Abstract
BackgroundPlatelets have been involved in both immune surveillance and host defense against severe infection. To date, whether platelet phenotype or other hemostasis components could be associated with predisposition to sepsis in critical illness remains unknown. The aim of this work was to identify platelet markers that could predict sepsis occurrence in critically ill injured patients.MethodsThis single-center, prospective, observational, 7-month study was based on a cohort of 99 non-infected adult patients admitted to ICUs for elective cardiac surgery, trauma, acute brain injury, and post-operative prolonged ventilation and followed up during ICU stay. Clinical characteristics and severity score (SOFA) were recorded on admission. Platelet activation markers, including fibrinogen binding to platelets, platelet membrane P-selectin expression, plasma soluble CD40L, and platelet-leukocytes aggregates were assayed by flow cytometry at admission and 48 h later, and then at the time of sepsis diagnosis (Sepsis-3 criteria) and 7 days later for sepsis patients. Hospitalization data and outcomes were also recorded.MethodsOf the 99 patients, 19 developed sepsis after a median time of 5 days. These patients had a higher SOFA score at admission; levels of fibrinogen binding to platelets (platelet-Fg) and of D-dimers were also significantly increased compared to the other patients. Levels 48 h after ICU admission no longer differed between the two patient groups. Platelet-Fg % was an independent predictor of sepsis (P = 0.0031). By ROC curve analysis, cutoff point for Platelet-Fg (AUC = 0.75) was 50%. In patients with a SOFA cutoff of 8, the risk of sepsis reached 87% when Platelet-Fg levels were above 50%. Patients with sepsis had longer ICU and hospital stays and higher death rate.ConclusionsPlatelet-bound fibrinogen levels assayed by flow cytometry within 24 h of ICU admission help identifying critically ill patients at risk of developing sepsis.
Highlights
Platelets have been involved in both immune surveillance and host defense against severe infection
It has been shown that activated platelets facilitate the clearance of adherent Streptococci in experimental infective endocarditis [12]; β-defensins released from platelets activated by the Staphylococcus aureus α-toxin impair bacterial growth and induce neutrophil extracellular trap formation [13]
The major findings of this study concern the clear relationship between patient levels of fibrinogen binding to circulating platelets measured upon intensive care unit (ICU) admission and sepsis occurrence, regardless of the patient’s baseline clinical characteristics
Summary
Platelets have been involved in both immune surveillance and host defense against severe infection. The Third International Consensus Task Force (Sepsis-3) defines sepsis as a “life-threatening organ dysfunction caused by a dysregulated host response to infection”. In this concept, growing experimental and preclinical evidence indicates that platelets could play an active role either in immune surveillance or in the response to infection. Platelets may contain infection both directly and through functional interactions with immune cells [8]. Platelets express CD40L, an essential player in host defense against infection that mediates interactions between platelets, antigenpresenting cells, and lymphocytes [15]
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