Small Animal Clinical Pharmacology - CYF MEDICAL DISTRIBUTION

CLASSES OF DRUGS USED TO TREAT OCULAR INFLAMMATION
allowing penetration of drugs into the eye. As inflammation
subsides, the impermeability of the blood–eye
barrier is restored.
Drug characteristics
There are a number of drug factors that need to be
considered when treating the eye, including drug pH,
tonicity, viscosity and use of wetting agents.
Drug pH
Dogs have a tear pH of approximately 6.5. If a drug is
to be nonirritant to the eye, the drug solution should be
buffered to this pH. Some drugs, such as pilocarpine,
can be very irritating and need to be buffered with the
vehicle solution. Drug pH can affect drug penetrability
and shelf-life.
Tonicity
Ophthalmic drugs should be isotonic with the precorneal
tear film. Generally, small animals will tolerate a
wide variation in tonicity. Some drugs need to be in
relatively high concentrations to be effective but may be
irritating. Ointments appear to be less irritating than
drops for highly concentrated drugs.
Viscosity
Drugs that are contained in viscous vehicles have much
longer contact times, resulting in greater intraocular
penetration. This is seen most commonly in artificial
tear preparations used to treat dry eye. Viscous preparations
such as Visco Tears and Liquifilm Forte remain in
contact with the cornea for substantially longer than
normal artificial tears. As a result these drugs can be
used less frequently, which in veterinary practice often
means better owner compliance and improved clinical
outcome.
Wetting agents
Drugs that act as wetting agents do so by reducing the
surface tension. These compounds can be added to ophthalmic
preparations to increase corneal penetration of
ionized drugs.
ANTI-INFLAMMATORY OCULAR
THERAPY
Inflammation occurs in many common ocular conditions
and can be beneficial and protective. However, the
eye is especially prone to excessive inflammation, which
can destroy vision. Prompt and judicious use of antiinflammatory
drugs is essential in clinical ophthalmic
practice.
Uncontrolled inflammation in the eye can result in a
number of adverse sequelae, including vision loss from
retinal and optic nerve damage, glaucoma from obstruction
of aqueous outflow, cataract formation and phthisis
bulbi (shrinkage of the eye). Such outcomes can be
reduced by the correct use of anti-inflammatory drugs.
In clinical ophthalmic practice anti-inflammatory drugs
are generally underused.
Relevant pathophysiology
Ocular inflammation is generally considered to be primarily
mediated by prostaglandins. Injury to cell membranes
can cause release of arachidonic acid from the
phospholipid layer of the cell membrane. This results in
a cascade of reactions, ultimately leading to production
of leukotrienes, prostaglandins and free radicals. The
cascade can be blocked by use of corticosteroids and
nonsteroidal anti-inflammatory drugs (NSAIDs). Corticosteroids
act by inhibiting the release of arachidonic
acid from the cell membrane (see Chapter 11). NSAIDs
act by inhibiting the enzyme cyclo-oxygenase which
converts arachidonic acid into prostaglandins and free
radicals (see Chapter 13).
Specifically in the eye, anti-inflammatory drugs reduce
vasodilation and vascular permeability of ocular blood
vessels. They also reduce migration of inflammatory
cells into the eye. Topical anti-inflammatory drugs can
be used to reduce corneal vascularization and minimize
scar tissue formation.
Clinical applications
Anti-inflammatory drug therapy is most commonly used
for the treatment of uveitis (Table 25.3). It is also used
to treat ocular inflammation caused by allergies and to
reduce scarring following the healing phase of corneal
ulceration.
CLASSES OF DRUGS USED TO TREAT
OCULAR INFLAMMATION
Corticosteroids
Mode of action
The beneficial effects of corticosteroids in the eye include
anti-inflammatory effects and reduction in the vascular
and cellular response to injury.
Decreased vascular response
Decreasing the vascular response is an important effect
in the eye. In inflammation, the blood–eye barrier is
reduced. Clinically this manifests as aqueous flare
(protein and inflammatory cells in the aqueous humor).
In severe cases hyphema (blood in the anterior chamber)
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