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Understanding and recognizing the patho- physi olog y of BRASH syndro me as a disti nct entity may improve patient outcomes. Treatment includes fluid resuscitation, hyper- kale mia ther apie s (int rav enou s calc ium, insul in/gl ucose, beta agonists, diuresis), management of bradycardia (which may necessitate epinephrine infusion), and more advanced therapies if needed (lipid emulsion, glucagon, or high-dose insulin infusion). BRASH syndrome should be differentiated from iso- late d hype rkal emia and over dose of A V -nod al bloc king medications. Pa tie nts ca n pre sen t wit h a va rie ty of sym pto ms ranging from asymptomatic bradycardia to multiorgan fail- ure.
Left untreated, this may result in deteriorating renal function, worsening hyperkalemia, and hemodynamic insta- bil ity. The most comm on prec ipita nt is hypo vo- lemi a or medi cati ons prom otin g hype rkal emia or rena l injury. Discussion: BRASH syndrome is initiated by synergistic bradycardia due to the combination of hyperkalemia and medications that block the atrioven- tric ular (A V) node. Obje ctiv e: We sought to define and review BRASH syndrome and identify specific management techniques that differ from the syndromes as they present individually. However, there is little emergency medicine and critical care literatur e specif- ical ly eva luat ing this cond itio n. Abstract-Ba ckground: BRASH syndrome, or Brady- cardia, Renal Failure, AV blockade, Shock, and Hyperkale- mia, has rec ent ly bec om e rec og niz ed as a col lec tio n of obje ctiv e findin gs in a speci fic clini cal context pertain ing to emergency medicine and critical care.
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