Corneal Thinning after Topical Ketorolac and Bandage Contact Lens in a Diabetic Post-PRK Patient

Mechanism

Topical NSAIDs inhibit cyclooxygenase and reduce prostaglandin synthesis. Prostaglandins are not merely inflammatory mediators; they support corneal epithelial migration, mitosis, and stromal wound repair. Excessive COX inhibition shifts the balance toward matrix metalloproteinase activity and impaired healing, producing sterile corneal thinning or 'melt'.

Contributing factors in this case

• Diabetes: hyperglycemia and diabetic neuropathy impair epithelial adhesion and corneal nerve-derived trophic support; HbA1c 8.9% is poorly controlled.
• Overuse: every 2 hours instead of four times daily markedly increases exposure.
• Preservative: ketorolac 0.5% contains benzalkonium chloride, which is toxic to epithelium, especially under a bandage lens.
• Bandage contact lens: traps preservative and creates a closed environment; lens wear with frequent preserved NSAID increases melt risk.
• Open bottle for a month: contamination risk and possible concentration changes; not the main cause of sterile melt but relevant.
• High myopia/PRK: deeper ablation and larger epithelial defect increase healing demand.

Interpretation

The absence of infiltrate and the sterile, progressive thinning point to NSAID-associated keratolysis rather than infection. The pain out of proportion to findings may be neuropathic.

Immediate actions

1. Stop ketorolac immediately; do not substitute another preserved NSAID or a 'stronger' NSAID drop.
2. Remove or exchange the bandage contact lens if it is not essential; if kept for comfort, use a preservative-free lens and preservative-free drops only.
3. Start aggressive preservative-free lubrication (non-preserved artificial tears or ointment) and consider a topical corticosteroid such as fluorometholone 0.1% or prednisolone acetate 1% to reduce inflammation and MMP activity, but only after infection is excluded and with close monitoring because steroids can also impair healing.
4. Consider oral doxycycline 100 mg twice daily for its MMP-inhibitory and anti-inflammatory effects, plus vitamin C and adequate glycemic control.
5. If thinning progresses below 50% or perforation threatens, use amniotic membrane grafting or cyanoacrylate glue with ophthalmology input.

Pain control

Use preservative-free lubricants, oral analgesia (e.g., paracetamol or tramadol), and consider a short course of oral gabapentin for neuropathic pain. Topical anesthetic drops are contraindicated for pain control because of epithelial toxicity.

Monitoring

Daily slit lamp until thinning stabilizes; measure defect size and stromal thickness; culture only if infiltrate appears.

Addressing the request

Explain clearly that stronger NSAID or anesthetic drops would accelerate melting and could cause perforation. The pain is a warning symptom, not a reason to intensify the offending drug. Validate her discomfort and offer a structured analgesic plan.

Prevention counseling

• Topical NSAIDs should be used at the lowest effective frequency and shortest duration, generally no more than 3–4 days after PRK, and avoided in diabetics, neurotrophic corneas, and patients wearing bandage lenses when possible.
• Never use preserved NSAIDs more often than prescribed; shake and store bottles correctly; discard after the labeled expiry.
• Keep diabetes controlled before and after refractive surgery; HbA1c 8.9% is a modifiable risk factor.
• Report increasing pain, redness, or vision loss immediately rather than self-adjusting drops.

Reporting and systems

Document the adverse drug reaction as topical NSAID-associated corneal melt in the chart and report it to the institutional pharmacovigilance system and national adverse drug reaction reporting program. Notify the prescribing surgeon and review clinic protocols for post-PRK NSAID duration and patient selection.

Follow-up

Weekly review until re-epithelialization; refractive outcome may be compromised, so counsel about possible haze and delayed visual recovery.