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Related Concept Videos

Coagulation01:09

Coagulation

The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
Coagulation01:06

Coagulation

Colloidal solids are solid particles suspended in solution. They are usually negatively charged, attracting a compact primary layer of positively charged ions, which attract more counterions to form an electrical double layer. Electrostatic repulsion between the charged double layers prevents the particles from colliding, stabilizing the colloids. These solids are often undesirable because they can contain toxins that are difficult to remove. Coagulation is a technique that helps aggregate and...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Introduction to Hemostasis01:05

Introduction to Hemostasis

Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized, and...
Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...

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Related Experiment Video

Updated: May 29, 2026

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation
06:50

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

Published on: June 10, 2020

Traumatic Inflammatory-Coagulation Coactivation Occurs Early After Injury and Impacts Mortality.

Julia Riccardi1, Anamaria J Robles1, James T Ross2,3

  • 1Department of Surgery, University of California Davis, Sacramento, CA.

Critical Care Medicine
|May 28, 2026
PubMed
Summary

Early coactivation of coagulation and inflammation pathways after severe injury is linked to increased 30-day mortality. Identifying these complex biomarker phenotypes is crucial for understanding trauma outcomes.

Keywords:
coagulationinflammationinflammatory reactioninjurytrauma

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Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

Area of Science:

  • Trauma research
  • Coagulation and inflammation pathways
  • Biomarker discovery

Background:

  • Acute traumatic coagulopathy is a known early complication of severe injury.
  • The specific roles of pro- and anti-inflammatory cytokines in this process remain unclear.
  • Understanding these pathways is critical for improving patient outcomes.

Purpose of the Study:

  • To investigate the interplay between inflammatory and coagulation pathways following severe injury.
  • To determine the relationship between these pathways and 30-day mortality.
  • To identify key biomarker phenotypes associated with mortality.

Main Methods:

  • Secondary analysis of the PROPPR study involving 680 severely injured patients.
  • Utilized Principal Component Analysis (PCA) on 48 coagulation and inflammatory biomarkers.
  • Least Absolute Shrinkage and Selection Operator (LASSO) regression identified mortality predictors.

Main Results:

  • 14 distinct biomarker phenotypes were identified, explaining 83% of pathophysiologic variability.
  • Coagulopathy and mixed inflammatory phenotypes were significantly associated with 30-day mortality.
  • Mortality was predominantly driven by coagulopathy phenotype 1 and mixed inflammatory phenotype 3, even after controlling for bleeding.

Conclusions:

  • Coagulation and inflammation are coactivated early after severe injury, contributing to poor outcomes.
  • The complex, integrated activation involves cytokines, coagulation factors, and platelet markers.
  • This study identified key biologic phenotypes linked to mortality in severe trauma using a comprehensive biomarker array.