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Compendium October 2009 (Vol 31, No 10)

Canine Glaucoma: Pathophysiology and Diagnosis

by Shelby L. Reinstein, DVM, MS, Amy Rankin, DVM, MS, DACVO, Rachel Allbaugh, DVM, MS, DACVO

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    Abstract

    Canine glaucoma encompasses a diverse group of diseases associated with an increase in intraocular pressure that results in retinal ganglion cell death and eventual blindness. Dogs may have congenital, primary, or secondary glaucoma. The diagnosis is made by recognizing clinical signs, interpreting ophthalmic examination findings, and determining intraocular pressure. Identifying the underlying cause of the glaucoma is essential to providing appropriate treatment recommendations.

    Aqueous humor is produced by the ciliary body and flows through the pupil into the anterior chamber of the eye. In dogs, most aqueous humor exits the eye through the iridocorneal angle; approximately 10% to 15% exits the eye through uveoscleral outflow.1 Normal intraocular pressure (IOP; range: 10 to 25 mm Hg2-4) is maintained by an equilibrium between aqueous humor production and drainage. Canine glaucoma is usually due to a disturbance in the conventional outflow pathway that results in an increased IOP.

    Canine Glaucoma

    Traditionally, glaucoma has been defined as an elevated IOP beyond that which permits normal visual function.2 Recent research has indicated that canine glaucoma is a common end point of several ophthalmic diseases. Canine glaucoma can be classified as congenital, primary, or secondary.

    Congenital glaucoma is rare in dogs. It is caused by abnormalities in the aqueous humor outflow pathways. Puppies generally present young (3 to 6 months of age) with an acute onset of buphthalmia and corneal edema. The disease may be unilateral or bilateral and may be associated with other ocular anomalies.2

    Primary glaucoma is considered a heritable condition in some breeds2 (BOX 1). The disease is progressive and may result from changes in the iridocorneal angle or from abnormal metabolism of the trabecular cells within the outflow pathway.2 Primary glaucoma is further classified as open-, narrow-, or closed-angle, based on the appearance of the drainage angle.2,5 It is always a bilateral condition.

    Secondary glaucoma results when another condition disrupts aqueous humor outflow. Several disease conditions can lead to secondary glaucoma, including cataract, lens luxation, hyphema, intraocular neoplasia, retinal detachment, and uveitis.2 In some of these conditions, the release of vasoactive factors may lead to the formation of a preiridal fibrovascular membrane and subsequent secondary glaucoma.2 Although secondary glaucoma is not considered heritable, some of the inciting causes do have a genetic basis (e.g., cataract, lens luxation). Dogs of breeds that are predisposed to these conditions that have developed a high IOP in one eye should have the contralateral eye routinely monitored for the development of disease.6,7 Additionally, if cataract surgery is performed, postoperative glaucoma is a potential complication that can be vision threatening.8,9 If secondary glaucoma can be diagnosed early and managed appropriately, vision may be preserved.

    Diagnosis

    The history, clinical presentation, and ophthalmic examination findings assist in diagnosing glaucoma. It is crucial for the veterinarian to determine the stage of the glaucoma (acute or chronic) to provide appropriate treatment.

    Clinical Signs

    Glaucoma can be a painful condition. Signs of ocular pain include blepharospasm, epiphora, and an elevated third eyelid. Episcleral congestion or corneal edema may also be present, and owners may describe the eye as reddish or blue.2,10 Dogs may also present without vision, lacking menace responses, pupillary light reflexes (PLRs), and dazzle reflexes.11

    Unfortunately, most subtle or transient increases in IOP lack overt clinical signs in the acute phases, and most dogs present with chronic glaucoma. IOP, corneal edema, and visual status may be similar in acute and chronic glaucoma. Globe size and fundic examination help determine the duration of the disease. Signs of acute glaucoma may include a normal-sized globe with corneal edema, mydriasis, and a relatively normal retina. Dogs with chronic glaucoma generally present with buphthalmia, blindness, corneal edema, and fixed, dilated pupils in one or both eyes. Fundic examination may reveal retinal degeneration and optic disc cupping.2,12

    Ophthalmic Examination

    The first objective of the ophthalmic examination is to determine the visual status and potential of each eye. Menace responses and direct and consensual PLRs should be assessed. If these responses are absent, dazzle reflexes should be assessed by shining a bright light into each eye in turn and monitoring for a blink response. A recent study11 demonstrated that dogs with acute glaucoma and absent menace responses, PLRs, and dazzle reflexes may regain some visual function in days to weeks if aggressive medical or surgical management is pursued early in the course of the IOP elevation.

    Determination of IOP in both eyes involves proper restraint (avoiding neck pressure) and correct use of equipment to obtain accurate measurements.4 A recent study13 demonstrated that body position can affect IOP readings in dogs without glaucoma; therefore, it is important to keep the dog's body position consistent during IOP measurement. There are three methods of measuring IOP: indentation, applanation, and rebound tonometry. Indentation tonometers, such as the Schiotz, indent the corneal surface and provide a measurement that can be converted for use in dogs by using the accompanying human conversion table.14 Applanation tonometers, such as the Tono-Pen VET (Reichert), measure IOP by flattening the corneal surface and are commonly used in general practice. Rebound tonometers (e.g., TonoVet, Icare) measure IOP by projecting a small probe at the corneal surface and analyzing the characteristics of its rebound. Rebound tonometers have been shown to be as accurate and easy to use as applanation tonometers.3,15 Because IOP measurements obtained using different instruments vary,15 it is recommended that the same instrument be consistently used when monitoring a patient.  TABLE 1 compares the three most commonly used tonometers.

    Canine glaucoma does not usually present symmetrically, and because primary glaucoma is always a bilateral disease, it is critical to thoroughly evaluate and routinely monitor the contralateral eye. Depending on the breed of dog, primary glaucoma usually manifests in middle or old age2; therefore, routine monitoring of at-risk puppies is not useful. When a dog presents with unilateral glaucoma, gonioscopy (iridocorneal angle examination) can be performed by a veterinary ophthalmologist to determine if the drainage angle is abnormal. This information helps differentiate primary and secondary glaucoma. Prophylactic medical therapy in the contralateral eye of an affected dog can significantly prolong visual status.16 In a multicenter clinical trial,16 topical 0.5% betaxolol twice daily or topical 0.25% demecarium bromide once daily and a topical corticosteroid once daily significantly delayed or prevented the onset of glaucoma in the second eye. Untreated control dogs developed glaucoma in the second eye earlier (median: 8 months) than eyes treated with prophylactic medication (median: approximately 31 months). Sharing this timeline with owners of dogs with primary closed-angle glaucoma helps keep the progressive nature of the disease in perspective and provides motivation to maintain compliance with the recommended prophylactic medications.

    Conclusion

    Canine glaucoma may be congenital, primary, or secondary in origin. It is crucial to determine the underlying cause of the glaucoma, the chronicity of the condition, and the visual potential of the affected eye because these factors decide the appropriate treatment recommendations and affect prognosis.

    Read the companion article, "Canine Glaucoma: Medical and Surgical Treatment Options".

    Downloadable PDF

    1. Abrams KL. Medical and surgical management of the glaucoma patient. Clin Tech Small Anim Pract 2001;16(1):71-76.

    2. Gelatt KN, Brooks DE, Kallberg ME. The canine glaucomas. In: Gelatt KN, ed. Veterinary Ophthalmology. 4th ed. Ames, Iowa: Blackwell Publishing; 2007:753-811.

    3. Knollinger AM, La Croix NC, Barrett PM, Miller PE. Evaluation of a rebound tonometer for measuring intraocular pressure in dogs and horses. JAVMA 2005;227(2):244-248.

    4. Pauli AM, Bentley E, Diehl KA, Miller PE. Effects of the application of neck pressure by a collar or harness on intraocular pressure in dogs. JAAHA 2006;42(3):207-211.

    5. Reilly CM, Morris R, Dubielzig RR. Canine goniodysgenesis-related glaucoma: a morphologic review of 100 cases looking at inflammation and pigment dispersion. Vet Ophthalmol 2005;8(4):253-258.

    6. Gelatt KN, MacKay EO. Secondary glaucomas in the dog in North America. Vet Ophthalmol 2004;
    7(4):245-259.

    7. Johnsen DA, Maggs DJ, Kass PH. Evaluation of risk factors for development of secondary glaucoma in dogs: 156 cases (1999-2004). JAVMA 2006;229(8):1270-1274.

    8. Lannek EB, Miller PE. Development of glaucoma after phacoemulsification for removal of cataracts in dogs: 22 cases (1987-1997). JAVMA 2001;218(1):70-76.

    9. Biros DJ, Gelatt KN, Brooks DE, et al. Development of glaucoma after cataract surgery in dogs: 220 cases (1987-1998). JAVMA 2000;216(11):1780-1786.

    10. Gelatt KN. The canine glaucomas. In: Essentials of Veterinary Ophthalmology. Ames, Iowa: Blackwell Publishing; 2005:165-196.

    11. Grozdanic SD, Matic M, Betts DM, et al. Recovery of canine retina and optic nerve function after acute elevation of intraocular pressure: implications for canine glaucoma treatment. Vet Ophthalmol 2007;10(suppl 1):101-107.

    12. Martin CL. Evaluation of patients with decreased vision or blindness. Clin Tech Small Anim Pract 2001;16(1):62-70.

    13. Broadwater JJ, Schorling JJ, Herring IP, Elvinger F. Effect of body position on intraocular pressure in dogs without glaucoma. Am J Vet Res 2008;69(4):527-530.

    14. Miller PE, Pickett JP. Comparison of the human and canine Schiotz tonometry conversion tables in clinically normal dogs. JAVMA 1992;201(7):1021-1025.

    15. Gorig C, Coenen RT, Stades FC, et al. Comparison of the use of new handheld tonometers and established applanation tonometers in dogs. Am J Vet Res 2006;67(1):134-144.

    16. Miller PE, Schmidt GM, Vainisi SJ, et al. The efficacy of topical prophylactic antiglaucoma therapy in primary closed angle glaucoma in dogs: a multicenter clinical trial. JAAHA 2000;36(5):431-438.

    References »

    NEXT: Case Report — Surgical Stabilization of a Craniocervical Junction Abnormality With Atlanto-Occipital Overlapping in a Dog

    CETEST This course is approved for 3.0 CE credits

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