Inflammation-related glaucoma is a secondary glaucoma that often combines angle-closure and open-angle components. The mechanism of inflammation-related secondary open-angle glaucoma may be caused by trabecular meshwork edema, corneal endothelial cell dysfunction, uveal fibrinous exudates and inflammatory cells blocking the trabecular meshwork, and prostaglandin mediation, as well as inflammation destroying the blood-aqueous barrier to produce serous aqueous humor, causing aqueous humor drainage obstruction. Inflammation-related secondary angle-closure glaucoma may be caused by the destruction of the blood-aqueous barrier, the increase of protein and fibrinous exudates in the aqueous humor, and the deposition in the eye to form posterior iris synechiae. If not treated in time, it may eventually form iris bulging and secondary angle closure. At the same time, peripheral iris tissue edema and inflammatory debris at the iridocorneal angle are prone to form peripheral anterior synechia (PAS) after organization. Gonioscopy shows that the PAS left over from inflammation has different shapes and heights, which can be distinguished from primary angle-closure glaucoma. During eye inflammation, ciliary body swelling and anterior rotation can cause uveal exudation, which in turn causes the iridocorneal angle to become shallow and closed. Inflammatory large KP blocks the iridocorneal angle, and severe posterior uveitis can manifest as secondary extensive exudative retinal detachment and anterior displacement of the irido-lens septum, which can also lead to angle-closure glaucoma.