Sepsis-Associated Encephalopathy (SAE) as an Early Predictor of Mortality: Using Neurological Status (GCS or Delirium Scores) upon ED Admission to Predict Long-Term Outcomes in Septic Patients.
Keywords:
Sepsis, Emergency Department, Delirium, Clinical KnowledgeAbstract
Background:
Sepsis-Associated Encephalopathy (SAE) is a dangerous and multifactorial complication of sepsis, causing diffuse dysfunction of the brain, and is a common presentation in the Emergency Department (ED). Sepsis-associated encephalopathy (SAE) presents a spectrum from mild cognitive deficits to deep coma. However, the lack of specific biomarkers and the confounding effects of sedation make SAE a challenging diagnosis of exclusion. It requires the systematic elimination of alternative etiologies for altered mentation in the febrile, critically ill patient.
OBJECTIVE:
To evaluate the efficacy of neurological assessment tools and biochemical markers at ED admission as early predictors of Sepsis-Associated Encephalopathy and long-term patient outcomes.
METHODOLOGY:
A comprehensive analysis of studies showing the GCS scores and Delirium screening in ED during admission for early identification of SEA and determination of 28-day mortality and long-term cognitive outcomes based on data from published literature.
RESULT:
The analysis of literature reveals that SEA affects 53% to 70% of patients. A GCS score of ≤14 on average during admission carries a 49.3% mortality rate, while GCS scores between 3–8 increases the risk to 63%. Delirium increases mortality by 4.3-fold, showing a 15.8% mortality after 28 days and long-term cognitive decline.
CONCLUSION:
Early identification of Sepsis-Associated Encephalopathy clinically calculating the GCS scores and delirium screening on arrival in the ED is essential and beneficial as these assessments serve as powerful independent and non-invasive predictors of 28-day mortality and long-term cognitive impairment, enabling clinicians to implement critical neuroprotective strategies and improve prognostic chances immediately upon admission.
References
1) Chaudhry, N., & Duggal, A. K. (2014). Sepsis associated encephalopathy. Advances in Medicine, 2014, 1–16. https://doi.org/10.1155/2014/762320
2) Gofton, T. E., & Young, G. B. (2012). Sepsis-associated encephalopathy. Nature Reviews Neurology, 8(10), 557–566. https://doi.org/10.1038/nrneurol.2012.183
3) Chaudhry, N., & Duggal, A. K. (2014b). Sepsis associated encephalopathy. Advances in Medicine, 2014, 1–16. https://doi.org/10.1155/2014/762320
4) Ito, H., Hosomi, S., Koyama, Y., Matsumoto, H., Imamura, Y., Ogura, H., & Oda, J. (2022). Sepsis-Associated Encephalopathy: A Mini-Review of inflammation in the brain and body. Frontiers in Aging Neuroscience, 14, 912866. https://doi.org/10.3389/fnagi.2022.912866
5) Krzyżaniak, K., Szymczyk, A., Wściślak, A., Szczygieł, N., Zembrzuska, S., Abramczyk-Suszek, A., Krion, R., Remisiewicz, M., & Siemiński, M. (2025). Prevalence, symptoms, risk factors and impact of sepsis-associated encephalopathy in emergency department patients: a case-control study. BMC Emergency Medicine, 25(1), 262. https://doi.org/10.1186/s12873-025-01385-8
6) Chaudhry, N., & Duggal, A. K. (2014c). Sepsis associated encephalopathy. Advances in Medicine, 2014, 1–16. https://doi.org/10.1155/2014/762320
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