Literature DB >> 34905531

Shock-Induced Endothelial Dysfunction is Present in Patients With Occult Hypoperfusion After Trauma.

Heather R Kregel1,2,3, Gabrielle E Hatton1,2,3, Kayla D Isbell1,2,3, Hanne H Henriksen4, Jakob Stensballe4,5, Per I Johansson4, Lillian S Kao1,2,3, Charles E Wade1,3.   

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.

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Year:  2022        PMID: 34905531      PMCID: PMC9148678          DOI: 10.1097/SHK.0000000000001866

Source DB:  PubMed          Journal:  Shock        ISSN: 1073-2322            Impact factor:   3.533


  37 in total

1.  Endotheliopathy of Trauma is an on-Scene Phenomenon, and is Associated with Multiple Organ Dysfunction Syndrome: A Prospective Observational Study.

Authors:  David N Naumann; Jon Hazeldine; David J Davies; Jon Bishop; Mark J Midwinter; Antonio Belli; Paul Harrison; Janet M Lord
Journal:  Shock       Date:  2018-04       Impact factor: 3.454

2.  Sympathoadrenal activation and endotheliopathy are drivers of hypocoagulability and hyperfibrinolysis in trauma: A prospective observational study of 404 severely injured patients.

Authors:  Sisse R Ostrowski; Hanne H Henriksen; Jakob Stensballe; Mikkel Gybel-Brask; Jessica C Cardenas; Lisa A Baer; Bryan A Cotton; John B Holcomb; Charles E Wade; Pär I Johansson
Journal:  J Trauma Acute Care Surg       Date:  2017-02       Impact factor: 3.313

Review 3.  Optimal trauma resuscitation with plasma as the primary resuscitative fluid: the surgeon's perspective.

Authors:  John B Holcomb; Shibani Pati
Journal:  Hematology Am Soc Hematol Educ Program       Date:  2013

Review 4.  Effectiveness of prehospital trauma triage systems in selecting severely injured patients: Is comparative analysis possible?

Authors:  Eveline A J van Rein; Rogier van der Sluijs; R Marijn Houwert; Amy C Gunning; Rob A Lichtveld; Luke P H Leenen; Mark van Heijl
Journal:  Am J Emerg Med       Date:  2018-02-01       Impact factor: 2.469

5.  The protective role of estrogen on endothelial and glycocalyx barriers after shock conditions: A microfluidic study.

Authors:  Lawrence N Diebel; Madison Wheaton; David M Liberati
Journal:  Surgery       Date:  2020-09-25       Impact factor: 3.982

6.  Modulating the endotheliopathy of trauma: Factor concentrate versus fresh frozen plasma.

Authors:  Shibani Pati; Daniel R Potter; Gyulnar Baimukanova; David H Farrel; John B Holcomb; Martin A Schreiber
Journal:  J Trauma Acute Care Surg       Date:  2016-04       Impact factor: 3.313

7.  Hypotension begins at 110 mm Hg: redefining "hypotension" with data.

Authors:  Brian J Eastridge; Jose Salinas; John G McManus; Lorne Blackburn; Eileen M Bugler; William H Cooke; Victor A Convertino; Victor A Concertino; Charles E Wade; John B Holcomb
Journal:  J Trauma       Date:  2007-08

8.  Antithrombin III Contributes to the Protective Effects of Fresh Frozen Plasma Following Hemorrhagic Shock by Preventing Syndecan-1 Shedding and Endothelial Barrier Disruption.

Authors:  Ernesto Lopez; Zhanglong Peng; Rosemary A Kozar; Yanna Cao; Tien C Ko; Charles E Wade; Jessica C Cardenas
Journal:  Shock       Date:  2020-02       Impact factor: 3.454

9.  Sympathoadrenal activation and endothelial damage are inter correlated and predict increased mortality in patients resuscitated after out-of-hospital cardiac arrest. a post Hoc sub-study of patients from the TTM-trial.

Authors:  Pär I Johansson; John Bro-Jeppesen; Jesper Kjaergaard; Michael Wanscher; Christian Hassager; Sisse R Ostrowski
Journal:  PLoS One       Date:  2015-03-19       Impact factor: 3.240

10.  Traumatic Endotheliopathy: A Prospective Observational Study of 424 Severely Injured Patients.

Authors:  Pär I Johansson; Hanne H Henriksen; Jakob Stensballe; Mikkel Gybel-Brask; Jessica C Cardenas; Lisa A Baer; Bryan A Cotton; John B Holcomb; Charles E Wade; Sisse R Ostrowski
Journal:  Ann Surg       Date:  2017-03       Impact factor: 12.969

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