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Related Concept Videos

Inflammatory Response01:28

Inflammatory Response

17.9K
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.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
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Inflammation01:38

Inflammation

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Overview
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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

Inflammatory Response II: Inflammatory Exudate and Tissue Repair

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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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Phases of Wound Repair01:28

Phases of Wound Repair

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Following injury, the integrity of the injured tissues must be reestablished. For example, in skin tissue, wound repair involves coordination among resident skin cells, blood mononuclear cells, extracellular matrix, growth factors, and cytokines to complete the healing cascade.
Formation of Blood Clot
In case of deep injuries, trauma to blood vessels results in blood loss. In the meantime, phospholipids released from the ruptured endothelial cellular membrane are converted into arachidonic...
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Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

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Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
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Updated: Mar 11, 2026

Pseudofracture: An Acute Peripheral Tissue Trauma Model
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Pseudofracture: An Acute Peripheral Tissue Trauma Model

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Postinjury Inflammation and Organ Dysfunction.

Angela Sauaia1, Frederick A Moore2, Ernest E Moore3

  • 1University of Colorado Denver, 655 Broadway #365, Denver, CO 80203, USA.

Critical Care Clinics
|November 30, 2016
PubMed
Summary
This summary is machine-generated.

Trauma triggers opposing inflammatory responses, influencing organ dysfunction (OD). Understanding this balance is key to preventing severe complications and improving patient outcomes.

Keywords:
CARSOrgan dysfunctionPICSPostinjury inflammationSARSSIRS

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Area of Science:

  • Immunology
  • Critical Care Medicine
  • Pathophysiology

Background:

  • Organ dysfunction (OD) arises from complex inflammatory responses post-trauma.
  • Imbalances in pro- and anti-inflammatory pathways contribute to both early and late OD.
  • Persistent inflammation-immunosuppression catabolism syndrome can develop in patients with low-level OD.

Purpose of the Study:

  • To elucidate the role of inflammatory response dynamics in trauma-induced organ dysfunction.
  • To highlight the mechanisms leading to early and late OD.
  • To emphasize the importance of prevention strategies for OD.

Main Methods:

  • Review of inflammatory processes following trauma.
  • Analysis of innate and adaptive immune system roles.
  • Examination of apoptosis and its consequences.

Main Results:

  • Early proinflammation can lead to early OD.
  • Anti-inflammation may cause immunoparalysis, infections, and late OD.
  • While multiple organ failure incidence decreased, single OD, like acute lung injury, remains prevalent.

Conclusions:

  • The balance between simultaneous, opposing inflammatory responses is critical in trauma-induced OD.
  • Prevention strategies are crucial as treatment options for OD are limited.
  • Further research into managing the inflammatory cascade is needed.