TY - JOUR
T1 - The Host Response in Patients with Sepsis Developing Intensive Care Unit-acquired Secondary Infections
AU - van Vught, Lonneke A.
AU - Wiewel, Maryse A.
AU - Hoogendijk, Arie J.
AU - Frencken, Jos F.
AU - Scicluna, Brendon P.
AU - Klein Klouwenberg, Peter M. C.
AU - Zwinderman, Aeilko H.
AU - Lutter, Rene
AU - Horn, Janneke
AU - Schultz, Marcus J.
AU - Bonten, Marc M. J.
AU - Cremer, Olaf L.
AU - van der Poll, Tom
PY - 2017
Y1 - 2017
N2 - Rationale: Sepsis can be complicated by secondary infections. We explored the possibility that patients with sepsis developing a secondary infection while in the intensive care unit (ICU) display sustained inflammatory, vascular, and procoagulant responses. Objectives: To compare systemic proinflammatory host responses in patients with sepsis who acquire a new infection with those who do not. Methods: Consecutive patients with sepsis with a length of ICU stay greater than 48 hours were prospectively analyzed for the development of ICU-acquired infections. Twenty host response biomarkers reflective of key pathways implicated in sepsis pathogenesis were measured during the first 4 days after ICU admission and at the day of an ICU-acquired infection or noninfectious complication. Measureinents and Main Results: Of 1,237 admissions for sepsis (1,089 patients), 178 (14.4%) admissions were complicated by ICU-acquired infections (at Day 10 [6-13]; median with interquartile range). Patients who developed a secondary infection showed higher disease severity scores and higher mortality up to 1 year than those who did not. Analyses of biomarkers in patients who later went on to develop secondary infections revealed a more dysregulated host response during the first 4 days after admission, as reflected by enhanced inflammation, stronger endothelial cell activation, a more disturbed vascular integrity, and evidence for enhanced coagulation activation. Host response reactions were similar at the time of ICU-acquired infectious or noninfectious complications. Conclusions: Patients with sepsis who developed an ICU-acquired infection showed a more dysregulated proinflammatory, and vascular host response during the first 4 days of ICU admission than those who did not develop a secondary infection
AB - Rationale: Sepsis can be complicated by secondary infections. We explored the possibility that patients with sepsis developing a secondary infection while in the intensive care unit (ICU) display sustained inflammatory, vascular, and procoagulant responses. Objectives: To compare systemic proinflammatory host responses in patients with sepsis who acquire a new infection with those who do not. Methods: Consecutive patients with sepsis with a length of ICU stay greater than 48 hours were prospectively analyzed for the development of ICU-acquired infections. Twenty host response biomarkers reflective of key pathways implicated in sepsis pathogenesis were measured during the first 4 days after ICU admission and at the day of an ICU-acquired infection or noninfectious complication. Measureinents and Main Results: Of 1,237 admissions for sepsis (1,089 patients), 178 (14.4%) admissions were complicated by ICU-acquired infections (at Day 10 [6-13]; median with interquartile range). Patients who developed a secondary infection showed higher disease severity scores and higher mortality up to 1 year than those who did not. Analyses of biomarkers in patients who later went on to develop secondary infections revealed a more dysregulated host response during the first 4 days after admission, as reflected by enhanced inflammation, stronger endothelial cell activation, a more disturbed vascular integrity, and evidence for enhanced coagulation activation. Host response reactions were similar at the time of ICU-acquired infectious or noninfectious complications. Conclusions: Patients with sepsis who developed an ICU-acquired infection showed a more dysregulated proinflammatory, and vascular host response during the first 4 days of ICU admission than those who did not develop a secondary infection
U2 - https://doi.org/10.1164/rccm.201606-1225OC
DO - https://doi.org/10.1164/rccm.201606-1225OC
M3 - Article
C2 - 28107024
SN - 1073-449X
VL - 196
SP - 458
EP - 470
JO - American journal of respiratory and critical care medicine
JF - American journal of respiratory and critical care medicine
IS - 4
ER -