title: Trauma-associated lung injury differs clinically and biologically from acute lung injury due to other clinical disorders.
abstract: OBJECTIVE
  Patients with trauma-associated acute lung injury have better outcomes than patients with other clinical risks for lung injury, but the mechanisms behind these improved outcomes are unclear. We sought to compare the clinical and biological features of patients with trauma-associated lung injury with those of patients with other risks for lung injury and to determine whether the improved outcomes of trauma patients reflect their baseline health status or less severe lung injury, or both.
  
  
  METHODS
  Analysis of clinical and biological data from 1,451 patients enrolled in two large randomized, controlled trials of ventilator management in acute lung injury.
  
  
  RESULTS
  Compared with patients with other clinical risks for lung injury, trauma patients were younger and generally less acutely and chronically ill. Even after adjusting for these baseline differences, trauma patients had significantly lower plasma levels of intercellular adhesion molecule-1, von Willebrand factor antigen, surfactant protein-D, and soluble tumor necrosis factor receptor-1, which are biomarkers of lung epithelial and endothelial injury previously found to be prognostic in acute lung injury. In contrast, markers of acute inflammation, except for interleukin-6, and disordered coagulation were similar in trauma and nontrauma patients. Trauma-associated lung injury patients had a significantly lower odds of death at 90 days, even after adjusting for baseline clinical factors including age, gender, ethnicity, comorbidities, and severity of illness (odds ratio, 0.44; 95% confidence interval, 0.24-0.82; p = .01).
  
  
  CONCLUSIONS
  Patients with trauma-associated lung injury are less acutely and chronically ill than other lung injury patients; however, these baseline clinical differences do not adequately explain their improved outcomes. Instead, the better outcomes of the trauma population may be explained, in part, by less severe lung epithelial and endothelial injury.
authors.affiliation: Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California-San Francisco, 505 Parnassus Avenue, San Francisco, CA 94143, USA. carolyn.calfee@ucsf.edu
authors.forename: Carolyn S
authors.initials: CS
authors.lastname: Calfee
authors.forename: Mark D
authors.initials: MD
authors.lastname: Eisner
authors.forename: Lorraine B
authors.initials: LB
authors.lastname: Ware
authors.forename: B Taylor
authors.initials: BT
authors.lastname: Thompson
authors.forename: Polly E
authors.initials: PE
authors.lastname: Parsons
authors.forename: Arthur P
authors.initials: AP
authors.lastname: Wheeler
authors.forename: Anna
authors.initials: A
authors.lastname: Korpak
authors.forename: Michael A
authors.initials: MA
authors.lastname: Matthay
mesh_terms: D000328:Adult; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012121:Respiration, Artificial; D012128:Respiratory Distress Syndrome / Q000097:blood / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D012307:Risk Factors; D012720:Severity of Illness Index; D016896:Treatment Outcome; D014947:Wounds and Injuries / Q000150:complications*