Read the German translation: Wenn Die Hornhaut Ulzeriert
A corneal ulcer is a focal defect in the corneal epithelium and possibly the stroma. It is diagnosed by applying fluorescein dye to the corneal surface where it adheres to the exposed corneal stroma. There are different types of corneal ulcers and they require different specific treatments depending on a variety of factors like size, depth, duration etc.
The Simple Superficial Ulcer
A superficial ulcer involves mostly the epithelium and very little of the stroma.
Caused by: Mechanical trauma, exposure, desiccation, severe edema.
Clinical signs: Blepharospasm, excessive lacrimation, photophobia, conjunctival hyperaemia, chemosis, irregular corneal surface.
Treatment: Treat underlying cause. Topical broad spectrum antibiotic solution or ointment, topical atropine sulfate 1%, topical Vitamine A.
Any superficial ulcer which does not show significant improvement within 3-5 days of commencing treatment should be re-evaluated. Some may fall into the category of refractory ulcers, while in others, foreign bodies or infection may still be present.
The Refractory or Indolent Superficial Ulcer
This is a very specific condition/type of ulcer, also called spontaneous chronic corneal epithelial defects. Especially seen in older animals and in Boxers, Corgis.
Caused by: Mechanical trauma to the epithelium may be inciting factor, can occur spontaneously. Age-related degeneration of the basement membrane with no or slow repair of the basement membrane. Abnormal superficial stroma. Epithelial cells fail to adhere to underlying layers.
Clinical signs: Blepharospasm, excessive lacrimation, photophobia, conjunctival hyperaemia, superficial corneal ulcer, mild corneal edema, loose epithelial tags at edge of ulcer. Takes up to 7 weeks or longer for blood vessels to appear and often results in exuberant granulation.
Treatment: The loose epithelial cells are removed under topical anaesthesia with proparacaine (debridement). Dry cotton tips are used to debride the loose, necrotic epithelium from the edge and surface of the ulcer until no more cells can be removed. Topical broad spectrum antibiotic solution, 5% NaCl drops or ointment q8-12h to reduce edema. If the ulcer is not healing in 7-10 days treatment with a multiple punctate or striate keratotomy is recommended. An alternate treatment is a superficial keratectomy.
Feline Herpes Keratitis
Caused by: feline herpes virus-1 (FHV-1)
Clinical signs: In kittens, it causes conjunctivitis from mild to necrotic with pseudodiphtheric membrane formation, upper respiratory disease, ophthalmia neonatorum.
In older cats it causes keratoconjunctivitis, upper respiratory tract infection, has a tropism for epithelium of the conjunctiva, cornea, and the nasal tract. Virus may persist latent in trigeminal ganglion. Stress and steroids re-activate the virus. Infected cats have a poor long-term immunity. Chronic and secondary infections: conjunctivitis with or without keratitis. Usually, superficial dendritic corneal ulceration accompanies conjunctivitis. Microdendrites coalesce into dendritic ulcers which progress to become map-like geographic ulcers. This progresses, if untreated, to stromal keratitis. Secondary bacterial infections may lead to deep ulcer and descemetocele formation.
Associated diseases: Symblepharon, entropion, corneal sequestrum, eosinophilic keratitis
Treatment: Conjunctivitis: topical antibiotics (oxytetracycline, chloramphenicol, erythromycin). Keratitis--topical antiviral treatment when disease is active with trifluridine, idoxuridine, vidarabine or others. Very frequent treatments necessary. Also, systemic L-Lysine orally, or topical or systemic interferon 2 alpha or gamma.
The Deep Ulcer
A deep ulceration involves the stromal layers of the cornea.
Caused by: The same etiologies as superficial ulcers, but after the initial trauma bacteria infect the stroma and cause deepening of the lesion. Any ulcer extending into the corneal stroma should be considered threatening with regards to maintenance of a visual eye.
Clinical signs: Blepharospasm, lacrimation, photophobia, conjunctival and scleral hyperaemia, mucopurulent discharge is suggestive of bacterial infection. Change in corneal contour with an obviously depressed area of corneal surface, corneal edema, corneal cellular infiltrates, corneal vascularisation, uveitis, sometimes hypopyon.
Vascularisation is beneficial to the healing of the ulcer. Certain drugs appear clinically to retard this process (N.S.A.I.D.) and their uses for relief of pain and uveitis must be balanced with their effects on the healing process. Invariably there is secondary uveitis present with deep ulcers.
Treatment: E-collar, elimination of the predisposing causes, topical broad spectrum antibiotics, topical atropine 1%, systemic anti-inflammatory therapy with NSAIDs. When the infection is under control and the ulcerated area needs support: conjunctival flap or cornea-conjunctival transposition.
The "Melting" Ulcer
The melting refers to the breakdown of the corneal collagen lamellae due to protease, hydrolase and collagenase activities.
Caused by: These enzymes are produced by bacteria, neutrophils, epithelial cells, dying keratocytes, and macrophages as part of the response to corneal injury and infection. This process is considerably enhanced by corticosteroids!
Usually the melting occurs in association with a bacterial infection of the stroma (Pseudomonas, Streptococcus), but can also be caused by acute severe damage to the keratocytes. This is a very serious condition. This form of a deep ulcer with rapid progression can lead to corneal perforation within 24 hours of ulceration.
Clinical signs: Pain, inflammation of the conjunctiva and sclera, the corneal tissue in the ulcerated area becomes gel-like, thickened, soft, white to yellowish. Usually accompanied by secondary uveitis with hypopyon and miotic pupil.
Treatment: The same treatments as for deep ulcers but also: topical serum to reduce melting. A bacterial infection is assumed and intensive antibiotic therapy is recommended with broad spectrum antibiotics given as often as hourly. A combination of antibiotics can be used to broaden the spectrum (aminoglycosides or fluoroquinolones and cephalosporins). Systemic antibiotics can be given in addition to the topical treatments. Corticosteroids should not be used topically or systemically in melting ulcers. Surgical removal of the melting cornea followed by a conjunctival flap is performed if a rupture is expected otherwise.
A descemetocele is a very deep ulcer in which only Descemet's membrane (and endothelium) remains as barrier between the anterior chamber and the outside world.
Caused by: This is usually the result of a fast progressing deep ulcer or a melting ulcer.
Clinical signs: Pain, conjunctival and scleral hyperaemia, a very deep ulcer /crater with a clear central portion that may be bulging because of the intraocular pressure, cornea edema surrounding it. Descemet's membrane is fluorescein negative but the stroma in the wall of the crater will retain the fluorescein dye.
Treatment: Descemetoceles should be regarded as ophthalmic emergencies. E-collar.
Medical treatment alone: Generally only in very young animals with a small descemetocele, or patients with a high anaesthetic risk, the same therapeutic regimen as for a deep/melting ulcer. Close observation and daily rechecks required.
Surgical and medical treatment is recommended: a conjunctival flap provides excellent blood supply and enables continued medication of the cornea. The eye can be evaluated quite well especially with a pedicle shaped conjunctival flap. A corneoconjunctival transposition is a sliding graft of normal cornea and conjunctiva into the area of the defect. It provides support and brings blood supply closer to the affected area. Cyanoacrylate tissue adhesive is sometimes used if long anaesthesia is not feasible or if the descemetocele is very small. Third eyelid flap or temporary tarsorrhaphy is not recommended in this situation. It can lead to the rupture of the cornea.
Corneal Perforation and Iris Prolapse
When the cornea develops a fully penetrating defect, the aqueous humour is lost and iris tissue may prolapse into the wound.
Caused by: It is the result of an uncontrolled deep ulceration or a trauma.
Clinical signs: Inflamed and painful eye with severe hyperaemia, hemorrhagic ocular discharge, corneal defect often with protruding mass of darkly pigmented iris and yellow-red fibrin and haemorrhage, possibly a flat or shallow anterior chamber, miotic pupil (secondary uveitis), anterior synechiae, and hyphema.
Treatment: Surgical and medical therapy indicated: direct corneal suturing of very small perforations, conjunctival flap or corneoconjunctival transposition with larger defects. The prolapsed iris must be trimmed or repositioned in the eye, and the anterior chamber reformed. Devitalized tissue and especially melting stroma may not hold the sutures well. Careful debridement is necessary. Appropriate medical therapy as needed for deep ulcers and uveitis. Often the cornea is treated medically for 12-24 hrs prior to surgery with topical antibacterial and atropine and the patient receives systemic antibiotics and anti-inflammatory treatments.
Very rarely and usually only in very young animals can a corneal perforation heal without surgery with preservation of the globe and even vision. Is the eye badly damaged, the loss of cornea very large or the laceration involves the sclera, the eye should be enucleated.