scleritis
Introduction
Introduction to scleritis Scleritis is a scleral infection characterized by redness and decreased vision as the initial symptom and severe eye pain. Also known as deep scleritis. It is rarer than superficial scleritis. Acute onset, often accompanied by cornea and uveitis, poor prognosis. According to the location of the disease can be divided into anterior scleritis and posterior scleritis. More common in women, both eyes can occur simultaneously or simultaneously. Mainly caused by endogenous antigen-antibody immune complexes, commonly found in connective tissue diseases such as rheumatoid arthritis, Wegener granulomatosis, recurrent polychondritis, systemic lupus erythematosus, Reiter disease, etc., also seen in herpes zoster After viral infection, syphilis, gout or eye surgery. basic knowledge The proportion of illness: 0.1%-0.3% Susceptible people: good for women Mode of infection: non-infectious Complications: corneal disease, cataract, glaucoma
Cause
Cause of scleritis
Wegener granuloma (30%):
Its pathology is characterized by inflammation of the blood vessel wall, mainly invading the upper and lower respiratory tract and the kidney, usually starting with focal granulomatous inflammation of the nasal mucosa and lung tissue, and then progressing to diffuse necrotizing granulomatous inflammation of the blood vessel. . Clinical manifestations of nasal and paranasal sinusitis, lung disease and progressive renal failure.
Recurrent polychondritis (35%):
Progressive inflammatory destructive lesions with recurrent and remission, involving cartilage and other systemic connective tissues, including the ear, nose, eyes, joints, respiratory tract, and cardiovascular system. Clinical manifestations include ear, nose, and respiratory chondritis, accompanied by symptoms of organ involvement in the eyes, vestibules, and the like.
Herpes zoster (25%):
Chickenpox occurs when a virus-free child is infected. Some patients become infected with a virus without symptoms. Because the virus is neurotropic, it can be lurking in the neurons of the posterior root ganglia of the spinal cord for a long time after infection. When the resistance is low or tired, infected, or caught, the virus can grow and reproduce and move along the nerve fibers to the skin. Causes intense inflammation of the affected nerves and skin.
Prevention
Scleritis prevention
This disease is often a concomitant disease of some systemic diseases. Once it occurs, it should actively find the relevant primary disease and treat the primary disease to effectively control the disease.
Complication
Scleritis complications Complications keratopathy cataract glaucoma
Scleritis has more ocular complication, and it is more common in the late stage of inflammation. The comorbidity depends on the severity and nature of inflammation. The surface scleritis accounts for about 15%, and the scleritis is higher than 57%, especially in the severe necrotizing sclera. Inflammation, in the spread of inflammation and secondary endophthalmitis, the comorbidities include various keratitis or keratopathy, cataract, uveitis, glaucoma and scleral thinning (defect).
(a) sclerosing keratitis
Sclerosing keratitis, also known as esclero-perikeratitis, is mostly female, older, often affected by both eyes, recurrent, causing the entire cornea to be affected and complicated by the iris ciliary body Inflammation or glaucoma, leading to serious consequences.
The lesion is characterized by edema and invasive changes in the scleral tissue surrounding the limbus, and forms a dense angiogenesis phenomenon. The corneal margin is immersed in the deep tissue of the cornea, causing corneal opacity, which often occurs in the limbus of the cornea, but it can also Occurred in the central or parenchymal layer of the cornea, and not associated with the lesion of the sclera, corneal opacity began to appear gray or grayish yellow, then turned white, typically tongue or triangle, tip to the center of the cornea, and common in the corneal stroma The layer is turbid and turbid in the layer, and the appearance is like ceramic. Once this turbidity appears, it will never disappear. In severe cases, turbidity can gradually develop into a ring shape, leaving only a transparent area in the center of the cornea, and even the central transparent area disappears. It is completely turbid and forms a so-called "sclerosing cornea". In some cases, it develops into a limbal ulcer of the cornea during the course of the disease.
The so-called "sclerosing cornea" means that the corneal tissue of the lesion becomes a ceramic-like appearance and resembles a sclera, and there is no pathological change of sclerosing.
(B) corneal dissolution or stratum corneum separation (keratolysis)
The disease is characterized by the presence of severe necrotizing scleritis or perforated scleral softening, the original transparent corneal surface, separation of the stratum corneum, dissolution and shedding, sometimes falling off a few millimeters, in severe cases, the posterior elastic layer bulging thin It can be broken at one touch, and tissue dissolution and shedding can occur in the sclera of the lesion. For this dissolution, treatment with corticosteroids can prevent its development, indicating that inhibition of collagen activity also inhibits the disease.
(c) scleral defect
Only in the most severe cases of scleral necrosis, if necrotizing scleritis is associated with inflammation, the upper scleral blood vessels disappear, and the underlying scleral tissue becomes non-perfused, eventually becoming necrotic tissue, and cases of perforating scleral softening can be Tissue necrosis occurs without any aura, and once the necrosis occurs, the sclera becomes thin and transparent, and perforation occurs.
(four) uveitis
According to the statistics of most scholars, about 35% of patients with scleral disease are complicated by uveitis and retinitis. For patients with anterior and posterior uveitis, they should be highly alert to whether there is scleritis and vice versa. Concurrent uveitis is fierce and often involves retinal detachment. It has also been reported that there are inflammatory cells in the anterior chamber and vitreous. Wilhelmus has histologically found inflammation of the choroidal capillaries; central retinal artery and its small arteries, and posterior ciliary There is a sleeve-like infiltration around the blood vessels.
(5) Glaucoma
In all stages of scleritis, elevated intraocular pressure can occur. The reasons are as follows: (1) ciliary choroidal exudation leads to iris-lens separation, which causes the angle of the anterior chamber to close and acute angle-closure glaucoma; 2 inflammatory cell infiltration in the anterior chamber Beam net and corner; 3 surface scleral blood vessels around the sleeve sleeve infiltration, causing scleral venous pressure rise; 4Sehlemm tube surrounding lymphocytes sleeve-like infiltration, affecting the rate of aqueous outflow; 5 local, periocular or systemic long-term application of cortex Steroids induce corticosteroid glaucoma.
Symptom
Scleral inflammation symptoms Common symptoms Eye pain periodic episodes of scleral congestion Eye congestion Schistosema edema Morning upper and lower eyelid adhesion Eyeball Highlights Dusk gray nodules Eyeball tenderness ptosis
Scleritis or deep scleritis is rarer than superficial scleritis, but it is acute, and often accompanied by cornea and uveitis, it is more serious than superficial scleritis, poor prognosis, and generally less superficial scleritis Invasion of the sclera, scleritis invades the sclera itself, scleritis occurs in the anterior sclera of the blood vessels through the sclera, and scleritis in the posterior equator, because it can not be seen directly and less blood vessels, the incidence is less, easy Neglected, scleritis can be divided into anterior scleritis and posterior scleritis. anterior scleritis is common in scleritis, mostly in young adults or adults, more women than men, and both eyes can be diagnosed simultaneously or simultaneously.
Scleritis is mainly caused by endogenous antigen-antibody immune complexes, and is often accompanied by systemic collagen disease. Therefore, it belongs to the category of collagen diseases and is related to autoimmunity. Benson (1988) attributed immunogenicity to inflammation directly invading collagen itself. Or scleral matrix (aminodextran), patients with primary necrotizing anterior scleritis may have altered tolerance to scleral-specific antigens, and have delayed-type hypersensitivity to scleral soluble antigen in rheumatoid arthritis The discovery of immune complexes is support for this theory, but most scleritis is difficult to find the cause.
1, anterior scleritis
(1) diffuse anterior scleritis (diffuse anterior scleritis): This disease is the most benign of scleritis, rarely combined with severe systemic diseases.
The clinical symptoms are sudden diffuse hyperemia and swelling of the sclera, and the sclera cannot be ascertained. In severe cases, the conjunctiva can be highly edematous, so it is necessary to drop 1:1000 adrenaline into the conjunctival sac to confirm the presence or absence of deep vascular congestion. Nodules, diffuse more easily than nodular spread, lesions can be limited to one quadrant or occupy the front of the whole eye, and more with scleral epidermitis.
(2) nodular anterior scleritis (nodular anterior scleritis): the clinical symptoms of conscious eye pain is quite intense, and radiated around the eyelids, accounting for half of the patients have eye tenderness, inflammatory nodules are dark red can not move, but The boundary between the scleral tissue and the upper sclera is clear, the surface of the blood vessels is raised by the nodules, the nodules can be single or multiple, and the infiltrating nodules can spread around the cornea to form a circular scleritis. At this time, the whole eyeball is It is dark purple with gray-white nodules. After absorption, it leaves dark and thin. The disease is shorter for weeks or months. The elderly can reach several years. The infiltration is gradually absorbed without rupture. The sclera is thin and dark purple or magnetic. White, due to the inferior eye pressure to form part of scleral bulging or grape swollen, deep scleral congestion of the upper sclera is purple-red, blood vessels can not move, the surface layer and deep scleral vascular network, distortion of the distortion, between the deep blood vessels Large anastomotic branch, thus showing a bead-like expansion and filling of the blood vessels, such as the appearance of shame, tearing, should be considered with keratitis and uveitis, the results often seriously impaired vision
(3) necrotizing anterior scleritis: This disease is also known as inflammatory necrotizing scleritis. This type is rare in clinical practice, but it is the most destructive. It is also a precursor to severe collagen disease. Slow, about half of the patients have complications and decreased vision.
The clinical symptoms are characterized by limited inflammatory infiltration in the early stage of the lesion, sharp hyperemia in the lesion, variceal and obstruction of the vessel, and typical manifestations of a localized flaky avascular region in which the scleral edema is below or near the avascular region. Displacement (this sign is easy to find with no red light), the development of the lesion can be limited to a small range, can also develop into a large area of necrosis, or from the original lesion around the side of the eyeball development, and finally damage the entire front of the eyeball, After the lesion is cured, the sclera continues to thin, and the uveal pigment is blue-violet. Unless the intraocular pressure continues to be as high as 4.0 kPa (30 mmHg), no general swelling is formed. If the necrotic area is small, the new collagen fiber can be used. Repair, if the conjunctiva above it is damaged, it will produce concave scars, and eyeball tenderness accounts for about half.
Ye Linan et al (1980) reported 2 cases of nodular necrotizing scleritis. The sclera had progressive necrotizing yellow nodules with obvious inflammation and severe pain. The sclera was thin blue-violet in the lesion area, and the pathological section was clearly diagnosed. After the general therapy was ineffective, the lesions were resected and lamellar keratoplasty. The results were improved and one case recurred. Li Yingzhan (1980) reported immunosuppressive therapy for 1 case of nodular sclerosing scleritis. The eye is ulcerative, the left eye is nodular, the right eye localized depressed ulcer and the left eye bulging yellow nodule are 4 mm from the limbus. The sclera is purple and hyperemia around the lesion, and the local rejection is suppressed. The agent treats the condition to relieve.
(4) scleromalacia perforans: also known as non-inflammatory necrotic scleritis, is a rare type of special type of scleritis, concealed, almost asymptomatic, about half of patients with rheumatoid arthritis or It is related to ankylosing polyarthritis. The eye disease can precede arthritis. The majority of patients are women over 50 years old. The lesions are bilateral, but their performance is different. The course of disease is slow, but there are also sharp performances. The person who caused blindness during the week.
The disease is rarely accompanied by inflammation or pain response. The lesion is characterized by the presence of yellow or gray spots on the sclera between the limbus and the equator. In the most severe cases, the local sclera gradually becomes carrion-like and falls into necrotic changes. Necrotic tissue can disappear completely after shedding the sclera. The blood vessels in the residual scleral tissue are obviously reduced. It looks white enamel from the outside. About half of the patients have more than one necrotic lesion. The sclera defect caused by necrosis can be layered. It may be covered by very thin connective tissue of the conjunctiva. Unless the intraocular pressure is increased, there is generally no swelling of the gland, and no case of eye tenderness, and one of the corneas is not affected.
There is no tissue regeneration repair in the defect area, which eventually leads to perforation and uveal detachment.
Gong Chunhui (1985) reported 1 case, perforated scleral softening, the patient had a history of arthritis for 5 to 6 years, the left middle finger proximal knuckle soft tissue fusiform swelling, local no redness and tenderness, X-ray film showed no bone sparse And the joint cavity stenosis, etc., the left eye is reddish secondary to corneal opacity, the inner scleral ulcer is purple-blue, the irritation symptoms are not obvious. After 6 months, the sclera is 4×5 mm round from the cornea 5 mm above the end of the medial rectus. Shape ulcers, blue sclera and purple-black choroidal tissue can be seen through the conjunctiva. The cornea festers from the edge of 12 to 5 o'clock, the fundus is normal, and it is repaired by corticosteroid and lamellar keratoplasty.
2, posterior scleritis
Posterior scleritis refers to inflammation that occurs in the posterior equator and around the optic nerve and is severe enough to cause destruction of the posterior lens of the eye. Due to the diversity of the disease and its seldom considered in diagnosis, The disease is not combined with anterior scleritis, and there are no obvious signs in the external eye. Therefore, this disease is one of the most easily treatable diseases in the eye. However, when many eyeballs are removed, the primary posterior sclera is found. Inflammation or anterior scleritis extended eyeballs are not uncommon, indicating the clinical concealment of posterior scleritis. This disease is also more common in women than in men and is common in middle-aged people.
(1) Clinical symptoms: The most common symptoms of posterior scleritis are pain of varying degrees, vision loss, redness, but some people have no obvious symptoms, or only one of these symptoms, severe cases of eyelid edema, conjunctiva Edema, eyeball protrusion or double vision, or both, the symptoms are difficult to distinguish from eyelid cellulitis, the point of identification is that the degree of edema of this disease is more obvious than cellulitis, while the eyeball of cellulitis is prominent. Posterior scleritis is significant, pain is moderate, some are very light, and some are extremely painful, often proportional to the severity of anterior scleritis involvement, the patient may complain that the eye itself is painful or painful involving the eyebrows, ankles or sputum Crotch.
Vision loss is a common symptom, which is accompanied by optic nerve retinopathy. Some people complain of visual fatigue caused by myopia reduction or increased hyperopia. This is caused by diffuse thickening of the posterior sclera leading to shortening of the eye axis.
Clinical and pathological aspects can be seen, patients with posterior scleritis have anterior sclera involvement, manifested as superficial scleral vasodilation, patchy anterior scleritis, nodular anterior scleritis, or no eye congestion, but There is a history of pain and eye congestion, or may have been treated with topical corticosteroids.
Eyeballs, ptosis and eyelid edema, can be seen in severe pericarditis, this inflammation often spread to the extraocular muscles or eyelids, because the extraocular muscle inflammation can have eyeball pain or diplopia, these symptoms are combined Known as periorbital inflammation, scleral bulbar fasciitis and acute anterior inflammatory pseudotumor.
In addition, there is a lesion that is more superficial, showing obvious ocular fasciitis, while the sclera has no obvious inflammation. James calls it jelly-like ocular fasciitis, and the conjunctiva is semi-gelatinous orange-red edema, such as Fish-like, slightly hard to touch, mild depression when pressed, lesions can extend to the limbus, and the eye is still normal, but there are also serious cases, the lesion can invade the sclera and become jelly-like scleritis.
(2) fundus lesions:
1 Clearly defined fundus mass: Localized scleral swelling can cause choroidal bulging, usually surrounded by concentric choroid folds or retinal streaks. These inflammatory nodules are often accompanied by pain around the ankle, but can also be diseased without obvious symptoms. Found in routine inspections.
2 choroidal folds, retinal streaks and optic disc edema: This is the main fundus manifestation of scleritis, patients often accompanied by mild pain or superficial vascular congestion of the occipital eye, scleral inflammation adjacent to the optic disc, can even cause optic disc edema.
3 annular choroidal detachment: in some cases, a slightly spherical choroidal detachment is seen near the scleritis lesion, but the annular ciliary choroidal detachment is more common.
4 exudative macular detachment: young women with posterior scleritis can cause post-polar blood-retinal detachment, this detachment is limited to the posterior pole, fundus fluorescein angiography can be seen at multiple needle tip size leakage areas, ultrasound scan shows the posterior pole Thickening of the layers and edema of the eyeball fascia.
Based on the above, Benson (1982) pointed out that for angle-closure glaucoma of unknown cause, choroidal wrinkles, optic disc edema, clear-eyed masses, choroidal detachment and spastic retinal detachment, the possibility of this disease should be considered.
Examine
Scleritis examination
Because scleritis is more common in immunogenicity and allergenicity, it is necessary to perform a corresponding systemic examination and laboratory examination in addition to the history of the disease and the general and local characteristics of the disease before treatment.
(1) Systemic examination
X-ray examination of the chest, spine, and ankle.
(2) Laboratory inspection
Blood routine, erythrocyte sedimentation rate, liver function, serum uric acid determination, syphilis serological test, tuberculin intradermal test, etc., immunological indicators: rheumatoid factor, peripheral blood T lymphocyte subsets, peripheral blood immunoglobulin, immune complex determination , anti-nuclear antibodies, complement C3 and so on.
(c) anterior fluorescein angiography of scleritis
Watson (1984) first applied fluorescein angiography to the diagnosis of scleritis, suggesting: typical diffuse or nodular scleritis, fluorescent angiography showing increased fluorescence of the vascular bed and reduced transit time, ie, in congested blood vessels only Little or no blood passes, its filling form is abnormal, because abnormal anastomosis is open, vascular short circuit is formed, fluorescein leaks into deep scleral tissue early, vascular filling is delayed, but if the blood vessels are patency, blood circulation It will eventually recover, but if the blood vessels are blocked, it will rarely reopen and eventually be replaced by newly formed blood vessels, which is particularly significant in diffuse, nodular and necrotic scleritis with significant inflammation. The occlusion is a small vein, and in the perforated sclera softening, it is a small artery, especially a small artery of the deep scleral plexus, so the result is not damaged by inflammatory cells like other types of necrotizing scleritis. The tissue is actively removed and replaced by sparse fibrous tissue, but the tissue is infarcted and separated, gradually Absorption cleared.
Although there is still controversy surrounding the normal filling of these blood vessels and the lack of filling of some major blood vessels, it is possible to identify benign superficial scleritis and severe by observing the inflamed vascular layer and the vascular displacement that occurs with scleral edema. Scleritis helps early diagnosis and further study of scleritis.
(four) fundus fluorescein angiography
In patients with subretinal exudate, the choroidal background fluorescence is mottled in the early stage of fluorescein angiography, followed by multiple fluorescent regions with large needle tip size, and then the strong fluorescent region gradually becomes larger and brighter, and fluorescein infiltration of these lesions in the late angiography In the subretinal fluid, of course, this fluorescein imaging is not specific to the posterior sclera, but these manifestations contribute to the diagnosis of posterior scleritis.
(5) Ultrasound scanning inspection
Ultrasound scanning is an indispensable method for scleral inflammatory hypertrophy after diagnosis in recent years. B-mode ultrasound scan shows that the posterior part of the ball is flattened, the layers in the posterior part of the eyeball become thicker, and the posterior edema of the ball. If the posterior edema of the ball surrounds the optic nerve, the "T" can be seen. Signs, this sign indicates that the edema that extends along the sclera is at right angles to the normal circular optic nerve shadow.
(6) CT scan examination
CT showed scleral thickness, injection enhancer can enhance the image, but also after the ball edema, but idiopathic inflammatory pseudotumor, acute scleral inflammation and sputum cellulitis cases can also have similar performance.
Diagnosis
Diagnosis of scleritis
The disease can also be complicated by cataract and glaucoma. The disease should be differentiated from the eyelid cellulitis. The latter is characterized by eyeball diagnosis and treatment. The obvious conjunctival edema is more difficult than the posterior scleritis and the eyeball fascia. Young people can also be called sclerotienitis, but extraocular muscle paralysis occurs in the early stage of ocular fascia.
