Canine Glaucoma

Chapter 251


Canine Glaucoma



Glaucoma is a common cause of blindness in dogs, with an incidence of 0.5% using the Veterinary Medical Data Base (VMDB). Glaucoma generally is characterized by the death of the retinal ganglionic cells leading to rapid loss of vision. The definition of glaucoma has evolved over the years to become more than simply elevated intraocular pressure (IOP). The retinal ganglionic cells, the cells that lead to the formation of the optic nerve, are exquisitely sensitive to changes in IOP, vascular abnormalities, and movement of the posterior scleral lamina cribrosa. The normal IOP in dogs can vary, but a general guideline for a normal range of IOP is between 15 and 25 mm Hg. Glaucoma usually is associated with an IOP much higher than these published numbers, and elevated IOP is a major risk factor for further optic nerve damage and subsequent blindness.


The main goals of management for the general practitioner are to diagnose the presence of glaucoma accurately, to distinguish primary from secondary causes of glaucoma, and to assess the potential for return or maintenance of vision or relief of ocular pain. Acute glaucoma truly is an ophthalmic emergency. This chapter provides practicing veterinarians with a framework for understanding the causes, diagnosis, and treatment of glaucoma in the dog.



Causes and Pathogenesis


Glaucoma can arise from both primary and secondary causes that are associated with increased IOP, which damages primarily the inner retina and the retinal ganglionic cells. Primary glaucoma has been observed in many breeds (Box 251-1) and is defined as an increase in IOP in the absence of concurrent ocular disease. It demonstrates a strong genetic basis with bilateral ocular involvement. Both primary open-angle and primary angle-closure glaucoma are identified in dogs. Primary angle-closure glaucoma is eight times more common than primary open-angle glaucoma in dogs. There is also a more than twofold higher frequency of primary angle-closure glaucoma in female dogs than in males. Secondary glaucoma occurs two times more frequently than primary canine glaucoma and may be related to disorders of the lens (cataract, intumescence, lens rupture or trauma, lens-induced uveitis), uveitis (see Chapter 249), hyphema, intraocular neoplasia, iridociliary cysts, misdirection of the vitreous, chronic retinal detachments, intraocular pigment dispersion or melanosis, and trauma.



A balance exists between aqueous humor production and aqueous outflow to maintain the normal shape and function of the eye. Aqueous humor is produced by the nonpigmented epithelium of the ciliary body through both active ionic transport and hydrostatic and colloidal diffusion of fluid. Carbonic anhydrase catalyzes the combination of carbon dioxide and water to form carbonic acid and is the key enzyme in the active production of aqueous humor. The IOP remains constant because of the equilibrium between aqueous production and aqueous outflow. This has importance for therapy because reduction in the production or increase in the outflow of aqueous humor can be accomplished medically with a number of oral and topical pharmaceuticals.


Two outlets for drainage of the aqueous humor are available: the conventional outflow through the iridocorneal angle and the unconventional outflow through the uveoscleral route. After production at the ciliary body, the aqueous fluid migrates into the posterior chamber (between the iris and the anterior portion of the lens), through the pupil, and into the anterior chamber, with the vast majority of fluid leaving through the iridocorneal angle into the trabecular meshwork. The conventional outflow is pressure sensitive and comprises 85% of the aqueous outflow in dogs. The uveoscleral outflow allows aqueous to drain through the iris stroma, ciliary body, and choroid into the posterior venous circulation and is independent of the IOP. Glaucoma occurs because of an obstruction to the outflow of aqueous. Overproduction of aqueous humor by the ciliary body does not occur.



Clinical Signs and Diagnosis


Clinical signs of glaucoma differ for acute and chronic glaucoma (Table 251-1). However, the IOP should be evaluated in all cases of a red eye with a dilated pupil.



Commonly observed ocular signs of acute glaucoma in dogs include a red eye caused by episcleral injection, squinting, diffuse corneal edema, a fixed or dilated pupil, and loss of vision to complete blindness (Figure 251-1). Fundus evaluation may demonstrate a swollen or edematous optic nerve head with or without peripapillary retinal edema or separation.



Clinical signs that may be observed in patients with chronic glaucoma include a red eye, corneal edema, corneal striae (caused by fractures in Descemet’s membrane), a normal to enlarged globe (the latter called buphthalmos), a midsized to dilated pupil, a subluxated to completely luxated lens, degeneration of the optic nerve head with or without cupping, and tapetal hyperreflectivity (Figures 251-2 and 251-3).




The diagnosis of glaucoma usually is entertained based on the classic clinical signs (red eye, corneal edema, dilated pupil, loss of vision), breed predisposition (in cases of primary glaucoma), ophthalmoscopic findings, and measurement of IOP. Gonioscopic evaluation, high-frequency ocular ultrasonography, and occasionally advanced radiologic imaging may be useful in understanding the cause and differential diagnoses. Tonometry, the measurement of the IOP, can be performed with various tonometers such as by use of an indentation instrument (Schiøtz tonometer), by applanation (Tono-Pen), and by the rebound process (TonoVet) as discussed in Chapter 242. There should not be a difference of more than 2 to 4 mm Hg between the two eyes. Gonioscopy is a procedure usually performed by a veterinary ophthalmologist in which a special lens is used to view the iridocorneal angle to classify glaucoma based on the degree of angle opening (normal, narrowed, closed, and dysplastic). High-frequency ultrasonography (35 to 50 MHz) can be used to evaluate the iridocorneal angle and ciliary cleft as well as the relationship between the iris and the anterior lens capsule.


Fundus examination is extremely important to evaluate for optic nerve damage and retinal changes. Both direct and indirect ophthalmoscopy should be employed. The PanOptic Ophthalmoscope is highly recommended to the general practitioner because of its ease of use. This instrument allows thorough fundus evaluation, particularly for the examiner who is uncomfortable performing posterior segment evaluations. With this ophthalmoscope, the optic nerve and peripapillary region can be assessed readily for glaucomatous alterations.



Treatment


The treatment goals depend on whether the glaucoma is primary or secondary, whether it is acute or chronic, and whether saving vision is an attainable goal. The optimal cases for referral to a veterinary ophthalmologist are those in which glaucoma has been diagnosed rapidly in the early stage of disease. If the IOP remains elevated for as few as 24 to 48 hours, irreversible blindness may ensue. As stated earlier, acute glaucoma is a true ophthalmic emergency and requires immediate attention from a veterinary ophthalmologist.


The three main therapeutic goals are maintenance of vision, control of the IOP, and maintenance of the health of the retinal ganglionic cells. Additional therapeutic considerations in subacute glaucoma are the potential to preserve vision and relief of ocular pain when vision has already been lost. Once glaucoma is diagnosed, medical therapy is instituted to lower the IOP rapidly. This includes the use of hyperosmotic agents (mannitol or glycerol), oral and topical carbonic anhydrase inhibitors, topical miotic agents, β-blockers, and prostaglandin analogs as well as neuroprotective agents (Table 251-2). Often multiple medications are required.


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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Canine Glaucoma

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