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  • 1
    In: Acta Anaesthesiologica Scandinavica, Wiley, Vol. 65, No. 4 ( 2021-04), p. 551-557
    Kurzfassung: Traumatic injury accounts for 800 000 deaths in the European Union annually. The main causes of deaths in trauma patients are exsanguination and multiple organ failure (MOF). We have studied 〉 1000 trauma patients and identified shock‐induced endotheliopathy (SHINE), the pathophysiological mechanism responsible for MOF and high mortality. Pilot studies indicate that low‐dose iloprost (1 ng/kg/min) improves endothelial functionality in critically ill patients suggesting this intervention may improve patient outcome in traumatic SHINE. Material and Methods This is a multicentre, randomized, blinded clinical investigator‐initiated phase 2B trial in trauma patients with haemorrhagic shock‐induced endotheliopathy. Patients are randomized 1:1 to 72 hours infusion of iloprost 1 ng/kg/min or Placebo (equal volume of saline). A total of 220 trauma patients will be included. The primary endpoint is the number of intensive care unit (ICU)‐free days, within 28 days of admission. Secondary endpoints include 28‐ and 90‐day all‐cause mortality, hospital length of stay, vasopressor‐free days in the intensive care unit (ICU) within 28 days, ventilator‐free days in the ICU within 28 days, renal replacement‐free days in the ICU within 28 days, number of serious adverse reactions and serious adverse events within the first 4 days of admission. Discussion This trial will test the safety and efficacy of administration of iloprost vs placebo for 72 hours in trauma patients with haemorrhagic shock‐induced endotheliopathy. Trial endpoints focus on the potential effect of iloprost to reduce the need for ICU stay secondary to mitigation of organ failure. Trial registration SHINE‐TRAUMA trial—EudraCT no. 2019‐000936‐24—Clinicaltrials.gov: NCT03903939 Ethics Committee no. H‐19014482.
    Materialart: Online-Ressource
    ISSN: 0001-5172 , 1399-6576
    URL: Issue
    RVK:
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2021
    ZDB Id: 2004319-3
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    In: Journal of Trauma and Acute Care Surgery, Ovid Technologies (Wolters Kluwer Health), Vol. 96, No. 3 ( 2024-3), p. 476-481
    Kurzfassung: A main cause of trauma morbidity and mortality is multiple-organ failure, and endotheliopathy has been implicated. Pilot studies indicate that low-dose prostacyclin improves endothelial functionality in critically ill patients, suggesting that this intervention may improve trauma patient outcome. METHODS We conducted a multicenter, randomized, blinded, clinical investigator-initiated trial in 229 trauma patients with hemorrhagic shock who were randomized 1:1 to 72 hours infusion of the prostacyclin analog iloprost (1 ng/kg/min) or placebo. The primary outcome was the number of intensive care unit (ICU)–free days alive within 28 days of admission. Secondary outcomes included 28-day all-cause mortality and hospital length of stay. RESULTS The mean number of ICU-free days alive within 28 days was 15.64 days in the iloprost group versus 13.99 days in the placebo group (adjusted mean difference, −1.63 days [95% confidence interval (CI), −4.64 to 1.38 days]; p = 0.28). The 28-day mortality was 18.8% in the iloprost group versus 19.6% in the placebo group (odds ratio, 1.01 [95% CI, 0.51–2.0]; p = 0.97). The mean hospital length of stay was 19.96 days in the iloprost group versus 27.32 days in the placebo group (adjusted mean difference, 7.84 days [95% CI, 1.66–14.02 days], p = 0.01). CONCLUSION Iloprost did not result in a statistically significant increase in the number of ICU-free days alive within 28 days of admission, whereas it was safe and a statistically significant reduction in hospital length of stay was observed. Further research on prostacyclin in shocked trauma patients is warranted. LEVEL OF EVIDENCE Therapeutic/Care Management; Level II.
    Materialart: Online-Ressource
    ISSN: 2163-0763 , 2163-0755
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2024
    ZDB Id: 2651313-4
    Standort Signatur Einschränkungen Verfügbarkeit
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