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Related Concept Videos

Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

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The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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Inflammatory Response II: Inflammatory Exudate and Tissue Repair01:24

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The immune system's inflammatory response destroys the invading pathogen, permitting the tissue to heal. The changes during the cellular and vascular stages allow exudate formation at the site of inflammation. The inflammatory exudate released from the wound has high protein content and a specific gravity above 1.020.
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the...
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Inflammatory Response01:28

Inflammatory Response

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An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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Inflammation01:38

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Endocarditis II: Clinical Features of Infective Endocarditis01:25

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Endocarditis can present various clinical features depending on the causative organism and the patient's underlying health conditions. Initially, the clinical features of infective endocarditis develop gradually, presenting with nonspecific symptoms that can be easily mistaken for other illnesses.General SymptomsEarly symptoms of infective endocarditis are fever, chills, weakness, malaise, fatigue, and weight loss. These symptoms reflect the systemic nature of the infection and the body's...
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Pneumonia II: Pathophysiology01:29

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The pathophysiology of pneumonia involves the following steps:
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Updated: Dec 19, 2025

A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats
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Thromboinflammatory response in SARS-CoV-2 sepsis.

Aniello Maiese1, Giovanna Passaro2, Alessandra DE Matteis3

  • 1Department of Surgical Pathology, Medical, Molecular and Critical Area, Institute of Legal Medicine, University of Pisa, Pisa, Italy.

The Medico-Legal Journal
|June 4, 2020
PubMed
Summary

Viral sepsis, though rare, can arise from SARS-CoV-2 infections. Early immunomodulator therapy and revised anticoagulant strategies are suggested to manage this severe condition.

Keywords:
Sars-CoV-2sepsis, COVID-19, Thrombosis, Coagulopathy

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Area of Science:

  • Infectious Diseases
  • Critical Care Medicine
  • Immunology

Background:

  • Viral sepsis is an uncommon but severe complication of viral infections.
  • Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) infection is associated with significant pro-inflammatory cytokine release.
  • This cytokine storm can exacerbate interstitial pneumonia and lead to viral sepsis with hypercoagulability.

Purpose of the Study:

  • To highlight the underrecognized incidence and pathophysiology of viral sepsis.
  • To emphasize the role of SARS-CoV-2 in triggering sepsis and hypercoagulability.
  • To propose therapeutic strategies for managing viral sepsis.

Main Methods:

  • Review of clinical observations and existing literature on SARS-CoV-2 and sepsis.
  • Analysis of the inflammatory and coagulation pathways involved in severe COVID-19.
  • Conceptual framework for early therapeutic interventions.

Main Results:

  • SARS-CoV-2 infection can precipitate viral sepsis through a pronounced inflammatory response.
  • Hypercoagulability is a significant feature of SARS-CoV-2-induced viral sepsis.
  • Current understanding suggests a need for proactive management.

Conclusions:

  • Early immunomodulatory therapy may be beneficial in managing viral sepsis.
  • Prophylactic anticoagulant therapy requires reevaluation in the context of viral sepsis.
  • Further research into the incidence and optimal treatment of viral sepsis is warranted.