PO21 | Exploring endothelial damage: the interplay between coagulopathy, capillary leak and vasoplegia in sepsis

M. Facci¹, G. Turcato¹, A. Zaboli², L. Filippi¹, P. Ferretto¹, M. Maggi¹, F. Lucente¹, D. Milazzo¹, A. Bresolin¹, M. Marchetti¹ | ¹UOC Medicina Generale, Ospedale Alto Vicentino, Santorso, (VI); ²Innovation, Research and Teaching Service “SABES-ASDAA” of Azienda Sanitaria dell’Alto Adige, Italy

Background: Sepsis-Induced Coagulopathy (SIC) is a severe complication characterized by alterations in hemostasis, associated with increased mortality. Endothelial damage, triggered by cytokine storm, plays a crucial role in SIC. Endothelial damage is also known to cause increased capillary permeability and vasoplegia. The interconnection between these phenomena remains clinically unexplored. Aim: To evaluate the clinical relationship between tissue permeability alteration, coagulopathy, and vasoplegia caused by sepsis-induced endothelial damage.

Methods: A prospective single-center study conducted on 75 patients with community-acquired sepsis admitted to the Intermediate Care Unit. The following were analyzed: SIC score (according to ISTH criteria), serum albumin (a surrogate for capillary leak), Total Peripheral Resistance Index (TPRI) (a surrogate for vasoplegia), obtained through NICaS hemodynamic monitoring. Structural Equation Modeling (SEM) was performed to explore the relationship between variables, hypothesizing a common latent factor (endothelial damage). Principal Component Analysis (PCA) was used to assess the presence of a common component among variables explaining their variance.

Results: The mean SIC score was 3.4 (SD 1.3), with 44% of patients affected by SIC. TPRI and albumin showed mean values of 1954 (SD 738) and 2.58 (SD 0.59), respectively, both negatively correlated with SIC: TPRI -0.263 (p=0.023) and albumin -0.454 (p<0.001). SEM revealed that SIC, albumin, and TPRI are associated with a latent factor (endothelial damage), which explains 68% of the variance. The model showed excellent fit (CFI=1.000, RMSEA=0.000) with SIC as the reference variable, albumin inversely correlated with the latent factor (p=0.004) and TPRI significantly associated (p=0.003). PCA identified three principal components explaining the variance: albumin (58.95% of variance, loading=0.606), representing metabolic state; SIC (23.24% of variance, loading=-0.590), representing coagulation state; TPRI (17.81% of variance, loading=0.534), representing hemodynamic state.

Conclusions: SEM and PCA highlight interconnections among permeability, coagulation, and hemodynamics, hypothesizing endothelial damage as a common factor.