Close this window to return to IVIS www.ivis.org

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

Reprinted in IVIS with the permission of WSAVA Close this window to return to IVIS

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