Stromal keratitis

Introduction to corneal stroma Corneal stroma inflammation or interstitial keratitis (interstitial keratitis), also known as non-ulcerative keratitis, is synonymous, meaning non-ulcerative and non-suppurative inflammation in the corneal stroma, mainly as Corneal stromal cells exudate, infiltrate, and often accompanied by deep vascularization, and the corneal epithelium and shallow stromal layers are generally unaffected. basic knowledge The proportion of illness: 0.006%-0.009% Susceptible people: no special people Mode of infection: non-infectious Complications: retinitis optic atrophy deafness

Cause of corneal stroma

(1) Causes of the disease

Keratitis may be associated with bacterial, viral, and parasitic infections. Treponema pallidum, leprosy, tuberculosis, and herpes simplex virus infections are common causes, although pathogenic microorganisms can directly invade the corneal stroma, but most corneal lesions are associated with infection. It is related to the immunoreactive inflammation caused by the original.

Treponema pallidum is the causative agent of syphilis. The spirochete is snail-like, less than 0.2m in diameter and 5-10m in length. It is difficult to culture in vitro and can only be cultured in experimental animals. It is divided into congenital and acquired according to different infection routes. Two kinds of congenital syphilis are directly inoculated into the newborn through the placenta or delivery, and the acquired syphilis is derived from the mucosal contact infection of the active diarrhea.

Mycobacterium tuberculosis is a less common cause of corneal stroma inflammation. Tuberculosis protein is a component of the cell wall and provides an antigenic stimulating substance for immune response. M. leprae and tuberculosis are both acid-fast bacilli. In the United States, leprosy is very rare. Most provinces have been rare in recent years.

(two) pathogenesis

The pathogenesis of the disease is recognized as the host's immune response to the infectious agent, rather than the direct result of pathogenic infection, which is a type IV (late type) allergy.

Corneal stroma inflammation prevention

There is no effective preventive measure for this disease. Early detection and early diagnosis are the key to the prevention and treatment of this disease.

Corneal stroma inflammation Complications retinitis optic atrophy deafness

Choroidal retinitis, optic atrophy, deafness, etc.

Symptoms of corneal stroma Symptoms common symptoms of lacrimal keratitis, corneal opacity, and triad nodules, the size of the cornea varies...

1. General clinical signs: pain in the eyes, tearing and photophobia, accompanied by watery secretions and eyelids, mild to severe visual acuity, ciliary congestion and so on.

2. Corneal lesions: Depending on the stage and duration of the disease, in general, the epithelium is intact but often in an edema state. In the early stage, there may be diffuse or fan-shaped, low-level matrix infiltration, and endothelial layer With or without KP, with the aggravation of stromal layer inflammation, edema of the stromal layer and epithelial layer is intensified, often with a ground-glass appearance, anterior chamber reaction can also be aggravated, patients' symptoms are also aggravated, and new blood vessels often invade the stromal layer. .

Depending on the severity, the entire lesion may be confined to the periphery of the cornea, or it may spread to the entire cornea. If it is not treated after weeks or even months, the inflammation and vascularization of the matrix will reach a peak and then subside, gradually The blood vessels are occluded and the cornea forms a permanent scar.

3. Specific signs

(1) syphilitic keratitis can be divided into three phases:

1 infiltration period.

2 angiogenesis.

3 regression period.

The first significant sign of active syphilitic stromitis is mild stromal edema, a small amount of endothelial KP, severe pain, clear and transparent secretions, and photophobia, indicating the onset of inflammatory infiltration.

Typical stromal layer inflammation often starts from the periphery and is fan-shaped at the top. The sparse, gray-white matrix layer is infiltrated and fused. In this stage, epithelial edema and small blister formation may occur. This process may be limited to a certain part of the cornea. Or the whole cornea becomes turbid, showing a typical ground-glass appearance. During the neovascular phase, the infiltration becomes more dense, and the blood vessels invade the deep stromal layer from the peripheral part. The endovascular growth and inflammation may be limited to a fan shape in the peripheral part, or in a few weeks. Even a few months later, the central corneal invasion of the entire cornea, in red tones, called Hutchinson orange erythema.

Once the entire cornea is vascularized, the course may have reached its peak, indicating that it will enter the absorption phase. After 1 to 2 years, if it is not treated, the inflammation will begin to subside, the peripheral part will begin to become transparent, the corneal vessels will be occluded, the corneal scar will persist, and the endothelial cell layer will continue. The posterior elastic layer may have persistent wrinkles, sputum sputum, posterior corneal sputum, and fiber bundles that can continue into the anterior chamber. This phenomenon is usually only seen during the stationary phase of the lesion.

Congenital syphilitic keratitis usually involves bilateral corneas. More than 75% of patients begin to develop in the second eye within 1 year. About 9% of patients have recurrence of inflammation. Acquired keratitis usually has a milder onset. Limitations.

In addition, congenital syphilitic keratitis, often with other typical features of congenital syphilis, namely Hutchison teeth and hearing (or deafness) together with corneal stroma, called the Hutchinson triad.

(2) Mycobacterium tuberculosis is rarely associated with corneal stroma inflammation. However, the possibility of this bacterial infection should be ruled out. This stromal keratitis tends to the peripheral part and is often fan-shaped and associated with scalloped scleritis, unlike syphilis. In keratitis, the inflammation of this keratitis affects the anterior stromal layer, with dense infiltrates predominating, sometimes nodular, abscess-like infiltration, and vascularization usually limited to the anterior stromal layer; however, the vascular diameter is usually large. It is curved, the disease course is prolonged, and the residual corneal scar is thicker because the severe inflammatory reaction leads to more serious corneal cell necrosis.

(3) Leprosy involves the cornea in a variety of ways. Corneal dysfunction or changes in the structure of the eyelids lead to corneal exposure. Surface avascular keratitis is a characteristic lesion of leprosy, usually starting from the supraorbital quadrant. The dispersed epithelial turbidity or turbidity of the anterior stromal layer is later fused into a diffuse anterior stromal layer turbidity, and finally the vascular invasion and extension to the corneal opacity area, forming a characteristic leprosy vasospasm.

Examination of corneal stroma

Mainly for the experimental examination of syphilis and tuberculosis, such as the complement fixation test and precipitation test of syphilis hematology test and tuberculosis test.

Corneal microscopy revealed localized or diffuse lymphocytic infiltration in the corneal stroma, and pathological examination of skin nodules in leprosy patients to confirm the diagnosis.

Diagnosis and differentiation of keratitis

Diagnose based on

1. More common in young patients, both eyes are sick and easy to relapse.

2. Other signs of congenital syphilis, such as saddle nose, Hekinson's teeth, etc., blood Kang-Fahrenheit reaction is mostly positive.

3. Corneal opacity and edema, deep blood vessels invade.

Differential diagnosis

1. Acute syphilitic keratitis is one of the late manifestations of congenital syphilis, most of which occurs in 5 to 20 years old, but can also be as early as birth, as late as 50 years old, syphilis serological test positive, eye signs including "Pepper salt"-like chorioretinitis or optic atrophy, accompanied by other advanced symptoms of congenital syphilis, suggest the presence of this disease, some other advanced syphilis manifestations, including Hutchinson's teeth and bone deformities, VIII Cerebral nerve involvement leads to deafness, mental retardation and behavioral abnormalities.

A history of sexually transmitted diseases, central nervous system symptoms or cardiovascular involvement, plus a positive serological test for syphilis can confirm the diagnosis of acquired syphilis.

Commonly used syphilis serological tests are complement fixation tests (such as the Wasserman test) and precipitation tests (such as the Kahn test). These tests are important for the diagnosis of various stages of syphilis, the judgment of therapeutic effects, and the discovery of recessive syphilis.

2. The etiology of tuberculous keratitis is determined by the eye, the serological serological test results are negative, the tuberculin test is positive, and the history of systemic tuberculosis infection.

3. The etiology of leprosy keratitis is difficult for ophthalmologists to make a new diagnosis. According to the assistance of a dermatologist, the face has a typical "lion-like face", thickening of the eyelid skin, acne, facial nerve palsy is a common late stage. Symptoms can form rabbit eyes and valgus valgus, corneal nerve can be segmental thickening, forming a "bead" shape, small stone-like milky white nodules can appear on the surface of the iris, and the scleral side of the sclera at the cleft palate A yellow gel-like nodule and a shallow vasospasm on the temporal side of the cornea can be used to determine the diagnosis.

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