

Volume

166

Issue

4 Suppl

First Page

A762

Comments

Chest 2024 Annual Meeting, October 6-9, 2024, Boston, MA

Last Page

A763

DOI

10.1016/j.chest.2024.06.516

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