Resuscitation-associated endotheliopathy (RAsE): a conceptual framework based on a systematic review and meta-analysis.

Autor: Obonyo NG; Critical Care Research Group, The Prince Charles Hospital, Brisbane, Australia. g.obonyo@uq.edu.au.; Faculty of Medicine, The University of Queensland, Brisbane, Australia. g.obonyo@uq.edu.au.; Initiative to Develop African Research Leaders (IDeAL), Kilifi, Kenya. g.obonyo@uq.edu.au.; KEMRI-Wellcome Trust Research Programme, Kilifi, Kenya. g.obonyo@uq.edu.au.; Wellcome Trust Centre for Global Health Research, Imperial College London, London, UK. g.obonyo@uq.edu.au.; Institute of Molecular Bioscience, The University of Queensland, Brisbane, Australia. g.obonyo@uq.edu.au., Sela DP; Critical Care Research Group, The Prince Charles Hospital, Brisbane, Australia.; Faculty of Medicine, The University of Queensland, Brisbane, Australia.; Institute of Molecular Bioscience, The University of Queensland, Brisbane, Australia., Raman S; Critical Care Research Group, The Prince Charles Hospital, Brisbane, Australia.; Faculty of Medicine, The University of Queensland, Brisbane, Australia.; Child Health Research Centre, The University of Queensland, Brisbane, QLD, Australia.; Paediatric Intensive Care Unit, Queensland Children's Hospital, South Brisbane, QLD, Australia., Rachakonda R; Critical Care Research Group, The Prince Charles Hospital, Brisbane, Australia.; Faculty of Medicine, The University of Queensland, Brisbane, Australia., Schneider B; Critical Care Research Group, The Prince Charles Hospital, Brisbane, Australia.; Faculty of Medicine, The University of Queensland, Brisbane, Australia., Hoe LES; Critical Care Research Group, The Prince Charles Hospital, Brisbane, Australia.; Faculty of Medicine, The University of Queensland, Brisbane, Australia., Fanning JP; Critical Care Research Group, The Prince Charles Hospital, Brisbane, Australia.; Faculty of Medicine, The University of Queensland, Brisbane, Australia.; Division of Cardiac Surgery, Department of Surgery, Johns Hopkins School of Medicine, Baltimore, MD, USA.; Nuffield Department of Population Health, University of Oxford, Oxford, UK.; Intensive Care Unit, St. Andrews War Memorial Hospital, Brisbane, QLD, Australia., Bassi GL; Critical Care Research Group, The Prince Charles Hospital, Brisbane, Australia.; Faculty of Medicine, The University of Queensland, Brisbane, Australia.; Institute of Molecular Bioscience, The University of Queensland, Brisbane, Australia.; Intensive Care Unit, St. Andrews War Memorial Hospital, Brisbane, QLD, Australia., Maitland K; KEMRI-Wellcome Trust Research Programme, Kilifi, Kenya.; Imperial College London, London, UK., Suen JY; Critical Care Research Group, The Prince Charles Hospital, Brisbane, Australia.; Faculty of Medicine, The University of Queensland, Brisbane, Australia.; Institute of Molecular Bioscience, The University of Queensland, Brisbane, Australia., Fraser JF; Critical Care Research Group, The Prince Charles Hospital, Brisbane, Australia.; Faculty of Medicine, The University of Queensland, Brisbane, Australia.; Institute of Molecular Bioscience, The University of Queensland, Brisbane, Australia.; Intensive Care Unit, St. Andrews War Memorial Hospital, Brisbane, QLD, Australia.
Jazyk: angličtina
Zdroj: Systematic reviews [Syst Rev] 2023 Nov 22; Vol. 12 (1), pp. 221. Date of Electronic Publication: 2023 Nov 22.
DOI: 10.1186/s13643-023-02385-0
Abstrakt: Introduction: Shock-induced endotheliopathy (SHINE), defined as a profound sympathoadrenal hyperactivation in shock states leading to endothelial activation, glycocalyx damage, and eventual compromise of end-organ perfusion, was first described in 2017. The aggressive resuscitation therapies utilised in treating shock states could potentially lead to further worsening endothelial activation and end-organ dysfunction.
Objective: This study aimed to systematically review the literature on resuscitation-associated and resuscitation-induced endotheliopathy.
Methods: A predetermined structured search of literature published over an 11-year and 6-month period (1 January 2011 to 31 July 2023) was performed in two indexed databases (PubMed/MEDLINE and Embase) per PRISMA guidelines. Inclusion was restricted to original studies published in English (or with English translation) reporting on endothelial dysfunction in critically ill human subjects undergoing resuscitation interventions. Reviews or studies conducted in animals were excluded. Qualitative synthesis of studies meeting the inclusion criteria was performed. Studies reporting comparable biomarkers of endothelial dysfunction post-resuscitation were included in the quantitative meta-analysis.
Results: Thirty-two studies met the inclusion criteria and were included in the final qualitative synthesis. Most of these studies (47%) reported on a combination of mediators released from endothelial cells and biomarkers of glycocalyx breakdown, while only 22% reported on microvascular flow changes. Only ten individual studies were included in the quantitative meta-analysis based on the comparability of the parameters assessed. Eight studies measured syndecan-1, with a heterogeneity index, I 2  = 75.85% (pooled effect size, mean = 0.27; 95% CI - 0.07 to 0.60; p = 0.12). Thrombomodulin was measured in four comparable studies (I 2  = 78.93%; mean = 0.41; 95% CI - 0.10 to 0.92; p = 0.12). Three studies measured E-selectin (I 2  = 50.29%; mean =  - 0.15; 95% CI - 0.64 to 0.33; p = 0.53), and only two were comparable for the microvascular flow index, MFI (I 2  = 0%; mean =  - 0.80; 95% CI - 1.35 to - 0.26; p < 0.01).
Conclusion: Resuscitation-associated endotheliopathy (RAsE) refers to worsening endothelial dysfunction resulting from acute resuscitative therapies administered in shock states. In the included studies, syndecan-1 had the highest frequency of assessment in the post-resuscitation period, and changes in concentrations showed a statistically significant effect of the resuscitation. There are inadequate data available in this area, and further research and standardisation of the ideal assessment and panel of biomarkers are urgently needed.
(© 2023. The Author(s).)
Databáze: MEDLINE
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