The blood supply of iris and ciliary body is large iris ring, so both of them are often inflamed at the same time, which is called iridocyclitis. If the choroid is also inflamed, it is called uveitis. The nutrition of the outer layer of retina is supplied by choroid, and the inflammation of the latter often affects the retina, forming chorioretinitis.

Pigment membrane is an important tissue that nourishes the eyeball and can secrete aqueous humor. If it is inflamed, it will affect the nutrition of the eyeball. Because the iris and ciliary body are close to the angle of anterior chamber, when inflamed, not only a large amount of exudate enters the anterior chamber, posterior chamber or vitreous body to produce turbidity, which will reduce vision, but also affect the circulation of aqueous humor, causing secondary glaucoma, which will seriously damage vision and even blindness. So uveitis is one of the main causes of blindness.

The etiology of many uveitis is not easy to determine, and can only be considered according to the clinical manifestations of the whole body and eyes, combined with medical history and related laboratory tests. Common reasons are as follows:

1. There are three sources of infection:

(1) Exogenous bacteria directly enter the eye through trauma or surgical wound;

(2) Secondary inflammation is caused by the diffusion of adjacent eye tissues, such as severe keratitis or ulcer, which can cause iriditis;

(3) Endogenous metastasis from infected lesions in other parts of the body, such as suppurative metastatic ophthalmia, or pigment membrane infection caused by systemic tuberculosis, syphilis, leprosy and other diseases.

2. Immune factors In recent years, due to the development of immunology, it has been found that many diseases are related to immune mechanism. Bacterial antigens, especially streptococcus infection, can produce immune inflammation, so many scholars believe that most non-specific endogenous uveitis is related to immunity. Some uveitis begins with infection and then develops delayed hypersensitivity. Rahi( 1979) believes that uveitis is an allergic disease and immune complex disease in many tissues such as muscles, nerves and blood vessels. At present, autoimmune uveitis is considered as allergic endophthalmitis and sympathetic ophthalmia, and HLA is closely related to some types of uveitis. The relationship between immune factors uveitis and immunity can be tested by immunological tests.

3. Repeated old bleeding of eyes, poisoning or stimulation of old retinal detachment, and toxicity and chemical stimulation of malignant pigmented tumor necrosis tissue can all cause uveitis.

4. Inflammation caused by traumatic reactive ocular contusion is a reflection of blood vessels and nerves. Firstly, arterioles contract rapidly, causing local hypoxia, and secondly, reflex capillary dilation, increasing permeability, causing tissue edema and exudation and other inflammatory manifestations.

5. Sarcoma, rheumatoid arthritis, multiple sclerosis and some skin diseases with systemic non-infectious diseases can be complicated with uveitis.

In recent years, many scholars have noticed the action mechanism of prostaglandin. Effect of PG) on pigment membrane inflammation. It was found that there was a large amount of prostaglandin in aqueous humor of acute anterior uveitis, but it did not exist in aqueous humor of cataract patients without inflammation. Therefore, it is speculated that the inflammatory manifestations of pigment membrane are caused by vasodilation and permeability enhancement caused by prostaglandin. The therapeutic mechanism of indomethacin or corticosteroids on uveitis is also due to the inhibition of prostaglandin production, thus controlling inflammation.

Uveitis can be classified in many ways. According to the inflammatory site, it can be divided into anterior, posterior, peripheral and panpigmented membranitis; According to the specific causes, it can be divided into tuberculosis, syphilis and leprosy. This classification method is ideal, but the exact causes of many uveitis are still unclear. According to the course of disease, it can be divided into acute, subacute, chronic and obsolete. There are purulent and exudative. According to the nature of exudate, the latter is divided into serous and cellulosic. In addition, according to the nature of inflammation, it can be divided into two categories: granulomatous and non-granulomatous; The former is caused by the actual invasion of pathogens, mainly proliferative lesions, often accompanied by systemic granulomatous infectious diseases, while the latter is mainly caused by immune response, including physical and chemical and toxic substances. However, these two types are sometimes difficult to distinguish in clinic and sometimes coexist. So this classification is not ideal.

clinical picture

1. Anterior uveitis (iritis, cyclophilitis and iridocyclitis)

(1) Pain is caused by contraction of ciliary muscles, swelling and congestion of tissues and stimulation of ciliary nerve endings by toxic substances. Pain often radiates to the eyebrow arch and cheeks; It is more obvious in light stimulation or eyeball compression, and it is heavier at night. Chronic inflammation can be dull pain. In acute inflammation, pain is obvious and often accompanied by shame and tears.

(2) Inflammatory cells and cellulose exudates in aqueous humor and vitreous before vision loss, deposits on the posterior wall of cornea and lens surface affect refractive stroma, and myopia caused by ciliary muscle spasm can affect vision. Late cataracts or secondary glaucoma make vision extremely poor and even blind.

(3) Acute anterior uveitis with ciliary congestion generally has obvious ciliary congestion, and in severe cases, it can also form mixed congestion, often accompanied by conjunctival edema.

(4) According to the nature, severity and duration of inflammation, keratinized deposits (K.P.) vary in size, shape, quantity and location. Generally located in the lower central part of the cornea, it is often arranged in a triangle, with the tip facing the center of the cornea (Figure 13- 1). This is because the outside air temperature is lower than the body temperature, inflammatory cells rise in the back of the anterior chamber with the convection of aqueous humor, and fall in the front, and corneal endothelial cells are easy to deposit on the posterior wall of the cornea when they are swollen and necrotic. The large gray-white boule de suif-like K.P. is a characteristic of chronic inflammation, which is more common in granulomatous uveitis, mostly deposited in the center and below the cornea, and occasionally seen in the anterior chamber angle. Gray K.P. is seen in acute or allergic non-granulomatous diseases.

(5) Turbidity of aqueous humor is caused by protein in inflammatory aqueous humor, which shows light gray or gray reflection light band under slit lamp, which is called Tindal sign, indicating active inflammation.

There are planktonic cells and fiber exudation in aqueous humor. The latter is generally linear, flaky, reticulate or even membranous, and the light one only occupies a small amount in or below the pupil area, and the heavy one fills the anterior chamber, which is the manifestation of so-called formative iridocyclitis.

There may also be hyphema or pus accumulation, forming a horizontal plane below the anterior chamber. Hyphema is more common in acute inflammation of herpes and gonorrhea, grayish yellow hyphema (Figure 13-2), bacterial infectious inflammation, Behcet's disease and endophthalmitis of lens. After the malignant tumor enters the anterior chamber, it can also form false hyphema.

(6) Ill-textured iris tissues are like sponges. Once inflamed, due to congestion and edema, the texture is unclear and the color darkens. Compared with healthy eyes, it is not difficult to find abnormalities.

(7) Iris nodules are more common in granulomatous uveitis, and there are two types: superficial and deep. The former is more common in subacute or chronic inflammation, and it is a translucent small gray mass. Koeppe nodules, located at the edge of the pupil, often appear in the early stage of inflammation, varying in number, and can disappear within a few days, but if the inflammation does not subside, new nodules can appear again. Sometimes the iris forms extensive posterior adhesions. Nodules located on the anterior surface of iris are called Bu8acca nodules. Most of them are near the iris curl wheel. Sometimes it disappears quickly, but it can last for several months, and occasionally it forms a mass, which causes organization and angiogenesis. Located at the iris root, it is easy to form anterior iris adhesion. Deep iris nodules are granulomatous nodules formed by infiltration of local inflammatory cells in iris tissue, such as miliary or spherical tuberculosis nodules and sarcomatoid iris nodules. Most of these nodules are large, obviously raised, gray or yellow-gray, with blood vessels nearby. If it does not disappear for a long time, it may become glassy or form localized atrophy.

(8) Pupil shrinkage is caused by congestion, edema, cell infiltration and toxin stimulation of exudate in iris tissue, which makes the pupil shrink and slows down the reflection of light. Although the pupil sphincter and pectoralis major muscle are stimulated at the same time, the pupil is narrowed because the pupil sphincter is dominant.

Anterior uveitis can cause the following complications and complications:

(1) Long-term inflammation of the pigment membrane before corneal opacity almost always leads to wrinkles in the posterior elastic layer. When inflammation involves corneal endothelial cells and destroys corneal hydration, it will cause corneal epithelial edema, bullae and bullous changes, and persistent edema will cause pannus and neovascularization around corneal parenchyma. When corneal endothelial cells are severely edematous and extensively exfoliated, exudate is deposited at the exfoliated site and gradually becomes organized, leaving permanent turbidity. In addition, vitreous degeneration can also occur, forming transparent deposits. Corneal zonation opacity occurs in the late stage of the disease and is more common in young patients.

(2) Posterior adhesion and anterior adhesion of iris This is due to the organization of inflammatory cells, fibroblasts and protein solution, which makes the iris adhere to the anterior surface of the lens to form posterior adhesion or anterior adhesion to the anterior chamber angle tissue. Chronic inflammation is sometimes easier to cause than acute inflammation. The initial posterior adhesion can be opened with mydriatic, but after opening, iris pigment epithelium is often left on the anterior surface of lens as a trace of inflammatory sequelae. If the exudate is organized and firmly adhered, it is not easy to open it with a mydriatic agent. After mydriasis, the pupil is partially adhered, with plum blossom shape and uneven edge (Figure 13-3). Annular total posterior adhesion occurs at the pupil edge.

When the iris is completely attached to the anterior surface of the lens, the obstruction of anterior and posterior aqueous humor is called pupillary atresia. In the former, aqueous humor stays in the posterior chamber, and the pressure in the posterior chamber increases, which pushes the iris forward and forms an iris bullet (Figure 13-4 (1)). The latter does not cause iris swelling (Figure 13-4(2)). When the exudate forms a white fibrous membrane in the pupil area and blocks the pupil, it is called pupillary atresia (Figure 13-4(3)). Unless the secretory function of ciliary body is destroyed, the above situation will generally cause secondary glaucoma. The iris bulges forward, which narrows the angle of anterior chamber and causes anterior chamber adhesion; Inflammatory exudate from the anterior chamber angle gradually pulls the iris root to the anterior chamber angle or causes inflammation and edema of the iris root, and contact with the peripheral part of the cornea can also form anterior adhesion. Secondary glaucoma is caused by anterior chamber adhesion that affects aqueous humor drainage.

(3) The toxic effect of complicated cataract inflammation can cause cataract. If the toxin damages the epithelium, invades the cortex, or the lens epithelium degenerates or proliferates due to the posterior adhesion of iris, the front part of the lens will be turbid. Turbidity often first appears in the cortex near the subcutaneous area of the posterior capsule, which is caused by the weakness of the posterior capsule and no epithelium. In severe cases, there is opacity in the anterior and posterior cortex of the lens, which will soon form a complete cataract.

(4) Pigment membrane inflammation before vitreous opacification is often accompanied by vitreous opacification, usually in the form of tiny spots, which can be seen in front of the vitreous body under slit lamp. In the late stage of chronic inflammation, due to the destruction of vitreous colloid structure, thin strip opacification can be formed.

(5) It is very rare that uveitis affects the retina before the fundus changes, but in severe cases, macular edema or cystic changes may occur, sometimes accompanied by vasculitis.

(6) Changes in intraocular pressure The intraocular pressure can be high or low. In acute inflammation, blood vessels dilate, plasma leaks out, the viscosity of aqueous humor in anterior chamber increases, and exudate blocks the anterior chamber angle, causing glaucoma. Inflammation can cause trabecular fibrosis, schlemmon's canal atresia or narrowing, and iris adhesion before and after can cause secondary glaucoma. On the contrary, the intraocular pressure is very low in many cases. This is due to ciliary inflammation and decreased aqueous humor production. Hypotension is transient and more common in the early stages of the disease. Once the inflammation disappears, the intraocular pressure returns to normal.

Eye atrophy This is the last stage of severe uveitis. The exudate is organized near the ciliary body, forming a fibrous membrane (ciliary body membrane) to pull the retina apart and destroy the ciliary body, so as to reduce aqueous humor secretion and intraocular pressure. In addition, the ciliary body itself becomes scar tissue due to repeated inflammatory attacks, and finally the eyeball shrinks and loses vision, which is called eyeball atrophy.

2. Posterior uveitis (chorioretinitis)

(1) Patients with self-conscious symptoms have no irritating symptoms such as pain and tears, and most of them seek medical treatment because of visual impairment. At the early stage of the disease, due to the stimulation of retinal cells, a sense of flash often appears in the corresponding field of vision of the disease. When the lesion develops further, visual impairment will occur. Because retinal edema has irregular protrusions, imaging disorder and vision distortion. If the exudation between visual cells increases the cell spacing, the imaging becomes smaller, which is called microvision. On the other hand, if the visual cells are piled up together, the imaging becomes larger, which is macropsia. The symptoms of macular lesions are extremely obvious, which is equivalent to conscious scotoma (solid scotoma) at the lesion site. In the later stage of severe cases, the corresponding retina is seriously damaged, and the visual impulse is no longer produced, and the so-called virtual scotoma is produced in the corresponding part. At this time, the patient may be unconscious, but the corresponding dark spots can be found during the examination.

(2) fundus changes choroidal lesions of different sizes and shapes can be seen in different parts of the fundus. Generally, fresh exudation lesions are white, yellowish white or grayish white, round or plastic, with unclear boundaries and sometimes slight uplift. If the retinal edema in the lesion area is obvious, it is white or grayish white; If there is no edema, patients with less dense pigment in the pigment epithelium are pale yellow or white lesions, and the center is yellow or grayish yellow.

After the acute phase passed, the atrophic phase began, and the boundary of the lesion gradually became clear. White spots appeared due to the systematization of exudate and the formation of fibrous tissue, or the white sclera was exposed due to the atrophy and thinning of choroidal tissue, and finally disappeared. In addition, due to the hyperplasia of pigment epithelium, black plaques appear in the lesion area, especially around the lesion. This is the manifestation of the old lesion.

Choroiditis has vitreous opacity. Patients complain of floaters, and the degree of opacity varies according to the severity of inflammation. In severe cases, the vision is seriously impaired. Some uveitis, such as Harada's disease, Koyanagi's disease, sympathetic ophthalmia and peripheral uveitis, may cause retinal or choroidal detachment.

It is generally best to treat the cause, but because the cause is very complicated and unknown, the treatment methods are different, so it is difficult to elaborate. The general principle processing method is briefly described as follows:

1. mydriasis is very important. Atropine drugs are mainly used to relax ciliary muscles, reduce arterial pressure, enhance blood circulation of pigment membrane, reduce capillary permeability, reduce exudation, play an anti-inflammatory role, rest tissues and play an analgesic role. In addition, mydriasis can also open and prevent posterior adhesion of iris. Before acute onset of mydriasis, adults should use 1% atropine solution 2 ~ 3 times a day, and at night, use 1 ~ 3% atropine ointment. If the inflammation has been relieved, you can use 1% atropine ointment 1 ~ 2 times a day 1 time. In order to prevent recurrence, after the inflammation subsides, it is still necessary to continue mydriasis for about 2 weeks to consolidate. For those allergic to atropine, 0.25 ~ 0.5% scopolamine can be used instead, and the usage is the same as atropine. If atropine can not fully dilate the pupil, 4 ~ 10% Novolin solution can be added to stimulate the pupil-opening muscle and enhance the mydriasis effect. People with posterior iris adhesion can inject 0. 1 ~ 0.2ml mydriatic agent (containing 1% atropine, 4% cocaine, 1: 1 000 adrenaline) or use a new mixed mydriatic agent with stronger mydriatic force and shorter action time. Attention should be paid to intraocular pressure when using mydriatic. For elderly patients with shallow anterior chamber, 2% atropine can be tried first to prevent acute glaucoma attack, and atropine can be used again after dropping the medicine without increasing intraocular pressure to ensure safety. For patients with chronic uveitis, drugs with short action time and strong mydriasis can be used alternately, such as 2% houmatopine and 4 ~ 10% neoforin, to make the pupil have room for movement and prevent the pupil from forming fixed adhesion again in the state of mydriasis.

2. Hot compress methods include wet hot compress, hot air, wax therapy and electric heating. It can promote eye blood circulation, absorb inflammatory products, increase antibodies and have analgesic effect.

You can wear colored glass glasses to avoid strong light stimulation, especially after mydriasis and in the sun.

3. Corticosteroid therapy In order to control inflammation, corticosteroids can be applied immediately, and their non-specific anti-inflammatory and anti-allergic effects can be used to prevent further damage to eye tissue and protect visual function. However, when used in large doses, it can inhibit the antigen-antibody reaction and even the formation of antibodies, that is, inhibit the body's defense function and enable bacteria to multiply. Therefore, anti-infective drugs must be added at the same time for infectious uveitis. Administration method: sufficient amount should be given at the beginning to control inflammation quickly. After the condition improves, it can be gradually reduced. Don't stop taking medicine suddenly, so as not to rebound and make inflammation relapse. Finally, the minimum maintenance dose was used until the inflammatory activity completely disappeared. In most cases of anterior uveitis, only local eye drops or subconjunctival injection can be used. However, for patients with uveitis or choroiditis, it is best to add retrobulbar injection combined with systemic administration, which is enough to reach the intraocular tissue.

Precautions when using corticosteroids ① Check blood pressure, urine sugar and weight regularly, pay attention to edema, diabetes or hypertension, and pay attention to mental state. ② Pay attention to prevent electrolyte balance disorder, especially hypokalemia. Long-term users should take potassium chloride orally, once 1 g, three times a day or 10% potassium citrate, 10 ml, three times a day. ③ For patients who take medicine for a long time, especially the elderly, osteoporosis should be prevented and pathological fractures should be avoided. ④ Prevention of infection. Pay attention to whether there are potential lesions. Long-term use of broad-spectrum antibiotics can lead to serious mold infection, which should be paid attention to. ⑤ Prevent adrenal cortical hypofunction. Those who need long-term medication should try to reduce the maintenance dose or take the method of administration every other day, that is, take it for 2 days at 8 o'clock every other day. It is suggested to switch to ACTH for 7 days every 3 months, 25 units a day, or to use ACTH for 7 days after treatment. ⑥ Glaucoma and cataract caused by attention. ⑦ Patients with severe hypertension, arteriosclerosis, tuberculosis, diabetes, peptic ulcer, myocardial infarction, severe psychosis, eclampsia, osteoporosis, fungal infection, early pregnancy and other diseases are prohibited or used with caution.

4. The application of non-corticosteroid anti-inflammatory drugs sodium salicylate and indomethacin has analgesic and anti-inflammatory effects. However, these drugs may cause side effects: sodium salicylate can reduce prothrombin, leading to bleeding, and patients with liver and kidney diseases are prohibited. Indomethacin can cause headache, dizziness, insomnia and gastrointestinal symptoms, so it is forbidden for patients with digestive tract ulcer and pregnant women. In addition, calcium chloride and calcium gluconate can reduce vascular permeability, thus reducing inflammation.

5. Application of immunosuppressants For some serious cases of uveitis such as sympathetic ophthalmia and Behcet's disease, when corticosteroid therapy is ineffective or ineffective, we can consider trying immunosuppressants as appropriate. Some of these drugs are screened from drugs for treating tumors, which are often cytotoxic, and can inhibit the growth and development of related cells or antibodies during the immune process, thus achieving the purpose of treating inflammation. But it must be used with caution, and the blood picture should be checked frequently during the application. The following briefly introduces the usage of several commonly used immunosuppressants.

(1) cyclophosphamide (cyclophosphamide) can be used in combination with corticosteroids or alone to treat intractable uveitis. Usually, the oral dosage is 50 ~ 100 mg, taken orally before breakfast every day 1 hour or twice in the morning and evening. Generally two weeks is a course of treatment. Dissolve 100 ~ 200mg in 20ml normal saline once a day or every other day during intravenous injection. The most common side effects are hair loss, nausea and vomiting. It can inhibit hematopoietic function, so check the blood picture frequently. When the total number of white blood cells is less than 4000, drug withdrawal should be considered. This product is unstable after being dissolved in water and should be used within 30 minutes after being dissolved.

(2) Oral administration of chlorambucil 2 ~10 mg per day can slightly inhibit hematopoietic function, with occasional nausea, vomiting and loss of appetite. Generally, it starts from 2 mg per day and gradually increases the amount.

(3) Jining (6- mercaptopurine, referred to as 6- mercaptopurine, 6-MP) takes 50 ~ 100 mg daily, and takes it twice or three times. It can reduce white blood cells and platelets, and occasionally has side effects such as stomatitis, diarrhea and gastrointestinal discomfort.

(4) Azathioprine (imuran) should be taken orally 50 ~ 100 mg per day, and the drug should be stopped if 10 day fails. The side effects affecting blood are the same as above, and large doses can lead to toxic hepatitis. Liver and renal insufficiency, pregnant women should use it with caution or disable it.

6. Isoprotein therapy intramuscular injection of milk or intravenous injection of typhoid vaccine causes fever, which can also reduce inflammation. This is an ancient treatment, often used for suppurative eye disease or uveitis. Although it is not as good as corticosteroids at present, it is still one of the commonly used therapies.

In addition, it is also important to pay attention to physical and mental rest, strengthen exercise and nutrition and improve resistance. According to the immune status of patients, transfer factors can be applied.

The clinical types of uveitis are generally divided into three categories according to the etiology, clinical manifestations or pathological changes, namely suppurative, exudative and special.

Pyogenic uveitis

Suppurative uveitis can start from the front or the back. It is characterized by violent onset, rapid development and a large amount of purulent exudate. If not treated in time, it will soon invade panuveitis, form panophthalmia, and the eyeball tissue will be completely destroyed. The development degree of inflammation mainly depends on the resistance of the whole body and eyes or the number and virulence of invading bacteria, and whether it is treated in time.

Etiology can be divided into two categories: exogenous and endogenous. Exogenous bacteria directly enter the eye from the outside, such as penetrating injury of eyeball, infection after intraocular surgery or perforation of suppurative keratitis. Endogenous factors are generally caused by purulent lesions in other parts of the body, such as puerperal fever, cellulitis and bacteria from some acute infectious diseases entering the intraocular blood vessels, so it is also called metastatic ophthalmia.

The clinical manifestations vary with the lesion site.

1. Ophthalmalgia occurs in the early stage of suppurative iridocyclitis, and the visual acuity decreases rapidly with the increase of exudate. Eyelid swelling, conjunctival congestion, edema, corneal opacity, a large amount of exudate in the anterior chamber, forming hyphema. If the toxicity of infection is weak or treated in time, inflammation may be limited or disappear, but in severe cases, pupillary atresia or pupillary membrane closure may be caused by the organization of anterior chamber exudate. If the inflammation spreads to panuveitis, panophthalmia will occur.

2. Suppurative choroiditis and suppurative endophthalmitis The pathological changes of suppurative choroiditis are limited to vitreous body and choroid, and are often caused by foreign bodies penetrating into vitreous body. Vitreous body is the best culture medium for bacteria, which can quickly aggravate inflammation and form vitreous abscess, but there are few endogenous ones. Except for decreased vision, there is no obvious inflammation in the anterior segment, but light yellow or grayish yellow reflection can often be seen from the pupil area, which is called pseudo-black cat eyes. If it happens to children, it must be distinguished from the real black cat eye, that is, retinoblastoma. If you can't distinguish, there is no hope of vision recovery, you can remove the eyeball to avoid delaying the illness. If inflammation involves panchromatic membrane, it is called suppurative uveitis or suppurative endophthalmitis. The patient suffered from severe pain, pus in the anterior chamber and glass volume, and his vision was completely lost. If inflammation continues to develop, panophthalmia can be formed.

3. Panophthalmia is caused by virulent purulent bacteria, mostly external causes. The disease develops rapidly and is difficult to control. You can be blind within 24 hours. People infected with mold may start unconsciously and make slow progress. The reason why suppurative uveitis develops into panophthalmia is that inflammation spreads to the tissues on the fascia and sclera of the eyeball through the scleral aqueduct, causing edema and infiltration of tissues inside and outside the eye.

The clinical manifestations are as follows: ① The pain is unbearable. ② Total loss of vision. (3) Elevated body temperature, headache, nausea and vomiting. Until surgery or spontaneous perforation of the eyeball. ④ The eyelid is highly swollen, especially the upper eyelid. ⑤ The bulbar conjunctiva is highly edema and hyperemia, even exposed to cracks. ⑥ exophthalmos: the orbital tissue is edema and infiltration, and the eyelids cannot be closed. ⑦ Eye movement limitation: due to the involvement of extraocular muscles, eyeball fascia and adjacent tissues.

In the late stage of the disease, the eyeball wall infiltrates, which leads to the rupture of the eyeball, the discharge of pus and eye contents, and finally the eyeball is completely organized and smaller, forming eyeball tuberculosis. The prognosis of this disease is extremely poor. If the diagnosis and treatment are timely, patients with suppurative iridocyclitis can retain certain vision, while patients with suppurative choroid or endophthalmitis can only retain one blind eyeball. Endogenous cases are often more serious, because there is sepsis all over the body, and unless antibiotics highly sensitive to pathogenic bacteria are used in time, it will be life-threatening.

Treatment should first actively control inflammation. In order to rescue patients with severe intraocular infection, antibiotics and corticosteroids can be injected into anterior chamber or vitreous body at the same time when necessary. Generally, 400 micrograms of gentamicin and 350 micrograms of dexamethasone are commonly used. At the same time, samples were collected for culture. Antifungal drugs such as amphotericin 3 ~ 5 micrograms can also be injected into the glass body.

While applying broad-spectrum antibiotics, bacterial culture and drug sensitivity test of conjunctival sac were performed on exogenous patients, and blood culture was performed on endogenous patients to treat pathogens. In addition to antibiotics, corticosteroid therapy can inhibit inflammation and prevent further damage to eyeball tissue. After active treatment, inflammation continued to progress and vision was completely lost. If there is no hope of recovery, the eyeball should be removed to avoid the development of panophthalmia. If panophthalmia has formed, the eyeball contents are removed.

Exudative uveitis

Exudative uveitis (exudative uveitis 8) generally has the following types:

1. The clinical course of acute iritis varies with the severity of the disease, with an average of 3 ~ 6 weeks. Mild symptoms and signs are not obvious. Typical seizures are sudden congestion of ciliary body, gray deposition on the posterior wall of cornea, unclear dark tissue of iris, and slow response of pupil contraction to light. The exudate is mainly in the anterior chamber, and the eyeball tenderness is not obvious. If treated early and timely, the condition will improve rapidly, otherwise it will leave posterior adhesion of iris and even cause various complications.

2. The clinical symptoms of acute iridocyclitis are the same as those of acute iridocyclitis. However, because inflammation involves the ciliary body, exudate is found not only in the anterior chamber, but also in the vitreous body: acute onset, severe symptoms, obvious pain and ciliary body tenderness, long course of disease, common macular edema and papillitis. If not treated in time, it can cause pupillary atresia, membranous closure and secondary glaucoma, and in severe cases, eyeball atrophy.

3. Chronic cyclophilitis is a very stubborn chronic inflammation with no acute symptoms and slow progress, even after a long illness. Maybe it's allergies. The clinical symptoms are not obvious, with a small amount of posterior corneal deposition, which is periodically aggravated, eventually leading to ciliary membrane and cataract, and the eyeball gradually shrinks after many years.

4. According to the scope and shape of the lesion, exudative choroiditis can usually be divided into three types:

(1) Diffuse choroiditis is rare and can be caused by syphilis, tuberculosis and some acute infectious diseases, but the etiology of many cases is unknown. At the early stage of the disease, there were several exudation points, the lesions gradually expanded and merged with each other, most of the fundus was involved, and the old and new lesions coexisted. At the same time, there is pigment disorder and accumulation in the pigment epithelium, which is similar to the form of retinitis pigmentosa and is called secondary retinitis pigmentosa. Sometimes there are centripetal annular scotoma and night blindness.

(2) Disseminated choroiditis is common, and isolated lesions are scattered all over the fundus. The acute exudation period is very short, so the cases seen in clinic are often atrophic lesions, and sometimes old and new lesions coexist. Vitreous opacity, congestion and edema of optic papilla often occur in acute stage, and optic atrophy may occur in the future.

(8) Localized exudative choroiditis is the most common type. It is a localized lesion with one or two or three exudation points, which is larger than disseminated inflammation. Lesions can occur in any part of the fundus. There are two important people in clinic:

1) The patients with myopic papillary choroiditis (Jen8en disease) are mostly young people, which is generally thought to be caused by tuberculosis. In recent years, many cases reported abroad are positive for toxoplasmosis. The lesions near the optic papilla are mostly oval or larger than the optic papilla, and other parts of the fundus are normal, often accompanied by vitreous opacity and visual field defect of nerve fiber bundles. The focus is the fan-shaped defect on the nasal side of the optic papilla, the Bjerrum scotoma on the temporal side, and the central blind spot if it invades the macula bundle of the papilla. The course of the disease is slow, and finally atrophy spots are left.

2) Central choroiditis This refers to choroidal invasion of macula. Lesions are the same as other localized choroiditis. Its severity lies in the appearance of central scotoma, which greatly affects vision. Generally, it is a single lesion, which is relatively large and nearly round. After the inflammation subsided, pigment hyperplasia gradually formed atrophic spots. In recent years, some people think that old choroiditis in macula is often a typical change of congenital toxoplasmosis.

5. Uveitis (chronic posterior ciliary inflammation) Uveitis 8 is a chronic inflammation of the flat part of the ciliary body and the peripheral part of the choroid. This is common, mostly bilateral youth, and the reason is unknown. It is characterized by colloidal exudate around the fundus, which progresses slowly and is easy to cause organic changes.

The clinical manifestations of this disease are complex, and the severity and duration of the disease vary. In the early stage, there was no change or only mild inflammation in the anterior segment of the eye, and tiny punctate or oily gray deposits appeared in the posterior part of the cornea, and the anterior chamber flash was weakly positive, with a small amount of plankton. The colloidal yellow-gray exudation at the corner of the room is easy to form anterior adhesion of iris root by gonioscopy. This exudation can sometimes be seen when the anterior segment is normal. There are yellow exudative masses at the serrated edge, the flat part of ciliary body and the peripheral part of retina, which are often accompanied by vasculitis at the end of retina, white sheath beside blood vessels or vascular occlusion. With the progress of the course of the disease, the exudative mass merged into a large piece, covering the underlying tissue, and the exudation around it increased, extending to the lower part of the fundus. The exudate can fall off from the agglutination block or around the blood vessels, and before it enters the vitreous body near the retina, it appears as a white or yellowish flocculent snow block, showing snowball-like vitreous opacity. Macular edema and pigment disorder often occur for a long time. The rapid leakage of fluorescein from fluorescein angiography into vitreous body is also one of the typical manifestations of this disease.

According to the clinical course, the disease can be divided into the following types:

(1) Benign type has a good prognosis. After several months, exudation disappears or there is only slight peripheral choroidal atrophy and a small amount of anterior adhesion residue.

(2) The secondary choroidal retinal detachment is mainly located in the peripheral part of the fundus, which is caused by exudation and may be accompanied by secondary retinal detachment without perforation. This type must be differentiated from primary retinal detachment. In some cases, after several months of corticosteroid treatment, the inflammation subsided, the retina detached and the vision recovered. The prognosis of surgical treatment is not good.

(3) The type of ciliary body membrane formation is malignant and progressive, with a large amount of grayish yellow exudation at the serrated edge. After several months, there are new blood vessels from the ciliary body in the exudate, which gradually develop and invade the equatorial part of the lens and proliferate on the posterior capsule of the lens to form the ciliary body membrane. At this time, complicated cataract began, vitreous opacity also increased, and the retina was often pulled open by the ciliary body membrane. The further systematization of pathological tissue can make the iris septum of lens move forward and the angle of chamber close, resulting in secondary glaucoma.

(4) Vascular atresia is mainly manifested as vascular changes. Vasculitis develops from the peripheral part to the optic papilla, sometimes the sheath around the vein is too dense to see the blood column clearly, and sometimes the vein is occluded.