bubble_chart Overview

Anterior uveitis, also known as iridocyclitis, involves inflammation of the iris that often affects the ciliary body. Therefore, isolated cases of iritis or cyclitis are rare in clinical practice, and they usually occur simultaneously.

bubble_chart Clinical Manifestations

1. Subjective Symptoms

Pain, photophobia, tearing, and decreased vision are the main features of this disease.

The pain is caused by toxic stimulation of the trigeminal nerve endings in the iris and ciliary body, contraction of the ciliary muscle, and pressure from swollen tissues, which can radiate to the eyebrow and cheek. There is obvious tenderness in the ciliary body, and the pain worsens at night. In the acute phase, it is often accompanied by corneal inflammation, resulting in photophobia, tearing, and a sudden decrease in vision. This is due to corneal edema, keratic precipitates, and inflammatory exudates affecting light entry. The ciliary body, stimulated by inflammation, undergoes reflex spasm, causing pseudomyopia. In advanced stages, it may be complicated by macular edema and optic neuritis.

2. Signs

1. Ciliary congestion: There is obvious ciliary congestion, and in severe cases, mixed congestion and conjunctival edema may occur.

2. Keratic precipitates (KP): Inflammatory cells and pigments in the aqueous humor adhere to the rough corneal endothelium due to the temperature difference between the back of the cornea and the surface of the iris, influenced by the centrifugal force and gravity of the aqueous humor convection in the anterior chamber. The precipitates mostly deposit in the lower central part of the cornea, forming a triangular distribution with the apex towards the pupil area, with larger particles below and smaller particles above.

Depending on the nature of the inflammation, the severity and duration of the exudates, and the size, shape, and quantity, the manifestations vary. Large, gray-white, suet-like KP is characteristic of chronic inflammation; fine, gray, dust-like KP is more common in acute or allergic granulomatous diseases. Occasionally, white KP can be seen in normal individuals without signs of iritis, known as physiological KP, so it should be differentiated and confirmed in combination with other clinical signs.

3. Aqueous humor turbidity: Due to inflammation, the protein content in the aqueous humor increases, making it turbid. Under the slit lamp, the aqueous humor shows a faint gray reflective band, known as the Tyndall sign, indicating active inflammation. In severe cases, fibrinous and purulent exudates may appear, settling in the lower part of the anterior chamber due to gravity, forming a fluid level known as hypopyon. If blood vessels rupture, red blood cells may extravasate, causing hyphema.

4. Blurred iris texture: In iritis, iris blood vessels dilate, followed by edema infiltration, darkening of the color, and blurred surface texture. In granulomatous iridocyclitis, iris nodules can be seen, with deep and superficial types. Deep nodules, located at the pupillary margin, appear as translucent small gray masses called Koeppe nodules, mostly seen in the early stages of subacute or chronic inflammation, varying in number and disappearing within a few days. Superficial nodules are mostly near the iris contraction furrow, known as Busacca nodules. These nodules can disappear quickly, occasionally forming aging and neovascularization. With recurrent inflammation, the iris atrophies, forming organized membranes and new blood vessels on its surface, indicating a state of iris repair.

5. Miosis: In the early stages of iritis, due to iris congestion, edema, cell infiltration, and the toxic stimulation of exudates, both the sphincter and dilator muscles of the pupil contract, resulting in miosis and a sluggish light reflex.

6. Vitreous opacity: The ciliary body is adjacent to the vitreous, and fine dust and flocculent exudates from iridocyclitis can invade the posterior chamber of the lens and the anterior vitreous, causing opacity.

bubble_chart Treatment Measures

Acute iridocyclitis must be accurately diagnosed and promptly treated to eliminate the risk of blindness and preserve good vision. The treatment principles are as follows:

1. Mydriasis: Once the diagnosis is confirmed, immediate mydriasis should be performed to dilate the pupil. This is the primary critical measure in treatment. Any delay will inevitably lead to irreversible consequences.

Mydriatic drugs mainly include atropine, such as 1% atropine eye drops, administered 3-6 times daily. Once the pupil is dilated and inflammation slightly subsides, reduce to 1-2 times daily to maintain pupil dilation until half a month to one month after the inflammation subsides, to consolidate the effect.

The main effect of atropine is to relax the ciliary muscle, reducing pressure on the stirred pulse, enhancing blood circulation in the pigment membrane, and decreasing capillary permeability, thereby reducing exudation and exerting anti-inflammatory effects, promoting inflammation absorption. Additionally, dilating the pupil prevents posterior synechia of the iris or eliminates already formed adhesions, relieving or reducing spasms of the pupillary sphincter and ciliary muscle, allowing the eye to rest well and achieving pain relief.

When using atropine, it is essential to compress the lacrimal sac area to avoid poisoning from absorption by the lacrimal sac and nasal membrane, especially with caution in children and the elderly, particularly those with narrow anterior chambers and a predisposition to glaucoma.

If atropine cannot dilate the pupil, a mixture of 1% cocaine and 0.1% adrenaline in equal parts, 0.3ml, can be injected subconjunctivally near the adhesion, known as forceful mydriasis.

2. Application of corticosteroids: Corticosteroids can reduce and control inflammation, exert anti-inflammatory and anti-allergic effects, decrease capillary permeability, reduce tissue edema and exudation, and lessen fibrous tissue proliferation and collagen deposition, inhibiting allergic reactions. Do not abruptly stop medication after more than two weeks of use; reduce dosage as appropriate.

Administration methods: oral medication, eye drops, or subconjunctival injections. Start with a sufficient dose of oral medication to quickly control inflammation, then maintain with the minimum dose until the inflammatory activity completely subsides.

For anterior uveitis, local application of 0.5% cortisone or 0.05% dexamethasone, 4-5 times daily, or hourly during the convalescence stage, can be reduced. Sometimes, subconjunctival injection is also possible.

For panuveitis or choroiditis patients, 0.025% dexamethasone 0.3ml can be injected subconjunctivally or subtenon, or combined with systemic administration. For severe cases, hydrocortisone 200-250mg or dexamethasone 5-10mg can be intravenously dripped once daily to ensure sufficient dosage reaches the intraocular tissues.

3. Non-steroidal anti-inflammatory drugs: Sodium salicylate, phenylbutazone, and indomethacin have analgesic and anti-inflammatory effects, mainly inhibiting the increase of prostaglandins in the anterior chamber during uveitis to achieve anti-inflammatory or hypotensive effects. Commonly used aspirin 0.5g, three times daily, and indomethacin 25mg, three times daily.

4. Antibiotics: For suppurative anterior uveitis, broad-spectrum antibiotics can be applied locally or systemically.

5. Immunotherapy: For severe uveitis and sympathetic ophthalmia, when steroids are ineffective, consider using immunosuppressants or immunoenhancers to adjust abnormal immune functions. Commonly used immunosuppressants include:

⑴ Cyclophosphamide: Can be used alone or in combination with steroids. Common oral dose is 50-100mg, twice daily, for two weeks as a course. Intravenous injection of 100-200mg dissolved in 20ml of saline, once daily or every other day. Monitor blood count to prevent side effects.

⑵ Ethylenedimethanesulfonate (AT-1727), 0.4g each time, three times daily, for 2-3 weeks, stop for one week, then repeat for 1-2 courses.

⑶ Chlorambucil (Chlorambucil, Leukeran, chlorambucil): The usual starting dose is 2 mg daily, increasing to 2-10 mg daily, with a maximum dose not exceeding 20 mg per day.

Common immunostimulants include levamisole, used for individuals with compromised immune function.

6. Hot compress or shortwave therapy: dilates blood vessels, promotes blood circulation, and enhances the absorption of inflammation.

7. Symptomatic treatment

⑴ For secondary glaucoma, oral vinegar acetazolamide can be administered to reduce intraocular pressure.

⑵ For iris bombe, iris puncture or iridectomy can be performed.

⑶ For secondary glaucoma caused by peripheral iris adhesions, peripheral iridectomy can be performed.

⑷ For concurrent internal visual obstruction, internal visual obstruction removal surgery can be performed after inflammation is controlled.

bubble_chart Complications

1. Corneal membrane opacity: Descemet's membrane folds and corneal epithelial edema with bullous keratopathy, advanced stage develops band-shaped keratopathy.

2. Posterior synechia of the iris: During iritis, due to fibrinous exudation, adhesions form between the pupillary margin of the iris and the anterior lens capsule. Early adhesions can be separated with mydriatics. If the exudate has organized and the adhesions are firm, it is difficult to separate them with mydriatics, or the separated part of the pupil may have a petaloid irregular edge.

3. Seclusion of the pupil: After complete fibrosis of posterior synechia of the iris, it can never be separated, and the iris around the pupil is completely adherent to the anterior surface of the lens, interrupting the circulation of aqueous humor between the anterior and posterior chambers.

4. Peripheral anterior synechia of the iris or goniosynechia: Due to increased posterior chamber pressure or accumulation of exudate, the peripheral iris or iris root adheres to the posterior surface of the cornea.

5. Occlusion of the pupil: A large amount of exudate deposits in the pupillary area, forming a thin membrane covering the anterior surface of the lens.

6. Iris bombe: Because the aqueous humor cannot flow from the posterior chamber to the anterior chamber, it is blocked in the posterior chamber, increasing the posterior chamber pressure. The accumulation of aqueous humor pushes the iris forward, causing it to bulge.

7. Complicated cataract: During iritis, changes in the composition of the aqueous humor and inflammatory toxins alter the external environment of the lens, disrupting its normal physiological metabolism. This leads to opacification of both the anterior and posterior cortex of the lens, rapidly forming a complete cataract.

8. Secondary glaucoma: Due to goniosynechia, seclusion of the pupil, vascular dilation during acute inflammation, plasma exudation, and increased viscosity of the aqueous humor, intraocular pressure rises, leading to secondary glaucoma.

9. Fundus lesions: In the late stage [third stage] or severe cases, complications may include macular edema or cystoid degeneration, or associated optic disc vasculitis.

10. Phthisis bulbi: Exudative organized tissue near the ciliary body forms fibrous membranes, causing retinal detachment and damaging the ciliary body, reducing aqueous humor secretion and lowering intraocular pressure. Additionally, repeated inflammation of the ciliary body leads to necrosis, causing the eyeball to shrink and atrophy. {|109|}