Neurotrophic keratitis

Neurotrophic keratitis. It is characterized by epithelial destruction and epithelial healing disorder, due to loss of corneal sensitivity . The most common pathogenic mechanism is injury to the trigeminal corneal innervation, and there are multiple ocular and neurological causes that can cause it, either at the level of the nucleus located in the protuberance, the Gasserian ganglion , the ophthalmic trigeminal branch , the nasociliary nerve or the fibers of the long ciliary nerve .


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  • 1 Causes
  • 2 Symptoms
  • 3 Critical sign
  • 4 Other signs
  • 5 Diagnostic protocol
  • 6 Treatment protocol
    • 1 Medical treatment
    • 2 Surgical treatment
  • 7 Follow-up
  • 8 Sources


  • Eye diseases: herpes simplex and herpes zoster eye infections, abuse of topical anesthetics, non-steroidal anti-inflammatory drugs, chemical burns, etc.
  • Trauma.
  • Systemic diseases: diabetes mellitus , leprosy .
  • Congenital processes: familial dysautonomia, Möbius syndrome , syndrome Riley-Day , ectodermal dysplasia and neuropathy sensory hereditary.
  • Neurological processes: any surgical or radiotherapy technique that acts iatrogenically on the trigeminal ganglion or the trigeminal nerve , stroke, tumor (especially acoustic neuroma), aneurysm , involvement of the VII cranial nerve.
  • Post-surgical processes: refractive surgery , penetrating keratoplasty , cataract extraction .


  • Red eye .
  • Photophobia .
  • Reflex tearing .
  • Foreign body sensation.
  • Decreased visual acuity.

Critical sign

  • Decreased corneal sensitivity ( hypoesthesia or corneal anesthesia ).

Other signs

  • Early: decreased tear production, superficial punctate keratopathy accompanied by conjunctival hyperemia and loss of corneal brightness.
  • Delayed: central corneal ulcer , rounded, raised, grayish-white, thinning and even corneal perforation.

Diagnostic protocol

  • History : history of trauma, herpes episodes, previous eye surgery, if radiation , hearing problems.
  • Verify bilateral corneal sensitivity with a sterile cotton swab (less than 5 mm is clinically significant).
  • Look for signs of corneal exposure: alterations of the eyelid closure, absence of Bell’s phenomenon , paralysis of the VII cranial nerve.
  • Fluorescein stained slit lamp biomicroscopy of the anterior segment : dotted keratopathy in the interpalpebral area, with irregular appearance of the epithelium and opacity thereof, an epithelial defect with stromal edema and superimposed infection can be seen, and in severe cases, perforation.
  • If no other causes are found, a space-occupying lesion in the central nervous system should be ruled out , computed tomography and magnetic resonance imaging performed .

Treatment protocol

Medical treatment

  • Mild and initial cases: artificial eye drops, preferably without preservation, apply 3-4 times a day and artificial gel tears at night, and mechanical ocular occlusion.
  • For epithelial defects: antibiotic ointment (eg chloramphenicol , erythromycin or tetracycline ) 3-4 times a day for 5-7 days or until resolution. Compressive occlusion on the first day (optional). Chronic treatment with artificial tears is generally required.
  • In the case of a sterile ulcer , a cycloplegic mydriatic should be applied (eg homatropin 2%, atropine 1%) 1 drop plus antibiotic ointment and occlusion for 24 h. Repeat this procedure until complete healing is achieved.

Surgical treatment

  1. Temporary or permanent tarsorrhaphy , depending on the case.
  2. Tear spots occlusion and therapeutic soft contact lenses. Good option in facial paralysis , as long as strict monitoring is done, but not in trigeminal paralysis due to its high risk of infection.
  3. Conjunctival or amniotic membrane coating.
  4. Small perforations: cyanoacrylate tissue adhesive and therapeutic soft contact lenses.
  5. Large perforations: keratoplasty .


  • Mild and initial cases: see evolution after 5 days.
  • Epithelial defects: follow-up every 2-3 days until improvement, then weekly.


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