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.
J Trauma Acute Care Surg. 2019 Jul;87(1S Suppl 1):S91-S100. doi: 10.1097/TA.0000000000002227.
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.
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.
(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.
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.
Animal research.
烟雾吸入性损伤（SII）导致 30%-40%的死亡率，并将随着延长野外护理时间而增加死亡原因。我们使用与战场相关的 SII 引起的急性呼吸窘迫综合征模型来研究通气-灌注（V/Q）匹配、计算机断层扫描（CT）扫描数据和组织病理学的时间变化，并假设 SII 导致分流（Qshunt）增加、V/Q 不匹配、肺实变和弥漫性肺泡损伤。
猪遭受严重的 SII 和气道压力释放通气（APRV，n=6）或常规 ARDSNet 机械通气（MV）（CMV，n=8）。无损伤的对照组接受容量控制 MV（CTRL，n=6）。在损伤后 0.5 小时、1 小时、2 小时、24 小时和 48 小时进行多次惰性气体消除技术和 CT。死后进行弥漫性肺泡损伤评分。p<0.05 表示有统计学意义：APRV 与 CTRL；CMV 与 CTRL；APRV 与 CMV*；表示与 BL 相比的变化。
（1）SII 导致分流增加，APRV 组比 CMV 组更明显。CTRL 组的 Qshunt 没有变化。（2）APRV 组的 PaO2 与 FIO2 比值（PFR）在 2 小时（375±62‡ 与 549±40）和 24 小时（126±34‡* 与 445±5）和 48 小时（120±41‡& 与 430±13）时均低于 CTRL。在 CMV 动物中，PFR 在 24 小时（238±33）和 48 小时（98±27）时低于 CTRL 和 BL。Qshunt 与 PFR 相关（r=0.75，p<0.0001，APRV 和（r=0.65，p<0.0001，CMV）。CT 显示正常充气肺减少，而充气不良和非充气肺增加。
烟雾吸入性损伤导致早期分流、V/Q 不匹配、肺实变和弥漫性肺泡损伤的发生。这些数据证实了在延长野外护理环境中需要对损伤点进行新的干预。
动物研究。
