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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 main contributor towards the fatality in these patients. <ref name="Menter Haslbauer Nienhold Savic p. ">{{cite journal | last=Menter | first=T. | last2=Haslbauer | first2=J.D. | last3=Nienhold | first3=R. | last4=Savic | first4=S. | last5=Hopfer | first5=H. | last6=Deigendesch | first6=N. | last7=Frank | first7=S. | last8=Turek | first8=D. | last9=Willi | first9=N. | last10=Pargger | first10=H. | last11=Bassetti | first11=S. | last12=Leuppi | first12=J.D. | last13=Cathomas | first13=G. | last14=Tolnay | first14=M. | last15=Mertz | first15=K.D. | last16=Tzankov | first16=A. | title=Post‐mortem examination of COVID19 patients reveals diffuse alveolar damage with severe capillary congestion and variegated findings of lungs and other organs suggesting vascular dysfunction | journal=Histopathology | publisher=Wiley | date=2020-05-04 | issn=0309-0167 | doi=10.1111/his.14134 | page=}}</ref> <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> Various studies have described Virchow's triad to be the main component of the hypercoagulable state in these patients.
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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
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| * Endothelial cells dysfunction: 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.<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> 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. Reduced ACE2 activity leads to activation of kallikrein-bradykinin pathway, which increases the vascular permeability. 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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| ===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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