Trauma-associated Acute Lung Injury Differs Clinically and Biologically From Acute Lung Injury Due to Other Clinical Disorders

Greg Martin, MD, MSc

Medscape Critical Care.  2007; ?2007 Medscape
Posted 12/03/2007

Trauma-associated Acute Lung Injury Differs Clinically and Biologically from Acute Lung Injury Due to Other Clinical Disorders

Calfee CS, Eisner MD, Ware LB, et al
Crit Care Med. 2007;35:2243-2250

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are related and lethal forms of acute respiratory failure, with a mortality rate of 30%-50%.[1,2] It has long been recognized that traumatically injured patients in whom ALI or ARDS develop have a greater chance of surviving than patients in whom ALI or ARDS develop from other causes (most frequently, sepsis).[3,4] The authors sought to determine how trauma-associated ALI and ARDS was different from ALI and ARDS due to other causes. This study evaluated data from a database of 1451 patients with ALI or ARDS enrolled in 2 large ARDS Network clinical studies. As previously shown, patients with trauma-associated ALI or ARDS were younger and had fewer chronic comorbid medical conditions. Of interest, they were also less acutely ill (as measured by the Acute Physiology and Chronic Health Evaluation score). These differences translated into significant biologic differences in a variety of markers, including those for cell adhesion, endothelial and epithelial injury, and inflammation. Even after adjusting for differences in the clinical condition of the patients (ie, age, gender, ethnicity, comorbidities, and severity of illness), patients with trauma-associated ALI or ARDS were more likely to survive for at least 90 days.

Viewpoint

The primary finding of this study -- that patients with trauma-associated ALI or ARDS are less likely to die -- is not surprising given that most previous studies have produced the same results.[5-8] In fact, at least 1 study has suggested that the development of ALI or ARDS in trauma patients does not alter the risk of death at all, but rather that death is solely determined by the acute traumatic injury and its attendant complications (excluding ALI or ARDS).[9] The importance of this study lies in the fact that such a large group of patients with combined clinical and biologic data was available for analysis. By combining these data, the authors were able to show that trauma-associated ALI and ARDS have a lower mortality because of different clinical factors (ie, younger age, less severely ill, fewer comorbid conditions) and biologic factors (ie, differences in inflammatory cytokine expression). An important unresolved question is how much of the biologic difference is explained by the identified clinical factors. For example, does the presence of chronic comorbid medical conditions produce a milieu that will inevitably elaborate greater cytokine concentrations? Or, are trauma-associated ALI and ARDS truly biologically different phenomena, with particular differences in systemic inflammation and disordered coagulation? If the latter is true, then both the study and management of ALI and ARDS should take into account the underlying disorder rather than focusing on the ALI and ARDS. However, regardless of these findings and the remaining questions, the existing data show that low-tidal volume ventilation (the foundation for optimal patient care in this condition) is broadly applicable in ALI and ARDS, irrespective of the cause.[8]

References

  1. Fowler AA, Hamman RF, Good JT, et al. Adult respiratory distress syndrome: risk with common predispositions. Ann Intern Med. 1983;98:593-597.  
  2. Baumann WR, Jung RC, Koss M, et al. Incidence and mortality of adult respiratory distress syndrome: a prospective analysis from a large metropolitan hospital. Crit Care Med. 1986;14:1-4.  
  3. Bernard GR, Artigas A, Brigham KL, et al. The American-European Consensus Conference on ARDS: definitions, mechanisms, relevant outcomes, and trial coordination. Am J Respir Crit Care Med. 1994;149:818-824.  
  4. Stapleton RD, Wang BM, Hudson LD, et al. Causes and timing of death in patients with ARDS. Chest. 2005;128:525-532.  
  5. Hudson LD, Milberg JA, Anardi D, et al. Clinical risks for development of the acute respiratory distress syndrome. Am J Respir Crit Care Med. 1995;151:293-301.  
  6. Rubenfeld GD, Caldwell E, Peabody E, et al. Incidence and outcomes of acute lung injury. N Engl J Med. 2005;353:1685-1693.  
  7. Estenssoro E, Dubin A, Laffaire E, et al. Incidence, clinical course, and outcome in 217 patients with acute respiratory distress syndrome. Crit Care Med. 2002;30:2450-2456.  
  8. Eisner MD, Thompson T, Hudson LD, et al. Efficacy of low tidal volume ventilation in patients with different clinical risk factors for acute lung injury and the acute respiratory distress syndrome. Am J Respir Crit Care Med. 2001;164:231-236.  
  9. Treggiari MM, Hudson LD, Martin DP, et al. Effect of acute lung injury and acute respiratory distress syndrome on outcome in critically ill trauma patients. Crit Care Med. 2004;32:327-331.

Greg Martin, MD, MSc, Assistant Professor of Medicine, Emory University, Atlanta, Georgia; Director, Medical and Coronary Intensive Care, Grady Memorial Hospital, Atlanta, Georgia

Disclosure: Greg Martin, MD, MSc, has disclosed no relevant financial relationships.