Background: BRASH syndrome, or Bradycardia, Renal Failure, AV blockade, Shock, and Hyperkalemia, has recently become recognized as a collection of objective findings in a specific clinical context pertaining to emergency medicine and critical care. However, there is little emergency medicine and critical care literature specifically evaluating this condition. Objective: We sought to define and review BRASH syndrome and identify specific management techniques that differ from the syndromes as they present individually. Discussion: BRASH syndrome is initiated by synergistic bradycardia due to the combination of hyperkalemia and medications that block the atrioventricular (AV) node. The most common precipitant is hypovolemia or medications promoting hyperkalemia or renal injury. Left untreated, this may result in deteriorating renal function, worsening hyperkalemia, and hemodynamic instability. Patients can present with a variety of symptoms ranging from asymptomatic bradycardia to multiorgan failure. BRASH syndrome should be differentiated from isolated hyperkalemia and overdose of AV-nodal blocking medications. Treatment includes fluid resuscitation, hyperkalemia therapies (intravenous calcium, insulin/glucose, 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). Understanding and recognizing the pathophysiology of BRASH syndrome as a distinct entity may improve patient outcomes. Conclusions: BRASH syndrome can be a difficult diagnosis and is due to a combination of hyperkalemia and medications that block the AV node. Knowledge of this condition may assist emergency and critical care providers. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http:// creativecommons.org/licenses/by-nc-nd/4.0/).
Many mouse models of allergic asthma exhibit eosinophil-predominant cellularity rather than the mixed granulocytic cytology in steroid-unresponsive severe disease. Therefore, we sought to implement a novel mouse model of antigen-driven, mixed-granulocytic, severe allergic asthma to determine biomarkers of the disease process and potential therapeutic targets. C57BL/6J, IL-6-/-, and IL-6R-/- mice were injected with an emulsion of Complete Freund's Adjuvant and House Dust Mite antigen (CFA/HDM) on day 1. Dexamethasone, a lymphocyte-depleting biological, or anti-IL-17A were administered during intranasal HDM challenge on days 19-22. On day 23, the CFA/HDM model elicited mixed bronchoalveolar lavage (BAL) cellularity (typically 80% neutrophils and 10% eosinophils), airway hyperresponsiveness (AHR) to methacholine, diffusion impairment, lung damage, body weight loss, corticosteroid resistance, and elevated levels of serum amyloid A (SAA), pro-inflammatory cytokines, and Th1/Th17 cytokines compared to eosinophilic models of HDM-driven allergic airway disease. BAL cells in IL-6- or IL-6R-deficient mice were predominantly eosinophilic and associated with elevated Th2 and reduced Th1/Th17 cytokine production, along with an absence of SAA. Nevertheless, AHR remained in IL-6-deficient mice even when administered dexamethasone. However, combined administration of anti-IL-17A and systemic corticosteroid significantly attenuated both overall and neutrophilic airway inflammation, and also reduced AHR and body weight loss. Inhibition of IL-17A combined with systemic corticosteroid treatment during antigen-driven exacerbations may provide a novel therapeutic approach to prevent the pathological pulmonary and constitutional changes that greatly impact patients with the mixed-granulocytic endotype of severe asthma.
Results from major clinical trials have shown significant cardiorenal-protective benefits of SGLT2 inhibitors in patients with type 2 diabetes (T2DM), leading to increased popularity. A rare but serious side effect of SGLT2 inhibitors is euglycemic diabetic ketoacidosis (EDKA), which presents more covertly but has been described. Identification and report of modifiable risk factors would be an important step in helping clinicians appropriately counsel patients. In this case report, we present DKA in a patient on an SGLT2 inhibitor and ketogenic diet (KD). A 47-year-old male with a history of poorly controlled T2DM on metformin and empagliflozin presented to the emergency department (ED) with several days of pharyngitis, dyspnea, emesis, abdominal pain, and anorexia. Of note, one month prior to this event, he presented to the ED with malaise and was found to have an anion gap of 21, a bicarbonate level of 13 mmol/L, a pH level of 7.22, 3+ ketonuria, and a glucose level of 7 mmol/L (127 mg/dl). Additional workup was negative, and findings were attributed to his KD. His use of empagliflozin was not identified on his medication list. At second presentation, the patient was tachypneic and tachycardic and had mild abdominal tenderness. Labs revealed anion gap 28, bicarbonate 5 mmol/l, pH 6.94, 3+ ketonuria, glucose 14.9 mmol/L (269 mg/dl), and beta-hydroxybutyrate 8.9 mmol/L. The patient was diagnosed with DKA and was treated accordingly. With closure of anion gap, the patient was transitioned to insulin and metformin, and his empagliflozin was discontinued indefinitely. Before prescribing this medication class, physicians should inquire about low-carbohydrate diets given the higher risk for DKA, though knowledge of this risk is still not widespread.
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