Tear Film Disease

Keratokonjunctivitis Sicca (KCS)

In veterinary ophthalmology the diagnosis of Keratoconjunctivitis Sicca (KCS) has almost always been based on the result of a Schirmers Tear Test (STT). It is assumed that STT is an indication of both the reflex as well as the basal aqueous tear secretion. In this section KCS will be described, and sections following will describe qualitative tear film disease in the canine will be reviewed. In the dog KCS is most often diagnosed after relapses of bacterial conjunctivitis (Kaswan et al 1995) with mucous piling up in the fornix and appearing at the medial canthus. Mucin produced by the goblet cells is not dispersed by the aqueous tears and therefore accumulates (Kaswan and Salisbury 1990). Often the dog will exhibit pruritus and rub the eye(s) against the paw, furniture etc.

In chronic cases of KCS corneal vascularization is often seen, which can result in a chronic pigmentary keratitis. The corneal nerves can become insensitive in chronic KCS resulting in a further reduction in the tearing (no reflex tearing) (Kaswan et al 1995). Several breeds are predisposed with the most common breeds being:, Bulldog (English), Cocker Spaniel, Lahsa apso, Miniature Schnauzer, Pekingese, Shi Tzu, Standard schnauzer, West highland white terrier and Yorkshire terrier (ACVO 1996). KCS can be caused by a variety of conditions, most commonly thought to be an immune mediated disease (Kaswan et al 1998). Loss of sex hormones following castration or ovariohysterectomy predisposes older dogs to quantitative tear deficiency (Kaswan et al 1998). Dogs of 10 years of age or over are significantly more likely to exhibit deficient tearing (Kaswan et al 1998).

KSC can be induced by medication:

· atropine (Hollingsworth et al 1992)

· trimethoprim-sulfadiazine ( Berger et al 1995, Bedford 1985).

The treatment of KCS is cyclosporine A. Studies have been evaluating 2% and 1% cyclosporine in various oils, all showing promising results (Olivero el al 1991, Morgan and Abrams 1991, . Only one commercial ophthalmic drug with cyclosporine A (0.2%) is available (Optimmune®, Schering-Plough Animal Health) but a 1% or 2% solution can be made from dilution of Sandimmun® (Novartis) in vegetable oils (olive etc.). The inflammation of lacrimal glands in patients with KCS (Kaswan et al 1984) is supressed by the action of cyclosporine A, a T-cell depressent. There is evidence that cyclosporine also has a lacrimimetic effect by a hormonal mechanism (Kaswan and Salisbury 1990). In human Dry Eye Disease various lacrimal substitutes have been investigated over the years. A tear substitute may be used in conjunction with cyclosporine A if the KCS is very marked (eg. 1-2mm/min), but a time period must ellapse between installation of several topical ophthalmic medications, or the second application may cause a reflex wash out of the first applied drug. If the STT value is very low cyclosporine A may be applied to the cornea bid; if the STT value is 5-10mm/min, sid cyclosporine therapy should be sufficient. If no effect of cyclosporine is observed after 4-6 weeks of therapy, Parotid duct transposition (PDT) may be considered (Kaswan and Salisbury 1990).

Meibomianitis

Infection of the palpebrae will often include marginal blepharitis with the consequence of affecting the meibomian glands, thus causing interference with the secretion of the outer layer of the tear film. Inflammatory diseases of the canine eyelids can be caused by gram-positive aerobic bacteria and yeasts (Moore 1990). Dogs with meibomianitis typically have swollen eyelid margins with slight poiting of the orifices (Moore 1990). Chronic meibomianitis may result in rupture and chalazia formation (Moore 1990). "Normal meibomain lipid appears as a clear viscous oil similar in appearance to clear vegetable oil. Abnormal meibomian secretions are typically thick and opaque or may appear inspissated with a cheesy consistency. Expression of coiled semisolid strands of abnormal lipid is not uncommon with chronic meibomian disease" (Moore 1990). Culture should be undertaken directly from expressed secretions from the meibomian glands (Moore 1990).

Conjunctivitis -Goblet cells deficiency

Diffuse infiltration of chronic inflammatory cells into conjunctival mucosa and submucosa may markedly reduce or eliminate goblet cells (Moore 1990). Conjunctival biopsy makes a quantification of epithelial goblet cells possible, which is an indirect measure of mucin production (Moore 1990). The BUT(Tear Break-up time) is 19±5 seconds for normal (anaesthetized) beagle dogs (Moore et al 1987). Moore et al (1987) suggested that there might be a direct relationship between surface hydration and the number of goblet cells in the conjunctiva.

This page was authored by T. F. Evans October 2000.