Syndecan-1 Levels in Trauma and Burn Patients Remain Elevated During Resuscitation and Correlate With Coagulopathy

Grace Bonson1, Peter Callas2, Maria-Cristina Bravo3

  • 1Department of Emergency Medicine, University of Vermont, Burlington, Vermont, USA.

Insights

Elevated levels of syndecan-1 (SDC-1) in severe trauma patients peak early and persist, indicating a higher risk of coagulopathy. This finding highlights SDC-1 as a potential biomarker for trauma-induced coagulopathy.

Area of Science:

  • Biochemistry
  • Trauma Medicine
  • Hematology

Background:

  • Syndecan-1 (SDC-1) shedding from vascular endothelium into circulation in severe trauma is linked to mortality.
  • The temporal profile of SDC-1 elevation in trauma patients remains underexplored.

Purpose of the Study:

  • To characterize the longitudinal pattern of SDC-1 elevation in trauma patients within 120 hours of resuscitation.
  • To investigate the association between elevated SDC-1 levels (endotheliopathy) and trauma-induced coagulopathy (INR ≥ 1.4).

Main Methods:

  • Prospective observational study of 301 severely injured adults across 3 trauma centers.
  • Blood samples collected at multiple time points (0-120 hours); SDC-1 quantified by ELISA (≥40 ng/mL considered elevated).
  • Coagulopathy defined as INR ≥ 1.4; association analyzed using logistic regression, adjusting for covariates.

Main Results:

  • SDC-1 levels were significantly higher in patients with coagulopathy.
  • Elevated SDC-1 (≥40 ng/mL) strongly predicted coagulopathy (adjusted OR 17.88, P < .05).
  • High SDC-1 levels were most prominent at initial presentation and tended to remain elevated.

Conclusions:

  • Plasma SDC-1 levels peak early and remain elevated throughout the initial 120 hours in most trauma patients with mechanical and/or burn injuries.
  • Elevated SDC-1 is independently associated with an increased risk of coagulopathy, regardless of injury severity.
Abstract

Related Concept Videos

Acute Inflammation II: Local and Systemic Effects01:25

Acute Inflammation II: 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...
7
Phases of Wound Repair01:28

Phases of Wound Repair

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...
10.0K
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,...
19.5K
Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

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...
2.2K
Blood Studies for Cardiovascular System I: Cardiac Biomarkers01:20

Blood Studies for Cardiovascular System I: Cardiac Biomarkers

Cardiac biomarkers are enzymes, proteins, and hormones released into the blood when cardiac cells are injured. They are powerful tools for triaging.
The essential diagnostic tools for detecting myocardial necrosis and monitoring individuals suspected of having acute coronary syndrome (ACS) include:
Troponins
Troponins, particularly cardiac troponins I and T, are the most precise and sensitive markers of myocardial injury. They are detectable within 4-6 hours of myocardial injury and remain...
1.2K
Inflammatory Response II: Inflammatory Exudate and Tissue Repair01:24

Inflammatory Response II: Inflammatory Exudate and Tissue Repair

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...
9.8K