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The Metabolic Subphenotype: A Protective Factor in Ards Secondary to Sepsis or Pneumonia
Critical Care Medicine ; 51(1 Supplement):603, 2023.
Article in English | EMBASE | ID: covidwho-2190684
ABSTRACT

INTRODUCTION:

Poor metabolic health increases the risk of COVID-19 acute respiratory distress syndrome (ARDS), however, its relationship with non-COVID-19 ARDS remains controversial. ARDS is often considered a heterogeneous disease caused by sepsis, pneumonia, trauma, transfusions, and aspiration. In this study, we hypothesized that metabolic inflammation may contribute to differential outcomes in ARDS primarily caused by infection. METHOD(S) This was a secondary analysis of seven studies from the ARDS and Prevention and Early Treatment of Acute Lung Injury network trials within the Biologic Specimen and Data Repository Information Coordinating Center database. A metabolic subphenotype, defined by obesity, diabetes, and hypertension, was compared to a control population. The overall results showed lower adjusted mortality with this subphenotype. In this report, we performed stratified analyses to estimate effect modification by the metabolic subphenotype. We considered metabolic inflammation to reside along the causal pathway between infection and ARDS outcomes, and as such, stratified for primary ARDS etiology (e.g., sepsis or pneumonia as compared to other primary etiologies). The primary outcome was 28-day mortality. Secondary outcomes included 90-day mortality, ventilator free days, organ-failure free days, ICU free days, and length of hospital stay. RESULT(S) Among 4,288 ARDS trial participants, 3,205 (74.7%) had primary ARDS etiologies sepsis or pneumonia and 1,083 (25.3%) aspiration, trauma, transfusions, or other causes. of those with sepsis or pneumonia, 364 (11.4%) met criteria for the subphenotype versus 2,841 (88.6%) control. In the non-infectious cohort, 90 (8.3%) met subphenotype criteria versus 993 (91.7%) control. In adjusted analyses, the subphenotype stratified by sepsis and pneumonia was associated with lower 28- and 90-day mortality (adjusted odds ratio [aOR] 0.64 [95%CI, 0.48-0.84] and aOR 0.69 [95%CI, 0.53-0.89], respectively). However, in ARDS due to other causes, analyses were not significant (mortality at 28 days, aOR 1.18 [95% CI, 0.70-1.99] and 90 days, aOR 1.26 [95% CI, 0.77-2.06]). Secondary outcomes were not significantly different. CONCLUSION(S) A metabolic subphenotype of ARDS is associated with lower risk of mortality in non-COVID ARDS primarily caused by sepsis or pneumonia.
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Full text: Available Collection: Databases of international organizations Database: EMBASE Type of study: Etiology study Language: English Journal: Critical Care Medicine Year: 2023 Document Type: Article

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Full text: Available Collection: Databases of international organizations Database: EMBASE Type of study: Etiology study Language: English Journal: Critical Care Medicine Year: 2023 Document Type: Article