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BRASH syndrome is a rare but potentially life-threatening medical condition that is often under-recognized among healthcare providers. It is characterized by a cluster of five clinical features, namely bradycardia, renal failure, AV blockade, shock, and hyperkalemia. The current algorithms for bradycardia may not be effective in treating it, making early recognition and appropriate management critical. Hereby, we present a case of a patient on hemodialysis presenting with this collection of findings, with its evaluation and management.
A 64-year-old male patient arrived at the Cardiology unit with a history of bradycardia and dyspnea within the past week, accompanied by chest pain during dialysis. He had been undergoing regular outpatient hemodialysis (HD) for the last 12 years at a different center due to diabetic kidney disease (DKD), through an arteriovenous fistula (AVF). He had a medical history of smoking, diabetes, hypertension, and chronic coronary artery disease, which has led to heart failure with reduced ejection fraction (HFrEF). His previous medical regimen included hydralazine, metoprolol, nitrates, rosuvastatin, and dual antiplatelet therapy.
Upon admission, the EKG revealed a first-degree atrial-ventricular blockade associated with a heart rate of 45 bpm, hyperkalemia (with a serum potassium of 8.4), and signs of cardiogenic shock while on beta-blocker use. This combination of signs and symptoms constitutes the BRASH syndrome, a clinical entity with a synchrony of pathophysiological factors, especially a vicious circling feedback promoting life-threatening bradycardia. He underwent urgent dialysis, improving the heart frequency and hemodynamic status, but quickly recurred hyperkalemia 4 hours after HD.
In the follow-up for this patient, his Kt/V per session ranged from 0.38-0.51. We performed a Doppler scan of his AVF while investigating persistent hyperkalemia even after HD sessions in our center. We found a significant stenosis on his AVF. He underwent an angioplasty of the vascular access, with improvement in the post-dialysis laboratory and no recurring bradycardia episodes. In agreement with the Cardiology team, it was opted to return the use of guideline-directed therapy for HFrEF, seen as beneficial for relevant clinical outcomes in his case.
This case highlights the dangerous combination of BRASH syndrome, particularly for patients undergoing kidney replacement therapy. Quick identification of hyperkalemia promoted its management, an action that is not considered in the ACLS bradycardia algorithm. By promptly intervening with HD, suspending beta-blockers, and recognizing the cause of persistent hyperkalemia related to AVF dysfunction, we stopped the pathophysiological cycle. This controlled the patient’s symptoms and allowed the use of outcome-modifying drugs for HFrEF on the long term.