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Updated: May 14, 2026
06:47
Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Platelets are dominant contributors to hypercoagulability after injury
Jeffrey N Harr1, Ernest E Moore, Theresa L Chin
1Department of Surgery, University of Colorado Denver, Aurora, Colorado, USA.
The Journal of Trauma and Acute Care Surgery
|February 22, 2013
Summary
Thrombelastography-guided prophylaxis using escalating low-molecular weight heparin (LMWH) and aspirin did not reduce venous thromboembolism (VTE) incidence in trauma patients. However, platelet count significantly correlated with clot strength, suggesting a role for antiplatelet therapy in VTE prevention.
Area of Science:
- Trauma critical care
- Hematology
- Pharmacology
Background:
- Venous thromboembolic (VTE) disease is common after trauma, but optimal prophylaxis remains debated.
- Thrombelastography (TEG) is proposed for guiding VTE prophylaxis.
- A phase II trial investigated TEG-guided prophylaxis to reduce VTE incidence.
Purpose of the Study:
- To test the hypothesis that TEG-guided prophylaxis with escalating low-molecular weight heparin (LMWH) and antiplatelet therapy reduces VTE incidence in trauma patients.
- To evaluate the role of TEG in guiding VTE prophylaxis strategies.
Main Methods:
- A randomized controlled trial involving 50 surgical intensive care unit trauma patients.
- Patients received either daily LMWH (control) or TEG-guided prophylaxis with escalating LMWH and aspirin.
- In vitro studies assessed platelet contribution to clot strength.
Main Results:
- No significant difference in VTE incidence between control and TEG-guided groups.
- Increased LMWH did not significantly affect clot strength.
- Platelet count showed the strongest correlation with clot strength over time.
- In vitro studies confirmed that increased platelets enhance clot strength, thrombus generation, and fibrin production.
Conclusions:
- TEG-guided prophylaxis with escalating LMWH and aspirin did not reduce VTE incidence in this cohort.
- Platelet count is a key determinant of clot strength in trauma patients.
- Findings suggest a potential role for antiplatelet therapy in VTE prophylaxis, especially after 48 hours post-trauma.
Related Concept Videos
01:22Formation 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...
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...
01:05Introduction 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...
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...
01:09Coagulation
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...
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01:18Structure and Function of Platelets
The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...
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01:20Extrinsic 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
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01:16Clot 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.