Original Article
Pulmonary mechanics and gas exchange characteristics in uncommon etiologies of acute respiratory distress syndrome
Abstract
Background: Common causes of acute respiratory distress syndrome (ARDS) include pneumonia, aspiration, non-pulmonary sepsis and trauma. Little is known about pulmonary mechanics and gas exchange in less-common etiologies of ARDS, which comprises 12–23% of cases. Our hospital’s ARDS quality assurance database contained a substantial number of these cases. This descriptive study examines the pulmonary mechanics, and gas exchange characteristics of this diverse cohort of ARDS subjects.
Methods: Between March 2010 and April 2017 we identified 94 subjects with less common etiologies of ARDS who had dead space fraction (VD/VT) and respiratory system compliance (CRS) measured within 24 hours of ARDS onset; 86 of whom did not have sepsis as a co-diagnosis. There were 18 identifiable sources of ARDS. For descriptive purposes these were subsumed under 10 etiologic categories: pancreatitis (n=16), hemorrhagic shock/reperfusion injury (n=9), transfusion-associated acute lung injury (TRALI) (n=3), drug overdose (n=13), inhalation injury (n=10), idiopathic (n=10), neurogenic (n=8), pulmonary toxicity (n=3), hyper-immune response (n=4), hepatic failure (n=7), and 3 other cases: 2 cutaneous burns and one case of malaria. VD/VT was measured using the Enghoff-Bohr equation. Arterial blood gases were drawn simultaneously with mixed expired CO2 using volumetric capnography and standard pulmonary mechanics measurements. Data are expressed as median (IQR). Comparisons between groups used Kruskal-Wallis and Dunn’s post-tests, Mann-Whitney tests or Fisher exact tests.
Results: The majority of less common ARDS were from indirect sources (79%) with 9% attributed to direct causes and 11% idiopathic. Because of the small sample sizes, there were no differences in pulmonary mechanics or gas exchange between subgroups classified as indirect, direct and idiopathic, or between subgroups sharing common lung injury mechanisms. Nevertheless, salient trends were apparent particularly in CRS and VD/VT. CRS was most severely reduced in the toxicity subgroup and least impaired in the idiopathic subgroup [18 (11 to 22), and 40 (30 to 43) mL/cmH2O respectively]. VD/VT was extraordinarily high in the hepatic failure subgroup and lowest in pancreatitis [0.78 (0.57 to 0.79) and 0.54 (0.47 to 0.65) respectively]. There was less distinction in oxygenation as median values for all subgroups met moderate ARDS criteria. For the entire cohort, only VD/VT was statistically different between non-survivors and survivors: 0.66 (0.57 to 0.78) vs. 0.59 (0.51 to 0.68), P=0.012.
Conclusions: Within a diverse cohort having less common presentations of ARDS, there was apparent variability in the distribution of CRS, VD/VT compared to differences oxygenation dysfunction. Elevated pulmonary dead space still identified patients with higher mortality, as is the case with more common causes of ARDS.
Methods: Between March 2010 and April 2017 we identified 94 subjects with less common etiologies of ARDS who had dead space fraction (VD/VT) and respiratory system compliance (CRS) measured within 24 hours of ARDS onset; 86 of whom did not have sepsis as a co-diagnosis. There were 18 identifiable sources of ARDS. For descriptive purposes these were subsumed under 10 etiologic categories: pancreatitis (n=16), hemorrhagic shock/reperfusion injury (n=9), transfusion-associated acute lung injury (TRALI) (n=3), drug overdose (n=13), inhalation injury (n=10), idiopathic (n=10), neurogenic (n=8), pulmonary toxicity (n=3), hyper-immune response (n=4), hepatic failure (n=7), and 3 other cases: 2 cutaneous burns and one case of malaria. VD/VT was measured using the Enghoff-Bohr equation. Arterial blood gases were drawn simultaneously with mixed expired CO2 using volumetric capnography and standard pulmonary mechanics measurements. Data are expressed as median (IQR). Comparisons between groups used Kruskal-Wallis and Dunn’s post-tests, Mann-Whitney tests or Fisher exact tests.
Results: The majority of less common ARDS were from indirect sources (79%) with 9% attributed to direct causes and 11% idiopathic. Because of the small sample sizes, there were no differences in pulmonary mechanics or gas exchange between subgroups classified as indirect, direct and idiopathic, or between subgroups sharing common lung injury mechanisms. Nevertheless, salient trends were apparent particularly in CRS and VD/VT. CRS was most severely reduced in the toxicity subgroup and least impaired in the idiopathic subgroup [18 (11 to 22), and 40 (30 to 43) mL/cmH2O respectively]. VD/VT was extraordinarily high in the hepatic failure subgroup and lowest in pancreatitis [0.78 (0.57 to 0.79) and 0.54 (0.47 to 0.65) respectively]. There was less distinction in oxygenation as median values for all subgroups met moderate ARDS criteria. For the entire cohort, only VD/VT was statistically different between non-survivors and survivors: 0.66 (0.57 to 0.78) vs. 0.59 (0.51 to 0.68), P=0.012.
Conclusions: Within a diverse cohort having less common presentations of ARDS, there was apparent variability in the distribution of CRS, VD/VT compared to differences oxygenation dysfunction. Elevated pulmonary dead space still identified patients with higher mortality, as is the case with more common causes of ARDS.
