Causes and attributable fraction of death from ARDS in inflammatory phenotypes of sepsis.

Autor: Evrard B; Division of Pulmonary, Critical Care, Allergy and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, CA, USA. bruno.evrard@chu-limoges.fr.; Inserm CIC 1435, Dupuytren Teaching Hospital, 87000, Limoges, France. bruno.evrard@chu-limoges.fr., Sinha P; Division of Clinical and Translational Research, Washington University School of Medicine, Saint Louis, MO, USA.; Department of Anesthesia, Division of Critical Care, Washington University, Saint Louis, MO, USA., Delucchi K; Department of Psychiatry and Behavioral Sciences, University of California San Francisco, San Francisco, CA, USA., Hendrickson CM; Division of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Zuckerberg San Francisco General Hospital and Trauma Center, San Francisco, CA, USA., Kangelaris KN; Division of Hospital Medicine, Department of Medicine, University of California San Francisco, San Francisco, CA, USA., Liu KD; Division of Nephrology, Department of Medicine, University of California San Francisco, San Francisco, CA, USA.; Department of Anesthesia, University of California San Francisco, San Francisco, CA, USA., Willmore A; Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA, USA., Wu N; Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA, USA., Neyton L; Division of Pulmonary, Critical Care, Allergy and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, CA, USA., Schmiege E; Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA, USA., Gomez A; Division of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Zuckerberg San Francisco General Hospital and Trauma Center, San Francisco, CA, USA., Kerchberger VE; Division of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.; Department of Biomedical Informatics, Vanderbilt University Medical Center, Nashville, TN, USA., Zalucky A; Division of Pulmonary, Critical Care, Allergy and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, CA, USA., Matthay MA; Division of Pulmonary, Critical Care, Allergy and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, CA, USA.; Department of Anesthesia, University of California San Francisco, San Francisco, CA, USA.; Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA, USA., Ware LB; Division of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.; Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA., Calfee CS; Division of Pulmonary, Critical Care, Allergy and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, CA, USA.; Department of Anesthesia, University of California San Francisco, San Francisco, CA, USA.; Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA, USA.
Jazyk: angličtina
Zdroj: Critical care (London, England) [Crit Care] 2024 May 14; Vol. 28 (1), pp. 164. Date of Electronic Publication: 2024 May 14.
DOI: 10.1186/s13054-024-04943-x
Abstrakt: Background: Hypoinflammatory and hyperinflammatory phenotypes have been identified in both Acute Respiratory Distress Syndrome (ARDS) and sepsis. Attributable mortality of ARDS in each phenotype of sepsis is yet to be determined. We aimed to estimate the population attributable fraction of death from ARDS (PAF ARDS ) in hypoinflammatory and hyperinflammatory sepsis, and to determine the primary cause of death within each phenotype.
Methods: We studied 1737 patients with sepsis from two prospective cohorts. Patients were previously assigned to the hyperinflammatory or hypoinflammatory phenotype using latent class analysis. The PAF ARDS in patients with sepsis was estimated separately in the hypo and hyperinflammatory phenotypes. Organ dysfunction, severe comorbidities, and withdrawal of life support were abstracted from the medical record in a subset of patients from the EARLI cohort who died (n = 130/179). Primary cause of death was defined as the organ system that most directly contributed to death or withdrawal of life support.
Results: The PAF ARDS was 19% (95%CI 10,28%) in hypoinflammatory sepsis and, 14% (95%CI 6,20%) in hyperinflammatory sepsis. Cause of death differed between the two phenotypes (p < 0.001). Respiratory failure was the most common cause of death in hypoinflammatory sepsis, whereas circulatory shock was the most common cause in hyperinflammatory sepsis. Death with severe underlying comorbidities was more frequent in hypoinflammatory sepsis (81% vs. 67%, p = 0.004).
Conclusions: The PAF ARDS is modest in both phenotypes whereas primary cause of death among patients with sepsis differed substantially by phenotype. This study identifies challenges in powering future clinical trials to detect changes in mortality outcomes among patients with sepsis and ARDS.
(© 2024. The Author(s).)
Databáze: MEDLINE
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