Romain Sonneville1,2, Etienne de Montmollin3,4, Julien Poujade5, Maïté Garrouste-Orgeas3,6, Bertrand Souweine7, Michael Darmon8,9, Eric Mariotte10, Laurent Argaud11, François Barbier12, Dany Goldgran-Toledano13, Guillaume Marcotte14, Anne-Sylvie Dumenil15, Samir Jamali16, Guillaume Lacave17, Stéphane Ruckly3, Bruno Mourvillier5,3, Jean-François Timsit5,3. 1. Department of Intensive Care Medicine and Infectious Diseases, Hôpital Bichat-Claude Bernard, 46 rue Henri Huchard, 75877, Paris Cedex, France. romain.sonneville@aphp.fr. 2. UMR1148, LVTS, Sorbonne Paris Cité, Inserm/Paris Diderot University, Paris, France. romain.sonneville@aphp.fr. 3. UMR 1137, IAME Team 5, DeSCID: Decision Sciences in Infectious Diseases, Control and Care, Sorbonne Paris Cité, Inserm/Paris Diderot University, Paris, France. 4. Medical-Surgical Intensive Care Unit, Delafontaine Hospital, Saint-Denis, France. 5. Department of Intensive Care Medicine and Infectious Diseases, Hôpital Bichat-Claude Bernard, 46 rue Henri Huchard, 75877, Paris Cedex, France. 6. Medical-Surgical Intensive Care Unit, Saint-Joseph Hospital Network, Paris, France. 7. Medical Intensive Care Unit, Gabriel Montpied University Hospital, Clermont-Ferrand, France. 8. Medical Intensive Care Unit, Saint Etienne University Hospital, Saint-Etienne, France. 9. Jacques Lisfranc Medicine University, Jean Monnet University, Saint-Etienne, France. 10. Medical Intensive Care Unit, AP-HP, Saint Louis Hospital, Paris, France. 11. Medical Intensive Care Unit, Lyon University Hospital, Lyon, France. 12. Medical Intensive Care Unit, La Source Hospital, Orléans, France. 13. Medical-Surgical Intensive Care Unit, Gonesse Hospital, Gonesse, France. 14. Surgical ICU, Edouard Herriot University Hospital, Lyon, France. 15. Medical-Surgical Intensive Care Unit, AP-HP, Antoine Béclère University Hospital, Clamart, France. 16. Medical-Surgical Intensive Care Medicine Unit, Dourdan Hospital, Dourdan, France. 17. Medical Intensive Care Unit, André Mignot Hospital, Versailles, France.
Abstract
PURPOSE: Identifying modifiable factors for sepsis-associated encephalopathy may help improve patient care and outcomes. METHODS: We conducted a retrospective analysis of a prospective multicenter database. Sepsis-associated encephalopathy (SAE) was defined by a score on the Glasgow coma scale (GCS) <15 or when features of delirium were noted. Potentially modifiable risk factors for SAE at ICU admission and its impact on mortality were investigated using multivariate logistic regression analysis and Cox proportional hazard modeling, respectively. RESULTS: We included 2513 patients with sepsis at ICU admission, of whom 1341 (53%) had sepsis-associated encephalopathy. After adjusting for baseline characteristics, site of infection, and type of admission, the following factors remained independently associated with sepsis-associated encephalopathy: acute renal failure [adjusted odds ratio (aOR) = 1.41, 95% confidence interval (CI) 1.19-1.67], hypoglycemia <3 mmol/l (aOR = 2.66, 95% CI 1.27-5.59), hyperglycemia >10 mmol/l (aOR = 1.37, 95% CI 1.09-1.72), hypercapnia >45 mmHg (aOR = 1.91, 95% CI 1.53-2.38), hypernatremia >145 mmol/l (aOR = 2.30, 95% CI 1.48-3.57), and S. aureus (aOR = 1.54, 95% CI 1.05-2.25). Sepsis-associated encephalopathy was associated with higher mortality, higher use of ICU resources, and longer hospital stay. After adjusting for age, comorbidities, year of admission, and non-neurological SOFA score, even mild alteration of mental status (i.e., a score on the GCS of 13-14) remained independently associated with mortality (adjusted hazard ratio = 1.38, 95% CI 1.09-1.76). CONCLUSIONS: Acute renal failure and common metabolic disturbances represent potentially modifiable factors contributing to sepsis-associated encephalopathy. However, a true causal relationship has yet to be demonstrated. Our study confirms the prognostic significance of mild alteration of mental status in patients with sepsis.
PURPOSE: Identifying modifiable factors for sepsis-associated encephalopathy may help improve patient care and outcomes. METHODS: We conducted a retrospective analysis of a prospective multicenter database. Sepsis-associated encephalopathy (SAE) was defined by a score on the Glasgow coma scale (GCS) <15 or when features of delirium were noted. Potentially modifiable risk factors for SAE at ICU admission and its impact on mortality were investigated using multivariate logistic regression analysis and Cox proportional hazard modeling, respectively. RESULTS: We included 2513 patients with sepsis at ICU admission, of whom 1341 (53%) had sepsis-associated encephalopathy. After adjusting for baseline characteristics, site of infection, and type of admission, the following factors remained independently associated with sepsis-associated encephalopathy: acute renal failure [adjusted odds ratio (aOR) = 1.41, 95% confidence interval (CI) 1.19-1.67], hypoglycemia <3 mmol/l (aOR = 2.66, 95% CI 1.27-5.59), hyperglycemia >10 mmol/l (aOR = 1.37, 95% CI 1.09-1.72), hypercapnia >45 mmHg (aOR = 1.91, 95% CI 1.53-2.38), hypernatremia >145 mmol/l (aOR = 2.30, 95% CI 1.48-3.57), and S. aureus (aOR = 1.54, 95% CI 1.05-2.25). Sepsis-associated encephalopathy was associated with higher mortality, higher use of ICU resources, and longer hospital stay. After adjusting for age, comorbidities, year of admission, and non-neurological SOFA score, even mild alteration of mental status (i.e., a score on the GCS of 13-14) remained independently associated with mortality (adjusted hazard ratio = 1.38, 95% CI 1.09-1.76). CONCLUSIONS:Acute renal failure and common metabolic disturbances represent potentially modifiable factors contributing to sepsis-associated encephalopathy. However, a true causal relationship has yet to be demonstrated. Our study confirms the prognostic significance of mild alteration of mental status in patients with sepsis.
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