What Is Iridocyclitis?

Iris ciliary body inflammation is also called anterior uveitis. The inflammation of the iris often affects the ciliary body, so iritis or ciliary body inflammation alone is rarely seen clinically. Often at the same time.

Basic Information

nickname
Anterior uveitis
English name
iridocyclitis
Visiting department
Ophthalmology
Common locations
eye
Common causes
Infectious and non-infectious factors
Common symptoms
Pain, photophobia, tearing, and vision loss

Causes of iris ciliary body inflammation

There are many causes of iris ciliary body inflammation. In addition to ocular trauma, bacteria, viruses, foreign bodies, chemicals, etc. directly enter the eye and cause inflammation, systemic diseases such as tuberculosis, leprosy, rheumatism, and apical spirochondria cause iris and eyelashes. An important cause of stigmatitis. Other eye tissues near the iris and ciliary body, such as keratitis and scleritis, can also cause this disease.

Clinical manifestations of iridocyclitis

Symptoms
Pain, photophobia, tearing, and vision loss are the main features of the disease.
The trigeminal nerve of the iris ciliary body is not slightly toxic. The pain caused by the contraction of the ciliary muscles and the compression of the swollen tissue can be reflected to the arch and cheeks. There is obvious tenderness in the ciliary body. It is often accompanied by corneal inflammation and shame, tearing vision may suddenly drop. This is due to intra-corneal edema, post-corneal deposits and inflammatory exudation affecting the entry of light, and the ciliary body is caused by inflammation to cause reflex spasm and cause false Myopia, late stage can be associated with macular edema and optic neuroretinitis.
2. Signs
(1) Ciliary congestion There is obvious ciliary congestion, and severe congestion and conjunctival edema can also form in severe cases.
(2) Post-corneal deposits. Edema. Inflammatory cells and pigments. Due to the temperature difference between the back of the cornea and the surface of the iris, the centrifugal force and gravity of the anterior aqueous convection affect the adhesion to the rough corneal endothelium after inflammation, that is, post-corneal deposits. The deposits are mostly triangularly distributed at the lower part of the cornea center, with the tip facing the pupil area, with large particles below and small particles above.
Depending on the nature of the inflammation, the severity of the exudate, the length of time, the size, shape, and quantity vary, large gray-white sheep fat-like KP is characteristic of chronic inflammation; small gray dust-like KP is more common in acute or allergic granulation Swollen diseases, white KP can also be seen in some normal people, but without the manifestation of iris, it is physiological KP, so it should be diagnosed in combination with other clinical signs.
(3) Turbid aqueous humor Due to inflammation, the protein content in aqueous humor increases, the aqueous humor becomes mixed, and a light-colored reflective reflective band appears in the aqueous humor under the slit lamp. It is called Tyndall sign, which is an active inflammation sign. It can appear in severe cases. Cellulose and purulent exudates are deposited in the lower part of the anterior chamber due to gravity, showing a fluid level in the anterior chamber. If blood vessels rupture and red blood cells overflow, anterior chamber hemorrhage occurs.
(4) When the texture of the iris is unclear , the iris vasodilatation infiltrates with edema, the color becomes dark, and the texture of the iris surface is unclear. In granulomatous iris ciliary body inflammation, iris nodules can be expected, with deep and There are two types of superficial layers, the deeper ones are located at the edge of the pupils and are translucent small gray clusters. They are called koeppew nodules, which are more common in the early stages of subacute or chronic inflammation. The number varies and can disappear within a few days. The superficial nodules are mostly in the iris volume. In the vicinity of the retraction wheel, it is a Busacca nodule. This nodule can quickly disappear and occasionally form aging and new blood vessels. When inflammation recurs, the iris shrinks, and the surface forms an organic membrane and new blood vessels, which is for iris repair. status.
(5) Pupil shrinkage In the early stage of iris inflammation, due to iris congestion and edema, cell infiltration, and exudate toxins stimulate the pupil sphincter and sphincter to contract at the same time, showing pupil shrinkage and slow response to light.
(6) Opaque vitreous The ciliary body is adjacent to the vitreous body, and the fine dusty Egyptian floc exudates of the iris and ciliary total inflammation can invade the posterior cavity of the lens and the front of the vitreous body, making it cloudy.

Examination of iridocyclitis

Check vision, fundus, and intraocular pressure.

Diagnosis of iridocyclitis

1. There may be infection lesions, systemic connective tissue diseases, etc.
2. Vision loss with eye pain, photophobia, and tearing.
3. Ciliary or mixed hyperemia, tenderness in the ciliary area.
4. Gray-white or brown-gray deposits behind the cornea, mostly below.
5. Turbidity in the anterior chamber, flocculent exudation or pus in the anterior chamber.
6. The texture of the iris is unclear, there may be nodules or atrophy lines, the pupils shrink, the response to light is slow, the pupils are stuck behind the edge of the pupil, or the anterior iris is stuck.
7. Can cause corneal edema, complicated cataract and vitreous opacity.
8. Differentiation from acute angle-closure glaucoma and acute conjunctivitis during acute inflammation.
If ciliary congestion is found, pupils are diminished (due to drug exclusion), and ciliary tenderness, the disease should be highly suspected. The diagnosis can be confirmed if the leakage in the anterior chamber water can be observed with a slit lamp microscope.

Differential diagnosis of iridocyclitis

Acute conjunctivitis
Acute onset, foreign body sensation, burning sensation, and little secretion. Examination showed swelling of the eyelid and conjunctival congestion. These manifestations were significantly different from photophobia, tearing, blurred vision, ciliary congestion, and anterior chamber reactions in acute anterior uvitis.
2. Acute angle-closure glaucoma
Acute onset, sudden vision loss, headache, nausea, vomiting, corneal epithelial edema, shallow anterior chamber, anterior chamber flashes, etc., but no anterior chamber inflammatory cells, pupils are oval-shaped spreading, increased intraocular pressure, and acute anterior grape The corneal inflammation of the membrane is transparent, a large number of KP, the anterior chamber depth is normal, a large number of inflammatory cells in the aqueous humor, the pupils are narrowed, and the pressure of the eye is normal or low.
3. Differentiated from intraocular tumors
Some primary intraocular tumors or intraocular metastases of tumors can cause changes in atrial abscess, but they can be distinguished from medical history, clinical examination of systemic lesions, X-rays, ultrasound, CT and other MRI examinations. .
4. Differentiation from pan-uveal inflammation that can cause pre-uveal inflammation
Some types of uveitis, such as Behcet's disease uveitis, Vogt-Koyanagi Harada disease, etc. can be manifested as whole uveitis, so attention should be paid to the identification during diagnosis.

Complications of iridocyclitis

Corneal opacity
Posterior elastin folds and corneal epithelial vesicular-like keratitis lesions, before the corneal shingles occur later.
2. Post-iris adhesions
In the case of irisitis, due to the fibrous exudation, adhesions occur between the pupil edge of the iris and the anterior capsule of the lens. Early adhesion can be pulled apart by the pupil dilator. If the exudate has been mechanicalized, the adhesion is firm, and it is not easy to pull with the pupil dilator. Open, or pull apart part of the pupils with petal-like edges and irregular edges.
3. Pupil atresia
After the iris adhesions are completely fibrotic, they can never be pulled apart, and the iris around the pupil is completely adhered to the front surface of the lens, and the aqueous humor circulation is interrupted.
4. Adhesion around the iris or corner adhesion
Due to increased posterior chamber pressure or accumulation of exudate, the peripheral iris or root of the iris adheres to the back of the cornea.
5. Pupil membrane closure
A large amount of exudate is deposited in the pupil area to form a thin film, covering the front surface of the lens.
6.Iris bulging
Because the aqueous humor cannot flow forward from the posterior chamber and is blocked in the posterior chamber, the pressure in the posterior chamber increases, and the accumulation of aqueous humor causes the iris to move forward and become swollen.
7. Concurrent cataract
When the iris is inflamed, the properties of the aqueous humor change. The inflammation in the aqueous humor changes the external environment of the crystal, which also changes the normal physiological metabolism of the crystal, causing the turbidity of the cortex before and after the crystal, and the formation of a complete cataract soon.
8. Secondary glaucoma
Because of angular adhesion, pupil closure, coupled with vasodilation in the acute inflammatory phase, plasma leakage, an increase in the viscosity of the anterior aqueous solution leads to increased intraocular pressure and secondary glaucoma.
9. Fundus Lesions
Late or severe cases may be accompanied by macular edema or cystoid degeneration, or with optic disc vasculitis.
10. Eyeball atrophy
Exudative mechanized tissue near the ciliary body forms a fibrous membrane to pull the retinal detachment, destroying the ciliary body to reduce the secretion of aqueous humor, reducing intraocular pressure, and the repeated inflammation of the ciliary body itself becomes necrotic tissue, causing the eyeball to shrink and shrink.

Iris ciliaryitis treatment

Drug treatment
There are oral medication, eye drops or subconjunctival injection. Oral medicine should be given in sufficient amount at the beginning to quickly control inflammation, and finally maintain the minimum amount until inflammation activity completely subsides.
For anterior uveitis, use 0.5% cortisone or 0.05% dexamethasone, 4 to 5 times a day, or once an hour. The recovery period is reduced. Sometimes subconjunctival injection is sufficient.
For patients with panuveitis or choroiditis, 0.025% dexamethasone can be injected under the conjunctiva or subocular fascia, or combined with systemic administration. In severe cases, hydrocortisone or dexamethasone is administered intravenously once a day. In this way, sufficient amount can reach the eye tissue.
(1) Non-hormonal anti-inflammatory agent Sodium salicylic acid and baitazone have analgesic and anti-inflammatory effects. It mainly inhibits the increase of prostaglandin in the anterior chamber during uveitis to achieve anti-inflammatory or hypotensive effects. Aspirin is commonly used.
(2) Antibiotics If the department is purulent anterior uveitis, a broad-spectrum antibiotic can be applied locally or systemically.
(3) Immunotherapy For severe uveitis and sympathetic ophthalmia, immunosuppressants or immune enhancers can be considered when hormones are not effective. To adjust abnormal immune function, commonly used immunosuppressants are: Cyclophosphamide can be used alone or in combination with steroids. Ethomorpholine three times a day, continuously for 2 to 3 weeks, stop iris ciliary body inflammation medicine for 1 week, and then use 1 to 2 courses. Painfulness.
Commonly used immune enhancers are levamisole, which is used for those with low immune function.
2. Hot compress or short wave therapy
Dilate blood vessels, promote blood circulation, and strengthen inflammation absorption.
3. Symptomatic treatment
(1) For patients with secondary glaucoma, acetaminophen can be taken orally to reduce intraocular pressure.
(2) For iris swelling, iris puncture or iris removal is feasible.
(3) Peripheral iris resection is feasible for secondary glaucoma caused by adhesions around the iris.
(4) Cataract extraction can be performed under the control of inflammation for patients with cataract.

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