January-February 2020

CORNEA

Presentation Spotlight
Successful management of neurotrophic corneal ulcer


by Stefanie Petrou Binder, MD Contributing Writer


Neurotrophic keratitis characterized by smooth edges
Source: Chiara Bonzano, MD

 

Out-of-the-ordinary case studies are not only instructional but they can help clinicians decide what to do if they ever find themselves in a similar bind. Chiara Bonzano, MD, discussed a challenging case of neurotrophic ulcer after retinal surgery and how she managed this patient.
Dr. Bonzano reported in a presentation the case of a 55-year-old Caucasian male who came to the corneal department because of blurry vision that he experienced in the week prior. The patient was on antiviral therapy that was prescribed by an outside ophthalmologist, without any sign of visual improvement. Upon examination, she identified a neurotrophic corneal ulcer, with evidence of confluent chorioretinal scarring from endolaser treatments that the patient received in two meridians.
The complicated patient history revealed a 23-gauge pars plana vitrectomy and a Densiron 68 tamponade (Fluoron), undertaken for a primary inferior rhegmatogenous retinal detachment. The patient was on antiglaucoma medication (bimatoprost QD) to keep IOP under control following the vitrectomy. Within 12 weeks of the initial surgery, oil removal was carried out and barrier endolaser was applied to the affected eye as augmentation. Six weeks later, cystoid macular edema occurred. The patient took topical NSAIDs for 1 month, which may have contributed to ulcer development.
The patient had no history of previous corneal surgery, intraoperative epithelial debridement, 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 examination of the right eye that revealed conjunctival 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 pupil 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 uncontrolled IOP made the clinical decision very challenging. We decided on a medication switch that allowed us to achieve faster corneal healing,” Dr. Bonzano said.
Studies have shown that the postoperative use of topical PGAs was found to be associated with an incidence of CME1 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 toxicity. 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 antibiotic and vitamin ointments and the eye was frequently monitored on an outpatient basis, pending improvement.
Dr. Bonzano reported corneal ulcer improvement within the first few days and a markedly ameliorated cornea after roughly 15 days. The new treatment regimen increased visual acuity and resulted in minimal residual CME and good IOP control.
“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, aneurysm, 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 keratopathy 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 hypertension 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 testing 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 perforation and visual loss.

About the doctor

Chiara Bonzano, MD
Clinica Oculistica
Policlinico San Martino
University of Genoa
Genoa, Italy

References

1. Wendel C, et al. Association of postoperative topical prostaglandin analog or beta-blocker use and incidence of pseudophakic cystoid macular edema. J Glaucoma. 2018;27:402–406.
2. Iwamoto S, et al. Non-steroidal anti-inflammatory drug delays corneal wound healing by reducing production of 12-hydroxyheptadecatrienoic acid, a ligand for leukotriene B4 receptor 2. Sci Rep. 2017;7:13267.

Relevant disclosures

Bonzano: None

Contact

Bonzano: oculistabonzano@gmail.com

Successful management of neurotrophic corneal ulcer Successful management of neurotrophic corneal ulcer
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