bubble_chart Overview

Posterior uveitis, also known as choroiditis, occurs because the blood vessels of the choroid originate from the short posterior ciliary arteries, allowing it to develop independently. However, since the choroid is closely attached to the retina and supplies blood to the outer layers of the retina, it often affects the retina, leading to retinochoroiditis.

bubble_chart Clinical Manifestations

1. Based on the extent and morphology of the lesions, choroiditis can be classified into three types: localized choroiditis, disseminated choroiditis, and diffuse choroiditis. These three types of choroiditis may occur independently or represent stages of inflammatory progression.

1. Localized choroiditis: This occurs when a balance is maintained between the pathogenic factors and the body's tissues, confining the lesion to a specific area. It can occur in the macular region, near the optic disc, or in the peripheral fundus.

2. Disseminated choroiditis: This arises when the pathogenic factors become more aggressive or the body's resistance decreases, resulting in multiple lesions appearing simultaneously on the choroid.

3. Diffuse choroiditis: As the condition progresses, lesions merge to form large areas of inflammation, presenting as a uniform reddish fundus resembling a sunset glow.

2. Clinical Manifestations

1. Subjective Symptoms

Primarily include decreased vision, flashes of light, and floating black shadows in the visual field, sometimes accompanied by micropsia or macropsia.

2. Signs

⑴ Vitreous opacity, composed of lymphocytes and fibrin, appearing as star-shaped, filamentous, dust-like, or snowball-like opacities.

⑵ Choroidal vascular dilation, increased exudation, tissue infiltration, and edema. The fundus shows scattered, diffuse grayish-white or grayish-yellow lesions, round or oval in shape, varying in size, with blurred edges, grade I elevation, and may appear singly or merge into multiple lesions. The surrounding retina may exhibit edema or occasionally hemorrhage.

⑶ After the acute phase, the lesions gradually turn white, forming well-defined atrophic patches with central black patches surrounded by pigment. Sclerotic choroidal vessels may be visible within these atrophic lesions.

bubble_chart Treatment Measures

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

1. **Mydriasis**: Once the diagnosis is confirmed, immediate dilation of the pupil is the primary and critical measure. Any delay will inevitably lead to irreversible consequences.

Mydriatic drugs mainly include atropine derivatives, 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 dilation until 2 weeks to 1 month after the inflammation resolves, ensuring consolidation.

The primary effects of atropine are relaxing the ciliary muscle to reduce pressure on the **stirred pulse**, enhancing blood circulation in the **pigment membrane**, reducing capillary permeability to decrease exudation, exerting anti-inflammatory effects, and promoting inflammation absorption. Additionally, it dilates the pupil, prevents posterior synechiae of the iris, resolves existing adhesions, and relieves spasms of the pupillary sphincter and ciliary muscles, allowing the eye to rest and achieving pain relief.

When applying atropine, pressure must be applied to the lacrimal sac to prevent systemic absorption and toxicity, especially in children. Caution is also required for elderly individuals, particularly those with narrow anterior chambers or a predisposition to glaucoma.

If atropine fails to dilate the pupil, a mixture of 1% cocaine and 0.1% adrenaline (0.3 ml) can be injected subconjunctivally near the adhesion site for **forced mydriasis**.

2. **Corticosteroid Therapy**: Corticosteroids can alleviate and control inflammation, exerting anti-inflammatory and anti-allergic effects, reducing capillary permeability, minimizing tissue **edema** and exudation, and mitigating fibrous tissue proliferation and collagen deposition. They also suppress allergic reactions. If used for over 2 weeks, abrupt discontinuation should be avoided; instead, gradual tapering is recommended.

**Administration Methods**: Options include oral medication, eye drops, or subconjunctival injections. Oral therapy should start with a sufficient dose to rapidly control inflammation, followed by the minimal maintenance dose until complete resolution.

For anterior uveitis, topical 0.5% cortisone or 0.05% dexamethasone eye drops can be used 4–5 times daily or hourly, tapering during the **convalescence stage**. Subconjunctival injections may also be employed.

For panuveitis or choroiditis, 0.3 ml of 0.025% dexamethasone can be injected subconjunctivally or beneath Tenon’s capsule. Systemic administration may also be combined. Severe cases may require intravenous hydrocortisone (200–250 mg) or dexamethasone (5–10 mg) once daily to ensure adequate ocular tissue penetration.

3. **Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)**: Sodium salicylate, phenylbutazone, and indomethacin provide analgesic and anti-inflammatory effects by suppressing elevated prostaglandins in the anterior chamber during uveitis, reducing inflammation or intraocular pressure. Common regimens include aspirin (0.5 g, 3 times daily) or indomethacin (25 mg, 3 times daily).

4. **Antibiotics**: For suppurative anterior uveitis, broad-spectrum antibiotics can be administered topically or systemically.

5. **Immunotherapy**: For severe uveitis or sympathetic ophthalmia unresponsive to steroids, immunosuppressants or immunomodulators may be considered to regulate abnormal immune function. Common immunosuppressants include:

(1) **Cyclophosphamide**: Can be used alone or with steroids. Oral dosage: 50–100 mg twice daily for 2 weeks per course. Intravenous injection: 100–200 mg dissolved in 20 ml saline, administered daily or every other day. Monitor blood counts to prevent **side effects**.

(2) **Bimolane (AT-1727)**: 0.4 g three times daily for 2–3 weeks, followed by a 1-week break, then repeated for 1–2 courses.

(3) Chlorambucil (Chlorambucil, Leukeran, phenylbutyric acid nitrogen mustard): Generally start with 2mg per day, increase to 2~10mg per day, the maximum dose should not exceed 20mg 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 inflammation absorption.

7. Symptomatic treatment

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

⑵ For iris bombé, iris puncture or iridectomy may be performed.

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

⑷ For complicated cataracts, cataract extraction may be performed after inflammation is controlled.

bubble_chart Complications

1. Macular surface folds: The macular area of the preretinal fibrous membrane shows a pearl-like reflection.

2. Macular papilledema: Edema in the macular region often leads to cystic degeneration or even holes.

3. Retinal vasculitis: Such as toxoplasmosis-induced perivasculitis with obvious vascular pulsation.

4. Retinal detachment: Caused by inflammatory exudation and vitreous traction due to organization.