INTRODUCTION: 14-53% of coronavirus disease 2019 (COVID-19) patients have elevated alanine aminotransferase(ALT) and aspartate aminotransferase (AST).[1] We present a case of COVID-19 who developed severe metabolic acidosis from acute liver failure.
Standard biomarkers have been widely used for COVID-19 diagnosis and prognosis. We hypothesize that thrombogenicity metrics measured by thromboelastography will provide better diagnostic and prognostic utility versus standard biomarkers in COVID-19 positive patients. In this observational prospective study, we included 119 hospitalized COVID-19 positive patients and 15 COVID-19 negative patients. On admission, we measured standard biomarkers and thrombogenicity using a novel thromboelastography assay (TEG-6s). In-hospital all-cause death and thrombotic occurrences (thromboembolism, myocardial infarction and stroke) were recorded. Most COVID-19 patients were African--Americans (68%). COVID-19 patients versus COVID-19 negative patients had higher platelet-fibrin clot strength (P-FCS), fibrin clot strength (FCS) and functional fibrinogen level (FLEV) (
P
≤ 0.003 for all). The presence of high TEG-6 s metrics better discriminated COVID-19 positive from negative patients. COVID-19 positive patients with sequential organ failure assessment (SOFA) score at least 3 had higher P-FCS, FCS and FLEV than patients with scores less than 3 (
P
≤ 0.001 for all comparisons). By multivariate analysis, the in-hospital composite endpoint occurrence of death and thrombotic events was independently associated with SOFA score more than 3 [odds ratio (OR) = 2.9,
P
= 0.03], diabetes (OR = 3.3,
P
= 0.02) and FCS > 40 mm (OR = 3.4,
P
= 0.02).
This largest observational study suggested the early diagnostic and prognostic utility of thromboelastography to identify COVID-19 and should be considered hypothesis generating. Our results also support the recent FDA guidance regarding the importance of measurement of whole blood viscoelastic properties in COVID-19 patients. Our findings are consistent with the observation of higher hospitalization rates and poorer outcomes for African--Americans with COVID-19.
BRASH syndrome is characterized by bradycardia, renal failure, AV nodal blockade, shock, and hyperkalemia. The proposed mechanism involves a vicious cycle between AV nodal blockers, hyperkalemia, and renal failure and was first described in 2016. We present a case of a 52-year-old woman who presented with progressively worsening shortness of breath and hypertensive urgency who subsequently developed profound bradycardia and shock that was refractory to resuscitative measures, she was diagnosed with BRASH syndrome. In this article, we explore the predisposing factors and challenges faced during the management of patients with BRASH syndrome.
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