Corneal Ulcer - Horse

Also known as: Equine Corneal Ulcers

Introduction

Corneal ulceration is a very common disease of the equine eye and can have sight threatening consequences. Aggressive treatment is always indicated, as even apparently mild ulcers can progress quickly, causing serious complications.

Aetiology

A distinct cause for initial ulceration is not commonly found, although in many cases it can be assumed to be traumatic in origin. The horse’s eye is especially vulnerable to trauma due to its prominent position, compared with other species.

Exposure keratitis can occur in the horse, most commonly secondary to facial nerve paralysis. Hospitalised animals have been shown to have a decreased corneal reflex, and this corresponds to an increased incidence of ulcers in the hospitalised population. Foreign bodies embedded in the palpebral conjunctiva, or the nictitating membrane can cause persistent irritation and ulceration. Often the shape/distribution of the lesion is suggestive of this aetiology, but even in the absence of a characteristic lesion their presence should be considered and sought out.

Bacterial (+/- fungal) infection occurs readily after initial ulceration, as disruption of the corneal epithelium allows attachment and colonisation of the underlying tissues by normal corneal commensals. Commonly isolated bacteria include Staphylococcus spp., Streptococcus spp. and Pseudomonas spp., and empirical anti-microbial therapy should be effective against these bacteria.

Clinical Signs

These include: ocular pain manifested as blepharospasms, increased lacrimation and photophobia. Corneal oedema, scleral injection and conjunctivitis are also often present.

Signs of infection may include: necrotic edges, a cratered base, severe manifestations of pain and inflammation.

Diagnostics

Differential diagnoses for the painful equine eye include: ulceration, uveitis, blepharitis, conjunctivitis, glaucoma, dacryocystitis.

A full ophthalmic exam should be performed.

Fluoroscein staining is usually diagnostic for corneal ulcers, although staining with Rose Bengal is also recommended as it can pick up early viral/fungal lesions, which will appear as multifocal disturbances to the tear film.

Cytology, culture and sensitivity is recommended for rapidly progressive or deep corneal ulcers. Cotton swabbing is often inadequate, and corneal scraping, for example, with the blunt side of a scalpel blade is usually required. This can be greatly facilitated by the use of local nerve blocks and topical anaesthesia.

There is almost invariably a secondary uveitis present with corneal ulceration, and signs of this may also be seen: miosis, corneal oedema, aqueous flare, hypopyon, intra ocular pressure (IOP) changes.

Treatment

Medical therapy should be based upon the severity of disease initially, and then by the response to therapy. The aims of initial therapy are:

Antibiosis

Analgesia

Anti-inflammatory medication

Mydriasis

The initial choice of antibiotic depends upon personal choice, experience and availability, but could include chloramphenicol, chlortetracycline, bacitracin-neomycin-polymyxin (BNP), ciprofloxacin, ofloxacin and tobramycin. Topical gentamicin formulations are also available, but in the opinion of some, should be reserved for cases with stromal melting. Frequency of application can vary from q1h to q8h, depending on both the severity of the lesion, and the formulation used (ointment vs. drops).

Much of the pain associated with corneal ulceration is due to the secondary uveitis and miosis, and effective relief can often be gained with topical atropine(1%), leading to mydriasis. Dosing is generally q4h initially, and then as required to maintain dilation. Mydriasis is also important to avoid some of the complications associated with uveitis, such as synechiae formation and glaucoma. Pain is also associated with inflammatory response occurring in the adjacent sclera and conjunctiva, and systemic analgesia in the form of NSAIDs is usually indicated, for example, flunixin meglumin. Topical NSAIDs are available (diclofenac, flurbiprofen) and effective, but have been shown to increase corneal healing time.

In horses that are difficult to treat, or in cases that require very frequent treatment, then placement of a sub-palpebral lavage system can be very useful. As an adjunct to therapy, physical protection of the eye may be required, in the form of a mask. Some horses will rub their eyes in response to pain, and this can cause further corneal damage. Box rest is also vital, as over-exertion has been linked to intra-ocular haemorrhage and increased severity of uveitis.

Success in your therapeutic regime can be judged by a reduction in pain, and a decrease in size of the ulcer. Healing generally occurs rapidly at first, followed by a slowing after 5-7 days. As a rough guide, a non-infected ulcer can be expected to heal at approximately 0.6mm/day.

Complications

Non-healing ulcer

This may be due to the following causes:

Persistent source of irritation: such as a foreign body, self trauma, iatrogenic

Infection: antibiotic therapy should be reviewed, culture and sensitivity performed

Immunosuppression: due to Cushing’s, steroid therapy

Compliance: check that treatment is being administered effectively

None of the above: abnormal epithelium may have formed, keratectomy may be appropriate.

Melting Ulcer

Melting ulcers reflect inappropriate collagenolysis of the corneal stroma, by matrix-metalloproteinases (MMPs). Bacterial pathogens (especially Pseudomonas and β-haemolytic Streptococcus) induce the corneal epithelial cells and resident leucocytes to upregulate pro-inflammatory, and MMP-activating cytokines (IL-1,-6 and -8). These bacteria can also produce their own proteinases. The combination of exogenous, and upregulated endogenous, proteinases leads to a rapid breakdown of collagen, with the characteristic melting appearance. Untreated, this can lead to perforation within 12 hours (so act hard and fast!). There are several therapeutic options for inhibiting MMPs:

Autogenous serum – administer topically as often as possible. Keep refrigerated and change every 8 days.

EDTA - 0.05% q1h

Acetylcysteine – 5-10% q1h

Tetracyclines – Doxycycline especially has been shown to have anti-MMP effects

Tetanus antitoxin – can be delivered sub-conjunctivally. It contains macroglobulins with anti-collagenase effects.

A combination of the above may be necessary early in the disease course. Effective antibiosis is also paramount, and gentamicin is a good empirical choice (although there are some reports of gentamicin-resistant Pseudomonas species). Obviously, treating an eye this frequently in practice will be difficult, so referral is probably the best option.

MMPs can be further activated iatrogenically, by treatment (topical or systemic) with corticosteroids. Steroids also reduce the immune defences of the eye, so just in case you forgot...

Steroids are contraindicated in the treatment of corneal ulcers!

Corneal Rupture

The appearance of a descematocoele should alert you to the danger of the eye rupturing. Put a donut bandage over the eye, and give some broad spectrum antibiosis in case it ruptures on the way to the referral centre! Enrofloxacin is probably a good choice as it has good ocular penetration.

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