Acute anterior uveitis, also known as iritis, is the inflammation of the anterior or posterior chamber and iris. It is not a true ocular emergency, and with proper treatment and follow-up, it has a good prognosis.
Uveitis is subdivided into anterior and posterior components.
The anterior tract is composed of the iris and ciliary body.
The posterior tract includes choroid.
Uveitis may involve inflammation of any of these components and also can include other surrounding tissues such as the optic nerve, sclera, and retina. Uveitis is often idiopathic, but it may be triggered by genetic, immune, traumatic, or infectious mechanisms.
Symptoms of uveitis depend on the type (anterior, posterior, or intermediate) and duration (acute or chronic).
Most cases of iritis are idiopathic, while 20% are due to blunt force trauma. Nontraumatic iritis often is associated with systemic diseases including juvenile rheumatoid arthritis, ulcerative colitis, Reiter syndrome, sarcoidosis, and ankylosing spondylitis. Infectious causes also include tuberculosis, herpes simplex, toxoplasmosis, varicella-zoster virus, and syphilis.
Anterior uveitis is the most common form of uveitis (occurring every 12 per 100 000 cases). It predominantly occurs in young and middle-aged people. In western countries, 50% to 70% of all uveitis cases are classified as anterior uveitis.
Eye pain is thought to be due to irritation of the ciliary nerves and ciliary muscle spasm. Photophobia is caused by irritation of the trigeminal nerve from the ciliary spasm. Increased permeability of blood vessels in anterior chamber allows proteinaceous transudate ("flare") and WBCs ("cells"), the characteristic 'flare and cells' seen with the slit lamp.
The majority of cases of uveitis are idiopathic, however, a systemic cause must always be considered.
Pain, redness, photophobia, tearing, and decreased vision with pain developing over a few hours or days except in cases of trauma.
Blurred vision, mild redness with little pain or photophobia except during an acute episode.
Blurred vision, floaters, with absence of symptoms of anterior uveitis such as pain, redness, and photophobia.
If there are symptoms of posterior uveitis and also pain this suggests anterior chamber involvement, posterior scleritis, or bacterial endophthalmitis.
Similar to posterior uveitis with painless floaters and decreased vision and minimal external inflammation or photophobia.
Given the wide range of causes for iritis, a thorough ophthalmic, medical, and family history including recent trauma, infection, or medication is important for proper evaluation. A complete review of the system also will be important as complaints of systemic symptoms can alert the health care provider to the need for further workup. The patient will complain of unilateral pain which is bilateral with systemic disease. Other common findings may include conjunctival injection, consensual photophobia, and decreased vision.
Physical exams should include a penlight exam, visual acuity, and intraocular pressure readings. Typical history and "cell and flare" (WBCs and/or proteinaceous fluid in the anterior chamber) seen on slit lamp examination is diagnostic for anterior uveitis.
If systemic involvement or infectious disease is suspected to be the underlying cause, further laboratory tests or imaging may be required.
Chest radiography may be considered if sarcoidosis or tuberculosis as the underlying cause of uveitis is a consideration.
Laboratory workup is usually not necessary. In mild unilateral nongranulomatous uveitis with trauma or no evidence of systemic disease laboratory studies are unlikely to be helpful.
Treatment is primarily aimed at reducing inflammation and pain and preventing complications. First-line treatment involves topical cycloplegics (dilate the pupil, prevent ciliary body and pupillary spasm) and topical steroids (decrease inflammation). The patient should be referred to an ophthalmologist within 24 to 48 hours.
Sustained-release corticosteroid vitreous implants (fluocinolone acetonide, dexamethasone) is available for the treatment of inflammation-induced cases of panuveitis, intermediate uveitis, and posterior uveitis.
Corticosteroids should be initiated only in conjunction with approval of an ophthalmologist because uveitis is a diagnosis of exclusion.
Steroids can have adverse effects, such as causing intraocular pressure, cataract formation, steroid-induced glaucoma, and development of herpes keratitis.
Potassium-sparing drugs should be used when chronic steroid use is required to control inflammation. Approximately half of the patients with uveitis need treatment beyond corticosteroid treatment to prevent vision loss.
Block nerve impulses to the ciliary muscles and pupillary sphincter to decrease photophobia and pain.
Induces cycloplegia in 30 to 90 minutes.
Induces mydriasis in 10 to 30 minutes.
Effects last 10 to 48 hours for cycloplegia and 6 to 96 hours for mydriasis, but duration may be less if severe anterior chamber reaction.
Homatropine is agent of choice for uveitis.
Induces cycloplegia in 25 to 75 minutes.
Induces mydriasis in 30 to 60 minutes.
Less attractive for treating uveitis than homatropine.
Corticosteroids decrease inflammation. Treatment should only be initiated after consultation with an ophthalmologist.
Strongest steroid and best choice for uveitis.
Decreases inflammation by reversing increased capillary permeability and suppressing migration of polymorphonuclear leukocytes.
Infliximab or adalimumab may be used as second-line treatment for patients with vision-threatening chronic uveitis caused by seronegative spondyloarthropathy.
The prognosis is good with appropriate treatment.
To have the best prognosis, follow-up care with an ophthalmologist within 24 hours is imperative.
Monitoring should include repeat slit-lamp and intraocular pressure checks every few days.
When the condition is stable, monitoring may be every 1-6 months.
The prognosis becomes worse if there is an acute rise in intraocular pressure secondary to pupillary block, inflammation, or topical corticosteroid.
Incorrectly treating with steroids is dangerous; the clinician should be sure of the diagnosis prior to start steroids.
A rise in intraocular pressure can result in optic nerve atrophy and catastrophic permanent vision loss.
If untreated, complications can include decreased visual acuity and/or blindness, glaucoma, cataracts, and irregular pupil.
The management of a patient with iritis is multidisciplinary. Whenever a patient presents with eye pain, tearing, photophobia, vision loss and a red eye in the absence of trauma, the patient must be referred to an ophthalmologist as soon as possible. The treatment of iritis is primarily aimed at reducing inflammation and pain and preventing complications. First-line treatment involves topical cycloplegics (dilate the pupil, prevent ciliary body and pupillary spasm) and topical steroids (decrease inflammation). Depending on the cause, most patients respond well to treatment and retain full vision. However, at least 10-30% of patients may need treatment beyond steroids to prevent vision loss. (Level V) Once discharged, the patient may follow up with the ophthalmic nurse, primary care provider or the ophthalmologist.