Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Extrinsic and Intrinsic Pathways of Hemostasis

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...

Coagulation

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...

Clot Retraction and Fibrinolysis

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...

Burn Injuries

Burn Injuries

Burn injuries occur when the skin and underlying tissues are damaged due to exposure to heat, electricity, chemicals, radiation, or friction. They can vary in severity, from minor superficial burns to severe deep burns that can be life-threatening.
The damage results in the death of skin cells, which can lead to a massive loss of fluid. Dehydration, electrolyte imbalance, and renal and circulatory failure follow, which can be fatal. Burn patients are treated with intravenous fluids to offset...

Formation of the Platelet Plug

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Balanced crystalloids versus saline and mortality in hospitalized patients: a hierarchical Bayesian meta-analysis of cluster-randomized trials.

Journal of critical care·2026

Same author

Patient blood management in cardiac valve surgery: combined effects of preoperative hemoglobin optimization and intraoperative blood conservation.

Minerva anestesiologica·2026

Same author

High inappropriate red blood cell transfusion rate despite low overall use: a real-world multicenter study in 43 Spanish hospitals.

Frontiers in medicine·2026

Same author

PHOENICS trial: robust methods, outdated question.

European journal of anaesthesiology·2026

Same author

N-terminal proBNP adds prognostic value to high-sensitivity cardiac troponin I in elective thoracic surgery: an observational cohort study.

BMJ open·2026

Same author

Distinct patterns of intraoperative hemodynamic behavior and postoperative outcomes after major abdominal surgery.

Journal of clinical anesthesia·2026

Search research articles

Related Experiment Video

Updated: Jun 23, 2025

Author Spotlight: A Multi-Depth Porcine Model for Comprehensive Study of Burn Injuries and Healing Processes

Author Spotlight: A Multi-Depth Porcine Model for Comprehensive Study of Burn Injuries and Healing Processes

Published on: February 23, 2024

Factor XIII in major burns coagulation.

Patricia Guilabert¹, Luis Abarca¹, Gemma Usúa¹

¹Anesthesia and Critical Care Department. University Hospital Vall d'Hebron, Autonomous University of Barcelona, Barcelona, Spain.

Burns : Journal of the International Society for Burn Injuries

|June 20, 2024

Summary

This summary is machine-generated.

Major burn patients experience significant declines in Factor XIII (FXIII) levels, impacting clot stability and wound healing. These low FXIII levels, crucial for coagulation, may not be detected by standard tests.

Keywords:

Blood coagulation Blood coagulation disorders Blood coagulation test Burns Factor XIII Thrombelastography

More Related Videos

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

Published on: February 14, 2017

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

Related Experiment Videos

Last Updated: Jun 23, 2025

Author Spotlight: A Multi-Depth Porcine Model for Comprehensive Study of Burn Injuries and Healing Processes

Author Spotlight: A Multi-Depth Porcine Model for Comprehensive Study of Burn Injuries and Healing Processes

Published on: February 23, 2024

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

Published on: February 14, 2017

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

Area of Science:

Biochemistry
Trauma Surgery
Hematology

Background:

Major burn patients (MBPs) often develop acute burn-induced coagulopathy, a complex disorder affecting blood clotting.
While many coagulation factors have been studied in MBPs, Factor XIII (FXIII), essential for clot stabilization and wound healing, remains under-investigated.

Purpose of the Study:

To investigate the dynamic changes (kinetics) of FXIII and other coagulation factors in MBPs.
To elucidate the role of FXIII in the coagulopathy of MBPs.
To explore the potential association between FXIII levels and surgical bleeding in MBPs.

Main Methods:

A prospective observational pilot study was conducted.
The study monitored the kinetics of FXIII and other coagulation factors and cofactors in MBPs.
Data collection spanned the initial 30 days following burn injury.

Main Results:

Factor XIII (FXIII) levels significantly decreased by 75.10% between burn injury and surgery, and by 87.70% within 24 hours post-surgery.
Patients presented with critically low median antigenic FXIII levels of 32% at the time of surgery.
Most coagulation factors showed significant decreases 24 hours post-burn injury.

Conclusions:

MBPs exhibit a marked reduction in plasma FXIII levels from admission through 24 hours post-surgery.
Substantially low FXIII levels were detected during surgery, potentially missed by other coagulation assays.
The observed decrease in most factors at 24 hours may be attributed to fluid resuscitation dilution.