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Proceedings of the 36th World Small Animal Veterinary Congress
WSAVA
Oct. 14 - 17, 2011 Jeju, Korea
Next Congress:
Reprinted in IVIS with the permission of WSAVA http://www.ivis.org
OP-B18
GLAUCOMA IN DOGS AND CATS: RECOGNIZING THE SIGNS
AND DETERMINING THE CAUSE
Gillian j. McLellan, BVMS, PhD, DVOphthal, DECVO, DACVO, MRCVS
School of Medicine & Public Health and School of Veterinary Medicine
University of Wisconsin-Madison, WI, USA
Introduction:Glaucoma is not a single disease entity. “The glaucomas” represent a large, diverse group of disorders,
unified in a final common pathway of characteristic optic nerve and retinal damage that results in loss of vision.
The single most important risk factor for the development of glaucoma in animals is elevated intraocular
pressure (IOP). Normal IOP is dependent on the equilibrium between production of aqueous humor by the
ciliary body processes, and its unimpeded drainage. Outflow of aqueous proceeds through the pupil from the
posterior to anterior chamber of the eye, and subsequently to the trabecular meshwork located within the irido-
corneal angle and ciliary cleft, thence to collector channels in the episclera and sclera which are continuous with
the episcleral and scleral vasulature. Perturbation of this normal route for aqueous outflow results in elevated
IOP and glaucomatous damage.
Early recognition and prompt, appropriate therapy, are essential if vision is to be retained, as damage
sustained by the optic nerve and retina rapidly becomes irreversible.
Recognizing the signs:
Clinical SignsClinical signs of glaucoma (outlined in Table 1) will vary depending on the speed of onset, duration and
degree of IOP elevation, and age of the animal (the sclera of young animals is more compliant and distensible,
so globe enlargement can be dramatic). Clinical signs in individual animals will also vary according to the
underlying cause (e.g. signs of uveitis or an intraocular mass)
Ancillary DiagnosticsTonometry: Clinicians should be familiar with the normal range of IOP for the tonometer type available to
8092011 WSAVA·FASAVA World Congress Proceedings
14(Fri) ~ 17(Mon) October 2011
ICC Jeju, Korea
2011 WSAVA·FASAVA World Congress
www.wsava2011.org
Reprinted in IVIS with the permission of WSAVA Close this window to return to IVIS
36th World Small Animal Veterinary Congress 2011 - Jeju, Korea
them. Caution should be exercised in diagnosing glaucoma based solely on a single, elevated IOP reading.
Elevated IOP in the absence of clinical evidence of glaucomatous optic nerve and retinal damage is termed
“ocular hypertension”, to distinguish it from overt glaucoma. IOP is influenced by age, positioning and manual
restraint of the patient and breed of dog. Conversely, IOP may be normal, or even low, in animals with
glaucoma, particularly in patients with chronic glaucoma, or animals with concurrent uveitis.
Gonioscopy: This technique allows evaluation of the opening of the ciliary cleft and anterior-most portion
of the trabecular meshwork. A contact lens applied to the corneal surface allows visualization of the pectinate ligament using focal illumination and magnification.
High Resolution Ultrasonography: of the ciliary cleft.
Where’s the block?When selecting a treatment strategy, it is important to determine the underlying mechanism of IOP
elevation. As all cases of glaucoma in dogs and cats are caused by obstruction of aqueous humor outflow,
determining the location of this obstruction should be a goal of the clinical examination. Note that aqueous
outflow is often obstructed at multiple locations in individual patients The mechanisms proposed (Table 2)
should not be considered mutually exclusive.
Table 1. Clinical Signs of Glaucoma in Dogs
ACUTE CHRONIC
PAINMay be severe (squinting, tearing, rubbing, lethargy, innappetance)
SIGNS OF DISCOMFORT VariableLess frequent in cats
EPISCLERAL INJECTIONOften accompanied by conjunctival injection
EPISCLERAL INJECTIONMay also see scleral thinning / staphyloma
CORNEAL VASCULARIZATIONDeep 360o limbal “brush border”
CORNEAL VASCULARIZATIONMay be exposure keratitis, with ulceration, branching vascularization and pigment
CORNEAL EDEMA CORNEAL EDEMA & STRIAE
MYDRIASIS
LENS SUBLUXATIONAphakic crescentDifferentiate from primary lens luxationCATARACT
OPTIC DISC CHANGESMay be “cupped” or more often swollen in acute cases
OPTIC DISC CUPPING & ATROPHY
LOSS OF VISIONAbsent direct & consensual Pupillary Light ReflexAbsent Menace ResponseAbsent Dazzle Reflex
LOSS OF VISIONUsually Complete, irreversible, with mydriasis
BUPHTHALMOS OR PHTHISIS BULBI Enlarged, or end stage, shrunken globe
810 2011 WSAVA·FASAVA World Congress Proceedings
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36th World Small Animal Veterinary Congress 2011 - Jeju, Korea
Table 2: Potential Locations of Obstruction to Aqueous Humor Outflow
Block at the ciliary Body/ posterior chamber/ Vitreous
“Crowding” of posterior chamber by:• Intraocular neoplasia• Cilio-vitreo-lenticular block (condensed anterior vitreous) • Iridociliary cystsVitreous expanded or pushed forward ( “malignant” glaucoma):• Posterior misdirection of aqueous• Choroidal effusion
Pupil block
Obstruction to flow of aqueous through pupil by:• Posterior synechiae / iris bombé (absolute block)• Lens within pupil / lens and iris anatomically apposed (relative block) : posterior misdirection of aqueous,lens luxation/ subluxation,
intumescent lens (phacomorphic), spherophakia• Vitreous within pupil
Block at the level of the irido-corneal angle
Primary angle-closure • narrow-angle glaucoma• Pectinate ligament dysplasiaSecondary angle closure• Due to anterior “pull” by peripheral anterior synechiae or pre-iridal fibrovascular membrane• Due to posterior “push” e.g. by posteriorly misdirected aqueous humor or mass effect in the posterior chamber
Trabecular Meshwork obstructions
Primary malformation of the ciliary cleft• Primary congenital glaucomaSecondary to obstruction of a conformationally “open angle” by • Inflammatory cells• Neoplastic cells• Pre-iridal fibrovascular membrane (iris neovasc.)• Erythrocytes (both intact and “ghost cells”)• Vitreous• Proteins including fibrin (uveitis) or globulin (hyperviscosity syndrome)
Post-trabecular block / Increased episcleral and/or scleral venous pressure
Innapropriate restraint• E.g. tight neck collars or a stress responseFeline primary open-angle glaucoma• Myxomatous change around vessels of outflow pathwayOrbital space occupying lesions• Increasing episcleral venous pressureInfiltration of the episclera and / or sclera• Inflammatory• Neoplastic
[Adapted from: McLellan, GJ & Miller PE. 2011. Feline Glaucoma: A Comprehensive Review. Veterinary Ophthalmology (in press)]
8112011 WSAVA·FASAVA World Congress Proceedings
GLAUCOMA IN DOGS AND CATS: RECOGNIZING THE SIGNS AND DETERMINING THE CAUSE
Reprinted in IVIS with the permission of WSAVA Close this window to return to IVIS
36th World Small Animal Veterinary Congress 2011 - Jeju, Korea
In summary, glaucoma may be considered either primary (occurring in the absence of other underlying
ocular disease; and relatively common in purebred dogs) or secondary (most commonly associated with uveitis
or intraocular tumors, particularly in cats, or with lens disease). However, this classification scheme is perhaps
too simplistic. It is more important, when selecting treatment for glaucoma, that different mechanisms of
aqueous humor outflow obstruction are identified and addressed.
812 2011 WSAVA·FASAVA World Congress Proceedings
14(Fri) ~ 17(Mon) October 2011
ICC Jeju, Korea
2011 WSAVA·FASAVA World Congress
www.wsava2011.org
Reprinted in IVIS with the permission of WSAVA Close this window to return to IVIS
36th World Small Animal Veterinary Congress 2011 - Jeju, Korea
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