Tuberculous scleritis

Introduction to tuberculous scleritis Tuberculosis is an ancient infectious disease, and tuberculosis has been found in human bones during the Neolithic period. This has a more detailed clinical description in 460 BC. China's book in the Spring and Autumn Period and the Warring States Period's masterpiece "The Yellow Emperor's Internal Classic" has a detailed record. In 1882, Koch discovered M. tuberculosis, which provides a reliable basis for the diagnosis, treatment and prevention of tuberculosis. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: body fluid transmission Complications: swelling optic disc edema macular cystic edema choroiditis optic discitis retinal detachment acute angle-closure glaucoma cystoid edema

Causes of tuberculous scleritis

Causes:

Mycobacterium tuberculosis belongs to mycobacteria and is a specialized intracellular parasite. It has the same characteristics and dyeing characteristics as other mycobacteria. It is mainly divided into human, bovine, bird, and mouse. It is most common in human diseases.

Pathogenesis:

The most frequently invaded part of Mycobacterium tuberculosis is the tip of the lung, but the lower lobe and any other area can be affected. Most cases are active tuberculosis obtained several months or a year ago, instead of reinfection or the first infection of Mycobacterium tuberculosis. Infection, the basic changes of tuberculosis infection are allergic reactions, exudation reactions and proliferative reactions. Due to the strength of the body's resistance and the degree of allergies, the disease progresses to both improvement and deterioration. The improvement is the absorption of the lesions, and even Complete disappearance and induration and calcification, the deterioration manifests as the infiltration progression and dissolution and spread of the lesion. Tuberculosis can spread to distant organs, such as through lymph or blood to the eye, producing scleritis or scleral inflammation, tuberculous sclera Inflammation can be caused by direct infection of the sclera by Mycobacterium tuberculosis or by an immune response to tuberculoprotein.

Tuberculous scleritis prevention

BCG vaccination: tuberculosis is a chronic consumptive infectious disease caused by Mycobacterium tuberculosis. The treatment should be based on the whole. The use of anti-tuberculosis drugs must increase the body's resistance and strengthen nutrition. It can replenish patients with sufficient heat and nutrients to meet the needs of tuberculosis repair. Enhance the body's resistance.

In addition, you need to add enough vitamins, vitamin A to enhance the body's immunity, vitamin D to promote calcium absorption, vitamin C is conducive to the healing of the lesion and hemoglobin synthesis, B vitamins have the effect of improving appetite. Fresh vegetables and fruits are also the main source of vitamins. In addition, foods such as milk, eggs, and internal organs are rich in vitamin A, and peanuts, beans, and lean meat are rich in vitamin B.

Tuberculous scleritis complications Complications, swollen optic disc edema, cystoid macular edema, choroiditis, optic discitis, retinal detachment, acute angle-closure glaucoma, macular cystic edema

Fundus manifestations of tuberculous scleritis:

1 subretinal mass: limited to the scleral swelling area, the boundary is clear, can cause choroidal uplift, the color of the mass is orange-red like the adjacent normal retinal epithelium, the choroidal blood vessels at the mass are normal, with a normal checkerboard appearance, the mass is often concentric choroid Wrinkles or retinal stripes surround, and some of the masses may have diffuse local yellow-white spots on the surface.

2 choroidal wrinkles or retinal streaks: manifested as a line-like change between the light and dark of the posterior pole, more common in the temporal side, rarely beyond the equator, often horizontally surrounding the subretinal mass, or vertically aligned, or oblique Or irregular arrangement, may be caused by thickening of the scleral choroid, resulting in the swelling of the Bruch membrane and retinal pigment epithelium.

3 optic disc edema, cystoid macular edema: sclera and choroidal inflammation can cause optic discitis, especially posterior scleritis adjacent to the optic nerve is easy to cause optic disc edema, optic discitis, similarly, scleral and choroidal inflammation spread to the retina, can cause macular cystic Edema, this patient usually does not have exudative retinal detachment.

4 annular choroidal detachment and retinal detachment: posterior scleritis invades the choroid causing fluid exudation, ring choroidal detachment and/or multiple retinal pigment epithelial detachment, and/or exudative retinal detachment, ring choroidal detachment , can make the iris-crystal lens advance, block the angle of the anterior chamber, cause acute angle-closure glaucoma, choroiditis can cause multiple retinal pigment epithelial detachment or damage the cells of the retinal pigment epithelium, resulting in exudative retinal detachment When the posterior pole is located, the macula is detached or confined to the periphery and is spherical, forming a vesicular retinal detachment.

Tuberculous sclera symptoms common symptoms tears nodules repeated bleeding high intraocular pressure uveitis sclerosing keratitis herpes scleral edema eye pain

Tuberculosis can involve all ocular tissues except the lens. The incidence of ocular tuberculosis is 0.5% to 1.4%. Eyelids, conjunctiva, and lacrimal vessels can be infected by Mycobacterium tuberculosis to form primary tumors, but rare, generally secondary. In tuberculous lesions in other parts of the body, the tissue reaction after ocular infection is divided into two types of hypertrophic and exudative. The two types of different reactions are related to whether the body has had tuberculosis infection. Among the cases in which no infection has occurred, mainly Chronic progressive inflammation, which is mainly caused by proliferative reactions, has been infected with tuberculosis or its toxic protein. If re-infected, it causes acute non-specific exudative inflammation. The degree of tissue damage produced during development is related to the number of tuberculosis, virulence and immune status of tissues and body resistance.

Eyelid tuberculosis is caused by direct infection of eyelid skin damage or dissemination of tuberculosis lesions in the body. It begins with sclerosing nodules of varying sizes, and later undergoes cheese-like changes, surface ulceration and perforation, formation of fistulas, prolonged healing, ulcers After healing, scar formation and valgus are formed. Conjunctival tuberculosis is more common in young women. Monocular, manifested as tuberculosis, tuberculous lupus, herpetic tuberculous keratitis, etc., early symptoms are mild, only eye discomfort, when the condition is aggravated Conjunctival hyperemia, photophobia, tearing, etc., corneal tuberculosis is more common in young women, easy to relapse, and more secondary to adjacent tissues, clinical manifestations similar to tuberculous corneal ulcers of lame corneal ulcer, stromal keratitis, vesicular keratitis, Deep central keratitis, tuberculous uveitis is one of endogenous uveitis, manifested as tuberculous anterior uveitis, tuberculous choroiditis, chronic tuberculous uveitis, etc., most of the retinal tuberculosis due to other parts of the body Mycobacterium tuberculosis in tuberculosis is transmitted to the retina through blood circulation or spread to the retina in adjacent tissues. Males are more common, mainly manifested as tuberculosis Tuberculous retinitis and retinal vein inflammation, if repeated bleeding, can lead to proliferative vitreoretinopathy or secondary retinal detachment, tuberculous tuberculous tuberculous periostitis is more common, local skin ulcers, bone destruction, The fistula is formed, and the skin and the periosteum are adhered.

Scleritis

The incidence of tuberculosis in patients with scleritis is 1.92%. Tuberculosis that spreads from the tuberculosis to the blood directly invades the sclera or local infection caused by direct damage or adjacent tissues such as cornea, conjunctiva or iris lesions cause scleritis.

2. Nodular anterior scleritis

Early stage of nodular anterior scleritis, symptoms include: almost all patients have red eyes, tears, photophobia, conjunctival sac secretions, 60% of patients have severe eye pain, pain radiates along the branches of the trigeminal nerve, patients often suffer from pain Can not fall asleep, and have varying degrees of visual decline, the main signs are deep sclera localized inflammatory nodules, purple red, can not push, and the pain refused to press, the nodule and its superficial tissue boundary clear, nodules to the conjunctiva and its The blood vessels and nodules may be single or multiple, and the infiltrating nodules may also be spread around the limbus to form a circular scleritis. The scleral blood vessels have no mobility, the surface blood vessels are twisted, expanded and nodules are jacked up.

3. Necrotizing anterior scleritis

If the treatment is not timely, nodular anterior scleritis can develop into necrotizing anterior scleritis, which is extremely destructive, and the eye pain is intensified. Most patients have obvious vision loss, 60% of patients have complications, and the lesion begins sclera. It is characterized by localized inflammatory infiltration. The most characteristic manifestation is the localized flaky avascular area of the sclera. The lesion can be further limited to a large area of necrosis, which can damage all the front sclera, scleral edema around the lesion, and superficial sclera. Vascular tortuosity, dilatation, displacement, lesions after treatment subsided thin, transparent, uveal exposure, unless high intraocular pressure for a long time, generally does not form grape swelling.

4. Posterior scleritis

Tuberculous posterior scleritis is one of the most easily diagnosed diseases in ophthalmology. It is more common in women. The incidence of posterior scleritis accounts for 2% to 12% of scleritis. Because of the involvement of anterior scleritis, posterior scleritis is easily ignored. The eyeball that has suffered from primary posterior scleritis or anterior scleritis extends 43% to 62%, and 1/2 of the anterior and posterior scleritis.

The most common symptoms of posterior scleritis are redness, pain, and loss of vision, but many people have no symptoms, or only one of these symptoms. In the early stages of the disease, persistent eye pain is a valuable measure before vision impairment. Symptoms, pain and severity, some very light, some extreme pain, often proportional to the degree of scleral involvement, may complain of eye pain itself, but more unique is the pain involved in the eyebrows, ankle and humerus, vision loss Sometimes it is the only important manifestation. The most common causes are exudative retinal detachment, macular degeneration caused by scleral mass, cystoid macular edema and optic neuritis. In some patients, visual fatigue caused by myopia reduction or hyperopia is due to sclera. Diffuse thickening leads to shortening of the eye axis.

The main signs of posterior scleritis are: superficial scleral vasodilatation of the ankle is the manifestation of the anterior sclera. In severe cases, there are prominent eyes, ptosis of the upper eyelid and edema of the eyelids. The inflammation often spreads to the extraocular muscles and eyelids, which can produce eyeball rotation. Pain, limited eye movement and diplopia are caused by inflammation of the extraocular muscles. These comorbidities are called periscleritis, scleral tenonitis, and acute anterior orbital inflammatory pseudotumor.

5. Scleral outer inflammation

Mycobacterium tuberculosis can invade the superficial sclera, leading to simple scleral inflammation or nodular scleral inflammation. The scleral outer layer is suddenly onset, red eyes, lighter pain, occasional photophobia, tearing, and unaffected vision. The common point of simple or nodular scleral inflammation is that the edema or infiltration is all located in the superficial sclera; the sclera itself is not involved, the superficial plexus of the superficial sclera is congested, and the deep vascular plexus is very light. The blood vessels of the conjunctiva also have a certain degree of hyperemia. The superficial sclera of the sclera has obvious hyperemia of the superficial sclera. The superficial sclera of the sclera remains radial, but the blood color is from reddish to flaming, but not Fuchsia, depth of edema and changes in vascular plexus, easily identified by narrow light of slit lamp, 69% of lesions are limited to one quadrant, 31% of patients with wide range, 1/3 of patients with eyeball tenderness, nodular sclera The outer layer of inflammation and infiltration is limited. The nodule is located in the superficial sclera. It is surrounded by congestion and can move on the sclera. The sclera is not affected by edema. The scleral plexus is deep in the nodule. The department is clearly visible and maintains a normal state. The nodules are mostly single-shot, round or elliptical, with a diameter of 2 to 3 mm. 40% of the patients have tenderness in the eyeball.

6. Immune-mediated scleritis

Immune-mediated tuberculous scleritis, often accompanied by stromal or vesicular keratitis or keratoconjunctivitis, caused by a series of immune responses to the cell wall protein component of Mycobacterium tuberculosis, occasionally Scleral epithelial inflammation occurs, and the pathogenesis is related to type IV immune response, which is highly sensitive to these antigens. Immune-mediated tuberculous scleritis is often associated with systemic active tuberculosis, and histomorphology of scleral slices shows no activity against acid-fast bacilli. Sexual granuloma, tuberculous stromal keratitis (tuberculous interstitial keratitis) unilateral, fan-shaped development to the margin, affecting only the superficial and middle stromal tissue, manifested as nodular infiltration of superficial neovascularization, clinical time, leaving The scar of the cornea is different from the luetic interstitial keratitis that invades the deep matrix. Phluctenular keratoconjunctivitis can develop into a vesicle of the limbar conjunctiva and cornea, which evolves into a nodule. Denatured and healed, corneal vesicles expand toward the center, creating scars and new blood vessels Characterized in unrestricted mesh structure, from the center to the edge gradually heal without scarring conjunctiva vesicles heal.

Tuberculous scleritis examination

Pathogen examination

There are several innovative ways to quickly diagnose tuberculosis, the most promising of which is:

1 Using an enzyme-linked immunosorbent assay (ELISA) to detect specific antigens with antibody-sensitive particles.

2 using a probe and polymerase chain reaction (PCR).

3 The presence of tuberculous stearic acid was confirmed by chromatography and chromatography. This method is especially useful for the detection of liquids such as cerebrospinal fluid (CSF).

2. Pathological examination

Scleral sections are characterized by multinucleated giant cells and cheese-like granuloma characterized by acid-fast bacilli.

3. Ultrasound scan

B superficial visible posterior sclera thickening, bulging, protruding into the vitreous cavity and post-balloon edema; can be seen due to posterior scleritis caused by chorioretinal detachment, posterior edema around the optic nerve can be seen "T" shape signs, A super shows the eye wall The back is thickened and the high-quality "ear" echo is expressed.

4.CT, MRI examination

CT scan showed thickening of the posterior eye ring, also showed thickening of the optic nerve and the eyeball junction, eyeball protrusion, edema after the ball was visible at the same time, the injection enhancer can make the image clearer, MRI scan also shows the posterior eye wall thickening, With long T1 and T2 signals, enhanced scanning can be enhanced. The weight of the image signal can distinguish the choroid and retina, which is valuable for the diagnosis of post-sclera.

5. FFA can show retinal pigment epithelial detachment, exudative retinal detachment, optic disc edema, cystoid macular edema, early appearance of mottled choroidal background fluorescence in exudative retinal detachment, diffuse multiple apex glare in the middle Area, late retinal fluid color development, choroidal folds appear as fringes in the fluorescent and weakly fluorescent regions, retinal streaks can not show fluorescence, FFA of posterior scleritis is non-specific.

Diagnosis and diagnosis of tuberculous scleritis

Tuberculosis can be diagnosed by Ziehl-Neelsen staining of sputum, urine, ocular tissue and other body fluids and acid-fast bacilli and Löwenstein-Jensen culture at 37 °C to find the Mycobacterium tuberculosis. Intradermal test and chest X-ray are helpful for diagnosis. It takes only a few weeks to be positive, as long as the acid-fast bacilli are found in the eye tissue and sputum to make a speculative diagnosis of systemic tuberculosis, if necessary, for diagnostic treatment, Jackson's protocol is ethylamine butanol 400mg, 2 times / d; Isoniazid 300mg, 1 time / d; rifampicin 600mg, 1 time / d or vitamin B6 (pyridoxine) 50mg, 1 time / d, treatment for 6 months, if symptoms and signs improve, can make a diagnosis, tuberculous sclera The diagnosis of inflammation requires biopsy, and acid-fast bacilli are found in the scleral tissue, but sputum and other body fluids are not characteristic of localized tuberculosis. Most of the diagnosis of immune-mediated tuberculous scleritis is difficult or impossible to diagnose, depending on the accompanying The ocular manifestations were positive by positive PPD, chest X-ray and sputum culture, to determine past or existing systemic tuberculosis.

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