Coronavirus Disease 2019 Sepsis

Yataco, Angel O. Coz; Simpson, Steven Q.

doi:10.1016/j.chest.2020.07.023

Cited by 20 publications

(10 citation statements)

References 4 publications

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“…The systemic proinflammatory response, that in extreme cases may lead to disseminated coagulopathy, is reminiscent of the cytokine plethora and kinetics of septic conditions [15], pointing to viral SARS-CoV-2 sepsis in critical forms of COVID-19 [16,17].…”

Section: Clinical Evidence Of Microvascular and Thromboinflammatory Amentioning

confidence: 99%

From angiotensin-converting enzyme 2 disruption to thromboinflammatory microvascular disease: A paradigm drawn from COVID-19

Vinci

Pedicino

Andreotti

et al. 2021

International Journal of Cardiology

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We concisely review clinical, autopsy, experimental and molecular data of 2019 coronavirus disease (COVID-19). Angiotensin-converting enzyme 2 disruption and thromboinflammatory microangiopathy emerge as distinctive features. Briefly, entry of the virus into microvessels can profoundly disrupt the local renin-angiotensin system, cause endothelial injury, activate the complement cascade and induce powerful thromboinflammatory reactions, involving, in particular, von Willebrand factor, that, if widespread, may lead to microvascular plugging, ischemia and, ultimately, organ failure. We believe the current COVID-19 data consolidate a widely unrecognised paradigm of potentially fatal thromboinflammatory microvascular disease.

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Section: Clinical Evidence Of Microvascular and Thromboinflammatory Amentioning

confidence: 99%

From angiotensin-converting enzyme 2 disruption to thromboinflammatory microvascular disease: A paradigm drawn from COVID-19

Vinci

Pedicino

Andreotti

et al. 2021

International Journal of Cardiology

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show abstract

Section: Final Remarks On Covid-19 and Sepsismentioning

confidence: 99%

“…Sepsis is a life-threatening organ dysfunction that results from dysregulated host responses to infection and impaired immune homeostasis [ 75 ]. Sepsis has high mortality rates and can be caused by bacteria, fungi, or viruses such as SARS-CoV-2, the causative agent of COVID-19 [ 75 ]. The clinical features of sepsis include uncontrolled systemic inflammation that is characterized by a storm of inflammation associated with the release of proinflammatory and anti-inflammatory biomarkers such as IL-6, IL-1, TNF-α, PCT, and CRP [ 30 ].…”

Section: Final Remarks On Covid-19 and Sepsismentioning

confidence: 99%

“…Patients presenting with bacterial sepsis and patients with COVID-19 had similar patterns of MOF. Since SARS-CoV-2 is an infectious pathogen, it is reasonable to conclude that severe COVID-19 is sepsis that is caused by SARS-CoV-2 rather than an uncomplicated inflammatory process [ 75 ]. Therapies that prove to be efficacious against COVID-19 should also be successful in treating sepsis through the reduction of the inflammatory response and the anticoagulant effect.…”

Section: Final Remarks On Covid-19 and Sepsismentioning

confidence: 99%

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Severe COVID-19 and Sepsis: Immune Pathogenesis and Laboratory Markers

2021

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The ongoing outbreak of the novel coronavirus disease 2019 (COVID-19), induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has taken a significant toll on people and countries all over the world. The pathogenesis of COVID-19 has not been completely elucidated yet. This includes the interplay between inflammation and coagulation which needs further investigation. The massive production of proinflammatory cytokines and chemokines results in the so-called cytokine storm, leading to plasma leakage, vascular hyperpermeability, and disseminated vascular coagulation. This is usually accompanied by multiorgan failure. The extensive changes in the serum levels of cytokines are thought to play a crucial role in the COVID-19 pathogenesis. Additionally, the viral load and host inflammation factors are believed to have a significant role in host damage, particularly lung damage, from SARS-CoV-2. Interestingly, patients exhibit quantitative and qualitative differences in their immune responses to the virus, which can impact the clinical manifestation and outcomes of COVID-19. There needs to be a better understanding of the dynamic events that involve immune responses, inflammatory reactions, and viral replication in the context of the COVID-19 infection. Here, we discuss the main aspects of COVID-19 pathogenesis while supporting the hypothesis that inflammatory immune responses are involved in the progression of the disease to a more critical and fatal phase. We also explore the similarities and differences between severe COVID-19 and sepsis. A deeper understanding of the COVID-19 clinical picture as it relates to better-known conditions such as sepsis can provide useful clues for the management, prevention, and therapy of the disease.

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“…Critical care physicians have written that patients suffering from severe COVID-19 infection should be considered as viral sepsis (Coz Yataco et al 2020). The knowledge and experience in treating bacterial sepsis provide guidance for infection control and treatment using anti-viral medications (e.g.…”

mentioning

confidence: 99%