Gut dysbiosis‑derived butyrate loss predicts feeding intolerance: Multiomics evidence guiding nurse‑driven microbiota‑supportive interventions (Review).

چکیده اصلی

Feeding intolerance (FI) is a common and debilitating challenge among critically ill patients that is linked to a pathway involving the collapse of the gut microbial ecology. The present review synthesizes multiomics evidence supporting a framework whereby critical illness‑associated gut dysbiosis results in a functional deficit of a microbially derived short‑chain fatty acid butyrate, a pivotal metabolite involved in maintaining intestinal barrier integrity, immuneoregulation and gastrointestinal motility. The loss of butyrate‑producing bacteria and their genetic pathways is strongly correlated with FI and may represent a contributory pathogenic mechanism. Key butyrate‑producing organisms diminished during this process include Faecalibacterium prausnitzii and Roseburia spp. Building upon this mechanistic framework, a pragmatic, nurse‑driven intervention model aimed at preserving and restoring microbial health in critically ill patients was proposed. This model is founded on four principal strategies: Minimizing iatrogenic harm (such as antibiotic/proton pump inhibitor stewardship), targeted microbiota nourishment (pre/synbiotics), cautious microbial restoration (probiotics/fecal microbiota transplantation) and innovative monitoring approaches. By integrating principles of microbial ecology with clinical nursing science, the present review provides a framework for developing nurse‑driven protocols designed to address the underlying pathophysiology of FI and improve patient outcomes.

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