Systematic Review with Qualitative Synthesis of Gut Microbiota Alterations after Acute Brain Injury

Abstract

Acute brain injury (ABI), traumatic or nontraumatic, profoundly disrupts the gut microbiota (GM). To provide intensive care physicians with a clearer understanding of this phenomenon, we conducted a systematic review with qualitative synthesis. Due to significant heterogeneity in study designs, populations, and outcomes, a meta-analysis was not feasible. Instead, findings were synthesized thematically, focusing on study types, microbiota metrics, and clinical associations. Across studies, ABI is consistently associated with reduced microbial diversity, a decline in the relative abundance of several species, and increased interindividual variability in GM composition. Notably, phyla, such as Pseudomonadota, Bacteroidota, and Verrucomicrobiota, are frequently enriched, whereas Bacillota tends to be depleted. These patterns of dysbiosis appear largely consistent regardless of ABI etiologies. Furthermore, GM alterations can occur within a few hours postinjury and often return to baseline levels within months. The review highlights the metabolic, immune, and neuronal disruptions induced by ABI, which may contribute to gastrointestinal dysfunction and negatively influence patient prognosis. Moreover, standard intensive care unit (ICU) therapies may exacerbate GM disturbances. Importantly, dysbiosis has been linked to adverse clinical outcomes (delayed recovery, increased mortality). Emerging therapeutic strategies (metabolite supplementation, fecal microbiota transplantation) have shown potential to modulate the GM and support postinjury recovery. However, the underlying mechanisms of ABI-related dysbiosis and its consequences remain incompletely understood. Future research should aim to clarify the pathophysiological drivers of GM disruption, explore the potential prognostic value of GM dynamics, and assess how ICU therapies influence GM evolution. Developing GM-targeted interventions may offer novel opportunities to modulate ABI-related complications and improve patient outcomes.