Shock-Induced Endothelial Dysfunction is Present in Patients With Occult Hypoperfusion After Trauma
- PMID: 34905531
- PMCID: PMC9148678
- DOI: 10.1097/SHK.0000000000001866
Shock-Induced Endothelial Dysfunction is Present in Patients With Occult Hypoperfusion After Trauma
Abstract
Background: Shock-induced endothelial dysfunction, evidenced by elevated soluble thrombomodulin (sTM) and syndecan-1 (Syn-1), is associated with poor outcomes after trauma. The association of endothelial dysfunction and overt shock has been demonstrated; it is unknown if hypoperfusion in the setting of normal vital signs (occult hypoperfusion [OH]) is associated with endothelial dysfunction. We hypothesized that sTM and Syn-1 would be elevated in patients with OH when compared to patients with normal perfusion.
Methods: A single-center study of patients requiring highest-level trauma activation (2012-2016) was performed. Trauma bay arrival plasma Syn-1 and sTM were measured by enzyme-linked immunosorbent assay. Shock was defined as systolic blood pressure (SBP) <90 mm Hg or heart rate (HR) ≥120 bpm. OH was defined as SBP ≥ 90, HR < 120, and base excess (BE) ≤-3. Normal perfusion was assigned to all others. Univariate and multivariable analyses were performed.
Results: Of 520 patients, 35% presented with OH and 26% with shock. Demographics were similar between groups. Patients with normal perfusion had the lowest Syn-1 and sTM, while patients with OH and shock had elevated levels. OH was associated with increased sTM by 0.97 ng/mL (95% CI 0.39-1.57, p = 0.001) and Syn-1 by 14.3 ng/mL (95% CI -1.5 to 30.2, p = 0.08). Furthermore, shock was associated with increased sTM by 0.64 (95% CI 0.02-1.30, p = 0.04) and with increased Syn-1 by 23.6 ng/mL (95% CI 6.2-41.1, p = 0.008).
Conclusions: Arrival OH was associated with elevated sTM and Syn-1, indicating endothelial dysfunction. Treatments aiming to stabilize the endothelium may be beneficial for injured patients with evidence of hypoperfusion, regardless of vital signs.
Copyright © 2021 by the Shock Society.
Conflict of interest statement
CEW receives funding from the William Stamps Farish Fund, the Howell Family Foundation, and the James H. “Red” Duke Professorship. GEH and HRK are supported by the National Institute of General Medical Sciences of the National Institutes of Health [5T32GM008792]. All others have no potential conflicts of interest to report.
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- Halbgebauer R, Braun CK, Denk S, Mayer B, Cinelli P, Radermacher P, Wanner GA, Simmen HP, Gebhard F, Rittirsch D, Huber-Lang M: Hemorrhagic shock drives glycocalyx, barrier and organ dysfunction early after polytrauma. J Crit Care 44:229–237, 2018. - PubMed
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