Effects of fluid balance on prognosis of acute respiratory distress syndrome patients secondary to sepsis

BACKGROUND:Fluid management is crucial to acute respiratory distress syndrome(ARDS)secondary to sepsis.However,choices of fluid resuscitation strategies and fluid input volumes remain a thorny problem.Our study aimed to elucidate the relationship between fluid balance and prognosis of ARDS patients secondary to sepsis.METHODS:Our study included 322 sepsis patients from Ruijin Hospital between 2014 and 2018,and 84 patients were diagnosed as ARDS within 72 hours after onset of sepsis according to Berlin ARDS Defi nition.RESULTS:Among the 322 sepsis patients,84(26.1%)were complicated with ARDS within 72 hours.ARDS patients had a lower oxygenation index(PaO2/FiO2166.4±71.0 vs.255.0±91.2,P<0.05),longer duration of mechanical ventilation(11[6-24]days vs.0[0-0]days,P<0.05)than those without ARDS.Sepsis patients with ARDS showed daily positive net fl uid balance during seven days compared with those without ARDS who showed daily negative net fluid balance since the second day with signifi cant statistical differences.Among the 84 sepsis patients with ARDS,58(69.0%)died.Mean daily fl uid input volumes were much lower in survivors than in non-survivors(43.2±16.7 mL/kg vs.51.0±25.2 mL/kg,P<0.05)while output volumes were much higher in survivors(45.2±19.8 mL/kg vs.40.2±22.7 mL/kg,P<0.05).Using binary logistic regression analysis,we found that the mean daily fl uid balance was independently associated with mortality of sepsis patients complicating with ARDS(P<0.05).CONCLUSIONS:Early negative fluid balance is independently associated with a better prognosis of sepsis patients complicated with ARDS.

Vitamin C Attenuates Hemorrhagic Shock-induced Dendritic Cell-specific Intercellular Adhesion Molecule 3-grabbing Nonintegrin Expression in Tubular Epithelial Cells and Renal Injury in Rats

Background： The expression of dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin （DC-SIGN） in renal tubular epithelial cells has been thought to be highly correlated with the occurrence of several kidney diseases, but whether it takes place in renal tissues during hemorrhagic shock （HS） is unknown. The present study airned to investigate this phenomenon and the inhibitory effect of Vitamin C （VitC）. Methods： A Sprague Dawley rat HS model was established in vivo in this study. The expression level and location of DC-SIGN were observed in kidneys. Also, the degree of histological damage, the concentrations of tumor necrosis factor-or and interleukin-6 in the renal tissues, and the serum concentration of blood urea nitrogen and creatinine at different times （2-24 h） alter HS （six rats in each group）, with or without VitC treatment belbre resuscitation, were evaluated. Results： HS induced DC-SIGN expression in rat tubular epithelial cells. The proinflarnmatory cytokine concentration, histological damage scores, and functional injury of kidneys had increased. All these phenornena induced by HS were relieved when the rats were treated with VitC before resuscitation. Conclusions： The results of the present study illustrated that HS could induce tubular epithelial cells expressing DC-SIGN, and the levels of proinflarnmatory cytokines in the kidney tissues improved correspondingly. The results also indicated that VitC could suppress the DC-SIGN expression in the tubular epithelial cells induced by HS and alleviate the inflammation and functional injury in the kidney.