THE PAINFUL RED EYE PART 4 ANTERIOR UVEITIS Lorrimer Esselaar

ANATOMY The uvea is the pigmented vascular layer of the eye. It consists of 3 parts:

UVEITIS DEFINITION CLASSIFICATION ANATOMICAL TEMPORAL Uveitis = intraocular inflammation. Because vascular tissue is the main mediator of inflammation, the uvea is usually involved in any inflammatory process within the eye. Consequently the term uveitis is used to denote any intraocular inflammation, and not only inflammation of the uvea. This includes all tissues internal to the sclera. The optic disc is not included. CLASSIFICATION ANATOMICAL The designation is determined by the part of the uvea which is involved. TEMPORAL Acute Chronic Recurrent

EPIDEMIOLOGY NONINFECTIVE CAUSES There are many causes of anterior uveitis. Although it is usually noninfective, uveitis may be caused by a wide variety of microorganisms: viruses, bacteria, fungi, protozoa and parasites. It is often not an isolated intraocular inflammation but part of a systemic inflammatory disease that requires further investigation and treatment. The tissues involved are very seldom available for histopathological or microbiological investigation. Consequently aetiological diagnoses are frequently presumptive, and an aetiological classification is not yet practical. NONINFECTIVE CAUSES Sarcoidosis: anterior uveitis is common. Ankylosing spondylitis: anterior uveitis is common. Juvenile chronic arthritis: anterior uveitis is common. Reiter’s syndrome: although more often characterised by conjunctivitis, anterior uveitis may occur. Large joint arthritis and urethritis or cervicitis complete the triad. Behçet’s syndrome: the triad of severe anterior uveitis with hypopion formation, aphthous mouth ulcers and genital ulcers. Trauma: the commonest cause of anterior uveitis in children.

PATHOLOGY INFECTIVE CAUSES Sympathetic ophthalmia: this is a rare, bilateral, chronic panuveitis that occurs after a substantial penetrating injury to one eye. The onset is 10 days to 50 years after the exciting trauma, and it does not occur if the injured eye is removed within 10 days of the original injury. The disease is almost certainly of autoimmune origin. The prognosis is poor as the inflammation is recurrent and difficult to treat, and usually results in relentlessly progressive ocular damage. Thus an injured blind eye should be removed within 10 days of the injury to prevent future progressive immune damage to the only remaining seeing eye. Infection elsewhere in the body may cause a uveitis on a hypersensitivity basis e.g. tooth abscess, sinusitis. Many others. INFECTIVE CAUSES Tuberculosis: inflammation may occur both on a hypersensitivity or infective basis. Syphilis: Anterior uveitis may occur in the secondary stage of the acquired disease. Many others such as Herpes simplex, Herpes zoster, cytomegalovirus, meningococcus, candida. PATHOLOGY As in any inflammation, the ocular pathology is the result of vascular dilation, extravascular fluid leakage, and leucocyte infiltration.

CLINICAL CHARACTERISTICS Anterior uveitis may cause extensive and irreversible intraocular damage. Adequate evaluation can only be done by an ophthalmologist. SYMPTOMS Dull vision Redness Deep seated eye pain. Note that pain is often inexplicably absent in children. Photophobia Tearing SIGNS Decrease in visual acuity: usually mild to moderate. Ciliary (circumcorneal) injection. Anterior chamber flare (light reflected from aqueous protein) and cells are easily seen with a slit lamp. Only in very severe uveitis can this anterior chamber haze be seen with the naked eye, when it also makes the iris appear dull and lighter in colour.

Keratic precipitates (KP) are deposits on the inferior corneal endothelium in a triangular pattern, base down. They appear as white, yellow or brown spots, and consist of precipitated white cells, fibrin, pigment and débris from the aqueous humour. Hypopyon if severe: white cells and fibrin precipitate in the inferior anterior chamber angle. Miosis. Positive tests for iritis. Discomfort not relieved by local anaesthetic. Dull view of the fundus.

COMPLICATIONS 1 Posterior synechiae. Adhesions of the posterior surface of the iris to the anterior lens capsule tend to produce an irregular and fixed pupil. When extensive, they may obstruct the flow of aqueous through the pupil sufficiently to cause anterior bulging of the iris and secondary acute angle closure. Effects on the trabeculum retard drainage of aqueous to cause increased intraocular pressure and eventually chronic open angle glaucoma. (a) Blockage of the trabeculum by cells and débris. Trabeculitis leading to trabecular sclerosis. 3 Cataract if chronic.

MANAGEMENT 1 Referral: any uveitis must be investigated and treated by an ophthalmologist. 2 If the cause of the uveitis is known, specific treatment is administered. 3 A topical mydriatic/cycloplegic is used in anterior uveitis for the following reasons: (a) Dilation and movement of the pupil decrease the probability of posterior synechiae developing. The iris and anterior lens capsule are usually least in contact in the fully dilated position. (b) Pain is caused by ciliary muscle and iris sphincter spasm, and relaxation of these leads to pain relief. For cycloplegia use Cyclopentolate HCI (Cyclogyl ®) 1% tid. This is because a fairly strong cycloplegic is needed for pain relief, but some movement of the pupil is desired as there is a strong tendency to form posterior synechiae. Omit a dose once every few days to allow the pupil to constrict further and break incipient posterior synechiae. Do not use tropicamide (Mydriacyl®). It is too weak and too short acting. Do not use atropine. It is too potent and too long acting and so produces an absolutely static pupil conducive to formation of posterior synechiae. 4 Steroidal and/or nonsteroidal antiinflammatory agents are used to suppress the inflammation. Steroids are the cornerstone of treatment and may be administered topically, subconjunctivally or systemically. 5 Management of complications.

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