Abstract

ABSTRACT This study aims to describe a challenging clinical case of a patient with a neurotrophic and exposure corneal ulcer. A 75-year-old male patient, with history of right eye (RE) limbic stem-cell insuficiency due to complications of recurrent herpetic keratitis, underwent successful limbic stem-cell transplantation in 2008. In 2010, an uneventful penetrating keratoplasty was performed. After a cataract phacoemulsification surgery with intraocular lens implantation done in 2011, best corrected visual acuity was 20/20, and remained stable until 2015. In July 2015, the patient developed right facial nerve palsy and two months later, presented with an extensive central corneal ulcer, with a significant thinning of central stroma, without infection signs, but with an imminent risk of perforation. Treatment with topical ofloxacin and intensive ocular lubrification was started in association with permanent ocular oclusion. Due to lack of any clinical improvement, treatment with RGTA [Poli (carboximetilglucose) sulfate, dextrano T40] (Cacicol®, Thea) was started. After two weeks of treatment, a complete reepithelization and partial stromal filling was observed. Continued monitoring and treatment with artificial tears was maintained, with no recurrence observed. There is an unmet need for a medical therapy that could help corneal neurotrophic ulcers to heal. The presented clinical case shows that the approach of targeting extracellular matrix can be effective in the reepithelialization of neurotrophic and exposure corneal ulcer that do not respond to conventional treatments.

Highlights

  • Corneal lesions that progress towards stromal ulceration are an important clinical problem as they impose a considerable risk of corneal stromal melting and perforation.(1) Many conditions can cause stromal ulceration, including neurotrophic keratitis

  • Other iatrogenic causes are the irradiation of the ocular surface, neurosurgery, corneal surgery or ciliary body ablation.(1) These ulcers result from loss of the sensory innervation of the cornea, which leads to a decrease in the number of corneal stem cells, decreased metabolic and mitotic rates in the corneal epithelium, and reduced acetylcholine and choline acetyltransferase concentrations.(2)

  • The standard treatments consist of instillation of artificial tears, elimination of toxic agents, preservatives, covering the eye with a patch or a soft contact lens, tarsorrhaphy, constructing a conjunctival flap, amniotic membranes and lamellar or penetrating keratoplasty.(1) these procedures are often ineffective, and the outcome is usually a severe impairment of vision

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Summary

Introduction

Corneal lesions that progress towards stromal ulceration are an important clinical problem as they impose a considerable risk of corneal stromal melting and perforation.(1) Many conditions can cause stromal ulceration, including neurotrophic keratitis. This last disease is associated to corneal hypoesthesia or total anesthesia and can be secondary to tumors that damage V nerve (neurinoma, meningioma), demyelinating disease (multiple sclerosis), cerebral infarct, aneurisms, herpes simplex or zoster. Bell’s palsy (or idiopathic facial nerve palsy) increases the risk of corneal exposure. Neurotrophic and corneal exposure ulcers remain difficult to treat. The standard treatments consist of instillation of artificial tears, elimination of toxic agents, preservatives, covering the eye with a patch or a soft contact lens, tarsorrhaphy, constructing a conjunctival flap, amniotic membranes and lamellar or penetrating keratoplasty.(1) these procedures are often ineffective, and the outcome is usually a severe impairment of vision.

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