The Role of Immune Cell Subsets in the Development of Postoperative Cognitive Dysfunction in Surgical Patients Under Anesthesia.

Abstract

Postoperative cognitive dysfunction (POCD) affects 10-54% of surgical patients, particularly elderly populations. This review discusses immune cell contributions to POCD pathogenesis through neuroinflammation mechanisms. While physiological postoperative inflammatory responses promote wound healing and tissue repair, pathological hyperactivation of immune pathways drives POCD development. Surgical trauma triggers systemic inflammation, disrupting blood-brain barrier integrity and facilitating immune cell infiltration. Innate immune cells, including activated microglia, infiltrating monocytes, and neutrophils, initiate neuroinflammatory cascades through cytokine release. Adaptive immune responses involve dysregulated T cell homeostasis with elevated Th17 cells and reduced regulatory T cells. Key molecular pathways include damage-associated molecular patterns, complement activation, and neurotrophin signaling disruption. Clinical biomarkers, particularly IL-6, TNF-α, and S100B, enable risk stratification with sensitivity ranging from 65-85% and specificity from 75-90%. Therapeutic strategies focus on immunomodulation through dexmedetomidine, anti-inflammatory agents, and perioperative optimization. Understanding these immune mechanisms provides foundations for targeted interventions to prevent this debilitating complication and improve perioperative cognitive outcomes.