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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Sepsis is a heterogeneous clinical syndrome with distinct phenotypes that influence prognosis and therapeutic response. Molecular profiling using accessible biomarkers enables personalized interventions. Five principal phenotypes have been identified: Immunoparalysis, Endothelial activity, Hepatobiliary dysfunction, Macrophage Activation Syndrome (MAS), and Mixed. Additionally, five dynamic subtypes of endothelial activity are recognized: TTP-like, HUS, SIC, Fibrinolytic, and Thrombotic. This case series illustrates how biomarker-guided stratification informs extracorporeal therapies, transitioning from empirical care to precision medicine.
Phenotypic classification followed a two-phase approach. First, patients were stratified by risk using SOFA score and Severity Criteria biochemical markers. This allowed classification into low, moderate, and high-risk groups (Figure 1). Second, sepsis phenotypes were defined based on accessible biomarkers. Interventions such as immunostimulation, anticoagulation, extracorporeal support, and cytokine modulation were guided by the identified profile (Figure 2). To demonstrate this approach, we present three representative cases with distinct phenotypes (Figure 3).
Case 1: A 70-year-old woman with septic shock due to intestinal perforation showed a mixed endothelial-hepatobiliary phenotype. She evolved from an initial thrombotic state to terminal SIC (sepsis-induced coagulopathy) and liver failure, resulting in death despite extracorporeal support.
Case 2: A 45-year-old man with H1N1 pneumonia and rhabdomyolysis developed an endothelial-thrombotic phenotype with extreme hyperfibrinogenemia and hyperviscosity. He underwent therapeutic plasma exchange with marked improvement and full recovery.
Case 3: A 49-year-old woman with extensive burns and respiratory sepsis had coexisting immunoparalysis and thrombotic endothelial activity. Managed conservatively, she recovered fully without extracorporeal interventions.
Case 1: This temporal evolution was directly related to inadequate abdominal focus control, demonstrating that persistent infectious sources drive continuous phenotype progression and determine therapeutic refractoriness. The failure to achieve optimal source control resulted in sustained inflammatory stimulation, perpetuating the coagulation cascade activation and ultimately leading to consumptive coagulopathy.
Case 2: Therapeutic plasma exchange achieved immediate mechanical removal of 90% of pathological fibrinogen, elimination of circulating inflammatory mediators, and replacement of natural anticoagulants. This targeted approach effectively reversed the thrombotic endothelial phenotype, allowing for rapid stabilization.
Case 3: Immunoparalysis acts as a protective mechanism against cytokine storm and severe multiorgan damage, while the prothrombotic state remains at controlled levels that do not require extracorporeal intervention.
The sepsis phenotype model represents a significant advance toward personalized medicine in critical care. Classification of the 5 sepsis phenotypes enables:
· Precise differential diagnosis of coagulopathies
· Phenotype-specific targeted therapies
· Improved prognostic stratification
· Personalized molecular monitoring
· Reduced sepsis mortality
