Pulmonary Angiopathy in Severe COVID-19: Physiologic, Imaging, and Hematologic Observations
Pulmonary Angiopathy in Severe COVID-19: Physiologic, Imaging, and Hematologic Observations
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DOI：
10.1164/rccm.202004-1412oc
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发表时间：
2020-09-01
影响因子：
24.7
通讯作者：
Desai, Sujal R.
中科院分区：
文献类型：
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作者：
Patel, Brijesh, V;Arachchillage, Deepa J.;Desai, Sujal R.
基本原理：冠状病毒病（COVID-19）的临床和流行病学数据自爆发以来迅速增加，但很少涉及潜在的病理生理学。目的：确定严重COVID-19肺炎肺损伤的生理学，血液学和影像学基础。方法：整理临床，生理学和实验室数据。评价了放射学（计算机断层扫描（CT）肺血管造影[n = 39]和双能量CT [DECT，n = 20]）研究：观察者量化了CT模式（包括异常肺的范围以及扩张的外周血管的存在和范围）和DECT上的灌注缺损。凝血状态采用血栓弹力图进行评估。测量和结果：在39例连续患者中，（男：女，32：7;平均年龄，53 +/- 10岁[范围，29-79岁];黑人和少数民族，n = 25 [64%]），存在显著的血管灌注异常和生理死腔增加（动态顺应性，33.7 +/- 14.7 ml/cm H2O; Murray肺损伤评分，3.14 +/- 0.53;平均舒张比，2.6 +/- 0.8），有高凝状态和纤溶“关闭”的证据。正常充气肺、磨玻璃样阴影和致密实质阴影的平均CT范围（+/- SD）分别为23.5 +/-16.7%、36.3 +/-24.7%和42.7 +/-27.1%。21/33例（63.6%）患者存在外周血管扩张，至少有两个可评估的肺叶（包括10/21例[47.6%]，无急性肺栓塞证据）。所有患者（楔形，n = 3;斑点状，n = 9;混合型，n = 6）均存在DECT灌注缺陷（18/20 [90%]可评估）。结论：生理学、血液学和成像数据显示，严重COVID-19肺炎不仅存在高凝表型，而且可能由肺血管病和血栓形成引起的肺灌注明显受损。
Rationale: Clinical and epidemiologic data in coronavirus disease (COVID-19) have accrued rapidly since the outbreak, but few address the underlying pathophysiology.Objectives: To ascertain the physiologic, hematologic, and imaging basis of lung injury in severe COVID-19 pneumonia.Methods: Clinical, physiologic, and laboratory data were collated. Radiologic (computed tomography (CT) pulmonary angiography In = 39] and dual-energy CT [DECT, n = 20]) studies were evaluated: observers quantified CT patterns (including the extent of abnormal lung and the presence and extent of dilated peripheral vessels) and perfusion defects on DECT. Coagulation status was assessed using thromboelastography.Measurements and Results: In 39 consecutive patients (male: female, 32:7; mean age, 53 +/- 10 yr [range, 29-79 yr]; Black and minority ethnic, n = 25 [64%]), there was a significant vascular perfusion abnormality and increased physiologic dead space (dynamic compliance, 33.7 +/- 14.7 ml/cm H2O; Murray lung injury score, 3.14 +/- 0.53; mean ventilatory ratios, 2.6 +/- 0.8) with evidence of hypercoagulability and fibrinolytic "shutdown". The mean CT extent (+/- SD) of normally aerated lung, ground-glass opacification, and dense parenchymal opacification were 23.5 +/- 16.7%, 36.3 +/- 24.7%, and 42.7 +/- 27.1%, respectively. Dilated peripheral vessels were present in 21/33 (63.6%) patients with at least two assessable lobes (including 10/21 [47.6%] with no evidence of acute pulmonary emboli). Perfusion defects on DECT (assessable in 18/20 [90%]) were present in all patients (wedge-shaped, n = 3; mottled, n = 9; mixed pattern, n = 6).Conclusions: Physiologic, hematologic, and imaging data show not only the presence of a hypercoagulable phenotype in severe COVID-19 pneumonia but also markedly impaired pulmonary perfusion likely caused by pulmonary angiopathy and thrombosis.