Urinary Tract Infection Causing Bradycardia, Renal Failure, Atrioventricular Nodal Blockade, Shock, and Hyperkalemia (BRASH) Syndrome: A Case Report and a Brief Review of the Literature

Abstract

Bradycardia, renal failure, atrioventricular (AV) nodal blockade, shock, and hyperkalemia (BRASH) syndrome commonly occurs in the elderly population with compromised renal function and a history of taking AV nodal blocking agents on a regular basis. Hypovolemia and worsening of renal function are considered to be the major risk factors. BRASH syndrome should be differentiated from pure intoxication with AV nodal blocking agents, as the therapeutic goals of these conditions are different from each other. It encompasses a vicious cycle of bradycardia and decreased cardiac output leading to organ dysfunction including renal failure with hyperkalemia, further augmenting bradycardia. It is usually associated with high morbidity and mortality. Typically, the treatment involves increasing renal blood flow by augmenting cardiac output using catecholamine infusion. Very rarely, interventions such as intralipid emulsion and continuous renal replacement therapy (CRRT) may be required on a case-to-case basis. Promptly recognizing the symptoms of BRASH syndrome can help to avoid diagnostic delays and reduce mortality rates.

Life-threatening Complication in a Patient with Chronic Kidney Disease: BRASH Syndrome

“…Patients with BRASH syndrome may also develop life-threatening bradycardia, even with moderately high potassium levels, because of the effect of AV nodal blocking agents which inhibit any compensatory increase in the HR. [1][2][3] The most commonly implicated AV nodal blocking agents are β blockers and CCBs, as seen in the present case. 4,5 Certain factors have been identified which may precipitate the BRASH syndrome.…”

“…1 Since then, a few case reports have been published highlighting the significance of this syndrome. [2][3][4][5][6][7][8] The suggested mechanism in BRASH syndrome is the synergistic effect of hyperkalemia and AV-nodal blocking agents causing refractory bradycardia and hypotension. 1 This leads to hypoperfusion and further worsening of renal function leading to reduced drug elimination and hyperkalemia, initiating a vicious cycle (Fig.…”

“…2,6 ECG picture may vary from only sinus bradycardia to the presence of junctional rhythm and varying degrees of AV blocks. 3,[6][7][8] Even though any sign of hyperkalemia may be present on ECG, bradycardia without the presence of typical signs like peaked T waves or widened QRS may indicate BRASH syndrome. 1,2 Early identification of this syndrome is imperative as it may not respond to the standard advanced cardiac life support (ACLS) protocols, and the bradycardia may be refractory to commonly employed therapies, including intravenous atropine and cardiac pacing.…”

“…1,2 Early identification of this syndrome is imperative as it may not respond to the standard advanced cardiac life support (ACLS) protocols, and the bradycardia may be refractory to commonly employed therapies, including intravenous atropine and cardiac pacing. 2,3 Due attention should be on the identification and correction of the underlying precipitating factor, especially hypovolemia, and breaking the vicious cycle with the correction of hyperkalemia and shock until the drug effect wears off. Hypotension should be aggressively managed with intravenous fluids and vasopressors to ensure adequate renal perfusion.…”

BRASH Syndrome: A Case Report and Literature Review

“…The proposed combination of signs and symptoms is thought to originate with an insult, such as dehydration, that induces prerenal acute kidney injury and associated hyperkalemia [3]. Impaired renal clearance leads to the accumulation of AV nodal blocking agents such as beta-blockers [4]. The synergistic effect of hyperkalemia and increased systemic levels of AV node blockers induce significant bradycardia and decreased cardiac output, leading to signs of shock [5].…”