1. Anterior chamber pus Severe cases are often combined with iridocyclitis. As a result of the leukocytes leaking from the iris ciliary body, the anterior atrial fluid becomes cloudy and settles in the lower part of the anterior chamber angle, called anterior chamber pus. The pus in the anterior chamber may be completely absorbed (the thinner it is, the more easily it is absorbed). The fibrous exudate may form connective tissue and produce anterior or posterior adhesions around the iris, even causing pupillary atresia. There are deposits on the posterior corneal wall in those with ciliary body involvement. 2, posterior elastic membrane bulge Because corneal ulcers can progress deeper, when the cornea will be perforated, a thin layer of clear tissue can appear at the base of the ulcer, shaped like a “black” vesicle protruding forward, which is rarely seen in young and young children, as it is often perforated by transient increases in intraocular pressure such as coughing, sneezing, and eyelid spasms. Careless examination of the eyelid by forceful separation of the eyelid also often results in perforation. 3, corneal perforation When the cornea is perforated, the patient feels violent pain and hot tears (atrial fluid) outflow, but the original pain symptoms disappear; after the perforation, the atrial fluid overflows, first the anterior chamber becomes shallow or even disappears, then the iris and lens move forward and contact with the posterior wall of the cornea, and the eye becomes soft. After corneal perforation, the outcome varies according to the size and location of the perforation. 4. Anterior pole cataract If the perforation is small and located in the central part of the cornea, the iris may begin to heal without detachment. When the atrial water flows out and the perforation is not yet blocked by thick enough fibrous exudate, the lens is in continuous contact with the posterior corneal wall. When the anterior chamber is formed and the anterior capsule of the lens is out of contact with the posterior corneal wall, the surface of the anterior capsule and subcapsular tissue in the central part of the lens have become permanently clouded, forming an acquired anterior pole cataract. 5. iris prolapse If the perforation occurs far from the central cornea, the iris is bound to block the ruptured hole. At this point the exudate fuses and fixes with the edge of the ulcer, isolating the anterior chamber from the outside world. At this point the anterior chamber recovers rapidly and scarring begins to form. The iris detachment gradually heals and subsides. The iris is permanently fixed within the perforation. Although the clinical picture is of a corneal scar, part of the iris actually becomes scarred as well. Sometimes the embedding is so minimal that it cannot be seen with the naked eye (if a brownish-yellow pigmented spot is found on the corneal white spot, this indicates that the iris is embedded within the scar). Some scarring is thick and self, which is called corneal adhesions white spots. 6, corneal chyloma After corneal ulcer perforation and iris prolapse, normal intraocular pressure is sufficient to make the prolapsed iris protrude from the corneal surface. During the healing period, the scar can be fixed in place so that there is a half spherical or conical bulge on the normal corneal surface, which is grayish in color, called partial corneal staphyloma. This lesion mostly occurs near the edge of the cornea, while the pupil is normal or only partially involved, vision is reduced and intraocular pressure is not high. 7, corneal fistula Sometimes corneal fistula is formed after incomplete healing of corneal perforation. In the center of the white spot at the rupture, a small, dark black bulge appears, while the anterior chamber disappears and the eye becomes soft. The eye immediately compensates by increasing atrial aqueous production in order to maintain the normal hardness of the eye. If this bulge is closed by the new membrane, the increased atrial aqueous production will gradually increase the intraocular pressure and cause secondary glaucoma. If the pressure continues to rise, the symptoms of an acute glaucoma attack can be caused, and the membrane breaks through, the symptoms disappear, and the eye becomes soft again. However, soon after the fistula is closed again by the new membrane, and the IOP increases again. Eventually, endophthalmitis, full-blown septicemia, or intraocular hemorrhage occurs due to fierce bacterial infection, and the eye eventually atrophies. There is also the end because of the long-term softening of the eye, flattening of the cornea, clouding of the lens, and even the occurrence of retinal detachment. 8, formation of corneal vessels Corneal inflammation is often accompanied by vascular proliferation, mostly reticular, occurring at the edge of the cornea near the ulcer. These are superficial vessels, but deep ulcers also have deep vessels. Initially, the vessels advance radially toward the ulcer and then widen as the ulcer begins to heal. This is extremely important for the healing of the ulcer. However, sometimes ulcers heal without vascularization. The vessels gradually disappear after the ulcer heals, but they may never disappear, especially in the presence of preiris adhesions. Sometimes the vessels are accompanied by inflammation, resembling exudate, into the cornea, as seen in parenchymal keratitis and corneal vascular opacification. Determining the location of the vessels is important in identifying keratoconus and can often be used to diagnose the type of keratitis.