Traumatic Iritis

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Article initiated by:

A. Paula Grigorian, MD, Nathan Carpenter

All contributors:

Alpa S. Patel, M.D., Douglas M. Wisner, MD, Alan Palestine, MD, Anna Murchison, MD, MPH, Fasika A. Woreta, MD, Jennifer Cao, MD, A. Paula Grigorian, MD, Boonkit Purt, MD

Assigned editor:

Boonkit Purt, MD, Jennifer Cao, MD

Review:

Assigned status Up to Date

 by Boonkit Purt, MD on November 13, 2024.

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Disease Entity

Traumatic iritis is inflammation of the iris due to trauma.

Disease

It is a subtype of uveitis localized to the iris also called anterior uveitis. Iridocyclitis is inflammation that affects both the iris and the ciliary body.

Etiology

Traumatic iritis is typically caused by blunt eye injury, but has been reported after injury from other sources including including firecrackers, pellet gun projectiles, motor vehicle accidents , amongst many others.

Epidemiology

Trauma is one of the most common causes of anterior uveitis.

• The incidence of iritis is estimated at 12 per 100,000 in the United States.
• Iritis accounts for 90% of uveitis.
• Traumatic iritis accounts for 20% of iritis.
• Younger patients are affected more than older patients.
• Males tend to be affected more than females.

Trauma to the eye causes injury and death to cells that subsequently form necrotic products. These necrotic products stimulate an inflammatory reaction. Increased permeability of blood vessels in the eye allow inflammatory cells (WBCs), inflammatory mediators (proteins, etc.), and other blood contents to enter the eye tissue and eye media.

Primary prevention

Wearing eye protection when risk of injury to eye is increased (e.g. pellet guns, fishing, metal or woodworking) may prevent initial inciting trauma.

Diagnosis

Signs

• Traumatic iritis typically presents with unilateral ocular involvement in the context of recent history of blunt ocular trauma.
• It may present with white blood cells and/or proteinaceous fluid in the anterior chamber; known as “cell and flare” or “anterior chamber reaction”.
• Visualization of cell and flare can be achieved with an intense, short, narrow slit beam of light at an oblique angle directed into the anterior chamber. These inflammatory products may deposit and be visualized on the endothelium of the cornea as keratic precipitates (KP).
• A Vossius ring of iris pigment deposited on the anterior lens capsule may be present from impression of the posterior iris on the lens produced by the concussive force driving the iris posteriorly onto the lens.
• Precipitates may also collect in dependent areas to form a hypopyon.
• Decreased visual acuity, perilimbal conjunctival injection (redness of the eye/ciliary flush), and change in intraocular pressure (IOP) are also associated with traumatic iritis.
• IOP may be increased due to the inflammatory process, damage to the trabecular meshwork, and/or it may be decreased due to damage of the ciliary body’s ability to produce aqueous humor.,
• Miosis may result as nociceptive reflex of photophobia or mydriasis due to iris sphincter tears.
• Inflammation of the iris may cause synechial formations between the inflamed, miotic iris and anterior lens. *Circumferential synechia may block the flow of aqueous fluid from exiting the posterior chamber causing increased pressure and may distend the iris forward like an umbrella to form what is called an iris bombé.
• Intractable secondary glaucoma may also result following traumatic iritis.

Symptoms

• Photophobia (pain when light enters eye; pain with miosis)
• Decreased visual acuity
• Floaters
• Ocular pain (typically dull achy or throbbing) not relieved by topical anesthetic; typically occur within the first 3 days of the traumatic event.

Clinical diagnosis

• Obtain a complete ophthalmic history; especially regarding any recent trauma, infection, or medication that could be the cause of present illness.
• Inquire about past medical history, family history, or history of iritis.
• A penlight exam should be performed to assess pupils, redness, and/or discharge.
• Visual acuity testing should be performed to detect vision changes.
• Obtain intraocular pressure (IOP) readings and perform dilated fundus examination.
• The slit lamp should be utilized to examine the dilated eye and to rule out any anterior chamber reaction.

Laboratory test

If the cause is known and there is no suspicion of systemic involvement, there is no need for laboratory testing.

Differential diagnosis

Traumatic hyphen and a corneal abrasion may have a similar presentation to traumatic iritis.

• A hyphema presents with red blood cells in the anterior chamber and blurred vision whereas iritis presents with photophobia and potentially white blood cells in anterior chamber. Hyphema presents earlier than traumatic iritis.
• Corneal abrasion presents with photophobia, foreign body sensation; especially when blinking, fluorescein staining, and typically no blood cells in anterior chamber.
• It is important to rule out an open globe and/or subsequent endophthalmitis as the root cause of inflammation, as the treatment algorithm would be vastly different.

Other causes of iritis include idiopathic (of unknown origin) iritis, infectious (herpes zoster, toxoplasmosis, tuberculosis, histoplasmosis, syphilis) iritis, genetic (HLA-B27, ankylosing spondylitis, reactive arthritis (formerly Reiter’s syndrome), psoriatic arthritis), medications (antibiotics, antivirals), associated with systemic diseases (juvenile rheumatoid arthritis, inflammatory bowel disease, down’s syndrome, Behcet’s syndrome), nongranulomatous anterior uveitis, extension of posterior uveitis, hyphema, corneal abrasion, or retinal detachment.

Management

Medical therapy

• Topical cycloplegics (e.g. cyclopentalate 2% bid-tid, scopolamine 0.25% bid) will dilate the pupil and prevent synechiae to the lens. They also stabilize the blood-aqueous barrier to prevent further protein leakage (flare). Topical cycloplegics will also prevent ciliary body and pupillary spasm that causes pain and discomfort.
• Topical steroids (e.g. prednisolone acetate 1% qid) are used to decrease inflammation. They are avoided if there is a corneal epithelial defect.
• Topical beta-blockers (e.g. timolol maleate 0.5% bid) may be beneficial if secondary glaucoma is present and there are no other contraindications to beta-blocker usage.

Follow-up

It is recommended to follow up in 5-7 days of the initial traumatic event. If iritis is resolved, cycloplegia may be discontinued and steroid may be tapered then discontinued. The risk of rebound iritis increases if steroid is not tapered. Traumatic iritis is generally much more responsive to topical steroids than anterior uveitis and steroids may generally be tapered more rapidly (e.g. over the course of 2 weeks).

Follow up should also occur at 1 month. Gonioscopy should be performed to rule out angle recession at this visit. Indirect ophthalmoscopy should be performed using scleral depression to rule out retinal breaks and retinal detachments. Particular care should be taken to rule out retinal dialysis in younger individuals as they often have delayed presentation.

Prognosis

Most patients respond well to current standard treatments. Some patients will have recurrence or lingering signs and symptoms. Complications can include decreased visual acuity and/or blindness, glaucoma, cataracts (duration of inflammation is directly related to risk), irregular pupil (due to synechia formation, tearing, and sloughing of inflamed iris), band keratopathy, and cystoid macular edema.

Additional Resources

• AAO, Basic and Clinical Science Course. Section 8: External Disease and Cornea, 2013-2014.