Equine Corneal Ulcers are one of the most common eye conditions, and because of their potential severity and difficulty in distinguishing them from other eye conditions, they should never be neglected or underestimated.
The horse’s cornea consists of 4 main layers; from front to back these are:
1. Corneal Epithelium – The outer surface, consisting of 8-10 layers of flattened cells which don’t absorb water
2. Corneal Stroma – The bulk of the cornea (>90%), consisting mainly of loosely arranged lamella of collagen fibres. The fibres are aligned in the same direction creating optical clarity and will absorb water.
3. Descemet’s Membrane – This is a thin acellular layer of protein attaching the stroma to the endothelium
4. Endothelium – A single layer of cells that forms the inside of the cornea. Importantly, both the Descemets and endothelium do not absorb water but pump water out of the cornea keeping it dehydrated, as any water within the stroma would render it opaque.
A corneal ulcer occurs when the corneal epithelium is disrupted to the extent that corneal stroma is exposed. A shallow ulcer involves just disruption of epithelial cells, while a deep ulcer would involve additional significant loss of stroma. Extremely deep ulcers can entirely remove corneal epithelium and corneal stroma, exposing Descemet’s Membrane. This is known as a descemetocoele and is an extremely serious condition.
In the majority of cases there is no obvious cause of ulceration, and it is assumed some form of trauma initiated it. Less commonly ulcers can be caused by a foreign body stuck to the inside of either the eyelids or the 3rd eyelid. These cases often have characteristic linear ulceration where the foreign body is swept across the cornea. Corneal ulcers can also be seen secondary to problems with blinking, most often due to facial nerve paralysis, although extremely uncommon, or with abnormally developed eyelashes (ectopic) irritating the cornea.
The signs of a corneal ulcer are very similar to signs seen with any other form of ocular pain, namely:
- Blepharospasm – a closed eyelid
- Photophobia – avoiding light
- Lacrimation – more tears being produced
- Miosis – a closed pupil
If your horse’s eye is open, you may also be able to see a small cloudy area on the cornea.
Once suspected your vet will carry out a comprehensive ocular examination. A vital stage is the application of a non-painful fluoroscein dye. This dye does not stain a corneal epithelium, but will stain corneal stroma. If the epithelium has been damaged and an ulcer created, the stroma will be exposed and become stained as a green area centrally with an often paler rim surrounding. This is where epithelium is still intact, but the dye has diffused through the stroma underneath the epithelium. In the case of a descemetocoele, then a similar staining pattern will be seen. However, there will be a central dark area that does not pick up dye. This is because Descemet’s membrane does not stain.
A second important part of examining an ulcerated eye is determining whether pupillary light responses are present. Even if the pupil in the affected eye is miotic/closed or not visible due to opacities, a consensual response to the opposite eye can be evaluated. Here shining a strong light into the affected eye, should provoke the opposite pupil to constrict. Absence of this response warrants a poor prognosis for restoration of vision implying disease of the deeper ocular structures, such as the retina and optic nerve.
The surface of the horse’s eye normally has a population of “friendly” bacteria that live within the conjunctival sacs. They cause no problems here, and the corneal epithelium prevents them from establishing infection. However, if the protective barrier of the epithelium is breached, with an ulcer, then infection can set up rapidly with serious consequences. The bacteria release, and induce the horse to release, certain enzymes that break down protein (Matrix Metallo-Proteinases or MMPs) into its constituent amino acids. The corneal stroma is made up primarily of collagen protein, and these enzymes can rapidly destroy the stromal integrity, and the cornea itself, predisposing eyeball. This is known as a melting corneal ulcer. The activation of these MMPs, and effects on the corneal stroma must be stopped before this occurs.
The formation of an ulcer also creates significant inflammation. Inflammation is a primarily vascular process, but due to the lack of blood vessels in the normal cornea does not occur here, instead “spilling over” into nearby structures seen as HYPERLINK “http://www.equine-vets.com/fact-sheets/eyes/conjunctivitis” \o “conjunctivitis” conjunctivitis, with reddening and swelling of the conjunctiva. Unfortunately, this inflammation will travel into the eye, and is seen as inflammation of the iris, ciliary body and choroid, together known as uveitis. This is an extremely painful process, and is usually seen as a constricted pupil with blepharospasm and photophobia. In severe cases inflammatory cells and proteins can be seen floating in the front of the eye. Unless treated, this can cause iris adhesions and permanent visual problems.
Corneal ulcers progress rapidly (within hours), so early and aggressive treatment is always indicated even for seemingly minor ulcers. The primary targets for treatment are:
- Reduce ocular pain
- Prevent and/or treat infection
- Prevent and/or reverse proteolytic enzyme activation
- Reduce inflammation internally and externally
The treatments commonly used are:
- Systemic anti-inflammatory and painkillers
- Flunixin has the greatest effect on the eye, so is most commonly used as a paste, powders or intravenously
- Topical Antibiotic
- Topical antibiotic cream (Chloramphenicol ointment commonly) or drops may be used. Creams have poorer penetration but do not need to be applied as frequently as drops.
- Oral or injectable antibiotics are rarely used as they will not reach sufficient concentration at the target site
Atropine is a parasympatholytic, meaning it has effects typically associated with a “fight or flight” response. In a fight/flight situation the pupil would normally dilate, allowing for greatest vision, so atropine dilates the pupil (and paralyzes the ciliary body in iridocycloplegia). Pupil dilation is important to relieve pain and to prevent iris adhesions. Overuse can be associated with impaction HYPERLINK “http://www.equine-vets.com/fact-sheets/colic” \o “colic” colic, so it is used sparingly to keep the pupil dilated and faecal output should be closely monitored while under treatment.
Topical Anti-Protease Treatment
There are several options to achieve this, including plasma extracted from your horse’s blood or topical EDTA (an anti-protease mixed with horses’ blood).
In severe cases, several different anti-protease treatments are used.
The key to successful medical management is frequent drug administration, in severe cases, hourly. When treating a horse’s eye this frequently they can become resentful and head shy, so placement of a Sub-Palpebral-Lavage-System (SPLS) may be needed. This allows delivery of treatments into the eye via a tube attached to the mane. The catheters are inserted through the eyelid under sedation, and desensitisation with anaesthetic.
In the most severe cases of ulceration, and especially with melting ulcers and descemetocoeles, or if the medical therapy fails, surgical treatment may be necessary. The latest surgical treatments include conjunctival pedicle grafts, where a piece of conjunctiva is used to cover the ulcer, following removal of the infected cornea by surgical keratectomy, or repair of the defect using pieces of amniotic membrane. Previously 3rd eyelid or conjunctival flaps were performed, where the 3rd eyelid was sutured across the ulcer to protect and to provide a blood supply. These are rarely performed now as it does not allow corneal examination, and the newer techniques are more successful.
In the initial stages of managing a corneal ulcer, your vet will want to re-examine your horse’s eye regularly to ensure treatment is working and there are no complications. This is vital, as any complications must be dealt with to ensure a positive outcome.
Uncomplicated corneal ulcers heal quickly, leaving minor scarring. New corneal epithelium migrates inwards from the ulcer edge at a rate of approximately 1mm/day. A 10mm diameter ulcer therefore heals in 5 days (as migration occurs from all edges). If healing has not occurred within the expected time frame, then there may be a problem. Potential reasons for slow healing are numerous including old age, immunosuppression (Cushing’s Disease) and other infections. Of these fungal infections are most concerning with a fungal keratitis’ appearing very similar to a bacterial keratitis. Fungal keratitis is however, less common than bacterial keratitis, and is often associated with previous topical steroid use. However, either can cause rapid loss of vision. Immediate aggressive diagnostics and treatment are again critical with corneal scraping for cytology and culture, and possibly biopsy required for precise diagnosis. Other causes for healing failure include viral infection, foreign body, underlying ocular disease, and epithelial dystrophy. While rarely reported, equine herpesvirus has been documented to cause keratitis. Slit lamp biomicroscopy assists with detection of small foreign bodies. Nearly any intraocular disease, such as uveitis and glaucoma, has detrimental effects on the cornea and can cause an ulcer to become refractory to treatment. Lastly, epithelial dystrophy will cause an ulcer to be refractory. This type of ulcer usually has a rim of non-adherent epithelium at its periphery, and the eye may be relatively comfortable. Electron microscopy has shown this condition is due to basement membrane abnormalities in humans and dogs with the same probably true in other species. This condition requires surgical intervention. A multiple punctate or grid keratotomy can be done standing, and is about 80% successful. The success of surgical keratectomy approaches 100%, and is used in the event that simpler procedures fail.