Entropion

Entropion refers to a conformational defect in which the eyelid margin rolls inward, threatening corneal and conjunctival health from contact with facial hairs. The condition occurs infrequently in the cat. With the exception of a breed-related predisposition in the Persian and other brachycephalic breeds, feline entropion is usually spastic, commonly accompanying chronic herpetic conjunctivitis and/or keratitis. Over time, the spastic component gives rise to cicatricial characteristics that require surgical correction. Repair is simple using a conventional Hotz-Celsus technique, but failure to recognise and control the precipitating keratoconjunctivitis can result in recurrence of the entropion.

Deep Corneal Ulceration

While cats are probably best known for superficial corneal erosions associated with herpesvirus, an epithelial defect also provides opportunistic bacteria normally present on the ocular surface the opportunity to adhere to the injured tissue and further complicate the healing process through concurrent enzymatic destruction of deeper corneal stroma. The resulting deep ulcer requires aggressive management to salvage both globe and vision. Fortunately, cats have a remarkable ability to remodel damaged corneal tissue, minimising the final scarring much more effectively than the dog.

A host of factors may retard corneal wound healing and set the stage for progressive stromal loss. Brachycephalic breeds demonstrate the variety of adnexal abnormalities that can influence healing in any species: exophthalmos, lagophthalmos, corneal insensitivity, reduced blink rate, medial entropion and nasal fold/medial canthal trichiasis. Local factors include inadequate tear production, occult foreign bodies and toxicity of topical medications. Progression and/or recurrence are virtually guaranteed if the underlying anatomical and physiological factors are not addressed.

A 'melting' ulcer describes the rapid stromal destruction caused by enzymatic degradation of the cornea's collagen lamellae. Collagenolytic enzymes of bacterial and corneal origin are equally responsible for the devastating corneal damage. Pseudomonas aeruginosa is a virulent corneal pathogen owing to production of several proteases and toxins that damage tissue and interfere with host defence mechanisms. The organism produces at least two major matrix metalloproteinases that degrade corneal collagen and proteoglycans. Some streptococcal isolates are equally destructive. This destructive cascade can become autonomous once initiated and continue despite successful eradication of the bacteria. Damaged epithelial cells, stromal tissue and polymorphonuclear leucocytes release additional enzymes, increasing the rate of tissue destruction and stromal melting. Collagenase-associated ulcers are frequently central or paracentral in location. The affected stroma appears grey and mucinous in the early stages. Pain associated with the corneal lesion may actually diminish when the ulcer depth erodes beyond the superficial nerve endings. As the stroma liquefies and the hydrophobic Descemet's membrane is exposed, the ulcer clears. Unchecked, corneal liquefaction can lead to perforation, sometimes in a matter of hours.

The management of deep ulcers requires a four-tiered approach:

1.  Elimination of the inciting cause

2.  Arrest of corneal destruction

3.  Control of uveitis

4.  Support or reconstruction of the weakened cornea

Anterior Uveitis

Ocular disease can occur in conjunction with systemic signs or may appear alone as the sole sign of feline infectious peritonitis (FIP), primarily in young adult cats. Because FIP severely compromises the blood-ocular barrier, accumulations of inflammatory cells and fibrin are customary within the anterior chamber. The clinical diagnosis of FIP is made by an evaluation of the history, clinical signs, and results of fluid analysis, complete blood count (CBC), serum protein electrophoresis, serum chemical analysis and serology. Because antibodies for all strains of feline coronavirus cross-react with each other, determination of an antibody titre should be used as an aid (and nothing more) in diagnosis. Without histology, a diagnosis of FIP is considered presumptive.

Lens Luxation

Clinical signs associated with anterior lens displacement include discomfort, focal corneal oedema and iris tremor. Olivero and his colleagues described a breed predisposition for primary lens luxation in the Siamese cat. The most common age at presentation was 7-9 years, with a disproportionate number of male cats affected. However, most feline lens luxations occur in patients with chronic uveitis and/or glaucoma. Although the displaced lens is ideally removed surgically, the anterior chamber of the cat is usually able to accommodate the lens without the pressure rise that occurs in the dog.

Glaucoma

Glaucoma is often defined as an increase in intraocular pressure beyond that compatible with normal vision and ocular physiology. The normal intraocular pressure (IOP) in companion animals ranges between 8 and 18 mmHg (based on our clinical experience with the Tonopen) and is a delicate balance between production of aqueous humour and its subsequent drainage from the eye. In conventional outflow, aqueous exits through the iridocorneal (or drainage) angle, the boundaries of which are formed by the base of the iris-ciliary body and the inner surfaces of the cornea and sclera. A small percentage of aqueous humour (3% in the cat) drains from the eye via uveoscleral flow, passing through the iris stroma and/or between the ciliary muscle fibres from the trabecular meshwork to reach the supraciliary and suprachoroidal spaces where it is absorbed by the vessels of the iris, ciliary body and choroid.

Glaucoma in the dog results from a decrease in aqueous humour outflow, most commonly within the iridocorneal angle. The pathogenesis of glaucoma is more likely secondary to chronic uveitis in the cat, so obstruction to outflow can occur at the pupil secondary to synechiae or within the iridocorneal angle as a consequence of scarring.

The clinical signs of glaucoma may be subtle enough in cats that owners do not recognise a problem until the advanced stages of disease. In a large retrospective study, the most common presenting complaints were increased globe size, cloudy appearance of the eye and pupillary dilation. These clinical signs had been present an average of 7 months prior to presentation. Seventy-two percent of eyes were blind by the time of referral to an ophthalmologist.

Treatment of glaucoma in cats can be challenging. Response to treatment is often unpredictable and cats are generally intolerant of frequent and/or long-term therapy. Topical carbonic anhydrase inhibitors applied two to three times daily are often effective in the early stages of glaucoma but response declines in chronically affected cats. Dorzolamide's metallic taste may cause salivation or anorexia, so the author prefers brinzolamide to minimise the cat's aversion to therapy. Cats may be more sensitive to oral carbonic anhydrase inhibitors, the side effects of which include anorexia, lethargy, metabolic acidosis and hypokalaemia. Topical 0.5% timolol maleate applied three times daily is well tolerated, but care should be used in patients with a history of asthma. Topical prostaglandin analogues such as latanoprost (Xalatan) and topical parasympathomimetics such as pilocarpine are generally contraindicated in the management of feline glaucoma due to their potential to exacerbate concurrent anterior uveitis. Cyclodestructive procedures using cryotherapy or diode laser are relatively ineffective in cats. Chemical ablation of the ciliary body by intravitreal injection should be avoided owing to the potential risk of post-traumatic sarcoma.

Chronically glaucomatous, blind eyes are best treated surgically by enucleation or insertion of an intrascleral prosthesis.

References

1.  Olivero DK, Riis RC, Dutton AG, et al. Feline lens displacement. A retrospective analysis of 345 cases. Progress in Veterinary and Comparative Ophthalmology 1991; 1:239-244.