Dr. Kristen Zubel HCA Citrus Florida, United States
Introduction: BRASH syndrome (bradycardia, renal failure, atrioventricular nodal blocker medication, shock, and hyperkalemia) is a syndrome noted to be a consequence of a positive loop bradycardia due to AV-nodal blockers and hyperkalemia secondary to renal insufficiency. We present to you a case of a 57 year old gentleman who presented with BRASH syndrome.
Description: 57 year old gentleman who was brought in to the ED by EMS due to worsening weakness, fatigue, and was unable to ambulate from his chair at home. Of note, patient was also having worsening shortness of breath and difficulty urinating for about one month. He denied any symptoms of chest pain, palpitations, and no episodes of syncope were mentioned.
Labs were significant for potassium 8.8, sodium 128, bicarbonate 14, glucose 375, BUN 74, Cr 4.9, lactic acid 3.43, troponin 0.187. ABG revealed pH 7.199, pCO2 28.2, pO2 140.5, and bicarbonate 11. Due to the presenting symptoms, findings mentioned above, and long term use of sotalol, presumptive diagnosis of BRASH syndrome was made. Patient was given 1g calcium gluconate, 10U regular insulin, 50mEq bicarbonate, and 5mg glucagon for Sotalolreversal. Minimal improvement to BP and heart rate after intervention, patient was then started on epinephrine and D5W drip with 150 mEqof bicarbonate. Nephrology was consulted for urgent hemodialysis. Patient was also upgraded to the ICU for closer monitoring. During ICU stay, the patient underwent 2 hemodialysis sessions with resolution of electrolyte abnormalities and subsequently downgraded.
Discussion: The combination of hyperkalemia (secondary to renal failure) and accumulation of AV nodal blockers synergistically cause bradycardia and hypoperfusion, leading to worsening of renal failure. This positive feedback loop may also lead to shock and multiorganfailure if left untreated or misdiagnosed. In the case presented, patient has been taking sotalol40 mg twice daily for management of atrial fibrillation. The goal of treatment is to correct potassium levels, hemodynamically stabilize the patient, and cessation of AV nodal blocking agents. The case presented, patient did have symptomatic bradycardia and evidence of hyperkalemia, persistent despite pharmacological intervention.
