BACKGROUND: ARDS is an important cause of respiratory failure and continues to be associated with a high mortality rate. Numerous therapeutic interventions have been employed to improve patient outcomes, including inhaled epoprostenol. METHODS: We examined subjects with ARDS treated with epoprostenol. We compared hospital survivors with nonsurvivors to identify predictors of mortality. RESULTS: Among the cohort (n=216), there were 80 (37%) hospital survivors and 136 (63%) hospital nonsurvivors. Logistic regression revealed 5 variables associated with hospital mortality: trauma as the etiology for ARDS (adjusted odds ratio [AOR] 0.09, 95% CI 0.04–0.22, P=.006), presence of both pulmonary and nonpulmonary sources of sepsis (AOR 3.06, 95% CI 1.98-4.74, P.01), an international normalized ratio of > 1.5 (AOR 3.15, 95% CI 2.19-4.54, P=.002), body mass index (1-unit increments, AOR 0.95, 95% CI 0.936-0.965, P=.001), and an incremental change in PaO2/FIO2 during the first 24 h of treatment with epoprostenol (AOR 0.99, 95% CI 0.988-0.994, P=.002). An analysis for 90-d mortality identified the same predictors, with the addition of cumulative fluid balance during treatment with epoprostenol of > 4 L also being an independent predictor (AOR 2.36, 95% CI 1.66-3.37, P=.02). CONCLUSIONS: Although the use of epoprostenol in ARDS remains a therapeutic challenge, we were able to identify predictors of mortality for this important cohort of patients. These predictor variables could be employed in the design of future trials of epoprostenol in ARDS.
BACKGROUND: ARDS is an important cause of respiratory failure and continues to be associated with a high mortality rate. Numerous therapeutic interventions have been employed to improve patient outcomes, including inhaled epoprostenol. METHODS: We examined subjects with ARDS treated with epoprostenol. We compared hospital survivors with nonsurvivors to identify predictors of mortality. RESULTS: Among the cohort (n=216), there were 80 (37%) hospital survivors and 136 (63%) hospital nonsurvivors. Logistic regression revealed 5 variables associated with hospital mortality: trauma as the etiology for ARDS (adjusted odds ratio [AOR] 0.09, 95% CI 0.04–0.22, P=.006), presence of both pulmonary and nonpulmonary sources of sepsis (AOR 3.06, 95% CI 1.98-4.74, P.01), an international normalized ratio of > 1.5 (AOR 3.15, 95% CI 2.19-4.54, P=.002), body mass index (1-unit increments, AOR 0.95, 95% CI 0.936-0.965, P=.001), and an incremental change in PaO2/FIO2 during the first 24 h of treatment with epoprostenol (AOR 0.99, 95% CI 0.988-0.994, P=.002). An analysis for 90-d mortality identified the same predictors, with the addition of cumulative fluid balance during treatment with epoprostenol of > 4 L also being an independent predictor (AOR 2.36, 95% CI 1.66-3.37, P=.02). CONCLUSIONS: Although the use of epoprostenol in ARDS remains a therapeutic challenge, we were able to identify predictors of mortality for this important cohort of patients. These predictor variables could be employed in the design of future trials of epoprostenol in ARDS.
Authors: Brian M Fuller; Nicholas M Mohr; Lee Skrupky; Susan Fowler; Marin H Kollef; Christopher R Carpenter Journal: Chest Date: 2015-06 Impact factor: 9.410
Authors: Christophe Guervilly; Magali Bisbal; Jean Marie Forel; Malika Mechati; Samuel Lehingue; Jeremy Bourenne; Gilles Perrin; Romain Rambaud; Melanie Adda; Sami Hraiech; Elisa Marchi; Antoine Roch; Marc Gainnier; Laurent Papazian Journal: Intensive Care Med Date: 2016-12-24 Impact factor: 17.440
Authors: Jayesh Dhanani; John F Fraser; Hak-Kim Chan; Jordi Rello; Jeremy Cohen; Jason A Roberts Journal: Crit Care Date: 2016-10-07 Impact factor: 9.097