Sandbox:Usman Shah
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."COVID-19 | Radiology Reference Article | Radiopaedia.org".
- 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.Iannaccone G, Scacciavillani R, Del Buono MG, Camilli M, Ronco C, Lavie CJ, Abbate A, Crea F, Massetti M, Aspromonte N (June 2020). "Weathering the Cytokine Storm in COVID-19: Therapeutic Implications". Cardiorenal Med: 1–11. doi:10.1159/000509483. PMC 7360507 Check
|pmc=value (help). PMID 32599589 Check|pmid=value (help).
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| 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.
- ↑ 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.