The normal horse cornea is made up of 4 layers; epithelium, stroma, Descemet’s membrane, and corneal endothelium. Corneal nutrition is supplied by the precorneal tear film anteriorly and the aqueous humour posteriorly and consists of oxygen, glucose and electrolytes. The tissue of the cornea is transparent and doesn’t contain any blood vessels, however, it is richly innervated superficially with sensory endings of the Trigeminal nerves.
Corneal ulcers occur when there is a loss of the corneal epithelium and in more severe cases the corneal stromal tissues. Horses are more susceptible to corneal disease due to having a large exposed cornea, high exposure to environmental bacteria and/or fungi and increased risk of trauma due to modern housing practices. Causes of corneal ulceration include exogenous trauma, endogenous eyelid disease including entropion, dystrichiasis, ectopic cilia or eyelid tumors. Other causes include foreign body such as a grass seed, disease of tear film production, reduce eyelid function including cranial nerve VII or V paralysis, or lastly primary pathogens include herpesvirus, however rarely seen in horses. As the cornea is a highly innervated structure, ulcers are very painful and can often result in reflex uveitis, which is inflammation of the middle layer of the eye, extending from the iris at the front to the retina.
Bacterial keratitis is the more common form of corneal ulceration. This is where a corneal ulcer is colonized by commensal flora and cause damage to the corneal epithelium. Common bacterial pathogens include gram negative Pseudomonas spp, Klebsiella spp, and Enterobacter spp and gram-positive species Staphylococcus spp, ¬B-hameolytic spp, Streptococus spp and Clostridium spp.
Fungal keratitis (Keratomycosis) is where the stroma of the corneal has been colonized by fungus and should always be considered in complicated corneal ulcer cases that do not respond to antimicrobial therapy. Common fungi associated with corneal ulceration include Aspergillus spp, Alteraria spp, Fusarium spp, and yeasts including Candida albicans.
‘Melting’ corneal ulcers (or malacia) are caused by collagenase activity and is an emergency. These type of corneal ulcers can deteriorate quickly with stromal loss and have devasting consequences. Collagenases are produced from bacteria, fungi and degranulated neutrophils that have migrated to the infected site.
The classification of corneal ulceration is important and is dependent on depth and presentation.
• Superficial ulceration
• Deep ulceration
• Descemetocele
• Iris prolapse
• Melting ulcers
Simple ulcers should re-epithelialized and fluorescein stain negative after 7 days of treatment. If the ulcer fails to respond to treatment or healing is abnormal, then it is classified as a complicated ulcer and most likely will involve the stroma, have a collagenase component, may involve a foreign body and/or has become infected. If left untreated, the horse may lose their eye within 24-48 hours and referral for surgery would be the recommended intervention.
Clinical signs of corneal ulceration include painful responses including blepharospasm (involuntary closure of the eye), epiphora (excessive watering of the eye) and photophobia (sensitivity to light). Corneal oedema (when the cornea appears cloudy or blue), conjunctival and episcleral hyperemia (reddening) may also become apparent along with the development of neovascularization. Commons signs the corneal ulcer has become infected include hypopyon (accumulation of stromal inflammatory cells), purulent (pus) discharge, severe anterior (front) uveitis (inflammation) and/or stromal necrosis (tissue that has died). In very severe cases where the ulcer has begun to melt, the corneal stroma will appear gelatinous yellow to white.
Diagnosis of the type of ulcer is based on initial examination of the cornea, collection of a corneal sample for further testing and fluorescein stain testing. The cornea is assessed using an ophthalmoscope for any deviations in the epithelium and the anterior chamber is assessed for anterior uveitis. Fluorescein dye sticks to the hydrophilic corneal stroma when the corneal epithelium is lost and fluoresces bright green. Cytology (examination of cells) can then be performed in-house on the corneal swab to determine the type of cells present within the ulcer and help determine the type of medication required to treat the infection.
Before treatment can begin for corneal ulceration, it is important to rule out the presence of a foreign body such as a grass seed. Culture and sensitivity should be assessed before the administration of any topical treatment. If the causative agent is known antimicrobial or antifungal therapy can be started through the application of topical ointments such as Tricin, Chlorsig, Illium Optigen and Illium Opticin. Each of these has different active ingredients and should only be administered under the guidance and instructions of a vet. Due to the nature of the tissue of the cornea, the topical application needs to be frequent, and severe corneal ulceration may even need to be administered up to every 2 hours. A sub-palpebral lavage can be placed under the eyelid to help with the administration of medication. Your horse my also benefit from systemic analgesia such as NSAIDs (Phenylbutazone) for more severe cases.
Secondary uveitis often develops due to marked pain associated with corneal ulceration and can result in significant ‘reflex’ anterior uveitis with miosis, aqueous flare and painful ciliary spasm and the animal will often rub their eye and cause more trauma to the area. Mydriatics (most commonly used is 1% atropine to effect) are used to provide analgesia and cause pupil dilation. Once the pupil has been fully dilated it is important to ensure the pupil to protected from light for the duration of treatment.
Extremely important to avoid the use of corticosteroids as these are contraindicated for corneal ulceration as they predispose the area to infection, delayed healing and potentiate enzymatic destruction of corneal stroma.
The prognosis for corneal ulceration is varied depending on the severity. Small uncomplicated ulcers heal within 5-7 days, require minimal treatment and produce minimal scarring. If the ulcer has not improved in this time it is classified as severe and requires further investigation for corneal swabs and thorough ophthalmic examination. If a stromal abscess develops (abscess within the stroma of the cornea), the treatment time will be extended and it is likely a corneal scar will develop.
The sooner corneal ulcers are diagnosed and treated, the more likely a better prognosis will be seen.