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@article{Patel:2020:10.1164/rccm.202004-1412oc,
author = {Patel, BV and Arachchillage, DJ and Ridge, CA and Bianchi, P and Doyle, JF and Garfield, B and Ledot, S and Morgan, C and Passariello, M and Price, S and Singh, S and Thakuria, L and Trenfield, S and Trimlett, R and Weaver, C and Wort, SJ and Xu, T and Padley, SPG and Devaraj, A and Desai, SR},
doi = {10.1164/rccm.202004-1412oc},
journal = {American Journal of Respiratory and Critical Care Medicine},
pages = {690--699},
title = {Pulmonary angiopathy in severe COVID-19: physiologic, imaging and hematologic observations},
url = {http://dx.doi.org/10.1164/rccm.202004-1412oc},
volume = {202},
year = {2020}
}

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TY  - JOUR
AB  - Rationale: Clinical and epidemiologic data in coronavirus disease 2019 (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 pulmonary angiography [CTPA, n=39] and dual-energy CT [DECT, n=20]) studies were evaluated: observers quantified CT patterns (including the extent of abnormal lung and the presence/extent of dilated peripheral vessels) and perfusion defects on DECT. Coagulation status was assessed using thromboelastography (TEG). Measurements and Results: In 39 consecutive patients (M:F 32:7; mean age, 53±10 years [range 29-79 years]; black and ethnic minority, n=25 [64%]), there was a significant vascular perfusion abnormality and increased physiologic dead-space (dynamic compliance, 33.7±14.7 mls/cmH2O; 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.
AU  - Patel,BV
AU  - Arachchillage,DJ
AU  - Ridge,CA
AU  - Bianchi,P
AU  - Doyle,JF
AU  - Garfield,B
AU  - Ledot,S
AU  - Morgan,C
AU  - Passariello,M
AU  - Price,S
AU  - Singh,S
AU  - Thakuria,L
AU  - Trenfield,S
AU  - Trimlett,R
AU  - Weaver,C
AU  - Wort,SJ
AU  - Xu,T
AU  - Padley,SPG
AU  - Devaraj,A
AU  - Desai,SR
DO  - 10.1164/rccm.202004-1412oc
EP  - 699
PY  - 2020///
SN  - 1073-449X
SP  - 690
TI  - Pulmonary angiopathy in severe COVID-19: physiologic, imaging and hematologic observations
T2  - American Journal of Respiratory and Critical Care Medicine
UR  - http://dx.doi.org/10.1164/rccm.202004-1412oc
UR  - https://www.atsjournals.org/doi/10.1164/rccm.202004-1412OC
UR  - http://hdl.handle.net/10044/1/80773
VL  - 202
ER  -

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