What is posterior uveitis?
Posterior uveitis is a group of inflammatory diseases involving the choroid, retina, retinal vasculature and vitreous, clinically including chorioretinitis, uveitis, chorioretinitis, retinal chorioretinitis and retinal vasculitis. Posterior uveitis is generally characterized by the absence of pain, with loss of vision and significant dark shadows in front of the eyes.
What are the principles of treatment for posterior uveitis?
(1) Those determined to be due to infectious factors should be given the appropriate anti-infective treatment.
(2) Inflammation caused by immune factors is treated primarily with immunosuppressive agents.
(3) Unilateral involvement can be treated with glucocorticoids followed by Tenon subcapsular injection.
(4) For bilateral involvement or unilateral involvement where posterior Tenon subcapsular injection is not appropriate, oral glucocorticoids, nitrogen mustard phenylbutyrate, cyclophosphamide and cyclosporine A are appropriate.
What is total uveitis?
Total uveitis is an inflammation that involves the entire uvea, often with inflammation of the retina and vitreous. The main common types of total uveitis are Vogt-Koyanagi Harada disease and Behcet’s pathology. Because some types of allogranulomatous uveitis are more recalcitrant, immunosuppressive agents should be applied for a long enough period of time, and the combination of drugs often reduces the side effects and enhances the efficacy. Kidney function and blood work should be checked regularly during treatment to avoid serious side effects.
What is sympathetic ophthalmia?
Sympathetic uveitis is a non-suppurative uveitis that occurs after a penetrating ocular trauma (or surgery) to one eye. Acute diffuse inflammation of the same nature occurs in the uvea of the healthy eye. The injured eye is called the irritated eye, the uninjured eye is called the sympathetic eye, and sympathetic uveitis is the general term for it. The etiology of sympathetic ophthalmia is unknown, but it is now believed that its development is related to immune factors.
What are the clinical manifestations of sympathetic ophthalmia?
The incubation time of sympathetic ophthalmia after trauma varies from a few hours to more than 40 years, with 90% occurring within 1 year and the most dangerous time being 4-8 weeks after the injury. In particular, it is more likely to occur when the ciliary body is injured or when there is an embedded uvea in the wound, or when there is a foreign body in the eye.
Presentation of irritated eye: poor wound healing after injury to the eye, or persistent inflammation after healing, persistent ciliary congestion, along with acute irritation, edema in the posterior pole of the fundus, optic disc congestion, lambdoid KP behind the cornea, cloudy atrial fluid, and thickening and darkening of the iris.
Sympathetic eye manifestations: at first there are mild self-conscious symptoms, ocular pain, photophobia, tearing, blurred vision, progressively more pronounced irritation, mild ciliary congestion, cloudy atrial fluid, fine KP, as the disease progresses a formative inflammatory reaction, indistinct iris texture, pupil narrowing and post-iris adhesions, pupillary rim nodules, pupillary atresia, cloudy vitreous, and congested and edematous optic papillae.
Small yellowish-white foci resembling vitreous warts are seen in the peripheral choroid, gradually fusing and expanding and spreading to the entire choroid, leaving pigmentation, depigmentation and pigment disorder in the fundus after the recovery period, and evening hazel-like changes may appear in the fundus.
Acute retinal necrosis syndrome
Acute retinal necrosis syndrome is caused by herpes virus infection and presents with retinal necrosis, vasculitis mainly retinal arteritis, vitreous clouding and late retinal detachment. It can occur at any age, but is more common between the ages of 15 and 75 years, with little gender difference, and most often involves one eye.
The disease course is divided into three stages: acute, degenerative, and terminal. The course of the disease is regular and does not recur, and the disease is mild or severe. In severe cases, the retina is necrotic, with numerous small and large fissures, and the retina is shaped like a rag or fishnet, and eventually the eye atrophies, and about 1/3 of the patients are completely blind. In mild cases, the prognosis is still good with timely treatment.
What are the treatments for acute retinal necrosis syndrome?
(1) Antiviral agents: acyclic guanosine, 15mg/kg, intravenous drip, 3 times a day for 10-21d, changed to 400-800mg orally, 5 times a day for 4-6 weeks.
(2) Anticoagulant: Heparin can be used, or small doses of aspirin can be used orally.
(3) Glucocorticoid: Prednisone 1mg/(kg/d) can be used in parallel with antiviral treatment for 4 weeks.
(4) Laser photocoagulation: Photocoagulation may have a role in preventing retinal detachment.
(5) In case of retinal detachment, vitrectomy combined with vitreous gas filling and silicone oil filling should be performed.
What is Vogt-Koyanagi Harada disease?
Vogt-Koyanagi-Harada disease, also known as Vogt-Koyanagi-Harada syndrome, is a bilateral uveitis with hair whitening, hair loss, skin discoloration and hearing impairment. The disease is usually seen in yellow people and is prone to recurrence, with a duration of several years or even decades. The disease may be preceded by fever, headache, dizziness, nausea, vomiting, and neck stiffness.
What are the clinical manifestations of Vogt-Koyanagi Harada disease?
The disease has a typical clinical progression.
(1) The prodromal phase ( about 1 week before the onset of uveitis), patients may have changes such as cervical tonicity, headache, tinnitus, hearing loss and scalp allergy;
The posterior uveitis phase (2 weeks after the onset of uveitis) typically presents with bilateral diffuse chorioretinitis, chorioretinitis, optic papillitis, and superficial neuroepithelial detachment;
(iii) The anterior uveal involvement phase (about 2 weeks-2 months after onset) is often accompanied by exudative retinal detachment and non-granulomatous anterior uveitis changes, in addition to the manifestations of the posterior uveitis phase;
④ The recurrent anterior uveitis stage (approximately 2 months after onset) typically presents with recurrent granulomatous anterior uveitis, often with late haze fundus changes, Dalen-Fuchs nodules, and ocular complications. These 4 stages are not present in all patients, and timely treatment may lead to discontinuation of the disease at stage 1 and possible cure. In addition to these manifestations, extraocular changes such as alopecia areata, hair whitening, and vitiligo may occur at different stages of the disease. Common complications include concurrent cataract, excitation glaucoma, and exudative retinal detachment.
Treatment of Vogt-Koyanagi Harada disease?
Prednisone is mainly given orally for the first episode, usually at a starting dose of 1-1.2 mg/(kg・d), with a reduction starting at 10-14 d. The maintenance dose is 15-20 mg/d (adult dose), and treatment mostly takes more than 8 months. For patients with recurrence, other immunosuppressive agents such as azelaic acid, cyclophosphamide, cyclosporine A, etc. should generally be given, or combined with low-dose glucocorticoid therapy; for secondary glaucoma and cataract, appropriate drug and surgical treatment should be given.