Stage ⒉ is the ulcer formation stage. The corneal tissue in the infiltration area undergoes degeneration and necrosis due to damage and nutritional disorders caused by toxins secreted by bacteria or enzymes released by the tissue. The necrotic tissue falls off to form a corneal ulcer. With the development of inflammation, corneal tissue necrosis and shedding worsen, ulcers gradually deepen, and the corneal stroma gradually becomes thinner. If the lesion breaks through the Descemet's membrane, a corneal perforation occurs. If the perforation is located in the center of the cornea, it often causes aqueous humor to continuously flow out, causing the perforation area to fail to heal completely, and corneal fistula can form.

Stage 4 is the healing period. The superficial scarring opacity is as thin as a cloud, and the texture of the iris behind can still be clearly seen through the opacity, which is called corneal pannus; If the turbidity is slightly white, but the iris can still be seen through, it is called corneal nebula; If the turbidity is very thick and porcelain white, and the iris cannot be seen through, it is called leukoplakia. If there is iris tissue embedded in the corneal scar tissue, adhesive leukoplakia will form, indicating a history of corneal perforation.

Even if corneal perforation does not occur in fungal keratitis, fungi can invade the eye and cause fungal intraocular infection.

Bacterial keratitis refers to corneal inflammation caused by bacterial infection, leading to corneal epithelial defect and corneal stromal necrosis, also known as bacterial corneal ulcer.

clinical manifestations

Diagnosis: Before starting drug treatment, scrape the diseased tissue from the infiltration focus and apply staining to search for bacteria, which will help early diagnosis of the cause. definite disease The original diagnosis requires bacterial culture and drug sensitivity testing at the same time to provide a basis for screening sensitive antibiotics.

treat

Clinical manifestations: slow onset, sub-acute course, mild irritation symptoms, accompanied by visual impairment. The corneal infiltration focus is white or milky white, dense, lacks luster, has a toothpaste-like or moss-like appearance, and there is matrix dissolution around the ulcer. The shallow groove formed by solution or the immune loop formed by antigen-antibody reaction. Sometimes "pseudopodia" or satellite-like infiltration foci can be seen next to the corneal infection foci.

Diagnosis: Laboratory tests can confirm the diagnosis by finding fungi and hyphae. Commonly used rapid diagnostic methods include corneal scraping Gram and Giemsa staining. For fungal culture, blood agar is used.

Treatment: ①Topical antifungal drug treatment; ②For severe cases, systemic antifungal drugs can be used in combination; ③For those who are complicated by iridocyclitis, 1% atropine eye drops or eye ointment should be used to dilate the pupils; ④ Even after timely medical treatment, 15% to 27% of patients still cannot control their condition. At this time, surgical treatment, including debridement, needs to be considered. surgery, conjunctival flap coverage and corneal transplantation.

Its clinical characteristics are repeated attacks, and multiple attacks gradually worsen the corneal opacity, which can eventually lead to blindness.

clinical manifestations

Treatment: Discoid keratitis caused by an immune response can be treated with hormones.

Acanthamoeba keratitis: Caused by infection with Acanthamoeba protozoa, it is a serious vision-threatening keratitis. The disease often manifests as a chronic, progressive corneal ulcer that can last for several months.

Clinical manifestations: central or paracentral annular infiltration in the cornea, which may be accompanied by epithelial defects. In the late stage, the release of proteases and collagenases in the tissue leads to matrix dissolution, abscess formation, corneal ulcers and even perforation.

Clinical manifestations: Typical fan-shaped or diffuse corneal inflammatory infiltrates can be seen in the early stage, which may be accompanied by or without retrocorneal precipitates (KP).

Neuroplegic keratitis occurs when the trigeminal nerve is damaged by trauma, surgery, inflammation, or tumors.

Clinical manifestations: Point-like detachment of corneal epithelium exposed to the palpebral fissure. Once secondary infection occurs, it will evolve into purulent corneal ulcer, which is easily perforated. The reflex blinking of the affected eye is reduced and can Accompanied by congestion, decreased vision, increased secretions, etc.

Treatment: Amniotic membrane covering, wearing soft contact lenses or bandaging the affected eye can promote the healing of corneal defects. Blepharoplasty can be performed to protect the cornea.

Seen in facial nerve paralysis, deep anesthesia or coma.

Clinical manifestations: In the early stage, the cornea and conjunctival epithelium are dry and rough, the exposed parts of the conjunctiva are congested and hypertrophic, the corneal epithelium gradually merges from punctate erosion into large defects, and new blood vessels form. secondary infection Symptoms and signs of purulent corneal ulcer may appear.

Treatment: The goals of treatment are to remove exposure factors, protect the corneal epithelium, and maintain ocular surface moisture. According to the cause of corneal exposure, eyelid defect repair, eyelid skin grafting, eyelid reconstruction, etc. are performed.

Clinical manifestations: The disease progresses slowly. The main symptoms include severe eye pain, photophobia, tearing and decreased vision. The ulcer develops in a ring shape along the limbus of the cornea and moves toward the middle Infiltration occurs in the central area, and the infiltration edge is submerged and slightly raised, and may eventually involve the entire cornea.

Treatment: Topical glucocorticoids or collagenase inhibitors (such as 2% cysteine ​​eye drops) can be used for eye drops.

Marginal corneal degeneration is also called Terrien marginal degeneration. The male-to-female incidence ratio is 3:1, and it often begins in youth (20 to 30 years old).

Clinical manifestations: generally no pain, photophobia, and chronic progressive decline in vision. Symmetrical corneal edge thinning and dilation in one or both eyes, more common in the upper nasal quadrant.

Treatment: Lamellar corneal transplantation is possible.

Clinical manifestations: Gray-white dots or patches, map-like and fingerprint-like particles can be seen in the central corneal epithelium and basement membrane. line. Recurrent epithelial denudation may occur.

Fuchs corneal endothelial dystrophy is a typical posterior corneal dystrophy characterized by progressive damage to the corneal endothelium and eventually the development of corneal endothelial decompensation. It is autosomal dominant inheritance. Histopathology showed scattered focal thickening of the corneal Descemet's lamina, forming corneal droplets.

Clinical manifestations: It is more common in menopausal women. Pain, photophobia and tearing occur when bullous keratopathy develops.