The Glycocalyx Shedding Influences Hemodynamic and Metabolic Response to Fluid Load in Septic Shock

Sepsis-associated endothelial dysfunction and degradation result in release of inflammatory mediators, compromise endothelial permeability, and impair alveolar fluid clearance leading to pulmonary edema. Excessive fluid therapy in septic shock damage the endothelial glycocalyx which will increase capillary leakage. The aim of our study was to assess the relationship of endothelial glycocalyx shedding with hemodynamic and metabolic response to fluid load in patients with septic shock.

Eighteen adult patients were included in prospective observational study. To predict the response to infusion, we performed fluid load test by using crystalloids 7 mL kg-1 for 10 minutes. The plasma concentrations of endothelial glycocalyx components including heparan sulfate proteoglycan and syndecan 1 were measured at baseline, 2, 24 hours after fluid load test.

We observed associations of syndecan 1 with extravascular lung water index (rho = 0.48, P =.04) at baseline and of heparan sulfate proteoglycan with extravascular lung water index (rho= -0.56, P = .03) and pulse pressure variation (rho = 0.53, P = .04) at 24 hours after fluid load test. The plasma concentration of syndecan 1 correlated with lactate at baseline (rho = 0.51, P = .02) and at 24 hours after fluid load test (rho = 0.76, P = .009). At 2 hours after fluid load test, the concentration of syndecan 1 correlated with global end-diastolic volume index (rho= 0.93, P = .001) in normovolemic patients.

The shedding of endothelial glycocalyx after fluid load test in septic shock is associated with hemodynamic and metabolic responses and related with the severity of pulmonary edema.