abstract

Scleral is a tissue with few cells and blood vessels, and most of it is composed of collagen. Its surface is covered by bulbar conjunctiva and bulbar fascia, and it is not in direct contact with the external environment, so it rarely gets sick. According to the statistics of most scholars, its incidence rate only accounts for about 0.5% of the total number of patients with eye diseases. Due to the collagen nature of the basic components of sclera, its pathological process is slow and the collagen disorder caused by it is difficult to repair. The eyeball is the "window" of collagen, so scleritis is often the ocular manifestation of systemic connective tissue diseases.

Treatment measures

The treatment principle of scleritis should first be to clarify the cause, treat the cause and prevent recurrence. It is also necessary to strengthen nutrition and improve the general condition.

(1) surface scleritis

Superficial scleritis, whether simple or nodular, is a benign and recurrent mild disease with self-limitation, and the course of disease is more than 1 ~ 2 weeks, so it can be left untreated. However, in order to cure as soon as possible, topical corticosteroid eye drops can be used to relieve symptoms and scleral injury by its non-specific anti-inflammatory effect. Or the use of non-corticosteroid anti-inflammatory drugs, such as indomethacin, phenylbutazone, etc., can also achieve therapeutic effects. Other topical eye drops should be routinely used in the treatment of various types of scleritis, such as scleritis complicated with iridocyclitis, atropine should be dripped in time to fully dilate the pupils.

Gout is an exception, and its pathogenesis is due to the rupture of phagocytic vacuoles, so it should be treated with uric acid urine. If necessary, corticosteroids should be given locally.

(2) scleritis

Diffuse and nodular scleritis, the vascular plexus in the affected area is open, but the course of disease is lingering. In addition to local administration, corticosteroids should also be taken. If complicated with uveitis, pupils should be dilated in time.

(3) necrotizing scleritis

The condition is serious, and most of the vascular plexus is occluded. Such as syphilis, tuberculosis and leprosy. Specific treatment and short-term systemic non-corticosteroid anti-inflammatory drugs should be given according to the etiology. For example, if oral oxycodone or indomethacin is ineffective within 1 week, and there is no vascular area in the sclera, a sufficient dose of corticosteroid preparation, such as prednisone or dexamethasone, should be taken orally to inhibit the necrosis process of the lesion. Once the disease is controlled, it will be reduced to maintenance until the disease subsides.

Subconjunctival injection should be regarded as a taboo for patients with deep scleritis to prevent scleral perforation. However, systemic or retrobulbar corticosteroid injection can usually relieve scleritis, periscleral inflammation, scleral fasciitis and acute inflammatory orbital pseudotumor, which is very effective in relieving severe pain without complications.

Severe cases sometimes require the use of strong immunosuppressants, such as cyclophosphamide. Sometimes, it is used as a corticosteroid reliever, or an increase in non-steroidal anti-inflammatory drugs for prostaglandins, thus reducing the systemic steroid dose to an acceptable level. However, it is generally believed that patients with real perforated sclerosis and malacia caused by partial anterior arteriolar occlusion should be treated long before necrosis occurs. For patients with systemic immune system diseases (such as Wegener's granulomatosis), the purpose of treatment is to inhibit the production of lymphocytes. The combination of immunosuppressants and glucocorticoids has the best effect, while for other patients with systemic vasculitis or diseases with only circulating immune complexes, only glucocorticoids are needed.

Surgical treatment is only suitable for affirming that the root of inflammation is autoimmune disease. Removing necrotic tissue can eliminate the source of antigen and implant allogenic sclera, which is also an effective treatment.

In recent years, it has been reported that cyclosporine A is a new powerful immunosuppressant, which can selectively act on helper T lymphocytes and exert its immunosuppressive effect without bone marrow toxicity. It was first used in ophthalmology to treat keratolysis syndrome. In recent years, it has achieved positive effects on necrotizing scleritis, silkworm-eroded corneal ulcer and corneal transplant rejection. It has been made into local eye drops for clinical application.

etiology

The cause of scleritis is unknown, sometimes it is not only impossible to find the cause, but also unclear whether the primary site of inflammation is in the sclera, upper sclera, bulbar fascia or other parts of the orbit. For example, posterior scleritis is difficult to distinguish from acute inflammatory orbital pseudotumor.

(1) Exogenous infection

Exogenous factors are rare and can be directly caused by bacteria, viruses and fungi through conjunctival infection, trauma and surgical wounds.

(2) Endogenous infection

1. pyogenic metastasis (pyogenic bacteria).

2. Non-suppurative granuloma (tuberculosis, syphilis, leprosy).

(3) Eye manifestations of connective tissue diseases

Connective tissue disease (collagen disease) is related to autoimmune diseases, such as rheumatoid arthritis, necrotizing nodular lupus erythematosus, nodular periarteritis, sarcoidosis (sarcoidosis), Wegener's granuloma, recurrent polychondritis and other complex scleritis, which causes fibrotic necrotic changes in the sclera, which is essentially similar to connective tissue disease. The incidence of complications of painstaking scleritis is above 50%, and the incidence of complications of perforated sclera softening is higher. Other patients, such as ankylosing spondylitis, Bencet disease, dermatomyositis, IgA nephropathy, temporal arteritis and porphyrin, have also reported scleritis. Watson( 1982) pointed out that this type of granulomatous change may indicate that the lesion is a type III hypersensitivity caused by the deposition of local antigen (IV delayed hypersensitivity) or circulating immune complex in the eye, thus inducing immune response. In type ⅲ hypersensitivity, vascular reaction is the result of the combination of antigen and antibody on the vascular wall. These complexes are deposited on the wall of venules and activate complement, thus causing acute inflammatory reaction. Therefore, collagen disease is an autoimmune disease with immune mechanism disorder related to individual genes, or one of its manifestations.

pathological change

Biopsy of scleral lesions is dangerous and often done. Only when the eyeball is removed or the diseased tissue is removed during the operation can the lesion be studied. Infiltration, hypertrophy and nodules in scleritis are chronic granulomatous lesions, which are characterized by painstaking efforts of fibrin-like blank and destruction of collagen. Suppurative inflammation is rare except for external infection or metastasis of adjacent suppurative lesions. Local inflammation can occur at the entrance and exit of blood vessels.

Granulomatous inflammation is limited to local and diffuse inflammation, but the essence is the same, that is, the affected sclera shows chronic inflammatory cell infiltration, including polymorphonuclear leukocytes, lymphocytes and macrophages, forming nodular and diffuse hypertrophic lesions. There are multinucleated epithelioid giant cells and new and old blood vessels around granuloma, and some blood vessels have thrombosis, which is characterized by vasculitis. These changes sometimes spread around, far beyond the site of granuloma, and first involve scleral mucopolysaccharide far away from the lesion, which indicates that colloidal iron staining is weakened. Fibers are pushed away by myxedema at the site where granulomas are received, while mucopolysaccharides can only form plaque staining. Under the electron microscope, it can be seen that collagen fibers also absorb dyes. The cell change here is that the number and activity of collagen fiber cells increase obviously, while in granuloma, the cell composition increases obviously. This area is infiltrated by plasma cells, lymphocytes and macrophages, some of which aggregate into giant cells. Scleral collagen fibers lose birefringence under polarized light. In the necrotic area, the infiltrated cell group dominated by plasma cells can be seen, and the cell blank is painstaking, and collagen fibers proliferate. Clusters of new blood vessels are formed in the upper sclera or choroid of this area. Both old and new blood vessels have middle necrosis, mucopolysaccharide deposition and thrombosis. Fibrin deposits are found in and around many blood vessels.

When the lesion is superficial, both subconjunctival and superficial sclera are invaded, scleral edema can be stratified, interstitial lymphocytes infiltrate, while superficial sclera blood vessels are congested and lymphatic vessels dilate. Mild patients leave no trace after recovery. Inflammation that invades the anterior part of the sclera will also spread to the cornea. Conversely, hyphema keratitis can also spread to the sclera, resulting in superficial scleritis. Deep scleritis also involves superficial sclera. In necrotizing scleritis, celluloid necrosis occurs in the center of the lesion, surrounded by large mononuclear cells, like a fence. In severe cases, there may be a flaky avascular area (arterial occlusion) in the center of inflammatory cell infiltration, and the tissue degeneration is painful, and then fatty degeneration, vitreous degeneration and calcification may occur. The necrotic part gradually absorbs fibrosis to form scar, local sclera thins and expands, or tissue thickens to form so-called "hypertrophic scleritis" (Sch? bl， 1889).

clinical picture

According to the location, symptoms and prognosis of inflammation invading sclera or superficial sclera tissue, it is generally considered that scleritis is classified reasonably.

(1) surface scleritis

Scleral episcleritis is an inflammation of the surface layer (or superficial layer) of the sclera, which is mostly located in the front of the equator between the corneal limbus and the attachment line of rectus muscle. Have a history of periodic attacks, and leave no trace after recovery. Both men and women can get sick, but women are more common, and patients are mostly monocular.

The etiology is often unknown, which is more common in allergic reactions caused by exogenous antigens and antibodies, as well as other systemic diseases such as metabolic diseases-gout. This disease mostly occurs in women's menstrual period and is also related to endocrine disorders. The anterior superficial sclera is prone to allergic reaction, which is related to the fact that the superficial sclera tissue is mainly composed of collagen fibers and elastic fibers, with rich vascular network and lymphatic vessels, which is suitable for the accumulation and deposition of various immune components.

Superficial scleritis is clinically divided into two types:

1. Simple episcleritis: also known as recurrent periodontitis.

The clinical symptom is sudden diffuse hyperemia and edema of the superficial sclera and bulbar conjunctiva at the lesion site, with red color, limited hyperemia range or fan shape. Most lesions are confined to a certain quadrant, and a wide range is rare. The superficial blood vessels of the upper sclera are tortuous and dilated, but they still remain radial, with no purple tone of deep blood vessel congestion and no localized nodules.

The disease has the characteristics of periodic recurrence, sudden attack, short attack time and recovery in a few days. Half of the patients have mild pain, but they often have burning sensation and tingling discomfort. Occasionally, pupil contraction and temporary myopia are caused by spasm of iris sphincter and ciliary muscle. Neurovascular reactive edema of eyelid can also occur during the attack. Severe cases may be accompanied by periodic migraine, and vision generally has no effect.

2. Nodular episcleritis Nodular episcleritis is a superficial scleritis characterized by localized nodules. It is often acute, with symptoms such as jealousy, pain, shame, tears and tenderness. Edema and infiltration quickly appeared on the superficial sclera of corneal limbus, forming reddish to flaming local nodules. The diameter of the nodule varies from small to large by several millimeters. The bulbar conjunctiva above the nodule can be pressed at will with tenderness.

The vascular plexus of bulbar conjunctiva is congested with red lesions, while the vascular plexus of upper sclera is congested with flaming red. It can be identified by anterior segment fluorescence angiography.

Nodules are round or oval, mostly single, sometimes reaching the size of peas. Nodules are located in the upper sclera tissue and can be pushed on the sclera, indicating that it has nothing to do with the deep sclera. Scleral vascular plexus remains normal in the lower part of nodule.

The course of the disease is about 2 weeks, and the nodule changes from fiery red to pink, and the shape also changes from round or oval to flat, and finally it can be completely absorbed, leaving traces of bluish gray tone on the surface. Inflammation here can also be secondary to other places after healing, and a nodule will appear after it subsides, and the recurrence of sputum can last for several months. Because of repeated attacks in different parts, an annular pigment ring can finally be formed around the sclera around the cornea. Eye pain is the most severe at night, and some people have no obvious pain. Vision is generally unaffected. Mild keratitis is the only complication of superficial scleritis. If there are tears of shame, it means that it is mild keratitis, which is more common in the limbus of cornea near nodules.

(2) scleritis

Sclerosis or deep scleritis. Shallow scleritis is rare, but the onset is urgent, often accompanied by corneal and uveitis, so shallow scleritis is serious and the prognosis is not good. Generally, superficial scleritis rarely invades the sclera tissue, while scleritis invades the sclera itself. Sclerosis often occurs where blood vessels pass through the anterior sclera, while scleritis at the posterior equator is easily overlooked because it can't be seen directly and there are few blood vessels. Sclerosis can be divided into anterior scleritis and posterior scleritis according to the site. Prescleritis is common in scleritis. More common in young people or adults, women are more than men, and both eyes can be affected successively or at the same time.

Sclerosis is mainly caused by endogenous antigen-antibody immune complex, often accompanied by systemic collagen disease, so it belongs to the category of collagen disease and is related to autoimmunity. Benson( 1988) attributed the immunogenicity to the direct invasion of collagen itself or scleral matrix (glucosamine) by inflammation. The tolerance of patients with primary necrotizing scleritis to scleral specific antigen may change, and they show delayed hypersensitivity to scleral soluble antigen. The discovery of immune complexes in rheumatoid arthritis supports this theory. But most scleritis is difficult to find the cause.

1. anterior scleritis

⑴ Diffuse anterior scleritis: This disease is the most benign scleritis, rarely complicated with serious systemic diseases.

The clinical symptom is sudden diffuse congestion and swelling of the tissues on the sclera, and the sclera cannot be determined. In severe cases, the conjunctiva can be highly edematous, so it is necessary to drip 1: 1000 epinephrine into the conjunctival sac to confirm whether there are deep vascular congestion and nodules. Diffuse is easier to spread than nodular. Lesions can be confined to one quadrant or occupy the front of the whole eyeball, often accompanied by episcleritis.

⑵ Nodular anterior scleritis: The clinical symptom is that the conscious eye pain is quite intense and radiates around the orbit. Half of the patients have eye tenderness. Inflammatory nodules are dark red and completely motionless, but the boundary with the upper sclera tissue is clear. The blood vessels on the surface are pushed up by nodules. Nodules can be single or multiple. Infiltrating nodules can spread around the cornea to form annular scleritis. At this time, the whole eyeball is dark purple with gray nodules, leaving a thin scar after absorption. The course of the disease can be as short as weeks or months, and the elderly can be as long as several years. Infiltration is gradually absorbed without rupture, and the sclera becomes thin, dark purple or magnetic white. Part of scleral swelling or grape swelling caused by high intraocular pressure. The deep vascular plexus of the upper sclera is congested and purple, and the blood vessels cannot move. The vascular network outside the superficial and deep sclera is abnormally distorted, and there are large anastomotic branches between the deep blood vessels, which shows that the blood vessels are beaded. If you have symptoms of shame and tears, you should consider keratitis and uveitis, which often seriously damage your vision.

⑶ Necrotizing anterior scleritis: This disease is also called inflammatory necrotizing scleritis. Although this type is rare in clinic, it is the most destructive and a precursor of severe systemic collagen disease. The course is slow. About half of the patients have complications and decreased vision.

The clinical symptoms are local inflammatory infiltration, acute congestion, tortuous blood vessels and occlusion in the early stage of the disease. The typical manifestation is a local flaky avascular area. Scleral edema occurs below or near this avascular area, and the superficial scleral blood vessels move forward (this sign is easy to find with red light). The development of the lesion can be limited to a small area, can also develop into a large area necrosis, can also develop from the periphery of the original lesion to both sides of the eyeball, and finally damage the entire anterior part of the eyeball. After the lesion healed, the sclera continued to become thinner and the uveal pigment was blue-purple. Unless the intraocular pressure continues to be as high as 4.0kpa(30mmHg), staphyloma generally does not form. If the necrotic area is small, new collagen fibers can repair it. If the conjunctiva above it is damaged, it will produce a sunken scar. Eye tenderness accounts for about half.

Ye Linan et al. (1980) reported two cases of nodular necrotizing scleritis, both of which were progressive necrotic yellow nodules with obvious inflammation and severe pain. The sclera in the lesion area was thin and blue-purple. Pathological examination confirmed the diagnosis. After the comprehensive treatment failed, 2 cases underwent focal resection and lamellar keratoplasty. Results 1 case improved, 1 case recurred. Li (1980) reported 1 case of nodular necrotizing scleritis treated with immunosuppressants. In this case, both eyes are affected, the right eye is in ulcer stage and the left eye is in nodule stage. The local sunken ulcer focus in the right eye and the yellow nodule raised in the left eye are all 4mm away from the corneal edge, and the sclera around the focus is purple and red with congestion, and local compression is refused. The case was relieved by immunosuppressant treatment.

⑷ Perforated scleromalacia: also known as non-inflammatory necrotizing scleritis, it is a rare special type of scleritis, and its condition is hidden and almost asymptomatic. About half of the patients are related to rheumatoid arthritis or ankylosing polyarthritis. Eye disease may precede arthritis. Most patients are women over 50 years old. At first glance, the lesion is bilateral, but its manifestations are different. The course of the disease develops slowly, but there are also cases of rapid performance, which leads to blindness within a few weeks.

This disease is rarely accompanied by inflammation or painful reaction. The lesion is characterized by yellow or gray spots on the sclera between the corneal limbus and the equator. In the most severe cases, the local sclera gradually appears carrion-like and falls into necrotic changes. Once the necrotic tissue falls off, the sclera can disappear completely. The blood vessels in the residual sclera tissue are obviously reduced, which looks like white enamel from the outside. About half of the patients have more than one necrotic focus. Scleral defect caused by necrosis can be covered by a thin layer of connective tissue, which may come from conjunctiva. Unless the intraocular pressure increases, there is generally no staphyloma. None of them have any eye tenderness. A part of the cornea is not affected.

There is no tissue regeneration and repair in the defect area, which eventually leads to perforation and uveal prolapse.

Gong Chunhui (1985) reported 1 case of perforated chondromalacia. The patient has a history of arthritis for 5-6 years, and the soft tissue of the proximal phalanx of the left middle finger is spindle-shaped with no redness and tenderness locally. X-ray film showed no bone thinning and joint cavity stenosis. The redness and swelling of the left eye is secondary to corneal opacity, and the medial sclera ulceration is purple-blue, and the irritation symptoms are not obvious. Six months later, a 4× 5mm circular ulcer appeared in the sclera 5 mm above the medial rectus muscle, and blue sclera and purple-black choroid tissue could be seen through the conjunctiva. At 12 ~ 5 o'clock, the corneal edge ulcerated and the fundus was normal. Corticosteroids and lamellar keratoplasty controlled the disease.

2. Posterior scleritis

Posterior scleritis refers to the inflammation of the sclera around the posterior equator and optic nerve. It is serious enough to cause damage to the posterior tissue of the eyeball. Because of its diversity of manifestations and little consideration in diagnosis, it is one of the most easily missed curable diseases in eyes without anterior scleritis and no obvious signs in the outer eye. However, it is not uncommon for many eyeballs to have primary posterior scleritis or anterior scleritis, which shows the clinical concealment of posterior scleritis. This disease is also common in women and men, especially in middle-aged people.

⑴ Clinical symptoms: The most common symptoms of posterior scleritis are different degrees of pain, decreased vision and jealousy, but some people have no obvious symptoms or only one of them. Severe cases include eyelid edema, bulbar conjunctival edema, exophthalmos or diplopia, or both. Symptoms are indistinguishable from orbital cellulitis. The difference is that the degree of edema of this disease is more obvious than that of cellulitis, and the exophthalmos of cellulitis is more obvious than that of posterior scleritis. Pain varies from mild to extreme, and is usually directly proportional to the severity of anterior scleritis. Patients may complain that the eyeball itself hurts or the pain involves eyebrows, temples or cheekbones.

Vision loss is a common symptom, which is caused by optic neuropathy and retinopathy. Some people complain that vision fatigue is caused by decreased myopia or increased hyperopia, which is caused by diffuse thickening of posterior sclera. Replacing lenses can relieve symptoms.

Clinically and pathologically, all patients with posterior scleritis have anterior sclera involvement, which is characterized by superficial scleral vasodilation, patchy anterior scleritis and nodular anterior scleritis. Or there may be no bloodshot eyes. But he has a history of pain and bloodshot eyes, or he may have been treated with topical corticosteroids.

Severe periscleral inflammation can be seen as exophthalmos, ptosis and eyelid edema, which often spread to extraocular muscles or orbit. Because of inflammation of extraocular muscles, eye movement pain or diplopia may occur. These symptoms are collectively called periscleral inflammation, scleral fasciitis and acute anterior inflammatory pseudotumor.

In addition, there is a more superficial lesion, which is characterized by obvious eyeball fasciitis, but there is no obvious inflammation in the sclera, which James calls jelly eyeball fasciitis. The bulbar conjunctiva is semi-jelly-like orange-red edema, such as fish-like, slightly hard to touch, slightly depressed when pressed, and the lesion can extend to the corneal limbus, but the eyeball is still normal. But in some cases, the lesion can invade the sclera and become jelly scleritis.

(2) fundus lesions:

① Fundus mass with clear boundary: localized scleral swelling area can cause choroidal uplift. Usually surrounded by concentric choroidal folds or retinal stripes. This kind of inflammatory nodule is often accompanied by periorbital pain, but it can also occur without obvious symptoms before routine examination is found.

② Choroidal folds, retinal stripes and optic disc edema: these are the main fundus manifestations of scleritis. Patients are often accompanied by mild pain or congestion of ocular surface vessels in the fornix. Scleral inflammation near the optic disc occasionally causes edema of the optic disc.

③ Annular choroidal detachment: In some cases, slightly spherical choroidal detachment can be seen near scleritis focus, but annular ciliary choroidal detachment is more common.

④ exudative macular detachment: young women's posterior scleritis can cause retinal detachment in the posterior pole, which is limited to the posterior pole. Fundus fluorescein angiography showed many needle tip-sized leakage areas. Ultrasonic scanning showed that the layers of posterior pole of eye were thickened and the fascia of eyeball was edema.

Based on the above, Benson( 1982) pointed out that the possibility of this disease should be considered for angle-closure glaucoma, choroidal folds, optic disc edema, well-defined fundus masses, choroidal detachment and retinal detachment with unknown causes.

complication

There are many ocular complications of scleritis, and most of them occur in the late stage of inflammation. Complications depend on the severity and nature of inflammation. Superficial scleritis accounts for about 15%, and scleritis is higher than 57%, especially severe necrotizing scleritis. When inflammation spreads and secondary endophthalmitis occurs, complications include keratitis or keratopathy, cataract, uveitis, glaucoma and scleral thinning (defect).

Sclerosing keratitis

Sclerosing keratitis, also called progressive sclerosing keratitis. Most of the patients are women, who are older, often suffer from binocular involvement and recurrent attacks, which affect the whole cornea, complicated with iridocyclitis or glaucoma, leading to serious consequences.

The pathological changes are edema and invasive changes of sclera tissue around corneal limbus, forming dense angiogenesis, and infiltrating into deep corneal tissue from corneal limbus, causing corneal opacity, which often occurs at corneal limbus. But it can also occur on the surface or substance of the central cornea, which has nothing to do with scleral lesions. Corneal opacity begins with grayish white or grayish yellow, and then turns white. The typical shape is tongue or triangle, and the tip points to the center of cornea. It is common that linear opacity remains in corneal stroma, which looks like ceramics and will never disappear once it appears. In severe cases, the opacity can gradually develop into a ring, leaving only a transparent area in the center of the cornea, or even the central transparent area disappears and is completely turbid, forming the so-called "sclerosing cornea". There are also some cases that develop into corneal limbal ulcer in the pathological process.

The so-called "sclerosing cornea" means that the diseased corneal tissue becomes a ceramic-like appearance, which looks like a sclera, not a sclerosing lesion.

(2) Corneal lysis or keratosis

The characteristic of this disease is that when severe necrotizing scleritis or perforated sclera softening occurs, the original transparent corneal surface layer is separated, dissolved and detached, and the detachment range is sometimes more than several millimeters. In severe cases, the back elastic layer expands so thin that it breaks when touched. Tissue dissolution and shedding may also occur in the diseased sclera. For this dissolution, corticosteroid therapy can prevent its development, indicating that inhibiting collagen activity can also inhibit the disease.

(3) Scleral defect

Only the most severe cases of scleral necrosis can be seen. If necrotizing scleritis is complicated with inflammation, the blood vessels in the upper part of the sclera disappear, and the sclera tissue under it becomes a perfusion-free area and eventually becomes necrotic tissue. In the case of perforated sclera softening, tissue necrosis can occur without any warning. Once necrosis occurs, the sclera becomes thin and transparent, and sometimes perforation occurs.

(IV) Uveitis

According to the statistics of most scholars, about 35% scleroderma patients are complicated with uveitis and retinitis. Patients with anterior and posterior uveitis should be highly alert to scleritis, and vice versa. Posterior scleritis, if complicated with uveitis, has fierce symptoms and often complicated with retinal detachment. Inflammatory cells were also reported in the anterior chamber and vitreous body. Wilhelmus found inflammation in choroidal capillaries histologically; Sleeve infiltration was formed around the central retinal artery and its arterioles and the posterior ciliary vessels.

(5) Glaucoma

In all stages of scleritis, intraocular pressure will increase. The reasons are as follows: ① Iris-lens septum moves forward due to choroidal exudation of ciliary body, which leads to the closure of the angle of the room and the occurrence of acute angle-closure glaucoma; ② Inflammatory cells in anterior chamber infiltrated and blocked trabecular meshwork and angle; (3) Sleeve infiltration of lymphocytes around superficial sclera blood vessels leads to the increase of scleral venous pressure; ④ Sleeve infiltration of lymphocytes around the sheath affects the outflow velocity of aqueous humor; ⑤ Long-term local, periocular or systemic application of corticosteroids can induce corticosteroid glaucoma.

accessory examination

Because scleritis is common in immunogenicity and sensitization, before treatment, in addition to medical history and systemic and local characteristics and signs, corresponding general examination and laboratory examination are needed.

(1) General inspection

X-ray examination of chest, spine and sacroiliac joint.

(2) Laboratory inspection

Blood routine, erythrocyte sedimentation rate, liver function, serum uric acid determination, syphilis serological test, tuberculin intradermal test, etc. Immune indicators: rheumatoid factor, peripheral blood T lymphocyte subsets, peripheral blood immunoglobulin, determination of immune complex, antinuclear antibody, complement C3, etc.

(3) Anterior segment fluorescence angiography of scleritis

Watson( 1984) first applied fluorescence angiography to the diagnosis of scleritis, and proposed that: typical diffuse or nodular scleritis, fluorescence angiography shows that the fluorescence of vascular bed is enhanced and the transit time is reduced, that is, little or no blood passes through congested blood vessels. Its filling shape is abnormal because there are abnormal anastomotic branches opening, forming a short circuit of blood vessels. Fluorescein leaked into the deep sclera in the early stage, and the blood vessel filling was delayed. But if the blood vessels in the disease are unobstructed, the blood circulation will eventually recover. However, if blood vessels are blocked, they rarely reopen and are eventually replaced by newly formed blood vessels. It is particularly significant that in diffuse scleritis, nodular scleritis and necrotizing scleritis with obvious inflammation, venules are blocked, while in perforated scleromalacia, arterioles are blocked, especially in deep scleral plexus. Therefore, unlike other types of necrotizing scleritis, the damaged tissue is not actively removed by inflammatory cells, but replaced by sparse fibrous tissue, but is infarcted, separated and gradually absorbed and removed.

At present, although the normal filling of these vessels and the non-filling of some major vessels are still controversial, we can distinguish benign superficial scleritis from severe scleritis by observing the inflammatory vascular layer and the vascular displacement with scleral edema, which is helpful for early diagnosis and further study of scleritis.

(4) fluorescein fundus angiography

In patients with subretinal exudate, the choroidal background was mottled with fluorescence in the early stage of fluorescence angiography, and then many strong fluorescence areas with the size of needle tips appeared, which gradually became larger and brighter. In the late stage of angiography, fluorescein from these lesions infiltrated into subretinal fluid. Of course, the results of this fluoroscopy are not unique to the posterior sclera. But these manifestations are helpful to the diagnosis of posterior scleritis.

(5) Ultrasonic scanning inspection

Ultrasound scanning is an indispensable method to diagnose posterior scleritis hypertrophy in recent years. B-ultrasound scan showed that the back of eyeball was flat, the layers at the back of eyeball were thickened, and retrobulbar edema was seen. If there is retrobulbar edema around the optic nerve, you can see the "T" sign. This sign shows that the edema spreading along the sclera is at right angles to the normal circular optic nerve shadow.

(6) CT scanning examination

CT shows the thickness of sclera, and injection of enhancer can enhance the image. Retrobulbar edema is also seen. However, cases of idiopathic inflammatory orbital pseudotumor, acute periscleritis and orbital cellulitis can also have similar manifestations.

Ye Rongkun (1983) reported a case of unilateral exophthalmos caused by posterior scleritis: female, 46 years old. Due to the visual acuity of the left eye decreased for 5 months, exophthalmos 1 month, eye movement limitation, diffuse congestion of bulbar conjunctiva, and nodules between local dark red congestion in the temporal equator, which caused obvious tenderness. The optic disc of the fundus was hyperemia and edema, and it bulged for 2.0D days, and the macular edema was mild. After systemic and local antibiotics and corticosteroids treatment, the condition was relieved. Liu et al. (1982) reported 1 case of posterior scleritis, with the contralateral eyeball slightly protruding > 2mm, conjunctival congestion and edema, and the pain aggravated during eye movement. The boundary of the optic disc is blurred, red and convex, the central vein is tortuous, the retina is slightly edematous, there are radial folds in the macular area, and the fovea is reflective (-). Adequate corticosteroids, vasodilators and neurotrophics were given for treatment. Vision improved from 0.3 to 0.8. No recurrence was found within two years.