Inflammation-associated glaucoma

Inflammation-associated glaucoma is secondary glaucoma, which often combines two types of closed-angle and open-angle glaucoma. The mechanism of inflammation-related secondary open-angle glaucoma can be caused by trabecular meshwork edema, corneal endothelial cell dysfunction, cellulosic exudate of uveal membrane and inflammatory cells blocking trabecular meshwork, and prostaglandin-mediated, Inflammation damages the blood-aqueous aqueous barrier to produce a serous-like aqueous humor that prevents drainage of the aqueous humor. Inflammation-related secondary angle-closure glaucoma can be caused by the destruction of the blood-aqueous aqueous barrier, protein and cellulosic exudates in the aqueous humor components, and deposits in the eyes to form adhesions after iris. Formation of iris swelling and secondary angle closure. At the same time, peripheral iris tissue edema and the inflammatory debris at the iris cornea corner are mechanized, and it is easy to form peripheral anterior synechia (PAS). A keratoscopy shows the PAS morphology and the height of the preadhesion left by inflammation. Different, can be distinguished from primary angle-closure glaucoma. Swelling and forward rotation of the ciliary body during eye inflammation can cause uveal exudation, which in turn causes the corneal angle of the iris to become shallow and closed. Inflammatory large-scale KP obstructs the iridocorneal horn, and severe posterior uveitis can be manifested by secondary extensive exudative retinal detachment, anterior iris-lens displacement, and angle-closure glaucoma.