Don't Be-RASH: A case report

Background

Bradycardia, renal failure, atrioventricular (AV) blockade, shock, and hyperkalemia is reported as a constellation of symptoms in critical care medicine known as “BRASH Syndrome.” It is reportedly a complex clinical scenario in which accumulated AV blockers and hyperkalemia result in bradycardia, renal failure, and shock interacting with each other synergistically.

Case report

A 70-year-old male taking metoprolol at home presented to the emergency department with hyperkalemia, cardiogenic shock, bradycardia, and renal failure. The patient was treated with routine treatment for shock (vasopressors), hyperkalemia (cardiac membrane stabilization, electrolyte temporization, and diuresis), and renal failure (dialysis) with eventual clinical resolution. A serum metoprolol concentration was obtained which was consistent with a therapeutic concentration. Why should the emergency physician be aware of this? The proposed BRASH syndrome may over-emphasize the role of AV nodal blockade in the presentation of patients with renal failure, hyperkalemia, and bradycardia. There is a limited list of renally-cleared medications that would be directly impacted by acute renal insufficiency. A common memory device for renally cleared beta blockers is NASA (nadolol, atenolol, sotalol, acebutolol). The suggestion of synergistic effect of hyperkalemia and therapeutic AV nodal blockade is speculative and lacks empiric evidence. The implication of potential supratherapeutic drug concentrations or even enhanced synergistic effects of a drug suggests a relative toxicity, which could mislead a clinician into considering toxicity state specific therapies such as high insulin euglycemia, glucagon, or lipid emulsion which carry adverse effect profiles and generally lack evidence to support use in these clinical presentations.