Pulmonary Disorders and COVID-19: Difference between revisions
Jump to navigation
Jump to search
| Line 14: | Line 14: | ||
===Pulmonary embolism=== | ===Pulmonary embolism=== | ||
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 | 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> | ||
==== Pathogenesis ==== | ==== Pathogenesis ==== | ||
| Line 23: | Line 23: | ||
* 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. | * 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. | ||
* 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. | * 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 | * Reduced ACE2 activity leads to activation of kallikrein-bradykinin pathway, which increases 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> | * 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> | ||
===== Stasis ===== | ===== Stasis ===== | ||
Most hospitalized critically ill immobile COVID-19 patients | 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. | ||
===== Hypercoagulable state ===== | ===== Hypercoagulable state ===== | ||
Various clinical studies have reported different prothrombotic factors in patients | 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> | ||
* Elevation of d-dimers | * Elevation of d-dimers | ||
| Line 40: | Line 40: | ||
==== Clinical Features ==== | ==== Clinical Features ==== | ||
<br /> | <br /> | ||
===Hypoxemia=== | ===Hypoxemia=== | ||
Revision as of 07:02, 19 June 2020
To go to the COVID-19 project topics list, click here.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Mohsin, M.D.[2]
Overview
Covid-19 infection is 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 pulmonary disease such as chronic obstructive pulmonary disease (COPD).
Complications
Acute respiratory distress syndrome
Pneumonia
Pulmonary embolism
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.[1]
Pathogenesis
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
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.
- 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 vascular permeability.
- The activated neutrophils migrate towards the pulmonary endothelial cells and produce cytotoxic mediators including reactive oxygen species. [2]
Stasis
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.
Hypercoagulable state
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. [3]
- Elevation of d-dimers
- Elevation of C-reactive protein
- Elevated factor VIII and von Willebrand factor
- Decrease in Antithrombin level
- Increased fibrinogen levels
Clinical Features
Hypoxemia
Superinfection
Respiratory failure
Increased mortality in COPD patients
- According to a study conducted in China, having an underlying comorbidity such as chronic obstructive pulmonary disease (COPD) conferred a mortality hazard ratio of 2.681, even after adjusting for smoking status.
References
- ↑ Wichmann, Dominic; Sperhake, Jan-Peter; Lütgehetmann, Marc; Steurer, Stefan; Edler, Carolin; Heinemann, Axel; Heinrich, Fabian; Mushumba, Herbert; Kniep, Inga; Schröder, Ann Sophie; Burdelski, Christoph; de Heer, Geraldine; Nierhaus, Axel; Frings, Daniel; Pfefferle, Susanne; Becker, Heinrich; Bredereke-Wiedling, Hanns; de Weerth, Andreas; Paschen, Hans-Richard; Sheikhzadeh-Eggers, Sara; Stang, Axel; Schmiedel, Stefan; Bokemeyer, Carsten; Addo, Marylyn M.; Aepfelbacher, Martin; Püschel, Klaus; Kluge, Stefan (2020-05-06). "Autopsy Findings and Venous Thromboembolism in Patients With COVID-19". Annals of Internal Medicine. American College of Physicians. doi:10.7326/m20-2003. ISSN 0003-4819.
- ↑ Teuwen, Laure-Anne; Geldhof, Vincent; Pasut, Alessandra; Carmeliet, Peter (2020-05-21). "COVID-19: the vasculature unleashed". Nature Reviews Immunology. Springer Science and Business Media LLC. doi:10.1038/s41577-020-0343-0. ISSN 1474-1733.
- ↑ Panigada, Mauro; Bottino, Nicola; Tagliabue, Paola; Grasselli, Giacomo; Novembrino, Cristina; Chantarangkul, Veena; Pesenti, Antonio; Peyvandi, Fora; Tripodi, Armando (2020-04-17). "Hypercoagulability of COVID‐19 patients in Intensive Care Unit. A Report of Thromboelastography Findings and other Parameters of Hemostasis". Journal of Thrombosis and Haemostasis. Wiley. doi:10.1111/jth.14850. ISSN 1538-7933.