Anterior uveitis, also known as iridocyclitis, is an inflammation of the iris that often affects the ciliary body, so it is rare to see iritis or ciliary body alone. It often develops simultaneously.
Anterior uveitis, also known as iridocyclitis, includes iritis, ciliary body inflammation, and iridocyclitis. Because the iris and ciliary body are anatomically interconnected and closely related, and because they supply blood to the same large ring of the iris, the iris and ciliary body are often inflamed at the same time. Iridocyclitis is one of the common blinding eye diseases and is the most common form of uveitis. The main clinical manifestations are ocular redness and pain, decreased visual acuity, cloudy atrial fluid and posterior corneal deposits. If not treated promptly, serious complications such as secondary glaucoma, concurrent cataract and ocular atrophy may occur and lead to blindness.
Clinical manifestations
I. Self-perceived symptoms
Pain, photophobia, lacrimation and vision loss are the main features of this disease.
The trigeminal nerve endings of the iris ciliary body are stimulated by toxicity, and the pain produced by the contraction of the ciliary muscle and the compression of the swollen tissue can be reflected to the arch of the eyebrow and the cheek, and there is obvious pressure pain in the ciliary body, and the pain increases at night. The acute phase is often accompanied by inflammatory reaction of the cornea with shyness, lacrimation and sudden loss of vision, which is due to intracorneal edema, posterior corneal deposits and inflammatory exudation that affects the entry of light, and reflex spasm of the ciliary body stimulated by inflammation that causes pseudomyopia. In late stages, macular edema and optic nerve retinitis may be combined.
Physical signs
1. Ciliary congestion: there is obvious ciliary congestion, and in severe cases, mixed congestion and conjunctival edema may form.
2, posterior corneal deposits (kerato-precipitates, KP): atrial edema inflammatory cells and pigments due to the temperature difference between the back of the cornea and the iris surface, with the centrifugal force and gravitational influence of the anterior atrial convection adhering to the rough corneal endothelium after inflammation, that is, posterior corneal deposits. The deposits are mostly deposited in the lower part of the corneal center in a triangular distribution with the tip toward the pupil area, with large particles at the bottom and small particles at the top.
According to the nature of inflammation, the exudate is light and heavy, the length of time, the size of the morphology, the number of different performance. Large grayish lambda-like KP is characteristic of chronic inflammation; fine gray dusty KP is seen in acute or allergic granulomatous disorders. The white KP can also be seen in individual normal people, without the performance of iritis, as physiological KP, so it should be combined with other clinical signs to differentiate the diagnosis.
3. cloudy atrial fluid: due to inflammation, the protein content in the atrial fluid increases, and the atrial fluid becomes mixed, showing a pale reflective reflective band in the atrial fluid under the slit lamp, called Tyndall’s sign. This is indicated as a sign of active inflammation. In severe cases, fibrinous and purulent exudate may appear, which is deposited in the lower part of the anterior chamber due to gravity, showing a plane of fluid known as anterior chamber pus (hypopion). If the blood vessels rupture and the red blood cells spill out, it will produce an anterior chamber hematoma (hyphema).
An exudate in the anterior chamber fluid is an important sign of iridocyclitis, but requires a skilled ophthalmologist to recognize it under a slit-lamp microscope. There are three manifestations, which are usually present simultaneously but not exclusively.
(1) Floaters in the atrial water: In inflammation, the atrial water has swimming microscopic particles of exuding inflammatory cells.
(2) Positive atrial water glitter: Atrial water glitter is Tyndall’s phenomenon. Under normal conditions, Tyndall’s phenomenon is negative. Due to inflammation, the number of proteins and cells in the atrial fluid increases. When the slit lamp point light source is shone onto the cornea, a beam of light appears in the atrial fluid, connecting the cornea and the crystal into a band of light, just as seen in a room full of flying dust shot into a beam of light.
(3) posterior corneal wall deposits: KP for short, composed of lymphocytes and plasma cells, small dots, grayish white when fresh inflammation, darkening as the inflammation subsides. Numerous dots are arranged in a triangular shape in the posterior corneal wall, with the base of the triangle facing downward.
4. Iris texture is unclear: In iriditis, the iris is dilated and subsequently infiltrated with edema, the color darkens, and the iris surface texture is unclear. The deep layers are located at the pupillary margin in small translucent gray clusters called koeppew nodules, which are mostly seen in the early stages of subacute or chronic inflammation and vary in number and may disappear within a few days. The superficial nodules are mostly in the vicinity of the iris convoluted wheel, hence Busacca’s nodule. This nodule may disappear quickly and may occasionally form aging and neovascularization. With recurrent inflammation, the iris undergoes atrophy and its surface forms mechanized membranes and neovascularization, which is the state of iris repair.
5, pupil narrowing: in the early stages of iris inflammation, due to iris congestion and edema, cellular infiltration, and exudate toxins stimulate the pupillary sphincter and open muscle contraction at the same time, and exhibit pupil narrowing, no reflex to light or Liu light response insensitive. If the posterior adhesions are extensive into a week, it is called pupillary atresia, and secondary glaucoma can occur because atrial fluid cannot flow from the posterior chamber to the anterior chamber. A large amount of inflammatory exudate covers the pupil area, and after mechanization is called pupillary membrane closure.
6, vitreous clouding: ciliary body and vitreous adjacent, iridocyclitis of fine dust and flocculent exudate can invade the posterior chamber of the crystal and the anterior part of the vitreous, making it cloudy and
7. Ciliary pressure pain, which refers to pressure pain in the ciliary area. During the examination, the patient is asked to look down, and the presser touches the eyeball with a finger on the upper lid, and when there is pain, it is positive for ciliary pressure pain, which is a manifestation of inflammation in the ciliary body part.
Treatment measures]
Acute iridocyclitis must be diagnosed accurately and treated promptly and properly to eliminate the crisis of blindness and to preserve better vision.
1, dilate the pupil: once the diagnosis is clear, immediately dilate the pupil, so that the pupil dilates, which is the first critical measure of treatment. If delayed, it will inevitably result in irreversible consequences.
The main pupil-diluting drug is atropine, 1% atropine eye drops, 3 to 6 times a day, after the pupil is dilated and the inflammation is slightly resolved, 1 to 2 times a day to keep the pupil dilated until half a month to 1 month after the inflammation has subsided. For consolidation.
The effect of atropine is mainly ciliary machine relaxation to reduce the pressure on the arteries to enhance blood circulation in the uvea, reduce capillary permeability, reduce exudation, play an anti-inflammatory role, and promote the absorption of inflammation. In addition, the pupil is dilated to prevent post-iris adhesions or to eliminate, release or reduce the spasm of the pupillary sphincter and ciliary muscle that has formed. The eye is made to rest well for pain relief purposes.
When using atropine drops, the tear sac must be compressed to avoid poisoning after absorption by the tear sac and nasal membrane, and it should be used with caution especially for children, and with caution for the elderly, especially those with anterior chamber stenosis with glaucomatous qualities. If atropine does not expand the pupil, you can add 1% cocaine and 0, 1% adrenal equivalent mixture of 0, 3ml, subconjunctival injection in the vicinity of the adhesions, the so-called strong pupil dilation.
2, the application of corticosteroids: the use of corticosteroids can reduce and control inflammation, play an anti-inflammatory and anti-allergic role, reduce capillary permeability, reduce tissue edema and exudation, reduce fibrous tissue hyperplasia and collagen deposition. Inhibit allergic reactions. Do not stop the drug abruptly in those who have been on it for more than 2 weeks. Reduce the dosage as appropriate.
Method of administration.
There are oral medications, eye drops or subconjunctival injections: oral medications should be given in adequate amounts at the beginning for rapid control of inflammation and finally with minimal most maintenance until the inflammatory activity has completely subsided mainly. Topical drops of 0,5% of pine or 0,05% of dexamethasone are used for anterior uveitis, 4-5 times a day, or once an hourly point, with a reduction in the recovery period. Sometimes subconjunctival injection is also sufficient. For patients with total uveitis or chorioretinitis, 0,025% dexamethasone 0,3ml can be used with subconjunctival or subfascial injection of the eye, or combined with systemic administration, hydrocortisone 200-250mg or dexamethasone 5-10mg intravenous drip once a day in severe cases, so that a sufficient amount can reach the intraocular tissue.
3.Non-hormonal anti-inflammatory agents: sodium salicylate ploctone and anti-inflammatory pain have analgesic and anti-inflammatory effects. Mainly inhibit the increase of prostaglandin in the anterior chamber during uveitis to achieve anti-inflammatory or hypotensive effects, commonly used aspirin 0,5g, three times a day, and anti-inflammatory pain 25mg, three times a day.
4, antibiotics: If it is septic anterior uveitis can be local or systemic application of broad-spectrum antibiotics.
5, immunotherapy: for severe uveitis and sympathetic ophthalmia, the use of hormones is not effective, consider the use of immunosuppressants or immune enhancers. To adjust the abnormal immune function, the commonly used immunosuppressants are.
(1) cyclophosphamide (cyclophosphamide): can be used alone or with steroid therapy, commonly used oral dose of 50-100mg, twice daily divided, even 2 weeks as a course of treatment. For intravenous injection, dissolve 100-200mg in 20ml of physiological brine, once daily or every other day. Blood picture should be checked to prevent side effect attacks.
(2) Ethylene double morpholine (AT-1727), 0,4g each time, three times a day, for 2-3 weeks, stop for 1 week, then 1 or 2 courses of treatment.
(3) Painconin (chlocambucil, Leukeuan, aminoglutethimide benzoate): generally start with 2mg per day, aggravate 2-10mg per day, the maximum dose should not exceed 20mg per day.
Commonly used immune enhancers are levamisole, used for immunocompromised people.
6.Hot compress or short wave therapy: dilate blood vessels, promote blood circulation and enhance inflammation absorption.
7.Symptomatic treatment
(1) For secondary glaucoma, oral acetamide can be given to make the IOP drop.
(2) For iris bulge, iris puncture or iridectomy is feasible.
(3) For secondary glaucoma caused by peripheral iris adhesions, peripheral iris resection is feasible.
(4) Cataract extraction can be performed under inflammatory control in cases of complicated cataract.
Complications
1, corneal clouding: posterior elastic layer folds and corneal epithelial blister-like keratitis lesions, late occurrence of corneal herpes zoster anterior.
2, post-iris adhesions: In iritis, adhesions are created between the pupillary margin of the iris and the anterior capsule of the lens due to fibrinous exudation. Early adhesions can be pulled apart with pupil dilators. If the exudate is mechanized and the adhesions are strong, it is not easy to pull them apart with pupil dilators, or if the adhesions are partially pulled apart, the pupil is petal-like with uneven edges.
3. In seclusion of the pupil, the posterior iris adhesions are all fibrotic and can never be pulled apart, and the iris of the pupil is completely adhered to the front surface of the lens, interrupting the anterior and posterior atrial circulation.
4. goniosynechia (adhesions in the periphery of the iris or atrial angle). The peripheral iris or the root of the iris adheres to the back of the cornea due to increased posterior atrial pressure or exudate accumulation.
5.Pupillary membrane closure (oclusion of pupil): A large amount of exudate is deposited in the pupil area to form a film covering the front surface of the lens.
6.Iris bombe: The iris bombe is bulging because the atrial water cannot flow forward from the posterior chamber and is obstructed in the posterior chamber, which increases the posterior chamber pressure and causes the atrial water to accumulate and push the iris forward.
7.Complicated cataract: When the iris is inflamed, the nature of the atrial water changes, and the inflammatory toxicity in the atrial water changes the external environment of the crystal, thus also changing the normal physiological metabolism of the crystal, resulting in clouding of both the anterior and posterior cortices of the crystal, and soon forming a complete cataract.
8, secondary glaucoma: secondary glaucoma due to atrial angle adhesions, pupil atresia, coupled with vasodilatation and plasma leakage during the acute inflammatory phase, and increased viscosity of anterior atrial aqueous leads to increased intraocular pressure.
9, fundus lesions: late lesions or severe cases can be complicated by macular edema or cystic degeneration, or accompanied by optic disc vasculitis.
10, eye atrophy: exudative mechanized tissue near the ciliary body forms fibrous membrane traction retinal detachment, which destroys the ciliary body to reduce atrial aqueous secretion and reduce intraocular pressure. Together with the repeated inflammation of the ciliary body itself into necrotic tissue, resulting in shrinkage and atrophy of the eye.
Diagnostic points]
1. There may be infectious lesions, systemic collagen diseases, etc.
2, vision loss with ocular pain and photophobia and tearing.
3, ciliary or mixed congestion, ciliary area may have pressure pain.
4.Posterior corneal gray or brownish gray deposits, more below.
5, anterior chamber clouding, flocculent exudate or anterior chamber pus accumulation.
6.Iris texture is unclear, there may be nodules or atrophic lines, pupil narrowing, blunted response to light, posterior adhesions at the pupil margin, or anterior adhesions at the periphery of the iris.
7. It may cause corneal edema, concurrent cataract and vitreous clouding.
8. Differentiate from acute angle-closure glaucoma and acute conjunctivitis in case of acute inflammation.
The disease should be highly suspected if ciliary congestion, pupil narrowing