ARDS is a pulmonary edema injury. Among its etiologies, it can be secondary to septic shock. Managing septic shock involves hemodynamic optimization with significant fluid and sodium inputs. Fluid and sodium inputs in ARDS worsen respiratory failure through capillary leakage, and a restrictive input strategy is clinically beneficial (reduced mechanical ventilation duration and ICU stay). Predicting ARDS onset in septic shock allows for optimized fluid and sodium input management, adopting a restrictive rather than liberal approach to minimize deterioration in respiratory function.
Septic shock remains highly fatal, causing multi-organ failure including hemodynamic, pulmonary, neurological, renal, hematologic, and hepatic. These failures stem from generalized inflammatory aggression leading to endothelial dysfunction, especially at the capillary level. Pulmonary failure secondary to septic shock is characterized by edema, with ARDS being the most severe form. Sepsis is the second most common cause of ARDS after pneumonia. The incidence of ARDS in severe sepsis is about 6%, and its occurrence is an independent factor contributing to increased mortality. These failures significantly impact the management of septic shock, where early and often agressive, vascular filling is standard for hemodynamic failure. Conversely, the onset of ARDS onset warrants limiting hydro-sodium inputs. Currently, there are no data predicting the occurrence of ARDS patients with septic shock.
Study Type
OBSERVATIONAL
Enrollment
100
CHI Andre Gregoire
Montreuil, France
Measurement of proteinuria in the first 24 hours (H0 and H24) of septic shock.
relationship between proteinuria kinetics in the first 24 hours (H0 and H24) of septic shock and presence of ARDS at H72
Time frame: 24 hours
measurement of albuminuria urinary IgG at H0 and H24
Evaluation of the association between proteinuria kinetics and the onset of hemodynamic failure, renal failure, duration of mechanical ventilation, ICU stay, and hospital mortality
Time frame: 24 hours
measurement of alpha-1-microglobulin at H0 and H24
Evaluation of the association between proteinuria kinetics and the onset of hemodynamic failure, renal failure, duration of mechanical ventilation, ICU stay, and hospital mortality
Time frame: 24 hours
measurement of urinary IgG at H0 and H24
Evaluation of the association between proteinuria kinetics and the onset of hemodynamic failure, renal failure, duration of mechanical ventilation, ICU stay, and hospital mortality
Time frame: 24 hours
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