PURPOSE: Patients with a history of alcohol abuse (AA) are at increased risk for developing and dying from acute lung injury (ALI). Accumulation of extravascular lung water (EVLW) is an integral part of ALI, and AA leads to alterations in epithelial cell permeability and decreased alveolar liquid clearance in animal models. We hypothesized that AA in humans may accentuate alveolar-capillary barrier dysfunction with consequent greater accumulation of EVLW.
METHODS: Patients at an academic hospital were prospectively enrolled within 3 days of meeting the American-European consensus definition of ALI. The PiCCO™ thermodilution system (Pulsion Medical, Munich) was used to measure cardiovascular hemodynamics and EVLW (indexed to actual body weight). AUDIT and SMAST questionnaires were employed to diagnose AA. Pulmonary vascular permeability index (PVPI) was calculated as the ratio of EVLW to global end-diastolic volume (GEDV).
RESULTS: Twelve patients were enrolled; 5 met criteria of AA. Mean AUDIT and SMAST scores with AA were 5.8 and 19.6, while for non-AA they were 0.3 and 0.4 respectively (p<0.01). There were no statistically significant differences in age, creatinine, albumin, Lung Injury Score, APACHE II score, or cause of ALI between the groups. The mean net fluid balance over the study period was not different between groups (8980mL vs. 8390mL), nor was mean cardiac index, stroke volume variation, or GEDV. Mean EVLW at enrollment was slightly higher in AA than non-AA group (14.2mL/kg vs. 11.0mL/kg, p=0.14). Mean PVPI over the study period was also higher in AA patients (0.63 vs. 0.52, p=0.09). EVLW increased during the 5-day study period in AA patients (+1.5mL/kg) compared to a mean loss in non-AA patients (−0.3mL/kg, p<0.01).
CONCLUSION: In patients who develop ALI, alcohol abuse is associated with increased pulmonary vascular permeability and greater accumulation of lung water.
CLINICAL IMPLICATIONS: Alcohol abuse in humans may exacerbate alveolar-capillary barrier dysfunction, resulting in greater accumulation of extravascular lung water in ALI. Interventions targeted to barrier repair or edema reduction in this population may improve outcomes.
DISCLOSURE: Pajman Danai, None.