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| __NOTOC__
| | #REDIRECT [[COVID-19 Pulmonary Complications]] |
| To go to the COVID-19 project topics list, click '''[[COVID-19 Project Topics|here]]'''.
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| {{CMG}} {{AE}} {{S.M.}}
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| ==Overview==
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| [[Covid19|Covid-19]] [[infection]] is [[Association (statistics)|associated]] with [[pulmonary]] [[complications]] such as [[acute respiratory distress syndrome]], [[pneumonia]], [[pulmonary embolism]], [[hypoxemia]], [[superinfection]], [[respiratory failure]], and increased [[mortality]] in [[patients]] with an [[Underlying representation|underlying]] [[pulmonary disease]] such as [[chronic obstructive pulmonary disease]] ([[Chronic obstructive pulmonary disease|COPD]]).
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| ==Complications==
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| ===Acute respiratory distress syndrome===
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| *
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| ===Pneumonia===
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| ===Pulmonary embolism===
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| In May 2020, various autopsies studies revealed pulmonary embolism to be the common cause of death in these patients. These patients in their mid-70s had preexisting medical conditions such as cardiac diseases, hypertension, diabetes, and obesity. These studies highlight the role of hypercoagulability as the main contributor to the fatality in these patients. Various studies have described Virchow's triad to be the main component of the hypercoagulable state in these patients.<ref name="Wichmann Sperhake Lütgehetmann Steurer p. ">{{cite journal | last=Wichmann | first=Dominic | last2=Sperhake | first2=Jan-Peter | last3=Lütgehetmann | first3=Marc | last4=Steurer | first4=Stefan | last5=Edler | first5=Carolin | last6=Heinemann | first6=Axel | last7=Heinrich | first7=Fabian | last8=Mushumba | first8=Herbert | last9=Kniep | first9=Inga | last10=Schröder | first10=Ann Sophie | last11=Burdelski | first11=Christoph | last12=de Heer | first12=Geraldine | last13=Nierhaus | first13=Axel | last14=Frings | first14=Daniel | last15=Pfefferle | first15=Susanne | last16=Becker | first16=Heinrich | last17=Bredereke-Wiedling | first17=Hanns | last18=de Weerth | first18=Andreas | last19=Paschen | first19=Hans-Richard | last20=Sheikhzadeh-Eggers | first20=Sara | last21=Stang | first21=Axel | last22=Schmiedel | first22=Stefan | last23=Bokemeyer | first23=Carsten | last24=Addo | first24=Marylyn M. | last25=Aepfelbacher | first25=Martin | last26=Püschel | first26=Klaus | last27=Kluge | first27=Stefan | title=Autopsy Findings and Venous Thromboembolism in Patients With COVID-19 | journal=Annals of Internal Medicine | publisher=American College of Physicians | date=2020-05-06 | issn=0003-4819 | doi=10.7326/m20-2003 | page=}}</ref>
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| ==== Pathogenesis ====
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| As data on COVID-19 has been incomplete and evolving, the pathogenesis of pulmonary embolism has not yet been completely understood. Various contributors to the pathogenesis of pulmonary embolism in these patients are listed as following
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| ===== Endothelial cells dysfunction: =====
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| * It has been proposed that endothelial cells contribute towards the initiation and propagation of ARDS by changing the vascular barrier permeability, increasing the chance of procoagulative state that leads to endotheliitis and infiltration of inflammatory cells in the pulmonary vasculature.
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| * It has been proposed that COVID-19 can directly affect endothelial cells leading to widespread endotheliitis. SARS-CoV-2 also binds to the ACE2 receptors which alter the activity of ACE2.
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| * Reduced ACE2 activity leads to activation of kallikrein-bradykinin pathway, which increases vascular permeability.
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| * The activated neutrophils migrate towards the pulmonary endothelial cells and produce cytotoxic mediators including reactive oxygen species. <ref name="Teuwen Geldhof Pasut Carmeliet p.">{{cite journal | last=Teuwen | first=Laure-Anne | last2=Geldhof | first2=Vincent | last3=Pasut | first3=Alessandra | last4=Carmeliet | first4=Peter | title=COVID-19: the vasculature unleashed | journal=Nature Reviews Immunology | publisher=Springer Science and Business Media LLC | date=2020-05-21 | issn=1474-1733 | doi=10.1038/s41577-020-0343-0 | page=}}</ref>
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| ===== Stasis =====
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| Most hospitalized critically ill immobile COVID-19 patients are prone to stasis of blood flow leading to another contributor towards the pathogenesis of pulmonary embolism.
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| ===== Hypercoagulable state =====
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| Various clinical studies have reported different prothrombotic factors in patients who are critically ill and are hospitalized due to COVID-19. These studies report various key lab factors that play an important role in the pathogenesis of pulmonary embolism. <ref name="Panigada Bottino Tagliabue Grasselli p. ">{{cite journal | last=Panigada | first=Mauro | last2=Bottino | first2=Nicola | last3=Tagliabue | first3=Paola | last4=Grasselli | first4=Giacomo | last5=Novembrino | first5=Cristina | last6=Chantarangkul | first6=Veena | last7=Pesenti | first7=Antonio | last8=Peyvandi | first8=Fora | last9=Tripodi | first9=Armando | title=Hypercoagulability of COVID‐19 patients in Intensive Care Unit. A Report of Thromboelastography Findings and other Parameters of Hemostasis | journal=Journal of Thrombosis and Haemostasis | publisher=Wiley | date=2020-04-17 | issn=1538-7933 | doi=10.1111/jth.14850 | page=}}</ref>
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| * Elevation of d-dimers
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| * Elevation of C-reactive protein
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| * Elevated factor VIII and von Willebrand factor
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| * Decrease in Antithrombin level
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| * Increased fibrinogen levels
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| ==== Clinical Features ====
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| Pulmonary embolism can present with no symptoms to shock and even sudden cardiac arrest. The most common symptoms that were observed in Prospective Investigation of Pulmonary Embolism Diagnosis II (PIOPED II) trial include, dyspnea that is sudden in onset at rest or exertion (73%), , pleuritic pain (44%), calf or thigh pain (44%), calf or thigh swelling (41%), and cough (34%). <ref name="Stein Beemath Matta Weg 2007 pp. 871–879">{{cite journal | last=Stein | first=Paul D. | last2=Beemath | first2=Afzal | last3=Matta | first3=Fadi | last4=Weg | first4=John G. | last5=Yusen | first5=Roger D. | last6=Hales | first6=Charles A. | last7=Hull | first7=Russell D. | last8=Leeper | first8=Kenneth V. | last9=Sostman | first9=H. Dirk | last10=Tapson | first10=Victor F. | last11=Buckley | first11=John D. | last12=Gottschalk | first12=Alexander | last13=Goodman | first13=Lawrence R. | last14=Wakefied | first14=Thomas W. | last15=Woodard | first15=Pamela K. | title=Clinical Characteristics of Patients with Acute Pulmonary Embolism: Data from PIOPED II | journal=The American Journal of Medicine | publisher=Elsevier BV | volume=120 | issue=10 | year=2007 | issn=0002-9343 | doi=10.1016/j.amjmed.2007.03.024 | pages=871–879}}</ref>
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| ===Hypoxemia===
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| ===Superinfection===
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| ===Respiratory failure===
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| ===Increased mortality in COPD patients===
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| *According to a [[Study design|study]] [[Conduct|conducted]] in China, having an [[Underlying representation|underlying]] [[comorbidity]] such as [[chronic obstructive pulmonary disease]] ([[Chronic obstructive pulmonary disease|COPD]]) conferred a [[mortality]] [[hazard ratio]] of 2.681, even after adjusting for [[smoking]] status.
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| ==References==
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| <references />
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