SEPSIGN: early identification of sepsis signs in emergency department
Because 20-30% of patients with sepsis deteriorate to critical illness, biomarkers that provide accurate early prognosis may identify which patients need more intensive treatment versus safe early discharge. The objective was to test the performance of sVEGFR2, suPAR and PCT, alone or combined with...
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creator | Lafon, Thomas Cazalis, Marie-Angélique Hart, Kimberly W Hennessy, Cassandra Tazarourte, Karim Self, Wesley H Akhavan, Arvin Radfar Laribi, Saïd Viglino, Damien Douplat, Marion Ginde, Adit A Tolou, Sophie Mahler, Simon A Le Borgne, Pierrick Claessens, Yann-Erick Yordanov, Youri Le Bastard, Quentin Pancher, Agathe Ducharme, Jim Lindsell, Christopher J Shapiro, Nathan I |
description | Because 20-30% of patients with sepsis deteriorate to critical illness, biomarkers that provide accurate early prognosis may identify which patients need more intensive treatment versus safe early discharge. The objective was to test the performance of sVEGFR2, suPAR and PCT, alone or combined with clinical signs and symptoms, for the prediction of clinical deterioration. This prospective observational study enrolled patients with suspected infection who met SIRS criteria without organ dysfunction (delta SOFA |
doi_str_mv | 10.1007/s11739-024-03802-5 |
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The objective was to test the performance of sVEGFR2, suPAR and PCT, alone or combined with clinical signs and symptoms, for the prediction of clinical deterioration. This prospective observational study enrolled patients with suspected infection who met SIRS criteria without organ dysfunction (delta SOFA <2 from baseline) from 16 emergency departments. The primary endpoint was clinical deterioration (increased SOFA score ≥2 points, new or increased organ support, or death) within 72 hours of enrollment. Diagnosis and classification of infection status were adjudicated. 724 patients were enrolled, (54% men, median age 55 [38-70] y-o). Infection origin was abdominopelvic (21%), skin and soft tissues (17%), urinary (16%) and pulmonary (15%). 176 (24%) patients deteriorated, with a 28-day mortality of 1.4%. They had lower sVEGFR2 level (6.17 [5.00-7.40] vs 6.52 [5.40-7.84], p=0.024), higher circulating suPAR (5.25 [3.86-7.50] vs 4.18 [3.16-5.68], p<0.001) and higher PCT level (0.32 [0.08-1.80] vs 0.18 [0.05-0.98], p=0.004). suPAR demonstrated superior performance (AUC=0.65 [0.60-0.70]), compared to other biomarkers (PCT, AUC=0.57 [0.52-0.62] and sVEGFR2, AUC=0.58 [0.53-0.64]). Maximum accuracy was achieved from the combination of clinical information, sVEGFR2 and suPAR, yielding an AUC of 0.74 [0.69-0.78] and NPV 0.90 [0.88-0.94]. sVEGFR2 and suPAR were insufficiently accurate to rule out clinical deterioration. Panels of biomarkers will likely be needed to capture the heterogeneous mechanistic pathways involved in sepsis-related organ failure.</description><identifier>ISSN: 1828-0447</identifier><identifier>ISSN: 1970-9366</identifier><identifier>EISSN: 1970-9366</identifier><identifier>DOI: 10.1007/s11739-024-03802-5</identifier><identifier>PMID: 39477836</identifier><language>eng</language><publisher>Italy: Springer</publisher><subject>Life Sciences</subject><ispartof>Internal and emergency medicine, 2024-10</ispartof><rights>2024. The Author(s), under exclusive licence to Società Italiana di Medicina Interna (SIMI).</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c218t-1271b59a028b01a01b2bfd3b6343212c36760a481b16452ebd7a8ef658b0d65e3</cites><orcidid>0000-0003-4424-8107 ; 0000-0001-6930-0720</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39477836$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-04794066$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Lafon, Thomas</creatorcontrib><creatorcontrib>Cazalis, Marie-Angélique</creatorcontrib><creatorcontrib>Hart, Kimberly W</creatorcontrib><creatorcontrib>Hennessy, Cassandra</creatorcontrib><creatorcontrib>Tazarourte, Karim</creatorcontrib><creatorcontrib>Self, Wesley H</creatorcontrib><creatorcontrib>Akhavan, Arvin Radfar</creatorcontrib><creatorcontrib>Laribi, Saïd</creatorcontrib><creatorcontrib>Viglino, Damien</creatorcontrib><creatorcontrib>Douplat, Marion</creatorcontrib><creatorcontrib>Ginde, Adit A</creatorcontrib><creatorcontrib>Tolou, Sophie</creatorcontrib><creatorcontrib>Mahler, Simon A</creatorcontrib><creatorcontrib>Le Borgne, Pierrick</creatorcontrib><creatorcontrib>Claessens, Yann-Erick</creatorcontrib><creatorcontrib>Yordanov, Youri</creatorcontrib><creatorcontrib>Le Bastard, Quentin</creatorcontrib><creatorcontrib>Pancher, Agathe</creatorcontrib><creatorcontrib>Ducharme, Jim</creatorcontrib><creatorcontrib>Lindsell, Christopher J</creatorcontrib><creatorcontrib>Shapiro, Nathan I</creatorcontrib><title>SEPSIGN: early identification of sepsis signs in emergency department</title><title>Internal and emergency medicine</title><addtitle>Intern Emerg Med</addtitle><description>Because 20-30% of patients with sepsis deteriorate to critical illness, biomarkers that provide accurate early prognosis may identify which patients need more intensive treatment versus safe early discharge. The objective was to test the performance of sVEGFR2, suPAR and PCT, alone or combined with clinical signs and symptoms, for the prediction of clinical deterioration. This prospective observational study enrolled patients with suspected infection who met SIRS criteria without organ dysfunction (delta SOFA <2 from baseline) from 16 emergency departments. The primary endpoint was clinical deterioration (increased SOFA score ≥2 points, new or increased organ support, or death) within 72 hours of enrollment. Diagnosis and classification of infection status were adjudicated. 724 patients were enrolled, (54% men, median age 55 [38-70] y-o). Infection origin was abdominopelvic (21%), skin and soft tissues (17%), urinary (16%) and pulmonary (15%). 176 (24%) patients deteriorated, with a 28-day mortality of 1.4%. They had lower sVEGFR2 level (6.17 [5.00-7.40] vs 6.52 [5.40-7.84], p=0.024), higher circulating suPAR (5.25 [3.86-7.50] vs 4.18 [3.16-5.68], p<0.001) and higher PCT level (0.32 [0.08-1.80] vs 0.18 [0.05-0.98], p=0.004). suPAR demonstrated superior performance (AUC=0.65 [0.60-0.70]), compared to other biomarkers (PCT, AUC=0.57 [0.52-0.62] and sVEGFR2, AUC=0.58 [0.53-0.64]). Maximum accuracy was achieved from the combination of clinical information, sVEGFR2 and suPAR, yielding an AUC of 0.74 [0.69-0.78] and NPV 0.90 [0.88-0.94]. sVEGFR2 and suPAR were insufficiently accurate to rule out clinical deterioration. 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The objective was to test the performance of sVEGFR2, suPAR and PCT, alone or combined with clinical signs and symptoms, for the prediction of clinical deterioration. This prospective observational study enrolled patients with suspected infection who met SIRS criteria without organ dysfunction (delta SOFA <2 from baseline) from 16 emergency departments. The primary endpoint was clinical deterioration (increased SOFA score ≥2 points, new or increased organ support, or death) within 72 hours of enrollment. Diagnosis and classification of infection status were adjudicated. 724 patients were enrolled, (54% men, median age 55 [38-70] y-o). Infection origin was abdominopelvic (21%), skin and soft tissues (17%), urinary (16%) and pulmonary (15%). 176 (24%) patients deteriorated, with a 28-day mortality of 1.4%. They had lower sVEGFR2 level (6.17 [5.00-7.40] vs 6.52 [5.40-7.84], p=0.024), higher circulating suPAR (5.25 [3.86-7.50] vs 4.18 [3.16-5.68], p<0.001) and higher PCT level (0.32 [0.08-1.80] vs 0.18 [0.05-0.98], p=0.004). suPAR demonstrated superior performance (AUC=0.65 [0.60-0.70]), compared to other biomarkers (PCT, AUC=0.57 [0.52-0.62] and sVEGFR2, AUC=0.58 [0.53-0.64]). Maximum accuracy was achieved from the combination of clinical information, sVEGFR2 and suPAR, yielding an AUC of 0.74 [0.69-0.78] and NPV 0.90 [0.88-0.94]. sVEGFR2 and suPAR were insufficiently accurate to rule out clinical deterioration. Panels of biomarkers will likely be needed to capture the heterogeneous mechanistic pathways involved in sepsis-related organ failure.</abstract><cop>Italy</cop><pub>Springer</pub><pmid>39477836</pmid><doi>10.1007/s11739-024-03802-5</doi><orcidid>https://orcid.org/0000-0003-4424-8107</orcidid><orcidid>https://orcid.org/0000-0001-6930-0720</orcidid></addata></record> |
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title | SEPSIGN: early identification of sepsis signs in emergency department |
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