by Noelle La Croix, DVM, Dip. ACVO
Keratoconjunctivitis Sicca – Part 2: Clinical signs and treatment of KCS
Clinical signs of KCS
The manifestations of precorneal tear film dysfunction vary greatly from patient to patient. Levels of discomfort, and the severity of secondary ocular pathology do not simply equate with levels of dryness. Brachycephalic dogs have decreased corneal sensitivity when compared to dolichocephalic and mesaticephalic breeds. These short-nosed dogs (e.g., Shih Tzu, pug) can be quite comfortable despite severe KCS and/or corneal pathology. Animals with acute KCS are typically more uncomfortable than those who adapt to a slower progressive dryness.
Ocular discharge is often the first clinical sign of KCS appreciated by companion animal owners (Figure 1). This sticky mucopurulent discharge is secondary to the collapse and blending of the mucous and lipid layers of the tear film. The conjunctival surface is usually hyperemic and chemotic because of decreased oxygenation and inflammation from the disordered tear film. Varying degrees of blepharospasm and third eyelid elevation are also commonly appreciated in patients with KCS. This is due to increases in frictional irritation between the eyelids and the desiccated corneal surface.
In the absence of protective tears the corneal epithelia may become exposed allowing corneal infections to develop in the underlying stroma. Endophthalmitis, corneal perforations, corneal vascularization, and corneal pigmentation may also develop secondary to KCS. Corneal vascularization arises with decreased oxygenation of the tear film and/or secondary corneal ulceration. Corneal pigmentation is thought to be secondary to corneal stem cell exhaustion associated with chronic ulceration. Pigmented conjunctival cells migrate to the cornea to close these epithelial wounds. All of these processes can lead to a loss of vision. A drying of the ipsilateral nostrils is associated with neurogenic KCS. In some cases of KCS, chronic meibomian gland impaction and infection may also decrease production of the lipid layer of the tear film and/or accelerate tear film evaporation.
Diagnoses of KCS – evaporative tear syndrome and aqueous tear deficiency
Keratoconjunctivitis sicca can be diagnosed as an evaporative tear syndrome or as an aqueous tear deficiency. Schirmer’s tear testing will establish KCS, but the tearing rates should be evaluated in the context of other clinical signs.
Evaporative tear syndrome is classically diagnosed with a tear film break-up time (TBUT) test. The TBUT test is performed by staining the eye with a fluorescent dye (fluorescein), and then (with the eyelids spread apart) observing the eye with a slit lamp until small dry spots first appear in the tear film. The initial break-up of the tear film is typically within one minute in a normal dog. Faster times are indicative of KCS because of accelerated tear film evaporation. Evaporative tear film dysfunction is also suspected when corneal vascularization and/or pigmentation is appreciated even if TBUT and/or Schirmer’s tear test values are within normal limits. Evaporative tear syndrome can be the result of both intrinsic (e.g., lagophthalmos, trichiasis, meibomian gland impaction, facial nerve paralysis, abnormal blinking, decreased number of goblet cells) or extrinsic (e.g., allergies, toxin exposure, increased air flow, increased temperature, decreased humidity) factors.
Aqueous tear deficiency is classically diagnosed when a patient’s Schirmer tear test values are less than 10 mm/min. This deficiency is generally idiopathic or neurologic. In dogs, idiopathic KCS is histologically characterized by varying degrees of lymphocytic and plasmacytic infiltrations of the lacrimal glands. These histologic features suggest that idiopathic KCS is due to an immune-mediated destruction of lacrimal cells. Idiopathic KCS may therefore respond to lifelong immunomodulating therapies.
Neurologic KCS is characterized by either abnormal afferent corneal sensitivity or abnormal parasympathetic efferent stimulation of the lacrimal glands. Changes in parasympathetic stimulation can also affect mucin production, and so many cases of neurologic KCS lack significant ocular discharge. Neurologic KCS can result from injuries to the parasympathetic nuclei of facial nerves, pterygopalatine ganglia, and/or pre-/postganglionic parasympathetic nerves. Other causes of neurologic KCS include otitis media and otitis interna. These disorders are associated with damage to preganglionic parasympathetic nerves, and often facial nerve damage causing concurrent facial paralysis. The parasympathetic aspects of the facial nerves also stimulate the lateral nasal glands. Therefore, facial nerve damage associated with a dry nose (xeromycteria) is also associated with neurogenic KCS.
Treatment of KCS
The first step in treating KCS is to determine its etiology as an aqueous tear deficiency or evaporative tear syndrome. Cases with an aqueous tear dysfunction are prescribed tear stimulants (1 to 2% cyclosporine, 0.02% tacrolimus, or a compounded combination of both). In severe cases, oral prednisone or topical steroids may help reduce corneal surface inflammation and discomfort. Topical tear supplementation is prescribed to moisten the eye until aqueous tear production improves. A patient’s ears should also be examined to see if nerve damage is related to a neurologic KCS. Neurologic KCS may resolve quickly when treating these related disorders.
An evaporative tear syndrome is characterized by abnormal mucin production, lipid production, or eyelid conformation/ function. Anti-inflammatories (topical/oral steroids and/or cyclosporine) are prescribed to reduce corneal surface inflammation and thereby increase mucin and subsequent tear film production. Inflammation of meibomian glands can also be controlled with oral cyclosporine, steroids, and/or antibiotics. The lipid layer of the tear film can be re-established by the lanolin within artifical tear supplementation. The hygroscopic properties of sodium hyaluronate are also used within tear supplements to moisturize the cornea. Evaporative tear dysfunction caused by disorders of the eyelids may require surgical repair by a veterinary ophthalmologist.
Owners of companion animals with KCS typically face an overwhelming array of medications and dosing schedules. Tear supplements should generally only be prescribed until tear stimulants become effective. Owner compliance with dosing schedules will be greatest when limited to once or twice daily, and ineffective or unnecessary medications should be quickly discontinued. Although frustrating to owners, KCS can be controlled in many patients. As responses vary greatly, routine re-evaluations are necessary for adjustments to drug regimens.
If you have further questions regarding the diagnosis and treatment of KCS, please feel free to consult a veterinary ophthalmologist.
Noelle La Croix, DVM, Dip. ACVO
Veterinary Medical Center of Long Island
75 Sunrise Highway
West Islip, New York 11795
(631) 587-0800; fax (631) 587-2006
Figure 1: Ocular discharge is often the first clinical sign of KCS appreciated by companion animal owners.