Objectives: Diabetes has been associated with decreased development of acute respiratory distress syndrome in some, but not all, previous studies. Therefore, we examined the relationship between diabetes and development of acute respiratory distress syndrome and whether this association was modified by type of diabetes, etiology of acute respiratory distress syndrome, diabetes medications, or other potential confounders.
Design: Observational prospective multicenter study.
Setting: Four adult ICUs at two tertiary academic medical centers.
Patients: Three thousand eight hundred sixty critically ill patients at risk for acute respiratory distress syndrome from sepsis, pneumonia, trauma, aspiration, or massive transfusion.
Measurements and Main Results: Diabetes history was present in 25.8% of patients. Diabetes was associated with lower rates of developing acute respiratory distress syndrome on univariate (odds ratio, 0.79; 95% CI, 0.66–0.94) and multivariate analysis (adjusted odds ratio, 0.76; 95% CI, 0.61–0.95). After including diabetes medications into the model, diabetes remained protective (adjusted odds ratio, 0.75; 95% CI, 0.59–0.94). Diabetes was associated with decreased development of acute respiratory distress syndrome both in the subgroup of patients with sepsis (adjusted odds ratio, 0.77; 95% CI, 0.61–0.97) and patients with noninfectious etiologies (adjusted odds ratio, 0.30; 95% CI, 0.10–0.90). The protective effect of diabetes on acute respiratory distress syndrome development is not clearly restricted to either type 1 (adjusted odds ratio, 0.50; 95% CI, 0.26–0.99; p = 0.046) or type 2 (adjusted odds ratio, 0.77; 95% CI, 0.60–1.00; p = 0.050) diabetes. Among patients in whom acute respiratory distress syndrome developed, diabetes was not associated with 60-day mortality on univariate (odds ratio, 1.11; 95% CI, 0.80–1.52) or multivariate analysis (adjusted odds ratio, 0.81; 95% CI, 0.56–1.18).
Conclusions: Diabetes is associated with a lower rate of acute respiratory distress syndrome development, and this relationship remained after adjusting for clinical differences between diabetics and nondiabetics, such as obesity, acute hyperglycemia, and diabetes-associated medications. In addition, this association was present for type 1 and 2 diabetics and in all subgroups of at-risk patients.
1Division of Critical Care Medicine, Department of Medicine, Jay B. Langner Critical Care Service, Montefiore Medical Center, Bronx, NY.
2Pulmonary and Critical Care Unit, Department of Medicine, Massachusetts General Hospital, Boston, MA.
3Environmental Health Department, Environmental and Occupational Medicine and Epidemiology Program, Harvard School of Public Health, Boston, MA.
4Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY.
* See also p. 2822.
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Supported, in part, by research grants R01 HL086667, R01 HL060710, and U01 HL108712 from the National Heart, Lung, and Blood Institute.
Dr. Christiani received grant support from NHLBI and funding from NIH. Dr. Thompson received grant support from NHLBI and funding from NIH. Dr. Gong received funding from NIH. The remaining authors have disclosed that they do not have any potential conflicts of interest.
Address requests for reprints to: Michelle Ng Gong, MD, MS, Division of Critical Care Medicine, Department of Medicine, Jay B. Langner Critical Care Service, Montefiore Medical Center, 111 East 210th Street, Bronx, NY 10467. E-mail: firstname.lastname@example.org