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* Cellular infection and viral replication cause activation of the inflammasome in the host cell, leading to the release of pro-inflammatory cytokines and cell death by pyroptosis with ensuing release of a damage-associated molecular pattern, further amplifying the inflammatory response.<ref name="IannacconeScacciavillani2020">{{cite journal|last1=Iannaccone|first1=Giulia|last2=Scacciavillani|first2=Roberto|last3=Del Buono|first3=Marco Giuseppe|last4=Camilli|first4=Massimiliano|last5=Ronco|first5=Claudio|last6=Lavie|first6=Carl J.|last7=Abbate|first7=Antonio|last8=Crea|first8=Filippo|last9=Massetti|first9=Massimo|last10=Aspromonte|first10=Nadia|title=Weathering the Cytokine Storm in COVID-19: Therapeutic Implications|journal=Cardiorenal Medicine|year=2020|pages=1–11|issn=1664-3828|doi=10.1159/000509483}}</ref> | * Cellular infection and viral replication cause activation of the inflammasome in the host cell, leading to the release of pro-inflammatory cytokines and cell death by pyroptosis with ensuing release of a damage-associated molecular pattern, further amplifying the inflammatory response.<ref name="IannacconeScacciavillani2020">{{cite journal|last1=Iannaccone|first1=Giulia|last2=Scacciavillani|first2=Roberto|last3=Del Buono|first3=Marco Giuseppe|last4=Camilli|first4=Massimiliano|last5=Ronco|first5=Claudio|last6=Lavie|first6=Carl J.|last7=Abbate|first7=Antonio|last8=Crea|first8=Filippo|last9=Massetti|first9=Massimo|last10=Aspromonte|first10=Nadia|title=Weathering the Cytokine Storm in COVID-19: Therapeutic Implications|journal=Cardiorenal Medicine|year=2020|pages=1–11|issn=1664-3828|doi=10.1159/000509483}}</ref> | ||
*The [[cytokine]] storm and the deadly uncontrolled [[systemic]] [[inflammatory]] response resulting from the release of large amounts of [[proinflammatory]] [[cytokines]] including [[interferons]] and [[interleukins]] and, [[chemokines]] by [[immune]] effector cells resulting in [[acute]] [[inflammation]] within the alveolar space. The [[exudate]] containing [[plasma proteins]], including [[albumin]], [[fibrinogen]], [[proinflammatory]] [[cytokines]] and [[coagulation factors]] will increase [[alveolar]]-[[capillary]] [[permeability]] and decrease the normal [[gas exchange]] and [[plasma proteins]], including [[albumin]], [[fibrinogen]], proinflammatory cytokines and coagulation factors.<ref name="MeduriAnnane2009">{{cite journal|last1=Meduri|first1=G. Umberto|last2=Annane|first2=Djillali|last3=Chrousos|first3=George P.|last4=Marik|first4=Paul E.|last5=Sinclair|first5=Scott E.|title=Activation and Regulation of Systemic Inflammation in ARDS|journal=Chest|volume=136|issue=6|year=2009|pages=1631–1643|issn=00123692|doi=10.1378/chest.08-2408}}</ref> | *The [[cytokine]] storm and the deadly uncontrolled [[systemic]] [[inflammatory]] response resulting from the release of large amounts of [[proinflammatory]] [[cytokines]] including [[interferons]] and [[interleukins]] and, [[chemokines]] by [[immune]] effector cells resulting in [[acute]] [[inflammation]] within the alveolar space. The [[exudate]] containing [[plasma proteins]], including [[albumin]], [[fibrinogen]], [[proinflammatory]] [[cytokines]] and [[coagulation factors]] will increase [[alveolar]]-[[capillary]] [[permeability]] and decrease the normal [[gas exchange]] and [[plasma proteins]], including [[albumin]], [[fibrinogen]], proinflammatory cytokines and coagulation factors.<ref name="MeduriAnnane2009">{{cite journal|last1=Meduri|first1=G. Umberto|last2=Annane|first2=Djillali|last3=Chrousos|first3=George P.|last4=Marik|first4=Paul E.|last5=Sinclair|first5=Scott E.|title=Activation and Regulation of Systemic Inflammation in ARDS|journal=Chest|volume=136|issue=6|year=2009|pages=1631–1643|issn=00123692|doi=10.1378/chest.08-2408}}</ref> | ||
*In line with this, recent studies have shown that patients with COVID-19 have high levels of inflammatory cytokines, such as interleukin (IL)-1β, IL-2, IL-6 IL-7, IL-8, IL-9, IL-10, IL-18, tumor necrosis factor (TNF)-α, granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor, fibroblast growth factor, macrophage inflammatory protein 1, compared to healthy individuals. | |||
*Circulating levels of IL-6, IL-10, and TNF-α also correlated with illness severity as they were significantly higher in intensive care unit (ICU) patients compared to mild/moderate cases. In particular, IL-6 may suppress normal T-cell activation and TNF-α can promote T-cell apoptosis via interacting with its receptor TNF receptor 1, and their upregulation may in part contribute to lymphocytopenia, a feature often encountered in COVID-19, with a more pronounced decline in severe cases <ref name="IannacconeScacciavillani2020" /> | |||
*This [[inflammatory]] process leads to the [[fibrin]] deposition in the air spaces and [[lung]] parenchyma and contributes to hyaline-membrane formation and subsequent [[alveolar]] [[fibrosis]].<ref name="BertozziAstedt1990">{{cite journal|last1=Bertozzi|first1=Paul|last2=Astedt|first2=Birgir|last3=Zenzius|first3=Laura|last4=Lynch|first4=Karen|last5=LeMaire|first5=Françoise|last6=Zapol|first6=Warren|last7=Chapman|first7=Harold A.|title=Depressed Bronchoalveolar Urokinase Activity in Patients with Adult Respiratory Distress Syndrome|journal=New England Journal of Medicine|volume=322|issue=13|year=1990|pages=890–897|issn=0028-4793|doi=10.1056/NEJM199003293221304}}</ref> | |||
Revision as of 17:29, 20 July 2020
Covid-19 Associated ARDS
Overview
Historical Perspective
- On 31 December 2019, the World Health Organization (WHO) was formally notified about a cluster of cases of pneumonia in Wuhan City.[1]
- Ten days later, WHO was aware of 282 confirmed cases, of which four were in Japan, South Korea and Thailand
- The virus responsible was isolated on 7 January and its genome shared on 12 January.The cause of the severe acute respiratory syndrome that became known as COVID‐19 was a novel coronavirus, SARS‐CoV‐2
- ARDS is one of the most important causes of hospital and ICU admission due to COVID.
- Many autopsies studies reported ARDS to be the cause of death in patients dying due to respiratory complications of COVID.
- As of July 19 2020 the number of total cases worldwide are 14,043,176 including 597,583 deaths, reported to WHO.
Classification
Authors in a case report highlighted the nonuniformity of patients with COVID-19-associated ARDS and proposed the existence of two primary phenotypes:
- Type L (low values of elastance, pulmonary ventilation/ perfusion ratio, lung weight, and recruitability).
- Type H (high values of elastance, right-to-left shunt, lung weight, and recruitability), more consistent with typical severe ARDS.[2]
ARDS is divided into three categories based on oxygenation index (PaO2/FiO2) on PEEP ≥ 5 cmH2O:
- mild (200 mmHg ≤ PaO2/FiO2 < 300 mmHg),
- mild-moderate (100 mmHg ≤ PaO2/FiO2 < 200 mmHg), and
- moderate-severe (PaO2/FiO2 < 100 mmHg).[3]
Pathophysiology
- The SARS-CoV-2 virus, like the closely-related MERS and SARS coronaviruses, effects its cellular entry via attachment of its virion spike protein (a.k.a. S protein) to the angiotensin-converting enzyme 2 (ACE2) receptor.[4]
- This receptor is commonly found on alveolar cells of the lung epithelium.It suggested that injury to the alveolar epithelial cells was the main cause of COVID-19-related ARDS.
- Cellular infection and viral replication cause activation of the inflammasome in the host cell, leading to the release of pro-inflammatory cytokines and cell death by pyroptosis with ensuing release of a damage-associated molecular pattern, further amplifying the inflammatory response.[5]
- The cytokine storm and the deadly uncontrolled systemic inflammatory response resulting from the release of large amounts of proinflammatory cytokines including interferons and interleukins and, chemokines by immune effector cells resulting in acute inflammation within the alveolar space. The exudate containing plasma proteins, including albumin, fibrinogen, proinflammatory cytokines and coagulation factors will increase alveolar-capillary permeability and decrease the normal gas exchange and plasma proteins, including albumin, fibrinogen, proinflammatory cytokines and coagulation factors.[6]
- In line with this, recent studies have shown that patients with COVID-19 have high levels of inflammatory cytokines, such as interleukin (IL)-1β, IL-2, IL-6 IL-7, IL-8, IL-9, IL-10, IL-18, tumor necrosis factor (TNF)-α, granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor, fibroblast growth factor, macrophage inflammatory protein 1, compared to healthy individuals.
- Circulating levels of IL-6, IL-10, and TNF-α also correlated with illness severity as they were significantly higher in intensive care unit (ICU) patients compared to mild/moderate cases. In particular, IL-6 may suppress normal T-cell activation and TNF-α can promote T-cell apoptosis via interacting with its receptor TNF receptor 1, and their upregulation may in part contribute to lymphocytopenia, a feature often encountered in COVID-19, with a more pronounced decline in severe cases [5]
- This inflammatory process leads to the fibrin deposition in the air spaces and lung parenchyma and contributes to hyaline-membrane formation and subsequent alveolar fibrosis.[7]
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![[1]](https://commons.wikimedia.org/w/index.php?search=covid&title=Special%3ASearch&go=Go&ns0=1&ns6=1&ns12=1&ns14=1&ns100=1&ns106=1#/media/File:Covid-19_San_Salvatore_02.jpg){kind=link}
| Criteria | Symptomatic WM | Asymptomatic WM | IgM-Related Disorders | MGUS |
|---|---|---|---|---|
| IgM monoclonal protein | + | + | + | + |
| Bone marrow infiltration | + | + | - | - |
| Symptoms attributable to IgM | + | - | + | - |
| Symptoms attributable to tumor infiltration | + | - | - | - |
|
Infra-Hisian Block Microchapters |
References
- ↑ 1.0 1.1 Chaplin, Steve (2020). "COVID
‐19: a brief history and treatments in development". Prescriber. 31 (5): 23–28. doi:10.1002/psb.1843. ISSN 0959-6682. line feed character in
|title=at position 6 (help) - ↑ Fan, Eddy; Beitler, Jeremy R; Brochard, Laurent; Calfee, Carolyn S; Ferguson, Niall D; Slutsky, Arthur S; Brodie, Daniel (2020). "COVID-19-associated acute respiratory distress syndrome: is a different approach to management warranted?". The Lancet Respiratory Medicine. doi:10.1016/S2213-2600(20)30304-0. ISSN 2213-2600.
- ↑ Li, Xu; Ma, Xiaochun (2020). "Acute respiratory failure in COVID-19: is it "typical" ARDS?". Critical Care. 24 (1). doi:10.1186/s13054-020-02911-9. ISSN 1364-8535.
- ↑ "COVID-19 | Radiology Reference Article | Radiopaedia.org".
- ↑ 5.0 5.1 Iannaccone, Giulia; Scacciavillani, Roberto; Del Buono, Marco Giuseppe; Camilli, Massimiliano; Ronco, Claudio; Lavie, Carl J.; Abbate, Antonio; Crea, Filippo; Massetti, Massimo; Aspromonte, Nadia (2020). "Weathering the Cytokine Storm in COVID-19: Therapeutic Implications". Cardiorenal Medicine: 1–11. doi:10.1159/000509483. ISSN 1664-3828.
- ↑ Meduri, G. Umberto; Annane, Djillali; Chrousos, George P.; Marik, Paul E.; Sinclair, Scott E. (2009). "Activation and Regulation of Systemic Inflammation in ARDS". Chest. 136 (6): 1631–1643. doi:10.1378/chest.08-2408. ISSN 0012-3692.
- ↑ Bertozzi, Paul; Astedt, Birgir; Zenzius, Laura; Lynch, Karen; LeMaire, Françoise; Zapol, Warren; Chapman, Harold A. (1990). "Depressed Bronchoalveolar Urokinase Activity in Patients with Adult Respiratory Distress Syndrome". New England Journal of Medicine. 322 (13): 890–897. doi:10.1056/NEJM199003293221304. ISSN 0028-4793.
- ↑ Kiran U, Aggarwal S, Choudhary A, Uma B, Kapoor PM (2017). "The blalock and taussig shunt revisited". Ann Card Anaesth. 20 (3): 323–330. doi:10.4103/aca.ACA_80_17. PMC 5535574. PMID 28701598.