Erosive corneal ulcer

Introduction to Moorenic Corneal Ulcer Mossy (or chronic limp) corneal ulcers, first reported by Mooren (1867), are also called Mooren's corneal ulcers. The disease is more common in the clinic, but because of the unclear etiology, stubborn condition, and no specific treatment, it is still regarded as an extremely serious blind eye disease. The ulcer is a typical furrow or silkworm type, which undergoes edge infiltration, bulging, deep ulcers and about one-half of the thickness of the anterior matrix. Sometimes it can be worn into the posterior elastic layer, and the ulcer can be extended in the center and both ends of the cornea. At the same time, the bottom is covered by epithelial repair and neovascularization. Although corneal perforation is rare, the disease progresses slowly and stubbornly. It is characterized by peripheral corneal periplasmic dissolution, leaving only the central cornea to eventually erode the entire cornea. basic knowledge Sickness ratio: 0.0001% Susceptible people: no specific people Mode of infection: non-infectious Complications: herpes simplex iridocyclitis

Causes of Mooren's Corneal Ulcer

The exact cause is unknown. For a long time, many scholars have proposed a variety of pathogenic factors, but they have not been confirmed. Some factors have a certain relationship with the occurrence of this disease, but not a fundamental cause. Several statements:

1. Infection: At the beginning of this century, it was suggested that Mooren's corneal ulcer is caused by a special Gram-positive double bacillus, and Koppe (1918) is cured with tuberculin in 3 cases, which is considered to be the cause of tuberculosis, Rodigina (1934) A Zur Nedden-negative bacillus was isolated from the tissue of Mooren's corneal ulcer and appeared to support this infection, but it was not confirmed in other cases.

In the 1940s, many scholars believed that Mooren's corneal ulcer was associated with certain viral infections. It is believed that this lesion has the characteristics of a viral disease, such as no response to antibiotic treatment; the pathological change of ulcer is localized tissue necrosis. The appearance of large mononuclear cells; intracellular or intracytoplasmic inclusions can be found in the conjunctiva and corneal epithelium of the lesion; in some cases, conjunctival follicular proliferation or regional lymphadenopathy is associated.

believes that the virus causing Mooren's corneal ulcer does not have neurotropic, so the corneal perception is normal. It is speculated that this virus may belong to the skin-like cell type or the variant skin-skin virus. Corneal trauma is a direct infection of the virus. Or an indirect cause, the virus or its toxin invades from the injury or with the vascular network around the cornea and its neovascularization, and develops with the expansion of the blood vessel. However, it has not been isolated from the diseased tissue so far. .

2, the body toxins said uriakose (1963): found 6 cases of mooring corneal ulcer without combined hookworm disease, after treatment with tetrachloroethylene anthelmin, ulcers are cured at the same time, it is considered to be related to intestinal parasitic worms, Givner (1963) To the phyfopharmacologic test, it was confirmed that the blood of patients with Mooren's corneal ulcer contains toxins that hinder the growth of the roots of white lentils. It is believed that this toxin is related to the occurrence of ulcers, and it is speculated that the toxins produced by intestinal parasites can also To promote the occurrence of ulcers, it is believed that the toxins produced by intestinal parasites are absorbed into the blood circulation, accumulating in the iliac crest around the limbus, and sufficient virulence can cause ulceration of the limbus. (1965) pointed out that Kuriakose The hypothesis that hookworm toxins cause ulceration due to vascular exudation, although it cannot explain the case of sclerosing corneal ulcers in which no hookworms are present, there is a possibility that pathological agents are affected by certain toxins, such as the slow progress of ulcers. With the front end of the vascular invasion department, the hairy, necrotizing pathological changes and non-lesional The complete boundary of the area indicates that this pathological process is related to the role of toxic products. Therefore, this statement has been valued by many researchers.

3, local nutritional metabolism disorders: Many people have suggested that Mooren's corneal ulcer is caused by trigeminal dystrophies, vitamin B1 deficiency or related to local nutritional disorders, the above findings and the majority of patients with systemic nutritional status and health status Contradictory, it is difficult to understand that the dystrophic disorder is limited to a part of the stenosis of the limbus. In addition, the perception of the corneal ulcer area does not conform to the damage of the lesion based on the trigeminal nerve.

It is also believed that there are vascular dysfunction factors in the mooring corneal ulcer, which is related to nodular arteritis, Wegener's internal bud, and on top of it, local dystrophies, however, clinically or histopathologically. There is no exact basis.

4, collagenase said: Brown (1969) found that the collagenase activity in the conjunctival tissue of the ulcerative corneal ulcer is significantly increased, and that the occurrence of this disease is closely related to the collagenase activity in the conjunctival tissue, from 1972 to 1975, he Further study of the conjunctival histopathology of adjacent ulcers and determination of collagenase, plasmin, and the use of collagenase inhibitor and lesion conjunctival resection in 7 cases of 10 eyes of mooring corneal ulcer, the results cured 8 eyes, and confirmed lesions of the conjunctiva, The metabolites produced in the corneal stroma and epithelial tissue of the ulcer can degrade the glycoprotein of collagen and cornea. Brown also believes that the accumulation of a large number of plasma cells in the conjunctival specimen may be the source of collagenase, lysozyme, or Other inducers of enzyme-producing cells, it is also believed that active neutrophils in the ulcer and its adjacent tissues are the source of ulcerase, and the granules of the neutral cells are a special form of primary lysosomes. The body contains a variety of hydrolases, including collagenase and glycoproteinase, and the debate about the source of ulcerase remains to be confirmed.

This collagenase theory is the direct cause of mooring corneal ulcer or the consequence of ulceration. It has not yet been fully clarified. In other chronic corneal ulcers and alkali burned corneal epithelium, the activity of collagenase is also increased. Therefore, collagenase is used. Increased activity to explain the occurrence of moxibustion ulcers is not specific.

5. Autoimmune theory: Studies in the past decade have shown that there are evidences of autoimmune phenomena and immunopathology in cases of Mooren's corneal ulcers. Most scholars believe that this disease is likely to be an autoimmune disease, Schaap ( 1969) First, an indirect immunofluorescence technique was used to detect a circulating antibody to the corneal epithelium in a patient with mooring corneal ulcer. Brown (1975) found that a large number of plasma cells in the subepithelial tissue of the conjunctiva showed an antibody-dependent effect. After that, immunoglobulin (IgG, IgM) was found in the conjunctival epithelial cells of 3 cases of Mooren's corneal ulcer by direct immunofluorescence technique. In addition, complement (C3) and immunoglobulin were found in 2 patients with ulcer activity. simultaneously exist.

Mondino et al (1978) used a macrophage migration inhibitory factor test in seven patients with Mooren's corneal ulcer, and six of them were positive for corneal antigens. It may play an important role in mediating autoimmune umbilical corneal ulcers.

Some scholars believe that the immune phenomenon of Mooren's corneal ulcer, the production of antibodies is probably due to the damage of the antigen of the conjunctiva and the cornea under the action of ocular tissue damage or sensory factors, and the antibodies occur, but not really " Autologous "immunization" is a spontaneous autoimmune. The pathological process of ulcer development is autoimmune dissolution from the corneal epithelium, which in turn releases collagenase, which aggravates the dissolution and destruction of collagen in the corneal lamellar layer.

Rahi (1976) suggested that the immune phenomenon in Mooren's corneal ulcer depends on the activity of the complement system, and there is C3 in the living tissue specimen, so this immune response should be attributed to complement-dependent allergy (type II allergy).

Morphological ulcer of the cornea is a progressive necrotizing lesion of the cornea, often accompanied by chronic inflammatory changes. Ulcer and tissue necrosis are often confined to the first half of the cornea, and the slow progress of the ulcer coincides with the repair process of the tissue. Characteristic histopathological changes are formed.

Histopathological findings, the main cause of ulceration is leukocyte infiltration, most of which are lymphocytes, a few cells and polynuclear leukocytes, occasionally eosinophils, where the cornea is thickened, epithelial swelling and hyperplasia, collagen fiber necrosis, ulcer overhang The anterior corneal elastic membrane is intact, and the anterior 1/3 or 1/2 of the cornea in the ulcer area is missing from the anterior elastic membrane.

In the healing ulcer area, the frontal elastic membrane is destroyed, and the first 1/3 to 1/2 of the corneal stroma is lost due to necrosis. It is filled by most vascularized tissues. Lymphocytes are aggregated in the early stage around the blood vessels, and replaced by fibers at the later stage. Irregular The bottom surface is covered with thickened epithelial cells (7-10 layers), and underneath it is a layer of non-thin scar tissue. Under the light microscope, a large number of lymphocytes, a few plasma cells, and occasionally giant cells are visible in this area.

The deep stromal layer is almost normal, and the posterior elastic membrane and endothelium are intact.

The conjunctival subepithelial tissue adjacent to the ulcer area is filled with plasma cells, occasionally multinucleated cells and monocytes, round cell infiltration around the upper scleral blood vessels, partial granulation tissue proliferation and scleral tissue defects.

Cell infiltration is dense with conjunctival gallbladder adjacent to the ulcerated area, and gradually sparse toward the center of the cornea and the periphery of the bulbar conjunctiva.

Under electron microscopy, vacuoles appear in the nucleus of conjunctival epithelial cells in some lesions. There are many rod-like and racquet-like Birbeck's particles in the epithelial cell space. In some cases, plasmacytoid cells (Russell body) can also be found.

In recent years, immunopathological studies of mooring corneal ulcers have shown that immunoglobulin content is increased and IgG is generally increased in lesions and conjunctival living tissue specimens. Brown et al. (1976) found that there is immunity in conjunctival subepithelial and epithelial tissues during active ulceration. Globulin (IgG, IgM) and complement (C3) are present in combination, and circulating antibodies in the conjunctiva and corneal epithelium are confirmed by indirect immunofluorescence techniques.

The above-mentioned histopathological and immunopathological findings indicate that the Mooren's corneal ulcer meets the pathological changes of autoimmune or cross-immune reaction caused by viral infection and the pathological changes of chronic inflammatory necrosis.

Moxibustion corneal ulcer prevention

The disease is an intractable corneal edge ulcer with unknown etiology. Various treatments can not completely prevent recurrence. Benign or mild cases should be treated with drugs first. Surgical treatment should be considered when progressing or disease progression. People should be treated in daily life. Pay attention to labor protection. In case of eye trauma, you must go to the hospital immediately and be treated by professionals. Also, avoid using unpleasant eye drops such as dioxin, dicaine, cortisone, or even sulfonamide, penicillin or fluorescein. In the case of corneal damage, eye drops after several days of storage are used, and special fluorescein liquid examination is dangerous.

Complications of Mooren's corneal ulcer Complications herpes simplex iridocyclitis

The deeper the corneal ulcer, the more severe the symptoms and complications. When the corneal ulcers heal, corneal scars are formed, which leads to corneal opacity, which leads to vision loss. Irritation may occur in corneal ulcers, iritis, iridocyclitis, corneal perforation. With iris prolapse, anterior chamber empyema, total ocular inflammation, and even destruction of eyeballs and other complications, corneal ulcer caused by fungi is painless but serious, and corneal ulcer caused by Pseudomonas aeruginosa is particularly ferocious, herpes simplex keratitis Corneal ulcers are particularly difficult to treat, and corneal ulcers should be urgent and need to be treated by an ophthalmologist.

Moxibustion corneal ulcer symptoms common symptoms tearing corneal ulcer photophobia granuloma eye congestion corneal erosion eye pain

According to the history of chronic progressive development, the typical ulcer lesion image, clinical diagnosis is not difficult, but in the early stage of the disease with simple marginal corneal ulcer, corneal limb degeneration, Wegener's granulomatosis, nodular polyarteritis Or the keratotic inflammatory ulcer associated with lupus erythematosus is differentiated from granuloma.

Inflammation or ulceration caused by degeneration of the cornea edge, the symptoms are light, the development is slow, the edge is not sneaked, the epithelium of the degeneration area is intact, and the elastic membrane is prone to bulging due to degeneration, which occurs in the upper edge of the cornea.

The lesion of Wegener's granuloma is biased toward the scleral side. The sclera of the sclera is granuloma, and the thicker blood vessels extend into the lesion along the corneoscleral margin. The ulcer is furrow-like and has no potential for excavation.

Moss-eroding corneal ulcers occur all over the world, and the incidence of colored people is slightly higher. Black people are significantly higher than whites. It has also been reported in China, accounting for 0.03% of ophthalmological cases.

All ages can be affected, blacks in the tropics are younger, and more common in young adults or middle-aged. China often occurs in the elderly and the elderly, and there are also young and middle-aged people. The minimum age of onset is 3 to 5 years old. There is a slightly more male incidence, and the ratio of male to female patients is about 3:2.

Most of them are monocular, and some cases occur simultaneously in both cases. Many cases involve another eye after a few years of illness. Foreign data reports that the incidence of both eyes is about 25%, and domestic reports are 8-40%.

The course of the disease often develops, starting from the corneal margin of the cleft palate, which develops into a marginal ulcer by shallow gray infiltration and gradually spreads to the central part of the cornea. The early stage of ulcer is not easy to distinguish from simple marginal corneal ulcer. After 2 to 3 weeks, the edge of the ulcer appeared in the sulcus and furrow of the sulcus, and the mooring was present. In a few cases, the ulceration occurred due to the progressive development of the cornea. The depth of ulcer erosion accounted for the stromal layer. 1/2, often does not develop to the deep part of the post-elastic film bulging or perforation is rare.

As the edge of the scabbard ulcer advances, the remaining ulcerated base is gradually covered by the neovascular tissue and epithelium from the limbus. The surface is uneven, slightly bite-shaped, with granulation tissue bulging and scattered infiltration small lesions. The case was scar-like, and there was a gray-white infiltrating line at the edge of the ulcer. The unaffected cornea remained intact and transparent, and the ulcer continued, which was not easily controlled by the drug, and eventually eroded the entire cornea and caused blindness. The whole course can reach 3 to 9 months.

Under the slit lamp, the above-mentioned lesion process is more clearly visible. Except for hundreds of secondary infections, it is generally not accompanied by anterior chamber empyema, usually without atrial water flash and iris inflammatory reaction.

From the beginning of the lesion, it is characterized by severe primary symptoms, severe pain, photophobia, tearing, pain often radiated along the trigeminal eye branch area, local anesthetics and oral painkillers are not easy to relieve symptoms, severe primary symptoms often It is not commensurate with the mild degree of congestion around the cornea.

Clinically, some people have prescribed Mooren's ulcers in two different types:

1. Malignant type: more common in young patients, the incidence of both eyes, the lesions are persistent and persistent, the main symptoms are heavy, the ulcer progresses quickly, often involving the sclera, the incidence of perforation is high, and the prognosis is poor.

2, benign type: more common in elderly patients, monocular onset, the course of disease is relatively slow, after a certain surgical treatment (such as conjunctival resection or lamellar keratoplasty) can often control the progression of the disease, the prognosis is relatively good.

Examination of mooring corneal ulcer

The ulcer is a typical furrow or silkworm type, which undergoes edge infiltration, bulging, deep ulcers and about one-half of the thickness of the anterior matrix. Sometimes it can be worn into the posterior elastic layer, and the ulcer can be extended in the center and both ends of the cornea. At the same time, the bottom is covered by epithelial repair and neovascularization. Although corneal perforation is rare, the disease progresses slowly and stubbornly. It is characterized by peripheral corneal periplasmic dissolution, leaving only the central cornea to eventually erode the entire cornea.

Pathological examination: a large number of lymphocytes and plasma cells were found in the hypertrophic conjunctiva of the lesion area and adjacent sclera; IgG, IgM, complement C and circulating antibodies were found in the conjunctival epithelial cell space and cytoplasm.

Diagnosis and differential diagnosis of mooring corneal ulcer

diagnosis

Diagnosis can be performed based on clinical performance and laboratory tests.

Differential diagnosis

Identification of ulcers with Pseudomonas aeruginosa corneal ulcers, bacterial corneal ulcers, and other ocular lesions.

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