Abstract: Late-onset capsular block syndrome (LCBS) is an ocular syndrome following cataract surgery characterized by capsular bag distension, intraocular lens (IOL) anterior displacement, and refractive shift, resulting from fluid accumulation within a sealed compartment formed by adhesions between the IOL and a small-diameter continuous curvilinear capsulorhexis (CCC) opening. Its pathogenesis involves three key mechanisms: (1) proliferation of lens epithelial cells secreting αB/βB crystallins and calcium ions to drive osmotic gradient formation; (2)latent Propionibacterium acnes infection inducing chylous opacity; and (3) inflammatory cytokines (TNF-α, IL-1β, BFGF, IL-8) mediating blood-aqueous barrier disruption. Diagnosis, beyond conventional ultrasound biomicroscopy (UBM) and anterior segment optical coherence tomography (AS-OCT), now leverages multimodal imaging to enhance differential diagnostic accuracy. Therapeutic strategies primarily include laser therapy: Nd:YAG laser anterior capsulotomy is indicated for cases without posterior capsular opacification (PCO); posterior capsulotomy proves more effective for PCO-associated LCBS; combined capsulotomy reduces recurrence rates, and femtosecond laser treatment with intraoperative OCT overcomes traditional localization limitations; and surgical intervention involves anterior capsular release with fluid aspiration to preserve the posterior capsular barrier, and pars plana vitrectomy combined with posterior continuous curvilinear capsulorhexis (PCCC) for severe PCO or infected cases, with future efforts focused on individualized prevention and management.

Key words: Late-onset capsular block syndrome, Pathogenesis, Treatment