Treating the Results of Neurotrophic Keratitis
BY WILLIAM L. MILLER, OD, PHD, FAAO
Neurotrophic keratitis is a secondary disease outcome from an array of primary disease entities. The fundamental cause is that the primary disease interferes with normal innervation along the course of the trigeminal nerve from its nucleus. This lack of sensation and disruption of normal trophic feedback can lead to corneal ulceration.
Causes and Stages
Two primary causes for neurotrophic keratitis are varicella-zoster and herpes simplex keratitis. Traumatic damage to the ophthalmic branch may also be a cause along with a host of other disease processes including irradiation of the eye or adnexa, stroke, multiple sclerosis, chemical/pharmaceutical toxicity to the cornea, and low-Dk lenses.
A temporary cause is LASIK, with most lasting a few months. It's sometimes called LASIK-induced neurotrophic epitheliopathy (LINE). However, some LASIK patients may have lingering effects and require therapeutic intervention. Patients who have pre-existing dry eye are more at risk of developing LINE.
Neurotrophic keratitis is divided into three stages. Stage 1 includes surface irregularities with punctate keratitis. This can progress to an epithelial defect with stromal inflammation (Stage 2). The most debilitating, Stage 3, consists of stromal melting and possible corneal perforation.
In the disease's early stages patients may complain of red eyes and mucous production and show clinical symptoms similar to ocular surface or dry eye syndrome.
Treatment regimens are similar regardless of cause, but are tailored to the severity of the keratitis. Prompt intervention is essential. The ultimate goal is to protect the cornea's fragile surface because the homeostatic feedback between corneal sensation and tear production is not functional. Another goal is to promote healing and epithelial mitosis through your treatment.
Treat early or mild cases the way you would treat a dry eye syndrome patient. Tear supplements, punctal occlusion, and ointment at bedtime all would be good starts for treatment. Preservative-free brands may be the best for the health of corneal cells. Oral administration of essential fatty acids may also help.
More moderate cases may require ointment with patching. A mild topical corticosteroid may be indicated to reduce corneal scarring. However, pay attention to these patients to prevent further lysis of the corneal stroma.
Bandage soft lenses can protect your patient's cornea, which continues to undergo epithelial defects and stromal lysis. Topical antibiotics may also protect the disrupted corneal surface from opportunistic bacteria. Several reports have also supported GP scleral lens use such as the Boston keratoprosthesis as a means to protect the cornea and bathe it in a reservoir of tear fluid.
Topical cyclosporine has been suggested as an early management strategy (Reynolds and Kabat, 2006). Autologous serum has been reported to help by providing growth factors to the compromised cornea, aiding in corneal epithelial cell regeneration. However, deriving autologous serum requires specialized preparation.
Other factors such as substance-P and nerve growth factor have been tried in animals and humans with limited success. Conjunctival flaps and amniotic membrane as patch grafts have also had success in severe forms of neurotrophic keratitis. CLS
For references, please visit www.clspectrum.com/references.asp and click on document #173.
Dr. Miller is an associate professor and chair of the Clinical Sciences Department at the University of Houston College of Optometry. He is a member of the American Optometric Association and serves on its Journal Review Board. You can reach him at email@example.com.