Traumatic iritis

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Disease Entity[edit | edit source]

Traumatic iritis is inflammation of the iris due to trauma.

Disease[edit | edit source]

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[edit | edit source]

Traumatic iritis is usually caused by blunt eye injury, but can result form any other type of injury,[1] like firecrackers, pellet gun projectile, electric shock from taser, fishing hook weight, motor vehicle accidents, batteries, water balloon sling-shots, as well as many others.[2],[3]

Epidemiology[edit | edit source]

Trauma is one of the most common causes of anterior uveitis.[4]

  • The incidence of iritis is estimated at 12 per 100,000 in the United States.[4]
  • Iritis accounts for 90% of uveitis.[5]
  • Traumatic iritis accounts for 20% of iritis.[5]
  • Younger patients are affected more than older patients.[4]
  • Males tend to be affected more than females.[4]


Trauma to the eye causes injury and death to cells that subsequently form necrotic products.[6],[4] 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.[6],[4]

Primary prevention[edit | edit source]

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

Diagnosis[edit | edit source]

Signs[edit | edit source]

  • Traumatic iritis typically presents with unilateral ocular involvement.
  • It may present with white blood cells and/or proteinaceous fluid in the anterior chamber; known as “cell and flare” or “anterior chamber reaction”.[6],[4],[7]
  • Visualization of cell and flare can be achieved with an intense, 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).[8]
  • A vossius ring of iris pigment 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 posterior onto the lens.[1]
  • Precipitates may also collect in dependent areas to form a hypopyon.[9]
  • Decreased visual acuity, perilimbal conjunctival injection (redness of the eye/ciliary flush), and change in intraocular pressure (IOP) are also associated with traumatic iritis.[6],[4]
  • IOP may be increased due to inflammatory process or it may be decreased due to damage of the ciliary body’s ability to produce aqueous humor.[10],[4]
  • Miosis may result as nociceptive reflex of photophobia or mydriasis due to iris sphincter tears.[10]
  • Inflammation of the iris may cause synechial formations between the inflamed, miotic iris and anterior lens.[6],[4],[9] *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.[9]
  • Intractable secondary glaucoma may also result following traumatic iritis.[9]

Symptoms[edit | edit source]

  • Photophobia (pain when light enters eye; pain with miosis)
  • Decreased visual acuity
  • Floaters
  • Tearing
  • Ocular pain (typically dull achy or throbbing) not relieved by topical anesthetic; typically occur within the first 3 days of the traumatic event.[6],[10],[4]

Clinical diagnosis[edit | edit source]

  • 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.[6],[10]
  • A penlight exam should be performed to assess pupils, redness, and/or discharge.[6],[10],[4]
  • Visual acuity testing should be performed to detect vision changes.
  • Obtain intraocular pressure (IOP) readings and perform dilated fundus examination. .[6],[10],[4]
  • The slit lamp should be utilized to examine the dilated eye and to rule out any anterior chamber reaction.


Laboratory test[edit | edit source]

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

Differential diagnosis[edit | edit source]

Traumatic hyphema, traumatic corneal abrasion, and traumatic retinal detachment have similar presentation to traumatic iritis.[10]

  • 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.[10] Hyphema presents earlier than traumatic iritis.[10]
  • Corneal abrasion presents with photophobia, foreign body sensation; especially when blinking, fluorescein staining, and typically no blood cells in anterior chamber.[10]
  • Retinal detachment presents with flashes of light, decreased field of vision and may not be painful.[10]


Other causes of iritis include idiopathic (of unknown origin) iritis, infectious (herpes zoster, toxoplasmosis, tuberculosis, histoplasmosis, syphilis) iritis, genetic (HLA-B27, ankylosing spondylitis, 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.[10] 

Management[edit | edit source]

Medical therapy[edit | edit source]

  • Topical cycloplegics (e.g. cyclopentalate 2% 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).[4] Topical cycloplegics will also prevent ciliary body and pupillary spasm that causes pain and discomfort.[6]
  • Topical steroids (e.g. prednisolone acetate 0.125-1% 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.[4]

Follow up[edit | edit source]

Add text here 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.[6],[10],[4]

Follow up should also occur at 1 month.[10] Gonioscopy should be performed to rule out angle recession at this visit.[10] Indirect ophthalmoscopy should be performed using scleral depression to rule out retinal breaks and retinal detachments.[10] 

Prognosis[edit | edit source]

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.1[6],[10],[4]

Additional Resources[edit | edit source]

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

References[edit | edit source]

  1. 1.0 1.1 Augsburger JJ, Corrêa ZM. Chapter 19. Ophthalmic Trauma. In: Riordan-Eva P, Cunningham, Jr. ET, eds. Vaughan & Asbury's General Ophthalmology. 18th ed. New York, NY: McGraw-Hill; 2011:371-382
  2. Ramstead C, Ng M, Rudnisky CJ. Ocular injuries associated with Airsoft guns: a case series. Canadian Journal of Ophthalmology. 2008. 43(5):584-587
  3. Seth RK, Abedi G, Daccache AJ, Tsai JC. Cataract secondary to electrical shock from a Taser gun. Journal of Cataract and Refractive Surgery. 2007. 33(9):1664-1665
  4. 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 4.13 4.14 4.15 4.16 Alexander KL, Dul MW, Lalle PA, Magnus DE. Onofrey B. Optometric Clinical Practice Guideline: Care of the Patient with Anterior Uveitis. St. Louis, MO: American Optometric Association; 1994:3-29.
  5. 5.0 5.1 Gutteridge IF, Hall AJ. Acute anterior uveitis in primary care. Clinical and Experimental Optometry. 2007. 90(2):70-82.
  6. 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 6.11 Reidy JJ. Section 08: External Disease and Cornea. Basic and Clinical Science Course. San Francisco, CA: American Academy of Ophthalmology; 2012: 363.
  7. Trobe JD. The Physician’s Guide to Eye Care. San Francisco, CA: American Academy of Ophthalmology; 2006:50-51
  8. Bartley GB, Liesegang TJ. Essentials of Ophthalmology. Philadelphia, PA: JB Lippincott Company; 1992:156-157
  9. 9.0 9.1 9.2 9.3 Trevor-Roper PD, Curran PV. The Eye and Its Disorders. Boston, MA: Blackwell Scientific Publications; 1984:489-507
  10. 10.00 10.01 10.02 10.03 10.04 10.05 10.06 10.07 10.08 10.09 10.10 10.11 10.12 10.13 10.14 10.15 10.16 Ehlers JP, Shah CP, Fenton GL, Hoskins EN. Chapter 03: Trauma. The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:19-22