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 25-28 September, 2018 | Singapore
WSV18-0273
OPHTHALMOLOGY
CANINE KERATOCONJUNCTIVITIS SICCA – WHAT DO I DO WHEN CYCLOSPORINE DOES NOT WORK?
D. Maggs1
1Professor Ophthalmology, University of California Davis, USA. Introductory Philosophy
Prior to and especially since the introduction of cyclosporine as a treatment for canine dry eye, I
think we have had a strong tendency to consider keratoconjunctivitis sicca (KCS) as a simple deficiency
of aqueous tear production. To be sure, this is justified (and reinforced on a daily basis in our clinics) because the vast majority of our canine patients respond so remarkably to topical administration of cyclosporine. Therefore, we sometimes need to remind ourselves that the nasolacrimal system consists of complex secretory, distributional, and drainage components all of which must act in superb harmony to effectively protect the corneal and conjunctival surfaces. In some ways, the fact that 0.2% cyclosporine ointment (Optimmune®) is
so effective in the majority of KCS patients has made treating tear film disease truly fascinating. I enjoy the challenge of thinking about and better managing those less common cases that are unresponsive or only partially responsive to immunomodulatory stimulation of aqueous tear production. A complete but brief review of nasolacrimal anatomy and physiology is a necessary first step.
A CLINICIAN’S APPROACH TO THE LACRIMAL UNIT Secretion
· Orbital and third eyelid lacrimal glands that produce the aqueous component of tears
· Tarsal (or meibomian) glands, which are modified sebaceous glands that secrete an oily fluid similar to sebum and responsible for reducing evaporation of the aqueous component of the tears.
· Conjunctival goblet cells, especially those in the ventral fornix, that produce mucin, which improves retention of the aqueous tears by the hydrophobic corneal epithelium.
Distribution and loss
The composite preocular tear film produced by lacrimal, tarsal and conjunctival glands is critical for corneal, conjunctival, and general ocular health. It is distributed by normal blinking and movements of the third eyelid and globe before pooling in a space referred to as the “lacrimal lake” between the anterior faces of the cornea and third eyelid and the posterior margin of the lower eyelid. A percentage of tears determined in large part by tearfilm stability (and therefore composition), ocular surface topography, and blink rate (determined in part by skull shape, corneal sensitivity, emotional state) then
evaporates or is lost over the eyelid margins. Excess tears drain via upper or lower nasolacrimal puncta into the nasolacrimal system.
Qualitative vs. Quantitative Tear Film Deficiencies
Classically, qualitative deficiencies describe biochemical alteration of a component of the tear film, while quantitative deficiencies describe decreased volume
of a tear component. Because the aqueous component of tears comprises the major volume of the tear film, qualitative tear film disturbance and KCS are sometimes considered synonymous. The majority of canine KCS
is believed to be due to an idiopathic, but immune mediated dacryoadenitis involving the lacrimal glands. These cases are most likely to respond to therapy with topical cyclosporine A (CsA). This treatment is so reliably successful in immune-mediated dacryoadenitis, that
I wonder if failure to consider other causes of KCS is possibly the most common cause of poor response to this standard therapy.
using the “DAMNIT” list to direct examination and testing
As the internists have taught us, a logical approach to apparently idiopathic or disease or cases unresponsive to “best guess” therapy is very wise. I think this is particularly true for canine dry eye patients unresponsive to topical administration of CsA. Here’s a few causes I consider (for completeness, I have included feline as well as canine causes):
Developmental KCS (acinar hypoplasia) is reasonably common in Yorkshire terriers and other toy breeds and is often associated with absolute sicca (STT = 0). Curiously, this can be unilateral. As might be expected, this form
of KCS is unlikely to respond to topical CsA and is one of the more challenging forms to treat, usually requiring parotid duct transposition.
Autoimmune disease with mononuclear cell infiltration and fibrosis of the lacrimal gland is the most common etiology for KCS in dogs. The stimulus for this disease
is unknown, however the observation that it occurs
more commonly in some breeds suggests that a familial predisposition may exist. Commonly-affected breeds
are West Highland White Terriers, Bulldogs, and Cocker Spaniels. These patients seem the most likely to respond to CsA.
Metabolic causes of KCS are limited. Although
some studies suggest an association between KCS
and certain endocrine diseases such as diabetes
and hypothyroidism, this is not universally proven. Regardless, concurrent treatment of any endocrinopathy and topical application of CsA would appear wise and may improve prognosis.
Neoplasia of the lacrimal glands is rare; however glandular dysfunction can be seen in association with
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43RD WORLD SMALL ANIMAL VETERINARY ASSOCIATION CONGRESS AND 9TH FASAVA CONGRESS






























































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