Eyeworld

68 | EYEWORLD | JANUARY/FEBRUARY 2020 C ORNEA Contact Bonzano: oculistabonzano@gmail.com "Corneal sensation is derived from the ophthalmic branch of the trigeminal nerve," she explained. "It is important to understand that damage to the long ciliary nerves can lead to an impairment in corneal innervation. Ciliary or ophthalmic nerve injury can be caused by orbital surgery or trauma, and fifth cranial nerve palsy due to trigeminal lesions in the posterior fossa can be caused by acoustic neuroma, aneu- rysm, or posterior fossa meningioma. Brainstem disease like cerebrovascular disease or multiple sclerosis can also contribute," Dr. Bonzano said. According to Dr. Bonzano, there were several contributing factors in the development of the neurotropic corneal ulcer. "The temporal relationship between the onset of the keratopa- thy favors endolaser damage over oil toxicity as the main cause. The oil could play an important role in the IOP elevation and its removal might have caused the cystoid macular edema. The treatments for macular edema and ocular hy- pertension didn't take into account the corneal impairment, and they could have delayed the ulcer healing," she said. Dr. Bonzano thinks that retinal surgeons should be mindful of the long ciliary nerves and, where possible, avoid heavy confluent laser treatments at these sites. Corneal sensitivity test- ing is quick and helpful to determine the extent of nerve involvement. If corneal anesthesia occurs, it is important to recognize it early and treat promptly. Careful management will ensure the prevention of complications such as perfo- ration and visual loss. took topical NSAIDs for 1 month, which may have contributed to ulcer development. The patient had no history of previous corneal surgery, intraoperative epithelial de- bridement, or herpetic eye disease. He had mild hypertension and no diabetes. His family history revealed that his father died of stroke. The patient was negative for alcohol, smoking, and drugs. Dr. Bonzano performed a slit lamp ex- amination of the right eye that revealed con- junctival hyperemia, a paracentral corneal ulcer 4.5 mm in diameter, and a quiet, deep anterior chamber. Closer inspection using fluorescein for corneal staining showed an area of corneal de-epithelialization with a 5-mm diameter. She evaluated corneal sensitivity by using a corneal Cochet-Bonnet contact aesthesiometer, and it resulted decreased. The patient had low visual acuity classified as hand motion, an irregular pu- pil shape, increased IOP, and decreased corneal sensitivity. The left eye was within normal limits. Treatment "Decreased corneal sensitivity, neurotropic corneal ulcer, cystoid macular edema, and un- controlled IOP made the clinical decision very challenging. We decided on a medication switch that allowed us to achieve faster corneal heal- ing," Dr. Bonzano said. Studies have shown that the postoperative use of topical PGAs was found to be associated with an incidence of CME 1 and that NSAIDs have been seen to delay corneal wound healing. 2 Dr. Bonzano discontinued nepafenac in the patient, due to the lack of treatment response, as well as bimatoprost to avoid epithelial toxici- ty. She started the patient on acetazolamide 250 mg tablets 2x/day plus a corticosteroid depot injection to avoid potential complications of corneal ulceration and corneal melting. The patient's eye was patched with anti- biotic and vitamin ointments and the eye was frequently monitored on an outpatient basis, pending improvement. Dr. Bonzano reported corneal ulcer im- provement within the first few days and a mark- edly ameliorated cornea after roughly 15 days. The new treatment regimen increased visual acuity and resulted in minimal residual CME and good IOP control. continued from page 67 References 1. Wendel C, et al. Association of postoperative topical prostaglan- din analog or beta-blocker use and incidence of pseudophakic cystoid macular edema. J Glauco- ma. 2018;27:402–406. 2. Iwamoto S, et al. Non-steroidal anti-inflammatory drug delays corneal wound healing by reduc- ing production of 12-hydroxy- heptadecatrienoic acid, a ligand for leukotriene B4 receptor 2. Sci Rep. 2017;7:13267. Relevant disclosures Bonzano: None Neurotrophic keratitis characterized by smooth edges Source: Chiara Bonzano, MD

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