Page 261 - WSAVA2018
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Minimization of tear loss and maximization of tear distribution
Minimization of tear loss and maximization of tear distribution relies on a thorough assessment of lid anatomy and function. Many dogs with only marginal tear production can be made more comfortable with correction of mild ectropion or entropion, removal of distichia, and/or reduction of palpebral fissure size.
Stimulation of normal tear production remains the main goal of medical therapy
Tear replacement products are no substitute for improved production of endogenous tears with their multitude of immunologic and nutritive factors, and appropriate pH and osmolarity. Cyclosporine remains the most effective drug for this purpose in my opinion.
In addition to its ability to reduce immune-mediated infiltration of the lacrimal gland, this compound has a direct lacrimogenic function, and it promotes mucin production from conjunctival goblet cells. Its direct lacrimogenic function appears to rely on frequent application, while immunosuppression and remodeling of glandular tissue presumably require more chronic use. Therefore, in most cases this drug should be instituted twice daily and the patient rechecked in approximately
2 weeks. It is important that the client be instructed
to apply CsA as scheduled right up until the time of recheck examination. Omitting the morning treatment because the dog was going to be examined later that day may cause an artificial depression in STT values. Clients should also be advised that initial response to therapy is best judged by change in STT values, mucoid discharge, and ocular comfort, rather than decrease in pigmentation or corneal vascularization. Improvement
in these corneal changes occurs at a similar rate to
that which they occurred – slowly. Tapering of dose frequency or product concentration is typically not possible and should be based on clinical and measured (STT) responses. Failure to respond to 0.2% CsA BID is a reason to trial a higher concentration such as 1% or 2%. In my experience, increased frequency beyond BID does not have a satisfactory effect.
Information regarding tacrolimus is encouraging. This drug acts by a similar mechanism to CsA but is more potent and operates via a different cellular receptor. Reports confirm that it is effective in some cases that are unresponsive to CsA. It is compounded in various ways by many pharmacies. To date I am aware of data for a 0.02% aqueous and a 0.03% suspension in olive oil only. Although its safety and efficacy as an ophthalmic drug in dogs have been preliminarily tested, an FDA alert in the USA suggests that topical application of this drug as a dermatologic preparation in humans, especially children, may be associated with development of lymphoma
and squamous cell carcinoma. The FDA currently recommends that tacrolimus be used only when other
drugs have failed or not been tolerated, and then with caution. I follow this guideline for our veterinary patients too. Consider recommending that clients wear gloves when handling this product and that children do not administer the drug to their pets.
Some advocate use of topical corticosteroids to further reduce dacryoadenitis. This has some rationale but requires caution in an eye that is already more prone
to ulceration. Addition of a topical, penetrating steroid such as dexamethasone or prednisolone after initial treatment with CsA has successfully promoted some tear production and improved corneal health may be justified.
Cholinergic agents such as pilocarpine may be used
to provide parasympathetic stimulation of the lacrimal gland. This alternative mechanism might be expected
to be more physiologic and therefore likely to succeed in cases of neurogenic KCS than more common cases of immune-mediated dacryoadenitis. Topical use of this drug is very irritating, produces a noticeable uveitis,
and may not provide adequate drug concentrations at neurologic synapses. This has led to the suggestion that oral dosing on an empirical but individualized basis is necessary. This requires that the dose be titrated to just below systemic toxicity in each animal. Signs of toxicity include vomiting, diarrhea, and bradycardia. Ophthalmic pilocarpine is used orally usually via a doctored food bolus. One dosage recommendation (credit Dr. Randy Scagliotti) is that 1% pilocarpine is used for dogs < 4
kg, 2% for dogs weighing 4-20 kg, and 4% pilocarpine
for dogs > 20 kg. The initial dose is one drop PO twice daily for three days. This dose is increased by one drop every three days until the earliest signs of toxicity (usually vomiting or anorexia without diarrhea) are observed.
The drug is discontinued for 24 hours or until GI signs abate and then re-instituted at the highest dose which did not produce signs of toxicity. Because of the different mechanism by which CsA acts and because of its additional desirable effects, the two drugs are expected to be synergistic. There is a case report supporting the addition of a topical sympathomimetic eye drop to this regimen, and my personal experience supports this.
I use 2.5% phenylephrine. While this seems counter- intuitive at first, it appears that there are smooth muscle fibers associated with the lacrimal glands that act via contraction to express tears over the eyes. Thus the initial use of pilocarpine to stimulate tear production followed by the addition of phenylephrine to stimulate tear secretion has been advocated by some. We have tried this with remarkable results in a small number of dogs.
Artificial tears
Supplementation of tears has traditionally been provided in one of three forms: aqueous (“artificial tear”) solutions, more viscous polymers or methylcellulose solutions,
and ointments in a petrolatum base. However, no
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