Citation

Batchinsky AI, Wyckoff R, Choi JH, Burmeister D, Jordan BS, Necsoiu C, Burkett SE, Morris MJ, Chung KK, Cancio LC. J. Trauma Acute Care Surg. 2019; 87(Suppl 1): S91-S100.

Affiliation

From the The Geneva Foundation (A.I.B., J.H.C.), Tacoma, Washington; Unites States Army Institute of Surgical Research (A.I.B., J.H.C., D.B., B.S.J., C.N., L.C.C.), JBSA Ft. Sam Houston, Texas, West Florida Hospital, Department of Internal Medicine (R.W.), Pensacola, Florida; Pulmonary/Critical Care Service, Department of Medicine (S.E.B.), Dwight D. Eisenhower Army Medical Center, Fort Gordon, Georgia; Department of Medicine (M.J.M., K.K.C.), Brooke Army Medical Center, JBSA Ft. Sam Houston, Texas.

Copyright

(Copyright © 2019, Lippincott Williams and Wilkins)

DOI

10.1097/TA.0000000000002227

PMID

31246912

Abstract

BACKGROUND: Smoke inhalation injury (SII) causes 30% to 40% mortality and will increase as a cause of death during prolonged field care. We used a combat relevant model of acute respiratory distress syndrome due to SII to study temporal changes in ventilation-perfusion (V/Q) matching, computed tomography (CT) scan data, and histopathology and hypothesized that SII leads to increase in shunt (Qshunt), V/Q mismatch, lung consolidation, and diffuse alveolar damage.

METHODS: Swine received severe SII and airway pressure release ventilation (APRV, n = 6), or conventional ARDSNet mechanical ventilation (MV) (CMV, n = 8). A control group without injury received volume controlled MV (CTRL, n = 6), The multiple inert gas elimination technique and CT were performed at baseline (BL), 0.5 hours, 1 hours, 2 hours, 24 hours, and 48 hours after injury. Diffuse alveolar damage scoring was performed post mortem. Significance at p less than 0.05: APRV versus CTRL; CMV versus CTRL; APRV versus CMV*; denotes changes versus BL.

RESULTS: (1) SII caused increases in Qshunt more so in APRV than CMV group. Qshunt did not change in CTRL. (2) PaO2-to-FIO2 ratio (PFR) was lower in APRV versus CTRL at 2 hours (375 ± 62‡ vs. 549 ± 40) and 24 hours (126 ± 34‡* vs. 445 ± 5) and 48 hours (120 ± 41‡& vs. 430 ± 13). In CMV animals, PFR was lower versus CTRL and BL at 24 hours (238 ± 33) and 48 hours (98 ± 27). Qshunt correlated with PFR (r = 0.75, p < 0.0001, APRV and (r = 0.65, p < 0.0001, CMV). CT showed decrease in normally aerated lung, while poorly and nonaerated lung increased.

CONCLUSION: Smoke inhalation injury leads to early development of shunt, V/Q mismatch, lung consolidation, and diffuse alveolar damage. These data substantiate the need for new point of injury interventions in the prolonged field care setting. LEVEL OF EVIDENCE: Animal research.

Language: en