# Clinical Challenges in Managing Bilateral Acute Iris Transillumination: Insights From a Case Triggered by Fluoroquinolone Therapy

## TL;DR

This paper reports a rare case of bilateral acute iris transillumination triggered by moxifloxacin, highlighting its severe and persistent complications.

## Contribution

The study provides clinical insights into managing BAIT, emphasizing differentiation from BADI and the role of fluoroquinolones.

## Key findings

- BAIT can be triggered by moxifloxacin and presents with severe photophobia and intraocular hypertension.
- Long-term management with carbonic anhydrase inhibitors and alpha-adrenergic blockers helps stabilize IOP.
- Persistent iris atrophy and pigment dispersion may occur despite treatment.

## Abstract

Bilateral acute iris transillumination (BAIT) is a rare ocular condition characterized by acute pigment dispersion from the iris pigment epithelium (IPE), resulting in diffuse iris transillumination, atonic mydriatic pupils, and intraocular hypertension. BAIT is often associated with severe photophobia and requires extended medical management. Differentiating BAIT from related conditions such as bilateral acute depigmentation of the iris (BADI) is critical, as BAIT presents with a more severe clinical course and lasting complications. Trigger factors include respiratory infections and fluoroquinolone use, particularly moxifloxacin. This report details a case of BAIT following oral moxifloxacin use. A 69-year-old male patient presented with bilateral ocular redness, pain, and severe photophobia one day after receiving an influenza vaccination and one-week post-moxifloxacin treatment. Examination revealed bullous keratopathy and bilateral iris depigmentation with transillumination. Moreover, Goldmann applanation tonometry showed an elevated intraocular pressure (IOP) exceeding 35 mmHg. Initial management included antiviral, anti-inflammatory, and IOP-lowering agents, which improved symptoms but revealed persistent pigment dispersion, atonic pupils, and recurrent IOP elevation during corticosteroid tapering. Long-term treatment with carbonic anhydrase inhibitors and alpha-adrenergic blockers stabilized IOP, but persistent iris atrophy and pigment dispersion were noted after one year. Therefore, this case underscores the severe and persistent nature of BAIT, emphasizing the importance of distinguishing it from BADI and other conditions with overlapping features. Corticosteroid management requires careful tapering to prevent symptomatic recurrences, and long-term monitoring is crucial to avoid sequelae such as glaucomatous damage. The association with moxifloxacin highlights the need for caution when prescribing fluoroquinolones, especially in at-risk populations, to mitigate potential ocular morbidity.