Traumatic iritis is a condition in which blunt external force damages the iris and ciliary body, causing inflammation in the anterior chamber. It is also called iridocyclitis and is classified as a type of anterior uveitis.
Blunt ocular trauma is the most common cause. Mechanisms of injury vary widely, including sports injuries, traffic accidents, and impact from airbag deployment. In sports-related eye injuries, anterior segment damage is the most frequent, accounting for 72% of all cases.
The incidence of iritis in the United States is estimated at approximately 12 per 100,000 people. Iritis accounts for 90% of all uveitis cases, and traumatic iritis represents about 20% of those. It is more common in younger individuals than in older adults, and more frequent in men than in women.
It usually develops only in the injured eye. If both eyes are injured simultaneously, it can be bilateral. There have been reports of bilateral traumatic iritis following airbag deployment in traffic accidents.
Symptoms of traumatic iritis usually appear within 3 days after injury.
Slit-lamp microscopy is central to diagnosis. Blunt trauma causes microscopic tissue damage to the iris and ciliary body, disrupting the blood-aqueous barrier. This results in the release of inflammatory cells and proteins into the anterior chamber.
Anterior Chamber Findings
Cells and flare: Leukocyte suspension and protein leakage in the anterior chamber. Observed with a slit lamp using oblique illumination.
Keratic precipitates (KP): Inflammatory deposits on the corneal endothelium. Typically present as fine, non-granulomatous KP.
Hypopyon: Accumulation of deposits in the lower part of the anterior chamber. Seen in severe cases.
Iris and Pupil Findings
Vossius ring: Annular deposition of iris pigment on the anterior lens capsule. Caused by the iris being pressed against the lens due to blunt trauma.
Miosis: Due to nociceptive reflex to photophobia.
Mydriasis: Occurs when there is a rupture of the iris sphincter muscle. The light reflex is diminished to absent.
Posterior synechiae: Adhesion between the miotic iris due to inflammation and the anterior lens surface.
Intraocular pressure may increase or decrease. Inflammation and trabecular meshwork damage cause elevated intraocular pressure, while reduced aqueous humor production by the ciliary body leads to decreased intraocular pressure.
Aqueous humor outflow from the posterior chamber is blocked, causing increased intraocular pressure. This may form an iris bombe, where the iris bulges forward, leading to refractory secondary glaucoma. Prevention of synechiae with mydriatic agents is important.
Blunt ocular trauma is the direct cause. When external force is applied to the eye, such as from a ball injury, the eyeball wall deforms, exerting stretching forces on the iris and ciliary body. This results in microtissue damage and disruption of the blood-aqueous barrier, leading to inflammatory cell migration into the anterior chamber.
Typical mechanisms of injury are as follows:
A recent history of eye trauma provides a clue for diagnosis. The examination proceeds as follows.
The SUN (Standardization of Uveitis Nomenclature) classification is used to assess anterior chamber inflammation.
| Grade | Cell count (1×1mm beam) | Flare |
|---|---|---|
| 0 | <1 | None |
| 1+ | 6–15 | Slight |
| 2+ | 16–25 | Moderate |
| 3+ | 26–50 | Severe |
| 4+ | >50 | Fibrin deposition |
If globe rupture is suspected (e.g., severe conjunctival edema, low intraocular pressure, subconjunctival hemorrhage), perform CT or MRI imaging. MRI is contraindicated if a metallic foreign body is suspected.
Traumatic iritis requires differentiation from the following conditions.
Other causes of iritis include infectious (herpes zoster, syphilis, etc.), hereditary (HLA-B27-associated), drug-induced, and systemic disease-related (Behçet’s disease, juvenile rheumatoid arthritis, etc.). If there is a clear history of trauma and no systemic involvement is suspected, clinical testing is unnecessary.
Hyphema presents mainly with red sedimentation due to red blood cells and blurred vision, appearing earlier than iritis. Iritis is characterized by white blood cell-induced cell and flare and photophobia. Both can occur together.
The basic treatment is anti-inflammatory therapy using a combination of mydriatic agents and steroid eye drops.
Standard prescriptions are shown below.
If intraocular pressure elevation is severe, add oral Diamox tablets (250 mg) 2 tablets twice daily (after breakfast and dinner). In that case, co-administer Aspara-K tablets (300 mg) 2 tablets twice daily to prevent hypokalemia.
Re-examine 5–7 days after injury. If inflammation has resolved, discontinue mydriatic agents. Taper steroids over approximately 2 weeks, then discontinue.
At the 1-month follow-up after injury, check the following:
It usually resolves within 1 to 2 weeks. Traumatic iritis responds better to steroids compared to other types of anterior uveitis, and tapering can be done relatively quickly. In severe cases, posterior synechiae may remain after fibrin resolution.
When blunt force is applied to the eye, deformation of the ocular wall causes stretching or shearing forces on the iris and ciliary body. Intraocular pressure transiently increases, the limbus stretches, and aqueous humor moves posteriorly and into the angle. This leads to the following pathological changes in a stepwise manner.
When a stronger force is applied, the following structural damage may occur.
There are multiple mechanisms of intraocular pressure elevation. These include trabecular meshwork dysfunction due to inflammation, obstruction of aqueous outflow by red blood cell breakdown products after hyphema (ghost cell glaucoma), and pupillary block due to posterior synechiae. On the other hand, cyclodialysis and decreased aqueous production by the ciliary body cause hypotony.
Some patients develop elevated intraocular pressure several years after injury due to trabecular meshwork damage and secondary degeneration associated with angle recession. Patient education and regular intraocular pressure monitoring are important.
Visual prognosis is generally good. Complications include vision loss, glaucoma, cataract (duration of inflammation directly correlates with risk), irregular pupil (due to synechiae formation or sphincter rupture), band keratopathy, and cystoid macular edema (CME).
