Recurrent Erosion, Neurotrophic Keratopathy and Vitamin A Deficiency
Key Takeaways
Morning recurrence suggests epithelial attachment failure, whereas reduced sensation suggests neurotrophic disease.
Persistent defects require assessment for exposure, toxicity, infection and stromal thinning.
EU cenegermin treatment has an adult moderate/severe indication and a specific eight-week regimen.
Vitamin A deficiency requires systemic cause assessment and age-appropriate replacement, with urgent care for keratomalacia.
Three different routes to epithelial failure
Corneal epithelium can fail because it does not attach securely, because its sensory and trophic support is impaired, or because a systemic nutritional problem alters the surface. A persistent defect therefore requires more than another antibiotic bottle. Determine onset, pain, recurrence, sensation, exposure, lid closure, tear function and stromal integrity. An epithelial defect can become infected irrespective of its original mechanism, and significant thinning changes urgency.
Recurrent corneal erosion
Recurrent corneal erosion (RCE) produces repeated epithelial breakdown, often with pain on waking. Prior abrasion and epithelial basement membrane dystrophy are important associations. Abnormal attachment and nocturnal lid adherence can lead to epithelial avulsion when the eye opens. Between attacks the cornea may appear nearly normal or show map-dot-fingerprint changes. Examine both eyes and record whether the current problem is an active defect, residual irregularity or recurrent pain without a visible break.
During an episode, assess for infection and provide lubrication, pain relief and suitable epithelial protection. A bandage contact lens can help in selected cases but carries infection risk and needs follow-up. Long-term lubrication or hypertonic preparations may reduce recurrence in appropriate eyes; lid disease and tear dysfunction should also be addressed. Do not provide repeated take-home topical anaesthetic as routine therapy: misuse can produce severe epithelial and stromal damage.
Persistent recurrence can lead to epithelial debridement with diamond-burr polishing, phototherapeutic keratectomy (PTK) or selected anterior stromal puncture. Choose by lesion location, optical importance, thickness and previous treatment. Stromal puncture can create visible scars and is usually avoided in the central visual axis. The randomised diamond-burr study supports this approach in a defined RCE population, but does not make it mandatory for every first episode. Discuss haze, refractive change and the possibility of further recurrence with laser treatment.
Neurotrophic keratopathy
Neurotrophic keratopathy follows reduced trigeminal sensory/trophic support. Causes include herpes infection, diabetes, surgery, trauma and proximal nerve disease. A relatively painless persistent defect in an eye with reduced sensation should raise suspicion; absence of pain does not imply low risk. Test sensation before anaesthetic and assess blink, tear function and exposure. A defect may progress to stromal ulceration, melt or perforation.
A commonly used staging approach separates epithelial irregularity, persistent epithelial defect and stromal ulceration/thinning. It helps describe severity but does not replace measurement of the actual defect and depth. Remove avoidable toxic medications and treat exposure or lid problems. Preservative-free lubrication, serum-derived preparations, amniotic membrane, a suitable protective lens or tarsorrhaphy may support healing, depending on the eye. Exclude and treat infection and reassess the underlying nerve cause.
Cenegermin is recombinant human nerve growth factor. In the EU, Oxervate is authorised for adults with moderate or severe neurotrophic keratitis, with one drop every two hours six times daily for eight weeks. It is a specialist-supervised treatment, not a general dry-eye prescription. Storage, vial preparation and timing must follow the current product information. The EMA Oxervate information identifies the indication and regimen; it does not guarantee recovery of every scarred or thinned cornea.
Vitamin A deficiency and xerophthalmia
Vitamin A is required for normal epithelial differentiation and the visual cycle. Deficiency can produce night blindness, conjunctival xerosis, Bitot spots, corneal xerosis and, in severe disease, keratomalacia. Consider malnutrition, malabsorption, restrictive diets, bariatric or intestinal disease and liver-related contexts. A child can have systemic malnutrition requiring urgent care as well as ocular disease. Night blindness alone has other causes, including inherited retinal disorders.
Keratomalacia can destroy tissue rapidly and may be associated with poor sensation or limited symptoms. Arrange urgent systemic assessment and vitamin replacement under an appropriate age- and pregnancy-specific regimen, together with ocular protection and infection assessment. Do not improvise high-dose vitamin A during pregnancy or assume that ordinary lubricants correct the nutritional mechanism. Treat the reason for deficiency to prevent recurrence.
| Presentation | Most useful discriminator | Main treatment objective |
|---|---|---|
| Recurrent painful episode on waking | Attachment disorder and prior abrasion/EBMD | Heal the defect and improve durable attachment |
| Persistent relatively painless defect | Reduced sensation or exposure | Restore protection and trophic support; prevent melt |
| Night blindness with xerosis/systemic risk | Nutritional or malabsorption history | Correct systemic deficiency and protect the surface |
Choosing the next step
An adult with previous HSV and a painless defect needs sensation testing and neurotrophic management even if there is no active dendrite. A patient with repeated morning pain and normal sensation may need an attachment-focused approach. A malnourished child with xerosis requires urgent systemic treatment. For every pattern, document acuity, size, stromal depth and infection findings, and arrange a review interval that reflects the risk of deterioration. Healing the epithelium is the immediate goal; durable prevention requires correcting its specific failure mechanism.
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