Pulmonary Angiopathy in Severe COVID-19: Physiologic, Imaging, and Hematologic Observations.

Tytuł:: Pulmonary Angiopathy in Severe COVID-19: Physiologic, Imaging, and Hematologic Observations.
Autorzy:: Patel BV; Division of Anaesthetics, Pain Medicine, and Intensive Care, Department of Surgery and Cancer.; Centre for Haematology, Department of Immunology and Inflammation, and.
Arachchillage DJ; National Heart and Lung Institute, Imperial College London, London, United Kingdom.; Department of Adult Intensive Care.
Ridge CA; Department of Haematology.; Department of Radiology.
Bianchi P; Department of Adult Intensive Care, and.
Doyle JF; Department of Adult Intensive Care, and.
Garfield B; Department of Adult Intensive Care, and.
Ledot S; Department of Adult Intensive Care, and.
Morgan C; Department of Adult Intensive Care, and.
Passariello M; Department of Adult Intensive Care, and.
Price S; Department of Haematology.; Department of Adult Intensive Care, and.
Singh S; Division of Anaesthetics, Pain Medicine, and Intensive Care, Department of Surgery and Cancer.; Department of Adult Intensive Care, and.
Thakuria L; Department of Adult Intensive Care, and.
Trenfield S; Department of Adult Intensive Care, and.
Trimlett R; Department of Adult Intensive Care, and.
Weaver C; Department of Adult Intensive Care, and.
Wort SJ; Department of Haematology.; The Pulmonary Hypertension Service, Royal Brompton & Harefield NHS Foundation Trust, London, United Kingdom.
Xu T; Department of Adult Intensive Care, and.
Padley SPG; Department of Haematology.; Department of Radiology.
Devaraj A; Department of Haematology.; Department of Radiology.
Desai SR; Department of Haematology.; Department of Radiology.
Źródło:: American journal of respiratory and critical care medicine [Am J Respir Crit Care Med] 2020 Sep 01; Vol. 202 (5), pp. 690-699.
Typ publikacji:: Journal Article; Observational Study
Język:: English
Imprint Name(s):: Publication: 2000- : New York, NY : American Thoracic Society
Original Publication: New York, NY : American Lung Association, c1994-
MeSH Terms:: Betacoronavirus*
Coronavirus Infections/*complications
Lung/*blood supply
Pneumonia, Viral/*complications
Pulmonary Circulation/*physiology
Vascular Diseases/*etiology
Adult ; Aged ; COVID-19 ; Coronavirus Infections/epidemiology ; Female ; Humans ; Lung/diagnostic imaging ; Male ; Middle Aged ; Pandemics ; Pneumonia, Viral/epidemiology ; SARS-CoV-2 ; Tomography, X-Ray Computed ; Vascular Diseases/diagnosis ; Vascular Diseases/physiopathology
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Contributed Indexing:: Keywords: acute respiratory distress syndrome; mechanical ventilation; novel coronavirus disease 2019; pulmonary perfusion; thoracic imaging
Entry Date(s):: Date Created: 20200716 Date Completed: 20200917 Latest Revision: 20240330
Update Code:: 20240330
PubMed Central ID:: PMC7462405
DOI:: 10.1164/rccm.202004-1412OC
PMID:: 32667207
: Czasopismo naukowe

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 [ 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 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 H 2 O; 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.

Comment in: Am J Respir Crit Care Med. 2020 Sep 1;202(5):642-644. (PMID: 32687386)
Comment in: Am J Respir Crit Care Med. 2021 Jan 15;203(2):258-259. (PMID: 33085901)
Comment in: Am J Respir Crit Care Med. 2021 Jan 15;203(2):260-261. (PMID: 33085902)
Comment in: Am J Respir Crit Care Med. 2021 Jan 15;203(2):261-263. (PMID: 33085905)
Comment in: Am J Respir Crit Care Med. 2021 Jan 15;203(2):259-260. (PMID: 33085907)
Comment in: Am J Respir Crit Care Med. 2021 Jan 15;203(2):257-258. (PMID: 33085908)

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