Neurotrophic Keratitis Recurrent Corneal Erosion Syndrome
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Neurotrophic Keratitis Dr Sue Ormonde Learning objectives: 1. Describe the aetiologies of recurrent corneal erosions 2. Understand the therapeutic options for recurrent corneal erosions 3. Identify the causes of exposure keratopathy 4. Understand management strategies for exposure keratopathy 5. Recognise and discuss the management of neurotrophic corneal ulcers Suggested reading: Davis EA. Dohlman CH. Neurotrophic keratitis. International Ophthalmology Clinics. 41(1):1-11, 2001. Das S. Seitz B. Recurrent corneal erosion syndrome. Survey of Ophthalmology. 53(1):3-15, 2008 Jan-Feb. Neurotrophic or neuropathic keratopathy occurs in anaesthetic cornea Corneal sensory nerves key to corneal metabolic activity & epithelial health Loss of neural influence promotes oedema & exfoliation of epithelial cells Acquired causes: - Herpes Simplex - Herpes Zoster - Transection CN 5 - Diabetes - Leprosy - Acoustic neuroma Congenital causes: - Familial dysautonomia (Riley-Day) - Anhidrotic ectodermal dysplasia - Congenital insensitivity to pain Diagnosis: - Often presents late as painless initially - Early - punctate keratopathy, epithelial irregularity - Later - persistent epithelial defect, round/oval, usually central/superior half, surrounding opaque epithelium with smooth rolled edges, may progress to corneal melt esp. if secondary infection or steroid use Treatment: - Preservative free lubricants, prophylactic preservative free antibiotics - Tarsorrhaphy or botulinum toxin ptosis. Patching ineffective. Recurrent corneal erosion syndrome • Epithelial basement membrane complex anchors corneal epithelium • Disturbance of this complex results in defective adhesion and “recurrent epithelial erosion” Aetiology 1. Corneal trauma 2. Corneal dystrophies – Map dot fingerprint (Cogan’s dystrophy, or epithelial basement membrane dystrophy) – Reis Bucklers dystrophy – Lattice Map dot fingerprint: Most common anterior dystrophy Grey patches,cysts,fingerprints Only 10% become symptomatic However 50% RCES have MDF Genetics Autosomal dominant No definite information available about genetic linkage Clinical presentation • Possible past history: trauma/RCES • Unilateral • Severe ocular pain on awakening • Lacrimation ++ • Resolve in hours to days • May last months or years • Worse in diabetics • Corneal abrasion of variable size • Stains strongly with fluorescein • May be microcysts or pseudodendrite • Exclude MDF in other eye Management • Acute erosions • Patching • Cycloplegic • Oc Chloramphenicol • Debridement • Prophylaxis • Lubrication QDS for 3 months • Ointment nocte for 6 months • Bandage contact lens • Excimer laser PTK • Anterior stromal puncture Exposure Keratopathy Inadequate wetting of cornea, despite normal tear production Inability of lids to resurface cornea with each blink 1. Facial nerve palsy 2. Severe ectropion 3. Proptosis 4. Nocturnal exposure Signs – Mild to severe – Inferior punctate epitheliopathy – Corneal ulceration – Infective keratitis – Neovascularisation – Corneal perforation Treatment – Artificial tears by day – Lubricant ointment by night – Taping of eyelids (temporary) – Botox ptosis – Corrective lid surgery .