INTRODUCTION:As a relatively new entity that has come into the literature, BRASH syndrome is an acronym for a collection of objective findings inclusive of bradycardia, renal failure, atrioventricular (AV) nodal block, shock, and hyperkalemia. It is a distinct process arising from the synergistic effects of hyperkalemia and an AV-nodal blocker in the setting of renal insufficiency. Patients often are treated as isolated hyperkalemia or AV-node blocker overdose. Hereby, we present a case of BRASH syndrome and aim to point out the importance of initial workup and management of this syndrome.
CASE PRESENTATION:A 66-year-old male with a history of hypertension, presented to the emergency room with altered mental status. His was bradycardic to 47 with a blood pressure of 101/67 mmHg. Initial laboratory work noted a serum potassium level of 6.3 mEq/L, sodium of 138 mEq/L, creatinine of 1.7 mg/L, serum bicarbonate of 18 mEq/L and corrected calcium level of 8.8 mEq/L. Electrocardiogram (ECG) demonstrated sinus bradycardia without hyperacute T-waves (figure1). Patient's home medication regimen review revealed he had been started on metoprolol tartrate 50 mg twice daily about a week prior to presentation. Beta blocker was held, and IV calcium gluconate was administered with resolution of bradycardia.DISCUSSION: Initial presentation of BRASH syndrome varies from mild hyperkalemia to hemodynamic compromise. Bradycardia directly reduces the cardiac output, which worsens the renal perfusion with activation of the RAAS system resulting in hyperkalemia. Furthermore, hyperkalemia affects the repolarization phase of action potential in cardiac pacemaker cells inducing more bradycardia by decreasing the potassium gradient across sinoatrial nodal cell membranes. Isolated hyperkalemia usually does not result in bradycardia until serum potassium level reach 7 mEq/L (1). However, with concurrent use of AV node blockers, bradycardia can occur in patients with a lower serum potassium level. Evidence of supratherapeutic levels of AV blockers is not a part of diagnosing BRASH syndrome (2). Isolated AV blockade intoxication can be differentiated from BRASH syndrome by normal serum level of the medication. Bradycardia related to BRASH syndrome is often resistant to atropine and should be addressed with intravenous calcium. Intravenous insulin and dextrose or epinephrine infusion can prevent the need for invasive measures such as intravenous pacing or dialysis (3). Fluid resuscitation should be individually evaluated for each patient to avoid volume overload.
CONCLUSIONS:The vicious cycle of bradycardia, hyperkalemia and renal insufficiency can lead to hemodynamic compromise and shock. The geriatric population is on the rise in the United States and is considered high risk for BRASH syndrome due to chronic kidney disease. It is important for clinicians to be cautious with use of AV nodal blockers in this patient population.
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