Description of a Case of BRASH Syndrome

BRASH syndrome is a combination of bradycardia, renal failure, atrioventricular nodal block, shock, and hyperkalemia. It was first described in the late 2010s in patients who presented with nonspecific symptoms due to hypoperfusion, including general fatigue, headache, dizziness, and syncope.

BRASH syndrome is often triggered by medications affecting the conduction system of the heart and specifically the atrioventricular (AV) node. The effects of AV node-blocking agents and hyperkalemia on heart rate lead to reduced cardiac output, resulting in shock and kidney injury. This, in turn, leads to decreased renal clearance of AV-blocking agents and worsening hyperkalemia, so the cycle repeats. Discovering BRASH syndrome early is crucial to its management.

In a report published in Cureus, Allan E. Santos Argueta and coauthors described the case of a 70-year-old female who presented with BRASH syndrome-induced atrial fibrillation (AFib) with a slow ventricular response. The patient had hypertension and type 2 diabetes and was taking losartan 50 mg, metoprolol succinate 50 mg, amlodipine 5 mg, rosuvastatin 10 mg, and insulin therapy.

She was experiencing fatigue, lightheadedness, and palpitations for 1 day. In the emergency room, she was found to be hypotensive, with a blood pressure of 72/35 mm Hg and an erratic heart rate of 40 beats per minute. There were no signs of volume overload on her physical exam, but AFib with a slow ventricular response was noted in the electrocardiogram (ECG) with associated peak T waves.

The patient received three doses of atropine 1 mg and intravenous (IV) fluid boluses, but improvement was minimal. Next, she was given calcium gluconate, and subsequently was managed in the intensive care unit with insulin infusion, albuterol, sodium bicarbonate, and sodium polystyrene. Cardiology was consulted and anticoagulation was not recommended, since new-onset AFib was likely secondary to severe hyperkalemia and acute illness. The patient’s creatinine level improved to baseline, achieving hemodynamic stability and normalizing potassium levels. A repeat ECG within 48 hours of admission found normal sinus rhythm. The patient was discharged and instructed to follow up with cardiology for additional monitoring.

Given the nonspecific symptoms and signs associated with BRASH syndrome, the authors noted, a high level of clinical suspicion is necessary for diagnosis. The most common electrographic findings are junctional rhythm and bradycardia, with or without ECG changes suggesting hyperkalemia, while laboratory findings include significantly elevated creatinine and moderate to severe hyperkalemia with or without other electrolyte abnormalities.

The goal of treatment is to stabilize the cardiac membrane with calcium gluconate and hemodynamic support with IV fluids and vasopressors if required. Underlying hyperkalemia also needs to be managed with treatments that reduce total potassium.

“This case highlighted an atypical ECG finding in a patient diagnosed with BRASH syndrome who was not started on anticoagulation, given the reversible underlying condition in an acute illness setting,” the authors wrote. “Further studies are required to determine the long-term outcomes of recurrence and thromboembolic events in patients with paroxysmal AFib induced by BRASH syndrome.”

Source: Cureus