Cognitive Impairment and Mortality after Hospitalization for Community-Acquired Pneumonia

Abstract

Community-acquired pneumonia (CAP) affects approximately 1.5 million patients annually in the United States, leading to significant acute and long-term clinical outcomes. CAP is increasingly recognized as a multisystemic disease with potential sequelae affecting various organ systems, including the neurologic, pulmonary, cardiovascular, musculoskeletal, metabolic, and renal systems. The primary objective of this study is to review literature on long-term cognitive impairment, dementia, and decreased survival following CAP hospitalization. Additionally, the potential role of the gut-lung-brain axis in the pathogenesis of these outcomes is explored. A comprehensive review of existing literature was conducted, focusing on studies that examined cognitive impairment, dementia, and mortality in patients hospitalized for CAP. Relevant studies were identified through a systematic search of medical databases, and data were extracted on study design, population characteristics, cognitive assessments, and outcomes. The review also incorporated mechanistic insights into the gut-lung-brain axis to hypothesize its role in the long-term sequelae of CAP. The review identified multiple studies demonstrating an increased risk of cognitive impairment and dementia following CAP hospitalization. Patients hospitalized for CAP had a 1.5 to 2.5 times higher risk of developing cognitive deficits compared to controls. This cognitive decline was not limited to elderly patients but spanned all adult age groups. Furthermore, CAP was associated with a significant reduction in life expectancy. Patients discharged after CAP hospitalization reached 50% mortality within three years, compared to seven years for those hospitalized for other reasons. The most pronounced decrease in survival was observed in CAP patients requiring ICU admission and immunocompromised patients. CAP is associated with significant long-term cognitive impairment and decreased survival. The proposed gut-lung-brain axis mechanism suggests that CAP-related dysbiosis leads to chronic systemic inflammation and neuroinflammation, potentially contributing to cognitive decline and increased mortality. Understanding the role of this axis may offer new therapeutic strategies for managing the long-term neurological consequences of CAP. Future research should focus on high-risk populations to develop targeted interventions aimed at mitigating these severe outcomes.