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any form of orbital disease, particularly cellulitis or space-occupying masses. Exophthalmos or strabismus with reduced globe retropulsion should arouse suspicion of such a cause and prompt orbital imaging. Hypovitaminosis A has been associated with nutritional KCS; however this is most common in food animals.
Infectious etiologies of reduced aqueous production include distemper virus in dogs and feline herpesvirus (FHV-1) in cats. In these diseases, signs of KCS are usually overshadowed by more overt ocular or systemic lesions. However, assessment of tear production and supplementation of the tear film when necessary should be a routine part of management of these diseases. Unlike other causes of KCS, tear production usually resumes if the primary infectious etiology is resolved. Perhaps of more relevance is the way in which infectious diseases may affect tear quality through destruction
or dysfunction of the conjunctival goblet cells and meibomian glands. For example, conjunctivitis of any cause, is often associated with reduction in goblet cell density, an unstable tear film and worsening conjunctival (and sometimes corneal) disease – thus setting up a “vicious cycle”. Likewise, bacterial blepharoconjunctivitis or orbital cellulitis may also extend to the tarsal and orbital lacrimal glands respectively. Surgical removal
of the third eyelid gland following third eyelid gland prolapse (or cherry eye) can be an iatrogenic cause of KCS.
Traumatic disruption of the lacrimal gland, its blood supply, or innervation (CN V or VII) is a known cause of KCS. Trauma may be anatomically distant from the gland if the nerve or vascular supply is involved. Possibly one of the most common causes of neurologic KCS is injury to the facial nerve, particularly in association with middle ear disease. Neurogenic reduction or failure of blinking due to facial nerve dysfunction and/or dysfunction of the sensory fibers of the trigeminal nerve can exacerbate KCS in these cases. Concurrent desiccation and crusting of the ipsilateral nostril (xeromycteria) strongly suggests neurogenic dysfunction. The most commonly incriminated toxic causes of KCS are sulphur drugs
and atropine; however etodolac (Etogesic®) appears to be associated with a rapid onset of usually absolute sicca poorly responsive to cessation of the drug and/or administration of cyclosporine. General anesthesia and sedation can also cause a temporary depression of STT values.
Regardless of cause, the pathogenesis and end result of deficient aqueous production is multifactorial. Surface dehydration, hypoxia and necrosis of surface tissues, accumulation of exudates, and secondary infections are important mechanisms.
Clinical signs
Clinical signs will always be the initial alert that tear film
dysfunction should be considered. The classic signs
of aqueous tear film deficiency are familiar, with the hallmark clinical sign being accumulation of tenacious, adherent mucopurulent discharge over the corneal surface, conjunctiva, and eyelids. The mechanisms underlying this are likely over-production of mucins to compensate for aqueous deficiency as well as reduced hydration and flushing of those mucins secreted.
It should come as no surprise to us therefore that analogous mechanisms are at play in mucin or lipid deficiency. For example, reductions in the quantity or quality of ocular surface mucins should be expected to cause a compensatory increase in aqueous production (and likely a less visible increase in lipid production)
as well as a tear film that is less well “anchored” to
the ocular surface. In other words one of the signs of qualitative tear film deficiency may well be... epiphora!!
Somewhat irrespective of which tear component is deficient, the secondary corneal changes are relatively non-specific and reflect the chronic, irritating nature of the disease. These include a lackluster corneal surface (especially with aqueous deficiency), superficial corneal vascularization and pigmentation, and sometimes (if
the onset of dry eye is acute) corneal ulceration. Ocular discomfort and conjunctival thickening due to squamous metaplasia are also common.
I am always careful to thoroughly assess all visible conjunctival regions (especially the deep fornicial regions) using both diffuse and a slit beam. In particular, I look for evidence of thickening/cellular infiltrate, chemosis, hyperemia, follicles, papillary conjunctivitis, or excessive folding. I also pay particular attention to the meibomian gland profiles visible through the palpebral conjunctiva and any glandular secretions naturally occurring or forcibly expressed from the gland orifices. Look particularly for secretions that are more difficult
to express, more opaque than translucent, thicker
or “waxier” than normal, or those that form a small inspissated “bubble” from the orifice (so-called “choked” meibomian glands)
Diagnostic testing
The “workhorse” of dry eye testing in veterinary medicine is of course is Schirmer’s tear test type 1 (STT-1). In dogs, I consider STT values less than 15 mm/ minute in conjunction with consistent clinical signs diagnostic. However, it is important to recall that the STT-1 result merely reflects the volume of tear film in the lacrimal lake plus the volume of reflex tears stimulated to be produced and released by the STT strip gently abrading the cornea. It is interesting to ponder, therefore, the effects of lid conformation, emotional state, corneal sensitivity, placement of the STT strip (medially,
centrally or laterally in the ventral conjunctival fornix), lacrimal gland function, and patency of the lacrimal
gland ductules. I am confident that a patient cold have
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