de Beer Friso M, Wieske Luuk, van Mierlo Gerard, Wouters Diana, Zeerleder Sacha, Bos Lieuwe D, Juffermans Nicole P, Schultz Marcus J, van der Poll Tom, Lagrand Wim K, Horn Janneke
Department of Intensive Care Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands.
Laboratory of Experimental Intensive Care and Anesthesiology (LEICA), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands.
Intensive Care Med Exp. 2020 Dec 18;8(Suppl 1):74. doi: 10.1186/s40635-020-00356-6.
Mechanical ventilation can induce or even worsen lung injury, at least in part via overdistension caused by too large volumes or too high pressures. The complement system has been suggested to play a causative role in ventilator-induced lung injury.
This was a single-center prospective study investigating associations between pulmonary levels of complement activation products and two ventilator settings, tidal volume (V) and driving pressure (ΔP), in critically ill patients under invasive ventilation. A miniature bronchoalveolar lavage (BAL) was performed for determination of pulmonary levels of C5a, C3b/c, and C4b/c. The primary endpoint was the correlation between BAL fluid (BALF) levels of C5a and V and ΔP. Levels of complement activation products were also compared between patients with and without ARDS or with and without pneumonia.
Seventy-two patients were included. Median time from start of invasive ventilation till BAL was 27 [19 to 34] hours. Median V and ΔP before BAL were 6.7 [IQR 6.1 to 7.6] ml/kg predicted bodyweight (PBW) and 15 [IQR 11 to 18] cm HO, respectively. BALF levels of C5a, C3b/c and C4b/c were neither different between patients with or without ARDS, nor between patients with or without pneumonia. BALF levels of C5a, and also C3b/c and C4b/c, did not correlate with V and ΔP. Median BALF levels of C5a, C3b/c, and C4b/c, and the effects of V and ΔP on those levels, were not different between patients with or without ARDS, and in patients with or without pneumonia.
In this cohort of critically ill patients under invasive ventilation, pulmonary levels of complement activation products were independent of the size of V and the level of ΔP. The associations were not different for patients with ARDS or with pneumonia. Pulmonary complement activation does not seem to play a major role in VILI, and not even in lung injury per se, in critically ill patients under invasive ventilation.
机械通气可诱发甚至加重肺损伤，至少部分是通过过大的潮气量或过高的压力导致的过度膨胀所致。有研究表明补体系统在呼吸机诱发的肺损伤中起致病作用。
这是一项单中心前瞻性研究，旨在调查有创通气的重症患者肺内补体激活产物水平与两种通气设置（潮气量[V]和驱动压力[ΔP]）之间的关联。进行微型支气管肺泡灌洗（BAL）以测定肺内C5a、C3b/c和C4b/c的水平。主要终点是支气管肺泡灌洗液（BALF）中C5a水平与V和ΔP之间的相关性。还比较了有或无急性呼吸窘迫综合征（ARDS）或有或无肺炎患者的补体激活产物水平。
纳入72例患者。从开始有创通气到进行BAL的中位时间为27[19至34]小时。BAL前的中位V和ΔP分别为6.7[四分位间距6.1至7.6]ml/kg预测体重（PBW）和15[四分位间距11至18]cmH₂O。有或无ARDS的患者之间以及有或无肺炎的患者之间，BALF中C5a、C3b/c和C4b/c的水平均无差异。BALF中C5a以及C3b/c和C4b/c的水平与V和ΔP均无相关性。有或无ARDS的患者之间以及有或无肺炎的患者之间，BALF中C5a、C3b/c和C4b/c的中位水平以及V和ΔP对这些水平的影响均无差异。
在这组有创通气的重症患者中，肺内补体激活产物水平与V的大小和ΔP的水平无关。ARDS患者或肺炎患者的相关性无差异。在有创通气的重症患者中，肺补体激活似乎在呼吸机诱发的肺损伤中不起主要作用，甚至在肺损伤本身中也不起主要作用。
